Persistence Of Asthma Research Articles

Asthma and the risk of panic attacks among adults in the community.

The study was designed to determine the association between self-reported asthma and the risk, persistence and severity of panic attacks among adults in the community. Data were drawn from waves 1 and 2 of the Baltimore site of the Epidemiologic Catchment Area (ECA) Study (N = 2768), which included self-report information on asthma, treatment for asthma and panic attacks in 1981 and 1982. Multiple logistic regression analyses were used to calculate odds ratios comparing the prevalence of panic attack at baseline and follow-up by asthma status at baseline. Linear regression analyses were used to examine the relationship between self-reported asthma status and the number of panic symptoms during a panic attack. Self-report asthma was associated with significantly increased likelihood of having panic attacks at baseline (1981) (12.1% v. 7.3%, P < 0.05) and of having panic attacks at both baseline and follow-up (15.9% v. 7.3%, P < 0.05), compared to those without asthma at baseline. Adults receiving treatment for asthma at baseline had an increased risk of incident panic attacks at follow-up (OR = 2.65 (1.11, 6.34)) and at baseline and follow-up (OR = 5.88 (2.21, 15.62)), though untreated asthma did not appear to increase risk of incident panic at follow-up. Similarly, the risk of panic at follow-up was not increased among those with asthma at baseline who did not report asthma at follow-up, compared with those without asthma at baseline. Treated asthma was associated with having more panic symptoms during panic attacks, compared to those without asthma (P < 0.001). These findings are consistent with and extend previous results suggesting that self-reported asthma is associated with an increased risk of panic attacks among adults in the general population, and that there is a consistent relation between severity and persistence of asthma and panic attacks. The lack of association between remitted asthma and panic attack may reveal a need for further research to determine whether asthma may be a causal risk factor for panic attacks, or whether a third factor (genetic or environmental) may be associated with increased risk of the cooccurrence of asthma and panic attacks. Replication of these results using alternative methodology with corroborative data on asthma and panic attacks is needed next.

Mechanisms of asthma

Airway inflammation is a key factor in the mechanisms of asthma. Articles published in the Journal of Allergy and Clinical Immunology this past year have highlighted the utility of investigative bronchoscopy with segmental antigen challenge and induced sputum analyses to evaluate features of airway inflammation in relationship to asthma severity. Peripheral blood cell generation of cytokines IFN-γ (TH1) and IL-5 (TH2) was used to evaluate the relationship of the balance of TH1/TH2 cytokines to asthma persistence and severity in a 42-year, longitudinal study. Chemokines, including thymus and activation-regulated chemokine, are important to the regulation of inflammation and IgE synthesis. Their potential role in asthma has also been evaluated. Finally, albuterol (R)- and (S)-enantiomers may have distinct effects on airway relaxation and regulation of inflammation, suggesting the possibility that monoisomeric therapy has therapeutic advantages. The potential contribution of genetic factors and mechanisms to airway inflammation and remodeling also continues to be an area of intense investigation. During the past year a number of articles published in the Journal of Allergy and Clinical Immunology have identified and clarified potential genetic mechanisms in asthma. The contribution of genetics to asthma has been examined in a wide variety of studies, ranging from epidemiologic association and twin studies all the way to molecular analysis through microarray gene expression experiments. (J Allergy Clin Immunol 2003;111:S799-804.)

Quoi de neuf en allergologie pédiatrique en 2002 ? Une revue de la littérature internationale d'octobre 2001 à octobre 2002

Most epidemiological studies suggest that immunological responses to environmental factors are largely dependent on genetic factors, including responses induced by allergenic and non-allergenic factors in utero. While avoidance of allergenic and non-allergenic factors predisposing to atopy and/or asthma during pregnancy, the perinatal period and infancy is effective, although often unachievable, moderate exposure to environmental antigens and allergens may induce tolerance in atopy- and/or asthma-predisposed children. On the other hand, syncytial respiratory virus is a powerful eosinophilopoietic agent and induces resistance to corticosteroids. Also, the influence of mycobacterial antigens on immune responses to unrelated antigens and allergens is highly dependent on genetic inheritance. The risk of persistence or relapse of asthma in adulthood is significantly and positively correlated with the severity of asthma during childhood. Thus, adequate treatment of asthmatic chidren with inhaled anti-inflammatory drugs (e.g., corticosteroids) and specific immunotherapy is mandatory. The diagnostic and predictive values of skin test reactivity and serum specific IgE levels are good in children with IgE-dependent peanut allergy. However, mean wheal diameters and mean values of specific IgE vary among ethnic groups and are not similar in children with urticaria, angioedema or anaphylaxis and in children with atopic dermatitis. The diagnostic value of patch tests in children with non IgE-dependent food hypersensitivity is discussed. Finally, the diagnostic value of skin and serological tests in children with suspected allergy to vaccines and gelatin-containing suppositories is probably high.

