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Original Research: ASTHMA |

Obesity and Asthma*: A Specific Phenotype? FREE TO VIEW

Andréa Lessard, BSc; Hélène Turcotte, MSc; Yvon Cormier, MD; Louis-Philippe Boulet, MD, FCCP
Author and Funding Information

*From the Centre de Recherche, Hôpital Laval, Institut de cardiologie et de pneumologie de l’Université Laval, Québec, QC, Canada.

Correspondence to: Louis-Philippe Boulet, MD, FCCP, Hôpital Laval, 2725 Chemin Sainte-Foy, Québec, QC Canada, G1V 4G5; e-mail: lpboulet@med.ulaval.ca



Chest. 2008;134(2):317-323. doi:10.1378/chest.07-2959
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Background: Obesity is associated with an increased prevalence of asthma, especially in women, and appears to be more severe in the obese. This study aimed to determine if obese subjects have a specific asthma phenotype.

Methods: Forty-four consecutive obese subjects (body mass index [BMI] ≥ 30 kg/m2) and 44 consecutive nonobese subjects (BMI < 25 kg/m2), all with asthma, completed an asthma control questionnaire, and underwent methacholine challenge with symptom perception scores, and sputum induction for differential cell count. BMI, waist circumference, and waist-to-hip ratio also were measured.

Results: Despite similar expiratory flows, bronchodilator response, airway responsiveness to methacholine, and symptom perception scores, asthma control was poorer in obese subjects than in nonobese subjects (p = 0.005). Total lung capacity (p = 0.01), expiratory reserve volume (p < 0.0001), functional residual capacity (p < 0.0001), and residual volume (p = 0.006) were lower in obese subjects than in nonobese subjects. Induced-sputum eosinophil and neutrophil counts were similar in both groups, although there was an inverse correlation between sputum eosinophils and waist circumference and a trend for a similar relationship for BMI. Blood serum C-reactive protein (p = 0.009) and fibrinogen (p = 0.0004) levels were higher in obese subjects than in nonobese subjects.

Conclusion: Obese people with asthma had poorer asthma control than nonobese asthmatics despite similar symptoms perception. Bronchial and systemic inflammatory characteristics and the specific pattern of pulmonary function changes suggest a different phenotype of asthma in these subjects.

Trial registration: Clinicaltrials.gov Identifier: NCT00532363 and NCT00532831.

Figures in this Article

In the last 2 decades, the prevalence of both asthma and obesity has increased worldwide.1Obesity promotes a systemic inflammatory state. Adipocytes may release proinflammatory hormones that in turn could contribute to the reported increase and severity of asthma in the obese population,2especially in women.35 Other factors such as changes in pulmonary mechanics or common genetic determinants may also be involved in this correlation. For example, obesity may be associated with a reduced expiratory reserve volume (ERV), functional residual capacity (FRC), and tidal volume.6Furthermore, obesity in nonasthmatic subjects is associated with a reduction in the bronchoprotection of deep inspiration during induced bronchoconstriction.7 However, the mechanisms by which obesity may enhance the clinical expression of asthma-related physiologic changes have not been fully elucidated.

Some observations suggest that asthma in obese subjects may differ from the classical phenotype of asthma. These include the fact that weight loss is associated with a significant reduction of asthma symptoms even without improvement of airway responsiveness.810 Moreover, obese subjects referred for severe asthma often seem to have poorly controlled asthma,1112 and often show a reduced response to standard asthma medications.1315

The purpose of the present study was to examine obese and nonobese subjects with a confirmed diagnosis of asthma based on bronchodilator response or airway responsiveness measurements and compare the following: (1) the level of asthma control; (2) pulmonary function and airway responsiveness to methacholine; (3) perception of asthma symptoms; and (4) airway and systemic inflammation. The goal was to determine if obese and nonobese people with asthma have different phenotypes of asthma.

