Huichu Li1, Jing Cai1, Renjie Chen1, Zhuohui Zhao1, Zhekang Ying1, Lin Wang1, Jianmin Chen1, Ke Hao1, Patrick L Kinney1, Honglei Chen1, Haidong Kan2. 1. From School of Public Health, Key Lab of Public Health Safety of the Ministry of Education and Key Lab of Health Technology Assessment of the Ministry of Health, Fudan University, Shanghai, China (H.L., J.C., R.C., Z.Z., Z.Y., H.K.); Shanghai Key Laboratory of Atmospheric Particle Pollution and Prevention (LAP3), Fudan University, China (J.C., R.C., Z.Y., L.W., J.C.); Department of Genetics and Genomics Sciences, Icahn School of Medicine at Mount Sinai, New York, NY (K.H.); The Icahn Institute for Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, NY (K.H.); Department of Respiratory Medicine, Shanghai Tenth People's Hospital, Tongji University, China (K.H.); Department of Environmental Health, School of Public Health, Boston University, MA (P.L.K.); Department of Epidemiology and Biostatistics, College of Human Medicine, Michigan State University, East Lansing (H.C.); and Key Laboratory of Reproduction Regulation of NPFPC, SIPPR, IRD, Fudan University, Shanghai, China (H.K.). 2. From School of Public Health, Key Lab of Public Health Safety of the Ministry of Education and Key Lab of Health Technology Assessment of the Ministry of Health, Fudan University, Shanghai, China (H.L., J.C., R.C., Z.Z., Z.Y., H.K.); Shanghai Key Laboratory of Atmospheric Particle Pollution and Prevention (LAP3), Fudan University, China (J.C., R.C., Z.Y., L.W., J.C.); Department of Genetics and Genomics Sciences, Icahn School of Medicine at Mount Sinai, New York, NY (K.H.); The Icahn Institute for Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, NY (K.H.); Department of Respiratory Medicine, Shanghai Tenth People's Hospital, Tongji University, China (K.H.); Department of Environmental Health, School of Public Health, Boston University, MA (P.L.K.); Department of Epidemiology and Biostatistics, College of Human Medicine, Michigan State University, East Lansing (H.C.); and Key Laboratory of Reproduction Regulation of NPFPC, SIPPR, IRD, Fudan University, Shanghai, China (H.K.). kanh@fudan.edu.cn.
Abstract
BACKGROUND:Exposure to ambient particulate matter (PM) is associated with a number of adverse health outcomes, but potential mechanisms are largely unknown. Metabolomics represents a powerful approach to study global metabolic changes in response to environmental exposures. We therefore conducted this study to investigate changes in serum metabolites in response to the reduction of PM exposure among healthy college students. METHODS: We conducted a randomized, double-blind crossover trial in 55 healthy college students in Shanghai, China. Real and sham air purifiers were placed in participants' dormitories in random order for 9 days with a 12-day washout period. Serum metabolites were quantified by using gas chromatography-mass spectrometry and ultrahigh performance liquid chromatography-mass spectrometry. Between-treatment differences in metabolites were examined using orthogonal partial least square-discriminant analysis and mixed-effect models. Secondary outcomes include blood pressure, corticotropin-releasing hormone, adrenocorticotropic hormone, insulin resistance, and biomarkers of oxidative stress and inflammation. RESULTS: The average personal exposure to PMs with aerodynamic diameters ≤2.5 μm was 24.3 μg/m3 during the real purification and 53.1 μg/m3 during the sham purification. Metabolomics analysis showed that higher exposure to PMs with aerodynamic diameters ≤2.5 μm led to significant increases in cortisol, cortisone, epinephrine, and norepinephrine. Between-treatment differences were also observed for glucose, amino acids, fatty acids, and lipids. We found significantly higher blood pressure, hormones, insulin resistance, and biomarkers of oxidative stress and inflammation among individuals exposed to higher PMs with aerodynamic diameters ≤2.5 μm. CONCLUSIONS: This study suggests that higher PM may induce metabolic alterations that are consistent with activations of the hypothalamus-pituitary-adrenal and sympathetic-adrenal-medullary axes, adding potential mechanistic insights into the adverse health outcomes associated with PM. Furthermore, our study demonstrated short-term reductions in stress hormone following indoor air purification. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT02712333.
RCT Entities:
BACKGROUND: Exposure to ambient particulate matter (PM) is associated with a number of adverse health outcomes, but potential mechanisms are largely unknown. Metabolomics represents a powerful approach to study global metabolic changes in response to environmental exposures. We therefore conducted this study to investigate changes in serum metabolites in response to the reduction of PM exposure among healthy college students. METHODS: We conducted a randomized, double-blind crossover trial in 55 healthy college students in Shanghai, China. Real and sham air purifiers were placed in participants' dormitories in random order for 9 days with a 12-day washout period. Serum metabolites were quantified by using gas chromatography-mass spectrometry and ultrahigh performance liquid chromatography-mass spectrometry. Between-treatment differences in metabolites were examined using orthogonal partial least square-discriminant analysis and mixed-effect models. Secondary outcomes include blood pressure, corticotropin-releasing hormone, adrenocorticotropic hormone, insulin resistance, and biomarkers of oxidative stress and inflammation. RESULTS: The average personal exposure to PMs with aerodynamic diameters ≤2.5 μm was 24.3 μg/m3 during the real purification and 53.1 μg/m3 during the sham purification. Metabolomics analysis showed that higher exposure to PMs with aerodynamic diameters ≤2.5 μm led to significant increases in cortisol, cortisone, epinephrine, and norepinephrine. Between-treatment differences were also observed for glucose, amino acids, fatty acids, and lipids. We found significantly higher blood pressure, hormones, insulin resistance, and biomarkers of oxidative stress and inflammation among individuals exposed to higher PMs with aerodynamic diameters ≤2.5 μm. CONCLUSIONS: This study suggests that higher PM may induce metabolic alterations that are consistent with activations of the hypothalamus-pituitary-adrenal and sympathetic-adrenal-medullary axes, adding potential mechanistic insights into the adverse health outcomes associated with PM. Furthermore, our study demonstrated short-term reductions in stress hormone following indoor air purification. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT02712333.
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