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Asbestos Exposure and Mesothelioma

The association between mesothelioma and prior exposure is undisputed. Dodson et al. (2011) cite mesothelioma as a signal tumor for asbestos exposure and typically occurs decades after first exposure to asbestos (Dodson, Hammar, &Poye, 2011). Welch (2007) also states that there is no debate that asbestos causes mesothelioma, and that the great majority of mesotheliomas are demonstrably caused by asbestos. Repeated studies have shown that all levels of exposure increase the risk of mesothelioma. Unlike many other cancers, for which there are multiple, well-documented causal factors, mesothelioma is overwhelmingly caused by asbestos (Welch, 2007). Smoking has no influence on the risk of mesothelioma (Finnish Institute of Occupational Health, 1997).

Wood et al. (1935) reported a case report of a worker exposed to asbestos contracting lung cancer and also having “chronic fibrous thickening of the pleura” (Lynch & Smith, 1935). Asbestos exposure was identified as a causative agent for lung cancer by Hueper in 1942 (Hueper, 1942). Various other authors continued to identify asbestos as causative of lung cancer, including the American Medical Association (Editorial, 1949).

One case of pleura mesothelioma in asbestos miners was reported in 1952. Several other scientists had related asbestos as a cause of mesothelioma, prior to the mid-1960s (Wagner, Sleggs, & Marchand, 1960; Eisenstadt & Wilson, 1960). Dr. Selikoff (1964) brought further national attention to the relationship between asbestos exposure and mesothelioma (Selikoff, Churg, & Hammond, 1964). Newhouse and Thompson (1965) clearly demonstrated mesothelioma in workers making filters, pipe insulation, brake linings, and rubber compounding (Newhouse & Thompson, 1965).

Although there are four types of asbestiform mineral fibers that have been in industrial use, only three have been used in the United States: amosite, chrysotile, and crocidolite. The fourth, anthophyllite, is mined and used in Finland. Of the three asbestos types that have been used in North America, Canadian chrysotile has formed 95% of all natural mineral fibers used, with amosite and crocidolite (both imported from South Africa) constituting the other 5%. Chrysotile is classified as a serpentine mineral, whereas the other three asbestos types are amphiboles (ACGIH, 2001).

All types of malignant mesothelioma can be induced by all asbestos fiber types; however, there is evidence that peritoneal mesotheliomas are associated with higher levels of asbestos than pleural mesotheliomas (Finnish Institute of Occupational Health, 1997).

Welch et al. (2007), along with 51 other scientists, reviewed the scientific literature as it relates to the exposure of brake mechanics to asbestos, resulting in occupational diseases including mesothelioma. They concluded that:

    1. Asbestos, in any of its forms (including serpentines and amphiboles) can cause occupational diseases, including mesothelioma.

    1. The scientific community is in consensus that brief and low-level exposures to asbestos can cause mesothelioma.

Awad (2011) analyzed and studied the Egyptian literature on air concentrations and mesothelioma victims living in the vicinity of two industrial plants producing products in Cairo, Egypt. They concluded that chrysotile was the main cause of mesothelioma in Egypt (Awad, 2011).

As noted above, Welch et al. (2007)concluded that there is a consensus among the scientific community that brief and low-level exposures to asbestos can cause mesothelioma. Furthermore, the mainstream scientific community has long recognized and continues to recognize today that there is no known “safe” level of exposure to asbestos. All levels of occupational exposure to asbestos increase the risk of mesothelioma(Welch, 2007).

OSHA has recognized for several years that its PEL for asbestos was not protective against mesothelioma. In its 1972 emergency temporary standard, OSHA states: “It appears that levels of exposure which may be safe with regard to asbestosis are not safe with regard to mesothelioma” (OSHA,1972).

In its Revised Recommended Asbestos Standard, NIOSH (1976) states: “Excessive cancer risks have been demonstrated at all fiber concentrations studied to date. Evaluation of all available human data provides no evidence for a threshold or for a ‘safe’ level of asbestos exposure” (NIOSH, 1976).

In its Review and Recommendations to Workplace Exposure to Asbestos, NIOSH (1980) states: “All levels of asbestos exposure studied to date have demonstrated asbestos-related disease…there is no level of exposure below which clinical effects do not occur” (NIOSH, November 1980).

OSHA recognizes that there is no assurance of a safe exposure for a substance with known carcinogenic properties, in this case, asbestos, and thus, there should be no detectable concentrations (OSHA,1975). However, OSHA is required to establish standards to the extent feasible and take into consideration technological and economic factors. Therefore, OSHA had to promulgate a standard based on the limit of detection of available sampling and analytical methods for determining asbestos exposure rather than based on health effects.

In OSHA’s preamble to 29 CFR1926.1101, Occupational Exposure to Asbestos, OSHA states that a significant risk remains at a Permissible Exposure Limit (PEL) of 0.1f/cc (OSHA, 1994).

The World Health Organization (1998) states: “Exposure to chrysotile asbestos poses increased risks for asbestosis, lung cancer, and mesothelioma in a dose-response manner. No threshold has been identified for carcinogenic effects”(WHO, 1998).

NIOSH reported in its Report to Congress on Workers’ Home Contamination Study (1995) that mesothelioma has occurred following short-term asbestos exposures of only a few weeks and can result from very low levels of exposure. NIOSH (1995) further reported that there may be a latency period of 40 years or longer between exposure and clinical disease(NIOSH, September 1995).

