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Background The disrupted skin barrier in eczema has been associated with an increased risk of immunoglobulin E (IgE) sensitization in childhood. However, it is unclear whether eczema, independent of atopy, is a risk factor for the development of allergic sensitization in adulthood. Objective To determine if skin barrier dysfunction, independent of atopy, is a risk factor for incident sensitization in adult workers at a mouse production and research facility. Methods New employees at The Jackson Laboratory enrolled in a cohort study and underwent skin-prick testing (SPT) at baseline and every 6 months to mouse and to a panel of aeroallergens (net wheal ≥3 mm indicated a positive SPT result). Mouse allergen exposure was measured every 6 months by using personal air monitors. Physician-diagnosed eczema was defined as self-reported physician-diagnosed eczema. Cox proportional hazard modeling was used to examine the association between baseline physician-diagnosed eczema and incident mouse skin test sensitization and adjusted for potential confounders. Results The participants (N = 394) were followed up for a median of 24 months. Fifty-four percent were women, 89% were white, and 64% handled mice. At baseline, 7% of the participants reported physician-diagnosed eczema and 9% reported current asthma; 61% had at least one positive skin test result. At 30 months, 36% of those with eczema versus 14% of those without eczema had developed a positive mouse skin test result (p = 0.02, log-rank test). After adjusting for age, race, sex, smoking status (current, former, never), current asthma, hay fever, the number of positive SPT results at baseline, and mouse allergen exposure, physician-diagnosed eczema was an independent risk factor for incident mouse SPT sensitization (hazard ratio 5.6 [95% confidence interval, 2.1-15.2]; p = 0.001). Conclusion Among adult workers at a mouse production and research facility, physician-diagnosed eczema was a risk factor for incident mouse sensitization, independent of atopy, which indicated that a defect in skin barrier alone may increase the risk of skin sensitization, not just in childhood, but throughout life.

Background Whether concomitant home exposures modify the effectiveness of mouse allergen reduction among mouse-sensitized children with asthma is unknown. Objective To determine whether a lower baseline home mouse allergen level, lower particulate matter 10 μ or less (PM10), and the absence of sensitization and exposure to other indoor allergens are associated with greater improvements in asthma associated with mouse allergen reduction. Methods A secondary analysis of a randomized clinical trial of a home mouse allergen intervention was performed to examine the effect of 3 indoor factors on the relationship between mouse allergen reduction and a range of asthma outcomes. Results Participants (N = 297) were predominantly minority (78% African American, 22% Hispanic) and publicly insured (88%). Higher baseline mouse allergen levels were associated with a greater response to mouse allergen reduction for several symptom and exacerbation outcomes. Lower indoor PM10 levels were associated with a greater response to mouse allergen reduction for several symptom outcomes, but not exacerbation outcomes. Overall, sensitization and exposure to other indoor allergens did not appear to modify the effect of mouse allergen reduction. Conclusions In this population of predominantly low-income children with persistent asthma and mouse sensitization, mouse allergen reduction was associated with improvements in asthma, especially among those with high baseline mouse allergen exposure. Lower indoor PM10 was associated with greater improvements in asthma symptoms.

BACKGROUND: Current childhood asthma therapies have little effect on lung function trajectory. OBJECTIVE: To determine if mouse allergen exposure reduction is associated with lung function growth in mouse-sensitized/exposed asthmatic children. METHODS: 350 mouse-sensitized/exposed asthmatic children (5–17y) were enrolled in a 1-year randomized trial of integrated pest management+education versus education alone. Pre-/post-bronchodilator (BD) spirometry was performed at baseline, 6 and 12 months, and bedroom floor mouse allergen was measured every 3 months. Mouse allergen reduction was defined as ≥75% decrease in mouse allergen from baseline. Treatment groups were combined for analyses, as there were no differences in outcomes between groups. Changes in lung function over time were modeled, adjusting for age, gender, race, atopy, group, BD reversibility and including an interaction term (allergen reduction*time). RESULTS: The study population was predominantly black (79.4%) and low-income (66.3%

