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Human disease consequences of fiber exposures: a review of human lung pathology and fiber burden data

Our plain-English summary of Human disease consequences of fiber exposures: a review of human lung pathology and fiber burden data, by V.L. Roggli (Environmental Health Perspectives, 1990).

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The study

Abstract

Inhalation of asbestos fibers results in a variety of neoplastic and nonneoplastic diseases of the respiratory tract. Some of these diseases, such as asbestosis, generally occur after prolonged and intensive exposure to asbestos, whereas others, such as pleural mesothelioma, may occur following brief exposures. Inhalation of nonasbestiform mineral fibers can occur as well, and these fibers can be recovered from human lung tissue. Thus, there has been considerable interest in the relationship between mineral fiber content of the lung and various pathologic changes. Techniques for fiber analysis of human tissues have not been standardized, and consequently results may differ appreciably from one laboratory to another. In all reported series, extremely high fiber burdens are found in the lungs of individuals with asbestosis. Although there is a correlation between the tissue concentration of asbestos fibers and the severity of pulmonary fibrosis, further studies of the mineralogic correlates of fiber-induced pulmonary fibrosis are needed. Mesothelioma may occur with fiber burdens considerably less than those necessary to produce asbestosis. More information is needed regarding the migration of fibers to the pleura and the numbers, types, and dimensions of fibers that accumulate at that site. Patients with asbestosis have a markedly increased risk for lung cancer, but the risk of lung cancer attributable to asbestos in exposed workers without asbestosis who also smoke is controversial. Combined epidemiologic-mineralogic studies of a well-defined cohort are needed to resolve this issue. In addition, more information is needed regarding the potential role of nonasbestos mineral fibers in the pathogenesis of lung cancer.

In plain English

This article reviewed published studies that measured asbestos and other mineral fibers in human lung tissue and related them to lung and pleural diseases. The author noted that laboratory techniques varied and that results could differ strikingly between laboratories even for the same sample. In the reviewed asbestosis series, uncoated fiber counts exceeded one million per gram of dried lung in all five studies (medians, except one study reporting only a mean), extremely high compared with general-population background levels. The reviewed studies indicated that mesothelioma may occur with fiber burdens considerably lower than those needed to produce asbestosis. One reported exception was chrysotile miners and millers, in whom those with mesothelioma had greater total fiber burdens than those with asbestosis. Patients with parietal pleural plaques had, on average, substantially lower burdens than patients with asbestosis. For lung cancer in exposed patients without asbestosis, the author wrote that the reviewed studies did not prove whether asbestos was a substantial contributing factor. The author concluded that more research was needed, including fiber-burden studies in cohorts of asbestos workers without asbestosis.

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 human lung fiber burden (tissue mineral analysis) studies and their relation to disease. Several of the reviewed series were the author's own earlier work.
  • Who was studied: Published series of lung tissue analyses from patients with asbestosis, mesothelioma, benign asbestos-related pleural disease (mostly parietal pleural plaques, plus diffuse pleural fibrosis) and lung cancer, and from reference or control populations. These are summarized in Tables 2 to 6.
  • Exposure: Inhaled asbestos fibers: chrysotile (serpentine) and the amphiboles amosite and crocidolite (commercial), plus actinolite, anthophyllite and tremolite (contaminants). Nonasbestiform fibers found in lung tissue were also discussed, including talc and other silicates, silica, carbon, metal oxides, zeolites and man-made mineral fibers.
  • Main results:
    • Interlaboratory comparison trials showed that results could differ strikingly between laboratories even when the same sample was analyzed.
    • In the reviewed series of patients with asbestosis, the uncoated fiber count exceeded one million fibers per gram of dried lung in all five studies. According to the Table 2 footnote, these values are medians except for the study of Wagner et al., for which only a mean could be obtained.
    • Compared with general-population background levels, patients with asbestosis generally had extremely high fiber burdens.
    • For diagnosing asbestosis when asbestos bodies are not found in tissue sections, the author wrote that the data suggest at least a million fibers 5 micrometers or longer per gram of dry lung should be present.
    • Fiber burden correlated with the severity of pulmonary interstitial fibrosis, but with wide scatter. The author took this to indicate that factors other than fiber burden are involved.
    • Fiber counts overlapped considerably between patients with asbestosis and patients with mesothelioma. Studies comparing the two groups showed that mesothelioma may occur with fiber burdens considerably less than those required to produce asbestosis.
    • Exception reported in chrysotile miners and millers: those with mesothelioma had a total fiber burden considerably greater than the median in workers with asbestosis. They also had a greater ratio of tremolite to chrysotile in their lungs.
    • Patients with parietal pleural plaques had tissue fiber burdens that were on average substantially lower than those of patients with asbestosis. Their burdens were somewhat lower than, but of about the same order of magnitude as, those of patients with mesothelioma.
    • Two reviewed studies of patients with plaques found significantly increased concentrations of commercial amphiboles (amosite or crocidolite) compared with a reference population. They found no significant differences for chrysotile or noncommercial amphiboles.
    • For lung cancer, the reviewed studies indicated little evidence for a contributing role of asbestos in populations with no appreciable occupational exposure and substantial smoking. Occupationally exposed patients without asbestosis had greater tissue asbestos burdens than the general population. The author stated that these studies do not prove whether asbestos is a substantial contributing factor in exposed patients without asbestosis.
    • Citing earlier literature, the author stated that somewhere between 40 and 65% of individuals with asbestosis ultimately die of carcinoma of the lung.
  • The authors' conclusion: The author concluded that whether asbestos contributes to lung cancer in exposed workers without asbestosis can only be resolved by studying tissue fiber burdens in cohorts of asbestos workers who do not have asbestosis. The author also called for further studies of the mineral correlates of fibrosis, of fiber migration to the pleura, and of nonasbestos mineral fibers in lung cancer. The author stressed that fiber burden findings in any disease group should be compared with a reference population analyzed by the same technique.
  • Limitations the authors state:
    • Techniques for fiber analysis were not standardized. Variation between and within laboratories makes results from different laboratories difficult to compare.
    • Fiber burden is measured at a single point in time, usually when disease is advanced. It may not reflect tissue fiber content while the disease was developing.
    • Reported values in the lung cancer series depend on how cases were selected as well as on the analytical techniques used.
    • No comparable data existed on fiber content of the visceral and parietal pleura in the general population.

Topics

Medical terms in this study, explained in our Lexicon: Pathology, Fiber Burden, Pleural Mesothelioma, Non-Asbestiform, Mineral Fiber, Pulmonary Fibrosis, Mesothelioma, Pleura.

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How to cite it

Cite the study

V.L. Roggli. Human disease consequences of fiber exposures: a review of human lung pathology and fiber burden data. Environmental Health Perspectives 1990;88:295-303. doi:10.1289/ehp.9088295. PMID: 2272326.

Cite our summary

“Human disease consequences of fiber exposures: a review of human lung pathology and fiber burden data.” AsbestosClaims.Law Library. https://asbestosclaims.law/library/research/human-disease-consequences-of-fiber-exposures-a-review-of-human-lung.

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