Atopy and Pulmonary Function Among Healthy-weight and Overweight/ Obese Children with Asthma

Abstract

Introduction:

Epidemiologic studies have found low/ absence of atopy in obese asthmatic children, but the association or lack thereof of atopy with disease morbidity, including pulmonary function, in obese asthma is not well understood. We sought to define the association of atopy with pulmonary function in overweight/obese minority children with asthma.

Methods:

In a retrospective chart review of 200 predominantly minority children evaluated at an academic Pediatric Asthma Center over 5 years, we compared the prevalence of atopy, defined as ≥1 positive skin prick test or serum-specific IgE quantification to environmental allergens, and its association with pulmonary function in overweight/obese (body mass index (BMI) >85%) (n=99) to healthy-weight children (BMI 5–85% for age) (n=101).

Results:

In a cohort comprised of 47.5% Hispanics and 39.5% African Americans, 81% of overweight/obese and 74% of healthy-weight children were atopic. While atopic healthy-weight children had lower percent-predicted FEV₁ (93±13.6 vs. 107%±33.2, p =0.03) and lower percent-predicted FVC (93%± 12.2 vs 104%±16.1, p=0.01) as compared to non-atopic children, atopy was not associated with FEV₁ (p=0.7) or FVC (p=0.17) in overweight/obese children. Adjusting for demographic and clinical variables, atopy was found to be an independent predictor of FEV₁ and FVC in healthy-weight (β=−2.4, p=0.07 and β= −1.7, p=0.04, respectively) but not in overweight/obese children (β=0.6, p=0.5 and β= 0.8, p=0.3).

Conclusions:

Atopy is associated with lower lung function in healthy-weight asthmatics but not in overweight/obese asthmatics, supporting the role of non-allergic mechanisms in disease burden in pediatric obesity-related asthma.

Introduction

The prevalence of obesity in the pediatric population has been increasing over the past several decades such that 18.5% of U.S. children, aged 2–19 years old, are obese¹. The obesity burden is disproportionately higher in inner-cities and urban communities, including African Americans and Hispanics. In 2015–2016, 25.8% of all Hispanic and 22% of all African American children were obese¹.

Obesity is an independent risk factor for asthma^2,3. Obese children with asthma have a substantial clinical and economic healthcare burden. They report more frequent use of rescue medication, greater shortness of breath, and poor responsiveness to asthma controller medications^4–6. Obese children are at greater odds of being bronchodilator unresponsive compared to non-obese⁴. They also have more frequent asthma exacerbations requiring emergency department visits and/or treatment with oral corticosteroids⁷, and have higher odds of having longer hospital stays and requiring mechanical ventilation compared to the non-obese⁸.

Although childhood asthma is consistently associated with allergic sensitization, there is conflicting data regarding the role of allergic sensitization in childhood obesity-related asthma. Early reports of data from the National Health and Nutrition Examination Study III (NHANES III) indicated that the prevalence of childhood asthma, but not atopy, increased with higher BMI quartiles⁹. Another cross sectional analysis of more recent NHANES data reported an association between adiposity and asthma among non-atopic, but not atopic children¹⁰. In a birth cohort of 731 children followed up to 8 years old, Murray et al. found that overweight status was associated with increased risk of asthma and eczema, but no association was found between BMI and atopy¹¹. Similarly, Kattan et al. found no relationship between adiposity or adipokines and total IgE and blood eosinophil levels in adolescents in the Inner-City Asthma Consortium¹². Other studies on predominantly minority, low-income populations showed that atopy, but not obesity, was associated with worse asthma control and severity^13,14. In addition, overweight/obese children were found to have lower odds of allergen sensitization when compared to normal weight asthmatic children¹⁵. Contrary to these findings, an Italian and a Taiwanese study found higher prevalence of allergic sensitization in overweight/obese compared with healthy-weight children^16,17. With few exceptions^12–14, the majority of these studies are in populations with small proportions of Hispanic and African American children. Thus, there is paucity of data on the patterns of allergic sensitization among urban minority obese children with asthma.

One of the mechanisms by which obesity is associated with asthma is through its effect on pulmonary function. Several studies have reported low FEV₁ and FEV₁/FVC ratio among obese children as compared to normal-weight children with asthma¹⁸. However, few studies have investigated the direct association of allergic sensitization with pulmonary function deficits in obese children with asthma¹⁹. Although one study investigated the association in children residing in Puerto Rico¹⁹, there are no studies that have investigated the association of allergic sensitization with pulmonary function in mainland US minority children with obesity-related asthma.

