Looking through the particles: a narrative review of air pollution and lung cancer
Review Article

Looking through the particles: a narrative review of air pollution and lung cancer

Darren Turner1 ORCID logo, David Hedrick1, Sandra L. Starnes1, Robert M. Van Haren1,2

1Division of Cardiothoracic Surgery, Department of Surgery, University of Cincinnati College of Medicine, Cincinnati, OH, USA; 2Cincinnati Research in Outcomes and Safety in Surgery (CROSS), Department of Surgery, University of Cincinnati College of Medicine, Cincinnati, OH, USA

Contributions: (I) Conception and design: D Turner, RM Van Haren; (II) Administrative support: SL Starnes, RM Van Haren; (III) Provision of study materials or patients: D Turner, RM Van Haren; (IV) Collection and assembly of data: D Hedrick; (V) Data analysis and interpretation: D Turner, D Hedrick; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors.

Correspondence to: Darren Turner, MD. Division of Cardiothoracic Surgery, Department of Surgery, University of Cincinnati College of Medicine, 231 Albert Sabin Way, ML 0556, Cincinnati, OH, USA. Email: turne2de@ucmail.uc.edu.

Background and Objective: Air pollution, particularly fine particulate matter ≤2.5 µm (PM2.5), has emerged as a significant public health concern with established carcinogenic properties. Lung cancer incidence among patients who have never smoked cigarettes has doubled from 8% to 15% of cases since the 1990s, with stronger correlations observed between poor air quality and cancer development. This review synthesizes epidemiological evidence linking PM2.5 exposure to lung cancer development, focusing on molecular mechanisms and clinical outcomes in those who have never smoked.

Methods: A systematic literature search was conducted in PubMed and Scopus using search terms related to PM2.5 epidemiology and lung cancer in never-smokers. Articles were limited to original research, reviews, and meta-analyses published in English between 2004 and 2024. Of 198 articles identified, 45 were selected as relevant.

Key Content and Findings: PM2.5 particles penetrate into alveoli, triggering inflammatory pathways including PI3K/Akt, NF-κB, JAK/STAT, and MAPK signaling, leading to oxidative stress, DNA damage, and oncogenic mutations. Non-tobacco user lung cancers demonstrate higher rates of epidermal growth factor receptor (EGFR) mutations, with PM2.5 promoting carcinogenesis by acting on cells with pre-existing EGFR mutations through interleukin-1β release and macrophage activation. Post-treatment outcomes are significantly impacted by continued PM2.5 exposure, particularly in populations with higher proportions of non-white patients, with higher exposure levels associated with increased mortality risk following surgical resection.

Conclusions: There has been an increased incidence of lung cancer in patients who have never smoked and can be associated with the increase in air pollution, particularly PM2.5. Furthermore, PM2.5 exposure is associated with worse outcomes after treatment of lung cancer. Because of this linkage between PM2.5 and lung cancer, further research is needed to identify PM2.5 exposure reduction strategies and improve post-treatment outcomes.

Keywords: Lung cancer in never smokers; air pollution; particulate matter ≤2.5 µm (PM2.5); lung cancer outcomes

Submitted Sep 02, 2025. Accepted for publication Nov 21, 2025. Published online Dec 29, 2025.

doi: 10.21037/jtd-2025-1800

Introduction

Air pollution is a byproduct of industrialization, and as urban development increases in all countries, so too does the global burden of air pollution. Air pollution’s pathogenicity depends on its size and composition and can be broadly categorized into gaseous products or particulate matter (PM).

While various air pollutants, including volatile organic compounds and nitrogen oxides, have been associated with lung cancer risk, PM, specifically of size ≤2.5 µm (PM2.5), is of specific interest because of its smaller size and its capacity to injure the lower respiratory tract (1,2). This is linked to increased prevalence and exacerbations of chronic respiratory conditions and increased incidence of lung cancer (3). Because of this, the World Health Organization (WHO) has revised its annual mean air quality guideline for PM2.5 and reduced the acceptable range of exposure from 10 to 5 µg/m3 in 2021 (4). And while the global levels of PM2.5 have slightly decreased, the burden of disease associated with PM2.5 has increased, particularly lung cancer in individuals who have never smoked tobacco (NS), emphasizing the need for further study and intervention.

