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Acute Asthma Among Adults Presenting to the Emergency Department
Acute Asthma Among Adults Presenting to the Emergency Department* The Role of Race/Ethnicity and Socioeconomic Status Edwin D. Boudreaux, PhD; Stephen D. Emond, MD; Sunday Clark, MPH; and Carlos A. Camargo, Jr, MD, DrPH, FCCP†
Objectives: To investigate racial/ethnic differences in acute asthma among adults presenting to the emergency department (ED), and to determine whether observed differences are attributable to socioeconomic status (SES). Design: Prospective cohort studies performed during 1996 to 1998 by the Multicenter Airway Research Collaboration. Using a standardized protocol, researchers provided 24-h coverage for a median duration of 2 weeks per year. Adults with acute asthma were interviewed in the ED and by telephone 2 weeks after hospital discharge. Participants: Sixty-four North American EDs. Results: A total of 1,847 patients were enrolled into the study. Black and Hispanic asthma patients had a history of more hospitalizations than did whites (ever-hospitalized patients: black, 66%; Hispanic, 63%; white, 54%; p < 0.001; patients hospitalized in the past year: black, 31%; Hispanic, 33%; white, 25%; p < 0.05) and more frequent ED use (median use in past year: black, three visits; Hispanic, three visits; white, one visit; p < 0.001). The mean initial peak expiratory flow rate (PEFR) was lower in blacks and Hispanics (black, 47%; Hispanic, 47%; white, 52%; p < 0.001). For most factors, ED management did not differ based on race/ethnicity. After accounting for several confounding variables, blacks and Hispanics were twice as likely to be admitted to the hospital. Blacks and Hispanics also were more likely to report continued severe symptoms 2 weeks after hospital discharge (blacks, 24%; Hispanic, 31%; white, 19%; p < 0.01). After adjusting for sociodemographic factors, the race/ethnicity differences in initial PEFR and posthospital discharge symptoms were markedly reduced. Conclusion: Despite significant racial/ethnic differences in chronic asthma severity, initial PEFR at ED presentation, and posthospital discharge outcome, ED management during the index visit was fairly similar for all racial groups. SES appears to account for most of the observed acute asthma differences, although hospital admission rates were higher among black and Hispanic patients after adjustment for confounding factors. Despite asthma treatment advances, race/ethnicity-based deficiencies persist. Health-care providers and policymakers might specifically target the ED as a place to initiate interventions designed to reduce race-based disparities in health. (CHEST 2003; 124:803– 812) Key words: adults; asthma; ethnicity; quality of care; race; socioeconomic status Abbreviations: CI ⫽ confidence interval; ED ⫽ emergency department; IQR ⫽ interquartile range; MARC ⫽ Multicenter Airway Research Collaboration; OR ⫽ odds ratio; PCP ⫽ primary care provider; PEFR ⫽ peak expiratory flow rate; SES ⫽ socioeconomic status
the United States, asthma does not affect all I nracial/ethnic groups equally. Population studies have repeatedly found higher asthma prevalence among blacks compared to whites.1–7 Black patients with asthma also experience greater morbidity8 –18 and mortality.19 –23 Hispanic patients, especially those of Puerto Rican descent, likewise bear a greater asthma burden than whites.5,9,10,24 –26 The reasons for racial/ethnic differences in asthma prevalence, morbidity, and mortality remain unclear. www.chestjournal.org
While evidence for the genetic basis of asthma (or asthma susceptibility) is clear,27,28 information about the contribution of genetic factors to race/ethnicity differences in asthma is lacking.2,29 –32 Rather, other nongenetic factors have been implicated, such as lower socioeconomic status (SES) and its correlates, including greater allergen and irritant exposure and poor access to and compliance with state-of-the-art medical management.2– 8,12,13,17,18,33– 41 Most published studies on emergency department CHEST / 124 / 3 / SEPTEMBER, 2003
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(ED) utilization by asthmatic adults of different racial/ethnic backgrounds have used retrospective reviews of archived or billing data.18,33 This restricts the range of variables that can be examined and leads to an incomplete picture of what actually happens to patients while they are in the ED. To further examine the role of race/ethnicity in asthma among adults presenting to the ED, we examined prospective data from the Multicenter Airway Research Collaboration (MARC). Based on previous research, we hypothesized that black and Hispanic asthma patients would be (1) in more severe respiratory distress on arrival to the ED, (2) more likely to receive substandard care while in the ED, (3) hospitalized more often during their index ED visit, and (4) more likely to relapse or have continued symptoms during the 2 weeks after hospital discharge. We further hypothesized that, after statistically controlling for factors thought to be confounders of the relation between race/ethnicity and illness severity (ie, education level, income, insurance status, and access to a primary care provider [PCP]), the observed racial/ethnic differences either would disappear or be dramatically reduced.
Materials and Methods We analyzed data from three prospective cohort studies performed from 1996 to 1998 as part of the MARC (http:// healthcare.partners.org/marc). The purpose of the MARC was to try to define the characteristics of patients presenting to the ED for acute asthma, to describe their management and outcome, and to follow their course after hospital discharge. Using a standardized protocol, researchers at 64 EDs in 21 US states and 4 Canadian provinces provided 24-h coverage for a median duration of 2 weeks and consecutively enrolled adult patients. The following criteria were used to determine eligibility: (1) *From the Department of Emergency Medicine (Dr. Boudreaux), Cooper Hospital and University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, Camden, NJ; Emergency Department (Dr. Emond), Kaiser Permanente, Santa Clara Medical Center, Santa Clara, CA; and Department of Emergency Medicine (Mr. Clark and Dr. Camargo), Massachusetts General Hospital and Channing Laboratory, Boston, MA. †A complete list of the MARC investigators is located in the Appendix. Dr. Camargo is supported by grant HL-63841 from the National Institutes of Health (Bethesda, MD). The Multicenter Airway Research Collaboration was supported by grant HL-63253 from the National Institutes of Health, and by unrestricted grants from GlaxoSmithKline Inc (Research Triangle Park, NC) and Monaghan Medical Corporation (Syracuse, NY). Manuscript received August 1, 2002; revision accepted March 13, 2003. Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (e-mail: [email protected]). Correspondence to: Edwin D. Boudreaux, PhD, Emergency Medicine Residency Program, Cooper Hospital, One Cooper Plaza, Camden, NJ 08103-1489; e-mail: boudreaux-edwin@ cooperhealth.edu 804
physician-diagnosed asthma (including new diagnoses by the ED physician or patient reported history); (2) current ED visit was due to an exacerbation; (3) age 18 to 54 years (truncated at 54 in order to help rule out COPD); and (4) the ability to give informed consent. Repeat visits by individual patients were excluded. All patients were managed at the discretion of the treating physician. The site investigators were not informed that we intended to compare presentation/management/outcome by race/ethnicity. Therefore, they were blinded to the specific hypotheses studied in this investigation. The institutional review board at each hospital approved the study. Public hospitals constituted 36% of sites. The remainder of the sites were private or not-for-profit hospitals. The median number of annual hospital admissions was 23,427, the median number of annual ED visits was 54,000, and the median number of annual visits for asthma was 1,500. Data Collection The ED interview assessed patients’ sociodemographic characteristics, asthma history, and details of their current asthma exacerbation. Data on ED management, disposition, and hospital discharge medications were obtained by chart review. Follow-up data were collected by telephone interview 2 weeks later. Research personnel used “best numbers” and “best times” solicited during the ED interview to guide their calls. A minimum of five attempts to reach the patient were made, spaced across at least 3 days. All forms were reviewed for accuracy, completeness, and legibility by site investigators before submission to the MARC Coordinating Center in Boston, MA, where they underwent further review by trained personnel. Incomplete, contradictory, or illegible data were returned to the site investigator for reconciliation. The data were double-entered. Sociodemographic Factors: Age, sex, level of education, and insurance status were recorded. Consistent with other literature in this area,10,11,13,17,18,33,38 the median family income was estimated using patients’ home ZIP codes.42 Race/ethnicity was assigned by self-report to standard US Census categories. For the purpose of this analysis, mutually exclusive categories were determined as follows: black (ie, African American or nonHispanic); Hispanic; or white (ie, non-Hispanic). Patients designated as Asian or “other” ethnicity were excluded due to small numbers. While the limitations of self-report have been discussed in the literature,43– 46 it remains the most common and efficient manner by which to classify patients’ race/ethnicity. Patients were asked whether they had a PCP. Chronic Asthma History: We also assessed patients’ asthma medication use, including oral corticosteroids, rescue inhalers, and inhaled corticosteroids. We measured health-care utilization via hospitalization history (ever hospitalized and hospitalized in the past year), the number of ED visits made in the past year, and the source of their primary asthma care and prescriptions. Smoking status also was assessed. To examine further disease self-management, we assessed whether the patient owned a spacer device, peak flowmeter, and a written action plan. Finally, we recorded whether a comorbid medical condition was present (eg, congestive heart failure or COPD). ED Course: We collected both subjective and objective measures of acute asthma severity. Severe symptoms was assigned to patients who reported asthma symptoms “most of the time” or had experienced “severe” discomfort and distress due to their asthma during the past 24 h. Peak expiratory flow rate (PEFR) was expressed as the percentage of the patient’s predicted value, based on race, age, sex, and height.47 Initial measurement and change in PEFR were recorded. The number of inhaled agonist treatments received prior to arrival in the ED, the number of treatments received during the ED visit (ie, within the Clinical Investigations
first hour and the total number), and whether the patient received oral corticosteroids were abstracted from the chart. We calculated ED length of stay and recorded ED disposition. Hospital discharge medications were recorded, including systemic and inhaled corticosteroids. However, prescription for inhaled corticosteroids at hospital discharge was systematically collected for only two of the three cohorts (566 patients). Two-Week Follow-up: All patients were called 2 weeks after their discharge from the ED. Relapse was defined as any urgent visit to an ED or clinic for worsening of asthma during the 2-week follow-up period. The number of days between discharge from the ED and the date of relapse was recorded. An ongoing exacerbation classification was assigned to patients who reported “severe symptoms” during the 24-h period preceding the phone call on any one of two questions (ie, asthma symptoms “most of the time” or “severe” discomfort and distress due to their asthma) or to those who stated that their asthma was “about the same” or “worse” than at the time of their ED presentation. Statistical Analysis All statistical analyses were performed using a statistical software package (STATA, version 7.0; StataCorp; College Station, TX). The data are presented as proportions, means (with SD), or medians (with interquartile range [IQR]). The association between race/ethnicity and other factors was examined using 2 test, analysis of variance, and Kruskal-Wallis test, as appropriate. Three multivariate models were derived to predict the initial PEFR, hospitalization, and posthospital discharge outcome. Each of these final models included the following variables: age; sex; education; median household income; insurance status; PCP status; and recent inhaled corticosteroid use. Other salient variables then were added based on the particular dependent variable (eg, initial PEFR and change in PEFR were used to predict hospitalization). The race/ethnicity variable was added to the three models as one variable. All interpretations of the odds ratios (ORs) for blacks and Hispanics were based on the reference group (whites). The possibility of a period effect was examined by adjusting for the period of enrollment, but this did not materially affect any of the results that follow (data not shown). All ORs are presented with 95% confidence intervals (CIs). All p values are two-sided. Considering the large sample size and the risk of multiple testing error, p ⬍ 0.01 was considered to be statistically significant.
