Extreme ambient temperatures have been linked to preterm birth. Preterm premature rupture of membranes is a common precursor to preterm birth but is rarely studied in relation to temperature.
We linked 15 381 singleton pregnancies with premature rupture of membranes from a nationwide US obstetrics cohort (2002-2008) to local temperature. Case–crossover analyses compared daily temperature during the week preceding delivery and the day of delivery to two control periods, before and after the case period. Conditional logistic regression models calculated the odds ratio (OR) and 95% confidence intervals (CI) of preterm and term premature rupture of membranes for a 1˚C increase in temperature during the warm (May-September) and cold (October-April) season separately after adjusting for humidity, barometric pressure, ozone and particulate matter.
During the warm season, 1˚C increase during the week before delivery was associated with a 5% (95% CI: 3-6%) increased preterm premature rupture of membranes risk, and a 4% (95% CI: 3-5%) increased term premature rupture of membranes risk. During the cold season, 1˚C increase was associated with a 2% decreased risk for both preterm (95% CI: 1-3%) and term premature rupture of membranes (95% CI: 1-3%). The day-specific associations for the week before delivery were similar, but somewhat stronger for days closer to delivery.
Relatively small ambient temperature changes were associated with the risk of both preterm and term premature of membranes. Given the adverse consequences of premature rupture of membranes and concerns over global climate change, these findings merit further investigation.
Funding: This work was supported by the Intramural Research Program of the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health; including Contract No. HHSN267200603425C (Consortium on Safe Labor), Contract No. HHSN275200800002I, and Task Order No. HHSN27500008 (Air Quality and Reproductive Health). Although the NICHD cleared this manuscript for publication, it had no role in the design, conduct, or writing of this manuscript.
Acknowledgements: We thank all the participants and participating clinical centers involved in the Consortium on Safe Labor: Baystate Medical Center, Springfield, MA; Cedars-Sinai Medical Center Burnes Alllen Research Center, Los Angeles, CA; Christiana Care Health System, Newark, DE; Georgetown University Hospital, MedStar Health, Washington, DC; Indiana University Clarian Health, Indianapolis, IN; Intermountain Healthcare and the University of Utah, Salt Lake City, UT; Maimonides Medical Center, Brooklyn, NY; MetroHealth Medical Center, Cleveland, OH; University of Illinois at Chicago, Chicago, IL; University of Miami, Miami, FL; Summa Health Care, Akron, OH; and University of Texas Health Science Center at Houston, Houston, TX. We also thank the Emmes Corporation, Rockville, MD, which provided data coordination; and the Texas A&M Supercomputing Facility and the Texas Advanced Computing Center, which provided computing resources essential to completing exposure estimations in this study. This research had been approved by IRB from all participating institutions.
The authors also wish to thank Dr. Enrique Schisterman for his expert advice on the case-crossover design.
Conflicts of interest: The authors have declared no actual or potential conflict of interest.
Data availability: The data of this study are currently not publicly available. A data use agreement is required and can be obtained from the corresponding author.
*Corresponding author: Pauline Mendola, PhD, Epidemiology Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, NIH, 6710B Rockledge Drive Room 3119, MSC 7004, Bethesda, MD 20892, Phone: 301-496-5267, Mobile: 301-905-6118, Fax: 301-402-2084, Email: email@example.com
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