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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 |Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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 Colu...
Source: Science Selections from EHP - November 1, 2009 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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.]. Preeclampsi...
Source: Science Selections from EHP - November 1, 2009 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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 part...
Source: Science Selections from EHP - November 1, 2009 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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 a...
Source: Science Selections from EHP - November 1, 2009 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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 |Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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 eg...
Source: Science Selections from EHP - August 31, 2009 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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 recommenda...
Source: Science Selections from EHP - August 31, 2009 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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 ...
Source: Science Selections from EHP - August 31, 2009 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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...
Source: Science Selections from EHP - August 31, 2009 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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 |Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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 dem...
Source: Science Selections from EHP - July 31, 2009 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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...
Source: Science Selections from EHP - July 31, 2009 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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, Ev...
Source: Science Selections from EHP - July 31, 2009 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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...
Source: Science Selections from EHP - July 31, 2009 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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 |Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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 repo...
Source: Science Selections from EHP - June 30, 2009 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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 ...
Source: Science Selections from EHP - June 30, 2009 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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 ...
Source: Science Selections from EHP - June 30, 2009 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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...
Source: Science Selections from EHP - June 30, 2009 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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 |Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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 reporte...
Source: Science Selections from EHP - June 1, 2009 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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 TillettEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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 thre...
Source: Science Selections from EHP - June 1, 2009 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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 WashamEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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�92...
Source: Science Selections from EHP - June 1, 2009 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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 SpiveyEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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 ...
Source: Science Selections from EHP - June 1, 2009 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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. BarrettEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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...
Source: Science Selections from EHP - May 1, 2009 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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 TillettEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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 wa...
Source: Science Selections from EHP - May 1, 2009 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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 WeinholdEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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 Universit...
Source: Science Selections from EHP - May 1, 2009 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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. BarrettEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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...
Source: Science Selections from EHP - April 1, 2009 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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. TenenbaumEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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 e...
Source: Science Selections from EHP - April 1, 2009 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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 SpiveyEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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 fo...
Source: Science Selections from EHP - April 1, 2009 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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 KesslerEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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 ...
Source: Science Selections from EHP - March 1, 2009 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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 MeadEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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 o...
Source: Science Selections from EHP - March 1, 2009 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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 MeadEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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 phon...
Source: Science Selections from EHP - March 1, 2009 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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 WashamEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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...
Source: Science Selections from EHP - February 1, 2009 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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. BettsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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; H...
Source: Science Selections from EHP - February 1, 2009 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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 WeinholdEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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 acquire...
Source: Science Selections from EHP - January 1, 2009 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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 PoteraEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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 func...
Source: Science Selections from EHP - January 1, 2009 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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 PoteraEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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.]....
Source: Science Selections from EHP - January 1, 2009 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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 TillettEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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 adip...
Source: Science Selections from EHP - December 1, 2008 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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 MeadEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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 "Contaminan...
Source: Science Selections from EHP - December 1, 2008 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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 DahlEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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 conclu...
Source: Science Selections from EHP - December 1, 2008 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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 WashamEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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 l...
Source: Science Selections from EHP - November 1, 2008 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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 PoteraEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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 alter...
Source: Science Selections from EHP - November 1, 2008 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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 WashamEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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 e...
Source: Science Selections from EHP - November 1, 2008 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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. BrownEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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 li...
Source: Science Selections from EHP - October 1, 2008 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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. TaylorEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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 li...
Source: Science Selections from EHP - October 1, 2008 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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 WashamEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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 ...
Source: Science Selections from EHP - October 1, 2008 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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 |Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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...
Source: Science Selections from EHP - September 1, 2008 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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 PoteraEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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 ...
Source: Science Selections from EHP - September 1, 2008 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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 PoteraEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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...
Source: Science Selections from EHP - September 1, 2008 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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 WashamEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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 i...
Source: Science Selections from EHP - September 1, 2008 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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 TillettEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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 an...
Source: Science Selections from EHP - August 1, 2008 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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 SpiveyEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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...
Source: Science Selections from EHP - August 1, 2008 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals

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 MeadEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
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...
Source: Science Selections from EHP - August 1, 2008 Category: Environmental Health Authors: webmaster at ehp.niehs.nih.gov Source Type: journals