Jian Hou1, Yanying Duan2, Xiaotian Liu1, Ruiying Li1, Runqi Tu1, Mingming Pan1, Xiaokang Dong1, Zhenxing Mao1, Wenqian Huo1, Gongbo Chen3, Yuming Guo4, Shanshan Li5, Chongjian Wang6. 1. Department of Epidemiology and Biostatistics, College of Public Health, Zhengzhou University, Zhengzhou, Henan, China. 2. Department of Occupational and Environmental Health, Xiangya School of Public Health, Central South University, Changsha 410078, China. 3. Department of Global Health, School of Health Sciences, Wuhan University, Wuhan, China. 4. Department of Epidemiology and Biostatistics, College of Public Health, Zhengzhou University, Zhengzhou, Henan, China; Department of Epidemiology and Preventive Medicine, School of Public Health and Preventive Medicine, Monash University, Melbourne, Australia. 5. Department of Epidemiology and Preventive Medicine, School of Public Health and Preventive Medicine, Monash University, Melbourne, Australia. Electronic address: Shanshan.Li@monash.edu. 6. Department of Epidemiology and Biostatistics, College of Public Health, Zhengzhou University, Zhengzhou, Henan, China. Electronic address: tjwcj2008@zzu.edu.cn.
Abstract
BACKGROUND: Long-term exposure to air pollutants relate to increase risk of cardiovascular diseases that may be partially attributable to platelet dysfunction. Physical activity (PA) may attenuate inflammation to modulate platelet function. Thus, this study aimed to evaluate associations of air pollutants and PA with platelet traits of cardiovascular risk. METHODS: A total of 31,282 participants were obtained from the Henan Rural Cohort (n = 39,259). The concentrations of particulate matter (PM) (PM with an aerodynamic diameter ≤1.0 μm (PM1), ≤2.5 μm (PM2.5), or ≤10 μm (PM10)) and nitrogen dioxide (NO2) were evaluated by using a spatiotemporal model incorporated into satellites data. Independent and combined effects of air pollutants and PA on platelet traits were analyzed by linear mixed models. RESULTS: Positive associations of PM1, PM2.5, PM10 and NO2 with platelet indices (mean platelet volume (MPV), platelet distribution width (PDW) and platelet large cell ratio (P-LCR), the MPV to platelet counts (PLT) ratio (MPVP)) were observed, whereas negative associations of PM10 and NO2 with PLT or plateletcrit (PCT) were observed; negative interaction effects of PM2.5 PM10 and NO2 and PA on MPV, PDW or P-LCR were found; negative interaction effects of PM1, PM2.5 and PM10 and PA on PCT were observed. CONCLUSIONS: Long-term exposure to air pollutants were related to increase platelet size and these associations were attenuated by increased PA, implying that PA is a costless and affordable method to decrease adverse effects on platelet traits in relation to air pollutants.
BACKGROUND: Long-term exposure to air pollutants relate to increase risk of cardiovascular diseases that may be partially attributable to platelet dysfunction. Physical activity (PA) may attenuate inflammation to modulate platelet function. Thus, this study aimed to evaluate associations of air pollutants and PA with platelet traits of cardiovascular risk. METHODS: A total of 31,282 participants were obtained from the Henan Rural Cohort (n = 39,259). The concentrations of particulate matter (PM) (PM with an aerodynamic diameter ≤1.0 μm (PM1), ≤2.5 μm (PM2.5), or ≤10 μm (PM10)) and nitrogen dioxide (NO2) were evaluated by using a spatiotemporal model incorporated into satellites data. Independent and combined effects of air pollutants and PA on platelet traits were analyzed by linear mixed models. RESULTS: Positive associations of PM1, PM2.5, PM10 and NO2 with platelet indices (mean platelet volume (MPV), platelet distribution width (PDW) and platelet large cell ratio (P-LCR), the MPV to platelet counts (PLT) ratio (MPVP)) were observed, whereas negative associations of PM10 and NO2 with PLT or plateletcrit (PCT) were observed; negative interaction effects of PM2.5 PM10 and NO2 and PA on MPV, PDW or P-LCR were found; negative interaction effects of PM1, PM2.5 and PM10 and PA on PCT were observed. CONCLUSIONS: Long-term exposure to air pollutants were related to increase platelet size and these associations were attenuated by increased PA, implying that PA is a costless and affordable method to decrease adverse effects on platelet traits in relation to air pollutants.