Asbestos workplace exposure

The relationship between workplace exposure to airborne asbestos fibers and respiratory diseases is one of the most widely studied subjects of modern epidemiology (37—39). Asbestos-related health concerns were first raised at the beginning of the century in the UK and the latter appears to have been the first country to regulate the asbestos-user industry (40). However, at that time, infectious respiratory diseases were a much greater concern than those arising from poor industrial hygiene practices. 

The relationship between workplace exposure to airborne asbestos fibers and respiratory diseases is one of the most widely studied subjects of modern epidemiology. 

Only in the case of ultra high speed burnishing was the OSHA PEL exceeded. However, this was due to the generation of nonasbestos particles during the burnishing process and therefore do not reflect actual asbestos exposure. This example underscores the limitations of PCM in interpreting workplace exposure. 

The effect of this new policy will be the development, whenever possible, of quantitative RELs that are based on human and/or animal data, as well as on the consideration of technological feasibility for controlling workplace exposures to the REL. Under the old policy, RELs for most carcinogens were non-quantitative values labeled lowest feasible concentration (LFC). [Note There are a few exceptions to LFC RELs for carcinogens (e.g., RELs for asbestos, formaldehyde, benzene, and ethylene oxide are quantitative values based primarily on analjdical limits of detection or technological feasibility). Also, in 1989, NIOSH adopted several quantitative RELs for carcinogens from OSHA s permissible exposure limit (PEL) update.]... 

Workplace exposure is usually assessed by personal sampling in which a known volume of air is sucked through a membrane filter which is subsequently prepared for examination by phase-contrast optical microscopy, and respirable fibres counted using predetermined rules (HSE, 1990). 0.5 0.2 f/ml control limits for chrysotile and amphibole asbestos exposure respectively has been introduced in the UK, and a 2f/ml maximum exposure to MMMF has been agreed, running in parallel with a 5mg/m gravimetric limit. 

Workplaces can use a variety of solvents, such as methyl ethyl ketone, acetone, and Stoddard solvent. Workers who come into contact with solvents should wear recommended PPE. Most solvents can remove the natural fats and oils from the skin and some pose absorption risks. Organizations must store flammable solvents in approved containers. Provide local exhaust ventilation, and as needed use enclosures to control workplace exposures. When selecting appropriate engineering or other controls, safety personnel must consider the toxicity, flammability, and explosion potential of the material. Remove asbestos using only fully trained personnel adhering to the methods and protective equipment mandated by OSHA and EPA asbestos standards. OSHA 29 CFR 1910.1001 contains standards addressing working in or near in-place asbestos. 

In accordance with demonstrated differences between the various asbestos fiber types, the workplace regulation in many countries specifies different exposure limits for chrysotile and the amphiboles (45). Moreover, to alleviate estabHshed, or apprehended, risk from substitute fibers, the regulation often specifies maximum exposure limits for synthetic fibers (46) values of exposure limits adopted in leading industrial countries are coUected in Table 8. 

Table 8. Exposure Limits for Asbestos Fibers, Synthetic Mineral Fibers (SMF) and Nuisance Dust in the Workplace ...

Total frequencies of environmental illness are difficult to measure. When causes can be identified, however, scientists observe that frequencies of occurrence of a particular illness vary directly with the severity and extent of exposure. Particularly frequent in the workplace are skin lesions from many different causes and pulmonary diseases related to the inhalation of various dusts, such as coal dust (black lung), cotton dust (brown lung), asbestos fibers (asbestosis), and silica dust (silicosis). Environmental agents can also cause biological effects without overt clinical illness (for example, chromosome damage from irradiation). 

In 1971 the National Academy of Science published a 40-page report, Asbestos The Need for and Feasibility of Air Pollution Controls, (Cooper, 1971) summarizing the illnesses associated with occupational exposure to asbestos and the risks of developing asbestosis, pleural calcifications, and cancers of the pulmonary and gastrointestinal tracts and thoracic cavity. Based on the evidence, the committee recommended control and reduction of dust containing fibrous inorganic materials in the workplace it also discussed nonoccupational exposure to asbestos. 

Regulation. The identification of health risks associated with asbestos fibers, together with the fact that huge quantities of these minerals were used ( 5 x 06 Uyr) m a variety of applications, has prompted strict regulations to limit the maximum exposure of air-borne fibers in workplace environments. 

Units of Exposure. Consideration and comparison of quantitative data on asbestos inhalation studies are complicated by the fact that a number of different methods have been used to measure asbestos levels in air. Currently, the standard method for measuring asbestos concentrations in workplace air employs phase contrast microscopy (PCM). A particle visible under PCM is counted as a fiber if it is 5 micrometers (pm) long and has a length/thickness ratio of 3 1. However, the method cannot detect fibers thinner than about 0.3 pm and caimot distinguish between asbestos fibers and other fibers (NIOSH 1987). 

Analyses of trends in mesothelioma mortality in Britain and Western Europe (Peto et al. 1995, 1999) indicate that the worst-affected birth cohort is men bom around 1945-1950 (1/150 were projected to die of mesothelioma), whereas similar analyses of trends in the United States (Price 1997) indicate that the worst affected cohort is the 1925-1929 male birth cohort (with an estimated lifetime risk of 2/1,000). These trends mirror trends in raw asbestos consumption and a reduction in workplace airborne asbestos levels, with maximum exposure in the United States from the 1930s to the 1960s and in Britain and Western Europe in the 1970s (Peto et al. 1995, 1999 Price 1997). NIOSH (1999) has reported that age-adjusted mortality rates for malignant neoplasm of the pleura in U.S. males showed a decline during the 1987-1996 period from 3.61 per million in 1987 to 2.87 per million in 1996. 

Asbestos fibers have also been measured in urine (see Section 7.1), and limited data indicate that above average exposures in the workplace (Finn and Hallenbeck 1984) and through drinking water (Cook and Olson 1979) can be detected by this means. However, only a tiny fraction of inhaled or ingested fibers is... 

Immunotoxicity. There are numerous studies of the immune system in workers (active or retired) exposed to asbestos in workplace air (deShazo et al. 1988 Froom et al. 2000 Kagan et al. 1977 Pemis et al. 1965 Sprince et al. 1991, 1992 Warwick et al. 1973). These studies indicate that the immune system may be depressed in individuals who have developed clinical signs of injury, such as asbestosis or cancer. However, the cause-effect relationship between the immunological changes and the asbestos-related diseases is not certain. Also, it is not known if similar effects occur after oral exposure, or if the effects are inhalation specific. Prospective studies on this subject may be useful, both in discerning the importance of... 

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