title: Genetics of asthma: potential implications for reducing asthma disparities.
abstract: Although genetic factors may partly explain the differences in asthma prevalence, morbidity, and mortality among ethnic groups in the United States, few studies of the genetics of asthma have included members of ethnic minority groups. Only one genome-wide linkage analysis of asthma and/or asthma-related phenotypes (conducted by the Collaborative Study on the Genetics of Asthma) has included any members of ethnic minority populations. The interpretation of the findings of genetic association studies of asthma in ethnic minority groups is complicated by reduced statistical power due to small sample sizes; the failure to correct for multiple comparisons; a lack of homogeneity of the populations studied with regard to area of residence, ancestral background, and/or country of origin; a lack of measurement of relevant environmental exposures; and (for case-control studies of genetic association) a lack of detection and control of potential population stratification. Genetic studies may improve our understanding of asthma and lead to new methods to prevent, diagnose, and treat this disease. Limited study of asthma genetics in ethnic minority populations is unacceptable, as it may prevent these groups from benefiting from future developments in asthma management and thus widen existing disparities in asthma care. Future genetic association studies of asthma among ethnic minorities in the United States should include large samples of populations that have been adequately defined with regard to area of residence, self-designated ancestry, and country of origin. These studies should also include an adequate assessment of potentially relevant environmental exposures and (for case-control association studies) population stratification.
authors.affiliation: Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA.
authors.forename: Christina V
authors.initials: CV
authors.lastname: Scirica
authors.forename: Juan C
authors.initials: JC
authors.lastname: Celedón
mesh_terms: D051722:ADAM Proteins / Q000235:genetics; D001741:Black or African American / Q000235:genetics; D001249:Asthma / Q000208:ethnology* / Q000235:genetics* / Q000517:prevention & control; D002874:Chromosome Mapping; D005006:Ethnicity / Q000235:genetics*; D020022:Genetic Predisposition to Disease; D054624:Health Status Disparities; D006801:Humans; D015847:Interleukin-4 / Q000235:genetics; D018343:Receptors, Adrenergic, beta-2 / Q000235:genetics; D011971:Receptors, Immunologic / Q000235:genetics; D019948:Receptors, Interleukin-4 / Q000235:genetics; D011982:Receptors, Prostaglandin / Q000235:genetics; D051193:Toll-Like Receptors / Q000235:genetics
chemical_list: D018343:Receptors, Adrenergic, beta-2; D011971:Receptors, Immunologic; D019948:Receptors, Interleukin-4; D011982:Receptors, Prostaglandin; D051193:Toll-Like Receptors; D015847:Interleukin-4; D051722:ADAM Proteins; C450441:ADAM33 protein, human; C036293:prostaglandin D2 receptor