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The article discusses a scientific study of lung function in individuals from infancy to late adolescence with a focus on what factors are associated with changes in function. Topics include the impact that gender, asthma, and maternal asthma have on lung function, the correlation between infant onset atopy, maternal smoking, and low lung function, and expiratory flow limitation in lung function.

Objective: The objective of this study is to compare the effects of inhaled beclomethasone with oral montelukast in long term management of moderate persistent asthma in children. Design: Quasi experimental study. Period: 6 months, from July 20,2007 to January 20, 2008. Settings: Out patient paediatric department at Fauji Foundation hospital, Rawalpindi. Material and Methods: 80 children between 5-12yrs of age presenting with moderate persistent asthma, divided in two groups of 40 each. Group A treated with beclomethasone inhaler while Group B was started on oral montelukast. Drugs effect was recorded on a 2 wkly proforma for 8 weeks. Results: There were 54(67.5%) male and 26(33%) female. Most common triggering factor seen in 54(67.5%) patients was recent history of respiratory tract infection, exposure to carpet dust in 43(53.75%), cigarette smoke in 42(52.5%),recent psychological stress in 28(35%) , pollen allergy in 26 (32.5%) , pets exposure in 8 (10%) and to mite was noticed in 5(6.25%) children. Marked improvement was observed in day time cough in group A with 10(25%) patients being free of cough with inhaler, while 20(50%) showed mild intermittent symptoms. 1(2.5%) showed mild persistent symptoms. In Group B 3(7.5%) patients were symptom free, 23(57.5%)with mild intermittent and 4(10%) with mild persistant symptoms while 6(15%) continued to have moderate persistent symptoms. P value was 0.01. Regarding day time breathlessness, P value was significant of 0.258. Similarly marked improvement was observed in night symptoms of breathlessness, cough and sleeplessness in both groups. P value was less than 0.05 in majority of the variables showing statistically significant improvement with inhaled beclomethasone than with oral montelukast. Conclusions: Inhaled beclomethasone is superior to oral montelukast in controlling chronic symptoms of childhood asthma. [ABSTRACT FROM AUTHOR]

This study was undertaken to determine whether there was a correlation between fine particles (PM2.5) levels and hospital admissions for asthma in Taipei, Taiwan. Hospital admissions for asthma and ambient air pollution data for Taipei were obtained for the period of 2006–2010. The relative risk of hospital admissions for asthma was estimated using a case-crossover approach, controlling for weather variables, day of the week, seasonality, and long-term time trends. For the single-pollutant model (without adjustment for other pollutants), increased asthma admissions were significantly associated with PM2.5levels both on warm days (>23°C) and cool days (<23°C), with an interquartile range rise associated with a 12% (95% CI = 6–18%) and 3% (95% CI = 0–8%) elevation in admissions for asthma, respectively. In the two-pollutant models, PM2.5levels remained significant for increased asthma admissions after inclusion of SO2or O3both on warm and cool days. This study provides evidence that higher levels of PM2.5elevate the risk of hospital admissions for asthma in Taiwan. [ABSTRACT FROM PUBLISHER]

Background Allergic reactions to the common house plant Hoya compacta (HC) have not previously been described. Aims To confirm HC as the cause of rhinoconjunctivitis in three horticultural workers. Methods Greenhouse working conditions were reproduced in our challenge chamber. Results All three cases developed rhinoconjunctivitis when working with HC plants. A control challenge was performed in two cases with iceberg lettuce causing no symptoms. Nasal volume measured by acoustic rhinometry (AR) fell after all three active challenges, but also after one of the control challenges. Conclusions Our study confirms that HC may cause occupational rhinoconjunctivitis and asthma through a Type I hypersensitivity reaction. Specific inhalation challenges, nasal nitric oxide measurement and AR may be useful additional tools in supporting such diagnoses for occupational physicians to consider. [ABSTRACT FROM AUTHOR]

Objective To investigate the relationship between inflammatory cytokine levels and airway remodeling in bronchial asthma patients. Methods 106 patients with bronchial asthma were divided into exacerbation group and stable groups, there were 61 cases, 45 cases, separately, 40 cases of healthy people were selected as control group. IL-2, IL-5, VEGF, bFGF, TGF-β 1 levels were detected. Results Compared with the control group, the levels of VEGF, bFGF, TGF-β1 in stable group were significantly increased ( P < 0.05) . Compared with the control group and the stable group, the levels of VEGF, bFGF, TGF-β1 in exacerbation group were significantly increased ( P < 0.05) . The levels of IL-5 in stable group patients were significantly higher than the control group (P< 0.05) . The levels of IL-2 and IL-5 in exacerbation group patients were significantly higher than than those in the control group and the stable group patients (P < 0.05) . IL-2 and TGF-β1 showed a significant positive correlation (F < 0.05), IL-5 and VEGF, bFGF, and TGF-β1 showed significant positive correlation (P< 0.05) . Conclusion The imbalance of inflammatory cytokine levels is closely related to airway fibrosis induced by VEGF, bFGF and TGF-β1 in bronchial asthma patients, these two factors work together to lead to bronchial asthma progress. [ABSTRACT FROM AUTHOR]

Linker for activation of T cells (LAT) is a key adaptor in the T cell receptor (TCR) signaling pathway. The expression of LAT is lower in asthmatic patients than that in healthy people, but there is little knowledge about the mechanism underlying this phenomenon. This study was aimed to determine whether LAT-PLC-γ1 interaction was involved in the development of asthma. It was shown that the phosphorylation of PLC-γ1 decreased in the asthmatic mouse model and Th2 cell differentiated CD4+ T cells. In addition, depleted endogenous PLC-γ1 promoted CD4+ T cells to differentiate into IL-4-Productor. It was therefore concluded that the low level of LAT-PLC-γ1 interaction was associated with Th2 polarized differentiation, and this may contribute to the etiology of asthma. [ABSTRACT FROM AUTHOR]

Dampness and visible mold in homes are associated with asthma development, but causal mechanisms remain unclear. The goal of this research was to explore associations among measured dampness, fungal exposure, and childhood asthma development without the bias of culture-based microbial analysis. In the low-income, Latino CHAMACOS birth cohort, house dust was collected at age 12 months, and asthma status was determined at age 7 years. The current analysis included 13 asthma cases and 28 controls. Next-generation DNA sequencing methods quantified fungal taxa and diversity. Lower fungal diversity (number of fungal operational taxonomic units) was significantly associated with increased risk of asthma development: unadjusted odds ratio ( OR) 4.80 (95% confidence interval ( CI) 1.04-22.1). Control for potential confounders strengthened this relationship. Decreased diversity within the genus Cryptococcus was significantly associated with increased asthma risk ( OR 21.0, 95% CI 2.16-204). No fungal taxon (species, genus, class) was significantly positively associated with asthma development, and one was significantly negatively associated. Elevated moisture was associated with increased fungal diversity, and moisture/mold indicators were associated with four fungal taxa. Next-generation DNA sequencing provided comprehensive estimates of fungal identity and diversity, demonstrating significant associations between low fungal diversity and childhood asthma development in this community. [ABSTRACT FROM AUTHOR]

The article discusses epidemiology, clinical characteristics, and management of occupational asthma. Topics explored include common agents that cause asthma such as animal allergens, plant products, and enzymes, the occupational asthma risks faced by farmers, office workers, and pharmaceutical industry employees, and the effectiveness of immunotherapy in addressing asthma symptoms.

