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American Journal of Epidemiology Advance Access originally published online on October 24, 2006
American Journal of Epidemiology 2007 165(1):53-62; doi:10.1093/aje/kwj343
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American Journal of Epidemiology Copyright © 2006 by the Johns Hopkins Bloomberg School of Public Health All rights reserved; printed in U.S.A.

ORIGINAL CONTRIBUTIONS

Exposure to Diesel and Gasoline Engine Emissions and the Risk of Lung Cancer

Marie-Élise Parent1, Marie-Claude Rousseau1, Paolo Boffetta2, Aaron Cohen3 and Jack Siemiatycki4

1 INRS-Institut Armand-Frappier, University of Quebec, Laval, Quebec, Canada
2 Gene-Environment Epidemiology Group, International Agency for Research on Cancer, Lyon, France
3 Health Effects Institute, Cambridge, MA
4 Department of Social and Preventive Medicine, University of Montreal, Montreal, Quebec, Canada

Correspondence to Dr. Marie-Élise Parent, Epidemiology and Biostatistics Unit, INRS-Institut Armand-Frappier, 531 Boul. des Prairies, Laval, Quebec, H7V 1B7 Canada (e-mail: marie-elise.parent{at}iaf.inrs.ca).

Received for publication June 23, 2005. Accepted for publication May 17, 2006.


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 APPENDIX
 References
 
Pollution from motor vehicles constitutes a major environmental health problem. The present paper describes associations between diesel and gasoline engine emissions and lung cancer, as evidenced in a 1979–1985 population-based case-control study in Montreal, Canada. Cases were 857 male lung cancer patients. Controls were 533 population controls and 1,349 patients with other cancer types. Subjects were interviewed to obtain a detailed lifetime job history and relevant data on potential confounders. Industrial hygienists translated each job description into indices of exposure to several agents, including engine emissions. There was no evidence of excess risks of lung cancer with exposure to gasoline exhaust. For diesel engine emissions, results differed by control group. When cancer controls were considered, there was no excess risk. When population controls were studied, the odds ratios, after adjustments for potential confounders, were 1.2 (95% confidence interval: 0.8, 1.8) for any exposure and 1.6 (95% confidence interval: 0.9, 2.8) for substantial exposure. Confidence intervals between risk estimates derived from the two control groups overlapped considerably. These results provide some limited support for the hypothesis of an excess lung cancer risk due to diesel exhaust but no support for an increase in risk due to gasoline exhaust.

case-control studies; environmental pollutants; gasoline; lung neoplasms; motor vehicles; occupational exposure; vehicle emissions


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 APPENDIX
 References
 
Pollution from motor vehicles constitutes one of the most ubiquitous environmental health problems of our era (1, 2). There has been increasing recognition, based in part on studies of workers exposed to diesel engine emissions, that such exposure may be carcinogenic to humans (3–12). However, drawing inferences regarding effects of diesel exhaust is difficult because of methodological limitations and the indirect nature of the evidence. Namely, most studies have used job titles (such as truck driver or railroad worker) as proxies for occupational exposure to diesel exhaust, but job titles can be misleading (13). Few studies were able to control for the potential confounding effect of the most powerful risk factor for lung cancer, cigarette smoking, and of other occupational exposures such as asbestos. Many of the studies had low statistical power. The number of diesel-powered vehicles is increasing in many countries. Given the significant scientific and public policy implications (14, 15), it is important to derive more definitive inferences regarding the potential human carcinogenicity of diesel emissions.

Because of the predominant role of gasoline as a motor vehicle fuel, the effects of gasoline engine emissions are potentially an even greater problem. However, there has been less research on possible carcinogenic effects of gasoline exhaust than on diesel exhaust. The purpose of this paper is to present epidemiologic evidence on the lung carcinogenic effects of diesel and gasoline engine emissions from a unique data set in which both of these substances could be measured and their effects contrasted.

