Abstract

BACKGROUND AND AIM: Although the biological mechanisms remain uncertain, non-optimal air temperatures have been associated with cardiovascular mortality. Dietary intake of omega-3 fatty acids (n-3 FA) has been correlated with cardiovascular health. This panel study aimed to examine whether n-3 FA would modify associations between ambient air temperature and autonomic function measured by changes in heart rate variability (HRV). METHODS: Six-two healthy adults (age: 25–55 years) residing in North Carolina, U.S. were recruited into low (n=28) and high (n=34) omega-3 groups based on dietary n-3 FA intake and blood levels of omega-3 index. Each participant underwent 3-5 examinations separated by at least one week between October 2016 and September 2019. HRV was measured using 5-minute resting electrocardiography recorded at each examination. Daily meteorological data were obtained from a central air monitoring station. We applied mixed-effects models with a distributed lag non-linear approach to assess associations between air temperature (lag 0-6 days) and HRV stratified by omega-3 levels. RESULTS:We observed inverse U-shape relationships between HRV indices and temperature in the low omega-3 group, which were significant for high temperatures. No associations were observed in the high omega-3 group. An increase from 10 °C (approximate optimum temperature) to the 95th percentile (28 °C) of temperature was associated with decreases in standard deviation of NN intervals [SDNN, -40.6% (95% CI: -63.7, -2.7)], root mean square of successive RR interval differences [RMSSD, -63.9% (95% CI: -82.7, -24.8)], and high-frequency power [HF, -82.7% (95% CI: -97.2, 5.2)]. The between-group differences were significant for RMSSD and HF. CONCLUSIONS:Non-optimal air temperatures, especially high temperatures were associated with decreased parasympathetic autonomic function that might explain the temperature effects on cardiovascular events. In addition, n-3 FA intake was associated with beneficial effects on autonomic function against non-optimal temperatures. This abstract does not necessarily reflect EPA policy. KEYWORDS: Cardiovascular diseases, Climate, Environmental epidemiology, Short-term exposure, Temperature

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