Asthma Triggers Research Articles

Molecular and immunological characterization of Asp f 34, a novel major cell wall allergen of Aspergillus fumigatus

Although fungal spores have been recognized as triggers of respiratory allergy and asthma, only two allergenic fungal cell wall components have so far been described. Eighty-one sequences derived from an Aspergillus fumigatus cDNA library encoding putative allergens were examined for the presence of cell wall components. A new allergen (Asp f 34) was evaluated by Western blots, enzyme-linked immunosorbent assay (ELISA), peripheral blood mononuclear cell (PBMC) proliferation assays, and skin prick test (SPT). The cDNA encoding Asp f 34 contained an open reading frame predicting a protein of 185 amino acids with a molecular weight of 19.38 kDa, showing sequence homology to phiA, an essential protein for the formation of conidia in the genus Aspergillus. The recombinant Asp f 34 was binding IgE from sensitized individuals in Western blots. An ELISA survey showed that 94% of the ABPA and 46% of the A. fumigatus-sensitized individuals tested had Asp f 34-specific serum IgE. Asp f 34 induced allergen-specific proliferation exclusively of PBMCs from patients sensitized to the allergen. Eight patients with anti-Asp f 34 serum IgE tested reacted positively in SPT, whereas four A. fumigatus-sensitized individuals without Asp f 34-specific IgE and eight healthy controls scored negatively. A cell wall protein of the phialides of A. fumigatus was identified as a major allergen. Asp f 34 belongs to the Aspergillus-specific proteins of the phiA family and has relevant potential for a specific diagnosis of Aspergillus sensitization.

A sensory neuronal ion channel essential for airway inflammation and hyperreactivity in asthma

Asthma is an inflammatory disorder caused by airway exposures to allergens and chemical irritants. Studies focusing on immune, smooth muscle, and airway epithelial function revealed many aspects of the disease mechanism of asthma. However, the limited efficacies of immune-directed therapies suggest the involvement of additional mechanisms in asthmatic airway inflammation. TRPA1 is an irritant-sensing ion channel expressed in airway chemosensory nerves. TRPA1-activating stimuli such as cigarette smoke, chlorine, aldehydes, and scents are among the most prevalent triggers of asthma. Endogenous TRPA1 agonists, including reactive oxygen species and lipid peroxidation products, are potent drivers of allergen-induced airway inflammation in asthma. Here, we examined the role of TRPA1 in allergic asthma in the murine ovalbumin model. Strikingly, genetic ablation of TRPA1 inhibited allergen-induced leukocyte infiltration in the airways, reduced cytokine and mucus production, and almost completely abolished airway hyperreactivity to contractile stimuli. This phenotype is recapitulated by treatment of wild-type mice with HC-030031, a TRPA1 antagonist. HC-030031, when administered during airway allergen challenge, inhibited eosinophil infiltration and prevented the development of airway hyperreactivity. Trpa1(-/-) mice displayed deficiencies in chemically and allergen-induced neuropeptide release in the airways, providing a potential explanation for the impaired inflammatory response. Our data suggest that TRPA1 is a key integrator of interactions between the immune and nervous systems in the airways, driving asthmatic airway inflammation following inhaled allergen challenge. TRPA1 may represent a promising pharmacological target for the treatment of asthma and other allergic inflammatory conditions.

Triggers in adult asthma: are patients aware of triggers and doing right?

BackgroundAs triggers have a potential to induce asthma exacerbations, awareness of the patients to individual triggers as well as protective measures might be helpful to prevent asthma attacks. Though allergens and allergen avoidance have been studied extensively, there are only few studies on non-allergic triggers and their avoidance for adult patients with asthma. In this study, we wanted to investigate asthma triggers and compliance to the preventive measures in an adult population. MethodsOne hundred and thirty one adult asthma patients were enrolled into the study. A face to face interview was done by using a questionnaire including individual asthma triggers, prevention measures against major modifiable triggers and knowledge sources of the cases. ResultsRegardless of asthma severity, 59.5 % of the subjects reported to be triggered by more than 10 factors. The most common triggers were air pollutants (89.3 %) and weather changes (81.7 %). Severe group was more frequently affected by medications, emotional stress, weather changes and indoor pollutants than other severity groups (p=0.017, 0.014, 0.049 and 0.018, respectively) whereas stress was reported more frequently by females than males. Prevention measures were insufficient regarding some major triggers. ConclusionAdult patients are vulnerable to several triggers regardless from underlying severity of the illness. Insufficient compliance to the major preventive measures indicates that new strategies are needed to prevent asthma attacks caused by modifiable triggers.

