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Rationale: Indoor particulate matter is associated with worse chronic obstructive pulmonary disease (COPD) outcomes. It remains unknown whether reductions of indoor pollutants improve respiratory morbidity. Objectives: To determine whether placement of active portable high-efficiency particulate air cleaners can improve respiratory morbidity in former smokers. Methods: Eligible former smokers with moderate-to-severe COPD received active or sham portable high-efficiency particulate absolute air cleaners and were followed for 6 months in this blinded randomized controlled trial. The primary outcome was 6-month change in St. George's Respiratory Questionnaire (SGRQ). Secondary outcomes were exacerbation risk, respiratory symptoms, rescue medication use, and 6-minute-walk distance (6MWD). Intention-to-treat analysis included all subjects, and per-protocol analysis included adherent participants (greater than 80% use of air cleaner). Measurements and Main Results: A total of 116 participants were randomized, of which 84.5% completed the study. There was no statistically significant difference in total SGRQ score, but the active filter group had greater reduction in SGRQ symptom subscale (β, -7.7 [95% confidence interval (CI), -15.0 to -0.37]) and respiratory symptoms (Breathlessness, Cough, and Sputum Scale, β, -0.8 [95% CI, -1.5 to -0.1]); and lower rate of moderate exacerbations (incidence rate ratio, 0.32 [95% CI, 0.12-0.91]) and rescue medication use (incidence rate ratio, 0.54 [95% CI, 0.33-0.86]) compared with sham group (all P  < 0.05). In per-protocol analysis, there was a statistically significant difference in primary outcome between the active filter versus sham group (SGRQ, β -4.76 [95% CI, -9.2 to -0.34]) and in moderate exacerbation risk, Breathlessness, Cough, and Sputum Scale, and 6MWD. Participants spending more time indoors were more likely to have treatment benefit. Conclusions: This is the first environmental intervention study conducted among former smokers with COPD showing potential health benefits of portable high-efficiency particulate absolute air cleaners, particularly among those with greater adherence and spending a greater time indoors.

Background: Indoor fine particulate air pollution (PM 2.5 ) is linked to asthma morbidity; however, whether vitamin D status influences individual susceptibility to airborne exposures is unclear., Objective: We aimed to determine if vitamin D modifies the effects of indoor PM 2.5 on asthma symptoms in urban children., Methods: A total of 120 children aged 5 to 12 years with physician-diagnosed asthma were evaluated at baseline and every 3 months for 9 months. Indoor PM 2.5 , serum 25-hydroxy vitamin D (25-OH D) levels, and asthma symptoms were simultaneously assessed at each time point. Adjusting for confounders, generalized estimating equations assessed the 3-way interaction effects of 25-OH D, obesity, and PM on asthma symptoms., Results: Children were of mean (standard deviation [SD]) age 9.7 (2.2) years, 36% were obese, and 95% self-reported black race. Mean (SD) PM 2.5 indoor exposure was 38.2 (42.9) μg/m 3 and 25-OH D was 19.1 (7.5) ng/mL. Three-way interaction models demonstrated significantly greater PM 2.5 -associated effects on daytime asthma symptoms only among obese children with low 25-OH D levels (odds ratio [OR] PM2.5  = 1.26, P = .049 at vitamin D = 15.5 ng/mL, increasingly stronger PM effects at levels <15.5 ng/mL). In homes with increased PM 2.5 , higher 25-OH D was associated with decreased symptom odds (eg, OR Vitamin D  = 0.87; P = .049 at PM 2.5  = 52.5 μg/m 3 , increasingly protective effects >52.5 μg/m 3 ) among obese children., Conclusions: Among obese urban children with asthma, low individual 25-OH D enhanced adverse respiratory effects associated with indoor PM 2.5 . In high PM 2.5 environments, 25-OH D was protective against asthma symptoms. Optimizing vitamin D status in children may help reduce asthma morbidity driven by indoor air pollution., (Copyright © 2019 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.)

