Mouse Sensitization and Exposure Are Associated with Asthma Severity in Urban Children.

BACKGROUND: Mouse sensitization and exposure are associated with uncontrolled asthma, but whether they are associated with asthma severity, an intrinsic disease characteristic and long-term outcome predictor, is unclear. OBJECTIVE: To examine relationships between mouse sensitization and/or exposure and asthma severity in urban children. METHODS: A total of 645 children (5-17 years) with uncontrolled asthma underwent mouse sensitization evaluation. Sensitized children had mouse allergen measured in bedroom dust. Relationships between mouse sensitization, allergen levels, and asthma severity measures (treatment step and Composite Asthma Severity Index [CASI]) were examined using regression models adjusted for age, sex, atopy, study site, race, ethnicity, and insurance. RESULTS: The study population was predominantly minority (69.6% black, 20.8% Hispanic), low income (61.8%), and mouse sensitized (54.4%). Mean ± SD treatment step was 3.2 ± 1.6, equivalent to medium-dose inhaled corticosteroid. Mean ± SD CASI was 6.5 ± 3.4, reflecting moderate persistent asthma. Mouse sensitization was associated with higher treatment step (3.5 vs 2.9, mouse-sensitized vs nonsensitized, P < .001), independent of potential confounders (ß [95% CI], 0.36 [0.07-0.64]; P = .01). Mouse sensitization was associated independently with CASI (ß [95% CI], 0.82 [0.16-1.47]; P = .02). Among mouse-sensitized participants, higher bedroom floor and bed Mus m 1 were independently associated with treatment step (ß [95% CI], 0.26 [0.09-0.43]; P = .002 and ß [95% CI], 0.22 [0.01-0.43]; P = .04), respectively. Higher bedroom floor Mus m 1 was independently associated with CASI (ß [95% CI], 0.43 [0.05-0.81]; P = .03). CONCLUSIONS: Mouse sensitization and exposure are associated with asthma severity, among low-income, minority children. Further studies are needed to determine whether reducing allergen exposure among mouse-sensitized patients with asthma can reduce severity, ultimately altering childhood asthma natural history.

Respiratory Effects of Indoor Heat and the Interaction with Air Pollution in Chronic Obstructive Pulmonary Disease.

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.

Indoor pollutant exposures modify the effect of airborne endotoxin on asthma in urban children.

RATIONALE: The effect of endotoxin on asthma morbidity in urban populations is unclear. OBJECTIVES: To determine if indoor pollutant exposure modifies the relationships between indoor airborne endotoxin and asthma health and morbidity. METHODS: One hundred forty-six children and adolescents with persistent asthma underwent repeated clinical assessments at 0, 3, 6, 9, and 12 months. Home visits were conducted at the same time points for assessment of airborne nicotine, endotoxin, and nitrogen dioxide (NO2) concentrations. The effect of concomitant pollutant exposure on relationships between endotoxin and asthma outcomes were examined in stratified analyses and statistical models with interaction terms. MEASUREMENTS AND MAIN RESULTS: Both air nicotine and NO2 concentrations modified the relationships between airborne endotoxin and asthma outcomes. Among children living in homes with no detectable air nicotine, higher endotoxin was inversely associated with acute visits and oral corticosteroid bursts, whereas among those in homes with detectable air nicotine, endotoxin was positively associated with these outcomes (interaction P value = 0.004 and 0.07, respectively). Among children living in homes with lower NO2 concentrations (<20 ppb), higher endotoxin was positively associated with acute visits, whereas among those living in homes with higher NO2 concentrations, endotoxin was negatively associated with acute visit (interaction P value = 0.05). NO2 also modified the effect of endotoxin on asthma symptom outcomes in a similar manner. CONCLUSIONS: The effects of household airborne endotoxin exposure on asthma are modified by coexposure to air nicotine and NO2, and these pollutants have opposite effects on the relationships between endotoxin and asthma-related outcomes.

Mouse allergen is the major allergen of public health relevance in Baltimore City.

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.

Guideline-recommended fractional exhaled nitric oxide is a poor predictor of health-care use among inner-city children and adolescents receiving usual asthma care.

BACKGROUND: American Thoracic Society guidelines support using fractional exhaled nitric oxide (FENO) measurements in patients with asthma and highlight gaps in the evidence base. Little is known about the use of FENO levels to predict asthma exacerbations among high-risk, urban, minority populations receiving usual care. METHODS: Children with persistent asthma (n = 138) were enrolled in a prospective, observational cohort study and skin tested at baseline (a wheal ≥ 3 mm indicated a positive skin-prick test). FENO levels, lung function, and asthma-related health-care use were assessed at baseline and every 3 months thereafter for 1 year. Relationships between FENO levels and health-care use in the subsequent 3 months were examined. Final models accounted for repeated outcome measures and were adjusted for age, sex, and lung function. RESULTS: The mean age of the children was 11 years (range, 5-17 years), and most were male (57%), black (91%), and atopic (90%). At baseline, the median FENO level was 31.5 parts per billion (interquartile range, 16-61 ppb) and mean FEV1/FVC was 80.7% (SD, ± 9.6%). There were 237 acute asthma-related health-care visits, 105 unscheduled doctor visits, 125 ED visits, and seven hospitalizations during the follow-up period. FENO level was not a significant predictor of acute visits, ED visits, unscheduled doctor visits, or hospitalization in either unadjusted or adjusted analyses. Use of recommended cut points did not improve the predictive value of the FENO level (positive predictive value, 0.6%-32.8%) nor did application of the guideline-based algorithm to assess change over time. CONCLUSIONS: FENO level may not be a clinically useful predictor of health-care use for asthma exacerbations in urban minority children with asthma.

In-home air pollution is linked to respiratory morbidity in former smokers with chronic obstructive pulmonary disease.

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 = 84) had moderate or severe COPD with a mean FEV1 of 48.6% predicted. The mean (± SD) indoor PM(2.5) and NO(2) concentrations were 11.4 ± 13.3 µg/m(3) and 10.8 ± 10.6 ppb in the bedroom, and 12.2 ± 12.2 µg/m(3) and 12.2 ± 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.

Being overweight increases susceptibility to indoor pollutants among urban children with asthma.

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.