Private drinking water wells as a source of exposure to perfluorooctanoic acid (PFOA) in communities surrounding a fluoropolymer production facility

Background

The C8 Health Project was established in 2005 to collect data on perfluorooctanoic acid (PFOA, or C8) and human health in Ohio and West Virginia communities contaminated by a fluoropolymer production facility.

Objective

We assessed PFOA exposure via contaminated drinking water in a subset of C8 Health Project participants who drank water from private wells.

Methods

Participants provided demographic information and residential, occupational, and medical histories. Laboratory analyses were conducted to determine serum-PFOA concentrations. PFOA data were collected from 2001 through 2005 from 62 private drinking water wells. We examined the relationship between drinking water and PFOA levels in serum using robust regression methods. As a comparison with regression models, we used a first-order, single-compartment pharmacokinetic model to estimate the serum:drinking-water concentration ratio at steady state.

Results

The median serum PFOA concentration in 108 study participants who used private wells was 75.7 μg/L, approximately 20 times greater than the levels in the U.S. general population but similar to those of local residents who drank public water. Each 1 μg/L increase in PFOA levels in drinking water was associated with an increase in serum concentrations of 141.5 μg/L (95% confidence interval, 134.9–148.1). The serum:drinking-water concentration ratio for the steady-state pharmacokinetic model was 114.

Conclusions

PFOA-contaminated drinking water is a significant contributor to PFOA levels in serum in the study population. Regression methods and pharmacokinetic modeling produced similar estimates of the relationship.     

Perfluorinated chemicals and fetal growth: a study within the Danish National Birth Cohort

Background

Perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) are man-made, persistent organic pollutants widely spread throughout the environment and human populations. They have been found to interfere with fetal growth in some animal models, but whether a similar effect is seen in humans is uncertain.

Objectives

We investigated the association between plasma levels of PFOS and PFOA in pregnant women and their infants’ birth weight and length of gestation.

Methods

We randomly selected 1,400 women and their infants from the Danish National Birth Cohort among those who completed all four computer-assisted telephone interviews, provided the first blood samples between gestational weeks 4 and 14, and who gave birth to a single live-born child without congenital malformation. PFOS and PFOA were measured by high performance liquid chromatography–tandem mass spectrometer.

Results

PFOS and PFOA levels in maternal plasma were on average 35.3 and 5.6 ng/mL, respectively. Only PFOA levels were inversely associated with birth weight (adjusted β = −10.63 g; 95% confidence interval, −20.79 to −0.47 g). Neither maternal PFOS nor PFOA levels were consistently associated with the risk for preterm birth or low birth weight. We observed no adverse effects for maternal PFOS or PFOA levels on small for gestational age.

Conclusion

Our nationwide cohort data suggest an inverse association between maternal plasma PFOA levels and birth weight. Because of widespread exposure to these chemicals, our findings may be of potential public health concern.     

Do Perfluoroalkyl Compounds Impair Human Semen Quality?

Background

Perfluoroalkyl acids (PFAAs) are found globally in wildlife and humans and are suspected to act as endocrine disruptors. There are no previous reports of PFAA levels in adult men from Denmark or of a possible association between semen quality and PFAA exposure.

Objectives

We investigated possible associations between PFAAs and testicular function. We hypothesized that higher PFAA levels would be associated with lower semen quality and lower testosterone levels.

Methods

We analyzed serum samples for levels of 10 different PFAAs and reproductive hormones and assessed semen quality in 105 Danish men from the general population (median age, 19 years).

Results

Considerable levels of perfluorooctane sulfonic acid (PFOS), perfluorooctanoic acid (PFOA), and perfluorohexane sulfonic acid were found in all young men (medians of 24.5, 4.9, and 6.6 ng/mL, respectively). Men with high combined levels of PFOS and PFOA had a median of 6.2 million normal spermatozoa in their ejaculate in contrast to 15.5 million among men with low PFOS–PFOA (p = 0.030). In addition, we found nonsignificant trends with regard to lower sperm concentration, lower total sperm counts, and altered pituitary–gonadal hormones among men with high PFOS–PFOA levels.