Allergen-induced bronchial inflammation in house dust mite-allergic patients with or without asthma.

It is presently unknown which factors determine the occurrence and persistence of asthma in house dust mite-allergic individuals. The level of allergen-specific IgE antibodies does not seem to be decisive for asthmatic symptoms. Moreover, levels of exposure to mite allergens do not seem to differ significantly between asthmatic and non-asthmatics individuals. It was hypothesized that the presence or absence of asthmatic symptoms in house dust mite-allergic patients is associated with quantitative or qualitative differences in the cellular bronchial inflammatory response during the late phase of the allergic reaction. This hypothesis was tested in the bronchial allergen challenge model. Whole lung challenges with house dust mite extract were performed in 52 house dust mite-allergic subjects, of whom 26 had asthma and 26 had perennial rhinitis without asthmatic symptoms. Primary outcomes were parameters for bronchial inflammation in serial samples of induced sputum (cell differentials, eosinophil cationic protein (ECP), interleukin-8 (IL-8), myeloperoxydase (MPO)). In addition, lung function, non-specific bronchial hyper-responsiveness and serial blood samples (eosinophils and IL-5) were analysed. At baseline sputum eosinophils and ECP were similar in both groups but neutrophils and IL-8 were higher in asthmatics. The early bronchoconstriction after allergen challenge was similar in asthma and non-asthmatic rhinitis (median decrease in FEV1: asthma -31.7% vs. non-asthmatics -29.1%, P > 0.1). The late phase bronchoconstriction was significantly greater in asthma (median decrease in FEV1: asthma -27.6% vs. non-asthmatics -18.9%, P = 0.02). Induction of bronchial hyper-responsiveness was similar in both groups. Bronchial allergen challenge elicited significant increases in sputum eosinophils and ECP, which were indistinguishable for both groups (P > 0.1 and P = 0.07, respectively). In contrast, higher numbers of neutrophils persisted in asthma 24h after challenge and were accompanied by significant increases in IL-8 and MPO, which were absent in non-asthmatics (difference between groups P = 0.007 and P = 0.05, respectively). Allergen challenge inducedvery similar increases in eosinophils and ECP in induced sputum in allergic asthmatics and in allergic non-asthmatic patients. The difference in bronchial inflammation between asthma and non-asthmatic rhinitis appeared to be more closely related to indices for neutrophilic inflammation.

Bébés siffleurs : qui traiter ?

Wheezing in babies is an important clinical problem. Differential diagnosis and prognosis are uncertain as there are no reliable markers for separating non-atopic wheezing from atopic “asthmatic” wheezing. Bronchial hyperresponsiveness cannot be ascertained easily in this age group and, moreover, it is not a reliable predictor of persistence of asthma. Serum markers that will forecast the development of asthma are not sufficiently sensitive. Allergic sensitisation, family history and evidence of atopy in the child are at present the most reliable indicators of future asthma. In babies where these factors exist, long-term treatment with an inhaled steroid is warranted. The possibility of dose-dependent systemic side effects, for which babies are particularly vulnerable, must be taken into account.

De la bronchiolite àl'asthme

Relationships between lower respiratory diseases with wheezing during infancy and asthma at school-age remain debatted. Indeed, although epidemiologic studies show that wheezy infants most often become asymptomatic before entry to school, they also demonstrate that severe bronchiolitis during infancy is a significant risk factor for persistence of wheezing episodes at school-age. One of the most important factors demonstrated to enhance the risk for persistence of asthma is an early allergic sensitization.