The goal of this article is to review the literature to better understand the relationship of PM2.5 exposure to lung cancer. We will review current literature regarding PM2.5 epidemiology and lung cancer carcinogenesis as it pertains to PM2.5. Then we will conclude with a brief discussion of lung cancer outcomes. We present this article in accordance with the Narrative Review reporting checklist (available at https://jtd.amegroups.com/article/view/10.21037/jtd-2025-1800/rc).

Methods

The following search strategy was employed to focus on PM2.5 epidemiology, mechanisms of oncogenesis, lung cancer, and outcomes (Table 1). We used several terms for our literature search in PubMed and Scopus. Furthermore, we utilized references that we had used for previous research and publications. We used the following terms and strings of terms: PM2.5 epidemiology; PM2.5 AND carcinogenesis; people who have never smoked AND lung cancer carcinogenesis; Lung cancer in people who have never smoked AND outcomes; Lung cancer in people who have never smoked AND surgical outcomes. We limited our selection to those articles that included original research, systematic and other types of review articles, and meta-analyses published between 2004 and 2024. We excluded those studies that were not published in English. Of the 198 articles identified, 45 were identified as relevant to the topic of air pollution epidemiology, carcinogenesis, and outcomes.

Table 1

Research strategy summary

Items Specifications
Date of search 05/01/2025
Databases searched PubMed, Scopus
Search terms and strings used PM2.5 epidemiology; PM2.5 AND carcinogenesis; never smokers AND lung cancer carcinogenesis; lung cancer in never smokers AND outcomes; lung cancer in never smokers AND surgical outcomes
Timeframe 2004–2025
Inclusion and exclusion criteria Inclusion: English language, primary research, review articles, and meta-analyses
Exclusion: non-English language
Selection process Articles were selected though relevancy by authors

PM2.5, particulate matter ≤2.5 µm.

PM2.5 epidemiology

Ambient air pollution has emerged as a critical area of investigation due to its ubiquitous nature and association with urbanization and industrial development. The complex mixture of air pollutants comprises two principal categories: gaseous pollutants and PM. Gaseous pollutants, which constitute approximately 90% of airborne contaminants, include ozone (O3), nitrogen dioxide (NO2), volatile organic compounds such as benzene, carbon monoxide (CO), and sulfur dioxide (SO2) (5). PM is classified by aerodynamic diameter, with PM2.5 and PM10 representing the most clinically relevant size fractions. The toxicological effects of these pollutants are primarily determined by particle size distribution and chemical composition, with PM2.5 demonstrating a strong association with adverse health outcomes through cardiovascular and systemic inflammatory pathways (6).

PM2.5 concentrations are highest in areas with significant population density, particularly in major urban centers where air pollution poses the greatest risk. Six of the top ten cities with the highest of PM2.5 concentration are in India (Figure 1A) (7). Still, other factors such as wildfires, agricultural practices, or natural dust, can also contribute and likely explain how some of the relatively unpopulated USA cities have some of the highest concentrations of PM2.5 in the country (Figure 1B) (7). Though some countries have seen a decline in concentrations of PM2.5 between 1980 and 2010, other countries have seen an increase of PM2.5 likely because of industrialization, population growth, and lack of pollution controls (8,9).

Figure 1 Listing of cities and associated pollution levels. (A) Cities in the world with the top 10 highest PM2.5 levels. (B) Cities in the United States with the top 10 highest PM2.5 levels. PM2.5, particulate matter ≤2.5 µm.

Epidemiological evidence linking air pollution to lung cancer, particularly with PM2.5, has accumulated progressively over the past several decades (10-13). Early longitudinal studies in the United States first established associations between long-term exposure to combustion-related PM2.5 and increased lung cancer mortality (14). This study and others contributed to the WHO’s International Agency for Research on Cancer (IARC) classifying outdoor air pollution and its PM components as Group 1 carcinogens (15,16). Subsequent epidemiological investigations have consistently demonstrated positive associations between ambient PM2.5 exposure and lung cancer incidence, with statistical significance maintained after adjustment for smoking status and other established risk factors (17,18). Moreover, Bowe et al. demonstrated that the number of lung cancer cases globally that can be attributed to PM2.5 exposure has increased by 30% since 2007 (19).

