This parameter was developed by the Joint Task Force on Practice Parameters, representing the American Academy of Allergy, Asthma & Immunology (AAAAI); the American College of Allergy, Asthma & Immunology (ACAAI); and the joint Council of Allergy, Asthma & Immunology. The AAAAI and the ACAAI have jointly accepted responsibility for establishing “Environmental assessment and remediation: a practice parameter.” This is a complete and comprehensive document at the current time. The medical environment is a changing environment, and not all recommendations will be appropriate for all patients. Because this document incorporated the efforts of many participants, no single person, including those who served on the Joint Task Force, is authorized to provide an official AAAAI or ACAAI interpretation of these practice parameters. Any request for information about or an interpretation of these practice parameters by the AAAAI or ACAAI should be directed to the Executive Offices of the AAAAI, the ACAAI, and the Joint Council of Allergy, Asthma & Immunology. These parameters are not designed for use by pharmaceutical companies in drug promotion. The findings and conclusions in this manuscript are those of the authors and do not necessarily represent the official position of the Centers for Disease Control and Prevention (CDC).
Allergy; cockroach; sensitization; disease; morbidity
Orally administered, food-specific immunotherapy appears effective in desensitizing and potentially permanently tolerizing allergic individuals.
We sought to determine whether milk oral immunotherapy (OIT) is safe and efficacious in desensitizing children with cow’s milk allergy.
Twenty children were randomized to milk or placebo OIT (2:1 ratio). Dosing included 3 phases: the build-up day (initial dose, 0.4 mg of milk protein; final dose, 50 mg), daily doses with 8 weekly in-office dose increases to a maximum of 500 mg, and continued daily maintenance doses for 3 to 4 months. Double-blind, placebo-controlled food challenges; end-point titration skin prick tests; and milk protein serologic studies were performed before and after OIT.
Nineteen patients, 6 to 17 years of age, completed treatment: 12 in the active group and 7 in the placebo group. One dropped out because of persistent eczema during dose escalation. Baseline median milk IgE levels in the active (n = 13) versus placebo (n = 7) groups were 34.8 kUa/L (range, 4.86–314 kUa/L) versus 14.6 kUa/L (range, 0.93–133.4 kUa/L). The median milk threshold dose in both groups was 40 mg at the baseline challenge. After OIT, the median cumulative dose inducing a reaction in the active treatment group was 5140 mg (range 2540-8140 mg), whereas all patients in the placebo group reacted at 40 mg (P = .0003). Among 2437 active OIT doses versus 1193 placebo doses, there were 1107 (45.4%) versus 134 (11.2%) total reactions, with local symptoms being most common. Milk-specific IgE levels did not change significantly in either group. Milk IgG levels increased significantly in the active treatment group, with a predominant milk IgG4 level increase.
Milk OIT appears to be efficacious in the treatment of cow’s milk allergy. The side-effect profile appears acceptable but requires further study.
Cow’s milk; food allergy; IgE; prognosis; desensitization; tolerance; oral immunotherapy
Endocrine-disrupting compounds (EDCs) have immune-modulating effects. We were interested in determining their association with allergic sensitization.
To determine the association between EDCs and allergic sensitization and if this relationship depended on the antimicrobial properties of the EDCs and/or gender.
Data were obtained from the 2005–2006 National Health and Nutrition Examination Survey in which urinary bisphenol A, triclosan, benzophenone-3, and propyl, methyl, butyl and ethyl paraben, and specific IgE were available on 860 children. Aeroallergen and food sensitization were defined as having at least one positive (≥0.35 kU/L) specific IgE to an aeroallergen or a food. Logistic regression was used to determine the association of EDCs and sensitization. Analyses were adjusted for urinary creatinine, age, ethnicity, and poverty index ratio.
The odds of aeroallergen sensitization significantly increased with the level of the antimicrobial EDCs triclosan and propyl and butyl paraben (p≤0.04). The odds of food sensitization significantly increased with the level of urinary triclosan among male subjects (odds ratio for 3rd versus 1st tertile 3.9, p=0.02 for trend). There was a significant interaction between gender and triclosan, with males being more likely to be food sensitized with exposure (p=0.03). Similar associations were not identified for the non-antimicrobial EDCs bisphenol A and benzophenone-3 (p>0.2).
As a group, EDCs are not associated with allergen sensitization. However, levels of the antimicrobial EDCs triclosan and parabens were significantly associated with allergic sensitization. The potential role of antimicrobial EDCs in allergic disease warrants further study as they are commonly used in Western society.
Triclosan; paraben; benzophenone; bisphenol A; endocrine disrupting compound; aeroallergen; sensitization; food; allergy
Season of birth has been reported as a risk factor for food allergy, but the mechanisms by which it acts are unknown.