Conclusion

High PFAA levels were associated with fewer normal sperm. Thus, high levels of PFAAs may contribute to the otherwise unexplained low semen quality often seen in young men. However, our findings need to be corroborated in larger studies.     

Prenatal exposure to perfluorooctanoate (PFOA) and perfluorooctanesulfonate (PFOS) and maternally reported developmental milestones in infancy

Background

Perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) are fluorinated organic compounds present in the general population at low concentrations. Animal studies have shown that they may affect neuromuscular development at high concentrations.

Objectives

We investigated the association between plasma levels of PFOS and PFOA in pregnant women and motor and mental developmental milestones of their children.

Methods

We randomly selected 1,400 pairs of pregnant women and their children from the Danish National Birth Cohort. PFOS and PFOA were measured in maternal blood samples taken in early pregnancy. Apgar score was abstracted from the National Hospital Discharge Register in Denmark. Developmental milestones were reported by mothers using highly structured questionnaires when the children were around 6 months and 18 months of age.

Results

Mothers who had higher levels of PFOA and PFOS gave birth to children who had similar Apgar scores and reached virtually all of the development milestones at the same time as children born to mothers with lower exposure levels. Children who were born to mothers with higher PFOS levels were slightly more likely to start sitting without support at a later age.

Conclusion

We found no convincing associations between developmental milestones in early childhood and levels of PFOA or PFOS as measured in maternal plasma early in pregnancy.     

Predictors of PFOA Levels in a Community Surrounding a Chemical Plant

Background

Perfluorooctanoic acid (PFOA) is considered a probable human carcinogen by the U.S. Environmental Protection Agency. It does not exist in nature but has been used widely since World War II. It is present in the serum of most Americans at about 4–5 ng/mL, although the routes of exposure remain unknown.

Objectives

We examined predictors of PFOA in mid-Ohio Valley residents living near a chemical plant that until recently released large quantities of PFOA into the environment, contaminating drinking water.

Methods

We studied 69,030 residents in six contaminated water districts who participated in a 2005–2006 survey involving a questionnaire and blood tests. Of these, 64,251 had complete data on PFOA and covariates. We also analyzed a subset (71%) for whom we had occupational history. We ran linear regression models to determine serum PFOA predictors.

Results

Mean PFOA serum level was 83.0 ng/mL (median, 28.2). The most important predictors were current (median for all districts, 38.4; highest district, 224.1) and past (median, 18.6) residence in contaminated water districts, and current (median, 147.8) and past (median, 74.9) employment at the chemical plant (R² model = 0.55). PFOA was higher for males, those consuming local vegetables, and those using well water rather than public water, and lower for those using bottled water. PFOA was higher at younger and older ages.

Conclusions

PFOA levels in this population varied with distance of residence from the plant and employment at the plant. Effects of age and sex reflected prior findings. Effects of other demographic and lifestyle covariates were relatively weak.     

Accumulation and Clearance of Perfluorooctanoic Acid (PFOA) in Current and Former Residents of an Exposed Community

Background

Perfluorooctanoic acid (PFOA) is a perfluoroalkyl acid found in > 99% of Americans. Its health effects are unknown. Prior estimates of serum half-life range from 2.3 to 3.8 years.

Objectives

We assessed the impact of years of residence and years since residing in the study area on serum PFOA concentration in a sample of current and former residents who were exposed to PFOA emissions from an industrial facility in six water districts in West Virginia and Ohio.

Methods

Serum samples and questionnaires, including residential history, were collected in 2005–2006. We modeled log serum PFOA (nanograms per milliliter) for current residents as a function of years of residence in a water district, adjusted for a variety of factors. We modeled the half-life in former residents who lived in two water districts with high exposure levels using a two-segment log-linear spline.

