- Email: [email protected]
Heterogeneity of risk within racial groups, a challenge for public health programs
Preventive Medicine 55 (2012) 405–408
Contents lists available at SciVerse ScienceDirect
Preventive Medicine journal homepage: www.elsevier.com/locate/ypmed
Heterogeneity of risk within racial groups, a challenge for public health programs Sean A. Valles ⁎ Lyman Briggs College and Department of Philosophy, Michigan State University, Holmes Hall, 919 E. Shaw Lane, Room W25-C, East Lansing, MI 48825, USA
a r t i c l e
i n f o
Available online 8 September 2012 Keywords: Bioethics Cystic fibrosis Hypertension Population groups Genetic testing Diet Sodium-restricted
a b s t r a c t Targeting high-risk populations for public health interventions is a classic tool of public health promotion programs. This practice becomes thornier when racial groups are identified as the at-risk populations. I present the particular ethical and epistemic challenges that arise when there are low-risk subpopulations within racial groups that have been identified as high-risk for a particular health concern. I focus on two examples. The black immigrant population does not have the same hypertension risk as US-born African Americans. Similarly, Finnish descendants have a far lower rate of cystic fibrosis than other Caucasians. In both cases the exceptional nature of these subpopulations has been largely ignored by the designers of important public health efforts, including the recent US government dietary recommendations. I argue that amending the publicly-disseminated risk information to acknowledge these exceptions would be desirable for several reasons. First, recognizing low-risk subpopulations would allow more efficient use of limited resources. Communicating this valuable information to the subpopulations would also promote truth-telling. Finally, presenting a more nuanced empirically-supported representation of which groups are at known risk of diseases (not focusing on mere racial categories) would combat harmful biological race essentialist views held by the public. © 2012 Elsevier Inc. All rights reserved.
Introduction Public health interventions are often targeted to identifiable highrisk populations. This raises philosophical issues such as what it means for a population to be at risk and what ethical considerations should guide programs. These challenges become considerably more complex when the target populations are racial groups. As Troy Duster lays out in a 2006 paper on the use of race in medicine: The unenviable task has been to try to walk a tightrope—to figure out a way to effectively deploy in research the concept of race (or population groups designated by race) without endowing “race” with a false sense of genetic essentialism (Duster, 2006, p. 488). This danger is a quite real one, as misperceptions of the biological basis of race abound in the United States. More importantly, psychological data suggests, “[the] belief that social categories have an underlying nature/natural foundation” is one central basis for the formation and endorsement of stereotypes and prejudice” (Keller, 2005, pp. 686, 699). On the other hand, “this implies that one possible way of combating stereotyping and prejudice is to challenge the belief in genetic determinism and biological essentialism” (Keller, 2005, p. 699). The danger of promoting race essentialism (the view that racial categories demarcate deep intrinsic similarities among members of a race and corresponding
⁎ Corresponding author. Fax: +1 517 432 2758. E-mail address: [email protected]. 0091-7435/$ – see front matter © 2012 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.ypmed.2012.08.022
differences between members of different races) does not automatically preclude the public application of race categories in medicine – Nancy Krieger has effectively argued why entirely ignoring race would “preclud[e] possibilities for monitoring progress and setbacks in reducing” “racial/ethnic inequalities” (2000, p. 213) – but that danger should be a guiding ethical consideration during deliberations about such medical uses. I will show how information about racial groups' disease risks has been mishandled in two cases and make recommendations for ameliorating those missteps. In both cases, the designers of public health efforts have downplayed data that complicates their broad statements about racial groups being at elevated risk for particular diseases. I will focus on the black immigrant exception to the high rates of hypertension among African Americans and the Finnish exception to the high rates of cystic fibrosis among Caucasians. In these two cases there is ample data to support more nuanced (yet still simple and practical) characterizations of the at-risk populations—US-born African Americans are at elevated risk of hypertension and non-Finnish Caucasians are at elevated risk of cystic fibrosis. Yet, the unmodified racial categories continue to be used instead. This creates the unique situation in which low-risk subpopulations have had their interests marginalized during the propagation of broad claims about race-wide disease risks. Hence, we have two distinct problems that overlap in practice: the problem of ignoring low-risk islands within seas of high risk (so to speak) and the problem of privileging mere race when delineating which populations have public health risks. Together, the two problems combine to impede the dissemination of more nuanced data about heterogeneity of risk within racial groups.
