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      Comments on Vimercati et al., 2019, “Asbestos exposure and malignant mesothelioma of the tunica vaginalis testis: a systematic review and the experience of the Apulia (southern Italy) mesothelioma register”

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          Abstract

          We read with interest the review by Vimercati et al. [1] of the scientific literature on malignant mesothelioma of the tunica vaginalis testis (MMTVT). The authors reviewed case series and case reports, and primarily focused their discussion on diagnostic and prognostic characteristics of MMTVT and options for MMTVT treatment. The authors also briefly discussed the potential etiologic role of asbestos exposure in MMTVT development, and declared, “[T]he only causal factor so far ascertained is asbestos exposure, and exposure to different asbestos-containing materials is the only well-documented risk factor, as stated by IARC [International Agency for Research on Cancer].” In this context, the authors referenced our recent review of the epidemiologic literature on mesothelioma of the pericardium and MMTVT [2], stating, “Nevertheless, there are authors [2] who do not agree with the absence, until today, of analytical case-control epidemiologic studies to test this relationship.” In response to this statement, we note several points. In our systematic literature review and complementary analysis of U.S. registry-based incidence rates of MMTVT [2], we assessed relevant epidemiologic findings regarding the potential etiologic role of asbestos exposure in MMTVT development. We acknowledged the lack of analytical epidemiologic studies, including case-control studies, to test this hypothesis but pointed to several lines of scientific evidence that support our conclusion that the available epidemiologic literature does not support an association, let alone a causal association, between inhaled asbestos exposure and the risk of developing MMTVT. First, in large occupational cohorts with heavy workplace exposures to asbestos, no cases of MMTVT have been reported (e.g., [3]). Second, registry-based incidence rates of MMTVT in the U.S. do not show temporal or geographical trends that would correspond with trends in commercial asbestos use, with due consideration of latency, nor do they reflect incidence rates of pleural malignant mesothelioma, for which asbestos historically played an etiologic role in a substantial fraction of male cases [2, 4]. Third, the incidence of extra-pleural mesothelioma, including MMTVT, in a recent study using the National Mesothelioma Register in Italy does not demonstrate an exposure-response relationship, as MMTVT cases were not reported in some of the highest-risk industries (e.g., asbestos cement, national defense, shipbuilding, and railway industries) [5]. If inhaled asbestos caused MMTVT, the highest risk of MMTVT would be expected in industries with the highest exposure; no such exposure-response relationship is reported (see Mezei et al. [2] for the details of this argument). Interestingly, Vimercati et al. [1] did not reference their Italian colleagues in their article. We also note that case reports and case series are not epidemiologic studies; they cannot establish associations, let alone causal relationships, between exposure and disease. Nevertheless, we found that a substantial proportion of MMTVT cases reported in the published literature did not have documented asbestos exposure [2]. Vimercati et al. [1] also referenced the most recent IARC monograph (2012) on the carcinogenic risks of asbestos [6] in support of their view that asbestos is an established cause of MMTVT. The IARC monograph (2012) does not contain a single mention of MMTVT (or of mesothelioma of the pericardium) either in the main text or in the reference list. Thus, the IARC monograph (2012) does not and cannot conclude that asbestos causes these rare extra-pleural forms of malignant mesothelioma. While an earlier version of the IARC monograph (1987) concerning asbestos mentions MMTVT and pericardial mesothelioma [7], the three references cited in a single sentence are case reports. In addition, contrary to the opinion expressed by Vimercati et al. [1], there is considerable evidence that in addition to asbestos and some other fibers such as erionite, ionizing radiation increases the risk of malignant mesothelioma (e.g., [8]). Finally, the current paradigm of carcinogenesis as a process of mutation accumulation implies that all cancers, including malignant mesothelioma can and do occur spontaneously without exposure to any external agents (e.g., [9, 10]). In summary, we conclude that the available epidemiology provides no evidence that inhaled asbestos exposure is a risk factor for the development of MMTVT. Vimercati et al. [1] provide no evidence to the contrary. We look forward to the results of the forthcoming Italian case-control study mentioned by the authors.

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          Stem cell divisions, somatic mutations, cancer etiology, and cancer prevention

          Cancers are caused by mutations that may be inherited, induced by environmental factors, or result from DNA replication errors (R). We studied the relationship between the number of normal stem cell divisions and the risk of 17 cancer types in 69 countries throughout the world. The data revealed a strong correlation (median = 0.80) between cancer incidence and normal stem cell divisions in all countries, regardless of their environment. The major role of R mutations in cancer etiology was supported by an independent approach, based solely on cancer genome sequencing and epidemiological data, which suggested that R mutations are responsible for two-thirds of the mutations in human cancers. All of these results are consistent with epidemiological estimates of the fraction of cancers that can be prevented by changes in the environment. Moreover, they accentuate the importance of early detection and intervention to reduce deaths from the many cancers arising from unavoidable R mutations.
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            Mesothelioma: Scientific clues for prevention, diagnosis, and therapy

