Smoking and environmental exposures on the onset of pulmonary fibrosis
DOI:
https://doi.org/10.70577/asce.v5i2.808Keywords:
pulmonary fibrosis; smoking; pollutants; oxidative stressAbstract
Pulmonary fibrosis (PF) is a progressive interstitial disease characterized by pulmonary remodeling, loss of elasticity, and high morbidity and mortality. Its development is associated with persistent inflammation and external factors such as smoking and exposure to environmental pollutants. This descriptive, retrospective study involved a review of the current literature through scientific databases using MeSH and DeCS terms. Thirty-four references from the past 5 years were included, comprising 10 primary studies selected using a PRISMA 2020 flowchart.
The evidence demonstrated that tobacco smoke, particulate matter (PM2.5 and PM10), nanoparticles, and other environmental toxins lead to oxidative stress and epithelial damage, activating profibrotic pathways such as TGF-β1, p38 MAPK, Wnt/β-catenin, and PI3K-Akt. The involvement of LINC00665 and NAT10-mediated stabilization of TGF-β1 is also highlighted, as these promote epithelial-mesenchymal transition and fibroblast proliferation. The combined action of tobacco and pollutants reduces macrophage clearance and contributes to lung deterioration.
Studies agree that long-term oxidative stress and fibroblast activation are key processes in the progression of PF. It is concluded that smoking and environmental pollutants are decisive factors in its pathogenesis and that their combined effect worsens the prognosis, highlighting the need to detect and reduce these exposures early on.
Downloads
References
Afthab, M., Hambo, S., Kim, H., Alhamad, A., & Harb, H. (2024). Particulate matter-induced epigenetic modifications and lung complications. In European Respiratory Review (Vol. 33, Number 174). European Respiratory Society. https://doi.org/10.1183/16000617.0129-2024
Calle, C. A., Rosales, M. F., & Macías Eddyn, R. (2022). Caracterización clínica de pacientes con fibrosis pulmonar idiopática en un hospital de tercer nivel en la ciudad de Quito-Ecuador. Revista Americana de Medicina Respiratoria, 22.
Casal, A., Suárez-Antelo, J., Riveiro, V., Ferreiro, L., Rodríguez-Núñez, N., Toubes, M. E., & Valdés, L. (2024). Smoking-related interstitial lung disease: A narrative review. Chronic Respiratory Disease, 21. https://doi.org/10.1177/14799731241291538
Douglas, D., Keating, L., Strykowski, R., Lee, C. T., Garcia, N., Selvan, K., Kaushik, N., Ventura, I. B., Jablonski, R., Vij, R., Chung, J. H., Bellam, S., Strek, M. E., & Adegunsoye, A. (2023). Tobacco smoking is associated with combined pulmonary fibrosis and emphysema and worse outcomes in interstitial lung disease. American Journal of Physiology - Lung Cellular and Molecular Physiology, 325(2), L233–L243. https://doi.org/10.1152/ajplung.00083.2023
Gandhi, S., Tonelli, R., Murray, M., Samarelli, A. V., & Spagnolo, P. (2023). Environmental Causes of Idiopathic Pulmonary Fibrosis. In International Journal of Molecular Sciences (Vol. 24, Number 22). Multidisciplinary Digital Publishing Institute (MDPI). https://doi.org/10.3390/ijms242216481
Geng, Y., Li, L., Yan, J., Liu, K., Yang, A., Zhang, L., Shen, Y., Gao, H., Wu, X., Noth, I., Huang, Y., Liu, J., & Fan, X. (2022). PEAR1 regulates expansion of activated fibroblasts and deposition of extracellular matrix in pulmonary fibrosis. Nature Communications, 13(1). https://doi.org/10.1038/s41467-022-34870-w
Ghio, A. J., Stewart, M., Sangani, R. G., Pavlisko, E. N., & Roggli, V. L. (2025). Cigarette smoking decreases macrophage-dependent clearance to impact the biological effects of occupational and environmental particle exposures. In Frontiers in Public Health (Vol. 13). Frontiers Media SA. https://doi.org/10.3389/fpubh.2025.1558723
Glass, D. S., Grossfeld, D., Renna, H. A., Agarwala, P., Spiegler, P., DeLeon, J., & Reiss, A. B. (2022). Idiopathic pulmonary fibrosis: Current and future treatment. The Clinical Respiratory Journal, 16(2), 84–96. https://doi.org/10.1111/crj.13466
Hu, Y., Huang, Y., Zong, L., Lin, J., Liu, X., & Ning, S. (2024). Emerging roles of ferroptosis in pulmonary fibrosis: current perspectives, opportunities and challenges. Cell Death Discovery, 10(1), 301. https://doi.org/10.1038/s41420-024-02078-0
