2017
DOI: 10.1016/j.tiv.2017.05.021
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Comparison of in vitro toxicological effects of biomass smoke from different sources of animal dung

Abstract: Worldwide, over 4 million premature deaths each year are attributed to the burning of biomass fuels for cooking and heating. Epidemiological studies associate household air pollution with lung diseases, including chronic obstructive pulmonary disease, lung cancer, and respiratory infections. Animal dung, a biomass fuel used by economically vulnerable populations, generates more toxic compounds per mass burned than other biomass fuels. The type of animal dung used varies widely depending on local agro-geography… Show more

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Cited by 16 publications
(15 citation statements)
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“…McCarthy et al, found that in pneumocytes wood smoke activates the aryl hydrocarbon receptor [ 87 ]. They did not inhibit hydrocarbon receptor signaling so it is not possible to ascertain the extent of the involvement of signaling via this receptor in response to biomass smoke.…”
Section: Other Potential Mechanismsmentioning
confidence: 99%
See 1 more Smart Citation
“…McCarthy et al, found that in pneumocytes wood smoke activates the aryl hydrocarbon receptor [ 87 ]. They did not inhibit hydrocarbon receptor signaling so it is not possible to ascertain the extent of the involvement of signaling via this receptor in response to biomass smoke.…”
Section: Other Potential Mechanismsmentioning
confidence: 99%
“…An alternative is to use systems where epithelial cells are cultured at an air liquid interface and expose these to gaseous biomass. McCarthy et al made dung cigarettes, and utilised a commercial smoking machine (Baumgartner-Jaeger CSM2072i, CH Technologies, Westwood, NJ, USA) to generate smoke and expose small airway epithelial cells, which had been at air: liquid interface for 24 h [ 87 ]. The obvious drawback to this particular system is that cigarettes were made with a filter, as used in a tobacco cigarette.…”
Section: How Should In Vitro and In Vivo Models Of Biomass Smoke mentioning
confidence: 99%
“…Understanding the mechanisms underlying smoke-related health effects, such susceptibility to pulmonary infection and chronic lung disease, is not thoroughly understood, but such knowledge is key in providing biological evidence that public health interventions are needed to address the harm associated with the use of this fuel source. Toxicological studies are however making progress, characterising heightened inflammatory responses and impaired immune defences [ 52 , 53 , 55 ], and in doing so, suggest a mechanism by which HAP can directly cause lung diseases and promote increased susceptibility to infection. For example, in providing direct evidence that the use of cleaner burning cookstoves by women reduces alveolar macrophage black carbon loading, Whitehouse et al .…”
Section: Discussionmentioning
confidence: 99%
“…Subchronic exposures (50 μg × 3/week for 8 weeks, nose aspiration), however, induced eosinophilic inflammation, PM-specific antibody responses and alveolar destruction, which was greatest in wood PM-exposed mice. The potentially greater toxicity of cow dung biomass smoke, on the basis of oxidative capacity, particulates per mass of fuel burned and concentrations of microbial products, compared to other combustion products [ 49 , 53 , 54 ], has prompted an examination of six different types of dung biomass smoke on lung cells [ 55 ]. Since the type of animal dung used varies widely depending on local agro-geography, the types tested included horse ( Equus caballus ), US domestic cow ( Bos taurus taurus ), Indian domestic cow ( Bos taurus indicus ), African elephant ( Loxodonta africana ), goat ( Capra hircus ) and white rhinoceros ( Ceratotherium simum ).…”
Section: Household Air Pollutionmentioning
confidence: 99%
“…However, other studies have not reproduced these conclusions and most probably this is related to the lack of standardization of the assays, the characteristics of the exposure to biomass and the cells and tissues examined. The axis: stress, autoimmunity and mitochondrial dysfunction already clearly involved in the pathogenesis of COPD associated with smoking has not been investigated in the COPD phenotype associated with biomass [107,108].…”
Section: Pathogenic Mechanismsmentioning
confidence: 99%