Abstract
BACKGROUND AND AIM: Dioxins, polychlorinated biphenyls (PCBs) and lead are widespread environmental pollutants. Peripubertal exposure is associated with altered age of pubertal onset and sexual maturity in boys, but its impact on pubertal progression is unknown. METHODS: The Russian Children’s Study is a prospective cohort of 516 boys residing in an industrial city historically contaminated with organochlorine pollutants, who were enrolled in 2003-2005 and followed annually from ages 8-19 years. At enrollment, blood was obtained to quantify serum dioxin-like toxic equivalents (TEQs), non-dioxin-like PCBs (NDL-PCBs) and blood lead levels (BLLs). At enrollment and annually thereafter, we assessed boys' pubertal Tanner stage and testicular volume (TV) via Prader orchidometer. To distinguish subgroups with similar pubertal trajectories, we applied group-based trajectory modeling to TV from ages 8-19 years. We used multinomial logistic regression to model the association of peripubertal serum TEQs, NDL-PCBs and BLL with pubertal progression subgroups. RESULTS:This Russian cohort had lower prevalence of obesity and higher serum organochlorine chemicals relative to other pediatric populations. We identified three pubertal trajectories: slower, moderate and accelerated. Higher peripubertal serum TEQs were associated with decreased odds of being in the accelerated (OR 0.56, 95% CI 0.32-0.99) or slower (OR 0.85, 95% CI 0.53-1.35) trajectories versus the moderate, but with increased odds of being in the slower trajectory versus the accelerated (OR 1.51, 95% CI 0.82, 2.79). However, higher NDL-PCBs were associated with increased odds of being in the accelerated trajectory, versus the moderate (OR 2.56, 95% CI 0.91-7.20) or slower (OR 3.31, 95% CI 1.07, 10.25). Higher BLLs were associated with increased odds of being in the slower trajectory versus the accelerated (OR 1.48, 95% CI 0.89, 2.45) or moderate (OR 1.21, 95% CI 0.83, 1.75). CONCLUSIONS:Boys with higher peripubertal serum dioxins, NDL-PCBs and lead may have either accelerated or slower pubertal progression, depending on the specific exposure. KEYWORDS: Biomarkers of Exposure, Endocrine disrupting chemicals, Children's environmental health, Male, Reproductive outcomes, Modeling
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