Status of TNF-α and IL-6 as pro-inflammatory cytokines in exhaled breath condensate of late adolescents with asthma and healthy in the dust storm and non-dust storm conditions

Exposure to airborne particulate matter (PM) can be considered as an important risk factor for human health. Some cytokines have been recognized as the biomarkers of exposure to air pollution. Experimental studies indicate that PM exposure could be associated with inflammation. Thus, the purpose of this study was to evaluate whether the exposure to air PM is associated with biomarkers of inflammation. The specific aim of this study was to determine the correlation between airborne PM levels and IL-6 and TNF-α as airway inflammation biomarkers among two groups of late adolescents in northwest of Iran. This study included 46 subjects, comprising 23 asthmatic subjects and 23 non-asthmatic persons. Environmental PM (PM10, PM2.5 and PM1) levels were measured in dust storm and non-dust storm days during both cold and warm seasons. Following the sampling of PM, Two pro-inflammatory cytokines of IL-6 and TNF-α in exhaled breath condensate (EBC) were also determined in the EBC samples via commercial ELISA kits. Daily mean ambient air PM10, PM2.5 and PM1 concentrations during the dust storm days was 221.79, 93.13 and 25.52 μg m−3 and in non-dusty days 48.37, 18.54 and 6.1 μg m−3, respectively. Biomarkers levels were significantly (p < 0.001) higher in asthmatic students compared to the non-asthmatic subjects. EBC cytokines levels were increased in dust storm days compared to the non-dusty days (p < 0.001) and were positively correlated with different size of ambient PM concentration. Dust storm conditions can increase the pro-inflammatory cytokines and cause adverse effects on pulmonary health and lung tissue damage. [Display omitted] •We evaluated the effects of air pollution on pro-inflammatory cytokines in EBC.•Pro-inflammatory cytokines levels were increased in dust storm days.•Air pollution was associated with increased TNF-α and IL-6 levels.•Air pollutants increase inflammation, especially among in asthmatic subjects.