Results Among the eligible patients, 588 refused study entry, were missed, or were not enrolled for another
reason, and 1,847 were enrolled into the study. Three patients were excluded because race/ethnicity data were missing. Patients identified as Asian or “other” race/ethnicity (44 patients) were excluded, since the purpose of the study was to investigate blacks and Hispanics. Patients who were enrolled did not differ from those who were not enrolled according to demographic factors, available chronic asthma factors, ED course (except for the administration of steroids in the ED, which was more likely among those who were enrolled in the study [68% vs 62%, respectively; p ⫽ 0.01]), or disposition. Among the 1,800 patients used in these analyses, 935 (52%) were black, 411 (23%) were Hispanic, and 454 (25%) were white. Since the US sites had a high proportion of black and Hispanic patients and the Canadian sites had a high proportion of white patients, we re-ran all the analyses excluding the Canadian sites. We found no significant differences in the results. Sociodemographics Sociodemographic characteristics by race/ethnicity are presented in Table 1. Trends show that black and Hispanic asthma patients were from lower SES households and were less likely to have a PCP. Chronic Asthma History Chronic asthma history by race/ethnicity also is presented in Table 2. Black and Hispanic patients were more likely to have a history of hospitalization and reported a greater number of ED visits. They were more likely to state that they used the ED as their primary source of asthma care and prescriptions. The three groups were equally likely to have recently used systemic corticosteroids and inhaled bronchodilators, but black and Hispanic patients were less likely to have used inhaled corticosteroids. Black patients and, especially, Hispanic patients were less likely to own a spacer and a peak flowmeter, while action plans were low across all three
Table 1—Demographic Characteristics of Adults with Acute Asthma According to Race/Ethnicity* Characteristics
Black (n ⫽ 935)
Hispanic (n ⫽ 411)
White (n ⫽ 454)
p Value
Age,† yr Female High school graduate Estimated household income‡ Insurance status Private Medicaid Other public None Primary care provider
35 ⫾ 10 62 68 26,288 (18,999–34,487)
35 ⫾ 10 66 53 25,185 (17,364–32,849)
34 ⫾ 10 71 81 35,336 (27,190–43,291)
0.80 0.002 ⬍ 0.001 ⬍ 0.001 ⬍ 0.001
26 29 10 35 61
21 41 10 29 62
40 14 24 21 77
⬍ 0.001
*Values given as %, unless otherwise indicated. †Values given as mean ⫾ SD. ‡Values given as median (IQR). www.chestjournal.org
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Table 2—Chronic Asthma Characteristics of Adults with Acute Asthma According to Race/Ethnicity* Characteristics
Black (n ⫽ 935)
Hispanic (n ⫽ 411)
White (n ⫽ 454)
p Value
74 66 18 27 58 34 85 42 35 3 (1–5) 38 42 29 31 79 52
68 63 17 38 59 31 86 39 33 3 (0–5) 30 30 32 33 78 54
74 54 12 25 74 41 87 53 39 1 (0–3) 43 45 33 25 61 25
0.09 ⬍ 0.001 0.02 0.001 ⬍ 0.001 0.01 0.59 ⬍ 0.001 0.11 ⬍ 0.001 ⬍ 0.001 ⬍ 0.001 0.42 0.02 ⬍ 0.001 ⬍ 0.001
Ever taken steroid medicine for asthma Ever hospitalized for asthma Ever intubated for asthma Recent use of home nebulizer† Hay fever Current smoker Inhaled -agonist during past 4 wk Inhaled corticosteroid during past 4 wk Other asthma medication during past 4 wk ED visits in past year‡ Owns a spacer Owns a peak flowmeter Has a written action plan Admitted for asthma in past year ED usual site of care for asthma problems ED usual source of asthma prescriptions *Values given as %, unless otherwise indicated. †Limited to two cohorts (1,281 patients). ‡Values given as median (IQR).
groups. Comorbid medical conditions were equally likely (blacks, 9%; Hispanics, 4%; whites, 8%; p ⫽ 0.03). Acute Presentation and ED Course Data on acute asthma presentation and ED course are presented in Table 3. Black and Hispanic patients exhibited more severe objective airway obstruction (based on PEFR), but blacks reported
slightly less severe subjective distress. Black and Hispanic patients received more inhaled bronchodilator doses during the first hour following triage, and black patients were most likely to have received systemic corticosteroid treatment. All race/ethnicity groups were equally likely to be discharged from the ED with a prescription for inhaled corticosteroids (566 patients; black, 39%; Hispanic, 37%; white, 48%; p ⫽ 0.15). When the sample was restricted to
Table 3—Acute Asthma Presentation and ED Course According to Race/Ethnicity*
Presentation Duration of symptoms ⬍ 24 h Severe symptoms† ED course Initial PEFR, % predicted Initial PEFR ⬍ 50% 50–79% ⱖ 80% Inhaled -agonist doses in first hour, No. Inhaled -agonist doses over ED stay, No. Given steroid treatment Received other asthma treatments in the ED Final PEFR, % predicted Change in PEFR, % predicted ED length of stay, min Sent home on systemic corticosteroids‡ Admitted
Black (n ⫽ 935)
Hispanic (n ⫽ 411)
White (n ⫽ 454)
53 71
56 77
56 79
47 ⫾ 21
47 ⫾ 18
52 ⫾ 21
59 33 8 1.8 ⫾ 0.9 3.3 ⫾ 1.9 72 27 72 ⫾ 23 25 ⫾ 19 182 (128–262) 70 20
62 33 5 1.9 ⫾ 1.0 3.1 ⫾ 1.7 64 25 73 ⫾ 22 26 ⫾ 19 187 (125–270) 61 21
51 39 10 1.6 ⫾ 0.9 3.1 ⫾ 2.4 66 35 75 ⫾ 23 22 ⫾ 20 180 (134–256) 65 19
p Value 0.52 0.002 ⬍ 0.001 0.02
⬍ 0.001 0.42 0.008 0.003 0.12 0.06 0.97 0.02 0.77
*Values given as %, mean ⫾ SD, or median (IQR), unless otherwise indicated. †See “Materials and Methods” section for details. ‡Restricted to patients sent home from ED (1,442 patients). 806
Clinical Investigations
Table 4 —Two-Week Follow-up According to Race/Ethnicity* Variables Hospital length of stay, d Relapse within 2 wk of ED visit† Days to relapse Ongoing exacerbation‡ Relapse or ongoing exacerbation
Black
Hispanic
White
p Value
2 (1–5) 13 7 (4–11) 24 31
3 (2–4) 17 2 (2–10) 31 40
2 (1–3) 15 3 (1–8) 19 31
0.30 0.31 ⬍0.001 0.003 0.008
*Values given as median (IQR) or %, unless otherwise indicated; n ⫽ 1,308. †Relapse event based on patient reporting a “worsening of asthma symptoms” that led to an urgent care visit. ‡See “Materials and Methods” section for details.
only those patients who were not already receiving inhaled corticosteroids, we again found no differences (black, 12%; Hispanic, 11%; white, 13%; p ⫽ 0.86). After controlling for seven factors (ie, age, sex, education, estimated household income, insurance status, PCP status, and recent use of inhaled steroids) using multiple linear regression analysis, we found that the initial PEFR no longer differed significantly by race/ethnicity (black vs white: difference, ⫺0.03; 95% CI, ⫺0.06 to ⫺0.004; p ⫽ 0.05; Hispanic vs white: difference, ⫺0.03; 95% CI, ⫺0.07 to ⫺0.001; p ⫽ 0.05). At the univariate level, hospitalization did not differ by race/ethnicity. However, the logistic regression model predicting hospitalization demonstrated that, all things being equal, black and Hispanic patients were more likely to be admitted to the hospital (black vs white: OR, 2.1; 95% CI, 1.2 to 3.6; p ⫽ 0.005; Hispanic vs white: OR, 2.6; 95% CI, 1.4 to 4.7; p ⫽ 0.002). Two-Week Follow-up A total of 1,308 patients (71% of total) were reached for telephone follow-up. Blacks were the least likely to be reached (likelihood: black, 66%; Hispanic, 72%; white, 80%; p ⬍ 0.001). Univariate results are presented in Table 4. Race/ethnicity was not related to the likelihood of short-term relapse,
although time to relapse among those who did relapse appeared to be longer for blacks. Blacks and, especially, Hispanics were the most likely to have ongoing symptoms at the univariate level. However, when the data were controlled for several factors (ie, age, sex, education, estimated household income, insurance status, PCP status, recent use of inhaled steroids, ED steroid treatment, and final PEFR), there was no statistically significant difference according to race/ethnicity (black vs white: OR, 1.3; 95% CI, 0.9 to 1.9; p ⫽ 0.17; Hispanic vs white: OR, 0.8; 95% CI, 0.5 to 1.2; p ⫽ 0.24). Approximately 33% of adults reported a relapse event or an ongoing exacerbation. Discussion It is widely recognized that black and Hispanic asthma patients receive substandard outpatient care, visit the ED more frequently, and are hospitalized at greater rates than are whites.8 –18,48 However, little is known about whether racial/ethnic differences exist during the course and treatment of exacerbations while in the ED or whether racial/ethnic differences exist in relapse and outcome after discharge from the ED. Because we prospectively enrolled patients during their ED visit and observed them after their ED discharge, rather than using archival or billing data, our study helps to answer these questions.
