Evaluation of the cardiovascular effects of methylmercury exposures: current evidence supports development of a dose-response function for regulatory benefits analysis

Background

The U.S. Environmental Protection Agency (U.S. EPA) has estimated the neurological benefits of reductions in prenatal methylmercury (MeHg) exposure in past assessments of rules controlling mercury (Hg) emissions. A growing body of evidence suggests that MeHg exposure can also lead to increased risks of adverse cardiovascular impacts in exposed populations.

Data extraction

The U.S. EPA assembled the authors of this article to participate in a workshop, where we reviewed the current science concerning cardiovascular health effects of MeHg exposure via fish and seafood consumption and provided recommendations concerning whether cardiovascular health effects should be included in future Hg regulatory impact analyses.

Data synthesis

We found the body of evidence exploring the link between MeHg and acute myocardial infarction (MI) to be sufficiently strong to support its inclusion in future benefits analyses, based both on direct epidemiological evidence of an MeHg–MI link and on MeHg’s association with intermediary impacts that contribute to MI risk. Although additional research in this area would be beneficial to further clarify key characteristics of this relationship and the biological mechanisms that underlie it, we consider the current epidemiological literature sufficiently robust to support the development of a dose–response function.

Conclusions

We recommend the development of a dose–response function relating MeHg exposures with MIs for use in regulatory benefits analyses of future rules targeting Hg air emissions.     

Ten Years of Addressing Children’s Health through Regulatory Policy at the U.S. Environmental Protection Agency

Background

Executive Order (EO) 13045, Protection of Children From Environmental Health Risks and Safety Risks, directs each federal agency to ensure that its policies, programs, activities, and standards address disproportionate environmental health and safety risks to children.

Objectives

We reviewed regulatory actions published by U.S. Environmental Protection Agency (EPA) in the Federal Register from April 1998 through December 2006 to evaluate applicability of EO 13045 to U.S. EPA actions and consideration of children’s health issues in U.S. EPA rulemakings.

Discussion

Although virtually all actions discussed EO 13045, fewer than two regulations per year, on average, were subject to the EO requirement to evaluate children’s environmental health risks. Nonetheless, U.S. EPA considered children’s environmental health in all actions addressing health or safety risks that may disproportionately affect children.

Conclusion

The EO does not apply to a broad enough set of regulatory actions to ensure protection of children’s health and safety risks, largely because of the small number of rules that are economically significant. However, given the large number of regulations that consider children’s health issues despite not being subject to the EO, other statutory requirements and agency policies reach a larger set of regulations to ensure protection of children’s environmental health.     

Lead exposures in U.S. Children, 2008: implications for prevention

Objective

We reviewed the sources of lead in the environments of U.S. children, contributions to children’s blood lead levels, source elimination and control efforts, and existing federal authorities. Our context is the U.S. public health goal to eliminate pediatric elevated blood lead levels (EBLs) by 2010.

Data sources

National, state, and local exposure assessments over the past half century have identified risk factors for EBLs among U.S. children, including age, race, income, age and location of housing, parental occupation, and season.

Data extraction and synthesis

Recent national policies have greatly reduced lead exposure among U.S. children, but even very low exposure levels compromise children’s later intellectual development and lifetime achievement. No threshold for these effects has been demonstrated. Although lead paint and dust may still account for up to 70% of EBLs in U.S. children, the U.S. Centers for Disease Control and Prevention estimates that ≥30% of current EBLs do not have an immediate lead paint source, and numerous studies indicate that lead exposures result from multiple sources. EBLs and even deaths have been associated with inadequately controlled sources including ethnic remedies and goods, consumer products, and food-related items such as ceramics. Lead in public drinking water and in older urban centers remain exposure sources in many areas.

Conclusions

Achieving the 2010 goal requires maintaining current efforts, especially programs addressing lead paint, while developing interventions that prevent exposure before children are poisoned. It also requires active collaboration across all levels of government to identify and control all potential sources of lead exposure, as well as primary prevention.     

