Chest Diseases, Inc., P.S. Everett, WA 98203
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INTRODUCTION |
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Most physicians and epidemiologists are unaware of the bias created from using such historical data. The membrane filter, phase-contrast method of counting asbestos fibers began in the 1960s, and the Asbestos Research Council attempted to standardize the method in 1968. The Council published a more detailed method in 1971. During this time, the method has undergone various revisions to improve its precision, including use of a specialized eyepiece graticule, test slides, and improved mounting techniques. Finally, improved counting methods have resulted in an approximately 10-fold increase in the fiber counts measured on the same filter. This development was commented on by Rogers (2) and by the Health Effects InstituteAsbestos Research study entitled Asbestos in Public and Commercial Buildings (3
). It would have been useful if the authors (1
) had related the historical levels measured in Swedish workplaces between 1969 and 1973 and the change in the fiber counts that would have occurred if these same membrane filters were reevaluated by using more modern methodology such as electron microscopy.
In table 3 of their paper, Gustavsson et al. (1) evaluated exposure intensity classes and the relative risks of lung cancer subdivided by the highest intensity class of exposure of at least 1 year's duration in Stockholm County, Sweden, between 1985 and 1990. Most experts would agree that, because of the long latency period required for lung cancers to develop, one would like to have a latency period of at least 20 years from the date of the last exposure before assessing the risk of cancer. The other problem with the authors' data is that while they do include the mean duration of exposure in each class, they use the measurement of intensity of the more recent exposures to classify the intensity of the exposure; however, we know that earlier exposures, prior to 1985, were much more likely to contain much more hazardous concentrations of asbestos and other carcinogens. Therefore, I find this type of data uninterpretable.
One would expect that the relative risk of lung cancer would be dose related to a carcinogen, such as asbestos. Table 5 of the paper (1) does not show an increasing relative risk of lung cancer with increasing duration of exposure, suggesting that other factors may have created bias in the risk estimates of the effects of asbestos exposure.
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REFERENCES |
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Department of Occupational Health Stockholm County Council S-171 76 Stockholm, Sweden
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INTRODUCTION |
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Our asbestos exposure assessments were based mainly on a large, previous survey of asbestos exposure in Swedish workplaces, performed in 19691973. Samples were taken by the membrane filter method and were analyzed by phase contrast microscopy (3) using criteria specified by the American Conference of Governmental Industrial Hygienists in 1973 (4
). The Rogers letter (5
), cited by Dr. Smith (1
), deals with problems in interpreting samples analyzed by an older method (long running thermal precipitator method) used in the 1960s and is not relevant to interpreting our study (2
). Indeed, fiber analysis is an area of continuous development, and techniques based on electron microscopy offer enhanced possibilities to identify small fibers as well as to differentiate asbestos fiber types. We agree that the fiber analysis method must be considered in dose-response analyses of asbestos, but the fiber levels reported in our study were based on methods similar to those used in most other modern studies of lung cancer and asbestos. In addition, phase contrast microscopy is still specified for compliance with threshold limit values, both in the United States (6
) and in Sweden (7
).
A long latency period does not imply that recent exposures would be less important to disease risk. This is clearly illustrated by a large number of studies of tobacco smoking and lung cancer demonstrating a drop in risk after cessation of smoking (showing that late exposures are important) even though at least 1520 years must pass from first exposure until an excess risk appears. The relevance of late exposures depends on whether the agent under study acts as an early- or late-stage carcinogen, or both. There are studies indicating that late exposures to asbestos are important (8, 9
), and cumulative dose, integrated over all work periods, has very strong support as a dose measure for asbestos in studies of bronchial carcinoma (10
, 11
). Asbestos exposure levels in Sweden diminished dramatically when asbestos was banned in 1974, and most of the contribution to the cumulative dose in our study (2
) came from the years before 1974. Thus, we find the argument that a long induction/latency speaks against the relevance of cumulative dose theoretically wrong, with no bearing on interpretation of the present results.
Finally, it has been said that the lack of correlation of risk with duration of asbestos exposure would speak against a causal relation. Duration of exposure is often a poor surrogate for cumulative exposure, especially if exposure levels have changed considerably over time. In view of the dramatic fall in asbestos levels during the mid-1970s in Sweden, the lack of correlation with duration is not surprising. The risk correlated with both exposure intensity and cumulative exposure. We find Dr. Smith's suggestion that "other factors may have created bias in the risk estimates" (1, p. 1029) is a misinterpretation of the findings (2
). Our findings fit in well with the massive evidence that asbestos is a human lung carcinogen.
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