Background Cockroach and mouse allergens have both been implicated as causes in inner-city asthma morbidity in multicenter studies, but whether both allergens are clinically relevant within specific inner-city communities is unclear. Objective: Our study aimed to identify relevant allergens in Baltimore City. Methods One hundred forty-four children (5–17 years old) with asthma underwent skin prick tests at baseline and had clinical data collected at baseline and 3, 6, 9, and 12 months. Home settled dust samples were collected at the same time points for quantification of indoor allergens. Participants were grouped based on their sensitization and exposure status to each allergen. All analyses were adjusted for age, sex, and serum total IgE level. Results Forty-one percent were mouse sensitized/exposed, and 41% were cockroach sensitized/exposed based on bedroom floor exposure data. Mouse sensitization/exposure was associated with acute care visits, decreased FEV1/forced vital capacity percentage values, fraction of exhaled nitric oxide levels, and bronchodilator reversibility. Cockroach sensitization/exposure was only associated with acute care visits and bronchodilator reversibility when exposure was defined by using bedroom floor allergen levels. Mouse-specific IgE levels were associated with poor asthma health across a range of outcomes, whereas cockroach-specific IgE levels were not. The relationships between asthma outcomes and mouse allergen were independent of cockroach allergen. Although sensitization/exposure to both mouse and cockroach was generally associated with worse asthma, mouse sensitization/exposure was the primary contributor to these relationships. Conclusions In a community with high levels of both mouse and cockroach allergens, mouse allergen appears to be more strongly and consistently associated with poor asthma outcomes than cockroach allergen. Community-level asthma interventions in Baltimore should prioritize reducing mouse allergen exposure.

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 ...

Background Both being overweight and exposure to indoor pollutants, which have been associated with worse health of asthmatic patients, are common in urban minority populations. Whether being overweight is a risk factor for the effects of indoor pollutant exposure on asthma health is unknown. Objectives We sought to examine the effect of weight on the relationship between indoor pollutant exposure and asthma health in urban minority children. Methods One hundred forty-eight children (age, 5–17 years) with persistent asthma were followed for 1 year. Asthma symptoms, health care use, lung function, pulmonary inflammation, and indoor pollutants were assessed every 3 months. Weight category was based on body mass index percentile. Results Participants were predominantly African American (91%) and had public health insurance (85%). Four percent were underweight, 52% were normal weight, 16% were overweight, and 28% were obese. Overweight or obese participants had more symptoms associated with exposure to fine particulate matter measuring less than 2.5 μm in diameter (PM2.5) than normal-weight participants across a range of asthma symptoms. Overweight or obese participants also had more asthma symptoms associated with nitrogen dioxide (NO2) exposure than normal-weight participants, although this was not observed across all types of asthma symptoms. Weight did not affect the relationship between exposure to coarse particulate matter measuring between 2.5 and 10 μm in diameter and asthma symptoms. Relationships between indoor pollutant exposure and health care use, lung function, or pulmonary inflammation did not differ by weight. Conclusion Being overweight or obese can increase susceptibility to indoor PM2.5 and NO2 in urban children with asthma. Interventions aimed at weight loss might reduce asthma symptom responses to PM2.5 and NO2, and interventions aimed at reducing indoor pollutant levels might be particularly beneficial in overweight children.

Home mouse allergen exposure is associated with asthma morbidity, but little is known about the shape of the dose-response relationship or the relevance of location of exposure within the home. Asthma outcome and allergen exposure data were collected every three months for 1 year in 150 urban children with asthma. Participants were stratified by mouse sensitization and relationships between continuous measures of mouse allergen exposure and outcomes of interest were analyzed. Every ten-fold increase in the bed mouse allergen level was associated with an 87% increase in the odds of any asthma-related health care use among mouse sensitized (OR (95% CI): 1.87 (1.21–2.88)), but not non-mouse sensitized participants. Similar relationships were observed for emergency department visit and unscheduled doctor visit among mouse sensitized participants. Kitchen floor and bedroom air mouse allergen concentrations were also associated with greater odds of asthma-related healthcare utilization; however, the magnitude of the association was less than that observed for bed mouse allergen concentrations. In this population of urban children with asthma, there is a linear dose-response relationship between mouse allergen concentrations and asthma morbidity among mouse-sensitized asthmatics. Bed and bedroom air mouse allergen exposure compartments may have a greater impact on asthma morbidity than other compartments.