Background It is unknown whether caregiver perception of a child's asthma control, independent of guideline-based asthma control assessment, is a predictor of future acute visits. Objective To determine whether caregiver-reported asthma control is an indicator of future risk of acute visit. Methods Two study populations of low-income, minority 5- to 17-year-old children with persistent asthma were included. Questionnaires administered at baseline and at 3, 6, 9, and 12 months captured symptoms, short-acting β-agonist use, acute visits in the previous 3 months, and caregiver-reported asthma control. Well-controlled, not well-controlled, and very poorly controlled asthma were defined using National Asthma Education and Prevention Program guideline-based assessment. Relationships between caregiver-reported control and acute visits in the subsequent 3 months were examined. Results At baseline, both populations were predominantly black/African American (91% and 79%) with public insurance (85% and 88%) and very poorly controlled asthma (47% and 50%). In both populations, most caregivers reported that their child's asthma was well controlled (73% and 69%). In both populations, participants whose caregivers reported that their child had uncontrolled asthma had greater odds of having an acute visit in the following 3 months as compared with participants whose caregivers reported that their child's asthma was well controlled, independent of guideline-based control, age, sex, race, controller medication, insurance, and atopy (odds ratio [95% CI], 2.4 [1.4-4.2] and 1.6 [1.1-2.4]). Conclusions Among predominantly low-income minority children with asthma, caregiver-reported asthma control may provide information about the risk of future acute visit for asthma that is complementary to guideline-based control assessment.

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.

Chronic obstructive pulmonary disease (COPD) guidelines make no recommendations for allergy diagnosis or treatment.To determine whether an allergic phenotype contributes to respiratory symptoms and exacerbations in patients with COPD.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 = 1,381) defined as age40 years, history of smoking, FEV1/FVC0.70, and no diagnosis of asthma were identified. The presence of an allergic phenotype (n = 296) was defined as self-reported doctor diagnosed hay fever or allergic upper respiratory symptoms. In CODE, former smokers with COPD (n = 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.In NHANES III, multivariate analysis revealed that individuals with allergic phenotype were more likely to wheeze (odds ratio [OR], 2.1; P0.01), to have chronic cough (OR, 1.9; P = 0.01) and chronic phlegm (OR, 1.5; P0.05), and to have increased risk of COPD exacerbation requiring an acute doctor visit (OR, 1.7; P = 0.04). In the CODE cohort, multivariate analysis revealed that sensitized subjects reported more wheeze (OR, 5.91; P0.01), more nighttime awakening due to cough (OR, 4.20; P = 0.03), increased risk of COPD exacerbations requiring treatment with antibiotics (OR, 3.79; P = 0.02), and acute health visits (OR, 11.05; P0.01). An increasing number of sensitizations was associated with a higher risk for adverse health outcomes.Among individuals with COPD, evidence of an allergic phenotype is associated with increased respiratory symptoms and risk of COPD exacerbations.

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 3 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 tenfold 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 [Odds Ratio (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.