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S.A. Valles / Preventive Medicine 55 (2012) 405–408
I will argue that using available data to present more nuanced/specific representations of the relevant at-risk populations, beyond statements about racial groups broadly, would yield substantial benefits and also mitigate some of the harms associated with using race in medicine. Further nuance would preempt public overestimates of the biomedical significance of race, better serve the interests of the low-risk Finnishdescended and black immigrant subpopulations, improve the efficiency of public health resource usage (e.g. funds for testing people for recessive cystic fibrosis mutations) and promote truth-telling—the race-level data now provided is technically true, but is misleading for the low-risk subpopulations unless accompanied by the more nuanced available information. While I focus on analyzing the two aforementioned cases, the analysis suggests that more attention to low-risk subpopulations is warranted and that the privileging of data at the level of broad racial categories is an important obstacle to pursuing more nuanced representations of the heterogeneity of risk within racial categories. The problem of heterogeneity of risk Katherine Frohlich and Louise Potvin raise the problem of withinpopulation heterogeneity of risk in their critique of Geoffrey Rose's influential “population strategy” of public health programs, which emphasizes small reductions of harm across entire populations, rather than large reductions of harm within limited high-risk subpopulations, the “high-risk strategy” (Frohlich and Potvin, 2008; Rose, 1992). It is beyond the scope of this paper to address the general merits of Rose's approach or of Frohlich and Potvin's critique, but I would like to highlight Frohlich and Potvin's observation about the problem of subpopulations with varying experiences/risks. They argue that Rose's approach can effectively erect blinders that prevent public health practitioners from detecting and addressing underlying causal complexities: “moderate correlations between several risk factor exposures in the general population may mask highly differentiated experiences in specific subpopulations” (Frohlich and Potvin, 2008, p. 219). A statistical correlation or average at the level of a large population can conceal enormous variability among its subpopulations. Interestingly, Rose himself worries about a similar problem, noting that individual experiences will vary in unpredictable ways among members of even a well-established at-risk subpopulation (Rose, 1992, pp. 49–50). Rose sees substantial weaknesses in the high-risk strategy, but notes that two of its main advantages are its potentially “cost-effective use of resources” and its favorable “benefit-to-risk ratio” when interventions carry some risk of harmful side effects (Rose, 1992, pp. 44–46). Both are advantages of targeting resources to those who stand to benefit the most, even if there is still unpredictable heterogeneity of risk within that group. However, if we lump in known low-risk populations with known high-risk populations during the crafting of interventions then we lose both benefits. This is problematic even within a utilitarian view of public health ethics, seeking to maximize net health benefits within a given group of people (a common general approach among public health practitioners). We would be spending resources (e.g. subsidizing testing) on subpopulations that have little need for such resources, while also exposing that subpopulation to any undesirable side effects (e.g. spending additional personal funds on a special diet). Dietary salt among African Americans The joint U.S. Department of Agriculture and Health and Human Services publication Dietary Guidelines for Americans 2010 recommends a reduced-sodium diet for all African Americans, responding to a large body of data identifying the group as having relatively high risk of hypertension and its various cardiovascular sequelae, including stroke (Read et al., 2005). Reduce daily sodium intake to less than 2300 milligrams (mg) and further reduce intake to 1500 mg among persons who are 51 and
older and those of any age who are African American or have hypertension, diabetes, or chronic kidney disease (US Department of Agriculture and US Department of Health and Human Services, 2010, p. x). The problem is that this clumsily portrays African-Americanness, (and by implication, Africanness) as a weighty biological and medical category, on par with being diabetic. Race and bioethics scholar Osagie Obasogie drew attention to this advice in a recent article for Slate, highlighting the problem of its tacit support for biological race essentialism (2011). Still, it is at least conceivable that the recommendation's implied support for biological race essentialism could be justified on the grounds that it is an accurate and practically useful representation of salt-related disease risks. It is not. Highlighting the problem of heterogeneity of risk among subpopulations, Read et al. point out that the well-known broad “black-white health disparities” actually conceal substantial “heterogeneity in the health status of black Americans”, especially the variation introduced by black immigrants (2005, p. 205, 208). According to a longitudinal study of 300,910 subjects, “foreign-born non-Hispanic blacks” had strikingly lower hypertension rates than “US-born non-Hispanic blacks”, 16.75% vs. 25.45% (Singh and Siahpush, 2002, p. 89). In fact, when adjusted for income, age, etc., “black immigrants had… 55% lower mortality from [cardiovascular disease] than US-born whites” (Singh and Siahpush, 2002, p. 97). 1 The causes of the foreign-born vs. US-born disparity remain hazy. A meta-analysis of the data on immigrants' blood pressure changes demonstrates that “acculturation to Western society is a risk factor for increased [blood pressure]”, and that “the majority of the acculturation effect appears to happen within the first 3 years of interaction with the new culture” (Steffen et al., 2006, p. 394). However, according to the previously mentioned longitudinal study, even those immigrating more than 15 years ago were still “19% less likely to report having high blood pressure than their US-born counterparts”, suggesting that acculturation during the early years of US residency has a limited effect on diminishing the disparity (Singh and Siahpush, 2002, p. 101). Overall, existing research suggests that black immigrants, on average, simply do not seem to be at the same elevated risk of hypertension (among other cardiovascular diseases) as US-born blacks, so it is problematic to create a dietary public health intervention that fails to distinguish between the two groups. 2 One could object that the dietary guidelines partly address my concern about promoting naive biological essentialism through using the term “African American”, which it leaves undefined, but is interpretable as a largely sociocultural term that could exclude most black immigrants. But, the fact that “African American” has a hazy and debatable mixture of racial, ethnic and cultural connotations means that, for example, a Nigerian-born permanent resident of the US would be forced to decipher whether the term applies to him or her. It is a term, after all, that is used alongside “black” and “negro” in the “race” section of the 2010 US census form. In short, imprecision is the problem here, not the solution. Cystic fibrosis risk among Finnish descendants During debates over the benefits and drawbacks of using race in medicine, discussion almost always focuses on minority or underprivileged groups. Indeed, this is a good thing. However, misapplications 1 Philosopher of science Jonathan Kaplan uses similar data (also co-authored by Singh) to undermine genetic arguments for black-white health disparities (Kaplan, 2010; Singh and Miller, 2004). 2 Even under the controversial “slavery hypothesis”, according to which African slaves underwent a unique natural selection event favoring the increased storage of dietary salt during the deadly transatlantic voyage, black immigrants are still deserving of special consideration (Kaufman and Hall, 2003). By hypothesis, they would be genetically distinct from the US-born descendants of slaves.
