Bronchiolitis caused by occupational and ambient atmospheric particles

Our plain-English summary of Bronchiolitis caused by occupational and ambient atmospheric particles, by A. Churg, J.L. Wright (Seminars in Respiratory and Critical Care Medicine, 2003).

The study

• Authors: A. Churg, J.L. Wright
• Journal: Seminars in Respiratory and Critical Care Medicine
• Published: 2003;24(5):577-84
• Cited by: 16 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Occupationally encountered mineral dusts such as asbestos, silica, silicates (talc, mica), and metals can produce a distinctive pattern of fibrosis and distortion of the small airways, particularly the distal membranous bronchioles (MB) and the respiratory bronchioles (RB). Recent reports show that the same types of changes, accompanied by considerable muscle hyperplasia, are found in individuals living in regions with high levels of particulate air pollutants (PM). Models and actual measurements suggest that these changes occur because the small airways are sites of high particle deposition, and inhaled and deposited particulates, including PM, enter the airway walls. Studies from our laboratory using a tracheal explant model have shown that, for many types of particles, entry into the airway wall causes expression of mediators that lead to airway wall fibrosis and airway wall smooth muscle hyperplasia, probably through oxidant mechanisms. These reactions are intrinsic properties of the particles and do not require exogenous inflammatory cells. There is considerable evidence that individuals with occupational exposure to a wide variety of mineral dusts, as well as individuals with chronic exposure to high levels of PM, develop chronic airflow obstruction. The type of small airway remodeling seen in particle-induced bronchiolitis appears to be one cause of chronic airflow obstruction in this setting.

In plain English

This article reviewed the small-airway damage that mineral dusts and air pollution particles can cause. The authors called this damage particle-induced small airways disease (PSAD) and reviewed their own and other groups' studies. It described scar-like (fibrotic) thickening and distortion of the smallest airways, the bronchioles. These changes were seen in workers heavily exposed to asbestos, coal, talc, mica, silica and metal oxides, and in people living with high air pollution. In the authors' earlier grading studies, severely fibrotic respiratory bronchioles made up 4% of those from smokers, compared with 48% from smoking asbestos workers and 31% from other dust-exposed smokers. In cited autopsy series, PSAD was found in 21 of 244 lungs (9%) from people exposed to amphibole asbestos and in 95 of 247 (39%) chrysotile asbestos miners, who had extremely high exposure. In rat windpipe tissue experiments, amosite asbestos increased signals linked to scarring. The authors concluded that this airway remodeling appears to be one cause of chronic airflow obstruction. They noted that the changes overlap with smoking damage and that data on how common PSAD is are hard to obtain.

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, drawing on the authors' own earlier pathology, particle-measurement and animal-tissue studies as well as studies by other groups
• Who was studied: Studies reviewed covered workers with high occupational dust exposure, people living in high air-pollution regions (e.g. never-smoking women in Mexico City compared with Vancouver residents), and rat tracheal explants
• Exposure: Asbestos (amphibole, chrysotile, and amosite in the explant experiments), coal, sheet silicates (talc, mica), aluminum oxide, iron oxide, silica (quartz), and ambient particulate pollutants (PM)
• Main results:
  • In the authors' earlier visual grading studies, severely fibrotic respiratory bronchioles were seen in 4% of respiratory bronchioles from smokers, 48% from smoking asbestos workers, and 31% from other dust-exposed smokers
  • In a cited series of 244 autopsy lungs from patients with amphibole asbestos exposure, 21 (9%) had PSAD
  • In a cited series of 247 sequential autopsies on chrysotile asbestos miners, 95 (39%) had PSAD; this cohort had extremely high asbestos exposure
  • In a cited series of 174 lung resection specimens, 13 of the 53 patients with occupational dust exposure (25%) had PSAD
  • In a cited study of asbestos-exposed workers, higher particle concentrations in the small airways correlated with greater airway wall fibrosis
  • In rat tracheal explants, amosite asbestos increased gene expression of fibrogenic (scar-promoting) growth factors and procollagen, and increased tissue collagen content
  • In the cited lung resection study, patients with PSAD had significant abnormalities in lung function tests compared with age- and smoking-matched dust-exposed subjects without PSAD
  • In a cited study, never-smoking women from Mexico City (high PM) had greater airway fibrosis and muscle in the small airways than Vancouver residents (low PM)
• The authors' conclusion: The authors concluded that the small airway remodeling seen in particle-induced bronchiolitis appears to be one cause of chronic airflow obstruction in people exposed to mineral dusts or high air pollution
• Limitations the authors state:
  • PSAD can be hard to tell apart from small airway changes caused by cigarette smoke
  • Prevalence data are difficult to obtain, and biopsy and autopsy series suffer from extreme selection bias
  • Direct data on the effects of PSAD on lung function are sparse
  • Rat tracheal explants have little smooth muscle, so they cannot show effects on muscle overgrowth

Topics

Medical terms in this study, explained in our Lexicon: Silicate, Talc, Mica, Fibrosis, Deposition, Occupational Exposure, Obstructive Lung Disease.

Related studies

• Observations an atmospheric air pollution caused by asbestos — A. Laamanen, L. Noro, et al. (1965)
• Treatment of airborne asbestos and asbestos-like microfiber particles using atmospheric microwave air plasma — A. Averroes, H. Sekiguchi, et al. (2011)
• Inhalable particles and pulmonary host defense: in vivo and in vitro effects of ambient air and combustion particles — G.E. Hatch, E. Boykin, et al. (1985)
• Airway wall remodeling induced by occupational mineral dusts and air pollutant particles — A. Churg, J.L. Wright (2002)
• Macrophage fusion caused by particle instillation — K.L. Trout, A. Holian (2020)
• The Impact of Ambient Environmental and Occupational Pollution on Respiratory Diseases — C. Nishida, K. Yatera (2022)

Browse more research in Seminars in Respiratory and Critical Care Medicine, or return to medical research.