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* From the Departments of Pulmonary and Critical Care (Dr. Thomson) and Emergency Medicine (Ms. Clark and Dr. Camargo), Massachusetts General Hospital, Boston, MA.
Correspondence to: Carlos A. Camargo, Jr, MD, DrPH, FCCP, Director, EMNet Coordinating Center, Department of Emergency Medicine, Massachusetts General Hospital, 55 Fruit St, Clinics Building 397, Boston, MA 02114; e-mail: marc{at}partners.org
| Abstract |
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Design: Multicenter, prospective cohort study.
Setting: Twenty-six North American EDs.
Participants: Five hundred seventy-two patients aged 18 to 54 years presenting with acute asthma.
Interventions: None.
Measurements and results: A standardized interview assessed demographic characteristics, asthma history, and details of the current asthma exacerbation. Data on ED medical management and disposition were obtained by chart review. Three of four asthmatic patients were either overweight (BMI, 25 to 29.9; 30%) or obese (BMI,
30; 44%). Normal weight/underweight, overweight, and obese patients did not differ on several markers of chronic asthma severity; obese subjects tended to rate symptoms more severely and to use more inhaled ß-agonists in the 6 h hours prior to ED presentation despite a significantly higher initial percentage of predicted peak expiratory flow (PEF) [44%, 45%, and 51%, respectively; p < 0.05]. The three BMI groups responded similarly to acute therapy in the ED, with all groups demonstrating reversible airway obstruction. The sex distribution by BMI group differed markedly (p < 0.001), with women less often overweight (40% vs 24%) and more often obese (30% vs 52%). Since women were more likely have a higher initial PEF (45% vs 53%, p < 0.001), we stratified by sex to further examine the relation of BMI to asthma severity. The observed BMI-asthma associations were due largely, but not entirely, to confounding by sex.
Conclusions: Despite lingering concerns about the veracity of "asthma" among obese individuals, asthma exacerbations among obese and nonobese adults were remarkably similar. Potential differences (eg, in symptom perception, use of inhaled ß-agonists before ED presentation, initial PEF rate) were due, in large part, to confounding by sex.
Key Words: asthma, adult body mass index obesity sex
| Introduction |
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30.3
4
The National Health and Nutrition Examination Survey III (from 1988 to 1994)3
estimated the prevalence of adult obesity in the United States as 18 to 23%, while more recent national survey data (1999)5
estimate 27%; the Behavioral Risk Factor Surveillance System (BRFSS) [2000] indicates an obesity prevalence of 20%.6
7
Increases in obesity are largest among women and minority groups.8
9
10
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In the United States, obesity costs approximately $99 billion, of which 52% is due to medical costs.12 Asthma is another common, chronic disorder, and its prevalence also is rising in the United States and worldwide.13 14 Between 1980 and 1994, the prevalence of self-reported asthma increased from 31 to 55 per 1,000 population.2 Like obesity, asthma increased more among women and minority groups.9 15 16 17 In the United States, asthma costs approximately $11 billion according to most recent estimates.18 19
The concomitant rise in both obesity and asthma has led several groups to examine a possible causal relation between these conditions.8 20 21 22 23 24 25 26 27 Some groups have raised concerns that the "asthma" of obese individuals may not be real, or that it may differ, on a pathophysiologic basis, from that of nonobese people. Specifically, these groups propose that "obese asthma" may not involve bronchial hyperresponsiveness or reversible airway obstruction but instead reflect dyspnea related to excess weight and subsequent misdiagnosis.24 25 Along those lines, the relationship between BMI and acute asthma is not known. In this multicenter, prospective study, we determined the prevalence of obesity among 572 adults presenting to urban emergency departments (EDs) with acute asthma, and examined the relationship between BMI and acute and chronic asthma severity in this high-risk population.
| Materials and Methods |
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Data Collection
The ED interview assessed demographic characteristics, asthma history, and details of the current asthma exacerbation. Data on ED management and disposition were obtained by chart review. All forms were reviewed by site investigators before submission to the MARC Coordinating Center in Boston, where they underwent further review by trained personnel and then double-data entry.
BMI was used as a measure of excess body fat.4
29
Normal/underweight is defined as a BMI < 25, overweight is defined as a BMI of 25 to 29.9, and obesity is defined as a BMI
30. Median family income was estimated using home ZIP codes obtained from hospital administration.30
31
Primary care provider status was assigned on the basis of the following question: "Do you have a primary care provider (such as a family doctor, internist, or nurse practitioner)?" If yes, patients were asked to provide the name and address of their provider. Smoking status was coded as never smoker, former smoker, and current smoker. The severe symptoms classification was assigned to patients who reported severe symptoms during the 24 h preceding the ED visit on at least one of two questions (ie, asthma symptoms "most of the time" or "severe" discomfort and distress due to their asthma).
Peak expiratory flow (PEF) was used to assess acute asthma severity, and is expressed as percentage of the value, based on age, sex, race, and height.32 Changes in PEF are expressed as the relative change in percentage of predicted (eg, an improvement from 40% predicted to 70% predicted would be expressed as a change of 75%).
