Effects of PM2.5 emissions from household fuel combustion on biomarkers and pulmonary function in rural areas of Fenwei Plain, China

Rural household solid fuel combustion poses serious health risks in China. This study investigated the effects of PM2.5 and its organic carbon (OC) and elemental carbon (EC) emissions from various solid fuel combustion on biomarkers (i.e., interleukin-6 [IL-6], 8-hydrox-2 '-deoxyguanosine [8-OHdG], and vascular endothelial growth factor [VEGF]) in human urine (u) and saliva (s) as well as on lung function. A total of 148 villagers burned various solid fuels (i.e., clean briquette coal, raw coal chunk, and biomass) in rural areas of Fenwei Plain in China were selected. The biomass group demonstrated the highest u-IL-6, s-IL-6, and s-8-OHdG levels, which were 1.2-3.1 times those of coal groups, whereas the clean briquette coal group exhibited the highest u-8-OHdG, and u-VEGF levels. In linear regression controlled for variables, a 1 g kg-1 increase in PM2.5 emission factor (EF) resulted in a decline in u-VEGF levels by 0.553 mu g mol-1 UCr and increases in s-IL-6 and s-8-OHdG levels by 0.119 and 0.545 mu g mol-1 UCr, respectively. A 1 g kg -1 increase in OC EF was associated with the upregulation of s-IL-6 and s-8-OHdG levels by 0.187 and 14.421 pg mL-1, respectively, a 1 g kg -1 increase in EC EF led to an increase in s-IL-6 by 0.354 pg mL-1. No significant differences in pulmonary function were observed among the three groups, nor did PM2.5 and its OC and EC significantly affect lung function. Through noninvasive tests, this study provided evidence on the effect of PM2.5 emitted from household fuel combustion emissions on human inflammation and oxidative stress responses.