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Background: Perfluoroalkyl acids (PFASs) are suspected thyroid toxicants, but results from epidemiological studies are inconsistent. Objectives: We examined associations between serum PFASs and thyroid hormones (THs) in a representative, cross-sectional sample of U.S. adults. We hypothesized that people with high thyroid peroxidase antibodies and low iodine would be more susceptible to PFAS-induced thyroid disruption. Methods: Our sample included 1,525 adults ([greater than or equal to] 18 years) from the 2007-2008 NHANES study with available serum PFASs and THs. We examined associations between four serum PFASs [perfluorohexane sulfonate (PFHxS), perfluorononanoate (PFNA), perfluorooctanoate (PFOA), and perfluorooctane sulfonate (PFOS)], and serum THs [free triiodothyronine (fT3), free thyroxine (fT4), fT3/fT4, thyroid-stimulating hormone (TSH), total T3 (TT3), and total T4 (TT4)] using multivariable linear regression. We stratified subjects into four groups by two indicators of thyroid 'stress': thyroid peroxidase antibody (TPOAb > 9 IU/mL) and iodine status (< 100 µg/L urine). Results: Of 1,525 participants, 400 (26%) had low iodine only (T0I1), 87 (6%) had high TPOAb only (T1I0), and 26 (2%) had both high TPOAb and low iodine (T1I1). In general, associations were similar among participants in the groups with neither (T0I0) or only one thyroid stressor (T0I1 or T1I0), suggesting that PFA--TH associations were not modified by high TPOAb or low iodine alone. However, PFHxS and PFOS were negatively associated (p < 0.05) with fT4, and all four PFASs were positively associated (p < 0.05) with fT3, fT3/fT4, TSH, and TT3 in the group with joint exposure to high TPOAb and low iodine (T1I1). Conclusions: We found evidence of PFAS-associated thyroid disruption in a subset of U.S. adults with high TPOAb (a marker of autoimmune hypothyroidism) and low iodine status, who may represent a vulnerable subgroup. However, the small sample size, cross-sectional design, and possibility of reverse causation are limitations of this work. http://dx.doi.org/10.1289/ehp.1409589, Introduction Perfluoroalkyl acids (PFASs), which are used as stain, water, and grease repellents in paper food packaging, carpets, carpet- and upholstery-cleaning liquids, fire-fighting foams, paints, and many other consumer products [...]

Abstract Background The major aim of this study was to investigate whether maternal risk factors associated with socioeconomic status and small for gestational age (SGA) might be viable targets of interventions to reduce differential risk of SGA by socioeconomic status (socioeconomic SGA inequality) in the metropolitan area of Vancouver, Canada. Methods This study included 59,039 live, singleton births in the Vancouver Census Metropolitan Area (Vancouver) from January 1, 2006 to September 17, 2009. To identify an indicator of socioeconomic SGA inequality, we used hierarchical logistic regression to model SGA by area-level variables from the Canadian census. We then modelled SGA by area-level average income plus established maternal risk factors for SGA and calculated population attributable SGA risk percentages (PAR%) for each variable. Associations of maternal risk factors for SGA with average income were investigated to identify those that might contribute to SGA inequality. Finally, we estimated crude reductions in the percentage and absolute differences in SGA risks between highest and lowest average income quintiles that would result if interventions on maternal risk factors successfully equalized them across income levels or eliminated them altogether. Results Average income produced the most linear and statistically significant indicator of socioeconomic SGA inequality with 8.9% prevalence of SGA in the lowest income quintile compared to 5.6% in the highest. The adjusted PAR% of SGA for variables were: bottom four quintiles of height (51%), first birth (32%), bottom four quintiles of average income (14%), oligohydramnios (7%), underweight or hypertension, (6% each), smoking (3%) and placental disorder (1%). Shorter height, underweight and smoking during pregnancy had higher prevalence in lower income groups. Crude models assuming equalization of risk factors across income levels or elimination altogether indicated little potential change in relative socioeconomic SGA inequality and reduction in absolute SGA inequality for shorter height only. Conclusions Our findings regarding maternal height may indicate trans-generational aetiology for socioeconomic SGA inequalities and/or that adult height influences social mobility. Conditions affecting foetal and childhood growth might be viable targets to reduce absolute socioeconomic SGA inequality in future generations, but more research is needed to determine whether such an approach is appropriate.

