Jul 2026· Electronic Journal of Medical Research· 0 citations· 69 references
TL;DR
The complex relationship between air pollution, the human microbiome, and lung cancer within a One Health framework is explored, highlighting the mechanistic links between air pollution-induced microbial dysbiosis and lung carcinogenesis.
Abstract
Lung cancer remains one of the leading causes of cancer-related mortality worldwide, with increasing evidence highlighting the role of environmental and biological interactions in its development. This review explores the complex relationship between air pollution, the human microbiome, and lung cancer within a One Health framework. While smoking remains a major risk factor, air pollution has emerged as a significant modifiable environmental contributor, particularly in urbanized and industrial regions. Pollutants such as particulate matter (PM2.5 and PM10), nitrogen dioxide, and volatile organic compounds are associated with increased lung cancer incidence through mechanisms involving oxidative stress, chronic inflammation, and genetic damage. Recent research has also identified the lung microbiome as an important factor in respiratory health. Once considered sterile, the lungs are now known to host diverse microbial communities that play a role in immune regulation and inflammatory balance. Environmental exposure, particularly polluted air, can disrupt this microbial balance, leading to dysbiosis. Such microbial alterations may contribute to impaired immune responses and enhanced susceptibility to disease. This review further highlights the mechanistic links between air pollution-induced microbial dysbiosis and lung carcinogenesis. Key pathways include chronic inflammation, immune dysregulation, oxidative stress, epigenetic changes, and alterations in the tumor microenvironment. The interaction between the lung and gut microbiome (lung–gut axis) further emphasizes the systemic impact of environmental exposures. The One Health approach provides an integrated framework to understand these interconnected systems, emphasizing the relationship between environmental health, microbial ecosystems, and human disease. However, current research remains fragmented, with gaps in longitudinal data and integrated multi-omics studies.
Despite advances in medical care, respiratory tract infections continue to be a leading cause of morbidity and mortality in children worldwide. In addition to posing a healthcare burden, infections acquired early in life are associated with long‐term detrimental effects on lung and immune function. This narrative review examines evidence on how environmental factors, such as air pollution and microbes, can affect children's susceptibility to upper and lower airway infections. Epidemiological studies correlate elevated concentrations of ambient and indoor air pollution with a higher frequency of acute upper and lower respiratory tract infections in pediatric populations. Experimental investigations of individual criteria air pollutants such as PM2.5 demonstrate compromised lung epithelial barrier integrity, oxidative stress and inflammation, and impaired innate and adaptive immune cell function with exposure, all of which may contribute to enhanced infection rates. Concomitantly, the developing respiratory microbiome plays a central role in shaping mucosal immunity; balanced communities provide colonization resistance and support immune education, while dysbiosis driven by antibiotic exposures, air pollution, or other perturbations can predispose to infection and chronic respiratory disease such as asthma. Exposure to diverse environmental microbes, including certain fungi, may also be protective against respiratory illness, and specific microbial signals can confer antiviral benefits. Collectively, the interplay between environmental exposures and infection risk is complex and likely influenced by developmental factors. Policies aimed at improving air quality and strategies to support a healthy microbiome in early life can mitigate the risk of respiratory infections and promote lifelong lung health.
Olivia H Rice, Lisa A Miller· Pediatric Pulmonology· 0 citations
It is suggested that air pollution may promote lung cancer partly through metabolic pathways related to inflammatory and oxidative processes, providing key insights into potential mechanisms and targets for prevention.
Sabrina S. Chow, Ying Wang, J. Sarnat et al.· Nature Communications· 0 citations
Inflammatory bowel disease (IBD) is rising at an alarming rate in parallel with rapid urbanization in newly industrialized parts of the world, including East Asia. Simultaneously, environmental pollutants are also an escalating problem in these regions. Recent studies have reported on associations between environmental pollutants and IBD, however, data on this topic specific to East Asia are limited. In this review, we summarize available data on environmental pollutants and related exposures in East Asia and their relationship with IBD. Motor vehicle emissions and industrial wastes are key sources of air pollution, while drinking water, seafood and vegetable produce constitute main sources of heavy metal and pesticide exposure. Microplastics are even more ubiquitous and pervasive toxicants. Mechanistic data suggest that environmental pollutants may influence IBD risk and outcomes through microbial dysbiosis and intestinal barrier disruption, ultimately leading to intestinal inflammation. Understanding the impact of environmental exposures and outcomes is key to potentially identify modifiable factors and inform strategies to predict, prevent and mitigate the rising burden of IBD in East Asia.
