Educational intervention decreases exhaled nitric oxide in farmers with occupational asthma. Occupational asthma: a longitudinal study on the clinical and socioeconomic outcome after diagnosis. Follow-up study of 232 patients with occupational asthma caused by western red cedar (Thuja plicata). [Follow-up of latex-induced occupational asthma]. Clinical and socio-professional fate of isocyanate-induced asthma. [The response to a specific bronchial provocation test and the evolution of occupational asthma. A longitudinal study in subjects with toluene diisocyanate-induced asthma]. Bronchial responsiveness decreases in relocated aluminum potroom workers compared with workers who continue their potroom exposure. Clinical and socioeconomic features of subjects with red cedar asthma. A follow-up study. Occupational asthma: fate and management after the diagnosis. [Course of isocyanate-induced asthma in relation to exposure cessation: longitudinal study of 50 subjects]. Long-term follow-up of toluene diisocyanate-induced asthma. Clinical features and natural history of occupational asthma due to western red cedar (Thuja plicata). Occupational asthma in electronics workers caused by colophony fumes: follow-up of affected workers. [Course of bronchial hyperresponsiveness in patients with occupational asthma caused by exposure to persulfate salts]. Persistent asthma due to isocyanates. A follow-up study of subjects with occupational asthma due to toluene diisocyanate (TDI). Longitudinal decline in lung function in patients with occupational asthma due to western red cedar. Follow-up study of patients with respiratory disease due to toluene diisocyanate (TDI). Outcome of occupational asthma due to cobalt hypersensitivity.
Allergic occupational asthma is frequent in farming populations. As educational interventions can improve disease management, the short-term effect of an educational intervention in asthmatic farmers was evaluated on the basis of spirometric indices and exhaled nitric oxide fraction (F(eNO)). Farmers with occupational asthma (n = 81), mostly sensitised against cow dander and storage mites, participated in a 1-day educational programme. Outcome measures were assessed at baseline and after 4-6 weeks, using F(eNO), lung function and a questionnaire. Results were compared with those of a control group without intervention (n = 24). In the educational group, the proportion of subjects reporting work-related symptoms was reduced after the intervention. The F(eNO) decreased from a geometric mean of 28.2 to 25.7 ppb, and, in subjects with an elevated (>35 ppb) baseline F(eNO) (n = 32), from 59.7 to 49.2 ppb. The corresponding changes in the control group were 25.6 versus 27.7 ppb and 49.5 versus 48.1 ppb. Spirometric results were unaltered in the two groups. Thus exhaled nitric oxide fraction, a marker of allergic airway inflammation, indicated a beneficial effect of a short-term educational intervention in farmers with occupational asthma. This suggests a potential for exhaled nitric oxide fraction in assessing the efficacy of preventive measures within a short time with higher sensitivity than spirometry. To evaluate the clinical outcome and socioeconomic consequences of occupational asthma (OA).
                Twenty-five patients with OA both to high- and low-molecular-weight agents (3 and 22, respectively) confirmed by specific inhalation challenge were followed up for 12 months after the diagnosis. Upon diagnosis, each patient received a diary on which to report peak expiratory flow rate (PEFR), symptoms, drug consumption, expenses directly or indirectly related to the disease, as well as information regarding personal socioeconomic status. At each follow-up visit (1, 3, 6, and 12 months), the patients underwent clinical examination, spirometry, methacholine (Mch) challenge, and assessment of diary-derived parameters and socioeconomic status. Asthma severity (AS) was classified into four levels, based on symptoms, drug consumption, and PEFR variability.