Two populations were studied; 5862 children from the National Health and Nutrition Examination Survey (NHANES) III, 1514 well-characterized food allergic children from the Johns Hopkins Pediatric Allergy Clinic (JHPAC). Food allergy was defined as self report of an acute reaction to a food (NHANES), or as milk, egg and peanut allergy. Logistic regression compared fall or non-fall birth between (1) food allergic and non-allergic subjects in NHANES, adjusted for ethnicity, age, income and sex, and (2) JHPAC subjects and the general Maryland population. For NHANES, stratification by ethnicity and for JHPAC, eczema, was examined.
Fall birth was more common among food allergic subjects in both NHANES (OR: 1.91, 95%CI: 1.31–2.77) and JHPAC/Maryland (OR: 1.31, 95%CI: 1.18–1.47). Ethnicity interacted with season (OR 2.34, 95%CI 1.43–3.82 for Caucasians, OR 1.19, 95%CI 0.77–1.86 for non-Caucasians, p=0.04 for interaction), as did eczema (OR 1.47, 95%CI 1.29–1.67 with eczema, OR 1.00, 95%CI 0.80–1.23 without eczema, p=0.002 for interaction).
Fall birth is associated with increased risk of food allergy, and this risk is greatest among those most likely to have seasonal variation in vitamin D during infancy (Caucasians) and those at risk for skin barrier dysfunction (subjects with a history of eczema), suggesting that vitamin D and the skin barrier may be implicated in seasonal associations with food allergy.
food allergy; season of birth; eczema; vitamin D
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.
allergen-specific antibody responses; laboratory animal allergy; mouse allergen
Folic acid is known to be associated with inflammatory diseases, but the relationship between folic acid and allergic diseases is unclear.
The purpose of the study was to examine the relationship between serum folate levels and markers of atopy, wheeze, and asthma.
Data were obtained from the 2005–2006 National Health and Nutrition Examination Survey (NHANES) in which serum folate and total IgE levels were measured in 8,083 subjects 2 years of age and older. A high total IgE level was defined as >100kU/L. Allergen-specific IgE levels were measured for a panel of 5 common aeroallergens. Atopy was defined as at least 1 positive allergen-specific IgE level. Doctor-diagnosed asthma and wheeze in the previous 12 months were assessed by questionnaire.
Serum folate levels were inversely associated with total IgE levels (p<.001). The odds of a high total IgE, atopy, and wheeze decreased across quintiles of serum folate, indicating a dose-response relationship between serum folate levels and these outcomes. Each of these associations remained statistically significant after adjusting for age, sex, race/ethnicity and poverty index ratio. Adjusted odds ratios[95% confidence intervals] associated with the fifth quintile (Q5) of folate relative to the first quintile (Q1) were as follows: High IgE: 0.70[0.53–0.92]; atopy: 0.69[0.57–0.85]; and wheeze: 0.60[0.44–0.82]. Higher folate levels were also associated with a lower risk of doctor-diagnosed asthma, but this finding was not statistically significant (OR[95% CI] for Q5 vs. Q1: 0.84 [0.70–1.02]).
Serum folate levels are inversely associated with high total IgE, atopy, and wheeze.
Folic acid status may influence the development and/or progression of atopy and wheeze.
asthma; allergy; atopy; folate; NHANES; Centers for Disease Control
Immigrants to developed countries have low rates of aeroallergen sensitization and asthma, but less is known about both food allergy and the role of parental immigration status.
To evaluate the relationship between personal and parental nativity on the risk of food sensitization.
3550 subjects <21 years old from the National Health and Examination Survey 2005-2006 were included. Odds ratios were generated using logistic regression which adjusted for race/ethnicity, gender, age, and household income, and accounted for the complex survey design. Nativity was classified as US-born or foreign-born and the age of immigration was estimated. Head of household nativity was used as a proxy for parental nativity. Food sensitization was defined as at least one specific-IgE ≥ 0.35 kU/L to milk, egg or peanut. Aeroallergen specific sensitizations, and the presence of asthma, allergic rhinitis or eczema were also assessed.
Compared to those born outside the US, US-born children and adolescents had higher odds of sensitization to any food (OR 2.05, 95% CI 1.49-2.83, p<0.001). Among the foreign-born, those who arrived before 2 years of age had higher odds of food sensitization than those who arrived later (OR 2.68, 95% CI 1.19-6.08, p=0.02). Within the US-born group, in contrast, children of immigrants were at the highest risk (OR 1.53, 95% CI 1.05-2.24, p=0.02).
While foreign-born children and adolescents are at lower risk of food sensitization compared to those born in the US, among those born in the US, the children of immigrants are at the highest risk.