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of blunt racial categories can also harm white residents of the United States or Europe. Whiteness/Caucasianness is no less hazy a category than African Americanness, so it should come as no surprise that misapplications of the Caucasian racial category in medicine can lead to serious problems. In this case I will focus on the partly misleading representation of Caucasianness as a risk factor for cystic fibrosis. The recessive genetic disease cystic fibrosis, a lethal condition damaging lung function (among many other effects), is “often characterized as a ‘white’ disease though it occurs in many populations” (Lindee and Mueller, 2011, p. 317). Its representation as a “‘white’ disease” is based on the striking variation in cystic fibrosis rates across world populations. In general, Caucasians have cystic fibrosis rates of ~1/2500, which is many times greater than the rate of ~1/40,000–1/100,000 in India, to choose just one example (Langfelder-Schwind et al., 2005, p. 10; Calafell et al., 2004, p. 15). The data indeed support an association between cystic fibrosis risk and Caucasianness/whiteness. But, the association does not hold uniformly across all Caucasian subpopulations. People of Finnish ancestry have a cystic fibrosis rate of ~1/25,000, ten times lower than the rate for Caucasians in general (Calafell et al., 2004, p. 15). This exceptionally low rate within a substantially sized and identifiable Caucasian subpopulation clearly undermines portrayals of Caucasianness per se as a risk factor for cystic fibrosis.3 Strangely, two recent sets of recommendations about cystic fibrosis testing, both from major North American medical organizations, ignore or downplay the Finnish-descended subpopulation in their recommendations. This is unfortunate, as the costs of testing individuals for the recessive mutations (such as when a couple is planning conception) are substantial. According to a 2008 review, “cost per test… ranged from US$28 to US$240” – cheaper versions of the tests yield more false negatives – in addition to the variable additional costs of advertising, pre- and post-test counseling, etc. (Radhakrishnan et al., 2008, p. 141–142). Though, those figures do not reflect costs such as the discomfort of undergoing medical tests, the stress of waiting for results, etc. This set of costs is not trivial, and the expected benefits for Finnish descendants are low. A recent statement by the American College of Obstetricians and Gynecologists on carrier screening for cystic fibrosis discusses the different frequencies among various races/ethnicities: “cystic fibrosis is most common in non-Hispanic white individuals and people of Ashkenazi Jewish ancestry”, yet points out, “it is becoming increasingly difficult to assign a single ethnicity to individuals”, and so, “it is reasonable, therefore, to offer CF carrier screening to all patients” (Committee on Genetics, 2011, p. 1030). The advice, then, is that carrier screening should be offered to all, but that the expected benefits will vary depending on the patient's background. But the statement does not mention Finnish-descended patients' anomalously low rate. A similar statement by the National Society of Genetic Counselors mentions the low rate among Finnish descendants, which is encouraging, but then oddly sets the phenomenon aside (Langfelder-Schwind et al., 2005). The text dismisses the existing data regarding heterogeneous rates within large populations, saying, “it is difficult to determine precisely which ethnic subgroup to assign a patient, and reliable risk data is not available for many populations”, so, “genetic counselors are urged to use” the text's “reliable” chart, listing a single carrier (heterozygote) frequency for “Caucasian:” 1/25 (Langfelder-Schwind et al., 2005, p. 10). But, the carrier frequency for Finnish Caucasians is approximately 1/77 (Kere et al., 1989). The statement is correct that there is little or no data on cystic fibrosis prevalence data for many subpopulations, yet the Finn-specific phenomenon has been established for decades (Kere et al., 1989; Calafell et al., 2004). Even if the specific detection and error rates for tests of Finnish descendants are not so firmly established, those Finnish descendants still deserve to know about the strikingly low benefits of getting tested in the first place. 3 Middle eastern and Ashkenazi Jewish populations introduce additional classificatory and demographic complexities, raise another set of complications that, unfortunately, cannot be adequately addressed here.
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The National Society of Genetic Counselors' resistance to contending with the unique Finnish subpopulation is incompatible with its conclusion. To some patients, [cystic fibrosis] screening may provide an opportunity that can give them important information about a current or future pregnancy. To others, it may provoke unwelcome anxiety or require a painful decision about the pregnancy. Genetic counselors will play an important role in providing information and support sufficient to allow people to make choices that are consistent with patient values and based on the best available information (Langfelder-Schwind et al., 2005). I fully endorse this conclusion, especially the importance of genetic counselors using the “best available information”. But, in the cases of both the American College of Obstetricians and Gynecologists (which ignores Finns entirely) and the National Society of Genetic Counselors (which mentions Finns then sidelines them), this goal has been held back by a narrow focus on representing disease risk data at the Caucasian/white level, even when more specific and directly relevant evidence is available. Failing to disseminate the information about Finnish descendants is both wasteful of resources and obstructs truth-telling. Finnishdescended patients are not being provided with the most relevant risk data available, meaning that they (and their physicians) are likely to make their testing decisions based on the relatively well-disseminated Caucasian high-risk data.4 This leads to cost-benefit analyses assuming an overestimated benefit. Thus, information about Finnish descendants' cystic fibrosis risk is being downplayed by the very organizations that should be actively disseminating it. Choosing a level of specificity Any demand for recognition of a further level of specificity in delineating a public health target population invites two important questions: 1) why increase the level of specificity beyond its current level? and 2) why stop at this level of specificity and not some other level? The first question has several answers. Increasing the specificity of at-risk population characterizations corrects the misleading, though not technically false, risk assessments communicated to low-risk subpopulations. Unnecessarily blunt assessments of race-wide risks engender wasteful use of resources, such as funds for cystic fibrosis carrier testing or the personal funds/ effort required to follow a very low-sodium diet. They also obstruct truth-telling, as important information has not been provided to patients. These harms are consequences of imprecision, though they are generic in the sense that similar harms would result from any sort of miscommunication of a subpopulation's risk. However, race brings in a unique challenge: racial categories themselves are problematic even prior to their application in public health contexts. A separate benefit of raising the level of specificity beyond the level of racial categories is that it not only fails to bolster naive biological race essentialism, it actively undermines it. Race essentialism is a concept that does not easily admit complications or exceptions. A small adjustment to the list of vulnerable populations needing decreased dietary salt would make all the difference in the support or rejection of biological essentialism for African descendants. Simply changing “African Americans” to “US-born African Americans” would actually help to correct the misguided essentialism so prevalent among Americans. It would deny the homogeneity of African Americans while simultaneously blunting the particular representation of African Americanness, 4 If we rely on Finnish descendants to self-identify (an imperfect system, though standard practice in the collection of demographic data) then we would also limit the problem of increasing costs through pursuing the added specificity. Systematically checking Caucasian patients for Finnish ancestry would not be entirely free, but it would presumably be very low-cost.
