Lung inflammation caused by inhaled toxicants: a review

Our plain-English summary of Lung inflammation caused by inhaled toxicants: a review, by J. Wong, B.E. Magun, L.J. Wood (International Journal of Chronic Obstructive Pulmonary Disease, 2016).

The study

• Authors: J. Wong, B.E. Magun, L.J. Wood
• Journal: International Journal of Chronic Obstructive Pulmonary Disease
• Published: 2016;11:1391-401
• Type of article: Review
• Cited by: 154 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Exposure of the lungs to airborne toxicants from different sources in the environment may lead to acute and chronic pulmonary or even systemic inflammation. Cigarette smoke is the leading cause of chronic obstructive pulmonary disease, although wood smoke in urban areas of underdeveloped countries is now recognized as a leading cause of respiratory disease. Mycotoxins from fungal spores pose an occupational risk for respiratory illness and also present a health hazard to those living in damp buildings. Microscopic airborne particulates of asbestos and silica (from building materials) and those of heavy metals (from paint) are additional sources of indoor air pollution that contributes to respiratory illness and is known to cause respiratory illness in experimental animals. Ricin in aerosolized form is a potential bioweapon that is extremely toxic yet relatively easy to produce. Although the aforementioned agents belong to different classes of toxic chemicals, their pathogenicity is similar. They induce the recruitment and activation of macrophages, activation of mitogen-activated protein kinases, inhibition of protein synthesis, and production of interleukin-1 beta. Targeting either macrophages (using nanoparticles) or the production of interleukin-1 beta (using inhibitors against protein kinases, NOD-like receptor protein-3, or P2X7) may potentially be employed to treat these types of lung inflammation without affecting the natural immune response to bacterial infections.

In plain English

This article was a narrative review, not a new study. The authors summarized research on lung inflammation after breathing in cigarette smoke, mycotoxins (fungal toxins) and ricin. Their aim was to find shared pathways and possible drug targets. Asbestos got only brief attention. The authors wrote that asbestos, crystalline silica, alloy particles and carbon nanotubes can also activate MAPKs (signaling proteins) and the inflammasome (a protein complex). They wrote that macrophages, immune cells that engulf particles, may play an important role in the response to these particles. A table listed inflammatory signaling molecules, including IL-1β and TNF-α, reported for asbestos in earlier studies. The main text did not distinguish asbestos fiber types or discuss asbestos-related diseases; chrysotile and Libby amphiboles appeared only in cited paper titles. Overall, the authors wrote that the toxicants they described all activate MAPKs, inhibit protein synthesis, and use the NLRP3 inflammasome to produce IL-1β. The authors concluded that ZAK, P2X7 and NLRP3 are promising targets for treating COPD and lung inflammation. They noted that some proposed macrophage-targeting strategies had not been tested in lung inflammatory 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
• Who was studied: No study population of its own. The authors reviewed published laboratory, animal and human research. The article does not report a search method or the number of studies reviewed.
• Exposure: Mainly cigarette smoke, mycotoxins and ricin. Airborne particulates of asbestos, silica and heavy metals, plus volatile organic compounds and carbon nanotubes, were mentioned briefly. The main text did not distinguish asbestos fiber types or name products, jobs or doses. Chrysotile asbestos and Libby "six-mix" amphiboles are named only in the titles of cited references.
• Main results:
  • Based on the literature reviewed, the authors wrote that asbestos, crystalline silica, alloy particles and carbon nanotubes can also activate MAPKs (signaling proteins) and the inflammasome.
  • The authors wrote that macrophages may play an important role in the inflammatory response to inhaling these particulates, including asbestos.
  • A table of cytokines and chemokines induced by inhaled toxicants in vivo listed, for asbestos, IL-1β, IL-6, TNF-α, CCL4, CCL6 and CCL10, drawn from earlier published studies.
  • Across the reviewed toxicants, the authors wrote that all activate the MAPK cascade, inhibit protein synthesis, and use the NLRP3 inflammasome to process IL-1β.
• The authors' conclusion: The authors concluded that their review identified several promising targets to treat COPD and lung inflammation, in particular ZAK, P2X7 and NLRP3.
• Limitations the authors state:
  • The authors noted that recent macrophage-targeting strategies (nanoparticle delivery of small interfering RNA, or simvastatin) had not been tested on lung inflammatory diseases.

Topics

Medical terms in this study, explained in our Lexicon: Inflammation, Macrophage.

Related studies

• Persistent effects of Libby amphibole and amosite asbestos following subchronic inhalation in rats — S.H. Gavett, C.U. Parkinson, et al. (2016)
• Inhalation of rod-like carbon nanotubes causes unconventional allergic airway inflammation — E.M. Rydman, M. Ilves, et al. (2014)
• Inhalation and Oropharyngeal Aspiration Exposure to Rod-Like Carbon Nanotubes Induce Similar Airway Inflammation and Biological Responses in Mouse Lungs — P. Kinaret, M. Ilves, et al. (2017)
• Carbon Nanotube and Asbestos Exposures Induce Overlapping but Distinct Profiles of Lung Pathology in Non-Swiss Albino CF-1 Mice — E.A. Frank, V.S. Carreira, et al. (2016)
• Effects of cigarette smoke exposure on retention of asbestos fibers in various morphologic compartments of the guinea pig lung — A. Churg, V. Tron, et al. (1987)
• Patterns of inflammation, cell proliferation, and related gene expression in lung after inhalation of chrysotile asbestos — T.R. Quinlan, K.A. BéruBé, et al. (1995)

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