Pesticides exposures are aspects of the human exposome that have not been sufficiently studied for their contribution to risk for preterm birth. We investigated risks of spontaneous preterm birth from potential residential exposures to 543 individual chemicals and 69 physicochemical groupings that were applied in the San Joaquin Valley of California during the study period, 1998–2011.
The study population was derived from birth certificate data linked with Office of Statewide Health Planning and Development maternal and infant hospital discharge data. After exclusions, the analytic study base included 197,461 term control births and 27,913 preterm case births. Preterm cases were more narrowly defined as 20–23 weeks (n = 515), 24–27 weeks (n = 1,792), 28–31 weeks (n = 3,098), or 32–36 weeks (n = 22,508).
The frequency of any (versus none) pesticide exposure was uniformly lower in each preterm case group relative to the frequency in term controls, irrespective of gestational month of exposure. All odds ratios were below 1.0 for these any versus no exposure comparisons. The majority of odds ratios were below 1.0, many of them statistically precise, for preterm birth and exposures to specific chemical groups or chemicals.
This study showed a general lack of increased risk of preterm birth associated with a range of agriculture pesticide exposures near women’s residences.
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From the aMarch of Dimes Prematurity Research Center at Stanford University, Department of Pediatrics, Division of Neonatal and Developmental Medicine, Stanford University School of Medicine, Stanford, CA; bPublic Health Institute, Oakland, CA; cPesticide Research Institute, Berkeley, CA; and dCalifornia Department of Public Health, Richmond, CA.
Submitted March 15, 2017; accepted September 14, 2017.
The data are publicly available from the Office of Statewide Health Planning and Development (OSHPD). The data are not available for replication because specific approvals from OSHPD and the California Committee for the Protection of Human Subjects must be obtained in order to access them.
The authors report no conflicts of interest.
Supported by NIH (R01HD075761) with additional support from the March of Dimes Prematurity Research Center at Stanford University (MOD PR625253) and the Stanford Child Health Research Institute.
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Correspondence: Gary M. Shaw, Department of Pediatrics, Stanford University, 1265 Welch Road, Rm X159, Stanford, CA 94305. E-mail: firstname.lastname@example.org.