Am J Respir Cell Mol Biol. 2013 Oct 8.
Source of Biomass Cooking Fuel Determines Pulmonary Response to Household Air Pollution.
Sussan TE, et al. Johns Hopkins University School of Public Health, Environmental Health Sciences, Baltimore, Maryland, United States; tsussan@jhsph.edu.
Abstract – Approximately 3 billion people, half the worldwide population, are exposed to extremely high concentrations of household air pollution (HAP) due to the burning of biomass fuels on inefficient cookstoves, accounting for 4 million annual deaths globally. Yet, our understanding of the pulmonary responses to HAP exposure and the underlying molecular and cellular events are limited.
The two most prevalent biomass fuels in India are wood and cow dung, and typical 24-h mean particulate matter (PM) concentrations in homes that use these fuels are 300-5,000 µg/m3. We dissected the mechanisms of pulmonary responses in mice after either acute or sub-chronic exposure to wood or cow dung PM collected from rural Indian homes during biomass cooking.
Acute exposures resulted in robust pro-inflammatory cytokine production, neutrophilc inflammation, airway resistance and hyper-responsiveness, all of which were significantly higher in mice exposed to PM from cow dung. On the contrary, sub-chronic exposures induced eosinophilic inflammation, PM-specific antibody responses, and alveolar destruction that was highest in wood PM-exposed mice. To understand the molecular pathways that trigger biomass PM-induced inflammation, we exposed TLR2, 3, 4, 5, and IL-1R deficient mice to PM, and found that IL-1R, TLR4 and TLR2 are the predominant receptors that elicit inflammatory responses via MyD88 in mice exposed to wood or cow dung PM.
In conclusion this study demonstrates that sub-chronic exposure to PM collected from households burning biomass fuel elicits a persistent pulmonary inflammation largely through activation of TLR and IL-1R pathways, which could increase the risk for chronic respiratory diseases.
