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Background: The occupational uses of latex gloves may be associated with asthma. Hypersensitivity to latex has been shown to be IgE-mediated. The asthmatic reaction to latex is usually early; however, the natural history of latex asthma is still unknown. Objective: The purposes of this study were to investigate asthmatic responses induced by natural rubber latex and to assess the long-term respiratory consequences of latex-induced asthma after removal from exposure. Methods: This report describes the clinical and immunologic study of six nurses with work-related respiratory and skin disorders induced by the use of latex gloves. To determine whether the symptoms induced by latex gloves were IgE-mediated, we assessed latex IgE antibody levels by skin prick tests (SPTs) and RASTs with latex extracts. To confirm work-related latex reactions, we assessed respiratory symptoms, skin reactions, and FEV 1 after a glove exposure test and an inhalation provocation test with latex gloves. All subjects were followed up for 7 months to 7 years after the first observation. Results: All subjects had positive SPT and RAST responses to latex extracts, positive double prick test responses to latex gloves, and negative SPT responses to cornstarch and common allergens. Ten atopic and 10 nonatopic control subjects had negative SPT responses to latex and cornstarch extracts and negative double prick test responses to latex gloves. In three subjects latex allergy was associated with allergy to fruit (banana and chestnut). After the glove exposure test, four of six subjects had contact urticaria, all had rhinoconjunctivitis, and two had a late asthmatic response. The inhalation provocation test was performed on four subjects: all had rhinoconjunctivitis, two had urticaria and late asthmatic response, and one had laryngeal edema. A late asthmatic response was recorded in four subjects. Three subjects continued to have chronic asthma, and four subjects had increased nonspecific bronchial responsiveness 7 months to 7 years after being assigned to duties not involving latex gloves. Conclusions: This study of six nurses shows that latex is a potential cause of occupational asthma, rhinoconjunctivitis, and urticaria-angioedema. Latex seems to include antigens that elicit IgE-mediated hypersensitivity and may cause a late asthmatic reaction. Occupational asthma caused by latex may lead to permanent respiratory disability, even after removal from exposure. (J ALLERGY CLIN IMMUNOL 1995;96;457-64.)

Asthma education programs result in clinical improvement. However, most studies involved programs of up to 1 year of follow-up, and their efficacy in improving quality of life (QoL) is still controversial. The aim of this study was to evaluate the effectiveness of a program of patient education in asthmatics over 2 years. Thirty-seven asthmatic patients were randomly allocated to group A (usual treatment) and 32 to group B (usual treatment plus patient education program). The effectiveness of the education program was evaluated by comparing morbidity outcomes at baseline and 12 and 24 months afterwards. At baseline, no intergroup difference emerged in age, sex, smoking, asthma severity, atopy, FEV1, symptom-free days, use of rescue salbutamol, and QoL. One year later, group B subjects had an improvement in the overall QoL (from 5.8 +/- 0.8 to 6.1 +/- 0.7, p < 0.005), and in "Activities" (from 5.3 +/- 0.9 to 5.7 +/- 0.8, p < 0.05) and "Environment" (from 6.4 +/- 1.0 to 6.8 +/- 0.4, p < 0.05) domains. Two years later the "Activities" domain score increased in group B (from 5.3 +/- 0.9 to 5.7 +/- 1.1, p < 0.05). QoL did not vary in group A. The education program was ineffective in all other parameters at both follow-up time-points. In group A, a significant increase in medication expenses and a significant decrease in rescue salbutamol use was found 1 and 2 years after baseline, respectively. In conclusion, this education program improved QoL for 1 year, but the improvement was not sustained in the 2nd year.

Asthma educational programs have been shown to reduce the use of emergency room, frequency of severe asthma attacks and hospitalization. However, its effectiveness in other morbidity parameters and on quality of life has yet to be fully understood. This prospective randomized control trial evaluated the effectiveness of a patient education program in 77 asthmatics according to “Teach Your Patients About Asthma: A Clinician's Guide”(1992). Forty asthmatic patients were randomly allocated to Group A (usual treatment) and 37 to Group B (usual treatment plus a patient education program). The effectiveness of the educational program was evaluated by comparing morbidity outcomes at baseline and 3 months after initial evaluation. At enrolment, the two groups were not different with regard to age, sex, smoking, asthma severity, atopy, FEV1, symptom-free days, use of rescue salbutamol and quality of life. Three months later, subjects in Group B showed a significant improvement in the overall quality of life (p

For difficult asthma, treatment is aimed at improving airway obstruction and minimizing adverse effects of systemic corticosteroids. The combination of troleandomycin (TAO) with methylprednisolone (MP) reportedly has a beneficial steroid-sparing effect on difficult asthma.To test the steroid-sparing effect of TAO, 14 subjects with severe corticosteroid-dependent asthma were studied before and during treatment with MP and TAO.Treatment with MP and TAO resulted in a clear reduction in respiratory symptoms, asthmatic attacks, corticosteroid and hospitalization requirements, improvement in pulmonary function tests, and a remarkable decrease in peak expiratory flow rate circadian variability when compared with the period before TAO treatment (with corticosteroids). Treatment with MP and TAO was fairly well tolerated. Only a reduction (-5.2%, p0.01) in bone mineral content and an increase in plasma glucose levels (from 81.7 to 94.3 mg/dl, p0.05) were found, in comparison with pre-TAO values. One subject discontinued MP-TAO treatment because of a mild but persistent increase in serum alanine aminotransferase. In an evaluation of the clinical and pulmonary function test results, eight of the 14 subjects were responders and six were nonresponders. During follow-up three subjects discontinued TAO and consequently had an asthmatic attack after 4, 7, or 15 days, respectively.This study confirms that treatment with MP and TAO has a beneficial effect in a subgroup of severely steroid-dependent asthma patients.

The pathogenetic mechanisms of occupational asthma (OA) due to low-molecular-weight compounds have been poorly defined, and further studies are required to clarify the role of immunologic mechanisms in OA. Until now cellular mechanisms have been less investigated than humoral ones. We have evaluated interleukin-1 (IL-1) and tumor necrosis factor (TNF) production by peripheral blood monocytes (PBM), and peripheral T-cell subpopulations in 22 subjects with possible OA before and after specific bronchoprovocation test (SBPT). After SBPT, three subjects had an immediate reaction, seven a late reaction, and two a dual reaction. Ten subjects had no asthmatic reaction to SBPT. Spontaneous release of IL-1 from PBM did not change significantly after SBPT. TNF activity was increased 48 h after SBPT in immediate reactions, and 72 h after SBPT in late-dual reactions. These results suggest that exposure to occupational agents may induce activation of PBM with increased spontaneous release of cytokines, such as TNF.

Ventilatory capacity tests and standardized respiratory questionnaires were used in 1973 and in 1980 to measure the effect of mixed dust exposure in the asbestos cement industry on respiratory symptoms and lung function in 65 exposed workers and 30 controls (exposed to polyvinyl chloride but not to asbestos). Workers exposed to asbestos had 1) a higher prevalence of breathlessness and chest pain, and a higher incidence of breathlessness; 2) lower 1980 values of forced vital capacity (FVC) (0.27-0.83 liters) and forced expiratory volume in 1 sec (FEV1) (0.23-0.62 liters); and 3) a faster decline (nearly 40 ml/year) in FVC and FEV1 between 1973 and 1980. The FVC annual decrease was 52.5 ml in the subjects with more than 15 years since first asbestos exposure, whereas it was 24.3 ml in those with less than 15 years, suggesting a faster decline after 15 years of exposure. The effect of asbestos exposure and smoking habits was less than additive as regards pulmonary function.