Monday, December 8, 2014
Few studies have comprehensively examined the role the school environment plays in asthma and how effectively changing the environment may reduce morbidity, when adjusting for exposures in the home. In their review, Huffaker and Phipatanakul summarize the importance and common challenges of school-based environmental assessment and intervention studies linked to health effects (J Allergy Clin Immunol 2014; 134: 1232-1237). They discuss the challenges and potential benefits of comprehensive environmental assessment and health outcomes in inner-city schools.
The school environment has been shown to be a significant reservoir for allergens and pollutants. Indoor allergens known to be important in urban home environments may also be important in schools, including cockroach, cat, dog, mouse, dust-mite, and molds. Studies have identified children with asthma in inner-cities have markedly higher levels of mouse allergen in their schools compared to levels in their individual bedrooms. Given the paucity of comprehensive data on school-based environmental interventions and health outcomes, successful home-based strategies currently serve as the model for school-based interventions. For example, practical interventions to reduce environmental exposures at home such as the use of air filtration systems and integrated pest management can be utilized in schools.
Despite the challenges associated with implementing environmental interventions in schools, evidence supports the importance of school and classroom exposures and health outcomes. School-based interventions have the potential to reduce exposures for many symptomatic children, in contrast to the individual families impacted by home-based interventions. If effective, results from school-based interventional studies could inform public policy change, funding and initiatives. If it can be demonstrated that reduction of classroom-specific exposures leads to improved asthma outcomes, then findings can be translated into efficient and cost-effective strategies to benefit communities of children through improvement of the school environment, where children in America spend the majority of their day.
Approximately 36,000 children miss school each day due to asthma which ultimately affects a child’s ability to learn. In fact, according to a U.S National Interview Survey, children with asthma missed three times more school and had a 1.7 times greater risk of having a learning disability compared to well children. Moreover, students attending schools with the highest proportions of low income students are more likely to miss school because of asthma. In their review article, Cicutto et al discuss how asthma and associated causal pathways can have interactive and synergistic effects that result in a complex situation that must be addressed collectively through a coordinated and partnered approach (J Allergy Clin Immunol 2014; 134: 1223-1230). School-centered interventions are thus directed at improving asthma control and reducing asthma-related absenteeism.
Asthma management at schools is important for pediatric pulmonologists and allergists, primary care providers and the whole interdisciplinary team working alongside them to provide quality asthma care. Several studies and systematic reviews demonstrate that students with asthma when supported through school-centered asthma care programs can have improvements in asthma knowledge, confidence in and actual practice of asthma management skills, regular use of preventive asthma medications, reduced school absenteeism, better school performance, and the use of urgent and emergent asthma care. Collectively, available research demonstrates that programs that either provide asthma care directly at-school and/or ensure adequate links between school, family and asthma care provider have achieved a reduction in asthma morbidity. The authors indicate that the synergy created by collaborative and coordinated efforts of schools and asthma care providers assists students and their families to achieve asthma control and reduce associated morbidity.
Future research is needed to determine the cost effectiveness of school-centered asthma programs and how to sustain program implementation once research funding no longer exists. Nonetheless, community asthma care providers are essential to successful asthma management across home and school settings.
Question for the authors:
You emphasize that clinicians must be advocates for appropriate services within inner city schools. What approaches can you suggest clinicians utilize to educate local school administrators?
Schools, especially inner city schools, are very limited in resources that they can devote to health care. Therefore, clinicians can provide a valuable service by partnering with schools in varying ways. The first step would be for the clinician to set up a dialogue with the school nurse that is responsible for a high proportion of the children in their practice.
A multitude of things can be done once this step is taken. First, an understanding of the challenges the nurse faces in delivering medications in school would be a start to the conversation. Many school action plans are not provided to the school nurse and many are not written for the school nurse. Also, availability of and access to rescue medications at school can be a challenge. A dialogue between the school nurse and clinician can help resolve these problems at the core level. Next, steps could be taken to assist the school nurse with education of school staff around medication administration and recognizing symptoms of asthma. The rest will depend on the clinician’s time and interest in improving asthma care in the school setting and developing a sense of community engagement.