Sources of Mercury Exposure for U.S. Seafood Consumers: Implications for Policy

Background

Recent policies attempting to reduce adverse effects of methylmercury exposure from fish consumption in the United States have targeted reductions in anthropogenic emissions from U.S. sources.

Objectives

To analyze the prospects for future North American and international emissions controls, we assessed the potential contributions of anthropogenic, historical, and natural mercury to exposure trajectories in the U.S. population over a 40-year time horizon.

Methods

We used models that simulate global atmospheric chemistry (GEOS-Chem); the fate, transport, and bioaccumulation of mercury in four types of freshwater ecosystems; and mercury cycling among different ocean basins. We considered effects on mercury exposures in the U.S. population based on dietary survey information and consumption data from the sale of commercial market fish.

Results

Although North American emissions controls may reduce mercury exposure by up to 50% for certain highly exposed groups such as indigenous peoples in the Northeast, the potential effects of emissions controls on populations consuming marine fish from the commercial market are less certain because of limited measurements.

Conclusions

Despite uncertainties in the exposure pathway, results indicate that a combination of North American and international emissions controls with adaptation strategies is necessary to manage methylmercury risks across various demographic groups in the United States.     

A Framework for Widespread Replication of a Highly Spatially Resolved Childhood Lead Exposure Risk Model

Background

Preventive approaches to childhood lead poisoning are critical for addressing this longstanding environmental health concern. Moreover, increasing evidence of cognitive effects of blood lead levels < 10 μg/dL highlights the need for improved exposure prevention interventions.

Objectives

Geographic information system–based childhood lead exposure risk models, especially if executed at highly resolved spatial scales, can help identify children most at risk of lead exposure, as well as prioritize and direct housing and health-protective intervention programs. However, developing highly resolved spatial data requires labor-and time-intensive geocoding and analytical processes. In this study we evaluated the benefit of increased effort spent geocoding in terms of improved performance of lead exposure risk models.

Methods

We constructed three childhood lead exposure risk models based on established methods but using different levels of geocoded data from blood lead surveillance, county tax assessors, and the 2000 U.S. Census for 18 counties in North Carolina. We used the results to predict lead exposure risk levels mapped at the individual tax parcel unit.

Results

The models performed well enough to identify high-risk areas for targeted intervention, even with a relatively low level of effort on geocoding.

Conclusions

This study demonstrates the feasibility of widespread replication of highly spatially resolved childhood lead exposure risk models. The models guide resource-constrained local health and housing departments and community-based organizations on how best to expend their efforts in preventing and mitigating lead exposure risk in their communities.     

Evaluating and regulating lead in synthetic turf

Background

In 2007, a synthetic turf recreational field in Newark, New Jersey, was closed because lead was found in synthetic turf fibers and in surface dust at concentrations exceeding hazard criteria. Consequently, public health professionals across the country began testing synthetic turf to determine whether it represented a lead hazard. Currently, no standardized methods exist to test for lead in synthetic turf or to assess lead hazards.

Objectives

Our objectives were to increase awareness of potential lead exposure from synthetic turf by presenting data showing elevated lead in fibers and turf-derived dust; identify risk assessment uncertainties; recommend that federal and/or state agencies determine appropriate methodologies for assessing lead in synthetic turf; and recommend an interim standardized approach for sampling, interpreting results, and taking health-protective actions.

Discussion

Data collected from recreational fields and child care centers indicate lead in synthetic turf fibers and dust at concentrations exceeding the Consumer Product Safety Improvement Act of 2008 statutory lead limit of 300 mg/kg for consumer products intended for use by children, and the U.S. Environmental Protection Agency’s lead-dust hazard standard of 40 μg/ft² for floors.

Conclusions

Synthetic turf can deteriorate to form dust containing lead at levels that may pose a risk to children. Given elevated lead levels in turf and dust on recreational fields and in child care settings, it is imperative that a consistent, nationwide approach for sampling, assessment, and action be developed. In the absence of a standardized approach, we offer an interim approach to assess potential lead hazards when evaluating synthetic turf.     

