Year : 2018  |  Volume : 22  |  Issue : 2  |  Page : 113--114

Asbestos and mesothelioma: A comment

Sergei V Jargin 
 Department of Pathology, Peoples' Friendship University of Russia, Moskva, Russia

Correspondence Address:
Dr. Sergei V Jargin
Department of Pathology, Peoples' Friendship University of Russia, Moskva

How to cite this article:
Jargin SV. Asbestos and mesothelioma: A comment.Indian J Occup Environ Med 2018;22:113-114

How to cite this URL:
Jargin SV. Asbestos and mesothelioma: A comment. Indian J Occup Environ Med [serial online] 2018 [cited 2020 Apr 2 ];22:113-114
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Full Text

This letter is an updated summary of several preceding papers.[1] Asbestos-related risks have been estimated on the basis of extrapolations from the past in industrial settings, where exposures were three to four orders of magnitude higher than the current level of airborne fibers in the environment.[2] Inhalation and discharge of fibers are probably in a dynamic equilibrium; accordingly, there may be a safe exposure level (threshold). However, the linear no-threshold dose-response pattern has been assumed for low exposure levels, although its applicability has never been proven. By analogy with radiation-related diseases,[3] the screening must have contributed to the enhanced registered incidence of asbestos-related diseases in exposed populations and exaggeration of dose-response relationships. In particular, mesothelioma was sought in exposed populations, and correspondingly, more often found. Mesothelioma can be spontaneous and/or can occur when asbestos fibres are present in the pulmonary or pleural tissues, which does not necessarily imply a cause–effect relationship. The diagnosis of malignant mesothelioma (MM) remains difficult being one of the greatest challenges faced by a surgical pathologist.[4] The current status of MM biomarkers is not satisfactory.[5] Histologically, MM can resemble various cancers. Some cancers can undergo de-differentiation, becoming histologically similar to MM. Misdiagnosis of MM is a worldwide problem; revisions of archives regularly found inaccurately classified cases, while sometimes no clear-cut entity diagnosis was possible.[6] Screening has been performed in asbestos-exposed populations with a well-aimed search for MM. Accordingly, more MMs are found, questionable or borderline cases being sometimes diagnosed as such. Other bias is not infrequent in asbestos research, e.g., detection of fibers in pulmonary or pleural tissues attributing the neoplasm to asbestos, although a cause–effect relationship remains unproven. Some studies rely on the work or residence histories of questionable reliability, interviews with relatives, etc. Bias due to litigation may further compromise objectivity. Asbestos-related diseases have been broadly studied in the former Soviet Union; the prevailing opinion is that, if necessary precautions are observed, modern technologies of asbestos production and processing are acceptably safe. Some experts admitted that the concept of much higher toxicity of inhaled amphibole fibres compared to chrysotile has not been confirmed. Carcino-, fibro-, mutagenicity, and cytotoxicity of chrysotile was demonstrated both in experiments and epidemiological studies;[7] more details and references are in.[1] At the same time, there are strong industrial interests behind chrysotile. In experiments, chrysotile was reported to possess acute toxicity, inducing a granulomatous tissue reaction; its carcinogenicity did not differ significantly from that of the amphiboles. Chrysotile clearance from the lung may partly result from fiber splitting and movement to the pleura. Carcinogenic effects depend not only on bio-persistence but also on dimensions of fibers of different types, which is an additional argument in favor of the “all fibers equal” approach to asbestos and its substitutes.[1] This concept can be used provisionally, pending reliable evidence. The “all fibers equal” basis of safety regulations is technically most plausible, being largely compatible with the current knowledge conflicting as it is. Substitution of asbestos by artificial fibers would not necessarily eliminate health risks. Considering economic interests behind chrysotile, and newly also some artificial fibers, any deviation from the “all fibers equal&” concept must be based on high-quality, independent research, e.g., large-scale chronic bioassays. In conclusion, some epidemiological studies are biased due to the screening effect in asbestos-exposed populations, over-diagnosis, biased exposure histories, unclear demarcation of mesothelioma from other cancers, as well as industrial interests. It can be reasonably assumed that nonuse of asbestos-containing materials (brake linings, fire-resisting, and thermal insulation) augmented the numbers of victims of traffic accidents, fires, terrorist attacks, etc. Bans and restrictions of asbestos should be revaluated on the basis of independent research.

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