Food allergy; food sensitization; immigration; nativity; child; hay fever; asthma; eczema; aeroallergen
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; pollutants; particulate matter; nitrogen dioxide; sulfur dioxide; secondhand smoke; ozone; allergens
The role of natural aeroallergen exposure in modulating allergen-specific immune responses is not well understood.
To examine relationships between mouse allergen exposure and mouse-specific immune responses.
New employees (n=179) at a mouse facility underwent repeated assessment of mouse allergen exposure, skin prick testing (SPT), and measurement of mouse-specific IgG. Relationships between the mean level of exposure, variability of exposure (calculated as log standard deviation), and time to development of immunologic outcomes were examined using Cox proportional hazards models.
By 24 months, 32 (23%) participants had developed a +SPT and 10 (8%) had developed mouse-specific IgG4. The incidence of a +SPT increased as levels of exposure increased from low to moderate, peaking at 1.2 ng/m3 and decreased beyond this point (p=.04). The more variable the exposure was across visits, the lower the incidence of a +SPT (HR [95% CI]: 0.17 [0.07–0.41]). Variability of exposure was an independent predictor of +SPT in a model that included both exposure metrics. In contrast, the incidence of mouse-specific IgG4 increased with increasing levels of mouse allergen exposure (2.9 [1.4–6.0]), and there was evidence of a higher risk of mouse-specific IgG4 with greater variability of exposure (6.3 [0.4–95.2]).
Both level and variability of mouse allergen exposure influence the humoral immune response, with specific patterns of exposure associated with specific immunophenotypes. Exposure variability may be a more important predictor of +SPT, while average exposure level may be a more important predictor of mouse-specific IgG4.
mouse allergen; IgE; IgG4; laboratory animal allergy
NQO1 and HO-1 expression in nasal epithelium are inversely correlated indicating that non-NRF2 mechanisms may play an important role in regulation of these genes. Further, NQO1 and HO-1 expression have opposing relationships with upper and lower airways symptoms, suggesting that induction of phase II enzymes could result in pleiotropic clinical effects.
NQO1; HO-1; NRF2; Oxidative Stress; Asthma; Nasal Epithelium
Vitamin D; wheeze; asthma; age
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, NO2, 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.
particulate matter; air pollution; pediatric; urban; bronchial hyperreactivity
MOIT can be effective in desensitizing children with severe IgE-mediated CMA, with most tolerating markedly increased amounts of cow’s milk protein over time and demonstrating changes in serologic markers.
Cow’s milk; food allergy; IgE; prognosis; desensitization; tolerance; oral immunotherapy
Our work group report details the importance of pest allergen exposure in inner-city asthma. We will focus specifically on mouse and cockroach exposure. We will discuss how exposure to these pests is common in the inner city and what conditions exist in urban areas that might lead to increased exposure. We will discuss how exposure is associated with allergen sensitization and asthma morbidity. Finally, we will discuss different methods of intervention and the effectiveness of these tactics.
Asthma; allergies; environmental allergens; indoor allergens; pest; rodents; inner city; abatement; mouse; cockroach
There is a need for a readily available, non-invasive source of biomarkers that predict poor asthma control.
We sought to determine if there is an association between the salivary inflammatory profile and disease control in children and adults with asthma.
In this cross-sectional study, we collected demographic and clinical information from two independent populations at different sites, resulting in convenience samples of 58 pediatric and 122 adult urban asthmatics. Control was assessed by symptom questionnaire (children) and by Asthma Control Questionnaire and current exacerbation (adults). Saliva was collected in all subjects. We applied principal component analysis to a 10-plex panel of relevant inflammatory markers to characterize marker profiles and determined if profiles were associated with asthma control.
There were similar, strong correlations amongst biologically related markers in both populations: eosinophil-related: eotaxin-1/CCL11, RANTES/CCL5, and IL-5 (p<.001); myeloid/innate: IL-1β, IL-6, MCP-1/CCL2, and IL-8/CXCL8 (p<.001). The first three principal components captured ≥74% of variability across all ten analytes in both populations. In adults, the Principal Component 1 score, broadly reflective of all markers, but with greater weight given to myeloid/innate markers, was associated with Asthma Control Questionnaire score and exacerbation. The Principal Component 3 score, reflective of IP-10/CXCL10, was associated with current exacerbation. In children, the Principal Component 1, 2, and 3 scores were associated with recent asthma symptoms. The Principal Component 2 score, reflective of higher eosinophil markers, was inversely correlated with symptoms. The Principal Component 3 score was positively associated with all symptom outcomes.
The salivary inflammatory profile is associated with disease control in children and adults with asthma.
