Original article
Asthma, lower airway diseases
Poor asthma control and exposure to traffic pollutants and obesity in older adults

https://doi.org/10.1016/j.anai.2012.04.009Get rights and content

Abstract

Background

Environmental and host predictors of asthma control in older asthmatic patients (>65 years old) are poorly understood.

Objective

To examine the effects of residential exposure to traffic exhaust and other environmental and host predictors on asthma control in older adults.

Methods

One hundred four asthmatic patients 65 years of age or older from allergy and pulmonary clinics in greater Cincinnati, Ohio, completed the validated Asthma Control Questionnaire (ACQ), pulmonary function testing, and skin prick testing to 10 common aeroallergens. Patients had a physician's diagnosis of asthma, had significant reversibility in forced expiratory volume in 1 second or a positive methacholine challenge test result, and did not have chronic obstructive pulmonary disease. The mean daily residential exposure to elemental carbon attributable to traffic (ECAT) was estimated using a land-use regression model. Regression models were used to evaluate associations among independent variables, ACQ scores, and the number of asthma exacerbations, defined as acute worsening of asthma symptoms requiring prednisone use, in the past year.

Results

In the adjusted model, mean daily residential exposure to ECAT greater than 0.39 μg/m3 was significantly associated with poorer asthma control based on ACQ scores (adjusted β = 2.85; 95% confidence interval [CI], 0.58–5.12; P = .02). High ECAT levels were also significantly associated with increased risk of asthma exacerbations (adjusted odds ratio, 3.24; 95% CI, 1.01–10.37; P = .05). A significant association was found between higher body mass index and worse ACQ scores (adjusted β = 1.15; 95% CI, 0.53–1.76; P < .001). Atopic patients (skin prick test positive) had significantly better ACQ scores than nonatopic patients (adjusted β = −0.39; 95% CI, −0.67 to −0.11; P < .01).

Conclusion

Higher mean daily residential exposure to traffic exhaust, obesity, and nonatopic status are associated with poorer asthma control among older asthmatic patients.

Introduction

The burden of asthma on adults 65 years and older is substantial and underappreciated.[1], [2], [3] Up to two-thirds of asthma-related deaths occur in adults 65 years and older.[4], [5] The prevalence of asthma in this age group is as high as 10%.[3], [4] High morbidity rates and decreased quality of life associated with asthma are also characteristic of this population.[1], [6] Despite evidence suggesting that older asthmatic patients may represent a more severe clinical phenotype with distinct mechanisms of airways inflammation, studies regarding the causes of high morbidity and mortality are lacking.[2], [3]

Environmental exposures and host factors contributing to poor asthma control in older asthmatic patients are poorly understood.[1], [3] Because of age-related decline in antioxidant defenses, older asthmatic patients may be especially susceptible to the effects of air pollutants, including traffic exhaust.7 Older asthmatic patients may be at increased risk of hospital admissions and reduced lung function due to acute elevations in nitrogen dioxide, ozone, and particles with diameters less than 2.5 μm.[8], [9] Previous studies also indicate that they might be at higher risk for poorly controlled asthma due to long-term exposure to nitrogen dioxide and ozone.[10], [11] Notably, these studies did not evaluate the effect of ultrafine particles (<100 nm), an important component of diesel exhaust exhibiting a strong spatial gradient and associated with significant health consequences in younger populations.12 In addition, these studies did not incorporate validated measures of asthma control.[13], [14] Thus, further study regarding the effect of long-term, residential exposure to traffic pollutants, including diesel exhaust, on asthma control in older adults is warranted.[1], [11]

The objective of this study was to examine the relationship between mean daily residential exposure to traffic exhaust and asthma control in asthmatic patients 65 years and older. Our hypothesis was that higher mean daily exposure to elemental carbon attributable to traffic (ECAT), a surrogate for diesel particulate exposure, would be significantly associated with poorer asthma control.[15], [16]

Section snippets

Study participants

To test this hypothesis, we conducted a study of 104 asthmatic patients 65 years or older recruited from 2 allergy and pulmonary clinical practices in greater Cincinnati, Ohio, and from the Cincinnati Veterans Administration Allergy Clinic. These practices included patient residences that were distributed across the greater Cincinnati area, had approximately equal numbers of males and females (in aggregate), and provided a study sample that was enriched for more severe asthma phenotypes. All

Cohort description

Characteristics of the 104 patients and their mean 6-item ACQ scores are presented in Table 1. Approximately half were female, the mean age was 74 years, and the cohort included 83 whites, 17 African Americans, 3 Hispanics, and 1 Asian, which is representative of the greater Cincinnati area. The median income was approximately $40,000. Most were overweight (BMI = 25), with 24% classified as obese and 18% considered morbidly obese. Comorbid gastroesophageal reflux disease (GERD) occurred in 60%.

Discussion

There are 3.1 million asthmatics 65 years of age and older in the United States, with that number expected to double in the next 25 years.28 Although mortality from asthma overall is less than 2.2 per 100,000 population, asthma-related mortality among older adults is almost 5 times greater, with 10.5 per 100,000 seniors dying of asthma.4 Predictors of asthma control among adults 65 years or older remain poorly understood, despite the increasing prevalence of and high rates of morbidity from

Acknowledgments

We thank the clinical research staff at the Bernstein Clinical Research Center, the Cincinnati Veterans Administration Clinical Research Unit, Abraham Research Center, and the University of Cincinnati Immunology Clinical Research Center. We are especially grateful to the patients who participated in this study from the Bernstein Allergy Group, the Cincinnati VA Medical Center, and the Fragge Allergy & Asthma Clinic.

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    Disclosures: Authors have nothing to disclose.

    Funding Sources: This study was funded by National Institute of Environmental Health Services grants P30-ES006096 and ES11170, US Public Health Service grant UL1 RR026314. The project described was supported by the National Center for Research Resources and the National Center for Advancing Translational Sciences, National Institutes of Health, through grant 8KL2 TR000078-04. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

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    Copyright © 2012 American College of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.