Household air pollution (HAP) from solid biomass fuel and lung inflammation: An exposure study in rural high altitude households of Nepal.

Abstract

Background/Aim Biomass smoke exposure is the leading cause of morbidity and mortality worldwide, disproportionately affecting low and middle income countries. The domestic smoke exposure pattern and its pulmonary effect have not been explored in high altitude Himalayan regions. This study aimed to (i) monitor the status of HAP in homes using biomass fuel in one rural high altitude (4000 m) Nepalese village and (ii) assess the short term effect of exposure on lung inflammation.Methods Real-time cooking period exposure to particulate matter (PM2.5) and carbon monoxide (CO) was monitored in 14 households specifically 9 households with improved cook stove (ICS) and 5 households with traditional cook stove (TCS). Simultaneously with the exposure monitoring, biomass smoke sample was collected in cell and tissue culture media (DMEM). The samples were used to stimulate ex vivo human lung tissue in a short term exposure tissue culture model and pro-inflammatory cytokines were measured in the resulting culture supernatant.Results The cooking period average PM2.5 and CO concentration were significantly reduced from 746 µg/m3 (95% CI: 350, 1142) to 91.2 µg/m3 (95% CI: 37.3, 145.2) and 12.56 ppm (95%CI: 6.7, 18.4) to 2.6 ppm (95% CI: 1.74, 3.6) among household using TCS and ICS respectively. A range of pro-inflammatory cytokines were detected with the fold stimulation of ~2 fold for IL-8 and IL-6, ~2.5 fold for IL-1β and ~3.5 fold for TNF-α. However, no significant variations in the levels of these cytokines were observed among the samples from two stove designs.Conclusions The increased level of inflammatory cytokines from lung tissue revealed short term exposure to high levels of indoor pollutants elicits marked airway inflammation. The people using ICS in this region are exposed to lower concentration of indoor pollutant; however remain likely to be at risk of developing airway inflammation despite ownership of ICS.