Wednesday, November 5, 2014
Despite the improvement of air quality in the U.S. since the enhancement of the Clean Air Act in 1990, exposures to outdoor and indoor air pollution remain a significant risk factor for both the development of asthma and the triggering of asthma symptoms. Clinical studies have shown that significant asthma exacerbations were attributable to air pollution exposure, as a result of living in densely populated cities with elevated ambient fine particulate matter (PM2.5) and ozone (O3). In their review, Miller and Peden highlight new data on the effects of pollutant exposure on the innate and adaptive immune responses, genetic and epigenetic modifiers of response to pollutants, and potential interventions to mitigate these effects (J Allergy Clin Immunol 2014; 134(5): 1001-1008).
Several studies have determined that the effects of air pollution are heightened during the prenatal period. This suggests that there is greater vulnerability of the growing lungs and the developing immune system, thus predisposing towards more airway inflammation later in life. Similarly, studies suggest that factors such as chronic low-grade inflammation associated with obesity and stress may predispose towards asthma. Furthermore, the authors describe evidence that the mechanism behind these effects alter the innate and adaptive immunity, inducing a heightened immune response. Another emerging area of investigation is the effects of the environment on oxidative stress genes such as glutathione S-transferase (GST) genes as well as genes associated with Toll-like receptors of the innate immune system. Newer mechanistic lines of investigation focus on epigenetic regulation, and identifying asthma genes whose imprinting may be disrupted by environmental exposures.
Pollutant induced asthma exacerbations are less frequent in patients that use inhaled corticosteroids, suggestive that interventions that target acute inflammatory responses are beneficial, however future studies are required to test the efficacy of interventions in this population. Actively minimizing both indoor and outdoor pollutants and government air care regulations could decrease pollutant impacts on allergic lung disease.
Question for the authors:
How has the improved air quality over recent decades relate to the incidence of pollution related asthma exacerbations?
In studies of both the Atlanta and Beijing Olympic Games, interventions that decreased automotive and point-source combustion were associated with decreased asthma morbidity. Future studies are needed to investigate more thoroughly whether improvements in air quality contribute to fewer asthma exacerbations. This remains a difficult challenge to show as even the best designed epidemiological studies are unable to prove causality.
In the U.S., ethnic minorities and the economically disadvantaged are disproportionately exposed to chronic psychological stressors such as poverty, discrimination and violence. Recent findings support a causal link between exposure to these stressors at the individual or community level and asthma morbidity. Moreover, current evidence suggests that the relation between stress and asthma is complex and partially mediated or modified by environmental exposures, adherence with treatment, co-morbidities and coping mechanisms.
In a review article, Rosenberg et al discuss recent findings suggesting potential biologic mechanisms for stress-related asthma, including changes in the methylation and expression of genes that regulate behavioral, autonomic, neuroendocrine, and immunologic responses to stress (J Allergy Clin Immunol 2014; 134(5): 1009-1015). For example, there may be susceptibility genes that predispose chronically stressed youth to both post-traumatic stress disorder and asthma. Moreover, recent studies show that low socioeconomic status in early life may program sustained resistance to glucocorticoid signaling, which could undermine the efficacy of steroid therapy in subjects who develop asthma.
Wednesday, October 8, 2014
In the October 2014 issue of Journal of Allergy and Clinical Immunology, Brough et al show that early environmental peanut exposure from house dust increases the risk of peanut allergy in children with impaired skin barrier. Children were assessed for peanut allergy and had genetic studies to determine whether they could produce normal filaggrin levels. Dust samples were collected and analyzed for peanut concentration to determine in which groups of children environmental peanut exposure influenced the development of peanut allergy. In normal children environmental peanut exposure did not influence the development of peanut allergy. In contrast, in filaggrin deficient children the risk of peanut allergy increased as peanut concentration in the house dust increased. To read the full article, please click here: http://bit.ly/1qkfHeY
Thursday, October 2, 2014
Atopic eczema (AE, syn. atopic dermatitis) is a major medical condition that causes substantial burden to patients, their families, and society. Various different interventions exist, many of which have been assessed in randomized controlled trials (RCTs). However, there is a lack of core outcome sets for atopic eczema (AE) which is a major obstacle for advancing evidence-based treatment. There are several different instruments identified to assess clinical signs of AE and the global Harmonizing Outcome Measures for Eczema (HOME) initiative has already defined clinical signs, symptoms, quality of life, and long-term control of flares as core outcome domains for AE-trials. To resolve the current lack of standardization of the assessment of clinical signs of AE, the HOME initiative followed a structured process of systematic reviews and international consensus sessions to identify one core outcome measurement instrument to assess clinical signs in all future AE-trials (J Allergy Clin Immunol 2014; 134(4): 800-807).
