Cigarette smoking decreases macrophage-dependent clearance to impact the biological effects of occupational and environmental particle exposures

Our plain-English summary of Cigarette smoking decreases macrophage-dependent clearance to impact the biological effects of occupational and environmental particle exposures, by A.J. Ghio, M. Stewart, R.G. Sangani, et al (Frontiers in Public Health, 2025).

The study

• Authors: A.J. Ghio, M. Stewart, R.G. Sangani, E.N. Pavlisko, V.L. Roggli
• Journal: Frontiers in Public Health
• Published: 2025;13:1558723
• Type of article: Review
• Cited by: 6 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

The retention of occupational and environmental particles in the lung is a primary determinant of biological effects. In the distal respiratory tract, particle clearance includes phagocytosis by alveolar macrophages (AMs), migration to the terminal bronchiole, and transport of AMs and particles by the mucociliary escalator. With increasing particle exposure, a focal collection of particle-laden macrophages results at the respiratory bronchiole (RB) which is that site in the clearance pathway demanding the greatest traverse by these cells after a commencement from the alveoli. With the greatest particle doses, there is "particle overload" and impaired mobility which is reflected by an excess accumulation of particle-laden macrophages throughout the RBs, alveolar ducts, and alveoli. With deposition of fibrous particles in the distal respiratory tract, the AM is unable to extend itself to enclose fibers with a major diameter of 10-20 microns or longer resulting in "frustrated phagocytosis" and longer retention times. Clearance pathways for particles are shared. There can be a summation of particle exposures with exhaustion in the capacity of the AMs for transport. Cigarette smoking (CS) is the greatest particle challenge humans encounter. Associated with its enormous magnitude, CS profoundly impacts the clearance pathways and subsequently interacts with other particle exposures to increase biological effects. Interstitial lung disease, pulmonary function, chronic obstructive pulmonary disease, infections, lung cancer, and mortality can be altered among smokers exposed to occupational and environmental particles (e.g., silica, coal mine dust, air pollution particles, other particles, and asbestos). It is concluded that both decreasing CS and controlling particle exposures are of vital importance in occupational and environmental lung disease.

Copyright © 2025 Ghio, Stewart, Sangani, Pavlisko and Roggli.

In plain English

In this review, the authors described particle clearance, which in the deepest parts of the lung depends on cells called alveolar macrophages, and summarized earlier research on how cigarette smoking interacts with silica, coal mine dust, air pollution particles, other dusts, and asbestos. For asbestos, they explained that macrophages cannot fully enclose fibers with a major diameter of 10–20 microns or longer, so these fibers stay in the lung longer. They also explained that asbestosis typically appears as small irregular opacities in the lower lobes. Citing earlier studies, the review reported that among asbestos-exposed people, smoking was linked to more small lung opacities, more pleural thickening or plaques, and greater loss of lung function. For lung cancer, it described interactions ranging from additive to multiplicative. US Navy surveillance data showed definite radiologic parenchymal abnormalities (ILO category 1/0 or higher) in 3.10 percent of 32,233 smokers versus 1.09 percent of 13,414 non-smokers. Some increases in opacities among smokers have been attributed to diffuse interstitial fibrosis. The authors concluded that smoking almost always increases the risk for or worsens many particle-related lung diseases.

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 of published research. No new data were collected.
• Who was studied: No study population of its own. The review drew on earlier human, pathology and animal studies of smokers and non-smokers exposed to occupational and environmental particles.
• Exposure: Cigarette smoking combined with silica, coal mine dust, air pollution particles, other particles (such as vermiculite, talc, flour and cotton dust), and asbestos. Specific asbestos fiber types were not distinguished in the review's discussion.
• Main results:
  • The review described two clearance pathways. In the conducting airways the main pathway is the mucociliary escalator. In the distal respiratory tract, clearance depends on phagocytosis and transport by alveolar macrophages.
  • The review explained that macrophages cannot fully enclose longer fibers (described as a major diameter of 10–20 microns or longer), which leads to longer retention in the lung.
  • Asbestosis was described as small irregular opacities, bilateral and commonly in the lower lobes, unlike silicosis and coal workers' pneumoconiosis.
  • The dust dose retained in the lungs in asbestosis was described as milligrams, compared with grams or tens of grams in silicosis and coal workers' pneumoconiosis.
  • Citing earlier studies, the review reported an interaction between smoking and asbestos exposure in the occurrence of small opacities on chest X-ray, CT and pathology specimens.
  • In the US Navy's Asbestos Medical Surveillance Program, definite radiologic parenchymal abnormalities (ILO category 1/0 or higher) were found in 3.10 percent of 32,233 smokers versus 1.09 percent of 13,414 non-smokers.
  • The review noted that increases in the profusion of asbestosis with smoking have been attributed to diffuse interstitial fibrosis.
  • Earlier studies were cited as showing that smoking can increase the risk for pleural thickening or plaques.
  • Among insulators, reductions in FVC and FEV1/FVC were more frequent in smokers than in non-smokers or in smokers in the general population. One cited study found additive but not synergistic effects of smoking and asbestos on manifestations of asbestosis.
  • For lung cancer, the review described an interaction between smoking and asbestos exposure that ranged from additive to supra-additive to multiplicative across cited studies.
• The authors' conclusion: The authors concluded that smoking interacts with other particles through its effect on clearance, and that it almost always increases the risk for or exacerbates many particle-related lung diseases. They also concluded that both decreasing smoking and controlling particle exposures are of vital importance in occupational and environmental lung disease.
• Limitations the authors state:
  • The authors stated that research on interactions between coal mine dust and smoking has been limited.

Topics

Medical terms in this study, explained in our Lexicon: Macrophage, Phagocytosis, Alveolar Macrophage, Mucociliary Clearance, Alveoli, Deposition, Frustrated Phagocytosis, Retention TIme.

Related studies

• Smoking, occupational exposures, and idiopathic pulmonary fibrosis among Swedish construction workers — M. Andersson, P.D. Blanc, et al. (2021)
• Risk assessment due to environmental exposures to fibrous particulates associated with taconite ore — R. Wilson, E.E. McConnell, et al. (2008)
• Differential responses of murine alveolar macrophages to elongate mineral particles of asbestiform and non-asbestiform varieties: Cytotoxicity, cytokine secretion and transcriptional changes — T.O. Khaliullin, E.R. Kisin, et al. (2020)
• Apportionment of risk among environmental exposures: application to asbestos exposure and cigarette smoking — R.C. Grimson (1987)
• The Role of Occupational and Environmental Exposures in the Pathogenesis of Idiopathic Pulmonary Fibrosis: A Narrative Literature Review — S.P. Trethewey, G.I. Walters (2018)
• Synergistic effects of mineral fibres and cigarette smoke on the production of tumour necrosis factor by alveolar macrophages of rats — Y. Morimoto, M. Kido, et al. (1993)

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