Epidemiologic studies have shown an association between mouse allergen exposure and asthma morbidity among urban populations, but confirmatory challenge studies in community populations have not been performed. This study was designed to examine the clinical relevance of mouse sensitization using a nasal challenge model. Forty-nine urban adults with asthma underwent skin-prick testing (SPT) and intradermal testing (IDT) with mouse epithelia extract. A positive SPT was defined as a net wheal size ≥3 mm and a positive IDT was defined as a net wheal size ≥6 mm using a 1:100 dilution of extract (1:10 w/v was obtained from Greer Laboratories (Lenoir, NC) as a single lot [Mus m 1 concentration = 2130 ng/mL]). Mouse-specific IgE (m-IgE) was measured by ImmunoCAP (Phadia, Uppsala, Sweden). Nasal challenge was performed with increasing concentrations of mouse epithelia extract and symptoms were assessed by visual analog scale. A positive challenge was defined as a 20-mm increase in the scale. The age range of the 49 participants was 18-50 years; 41% were men and 86% were black. Fourteen participants were SPT(+) to mouse, 15 participants were SPT(-) but (IDT(+)), and 20 participants were negative on both SPT(-) and IDT(-) (SPT(-)/IDT(-)). Sixty-four percent of the SPT(+) group, 40% of the IDT(+) group, and 20% of the SPT(-)/IDT(-) group had a positive nasal challenge. Sixty-seven percent (10/15) of those who were either SPT(+) or m-IgE(+) had a positive nasal challenge. SPT or the combination of SPT plus m-IgE performed best in diagnosing mouse allergy. The great majority of mouse-sensitized urban adults with asthma appear to have clinically relevant sensitization. Urban adults with asthma should be evaluated for mouse sensitization using SPT or SPT plus m-IgE testing.

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 PM2.5–10 (PM with aerodynamic diameter 2.5–10 μm) and PM2.5 (aerodynamic diameter < 2.5 μm) concentrations were 17.4 ± 21.0 and 40.3 ± 35.4 μg/m3. In adjusted models, 10-μg/m3 increases in indoor PM2.5–10 and PM2.5 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 μg/m3 in indoor and ambient PM2.5 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 PM2.5–10 and PM2.5 were associated with respiratory symptoms and rescue medication use. Increases in in-home and ambient PM2.5 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.

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.

Background The effect of indoor nitrogen dioxide concentrations on asthma morbidity among inner-city preschool children is uncertain. Objectives Our goal was to estimate the effect of indoor NO2 concentrations on asthma morbidity in an inner-city population while adjusting for other indoor pollutants. Methods We recruited 150 children (2–6 years of age) with physician-diagnosed asthma from inner-city Baltimore, Maryland. Indoor air was monitored over a 72-hr period in the children’s bedrooms at baseline and 3 and 6 months. At each visit, the child’s caregiver completed a questionnaire assessing asthma symptoms over the previous 2 weeks and recent health care utilization. Results Children were 58% male, 91% African American, and 42% from households with annual income < $25,000; 63% had persistent asthma symptoms. The mean (± SD) in-home NO2 concentration was 30.0 ± 33.7 (range, 2.9–394.0) ppb. The presence of a gas stove and the use of a space heater or oven/stove for heat were independently associated with higher NO2 concentrations. Each 20-ppb increase in NO2 exposure was associated significantly with an increase in the number of days with limited speech [incidence rate ratio (IRR) = 1.15; 95% confidence interval (CI), 1.05–1.25], cough (IRR = 1.10; 95% CI, 1.02–1.18), and nocturnal symptoms (IRR = 1.09; 95% CI, 1.02–1.16), after adjustment for potential confounders. NO2 concentrations were not associated with increased health care utilization. Conclusions Higher indoor NO2 concentrations were associated with increased asthma symptoms in preschool inner-city children. Interventions aimed at lowering NO2 concentrations in inner-city homes may reduce asthma morbidity in this vulnerable population.

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.

Innercity Black children are at high risk for asthma morbidity. Asthma specialists may improve asthma outcomes. Understanding specialist use among innercity Black children may provide insight into asthma care in this population. We hypothesized that increased asthma morbidity would be associated with increased use of and parental desire for specialist care. Participants were recruited from Baltimore City health plans. Parents of children (2–6 years of age) with asthma were surveyed about their child's asthma, including use of or desire for asthma specialist care. We compared asthma specialist care status (yes or no) and desire for specialist care to asthma morbidity and criteria for specialist referral based on national asthma guidelines. Of 135 children, 23% had severe asthma, but 9% had seen a specialist and 43% met criteria for asthma specialist referral. Forty percent of parents of children not seen by a specialist expressed a desire to see one. Compared to children of parents who did not desire a spe...

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.

