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Role of Autonomic Reflex Arcs in Cardiovascular Responses to Air Pollution Exposure
Citation:
Perez, C., M. Hazari, AND A. Farraj. Role of Autonomic Reflex Arcs in Cardiovascular Responses to Air Pollution Exposure. Cardiovascular Toxicology. Humana Press Incorporated, Totowa, NJ, 15(1):69-78, (2015).
Impact/Purpose:
Our understanding of the mechanisms underlying air pollution-induced cardiovascular dysfunction has increased substantially since the first epidemiological studies discovered a clear link between PM exposure and increased cardiovascular morbidity/mortality. While multiple theories have been proposed, there are three widely-accepted hypothesized mechanisms of action that overlap among gaseous and particulate pollutants, including systemic inflammation-induced vascular dysfunction, direct effects of PM constituents, and autonomic dysfunction. While evidence exists for all three mechanisms, changes in cardiac autonomic tone are often the most immediate consequences of air pollution exposure and involve several different reflex arcs. These include pulmonary pathways that respond to sensory activation/irritation, baroreceptor reflexes that respond to changes in blood pressure, and chemoreceptor-initiated reflex responses to changes in pCO2, pO2, pH, and temperature. Given the growing interest in mechanisms that mediate acute cardiovascular effects of air pollution, this review will discuss (1) the impacts of autonomic modulation on cardiovascular function, (2) evidence linking these three prominent autonomic reflex arcs to the cardiovascular effects associated with exposure to air pollution, and (3) how these responses are integrated. Increased understanding of the mechanisms that mediate adverse cardiovascular effects of air pollution will help to reduce uncertainty in standard setting and facilitate assessment of risk associated with exposure to specific air sheds.
Description:
The body responds to environmental stressors by triggering autonomic reflexes in the pulmonary receptors, baroreceptors, and chemoreceptors to maintain homeostasis. Numerous studies have shown that exposure to various gases and airborne particles can alter the functional outcome of these reflexes, particularly with respect to the cardiovascular system. Modulation of autonomic neural input to the heart and vasculature following direct activation of sensory nerves in the respiratory system, elicitation of oxidative stress and inflammation, or through other mechanisms is one of the primary ways that exposure to air pollution affects normal cardiovascular function. Any homeostatic process that utilizes the autonomic nervous system to regulate organ function might be affected. Thus, air pollution and other inhaled environmental irritants have the potential to alter both local airway function and baro- and chemoreflex responses, which modulate autonomic control of blood pressure and detect concentrations of key gases in the body. While each of these reflex pathways causes distinct responses, the systems are heavily integrated and communicate through overlapping regions of the brainstem to cause global effects. This short review summarizes the function of major pulmonary sensory receptors, baroreceptors, and carotid body chemoreceptors and discusses the impacts of air pollution exposure on these systems.
