Rationale: Chronic obstructive pulmonary disease (COPD) guidelines make no recommendations for allergy diagnosis or treatment. Objectives: To determine whether an allergic phenotype contributes to respiratory symptoms and exacerbations in patients with COPD. Methods: Two separate cohorts were analyzed: National Health and Nutrition Survey III (NHANES III) and the COPD and domestic endotoxin (CODE) cohort. Subjects from NHANES III with COPD (n ¼ 1,381) defined as age . 40 years, history of smoking, FEV 1 /FVC , 0.70, and no diagnosis of asthma were identified. The presence of an allergic phenotype (n ¼ 296) was defined as self-reported doctor diagnosed hay fever or allergic upper respiratory symptoms. In CODE, former smokers with COPD (n ¼ 77) were evaluated for allergic sensitization defined as a detectable specific IgE to perennial allergens. Bivariate and multivariate models were used to determine whether an allergic phenotype was associated with respiratory symptoms and exacerbations. Measurements and Main Results: In NHANES III, multivariate analysis revealed that individuals with allergic phenotype were more likely to wheeze (odds ratio [OR], 2.1; P , 0.01), to have chronic cough (OR, 1.9; P ¼ 0.01) and chronic phlegm (OR, 1.5; P , 0.05), and to have increased risk of COPD exacerbation requiring an acute doctor visit (OR, 1.7; P ¼ 0.04). In the CODE cohort, multivariate analysis revealed that sensitized subjects reported more wheeze (OR, 5.91; P , 0.01), more nighttime awakening due to cough (OR, 4.20; P ¼ 0.03), increased risk of COPD exacerbations requiring treatment with antibiotics (OR, 3.79; P ¼ 0.02), and acute health visits (OR, 11.05; P , 0.01). An increasing number of sensitizations was associated with a higher risk for adverse health outcomes. Conclusions: Among individuals with COPD, evidence of an allergic phenotype is associated with increased respiratory symptoms and risk of COPD exacerbations.Keywords: atopy; allergic sensitization; allergy; chronic obstructive pulmonary disease Chronic obstructive pulmonary disease (COPD), a chronic disease of the airways, is caused by tobacco smoke and other air pollutant exposures (1). In the United States, COPD affects 14% of the adult population and is the third leading cause of death (2). Annually, COPD is responsible for 726,000 hospitalizations and over $32 billion in estimated cost, reflecting a large public health burden (3). Patients with COPD suffer significant morbidity, including respiratory symptoms that adversely affect quality of life and limit activity (4). Given the significant morbidity, understanding the different factors that contribute to symptom burden in COPD is an important focus of research.Allergic sensitization, assessed by allergen-specific IgE or skin prick testing, is a known risk factor for asthma (5, 6), and exposure to specific allergens in sensitized patients with asthma is known to worsen pulmonary symptoms (7,8). National and international guidelines recommend assessment of allergic sensitization and environmental exposur...

Rationale: The effect of indoor air pollutants on respiratory morbidity among patients with chronic obstructive pulmonary disease (COPD) in developed countries is uncertain. Objectives: The first longitudinal study to investigate the independent effects of indoor particulate matter (PM) and nitrogen dioxide (NO 2 ) concentrations on COPD morbidity in a periurban community. Methods: Former smokers with COPD were recruited and indoor air was monitored over a 1-week period in the participant's bedroom and main living area at baseline, 3 months, and 6 months. At each visit, participants completed spirometry and questionnaires assessing respiratory symptoms. Exacerbations were assessed by questionnaires administered at clinic visits and monthly telephone calls. Measurements and Main Results: Participants (n ¼ 84) had moderate or severe COPD with a mean FEV 1 of 48.6% predicted. The mean (6 SD) indoor PM 2.5 and NO 2 concentrations were 11.4 6 13.3 µg/m 3 and 10.8 6 10.6 ppb in the bedroom, and 12.2 6 12.2 µg/m 3 and 12.2 6 11.8 ppb in the main living area. Increases in PM 2.5 concentrations in the main living area were associated with increases in respiratory symptoms, rescue medication use, and risk of severe COPD exacerbations. Increases in NO 2 concentrations in the main living area were independently associated with worse dyspnea. Increases in bedroom NO 2 concentrations were associated with increases in nocturnal symptoms and risk of severe COPD exacerbations. Conclusions: Indoor pollutant exposure, including PM 2.5 and NO 2 , was associated with increased respiratory symptoms and risk of COPD exacerbation. Future investigations should include intervention studies that optimize indoor air quality as a novel therapeutic approach to improving COPD health outcomes.Keywords: indoor air; chronic obstructive pulmonary disease; particulate matter; nitrogen dioxide; exacerbations Chronic obstructive pulmonary disease (COPD), the third leading cause of death in the United States and the fifth leading cause worldwide, is expected to become increasingly prevalent in upcoming decades (1, 2). Most COPD is caused by environmental exposures; in developed countries, this exposure is primarily cigarette smoke. After COPD begins, evidence indicates that it can be worsened by other environmental exposures. For example, outdoor particulate matter (PM) concentrations have been associated with an increase in COPD hospitalizations and mortality (3, 4). Similarly, outdoor nitrogen dioxide (NO 2 ) exposure has been linked to worse COPD morbidity, including higher rates of exacerbations (4-6).Although substantial evidence shows that outdoor air pollutants impact COPD, there is much less evidence for the impact of indoor air on COPD, especially in developed countries. Although the Global Initiative for Chronic Obstructive Lung Disease guidelines identify indoor air pollution resulting from burning wood and other biomass fuels as a major risk factor for COPD (7), exposures under these conditions are two to three orders of magnitude higher ...

