Malignant Mesothelioma - Asbestos Dust, Crocidolite
Asbestos, mesothelioma death rates
The difficulty of determining the cause of mesothelioma is also determined by the evidence that the latent period of mesothelioma is extremely long: the tumour is believed to appear 20, 30, or even up to 50 years after the first exposure. After so many years correlation to exposure is difficult and often impossible in the absence of records of dustiness decades ago, and considering the unreliability of human memory. In studies in which the relation to measured asbestos exposures is investigated there is evidence that the incidence of human mesothelioma is dose-related (table 4), and it is a common experience confirmed by all epidemiologic studies that there were levels of occupational exposures to asbestos at which no mesothelioma developed. This is true for all kinds of asbestos. The documented existence of such a level gives hope that a practical threshold for causing mesothelioma can be identified.
Table 4. Mesothelioma death rates
| Exposure category and duration | Pleura | Peritoneum | S years | Rate per 100,000 (years) S years |
| Males | ||||
| Low to moderate | ||||
| < 2 | 3 | 1 | 12,031 | 33 |
| > 2 | 3 | 4 | 7,500 | 93 |
| Severe | ||||
| < 2 | 6 | 10 | 15,428 | 104 |
| > 2 | 7 | 12 | 7,827 | 243 |
| Laggers | ||||
| < 2 | 3 | 2 | 7,893 | 63 |
| > 2 | 1 | 4 | 2,690 | 186 |
| Females | ||||
| Low to moderate | 1 | 0 | 2,066 | 48 |
| Severe | ||||
| < 2 | 8 | 5 | 9,538 | 136 |
| > 2 | 4 | 3 | 4,388 | 360 |
| From: Newhouse, M. L.; Berry, G. "Patterns of mortality in asbestos factory workers in London". Annals of the New York Academy of Sciences (New York), 1979, 330 (53-60). | ||||
Occasional cases are brought up of mesothelioma linked with indirect or non-occupational exposures to asbestos. The assumption is made that the persons involved were exposed to low levels of dustiness, certainly less than industrial "asbestos workers". Certain cases may be regarded as cases of para-occupational exposure, i.e. in persons who had worked next to an asbestos worker. In shipbuilding cases are known of welders whose mesothelioma is linked with exposure to asbestos from a fellow worker applying insulation nearby. Exposure in these cases clearly cannot be considered low; in addition a possible carcinogenic effect of high levels of exposure to iron fumes was postulated by some authors, as one hypothesis to explain the higher risk of mesothelioma generally observed in shipyards. Accumulations of cases of mesothelioma have also been observed among members of the general population in the vicinity of asbestos factories and mines. It is questionable if the exposure of these neighbourhood cases had been low. The vicinity of the South African crocidolite mines was notoriously dry and dusty and the factory exhaust ventilation systems were said to have blown asbestos into the streets around the asbestos factories in Hamburg and London. No accumulation of any cancer could be found to be linked with dustiness around chrysotile mines in Canada or around the amosite factory in New Jersey. Perhaps most conspicuous are the household cases of mesothelioma in members of the family of asbestos workers who themselves had never been occupationally exposed to asbestos. Asbestos dust brought home from the job on the worker's clothes is considered to be the cause. Again it is doubtful whether exposure of the members of the family was necessarily low. Years of the bad practice of coming home in industrial work clothes could contaminate the household substantially. In fact levels of asbestos as high as 5 000 mg/m3 of air were measured in the homes of asbestos workers, which is 1 to 3 orders of magnitude higher than levels measured at 800 m from asbestos spray sites. Less clear are cases which developed many years after a very short period of exposure. It seems probable that such exposures, although short, were very high.
In animal experiments all kinds of asbestos cause malignant mesothelioma in a certain number of animals, when introduced into the pleural or peritoneal cavity, and the higher the dose of asbestos introduced the more tumours resulted, i.e. a dose-response was established also in animals. There were doses with which no cases, or no excess of tumours was seen (table 5). Another important observation was made by Stanton and confirmed by others. Carcinogenic potency in animals did not depend on the chemical composition as much as on the size and shape of the fibre. Only very thin and comparatively long fibres were carcinogenic, the diameter < 1.5 micron and length > 8 micron appearing critical. Asbestos fibres occur in this size but most other natural and man-made fibres are thicker than the critical diameter. If, however, a non-asbestos fibre is made thin enough, and long enough, as is the case of some newer man-made fibres, they appear to be as carcinogenic as asbestos. An interesting conclusion is that we are dealing here with physical rather than chemical carcinogenicity. The practical conclusion is much more important: possible substitutes for asbestos may be equally carcinogenic, if we assume that their ability to replace asbestos is based on their similar technological properties, which in turn may well depend on their similar fibres sizes and shapes.