Subjects and Design

We recruited obese and nonobese subjects from Laval Hospital outpatient clinics and advertisements. Participants were eligible if they had documented physician-diagnosed asthma with airway responsiveness to methacholine < 16 mg/mL, were ≥ 18 years old, were obese (body mass index [BMI] ≥ 30 kg/m2) or nonobese (BMI < 25 kg/m2) according to the criteria of the current international classification,1 and were nonsmokers or ex-smokers for > 6 months. We aimed at recruiting patients receiving a bronchodilator with or without regular maintenance therapy. Subjects unable to provide an informed consent, or who were pregnant, or had a comorbid illness that could interfere with the proposed tests were excluded. The results were blinded to the subjects and to the investigators who performed the analysis. Obese and nonobese subjects were paired for age, sex, and maintenance treatment of asthma. The study was approved by our local Ethic Committee, and all subjects signed an informed consent form.

Measurements

On first visit, height, weight, waist, and hip circumferences were measured, and BMI and waist-to-hip ratio were calculated. After a physical examination conducted by a physician, participants completed the Asthma Control Questionnaire (ACQ).16 The ACQ was designed to evaluate asthma control by asking subjects to recall symptoms and β2-agonist use in the last week, and their FEV1.,16 The questionnaire includes seven items rated on a 7-point scale (0 = good control, 6 = poor control). The patients were also given skin-prick tests with a battery of 24 common aeroallergens. Atopy was defined as at least one positive skin response (wheal diameter ≥ 3 mm) after 15 min.

Spirometry with bronchodilator response and sputum induction were also conducted in the first visit, and venous blood samples were drawn. The pulmonary function tests were performed according to American Thoracic Society criteria,17and predicted values were obtained from the work of Knudson et al.18Postbronchodilator measurements were made 15 min after the administration of 200 μg of inhaled salbutamol. Sputum induction was performed using the method described by Pin et al19and modified by Pizzichini et al.20 Induced-sputum samples were analyzed for counts of eosinophils, neutrophils, macrophages, and lymphocytes. The serum samples were analyzed for levels of IgE (IgE), eosinophils, C-reactive protein (CRP), and fibrinogen.

On the second visit, lung volumes were obtained by body plethysmography according to standardized methods.21Methacholine inhalation testing with perception of respiratory symptoms also was conducted, as described by Hargreave et al.22Airway responsiveness to methacholine was expressed as the provocative concentration of methacholine that induces a 20% fall in FEV1 (PC20). The severity of wheezing, phlegm production, chest tightness, breathlessness, and cough following methacholine inhalation were self-evaluated by the subjects on a modified Borg scale (from 0 to 10 for each symptom, with 0 = “nothing at all” and 10 = maximum symptoms).23 The perception score corresponding to the PC20 was intrapolated for each symptom.

Statistical Methods

The sample size was derived from a pilot project on a small group of obese vs nonobese subjects and on previous studies published. Based on previous results, the study was designed to have 80% power to detect a significant relationship between BMI and asthma control score (ACQ) with a type I error of 5%. To achieve this power, 30 subjects were needed in each group. Categorical variables were expressed as percentages and compared using Fisher exact test. Continuous variables were expressed using mean ± SD and were compared using the Student’s paired t test. For some variables, graphical analysis of residuals with predicted values revealed a relationship between the variances of the observations and the means for these variables. In these cases, the logarithm transformation was the appropriate test, and hence the relevant statistical results were expressed using the log-transformed values. Because of missing data, unpaired comparisons were used to compare sputum induction differential cell counts between obese and nonobese subjects. Relationships between variables were measured using the Spearman correlation coefficient or linear regression and were adjusted with first-order partial correlations. A p value < 0.05 using a two-tailed test was taken as significant for all statistical tests. Data analysis was performed using statistical software (SAS v9.1.3 and StatView v5.0.1; SAS Institute; Cary, NC).

