Sir,
We have read with interest and concern the recent article in the BJC by McCormack et al (2012), Estimating the asbestos-related lung cancer burden from mesothelioma mortality. The article puts forth erroneous estimates and conclusions by omitting newer data, relying on incomplete and/or outdated data, omitting critiques of data relied upon, and drawing conclusions using heterogeneous data sets that are not adequately controlled for latency and/or exposure. These shortcomings undermine conclusions and recommendations in the report.
While several authors of the McCormack et al (2012) article are employees or affiliated with IARC, their article omits relevant data identified and published by 2009 when, during 17–24 March 2009, the IARC Working Group on the Evaluation of Carcinogenic Risks to Humans met in Lyon, France (Straif et al, 2009; IARC, 2012). Specific to our concerns regarding chrysotile asbestos, McCormack et al (2012) omit the most recent update by Mirabelli et al (2008) on the Italian chrysotile asbestos mining cohort and discussed in the evaluation of the 2009 IARC monograph working group. The update by Mirabelli et al (2008) found a total of 27 cases of mesothelioma associated with the site, including not only miners, but also relatively low-dose ‘white collar’ and environmental cases stemming from the mine. McCormack et al (2012) exclude this information resulting in attentuation of the risk estimates. Instead, they cite an older study: the 1990 cohort study by Piolatto et al (1990), in which only two mesothelioma cases in miners had been reported. This mine’s asbestos was ‘pure’ chrysotile without amphiboles of any type. (IARC, 2012).
McCormack et al (2012) also cite and rely on outdated data from IARC (1987), Overall evaluations of carcinogenicity: an updating of IARC Monographs, ignoring newer and more relevant data presented at the 2009 IARC meeting and included in IARC’s latest monograph on asbestos pertaining to chrysotile (IARC, 2012). These newer data have important implications as both latency and dose are major factors in the aetiology of mesothelioma occurrence, neither adjusted for nor adequately addressed.
Bignon et al (2002) concluded ‘very few studies have focused on the time-related pattern of occupational exposure as a significant factor in the occurrence of mesothelioma,’ and multiple studies cited by McCormack et al (2012) suffer from this lack of focus. One of the McCormack et al (2012) authors (Boffetta) acknowledges elsewhere the importance of latency as the main determining risk factor (La Vecchia and Boffetta, 2011). The current paper includes studies having insufficient latency for mesothelioma to manifest (Zasadzinski et al, 2013).
McCormack et al (2012) also refer to studies of earlier potency estimates reported by Hodgson and Darnton (2000) while ignoring the significantly revised estimates lowering the potency differences between chrysotile and amphibole asbestos by these same authors (Hodgson and Darnton, 2009).
The authors fail to impose quality control standards to their study, as required when dealing with hetrogeneous data sets and as demonstrated by Lenters et al (2011) in their meta-analysis, which included only studies adequately controlled for exposure.
McCormack et al (2012) further state that figures showing mesotheliomas related to chrysotile asbestos exposure may be erroneously over-reported, but give no explanation for their statement that ‘the lung cancer excess depends critically on the rates on which the SMR is based’. Such an effect would be true for all asbestos types, including the amphibole and mixed exposure cohorts, especially given the inadequate coding scheme for mesothelioma and under-reporting due to a variety of country-to-country reporting errors (Delgermaa et al, 2011) over the time frames covered by the cited epidemiology studies of McCormack et al (2012). Until recently, the coding for mesothelioma was unspecific until the implementation of the International Classification of Diseases-10 in 1994, which gave mesothelioma its own specific codes.
The McCormack et al (2012) conclusion that mesothelioma occurring in chrysotile-exposed cohorts is due to other asbestos types lacks justification, as it is based on lung-burden analysis alone.
In particular, the study by Frank et al (1998) using tremolite-free UICC Chrysotile B (Canadian chrysotile) has shown all forms of asbestos to cause disease, including mesothelioma. In an inhalation study (Wagner et al, 1974) chrysotile, caused as many mesotheliomas as did crocidolite in an inhalation study. To suggest causal inference from amphiboles found in the lung parenchyma while ignoring the predominant finding of chrysotile in the pleura, where mesotheliomas occur, seems scientifically questionable (Stayner et al, 1996).
