Does the social environment contribute to asthma?

The impact of the social environment on asthma has recently begun to receive increasing attention. This article reviews the current literature to investigate the impact of the social environment at three levels-the neighborhood level, the peer level, and the family level-and to explore pathways through which the social environment "gets under the skin" to impact asthma onset and morbidity. Research to date suggests that adverse social conditions at the neighborhood and family levels impact asthma morbidity through direct effects on physiologic systems as well as by altering health behaviors. The impact on asthma of social networks, such as friendships, is less clear and will need to be investigated further. Future research will need to take into account the impact of the social environment to develop more comprehensive models of asthma pathogenesis.     

Obesity and asthma, what are the links?

PURPOSE OF REVIEW: Obesity is a major cause of morbidity accounting for approximately 300 000 deaths each year and about 7% of the health care budget with an economic impact greater than US dollar 100 billion annually in the United States. Obesity and its sequelae such as cardiovascular disease, diabetes, arthritis or cancer have been on the rise over the last decades. The parallel time trend with an increasing prevalence of asthma has induced a lively debate about a potential link between both conditions. RECENT FINDINGS: A number of prospective studies have shown that weight gain can antedate the development of asthma. Effect modification by sex may occur as some studies have shown effects of body mass index on asthma only among females. However, sex differences are not consistent. Several hypotheses have been proposed to explain the epidemiological associations including alterations in airway mechanics and immune responses, hormonal influences and genetic factors. SUMMARY: There is evidence that obesity and overweight are associated with the development of asthma. Yet, the mechanisms underlying this relation are unclear. Weight reduction among asthmatic patients can result in improvements of lung function demonstrating the potential clinical impact of the findings.     

Do vaccines modify the prevalence of asthma and allergies?

Epidemiological studies suggest the hypothesis that the increase in asthma and allergies in the industrialized world can be explained by a decline in the number of infectious diseases occurring during childhood. In the context of this 'hygiene hypothesis', is immunization in early life a risk factor for promoting allergic diseases? The majority of studies, especially those conducted with more extensive populations, have not found an increased risk, and although 'not finding an increased risk' is not the same as 'the non-existence of any risk at all', it seems that the evidence is tipped in favor of the absence of risk. Conversely, although some surveys have described a protective effect of vaccination, the majority refuted this result. If there is any effect, it is probably a weak one.     

Can inhaled corticosteroids influence the natural history of asthma?

PURPOSE OF REVIEW: Asthma is characterised by variable airflow obstruction, airway inflammation and hyper-responsiveness. Persistent inflammation is thought to lead to 'remodelling' of the airway, which in turn leads to the progressive loss of lung function seen in asthmatics. It would appear logical that anti-inflammatory drugs such as inhaled corticosteroids (ICS) would influence the natural history of asthma by reducing inflammation, subsequent remodelling, and thus preventing the decline in lung function. This review will summarise the effects of ICS on the secondary prevention of asthma, lung function and remodelling. RECENT FINDINGS: Many published studies show a reduction in airway inflammation, improvement in clinical symptoms and prebronchodilator lung function whilst taking ICS. Few studies, however, examine their effect on the natural history of asthma. Several recent studies have targeted very young children with asthma using ICS, and despite their differing target populations and treatment strategies, have failed to show any difference in lung function. Studies in adults with mild persistent asthma show similar findings. ICS appear to reverse some of the processes involved in airway remodelling, but not all. SUMMARY: Although ICS are effective in controlling symptoms they do not appear to alter the natural history of asthma.     

What are the best estimates of pediatric asthma control?

PURPOSE OF REVIEW: To evaluate asthma outcome measures in the face of the variable nature of asthma. The outcome measures are divided into objective and subjective clinical measures, humanistic measures such as quality of life, and costs of asthma control. RECENT FINDINGS: Objective measures of asthma include those traditionally used such as spirometry, peak expiratory flow rate, and airway hyperresponsiveness. Recently, more attention has been geared towards markers of inflammation including exhaled nitric oxide and sputum eosinophils. Subjective measures of asthma control include patient-derived parameters such as number of wheezing episodes, nocturnal symptoms, exercise-induced symptoms, short-acting beta-agonist use, steroid bursts, emergency-department visits, and hospitalizations. Asthma-related quality of life is related to asthma morbidity, and patients with better baseline quality of life have improved outcomes. Asthma-related costs include direct costs mostly comprised of hospitalizations and emergency-room visits, and indirect costs including school absenteeism. SUMMARY: There is no ideal outcome measure for evaluating pediatric asthma control, but each of these outcome measures must be used together to evaluate a patient at each outpatient visit. Patient-centered measures of asthma control must also be further incorporated into office visits for improved asthma management.     

Allergic vs nonallergic asthma: what makes the difference?