To address these gaps in knowledge, we compared the prevalence of allergic sensitization and its association with pulmonary function in obese asthmatic and healthy-weight asthmatic children of African American and Hispanic backgrounds residing in an urban environment. We hypothesized that obese asthmatic children have lower prevalence of allergic sensitization to common indoor and outdoor allergens as compared to healthy-weight children with asthma. We also hypothesized that allergic sensitization correlates with pulmonary function in healthy-weight but not in obese children.

Methods

Study population

We conducted a retrospective analysis of medical records of outpatient visits of pediatric patients aged 5 to 21 years old evaluated from July 1^st, 2011, to June 30^th, 2016 at the pediatric Asthma Center at the Children’s Hospital at Montefiore (CHAM), a consultative center staffed by a pediatric pulmonologist and allergist. Asthma was defined as two or more episodes of bronchial hyper-responsiveness, responsive to short acting bronchodilator, with or without systemic steroids. Patients seen for outpatient visits on specific Asthma Center clinic dates were identified through Looking Glass^™ Clinical Analytics (Streamline Health, Atlanta, Georgia), which is a patented, user-friendly software application that extracts data from clinical and administrative data sets²⁰. Of the 325 charts reviewed, 200 were included for the final analysis. The remainder were excluded due to not being Asthma Center patients (n=58), missing/ incomplete atopic sensitization data (n=43), or due to the presence of co-morbid conditions including underlying immunodeficiency, multiple congenital abnormalities, connective tissue disorders, or sickle cell disease (n=24) (Supplemental Figure 1). The study was approved by the Institutional Review Board at Albert Einstein College of Medicine, Bronx, NY.

Clinical and demographic variables

Data was collected on demographic variables and measures of asthma disease burden. Demographic variables collected included patient age, sex, ethnicity/race, height, weight, and BMI. Healthy weight was defined as BMI 5–85^th%, overweight as BMI >85–95^th%, and obese as BMI>95^th percentile for age and sex, as per the Center for Disease Control (CDC) classification²¹. As a measure of asthma disease burden, we collected data on asthma severity classified as per the National Heart Lung and Blood Institute guidelines²². Among children aged 4 to 11 years old, patient’s asthma control was assessed via the Childhood Asthma Control Test²³, while the Asthma Control Test (ACT) was used for those 12 years and older. A score of <19 on either test was suggestive of poor asthma control²³. We also quantified the number of emergency room visits for asthma and oral steroid courses received over the prior year.

Pulmonary function testing (PFTs)

Pulmonary function tests (PFTs) were performed at the CHAM Pulmonary Function Test Laboratory. Experienced technicians performed the testing according to the American Thoracic Society guidelines using the CareFusion Vmax Encore 229C E spirometer and CareFusion Vmax Autobox 62 J body plethysmography. PFT values, including forced vital capacity (FVC), forced expiratory volume in the first second (FEV₁), FEV₁/FVC ratio, and mid-expiratory flow rates (FEF_25–75%), were abstracted from the test done at the clinic visit when allergy testing was performed. Short acting beta agonists were withheld on the day of pulmonary function testing but long acting beta agonists, as part of controller therapy, were continued as per schedule. Percent predicted values, obtained by comparing observed values with predicted values for patients’ age, sex, and height were included in the analysis²⁴. All included PFTs met ATS criteria for reproducibility and acceptability²⁵.

Allergen sensitization and atopy

Results of skin prick testing (SPT) and serum levels of specific IgE to the most common indoor and outdoor allergens to the Northeastern United States were abstracted. Testing included up to 28 allergens. SPT was performed using commercially available allergen extracts and analyzed wheal-and-flare responses were resulted by an allergist at the clinic visit. A wheal response 3 mm larger than the negative control was considered positive²⁶. When SPT was not done, either due to acute asthma exacerbation, recent use of antihistamines, or other causes, serum-specific IgE was quantified by Quest Diagnostics and IgE levels above 0.35 kU/L were considered positive. Allergen sensitization was further sub-grouped into sensitization to indoor allergens (cockroach, cat, dog, dust mites, feather, rodents (mouse or rat), or guinea pig) and outdoor allergens (grass, trees, or weed pollen). Molds were excluded from sub-grouping, as certain types could be both indoor and outdoor allergens. Positive allergy to trees included at least one of 9 types of allergens (elm, ash, beech, birch, oak, maple, cedar, hickory, or tree mix); allergens for weeds included ragweed, weed mix, sorrel, lambs quarter, cocklebur, and English plantain; grasses included Northern grass or grass mix; mold included mold mix, Alternaria alternata, Cladosporium herbarum, Aspergillus fumigatus, or Penicillium.

