Assessment of the biological consequences of controlling indoor solid fuel smoke emissions in Nepal

Household air pollution (HAP) exposure and its consequences for human health have been a topic of interest in the medical and engineering research world for many years. Large populations in low and middle-income countries (LMICs) are exposed to HAP as a result of the combustion of solid biomass fuel, especially for household cooking. Short-term exposure to HAP may increase respiratory symptoms including cough and breathlessness, which on more prolonged exposure may cause serious respiratory damage and lead to premature death. Airway inflammation following exposure to inhaled pollutants is likely to be a key step in this process, and little is known about the mechanisms underlying responses to biomass smoke in human lung. The main aims of this thesis were to (i) quantify ‘real-life’ exposure to particulate matter of aerodynamic diameter smaller than 2.5 µm (PM2.5) and carbon monoxide (CO) measured during cooking on stoves in rural areas of Nepal in different geographical settings, (ii) assess the potential effect of biomass smoke extract generated in real life cooking on inflammatory responses in human lung tissue, and (iii) investigate the consequences of controlling biomass smoke exposure using improved cook stoves (with a flue to vent smoke out of the room) (ICS) on inflammatory responses in human lung tissue. Using eight different types of biomass fuels, it was identified that PM2.5 and CO emissions were higher with agricultural residue and cow dung compared to fuel wood. The real-life exposure was measured during cooking on a range of stoves in 103 households in 4 different Nepalese villages situated at altitudes between ~100 m to 4000 m above sea level. It was found that in a range of settings in rural Nepal from villages at all altitudes high levels of personal exposures to indoor pollutants occur and that the exposures are higher in villages at higher altitude. I demonstrated that the biomass smoke samples collected in a real-life environment from rural Nepal have pro-inflammatory effects in both human lung tissue and HBEC. An elevated level of pro-inflammatory cytokines and chemokines measured in the cell and tissue culture supernatant following biomass smoke exposure suggests that high levels of indoor exposures are likely to produce lung inflammation. The use of ICS was effective in reducing the overall indoor exposure, and the exposure reduction was about 51%. However, the use of ICS does not prevent pro-inflammatory responses in human lung as a similar pattern of inflammatory mediators was observed with the samples from ICS cooking. Overall, this study supports the need to reduce exposures in order to improve respiratory health in this setting. Furthermore, it suggests that additional methods other than those currently being trialled may be needed to reduce exposures to levels which will prevent lung inflammation from occurring in real-life settings.