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Relation between lung asbestos fibre burden and exposure indices based on job history.

Takahashi, K, Case, B W, Dufresne, A, Fraser, R, Higashi, T, Siemiatycki, J·1994·Occupational and Environmental Medicine
DOI 10.1136/oem.51.7.461
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Abstract

Lung asbestos burden was compared with exposure indices derived from job history interviews in 42 male subjects originating from the Montréal Case-Control Study project, 12 of whom had documented asbestos exposed job histories. Job interview data consisting of a chronological timetable of job histories were translated into detailed exposure indices by an expert group of hygienists and chemists. Total and individual asbestos fibre type concentrations were quantified by transmission electron microscopy with fibre identification by energy dispersive chi ray spectrometry after deparaffinisation of tissue blocks and low temperature plasma ashing. Geometric mean or median asbestos content was higher in subjects with an asbestos exposed job history than those without for retained dose of amosite, total commercial amphiboles, and total asbestos fibre. Except for crocidolite fibre diameter, which was significantly less in the lungs of exposed workers, no consistent differences were found in measurements of fibre dimension for any fibre type. Subgroups of subjects exposed to silica, metals, or smokers and non-smokers without significant occupational exposure showed varying patterns of lung asbestos fibre type deficit compared with the asbestos exposed subgroup. There was an overall trend for higher lung asbestos content proportional to higher exposure indices for asbestos representing concentration, frequency, and reliability. These exposure indices as well as duration of exposure (in years) were independent predictors of total asbestos content in regression analyses when combined in a model with age. Stepwise regression indicated that exposure concentration was the most important variable, explaining 32% of the total variation in total asbestos content. Smoking, whether expressed in ever or never smoked dichotomy or in smoked-years, had no relation to lung asbestos content in this model.

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Research works printed but not linked: 21

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  2. Dufresne A, Perreault G, Case BW, Fraser R. A protocol for lung particulate analysis by transmission electron microscopy. In: McCallum I, Dodgson J, eds. Seventh international symposium on inhaled particles. London: Pergamon Press, 1994 (in press).
  3. Case BW, Dufresne A, Fraser R, Siemiatycki J, Perrault G, Takahashi K. Decoding occupational history from total particulate analysis: concordance between physicochemical analysis and occupational histories. In: McCallum R, Dodgson J, eds. Seventh international symposium on inhaled particles. London: Pergamon Press, 1984 (in press).
  4. Case BW. Lung fibre content as a marker of low-level asbestos exposure. In: Gibbs G, Dunnigan J, Kido M, Higashi T, eds. Health risksfrom exposure to mineralfibres: an international perspective. North York, Ontario: Captus University Press, 1993:326-33.
  5. Case BW, Sibastien P. Environmental and occupational exposures to chrysotile asbestos: a comparative microanalytic study. Arch Environ Health 1987;42:185-91.
  6. Case BW. Biological indicators of chrysotile exposure. In: Gibbs GW, Valic F, Browne K, eds. Health risks associated with chrysotile asbestos: a report on a workshop held in Jersey, Channel Islands. Ann Occup Hyg 1994 (in press).
  7. Churg A, Wood P. Observations on the distribution of asbestos fibres in human lungs. Environ Res 1983; 31:374-80. · DOI
  8. Sebastien P, McDonald JC, McDonald AD, Case B, Harley R. Respiratory cancer in chrysotile textile and mining industries: exposure inferences from lung analysis. BrJInd Med 1989;46:180-7.
  9. McDonald JC, Case BW, Enterline PE, et al. Lung dust analysis in the assessment of past exposure of manmade mineral fibre workers. Ann Occup Hyg 1990;34: 427-41.
  10. McDonald JC, Armstrong B, Case BW, et al. Mesothelioma and asbestos fiber type: evidence from lung tissue analyses. Cancer 1989;63:1544-7. · DOI
  11. Roggli VL, Pratt PC, Brody AR. Asbestos content of lung tissue in asbestos associated diseases: a study of 110 cases. BrJt Ind Med 1986;43:18-28.
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  13. Hulka BS, Wilcosky TW. Biological markers of disease. Arch Environ Health 1987;43:83-9. · DOI
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  15. Siemiatycki J, Day NE, Fabry J, Cooper JA. Discovering carcinogens in the occupational environment: a novel epidemiologic approach. _J Natl Cancer Inst 1981;66: 217-25.
  16. Siemiatycki J, Richardson L, Gcrin M, et al. Associations between several sites of cancer and nine organic dusts: results from an hypothesis-generating case-control study in Montreal, 1979-1983. Am _J Epidemiol 1986;123: 235-49. · DOI
  17. Siemiatycki J, Wacholder S, Richardson L, Dewar R, Gerin M. Discovering carcinogens in the occupational environment: methods of data collection and analysis of a large case-referent monitoring system. Scand J Work Environ Health 1987;13:486-92. · DOI
  18. Goldberg MS, Siemiatycki I, Gerin M. Inter-rater agreement in assessing occupational exposure in a case-control study. BrJ Ind Med 1986;43:667-76.
  19. Baker D. Limitations in drawing etiologic inferences based on measurement of asbestos fibers from lung tissue. Ann NYAcad Sci 1991;643:61-70. · DOI
  20. Case BW. Asbestos: an autopsy series, and epidemiology [abstract]. Canadian Congress on Laboratory Medicine 1993;44:87.
  21. Weill HW, Abraham J, Balmes J, et al. Health effects of tremolite. Am Rev Respir Dis 1990;142:1453-8. · DOI

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Metadata

Authors
Takahashi, K., Case, B. W., Dufresne, A., Fraser, R., Higashi, T., & Siemiatycki, J.
Venue
Occupational and Environmental Medicine
Publisher
BMJ
Published
1994-07
Volume
51
Issue
7
Pages
461-469
ISSN
  • 1351-0711
  • 1470-7926
DOI
10.1136/oem.51.7.461
Cited by
22
References
0
Language
en

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