BACKGROUND: Animal data demonstrate associations of dioxin, furan, and polychlorinated biphenyl (PCB) exposures with altered male gonadal maturation. It is unclear whether these associations apply to human populations.
OBJECTIVES: We investigated the association of dioxins, furans, PCBs, and corresponding toxic equivalent (TEQ) concentrations with pubertal onset among boys in a dioxin-contaminated region.
METHODS: Between 2003 and 2005, 499 boys 8-9 years of age were enrolled in a longitudinal study in Chapaevsk, Russia. Pubertal onset [stage 2 or higher for genitalia (G2+) or testicular volume (TV) > 3 mL] was assessed annually between ages 8 and 12 years. Serum levels at enrollment were analyzed by the Centers for Disease Control and Prevention, Atlanta, Georgia, USA. We used Cox proportional hazards models to assess age at pubertal onset as a function of exposure adjusted for potential confounders. We conducted sensitivity analyses excluding boys with pubertal onset at enrollment.
RESULTS: The median (range) total serum TEQ concentration was 21 (4-175) pg/g lipid, approximately three times higher than values in European children. At enrollment, boys were generally healthy and normal weight (mean body mass index, 15.9 kg/m2), with 30% having entered puberty by G2+ and 14% by TV criteria. Higher dioxin TEQs were associated with later pubertal onset by TV (hazard ratio = 0.68, 95% confidence interval, 0.49-0.95 for the highest compared with the lowest quartile). Similar associations were observed for 2,3,7,8-tetrachlorodibenzo-/>-dioxin and dioxin concentrations for TV but not G2+. Results were robust to sensitivity analyses.
CONCLUSIONS: Findings support an association of higher peripubertal serum dioxin TEQs and concentrations with later male pubertal onset reflected in delayed testicular maturation.
KEY WORDS: children, dioxins, furans, growth, PCBs, polychlorinated biphenyls, pubertal stage, puberty, testicular volume. Environ Health Perspect 119:1339-1344 (2011). http://dx.doi.org/10.1289/ehp.l003102 [Online 28 April 2011]
The transition from prepuberty to sexual maturity entails rapid physical, hormonal, and behavioral development. Alterations in the timing of pubertal onset or pace of its progression can adversely affect not only physical and sexual maturation, but also social, cognitive, and behavioral development and adult health (Graber et ill. 2004; Michaud et al. 2006). For example, earlier puberty incurs risk for metabolic syndrome and obesity in later life, and delayed puberty is associated with decreased bone mineral density in adults, raising concerns about increased fracture risk (Biro et al. 2003; Finkelstein et al. 1996; Van Lenthe et al. 1996).
In recent decades, suggestive evidence of earlier onset of breast development and age at menarche has been observed in girls, but data in boys are limited (Biro et al. 2010; Euling et al. 2008; Herman-Giddens et al. 1997, 2001; Sorensen et al. 2010). Explanations for this possible trend include changes in diet and activity and/or environmental exposures. Chemicals chat can disrupt gonadal steroidogenesis and neuroendocrine pathways, such as organochlorine pollutants including dioxins, furans, and polychlorinated biphenyls (PCBs), are of particular concern Jacobson-Dickman and Lee 2009; Schoeters et al. 2008). Despite efforts to limit dioxin emissions, and longstanding bans on PCB manufacture and use, human exposure is ongoing, primarily through diet. For example, fish...