Exposure to motor vehicle emissions is so widespread in urban environments that it is difficult to discriminate among subjects with differing degrees of historic lifetime exposure to such emissions in the general environment. Occupational exposure can provide an alternative setting in which to estimate the effects of different emission sources (16).

In the 1980s, we conducted a large, community-based case-control study to assess the role of occupational exposures in cancer incidence. We interviewed more than 4,000 cancer patients and population controls to elicit covariate information and detailed job histories, and a team of industrial hygienists translated the job histories into histories of occupational exposures. This data set enabled us to analyze the possible associations between many occupational exposures and sites of cancer. Partial results of this study have previously been presented as part of a sweeping analysis of the relation between 13 sites of cancer and 10 types of combustion products (17). Results from that earlier analysis, based on cancer controls as referents, suggested that exposure to either gasoline or diesel exhaust was associated with a 20 percent excess risk of lung cancer. Given the importance and controversy surrounding the debate about lung carcinogenicity of vehicle emissions, we aimed to improve the quality of the evidence from our study. Compared with our previous study, the present one entails several improvements: 1) in preparation for this analysis, our team conducted an exhaustive revision of the exposure assessment, increasing substantially the total cumulated person-time of experts involved in the exposure assessment of these substances; 2) we exploited the availability of both population controls and cancer controls; and 3) we minimized the potential confounding effect of smoking by using a better parameterization of smoking variables.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 APPENDIX
 References
 
The study design and data collection methods have been presented in detail elsewhere (18–20). A total of 19 cancer sites were selected for study among males 35–70 years of age residing in the Montreal area. Given the presence of a universal national health system in Canada, participation of all large hospitals in the study area assured virtually complete population-based ascertainment of cancer patients. Between 1979 and 1985, 3,730 histologically confirmed cancer patients (82 percent response rate) and 533 population controls selected from electoral lists (71 percent response rate) were successfully interviewed, mostly face-to-face. Over 82 percent of the subjects responded for themselves; proxies provided information for the rest. An institutional review board approved the study, and informed consent was obtained from study participants.

Lung cancer case and control series
There were 857 lung cancers (359 squamous cell carcinomas, 167 adenocarcinomas, 159 small cell carcinomas, and 172 other cell types or unclassified). For the present analysis, we used two different sets of controls: the 533 population controls and 1,349 cancer patients (referred to as "cancer controls") who had been ascertained in the same years and hospitals as the lung cancer cases and selected so that none of the 19 individual cancer sites represented more than 20 percent of the overall pool of cancers. The main cancer sites represented among cancer controls were colorectal (n = 261), bladder (n = 243), prostate (n = 162), stomach (n = 147), non-Hodgkin's lymphoma (n = 129), and kidney (n = 100).

Data collection
The questionnaire had two parts: a structured section requesting information on sociodemographic and lifestyle characteristics, and a semistructured section designed to obtain a detailed description of each job the subject had held in his working lifetime. For each job held, a specially trained interviewer asked the subject about the company, its products, the nature of the work site, the subject's main and subsidiary tasks, and any additional information (e.g., equipment maintenance, use of protective equipment, activities of coworkers) that could furnish clues about possible exposures. For some occupations, supplementary questionnaires were used to assist interviewers with detailed technical probing (21).

A team of chemists and industrial hygienists examined each completed questionnaire and translated each job into a list of potential exposures by using a checklist that mentioned some 300 substances, including gasoline and diesel engine emissions. This team of coders spent about 40 person-years on this project, including helping to develop the methodology, monitoring the quality of the interviewing, conducting background research on exposures in different occupations, coding the files, and recoding after the first complete round of coding was finished. The final codes given to a file were based on consensus among the coders. Chemical coders were blinded with regard to the subject's disease status.

