Background: Ambient air pollution has been linked to the development of gestational diabetes mellitus (GDM). However, evidence of the association is very limited, and no study has estimated the effects of ozone.

Objective: Our aim was to determine the association of prenatal exposures to particulate matter ≤ 2.5 μm (PM_2.5) and ozone (O₃) with GDM.

Methods: We used Florida birth vital statistics records to investigate the association between the risk of GDM and two air pollutants (PM_2.5 and O₃) among 410,267 women who gave birth in Florida between 2004 and 2005. Individual air pollution exposure was assessed at the woman’s home address at time of delivery using the hierarchical Bayesian space–time statistical model. We further estimated associations between air pollution exposures during different trimesters and GDM.

Results: After controlling for nine covariates, we observed increased odds of GDM with per 5-μg/m³ increase in PM_2.5 (OR_Trimester1 = 1.16; 95% CI: 1.11, 1.21; OR_Trimester2 = 1.15; 95% CI: 1.10, 1.20; OR_Pregnancy = 1.20; 95% CI: 1.13, 1.26) and per 5-ppb increase in O₃ (OR_Trimester1 = 1.09; 95% CI: 1.07, 1.11; OR_Trimester2 = 1.12; 95% CI: 1.10, 1.14; OR_Pregnancy = 1.18; 95% CI: 1.15, 1.21) during both the first trimester and second trimester as well as the full pregnancy in single-pollutant models. Compared with the single-pollutant model, the ORs for O₃ were almost identical in the co-pollutant model. However, the ORs for PM_2.5 during the first trimester and the full pregnancy were attenuated, and no association was observed for PM_2.5 during the second trimester in the co-pollutant model (OR = 1.02; 95% CI: 0.98, 1.07).

Conclusion: This population-based study suggests that exposure to air pollution during pregnancy is associated with increased risk of GDM in Florida, USA.

Citation: Hu H, Ha S, Henderson BH, Warner TD, Roth J, Kan H, Xu X. 2015. Association of atmospheric particulate matter and ozone with gestational diabetes mellitus. Environ Health Perspect 123:853–859;  http://dx.doi.org/10.1289/ehp.1408456

Address correspondence to X. Xu, University of Florida, College of Public Health and Health Professions and College of Medicine, Department of Epidemiology, 2004 Mowry Rd., CTRB 4219, Gainesville, FL 32610 USA. Telephone: (352) 273-5362. E-mail: xhxu@phhp.ufl.edu

This work was supported by grant K01ES019177 from the National Institute of Environmental Health Sciences, National Institutes of Health (NIEHS/NIH). The data were provided by the Bureau of Vital Statistics, Florida Department of Health (DOH).

All conclusions are the authors’ own and do not necessarily reflect the opinion of the NIEHS/NIH or the Florida DOH.

The authors declare they have no actual or potential competing financial interests.

Received: 21 March 2014 Accepted: 17 March 2015 Advance Publication: 20 March 2015 Final Publication: 1 September 2015

Note to readers with disabilities: EHP strives to ensure that all journal content is accessible to all readers. However, some figures and Supplemental Material published in EHP articles may not conform to 508 standards due to the complexity of the information being presented. If you need assistance accessing journal content, please contact ehp508@niehs.nih.gov . Our staff will work with you to assess and meet your accessibility needs within 3 working days.

Note to readers with disabilities: EHP has provided a 508-conformant table of contents summarizing the Supplemental Material for this article (see below) so readers with disabilities may determine whether they wish to access the full, nonconformant Supplemental Material. If you need assistance accessing this or any other content on this site, please contact ehp508@niehs.nih.gov . Our staff will work with you to assess and meet your accessibility needs within 3 working days.

Supplemental Table of Contents PDF (113 KB)