Asthma is common among children in the United States, especially those who are racial/ethnic minorities living in inner cities (Centers for Disease Control and Prevention 2004). Although definitive causes of asthma remain to be discovered, substantial evidence points to environmental exposures, which may in turn interact with individual genetic susceptibility—a phenomenon often called gene–environment interaction. Some evidence points to the heritability of asthma, because it occurs more commonly in children whose parents have asthma and in affected twins (Laitinen et al. 1998). Because not all cases of asthma arise in people with affected first-degree relatives, however, it leaves open the possibility that asthma results from high exposure to environmental factors. Evidence to support asthma causation through high exposure alone can come from studies that compare the environment of people with and without asthma. Environmental studies of inner-city children are especially important for understanding asthma disparities among African Americans. Asthma prevalence is 39% higher among African Americans than whites, and African Americans are more likely than whites to live in urban areas (86% vs. 70% of the respective populations), areas which are at high risk for air pollution (American Lung Association 2005). Indeed, 65% of African Americans live in counties that failed to meet at least one of the U.S. Environmental Protection Agency’s (EPA) outdoor air quality standards (American Lung Association 2005). The home indoor environment is especially relevant for studying inner-city childhood asthma, because some pollutants, such as ambient particulate matter (PM), penetrate from the outside, and some are generated and remain indoors, such as particles and gases from smoking, heating, cooking, and cleaning (Abt et al. 2000; Howard-Reed et al. 2000; Long et al. 2000; National Research Council and Committee on Research Priorities for Airborne Particulate Matter 2004; Rea et al. 2001; Vette et al. 2001). Remarkably, a previously published study from the Center for Childhood Asthma in the Urban Environment, conducted in older children from inner-city Baltimore (90% African American), has already shown that children are exposed to concentrations of indoor PM that are three times the concentrations found in outdoor air (Breysse et al. 2005). Such concentrations would frequently exceed the outdoor limits set by the U.S. EPA (Breysse et al. 2005). Furthermore, the indoor environment may be especially critical to study because Americans, including preschool children, spend the vast majority of time indoors. Studies are urgently needed to determine the causes of the asthma epidemic, and in response to this need, there has been support for research from the U.S. federal government to uncover the role of environmental exposures in the etiology and prevention of prevalent disorders, such as asthma, in children (National Institute of Environmental Health Sciences 2003). To address this issue, the Johns Hopkins Center for Childhood Asthma in the Urban Environment conducted a study to determine whether indoor home environmental pollutants are greater in homes of preschool children with asthma compared with homes of children without asthma.

We conducted this study to compare environmental exposures in suburban homes of children with asthma to exposures in inner city homes of children with asthma, to better understand important differences of indoor pollutant exposure that might contribute to increased asthma morbidity in the inner city. Indoor PM(10), PM(2.5), NO(2), O(3), and airborne and dust allergen levels were measured in the homes of 120 children with asthma, 100 living in inner city Baltimore and 20 living in the surrounding counties. Home conditions and health outcome measures were also compared. The inner city and suburban homes differed in ways that might affect airborne environmental exposures. The inner city homes had more cigarette smoking (67% vs. 5%, p.001), signs of disrepair (77% vs. 5%, p.001), and cockroach (64% vs. 0%, p.001) and mouse (80% vs. 5%, p.001) infestation. The inner city homes had higher geometric mean (GM) levels (p.001) of PM(10) (47 vs. 18 microg/m(3)), PM(2.5) (34 vs. 8.7 microg/m(3)), NO(2) [19 ppb vs. below detection (BD)], and O(3) (1.9 vs. .015 ppb) than suburban homes. The inner city homes had lower GM bedroom dust allergen levels of dust mite (.29 vs. 1.2 microg/g, p = .022), dog (.38 vs. 5.5 microg/g, p.001) and cat (.75 vs. 2.4 microg/g, p = .039), but higher levels of mouse (3.2 vs. .013 microg/g, p.001) and cockroach (4.5 vs. .42 U/g, p.001). The inner city homes also had higher GM airborne mouse allergen levels (.055 vs. .016 ng/m(3), p = .002). Compared with the homes of suburban children with asthma, the homes of inner city Baltimore children with asthma had higher levels of airborne pollutants and home characteristics that predispose to greater asthma morbidity.