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and by implication all Africanness, as a negative biomedical trait. It seems that the strongest defense of the status quo here is that public health programs, especially public education programs, demand simplicity; we are better off keeping the story simple than complicating it and confusing the audience. I argue that adding only a small measure of increased complexity would yield disproportionately large benefits. The remaining question is why, for example, we should specify US-born vs. foreign-born in dietary salt recommendations and not specify even further. In principle, one could always demand more and more specificity in delineating which populations are really the at-risk/vulnerable ones (see discussion in Rose, 1992, p. 49–50). For example, there is data suggesting that black immigrants from Africa are generally healthier than black immigrants from the West Indies, who are in turn healthier than black immigrants from Europe (Read et al., 2005). In practice, though, increasing specificity cannot go on ad infinitum—limitations of data availability and pragmatic effectiveness intervene. For example, in the Read et al. data, the study's quite small sample of black European immigrant subjects weakens the inferences we can make about the black European immigrant population generally (2005). In the cystic fibrosis case, even if it were statistically feasible, it would not be practical to expect Finnish-descended patients to consult a massive diagram of the differing relative risks for inhabitants of various regions of Finland and then decide (according to their family histories) whether to pursue cystic fibrosis testing. My recommendation is not that we increase the target population specificity to recognize Finnish descendants and black immigrants and then immediately stop. My plea is that our specificity must go at least that far. We should at least amend dietary salt guidelines to reflect that the risk is for “US-born African Americans” and cystic fibrosis testing literature to reflect that the known risk is for “non-Finnish Caucasians”. Once these public health programs escape from overreliance on mere race then any further calls for specificity can be handled on a case-by-case basis. Conclusion Mere race has been treated as a privileged level of specificity in defining cardiovascular disease risk and cystic fibrosis risk. This is quite unfortunate. Of all the possible levels of population specificity, race is probably the choice that introduces the most unintended harm, primarily due to its tacit reinforcement of biological race essentialism. Adding one more level of specificity beyond mere race would leave the target population delineations simple enough to be accessible to laypeople and also limit the socially detrimental side-effects of using racial categories in medicine. In fact, it offers an opportunity to combat prejudice through undercutting essentialism. It is important to stress that this paper is not a call to rewrite science for political ends. Rather, it is a call for biomedical experts to responsibly use the scientific data already available to them. I focus on only the two aforementioned cases, but believe that these two cases point to larger problems with the unconscious privileging of broad racial categories
in the reporting of public health information, and particularly the potential harms that result from (unconsciously) concealing information about low-risk subpopulations. Conflict of interest statement The author declares there is no conflict of interest.
Acknowledgments I have been greatly aided by feedback from Jim Nelson, Lisa Lloyd, Ryan Ketcham, Andrea Smith, Kristie Dotson, the participants of the 2012 UT-Dallas Science-Policy Interactions and Social Values Conference and this journal's two anonymous reviewers. References Calafell, F., Cutting, G., Dodge, J., Des Georges, M., Dörk, T., Durie, P., et al., 2004. The Molecular Genetic Epidemiology of Cystic Fibrosis: Report of a Joint Meeting of WHO/ECFTN/ICF(M)A/ECFS Genoa, Italy, 19 June 2002 World Health Organization. Chronic Diseases and Health Promotion, Human Genetics Programme, Geneva. Committee on Genetics, 2011. Update on carrier screening for cystic fibrosis. Obstet. Gynecol. 117, 1028–1031. Duster, T., 2006. Lessons from history: why race and ethnicity have played a major role in biomedical research. J. Law Med. Ethics 34, 487–496. Frohlich, K.L., Potvin, L., 2008. Transcending the known in public health practice—the inequality paradox: the population approach and vulnerable populations. Am. J. Public Health 98, 216–221. Kaplan, J.M., 2010. When socially determined categories make biological realities: understanding black/white health disparities in the U.S. Monist 93, 281–297. Kaufman, J.S., Hall, S.A., 2003. The slavery hypertension hypothesis: dissemination and appeal of a modern race theory. Epidemiology 14, 111–118. Keller, J., 2005. In genes we trust: the biological component of psychological essentialism and its relationship to mechanisms of motivated social cognition. J. Pers. Soc. Psychol. 88, 686–702. Kere, J., Norio, R., Savilahti, E., Estivill, X., de la Chapeile, A., 1989. Cystic fibrosis in Finland: a molecular and genealogical study. Hum. Genet. 83, 20–25. Krieger, N., 2000. Refiguring “race”: epidemiology, racialized biology, and biological expressions of race relations. Int. J. Health Serv. 30, 211–216. Langfelder-Schwind, E., Kloza, E., Sugarman, E., Pettersen, B., Brown, T., Jensen, K., et al., 2005. Cystic fibrosis prenatal screening in genetic counseling practice: recommendations of the national society of genetic counselors. J. Genet. Couns. 14, 1–15. Lindee, S., Mueller, R., 2011. Is cystic fibrosis genetic medicine's canary? Perspect. Biol. Med. 54, 316–331. Obasogie, O.K., 2011. Black Salt. Slate, The Slate Group, Online. Radhakrishnan, M., van Gool, K., Hall, J., Delatycki, M., Massie, J., 2008. Economic evaluation of cystic fibrosis screening: a review of the literature. Health Policy 85, 133–147. Read, J.G., Emerson, M.O., Tarlov, A., 2005. Implications of black immigrant health for U.S. racial disparities in health. J. Immigr. Health 7, 205–212. Rose, G., 1992. The Strategy of Preventive Medicine. Oxford University Press, New York. Singh, G.K., Miller, B.A., 2004. Health, life expectancy, and mortality patterns among immigrant populations in the United States. Can. J. Public Health 95, I14–I21. Singh, G.K., Siahpush, M., 2002. Ethnic-immigrant differentials in health behaviors, morbidity, and cause-specific mortality in the United States: an analysis of two national data bases. Hum. Biol. 74, 83–109. Steffen, P.R., Smith, T.B., Larson, M., Butler, L., 2006. Acculturation to western society as a risk factor for high blood pressure: a meta-analytic review. Psychosom. Med. 68, 386–397. US Department of Agriculture, US Department of Health and Human Services, 2010. Dietary guidelines for Americans, In: US Department of Agriculture, US Department of Health and Human Services (Eds.), 7th Edition. U.S. Government Printing Office, Washington, DC.
