Module 4: Asbestos And Disease - Note (Continued)

FIBRE TYPES, AND DOSE-RESPONSE RELATIONSHIPS AND STATUTORY CONTROLS:

Asbestos related disease conforms to the normal toxicological model in that the greater the exposure of a population, the higher the incidence of disease. Dose-response models are the basis of risk assessment, projections of future disease (including for litigation purposes) and the setting of occupational exposure limits.

In general, the risk of asbestos related diseases have been found to depend on:

• Duration of exposure;
• Concentration of fibres in air (fibres/ml); (together these two make up "cumulative exposure");
• Time elapsed since exposure began (or ended) - so called "latency".

Other factors influencing risk include:

• Fibre dimensions. Fibres > 5 microns in length and < 0.2 microns in diameter are most hazardous.
• Specific industry e.g. asbestos textile manufacturing has a higher lung cancer risk than mining for a given exposure;

• Smoking, for lung cancer and asbestosis.

  Relative risk of developing cancer of the lung with exposure to cigarettes and/or asbestos:
  12 051 men exposed > 20 years to asbestos.

  Exposure status	No asbestos exposure	Asbestos exposure
  No smoking exposure	1	5.17
  Smoking exposure	10.85	53.24
  Source: Hammond et. al.

  Note "multiplicative" interaction between smoking and asbestos).

• Fibre type, specifically for mesothelioma. There is consensus on the highly carcinogenic nature of amphiboles (crocidolite and amosite) with regard to mesothelioma, but controversy has surrounded the relative carcinogenicity of chrysotile for mesothelioma. In vitro and animal experiments using various routes of administration have shown that all fibres have similar mutagenic and carcinogenic effects. However, chrysotile is much shorter lived in the lung than the amphiboles. Epidemiologically in South Africa, the gradient of ability to cause mesothelioma appears as crocidolite > amosite > chrysotile. (See reading by Rees et al.).

Given that only chrysotile is now produced commercially, and that the occupational exposure limits are much lower than in the past (too low to cause asbestosis), the question has shifted to whether there is any safe level or threshold for the carcinogenic effects of chrysotile. (Low or very short term exposure to crocidolite has been associated with mesothelioma suggesting a very low threshold. However, the statement that "one fibre kills" that one sometimes hears has no meaning in that such an effect could never be observed. In addition, the usual model for carcinogenesis is that it takes multiple "hits" to initiate carcinogenesis).

As in all risk assessment models, there is the problem of extrapolating from relatively high historical or occupational exposures for which there are more data to low exposures which are more likely to approximate current and future situations, including "bystander" exposure in houses and buildings.

Occupational exposure levels have been progressive lowered, as the regulating authorities have adopted a more preventive approach in the face of data on the risk of asbestos related disease rather than compromise with industrial interests. The current OEL in the South African Asbestos Regulations is 0.2 fibres/ml, having been lowered from 1 fibre/ml in the 1986 Regulations.

This modern standard can be compared with exposures in the mines and mills of > 100 fibres/ml in the 1940s, around 50 fibres/ml in the 1950s and below 2 fibres/ml by the 1980s. Industry probably lagged behind the mines with regard to control, with higher exposures persisting into the 1980s.