Table 5—Relation of Black or Hispanic (vs White) Race/Ethnicity to Risk of Hospital Admission Among Adults With Acute Asthma Black
Hispanic
Variables
OR
95% CI
p Value
OR
95% CI
p Value
Model 1 (adjusted for age ⫹ sex) Model 2 (adjusted for above ⫹ education, median income, insurance status) Model 3 (adjusted for above ⫹ PCP status) Model 4 (adjusted for above ⫹ recent inhaled steroid use) Model 5 (adjusted for above ⫹ initial PEFR) Model 6 (adjusted for above ⫹ change in PEFR)
1.1 1.2
0.8–1.5 0.9–1.7
0.53 0.22
1.1 1.1
0.8–1.6 0.8–1.7
0.43 0.49
1.3 1.3
0.9–1.8 0.9–1.8
0.14 0.11
1.2 1.2
0.8–1.8 0.8–1.8
0.37 0.30
1.5 2.1
1.0–2.3 1.2–3.6
0.05 0.005
1.4 2.6
0.9–2.3 1.4–4.7
0.16 0.002
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Racial/Ethnic Differences in Asthma on Presentation to the ED We hypothesized that black and Hispanic patients would present to the ED in more severe respiratory distress than white patients. Consistent with this hypothesis, black and Hispanic patients in our sample presented to the ED with an average PEFR of 47% of the predicted value, compared to 52% for white patients. Our analyses indicate that this difference is not likely due to chance. Moreover, if an individual improved from 47 to 52%, this would represent a ⬎ 10% change in the patient’s PEFR, which generally is considered clinically significant. Arguably, using the mean PEFR may have blurred very sick and very mild cases together, potentially hiding a trend for a continued greater rate of mild cases among black and Hispanic patients. To help explore this possibility, we further subdivided the PEFR into three groups based on National Asthma Education and Prevention Program guidelines. This distribution showed that white patients, rather than black and Hispanic patients, tended to be more likely to present with mild exacerbations. Our multivariate analyses indicated that adjusting for demographic factors and SES markedly reduced the size of the discrepancy in severity of acute asthma by race/ethnicity. The extant literature is contradictory regarding the role that SES plays in the race/ethnic disparities observed in asthma severity, morbidity, and management. Some have found33 results similar to ours, with all or most of the race/ethnicity-based disparities being accounted for by SES. Most others have found that race/ethnicitybased differences persist even after adjusting for SES indicators, such as annual income,11,17,18 urban nature of residence,9,10 and insurance status.18 However, to conclude that SES is not an important mediator of race/ethnicity-based asthma disparities based on these later studies alone would be to oversimplify a very complex issue. Many of these studies found that SES was substantially related to at least some of the disparities noted, and none concluded that SES was unrelated to race-based disparities or was unimportant in understanding why such disparities occur. They simply concluded that SES was not the only factor accounting for racial/ethnic disparities. The persisting race/ethnicity differences in morbidity and mortality, even after controlling for SES, possibly can be explained by cultural differences in the tendency to use a short-term treatment approach rather than preventive treatment approaches. However, to date, convincing data for this hypothesis have not been published in the asthma literature. Furthermore, it is clear that, by focusing on only one 808
indicator such as insurance status or annual income, many studies simply did not sufficiently account for SES, which is a multifaceted construct. Kaufman and colleagues49 have cautioned that residual confounding can be a significant problem when studying the health correlates of SES. For example, Zoratti and colleagues18 found that, even among members of the same managed care organization, blacks still earned less than whites. When they isolated their sample to include only those patients who had low incomes, many (but not all) of their race/ethnicity-based discrepancies in health-care utilization and prescription medication usage disappeared or were markedly attenuated. Racial/Ethnic Differences in ED Course and Management Many of our results on ED course and management ran counter to the trends noted in outpatient settings. Black and Hispanic patients received more doses of inhaled -agonists within the first hour of presentation, and black patients were more likely to receive oral corticosteroids than were white patients. This more aggressive treatment possibly reflects an appropriate response to the aforementioned greater severity on presentation and worse chronic history of asthma among minorities. These trends, combined with the fact that the total number of inhaled -agonist treatments, the final PEFR, change in PEFR, ED length of stay, and ED discharge medications did not differ among racial/ethnic groups, indicates that patients received similar care and achieved comparable resolution of symptoms while in the ED. Other studies50,51 have shown that the quality of ED asthma care frequently diverges from national guidelines. However, these studies did not specifically investigate whether ED care for minorities diverged to a greater degree than that of whites, making it difficult to integrate our results. Importantly, our results affirm the common perception that the ED is a “safety net” for individuals with asthma, regardless of race/ethnicity. Racial/Ethnic Differences in Hospitalization During the Index ED Visit Studies9 –11,14,17,18,38 have found that hospitalization rates among minorities are three to five times that for whites during a given period. However, we could not identify any published studies that actually have investigated racial/ethnic differences in hospital admission rates during an index ED visit. We expected moderate-to-large racial/ethnic differences in hospitalization at the index visit. To the contrary, we found almost identical rates, in absolute terms, Clinical Investigations
among all three groups. Approximately 20% of all blacks, Hispanics, and whites were hospitalized during their index visit. The discrepancy between hospitalization point incidence (ie, at the index ED visit) and period incidence (ie, 1 year) is difficult to explain. It seems likely that it is due, at least in part, to a base-rate effect. Even though black and Hispanic patients have the same risk of being hospitalized during a given ED visit, they may have a markedly greater incidence of hospitalization over a given period, because they experience severe exacerbations warranting emergency care more frequently. This can be conceptualized in probabilistic terms. The chance of rolling a six on any roll of a die is identical. Nevertheless, one has a better chance of rolling at least one six during a given period of time if allowed to roll the die three times instead of only once. Even though a black patient has a similar probability of being admitted to the hospital at a given visit, if that patient presents three times over the course of a year and a white patient presents only once, the black patient will be more likely to be admitted to the hospital during that year. Although the absolute rates of hospitalization were roughly equivalent, our multivariate analyses revealed an interesting trend. Once all sociodemographic factors, initial PEFR, and change in PEFR were controlled for, black and Hispanic patients were more than twice as likely to have been admitted to the hospital. The inclusion of PEFR indexes in the last step of the model appeared to have the largest impact on the race/ethnicity-hospitalization relationship. This finding seems to suggest that, at equivalent levels of symptom resolution, black and Hispanic patients are more likely to be admitted to the hospital than whites. The reasons for this association are difficult to determine and await further empirical validation. The Role of Race/Ethnicity and Posthospital Discharge Outcome The posthospital discharge outcomes present a mixed picture. Blacks and Hispanics sought urgent medical care within the 2 weeks after hospital discharge at approximately the same rate as whites (approximately 15%), although blacks appeared to have a longer delay before seeking such care. Whether this is due to a delay in seeking treatment or a delay in experiencing an exacerbation severe enough to warrant treatment is not clear. Our relapse rates were comparable to those reported by other single-center studies.52–54 Treatment failure, defined by the continued self-report of severe symptoms, occurred more frequently in minorities, particularly Hispanics. As with the racial/ethnic differwww.chestjournal.org
ences noted in initial PEFR on presentation to the ED, the race-based discrepancy in treatment failure appears to be associated primarily with racial/ethnic differences in sociodemographic factors, including SES. Potential Limitations In evaluating our results, several potential limitations should be considered. First, we recognize that the race/ethnicity designation, though ubiquitous in epidemiologic research, may be misleading, and that standard census classification is simplistic. Nevertheless, our designations are consistent with those used in prior studies cited throughout our article. Such research remains common and is important in order to further understand and eventually to modify the reasons why such differences exist. The fact that race/ethnicity is difficult to operationalize does not mean we should not study it. Research such as ours is important in raising public awareness and may help providers to counteract any implicit racism that may be present. Second, our sample size was large, which enabled us to detect small differences that were not necessarily clinically meaningful. We were sensitive to this fact, however, and emphasized only those trends that appeared clinically significant, noting in the text when such a problem might exist. Third, the EDs that comprised our sample are predominantly urban, academically affiliated hospitals. This may make our results less generalizable to community hospitals without academic affiliation. Future studies need to address this issue. Fourth, we noted a paradoxical trend in initial severity. Despite presenting with worse PEFR, black patients reported slightly less severe symptoms than whites. The reason for this is unclear. The differences were not likely due to chance, but the magnitude was small and may not be clinically meaningful. The observation awaits validation by other studies. It is a potentially important area, since blunted perception of dyspnea has been associated with the increased risk of near-fatal asthma.55,56 Finally, we found that hospital discharge medications did not differ based on race. However, since black and Hispanic patients had more severe chronic asthma, the fact that the ED discharge rates were equal for inhaled corticosteroids is somewhat disconcerting. Under these conditions, one would logically expect that the ED discharge rates for inhaled corticosteroids should be greater for blacks and Hispanic patients. Consequently, the equal rates of ED discharge on inhaled corticosteroids may actually be interpreted to mean that blacks and Hispanics were undertreated on ED discharge. CHEST / 124 / 3 / SEPTEMBER, 2003