Contents lists available at SciVerse ScienceDirect
Preventive Medicine journal homepage: www.elsevier.com/locate/ypmed
Heterogeneity of risk within racial groups, a challenge for public health programs Sean A. Valles ⁎ Lyman Briggs College and Department of Philosophy, Michigan State University, Holmes Hall, 919 E. Shaw Lane, Room W25-C, East Lansing, MI 48825, USA
a r t i c l e
i n f o
Available online 8 September 2012 Keywords: Bioethics Cystic fibrosis Hypertension Population groups Genetic testing Diet Sodium-restricted
a b s t r a c t Targeting high-risk populations for public health interventions is a classic tool of public health promotion programs. This practice becomes thornier when racial groups are identified as the at-risk populations. I present the particular ethical and epistemic challenges that arise when there are low-risk subpopulations within racial groups that have been identified as high-risk for a particular health concern. I focus on two examples. The black immigrant population does not have the same hypertension risk as US-born African Americans. Similarly, Finnish descendants have a far lower rate of cystic fibrosis than other Caucasians. In both cases the exceptional nature of these subpopulations has been largely ignored by the designers of important public health efforts, including the recent US government dietary recommendations. I argue that amending the publicly-disseminated risk information to acknowledge these exceptions would be desirable for several reasons. First, recognizing low-risk subpopulations would allow more efficient use of limited resources. Communicating this valuable information to the subpopulations would also promote truth-telling. Finally, presenting a more nuanced empirically-supported representation of which groups are at known risk of diseases (not focusing on mere racial categories) would combat harmful biological race essentialist views held by the public. © 2012 Elsevier Inc. All rights reserved.
Introduction Public health interventions are often targeted to identifiable highrisk populations. This raises philosophical issues such as what it means for a population to be at risk and what ethical considerations should guide programs. These challenges become considerably more complex when the target populations are racial groups. As Troy Duster lays out in a 2006 paper on the use of race in medicine: The unenviable task has been to try to walk a tightrope—to figure out a way to effectively deploy in research the concept of race (or population groups designated by race) without endowing “race” with a false sense of genetic essentialism (Duster, 2006, p. 488). This danger is a quite real one, as misperceptions of the biological basis of race abound in the United States. More importantly, psychological data suggests, “[the] belief that social categories have an underlying nature/natural foundation” is one central basis for the formation and endorsement of stereotypes and prejudice” (Keller, 2005, pp. 686, 699). On the other hand, “this implies that one possible way of combating stereotyping and prejudice is to challenge the belief in genetic determinism and biological essentialism” (Keller, 2005, p. 699). The danger of promoting race essentialism (the view that racial categories demarcate deep intrinsic similarities among members of a race and corresponding
⁎ Corresponding author. Fax: +1 517 432 2758. E-mail address: [email protected]. 0091-7435/$ – see front matter © 2012 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.ypmed.2012.08.022
differences between members of different races) does not automatically preclude the public application of race categories in medicine – Nancy Krieger has effectively argued why entirely ignoring race would “preclud[e] possibilities for monitoring progress and setbacks in reducing” “racial/ethnic inequalities” (2000, p. 213) – but that danger should be a guiding ethical consideration during deliberations about such medical uses. I will show how information about racial groups' disease risks has been mishandled in two cases and make recommendations for ameliorating those missteps. In both cases, the designers of public health efforts have downplayed data that complicates their broad statements about racial groups being at elevated risk for particular diseases. I will focus on the black immigrant exception to the high rates of hypertension among African Americans and the Finnish exception to the high rates of cystic fibrosis among Caucasians. In these two cases there is ample data to support more nuanced (yet still simple and practical) characterizations of the at-risk populations—US-born African Americans are at elevated risk of hypertension and non-Finnish Caucasians are at elevated risk of cystic fibrosis. Yet, the unmodified racial categories continue to be used instead. This creates the unique situation in which low-risk subpopulations have had their interests marginalized during the propagation of broad claims about race-wide disease risks. Hence, we have two distinct problems that overlap in practice: the problem of ignoring low-risk islands within seas of high risk (so to speak) and the problem of privileging mere race when delineating which populations have public health risks. Together, the two problems combine to impede the dissemination of more nuanced data about heterogeneity of risk within racial groups.
