NHLBI workshop summary. Environmental lung diseases. Relationship between acute inflammatory responses to air pollutants and chronic lung disease

Our plain-English summary of NHLBI workshop summary. Environmental lung diseases. Relationship between acute inflammatory responses to air pollutants and chronic lung disease, by J. Crapo, F.J. Miller, B. Mossman, et al (The American Review of Respiratory Disease, 1992).

The study

• Authors: J. Crapo, F.J. Miller, B. Mossman, W.A. Pryor, J.P. Kiley
• Journal: The American Review of Respiratory Disease
• Published: 1992;145(6):1506-12
• Cited by: 22 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Summary of the article

This report summarized a workshop held by the Division of Lung Diseases, National Heart, Lung and Blood Institute, on May 29 and 30, 1991, in Bethesda, Maryland, cosponsored by the National Institute of Environmental Health Sciences. Participating scientists reviewed current knowledge of how acute inflammatory responses to environmental air pollutants may contribute to chronic lung diseases such as fibrosis, emphysema, chronic bronchitis and lung cancer. They also identified gaps in knowledge. Topics included microdosimetry of inhaled gases and particles, the transfer of ozone and nitrogen dioxide across the air-tissue interface, oxidative reactions involving nitric oxide, early events leading to lung fibrosis, chronic injury in the proximal alveolar region, pollutant mixtures and diesel exhaust. For asbestos, the summary reported that fibers had a superadditive effect with radiation on transformation of C3H10T1/2 cells. It also reported that iron in asbestos accelerated hydroxyl radical production in vitro. The mechanisms linking reactive oxygen species to asbestosis, lung cancer or mesothelioma were described as unclear. The interaction of asbestos with cigarette smoke was described as particularly hazardous but poorly understood. The participants made 15 recommendations, including better anatomical and dosimetry models, studies of genetic and molecular responses, and work on reactive species and asbestos-smoke synergy. They concluded that extrapolation from animals to humans required a mechanistic understanding linking exposure, dose and response.

PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

In plain English

This article was not a research study. It summarized a National Heart, Lung and Blood Institute workshop held in Bethesda, Maryland, on May 29-30, 1991. Participating scientists reviewed how air pollutants, including ozone, nitrogen dioxide, diesel exhaust and asbestos, might lead from acute lung inflammation to chronic lung disease, and they listed research needs. Ozone and nitrogen dioxide were prominent examples. In one laboratory cell assay, asbestos fibers could not transform cells alone but had a superadditive effect when combined with radiation. Asbestos fibers were described as nonmutagenic in most bioassays. Iron in asbestos sped up production of the hydroxyl radical in laboratory tests. The report also stated that asbestos, like cigarette tar, accumulates in lung cells, prompts release of factors that recruit phagocytes (scavenger cells), and produces lung damage over long periods. It stated that how these mechanisms relate to asbestosis, lung cancer or mesothelioma was unclear, and that the hazardous interaction of asbestos with cigarette smoke was poorly understood. The authors concluded that extrapolating from animals to humans required a mechanistic understanding linking exposure, dose and response.

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: Workshop summary report (a review of discussions and presentations, not an original study)
• Who was studied: Scientists attending a National Heart, Lung and Blood Institute workshop on environmental lung disease, held in Bethesda, Maryland, May 29-30, 1991
• Exposure: Environmental air pollutants discussed, including ozone, nitrogen dioxide, sulfur dioxide, lead, particulate matter, diesel exhaust, acid aerosols, and fibrous materials such as asbestos
• Main results:
  • In a laboratory cell transformation assay, radiation transformed cells. Asbestos fibers could not transform the cells alone but had a superadditive effect on transformation.
  • Asbestos fibers were described as nonmutagenic in most bioassays
  • Studies using the electron spin resonance spin trapping method showed that iron in asbestos accelerates production of the hydroxyl radical in vitro
  • Cigarette tar and asbestos were described as accumulating in lung cells, causing release of chemotactic factors that recruit phagocytes, and producing lung damage over long time periods
  • The cellular and molecular mechanisms of asbestos injury, and their relationship to asbestosis, lung cancer or mesothelioma, were described as not clear
  • The interaction of asbestos with cigarette smoke was described as known to be particularly hazardous, but understanding of this synergy was described as limited
  • Exercising humans were reported to receive an ozone dose to the deep lung three to four times greater than resting rats
• The authors' conclusion: The authors concluded that the ability to extrapolate from laboratory animals to humans must be strengthened by developing a mechanistic understanding that links exposure to dose and to response
• Limitations the authors state:
  • The authors noted that interpreting data on environmental air pollutants and chronic disease is difficult, partly because confounding variables such as cigarette smoking, genetic susceptibility and socioeconomic status have substantial effects

Topics

Medical terms in this study, explained in our Lexicon: Fibrosis, Emphysema, Lung Cancer, Hydroxyl Radical, Reactive Oxygen Species (ROS), Mesothelioma.

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