Science Selections from EHP via MedWorm.com MedWorm.com provides a medical RSS filtering service. Over 6000 RSS medical sources are combined and output via different filters. This feed contains the latest items from the 'Science Selections from EHP' source. Thu, 31 Dec 2009 15:39:14 +0100 youa'> You Are Where You Live The Interrelationship of Air Pollution, Address, and Walkability Exposure to air pollution adversely affects human health by triggering or exacerbating a number of conditions such as asthma and heart disease. Likewise, physical inactivity has been linked to negative health consequences including heart disease and diabetes. Now for the first time a new study offers a quantitative analysis of the intersection between neighborhood �walkability��or how conducive the neighborhood is to walking�and exposure to air pollutants [EHP 117:1752�1759; Marshall et al.]. man walking in Vancouver, British Columbia Vancouver, British Columbia image: � Philip and Karen Smith/Getty Images The authors analyzed concentration estimates of nitric oxide (NO), a marker of fresh vehicle exhaust, and ozone (O3), a secondary pollutant formed in the atmosphere from vehicle emissions and other pollutants. Concentrations were estimated for the months of May�September. The authors then compared those levels against neighborhood walkability scores, which they calculated for 89% of the postal codes in Vancouver, British Columbia (the average postal code for the city comprises 39 people or 0.05 km2). Walkability scores were calculated based on residential density, intersection density, retail floor-area, and land-use mix of the postal code area. The study did not measure people�s daily exercise levels or their exposure to air pollution�both of which may vary within a neighborhood and even within a single household. The authors report that lower-income areas tended to have higher walkability scores and lower O3 concentrations than did higher-income areas, but had higher NO concentrations. That finding reflects the tendency of lower-income areas to fall in busier urban areas whereas middle-income areas tend to fall farther from the city center. �Sweet spot� neighborhoods with high walkability and low pollution tended to be located near but not at the city center. They typically featured highly connected streets, mixed land uses, sidewalks, and an absence of large parking lots; they also tended to be in higher-income areas. �Sour spot� neighborhoods with high pollution and low walkability tended to be located far from the city center. The findings indicate that walkable urban settings can offer health benefits but may also come with health costs when exposure to air pollution is considered. The authors write that high NO exposure may occur in low-income areas and in areas where walking, biking, and other forms of �active transportation� are encouraged, and that strategies are required to mitigate exposure to high concentrations of air pollutants. This type of analysis could be used to monitor changes over time in future urban development and redevelopment projects. Tanya Tillett, MA, of Durham, North Carolina, is a writer/editor for EHP. She has been with EHP since 2000 and has represented the journal at national and international conferences. spacer | Purchase This Issue | http://www.medworm.com/index.php?rid=2950074&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeedproxy.google.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2FDQi7TRP29rA%2Fss.html youa"> You Are Where You Live The Interrelationship of Air Pollution, Address, and Walkability Exposure to air pollution adversely affects human health by triggering or exacerbating a number of conditions such as asthma and heart disease. Likewise, physical inactivity has been linked to negative health consequences including heart disease and diabetes. Now for the first time a new study offers a quantitative analysis of the intersection between neighborhood �walkability��or how conducive the neighborhood is to walking�and exposure to air pollutants [EHP 117:1752�1759; Marshall et al.]. Vancouver, British Columbia image: � Philip and Karen Smith/Getty Images The authors analyzed concentration estimates of nitric oxide (NO), a marker of fresh vehicle exhaust, and ozone (O3), ... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2950074 Sun, 01 Nov 2009 00:00:00 +0100 2950074 deli'> Delivering New Data Local Traffic Pollution and Pregnancy Outcomes Up to 35% of preterm births are due to preeclampsia, a complication in 2�8% of pregnancies that is characterized by maternal high blood pressure, edema, protein in the urine, and abnormal liver function. Exposure to certain air pollutants is associated with prematurity and may also be linked with preeclampsia. A new study is the first to home in on specific components of air pollution�those generated by traffic�as being associated with preeclampsia and further supports their role in preterm birth [EHP 117:1773�1779; Wu et al.]. Preeclampsia, which resolves only with delivery of the baby, can cause maternal illness and death, intrauterine growth restriction, preterm birth, and infant death. Each year more than half a million infants in the United States are born prematurely (at less than 37 weeks� gestation) and consequently face increased risks for developmental delays, lifelong health problems, and neonatal death. These challenges are particularly severe for infants born prior to 30 weeks� gestation. The study was based upon 81,186 singleton births that occurred during 1997�2006 at four Southern California hospitals within the same health care system. The system�s database provided information on the mothers� demographic characteristics, medical history, and pregnancy complications; their home address at the time they gave birth; and their infants� gestational age, sex, and birth weight. Traffic pollution generated within a 3-km radius of each mother�s residence was estimated using a comprehensive dispersion model that incorporated meteorologic variables (such as atmospheric stability and wind), roadway geometry, traffic counts, and vehicle emission factors. The exhaust components nitrogen oxides (NOx) and particulate matter smaller than 2.5 �m (PM2.5) served as surrogates for local traffic pollution in the model. The researchers estimated average exposures over the entire pregnancy at approximately 7 ppb for NOx and 2 �g/m3 for PM2.5. After accounting for other factors that might be related to preeclampsia and exposure, the authors estimated that pregnant women in the highest quartile of PM2.5 exposure had a 42% increased relative risk of preeclampsia compared with women in the lowest quartile, and those in the highest quartiles of NOx and PM2.5 exposure had 128% and 81% higher relative risk than women in the lowest quartiles, respectively, for delivery at less than 30 weeks� gestation. The sophisticated dispersion model and detailed individual clinical data are particular strengths of the study, but the findings are limited by information that was not available, such as workplace exposures, changes in residence during pregnancy, and maternal smoking. The researchers speculate that the toxic mechanisms described in air pollution studies of respiratory and cardiovascular diseases�specifically, oxidative stress and a generalized inflammatory response�might also partly explain preterm delivery and preeclampsia. They emphasize that the current study does not specifically indict NOx and PM2.5, although the results support a connection between traffic-related air pollution and adverse reproductive outcomes. Julia R. Barrett, MS, ELS, a Madison, Wisconsin�based science writer and editor, has written for EHP since 1996. She is a member of the National Association of Science Writers and the Board of Editors in the Life Sciences. http://www.medworm.com/index.php?rid=2950073&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeedproxy.google.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2FrToH6MajnEc%2Fss.html deli"> Delivering New Data Local Traffic Pollution and Pregnancy Outcomes Up to 35% of preterm births are due to preeclampsia, a complication in 2�8% of pregnancies that is characterized by maternal high blood pressure, edema, protein in the urine, and abnormal liver function. Exposure to certain air pollutants is associated with prematurity and may also be linked with preeclampsia. A new study is the first to home in on specific components of air pollution�those generated by traffic�as being associated with preeclampsia and further supports their role in preterm birth [EHP 117:1773�1779; Wu et al.]. Preeclampsia, which resolves only with delivery of the baby, can cause maternal illness and death, intrauterine growth restriction, preterm birth, and infant death. Each year more t... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2950073 Sun, 01 Nov 2009 00:00:00 +0100 2950073 micr'> Micro Management Understanding How Diesel Exhaust Particles Alter Cellular Processes Scientists have known for decades that people living in cities are more susceptible to certain respiratory diseases than are their countryside counterparts. But they haven�t been able to explain why one urbanite develops severe asthma while his neighbor breathing the same city air has healthy lungs. Now researchers are beginning to solve that riddle as they delve into epigenetics, the emerging science of how environmental factors alter gene expression [EHP 117:1745�1751; Jardim et al.]. This new study focuses on airborne particulate matter, which has long been linked with respiratory disease. Emissions from diesel engines are a prominent source of particulate matter, and diesel exhaust particles (DEP) are classified by the U.S. Environmental Protection Agency as a likely carcinogen. DEP also has been associated with several respiratory disorders including pulmonary inflammation, asthma, and chronic obstructive pulmonary disease. The authors speculated that pulmonary inflammation due to DEP exposure could be the result of altered microRNA (miRNA) expression, or activation, in cells lining the respiratory tract. MiRNAs are small molecules that regulate gene expression. Studies have connected aberrant miRNA expression with several diseases including cancer, heart disease, neurodegenerative disorders, and congenital organ defects. Few studies, though, have examined whether exposures to environmental contaminants alter miRNA expression. The authors studied miRNA expression in bronchial epithelial cells, one of the first targets of inhaled particulates. They collected the cells from the airways of healthy, nonsmoking adults and cultured them in a novel air�liquid interface in which differentiated cells were exposed on one side to air, mimicking the environment of the human airway. DEP generated by a diesel automobile engine was suspended in a liquid that was poured on the cell culture. MiRNA expression changed significantly following DEP exposure. Expression increased in many of the miRNAs and decreased in others. Software identified interrelations between the expression of different miRNAs to assess whether the pattern of up- and down-regulation was consistent with specific biologic pathways. The authors report that pathways involved in inflammation and tumorigenicity are implicated by the patterns they observed. Earlier studies have shown that DEP prompts the release of several proinflammatory immunoregulatory proteins called cytokines. The authors of the current study suggest this response may be at least partly regulated by changes in the pattern of miRNA expression. The authors believe these alterations may be the first steps toward respiratory disease, and they predict future studies will provide a clearer picture of how expression patterns relate to disease. Cynthia Washam writes for EHP, Oncology Times, and other science and medical publications from South Florida. http://www.medworm.com/index.php?rid=2950072&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeedproxy.google.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F-Hn6PGeGJSY%2Fss.html micr"> Micro Management Understanding How Diesel Exhaust Particles Alter Cellular Processes Scientists have known for decades that people living in cities are more susceptible to certain respiratory diseases than are their countryside counterparts. But they haven�t been able to explain why one urbanite develops severe asthma while his neighbor breathing the same city air has healthy lungs. Now researchers are beginning to solve that riddle as they delve into epigenetics, the emerging science of how environmental factors alter gene expression [EHP 117:1745�1751; Jardim et al.]. This new study focuses on airborne particulate matter, which has long been linked with respiratory disease. Emissions from diesel engines are a prominent source of particulate matter, and diesel exhaust partic... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2950072 Sun, 01 Nov 2009 00:00:00 +0100 2950072 sent'> Sentinel Symptoms of Climate Change Indicators for Related Health Effects Greenhouse gas emissions are widely acknowledged to be contributing to climate change�related health effects that vary by location, and are expected to continue doing so for many years, even if substantial emission cuts occur. A workgroup of the Council of State and Territorial Epidemiologists has identified a set of indicators that it says will allow national and local officials in the United States to better predict any such changes and consequences and to take appropriate action as it becomes warranted [EHP 117:1673�1681; English et al.]. The team also identified the data needed for tracking these indicators and ascertained whether the data exist, must be improved, or must be generated. They say this is the first effort to synthesize and evaluate related information published by many sources. photo collage showing flooding, pathogens, fire and waste. images (clockwise from lower left): AP Photo/Francis Specker; AP Photo/Bullit Marquez; � 2009 Dennis Kunkel Microscopy; � Kevin Schafer/Corbis The team determined the best indicators of environmental changes due to climate change are quantity of greenhouse gas emissions, air quality (in particular ozone), air mass stagnation events (such as those caused by temperature inversions), temperature and humidity, pollen loads, ragweed occurrence, drought incidence, drinking water scarcity, and occurrence of wildfires and harmful algal blooms. Data for some of these indicators are strong and/or expected to improve soon, as in the case of greenhouse gases, temperature, air mass stagnation events, and drought. Data on other indicators, such as pollen, harmful algal blooms, and ozone, require substantial improvement. For indicators of human death and illness, the authors recommend tracking excess numbers of each that can be attributed to events related to climate change. Doing so will require significant improvements in existing data and methods, such as more comprehensive reporting of emergency room visits and hospitalizations related to heat waves, floods, and other extreme weather events. For infectious diseases, the targeted culprits are West Nile virus, Lyme disease, dengue fever, coccidioidomycosis, and hantavirus cardiopulmonary syndrome. The authors note that some segments of the population may be especially vulnerable to certain effects of climate change. These groups include children; the elderly; pregnant and nursing women; those with disabilities and preexisting conditions such as asthma, chronic obstructive pulmonary disease, and obesity; people living in poverty or social isolation or without access to transportation; and those living within 5 km of a coast that is highly vulnerable to sea level rise, or in a 100- or 500-year flood zone. Awareness of these vulnerable subpopulations will be important in planning appropriate prevention and intervention activities. Data for indicators of adaptability are sparse because most efforts so far have focused on mitigating climate change, not adapting to it. The authors propose that such indicators might include access to public cooling centers during heat waves, the existence of early warning systems for heat waves, mitigation plans to reduce urban heat islands, the number and quality of surveillance systems available to collect data on climate�health effects, and the availability of local public health workers and task forces trained in climate change research, surveillance, and adaptation. Bob Weinhold, MA, has covered environmental health issues for numerous outlets since 1996. He is a member of the Society of Environmental Journalists. http://www.medworm.com/index.php?rid=2950071&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeedproxy.google.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F9p7JayG4fR0%2Fss.html sent"> Sentinel Symptoms of Climate Change Indicators for Related Health Effects Greenhouse gas emissions are widely acknowledged to be contributing to climate change�related health effects that vary by location, and are expected to continue doing so for many years, even if substantial emission cuts occur. A workgroup of the Council of State and Territorial Epidemiologists has identified a set of indicators that it says will allow national and local officials in the United States to better predict any such changes and consequences and to take appropriate action as it becomes warranted [EHP 117:1673�1681; English et al.]. The team also identified the data needed for tracking these indicators and ascertained whether the data exist, must be improved, or must be generated. They say this ... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2950071 Sun, 01 Nov 2009 00:00:00 +0100 2950071 dang'> Dangerous Delicacy Contaminated Sea Turtle Eggs Pose a Potential Health Threat The eggs of the green turtle (Chelonia mydas) and other sea turtle species are a popular food in areas such as Peninsular Malaysia�so popular, in fact, that nesting populations in the region have declined by more than 80% since the 1950s, largely because of their eggs being collected for human consumption. Persistent organic pollutants (POPs) and heavy metals have been reported in the eggs of a number of C. mydas populations. Now a team of Australian and Malaysian scientists reports that the concentrations of POPs found in C. mydas eggs from markets in Peninsular Malaysia could pose a considerable threat to human health [EHP 117:1397�1401; van de Merwe et al.]. C. mydas eggs for sale in Kuala Terengganu, Peninsular Malaysia C. mydas eggs for sale in Kuala Terengganu, Peninsular Malaysia image: Christian Amodeo In August 2006, the investigators surveyed 33 markets along 730 miles of coastal Peninsular Malaysia. C. mydas eggs were available in 9 of these 33 markets. A random sample of 3�13 eggs was purchased from each market where they were sold. In total, 55 eggs were collected and frozen until they could be analyzed. The eggs were analyzed for numerous POPs, among them 83 polychlorinated biphenyls (PCBs), 23 organochlorine pesticides, and 19 polybrominated diphenyl ethers. Eggs were also analyzed for zinc, copper, cobalt, selenium, arsenic, cadmium, lead, and mercury. For each metal and category of POP, the authors calculated the percentage of the acceptable daily intake (ADI) found in the eggs, providing an estimate of potential human health risks involved in consuming the eggs. ADIs are set by the World Health Organization. The concentrations of POPs and metals measured were generally lower than those reported elsewhere for loggerhead sea turtle (Caretta caretta) eggs. Nevertheless, all the eggs analyzed had at least 3 times the ADI of coplanar PCBs, which are among the most toxic members of their chemical family. One egg had 300 times the ADI for this contaminant. The authors note that the rate of C. mydas egg consumption in Peninsular Malaysia was not investigated in the present study, nor has it been well quantified. However, there is a cultural perception in this area that sea turtle eggs have medicinal qualities. The authors write that a public education campaign could highlight the health consequences of consuming contaminated eggs. This in turn could reduce egg collection pressure and hence potentially contribute to the recovery of the C. mydas populations in this region. John Tibbetts, based in Charleston, South Carolina, has written for EHP since 1995. Editor of Coastal Heritage, the magazine of the South Carolina Sea Grant Consortium, he is a member of the Society of Environmental Journalists. spacer | Purchase This Issue | http://www.medworm.com/index.php?rid=2750875&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeedproxy.google.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2FiDPKMs8nsQ0%2Fss.html dang"> Dangerous Delicacy Contaminated Sea Turtle Eggs Pose a Potential Health Threat The eggs of the green turtle (Chelonia mydas) and other sea turtle species are a popular food in areas such as Peninsular Malaysia�so popular, in fact, that nesting populations in the region have declined by more than 80% since the 1950s, largely because of their eggs being collected for human consumption. Persistent organic pollutants (POPs) and heavy metals have been reported in the eggs of a number of C. mydas populations. Now a team of Australian and Malaysian scientists reports that the concentrations of POPs found in C. mydas eggs from markets in Peninsular Malaysia could pose a considerable threat to human health [EHP 117:1397�1401; van de Merwe et al.]. C. mydas eggs for sale in Kuala Teren... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2750875 Mon, 31 Aug 2009 23:00:00 +0100 2750875 acom'> A Complex Relationship Psychosocial Stress, Pollution, and Health In recent years, a growing body of work has shown that psychosocial stress may exacerbate susceptibility to the adverse effects of pollutants such as lead, polychlorinated biphenyls, and combustion emissions. To accurately measure and evaluate the effects of stress on people�s susceptibility to pollutants, researchers need to rely on the tools and findings of both social epidemiology and environmental health science, according to a review of the research to date [EHP 117:1351�1358; Clougherty and Kubzansky]. The authors offer specific recommendations for how researchers can combine techniques from these fields to investigate the links between stress, pollution, and health. In the authors� own earlier studies, they found that stress seemed to exacerbate effects of pollution, which suggests that stress increases susceptibility to environmental exposures. However, they also noted that the interaction between stress and pollution was no longer evident beyond a certain range of exposure, a phenomenon they refer to as the saturation effect. For example, if air pollution levels are very high, stress may have no additional effect on the likelihood of asthma symptoms occurring, and vice versa. It�s also important to pay attention to differences in spatial patterns of social and physical exposures. As an example, the authors write, �spatial epidemiologists are challenged to differentiate health effects of traffic-related pollution from those of spatially correlated noise, stress, or poverty.� It can be particularly difficult to separate the effects of different exposures if they affect the same health outcomes. Moreover, not every individual within this sample neighborhood would necessarily experience high levels of stress, nor would every individual receive the same traffic-related pollution exposures, which the authors point out vary dramatically within 50�200 m of major roadways. To understand the combined effects of stress and pollutant exposures, timing is everything because acute and chronic stress can produce different results. Acute stress can produce �fight-or-flight� responses that might counterbalance the effects of pollution�for example, stress-induced bronchodilation might temporarily reduce or mask bronchial constriction caused by air pollution. Chronic stress is more likely to gradually weaken the immune system, increasing susceptibility to pollution-related illness. Stress is also multidimensional; it includes the stimulus that poses the challenge, the person�s appraisal of the stressor, and finally the psychological and physiological response. When measuring stress, researchers must consider what stage of the stress experience they are observing. They also must track the relative timing of study participants� exposures to determine whether the stress occurred before, after, or during the pollutant exposure. In all, the authors write, �These topics are exceedingly complicated, and accurately characterizing both social and physical exposures is a significant challenge, one which must be performed carefully . . . before analyzing and interpreting interactions.� Tina Adler first wrote for EHP about the Clinton�Gore environmental agenda in 1993. She is a member of the National Association of Science Writers and the American Society of Journalists and Authors. http://www.medworm.com/index.php?rid=2750874&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeedproxy.google.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2FP1chhBoORvU%2Fss.html acom"> A Complex Relationship Psychosocial Stress, Pollution, and Health In recent years, a growing body of work has shown that psychosocial stress may exacerbate susceptibility to the adverse effects of pollutants such as lead, polychlorinated biphenyls, and combustion emissions. To accurately measure and evaluate the effects of stress on people�s susceptibility to pollutants, researchers need to rely on the tools and findings of both social epidemiology and environmental health science, according to a review of the research to date [EHP 117:1351�1358; Clougherty and Kubzansky]. The authors offer specific recommendations for how researchers can combine techniques from these fields to investigate the links between stress, pollution, and health. In the authors� own earlier studies,... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2750874 Mon, 31 Aug 2009 23:00:00 +0100 2750874 poly'> Polycarbonate Plastics and Human BPA Exposure Urinary Levels Rise with Use of Drinking Bottles Public and scientific concerns about exposure to bisphenol A (BPA) have risen in the last few years, with Canada and some U.S. states and cities banning BPA from polycarbonate baby bottles and other products sold for use by infants and children. Despite these concerns, little is known about whether the use of polycarbonate food or beverage containers actually contributes to BPA body burden in people. A new study of human exposure to BPA from drinking containers now shows that study participants� urinary concentrations of the molecule increased by two-thirds after they used polycarbonate drinking bottles for 1 week [EHP 117:1368�1372; Carwile et al.]. Rodent studies have associated prenatal and neonatal exposure to BPA with early onset of sexual maturation, reproductive tract lesions, and altered development of the mammary gland, among other reproductive abnormalities. However, limited information is available on human health effects. Nevertheless, human exposure to BPA is widespread: the chemical was detected in the urine of more than 92% of the participants aged 6 years and older in the 2003�2004 National Health and Nutrition Examination Study (NHANES). Not all polycarbonate plastics contain BPA, but nearly three-quarters of the BPA used in the United States in 2003 went into the manufacture of this one material. The hard, nearly shatterproof plastic is widely used in drinking bottles, baby bottles, and nonfood uses ranging from eyeglasses to labware. Earlier studies of polycarbonate drinking containers containing BPA have shown that under normal use�washing, rinsing, and exposure to high temperatures or to alkali or acid solutions�the plastic can degrade and release small amounts of the constituent chemical. BPA is believed to be rapidly metabolized and eliminated. Therefore, in the current study, 77 college students aged 18�22 underwent a weeklong �washout� to minimize any preexisting BPA load that could have arisen from the use of polycarbonate drinking bottles. During the washout, participants were instructed to drink any cold beverages only from stainless steel bottles and to avoid drinking water from the polycarbonate dispensers in the college dining halls. After the washout, the group switched to drinking cold drinks only from 2 new researcher-provided polycarbonate bottles for 1 week. Exposure to other BPA sources was not controlled; thus, the study yielded a conservative estimate of the potential for BPA exposure via polycarbonate drinking bottles. Comparison of urine samples collected throughout the study showed that after using polycarbonate bottles for 1 week, participant�s mean urinary BPA concentrations increased by more than two-thirds to 2.1 �g/L, compared with the mean of 2.6 �g/L observed in the NHANES 2003�2004 study. The authors anticipate higher urinary BPA concentrations would result from drinking hot beverages stored in the same bottles. Victoria McGovern, based in Durham, North Carolina, has written for EHP since 2000. She is a member of the National Association of Science Writers. http://www.medworm.com/index.php?rid=2750873&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeedproxy.google.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2FC4GRrq8V9Zw%2Fss.html poly"> Polycarbonate Plastics and Human BPA Exposure Urinary Levels Rise with Use of Drinking Bottles Public and scientific concerns about exposure to bisphenol A (BPA) have risen in the last few years, with Canada and some U.S. states and cities banning BPA from polycarbonate baby bottles and other products sold for use by infants and children. Despite these concerns, little is known about whether the use of polycarbonate food or beverage containers actually contributes to BPA body burden in people. A new study of human exposure to BPA from drinking containers now shows that study participants� urinary concentrations of the molecule increased by two-thirds after they used polycarbonate drinking bottles for 1 week [EHP 117:1368�1372; Carwile et al.]. Rodent studies have associated p... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2750873 Mon, 31 Aug 2009 23:00:00 +0100 2750873 newf'> New Face of a Well-Known Hazard Arsenic Alters H1N1 Response in Mice One of the puzzles of the 2009 pandemic of novel H1N1 influenza virus is why some populations are being hit harder than others�a reminder that known susceptibility factors cannot always explain why otherwise healthy people succumb to diseases that others survive. A team of researchers from Dartmouth Medical School may have uncovered a potential previously unrecognized susceptibility factor, demonstrating that exposure to arsenic significantly weakened mice�s immune response to a mouse-adapted subtype of H1N1 flu [EHP 117:1441�1447; Kozul et al.]. Influenza A Virus Influenza A virus image: � Dennis Kunkel Microscopy, Inc. The team believes their study is the first to link flu morbidity to arsenic, which occurs naturally in the drinking water of hundreds of millions of people worldwide. In the United States public drinking water must meet the U.S. Environmental Protection Agency (EPA) arsenic limit of 10 ppb, but private well water is unregulated. Up to 25 million Americans with private wells may be exposed to arsenic levels above the EPA limit. In many regions of the United States and in Mexico, where the novel H1N1 outbreak began, arsenic levels in well water commonly exceed the EPA limit by tenfold or more. The current study was inspired by recent epidemiologic research indicating that chronic exposure to arsenic increased the risk for a variety of pulmonary diseases including impaired lung function, cancer, and bronchiectasis. Other studies, including recent work by members of this research team [EHP 117:1108�1115 (2009)], have indicated that arsenic exposure can suppress the innate immune system. Impairment of the immune cells in the lungs as a result of arsenic exposure could also alter the ability to fight other infectious challenges. The researchers tested their hypothesis that arsenic could suppress the innate immune response and thereby intensify H1N1 flu infection by giving mice drinking water containing 100 ppb arsenic for 5 weeks. After 5 weeks, the researchers inoculated the arsenic-exposed mice and a group of control mice with the H1N1 virus, and flu morbidity was measured as weight loss. Control mice experienced moderate weight loss but returned to their original weight by day 16 postinfection. The arsenic-exposed mice had a more dramatic weight loss of up to 20% of their body weight by day 8 postinfection, at which point the researchers euthanized them to prevent suffering, in compliance with institutional animal care standards. In subsequent analyses at day 7 postinfection, examination of the exposed mice�s lungs revealed hemorrhaging, edema, and 10 times more virus than was seen in the lungs of control mice. Millions of people worldwide are infected with seasonal flu each year, and hundreds of thousands die. Understanding the risk factors that may increase flu cases and deaths could have a potentially significant impact on preventing and treating this common disease. Cynthia Washam writes for EHP, Oncology Times, and other science and medical publications from South Florida. http://www.medworm.com/index.php?rid=2750872&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeedproxy.google.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2Fr2JYQ9RqrLk%2Fss.html newf"> New Face of a Well-Known Hazard Arsenic Alters H1N1 Response in Mice One of the puzzles of the 2009 pandemic of novel H1N1 influenza virus is why some populations are being hit harder than others�a reminder that known susceptibility factors cannot always explain why otherwise healthy people succumb to diseases that others survive. A team of researchers from Dartmouth Medical School may have uncovered a potential previously unrecognized susceptibility factor, demonstrating that exposure to arsenic significantly weakened mice�s immune response to a mouse-adapted subtype of H1N1 flu [EHP 117:1441�1447; Kozul et al.]. Influenza A virus image: � Dennis Kunkel Microscopy, Inc. The team believes their study is the first to link flu morbidity to arsenic, which occurs naturally i... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2750872 Mon, 31 Aug 2009 23:00:00 +0100 2750872 sout'> Southern Discomfort? PON1 Variation May Help Explain Regional CVD Risk Age-associated rates of cardiovascular disease (CVD) are higher in the Southern states (except Florida) than anywhere else in the United States, and higher among Southern blacks than Southern whites. Animal studies suggest that higher levels of activity of the enzyme paraoxonase-1 (PON1) may lower the risk of CVD, specifically atherosclerosis, but evidence linking functional variations in PON1 to atherosclerosis risk in humans has been ambiguous. New research correlates functional variation in PON1 activity with race, which may help explain demographic variation in CVD prevalence [EHP 117:1226 1231; Davis et al.]. a black man and a white man embracing PON1 helps break down pesticides in the body. image: Getty Images PON1 is carried by high-density lipoprotein in the blood and is involved in the hydrolysis, or breakdown, of oxidized low-density lipoprotein, whose buildup is considered an early step in the development of atherosclerosis. PON1 is also involved in the hydrolysis of the toxic oxon metabolites of certain organophosphate insecticides. A single-nucleotide polymorphism at position 192 on the PON1 gene results in two functional variations of the enzyme, the Q and R forms. Other studies have associated the R form with a greater risk of atherosclerosis. The R form also hydrolyzes chlorpyrifos oxon more effectively than the Q form, whereas both alloforms are equally effective at metabolizing diazoxon; neither hydrolyzes paraoxon quickly enough to offer protection. PON1 activity is also linked to the quantity of the enzyme in the blood, which is controlled in part by polymorphisms in the gene s promoter region and may vary by at least 13-fold among individuals. The researchers analyzed serum samples for 200 adult black and white men and women (50 in each sex race group) obtained from blood banks in Alabama and Tennessee. The team determined PON1 functional genotypes RR, QR, or QQ by measuring rates of hydrolysis of paraoxon and diazoxon. They also analyzed arylesterase activity (another measure of PON1 activity), levels of cotinine (a biomarker of smoking, which can affect PON1 levels), and C-reactive protein (a biomarker of inflammation associated with greater risk of CVD). Forty-four percent of black subjects had higher in vitro rates of paraoxon hydrolysis and lower rates of diazoxon hydrolysis, consistent with the RR genotype that has been hypothesized to increase the risk of CVD. In contrast, only 7% of white subjects had activity levels consistent with the RR genotype. Black subjects also had higher levels of C-reactive protein, consistent with a greater risk of CVD. However, levels of C-reactive protein were not associated with PON1 activity. Cotinine levels indicated that all study participants were nonsmokers possibly the result of the blood banks having screened out smokers. The authors conclude their data support the idea that the functional RR genotype is less protective of cardiovascular health. They are working on a follow-up study of Southerners of both races and sexes where there is more information about participants health status and medical history. Kris S. Freeman has written for Encarta encyclopedia, NIH, ABCNews.com, and the National Park Service. Her research on the credibility of online health information appeared in the June 2009 IEEE Transactions on Professional Communication. spacer | Purchase This Issue | http://www.medworm.com/index.php?rid=2670032&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeedproxy.google.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2FlmJvOsqxXK4%2Fss.html sout"> Southern Discomfort? PON1 Variation May Help Explain Regional CVD Risk Age-associated rates of cardiovascular disease (CVD) are higher in the Southern states (except Florida) than anywhere else in the United States, and higher among Southern blacks than Southern whites. Animal studies suggest that higher levels of activity of the enzyme paraoxonase-1 (PON1) may lower the risk of CVD, specifically atherosclerosis, but evidence linking functional variations in PON1 to atherosclerosis risk in humans has been ambiguous. New research correlates functional variation in PON1 activity with race, which may help explain demographic variation in CVD prevalence [EHP 117:1226 1231; Davis et al.]. PON1 helps break down pesticides in the body. image: Getty Images PON1 is carried by high-densit... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2670032 Fri, 31 Jul 2009 23:00:00 +0100 2670032 afra'> A Framework to Monitor Toxics Measuring the Health Impact of Chemical Bans One of the tasks mandated by the Stockholm Convention on Persistent Organic Pollutants is to determine if bans on toxic substances are effective in reducing contamination in people. But assessing such trends in diverse global populations is difficult because researchers must use changes in the average levels of contaminants measured in groups of people at different points in time known as cross-sectional trend data to estimate how levels are changing in individuals over time. A team of Swiss researchers has developed a pharmacokinetic model framework that may help improve the use of cross-sectional trend data in assessing the effects of chemical bans [EHP 117:1280 1286; Ritter et al.]. Among the parameters required by the model are the rate of elimination of the contaminant from the body and the rate of decline of individual intake of the contaminant once a ban takes effect. Additional parameters include body weight and the fraction of the body weight that is lipid. The authors tested their formulas with sample cases involving p,p -DDT and p,p -DDE from selected Swedish and U.K. populations, and found that the outcomes matched fairly well with concentrations identified in earlier studies. As with any model, however, a key to its successful application is good data for the variables included in the model. The authors note that total diet studies, which are regularly conducted in a number of countries, are a good source of data to estimate changes in contaminant intake over time, because food is typically the primary source of ongoing exposures in postban situations. The model assumes that cross-sectional averages used to estimate changes in contaminant levels over time are based on data from populations that are similar in age and other factors that would influence initial body burden and contaminant intake and elimination. The key is that changes in intakes be reasonably consistent among members of the population, but they need not be consistent for the population over time if data are available to estimate changes in dietary intake. Modeling data from populations that are reasonably similar with regard to these characteristics also means that results from the model will be population-specific and not necessarily applicable to other populations. Still, the authors say the model is broadly adaptable, and the formulas can be modified to factor in considerations such as pathways other than ingestion, storage in body reservoirs other than fat tissue, and different elimination rates. To optimize the use of this model, the authors recommend that efforts to monitor toxics include regular data collection, including total diet data to estimate background levels of ongoing exposure, in young adult populations. Bob Weinhold, MA, has covered environmental health issues for numerous outlets since 1996. He is a member of the Society of Environmental Journalists. http://www.medworm.com/index.php?rid=2670031&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeedproxy.google.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2FsstM7GzhgAI%2Fss.html afra"> A Framework to Monitor Toxics Measuring the Health Impact of Chemical Bans One of the tasks mandated by the Stockholm Convention on Persistent Organic Pollutants is to determine if bans on toxic substances are effective in reducing contamination in people. But assessing such trends in diverse global populations is difficult because researchers must use changes in the average levels of contaminants measured in groups of people at different points in time known as cross-sectional trend data to estimate how levels are changing in individuals over time. A team of Swiss researchers has developed a pharmacokinetic model framework that may help improve the use of cross-sectional trend data in assessing the effects of chemical bans [EHP 117:1280 1286; Ritter et al.]. Among the parameters ... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2670031 Fri, 31 Jul 2009 23:00:00 +0100 2670031 chem'> Chemicals Policy Gap Toward Stronger Regulation in the United States Chemicals policy in the United States is in need of profound change for both environmental health and economic reasons, according to a review of how the U.S. chemical industry currently is regulated [EHP 117:1202 1209; Wilson and Schwarzman]. The 1976 Toxic Substances Control Act (TSCA), which provides the chief legal authority for regulating industrial chemicals in the United States, is antiquated and ineffective, according to the authors. Reform of TSCA is especially urgent in view of the European Union s passage in 2006 of the Registration, Evaluation, Authorisation and Restriction of Chemicals (REACH) legislation. REACH s more stringent and transparent rules for regulating industrial chemicals could put the United States at risk of becoming a market for hazardous chemicals that become banned in Europe. Without a parallel transformation in U.S. chemicals policy and a strong commitment to green chemistry, the United States could face growing health and environmental problems and will have difficulty meeting the challenges of environmental and economic sustainability, the authors write. TSCA currently requires chemical producers to disclose little toxicologic or other test data, creating a data gap that prevents the public and downstream users of chemicals from making informed purchasing decisions. The U.S. Environmental Protection Agency bears the burden of proving that a chemical should be regulated (as opposed to the manufacturer proving that the chemical need not be regulated), and a lack of governmental tools to evaluate and mitigate chemical hazards has produced a safety gap. In concert with the first two gaps, the lack of investment in green chemistry research and development has produced a technology gap, with the United States at risk of falling behind the European Union and other industrialized nations in this area. The authors argue that the three gaps have produced a chemicals market that values function, price, and performance over safety while externalizing the costs of chemically related health and environmental damage to the public. These market and regulatory conditions also pose a key barrier to the scientific and commercial success of green chemistry in the United States and could hinder the U.S. chemical industry s global competitiveness as green chemistry technologies accelerate under REACH. Global chemical production is expected to double in the next 24 years, according to the United Nations and other sources, and the Environmental Protection Agency has estimated the United States will need 217,000 new hazardous waste sites in the next 20 years. Concluding that the vast potential of green chemistry remains untapped, the authors call for a chemicals policy that departs markedly from the federal policies of the last 30 years, of which TSCA is emblematic. Taking advantage of this opportunity, they write, would propel the United States toward new chemistries that are safer for occupational, environmental, and public health the cornerstone of a truly sustainable society. Valerie J. Brown, based in Oregon, has written for EHP since 1996. In 2009 she won a Society of Environmental Journalists Outstanding Explanatory Reporting award for her writing on epigenetics. http://www.medworm.com/index.php?rid=2670030&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeedproxy.google.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2FreGojJkyVY8%2Fss.html chem"> Chemicals Policy Gap Toward Stronger Regulation in the United States Chemicals policy in the United States is in need of profound change for both environmental health and economic reasons, according to a review of how the U.S. chemical industry currently is regulated [EHP 117:1202 1209; Wilson and Schwarzman]. The 1976 Toxic Substances Control Act (TSCA), which provides the chief legal authority for regulating industrial chemicals in the United States, is antiquated and ineffective, according to the authors. Reform of TSCA is especially urgent in view of the European Union s passage in 2006 of the Registration, Evaluation, Authorisation and Restriction of Chemicals (REACH) legislation. REACH s more stringent and transparent rules for regulating industrial chemicals could put the U... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2670030 Fri, 31 Jul 2009 23:00:00 +0100 2670030 thev'> The Vulnerability of the Older Child A New Approach to Identifying Ages When Children Are Most Susceptible to Lead Effects Watch a toddler, and you quickly see why small children are so vulnerable to environmental exposures: most of what they touch goes right into their mouths. It s no wonder, then, that lead levels generally peak at age 2 years, which is when health officials recommend children be tested for elevated blood lead. But new research shows that 5- to 6-year-olds may be particularly vulnerable to the cognitive and behavioral effects of lead and should be tested as well if such problems are apparent [EHP 117:1309 1312; Hornung et al.]. older childs hand on a painted window ledge Although blood lead concentrations tend to decline after toddlerhood, older children may be more susceptible to adverse effects of exposure. image: iStockphoto Previous studies have suggested that IQ scores at ages 5 7 years are more strongly associated with concurrent blood lead concentrations than with concentrations measured at age 2. However, children s blood lead concentrations during infancy are strongly associated with concentrations at older ages meaning, for instance, a highly exposed toddler still tends to be highly exposed at age 6. This serial correlation makes it difficult to determine whether lead has a cumulative effect or whether effects of lead differ according to age. In the current study, researchers analyzed blood lead concentration data for 462 children who participated in either the Cincinnati Lead Study, which enrolled children from 1979 to 1984, or the Rochester Longitudinal Study, which enrolled children from 1994 to 1995. In both studies the children s blood lead was measured every year from infancy to age 6. The children also took IQ tests around age 6. To study effects of lead at different ages while accounting for correlations in lead levels over time, the researchers estimated effects of the ratio of the child s blood lead at age 2 relative to his or her blood lead at each subsequent age (3 6 years). As the ratio of age 6:age 2 blood lead increased, IQs declined even after controlling for average lead exposure at all ages as well as a range of other covariates. In addition, children who had relatively higher lead exposure at age 5 or 6 compared with age 2 had significantly higher arrest rates for criminal behavior in adulthood than other children. The results suggest that blood lead testing and efforts to reduce exposure should continue as children reach school age. Moreover, lead testing of school-age children with cognitive or behavioral problems may help identify underlying causes of difficulties teachers or parents are seeing. Tina Adler first wrote for EHP about the Clinton Gore environmental agenda in 1993. She is a member of the National Association of Science Writers and the American Society of Journalists and Authors. http://www.medworm.com/index.php?rid=2670029&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeedproxy.google.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2FaxtuYwsshZg%2Fss.html thev"> The Vulnerability of the Older Child A New Approach to Identifying Ages When Children Are Most Susceptible to Lead Effects Watch a toddler, and you quickly see why small children are so vulnerable to environmental exposures: most of what they touch goes right into their mouths. It s no wonder, then, that lead levels generally peak at age 2 years, which is when health officials recommend children be tested for elevated blood lead. But new research shows that 5- to 6-year-olds may be particularly vulnerable to the cognitive and behavioral effects of lead and should be tested as well if such problems are apparent [EHP 117:1309 1312; Hornung et al.]. Although blood lead concentrations tend to decline after toddlerhood, older children may be more susceptible to adverse effects of expo... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2670029 Fri, 31 Jul 2009 23:00:00 +0100 2670029 rain'> Rainy Day Reaction Human West Nile Viruses Cases Respond to Weather Patterns Piecemeal evidence suggests weather may have played a role in the rapid spread of West Nile virus (WNV) across the United States and into Canada and Central America following its detection in New York City in 1999. A team of U.S. and Canadian researchers has looked more comprehensively at the evidence by analyzing a spectrum of weather factors for 17 climatically diverse states, and found several significant links with the incidence of human WNV cases [EHP 117:1049�1052; Soverow et al.]