Peripheral blood monocytes (PBMCs) display innate antiviral response to rhinovirus (RV) infected bronchial epithelial cells (133.44)

Abstract Rhinovirus (RV) infection is an important trigger of acute asthma and COPD. Study objectives; were to characterise the response of PBMCs and CD8 lymphocytes when exposed to RV infected bronchial epithelial cells. Methods; Human Calu3 cells were used as a model for bronchial epithelial cells and infected with RV-43 and RV-1B. PBMCs were obtained from healthy individuals and separated by Ficoll-Paque centrifugation. CD8 lymphocytes were identified as CD3+, CD8+ by flow cytometry. PBMCs were exposed to infected Calu3 cells, cells exposed to UV inactive RV, PHA and TLR3 agonist PolyI:C. Response was measured by ELISA for release of interferon(IFN)-γ and TNF-α. CD8 activation with expression of perforin or proliferation measured by carboxyfluorescein succinimidyl ester assay. Results: Exposure of PBMCs to Calu3 cells infected with both RV led to significant release of IFN-γ and TNF-α, smaller release was seen in response to UV inactive RV. Exposure to PolyI:C also led to a similar release. CD8+ cells were found to be the primary source of IFN-γ release. CD8+ cells did not show an increase in perforin expression or evidence of proliferation. Conclusions; exposure of PBMCs and CD8+ cells to an RV infected bronchial epithelium alone results in an innate immune response mediated by TLR3 without evidence of a CD8 adaptive immune response.

Diversity in the bronchial epithelial cell response to infection with different rhinovirus strains

Infection with rhinovirus (RV) is the most common trigger for acute asthma and COPD. The aim of this study was to characterize the variability in the response of primary bronchial epithelial cells to infection with several strains of RV. RV strains, RV-43, RV-48 (major group RV), RV-47 (minor) and EV-68 (enterovirus), were cultured from subjects with acute asthma and compared with the laboratory RV strains, RV-16, RV-14 (major) and RV-1B (minor). Primary bronchial epithelial cells were obtained from healthy control and asthmatic subjects by endobronchial brushing. Response to infection was assessed by the release of IL-6, interferon (IFN)-gamma induced protein (IP)-10 and IFN-beta, as measured by ELISA. Viral replication was assessed by serial titration assays and cell viability by flow cytometry. Major group RV strains and EV-68 all efficiently infected and replicated in epithelial cells causing little cell death. The clinical major group RV strains caused greater release of IL-6 and IP-10 compared with laboratory major group RV strains. Infection with minor group RV resulted in greater release of IP-10, IL-6 and IFN-beta that was associated with induction of apoptosis and less efficient viral replication. Asthmatic bronchial epithelial cells were less able to respond by releasing IFN-beta following infection with RV-1B. Considerable diversity exists in the response to RV strains, especially between minor and major group RV. The impaired IFN-beta response in asthmatic bronchial epithelial cells may make them particularly susceptible to minor group RV.

