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Mild sleep disruption exaggerates cardiovascular responses to eucalyptus wood smoke in rats
Citation:
Martin, W., Mette C. Schladweiler, W. Oshiro, C. King, M. Valdez, C. Miller, D. Freeborn, Ian Gilmour, U. Kodavanti, Prasada Rao Kodavanti, M. Hazari, AND A. Farraj. Mild sleep disruption exaggerates cardiovascular responses to eucalyptus wood smoke in rats. Annual Meeting of the Society of Toxicology- Virtual, NA, NA-Virtual, March 14 - 26, 2021.
Impact/Purpose:
Poor sleep, which impacts millions of people worldwide, may be a previously undescribed factor that modifies responsiveness to air pollution. Defining the magnitude of this factor as it relates to its potential interactive effects with air pollution may help identify factors other than ambient air pollutant concentrations that determine adversity and may in the long run help reduce uncertainty in standard setting.
Description:
Cardiovascular (CV) disease remains the paramount cause of premature death worldwide, and its incidence and progression are influenced heavily by exposure to environmental agents as well as hereditary and lifestyle factors. As a lifestyle factor, poor sleep status is associated with increased CV morbidity and mortality and may exaggerate sensitivity to non-specific stressors of the cardiovascular system, including air pollution, further increasing CV risk. To probe the role that sleep status may play in exacerbating CV responses to air pollution we designed a study to evaluate the impact that mild sleep loss in the form of gentle handling (5 s every 30 min for 5 h) may exert on the CV responses to eucalyptus wood smoke (1 mg/m3 for 1h) in adult, male SD rats. We previously demonstrated that gentle handling disrupts sleep, as evidenced by increased locomotor activity to levels that mirrored those of the preceding wake period, and by increases in systolic and diastolic blood pressure (BP), heart rate (HR), and body temperature. Each wood smoke exposure in the current study occurred immediately following the handling period 2x/week for 4 weeks and CV responses (the electrocardiogram, HR, BP, baroreceptor reflex, HRV, etc.) were monitored using radiotelemetry for the duration of the study. Preliminary data indicates wood smoke exposure significantly increased HR (+58 bpm, p=0.0135), systolic BP (+11 mmHg, p=0.0373), diastolic BP (+ 10 mmHg, p=0.0163), and decreased QA interval (an indirect, inverse metric of cardiac contractility; +4 ms, p=0.0027) among the sleep disrupted animals, but not the rested controls beginning after the first exposure. Interestingly, this difference was most pronounced as the rats transitioned into their active/awake period (lights off), an interval during which ischemic CV events occur disproportionately in humans (e.g., morning stroke risk). These results suggest that mild sleep loss may transiently open a window of increased sensitivity to the harmful CV effects of environmental stressors such as air pollution, further implicating sleep loss as an important risk factor for CV disease. (This abstract does not reflect U.S. E.P.A policy).