. The analysis was based on 16,298 WNV cases reported to the Centers for Disease Control and Prevention from 2001 to 2005, as well as year-round temperature, precipitation, and dew point data from 351 weather stations in close proximity to the infected people. A 12�F increase in maximum daily temperature was associated with a 45�72% increase in WNV case reports within a 1-month period. Precipitation was also associated with WNV, which increased 29�66% in association with a single-day rainfall of at least 50 mm within 3 weeks of diagnosis. Smaller amounts of precipitation were associated with smaller increases in WNV cases, consistent with a dose�response effect. Increases in cumulative weekly precipitation and mean weekly dew point temperature (a measure of relative humidity) were also associated with an increase in WNV cases. The findings, which hold up across season and location, generally mesh with what is known about the biology of WNV, humans, mosquito vectors, and bird reservoir hosts. The authors write that additional research will be needed to address some limitations of their work�notably gaps in data from a number of geographic regions and the influence of localized interactions of factors such as bird populations, vegetation, mosquito control efforts, and acquired immunity in both humans and animals. If these weather�disease links are confirmed, and if climate changes in North America unfold as predicted with increases in temperature and precipitation, public health officials may be better able to prevent or mitigate outbreaks in the future. Bob Weinhold, MA, has covered environmental health issues for numerous outlets since 1996. He is a member of the Society of Environmental Journalists. spacer | Purchase This Issue | http://www.medworm.com/index.php?rid=2559645&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeedproxy.google.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F6r_Gtr3DnGI%2Fss.html rain"> Rainy Day Reaction Human West Nile Viruses Cases Respond to Weather Patterns Piecemeal evidence suggests weather may have played a role in the rapid spread of West Nile virus (WNV) across the United States and into Canada and Central America following its detection in New York City in 1999. A team of U.S. and Canadian researchers has looked more comprehensively at the evidence by analyzing a spectrum of weather factors for 17 climatically diverse states, and found several significant links with the incidence of human WNV cases [EHP 117:1049�1052; Soverow et al.]. The analysis was based on 16,298 WNV cases reported to the Centers for Disease Control and Prevention from 2001 to 2005, as well as year-round temperature, precipitation, and dew point data from 351 weather stations i... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2559645 Tue, 30 Jun 2009 23:00:00 +0100 2559645 aluc'> A Lucrative Investment Controlling Lead Paint Yields Big Dividends Fewer children today have the high blood lead levels seen in kids a few decades ago, when gasoline and paint still came fully leaded. But a surprising number of children still have blood lead levels that may place them at risk for a variety of cognitive, emotional, and behavioral problems. The good news is that boosting current efforts to protect U.S. children from one major source of lead�the house paint used prior to a 1978 ban, which still appears in many homes�may pay for itself many times over [EHP 117:1162�1167; Gould]. old building with lead paint It can cost a homeowner more than $200,000 to clean up lead contamination after uncontrolled power sanding, compared with about $1,200 to incorporate lead-safe work practices into repainting. image: AP Photo/Stew Milne According to National Health and Nutritional Examination Survey data from 2003 to 2006, an estimated 25% of the 28 million U.S. children aged 6 years and younger have blood lead levels between 2 and 10 g/dL, a range in which persistent cognitive damage is known to occur. Another 200,000 children are estimated to have levels over 10 g/dL. Using data from published studies, the author performed a cost�benefit analysis of the effects of controlling children�s exposure to lead paint. She calculated that controlling lead paint in the approximately 1 million worst-case housing units would cost between $1.2 billion and $11 billion, depending on many factors including local costs of lead abatement. But the benefits to be derived from controlling lead hazards could range from $181 billion to $269 billion. For example, abatement could save $11�53 billion in immediate medical treatment and $30�146 million in special education costs. Reducing the incidence of attention deficit/hyperactivity disorder (ADHD) related to lead paint exposure might save $267 million; and because both ADHD and lead exposure have been associated with criminal behavior, crime-related costs could shrink by $1.7 billion with efforts to eliminate and contain lead-laden paint. The author concludes that every dollar spent to limit U.S. children�s exposure to lead paint�such as through paint stripping, replacement, and covering with a special encapsulant coating�could net $17�221. By comparison, vaccination against the most common childhood diseases is estimated to save $5.30�16.50 for every dollar spent on immunizations. The author noted that the cost savings from better lead mitigation could be even higher than estimated in the current study. For one thing, the calculations of potential benefit pertain only to children under age 6. Yet getting rid of lead paint would benefit other segments of the population as well. Also, the analysis excluded many potential costs of lead exposure, including future health care expenses and the indirect costs of criminal activity. U.S. public health and housing policies have been slow to address the lingering problems related to lead paint, the author asserts. Given the huge projected savings and income in terms of health care, crime prevention, education, lifetime earnings, and tax revenues, she writes, the time for proactive and universal lead control has never been better. Tina Adler first wrote for EHP about the Clinton�Gore environmental agenda in 1993. She is a member of the National Association of Science Writers and the American Society of Journalists and Authors. http://www.medworm.com/index.php?rid=2559644&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeedproxy.google.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F-fJcp8FNhRM%2Fss.html aluc"> A Lucrative Investment Controlling Lead Paint Yields Big Dividends Fewer children today have the high blood lead levels seen in kids a few decades ago, when gasoline and paint still came fully leaded. But a surprising number of children still have blood lead levels that may place them at risk for a variety of cognitive, emotional, and behavioral problems. The good news is that boosting current efforts to protect U.S. children from one major source of lead�the house paint used prior to a 1978 ban, which still appears in many homes�may pay for itself many times over [EHP 117:1162�1167; Gould]. It can cost a homeowner more than $200,000 to clean up lead contamination after uncontrolled power sanding, compared with about $1,200 to incorporate lead-safe work practices into re... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2559644 Tue, 30 Jun 2009 23:00:00 +0100 2559644 moth'> Mother Load Arsenic May Contribute to Gestational Diabetes Chronic exposure to arsenic�usually via drinking water contaminated with inorganic arsenic�has been associated with an increased risk of type 2 diabetes mellitus in countries around the world. New research shows that arsenic exposure may be an environmental risk factor for gestational diabetes as well [EHP 117:1059�1064; Ettinger et al.]. pregnant woman drinking a glass of water Millions of people worldwide may be exposed to naturally occurring arsenic in drinking water. image: Veer Arsenic may promote type 2 diabetes by increasing insulin resistance (inability to utilize insulin at the cellular level) and impairing insulin production. Insulin resistance is also a central feature of gestational diabetes, a potential complication during pregnancy that can lead to a 30�60% increased risk for the mother of developing lifelong diabetes, as well as impaired glucose tolerance, adverse birth outcomes, and obesity in her child. The study was conducted near the Tar Creek Superfund site in Ottawa County, Oklahoma, whose residents include many Native Americans, a population already at elevated risk for type 2 diabetes. The area, once active in lead and zinc mining, has an above-average poverty rate compared with the rest of Oklahoma and the nation. Mine waste contaminated with assorted metals is still present and has been used to build roads, playgrounds, driveways, and house foundations. Moreover, 25% of drinking water samples tested in the area have naturally occuring arsenic levels exceeding the Environmental Protection Agency maximum contaminant level of 10 �g/L. Total arsenic concentrations were measured in blood and hair samples collected at delivery from 532 women; blood was available from all women and hair from a subset of 179. Routine prenatal glucose tolerance tests conducted between weeks 24 and 28 of pregnancy yielded plasma glucose measurements, and questionnaires and medical record review provided data on sociodemographic characteristics, potential sources of arsenic exposure, and pregnancy history. Blood arsenic concentrations, a measure of biologically active arsenic, were between 0.2 and 24.1 �g/L, whereas hair arsenic concentrations, an indicator of cumulative exposure, were 1.1�724.4 ng/g. Blood glucose levels ranged from 40 to 284 mg/dL. At a cut-off value of > 140 mg/dL, 12% of the women were identified as having impaired glucose tolerance; a cut-off value of 130 mg/dL yielded a prevalence of more than 20%. A statistically significant relationship existed between each increasing quartile of blood arsenic exposure and impaired glucose tolerance after controlling for health and demographic factors. Depending on the glucose test cut-off value, women in the highest quartile of arsenic exposure were 2.4�2.8 times more likely to have impaired glucose tolerance than women in the lowest quartile of exposure. These results suggest that chronic arsenic exposure may increase the risk of developing gestational diabetes. A better understanding of this and other factors through further research may identify modifiable risk factors this condition. Julia R. Barrett, MS, ELS, a Madison, Wisconsin�based science writer and editor, has written for EHP since 1996. She is a member of the National Association of Science Writers and the Board of Editors in the Life Sciences. http://www.medworm.com/index.php?rid=2559643&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeedproxy.google.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2FzN5CBt2kLwQ%2Fss.html moth"> Mother Load Arsenic May Contribute to Gestational Diabetes Chronic exposure to arsenic�usually via drinking water contaminated with inorganic arsenic�has been associated with an increased risk of type 2 diabetes mellitus in countries around the world. New research shows that arsenic exposure may be an environmental risk factor for gestational diabetes as well [EHP 117:1059�1064; Ettinger et al.]. Millions of people worldwide may be exposed to naturally occurring arsenic in drinking water. image: Veer Arsenic may promote type 2 diabetes by increasing insulin resistance (inability to utilize insulin at the cellular level) and impairing insulin production. Insulin resistance is also a central feature of gestational diabetes, a potential complication during pregnancy that... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2559643 Tue, 30 Jun 2009 23:00:00 +0100 2559643 smok'> Smoking Gain? Secondhand Smoke Exposure Influences Body Weight, Lipid Profiles in Offspring An estimated 780,000 U.S. women continue smoking throughout pregnancy each year despite warnings about the elevated risk of birth defects in the children of female smokers. A new mouse study provides experimental evidence that exposure to secondhand cigarette smoke during pregnancy may lead to weight gain in offspring as well as changes in lipid profiles that may increase the chances of cardiovascular disease later in life [EHP 117:1042�1049; Ng et al.]. Oxidants in cigarette smoke have previously been shown to promote local and systemic inflammation and increase the risk of cardiovascular disease in both smokers and those exposed to secondhand smoke. Lipid oxidation in particular has been associated with cardiovascular diseases. Women have a higher risk of dying from cardiovascular disease than men and are more likely to die following a heart attack. The current study may shed light on this observed sex-specific difference. Female pups of mice that were exposed to cigarette smoke for 4 hours a day, 5 days a week, throughout pregnancy grew up to have a higher body weight than their unexposed peers and had significant increases in plasma high-density lipoprotein (HDL), low-density lipoprotein (LDL), and total protein. However, these differences were not observed when the adult female offspring were fed a high-fat diet instead of a regular diet. On the other hand, smoke-exposed male pups gained more weight and displayed altered lipid profiles compared with their sex-matched, unexposed counterparts when they were fed a high-fat diet but showed little evidence of an effect of smoke exposure when fed a normal diet. Although maternal exposure to cigarette smoke appeared to influence weight gain and lipid profiles in their offspring, lipid parameters in the dams themselves showed little change in response to smoke exposure. Additional work is necessary to understand why lipoprotein levels�which reflect cholesterol metabolism�are altered in the offspring in response to cigarette smoke exposure during pregnancy. Abnormal body weight and dyslipidemia (abnormal plasma lipoprotein levels) are among the best-established risk factors for cardiovascular diseases. Although the new study does not investigate the mechanisms of the observed changes, it does suggest that prevention programs that emphasize avoidance of cigarette smoke during pregnancy could reap long-range health benefits for the newborn. Victoria McGovern, based in Durham, North Carolina, has written for EHP since 2000. She is a member of the National Association of Science Writers. http://www.medworm.com/index.php?rid=2559642&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeedproxy.google.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2FOVrwzuew-Mc%2Fss.html smok"> Smoking Gain? Secondhand Smoke Exposure Influences Body Weight, Lipid Profiles in Offspring An estimated 780,000 U.S. women continue smoking throughout pregnancy each year despite warnings about the elevated risk of birth defects in the children of female smokers. A new mouse study provides experimental evidence that exposure to secondhand cigarette smoke during pregnancy may lead to weight gain in offspring as well as changes in lipid profiles that may increase the chances of cardiovascular disease later in life [EHP 117:1042�1049; Ng et al.]. Oxidants in cigarette smoke have previously been shown to promote local and systemic inflammation and increase the risk of cardiovascular disease in both smokers and those exposed to secondhand smoke. Lipid oxidation in particular has ... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2559642 Tue, 30 Jun 2009 23:00:00 +0100 2559642 fatc'> Fat Chance? A High-Fat Diet May Offset the Effects of Developmental Neurotoxicity Widespread exposure to a variety of neurotoxic chemicals has been posited as one potential factor behind what has been called a �silent pandemic� of autism spectrum disorders, learning disabilities, and other neurodevelopmental disorders. Exposure to organophosphate insecticides is of particular concern because these widely used compounds have been shown in rodents to induce persistent synaptic abnormalities in neural acetylcholine (ACh) systems at doses too low to cause symptoms of systemic exposure. Pilot studies have reported some evidence of improvement when a �ketogenic� diet�high in fat and low in carbohydrates�was used to treat certain neurologic disorders. Drawing from this preliminary clinical research, researchers have now demonstrated that many of the abnormalities in ACh systems produced by neonatal organophosphate exposure were not evident in adult rats fed a high-fat diet [EHP 117:916�922; Slotkin et al.]. Rats were injected with the organophosphate parathion on each of postnatal days 1�4, at doses of 0.1 or 0.2 mg/kg/day�these dosages straddle the threshold at which cholinesterase inhibition is first detectable. In adulthood, half the animals were switched to a high-fat diet for 8 weeks. The investigators then examined brain regions of the rats to assess specific aspects of ACh synaptic function, including nicotinic ACh receptor binding, choline acetyltransferase activity, and hemicholinium-3 binding to the presynaptic choline transporter. Adult rats on a standard lab chow diet showed multiple abnormalities in regional ACh synaptic markers following parathion exposure. All seven abnormalities observed in parathion-exposed females on the standard diet were absent in exposed females on the high-fat diet, and eight of ten abnormalities observed in parathion-exposed males on the standard diet were absent in exposed males on the high-fat diet. The results suggest that diet may offer a way to ameliorate the effects of developmental neurotoxicant exposure. However, the authors offer several caveats. Their earlier work showed that neonatal exposure to organophosphates produced long-term changes in metabolic function that have been linked with obesity, prediabetes, and cardiovascular risk factors such as elevated serum lipids. Because these metabolic abnormalities could be exacerbated by a high-fat diet, future studies should seek to uncover whether and how specific aspects of the diet influence abnormalities in ACh systems. Moreover, although this study showed that dietary modifications may offset synaptic changes, future studies will need to determine whether such modifications can actually lead to improved neurobehavioral outcomes. The authors also highlight a potential connection between early-life toxicant exposure and subsequent diet-related disease. If a high-fat diet can indeed ameliorate the impact of developmental neurotoxicants, then this might serve as an underlying, subconscious reinforcement to consume a high-fat diet as a way of self-remediating underlying neurobehavioral deficits�potentially expanding the public health implications of the developmental effects of neurotoxicant exposure. Angela Spivey spacer | Purchase This Issue | http://www.medworm.com/index.php?rid=2454932&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeedproxy.google.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2FGaIF7nvCla0%2Fss.html fatc"> Fat Chance? A High-Fat Diet May Offset the Effects of Developmental Neurotoxicity Widespread exposure to a variety of neurotoxic chemicals has been posited as one potential factor behind what has been called a �silent pandemic� of autism spectrum disorders, learning disabilities, and other neurodevelopmental disorders. Exposure to organophosphate insecticides is of particular concern because these widely used compounds have been shown in rodents to induce persistent synaptic abnormalities in neural acetylcholine (ACh) systems at doses too low to cause symptoms of systemic exposure. Pilot studies have reported some evidence of improvement when a �ketogenic� diet�high in fat and low in carbohydrates�was used to treat certain neurologic disorders. Drawing from this prel... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2454932 Mon, 01 Jun 2009 04:00:00 +0100 2454932 thep'> The Price of Progress Modern Environmental Health Hazards in Africa With the spread of industrialization to all areas of the globe, scientists and policymakers alike have voiced mounting concerns over the ability of developing countries to limit the public health impacts of unchecked development. African nations, for example, have experienced rapid urbanization as well as tremendous expansion in industry and technology in an attempt to raise living standards and keep pace with the global community. But this trend has also exposed these nations to numerous modern environmental health hazards (MEHHs)�health threats that tend to accompany rapid development in the absence of health and environmental safeguards. A review of the scientific literature suggests that such hazards have added considerably to Africa�s disease burden and are increasing in public health significance [EHP 117:863�870; Nweke and Sanders]. sources of BPA Leaded gas is now banned in sub-Saharan Africa but is still sold in some northern nations. image: � Black Star/Alamy The authors wrote that ongoing exposures to emerging MEHHs may soon rival the contributions of more traditional hazards�including malaria, poor access to safe drinking water, and lack of basic sanitation�that have long troubled Africa. Furthermore, poor and malnourished populations may be more vulnerable to the impacts of MEHHs, given that malnutrition increases susceptibility to toxicologic challenges. According to the United Nations Industrial Development Organization, Africa�s pollution intensity (pollution generated per unit of production output) is among the highest in the world. Reviewing published epidemiologic, exposure, and environmental studies of chemical agents, the researchers noted ongoing occupational and nonoccupational exposures to organochlorine pesticides such as DDT and to heavy metals such as lead and mercury. All these pollutants are known to persist in the environment and accumulate in the food chain over time, as confirmed by biomonitoring studies of farmworker populations in several African nations. The authors also presented evidence of existing and emerging air toxics issues related to both indoor and outdoor air pollution, pervasiveness of toxic chemicals in consumer products (such as arsenic and chromium in canned beverages), and inadequate management of domestic and industrial waste streams. Relatively robust exposure data for lead showed elevated body burdens in African populations exposed to lead-bearing soil, dust, and paint, offering suggestive evidence of ongoing exposures to MEHHs at biological levels associated with adverse health impacts. Some studies found elevated body burdens of mercury in exposed populations such as miners, workers involved in ore processing, children who resided in mining communities, and women who habitually used soaps that contain high concentrations of inorganic mercury (such soaps are marketed as skin and hair lighteners). However, very few body burden studies have provided conclusive evidence of the relationship between heavy metal exposures and increased disease risks in African populations. Management of MEHHs in many African nations has long been hampered by a lack of various safeguards for environmental health, such as stable institutions, adequate infrastructure, monitoring capacity, and regulatory frameworks. The researchers proposed that MEHHs should occupy a priority spot on Africa�s public health and policy agenda, and emphasized that future public health policy should consider these newer environmental health risks in tandem with other longstanding public health issues. Tanya Tillett http://www.medworm.com/index.php?rid=2454931&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeedproxy.google.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2FQR7s190WfFA%2Fss.html thep"> The Price of Progress Modern Environmental Health Hazards in Africa With the spread of industrialization to all areas of the globe, scientists and policymakers alike have voiced mounting concerns over the ability of developing countries to limit the public health impacts of unchecked development. African nations, for example, have experienced rapid urbanization as well as tremendous expansion in industry and technology in an attempt to raise living standards and keep pace with the global community. But this trend has also exposed these nations to numerous modern environmental health hazards (MEHHs)�health threats that tend to accompany rapid development in the absence of health and environmental safeguards. A review of the scientific literature suggests that such hazards have ... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2454931 Mon, 01 Jun 2009 04:00:00 +0100 2454931 lega'> Legacy for Young Men PFAAs and Human Sperm Recent studies suggest that men�s capacity for sperm production may be harmed by toxic exposures in both fetal and later life. Among the potential chemical culprits are the perfluoroalkyl acids (PFAAs), highly persistent degradation products of the polyfluorinated compounds used in products including nonstick cookware and water-resistant coatings for carpeting, clothing, and other textiles. Findings from a new Danish study suggest that exposure to PFAAs may help account for the otherwise unexplained poor semen quality observed in many young men today [EHP 117:923�927; Joensen et al.]. sperm illustration Men with the highest PFAA scores also had the highest percentages and numbers of morphologically abnormal sperm. image: Daniel Cooper Studies in the 1990s found that PFAAs diminished testosterone levels and increased estradiol levels in male rats. In human studies, men have appeared to have higher serum PFAA concentrations than women, and younger men may have even higher levels compared with those of older men. Young men may therefore be at higher risk for any potential adverse effects posed by these chemicals. Inspired by such observations, the Danish team designed what they believe is the first study of the effects of PFAAs on sperm quality in humans. They focused their investigation on perfluorooctanoic acid (PFOA) and perfluorooctane sulfonic acid (PFOS) because of these compounds� prevalence, their long half-lives, and existing evidence that they act as endocrine disruptors. The subjects included 105 young men from the general population who had provided semen samples in 2003 as part of Denmark�s compulsory military draft examination. These men had the highest and lowest testosterone counts of 546 potential subjects considered. Serum levels of PFOA and PFOS were combined to give each man a PFAA score. These scores were used to classify subjects into low-, intermediate-, and high-PFAA groups. Sperm quality varied markedly among all three groups. Compared with the low- and intermediate-PFAA groups, men in the high-PFAA group showed significantly poorer sperm quality in terms of both percentage and total numbers of morphologically normal sperm. Ejaculate from men in the low-PFAA group had a median count of 15.5 million normal sperm compared with 10 million and 6.2 million normal sperm in the intermediate- and high-PFAA groups, respectively. Average sperm concentration and motility also were lower in the high-PFAA group, but not significantly so. PFAAs were not inversely associated with testosterone levels, a finding that was contrary to expectations based on previous animal research. The researchers note that humans and wildlife will be exposed to persistent PFAAs for years to come. They speculate that high exposures to PFAAs may be contributing to low semen quality and subfertility reported in other studies. However, they caution, results from this preliminary study should be corroborated in larger studies. Cynthia Washam http://www.medworm.com/index.php?rid=2454930&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeedproxy.google.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2FVPINual8DJI%2Fss.html lega"> Legacy for Young Men PFAAs and Human Sperm Recent studies suggest that men�s capacity for sperm production may be harmed by toxic exposures in both fetal and later life. Among the potential chemical culprits are the perfluoroalkyl acids (PFAAs), highly persistent degradation products of the polyfluorinated compounds used in products including nonstick cookware and water-resistant coatings for carpeting, clothing, and other textiles. Findings from a new Danish study suggest that exposure to PFAAs may help account for the otherwise unexplained poor semen quality observed in many young men today [EHP 117:923�927; Joensen et al.]. Men with the highest PFAA scores also had the highest percentages and numbers of morphologically abnormal sperm. image: Daniel Cooper Studies in ... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2454930 Mon, 01 Jun 2009 04:00:00 +0100 2454930 pren'> Prenatal Preview Early Bisphenol A Exposure May Spawn Late-Life Reproductive Problems Scientists increasingly find that exposure to toxicants during critical periods of pre- and perinatal development can have long-lasting effects that increase the risk of reduced fertility, reproductive tumors, and breast cancer later in life. Some animal studies have suggested that very low doses of bisphenol A (BPA) in a range relevant to human exposures can cause abnormalities in the uterus, vagina, and ovary when those exposures occur during early development. To date, however, evidence for a carcinogenic effect of low-dose BPA on the female reproductive tract has been lacking; studies examining carcinogenic susceptibility to BPA have focused only on the mammary and prostate glands. Now a report from researchers at the NIEHS indicates that low prenatal doses of BPA in mice may cause potentially carcinogenic alterations in female reproductive tissues [EHP 117:879�885; Newbold et al.]. Widespread human exposure to BPA is a cause for concern because of the compound�s chemical similarity to diethylstilbestrol (DES), an antinausea drug that caused harmful reproductive effects in women whose mothers took it during pregnancy. This study used an experimental animal model (the CD-1 mouse) that has been useful in studying the effects of prenatal exposure to DES. On gestational days 9�16, pregnant mice were injected with relatively low dosages of BPA�0.1, 1, 10, 100, or 1,000 �g/kg/day, which are considered by the authors and other researchers to be within an environmentally relevant range. When the dams� offspring reached late adulthood (16�18 months), their reproductive tissues were evaluated. Some of the BPA-exposed offspring developed both benign and malignant lesions in late adulthood. In the pups that received 1 �g/kg/day, the incidence of benign ovarian cysts was 67%�similar to what the same team had previously observed for neonatal exposure to BPA. In addition, more severe ovarian lesions were found in the groups that received 10, 100, or 1,000 �g/kg/day but not in control animals. The occurrence of progressive proliferative lesions of the oviduct seemed to increase following BPA exposure, similar to effects seen in previous studies following prenatal exposure to DES. Because DES appears to delay the expression of genes that guide the development of the reproductive tract, the authors suggest that molecular �misprogramming� is the most likely reason for both DES- and BPA-induced lesions of the oviduct. Malignant changes in the uterus also were found in exposed mice, although the incidence of those lesions was not statistically different from that seen in controls. In addition, more severe pathologies were observed in exposed animals but not in controls. These included atypical hyperplasia and stromal polyps of the uterus, sarcoma of the uterine cervix, and mammary adenocarcinoma. According to the authors, this study is the first to find both benign and malignant lesions in reproductive tissues of senescent female mice exposed prenatally to BPA over a wide dosage range thought to be relevant to human exposure. The study adds to the growing body of literature showing adverse effects following developmental exposure to low doses of BPA and suggests that exposure during critical periods of fetal development may result in adverse reproductive and carcinogenic changes over the long term. Angela Spivey http://www.medworm.com/index.php?rid=2454929&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeedproxy.google.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2FI5ZPKT-CoS8%2Fss.html pren"> Prenatal Preview Early Bisphenol A Exposure May Spawn Late-Life Reproductive Problems Scientists increasingly find that exposure to toxicants during critical periods of pre- and perinatal development can have long-lasting effects that increase the risk of reduced fertility, reproductive tumors, and breast cancer later in life. Some animal studies have suggested that very low doses of bisphenol A (BPA) in a range relevant to human exposures can cause abnormalities in the uterus, vagina, and ovary when those exposures occur during early development. To date, however, evidence for a carcinogenic effect of low-dose BPA on the female reproductive tract has been lacking; studies examining carcinogenic susceptibility to BPA have focused only on the mammary and prostate glands. Now a re... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2454929 Mon, 01 Jun 2009 04:00:00 +0100 2454929 they'> The Yin and Yang of Exposure Chemical Combinations May Explain Feminization of Wild Fish More than 100,000 substances occur in wastewater effluent, including an array of endocrine disruptors such as human and veterinary pharmaceuticals, natural and synthetic hormones, detergents, and industrial chemicals. Studies have linked estrogenic wastewater pollution with feminization of males in downstream fish populations. However, findings from rodent models of testicular dysgenesis syndrome, a spectrum of environmentally linked male reproductive disorders in humans, indicate that both estrogens and antiandrogens may be contributing to health effects in tandem. A new study that models exposure to both estrogenic and antiandrogenic compounds in wild fish now suggests that combinations of these compounds, rather than estrogenic compounds alone, may be responsible for the endocrine disruption observed in these animals as well [EHP 117:797�802; Jobling et al.]. sources of BPA The micrograph on the left shows normal testis tissue from an adult male roach (Rutilis rutilis). On the right is the testis of a severely feminized male roach; the large circular inclusions are oocytes. image: Catherine Harris and Tamsin Runnalls/Brunel University To help elucidate the complex relationships and interactions among the various types of endocrine disruptors (estrogenic, antiestrogenic, androgenic, and antiandrogenic), the authors created statistical models based on 1) the chemicals� known hormonal activities in recombinant yeast screen assays and 2) concentrations measured during an earlier national survey in effluent from U.K. wastewater treatment plants. The models also included hydrologic data to enable estimation of river-water chemical concentrations at specific sites and national survey data on the location and prevalence of feminized male fish. The statistical models first accounted for estrogenic effects observed in fish, then included effects associated with antiandrogens and other compounds. The authors previously found a very strong correlation between the predicted steroid estrogen content of U.K. rivers and feminization in male wild fish. In the current study they focused on four specific traits of feminization: elevated plasma levels of vitellogenin (an egg yolk precursor protein normally produced only in females), feminized reproductive ducts, oocyte (egg cell) development in the testes, and the number of oocytes found in the testes. Once the main factors accounting for variation were identified, the researchers were able to distinguish the respective contributions of estrogens and antiandrogens to biologic responses and explore potential interactions. Model estimates suggested that male fish exposed to the highest concentrations of estrogens or antiandrogens were the most likely to be feminized. However, chemical combinations were also important. Estrogens and antiandrogens acted additively with regard to oocytes in the testes, but estrogens appeared to antagonize effects of antiandrogens on feminization of the reproductive duct. The authors note that combined effects were not necessarily due to simultaneous exposure; for example, one compound could serve as an initiator early in life while another could act as a promoter later in life. On the basis of these analyses, the authors suggest that sexual disruption in male wild fish populations may be related to exposure to a combination of both estrogenic and antiandrogenic compounds, a relationship that may also hold true for humans. Julia R. Barrett http://www.medworm.com/index.php?rid=2385955&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2009%2F117-5%2Fss.html%23they they"> The Yin and Yang of Exposure Chemical Combinations May Explain Feminization of Wild Fish More than 100,000 substances occur in wastewater effluent, including an array of endocrine disruptors such as human and veterinary pharmaceuticals, natural and synthetic hormones, detergents, and industrial chemicals. Studies have linked estrogenic wastewater pollution with feminization of males in downstream fish populations. However, findings from rodent models of testicular dysgenesis syndrome, a spectrum of environmentally linked male reproductive disorders in humans, indicate that both estrogens and antiandrogens may be contributing to health effects in tandem. A new study that models exposure to both estrogenic and antiandrogenic compounds in wild fish now suggests that combinations of... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2385955 Fri, 01 May 2009 04:00:00 +0100 2385955 bisp'> Bisphenol A, Chapter 2 New Data Shed Light on Exposure, Potential Bioaccumulation Bisphenol A (BPA), an industrial chemical used in a variety of consumer products, is ubiquitous in the modern environment, with residues found in the urine of an estimated 93% of Americans over 6 years of age, according to data from the 2003�2004 National Health and Nutrition Examination Survey (NHANES). Recent research indicates that BPA acts as an endocrine disruptor and may increase the risk of heart disease, diabetes, and liver problems in adults. Until now, most exposure was thought to occur through diet, and the chemical was thought to clear the body quickly and completely. But a new study shows that urine BPA levels of subjects who had fasted for several hours were not as low as expected, suggesting either nondietary exposures or accumulation in fatty tissue, or both [EHP 117:784�789; Stahlhut et al.]. sources of BPA New findings raise the possibility that nonfood BPA exposure may be more substantive than previously thought. images: (Clockwise from top left) Danil Vachegin/iStockphoto; Serhiy Zavalnyuk/iStockphoto; Corbis; Danish Khan/iStockphoto Although BPA is fat-soluble and thus can accumulate in fatty tissues, animal and human data suggest it tends to be rapidly metabolized, with elimination thought to be virtually complete within 24 hours of acute exposure. To gain a better understanding of how BPA clears the body, investigators in the current study used data from 1,469 adult participants in the 2003�2004 NHANES. Study participants (excluding children and insulin-dependent diabetics) had been asked to fast for at least 6�9 hours. Using the urine drawn from each study participant, the investigators modeled log BPA concentration against fasting time, adjusting for urine creatinine and other confounders, to estimate what they called the �population-based half-life� of BPA for a 0- to 24-hour fasting period. Previous studies have reported that BPA has a urinary elimination half-life of only 4�5 hours, but BPA levels in this population declined much more slowly, showing a drop from adjusted population peak to trough levels of only 46% by 17 hours. Although there was a relatively rapid decline in BPA levels during the 4.5- to 8.5-hour fasting interval, the BPA slope was essentially flat between 8.5 and 24 hours, suggesting very slow or minimal elimination during that time. The findings are consistent with two possible explanations�first, that BPA exposure occurs through means other than food, and second, that BPA accumulates in body fat, from which it is gradually released over time. The authors conclude that their findings highlight the need for additional research on chronic BPA exposure, identification of significant nonfood sources of exposure (which may include dental composites and sealants, household dusts, air, recycled and carbonless paper, and the PVC pipe approved for use in residential water supply lines in many cities), and confirmation of reported data on bioaccumulation of the xenoestrogen in human adipose tissue. Confirmation of the current findings could lead to a reevaluation of BPA exposures in risk assessment studies. Tanya Tillett http://www.medworm.com/index.php?rid=2385954&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2009%2F117-5%2Fss.html%23bisp bisp"> Bisphenol A, Chapter 2 New Data Shed Light on Exposure, Potential Bioaccumulation Bisphenol A (BPA), an industrial chemical used in a variety of consumer products, is ubiquitous in the modern environment, with residues found in the urine of an estimated 93% of Americans over 6 years of age, according to data from the 2003�2004 National Health and Nutrition Examination Survey (NHANES). Recent research indicates that BPA acts as an endocrine disruptor and may increase the risk of heart disease, diabetes, and liver problems in adults. Until now, most exposure was thought to occur through diet, and the chemical was thought to clear the body quickly and completely. But a new study shows that urine BPA levels of subjects who had fasted for several hours were not as low as expected, ... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2385954 Fri, 01 May 2009 04:00:00 +0100 2385954 acle'> A Clearer View of TCE Evidence Supports Autoimmune Link More than 80 known or suspected autoimmune disorders�such as Crohn disease, multiple sclerosis, and rheumatoid arthritis�affect 5�8% of the U.S. population, according to the National Institute of Allergy and Infectious Diseases. The underlying causes of these disorders remain largely unknown, but one agent suspected to play a role is trichloroethylene (TCE), a solvent widely used in industrial and household applications. Researchers from the U.S. Environmental Protection Agency�s National Center for Environmental Assessment and the Medical University of South Carolina searched the scientific literature for studies linking TCE with selected immunologic connections, including immunosuppression, hypersensitivity, and autoimmune-related effects [EHP 117:696�702; Cooper et al.]. On the basis of their review, the authors concluded that the evidence to date in mice and humans supports an etiologic role of TCE in autoimmune disorders. Substantial evidence from mechanistic, clinical, and epidemiologic studies indicates that exposure to TCE and/or its metabolites (including chloral hydrate, trichloracetic acid, trichloracetaldehyde hydrate, and dichloracetyl chloride) could influence the incidence of autoimmune disorders. Research on autoimmune mouse models, including the MRL+/+ lupus mouse, has provided strong and consistent support for a role of TCE; this has included studies of exposures at environmentally relevant concentrations through multiple routes (inhalational, dermal, and oral). Studies of humans with high occupational or environmental exposures have also shown links between TCE and inflammatory immune responses, systemic sclerosis (scleroderma), and a severe generalized hypersensitivity skin disorder. However, the authors also point out major gaps in our knowledge of TCE�s effects on the immune system. In particular, data pertaining to measures of immunosuppression in humans are very limited, and potential effects of age or sex on susceptibility to autoimmune-related effects of TCE exposures, as well as effects of variation in exposure dose, timing, and duration, have yet to be established. Because individual autoimmune diseases are relatively rare, it is difficult to assemble enough cases to conduct adequately powered epidemiologic research. However, the authors assert that the findings of recent experimental and observational studies of TCE provide a strong rationale for developing multisite collaborations to address the potential influence of TCE and other solvents on the incidence of autoimmune disorders. Such research would be facilitated by the establishment of state and national autoimmune disease registries. Bob Weinhold http://www.medworm.com/index.php?rid=2385953&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2009%2F117-5%2Fss.html%23acle acle"> A Clearer View of TCE Evidence Supports Autoimmune Link More than 80 known or suspected autoimmune disorders�such as Crohn disease, multiple sclerosis, and rheumatoid arthritis�affect 5�8% of the U.S. population, according to the National Institute of Allergy and Infectious Diseases. The underlying causes of these disorders remain largely unknown, but one agent suspected to play a role is trichloroethylene (TCE), a solvent widely used in industrial and household applications. Researchers from the U.S. Environmental Protection Agency�s National Center for Environmental Assessment and the Medical University of South Carolina searched the scientific literature for studies linking TCE with selected immunologic connections, including immunosuppression, hypersensitivity, and a... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2385953 Fri, 01 May 2009 04:00:00 +0100 2385953 dram'> Dramatic Devices? Medical Procedures May Expose Infants to BPA The industrial chemical bisphenol A (BPA) is widely used to make polycarbonate plastic and epoxy resins. Low-level exposure to BPA has been shown to cause endocrine disruption in animal experiments, resulting in abnormal development of the prostate and mammary glands, among other adverse outcomes. Interpreting these studies with regard to human health has generated substantial debate, one heightened by growing awareness of the widespread nature of BPA exposure. In this report, researchers describe evidence of substantial exposure to BPA and other potential endocrine disruptors through medical treatment of premature infants [EHP 117:639�644; Calafat et al.]. In an earlier study by the same group [EHP 113:1222�1225 (2005)], urine samples were collected from 54 premature infants in neonatal intensive care units at two institutions. The infants required medical interventions such as ventilation, enteral feeding, parenteral feeding, and indwelling catheterization. Some of the medical devices used in these procedures contained the plasticizer di(2-ethylhexyl) phthalate (DEHP), and urine sample analysis revealed that concentrations of DEHP metabolites correlated with the relative intensity (low, medium, or high) of medical device use�that is, the variety, invasiveness, and duration of the procedure(s) that each infant underwent. In the current study, the team used some of those same urine samples to assess exposure to several other potential endocrine disruptors, including BPA, the antimicrobial triclosan, the preservatives methyl paraben and propyl paraben (found in personal care products), and benzophenone-3, a sunscreen agent. For each chemical, urinary concentrations of the free (unmetabolized) and total (both free and conjugated, or metabolized) compounds were measured. The detection of BPA and both parabens in the urine of all the samples analyzed suggested that all the infants had been exposed to those chemicals. Benzophenone-3 was detected in the urine of all but 2 infants, whereas triclosan was detected in only 8 infants. Urinary concentrations of BPA correlated with those of DEHP, suggesting a common pathway of exposure. Of the chemicals assessed in the current study, only BPA correlated significantly with the intensity of medical device use, although the authors have no information about whether or how BPA is used in these devices. The median urinary BPA concentration in these infants was almost 10 times higher than levels reported elsewhere for 6- to 11-year-old children in the general population. The fact that more than 90% of the BPA was conjugated suggests that premature infants are able to metabolize the compound even though metabolic pathways typically do not function at an adult level for some months after birth. The authors suggest that, given concerns over BPA toxicity and the demonstrated exposure, use of BPA-free products may be justified in this developmentally vulnerable population. Julia R. Barrett http://www.medworm.com/index.php?rid=2322242&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2009%2F117-4%2Fss.html%23dram In this report, researchers describe evidence of substantial exposure to BPA and other potential endocrine disruptors through medical treatment of premature infants [EHP 117:639�644; Calafat et al.]. In an earlier study by the same group [EHP 113:1222�1225 (2005)], urine samples were collected from 54 premature infants in neonatal intensive care units at two institutions. The infants required medical interventions such as ventilation, enteral feeding, parenteral feeding, and indwelling catheterization. Some of the medical devices used in these procedures contained the plasticizer di(2-ethylhexyl) phthalate (DEHP), and urine sample analysis revealed that concentrations of DEHP metabolites correlated with the relative intensity (low, medium, or high) of medical device use�that is, the... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2322242 Wed, 01 Apr 2009 04:00:00 +0100 2322242 ital'> It All Adds Up over Time Cumulative Lead Exposure and Cognition in Older Women Many older people in the U.S. population were chronically exposed to lead from paint and gasoline prior to the 1980s. To date, most of the research on lead and cognitive functioning in older age has focused on men, despite the fact that women live longer on average and therefore may be more likely to develop dementia over the course of their life span. Now, in a prospective look at a subset of data from the Nurses� Health Study�which began in 1976 and included 121,700 registered nurses aged 30�55 years�researchers report that even low-level cumulative lead exposure may exacerbate cognitive decline in older women [EHP 117:574�580; Weuve et al.]. The study looked at 587 women (now aged 47�74 years) who had undergone bone lead evaluations as part of two studies during the 1990s; to assess long-term exposures, bone lead concentrations were determined at each woman�s mid-tibial shaft (shin bone) and patella (kneecap). All but 6 of those individuals had also provided blood samples for assessment of more recent lead exposure. Trained interviewers conducted telephone interviews an average of 5 years after the lead measurements were taken to obtain cognitive data. The interviewers asked participants to perform a variety of tasks related to memory and verbal abilities. The researchers found a significant positive association between cognitive deficits and higher lead levels in the tibia but not in the patella or blood. Because the type of bone in the tibia is known to provide a longer record of lead exposure than other tissues, the research points to long-term exposure to lead�but not to current or recent exposures�as the most likely source of deterioration in cognitive functioning in this population. One standard deviation increase in lead exposure produced, on average, as much decrement in cognitive functioning as 3 years of aging in the women in the study. Lead may damage brain neurons through a range of mechanisms, including oxidative damage and programmed cell death. As the population of older adults grows, it becomes ever more critical to understand ways to ward off dementia. Clues to this understanding may come from studying subtle decreases in cognitive functioning, which, as several researchers have found, often precedes the development of dementia. If other studies confirm the observed relationship between cumulative lead exposure and impaired cognition, measures to minimize exposure or reduce the body�s lead burden could have a substantial impact on aging-related cognitive impairment. David J. Tenenbaum http://www.medworm.com/index.php?rid=2322239&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2009%2F117-4%2Fss.html%23ital ital"> It All Adds Up over Time Cumulative Lead Exposure and Cognition in Older Women Many older people in the U.S. population were chronically exposed to lead from paint and gasoline prior to the 1980s. To date, most of the research on lead and cognitive functioning in older age has focused on men, despite the fact that women live longer on average and therefore may be more likely to develop dementia over the course of their life span. Now, in a prospective look at a subset of data from the Nurses� Health Study�which began in 1976 and included 121,700 registered nurses aged 30�55 years�researchers report that even low-level cumulative lead exposure may exacerbate cognitive decline in older women [EHP 117:574�580; Weuve et al.]