Jiang, M., Bu, W., Wang, X., Ruan, J., Shi, W., Yu, S., Huang, L., Xue, P., Tang, J., Zhao, X., Su, L., & Cheng, D. (2025). Pulmonary fibrosis: from mechanisms to therapies. In Journal of Translational Medicine (Vol. 23, Number 1). BioMed Central Ltd. https://doi.org/10.1186/s12967-025-06514-2
Jo, Y. S., & Song, J. W. (2025). Air Pollution and Interstitial Lung Disease. Tuberculosis and Respiratory Diseases, 88(1), 45–55. https://doi.org/10.4046/trd.2024.0116
Johannson, K. A., Adegunsoye, A., Behr, J., Cottin, V., Glanville, A. R., Glassberg, M. K., Goobie, G. C., Jenkins, R. G., Kim, J. S., Lee, C. T., Redlich, C. A., Richeldi, L., Salisbury, M. L., Tetley, T., & Corte, T. J. (2025). Impact of Environmental Exposures on the Development and Progression of Fibrotic Interstitial Lung Disease. American Journal of Respiratory and Critical Care Medicine, 211(4), 560–568. https://doi.org/10.1164/rccm.202409-1730PP
Kumar, A., Cherian, S. V., Vassallo, R., Yi, E. S., & Ryu, J. H. (2018). Current Concepts in Pathogenesis, Diagnosis, and Management of Smoking-Related Interstitial Lung Diseases. Chest, 154(2), 394–408. https://doi.org/10.1016/j.chest.2017.11.023
Luo, C., Wu, X., Zhang, S., Tan, J., Song, X., Ning, B., Tang, Q., Huo, Y., Li, J., Ye, Y., & Wang, F. (2025). Effects of air pollutants on the incidence, progression, and mortality of idiopathic pulmonary fibrosis: a systematic review and meta-analysis. In BMC Public Health (Vol. 25, Number 1). BioMed Central Ltd. https://doi.org/10.1186/s12889-025-24158-1
Majewski, S., & Piotrowski, W. J. (2021). Air pollution—an overlooked risk factor for idiopathic pulmonary fibrosis. In Journal of Clinical Medicine (Vol. 10, Number 1, pp. 1–15). MDPI. https://doi.org/10.3390/jcm10010077
Makena, P., Kikalova, T., Prasad, G. L., & Baxter, S. A. (2023). Oxidative Stress and Lung Fibrosis: Towards an Adverse Outcome Pathway. In International Journal of Molecular Sciences (Vol. 24, Number 15). Multidisciplinary Digital Publishing Institute (MDPI). https://doi.org/10.3390/ijms241512490
Pardo, A., & Selman, M. (2021). The Interplay of the Genetic Architecture, Aging, and Environmental Factors in the Pathogenesis of Idiopathic Pulmonary Fibrosis. American Journal of Respiratory Cell and Molecular Biology, 64(2), 163–172. https://doi.org/10.1165/rcmb.2020-0373PS
Platenburg, M. G. J. P., van der Vis, J. J., Kazemier, K. M., Grutters, J. C., & van Moorsel, C. H. M. (2022). The detrimental effect of quantity of smoking on survival in progressive fibrosing ILD. Respiratory Medicine, 194, 106760. https://doi.org/10.1016/j.rmed.2022.106760
Ren, L.-L., Miao, H., Wang, Y.-N., Liu, F., Li, P., & Zhao, Y.-Y. (2023). TGF-β as A Master Regulator of Aging-Associated Tissue Fibrosis. Aging and Disease, 14(5), 1633. https://doi.org/10.14336/AD.2023.0222
Savin, I. A., Zenkova, M. A., & Sen’kova, A. V. (2022). Pulmonary Fibrosis as a Result of Acute Lung Inflammation: Molecular Mechanisms, Relevant In Vivo Models, Prognostic and Therapeutic Approaches. International Journal of Molecular Sciences, 23(23), 14959. https://doi.org/10.3390/ijms232314959
Shahabi, R., Dehghani, M., Javad Moosavi, S. A., Shahabi, B., Poordakan, O., Sadeghi, M., Aryan, L., Ghasempoor, A., Aghanasiri, F., Mohseni, M., & Mehravi, B. (2022). The effect of nanoparticles on pulmonary fibrosis: a systematic review and Meta-analysis of preclinical studies. Archives of Environmental and Occupational Health, 77(8), 684–694. https://doi.org/10.1080/19338244.2021.2001637
Song, M., Shen, Q., Ouyang, X., Zhou, Z., Luo, H., & Peng, H. (2023). CSE regulates LINC000665/XBP-1 in the progress of pulmonary fibrosis. Tobacco Induced Diseases, 21(December). https://doi.org/10.18332/tid/175004
Spagnolo, P., Ryerson, C. J., Guler, S., Feary, J., Churg, A., Fontenot, A. P., Piciucchi, S., Udwadia, Z., Corte, T. J., Wuyts, W. A., Johannson, K. A., & Cottin, V. (2023). Occupational interstitial lung diseases. Journal of Internal Medicine, 294(6), 798–815. https://doi.org/10.1111/joim.13707
Sung, J. S., Ko, I. G., Hwang, L., Kim, S. H., Han, J. H., Jeon, J. W., Kim, S. R., Lee, J. M., & Choi, C. W. (2025). Pirfenidone Alleviates Against Fine Particulate Matter-Induced Pulmonary Fibrosis Modulating via TGF-β1/TAK1/MKK3/p38 MAPK Signaling Pathway in Rats. Biomedicines, 13(4). https://doi.org/10.3390/biomedicines13040989