Polycyclic aromatic hydrocarbons (PAHs), the by-products of incomplete combustion of organic materials, are commonly found on particulate matter (PM) and have been associated with the development of asthma and asthma exacerbation in urban populations. We examined time spent in the home and outdoors as predictors of exposures to airborne PAHs and measured urinary 1-hydroxypyrene-glucuronide (1-OHPG) as internal dose of PAHs in 118 children aged 5–12 years from Baltimore, MD. During weeklong periods (Saturday–Saturday) in each of four seasons: daily activities were assessed using questionnaires, indoor air nicotine and PM concentrations were monitored, and urine specimens were collected on Tuesday (day 3) and Saturday (day 7) for measurement of 1-OHPG. Time spent in non-smoking homes was associated with significantly decreased 1-OHPG concentration in urine (β = −0.045, 95% CI (−0.076, −0.013)), and secondhand smoke (SHS) exposures modified these associations, with higher urinary 1-OHPG concentrations in children spending time in smoking homes than non-smoking homes (P-value for interaction = 0.012). Time spent outdoors was associated with increased urinary 1-OHPG concentrations (β=0.097, 95% CI (0.037, 0.157)) in boys only. Our results suggest that SHS and ambient (outdoor) air pollution contribute to internal dose of PAHs in inner city children.

Current guidelines recommend environmental control practices (ECPs) as part of asthma management. We investigated the relationship of caregiver health beliefs and asthma experiences to ECP use in homes of children with asthma. Caregivers of children with asthma (ages 2 to 6 years) completed a survey about indoor environmental exposures, ECPs, physician ECP recommendations, caregiver health beliefs and experiences (outcome expectancy, self-efficacy, emotional bother) regarding ECPs, child's respiratory symptoms, and medication use. Allergic sensitization was determined by skin prick testing. Children (n = 150) were 58% male, 91% African American, 42% from households with annual income

Background Room characteristics predicting indoor allergen exposure in suburban homes have not been clearly identified. Objective To examine relationships between room characteristics and concentrations of indoor allergens in homes of suburban asthmatic patients. Methods The homes of 339 asthmatic children ages 6 to 17 years were studied. Home inspections were conducted by a trained technician, and dust samples were analyzed for indoor allergen content. A high allergen concentration was defined as 8 μg (U)/g or more of fine dust. Results Infrequent sheet washing and wall-to-wall carpet were risk factors for high bedroom dust mite concentrations. Infrequent sheet washing was also a risk factor for high Fel d 1 concentrations. Food remains in the bedroom was a risk factor for high bedroom Bla g 1 levels, and exposed food, leaks, and dirty pots were all risk factors for high kitchen Bla g 1 levels. The combination of lack of mattress or pillow encasements, infrequent sheet washing, and carpeting was associated with a 24-fold increase in odds of a high dust mite concentration (odds ratio [OR], 24.1; 95% confidence interval [CI], 3.2-181.4). Among non-cat owners, the combination of stuffed toys on the bed, lack of mattress or pillow encasements, and infrequent sheet washing was associated with a 49-fold increase in odds of a high Fel d 1 level (OR, 49.4; 95% CI, 2.8-887.3). The combination of leaks, exposed food, and dirty pots was associated with a high kitchen Bla g 1 concentration (OR, 10.6; 95% CI, 2.8-40.5). Conclusions Specific room characteristics predict high indoor allergen exposure among children with asthma, and a combination of these characteristics may further increase the risk of high allergen exposure.

