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How COPD associated with household biomass smoke differs from COPD induced by cigarette smoke

A review examined the ways in which biomass smoke-associated chronic obstructive pulmonary disease (COPD) was associated with a slower decline in lung function, more airway involvement, and less emphysema, suggesting a different phenotype and different pathophysiology of COPD induced by cigarette smoke.

“Despite the high biomass-associated burden of COPD, the molecular, genetic, and epigenetic mechanisms underlying its pathogenesis are poorly understood,” the authors of this review wrote. “This review describes the pathogenic mechanisms potentially involved in lung damage, the development of COPD associated with exposure to wood smoke, and the influence of genetic and epigenetic factors on the development of this disease.”

This review was posted on cells.

Household use of solid fuels for cooking and heating, particularly wood, are the most widespread sources of indoor air pollution. About 2.8 billion people (36% of the world’s population) use solid fuels as their primary energy source. In addition, the proportion of people using polluting fuels for cooking is 61% in rural areas and 20% in urban areas.

Wood smoke is known to contain hundreds of volatile chemicals with toxic, carcinogenic, and irritating properties, and respirable particulate matter (PM), which can cause airway inflammation, exacerbated respiratory symptoms, lung inflammation, cell toxicity, and mucin expression. .

One study found that the overall risk of COPD due to exposure to indoor air pollution, such as wood smoke, was higher among women (3.2; 95% CI, 2.3-4.8) than among men (1.8; 95% CI, 1.0-3.2).

Chronic exposure to these indoor air pollutants is associated with a higher prevalence of respiratory symptoms, reduced lung function, and the development of COPD, according to multiple cross-sectional studies.

A study comparing smoking-related COPD with COPD induced by biomass smoke included a 15-year follow-up of 112 COPD patients who were chronically exposed to wood smoke during cooking (87% women) and 302 smokers. with COPD (26% female). The results of this study showed a slower decline in lung function, no rapid declines, and less variability in lung function in the exposed group compared to the smoking group.

Other in vitro studies have consistently shown that wood smoke induces an inflammatory response, oxidative stress, cytotoxicity, genotoxicity, mitochondrial dysfunction, mucin expression, decreased epithelial barrier function, lung parenchymal damage, and endoplasmic reticulum stress.

Exposure to indoor air pollution is also higher among people living in poverty and underdeveloped countries. People living in sub-Saharan Africa are most at risk (around 84%), followed by Central Asia and South Asia (around 30%). By contrast, the proportion of people using solid fuels indoors in North America and Europe is around 6%.

There are additional studies that have shown strong evidence for the association of multiple genes with lung function and susceptibility to COPD. A European study included COPD patients who were heavy smokers and COPD patients who had never smoked. The researchers were able to identify 6 new genome-wide significant signals with extremes of forced expiratory volume within 1 second in both groups, regardless of smoking history.

This review identified key differences in COPD induced by biomass smoke and COPD induced by smoking that suggest that COPD related to indoor air pollutants involves a combination of intrinsic factors, and the reviewers believe that more specific treatments are needed. for COPD induced by biomass smoke.

“In conclusion, further research is needed to elucidate the mechanisms of biomass-induced pathogenesis and susceptibility in COPD and other lung conditions,” the reviewers wrote. “In addition, more data on exposure-response relationships are needed from well-designed longitudinal studies in children, adolescents, and adults to capture the adverse effects associated with exposure to biomass before birth and at an early age and the natural history of development of COPD. ”

Reference

Ortiz-Quintero B, Martínez-Espinosa I, Pérez-Padilla R. Mechanisms of lung damage and development of COPD due to exposure to smoke from domestic biomass: inflammation, oxidative stress, microRNA and gene polymorphisms. cells. 2022;12(1):67. doi:10.3390/cells12010067