Prior studies have related community violence to depression among children, but few studies have examined this relationship among adults. We hypothesized that victimization, awareness, and fear of neighborhood violence would increase the odds of depression among adult caregivers of children with asthma. We surveyed caregivers in the Baltimore Indoor Environment Study of Asthma in Kids (BIESAK), USA. The primary outcome was screening positive for depression on the Center for Epidemiological Studies Depression index. We assessed victimization, awareness, and fear of neighborhood violence, and conducted spatial analysis identifying subject homes within 500 ft of a homicide to validate survey measures of neighborhood violence. A multilevel logistic model with clustering by neighborhood estimated odds ratios and 95% confidence intervals. Survey responses about fear of neighborhood violence were strongly predicted by having a home within 500 ft of a homicide. Of 150 caregivers of children with asthma, 49% were aware of a neighborhood violent event, 36% were fearful of neighborhood violence, 22% reported victimization, and 27% had a homicide within 500 ft of the home. In our multilevel model, fear of violence increased the odds of depression by 6.7. Victimization was associated with a possible trend towards depression, and awareness of neighborhood violence did not increase the odds of depression. Based on our findings, personal experience with neighborhood violence may be more important than simple awareness. Health care workers should consider screening for depression among patients exposed to community violence.
CES-D; Community; Inner-city; Mental health; Survey; USA
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.
This study was designed to investigate the effect of in-home PM on asthma morbidity.
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.
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.
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.
air pollution; asthma; indoor; particulate matter; pediatric; urban
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 PM2.5 and PM10 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 PM2.5 and PM10 concentrations were 39.5±34.5 μg/m3 and 56.2±44.8 μg/m3, compared to the simultaneously measured ambient PM2.5 and PM10 (15.6±6.9 and 21.8±9.53 μg/m3, 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.
Particulate matter; Air pollution; Asthma; Pediatric; Urban
The effect of indoor nitrogen dioxide concentrations on asthma morbidity among inner-city preschool children is uncertain.
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.
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.
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.
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; indoor pollutants; inner city; nitrogen dioxide; preschool
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.
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 ≤ 2.5 and ≤ 10 μm in aerodynamic diameter (PM2.5, PM10), nitrogen dioxide, and ozone. Median baseline values were compared for children with (n = 150) and without (n = 150) asthma. Housing characteristics related to indoor air pollution were assessed by caregiver report and home inspection. In addition, indoor allergen levels were measured in settled dust.
Children were 58% male, 91% African American, and 88% with public health insurance. Housing characteristics related to pollutant exposure and bedroom air pollutant concentrations did not differ significantly between asthmatic and control subjects [median: PM2.5, 28.7 vs. 28.5 μg/m3; PM10, 43.6 vs. 41.4 μg/m3; NO2, 21.6 vs. 20.9 ppb; O3, 1.4 vs. 1.8 ppb; all p > 0.05]. Settled dust allergen levels (cat, dust mite, cockroach, dog, and mouse) were also similar in bedrooms of asthmatic and control children.
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.
African American; air pollution; allergens; asthma; particulate matter; pediatric; urban
There is an association between adiposity and asthma prevalence, but the relationship to asthma control is unclear.
To understand the relationships among adiposity, gender, and asthma control in inner-city adolescents with asthma.
We prospectively followed 368 adolescents with moderate to severe asthma (ages 12–20 years) living in 10 urban areas for one year. Asthma symptoms and exacerbations were recorded, and pulmonary function and exhaled nitric oxide were measured every 6 weeks. Adiposity measures (BMI, DEXA scans) were made, and blood was collected for allergy markers, adiponectin, leptin, TNF-α, IL-6 and CRP.
More than 60% of females and 50% of males were above the 85th percentile of BMI-for-age. Higher BMI was associated with more symptom days (R= 0.18, P<0.01) and exacerbations (R=0.18, P=0.06) among females only. Adiponectin was inversely related to asthma symptoms (R=− 0.18, P<0.05) and exacerbations (R=− 0.20, P<0.05) and positively with FEV1/FVC (R=0.15, P<0.05) in males only, independent of body size. There was no relationship between adiposity or adipokines and total IgE, blood eosinophils and exhaled nitric oxide. DEXA provided little additional value in relating adiposity to asthma outcome in this population of adolescents.
Adiposity is associated with poorer asthma control in females. Adiponectin is associated with improved asthma control in males.
Obesity; Asthma; Adipokines; Leptin; Adiponectin
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 (PM2.5) 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 PM2.5, AN and cotinine concentrations were detected in households where the caregiver was the smoker (caregiver smoker: PM2.5 μg/m3: 44.16, AN: 1.79 μg/m3, cotinine: 27.39 ng/ml; caregiver non-smoker: PM2.5: 28.88 μg/m3, AN: 0.71 μg/m3, 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.
Asthma; Children; Cotinine; Particulate matter; Air Nicotine