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Integration The associations among race/ethnicity, SES, and various measures of asthma severity and morbidity are complex. We found marked racial/ethnic differences in chronic asthma management. Black and Hispanic asthma patients lacked PCPs more often, reported a greater likelihood of lifetime hospitalization, and reported more numerous ED visits in the past year. Importantly, they also were less likely to use inhaled corticosteroids and less frequently owned a spacer and a peak flowmeter. Not only do they present to the ED more often, but also our data show that they presented to the ED with somewhat more severe exacerbations. However, their course and treatment during the ED visit did not seem to differ dramatically, they were not hospitalized during their index ED visit at greater rates than whites (except when controlling for confounding factors), and they did not seek urgent medical care within the 2 weeks after hospital discharge more frequently than whites. As mentioned earlier, the reason that minorities exhibit such deficient chronic asthma management is probably, at least in part, due to SES and the substandard health care that accompanies lower SES. Other environmental factors associated with low SES may lead to deficient chronic disease management, such as increased risk of respiratory infections due to overcrowding, and greater exposure to allergens and irritants,13,35,38,41 but these were not assessed in our study. Although we found that most differences were attributable to differences in SES, other research49 suggests that residual race/ethnicity differences may still be present even after adjusting for SES. This implicates other sociocultural and psychological factors. Some authors have speculated that racial/ethnic discrimination among health-care providers is a possible cause for the inequities observed in health care,43,57 although it is probably not conscious or deliberate.58 Several other explanations have been mentioned in the literature but have not been researched well enough to form conclusions. At best they offer direction for future research. These include race-based differences in health beliefs and practices emphasizing rescue rather than preventive strategies,18,59,60 impaired illness perception and judgment of disease severity,13,61– 63 lower selfefficacy regarding asthma management,64 – 67 and greater comorbid psychopathology, such as depression, anxiety, and panic disorders.64,65 The elimination of health disparities by race/ ethnicity is an overarching goal of Healthy People 2010. Although race-based disparities are trenchant and difficult to address, they can and should be eliminated. Evidence68 has shown that the deficient asthma care in economically disadvantaged health810
care facilities can be rectified with education and supportive programs. The necessary changes are unlikely to occur on a broad scale, however, without massive, coordinated, and sustained effort by all concerned parties, including the federal government, health-care providers and organizations, the pharmaceutical industry, community and civic associations, patient-advocacy groups, and the patients themselves. Appendix: MARC Emergency Medicine Network Steering Committee Edwin D. Boudreaux, PhD; Barry E. Brenner, MD, PhD; Carlos A. Camargo, Jr, MD (Chair); Rita K. Cydulka, MD; Theodore J. Gaeta, DO, MPH; and Michael S. Radeos, MD, MPH. Emergency Medicine Network 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, MA). Principal Investigators at the 64 Participating Sites F.C. Baker, III (Maine Medical Center, Portland, ME); J.M. Basior (Buffalo General Hospital, Buffalo, NY); C.A. Bethel (Mercy Hospital, Philadelphia, PA); L. Bielory (University Hospital, Newark, NJ); M.P. Blanda (Summa Health System, Akron, OH); D. Bond (Gray Nun’s Community Hospital, Edmonton, AB, Canada); G.W. Bota (Sudbury General Hospital, Sudbury, BC, Canada); E.D. Boudreaux (Earl K. Long Memorial Hospital, Baton Rouge, LA); B.E. Brenner (The Brooklyn Hospital Center, Brooklyn, NY); J. Brown (Misericordia Community Hospital, Edmonton, AB, Canada); C.A. Camargo, Jr (Massachusetts General Hospital, Boston, MA); F.L. Counselman (Sentara Norfolk General Hospital, Norfolk, VA); G. Ramalanjaona (Newark Beth Israel Hospital, Newark, NJ); R.K. Cydulka (MetroHealth Medical Center, Cleveland, OH); D.J. Dire (University of Oklahoma Medical Center, Oklahoma City, OK); N. El Sanadi (Broward General Hospital, Ft. Lauderdale, FL); S.D. Emond (St. Luke’s/ Roosevelt Hospital Center, NY, NY); T.J. Gaeta (Methodist Hospital, Brooklyn, NY); T.J. Gaeta (St. Barnabas Hospital, Bronx, NY); M.A. Gibbs (Carolinas Medical Center, Charlotte, NC); T.E. Glynn (Brooke Army Medical Center, Fort Sam Houston, TX); L.G. Graff IV (New Britain General Hospital, New Britain, CT); R.O. Gray (Hennepin County Medical Center, Minneapolis, MN); S.K. Griswold (Thomas Jefferson University Hospital, Philadelphia, PA); A. Guttman (Sir Mortimer B. Davis Jewish General Hospital, Montreal, QC, Canada); J.P. Hanrahan (Beth Israel Hospital, Boston, MA); F. Harchelroad (Allegheny General Hospital, Pittsburgh, PA); R. Harrigan (Temple University Hospital, Philadelphia, PA); S.E. Hughes (Albany Medical College, Albany, NY); A.H. Idris (University of Florida Health Center, Gainesville, FL); G.D. Innes (St. Paul’s Hospital, Vancouver, BC, Canada); M.E. Johnson (Jackson Memorial Hospital, Miami, FL); D.M. Joyce (University Hospital, SUNY HSC, Syracuse, NY); L.W. Kreplick (Christ Hospital & Medical Center, Oak Lawn, IL); E.C. Leibner (Detroit Receiving Hospital, Detroit, MI); J. Li (Charity Hospital, New Orleans, LA); L.F. Clinical Investigations
Lobon (Beth Israel Medical Center, New York, NY); A. Mangione (Albert Einstein Medical Center, Philadelphia, PA); M.F. McDermott (Cook County Hospital, Chicago, IL); J.S. Myslinski (Richland Memorial Hospital, Columbia, SC); E.S. Nadel (Brigham and Women’s Hospital, Boston, MA); R.M. Nowak (Henry Ford Hospital, Detroit, MI); C.V. Pollack, Jr (Maricopa Medical Center, Phoenix, AZ); M.S. Radeos (Lincoln Medical Center, Bronx, NY); D.J. Robinson (University of Maryland Medical Center, Baltimore, MD); R.M. Rodriguez (Southwestern Medical Center, Dallas, TX); B.H. Rowe (University of Alberta Hospital, Edmonton, AB, Canada); G. Rudnitsky (Allegheny University-MCP Division, Philadelphia, PA); R.E. Sapien (University of New Mexico Health Sciences Center, Albuquerque, NM); D. Schreiber (Stanford University Medical Center, Stanford, CA); R.A. Silverman (Long Island Jewish Medical Center, New Hyde Park, NY); H. Smithline (Baystate Medical Center, Springfield, MA); S. Stahmer (Hospital of the University of Pennsylvania, Philadelphia, PA); D. Stewart (Bronson Medical Center, Kalamazoo, MI); A. Sucov (University of Rochester Hospital, Rochester, NY); D.M. Taylor (University of Pittsburgh Medical Center, Pittsburgh, PA); C.A. Terregino (Cooper Hospital/University Medical Center, Camden, NJ); J.L. Larson (University of North Carolina Hospitals, Chapel Hill, NC); A. Walker (Royal Alexandria Hospital, Edmonton, AB, Canada); J. Walter (University of Chicago Hospital, Chicago, IL); E.J. Weber (University of California San Francisco Medical Center, San Francisco, CA); L. White (Akron General Medical Center, Akron, OH); and J.L. Zimmerman (Ben Taub General Hospital, Houston, TX).
References 1 National Center for Health Statistics. Raw data from the National Health Interview Survey: United States, 1997–1998. Notes: Analysis by the American Lung Association Best Practices Division, Using SPSS and SUDAAN software 2 Aligne A, Auinger P, Byrd R, et al. Risk factors for pediatric asthma: contributions of poverty, race, and urban residence. Am J Respir Crit Care Med 2000; 162:873– 877 3 Cunningham J, Dockery D, Speizer F. Race, asthma, and persistent wheeze in Philadelphia schoolchildren. Am J Public Health 1996; 86:1406 –1409 4 Fagan J, Scheff P, Hryhorczuk D, et al. Prevalence of asthma and other allergic diseases in an adolescent population: association with gender and race. Ann Allergy Asthma Immunol 2001; 86:177–184 5 Litonjua A, Carey V, Weiss S, et al. Race, socioeconomic factors, and area of residency are associated with asthma prevalence. Pediatr Pulmonol 1999; 28:394 – 401 6 Schwartz J, Gold D, Dockery D, et al. Predictors of asthma and persistent wheeze in a national sample of children in the United States: association with social class, perinatal events, and race. Am Rev Respir Dis 1990; 142:555–562 7 Weitzman M, Gortmaker S, Sobol A. Racial, social, and environmental risks for childhood asthma. Am J Dis Child 1990; 144:1189 –1194 8 Bosco L, Gerstman B, Tomita D. Variations in the use of medication for the treatment of childhood asthma in the Michigan Medicaid population, 1980 to 1986. Chest 1993; 104:1727–1733 9 Carr W, Zeital L, Weiss K. Variations in asthma hospitalizations and deaths in New York City. Am J Public Health 1992; 82:59 – 65 10 DePalo VA, Mayo P, Friedman P, et al. Demographic influences on asthma hospital admission rates in New York City. Chest 1994; 106:447– 451 www.chestjournal.org
11 Lin S, Fitzgerald E, Hwang S, et al. Asthma hospitalization rates and socioeconomic status in New York State (1987– 1993). J Asthma 1999; 36:239 –251 12 Lozano P, Connell F, Koepsell T. Use of health services by African-American children with asthma on Medicaid. JAMA 1995; 274:469 – 473 13 Marder D, Targonski P, Orris P, et al. Effect of racial and socioeconomic factors on asthma mortality in Chicago. Chest 1992; 101:426S– 429S 14 Asthma hospitalizations and readmissions among children and young adults: Wisconsin, 1991–1995. MMWR Morb Mortal Wkly Rep 1997; 46:726 –729 15 The National Heart, Lung, and Blood Institute Working Group. Respiratory diseases disproportionately affecting minorities. Chest 1995; 108:1380 –1392 16 Perrin J, Homer CBD, Woolf A, et al. Variations in rates of hospitalization of children in three urban communities. N Engl J Med 1989; 320:1183–1187 17 Ray N, Thamer M, Fadillioglu B, et al. Race, income, urbanicity, and asthma hospitalization in California: a small area analysis. Chest 1998; 113:1277–1284 18 Zoratti E, Havstad S, Rodriguez J, et al. Health service use by African Americans and Caucasians with asthma in a managed care setting. Am J Respir Crit Care Med 1998; 158:371–377 19 Grant E, Lyttle C, Weiss K. The relation of socioeconomic factors and racial/ethnic differences in US asthma mortality. Am J Public Health 2000; 90:1923–1925 20 Asthma mortality and hospitalization among children and young adults: United States, 1980 –1993. MMWR Morb Mortal Wkly Rep 1996; 45:350 –353 21 Schleicher N, Koziol J, Christiansen S. Asthma mortality rates among California youths. J Asthma 2000; 37:259 –265 22 Sly R, O’Donnell R. Stabilization of asthma mortality. Ann Allergy Asthma Immunol 1997; 78:347–354 23 Weiss K, Wagener D. Changing patterns of asthma mortality: Identifying target populations at high risk. JAMA 1990; 264:1683–1687 24 Beckett W, Belanger K, Gent J, et al. Asthma among Puerto Rican Hispanics: a multi-ethnic comparison study of risk factors. Am J Respir Crit Care Med 1996; 154:894 – 899 25 Carter-Pokras O, Gergen P. Reported asthma among PuertoRican, Mexican-American, and Cuban children 1982 through 1984. Am J Public Health 1993; 83:580 –582 26 Colp C, Pappas J, Moran D, et al. Variants of A1-antirypsin in Puerto Rican children with asthma. Chest 1993; 103:812– 815 27 The Collaborative Study on the Genetics of Asthma. A genome-wide search for asthma susceptibility loci in ethnically diverse populations. Nat Genet 1997; 15:389 –392 28 Holberg C, Elston R, Halonen M, et al. Segregation analysis of physician-diagnosed asthma in Hispanic and Non-Hispanic white families: a recessive component? Am J Respir Crit Care Med 1996; 154:144 –150 29 Feldman C, Weltman M, Wadee A, et al. A study of immunoglobulin G subclass levels in black and white patients with various forms of obstructive lung disease. S Afr Med J 1993; 83:9 –12 30 Gaillard M, Zwi S, Nogueira C, et al. Ethnic differences in the occurrence of the M1 (ala213) haplotype of alpha-1-antitrypsin in asthmatic and non-asthmatic black and white South Africans. Clin Genet 1994; 45:122–127 31 Sanford A, Weir T, Pare P. The genetics of asthma. Am J Respir Crit Care Med 1996; 153:1749 –1765 32 Smith J, Cadoret R, Burns T, et al. Asthma and allergic rhinitis in adoptees and their adoptive parents. Ann Allergy Asthma Immunol 1998; 81:135–139 33 Apter A, Reisine S, Kennedy D, et al. Demographic predictors of asthma treatment site: outpatient, inpatient, or emerCHEST / 124 / 3 / SEPTEMBER, 2003
