Bora Plaku-Alakbarova1, Oleg Sergeyev2, Paige L Williams3, Jane S Burns4, Mary M Lee5, Russ Hauser6, Susan A Korrick7. 1. Department of Environmental Health, Harvard T. H. Chan School of Public Health, 677 Huntington Ave, Boston, MA, 02115, USA. Electronic address: bop020@mail.harvard.edu. 2. Belozersky Research Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Leninskye Gory 1, Building 40, 119234, Moscow, Russia; Chapaevsk Medical Association, Meditsinskaya Str. 3a, 446100, Chapaevsk, Samara Region, Russia. Electronic address: olegsergeyev1@yandex.ru. 3. Department of Biostatistics, Harvard T. H. Chan School of Public Health, 655 Huntington Ave, Boston, MA, 02115, USA; Department of Epidemiology, Harvard T. H. Chan School of Public Health, 655 Huntington Ave, Boston, MA, 02115, USA. Electronic address: paige@hsph.harvard.edu. 4. Department of Environmental Health, Harvard T. H. Chan School of Public Health, 677 Huntington Ave, Boston, MA, 02115, USA. Electronic address: jburns@hsph.harvard.edu. 5. Nemours AI duPont Hospital for Children, 1600 Rockland Road, Wilmington, DE, USA; Sidney Kimmel Medical College, Jefferson University, Philadelphia, PA, USA. Electronic address: mary.lee@nemours.org. 6. Department of Environmental Health, Harvard T. H. Chan School of Public Health, 677 Huntington Ave, Boston, MA, 02115, USA; Department of Epidemiology, Harvard T. H. Chan School of Public Health, 655 Huntington Ave, Boston, MA, 02115, USA. Electronic address: rhauser@hsph.harvard.edu. 7. Department of Environmental Health, Harvard T. H. Chan School of Public Health, 677 Huntington Ave, Boston, MA, 02115, USA; Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, 02115, USA. Electronic address: susan.korrick@channing.harvard.edu.
Abstract
BACKGROUND: Dioxins, furans and polychlorinated biphenyls (PCBs) are endocrine disruptors with half-lives of months to years in humans. Peripubertal exposure to these chemicals may disrupt pubertal timing. Biomarker exposure metrics like the sum of non-dioxin-like PCBs in serum (∑NDL-PCBs) involve chemicals with different hypothetical effects. Empirical exposure metrics represent an alternative that requires no knowledge of biological mechanisms. METHODS: From 2003 to 2005, 516 Russian boys aged 8-9 residing near a plant that historically produced organochlorine pesticides were enrolled in the Russian Children's Study. At enrollment, blood was collected for measurement of organochlorine chemicals by the Centers for Disease Control and Prevention (CDC). Variable cluster analysis was used to empirically group serum levels of 45 dioxins, furans and PCBs into eight cluster scores. These scores were compared to the sum of dioxin-like toxic equivalents (∑TEQs) and ∑NDL-PCBs using Spearman correlation coefficients. RESULTS: Clustering appeared to reflect number and position of chlorine atoms. Clusters 4, 7 and 1 contained, respectively, tri/tetra-, tetra/penta-, and hexa/hepta-chlorinated PCBs with chlorines at the 4,4' positions. Clusters 2, 8 and 5 contained, respectively, tetra-to hexa-, hexa/hepta-, and hepta/octa-chlorinated PCBs with chlorines at the 2,2' positions. ∑NDL-PCBs were highly correlated with 4,4'-chlorinated clusters 1 and 7 (Spearman's ρ = 0.8) and less so with all other clusters (Spearman's ρ = 0.4-0.5). CONCLUSIONS: In this cohort of Russian boys, baseline serum dioxins, furans and PCBs seemed to cluster by chlorination pattern, possibly reflecting shared persistence, metabolism or source of exposure. The widely used measure ∑NDL-PCB seemed most representative of 4,4'-chlorinated PCBs.
BACKGROUND: Dioxins, furans and polychlorinated biphenyls (PCBs) are endocrine disruptors with half-lives of months to years in humans. Peripubertal exposure to these chemicals may disrupt pubertal timing. Biomarker exposure metrics like the sum of non-dioxin-like PCBs in serum (∑NDL-PCBs) involve chemicals with different hypothetical effects. Empirical exposure metrics represent an alternative that requires no knowledge of biological mechanisms. METHODS: From 2003 to 2005, 516 Russian boys aged 8-9 residing near a plant that historically produced organochlorine pesticides were enrolled in the Russian Children's Study. At enrollment, blood was collected for measurement of organochlorine chemicals by the Centers for Disease Control and Prevention (CDC). Variable cluster analysis was used to empirically group serum levels of 45 dioxins, furans and PCBs into eight cluster scores. These scores were compared to the sum of dioxin-like toxic equivalents (∑TEQs) and ∑NDL-PCBs using Spearman correlation coefficients. RESULTS: Clustering appeared to reflect number and position of chlorine atoms. Clusters 4, 7 and 1 contained, respectively, tri/tetra-, tetra/penta-, and hexa/hepta-chlorinated PCBs with chlorines at the 4,4' positions. Clusters 2, 8 and 5 contained, respectively, tetra-to hexa-, hexa/hepta-, and hepta/octa-chlorinated PCBs with chlorines at the 2,2' positions. ∑NDL-PCBs were highly correlated with 4,4'-chlorinated clusters 1 and 7 (Spearman's ρ = 0.8) and less so with all other clusters (Spearman's ρ = 0.4-0.5). CONCLUSIONS: In this cohort of Russian boys, baseline serum dioxins, furans and PCBs seemed to cluster by chlorination pattern, possibly reflecting shared persistence, metabolism or source of exposure. The widely used measure ∑NDL-PCB seemed most representative of 4,4'-chlorinated PCBs.
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