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Effects of Temperature and Relative Humidity on DNA Methylation

Bind, Marie-Abelea,b; Zanobetti, Antonellaa; Gasparrini, Antonioc; Peters, Annettea,d; Coull, Brentb; Baccarelli, Andreaa; Tarantini, Letiziae; Koutrakis, Petrosa; Vokonas, Pantelf; Schwartz, Joela

doi: 10.1097/EDE.0000000000000120

Background: Previous studies have found relationships between DNA methylation and various environmental contaminant exposures. Associations with weather have not been examined. Because temperature and humidity are related to mortality even on non-extreme days, we hypothesized that temperature and relative humidity may affect methylation.

Methods: We repeatedly measured methylation on long interspersed nuclear elements (LINE-1), Alu, and 9 candidate genes in blood samples from 777 elderly men participating in the Normative Aging Study (1999–2009). We assessed whether ambient temperature and relative humidity are related to methylation on LINE-1 and Alu, as well as on genes controlling coagulation, inflammation, cortisol, DNA repair, and metabolic pathway. We examined intermediate-term associations of temperature, relative humidity, and their interaction with methylation, using distributed lag models.

Results: Temperature or relative humidity levels were associated with methylation on tissue factor (F3), intercellular adhesion molecule 1 (ICAM-1), toll-like receptor 2 (TRL-2), carnitine O-acetyltransferase (CRAT), interferon gamma (IFN-γ), inducible nitric oxide synthase (iNOS), and glucocorticoid receptor, LINE-1, and Alu. For instance, a 5°C increase in 3-week average temperature in ICAM-1 methylation was associated with a 9% increase (95% confidence interval: 3% to 15%), whereas a 10% increase in 3-week average relative humidity was associated with a 5% decrease (−8% to −1%). The relative humidity association with ICAM-1 methylation was stronger on hot days than mild days.

Conclusions: DNA methylation in blood cells may reflect biological effects of temperature and relative humidity. Temperature and relative humidity may also interact to produce stronger effects.

Supplemental Digital Content is available in the text.

From the aDepartment of Environmental Health, Harvard School of Public Health, Boston, MA; bDepartment of Biostatistics, Harvard School of Public Health, Boston, MA; cDepartment of Medical Statistics, London School of Hygiene and Tropical Medicine, London, United Kingdom; dInstitute of Epidemiology, Helmholtz Zentrum München German Research Center for Environmental Health, Neuherberg, Germany; eCenter of Molecular and Genetic Epidemiology, University of Milan, Milan, Italy; and fVA Boston Healthcare System and the Department of Medicine, Boston University School of Medicine, Boston, MA.

Submitted 12 June 2013; accepted 31 December 2013; posted 7 May 2014.

The authors report no conflicts of interest.

This work was supported by the following US EPA grants RD-827353 and RD-832416; NIEHS grants RO1-ES015172, 2RO1-ES015172, R21 AG0H0027, ES014663, ES00002, and Clean Air Act grant RD83479701, and by a grant from Medical Research Council-UK G1002296. The Normative Aging Study is supported by the Cooperative Studies Program/Epidemiology Research and Information Center of the U.S. Department of Veterans Affairs and is a component of the Massachusetts Veterans Epidemiology Research and Information Center, Boston, MA.

Supplemental digital content is available through direct URL citations in the HTML and PDF versions of this article ( This content is not peer-reviewed or copy-edited; it is the sole responsibility of the author.

Correspondence: Marie-Abele Bind, Department of Environmental Health, 401 Park Drive, Landmark Center, Suite 415, Boston, MA 02115. E-mail:

© 2014 by Lippincott Williams & Wilkins, Inc