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gency department. Ann Allergy Asthma Immunol 1997; 79: 353–361 Butz A, Malveaux F, Eggleston P, et al. Use of community health workers with inner-city children who have asthma. Clin Pediatr (Phila) 1994; 33:135–141 Call R, Smith T, Morris E, et al. Risk factors for asthma in inner city children. J Pediatr 1992; 121:862– 866 Diette G, Wu A, Skinner E, et al. Treatment patterns among adult patients with asthma: factors associated with overuse of inhaled beta-agonists and underuse of inhaled corticosteroids. Arch Intern Med 1999; 159:2697–2704 Evans D, Mellins R, Lobach K, et al. Improving care for minority children with asthma: professional education in public health clinics. Pediatrics 1997; 99:157–163 Gottlieb D, Beiser A, O’Connor G. Poverty, race, and medication use are correlates of asthma hospitalization rates: a small area analysis in Boston. Chest 1995; 108:28 –35 Haas J, Cleary P, Guadagnoli E, et al. The impact of socioeconomic status on the intensity of ambulatory treatment and health outcomes after hospital discharge for adults with asthma. J Gen Intern Med 1994; 9:121–126 McDermott M, Silva J, Rydman R, et al. Practice variations in treating urban minority asthmatics in Chicago. J Med Syst 1996; 20:255–266 Sarpong S, Hamilton R, Eggleston P, et al. Socioeconomic status and race as risk factors for cockroach allergen exposure and sensitization in children with asthma. J Allergy Clin Immunol 1996; 97:1393–1401 Health Canada. Federal census data: statistic Canada. Ottawa, ON, Canada: Health Canada, 1996 Freeman H, Payne R. Racial injustice in health care. N Engl J Med 2000; 342:1045–1046 Krieger N. Counting accountably: implications of the new approaches to classifying race/ethnicity in the 2000 census. Am J Public Health 2000; 90:1687–1689 Lillie-Blaton M, Parsons P, Gayle H, et al. Racial differences in health: not just black and white, but shades of gray. Annu Rev Public Health 1996; 17:411– 448 Schwartz R. Racial profiling in medical research. N Engl J Med 2001; 344:1392–1393 Hankinson J, Odencrantz J, Fedan K. Spirometric reference values from a sample of the general US population. Am J Respir Crit Care Med 1999; 159:179 –187 Finkelstein J, Brown R, Schneider L, et al. Quality of care for preschool children with asthma: the role of social factors and practice setting. Pediatrics 1995; 95:389 –394 Kaufman J, Cooper R, McGee D. Socioeconomic status and health in blacks and whites: the problem of residual confounding and the resiliency of race. Epidemiology 1997; 8:621– 628 Grunfeld A, Beveridge R, Berkowitz J, et al. Management of acute asthma in Canada: an assessment of emergency physician behavior. J Emerg Med 1997; 15:547–556 Milks C, Oppenheimer J, Bielory L. Comparison of emer-
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gency room asthma care to National Guidelines. Ann Allergy Asthma Immunol 1999; 83:208 –211 Emerman C, Cydulka R. Factors associated with acute relapse after emergency department treatment for acute asthma. Ann Emerg Med 1995; 26:6 –11 Fischl M, Pitchenik A, Gardner L. An index predicting relapse and need for hospitalization in patients with acute bronchial asthma. N Engl J Med 1981; 305:783–789 Worthington J, Ahuja J. The value of pulmonary function tests in the management of acute asthma. Can Med Assoc J 1989; 140:153–156 Kikuchi Y, Okabe S, Tamura G, et al. Chemosensitivity and perception of dyspnea in patients with a history of near-fatal asthma. N Engl J Med 1994; 330:1383–1384 Ruffin R, Latimer K, Schembri D. Longitudinal study of near fatal asthma. Chest 1991; 99:77– 83 Geiger H. Race and health care: an American dilemma. N Engl J Med 1996; 335:815– 816 Epstein A, Ayanian J. Racial disparities in medical care. N Engl J Med 2001; 344:1471–1472 Blendon R, Scheck A, Donelan K, et al. How white and African Americans view their health and social problems: different experiences and different expectations. JAMA 1995; 273:341–346 Haire-Joshu D, Fisher E, Munro J, et al. A comparison of attitudes toward asthma self-management among acute and preventive care services. J Asthma 1993; 30:359 –371 Hardie G, Janson S, Gold W, et al. Ethnic differences: word descriptors used by African-American and white asthma patients during induced bronchoconstriction. Chest 2000; 117:935–943 Strunk R. Identification of the fatality-prone subject with asthma. J Allergy Clin Immunol 1988; 83:477– 485 Miller B, Strunk R. Circumstances surrounding the deaths of children due to asthma: a case-control study. Am J Dis Child 1989; 143:1294 –1299 Mancuso C, Rincon M, McCulloch C, et al. Self-efficacy, depressive symptoms, and patients’ expectations predict outcomes in asthma. Med Care 2001; 39:1326 –1338 Nouwen A, Freeston M, Labbe R, et al. Psychological factors associated with emergency room visits among asthmatic patients. Behav Modif 1999; 23:217–233 Scherer Y, Bruce S. Knowledge, attitudes, and self-efficacy and compliance with medical regimen, number of emergency department visits, and hospitalizations in adults with asthma. Heart Lung 2001; 30:250 –257 van der Palen J, Klein J, Seydel E. Are high generalized and asthma-specific self-efficacy predictive of adequate selfmanagement behaviour among adult asthma patients? Patient Educ Couns 1997; 23(suppl):S35–S41 Evans D, Mellins R, Lobach K, et al. Improving care for minority children with asthma: professional education in public health clinics. Pediatrics 1997; 99:157–163
Clinical Investigations
Objectives: To investigate racial/ethnic differences in acute asthma among adults presenting to the emergency department (ED), and to determine whether observed differences are attributable to socioeconomic status (SES). Design: Prospective cohort studies performed during 1996 to 1998 by the Multicenter Airway Research Collaboration. Using a standardized protocol, researchers provided 24-h coverage for a median duration of 2 weeks per year. Adults with acute asthma were interviewed in the ED and by telephone 2 weeks after hospital discharge. Participants: Sixty-four North American EDs. Results: A total of 1,847 patients were enrolled into the study. Black and Hispanic asthma patients had a history of more hospitalizations than did whites (ever-hospitalized patients: black, 66%; Hispanic, 63%; white, 54%; p < 0.001; patients hospitalized in the past year: black, 31%; Hispanic, 33%; white, 25%; p < 0.05) and more frequent ED use (median use in past year: black, three visits; Hispanic, three visits; white, one visit; p < 0.001). The mean initial peak expiratory flow rate (PEFR) was lower in blacks and Hispanics (black, 47%; Hispanic, 47%; white, 52%; p < 0.001). For most factors, ED management did not differ based on race/ethnicity. After accounting for several confounding variables, blacks and Hispanics were twice as likely to be admitted to the hospital. Blacks and Hispanics also were more likely to report continued severe symptoms 2 weeks after hospital discharge (blacks, 24%; Hispanic, 31%; white, 19%; p < 0.01). After adjusting for sociodemographic factors, the race/ethnicity differences in initial PEFR and posthospital discharge symptoms were markedly reduced. Conclusion: Despite significant racial/ethnic differences in chronic asthma severity, initial PEFR at ED presentation, and posthospital discharge outcome, ED management during the index visit was fairly similar for all racial groups. SES appears to account for most of the observed acute asthma differences, although hospital admission rates were higher among black and Hispanic patients after adjustment for confounding factors. Despite asthma treatment advances, race/ethnicity-based deficiencies persist. Health-care providers and policymakers might specifically target the ED as a place to initiate interventions designed to reduce race-based disparities in health. (CHEST 2003; 124:803– 812) Key words: adults; asthma; ethnicity; quality of care; race; socioeconomic status Abbreviations: CI ⫽ confidence interval; ED ⫽ emergency department; IQR ⫽ interquartile range; MARC ⫽ Multicenter Airway Research Collaboration; OR ⫽ odds ratio; PCP ⫽ primary care provider; PEFR ⫽ peak expiratory flow rate; SES ⫽ socioeconomic status
the United States, asthma does not affect all I nracial/ethnic groups equally. Population studies have repeatedly found higher asthma prevalence among blacks compared to whites.1–7 Black patients with asthma also experience greater morbidity8 –18 and mortality.19 –23 Hispanic patients, especially those of Puerto Rican descent, likewise bear a greater asthma burden than whites.5,9,10,24 –26 The reasons for racial/ethnic differences in asthma prevalence, morbidity, and mortality remain unclear. www.chestjournal.org
While evidence for the genetic basis of asthma (or asthma susceptibility) is clear,27,28 information about the contribution of genetic factors to race/ethnicity differences in asthma is lacking.2,29 –32 Rather, other nongenetic factors have been implicated, such as lower socioeconomic status (SES) and its correlates, including greater allergen and irritant exposure and poor access to and compliance with state-of-the-art medical management.2– 8,12,13,17,18,33– 41 Most published studies on emergency department CHEST / 124 / 3 / SEPTEMBER, 2003
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(ED) utilization by asthmatic adults of different racial/ethnic backgrounds have used retrospective reviews of archived or billing data.18,33 This restricts the range of variables that can be examined and leads to an incomplete picture of what actually happens to patients while they are in the ED. To further examine the role of race/ethnicity in asthma among adults presenting to the ED, we examined prospective data from the Multicenter Airway Research Collaboration (MARC). Based on previous research, we hypothesized that black and Hispanic asthma patients would be (1) in more severe respiratory distress on arrival to the ED, (2) more likely to receive substandard care while in the ED, (3) hospitalized more often during their index ED visit, and (4) more likely to relapse or have continued symptoms during the 2 weeks after hospital discharge. We further hypothesized that, after statistically controlling for factors thought to be confounders of the relation between race/ethnicity and illness severity (ie, education level, income, insurance status, and access to a primary care provider [PCP]), the observed racial/ethnic differences either would disappear or be dramatically reduced.
