A randomized trial of air cleaners and a health coach to improve indoor air quality for inner-city children with asthma and secondhand smoke exposure.

OBJECTIVE: To test an air cleaner and health coach intervention to reduce secondhand smoke exposure compared with air cleaners alone or no air cleaners in reducing particulate matter (PM), air nicotine, and urine cotinine concentrations and increasing symptom-free days in children with asthma residing with a smoker. DESIGN: Randomized controlled trial, with randomization embedded in study database. SETTINGS: The Johns Hopkins Hospital Children's Center and homes of children. PARTICIPANTS: Children with asthma, residing with a smoker, randomly assigned to interventions consisting of air cleaners only (n = 41), air cleaners plus a health coach (n = 41), or delayed air cleaner (control) (n = 44). MAIN OUTCOME MEASURES: Changes in PM, air nicotine, and urine cotinine concentrations and symptom-free days during the 6-month study. RESULTS: The overall follow-up rate was high (91.3%). Changes in mean fine and coarse PM (PM(2.5) and PM(2.5-10)) concentrations (baseline to 6 months) were significantly lower in both air cleaner groups compared with the control group (mean differences for PM(2.5) concentrations: control, 3.5 µg/m(3); air cleaner only, -19.9 µg/m(3); and air cleaner plus health coach, -16.1 µg/m(3); P = .003; and PM(2.5-10) concentrations: control, 2.4 µg/m(3); air cleaner only, -8.7 µg/m(3); and air cleaner plus health coach, -10.6 µg/m(3); P = .02). No differences were noted in air nicotine or urine cotinine concentrations. The health coach provided no additional reduction in PM concentrations. Symptom-free days were significantly increased [corrected] in both air cleaner groups compared with the control group (P = .03). CONCLUSION: Although the use of air cleaners can result in a significant reduction in indoor PM concentrations and a significant increase in symptom-free days, it is not enough to prevent exposure to secondhand smoke.

Both the variability and level of mouse allergen exposure influence the phenotype of the immune response in workers at a mouse facility.

BACKGROUND: The role of natural aeroallergen exposure in modulating allergen-specific immune responses is not well understood. OBJECTIVE: We sought to examine relationships between mouse allergen exposure and mouse-specific immune responses. METHODS: New employees (n = 179) at a mouse facility underwent repeated assessment of mouse allergen exposure, skin prick tests (SPTs), and measurement of mouse-specific IgG levels. Relationships between the mean level of exposure, variability of exposure (calculated as log deviation), and time to development of immunologic outcomes were examined by using Cox proportional hazards models. RESULTS: By 24 months, 32 (23%) participants had experienced a positive SPT response, and 10 (8%) had mouse-specific IgG4. The incidence of a positive SPT response increased as levels of exposure increased from low to moderate, peaking at 1.2 ng/m³, and decreased beyond this point (P = .04). The more variable the exposure was across visits, the lower the incidence of a positive SPT response (hazard ratio [HR], 0.17; 95% CI, 0.07-0.41). Variability of exposure was an independent predictor of a positive SPT response in a model that included both exposure metrics. In contrast, the incidence of mouse-specific IgG4 increased with increasing levels of mouse allergen exposure (HR, 2.9; 95% CI, 1.4-6.0), and there was evidence of a higher risk of mouse-specific IgG4 with greater variability of exposure (HR, 6.3; 95% CI, 0.4-95.2). CONCLUSION: Both the level and variability of mouse allergen exposure influence the humoral immune response, with specific patterns of exposure associated with specific immunophenotypes. Exposure variability might be a more important predictor of a positive SPT response, whereas the average exposure level might be a more important predictor of mouse-specific IgG4.

Household smoking behavior: effects on indoor air quality and health of urban children with asthma.

