Pulmonary function in asbestos cement workers: a dose-response study

Our plain-English summary of Pulmonary function in asbestos cement workers: a dose-response study, by M. Finkelstein (British Journal of Industrial Medicine, 1986).

The study

• Author: M. Finkelstein
• Journal: British Journal of Industrial Medicine
• Published: 1986;43(6):406-13
• Cited by: 9 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text
• In J-M's library: Johns-Manville's company medical library held a copy (J-M no. 000391).

Abstract

This study has found that residence time weighted exposure (asbestos dose) may be used to model the risk and extent of pulmonary function abnormalities in a cohort of asbestos cement workers. This parameter, which incorporates both exposure concentration and latency, had previously proved useful for modelling the risk of radiographic abnormalities in this cohort. Asbestos dose and smoking were independent and additive contributors to decreased pulmonary function. It was also found that lung function results could be used as surrogates for dose in the assessment of mortality risk in this cohort.

In plain English

This study examined lung function tests of production workers at an Ontario asbestos cement factory. The workers were exposed to dusts of chrysotile and crocidolite asbestos, silica and cement. Of 180 eligible long-term workers, 138 had test results. The author measured exposure as "dose", weighting each year's exposure by how long fibres stay in the lung. For the tests examined, the dose-response relationship did not differ significantly by time since first exposure (20 to 34 years); this could not be tested for diffusing capacity. After accounting for smoking, forced vital capacity (FVC) fell by 170 ml, or 4% of predicted, per 1000 fibres/ml × years squared. Smoking and asbestos dose were independent, additive contributors to lower lung function. The share of men with abnormal FVC rose with dose. Among 115 men tested 20 to 24 years after first exposure, lower FVC and FEV1 were significantly associated with death from all causes and from asbestos-associated cancers. The author concluded that this single dose measure could replace cumulative exposure plus time in modelling these relationships. The author noted that dose estimates are probably more uncertain than cumulative exposure estimates.

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: Dose-response study of pulmonary function in a cohort of asbestos cement workers, using test results collected for routine workforce surveillance and workers' compensation assessments; multiple linear regression, plus Cox regression for mortality
• Who was studied: Male production workers at an Ontario asbestos cement factory who were hired before 1960, employed nine years or more, and had at least 12 months in asbestos-exposed jobs; 180 men eligible, 138 (77%) with lung function measurements (testing began in 1970); mean age 58; 95 smokers and 43 non-smokers
• Exposure: Dusts of chrysotile and crocidolite asbestos, silica and cement. Asbestos exposure was expressed as "dose" (residence time weighted exposure), in fibres/ml × years squared
• Main results:
  • When pooled data were tested, adding terms for latency interval (20 to 24, 25 to 29, 30 to 34 years since first exposure) did not significantly improve the fit of the dose-response models. Latency independence could not be tested for diffusing capacity and was assumed
  • After accounting for smoking, FVC was reduced by 170 ml (or 4% of predicted) per 1000 fibres/ml × years squared of asbestos dose
  • Asbestos dose and smoking were independent and additive contributors to decreased pulmonary function; all dose-smoking interaction terms were not statistically significant
  • Asbestos dose was associated with significantly lower total lung capacity (TLC). The association with decreased diffusing capacity was of borderline statistical significance
  • Smoking-adjusted abnormal FVC (Knudson reference equation) rose from 3 of 37 men (8%) in the lowest dose interval (0 to under 1200) to 6 of 10 men (60%) at 4800 or more fibres/ml × years squared (test for trend chi-square 14.2, p less than 0.01)
  • For carbon monoxide diffusing capacity, a dose-response relation was found only among smokers, and the prevalence of abnormal results did not vary significantly with dose
  • Average lung function results tended to worsen as the chest radiograph appearance worsened
  • Among the 75 men with a small-opacity score of 0/0, there was no significant difference in lung function between the 12 men with bilateral pleural thickening and the 63 men without
  • In a Cox regression mortality analysis of 115 men tested at 20 to 24 years since first exposure, decreased FVC and FEV1 were significantly associated with all-cause mortality and with death from asbestos-associated cancers (mesothelioma, lung, gastrointestinal)
  • Men with FVC at the lower limit of normal were estimated to have about twice the risk of death of men whose results matched the predicted value
• The authors' conclusion: The authors concluded that residence time weighted exposure (dose) gave dose-response estimates that did not depend on latency, and that this one parameter could replace cumulative exposure plus time in modelling dose-response relations in the pneumoconioses. The author said this should be verified in other cohorts
• Limitations the authors state:
  • Dose estimates are probably more uncertain than cumulative exposure estimates, which were themselves considered accurate only to within a factor of three to five
  • 42 of the 180 eligible men had no measurements. The author judged that this could underestimate the dose-response slope, but that the bias was unlikely to be large
  • There were few diffusing capacity measurements, so whether its dose-response was independent of latency could not be tested; this was assumed
  • Possible effects of the other dusts on asbestos clearance from the lung could not be assessed

Topics

Medical terms in this study, explained in our Lexicon: Asbestos-Cement, Dose-response relationship, Latency.

Related studies

• Relation between lung function, exercise capacity, and exposure to asbestos cement — P. Wollmer, L. Eriksson, et al. (1987)
• Risk and significance of chest radiograph and pulmonary function abnormalities in an elderly cohort of former nuclear weapons workers — M.A. Mikulski, P.G. Hartley, et al. (2011)
• Final results from a 90-day quantitative inhalation toxicology study evaluating the dose-response and fate in the lung and pleura of chrysotile-containing brake dust compared to TiO2, chrysotile, crocidolite or amosite asbestos: Histopathological examination, confocal microscopy and collagen quantification of the lung and pleural cavity — D.M. Bernstein, B. Toth, et al. (2021)
• A study of dose-response relationships for asbestos associated disease — M.M. Finkelstein (1985)
• Correlation between respiratory symptoms and pulmonary function in asbestos-exposed workers — C.A. Brodkin, S. Barnhart, et al. (1993)
• Smoking, morbidity, and pulmonary function in a group of ex-asbestos workers: a pilot study — E.D. Richter, H. Tuch, et al. (1986)

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