The Journal of Allergy and Clinical Immunology
Volume 121, Issue 3 , Pages 620-621, March 2008

The Editors' Choice

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Childhood asthma varies widely by neighborhood 

Asthma is already the most prevalent chronic disease of childhood in the United States, with an estimated 8.9 million children being affected. Childhood asthma prevalence has been shown to be higher in urban communities overall without an understanding of differences by neighborhood. As part of the Chicago Initiative to Raise Asthma Health Equity (CHIRAH) study, Gupta et al (p 639) analyzed the asthma status of 48,917 Chicago schoolchildren and geocoded the results by Chicago neighborhoods. Overall asthma prevalence was 12.9%; however, rates varied from almost 0% to 44%, depending on the child's neighborhood (see Figure). Childhood asthma rates in predominantly black neighborhoods varied from 4% to 44%, those in predominantly white neighborhoods varied from 2% to 30%, and those in predominantly Hispanic neighborhoods varied from 0% to 29%. Although sex, age, household members with asthma, and neighborhood income significantly affected asthma prevalence, these factors did not explain the differences seen among neighborhoods. Race/ethnicity explained a significant proportion, but not all, of the neighborhood variation. Understanding neighborhood attributes associated with asthma rates might lend insight into the important public health problem of “urban asthma” and help reduce childhood asthma morbidity.

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Children's respiratory health in the aftermath of Hurricane Katrina 

Rabito et al (p 622) conducted a study examining indoor air mold levels and indices of respiratory health in a cohort of children living in New Orleans shortly after Hurricane Katrina. The cohort comprised a select sample of children—namely, those attending a private primary school that had the ability to reopen in January 2006, relatively soon after the storm. Although only 37% of the children's homes were flooded, nearly all (96%) of the families reported some type of hurricane damage to the home. The study results showed that indoor mold levels were low and children's lung function was normal despite hurricane damage (see Figure). Overall declines in mold levels and respiratory symptoms were observed during the study period. A higher proportion of children had upper and lower respiratory symptoms at the baseline post-Katrina measurement in comparison with symptoms reported before Hurricane Katrina and at the follow-up measurement 2 months later. The authors suggest that this transient spike in symptoms could be due to a possible short-term storm damage–related environmental influence. Increased exposure to rotting debris and particles generated by the removal of drywall, roofing material, and outdoor vegetation may have contributed to respiratory irritation and congestion.

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Delay in DPT vaccination reduces the risk of asthma 

Diphtheria-pertussis-tetanus (DPT) immunization stimulates a TH2-type immune response and decreases microbial burden, potentially shifting the balance between TH1 and TH2 immunity in early childhood. The epidemiologic evidence linking DPT immunizations to childhood asthma is inconsistent. Research was undertaken by McDonald et al (p 626) to determine whether the timing of DPT immunization has an effect on the development of asthma. They performed a retrospective longitudinal study of the complete immunization and health care records of children born in Manitoba, Canada, in 1995. The odds ratio for asthma at age 7 years according to timing of whole-cell DPT immunization was computed from logistic regression, adjusting for well-known asthma risk factors. Among 11,531 children who received at least 4 doses of DPT, the risk of asthma was reduced to one half in children whose first dose of DPT was delayed by more than 2 months compared with children whose first dose was given on schedule at 2 months. The likelihood of asthma in children with delays in all 3 doses was 0.39 (95% CI, 0.18-0.86). This protective effect may be subsequent to vaccine-induced fever, which is greater with whole-cell pertussis vaccine. Further research is required with acellular DPT vaccine. The benefits of altering immunization schedules need to be weighed against the risks.

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Risk factors for anaphylaxis to peanuts and tree nuts 

Although allergies to peanuts and tree nuts are relatively common, fatalities after ingestion of these foods are rare, occurring in less than 1 in a million people. Unfortunately, most life-threatening or fatal allergic (anaphylactic) reactions are unpredictable, making management and reassurance of patients with these nut allergies difficult. In a study of more than 1000 patients with peanut and tree nut allergies over a 12-year period, Summers et al (p 632) show that the nature and severity of anaphylactic symptoms correlates with the patient's atopic disease. Inasmuch as severe nut allergy–induced bronchospasm was 7 times more likely in patients with severe asthma, the authors suggest that optimizing asthma control may be crucial in reducing the chances of patients developing this potential complication. Severity of allergic reactions did not correlate with specific serum IgE or skin prick wheal measurements, but severe pharyngeal edema was 10-fold more likely in patients with low blood angiotensin-converting enzyme (ACE) levels (see Figure). As ACE is the major enzyme involved in breakdown of bradykinin, Summers et al suggest that this inflammatory mediator contributes to the induction of life-threatening pharyngeal edema. Thus, the study also provides a potentially novel insight into the etiology and management of nut allergy–induced upper airway obstruction.

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Sensitization does not develop in utero 

It has been hypothesized that allergen-specific sensitization might occur in utero. This concept has led to interventional trials and current recommendations aimed at allergy prevention through allergen avoidance during pregnancy. In this issue of the Journal, Bønnelykke and coauthors (p 646) demonstrate the presence of allergen-specific IgE in 14% of cord blood samples from a birth cohort of asthmatic mothers. However, this specific IgE was no longer present at 6 months of age, which shows that it did not represent clinically relevant sensitization in infancy. Furthermore, specific IgE in cord blood completely matched specific IgE in maternal blood with respect to allergen specificity (see Figure), level of specific IgE, and ratio of total IgE/specific IgE. Finally, specific IgE was associated with IgA in cord blood. Taken together, this evidence strongly suggests that allergen-specific IgE in cord blood is the result of transfer of IgE from mother to fetus rather than of intrauterine production. This leads the authors to question the existence of intrauterine sensitization and to suggest that guidelines recommending allergen avoidance during pregnancy be withdrawn.

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Increased TH1 apoptosis as a mechanism for TH2 predominance in atopic disease 

Given the chronic-ongoing-memory type immunologic nature of atopic disease, models that envisage responsible nuclear factors for naive T-cell differentiation might not fully explain the TH2 response in atopy. Although there is an enormous amount of T-cell infiltration in the dermis in atopic dermatitis and very active skin-homing and dehoming of T cells, there is no evidence for the expansion of lymphocytes in peripheral blood in patients. This raises the interesting possibility that unequal apoptosis of TH1 and TH2 effector cells might lead to preferential deletion of one subset over the other. Akkoc et al (p 652) investigated the differences and mechanisms of TH1 and TH2 cell apoptosis in polyallergic atopic individuals with high total IgE. They found that TH1 cells, particularly their high IFN-γ–producing fraction, as well as the CXCR3+ T cells, show significantly increased apoptosis in atopic individuals. Neutralization experiments demonstrated a dominant role of IFN-γ and Fas-Fas-ligand interaction–mediated TH1 cell apoptosis.

PII: S0091-6749(08)00149-8

doi:10.1016/j.jaci.2008.01.017

The Journal of Allergy and Clinical Immunology
Volume 121, Issue 3 , Pages 620-621, March 2008