. The study looked at 587 women (now aged 47�74... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2322239 Wed, 01 Apr 2009 04:00:00 +0100 2322239 wide'> Widening the Pool of Factors Studies Needed to Assess Asthma�Swimming Link Several epidemiologic studies have suggested an association between childhood asthma and exposure to disinfection by-products (DBPs) in the swimming pool environment. In August 2007 a group of clinicians, epidemiologists, exposure scientists, pool operations experts, and analytical chemists met to discuss the literature on childhood asthma and swimming pools, and to develop recommendations for future research. In a review based on the results of that workshop, the authors state that current evidence, while suggestive, is inconclusive for an association with childhood asthma, and they point to several substantial data gaps that must be filled [EHP 117:500�507; Weisel et al.]. smog near a busy street A number of variables still must be studied in greater detail to better characterize exposure to pool-related chemicals. image: Benis Arapovic/Shutterstock The authors articulate several variables that must be measured in more detail to properly characterize inhalation exposure to chemicals around pools. The review calls for a comprehensive assessment of a substantially larger number of chemicals in the pool area than the limited number of DBPs studied to date. Earlier epidemiologic studies suggested trichloramine as a DBP of interest, but one 2007 study revealed previously unknown volatile DBPs in the air surrounding swimming pools. The frequency and extent of exposure to chemicals around pools also must be studied. In research to date, only simple exposure indices have been used, including whether the pool was indoors or outdoors, specific disinfection treatment, whether the child swam in or was simply present at an indoor pool, and cumulative duration of swimming. But to evaluate the breathing rate and DBP dose delivered to the lungs, more detailed, validated assessments of activity levels are needed. To obtain these data, the authors recommend that future studies use prospective questionnaires in which participants report their pool use and activity levels over time as they occur. The authors also point to the need for studies that define asthma cases in a rigorous, reproducible way, utilizing the International Study of Asthma and Allergy in Children questionnaire. Previous studies have often used clinical diagnoses, but this may be insufficient for epidemiologic studies because asthma is a heterogeneous disease with no single reliable diagnostic test. Additional needs include development and validation of new biomarkers for asthmatic reactivity and studies designed to refine guidelines for proper pool maintenance and disinfection to reduce levels of DBPs. The authors conclude this research area requires studies across multiple disciplines. Once chemicals of interest are identified, studies of the mechanisms behind the possible association�such as oxidative stress, inflammation, and changes in lung permeability�may be useful. But long-range prospective studies starting in early childhood will be needed to better gauge the relationship between swimming pools and childhood asthma. Absent conclusive studies, the authors say children�s exposures should be minimized. Pool managers must be well educated about pool chemistry so they can understand the potential dangers of disinfectants and DBPs. Swimmers, too, must be educated about the need for proper pool hygiene (for example, showering before swimming and not urinating in the pool), as swimmer hygiene can affect the formation of DBPs and the amount of disinfectant used. Angela Spivey http://www.medworm.com/index.php?rid=2322236&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2009%2F117-4%2Fss.html%23wide wide"> Widening the Pool of Factors Studies Needed to Assess Asthma�Swimming Link Several epidemiologic studies have suggested an association between childhood asthma and exposure to disinfection by-products (DBPs) in the swimming pool environment. In August 2007 a group of clinicians, epidemiologists, exposure scientists, pool operations experts, and analytical chemists met to discuss the literature on childhood asthma and swimming pools, and to develop recommendations for future research. In a review based on the results of that workshop, the authors state that current evidence, while suggestive, is inconclusive for an association with childhood asthma, and they point to several substantial data gaps that must be filled [EHP 117:500�507; Weisel et al.]. A number of variables st... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2322236 Wed, 01 Apr 2009 04:00:00 +0100 2322236 from'> From Dust to Blood Studies Predict Lead Intake in Children Lead concentrations in U.S. children�s blood have decreased markedly in recent decades, thanks largely to lower industrial emissions, voluntary elimination of lead solder in food cans, and legislation barring lead from gasoline and new paint. The main source of lead exposure for today�s children is deteriorating lead-based paint, which contributes to lead-laden dust in older homes. Two studies, the first of their kind to use nationally representative data from U.S. homes, predict how varying degrees of lead contamination of floor and windowsill dust may affect the blood lead levels of resident children [EHP 117:461�467; Gaitens et al.; EHP 117:468�474; Dixon et al.]. Despite reductions in child blood lead levels, the U.S. Centers for Disease Control and Prevention (CDC) estimates on the basis of 1999�2002 data that some 310,000 children still have levels above the agency�s threshold of concern, 10 �g/dL. Such children are at increased risk for cognitive impairment and behavioral problems. Mounting evidence [e.g., EHP 116:243�248 (2008)] has linked even lower blood lead levels with adverse effects. The current studies examined lead- and housing-related data for a nationally representative group of 2,155 children aged 1�5 years, drawn from the National Health and Nutrition Examination Survey (NHANES) from 1999 through 2004. In addition to blood lead data, dust samples had been collected from floors and windowsills in the children�s homes and analyzed for lead content. The study by Gaitens et al. showed that dust lead levels in the great majority of homes met or exceeded federal standards: just 0.16% of homes failed the standard for floors of 40 �g/ft2, and 4.0% failed the standard for windowsills of 250 �g/ft2. Income, race/ethnicity, floor condition, windowsill dust lead content, year of home construction, recent renovation, smoking, and survey year all were significant predictors of floor dust lead loading, which was more predictive than windowsill dust lead of elevated blood lead in residents. Dixon et al. examined blood lead levels for the same 2,155 children and used a linear regression model to predict children�s blood lead given a range of floor dust lead concentrations from very low (0.25 �g/ft2) up to the federal standard of 40 �g/ft2. Based on logistic regression models, the authors estimated that among children living in pre-1978 homes with floor dust lead levels of 12 �g/ft2, 4.6% would have a blood lead level of at least 10 �g/dL, whereas 27% would have a level of at least 5 �g/dL. Because the blood lead and dust lead levels observed in the NHANES data set were relatively low, the researchers verified the models� predictive capacity by analyzing data from three high-risk populations with higher levels of both blood lead and floor dust lead than those observed in NHANES. The studies indicate that most U.S. homes already meet federal standards for floor and windowsill dust lead levels, but also suggest that further tightening of the standards would afford greater protection for today�s children. However, although data for both studies came from a nationally representative sample of children, the homes may not necessarily represent the U.S. housing stock. The authors cite the need for an integrated health and housing survey that is representative of both the population and the housing stock, similar to surveys recently conducted in Europe. Rebecca Kessler http://www.medworm.com/index.php?rid=2256369&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2009%2F117-3%2Fss.html%23from from"> From Dust to Blood Studies Predict Lead Intake in Children Lead concentrations in U.S. children�s blood have decreased markedly in recent decades, thanks largely to lower industrial emissions, voluntary elimination of lead solder in food cans, and legislation barring lead from gasoline and new paint. The main source of lead exposure for today�s children is deteriorating lead-based paint, which contributes to lead-laden dust in older homes. Two studies, the first of their kind to use nationally representative data from U.S. homes, predict how varying degrees of lead contamination of floor and windowsill dust may affect the blood lead levels of resident children [EHP 117:461�467; Gaitens et al.; EHP 117:468�474; Dixon et al.]. Despite reductions in child blood lead levels... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2256369 Sun, 01 Mar 2009 05:00:00 +0100 2256369 prot'> Protein Baggage Toxicity of Organotin Tied to Proteasome Interference Organotins have been widely used as agricultural pesticides, antifungal agents, polyvinyl chloride stabilizers, industrial catalysts, and antifouling additives in boat paints. These tin-based chemicals, which have been detected in various environmental media, are lipophilic and thus capable of becoming increasingly concentrated as they pass up the food chain. A new study suggests that the toxic effects of organotins on living cells are mediated in part by inhibiting the function of the proteasome, a molecular structure that degrades unneeded or damaged proteins [EHP 117:379�386; Shi et al.]. In eukaryotic organisms (animals, plants, fungi, algae, and plankton), more than 80% of intracellular proteins are degraded through the proteasome-mediated pathway. By interfering with proteasome function, organotins enable proteins to accumulate inappropriately. Because normal immune function and many cellular processes depend on the proteasome pathway, the organotin�proteasome interaction could help explain some of the adverse health effects of organotins�notably endocrine disruption, infertility, and immune dysfunction�that have been observed in wildlife and in animal studies. In addition, human exposure to organotins has been proposed as a possible risk factor for cancer (by inhibiting the cytotoxic function of natural killer cells), neurotoxicity, obesity, allergies, asthma, and altered reproductive development. The researchers provide several lines of evidence suggesting that triphenyltin (TPT), a common organotin, binds to and blocks the activity of the proteasome by irreversibly inhibiting its protein-degrading activity. TPT was shown to have greater potency in this regard than seven other organotins examined by the authors. The investigators deduced that the tin present in TPT interacts with the N-terminal threonine of the proteasomal 5 subunit, possibly providing a specific target for organotins. Organotins have long been known to induce necrosis; the authors propose this may occur through caspase-dependent, DNA damage�independent cell death. In addition, the researchers assert that organotins most likely kill cells via a p53-independent pathway. The new findings suggest that other previously identified potential targets of organotins, such as the transcription factor NF B and the pro-apoptotic protein Bax, might be downstream of proteasome inhibition. The investigators further posit that inhibition of aromatase activity observed in organotin-exposed humans and animals�an effect linked to altered reproductive development�may be due to proteasome inhibition because such inhibition causes up-regulation of factors that suppress transcription of the hCYP19/aromatase gene. M. Nathaniel Mead http://www.medworm.com/index.php?rid=2256368&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2009%2F117-3%2Fss.html%23prot prot"> Protein Baggage Toxicity of Organotin Tied to Proteasome Interference Organotins have been widely used as agricultural pesticides, antifungal agents, polyvinyl chloride stabilizers, industrial catalysts, and antifouling additives in boat paints. These tin-based chemicals, which have been detected in various environmental media, are lipophilic and thus capable of becoming increasingly concentrated as they pass up the food chain. A new study suggests that the toxic effects of organotins on living cells are mediated in part by inhibiting the function of the proteasome, a molecular structure that degrades unneeded or damaged proteins [EHP 117:379�386; Shi et al.]. In eukaryotic organisms (animals, plants, fungi, algae, and plankton), more than 80% of intracellular proteins are de... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2256368 Sun, 01 Mar 2009 05:00:00 +0100 2256368 toug'> Tough Call Challenges to Assessing Cancer Effects of Mobile Phone Use Mobile phone use worldwide has exploded in the past decade, with many countries fast approaching a usage prevalence of 100%. Even as mobile phone use grows exponentially, questions remain regarding the health impact of frequent exposure to the electromagnetic fields (EMFs) associated with mobile phone use. A review of 33 peer-reviewed epidemiologic studies suggests that a number of study design issues may result in an underestimate of the relative risk of brain tumors among mobile phone users [EHP 117:316-324; Kundi]. smog near a busy street A review of mobile phone use and cancer reveals areas where study design can be strengthened. image: Corbis Recall bias is a widely cited concern that could lead to biased risk estimates in case�control studies of ipsilateral exposure (i.e., tumors occurred on the same side of the head where the phone was usually held); the review author notes that cancer patients may tend to either attribute their disease to their mobile phone use or to dismiss a relationship between the two. But ipsilateral risks also carry greater biologic plausibility, since one 2008 study showed that nearly 99% of the total electromagnetic energy deposited in the brain is absorbed at the side of the head where the phone is held during calls. According to the author�s analysis, more than half of mobile phone users among cases and none among controls would have to incorrectly identify which ear they usually hold their phone to in order to nullify the observed increased risk. Another source of potential bias concerns the comparison groups used. In the widely cited Interphone study, a case�control study spanning 13 countries, the unexposed group included people who used cordless phones. However, according to the author, cordless and mobile phones users receive about the same EMF exposure, and cordless phones are generally used for longer periods of time than mobile phones. This may help explain why Interphone has consistently reported either no effect or even a protective effect of mobile phone use. Finally, methods of data acquisition, which have differed substantially between Interphone and other studies, may also introduce bias. Memory performance may be altered in patients with aggressive gliomas, malignant brain tumors that have been associated with mobile phone use in some studies. The author also suggests that exposure assessment may be biased if conducted by phone interviews (as in the Interphone study) compared with the mailed questionnaire method. According to the review author, results of the research to date suggest an association between mobile phone use and glioma risk that falls in the range of magnitude delineated for passive smoking and lung cancer. Confidence in a causal relationship is bolstered by two key findings: longer latencies are associated with higher risk estimates, and living in a rural area�where mobile phones typically radiate at higher intensities�also is associated with elevated risk. Even a modest cancer risk could have major public health implications because of the vast number of mobile phone users. On the other hand, as this review points out, the individual risk perspective is less dramatic: in industrialized countries, the prevailing life-time brain tumor risk is 4�8 per 1,000, and thus individual risk is still low if mobile phone use increases the risk even 50% to 6�12 per 1,000. M. Nathaniel Mead http://www.medworm.com/index.php?rid=2256367&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2009%2F117-3%2Fss.html%23toug toug"> Tough Call Challenges to Assessing Cancer Effects of Mobile Phone Use Mobile phone use worldwide has exploded in the past decade, with many countries fast approaching a usage prevalence of 100%. Even as mobile phone use grows exponentially, questions remain regarding the health impact of frequent exposure to the electromagnetic fields (EMFs) associated with mobile phone use. A review of 33 peer-reviewed epidemiologic studies suggests that a number of study design issues may result in an underestimate of the relative risk of brain tumors among mobile phone users [EHP 117:316-324; Kundi]. A review of mobile phone use and cancer reveals areas where study design can be strengthened. image: Corbis Recall bias is a widely cited concern that could lead to biased risk estimates in ... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2256367 Sun, 01 Mar 2009 05:00:00 +0100 2256367 doub'> Double Trouble Flu Intensifies Effects of Ozone Environmental health scientists have long speculated that the influenza virus could intensify the pulmonary effects of air pollution or vice versa. Like air pollution, influenza affects primarily the respiratory system, and ambient air pollutants may either lower resistance to viral infection or provide a vehicle that facilitates the spread of the virus, or both. There have been a number of laboratory-based animal studies on this potential relationship but no epidemiologic research. Researchers at the University of Hong Kong, in the first study of the influenza?air pollution interaction in humans, now report that respiratory hospitalizations and mortality significantly increased when ozone (O3) levels rose during flu season [EHP 117:248?253; Wong et al.]. smog near a busy street Influenza appeared to exacerbate the health effects of ozone pollution in Hong Kong. image: Mike Clarke/AFP/Getty Images The authors conducted a retrospective population-based study focusing on hospitalization and mortality rates for respiratory and cardiovascular disease. Medical data on patients diagnosed with respiratory or cardiovascular disease between 1996 and 2002 came from 14 Hong Kong hospitals. The authors determined ?influenza intensity? during the same period as the percentage of respiratory specimens that tested positive for influenza each week. The Hong Kong Environmental Protection Department provided data on average daily concentrations of nitrogen dioxide (NO2), sulfur dioxide (SO2), particulate matter smaller than 10 ?m (PM10), and O3. As O3 levels increased during times of high influenza intensity, so did the number of hospitalizations and deaths from respiratory disease. The association was stronger in women than men, the researchers reported. There was no significant relationship between O3 and cardiovascular disease hospitalizations or mortality, and the data reflected no significant modification by influenza on the health effects of the other pollutants studied. Hong Kong has two flu seasons, peaking in January?February and May?July. O3 levels in Hong Kong typically peak in the sunniest months of September?December, when ultraviolet radiation reacts with nitrogen oxides and volatile organic compounds to form the noxious gas. A surprising finding was a decrease in hospitalization for respiratory illness when peak PM10 concentrations coincided with flu outbreaks, whereas PM10 increases at other times were associated with increased hospitalizations. The researchers hypothesize that PM10 may diminish the flu effect by limiting the amount of ultraviolet light entering the atmosphere, which in turn would reduce the production of ozone. The authors found weak interactions between influenza and both NO2 and SO2, but cautioned against drawing conclusions about individual pollutants that react in the atmosphere. NO2, for example, can combine with oxygen to form O3. The researchers propose that future studies focus on influenza?s potential interactions with a combination of pollutants in the atmosphere. Cynthia Washam http://www.medworm.com/index.php?rid=2152379&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2009%2F117-2%2Fss.html%23doub doub"> Double Trouble Flu Intensifies Effects of Ozone Environmental health scientists have long speculated that the influenza virus could intensify the pulmonary effects of air pollution or vice versa. Like air pollution, influenza affects primarily the respiratory system, and ambient air pollutants may either lower resistance to viral infection or provide a vehicle that facilitates the spread of the virus, or both. There have been a number of laboratory-based animal studies on this potential relationship but no epidemiologic research. Researchers at the University of Hong Kong, in the first study of the influenza?air pollution interaction in humans, now report that respiratory hospitalizations and mortality significantly increased when ozone (O3) levels rose during flu season [EHP 11... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2152379 Sun, 01 Feb 2009 05:00:00 +0100 2152379 phth'> Phthalates in Prescription Drugs Some Medications Deliver High Doses Until recently, most of the concern surrounding the health risks of phthalates has focused on the use of these plasticizers in toys, personal care products, food packaging, and medical equipment such as intravenous tubing. A case report in 2004 raised the possibility that certain prescription medications may also be a source of phthalate exposure for some people [EHP 112:751?753 (2004)]. That finding prompted a systematic investigation that links phthalate-containing medications with high internal exposure to these chemicals [EHP 117:185?189; Hern?ndez-D?az et al.]. The 2004 case study pinpointed Asacol?, a medication for treating ulcerative colitis, as a probable source of phthalate exposure. Asacol is covered with an enteric coating of dibutyl phthalate (DBP) that prevents the medication from degrading before it reaches the small intestine. Concentrations of the main metabolite of DBP in the urine of the case study subject corresponded to an uptake of DBP exceeding by two orders of magnitude the 95th percentile reported by the Centers for Disease Control and Prevention in the general population. The concentrations also surpassed the reference dose established for DBP by the U.S. Environmental Protection Agency (EPA) on the basis of animal testing. To assess possible links between phthalate-containing prescription medication usage and excreted metabolites, the investigators searched National Health and Nutrition Examination Survey (NHANES) data from survey periods between 1999 and 2004 when urine samples were tested for phthalate metabolites and participants were asked about their use of prescription medications. Various enteric-coated medications identified as likely to contain phthalates included mesalamine (the generic form of Asacol), didanosine (an antiretroviral agent), omeprazole (which inhibits gastric acid secretion), and theophylline (used to treat asthma and other lung diseases). Among the 6 documented mesalamine users, average urine concentrations of DBP metabolites were 50 times higher than those of nonusers. For 2 of the 6 mesalamine users, the DBP metabolite concentrations pointed to uptake exceeding the EPA?s reference dose. Users of the other phthalate-containing medications also had significantly higher concentrations of some metabolites than did nonusers, though the gaps between users and nonusers were considerably smaller than for mesalamine. The NHANES data also showed that at least 3 women who reported taking phthalate-containing medications were pregnant. These findings call for more investigation, the authors write, particularly because some phthalates cross the placenta and cause reproductive and developmental effects in laboratory animals. In one study of male infants, increasing prenatal exposure to background levels of phthalates was associated with a decrease in the distance between the anus and base of the penis, indicating incomplete male reproductive development [EHP 113:1056?1061 (2005)]. The authors of the new study write that phthalate-containing medications are among some of the most widely prescribed drugs in the United States, which implies that many people, including pregnant women, may be exposed to high concentrations of phthalates. Kellyn S. Betts http://www.medworm.com/index.php?rid=2152378&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2009%2F117-2%2Fss.html%23phth phth"> Phthalates in Prescription Drugs Some Medications Deliver High Doses Until recently, most of the concern surrounding the health risks of phthalates has focused on the use of these plasticizers in toys, personal care products, food packaging, and medical equipment such as intravenous tubing. A case report in 2004 raised the possibility that certain prescription medications may also be a source of phthalate exposure for some people [EHP 112:751?753 (2004)]. That finding prompted a systematic investigation that links phthalate-containing medications with high internal exposure to these chemicals [EHP 117:185?189; Hern?ndez-D?az et al.]. The 2004 case study pinpointed Asacol?, a medication for treating ulcerative colitis, as a probable source of phthalate exposure. Asacol is covere... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2152378 Sun, 01 Feb 2009 05:00:00 +0100 2152378 game'> Gamete Gamble Phthalate Alters Germ Cell Development Di-2-ethylhexyl phthalate (DEHP), one of the most abundant phthalates produced, has been incorporated into flexible plastic products such as food containers and packaging, toys, medical equipment, and home and garden products. DEHP is being phased out of some products because of growing concern about its potential health effects. A French team has now established the first tangible link between one phthalate, the DEHP metabolite mono-2-ethylhexyl phthalate (MEHP), and altered human germ cell development [EHP 117:32?37; Lambrot et al.]. The French team acquired testes from morphologically normal fetuses of women undergoing legal abortion during weeks 7 to 12 of gestation. Using an organotypic culture system, they exposed the testes for 3 days to one of three concentrations of MEHP: 10?6, 10?5, or 10?4 M. The highest concentration was 2 orders of magnitude higher than that known by the authors to occur in humans; the lowest was the same order of magnitude as that found in human milk in Finland, which reached 1,410 ?g/L. Biomonitoring data for 2005 published by the Centers for Disease Control and Prevention (CDC) showed that MEHP in the urine of U.S. residents reached 52.1 ?g/L (or 10?8 M). At the highest concentration, the authors found that exposure reduced germ cell numbers by 40%. The sharp reduction occurred via an increase in apoptosis, or programmed cell death, without any effect on proliferation. The authors note that the plunge in numbers is crucial because the germ cells formed during fetal life?which will go on to become ova or sperm?help determine adult fertility. The highest concentration of MEHP also significantly reduced the messenger RNA expression of anti-M?llerian hormone, which plays a key role in the development of certain cells into male reproductive organs, usually during week 8 of fetal development. The lowest concentration of MEHP tested didn?t show adverse effects for the pathways analyzed. The general population is routinely exposed to many types of phthalates, with at least one metabolite, monoethyl phthalate, documented in urine by the CDC at concentrations of 10?6 M. The authors suggest that researchers should investigate additional phthalates and interactive effects, other concentrations and periods of exposure, different time periods of fetal development, and additional pathways. They also note that their findings conflict with some results from animal studies. For instance, there were no MEHP effects on testosterone production in this study, but testosterone suppression has occurred in rats exposed to phthalates. Such discrepancies may be due to differences between species, they say. Bob Weinhold http://www.medworm.com/index.php?rid=2072302&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2009%2F117-1%2Fss.html%23game game"> Gamete Gamble Phthalate Alters Germ Cell Development Di-2-ethylhexyl phthalate (DEHP), one of the most abundant phthalates produced, has been incorporated into flexible plastic products such as food containers and packaging, toys, medical equipment, and home and garden products. DEHP is being phased out of some products because of growing concern about its potential health effects. A French team has now established the first tangible link between one phthalate, the DEHP metabolite mono-2-ethylhexyl phthalate (MEHP), and altered human germ cell development [EHP 117:32?37; Lambrot et al.]. The French team acquired testes from morphologically normal fetuses of women undergoing legal abortion during weeks 7 to 12 of gestation. Using an organotypic culture system, they exposed the t... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2072302 Thu, 01 Jan 2009 05:00:00 +0100 2072302 pcbs'> PCBs Make Their Mark Review Pinpoints Cognitive Profile of Prenatal Exposure Prenatal exposure to polychlorinated biphenyls (PCBs) impairs cognitive development in infants and children, according to numerous studies of these ubiquitous environmental pollutants. Studies of PCB damage have considered many different end points, but the results of these different studies have never been coordinated to pinpoint the neuropsychologic functions most likely to be damaged by prenatal exposure to PCBs. However, a review of longitudinal birth cohort studies in the medical literature reveals that impairment of executive functions?high-order brain processes responsible for planning, flexible thinking, abstract reasoning, problem solving, and inhibition of inappropriate actions?most consistently reflects prenatal PCB exposure [EHP 117:7?16; Boucher et al.]. The review authors selected nine longitudinal birth cohort studies performed between 1959 to 2008 in North America, Europe, and Japan. Consumption of fish, whale blubber, and dairy products by pregnant women was the main source of prenatal PCB exposure as reflected by maternal serum concentrations that ranged from 23 to 450 ng/g of fat. All combined, about 4,000 children were monitored at different ages, from as early as 3 months to as late as 11 years, depending on the study. The types of tests conducted in the various studies included assessments of mental and psychomotor development of infants, IQ tests, and specific measures of verbal skills, visual?spatial ability, memory, attention, and executive functions. No one study measured all these neuropsychologic skills. Such a comprehensive evaluation would require a battery of complicated and expensive procedures. The overall analysis found that executive functions are especially sensitive to PCB exposure. Three studies involving about 1,000 children specifically documented executive functions, and they all found that poor response inhibition was consistently related to prenatal PCB exposure. In one of these studies, children were exposed to some of the lowest doses of PCBs among the reviewed cohorts. Some of the studies reported that processes similar to executive functions?such as task planning, speed of information processing, verbal abilities, and visual recognition memory?were negatively impacted by prenatal exposure to PCBs as well. The authors conclude that executive functions in particular should be assessed in future cohort studies of the neurotoxic effects of PCBs and other organochlorine compounds. Carol Potera http://www.medworm.com/index.php?rid=2072301&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2009%2F117-1%2Fss.html%23pcbs pcbs"> PCBs Make Their Mark Review Pinpoints Cognitive Profile of Prenatal Exposure Prenatal exposure to polychlorinated biphenyls (PCBs) impairs cognitive development in infants and children, according to numerous studies of these ubiquitous environmental pollutants. Studies of PCB damage have considered many different end points, but the results of these different studies have never been coordinated to pinpoint the neuropsychologic functions most likely to be damaged by prenatal exposure to PCBs. However, a review of longitudinal birth cohort studies in the medical literature reveals that impairment of executive functions?high-order brain processes responsible for planning, flexible thinking, abstract reasoning, problem solving, and inhibition of inappropriate actions?most consistent... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2072301 Thu, 01 Jan 2009 05:00:00 +0100 2072301 extr'> Extra Protection for Pregnant Women Calcium Supplement Reduces Blood Lead Lead, like calcium, is stored in bones and generally does not circulate throughout the body. But the demands of pregnancy and lactation trigger the release of calcium, which also releases lead into the maternal blood stream. Researchers previously showed that daily calcium supplementation during lactation reduced maternal blood lead by 15?20% and lead in breast milk by 5?10%. A new study by the same team shows that taking inexpensive calcium supplements daily also reduces blood lead levels during pregnancy [EHP 117:26?31; Ettinger et al.]. Such supplementation could help mitigate the adverse effects of prenatal lead exposure, which include low birth weight, lower intelligence scores, and impaired motor and visual skills. woman cooking a tortilla on pottery The greatest reduction in blood lead was seen in women who were most compliant with the calcium regimen and who used lead-glazed pottery. image: Danita Delimont/Alamy The study included 557 women recruited in the first trimester of pregnancy from prenatal clinics in Mexico City. The women were recruited from 2001 to 2003; Mexico completed the phase-out of leaded gasoline in 1997, so women enrolled in the study had been exposed for many years to high environmental lead levels prior to becoming pregnant. In addition, just over one-third of the women used the traditional lead-glazed pottery that is common in Mexico. Half the women received 1,200 mg of calcium daily and the others received placebos. Blood lead levels were checked in the first (baseline), second, and third trimesters of pregnancy. The Mexican women enrolled in the current study had an estimated average dietary calcium intake of 900 mg per day, which parallels national surveys of U.S. women. (The U.S. Institute of Medicine advises 1,000 mg of calcium daily for pregnant and lactating women aged 19?50 years and 1,300 mg/day for pregnant and lactating women under age 19 years.) Blood lead levels declined more in the second trimester than in the third, with reductions averaging 14% and 8%, respectively. Women who were more compliant with the calcium regimen had higher reductions in blood lead relative to the placebo group. The most compliant women?those who took at least 75% of their calcium supplements?showed a 24% drop in blood lead levels over the course of pregnancy, with the greatest reduction (31%) occurring in women who were most compliant and who also cooked, served, or stored food in lead-glazed pottery, and who had the highest bone lead levels. The investigators conclude that calcium supplements should be considered as a low-risk, cost-effective means for lowering fetal lead exposure. Carol Potera http://www.medworm.com/index.php?rid=2072300&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2009%2F117-1%2Fss.html%23extr extr"> Extra Protection for Pregnant Women Calcium Supplement Reduces Blood Lead Lead, like calcium, is stored in bones and generally does not circulate throughout the body. But the demands of pregnancy and lactation trigger the release of calcium, which also releases lead into the maternal blood stream. Researchers previously showed that daily calcium supplementation during lactation reduced maternal blood lead by 15?20% and lead in breast milk by 5?10%. A new study by the same team shows that taking inexpensive calcium supplements daily also reduces blood lead levels during pregnancy [EHP 117:26?31; Ettinger et al.]. Such supplementation could help mitigate the adverse effects of prenatal lead exposure, which include low birth weight, lower intelligence scores, and impaired motor and... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2072300 Thu, 01 Jan 2009 05:00:00 +0100 2072300 bisp'> Bisphenol A Suppresses Release of Adipose Hormone Exposure May Contribute to Metabolic Syndrome Bisphenol A (BPA), a chemical used in the manufacture of numerous consumer products, is ubiquitous throughout the environment, and its widespread presence in human serum has been well documented. Although animal research indicates that BPA can alter several metabolic functions, interpretation of human data has been more controversial. A new study now presents evidence confirming that exposure of human adipose tissue and isolated fat cells to environmentally relevant levels of BPA suppresses release of the hormone adiponectin [EHP 116:1642?1647; Hugo et al.]. A high-calorie diet and sedentary lifestyle have both traditionally been linked to metabolic syndrome?the presence of a constellation of metabolic risk factors including insulin resistance, hypertension, and elevated blood sugar and lipid levels?but researchers are now examining environmental factors as additional causes. Adiponectin increases insulin sensitivity and reduces tissue inflammation, so suppression of its release could lead to insulin resistance and increased susceptibility to metabolic syndrome, the authors write. The study examined three types of adipose tissue samples taken during breast reduction, abdominoplasty, and gastric bypass surgery. The research team incubated each type of tissue for 6 hours in BPA or estradiol (E2), an endogenous human estrogen. They used enzyme-linked immunosorbent assay to measure secreted adiponectin. They also used quantitative real-time polymerase chain reaction to compare the expression of estrogen receptors?and estrogen-related receptors in these tissues. In all three tissue types, exposure to low-nanomolar concentrations of BPA suppressed adiponectin as effectively or more effectively compared with equimolar concentrations of E2. The authors also showed that the dose response to BPA was nonmonotonic, meaning lower doses caused different effects than higher doses. Finally, they report for the first time similar mRNA expression levels for several estrogen receptors in visceral adipose tissue, although the role of these receptors in the suppressive nature of BPA and E2?has yet to be determined. The results of the data are limited by the relatively small sample size in each tissue category, as well as the potential unknown effects of age or obesity on tissue responsiveness. However, the authors write that their data present clear evidence that BPA suppresses adiponectin, potentially leading to a much higher risk of developing metabolic syndrome and its resultant adverse health effects. They conclude that with BPA's persistence in the environment, more research should be done to determine the mechanism by which the chemical suppresses adiponectin. Tanya Tillett http://www.medworm.com/index.php?rid=2004074&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2008%2F116-12%2Fss.html%23bisp bisp"> Bisphenol A Suppresses Release of Adipose Hormone Exposure May Contribute to Metabolic Syndrome Bisphenol A (BPA), a chemical used in the manufacture of numerous consumer products, is ubiquitous throughout the environment, and its widespread presence in human serum has been well documented. Although animal research indicates that BPA can alter several metabolic functions, interpretation of human data has been more controversial. A new study now presents evidence confirming that exposure of human adipose tissue and isolated fat cells to environmentally relevant levels of BPA suppresses release of the hormone adiponectin [EHP 116:1642?1647; Hugo et al.]. A high-calorie diet and sedentary lifestyle have both traditionally been linked to metabolic syndrome?the presence of a constel... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2004074 Mon, 01 Dec 2008 05:00:00 +0100 2004074 amea'> A Measure for Mothers Model Predicts Lactational Transfer of PCB-153 Breastfed infants sit at the top of the food chain for the simple reason that their nourishment comes from other humans. Through biomagnification, environmental chemicals such as polychlorinated biphenyls (PCBs) are passed up the food chain to the nursling. Although epidemiologic studies have established an association between prenatal PCB exposures and neurodevelopmental and neurobehavioral problems, the potential health risks of xenobiotic exposures via human milk are less clear and remain an area of intense research interest [see 'Contaminants in Human Milk: Weighing the Risks against the Benefits of Breastfeeding,' EHP 116:A426?A434 (2008)]. Researchers have now developed a physiologically based pharmacokinetic model of PCB-153 in women to predict the transfer of this compound via lactation [EHP 116:1629?1634; Redding et al.]. PCB-153 was selected for study because it is the most prevalent PCB congener in human tissues. To predict the concentration of PCB-153 in human milk, physiological parameters were obtained from a Taiwanese cohort and from reference values in published studies. Partition coefficients were estimated based on chemical structure and the lipid content in various body tissues as reported in the literature: liver, fat, mammary tissue, and the 'rest of the body' (an average of brain, skin, and muscle), as well as a mixed blood compartment. The investigators predicted the acquired body burden of PCB-153 from birth over a 25-year period on the basis of estimates of exposure via diet using data from Japanese population studies. They then compared the model's predictions with measurements from published studies in multiple countries. Blood and tissue concentrations for a 25-year-old woman generated by the model were found to fall within ranges reported in the literature, assuming that dietary intake of PCB-153 was the principal source of this chemical in human milk. Additionally, the researchers demonstrated the use of the model for reverse dosimetry, also referred to as 'exposure reconstruction,' for possible exposure scenarios in Canadian Inuits, who consume extremely high levels of PCB-153 through their traditional high-fat diet. This human, population-scale lactational model for PCB-153 is the first to successfully predict a range of results that encompass human biomonitoring data of milk PCB-153 content from all over the world. The primary value of this model will be its ability to describe the distribution, absorption, metabolism, and elimination of PCB-153 in nursing women. The new tool could also be useful for reverse dosimetry modeling to enable retrospective analyses of potential health effects of PCB exposures in breastfed individuals. M. Nathaniel Mead http://www.medworm.com/index.php?rid=2004073&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2008%2F116-12%2Fss.html%23amea amea"> A Measure for Mothers Model Predicts Lactational Transfer of PCB-153 Breastfed infants sit at the top of the food chain for the simple reason that their nourishment comes from other humans. Through biomagnification, environmental chemicals such as polychlorinated biphenyls (PCBs) are passed up the food chain to the nursling. Although epidemiologic studies have established an association between prenatal PCB exposures and neurodevelopmental and neurobehavioral problems, the potential health risks of xenobiotic exposures via human milk are less clear and remain an area of intense research interest [see "Contaminants in Human Milk: Weighing the Risks against the Benefits of Breastfeeding," EHP 116:A426?A434 (2008)]. Researchers have now developed a physiologically based pharmacokin... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2004073 Mon, 01 Dec 2008 05:00:00 +0100 2004073 angl'> Angling for Thyroid Answers Study Links PBDEs to Hormone Disruption in Male Sport-Fish Consumers Levels of polybrominated diphenyl ethers (PBDEs) measured in human samples have increased in recent years, but the health effects of these compounds are not well studied. A group of persistent pollutants similar in structure to polychlorinated biphenyls (PCBs), PBDEs are thought to affect endocrine function, but this relationship has only been examined in several small studies. A new study significantly expands this knowledge base by analyzing PBDE exposure among a large cohort of male sport-fish consumers and concluding that these exposures are associated with increased thyroglobulin antibodies and increased thyroxine (T4) in adult males independent of PCB exposure [EHP 116:1635?1641; Turyk et al.]. man fishing in Lake Michigan EPA data show that contaminant levels in fish from Lake Michigan (above) and the other Great Lakes, while still high, have declined consistently since 1990. image: Bill Raboin/iStockphoto The study examined 405 adult males who consumed sport fish from the Great Lakes during the early 1990s. Researchers gathered data on the subjects' levels of fish consumption, medical diseases, and use of medications, and took serum samples that were tested for PBDEs, PCBs, and DDE, a metabolite of DDT that may affect thyroid hormones. Total and free T4 and triiodothyronine (T3) were measured in serum and urine. PBDE concentrations were positively associated with increased T4 and reverse T3, and inversely correlated with total T3 and thyroid-stimulating hormone (TSH). In addition, PBDEs were positively related to the percentage of T4?bound to albumin, a carrier protein. An observed increase in thyroglobulin antibodies in men with the highest PBDE exposures may indicate an increased susceptibility to autoimmune thyroiditis among people who have been exposed to PBDEs, according to the authors. The findings of a positive association of PBDEs with T4 are not consistent with results of animal studies that have shown decreased T4?in rats and mice exposed to PBDE. However, the results do align with those of several smaller human studies. The authors speculate the disparity may be attributable to the fact that, while thyroid hormone regulation is similar among vertebrates, some functions differ by species. A major strength of the study is the measurement of the effects of PBDEs on multiple hormones and the consideration of other environmental exposures that can affect thyroid hormones. The authors point out that their findings provide a rationale for future mechanistic studies related to PBDE exposure, including how those exposures may be linked to changes in thyroid hormone metabolism and binding of T4 to serum-binding proteins. Also needed, they write, are larger studies to determine whether PBDE exposure is related to thyroid disease in human populations. Richard Dahl http://www.medworm.com/index.php?rid=2004072&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2008%2F116-12%2Fss.html%23angl angl"> Angling for Thyroid Answers Study Links PBDEs to Hormone Disruption in Male Sport-Fish Consumers Levels of polybrominated diphenyl ethers (PBDEs) measured in human samples have increased in recent years, but the health effects of these compounds are not well studied. A group of persistent pollutants similar in structure to polychlorinated biphenyls (PCBs), PBDEs are thought to affect endocrine function, but this relationship has only been examined in several small studies. A new study significantly expands this knowledge base by analyzing PBDE exposure among a large cohort of male sport-fish consumers and concluding that these exposures are associated with increased thyroglobulin antibodies and increased thyroxine (T4) in adult males independent of PCB exposure [EHP 116:1635?164... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=2004072 Mon, 01 Dec 2008 05:00:00 +0100 2004072 grow'> Growing Weight of OP Evidence Parathion Linked to Metabolic Effects in Rats Parathion and other organophosphate pesticides, the most widely used class of insecticides, have long been known as neurotoxicants but were only recently linked to metabolic disorders. A new study adds to the growing evidence that parathion may be contributing to epidemics of obesity and diabetes [EHP 116:1456?1462; Lassiter et al.]. Obesity and type 2 diabetes have surged in recent decades to the point where two-thirds of U.S. adults are now overweight and approximately 26% have diabetes or prediabetes (elevated fasting blood glucose level below the level considered diabetic). These conditions also are increasing in children, and a growing body of evidence suggests that perinatal exposures to a variety of compounds may have a significant impact on metabolic programming. The authors were prompted to focus on the role of pesticides in these conditions after noting that subpopulations with the highest rates of diabetes and obesity?impoverished residents of inner cities and residents of farming communities?also tended to have the highest pesticide exposures. The researchers chose parathion as a representative organophosphate. Rats received daily injections of the compound during their first 4 days of life, a developmental period that corresponds to the second to early third trimester in human gestation. Half the treated rats were given a dose (0.1 mg/kg/day) just below the threshold for symptoms of exposure. The other half were given a dose (0.2 mg/kg/day) just above the threshold. Both doses altered the rats' metabolism into adulthood, but the effects differed in males and females. Male rats given the lower dose ate about as much as control rats, but outweighed them throughout the 22-week study. Equally important, they showed signs of prediabetes, with elevated fasting serum glucose levels and impaired fat metabolism. High-dose males weighed about as much as controls while consuming less food. In contrast, both high- and low-dose females weighed less than controls although they consumed at least as much food, indicating a 'wasting' condition. This was confirmed by a demonstrated disruption of both glucose and lipid metabolism at both doses. After reaching adulthood, half the rats were switched to a high-fat diet. Increased fat intake exaggerated parathion's metabolic effects, particularly in females. The researchers believe early-life exposure to parathion and other chemicals might similarly disrupt human metabolism, thereby contributing to obesity and diabetes. They recommend further studies on the metabolic influence of environmental chemical exposures. Cynthia Washam http://www.medworm.com/index.php?rid=1929531&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2008%2F116-11%2Fss.html%23grow grow"> Growing Weight of OP Evidence Parathion Linked to Metabolic Effects in Rats Parathion and other organophosphate pesticides, the most widely used class of insecticides, have long been known as neurotoxicants but were only recently linked to metabolic disorders. A new study adds to the growing evidence that parathion may be contributing to epidemics of obesity and diabetes [EHP 116:1456?1462; Lassiter et al.]. Obesity and type 2 diabetes have surged in recent decades to the point where two-thirds of U.S. adults are now overweight and approximately 26% have diabetes or prediabetes (elevated fasting blood glucose level below the level considered diabetic). These conditions also are increasing in children, and a growing body of evidence suggests that perinatal exposures to a variety... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=1929531 Sat, 01 Nov 2008 04:00:00 +0100 1929531 thei'> The Irritation of House Dust DEHP Heightens Inflammatory Response in Allergy Sufferers Past research has suggested that di(2-ethylhexyl) phthalate (DEHP), a commonly used plasticizer, contributes to asthma symptoms in children [EHP 116:98?103 (2008)] and to dermatitis caused by dust mite allergens in mice [EHP 114:1266?1268 (2006)]. Both the prevalence of allergic diseases and environmental exposure to phthalates have increased dramatically in the past several decades, but few studies have examined how people's mucosal airways respond to inhaled DEHP. A new study reveals that exposure to DEHP in house dust altered the response of nasal mucosa in allergic people but not in nonallergic people [EHP 116:1487?1493; Deutschle et al.]