406
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I will argue that using available data to present more nuanced/specific representations of the relevant at-risk populations, beyond statements about racial groups broadly, would yield substantial benefits and also mitigate some of the harms associated with using race in medicine. Further nuance would preempt public overestimates of the biomedical significance of race, better serve the interests of the low-risk Finnishdescended and black immigrant subpopulations, improve the efficiency of public health resource usage (e.g. funds for testing people for recessive cystic fibrosis mutations) and promote truth-telling—the race-level data now provided is technically true, but is misleading for the low-risk subpopulations unless accompanied by the more nuanced available information. While I focus on analyzing the two aforementioned cases, the analysis suggests that more attention to low-risk subpopulations is warranted and that the privileging of data at the level of broad racial categories is an important obstacle to pursuing more nuanced representations of the heterogeneity of risk within racial categories. The problem of heterogeneity of risk Katherine Frohlich and Louise Potvin raise the problem of withinpopulation heterogeneity of risk in their critique of Geoffrey Rose's influential “population strategy” of public health programs, which emphasizes small reductions of harm across entire populations, rather than large reductions of harm within limited high-risk subpopulations, the “high-risk strategy” (Frohlich and Potvin, 2008; Rose, 1992). It is beyond the scope of this paper to address the general merits of Rose's approach or of Frohlich and Potvin's critique, but I would like to highlight Frohlich and Potvin's observation about the problem of subpopulations with varying experiences/risks. They argue that Rose's approach can effectively erect blinders that prevent public health practitioners from detecting and addressing underlying causal complexities: “moderate correlations between several risk factor exposures in the general population may mask highly differentiated experiences in specific subpopulations” (Frohlich and Potvin, 2008, p. 219). A statistical correlation or average at the level of a large population can conceal enormous variability among its subpopulations. Interestingly, Rose himself worries about a similar problem, noting that individual experiences will vary in unpredictable ways among members of even a well-established at-risk subpopulation (Rose, 1992, pp. 49–50). Rose sees substantial weaknesses in the high-risk strategy, but notes that two of its main advantages are its potentially “cost-effective use of resources” and its favorable “benefit-to-risk ratio” when interventions carry some risk of harmful side effects (Rose, 1992, pp. 44–46). Both are advantages of targeting resources to those who stand to benefit the most, even if there is still unpredictable heterogeneity of risk within that group. However, if we lump in known low-risk populations with known high-risk populations during the crafting of interventions then we lose both benefits. This is problematic even within a utilitarian view of public health ethics, seeking to maximize net health benefits within a given group of people (a common general approach among public health practitioners). We would be spending resources (e.g. subsidizing testing) on subpopulations that have little need for such resources, while also exposing that subpopulation to any undesirable side effects (e.g. spending additional personal funds on a special diet). Dietary salt among African Americans The joint U.S. Department of Agriculture and Health and Human Services publication Dietary Guidelines for Americans 2010 recommends a reduced-sodium diet for all African Americans, responding to a large body of data identifying the group as having relatively high risk of hypertension and its various cardiovascular sequelae, including stroke (Read et al., 2005). Reduce daily sodium intake to less than 2300 milligrams (mg) and further reduce intake to 1500 mg among persons who are 51 and
older and those of any age who are African American or have hypertension, diabetes, or chronic kidney disease (US Department of Agriculture and US Department of Health and Human Services, 2010, p. x). The problem is that this clumsily portrays African-Americanness, (and by implication, Africanness) as a weighty biological and medical category, on par with being diabetic. Race and bioethics scholar Osagie Obasogie drew attention to this advice in a recent article for Slate, highlighting the problem of its tacit support for biological race essentialism (2011). Still, it is at least conceivable that the recommendation's implied support for biological race essentialism could be justified on the grounds that it is an accurate and practically useful representation of salt-related disease risks. It is not. Highlighting the problem of heterogeneity of risk among subpopulations, Read et al. point out that the well-known broad “black-white health disparities” actually conceal substantial “heterogeneity in the health status of black Americans”, especially the variation introduced by black immigrants (2005, p. 205, 208). According to a longitudinal study of 300,910 subjects, “foreign-born non-Hispanic blacks” had strikingly lower hypertension rates than “US-born non-Hispanic blacks”, 16.75% vs. 25.45% (Singh and Siahpush, 2002, p. 89). In fact, when adjusted for income, age, etc., “black immigrants had… 55% lower mortality from [cardiovascular disease] than US-born whites” (Singh and Siahpush, 2002, p. 97). 1 The causes of the foreign-born vs. US-born disparity remain hazy. A meta-analysis of the data on immigrants' blood pressure changes demonstrates that “acculturation to Western society is a risk factor for increased [blood pressure]”, and that “the majority of the acculturation effect appears to happen within the first 3 years of interaction with the new culture” (Steffen et al., 2006, p. 394). However, according to the previously mentioned longitudinal study, even those immigrating more than 15 years ago were still “19% less likely to report having high blood pressure than their US-born counterparts”, suggesting that acculturation during the early years of US residency has a limited effect on diminishing the disparity (Singh and Siahpush, 2002, p. 101). Overall, existing research suggests that black immigrants, on average, simply do not seem to be at the same elevated risk of hypertension (among other cardiovascular diseases) as US-born blacks, so it is problematic to create a dietary public health intervention that fails to distinguish between the two groups. 2 One could object that the dietary guidelines partly address my concern about promoting naive biological essentialism through using the term “African American”, which it leaves undefined, but is interpretable as a largely sociocultural term that could exclude most black immigrants. But, the fact that “African American” has a hazy and debatable mixture of racial, ethnic and cultural connotations means that, for example, a Nigerian-born permanent resident of the US would be forced to decipher whether the term applies to him or her. It is a term, after all, that is used alongside “black” and “negro” in the “race” section of the 2010 US census form. In short, imprecision is the problem here, not the solution. Cystic fibrosis risk among Finnish descendants During debates over the benefits and drawbacks of using race in medicine, discussion almost always focuses on minority or underprivileged groups. Indeed, this is a good thing. However, misapplications 1 Philosopher of science Jonathan Kaplan uses similar data (also co-authored by Singh) to undermine genetic arguments for black-white health disparities (Kaplan, 2010; Singh and Miller, 2004). 2 Even under the controversial “slavery hypothesis”, according to which African slaves underwent a unique natural selection event favoring the increased storage of dietary salt during the deadly transatlantic voyage, black immigrants are still deserving of special consideration (Kaufman and Hall, 2003). By hypothesis, they would be genetically distinct from the US-born descendants of slaves.
