Abstract

INTRODUCTION

Childhood atopic diseases, including asthma, cause significant morbidity and mortality and are common in the westernized world.[1] In particular, asthma is the most common chronic disease in childhood and has increased in frequency over the last several decades with half of the current cases of asthma in the United States being attributable to atopy.[2] It is also estimated that the majority (54.3%) of the United States population is atopic (sensitized to ≥1 allergen) – a prevalence that is 2.1–5.5 times higher than the prevalence from a decade earlier.[3] Therefore prevention of atopy has been considered a leading strategy to decrease asthma.[2,4]

Racial disparities in allergic disease outcomes have been reported with African Americans suffering disproportionately compared to White individuals.[3,5–11] Sources of racial differences in allergic disease may not be fully explained by social and economic status (SES). For example, our research group has shown that even among middle class children, African Americans may be more susceptible to asthma.[12,13] Based on census and health interview survey data in Rhode Island, Black children were more likely to have asthma than either their White or Hispanic counterparts even after adjusting for measures of family and neighborhood socioeconomic position.[14]

Our goal was to examine whether racial disparities are present as early as age 2 years in a racially diverse birth cohort established in the Detroit metropolitan area. Additionally, we sought to determine whether any observed racial differences could be explained, either fully or in part, by various components of SES.

METHODS

RESULTS

There were 223 White children and 466 African American children who participated in the clinic visit and thus the proportion of cohort subjects included in the analyses were 66% and 58%, respectively. Among White children, those who participated in the clinic visit at age 2 years tended to have higher family income and maternal education. They also tended to have greater birthweight and be born in the winter and spring and had a slightly higher maternal age at enrollment (Table 1). Among African American children, those included tended to have higher maternal education, were more likely to have mothers who kept indoor pets during pregnancy, were more likely to have mothers who were married or living as married, be less likely to live with a smoker and had slightly older mothers at enrollment (Table 1). Table 1 indicates that while there are overall differences in the distributions of income and maternal education between White and African American households, all income and maternal education levels are represented in the included study samples of White and African American children.

DISCUSSION

Racial disparities in each of the allergic disease outcomes examined, with the exception of wheeze, were apparent in our study population at age 2 years with African American children experiencing higher rates/levels of each of the outcomes examined compared to White children. These findings indicate that potential sources of disparities may occur, at least in part, in very early life including the prenatal period and the first 2 years of life. A major implication of this finding is that the focus of future investigations into sources of racial disparities and allergic disease causation must begin during pregnancy and infancy.

There is some prior documentation of racial differences in the outcomes investigated; however, our data provide the earliest indication of the disparities. In an analysis of NHANES II data, African American children ages 6–16 years were more likely to be SPT+ for German cockroach, dust mite and the mold Alternaria compared with White children.[8] NHANES III data indicated that Black individuals ages 6–59 years were more likely than White individuals to have had a positive skin prick test to at least one of ten allergens (adjusted OR=1.6, 95% CI 1.4, 1.9).[3] In their study of 882 pregnant women (169 were Black and 577 were White), Litonjua et al. reported higher total IgE for Black women compared with White women.[9] Black women were also approximately 2.5 times more likely than White women to be sensitized to ≥3 allergens. Results from the 2003 National Survey of Children’s Health reported the odds of having had a doctor’s diagnosis of AD was almost double among African American children under 18 years of age compared to White children.[10] Black individuals were twice as likely as White individuals to seek treatment for AD (54.4 versus 25.7 visits per 10,000 population) in the United States based on the 1990–1998 National Ambulatory Medical Care Survey (not limited to any age group).[11]

In the CDC’s May 3, 2011 Morbidity and Mortality Weekly Report, it was reported that asthma was most common in non-Hispanic Black children and had increased from 2001 to 2009 (17.0% from 11.4% in 2001).[6] The prevalence among White children was reported as 8.5%.[6] Based on data from numerous national surveys and health statistic reports (1980–2007), Akinbami et al. reported that 1 in 11 children in the United States has asthma and that Black children were 1.6 times as likely as White children to have asthma.[5] The disproportionately higher prevalence of severe childhood asthma and its medical consequences (emergency department and acute care visits) among African Americans have been well documented.[7]

With or without adjustment for SES and other factors, the rates of wheeze in this study did not differ tremendously between African American and White children at this early age. We did not collect information on repeated wheeze and this was a limitation. We only asked whether the child ever wheezed. This lack of specificity about wheezing could have contributed to its moderate to weak observed associations.

Our analyses also found that SES factors and other key variables that sometimes differ by race used in our analyses could not fully explain the racial differences in allergic outcomes – associations between race and the outcomes persisted even after adjusting for these common SES and other variables. However, while the sources of well-documented racial disparities have not been thoroughly studied, racial disparities in management of allergic diseases, especially asthma, have garnered much attention from researchers.[18–21] Our work focused on racial disparities in disease incidence rather than racial disparities in disease management. Factors related to causation are poorly understood and novel hypotheses are needed to address this problem. As our research group has proposed, prevention is as important as disease management if racial disparities in asthma are to be eliminated.[22]

Our results further suggest that other potential sources of these racial disparities, beyond frequently collected SES data, should be investigated. Genetic variations by race have been an exciting research area [23,24]; additional avenues should be pursued. For example, vitamin D represents a clear opportunity for research as it has received much recent attention in the area of allergic disease causation.[25–34] There is an epidemic of vitamin D deficiency that may have been caused by changes in lifestyles in westernized cultures, especially the United States, over the last several decades.[35,36] The epidemic has also disproportionately affected African Americans compared to lighter skinned individuals. In NHANES 2001–2004, Black children ages 1–21 years were more than 20 times as likely as White children to have 25(OH)D deficiency (defined as <15 ng/ml) (age and gender adjusted odds ratio (OR)=24.2, 95% confidence interval (CI) 15.9, 36.9).[35] Lack of exercise, nutrition, and inner city air pollution, especially diesel exhaust, are also possible causes of increased asthma prevalence among African Americans living in cities.

We do not have data on all environmental exposures including airborne particulates. The racial disparities observed could be caused by environmental differences since they would be part of the child’s early exposures. However, in this study, adjustments for endotoxin and some allergen (dog, cat, cockroach) levels in the home did not explain the observed racial disparities. Further, our prior research on racial disparities in children in suburban Detroit would suggest that the environment does not fully explain observed racial differences.[12]

There were additional limitations to our study. Ideally, we would have examined the association with race separately for urban and suburban residents; however, this was not possible. Participation rates for the clinic visit at age 2 years were not as high as we had hoped for; however, the factors that differed between included and excluded children were considered in our analyses. Following diverse cohorts is important, but a challenge; our participation rates at 2 years of age are similar to those of other NIH-funded birth cohort studies in the United States comprised of urban and suburban women not selected by allergic status.[37] Further, those included in the analyses tended to be more educated and have higher income. These and other observed differences should be considered when comparing our results to other populations.

In summary, racial disparities in allergic disease related outcomes were seen as early as age 2 years in our cohort study with African American children being more likely to have: a positive skin prick test, an elevated allergen-specific IgE and atopic dermatitis. African American children also tended to have higher total IgE. The associations between race and these outcomes could not be explained by family income, maternal education or marital status, family housing payment, prenatal exposure to indoor pets, living with a smoker, breastfeeding or a host of other factors. A less marked association between race and wheeze dissipated when adjusted for all the SES and other factors. Novel hypotheses beyond those related to SES (or better ways of measuring SES) are needed to explain the causes of these racial disparities and investigations of the causation of disparities must include information from very early life.

Acknowledgments

Footnotes

References