Eighty-eight of the 96 subjects who agreed to take part in the study were eligible. Three obese and three nonobese subjects had a PC20 ≥ 16 mg/mL and thus were excluded. One participant was unable to perform the methacholine challenge, and another failed to attend the second visit. Half of the subjects (n = 44) used monotherapy with short-acting β2-agonists (SABAs), and the other half took SABAs combined with inhaled corticosteroids (ICS). The mean dose of ICS taken by subjects using these medications was equivalent to 827 ± 282 μg/d of chlorofluorocarbon-beclomethasone among the obese subjects, and 814 ± 247 μg/d among the nonobese subjects. Subject characteristics are summarized in Table 1 .

Total ACQ scores were significantly higher for the obese subjects than for the nonobese participants (p = 0.005). Obese subjects also reported significantly more activity limitation (p = 0.003), breathlessness (p = 0.009), and wheezing (p = 0.005) in the previous week than did their nonobese counterparts. The number of awakenings per night due to asthma-related symptoms (p = 0.15), frequency of presence of symptoms on waking (p = 0.10), and amount of SABA use (p = 0.11) were not significantly different in obese and nonobese subjects. As a whole, ACQ total score was positively correlated with BMI (p = 0.01, r = 0.27) and waist circumference (p = 0.03, r = 0.24), but not with waist-to-hip ratio (p = 0.93, r = 0.01). Small differences between groups were noted in regard to asthma duration, smoking, and atopy, but when adjusting for those variables, results of the analysis were unchanged.

Spirometry and lung volumes results are summarized in Table 2 . FEV1, FVC, FEV1/FVC, and forced expiratory flow between 25% and 75% of FVC (FEF25–75%) were similar in both groups (p > 0.05). However, ERV, FRC, total lung capacity (TLC), residual volume (RV), and inspiratory capacity (IC) were significantly different in obese and in nonobese subjects. Correlations of these parameters with BMI, waist circumference, and waist-to-hip ratio are presented in Figure 1 . Moreover, ERV was correlated with total ACQ score (p = 0.03, r = − 0.22), but this association was no longer significant after adjusting for BMI and waist circumference. Among obese subjects, ERV and FRC did not differ significantly between subjects taking ICS and those using only SABAs to control their asthma (p = 0.84 and p = 0.20, respectively); they also were not significantly correlated with PC20 (p = 0.33 and p = 0.31).

Airway responsiveness to methacholine was higher in subjects with ICS treatment, but there was no significant difference between the airway responsiveness of obese and nonobese subjects (Fig 2 ). At 20% fall in FEV1 during the methacholine challenge, obese and nonobese subjects reported the same amount of wheezing (p = 0.22), phlegm production (p = 0.11), chest tightness (p = 0.35), breathlessness (p = 0.64), and cough (p = 0.21).

Sputum induction was successful in 28 obese and in 23 nonobese subjects. The differential cell counts are presented in Table 3 ; there was no significant difference between both groups (Fig 3 ). Globally, the percentage of eosinophils in the induced-sputum samples was significantly correlated with waist circumference (p = 0.01, r = − 0.36), and there was such trend for BMI (p = 0.06, r = − 0.26).

Obese subjects had a mean serum IgE of 216 ± 367 IU/mL, while in nonobese subjects it was 219 ± 245 IU/mL (p = 0.96). Blood eosinophil percentages were similar in both groups (p = 0.32). Mean serum level of CRP was significantly higher in the obese subjects (4.3 ± 3.2 mg/L) than in the nonobese subjects (2.4 ± 3.4 mg/L) [p = 0.001], and was significantly correlated with BMI (p = 0.0004, r = 0.39), waist circumference (p < 0.0001, r = 0.45), and waist-to-hip ratio (p = 0.03, r = 0.23) in both groups. The mean serum level of fibrinogen was also significantly higher in obese (3.7 ± 0.7 g/L) than in nonobese subjects (3.1 ± 0.6 g/L; p = 0.0002). Furthermore, it was correlated with BMI (p = 0.0003, r = 0.39), and waist circumference (p = 0.0009, r = 0.36), but not with waist-to-hip ratio (p = 0.36, r = 0.01). In all subjects taken together, induced sputum eosinophil count was negatively correlated with blood CRP titer (p = 0.009, r = − 0.37). This correlation remained significant after adjusting for BMI (p = 0.03, r = − 0.30) and waist-to-hip ratio (p = 0.02, r = − 0.33), but not after adjusting for waist circumference (p = 0.08, r = − 0.25).