. DEHP is found in polyvinyl chloride pipes, flooring, food containers, and other household products. Oral intake is the main route of exposure, but inhalation offers an alternative route. DEHP vaporizes from consumer products directly into the home and attaches to inhalable airborne dust particles. The subjects included 16 controls and 16 people who were allergic to house dust mites. The researchers exposed the subjects to one of two house dust samples?vacuumed samples containing 0.41 mg/g (DEHPlow) or augmented samples containing 2.09 mg/g (DEHPhigh)?for 3 hours. Nasal fluid was collected after exposure to measure biomarkers of allergic inflammation, including interleukin (IL)-2, -4, -5, -6, and -8, granulocyte colony?stimulating factor (G-CSF), and eosinophilic cationic protein (ECP). The expression of 1,232 genes was analyzed by microarrays in biopsies obtained from one nostril. Following either DEHP dose, the nonallergic group experienced no changes in nasal mucosa, and biomarker levels did not change significantly. However, DEHP exposure was associated with biomarker changes in the allergic group: half the allergic subjects challenged with DEHPlow showed significantly elevated levels of G-CSF, ECP, IL-5, and IL-6, whereas other allergic subjects exposed to DEHPhigh?showed significantly diminished levels of G-CSF and IL-6, suggesting a reduced immune response. DEHP is a known modulator of gene expression, as illustrated by the current study results. Among healthy subjects, between the two exposure groups, 6 genes were upregulated and 4 were downregulated. Among allergic subjects, between the two exposure groups, 8 genes were upregulated and 8 were downregulated. One of the genes elevated by DEHP was anti-M?llerian hormone, which is associated with proper gonad development in males. DEHP dampened the expression of lactate dehydrogenase A and fibroblast growth factor 9, regulators of testis formation. Although the gene expression data shed little light on allergic reactions, they support earlier evidence for phthalates' action as endocrine disruptors that can impair reproductive tract development. Carol Potera http://www.medworm.com/index.php?rid=1929530&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2008%2F116-11%2Fss.html%23thei thei"> The Irritation of House Dust DEHP Heightens Inflammatory Response in Allergy Sufferers Past research has suggested that di(2-ethylhexyl) phthalate (DEHP), a commonly used plasticizer, contributes to asthma symptoms in children [EHP 116:98?103 (2008)] and to dermatitis caused by dust mite allergens in mice [EHP 114:1266?1268 (2006)]. Both the prevalence of allergic diseases and environmental exposure to phthalates have increased dramatically in the past several decades, but few studies have examined how people's mucosal airways respond to inhaled DEHP. A new study reveals that exposure to DEHP in house dust altered the response of nasal mucosa in allergic people but not in nonallergic people [EHP 116:1487?1493; Deutschle et al.]. DEHP is found in polyvinyl chloride pipes, floori... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=1929530 Sat, 01 Nov 2008 04:00:00 +0100 1929530 back'> Backpack on Board Individual Air Monitoring Predicts Prenatal Exposure to PAHs Scientists studying human exposure to air pollutants have traditionally had to rely on data from stations monitoring ambient pollution levels. These stations are unable to account for neighborhood variation of or indoor exposure to pollutants such as tobacco smoke, and thus do not capture personal exposures. An international group of researchers studying pregnant women in Krakow, Poland, found they could accurately predict individual exposures by using data from personal air monitors, allowing the development of a predictive model of exposure that may be generalizable to pregnant women in similar exposure settings [EHP 116:1509?1518; Choi et al.]. Moreover, they found most of the women's exposure was to outdoor pollutants that penetrated indoors. pregnant Polish woman A study of Polish women offers insight into gestational PAH exposure. image: Hyunok Choi/Harvard School of Public Health The researchers assessed the exposure of 341 nonsmoking pregnant women to airborne polycyclic aromatic hydrocarbons (PAHs). PAHs are ubiquitous carcinogenic compounds formed by the incomplete burning of wood, coal, oil, and other organic substances. The eight PAHs selected for analysis are associated with a variety of health effects including cancer, developmental abnormalities, and asthma. PAHs are known to cross the placenta and have been demonstrated to pose significant harm to developing fetuses. Pregnant women were recruited from prenatal clinics in the center and outskirts of the city. Each was given a backpack equipped with an air monitor to wear for a 48-hour period during the second trimester. Before they went to sleep, the subjects placed the device alongside their beds. A subset of 78 women also used the device for 48-hour periods in their first and third trimesters. To account for seasonal variations in pollution, an approximately equal number of women were enrolled each season. Subjects also completed questionnaires about their health and lifestyle, including exposure to secondhand tobacco smoke. The results revealed that although most of the women spent less than 3 hours a day outdoors, their personal PAH exposure correlated closely with outdoor levels of the pollutants. The data also showed exposure increased significantly during the winter months with levels declining in the summer, appearing to confirm that coal-burning municipal furnaces and industries were the source of most ambient PAHs in the city. Using data from the monitors and questionnaires, the researchers reported they could accurately predict personal PAH exposure throughout pregnancy based on the outdoor mean PAH concentration at any given month of the year. They note, however, that indoor data are more accurate for assessing short-term (48 hours or less) individual exposure. Cynthia Washam http://www.medworm.com/index.php?rid=1929529&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2008%2F116-11%2Fss.html%23back back"> Backpack on Board Individual Air Monitoring Predicts Prenatal Exposure to PAHs Scientists studying human exposure to air pollutants have traditionally had to rely on data from stations monitoring ambient pollution levels. These stations are unable to account for neighborhood variation of or indoor exposure to pollutants such as tobacco smoke, and thus do not capture personal exposures. An international group of researchers studying pregnant women in Krakow, Poland, found they could accurately predict individual exposures by using data from personal air monitors, allowing the development of a predictive model of exposure that may be generalizable to pregnant women in similar exposure settings [EHP 116:1509?1518; Choi et al.]. Moreover, they found most of the women's exposure was t... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=1929529 Sat, 01 Nov 2008 04:00:00 +0100 1929529 deve'> Developing Story No Link Observed between Prenatal PFOA/PFOS Exposure and Milestone Achievement Perfluorooctanoate (PFOA; also known as perfluorooctanoic acid) and perfluorooctanesulfonate (PFOS), chemicals used in waterproofing fabrics and greaseproofing fast-food containers, among other applications, have been detected at low concentrations in 98% of the U.S. population. These chemicals have half-lives of several years, and children tend to have higher serum concentrations than adults. Animal and human studies have hinted at a link between PFOA and PFOS and developmental effects, but human studies have been limited. A new human study suggests that maternal plasma levels of PFOA and PFOS may not be associated with delayed early development in babies [EHP 116:1391?1395; Fei et al.]. The research team randomly selected 1,400 mother?baby pairs from the Danish National Birth Cohort comprising 100,000 women recruited during early pregnancy between 1996 and 2002. The team measured PFOA and PFOS levels in maternal blood samples taken in the first trimester of pregnancy. Each newborn's Apgar score was obtained from Danish hospital records; this assessment of viability taken immediately after birth measures heart rate, respiratory effort, reflex irritability, muscle tone, and skin color. When the children were 6 and 18 months old, their mothers provided data on gross and fine motor functioning, attention, cognitive function, language, and social-personal development via computer-assisted telephone interviews. The study was funded by the International Epidemiology Institute, which received money from the 3M Company, the original manufacturer of PFOA and PFOS, and the 3M Toxicology Laboratory performed the chemical analyses. Earlier human and animal studies suggested that PFOA and PFOS might reduce fetal growth, delay learning, accelerate or delay sexual maturation, and produce other developmental effects. The current study found no significant association between maternal PFOA/PFOS levels and child achievement of early developmental milestones such as walking without support, taking off socks and shoes when asked, and turning a picture book right side up. However, a statistically nonsignificant association was observed between higher maternal PFOS levels and delay of a child's ability to sit without support. PFOA and PFOS were significantly higher among first-time mothers than in women who had given birth previously. This may confound their results, because the presence of older siblings may accelerate the developmental progress of younger ones. Given animal studies showing potential adverse effects of PFOA and PFOS, and the limited data for humans, the authors write that additional studies should be conducted using more sensitive measures of early childhood development. Valerie J. Brown http://www.medworm.com/index.php?rid=1843676&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2008%2F116-10%2Fss.html%23deve deve"> Developing Story No Link Observed between Prenatal PFOA/PFOS Exposure and Milestone Achievement Perfluorooctanoate (PFOA; also known as perfluorooctanoic acid) and perfluorooctanesulfonate (PFOS), chemicals used in waterproofing fabrics and greaseproofing fast-food containers, among other applications, have been detected at low concentrations in 98% of the U.S. population. These chemicals have half-lives of several years, and children tend to have higher serum concentrations than adults. Animal and human studies have hinted at a link between PFOA and PFOS and developmental effects, but human studies have been limited. A new human study suggests that maternal plasma levels of PFOA and PFOS may not be associated with delayed early development in babies [EHP 116:1391?1395; Fei et a... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=1843676 Wed, 01 Oct 2008 04:00:00 +0100 1843676 some'> Sometimes Less Is More Perinatal Bacterial Exposure May Be More Important than Hepatitis for Liver Tumor Development Helicobacter hepaticus, a bacterium discovered in 1994 and widespread in many experimental mouse populations, is associated with a high incidence of liver tumors in aging mice. A new mouse study shows that perinatal exposure to this pathogen, rather than development of hepatitis itself, may be the single most important factor in the development of liver tumors caused by H. hepaticus [EHP 116:1352?1356; Diwan et al.]. The results support evidence from other studies that progressive hepatitis and liver tumors in older mice may stem from early-life exposure. The researchers isolated a strain of H. hepaticus from infected A/J mice. Female mice received injections with a single dose of the bacteria. Females testing positive for the bacteria were bred with uninfected males. The researchers assessed liver histopathologic findings and tumor growth in male offspring aged 2 weeks to 2 years. Uninfected weanling males from another lab were injected at 3?4 weeks. The results showed a significant incidence of liver tumors in the offspring after intraperitoneal maternal exposure to the bacteria: 33% developed liver tumors, usually multiple tumors, and 18% developed hepatocellular carcinoma. None of the mice injected with the bacteria as young adults developed any tumors. Another striking result was that tumor outcome was not closely linked to severity of hepatitis; mice that contracted hepatitis did not necessarily develop hepatic tumors. Rather, it appeared that early exposure to the bacteria, not the hepatitis itself, was key to fostering tumor growth. The type of additional perinatal event required to induce tumor development is unknown but could involve DNA damage at that vulnerable early stage, followed by subacute inflammation of the liver in response to H. hepaticus infection. The authors note that similar scenarios could apply to human infection with Helicobacter pylori and other pathogens linked with cancer. The results point to the need for further study of changes in perinatal tissues in response to such infections. David A. Taylor http://www.medworm.com/index.php?rid=1843675&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2008%2F116-10%2Fss.html%23some some"> Sometimes Less Is More Perinatal Bacterial Exposure May Be More Important than Hepatitis for Liver Tumor Development Helicobacter hepaticus, a bacterium discovered in 1994 and widespread in many experimental mouse populations, is associated with a high incidence of liver tumors in aging mice. A new mouse study shows that perinatal exposure to this pathogen, rather than development of hepatitis itself, may be the single most important factor in the development of liver tumors caused by H. hepaticus [EHP 116:1352?1356; Diwan et al.]. The results support evidence from other studies that progressive hepatitis and liver tumors in older mice may stem from early-life exposure. The researchers isolated a strain of H. hepaticus from infected A/J mice. Female mice received injections wit... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=1843675 Wed, 01 Oct 2008 04:00:00 +0100 1843675 asth'> Asthma among WTC Children Registry Yields First Child Health Report The World Trade Center Health Registry (WTCHR), comprising persons most likely to have been heavily exposed to traumatic events and air pollution related to the World Trade Center attacks of 11 September 2001, includes 3,184 children under age 18 years who were living or attending school in lower Manhattan at the time, who were otherwise near the World Trade Center that morning, or who assisted in recovery efforts. In the first report of children enrolled in this registry, researchers observe that preschoolers exposed to smoke and dust from the collapsing towers had asthma rates twice the national average following the 9/11 attack, whereas asthma rates in exposed older children remained about average [EHP 116:1383?1390; Thomas et al.]. Children in certain ethnic groups also experienced disproportionate asthma rates, although the reasons for this are unclear. wtc disaster Collapse of the World Trade Center towers, 11 September 2001 image: Reuters/Ray Stubblebine Data were collected in 2003 and 2004 by telephone interviews with parents of younger children or the children themselves if they had turned 18 since the attacks. More than half the children reported having respiratory symptoms after the attacks, including cough and sinus problems. Nearly 6% of all children reported having asthma diagnosed after 9/11. At the time of the interviews, 16% of children then aged 2?4 years had been diagnosed with asthma, more than twice the average of 7% for children that age in the Northeast. Asthma rates in older subjects, however, were just slightly higher than the Northeast rate. Childhood asthma normally develops in a child's first five years of life, often after exposure to an environmental irritant. Smoke and dust from the collapsing towers might have acted as such an early trigger in susceptible preschoolers. The researchers speculate that older youngsters could have had fewer new diagnoses because most susceptible children had been diagnosed before 9/11. The researchers noted racial disparities in asthma rates. Black and Hispanic children in the WTCHR were twice as likely to be diagnosed with asthma as whites or Asians, both before and after the attacks. Reasons for the racial disparities are unclear, although prior studies on ethnic disparities in asthma suggest that both genetics and environment may play a role in etiology of the disease. Children of all ages and ethnicities were more likely to develop asthma if they were caught in the cloud of cement dust created by the collapsing towers, as pulverized cement dust is known to irritate mucous membranes. The WTCHR data have several limitations, including lack of information on how long after 9/11 symptoms appeared and the presence of co-factors for asthma. Despite these limitations, findings from the WTCHR, which constitutes the largest collection of post-disaster data of children, could have broad impact, given that tens of thousands of New York City children may have been exposed to smoke and dust on 9/11. Researchers also expect their data to improve understanding of risks to children exposed to other polluting disasters, such as the California wildfires. Cynthia Washam http://www.medworm.com/index.php?rid=1843674&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2008%2F116-10%2Fss.html%23asth asth"> Asthma among WTC Children Registry Yields First Child Health Report The World Trade Center Health Registry (WTCHR), comprising persons most likely to have been heavily exposed to traumatic events and air pollution related to the World Trade Center attacks of 11 September 2001, includes 3,184 children under age 18 years who were living or attending school in lower Manhattan at the time, who were otherwise near the World Trade Center that morning, or who assisted in recovery efforts. In the first report of children enrolled in this registry, researchers observe that preschoolers exposed to smoke and dust from the collapsing towers had asthma rates twice the national average following the 9/11 attack, whereas asthma rates in exposed older children remained about average [EHP 116:13... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=1843674 Wed, 01 Oct 2008 04:00:00 +0100 1843674 meta'> 'Metal Detector' Gene May Influence Lead Absorption Variants Predict Higher Blood Lead Levels in Children An estimated 310,000 U.S. children between ages 1 and 5 have elevated blood lead levels despite efforts to reduce lead in the environment. Research in the past decade has begun to focus on factors that could make some children more susceptible to lead poisoning even at low levels of exposure. A new study explores one such possible factor?gene variants that influence lead absorption?linking variants in two iron metabolism genes to higher blood lead levels in children [EHP 116:1261-1266; Hopkins et al.]. When researchers analyzed umbilical cord blood from 422 children in Mexico, they found that the presence of two variants of the hemochromatosis (HFE) gene?HFE C282Y and HFE H63D?predicted blood lead levels 11% higher than those in children not carrying the variants. Moreover, the presence of either HFE variant combined with a variant form of the transferrin (TF) receptor gene?TF-P570S?predicted blood lead levels 50% higher than in children with none of the variants. Although the HFE and TF genes normally regulate iron metabolism, they may also influence blood lead levels because lead?like iron?is a divalent metal. Thus, the two metals can be 'mistaken' for each other during metabolic processes. The HFE gene regulates iron-binding proteins, including TF, and variant forms of this gene sometimes induce hemochromatosis, a disease characterized by increased intestinal absorption of iron that contributes to abnormally high iron stores in adulthood. The authors hypothesized that the HFE variants might similarly increase absorption of lead, a hypothesis supported by the results of this study. TF interacts with HFE to form a complex that down-regulates iron absorption. However, TF-P570S may interact with the HFE variants in ways that heighten metal absorption rates. Study results showed the TF and HFE variants produced higher lead levels than those predicted by either HFE variant alone. Previously published research by these investigators has shown that having the HFE variants predicted lower blood lead levels in elderly men compared with men without the variants. The contrasting findings, the authors speculate, may reflect age-specific differences in body iron stores and in the variants' effect on lead metabolism. Among children with low iron body stores and high iron needs, the variants predicted higher blood lead levels. But as iron stores accumulate with age, the variants down-regulated iron and lead absorption, leading to progressive declines in blood lead levels. The study's key implications are twofold: first, that children with variant iron-metabolizing genes may be especially susceptible to the effects of lead at low exposure levels, and second, that genetic variants may increase risk at one life stage and decrease it at others. Charles W. Schmidt spacer | Purchase This Issue | http://www.medworm.com/index.php?rid=1749541&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2008%2F116-9%2Fss.html%23meta meta"> "Metal Detector" Gene May Influence Lead Absorption Variants Predict Higher Blood Lead Levels in Children An estimated 310,000 U.S. children between ages 1 and 5 have elevated blood lead levels despite efforts to reduce lead in the environment. Research in the past decade has begun to focus on factors that could make some children more susceptible to lead poisoning even at low levels of exposure. A new study explores one such possible factor?gene variants that influence lead absorption?linking variants in two iron metabolism genes to higher blood lead levels in children [EHP 116:1261-1266; Hopkins et al.]. When researchers analyzed umbilical cord blood from 422 children in Mexico, they found that the presence of two variants of the hemochromatosis (HFE) gene?HFE C282Y and HFE H... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=1749541 Mon, 01 Sep 2008 04:00:00 +0100 1749541 disa'> Disaster Response Mental Health Effects among WTC Rescue and Recovery Workers The attacks on the World Trade Center (WTC) on 11 September 2001 exposed thousands of emergency responders and other recovery workers to a unique mix not only of airborne toxic pollutants but also psychological stressors. The physical consequences such as persistent respiratory ailments have been documented previously [e.g., EHP 114:1853-1858 (2006)]. The latest report from a 5-year study of health effects among WTC rescue and recovery workers describes a higher level of lingering mental health problems among these workers than in the general population [EHP 116:1248-1253; Stellman et al.]. rescue worker looking out on the WTC A worker surveys the WTC site, 25 September 2001 image: Mike Rieger/FEMA News Photo More than 10,000 WTC workers completed several standard mental health questionnaires 10-61 months after the attacks. About 90% of the respondents worked at the WTC site during the first 2 weeks after 9/11, and the majority remained onsite for 3 months or longer. On the basis of an analysis of their responses, and in the absence of a clinical evaluation, the researchers classified 11.1% of workers with probable post-traumatic stress disorder (PTSD), 8.8% with probable depression, 5.0% with probable panic disorder, and 62% with substantial stress reactions (such as nightmares, flashbacks, and insomnia). Overall, mental health problems declined gradually from 13.5% to 9.7% among WTC workers during the course of the study. The incidence of PTSD in WTC workers, which parallels that reported in soldiers returning from combat duty in Afghanistan, was about 4 times higher than that for the general population in the United States. Probable PTSD was associated with having lost family members or friends in the attacks; those with probable PTSD had a 17-fold greater likelihood of reporting disruption of family, work, and social life. About half those with probable PTSD also experienced probable panic disorder, depression, or both. Workers with probable PTSD also perceived their children as having more psychological symptoms (such as clinginess or trouble sleeping) and behavioral problems than workers without PTSD. Alcohol-related problems also were abundant in the study group. More than 17% reported symptoms of probable alcohol abuse. Nearly half reported drinking more heavily than usual during the period they worked at rescue and recovery efforts, and months later a third were still drinking more than usual. The authors conclude that the variety of persistent mental health problems in responders 'underscores the need for long-term mental health screening and treatment programs targeting this population.' Following future environmental disasters, they write, mental health problems are virtually certain to accompany physical effects of toxic exposures. Rescue and recovery workers therefore should receive behavioral health evaluations as well as medical evaluations to reduce adverse health and social consequences. Carol Potera http://www.medworm.com/index.php?rid=1749540&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2008%2F116-9%2Fss.html%23disa disa"> Disaster Response Mental Health Effects among WTC Rescue and Recovery Workers The attacks on the World Trade Center (WTC) on 11 September 2001 exposed thousands of emergency responders and other recovery workers to a unique mix not only of airborne toxic pollutants but also psychological stressors. The physical consequences such as persistent respiratory ailments have been documented previously [e.g., EHP 114:1853-1858 (2006)]. The latest report from a 5-year study of health effects among WTC rescue and recovery workers describes a higher level of lingering mental health problems among these workers than in the general population [EHP 116:1248-1253; Stellman et al.]. A worker surveys the WTC site, 25 September 2001 image: Mike Rieger/FEMA News Photo More than 10,000 WTC wor... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=1749540 Mon, 01 Sep 2008 04:00:00 +0100 1749540 thec'> The Cool Factor Season Modifies Cardiorespiratory Deaths in China Outdoor air pollution has been linked with increased risk of death from cardiorespiratory disease in epidemiologic studies in North America and Europe. Some studies have found that sex, age, or other modifying factors can cause increased susceptibility to air pollution in some individuals. However, few of these studies have been conducted in Asia. Now a new study of Shanghai residents reveals that the elderly, women, and individuals with lower educational backgrounds are especially vulnerable to outdoor air pollution during cooler weather [EHP 116:1183-1188; Kan et al.]. people in China riding bikes A study of Shanghai residents showed that cardiorespiratory deaths increased during the cool season, which runs from October through March. image: Mark Henley/Panos Pictures The researchers examined death certificates recorded between 1 January 2001 and 31 December 2004 in the central area of Shanghai and found an average of 119 nonaccidental deaths reported daily, with 49.1% due to cardiorespiratory disease. They collected daily air pollution data for particulate matter less than 10 ?m in diameter (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), and ozone (O3) from the Chinese government agency that tracks air pollutants and assessed how mortality and pollutant levels varied by sex, age, educational status, and season of the year. They found that most air pollutant levels peaked in the cool season (October through March, when the temperature averages 58?F), correlating with a peak in the death rate; the exception was O3, which had higher concentrations in the warm season (April through September, when the temperature averages 75?F). They observed a 2- to 3-times greater risk of death from cardiorespiratory disease in the cool season compared with the warm season, with SO2, NO2, and O3 particularly showing seasonal differences in association with cause of death. The same air pollutants were also associated with a 3- to 4-fold greater risk of cardiovascular death in the cool season than in the warm season, possibly because exposure to air pollutants is reduced by staying inside air-conditioned buildings. Additionally, people older than 65 were up to 5 times more likely than younger people to die of cardiorespiratory disease. Compared with men, deaths in women were twice as likely to be linked to elevated O3 and PM10 levels. This may be due to men's greater rate of smoking, the effects of which may override pollution-related effects in male smokers. Overall, people with less education were twice as likely as more educated residents to die during periods of elevated pollution. Educational level, a reflection of socioeconomic status, has been reported previously as a modifying factor for air pollution?related deaths in North America and Europe, but this is the first such report from mainland China, where the concentrations of PM10, SO2, and NO2 are much higher. Carol Potera http://www.medworm.com/index.php?rid=1749539&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2008%2F116-9%2Fss.html%23thec thec"> The Cool Factor Season Modifies Cardiorespiratory Deaths in China Outdoor air pollution has been linked with increased risk of death from cardiorespiratory disease in epidemiologic studies in North America and Europe. Some studies have found that sex, age, or other modifying factors can cause increased susceptibility to air pollution in some individuals. However, few of these studies have been conducted in Asia. Now a new study of Shanghai residents reveals that the elderly, women, and individuals with lower educational backgrounds are especially vulnerable to outdoor air pollution during cooler weather [EHP 116:1183-1188; Kan et al.]. A study of Shanghai residents showed that cardiorespiratory deaths increased during the cool season, which runs from October through March. im... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=1749539 Mon, 01 Sep 2008 04:00:00 +0100 1749539 ados'> A Dose of Defense? Omega-3 Supplements Appear Protective against PM Effects Omega-3 polyunsaturated fatty acids, believed to lessen the risk of many chronic ailments including arthritis, cancer, heart disease, and memory loss, may also help protect the heart against certain damaging effects of air pollution. In a new study by an international team of researchers, supplementation with omega-3s was associated with significantly reduced cardiac stress caused by particulate matter less than 2.5 microm in diameter (PM2.5) in a group of elderly individuals in Mexico City [EHP 116:1237-1242; Romieu et al.]. The study is the first to examine the effects of omega-3s on biomarkers of cellular response to the oxidative stress of air pollution. Exposure to high levels of particulates from vehicle exhaust and industrial emissions raises the risk of hypertension, heart arrhythmia, heart attack, and stroke, with the elderly being particularly susceptible. Some of the authors had previously shown both that PM2.5 promotes heart disease by diminishing heart-rate variability and that omega-3 supplementation could increase heart-rate variability. The current study was intended to find out how omega-3s achieve their effects. The study population of 52 elderly nursing home residents was chronically exposed to high PM2.5 levels; particulate levels inside the nursing home, where residents spent nearly all their time, correlated with the smoggy surroundings outside. For four months starting in 2001, half the participants in the double-blind study received fish oil supplements at doses typical for over-the-counter supplement users; the other half received soy oil supplements. The research team compared blood samples taken from subjects before and during supplementation and found that omega-3 use was associated with diminished oxidative damage in blood cells. The observed antioxidant effect of omega-3s was much greater in fish oil users than in soy oil users, a difference the investigators attribute to the different amounts and types of omega-3s in the two supplement types (docosahexaenoic acid and eicosapentaenoic acid in fish oil versus -linolenic acid in soy oil). The authors note limitations of their study, such as the small sample size and limited exposure assessment. However, the finding that omega-3s appear effective against oxidative stress related to PM2.5 exposure, with fish oil supplements offering more protection than soy oil supplements, merits further study in larger populations. Cynthia Washam http://www.medworm.com/index.php?rid=1749538&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2008%2F116-9%2Fss.html%23ados ados"> A Dose of Defense? Omega-3 Supplements Appear Protective against PM Effects Omega-3 polyunsaturated fatty acids, believed to lessen the risk of many chronic ailments including arthritis, cancer, heart disease, and memory loss, may also help protect the heart against certain damaging effects of air pollution. In a new study by an international team of researchers, supplementation with omega-3s was associated with significantly reduced cardiac stress caused by particulate matter less than 2.5 microm in diameter (PM2.5) in a group of elderly individuals in Mexico City [EHP 116:1237-1242; Romieu et al.]. The study is the first to examine the effects of omega-3s on biomarkers of cellular response to the oxidative stress of air pollution. Exposure to high levels of particulates from ... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=1749538 Mon, 01 Sep 2008 04:00:00 +0100 1749538 gett'> Getting Straight on What's Flushed 'Sewage Epidemiology' Measures Community Drug Consumption Active pharmaceutical agents and other chemicals in sewage pose a considerable concern when one considers the potential for inadvertent exposures through treated water. On the flip side, wastewater can also provide a wealth of economical and accessible epidemiologic data on common drug products consumed and excreted into community sewage systems. Now researchers have successfully tested a new 'sewage epidemiology' analysis strategy to obtain near real-time information on community usage rates of drugs, allowing trends and patterns to be promptly monitored [EHP 116:1027?1032; Zuccato et al.]. Many drug usage studies focus on prevalence data??reported use rates based on the integration of population surveys with medical records, drug production and seizure rates, and crime statistics. But obtaining information through these channels can often be time-consuming and the accuracy questionable, as the data are based partly on self-reported use. Using a novel approach first proposed in 2001, the researchers in the current study gathered data from sewage treatment plants in Milan (Italy), Lugano (Switzerland), and London (England) to obtain information on community-wide consumption of cocaine, heroin, cannabis, and amphetamines. The investigators collected composite samples of untreated wastewater from major sewage treatment plants in each of the cities every 20 minutes for 24 hours in a time-proportional mode and pooled the samples using a computer-controlled device. They also tested field data from a given treatment plant for reproducibility over time: samples were taken on consecutive days for 1 week on 3 different occasions in Milan and Lugano, and on 2 days at 2 major plants in London. Wastewater samples were analyzed by liquid chromatography?tandem mass spectrometry, which measured drug residues using a highly selective multiresidue assay. This new testing method enabled the research team to accurately measure the drugs in wastewater samples using objective quantitative data?drug concentration, wastewater flow rate, and population size?and to acquire near real-time reporting of results because of the short 1- to 2-day completion time for mass spectrometric analysis of samples. The new approach also makes it possible to integrate wastewater monitoring data with other information on drug use to obtain more refined estimates of community consumption patterns and user profiles. The authors note this approach has certain limitations, including lack of data regarding the number of drug users in a given community, but say that the results on overall consumption rates compare reasonably well with official prevalence-based figures. For the sake of accuracy, detailed information would be needed on the metabolism and kinetics of any compound for which the approach is used. Furthermore, it can be difficult to accurately characterize 'typical' users of certain pharmaceuticals or drugs. However, the authors state that with further testing, the method could be used in future research to provide real-time epidemiologic data for application to other public health issues. Tanya Tillett http://www.medworm.com/index.php?rid=1673922&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2008%2F116-8%2Fss.html%23gett gett"> Getting Straight on What's Flushed "Sewage Epidemiology" Measures Community Drug Consumption Active pharmaceutical agents and other chemicals in sewage pose a considerable concern when one considers the potential for inadvertent exposures through treated water. On the flip side, wastewater can also provide a wealth of economical and accessible epidemiologic data on common drug products consumed and excreted into community sewage systems. Now researchers have successfully tested a new "sewage epidemiology" analysis strategy to obtain near real-time information on community usage rates of drugs, allowing trends and patterns to be promptly monitored [EHP 116:1027?1032; Zuccato et al.]. Many drug usage studies focus on prevalence data??reported use rates based on the integration of... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=1673922 Fri, 01 Aug 2008 04:00:00 +0100 1673922 trac'> Tracking Down a Cause for Hypospadias Placental Malfunction May Contribute Hypospadias is a male birth defect in which the opening of the urethra is located on the underside of the penis instead of the tip. Although the defect is common and increasing in prevalence (2?8 cases per 1,000 live births in Western countries), the causes of most cases are unknown. Some studies suggest that reduced levels of the placental hormone human chorionic gonadotropin (hCG) may play a role; others suggest associations between hypospadias and conditions such as low birth weight, preterm birth, and preeclampsia that could be caused by malfunction of the placenta and subsequent abnormalities in hormone regulation and nutrition provided to the fetus (a condition known as placental insufficiency). A new study now presents additional evidence that hypospadias has its origins in malfunction of the placenta [EHP 116:1071?1076; Akre et al.]. Data on 292 cases of hypospadias and 427 controls were collected as part of a joint Danish?Swedish study of both hypospadias and cryptorchidism (undescended testes). In Sweden, hypospadias cases were recruited at a pediatric surgery clinic, and data were collected via self-administered questionnaires. In Denmark, cases were from the Danish National Birth Cohort, a population-based cohort of women and children. Mothers were interviewed while pregnant and twice after delivery. Matched controls were born within at least 6 months of each case and within the same county, and were randomly selected from national birth and population registries. The investigators found several conditions independently associated with increased hypospadias risk, most of which they say could be explained by impaired production of hormones by the placenta. Mothers without first-trimester nausea were twice as likely to bear sons with hypospadias, as were mothers who had a prepregnancy body mass index of 30 or greater. These findings support the theory that placental insufficiency contributes to hypospadias. Nausea is believed to be caused by an early surge of pregnancy hormones, and the absence of first-trimester nausea is associated with low hCG levels. A previous study showed that obese women have lower levels of a family of proteins called plasminogen activator inhibitors, some of which are derived from the placenta. The team also determined that a maternal diet lacking both fish and meat was associated with more than a fourfold increased risk of hypospadias in baby boys. This finding complements a 2000 study by other authors that showed a strong positive association between maternal vegetarian diet and hypospadias in offspring. The authors of the current study conclude that exclusion of animal proteins could increase the risk of a transient deficiency of some nutrient that's essential for formation of the organs or the placenta. Another explanation is that some protein sources in vegetarians' diets (such as soybeans) contain compounds with hormonal effects that may affect the development of the urogenital organs in humans. Angela Spivey http://www.medworm.com/index.php?rid=1673921&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2008%2F116-8%2Fss.html%23trac trac"> Tracking Down a Cause for Hypospadias Placental Malfunction May Contribute Hypospadias is a male birth defect in which the opening of the urethra is located on the underside of the penis instead of the tip. Although the defect is common and increasing in prevalence (2?8 cases per 1,000 live births in Western countries), the causes of most cases are unknown. Some studies suggest that reduced levels of the placental hormone human chorionic gonadotropin (hCG) may play a role; others suggest associations between hypospadias and conditions such as low birth weight, preterm birth, and preeclampsia that could be caused by malfunction of the placenta and subsequent abnormalities in hormone regulation and nutrition provided to the fetus (a condition known as placental insufficiency). A n... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=1673921 Fri, 01 Aug 2008 04:00:00 +0100 1673921 gast'> Gastronomical Delight Micronutrients Protect against Arsenic Lesions Studies in South Asia suggest that antioxidants may mediate many of the dermatologic symptoms associated with exposure to arsenic in drinking water. Nonetheless, the mitigating effects of diet on arsenic-related premalignant skin lesions are largely unknown, particularly in the context of the typical Bangladeshi diet. A new cross-sectional study using baseline data from the Health Effects of Arsenic Longitudinal Study (HEALS), 2000?2002, is the first systematic, population-based attempt to assess the association between micronutrient intake and the prevalence of arsenic-induced skin lesions [EHP 116:1056?1062; Zablotska et al.]. market selling vegetables and fruit A diet rich in B vitamins and antioxidants may counter some of the effects of chronic arsenic ingestion image: G.M.B. Akash/Panos Pictures As many as a third of the people living in Bangladesh have been exposed to arsenic-tainted water levels above the national limit of 50 ppb, with many levels as high as 800 ppb. Several studies have shown an association between drinking arsenic-rich water and development of skin lesions, a common outward sign of chronic arsenic exposure. HEALS is a population-based prospective cohort study in Araihazar, Bangladesh, using individual-level time-weighted measures of arsenic exposure via drinking water. The present study relied on detailed daily diet information obtained from all participants using a food frequency questionnaire along with U.S. Department of Agriculture nutritional tables. The analyses were aimed at clarifying the effects of the B vitamin group and antioxidants (vitamins A, C, and E) on the risk of arsenic-related skin lesions. Because supplements and food fortification are rare in Bangladesh, only dietary intakes of these micronutrients were considered. Skin lesions were identified among 10,628 subjects according to a structured clinical protocol during screening that was confirmed with further clinical review. Dietary intake of B1, B6, and B9 and all three antioxidants significantly reduced the risk of arsenic-related skin lesions. For example, for individuals with the highest vitamin intake, the risk of arsenic-induced skin lesions was significantly reduced by 60% for vitamin E. The investigators conclude that intakes of B vitamins and antioxidants at doses greater than the current recommended daily amounts for Bangladesh might lower the risk of arsenic-related skin lesions. However, the research team observed that there was a high prevalence of micronutrient deficiency in Bangladesh, with the potential protective modifying effects of these vitamins restricted to the medium and upper consumption levels. Public health measures to assist this population may need to include either supplementation or food fortification to achieve a significant degree of protection from chronic arsenic exposures. M. Nathaniel Mead http://www.medworm.com/index.php?rid=1673920&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2008%2F116-8%2Fss.html%23gast gast"> Gastronomical Delight Micronutrients Protect against Arsenic Lesions Studies in South Asia suggest that antioxidants may mediate many of the dermatologic symptoms associated with exposure to arsenic in drinking water. Nonetheless, the mitigating effects of diet on arsenic-related premalignant skin lesions are largely unknown, particularly in the context of the typical Bangladeshi diet. A new cross-sectional study using baseline data from the Health Effects of Arsenic Longitudinal Study (HEALS), 2000?2002, is the first systematic, population-based attempt to assess the association between micronutrient intake and the prevalence of arsenic-induced skin lesions [EHP 116:1056?1062; Zablotska et al.]. A diet rich in B vitamins and antioxidants may counter some of the effects of chr... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=1673920 Fri, 01 Aug 2008 04:00:00 +0100 1673920 neww'> New Window into Breast Cancer Risk Assessing Lifetime Exposures to POPs Persistent organic pollutants (POPs) such as polychlorinated biphenyls (PCBs) are ubiquitous chemical compounds that persist in the environment and bioaccumulate through the food web. Although experiments have shown that POPs stimulate the proliferation of human cancer cell lines, epidemiologic studies of POP-associated cancer risk have yielded inconsistent results, possibly because of the lack of tools for estimating lifetime exposures to these chemicals. Now, however, researchers have developed a new physiologically based pharmacokinetic (PBPK) modeling approach that can potentially be used in epidemiologic studies to simulate lifetime toxicokinetics of POPs in women [EHP 116:886?892; Verner et al.]. Previous biological assessments have been limited to measuring POP levels in blood or tissue samples collected around the time of breast cancer diagnosis. However, such assessments may not reflect the body burden during earlier, potentially critical exposure points in a woman's life such as the fetal, postnatal, and adolescent periods. In contrast, the new model integrates the relevant processes of absorption, distribution, metabolism, and elimination to estimate lifetime blood and tissue exposure and levels during any hypothesized time window of susceptibility in breast cancer development. The model also predicts how various types of relevant lifetime physiologic changes?such as body weight variation, pregnancy, excretion of POPs through lactation, and aging?will influence the kinetics of a compound in a woman throughout her life. The model enables the estimation of interindividual differences in POP exposures through the use of physiologic information obtained from questionnaires in epidemiologic studies. The researchers found that lactation and weight change histories had the greatest impact on the toxicokinetic profile throughout life. According to the model, the longer and later in life lactation occurred, the lower the woman's blood POP concentration at age 55 (a surrogate time representing the typical age at breast cancer diagnosis). Similarly, variations in body weight throughout life had a greater impact than average body weight on blood POP concentrations, possibly because weight loss is accompanied by unloading of POPs into the blood via lost adipose tissue. This means that quantitative information on both lactation and body weight histories is critical when evaluating past POP exposures. If, as some researchers hypothesize, breast cancer is related to POP exposures at specific time windows of susceptibility during a woman's lifetime, lactation and body weight histories must be considered in studies of POP exposures and breast cancer risk. Depending on when such physiologic events occur, women having similar POP concentrations at the age of diagnosis may have had completely different internal levels at a time that may be critical to the formation of breast cancer. The proposed PBPK modeling approach therefore could be used in environmental epidemiology research to circumvent limitations inherent in relying on late-life sampling for past exposure assessments. M. Nathaniel Mead http://www.medworm.com/index.php?rid=1559548&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2008%2F116-7%2Fss.html%23neww neww"> New Window into Breast Cancer Risk Assessing Lifetime Exposures to POPs Persistent organic pollutants (POPs) such as polychlorinated biphenyls (PCBs) are ubiquitous chemical compounds that persist in the environment and bioaccumulate through the food web. Although experiments have shown that POPs stimulate the proliferation of human cancer cell lines, epidemiologic studies of POP-associated cancer risk have yielded inconsistent results, possibly because of the lack of tools for estimating lifetime exposures to these chemicals. Now, however, researchers have developed a new physiologically based pharmacokinetic (PBPK) modeling approach that can potentially be used in epidemiologic studies to simulate lifetime toxicokinetics of POPs in women [EHP 116:886?892; Verner et al.]. Prev... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=1559548 Tue, 01 Jul 2008 04:00:00 +0100 1559548 isar'> Is Arsenic 'Lactation Intolerant'? Study Indicates Low Excretion in Breast Milk Arsenic is known to readily cross the placenta, but few data exist on postnatal exposure to arsenic in breast milk. Results of a study conducted in Bangladesh now suggest that infants who are exclusively breastfed are protected against arsenic, despite high maternal exposures [EHP 116:963?969; F?ngstr?m et al.]