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The analysis by Ahern et al of risk factors for preterm birth among African American and white women in San Francisco1 concluded that pregnant African American smokers are more prone to preterm delivery than white pregnant smokers. This conclusion is misleading. Firstly, the evidence of interaction between smoking and ethnicity was unconvincing—the difference in the odds ratios (ORs) was modest, and confidence intervals (CI) overlapped considerably (African American women: OR 1.77, 95% CI 1.12 to 2.79; white women: OR 1.25, 95% CI 1.01 to 1.55). Secondly, the authors did not consider residual confounding by factors such as maternal infection and previous preterm birth, which differ by ethnic group.2,3 Their assumption that the smoking-preterm birth association is linear seems biologically unlikely and problematic, as African American women in their study population smoked more than white women.
Such analyses raise a more fundamental issue: the limitations of using ethnicity/race in epidemiological studies of causality. There is no consensus as to what “ethnicity” means. To some, “ethnicity” describes cultural differences between populations definable by phenotype, while “race” signifies differences strictly under genetic influence. This separation is imperfect—“ethnic groups” differ in genetic mix, culture, and socioeconomic situation. The “catch all” quality of ethnicity makes its use in epidemiological research attractive, but is an obstacle to causal inference. Ethnic groups have qualitative and contextual differences that do not make them directly comparable. …