To assess the level of asbestos toxicity on human health, exposure assessments using models and simulations must be integrated as a starting point in understanding the short-term and long-term effects to which it contributes. For nearly a century, the presence of asbestos fibres lingering in the air has been acknowledged as a health hazard by the scientific community; consequently, an extensive amount of human exposure data exists in literature, both in occupational and natural environmental exposures (Erdal & Esmen, 1990). Like most toxicants, asbestos is only harmful when it enters the body; therefore, modeling its route of exposure must be evaluated prior to making assumptions that certain diseases are linked to its presence.
Although some mesotheliomas can occur without a history of exposure (Arblaster et al. 1999), nearly all cases reported in Canada are thought to be related to asbestos exposure. Unlike PAHs and DDT, asbestos is part of the natural environment; therefore, the likelihood of unintentional exposure should not come as a surprise, especially if one has lived or worked in a building that contained asbestos or came in contact with the clothing of industrial workers.
To identify the presence of asbestos fibres within a given location, ambient air samples are collected and observed for the following mineralogical properties: Morphology, crystallography, colour, appearance, optical properties, and hardness of a specimen (Erdal & Esmen, 1990). Compared to data obtained in occupational cohort-based studies, nonoccupational data is to some extent haphazard in terms of consistency. For instance, some studies indicate that a considerable amount of asbestos fibres exist in schools and public buildings, while data obtained from other sources are mainly scattered (Table 2). In a study conducted by Case et al. (2002), pleural mesothelioma among female residents of Québec’s asbestos mining regions were compared to controls for residential, domestic and occupational asbestos exposures. They learned that between 1970 and 1989, ten women suffering from mesothelioma resided in the mining region at the time they were diagnosed (ten cases or 22.7 cases per million), while 108 others lived elsewhere in Québec at the time of diagnosis (108 cases or 2.1 per million). Thus, women in the mining regions had 10.8 times more mesothelioma than women elsewhere in Québec. This study suggests that the risks associated with asbestos-exposure are higher in places where asbestos is more likely to be present, such as in an occupational or paraoccupational setting. This relationship is highlighted in Table 2, where amosite levels analyzed downwind of a factory were far greater than most public areas.
In a similar study conducted by Arblaster et al. (1999), it was investigated whether the amount of asbestos retained in the lungs of mesothelioma sufferers differed in three different groups: Occupational, paraoccupational, and residential exposure. Although many of the paraoccupational mesothelioma cases showed similar lung fibre concentrations to occupational, it was apparent that the nonoccupational mesothelioma cases ranged several orders of magnitude lower than occupational in fibre count. This study suggests that people who work in asbestos-based product manufacturing industries are more susceptible to asbestos exposure than nonoccupational groups. In addition, the author speculates that merely living near an industry that uses asbestos, such as the examined population, can increase the risk of developing mesothelioma.
The ingestion of asbestos fibres as a route of exposure has been investigated in past literature and also deserves mention. Generally, asbestos is introduced into water by the dissolution of asbestos-containing minerals, as well as from industrial effluents, atmospheric pollution, and erosion of asbestos-insulated pipes in water distribution systems (WHO, 1996). In a national survey of the water supplies of 77 communities in Canada, chrysotile was the predominant type of asbestos detected, with fibres ranging in length from 0.5–0.8 μm. It was estimated that concentrations were >1 million fibres per litre (MFL) in the water supplies of 25 percent of the population, >10 MFL for 5 percent of the population, and >100 MFL for 0.6 percent of the population. Concentrations were also higher in untreated water than in treated drinking water (WHO, 1996).