Materials and Methods We analyzed data from three prospective cohort studies performed from 1996 to 1998 as part of the MARC (http:// healthcare.partners.org/marc). The purpose of the MARC was to try to define the characteristics of patients presenting to the ED for acute asthma, to describe their management and outcome, and to follow their course after hospital discharge. Using a standardized protocol, researchers at 64 EDs in 21 US states and 4 Canadian provinces provided 24-h coverage for a median duration of 2 weeks and consecutively enrolled adult patients. The following criteria were used to determine eligibility: (1) *From the Department of Emergency Medicine (Dr. Boudreaux), Cooper Hospital and University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, Camden, NJ; Emergency Department (Dr. Emond), Kaiser Permanente, Santa Clara Medical Center, Santa Clara, CA; and Department of Emergency Medicine (Mr. Clark and Dr. Camargo), Massachusetts General Hospital and Channing Laboratory, Boston, MA. †A complete list of the MARC investigators is located in the Appendix. Dr. Camargo is supported by grant HL-63841 from the National Institutes of Health (Bethesda, MD). The Multicenter Airway Research Collaboration was supported by grant HL-63253 from the National Institutes of Health, and by unrestricted grants from GlaxoSmithKline Inc (Research Triangle Park, NC) and Monaghan Medical Corporation (Syracuse, NY). Manuscript received August 1, 2002; revision accepted March 13, 2003. Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (e-mail: [email protected]). Correspondence to: Edwin D. Boudreaux, PhD, Emergency Medicine Residency Program, Cooper Hospital, One Cooper Plaza, Camden, NJ 08103-1489; e-mail: boudreaux-edwin@ cooperhealth.edu 804
physician-diagnosed asthma (including new diagnoses by the ED physician or patient reported history); (2) current ED visit was due to an exacerbation; (3) age 18 to 54 years (truncated at 54 in order to help rule out COPD); and (4) the ability to give informed consent. Repeat visits by individual patients were excluded. All patients were managed at the discretion of the treating physician. The site investigators were not informed that we intended to compare presentation/management/outcome by race/ethnicity. Therefore, they were blinded to the specific hypotheses studied in this investigation. The institutional review board at each hospital approved the study. Public hospitals constituted 36% of sites. The remainder of the sites were private or not-for-profit hospitals. The median number of annual hospital admissions was 23,427, the median number of annual ED visits was 54,000, and the median number of annual visits for asthma was 1,500. Data Collection The ED interview assessed patients’ sociodemographic characteristics, asthma history, and details of their current asthma exacerbation. Data on ED management, disposition, and hospital discharge medications were obtained by chart review. Follow-up data were collected by telephone interview 2 weeks later. Research personnel used “best numbers” and “best times” solicited during the ED interview to guide their calls. A minimum of five attempts to reach the patient were made, spaced across at least 3 days. All forms were reviewed for accuracy, completeness, and legibility by site investigators before submission to the MARC Coordinating Center in Boston, MA, where they underwent further review by trained personnel. Incomplete, contradictory, or illegible data were returned to the site investigator for reconciliation. The data were double-entered. Sociodemographic Factors: Age, sex, level of education, and insurance status were recorded. Consistent with other literature in this area,10,11,13,17,18,33,38 the median family income was estimated using patients’ home ZIP codes.42 Race/ethnicity was assigned by self-report to standard US Census categories. For the purpose of this analysis, mutually exclusive categories were determined as follows: black (ie, African American or nonHispanic); Hispanic; or white (ie, non-Hispanic). Patients designated as Asian or “other” ethnicity were excluded due to small numbers. While the limitations of self-report have been discussed in the literature,43– 46 it remains the most common and efficient manner by which to classify patients’ race/ethnicity. Patients were asked whether they had a PCP. Chronic Asthma History: We also assessed patients’ asthma medication use, including oral corticosteroids, rescue inhalers, and inhaled corticosteroids. We measured health-care utilization via hospitalization history (ever hospitalized and hospitalized in the past year), the number of ED visits made in the past year, and the source of their primary asthma care and prescriptions. Smoking status also was assessed. To examine further disease self-management, we assessed whether the patient owned a spacer device, peak flowmeter, and a written action plan. Finally, we recorded whether a comorbid medical condition was present (eg, congestive heart failure or COPD). ED Course: We collected both subjective and objective measures of acute asthma severity. Severe symptoms was assigned to patients who reported asthma symptoms “most of the time” or had experienced “severe” discomfort and distress due to their asthma during the past 24 h. Peak expiratory flow rate (PEFR) was expressed as the percentage of the patient’s predicted value, based on race, age, sex, and height.47 Initial measurement and change in PEFR were recorded. The number of inhaled agonist treatments received prior to arrival in the ED, the number of treatments received during the ED visit (ie, within the Clinical Investigations
first hour and the total number), and whether the patient received oral corticosteroids were abstracted from the chart. We calculated ED length of stay and recorded ED disposition. Hospital discharge medications were recorded, including systemic and inhaled corticosteroids. However, prescription for inhaled corticosteroids at hospital discharge was systematically collected for only two of the three cohorts (566 patients). Two-Week Follow-up: All patients were called 2 weeks after their discharge from the ED. Relapse was defined as any urgent visit to an ED or clinic for worsening of asthma during the 2-week follow-up period. The number of days between discharge from the ED and the date of relapse was recorded. An ongoing exacerbation classification was assigned to patients who reported “severe symptoms” during the 24-h period preceding the phone call on any one of two questions (ie, asthma symptoms “most of the time” or “severe” discomfort and distress due to their asthma) or to those who stated that their asthma was “about the same” or “worse” than at the time of their ED presentation. Statistical Analysis All statistical analyses were performed using a statistical software package (STATA, version 7.0; StataCorp; College Station, TX). The data are presented as proportions, means (with SD), or medians (with interquartile range [IQR]). The association between race/ethnicity and other factors was examined using 2 test, analysis of variance, and Kruskal-Wallis test, as appropriate. Three multivariate models were derived to predict the initial PEFR, hospitalization, and posthospital discharge outcome. Each of these final models included the following variables: age; sex; education; median household income; insurance status; PCP status; and recent inhaled corticosteroid use. Other salient variables then were added based on the particular dependent variable (eg, initial PEFR and change in PEFR were used to predict hospitalization). The race/ethnicity variable was added to the three models as one variable. All interpretations of the odds ratios (ORs) for blacks and Hispanics were based on the reference group (whites). The possibility of a period effect was examined by adjusting for the period of enrollment, but this did not materially affect any of the results that follow (data not shown). All ORs are presented with 95% confidence intervals (CIs). All p values are two-sided. Considering the large sample size and the risk of multiple testing error, p ⬍ 0.01 was considered to be statistically significant.
Results Among the eligible patients, 588 refused study entry, were missed, or were not enrolled for another
reason, and 1,847 were enrolled into the study. Three patients were excluded because race/ethnicity data were missing. Patients identified as Asian or “other” race/ethnicity (44 patients) were excluded, since the purpose of the study was to investigate blacks and Hispanics. Patients who were enrolled did not differ from those who were not enrolled according to demographic factors, available chronic asthma factors, ED course (except for the administration of steroids in the ED, which was more likely among those who were enrolled in the study [68% vs 62%, respectively; p ⫽ 0.01]), or disposition. Among the 1,800 patients used in these analyses, 935 (52%) were black, 411 (23%) were Hispanic, and 454 (25%) were white. Since the US sites had a high proportion of black and Hispanic patients and the Canadian sites had a high proportion of white patients, we re-ran all the analyses excluding the Canadian sites. We found no significant differences in the results. Sociodemographics Sociodemographic characteristics by race/ethnicity are presented in Table 1. Trends show that black and Hispanic asthma patients were from lower SES households and were less likely to have a PCP. Chronic Asthma History Chronic asthma history by race/ethnicity also is presented in Table 2. Black and Hispanic patients were more likely to have a history of hospitalization and reported a greater number of ED visits. They were more likely to state that they used the ED as their primary source of asthma care and prescriptions. The three groups were equally likely to have recently used systemic corticosteroids and inhaled bronchodilators, but black and Hispanic patients were less likely to have used inhaled corticosteroids. Black patients and, especially, Hispanic patients were less likely to own a spacer and a peak flowmeter, while action plans were low across all three
Table 1—Demographic Characteristics of Adults with Acute Asthma According to Race/Ethnicity* Characteristics
Black (n ⫽ 935)
Hispanic (n ⫽ 411)
White (n ⫽ 454)
p Value
Age,† yr Female High school graduate Estimated household income‡ Insurance status Private Medicaid Other public None Primary care provider
35 ⫾ 10 62 68 26,288 (18,999–34,487)
35 ⫾ 10 66 53 25,185 (17,364–32,849)
34 ⫾ 10 71 81 35,336 (27,190–43,291)
0.80 0.002 ⬍ 0.001 ⬍ 0.001 ⬍ 0.001
26 29 10 35 61
21 41 10 29 62
40 14 24 21 77
⬍ 0.001
*Values given as %, unless otherwise indicated. †Values given as mean ⫾ SD. ‡Values given as median (IQR). www.chestjournal.org
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Table 2—Chronic Asthma Characteristics of Adults with Acute Asthma According to Race/Ethnicity* Characteristics
Black (n ⫽ 935)
Hispanic (n ⫽ 411)
White (n ⫽ 454)
p Value
74 66 18 27 58 34 85 42 35 3 (1–5) 38 42 29 31 79 52
68 63 17 38 59 31 86 39 33 3 (0–5) 30 30 32 33 78 54
74 54 12 25 74 41 87 53 39 1 (0–3) 43 45 33 25 61 25
0.09 ⬍ 0.001 0.02 0.001 ⬍ 0.001 0.01 0.59 ⬍ 0.001 0.11 ⬍ 0.001 ⬍ 0.001 ⬍ 0.001 0.42 0.02 ⬍ 0.001 ⬍ 0.001
Ever taken steroid medicine for asthma Ever hospitalized for asthma Ever intubated for asthma Recent use of home nebulizer† Hay fever Current smoker Inhaled -agonist during past 4 wk Inhaled corticosteroid during past 4 wk Other asthma medication during past 4 wk ED visits in past year‡ Owns a spacer Owns a peak flowmeter Has a written action plan Admitted for asthma in past year ED usual site of care for asthma problems ED usual source of asthma prescriptions *Values given as %, unless otherwise indicated. †Limited to two cohorts (1,281 patients). ‡Values given as median (IQR).