The clinical significance of lung cancer in those who have never smoked has also reached unprecedented levels, with approximately 10–15% of United States lung cancer cases now occurring in individuals with no smoking history. This represents a near-doubling from the early 1990s, when NS accounted for approximately 8% of cases, to the early 2010s, when this proportion reached 15% (20). Other studies have shown similar increases in non-tobacco user lung cancer incidence (21,22). The epidemiological burden of lung cancer in NS has become so substantial that, if considered as a distinct malignancy, it would rank among the leading causes of cancer-related mortality worldwide (22).

Furthermore, recent studies have demonstrated that lung cancer incidence in NS shows stronger correlations with poor ambient air quality (23-26). This trend is particularly pronounced among racial minority populations, raising important questions about environmental health disparities and social determinants of cancer risk (23). This demographic shift provides a compelling rationale to examine ambient air pollution as a significant oncogenic exposure in contemporary public health practice.

PM2.5 pathophysiology and mechanisms of carcinogenesis

PM2.5 is unique in that it is small enough to bypass the nasal cavity and upper respiratory tract, allowing it to penetrate deeply into the small airways and alveoli. Exposure to PM2.5 has been associated with upregulation of inflammatory pathways and inflammation of the upper and lower respiratory tract system. Some of these affected pathways are the PI3K/Akt, NF-kB, JAK/STAT, and MAPK signal pathways, which are all implicated is oxidative stress signaling (27-29). These findings supplemented earlier data showing increased reactive oxygen and reactive nitrogen species generation after exposure to PM (30). Furthermore, the increasing oxidative stress caused by PM2.5 has been linked to asthma development and worse exacerbations (31). Interestingly, oxidative and inflammatory effects can persist in lungs despite removal of PM2.5 exposure (32). This may be an explanation as to why, despite decreasing PM2.5 exposure globally, its effects on mortality have persisted. These triggered inflammatory pathways in the lungs contribute to oxidative stress and DNA damage, which can lead to epigenetic changes and carcinogenesis. Such targets include epidermal growth factor receptor (EGFR), which belongs to a group of transmembrane receptors that cause downstream intracellular signaling that promotes cell growth and division (33).

Early research generated data showing cancers in NS had a preponderance towards EGFR mutations, a distinct oncogenic profile from tobacco carcinogenesis, and this observation has been sustained over some years (34,35). Moreover, there have also been many retrospective analyses demonstrating that in NS, there were higher rates of EGFR mutations (33,36). There were also clinical studies observing that NS patients who were treated with the EGFR-targeting small molecules gefitinib or erlotinib exhibited a better response than those who did not smoke (37,38). These data suggested that disease in NS patients may be a unique entity from tobacco-associated lung cancer.

The EGFR pathway establishes a linkage between never-smoking patient oncogenesis and air pollution oncogenesis. A study conducted by Hill suggested that PM2.5 promotes lung cancer by acting on cells that have pre-existing EGFR mutations by increasing the number of interstitial macrophages in the lung that release interleukin-1β (18). This results in a progenitor-like cell state within type 2 alveolar cells, which have mutant EGFR signaling. Wang et al. proposed another mechanism whereby PM2.5 directly promotes tumor progression through activation of EGFR (39). Taken together, these studies provide a potential explanation for the increased incidence of EGFR tumors in NS patients and PM2.5 (40,41).

Osimertinib is a tyrosine kinase inhibitor that was found to have superior outcomes compared to gefitinib and erlotinib, leading it to become the standard of care for EGFR-positive advanced non-small cell lung cancer (NSCLC) (42). Its efficacy in both the adjuvant and neoadjuvant settings has been demonstrated in two trials: ADAURA and NEOADAURA (Table 2). In 2020, the ADAURA trial described the outcomes of stage 1b to 3A EGFR-positive NSCLC when osimertinib was used as adjuvant therapy following surgery and chemotherapy as compared to surgery and chemotherapy alone (43). The 2-year survival was 89% for the treatment group versus 52% for placebo. The NEOADAURA trial investigated the use of osimertinib versus chemotherapy as neoadjuvant therapy for EGFR-positive NSCLC (44). There were 3 treatment arms: osimertinib with chemotherapy, osimertinib therapy alone, and chemotherapy alone. Because many patients were also given osimertinib as adjuvant therapy, the primary endpoint was major pathological response. This study concluded that neoadjuvant osimertinib with or without chemotherapy demonstrated significantly increased major pathological response (26%, 25% vs. 2%), with odds ratios of 19.82 (95.002% CI: 4.60 to 85.33; P<0.0001) and 19.28 (99.9% CI: 1.71 to 217.39; P<0.0001), respectively. While these advances in targeted therapy represent significant contributions to the treatment of EGFR NSCLC, the continued impact of air pollution on lung cancer prevalence underscores the necessity of therapeutic innovation and environmental regulation to decrease overall disease burden.