We found that obese subjects reported poorer asthma control than nonobese subjects. This was despite a similar perception of asthma symptoms during the methacholine challenge and comparable maintenance treatment of their asthma. It suggests no impairment or increase in acute symptom report following bronchoconstriction. To our knowledge, this is the first study comparing self-perception of asthma symptoms between obese and nonobese subjects. Airway hyperresponsiveness was comparable in both groups, but differences in airway and systemic inflammatory parameters, and changes in pulmonary function with obesity, suggest a particular asthma phenotype in obese subjects. The blood level of CRP and waist circumference were correlated with lung volume changes and with decreased induced-sputum eosinophil, which could indicate a possible impact of fat distribution and systemic inflammatory state in people who are obese on the development and clinical presentation of asthma.

In agreement with our results indicating obese subjects have poorer asthma control than nonobese subjects, Lavoie et al11found a significant association between BMI and total ACQ score in 382 asthmatics. In addition, Saint-Pierre et al12showed that, compared with nonobese subjects, overweight and obese asthmatics were more likely to have poorly controlled asthma despite pharmacologic treatment. Other studies1315 looking at the efficiency of asthma medication also documented poorer control of asthma in obese subjects despite appropriate medication. However, obesity has been associated with a subjective increase in dyspnea.24 Therefore, even if obese patients were specifically questioned about breathlessness and activity limitation due to their asthma, obesity itself could have influenced the results.

Poor asthma control in obese individuals could also have been due to their having an altered perception of asthma symptoms. However, we found no significant difference in asthma symptom perception between individuals in both groups with the same degree of bronchoconstriction. A different phenotype of asthma, reduced response to treatment, or more severe asthma could explain the poorer asthma control in obese asthmatics.

It is well known that obesity is associated with a reduction in ERV and FRC.2527 Obesity also causes a reduction of both FEV1 and FVC with a preserved FEV1/FVC ratio. However, previous studies30 yielded contradictory data on whether obesity affects respiratory function in asthmatic subjects. We demonstrated that people who have asthma and are obese have a different pulmonary function profile than their nonobese counterparts. Although we have not tested specifically this hypothesis in the present study, obesity and insulin resistance may be the common pathways underlying lung function impairment and metabolic syndrome.29

Breathing near the airways closing volume has also been associated with increased airway responsiveness3132 and, as previously mentioned, obesity in nonasthmatic subjects is associated with a reduction in the bronchoprotection of deep inspiration during induced bronchoconstriction.7 Therefore, it is difficult to determine how much of the observed abnormalities is related to the mechanical effect of obesity or to an altered immune response that could have also influenced bronchoreactivity. Moreover, our findings suggest that lung volume changes are unlikely to be the sole cause of reduced asthma control in people who are obese. In this regard, there was no direct association between ERV or FRC and ICS use, or PC20 and ACQ score. This suggests that lung volume changes with obesity do not have a significant influence on asthma severity.

Mild-to-moderate asthma is classically associated with an eosinophilic inflammation of the airways, although some show either a neutrophilic inflammation or no inflammation at all when noninvasive assessment of airway inflammation with, for example, induced-sputum analysis is used.33Our study did not uncover a significant difference between groups in induced-sputum levels of eosinophils and neutrophils. This is consistent with the results recently obtained by Todd et al34 showing no difference in the total or differential cell counts between obese and nonobese participants when the data were analyzed according to BMI category, gender, dose of ICS, and presence or absence of asthma.

