Rationale: Exposure to biomass smoke is believed to increase the risk of developing chronic obstructive pulmonary disease. However, little is known about the mechanisms underlying responses to biomass smoke in human lungs. Objectives: This study had two objectives: first, to quantify "real-life" exposures to particulate matter <2 μm in diameter (PM2.5) and carbon monoxide (CO) measured during cooking on stoves in rural areas of Nepal in different geographical settings; and second, to assess the effect of biomass smoke extracts on inflammatory responses in ex vivo human lung tissue. Methods: Personal exposures to PM2.5 and indoor near-stove CO concentrations were measured during cooking on a range of stoves in 103 households in 4 different Nepalese villages situated at altitudes between ∼100 and 4,000 m above sea level. Inflammatory profiles to smoke extracts collected in the field were assessed by incubating extracts with human lung tissue fragments and subsequent Luminex analysis. Results: In households using traditional cooking stoves, the overall mean personal exposure to PM2.5 during cooking was 276.1 μg/m3 (standard deviation [SD], 265 μg/m3), and indoor CO concentration was 16.3 ppm (SD, 19.65 ppm). The overall mean PM2.5 exposure was reduced by 51% (P = 0.04) in households using biomass fuel in improved cook stoves, and 80% (P < 0.0001) in households using liquefied petroleum gas. Similarly, the indoor CO concentration was reduced by 72% (P < 0.001) and 86% (P < 0.0001) in households using improved cook stoves and liquefied petroleum gas, respectively. Significant increases occurred in 7 of the 17 analytes measured after biomass smoke extract stimulation of human lung tissue (IL-8 [interleukin-8], IL-6, TNF-α [tumor necrosis factor-α], IL-1β, CCL2, CCL3, and CCL13).Conclusions: High levels of real-life exposures to PM2.5 and CO occur during cooking events in rural Nepal. These exposures induce lung inflammation ex vivo, which may partially explain the increased risk of chronic obstructive pulmonary disease in these communities.
Rationale: Exposure to biomass smoke is believed to increase the risk of developing chronic obstructive pulmonary disease. However, little is known about the mechanisms underlying responses to biomass smoke in human lungs. Objectives: This study had two objectives: first, to quantify "real-life" exposures to particulate matter <2 μm in diameter (PM2.5) and carbon monoxide (CO) measured during cooking on stoves in rural areas of Nepal in different geographical settings; and second, to assess the effect of biomass smoke extracts on inflammatory responses in ex vivo human lung tissue. Methods: Personal exposures to PM2.5 and indoor near-stove CO concentrations were measured during cooking on a range of stoves in 103 households in 4 different Nepalese villages situated at altitudes between ∼100 and 4,000 m above sea level. Inflammatory profiles to smoke extracts collected in the field were assessed by incubating extracts with human lung tissue fragments and subsequent Luminex analysis. Results: In households using traditional cooking stoves, the overall mean personal exposure to PM2.5 during cooking was 276.1 μg/m3 (standard deviation [SD], 265 μg/m3), and indoor CO concentration was 16.3 ppm (SD, 19.65 ppm). The overall mean PM2.5 exposure was reduced by 51% (P = 0.04) in households using biomass fuel in improved cook stoves, and 80% (P < 0.0001) in households using liquefied petroleum gas. Similarly, the indoor CO concentration was reduced by 72% (P < 0.001) and 86% (P < 0.0001) in households using improved cook stoves and liquefied petroleum gas, respectively. Significant increases occurred in 7 of the 17 analytes measured after biomass smoke extract stimulation of human lung tissue (IL-8 [interleukin-8], IL-6, TNF-α [tumor necrosis factor-α], IL-1β, CCL2, CCL3, and CCL13).Conclusions: High levels of real-life exposures to PM2.5 and CO occur during cooking events in rural Nepal. These exposures induce lung inflammation ex vivo, which may partially explain the increased risk of chronic obstructive pulmonary disease in these communities.
Entities:
Keywords:
cytokine; exposure; household air pollution; lung inflammation; smoke extract
Authors: Sean Semple; Delan Devakumar; Duncan G Fullerton; Peter S Thorne; Nervana Metwali; Anthony Costello; Stephen B Gordon; Dharma S Manandhar; Jon G Ayres Journal: Environ Health Perspect Date: 2010-03-22 Impact factor: 9.031
Authors: Angela M Fonceca; Graeme R Zosky; Elizabeth M Bozanich; Erika N Sutanto; Anthony Kicic; Paul S McNamara; Darryl A Knight; Peter D Sly; Debra J Turner; Stephen M Stick Journal: Respir Res Date: 2018-01-22
Authors: Marco Checa; James S Hagood; Rafael Velazquez-Cruz; Victor Ruiz; Carolina García-De-Alba; Claudia Rangel-Escareño; Francisco Urrea; Carina Becerril; Martha Montaño; Semiramis García-Trejo; José Cisneros Lira; Arnoldo Aquino-Gálvez; Annie Pardo; Moisés Selman Journal: PLoS One Date: 2016-03-02 Impact factor: 3.240
Authors: Andy I Ritchie; Jonathon R Baker; Trisha M Parekh; James P Allinson; Surya P Bhatt; Louise E Donnelly; Gavin C Donaldson Journal: Am J Respir Crit Care Med Date: 2021-07-01 Impact factor: 21.405