Abstract: It has been suggested that mitochondrial dysfunction plays a role in the pathogenesis of asthma. To test whether mitochondrial variants influence the risk of asthma, we analyzed 16,158 mtSNPs in a sample of 372 asthmatic children and 395 healthy children using the DNA pooling technique and genome wide association analysis. Stratified analysis by sex was performed to explain the differences observed between sexes in the etiology of asthma. Different variants were detected to be significant in the sample of girls and boys with the smallest adjusted p values being 1.4×10−09 (mt5295) and 3.6×10−12 (mt16158), respectively. Most of the significant locations found in boys are within the CYB gene and the non-coding region. For girls, most of the significant mtSNPs lie within NADH-dehydrogenase-subunits. The variants reported here have not previously been described in connection with asthma. Although further studies in other cohorts are needed to confirm these findings our study highlights the importance of the mitochondria among the factors that contribute to the risk of asthma. [Copyright &y& Elsevier]

Background Hyperpolarised ³He MRI provides a way to visualise regional pulmonary functional abnormalities that in asthma are thought to be related to airway morphological abnormalities. However, the exact aetiology of ventilation defects in asthma is not well understood. Objective To better understand the determinants of ventilation defects in asthma, we evaluated wellestablished clinical as well as ³He MRI and X-ray CT airway measurements in healthy subjects and subjects with asthma. Methods Thirty-four subjects (n=26 subjects with asthma, n=8 healthy volunteers) underwent MRI, spirometry, plethysmography, fraction of exhaled nitric oxide analysis, methacholine challenge and CT for a region-of-interest proximal to ventilation defects. For subjects who consented to CT (n=18 subjects with asthma, n=5 healthy volunteers), we evaluated 3rd to 5th generation airway wall area and wall thickness per cent and lumen area. Results Seventeen subjects with asthma (17/26=65%) had visually obvious evidence of ³He ventilation defects prior to bronchoprovocation and nine subjects with asthma had no ventilation defects prior to bronchoprovocation (9/26=35%). Subjects with asthma with defects were older (p=0.01) with worse forced expiratory volume in 1 s (FEV1)/forced vital capacity (p=0.0003), airways resistance (p=0.004), fraction of exhaled nitric oxide (p=0.03), greater bronchoprovocation concentration of methacholine that reduced FEV1 by 20% ( p=0.008) and wall thickness per cent (p=0.02) compared with subjects with asthma without defects. There was a moderate correlation for wall area per cent with ventilation defect per cent (r=0.43, p=0.04). Conclusions Subjects with asthma with ³He ventilation defects were older with significantly worse airway hyperresponsiveness, inflammation and airway remodelling but similar FEV1 as subjects with asthma without defects; hyperpolarised ³He ventilation abnormalities were spatially and quantitatively related to abnormally remodelled airways. [ABSTRACT FROM AUTHOR]

In the majority of cases, asthma and chronic obstructive pulmonary disease (COPD) are two clearly distinct disease entities. However, in some patients there may be significant overlap between the two conditions. This constitutes an important area of concern because these patients are generally excluded from randomised controlled trials (mostly because of smoking history in the case of asthma or because of significant bronchodilator reversibility in the case of COPD). As a result, their pathobiology, prognosis and response to therapy are largely unknown. This may lead to suboptimal management and can limit the development of more personalised therapeutic options. Emerging genetic and molecular information coupled with new bioinformatics capabilities provide novel information that can pave the way towards a new taxonomy of airway diseases. In this paper we question the current value of the terms 'asthma' and 'COPD' as still useful diagnostic labels; discuss the scientific and clinical progress made over the past few years towards unravelling the complexity of airway diseases, from the definition of clinical phenotypes and endotypes to a better understanding of cellular and molecular networks as key pathogenic elements of human diseases (so-called systems medicine); and summarise a number of ongoing studies with the potential to move the field towards a new taxonomy of airways diseases and, hopefully, a more personalised approach to medicine, in which the focus will shift from the current goal of treating diseases as best as possible to the so-called P4 medicine, a new type of medicine that is predictive, preventive, personalised and participatory. [ABSTRACT FROM AUTHOR]

: In a systematic review and meta-analysis, Jasper Been and colleagues investigate the association between preterm birth and the development of wheezing disorders in childhood. Please see later in the article for the Editors' Summary [ABSTRACT FROM AUTHOR]

Background: Cockroach (CR) allergens frequently cause severe asthma in CR-sensitized subjects. Allergen-specific immunotherapy causes a shift of allergic Th2 responses towards Th1 and/or regulatory T cell (Treg) responses which reduce airway inflammation and prevent disease progression. Data are relatively limited on immunotherapy via CR allergy vaccine. Methods: The therapeutic efficacy of an intranasal liposome-adjuvant vaccine made of a refined Periplaneta americana arginine kinase (AK) was compared to the liposome-entrapped P. americana crude extract (CRE) vaccine. Adult BALB/c mice were rendered allergic to CRE. Three allergic mouse groups were immunized intranasally on alternate days with 8 doses of liposome-entrapped CRE (L-CRE), liposome-entrapped AK and placebo, respectively. One week later, all mice received a nebulized CRE provocation. Evaluation of vaccine efficacy was performed 1 day after provocation. Results: Liposome-entrapped native AK attenuated airway inflammation after the CRE provocation and caused a shift of allergic Th2 to Th1 and Treg responses. The L-CRE also induced a shift from the Th2 to the Th1 response but did not induce a Treg response and could not attenuate the airway inflammation upon allergen reexposure. Conclusions: Intranasal liposome-adjuvant CR allergy vaccine containing native AK (Per a 9) is better than L-CRE in attenuating allergic airway inflammation. The findings of this study not only document a more comprehensive and beneficial immune response induced by the refined allergen vaccine but also raise the point that the shift from the Th2 to the Th1 response alone might not correlate with improved airway histopathology, clinical outcome and quality of life. Copyright © 2013 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Abstract: Methylene diphenyl diisocyanate (MDI), a low molecular weight chemical important for producing polyurethane foam, coatings, and elastomers is a major cause of occupational asthma, however, mechanisms of disease pathogenesis remain poorly understood. This study characterizes the rearranged germline and hypervariable region cDNA of new anti-MDI secreting hybridomas derived from mice immunized with MDI-conjugated to autologous serum proteins. Six IgG1 secreting clones were identified in initial screening ELISAs, based on differential binding to MDI conjugated human albumin vs. mock exposed albumin. The mAbs secreted by the hybridomas also recognized MDI conjugated to other model proteins (e.g. ovalbumin, transferrin), but did not bind unconjugated proteins, or protein conjugates prepared with other isocyanates (e.g. TDI, HDI). The mAbs displayed MDI-dose dependent binding in ELISA and Western blot, and exhibited varying degrees of cross-competition, suggesting differences in epitope specificity. The cDNA encoding the monoclonal antibodies reveal clonal differences in the CDR3 regions, germline gene usage, and patterns of somatic hypermutation related to epitope specificity. Together, the data provide new insight into the molecular determinants of humoral MDI specificity, and characterize anti-MDI IgG1 mAbs that may be developed into useful diagnostic reagents. [Copyright &y& Elsevier]