A child was considered atopic if he/she tested positive by either serum IgE testing or SPT to at least one of the tested environmental allergens²⁶. Children were classified as non-atopic if they had at least 8 or more tests done and all tests were negative. Fourteen children (7 in each study group) were excluded from further analysis as less than 8 tests were done with all tests being negative.

Statistical Analysis

Our primary outcome of interest, the comparison of presence of atopic sensitization between overweight/obese and healthy-weight children with asthma, was conducted using χ² test. Student T test was applied to quantify the association of pulmonary function variables with atopy. Other demographic and clinical variables were analyzed using the Student T test if they were continuous variables and normally distributed or Mann-Whitney U test if not normally distributed. Categorical variables were analyzed using the χ² test other than race/ethnicity, which was analyzed using Fisher-exact test. Since age and pulmonary function variables differed between obese and healthy-weight children with asthma, we conducted linear regression analysis, adjusting for age, sex, and ethnicity (the latter two included for demographic significance) to quantify the association of atopic status with pulmonary function, independent of the demographic variables. Given the small proportions of children in the Asian and Non-Hispanic White category (Table 1), they were grouped into an “Others” category for the regression analysis. African American and Others category were included in the regression model, retaining the Hispanic category as the reference group. Regression diagnostics were conducted on the multivariable models. Statistical significance was set a priori at a p value of <0.05. Analysis was conducted on STATA statistical software, version 14.2.

Table 1:

Demographic and clinical characteristics of the study population

	Healthy-weight (BMI 5–85th %) (n=101)	Overweight/obese (BMI >85th %) (n=99)	P value*
Demographic characteristics
Age (years), mean ± SD	7.2 ± 4.1	9 ± 4.3	<0.01
Sex, n (%)			0.61
Male	56 (55)	56 (57)
Female	45 (45)	43 (43)
Race/Ethnicity, n (%)			0.56
Hispanic	46 (46)	49 (50)
African American	41 (41)	38 (38)
Asian	2 (2)	1 (1)
Non-Hispanic White	1 (1)	4 (4)
Other	11 (11)	7 (7)
Clinical characteristics
Asthma Severity, n (%)			0.72
Intermittent	9 (10)	6 (6)
Mild Persistent	34 (36)	37 (38)
Moderate Persistent	42 (44)	43 (43)
Severe Persistent	9 (10)	13 (13)
Asthma Control n (%)			0.04
Well controlled	52 (57)	39 (40)
Not well controlled	23 (25)	40 (41)
Poorly controlled	16 (18)	18 (19)
Medication Use, n (%)
ICS	78 (88)	71 (79)	0.08
ICS/LABA	13 (14)	21 (22)	0.12
Montelukast	54 (56)	66 (69)	0.06
ED visits in prior 12 months (median, IQR)	2 (1–3)	2 (1–4)	0.26
Steroid courses in prior 12 months (median, IQR)	2 (1–3)	2 (1–5)	0.23
Pulmonary function variables
FVC, mean ± SD	96.1 ± 13.9	96.2 ± 14.5	0.94
FEV1, mean ± SD	96.7 ± 21	87.3 ± 16.8	<0.01
FEV1/FVC, mean ± SD	88.3 ± 11.6	79.1 ± 9	<0.01
FEF25–75%, mean ± SD	89.2 ± 28.1	69.6 ± 24.5	<0.01

BMI, body mass index; SD, standard deviation; ICS, inhaled corticosteroid; ICS/LABA, combination inhaled corticosteroid and long-acting beta agonist; FVC, forced vital capacity; FEV1, forced expiratory volume in 1 second; FEV1/FVC, ratio of FEV1 and FVC; FEF_25–75%, forced expiratory flow rate at 25–75% of expiratory flow

^*Continuous variables were analyzed using Student’s T test other than ED visits and steroid courses, which were analyzed using Mann-Whitney U test; categorical variables were analyzed using χ² test other than ethnicity, which was analyzed using Fisher Exact Test.