A Systematic Review of Home-Based Multi-Trigger Multi-Component Environmental Interventions to Reduce Asthma Morbidity

RATIONALE: Interventions that target a wide variety of asthma triggers through home visits may be beneficial in improving asthma outcomes. CDC scientists and the Task Force on Community Preventive Services systematically reviewed the evidence of effectiveness of home-based multi-trigger multi-component environmental interventions in improving asthma-related morbidity. METHODS: We sought English language studies that evaluated interventions with at least one home visit, included more than one intervention component, were directed towards reducing multiple environmental asthma triggers, and met the minimum research quality for study design and execution. RESULTS: Twenty-five studies met inclusion criteria. In the 21 studies targeting children, asthma symptom days were reduced by 0.8 days/2weeks (Interquartile Interval or IQI: -0.9 to -0.6 days/2 weeks) equivalent to 21 symptom days/year, school days missed due to asthma were reduced by 11 days per year (IQI: -18.2 to -2.9 days), and the number of asthma acute care visits were modestly reduced by 0.57 visits per year (IQI -1.7 to -0.3). Only four studies reported outcomes among adults with asthma and found inconsistent results. CONCLUSIONS: Findings from this review indicate that home-based multi-trigger, multi-component, environmental interventions are effective in reducing symptom days, school days missed, and acute asthma visits in children with asthma. We cannot draw any conclusions on the effectiveness of this intervention in adults due to the small number of studies with inconsistent results. Additional studies are needed to evaluate 1) the effectiveness of this intervention in adults; 2) evaluate cost-effectiveness; and 3) determine the individual contributions of the various intervention components.

Community Health Workers and Environmental Interventions for Children with Asthma: A Systematic Review

Community health worker (CHW)–delivered, home-based environmental interventions for pediatric asthma were systematically reviewed. Seven PubMed/MEDLINE listed randomized controlled trials that encompassed the following intervention criteria were identified: (1) home-based; () delivered by a CHW; () delivered to families with children with asthma; and () addressed multiple environmental triggers for asthma. Details of research design, intervention type, and setting, interventionist, population served, and the evaluated outcomes were abstracted. Outcome assessment was broad and non-uniform. Categories included direct mediators of improved health outcomes, such as trigger-related knowledge, trigger reduction behaviors and allergen or exposure levels, and asthma-related health outcomes: change in lung function, medication use, asthma symptoms, activity limitations, and health care utilization. Indirect mediators of health outcomes, or psychosocial influences on health, were measured in few studies.Overall, the studies consistently identified positive outcomes associated with CHW-delivered interventions, including decreased asthma symptoms, daytime activity limitations, and emergency and urgent care use. However, improvements in trigger reduction behaviors and allergen levels, hypothesized mediators of these outcomes, were inconsistent. Trigger reduction behaviors appeared to be tied to study-based resource provision. To better understand the mechanism through which CHW-led environmental interventions cause a change in asthma-related health outcomes, information on the theoretical concepts that mediate behavior change in trigger control (self-efficacy, social support) is needed. In addition, evaluating the influence of CHWs as clinic liaisons that enhance access to health professionals, complement clinic-based teaching, and improve appropriate use of asthma medications should be considered, alongside their effect on environmental management. A conceptual model identifying pathways for future investigation is presented.

Managing Asthma Triggers in School

Managing Asthma Triggers in School

Clinical importance of identifying immunoglobulin E-mediated disease in patients with Asthma

The strong association between allergy and asthma is well documented; however, few practitioners-even asthma specialists-accurately estimate the percentage of patients with asthma who have clinically relevant allergies. Because allergen exposure can prompt airway inflammation, trigger asthma exacerbations, and possibly lead to negative health outcomes for patients with asthma, identifying allergies and immunoglobulin E (IgE)-mediated disease in patients with persistent asthma is crucial. Updated Expert Panel 3 asthma guidelines from the National Asthma Education and Prevention Program reinforce the need for clinicians to identify allergic sensitivities in patients with persistent asthma and determine their clinical relevance. Allergy testing can be useful in educating the patient with IgE-mediated asthma about the need for allergic trigger avoidance and can help determine optimal therapy for patients with concomitant asthma and allergy. Implementing this guideline recommendation, however, requires active clinical engagement. Data from a recent observational study indicate that there may be a substantial gap between guideline recommendations and actual clinical practice. These data also suggest that when clinicians participate in education about the role of IgE in asthma and begin testing their patients for allergy, the recognition of allergies among patients with asthma dramatically increases.