Atopic asthma is a chronic inflammatory disease of the lungs generally marked by excessive Th2 inflammation. The role of allergen-specific IgG in asthma is still controversial; however, a receptor of IgG-immune complexes (IgG-ICs), FcγRIII, has been shown to promote Th2 responses through an unknown mechanism. Herein, we demonstrate that allergen-specific IgG-ICs, formed upon reexposure to allergen, promoted Th2 responses in two different models of IC-mediated inflammation that were independent of a preformed T cell memory response. Development of Th2-type airway inflammation was shown to be both FcγRIII and TLR4 dependent, and T cells were necessary and sufficient for this process to occur, even in the absence of type 2 innate lymphoid cells. We sought to identify downstream targets of FcγRIII signaling that could contribute to this process and demonstrated that bone marrow-derived DCs, alveolar macrophages, and respiratory DCs significantly upregulated IL-33 when activated through FcγRIII and TLR4. Importantly, IC-induced Th2 inflammation was dependent on the ST2/IL-33 pathway. Our results suggest that allergen-specific IgG can enhance secondary responses by ligating FcγRIII on antigen-presenting cells to augment development of Th2- mediated responses in the lungs via an IL-33-dependent mechanism. [ABSTRACT FROM AUTHOR]

Increased airway smooth muscle (ASM) contractility and the development of airway hyperresponsiveness (AHR) are cardinal features of asthma, but the signaling pathways that promote these changes are poorly understood. Tyrosine phosphorylation is tightly regulated by the opposing actions of protein tyrosine kinases and phosphatases, but little is known about whether tyrosine phosphatases influence AHR. Here, we demonstrate that genetic inactivation of receptor-like protein tyrosine phosphatase J (Ptprj), which encodes CD148, protected mice from the development of increased AHR in two different asthma models. Surprisingly, CD148 deficiency minimally affected the inflammatory response to allergen, but significantly altered baseline pulmonary resistance. Mice specifically lacking CD148 in smooth muscle had decreased AHR, and the frequency of calcium oscillations in CD148-deficient ASM was substantially attenuated, suggesting that signaling pathway alterations may underlie ASM contractility. Biochemical analysis of CD148-deficient ASM revealed hyperphosphorylation of the C-terminal inhibitory tyrosine of SRC family kinases (SFKs), implicating CD148 as a critical positive regulator of SFK signaling in ASM. The effect of CD148 deficiency on ASM contractility could be mimicked by treatment of both mouse trachea and human bronchi with specific SFK inhibitors. Our studies identify CD148 and the SFKs it regulates in ASM as potential targets for the treatment of AHR. [ABSTRACT FROM AUTHOR]

Asthma is a public health problem; in Mexico asthma is included among the ten causes of hospital and medical care. Exacerbations of asthma (asthma attacks or acute asthma) are episodes of progressive increase in shortness of breath, coughing, wheezing, tightness in the chest, or a combination of these symptoms. It has been identified airway infections, as the major etiology of exacerbations. Microbiological study of the sputum of the 90 patients included in this study was performed. The results showed that pathogenic microorganisms associated to asthma exacerbations were isolated in almost 50% of the samples analyzed, the pathogens isolated were bacterias followed by virus. In contrast to previous studies, in this study bacterias were isolated in higher proportion than virus. However, we are not able to conclude that bacterias or virus infections are responsible of the exacerbations, because it was not possible to found a strong association between the severity of the crisis and the presence of some pathogens. [ABSTRACT FROM AUTHOR]

Introduction: Humidity is commonly associated with increased airway hyperresponsiveness in asthma. Objective: To examine mold sensitization in patients with allergic asthma or allergic rhinitis and self-reports of humidity as exacerbating factors of clinical symptoms. Methods: A retrospective, cross-sectional study at a University hospital outpatient allergy and asthma clinic was performed. A total of 106 patients with either allergic asthma or allergic rhinitis completed standard prick-puncture skin testing with 17 allergens and controls and completed standardized forms addressing trigger factors for clinical symptoms. Results: Allergic asthmatics sensitized to Cladosporium were more likely to have a more severe asthma severity class (odds ratio = 4.26, confidence interval = 1.30-16.93). Sensitization to Alternaria, Cladosporium, Helminthosporium, Aspergillus and Dermatophagoides pteronyssinus in asthma was associated with higher likelihood for previous hospitalization, while sensitization to Cladosporium, Helminthosporium, Aspergillus, Dermatophagoides pteronyssinus and cockroach in asthma was associated with higher likelihood of having reduced pulmonary function based on forced expiratory volume in 1 s. Furthermore, allergic asthmatics more commonly reported humidity as an exacerbating factor of symptoms than did patients only with allergic rhinitis (68.42% vs 42.86%, respectively; P < 0.05). Conclusion: Mold sensitization is highly associated with more severe asthma, while humidity is more of an exacerbating factor in patients with allergic asthma as compared with allergic rhinitis alone. Further delineation between mold sensitization and humidity is needed to determine whether these are independent factors in asthma. Please cite this paper as: Hayes D Jr, Jhaveri MA, Mannino DM, Strawbridge H and Temprano J. The effect of mold sensitization and humidity upon allergic asthma. Clin Respir J 2013; 7: 135-144. [ABSTRACT FROM AUTHOR]

Thunderstorm asthma is a term used to describe an observed increase in acute bronchospasm cases following the occurrence of thunderstorms in the local vicinity. The roles of accompanying meteorological features and aeroallergens, such as pollen grains and fungal spores, have been studied in an effort to explain why thunderstorm asthma does not accompany all thunderstorms. Despite published evidence being limited and highly variable in quality due to thunderstorm asthma being a rare event, this article reviews this evidence in relation to the role of aeroallergens, meteorological features and the impact of thunderstorm asthma on health services. This review has found that several thunderstorm asthma events have had significant impacts on individuals’ health and health services with a range of different aeroallergens identified. This review also makes recommendations for future public health advice relating to thunderstorm asthma on the basis of this identified evidence. [ABSTRACT FROM AUTHOR]

