Railroad workers with pleural plaques: I. Spirometric and nitrogen washout investigation on smoking and nonsmoking asbestos-exposed workers

Our plain-English summary of Railroad workers with pleural plaques: I. Spirometric and nitrogen washout investigation on smoking and nonsmoking asbestos-exposed workers, by U. Hjortsberg, P. Orbaek, M. Aborelius, et al (American Journal of Industrial Medicine, 1988).

The study

• Authors: U. Hjortsberg, P. Orbaek, M. Aborelius, J. Ranstam, H. Welinder
• Journal: American Journal of Industrial Medicine
• Published: 1988;14(6):635-41
• Cited by: 25 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. 000227).

Abstract

Eighty-seven workers exposed to asbestos in a railroad car repair shop, with characteristic asbestos-induced pleural plaques, underwent extensive lung-function examination. Vital capacity (VC) showed the greatest reduction among the static lung volumes, with an asymmetrical distribution of one-fourth of the subjects below 80% of the predicted value. Logistic regression demonstrated VC to be sufficient for optimal discrimination of asbestos-exposed subjects from a group of matched controls. No further discriminatory power was gained by additional spirometric measures, lung mechanics, blood gas analysis, or diffusing capacity. Smoking had an influence on dynamic but not on static lung volumes. In conclusion, reduced static lung volumes among smoking asbestos-exposed workers with pleural plaques should, in the absence of other lung diseases, be mainly attributed to the asbestos exposure.

In plain English

This Swedish study measured lung function in 87 men with asbestos-induced pleural plaques from the state railroad company's car repair shop in Malmo, examined during 1977-82. Railroad cars had been sprayed with asbestos for insulation in 1968-73. Chrysotile was used to insulate fans, water tanks and ventilation compartments, and small amounts of crocidolite had also been used. The men's results were compared with predicted values based on 200 healthy nonsmoking men. Among the static lung volumes, vital capacity (the air breathed out after a full breath) showed the greatest reduction, with a lower quartile of 81% of predicted. Smoking was not significantly related to vital capacity or other static lung volumes, but it was related to the airflow measure FEV1. Vital capacity alone best separated the exposed men from the reference group, and adding other tests did not significantly improve this. No lung function measure correlated with years of exposure. The authors concluded that tobacco smoking was not an important co-factor in the reduction of vital capacity in these men. They noted that a lack of statistical power could be considered as an explanation for the smoking finding.

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: Cross-sectional lung function study of asbestos-exposed men with pleural plaques. Results were compared with reference values from healthy nonsmoking men, using t-tests, multiple linear regression, and conditional logistic regression against hypothetical matched controls generated from reference equations.
• Who was studied: 87 men with asbestos-induced pleural plaques, identified among about 500 active and some retired asbestos-exposed workers at the Swedish state railroad company's repair shop in Malmo who had chest X-rays in 1977-80. Nine men who also had slight parenchymal changes were excluded. The men were aged 39-78 (median 57): 38 smokers, 27 ex-smokers and 22 never smokers. The reference group was 200 healthy nonsmoking men aged 20-70.
• Exposure: Work in a renovation shop for railroad engines and cars, with no personal dust protection. Cars were sprayed with asbestos for insulation in 1968-73. Chrysotile was used for insulation around fans, hot water tanks and ventilation compartments, and small amounts of crocidolite were also used. Air measurements from 1975 onward:
• background generally less than 0.1 fiber/ml
• personal samples rarely above 2 fibers/ml, most below 1 fiber/ml
• earlier levels were said to be considerably higher
  Exposure time ranged from 6 to 46 years (median 30).
• Main results:
  • Among static lung volumes in the 87 men, vital capacity (VC) showed the greatest reduction, with a lower quartile value of 81% of predicted. This distribution was unaffected by smoking habits.
  • Smoking index showed no significant relation to VC, TLC, FRC or RV/TLC in the exposed men.
  • FEV1 depended on smoking index (b = -0.01, p less than 0.05), and the FEV1/VC ratio did so even more strongly (p less than 0.001).
  • In never smokers, the FEV1/VC ratio was significantly higher than 100% of predicted, which the authors said indicated restrictive lung function impairment.
  • Diffusion capacity was pathologic more often among smokers (37%) than among ex-smokers (19%) and nonsmokers (18%). This difference was not statistically significant.
  • In logistic regression, the decrease in VC was by itself the strongest predictor of belonging to the asbestos-exposed group. Adding other lung function measurements did not significantly improve discrimination from the reference group.
  • No lung function measurement correlated with exposure time.
• The authors' conclusion: The authors concluded that tobacco smoking was not an important co-factor in the reduction of VC in asbestos-exposed men with pleural plaques. They also concluded that VC was the most sensitive indicator of asbestos-induced decrease of lung function in both smokers and nonsmokers.
• Limitations the authors state:
  • The authors noted that a lack of statistical power could be considered as an explanation for the nonsignificant link between VC and smoking. They argued, however, that the data were sufficient to show smoking's expected effects on airway measures.
  • Exposure levels before 1975 were difficult to assess.
  • The authors suggested the lack of association between exposure duration and lung function might be because the entire group had long been exposed.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Asbestosis, Pleural plaques and thickening, Railroads.

Medical terms in this study, explained in our Lexicon: Pleural Plaques, Diffusing Capacity (DLCO), Asbestos Exposure.

Related studies

• Railroad workers with pleural plaques: II. Small airway dysfunction among asbestos-exposed workers — U. Hjortsberg, P. Orbaek, et al. (1988)
• Asbestos-related pleural plaques and lung function — L.C. Oliver, E.A. Eisen, et al. (1988)
• Spirometric impairments in long-term insulators. Relationships to duration of exposure, smoking, and radiographic abnormalities — A. Miller, R. Lilis, et al. (1994)
• Asbestos-related disease in railroad workers. A cross-sectional study — L.C. Oliver, E.A. Eisen, et al. (1985)
• Pleural plaques and cigarette smoking in asbestos workers — W. Weiss, R. Levin, et al. (1981)
• Roentgenographic evidence of asbestos exposure in a select population of railroad workers — M.J. Sepulveda, J.A. Merchant (1983)

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