For each product considered present in each job, the coders noted three dimensions of information, each on a three-point scale: their degree of confidence that the exposure had actually occurred (possible, probable, definite), the frequency of exposure in a normal work week (<5 percent, 5–30 percent, >30 percent of the time), and the relative level of concentration of the agent (low, medium, high). Nonexposure was interpreted as exposure up to the level that can be found in the general environment. Although a subject's job title was certainly a factor in attributing exposure, the details of the subject's activities were taken into account, and there were many examples of subjects with the same job title having different exposure profiles; conversely, similar exposures were attributed to many subjects with different job titles.

Selected characteristics of lung cancer cases and the two control groups are shown in table 1. Although similar to controls in terms of age, cases had, on average, a lower income, were more often of French origin, and were more likely to have a proxy respond for them. The proportion of never smokers was markedly lower among cases, and cases were more often current smokers or had quit smoking only very recently. A greater proportion of cases than controls had ever had occupational exposure to asbestos and silica.


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  		TABLE 1 Selected characteristics of cases and controls studied regarding the association of exposure to diesel and gasoline engine emissions with risk of lung cancer, Montreal, Canada, 1979–1985

 
Exposure to gasoline and diesel exhaust
The potential exposure period of our study subjects was from the 1940s to the 1970s. Since gasoline and diesel exhaust have been ubiquitous features of urban environments for many decades, it was important to discriminate between subjects exposed at "environmental" levels and those exposed at higher levels. We decided that subjects whose exposure to traffic pollution was sporadic or recreational would be considered to have background environmental exposure. Furthermore, among those who spent a considerable amount of time "on the road," there was dissymmetry in the way we treated gasoline and diesel exhaust. Namely, such drivers were routinely attributed exposure to gasoline exhaust but not necessarily to diesel exhaust because diesel pollution has in the past represented a small fraction of vehicle-related pollution on roadways. To trigger an attribution of diesel exhaust exposure, we required that the subject drive a diesel-powered engine and that there was reason to believe that he was exposed to his own vehicle exhaust at a level considered above background environmental exposure.

An important factor in determining whether a worker was exposed to diesel exhaust was the era of work. There has been a shift from gasoline- to diesel-powered engines in many industries over the past 60 years, but it happened at different rates in different places for different industries (trucking, buses, automobiles, fire trucks, construction equipment, farm equipment, etc.). Although we found little formal documentation of these gradual shifts, we obtained useful guidance by consulting local experts and industry associations. Sometimes study subjects were able to provide information on the type of fuel used, and sometimes we had to infer it from the industry and the era.

Table 2 lists some of the main occupations in which these substances were coded. When our criteria were used, all vehicle drivers were considered exposed to gasoline exhaust, but only 37 percent were exposed to diesel exhaust. For diesel, it depended on the type of vehicle driven, the era, and the idiosyncratic details of the job. For motor vehicle mechanics, 78 percent were exposed to gasoline exhaust and 29 percent to diesel exhaust. This table also shows the typical coding of confidence, frequency, and concentration among exposed workers. Lest the reader infer that these were attributed in an automated way, the Appendix presents some examples showing that these typical codings were adapted to the idiosyncratic details of the job. There, it is shown that four different workers, all with the same 7-digit job code, were allocated different levels of exposure to diesel exhaust.


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  		TABLE 2 Proportion of workers exposed to gasoline and/or diesel emissions in selected occupations and usual exposure codings*,{dagger} Montreal, Canada, 1979–1985

 
Table 3 describes the exposure patterns to gasoline and diesel exhaust among controls. Gasoline exhaust was a much more common exposure than diesel exhaust (43.0 percent vs. 14.8 percent). Almost all of these persons were considered probably or definitely exposed, and a majority of those exposed had been exposed more than 30 percent of the day. However, much smaller fractions were considered to have high concentrations of exposure. Fifty-four percent of controls were unexposed to both types of exhaust, 31 percent were exposed to gasoline exhaust only, 3 percent were exposed to diesel exhaust only, and 11 percent were exposed to both gasoline and diesel exhaust. While the shift from gasoline to diesel happened in many industries, the main occupations for which the change occurred are truck drivers, among whom the prevalence of diesel exhaust exposure increased from 28 percent to 64 percent from pre–1959 to post–1959, and mechanics, among whom it increased from 27 percent to 39 percent in the same eras. Among those exposed, the mean durations of exposure for both gasoline and diesel exhaust were 20 years.


