Pleural plaques and exposure to mineral fibres in a male urban necropsy population

Our plain-English summary of Pleural plaques and exposure to mineral fibres in a male urban necropsy population, by A. Karjalainen, P.J. Karhunen, K. Lalu, et al (Occupational and Environmental Medicine, 1994).

The study

• Authors: A. Karjalainen, P.J. Karhunen, K. Lalu, A. Penttilä, E. Vanhala, P. Kyyrönen, A. Tossavainen
• Journal: Occupational and Environmental Medicine
• Published: 1994;51(7):456-60
• Cited by: 27 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Objectives: The study aimed to evaluate the risk of pleural plaques according to the degree of past exposure to asbestos, type of amphibole asbestos, and smoking, as well as to estimate the aetiologic fraction of asbestos as a cause of plaques among urban men.

Methods: The occurrence and extent of pleural plaques were recorded at necropsies of 288 urban men aged 33 to 69 years. The pulmonary concentration of asbestos and other mineral fibres was analysed with scanning electron microscopy. The probability of past exposure was estimated from the last occupation.

Results: Pleural plaques were detected in 58% of the cases and their frequency increased with age, probability of past occupational exposure to asbestos, pulmonary concentration of asbestos fibres, and smoking. The risk of both moderate and widespread plaques was raised among asbestos exposed cases, and the risk estimates were higher for widespread plaques than for moderate plaques. The age adjusted risk was higher for high concentrations of crocidolite/amosite fibres than for anthophyllite fibres. The aetiologic fraction of pulmonary concentration of asbestos fibres exceeding 0.1 million fibres/g was 43% for widespread plaques and 24% for all plaques. The median pulmonary concentrations of asbestos fibres were about threefold greater among cases with widespread plaques than among those without plaques. No increased risk of pleural plaques was associated with raised total concentrations of non-asbestos fibres.

Conclusion: The occurrence of pleural plaques correlated closely with past exposure to asbestos. The risk was dependent on the intensity of exposure. Due to methodological difficulties in detecting past exposures to chrysotile and such low exposures that may still pose a risk of plaques, the aetiologic fractions calculated in the study probably underestimate the role of asbestos.

In plain English

This Finnish autopsy study examined pleural plaques, thickened patches on the chest-wall lining. The men had died suddenly and unexpectedly in Helsinki and were autopsied between January 1991 and January 1992. Plaques were assessed in 288 men aged 33 to 69 and found in 58%. Lung fibres were counted by electron microscopy; exposure was also judged from last occupation. Men with over 1 million asbestos fibres per gram of dry lung tissue had an odds ratio of 8.1 (95% CI 2.7 to 24) for widespread plaques versus men under 0.1 million, adjusted for age and other fibres. After age adjustment, crocidolite/amosite levels, but not anthophyllite levels, were linked to significantly raised odds of plaques. Smokers and ex-smokers had raised odds of widespread plaques. Total non-asbestos fibre levels showed no increased risk, though individual types could not be analysed separately. The authors estimated that asbestos levels above 0.1 million fibres per gram of dry tissue accounted for 24% of all plaques and 43% of widespread plaques. They concluded these probably underestimate asbestos's role, partly because chrysotile is poorly detected.

