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Sleep disruption increases cardiovascular of risk wildfire-related smoke inhalation in rats
Citation:
Martin, W., Mette C Schladweiler, W. Oshiro, J. Smoot, C. King, W. Williams, M. Valdez, C. Miller, D. Freeborn, Yong Ho Kim, D. Davies, Ian Gilmour, U. Kodavanti, Prasada Rao Kodavanti, M. Hazari, AND A. Farraj. Sleep disruption increases cardiovascular of risk wildfire-related smoke inhalation in rats. 2023 Annual meeting of the Society of Toxicology, Nashville, TN, March 19 - 23, 2023.
Impact/Purpose:
Physiological sleep is necessary for normal health and well-being, but nearly a third of Americans report inadequate sleep, with disproportionate impacts among the disadvantaged. Perturbations in sleep patterns, including insomnia or disrupted sleep, increase risk of atherosclerosis, stroke, and blood pressure dysregulation and increase sensitivity to environmental stressors, although sleep disruption's influence on responsiveness to air pollution is unknown. The identification of poor sleep as a modifiable factor in the cardiovascular responsiveness to air pollution, as demonstrated in this study, may uncover a previously underappreciated risk factor in the health effects of air pollution that impacts a large segment of the population. This work also identifies factors in addition to air pollutant mass concentration that determine adversity and defines a biological basis for increased cardiovascular risk, potentially helping to substantiate epidemiological findings.
Description:
Poor sleep is associated with increased cardiovascular (CV) morbidity and mortality and may exaggerate sensitivity to non-specific stressors of the CV system, including air pollution. To determine whether sleep status impacts CV responses to air pollution, we evaluated the effects of mild sleep loss in the form of gentle handling (GH; 5 s every 30 min for 5 h during rest period) on the CV responses to single or repeated (twice/week for 4 weeks) inhalation exposure to eucalyptus wood smoke (ES; 1 mg/m3 for 1h), a key wildland fire air pollution source, in 12-week-old, adult, male Sprague Dawley rats. CV function, measured using blood pressure (BP) radiotelemetry and echocardiography, was evaluated along with assessments of lung and systemic inflammation, cardiac and hypothalamic gene expression, and heart rate variability (HRV), a measure of cardiac autonomic tone. GH disrupted sleep, as evidenced by active period-like locomotor activity, increases in BP, heart rate (HR), and body temperature, and increases in hypothalamic expression of the circadian gene PER2. A single bout of sleep disruption and ES, but not either alone, increased HR and BP as rats transitioned into their active/awake period (lights off), a period that is aligned with a critical early morning stroke risk window in humans. These responses were immediately preceded by reduced HRV, indicating increased cardiac sympathetic tone. In addition, only sleep disrupted rats exposed to ES had increased HR and BP during the final handling period and had increased cardiac output and left ventricular wall thickness. Disrupted rats also had increased cardiac expression of genes related to adrenergic function and the regulation of vasoconstriction and systemic blood pressure after final ES exposure. There was little evidence of lung or systemic inflammation. These results suggest that mild sleep loss may reduce the threshold for adverse cardiovascular outcomes caused by inhaled air pollution in part by increased sympathetic activity (Abstract does not reflect U.S. E.P.A policy).