Background Asthma guidelines recommend environmental control practices (ECPs) to improve asthma health. In the inner city, where asthma morbidity is high, it is not known whether children's health status affects the use of ECPs. Objective To investigate health status determinants of ECPs in the homes of children with asthma. Methods Caregivers of children aged 2 to 6 years with (n = 150) and without (n = 150) asthma completed a survey about ECPs. Atopic status was determined by means of skin prick testing. Results Most ECPs were similarly practiced, regardless of whether the child had asthma. Only pet avoidance was more common in children with asthma (30% vs 19%). Asthma severity and recent acute health care visits for asthma were not associated with ECP use. Most ECPs were not linked to allergen sensitization (eg, mite and mouse), although cockroach-sensitized children were more likely to have cockroach control than nonsensitized individuals (65% vs 45%). Caregivers of asthmatic children with rhinitis were more likely than those without rhinitis to report ECPs, including pet avoidance (44% vs 15%), smoking avoidance (78% vs 53%), cockroach control (65% vs 42%), mouse control (78% vs 42%), air-conditioning (45% vs 24%), and allergyproof covers (7% vs 0%). Conclusions The presence of asthma, asthma severity, and allergen sensitization seem to have little relationship to ECP use in the homes of inner-city children. Rhinitis was consistently linked to ECPs, which suggests that caregivers may make changes in the home environment for upper airway but not lower airway symptoms.

Airborne pollutants and indoor allergens increase asthma morbidity in inner-city children; therefore, reducing exposure, if feasible, should improve asthma morbidity.To conduct a randomized controlled trial of methods to reduce environmental pollutant and allergen exposure in the homes of asthmatic children living in the inner city.After the completion of questionnaires, spirometry and allergen skin tests, home inspection, and measurement of home air pollutant and allergen levels, 100 asthmatic children aged 6 to 12 years were randomized to the treatment group (home-based education, cockroach and rodent extermination, mattress and pillow encasings, and high-efficiency particulate air cleaner) or to the control group (treated at the end of the 1-year trial). Outcomes were evaluated by home evaluations at 6 and 12 months, clinic evaluation at 12 months, and multiple telephone interviews.In the treatment group, 84% received cockroach extermination and 75% used the air cleaner. Levels of particulate matter 10 microm or smaller declined by up to 39% in the treatment group but increased in the control group (P.001). Cockroach allergen levels decreased by 51% in the treatment group. Daytime symptoms increased in the control group and decreased in the treatment group (P = .04). Other measures of morbidity, such as spirometry findings, nighttime symptoms, and emergency department use, were not significantly changed.A tailored, multifaceted environmental treatment reduced airborne particulate matter and indoor allergen levels in inner-city homes, which, in turn, had a modest effect on morbidity.

This paper presents indoor air pollutant concentrations and allergen levels collected from the homes of 100 Baltimore city asthmatic children participating in an asthma intervention trial. Particulate matter (PM), NO2, and O3 samples were collected over 72 h in the child's sleeping room. Time-resolved PM was also assessed using a portable direct-reading nephelometer. Dust allergen samples were collected from the child's bedroom, the family room, and the kitchen. The mean PM10 concentration, 56.5+/-40.7 microg/m3, is 25% higher than the PM2.5 concentration (N=90), 45.1+/-37.5 microg/m3. PM concentrations measured using a nephelometer are consistent and highly correlated with gravimetric estimates. Smoking households' average PM2.5 and PM10 concentrations are 33-54 microg/m3 greater than those of nonsmoking houses, with each cigarette smoked adding 1.0 microm/m3 to indoor PM2.5 and PM10 concentrations. Large percentages of NO2 and O3 samples, 25% and 75%, respectively, were below the limit of detection. The mean NO2 indoor concentration is 31.6+/-40.2 ppb, while the mean indoor O3 concentration in the ozone season was 3.3+/-7.7 ppb. The levels of allergens are similar to those found in other inner cities. Results presented in this paper indicate that asthmatic children in Baltimore are exposed to elevated allergens and indoor air pollutants. Understanding this combined insult may help to explain the differential asthma burden between inner-city and non-inner-city children.