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: Autopsy (necropsy) series study of consecutive forensic autopsies, with lung fibre analysis by scanning electron microscopy and exposure estimated from last occupation; analysed with multinomial logistic regression
• Who was studied: All sudden, unexpected deaths of men aged 35 to 69 (two men aged 33 included by mistake) who died in Helsinki and were autopsied at the Department of Forensic Medicine, University of Helsinki, between 15 January 1991 and 30 January 1992. There were 300 autopsies, and plaques were assessed in 288. Relatives were interviewed in 167 cases, and smoking habits were known for 161.
• Exposure: Probability of asbestos exposure from last occupation (probable: construction; possible: other industrial; unlikely: office, health care, agricultural; unknown). Lung concentrations, in million fibres per gram of dry tissue, of asbestos fibres and of non-asbestos inorganic fibres. Asbestos fibres included anthophyllite and crocidolite/amosite, the last two counted together because they could not be told apart. Chrysotile was found in one sample and tremolite in six. Smoking was also studied.
• Main results:
  • Pleural plaques were found in 58% of the 288 men. Their frequency rose with age, probability of occupational asbestos exposure, lung asbestos fibre concentration, and smoking.
  • More than 80% of men with over 1 million asbestos fibres per gram had plaques. Plaques were also found in 43% of men whose occupation made exposure unlikely, and in 38% of men with under 0.1 million asbestos fibres per gram.
  • Compared with men under 0.1 million asbestos fibres per gram of dry lung tissue, men with more than 1 million had an odds ratio for widespread plaques of 8.1 (95% CI 2.7 to 24), the highest risk found. For 0.1 to 0.99 million fibres per gram the odds ratio for widespread plaques was 2.7 (1.2 to 6.2). These estimates were adjusted for age and for the lung concentration of non-asbestos inorganic fibres.
  • After adjusting for age, crocidolite/amosite concentrations were linked to significantly raised odds of plaques. For widespread plaques at the highest crocidolite/amosite level the odds ratio was 7.7. The odds ratios for anthophyllite were not significantly raised after age adjustment, though they were significant without it.
  • Compared with non-smokers, the odds ratio for widespread plaques was 5.6 (1.5 to 21) among smokers and 5.3 (1.1 to 26) among ex-smokers, adjusted for age and lung asbestos concentration. These figures come from the 161 men whose smoking habits were known.
  • Plaque frequency did not increase with the total lung concentration of inorganic fibres other than asbestos. Individual non-asbestos fibre types could not be analysed separately.
  • The estimated share of plaques attributable to lung asbestos concentrations above 0.1 million fibres per gram of dry tissue was 24% of all plaques and 43% of widespread plaques. Using last occupation (probable or possible exposure) instead, the figures were 26% and 29%. The corresponding figure was 12% each for anthophyllite and for crocidolite/amosite fibres.
  • Median lung asbestos concentrations were 0.16 million fibres per gram in men without plaques, 0.40 in men with moderate plaques and 0.57 in men with widespread plaques. These medians were not adjusted for age, and men with widespread plaques were on average about 8 years older than men without plaques.
• The authors' conclusion: The authors concluded that the occurrence of pleural plaques correlated closely with past asbestos exposure and that risk depended on the intensity of exposure. They also concluded that their attributable-fraction estimates underestimate the share of plaques due to asbestos.
• Limitations the authors state:
  • Plaques were identified by their appearance at autopsy only, without microscopic (histological) confirmation.
  • Chrysotile is poorly detected by scanning electron microscopy, which may have caused underestimation of the asbestos-attributable fraction.
  • Asbestos concentrations below 0.1 million fibres per gram, which may still carry some risk, could not be quantified with the method used.
  • Using last occupation as the exposure indicator probably caused misclassification, because of the long latency between exposure and plaques. The exposure criteria also mainly reflect occupational exposure, neglecting environmental and domestic exposure.
  • The analyses could adjust only for age, not directly for latency.
  • The smoking finding may have been confounded by differences in latency between smokers, ex-smokers and non-smokers.
  • Too few samples had raised levels of any single non-asbestos fibre to analyse those fibres separately, so the authors could not rule out that some of them cause plaques.
  • Amosite and crocidolite have almost identical x-ray spectra and could not be reported separately.

Topics

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

Medical terms in this study, explained in our Lexicon: Pleural Plaques, Autopsy, Amphibole Asbestos, Scanning Electron Microscopy (SEM), Occupational Exposure, Crocidolite, Amosite, Anthophyllite.

Related studies

• 'Black Spots' and hyaline pleural plaques on the parietal pleura of 150 urban necropsy cases — K. Mitchev, P. Dumortier, et al. (2002)
• Diachronic study of pleural plaques in rural population with environmental exposure to asbestos — L. Sichletidis, D. Chloros, et al. (2006)
• Pleural plaques as risk indicators for malignant pleural mesothelioma: a necropsy-based study — C. Bianchi, A. Brollo, et al. (1997)
• Coated and uncoated lung mineral fibres in subjects with and without pleural plaques at autopsy — A. Andrion, D. Bellis, et al. (1984)
• Aetiology of pleural plaques — V. Rous, J. Studený (1970)
• Asbestos bodies and pleural plaques in human lungs at necropsy — I. Hägerstrand, B. Seifert (1973)

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