Department of Epidemiology School of Public Health University of North Carolina at Chapel HillChapel Hill, NC 27599
Department of Preventive Medicine and Epidemiology Stritch School of Medicine Loyola University Maywood, IL 60153
The strategy of adjusting racial differentials for measures of social status to separate the "biologic" and "nonbiologic" pathways that produce these disparities has elicited significant criticism. The problems are numerous: Causal parameters for race effects of interest are not well defined (1). Deficiencies in the specification or measurement of causal intermediates can lead to spurious apparent race effects (2
). Measured intermediates are inherently inadequate because of incommensurability of social measures between racial groups (3
). Adjustment is made for factors that are causally subsequent to exposure (4
). Finally, even if race were considered a meaningful "exposure" and assumed (however absurdly) to be essentially randomized to individuals, this assumption would be sufficient only to identify total effects of race; effects transmitted through direct or indirect pathways still would not be separately identifiable without additional, unrealistic assumptions about factors affecting both measured intermediates and disease outcome (5
, 6
).
Despite these and other criticisms, the inferential strategy of positing biologic race effects by adjusting for social factors is unfortunately still quite commonly used. The paper by Robbins et al. in a recent issue of the Journal (7) seems to be distinguished from others in this category by the authors' many stated caveats and reservations, some of which appear self-contradictory. The authors agreed that there were serious problems with the analytical approach they pursued, but they nonetheless concluded that their results were "...consistent with the hypothesis that racial differences in rates of death from prostate cancer are due to biologic factors" (7, p. 414). The authors focused on their finding that the adjusted death rate ratio comparing Blacks with Whites was "larger" among younger men than among older men, even though the estimate for the older men (relative risk = 1.20) fell within the 95 percent confidence interval for the younger men (95 percent confidence interval: 1.15, 1.72) (7, table 2). In addition, since the death rate rises with age, a greater rate ratio may mean a smaller rate difference among the younger men (6
). The authors further stated that differences in ecologic socioeconomic status measures "accounted" for 100 percent of the racial difference in rates of death from causes other than prostate cancer among older men (ages
65 years) (7, p. 413). The reader is left to speculate as to whether taking older Black men from the poorest 15 percent of the census tracts and simply relocating them to the wealthiest 15 percent of the census tracts would really give these men survival probabilities equal to those of Whites for all causes of death other than prostate cancer.
Robbins et al. provided an extensive discussion of the weaknesses inherent in their methodological approach; nonetheless, they felt justified in speculating that Black men of all ages have some biologic (genetic?) abnormality, manifested as "more virulent tumors" of the prostate, which "explains" the observed survival disparity in prostate cancer mortality. Making an informal Bayes-like calculation in reverse, we can surmise only that the posterior emphasis on "biologic" differences between racial groups in this study, given methods so admittedly weak that they should not be very influential in transforming one's beliefs, implies that the authors began with a strong prior preference for "biologic" explanations. The pattern of higher incidence and shorter survival among Blacks compared with Whites, especially at younger ages, is not restricted to prostate cancer but is seen for many other common conditions, including hypertension, diabetes mellitus, coronary heart disease, stroke, breast cancer, and lung cancer, to name but a few. Although attributing the racial differentials for each of these conditions to "biologic factors" may sound plausible if the conditions are considered one at a time, the overall pattern is most compatible with Black exposure to a higher-risk social and physical environment. Robbins et al. ignore this obvious prior constraint on their etiologic conclusions.
REFERENCES
Department of Health Research and Policy Stanford University School of Medicine Stanford, CA 94305
Some lay people and scientists believe that social and environmental factors can completely explain racial and ethnic differences in rates of disease and death. This appears to be the case in the letter by Kaufman et al. (1), which pointedly repeats the limitations to causal inferences discussed at length in our paper (2
). Without presenting any supporting data, Kaufman et al. give a list of conditions for which they assert that the higher incidence and mortality of African Americans is "most compatible with Black exposure to a higher-risk social and physical environment" (1
). It is noteworthy that their list excludes sickle cell anemia. Also noteworthy is the absence of conditions such as cutaneous malignant melanoma and epithelial ovarian cancer, for which the death rates in African Americans are lower than those in Whites, and for which the racial differences cannot be explained by known environmental risk factors (3
). As a factual point, it must be noted that the words "genetic" and "abnormality," which the authors suggest we would invoke as a speculative explanation for the higher prostate cancer mortality in Blacks, do not appear in our paper.
We observed a sharp difference in the effect of adjustment for socioeconomic status (SES) on Black-White death rate ratiosa very large effect of SES adjustment for causes of death other than prostate cancer versus little effect of SES adjustment for death from prostate cancer. It was this observation, and not "a strong prior preference" as asserted by Kaufman et al., that led to the conclusions in our paper. On the contrary, we would have actually preferred to find that SES-associated differences entirely explained the elevated Black-White death rate ratios for death from prostate cancer as well as for death from other causes. The path toward a potential solution would have been clearer, since there are a number of potentially modifiable factors associated with SES, such as diet, physical activity, medical care, and level of social support.
Our data are consistent with the hypothesis that race-related biologic differences contribute to higher prostate cancer mortality in Blacks. We hope that our presenting these data will lead to further investigation resulting in a better understanding of the biology of prostate cancer, and ultimately a reduction in mortality for both Black and White men. To not allow for the possibility of a biologic basis for these results would be scientifically unwarranted.
REFERENCES