A comprehensive examination of the impact of environmental pollution on lung cancer: A review

Our plain-English summary of A comprehensive examination of the impact of environmental pollution on lung cancer: A review, by H. Zhang, H. Wei, S. Han, et al (Journal of Advanced Research, 2026).

The study

• Authors: H. Zhang, H. Wei, S. Han, L. Zheng, X. Chen, Z. Li, L. Wang
• Journal: Journal of Advanced Research
• Published: 2026;81:273-286
• Type of article: Review
• Cited by: 16 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Background: Lung cancer is a leading cause of death worldwide, with environmental factors playing critical roles in its development and progression. Respirable and food-borne contaminants are major contributors to lung cancer onset, influencing various physiological pathways that lead to lung injury and tumor formation.

Aim Of Review: This review aims to examine the effects of common environmental pollutants on lung cancer development, highlighting the role of specific contaminants, such as PM2.5 (particulate matter with aerodynamic diameter less than 2.5 µm) and nitrogen oxides, and warning people to pay more attention to environmental pollutants.

Key Scientific Concepts Of Review: Environmental pollutants play a significant role in increasing the susceptibility to lung cancer by triggering various biological mechanisms that lead to lung injury and tumorigenesis. Excessive PM2.5 exposure contributes to the overall burden of lung cancer via Wnt/β-catenin, Reactive oxygen species-DNA methyltransferases (ROS-DNMT), phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB/Akt), Janus kinase/signal transducers and activators of transcription (JAK/STAT) signalling pathways. The primary mechanisms by which NO contributes to the occurrence and development of pulmonary neoplasm revolve around the production and regulation of ROS. Occupational exposure and ecosystem pollution to hazardous substances, including microplastics, pesticides, asbestos, cadmium, and nickel, are the well-established risk factors for the development of lung cancer via DNA damage, oxidative stress, and inflammation pathways. This review emphasizes the importance of effective prevention strategies for lung cancer by reducing environmental pollution levels.

Copyright © 2025. Published by Elsevier B.V.

In plain English

This article was a narrative review, not a new study. The authors summarized published research on how environmental pollutants may contribute to lung cancer. They covered PM2.5 (fine particulate matter), nitrogen oxides, microplastics, passive smoking, polycyclic aromatic hydrocarbons, radon, asbestos, silica, cadmium, nickel and pesticides. The article did not describe how studies were found or chosen. Much of it covered laboratory and animal findings on oxidative stress, inflammation and DNA damage. The short asbestos section drew on an earlier review. It described asbestos fibers causing lung inflammation and damage to DNA and chromosomes, and linked genes such as BAP1, ALK and MET to pleural and lung disease. It named no fiber types and gave no asbestos risk figures. The review reported no new data of its own, and most of its figures were attributed to other studies. For example, a cited case-control study found an odds ratio of 4.41 (95% confidence interval 2.01 to 9.67) for lung cancer in the highest versus lowest cadmium quartile. The authors stated that occupational asbestos exposure had the highest carcinogenic intensity, with a lung cancer relative risk much higher than outdoor PM2.5 or passive smoking. They gave no figures for this comparison. They concluded that workplace carcinogens, including asbestos, warrant enhanced regulatory oversight.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Narrative review. No search method or study selection process is described.
• Who was studied: No study population of its own. The authors reviewed published cell, animal and human studies on environmental pollutants and lung cancer. They did not report the number of studies or the time period covered.
• Exposure: Multiple pollutants: PM2.5, nitrogen oxides, microplastics, passive smoking, polycyclic aromatic hydrocarbons, radon, asbestos, silica, cadmium, nickel and pesticides. Asbestos is discussed as 'asbestos fibers' without naming fiber types.
• Main results:
  • Citing an earlier review (reference 105), the authors described asbestos fibers as able to cause mutagenicity and genotoxicity. They described damage to DNA and chromosomes either directly or through reactive oxygen and nitrogen species.
  • Citing the same earlier review, the authors linked changes in certain genes, including BAP1, ALK and MET, to pleural and pulmonary disease.
  • In their conclusion, the authors stated that occupational asbestos exposure has the highest carcinogenic intensity. They said its relative risk of lung cancer is much higher than that of outdoor PM2.5 and indoor passive smoking. No figures were given for this comparison.
  • The authors described occupational asbestos exposure as having a narrower exposure range than outdoor PM2.5, mainly confined to employees of specific industries.
  • Citing a case-control study by Lener and colleagues, the authors reported that people in the top quartile of cadmium exposure had a lung cancer odds ratio of 4.41 (95% CI 2.01 to 9.67) compared with the bottom quartile.
  • The authors reported that each 100 Bq/m3 increase in radon was linked to increases of 11%, 19% and 13% in the likelihood of small cell lung cancer, adenocarcinoma and squamous cell carcinoma, respectively. This sentence carries no citation of its own.
  • Citing a meta-analysis of 37 studies, the authors reported that non-smokers living with smokers had a 24% increased lifetime risk of lung cancer.
• The authors' conclusion: The authors concluded that there is a robust association between environmental contaminants and lung cancer. They identified ambient air pollution, household pollutants and occupational exposure as primary causes. In their view, workplace carcinogens including asbestos and heavy metals warrant enhanced regulatory oversight and stringent safety protocols.
• Limitations the authors state:
  • Regarding PM2.5, the authors stated that the causal sequence between inflammatory pathways and cancer has not yet been determined.
  • Regarding pesticides, the authors stated that human epidemiological evidence on lung cancer remains inconclusive.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Lung cancer.

Medical terms in this study, explained in our Lexicon: Lung Cancer, Carcinogenesis, Reactive Oxygen Species (ROS), Neoplasm, Occupational Exposure, Oxidative Stress, Inflammation.

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