Results

We modeled serum PFOA concentration in 17,516 current residents as a function of years of residence (R² = 0.68). Years of residence was significantly associated with PFOA concentration (1% increase in serum PFOA/year of residence), with significant heterogeneity by water district. Half-life was estimated in two water districts comprising a total of 1,573 individuals. For the participants included in our analyses, we found that years since residing in a water district was significantly associated with serum PFOA, which yielded half-lives of 2.9 and 8.5 years for water districts with higher and lower exposure levels, respectively.

Conclusion

Years of residence in an exposed water district is positively associated with observed serum PFOA in 2005–2006. Differences in serum clearance rate between low- and high-exposure water districts suggest a possible concentration-dependent or time-dependent clearance process or inadequate adjustment for background exposures.     

Correlations between Prenatal Exposure to Perfluorinated Chemicals and Reduced Fetal Growth

Background

Perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA) are man-made, ubiquitous, and persistent contaminants in the environment, wildlife, and humans. Although recent studies have shown that these chemicals interfere with fetal growth in humans, the results are inconsistent.

Objectives

Our goal was to investigate the correlation between relatively low levels of PFOS and PFOA in maternal serum and birth weight and birth size.

Methods

We conducted a hospital-based prospective cohort study between July 2002 and October 2005 in Sapporo, Japan. A total of 428 women and their infants were involved in the study. We obtained characteristics of the mothers and infants from self-administered questionnaire surveys and from medical records. We analyzed maternal serum samples for PFOS and PFOA by liquid chromatography–tandem mass spectrometry (LC/MS/MS).

Results

After adjusting for confounding factors, PFOS levels negatively correlated with birth weight [per log₁₀ unit: β = −148.8 g; 95% confidence interval (CI), −297.0 to −0.5 g]. In addition, analyses stratified by sex revealed that PFOS levels negatively correlated with birth weight only in female infants (per log₁₀ unit: β = −269.4 g; 95% CI, −465.7 to −73.0 g). However, we observed no correlation between PFOA levels and birth weight.

Conclusion

Our results indicate that in utero exposure to relatively low levels of PFOS was negatively correlated with birth weight.     

Structure-Activity–Dependent Regulation of Cell Communication by Perfluorinated Fatty Acids using in Vivo and in Vitro Model Systems

Background

Perfluoroalkanoates, [e.g., perfluorooctanoate (PFOA)], are known peroxisome proliferators that induce hepatomegaly and hepatocarcinogenesis in rodents, and are classic non-genotoxic carcinogens that inhibit in vitro gap-junctional intercellular communication (GJIC). This inhibition of GJIC is known to be a function of perfluorinated carbon lengths ranging from 7 to 10.

Objectives

The aim of this study was to determine if the inhibition of GJIC by PFOA but not perfluoropentanoate (PFPeA) observed in F344 rat liver cells in vitro also occurs in F344 rats in vivo and to determine mechanisms of PFOA dysregulation of GJIC using in vitro assay systems.

Methods

We used an incision load/dye transfer technique to assess GJIC in livers of rats exposed to PFOA and PFPeA. We used in vitro assays with inhibitors of cell signaling enzymes and antioxidants known to regulate GJIC to identify which enzymes regulated PFOA-induced inhibition of GJIC.

Results

PFOA inhibited GJIC and induced hepatomegaly in rat livers, whereas PFPeA had no effect on either end point. Serum biochemistry of liver enzymes indicated no cytotoxic response to these compounds. In vitro analysis of mitogen-activated protein kinase (MAPK) indicated that PFOA, but not PFPeA, can activate the extracellular receptor kinase (ERK). Inhibition of GJIC, in vitro, by PFOA depended on the activation of both ERK and phosphatidylcholine-specific phospholipase C (PC-PLC) in the dysregulation of GJIC in an oxidative-dependent mechanism.

Conclusions

The in vitro analysis of GJIC, an epigenetic marker of tumor promoters, can also predict the in vivo activity of PFOA, which dysregulated GJIC via ERK and PC-PLC.     

