Occupational Exposure to Asbestos Fibres - Essay Example

Occupational Exposure to Asbestos Fibres Introduction: Asbestos is a fibrous mineral that has undeniable usefulness, but some resulted in catastrophic and widespread human health effects. The minerals known as "asbestos" represent a group of naturally occurring fibrous silicates, defined commercially much more easily than as "minerals." There are only three asbestos types of major commercial importance-chrysotile, the most widely used and only member of the magnesium-rich serpentine class, and the asbestos amphiboles "crocidolite", which is fibrous riebeckite and "amosite" that is fibrous cummingtonite-grunerite. Amosite and crocidolite are iron-rich fibrous silicates and have really no economic importance, and they belong to a group of 50 other iron-rich asbestos minerals (Bandli and Gunter, 2006, 949-962). Asbestos induces disease in man has been confirmed through clinical observations, pathological assessments of tissue, and epidemiological data obtained from exposed cohorts. The respiratory system is the primary portal of entry for asbestos into the human body. Therefore, like as it is relevant to understand the applicability of techniques and selected instrumentation for analysis of environmental samples, it is equally important in determination of asbestos content from biological samples. Based on its on its fibrous morphology, asbestos is recognized as being a pathogenically active dust. Once inhaled, asbestos has continuous influences on cellular, biochemical, and molecular events in the human body. These complementary stimuli in synergy with the fibrous morphology of asbestos can result in irreversible cellular damage and in some cases the development of tumors. Various countries have sought to deal with asbestos and public health through regulatory guidance documents. This is necessary since asbestos mixtures are frequently used in industry, particularly chrysotile with either amosite or crocidolite. Moreover, exposures to "contaminant" noncommercial amphiboles are common in miners and millers of chrysotile, talc, and vermiculite in some geographical locations. Therefore, there has been an acknowledged risk when the person is subjected to the exposure of asbestos, and these risks are health risks to create potential health problems even years after the exposure ceases. To prohibit these there are regulations from different authorities, which ideally would ascertain safety by eliminating and minimizing risks for the workers. These regulations should be guided by this risk and risk assessment approach. In this critical review, an assessment of different regulations will be done to examine how far these regulations have been guided by the concept of risk to control occupational exposure of asbestos (Bartrip, 2004, 72-76). Review: There is a perceived need for this critical review for various reasons. Practically, exposure to asbestos is very difficult to characterize. Moreover, there is a continued debate since there is an important confounding factor to determine the aetiology of any particular pathology. A strict separation of minerals goes beyond "asbestos" but involves two separate classes of the amphiboles, which collectively make up a great percentage of the earth's crust. The amphiboles occur in both forms and are not fibrous and do not look like asbestos, although they are basically asbestos. For those that are not fibrous and termed nonasbestiform, the United States Occupational Safety and Health Administration (OSHA) ruled in 1992 that "available evidence supports a conclusion that exposure to nonasbestiform cleavage fragments is not likely to produce a significant risk of developing asbestos-related disease" (OSHA, 1992) Similar problem has been reported from the British areas, but from the point of view of causation of the disease, this appears immaterial which form of asbestos has caused the disease. The grouping of the three commercial asbestos minerals is usually supplemented by the addition of the three "noncommercial" asbestiform amphiboles tremolite, actinolite, and anthophyllite, which are regulated in the United States. All are used commercially in Finland, but there is a tendency to recognise their principal health effects in the environmental settings or as occupational co exposures or even sometimes they are termed as contaminants with other minerals. Due to these issues related to taxonomic confusion and lack of standard operating definitions for fibers, it becomes very difficult to assign and assess a case to know whether it has been caused by any specific occupational exposure. Since the year 1973, asbestos production has declined in the United States (Virta, 2003a, 1-59) and in South Africa (Abratt et al., 2004, S3-S6). Western society has stopped mining and using asbestos. There will soon be commercial ban in all of the European Economic Community as well as in Australia, Argentina, and elsewhere. McDougall reports that through regulations, the United States and Canada the mining has ended effectively (McDougall, 2007, B1). Interestingly, mining and product manufacture appear conversely to be increasing elsewhere, for example, in China, Kazakhstan, Russia, and Zimbabwe, mainly due to increase in industrialization and availability of cheap labour. There are now stringent regulations of asbestos use in most parts of the developed world. Although there is confusion in published medical literature about the documented health effects of asbestiform minerals other than chrysotile and the common amphiboles, almost all regulations are based on the view that all including asbestiform amphiboles and some other fibrous minerals will have similar health effects. In Western industrialized countries, the widespread industrial use of asbestos has resulted now in an epidemic of asbestos-related illnesses. These include asbestos exposures affecting older workers, the current risk of the workforce engaged in occupations who manage the remaining hazards of building and facility maintenance, people engaged in asbestos abatement operations including those involving demolitions (Paris et al., 2002, 1167-1173). Assessments of risks, therefore, would need a comprehensive occupational and environmental history. The occupation history would, therefore, emphasize occupational and environmental avenues of exposure that occurred 15 years or more before presentation. Although short bursts of exposure for even a period of 1 month is enough to create asbestosis or any other chronic noncancerous diseases of the lungs, it usually needs exposure for at least 10 to 20 years. Therefore, a regulation that is in use today and is applicable to the person of this era may have involved a risk regulation approach for today, but the person has already started acquiring the disease many years back. Different varieties of exposures are segregated by differences in solubility of various types of asbestos fibers. These would affect the factors like fiber retention, body burden, and the risk of noncancerous chronic pulmonary disease. There is still no consensus about whether ingestion of asbestos