Cumulative exposure to environmental pollutants during early pregnancy and reduced fetal growth: the Project Viva cohort.

Document Type

Article

Publication Date

2-20-2018

Institution/Department

Pediatrics; Endocrinology & Diabetes; Center for Outcomes Research and Evaluation; Maine Medical Center Research Institute

Journal Title

Environmental health : a global access science source [electronic resource]

MeSH Headings

Adult, Alkanesulfonic Acids, Environmental Pollutants, Female, Fetal Development, Fluorocarbons, Humans, Massachusetts, Maternal Exposure, Pregnancy, Prospective Studies, Soot, Tobacco Smoke Pollution, Traffic-Related Pollution

Abstract

BACKGROUND: Reduced fetal growth is associated with perinatal and later morbidity. Prenatal exposure to environmental pollutants is linked to reduced fetal growth at birth, but the impact of concomitant exposure to multiple pollutants is unclear. The purpose of this study was to examine interactions between early pregnancy exposure to cigarette smoke, traffic pollution, and select perfluoroalkyl substances (PFASs) on birth weight-for-gestational age (BW/GA).

METHODS: Among 1597 Project Viva mother-infant pairs, we assessed maternal cigarette smoking by questionnaire, traffic pollution at residential address by black carbon land use regression model, and plasma concentration of select PFASs in early pregnancy. We calculated sex-specific BW/GA z-scores, an index of fetal growth, from national reference data. We fit covariate-adjusted multi-pollutant linear regression models and examined interactions between exposures, using a likelihood-ratio test to identify a best-fit model.

RESULTS: Two hundred six (13%) mothers smoked during pregnancy. Mean [standard deviation (SD)] for black carbon was 0.8 (0.3) μg/m

CONCLUSIONS: Concurrent prenatal exposures to maternal smoking, black carbon, and PFOS are additively associated with lower fetal growth, whereas PFNA may attenuate associations of smoking and black carbon with lower fetal growth. It is important to examine interactions between multiple exposures in relation to health outcomes, as effects may not always be additive and may shed light on biological pathways.

ISSN

1476-069X

First Page

19

Last Page

19

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