The goal of the study was to examine the association between biomarkers and environmental measures of second hand smoke (SHS) with caregiver, i.e. parent or legal guardian, report of household smoking behavior and morbidity measures among children with asthma. Baseline data were drawn from a longitudinal intervention for 126 inner city children with asthma, residing with a smoker. Most children met criteria for moderate to severe persistent asthma (63%) versus mild intermittent (20%) or mild persistent (17%). Household smoking behavior and asthma morbidity were compared with child urine cotinine and indoor measures of air quality including fine particulate matter (PM(2.5)) and air nicotine (AN). Kruskal-Wallis, Wilcoxon rank-sum and Spearman rho correlation tests were used to determine the level of association between biomarkers of SHS exposure and household smoking behavior and asthma morbidity. Most children had uncontrolled asthma (62%). The primary household smoker was the child's caregiver (86/126, 68%) of which 66 (77%) were the child's mother. Significantly higher mean PM(2.5), AN and cotinine concentrations were detected in households where the caregiver was the smoker (caregiver smoker: PM(2.5) µg/m(3): 44.16, AN: 1.79 µg/m(3), cotinine: 27.39 ng/ml; caregiver non-smoker: PM(2.5): 28.88 µg/m(3), AN: 0.71 µg/m(3), cotinine:10.78 ng/ml, all P ≤ 0.01). Urine cotinine concentrations trended higher in children who reported 5 or more symptom days within the past 2 weeks (>5 days/past 2 weeks, cotinine: 28.1 ng/ml vs. <5 days/past 2 weeks, cotinine: 16.2 ng/ml; P = 0.08). However, environmental measures of SHS exposures were not associated with asthma symptoms. Urban children with persistent asthma, residing with a smoker are exposed to high levels of SHS predominantly from their primary caregiver. Because cotinine was more strongly associated with asthma symptoms than environmental measures of SHS exposure and is independent of the site of exposure, it remains the gold standard for SHS exposure assessment in children with asthma.

Occupational mouse allergen exposure among non-mouse handlers.

This study assessed mouse allergen exposure across a range of jobs, including non-mouse handling jobs, at a mouse facility. Baseline data from 220 new employees enrolled in the Jackson Laboratory (JAXCohort) were analyzed. The baseline assessment included a questionnaire, allergy skin testing, and spirometry. Exposure assessments consisted of collection of two full-shift breathing zone air samples during a 1-week period. Air samples were analyzed for mouse allergen content, and the mean concentration of the two shifts represented mouse allergen exposure for that employee. The mean age of the 220 participants was 33 years. Ten percent reported current asthma and 56% were atopic. Thirty-eight percent were animal caretakers, 20% scientists, 20% administrative/support personnel, 10% materials/supplies handlers, and 9% laboratory technicians. Sixty percent of the population handled mice. Eighty-two percent of study participants had detectable breathing zone mouse allergen, and breathing zone mouse allergen concentrations were 1.02 ng/m³ (0.13-6.91) (median [interquartile range (IQR)]. Although mouse handlers had significantly higher concentrations of breathing zone mouse allergen than non-handlers (median [IQR]: 4.13 ng/m³ [0.69-12.12] and 0.21 ng/m³ [below detection (BD)-0.63], respectively; p < 0.001), 66% of non-handlers had detectable breathing zone mouse allergen. Mouse allergen concentrations among administrative/support personnel and materials/supplies handlers, jobs that generally do not entail handling mice, were median [IQR]: 0.23 ng/m³ [BD-0.59] and 0.63 ng/m³ [BD-18.91], respectively. Seventy-one percent of administrative/support personnel, and 68% of materials/supplies handlers had detectable breathing zone mouse allergen. As many as half of non-mouse handlers may have levels of exposure that are similar to levels observed among mouse handlers.

Childhood asthma and environmental exposures at swimming pools: state of the science and research recommendations.

OBJECTIVES: Recent studies have explored the potential for swimming pool disinfection by-products (DBPs), which are respiratory irritants, to cause asthma in young children. Here we describe the state of the science on methods for understanding children's exposure to DBPs and biologics at swimming pools and associations with new-onset childhood asthma and recommend a research agenda to improve our understanding of this issue. DATA SOURCES: A workshop was held in Leuven, Belgium, 21-23 August 2007, to evaluate the literature and to develop a research agenda to better understand children's exposures in the swimming pool environment and their potential associations with new-onset asthma. Participants, including clinicians, epidemiologists, exposure scientists, pool operations experts, and chemists, reviewed the literature, prepared background summaries, and held extensive discussions on the relevant published studies, knowledge of asthma characterization and exposures at swimming pools, and epidemiologic study designs. SYNTHESIS: Childhood swimming and new-onset childhood asthma have clear implications for public health. If attendance at indoor pools increases risk of childhood asthma, then concerns are warranted and action is necessary. If there is no such relationship, these concerns could unnecessarily deter children from indoor swimming and/or compromise water disinfection. CONCLUSIONS: Current evidence of an association between childhood swimming and new-onset asthma is suggestive but not conclusive. Important data gaps need to be filled, particularly in exposure assessment and characterization of asthma in the very young. Participants recommended that additional evaluations using a multidisciplinary approach are needed to determine whether a clear association exists.

