association of particulate air pollution and secondhand smoke on endothelium-dependent brachial artery dilation in healthy children

association of particulate air pollution and secondhand smoke on endothelium-dependent brachial artery dilation in healthy children

;Mohammad Hashemi;Mohammad Reza Afshani;Marjan Mansourian;Parinaz Poursafa;Roya Kelishadi
2017 ieee international conference on communication, networks and satellite, comnetsat 2017 - proceedings 2012 Vol. 17 pp. 317-321
242
hashemi2012journalassociation

Abstract

Background: This study aimed to determine the association of particulate matters with endothelial function, measured by flow mediated dilation (FMD) of brachial artery, in children with or without exposure to secondhand smoke. Methods: This cross-sectional study was conducted from January to March 2011 in Isfahan, which is the second large and air-polluted city in Iran. The areas of the city with lowest and highest air pollution were determined, and in each area, 25 prepubescent boys with or without exposure to daily tobacco smoke in home were selected, i.e. 100 children were studied in total. Results: FMD was significantly smaller in those living in high-polluted area and those exposed to secondhand smoke. Multiple linear regression analysis, adjusted for age and body mass index, showed that both passive smoking status and living area in terms of particulate air pollution were effective determinants of the brachial artery diameter. The standardized coefficient of passive smoking status was –0.36 (SD = 0.09, P < 0.0001) showing negative association with percent increase in FMD. Likewise, the percent increase in brachial artery diameter was lower in passive smoker children. Similar relationship was documented for PM 10 concentration with a regression coefficient of –0.32 (SD = 0.04, P < 0.0001). Without considering passive smoking variable, PM 10 concentration has significant independent effect on FMD level. Conclusion: Our findings provide evidence on the association of environmental factors on endothelial dysfunction from early life. Studying such associations among healthy children may help identify the underlying mechanisms. The clinical implications of environmental factors on early stages of atherosclerosis should be confirmed in longitudinal studies.

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