Institutional members access full text with Ovid®

Share this article on:

Dioxin and Polychlorinated Biphenyl Concentrations in Mother's Serum and the Timing of Pubertal Onset in Sons

Humblet, Oliviera; Williams, Paige L.b; Korrick, Susan A.a,c; Sergeyev, Olegd,e; Emond, Claudef; Birnbaum, Linda S.g; Burns, Jane S.a; Altshul, Larisah,i; Patterson, Donald G. Jr.j; Turner, Wayman E.k; Lee, Mary M.l; Revich, Borism; Hauser, Russa

doi: 10.1097/EDE.0b013e318230b0d1
Puberty

Background: Animal studies have demonstrated that timing of pubertal onset can be altered by prenatal exposure to dioxins or polychlorinated biphenyls (PCBs), but studies of human populations have been quite limited.

Methods: We assessed the association between maternal serum concentrations of dioxins and PCBs and the sons' age of pubertal onset in a prospective cohort of 489 mother–son pairs from Chapaevsk, Russia, a town contaminated with these chemicals during past industrial activity. The boys were recruited at ages 8 to 9 years, and 4 years of annual follow-up data were included in the analysis. Serum samples were collected at enrollment from both mothers and sons for measurement of dioxin and PCB concentrations using high-resolution mass spectrometry. The sons' pubertal onset—defined as pubertal stage 2 or higher for genitalia (G) or pubic hair (P), or testicular volume >3 mL—was assessed annually by the same physician.

Results: In multivariate Cox models, elevated maternal serum PCBs were associated with earlier pubertal onset defined by stage G2 or higher (4th quartile hazard ratio = 1.7 [95% confidence interval = 1.1– 2.5]), but not for stage P2 or higher or for testicular volume >3 mL. Maternal serum concentrations of dioxin toxic equivalents were not consistently associated with the sons' pubertal onset, although a dose-related delay in pubertal onset (only for G2 or higher) was seen among boys who breast-fed for 6 months or more.

Conclusions: Maternal PCB serum concentrations measured 8 or 9 years after sons' births—which may reflect sons' prenatal and early-life exposures—were associated with acceleration in some, but not all, measures of pubertal onset.

From the aEnvironmental and Occupational Medicine and Epidemiology Program, Department of Environmental Health, Harvard School of Public Health, Boston, MA; bDepartment of Biostatistics, Harvard School of Public Health, Boston, MA; cDepartment of Medicine, Channing Laboratory, Brigham and Women's Hospital and Harvard Medical School, Boston, MA; dDepartment of Physical Education and Health, Samara State Medical University, Samara, Russia; eChapaevsk Medical Association, Chapaevsk, Samara, Russia; fDepartment of Environmental and Occupational Health, Faculty of Medicine, University of Montreal, Montreal, Quebec, Canada; gDepartment of Health and Human Services, National Cancer Institute, National Institutes of Health, Bethesda, MD; hDepartment of Environmental Health, Harvard School of Public Health, Boston, MA; iEnvironmental Health and Engineering, Inc., Needham, MA; jEnviroSolutions Consulting, Inc., Jasper, GA; kCenters for Disease Control and Prevention, Atlanta, GA; lPediatric Endocrinology Division, Departments of Pediatrics and Cell Biology, University of Massachusetts Medical School, Worcester, MA; and mCenter for Demography and Human Ecology, Institute for Forecasting, Russian Academy of Sciences, Moscow, Russia.

Submitted 15 April 2011; accepted 16 June 2011.

The research described in this article has been reviewed by the National Institute of Environmental Health Sciences, and approved for publication. Approval does not signify that the contents necessarily reflect the views of the Agency, nor does the mention of trade names or commercial products constitute endorsement or recommendation for use.

The opinions expressed in this manuscript are those of the authors and do not necessarily reflect the official opinion of the Centers for Disease Control and Prevention.

This work was funded by U.S. EPA grant R82943701 and NIEHS grants ES014370, ES00002, and 5T32-ES07069-28. OH was supported by 5T32ES016645-02 from NIEHS/NHGRI. MML is a member of the UMass DERC (DK32520). CE is an International Consultant and the President of BioSimulation Consulting Inc. LA is a consultant for Environmental Health and Engineering, Inc. DGP is a consultant for Axys Analytical Solutions, Fluid Management Systems, Inc., and Exponent Inc.

The other authors reported no financial interests related to this research.

Correspondence: Russ Hauser, Environmental and Occupational Medicine and Epidemiology Program, Department of Environmental Health, Harvard School of Public Health, 665 Huntington Avenue, Building I, room 1405, Boston, MA 02115. E-mail: rhauser@hohp.harvard.edu.

© 2011 Lippincott Williams & Wilkins, Inc.