An examination of interventions to reduce respiratory health and injury hazards in homes of low-income families

We evaluated whether combining asthma trigger reduction with housing structural repairs, device disbursement and education in low-income households with children would improve self-reported respiratory health and reduce housing-related respiratory health and injury hazards (convenience sample of n=67 homes with 63 asthmatic and 121 non-asthmatic children). At baseline, a visual assessment of the home environment and a structured occupant interview were used to examine 29 potential injury hazards and 7 potential respiratory health hazards. A home-specific intervention was designed to provide the children's parents or caretakers with the knowledge, skills, motivation, supplies, equipment, and minimum housing conditions necessary for a healthy and safe home. The enrolled households were primarily Hispanic and owned their homes. On average, 8 injury hazards were observed in the homes at baseline. Four months following intervention, the average declined to 2.2 hazards per home ( p<0.001), with 97% of the parents reporting that their homes were safer following the interventions. An average of 3.3 respiratory health hazards were observed in the homes at baseline. Four months following intervention, the average declined to 0.9 hazards per home ( p<0.001), with 96% of parents reporting that the respiratory health of their asthmatic children improved. A tailored healthy homes improvement package significantly improves self-reported respiratory health and safety, reduces respiratory health and injury hazards, and can be implemented in concert with a mobile clinical setting.

Innate immunity in asthma

Asthma is a complex disorder and evidence now suggests that it is not solely attributable either to allergy or eosinophilia. Non-eosinophilic asthma accounts for up to one half of all cases and a large proportion have a non-allergic aetiology. The innate immune system responds to a variety of triggers, including viral and bacterial components which are known non-allergic triggers of asthma. The innate immune response may be involved in both the development of and protection against asthma. Factors which are likely to determine the nature of the response include the timing of the exposure (childhood or adulthood), baseline asthma inflammatory subtype (eosinophilic or non-eosinophilic) and the dose of the exposure. Gene-environment interactions are likely to modify the response. Further research is required to elucidate the specific mechanisms involved in the innate immune response in asthma and will be important in the identification of new targets for therapy and management.

Control of asthma triggers in indoor air with air cleaners: a modeling analysis

BackgroundReducing exposure to environmental agents indoors shown to increase asthma symptoms or lead to asthma exacerbations is an important component of a strategy to manage asthma for individuals. Numerous investigations have demonstrated that portable air cleaning devices can reduce concentrations of asthma triggers in indoor air; however, their benefits for breathing problems have not always been reproducible. The potential exposure benefits of whole house high efficiency in-duct air cleaners for sensitive subpopulations have yet to be evaluated.MethodsWe used an indoor air quality modeling system (CONTAM) developed by NIST to examine peak and time-integrated concentrations of common asthma triggers present in indoor air over a year as a function of natural ventilation, portable air cleaners, and forced air ventilation equipped with conventional and high efficiency filtration systems. Emission rates for asthma triggers were based on experimental studies published in the scientific literature.ResultsForced air systems with high efficiency filtration were found to provide the best control of asthma triggers: 30–55% lower cat allergen levels, 90–99% lower risk of respiratory infection through the inhalation route of exposure, 90–98% lower environmental tobacco smoke (ETS) levels, and 50–75% lower fungal spore levels than the other ventilation/filtration systems considered. These results indicate that the use of high efficiency in-duct air cleaners provide an effective means of controlling allergen levels not only in a single room, like a portable air cleaner, but the whole house.ConclusionThese findings are useful for evaluating potential benefits of high efficiency in-duct filtration systems for controlling exposure to asthma triggers indoors and for the design of trials of environmental interventions intended to evaluate their utility in practice.