Mediator release assay for assessment of biological potency of German cockroach allergen extracts.

BACKGROUND: Cockroach is an important allergen in inner-city asthma. The diagnosis and treatment of cockroach allergy has been impeded by the lack of standardized cockroach extracts. OBJECTIVE: We investigated the utility of a mediator release assay based on rat basophil leukemia (RBL) cells for comparing the potency of German cockroach extracts. METHODS: RBL cells (line 2H3) transfected with human FcepsilonRI were passively sensitized with sera from subjects with cockroach allergy and stimulated with serial dilutions of 3 commercial cockroach extracts (1:10 weight/volume). In addition, the in-house prepared extract was tested in separate experiments with pooled sera that produced optimal performance in the RBL assay. N-hexosaminidase release (NHR) was used as a marker of RBL cell degranulation and was examined in relation to the intradermal skin test (ID(50)EAL) and serum cockroach-specific and total IgE levels. RESULTS: The median cockroach-specific IgE concentration in 60 subjects was 0.72 kU(A)/L (interquartile range, 0.35-2.97 kU(A)/L); 19 sera (responders) produced a minimum 10% NHR to more than 1 extract. Responders had higher median cockroach-specific IgE (7.4 vs 1.0 kU(A)/L) and total IgE (429 vs 300 kU/L) levels than nonresponders. Ranking of extract potency was consistent between the mediator release assay and the ID(50)EAL. For the in-house prepared cockroach extract, the dose-response curves were shifted according to the concentration of the extract. NHR was reproducible between different experiments by using pooled sera. CONCLUSION: The mediator release assay measures biologic potency and correlates with the ID(50)EAL. It should be further evaluated to determine whether it could be used to replace intradermal skin test titration for assessing the potency of cockroach extract.

In-home particle concentrations and childhood asthma morbidity.

BACKGROUND: Although outdoor particulate matter (PM) has been linked to mortality and asthma morbidity, the impact of indoor PM on asthma has not been well established. OBJECTIVE: This study was designed to investigate the effect of in-home PM on asthma morbidity. METHODS: For a cohort of 150 asthmatic children (2-6 years of age) from Baltimore, Maryland, a technician deployed environmental monitoring equipment in the children's bedrooms for 3-day intervals at baseline and at 3 and 6 months. Caregivers completed questionnaires and daily diaries during air sampling. Longitudinal data analyses included regression models with generalized estimating equations. RESULTS: Children were primarily African Americans (91%) from lower socioeconomic backgrounds and spent most of their time in the home. Mean (+/- SD) indoor PM(2.5-10) (PM with aerodynamic diameter 2.5-10 microm) and PM(2.5) (aerodynamic diameter < 2.5 microm) concentrations were 17.4 +/- 21.0 and 40.3 +/- 35.4 microg/m(3). In adjusted models, 10-microg/m(3) increases in indoor PM(2.5-10) and PM(2.5) were associated with increased incidences of asthma symptoms: 6% [95% confidence interval (CI), 1 to 12%] and 3% (95% CI, -1 to 7%), respectively; symptoms causing children to slow down: 8% (95% CI, 2 to 14%) and 4% (95% CI, 0 to 9%), respectively; nocturnal symptoms: 8% (95% CI, 1 to 14%) and 6% (95% CI, 1 to 10%), respectively; wheezing that limited speech: 11% (95% CI, 3 to 19%) and 7% (95% CI, 0 to 14%), respectively; and use of rescue medication: 6% (95% CI, 1 to 10%) and 4% (95% CI, 1 to 8%), respectively. Increases of 10 microg/m(3) in indoor and ambient PM(2.5) were associated with 7% (95% CI, 2 to 11%) and 26% (95% CI, 1 to 52%) increases in exercise-related symptoms, respectively. CONCLUSIONS: Among preschool asthmatic children in Baltimore, increases in in-home PM(2.5-10) and PM(2.5) were associated with respiratory symptoms and rescue medication use. Increases in in-home and ambient PM(2.5) were associated with exercise-related symptoms. Although reducing PM outdoors may decrease asthma morbidity, reducing PM indoors, especially in homes of inner-city children, may lead to improved asthma health.

