Canadian Medical Association Journal Home

Table of Contents
Free eCMAJ TOC

Back issues
Supplements
Selected series

eLetters
About this journal
Info for authors

PubMed

A ban on asbestos must be based on a comparative risk assessment
Michel Camus
CMAJ 2001;164(4):491-4 [PDF]


See also:
   •  Chile bans asbestos, others to follow? [News]
   •  A call for an international ban on asbestos [Commentary]
   •  Should Canadian health care professionals support the call for a worldwide ban on asbestos? [Commentary]

In this issue (page 489), Joseph LaDou and colleagues on behalf of the Collegium Ramazzini1 call for an immediate and total ban on "asbestos" products because the current health risks associated with the use of "asbestos" are not acceptable, "controlled use" is not possible and "safer" substitutes are readily available. The logic is indisputable, but the premises are not. First, the risks associated with chrysotile, the type of asbestos used nowadays, are exaggerated by relying on a single and aberrant study. Second, the statements on controlled use and substitutes are supported neither by evidence nor by references. Finally, the Collegium fails to consider the technical efficiency of chrysotile and its substitutes when used in brakes and thermal insulation. A distortion of the evidence might result in a useless ban and possibly increased risk. This commentary presents critical evidence omitted by the Collegium and argues that any decision to ban "asbestos" should rely on a comparative risk assessment of chrysotile and its substitutes.

Which asbestos products are at stake specifically? "Asbestos" is a group of heterogeneous mineral fibres that have some common physical characteristics and commercial uses. The risk of developing asbestos-related diseases depends on the dose, dimensions, durability (biopersistence) and surface reactivity of inhaled materials. The greatest differences in the physicochemical properties are between curly chrysotile and the more biopersistent needle-like amphiboles (tremolite, amosite and crocidolite). These differences entail different industrial applications and different toxicities. For instance, amphibole fibres were heavily used in buildings, blast furnaces and ships until 1980 in Europe because they resist high temperatures and chemically aggressive environments better than chrysotile. These uses and the 25–50-year latency of mesothelioma are responsible for mesothelioma clusters in ship-building areas around the world and for the predicted peak of the mesothelioma epidemic at around 2020 in Europe.2 The much lower incidence of mesothelioma in chrysotile industries (mining, cement, textiles and friction products) probably results from the much shorter biopersistence and lower iron content of chrysotile.3,4 Yet, an "asbestos" ban will only replace short, and thus less toxic, chrysotile fibres with certain substitute materials in new high-density cement and friction products, or it will replace fibre-containing products with other products altogether (e.g., steel, polyvinyl chloride [PVC]). It will not address the main cause of the mesothelioma epidemic: extant friable products in buildings that contain amphibole fibres.

What risks are associated with chrysotile fibres? The Collegium claims that all asbestos fibres are associated with similar risks of lung cancer and asbestosis, and only marginally different risks of mesothelioma. Experienced scientists in the field strongly disagree with this view.5,6,7,8 Risk assessments and reviews generally attribute peritoneal mesotheliomas exclusively to amphibole fibres. The 47 cohorts of individuals working with asbestos reviewed in the most recent and comprehensive risk assessments9,10 show higher risks in those working with amphibole than in those working with chrysotile. Thus, excess lung cancers occur 3 times, pleural mesothelioma 12 times and peritoneal mesotheliomas 30 times more frequently in mainly amphibole than in chrysotile industries for an equal number of expected cases (see additional data in the Table). Exposure–response comparisons of studies with meaningful exposure data suggest that chrysotile workers were 4–24 times less at risk of asbestos-induced lung cancer than amphibole workers at equal exposure.11,12 To put this in perspective, based on the exposure–response estimate of the US Environmental Protection Agency (EPA), the lifetime risk of an asbestos-induced lung cancer in smoking male workers exposed for 20 years to 20 fibres per millilitre of air in primarily chrysotile industries was about 2%–10%, compared with 40% in smoking male workers in industries using amphiboles. Risk in nonsmoking asbestos workers was about 15 times lower in both cases.

