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The hazardous work environment
Published in Sue Reed, Dino Pisaniello, Geza Benke, Principles of Occupational Health & Hygiene, 2020
Charles Steer, Caroline Langley
Reliable data on the contributions of workplace conditions to ill-health in the community have traditionally been difficult to assemble, and this is a worldwide problem. Data on compensation for work-related ill-health is lacking, leading to a misleading impression of the true prevalence of occupational disease. Most work-related ill-health is the result not of accidents (falls, high-energy impacts, crushing or piercing injuries, etc.), but of exposure to hazardous chemicals or environmental conditions. Consider the following examples where the findings of epidemiological studies—sometimes conducted years after exposure first commenced—confirmed the need for the controls now widely demanded by law: The world’s worst single-event industrial disaster (with the probable exception of Chernobyl). At Bhopal, India in 1984, the inadvertent release of methyl isocyanate gas (an intermediate of manufacturing a pesticide) killed more than 3000 people and injured some 17,000 more who lived in the chemical factory environs. Although the cause of the disaster was soon evident, its true scale was not so immediately obvious.The United States’ worst individual industrial accident. Hawk’s Nest Tunnel in West Virginia, built to divert a river in the early 1930s, required drilling through silica rock. As a result of inhaling the resulting dust, more than 600 men died from silicosis within two to six years. Neither the cause of the illness nor its true prevalence were obvious at the time of the work.Australia’s worst industrial accident. Mining of blue asbestos at Wittenoom, Western Australia continued from 1937 to 1966. At that time, the link between asbestos fibre exposure and asbestosis, lung cancer and mesothelioma was not well defined. Workers, town residents and visitors developed these diseases over the ensuing decades and deaths are still occurring. The death toll could eventually exceed 2000. Worldwide, the death toll from asbestos exposure in the late twentieth and early twenty-first centuries could possibly reach into the millions.A further disturbing aspect of asbestos-related disease is that the number of new mesothelioma cases continues to be high. As the first wave of deaths from exposure during mining and processing prior to 1983 declines, a second wave of disease has emerged in tradespeople and workers in asbestos buildings (ASEA, 2016). Although these exposures were much lower, far more people were exposed, resulting in continuing high numbers of mesothelioma cases and deaths. Asbestos is covered in more detail in Chapter 7.
Autoantibodies and cancer among asbestos-exposed cohorts in Western Australia
Published in Journal of Toxicology and Environmental Health, Part A, 2021
Renee N Carey, Jean C Pfau, Marvin J Fritzler, Jenette Creaney, Nicholas de Klerk, Arthur W (Bill) Musk, Peter Franklin, Nita Sodhi-Berry, Fraser Brims, Alison Reid
Associations between asbestos exposure and autoantibody responses were previously reported (Pernis, Vigliani, and Selikoff 1965; Pfau et al. 2018), with an elevated frequency of ANA (Pfau et al. 2005; Pfau, Serve, and Noonan 2014; Reid et al. 2018) and an increased risk for systematic autoimmune diseases (SAID) observed in asbestos-exposed cohorts (Bunderson-Schelvan et al. 2011; Noonan et al. 2006; Pfau, Serve, and Noonan 2014). Studies in Libby, Montana USA found a higher relative frequency of positive ANAs among an asbestos-exposed compared with a reference population (Pfau et al. 2018, 2005). Similarly, elevated odds of ANA positivity were detected among those exposed to asbestos in Wittenoom, Western Australia, compared with an unexposed reference population (Reid et al. 2018). These investigators also demonstrated higher ANA titers in the asbestos-exposed compared with reference populations (Pfau et al. 2018, 2005; Reid et al. 2018). Both of these cohort studies examined populations that were exposed to an amphibole asbestos, Libby Amphibole in Libby and crocidolite or blue asbestos in Wittenoom. Amphibole asbestos types possess fibers that are long and straight, more readily inhaled, and thus the most carcinogenic form (Pfau, Serve, and Noonan 2014). To date, a link between elevated ANA and cancer rates in the Wittenoom population has not been investigated. It is possible that autoantibodies may serve as early markers to detect or predict the severity of adverse health outcomes in asbestos-exposed populations (Pfau et al. 2019), making this study a critical step in understanding their potential as markers in cancer identification.
Analysis of autoantibody profiles in two asbestiform fiber exposure cohorts
Published in Journal of Toxicology and Environmental Health, Part A, 2018
Jean C. Pfau, Christopher Barbour, Brad Black, Kinta M. Serve, Marvin J. Fritzler
The importance of this study is two-fold. First, it is an approach to fulfilling criteria needed for proposing that LAA, like crystalline silica, is an environmental trigger for systemic autoimmune disease by providing comparative data with another exposure (Miller et al. 2012b). Multiple large epidemiological studies were needed to make the case that crystalline silica is a trigger for SAID (Miller et al. 2012a), and there simply are no large cohorts for amphibole asbestos exposures in order to conduct similar experiments for amphibole asbestos, with the possible exception of the Wittenoom crocidolite exposure cohorts in Western Australia (Berry et al. 2012) where current studies are underway (Reid et al. 2018). There are currently few occupational exposure cohorts, and more environmental asbestos exposures, with the latter being more difficult to track subjects or assess exposure. More creative approaches are needed, and thus a statistical model was constructed to assess the ability of autoantibodies to predict exposure to LAA compared to predominantly chrysotile, and therefore to distinguish various types of asbestos exposure. It is essential to make that distinction due to the many differences being described in the health outcomes for LAA compared to chrysotile asbestos (Bernstein, Chevalier, and Smith 2005; Cyphert et al. 2016, 2012; Ferro et al. 2013; Li, Gunter, and Fukagawa 2012). Second, it sets the stage to begin studies that assess the pathogenic determinants of LAA that increase the risk for autoantibody production and for autoimmune diseases, and to evaluate the clinical rheumatic outcomes of exposure to different asbestiform fibers.