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Human prenatal exposure to polychlorinated biphenyls (PCBs) and risk behaviors in adolescence

Authors
  • Dickerson, Aisha S.1
  • Ransome, Yusuf2
  • Karlsson, Oskar3
  • 1 Department of Environmental Health, Harvard T.H. Chan School of Public Health, 665 Huntington Avenue, 1402, Boston, MA 02215, USA
  • 2 Department of Social and Behavioral Sciences, Yale School of Public Health, 60 College Street, LEPH 4th Floor, New Haven, CT 06510, USA
  • 3 Science for Life Laboratory, Department of Environmental Sciences and Analytical Chemistry, Stockholm University, Stockholm 114 18, Sweden
Type
Published Article
Journal
Environment international
Publication Date
May 27, 2019
Volume
129
Pages
247–255
Identifiers
DOI: 10.1016/j.envint.2019.04.051
PMID: 31146159
PMCID: PMC6605040
Source
PubMed Central
Keywords
License
Green

Abstract

Polychlorinated biphenyls (PCBs) are chemicals used in a variety of products before they were widely banned due to toxic effects in humans and wildlife. Because of continued persistence and ubiquity of these contaminants, risk of exposure to people living in industrialized countries is still high. Experimental research show that developmental exposure to PCB may alter function of brain pleasure centers and potentially influence disinhibitory behaviors, including tobacco and alcohol use. Yet, the potential effects of developmental PCB exposure on adolescent substance use have not been studied in humans. We used the Child Health and Development Studies (CHDS), a prospective birth cohort study in the Oakland and East Bay areas of California, to investigate associations between prenatal exposure to PCB congeners (66, 74, 99, 118, 138, 153, 170, 180, 187, and 203) and later disinhibitory behaviors in adolescents, specifically alcohol consumption and smoking, in a randomly selected sample( n = 554). Total prenatal PCB exposure was not associated with disinhibitory behaviors, among adolescents. However, the adjusted odds ratio (aOR) for being a current smoker, was higher in subjects within the third quartile of maternal PCB 66 exposure compared to those below the median (aOR = 1.93; 95% CI 1.05, 3.55). The aOR for drinking > 2 alcoholic beverages per week, were also higher for adolescents within the third (aOR = 1.46; 95% CI 0.86, 2.47) and fourth quartile of PCB 66 exposure (aOR = 1.39; 95% CI 0.83, 2.35), but the differences did not reach statistical significance. These results suggest that this specific PCB congener may play a role inducing neurodevelopmental alterations that could potentially increase the risk of becoming a long-term user of tobacco and possibly alcohol. There were no notable differences between magnitude or direction of effect between boys and girls. Future replicate analyses with larger longitudinal samples and animal experimental studies of potential underlying mechanisms are warranted.

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