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Small airways disease and mineral dust exposure. Prevalence, structure, and function

Our plain-English summary of Small airways disease and mineral dust exposure. Prevalence, structure, and function, by A. Churg, J.L. Wright, B. Wiggs, et al (The American Review of Respiratory Disease, 1985).

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The study

Abstract

Previously we described a lesion of the small airways that appears related to mineral dust exposure and is found in asbestos and nonasbestos dust-exposed populations. To determine the usefulness of this lesion as a marker for mineral dust exposure, and to determine whether it produces functional consequences, we examined a group of 53 workers who had been either hard rock miners or in the asbestos, construction, and shipyard industries. The specific lesion (mineral dust airways disease (MDAD] consists of marked fibrosis and pigmentation of the respiratory bronchioles and was found in 13 of 53 workers with dust exposure, but only in 1 of 121 without dust exposure. Compared with age and smoking-matched dust-exposed control subjects, patients with this lesion had significant abnormalities of forced expiratory volume in one second (FEV1), forced expiratory flow during the middle half of the forced vital capacity (FEF25-75), vital capacity (VC), and nitrogen washout. In addition to fibrosis in the walls of respiratory bronchioles, these patients also had significant increases of fibrosis in the walls of membranous bronchioles, indicating that changes in the small airways are widespread in this subset of workers. We conclude that markedly abnormal small airways are present in some workers with mineral dust exposure; pathologic observation of this lesion is a good indicator of dust exposure, and its presence is associated with abnormalities of air flow greater than those induced by smoking alone. The presence of this lesion in only a portion of dust-exposed workers may account for contradictory results in past studies that attempted to demonstrate air flow abnormalities associated with mineral dust exposure.

In plain English

Researchers in Vancouver examined lung tissue removed during lung cancer surgery from 174 consecutive patients. Fifty-three had worked at least 1 year in dusty jobs such as hard rock mining, shipyards, asbestos insulation or construction; 121 had no such history. The authors looked for a lesion they call mineral dust airways disease (MDAD): marked scarring and pigment in the walls of the smallest airways (respiratory bronchioles). It was found in 13 of the 53 dust-exposed patients and in 1 of the 121 others, whose lung nonetheless showed dust. The 13 patients with MDAD were compared with 13 dust-exposed patients without it, matched for age, sex and smoking. Those with MDAD had poorer breathing tests (mean FEV1 65% of predicted versus 87%) and more scarring in other small airways. The authors concluded the lesion is a highly specific but not very sensitive marker of dust exposure, associated with airflow abnormalities greater than smoking alone causes. Patients with asbestosis were excluded, and dust exposure was not matched.

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: Pathology and lung-function study of surgically removed lung tissue from consecutive lung cancer patients. It compared dust-exposed and unexposed patients, then compared 13 dust-exposed patients with the lesion against 13 matched dust-exposed patients without it.
  • Who was studied: 174 consecutive patients having lung resection for lung carcinoma at a University of British Columbia (Vancouver) hospital. 53 had a history of mineral dust exposure and 121 did not. Patients with interstitial fibrosis or asbestosis were excluded. The matched subgroups had 13 patients each, with a mean age of 64 in both. Study dates were not stated.
  • Exposure: Employment for 1 year or longer as a hard rock miner, coal miner, shipyard worker, pipefitter, lagger or asbestos insulation worker, welder, foundry worker, construction worker, or metal machinist. Asbestos fiber types and doses were not specified, and lung mineral content was not measured. Mean years of exposure were 20 in the MDAD group and 15 in the matched group.
  • Main results:
    • 13 of 53 patients (25%) with a history of mineral dust exposure had the MDAD lesion.
    • 1 of 121 patients (1%) without a history of dust exposure had the lesion; the authors reported the difference as highly significant (chi-square 24.8, p less than 0.001).
    • The one unexposed patient with the lesion was a vacuum cleaner repairman. His lung showed refractile dust in amounts comparable to those of patients with a dust exposure history.
    • As a marker of dust exposure, the lesion correctly excluded 120 of 121 unexposed patients (99.2%) and correctly predicted exposure in 13 of 14 patients with the lesion (92.9%). However, it detected only 13 of 53 exposed patients (24.5%).
    • Compared with matched dust-exposed patients without MDAD, the 13 patients with MDAD had significantly lower FEV1 (mean 65 versus 87% of predicted, p less than 0.001) and lower FEF25-75 (mean 34 versus 62% of predicted, p less than 0.002).
    • Total lung capacity was similar in both groups (mean 104% of predicted). In the MDAD group, vital capacity was significantly lower (mean 78 versus 98% of predicted, p less than 0.02) and RV/TLC was higher (p less than 0.002).
    • The MDAD group had an abnormal nitrogen washout test, with a marked increase in the Phase III nitrogen slope (mean 360 versus 231% of predicted, p less than 0.002). There were trends, approaching significance (p less than 0.06), for higher FRC and closing capacity/TLC.
    • Besides the respiratory bronchioles (the lesion used to select patients), the membranous bronchioles in the MDAD group also had higher fibrosis scores (mean 40 versus 26, p less than 0.009).
    • Emphysema grades did not differ statistically between the MDAD group and the matched group.
  • The authors' conclusion: The authors concluded that the MDAD lesion is a highly specific but not very sensitive indicator of a history of mineral dust exposure. They said its presence is associated with airflow abnormalities greater than those from smoking alone. They suggested this may explain conflicting results of earlier studies, because only some dust-exposed workers have the lesion.
  • Limitations the authors state:
    • The groups were not matched for dust exposure because there were too few cases.
    • The mineral content of the lungs was not analyzed because exposures were too varied to compare.
    • Cigarette smoking accounted for a large portion of the lung function changes in both groups.
    • Other workplace agents, such as fumes, could have contributed to airflow obstruction in some patients. The authors noted that only 1 test patient and 1 control appeared likely to have had much fume exposure.

Topics

Medical terms in this study, explained in our Lexicon: Fibrosis, FEV1.

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Cited on this site

How to cite it

Cite the study

A. Churg, J.L. Wright, B. Wiggs, P.D. Paré, N. Lazar. Small airways disease and mineral dust exposure. Prevalence, structure, and function. The American Review of Respiratory Disease 1985;131(1):139-43. doi:10.1164/arrd.1985.131.1.139. PMID: 3966701.

Cite our summary

“Small airways disease and mineral dust exposure. Prevalence, structure, and function.” AsbestosClaims.Law Library. https://asbestosclaims.law/library/research/small-airways-disease-and-mineral-dust-exposure-prevalence-structure.

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