Abstract: Background: The Saudi national asthma protocol (SNAP) for asthma management was released in 1995 in an attempt to streamline asthma management practices in Saudi Arabia and improve the quality of care for asthma. Up to our knowledge, few studies assessed the adherence of Saudi physicians to the national asthma guidelines. Objectives: The objective of this present study was to assess the level of adherence of pediatricians and primary care physicians (PCPs) to the current SNAP recommendations and identify barriers to physician adherence. Methodology: This is a cross-sectional study involving pediatricians and PCPs selected randomly from five major governmental hospitals in Riyadh, Saudi Arabia. Subjects were administered a self-administered questionnaire comprising 24 questions assessing their awareness of SNAP and their level of adherence to the recommendations. Results: The response rate was 38% (80/206). Out of most of the physicians who responded, 70% (56) were aware of SNAP, and only 78.2% (n =43) of them had modified their management of asthmatic patients according to the SNAP recommendations. The level of knowledge of the pharmacotherapy and diagnostic parts of the guidelines ranged between 41.5% and 90.7% in the pharmacotherapy part, and 53.7–59.6% in the diagnostic part. The most common barriers to adherence to SNAP were lack of awareness (25.2%), patient non- compliance (18.9%) and lack of resources (13.5%). There was no significant difference in awareness between pediatricians and PCPs (69.2%, 70.7% respectively). Conclusion: This study reveals a substantial gap between the actual care provided by pediatricians and PCPs to asthmatic patients and the recommendations formulated in the Saudi National Asthma Protocol (SNAP). Lack of awareness remains the most common barrier for adherence to the guidelines followed by patient non-compliance. To improve SNAP guideline adherence, tailored interventions that address barriers to adherence need to be implemented. [Copyright &y& Elsevier]

Abstract: The etiology of status asthmaticus (SA), a complication of severe asthma, is unknown. Fungal exposure, as measured by fungal atopy, is a major risk factor for developing asthma, but the relationship of fungi in SA per se has not previously been reported. In this five patient retrospective case series study, lower respiratory tract cultures were performed on bronchoalveolar lavage or tracheal aspirate fluid, comparing standard clinical laboratory cultures with a specialized technique in which respiratory mucus was removed prior to culture. We show that mucolytic treatment allows an increased detection of fungal growth, especially yeast, from the lower airways of all SA patients. We also demonstrate that inhalation of the yeast Candida albicans readily induces asthma-like disease in mice. Our observations suggest that SA may represent a fungal infectious process, and support additional prospective studies utilizing anti-fungal therapy to supplement conventional therapy, broad-spectrum antibiotics and high-dose glucocorticoids, which can promote fungal overgrowth. [Copyright &y& Elsevier]

Background: Toxocara canis and T. cati are parasites of dogs and cats, respectively, that infect humans and cause human toxocariasis. Infection may cause asthma-like symptoms but is often asymptomatic and is associated with a marked eosinophilia. Previous epidemiological studies indicate that T. canis infection may be associated with the development of atopy and asthma. Objectives: To investigate possible associations between Toxocara spp. seropositivity and atopy and childhood wheezing in a population of children living in non-affluent areas of a large Latin American city. Methods: The study was conducted in the city of Salvador, Brazil. Data on wheezing symptoms were collected by questionnaire, and atopy was measured by the presence of aeroallergen-specific IgE (sIgE). Skin prick test (SPT), total IgE and peripheral eosinophilia were measured. Toxocara seropositivity was determined by the presence of anti-Toxocara IgG antibodies, and intestinal helminth infections were determined by stool microscopy. Findings: Children aged 4 to 11 years were studied, of whom 47% were seropositive for anti-Toxocara IgG; eosinophilia >4% occurred in 74.2% and >10% in 25.4%; 59.6% had elevated levels of total IgE; 36.8% had sIgE≥0.70 kU/L and 30.4% had SPT for at least one aeroallergen; 22.4% had current wheezing symptoms. Anti-Toxocara IgG was positively associated with elevated eosinophils counts, total IgE and the presence of specific IgE to aeroallergens but was inversely associated with skin prick test reactivity. Conclusion: The prevalence of Toxocara seropositivity was high in the studied population of children living in conditions of poverty in urban Brazil. Toxocara infection, although associated with total IgE, sIgE and eosinophilia, may prevent the development of skin hypersensitivity to aeroallergens, possibly through increased polyclonal IgE and the induction of a modified Th2 immune reaction. [ABSTRACT FROM AUTHOR]

Adherence in asthma is an important cause for concern. Although nearly 50% of asthma patients are considered poorly adherent to therapeutic advices, adherence is still difficult to assess, understand and improve despite major medical consequences. In this review, we revisited the literature of the last 10 years related to adherence in severe asthma. The concepts have changed and 'compliance' is usually replaced by 'adherence'. Assessment of adherence is addressing ethical issues, but provides important insight into difficult-to-treat asthma. Different tools have been used but none is routinely recommended. Health-related outcomes (poor control, exacerbations, hospitalizations, lung function decline), which are clearly associated with severe asthma, are often worsened by non-adherence with consequences also on patient related outcomes (quality of life). The potential behaviour associated with non-adherence and all other related factors including easy-to-recognize psychological traits can help for patient's future management. Therapeutic educational interventions have been recognized with a scientifically proven efficiency even though evolution and improvements are needed. A multidisciplinary approach is required in severe asthma. Therapeutic adherence for a given patient is always a prerequisite to any other aspects when addressing severe asthma phenotypes. Severe asthma should be considered only in those who still experienced poor asthma outcomes despite optimal adherence. At a glance, poor adherence and severe asthma should be considered antinomic. Better understanding of the causes and customised management are potential future directions. [ABSTRACT FROM AUTHOR]

Objective. Many fungi may cause allergic reactions and increase asthma symptoms prevalence and severity. One susceptible, vulnerable population subgroup of increasing size in industrialized countries and of public health concern who spends the majority of their time at home is older adults. Older adults diagnosed with chronic obstructive pulmonary disease (COPD) are at risk of exposure to fungi. Currently, species identification is based on observation of microscopic and macroscopic morphologies, which may underestimate concentrations compared to quantitative polymerase chain reaction (qPCR)-based measurements which are toxicologically more relevant to exposure science. Methods. This article analyzes quantitative indoor exposure data on fungi in floor dust (cells/cm2 floor) by real-time qPCR-based detection with quantitative outcome data via field spirometry in a pilot community-based study in Visalia, Tulare County, California, between July 2009 and January 2010. Subjects ( n = 9, five females, four males) were Caucasian, English-speaking, nonsmoking older adults with doctor-diagnosed asthma and/or COPD. Results. While certain results did not reach statistical significance ( p ≤ .10) due to sample size-overall and by gender-we found consistent trends and statistically significant associations for total fungal DNA (summer data) with forced vital capacity and forced expiratory volume in 1 second. Conclusions. The results of this pilot study are novel and suggest adverse effects of exposure inside homes to certain fungal species. This pilot study supports the need for larger prospective epidemiologic studies of older adults with asthma and/or chronic bronchitis based on quantitative environmental and clinical measures. [ABSTRACT FROM AUTHOR]