Prenatal exposure to perfluorinated chemicals and behavioral or coordination problems at age 7 years

Objective

Potential neurotoxic effects of perfluorinated compounds (PFCs) have been reported in highly exposed animals, but whether these chemicals are neurotoxic in humans is not known. We therefore investigated whether prenatal exposure to perfluorooctanoic acid (PFOA) or perfluorooctane sulfate (PFOS), two of the most prevalent PFCs, are associated with behavioral or coordination problems in early childhood.

Methods

We used data from the Danish National Birth Cohort, which enrolled mothers in early pregnancy, and we measured maternal blood levels of PFOA and PFOS using specimens drawn around 8 weeks of gestation. When the children reached 7 years of age, mothers completed the Strengths and Difficulties Questionnaire (SDQ, n = 787) and the Developmental Coordination Disorder Questionnaire (DCDQ, n = 526) to assess behavioral health and motor coordination of their children. SDQ scores above the 90th percentile were a priori defined to identify behavioral problems and DCDQ scores below the 10th percentile were defined as a potential DCD.

Results

The median concentrations of PFOS and PFOA in maternal blood were 34.4 ng/mL [interquartile range (IQR), 26.6–44.5] and 5.4 ng/mL (IQR, 4.0–7.1), respectively, similar to distributions reported for populations without occupational exposure. We found no association between higher SDQ scores and maternal levels of PFOS or PFOA, nor did we see any statistically significant association with motor coordination disorders.

Conclusion

The findings suggest that background levels of PFOA and PFOS are not associated with behavioral and motor coordination problems in childhood. However, effects on other developmental end points, including cognitive, attentional, and clinical mental disorders not measured in this study, cannot be ruled out.     

Exposure to Polyfluoroalkyl Chemicals and Cholesterol,Body Weight,and Insulin Resistance in the General U.S. Population

Background

Polyfluoroalkyl chemicals (PFCs) are used commonly in commercial applications and are detected in humans and the environment worldwide. Concern has been raised that they may disrupt lipid and weight regulation.

Objectives

We investigated the relationship between PFC serum concentrations and lipid and weight outcomes in a large publicly available data set.

Methods

We analyzed data from the 2003–2004 National Health and Nutrition Examination Survey (NHANES) for participants 12–80 years of age. Using linear regression to control for covariates, we studied the association between serum concentrations of perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA), perfluorooctane sulfonic acid (PFOS), and perfluorohexane sulfonic acid (PFHxS) and measures of cholesterol, body size, and insulin resistance.

Results

We observed a positive association between concentrations of PFOS, PFOA, and PFNA and total and non-high-density cholesterol. We found the opposite for PFHxS. Those in the highest quartile of PFOS exposure had total cholesterol levels 13.4 mg/dL [95% confidence interval (CI), 3.8–23.0] higher than those in the lowest quartile. For PFOA, PFNA, and PFHxS, effect estimates were 9.8 (95% CI, −0.2 to 19.7), 13.9 (95% CI, 1.9–25.9), and −7.0 (95% CI, −13.2 to −0.8), respectively. A similar pattern emerged when exposures were modeled continuously. We saw little evidence of a consistent association with body size or insulin resistance.

Conclusions

This exploratory cross-sectional study is consistent with other epidemiologic studies in finding a positive association between PFOS and PFOA and cholesterol, despite much lower exposures in NHANES. Results for PFNA and PFHxS are novel, emphasizing the need to study PFCs other than PFOS and PFOA.     

Exploring indirect sources of human exposure to perfluoroalkyl carboxylates (PFCAs): evaluating uptake, elimination, and biotransformation of polyfluoroalkyl phosphate esters (PAPs) in the rat

Background

Perfluorinated carboxylic acids (PFCAs) are ubiquitous in human sera worldwide. Biotransformation of the polyfluoroalkyl phosphate esters (PAPs) is a possible source of PFCA exposure, because PAPs are used in food-contact paper packaging and have been observed in human sera.