Childhood Lead Exposure After the Phaseout of Leaded Gasoline: An Ecological Study of School-Age Children in Kampala,Uganda

Background

Tetraethyl lead was phased out of gasoline in Uganda in 2005. Recent mitigation of an important source of lead exposure suggests examination and re-evaluation of the prevalence of childhood lead poisoning in this country. Ongoing concerns persist about exposure from the Kiteezi landfill in Kampala, the country’s capital.

Objectives

We determined blood lead distributions among Kampala schoolchildren and identified risk factors for elevated blood lead levels (EBLLs; ≥ 10 μg/dL).

Analytical approach

Using a stratified, cross-sectional design, we obtained blood samples, questionnaire data, and soil and dust samples from the homes and schools of 163 4- to 8-year-old children representing communities with different risks of exposure.

Results

The mean blood lead level (BLL) was 7.15 μg/dL; 20.5% of the children were found to have EBLL. Multivariable analysis found participants whose families owned fewer household items, ate canned food, or used the community water supply as their primary water source to have higher BLLs and likelihood of EBLLs. Distance < 0.5 mi from the landfill was the factor most strongly associated with increments in BLL (5.51 μg/dL, p < 0.0001) and likelihood of EBLL (OR = 4.71, p = 0.0093). Dust/soil lead was not significantly predictive of BLL/EBLL.

Conclusions

Lead poisoning remains highly prevalent among school-age children in Kampala. Confirmatory studies are needed, but further efforts are indicated to limit lead exposure from the landfill, whether through water contamination or through another mechanism. Although African nations are to be lauded for the removal of lead from gasoline, this study serves as a reminder that other sources of exposure to this potent neurotoxicant merit ongoing attention.     

Comparative Analysis of State Fish Consumption Advisories Targeting Sensitive Populations

Objective

Fish consumption advisories are issued to warn the public of possible toxicological threats from consuming certain fish species. Although developing fetuses and children are particularly susceptible to toxicants in fish, fish also contain valuable nutrients. Hence, formulating advice for sensitive populations poses challenges. We conducted a comparative analysis of advisory Web sites issued by states to assess health messages that sensitive populations might access.

Data sources

We evaluated state advisories accessed via the National Listing of Fish Advisories issued by the U.S. Environmental Protection Agency.

Data extraction

We created criteria to evaluate advisory attributes such as risk and benefit message clarity.

Data synthesis

All 48 state advisories issued at the time of this analysis targeted children, 90% (43) targeted pregnant women, and 58% (28) targeted women of childbearing age. Only six advisories addressed single contaminants, while the remainder based advice on 2–12 contaminants. Results revealed that advisories associated a dozen contaminants with specific adverse health effects. Beneficial health effects of any kind were specifically associated only with omega-3 fatty acids found in fish.

Conclusions

These findings highlight the complexity of assessing and communicating information about multiple contaminant exposure from fish consumption. Communication regarding potential health benefits conferred by specific fish nutrients was minimal and focused primarily on omega-3 fatty acids. This overview suggests some lessons learned and highlights a lack of both clarity and consistency in providing the breadth of information that sensitive populations such as pregnant women need to make public health decisions about fish consumption during pregnancy.     

Blood Pressure Changes in Relation to Arsenic Exposure in a U.S. Pregnancy Cohort

Background

Inorganic arsenic exposure has been related to the risk of increased blood pressure based largely on cross-sectional studies conducted in highly exposed populations. Pregnancy is a period of particular vulnerability to environmental insults. However, little is known about the cardiovascular impacts of arsenic exposure during pregnancy.

Objectives

We evaluated the association between prenatal arsenic exposure and maternal blood pressure over the course of pregnancy in a U.S. population.