It has been pointed out that obesity is a risk factor for, and is involved in the exacerbation of asthma. Mounting evidence about adipose tissue-derived proteins (adipokines) gave rise to the current understanding of obesity as a systemic inflammatory disorder. In this review, we summarized the involvement of leptin, focusing on eosinophil functions. Several studies have indicated that leptin can restrain eosinophil apoptosis, enhance migration, increase adhesion molecules and induce cytokine production. Since leptin also acts on a variety of immune cells related to allergic response, increased leptin in obese individuals potentially explains the mechanism by which obesity leads to an exacerbation of asthma. Further studies targeting adipokines will delineate the association between obesity and eosinophil-associated diseases. Copyright © 2012 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Abstract: A daily moisturizing routine is a vital part of the management of patients with atopic dermatitis and other dry skin conditions. The composition of the moisturizer determines whether the treatment strengthens or deteriorates the skin barrier function, which may have consequences for the outcome of the dermatitis. One might expect that a patient''s impaired skin barrier function should improve in association with a reduction in the clinical signs of dryness. Despite visible relief of the dryness symptoms, however, the abnormal transepidermal water loss has been reported to remain high, or even to increase under certain regimens, whereas other moisturizers improve skin barrier function. Differing outcomes have also been reported in healthy skin: some moisturizers produce deterioration in skin barrier function and others improve the skin. Possible targets for barrier-influencing moisturizing creams include the intercellular lipid bilayers, where the fraction of lipids forming a fluid phase might be changed due to compositional or organizational changes. Other targets are the projected size of the corneocytes or the thickness of the stratum corneum. Moisturizers with barrier-improving properties may delay relapse of dermatitis in patients with atopic dermatitis. In a worst-case scenario, treatment with moisturizing creams could increase the risks of dermatitis and asthma. [Copyright &y& Elsevier]

Asthma is a T lymphocyte-controlled disease of the airway wall caused by inflammation, overproduction of mucus and airway wall remodeling leading to bronchial hyperreactivity and airway obstruction. The airway epithelium is considered an essential controller of inflammatory, immune and regenerative responses to allergens, viruses and environmental pollutants that contribute to asthma pathogenesis. Epithelial cells express pattern recognition receptors that detect environmental stimuli and secrete endogenous danger signals, thereby activating dendritic cells and bridging innate and adaptive immunity. Improved understanding of the epithelium's function in maintaining the integrity of the airways and its dysfunction in asthma has provided important mechanistic insight into how asthma is initiated and perpetuated and could provide a framework by which to select new therapeutic strategies that prevent exacerbations and alter the natural course of the disease. [ABSTRACT FROM AUTHOR]

Background: Allergic asthma is characterized by reversible airway obstruction and bronchial hyperresponsiveness associated with TH2 cell–mediated inflammation. Cysteinyl leukotrienes (CysLTs) are potent lipid mediators involved in bronchoconstriction, mucus secretion, and cell trafficking in asthmatic patients. Recent data have implicated CysLTs in the establishment and amplification of TH2 responses in murine models, although the precise mechanisms are unresolved. Objectives: Preliminary microarray studies suggested that human TH2 cells might selectively express cysteinyl leukotriene receptor 1 (CYSLTR1) mRNA. We sought to establish whether human TH2 cells are indeed a CysLT target cell type. Methods: We examined the expression of CYSLTR1 using real-time PCR in human TH1 and TH2 cells. We functionally assessed cysteinyl leukotriene receptor 1 protein (CysLT1) expression using calcium flux, cyclic AMP, and chemotaxis assays. Results: We show that human TH2 cells selectively express CYSLTR1 mRNA at high levels compared with TH1 cells after in vitro differentiation from naive precursors. Human TH2 cells are selectively responsive to CysLTs in a calcium flux assay when compared with TH1 cells with a rank order of potency similar to that described for CysLT1 (leukotriene [LT] D4 > LTC4 > LTE4). We also show that LTD4-induced signaling in TH2 cells is mediated through CysLT1 coupled to Gαq and Gαi proteins, and both pathways can be completely inhibited by selective CysLT1 antagonists. LTD4 is also found to possess potent chemotactic activity for TH2 cells at low nanomolar concentrations. Conclusions: These findings suggest a novel mechanism of action for CysLTs in the pathogenesis of asthma and provide a potential explanation for the anti-inflammatory effects of CysLT1 antagonists. [ABSTRACT FROM AUTHOR]

Background: Asthma morbidity and mortality rates are high among young inner-city children. Lack of routine primary care provider visits, poor access to care, and poor patient-physician communication might be contributing factors. Objective: This study evaluated the effects of providing Breathmobile services only, a Facilitated Asthma Communication Intervention (FACI) only, or both Breathmobile plus FACI on asthma outcomes relative to standard care. Methods: Children with asthma (n = 322; mean age, 4 years; 53% male; 97% African American) were recruited from Head Start programs in Baltimore City and randomized into 4 groups. Outcome measures included symptom-free days (SFDs), urgent care use (emergency department visits and hospitalizations), and medication use (courses of oral steroids and proportion taking an asthma controller medication), as reported by caregivers at baseline, 6-month, and 12-month assessments. Generalized estimating equations models were conducted to examine the differential treatment effects of the Breathmobile and FACI compared with standard care. Results: Children in the combined treatment group (Breathmobile plus FACI) had an increase of 1.7 (6.6%) SFDs that was not maintained at 12 months. In intent-to-treat analyses the FACI-only group had an increase in the number of emergency department visits at 6 months, which was not present at 12 months or in the post hoc as-treated analyses. No significant differences were found between the intervention groups compared with those receiving standard care on all other outcome measures. Conclusions: Other than a slight improvement in SFDs at 6 months in the Breathmobile plus FACI group, the intervention components did not result in any significant improvements in asthma management or asthma morbidity. [ABSTRACT FROM AUTHOR]