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  		TABLE 3 Prevalence of lifetime exposure to gasoline and diesel engine emissions, by degree of exposure,* Montreal, Canada, 1979–1985

 
Statistical analyses
Unconditional logistic regression models were used (22), retaining the following variables as potential confounders: age and socioeconomic status expressed as family income (linear terms), ethnicity (French, Anglo, Italian, Jewish, other European, other), respondent status (self, proxy), tobacco smoking, and occupational exposure to asbestos and crystalline silica. After an in-depth comparison of several parameterizations of the smoking variables in this data set (23, 24), we selected a three-variable model that provided the best fit: ever smoking, the natural logarithm of the number of cigarette-years, and number of years since quitting smoking.

For each of the two types of emissions, subjects were classified into one of four possible exposure categories based on the probability, timing, duration, and degree of exposure. The first category consisted of "unexposed" subjects. The second consisted of subjects with low confidence of exposure or with less than 5 years since first exposure; data for these persons were excluded from analyses. The remaining exposed subjects were divided into two exposure groups, nonsubstantial and substantial. Substantial exposure was assigned to those subjects with exposure at the medium or high concentration and frequency levels and who had been exposed for more than 5 years.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 APPENDIX
 References
 
The crude proportions of subjects exposed to gasoline exhaust were similar among cases (44.3 percent), population controls (43.3 percent), and cancer controls (42.3 percent). The proportion exposed to diesel exhaust was higher among cases (19.4 percent) than among population controls (12.8 percent) or cancer controls (15.3 percent). Table 4 shows the main adjusted odds ratios for the relation between lung cancer and occupational exposure to gasoline and diesel emissions based on data for population or cancer controls. These values were estimated by using a common reference category comprising subjects unexposed to both types of emissions. Results are shown for subjects exposed to both types and to each type of emission separately.


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  		TABLE 4 Odds ratios for the association of exposure to gasoline and diesel engine emissions with lung cancer, using data for population or cancer controls, Montreal, Canada, 1979–1985

 
Gasoline engine emissions
Exposure to gasoline exhaust was not associated with an increased risk of lung cancer. This finding held true when both control groups were considered and whether we looked at gasoline in the absence of diesel or gasoline irrespective of diesel. We conducted further analyses of the gasoline exposure data, looking at risks by histologic types, more detailed exposure categories, and the interaction with smoking. None showed a noteworthy departure from the null pattern evident in table 4.

Diesel engine emissions
The two control groups provided mixed messages about diesel exhaust and lung cancer. When population controls were considered, the adjusted odds ratios were 1.2 (95 percent confidence interval: 0.8, 1.8) and 1.6 (95 percent confidence interval: 0.9, 2.8) for any and substantial exposure, respectively. Of the covariates included in the models, smoking had the greatest effect on the adjusted odds ratios. Among workers exposed to diesel only, the numbers were small but still indicated excess risks. When we studied cancer controls, the odds ratios associated with exposure to diesel exhaust were close to 1.0, although there was a hint of excess risk for those exposed to diesel only. There was considerable overlap in confidence intervals between risk estimates derived from population and cancer controls data, indicating that the two apparently discrepant sets of results may reflect statistical variability from an underlying common relative risk. When we combined data for the two control groups and weighed them equally, the resulting odds ratios were 1.1 (95 percent confidence interval: 0.8, 1.4) for any exposure and 1.2 (95 percent confidence interval: 0.8, 1.8) for substantial exposure to diesel. The odds ratio for workers exposed to diesel only, based on the combined group of controls, was 1.5 (95 percent confidence interval: 0.9, 2.5).