Results

Characteristics of the study population

The demographic and clinical characteristics of the patients are summarized in Table 1. Of the 200 patients included in the analysis, 101 patients were healthy-weight and 99 were overweight/obese group. The BMI distribution of the cohort is summarized in Supplemental Figure 2. Patients in the overweight/obese group were older than in the healthy-weight group (p<0.01) but did not differ in other characteristics. The majority of patients in both groups were either Hispanic or African American with no between-group differences in the distribution of race or ethnicity. Asthma severity did not differ between the two study groups but a larger proportion of overweight/obese children had not-well controlled or poorly controlled asthma (p=0.04). There was no difference in the use of controller medications, prior ED visits, or steroid courses between the groups. Baseline FEV₁, FEV₁/FVC and FEF_25–75% were significantly lower in the overweight/obese patients compared to the healthy-weight patients.

Allergy testing profile of overweight/obese and healthy-weight children with asthma

Of the 200 patients, 129 patients underwent SPT and 71 underwent serum-specific IgE testing. Of the 28 potential allergens, there was no difference in the mean number of allergens that overweight/obese and healthy-weight groups (17 ± 7.2 vs 16.8 ± 6.9; p=0.76) were tested for. After removing the 7 children in each group that were tested for fewer than 8 allergens, the proportion of children with atopy was similar in both groups, with 81% (n=76) of overweight/obese asthmatics and 74% (n=73) in the healthy-weight asthmatics having one or more positive allergy test results to environmental allergens (p=0.3) (Table 2). The sensitization patterns did not differ between the study groups when testing was sub-grouped into indoor and outdoor allergens. However, when comparing sensitization to specific allergens, a higher number of overweight/obese asthmatics were sensitized to indoor allergens, cat and cockroach (p=0.03 and <0.01, respectively), compared to healthy-weight asthmatics.

Table 2:

Comparison of atopic status and sensitization to specific allergens between overweight/ obese and healthy-weight children with asthma

	Healthy-weight n (%)	Overweight/obese n (%)	P value
Atopic	73 (74)	76 (81)	0.29
Non-Atopic	25 (26)	18 (19)
Sensitization to indoor allergens	70 (71)	74 (76)	0.38
Sensitization to outdoor allergens	51 (52)	57 (58)	0.26
Sensitization to specific allergens
Cat	36 (38)	52 (54)	0.03
Dog	40 (41)	50 (53)	0.10
Dust mite	38 (38)	40 (43)	0.55
Roach	33 (34)	53 (55)	<0.01
Rodent	14 (20)	19 (28)	0.29
Grass	22 (25)	30 (33)	0.20
Tree	47 (49)	52 (56)	0.34
Weeds	31 (33)	32 (35)	0.83
Mold	19 (20)	26 (27)	0.27

Association of atopy with disease burden among overweight/obese and healthy-weight children with asthma

On univariate analysis, atopy was not associated with FEV₁ (p=0.7) or FVC (p=0.17) in overweight/obese asthmatic children (Figure 1). In contrast, atopic healthy-weight children had lower FEV₁ (93 ± 13.6 vs 107 ± 33.2, p=0.03) and FVC (93 ± 12.2 vs 104 ± 16.1, p=0.01) as compared to non-atopic children. Although overweight/ obese children had higher sensitization to cat and cockroach, sensitization to indoor allergens was associated with lower FEV₁ (105 ± 32 vs 93 ± 13, p=0.05) and FVC (102 ± 17.2 vs 94 ± 11.7, p=0.03) in healthy-weight children but not in overweight/obese (88 ± 14.5 vs 87 ± 17.2, p=0.9 and 94 ± 16 vs 97 ± 14.4, p=0.6, respectively). Sensitization to outdoor allergens was also associated with lower FVC (101 ± 14.1 vs 92 ± 12.5, p= 0.01) but not FEV₁ (101 ± 26 vs 92 ± 13.8, p= 0.08) in healthy-weight children; its association with FVC (91 ± 12.8 vs 99 ± 14.9, p= 0.05) or FEV₁ (84 ± 14.7 vs 89 ± 17.6, p=0.2) did not reach statistical significance in overweight/obese children. There was no association of atopy with FEV₁/FVC or FEF_25–75% among healthy-weight or overweight/obese children.

Figure 1.

The association of atopy with pulmonary function indices (FVC, FEV₁, FEV₁/FVC and FEF _25–75%) are compared between healthy-weight and overweight/ obese children with asthma.

