SYNOPSISObjectives. Optimistic predictions for the Healthy People 2010 goals of eliminating racial/ethnic disparities in health have been made based on absolute improvements in life expectancy and mortality. This study sought to determine whether there is evidence of relative improvement (a more valid measure of inequality) in life expectancy and mortality, and whether such improvement, if demonstrated, predicts future success in eliminating disparities.Methods. Historical data from the National Center for Health Statistics and the Census Bureau were used to predict future trends in relative mortality and life expectancy, employing an Autoregressive Integrated Moving Average (ARIMA) model. Excess mortality and time lags in mortality and life expectancy for blacks relative to whites were also estimated.Results. Based on data for 1945 to 1999, forecasts for relative black:white ageadjusted, all-cause mortality and white:black life expectancy at birth showed trends toward increasing disparities. From 1979, when the Healthy People initiative began, to 1998, the black:white ratio of age-adjusted, gender-specific mortality increased for all but one of nine causes of death that accounted for 83.4% of all US mortality in 1998. From 1980 to 1998, average numbers of
Although nearly all segments of the Black population experienced widened post-HAART disparities, disparities were not inevitable and tended to reflect pre-HAART levels. Public health policymakers should consider the hypothesis of unequal diffusion of the HAART innovation, with place effects rendering some communities more vulnerable than others to this potential problem.
The rationale that underlies the optimistic Healthy People 2010 forecasts, that future success can be built on a foundation of past success, is not supported when relative measures of inequality are used. There has been no sustained decrease in black-white inequalities in age-adjusted mortality or life expectancy at birth at the national level since 1945. Without fundamental changes, most probably related to the ways medical and public health practitioners are trained, evaluated, and compensated for prevention-related activities, as well as further research on translating the findings of prevention studies into clinical practice, it is likely that simply reducing disparities in access to care and/or medical treatment will be insufficient. Millions of premature deaths will continue to occur among African Americans.
Previous reports offer limited support for an association between cigarette smoking and Hodgkin's disease. The authors investigated dose-response effects for smoking in relation to the risk of Hodgkin's disease using data from the Selected Cancers Study. Cases (n = 343) were men aged 32-60 years identified from eight US population-based cancer registries in 1984-1988. Controls (n = 1,910) were men recruited by random digit telephone dialing and frequency matched to cases by age and registry. Conditional logistic regression was used to calculate odds ratios and 95% confidence intervals adjusted for age, registry, race/ethnicity, Jewish upbringing, education, and childhood domicile. Compared with never smokers, current smokers had a significantly increased risk of Hodgkin's disease (odds ratio (OR) = 1.8, 95% confidence interval (CI): 1.3, 2.9). Risks increased linearly (p < 0.001) with increasing packs per day (OR(>or=2) = 2.5, 95% CI: 1.6, 4.0), years (OR(>or=30) = 2.4, 95% CI: 1.5, 3.9), and pack-years (OR(>40) = 2.7, 95% CI: 1.8, 4.3) of smoking. These associations were significant for the nodular sclerosis and mixed cellularity subtypes but were much stronger for mixed cellularity. Stratified analyses by age (42 years) and subtype suggested that the effects of smoking are more closely related to histology than age. In contrast to findings from previous studies, these data suggest that smoking is an important preventable risk factor for Hodgkin's disease.
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