To further explore dose-response patterns with diesel exhaust, we evaluated risks of lung cancer separately in relation to frequency, concentration, and duration of exposure (table 5). Whereas no clear pattern emerged by frequency or duration, high concentration conferred an excess risk when both population controls (odds ratio = 2.8, 95 percent confidence interval: 1.0, 8.0) and cancer controls (odds ratio = 1.7, 95 percent confidence interval: 0.9, 3.3) were studied.


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  		TABLE 5 Odds ratios for the association of diesel engine emissions with lung cancer, by frequency, concentration, and duration of exposure, using data for population or cancer controls, Montreal, Canada, 1979–1985

 
Table 6 shows that, when the population controls were considered, the effect of diesel exhaust varied somewhat according to histologic types, with the highest odds ratio for squamous cell carcinoma (odds ratio = 1.5, 95 percent confidence interval: 0.9, 2.4). When cancer controls were studied, no excess risks were seen (not shown in table).


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  		TABLE 6 Odds ratios for the association of exposure to diesel engine emissions with lung cancer, by histologic types, using data for population controls, Montreal, Canada, 1979–1985

 
Table 7 shows the joint effects of smoking and diesel exhaust when population controls were considered. These analyses had low power because of few cases who did not smoke. In all four comparisons of diesel exposed with unexposed (nonsmokers/smokers and cancer/population controls), the odds ratios for diesel exposed were greater than the corresponding ones for diesel unexposed. To the extent that it is meaningful to evaluate the fit of these patterns to additive or multiplicative models of interaction, they are more compatible with the former.


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  		TABLE 7 Joint effects of diesel emissions and cigarette smoking on risk of lung cancer, using data for population controls, Montreal, Canada, 1979–1985

 
We analyzed lung cancer risks according to job titles for the main occupational groups that had exposure to gasoline and/or diesel exhaust. There was no evidence that excess risks were concentrated in one or two of those occupations; when population controls were considered, the excess was spread across workers with different job titles who had exposure to diesel exhaust.


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
APPENDIX
 References
 
This study benefited from the availability of a relatively large number of lung cancer cases, two different types of controls, complete lifetime job histories, information on other occupational exposures such as asbestos, a long follow-up period between exposure and possible effect (the mean date of beginning exposure was 1949 for gasoline exhaust and 1952 for diesel exhaust), and information on subjects' smoking histories. Smoking is by far the strongest predictor of lung cancer and a plausible confounder of relatively weak associations. We carefully selected a group of parameters that best fitted the available smoking data and described the range of smoking exposure patterns. Of the covariables included in the various models, smoking had the largest confounding effect and accounted for most of the difference between crude and adjusted odds ratios. Nevertheless, some residual confounding by smoking is still possible. It has been suggested that aspects of smoking behavior, such as tar intake or interpuff intervals, may induce residual confounding even after other smoking variables are considered (25). These smoking variables were not collected in the present study. Nevertheless, we consider it unlikely that such subtle aspects of smoking would have induced greater bias than variables such as duration and daily amount of smoking.

Exposures were attributed by a team of chemists and industrial hygienists on a case-by-case basis based on job descriptions obtained during the interview, taking into consideration the era of exposure, work practices, and so forth. It is difficult to validate retrospective exposure assessment. We have shown that the interview-based job histories were valid (26), that the exposure coding was reliable (27, 28), and, in a limited trial, that the exposure assessment reflected past measured exposures (29). This method is widely considered the reference method of exposure assessment for such a study design (30).

The present results, providing risk estimates for exposures incurred from a broad spectrum of occupations, entailed a wider range of exposure levels than those typically found in industrial cohort studies. Because our study cut across different occupational groups, it reduced the impact of confounders that may be specific to particular occupations (e.g., secondhand smoke for drivers, radon for miners).

Limitations of the study include exposure misclassification that inevitably occurred in the absence of objective measurements for study subjects; lack of quantitative data on exposure levels; and limited statistical power, despite the fact that ours is one of the largest case-control studies on this issue.