Complex interactions of pollutant and allergen exposures and their impact on people with asthma.

Pediatric asthma has many causes and can manifest differently in different children and at different times. Understanding the many factors related to the development and exacerbation of asthma is complicated by the complexity of the many environmental exposures related to asthma development and morbidity. Furthermore, the same environmental exposures that may cause increased symptoms at 1 point in time may be protective when the exposure occurs earlier or at high enough levels. We know that environmental exposures such as allergens, irritants, and pollutants are quite complex in their composition; further examination of this complexity may improve our understanding of this complex and highly prevalent disease.

Parent report of pests and pets and indoor allergen levels in inner-city homes.

BACKGROUND: Guidelines recommend allergen avoidance for patients with allergic asthma, but direct measurements of home allergen levels are not available to most physicians. Parent report of indoor allergen exposure is a potentially convenient and inexpensive surrogate measure of exposure, although validity of parent report to estimate indoor allergen levels is not well established. OBJECTIVE: To determine if parent-reported pest and pet exposures can identify patients with clinically relevant allergen exposure. METHODS: Parents of 300 inner-city children completed a survey about pests (cockroaches and mice) and furred pets (dogs and cats). Settled dust samples were obtained for Bla g 1, Mus m 1, Can f 1, and Fel d 1 from kitchens and bedrooms. RESULTS: Parent reports were associated with clinically relevant levels of Bla g 1, Mus m 1, Can f 1, and Fel d 1 (P < .001 for all). For example, when parents reported cockroaches were present, 86% of homes had settled dust Bla g 1 levels of 1 U/g or higher, and when they reported mice were present, 90% had Mus m 1 levels greater than 500 ng/g. Report of pets was also predictive of clinically meaningful allergen levels. Parent-reported absence of pets provided assurance that allergen levels were below relevant thresholds (negative predictive value, 80%-98%). However, parent-reported absence of pests did not provide assurance of low levels of these allergens (negative predictive value, 38%-75%). CONCLUSIONS: Since direct measurement of indoor allergens is not always feasible, especially in the inner city, parent report of pests and pets may be sufficient to recommend environmental control practices for sensitized children. Negative parent reports of pests are not sufficient evidence of low pest allergen exposure.

Management of asthma based on exhaled nitric oxide in addition to guideline-based treatment for inner-city adolescents and young adults: a randomised controlled trial.

BACKGROUND: Preliminary evidence is equivocal about the role of exhaled nitric oxide (NO) in clinical asthma management. We aimed to assess whether measurement of exhaled NO, as a biomarker of airway inflammation, could increase the effectiveness of asthma treatment, when used as an adjunct to clinical care based on asthma guidelines for inner-city adolescents and young adults. METHODS: We did a randomised, double-blind, parallel-group trial at ten centres in the USA. We screened 780 inner-city patients, aged 12-20 years, who had persistent asthma. All patients completed a run-in period of 3 weeks on a regimen based on standard treatment. 546 eligible participants who adhered to treatment during this run-in period were then randomly assigned to 46 weeks of either standard treatment, based on the guidelines of the National Asthma Education and Prevention Program (NAEPP), or standard treatment modified on the basis of measurements of fraction of exhaled NO. The primary outcome was the number of days with asthma symptoms. We analysed patients on an intention-to-treat basis. This trial is registered with clinicaltrials.gov, number NCT00114413. FINDINGS: During the 46-week treatment period, the mean number of days with asthma symptoms did not differ between the treatment groups (1.93 [95% CI 1.74 to 2.11] in the NO monitoring group vs 1.89 [1.71 to 2.07] in the control group; difference 0.04 [-0.22 to 0.29], p=0.780). Other symptoms, pulmonary function, and asthma exacerbations did not differ between groups. Patients in the NO monitoring group received higher doses of inhaled corticosteroids (difference 119 mug per day, 95% CI 49 to 189, p=0.001) than controls. Adverse events did not differ between treatment groups (p>0.1 for all adverse events). INTERPRETATION: Conventional asthma management resulted in good control of symptoms in most participants. The addition of fraction of exhaled NO as an indicator of control of asthma resulted in higher doses of inhaled corticosteroids, without clinically important improvements in symptomatic asthma control.