The relative lack of biopersistence of chrysotile asbestos in lung tissue can hardly be grounds for concluding that chrysotile asbestos does not cause mesothelioma, given the translocation and biopersistence of chrysotile in target sites of mesothelioma occurrence (Sebastien et al, 1980; Dodson et al, 1990; Suzuki and Yuen, 2001; Suzuki et al, 2005). After extensive hearings, the Royal Commission concluded that such data were lacking to implicate tremolite as the cause of mesothelioma in chrysotile asbestos-exposed miners (Dupré et al, 1984). To date, no more compelling data have been produced to conclude otherwise and, in fact, chrysotile’s role in the aetiology of mesothelioma is continually reaffirmed (IPCS, 1998; Straif et al, 2009; IARC, 2012).
The McCormack et al (2012) article omits criticisms regarding the Quebec industry-sponsored research, which they refer to and where the ‘amphibole hypothesis’ originated. In the study by Lenters et al (2011), this research did not meet their quality of exposure assessment standard and was excluded for that reason. In fact, a major international epidemiology organisation has also raised criticisms of this same Quebec research in their Position Statement on Asbestos (JPC-SE, 2012).
The McCormack et al (2012) study minimises the health risks posed by chrysotile asbestos and suggests that ‘strict regulation’ in lieu of eliminating all asbestos use is acceptable. The suggestion that continuing ‘controlled use’ of asbestos is realistic is the asbestos industry’s position and is contradictory to the World Health Organization’s recommendation that all use of asbestos should stop (WHO, 2006).
Finally, the authors’ inexplicable encouragement of a smoking cessation programme only for workers formerly exposed, and not for current asbestos workers, is an inconsistent public health position. The suggestion that ‘controlled use’ is effective has never been justified.
References
Bignon J, Iwatsubo Y, Galateau-Salle F, Valleron AJ (2002) History and Experience of Mesothelioma in Europe. In : Mesothelioma Bruce, WS, Robinson A eds. Philippe Chahinian. Martin Dunitz Ltd., Taylor & Francis Group: London. 29–53.
Delgermaa V, Takahashi K, Park E-K, Le GV, Toshiyuki H, Sorahan T (2011) Global mesothelioma deaths reported to the World Health Organization between 1994 and 2008. Bull World Health Organ 89: 716–724C.
Dodson RF, Williams MG Jr, Corn CJ, Brollo A, Bianchi C (1990) Asbestos content of lung tissue, lymph nodes, and pleural plaques from fromer shipyard workers. Am Rev Respir Dis 142 (4): 843–847.
Dupré JS, Mustard JF, Uffen RJ (1984) Report of the Royal Commission on Matters of Health and Safety Arising from the Use of Asbestos in Ontario, Ontario Ministry of the Attorney General, Queen’s Printer for Ontario,. Toronto.
Frank AL, Dodson RF, Williams MG (1998) Carcinogenic implications of the lack of tremolite in UICC reference chrysotile. Am J Industrial Med 34: 314–317.
Hodgson JT, Darnton A (2000) The quantitative risks of mesothelioma and lung cancer in relation to asbestos exposure. Ann Occup Hyg 44: 565–601.
Hodgson JT, Darnton A (2009) Mesothelioma risk from chrysotile. Occup Environ Med. 67 (6): 432.
IARC (1987) Overall evaluations of carcinogenicity: an updating of IARC Monographs volumes 1 to 42. IARC Monogr Eval Carcinogenic Risks Humans Suppl 7: 1–440.
IARC (2012) IARC Monographs—Arsenci, Metals, Fibres, and Dusts, Volume 100 C. A Reviews of Human Carcinogens. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. International Agency for Research on Cancer, World Health Organization.
IPCS (1998) Chrysotile Asbestos—Environmental Health Criteria 203. International Programme on Chemical Safety. World Health Organization: Geneva.
Joint Policy Committee of Societies of Epidemiology (JPC-SE),, Weiss SH, Hiatt RA et al (2012) Position Statement on Asbestos. Included in: Weiss SH (2012) A call to action: epidemiologists assert themselves with scientific data. Int J Occup Environ Health 18 (3): 167–178.
La Vecchia C, Boffetta P (2011) Role of stopping exposure and recent exposure to asbestos in the risk of mesothelioma. Eur J Cancer Prev 21 (3): 227–230.
Lenters V, Vermeulen R, Dogger S, Stayner L, Portengen L, Portengen L, Burdorf A, Heederik D (2011) A meta-analysis of asbestos and lung cancer: is better quality exposure assessment associated with steeper slopes of the exposure-response relationships? Environ Health Perspect 119: 1547–1555.