We also found, however, that the number of sputum eosinophils significantly decreases as waist circumference increases. This may be suggestive of a role of abdominal obesity in changing the inflammatory pattern in the airways and possibly then contributing to the development of the disease in obese individuals though other mechanisms. In this regard, obesity is commonly associated with systemic inflammation.35In our study, levels of blood CRP and fibrinogen—two nonspecific markers of systemic inflammation—were higher in obese than in nonobese subjects. Interestingly, levels of CRP also were inversely correlated with those of induced-sputum eosinophils. This suggests a possible influence of systemic inflammation on bronchial inflammation. Furthermore, since the type of systemic inflammation found in obesity seems to vary with fat distribution and body composition,3637 our data suggest an impact of abdominal obesity on the production of specific markers of systemic inflammation. This may in turn lead to, or modulate, a particular type of airway inflammation in various organs such as the airways, in subjects with abdominal obesity. Further studies with more specific markers of bronchial and systemic inflammation are needed to confirm these results. The impact of weight distribution and body composition on airway inflammation also needs to be further investigated.

Our study has some limitations. First, 84% of the people enrolled were women. This is expected because asthma is generally more often related to obesity in women than men.35 This may be considered to limit the generalizability of the results, although it brings gender-specific key information. Weight distribution and body composition between women and men could differentially affect lung volumes and level of systemic inflammation. Hormonal effects could also influence these parameters. However, this study was not designed to evaluate these issues. A second limitation could be the significant variability in BMI among the obese subjects, ranging from 30.0 to 49.5 kg/m2. Although the effects of obesity on asthma may vary with the degree of obesity, our data provide useful information on this overall population.6 A third possible limitation is the fact that obese subjects had more hypertension, type II diabetes, and gastroesophageal reflux disease than their nonobese counterparts, although these differences were not statistically significant. The impact of comorbidities on asthma in obese subjects needs further research. Moreover, some differences observed between obese and nonobese subjects could also have been due to the different smoking history between the two groups. However, there were no significant differences in this regard between both groups, and conclusions remained unchanged after adjusting for this parameter. Finally, not all subjects could produce a sputum sample, limiting the power of the study with respect to inflammatory parameters.

Overall, our results suggest a different phenotype of asthma in obese individuals. In addition, our study points to the need for studies of the cause of poorer asthma control in asthma subjects. Furthermore, the observed changes in lung volume, as well as the decrease in induced sputum eosinophil counts with increased waist circumference and CRP among obese people with asthma, provide the basis for additional studies on the role of obesity in the development and clinical expression of asthma. It is hoped that the results will help to provide better asthma management to subjects with comorbid obesity.

Abbreviations: ACQ = asthma control questionnaire; BMI = body mass index; CRP = C-reactive protein; ERV = expiratory reserve volume; FEF25–75% = forced expiratory flow between 25 and 75% of FVC; FRC = functional residual capacity; IC = inspiratory capacity; ICS = inhaled corticosteroids; PC20 = provocative concentration of methacholine inducing a 20% fall in FEV1; RV = residual volume; SABA = short-acting β2-agonist; TLC = total lung capacity

Potential financial conflicts of interest: advisory boards: Dr. Boulet (Altana, AstraZeneca, GlaxoSmithKline, Merck Frosst, Novartis); lecture fees: Dr. Boulet (3M, Altana, AstraZeneca, GlaxoSmithKline, Merck Frosst, Novartis); sponsorhip for investigator-generated research: Dr. Boulet (AstraZeneca, GSK, Merck Frosst, Schering); research funding for participating in multicenter studies: Dr. Boulet (3M, Altana, AsthmaTx, AstraZeneca, Boehringer-Ingelheim, Dynavax, Genentech, GlaxoSmithKline, IVAX, Merck Frosst, MedImmune, Novartis, Roche, Schering, Topigen, Wyeth); support for the production of educational materials: Dr. Boulet (AstraZeneca, GlaxoSmithKline, Merck Frosst); governmental: Dr. Boulet (Adviser for the Conseil du Médicament du Québec, Member of the Quebec Workmen Compensation Board Respiratory Committee); organizational: Dr. Boulet (Chair of the Canadian Thoracic Society Guidelines Dissemination and Implementation Committee). Dr. Cormier is president and chief medical officer of a biotech company whose objective is to develop a new drug for the treatment of asthma. Dr. Lessard and Dr. Turcotte have no conflicts of interest to declare.