The editors' choice

The editors' choice

Effect of continuing or finishing high-level sports on airway inflammation, bronchial hyperresponsiveness, and asthma: A 5-year prospective follow-up study of 42 highly trained swimmers

Abstract Background: Mild eosinophilic airway inflammation and bronchial hyperresponsiveness-ie, mild asthma-have been shown to affect a high proportion of endurance athletes. The persistence of airway inflammation, bronchial hyperresponsiveness, and asthma in this population is not known, however, inasmuch as follow-up studies of athletes' asthma have not been performed. Objective: The purpose of this study was to investigate effect of finishing high-level sports on airway inflammation, bronchial hyperresponsiveness, and asthma. Methods: Forty-two elite competitive swimmers, most of them from the Finnish national team (37/42; 88%), were followed for 5 years in a prospective manner. All of the swimmers completed questionnaires and underwent resting spirometry, histamine challenge testing, and skin prick tests at baseline and at follow-up. Twenty-nine swimmers (69%) also gave induced sputum samples on both occasions. Sixteen (38%) of the swimmers had continued their competitive careers during follow-up (active swimmers), but 26 (62%) had stopped competing more than 3 months before the follow-up examination (past swimmers). Results: Bronchial responsiveness was increased in 7 (44%) of the 16 active swimmers at baseline and in 8 (50%) of the 16 active swimmers at follow-up; it was increased in 8 (31%) of the 26 past swimmers at baseline and in 3 (12%) of the 26 past swimmers at follow-up (McNemar test, P = .025). The difference in the change in bronchial hyperresponsiveness between the study groups was significant (likelihood ratio test, P = .023). Current asthma (defined as bronchial hyperresponsiveness and exercise-induced bronchial symptoms monthly) was observed in 5 (31%) of the active swimmers at baseline and in 7 (44%) of the active swimmers at follow-up; of the past swimmers, it occurred in 6 (23%) at baseline and in 1 (4%) at follow-up (McNemar test, P = .025). The difference in the change in current asthma between the study groups was significant (likelihood ratio test, P = .0040). The sputum differential cell counts of eosinophils and lymphocytes increased significantly during the follow-up period in the active swimmers (Wilcoxon signed rank sum test; P = .033 and P = .0029, respectively); in the past swimmers, the sputum differential cell counts of eosinophils tended to decrease during the follow-up period ( P = .17), whereas the differential cell counts of lymphocytes did not change significantly. The changes in the sputum differential cell counts of eosinophils between the study groups differed significantly (Mann-Whitney U test, P = .019). Conclusion: In swimmers who had stopped high-level training, bronchial hyperresponsiveness and asthma attenuated or even disappeared. Mild eosinophilic airway inflammation was aggravated among highly trained swimmers who remained active during the 5-year follow-up. Our results suggest that athletes' asthma is partly reversible and that it may develop during and subside after an active sports career. (J Allergy Clin Immunol 2002;109:962-8.)

Effect of continuing or finishing high-level sports on airway inflammation, bronchial hyperresponsiveness, and asthma: a 5-year prospective follow-up study of 42 highly trained swimmers.

Mild eosinophilic airway inflammation and bronchial hyperresponsiveness-ie, mild asthma-have been shown to affect a high proportion of endurance athletes. The persistence of airway inflammation, bronchial hyperresponsiveness, and asthma in this population is not known, however, inasmuch as follow-up studies of athletes' asthma have not been performed. The purpose of this study was to investigate effect of finishing high-level sports on airway inflammation, bronchial hyperresponsiveness, and asthma. Forty-two elite competitive swimmers, most of them from the Finnish national team (37/42; 88%), were followed for 5 years in a prospective manner. All of the swimmers completed questionnaires and underwent resting spirometry, histamine challenge testing, and skin prick tests at baseline and at follow-up. Twenty-nine swimmers (69%) also gave induced sputum samples on both occasions. Sixteen (38%) of the swimmers had continued their competitive careers during follow-up (active swimmers), but 26 (62%) had stopped competing more than 3 months before the follow-up examination (past swimmers). Bronchial responsiveness was increased in 7 (44%) of the 16 active swimmers at baseline and in 8 (50%) of the 16 active swimmers at follow-up; it was increased in 8 (31%) of the 26 past swimmers at baseline and in 3 (12%) of the 26 past swimmers at follow-up (McNemar test, P =.025). The difference in the change in bronchial hyperresponsiveness between the study groups was significant (likelihood ratio test, P =.023). Current asthma (defined as bronchial hyperresponsiveness and exercise-induced bronchial symptoms monthly) was observed in 5 (31%) of the active swimmers at baseline and in 7 (44%) of the active swimmers at follow-up; of the past swimmers, it occurred in 6 (23%) at baseline and in 1 (4%) at follow-up (McNemar test, P =.025). The difference in the change in current asthma between the study groups was significant (likelihood ratio test, P =.0040). The sputum differential cell counts of eosinophils and lymphocytes increased significantly during the follow-up period in the active swimmers (Wilcoxon signed rank sum test; P =.033 and P =.0029, respectively); in the past swimmers, the sputum differential cell counts of eosinophils tended to decrease during the follow-up period (P =.17), whereas the differential cell counts of lymphocytes did not change significantly. The changes in the sputum differential cell counts of eosinophils between the study groups differed significantly (Mann-Whitney U test, P =.019). In swimmers who had stopped high-level training, bronchial hyperresponsiveness and asthma attenuated or even disappeared. Mild eosinophilic airway inflammation was aggravated among highly trained swimmers who remained active during the 5-year follow-up. Our results suggest that athletes' asthma is partly reversible and that it may develop during and subside after an active sports career.