Table 2

Comparison of ADAURA and NEOADAURA trials

Characteristics ADAURA NEOADAURA
Treatment Osimertinib Osimertinib
Treatment strategy Adjuvant therapy after surgery and chemotherapy Neoadjuvant therapy with/without chemotherapy vs. chemotherapy alone (3 arms)
Study population All stages EGFR+ NSCLC Stage II–IIIB EGFR+ NSCLC
Primary endpoint Disease-free survival among stage II–IIIA EGFR+ NSCLC Major pathological response
Secondary endpoints Disease-free survival in patients with stage IB–IIIA disease Event-free survival, pathological complete response, and nodal downstaging at surgery
Patients enrolled 682 358

EGFR, epidermal growth factor receptor; NSCLC, non-small cell lung cancer.

Outcomes and disparities

Notwithstanding that PM2.5 contributes to the development of a distinct genotype of lung cancer, it can also influence outcomes after treatment of lung cancer. Chandwani et al. sought to explore what environmental and social factors were associated with increased survival after resection of NSCLC in patients who never smoked (45). Significant factors associated with survival were longer distance from the road, the amount of surrounding green space, and PM exposure. Another study by Liu et al. investigated the correlation of PM2.5 exposure and survival of patients after lobectomy and found that an increasing amount of exposure to PM2.5 within 2 months after surgery is associated with an increased risk of death (46). Whitrock et al. also examined post-resection outcomes in relation to air pollution exposure, specifically PM2.5, providing insights into how environmental factors may influence recovery and long-term results following surgical intervention (47). The study concluded that PM2.5 exposure was independently associated with worse post-resection outcomes on univariate and multivariate analysis. Interestingly, PM2.5 exposure was an even more significant predictor of outcome than race or socioeconomic disadvantage. But the study also concluded that there was no difference in PM2.5 exposure between races.

The relationship between air pollution exposure and disparities was explored more thoroughly in a large national study by Jbaily et al. (48). This study showed that areas with higher than average white and native American populations have been consistently exposed to average PM2.5 levels, which are lower than areas with higher than average black, Asian, Hispanic, or Latino populations. They also showed that low-income populations have been consistently exposed to higher average PM2.5 levels than high-income groups from 2004–2016, consistent with another study conducted years later (23). These data suggest that interventions to reduce air pollution, particularly in communities disproportionately exposed, are an opportunity to improve cancer survival even after treatment.

Beyond direct pulmonary effects, PM2.5 may contribute to lung cancer risk through indirect metabolic pathways. Emerging evidence suggests that PM2.5 and its components function as obesogens, promoting weight gain and metabolic dysfunction (49-51). This is particularly relevant given that abdominal obesity has been associated with increased lung cancer risk in meta-analyses (52). This potential indirect carcinogenic pathway through metabolic disruption warrants further investigation, though the relative contribution compared to direct pulmonary mechanisms remains unclear.

Future studies

It is not clear whether the increased global incidence of lung cancer is simply because we are better at diagnosing it, but it is clear that the increased incidence of lung cancer in NS is a public health issue that can be meaningfully linked to air pollution, specifically PM2.5, and future work should explore strategies to continue to mitigate exposure to PM2.5. Because much of the data is correlative, more work is needed to better histologically or biochemically characterize tumors that can be significantly linked to air pollution to further stratify outcomes of those who use smoking tobacco and NS who are exposed to increased levels of PM2.5. This may be a phenomenon to explore when cumulative outdoor exposures to PM2.5 can be more accurately measured, accounting for indoor and outdoor exposure. Perhaps future screening guidelines could even make exceptions for patients who are at an increased ‘environmental risk’ of lung cancer, regardless of smoking status, given that some communities are disproportionately affected by air pollution.