Causative exposure criteria have been established by the International Expert Meeting on Asbestos, Asbestosis, and Cancer in 1997, also known as the Helsinki Criteria (Finnish Institute of Occupational Health, 1997). In their consensus report, they cite the criteria that need to be considered in the assessment of the occupational etiology of mesothelioma. Among the industrial hygiene issues most applicable are as follows:

    1. Mesothelioma can occur in cases with low asbestos exposure. However, very low background environmental exposures carry only an extremely low risk

    1. An occupational history of brief or low-level exposure should be considered sufficient for mesothelioma to be designated as occupationally related.

    1. A minimum of 10 years from the first exposure is required to attribute the mesothelioma to asbestos exposure, though in most cases, the latency interval is longer (e.g., on the order of 30 to 40 years).

Roggli et al. (2002) reported findings of 1445 cases of mesothelioma with known exposure history. The number of (total) mesothelioma cases by industry reported by the authors’ areas follows:

    1. Shipbuilding (289)

    1. U.S. Navy (175)

    1. Construction (134)

    1. Insulation (103)

    1. Oil and chemical (88)

    1. Power plant (60)

    1. Railroad (53)

    1. Automotive (51)

    1. Steel/metal (43)

    1. Asbestos manufacturing (39)

    1. Papermill (7)

    1. Ceramics/glass (6)

The number of (total) mesothelioma cases by occupation reported by the authors is as follows:

    1. Pipefitter (187)

    1. Boilermaker (112)

    1. Maintenance (90)

    1. Machinist (89)

    1. Electrician (81)

    1. Sheet metal (22)

    1. Other asbestos (23)

There were 89 cases (6.2%) that were household contacts of an asbestos worker, which was the most frequent, by far, among the non-occupational exposure categories. Roggli et al. (2002) further concluded that environmental or neighborhood exposures appear to be a very uncommon cause of mesothelioma (Roggli, Sharma, Butnor, Sporn, & Vollmer, 2002).

References

ACGIH. (2001). Documentations of the Threshold Limit Values for Asbestos, All Forms. Cincinnati, Ohio: ACGIH.

Awad, A. H. (2011). Airborne asbestos fibers and mesothelioma in the last 20 years in Egypt: a review. Atmospheric Pollution Research, Vol. 2, 445-451.

Dodson, R. F., Hammar, S. P., & Poye, L. W. (2011). Mesothelioma in an Individual Following Exposure to Crocidolite-containing Gaskets as a Teenager. International Journal of Occupational Health, Vol. 17, 190-194.

Editorial. (1949, May – August). The Journal of the American Medical Association, 140, 1219.

Eisenstadt, H., & Wilson, F. (1960, November). Primary Malignant Mesothelioma of the Pleura. The Journal Lancet, 511-514.

Finnish Institute of Occupational Health. (1997). Asbestos, asbestosis, and cancer: the Helsinki criteria for diagnosis and attribution. Scand J Work Environ Health, 23, 311-316.

Hueper, W. (1942). Occupational Tumors and Allied Diseases. Springfield, IL: Charles C. Thomas Publisher.

Lynch, K., & Smith, W. (1935).Pulmonary Asbestosis and Carcinoma of the Lung in Asbestos-Silicosis. The American Journal of Cancer, XXIV, 62.

Newhouse, M., & Thompson, H. (1965). Epidemiology of Mesothelial Tumors in the London Area. Annals of the NewYork Academy of Science, 132, 579-588.

NIOSH. (1976). Revised Recommended Asbestos Standard. Washington, D.C.: U.S. Government Printing Office.

NIOSH. (November 1980). Workplace Exposure to Asbestos: Review and Recommendations (No. 81-103). Washington, D.C.: U.S. Department of Health and Human Services.

NIOSH. (September 1995). Report to Congress on Workers’ Home Contamination Study Conducted.

Under The Workers’ Family Protection Act (29 U.S.C. 671a) (No. 95-123).Cincinnati, OH: U.S. Department of Health and Human Services.

OSHA. (1972). Standard for Exposure to Asbestos Dust, Federal Register, Volume 27, No. 110. Washington D.C.:OSHA.

OSHA. (1975, October 9). Occupational Exposure to Asbestos – Notice of Proposed Rule Making. Federal Register, 48(197), 47657.

OSHA. (1994). Preamble to Final Rule,29 CFR 1926.1101, Occupational Exposure to Asbestos. Federal Register. Washington, DC.

Roggli, V. L., Sharma, A., Butnor, K.J., Sporn, T., & Vollmer, R. T. (2002). Malignant Mesothelioma and Occupational Exposure to Asbestos: A Clinicopathological Correlation of 1445 Cases. Ultrastructural Pathology, 26,55-65.

Selikoff, I. J., Churg, J., & Hammond, E. C.(1964, April 6). Asbestos Exposure and Neoplasia. JAMA, 22-26.

Wagner, J. C., Sleggs, C. A., & Marchand, P. (1960). Diffuse Pleural Mesothelioma and Asbestos Exposure in the NorthWestern Cape Province. British Journal of Industrial Medicine, 17, 260-271.

Welch, L. S. (2007). Asbestos Exposure Causes Mesothelioma, But Not This Asbestos Exposure: An Amicus Brief to the Michigan Supreme Court. International Journal of Occupational Environmental Health, Vol. 13, No. 3,318-327.

WHO. (1998). Chrysotile Asbestos.Environmental Health Criteria 203.Geneva: World Health Organization.

 

 

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