After adjusting for demographic variables in multivariable linear regression analyses (Table 3), atopy remained an independent predictor of FEV₁ and FVC in healthy-weight (β= −13.25, p=0.03 and β= −10.23, p=0.01, respectively), i.e. mean percent predicted FEV₁ was 13.25 points and mean percent predicted FVC was 10.23 points lower among atopic as compared to non-atopic healthy weight children. Atopy was not found to be an independent predictor of FEV₁ (β=2.56, p=0.7) or FVC (β= 7.45, p=0.21) in overweight/obese children. Among the demographic variables, sex was a significant predictor of FEV₁ in healthy-weight children; girls had higher percent predicted FEV₁ relative to the boys. None of the demographic variables were predictors of FEV₁ or FVC among overweight/ obese children.

Table 3.

Multivariable regression analysis of the association of atopy with pulmonary function

a. Normal weight children
Predictor Variable	Percent-predicted FVC *	Percent-predicted FEV1*
Atopy	−10.23 (−18.31, −2.14), 0.01	−13.26 (−25.16, −1.35), 0.03
Age	−0.25(−1.17, 0.67), 0.59	−0.63(−1.99, 0.72), 0.35
Sex^	5.71 (−1.60, 13.02), 0.12	14.58 (3.81, 25.35), 0.01
Ethnicity^^
African Americans	2.84 (−5.03, 10.71), 0.47	10.19 (−1.41, 21.78), 0.08
Others	−7.74 (−19.79, 4.30), 0.20	−4.66 (−22.40, 13.09), 0.60
b. Overweight/obese children
Predictor Variable	Percent-predicted FVC *	Percent-predicted FEV1 *
Atopy	7.45(−4.25, 19.15), 0.21	2.56 (−10.84, 15.96), 0.70
Age	−0.37 (−1.32, 0.57), 0.43	−0.93 (−2.01, 0.16), 0.09
Sex^	4.44 (−2.77, 11.64), 0.22	8.25 (−0.01, 16.50), 0.05
Ethnicity^^
African Americans	3.43 (−4.26, 11.11), 0.38	.91 (−7.9, 9.71), 0.83
Others	−2.34 (−13.85, 9.17), 0.69	2.22 (−10.96, 15.41), 0.74

^*β (95% CI), p value)

^{^}Males were the reference group

^{^^}Hispanics were the reference group

Discussion

In this study, contrary to our hypothesis and existing literature, we found no difference in the prevalence of atopy to environmental aeroallergens between overweight/obese and healthy-weight minority children with asthma. While overweight/obese children had lower pulmonary function at baseline as compared to healthy-weight children with asthma, atopy was associated with lower pulmonary function in healthy-weight children, but not among the overweight/obese children. Together, these findings suggest that atopy is not contributing to lower pulmonary function, a measure of disease burden, among overweight/obese children²⁷.

Our findings in a predominantly minority cohort are relevant, since we report the lack of association between pulmonary function and atopy among a cohort of overweight/obese minority children that are typically predisposed to higher disease burden of atopic asthma^28,29. In keeping with prior studies that reported higher atopy as well as asthma severity and prevalence in African American and Hispanic children^28,29, we also observed high prevalence of atopy in our study sample, irrespective of their body weight status, with sensitization levels partially overlapping with those observed among children residing in Puerto Rico¹⁹ and higher than those previously reported in a Bronx cohort³⁰. Our observed association between atopy and lower pulmonary function in healthy-weight asthmatics, but not among overweight/obese asthmatics, provides a biological mechanism to explain observations by Lu et al. on a similar predominantly minority, low-income population from Baltimore and Boston where atopy, but not obesity, was associated with worse asthma control and severity¹³. Since obesity, independent of atopy, is associated with lower lung volumes, but not necessarily lower airway obstruction³¹, our findings, in context of the existing literature on minority children, suggest that mechanisms other than atopy underlie the higher disease burden, as measured by pulmonary function deficits, among obese asthmatics. Our study also extends findings from prior studies into Hispanic children.

