The Washington University-EPRI veterans' cohort mortality study: Preliminary results

This article presents the design of and some results from a new prospective mortality study of a national cohort of about 50,000 U.S. veterans who wer e diagnosed as hypertensive in the mid 1970s, based on approximately 21 yr of follow-up. This national cohort is male with an average age at recruitme nt of 51 +/- 72 yr; 35% were black and 81% had been smokers at one time. Be cause the subjects have been receiving care at various U.S. Veterans Admini stration (VA) hospitals, access to and quality of medical care are relative ly homogeneous. The health endpoints available for analysis include all-cau se mortality and specific diagnoses for morbidity during VA hospitalization s; only the mortality results are discussed here. Nonpollution predictor va riables in the baseline model include race, smoking (ever or at recruitment ), age, systolic and diastolic blood pressure (BP), and body mass index (BM I). Interactions of BP and BMI with age were also considered. Although this study essentially controls for socioeconomic status by design because of t he homogeneity of the cohort, selected ecological variables were also consi dered at the ZIP code and county levels, some of which were round to be sig nificant predictors. Pollutants were averaged by year and county for TSP, P M10, CO, O-3 and NO2; SO2 and Pb were considered less thoroughly. Both mean and peak levels were considered for gases. SO42- data from the AIRS databa se and PM2.5, coarse particles, PM15, and SO42- from the U.S. EPA Inhalable Particulate (IP) Network were also considered. Four relevant exposure peri ods were defined: 1974 and earlier (back to 1953 for TSP), 1975-1981, 1982- 1988, and 1989-1996. Deaths during each of the three most recent exposure p eriods were considered separately, yielding up to 12 combinations of exposu re and mortality periods for each pollutant. Associations between concurren t air quality and mortality periods were considered to relate to acute resp onses; delayed associations with prior exposures were considered to be embl ematic of initiation of chronic disease. Preexposure mortality associations were considered to be indirect (noncausal). The implied mortality risks of long-term exposure to air pollution were found to be sensitive to the deta ils of the regression model, the time period of exposure, the locations inc luded, and the inclusion of ecological as well as personal variables. Both positive and negative statistically significant mortality responses were fo und. Fine particles as measured in the 1979-1984 US. EPA Inhalable Particul ate Network indicated no significant (positive) excess mortality risk for t his cohort in any of the models considered. Among the positive responses, i ndications of concurrent mortality risks were seen for NO2 and peak O-3, wi th a similar indication of delayed risks only for NO2. The mean levels of t hese excess risks were in the range of 5-9%. Peak O-3 was dominant in two-p ollutant models and there was some indication of a threshold in response. H owever, it is likely that standard errors of the regression coefficients ma y have been underestimated because of spatial autocorrelation among the mod el residuals. The significant variability of responses by period of death c ohort suggests that aggregation over the entire period of followup obscures important aspects of the implied pollution-mortality relationships, such a s early depletion of the available pool of those subjects who may be most s usceptible to air pollution effects.