L’enfant siffleur de zéro à trois ans : place de l’enquête allergologique

Wheezing is frequently present during lower respiratory diseases in infancy. Viral infections are mostly responsible for these acute episodes. IgE-dependent mechanisms may however also contribute to the pathophysiology of infantile asthma. First, allergenic sensitization is more frequently observed in asthmatic infants than in the whole population within the same age range. Second, some studies argue for a predisposing role of an early allergenic sensitization to the appearance of an asthma in infants. When asthma is established, allergenic sensitization is associated with more acute episodes. Finally, the persistence of asthma from infancy to school age appears strongly influenced by personal or familial atopy.

Relationship of viral infections to wheezing illnesses and asthma.

Viral infections can influence both the development and the severity of asthma. In early life, viral infections can either increase or, remarkably, decrease the risk of subsequent asthma. In children and adults with existing asthma, viral respiratory infections frequently cause acute airway obstruction and wheezing. This article discusses the influence of viral infections on mechanisms of virus-induced airway inflammation in relationship to the development, persistence and severity of asthma.

CXCR2 Is Necessary for the Development and Persistence of Chronic Fungal Asthma in Mice

The role of CXCR during allergic airway and asthmatic diseases is yet to be fully characterized. Therefore, the present study addressed the role of CXCR2 during Aspergillus fumigatus-induced asthma. Mice deficient in CXCR2 (CXCR2-/-) and wild-type counterparts (CXCR2+/+) were sensitized to A. fumigatus Ags and challenged with A. fumigatus conidia, and the resulting allergic airway disease was monitored for up to 37 days. At days 3 and 7 after conidia, CXCR2-/- mice exhibited significantly greater methacholine-induced airway hyperreactivity than did CXCR2+/+ mice. In contrast, CXCR2-deficient mice exhibited significantly less airway hyperresponsiveness than the wild-type control groups at days 14 and 37 after conidia. At all times after conidia, whole lung levels of IL-4, IL-5, and eotaxin/CC chemokine ligand 11 were significantly lower in CXCR2-/- mice than in the wild-type controls. Eosinophil and T cell, but not neutrophil, recruitment into the airways of A. fumigatus-sensitized CXCR2-/- mice was significantly impaired compared with wild-type controls at all times after the conidia challenge. Whole lung levels of IFN-gamma, inflammatory protein-10/CXC ligand (CXCL) 10, and monokine induced by IFN-gamma (MIG)/CXCL9 were significantly increased in CXCR2-/- mice compared with CXCR2+/+ mice at various times after conidia. Interestingly, at day 3 after conidia, neutrophil recruitment and airway hyperresponsiveness in CXCR2-/- mice was mediated by inflammatory protein-10/CXCL10 and, to a lesser degree, MIG/CXCL9. Taken together, these data suggest that CXCR2 contributes to the persistence of asthmatic disease due to A. fumigatus.

The role of CC chemokine receptor 5 (CCR5) and RANTES/CCL5 during chronic fungal asthma in mice.