Objectives

We determined pharmacokinetic parameters for the PAP monoesters (monoPAPs) and PAP diesters (diPAPs), as well as biotransformation yields to the PFCAs, using a rat model.

Methods

The animals were dosed intravenously or by oral gavage with a mixture of 4:2, 6:2, 8:2, and 10:2 monoPAP or diPAP chain lengths. Concentrations of the PAPs and PFCAs, as well as metabolic intermediates and phase II metabolites, were monitored over time in blood, urine, and feces.

Results

The diPAPs were bioavailable, with bioavailability decreasing as the chain length increased from 4 to 10 perfluorinated carbons. The monoPAPs were not absorbed from the gut; however, we found evidence to suggest phosphate-ester cleavage within the gut contents. We observed biotransformation to the PFCAs for both monoPAP and diPAP congeners.

Conclusions

Using experimentally derived biotransformation yields, perfluorooctanoic acid (PFOA) sera concentrations were predicted from the biotransformation of 8:2 diPAP at concentrations observed in human serum. Because of the long human serum half-life of PFOA, biotransformation of diPAP even with low-level exposure could over time result in significant exposure to PFOA. Although humans are exposed directly to PFCAs in food and dust, the pharmacokinetic parameters determined here suggest that PAP exposure should be considered a significant indirect source of human PFCA contamination.     

Association of Perfluorooctanoic Acid (PFOA) and Perfluorooctane Sulfonate (PFOS) with Uric Acid among Adults with Elevated Community Exposure to PFOA

Background

Perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) are compounds that do not occur in nature, have been widely used since World War II, and persist indefinitely in most environments. Median serum levels in the United States are 4 ng/mL for PFOA and 21 ng/mL for PFOS. PFOA has been associated with elevated uric acid in two studies of chemical workers. Uric acid is a risk factor for hypertension and possibly other cardiovascular outcomes.

Methods

We conducted a cross-sectional study of PFOA and PFOS and uric acid among 54,951 adult community residents in Ohio and West Virginia, who lived or worked in six water districts contaminated with PFOA from a chemical plant. Analyses were conducted by linear and logistic regression, adjusted for confounders.

Results

Both PFOA and PFOS were significantly associated with uric acid. An increase of 0.2–0.3 mg/dL uric acid was associated with an increase from the lowest to highest decile of either PFOA or PFOS. Hyperuricemia risk increased modestly with increasing PFOA; the odds ratios by quintile of PFOA were 1.00, 1.33 [95% confidence interval (CI), 1.24–1.43], 1.35 (95% CI, 1.26–1.45), 1.47 (95% CI, 1.37–1.58), and 1.47 (95% CI, 1.37–1.58; test for trend, p < 0.0001). We saw a less steep trend for PFOS. Inclusion of both correlated fluorocarbons in the model indicated PFOA was a more important predictor than was PFOS.

Conclusion

Higher serum levels of PFOA were associated with a higher prevalence of hyperuricemia, but the limitations of cross-sectional data and the possibility of noncausal mechanisms prohibit conclusions regarding causality.     

Rate of Decline in Serum PFOA Concentrations after Granular Activated Carbon Filtration at Two Public Water Systems in Ohio and West Virginia

Background

Drinking water in multiple water districts in the Mid-Ohio Valley has been contaminated with perfluorooctanoic acid (PFOA), which was released by a nearby DuPont chemical plant. Two highly contaminated water districts began granular activated carbon filtration in 2007.

Objectives

To determine the rate of decline in serum PFOA, and its corresponding half-life, during the first year after filtration.

Methods

Up to six blood samples were collected from each of 200 participants from May 2007 until August 2008. The primary source of drinking water varied over time for some participants; our analyses were grouped according to water source at baseline in May–June 2007.

