The role of PM2.5 exposure in lung cancer: mechanisms, genetic factors, and clinical implications
Abstract Lung cancer is one of the most critical global health threats, as the second most common cancer and leading cause of cancer deaths globally. While smoking is the primary risk factor, an increasing number of cases occur in nonsmokers, with lung cancer in nonsmokers (LCNS) now recognized as t...
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| Format: | Article |
| Language: | English |
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Springer Nature
2024-11-01
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| Series: | EMBO Molecular Medicine |
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| Online Access: | https://doi.org/10.1038/s44321-024-00175-2 |
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| author | Chi-Yuan Chen Kuo-Yen Huang Chin-Chuan Chen Ya-Hsuan Chang Hsin-Jung Li Tong-Hong Wang Pan-Chyr Yang |
| author_facet | Chi-Yuan Chen Kuo-Yen Huang Chin-Chuan Chen Ya-Hsuan Chang Hsin-Jung Li Tong-Hong Wang Pan-Chyr Yang |
| author_sort | Chi-Yuan Chen |
| collection | DOAJ |
| description | Abstract Lung cancer is one of the most critical global health threats, as the second most common cancer and leading cause of cancer deaths globally. While smoking is the primary risk factor, an increasing number of cases occur in nonsmokers, with lung cancer in nonsmokers (LCNS) now recognized as the fifth leading cause of cancer mortality worldwide. Recent evidence identifies air pollution, particularly fine particulate matter (PM2.5), as a significant risk factor in LCNS. PM2.5 can increase oxidative stress and inflammation, induce genetic alterations and activation of oncogenes (including the epidermal growth factor receptor, EGFR), and contribute to lung cancer progression. This review summarizes the current understanding of how exposure to PM2.5 induces lung carcinogenesis and accelerates lung cancer development. It underscores the importance of prevention and early detection while calling for targeted therapies to combat the detrimental effects of air pollution. An integrated approach that combines research, public health policy, and clinical practice is essential to reduce the lung cancer burden and improve outcomes for those affected by PM2.5 exposurrre. |
| format | Article |
| id | doaj-art-54a6f16c92bb41d0835806b61b80ce8c |
| institution | Kabale University |
| issn | 1757-4684 |
| language | English |
| publishDate | 2024-11-01 |
| publisher | Springer Nature |
| record_format | Article |
| series | EMBO Molecular Medicine |
| spelling | doaj-art-54a6f16c92bb41d0835806b61b80ce8c2025-01-19T12:34:38ZengSpringer NatureEMBO Molecular Medicine1757-46842024-11-01171314010.1038/s44321-024-00175-2The role of PM2.5 exposure in lung cancer: mechanisms, genetic factors, and clinical implicationsChi-Yuan Chen0Kuo-Yen Huang1Chin-Chuan Chen2Ya-Hsuan Chang3Hsin-Jung Li4Tong-Hong Wang5Pan-Chyr Yang6Graduate Institute of Health Industry Technology and Research Center for Food and Cosmetic Safety, Chang Gung University of Science and TechnologyDepartment of Clinical Laboratory Sciences and Medical Biotechnology, College of Medicine, National Taiwan UniversityBioBank, Chang Gung Memorial Hospital at LinkouInstitute of Molecular and Genomic Medicine, National Health Research InstitutesNational Taiwan University YongLin Institute of Health, National Taiwan UniversityGraduate Institute of Health Industry Technology and Research Center for Food and Cosmetic Safety, Chang Gung University of Science and TechnologyNational Taiwan University YongLin Institute of Health, National Taiwan UniversityAbstract Lung cancer is one of the most critical global health threats, as the second most common cancer and leading cause of cancer deaths globally. While smoking is the primary risk factor, an increasing number of cases occur in nonsmokers, with lung cancer in nonsmokers (LCNS) now recognized as the fifth leading cause of cancer mortality worldwide. Recent evidence identifies air pollution, particularly fine particulate matter (PM2.5), as a significant risk factor in LCNS. PM2.5 can increase oxidative stress and inflammation, induce genetic alterations and activation of oncogenes (including the epidermal growth factor receptor, EGFR), and contribute to lung cancer progression. This review summarizes the current understanding of how exposure to PM2.5 induces lung carcinogenesis and accelerates lung cancer development. It underscores the importance of prevention and early detection while calling for targeted therapies to combat the detrimental effects of air pollution. An integrated approach that combines research, public health policy, and clinical practice is essential to reduce the lung cancer burden and improve outcomes for those affected by PM2.5 exposurrre.https://doi.org/10.1038/s44321-024-00175-2PM2.5InflammationDNA DamageEGFRLung Cancer |
| spellingShingle | Chi-Yuan Chen Kuo-Yen Huang Chin-Chuan Chen Ya-Hsuan Chang Hsin-Jung Li Tong-Hong Wang Pan-Chyr Yang The role of PM2.5 exposure in lung cancer: mechanisms, genetic factors, and clinical implications EMBO Molecular Medicine PM2.5 Inflammation DNA Damage EGFR Lung Cancer |
| title | The role of PM2.5 exposure in lung cancer: mechanisms, genetic factors, and clinical implications |
| title_full | The role of PM2.5 exposure in lung cancer: mechanisms, genetic factors, and clinical implications |
| title_fullStr | The role of PM2.5 exposure in lung cancer: mechanisms, genetic factors, and clinical implications |
| title_full_unstemmed | The role of PM2.5 exposure in lung cancer: mechanisms, genetic factors, and clinical implications |
| title_short | The role of PM2.5 exposure in lung cancer: mechanisms, genetic factors, and clinical implications |
| title_sort | role of pm2 5 exposure in lung cancer mechanisms genetic factors and clinical implications |
| topic | PM2.5 Inflammation DNA Damage EGFR Lung Cancer |
| url | https://doi.org/10.1038/s44321-024-00175-2 |
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