The distribution of amosite asbestos fibers in the lungs of workers with mesothelioma or carcinoma

Our plain-English summary of The distribution of amosite asbestos fibers in the lungs of workers with mesothelioma or carcinoma, by A. Churg, B. Wiggs (Experimental Lung Research, 1989).

The study

• Authors: A. Churg, B. Wiggs
• Journal: Experimental Lung Research
• Published: 1989;15(5):771-83
• Cited by: 8 articles, as counted by NIH iCite
• Read it: PubMed · Publisher
• In J-M's library: Johns-Manville's company medical library held a copy (J-M no. 002559).

Abstract

We have previously shown that there are differences in the sizes of fibers of amosite asbestos in different parts of the lung in workers with relatively high asbestos exposure and malignant pleural mesothelioma. To determine whether this distribution pattern is specific to cases of mesothelioma, we compared the fiber distribution in the lungs of 20 cases of mesothelioma and 10 cases of carcinoma of the lung. The two test groups were statistically identical in terms of age, and exposure period, and overall both groups had very similar mean fiber concentrations and mean fiber sizes. When individual sampling sites within the lung were considered, neither group showed preferential fiber concentration in any area. However, there were definite differences in the intrapulmonary fiber size distribution both within and between the two groups: Cases of mesothelioma showed accumulation of lung fibers in the peripheral upper lobe with shorter central upper lobe fibers. The lung cancer cases demonstrated a reverse pattern, with shorter fibers in the peripheral compared to central upper lobe, but accumulations of long fibers in the peripheral lower lobe. Fiber surfaces and masses showed similar differences among sample sites. We conclude that (1) there is no evidence for fiber concentration variations in different portions of the lung; (2) there is strong evidence for variations in fiber sizes in different portions of the lung, and these differences are most clearly related to fiber length, surface area, and mass; (3) contrary to data from experimental animals, there are no clear gravitational effects on fiber distribution in humans; and (4) there are reproducible differences in intrapulmonary fiber size distribution between mesothelioma and lung cancer cases. These differences may be a manifestation of individual handling of mineral particles because of structural variations in individual lungs.

In plain English

The authors compared where amosite asbestos fibers were found in the lungs of 20 shipyard and insulation workers with mesothelioma and 10 with lung cancer. All had at least 300,000 amosite fibers per gram of dry lung, and none had asbestosis. Four samples per case, from the outer and central parts of the upper and lower lobes, were examined by electron microscope. Fiber concentrations did not differ significantly between sampling sites or between the two diseases. Fiber sizes did differ: mesothelioma cases tended to have long fibers in the outer upper lobe, while lung cancer cases had their longest fibers in the outer lower lobe. Outer upper lobe fibers were longer than outer lower lobe fibers in 15 of 20 mesothelioma cases but in only 2 of 10 lung cancer cases. The authors found no evidence that gravity affected where fibers ended up. They stated their belief that these lung cancers were caused by smoking. They concluded, calling the evidence indirect, that individual differences in how lungs handle fibers may influence where fibers end up and which disease develops.

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: Comparative analysis of asbestos fibers in lung tissue, using records and lung specimens from the authors' mineral analysis laboratory; mesothelioma cases compared with lung cancer cases
• Who was studied: 20 mesothelioma cases (8 of them from the authors' earlier report) and 10 lung cancer cases. All were shipyard and insulation workers whose cases came to the authors' mineral analysis laboratory (University of British Columbia, Vancouver) over the previous 6 years. Cases with asbestosis were excluded.
• Exposure: Amosite asbestos, at a lung concentration of at least 300,000 fibers per gram of dry lung. The authors note that these workers also had historic high-level chrysotile exposure, which was not counted. Amosite fibers longer than 0.5 micrometers were measured, 50 to 100 per sampling site.
• Main results:
  • Across each group as a whole, fiber concentrations and most size measures were essentially identical in the mesothelioma and lung cancer groups.
  • Amosite fiber concentrations showed no significant differences among the four sampling sites, or between mesothelioma and lung cancer cases.
  • Fiber size measures showed highly significant differences among sampling sites within each disease group, and between the mesothelioma and lung cancer groups at particular sites.
  • In mesothelioma cases the peripheral (outer) upper lobe tended to accumulate long fibers. In lung cancer cases, peripheral upper lobe fibers were shorter than central upper lobe fibers, and the longest fibers were in the peripheral lower lobes.
  • Case by case, peripheral upper lobe fibers were on average longer than peripheral lower lobe fibers in 15 of 20 mesothelioma cases and in 2 of 10 lung cancer cases.
  • Differences among sampling sites were even more marked for fiber surface area and fiber mass. Differences in fiber width and aspect ratio were less marked and less consistent.
  • The authors found no evidence of gravitational effects on fiber distribution, unlike findings reported in rats.
  • None of the demographic variables correlated with case fiber concentrations or mean fiber lengths. All lung cancer patients had been smokers. 5 of the 20 mesothelioma patients had never smoked.
  • The authors stated their opinion that lung cancer is related to asbestos only when asbestosis is present, and their belief that the lung cancers in this study were all caused by smoking.
• The authors' conclusion: The authors concluded that, although the evidence remains indirect, their observations support the idea that individual variations in how the lung handles fibers may determine both where fibers end up and which patients get which diseases.
• Limitations the authors state:
  • The small number of eligible cases meant the two groups could not be matched case by case on demographics.
  • The study could not control for the timing or intensity of exposure, which might influence fiber deposition and clearance.
  • The chrysotile content of the lungs was ignored, although all the workers had historic high-level chrysotile exposure.
  • The authors had no information on how clearance over time changes fiber distribution. It is unclear whether the findings reflect initial deposition or later redistribution of fibers.
  • Emphysema was present to varying degrees in some cases but was not graded, because the lungs were not inflated.
  • Sampling the extremes of the lung (apex and base) might have shown differences not seen here.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Amosite, Lung cancer, Mesothelioma.

Medical terms in this study, explained in our Lexicon: Amosite, Mesothelioma, Carcinoma, Asbestos Exposure, Pleural Mesothelioma, Lung Cancer, Fiber Length.

Related studies

• Correlation of in vitro and in vivo methods by means of mass dose and fiber distribution for amosite and fibrous ferroactinolite — D.L. Coffin, L.D. Palekar, et al. (1983)
• Fiber burden and patterns of asbestos-related disease in workers with heavy mixed amosite and chrysotile exposure — A. Churg, S. Vedal (1994)
• The distribution of amosite asbestos in the periphery of the normal human lung — A. Churg (1990)
• Pulmonary endpoints (lung carcinomas and asbestosis) following inhalation exposure to asbestos — B.T. Mossman, M. Lippmann, et al. (2011)
• Pulmonary fibrosis, carcinoma, and ferruginous body counts in amosite asbestos workers. A study of six cases — V.L. Roggli, S.D. Greenberg, et al. (1980)
• Cigarette smoke increases amosite asbestos fiber binding to the surface of tracheal epithelial cells — A. Churg, J. Sun, et al. (1998)

Browse more research in Experimental Lung Research, or return to medical research.