Support was provided by Réseau en Santé Respiratoire du Fonds de Recherche en Santé du Québec.

Table Graphic Jump Location
Table 1. Demographics and Medical Characteristics*
* 

Data are presented as mean ± SD or No. (%). GERD = gastroesophageal reflux disease.

Table Graphic Jump Location
Table 2. Spirometry, Lung Volumes, and Methacholine Test Results*
* 

Data are presented as mean ± SD or geometric mean (95% confidence interval).

 

Obese vs nonobese subjects.

Figure Jump LinkFigure 1. Spearman correlations between lung volumes, BMI, waist-to-hip ratio, and waist circumference.Grahic Jump Location
Figure Jump LinkFigure 2. Pulmonary function results between obese and nonobese subjects. Light bars indicate obese subjects receiving SABAs and ICS. Light gray bars indicate obese subjects receiving SABAs. Darker gray bars indicate nonobese subjects receiving SABAs and ICS. Dark bars indicate nonobese subjects receiving SABAs.Grahic Jump Location
Table Graphic Jump Location
Table 3. Differential Cell Count in Induced Sputum*
* 

Data are presented as mean percentage of cells (± SD). No significant differences were found between groups for the various cell counts.

 

Median value 7.8 kg/m2.

Figure Jump LinkFigure 3. Differential cell count in induced sputum between obese and nonobese subjects. Light bars indicate obese subjects receiving SABAs and ICS. Light gray bars indicate obese subjects receiving SABAs. Darker gray bars indicate nonobese subjects receiving SABAs and ICS, Dark bars indicate nonobese subjects receiving SABAs.Grahic Jump Location

The authors thank Line Ringuette, Philippe Prince, Marie-Eve Boulay, and nurses from the research center for their invaluable help, and the Laval University statistics department as well as Serge Simard for statistical analysis.

Obesity: preventing and managing the global epidemic; report of a WHO consultation.World Health Organ Tech Rep Ser2000;894,i-253
 
Shore, SA, Johnston, RA Obesity and asthma.Pharmacol Ther2006;110,83-102. [PubMed] [CrossRef]
 
Chen, Y, Rennie, D, Cormier, Y, et al Sex specificity of asthma associated with objectively measured body mass index and waist circumference: the Humboldt study.Chest2005;128,3048-3054. [PubMed]
 
Hancox, RJ, Milne, BJ, Poulton, R, et al Sex differences in the relation between body mass index and asthma and atopy in a birth cohort.Am J Respir Crit Care Med2005;171,440-445. [PubMed]
 
Boulet, LP, Des, CA The link between obesity and asthma: a Canadian perspective.Can Respir J2007;14,217-220. [PubMed]
 
Parameswaran, K, Todd, DC, Soth, M Altered respiratory physiology in obesity.Can Respir J2006;13,203-210. [PubMed]
 
Boulet, LP, Turcotte, H, Boulet, G, et al Deep inspiration avoidance and airway response to methacholine: influence of body mass index.Can Respir J2005;12,371-376. [PubMed]
 
Schachter, LM, Salome, CM, Peat, JK, et al Obesity is a risk for asthma and wheeze but not airway hyperresponsiveness.Thorax2001;56,4-8. [PubMed]
 
Aaron, SD, Fergusson, D, Dent, R, et al Effect of weight reduction on respiratory function and airway reactivity in obese women.Chest2004;125,2046-2052. [PubMed]
 
Bustos, P, Amigo, H, Oyarzun, M, et al Is there a causal relation between obesity and asthma? Evidence from Chile.Int J Obes (Lond)2005;29,804-809. [PubMed]
 