Results

For Lubeck Public Service District customers, the average decrease in serum PFOA concentrations between May–June 2007 and May–August 2008 was 32 ng/mL (26%) for those primarily consuming public water at home (n = 130), and 16 ng/mL (28%) for those primarily consuming bottled water at home (n = 17). For Little Hocking Water Association customers, the average decrease in serum PFOA concentrations between November–December 2007 and May–June 2008 was 39 ng/mL (11%) for consumers of public water (n = 39) and 28 ng/mL (20%) for consumers of bottled water (n = 11). The covariate-adjusted average rate of decrease in serum PFOA concentration after water filtration was 26% per year (95% confidence interval, 25–28% per year).

Conclusions

The observed data are consistent with first-order elimination and a median serum PFOA half-life of 2.3 years. Ongoing follow-up will lead to improved half-life estimation.     

Epidemiologic Evidence on the Health Effects of Perfluorooctanoic Acid (PFOA)

Objective and sources

We reviewed the epidemiologic literature for PFOA.

Data synthesis

Perfluorooctanoic acid (PFOA) does not occur naturally but is present in the serum of most residents of industrialized countries (U.S. median, 4 ng/mL). Drinking water is the primary route of exposure in some populations, but exposure sources are not well understood. PFOA has been used to manufacture such products as Gore-Tex and Teflon. PFOA does not break down in the environment; the human half-life is estimated at about 3 years. PFOA is not metabolized in the body; it is not lipophilic. PFOA is not directly genotoxic; animal data indicate that it can cause several types of tumors and neonatal death and may have toxic effects on the immune, liver, and endocrine systems. Data on the human health effects of PFOA are sparse. There is relatively consistent evidence of modest positive associations with cholesterol and uric acid, although the magnitude of the cholesterol effect is inconsistent across different exposure levels. There is some but much less consistent evidence of a modest positive correlation with liver enzymes. Most findings come from cross-sectional studies, limiting conclusions. Two occupational cohort studies do not provide consistent evidence for chronic disease; both are limited by sample size and reliance on mortality data. Reproductive data have increased recently but are inconsistent, and any observed adverse effects are modest.

Conclusions

Epidemiologic evidence remains limited, and to date data are insufficient to draw firm conclusions regarding the role of PFOA for any of the diseases of concern.     

A Review of Advocate–Scientist Collaboration in Federally Funded Environmental Breast Cancer Research Centers

Background

The Long Island Breast Cancer Study Project was the first federally funded study of environmental causes of breast cancer. Although advocates were expected to participate in this study, the details of their participation were not adequately clarified in project guidelines, which resulted in confusion over their role in the project. The Breast Cancer and Environment Research Centers (BCERCs) are funded by the National Institute of Environmental Health Sciences and the National Cancer Institute; these centers continue to conduct research into environmental links to breast cancer and to clarify advocate–scientist guidelines for collaboration.

Objectives

Practitioners in community-based participatory research (CBPR) are grappling with how to improve CBPR projects for all groups involved in breast cancer and environmental studies. The ever-growing body of literature on CBPR elaborates on a number of factors that make CBPR particularly challenging, specifically regarding partnerships between advocate and scientific communities. This study draws on CBPR principles to evaluate advocate–scientist collaboration in the BCERCs.

Methods

We conducted surveys at BCERC annual meetings in 2005 and 2007 and 11 in-depth open-ended interviews with key stakeholders such as primary investigators within the centers to assess the perceptions of the advocates and scientists regarding collaboration between advocates and scientists who were engaged in CBPR studies.

Results

We found that although participatory guidelines were a focus of BCERCs, underlying differences between advocates and scientists with regard to paradigms of scientific inquiry, priorities, and desired outcomes need to be addressed for more effective collaboration to take place.

Conclusion

Our findings contribute to the broader CBPR literature by highlighting the role of underlying assumptions that may hinder the collaborative process and suggest the need for continued assessment research into participatory research projects on breast cancer and the environment.     

Ethical Issues in Measuring Biomarkers in Children’s Environmental Health

Background

Studying the impact of environmental exposures is important in children because they are more vulnerable to adverse effects on growth, development, and health. Assessing exposure in children is difficult, and measuring biomarkers is potentially useful. Research measuring biomarkers in children raises a number of ethical issues, some of which relate to children as research subjects and some of which are specific to biomarker research.

