Before characterizing the risks attributed to asbestos exposure, it is helpful to understand the relationship that exists between risk and probability. Risk is the probability of an event multiplied by the consequence. Hence, if the consequence is very large, such as developing a disease, the risk will be high even if the probability is very low. On the contrary, if the consequences are minor, the risk will be low even if the probability is very high. Since the consequences associated with asbestos-related illnesses lead to death, the exposure to asbestos poses great risk even through the probability of inhaling toxic doses is low.
Three methods are predominantly used to evaluate risk of a particular hazard, namely: (1) In vitro testing, where the effects of the substance are determined at the cellular level, (2) in vivo testing, where laboratory animals are exposed to substances under controlled conditions and monitored for the spontaneous development of a disease, and (3) cohort studies of humans exposed to a material, where the death rates and exposure levels are known (Gunter, 1994). Based on the majority of the results obtained in all three approaches, one aspect that remains consistent is that the greater the amount of exposure and the longer the time of exposure, the greater the risk of asbestos-related illnesses. Figure 5 depicts how the exposure to various asbestos fibre sizes can contribute to the number of deaths per 1000 workers. Unfortunately, the same problem exists with this model as in other models that suggest an association between exposure to asbestos and asbestosis, mesothelioma, and lung cancer, that is, there is a lack of consistent information indicating fibre type, size, and duration of exposure. This limits the ability to quantify the probability and to characterize the risks to humans, for both the hazard and exposure aspect of the risk equation (Kava, 2007).
Chyrsotile and amphibole asbestos are the types most commonly used in factories and commercial applications, and growing evidence suggests that they differ in respect to toxicity and their potential for disease production (Finley et al., 2008). According to the EPA, recent studies concluded that amphiboles are four times and 800 times as potent as chrysotile at inducing lung cancer and mesothelioma, respectively (Berman & Crump, 2003). Likewise, Darnton and Hodgson (2000) reported that the exposure specific risk of mesothelioma from the three most commonly used commercial asbestos – chrysotile, amosite, and crocidolite – is broadly estimated in the ratio 1:100:500, respectively.
Although there are dozens of published epidemiological studies quantifying the asbestos exposure-response relationship for lung cancer and mesothelioma (Finley et al., 2008), estimated no observed adverse effect levels (NOAEL) reported by some studies are highly inconsistent with ranges reported by other studies. For example, Fry et al. (1984) observed a significant increase in respiratory cancer when cohorts were exposed to <14 fibres per cubic centimetre per year (f/cm3-yr; equivalent to f/mL-yr). This effect level conflicts with other studies which range from >25 to 1600-3200 f/cm3-yr (Finley et al., 2008). Similarly, Brownet al. (1994) observed significant increases in lung cancer risk in cohorts who were exposed to a range of 2.7 to 6.8 f/cm3-yr (NOAEL: 1.4–2.7 f/cm3-yr); this is also inconsistent with lung cancer NOAELS reported in other studies. Surprisingly, one author, mentioned by Finley et al. (2008), reported that no increased risks occur at estimated cumulative asbestos exposures of 1600–3200 f/cm3-yr. This is well beyond the threshold values stated earlier. Finley et al. (2008) states that this variability may be due to a number of factors, including, and not limited to: (i) air sampling techniques, (ii) use of appropriate controls, (iii) cohort sizes, and (iv) biases. Overall, the accepted derived NOAELs for lung cancer and mesothelioma fall in the range of 25–1000 f/cm3-yr and 15–500 f/cm3-yr, respectively (Finley et al., 2008). Fortunately, this is well below the nonoccupational asbestos exposure levels listed in Table 2. Figure 6 shows a comparison of upper bound cumulative chyrsotile exposures from various studies analyzed by Finley et al. (2008).
Currently, the permissible exposure limit for asbestos is 0.1 f/cm3 of air averaged over an eight-hour work shift (29 CFR 1910.1001, OSHA) or 1.0 f/cm3 of air averaged over a sampling period of 30 minutes (29 CFR 1910.1001, OSHA). Although there is no safe level of exposure to any carcinogen such as asbestos, this standard would reduce worker asbestos-related illnesses to less than four cases per 1000 workers, half of the current illness rate. Moreover, the EPA (2009) specifies that water containing greater than seven MFL could increase one’s risk of developing benign intestinal polyps. Thus, depending on the accuracy of the method and reliability of the information supplied by Edmen & Erdal (1990) on chrysotile levels observed in Québec’s water quality (Table 2), drinking water in Québec could potentially be fatal.
As mentioned earlier, risk can also be evaluated using in vitro studies. In a study conducted by Layard et al. (1981), fibres of various sizes were implanted in the pleurae of rats for periods of more than one year. It was discovered that the probability for the development of pleural mesotheliomas was highest for fibres with a diameter of ≤0.25 µm and lengths ≥8 µm. Not surprisingly, these dimensions correlate with the average dimension of a single chrysotile fibril. Table 4 shows the correlation coefficients for the logit of tumour probability for the development of pleural mesotheliomas in rats. This discovery also correlates with Pott’s (1978) hypothesis on the carcinogenic potency of a fibre with respect to size (Figure 4).
Although much scientific progress has been made in understanding the mechanisms involved in asbestos-induced diseases, the EPA (2003) notes that at least two critical data gaps remain:
- No one has yet been able to track a specific lesion induced by asbestos in a specific cell through to the development of a specific tumor. Studies have demonstrated that tumors of the type that result from asbestos exposure exhibit patterns of DNA alteration (or other kinds of cellular damage) that are sometime (but not always) consistent with the earlier cellular changes associated with asbestos exposure. There are also studies that show that exposure to asbestos can lead ultimately to development of tumors. However, these types of studies have yet to be linked.
- The specific target cells that serve as precursors to tumors in various target tissues are not known with certainty.
Since researchers tend to report a broad range of tissue and cellular effects to denote the toxicity of asbestos-fibre exposure (EPA, 2003), there is no consistent endpoint to be used as a marker to track for asbestos-induced carcinogenesis. Consequently, this is a limitation on the hazard side of the risk assessment evaluation of asbestos (Kava, 2007).
Since asbestos abatement (removal) is a multibillion dollar industry and one in which many people have invested interest in (Gunter, 1994), innovative risk-based decision making must be based on factual matter and not one that is subject to ignorance, fear, and irrationality. Many developed countries, including Canada, have stopped using asbestos because of its detrimental effects to human health. However, is the removal of asbestos from existing building necessary? The two main issues involving this debate are the health risks associated with low-level exposure and the financial cost of removal (Gunter, 1994). To address the first issue, the NOAEL established by Finley et al. (2008) clearly indicates that what people are exposed to, on average, in buildings or schools (Table 2) is far lower than the threshold. Secondly, despite evidence showing it is unnecessary, the EPA estimates costs more than $53 billion over the next 30 years for the abatement of public and commercial buildings (Gunter 1994). It is now up to the stakeholders (tax-payers) to decide whether this is necessary or just a waste of time.