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Lung asbestos

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). [Pg.47]

Exposures of Children. Only a few small studies have assessed the lung asbestos fiber content of children (Case et al. 1988, 1994). Preliminary results from the most comprehensive of these studies indicate that asbestos bodies and lung fiber concentrations in children are one to two orders of magnitude lower than those found in adults. More data are needed on the levels of asbestos in children, and attempts should be made when these data are acquired to link the body burden with possible sources of exposure (e.g., residing in places with naturally elevated soil concentrations, in areas with mining or hazardous waste sites, or in housing with crumbling asbestos). [Pg.209]

Churg A. 1986b. Lung asbestos content in long-term residents of a chrysotile mining town. Am Rev RespirDis 134 125-127. [Pg.245]

De Vuyst P, Dumortier P, Moulin E, et al. 1988. Asbestos bodies in bronchoalveolar lavage reflect lung asbestos body concentration. Eur Resp J 1 362-367. [Pg.253]

Rogers AJ, Ixigh J, Berry G, et al. 1991. Relationship between lung asbestos fiber type and concentration and relative risk of mesothelioma. Cancer 67 1912-1920. [Pg.323]

Takahashi K, Case BW, Dufresne A, et al. 1994. Relation between lung asbestos fibre burden and exposure indices based on job history. Occup Environ Med 51 461-469. [Pg.333]

Wamock ML. 1989. Lung asbestos burden in shipyard and construction workers with mesothelioma Comparison with burdens in subjects with asbestosis or lung cancer. Environ Res 50 68-85. [Pg.341]

Inhalation of certain fine dusts may constitute a health hazard. Eor example, exposure to siUca, asbestos, and beryllium oxide dusts over a period of time results ki the potential risk of lung disease. OSHA regulations specify the allowable levels of exposure to kigestible and respkable materials. Material Safety Data Sheets, OSHA form 20, available from manufacturers, provide information about hazards, precautions, and storage pertinent to specific refractory products. [Pg.35]

The replacement of asbestos fibers by other fibrous materials has raised similar health issues in relation to substitute materials. However, since lung cancer has a latency period of approximately 25 years, and since the fiber exposure levels in contemporary industries is far lower than those which prevailed half a century ago, the epidemiological data on most substitutes is insufficient. A possible exception is slag fibers for which several studies on worker populations are available over extended periods (44) some results show a substantial increase in lung cancer occurrence. Consequentiy, the toxicity of asbestos substitute fibers remains a subject of active investigation. [Pg.356]

Asbestos and other fibers in a wide variety of bundle sizes or even individual fibrils are in commercial usage. The handling of asbestos and other fibers causes degradation of the larger fiber bundles to fibers having diameters less than two micrometers that remain airborne for extended periods of time. These airborne fibers are prone to inhalation and lung entrapment. The exact definition of harmfiil fibers and the mechanism by which they affect the body is not accurately known. [Pg.275]

Handling hazardous ehemieals has beeome part of most people s everyday living. Just eonsider gasoline, and how most people fill their own tanks. In the manufaeturing arena, ehemieals are eommonplaee. On hazardous waste sites there are a variety of unknown ehemieal substanees and other hazards that may take the form of a solid, liquid, or gas. The eflfeets of exposure to toxie ehemieals may either be immediate (e.g., aeid burns) or delayed (e.g., lung damage from inhaling asbestos). There are four routes of ehemieal exposure that exist ... [Pg.78]

Bronchogenic carcinoma A lung cancer associated with asbestos exposure. [Pg.1418]

The standard unit normally used for measuring dust particles is the micron (pm one-thousandth of a millimeter). The smallest particle visible to the unaided eye is between 50 and 100 pm and the most dangerous sizes are between 0.2 and 5 pm. Particles larger than this are usually unable to penetrate the lung defenses and smaller ones settle out too slowly. Some dusts can be both toxic and fibrous (e.g. asbestos) and are therefore harmful even outside these parameters. It may therefore be assumed that dusts which are visible (i.e. between 50 and 100 pm), are quite safe. However, this is not the case, as dust clouds never consist solely of particles of one size. Analysis would show percentages of all sizes, and it is for this reason that special care is needed in measuring dust clouds and concentrations. [Pg.764]

When asbestos is handled, microscopic fibers become suspended in the atmosphere and are breathed into the lungs. There, they lodge in lung tissue, where they remain for many years, causing irritation that eventually leads to loss of lung function. Asbestos, which was once used extensively as insulation, is now recognized as a significant health hazard. [Pg.618]

The a-tocopherol, P-carotene (ATBC) Cancer Prevention study was a randomised-controlled trial that tested the effects of daily doses of either 50 mg (50 lU) vitamin E (all-racemic a-tocopherol acetate), or 20 mg of P-carotene, or both with that of a placebo, in a population of more than 29,000 male smokers for 5-8 years. No reduction in lung cancer or major coronary events was observed with any of the treatments. What was more startling was the unexpected increases in risk of death from lung cancer and ischemic heart disease with P-carotene supplementation (ATBC Cancer Prevention Study Group, 1994). Increases in the risk of both lung cancer and cardiovascular disease mortality were also observed in the P-carotene and Retinol Efficacy Trial (CARET), which tested the effects of combined treatment with 30 mg/d P-carotene and retinyl pahnitate (25,000 lU/d) in 18,000 men and women with a history of cigarette smoking or occupational exposure to asbestos (Hennekens et al, 1996). [Pg.33]


See other pages where Lung asbestos is mentioned: [Pg.27]    [Pg.123]    [Pg.205]    [Pg.120]    [Pg.128]    [Pg.27]    [Pg.123]    [Pg.205]    [Pg.120]    [Pg.128]    [Pg.43]    [Pg.381]    [Pg.106]    [Pg.356]    [Pg.356]    [Pg.77]    [Pg.77]    [Pg.119]    [Pg.42]    [Pg.43]    [Pg.129]    [Pg.140]    [Pg.250]    [Pg.270]    [Pg.295]    [Pg.295]    [Pg.324]    [Pg.325]    [Pg.325]    [Pg.351]    [Pg.588]    [Pg.733]    [Pg.43]    [Pg.43]    [Pg.55]    [Pg.77]    [Pg.77]    [Pg.148]    [Pg.181]    [Pg.217]   
See also in sourсe #XX -- [ Pg.9 , Pg.22 , Pg.25 , Pg.85 , Pg.116 , Pg.118 , Pg.208 , Pg.214 ]




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