Accounting for smoking, occupational exposure was associated with COPD risk and, for those with established disease, shorter walk distance, greater breathlessness, worse quality of life, and increased exacerbation risk. Clinicians should obtain occupational histories from patients with COPD because work-related exposures may influence disease burden.

Rationale: There is limited evidence of the effect of exposure to heat on chronic obstructive pulmonary disease (COPD) morbidity, and the interactive effect between indoor heat and air pollution has not been established. Objectives:To determine the effect of indoor and outdoor heat exposure on COPD morbidity and to determine whether air pollution concentrations modify the effect of temperature.Methods: Sixty-nine participants with COPD were enrolled in a longitudinal cohort study, and data from the 601 participant days that occurred during the warm weather season were included in the analysis. Participants completed home environmental monitoring with measurement of temperature, relative humidity, and indoor air pollutants and simultaneous daily assessment of respiratory health with questionnaires and portable spirometry.Measurements and Main Results: Participants had moderate to severe COPD and spent the majority of their time indoors. Increases in maximal indoor temperature were associated with worsening of daily Breathlessness, Cough, and Sputum Scale scores and increases in rescue inhaler use. The effect was detected on the same day and lags of 1 and 2 days. The detrimental effect of temperature on these outcomes increased with higher concentrations of indoor fine particulate matter and nitrogen dioxide (P , 0.05 for interaction terms). On days during which participants went outdoors, increases in maximal daily outdoor temperature were associated with increases in Breathlessness, Cough, and Sputum Scale scores after adjusting for outdoor pollution concentrations.Conclusions: For patients with COPD who spend the majority of their time indoors, indoor heat exposure during the warmer months represents a modifiable environmental exposure that may contribute to respiratory morbidity. In the context of climate change, adaptive strategies that include optimization of indoor environmental conditions are needed to protect this high-risk group from the adverse health effects of heat.

Our goal was to investigate whether obesity increases susceptibility to the adverse effects of indoor particulate matter on respiratory morbidity among individuals with chronic obstructive pulmonary disease (COPD). Participants with COPD were studied at baseline, 3 and 6 months. Obesity was defined as a body mass index ≥30 kg·m−2. At each time point, indoor air was sampled for 5–7 days and particulate matter (PM) with an aerodynamic size ≤2.5 μm (PM2.5) and 2.5–10 μm (PM2.5–10) was measured. Respiratory symptoms, health status, rescue medication use, exacerbations, blood biomarkers and exhaled nitric oxide were assessed simultaneously. Of the 84 participants enrolled, 56% were obese and all were former smokers with moderate-to-severe COPD. Obese participants tended to have less severe disease as assessed by Global Initiative for Chronic Obstructive Pulmonary Disease stage and fewer pack-years of smoking. There was evidence that obesity modified the effects of indoor PM on COPD respiratory outcomes. Increases in PM2.5 and PM2.5–10 were associated with greater increases in nocturnal symptoms, dyspnoea and rescue medication use among obese versus non-obese participants. The impact of indoor PM on exacerbations, respiratory status and wheeze also tended to be greater among obese versus non-obese participants, as were differences in airway and systemic inflammatory responses to indoor PM. We found evidence that obesity was associated with exaggerated responses to indoor fine and coarse PM exposure among individuals with COPD.