Pleural plaques and exposure to asbestos: a mathematical model

Our plain-English summary of Pleural plaques and exposure to asbestos: a mathematical model, by B. Järvholm (International Journal of Epidemiology, 1992).

The study

• Author: B. Järvholm
• Journal: International Journal of Epidemiology
• Published: 1992;21(6):1180-4
• Cited by: 16 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

The objective of this study was to find a model to describe the relationship between the occurrence of pleural plaques and exposure to asbestos. A simple model based on the cumulative exposure was postulated and empirically tested on shipyard workers occupationally exposed to asbestos. Exposure time was used to approximate the cumulative dose. It was found that the incidence of pleural plaques could be described as K(t-w)a where 't' is time since onset of exposure; 'K' is a constant that would depend on the level of asbestos exposure; 'w' is a latency period and was around 13 years; 'a' is a constant that was 0.4. In subgroups of the workers, i.e. plumbers, fitters and platers, 'a' was 0.4, 0.6 and 0.2 respectively.

In plain English

This study proposed a mathematical model for how often pleural plaques appear after asbestos exposure. It tested the model on men working at shipyards in Göteborg, Sweden, who had chest x-rays and answered a questionnaire in 1977-1979. The analysis included 2423 men who started shipyard work before age 26. The article does not say which asbestos fibre types these shipyard workers were exposed to, and their exposure levels were not measured. Time since first exposure stood in for cumulative dose. Plaque prevalence began rising about 10 to 14 years after first exposure. The estimated minimum latency period was 13.1 years, but this estimate was unstable (95% confidence interval 1.9 to 16.1). The model's exponent 'a' was 0.43 for all workers, and 0.42, 0.61 and 0.19 for plumbers, fitters and platers. The author concluded that plaque incidence could be modelled with a latency of around 13 years, 'a' around 0.4, and a constant depending on exposure intensity. The author noted that the model's general applicability cannot be judged until it is tested on other data sets.

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: Mathematical modelling study, with the model tested against prevalence data from a cross-sectional chest x-ray examination of shipyard workers; constants estimated by maximum likelihood
• Who was studied: Men employed at shipyards in Göteborg, Sweden, examined 1977-1979 (chest x-ray, spirometry, questionnaire). The analysis was restricted to 2423 men who started work at the shipyards before age 26. Separate analyses were done for the three largest occupational groups: plumbers, fitters and platers.
• Exposure: Occupational asbestos exposure at shipyards. The fibre types these workers were exposed to are not specified. No fibre measurements were used: cumulative exposure was approximated by time since first exposure to asbestos, as reported by questionnaire. Exposure ended around 1972 for most workers.
• Main results:
  • Among all shipyard workers, the prevalence of pleural plaques began to increase about 10-14 years after onset of exposure.
  • The minimum latency period (w) was estimated at 13.1 years for all shipyard workers, but the estimate was rather unstable (95% likelihood-based confidence interval 1.9-16.1).
  • In the total group of shipyard workers, the constant a was estimated at 0.43 (slope a+1 of 1.43, standard error 0.10), and the coefficient k was 0.010.
  • Using a common latency of 13.1 years, a was estimated at 0.42 for plumbers, 0.61 for fitters and 0.19 for platers. The corresponding k values were 0.015, 0.0063 and 0.014. The article reports one difference as just significant (P = 0.05) and no other differences as significant.
  • Alternative models fitted the data significantly worse. These included using age instead of time since first exposure, a linear model of t or t squared, and logit or probit link functions.
• The authors' conclusion: The author concluded that the incidence of pleural plaques attributable to asbestos exposure can be modelled as K(t-w) raised to the power a, for t greater than w. In this model, K is a constant depending on the intensity of asbestos exposure, a is around 0.4, and w is a minimum latency period of around 13 years.
• Limitations the authors state:
  • Exposure was estimated only by time since onset of exposure. No measure of the level of exposure was available.
  • The model rests on assumptions, and its general applicability cannot be established until it is tested on other data sets.
  • The method used to determine the latency period, which excluded everyone with less than 15 years since onset of exposure, has its limitations. Latency estimates in the subgroups were quite unstable.
  • Chest x-ray diagnosis of pleural plaques is less than 100% specific, and the actual specificity in this study is not known.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Asbestosis.

Medical terms in this study, explained in our Lexicon: Pleural Plaques, Cumulative Exposure, Cumulative Dose, Asbestos Exposure, Latency.

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