Non-chemical stressors affect behavioral function and alter the cardiopulmonary response to acute extreme heat and wildfire smoke exposures
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Extreme heat events from climate change are classified as the leading cause of weather-related death in the United States and are associated with cardiovascular morbidity and mortality. The American Heart Association has also released a scientific statement describing the importance of living conditions on cardiovascular health and well-being and emphasized the impact of the broader physical and social environment. Thus, increased temperatures due to climate change and lack of housing enrichment represent two of the most serious non-chemical stressors facing large sectors of the population in the United States. Epidemiological evidence has shown that socio-economic status and psychosocial stress might act as modifying factors of the cardiopulmonary response to climate change-related phenomenon like extreme heat and wildfire smoke exposures. This represents a potentially hazardous interaction of non-chemical and chemical stressors on the body and its ability to adapt and respond to subsequent insults. Thus, this presentation will describe the impact of housing (i.e., depleted/increased psychosocial stress v. enriched) on behavioral outcomes in C57BL6/J mice, both in normal and high ambient living temperatures, and cardiovascular changes following a single flaming eucalyptus wildfire smoke exposure. Moreover, novel data on how housing/stress can alter the physiological response to acute extreme heat exposures will also be presented. Results from these studies indicate that increased ambient temperatures and extreme heat exposures contribute to altered cardiopulmonary, autonomic, arrhythmogenesis, and behavioral function, including measures of spatial learning, locomotor activity, and anxiety-like behavior. These outcomes are further impacted by housing/stress conditions that appear to be modifying the expression of genes important in environmental and heat sensing (specifically transient receptor potential vanilloid 1). In sum, this research has the potential to provide information on previously uncharacterized biological mechanisms driving the effects of non-chemical stressors (i.e., depleted housing/stress and heat) and their ability to modify the response to chemical stressors and the progression of underlying disease. (This abstract does not reflect EPA policy)