Statistical Analysis
All analyses were performed using STATA 7.0 (StataCorp; College Station, TX). Data are presented as proportion (95% confidence interval [CI]), mean ± SD, or median (interquartile range [IQR]). The prevalence of obesity in the study population was compared with the prevalence of obesity among adults from the general population, as reported in national studies.5
6
7
The association between BMI and asthma severity was examined using
2 test, analysis of variance, or Kruskal-Wallis test, as appropriate. Stratified analyses and multivariate linear and logistic regression models were performed. Factors associated with BMI (or with the outcome of interest) at p < 0.10 in univariate analysis were evaluated for inclusion in multivariate regression models. All odds ratios (ORs) are presented with 95% CIs. All p values are two sided, with p < 0.05 considered statistically significant.
| Results |
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Figure 1
shows the BMI classification of these patients, with three of every four patients either overweight (30%) or obese (44%). The high prevalence of BMI
25.0 did not materially differ by socioeconomic status. For example, the prevalence of overweight or obesity was comparable among those who had and had not graduated from high school (74% vs 73%, p = 0.83) and across quartiles of median household income (74%, 74%, 77%, and 73%, respectively; p = 0.83).
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Comparisons of the three BMI groups are shown in Table 1
. As previously noted, obese patients were significantly more likely to be female. Although the total with BMI
25 did not differ between the 196 men and 376 women (70% vs 76%, p = 0.10), the distribution within BMI categories did (p < 0.001): women were less often overweight (40% vs 24%) and more often obese (30% vs 52%). Overall, men had a mean BMI of 28.4 ± 5.8 while women had a mean BMI of 32.1 ± 9.3 (p < 0.001). Obese participants were slightly older, but did not differ according to several other important sociodemographic factors.
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Acute asthma presentation and ED course are shown in Table 2
. Compared to normal/underweight and overweight individuals, the obese groups had a significantly higher initial PEF (48% vs 53%, p < 0.04), despite a trend toward more severe subjective symptoms (76% vs 81%, p = 0.15) and more inhaled ß-agonist puffs within 6 h of presenting to the ED (four puffs vs six puffs, p = 0.03). Although nonobese subjects had a shorter duration of symptoms than their obese counterparts (duration
24 h, 38% vs 47%; p = 0.05), obese participants did not differ by ED management or clinical response (eg, change in PEF, hospital admission).
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Tables 3 , 4 show the relation of BMI to the more important asthma factors, with analyses stratified by sex. Obesity was not related to initial PEF among men (p = 0.72) or among women (p = 0.27). Among men, obese patients were more likely to report recent use of inhaled steroids and were least likely to be admitted to the hospital, but did not differ from normal/underweight or overweight patients according to other acute or chronic asthma severity measures. Among women, obese patients were least likely to report duration of symptoms of < 24 h, while overweight women had the shortest ED length of stay. Other acute and chronic asthma measures did not differ across BMI groups among women.
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| Discussion |
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For example, we found no association between obesity and chronic asthma severity, using several measures such as history of steroid use, hospitalizations, intubations, number of ED visits, and hospital admissions. Although data are sparse, if anything, prior studies22 25 suggest that obese participants with asthma reported increased severity of symptoms. Taken together, the medical literature does not support contentions that the asthma of obese individuals is of a lesser chronic severity or simply reflects misdiagnosed dyspnea.36
Although our study largely confirmed the absence of any important obesity-related differences, we did find that obese individuals had a higher initial percentage of predicted PEF at presentation to the ED. This finding was juxtaposed against a nonsignificant trend in tendency for obese subjects to rate their symptoms more severely and to use more inhaled ß-agonists in the 6 h prior to ED presentation. Might obese persons have a heightened awareness of their bronchoconstriction? Or is this evidence for a relatively greater dyspnea unrelated to bronchoconstriction, as posited by some groups?24 25 The comparable response to bronchodilator therapy, with documented airway reversibility in all three BMI groups, provides real-world evidence against claims that many obese individuals do not have "true" asthma. At least in the ED settingwith > 2 million annual visits in the United States alone13 the asthma exacerbations of obese individuals appear quite real and respond appropriately to bronchodilator therapy.
Several observations led us to explore potential confounding by sex of the obesity-PEF finding. As previously reported in another cohort of ED patients,39 we confirmed that women were almost twice common as men among ED patients with acute asthma, and that women presented with higher initial percentage of predicted PEF. In another prior publication by our group, we found that women were more likely than men to report severe asthma symptoms and activity limitations at similar levels of airflow obstruction.40 Since 77% of obese individuals in the current study were women, the potential for confounding was clear. Indeed, the relationship between obesity and initial PEF was due largely, but not entirely, to confounding by sex. In stratified analyses, the association between obesity and initial PEF was not significant in both men (p = 0.72) and women (p = 0.27), without evidence of any significant interaction by sex.