Conclusions

There has been an increased incidence of lung cancer in patients who have never smoked, which can be associated with the increase in air pollution, particularly PM2.5. Furthermore, PM2.5 exposure is associated with worse outcomes after treatment of lung cancer. Because of this linkage between PM2.5 and lung cancer, further research is needed to continue to improve PM2.5 exposure reduction strategies to decrease the associated lung cancers and improve post-treatment outcomes in patients who have never smoked or are at increased exposure to air pollution.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the Narrative Review reporting checklist. Available at https://jtd.amegroups.com/article/view/10.21037/jtd-2025-1800/rc

Peer Review File: Available at https://jtd.amegroups.com/article/view/10.21037/jtd-2025-1800/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://jtd.amegroups.com/article/view/10.21037/jtd-2025-1800/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

References

  1. Hamra GB, Laden F, Cohen AJ, et al. Lung Cancer and Exposure to Nitrogen Dioxide and Traffic: A Systematic Review and Meta-Analysis. Environ Health Perspect 2015;123:1107-12. [Crossref] [PubMed]
  2. Hussain MS, Gupta G, Mishra R, et al. Unlocking the secrets: Volatile Organic Compounds (VOCs) and their devastating effects on lung cancer. Pathol Res Pract 2024;255:155157. [Crossref] [PubMed]
  3. Lu X, Li R, Yan X. Airway hyperresponsiveness development and the toxicity of PM2.5. Environ Sci Pollut Res Int 2021;28:6374-91. [Crossref] [PubMed]
  4. WHO. WHO global air quality guidelines: Particulate matter (PM2.5 and PM10), ozone, nitrogen dioxide, sulfur dioxide and carbon monoxide. Geneva: World Health Organization; 2021.
  5. Münzel T, Gori T, Al-Kindi S, et al. Effects of gaseous and solid constituents of air pollution on endothelial function. Eur Heart J 2018;39:3543-50. [Crossref] [PubMed]
  6. Anderson JO, Thundiyil JG, Stolbach A. Clearing the air: a review of the effects of particulate matter air pollution on human health. J Med Toxicol 2012;8:166-75. [Crossref] [PubMed]
  7. IQAir. World’s Most Polluted cities in 2024 - PM2.5 Ranking [cited 2025 July 1]. Available online: https://www.iqair.com/us/world-most-polluted-cities
  8. Fann N, Kim SY, Olives C, et al. Estimated Changes in Life Expectancy and Adult Mortality Resulting from Declining PM2.5 Exposures in the Contiguous United States: 1980-2010. Environ Health Perspect 2017;125:097003. [Crossref] [PubMed]
  9. Shaddick G, Thomas ML, Mudu P, et al. Half the world’s population are exposed to increasing air pollution. Npj Clim Atmospheric Sci 2020;3:23.
  10. Shi L, Zanobetti A, Kloog I, et al. Low-Concentration PM2.5 and Mortality: Estimating Acute and Chronic Effects in a Population-Based Study. Environ Health Perspect 2016;124:46-52. [Crossref] [PubMed]
  11. Schwartz J, Dockery DW, Neas LM. Is daily mortality associated specifically with fine particles? J Air Waste Manag Assoc 1996;46:927-39.
  12. Lewis TC, Robins TG, Dvonch JT, et al. Air pollution-associated changes in lung function among asthmatic children in Detroit. Environ Health Perspect 2005;113:1068-75. [Crossref] [PubMed]
  13. Franklin M, Koutrakis P, Schwartz P. The role of particle composition on the association between PM2.5 and mortality. Epidemiology 2008;19:680-9. [Crossref] [PubMed]
  14. Feng Y, Li J, Wang Y, et al. Fine particulate matter exposure and cancer risk: a systematic review and meta-analysis of prospective cohort studies. Rev Environ Health 2025;40:792-819. [Crossref] [PubMed]
  15. Loomis D, Grosse Y, Lauby-Secretan B, et al. The carcinogenicity of outdoor air pollution. Lancet Oncol 2013;14:1262-3. [Crossref] [PubMed]