Methods

The New Hampshire Birth Cohort Study is an ongoing prospective cohort study in which > 10% of participant household wells exceed the arsenic maximum contaminant level of 10 μg/L established by the U.S. EPA. Total urinary arsenic measured at 24–28 weeks gestation was measured and used as a biomarker of exposure during pregnancy in 514 pregnant women, 18–45 years of age, who used a private well in their household. Outcomes were repeated blood pressure measurements (systolic, diastolic, and pulse pressure) recorded during pregnancy.

Results

Using linear mixed effects models, we estimated that, on average, each 5-μg/L increase in urinary arsenic was associated with a 0.15-mmHg (95% CI: 0.02, 0.29; p = 0.022) increase in systolic blood pressure per month and a 0.14-mmHg (95% CI: 0.02, 0.25; p = 0.021) increase in pulse pressure per month over the course of pregnancy.

Conclusions

In our U.S. cohort of pregnant women, arsenic exposure was associated with greater increases in blood pressure over the course of pregnancy. These findings may have important implications because even modest increases in blood pressure impact cardiovascular disease risk.

Citation

Farzan SF, Chen Y, Wu F, Jiang J, Liu M, Baker E, Korrick SA, Karagas MR. 2015. Blood pressure changes in relation to arsenic exposure in a U.S. pregnancy cohort. Environ Health Perspect 123:999–1006; http://dx.doi.org/10.1289/ehp.1408472     

Exposure of the U.S. Population to Acrylamide in the National Health and Nutrition Examination Survey 2003–2004

Background

The lifelong exposure of the population to acrylamide has raised concerns about the possible health effects of the chemical. Data on the extent of exposure to acrylamide and its primary metabolite, glycidamide, are needed to aid in the assessment of potential health effects.

Objectives

The aim of this study was to assess human exposure to acrylamide and glycidamide in the general U.S. population through the measurement of hemoglobin adducts of acrylamide (HbAA) and glycidamide (HbGA).

Methods

HbAA and HbGA were measured in 7,166 subjects from the National Health and Nutrition Examination Survey. Stratified HbAA and HbGA data were reported by sex, age groups, race/ethnicity (Mexican American, non-Hispanic black, non-Hispanic white), and smoking status based on serum cotinine levels. Covariate-adjusted geometric means for each demographic group were calculated using multiple regression analysis.

Results

HbAA and HbGA levels ranged from 3 to 910 and from 4 to 756 pmol/g hemoglobin, respectively, with smokers having the highest levels overall. Tobacco smoke exposure in nonsmokers had a small but significant effect on HbAA and HbGA levels. Adjusted geometric mean levels for children 3–11 years of age were higher than for adults ≥ 60 years of age [mean (95% confidence interval): HbAA, 54.5 (49.1–51.5) and HbGA, 73.9 (71.3–76.6) vs. HbAA, 46.2 (44.3–48.2) and HbGA, 41.8 (38.7–45.2)]. Levels were highest in Mexican Americans [HbAA: 54.8 (51.9–57.8), HbGA: 57.9 (53.7–62.5)], whereas non-Hispanic blacks had the lowest HbGA levels [43.5 (41.1–45.9)].

Conclusions

U.S. population levels of acrylamide and glycidamide adducts are described. The high variability among individuals but modest differences between population subgroups suggest that sex, age, and race/ethnicity do not strongly affect acrylamide exposure. Adduct concentration data can be used to estimate relative exposure and to validate intake estimates.     

Biological Monitoring for Depleted Uranium Exposure in U.S. Veterans

Background

As part of an ongoing medical surveillance program for U.S. veterans exposed to depleted uranium (DU), biological monitoring of urine uranium (U) concentrations is offered to any veteran of the Gulf War and those serving in more recent conflicts (post-Gulf War veterans).

Objectives

Since a previous report of surveillance findings in 2004, an improved methodology for determination of the isotopic ratio of U in urine (²³⁵U:²³⁸U) has been developed and allows for more definitive evaluation of DU exposure. This report updates previous findings.

Methods

Veterans provide a 24-hr urine specimen and complete a DU exposure questionnaire. Specimens are sent to the Baltimore Veterans Affairs Medical Center for processing. Uranium concentration and isotopic ratio are measured using ICP-MS at the Armed Forces Institute of Pathology.

