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Background: Consistent evidence has shown increased all-cause mortality, and mortality from broad categories of causes associated with airborne particles. Less is known about associations with specific causes of death, and modifiers of those associations. Aims: To examine these questions in 20 US cities, between 1989 and 2000. Methods: Mortality files were obtained from the National Center for Health Statistics. Air pollution data were obtained from the Environmental Protection Agency website. The associations between daily concentrations of particulate matter of aero-diameter ⩽10 μm (PM10) and daily mortality from all-cause and selected causes of death, were examined using a case-crossover design. Temporal effects of PM10 were examined using lag models, in first stage regressions. City specific modifiers of these associations were examined in second stage regressions. Results: All-cause mortality increased with PM10 exposures occurring both one and two days prior the event. Deaths from heart disease were primarily associated with PM10 on the two days before, while respiratory deaths were associated with PM10 exposure on all three days. Analyses using only one lag underestimated the effects for all-cause, heart, and respiratory deaths. Several city characteristics modified the effects of PM10 on daily mortality. Important findings were seen for population density, percentage of primary PM10 from traffic, variance of summer temperature, and mean of winter temperature. Conclusions: There was overall evidence of increased daily mortality from increased concentrations of PM10 that persisted across several days, and matching for temperature did not affect these associations. Heterogeneity in the city specific PM10 effects could be explained by differences in certain city characteristics.

Objectives The objective of this work was to apply the two-stage clonal expansion model, with the intention to expand the literature on epidemiological applications of the model and demonstrate the feasibility of incorporating biologically based modelling methods into the widely used retrospective cohort study. Methods The authors fitted the two-stage clonal expansion model model to three occupational cohort studies: (1) a cohort of textile workers exposed to asbestos and followed for lung cancer mortality; (2) a cohort of diatomaceous earth workers exposed to silica and also followed for lung cancer mortality; and (3) a cohort of automotive manufacturing workers exposed to straight metalworking fluid (MWF) and followed for larynx cancer incidence. The model allowed the authors to estimate exposure effects in three stages: cancer initiation (early effects), promotion or malignant transformation (late effects). Results In the first cohort, the authors found strong evidence for an early effect of asbestos on lung cancer risk. Findings from analyses of the second cohort suggested early and less evidently late effects of silica on lung cancer risk. In the MWF (third) cohort, there was only weak evidence of straight MWF exposure effects on both early and late stages. The authors also observed a late birth cohort effect on larynx cancer risk. Conclusions The findings for asbestos and silica were essentially confirmatory, supporting evidence for their earlyeffects onlung cancer from alargebody of literature. TheeffectofstraightMWFonlarynxcancerwaslessclear.

Aims: To re-examine aerodigestive cancer risk in a cohort of autoworkers exposed to metal working fluids (MWF), using improved case definition and more recently diagnosed cases. Methods: The autoworker cohort included 31 100 hourly workers alive on 1 January 1985 who worked at three automobile plants in Michigan. A case-cohort design was carried out that included incident cases of cancers of the larynx, oesophagus, and stomach, and a 10% sample of the cohort. A Cox proportional hazards model was used to estimate MWF exposure effects. The smoothing method of penalised splines was used to explore the shape of the underlying exposure-response curves. Results: The most important finding was the association between larynx cancer incidence and cumulative straight MWF exposure. The results for oesophageal cancer were less consistent. For stomach cancer there was no evidence of excess risk. Conclusion: This association between larynx cancer and straight MWF exposures was consistent with a previous finding in this cohort, providing further support for a causal relation.