Objectives: Postpartum amenorrhea (PA) affects the length of interbirth intervals and thus is intimately related to human life history strategies. PA duration appears to be influenced by maternal energetic status. In humans, as in other mammals, sons are costlier than daughters. Thus, we hypothesize that, in energetically constrained environments, a newborn's sex should be associated with PA duration. Methods: We analyzed data from two natural fertility populations in which mothers have differing energy budgets: Qom women (n = 121) from a periurban village in Argentina, who have a comparatively calorically dense diet and are sedentary (prepregnancy mean BMI = 24.8 ± 4.5 kg/m2 in 1997), and agropastoral Kaqchikel Maya women (n = 88), who have a comparatively calorically restricted diet and high physical activity levels (mean BMI = 21.8 ± 3.7 kg/m2). We predict that (a) mothers of sons exhibit longer PA duration than mothers of daughters and (b) this association between offspring sex and PA duration is stronger in the Maya, who have smaller energy budgets. Results: Maya mothers with sons exhibited estimated mean and median PA durations that were 1.34 times the estimated mean and median PA duration of mothers with daughters (p = 0.02). Among the Qom, mean, and median PA duration did not differ significantly in relation to offspring sex (p = 0.94). Conclusions: Maya mothers with sons exhibited longer PA duration than those with daughters. This phenomenon was not observed in the well‐nourished Qom, possibly due to "buffering" effects from larger energy budgets. Offspring sex may influence birth spacing and maternal life history strategies in energetically constrained environments. [ABSTRACT FROM AUTHOR]

Background: Early-life exposure to bisphenol A (BPA) may increase childhood obesity risk, but few prospective epidemiological studies have investigated this relationship. OBJECTIVE: We sought to determine whether early-life exposure to BPA was associated with increased body mass index (BMI) at 2-5 years of age in 297 mother-child pairs from Cincinnati, Ohio (HOME Study). METHODS: Urinary BPA concentrations were measured in samples collected from pregnant women during the second and third trimesters and their children at 1 and 2 years of age. BMI z-scores were calculated from weight/height measures conducted annually from 2 through 5 years of age. We used linear mixed models to estimate BMI differences or trajectories with increasing creatinine-normalized BPA concentrations. RESULTS: After confounder adjustment, each 10-fold increase in prenatal (β = -0.1; 95% CI: -0.5, 0.3) or early-childhood (β = -0.2; 95% CI: -0.6, 0.1) BPA concentrations was associated with a modest and nonsignificant reduction in child BMI. These inverse associations were suggestively stronger in girls than in boys [prenatal effect measure modification (EMM) p-value = 0.30, early-childhood EMM p-value = 0.05], but sex-specific associations were imprecise. Children in the highest early-childhood BPA tercile had lower BMI at 2 years (difference = -0.3; 95% CI: -0.6, 0.0) and larger increases in their BMI slope from 2 through 5 years (BMI increase per year = 0.12; 95% CI: 0.07, 0.18) than children in the lowest tercile (BMI increase per year = 0.07; 95% CI: 0.01, 0.13). All associations were attenuated without creatinine normalization. CONCLUSIONS: Prenatal and early-childhood BPA exposures were not associated with increased BMI at 2-5 years of age, but higher early-childhood BPA exposures were associated with accelerated growth during this period. Environ Health Perspect 122:1239-1245; http://dx.doi.org/10.1289/ehp.1408258, Introduction Child obesity is one of the greatest public health challenges worldwide (World Health Organization 2010). Excess food consumption and inadequate physical activity are major risk factors for obesity, but [...]