Results

Between January 2003 and June 2008, we received 1,769 urine specimens for U analysis. The mean urine U measure was 0.009 μg U/g creatinine. Mean urine U concentrations for Gulf War and post-Gulf War veterans were 0.008 and 0.009 μg U/g creatinine, respectively. Only 3 of the 1,700 (0.01%) specimens for which we completed isotopic determination showed evidence of DU. Exposure histories confirmed that these three individuals had been involved in “friendly fire” incidents involving DU munitions or armored vehicles.

Conclusions

No urine U measure with a “depleted” isotopic signature has been detected in U.S. veterans without a history of retained DU embedded fragments from previous injury. These findings suggest that future DU-related health harm is unlikely in veterans without DU fragments.     

Modification by ALAD of the Association between Blood Lead and Blood Pressure in the U.S. Population: Results from the Third National Health and Nutrition Examination Survey

Background

Environmental lead exposure has been found to be associated with an increased risk of hypertension. Individuals vary greatly in susceptibility to lead toxicity, and genetic susceptibility has often been cited as the probable cause for such variation.

Objective

The main objective is to determine the role of the aminolevulinic acid dehydratase (ALAD) gene, which encodes the main carrier protein of lead in blood, in the association between lead exposure and blood pressure (BP) and hypertension in the U.S. population.

Methods

We analyzed data from individuals ≥ 17 years of age who participated in the Third National Health and Nutrition Examination Survey for whom DNA was available (n = 6,016). Multivariable logistic and linear regressions stratified by race/ethnicity were used to examine whether hypertension and BP were associated with ALAD and blood lead levels (BLL).

Results

BLL was associated with systolic BP in non-Hispanic whites and with hypertension and systolic and diastolic BP in non-Hispanic blacks. BLL was not associated with BP outcomes in Mexican Americans. Non-Hispanic white ALAD2 carriers in the highest BLL quartile (3.8–52.9 μg/dL) had a significantly higher adjusted prevalence odds ratio for hypertension compared with ALAD1 homozygous individuals. We also found a significant interaction between lead concentration and the ALAD2 allele in non-Hispanic whites and non-Hispanic blacks in relation to systolic BP.

Conclusions

BLL may be an important risk factor for hypertension and increased systolic and diastolic BP. These associations may be modified by ALAD genotype.     

First Steps toward Harmonized Human Biomonitoring in Europe: Demonstration Project to Perform Human Biomonitoring on a European Scale

Background

For Europe as a whole, data on internal exposure to environmental chemicals do not yet exist. Characterization of the internal individual chemical environment is expected to enhance understanding of the environmental threats to health.

Objectives

We developed and applied a harmonized protocol to collect comparable human biomonitoring data all over Europe.

Methods

In 17 European countries, we measured mercury in hair and cotinine, phthalate metabolites, and cadmium in urine of 1,844 children (5–11 years of age) and their mothers. Specimens were collected over a 5-month period in 2011–2012. We obtained information on personal characteristics, environment, and lifestyle. We used the resulting database to compare concentrations of exposure biomarkers within Europe, to identify determinants of exposure, and to compare exposure biomarkers with health-based guidelines.

Results

Biomarker concentrations showed a wide variability in the European population. However, levels in children and mothers were highly correlated. Most biomarker concentrations were below the health-based guidance values.

Conclusions

We have taken the first steps to assess personal chemical exposures in Europe as a whole. Key success factors were the harmonized protocol development, intensive training and capacity building for field work, chemical analysis and communication, as well as stringent quality control programs for chemical and data analysis. Our project demonstrates the feasibility of a Europe-wide human biomonitoring framework to support the decision-making process of environmental measures to protect public health.

