Short-term effects of air temperature and mitochondrial DNA lesions within an older population.

BACKGROUND: Previous studies have linked both extreme and sub-optimal air temperature to cardiopulmonary morbidity and mortality, especially in older individuals. However, the underlying mechanisms are yet to be determined.

OBJECTIVES: We hypothesized that short-term increases in air temperature may induce blood mitochondrial DNA (mtDNA) lesions in older individuals, which could contribute to temperature-related pathogenesis.

METHODS: We repeatedly measured mtDNA lesions in blood samples from 654 participants in the Normative Aging Study from 1999 to 2013 (1142 observations) by quantitative long-amplicon polymerase chain reaction assay. Hourly temperature data were obtained from the Boston Logan Airport weather station (located approximately 12km from the clinical site). We calculated 2-, 7-, and 14-day moving averages of 24-hour mean and 24-hour variability of temperature. We fit covariate-adjusted linear-mixed models accounting for repeated measures to evaluate the association between short-term increases in mean and variability of temperature with mtDNA lesions within each season.

RESULTS: Interquartile increases in 7- and 14-day moving averages of 24-hour mean temperature in summer were associated with a 0.17 (95% CI: 0.07, 0.27; p=0.0007) and 0.21 (95% CI: 0.10, 0.32; p=0.0001) increase in the number of mtDNA lesions per 10kb, respectively. Results were similar when we further adjusted for temperature variability. We also observed significant associations between increases in temperature variability and mtDNA lesions independent of mean air temperature. An interquartile range increase in the 7-day moving average of 24-hour standard deviation in summer was associated with a 0.19 (95% CI: 0.07, 0.31; p=0.0023) increase in the number of mtDNA lesions per 10kb.

CONCLUSIONS: Short-term exposure to higher mean air temperature was associated with increased mtDNA lesions in older adults, supporting the hypothesis that sub-optimal meteorological conditions may induce pathophysiological responses among susceptible populations.