            Mesothelioma affects mostly older individuals who have been occupationally exposed to asbestos. The global mesothelioma incidence and mortality rates are unknown, because data are not available from developing countries that continue to use large amounts of asbestos. The incidence rate of mesothelioma has decreased in Australia, the United States, and Western Europe, where the use of asbestos was banned or strictly regulated in the 1970s and 1980s, demonstrating the value of these preventive measures. However, in these same countries, the overall number of deaths from mesothelioma has not decreased as the size of the population and the percentage of old people have increased. Moreover, hotspots of mesothelioma may occur when carcinogenic fibers that are present in the environment are disturbed as rural areas are being developed. Novel immunohistochemical and molecular markers have improved the accuracy of diagnosis; however, about 14% (high-resource countries) to 50% (developing countries) of mesothelioma diagnoses are incorrect, resulting in inadequate treatment and complicating epidemiological studies. The discovery that germline BRCA1-asssociated protein 1 (BAP1) mutations cause mesothelioma and other cancers (BAP1 cancer syndrome) elucidated some of the key pathogenic mechanisms, and treatments targeting these molecular mechanisms and/or modulating the immune response are being tested. The role of surgery in pleural mesothelioma is controversial as it is difficult to predict who will benefit from aggressive management, even when local therapies are added to existing or novel systemic treatments. Treatment outcomes are improving, however, for peritoneal mesothelioma. Multidisciplinary international collaboration will be necessary to improve prevention, early detection, and treatment.
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              The quantitative risks of mesothelioma and lung cancer in relation to asbestos exposure.

              Mortality reports on asbestos exposed cohorts which gave information on exposure levels from which (as a minimum) a cohort average cumulative exposure could be estimated were reviewed. At exposure levels seen in occupational cohorts it is concluded that the exposure specific risk of mesothelioma from the three principal commercial asbestos types is broadly in the ratio 1:100:500 for chrysotile, amosite and crocidolite respectively. For lung cancer the conclusions are less clear cut. Cohorts exposed only to crocidolite or amosite record similar exposure specific risk levels (around 5% excess lung cancer per f/ml.yr); but chrysotile exposed cohorts show a less consistent picture, with a clear discrepancy between the mortality experience of a cohort of xhrysotile textile workers in Carolina and the Quebec miners cohort. Taking account of the excess risk recorded by cohorts with mixed fibre exposures (generally<1%), the Carolina experience looks uptypically high. It is suggested that a best estimate lung cancer risk for chrysotile alone would be 0.1%, with a highest reasonable estimate of 0.5%. The risk differential between chrysotile and the two amphibole fibres for lunc cancer is thus between 1:10 and 1:50. Examination of the inter-study dose response relationship for the amphibole fibres suggests a non-linear relationship for all three cancer endpoints (pleural and peritoneal mesotheliomas, and lung cancer). The peritoneal mesothelioma risk is proportional to the square of cumulative exposure, lung cancer risk lies between a linear and square relationship and pleural mesothelioma seems to rise less than linearly with cumulative dose. Although these non-linear relationships provide a best fit ot the data, statistical and other uncertainties mean that a linear relationship remains arguable for pleural and lung tumours (but not or peritoneal tumours). Based on these considerations, and a discussion fo the associated uncertainties, a series of quantified risk summary statements for different elvels of cumulative exposure are presented.
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                Author and article information

                Contributors
                gmezei@exponent.com
                echang@exponent.com
                fmowat@exponent.com
                smoolgavkar@exponent.com
                Journal
                Environ Health
                Environ Health
                Environmental Health
                BioMed Central (London )
                1476-069X
                26 December 2019
                26 December 2019
                2019
                : 18
                : 111
                Affiliations
                [1 ]ISNI 0000 0000 9662 0001, GRID grid.418983.f, Exponent, Inc., ; 149 Commonwealth Drive, Menlo Park, CA 94025 USA
                [2 ]ISNI 0000 0000 9662 0001, GRID grid.418983.f, Exponent, Inc., ; 15735 SE 30th Place, Suite 250, Bellevue, WA USA
                Author information
                http://orcid.org/0000-0001-6562-7857
                Article
                552
                10.1186/s12940-019-0552-9
                6933728
                31878926
                00b921a8-0a3c-4d0c-ba5f-4ad9890739cd
                © The Author(s). 2019

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 18 October 2019
                : 6 December 2019
                Categories
                Letter to the Editor
                Custom metadata
                © The Author(s) 2019

                Public health
                malignant mesothelioma,tunica vaginalis testis,epidemiology,etiology
                Public health
                malignant mesothelioma, tunica vaginalis testis, epidemiology, etiology

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