Objective

As an international group with experience in pediatric research, biomarkers, and the ethics of research in children, we highlight the ethical issues of undertaking biomarker research in children in these environments.

Discussion

Significant issues include undertaking research in vulnerable communities, especially in developing countries; managing community expectations; obtaining appropriate consent to conduct the research; the potential conflicts of obtaining permission from an ethics review board in an economically developed country to perform research in a community that may have different cultural values; returning research results to participants and communities when the researchers are uncertain of how to interpret the results; and the conflicting ethical obligations of maintaining participant confidentiality when information about harm or illegal activities mandate reporting to authorities.

Conclusion

None of these challenges are insurmountable and all deserve discussion. Pediatric biomarker research is necessary for advancing child health.     

Attention Deficit/Hyperactivity Disorder and Childhood Autism in Association with Prenatal Exposure to Perfluoroalkyl Substances: A Nested Case–Control Study in the Danish National Birth Cohort

Background:

Perfluoroalkyl substances (PFASs) are persistent pollutants found to be endocrine disruptive and neurotoxic in animals. Positive correlations between PFASs and neurobehavioral problems in children were reported in cross-sectional data, but findings from prospective studies are limited.

Objectives:

We investigated whether prenatal exposure to PFASs is associated with attention deficit/hyperactivity disorder (ADHD) or childhood autism in children.

Methods:

Among 83,389 mother–child pairs enrolled in the Danish National Birth Cohort during 1996–2002, we identified 890 ADHD cases and 301 childhood autism cases from the Danish National Hospital Registry and the Danish Psychiatric Central Registry. From this cohort, we randomly selected 220 cases each of ADHD and autism, and we also randomly selected 550 controls frequency matched by child’s sex. Sixteen PFASs were measured in maternal plasma collected in early or mid-pregnancy. We calculated risk ratios (RRs) using generalized linear models, taking into account sampling weights.

Results:

Perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) were detected in all samples; four other PFASs were quantified in ≥ 90% of the samples. We did not find consistent evidence of associations between mother’s PFAS plasma levels and ADHD [per natural log nanograms per milliliter increase: PFOS RR = 0.87 (95% CI: 0.74, 1.02); PFOA RR = 0.98 (95% CI: 0.82, 1.16)] or autism [per natural log nanograms per milliliter increase: PFOS RR = 0.92 (95% CI: 0.69, 1.22); PFOA RR = 0.98 (95% CI: 0.73, 1.31)]. We found positive as well as negative associations between higher PFAS quartiles and ADHD in models that simultaneously adjusted for all PFASs, but these estimates were imprecise.

Conclusions:

In this study we found no consistent evidence to suggest that prenatal PFAS exposure increases the risk of ADHD or childhood autism in children.

Citation:

Liew Z, Ritz B, von Ehrenstein OS, Bech BH, Nohr EA, Fei CY, Bossi R, Henriksen TB, Bonefeld-Jørgensen EC, Olsen J. 2015. Attention deficit/hyperactivity disorder and childhood autism in association with prenatal exposure to perfluoroalkyl substances: a nested case–control study in the Danish National Birth Cohort. Environ Health Perspect 123:367–373; http://dx.doi.org/10.1289/ehp.1408412     

Exposure to Polyfluoroalkyl Chemicals and Attention Deficit/Hyperactivity Disorder in U.S. Children 12–15 Years of Age

Background

Polyfluoroalkyl chemicals (PFCs) have been widely used in consumer products. Exposures in the United States and in world populations are widespread. PFC exposures have been linked to various health impacts, and data in animals suggest that PFCs may be potential developmental neurotoxicants.

Objectives

We evaluated the associations between exposures to four PFCs and parental report of diagnosis of attention deficit/hyperactivity disorder (ADHD).

