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Research Paper|Volume 11, Issue 15|pp 5498—5517

Environmental exposure to polybrominated biphenyl (PBB) associates with an increased rate of biological aging

Sarah W. Curtis1, Dawayland O. Cobb2, Varun Kilaru2, Metrecia L. Terrell3, M. Elizabeth Marder4, Dana Boyd Barr4, Carmen J. Marsit4, Michele Marcus3,4,5, Karen N. Conneely6, Alicia K. Smith2,7
  • 1Genetics and Molecular Biology Program, Laney Graduate School, Emory University, Atlanta, GA 30322, USA
  • 2Department of Gynecology and Obstetrics, School of Medicine, Emory University, Atlanta, GA 30322, USA
  • 3Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, GA 30322, USA
  • 4Department of Environmental Health, Rollins School of Public Health, Emory University, Atlanta, GA 30322, USA
  • 5Department of Pediatrics, School of Medicine, Emory University, Atlanta, GA 30322, USA
  • 6Department of Human Genetics, School of Medicine, Emory University, Atlanta, GA 30322, USA
  • 7Department of Psychiatry and Behavioral Sciences, School of Medicine, Emory University, Atlanta, GA 30322, USA
Received: May 21, 2019Accepted: July 26, 2019Published: August 2, 2019
https://doi.org/10.18632/aging.102134

Copyright © 2019 Curtis et al. This is an open-access article distributed under the terms of the Creative Commons Attribution (CC BY) 3.0 License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Advanced age increases risk for cancer, cardiovascular disease, and all-cause mortality. However, people do not age at the same rate, and biological age (frequently measured through DNA methylation) can be older than chronological age. Environmental factors have been associated with the rate of biological aging, but it is not known whether persistent endocrine-disrupting compounds (EDCs) like polybrominated biphenyl (PBB) would associate with age acceleration. Three different epigenetic age acceleration measures (intrinsic, extrinsic, and phenotypic) were calculated from existing epigenetic data in whole blood from a population highly exposed to PBB (N=658). Association between serum PBB concentration and these measures was tested, controlling for sex, lipid levels, and estimated cell type proportions. Higher PBB levels associated with increased age acceleration (intrinsic: β=0.24, 95%CI=0.01-0.46, p = 0.03; extrinsic: β=0.39, 95%CI=0.12-0.65, p = 0.004; and phenotypic: β=0.30, 95%CI=0.05-0.54, p = 0.01). Neither age when exposed to PBB nor sex statistically interacted with PBB to predict age acceleration, but, in stratified analyses, the association between PBB and age acceleration was only in people exposed before finishing puberty and in men. This suggests that EDCs can associate with the biological aging process, and further studies are warranted to investigate other environmental pollutants’ effect on aging.