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Environmental Chemicals and Preterm Birth: Biological Mechanisms and the State of the Science

  • Environmental Epidemiology (J Braun, Section Editor)
  • Published:
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Abstract

Purpose of Review

Preterm birth is a significant worldwide health problem of uncertain origins. The extant body of literature examining environmental contaminant exposures in relation to preterm birth is extensive but results remain ambiguous for most organic pollutants, metals and metalloids, and air pollutants. In the present review, we examine recent epidemiologic studies investigating these associations and identify advances and the state of the science. Additionally, we highlight biological mechanisms of action in the pathway between chemical exposures and preterm birth, including inflammation, oxidative stress, and endocrine disruption, that deserve more attention in this context.

Recent Findings

Important advances have been made in the study of the environment and preterm birth, particularly in regard to exposure assessment methods, exploration of effect modification by co-morbidities and exposures, and in identification of windows of vulnerability during gestation. There is strong evidence for an association between maternal exposure to some persistent pesticides, lead, and fine particulate matter, but data on other contaminants is sparse and only suggestive trends can be noted.

Summary

Beyond replicating current findings, further work must be done to improve understanding of mechanisms underlying the associations observed between environmental chemical exposures and preterm birth. By examining windows of vulnerability, disaggregating preterm birth by phenotypes, and measuring biomarkers of mechanistic pathways in these epidemiologic studies, we can improve our ability to detect associations with exposure, provide additional evidence for causality in an observational setting, and identify opportunities for intervention.

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Ferguson, K.K., Chin, H.B. Environmental Chemicals and Preterm Birth: Biological Mechanisms and the State of the Science. Curr Epidemiol Rep 4, 56–71 (2017). https://doi.org/10.1007/s40471-017-0099-7

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