Boston University Superfund Research Program

Background: Exposure to air pollution has been associated with higher C-reactive protein (CRP) levels, suggesting an inflammatory response. Not much is known about this association in pregnancy.

Objectives: We investigated the associations of air pollution exposure during pregnancy with maternal and fetal CRP levels in a population-based cohort study in the Netherlands.

Methods: PM10 and NO2 levels were estimated at the home address using dispersion modelling for different averaging periods preceding the blood sampling (1 week, 2 weeks, 4 weeks, and total pregnancy). High-sensitivity CRP levels were measured in maternal blood samples in early pregnancy (n = 5067) and in fetal cord blood samples at birth (n = 4450).

Results: As compared to the lowest quartile, higher PM10 exposure levels for the prior one and two weeks were associated with elevated maternal CRP levels (>8 mg/L) in the first trimester (odds ratio (OR) 1.32, 95% confidence interval (CI) 1.08 to 1.61 for the fourth PM10 quartile for the prior week, and OR 1.28, 95% CI 1.06 to 1.56 for the third PM10 quartile for the prior two weeks), however, no clear dose-response relationships were observed. PM10 and NO2 exposure levels for one, two, and four weeks preceding delivery were not consistently associated with fetal CRP levels at delivery. Higher long-term PM10 and NO2 exposure levels (total pregnancy) were associated with elevated fetal CRP levels (>1 mg/L) at delivery (OR 2.18, 95% CI 1.08 to 4.38 and OR 3.42, 95% CI 1.36 to 8.58 for the fourth quartiles of PM10 and NO2, respectively; P-values for trend <0.05).

Conclusions: Our results suggest that exposure to air pollution during pregnancy may lead to maternal and fetal inflammatory responses.

Background: Perfluoroalkyl acids are persistent compounds used in various industrial applications. Of these compounds, perfluorooctanoate (PFOA) is currently detected in humans world-wide. A recent study on low dose developmental exposure to PFOA in mice reported increased weight and elevated biomarkers of adiposity in postpubertal female offspring. We examined whether those findings could be replicated in humans.

Methods: A prospective cohort of 665 Danish pregnant women was recruited in 1988-1989 with offspring follow-up at 20 years. PFOA was measured in serum from gestational week 30. Offspring body mass index (BMI) and waist circumference was recorded at follow-up (n=665) and biomarkers of adiposity were quantified in a sub-set (n=422) of participants.

Results: After adjustment for covariates, including maternal pre-pregnancy body mass index (BMI), smoking, education and birth weight, in utero exposure to PFOA was positively associated with anthropometry at 20 years in female but not male offspring. Adjusted relative risks comparing the highest to lowest quartile (median: 5.8 vs. 2.3ng/mL) of maternal PFOA concentration were 3.1 (95% confidence interval (CI): 1.4, 6.9) for overweight or obese (BMI≥25 kg/m2) and 3.0 (95%CI: 1.3, 6.8) for waist circumference >88 cm among female offspring. This corresponded to estimated increases of 1.6 kg/m2 (95%CI: 0.6, 2.6) and 4.3 cm (95%CI: 1.4, 7.3) in average BMI and waist circumference, respectively. In addition, maternal PFOA concentrations were positively associated with serum insulin and leptin levels, and inversely associated with adiponectin levels in female offspring. Similar associations were observed for males, although point estimates were less precise due to fever number of observations. Maternal PFOS, PFOSA and PFNA concentrations were not independently associated with offspring anthropometry at 20 years.

Conclusions: Our findings on low dose developmental exposures to PFOA are in line with experimental results suggesting obesogenic effects in female offspring at 20 years.

Obesity is rising steadily around the world. Convincing evidence suggests that diet and activity are not the only factors at work in this trend—chemical “obesogens” may alter human metabolism and predispose some people to gain weight.

BACKGROUND: Increasing global focus on improved cookstoves (ICS) and clean fuels arises from their potential for delivering triple dividends of (1) household health, (2) local environmental quality and (3) regional climate benefits. However, ICS and clean fuel dissemination programs have met with low rates of adoption.

OBJECTIVES: We review empirical studies on ICS and fuel choice to describe the literature, examine determinants of fuel and stove choice, and identify knowledge gaps.

METHODS: We conduct a systematic review of the literature on the adoption of ICS or cleaner fuels by households in developing countries. Results are synthesized through a simple vote-counting meta-analysis.

RESULTS: We identify 32 research studies that contain 146 separate regression analyses of ICS adoption (11 analyses) or fuel choice (135 analyses) from Asia (60%), Africa (27%), and Latin America (19%). Most studies apply multivariate regression methods to consider 7 – 13 determinants of choice. Income, education and urban location are positively associated with adoption in most (not all) studies. However, the influence of fuel availability and prices, household size and composition, and gender is unclear. Potentially important drivers such as credit, supply-chain strengthening and social marketing have been ignored.

CONCLUSIONS: Adoption studies of ICS or clean energy are scarce, scattered and of differential quality, even while global distribution programs are quickly expanding. Future research must examine an expanded set of contextual variables to improve implementation of stove programs that can realize the “win-win-win” associated with these technologies.

Background: There has been increasing interest in the concept that exposures to environmental chemicals may be contributing factors to the epidemics of diabetes and obesity. On January 11-13, 2011 the Division of the National Toxicology Program (NTP) organized a workshop to evaluate the current state of the science on these topics of increasing public health concern.

Objective: The main objective of the workshop was to develop recommendations for a research agenda following a critical analysis of the literature for humans and experimental animals exposed to certain environmental chemicals. The environmental exposures considered at the workshop were arsenic, persistent organic pollutants (POPs), maternal smoking/nicotine, organotins, phthalates, bisphenol A (BPA), and pesticides. High throughput screening data from Tox21 were also considered as a way to evaluate potential cellular pathways and generate hypotheses for testing which and how certain chemicals might perturb biological processes related to diabetes and obesity.

Conclusions: Overall, the review of the existing literature identified linkages between several of the environmental exposures and type 2 diabetes. There was also support for the “developmental obesogen” hypothesis, which suggests that chemical exposures may increase the risk of obesity by altering the differentiation of adipocytes or the development of neural circuits that regulate feeding behavior. The effects may be most apparent when the developmental exposure is combined with consumption of a high-calorie, high-carbohydrate, or high-fat diet later in life. Research on environmental chemical exposures and type 1 diabetes was very limited. This lack of research was considered a critical data gap. This workshop report outlines the major themes that emerged from the workshop and discusses activities that NIEHS and NTP are undertaking to address research recommendations. This report also serves as an introduction to a series of papers that will review the literature regarding specific exposures and outcomes in more detail.