In the present study, we explored the role of CC chemokine receptor 5 (CCR5) in a murine model of chronic fungal asthma induced by an intrapulmonary challenge with Aspergillus fumigatus conidia (or spores). Airway hyperresponsiveness was significantly lower in A. fumigatus-sensitized mice lacking CCR5 (CCR5-/-) compared with similarly sensitized wild-type (CCR5+/+) control mice at days 2, 21, 30, and 40 after the conidia challenge. CCR5-/- mice exhibited significantly less peribronchial T-cell and eosinophil accumulation and airway-remodeling features, such as goblet cell hyperplasia and peribronchial fibrosis, compared with CCR5+/+ mice at these times after conidia. However, both groups of mice exhibited similar allergic airway disease at day 12 after the conidia challenge. In CCR5-/- mice at day 12, the allergic airway disease was associated with airway hyperresponsiveness, peribronchial allergic inflammation, and goblet cell hyperplasia. Immunoneutralization of RANTES/CCL5 in sensitized CCR5+/+ and CCR5-/- mice for 12 days after the conidia challenge significantly reduced the peribronchial inflammation and airway hyperresponsiveness in comparison with control wild-type and knockout mice at this time. These data demonstrate that functional CCR5 and RANTES/CCL5 are required for the persistence of chronic fungal asthma in mice.

High levels of urinary eosinophil protein X in young asthmatic children predict persistent atopic asthma.

Levels of urinary eosinophil protein X (U-EPX) and eosinophil counts were measured in 32 children (12-36 months of age) who were hospitalized for acute asthma, and the U-EPX levels were measured in 20 healthy children of the same age. The ability of these parameters to predict persistent asthma (at least one wheezing episode during the last 6 months) and atopic asthma (a positive skin-prick test [SPT]), was evaluated at a follow-up 2 years later. On admission, levels of U-EPX were higher in children with asthma (median: 120 microg/mmol of creatinine; quartiles: 67-123 microg/mmol of creatinine) than in controls (60 microg/mmol of creatinine, 38-74 microg/mmol of creatinine; p< 0.001). The U-EPX level was higher in those with persistent atopic asthma at follow-up (173 microg/mmol of creatinine, 123-196 microg/mmol of creatinine, n = 16), than in those with persistent non-atopic asthma (73 microg/mmol creatinine, 46-105 microg/mmol of creatinine, n = 8; p< 0.05), and higher than in those with transient asthma (no symptoms at follow-up) (106 microg/mmol creatinine; 42-167 microg/mmol of creatinine, n = 8; p< 0.05). By multiple logistic regression analysis, U-EPX was the only parameter able to predict persistent atopic asthma; eosinophil counts, parental atopy, age or gender could not. Parental atopy was the only parameter predictive for persistent asthma, regardless of atopic status. In conclusion, levels of U-EPX, but not eosinophil counts, measured in young children hospitalized with acute asthma can predict the persistence of atopic asthma 2 years later.

Relationship between bronchial responsiveness and clinical evolution in infants who wheeze: a four-year prospective study.

Recurrent illness involving wheezing during the first years of life is transient in most children. The role of bronchial hyperresponsiveness as a factor influencing the persistence of wheezing from infancy to school age remains unknown. In a prospective study we investigated whether infants who wheezed and subsequently developed persistent asthma differed from infants who wheezed and later became asymptomatic either in the initial degree of bronchial hyperresponsiveness or in the persistence of bronchial hyperresponsiveness with age. One hundred and twenty-nine infants with three or more wheezing episodes before 2 yr of age were followed during 4 yr with a clinical evaluation and a methacholine challenge performed every 6 mo until the child was 4 yr old and once per year thereafter. The clinical score significantly improved with time in most children. The proportion of children with persistent wheezing after 2 and 4 yr of follow-up was only 31% and 20%, respectively. Persistent wheezers had significantly lower VmaxFRC values at initial evaluation and higher SRaw values at the end of follow-up than infants who became asymptomatic. We used transcutaneous oxygen tension (PtcO(2)) to measure the response to methacholine. No significant difference in PD(15) PtcO(2) between groups with subsequently different clinical progression was observed at initial evaluation. Bronchial hyperresponsiveness persisted 4 yr later in all children but children with persistent wheezing showed significantly lower PD(15) PtcO(2) values than children who became asymptomatic, as early as 30 mo of age. However, an acceptable early PD(15) PtcO(2) cut-off point predictive for subsequent clinical progression could not be identified. The level of bronchial hyperresponsiveness in infants who wheezed was not predictive of the persistence of asthma 4 yr later.

Onset and persistence of childhood asthma: predictors from infancy.

Onset and persistence of childhood asthma: predictors from infancy.