Characterization of Proteases, Proteins, and Eicosanoid-Like Substances in Soluble Extracts from Allergenic Pollen Grains

Background: Pollen is an important trigger of seasonal rhinitis, conjunctivitis, and/or allergic asthma, and an exacerbating factor in atopic dermatitis. Pollen grains contain allergen proteins, enzymes, and bioactive lipid mediators, the latter two possibly involved in the pathogenesis of allergic diseases through IgE-independent mechanisms. Methods: We analyzed the patterns of release of endopeptidases from allergenic pollen of Japanese cedar, Japanese cypress, and Rocky mountain juniper, which belong to the Cupressaceae/Taxodiaceae family, and birch, ragweed, and two grasses, Kentucky blue and cultivated rye, using synthetic substrates, class-specific inhibitors, and zymography. The proteins released were analyzed by gel electrophoresis. Eicosanoid-like substances were measured by enzyme-linked immunosorbent assays for prostaglandin E₂ and leukotriene B₄. Results: Major fractions of proteins, eicosanoid-like substances, and at least one molecular species of serine endopeptidase were released into phosphate-buffered saline from the pollen grains at 37°C within 25 min or 60 min without sonication. In the Cupressaceae/Taxodiaceae family, sonication was necessary for the release of other proteins and another serine endopeptidase. In birch, ragweed, and the grasses, most of the serine and cysteine endopeptidases were released without sonication. Proteases released within 25 min digested gelatin and/or casein differently among plant species. Conclusions: Grains of allergenic pollen release proteases, which can digest not only short synthetic substrates but also protein substrates, along with eicosanoid-like substances and proteins. The release of these components could contribute to the formation of a microenvironment optimum for initiation of the sensitization or the exacerbation of pollen allergy in tissues exposed to pollen grains.

Risk Factors for Repeat Adverse Asthma Events in Children After Visiting an Emergency Department

ObjectiveThe aim of this study was to identify risk factors for long-term adverse outcomes in children with asthma after visiting the emergency department (ED).MethodsA prospective observational study was conducted at the ED of a pediatric tertiary hospital in Ontario, Canada. Patient outcomes (ie, acute asthma episodes and ED visits) were measured at baseline and at 1- and 6-months post-ED discharge. Time trends in outcomes were assessed using the generalized estimating equations method. Multiple conditional logistic regressions were used to model outcomes at 6 months and examine the impact of drug insurance coverage while adjusting for confounders.ResultsOf the 269 children recruited, 81.8% completed both follow-ups. ED use significantly reduced from 39.4% at baseline to 26.8% at 6 months (P < .001), whereas the level of acute asthma episodes remained unchanged. Children with drug insurance coverage were less likely to have acute asthma episodes (adjusted odds ratio [AOR] = 0.36; 95% CI, 0.15–0.85; P < .02) or repeat ED visits (AOR = 0.45; 95% CI, 0.20–0.99; P < .05) at 6 months. Other risk factors for adverse outcomes included previous adverse asthma events and certain asthma triggers (eg, cold/sinus infection). Washing bed linens in hot water weekly was protective against subsequent acute asthma episodes.ConclusionsOur study demonstrated significant improvements in long-term outcomes in children seeking acute care for asthma in the ED. Future efforts remain in targeting the sustainability of improved outcomes beyond 6 months. Risk factors identified can help target vulnerable populations for proper interventions, which may include efforts to maximize insurance coverage for asthma medications and strategies to improve asthma self-management through patient and provider education.

Therapeutic effects of anti-B7-1 antibody in an ovalbumin-induced mouse asthma model

