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African ancestry, early life exposures, and respiratory morbidity in early childhood
Author(s) -
Kumar R.,
Tsai H.J.,
Hong X.,
Gignoux C.,
Pearson C.,
Ortiz K.,
Fu M.,
Pongracic J. A.,
Burchard E. G.,
Bauchner H.,
Wang X.
Publication year - 2012
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1111/j.1365-2222.2011.03873.x
Subject(s) - medicine , genetic genealogy , wheeze , demography , confounding , logistic regression , race (biology) , decile , prospective cohort study , asthma , cohort , respiratory sounds , pediatrics , population , environmental health , biology , statistics , botany , mathematics , sociology
Summary Background Racial disparities persist in early childhood wheezing and cannot be completely explained by known risk factors. Objective To evaluate the associations of genetic ancestry and self‐identified race with early childhood recurrent wheezing, accounting for socio‐economic status ( SES ) and early life exposures. Methods We studied 1034 children in an urban, multi‐racial, prospective birth cohort. Multivariate logistic regression was used to evaluate the association of genetic ancestry as opposed to self‐identified race with recurrent wheezing (>3 episodes). Sequential models accounted for demographic, socio‐economic factors and early life risk factors. Genetic ancestry, estimated using 150 ancestry informative markers, was expressed in deciles. Results Approximately 6.1% of subjects (mean age 3.1 years) experienced recurrent wheezing. After accounting for SES and demographic factors, A frican ancestry ( OR : 1.16, 95% CI : 1.02–1.31) was significantly associated with recurrent wheezing. By self‐reported race, hispanic subjects had a borderline decrease in risk of wheeze compared with A frican A mericans ( OR : 0.44, 95% CI : 0.19–1.00), whereas white subjects ( OR : 0.46, 95% CI : 0.14–1.57) did not have. After further adjustment for known confounders and early life exposures, both A frican ( OR : 1.19, 95% CI : 1.05–1.34) and E uropean ancestry ( OR : 0.84, 95% CI : 0.74–0.94) retained a significant association with recurrent wheezing, as compared with self‐identified race ( OR whites : 0.31, 95% CI : 0.09–1.14; OR hispanic : 0.47, 95% CI : 0.20–1.08). There were no significant interactions between ancestry and early life factors on recurrent wheezing. Conclusions and Clinical Relevance In contrast to self‐identified race, A frican ancestry remained a significant, independent predictor of early childhood wheezing after accounting for early life and other known risk factors associated with lung function changes and asthma. Genetic ancestry may be a powerful way to evaluate wheezing disparities and a proxy for differentially distributed genetic and early life risk factors associated with childhood recurrent wheezing.