Association of outdoor temperature with lung function in a temperate climate.

Acute exposure to cold dry air is a trigger of bronchoconstriction, but little is known about how daily outdoor temperature influences lung function.We investigated associations of temperature from a model using satellite remote sensing data with repeated measures of lung function among 5896 participants of the Framingham Heart Study Offspring and Third Generation cohorts residing in the Northeastern US. We further tested if temperature modified previously reported associations between pollution and lung function. We constructed linear mixed-effects models, and assessed departures from linearity using penalised splines.In fully adjusted linear models, 1-, 2- and 7-day average temperatures were all associated with lower lung function: each 5°C higher previous-week temperature was associated with a 20 mL lower (95% CI -34---6) forced expiratory volume in 1 s. There was significant effect modification by season: negative associations of temperature and lung function were present in winter and spring only. Negative associations between previous-day fine particulate matter and lung function were present during unseasonably warm but not unseasonably cool days, with a similar pattern for other pollutants.We speculate that temperature-related differences in lung function may be explained by behavioural changes on relatively warm days, which may increase outdoor exposures.
Competing Interests: Conflict of interest: M.B. Rice reports grants from the American Thoracic Society Foundation, American Lung Association and National Institutes of Environmental Health Sciences, during the conduct of the study; and she is the vice chair of the American Thoracic Society's Environmental Health Policy Committee. Conflict of interest: W. Li has nothing to disclose. Conflict of interest: E.H. Wilker reports grants from the National Institutes of Health and US Environmental Protection Agency, during the conduct of the study. Conflict of interest: D.R. Gold reports grants from the National Institutes of Health and US Environmental Protection Agency, during the conduct of the study. Conflict of interest: J. Schwartz has nothing to disclose. Conflict of interest: A. Zanobetti reports grants from the National Institutes of Health, US Environmental Protection Agency and Health Effect Institute, during the conduct of the study. Conflict of interest: P. Koutrakis reports a grant from US Environmental Protection Agency (RD-835872-01), during the conduct of the study. Conflict of interest: I. Kloog has nothing to disclose. Conflict of interest: G.R. Washko reports grants from the National Institutes of Health and BTG Interventional Medicine, grants and other support from Boehringer Ingelheim and Janssen Pharmaceuticals, other support from Genentech, Quantitative Imaging Solutions, PulmonX, Regeneron, ModoSpira, Toshiba and GlaxoSmithKline, outside the submitted work; G.R. Washko's spouse works for Biogen, which is focused on developing therapies for fibrotic lung disease. Conflict of interest: G.T. O'Connor reports personal fees from AstraZeneca and grants from Janssen Pharmaceuticals, outside the submitted work. Conflict of interest: M.A. Mittleman reports grants from the National Institutes of Health and US Environmental Protection Agency, during the conduct of the study.
(Copyright ©ERS 2019.)