Allergic asthma is a chronic inflammatory disorder of airways, which is characterized by attacks provoked by exposure to so-called asthma triggers, such as pet dander, second-hand tobacco smoke, dust mites, and mold spores. B7-1 (CD80), perhaps one of the most studied co-stimulatory molecules involved in asthma, plays a key role in regulating allergen-induced T cell activation in asthma, probably through T cell recruitment and Th cell differentiation upon allergen provocation. The present study was designed to test the hypothesis that anti-B7-1 antibody has therapeutic effects in asthma by blocking B7-1/CD28 pathway. The asthma model was established by ovalbumin (OVA) sensitization and challenging in female Balb/c mice. One hour after the last induction, mice were sacrificed and whole lung lavage was conducted. Cell numbers in bronchoalveolar lavage fluid (BALF) were determined and the expression levels of IFN-γ and IL-4 in supernatant were measured by an enzyme-linked immunosorbent assay method. Sedimental cells smears were stained with Wright's–Gimsa mixed coloring method. The B7-1 expression was detected by immunohistochemistry method with frozen tissue sections. The anti-B7-1 antibody treatment could alleviate asthmatic syndromes induced by OVA. The number of recoverable eosinophils in BALF in the anti-B7-1 antibody treated group was significantly lower than that in the control group ( P < 0.01) and the eosinophils peribronchial infiltration was remarkably reduced in anti-B7-1 treated asthmatic mice, based on histological evaluation. The treatment with the anti-B7-1 antibody induced IFN-γ expression and decreased IL-4 expression, compared with the asthmatic control group ( P < 0.01). In conclusion, the anti-B7-1 antibody approach may provide a novel therapy for allergic asthma.

Psychological triggers and hyperventilation symptoms in asthma

Anecdotal accounts have identified hyperventilation as one route through which psychological factors can trigger bronchoconstriction. However, little is known about the empirical association between psychological and other trigger factors and hyperventilation in asthma exacerbations. To study the cross-sectional association between perceived triggers and hyperventilation symptoms in 1 British and 1 German sample of patients with asthma who were recruited from the community and from primary care clinics. Patients completed relevant language versions of the Asthma Trigger Inventory and the Asthma Symptom Checklist. After controlling for demographics and asthma severity, perceived asthma triggers measured by subscales of the Asthma Trigger Inventory explained 12.5% to 37.3% of the variance in Asthma Symptom Checklist hyperventilation-hypocapnia symptoms. Psychological triggers accounted for 10.6% to 26.7% of the variance alone and 4.3% to 11.0% of the variance over and above other trigger factors. In contrast, perceived animal and pollen allergen triggers did not contribute unique variance to the hyperventilation symptom report. Psychological triggers did not explain variance in classic airway obstruction symptoms, thus arguing against a general bias toward inflated symptom reports in patients with psychologically induced asthma. Differences in perceived asthma triggers are substantially associated with hyperventilation symptoms, and patients with more frequent psychological triggers also tend to report that they experience more hyperventilation symptoms during their asthma symptom episodes.

Stress Effects on Lung Function in Asthma are Mediated by Changes in Airway Inflammation

To examine the association of changes in current negative mood and long-term daily hassles with changes in lung function and airway inflammation in patients suffering from asthma and in healthy controls. Associations between psychological factors and asthma symptoms have been documented, but the relationship between airway inflammation and psychological factors has been largely unexplored. Data were analyzed from 46 asthma patients and 25 controls who completed questionnaires on current mood and daily hassles at two assessments 3 months apart. Lung function was measured by spirometry (forced expiratory volume in the first second (FEV(1))) and airway inflammation by the fraction of nitric oxide in exhaled air (FeNO). Regression analyses controlling for allergen load and air pollution (ozone) were calculated to study the association between changes in psychological factors and changes in lung function and airway inflammation, and to examine the mediational role of airway inflammation in the stress-lung function association. In patients with asthma, increases in negative affect were associated with decreases in FEV(1) and increases in FeNO. For daily hassles, a reverse pattern of associations was found, with decreases in daily hassles linked to decreases in FEV(1) and increases in FeNO. Mediation analyses showed that FeNO was a significant mediator of the association of both negative affect and daily hassles with lung function changes. No significant associations were found for healthy controls. Psychological variables are consistently associated with spirometric lung function and airway inflammation in asthma patients. For asthma patients, effects of acute negative affect must be distinguished from more chronic distress due to daily hassles.