This study has some potential limitations. As in most prior studies, the temporal relation between obesity and asthma cannot be established using our study design. Although this issue was not our focus, we note that prospective studies of asthma incidence provide temporally correct evidence for a causal relation.8 36 37 38 Our hypothesis, supported by other investigators, is that exercise intolerance from asthma does not lead to obesity. Beckett et al23 investigated the relationship between obesity and incident asthma in a prospective study of 4,547 participants followed up for 10 years, and concluded physical inactivity did not explain the association between a gain in BMI and incident asthma found in women. Additionally, Chen et al41 assessed the relationship between energy expenditure and asthma in 16,813 patients, and determined that physical inactivity determined by energy expenditure failed to explain the relationship between obesity and asthma.
We focused instead on the remarkably high prevalence of ED patients with comorbid obesity and asthma. The addition of a nonasthmatic ED comparison group would have nicely complemented the national survey data since it is possible that ED patients, in general, are more obese; the prevalence of obesity is higher among individuals with a low socioeconomic status.42 However, the prevalence of obesity among ED patients with asthma was high regardless of socioeconomic status. Moreover, the presence or absence of additional comparison groups in no way detracts from our observation that three of every four ED patients with asthma are overweight or obese. Although these data may not be generalizable outside the acute setting, greater awareness of this public health problem might lead urgent-care staff to initiate a multidisciplinary approach for the prevention and treatment of both conditions.
In addition, because asthma is a common disease in the general population that still lacks a universally accepted definition, asthma overdiagnosis may have been common.43 Overdiagnosis of asthma among obese individuals would complicate interpretation of the apparent relationship between obesity and asthma. Although bronchoprovocation studies would be inappropriate in the ED setting, we provide evidence that clearly demonstrates comparable airway reversibility in all three BMI groups. This novel finding suggests, at least in the ED setting, that obese individuals with doctor-diagnosed asthma very likely have "asthma" by traditional definitions.
Another potential limitation of our study is reliance on self-reported height and weight to calculate BMI. Studies that have examined the accuracy of self-reported height and weight to determine overweight and obesity prevalence among adults have shown that this approach may lead to an underestimation of the prevalence in men and women.44 However, the relatively large sample size and almost complete absence of an association between BMI and several markers of chronic and acute asthma severity is consistent enough for us to believe that we have not missed any major associations.
| Conclusion |
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| Appendix |
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EMNet Coordinating Center
Keith Brinkley, MA; Carlos A. Camargo, Jr, MD (Director); Sunday Clark, MPH; Jennifer A. Emond, MS; Jessica L. Hohrmann, MPH; Sunghye Kim, MD (all at Massachusetts General Hospital, Boston).
Principal Investigators at the 30 Participating Sites
M.P. Blanda (Akron City Hospital, Akron, OH); E.D. Boudreaux (Earl K. Long Memorial Hospital, Baton Rouge, LA); J.C. Brancato (Connecticut Childrens Medical Center, Hartford, CT); B.E. Brenner (Arkansas Childrens Hospital, Little Rock, AR); B.E. Brenner (Brooklyn Hospital Center, Brooklyn, NY); B.E. Brenner (University of Arkansas for Medical Sciences, Little Rock, AR); C.A. Camargo Jr (Massachusetts General Hospital, Boston, MA); A.K. Chang (UC Irvine Medical Center, Orange, CA); F.L. Counselman (Sentara Norfolk General Hospital, Norfolk, VA); R.K. Cydulka (MetroHealth Medical Center, Cleveland, OH); C.O. Davis (University of Rochester Medical Center, Rochester, NY); T.J. Gaeta (New York Methodist Hospital, Brooklyn, NY); J.E. Gough (Pitt County Medical Center, Greenville, NC); R.O. Gray (Hennepin County Medical Center, Minneapolis, MN); A.H. Idris (Shands Hospital at the University of Florida, Gainesville, FL); A. Johnson (Jackson Memorial Hospital, Miami, FL); K. Jones (Detroit Receiving Hospital, Detroit, MI); E.C. Leibner (Maricopa Medical Center, Phoenix, AZ); S.J. Nairn and A.L. Nyce (Cooper Hospital/University Medical Center, Camden, NJ); J. Peters (University of Texas Health Science Center at San Antonio, San Antonio, TX); M.S. Radeos (Lincoln Medical Center, Bronx, NY); N. Schiebel (Mayo Clinic, Rochester, MN); D. Schreiber (Stanford University Medical Center, Stanford, CA); R.A. Schwab (Truman Medical Center, KS City, MO); N.I. Shapiro (Beth Israel Deaconess Medical Center, Boston, MA); P.C. Shukla (University of Texas Southwestern Medical Center, Dallas, TX); H. Smithline (Baystate Medical Center, Springfield, MA); B.K. Snyder (UCSD Medical CenterHillcrest, San Diego, CA); P.E. Sokolove (UC Davis Medical Center, Sacramento, CA); D. Teoh (Childrens Medical Center of Dallas, Dallas, TX).
| Acknowledgements |
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| Footnotes |
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Dr. Thomson is supported by grant HL-707427, and Dr. Camargo by grant HL-63841 from the National Institutes of Health (Bethesda, MD). The project was supported by grant HL-63253 from the National Institutes of Health, and by an unrestricted grant from GlaxoSmithKline (Research Triangle Park, NC).
Received for publication November 5, 2002. Accepted for publication February 12, 2003.
| References |
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