Citation

Den Hond E, Govarts E, Willems H, Smolders R, Casteleyn L, Kolossa-Gehring M, Schwedler G, Seiwert M, Fiddicke U, Castaño A, Esteban M, Angerer J, Koch HM, Schindler BK, Sepai O, Exley K, Bloemen L, Horvat M, Knudsen LE, Joas A, Joas R, Biot P, Aerts D, Koppen G, Katsonouri A, Hadjipanayis A, Krskova A, Maly M, Mørck TA, Rudnai P, Kozepesy S, Mulcahy M, Mannion R, Gutleb AC, Fischer ME, Ligocka D, Jakubowski M, Reis MF, Namorado S, Gurzau AE, Lupsa IR, Halzlova K, Jajcaj M, Mazej D, Snoj Tratnik J, López A, Lopez E, Berglund M, Larsson K, Lehmann A, Crettaz P, Schoeters G. 2015. First steps toward harmonized human biomonitoring in Europe: demonstration project to perform human biomonitoring on a European scale. Environ Health Perspect 123:255–263; http://dx.doi.org/10.1289/ehp.1408616     

Adult Women’s Blood Mercury Concentrations Vary Regionally in the United States: Association with Patterns of Fish Consumption (NHANES 1999–2004)

Background

The current, continuous National Health and Nutrition Examination Survey (NHANES) has included blood mercury (BHg) and fish/shellfish consumption since it began in 1999. NHANES 1999–2004 data form the basis for these analyses.

Objectives

This study was designed to determine BHg distributions within U.S. Census regions and within coastal and noncoastal areas among women of childbearing age, their association with patterns of fish consumption, and changes from 1999 through 2004.

Methods

We performed univariate and bivariate analyses to determine the distribution of BHg and fish consumption in the population and to investigate differences by geography, race/ethnicity, and income. We used multivariate analysis (regression) to determine the strongest predictors of BHg among geography, demographic factors, and fish consumption.

Results

Elevated BHg occurred more commonly among women of childbearing age living in coastal areas of the United States (approximately one in six women). Regionally, exposures differ across the United States: Northeast > South and West > Midwest. Asian women and women with higher income ate more fish and had higher BHg. Time-trend analyses identified reduced BHg and reduced intake of Hg in the upper percentiles without an overall reduction of fish consumption.

Conclusions

BHg is associated with income, ethnicity, residence (census region and coastal proximity). From 1999 through 2004, BHg decreased without a concomitant decrease in fish consumption. Data are consistent with a shift over this time period in fish species in women’s diets.     

Environmental Health Indicators of Climate Change for the United States: Findings from the State Environmental Health Indicator Collaborative

Objective

To develop public health adaptation strategies and to project the impacts of climate change on human health, indicators of vulnerability and preparedness along with accurate surveillance data on climate-sensitive health outcomes are needed. We researched and developed environmental health indicators for inputs into human health vulnerability assessments for climate change and to propose public health preventative actions.

Data sources

We conducted a review of the scientific literature to identify outcomes and actions that were related to climate change. Data sources included governmental and nongovernmental agencies and the published literature.

Data extraction

Sources were identified and assessed for completeness, usability, and accuracy. Priority was then given to identifying longitudinal data sets that were applicable at the state and community level.

Data synthesis

We present a list of surveillance indicators for practitioners and policy makers that include climate-sensitive health outcomes and environmental and vulnerability indicators, as well as mitigation, adaptation, and policy indicators of climate change.

Conclusions

A review of environmental health indicators for climate change shows that data exist for many of these measures, but more evaluation of their sensitivity and usefulness is needed. Further attention is necessary to increase data quality and availability and to develop new surveillance databases, especially for climate-sensitive morbidity.     

Dietary Intake Is Associated with Phthalate Body Burden in a Nationally Representative Sample

Background

Phthalates are compounds that are used in a wide range of consumer products. However, the contribution of dietary intake to phthalate exposure has not been well defined.

Objective

The objective of this study was to assess the contribution of different food types to phthalate exposure. Phthalates are chemicals of concern because of the high levels measured in people and the environment, as well as the demonstrated toxicity in animal studies and limited epidemiological studies. Previous research, although limited, has suggested that phthalates contaminate food in various countries.

