Abstract Body (Do not enter title and authors here): Introduction: Excessive deaths due to heat waves are overwhelmingly cardiovascular in origin. However, many previous studies only consider ambient temperature, which fails to capture the actual heat stress experienced by populations. Hot weather can interfere with a variety of biological processes including the promotion of systemic inflammatory responses, which play a critical role in the progression of cardiovascular disease. Our objective was to assess how short-term heat exposures are related to markers of inflammation and the immune response using physiologically-relevant heat metrics.
Methods: Adult participants, aged 20-70 years, were recruited from a neighborhood in Louisville, KY during the summer months of 2018 and 2019. Circulating cytokines and immune cells were measured in 624 participants at baseline. Heat metrics, including temperature, net effective temperature, and Universal Thermal Climate Index (UTCI) were calculated as the 24hr mean on the day of participants’ clinical visit. Linear regression models were used to estimate associations between heat metrics and each biomarker, adjusting for socio-demographic and behavioral factors.
Results: Participants were predominantly female (59%) and White (77%), with an average age of 49.5 years. The median daily temperature during study visits was 24.5 degrees C (IQR=3.8 degrees). The mean daily UTCI was positively associated with total circulating monocytes (4.2% per IQR; 95% CI: 0.3, 8.3), and classical monocytes (CD14^hiCD16^lo), while nonclassical monocytes (CD14^loCD16^hi) displayed a negative association. We also observed positive associations with eosinophils 9.5% per IQR (95% CI: 0.6, 19.1) and Natural Killer T-Cells 9.9% per IQR (95% CI:2.8, 17.5), and a negative association with B-cells -6.8% per IQR (95% CI: -12.1, -1.1). In our cytokine analysis, UTCI was positively associated with TNF-alpha 7.0% per IQR (95% CI:2.8, 11.4) as well as IL-5 and MIP-1α. Similar associations were observed using daily temperature and other heat metrics.
Conclusion: Short-term heat exposure may trigger an inflammatory response characterized by innate immune activation as evidenced by our results of higher total monocytes, classical monocytes, and TNF-alpha. Moreover, short-term heat exposure may impair adaptive immune response. These results suggest that exposure to high temperatures may increase susceptibility to infectious agents, environmental exposures, and accelerate the progression of cardiovascular disease.