Objectives: Secondhand smoke (SHS) and other air pollutants adversely affect the health of pregnant women and infants. A feasibility study aimed at reducing air pollution in homes of pregnant women or infants living with a smoker was completed., Methods: In collaboration with the Baltimore City Health Department, women ≥ 18 years of age and either pregnant nonsmokers, or post-partum (any smoking status) with an infant age 0-12 months were recruited. Homes had at least one smoker. Intervention included two air purifiers and secondhand smoke education. Outcomes included feasibility, change in fine particulate matter (PM 2.5 ), air nicotine, and salivary cotinine pre- and post-intervention., Results: Fifty women were enrolled (mean age 27 years, 92% African American, 71% single, 94% Medicaid eligible, 34% reported smoking) and 86% completed the study. Of the 50 women, 32 had infants and 18 were pregnant at time of enrollment. Post- intervention, 70% of participants reported smokers were less likely to smoke indoors, and 77% had at least one air purifier turned on at the final visit. Participant satisfaction was high (91%) and 98% would recommend air purifiers. Indoor PM 2.5 was significantly decreased (P < 0.001). Salivary cotinine was significantly decreased for non-smoking women (P < 0.01) but not infants, and no significant change in air nicotine occurred (P = 0.6)., Conclusions: Air purifiers with SHS education is a feasible intervention in homes of women and infants. These data demonstrate reduction in indoor PM 2.5 and salivary cotinine in non-smoking adults. Air purifiers are not an alternative for smoking cessation and a home/ car smoking ban. Smoking cessation should be strongly encouraged for all pregnant women, and nonsmoking mothers with infants should be counseled to completely avoid SHS exposure. This study provides support for a future intervention evaluating clinical endpoints., (Copyright © 2017. Published by Elsevier Inc.)

Exposure to nitrogen dioxide (NO 2 ), a byproduct of combustion, is associated with poor asthma control in children. We sought to determine whether gas-fueled kitchen appliance use is associated with 24-h indoor NO 2 concentrations and whether these concentrations are associated with asthma morbidity in children. Children aged 5-12 years old with asthma were eligible. Mean 24-h NO 2 concentration was measured in the kitchen over a four-day sampling period and gas stove use was captured in time activity diaries. The relationship between stove and oven use and daily NO 2 concentration was analyzed. Longitudinal analysis assessed the effect of daily NO 2 exposure on symptoms, inhaler use, and lung function. Multivariate models were adjusted for age, sex, season, and maternal education. Thirty children contributed 126 participant days of sampling. Mean indoor 24-h NO 2 concentration was 58(48)ppb with a median (range) of 45(12-276)ppb. All homes had gas stoves and furnaces. Each hour of kitchen appliance use was associated with an 18ppb increase in 24-h NO 2 concentration. In longitudinal multivariate analysis, each ten-fold increase in previous-day NO 2 was associated with increased nighttime inhaler use (OR = 4.9, p = 0.04). There were no associations between NO 2 and lung function or asthma symptoms. Higher previous-day 24-h concentration of NO 2 is associated with increased nighttime inhaler use in children with asthma., (Copyright © 2017 Elsevier Inc. All rights reserved.)

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.

Airborne contaminants produced by industrial agricultural facilities contain chemical and biological compounds that can impact the health of residents living in close proximity. Settled dust can be a reservoir for these contaminants and can influence long-term exposures. In this study, we sampled the indoor- and outdoor-settled dust from 40 homes that varied in proximity to industrial-scale dairies (ISD; industrial-scale dairy, a term used in this paper to describe a large dairy farm and adjacent waste sprayfields, concentrated animal feeding operation or animal feeding operation, that uses industrial processes) in the Yakima Valley, Washington. We analyzed settled dust samples for cow allergen (Bos d2, a cow allergen associated with dander, hair, sweat and urine, it is a member of the lipocalin family of allergens associated with mammals), mouse allergen (Mus m1; major mouse allergen, a mouse urinary allergen, in the lipocalin family), dust mite allergens (Der p1 (Dermatophagoides pteronissinus 1) and Der f1 (Dermatophagoides farinae 1)), and endotoxin (a component of the cell walls of gram negative bacteria, lipopolysaccharide, which can be found in air and dust and can produce a strong inflammatory response). A concentration gradient was observed for Bos d2 and endotoxin measured in outdoor-settled dust samples based on proximity to ISD. Indoor-settled dust concentrations of Bos d2 and endotoxin were also highest in proximal homes. While the associated health effects of exposure to cow allergen in settled dust is unknown, endotoxin at concentrations observed in these proximal homes (100 EU/mg) has been associated with increased negative respiratory health effects. These findings document that biological contaminants emitted from ISDs are elevated in indoor- and outdoor-settled dust samples at homes close to these facilities and extend to as much as three miles (4.8 km) away.