McCormack V, Peto J, Byrnes G, Straif K, Boffetta P (2012) Estimating the asbestos-related lung cancer burden from mesothelioma mortality. Br J Cancer 106: 575–584.
Mirabelli D, Calisti R, Barone-Adesi F, Fornero E, Merletti F, Magnani C (2008) Excess of mesotheliomas after exposure to chrysotile in Balangero, Italy. Occup Environ Med 65: 815–819.
Piolatto G, Negri E, La Vecchia C, Pira E, Decarli A, Peto J (1990) An update of cancer mortality among chrysotile asbestos miners in Balangero, northern Italy. Br J Ind Med 47: 810–814.
Sebastien P, Janson X, Gaudichet A, Hirsch A, Bignon J (1980) Asbestos retention in human respiratory tissues: comparative measurements in lung parenchyma and parietal pleura. In: Wagner JC ed. Biological Effects of Mineral Fibers. IARC: Lyon. 237–246.
Stayner LT, Dankovic DA, Lemen RA (1996) Occupational exposure to chrysotile asbestos and cancer risk: a review of the amphibole hypothesis. Am J Public Health 86: 179–186.
Straif K, Benbrahim-Talloa L, Baan R, Grosse Y, Secretan B, El Ghissassi F, Bouvard B, Guha N, Freeman C, Galichet L, Cogliano V (2009) Special Report: Policy. A review of human carcinogens–Part C: metals, arsenic, dusts, and fibres. Lancet Oncol 10: 453–454.
Suzuki Y, Yuen SR (2001) Asbestos tissue burden study on human malignant mesothelioma. Ind. Health 39: 150–160.
Suzuki Y, Yuen SR, Ashley R (2005) Short, thin asbestos fibres contribute to the development of human malignant mesothelioma: pathological evidence. Int J Hyg Environ Health 208: 201–210.
Wagner JC, Berry G, Skidmore JW, Timbrell V (1974) The Effects of the Inhalation of Asbestos in Rats. Br J Cancer 29 (3): 252–269.
WHO (2006) Elimination of Asbestos-Related Diseases. http://whqlibdoc.who.int/hq/2006/WHO_SDE_OEH_06.03_eng.pdf.
Zasadzinski JR, Weiss SH, Soskolne CL (2013) In the Epidemiology of Mesothelioma, Could 50 Years of Cohort Follow-Up After Exposure to Asbestos Be Insufficient? 2013 Annual Retreat on Cancer Research in New Jersey 23 May 2013; UMDNJ - Robert Wood Johnson Medical School: Piscataway, NJ.
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All authors are health professionals whose mandate is to advocate for health. Individually, and as part of his professional or academic duties, SHW serves as Chair of the Joint Policy Committee of the Societies of Epidemiology (JPC-SE), a consortium of 13 organisations described at www.jpc-se.org, which prepares evidence-based materials that are vetted through the individual societies for comment and possible endorsement. Both SHW and CLS played a role in the 2012 JPC-SE position statement on asbestos. RAL, BC, CLS and ALF are elected Fellows in the Collegium Ramazzini that advocates the banning of both asbestos products and mining, worldwide. BC and RAL have been advisors to the World Health Organization, which advocates against asbestos use worldwide. ALF, RAL and BC are members of the Science Advisory Board to the Asbestos Disease Awareness Organization, which advocates a worldwide ban on asbestos. RAL is retired from the National Institute for Occupational Safety and Health of the United States that recommended a ban on asbestos in the workplace as early as 1976. RAL was a Working Group member and primary author of the first International Agency for Research on Cancer (IARC) Monograph solely devoted to asbestos (Monograph 14, 1976), which determined that all forms of asbestos are carcinogenic. All authors have been retained and/or testified as expert witnesses in asbestos personal injury compensation claims, usually at the request of plaintiffs. Remuneration for such work has been donated by ALF and CLS to their respective employing institutions.
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Lemen, R., Frank, A., Soskolne, C. et al. Comment on ‘Estimating the asbestos-related lung cancer burden from mesothelioma mortality’ – IARC and Chrysotile Risks. Br J Cancer 109, 823–825 (2013). https://doi.org/10.1038/bjc.2013.301
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DOI: https://doi.org/10.1038/bjc.2013.301
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