Enhanced retention of asbestos fibers in the airways of human smokers

Our plain-English summary of Enhanced retention of asbestos fibers in the airways of human smokers, by A. Churg, B. Stevens (American Journal of Respiratory and Critical Care Medicine, 1995).

The study

• Authors: A. Churg, B. Stevens
• Journal: American Journal of Respiratory and Critical Care Medicine
• Published: 1995;151(5):1409-13
• Cited by: 40 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

To determine whether cigarette smoke increases the pulmonary retention of asbestos, we compared the asbestos-fiber burden in the airway mucosa of six cigarette smokers who had received heavy occupational asbestos exposure with that in a group of six subjects with similar exposure who were never smokers. The groups were matched in terms of age, sex, years of exposure, and mean parenchymal amosite burden. We found that the concentration of amosite in airway mucosa was significantly elevated (by approximately sixfold) in smokers (p < 0.02). Chrysotile parenchymal burdens were statistically similar in both groups, but the chrysotile airway burden was again higher (by approximately 50-fold) in smokers (p < 0.006). There were no differences in airway or parenchymal tremolite burdens between the two groups. Fibers of all three types of asbestos recovered from the airway mucosa or parenchyma of smokers were shorter than fibers recovered from nonsmokers, an observation in accord with experimental data suggesting that cigarette smoke leads to retention of shorter fibers. These findings indicate that cigarette smoking causes enhanced accumulation of both amosite and chrysotile in the airway mucosa. This process may play a role in potentiating the pathologic effects of asbestos.

In plain English

The authors compared asbestos fibers in autopsy lungs from men who had heavy work exposure to asbestos in the Pacific Northwest, in shipyards or as career insulators and in similar trades. They measured fibers in the lining of the airways (airway mucosa) and in the lung tissue (parenchyma) of six cigarette smokers and six never-smokers from their earlier study. All twelve were men. The groups were roughly matched by age, years of exposure and average amosite level in lung tissue. All the nonsmokers had mesothelioma. Of the smokers, two had mesothelioma and four had lung cancer. Amosite concentrations in the airway mucosa were about sixfold higher in smokers (p less than 0.02), and chrysotile concentrations about 50-fold higher (p less than 0.006). Tremolite levels did not differ. Amosite and tremolite fibers were significantly shorter in smokers. Chrysotile showed the same trend, but too few chrysotile fibers were found for statistical significance. The authors concluded that cigarette smoking causes enhanced accumulation of amosite and chrysotile in the airway mucosa. They noted that actual exposure levels were unknown and that their matching was less than ideal.

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: Comparison of asbestos fiber burden in autopsy lung tissue (airway mucosa and lung parenchyma) between smokers and never-smokers, measured by electron microscopy with X-ray spectroscopy
• Who was studied: 12 men with heavy occupational asbestos exposure whose autopsy lungs were referred to the authors' laboratory: six cigarette smokers (mean 35 plus or minus 22 pack-years) and six never-smokers from the authors' previous study. All nonsmokers had mesothelioma; two smokers had mesothelioma and four had lung cancer.
• Exposure: Occupational asbestos exposure in the Pacific Northwest (Oregon, Washington, British Columbia), in shipyards or as career asbestos insulators and similar trades; fibers measured were amosite, tremolite and chrysotile. Cigarette smoking was the factor compared.
• Main results:
  • Amosite concentration in airway mucosa was about sixfold higher in smokers than in nonsmokers (p < 0.02)
  • Chrysotile concentration in airway mucosa was about 50-fold higher in smokers (p < 0.006); in the parenchyma chrysotile was statistically similar between groups (described in the results as marginally higher in smokers, p < 0.07)
  • Chrysotile was found in 12 of 36 airway samples from smokers compared with 4 of 40 from nonsmokers (p < 0.04); amosite in 14 of 36 compared with 7 of 40 (p < 0.09, nearly significant)
  • Tremolite burdens in airways and parenchyma did not differ between smokers and nonsmokers
  • Amosite and tremolite fibers in the parenchyma and airways of smokers were significantly shorter than in nonsmokers
  • Chrysotile fibers showed the same trend toward shorter length in smokers, but the difference in length did not reach statistical significance because few chrysotile fibers were found
• The authors' conclusion: The authors concluded that cigarette smoking causes enhanced accumulation of both amosite and chrysotile in the airway mucosa, and that this may play a role in increasing the harmful effects of asbestos
• Limitations the authors state:
  • Actual asbestos exposure levels of the subjects were unknown
  • The groups were only crudely matched by age, years of exposure and mean amosite burden, which the authors called less than ideal
  • Matching on parenchymal amosite burden prevents conclusions about smoking-related changes in parenchymal fiber concentration
  • Time since last exposure was not known for two of the smokers (the authors argued this could not explain the chrysotile difference)
  • Disease distribution differed between groups, a potential confounder, though the authors considered it a less likely explanation than smoking
  • The source of the chrysotile in smokers' airways is unclear; it may partly reflect retention of environmental fibers from ambient air rather than only occupational fibers

Topics

The National Library of Medicine indexes this study under subjects our site covers: Amosite, Chrysotile, Tremolite.

Medical terms in this study, explained in our Lexicon: Fiber Burden, Asbestos Exposure, Amosite, Chrysotile, Tremolite, Parenchyma.

Related studies

• 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)
• Severe diffuse small airways abnormalities in long term chrysotile asbestos miners — J.L. Wright, A. Churg (1985)
• Pathologic changes in the small airways of the guinea pig after amosite asbestos exposure — D. Filipenko, J.L. Wright, et al. (1985)
• Early detection of central airway lung cancer in smokers with silicosis — A.I. Lo, Y. Huang, et al. (2011)
• Asbestos exposure increases paracellular transport of fibrin degradation products across human airway epithelium — T.J. Gross, S.M. Cobb, et al. (1994)
• Morphology of small-airway lesions in patients with asbestos exposure — J.L. Wright, A. Churg (1984)

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