Asthma & Allergy

Asthma & Allergy

Page 8

Cover Story

Asthma & Allergy


Contributing Roles of Environment, Ethnic Origin and Genes

Asthma, the most common chronic pediatric disease in the U.S., has since the mid-1980s killed or hospitalized African-American children at a greater rate than children of other racial groups, according to the Centers for Disease Control and Prevention.

Health officials have long pointed the finger of blame at house dust mites, cockroaches, tobacco smoke and other environmental risk factors known to trigger asthma in black (and Hispanic) children growing up in America’s economically distressed inner-cities.

Along with these factors, however, researchers are beginning to implicate nature as well as nurture for the alarming rise in asthma among racial minorities.

African-American children are more likely to have higher levels of the antibody IgE, according to a recent study appearing in CHEST. Higher serum IgE levels, along with racial differences in lung volume and airway responsiveness documented previously and confirmed in this study, may provide biological explanations for increased asthma prevalence and severity in African-American children.

“There is need for further study, but it would not be surprising if racial genetic differences accounted for part of the increased prevalence of asthma among blacks as compared with whites,” Michael Sly, MD, who heads the Section of Allergy and Immunology at Children’s National Medical Center in Washington, D.C., told ADVANCE.

Confounding Factors
Researchers at the Henry Ford Health System in Detroit sought to explore racial differences in physiologic factors associated with pediatric asthma severity. In an attempt to separate the confounding factors of poverty from physiologic factors, they selected 569 children from similar, middle-class socioeconomic backgrounds.

Seventy-nine children were African-American. The other 490 were described as European-American. All were between ages six and eight.

Investigators took medical histories, gave physical examinations, and employed allergen skin testing, spirometry and methacholine challenges. They measured total and allergen-specific IgE, the antibody that causes all allergic reactions. People with allergic diseases, including asthma, produce large amounts of IgE antibodies in response to any number of environmental factors.

The results of the study showed a significant difference in the geometric mean serum IgE in African-American children (60.63 IU/mL) versus that in European-American children (27.48 IU/mL). Racial differences were even greater when compared in those children with serum IgE levels of greater than 100 IU/mL: 40.6 percent for African-Americans and 16.2 percent for European- Americans.

In looking at just African-American children, the difference in serum IgE levels between those with asthma (74.44 IU/mL) and those without (59.15 IU/mL) was not significant. Differences among European-American children, on the other hand, were quite significant: 67.36 IU/mL for those with asthma and 24.78 for those without asthma.

In testing for sensitization to major indoor allergens, including cockroaches, the researchers found African-American children were more likely to be sensitized to ragweed and grass. They also noted lower pulmonary function levels. Only 75.9 percent of African-American children had FEV1 scores of more than 70 percent of predicted as compared to 99.2 percent of European-American children.

“In summary,” the researchers reported in the May 2000, issue of CHEST, “we found a significant racial difference in the relationship between total serum IgE and airway responsiveness and between serum IgE and asthma status. To our knowledge, this finding has not been reported in the literature. These differences are consistent with the hypothesis that African-American children may be predisposed to more severe asthma.”

More Studies Needed
Asked if he thought physiologic differences predispose African-American children to more severe asthma, Reynold Panettieri Jr., MD, an asthma specialist at the University of Pennsylvania Medical Center in Philadelphia, said:

“Right now, we don’t know. But many of us in the asthma business feel that racial differences in allergies exist. There might be differences in the inflammatory response. We know in other diseases­hypertension, for instance­that blacks respond differently to drugs than whites. More studies will give us greater insight.”

By contrast, many studies have already documented how adverse environmental factors contribute to asthma’s high morbidity and mortality among racial minorities. Today, according to the web site, blacks are twice as likely to die from asthma as whites.

“Poverty and single-parent households impact adversely upon the ability to purchase medications, reach physicians’ offices for care, monitor asthma, and minimize exposure to dust mites and cockroaches,” noted Sly, also a Professor of Pediatrics at The George Washington University School of Medicine and Health Sciences in Washington, D.C.

“Over-reliance on emergency rooms as the primary source of care for asthma contributes to inadequate asthma education and treatment. Insurance still does not cover costs of peak flow meters or allergen-proof encasings for mattresses and pillows, not to mention other precautions that may be necessary to reduce exposure to allergens.”

Improvements in care for such patients, he concluded, may depend on future governmental health care and taxation initiatives.

Michael Gibbons is an ADVANCE senior editor.

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