Tahara, M., Fujino, Y., Yamasaki, K., Oda, K., Kido, T., Sakamoto, N., Kawanami, T., Kataoka, K., Egashira, R., Hashisako, M., Suzuki, Y., Fujisawa, T., Mukae, H., Suda, T., & Yatera, K. (2021). Exposure to PM2.5 is a risk factor for acute exacerbation of surgically diagnosed idiopathic pulmonary fibrosis: a case–control study. Respiratory Research, 22(1). https://doi.org/10.1186/s12931-021-01671-6
Tomos, I., Dimakopoulou, K., Manali, E. D., Papiris, S. A., & Karakatsani, A. (2021). Long-term personal air pollution exposure and risk for acute exacerbation of idiopathic pulmonary fibrosis. Environmental Health: A Global Access Science Source, 20(1). https://doi.org/10.1186/s12940-021-00786-z
Tulmo Quimbita, J. E., & Salinas Velastegui, V. G. (2024). Factores de riesgo intrínsecos y extrínsecos que favorecen el desarrollo de fibrosis pulmonar en pacientes mayores de 65 años, revisión de la literatura. Mediciencias UTA, 8(1), 35–43. https://doi.org/10.31243/mdc.uta.v8i1.2307.2024
Vehar, S. J., Yadav, R., Mukhopadhyay, S., Nathani, A., & Tolle, L. B. (2023). Smoking-Related Interstitial Fibrosis (SRIF) in Patients Presenting with Diffuse Parenchymal Lung Disease. American Journal of Clinical Pathology, 159(2), 146–157. https://doi.org/10.1093/ajcp/aqac144
Wu, S., Yin, L., Han, K., Jiang, B., Meng, Q., Aschner, M., Li, X., & Chen, R. (2023). NAT10 accelerates pulmonary fibrosis through N4-acetylated TGFB1-initiated 1 epithelial-to-mesenchymal transition upon ambient fine particulate matter 2 exposure 3.
Xue, S., Broerman, M. J., Goobie, G. C., Kass, D. J., Fabisiak, J. P., Wenzel, S. E., & Nouraie, S. M. (2025). Gaseous Air Pollutants and Lung Function in Fibrotic Interstitial Lung Disease (fILD): Evaluation of Different Spatial Analysis Approaches. Environmental Science & Technology, 59(12), 5936–5945. https://doi.org/10.1021/acs.est.4c11275
Yoon, H. Y., Kim, H., Bae, Y., & Song, J. W. (2024). Smoking status and clinical outcome in idiopathic pulmonary fibrosis: a nationwide study. Respiratory Research, 25(1). https://doi.org/10.1186/s12931-024-02819-w
Yoon, H.-Y., Kim, S.-Y., Kim, O.-J., & Song, J. W. (2021). Nitrogen dioxide increases the risk of mortality in idiopathic pulmonary fibrosis. European Respiratory Journal, 57(5), 2001877. https://doi.org/10.1183/13993003.01877-2020
Zhang, J., Du, J., Liu, D., Zhuo, J., Chu, L., Li, Y., Gao, L., Xu, M., Chen, W., Huang, W., Xie, L., Chen, J., Meng, X., Zou, F., Cai, S., & Dong, H. (2024). Polystyrene microplastics induce pulmonary fibrosis by promoting alveolar epithelial cell ferroptosis through cGAS/STING signaling. Ecotoxicology and Environmental Safety, 277. https://doi.org/10.1016/j.ecoenv.2024.116357
Zhang, Y., Huang, W., Zheng, Z., Wang, W., Yuan, Y., Hong, Q., Lin, J., Li, X., & Meng, Y. (2021). Cigarette smoke-inactivated SIRT1 promotes autophagy-dependent senescence of alveolar epithelial type 2 cells to induce pulmonary fibrosis. Free Radical Biology and Medicine, 166, 116–127. https://doi.org/10.1016/j.freeradbiomed.2021.02.013
Downloads
Published
How to Cite
Issue
Section
License
Copyright (c) 2026 Ashly Mishel Aguilar R., Juana Karina Pineda A., Edgar Alexander Salazar C.
This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.
Eres libre de:
- Compartir : copiar y redistribuir el material en cualquier medio o formato
- Adaptar : remezclar, transformar y desarrollar el material
- El licenciante no puede revocar estas libertades siempre y cuando usted cumpla con los términos de la licencia.
En los siguientes términos:
- Atribución : Debe otorgar el crédito correspondiente , proporcionar un enlace a la licencia e indicar si se realizaron cambios . Puede hacerlo de cualquier manera razonable, pero no de ninguna manera que sugiera que el licenciante lo respalda a usted o a su uso.
- No comercial : no puede utilizar el material con fines comerciales .
- CompartirIgual — Si remezcla, transforma o construye sobre el material, debe distribuir sus contribuciones bajo la misma licencia que el original.
- Sin restricciones adicionales : no puede aplicar términos legales ni medidas tecnológicas que restrinjan legalmente a otros hacer algo que la licencia permite.