Background: Laryngopharyngeal reflux (LPR) can cause atypical symptoms, asthma, and pulmonary fibrosis. The aim of this study was to establish the normative data for LPR using hypopharyngeal multichannel intraluminal impedance-pH (HMII). Methods: Asymptomatic subjects underwent endoscopy followed by 24-h HMII using a specialized impedance catheter configured to detect LPR before and after a 2-week course of proton pump inhibitors (PPI). Subjects were excluded if they had esophageal pathology or a positive DeMeester score. A cohort of 24 LPR patients who had a complete response to treatment was used for comparison with the normative data. Results: Forty subjects were enrolled. Thirty-four subjects completed one, and 25 completed both HMII testing periods off and on PPI. There was no difference in the total number of reflux events between off and on PPI [22 (8-32) and 24 (10-28), respectively, p = 0.89]. The 95th percentiles of LPR off and on PPI were 0 and 1, respectively. All patients with treatment responsive LPR had pre-treatment HMII values of LPR greater than the 95th percentile. Conclusion: LPR events are rare in an asymptomatic population. One or more LPR events should be considered abnormal in patients with LPR symptoms regardless of whether there is a positive DeMeester score. [ABSTRACT FROM AUTHOR]

Abstract: Bronchial asthma is a chronic disorder characterized by airway inflammation, reversible airway obstruction, and airway hyperresponsiveness. Eosinophils are believed to play important roles in the pathogenesis of asthma through the release of inflammatory mediators. In refractory eosinophilic asthma, anti-IL-5 mAb reduces exacerbations and steroid dose, indicating roles of eosinophils and IL-5 in the development of severe eosinophilic asthma. Even in the absence of IL-5, it is likely that the “Th2 network”, including a cascade of vascular cell adhesion molecule-1/CC chemokines/GM-CSF, can sufficiently maintain eosinophilic infiltration and degranulation. Cysteinyl leukotrienes can also directly provoke eosinophilic infiltration and activation in the airways of asthma. Therefore, various mechanisms would be involved in the eosinophilic airway inflammation of asthma. In the pathogenesis of severe asthma, not only eosinophils but also mast cells or neutrophils play important roles. Mast cells are much infiltrated to smooth muscle in severe asthma and induce airway remodeling by release of inflammatory mediators such as amphiregulin. Treatment with anti-IgE Ab, which neutralizes circulating IgE and suppresses mast cell functions, reduces asthma exacerbations in severe asthmatic patients. Furthermore, infiltration of neutrophils in the airway is also increased in severe asthma. IL-8 plays an important role in the accumulation of neutrophils and is indeed upregulated in severe asthma. In the absence of chemoattractant for eosinophils, neutrophils stimulated by IL-8 augment the trans-basement membrane migration of eosinophils, suggesting that IL-8-stimulated neutrophils could lead eosinophils to accumulate in the airways of asthma. In view of these mechanisms, an effective strategy for controlling asthma, especially severe asthma, should be considered. [Copyright &y& Elsevier]

The glutathione S-transferases (GST) represent a superfamily of enzymes present in all aerobic organisms. There are three main families that are widely distributed in nature and are classified into cytosolic glutathione s transferases, mitochondrial and microsomal according to their location in the cell. Polymorphisms reported in the genes encoding these enzymes have been associated with the onset of diseases such as asthma under the influence of environmental contaminants. The frequency distribution of these polymorphisms is different in the populations and therefore the susceptibility of individuals to the diseases therefore the susceptibility of individuals to the diseases polymorphisms in GST and their relation with the respiratory diseases, we present a theoretical review updates on the properties and functions of glutathione S transferases, description of genetic polymorphisms and methodologies used for genotyping, as well as their participation in the pathogenesis of asthma. [ABSTRACT FROM AUTHOR]

Background: Experimental data suggest that asthma exacerbation by allergens is enhanced by exposure to environmental tobacco smoke (ETS); however, there is little supporting epidemiologic evidence. To our knowledge, few studies have assessed respiratory symptoms and allergies in this context. Objectives: To evaluate whether the association of exposure to animals (indicators of allergen and endotoxin exposure) with asthma-related symptoms is modified by ETS exposure in Chinese children. Methods: A cross-sectional study of 8,819 children in kindergarten was conducted in 25 districts in northern China. Information on respiratory health and exposure to indoor allergens was obtained using a standard questionnaire from the American Thoracic Society. Results: Among the children with ETS exposure in utero, the effects of exposure to animals were significant with respect to persistent cough [adjusted odds ratio (OR) 1.83; 95% confidence interval (CI) 1.12-2.99] and persistent phlegm (adjusted OR 2.40; 95% CI 1.28-4.54). The combined effect of in utero ETS exposure and animal exposure on doctor-diagnosed asthma was approximately as expected on the basis of their independent effects on an additive scale. There was no interaction between animal exposure and ETS exposure in the first 2 years of life or current ETS exposure. Conclusions: This study provides evidence that animal and ETS exposure increases the risk of asthma-related symptoms in children in kindergarten. ETS exposure in utero did modify the effect of animal exposure on persistent phlegm and persistent cough but not on doctor-diagnosed asthma among children. Copyright © 2010 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

2010 found a number of significant advances in environmental and occupational respiratory disease. The role of sensitization and the subsequent production of allergic disease have been explored. New allergens and their T- and B-cell epitopes have been characterized. Novel approaches to the diagnosis and evaluation of food allergy have been described. The role of pollutants as they affect respiratory disease and the effects of age extremes on sensitization and asthma have been addressed. Significant advances in the understanding of inflammatory changes in both the upper and lower respiratory systems occurred. Novel therapeutic approaches have been explored, including the development of hypoallergens from improved molecular biology techniques. New effective approaches to asthma therapy have been identified. Exposure reduction through air filtration and novel immunotherapy approaches, such as sublingual therapy, have made significant advances. [ABSTRACT FROM AUTHOR]

Patients with type 1 diabetes (a TH1 disease) have been reported to be at a lower risk of developing asthma (a TH2 disease). Both diseases are affected by environmental and genetic factors. Our objective is to examine this relationship in Lebanon, a Middle-Eastern country, where no previous similar studies are available. This is a cross-sectional observational study conducted at the Chronic Care Center, a referral medical center for type 1 diabetics. Patients with type 1 diabetes aged 6-39 years old, their unaffected siblings and age-matched control completed the International Primary Care Airways Group asthma screening questionnaire. The prevalence of asthma symptoms was compared among the three groups and separately within a subgroup of diabetics in relation to their carrier state of previously collected genetic data. Among 305 diabetics, 776 siblings and 187 controls, diabetics were at lower risk of having any asthma symptoms than controls; OR 0.48 (95% CI 0.32-0.72, p < 0.001) and siblings were at lower risk than diabetics and controls; OR 0.64 (95% CI 0.45-0.91, p = 0.01) and 0.28 (95% CI 0.19-0.42, p < 0.001), respectively. Among 66 diabetics, carriers of the HLA-DQB1*0201 allele were at lower risk of having any asthma symptoms than non-carriers (25.5 vs. 53.3%, p = 0.04). Only a statistically non-significant trend of higher risk was observed in carriers of HLA-DQB1*0301 and G allele at the 49 (A/G) nucleotide of CTLA-4 gene. The TH1-TH2 paradigm might partially explain these findings, since siblings were the least to report asthma symptoms. Future research is needed with diagnostic tests for asthma and extensive genetic testing. [ABSTRACT FROM AUTHOR]