  16. Hamra GB, Guha N, Cohen A, et al. Outdoor particulate matter exposure and lung cancer: a systematic review and meta-analysis. Environ Health Perspect 2014;122:906-11. [Crossref] [PubMed]
  17. Huang Y, Zhu M, Ji M, et al. Air Pollution, Genetic Factors, and the Risk of Lung Cancer: A Prospective Study in the UK Biobank. Am J Respir Crit Care Med 2021;204:817-25. [Crossref] [PubMed]
  18. Hill W, Lim EL, Weeden CE, et al. Lung adenocarcinoma promotion by air pollutants. Nature 2023;616:159-67. [Crossref] [PubMed]
  19. Bowe B, Xie Y, Yan Y, et al. Burden of Cause-Specific Mortality Associated With PM2.5 Air Pollution in the United States. JAMA Netw Open 2019;2:e1915834. [Crossref] [PubMed]
  20. Pelosof L, Ahn C, Gao A, et al. Proportion of Never-Smoker Non-Small Cell Lung Cancer Patients at Three Diverse Institutions. J Natl Cancer Inst 2017;109:djw295. [Crossref] [PubMed]
  21. Cufari ME, Proli C, De Sousa P, et al. Increasing frequency of non-smoking lung cancer: Presentation of patients with early disease to a tertiary institution in the UK. Eur J Cancer 2017;84:55-9. [Crossref] [PubMed]
  22. LoPiccolo J, Gusev A, Christiani DC, et al. Lung cancer in patients who have never smoked - an emerging disease. Nat Rev Clin Oncol 2024;21:121-46. [Crossref] [PubMed]
  23. Hutchings H, Wang A, Grady S, et al. Influence of air quality on lung cancer in people who have never smoked. J Thorac Cardiovasc Surg 2025;169:454-461.e2. [Crossref] [PubMed]
  24. Hvidtfeldt UA, Severi G, Andersen ZJ, et al. Long-term low-level ambient air pollution exposure and risk of lung cancer - A pooled analysis of 7 European cohorts. Environ Int 2021;146:106249. [Crossref] [PubMed]
  25. Chang ET, Lau EC, Moolgavkar SH. Smoking, air pollution, and lung cancer risk in the Nurses' Health Study cohort: time-dependent confounding and effect modification. Crit Rev Toxicol 2020;50:189-200. [Crossref] [PubMed]
  26. Myers R, Brauer M, Dummer T, et al. High-Ambient Air Pollution Exposure Among Never Smokers Versus Ever Smokers With Lung Cancer. J Thorac Oncol 2021;16:1850-8. [Crossref] [PubMed]
  27. Zhai X, Wang J, Sun J, et al. PM(2.5) induces inflammatory responses via oxidative stress-mediated mitophagy in human bronchial epithelial cells. Toxicol Res (Camb) 2022;11:195-205. [Crossref] [PubMed]
  28. Dou C, Zhang J, Qi C. Cooking oil fume-derived PM(2.5) induces apoptosis in A549 cells and MAPK/NF-кB/STAT1 pathway activation. Environ Sci Pollut Res Int 2018;25:9940-8. [Crossref] [PubMed]
  29. Xu Z, Wu H, Zhang H, et al. Interleukins 6/8 and cyclooxygenase-2 release and expressions are regulated by oxidative stress-JAK2/STAT3 signaling pathway in human bronchial epithelial cells exposed to particulate matter ≤2.5 μm. J Appl Toxicol 2020;40:1210-8. [Crossref] [PubMed]
  30. Valavanidis A, Vlachogianni T, Fiotakis K, et al. Pulmonary oxidative stress, inflammation and cancer: respirable particulate matter, fibrous dusts and ozone as major causes of lung carcinogenesis through reactive oxygen species mechanisms. Int J Environ Res Public Health 2013;10:3886-907. [Crossref] [PubMed]
  31. Sharma VJ, Iyengar AJ, Zannino D, et al. Protein-losing enteropathy and plastic bronchitis after the Fontan procedure. J Thorac Cardiovasc Surg 2021;161:2158-2165.e4. [Crossref] [PubMed]
  32. Barbier E, Carpentier J, Simonin O, et al. Oxidative stress and inflammation induced by air pollution-derived PM(2.5) persist in the lungs of mice after cessation of their sub-chronic exposure. Environ Int 2023;181:108248. [Crossref] [PubMed]
  33. Devarakonda S, Li Y, Martins Rodrigues F, et al. Genomic Profiling of Lung Adenocarcinoma in Never-Smokers. J Clin Oncol 2021;39:3747-58. [Crossref] [PubMed]
  34. Chen CY, Huang KY, Chen CC, et al. The role of PM2.5 exposure in lung cancer: mechanisms, genetic factors, and clinical implications. EMBO Mol Med 2025;17:31-40. [Crossref] [PubMed]