Our goal was to investigate whether obesity increases susceptibility to the adverse effects of indoor particulate matter on respiratory morbidity among individuals with chronic obstructive pulmonary disease (COPD). Participants with COPD were studied at baseline, 3 and 6 months. Obesity was defined as a body mass index ≥30 kg·m(-2). At each time point, indoor air was sampled for 5-7 days and particulate matter (PM) with an aerodynamic size ≤2.5 μm (PM2.5) and 2.5-10 μm (PM2.5-10) was measured. Respiratory symptoms, health status, rescue medication use, exacerbations, blood biomarkers and exhaled nitric oxide were assessed simultaneously. Of the 84 participants enrolled, 56% were obese and all were former smokers with moderate-to-severe COPD. Obese participants tended to have less severe disease as assessed by Global Initiative for Chronic Obstructive Pulmonary Disease stage and fewer pack-years of smoking. There was evidence that obesity modified the effects of indoor PM on COPD respiratory outcomes. Increases in PM2.5 and PM2.5-10 were associated with greater increases in nocturnal symptoms, dyspnoea and rescue medication use among obese versus non-obese participants. The impact of indoor PM on exacerbations, respiratory status and wheeze also tended to be greater among obese versus non-obese participants, as were differences in airway and systemic inflammatory responses to indoor PM. We found evidence that obesity was associated with exaggerated responses to indoor fine and coarse PM exposure among individuals with COPD., (Copyright ©ERS 2015.)

Previous research has found evidence of an association between indoor air pollution and asthma morbidity in children. Environmental intervention studies have been performed to examine the role of household environmental interventions in altering indoor air pollution concentrations and improving health. Previous environmental intervention studies have found only modest effects on health outcomes and it is unclear if the health benefits provided by environmental modification are comparable with those provided by medication. Traditionally, the statistical analysis of environmental intervention studies has involved performing two intention-to-treat analyses that separately estimate the effect of the environmental intervention on health and the effect of the environmental intervention on indoor air pollution concentrations. We propose a principal stratification approach to examine the extent to which an environmental intervention's effect on health outcomes coincides with its effect on indoor air pollution. We apply this approach to data from a randomized air cleaner intervention trial conducted in a population of asthmatic children living in Baltimore, Maryland, USA. We find that among children for whom the air cleaner reduced indoor particulate matter concentrations, the intervention resulted in a meaningful improvement of asthma symptoms with an effect generally larger than previous studies have shown. A key benefit of using principal stratification in environmental intervention studies is that it allows investigators to estimate causal effects of the intervention for sub-groups defined by changes in the indoor air pollution concentration., (Copyright © 2014 John Wiley & Sons, Ltd.)