Nitrogen dioxide (NO2 ), a by-product of combustion produced by indoor gas appliances such as cooking stoves, is associated with respiratory symptoms in those with obstructive airways disease. We conducted a three-armed randomized trial to evaluate the efficacy of interventions aimed at reducing indoor NO2 concentrations in homes with unvented gas stoves: (i) replacement of existing gas stove with electric stove; (ii) installation of ventilation hood over existing gas stove; and (iii) placement of air purifiers with high-efficiency particulate air (HEPA) and carbon filters. Home inspection and NO2 monitoring were conducted at 1 week pre-intervention and at 1 week and 3 months post-intervention. Stove replacement resulted in a 51% and 42% decrease in median NO2 concentration at 3 months of follow-up in the kitchen and bedroom, respectively (P = 0.01, P = 0.01); air purifier placement resulted in an immediate decrease in median NO2 concentration in the kitchen (27%, P0.01) and bedroom (22%, P = 0.02), but at 3 months, a significant reduction was seen only in the kitchen (20%, P = 0.05). NO2 concentrations in the kitchen and bedroom did not significantly change following ventilation hood installation. Replacing unvented gas stoves with electric stoves or placement of air purifiers with HEPA and carbon filters can decrease indoor NO2 concentrations in urban homes.Several combustion sources unique to the residential indoor environment, including gas stoves, produce nitrogen dioxide (NO2), and higher NO2 concentrations, are associated with worse respiratory morbidity in people with obstructive lung disease. A handful of studies have modified the indoor environment by replacing unvented gas heaters; this study, to our knowledge, is the first randomized study to target unvented gas stoves. The results of this study show that simple home interventions, including replacement of an unvented gas stove with an electric stove or placement of HEPA air purifiers with carbon filters, can significantly decrease indoor NO2 concentrations.

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 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.

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.

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 IgG 4 . The incidence of a positive SPT response increased as levels of exposure increased from low to moderate, peaking at 1.2 ng/m 3 , 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 IgG 4 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 IgG 4 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 IgG 4 .

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.

Few studies have assessed in home factors which contribute to airborne endotoxin concentrations. In 85 inner city Baltimore homes, we found no significant correlation between settled dust and airborne endotoxin concentrations. Certain household activities and characteristics, including frequency of dusting, air conditioner use and type of flooring, explained 36-42% of the variability of airborne concentrations. Measurements of both airborne and settled dust endotoxin concentrations may be needed to fully characterize domestic exposure in epidemiologic investigations.

Background Compared with atopic asthma, fewer environmental modifications are recommended for non-atopic asthma in children. Objective To better understand the role of indoor pollutants in provoking non-atopic asthma, we investigated the effect of in-home particulate matter on asthma symptoms among non-atopic and atopic children living in inner-city Baltimore. Methods A cohort of 150 children ages 2 to 6 years with asthma underwent home environmental monitoring for 3-day intervals at baseline, 3, and 6 months. Children were classified as non-atopic if they were skin test negative to a panel of 14 aeroallergens. Caregivers completed questionnaires assessing symptoms and rescue medication use. Longitudinal data analysis included regression models with generalized estimating equations. Results Children were primarily African American from lower socioeconomic backgrounds and spent most of their time in the home. Thirty-one percent were non-atopic, and 69% were atopic. Among non-atopic and atopic children, increased in-home fine (PM2.5) and coarse (PM2.5–10) particle concentrations were associated with significant increases in asthma symptoms and rescue medication use ranging from 7% (95% confidence interval [CI], 0–15) to 14% (95% CI, 1–27) per 10 μg/m 3 increase in particle concentration after adjustment for confounders. Conclusions In-home particles similarly cause increased symptoms of asthma in non-atopic and atopic children. Environmental control strategies that reduce particle concentrations may prove to be an effective means of improving asthma outcomes, especially for non-atopic asthma, for which there are few environmental control practice recommendations.