groups. Comorbid medical conditions were equally likely (blacks, 9%; Hispanics, 4%; whites, 8%; p ⫽ 0.03). Acute Presentation and ED Course Data on acute asthma presentation and ED course are presented in Table 3. Black and Hispanic patients exhibited more severe objective airway obstruction (based on PEFR), but blacks reported
slightly less severe subjective distress. Black and Hispanic patients received more inhaled bronchodilator doses during the first hour following triage, and black patients were most likely to have received systemic corticosteroid treatment. All race/ethnicity groups were equally likely to be discharged from the ED with a prescription for inhaled corticosteroids (566 patients; black, 39%; Hispanic, 37%; white, 48%; p ⫽ 0.15). When the sample was restricted to
Table 3—Acute Asthma Presentation and ED Course According to Race/Ethnicity*
Presentation Duration of symptoms ⬍ 24 h Severe symptoms† ED course Initial PEFR, % predicted Initial PEFR ⬍ 50% 50–79% ⱖ 80% Inhaled -agonist doses in first hour, No. Inhaled -agonist doses over ED stay, No. Given steroid treatment Received other asthma treatments in the ED Final PEFR, % predicted Change in PEFR, % predicted ED length of stay, min Sent home on systemic corticosteroids‡ Admitted
Black (n ⫽ 935)
Hispanic (n ⫽ 411)
White (n ⫽ 454)
53 71
56 77
56 79
47 ⫾ 21
47 ⫾ 18
52 ⫾ 21
59 33 8 1.8 ⫾ 0.9 3.3 ⫾ 1.9 72 27 72 ⫾ 23 25 ⫾ 19 182 (128–262) 70 20
62 33 5 1.9 ⫾ 1.0 3.1 ⫾ 1.7 64 25 73 ⫾ 22 26 ⫾ 19 187 (125–270) 61 21
51 39 10 1.6 ⫾ 0.9 3.1 ⫾ 2.4 66 35 75 ⫾ 23 22 ⫾ 20 180 (134–256) 65 19
p Value 0.52 0.002 ⬍ 0.001 0.02
⬍ 0.001 0.42 0.008 0.003 0.12 0.06 0.97 0.02 0.77
*Values given as %, mean ⫾ SD, or median (IQR), unless otherwise indicated. †See “Materials and Methods” section for details. ‡Restricted to patients sent home from ED (1,442 patients). 806
Clinical Investigations
Table 4 —Two-Week Follow-up According to Race/Ethnicity* Variables Hospital length of stay, d Relapse within 2 wk of ED visit† Days to relapse Ongoing exacerbation‡ Relapse or ongoing exacerbation
Black
Hispanic
White
p Value
2 (1–5) 13 7 (4–11) 24 31
3 (2–4) 17 2 (2–10) 31 40
2 (1–3) 15 3 (1–8) 19 31
0.30 0.31 ⬍0.001 0.003 0.008
*Values given as median (IQR) or %, unless otherwise indicated; n ⫽ 1,308. †Relapse event based on patient reporting a “worsening of asthma symptoms” that led to an urgent care visit. ‡See “Materials and Methods” section for details.
only those patients who were not already receiving inhaled corticosteroids, we again found no differences (black, 12%; Hispanic, 11%; white, 13%; p ⫽ 0.86). After controlling for seven factors (ie, age, sex, education, estimated household income, insurance status, PCP status, and recent use of inhaled steroids) using multiple linear regression analysis, we found that the initial PEFR no longer differed significantly by race/ethnicity (black vs white: difference, ⫺0.03; 95% CI, ⫺0.06 to ⫺0.004; p ⫽ 0.05; Hispanic vs white: difference, ⫺0.03; 95% CI, ⫺0.07 to ⫺0.001; p ⫽ 0.05). At the univariate level, hospitalization did not differ by race/ethnicity. However, the logistic regression model predicting hospitalization demonstrated that, all things being equal, black and Hispanic patients were more likely to be admitted to the hospital (black vs white: OR, 2.1; 95% CI, 1.2 to 3.6; p ⫽ 0.005; Hispanic vs white: OR, 2.6; 95% CI, 1.4 to 4.7; p ⫽ 0.002). Two-Week Follow-up A total of 1,308 patients (71% of total) were reached for telephone follow-up. Blacks were the least likely to be reached (likelihood: black, 66%; Hispanic, 72%; white, 80%; p ⬍ 0.001). Univariate results are presented in Table 4. Race/ethnicity was not related to the likelihood of short-term relapse,
although time to relapse among those who did relapse appeared to be longer for blacks. Blacks and, especially, Hispanics were the most likely to have ongoing symptoms at the univariate level. However, when the data were controlled for several factors (ie, age, sex, education, estimated household income, insurance status, PCP status, recent use of inhaled steroids, ED steroid treatment, and final PEFR), there was no statistically significant difference according to race/ethnicity (black vs white: OR, 1.3; 95% CI, 0.9 to 1.9; p ⫽ 0.17; Hispanic vs white: OR, 0.8; 95% CI, 0.5 to 1.2; p ⫽ 0.24). Approximately 33% of adults reported a relapse event or an ongoing exacerbation. Discussion It is widely recognized that black and Hispanic asthma patients receive substandard outpatient care, visit the ED more frequently, and are hospitalized at greater rates than are whites.8 –18,48 However, little is known about whether racial/ethnic differences exist during the course and treatment of exacerbations while in the ED or whether racial/ethnic differences exist in relapse and outcome after discharge from the ED. Because we prospectively enrolled patients during their ED visit and observed them after their ED discharge, rather than using archival or billing data, our study helps to answer these questions.
Table 5—Relation of Black or Hispanic (vs White) Race/Ethnicity to Risk of Hospital Admission Among Adults With Acute Asthma Black
Hispanic
Variables
OR
95% CI
p Value
OR
95% CI
p Value
Model 1 (adjusted for age ⫹ sex) Model 2 (adjusted for above ⫹ education, median income, insurance status) Model 3 (adjusted for above ⫹ PCP status) Model 4 (adjusted for above ⫹ recent inhaled steroid use) Model 5 (adjusted for above ⫹ initial PEFR) Model 6 (adjusted for above ⫹ change in PEFR)
1.1 1.2
0.8–1.5 0.9–1.7
0.53 0.22
1.1 1.1
0.8–1.6 0.8–1.7
0.43 0.49
1.3 1.3
0.9–1.8 0.9–1.8
0.14 0.11
1.2 1.2
0.8–1.8 0.8–1.8
0.37 0.30
1.5 2.1
1.0–2.3 1.2–3.6
0.05 0.005
1.4 2.6
0.9–2.3 1.4–4.7
0.16 0.002
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Racial/Ethnic Differences in Asthma on Presentation to the ED We hypothesized that black and Hispanic patients would present to the ED in more severe respiratory distress than white patients. Consistent with this hypothesis, black and Hispanic patients in our sample presented to the ED with an average PEFR of 47% of the predicted value, compared to 52% for white patients. Our analyses indicate that this difference is not likely due to chance. Moreover, if an individual improved from 47 to 52%, this would represent a ⬎ 10% change in the patient’s PEFR, which generally is considered clinically significant. Arguably, using the mean PEFR may have blurred very sick and very mild cases together, potentially hiding a trend for a continued greater rate of mild cases among black and Hispanic patients. To help explore this possibility, we further subdivided the PEFR into three groups based on National Asthma Education and Prevention Program guidelines. This distribution showed that white patients, rather than black and Hispanic patients, tended to be more likely to present with mild exacerbations. Our multivariate analyses indicated that adjusting for demographic factors and SES markedly reduced the size of the discrepancy in severity of acute asthma by race/ethnicity. The extant literature is contradictory regarding the role that SES plays in the race/ethnic disparities observed in asthma severity, morbidity, and management. Some have found33 results similar to ours, with all or most of the race/ethnicity-based disparities being accounted for by SES. Most others have found that race/ethnicitybased differences persist even after adjusting for SES indicators, such as annual income,11,17,18 urban nature of residence,9,10 and insurance status.18 However, to conclude that SES is not an important mediator of race/ethnicity-based asthma disparities based on these later studies alone would be to oversimplify a very complex issue. Many of these studies found that SES was substantially related to at least some of the disparities noted, and none concluded that SES was unrelated to race-based disparities or was unimportant in understanding why such disparities occur. They simply concluded that SES was not the only factor accounting for racial/ethnic disparities. The persisting race/ethnicity differences in morbidity and mortality, even after controlling for SES, possibly can be explained by cultural differences in the tendency to use a short-term treatment approach rather than preventive treatment approaches. However, to date, convincing data for this hypothesis have not been published in the asthma literature. Furthermore, it is clear that, by focusing on only one 808
indicator such as insurance status or annual income, many studies simply did not sufficiently account for SES, which is a multifaceted construct. Kaufman and colleagues49 have cautioned that residual confounding can be a significant problem when studying the health correlates of SES. For example, Zoratti and colleagues18 found that, even among members of the same managed care organization, blacks still earned less than whites. When they isolated their sample to include only those patients who had low incomes, many (but not all) of their race/ethnicity-based discrepancies in health-care utilization and prescription medication usage disappeared or were markedly attenuated. Racial/Ethnic Differences in ED Course and Management Many of our results on ED course and management ran counter to the trends noted in outpatient settings. Black and Hispanic patients received more doses of inhaled -agonists within the first hour of presentation, and black patients were more likely to receive oral corticosteroids than were white patients. This more aggressive treatment possibly reflects an appropriate response to the aforementioned greater severity on presentation and worse chronic history of asthma among minorities. These trends, combined with the fact that the total number of inhaled -agonist treatments, the final PEFR, change in PEFR, ED length of stay, and ED discharge medications did not differ among racial/ethnic groups, indicates that patients received similar care and achieved comparable resolution of symptoms while in the ED. Other studies50,51 have shown that the quality of ED asthma care frequently diverges from national guidelines. However, these studies did not specifically investigate whether ED care for minorities diverged to a greater degree than that of whites, making it difficult to integrate our results. Importantly, our results affirm the common perception that the ED is a “safety net” for individuals with asthma, regardless of race/ethnicity. Racial/Ethnic Differences in Hospitalization During the Index ED Visit Studies9 –11,14,17,18,38 have found that hospitalization rates among minorities are three to five times that for whites during a given period. However, we could not identify any published studies that actually have investigated racial/ethnic differences in hospital admission rates during an index ED visit. We expected moderate-to-large racial/ethnic differences in hospitalization at the index visit. To the contrary, we found almost identical rates, in absolute terms, Clinical Investigations