Allergy to rodents in the workplace is an important occupational health problem affecting research, pharmaceutical and toxicological sectors and can have a serious impact on employees working in this area. Despite measures to reduce aeroallergen exposures to rodents in the workplace, there are few signs that this occupational health problem is declining. Rodent allergens are well characterized and exposure-response relationships have been demonstrated to be complex. More recently, the importance of rodent allergens outside of the workplace has been demonstrated in several studies of individuals with asthma. This review focuses on rodent allergy both in the workplace and in the home and examines the complex exposure-response relationships between allergen exposure and sensitization and asthma. Risk factors for rodent allergy and mechanisms of tolerance to rodent allergens are discussed. Cite this as: H. Jeal and M. Jones, Clinical & Experimental Allergy, 2010 (40) 1593-1601. [ABSTRACT FROM AUTHOR]

Objectives: To determine the effect on patients' quality of life of functional endoscopic sinus surgery performed for chronic rhinosinusitis within a tertiary care centre in Montreal, Canada. Methods: A prospective cohort study was undertaken. Subjects were consecutive patients with a diagnosis of chronic rhinosinusitis who had failed medical treatment and were undergoing functional endoscopic sinus surgery. Questionnaires assessing general health outcomes (i.e. the second version of the Short Form 12 questionnaire) and disease-specific outcomes (i.e. the Chronic Sinusitis Survey) were completed pre-operatively and a minimum of three months post-operatively. Results: A total of 152 patients were enrolled over a seven-month period, of whom 120 completed the post-operative surveys. The most common co-morbidity was asthma (40 per cent). Of the 120 patients with completed questionnaires, 72 per cent reported clinical improvement, 12 per cent reported deterioration and 15 per cent remained unchanged. The average improvement in Chronic Sinusitis Survey score was 17 per cent. Conclusion: Patients with chronic rhinosinusitis achieved a significant improvement in disease-specific quality of life after functional endoscopic sinus surgery. There was no significant improvement in general health related quality of life, as measured using the Short Form 12 questionnaire. [ABSTRACT FROM AUTHOR]

Background The role in allergic asthma development of the immune response against fungi with concomitant exposure to other common aeroallergens has yet to be determined. In particular, there is little understanding of how inhaled fungi affect the host response to mite allergens. Objective To characterize the in vitro and in vivo effects of concurrent exposure of Aspergillus fumigatus ( Af) and Dermatophagoides farinae ( Derf) on dendritic cells (DCs) in the development of allergic asthma. Methods Murine bone marrow-derived DCs were pulsed with Derf and/or live or heat-inactivated Af. Cytokine production and the expression of pathogen recognition receptors (PRRs) were determined in vitro. Subsequently, these DCs were inoculated into the airway of naïve mice to assess the development of allergic airway inflammation in vivo. The effect of antibodies against PRRs was also evaluated. Results Live Af significantly enhanced IL-10 production and the expression of Toll-like receptor (TLR) 2 and Dectin-1 in Derf-pulsed DCs. Live Af infection significantly attenuated Derf-pulsed DC-induced allergic airway inflammation in vivo. Antibodies against either TLR2 or Dectin-1 significantly reversed the inhibitory effects of live Af in the development of Derf-pulsed DC-induced allergic airway inflammation. Conclusion Concurrent exposure of DCs to fungal antigens has profound influences on the subsequent mite allergen-induced allergic airway inflammation. Live Af could regulate the functions of airway DCs in the development of mite allergen-induced allergic airway inflammation via regulation of their PRRs. Our results suggest that concurrent exposure to pathogens such as fungi and mite allergens has profound influences on the subsequent allergen-induced allergic airway inflammation. Furthermore, modulating PRR signalling could provide a therapeutic regimen for the development of asthma. Cite this as: S. Fukahori, H. Matsuse, T. Tsuchida, T. Kawano, S. Tomari, C. Fukushima and S. Kohno, Clinical & Experimental Allergy, 2010 (40) 1507–1515. [ABSTRACT FROM AUTHOR]

This article offers information on occupational asthma. It notes the prevalence of occupational asthma in westernised industrial countries. Included is a list of occupations commonly reported as leading to occupational asthma. Particular focus is given to the pathophysiology of the condition. It cites rhinitis and nocturnal cough as the first symptoms of the condition during its early stages. Also included are information on the Control of Substances Hazardous to Health Regulations in Great Britain.

Abstract: It has been suggested that one possible contributor to the increasing prevalence of atopic (IgE-mediated) allergic diseases and asthma in Europe and the US is exposure to chemicals that may act as adjuvants. Certain commonly used phthalate plasticisers, such as di-(2-ethylhexyl) phthalate, have been implicated in this regard. The evidence for the ability of phthalates to impact on immune and allergic responses has been examined, encompassing epidemiological investigations and results deriving from studies using experimental animals and from analyses in vitro. The epidemiological data provide some evidence that exposure to phthalates may be associated with increased risk of development of allergies and asthma, however, the lack of objective exposure information limits the interpretation. A variety of studies have been performed in mice to examine the influence of phthalate (delivered via various routes of exposure) to impact on immune responses. Measurement of antibody responses is the commonest read out, although other parameters of inflammation such as eosinophil infiltration and cytokine production have been used also. Although certain phthalates, when delivered at appropriate doses, and via an appropriate route, have been reported to impact on immune and inflammatory function in rodents, as yet no consistent pattern has emerged. Results ranged from potentiation of immune or inflammatory responses, to the absence of any effect, to inhibitory or immunosuppressive activity. In addition, comparatively low doses of phthalates have been associated with immune effects only when routes of administration (subcutaneous or intraperitoneal) are used that do not reflect, and are much less relevant for, opportunities for human contact with phthalates. There is clearly a case to be made for the design of more definitive animal studies that will allow development of a more detailed understanding of whether and to what extent, and under what conditions, phthalates are able to effect meaningful changes in immune function that may in turn impact on human health. [Copyright &y& Elsevier]

