Lung cancer risk after exposure to polycyclic aromatic hydrocarbons: a review and meta-analysis

Environmental Health Perspectives, June 15, 2004 by Ben Armstrong, Emma Hutchinson, John Unwin, Tony Fletcher

We excluded the following:

* Studies of workplaces where PAHs were considered unlikely to be the predominant lung or bladder carcinogen, to reduce potential for confounded results. Such workplaces included those in the rubber industry; those where primary exposure was from diesel exhaust; foundries; and steel works (because of co-exposure to silica), unless there were separate analyses specifically of coke oven workers.

* Studies for which it was not possible to quantify exposure to PAHs. Hospital--and population-based case-control and registry studies were excluded for this reason.

* Studies of occupational exposure other than by inhalation.

* Superceded publications. Where repeated follow-ups of the same workforce were reported in several articles, only the most recent was included.

* Biomarker studies because it was difficult to deduce relationships of exposure concentration to cancer incidence.

* Proportional cancer analyses.

* Articles not written in English.

After these exclusions, 34 articles remained, of which 5 reported two distinct cohorts for which results were presented separately. Thus, there were 39 cohorts. For each included cohort we systematically extracted general descriptive information, information on potential modifiers of risk associated with PAHs, and information from which we estimated unit relative risk (URR) increments (see next two subsections).

Exposure Estimation

We distinguished studies according to author reports of the following:

* exposures to PAHs measured as BaP (10 cohorts)

* exposures to PAHs measured by a proxy that we could convert to BaP: benzene soluble matter (BSM), total PAHs, carbon black (6 cohorts)

* no measures of exposure (n = 23 cohorts)

For those studies with no exposure measures, we estimated exposure to PAHs for each workgroup for which cancer risk estimates were presented (e.g., for top-oven workers, side-oven workers). These exposure estimates were based on published exposure estimates in the same industries (IARC 1984; Lindstedt and Sollenberg 1982) and other published epidemiologic studies. Principle estimates thus derived are presented in Table 1.

Cumulative exposure. We sought to relate cancer risk to mean cumulative exposures to BaP (duration x time-weighted mean concentration). Where risk by cumulative exposure was not published, it was derived as the product of mean estimated concentration of exposure in each group for which risk was reported and the mean duration of exposure in that group. In the absence of information on duration of exposure, 20 years was assumed, representing the average found in studies for which duration was reported.

Dust exposure. At the inception of this study, we had not planned to seek information on potentially confounding exposures beyond those noted by the authors. However, interest has sharply increased recently in the hypothesis that inhaled dust carries a risk of lung cancer regardless of composition. We therefore sought to add information that we could find on dust exposure. Because few publications reported such estimates, we relied entirely on supplementary data and the judgment of the hygienists on the research team. We were aware that this would be a very rough assessment and chose a simple scale [low (< 1 mg/[m.sup.3] total dust); moderate (1-5 mg/[m.sup.3]); high (5-10 mg/[m.sup.3]); very high (10-25 mg/[m.sup.3])] and broad job groups or, in some cases, entire industries. Assessments are listed in the final column of Table 1. A list of references on which assessments were based is included in Appendix B4 of the full research report (Armstrong et al. 2002).