4.7 Article

Prenatal and early childhood exposure to tetrachloroethylene (PCE) and non-medical use of prescription drugs: A retrospective cohort study in Cape Cod, MA

Journal

ENVIRONMENTAL RESEARCH
Volume 196, Issue -, Pages -

Publisher

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.envres.2020.110384

Keywords

Tetrachloroethylene; Drinking water; Neurotoxicity; Early-life exposure; Non-medical use of prescription drugs& nbsp; (NMUPD)

Funding

  1. National Institute of Environmental Health Sciences Superfund Research Program [5P42ES00738]
  2. National Institutes of Environmental Health Sciences (NIEHS) [grantT32ES014562]

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This study examined the risk of non-medical use of prescription drugs (NMUPD) following prenatal and early childhood exposure to the chlorinated solvent tetrachloroethylene (PCE). The results showed a moderate increase in the risk of NMUPD associated with PCE exposure, with dose-related increased risks of specific categories of prescription drugs. Long-term neurotoxic effects of early life exposure to PCE should be further studied in longitudinal populations.
Background: Between 1968 and 1983, public drinking water supplies of Cape Cod, Massachusetts were contaminated with the chlorinated solvent tetrachloroethylene (PCE). We previously found an affinity for risktaking behaviors, including the use of illicit drugs, following prenatal and early childhood exposure to PCE. Using newly collected data, we investigated the risk of non-medical use of prescription drugs (NMUPD) following prenatal and early childhood PCE exposure. Methods: Participants were identified from a retrospective cohort study (Cape Cod Health Study?) via crossmatching birth certificates and water system data. The original self-administered questionnaire gathered data on demographics, work and medical history, and alcohol and illicit drug use from 618 individuals (363 exposed and 255 unexposed). The follow-up survey added questions on non-medical use of prescription pain relievers, tranquilizers, stimulants and sedatives. A validated leaching and transport model was used to estimate exposure to PCE exposure in drinking water. Results: There was a wide distribution of cumulative prenatal and early childhood PCE exposure levels (range: 0.04 g?3722.2 g). PCE exposed subjects had a 1.92-fold increase in risk of any non-medical use of prescription drugs [Adjusted RR: 1.92, (95% CI: 1.31, 2.83)]. Furthermore, the association followed a dose-response relationship where the risk of NMUPD was higher for those exposed to PCE levels greater than or equal the median level versus those exposed to levels less than the median [Adjusted RR: 2.05 (95% CI: 1.34, 3.15) vs. 1.83 (95% CI: 1.20, 2.79) (p-value for trend < 0.01)]. Additionally, we found moderate increases in risk by level of nonmedical use (any non-medical use, non-medical use of 1 or more categories of prescription drugs, or 2+ categories) as well as by category of drug for pain relivers, stimulants and tranquilizers. Conclusion: We found that prenatal and early childhood exposure to PCE was associated with a moderate increase in the risk of NMUPD. Exposed subjects had dose-related increased risks of NMUPD of pain relievers, tranquilizers, and stimulants. This study has a number of limitations and is the first to report this association. Additional longitudinal studies of populations exposed to PCE during early life should be conducted to examine its long-term neurotoxic effects.

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