Background: Indoor particulate matter (PM) has been linked to respiratory symptoms in former smokers with COPD. While subjects with COPD and atopy have also been shown to have more frequent respiratory symptoms, whether they exhibit increased susceptibility to PM as compared to their non-atopic counterparts remains unclear. The aim of this study was to determine whether atopic individuals with COPD have greater susceptibility to PM compared to non-atopic individuals with COPD., Methods: Former smokers with moderate to severe COPD were enrolled (n = 77). PM2.5, PM with diameter <2.5 micrometers, was measured in the main living area over three one-week monitoring periods at baseline, 3, and 6 months. Quality of life, respiratory symptoms and medication use were assessed by questionnaires. Serum was analyzed for specific IgE for mouse, cockroach, cat, dog and dust mite allergens. Atopy was established if at least one test was positive. Interaction terms between PM and atopy were tested and generalized estimating equation analysis determined the effect of PM concentrations on health outcomes. Multivariate models were adjusted for age, sex, education, race, season, and baseline lung function and stratified by atopic status., Results: Among atopic individuals, each 10 μg/m(3) increase in PM was associated with higher risk of nocturnal symptoms (OR, 1.95; P = 0.02), frequent wheezing (OR, 2.49; P = 0.02), increased rescue medication use (β = 0.14; P = 0.02), dyspnea (β = 0.23; P < 0.001), higher St. George's Respiratory Quality of Life score (β = 2.55; P = 0.01), and higher breathlessness, cough, and sputum score (BCSS) (β = 0.44; P = 0.01). There was no association between PM and health outcomes among the non-atopic individuals. Interaction terms between PM2.5 and atopy were statistically significant for nocturnal symptoms, frequency of rescue medication use, and BCSS (all P < 0.1)., Conclusions: Individuals with COPD and atopy appear to be at higher risk of adverse respiratory health effects of PM exposure compared to non-atopic individuals with COPD.

Unlabelled: 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%, P < 0.01) 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., Practical Implications: 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., (© 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

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.

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.

Background: Community exposures to environmental contaminants from industrial scale dairy operations are poorly understood. The purpose of this study was to evaluate the impact of dairy operations on nearby communities by assessing airborne contaminants (particulate matter, ammonia, and cow allergen, Bos d 2) associated with dairy operations inside and outside homes., Methods: The study was conducted in 40 homes in the Yakima Valley, Washington State where over 61 dairies operate., Results: A concentration gradient was observed showing that airborne contaminants are significantly greater at homes within one-quarter mile (0.4 km) of dairy facilities, outdoor Bos d 2, ammonia, and TD were 60, eight, and two times higher as compared to homes greater than three miles (4.8 km) away. In addition median indoor airborne Bos d 2 and ammonia concentrations were approximately 10 and two times higher in homes within one-quarter mile (0.4 km) compared to homes greater than three miles (4.8 km) away., Conclusions: These findings demonstrate that dairy operations increase community exposures to agents with known human health effects. This study also provides evidence that airborne biological contaminants (i.e. cow allergen) associated with airborne particulate matter are statistically elevated at distances up to three miles (4.8 km) from dairy operations.

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., (Copyright © 2011 Elsevier Inc. All rights reserved.)

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: 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., (Copyright © 2011. Published by Elsevier Inc.)

The purpose of this article is to review indoor air pollution factors that can modify asthma severity, particularly in inner-city environments. While there is a large literature linking ambient air pollution and asthma morbidity, less is known about the impact of indoor air pollution on asthma. Concentrating on the indoor environments is particularly important for children, since they can spend as much as 90% of their time indoors. This review focuses on studies conducted by the Johns Hopkins Center for Childhood Asthma in the Urban Environment as well as other relevant epidemiologic studies. Analysis of exposure outcome relationships in the published literature demonstrates the importance of evaluating indoor home environmental air pollution sources as risk factors for asthma morbidity. Important indoor air pollution determinants of asthma morbidity in urban environments include particulate matter (particularly the coarse fraction), nitrogen dioxide, and airborne mouse allergen exposure. Avoidance of harmful environmental exposures is a key component of national and international guideline recommendations for management of asthma. This literature suggests that modifying the indoor environment to reduce particulate matter, NO(2), and mouse allergen may be an important asthma management strategy. More research documenting effectiveness of interventions to reduce those exposures and improve asthma outcomes is needed.

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.

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.