These consistent findings among minority children differ from those among Italian and Asian cohorts, suggesting that ethnicity may potentially contribute to the observed differences between the association of allergic sensitization and disease burden in pediatric obesity-related asthma^16,17. Another potential explanation for the difference may be the chronology of onset of asthma versus obesity among children, which is not addressed in cross sectional studies, including ours. While asthma that is incident to obesity is frequently non-atopic³², children with classic allergic childhood asthma are at increased risk of becoming obese³³. In addition to the chronological relationship between obesity and asthma, the dynamics of weight gain in relationship to age, as a marker of somatic growth in children, may explain the lower FEV₁ in our overweight/obese cohort, which was younger than the Puerto Rican cohort in whom higher BMI, and to a lesser extent, percent body fat, was associated with higher FEV₁ and FVC¹⁹. Moreover, since BMI was included as a continuous variable in the analysis on the Puerto Rican cohort¹⁹, given the curvilinear relationship between body weight and asthma³⁴, we speculate that weight gain to a certain extent may be beneficial for pulmonary function in children¹⁸, but becomes deleterious when it reaches obese proportions, in light of lower FEV₁ observed in children who became obese in the Childhood Asthma Management Program cohort³⁵. Thus, longitudinal studies are needed to address the chronology of asthma and obesity onset as well as their relationship with age and extent and rapidity of weight gain in the different developmental stages of children, in addition to the association of disease burden with atopy.

The lack of association of lower pulmonary function with atopy in obese children suggests that the obesity-mediated effects on pulmonary physiology may underlie these pulmonary function deficits. Physiologic studies have shown that obesity affects lung mechanics by altering airflows (both FEV₁ and FVC)³⁶, along with changing respiratory system compliance, likely due to fatty infiltration of the chest wall, and excess soft tissue weight compressing the rib cage^36,37. Since not all obese children develop asthma or pulmonary function deficits³⁸, obesity-mediated inflammation, with elevated leptin and decreased adiponectin, and systemic non-allergic inflammation, with elevated interleukin (IL)-6, Tumor Necrosis factor (TNF) and Interferon-gamma (IFNγ)³⁹, is another potential underlying mechanism. Increased leptin levels have been associated with asthma and severity of exercise-induced bronchoconstriction in children⁴⁰. Similarly, non-allergic Th1 predominant systemic immune patterns found in obese asthmatics have been associated with lower pulmonary function in obese children with asthma^41,42. Given that obesity skews the inflammatory response from Th2 to Th1, based on our findings, we speculate that obesity may dampen airway inflammation in response to allergen exposure, leading to an attenuated effect of atopy on pulmonary function. This hypothesis is supported by the lack of an association between aeroallergen sensitization and elevated leptin or BMI in urban Puerto Rican children⁴³. In addition, obesity-mediated metabolic abnormalities have been linked with pulmonary function deficits in obesity-related asthma³¹. Therefore, mechanistic studies are needed to define the individual contributions of leptin, non-allergic systemic Th1 polarization, and metabolic dysregulation, to pulmonary physiology in the context of obesity.

We acknowledge multiple limitations to our study. First, it was a retrospective chart review rather than a prospective study. For this reason, we had access only to BMI and not to other measures of adiposity, such as waist circumference or subcutaneous fat distribution, and we acknowledge the limitations of using BMI as a measure of adiposity⁴⁴. However, since we included objective measures of atopy and pulmonary function, and the data abstraction approach was the same for the study samples, it is unlikely that the retrospective nature influenced our findings. Secondly, the sample size of our study was limited due to several children being excluded due to missing data or presence of co-morbidities. By taking such a stringent approach, we were able to remove the influence of these coexisting medical conditions. Since the data was collected from a real-life clinical setting, patients did not consistently have pulmonary function testing done at the time of the clinic visit or were tested for allergen sensitization using a limited panel, which further decreased the total number of PFTs included in the analysis. We also did not systematically test all children seen at the clinic for bronchodilator responsiveness, which limits our ability to address the contribution of inherent airway hyper-responsiveness relative to adiposity to the pulmonary function deficits observed in our cohort. Moreover, fractional exhaled nitric oxide was not available at our institution during all years included in the study, which would have provided an additional dimension on the association of allergic airway inflammation with pulmonary function in normal-weight and overweight/obese asthmatic children respectively.

Conclusion

In conclusion, we found that although overweight/obese children had lower pulmonary function relative to their healthy-weight counterparts, atopy was not associated with pulmonary function deficits in overweight/obese minority children with asthma. Our findings support the need for further investigation of the mechanisms that underlie pulmonary function deficits in overweight/obese children. As the obesity burden grows in the pediatric population, especially among minority children, it is imperative to develop a greater understanding of the underlying pathophysiology that underlies pulmonary disease burden associated with obesity, in order to develop and implement alternative treatment options for those not responsive to currently available therapies.

Supplementary Material

Sup fig S1

Supplemental Figure 1. Consort diagram summarizing the study cohort

Sup fig S2

Supplemental Figure 2. Distribution of BMI percentile among the children including in this study cohort.