Diet-induced obesity causes innate airway hyperresponsiveness to methacholine and enhances ozone-induced pulmonary inflammation

We previously reported that genetically obese mice exhibit innate airway hyperresponsiveness (AHR) and enhanced ozone (O(3))-induced pulmonary inflammation. Such genetic deficiencies in mice are rare in humans, and they may not be representative of human obesity. Thus the purpose of this study was to determine the pulmonary phenotype of mice with diet-induced obesity (DIO), which more closely mimics the cause of human obesity. Therefore, wild-type C57BL/6 mice were reared from the time of weaning until at least 30 wk of age on diets in which either 10 or 60% of the calories are derived from fat in the form of lard. Body mass was approximately 40% greater in mice fed 60 vs. 10% fat diets. Baseline airway responsiveness to intravenous methacholine, measured by forced oscillation, was greater in mice fed 60 vs. 10% fat diets. We also examined lung permeability and inflammation after exposure to room air or O(3) (2 parts/million for 3 h), an asthma trigger. Four hours after the exposure ended, O(3)-induced increases in bronchoalveolar lavage fluid protein, interleukin-6, KC, macrophage inflammatory protein-2, interferon-gamma-inducible protein-10, and eotaxin were greater in mice fed 60 vs. 10% fat diets. Innate AHR and augmented responses to O(3) were not observed in mice raised from weaning until 20-22 wk of age on a 60% fat diet. These results indicate that mice with DIO exhibit innate AHR and enhanced O(3)-induced pulmonary inflammation, similar to genetically obese mice. However, mice with DIO must remain obese for an extended period of time before this pulmonary phenotype is observed.

Outcomes of a Home-Based Environmental Remediation for Urban Children with Asthma

Increasing urban asthma prevalence and severity is found among minority, underserved populations. Improving asthma self-management includes home management of complex medical protocols as well as environmental trigger removal. To study the effectiveness of a low-cost approach to improve control of asthma symptoms in an urban population through lay educators who promote a generalized approach to asthma trigger avoidance in the bedrooms of children with asthma. Prospective, randomized controlled trial with two arms: historical controls and matched controls for each subject. Two-hundred-eighty-one patients living in an urban environment, randomized to receive home visits only (n = 128) or home visits with environmental remediation (n = 153). One-hundred-fifteen controls matched according to age, gender and ethnicity did not receive any intervention. In-home education visits covered asthma physiology, asthma trigger avoidance and asthma management. Environmental remediation was conducted together with the caregiver. Primary outcomes include length of hospital stay, number of emergency visits and number of sick visits. Secondary outcomes are symptom frequency, medication management and trigger reduction. Both intervention groups experienced reduction of hospitalizations, emergency room visits, sick visits and asthma symptoms. Both groups showed outcomes significantly superior to the matched control group. Intervention effectively reduced the presence of rodents and carpet in home and increased the use of mattress and pillow covers. This study shows that low-cost in-home education and environmental remediation improve outcomes for children with asthma. Lay educators can deliver effective asthma-specific education that results in improved asthma control.

Ambient Air Pollution and Daily Emergency Department Visits for Asthma in Edmonton, Canada

As demonstrated by many studies, emergency department (ED) visits for asthma can be associated with air pollution exposures. The aim of this study was to examine and assess the potential relations between ED visits for asthma and the concentrations of ambient air pollutants. Generalized linear mixed model was applied to study 62,563 ED visits for asthma (ICD-9: 493) in Edmonton, Canada. Two age groups, with 10 years of age as a separator, were considered by gender and season of the year: all (I-XII), warm (IV-IX) and cold (X-III). The percentage increase in daily ED visits for asthma was 17.8% (95% CI: 7.1-29.5) and 13.8% (95% CI: 3.3-25.3) for females below 10 years of age, in the period of IV-IX, for current day and 1-day lagged exposure to ozone (O(3)), respectively. The percentage increase was 19.2% (95% CI: 11.4-27.6) for males below 10 years of age, in the period of IV-IX, for 2-day lagged exposure to nitrogen dioxide (NO(2)). The findings provide support for the hypothesis that ED visits for asthma are associated with exposure to O(3). This study underlines the significant role of air pollutants as triggering asthma attacks.