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doi:10.1378/chest.06-2649
(Chest. 2007; 131:336-338)
© 2007 American College of Chest Physicians
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Environmental Asbestos Contamination

What Are the Risks?

Victor L. Roggli, MD, FCCP

Durham, NC
Dr. Roggli is Professor of Pathology, Duke University Medical Center.

Correspondence to: Victor L. Roggli, MD, FCCP, Professor of Pathology; Duke University Medical Center, Box 3712 Med Center, Durham, NC 27710; e-mail: Roggl002{at}mc.duke.edu

Malignant mesothelioma is a well-recognized risk of exposure to asbestos, and the disease may occur after relatively brief, low-level, or indirect exposures. Consequently, there have been concerns regarding exposures to asbestos contaminating the environment.1 One highly publicized example is contamination of the town of Libby, MT, by tremolite asbestos occurring in the nearby vermiculite mine.2 Recently, the Agency for Toxic Substances and Disease Registry convened an expert panel in Atlanta, GA, to discuss the potential risks of environmental asbestos contamination in communities throughout the United States. A number of questions remain unanswered. What is the magnitude of the risk (if any) to these communities? Can the risks be quantified, and what are the parameters that best predict the risk of mesothelioma? Are there gender differences in susceptibility, and are young children who are exposed to asbestos (eg, on playgrounds) at greater risk than adults?

The tragedy of Wittenoom, WA, Australia, has provided the opportunity to obtain some answers to these questions. Crocidolite (blue) asbestos was mined in this location from 1943 to 1966. As of 2002, 254 cases of mesothelioma had been reported from exposures at Wittenoom, accounting for about 5% of all cases of mesothelioma observed in Australia.3 Tailings from the mine and mill were used in the construction of roads, parking, school playgrounds, and a race course, and were even used in yards to suppress dust from red clay. Consequently, there was ample opportunity for environmental exposure to asbestos among the 4,768 residents of Wittenoom who never worked in the mine or mill and were never exposed occupationally elsewhere. Reid et al4 provide the most recent follow-up information concerning this cohort in the current issue of CHEST (see page 376).

The results are sobering. To date, there have been 67 cases of mesothelioma among the Wittenoom residents, including 31 cases in women. Twenty-seven of these women reported laundering the clothing of mine or mill workers, which is a well-recognized cause of mesothelioma among women in the United States.5 The relative risk of mesothelioma increased with duration of exposure, estimated dose, and latency interval. Women had a steeper dose-response curve, which was just significant at the p = 0.05 level, than men. However, there was no evidence of an increased susceptibility to mesothelioma among children.4

The estimated death rate from mesothelioma in this population was 710 cases per million person-years (see \?\Table 2 in the article), and the mean cumulative exposure was 5.5 fibers/mL/yr.4 If one assumes that the background death rate from mesothelioma is one case per million person-years,5 and further assuming that the risk is a linear dose response with no identifiable threshold,6 then exposure to Wittenoom blue asbestos doubles the background risk of mesothelioma at a cumulative level of 0.015 fiber/mL/yr. This is equivalent to approximately 2 months of exposure at the current Occupational Safety and Health Administration permissible exposure limit of 0.1 fiber/mL. Although these figures are rather alarming, it is reassuring that the vast majority (up to 95%) of asbestos used in the past in the United States was chrysotile (white) asbestos, and the best estimates indicate that a higher dose of white asbestos of several hundred times would be necessary to achieve a similar risk.78 It is possible that there is a threshold of exposure to asbestos below which mesothelioma will not occur, but such a level has yet to be identified.

Another important observation from the study of Reid et al4 is that the youngest individual in whom mesothelioma was diagnosed at Wittenoom was 26 years old at the time of diagnosis. This is the same age as the youngest mesothelioma case reported from another environmental tragedy that occurred in three small villages in the Anatolian region of Turkey, where an epidemic of mesothelioma followed environmental contamination with erionite, an asbestiform fibrous mineral.9 The present author’s consultation files include > 2,500 cases of mesothelioma, with lung fiber burden analyses performed in > 400 of these cases. The youngest age at diagnosis of a mesothelioma case confirmed to be asbestos related was 28 years.5 Taken together, these observations from three independent sources would indicate that mesothelioma occurring in individuals < 25 years of age is unlikely to be related to asbestos.10

Hopefully, tragedies such as those at Wittenoom and in the Anatolian region of Turkey can be avoided in the future. Studies such as the careful observations of Reid et al4 may provide useful information to help guide policymakers who are dealing with potential environmental contamination of communities with asbestos. Identification of the fiber type and the concentrations of asbestos in the ambient air along with the size and demographics of the exposed population can be used to predict the likelihood of future occurrence of asbestos-related disease, including mesothelioma.678 However, it is no trivial matter to determine what level of risk is "socially acceptable," and any means of dust suppression or avoidance of exposure is recommended, especially when exposures are to asbestos fiber types as dangerous as Australian blue asbestos.

Footnotes

The author has testified as an expert witness in asbestos litigation for both plaintiffs and defendants.

References

  1. Pan, X-l, Day, HW, Wang, W, et al (2005) Residential proximity to naturally occurring asbestos and mesothelioma risk in California. Am J Respir Crit Care Med 172,1019-1025[Abstract/Free Full Text]
  2. Noonan, CW Exposure matrix development for the Libby cohort. Inhal Toxicol 2006;18,963-967[CrossRef][ISI][Medline]
  3. Leigh, J, Driscoll, T Malignant mesothelioma in Australia, 1945–2002. Int J Occup Environ Health 2003;9,206-217[ISI][Medline]
  4. Reid, A, Berry, G, de Klerk, N, et al Age and sex differences in malignant mesothelioma after residential exposure to blue asbestos (crocidolite). Chest 2007;131,376-382
  5. Roggli, VL, Oury, TD, Moffatt, EJ Malignant mesothelioma in women. Rosen, PP Fechner, RE eds. Anatomic pathology 1998, 1997;vol 2,147-163 ASCP Press. Chicago, IL:
  6. Peto, J, Seidman, H, Selikoff, IJ Mesothelioma mortality in asbestos workers: implications for models of carcinogenesis and risk assessment. Br J Cancer 1982;45,124-135[ISI][Medline]
  7. Hodgson, JT, Darnton, A The quantitative risks of mesothelioma and lung cancer in relation to asbestos exposure. Ann Occup Hyg 2000;44,565-601[Abstract/Free Full Text]
  8. Berman DW, Crump KS. Technical support document for a protocol to assess asbestos-related risk: final draft. US Environmental Protection Agency, Washington, DC: Environmental Protection Agency, 2003; Publication No. 9345.4-06
  9. Selcuk, ZT, Emri, S, Sahin, AA, et al Malignant mesothelioma and erionite exposure. Eur Respir J 1999;14,480-481[CrossRef][ISI][Medline]
  10. Fraire, AE, Cooper, S, Greenberg, SD, et al Mesothelioma of childhood. Cancer 1988;62,838-847[CrossRef][ISI][Medline]




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