BACKGROUND: The aim of this work was to describe clinical similarities and differences between allergic and nonallergic asthmatics, notably concerning the nasosinusal involvement. METHODS: A total of 165 asthmatics (122 allergics and 43 nonallergics) and 193 controls (40 allergics and 153 nonallergics), recruited in the frame of EGEA study (Epidemiological study on the Genetics and Environment of Asthma, bronchial hyperresponsiveness and atopy), were included. Asthmatics were included on the basis of positive answer to four standardized items. To establish differences and similarities between allergic and nonallergic asthmatics, general characteristics (age, sex, smoking habits, history of hay fever and allergic dermatitis), history of asthma, severity and nasosinusal involvement were examined. Clinical assessment was based on the answers to a detailed questionnaire, and spirometry. RESULTS: Greater age, female sex, sinusal polyposis, and FEV1 below 80% of the predicted value increased the risk of displaying a nonallergic type of asthma, whereas history of hay fever, seasonal exacerbation of asthma, and asthma duration lowered this risk. Unexpectedly, we found no difference in terms of rhinitic symptoms between both groups, probably resulting from distinct causes. CONCLUSION: These results give new insights into the contrasts between clinical features of allergic and nonallergic asthma. The terminology of extrinsic asthma was first introduced by Rackeman in 1947 (1) and referred to the triggering role of allergens in asthma. By symmetry, he described intrinsic asthma as a disease characterized by later onset in life, female predominance, higher degree of severity, and more frequent association to nasosinusal polyposis. As these asthmatics were not improved by conventional treatment, this author considered their disease as caused by a nonallergic, unknown phenomenon. It is now widely admitted that nonallergic asthma can be objectively distinguished from allergic asthma based on negative skin tests to usual aeroallergens. On the other hand, positive skin test shows a tendency to produce IgE antibodies in response to low doses of allergens. "Atopy" and "atopic" are the terms used to describe this clinical trait and predisposition (2). Allergic clinical manifestations of atopy are of various types, for example rhinitis and asthma. Nowadays the terminology of "extrinsic" and "intrinsic" asthma should no longer be used, and should be replaced by the terminology of "allergic" or "nonallergic" asthma (2).     

Natural history of asthma: persistence versus progression-does the beginning predict the end?

Environmental exposures during the early years and airway obstruction that develops during this time, in conjunction with genetic susceptibility, are important factors in the development of persistent asthma in childhood. Established risk factors for childhood asthma include frequent wheezing during the first 3 years, a parental history of asthma, a history of eczema, allergic rhinitis, wheezing apart from colds, and peripheral blood eosinophilia, as well as allergic sensitization to aeroallergens and certain foods. Risk factors for the development of asthma in adulthood remain ill defined. Moreover, reasons for variability in the clinical course of asthma--persistence in some individuals and progression in others--remain an enigma. The distinction between disease persistence and disease progression suggests that these are different entities or phenotypes. There is currently no consensus on whether disease progression requires either airway inflammation or airway remodeling or the combination of the two. For patients with irreversible airway obstruction, inflammation might, in part, be necessary but perhaps not entirely sufficient to induce the irreversible component, some of which could be attributed to alterations in the structure of the bronchial wall. Intervening with intermittent or daily inhaled corticosteroids in high-risk infants and children does not prevent disease progression or impaired lung growth. These findings, however, might not apply to adults, and further study in adults is needed to determine the effect of inhaled corticosteroid therapy on disease progression.     

Do low testosterone levels contribute to the pathogenesis of asthma?

Asthma is a chronic inflammatory airway disorder that causes respiratory hypersensitivity and intermittent obstruction. Airway hyperresponsiveness to both specific and nonspecific stimuli is the hallmark of asthma. Although genetic susceptibility and airway inflammation are believed to play fundamental roles, etiology of asthma is unknown. In most cases, the treatment of asthma focuses on control of factors contributing to asthma severity and pharmacologic therapy including bronchodilator and anti-inflammatory agents. The prevalence of reported asthma is greater in prepubertal boys, with a change to a female predominance after puberty. Many epidemiological studies also suggest that women are at increased risk of developing adult-onset asthma and also suffer from more severe disease than men. This strongly suggests an important role for sex hormones in asthma. Previous articles provided us that, testosterone and/or its metabolites maintain the physiological balance of autoimmunity and protective immunity by preserving the number of regulatory cells. Testosterone is an immunosuppressant and is likely to be protective against immunological and inflammatory processes that trigger asthma. We hypothesized that the testosterone or selective androgen receptor modulators would have beneficial effects on asthma and could decrease the risk of asthmatic attacks.     

Is vitamin D deficiency to blame for the asthma epidemic?

In the 1960s, the prevalence of asthma and allergic diseases began to increase worldwide. Currently, the burden of the disease is more than 300 million people affected. We hypothesize that as populations grow more prosperous, more time is spent indoors, and there is less exposure to sunlight, leading to decreased cutaneous vitamin D production. Coupled with inadequate intake from foods and supplements, this then leads to vitamin D deficiency, particularly in pregnant women, resulting in more asthma and allergy in their offspring. Vitamin D has been linked to immune system and lung development in utero, and our epidemiologic studies show that higher vitamin D intake by pregnant mothers reduces asthma risk by as much as 40% in children 3 to 5 years old. Vitamin D deficiency has been associated with obesity, African American race (particularly in urban, inner-city settings), and recent immigrants to westernized countries, thus reflecting the epidemiologic patterns observed in the asthma epidemic. Providing adequate vitamin D supplementation in pregnancy may lead to significant decreases in asthma incidence in young children.     