There are pros and cons to both types of controls (20, 31), and we cannot say with certainty which type provides a more faithful representation of the parameter of interest—exposure prevalence in the study base from which cases were derived. For both types of controls, there are legitimate questions regarding selection and response rate biases. For population controls, there are also doubts about information bias when comparing responses from healthy and diseased people. However, our approach to exposure assessment, based not on self-reports of exposure but on assessments by a blinded team of experts, is less susceptible to such bias. For cancer controls, there are concerns about the possibility that diesel exhaust could be associated with one or more cancer sites in the control pool, although this possibility is speculative and would not have a great effect on the results unless the effect applied to many sites in the control pool. Bladder cancer, for example, has been associated with exposure to diesel exhaust in a number of studies (7). Excluding individual cancer sites from the cancer control pool had virtually no effect on the main results.

Sometimes it is justifiable to pool data to derive common estimates, and sometimes it is preferable to juxtapose the two sets of findings with a heuristic interpretation. In this paper, we chose to present the results separately. If the results provided by the control groups are similar, as they were for gasoline exhaust, then it increases confidence in the inferences. If they appear to differ, as they did for diesel exhaust, then we are confronted with the same inferential challenge as interpreting two different studies that give ostensibly different results.

Gasoline engine emissions
Although the toxicologic database for the health effects of gasoline emissions is limited, long-term inhalation studies do not indicate that this mixture is a lung carcinogen in animals (5, 32). A study of the mutagenicity of exhausts derived from different fuel/engine combinations suggests that it is lower for gasoline than for diesel emissions (33, 34).

There have been very few studies of workers whose predominant exhaust exposure has been from gasoline engines. Our findings suggest that occupational exposure to gasoline emissions does not confer an excess risk of lung cancer. There are two qualifications. Because exposure to gasoline exhaust is so widespread in the general population, the contrast between occupationally exposed and occupationally unexposed may not be large enough to engender a detectable risk. Another qualification concerns the fact that the study subjects worked mainly before the changeover from leaded to unleaded gasoline. Our findings are thus most relevant to carcinogenicity of exhausts from leaded gasoline.

Diesel engine emissions
When we considered population controls, the overall odds ratio of lung cancer for those exposed to diesel exhaust was elevated, as it was in several of the subgroups examined. The increases were of borderline statistical significance and were higher for men exposed at high concentration levels. When cancer controls were studied, the only increased risk was seen in the high concentration subgroup. The association with diesel exhaust was strongest for squamous cell tumors, a pattern similar to that for cigarette smoking (35). Moreover, we observed elevated risks with diesel exhaust exposure for both smokers and nonsmokers. The increased risk was not concentrated in any particular diesel-exposed occupation. These findings, although not persuasive by themselves, nevertheless support other epidemiologic and experimental findings.

There is convincing evidence that chronic exposure to a high concentration of whole diesel engine exhaust causes lung tumors in rats, whereas results for other rodent species have been mixed (32). The relevance of these toxicologic results for human exposure in most general and occupational environments is questionable (4). Carcinogenicity of diesel exhaust is hypothesized to originate from mutagenic and carcinogenic organic compounds adsorbed to the particles or from an overloading of particle clearance from the lung by macrophages, resulting in chronic inflammation, cell proliferation, and lung tumors (36).

Considerable epidemiologic data have accumulated on lung cancer risk in some occupations presumed to entail exposure to diesel emissions, such as railroad workers, miners, heavy-equipment operators, truck drivers, bus drivers, and vehicle and truck mechanics (3, 5, 7, 37–53). Several studies, including meta-analyses (10, 54), support the notion that these jobs are associated with an excess risk of lung cancer.

Our results are also in line with the positive associations reported in most studies that assessed diesel exhaust exposure per se by using either self-reports (50, 55), a job-exposure matrix (56), expert ratings (57–60), or indices based on fuel and equipment use (61). Previous null findings may have resulted from errors in self-reported exposure (62, 63) or from low exposure levels (64).