. Numerous studies have linked arsenic exposure in adults to various diseases, including cancer, cardiovascular disease, and diabetes mellitus. Exposure in school-age children has been associated with neurodevelopmental disorders. During fetal development, the brain is particularly vulnerable to arsenic exposure, as it readily crosses the placenta, possibly altering fetal programming and leading to a higher risk of susceptibility to disease later in life. The subjects in the current study included 98 mothers and their 3-month-old infants who participated in the Maternal and Infant Nutrition Interventions of Matlab in Bangladesh, one of the most severely affected countries in terms of high prevalence of extremely elevated levels of arsenic in drinking water supplies. The investigators evaluated nutritional status and arsenic exposure as reflected by arsenic metabolites in infant urine and maternal blood, urine, and saliva samples. They also analyzed breast milk samples at 2 months postpartum for arsenic. Questionnaires completed by the mothers provided data on infant feeding practices. The median sum of arsenic metabolites in infant urine was 1.2 ?g/L, with significantly lower concentrations in infants who were exclusively breastfed compared with those who received some solid food. Arsenic concentrations in breast milk were low (median 1.0 ?g/kg) and mostly in the form of trivalent inorganic arsenic. The researchers observed a significant association between arsenic in infant urine and breast milk, but noted that some mothers with low breast milk arsenic had infants with high urine concentrations, possibly because the infants had been given water to drink. Median maternal blood and urine concentrations were high (5.7 and 67 ?g/L, respectively), whereas median maternal saliva concentrations were low (1.3 ?g/L). Among infants who were exclusively breastfed, urine levels did not exceed 19 ?g/L inorganic arsenic and its metabolites, whereas infants who received infant formula prepared with local drinking water in addition to some breast milk had urine levels up to 1,100 ?g/L. The authors demonstrate for the first time that arsenic in human breast milk is mostly the inorganic arsenite form. Although there was a significant relationship between arsenic concentrations in milk and in maternal blood, arsenic concentrations in breast milk were relatively low despite the mothers' high exposures. The findings suggest that breastfeeding exclusively can protect infants from arsenic exposure during this critical development period, but the authors note that researchers have yet to determine the extent to which breastfeeding decreases the health risks associated with prenatal arsenic exposure. Tanya Tillett http://www.medworm.com/index.php?rid=1559547&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2008%2F116-7%2Fss.html%23isar isar"> Is Arsenic "Lactation Intolerant"? Study Indicates Low Excretion in Breast Milk Arsenic is known to readily cross the placenta, but few data exist on postnatal exposure to arsenic in breast milk. Results of a study conducted in Bangladesh now suggest that infants who are exclusively breastfed are protected against arsenic, despite high maternal exposures [EHP 116:963?969; F?ngstr?m et al.]. Numerous studies have linked arsenic exposure in adults to various diseases, including cancer, cardiovascular disease, and diabetes mellitus. Exposure in school-age children has been associated with neurodevelopmental disorders. During fetal development, the brain is particularly vulnerable to arsenic exposure, as it readily crosses the placenta, possibly altering fetal programming and leadi... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=1559547 Tue, 01 Jul 2008 04:00:00 +0100 1559547 shin'> Shining a Light on BP-3 Exposure Sunscreen Chemical Measured in U.S. Population Sunscreens provide important protection against sunburn and squamous cell cancer, particularly for individuals who work outdoors or in situations where sun exposure is unavoidable. The widespread use of the common sunscreen agent benzophenone-3 (BP-3) and its detection in the environment suggest the need for more information about the extent of human exposure. Results of a new study now provide the first nationally representative data on BP-3 exposure among the U.S. population [EHP 116:893?897; Calafat et al.]. lady applying sunscreen In an NHANES sample, women and light-skinned individuals had the highest concentrations of the sunscreen agent BP-3 image: Graca Victoria/Shutterstock BP-3 is used in personal care products to absorb and dissipate ultraviolet (UV) radiation. It is also used as a UV stabilizer in plastic surface coatings to prevent polymer or food photodegradation and has been approved by the Food and Drug Administration as an indirect food additive. Although BP-3 exposure has not been linked to adverse health effects in humans, results of animal studies by the National Toxicology Program have shown effects in liver, kidney, and reproductive organs, and studies by other groups have shown endocrine-disrupting effects. Using data from the National Health and Nutrition Examination Survey (NHANES) 2003?2004 conducted by the Centers for Disease Control and Prevention, the current research team analyzed 2,517 urine samples from three major racial/ethnic groups: non-Hispanic black, non-Hispanic white, and Mexican American. NHANES includes household interviews, medical histories, standardized physical examinations, and a collection of biologic specimens that can be used to assess exposure to environmental chemicals, as in the current study. The scientists detected BP-3 in 96.8% of the urine samples, with a mean concentration of 22.9 ?g/L and a concentration of 1,040 ?g/L in the 95th percentile. The high level of detection likely resulted from routine use of personal care products such as sunscreen, moisturizers, lipstick, and hairspray. Results of the current study suggest that females and non-Hispanic whites were the most highly exposed of all the demographic groups studied. Mean concentrations of BP-3 were significantly higher for females than for males, regardless of age, probably because women and girls use more sunscreen and other personal care products than men and boys do. At the 95th percentile of exposure, adult females had BP-3 concentrations 3.5 times greater than those of adult males. Mean concentrations also differed significantly among the different racial/ethnic groups. Non-Hispanic whites were 6.8 times more likely and Mexican Americans were 4 times more likely to have BP-3 concentrations above the 95th percentile compared with non-Hispanic blacks. These differences likely result from increased use of sunscreens by people with lighter skin pigmentation. According to the authors, the NHANES 2003?2004 data can be used to establish a nationally representative baseline assessment of exposure. Moreover, the data could aid risk assessments for BP-3 exposure if future toxicologic or epidemiologic studies suggest the need for such research, and may encourage further research to determine the potential public health impact of exposure at the levels reported. John Tibbetts http://www.medworm.com/index.php?rid=1559546&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2008%2F116-7%2Fss.html%23shin shin"> Shining a Light on BP-3 Exposure Sunscreen Chemical Measured in U.S. Population Sunscreens provide important protection against sunburn and squamous cell cancer, particularly for individuals who work outdoors or in situations where sun exposure is unavoidable. The widespread use of the common sunscreen agent benzophenone-3 (BP-3) and its detection in the environment suggest the need for more information about the extent of human exposure. Results of a new study now provide the first nationally representative data on BP-3 exposure among the U.S. population [EHP 116:893?897; Calafat et al.]. In an NHANES sample, women and light-skinned individuals had the highest concentrations of the sunscreen agent BP-3 image: Graca Victoria/Shutterstock BP-3 is used in personal care prod... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=1559546 Tue, 01 Jul 2008 04:00:00 +0100 1559546 meth'> Methylmercury Pause Study Suggests Long Latency for Neurotoxicity Methylmercury (MeHg) easily crosses the blood?brain barrier and accumulates in the central nervous system, where it is demethylated to inorganic mercury. Chronic perinatal exposure to environmentally relevant levels of MeHg is associated with the occurrence later in childhood of neurobehavioral problems such as impaired attention and fine motor function. Animal studies confirm this association, but epidemiologic evidence is mixed despite extensive study. Moreover, MeHg toxicity and the period of time before effects appear are not completely understood, as few studies have been conducted beyond the first months or years of life in either animals or humans. Researchers now demonstrate in a mouse model that effects from early exposure to methylmercury can occur years after early-life mercury levels in the brain have declined [EHP 116:746?751; Yoshida et al.]. In the current study, investigators used two strains of mice?the wild-type C57BL strain and the genetically manipulated metallothionein (MT)-null strain. The latter was used to examine potential genetic susceptibility to the toxic effects of MeHg exposure, as MT-null mice do not produce metallothionein-I and II proteins that can bind metals and protect against their toxic effects. Mice were exposed through diet to low levels of MeHg (5 ?g/g diet) from the first day of pregnancy through the tenth day after birth. Offspring of the treated mice were weaned at 28 days. At 12 and 52 weeks (roughly comparable to young adulthood and middle age in humans), the offspring underwent behavioral tests of their locomotor activity and learning ability. All animals were weighed biweekly, and mercury concentrations in the brains, livers, and kidneys were measured for 10-day-old mice and for the group tested at 12 weeks. In 10-day-old exposed mice, mercury concentrations in the brain were 0.5 ?g Hg/g body weight or lower, with no significant differences observed between exposed wild-type mice and MT-null mice. At 13 weeks, concentrations of mercury in the brain of exposed groups were similar to those of the unexposed groups. Except for one activity measure in female MT-null mice, exposure to MeHg did not significantly affect behavioral test responses at 12 weeks. At 52 weeks, however, investigators observed significant effects in all behavioral test responses, with MT-null mice being slightly more affected. After 28 weeks, wild-type male and all MT-null mice exposed to MeHg weighed significantly less than control mice, which may signal an emerging toxic effect. The authors demonstrate a long latency period after perinatal exposure to low levels of MeHg and show that this period may be influenced by genetic susceptibility, given the stronger effect of MeHg exposure in MT-null mice. The existence of a latency period suggests that a slow process, such as aging, plays a role in MeHg toxicity, although the actual damage occurs much earlier in life. Julia R. Barrett http://www.medworm.com/index.php?rid=1486999&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2008%2F116-6%2Fss.html%23meth meth"> Methylmercury Pause Study Suggests Long Latency for Neurotoxicity Methylmercury (MeHg) easily crosses the blood?brain barrier and accumulates in the central nervous system, where it is demethylated to inorganic mercury. Chronic perinatal exposure to environmentally relevant levels of MeHg is associated with the occurrence later in childhood of neurobehavioral problems such as impaired attention and fine motor function. Animal studies confirm this association, but epidemiologic evidence is mixed despite extensive study. Moreover, MeHg toxicity and the period of time before effects appear are not completely understood, as few studies have been conducted beyond the first months or years of life in either animals or humans. Researchers now demonstrate in a mouse model that effects f... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=1486999 Sun, 01 Jun 2008 04:00:00 +0100 1486999 brai'> Brain Effects Stick Around PFCs and Neural Cell Development Although some perfluorinated chemicals?manmade compounds used in such goods as nonstick cookware and stain protectors?are no longer manufactured, decoding the ways in which these chemicals affect humans and wildlife is important because of the stability of the compounds, their persistence in the environment, and their long retention times in living organisms. To date, the biological mechanisms through which these chemicals cause damage have not been well understood. Now, however, researchers have shown that four common perfluorinated chemicals?perfluorooctane sulfonamide (PFOSA), perfluorooctane sulfonic acid (PFOS), perfluorooctanoic acid (PFOA), and perfluorobutane sulfonic acid (PFBS)?affect developing PC12 cells in ways that suggest a variety of mechanisms of action at work [EHP116:716?722; Slotkin et al.]. The team studied whether the chemicals affected the cells' ability to synthesize DNA, the growth of the cells and their ability to reproduce, cell viability, and the tendency of the cells to manufacture dopamine and acetylcholine neurotransmitters as they differentiated into neural cells. The investigators also assessed the abilities of the chemicals to induce oxidative stress that can damage or kill cells. For a benchmark comparison, the research team compared the effects of PFOSA, PFOS, PFOA, and PFBS to those of chlorpyrifos, an insecticide and known developmental neurotoxicant. The PC12 cells, a model of neuronal development, were exposed to the chemicals in five concentrations ranging from 10 ?M to 250 ?M. The effects were assessed over six days?long enough for the cells to differentiate into neuronlike structures. The researchers demonstrated that all four perfluorinated chemicals affected the PC12 cells. PFOSA had the strongest effects on the health of the cells. Next most significant was PFOS, with PFBS and PFOA tied for third place. Despite similarities in their chemical structures, each chemical had a different effect on neurodevelopment, which suggests the adverse effects are likely mediated by different mechanisms. PFOSA behaved very differently from PFOA and PFOS. At all concentrations, PFOSA suppressed the production of DNA. At the highest concentration, almost all DNA production was prevented. In addition to PFOSA preventing the production of new cells, existing cells appeared to have been destroyed. Even at the lowest concentration, PFOSA caused more oxidative stress than that seen with a five-fold higher concentration of chlorpyrifos. At the highest PFOSA concentration, cell viability plummeted. The researchers offer one possible explanation for PFOSA being more toxic than the other perfluorinated chemicals?it is more hydrophobic and therefore crosses cell membranes more easily. This ability to enter cells could indicate that PFOSA and perfluorinated chemicals with similar properties are better able to cross the barriers that guard the placenta and developing brain tissues. Hence, these chemicals may warrant particular research attention. Scott Fields http://www.medworm.com/index.php?rid=1486998&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2008%2F116-6%2Fss.html%23brai brai"> Brain Effects Stick Around PFCs and Neural Cell Development Although some perfluorinated chemicals?manmade compounds used in such goods as nonstick cookware and stain protectors?are no longer manufactured, decoding the ways in which these chemicals affect humans and wildlife is important because of the stability of the compounds, their persistence in the environment, and their long retention times in living organisms. To date, the biological mechanisms through which these chemicals cause damage have not been well understood. Now, however, researchers have shown that four common perfluorinated chemicals?perfluorooctane sulfonamide (PFOSA), perfluorooctane sulfonic acid (PFOS), perfluorooctanoic acid (PFOA), and perfluorobutane sulfonic acid (PFBS)?affect developing PC12 cells in ... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=1486998 Sun, 01 Jun 2008 04:00:00 +0100 1486998 gett'> Getting a Handle on Biosolids New Model Estimates Microbial Exposure Risk Each year several million tons of treated sewage sludge ('biosolids') are applied to crop land, reclaimed surface mines, forests, parks, and various other land areas in the United States. Yet the public health risk from exposure to pathogens in biosolids has never been quantitatively assessed because of the lack of an appropriate model and a paucity of exposure data. Now researchers have developed a model that can estimate microbial exposure, starting with data on the content of certain pathogens in raw sewage sludge, through the treatment process, and ending with exposure to humans [EHP 116:727?733; Eisenberg et al.]. Generation, Treatment, Use, and Disposal of Sewage Sludge Source: Adapted from Environmental Regulations and Technology Report: Control of Pathogens and Vector Attraction in Sewage Sludge. EPA/625/R-92/013. Washington, DC: U.S. EPA, 2003; p. 1. (Matthew Ray/EHP) Untreated sewage sludge contains a wide variety of microbes and parasitic worms. Current federal standards for pathogen reduction in sewage sludge are based on levels of a few indicator organisms, such as Escherichia coli and enteroviruses. A National Research Council committee concluded in 2002 that while there was no evidence that the standards had failed to protect public health, there also had been no concerted effort to investigate health complaints and the potential for adverse human health effects from exposure to biosolids. In the current proof-of-concept article, the model was used to examine three pathogen exposure pathways?ingestion, drinking contaminated groundwater, and inhalation?using data for Class A biosolids, one of two EPA-designated categories of biosolids. Class A sludges have no detectible indicator organisms; low levels of indicator pathogens are permitted in class B sludges. The team used Class A biosolids data for testing. The authors demonstrated the model's utility by calculating human exposure in different settings. Using enterovirus concentration as a proxy for pathogens in general and beginning with data on raw sludge, they calculated the attenuation that resultedfrom anaerobic digestion with or without the use of lime to control the growth of pathogens. They also considered natural attenuation. The modeling suggests that treatment systems using two anaerobic digesters substantially reduce pathogen loads. The most hazardous exposure was seen with contaminated groundwater. Ingesting a 100-mg speck of treated sludge was the next-riskiest exposure, and aerosol exposure was the least risky. Although the new model was not developed with the intention of examining specific disease outcomes, it lays the foundation for future models that could address end points such as irritation of the skin, mucous membranes, and respiratory tract. The authors conclude that risk assessments for biosolids exposure are practical, even for Class A biosolids for which post-treatment monitoring data are below detectable limits. They also believe pathogens in biosolids can now be regulated similarly to water-related risks. Rebecca Renner http://www.medworm.com/index.php?rid=1486997&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2008%2F116-6%2Fss.html%23gett gett"> Getting a Handle on Biosolids New Model Estimates Microbial Exposure Risk Each year several million tons of treated sewage sludge ("biosolids") are applied to crop land, reclaimed surface mines, forests, parks, and various other land areas in the United States. Yet the public health risk from exposure to pathogens in biosolids has never been quantitatively assessed because of the lack of an appropriate model and a paucity of exposure data. Now researchers have developed a model that can estimate microbial exposure, starting with data on the content of certain pathogens in raw sewage sludge, through the treatment process, and ending with exposure to humans [EHP 116:727?733; Eisenberg et al.]. Source: Adapted from Environmental Regulations and Technology Report: Control of Pat... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=1486997 Sun, 01 Jun 2008 04:00:00 +0100 1486997 cook'> Cooking with Wood May Fuel Low Birth Weight Kitchen Smoke Puts Babies at Risk The etiology of low birth weight (LBW; defined as weighing less than 2.5 kg at birth) is complex, with demographic, nutritional, reproductive, and socioeconomic factors each potentially playing a role. Inhaled tobacco smoke is the leading cause of LBW in industrialized countries, and inhaled smoke from the world's most widely used cooking fuel, wood, can impair fetal growth much the same way. A team of researchers therefore launched a population-based study to examine the risk of LBW specifically in relation to use of wood fuel during pregnancy [EHP 116:543?549; Siddiqui et al.]. They found that maternal exposure to pollutants from wood smoke increases the risk of LBW, which is linked with myriad health problems including nutritional deficiencies, impaired psychomotor development, and chronic disease. cooking on a wood stove image: Rashmi Gill/iStockphoto Tobacco smoke and wood smoke work in two ways to thwart fetal development. One occurs when carbon monoxide combines with hemoglobin to cross the placenta. This causes hypoxia, or a decreased oxygen supply to tissue, which limits the ability of the placenta to transfer nutrients to the fetus. The other occurs when inhaled particulate matter from smoke impairs fetal growth by damaging cells through oxidative stress. The team of U.S.- and Pakistan-based researchers studied births in the latter country, where more than half the population cooks with wood and the 19% LBW rate is among the world's highest. The researchers studied 634 women who gave birth from 2000 through 2002 in the poor, semirural community of Rehri Goth. Interviewers collected data on the mothers' cooking habits and family demographics. The researchers also obtained pregnancy and delivery data from the mothers' and infants' medical records. Women who used wood fuel during pregnancy had a significantly higher risk of delivering LBW babies than those who cooked with natural gas?23% versus 15%. More time spent cooking was linked with increased LBW risk in wood users but not natural gas users. Wood users were poorer than users of natural gas; more of them lived in crowded, run-down houses; and they were more likely to be illiterate. Wood users also tended to weigh less than natural gas users. Although such socioeconomic factors may play a greater role in birth outcomes, cooking fuel is one factor that is relatively amenable to change. The authors now propose studies of the health impact of smoke-free stoves. The World Health Organization has predicted that if all Pakistani households cooking with wood converted to cleaner fuels, the incidence of LBW would fall from the current rate of 19% to just below the 15% target rate set by the organization. Cynthia Washam http://www.medworm.com/index.php?rid=1343301&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2008%2F116-4%2Fss.html%23cook cook"> Cooking with Wood May Fuel Low Birth Weight Kitchen Smoke Puts Babies at Risk The etiology of low birth weight (LBW; defined as weighing less than 2.5 kg at birth) is complex, with demographic, nutritional, reproductive, and socioeconomic factors each potentially playing a role. Inhaled tobacco smoke is the leading cause of LBW in industrialized countries, and inhaled smoke from the world's most widely used cooking fuel, wood, can impair fetal growth much the same way. A team of researchers therefore launched a population-based study to examine the risk of LBW specifically in relation to use of wood fuel during pregnancy [EHP 116:543?549; Siddiqui et al.]. They found that maternal exposure to pollutants from wood smoke increases the risk of LBW, which is linked with myriad healt... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=1343301 Tue, 01 Apr 2008 04:00:00 +0100 1343301 arse'> Arsenic and Erectile Dysfunction Drinking Contaminated Well Water Increases Risk Age is the most common risk factor for erectile dysfunction (ED), the consistent or recurrent inability to attain and/or maintain a penile erection sufficient for sexual performance. The correlation between age and ED is attributed to declines in testosterone levels; growing evidence links the condition to cardiovascular disease (CVD) as well. Now researchers from Taiwan have found a direct correlation between ED, the decline of testosterone, and exposure to arsenic via well water?a connection of potential concern for the millions of men worldwide who drink groundwater contaminated with naturally occurring arsenic [EHP 116:532?536; Hsieh et al.]. Besides its association with ED, CVD has also been linked to chronic arsenic exposure, perhaps by reducing the synthesis of nitric oxide (NO), which is involved in the control of smooth muscle in blood vessels. In the penis, NO activates cyclic guanosine monophosphate, which dilates blood vessels, allowing the penis to become engorged with blood. Testosterone can regulate activity of the enzyme nitric oxide synthase, which creates NO. The researchers measured free testosterone levels in the blood of 129 men with ED and 48 without. The average age of the study participants was about 67 years. Sixty-six of the participants were from an arsenic-endemic area in northeast Taiwan where residents have used contaminated artesian well water for more than 50 years. Arsenic exposure was determined by analysis of participants' well water. As arsenic exposure of participants increased, so did the risk of ED. The prevalence of ED was 83.3% among men from the arsenic-endemic area compared with 66.7% among men outside this area. Moreover, as the arsenic exposure of the participants increased, their testosterone levels decreased. The risk of carotid atherosclerosis increased with increasing levels of exposure, but only in men who drank well water containing arsenic concentrations higher than 50 ppb. These men also had a significantly higher risk of ED than men who drank water with arsenic concentrations below 50 ppb, even after adjustments for testosterone levels. Other risk factors for ED did not affect the associations. According to the authors, arsenic exposure appears to increase ED risk by decreasing testosterone levels. However, they speculate that other factors are at work, as decreases in testosterone did not account for all the ED found in men with high arsenic exposures. The presence of oxygen free radicals can inhibit the synthesis of NO and impair blood vessel function. Therefore, the researchers suggest that oxidative stress from high arsenic exposure may also increase ED risk. Kris Freeman http://www.medworm.com/index.php?rid=1343300&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2008%2F116-4%2Fss.html%23arse arse"> Arsenic and Erectile Dysfunction Drinking Contaminated Well Water Increases Risk Age is the most common risk factor for erectile dysfunction (ED), the consistent or recurrent inability to attain and/or maintain a penile erection sufficient for sexual performance. The correlation between age and ED is attributed to declines in testosterone levels; growing evidence links the condition to cardiovascular disease (CVD) as well. Now researchers from Taiwan have found a direct correlation between ED, the decline of testosterone, and exposure to arsenic via well water?a connection of potential concern for the millions of men worldwide who drink groundwater contaminated with naturally occurring arsenic [EHP 116:532?536; Hsieh et al.]. Besides its association with ED, CVD has also been l... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=1343300 Tue, 01 Apr 2008 04:00:00 +0100 1343300 bett'> Better than Eating Worms? Children's Dietary Exposure to OP Pesticides Widespread agricultural use of organophosphate (OP) pesticides frequently leads to low-level exposures in adults and children who eat conventionally grown foods. The frequently used one-time measurement of OP metabolites reveals only short-term exposures, thereby providing little evidence on long-term low-level exposures. A new article presents longitudinal evidence that foods grown in conventional fashion?that is, with the use of pesticides?may be a predominant source of exposure in children [EHP 116:537?542; Lu et al.]. girl eating image: Francisco Romero/iStockphoto The article sprang from the Children's Pesticide Exposure Study, which focused on two groups of children (3?11 years of age) in the Seattle and Atlanta areas from July 2003 to May 2004. For the present study, the researchers examined 23 children in Seattle (19 of whom completed the study) who normally consumed conventional diets. Parents tracked food consumption during the study and collected urine samples twice daily. During interventions over the course of the study, the children's conventional diets were replaced with organic diets and the differences in urinary metabolites of OP pesticides were measured. The organic diets substituted conventionally produced grain, fruit, juice, and vegetables with those produced without pesticides; meat and dairy products rarely contain OP pesticides and were not substituted. During the summer and fall 2003 intervention periods (15 and 12 days, respectively), the children consumed their regular diets from days 1 to 3 and organic diets from days 4 to 8. After day 8, the children resumed their regular diets. There was no organic diet intervention during the winter and spring 2004 sampling periods. Urine samples were analyzed for metabolites of malathion, chlorpyrifos, diazinon, coumaphos, and methyl pirimiphos; only chlorpyrifos and malathion metabolites were detected frequently enough for statistical analysis. These metabolite levels fell to nearly or fully nondetectable levels within days of the children beginning an organic diet intervention and rose when the children returned to conventional diets. Given that OP pesticides were reported by parents not to have been used in the home and that urinary metabolites were clearly affected by diet, the researchers conclude that conventionally produced foods were the primary source of OP pesticide exposure for the children in this study. They also attribute higher dietary exposures to imported produce eaten in the winter and spring when domestic produce is not available. This finding is supported by a 2006 Environmental Protection Agency report showing that OP residues on imported produce have risen since 1996 even as residues on domestically grown produce have fallen. The authors caution, however, that their findings do not promote limiting fresh produce or eating only organic items, as it is unknown whether the observed exposures are harmful. Additionally, the study group did not represent the general population. However, the findings do provide a basis for more accurate assessment of exposure and associated efforts to determine the effects of OP pesticides on Childrens Health. Julia R. Barrett http://www.medworm.com/index.php?rid=1343299&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2008%2F116-4%2Fss.html%23bett bett"> Better than Eating Worms? Children's Dietary Exposure to OP Pesticides Widespread agricultural use of organophosphate (OP) pesticides frequently leads to low-level exposures in adults and children who eat conventionally grown foods. The frequently used one-time measurement of OP metabolites reveals only short-term exposures, thereby providing little evidence on long-term low-level exposures. A new article presents longitudinal evidence that foods grown in conventional fashion?that is, with the use of pesticides?may be a predominant source of exposure in children [EHP 116:537?542; Lu et al.]. image: Francisco Romero/iStockphoto The article sprang from the Children's Pesticide Exposure Study, which focused on two groups of children (3?11 years of age) in the Seattle and At... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=1343299 Tue, 01 Apr 2008 04:00:00 +0100 1343299 taki'> Taking a Bite Out of Amalgam Concerns? Study Shows No Renal Effects in Children Dental amalgam is a major source of human exposure to inorganic mercury, which is thought to occur primarily when elemental mercury from the amalgam surface evaporates and is inhaled. Prior studies provide strong evidence that the central nervous system and the kidney are the primary targets of inorganic mercury. Data from the New England Children's Amalgam Trial (NECAT), a clinical trial designed to study the possible health effects in children of mercury-containing dental amalgam, now indicate that amalgam fillings' effects on renal function may be quite small [EHP 116:394 399; Barregard et al.] girl in dentist chair image: Stockbyte The study, launched in 1996 in Maine and Massachusetts, is one of two parallel randomized trials funded by the National Institute of Dental and Craniofacial Research. These trials provide the first rigorously designed clinical data on the effects of children's dental exposure to mercury, a known neuro- and nephrotoxicant. A group of 537 children aged 6 10 years at the start of the trial were followed for five years. Children began the trial with no pre-existing fillings and at least one cavity in a back tooth. The children were randomly assigned to two groups, one receiving only amalgam fillings in cavities in the back teeth and the other receiving only composite fillings in the back teeth. Both groups received the more aesthetically pleasing composite fillings in the front teeth, conforming to current standard dental practice. The children showed no statistically significant differences in several markers of toxicity to renal tubules studied including N-acetyl-beta-D-glucosaminidase and alpha-1-microglobulin, both early indicators of toxic exposure to mercury vapor, or in gamma -glutamyl transpeptidase, which has been shown to be affected by toxic heavy metal exposure regardless of whether their cavities were filled with amalgam or with composite. Microalbuminuria, the occurrence of small quantities of albumin in the urine, increased in 10 children treated with amalgam and in 2 treated with composite fillings, but it did not correlate with the number of amalgam fillings or with increasing concentrations of mercury excreted in urine. Because this difference is marginally significant, the authors note it may be due to chance. Moreover, microalbuminuria can occur transiently as a consequence of recent vigorous play. The results therefore appear to indicate that the use of amalgam fillings does not cause any clear, consistent damage to kidney function in young, developing children. Victoria McGovern http://www.medworm.com/index.php?rid=1274650&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2008%2F116-3%2Fss.html%23taki taki"> Taking a Bite Out of Amalgam Concerns? Study Shows No Renal Effects in Children Dental amalgam is a major source of human exposure to inorganic mercury, which is thought to occur primarily when elemental mercury from the amalgam surface evaporates and is inhaled. Prior studies provide strong evidence that the central nervous system and the kidney are the primary targets of inorganic mercury. Data from the New England Children's Amalgam Trial (NECAT), a clinical trial designed to study the possible health effects in children of mercury-containing dental amalgam, now indicate that amalgam fillings' effects on renal function may be quite small [EHP 116:394 399; Barregard et al.] image: Stockbyte The study, launched in 1996 in Maine and Massachusetts, is one of two parallel ... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=1274650 Sat, 01 Mar 2008 05:00:00 +0100 1274650 dust'> Dust Storm Fallout Tiniest Travelers Pose Greatest Infection Threat Dust isn't just a nuisance its ability to clog human airways and carry pathogens poses a human health problem. In the sub-Saharan region of Africa, the World Health Organization pinpointed dust storms exacerbated by the dry season and drought as a cause of outbreaks of meningococcal meningitis. Dust from Saharan storms can reach as far away as Florida, with particles smaller than 2.5 microm traveling the greatest distances. Studies have shown that human exposure to these tiny particles is associated with human mortality, and new research now shows that such particles are also more likely to carry health-threatening bacteria [EHP 116:292 296; Polymenakou et al.]. dust storm over eastern Mediterranean Sea The dust storm that provided samples for Polymenakou et al. obscures the eastern Mediterranean Sea, 25 February 2006 image: Jeff Schmaltz, MODIS Rapid Response Team, NASA/GSFC During a strong Saharan dust storm in 2006, researchers collected air samples in Heraklion, Crete, an area that often feels the effects of such storms. Particles from the samples were separated according to size (>7.9 microm, 3.3 7.9 microm, 1.6 3.3 microm, 1.0 1.6 microm, 0.55 1.0 microm, or The researchers identified clones that were genetically related to pathogens linked to human diseases such as pneumonia, meningitis, and bacteremia, or to pathogens suspected of inducing infections such as endocarditis. Of the sequenced clones related to bacteria that are dangerous to humans, almost half (43%) were found at particle sizes less than 3.3 microm. Spore-forming bacteria such as Firmicutes dominated the particle sizes larger than 3.3 microm. Most of these bacteria are nonpathogenic. The authors conclude that the prevalence of breathable bacteria on small dust particles may pose a significant, widespread health risk to humans, given that dust, especially the smallest particles, is known to travel across continents. To determine just how much of a threat these tiny travelers pose, long-term studies are needed to further investigate how pathogens are distributed across dust particle size, and the distances these pathogens can travel and still survive. Angela Spivey http://www.medworm.com/index.php?rid=1274649&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2008%2F116-3%2Fss.html%23dust dust"> Dust Storm Fallout Tiniest Travelers Pose Greatest Infection Threat Dust isn't just a nuisance its ability to clog human airways and carry pathogens poses a human health problem. In the sub-Saharan region of Africa, the World Health Organization pinpointed dust storms exacerbated by the dry season and drought as a cause of outbreaks of meningococcal meningitis. Dust from Saharan storms can reach as far away as Florida, with particles smaller than 2.5 microm traveling the greatest distances. Studies have shown that human exposure to these tiny particles is associated with human mortality, and new research now shows that such particles are also more likely to carry health-threatening bacteria [EHP 116:292 296; Polymenakou et al.]. The dust storm that provided samples for Polym... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=1274649 Sat, 01 Mar 2008 05:00:00 +0100 1274649 life'> Life after Lindane in California Water Concentrations, Poison Control Calls Drop Following Ban Lindane, a persistent, highly toxic, and bioaccumulative organochlorine insecticide, was used in agriculture and as a topical treatment for human head lice and scabies beginning in the 1940s. As its toxicity became better known, manufacture and use declined in the United States; in 2002, California banned the pharmaceutical use of lindane altogether. According to a new study, that ban appears to have resulted in steep drops in concentrations of lindane in Southern California's wastewater and a dramatic reduction in calls to the California Poison Control System [EHP 116:297 302; Humphreys et al.]. The most common adverse effects of lindane exposure in humans include seizures, dizziness, and headaches. High levels of exposure can be fatal. Although the U.S. Environmental Protection Agency has canceled all registrations for lindane-containing compounds in agriculture, the chemical is still available by prescription as a second-line treatment for head lice in states other than California. Its continued pharmaceutical use raises concerns about its potential presence in wastewater effluent and drinking water. The research team, part of the University of California, San Francisco, Pediatric Environmental Health Specialty Unit, examined historical lindane concentrations in several Southern California water pollution control plants and compared them before and after the ban. To assess the ban's impact on human exposures, they analyzed lindane-related calls to California's poison control hotline between 1998 and 2006. They searched the Medi-Cal fee-for-service pharmacy-paid claims database and obtained national data from Verispan, a commercial health industry data tracker, to determine the number of lindane prescriptions issued. The team also conducted a random survey of pediatricians to ascertain both their awareness of the ban and their current treatment preferences for scabies and head lice. In Los Angeles County, the average wastewater concentration of lindane in 1999 was 36 ppt. By 2006, concentrations had dropped to almost undetectable levels throughout California. In 1998, 135 per 100,000 calls to the Poison Control System concerned lindane; by 2006 such calls had declined to 2 per 100,000. Similarly, lindane prescriptions fell from 114,000 in 1997 to 34 in 2002. Medical providers reported few problems using alternative treatments such as pyrethrins. The study authors are encouraged by their findings but note that lindane is still used in many countries, mostly in the developing world, and that every ton of lindane manufactured produces about 9 tons of toxic waste. Although the U.S. Food and Drug Administration has not banned pharmaceutical lindane in the United States, the pesticide is currently under review for inclusion in the Stockholm Convention on Persistent Organic Pollutants, which could eventually lead to a worldwide ban. Valerie J. Brown http://www.medworm.com/index.php?rid=1274648&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2008%2F116-3%2Fss.html%23life life"> Life after Lindane in California Water Concentrations, Poison Control Calls Drop Following Ban Lindane, a persistent, highly toxic, and bioaccumulative organochlorine insecticide, was used in agriculture and as a topical treatment for human head lice and scabies beginning in the 1940s. As its toxicity became better known, manufacture and use declined in the United States; in 2002, California banned the pharmaceutical use of lindane altogether. According to a new study, that ban appears to have resulted in steep drops in concentrations of lindane in Southern California's wastewater and a dramatic reduction in calls to the California Poison Control System [EHP 116:297 302; Humphreys et al.]. The most common adverse effects of lindane exposure in humans include seizures, dizziness... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=1274648 Sat, 01 Mar 2008 05:00:00 +0100 1274648 revi'> Revisiting the DDE?Lactation Question Association Not Confirmed in Breastfeeding Mothers Breastfeeding is known to be protective of newborn health, for example by lowering infant mortality and risk of infectious diseases. But breastfeeding is on the decline in some locales, especially in developing countries. Some studies have reported a link between elevated maternal serum DDE (the primary metabolite of the pesticide DDT) and shorter breastfeeding duration, suggesting that exposure to DDT affects the ability to breastfeed. New research does not confirm this hypothesis, however, and suggests possible ways to refine our understanding of the association previously reported with DDE [EHP 116:179?183; Cupul-Uicab et al.]. woman smiling Good news for now. Data from a study of Mexican mothers do not support earlier concerns that DDT exposure might impede lactation. image: Sean Sprague/Panos Pictures Both DDT and DDE are retained in fatty tissue and excreted in breast milk. DDT was banned in the United States in 1972 but is still being used elsewhere to fight malaria. Given DDT's prominence in malaria prevention, it is important to determine whether it affects infant and maternal health. The current study involved 784 mother?son pairs from Tapachula, Chiapas, Mexico, where DDT had been used for about 40 years. The pairs had previously participated in a study of DDE's antiandrogenic effects, in which the mothers' serum levels of DDT and DDE were measured shortly after delivery. For the current study, the researchers interviewed each mother about every 2 months until her baby was weaned to determine the length of lactation. The Tapachula women's serum levels of DDE were about 15 times higher than recently measured levels in U.S. women. The team was not surprised to find higher DDE levels in first-time breastfeeders, because experienced breastfeeders would already have transferred some of their DDE body burden to earlier children. In the group as a whole, few women reported problems starting breastfeeding, and the median nursing duration was 10.8 months. The researchers found a statistically significant positive association between DDE and shorter duration of lactation, but only among women who had previously breastfed. This is consistent with some earlier research. But the team writes that it is probably an artifact rather than a causal link; otherwise, an association between DDE and shortened lactation would have been observed in both experienced and novice breastfeeders. Only 11 women could not breastfeed?too small a number for statistical significance?but these women did have higher median serum DDE concentrations than the other women in the study. Although the authors found no link between DDE and shortened breastfeeding duration, they write that DDT exposure may make it more difficult to initiate breastfeeding, perhaps because of endocrine disruption early in lactation. For the first 2?3 days, lactation is controlled by hormones. If DDE behaves like estrogen, it could suppress initial milk production but have a weaker effect on established lactation. Future research could focus on this avenue by which DDE may affect successful breastfeeding. Valerie J. Brown http://www.medworm.com/index.php?rid=1194366&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2008%2F116-2%2Fss.html%23revi revi"> Revisiting the DDE?Lactation Question Association Not Confirmed in Breastfeeding Mothers Breastfeeding is known to be protective of newborn health, for example by lowering infant mortality and risk of infectious diseases. But breastfeeding is on the decline in some locales, especially in developing countries. Some studies have reported a link between elevated maternal serum DDE (the primary metabolite of the pesticide DDT) and shorter breastfeeding duration, suggesting that exposure to DDT affects the ability to breastfeed. New research does not confirm this hypothesis, however, and suggests possible ways to refine our understanding of the association previously reported with DDE [EHP 116:179?183; Cupul-Uicab et al.]. Good news for now. Data from a study of Mexican mothers d... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=1194366 Fri, 01 Feb 2008 05:00:00 +0100 1194366 arse'> Arsenic Makes Its Mark Using Biomarkers to Track Noncancer Respiratory Effects Exposure to toxic levels of arsenic is a serious problem in many Asian countries, notably Bangladesh and India, where exposure to inorganic arsenic through naturally contaminated groundwater is widespread and often excessive. Scientists have long recognized the lung to be a major site of action of ingested arsenic, and most of the focus has been on risks associated with lung cancer. Nonetheless, habitual ingestion of high-arsenic drinking water also promotes many noncancer lung effects, and researchers are investigating the potential utility of biomarkers to identify such effects [EHP 116:190?195; Parvez et al.]. man collecting water from a well As it happens . . . Lung cancer isn't the only respiratory effect linked with drinking arsenic-contaminated water; noncancer effects also may occur. image: Heldur Netocny/Panos Pictures One of the challenges of pursuing connections between arsenic and respiratory illness is that assessments of respiratory symptoms may be prejudiced by interviewer bias if study participants show visible skin lesions, a hallmark sign of chronic arsenic poisoning. To overcome this obstacle, researchers have begun exploring the use of biomarkers for chronic respiratory disease such as serum levels of Clara cell protein CC16. This serum marker runs low in individuals with compromised lung conditions induced by chronic environmental exposures such as cigarette smoking or ozone. In the current study, investigators sought to determine the relationships of serum CC16 with well-water arsenic, total urinary arsenic, and urinary arsenic methylation indices in a population of 241 nonsmoking individuals exposed to arsenic-laden drinking water in Araihazar, Bangladesh. The mean arsenic concentration in drinking water was 134 ?g/L, and individuals with skin lesions consumed significantly more arsenic than those without (159 versus 105 ?g/L, respectively). In individuals with skin lesions (but not those without such lesions), there was a significant inverse association of CC16 with urinary arsenic as well as a marginally significant inverse association of CC16 with the cumulative arsenic exposure index, which estimates long-term exposure. The researchers speculate that individuals with skin lesions either are exposed to higher levels of arsenic or have a unique susceptibility to the respiratory effects of arsenic exposure for reasons unknown. The analysis also revealed positive associations of CC16 levels with the secondary arsenic methylation index (an indicator of arsenic methylation capability), particularly among individuals without skin lesions. This suggests that individuals with better methylation capacity may be less susceptible to the adverse respiratory effects of arsenic. Moreover, the inverse association of CC16 with the percentage of monomethylated arsenic (a commonly measured arsenic metabolite) in urine indicates that individuals with incomplete methylation may be more vulnerable to arsenic-induced respiratory problems. This cross-sectional investigation, the first to use biomarkers of arsenic exposure and lung injury in this way, is an important step toward further improving our understanding of arsenic-related nonmalignant respiratory illness. Serum CC16 shows promise as a biomarker for assessing early respiratory damage induced by arsenic, especially among individuals with skin lesions associated with the consumption of arsenic-contaminated drinking water. M. Nathaniel Mead http://www.medworm.com/index.php?rid=1194365&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2008%2F116-2%2Fss.html%23arse arse"> Arsenic Makes Its Mark Using Biomarkers to Track Noncancer Respiratory Effects Exposure to toxic levels of arsenic is a serious problem in many Asian countries, notably Bangladesh and India, where exposure to inorganic arsenic through naturally contaminated groundwater is widespread and often excessive. Scientists have long recognized the lung to be a major site of action of ingested arsenic, and most of the focus has been on risks associated with lung cancer. Nonetheless, habitual ingestion of high-arsenic drinking water also promotes many noncancer lung effects, and researchers are investigating the potential utility of biomarkers to identify such effects [EHP 116:190?195; Parvez et al.]. As it happens . . . Lung cancer isn't the only respiratory effect linked with drinkin... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=1194365 Fri, 01 Feb 2008 05:00:00 +0100 1194365 test'> Testing Lead's Limits Time for Another Reassessment of Guidelines? Cohort data during the 1980s linked blood lead levels of at least 10 ?g/dL with low cognitive test scores in children, prompting the decision by the Centers for Disease Control and Prevention to redefine the action level for elevated blood lead from 25 to 10 ?g/dL. Now, new data add to the growing evidence that the 10-?g/dL level may not be protective [EHP 116:243?248; Jusko et al.]. The investigators recruited children aged 24?30 months who had been previously enrolled in a dust control study. All the children were born between July 1994 and January 1995 and lived in Rochester, New York, with parents expressing no plans to relocate. To reduce the possibility of misclassification of exposure, blood samples were collected for measuring blood lead on up to 8 occasions (at ages 6, 12, and 18 months, and annually from age 2 through 6 years). The children were given the Wechsler Preschool and Primary Scale of Intelligence during their 6-year visit by an examiner trained in neurobehavioral testing and blinded to each child's blood lead level. These assessments were made at an age when IQ is measured reliably and is a significant predictor of IQ scores and educational and occupational success during adolescence and adulthood. The data analysis employed a regression model that controlled for family income; maternal education, race, prenatal smoking, and Stanford-Binet IQ score; child's birth weight; breastfeeding; crowding in the home; and quality of childrearing (using the Home Observation for Measurement of the Environment Inventory). The average blood lead level was 7.2 ?g/dL, and lead concentrations for more than half the children never exceeded the 10 ?g/dL mark. Even at these concentrations, blood lead levels were inversely related to IQ scores. The association was most pronounced for the Full-Scale and Performance IQ scores. Children whose blood lead levels measured in the 5- to 9.9-?g/dL range had significantly lower IQ scores than children with levels below 5 ?g/dL. A descriptive analysis of peak exposure throughout early childhood suggested an inverse association between maximal blood lead level and IQ at blood lead levels less than 3 ?g/dL; levels as low as about 2 ?g/dL were associated with significant IQ declines. These findings, reinforced by previous data gathered by the same research team, support the need for a further reassessment of standard guidelines for responding to blood lead in infants and children. M. Nathaniel Mead http://www.medworm.com/index.php?rid=1194364&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2008%2F116-2%2Fss.html%23test test"> Testing Lead's Limits Time for Another Reassessment of Guidelines? Cohort data during the 1980s linked blood lead levels of at least 10 ?g/dL with low cognitive test scores in children, prompting the decision by the Centers for Disease Control and Prevention to redefine the action level for elevated blood lead from 25 to 10 ?g/dL. Now, new data add to the growing evidence that the 10-?g/dL level may not be protective [EHP 116:243?248; Jusko et al.]