The mining and milling industry is most informative because fibre types are not mixed, and because it produces fibres of different sizes for all the asbestos industries. Of all the pleural mesotheliomas reported among chrysotile workers, 70% occurred among Quebec miners and millers, and most were traced to coexposures to amphiboles.13 The dose-specific risks of asbestosis,14,15 lung cancer and mesothelioma are 15–50 times lower in chrysotile miners than in amphibole miners.14,15 This seems true also for nonoccupationally exposed populations.16,17,18 In contrast to the Collegium's interpretation of our research, my colleagues and I found that the absence of excess lung cancers among residents of chrysotile mining towns implies a risk at least 15 times smaller than that predicted with the EPA model,17 and the number of mesotheliomas observed is at least 20 times smaller than that predicted by the EPA model.19

The Collegium discarded previous risk assessments and estimated risk from a single cohort of chrysotile textile workers.20,21 Yet this cohort may well be an unrepresentative outlier.22 The ratio of excess lung cancers to mesotheliomas is 3–10 times larger than in other asbestos studies. These workers were exposed to long amphibole fibres23 and to mineral oils. Moreover, rarely is anyone exposed to asbestos textile fibres today. On that precarious basis, the Collegium estimated 10 times the risk for chrysotile than that of any previous risk assessment, yet the latter assessments were based on 30%-amphibole exposures and were construed to overestimate the risks of chrysotile according to the EPA.24

Controlled occupational exposures today are about 1000 times lower than in the past.25 Accordingly, lifetime risks of asbestos-related deaths in today's chrysotile-exposed workers should be at least 1000 times lower than in individuals who worked with an "asbestos mixture" in the past, or less than 1–5 per 100 000 lives, that is, 20–100 times less than the Collegium's estimate. Such risks are comparable to or lower than risks accepted by the US National Institute for Occupational Safety and Health in the workplace. Risk estimates based only on chrysotile friction products and cement industries may be lower still.26

Are substitutes definitely "safer?" Chrysotile substitutes comprise p-aramid, polyvinyl alcohol (PVA), cellulose, polyacrylonitrile, glass fibres, graphite, polytetrafluoroethylene, ceramic fibres and silicon carbide whiskers. Epidemiological evidence concerning these substitutes is scarce, and the cohorts studied have been much less exposed than were asbestos workers in the past. Moreover, much lower exposures and doses are used in today's experiments on synthetic fibres and other substitutes than in past experiments on asbestos fibres.27 So, apparent differences cannot be taken at face value.

There are reasons to doubt the safety of substitutes for chrysotile. Glass and ceramic fibres, silicon carbide whiskers, and rock and slag wools have been classified by the International Agency for Research on Cancer as possible or probable carcinogens. Any fibre can carry chemical and biological contaminants such as cigarette tars deeply into the lung by adsorption. The lung cancer and fibrosis health risks of asbestos substitutes depend on the dose, dimensions, biopersistence and surface reactivity, as is the case for asbestos fibres, but they also depend on dissolution by-products.27 PVA and p-aramid (Kevlar) fibres are less respirable but more biopersistent than chrysotile, and p-aramid fibres have induced fibrosis and mesothelioma in inoculation studies.28 The biopersistence of cellulose exceeds that of chrysotile,29 cytotoxic effects have been observed30 and an epidemiological study has found chronic airflow limitations.31 Refractory ceramic fibres that complement p-aramid materials in brake pads may be more carcinogenic than chrysotile,32,33 although one experiment failed to replicate these findings.34 All man-made fibres are carcinogenic when inoculated into the peritoneum. One review concluded that they are at least as carcinogenic as "asbestos" fibres when inhaled.35 Another concluded that "synthetic vitreous fibres are not appreciably worse, fibre for fibre, than chrysotile," although mechanistic considerations suggest that glass wool might be "5 times less carcinogenic."36

Although the results of earlier US and European epidemiological studies were negative or not conclusive for lung cancer, a recent European cohort study found a dose-related excess of oral, pharyngeal and laryngeal cancers for individuals working with rock and slag wool (relative risk [RR] 1.5, 95% confidence interval [CI] 1.0–2.1) and a similar, but not statistically significant, relationship for those working with glass wool (RR 1.4, 95% CI 0.8–2.3).37 A contemporary German case–control study found an excess risk of lung cancer (odds ratio 1.5, 95% CI 1.2–1.9) among vitreous fibre insulators after controlling for smoking and asbestos exposure.38