Methods

We conducted an exploratory analysis of data collected as part of the 2003–2004 National Health and Nutrition Examination Survey (NHANES). Associations between dietary intake (assessed by a 24-hr dietary recall) for a range of food types (meat, poultry, fish, fruit, vegetable, and dairy) and phthalate metabolites measured in urine were analyzed using multiple linear regression modeling.

Results

We found that metabolites of di-(2-ethylhexyl) phthalate (DEHP) and high-molecular-weight phthalate metabolites were associated with the consumption of poultry. Monoethyl phthalate, the metabolite of diethyl phthalate (DEP), was associated with vegetable consumption, specifically tomato and potato consumption.

Discussion

These results, combined with results from previous studies, suggest that diet is an important route of intake for phthalates. Further research is needed to determine the sources of food contamination with these toxic chemicals and to describe the levels of contamination of U.S. food in a large, representative U.S. sample.     

Developmental neurotoxicants in e-waste: an emerging health concern

Objective

Electronic waste (e-waste) has been an emerging environmental health issue in both developed and developing countries, but its current management practice may result in unintended developmental neurotoxicity in vulnerable populations. To provide updated information about the scope of the issue, presence of known and suspected neurotoxicants, toxicologic mechanisms, and current data gaps, we conducted this literature review.

Data sources

We reviewed original articles and review papers in PubMed and Web of Science regarding e-waste toxicants and their potential developmental neurotoxicity. We also searched published reports of intergovernmental and governmental agencies and nongovernmental organizations on e-waste production and management practice.

Data extraction

We focused on the potential exposure to e-waste toxicants in vulnerable populations—that is, pregnant women and developing children—and neurodevelopmental outcomes. In addition, we summarize experimental evidence of developmental neurotoxicity and mechanisms.

Data synthesis

In developing countries where most informal and primitive e-waste recycling occurs, environmental exposure to lead, cadmium, chromium, polybrominated diphenyl ethers, polychlorinated biphenyls, and polycyclic aromatic hydrocarbons is prevalent at high concentrations in pregnant women and young children. Developmental neurotoxicity is a serious concern in these regions, but human studies of adverse effects and potential mechanisms are scarce. The unprecedented mixture of exposure to heavy metals and persistent organic pollutants warrants further studies and necessitates effective pollution control measures.

Conclusions

Pregnant women and young children living close to informal e-waste recycling sites are at risk of possible perturbations of fetus and child neurodevelopment.     

Impact of Environmental Chemicals on Lung Development

Background

Disruption of fundamental biologic processes and associated signaling events may result in clinically significant alterations in lung development.

Objectives

We reviewed evidence on the impact of environmental chemicals on lung development and key signaling events in lung morphogenesis, and the relevance of potential outcomes to public health and regulatory science.

Data sources

We evaluated the peer-reviewed literature on developmental lung biology and toxicology, mechanistic studies, and supporting epidemiology.

Data synthesis

Lung function in infancy predicts pulmonary function throughout life. In utero and early postnatal exposures influence both childhood and adult lung structure and function and may predispose individuals to chronic obstructive lung disease and other disorders. The nutritional and endogenous chemical environment affects development of the lung and can result in altered function in the adult. Studies now suggest that similar adverse impacts may occur in animals and humans after exposure to environmentally relevant doses of certain xenobiotics during critical windows in early life. Potential mechanisms include interference with highly conserved factors in developmental processes such as gene regulation, molecular signaling, and growth factors involved in branching morphogenesis and alveolarization.

Conclusions

Assessment of environmental chemical impacts on the lung requires studies that evaluate specific alterations in structure or function—end points not regularly assessed in standard toxicity tests. Identifying effects on important signaling events may inform protocols of developmental toxicology studies. Such knowledge may enable policies promoting true primary prevention of lung diseases. Evidence of relevant signaling disruption in the absence of adequate developmental toxicology data should influence the size of the uncertainty factors used in risk assessments.