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of blunt racial categories can also harm white residents of the United States or Europe. Whiteness/Caucasianness is no less hazy a category than African Americanness, so it should come as no surprise that misapplications of the Caucasian racial category in medicine can lead to serious problems. In this case I will focus on the partly misleading representation of Caucasianness as a risk factor for cystic fibrosis. The recessive genetic disease cystic fibrosis, a lethal condition damaging lung function (among many other effects), is “often characterized as a ‘white’ disease though it occurs in many populations” (Lindee and Mueller, 2011, p. 317). Its representation as a “‘white’ disease” is based on the striking variation in cystic fibrosis rates across world populations. In general, Caucasians have cystic fibrosis rates of ~1/2500, which is many times greater than the rate of ~1/40,000–1/100,000 in India, to choose just one example (Langfelder-Schwind et al., 2005, p. 10; Calafell et al., 2004, p. 15). The data indeed support an association between cystic fibrosis risk and Caucasianness/whiteness. But, the association does not hold uniformly across all Caucasian subpopulations. People of Finnish ancestry have a cystic fibrosis rate of ~1/25,000, ten times lower than the rate for Caucasians in general (Calafell et al., 2004, p. 15). This exceptionally low rate within a substantially sized and identifiable Caucasian subpopulation clearly undermines portrayals of Caucasianness per se as a risk factor for cystic fibrosis.3 Strangely, two recent sets of recommendations about cystic fibrosis testing, both from major North American medical organizations, ignore or downplay the Finnish-descended subpopulation in their recommendations. This is unfortunate, as the costs of testing individuals for the recessive mutations (such as when a couple is planning conception) are substantial. According to a 2008 review, “cost per test… ranged from US$28 to US$240” – cheaper versions of the tests yield more false negatives – in addition to the variable additional costs of advertising, pre- and post-test counseling, etc. (Radhakrishnan et al., 2008, p. 141–142). Though, those figures do not reflect costs such as the discomfort of undergoing medical tests, the stress of waiting for results, etc. This set of costs is not trivial, and the expected benefits for Finnish descendants are low. A recent statement by the American College of Obstetricians and Gynecologists on carrier screening for cystic fibrosis discusses the different frequencies among various races/ethnicities: “cystic fibrosis is most common in non-Hispanic white individuals and people of Ashkenazi Jewish ancestry”, yet points out, “it is becoming increasingly difficult to assign a single ethnicity to individuals”, and so, “it is reasonable, therefore, to offer CF carrier screening to all patients” (Committee on Genetics, 2011, p. 1030). The advice, then, is that carrier screening should be offered to all, but that the expected benefits will vary depending on the patient's background. But the statement does not mention Finnish-descended patients' anomalously low rate. A similar statement by the National Society of Genetic Counselors mentions the low rate among Finnish descendants, which is encouraging, but then oddly sets the phenomenon aside (Langfelder-Schwind et al., 2005). The text dismisses the existing data regarding heterogeneous rates within large populations, saying, “it is difficult to determine precisely which ethnic subgroup to assign a patient, and reliable risk data is not available for many populations”, so, “genetic counselors are urged to use” the text's “reliable” chart, listing a single carrier (heterozygote) frequency for “Caucasian:” 1/25 (Langfelder-Schwind et al., 2005, p. 10). But, the carrier frequency for Finnish Caucasians is approximately 1/77 (Kere et al., 1989). The statement is correct that there is little or no data on cystic fibrosis prevalence data for many subpopulations, yet the Finn-specific phenomenon has been established for decades (Kere et al., 1989; Calafell et al., 2004). Even if the specific detection and error rates for tests of Finnish descendants are not so firmly established, those Finnish descendants still deserve to know about the strikingly low benefits of getting tested in the first place. 3 Middle eastern and Ashkenazi Jewish populations introduce additional classificatory and demographic complexities, raise another set of complications that, unfortunately, cannot be adequately addressed here.
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The National Society of Genetic Counselors' resistance to contending with the unique Finnish subpopulation is incompatible with its conclusion. To some patients, [cystic fibrosis] screening may provide an opportunity that can give them important information about a current or future pregnancy. To others, it may provoke unwelcome anxiety or require a painful decision about the pregnancy. Genetic counselors will play an important role in providing information and support sufficient to allow people to make choices that are consistent with patient values and based on the best available information (Langfelder-Schwind et al., 2005). I fully endorse this conclusion, especially the importance of genetic counselors using the “best available information”. But, in the cases of both the American College of Obstetricians and Gynecologists (which ignores Finns entirely) and the National Society of Genetic Counselors (which mentions Finns then sidelines them), this goal has been held back by a narrow focus on representing disease risk data at the Caucasian/white level, even when more specific and directly relevant evidence is available. Failing to disseminate the information about Finnish descendants is both wasteful of resources and obstructs truth-telling. Finnishdescended patients are not being provided with the most relevant risk data available, meaning that they (and their physicians) are likely to make their testing decisions based on the relatively well-disseminated Caucasian high-risk data.4 This leads to cost-benefit analyses assuming an overestimated benefit. Thus, information about Finnish descendants' cystic fibrosis risk is being downplayed by the very organizations that should be actively disseminating it. Choosing a level of specificity Any demand for recognition of a further level of specificity in delineating a public health target population invites two important questions: 1) why increase the level of specificity beyond its current level? and 2) why stop at this level of specificity and not some other level? The first question has several answers. Increasing the specificity of at-risk population characterizations corrects the misleading, though not technically false, risk assessments communicated to low-risk subpopulations. Unnecessarily blunt assessments of race-wide risks engender wasteful use of resources, such as funds for cystic fibrosis carrier testing or the personal funds/ effort required to follow a very low-sodium diet. They also obstruct truth-telling, as important information has not been provided to patients. These harms are consequences of imprecision, though they are generic in the sense that similar harms would result from any sort of miscommunication of a subpopulation's risk. However, race brings in a unique challenge: racial categories themselves are problematic even prior to their application in public health contexts. A separate benefit of raising the level of specificity beyond the level of racial categories is that it not only fails to bolster naive biological race essentialism, it actively undermines it. Race essentialism is a concept that does not easily admit complications or exceptions. A small adjustment to the list of vulnerable populations needing decreased dietary salt would make all the difference in the support or rejection of biological essentialism for African descendants. Simply changing “African Americans” to “US-born African Americans” would actually help to correct the misguided essentialism so prevalent among Americans. It would deny the homogeneity of African Americans while simultaneously blunting the particular representation of African Americanness, 4 If we rely on Finnish descendants to self-identify (an imperfect system, though standard practice in the collection of demographic data) then we would also limit the problem of increasing costs through pursuing the added specificity. Systematically checking Caucasian patients for Finnish ancestry would not be entirely free, but it would presumably be very low-cost.