Finally, the most comprehensive and recent review27 of human and animal data on man-made mineral fibres
concludes that ceramic fibres, rock and slag wools are "probably" and glass wool is "possibly" carcinogenic, whereas the health effects of other man-made substitutes cannot be evaluated at the present time. The Institut National de la Santé et de la Recherche Médicale (INSERM) in France deplores27 the fact that man-made fibres have been tested without the dust-suppressing agents and binders normally added in the industrial process, and that experiments are now conducted at much lower doses than those used in past studies of asbestos fibres: they state that similar doses in carcinogenic assays of asbestos fibres would likely have resulted in absent or nonsignificant health effects. Finally, INSERM underlines that end points other than cancer such as lung irritation, fibroses and dermatoses have not been adequately considered and that the dissolution by-products of chrysotile substitutes can reach distant organs.

Are substitutes as efficient as chrysotile in safety applications? Some important product safety issues have been raised by ancillary sources. Asbestos–cement pipes are being replaced by PVC and ductile steel pipes. Yet, as mentioned in the 1991 ruling that overturned the EPA's asbestos ban, "The EPA agency concedes the population cancer risk for production of ductile iron pipe could be comparable to the population cancer risk for production of A/C pipe."39Apparently, PVC pipe systems in buildings can spread flames from floor to floor and can release hydrogen chloride gas, dioxin and other organochlorines in the case of a fire.40 Concerning brakes, the head of the Society of Automotive Engineers' Brake Committee stated, "P-aramid, glass fiber and several glass-like fibers have substantially higher friction wet than dry and provide less dimensional stability to friction materials, especially large drum brake lining segments."41 According to this engineer, substitute products have been responsible for brake problems with General Motors X-body cars and for the fracturing of thousands of heavy-truck brake drums each year. Asbestos brakes are now installed again in US luxury cars to lower insurance expenses.41 Substitutes may be more efficient in other safety applications, however, the performance risks of asbestos substitutes are poorly documented. Such safety issues cannot simply be ignored and should be addressed in a proper risk assessment of the substitutes for chrysotile.

Under what exposure conditions are substitutes safer? Although INSERM insists that exposure to asbestos substitutes should be kept as low as possible, the Collegium does not caution against such exposures and communicates a false sense of security that might result in higher exposure to substitutes than to chrysotile. Today's health standards tolerate 5–20 times more exposure to glass, rock and slag wools than to chrysotile fibres. If those standards were applied after an asbestos ban, the substitutes would have to be more than 5–20 times less toxic than chrysotile to reduce risk. If substitutes are less hazardous than chrysotile by an unknown factor, then the same exposure limits and standards should apply to substitutes as to chrysotile. Indeed, even present exposures to substitutes could entail greater health risks than chrysotile exposures.

Likewise, the critical problem of poorly controlled environments (e.g., developing countries) underlined by the Collegium cannot be solved by substitution alone. In addition to the risks of substitute materials, coexposures to carcinogens contained in asbestos products (e.g., respirable quartz) entail health risks; such exposures must be minimized by education and by enforcing laws and regulations. A ban is not a sufficient solution and product users must be warned about the need to apply similar safety controls and procedures to asbestos and its substitutes. The conditions of a ban are critical.

Over the last 20 years, risk assessment methods have been developed for regulating or recommending exposure standards. In this context, the uncertainties, inconsistencies and gaps in knowledge in risk assessments have been dealt with by the precautionary principle, namely, by making assumptions and choosing models that tend to overestimate risks. In this case, to ban is to substitute and one must apply the precautionary principle equally to chrysotile and to its substitutes. This comparative risk approach differs from traditional risk assessment. The Collegium applies the precautionary principle to chrysotile but not to its substitutes, with the result that the proposed ban could do more harm than good.

Other aspects not considered here involve the costs of sanitation piping to developing nations and the transfer of jobs from poor asbestos-producing countries to affluent nations producing substitutes. The Collegium's call to ban asbestos is insufficient in all respects. A ban must be assessed more thoughtfully following a comparative risk approach before being adopted. The progressive introduction of safe, efficient substitutes should proceed apace but with evidence-based safety assurance, in concordance with the precautionary principle.

Competing interests: None declared.

Acknowledgement: I thank Dr. Bruce Case, pathologist and epidemiologist at McGill University, for his helpful suggestions and critical comments.

This paper presents personal views that do not necessarily reflect the views or policies of Health Canada.


