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Exposure to PM2.5 Activates Hypothalamic-Pituitary-Adrenal Axis in Mouse Models and Humans
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A2274 - Exposure to PM2.5 Activates Hypothalamic-Pituitary-Adrenal Axis in Mouse Models and Humans
Author Block: Y. Xu1, M. Chen2, J. Zhou3, H. Li1, X. Zhang2, S. Liang2, X. Qin2, L. Qiu2, Q. Cao2, H. Kan1, Z. Ying4; 1Public Health, Fudan University, Shanghai, China, 2University of Maryland School of Medicine, Baltimore, MD, United States, 3Shanghai Key Laboratory of Meteorology and Health, Shanghai, China, 4University of Maryland, Baltimore, Baltimore, MD, United States.
Rationale: Exposure to ambient fine particulate matter (PM2.5) correlates to adverse cardiometabolic effects. The underlying mechanism has not yet been fully understood. Hypothalamic-pituitary-adrenal (HPA) axis is the central stress response system that regulates cardiometabolic homeostasis and is implicated in the development of adverse health effects due to inhalation exposure to airborne pollutants. In the present study, we investigated whether exposure to ambient PM2.5 activates HPA axis. Methods: To check the acute effect of PM2.5 on HPA axis, female C57Bl/6J mice were first intratracheally instilled with different concentrations of diesel exhaust PM2.5 (DEP), and plasma was harvested in different times. To determine which components of DEP activate HPA axis, C57Bl/6J mice were intratracheally instilled with water-soluble and -insoluble fractions of DEP. For the chronic effect of PM2.5, C57Bl/6J mice were exposed to filtered air (FA) or concentrated ambient PM2.5 (CAP) for 3 months using a versatile aerosol concentration enrichment system (VACES) that was modified for long-term exposures, and their urine and hair samples were collected for HPA axis activation assessment. In addition, a human double-blind two stage crossover trial study was also carried out using air purifier as the intervention. Results: Assessments of plasma stress hormone revealed that DEP instillation dose- and time-dependently increased mouse circulating corticosterone and adrenocorticotropic hormone (ACTH) levels, strongly supporting that DEP instillation activates HPA axis. Plasma analyses showed that water-insoluble but not -soluble fraction of DEP increased circulating corticosterone and ACTH levels. Consistently, exposure to concentrated ambient PM2.5 (CAP) significantly increased mouse urine and hair corticosterone levels, corroborating the activation of HPA axis by ambient PM2.5. Furthermore, reduction in ambient PM2.5 using air purifier significantly decreased urine cortisol levels in healthy college students, suggesting that ambient PM2.5 may also activate HPA axis in humans. Conclusion: The present study demonstrates that inhalation exposure to PM2.5 activates HPA axis, implicating the latter in the development of adverse health effects due to exposure to PM2.5.
Author Block: Y. Xu1, M. Chen2, J. Zhou3, H. Li1, X. Zhang2, S. Liang2, X. Qin2, L. Qiu2, Q. Cao2, H. Kan1, Z. Ying4; 1Public Health, Fudan University, Shanghai, China, 2University of Maryland School of Medicine, Baltimore, MD, United States, 3Shanghai Key Laboratory of Meteorology and Health, Shanghai, China, 4University of Maryland, Baltimore, Baltimore, MD, United States.
Rationale: Exposure to ambient fine particulate matter (PM2.5) correlates to adverse cardiometabolic effects. The underlying mechanism has not yet been fully understood. Hypothalamic-pituitary-adrenal (HPA) axis is the central stress response system that regulates cardiometabolic homeostasis and is implicated in the development of adverse health effects due to inhalation exposure to airborne pollutants. In the present study, we investigated whether exposure to ambient PM2.5 activates HPA axis. Methods: To check the acute effect of PM2.5 on HPA axis, female C57Bl/6J mice were first intratracheally instilled with different concentrations of diesel exhaust PM2.5 (DEP), and plasma was harvested in different times. To determine which components of DEP activate HPA axis, C57Bl/6J mice were intratracheally instilled with water-soluble and -insoluble fractions of DEP. For the chronic effect of PM2.5, C57Bl/6J mice were exposed to filtered air (FA) or concentrated ambient PM2.5 (CAP) for 3 months using a versatile aerosol concentration enrichment system (VACES) that was modified for long-term exposures, and their urine and hair samples were collected for HPA axis activation assessment. In addition, a human double-blind two stage crossover trial study was also carried out using air purifier as the intervention. Results: Assessments of plasma stress hormone revealed that DEP instillation dose- and time-dependently increased mouse circulating corticosterone and adrenocorticotropic hormone (ACTH) levels, strongly supporting that DEP instillation activates HPA axis. Plasma analyses showed that water-insoluble but not -soluble fraction of DEP increased circulating corticosterone and ACTH levels. Consistently, exposure to concentrated ambient PM2.5 (CAP) significantly increased mouse urine and hair corticosterone levels, corroborating the activation of HPA axis by ambient PM2.5. Furthermore, reduction in ambient PM2.5 using air purifier significantly decreased urine cortisol levels in healthy college students, suggesting that ambient PM2.5 may also activate HPA axis in humans. Conclusion: The present study demonstrates that inhalation exposure to PM2.5 activates HPA axis, implicating the latter in the development of adverse health effects due to exposure to PM2.5.
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