. The investigators recruited children aged 24?30 months who had been previously enrolled in a dust control study. All the children were born between July 1994 and January 1995 and lived in Rochester, New York, with parents expressing no plans to relocate. To reduce the possibility of misclassification of exposure, blood samples were ... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=1194364 Fri, 01 Feb 2008 05:00:00 +0100 1194364 scie'> Science in the Courtroom Examining Standards for Litigation-Based Research Over the last 20 years, the term 'junk science' has gained increasing use by defendants in toxic tort litigation as a pejorative phrase to discredit health effects data that do not meet some standard for scientific validity?or, some say, that are favorable to the interests of plaintiffs. Proponents of tort reform have argued that many large jury verdicts are the unjustified products of questionable scientific data presented by plaintiff lawyers to easily swayed jurors. Courts have responded by raising the bar that scientific evidence must exceed in order to be admitted as evidence. But has this change produced sound results? Is there really a distinction between litigation-based science and other science? In a mini-monograph in this issue, 5 articles examine these questions and others that arise when examining the juncture of science and litigation [EHP 116:116?147]. Acknowledging that conflicts of interest are an inherent component of science-based litigation, authors Ronald L. Melnick, Kristina A. Thayer, and John R. Bucher of the NIEHS conclude that public health decisions to allow exposure to possible carcinogens should not rely 'on untested hypotheses that are promoted to explain away adverse outcomes.' Their article focuses specifically on rodent carcinogenicity studies and examines how strict attention to design and evaluation can reduce inaccurate conclusions and provide data that are useful for evaluating human health risks. Litigation-Based Research image: Getty Images, Matthew Ray/EHP The authors cite early animal studies on benzene as an example of poor design that failed to detect carcinogenic effects, even though epidemiologic studies demonstrated a causal association between benzene exposure and leukemia in humans. Those early studies employed too few animals, insufficient controls, too short a study duration, and inadequate levels of exposure. In addition, the authors write, 'evaluations that are based on incomplete necropsy or histopathology, do not combine related tumor effects, fail to adjust for differences in animal survival, or incorrectly use historical control data would not be expected to produce reliable information on chemical carcinogenesis.' Courts, meanwhile, have also taken steps to reduce the likelihood of 'junk science' influencing juries. Two of the articles in the mini-monograph, the first by Leslie I. Boden and David Ozonoff of the Boston University School of Public Health and the other by Sheila Jasanoff of Harvard University?s Kennedy School of Government, examine the assertion that science conducted to support litigation must be held to tougher admissibility standards than other science. Appeals Court Judge Alex Kosinski made this claim in 1995 in response to the Supreme Court remand in Daubert v. Merrell-Dow Pharmaceuticals, Inc., deciding that judges were henceforth required to assume roles as gatekeepers with the responsibility of culling out unreliable expert evidence. As the authors describe, many courts following Daubert have held that research conducted specifically for the purpose of a litigation is inherently less reliable than other science. Boden and Ozonoff re-examine whether litigation-based science should be treated differently from other science offered as evidence in the courtroom. They conclude that it shouldn?t. Their contentions include an assertion that cross-examination by attorneys aided by competent experts, not just journal peer review, also serves the ends of justice. They further argue that any science is subject to a variety of biases; for example, they write, studies funded by pharmaceutical companies or investments by corporations in research agendas tend to favor their own economic interest. Finally, the authors argue that tougher standards for litigation-generated science unfairly burden plaintiffs. In her article, Jasanoff agrees that restrictions placed on litigation-based science following Daubert are misconceived because the scientific knowledge needed to resolve legal disputes often arises only in response to litigation. Rather than assign judges the role of gatekeeper, a more sensible approach, she writes, would be for judges to assume the position of referee. In this role, judges would 'focus on the process through which litigation science is generated rather than on its validity or invalidity. They would be in a position to structure agreements among the parties that would be most conducive to producing relevant and reliable knowledge.' In a fourth article, Carol J. Henry and James W. Conrad, Jr., of the American Chemistry Council focus on the role of federal agencies rather than that of the courts. They write that the quality of agency scientific research and testing is already subject to a variety of standards and practices (e.g., the Federal Information Quality Act, and peer review and transparency in research practices), and argue that these standards and practices allow agencies to judge the quality of work regardless of the reason for which it was created. They also point out that federal agencies are required to accept and fairly consider information provided by any interested person in the course of decision making. In the last paper, William R. Freudenburg of the University of California, Santa Barbara, takes a critical look at the nature of bias itself, concluding that scientists oftentimes are not conscious of its influence on them. Drawing from personal experience, Freudenburg describes litigation-based research he conducted for a company that never tried to censor his work and consistently praised him for being principled and credible. But he subsequently came to realize that praise for his objectivity actually encouraged him to interpret his findings in ways that would favor his corporate sponsors more than if they had tried to tell him what to say. The problem, he writes, was 'the temptation to start changing my own judgments . . . in response to their repeated insistence that it was precisely my independent and scientific credibility that they valued.' The articles in the mini-monograph share a common thread: when science is used to serve the purposes of litigation or administrative proceedings, great care is needed to ensure its proper deployment, and a courtroom judge is probably not the appropriate person to decide on the reliability and relevance of scientific evidence. Furthermore, the perception that bias is inherently bad or avoidable may itself be biased. Richard C. Dahl | Purchase This Issue | http://www.medworm.com/index.php?rid=1128239&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2008%2F116-1%2Fss.html%23scie scie"> Science in the Courtroom Examining Standards for Litigation-Based Research Over the last 20 years, the term "junk science" has gained increasing use by defendants in toxic tort litigation as a pejorative phrase to discredit health effects data that do not meet some standard for scientific validity?or, some say, that are favorable to the interests of plaintiffs. Proponents of tort reform have argued that many large jury verdicts are the unjustified products of questionable scientific data presented by plaintiff lawyers to easily swayed jurors. Courts have responded by raising the bar that scientific evidence must exceed in order to be admitted as evidence. But has this change produced sound results? Is there really a distinction between litigation-based science and other science?... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=1128239 Tue, 01 Jan 2008 05:00:00 +0100 1128239 clea'> Clear Reception Elucidating the Binding Characteristics of Bisphenol A Several studies have indicated that bisphenol A (BPA), which is widely used in polycarbonate plastic and epoxy resin manufacturing, can disrupt normal endocrine function. Given that BPA's estrogen receptor (ER) binding and interaction are 100?1,000 times weaker than those of endogenous hormones, researchers have hypothesized that BPA interacts with nuclear receptors other than ER. A recent study directly assayed BPA's interaction with estrogen-related receptor- (ERR- ), one of a family of 'orphan' nuclear receptors?those for which natural ligands are unknown?and clarified the structural requirements that enable BPA to bind this receptor [EHP 116:32?38; Okada et al.]. Earlier research by the same team demonstrated that BPA strongly binds ERR- . The research also showed that BPA preserves ERR- 's high constitutive activity. Receptors with constitutive activity trigger molecular events in the absence of a ligand; specific ligands known as inverse agonists can deactivate these receptors. The authors emphasize the importance of this investigation by noting that ERR- is very strongly expressed in the mammalian brain during development and in the brain, lung, and other tissues in adults; unpublished results from this group show the highest expression in the placenta. It is possible that BPA's binding ERR- could affect the receptor's role by activating transcription at the wrong times. Using tritium-labeled BPA, the researchers conducted the first saturation binding assay to precisely characterize how strongly BPA binds ERR- . They also ran competitive binding assays with BPA analogs and other industrial chemicals, including phenol derivatives, to identify which structural characteristics of the chemicals are critical for binding ERR- and maintaining its constitutive activity. They found specific, extremely high binding affinity of BPA for ERR- . BPA analogs varied in their ability to bind the receptor, and phenol derivatives were newly discovered to be potential candidates for ERR- ?mediated endocrine disruption. These findings raise the immediate question of whether reported BPA-related endocrine disruption might actually be mediated through ERR- rather than through ER. Additionally, the researchers stress the need to determine the normal physiologic roles of ERR- as well as the ways in which BPA might affect these roles. Given the strong expression of ERR- in the fetal brain and placenta, further information is especially urgent with regard to outcomes for newborns. Julia R. Barrett http://www.medworm.com/index.php?rid=1128238&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2008%2F116-1%2Fss.html%23clea clea"> Clear Reception Elucidating the Binding Characteristics of Bisphenol A Several studies have indicated that bisphenol A (BPA), which is widely used in polycarbonate plastic and epoxy resin manufacturing, can disrupt normal endocrine function. Given that BPA's estrogen receptor (ER) binding and interaction are 100?1,000 times weaker than those of endogenous hormones, researchers have hypothesized that BPA interacts with nuclear receptors other than ER. A recent study directly assayed BPA's interaction with estrogen-related receptor- (ERR- ), one of a family of "orphan" nuclear receptors?those for which natural ligands are unknown?and clarified the structural requirements that enable BPA to bind this receptor [EHP 116:32?38; Okada et al.]. Earlier research by the same team demonst... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=1128238 Tue, 01 Jan 2008 05:00:00 +0100 1128238 miti'> Mitigating Methylmercury Exposure Study Confirms Potential of NAC as Antidote and Biomarker Researchers have been searching for better ways to quantify and mitigate exposures to the neurotoxicant methylmercury (MeHg). Results from a new animal study confirm that N-acetylcysteine (NAC), already used to treat acetaminophen overdose, may serve as a quick-acting antidote for and biomarker of MeHg exposure [EHP 116:26?31; Aremu et al.]. MeHg is created when elemental mercury released through the burning of coal, waste incineration, and other industrial processes is metabolized by aquatic microorganisms such as anaerobic bacteria. It bioaccumulates rapidly, with concentrations in some top marine predators reaching 100,000 times that of surrounding seawater. Fish consumption is the major source of human exposure. MeHg can cause irreversible brain damage, and the developing brain is especially vulnerable to its effects. Treatments to mitigate MeHg exposure involve chelation, the administration of compounds that bind mercury, speeding its elimination from the body and thereby minimizing its toxicity. Current chelation methods can be nonspecific, depleting not only MeHg but also minerals required for normal cell function, such as calcium. illustration of rodent and chemical structure image: Indigo Fish/Shutterstock, Getty Images, Matthew Ray/EHP In contrast, chelation treatment with NAC does not affect levels of essential minerals. NAC, a derivative of the amino acid L-cysteine and a precursor of the antioxidant glutathione, is itself a potent antioxidant. NAC can be delivered intravenously or orally. In the current study, adult rats were injected with NAC (1 mmol/kg) 2 hours after being exposed to MeHg (0.1 ?mol/kg). The treated animals excreted about 5% of their body burden of MeHg within 2 hours, compared with less than 0.1% excreted by untreated animals. The response was transient and dose dependent, with larger doses of NAC resulting in higher rates of MeHg excretion. These effects were not seen in preweaned rats (age 15?19 days) treated with NAC. The researchers speculate that the transporter systems needed to move the MeHg?NAC complex through the kidney do not mature until animals reach adulthood (around 30 days of age). However, oral NAC treatment in pregnant rats (10 mg/mL in drinking water) did protect their fetuses, reducing concentrations in the placenta and the whole fetus by 70?90%. In the dams themselves, NAC also reduced MeHg concentrations by 70?90% in the brain, by about 20% in the kidney, and by 60?80% in the blood and liver. NAC's short half-life, about 2 hours, may allow it to serve as an accurate real-time biomarker of MeHg exposure. According to the researchers, such a quick-acting biomarker could provide critical early warning of possible acute exposures, where early treatment is critical to prevent neurological damage. In the current study, MeHg excretion in animals treated with NAC was proportionate to MeHg body burden at the time of treatment. In contrast, standard monitoring techniques, which use hair analysis, can provide only a history of exposure and cannot guide immediate treatment for acute exposures. The researchers propose that future studies test NAC in adult humans as a biomarker of exposure and a possible treatment for MeHg exposure, especially for pregnant women whose unborn children are in danger of prenatal MeHg exposure. Kris Freeman http://www.medworm.com/index.php?rid=1128237&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2008%2F116-1%2Fss.html%23miti miti"> Mitigating Methylmercury Exposure Study Confirms Potential of NAC as Antidote and Biomarker Researchers have been searching for better ways to quantify and mitigate exposures to the neurotoxicant methylmercury (MeHg). Results from a new animal study confirm that N-acetylcysteine (NAC), already used to treat acetaminophen overdose, may serve as a quick-acting antidote for and biomarker of MeHg exposure [EHP 116:26?31; Aremu et al.]. MeHg is created when elemental mercury released through the burning of coal, waste incineration, and other industrial processes is metabolized by aquatic microorganisms such as anaerobic bacteria. It bioaccumulates rapidly, with concentrations in some top marine predators reaching 100,000 times that of surrounding seawater. Fish consumption is the ma... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=1128237 Tue, 01 Jan 2008 05:00:00 +0100 1128237 uran'> Uranium in Drinking Water Low Dose Acts as Endocrine Mimic Uranium, the heaviest naturally occurring element, is well known as a radioactive toxicant capable of damaging the kidneys and DNA. A new study has shown for the first time that uranium also acts as an estrogen mimic in mice at concentrations below the U.S. EPA's safety limit of 30 ?g/L in drinking water [EHP 115:1711?1716; Raymond-Whish et al.]. Other metals, including arsenic, cadmium, lead, and mercury, also are known estrogen mimics. glass of tap water Mine memory. Navajo miners work the Kerr-McGee uranium mine, 7 May 1953. Today, uranium from unremediated abandoned mines contaminates nearby water supplies. image: AP Photo The researchers manipulated the reproductive status of female mice in several ways. They exposed one group of immature female mice to uranium as they matured, a second group of mature female mice to uranium at environmentally relevant concentrations for 30 days prior to breeding and through gestation, and a third group of female mice to uranium immediately after their ovaries were removed. In a fourth group, they removed the ovaries of female mice, then exposed subgroups of this cohort to either uranium or the synthethic estrogen diethylstilbestrol (DES) alone or in combination with the antiestrogen ICI 182,780. All uranium exposures were via the mice's drinking water at concentrations of 0.5 ?g/L?60.0 mg/L. Uranium had estrogen-like effects at varying dose ranges throughout the suite of experiments. In the first group, exposure resulted in fewer primary and more secondary ovarian follicles among adult females. In the second group, female pups of exposed dams had significantly fewer small primary ovarian follicles. The researchers conjecture that this primary-to-secondary follicle ratio may lead to fewer ovulated eggs and early-onset menopause. In the ovariectomized mice, the researchers found higher uterine weights and accelerated vaginal opening (indicators of earlier puberty onset). In addition, estrogenic activity was blocked in the mice exposed to ICI 182,780 after DES or uranium exposure. The current study is of immediate relevance to the Navajo Nation of Arizona and New Mexico, where many rural Navajo water supplies currently contain uranium at concentrations exceeding the U.S. EPA standard. The uranium boom of the 1950s and 1960s left thousands of abandoned mine sites and derelict milling operations on Navajo lands. Uranium mining has been banned there, but there are active efforts to revive uranium mining in the Navajo town of Crownpoint, New Mexico. The findings may also soon apply to other populations living amid the uranium boom now under way in central Colorado, Canada, Australia, and elsewhere. Valerie J. Brown http://www.medworm.com/index.php?rid=1066891&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2007%2F115-12%2Fss.html%23uran uran"> Uranium in Drinking Water Low Dose Acts as Endocrine Mimic Uranium, the heaviest naturally occurring element, is well known as a radioactive toxicant capable of damaging the kidneys and DNA. A new study has shown for the first time that uranium also acts as an estrogen mimic in mice at concentrations below the U.S. EPA's safety limit of 30 ?g/L in drinking water [EHP 115:1711?1716; Raymond-Whish et al.]. Other metals, including arsenic, cadmium, lead, and mercury, also are known estrogen mimics. Mine memory. Navajo miners work the Kerr-McGee uranium mine, 7 May 1953. Today, uranium from unremediated abandoned mines contaminates nearby water supplies. image: AP Photo The researchers manipulated the reproductive status of female mice in several ways. They exposed one group ... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=1066891 Sat, 01 Dec 2007 05:00:00 +0100 1066891 diet'> Dietary Dose Rodent Feed Affects ED Screening Results As the U.S. EPA begins its program to test endocrine-disrupting effects of pesticides, researchers caution that routine screening methods could distort results [EHP 115:1717?1726; Thigpen et al.]. The team discovered that some commercially available rodent diets can cause early sexual maturation similar to that induced by chemical endocrine disruptors. Furthermore, one rat strain commonly used by many researchers is not the most sensitive to the effects of endocrine disruptors and thus may not provide optimal results. illustration of rodent and chemical structure image: Matthew Ray/EHP The U.S. EPA Endocrine Disruptor Screening Program was mandated by Congress in 1996 amid mounting evidence that hormone-mimicking chemicals in the environment alter sexual traits in exposed wildlife. Research suggests these chemicals might also contribute to increases in human male reproductive disorders including poor sperm quality, cryptorchidism, and hypospadias. In June 2007 the U.S. EPA published a list of 73 suspect chemicals for initial screening. According to the authors of the current study, some rodent diets could distort screening results because they contain high levels of plant estrogens. The phytoestrogens genistein and daidzein are found in the soybeans used in many rodent diets. U.S. EPA guidelines allow a limited amount of genistein and daidzein in the diets of rodents used for screening. The authors report, however, that even approved levels of these compounds are sufficient to adversely impact sexual end points that researchers use to measure endocrine disruption. Furthermore, genistein and daidzein levels vary significantly among different batches of the same diet. Rats on a diet with the highest genistein and daidzein concentrations reached sexual maturity several days earlier than those fed a different batch of the same diet containing lower levels of the compounds. In addition, rodents on high-calorie diets grew faster and reached sexual maturity earlier than those fed a low-calorie diet. The researchers measured sexual maturity by observing the day each rodent's vagina opened. Vaginal opening provides a noninvasive measurement that does not require the animal to be sacrificed. In contrast, sexual maturity is typically measured by uterine weight, which increases at puberty. The results revealed that dietary estrogens had a lesser effect on the vaginal opening day of Sprague-Dawley rats than on Fischer 344 rats or CD-1 mice. This indicates that the latter two species may be more sensitive to exogenous estrogens and thus are preferable for screening. The authors call on scientists screening suspected endocrine disruptors to choose the most sensitive rodents, to minimize the animals' exposure to dietary estrogens, and to control their caloric intake. Only then, they write, will scientists obtain results that are the most accurate, reproducible, and easiest to compare among laboratories. Cynthia Washam http://www.medworm.com/index.php?rid=1066890&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2007%2F115-12%2Fss.html%23diet diet"> Dietary Dose Rodent Feed Affects ED Screening Results As the U.S. EPA begins its program to test endocrine-disrupting effects of pesticides, researchers caution that routine screening methods could distort results [EHP 115:1717?1726; Thigpen et al.]. The team discovered that some commercially available rodent diets can cause early sexual maturation similar to that induced by chemical endocrine disruptors. Furthermore, one rat strain commonly used by many researchers is not the most sensitive to the effects of endocrine disruptors and thus may not provide optimal results. image: Matthew Ray/EHP The U.S. EPA Endocrine Disruptor Screening Program was mandated by Congress in 1996 amid mounting evidence that hormone-mimicking chemicals in the environment alter sexual traits in e... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=1066890 Sat, 01 Dec 2007 05:00:00 +0100 1066890 keep'> Keep the Sprays Away? Home Pesticides Linked to Childhood Cancers Previous studies have suggested a link between pesticide use in the home and childhood hematopoietic tumors, the most common type of childhood cancer. A new epidemiologic study of French children diagnosed with leukemia or lymphoma in 2003 or 2004 suggests that a child has about twice the risk of developing acute leukemia (AL) or non-Hodgkin lymphoma (NHL) if his or her mother used insecticides in the home while pregnant [EHP 115:1787?1793; Rudant et al.]. The researchers interviewed 1,060 children diagnosed within the prior 6 months and 1,681 control children. When analyzing the data on the children, the team controlled for other factors that may alter a child's risk of getting cancer, including family cancer history and whether the child was breastfed. The children with cancer were part of the French National Registry of Childhood Blood Malignancies, begun in 1990, which documents all children in the country under age 15 year who have had hematopoietic tumors. The researchers asked the children's mothers about their use while pregnant of pesticides in their homes, on pets, and in the garden. They also asked about the father's use of pesticides while the mother was pregnant and after the child's birth. Just over 50% of the parents who had a child with AL or NHL had used pesticides at least once during the pregnancy, as did just under 40% of the parents of the control group. Children had 2.1 and 1.8 times the risk of developing AL or NHL, respectively, with maternal use of pesticides during pregnancy. Mothers' use of insecticides during pregnancy was significantly associated with childhood AL, NHL, and mixed-cell Hodgkin lymphomas (HLs). Use of pesticides by fathers was also related to AL and NHL. The association was stronger for common B-cell acute lymphoblastic leukemia (ALL) and acute myeloblastic leukemia than for T-cell ALL or mature B-cell ALL. It was also stronger for Burkitt lymphoma than for the other NHLs. Of the HLs, the study linked only the mixed-cell subtype to pesticide use. The strength of the association between pesticide use in the home and cancer did not change as the children grew older. This is the first study to tease out the different types of hematopoietic cancers as they relate to pesticide use in the home. Other studies have found a link between parents' occupational exposure to pesticides and childhood cancers, but few of the parents in the French study were exposed to pesticides at work or through farming. Whether a family was rural or urban didn't alter a child's risk of developing cancer. The two types of lymphoma associated with maternal pesticide use during pregnancy have also both been linked to the Epstein-Barr virus, which may suggest a link between pesticide exposure and susceptibility to a viral lymphoma. According to the authors, the consistency of the findings suggests pregnant women may want to avoid pesticide use. Tina Adler http://www.medworm.com/index.php?rid=1066889&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2007%2F115-12%2Fss.html%23keep keep"> Keep the Sprays Away? Home Pesticides Linked to Childhood Cancers Previous studies have suggested a link between pesticide use in the home and childhood hematopoietic tumors, the most common type of childhood cancer. A new epidemiologic study of French children diagnosed with leukemia or lymphoma in 2003 or 2004 suggests that a child has about twice the risk of developing acute leukemia (AL) or non-Hodgkin lymphoma (NHL) if his or her mother used insecticides in the home while pregnant [EHP 115:1787?1793; Rudant et al.]. The researchers interviewed 1,060 children diagnosed within the prior 6 months and 1,681 control children. When analyzing the data on the children, the team controlled for other factors that may alter a child's risk of getting cancer, including family cancer hi... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=1066889 Sat, 01 Dec 2007 05:00:00 +0100 1066889 drin'> Drink a Toast to Tap Water Study Suggests Water Consumption Benefit Outweighs THM Many water treatment systems use chlorine to disinfect drinking water. However, chlorine reacts with dissolved organic matter in water to create trihalomethanes (THMs), which have been associated with excess risk of bladder cancer in people who drink chlorinated water. Now, in a large study conducted in Spain, an international team of scientists has examined the role of tap water and total fluid intake in bladder cancer risk, while also assessing the effect of exposure to THMs in water [EHP 115:1569?1572; Michaud et al.]. The results suggest that higher water consumption is associated with lower risk of bladder cancer, regardless of THM exposure. glass of tap water Drink up! Despite the potential for THM exposure, water is still a healthy choice of beverage. image: BelleMedia/Shutterstock Some studies have linked high consumption of fluids including tap water with a lower risk of bladder cancer, perhaps because urinating more frequently allows more flushing of the bladder. Other studies suggest that high tap water consumption could increase bladder cancer risk if chlorination by-products or other water contaminants such as arsenic are elevated in the water source. Adding to this complexity is that still other studies have shown a THM-related excess risk of bladder cancer in men but not women. Between June 1998 and June 2001, researchers conducted a hospital-based case?control study of bladder cancer in multiple centers in Spain. Male and female bladder cancer patients aged 20?80 years were recruited from 18 participating hospitals. For the 397 bladder cancer cases available for this analysis, the team recruited 664 matched controls who had been admitted to the same hospitals around the same time for hernias, fractures, orthopedic problems, and other reasons. Trained interviewers collected information during each subject's hospitalization that included sociodemographic characteristics, family history of cancer, smoking history, occupational history, residential history, drinking water source at each residence, beverage consumption (including water), and medical history. The researchers used local government and water company data on annual average THM levels, water source history since 1920, and chlorination history to calculate average year-by-year THM exposure. These data were available for 78.5% of the total study person-years. The researchers examined the association between total fluid and water consumption and bladder cancer risk, while also examining the interaction between water intake and THM exposure. The results suggest that drinking more water, even from chlorinated sources with high THM levels, is beneficial in reducing risk of bladder cancer. The authors found a 53% lower risk of bladder cancer in people who drank 1,400 mL or more water per day compared with those who drank less than 400 mL per day after adjusting for known and potential confounders. This inverse association held across all strata of smoking status and THM exposure, and for both men and women. The study was strengthened by high response rates from cases and controls, detailed interview data on individual beverage consumption, detailed assessment of THM exposure, and detailed data on smoking, which is believed to be the greatest risk factor for bladder cancer. John Tibbetts http://www.medworm.com/index.php?rid=996337&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2007%2F115-11%2Fss.html%23drin drin"> Drink a Toast to Tap Water Study Suggests Water Consumption Benefit Outweighs THM Many water treatment systems use chlorine to disinfect drinking water. However, chlorine reacts with dissolved organic matter in water to create trihalomethanes (THMs), which have been associated with excess risk of bladder cancer in people who drink chlorinated water. Now, in a large study conducted in Spain, an international team of scientists has examined the role of tap water and total fluid intake in bladder cancer risk, while also assessing the effect of exposure to THMs in water [EHP 115:1569?1572; Michaud et al.]. The results suggest that higher water consumption is associated with lower risk of bladder cancer, regardless of THM exposure. Drink up! Despite the potential for THM exposure... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=996337 Thu, 01 Nov 2007 04:00:00 +0100 996337 vocs'> VOCs Turn Up in Well Water Sensitive Measure Reveals Groundwater Contaminant About 15% of the U.S. population get their drinking and household water from a largely unmonitored source: private residential wells. About 400,000 new wells are drilled every year. A new USGS study suggests that the water in a small percentage of domestic wells could contain unsafe levels of volatile organic compounds (VOCs) [EHP 115:1539?1546; Rowe et al.]. U.S. well chart Of 2,401 wells assayed by Rowe et al., 1% had water containing VOCs above EPA maximum contaminant levels. image: Barbara L. Rowe PAHs and PM2.5 are generated primarily by combustion of petroleum products, coal, wood, tobacco, trash, fat, and other substances. The concentrations of PAHs and PM2.5 in the two Czech Republic districts studied, Prachatice and Teplice, were similar to those found in many U.S., European, and Asian cities. VOCs come from a wide variety of sources, including gasoline, plastics, paints, dyes, solvents, adhesives, insecticides, and spot removers, and have wide-ranging health effects. The chemical and physical properties of VOCs allow the compounds to move between the atmosphere, soil, surface water, and groundwater. Once in the environment, some VOCs degrade quickly whereas others persist for decades. The USGS collected data on 55 VOCs primarily between 1991 and 2002. The team analyzed water samples before homeowners treated or filtered the water, which could help reduce VOCs. Many?possibly half of all well users?don't filter their water. The wells ranged in depth from 6 to 1,500 feet, with a median depth of about 140 feet. Of the 2,401 wells studied, 65% had detectable levels of VOCs, and 1% had levels above the EPA maximum contaminant level for the compound(s) observed. The most common compounds found were chloroform, toluene, 1,2,4-trimethylbenzene, and perchloroethene. Factors associated with the presence of VOCs were dissolved oxygen content, precipitation, the presence of a hazardous waste site within 1 km of the well, aquifer type, and water temperature. The authors note that identifying factors associated with VOC occurrence may aid in understanding the sources, transport, and fate of these compounds in groundwater. Tina Adler http://www.medworm.com/index.php?rid=996336&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2007%2F115-11%2Fss.html%23vocs vocs"> VOCs Turn Up in Well Water Sensitive Measure Reveals Groundwater Contaminant About 15% of the U.S. population get their drinking and household water from a largely unmonitored source: private residential wells. About 400,000 new wells are drilled every year. A new USGS study suggests that the water in a small percentage of domestic wells could contain unsafe levels of volatile organic compounds (VOCs) [EHP 115:1539?1546; Rowe et al.]. Of 2,401 wells assayed by Rowe et al., 1% had water containing VOCs above EPA maximum contaminant levels. image: Barbara L. Rowe PAHs and PM2.5 are generated primarily by combustion of petroleum products, coal, wood, tobacco, trash, fat, and other substances. The concentrations of PAHs and PM2.5 in the two Czech Republic districts studied, P... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=996336 Thu, 01 Nov 2007 04:00:00 +0100 996336 pfos'> PFOS and PFOA in Humans New Study Links Prenatal Exposure to Lower Birth Weight Scientists have accumulated a wealth of evidence that perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA, also known as perfluorooctanoic acid) accumulate in the environment and humans. Animal studies have shown these compounds to cause a variety of health effects, including reduced birth size and infant mortality. Now researchers are presenting the first evidence to suggest that human exposure to the chemicals is linked to reduced birth weight [EHP 115:1670?1676; Apelberg et al.]. PFOS, PFOA, and related polyfluoroalkyl compounds (PFCs) that can be transformed into these chemicals in the environment are used in a wide range of consumer applications, including oil and water repellents for fabric, apparel, and carpets, and paper coatings such as fast-food wrappers. The chemicals have been found in the blood of people throughout the world. The new study shows that infants born with higher concentrations of PFOS and/or PFOA in their umbilical cord serum (a measure the researchers used as a marker of in utero exposure) had lower birth weights. The authors calculate the reduction as ?69 g for PFOS and ?104 g for PFOA. The study population included 293 infants born in Baltimore, Maryland, in 2004 and 2005. In earlier research, PFOA had been found in all these infants, and PFOS had been found in 99% of them. Infants with higher levels of PFOS and PFOA also had smaller head circumferences and lower scores on the ponderal index, a measure of body mass at birth. The study was not designed to allow the cohort to be followed in the future. The results are consistent with those of toxicologic studies conducted with mice and rats that also have linked exposure to PFOS and PFOA with low birth weight?albeit at doses that resulted in much higher body burdens than those seen in the Baltimore infants. Both compounds have also been tied to developmental delays in animal studies. Previous studies in humans have correlated low birth weight with obesity, diabetes, and cardiovascular diseases later in life. The researchers stress that the effect was small but statistically significant. They also note that the concentrations of PFOS, PFOA, and other PFCs in the infants' blood were relatively low compared with levels tested in other studies. The results were statistically adjusted to consider other potential sources of altered birth weight, such as maternal smoking, diabetes, and hypertension. The new study did not find a correlation between levels of the compounds and socioeconomic status, as had previous research. The researchers also found no evidence of an association between the infants' exposure to the chemicals and their cholesterol or triglyceride levels, despite previous human and animal studies suggesting that these blood lipids are particularly sensitive to PFC exposure. Kellyn Betts http://www.medworm.com/index.php?rid=996335&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2007%2F115-11%2Fss.html%23pfos pfos"> PFOS and PFOA in Humans New Study Links Prenatal Exposure to Lower Birth Weight Scientists have accumulated a wealth of evidence that perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA, also known as perfluorooctanoic acid) accumulate in the environment and humans. Animal studies have shown these compounds to cause a variety of health effects, including reduced birth size and infant mortality. Now researchers are presenting the first evidence to suggest that human exposure to the chemicals is linked to reduced birth weight [EHP 115:1670?1676; Apelberg et al.]. PFOS, PFOA, and related polyfluoroalkyl compounds (PFCs) that can be transformed into these chemicals in the environment are used in a wide range of consumer applications, including oil and water repellents for... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=996335 Thu, 01 Nov 2007 04:00:00 +0100 996335 area'> A Reason to Rethink Groups New Approach Links PCBs, Thyroid Disruption The production of polychlorinated biphenyls (PCBs), once widely used in electrical transformers, plastics, and other products, has been banned in the United States since the 1970s. Nevertheless, most Americans carry measurable levels of PCBs because the compounds persist in the environment and bioaccumulate. Epidemiologic studies have linked prenatal PCB exposure with impaired neurodevelopment in infants and young children, and in animal studies, prenatal exposure caused decreased levels of the thyroid hormone thyroxine (T4). Given that thyroid hormones are essential for proper neurodevelopment, disruption of the thyroid system may be a pathway by which PCBs cause damage. New research using a novel method of grouping the chemicals now provides additional support for PCB-related thyroid disruption [EHP 115:1490?1496; Chevrier et al.]. PCBs include 209 congeners that vary based on the number and positions of chlorine atoms. These congeners have been grouped according to their potential mechanism of action (e.g., estrogenicity, antiestrogenicity, or microsomal enzyme induction). In the current study, researchers grouped congeners on the basis of their reported abilities to induce the enzymes UDP-GT, CYP1A, and CYP2B. UDP-GT has a role in T4 elimination, and compounds that induce CYP1A and CYP2A are also likely to induce UDP-GT. Thirty-four PCB congeners, in addition to other environmental chemicals, were measured in blood samples drawn from 285 pregnant women through the Center for the Health Assessment of Mothers and Children of Salinas, a longitudinal birth cohort study in the Salinas Valley, California. The women provided information through interviews on sociodemographic variables; alcohol, tobacco, drug, and caffeine consumption; and agricultural work history. Routine screening conducted by heel-stick blood collection yielded data on the infants' blood levels of thyroid-stimulating hormone (TSH), which is involved in the control of thyroid function. All of the infants had TSH levels within the normal range. However, levels were significantly higher in relation to specific PCB congeners in their mothers' blood. When the researchers considered total PCB levels and PCBs grouped by structure or dioxin-like activity, they found no association. There was, however, a significant positive association between TSH levels and PCBs grouped by their ability to induce UDP-GT, CYP1A, and CYP2B. The team found that TSH increased by 29% with each 10-fold increase of such PCBs. The researchers recommend that future studies evaluate whether any changes in neurodevelopment are associated with these PCB-related alterations in thyroid hormone levels. Their results suggest that grouping PCBs on the basis of hypothesized mechanism of action, rather than summing all congeners, may be important in understanding adverse effects of PCB exposure. Julia R. Barrett http://www.medworm.com/index.php?rid=917364&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2007%2F115-10%2Fss.html%23area area"> A Reason to Rethink Groups New Approach Links PCBs, Thyroid Disruption The production of polychlorinated biphenyls (PCBs), once widely used in electrical transformers, plastics, and other products, has been banned in the United States since the 1970s. Nevertheless, most Americans carry measurable levels of PCBs because the compounds persist in the environment and bioaccumulate. Epidemiologic studies have linked prenatal PCB exposure with impaired neurodevelopment in infants and young children, and in animal studies, prenatal exposure caused decreased levels of the thyroid hormone thyroxine (T4). Given that thyroid hormones are essential for proper neurodevelopment, disruption of the thyroid system may be a pathway by which PCBs cause damage. New research using a novel method of ... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=917364 Mon, 01 Oct 2007 04:00:00 +0100 917364 feel'> Feeling the Burn Combustion By-Products Put Kids at Risk One of the most extensive studies of the link between lower respiratory diseases and ambient concentrations of polycyclic aromatic hydrocarbons (PAHs), a class of widespread air pollutants, has found that the chemicals are a potent problem for preschool-age children [EHP 115:1510?1518; Hertz-Picciotto et al.]. The team of researchers also found that fine particles (PM2.5) pose a respiratory risk to very young children. PAHs and PM2.5 are generated primarily by combustion of petroleum products, coal, wood, tobacco, trash, fat, and other substances. The concentrations of PAHs and PM2.5 in the two Czech Republic districts studied, Prachatice and Teplice, were similar to those found in many U.S., European, and Asian cities. The study involved 1,133 children up to age 4.5 years. The team examined pediatric charts to determine those whom a doctor had diagnosed with a lower respiratory disease of acute bronchitis, tracheitis, or laryngitis. These children were among 7,502 born from May 1994 to December 1998 who were evaluated in previous studies, providing substantial data on factors such as fuels used for home heating and cooking; birth weight; and maternal education, age at birth, and smoking history. The current study collected information on breastfeeding, daycare attendance, and other factors that could either protect these children or increase their risk of respiratory disease. Pollution data were obtained from selected monitors in each district; readings were taken during each month anywhere from once each day to once every six days. This allowed analysis of all seasons and a wide range of intervals. The team found a statistically significant link between bronchitis, the most commonly diagnosed illness, and elevated ambient PAHs, escalating 56% in children aged 2 to 4.5 years for each 30-day-average increase of 100 ng/m3. The increase was 29% for children under age 2 years. For each 30-day-average increase in PM2.5 of 25 ?g/m3, bronchitis diagnoses rose 30% for children up to age 2 years. In children aged 2 to 4.5, it rose 23%. Some other pollutants that could play a role in respiratory illness, such as ozone, nitrogen oxides, sulfur dioxide, and metals, were not covered in the analysis. Certain weather variables, such as wind and humidity, also were not considered. However, the study was strengthened by the use of a doctor's diagnosis rather than parental reports or recalled incidents, and the likelihood of a sick child visiting a doctor was very high, given that health care was free and readily available. Consistency of diagnostic coding also appeared to be very good. The strengths of the study and the magnitude of the findings lead the authors to conclude that relatively short-term exposure to ubiquitous PAHs may pose a significant respiratory threat to children. Bob Weinhold http://www.medworm.com/index.php?rid=917363&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2007%2F115-10%2Fss.html%23feel feel"> Feeling the Burn Combustion By-Products Put Kids at Risk One of the most extensive studies of the link between lower respiratory diseases and ambient concentrations of polycyclic aromatic hydrocarbons (PAHs), a class of widespread air pollutants, has found that the chemicals are a potent problem for preschool-age children [EHP 115:1510?1518; Hertz-Picciotto et al.]. The team of researchers also found that fine particles (PM2.5) pose a respiratory risk to very young children. PAHs and PM2.5 are generated primarily by combustion of petroleum products, coal, wood, tobacco, trash, fat, and other substances. The concentrations of PAHs and PM2.5 in the two Czech Republic districts studied, Prachatice and Teplice, were similar to those found in many U.S., European, and Asian cities. ... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=917363 Mon, 01 Oct 2007 04:00:00 +0100 917363 auti'> Autism and Agricultural Pesticides Integrating Data to Track Trends The purpose of the CDC's Environmental Public Health Tracking Program is to integrate diverse data sources for surveillance and research. In a demonstration project by program grantees, a powerful convergence of data on births, social services, and agriculture allows researchers to ask highly focused questions about the relationship between environmental exposures to farm pesticides and autism spectrum disorders (ASDs) in children [EHP 115:1482?1489; Roberts et al.]. agricultural fields and a pregnant woman Data network. Combining existing birth, social service, and chemical use data in new ways may reveal new environmental connections. images (left to right): Brand X Pictures; Merrill Dyck/Shutterstock The study focused on ASDs in children whose mothers lived near well-defined sites of agricultural pesticide application in the California Central Valley, a 19-county swath spanning the Sacramento and San Joaquin River valleys. The team identified 465 children born in 1996?1998 who had received ASD-related diagnoses and services. They used state Department of Pesticide Regulation data to determine mothers' residential proximity to pesticide applications at the time they gave birth. Data from 6,975 non-ASD children whose mothers had been pregnant in the same time and region served as controls. The group set out to examine every combination of three factors: mother's residential distance from the site of pesticide application, type of pesticide(s) applied, and stage of gestation at the time of pesticide use. Three time windows were of special interest: the period leading up to and covering central nervous system embryogenesis (1 week before conception through 7 weeks after), the period leading up to and covering neural tube development (4 days before conception through 24 days after) and overall gestation (2 weeks before conception through birth). Because the number of possible combinations is high and the number of affected children relatively low, the study yielded only a preliminary view of how the three factors may interact. However one group of pesticides did stand out: organochlorines, including the commonly used dicofol and endosulfan, were associated with ASD out to a maternal residential distance of 1,750-meter from the site of application. Dicofol and endosulfan, which are used in the production of cotton, fruit, vegetables, beans, and nuts, account for 98% of the organochlorines applied in the Central Valley region. Although the association between organochlorine exposure and ASDs points to a connection between the two, it does not indicate causality and does not consider other factors that may be involved. For the residences nearest to the organochlorine application sites (where the ASD association was the strongest), data around exposures came from only 8 cases and 105 controls. Of those, the focus is on the quarter who lived nearest sites where the greatest amounts of chemicals were applied. Still, the work, which used data routinely collected for other public uses, marks the need for further analysis of the relationship between organochlorines and ASDs, and lays the groundwork for asking difficult environmental health questions using available geographic, public health, and social services records. Victoria McGovern http://www.medworm.com/index.php?rid=917362&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2007%2F115-10%2Fss.html%23auti auti"> Autism and Agricultural Pesticides Integrating Data to Track Trends The purpose of the CDC's Environmental Public Health Tracking Program is to integrate diverse data sources for surveillance and research. In a demonstration project by program grantees, a powerful convergence of data on births, social services, and agriculture allows researchers to ask highly focused questions about the relationship between environmental exposures to farm pesticides and autism spectrum disorders (ASDs) in children [EHP 115:1482?1489; Roberts et al.]. Data network. Combining existing birth, social service, and chemical use data in new ways may reveal new environmental connections. images (left to right): Brand X Pictures; Merrill Dyck/Shutterstock The study focused on ASDs in children whos... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=917362 Mon, 01 Oct 2007 04:00:00 +0100 917362 bari'> Baring Bone's Secrets Understanding How Lead Exposure Affects Skeletal Development Among lead's well-known developmental health effects is stunting of skeletal growth in children. Moreover, lead is known to delay fracture healing and may contribute to osteoporosis. Yet the exact mechanism by which lead affects normal cellular functions in bone and cartilage is poorly understood. A new study reports in vitro and in vivo effects of lead on cell signaling during differentiation of embryonic stem cells destined to form bone and cartilage [EHP 115:1276?1282; Zucsik et al]. x-ray of a human leg image: Eric Schmuttenmaer Chondrogenesis is the process by which a mesenchymal cell?a type of stem cell already assigned to become connective tissue or blood cells?turns into a cartilage cell, or chondrocyte. As chondrocytes mature, they differentiate further into bone and more specialized types of cartilage. Because the early embryo makes a cartilage model of the skull, spine, and limbs, chondrogenesis is vital to full skeletal development. The authors exposed mouse mesenchymal cells to lead in vitro and observed signaling changes in several proteins active in chondrogenesis: transforming growth factor-beta (TGF- ), bone morphogenetic protein (BMP), activating protein 1 (AP-1), and nuclear factor kappa B (NF B). They also implanted mesenchymal cells expressing BMP-2 in the thighs of living mice. Before implantation, the mice had been exposed to lead through their drinking water. The in vitro experiment revealed several dose-dependent effects. Lead stimulated chondrogenesis, influenced the regulation of chondrogenesis by BMP-2 and TGF- , and induced expression of three genes, also mediating the genes' regulation by BMP-2 and TGF- . Similarly, in the in vivo experiment, lead was associated with a dose-dependent induction of chondrogenesis at the implantation site. Lead also inhibited AP-1 signaling and induced NF B signaling. However, on the basis of previous research on AP-1 and NF B with opposite findings, the authors do not believe either of these pathways is responsible for the heightened chondrogenesis observed in the current study. TGF- proteins are mediated by members of the Smad family of transcription activators, and Smads also affect BMP signaling in some situations. In the current study, lead inhibited BMP-2 Smad signaling while stimulating the same in TGF- . Lead's inhibition of BMP-2 Smad signaling 'represents the most robust signaling effect identified to date in a skeletal cell type with regard to a candidate mechanism of [lead] toxicity,' the authors state. At the same time, this finding implies that lead's influence on chondrogenesis operates independently of Smad signaling. Given the importance of cartilage both in embryonic development and in fracture repair later in life, stimulation of chondrogenesis seems like a good thing; but if lead triggers the formation of too much cartilage at the wrong time, or prevents its further maturation into bone, this could explain lead's crippling effects on the skeleton. And because mesenchymal cells may differentiate into a variety of cell types in addition to cartilage, lead may also affect the development of other body systems. Valerie J. Brown http://www.medworm.com/index.php?rid=841252&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2007%2F115-9%2Fss.html%23bari bari"> Baring Bone's Secrets Understanding How Lead Exposure Affects Skeletal Development Among lead's well-known developmental health effects is stunting of skeletal growth in children. Moreover, lead is known to delay fracture healing and may contribute to osteoporosis. Yet the exact mechanism by which lead affects normal cellular functions in bone and cartilage is poorly understood. A new study reports in vitro and in vivo effects of lead on cell signaling during differentiation of embryonic stem cells destined to form bone and cartilage [EHP 115:1276?1282; Zucsik et al]. image: Eric Schmuttenmaer Chondrogenesis is the process by which a mesenchymal cell?a type of stem cell already assigned to become connective tissue or blood cells?turns into a cartilage cell, or chondrocyt... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=841252 Sat, 01 Sep 2007 04:00:00 +0100 841252 theb'> The Best Rodent for the Job NTP Workshop Compares Models Researchers have long used rats and mice to understand the potential links between environmental exposures and incidences of breast, ovarian, testicular, and prostate tumors. Concern exists, however, that rodent models are not optimal for detecting carcinogens that act through the hormone system. To address this concern, the National Toxicology Program (NTP) organized a workshop in May 2006 to evaluate the utility of current two-year rodent bioassays to adequately evaluate these hormonally mediated tumors and the relevance of the findings to humans [EHP 115:1351?1356; Thayer and Foster]. male and female reproductive organs image: Shutterstock The workshop, part of a series of events aimed at evaluating and refining the NTP's testing program, included representatives from academia, industry, government, and nonprofit groups, as well as a panel of invited experts in endocrinology, cancer biology, reproductive toxicology, statistics, and other fields. Workshop participants were concerned that many hormonally mediated tumors, such as those in the testes and breasts, are initiated in fetal or early neonatal life, yet these periods of exposure are not covered in the NTP's standard cancer bioassay. In response to this concern, the NTP has committed to routinely include perinatal exposures in these studies unless there is a specific justification not to do so. Furthermore, some rat and mouse strains used in testing either do not develop certain tumors or have a high incidence of spontaneous tumors. For example, the F344/N rat typically used by the NTP has high background incidences of testicular Leydig cell tumors and mononuclear cell leukemia, along with unresolved issues about declining fertility, sporadic seizures, and chylothorax (accumulation of lymphatic fluid in the pleural cavity, which can result from lymphoma). By press time, in response to this and other workshop findings, the NTP had selected the Wistar Han as its standard rat strain for cancer and noncancer end points, although other strains will be used when appropriate. Although rodent models are considered to have certain deficiencies and can be improved, they are considered valuable nonetheless. Rodent models for prostate and ovarian tumors are the most problematic for understanding human disease because of significant interspecies differences in anatomy and tumor prevalence. Participants in the workshop recommended using alternative models, such as genetically engineered models and in vitro systems, to address some of these deficiencies. They also recommended more in-depth investigation of how noncancerous changes observed in rodents might be relevant to human diseases. Julia R. Barrett http://www.medworm.com/index.php?rid=841251&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2007%2F115-9%2Fss.html%23theb theb"> The Best Rodent for the Job NTP Workshop Compares Models Researchers have long used rats and mice to understand the potential links between environmental exposures and incidences of breast, ovarian, testicular, and prostate tumors. Concern exists, however, that rodent models are not optimal for detecting carcinogens that act through the hormone system. To address this concern, the National Toxicology Program (NTP) organized a workshop in May 2006 to evaluate the utility of current two-year rodent bioassays to adequately evaluate these hormonally mediated tumors and the relevance of the findings to humans [EHP 115:1351?1356; Thayer and Foster]. image: Shutterstock The workshop, part of a series of events aimed at evaluating and refining the NTP's testing program, included ... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=841251 Sat, 01 Sep 2007 04:00:00 +0100 841251 aspa'> Aspartame Cancer Risks Revisited Prenatal Exposure May Be Greatest Concern Aspartame is an artificial sweetener used in more than 6,000 diet products, beverages, and pharmaceuticals. In March 2006, EHP published the first compelling experimental evidence for the carcinogenic effects of aspartame at a dose level within range of human daily intake [EHP 14:379?385; Soffritti et al.]. A second animal study by the same research team now indicates that the carcinogenic effects of aspartame are magnified when exposure begins during fetal life [EHP 115:1293?1297; Soffritti et al.]. The first study involved a much larger sample size than had been used in previous experiments. It showed a dose-related increase in the incidence of various malignant tumors in female rats fed aspartame from 8 weeks of age until natural death. The experiment was impressive for its long observation period and comprehensive assessment of aspartame's carcinogenic potential. Nevertheless, as the researchers acknowledged, the study did not take into account prenatal or perinatal exposures. In the new study, the investigators added aspartame to the standard diets of male and female Sprague-Dawley rats from the twelfth day of fetal life until natural death. Rats were fed in groups of 70 to 95 each at aspartame concentrations of 2,000, 400, and 0 ppm?approximately equivalent to a daily intake of 100, 20, or 0 mg/kg body weight. The current limits for acceptable daily intake are set at 50 mg/kg body weight in the United States and 40 mg/kg body weight in Europe. The researchers report that rats fed at the 400 ppm level showed nonsignificant increases in malignancies. For animals fed at the 2,000 ppm level, there was a significant increase in the incidence of lymphomas/leukemias and malignant mammary tumors. Furthermore, compared with the team's earlier study in which animals were dosed postnatally only, the incidence of animals bearing lymphomas/leukemias increased from 18.7% to 31.4%. The 2,000 ppm level corresponds to an assumed daily intake of 100 mg/kg body weight?approximately the equivalent of a 45-pound child drinking 5 cans of diet soda or a 150-pound adult consuming 14 packets of sweetener per day. Although recent epidemiologic studies have not found an association between aspartame and human cancers, those studies were not designed to measure cancer risks associated with fetal exposures. The public health implications of the new findings are considerable. Currently, more than 200 million people regularly consume aspartame, and children and women of childbearing age (which presumably includes many who are pregnant and breastfeeding) are among the major consumers. If the U.S. FDA were to conclude that exposure to aspartame causes cancer in rodents, the agency would be required by law to revoke its approval for the popular sweetener. M. Nathaniel Mead http://www.medworm.com/index.php?rid=841250&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2007%2F115-9%2Fss.html%23aspa aspa"> Aspartame Cancer Risks Revisited Prenatal Exposure May Be Greatest Concern Aspartame is an artificial sweetener used in more than 6,000 diet products, beverages, and pharmaceuticals. In March 2006, EHP published the first compelling experimental evidence for the carcinogenic effects of aspartame at a dose level within range of human daily intake [EHP 14:379?385; Soffritti et al.]. A second animal study by the same research team now indicates that the carcinogenic effects of aspartame are magnified when exposure begins during fetal life [EHP 115:1293?1297; Soffritti et al.]. The first study involved a much larger sample size than had been used in previous experiments. It showed a dose-related increase in the incidence of various malignant tumors in female rats fed aspartame from 8... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=841250 Sat, 01 Sep 2007 04:00:00 +0100 841250 reci'> Recipe for High Blood Pressure Synergistic Effects of Stress and Lead Human research has shown associations between lead exposure and hypertension as well as between stress and hypertension. A new study now shows for the first time that stress amplifies the effects of lead exposure on blood pressure in humans [EHP 115:1154?1159; Peters et al.]. National Heart, Lung, and Blood Institute guidelines define high blood pressure as systolic pressure over 140 mmHg or diastolic pressure over 80 mmHg. Systolic pressure tends to rise with age whereas diastolic pressure tends to decline. High readings of either type significantly raise the risk of stroke and coronary disease. A multi-institutional team examined data from 513 participants in the Normative Aging Study, a longitudinal study of men in the greater Boston area begun in 1963. Using data from the period 1987?1996, the researchers compared blood pressure status with self-reported stress levels (determined by questionnaires) and body burden of lead (determined by bone lead tests). About half the participants did not have hypertension; for this group the researchers analyzed follow-up data until 2004 or the participants developed hypertension, whichever came first. In the latter group, 97 new cases of hypertension were observed. The study participants averaged 66.9 years of age. This put them in the age group most likely to have high systolic pressure, and meant they were old enough to have been exposed to significant amounts of lead before public policy changes in the 1970s reduced environmental lead from gasoline, paint, and other sources. After accounting for other known hypertension risk factors, including age, body mass index, family history, and alcohol consumption, the researchers found that the effect of lead was 'most pronounced among highly stressed individuals, independent of demographic and behavioral risk factors.' Among those reporting high stress, the risk of developing hypertension was more than 2.5 times that of participants reporting low stress for each standard deviation increase in bone lead. The current study was consistent with previous research suggesting that lead and stress affect only systolic pressure. The authors note that their study does not address lead's potential effects at various life stages. For example, early exposure leading to neurological damage might make people more likely to experience events as stressful. In addition, the study was limited in that participants were all male, were 97% white, and had higher than median incomes. Given that both lead exposure and stress tend to be elevated in lower socioeconomic strata, their effects on blood pressure may be more serious in those populations. Valerie J. Brown http://www.medworm.com/index.php?rid=772743&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2007%2F115-8%2Fss.html%23reci reci"> Recipe for High Blood Pressure Synergistic Effects of Stress and Lead Human research has shown associations between lead exposure and hypertension as well as between stress and hypertension. A new study now shows for the first time that stress amplifies the effects of lead exposure on blood pressure in humans [EHP 115:1154?1159; Peters et al.]. National Heart, Lung, and Blood Institute guidelines define high blood pressure as systolic pressure over 140 mmHg or diastolic pressure over 80 mmHg. Systolic pressure tends to rise with age whereas diastolic pressure tends to decline. High readings of either type significantly raise the risk of stroke and coronary disease. A multi-institutional team examined data from 513 participants in the Normative Aging Study, a longitudinal study... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=772743 Wed, 01 Aug 2007 04:00:00 +0100 772743 sper'> Sperm Quality and Tap Water Disinfection By-Product Effects Not Supported Chemicals used to disinfect water often contain chlorine, which can react with organic matter in the water to form compounds such as trihalomethanes (THMs) and haloacetic acids (HAAs), known collectively as disinfection by-products (DBPs). DBP exposure has been implicated in reproductive abnormalities, and earlier human studies have found associations between DBPs and adverse pregnancy outcomes. A new study of DBP exposure now shows only weak evidence of sperm quality damage from exposures at or below regulatory limits [EHP 115:1169?1176; Luben et al.]. Earlier studies have revealed little about the degree of risk from DBP exposure, especially for male reproductive health, and there have been few epidemiologic studies of the possible effects on sperm quality. Rodent studies suggest that drinking water exposure to HAAs, particularly brominated species, could pose a threat to human sperm. Because some DBPs are considered carcinogens, there is also concern about DNA damage. The current study assessed 228 men recruited from couples participating in a project to determine whether DBPs affect spontaneous abortion. The study population was drawn from three locations: one with a water supply containing low overall DBPs, one with low brominated but moderate chlorinated DBPs, and one with low chlorinated but moderate brominated DBPs. 'Moderate' was defined as close to but below the U.S. EPA limits for four THMs and five HAAs. The study also analyzed total organic halides (TOX), a group that includes THMs, HAAs, and other organic halides that may not have been identified individually. Researchers surveyed participants to determine the amount of tap water they ingested and the frequency and length of their showers and baths, then calculated individual DBP exposure estimates. The men also provided semen samples, which the researchers analyzed for total sperm count, sperm maturity and morphology, and DNA integrity. Expecting more sperm damage at higher DBP exposures, the researchers found instead that the top 25th percentile for both THM and HAA exposure had higher sperm counts than those in the bottom 50th percentile of each group. Results for sperm morphology and DNA integrity were similar. Sperm concentration did decrease as exposure to TOX increased, consistent with findings that TOX may be a greater risk factor for pregnancy difficulties than the individual compounds or groups of compounds now regulated. However, if this were the case, an increase in abnormal sperm morphology with increasing TOX would be expected, and no such increase was observed. Because the study population was presumed fertile, a small decrease in sperm count might not be detectable against high background counts, and could explain the null results reported by the authors. Because only a few men were exposed to DBPs above regulatory limits, further clarification might be obtained by future studies including a wider range of exposures. Valerie J. Brown http://www.medworm.com/index.php?rid=772742&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2007%2F115-8%2Fss.html%23sper sper"> Sperm Quality and Tap Water Disinfection By-Product Effects Not Supported Chemicals used to disinfect water often contain chlorine, which can react with organic matter in the water to form compounds such as trihalomethanes (THMs) and haloacetic acids (HAAs), known collectively as disinfection by-products (DBPs). DBP exposure has been implicated in reproductive abnormalities, and earlier human studies have found associations between DBPs and adverse pregnancy outcomes. A new study of DBP exposure now shows only weak evidence of sperm quality damage from exposures at or below regulatory limits [EHP 115:1169?1176; Luben et al.]. Earlier studies have revealed little about the degree of risk from DBP exposure, especially for male reproductive health, and there have been few epidemio... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=772742 Wed, 01 Aug 2007 04:00:00 +0100 772742 when'> When the Attack Comes Before the Asthma Violence Increases Risk from Pollution Chronic physical or emotional stress is known to impair the immune system, a link that may explain some of the health disparities found among different socioeconomic groups. Researchers have also found that living in poor, urban communities or near highways is linked to a greater risk of developing childhood asthma and other breathing problems. A new study now reveals that psychosocial stressors may increase children's vulnerability to the effects of traffic-related air pollution [EHP 115:1140?1146; Clougherty et al.]. boy standing at a window Added burden. Stress can compound the physiological effects of environmental pollutants such as nitrogen dioxide. image: Rebecca Grabill/iStockphoto The researchers examined data from the Maternal?Infant Smoking Study of East Boston, which began in 1987 to establish a cohort of pregnant women. In 1997, parents or guardians of 417 children of the cohort, then aged 4 to 11.5, answered questions about the children's exposure to violence. Respondents were asked about the frequency with which the children had ever seen hitting, a shooting, or a stabbing, or heard domestic verbal abuse or gunshots. Other studies have suggested that residual trauma from witnessing episodic violence is a source of chronic stress for urban residents. About 45% of the children had witnessed at least one violent act, and almost 20% had witnessed at least two. Responses were generalized to account for variables that can affect the severity of such acts, including whether the child knew the victim or perpetrator. The researchers then acquired data collected between 1987 and 2004 on Boston levels of nitrogen dioxide (NO2), a constituent of vehicular exhaust with a known link to asthma. They used computerized mapping tools to estimate NO2 exposure at the children's residences in East Boston, a working-class urban neighborhood with highways running through it. About 25% of the children in the study had asthma. However, residential exposure to NO2 was linked to asthma only among children who were above the median for exposure to violence. The association between asthma and NO2 exposure disappeared when the researchers looked at the group as a whole. The authors conclude that their findings 'indicate ancillary effects of violence on children in addition to direct injury and post-traumatic stress.' Larger studies are needed to investigate other possible interactions among risk factors for asthma. It is also important to study the effects of other pollutants, including indoor air pollution. The authors observe that accurate reports about violence are difficult to obtain, and that violence exposures may be a sign of other problems with family stability that affect stress levels and health. Tina Adler http://www.medworm.com/index.php?rid=772741&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2007%2F115-8%2Fss.html%23when when"> When the Attack Comes Before the Asthma Violence Increases Risk from Pollution Chronic physical or emotional stress is known to impair the immune system, a link that may explain some of the health disparities found among different socioeconomic groups. Researchers have also found that living in poor, urban communities or near highways is linked to a greater risk of developing childhood asthma and other breathing problems. A new study now reveals that psychosocial stressors may increase children's vulnerability to the effects of traffic-related air pollution [EHP 115:1140?1146; Clougherty et al.]. Added burden. Stress can compound the physiological effects of environmental pollutants such as nitrogen dioxide. image: Rebecca Grabill/iStockphoto The researchers examined data... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=772741 Wed, 01 Aug 2007 04:00:00 +0100 772741 mang'> Manganese and Infant Mortality Well Water May Raise Death Rates in Bangladesh Many wells in Bangladesh exceed the WHO threshold for manganese of 0.4 mg/L?in the Araihazar region in eastern Bangladesh, 80% of the wells provide water with manganese concentrations above 0.5 mg/L. A new study now suggests that manganese exposure through drinking water may contribute to Bangladesh's extremely high infant mortality rate of 54 per 1,000 live births [EHP 115:1107?1112; Hafeman et al.]. mother and newborn Mother and newborn in Dhaka, Bangladesh image: Dieter Telemans/Panos Pictures Well water in Bangladesh already receives close scrutiny for its naturally high levels of arsenic, a known carcinogen. Manganese is also a concern, however, due to research showing associations between exposure and subclinical neurological effects in adults and decreased intellectual function in children. Additionally, neonatal animal studies have linked reduced weight gain and decreased survival to manganese exposure. An ongoing cohort study in Araihazar, the Health Effects of Arsenic Longitudinal Study (HEALS), provided the framework for investigating whether manganese might affect human infant survival. Of the HEALS participants, 1,628 women met the criteria for the current study: they married before age 40, drank from the same well for most of their reproductive years, and reported at least one live birth. The researchers considered concentrations of manganese and other metals in the wells used by the target population, the mothers' reproductive history and education, and the families' socioeconomic status and other factors that can affect infant survival. Although breastfeeding rates are high in Bangladesh, newborns are often given sugar water in place of colostrum, and most young infants receive complementary foods by age 6 months. Of the 3,824 infants born to the study group, nearly 85% were exposed to water manganese levels above 0.4 mg/L, and 335 died before age 1 year, an elevated risk of death not explained by measured covariates. The finding was more pronounced when restricted to women married after 1991, who appeared to give more complete reproductive histories; among these women, the infant death rate was 82 per 1,000 live births. No dose?response relationship was seen, though, and the association was not found when analysis was restricted to water samples collected for the current study. The researchers recommend designing a study specifically to investigate the role of manganese exposure in infant mortality, with particular attention to causes of mortality and potential routes of exposure. Julia R. Barrett http://www.medworm.com/index.php?rid=710461&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2007%2F115-7%2Fss.html%23mang mang"> Manganese and Infant Mortality Well Water May Raise Death Rates in Bangladesh Many wells in Bangladesh exceed the WHO threshold for manganese of 0.4 mg/L?in the Araihazar region in eastern Bangladesh, 80% of the wells provide water with manganese concentrations above 0.5 mg/L. A new study now suggests that manganese exposure through drinking water may contribute to Bangladesh's extremely high infant mortality rate of 54 per 1,000 live births [EHP 115:1107?1112; Hafeman et al.]. Mother and newborn in Dhaka, Bangladesh image: Dieter Telemans/Panos Pictures Well water in Bangladesh already receives close scrutiny for its naturally high levels of arsenic, a known carcinogen. Manganese is also a concern, however, due to research showing associations between exposure and subcl... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=710461 Sun, 01 Jul 2007 04:00:00 +0100 710461 resi'> Resisting Arrest Drug-Resistant Campylobacter Persists in Poultry Doctors use the fluoroquinolone class of antibiotics to treat food poisoning caused by Campylobacter. But after poultry farmers began using fluoroquinolones to treat respiratory disease in flocks, the drugs became less effective in people. In 2005, the FDA banned the use of fluoroquinolones on poultry farms because of these concerns. A new study now suggests that the ban may not be enough to fix the problem [EHP 115:1035?1039; Price et al.]. chickens image: Tony Campbell/Shutterstock A team of Johns Hopkins researchers made weekly trips to Baltimore supermarkets for 20 weeks in 2004 and 15 weeks in 2006. Each week, they bought chicken from each of five different producers. Three producers had never used any antibiotics; two were major conventional producers that declared they had ceased all use of fluoroquinolones in 2002, three years before the FDA ban. The scientists tested one piece of chicken from each package for Campylobacter, confirmed the bacterium's identity using DNA analysis, then tested for antibiotic resistance using the minimal inhibitory concentration method. The bacteria from conventional chicken were more likely to be fluoroquinolone-resistant than those from antibiotic-free products. The researchers compared each poultry producer to every other producer in a pair-wise fashion. In both 2004 and 2006, this statistical analysis showed that the Campylobacter strains from the conventionally produced chicken were more likely to be resistant than the strains from antibiotic-free samples. In addition, between 2004 and 2006, the proportion of antibiotic-resistant bacteria on the conventionally produced chicken showed no significant change, indicating that the prevalence of fluoroquinolone-resistant Campylobacter was not decreasing in chicken from these producers, even after four years. The results suggest that once antibiotic-resistant bacteria have developed, they may show up on grocery store shelves long after drug use stops. The authors note that they could not verify claims of voluntary fluoroquinolone prohibition because poultry producers are not required to report their use of drugs in food animals to regulatory agencies. Other studies have shown that resistant bacteria can linger in poultry farms' water distribution and ventilation systems and in reused litter. The authors state that additional interventions, such as requiring thorough disinfection and regular litter changing in poultry houses, may be necessary to reduce the public health burden of fluoroquinolone-resistant Campylobacter. Angela Spivey http://www.medworm.com/index.php?rid=710460&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2007%2F115-7%2Fss.html%23resi resi"> Resisting Arrest Drug-Resistant Campylobacter Persists in Poultry Doctors use the fluoroquinolone class of antibiotics to treat food poisoning caused by Campylobacter. But after poultry farmers began using fluoroquinolones to treat respiratory disease in flocks, the drugs became less effective in people. In 2005, the FDA banned the use of fluoroquinolones on poultry farms because of these concerns. A new study now suggests that the ban may not be enough to fix the problem [EHP 115:1035?1039; Price et al.]. image: Tony Campbell/Shutterstock A team of Johns Hopkins researchers made weekly trips to Baltimore supermarkets for 20 weeks in 2004 and 15 weeks in 2006. Each week, they bought chicken from each of five different producers. Three producers had never used any antibio... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=710460 Sun, 01 Jul 2007 04:00:00 +0100 710460 pman'> PM and Elevated Inflammation Markers More Support for Air Pollution?Heart Disease Link After evaluating about 1,000 Europeans already suffering from cardiovascular disease, researchers have found a relationship between elevated concentrations of airborne particulates (PM) and increases in two markers of inflammation that have strong links with cardiovascular diseases and deaths [EHP 115:1072?1080; R?ckerl et al.]. The cumulative number of people studied is the largest to date for PM and these inflammation indicators,with the findings generally consistent across diverse locales. The researchers evaluated about 100 to 200 myocardial infarction survivors in each of six cities around the continent: Athens, Augsburg, Barcelona, Helsinki, Rome, and Stockholm. The cities have a wide range of demographic profiles, climates, and air pollutant concentrations. The selected people tended to be male, elderly, overweight,and consumers of numerous prescription drugs. To evaluate inflammation,the researchers studied interleukin 6 (IL-6; thought to play a central role in triggering inflammation) and two proteins, fibrinogen and C-reactive protein (CRP), whose synthesis is stimulated by IL-6. They also considered the potentially confounding effects of many other variables, such as smoking status, presence of diabetes, time of day, and season. They found that IL-6 increased most when particle number concentration?an indicator of ultrafine particulates?was elevated 12 to 17 hours before a blood draw. They also found that increased fibrinogen was associated with cumulative five-day exposure to larger particulates (PM10). In addition, the results indicated associations between fine particulates (PM2.5) and fibrinogen, and between nitrogen dioxide and IL-6. There were a few anomalies that remain to be explained, such as the fact that the strongest link between PM10 exposures and increased fibrinogen after three days occurred in Helsinki, even though that city had the lowest PM10 concentrations of the six studied. There were no consistent patterns for CRP, although the results may have been skewed by the fact that most of the people studied consumed statins, cholesterol-lowering drugs known to reduce this protein. Much remains unknown about the links between the inflammation indicators tracked and subsequent health effects. Nonetheless, this study may help explain conflicting results of similar work, since it better addresses previous limitations such as lack of geographic diversity, small subject population, limited number of inflammation indicators tested, and variable health status. Bob Weinhold http://www.medworm.com/index.php?rid=710459&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Fwww.ehponline.org%2Fdocs%2F2007%2F115-7%2Fss.html%23pman pman"> PM and Elevated Inflammation Markers More Support for Air Pollution?Heart Disease Link After evaluating about 1,000 Europeans already suffering from cardiovascular disease, researchers have found a relationship between elevated concentrations of airborne particulates (PM) and increases in two markers of inflammation that have strong links with cardiovascular diseases and deaths [EHP 115:1072?1080; R?ckerl et al.]. The cumulative number of people studied is the largest to date for PM and these inflammation indicators,with the findings generally consistent across diverse locales. The researchers evaluated about 100 to 200 myocardial infarction survivors in each of six cities around the continent: Athens, Augsburg, Barcelona, Helsinki, Rome, and Stockholm. The cities have a wide r... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=710459 Sun, 01 Jul 2007 04:00:00 +0100 710459 atwi'> A Twist in the Ritalin Riddle Drug-Related Genomic Damage Not Confirmed in Children The frequently prescribed central nervous system stimulant methylphenidate (MPH), better known by brand names that include Ritalin, does not cause genomic damage in children, contrary to earlier reports, according to new work published this month [EHP 115:936 940; Walitza et al.]. In use for more than 50 years and now prescribed more than 5 million times a year in the United States, MPH is the drug of choice for attention deficit/hyperactivity disorder (ADHD). ADHD is the most frequently diagnosed psychiatric disorder in children and adolescents, with an estimated 6 12% of minors worldwide thus diagnosed. medicine bottle with pills image: Calvero, GFDL A 2005 report published in Cancer Letters had showed that gross genomic damage reflected by chromosome aberrations including sister chromatid exchanges and formation of micronuclei (smaller-than-normal cell nuclei containing partial genomes) was found in nucleated lymphocytes taken from peripheral circulation of children who had been taking the drug for only three months. Because large chromosomal breaks are associated with cancer, the study raised concerns about the potential for cancer risk in the millions of people who have taken the stimulant. That 2005 study found an increased frequency of chromosomal abnormalities in all of the 12 children whose lymphocytes were examined, lending urgency to future studies. The current study looked at micronuclei as an indicator of genomic damage in the lymphocytes of 38 children newly prescribed the drug, following some but not all of them out to six months. The children, 29 boys and 9 girls, took a variety of doses and formulations of the drug. Some subjects were lost to follow-up during the study; others switched to other medications or dropped out because they did not respond to the drug. Eight children stayed in the study through the whole six months. Overall, there was no significant increase in the formation of micronuclei at any time point, though some individual children had elevated numbers of micronucleated lymphocytes at one time point or another. Further, the lymphocytes of 9 children who had been taking the drug for more than six months at the start of the study did not show increased levels of micronucleation compared to the pretreatment levels seen in drug-naive children. The marked difference in results between the 2005 study and the current one raises the possibility of unexplained genetic differences between the study populations. Whereas the first study population included six white, four black, and two Hispanic children, the latter study focused on a more uniform group of ethnically German children. The authors say further work, especially on the long-terms effects of MPH, is called for. http://www.medworm.com/index.php?rid=648345&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F121361327%2Fss.html atwi"> A Twist in the Ritalin Riddle Drug-Related Genomic Damage Not Confirmed in Children The frequently prescribed central nervous system stimulant methylphenidate (MPH), better known by brand names that include Ritalin, does not cause genomic damage in children, contrary to earlier reports, according to new work published this month [EHP 115:936 940; Walitza et al.]. In use for more than 50 years and now prescribed more than 5 million times a year in the United States, MPH is the drug of choice for attention deficit/hyperactivity disorder (ADHD). ADHD is the most frequently diagnosed psychiatric disorder in children and adolescents, with an estimated 6 12% of minors worldwide thus diagnosed. image: Calvero, GFDL A 2005 report published in Cancer Letters had showed that gross genomi... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=648345 Fri, 01 Jun 2007 04:00:00 +0100 648345 chil'> Childhood Leukemia in Germany Cluster Identified near Nuclear Power Plant Childhood leukemia clusters have been observed at a number of sites near European nuclear facilities. With the identification of the largest cluster to date, a new German study underscores the need to clarify the association [EHP 115:947 952; Hoffmann et al.]. Krummel nuclear power plant image: vario images GmbH Co. KG/Alamy Between February 1990 and May 1991, five cases of leukemia were diagnosed in children living within 5 kilometers of the Krummel nuclear power plant in Geesthacht and a neighboring nuclear research operation along the Elbe River in northern Germany. By 2005, another nine cases of leukemia had been discovered in the area. Most of the cases were acute lymphatic leukemia in males under five years of age. Several expert commissions investigated, and found moderate levels of cesium in rainwater and air samples, along with plutonium and americium in household dust near the plant. There was also some evidence of chromosomal damage to lymphocytes among the local population. One panel deemed these observations consistent with fallout from a possible accident at the research facility that would have to have occurred around September 1986, but so far no such accident has been proved. Another panel suggested instead that chance or population mixing the commingling of local people with newcomers from various places might have caused the cluster. In the current study, researchers compared the number of observed leukemia cases in the sparsely populated Geesthacht area to the number of predicted cases based on nearby county and national incidence rates from 1990 to 2005. The five cases found in 1990 and 1991 significantly exceeded the expected incidence for that period of 0.45 cases. After studying medical records from all treatment facilities in the vicinity and in Hamburg, the team concluded that the Geesthacht cluster is the 'largest series of childhood leukemia cases reported to date' among European leukemia clusters near nuclear facilities, including those at Dounreay, Scotland; LeHague, France; and Sellafield, England. The authors state that population mixing is unlikely to account for the leukemia incidence because the population remained stable over the years studied. Nor would an alleged one-time release of radiation in 1986 readily explain the cluster, given that the excess incidence persisted over at least 15 years. Thus, they conclude, the elevated incidence of childhood leukemia around Geesthacht remains 'another piece in a growing puzzle' of childhood leukemia's association with nuclear installations and its severity and persistence emphasize the need to keep investigating. http://www.medworm.com/index.php?rid=648344&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F121361326%2Fss.html chil"> Childhood Leukemia in Germany Cluster Identified near Nuclear Power Plant Childhood leukemia clusters have been observed at a number of sites near European nuclear facilities. With the identification of the largest cluster to date, a new German study underscores the need to clarify the association [EHP 115:947 952; Hoffmann et al.]. image: vario images GmbH Co. KG/Alamy Between February 1990 and May 1991, five cases of leukemia were diagnosed in children living within 5 kilometers of the Krummel nuclear power plant in Geesthacht and a neighboring nuclear research operation along the Elbe River in northern Germany. By 2005, another nine cases of leukemia had been discovered in the area. Most of the cases were acute lymphatic leukemia in males under five years of age. Several ex... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=648344 Fri, 01 Jun 2007 04:00:00 +0100 648344 phth'> Phthalates and Metabolism Exposure Correlates with Obesity and Diabetes in Men The prevalence of obesity, insulin resistance, and diabetes has increased considerably in the past few decades. Many plausible contributing factors have been identified for this increase, among them low testosterone levels in men. Research has found that exposure to certain synthetic chemicals adversely affects testicular function in animals and possibly in humans. A new analysis looked for and found that exposure to one class of these chemicals, phthalates, correlated with two metabolic abnormalities in men: abdominal obesity and insulin resistance [EHP 115:876 882; Stahlhut et al.]. man measuring his waist image: Paul Cowan/ShutterStock Phthalates are commonly used in products such as cosmetics, soaps, pesticides, lubricants, plastics, and paints. They are widespread; indeed, more than 75% of the U.S. population carries detectable levels of several phthalate metabolites. Studies have also found associations between some phthalate metabolites and antiandrogenic effects in humans, including both infant and adult males. The authors used 1999 2002 data from the CDC National Health and Nutrition Examination Survey (NHANES) to look for a connection between phthalate exposure and metabolic disease in adult men. They compared urine concentrations of six phthalate metabolites to the participants' waist circumference and measures of insulin resistance. The analysis controlled for a variety of potential confounders, including age, ethnicity, fat and calorie consumption, physical activity, and smoking status. Four phthalate metabolites were significantly associated with greater waist circumference and three with increased insulin resistance. When the authors further controlled their models for measures of participants' kidney and liver function, the associations decreased somewhat but remained significant for all but one metabolite. The authors caution that this first look at phthalates, obesity, and insulin resistance is limited by the study's cross-sectional design and the single measurement of urine phthalate metabolites (an imperfect measure of long-term exposure). In addition, although the study was based on the hypothesis that phthalates cause metabolic abnormalities by decreasing androgen levels or function, the authors couldn't examine this mechanism, because the NHANES data do not contain measures of sex hormones in men. They note that other mechanisms could also be involved in a relationship between phthalates and metabolic disease. If phthalates are eventually shown conclusively to contribute to obesity or diabetes in men, it's still not clear how these chemicals would affect the opposite sex, since low testosterone has been associated with a lower (not higher) prevalence of metabolic disease in women. If further longitudinal studies confirm that phthalate exposure contributes to obesity, diabetes, and related disorders, actions to reduce phthalate exposure could effectively lessen the chemicals' contribution to metabolic disorders, because phthalates are quickly metabolized and excreted by the body. http://www.medworm.com/index.php?rid=648343&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F121361325%2Fss.html phth"> Phthalates and Metabolism Exposure Correlates with Obesity and Diabetes in Men The prevalence of obesity, insulin resistance, and diabetes has increased considerably in the past few decades. Many plausible contributing factors have been identified for this increase, among them low testosterone levels in men. Research has found that exposure to certain synthetic chemicals adversely affects testicular function in animals and possibly in humans. A new analysis looked for and found that exposure to one class of these chemicals, phthalates, correlated with two metabolic abnormalities in men: abdominal obesity and insulin resistance [EHP 115:876 882; Stahlhut et al.]. image: Paul Cowan/ShutterStock Phthalates are commonly used in products such as cosmetics, soaps, pesticides, lubric... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=648343 Fri, 01 Jun 2007 04:00:00 +0100 648343 shif'> Shift in the Sexes Are Endocrine Disruptors Changing Birth Ratios? According to demographic data compiled by the United Nations, an average of 105 boys are born for every 100 girls. The male proportion of births, equal to 0.515, varies slightly between years and populations, but these factors do not fully explain consistently shifting ratios in several industrialized countries over recent decades. A new study examines birth and fetal death sex ratios in Japan and the United States and reveals significant male-to-female shifts in both nations [EHP 115:941 946; Davis et al.]. new-born infant image: Brent Bossom The research team calculated birth and fetal death sex ratios in Japan based on 1949 1999 data from the Japanese Vital Statistics Bureau. The proportion of male births varied yearly before 1970 but declined steadily since then, from 0.5172 to 0.5135. Between 1960 and 1999, the male proportion of fetal deaths increased from 56% to 67.7%. The male fetal death rate is approximately four times higher in Japan than in the United States. For U.S. calculations, the researchers drew 1983 1995 fetal death data and 1970 2002 birth data from the National Center for Health Statistics. The proportion of male births dropped in the United States, from 0.5134 in 1970 to 0.5117 in 2002. There are significant racial differences, however: between 1970 and 2002 the proportion of non-Hispanic white male births fell from 0.5143 to 0.5122, whereas the proportion of black male births rose slightly from 0.5076 to 0.5079. The male proportion of black fetal deaths also increased, rising from 53.5% to 54.5%; among whites, the male proportion of fetal deaths rose by less than 0.5%. Why birth sex ratios differ so much between white and black women is unknown, but hormonal differences due to race and to incidence of obesity may be involved. A possible explanation for the increased ratio among black births may stem from improved prenatal and obstetric care in general, reducing the overall number of fetal deaths. The researchers speculate that parental exposures to endocrine-disrupting chemicals, including metalloestrogens such as methylmercury, might be factors undermining the conception and survival of male children. They suggest particular scrutiny of Japanese body burden of mercury and other metalloestrogens to understand this difference. Additionally, future investigations of declining sex ratios should consider the types and timing of prenatal and parental exposures to endocrine-disrupting chemicals. The researchers hypothesize that paternal exposures prior to conception might affect expression of the SRY gene on the Y chromosome. http://www.medworm.com/index.php?rid=648342&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F121361324%2Fss.html shif"> Shift in the Sexes Are Endocrine Disruptors Changing Birth Ratios? According to demographic data compiled by the United Nations, an average of 105 boys are born for every 100 girls. The male proportion of births, equal to 0.515, varies slightly between years and populations, but these factors do not fully explain consistently shifting ratios in several industrialized countries over recent decades. A new study examines birth and fetal death sex ratios in Japan and the United States and reveals significant male-to-female shifts in both nations [EHP 115:941 946; Davis et al.]. image: Brent Bossom The research team calculated birth and fetal death sex ratios in Japan based on 1949 1999 data from the Japanese Vital Statistics Bureau. The proportion of male births varied yearly befor... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=648342 Fri, 01 Jun 2007 04:00:00 +0100 648342 cott'> Cottonwood Clues in Fallon Tree Rings Reflect Tungsten, Cobalt Exposure The cause of a childhood leukemia cluster in Fallon, Nevada (population 8,000) has mystified investigators since it was first discovered in 2000. Sixteen children have been diagnosed with acute lymphocytic leukemia and one with acute myelocytic leukemia. Because known risk factors such as ionizing radiation and prenatal exposure to volatile organic compounds do not explain most acute lymphocytic leukemia cases, researchers suspect other environmental exposures in Fallon. Now a tree ring study reveals elevated environmental tungsten and cobalt levels in Fallon compared to other towns in the area in the years just prior to the onset of the cluster [EHP115:715–719; Sheppard et al.]. cottonwood tree Branching out. The cottonwoods around Fallon may add a new chapter to the story of the town's leukemia cluster. image: Paul R. Sheppard Among Fallon's potential sources of contamination are a tungsten carbide production facility, melon and alfalfa fields, and a naval air base jet fuel pipeline. The study team took core samples representing the years 1989 through 2002 from cottonwood trees around the Fallon processing plant and analyzed them for tungsten, cobalt (also used in tungsten carbide processing), and a range of other metals. For comparison, they also sampled trees in three nearby towns. In addition, the team tested trees in Sweet Home, Oregon, which also has a known local source of airborne tungsten, to test the dendrochemical technique independently. Before 1992, median tungsten levels in Fallon tree rings differed little from those in the comparison Nevada towns, but rose thereafter to levels significantly higher than those in the other towns. Median cobalt levels in Fallon were higher than in surrounding towns but remained constant over the study period. Other trace metals did not increase consistently over time. It is unknown whether tungsten causes cancer. The National Toxicology Program is currently assessing its disposition in rodents, with carcinogenicity studies planned. Cobalt has been associated with lung cancer, thyroid disorders, and lung disease, according to the CDC's 2005 Third National Report on Human Exposure to Environmental Chemicals. The International Agency for Research on Cancer has classified the combination of tungsten carbide and cobalt as a probable human carcinogen. By itself the tree-ring study does not establish a causal link between these elements and leukemia, but based on the temporal change in tungsten and the high level of cobalt found in the trees, further biomedical research is advisable. http://www.medworm.com/index.php?rid=584198&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F113325326%2Fss.html cott"> Cottonwood Clues in Fallon Tree Rings Reflect Tungsten, Cobalt Exposure The cause of a childhood leukemia cluster in Fallon, Nevada (population 8,000) has mystified investigators since it was first discovered in 2000. Sixteen children have been diagnosed with acute lymphocytic leukemia and one with acute myelocytic leukemia. Because known risk factors such as ionizing radiation and prenatal exposure to volatile organic compounds do not explain most acute lymphocytic leukemia cases, researchers suspect other environmental exposures in Fallon. Now a tree ring study reveals elevated environmental tungsten and cobalt levels in Fallon compared to other towns in the area in the years just prior to the onset of the cluster [EHP115:715–719; Sheppard et al.]