Methods

Data were obtained from the National Health and Nutrition Examination Survey (NHANES) 1999–2000 and 2003–2004 for children 12–15 years of age. Parental report of a previous diagnosis by a doctor or health care professional of ADHD in the child was the primary outcome measure. Perfluorooctane sulfonic acid (PFOS), perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA), and perfluorohexane sulfonic acid (PFHxS) levels were measured in serum samples from each child.

Results

Parents reported that 48 of 571 children included in the analysis had been diagnosed with ADHD. The adjusted odds ratio (OR) for parentally reported ADHD in association with a 1-μg/L increase in serum PFOS (modeled as a continuous predictor) was 1.03 [95% confidence interval (CI), 1.01–1.05]. Adjusted ORs for 1-μg/L increases in PFOA and PFHxS were also statistically significant (PFOA: OR = 1.12; 95% CI, 1.01–1.23; PFHxS: OR = 1.06; 95% CI, 1.02–1.11), and we observed a nonsignificant positive association with PFNA (OR = 1.32; 95% CI, 0.86–2.02).

Conclusions

Our results, using cross-sectional data, are consistent with increased odds of ADHD in children with higher serum PFC levels. Given the extremely prevalent exposure to PFCs, follow-up of these data with cohort studies is needed.     

Qualitative Environmental Health Research: An Analysis of the Literature, 1991–2008

Background

Recent articles have advocated for the use of qualitative methods in environmental health research. Qualitative research uses nonnumeric data to understand people’s opinions, motives, understanding, and beliefs about events or phenomena.

Objective

In this analysis of the literature, I report the use of qualitative methods and data in the study of the relationship between environmental exposures and human health.

Data sources

A primary search on ISI Web of Knowledge/Web of Science for peer-reviewed journal articles dated from 1991 through 2008 included the following three terms: qualitative, environ*, and health. Inclusion and exclusion criteria are described.

Data extraction

Searches resulted in 3,155 records. Data were extracted and findings of articles analyzed to determine where and by whom qualitative environmental health research is conducted and published, the types of methods and analyses used in qualitative studies of environmental health, and the types of information qualitative data contribute to environmental health.

Data synthesis

Ninety-one articles met inclusion criteria. These articles were published in 58 different journals, with a maximum of eight for a single journal. The results highlight a diversity of disciplines and techniques among researchers who used qualitative methods to study environmental health, with most studies relying on one-on-one interviews. Details of the analyses were absent from a large number of studies. Nearly all of the studies identified increased scientific understanding of lay perceptions of environmental health exposures.

Discussion and conclusions

Qualitative data are published in traditionally quantitative environmental health studies to a limited extent. However, this analysis demonstrates the potential of qualitative data to improve understanding of complex exposure pathways, including the influence of social factors on environmental health, and health outcomes.     

Prenatal Exposure to Lead, δ-Aminolevulinic Acid,and Schizophrenia: Further Evidence

Background

A previously conducted study of prenatal lead exposure and schizophrenia using δ-aminolevulinic acid, a biologic marker of Pb exposure, in archived maternal serum samples collected from subjects enrolled in the Childhood Health and Development Study (1959–1966) based in Oakland, California, suggested a possible association between prenatal Pb exposure and the development of schizophrenia in later life.

Objectives

In the present study we extend these findings using samples collected from the New England cohort of the National Collaborative Perinatal Project (1959–1966). Using similar methods, in this study we found results that suggest a comparable association in this cohort.

Methods

We pooled matched sets of cases and controls from both the California and New England sites using a multilevel random-intercept logistic regression model, accounting for matching and site structure as well as adjusting for maternal age at delivery and maternal education.

Results

The estimated odds ratio for schizophrenia associated with exposure corresponding to 15 μg/dL of blood Pb was 1.92 (95% confidence interval, 1.05–3.87; p = 0.03).

Conclusion

Although several limitations constrain generalizability, these results are consistent with previous findings and provide further evidence for the role of early environmental exposures in the development of adult-onset psychiatric disorders.