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A limitation of the registry based study was lack of accurate and complete lifetime occupational histories on individual cases and controls. Incomplete occupational data and lack of duration and intensity of occupational exposure to asbestos in the past made it difficult for us to evaluate occupational exposure to asbestos using common occupational exposure assessments such as job-exposure matrices and expert assessment for exposures. Although the CCR was supposed to record the patient's longest-held occupation and industry, it often listed only current or most recent occupation. Occupational exposure is the predominant cause of asbestos-induced mesothelioma. We should be cautious to explain our results because our assessment for occupational exposure to asbestos was based on incomplete occupational history on individual cases and control subjects.
Another limitation of the study was the lack of a reliable and acceptable job-exposure matrix for asbestos to characterize the potential of individual occupational exposure to asbestos based on occupation or job titles. Therefore we had to derive occupational exposure to asbestos based on incomplete information on occupations and industries. Misclassification for occupational exposure was unavoidable in this study. Although the National Institute for Occupational Safety and Health has reported asbestosis PMR for selected occupations and industries to reflect strength of occupational exposure to asbestos, it included only limited occupations and industries with higher occupational exposure to asbestos and more asbestosis cases (26). The job-exposure matrix for asbestos developed by Cocco and Dosemeci in 1998 lacked validation of occupational exposure to asbestos (27), and too many occupations were defined as exposed in a study of mesothelioma in Australia (31).
The study was also limited by the lack of complete lifetime residential history on individual cases and controls. When we calculated the distance to the nearest NOA from subject residential address at initial diagnosis, we had to assume that subject's residential address at initial diagnosis was the same as the longest residential address in his or her life. Exposure misclassification in our study could either decrease or increase the observed dose–response relationship. Incomplete residential data and lack of residential duration in one's lifetime made it difficult to accurately assess environmental exposure to naturally occurring and other asbestos sources. Reliable assessment of exposure to NOA using GIS approaches ideally depends on accurate and complete residential histories. A field study is needed to examine the relationship between actual asbestos exposure potential and the distance to the nearest asbestos sources. In additionally, consideration should be given to the impact of age of potential exposure, deposit size, residence duration, nature of human disturbance activity, meteorologic conditions, and other geologic/demographic attributes on the actual or potential exposure to NOA.Our study is based on ultramafic rock-specific GIS map, but not asbestos-specific GIS map for distribution of asbestos sources in California. A new digital map with more accurate and specific information about asbestos sources in California needs to be developed for further studies. It is essential for public health efforts to assess more accurately potential exposure to NOA. Some efforts should be increased to characterize the location of asbestos deposits using imaging spectroscopy to map ultramafic rocks, serpentinites, and tremolite-actinolite–bearing rocks in California (32).
Frequency matching was used to minimize confounding from age and sex. We were unable to control for potential confounding from domestic or residential exposure to asbestos because these data were not available for this study. Selection bias was limited because the data included all eligible cases from the population-based CCR and the control subjects were selected by stratified random sampling from the same population-based cancer registry. The data were collected in a similar manner for cases and control subjects; therefore, information bias from the data collection was limited, although some information bias cannot be avoided. For example, data on the longest occupation and industry were available for 74% of mesothelioma cases and 63% of pancreatic cancer cases in the CCR records. Because patients diagnosed with mesothelioma may be more likely to have been asked about occupational history and asbestos exposure, this may have led to overestimating occupational exposure to asbestos in this study.
We have found that residential proximity to NOA shows an independent and dose–response association with mesothelioma risk. The findings are biologically plausible in view of the known strong association of occupational asbestos exposure and mesothelioma, and the observation of an association of NOA and mesothelioma in other areas of the world (33). A prospective case–control study based on asbestos-specific GIS map in California should be done with incident mesothelioma cases. This would facilitate obtaining accurate and complete lifetime residential and occupational histories. Further research also is needed to develop a model to evaluate relationship between actual environmental exposure to NOA and major influencing factors, and to develop public health strategies to reduce exposure to asbestos from environmental sources.
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Correspondence and requests for reprints should be addressed to Marc B. Schenker, M.D., M.P.H., Division of Environmental & Occupational Health, Department of Public Health Sciences, University of California, Davis, One Shields Avenue, TB168 Davis, CA 95616-8638. E-mail: mbschenker@ucdavis.edu

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