. Branching out. The cottonwo... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=584198 Tue, 01 May 2007 04:00:00 +0100 584198 toxi'> Toxic Neighbors? Fetal Death Risk Near Hazardous Waste Sites The health effects associated with residential proximity to hazardous waste sites are uncertain, and findings on potential links between prenatal exposure to environmental toxicants and outcomes such as miscarriage are mixed. A recent exploratory study in Washington State finds no evidence for an overall association between hazardous waste sites and occurrence of fetal death, but pesticide-containing sites may be an exception [EHP 115:776–780; Mueller et al.]. hazardous waste sign image: Jeff Banke/Shutterstock Using state health department records, researchers examined the occurrence of fetal death, defined as pregnancy loss after 20 weeks' gestation, against the straight-line distance between a mother's home and the nearest hazardous waste site. The team used ten live births for each fetal death as controls and considered several factors that could affect pregnancy outcome, such as maternal smoking, alcohol consumption, age, medical conditions, and socioeconomic status. Between 1987 and 2001, the state recorded 7,054 fetal deaths; the team located maternal residences for 5,302 cases and 61,455 controls. Hazardous waste sites were characterized according to type of contaminant (solvents, metals, pesticides, or radioactive substances) and type of contaminated medium (air, water, or soil). Sites were also ranked as 'high priority' or 'low priority' depending on their potential hazard to public or environmental health. Maternal characteristics more common among women who experienced a fetal death included being unmarried and older than 35, having less than a high school education, drinking alcohol during pregnancy, and receiving government-funded medical assistance. Mothers who experienced fetal death were also more often of nonwhite race/ethnicity and less likely to have had a previous pregnancy or birth. In general, no association was seen between hazardous waste site proximity and fetal death. However, subanalysis by contaminant type showed a small but significant increase in fetal deaths within five miles of pesticide-contaminated sites, with a slightly increased risk with each mile nearer such waste sites. Subanalysis by priority type revealed a slight but nonsignificant increase in fetal death for mothers within two miles of a high-priority site. The authors describe several study limitations. No actual toxicant exposure measurements were available, potential occupational exposures and their duration were unknown, and fetal deaths and pertinent maternal health information may have been underreported. The findings do not negate the need for waste site remediation, however, and in light of other research showing health risks linked to prenatal pesticide exposure, the authors recommend that more attention be paid to pesticide-contaminated sites. http://www.medworm.com/index.php?rid=584186&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F113325325%2Fss.html toxi"> Toxic Neighbors? Fetal Death Risk Near Hazardous Waste Sites The health effects associated with residential proximity to hazardous waste sites are uncertain, and findings on potential links between prenatal exposure to environmental toxicants and outcomes such as miscarriage are mixed. A recent exploratory study in Washington State finds no evidence for an overall association between hazardous waste sites and occurrence of fetal death, but pesticide-containing sites may be an exception [EHP 115:776–780; Mueller et al.]. image: Jeff Banke/Shutterstock Using state health department records, researchers examined the occurrence of fetal death, defined as pregnancy loss after 20 weeks' gestation, against the straight-line distance between a mother's home and the nearest hazardous w... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=584186 Tue, 01 May 2007 04:00:00 +0100 584186 shor'> Short-Term Particulate Threat Pollution Standard May Not Protect Health Many studies have shown that particulate matter (PM) poses health risks, yet the attributes of PM that cause these effects remain uncertain. To address some of those critical nuances, especially the short-term effects of specific emissions, researchers used a refined approach, including new application of a pollutant distribution model, to assess links between deaths and two PM components, black carbon and sulfate particles [EHP 115:751–755; Maynard et al.]. They found that as the air concentration of either component increased, there were more deaths the following day. These results occurred even at concentrations below current U.S. standards for fine particulates. Boston, Massachusetts image: Dave Raboin/iStockphoto Sulfate exposure in the northeastern United States comes in large part from coal-fired power plants. Black carbon is a surrogate for vehicle-related pollution that varies significantly over short distances. The researchers used data from a central monitor at the Harvard School of Public Health to determine concentrations of sulfates and assumed there were homogenous concentrations throughout the study area, a premise other studies have validated. To estimate concentrations of black carbon, they used a model that began its calculations with daily data from another monitor at the school. The model then estimated black carbon concentrations at more than 80 representative sites in the Boston area, incorporating variables such as weather, season, day of week, traffic volume, proximity to major roadways, population density, and percent urbanization. The researchers also accounted for gender, education, income, and residence location for each death. In evaluating 107,925 deaths that occurred at Boston-area residences from 1995 through 2002, the researchers found that each interquartile increase in black carbon concentration on the day before death was linked with a 2.3% rise in deaths from any cause and a 4.4% increase in stroke deaths. A similar, though smaller, relationship existed for sulfate particles, with each interquartile increase the day before death linked with a 1.1% increase in death from any cause. The researchers also found that for both black carbon and sulfates, there were increases of similar magnitude for deaths from cardiovascular disease, respiratory diseases, and diabetes. The authors acknowledge that the black carbon estimation model still needs refinement, that the study was limited by its focus on just one city, and that there were relatively limited data for sulfates and some causes of death. Nonetheless, this work confirms past research implicating sulfates and black carbon in the PM–mortality association. As a result, the authors say their findings reinforce concerns that current and proposed fine particulate standards do not adequately protect public health. http://www.medworm.com/index.php?rid=584174&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F113325324%2Fss.html shor"> Short-Term Particulate Threat Pollution Standard May Not Protect Health Many studies have shown that particulate matter (PM) poses health risks, yet the attributes of PM that cause these effects remain uncertain. To address some of those critical nuances, especially the short-term effects of specific emissions, researchers used a refined approach, including new application of a pollutant distribution model, to assess links between deaths and two PM components, black carbon and sulfate particles [EHP 115:751–755; Maynard et al.]. They found that as the air concentration of either component increased, there were more deaths the following day. These results occurred even at concentrations below current U.S. standards for fine particulates. image: Dave Raboin/iStockphoto Sulfate e... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=584174 Tue, 01 May 2007 04:00:00 +0100 584174 arse'> Arsenic Upsets Heartbeat Possible Early Warning for Cardiovascular Risk Acute arsenic exposure can cause severe heartbeat abnormalities, and chronic exposure has been linked to coronary disease and cancer. Now researchers from Inner Mongolia, China, and the United States have begun to analyze the effects of chronic exposure on the electrical signals that regulate heartbeat [EHP 115:690–694; Mumford et al.]. They found a correlation between exposure via drinking well water and signal changes associated with arrhythmia and death. Ba Men residents pumping well water The heart of the exposure. Many residents of Ba Men, Inner Mongolia, use artesian well water containing high concentrations of arsenic. image: Judy Mumford Tens of millions of people worldwide drink groundwater contaminated with naturally occurring arsenic. Through metabolism, the inorganic arsenic found in drinking water is converted to more toxic methylated compounds. The research team focused on the QTc interval, a specific portion of the cardiac signal that corresponds to the active pumping (systole) phase of the heartbeat. QTc intervals of 0.45 second or longer are associated with cardiac risk. The team used electrocardiography to measure the QTc interval of 168 men and 145 women from four villages in Ba Men, an area of Inner Mongolia where the drilling of artesian wells in 1980 exposed residents to arsenic. Arsenic exposure was determined through analysis of toenail samples from participants and water samples from their wells. Arsenic exposure was categorized as low (21 µg/L or less), medium (100–300 µg/L), or high (430–609 µg/L). As exposure to arsenic increased, so did the occurrence of prolonged QTc interval, which was seen in 3.9% of the low exposure group, 11.1% of the medium exposure group, and 20.6% of the high exposure group. Women—who typically have a longer QTc interval than men—were more susceptible to this effect than men. Age, smoking, and pesticide exposure did not affect the association. The authors suggest that arsenic may affect QTc interval by altering the flow of potassium ions that are involved in cardiac signaling. They write that measurement of QTc interval may be useful in the early detection of cardiovascular risk among individuals exposed to arsenic, as well as in the identification of populations where such risk is high. The team is currently conducting a large follow-up study in the same population. Meanwhile, the Chinese government is helping to install water systems in the Ba Men area that will decrease arsenic exposure. http://www.medworm.com/index.php?rid=584168&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F113325323%2Fss.html arse"> Arsenic Upsets Heartbeat Possible Early Warning for Cardiovascular Risk Acute arsenic exposure can cause severe heartbeat abnormalities, and chronic exposure has been linked to coronary disease and cancer. Now researchers from Inner Mongolia, China, and the United States have begun to analyze the effects of chronic exposure on the electrical signals that regulate heartbeat [EHP 115:690–694; Mumford et al.]. They found a correlation between exposure via drinking well water and signal changes associated with arrhythmia and death. The heart of the exposure. Many residents of Ba Men, Inner Mongolia, use artesian well water containing high concentrations of arsenic. image: Judy Mumford Tens of millions of people worldwide drink groundwater contaminated with naturally occurring arseni... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=584168 Tue, 01 May 2007 04:00:00 +0100 584168 modi'> A Modified Effect on Asthma Ozone and Secondhand Smoke Outweigh Genetic Influence Individual variations in genes, known as single-nucleotide polymorphisms (SNPs), help to explain why some children are more susceptible to asthma and allergies. But does exposure to ozone or secondhand smoke alter this genetic susceptibility? Public health experts from Mexico and the United States report that, in 596 families with asthmatic children living in Mexico City, where ozone levels rank as the highest in North America, parental smoking can indeed modify the risk conferred by a particular SNP [EHP 115:616 622; Wu et al.]. man smoking around child Smoke screen? For certain people, secondhand smoke exposure may override genetic influence on asthma risk. image: Elena Kouptsova-Vasic/Shutterstock Complex interactions among genes and environmental triggers are known to contribute to asthma and allergic reactions in children. Exposure to ozone, for instance, turns on the TNF gene for the production of tumor necrosis factor- , a cytokine that causes airway inflammation. So does exposure to cigarette smoke. The children, who ranged in age from 4 to 17 years, largely had mild asthma. Half lived with a smoking parent. The researchers measured variations in TNF and the gene for lymphotoxin- (LTA) in the children and their parents. TNF and LTA lie next to each other on chromosome 6 and share receptors. Two SNPs for LTA and four for TNF capture most of the variation in these two genes. The team found that LTA was not associated with asthma risk, but one SNP for TNF (coded 308A) raised the risk by 50% among all children. This SNP and one other (238A) more than doubled the risk of asthma among children living with nonsmoking parents. None of the SNPs for LTA or TNF were linked to asthma among children living with smoking parents. In addition, allergic reactions generated with skin prick tests were not related to any of the SNPs tested. The researchers suspect that secondhand smoke and ozone may synergistically increase production of tumor necrosis factor- , an effect that overrides the minor influence of genetic variation. Therefore, the effects of certain SNPs on risk of asthma may stand out more clearly in children who are not exposed to secondhand smoke. http://www.medworm.com/index.php?rid=524775&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F106005737%2Fss.html modi"> A Modified Effect on Asthma Ozone and Secondhand Smoke Outweigh Genetic Influence Individual variations in genes, known as single-nucleotide polymorphisms (SNPs), help to explain why some children are more susceptible to asthma and allergies. But does exposure to ozone or secondhand smoke alter this genetic susceptibility? Public health experts from Mexico and the United States report that, in 596 families with asthmatic children living in Mexico City, where ozone levels rank as the highest in North America, parental smoking can indeed modify the risk conferred by a particular SNP [EHP 115:616 622; Wu et al.]. Smoke screen? For certain people, secondhand smoke exposure may override genetic influence on asthma risk. image: Elena Kouptsova-Vasic/Shutterstock Complex interactions am... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=524775 Sun, 01 Apr 2007 04:00:00 +0100 524775 door'> Door of Perception NIEHS Portal Shows Way to Better Disaster Response Hurricane Katrina which killed 1,300 people, disrupted the lives of 650,000, and produced an estimated $125 billion in recovery and reconstruction costs brought the need for better disaster response into sharp focus. In this issue, researchers introduce the NIEHS Portal, a state-of-the-art web-based system to improve decision making during disaster response [EHP 115:564 571; Pezzoli et al.]. destroyed house SOS. Nineteen months after Katrina, Gulf Coast residents are still in the storm's shadow. image: Laurie Barr/Shutterstock The portal was designed to fulfill three objectives: to monitor disaster-related human and environmental health impacts; to assess and reduce pollutant exposures caused by disasters; and to develop science-based recovery strategies. The portal does this by combining geographically referenced data on roads, power plants, contaminant release sources, flood measures, and local demography in a cyber-infrastructure called 'Telescience,' which was developed at the University of California, San Diego. This cyberinfrastructure lets users share computer power and storage over the Internet. A user-friendly interface provides access to project-relevant databases and data integration tools. High-speed network connections allow researchers to use supercomputing facilities and massive data storage sites as if they were on their desktop. A geographic information system (GIS) manages the data, and an accessible interface allows users to contribute new information and participate in online discussions and collaborative workspaces. Contributors are responsible for the accuracy of the data they provide. Access to data associated with any given research project is governed by the members of that research group. In its current deployment, the portal assembles GIS data for Texas, Louisiana, and Mississippi, and includes high-resolution data layers for the regions that were affected by Hurricanes Katrina and Rita in 2005. Scientists have begun exploring ways to use the system. One project supports ongoing efforts to study and mitigate the health effects of flood-induced indoor mold, particularly asthma among exposed children. Scientists link high mold concentrations with population information to identify locations of potential high exposures. The portal is also supporting studies of toxic sediments, particularly hot spots generated by the release of contaminants such as sewage and industrial chemicals during the storms. The authors stress how the portal can also address the research needs of exposure biology and gene environment interactions. The system's massive computing power can integrate population-level studies of genetics with real-time exposure monitoring and environmental sampling, advancing the NIEHS's goal of studying molecular processes in environmental health. http://www.medworm.com/index.php?rid=524774&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F106005736%2Fss.html door"> Door of Perception NIEHS Portal Shows Way to Better Disaster Response Hurricane Katrina which killed 1,300 people, disrupted the lives of 650,000, and produced an estimated $125 billion in recovery and reconstruction costs brought the need for better disaster response into sharp focus. In this issue, researchers introduce the NIEHS Portal, a state-of-the-art web-based system to improve decision making during disaster response [EHP 115:564 571; Pezzoli et al.]. SOS. Nineteen months after Katrina, Gulf Coast residents are still in the storm's shadow. image: Laurie Barr/Shutterstock The portal was designed to fulfill three objectives: to monitor disaster-related human and environmental health impacts; to assess and reduce pollutant exposures caused by disasters; and to develop scien... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=524774 Sun, 01 Apr 2007 04:00:00 +0100 524774 peri'> Peril of the Shallows? Elevated Arsenic in Kelp Supplements Kelp, widely consumed in Asian countries, is a growing part of the U.S. supplement market. It generally is marketed as a concentrated source of iodine and other essential minerals. Because kelp is a nutritional supplement and not a drug, the FDA does not require manufacturers to demonstrate safety or efficacy. Now researchers at the University of California, Davis, report the case of a woman who received toxic doses of arsenic from kelp supplements [EHP 115:606 608; Amster et al.]. kelp supplements Herbal loophole. As a dietary supplement, kelp is exempt from drug safety testing. image: Chris Reuther/EHP Arsenic occurs naturally in some soils, and can contaminate bodies of water. The metalloid concentrates in fish that eat arsenic-rich algae and can also be found in plants that absorb it from the soil or water in which they are grown. Human exposure typically comes from diet, contaminated drinking water, or occupational exposures, as in smelters; people ingest an average of 40 microg per day. The researchers investigated kelp supplements after a 54-year-old woman taking the pills was referred to the university's occupational medicine clinic. The patient had started taking kelp to treat minor memory loss and fatigue. She initially took the dose recommended on the bottle, then doubled it when her symptoms failed to improve. She took kelp for one year, during which her fatigue worsened to the point that she had to switch from full- to part-time work. She also experienced rash, diarrhea, vomiting, severe headaches, and hair loss. A urine test revealed an arsenic concentration of 83.6 microg/g creatinine. Creatinine, a muscle metabolite, is excreted at a relatively constant rate and is used for reporting urinary biomarkers, as an adjustment for the high variability of urine dilution. A normal arsenic concentration is less than 50 microg/g creatinine. The researchers sent the patient's kelp supplement, along with several other brands purchased from local health food stores, to be tested at a state lab after ruling out occupational, dietary, and drinking-water exposure. Only one of the nine samples tested contained no detectable arsenic. Concentrations among the other eight ranged from 1.59 ppm to 65.5 ppm by dry weight. Samples taken from three batches of the patient's brand had concentrations of 1.59, 2.28, and 34.8 ppm. The FDA tolerance level for arsenic is 2 ppm. Three weeks after she abandoned kelp, the woman resumed full-time work. Her urine arsenic concentration dropped more than a third in two months and was undetectable after another two months. Eventually all her syptoms resolved. Past studies have shown that many herbal remedies are contaminated with potential toxicants including mercury and lead. To prevent more inadvertent poisonings, the authors recommend that manufacturers be required to prove safety before marketing their products. http://www.medworm.com/index.php?rid=524773&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F106005735%2Fss.html peri"> Peril of the Shallows? Elevated Arsenic in Kelp Supplements Kelp, widely consumed in Asian countries, is a growing part of the U.S. supplement market. It generally is marketed as a concentrated source of iodine and other essential minerals. Because kelp is a nutritional supplement and not a drug, the FDA does not require manufacturers to demonstrate safety or efficacy. Now researchers at the University of California, Davis, report the case of a woman who received toxic doses of arsenic from kelp supplements [EHP 115:606 608; Amster et al.]. Herbal loophole. As a dietary supplement, kelp is exempt from drug safety testing. image: Chris Reuther/EHP Arsenic occurs naturally in some soils, and can contaminate bodies of water. The metalloid concentrates in fish that eat arsenic-rich ... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=524773 Sun, 01 Apr 2007 04:00:00 +0100 524773 meth'> Methylmercury and IQ Dose Response Estimate of Prenatal Effect Methylmercury, the most biologically active mercury compound, is well known to cause serious health effects, particularly to the developing fetal nervous system. Effects can include attention deficits as well as IQ, motor, memory, and language impairment. A new analysis now combines data from three earlier studies to produce an integrated estimate of the dose response relationship between maternal mercury exposure during pregnancy and lowered childhood IQ [EHP 115:609 615; Axelrad et al.]. illustration of pregnant woman cooking fish Smart move. A new analysis takes a first step toward quantifying the benefits of reducing mercury exposure, which may include avoiding IQ deficits. image: Imagezoo/Images.com/Corbis The authors analyzed combined IQ data from three longitudinal studies conducted in the Faroe Islands, the Seychelles Islands, and New Zealand. These studies measured a variety of neurodevelopmental end points, including IQ, attention, and motor skills. The range of prenatal exposures in the three populations is comparable to those of some U.S. populations. For example, a 2003 study found the lowest maternal blood mercury level in the Faroe Islands to be 0.53 microg/L, and the CDC reported in 2004 that more than half of U.S. women had blood mercury concentrations higher than this. Geometric mean blood concentrations in the United States from 1999 to 2002 were 0.92 microg/L for women of childbearing age; for children the mean was 0.33 microg/L. The New Zealand and Seychelles studies reported results in terms of ppm of hair mercury, whereas the Faroe Islands study reported effects in terms of ppb of cord blood mercury. So the team converted the Faroe Islands results to their equivalents in units of hair mercury. They found a childhood IQ decrease of 0.18 points for each ppm rise in maternal hair mercury. The team assumed a linear, nonthreshold dose response curve. However, they noted that if very low exposures produce a steeper curve, as has been found recently with childhood lead exposure, their calculation may underestimate the effects of prenatal mercury exposure. Similarly, certain cognitive abilities such as word retrieval and retention of verbally presented information are not captured by IQ scores, so relying only on IQ as a measure of cognitive function will also underestimate mercury's effects. Eating fish is the most common route of human exposure to methylmercury. In 2004 the FDA and the EPA issued a joint statement advising women of childbearing age and children to limit their weekly consumption of commercially caught fish to 12 oz (6 oz for locally caught fish) in order to avoid harmful exposure. The EPA has set a reference dose of 0.1 microg/kg/day for methylmercury as an estimate of the daily exposure unlikely to cause harm over a lifetime. Methylmercury's effect on IQ is separate from its effect on attention and motor skills. But because IQ is a well-established end point used in cost benefit and economic analyses of the effects of environmental contaminants, establishing the dose response relationship for IQ is a first step in quantifying the benefits of reducing mercury exposure. http://www.medworm.com/index.php?rid=524772&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F106005734%2Fss.html meth"> Methylmercury and IQ Dose Response Estimate of Prenatal Effect Methylmercury, the most biologically active mercury compound, is well known to cause serious health effects, particularly to the developing fetal nervous system. Effects can include attention deficits as well as IQ, motor, memory, and language impairment. A new analysis now combines data from three earlier studies to produce an integrated estimate of the dose response relationship between maternal mercury exposure during pregnancy and lowered childhood IQ [EHP 115:609 615; Axelrad et al.]. Smart move. A new analysis takes a first step toward quantifying the benefits of reducing mercury exposure, which may include avoiding IQ deficits. image: Imagezoo/Images.com/Corbis The authors analyzed combined IQ data from three ... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=524772 Sun, 01 Apr 2007 04:00:00 +0100 524772 Metal Duo Damages Lungs: Lead and Manganese in Fine Particulates http://www.medworm.com/index.php?rid=451079&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F97888104%2Fss.html Extensive evidence indicates that fine particulates can damage human lungs. But much remains unknown about exactly which components of these particulates are to blame. In a small study of Korean children, researchers have found that two metals, lead and manganese, are among the substances likely at fault [EHP 115: 430–434; Hong et al.]. Gotcha! In a study of Korean children scientists identified some of the health-damaging components of fine particulates. image: Photodisc To pin down the particulate culprits, the researchers evaluated 43 children who attended school on an island near Incheon City. The island has low traffic density and industrial emissions, but concentrations of fine particulates 2.5 µm in diameter or smaller were relatively high by U.S. standards, perhaps owing to nat... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=451079 Thu, 01 Mar 2007 05:00:00 +0100 451079 The Testosterone Test: Phthalate Inhibits Leydig Cell Aggregation http://www.medworm.com/index.php?rid=451078&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F97888103%2Fss.html Testicular cancer and low sperm count are adult disorders, but evidence increasingly suggests they have a fetal origin. Cryptorchidism and hypospadias, apparent at birth, also appear linked to prebirth events. According to the testicular dysgenesis syndrome (TDS) hypothesis, all four disorders, which by some reports have become more common in recent decades, partially stem from fetal abnormalities in testosterone-producing Leydig cells. An investigation now reveals that di(n-butyl) phthalate (DBP) and its metabolite monobutyl phthalate (MBP) suppress testosterone production in rats and primates [EHP 115:390–396; Hallmark et al.]. Attempts to establish in vitro models were unsuccessful, however. Testicular effect. The numbers and size of Leydig cells (in brown, above) increased in MBP-tr... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=451078 Thu, 01 Mar 2007 05:00:00 +0100 451078 Carbon Concerns: Nanotubes Cause Cardiovascular Damage http://www.medworm.com/index.php?rid=451077&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F97888102%2Fss.html Lung deposition of single-wall carbon nanotubes (SWCNTs), one of the most commonly used materials in nanotechnology, is already known to cause localized toxic effects. Now scientists have demonstrated that such deposition also leads to cardiovascular damage in mice, including accelerated formation of atherosclerotic plaques [EHP 115:377–382; Li et al.]. The findings add to concerns that exposure to SWCNTs could result in systemic toxic effects. Worming their way in? SWCNTs may cause systemic toxicity. image: Dennis Kunkel The team conducted a series of experiments, instilling SWCNTs into the lungs of mice. In an initial screen for extrapulmonary effects, Ho1-luc reporter transgenic mice were exposed to single SWCNT doses of 10 or 40 µg. Heme oxygenase-1 (HO-1) gene expression, a biomar... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=451077 Thu, 01 Mar 2007 05:00:00 +0100 451077 Breaking In through Critical Windows: p,p´-DDE May Alter Fetal Neurodevelopment http://www.medworm.com/index.php?rid=451076&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F97888101%2Fss.html DDT has been widely used to control mosquito-borne malaria since the late 1940s. The compound and metabolites such as p,p´-DDE linger in the environment for decades; even in areas where DDT has been banned, these neurotoxic chemicals are still detected in human blood, fat, breast milk, and umbilical cord blood. Researchers examined the possibility that prenatal exposure to p,p´-DDE damages early neurodevelopment, and present the first evidence that exposure during a critical window of development adversely affects infant psychomotor development. [EHP 115:435–439; Torres-Sánchez et al.] Back tracks. Long-ago pesticide spraying can still affect today's children. image: Aubrey Wade/Panos Pictures From January 2001 to June 2005, 1,585 reproductive-age women in the State of Morelos, Mexic... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=451076 Thu, 01 Mar 2007 05:00:00 +0100 451076 Mapping a Course for PFCs: Transfer Between Mothers' Milk and Serum http://www.medworm.com/index.php?rid=399545&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F84927092%2Fss.html Studies have found assorted perfluorinated compounds (PFCs)—the persistent chemicals in such products as nonstick coatings—in samples of human blood and milk, but what isn't clear is how efficiently the chemicals transfer between these two media. To address this gap, researchers in Sweden compared PFC levels in blood serum and milk samples to better understand the lactational transfer of these compounds [EHP 115: 226–230; Kärrman et al.]. Lactation equation. A new study shows that PFCs are transferred into breast milk at concentrations about 1% of maternal serum levels. image: Najin/Shutterstock Previous animal and human studies have shown that mothers can pass certain PFCs to fetuses and infants. That these compounds can find their ways into humans at the earliest stages is cause f... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=399545 Thu, 01 Feb 2007 07:00:00 +0100 399545 Another Look at Succimer: Cognitive Deficits May Be Reversible After All http://www.medworm.com/index.php?rid=399544&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F84927091%2Fss.html Clinicians for years have used chelation to treat lead poisoning without knowing whether it prevented cognitive impairment in lead-exposed children. A recent study of chelation therapy now brings new hope to parents of children exposed to lead [EHP 115:201–209; Stangle et al.]. The Cornell University study is thought to be the first to show that chelation can alleviate cognitive deficits caused by lead exposure. That finding contradicts the most comprehensive chelation study to date, in which scientists at the NIEHS found no cognitive benefits of the therapy. Succimer for success? A new rat study suggests that chelation may negate some cognitive effects of lead exposure. image: Photodisc Chelation's known effect is to cause lead and other metals to be removed quickly from the blood and... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=399544 Thu, 01 Feb 2007 07:00:00 +0100 399544 Chloramine Catch: Water Disinfectant Can Raise Lead Exposure http://www.medworm.com/index.php?rid=399543&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F84927090%2Fss.html Many water treatment systems around the nation have stopped using chlorine to disinfect drinking water. Chlorine reacts with dissolved organic matter in water to create by-products that are suspected of causing human health problems, including some forms of cancer. Many water treatment plants now use disinfectants called chloramines, combinations of chlorine and ammonia. But in some water systems this switch has coincided with an increase in lead in drinking water, perhaps because chloramines cause lead to leach from pipes, fixtures, and solder. Now a team of researchers from Duke University has measured the potential effect of switching from chlorine to chloramines on blood lead levels [EHP 115:221–225; Miranda et al.]. Trading effects? Chloramines do not create toxic by-products like ... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=399543 Thu, 01 Feb 2007 07:00:00 +0100 399543 Trickledown Effect?: Maternal Alcohol Consumption Linked to Cryptorchidism in Sons http://www.medworm.com/index.php?rid=399542&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F84927089%2Fss.html Cryptorchidism (undescended testes), the most frequently occurring genital malformation in newborn boys, is a risk factor for later testicular cancer and fertility problems. By some reports, incidence has increased in recent decades, with environmental and lifestyle factors as potential contributors. As part of a broader investigation of these factors, a study of alcohol consumption during pregnancy reveals that imbibing five or more drinks per week may increase the risk of cryptorchidism [EHP 115:272–277; Damgaard et al.]. Booze and boys. A new study links alcohol consumption during pregnancy with reproductive effects in sons. image: Tom Grill/Corbis Prenatal alcohol exposure has already been linked to low birth weight and fetal alcohol syndrome, a spectrum of neurological and developm... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=399542 Thu, 01 Feb 2007 07:00:00 +0100 399542 Signs for Girls: Biomarkers of Common Exposures http://www.medworm.com/index.php?rid=335894&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F68190161%2Fss.html Urinary biomarkers are useful measures of environmental agents in the body. However, little is known about levels of such biomarkers in children and how they may vary by race, age, body mass index, and sex. A three-city pilot study reported this month used urinary biomarkers to better characterize a number of exposures in young girls [EHP 115:116 121; Wolff et al.]. The discovery of detectable urine levels of a range of hormonally active substances in the children may shed light on how various biomarkers relate to pubertal development. Chemicals in kids. Scientists have identified useful biomarkers of girls' exposure to chemicals including agents found in antimicrobial soaps, shampoos, and other personal products. image credit: Robert Gubbins/Shutterstock The study authors measured pare... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=335894 Mon, 01 Jan 2007 05:00:00 +0100 335894 Ahead by a Hair: Preterm Delivery and Maternal Mercury Intake http://www.medworm.com/index.php?rid=335893&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F68190160%2Fss.html Pregnant women often receive confusing information about whether or not they should consume fish and fish oils. Protein and unsaturated fatty acids in fish confer health benefits. Yet numerous studies have suggested that fish consumption is a major source of mercury exposure, and scientists have raised concerns that mercury levels safe for adults could pose a hazard to the developing fetus. Now a new study suggests another possible hazard associated with mercury exposure during pregnancy: preterm delivery [EHP 115:42 47; Xue et al.]. Predictor of preemies? Measures of mercury in maternal hair may predict risk for preterm delivery. image credit: Millanovic/iStockPhoto The Pregnancy Outcomes and Community Health study, conducted by researchers at Michigan State University, is the first lar... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=335893 Mon, 01 Jan 2007 05:00:00 +0100 335893 Does Closeness Make the Heart Grow Weaker?: Heart Attacks and Proximity to Local Traffic http://www.medworm.com/index.php?rid=335892&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F68190159%2Fss.html Growing evidence links heart attacks with short-term exposures to vehicle exhaust from nearby streets. Now some of the first evidence that long-term exposures also are a culprit has been published by a team of Massachusetts researchers [EHP 115:53 57; Tonne et al.]. Cardiovascular disease, of which heart attacks are one major type, is the leading killer in the United States and much of the world. Hazard near home. New data link small increases in heart attack risk to living within 100 m of local traffic and major roads. image credit: image100/Alamy The team evaluated more than 5,000 cases of acute myocardial infarction that occurred in residents of the mid-sized city of Worcester, Massachusetts, from 1995 to 2003, to determine if there was any connection between the heart attacks and exp... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=335892 Mon, 01 Jan 2007 05:00:00 +0100 335892 Tamiflu Swan Song?: Building Resistance to Top Avian Flu Drug http://www.medworm.com/index.php?rid=335891&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F68190158%2Fss.html As the WHO has begun warning of the potential for an avian flu pandemic, governments worldwide have been stockpiling Tamiflu (oseltamivir phosphate). Tamiflu minimizes flu symptoms and duration by preventing the virus from escaping the cells it infects. It also reduces the likelihood of spreading the virus. Now British researchers are predicting that heavy use of Tamiflu, as during a pandemic, will expose wild waterfowl to enough of the antiviral agent to foster a resistant strain [EHP 115:102 106; Singer et al.]. Release and catch. Release of excreted Tamiflu into the environment could create drug-resistant strains of avian flu in wild waterfowl. image credit: Chris Reuther/EHP The risk that Tamiflu will promote a resistant virus comes from the drug's excreted metabolite, oseltamivir ca... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=335891 Mon, 01 Jan 2007 05:00:00 +0100 335891 Unwelcome Guest: Airborne Staph in Homes http://www.medworm.com/index.php?rid=301196&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F56172156%2Fss.html Staphylococcus aureus, one of the most prevalent causes of infections of the blood, skin, soft tissue, and lower respiratory tract, spreads through close contact with contaminated people and surfaces. Although a few studies hint that airborne transmission of the microbe may be involved in hospital infections, no studies have examined indoor levels of S. aureus outside of a hospital setting. The first study to monitor S. aureus bioaerosols in residences shows that strains of the bacterium are common inhabitants of indoor and outdoor air [EHP 114:1859 1864; Gandara et al.]. Moreover, indoor strains are particularly resistant to commonly prescribed antibiotics. Down in the west Texas town. A study in El Paso, Texas, shows evidence of antibiotic-resistant Staphylococcus aureus within residen... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=301196 Fri, 01 Dec 2006 07:00:00 +0100 301196 Adding Up to ADHD: Effects of Early Exposures http://www.medworm.com/index.php?rid=301195&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F56172155%2Fss.html Many studies have documented health risks of childhood exposures to lead and tobacco smoke. Both exposures have been implicated in the development of attention deficit/hyperactivity disorder (ADHD) in children. A team of researchers now confirms links between both neurotoxicants and ADHD development [EHP 114: 1904 1909; Braun et al.]. Exciting data. New findings shed light on links between ADHD and early exposure to lead or tobacco smoke. image: LWA/Dann Tardif/Alamy ADHD, one of the most common childhood disorders, may affect up to 8% of children, costing society an estimated $9.2 billion per year. However, the mechanisms for the development of the disorder are unclear. Previous research has implicated prenatal tobacco smoke exposure in its development, but the relative contribution of ... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=301195 Fri, 01 Dec 2006 07:00:00 +0100 301195 Picking Up on Preservatives: New Biomarkers for Gauging Paraben Exposure http://www.medworm.com/index.php?rid=301194&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F56172154%2Fss.html As scientists seek to characterize human exposures to chemicals, they need more valid, accurate biomarkers telltale molecular signatures that indicate a particular exposure has occurred. A team from the CDC has now provided the field with a new biomarker that could help researchers document exposures to a class of antimicrobial preservatives called parabens [EHP 114: 1843 1846; Ye et al.]. Biomarkers roll on. Scientists may have discovered a new way to measure exposure to parabens, an ingredient in many toiletries and cosmetics. image: Jim Boorman/Alamy Parabens are used in shampoos, cosmetics, moisturizers, medications, foods, and beverages. Concerns have arisen about the potential human health risks associated with the widespread use of these weakly estrogenic compounds, including wide... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=301194 Fri, 01 Dec 2006 07:00:00 +0100 301194 Thyroid Alert: Low Iodine and Perchlorate Effects in Women http://www.medworm.com/index.php?rid=301193&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F56172153%2Fss.html Perchlorate, an oxidizer in solid rocket fuel, is widely found in groundwater, drinking water, milk, vegetables, fruit, grain, and forage crops. Large doses of perchlorate have been shown to inhibit iodide uptake and reduce thyroid hormone production, which can contribute to metabolic problems in adults and abnormal neurodevelopment during gestation and infancy. Now, researchers at the CDC show that U.S. women with low iodine intake may be at risk for reduced thyroid function due to perchlorate exposure [EHP114:1865 1871; Blount et al.]. One thing leads to another. Thyroid tissue, with thyroglobulin, a protein used to produce T4, shown in orange. Perchlorate may interfere with iodide uptake by the thyroid, leading to altered thyroid hormone synthesis. image: Dee Breger/Drexel University ... Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=301193 Fri, 01 Dec 2006 07:00:00 +0100 301193 New Neurons at Risk: Genotoxicants and Brain Development http://www.medworm.com/index.php?rid=257542&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F43890774%2Fss.html (Source: Science Selections from EHP) Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=257542 Wed, 01 Nov 2006 21:44:01 +0100 257542 Fetal Lead Exposure: Timing Is Everything for Effects http://www.medworm.com/index.php?rid=257541&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F43890773%2Fss.html (Source: Science Selections from EHP) Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=257541 Wed, 01 Nov 2006 21:44:01 +0100 257541 Health on the Factory Floor: Occupational Phthalate Exposure Reduces Testosterone http://www.medworm.com/index.php?rid=257540&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F43890772%2Fss.html (Source: Science Selections from EHP) Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=257540 Wed, 01 Nov 2006 21:44:01 +0100 257540 Man's Worst Friend?: TCDD and Male Reproductive Effects http://www.medworm.com/index.php?rid=257539&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F43890771%2Fss.html (Source: Science Selections from EHP) Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=257539 Wed, 01 Nov 2006 21:44:01 +0100 257539 A Backpack's Worth of Data: Elevated Teen Cancer Risks Linked to Air Pollution http://www.medworm.com/index.php?rid=215027&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F29465105%2Fss.html (Source: Science Selections from EHP) Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=215027 Sat, 30 Sep 2006 12:23:01 +0100 215027 Faulty Folic Acid Assumptions: Prenatal Supplements Not Always a Good Idea http://www.medworm.com/index.php?rid=215026&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F29465104%2Fss.html (Source: Science Selections from EHP) Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=215026 Sat, 30 Sep 2006 12:23:01 +0100 215026 This Little PBDE Went to Market: Estimating Intake from Grocery Store Foods http://www.medworm.com/index.php?rid=215025&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F29465103%2Fss.html (Source: Science Selections from EHP) Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=215025 Sat, 30 Sep 2006 12:23:01 +0100 215025 Swimming in Allergens?: Pool Use and Asthma http://www.medworm.com/index.php?rid=215024&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F29465102%2Fss.html (Source: Science Selections from EHP) Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=215024 Sat, 30 Sep 2006 12:23:01 +0100 215024 Tiny Intensifiers: Nanoparticles Worsen Lung Effects of Bacterial Endotoxin http://www.medworm.com/index.php?rid=168082&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F18314790%2Fss.html (Source: Science Selections from EHP) Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=168082 Sat, 02 Sep 2006 02:27:01 +0100 168082 A Lethal Change in the Weather: Temperature Extremes and Premature Mortality http://www.medworm.com/index.php?rid=168081&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F18314789%2Fss.html (Source: Science Selections from EHP) Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=168081 Sat, 02 Sep 2006 02:27:01 +0100 168081 Heavy Traffic Can Be a Pain in the . . . Ear?: Vehicle Emissions Linked to Otitis Media http://www.medworm.com/index.php?rid=168080&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F18314788%2Fss.html (Source: Science Selections from EHP) Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=168080 Sat, 02 Sep 2006 02:27:01 +0100 168080 Pyrethroids in the Home: Nondietary Pesticide Exposure in Children http://www.medworm.com/index.php?rid=168079&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F18314787%2Fss.html (Source: Science Selections from EHP) Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=168079 Sat, 02 Sep 2006 02:27:01 +0100 168079 PAHs and Cognitive Impairment: Prenatal Exposure Catches Up with Toddlers http://www.medworm.com/index.php?rid=133602&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F8025770%2Fss.html (Source: Science Selections from EHP) Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=133602 Wed, 02 Aug 2006 20:37:02 +0100 133602 Hearing Loss, Loud and Clear: Combined Effect of Noise and Toluene in Workers http://www.medworm.com/index.php?rid=133601&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F8025769%2Fss.html (Source: Science Selections from EHP) Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=133601 Wed, 02 Aug 2006 20:37:02 +0100 133601 Ultrafines' Quick Neurological Hit: Particles Take a Direct Route to the Brain http://www.medworm.com/index.php?rid=133600&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F8025768%2Fss.html (Source: Science Selections from EHP) Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=133600 Wed, 02 Aug 2006 20:37:02 +0100 133600 A Liquid Path to Lung Disease: Early Arsenic Exposure and Effects in Young Adults http://www.medworm.com/index.php?rid=133599&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2F%7Er%2Fehpsciselectsummary%2F%7E3%2F8025767%2Fss.html (Source: Science Selections from EHP) Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=133599 Wed, 02 Aug 2006 20:37:02 +0100 133599 Remember Pfiesteria? : Occupational Exposure Unlikely to Cause Cognitive Effects http://www.medworm.com/index.php?rid=83502&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2Fehpsciselectsummary%3Fm%3D11 (Source: Science Selections from EHP) Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=83502 Fri, 30 Jun 2006 21:25:01 +0100 83502 Potential Immunotoxic Effect of Thimerosal : Compound Alters Dendritic Cell Response in Vitro http://www.medworm.com/index.php?rid=83501&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2Fehpsciselectsummary%3Fm%3D10 (Source: Science Selections from EHP) Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=83501 Fri, 30 Jun 2006 21:25:01 +0100 83501 A Killer Smell: Mold Toxin Destroys Olfactory Cells in Mice http://www.medworm.com/index.php?rid=83500&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2Fehpsciselectsummary%3Fm%3D9 (Source: Science Selections from EHP) Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=83500 Fri, 30 Jun 2006 21:25:01 +0100 83500 Near and Not-So-Dear TRI Facilities: Prenatal Proximity and Later Brain Cancer http://www.medworm.com/index.php?rid=83499&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2Fehpsciselectsummary%3Fm%3D8 (Source: Science Selections from EHP) Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=83499 Fri, 30 Jun 2006 21:25:01 +0100 83499 The Public Health Payoff of 'No Smoking Allowed' : Quantifying Decreases in SHS Exposure http://www.medworm.com/index.php?rid=69917&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2Fehpsciselectsummary%3Fm%3D7 (Source: Science Selections from EHP) Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=69917 Thu, 22 Jun 2006 02:15:23 +0100 69917 Putting a Load on Your Bones: Low-Level Cadmium Exposure and Osteoporosis http://www.medworm.com/index.php?rid=69916&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2Fehpsciselectsummary%3Fm%3D6 (Source: Science Selections from EHP) Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=69916 Thu, 22 Jun 2006 02:15:23 +0100 69916 PCBs Are Endocrine Disruptors: Mixture Affects Reproductive Development in Female Mice http://www.medworm.com/index.php?rid=69915&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2Fehpsciselectsummary%3Fm%3D5 (Source: Science Selections from EHP) Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=69915 Thu, 22 Jun 2006 02:15:23 +0100 69915 A Most Irregular Threat: Old Gas Regulators Can Present Mercury Exposure http://www.medworm.com/index.php?rid=69914&cid=s_29375_55_f&fid=29375&url=http%3A%2F%2Ffeeds.feedburner.com%2Fehpsciselectsummary%3Fm%3D4 (Source: Science Selections from EHP) Science Selections from EHP journals http://www.medworm.com/rss/comments.php?id=69914 Thu, 22 Jun 2006 02:15:23 +0100 69914