Animal studies have suggested that bisphenol-A (BPA) is a potential human endocrine disrupter; but evidence from human studies is needed. We conducted an occupational cohort study to examine the effect of occupational exposure to BPA on the risk of male sexual dysfunction. Current workers from BPA-exposed and control factories were recruited. The exposed workers were exposed to very high BPA levels in their workplace. Male sexual function was ascertained through in-person interviews using a standard male sexual function inventory. BPA-exposed workers had consistently higher risk of male sexual dysfunction across all domains of male sexual function than the unexposed workers. After controlling for matching variables and potential confounders, exposed workers had a significantly increased risk of reduced sexual desire [odds ratios (OR) = 3.9, 95% confidence interval: 1.8–8.6), erectile difficulty (OR = 4.5, 95% CI 2.1–9.8), ejaculation difficulty (OR = 7.1, 95% CI 2.9–17.6), and reduced satisfaction with sex life (OR = 3.9, 95% CI 2.3–6.6). A dose–response relationship was observed with an increasing level of cumulative BPA exposure associated with a higher risk of sexual dysfunction. Furthermore, compared with the unexposed workers, BPA-exposed workers reported significantly higher frequencies of reduced sexual function within 1 year of employment in the BPA-exposed factories. Our findings provide the first evidence that exposure to BPA in the workplace could have an adverse effect on male sexual dysfunction.

Background: Environmental pollutants such as polycyclic aromatic hydrocarbons (PAHs), lead, and mercury are released by combustion of coal and other fossil fuels. Objectives: In the present study we evaluated the association between prenatal exposure to these pollutants and child development measured by the Gesell Developmental Schedules at 2 years of age. Methods: The study was conducted in Tongliang, Chongqing, China, where a seasonally operated coal-fired power plant was the major source of ambient PAHs and also contributed lead and mercury to the air. In a cohort of nonsmoking women and their newborns enrolled between March 2002 and June 2002, we measured levels of PAH–DNA adducts, lead, and mercury in umbilical cord blood. PAH–DNA adducts (specifically benzo[a]pyrene adducts) provided a biologically relevant measure of PAH exposure. We also obtained developmental quotients (DQs) in motor, adaptive, language, and social areas. Results: Decrements in one or more DQs were significantly associated with cord blood levels of PAH–DNA adducts and lead, but not mercury. Increased adduct levels were associated with decreased motor area DQ (p = 0.043), language area DQ (p = 0.059), and average DQ (p = 0.047) after adjusting for cord lead level, environmental tobacco smoke, sex, gestational age, and maternal education. In the same model, high cord blood lead level was significantly associated with decreased social area DQ (p = 0.009) and average DQ (p = 0.038). Conclusion: The findings indicate that exposure to pollutants from the power plant adversely affected the development of children living in Tongliang; these findings have implications for environmental health policy.

Background: Associations between airborne particles and health outcomes have been documented worldwide; however, there is limited information regarding health effects associated with different particle sizes. Objectives: We explored the association between size-fractionated particle number concentrations (PNCs) and daily mortality in Shenyang, China. Methods: We collected daily data on cause-specific mortality and PNCs for particles measuring 0.25–10 μm in diameter between 1 December 2006 and 30 November 2008. We used quasi-Poisson regression generalized additive models to estimate associations between PNCs and mortality, and we used natural spline smoothing functions to adjust for time-varying covariates and long-term and seasonal trends. Results: Mean numbers of daily deaths were 67, 32, and 7 for all natural causes, cardiovascular diseases, and respiratory diseases, respectively. Interquartile range (IQR) increases in PNCs for particles measuring 0.25–0.50 μm were significantly associated with total and cardiovascular mortality, but not respiratory mortality. Effect estimates were larger for PNCs during the warm season than the cool season, and increased with decreasing particle size. IQR increases in PNCs of 0.25–0.28 μm, 0.35–0.40 μm, and 0.45–0.50 μm particles were associated with 2.41% (95% CI: 1.23, 3.58%), 1.31% (95% CI: 0.52, 2.09%), and 0.45% (95% CI: 0.04, 0.87%) higher total mortality, respectively. Associations were generally stable after adjustment for mass concentrations of ambient particles and gaseous pollutants. Conclusions: Our findings suggest that particles < 0.5 μm in diameter may be most responsible for adverse health effects of particulate air pollution and that adverse health effects may increase with decreasing particle size. Citation: Meng X, Ma Y, Chen R, Zhou Z, Chen B, Kan H. 2013. Size-fractionated particle number concentrations and daily mortality in a Chinese city. Environ Health Perspect 121:1174–1178; http://dx.doi.org/10.1289/ehp.1206398