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and by implication all Africanness, as a negative biomedical trait. It seems that the strongest defense of the status quo here is that public health programs, especially public education programs, demand simplicity; we are better off keeping the story simple than complicating it and confusing the audience. I argue that adding only a small measure of increased complexity would yield disproportionately large benefits. The remaining question is why, for example, we should specify US-born vs. foreign-born in dietary salt recommendations and not specify even further. In principle, one could always demand more and more specificity in delineating which populations are really the at-risk/vulnerable ones (see discussion in Rose, 1992, p. 49–50). For example, there is data suggesting that black immigrants from Africa are generally healthier than black immigrants from the West Indies, who are in turn healthier than black immigrants from Europe (Read et al., 2005). In practice, though, increasing specificity cannot go on ad infinitum—limitations of data availability and pragmatic effectiveness intervene. For example, in the Read et al. data, the study's quite small sample of black European immigrant subjects weakens the inferences we can make about the black European immigrant population generally (2005). In the cystic fibrosis case, even if it were statistically feasible, it would not be practical to expect Finnish-descended patients to consult a massive diagram of the differing relative risks for inhabitants of various regions of Finland and then decide (according to their family histories) whether to pursue cystic fibrosis testing. My recommendation is not that we increase the target population specificity to recognize Finnish descendants and black immigrants and then immediately stop. My plea is that our specificity must go at least that far. We should at least amend dietary salt guidelines to reflect that the risk is for “US-born African Americans” and cystic fibrosis testing literature to reflect that the known risk is for “non-Finnish Caucasians”. Once these public health programs escape from overreliance on mere race then any further calls for specificity can be handled on a case-by-case basis. Conclusion Mere race has been treated as a privileged level of specificity in defining cardiovascular disease risk and cystic fibrosis risk. This is quite unfortunate. Of all the possible levels of population specificity, race is probably the choice that introduces the most unintended harm, primarily due to its tacit reinforcement of biological race essentialism. Adding one more level of specificity beyond mere race would leave the target population delineations simple enough to be accessible to laypeople and also limit the socially detrimental side-effects of using racial categories in medicine. In fact, it offers an opportunity to combat prejudice through undercutting essentialism. It is important to stress that this paper is not a call to rewrite science for political ends. Rather, it is a call for biomedical experts to responsibly use the scientific data already available to them. I focus on only the two aforementioned cases, but believe that these two cases point to larger problems with the unconscious privileging of broad racial categories
in the reporting of public health information, and particularly the potential harms that result from (unconsciously) concealing information about low-risk subpopulations. Conflict of interest statement The author declares there is no conflict of interest.
Acknowledgments I have been greatly aided by feedback from Jim Nelson, Lisa Lloyd, Ryan Ketcham, Andrea Smith, Kristie Dotson, the participants of the 2012 UT-Dallas Science-Policy Interactions and Social Values Conference and this journal's two anonymous reviewers. References Calafell, F., Cutting, G., Dodge, J., Des Georges, M., Dörk, T., Durie, P., et al., 2004. The Molecular Genetic Epidemiology of Cystic Fibrosis: Report of a Joint Meeting of WHO/ECFTN/ICF(M)A/ECFS Genoa, Italy, 19 June 2002 World Health Organization. Chronic Diseases and Health Promotion, Human Genetics Programme, Geneva. Committee on Genetics, 2011. Update on carrier screening for cystic fibrosis. Obstet. Gynecol. 117, 1028–1031. Duster, T., 2006. Lessons from history: why race and ethnicity have played a major role in biomedical research. J. Law Med. Ethics 34, 487–496. Frohlich, K.L., Potvin, L., 2008. Transcending the known in public health practice—the inequality paradox: the population approach and vulnerable populations. Am. J. Public Health 98, 216–221. Kaplan, J.M., 2010. When socially determined categories make biological realities: understanding black/white health disparities in the U.S. Monist 93, 281–297. Kaufman, J.S., Hall, S.A., 2003. The slavery hypertension hypothesis: dissemination and appeal of a modern race theory. Epidemiology 14, 111–118. Keller, J., 2005. In genes we trust: the biological component of psychological essentialism and its relationship to mechanisms of motivated social cognition. J. Pers. Soc. Psychol. 88, 686–702. Kere, J., Norio, R., Savilahti, E., Estivill, X., de la Chapeile, A., 1989. Cystic fibrosis in Finland: a molecular and genealogical study. Hum. Genet. 83, 20–25. Krieger, N., 2000. Refiguring “race”: epidemiology, racialized biology, and biological expressions of race relations. Int. J. Health Serv. 30, 211–216. Langfelder-Schwind, E., Kloza, E., Sugarman, E., Pettersen, B., Brown, T., Jensen, K., et al., 2005. Cystic fibrosis prenatal screening in genetic counseling practice: recommendations of the national society of genetic counselors. J. Genet. Couns. 14, 1–15. Lindee, S., Mueller, R., 2011. Is cystic fibrosis genetic medicine's canary? Perspect. Biol. Med. 54, 316–331. Obasogie, O.K., 2011. Black Salt. Slate, The Slate Group, Online. Radhakrishnan, M., van Gool, K., Hall, J., Delatycki, M., Massie, J., 2008. Economic evaluation of cystic fibrosis screening: a review of the literature. Health Policy 85, 133–147. Read, J.G., Emerson, M.O., Tarlov, A., 2005. Implications of black immigrant health for U.S. racial disparities in health. J. Immigr. Health 7, 205–212. Rose, G., 1992. The Strategy of Preventive Medicine. Oxford University Press, New York. Singh, G.K., Miller, B.A., 2004. Health, life expectancy, and mortality patterns among immigrant populations in the United States. Can. J. Public Health 95, I14–I21. Singh, G.K., Siahpush, M., 2002. Ethnic-immigrant differentials in health behaviors, morbidity, and cause-specific mortality in the United States: an analysis of two national data bases. Hum. Biol. 74, 83–109. Steffen, P.R., Smith, T.B., Larson, M., Butler, L., 2006. Acculturation to western society as a risk factor for high blood pressure: a meta-analytic review. Psychosom. Med. 68, 386–397. US Department of Agriculture, US Department of Health and Human Services, 2010. Dietary guidelines for Americans, In: US Department of Agriculture, US Department of Health and Human Services (Eds.), 7th Edition. U.S. Government Printing Office, Washington, DC.