Disconnection of man and the soil: reason for the asthma and atopy epidemic?

Intense search has been going on to find factors responsible for the asthma and atopy epidemic in Western societies. Attention has increasingly been devoted to environmental saprophytes, which, in addition to gut commensals, might be the major players in the development and fine tuning of immunologic homeostasis. This review outlines current evidence for the role of environmental saprophytes in the development of atopic disease and considers the consequences of urbanization in reducing contacts with soil microorganisms. The major microbial components that have been shown to possess immunomodulatory capacity and their respective Toll-like receptors are also discussed, as are the possible mechanisms underlying the ability of saprophytes to confer protection against atopic disease.     

Progress on the study of nuclear factor-κB and asthma

The incidence of asthma is increasing year by year. Therefore, to effectively control asthma is critical for the quality of life of the patients. Recent studies have revealed that the pathogenesis of asthma includes airway inflammation and remodeling,which are closely related with the overexpression of a variety of inflammatory proteins. Nuclear factor κB(NF-κB) mediates the expression of these inflammatory proteins,thereby contributing to the pathological development of asthma. The specific inhibition of NF-κB pathway might lead to a new way to the treatment of asthma.     

Immunotherapy: an option in the management of occupational asthma?

PURPOSE OF REVIEW: To review clinical data on immunotherapy applied to occupational asthma. RECENT FINDINGS: There are very few studies on immunotherapy in occupational asthma. The best documented use of immunotherapy in this disorder corresponds to latex allergy among healthcare workers. There are anecdotic reports of non-well controlled studies using immunotherapy with wheat flour, African maple wood, sea squirt and rat epithelium extracts. Subcutaneous immunotherapy with natural rubber latex extract, at adequate doses, seems to be a useful treatment in reducing cutaneous and respiratory symptoms, but it should be considered as a high-risk treatment due to the appearance of systemic reactions. SUMMARY: At present, subcutaneous immunotherapy with latex extract can only be considered experimental and must be administered by experienced allergists in a hospital setting, similarly to venom immunotherapy. Nevertheless, systemic reactions responded well to treatment. Further clinical trials on efficacy, safety and long-term effectiveness in immunoglobulin E-mediated occupational rhinitis and asthma are clearly needed. Since allergen avoidance is not always possible, no other etiologic treatment but immunotherapy can be offered to patients with occupational rhinitis/asthma.     

Severe asthma in adults: what are the important questions?

The term severe refractory asthma (SRA) in adults applies to patients who remain difficult to control despite extensive re-evaluation of diagnosis and management following an observational period of at least 6 months by a specialist. Factors that influence asthma control should be recognized and adequately addressed prior to confirming the diagnosis of SRA. This report presents statements according to the literature defining SRA in order address the important questions. Phenotyping SRA will improve our understanding of mechanisms, natural history, and prognosis. Female gender, obesity, and smoking are associated with SRA. Atopy is less frequent in SRA, but occupational sensitizers are common inducers of new-onset SRA. Viruses contribute to severe exacerbations and can persist in the airways for long periods. Inflammatory cells are in the airways of the majority of patients with SRA and persist despite steroid therapy. The T(H)2 immune process alone is inadequate to explain SRA. Reduced responsiveness to corticosteroids is common, and epithelial cell and smooth muscle abnormalities are found, contributing to airway narrowing. Large and small airway wall thickening is observed, but parenchymal abnormalities may influence airway limitation. Inhaled corticosteroids and bronchodilators are the mainstay of treatment, but patients with SRA remain uncontrolled, indicating a need for new therapies.     

Progress on the study of nuclear factor-κB and asthma

The incidence of asthma is increasing year by year. Therefore, to effectively control asthma is critical for the quality of life of the patients. Recent studies have revealed that the pathogenesis of asthma includes airway inflammation and remodeling,which are closely related with the overexpression of a variety of inflammatory proteins. Nuclear factor κB(NF-κB) mediates the expression of these inflammatory proteins,thereby contributing to the pathological development of asthma. The specific inhibition of NF-κB pathway might lead to a new way to the treatment of asthma.     

Is TGF-beta1 the key to suppression of human asthma?

Transforming growth factor beta1 (TGF-beta1) is produced by many types of cells that are activated in the asthmatic response. Recent studies have highlighted this cytokine as an important negative regulator in an experimental model of asthma. Although the role of TGF-beta1 in human asthma remains obscure, data derived from animal models have encouraged the further investigation of such suppression mechanisms in order to develop novel therapies for asthma.