Does neighborhood violence lead to depression among caregivers of children with asthma?

Prior studies have related community violence to depression among children, but few studies have examined this relationship among adults. We hypothesized that victimization, awareness, and fear of neighborhood violence would increase the odds of depression among adult caregivers of children with asthma. We surveyed caregivers in the Baltimore Indoor Environment Study of Asthma in Kids (BIESAK), USA. The primary outcome was screening positive for depression on the Center for Epidemiological Studies Depression index. We assessed victimization, awareness, and fear of neighborhood violence, and conducted spatial analysis identifying subject homes within 500 ft of a homicide to validate survey measures of neighborhood violence. A multilevel logistic model with clustering by neighborhood estimated odds ratios and 95% confidence intervals. Survey responses about fear of neighborhood violence were strongly predicted by having a home within 500 ft of a homicide. Of 150 caregivers of children with asthma, 49% were aware of a neighborhood violent event, 36% were fearful of neighborhood violence, 22% reported victimization, and 27% had a homicide within 500 ft of the home. In our multilevel model, fear of violence increased the odds of depression by 6.7. Victimization was associated with a possible trend towards depression, and awareness of neighborhood violence did not increase the odds of depression. Based on our findings, personal experience with neighborhood violence may be more important than simple awareness. Health care workers should consider screening for depression among patients exposed to community violence.

Common household activities are associated with elevated particulate matter concentrations in bedrooms of inner-city Baltimore pre-school children.

Asthma disproportionately affects inner-city, minority children in the U.S. Outdoor pollutant concentrations, including particulate matter (PM), are higher in inner-cities and contribute to childhood asthma morbidity. Although children spend the majority of time indoors, indoor PM exposures have been less extensively characterized. There is a public health imperative to characterize indoor sources of PM within this vulnerable population to enable effective intervention strategies. In the present study, we sought to identify determinants of indoor PM in homes of Baltimore inner-city pre-school children. Children ages 2-6 (n=300) who were predominantly African-American (90%) and from lower socioeconomic backgrounds were enrolled. Integrated PM(2.5) and PM(10) air sampling was conducted over a 3-day period in the children's bedrooms and at a central monitoring site while caregivers completed daily activity diaries. Homes of pre-school children in inner-city Baltimore had indoor PM concentrations that were twice as high as simultaneous outdoor concentrations. The mean indoor PM(2.5) and PM(10) concentrations were 39.5+/-34.5 and 56.2+/-44.8 microg/m(3), compared to the simultaneously measured ambient PM(2.5) and PM(10) (15.6+/-6.9 and 21.8+/-9.53 microg/m(3), respectively). Common modifiable household activities, especially smoking and sweeping, contributed significantly to higher indoor PM, as did ambient PM concentrations. Open windows were associated with significantly lower indoor PM. Further investigation of the health effects of indoor PM exposure is warranted, as are studies to evaluate the efficacy of PM reduction strategies on asthma health of inner-city children.

Rodent allergen in Los Angeles inner city homes of children with asthma.