Dr. Camus is with the Health Environments and Consumer Safety Branch, Health Canada, Montreal, Que.

Correspondence to: Dr. Michel Camus, 10881 ave. Durham, Montreal QC H2C 2G8; fax 450 928-4102; mcamus@videotron.ca


References

    1.   LaDou J, Landrigan P, Bailar JC III, Foa V, Frank A, on behalf of the Collegium Ramazzini. A call for an international ban on asbestos. CMAJ 2001;164(4):489-90.
    2.   Peto J, Decarli A, La Vecchia C, Levi F, Negri E. The European mesothelioma epidemic. Br J Cancer 1997;79:666-72.
    3.   Case BW, Ip MP, Padilla M, Kleinerman J. Asbestos effects on superoxide production. An in vitro study of hamster alveolar macrophages. Environ Res 1986;39:299-306. [MEDLINE]
    4.   Kane AB, Boffetta P, Saracci R, Wilbourn JD, editors. Mechanisms of fibre carcinogenicity. Lyon (France): International Agency for Research on Cancer; 1996.
    5.   Doll R. Mineral fibres in the non-occupational environment: concluding remarks. In: Bignon J, Peto J, Saracci R, editors. Non-occupational exposure to mineral fibres. Lyon (France): International Agency for Research on Cancer; 1989. p. 511-8.
    6.   Davis JMG, McDonald JC. Low level exposure to asbestos: Is there a cancer risk? Br J Ind Med 1988;45:505-8. [MEDLINE]
    7.   McDonald JC, McDonald AD. The epidemiology of mesothelioma in historical context. Eur Respir J 1996;9:1932-42. [MEDLINE]
    8.   Wagner JC. The discovery of the association between blue asbestos and mesotheliomas and the aftermath. Br J Ind Med 1991;48:399-403. [MEDLINE]
    9.   Health Effects Institute – Asbestos Research Literature Review Panel. Asbestos in public and commercial buildings: a literature review and synthesis of current knowledge — final report. Cambridge (MA): The Institute; 1991.
    10.   Institut National de la Santé et de la Recherche Médicale (INSERM). Effets sur la santé des principaux types d'exposition à l'amiante — rapport de synthèse. Paris: INSERM; 1996.
    11.   Liddell FDK, Hanley JA. Relations between asbestos exposure and lung cancer SMRs in occupational cohort studies. Br J Ind Med 1985;42:389-96. [MEDLINE]
    12.   Lash TL, Crouch EA, Green LC. A meta-analysis of the relation between cumulative exposure to asbestos and relative risk of lung cancer. Occup Environ Med 1997;54:254-63. [MEDLINE]
    13.   McDonald AD, Case BW, Churg A, Dufresne A, Gibbs GW, Sebastien P, et al. Mesothelioma in Quebec chrysotile miners and millers: epidemiology and aetiology. Ann Occup Hyg 1997;41:707-19. [MEDLINE]
    14.   Becklake MR. The epidemiology of asbestosis. In: Liddell D, Miller K, editors. Mineral fibers and health. Boca Raton (FL): CRC Press; 1991. p. 104-19.
    15.   Camus M. Do asbestos risk assessments justify banning chrysotile or not? Can Mineralogist. In press.
    16.   Hansen J, de Klerk NH, Musk AW, Hobbs MS. Environmental exposure to crocidolite and mesothelioma: exposure-response relationships. Am J Respir Crit Care Med 1998;157:69-75. [MEDLINE]
    17.   Camus M, Siemiatycki J, Meek B. Nonoccupational exposure to chrysotile asbestos and the risk of lung cancer. N Engl J Med 1998;338:1565-71. [MEDLINE]
    18.   Camus M. Why experts disagree about risks of cancer due to exposure to environmental asbestos. In: Herzberg AM, Krupka I, editors. Statistics, science and public policy: hazards and risks. Kingston (ON): McGill-Queen's University Press; 1998. p. 19-26.
    19.   Case B, Camus M, Siemiatycki J. Mesothelioma mortality and diagnosis are increased among women in Quebec chrysotile/tremolite mining areas. Am J Crit Care Respir Med 1997;155:A808.
    20.   Dement JM, Brown DP. Lung cancer mortality among asbestos textile workers: a review and update. Ann Occup Hyg 1994;38:525-32. [MEDLINE]