  35. Chapman AM, Sun KY, Ruestow P, et al. Lung cancer mutation profile of EGFR, ALK, and KRAS: Meta-analysis and comparison of never and ever smokers. Lung Cancer 2016;102:122-34. [Crossref] [PubMed]
  36. Vasudevan S, Krishna V, Mehta A. Lung Cancer in Non-Smokers: Clinicopathological and Survival Differences from Smokers. Cureus 2022;14:e32417. [Crossref] [PubMed]
  37. Thatcher N, Chang A, Parikh P, et al. Gefitinib plus best supportive care in previously treated patients with refractory advanced non-small-cell lung cancer: results from a randomised, placebo-controlled, multicentre study (Iressa Survival Evaluation in Lung Cancer). Lancet 2005;366:1527-37. [Crossref] [PubMed]
  38. Shepherd FA, Rodrigues Pereira J, Ciuleanu T, et al. Erlotinib in previously treated non-small-cell lung cancer. N Engl J Med 2005;353:123-32. [Crossref] [PubMed]
  39. Wang TH, Huang KY, Chen CC, et al. PM2.5 promotes lung cancer progression through activation of the AhR-TMPRSS2-IL18 pathway. EMBO Mol Med 2023;15:e17014. [Crossref] [PubMed]
  40. Tseng CH, Chiang CJ, Tseng JS, et al. EGFR mutation, smoking, and gender in advanced lung adenocarcinoma. Oncotarget 2017;8:98384-93. [Crossref] [PubMed]
  41. Sonobe M, Manabe T, Wada H, et al. Mutations in the epidermal growth factor receptor gene are linked to smoking-independent, lung adenocarcinoma. Br J Cancer 2005;93:355-63. [Crossref] [PubMed]
  42. Soria JC, Ohe Y, Vansteenkiste J, et al. Osimertinib in Untreated EGFR-Mutated Advanced Non-Small-Cell Lung Cancer. N Engl J Med 2018;378:113-25. [Crossref] [PubMed]
  43. Wu YL, Tsuboi M, He J, et al. Osimertinib in Resected EGFR-Mutated Non-Small-Cell Lung Cancer. N Engl J Med 2020;383:1711-23. [Crossref] [PubMed]
  44. Tsuboi M, Weder W, Escriu C, et al. Neoadjuvant osimertinib with/without chemotherapy versus chemotherapy alone for EGFR-mutated resectable non-small-cell lung cancer: NeoADAURA. Future Oncol 2021;17:4045-55. [Crossref] [PubMed]
  45. Chandwani R, Brokamp C, Salfity H, et al. Impact of Environmental Exposures on Lung Cancer in Patients Who Never Smoked. World J Surg 2023;47:2578-86. [Crossref] [PubMed]
  46. Liu C, Yang D, Liu Y, et al. The effect of ambient PM(2.5) exposure on survival of lung cancer patients after lobectomy. Environ Health 2023;22:23. [Crossref] [PubMed]
  47. Whitrock JN, Carter MM, Pratt CG, et al. The Role of Environmental Exposures on Survival After Non-Small Cell Lung Cancer Resection. Ann Thorac Surg Short Rep 2024;2:618-23. [Crossref] [PubMed]
  48. Jbaily A, Zhou X, Liu J, et al. Air pollution exposure disparities across US population and income groups. Nature 2022;601:228-33. [Crossref] [PubMed]
  49. Heindel JJ, Alvarez JA, Atlas E, et al. Obesogens and Obesity: State-of-the-Science and Future Directions Summary from a Healthy Environment and Endocrine Disruptors Strategies Workshop. Am J Clin Nutr 2023;118:329-37. [Crossref] [PubMed]
  50. Heindel JJ, Lustig RH, Howard S, et al. Obesogens: a unifying theory for the global rise in obesity. Int J Obes (Lond) 2024;48:449-60. [Crossref] [PubMed]
  51. Peng Y, Zhao Y, Wang M, et al. Exposure to PM(2.5) and its components leads to obesity: role of socioeconomic status. Sci Rep 2025;15:114. [Crossref] [PubMed]
  52. Hidayat K, Du X, Chen G, et al. Abdominal Obesity and Lung Cancer Risk: Systematic Review and Meta-Analysis of Prospective Studies. Nutrients 2016;8:810. [Crossref] [PubMed]
Cite this article as: Turner D, Hedrick D, Starnes SL, Van Haren RM. Looking through the particles: a narrative review of air pollution and lung cancer. J Thorac Dis 2025;17(12):11369-11376. doi: 10.21037/jtd-2025-1800

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