Indoor air pollution represents a chronic and under-recognized risk factor for lung cancer, silently contributing to a substantial portion of global cases, given that people spend up to 90% of their time indoors[1]. Unlike the visible haze of outdoor smog, indoor contaminants such as radon gas (naturally released from soil and granite), fine particulate matter (PM2.5; e.g. from burning candles or incense), cooking fumes, biomass smoke (from fireplaces or wood-burning stoves), and second-hand tobacco smoke accumulate gradually over years or decades, often without causing symptoms that would prompt concern[2]. This slow and insidious exposure allows carcinogens, including polycyclic aromatic hydrocarbons (PAHs), volatile organic compounds (VOCs), and radioactive radon decay products, to inflict persistent damage on lung tissue — a risk particularly relevant for never-smokers, who represent a growing proportion of lung cancer diagnoses worldwide.
Household air pollution (HAP) arises primarily from routine domestic activities, especially in poorly ventilated homes. The use of coal, wood, crop residues or animal dung for cooking and heating remains common in many regions and generates high concentrations of carcinogenic particles[3]. Radon, which seeps into buildings from soil and construction materials, is the second leading cause of lung cancer after smoking. Long-term exposure increases lung cancer risk by 6% to 16% for every 100 Bq per cubic metre increase in radon concentration, often without detection. Fine particles such as PM2.5 penetrate deep into the alveoli, where they trigger chronic inflammation, oxidative stress, and DNA damage. These processes are closely associated with adenocarcinoma, the lung cancer subtype most frequently observed in never-smokers and most strongly linked to air pollution[4].
Epidemiological data underscore the scale of this risk. Among non-smoking women in Asia exposed to biomass fuels or traditional cooking methods, lung cancer odds ratios have been reported as high as 8.13. Studies in China have also documented significantly elevated particulate levels in affected individuals, with lung cancer risk increasing by approximately 45% for every 10 micrograms per cubic meter rise in particulate exposure[5]. The World Health Organization estimates that indoor air pollution contributes to approximately 4 million deaths annually, including about 6% from lung cancer, disproportionately affecting rural and low-income populations[6]. Even in urban environments, exposure to cooking fumes, incense smoke, and inadequate ventilation produces similar biological effects. The presence of airborne carcinogen biomarkers in lung tissue and pleural fluid provides direct evidence of long-term accumulation and biological impact.
At the cellular level, chronic exposure to indoor pollutants creates conditions that support cancer development. Fine particles stimulate immune cells such as macrophages to release inflammatory cytokines, including IL-1β, which promote genetic mutations and create a tumor-supportive microenvironment[7]. These processes frequently affect alveolar type II cells, where oncogenic pathways such as EGFR signaling may become activated. Because these changes develop slowly and without acute symptoms, the link between indoor air pollution and cancer often remains unrecognized. Although particulate matter has been classified as a Group 1 carcinogen by the International Agency Research on Cancer, indoor sources have historically received less regulatory attention than outdoor air pollution.
Prolonged Exposure to Household Pollutants: Inflammation and Cellular Damage
Long-term exposure to household pollutants drives persistent inflammation and cellular injury in the lungs. Fine particles and toxic gases generated by biomass combustion, cooking oils, and indoor chemical emissions penetrate deeply into lung tissue, where they disrupt epithelial integrity and generate excessive reactive oxygen species. This oxidative stress depletes protective antioxidants such as glutathione and causes damage to cellular lipids, proteins, and DNA, creating conditions conducive to malignant transformation[8].
This oxidative damage activates inflammatory pathways, including NF-κB signaling, in both epithelial and immune cells. This results in sustained release of pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α[9]. Over time, chronic inflammation impairs normal lung repair mechanisms, disrupts mitochondrial function, and promotes cellular senescence or apoptosis. Senescent cells further amplify inflammation and reinforce a cycle of ongoing tissue injury and immune dysregulation[10].
These biological changes are accompanied by epigenetic alterations, including telomere shortening and histone modification, which can silence tumor suppressor genes and promote genomic instability. Long-term exposure has also been linked to early fibrotic changes and precancerous lesions, particularly among populations exposed to biomass smoke for decades. Because these processes progress silently, damage often becomes apparent only after irreversible changes have occurred.
Encouragingly, interventions such as improved ventilation, clean fuels, and indoor air quality monitoring can significantly reduce exposure and interrupt these pathogenic mechanisms.
Why Domestic Environments Matter in Lung Cancer Prevention?
Domestic environments must play a central role in cancer prevention strategies. While tobacco control remains essential, indoor environmental exposures represent a significant and often overlooked source of risk.
Never-smokers now account for approximately 15% to 20% of global lung cancer cases, many linked to environmental exposures rather than tobacco use. Household air pollution contributes to millions of deaths annually, including a substantial number from lung cancer, particularly in low- and middle-income regions[11].
The risk is especially pronounced among populations exposed to biomass cooking fuels, poor ventilation, and radon infiltration. Biomarkers detected in lung tissue confirm that carcinogenic compounds originating within the home accumulate over time and reinforce the need to address domestic air quality as a core component of prevention efforts[12].
Reducing household air pollution represents one of the most actionable opportunities to lower lung cancer risk globally. Improving ventilation, transitioning to clean energy sources, testing for radon, and increasing awareness can significantly reduce long-term exposure. Recognizing the home as a critical environment for prevention is essential to addressing the full spectrum of lung cancer risk.
References:
1. Slater, K. D. (2025). Characterizing Associations Between Household Energy-Related Exposures to Air Pollution and Biological Indicators of Respiratory Health (Doctoral dissertation, Colorado State University).
2. Valavanidis, A. (2023). Indoor air pollution causes around 4 million premature deaths worldwide per year.
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4. Valavanidis, A. (2019). Oxidative stress and pulmonary carcinogenesis through mechanisms of reactive oxygen species. How respirable particulate matter, fibrous dusts, and ozone cause pulmonary inflammation and initiate lung carcinogenesis. In Oxidative Stress in Lung Diseases: Volume 1 (pp. 247-265). Singapore: Springer Singapore. doi: https://doi.org/10.1007/978-981-13-8413-4_13
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10. Liu, S., Xi, Q., Li, X., & Liu, H. (2025). Mitochondrial dysfunction and alveolar type II epithelial cell senescence: The destroyer and rescuer of idiopathic pulmonary fibrosis. Frontiers in Cell and Developmental Biology, 13, 1535601. doi: https://doi.org/10.3389/fcell.2025.1535601
11. Lai, P. S., Lam, N. L., Gallery, B., Lee, A. G., Adair-Rohani, H., Alexander, D., … & Ozoh, O. B. (2024). Household air pollution interventions to improve health in low-and middle-income countries: an official American thoracic society research statement. American Journal of Respiratory and Critical Care Medicine, 209 (8), 909-927. doi: https://doi.org/10.1164/rccm.202402-0398ST
12. Hudson-Hanley, B. A. (2022). Polycyclic Aromatic Hydrocarbons (PAH) Exposure Trends, and Evidence of Adverse Health Effects in Infants and Children from Prenatal/Early-Life PAH Exposure.