    21.   Stayner L, Smith R, Bailer J, Gilbert S, Steenland K, Dement J, et al. Exposure-response analysis of risk of respiratory disease associated with occupational exposure to chrysotile asbestos. Occup Environ Med 1997;54:646-52. [MEDLINE]
    22.   McDonald JC. Unfinished business: the asbestos textiles mystery [editorial]. Ann Occup Hyg 1998;42:3-5. [MEDLINE]
    23.   Case BW, Dufresne A, McDonald AD, McDonald JC, Sébastien P. Asbestos fibre type and length in lungs of chrysotile textile and production workers: fibres longer than 18µm. Inhal Toxicol 2000;12:411-8.
    24.   Nicholson WJ. Airborne asbestos health assessment update. Washington: Office of Health and Environmental Assessment, US Environmental Protection Agency; 1986. p. 166.
    25.   Rickards AL. Levels of workplace exposure. Ann Occup Hyg 1994;38:469-75. [MEDLINE]
    26.   Hughes JM. Human evidence: lung cancer mortality risk from chrysotile exposure. Ann Occup Hyg 1994;38:555-60. [MEDLINE]
    27.   INSERM Panel on the Health Effects of Asbestos. Effets sur la santé des fibres de substitution à l'amiante. Paris: Les Éditions INSERM; 1999.
    28.   Friemann J, Muller KM, Pott F. Mesothelial proliferation due to asbestos and man-made fibres: experimental studies on rat omentum. Pathol Res Pract 1990;186:117-23. [MEDLINE]
    29.   Muhle H, Bellmann B. Significance of the biodurability of man-made vitreous fibers to risk assessment. Environ Health Perspect 1997;105:1045-7. [MEDLINE]
    30.   Huuskonen SE, Hahn ME, Lindstrom-Seppa P. A fish hepatoma cell line (PLHC-1) as a tool to study cytotoxicity and CYP1A induction properties of cellulose and wood chip extracts. Chemosphere 1998;36:2921-32. [MEDLINE]
    31.   Christiani DC, Ye TT, Zhang S, Wegman DH, Eisen EA, Ryan LA, et al. Cotton dust and endotoxin exposure and long-term decline in lung function: results of a longitudinal study. Am J Ind Med 1999;35:321-31. [MEDLINE]
    32.   Hesterberg TW, Miller WC, Mast R, McConnell EE, Bernstein DM, Anderson R. Relationship between lung biopersistence and biological effects of man-made vitreous fibers after chronic inhalation in rats. Environ Health Perspect 1994;102:133-7. [MEDLINE]
    33.   McConnell EE. Synthetic vitreous fibers -- inhalation studies. Regul Toxicol Pharmacol 1994;20:S22-34. [MEDLINE]
    34.   Brown RC, Sébastien P, Bellmann B, Muhle H. Particle contamination in experimental fibre preparations and in workplace air. Inhal Toxicol 2000;12:99-107.
    35.   Infante PF, Schuman LD, Dement J, Huff J. Fibrous glass and cancer. Am J Ind Med 1994;26:559-84. [MEDLINE]
    36.   Wilson R, Langer AM, Nolan RP. A risk assessment for exposure to glass wool. Regul Toxicol Pharmacol 1999;30:96-109. [MEDLINE]
    37.   Boffetta P, Andersen A, Hansen J, Olsen JH, Plato N, Teppo L, et al. Cancer incidence among European man-made vitreous fiber production workers. Scand J Work Environ Health 1999;25:222-6. [MEDLINE]
    38.   Pohlabeln H, Jockel KH, Bruske-Hohlfeld I, Mohner M, Ahrens W, Bolm-Audorff U, et al. Lung cancer and exposure to man-made vitreous fibers: results from a pooled case-control study in Germany. Am J Ind Med 2000;
37:469-77. [MEDLINE]
    39.   Corrosion Proof Fittings v. EPA, 947 F2d 1201 (5th Cir 1991).
    40.   Wallace D. In the mouth of the dragon: toxic fires in the age of plastics. Garden City (NY): Avery Publishing Group; 1990.
    41.   Anderson A. Fibers in friction materials. Scientific evidence presented by Canada at World Trade Organization hearings on France's asbestos ban. 1999; Geneva.

 

 

Copyright 2001 Canadian Medical Association or its licensors