among all three groups. Approximately 20% of all blacks, Hispanics, and whites were hospitalized during their index visit. The discrepancy between hospitalization point incidence (ie, at the index ED visit) and period incidence (ie, 1 year) is difficult to explain. It seems likely that it is due, at least in part, to a base-rate effect. Even though black and Hispanic patients have the same risk of being hospitalized during a given ED visit, they may have a markedly greater incidence of hospitalization over a given period, because they experience severe exacerbations warranting emergency care more frequently. This can be conceptualized in probabilistic terms. The chance of rolling a six on any roll of a die is identical. Nevertheless, one has a better chance of rolling at least one six during a given period of time if allowed to roll the die three times instead of only once. Even though a black patient has a similar probability of being admitted to the hospital at a given visit, if that patient presents three times over the course of a year and a white patient presents only once, the black patient will be more likely to be admitted to the hospital during that year. Although the absolute rates of hospitalization were roughly equivalent, our multivariate analyses revealed an interesting trend. Once all sociodemographic factors, initial PEFR, and change in PEFR were controlled for, black and Hispanic patients were more than twice as likely to have been admitted to the hospital. The inclusion of PEFR indexes in the last step of the model appeared to have the largest impact on the race/ethnicity-hospitalization relationship. This finding seems to suggest that, at equivalent levels of symptom resolution, black and Hispanic patients are more likely to be admitted to the hospital than whites. The reasons for this association are difficult to determine and await further empirical validation. The Role of Race/Ethnicity and Posthospital Discharge Outcome The posthospital discharge outcomes present a mixed picture. Blacks and Hispanics sought urgent medical care within the 2 weeks after hospital discharge at approximately the same rate as whites (approximately 15%), although blacks appeared to have a longer delay before seeking such care. Whether this is due to a delay in seeking treatment or a delay in experiencing an exacerbation severe enough to warrant treatment is not clear. Our relapse rates were comparable to those reported by other single-center studies.52–54 Treatment failure, defined by the continued self-report of severe symptoms, occurred more frequently in minorities, particularly Hispanics. As with the racial/ethnic differwww.chestjournal.org
ences noted in initial PEFR on presentation to the ED, the race-based discrepancy in treatment failure appears to be associated primarily with racial/ethnic differences in sociodemographic factors, including SES. Potential Limitations In evaluating our results, several potential limitations should be considered. First, we recognize that the race/ethnicity designation, though ubiquitous in epidemiologic research, may be misleading, and that standard census classification is simplistic. Nevertheless, our designations are consistent with those used in prior studies cited throughout our article. Such research remains common and is important in order to further understand and eventually to modify the reasons why such differences exist. The fact that race/ethnicity is difficult to operationalize does not mean we should not study it. Research such as ours is important in raising public awareness and may help providers to counteract any implicit racism that may be present. Second, our sample size was large, which enabled us to detect small differences that were not necessarily clinically meaningful. We were sensitive to this fact, however, and emphasized only those trends that appeared clinically significant, noting in the text when such a problem might exist. Third, the EDs that comprised our sample are predominantly urban, academically affiliated hospitals. This may make our results less generalizable to community hospitals without academic affiliation. Future studies need to address this issue. Fourth, we noted a paradoxical trend in initial severity. Despite presenting with worse PEFR, black patients reported slightly less severe symptoms than whites. The reason for this is unclear. The differences were not likely due to chance, but the magnitude was small and may not be clinically meaningful. The observation awaits validation by other studies. It is a potentially important area, since blunted perception of dyspnea has been associated with the increased risk of near-fatal asthma.55,56 Finally, we found that hospital discharge medications did not differ based on race. However, since black and Hispanic patients had more severe chronic asthma, the fact that the ED discharge rates were equal for inhaled corticosteroids is somewhat disconcerting. Under these conditions, one would logically expect that the ED discharge rates for inhaled corticosteroids should be greater for blacks and Hispanic patients. Consequently, the equal rates of ED discharge on inhaled corticosteroids may actually be interpreted to mean that blacks and Hispanics were undertreated on ED discharge. CHEST / 124 / 3 / SEPTEMBER, 2003
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Integration The associations among race/ethnicity, SES, and various measures of asthma severity and morbidity are complex. We found marked racial/ethnic differences in chronic asthma management. Black and Hispanic asthma patients lacked PCPs more often, reported a greater likelihood of lifetime hospitalization, and reported more numerous ED visits in the past year. Importantly, they also were less likely to use inhaled corticosteroids and less frequently owned a spacer and a peak flowmeter. Not only do they present to the ED more often, but also our data show that they presented to the ED with somewhat more severe exacerbations. However, their course and treatment during the ED visit did not seem to differ dramatically, they were not hospitalized during their index ED visit at greater rates than whites (except when controlling for confounding factors), and they did not seek urgent medical care within the 2 weeks after hospital discharge more frequently than whites. As mentioned earlier, the reason that minorities exhibit such deficient chronic asthma management is probably, at least in part, due to SES and the substandard health care that accompanies lower SES. Other environmental factors associated with low SES may lead to deficient chronic disease management, such as increased risk of respiratory infections due to overcrowding, and greater exposure to allergens and irritants,13,35,38,41 but these were not assessed in our study. Although we found that most differences were attributable to differences in SES, other research49 suggests that residual race/ethnicity differences may still be present even after adjusting for SES. This implicates other sociocultural and psychological factors. Some authors have speculated that racial/ethnic discrimination among health-care providers is a possible cause for the inequities observed in health care,43,57 although it is probably not conscious or deliberate.58 Several other explanations have been mentioned in the literature but have not been researched well enough to form conclusions. At best they offer direction for future research. These include race-based differences in health beliefs and practices emphasizing rescue rather than preventive strategies,18,59,60 impaired illness perception and judgment of disease severity,13,61– 63 lower selfefficacy regarding asthma management,64 – 67 and greater comorbid psychopathology, such as depression, anxiety, and panic disorders.64,65 The elimination of health disparities by race/ ethnicity is an overarching goal of Healthy People 2010. Although race-based disparities are trenchant and difficult to address, they can and should be eliminated. Evidence68 has shown that the deficient asthma care in economically disadvantaged health810
care facilities can be rectified with education and supportive programs. The necessary changes are unlikely to occur on a broad scale, however, without massive, coordinated, and sustained effort by all concerned parties, including the federal government, health-care providers and organizations, the pharmaceutical industry, community and civic associations, patient-advocacy groups, and the patients themselves. Appendix: MARC Emergency Medicine Network Steering Committee Edwin D. Boudreaux, PhD; Barry E. Brenner, MD, PhD; Carlos A. Camargo, Jr, MD (Chair); Rita K. Cydulka, MD; Theodore J. Gaeta, DO, MPH; and Michael S. Radeos, MD, MPH. Emergency Medicine Network 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, MA). Principal Investigators at the 64 Participating Sites F.C. Baker, III (Maine Medical Center, Portland, ME); J.M. Basior (Buffalo General Hospital, Buffalo, NY); C.A. Bethel (Mercy Hospital, Philadelphia, PA); L. Bielory (University Hospital, Newark, NJ); M.P. Blanda (Summa Health System, Akron, OH); D. Bond (Gray Nun’s Community Hospital, Edmonton, AB, Canada); G.W. Bota (Sudbury General Hospital, Sudbury, BC, Canada); E.D. Boudreaux (Earl K. Long Memorial Hospital, Baton Rouge, LA); B.E. Brenner (The Brooklyn Hospital Center, Brooklyn, NY); J. Brown (Misericordia Community Hospital, Edmonton, AB, Canada); C.A. Camargo, Jr (Massachusetts General Hospital, Boston, MA); F.L. Counselman (Sentara Norfolk General Hospital, Norfolk, VA); G. Ramalanjaona (Newark Beth Israel Hospital, Newark, NJ); R.K. Cydulka (MetroHealth Medical Center, Cleveland, OH); D.J. Dire (University of Oklahoma Medical Center, Oklahoma City, OK); N. El Sanadi (Broward General Hospital, Ft. Lauderdale, FL); S.D. Emond (St. Luke’s/ Roosevelt Hospital Center, NY, NY); T.J. Gaeta (Methodist Hospital, Brooklyn, NY); T.J. Gaeta (St. Barnabas Hospital, Bronx, NY); M.A. Gibbs (Carolinas Medical Center, Charlotte, NC); T.E. Glynn (Brooke Army Medical Center, Fort Sam Houston, TX); L.G. Graff IV (New Britain General Hospital, New Britain, CT); R.O. Gray (Hennepin County Medical Center, Minneapolis, MN); S.K. Griswold (Thomas Jefferson University Hospital, Philadelphia, PA); A. Guttman (Sir Mortimer B. Davis Jewish General Hospital, Montreal, QC, Canada); J.P. Hanrahan (Beth Israel Hospital, Boston, MA); F. Harchelroad (Allegheny General Hospital, Pittsburgh, PA); R. Harrigan (Temple University Hospital, Philadelphia, PA); S.E. Hughes (Albany Medical College, Albany, NY); A.H. Idris (University of Florida Health Center, Gainesville, FL); G.D. Innes (St. Paul’s Hospital, Vancouver, BC, Canada); M.E. Johnson (Jackson Memorial Hospital, Miami, FL); D.M. Joyce (University Hospital, SUNY HSC, Syracuse, NY); L.W. Kreplick (Christ Hospital & Medical Center, Oak Lawn, IL); E.C. Leibner (Detroit Receiving Hospital, Detroit, MI); J. Li (Charity Hospital, New Orleans, LA); L.F. Clinical Investigations
Lobon (Beth Israel Medical Center, New York, NY); A. Mangione (Albert Einstein Medical Center, Philadelphia, PA); M.F. McDermott (Cook County Hospital, Chicago, IL); J.S. Myslinski (Richland Memorial Hospital, Columbia, SC); E.S. Nadel (Brigham and Women’s Hospital, Boston, MA); R.M. Nowak (Henry Ford Hospital, Detroit, MI); C.V. Pollack, Jr (Maricopa Medical Center, Phoenix, AZ); M.S. Radeos (Lincoln Medical Center, Bronx, NY); D.J. Robinson (University of Maryland Medical Center, Baltimore, MD); R.M. Rodriguez (Southwestern Medical Center, Dallas, TX); B.H. Rowe (University of Alberta Hospital, Edmonton, AB, Canada); G. Rudnitsky (Allegheny University-MCP Division, Philadelphia, PA); R.E. Sapien (University of New Mexico Health Sciences Center, Albuquerque, NM); D. Schreiber (Stanford University Medical Center, Stanford, CA); R.A. Silverman (Long Island Jewish Medical Center, New Hyde Park, NY); H. Smithline (Baystate Medical Center, Springfield, MA); S. Stahmer (Hospital of the University of Pennsylvania, Philadelphia, PA); D. Stewart (Bronson Medical Center, Kalamazoo, MI); A. Sucov (University of Rochester Hospital, Rochester, NY); D.M. Taylor (University of Pittsburgh Medical Center, Pittsburgh, PA); C.A. Terregino (Cooper Hospital/University Medical Center, Camden, NJ); J.L. Larson (University of North Carolina Hospitals, Chapel Hill, NC); A. Walker (Royal Alexandria Hospital, Edmonton, AB, Canada); J. Walter (University of Chicago Hospital, Chicago, IL); E.J. Weber (University of California San Francisco Medical Center, San Francisco, CA); L. White (Akron General Medical Center, Akron, OH); and J.L. Zimmerman (Ben Taub General Hospital, Houston, TX).
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