Asbestos exposure-cigarette smoking interactions among shipyard workers

Our plain-English summary of Asbestos exposure-cigarette smoking interactions among shipyard workers, by P.D. Blanc, J.A. Golden, G. Gamsu, et al (JAMA, 1988).

The study

• Authors: P.D. Blanc, J.A. Golden, G. Gamsu, D.R. Aberle, W.M. Gold
• Journal: JAMA
• Published: 1988;259(3):370-3
• Cited by: 33 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. 000192).

Abstract

We studied the roentgenograms, pulmonary function tests, and physical findings of 294 shipyard workers to evaluate asbestos exposure-cigarette smoking interactions. Roentgenographic parenchymal opacities, decreased pulmonary diffusing capacity for carbon monoxide, decreased flow at low lung volume, rales, and clubbing were each significantly related to the number of years elapsed since first exposure to asbestos and cigarette smoking status when analyzed by logistic regression. A dose-dependent cigarette smoking response that was consistent with synergism was present only for parenchymal opacities and decreased flow at low lung volume. These findings suggest that decreased flow at low lung volume, possibly reflecting peribronchiolar fibrosis, may be a functional corollary to smoking-associated parenchymal roentgenographic opacities among some asbestos-exposed individuals.

In plain English

The authors retrospectively reviewed the records of 294 shipyard workers. The US Department of Labor had referred them to the University of California, San Francisco, between 1978 and 1985 under a claims-related follow-up of West Coast shipyard employees. Lacking industrial hygiene data, the authors measured asbestos exposure as years since first shipyard employment. They grouped smokers as light (20 pack-years or less) or heavy (more than 20). In logistic regression, asbestos exposure and smoking together were significantly related to irregular parenchymal opacities on chest X-rays, reduced diffusing capacity, decreased airflow at low lung volume, rales and clubbing. They were not significantly related to reduced total lung capacity, reduced vital capacity, increased flow at high lung volume or pleural abnormality. Compared with nonsmokers, heavy smokers had significantly raised relative risks for all four abnormalities analyzed further. Light smokers did not appear to be at elevated risk of decreased low-volume flow compared with never smokers. In nonsmokers, decreased low-volume flow (47 of 85) was significantly related to years since first employment. The authors concluded that this decreased flow, possibly reflecting peribronchiolar fibrosis, may accompany smoking-associated opacities in some asbestos-exposed people. They cautioned that this referred group may not reflect shipyard workers generally.

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: Retrospective review of clinical records (cross-sectional analysis using logistic regression)
• Who was studied: 294 current and former West Coast shipyard workers referred by the US Department of Labor, under a claims-related regional medical follow-up program, to the Division of Pulmonary Medicine, University of California, San Francisco, between January 1, 1978 and December 31, 1985. All but four were men, more than one third were nonwhite, and mean age was 59.9 years. Chest X-rays were ILO-classified for 133 subjects. Lung function analyses were limited to 184 white men.
• Exposure: Shipyard asbestos exposure (fiber type not specified), measured as the number of years elapsed since first shipyard employment (mean 33.1 years; mean years of employment 23.2). Cigarette smoking was grouped as nonsmokers, light smokers (20 pack-years or less) and heavy smokers (more than 20 pack-years).
• Main results:
  • Decreased flow at low lung volume was the most frequent abnormality (141 of 284 subjects, 49.6%). Parenchymal opacities were found in 17 of 133 ILO-classified subjects (12.8%). Clubbing was the least frequent finding.
  • For all subjects, the combined asbestos exposure-cigarette smoking model was statistically significantly related to parenchymal opacities, reduced diffusing capacity (DLco), decreased flow at low lung volume, rales and clubbing.
  • Decreased total lung capacity, decreased vital capacity and increased flow at high lung volume were not significantly related to asbestos exposure and smoking.
  • Bilateral pleural abnormality only approached statistical significance. Unilateral pleural abnormality (70 of 133 ILO-classified cases, 52.6%) also approached but did not achieve significance (model chi-square 5.7, P greater than .05).
  • Compared with nonsmokers, and adjusted for years since first employment, heavy smokers had significantly elevated relative risks for parenchymal opacities, reduced DLco, decreased flow at low lung volume and rales.
  • Among light smokers, the relative risks for decreased DLco and rales were also significantly elevated, with estimates similar to those of heavy smokers. Light smokers did not seem to be at elevated risk of decreased flow at low lung volume relative to never smokers. Their point estimate for parenchymal opacities was elevated but far less than for heavy smokers and not statistically significant at the .05 level.
  • Because no cases of clubbing were seen among nonsmokers, clubbing was not analyzed further.
  • Among nonsmokers analyzed separately, decreased flow at low lung volume (47 of 85 nonsmoking subjects) was significantly related to years since first asbestos-related employment (model chi-square 4.7, P less than .05). Parenchymal opacities, decreased DLco and rales among nonsmokers were not statistically significantly related.
• The authors' conclusion: The authors suggested that decreased flow at low lung volume, possibly reflecting peribronchiolar fibrosis, may be a functional corollary to smoking-associated parenchymal opacities on chest X-rays among some asbestos-exposed individuals. They found a dose-dependent smoking response consistent with synergism only for parenchymal opacities and decreased flow at low lung volume.
• Limitations the authors state:
  • The study population came from disability evaluations. Because of the selection bias in such referrals, the authors did not infer that the data reflect the general prevalence of lung abnormalities among all shipyard workers.
  • Reliable, contemporary industrial hygiene data were not available, so years since first employment was used as the measure of asbestos exposure.

Topics

Medical terms in this study, explained in our Lexicon: Asbestos Exposure, Pulmonary Function Test (PFT), Diffusing Capacity (DLCO), Clubbing, Fibrosis.

Related studies

• Behavioral, attitudinal, and physiologic characteristics of smoking and nonsmoking asbestos-exposed shipyard workers — V.C. Li, Y.J. Kim, et al. (1983)
• Does smoking cessation lead to weight gain? The experience of asbestos-exposed shipyard workers — T.J. Coates, V.C. Li (1983)
• Interaction of asbestos, age, and cigarette smoking in producing radiographic evidence of diffuse pulmonary fibrosis — K.H. Kilburn, R. Lilis, et al. (1986)
• Mortality among workers exposed to asbestos at the shipyard of Genoa, Italy: a 55 years follow-up — D.F. Merlo, M. Bruzzone, et al. (2018)
• The effect of cigarette smoking on the detection of small radiographic opacities in inorganic dust diseases — P.D. Blanc, G. Gamsu (1988)
• Asbestosis: interstitial pulmonary fibrosis and pleural fibrosis in a cohort of asbestos insulation workers: influence of cigarette smoking — R. Lilis, I.J. Selikoff, et al. (1986)

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