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.To determine if parent-reported pest and pet exposures can identify patients with clinically relevant allergen exposure.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.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%).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.

Summary Background High levels of allergen-specific IgG have been associated with clinical efficacy in immunotherapy studies, but whether this antibody isotype is associated with clinical tolerance in the setting of environmental exposure remains unclear. Objective To determine if mouse allergen-specific IgG (mIgG) and IgG4 (mIgG4) levels are associated with mouse-related symptoms among IgE-sensitized laboratory workers. Methods Fifty-eight workers with either skin test or serologic evidence of IgE-mediated mouse sensitization were studied. Symptom data were obtained by a questionnaire. Serum levels of mouse-specific IgG, IgG4, and IgE were quantified by a solid-phase antigen-binding assay (IgG) and RAST (IgG4 and IgE), and the relationships between mouse-specific serologic responses and mouse-related symptoms were analysed. Results Twenty-three (39.7%) participants reported mouse-related symptoms. Mouse-specific IgG and IgG4 levels were not associated with mouse-related symptoms among the study population as a whole. Among the 29 (50%) participants with detectable mouse-specific IgE (mIgE), higher mouse-specific IgG and IgG4 levels were associated with a decreased risk of symptoms, after adjusting for mIgE level (odds ratio (OR) 0.3, 95% confidence interval (CI): 0.1–1.4, and OR 0.3, 95% CI: 0.04–2.6, respectively). Higher levels of mIgG and mIgG4 remained associated with a decreased risk of symptoms after additional adjustment for sex and handling of mice (OR 0.1, 95% CI: 0.02–0.7, and OR 0.2, 95% CI: 0.02–2.1, respectively). Higher mIgG : IgE and mIgG4 : IgE ratios were also associated with a decreased risk of symptoms after adjusting for these confounders (OR 0.1, 95% CI: 0.02–0.7, and OR 0.2, 95% CI: 0.02–0.92, respectively). Conclusion Among workers with detectable mIgE, higher mIgG and mIgG4 levels are associated with a decreased risk of mouse-related symptoms. High serum levels of mIgG or mIgG4 may be markers for clinical tolerance among laboratory mouse workers with detectable mIgE, but these findings need to be confirmed in larger, prospective studies.

Background: Exposure to cockroach allergen is prevalent in inner-city homes and is associated with an increased risk of cockroach sensitization. Objective: We sought to determine the prevalence of cockroach allergen exposure in suburban middle-class homes and to study its relationship to cockroach sensitization. Methods: Children with asthma, 6 to 17 years of age, were recruited from 3 pediatric practices located in counties surrounding Baltimore city and from 1 practice located within Baltimore city limits. Participants underwent skin prick testing and completed baseline questionnaires. In addition, their homes were inspected, and settled dust samples were collected for allergen analysis. Results: Forty-one percent of the total study population (n = 339) had kitchen Bla g 1 levels of greater than 1 U/g. Fortynine percent were white, 53% had annual incomes of greater than $50,000, and 48% of mothers had college degrees. Seventy-seven percent of the study population resided in a suburban or rural location, and 30% of kitchens in these homes had Bla g 1 levels of greater than 1 U/g. Among the suburban-rural subgroup, 21% were sensitized to cockroach compared with 35% of the city group. In multivariate analysis, exposure to kitchen Bla g 1 levels of greater than 1 U/g was associated with cockroach sensitization for both the total study population (odds ratio, 2.29; 95% CI, 1.28-4.11) and the suburban-rural subgroup (odds ratio, 2.37; 95% CI, 1.23-4.57). Conclusions: Cockroach allergen exposure might be more common in suburban middle-class homes of asthmatic children than previously thought. Moreover, the data suggest that low-level cockroach exposure is a risk factor for cockroach sensitization. (J Allergy Clin Immunol 2003;112:87-92.)

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 FEV 1 /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.