fibers lead to esophageal cancer or not, and despite that regulations point out esophageal cancers. Unfortunately, the clinician never ever is able to evaluate the solubility aspect of exposure, and there are no valid means to adjust the occupational history to take this factor into consideration. Solubility projects future risk for malignant disease, if there has been an exposure (Biggeri et al., 2004, 249-252). The Control of Asbestos Regulations 2006 came into force on 13 November 2006, which brought together three previous sets of Regulations that covered the prohibition of asbestos, the control of asbestos at work, and asbestos licensing. In all, they prohibit supply and use of all forms of asbestos. They continue the ban introduced for blue and brown asbestos 1985 and for white asbestos in 1999. In this regulation, the secondary use of asbestos products such as asbestos cement sheets and asbestos boards and tiles are prohibited. This prohibition also applies to new use of asbestos. If existing asbestos containing materials are in good condition, they may be left in place and their condition monitored and managed to ensure they are not disturbed. The discrepancy will be more highlighted in the regulation where the worker exposure must be below the airborne exposure limit of all types of asbestos of 0.1 fibres per cm3 of air (Health & Safety Executive., 1997). This leads to the other part of the regulation such as air monitoring and control, and the collection and analysis of samples to find out if a specific material contains asbestos. These are United Kingdom regulations, but the drift from the risk approach will be evident from the following analysis. The question of monitoring of asbestos-associated disease is complicated by requirements of occupational surveillance, and employers are required by regulations to monitor their employees during employment (Health & Safety Executive, 1992), but there is no provision in regulations to monitor them beyond the period of employment despite the known prevalence latency in development of asbestosis. Since the aim of the regulations is to limit exposure of asbestos, the target of the regulations is to reduce the exposure to as low as possible and as far as reasonably practicable, in order to prevent the spread of asbestos. The regulations specify the work methods and controls that are imperative to prevent exposure and spread. A control limit that has been decided is the maximum concentration of asbestos fibres in the air over any continuous 4 hour period that must not be exceeded, and it is required that worker exposure should not exceed 0.6 fibres per cm3 of air averaged over any continuous 10 minute period using respiratory protective equipment if exposure cannot be reduced sufficiently using other means. This is not a valid approach given the pathologic ways of asbestos particles, since the regulations set asbestos upper limit of exposure in order to control workplace exposure, does not take into consideration the biomarkers (Harrison and Sepai, 2000, 61-63). These take into account the toxicological, occupational, hygiene, and epidemiological data and are evidently influenced by socioeconomic judgments and the balancing act between worker health and the cost of effort of reducing exposure. Asbestos exposure in that sense can generate a biomarker which can reflect an interaction between human body and asbestos. These tools are used extensively in the occupational epidemiology in other areas and can serve as a powerful tool for surveillance of workers in terms of assessment of internal dose, early adverse effects, and risk (Bruno, Comba, Zona, 2006, 778-783). The UK legislation and for that matter no legislation in the world does not use this risk stratification approach for both occupational and environmental exposures. Appropriate regulations should incorporate the method of assessment of dose via biomarkers to assess the exposure that can track not only the amount of asbestos in environmental air, but also can detect absorption, distribution, toxicokinetics, and dynamic modeling to provide information on sampling time and sampling size. To sum up, the disease entities caused by exposure to asbestos were not unappreciated, even though conditions were unnamed and the knowledge about the conditions were incomplete. For the problem of mesothelioma, case reports began accumulating in the 1940s, and by the early 1950s there were studies relating asbestos to the development of this form of malignancy. Over the years, studies have shown that other forms of cancer can be caused by asbestos (Stayner, Dankovic, and Lemen, , 1996, 179-186). While there continues to be some controversy, it is generally accepted that gastrointestinal tract cancers, laryngeal cancers, and kidney cancers are all found in excess following exposure to asbestos the risk increasing with increasing exposure. In the United States various government agencies and organizations interested in cancer accept these findings. As more and more groups of individuals exposed to asbestos have been looked at, evidence of asbestos-induced disease is found. While there clearly appears to be a threshold phenomenon with regard to the development of asbestosis, no such threshold appears to exist for asbestos cancers, although a dose-response relationship exists. Studies have also indicated that asbestos related disease may also occur from environmental or bystander exposure, although most studies of asbestos and the development of human disease have focused on individuals occupationally exposed. Practically examined, taking the case of USA, there has been a substantial increase and then a leveling of male malignant mesothelioma incidence tracks asbestos use with a shift of 30-40 years (Hodgson and Darnton, 2000, 565-601). Male exposures generally were very high during the 1930s through the 1960s; for example, cumulative exposures were as great as 500 f/mL-yrs, sometimes higher (Mowat, Weidling, and Sheehan, 2007, 451-462). The mesothelioma trend reflects heavy occupational exposures after accounting for latency. Epidemiologic analysis of the data indicates that typical domestic and environmental exposures alone were insufficient to cause malignant mesothelioma, and hence a risk is established between occupational exposure and mesothelioma (Ladou, 2004, 285-290). In the USA, taking alone the case of mesothelioma, the peak for male cases is indicated in the 2000-2004 time-period and the decline to the spontaneous background level is projected to occur over the next 50 years. These have been possible due to regulations that led to reduction in asbestos use in manufacturing and tightening of workplace exposure limits initially imposed in 1971 by OSHA (OSHA, 1992). The current regulatory structure in the United States and voluntary reductions in asbestos use have been effective over the past 30 years in reducing asbestos-associated diseases, and will continue to be effective in the future due to this risk directed approach to develop regulations. Reference List Abratt RP, Vorobiof DA, (2004). 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