Recent studies have examined the presence of mouse allergen in inner city children with asthma. Researchers have found high levels of rodent allergen in homes sampled in the northeast and midwest United States, but there has been considerable variation between cities, and there have been few studies conducted in western states. We evaluated the frequency of rodent sightings and detectable mouse allergen and the housing conditions associated with these outcomes in inner city homes in Los Angeles. Two hundred and two families of school children, ages 6-16 living in inner city neighborhoods, participated in the study. Families were predominantly Latino (94%), and Spanish speaking (92%). At study entry, parents completed a home assessment questionnaire, and staff conducted a home evaluation and collected kitchen dust, which was analyzed for the presence of mouse allergen. Fifty-one percent of homes had detectable allergen in kitchen dust. All 33 families who reported the presence of rodents had detectable allergen in the home and were also more likely to have increased levels of allergen compared to those who did not report rodents. Unwashed dishes or food crumbs, lack of a working vacuum, and a caretaker report of a smoker in the home were all significantly associated with a greater risk of rodent sightings or detectable allergen (P<0.05). Detached homes were significantly more likely to have detectable allergen. The prevalence of allergen is common enough that it may have public health implications for asthmatic children, and detectable allergen was not routinely identified based on rodent sightings. Many of the predictors of rodent allergen are amenable to low-cost interventions that can be integrated with other measures to reduce exposure to indoor allergens.

The environment and asthma in US inner cities.

Poor, minority children living in US inner cities have increased rates of asthma morbidity and mortality. Factors that contribute to these increased rates are varied and complex, with current evidence suggesting that the environment is an important causative factor. Respiratory morbidity is often the result of allergens and air pollutants. Additionally, for children living in urban environments, underlying societal susceptibility factors specific to the inner city serve to increase asthma morbidity. Even though ambient pollutants have been declining in US cities, asthma morbidity and mortality rates have been increasing. Indoor pollutants are closely linked to increased asthma prevalence and morbidity. While the understanding of environmental influences is still relatively limited, we can say that indoor exposures are more important than ambient pollutants, and we know that bioaerosols containing allergenic proteins are especially important. Additionally, certain particulate aerosols and ozone cause inflammation individually and may act synergistically to enhance the acute and chronic IgE-mediated inflammation. The purpose of this article is to review the data relating exposure to environmental pollutants and airborne allergens, and the relationship of this exposure to asthma prevalence and morbidity in order to inform plans for public health programs to reduce an asthma burden.

Does current asthma control predict future health care use among black preschool-aged inner-city children?

OBJECTIVES: Factors predictive of future asthma must be identified among young inner-city children, who suffer disproportionately from asthma. We investigated whether current asthma control predicts future asthma-related health care use among inner-city preschool-aged children with asthma. METHODS: A total of 150 inner-city preschool-aged children with asthma were followed prospectively for 6 months. At baseline, symptom frequency and reliever-medication use were assessed to classify children into National Asthma Education and Prevention Program-derived control categories. Long-term controller-medication use was also assessed, as well as asthma-related health care use at baseline and at 3 and 6 months. RESULTS: The mean age was 4.4 years, 92% were black, and 39% reported long-term controller use. At baseline, 37% were classified as having mild-intermittent, 17% had mild-persistent, 21% had moderate-persistent, and 25% had severe-persistent asthma control. Significant changes in asthma control were observed over time, including 46% of children originally categorized with mild-intermittent asthma who had worsened asthma control by 3 months. Asthma control significantly predicted future health care use 3 months later but not 6 months later. Multivariate analyses showed that, once control status was known, reported use of long-term controller medication added little additional predictive value. CONCLUSIONS: Among inner-city preschool-aged children, significant fluctuations in asthma control occur as early as 3 months after assessment. Poor control but not long-term controller-medication use is an independent predictor of future asthma-related health care use at 3 months but is not significantly predictive of 6-month outcomes. Therefore, clinicians caring for inner-city children with asthma should consider reassessing asthma control at least every 3 months to identify those at highest future risk and to provide early interventions.

Home indoor pollutant exposures among inner-city children with and without asthma.

BACKGROUND: Evidence for environmental causes of asthma is limited, especially among African Americans. To look for systematic differences in early life domestic exposures between inner-city preschool children with and without asthma, we performed a study of home indoor air pollutants and allergens. METHODS: Children 2-6 years of age were enrolled in a cohort study in East Baltimore, Maryland. From the child's bedroom, air was monitored for 3 days for particulate matter 0.05]. Settled dust allergen levels (cat, dust mite, cockroach, dog, and mouse) were also similar in bedrooms of asthmatic and control children. CONCLUSIONS: Exposures to common home indoor pollutants and allergens are similar for inner-city preschool children with and without asthma. Although these exposures may exacerbate existing asthma, this study does not support a causative role of these factors for risk of developing childhood asthma.