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How Household Biomass Smoke–Associated COPD Differs From Cigarette Smoke–Induced COPD


Multiple studies suggest that the mechanisms of lung damage and chronic obstructive pulmonary disease (COPD) due to biomass smoke differ from COPD caused by smoking cigarettes.

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

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

This review was published in 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 a primary energy source. Furthermore, the proportion of people using polluting fuels for cooking is 61% in rural areas and 20% in urban environments.

Wood smoke is known to contain hundreds of chemical volatiles with toxic, carcinogenic, and irritant properties, and respirable particulate matter (PM), which can lead to airway inflammations, exacerbated respiratory symptoms, lung inflammation, cell toxicity, and mucin expression.

One study found 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 men (1.8; 95% CI, 1.0-3.2).

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

One study that compared smoking-related COPD with biomass smoke–induced COPD included a 15-year follow-up of 112 patients with COPD who were chronically exposed to wood smoke during cooking (87% female) and 302 smoking patients with COPD (26% female). The results of this study showed a slower decline in lung function, absence of rapid decliners, and less variability in lung function in the exposed group compared to the smoking group.

Other in vitro studies have consistently shown wood smoke to induce inflammatory response, oxidative stress, cytotoxicity, genotoxicity, mitochondrial disfunction, 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. Individuals living in sub-Saharan Africa are the most exposed (about 84%), followed by Central Asia and South Asia (about 30%). In contrast, the proportion of people using indoor solid fuel in North America and Europe is about 6%.

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

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

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


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

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