Lavoie, KL, Bacon, SL, Labrecque, M, et al Higher BMI is associated with worse asthma control and quality of life but not asthma severity.Respir Med2006;100,648-657. [PubMed]
 
Saint-Pierre, P, Bourdin, A, Chanez, P, et al Are overweight asthmatics more difficult to control?Allergy2006;61,79-84. [PubMed]
 
Dixon, AE, Shade, DM, Cohen, RI, et al Effect of obesity on clinical presentation and response to treatment in asthma.J Asthma2006;43,553-558. [PubMed]
 
Peters-Golden, M, Swern, A, Bird, SS, et al Influence of body mass index on the response to asthma controller agents.Eur Respir J2006;27,495-503. [PubMed]
 
Boulet, LP, Franssen, E Influence of obesity on response to fluticasone with or without salmeterol in moderate asthma. Respir Med. 2007; ;
 
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Figures

Figure Jump LinkFigure 1. Spearman correlations between lung volumes, BMI, waist-to-hip ratio, and waist circumference.Grahic Jump Location
Figure Jump LinkFigure 2. Pulmonary function results between obese and nonobese subjects. Light bars indicate obese subjects receiving SABAs and ICS. Light gray bars indicate obese subjects receiving SABAs. Darker gray bars indicate nonobese subjects receiving SABAs and ICS. Dark bars indicate nonobese subjects receiving SABAs.Grahic Jump Location
Figure Jump LinkFigure 3. Differential cell count in induced sputum between obese and nonobese subjects. Light bars indicate obese subjects receiving SABAs and ICS. Light gray bars indicate obese subjects receiving SABAs. Darker gray bars indicate nonobese subjects receiving SABAs and ICS, Dark bars indicate nonobese subjects receiving SABAs.Grahic Jump Location

Tables

Table Graphic Jump Location
Table 1. Demographics and Medical Characteristics*
* 

Data are presented as mean ± SD or No. (%). GERD = gastroesophageal reflux disease.

Table Graphic Jump Location
Table 2. Spirometry, Lung Volumes, and Methacholine Test Results*
* 

Data are presented as mean ± SD or geometric mean (95% confidence interval).

 

Obese vs nonobese subjects.

Table Graphic Jump Location
Table 3. Differential Cell Count in Induced Sputum*
* 

Data are presented as mean percentage of cells (± SD). No significant differences were found between groups for the various cell counts.

 

Median value 7.8 kg/m2.

References

Obesity: preventing and managing the global epidemic; report of a WHO consultation.World Health Organ Tech Rep Ser2000;894,i-253
 
Shore, SA, Johnston, RA Obesity and asthma.Pharmacol Ther2006;110,83-102. [PubMed] [CrossRef]
 
Chen, Y, Rennie, D, Cormier, Y, et al Sex specificity of asthma associated with objectively measured body mass index and waist circumference: the Humboldt study.Chest2005;128,3048-3054. [PubMed]
 
Hancox, RJ, Milne, BJ, Poulton, R, et al Sex differences in the relation between body mass index and asthma and atopy in a birth cohort.Am J Respir Crit Care Med2005;171,440-445. [PubMed]
 
Boulet, LP, Des, CA The link between obesity and asthma: a Canadian perspective.Can Respir J2007;14,217-220. [PubMed]
 
Parameswaran, K, Todd, DC, Soth, M Altered respiratory physiology in obesity.Can Respir J2006;13,203-210. [PubMed]
 
Boulet, LP, Turcotte, H, Boulet, G, et al Deep inspiration avoidance and airway response to methacholine: influence of body mass index.Can Respir J2005;12,371-376. [PubMed]
 
Schachter, LM, Salome, CM, Peat, JK, et al Obesity is a risk for asthma and wheeze but not airway hyperresponsiveness.Thorax2001;56,4-8. [PubMed]
 
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Obesity and asthma: current knowledge and future needs. Curr Opin Pulm Med Published online Nov 15, 2014.;
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