The authors determined that from 16 different instruments identified to assess clinical signs of AE, only the Eczema Area and Severity Index (EASI) and the objective Scoring Atopic Dermatitis Index (objective SCORAD) were identified as sufficiently tested for inclusion in the core outcome set. The EASI has adequate validity, responsiveness, internal consistency, and intra-observer reliability. The objective SCORAD has adequate validity, responsiveness, and inter-observer reliability, but unclear intra-observer reliability to measure clinical signs of AE. In an international consensus study, patients, physicians, nurses, methodologists, and pharmaceutical industry representatives agreed that EASI is the preferred core instrument to measure clinical signs in all future AE-trials. The EASI was chosen as the core outcome measure for clinical trials because (1) it only includes the 4 essential signs, (2) assesses the severity of AE signs at multiple body sites, rather than at a single representative site for each sign, and (3) gives the extent of AE lesions sufficient weighting.
The HOME initiative recommends that all investigators, pharmaceutical industry, and regulatory authorities observe this consensus and include the EASI in all future atopic eczema trials to enable improved evidence-based decision making and scientific communication in the future. This does not preclude the use of other scales in trials (such as SCORAD) in addition to the core outcome measure. Better training materials for use of EASI are in preparation and will be freely available via the HOME website (). Furthermore, the process of standardization and selection of measurement instruments for the assessment of the other core outcome domains of AE, i.e. symptoms such as pruritus and sleeping problems, quality of life and long-term control of flares, is currently underway.
Atopic dermatitis (AD) is the most common chronic inflammatory skin disease and often precedes the development of food allergy and asthma. The defective skin barrier in AD is thought to allow the absorption of allergens through the skin. This promotes systemic allergen sensitization, contributing to the development of food allergy and asthma, as well as skin infections such as Staphylococcus aureus and herpes simplex virus (HSV). This month’s JACI focuses on the importance of both genetic and acquired causes of epithelial skin barrier dysfunction in driving the natural history of AD. In their review, Donald Leung and Emma Guttman-Yassky summarize current insights into AD that may lead to new treatment approaches, including several articles published in this month’s journal (J Allergy Clin Immunol 2014; 134(4): 769-779).
The causes of AD are complex and driven by a combination of genetic, environmental and immunologic factors which likely account for heterogeneity of AD onset, severity and natural history of the disease. While there is currently no cure for AD, recent studies suggest prevention of AD can be achieved by early interventions that protect the skin barrier such as emollients and topical anti-inflammatory treatments. Importantly, the control of lesional AD may improve long term outcomes not only in AD, but in allergic diseases of the gastrointestinal and respiratory tracts as well, due to the reduction of associated allergen sensitization.
Although current treatment options for AD are limited, the authors explain that in addition to Th2 antagonists (i.e. the anti IL-4R drug dupilumab), determining the key role of TSLP-receptor signaling and IL-22 that involve clinical trials with agents that target TSLP, Th22, and TH17/IL-23 will be of interest. Furthermore, the selection of therapeutics for patients with differing degrees of disease severity and /or phenotypes should be guided by defining the extent of activation in the skin and blood. For example, anti IL-23/IL-17 might provide beneficial responses particularly in intrinsic AD patients. The individual contributions of the TH22, Th17, and Th2 immune pathways to the disease phenotype will be clarified through clinical trials coupled with mechanistic studies that are currently in progress. This comprehensive review highlights the importance of translational medicine, from animal models to clinical trials, and how this approach is advancing AD research.
Questions for the authors:
Recently, both basic science and clinical research have provided novel insights into the prevention, identification, and treatment options for AD. Do you anticipate these findings to improve outcomes for not only AD but other allergic diseases as well?
Yes, because the principle underlying causation of allergic diseases likely have in common a defective epithelial barrier and abberant immune response. This is modulated by different resident cells in each organ.
AD is most often a first step in a series of atopic diseases in the Atopic March that often leads to rhinitis, food allergy, and asthma. Could removing the first step in the Atopic March reduce the global burden of atopic disease?
Possibly. The studies in the current issue of JACI support the concept that skin barrier dysfunction enhances sensitization via environmental allergen exposure. A natural progression of this concept would be to correct the skin barrier defect to determine whether elimination of AD could prevent food allergy, asthma and allergic rhinitis.