Allergen-specific IgE as a biomarker of exposure plus sensitization in inner-city adolescents with asthma

Abstract

Background: Relationships among allergen-specific IgE levels, allergen exposure and asthma severity are poorly understood since sensitization has previously been evaluated as a dichotomous, rather than continuous characteristic.

Methods: Five hundred and forty-six inner-city adolescents enrolled in the Asthma Control Evaluation study underwent exhaled nitric oxide (FE(NO)) measurement, lung function testing, and completion of a questionnaire. Allergen-specific IgE levels and blood eosinophils were quantified. Dust samples were collected from the participants' bedrooms for quantification of allergen concentrations. Participants were followed for 12 months and clinical outcomes were tracked.

Results: Among sensitized participants, allergen-specific IgE levels were correlated with the corresponding settled dust allergen levels for cockroach, dust mite, and mouse (r = 0.38, 0.34, 0.19, respectively; P < 0.0001 for cockroach and dust mite and P = 0.03 for mouse), but not cat (r = -0.02, P = 0.71). Higher cockroach-, mite-, mouse-, and cat-specific IgE levels were associated with higher FE(NO) concentrations, poorer lung function, and higher blood eosinophils. Higher cat, dust mite, and mouse allergen-specific IgE levels were also associated with an increasing risk of exacerbations or hospitalization.

Conclusions: Allergen-specific IgE levels were correlated with allergen exposure among sensitized participants, except for cat. Allergen-specific IgE levels were also associated with more severe asthma across a range of clinical and biologic markers. Adjusting for exposure did not provide additional predictive value, suggesting that higher allergen-specific IgE levels may be indicative of both higher exposure and a greater degree of sensitization, which in turn may result in greater asthma severity.

Figure 1

Partial correlations of Specific IgE and Settled Dust Allergen Concentrations. Correlations of each specific IgE (y-axis) and matching exposures (x-axis) are depicted with regression lines and 95% confidence limits. The Partial Pearson correlations and P-values head each cell and are adjusted for gender, age, race, study group and income above $15 000 per year. IgE and exposure data are log base 10 transformed and only include subjects with detectable IgE levels (≥0.10 kUA/l). The Dust Max cell displays the maximum value of Der f 1- or Der p 1-specific IgE level and allergen concentrations.

Figure 2

Effects of Exposure and Allergen-specific IgE on Inflammatory Biomarkers. Beta coefficients and 95% Confidence intervals are depicted with ‘’ for allergen-specific IgE and with ‘’ for allergen exposure. The sample size is approximately 534 for all estimates and varies slightly due to randomly missing data across each outcome and predictor. All models adjust for income above $15 000 a year, study group, gender, age, and race. Both IgE and exposure measures are log base 10 transformed and entered as independent covariates in separate models.

Figure 3

Effects of Exposure and Allergen-specific IgE on Lung Function. Beta coefficients and 95% Confidence intervals are depicted with ‘’ for allergen-specific IgE and with ‘’ for allergen exposure. The sample size is approximately 534 for all estimates and varies slightly due to randomly missing data across each outcome and predictor. All models adjust for income above $15 000 a year, study group, gender, age, and race. Both IgE and exposure measures are log base 10 transformed and entered as independent covariates in separate models.

Figure 4

Linear relationships between Allergen-specific IgE levels and Biomarker and Lung Function Measures. The sample size is approximately 534 for all estimates and varies slightly due to randomly missing data across each outcome and predictor. All models adjust for income above $15 000 a year, study group, gender, age, and race.

Figure 5

Effects of Exposure and Allergen-specific IgE on Clinical Outcomes. Odds ratios and 95% Confidence intervals are depicted with ‘’ for allergen-specific IgE and with ‘’ for allergen exposure. The sample size is approximately 534 for all estimates and varies slightly due to randomly missing data across each outcome and predictor. All models adjust for income above $15 000 a year, study group, gender, age, and race. Both IgE and exposure measures are log base 10 transformed and entered as independent covariates in separate models.