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Nature Versus Nurture: Does Genetic Ancestry Alter the Effect of Air Pollution in Children with Asthma?



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  • Description:
    As one of the most common respiratory illnesses, asthma is also a disease characterized by striking ethnic disparities. The prevalence of asthma among black and Latino individuals is almost double that seen among white individuals. The differences in morbidity and mortality are even more significant: Child mortality rates in non-Hispanic black individuals are eightfold higher than in non-Hispanic white individuals. Unpacking the etiology of these differences is difficult, given the complex intersection between social, environmental, and heritable factors that modulate disease susceptibility and manifestations. Understanding the role of ethnicity is even harder, particularly in an admixed society where interracial marriage and multiethnic groups are increasingly common. In this issue of the Journal, Neophytou and colleagues (pp. 1271-1280) tackle this issue by exploring the interaction between environmental exposure and genetic variation in a study of minority adolescents with asthma. The authors focus their analysis on air pollution, a risk factor that has been repeatedly linked with adverse asthma-related outcomes. Because minorities tend to cluster in neighborhoods with poor air quality, they are expected to be particularly vulnerable to exposure. Although many epidemiologic studies have shown an association between incident asthma and poor symptom control, asthma-related hospitalizations, and reduced lung function, few of these studies have been performed in populations with a significant proportion of minorities. ... The conclusions that can be drawn from the analysis of effect modification by genetic ancestry are less clear. Superficially, this suggests that other psychosocial constructs of ethnicity may alter susceptibility to air pollution rather than genetic background. But modeling the effect of genetic ancestry by using an interaction term with pollutant concentration may be a statistical simplification of a complex biologic relationship. Interaction terms assume there is a multiplicative effect on the outcome, whereas in reality, the effect could be additive, synergistic, or effected by additional environmental factors. Moreover, defining genetic ancestry through the identification of single nucleotide polymorphisms is a crude estimation of the genetic diversity between different populations that may not capture significant biologic effects. If a rare polymorphism that confers increased susceptibility is found within a subset of an ancestral population, then the heterogeneity within the larger population can increase the likelihood of a false negative association. This is particularly true in African populations that tend to have complex geographical histories and a higher level of genetic diversity. An alternative approach would be to genotype the single nucleotide polymorphisms in individuals with low lung function, instead of relying on population-level genetics as a surrogate. More research is needed to determine the relative importance of the multiple socioeconomic and environmental risk factors that contribute to ethnic disparities in asthma, and to determine whether there may be certain heritable susceptibilities. Yet this article adds significantly to the literature and informs public policy by demonstrating a significant association between ambient air pollution and reduced lung function in minorities with asthma. By improving air quality, we could potentially reduce the burden of disease and improve asthma-related outcomes. [Description provided by NIOSH]
  • Subjects:
  • Keywords:
  • ISSN:
    1073-449X
  • Document Type:
  • Funding:
  • Genre:
  • Place as Subject:
  • CIO:
  • Topic:
  • Location:
  • Volume:
    193
  • Issue:
    11
  • NIOSHTIC Number:
    nn:20063736
  • Citation:
    Am J Respir Crit Care Med 2016 Jun; 193(11):1196-1198
  • Federal Fiscal Year:
    2016
  • Performing Organization:
    University of Washington
  • Peer Reviewed:
    False
  • Start Date:
    20050701
  • Source Full Name:
    American Journal of Respiratory and Critical Care Medicine
  • End Date:
    20250630
  • Collection(s):
  • Main Document Checksum:
    urn:sha-512:bf4a09cebc6c0aac4993d9e66e3d1da64ea519927b2e0938c3079c4cc1733bf9211d904a97a2d99f7aaf74cf127f7d2096d08361fb604bc6549e1b5e42e311f2
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  • File Type:
    Filetype[PDF - 440.17 KB ]
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