Abstract: Low income, multi-ethnic communities in Main South/Piedmont neighborhoods of Worcester, Massachusetts are exposed to cumulative, chronic built-environment stressors, and have limited capacity to respond, magnifying their vulnerability to adverse health outcomes. “Neighborhood STRENGTH”, our community-based participatory research (CBPR) project, comprised four partners: a youth center; an environmental non-profit; a community-based health center; and a university. Unlike most CBPR projects that are single topic-focused, our ‘holistic’, systems-based project targeted five priorities. The three research-focused/action-oriented components were: (1) participatory monitoring of indoor and outdoor pollution; (2) learning about health needs and concerns of residents through community-based listening sessions; (3) engaging in collaborative survey work, including a household vulnerability survey and an asthma prevalence survey for schoolchildren. The two action-focused/research-informed components were: (4) tackling persistent street trash and illegal dumping strategically; and (5) educating and empowering youth to promote environmental justice. We used a coupled CBPR-capacity building approach to design, vulnerability theory to frame, and mixed methods: quantitative environmental testing and qualitative surveys. Process and outcomes yielded important lessons: vulnerability theory helps frame issues holistically; having several topic-based projects yielded useful information, but was hard to manage and articulate to the public; access to, and engagement with, the target population was very difficult and would have benefited greatly from having representative residents who were paid at the partners’ table. Engagement with residents and conflict burden varied highly across components. Notwithstanding, we built enabling capacity, strengthened our understanding of vulnerability, and are able to share valuable experiential knowledge. [Copyright &y& Elsevier]

Background: Epidemiologic findings support a positive association between asthma and obesity. Objective: Determine whether obesity or increasing level of body mass index (BMI) are associated with worse asthma control in an ethnically diverse urban population. Methods: Cross-sectional assessment of asthma control was performed in patients with asthma recruited from primary care offices by using 4 different validated asthma control questionnaires: the Asthma Control and Communication Instrument (ACCI), the Asthma Control Test (ACT), the Asthma Control Questionnaire (ACQ), and the Asthma Therapy Assessment Questionnaire (ATAQ). Multiple linear regression analysis was performed to evaluate the association between obesity and increasing BMI level and asthma control. Results: Of 292 subjects with a mean age of 47 years, the majority were women (82%) and African American (67%). There was a high prevalence of obesity with 63%, with only 15% normal weight. The mean score from all 4 questionnaires showed an average suboptimal asthma control (mean score/maximum possible score): ACCI (8.3/19), ACT (15.4/ 25), ACQ (2.1/ 6), and ATAQ (1.3/ 4). Regression analysis showed no association between obesity or increasing BMI level and asthma control using all 4 questionnaires. This finding persisted even after adjusting for FEV1, smoking status, race, sex, selected comorbid illnesses, and long-term asthma controller use. Conclusion: Using 4 validated asthma control questionnaires, we failed to find an association between obesity and asthma control in an urban population with asthma. Weight loss may not be an appropriate strategy to improve asthma control in this population. [Copyright &y& Elsevier]

BACKGROUND: Epidemiological studies suggest that dietary intake of vitamins A, C and E may be associated with the occurrence of asthma. A systematic review and meta-analysis was conducted in accordance with MOOSE guidelines to determine whether vitamins A, C and E, measured as dietary intakes or serum levels, are associated with asthma. METHODS: MEDLINE, EMBASE, CINAHL, CAB abstracts and AMED (up to November 2007), conference proceedings and bibliographies of papers were searched to identify studies of asthma, wheeze or airway responsiveness in relation to intakes and serum concentrations of vitamins A, C and E. Pooled odds ratios (OR) or mean differences (MD) with 95% confidence intervals (CI) were estimated using random effects models. RESULTS: A total of 40 studies were included. Dietary vitamin A intake was significantly lower in people with asthma than in those without asthma (MD –182 µg/day, 95% CI –288 to –75; 3 studies) and in people with severe asthma than in those with mild asthma (MD –344 µg/day; 2 studies). Lower quantile dietary intakes (OR 1.12, 95% CI 1.04 to 1.21; 9 studies) and serum levels of vitamin C were also associated with an increased odds of asthma. Vitamin E intake was generally unrelated to asthma status but was significantly lower in severe asthma than in mild asthma (MD –1.20 µg/day, 95% CI –2.3 to –0.1; 2 studies). CONCLUSIONS: Relatively low dietary intakes of vitamins A and C are associated with statistically significant increased odds of asthma and wheeze. Vitamin E intake does not appear to be related to asthma status. [ABSTRACT FROM AUTHOR]

Bakers are frequently exposed to various irritant chemicals during work which can induce respiratory problems. In this study, pulmonary function tests and self-reported respiratory and allergic symptoms in bakers were compared with matched control subjects. The frequency of respiratory and allergic symptoms was evaluated in a sample of 58 Iranian bakers and 58 control subjects using a questionnaire. Pulmonary function tests (PFT) were also measured in all participants. All respiratory symptoms were significantly higher in bakers than control croup (p<0.05 to p<0.005). All allergic symptoms in bakers were also significantly greater than control group (p<0.05 to p<0.005). In addition, all respiratory (except sputum) and allergic (except urticaria) symptoms were significantly higher in bakers compared to rest period (p<0.05 to p<0.01) during work. Most PFT values except MEF25 were also significantly lower in bakers than control subjects (p<0.05 to p<0.001). These results showed that bakers have a higher frequency of work related respiratory symptoms and to a lesser extend allergic symptoms particularly during the work period. PFT values were also significantly reduced among bakers. [ABSTRACT FROM AUTHOR]

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Background: Asthma-associated morbidity is rising, especially in inner city children. Objective: We evaluated the allergen sensitivities, allergen exposures, and associated morbidity for participants in the Inner City Asthma Study. We also determined geographic variations of indoor allergen levels. Methods: Nine hundred thirty-seven inner city children 5 to 11 years old with moderate to severe asthma underwent allergen skin testing. Bedroom dust samples were evaluated for Der p 1, Der f 1, Bla g 1, Fel d 1, and Can f 1. Results: Skin test sensitivities to cockroach (69%), dust mites (62%), and molds (50%) predominated, with marked study site–specific differences. Cockroach sensitivity was highest in the Bronx, New York, and Dallas (81.2%, 78.7%, and 78.5%, respectively), and dust mite sensitivity was highest in Dallas and Seattle (83.7% and 78.0%, respectively). A majority of homes in Chicago, New York, and the Bronx had cockroach allergen levels greater than 2 U/g, and a majority of those in Dallas and Seattle had dust mite allergen levels greater than 2 μg/g. Levels of both of these allergens were influenced by housing type. Cockroach allergen levels were highest in high-rise apartments, whereas dust mite allergen levels were highest in detached homes. Children who were both sensitive and exposed to cockroach allergen had significantly more asthma symptom days, more caretaker interrupted sleep, and more school days missed than children who were not sensitive or exposed. Conclusion: Geographic differences in allergen exposure and sensitivity exist among inner city children. Cockroach exposure and sensitivity predominate in the Northeast, whereas dust mite exposure and sensitivity are highest in the South and Northwest. Cockroach allergen appears to have a greater effect on asthma morbidity than dust mite or pet allergen in these children. [ABSTRACT FROM AUTHOR]

A letter to the editor regarding clinical pharmacology study of formoterol fumarate dry powder inhalers and inhaled beclometasone dipropionate in asthmatic adolescents is presented.