If diesel exhaust is carcinogenic and operates through a mechanism similar to that of tobacco smoke, then one would expect their joint effect to be additive (65). In fact, the joint effect was close to additive in our data. This finding is compatible with most (57) but not all (66) previous results on the joint effects of smoking and urban air pollution on lung cancer.

While the evidence on diesel exhaust and lung cancer remains controversial (14, 25, 67–70), there is increasing evidence in favor of the hypothesis. However, there are still few data on the quantitative aspects of the diesel exhaust–lung cancer relation. What the relative risk might be at the low levels found in the general population remains speculative. Indeed, recall that the workers who we considered "unexposed" were in fact exposed to general environmental levels; if such levels in fact carry some excess risk of lung cancer, then our estimates would have underestimated the relative risks compared with a truly unexposed population. Nonetheless, given the complex nature of urban air pollution from diverse mobile and stationary sources, it is unlikely that epidemiologic methods alone will suffice to quantify the relative magnitude of the effects of specific causal components (71). In conclusion, results from this study provide some limited support for the hypothesis of an excess lung cancer risk due to diesel exhaust but no support for an increase in risk due to gasoline exhaust.


   APPENDIX
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 APPENDIX
References
 
The exposure coding in this study was based on not only the occupational codes that workers may be ascribed but also the unique characteristics of the job as related by the worker himself. To illustrate this point, consider four workers who were motor vehicle mechanics and who were all given the same 7-digit code (8581-110) according to the Canadian Classification and Dictionary of Occupations (1971 edition) (72). This 7-digit code applies to workers who repair automobiles, buses, and trucks.

Job 1: This mechanic worked from 1975 to 1984 in a big garage in which 12 mechanics worked on as many as 30 trucks at the same time. In this workplace, there was no venting of engine emissions to the outside. Our team attributed a high confidence score that exposure to diesel exhaust had occurred in this job, that the frequency of exposure was high (e.g., over 30 percent of the workday), and that the exposure concentration would have been high (compared with other jobs in our study).

Job 2: This mechanic worked from 1973 to 1979 in a big garage in which 10 mechanics worked on trucks. There was a policy of venting engine emissions to the outdoors by means of hoses attached to the exhaust pipes. However, the worker reported that there were nevertheless fumes in the garage because the exhaust hoses frequently leaked. Accordingly, our team attributed high confidence and high frequency of exposure to diesel exhaust to this job; however, the concentration was coded as medium rather than high because of the partial venting of fumes.

Job 3: This truck mechanic worked from 1953 to 1965 in a small truck garage that could handle four trucks and in which four mechanics worked at a time. This mechanic indicated that he worked exclusively on gasoline-powered trucks, and, given our knowledge of local conditions in that era, this was quite plausible. However, our experts had sufficient doubt about whether all of the mechanics in the garage would have worked on only gasoline-powered trucks that they coded exposure to diesel exhaust for this worker, but with a low confidence level. This worker's exposure to diesel exhaust would have been sporadic and quite indirect. He was given a frequency code of medium and a concentration code of low.

Job 4: This mechanic worked from 1960 to 1969 in a garage that repaired only automobiles. He was not assigned diesel exhaust exposure at all.

These examples illustrate that exposures were not attributed automatically according to job title. Rather, our experts evaluated the idiosyncratic nature of each job.


   ACKNOWLEDGMENTS
 
This study was supported by research and personnel support grants from Health Canada, the National Cancer Institute of Canada, the Institut de recherche en santé et sécurité au travail du Québec, the Fonds de la recherche en santé du Québec, and a Visiting Scientist Award from the International Agency for Research on Cancer.

The fieldwork was supervised by Lesley Richardson, and the chemical coding was carried out by Dr. Michel Gerin, Dr. Louise Nadon, Denis Begin, and Ramzan Lakhani.

The views set forth in this paper are the authors' and do not necessarily reflect those of the Health Effects Institute or its sponsors.

Conflict of interest: none declared.


   References
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 APPENDIX
 References
 

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