S. Shenoy, Mansi Chaubey, Eun Soo Kim et al.· Intestinal Research· 0 citations
Exposure to both outdoor and indoor air pollution poses significant global public health challenges at all life stages. As the respiratory system serves as the primary entry route for inhaled pollutants, extensive evidence has demonstrated the detrimental effects of various air pollutants on respiratory health. Air pollution is a well-established risk factor for the development, exacerbation, and mortality of chronic respiratory diseases (CRDs), including airway diseases such as asthma, chronic obstructive pulmonary disease, interstitial lung disease, and lung cancer. This review summarizes the epidemiological evidence linking air pollution to the incidence and progression of CRDs and examines the impact of air quality control interventions. With the growing recognition that air pollution is a potentially preventable risk factor contributing to high morbidity and mortality, increasing attention has been directed toward protective strategies. We discuss the recent evidence on non-pharmacological interventions aimed at reducing air pollution exposure, both at the individual and social levels, and emphasize the ongoing need for integrated efforts to improve air quality and respiratory health.
Suk-Jo Yong, Jin Woo Song· The Korean Journal of Intern...· 0 citations
BACKGROUND
While smoking is the leading cause of lung cancer, the increasing incidence among never-smokers is a growing concern, highlighting non-tobacco-related mechanisms of carcinogenesis. Emerging evidence suggests that respiratory microbial dysbiosis and associated inflammatory responses may contribute to lung tumorigenesis. We previously showed that elevated abundances of Selenomonas, Streptococcus, and Veillonella are correlated with lung cancer independent of smoking history. Here, we examine whether circulating microbial and inflammatory profiles are linked to lung cancer in never-smokers.
METHODS
Circulating bacterial DNA representing the three genera was quantified by droplet digital PCR, and seven systemic inflammatory cytokines were measured by ELISA in plasma of 56 ever-smoker lung cancer patients, 56 never-smoker lung cancer patients, and 78 healthy controls. Integrative statistical modeling was performed to evaluate relationships among bacterial DNA burden, inflammatory activation, smoking history, and cancer status.
RESULTS
Plasma DNA levels of Selenomonas, Streptococcus, and Veillonella, together with IL-6, TNF-α, IL-1β, IL-8, and IL-17A, were elevated in lung cancer patients compared with controls (all p < 0.05). No significant differences were observed between smoking and never-smoking lung cancer patients for bacterial DNA levels, IL-6, TNF-α, or IL-17A (all > 0.05), whereas modest but statistically significant differences were observed for IL-8 (P = 0.036) and IL-1β (P = 0.048). Bacterial DNA burden was correlated with systemic inflammatory cytokine activation independent of smoking history (all p < 0.05).
CONCLUSIONS
A smoking-independent microbial-inflammatory signature is associated with lung cancer and provides a foundation for future studies evaluating its biological significance and clinical utility for diagnosis and management.
P. Dhilipkannah, Feng Jiang· Lung Cancer· 0 citations
Air pollution is the leading environmental cause of disease burden worldwide and is increasingly recognized as a potent driver of accelerated biological aging. Rather than acting through organ-specific toxicity alone, air pollutants appear to affect the fundamental hallmarks of aging itself, including oxidative stress, chronic inflammation, epigenetic dysregulation, telomere attrition, mitochondrial dysfunction, and cellular senescence. The pollutants of greatest concern are fine and ultrafine particulate matter (PM2.5, PM0.1), traffic-related air pollution, and household combustion emissions. This review synthesizes epidemiological and mechanistic evidence linking ambient and household air pollution to biological aging across the full spectrum of biomarker classes, including molecular measures (epigenetic clocks, telomere length, transcriptomic signatures), system-level indices (composite clinical biomarkers, proteomic aging clocks, inflammatory markers), and whole-organism measures (frailty). The strength of evidence varies meaningfully across biomarker classes. System-level composite measures, particularly the Klemera-Doubal method biological age, PhenoAge, and frailty scores, show the most robust and consistent associations with air pollution. Causal mediation analyses across independent cohorts support the role of biological aging as a mechanistic pathway linking air pollution exposure to clinical disease outcomes, including cardiovascular disease, neuropsychiatric disorders, and chronic kidney disease. Epigenetic clock findings remain inconclusive at the meta-analytic level despite strong biological plausibility, likely reflecting differences in exposure assessment methods, study design, and cell composition of the target tissue. Life-course vulnerability windows are also examined, with prenatal and early-life exposures shown to shape biological aging trajectories that persist into later life. Key research gaps include underrepresentation of household air pollution and low-income settings, and the shortage of longitudinal multimarker or multi-omics study designs. Air quality improvements and clean cooking fuel transitions have been shown to partially reverse air pollution-associated aging acceleration, reinforcing the public health relevance of these findings. Reducing air pollution thus remains the most equitable strategy for slowing biological aging at the population level, and incorporating aging-focused endpoints into environmental health research and regulatory policy is both a scientific and public health priority.
P. Poursafa, J. Jylhävä· Ageing Research Reviews· 0 citations
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