Rôle des mécanismes IgE dépendants au cours de l’asthme du nourrisson

Infantile asthma, defined by the presence of three or more wheezing episodes before 2 years of age, is frequently considered as mainly being encouraged by small airways and passive tobacco smoke, and triggered by viral infections. IgE-dependent mechanisms may however also contribute to the pathophysiology of infantile asthma. First, allergenic sensitization is more frequently observed in asthmatic infants than in the whole population with the same age range. Second, some studies argue for a predisposing role of an early allergenic sensitization to the appearance of asthma in infants. When asthma is established, allergenic sensitization is associated with more acute episodes. Finally, the persistence of asthma from infancy to school age appears strongly influenced by personal or familial atopy.

Are peak flow and symptom measures good predictors of asthma hospitalizations and unscheduled visits?

Epidemiologic studies of pediatric respiratory health often include objective measures such as peak expiratory flow (PEF), and subjective measures such as symptom reports. These measures, however, are poorly correlated with each other, and there is little evidence that PEF is useful in predicting important health outcomes. Within a cohort of 791 inner-city children with asthma, we examined correlations between a series of five peak flow measures and five symptom scores obtained from 2-week diaries. The strongest correlations were found between "total peak flow lability" defined as: [(diary maximum - diary minimum)/diary mean] and "% of days with chest tightness" (r = 0.31). Logistic models evaluated peak flow and symptoms as predictors of an important health outcome: hospitalization or emergency department or unscheduled clinic visit for asthma within 30 days of starting the diary. Each of the peak flow and symptom measures was significantly related to utilization. However, the predictive power of each measure was low (range of area under ROC curve, 0.54-0.67). Models including only peak flow or symptoms had greater prediction than models with risk factors such as atopy, asthma persistence, and age. The prediction from a model with the risk factors and symptoms was not improved by adding a peak flow measure to the model (increase in area under ROC, 0.67-0.68). Stratified analyses suggest that prediction was similar in the fall vs. winter, spring, and summer months. Greater prediction of health outcomes was found among more persistent asthmatics and children who were nonatopic. These findings suggest that in a research setting, peak flow monitoring in children did not add prediction beyond that obtained from symptom reports. Pediatr Pulmonol. 2001; 31:190-197. Published 2001 Wiley-Liss, Inc.

The importance of allergens in the development of asthma and the persistence of symptoms

The importance of allergies and allergens in the development and persistence of asthma is suggested by 3 lines of evidence. First, a number of epidemiologic studies demonstrate that sensitization to indoor allergens and the spores of the outdoor seasonal fungus Alternaria is a risk factor for the development of asthma in both children and adults. Sensitivity to pollens, on the other hand, rarely constitutes a risk for asthma but does constitute a risk for seasonal allergic rhinitis. Second, several studies, again in both children and adults, have demonstrated that, in persons sensitive to indoor allergens, the severity of asthma symptoms will vary with the level of exposure. Third, the elimination of exposure to house-dust mites has produced a remarkable reversal of asthma in sensitive children and adults. Not only have symptoms and pulmonary function improved, but there has also been evidence of a reduction in airway inflammation and hyperresponsiveness. Taken together, these studies make a strong argument for the importance of allergy and allergen exposure as aggravating factors in asthma in both children and adults and reinforce the importance of the identification and treatment of these allergen sensitivities. (J Allergy Clin Immunol 2000;105:S628-32.)

Occupational asthma: a review.

Occupational asthma is the most common form of occupational lung disease in the developed world at the present time. In this review, the epidemiology, pathogenesis/mechanisms, clinical presentations, management, and prevention of occupational asthma are discussed. The population attributable risk of asthma due to occupational exposures is considerable. Current understanding of the mechanisms by which many agents cause occupational asthma is limited, especially for low-molecular-weight sensitizers and irritants. The diagnosis of occupational asthma is generally established on the basis of a suggestive history of a temporal association between exposure and the onset of symptoms and objective evidence that these symptoms are related to airflow limitation. Early diagnosis, elimination of exposure to the responsible agent, and early use of inhaled steroids may play important roles in the prevention of long-term persistence of asthma. Persistent occupational asthma is often associated with substantial disability and consequent impacts on income and quality of life. Prevention of new cases is the best approach to reducing the burden of asthma attributable to occupational exposures. Future research needs are identified.