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Neuroendocrine regulation of air pollution health effects: Emerging insights
Citation:
Snow, S., A. Henriquez, D. Costa, AND U. Kodavanti. Neuroendocrine regulation of air pollution health effects: Emerging insights. TOXICOLOGICAL SCIENCES. Society of Toxicology, RESTON, VA, 164(1):9-20, (2018). https://doi.org/10.1093/toxsci/kfy129
Impact/Purpose:
Although the mechanism(s) by which the lung communicates with the brain following air pollutant exposure remains to be fully elucidated, new studies demonstrate that air pollutants activate the neuroendocrine stress pathways involving the SAM and HPA axes, which produce widespread metabolic and innate immune changes in multiple organs.
Description:
Air pollutant exposure is linked to cardiopulmonary diseases, diabetes, metabolic syndrome, neurobehavioral conditions, and reproductive abnormalities. As such, there is growing investment in understanding how pollutants encountered by the lung might induce effects in distant organs. New evidence has recently emerged which implicates the role of neuroendocrine sympathetic-adrenal-medullary (SAM) and hypothalamus-pituitary-adrenal (HPA) stress axes in mediating a wide array of systemic and pulmonary effects. The systemic metabolic and immune effects of pollutants resemble those induced during the classic “fight-or-flight” homeostatic response. Our recent studies using ozone exposure as a prototypical air pollutant demonstrate that lung injury/inflammation and metabolic effects in the liver, pancreas, adipose tissues, and muscle results in increases in circulating adrenal-derived stress hormones (epinephrine and cortisol/corticosterone). When stress hormones are depleted by adrenalectomy in rats, most ozone effects, including lung injury/inflammation are diminished. Animals treated with antagonists for adrenergic and glucocorticoid receptors show depletion of the pulmonary and systemic effects of ozone, while treatment with agonists restore and exacerbate the ozone-induced injury/inflammation phenotype, implying the role of neuroendocrine activation. The neuroendocrine system is critical for normal homeostasis and allostatic activation; however, chronic exposure to stressors may lead to increases in allostatic load. Although autonomic sensory pathways from the lung to brain centers are well characterized, the role of neuroendocrine activation in mediating air pollution immune and metabolic effects are not well understood. Moreover, since the same responses are linked to both chemical and non-chemical stressors, the interactive influence of air pollutants, lifestyle, and environmental factors requires further study.
