How can race be a cause of something like asthma?

Though I’ve posed this posting around the question of “race and asthma,” the question here isn’t really about public health. It is rather concerned with the general question, how can a group characteristic be a causal factor in enhancing some other group characteristic?

Suppose the facts are these: that African-Americans have a higher probability of developing asthma, even controlling for income levels, education levels, age, and urban-suburban residence. (I don’t know if the facts support this statement, but it is the logic that I am concerned with here.) And suppose that the researcher summarizes his/her findings by saying that “being African-American causes the individual to have a higher risk of developing asthma.” How are we supposed to interpret this claim?

My preferred interpretation of statements like these is to hypothesize a causal mechanism, presently unknown, that influences African-American people differentially and produces a higher incidence of asthma. Here are a few possibilities:

  • (a) African-Americans as a population have a lower level of access to quality healthcare and are more likely to be uninsured. Asthma is a disease that is best treated on the basis of early diagnosis. Therefore African–Americans are more likely to suffer from undiagnosed and worsening asthma. This hypothesis is inconsistent with the assumed facts, however, in that the assertion is that the pattern persists even when we control for income.
  • (b) Asthma is an inner-city disease. It is stimulated by air pollution. African-Americans are more likely to live in inner-city environments because of the workings of residential segregation. So race causes exposure which in turn causes a higher incidence of the disease. (Again, this hypothesis is inconsistent with the stated facts that stipulate having controlled for residence.)
  • (c) There might be an unidentified gene that is more frequent in people with African ancestry than non-African ancestry and that makes one more susceptible to asthma. If this were correct, then we would expect the discrepancy to disappear if we control for frequency of this gene. Groups of white and black people randomly selected but balanced so that the frequency of the gene is the same in both groups should show the same incidence of asthma.
  • (d) It could be that there is a nutritional component to the onset of asthma, and it could be that cultural differences between the two communities lead the African-American population to have higher levels of exposure to the nutritional cause of the disease.

And of course we could proliferate possible mechanisms.

In each case the logic of the account is similar. We proceed by hypothesizing a factor or combination of factors that increase the likelihood of developing asthma; and then we try to determine whether this collalateral factor is more common in the African-American community. Some of these stories would amount to spurious correlations, while others would constitute stories in which the fact of race (as opposed to a factor with which race is accidentally correlated) plays an essential role in the causal story. (Reduced access to healthcare and inner city air pollution fall in this category, since it is institutional race segregation that causes the higher-than-normal frequency of urban residence for African-Americans.)

So this is a potential interpretation of the causal meaning of a statement like “race causes an increased risk of X.” But is this now a fact about individuals or groups? Do the causal interpretations here disaggregate from group to individual? Does “higher incidence in the population” disaggregate onto statements about the factors that influence the individual’s separate risk? It appears that this causal mechanism interpretation does in fact disaggregate to the individual level, since each describes a factor that pertains to the individual and that directly influences his/her likelihood of developing the disease.

What would be most perplexing is if there were multiple sets of causal mechanisms, each independent of the others and each creating a race-specific difference in incidence of the disease. For example, it might be that both exposure to air pollution and lack of health insurance lead to a higher incidence of the disease; and further, it might be that inner-city residents do in fact have adequate healthcare but exposure to inner-city pollution; while suburban African-Americans might have less healthcare and limited exposure to air pollution. In this set of facts, both African-American populations would display higher-than-normal incidence, but for different and unrelated reasons.

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