An analytical method of measuring nicotine in house dust was optimized and associations among three secondhand smoking exposure markers were evaluated, i.e., nicotine concentrations of both house dust and indoor air, and the self-reported number of cigarettes smoked daily in a household. We obtained seven house dust samples from self-reported nonsmoking homes and 30 samples from smoking homes along with the information on indoor air nicotine concentrations and the number of cigarettes smoked daily from an asthma cohort study conducted by the Johns Hopkins Center for Childhood Asthma in the Urban Environment. House dust nicotine was analyzed by isotope dilution gas chromatography-mass spectrometry (GC/MS). Using our optimized method, the median concentration of nicotine in the dust of self-reported nonsmoking homes was 11.7 ng/mg while that of smoking homes was 43.4 ng/mg. We found a substantially positive association (r=0.67, P<0.0001) between house dust nicotine concentrations and the numbers of cigarettes smoked daily. Optimized analytical methods showed a feasibility to detect nicotine in house dust. Our results indicated that the measurement of nicotine in house dust can be used potentially as a marker of longer term SHS exposure.

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.

Inner-city residents continue to suffer disproportionate asthma morbidity despite recent progress in reducing asthma morbidity and mortality in other strata of the United States population. Studies over the past decade indicate that the indoor environment is a strong contributor to poor asthma control and asthma-related health care use in inner-city populations. Certain indoor exposures are more common and occur in higher concentrations in inner-city communities than in suburban communities. Identification of "asthmagenic" indoor exposures has paved the way for the development of intervention strategies aimed at reducing asthma morbidity. This article reviews the growing body of evidence that certain indoor environmental exposures contribute to the burden of asthma in the inner city.

Management of asthma requires attention to environmental exposures both indoors and outdoors. Americans spend most of their time indoors, where they have a greater ability to modify their environment. The indoor environment contains both pollutants (eg, particulate matter, nitrogen dioxide, secondhand smoke, and ozone) and allergens from furred pets, dust mites, cockroaches, rodents, and molds. Indoor particulate matter consists of particles generated from indoor sources such as cooking and cleaning activities, and particles that penetrate from the outdoors. Nitrogen dioxide sources include gas stoves, furnaces, and fireplaces. Indoor particulate matter and nitrogen dioxide are linked to asthma morbidity. The indoor ozone concentration is mainly influenced by the outdoor ozone concentration. The health effects of indoor ozone exposure have not been well studied. In contrast, there is substantial evidence of detrimental health effects from secondhand smoke. Guideline recommendations are not specific for optimizing indoor air quality. The 2007 National Asthma Education and Prevention Program asthma guidelines recommend eliminating indoor smoking and improving the ventilation. Though the guidelines state that there is insufficient evidence to recommend air cleaners, air cleaners and reducing activities that generate indoor pollutants may be sound practical approaches for improving the health of individuals with asthma. The guidelines are more specific about allergen avoidance; they recommend identifying allergens to which the individual is immunoglobin E sensitized and employing a multifaceted, comprehensive strategy to reduce exposure. Outdoor air pollutants that impact asthma include particulate matter, ozone, nitrogen dioxide, and sulfur dioxide, and guidelines recommend that individuals with asthma avoid exertion outdoors when these pollutants are elevated. Outdoor allergens include tree, grass, and weed pollens, which vary in concentration by season. Recommendations to reduce exposure include staying indoors, keeping windows and doors closed, using air conditioning and perhaps high-efficiency particulate arrestor (HEPA) air filters, and thorough daily washing to remove allergens from one's person.

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.

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.

The burden of asthma for children in the United States is substantial and has continued to rise for the past 2 decades. There is growing evidence that the indoor environment may play an important role in the pathogenesis of childhood asthma. This article first reviews the effects of indoor allergen exposure and sensitization on asthma incidence and morbidity, focusing on dust mite, cockroach, pet, and rodent allergens. It then addresses the effects of indoor air pollutants (ozone, particulate matter, nitrogen dioxide, environmental tobacco smoke, sulfur dioxide, and carbon monoxide) on asthma morbidity.

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.

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.