                At 12 months, 13 patients (group A) had ceased exposure; the remaining 12 patients (group B) continued to be exposed. At diagnosis, FEV1 percent and provocative dose causing a 20% fall in FEV1 (PD20) of Mch were lower in group A than in group B; patients of group A were also characterized by significantly higher basal AS levels. At 12 months, no significant variation in FEV1 percent or PD20 was found for either group, while AS levels improved in both groups, the change being more marked for group A than group B. Pharmaceutical expense at 12 months significantly (p < 0.05) decreased, as compared with the first month, in group A, whereas it tended to increase in group B. In group A, 9 of 13 subjects had reported a deterioration of their socioeconomic status as compared with 2 of 12 in group B (p < 0.01). A significant loss of income was registered in patients of group A (median 21.45, 25th to 75th percentiles 16.9 to 25.8 Italian liras x 10(6) on the year preceding diagnosis and 15.498, 10.65 to 21.087 Italian liras x 10(6) on the year after diagnosis; p < 0.01), whereas no significant change was seen for patients in group B.
                In OA, cessation of exposure to the offending agent results in a decrease in asthma severity and in pharmaceutical expenses, but it is associated with a deterioration of the individual's socioeconomic status (professional downgrading and loss of work-derived income). There appears to be a great need for legislation that facilitates the relocation of these patients. A total of 232 patients with red cedar asthma diagnosed by inhalation provocation tests were observed an average of 4 years after the initial diagnosis. The status during the follow-up examination was as follows: 96 patients continued to work with red cedar, and 136 left the industry and had no further exposure to red cedar in their jobs or hobbies. Of the 136 patients who left the industry, only 55 (40.4%) recovered completely, whereas the remaining 81 (59.6%) continued to experience attacks of asthma of varying severity. The initial pulmonary function tests were significantly higher among the asymptomatic group compared to the symptomatic group (FEV1 99.3 +/- 2.7% versus 90.5 +/- 2.2% predicted, respectively). Methacholine PC20 during the initial examination was higher among the asymptomatic group than in the symptomatic group (1.46 +/- 3.96 mg/ml versus 0.77 +/- 4.52 mg/ml, respectively). These findings indicate that the patients in the asymptomatic group were diagnosed at an earlier stage of the disease. This observation was confirmed by the significantly shorter duration of symptoms before diagnosis among the asymptomatic patients compared to the symptomatic patients (1.6 +/- 1.9 versus 2.6 +/- 4.3 years). Race, smoking status, immediate skin reactivity, and presence of plicatic acid-specific IgE antibodies did not influence the outcome of these patients. Of the 96 patients who continued to work with red cedar, 47 were exposed daily, whereas 41 were exposed intermittently.(ABSTRACT TRUNCATED AT 250 WORDS) We studied 29 subjects with latex-induced occupational asthma in a follow-up of 5 +/- 3 years. Initial and follow-up visits included a questionnaire and measurement of lung volumes, bronchial responsiveness to methacholine (PD20FEV1), and latex-specific serum IgE levels. At follow-up, 17 subjects were no longer exposed to latex, whereas 12 subjects had reduced exposure. Asthma and rhinitis symptoms, use of steroids and bronchial hyperresponsiveness improved significantly at follow-up, whereas mean FEV1% and FVC% decreased (p < 0.05). Multiple regression analysis showed that the main determinant of FEV1 and PD20FEV1 at follow up were the values of these variables at diagnosis. Complete recovery of occupational asthma was observed in 7 subjects (24%), all in the non-exposed group. Latex-specific IgE did not exhibit significant changes. In conclusion latex-induced occupational asthma improves after a follow-up of 5 +/- 3 years, but a complete recovery occurs in a minority of subjects and is associated with cessation of exposure. Lung function measurements at follow up depend from their impairment at the time of diagnosis. Thirty-one patients with isocyanate-induced asthma were studied 6-54 months after diagnosis. Four had the same work conditions and unchanged or worse respiratory symptoms; seven had an alternative job or safer work conditions at the same work-place and suffered from mild to severe symptoms. The remaining twenty subjects were definitely removed from exposure; of these, ten (50%) remained symptomatic after being removed from exposure for an average of 19 months. Asymptomatic patients appeared to be younger and to have shorter durations of total and symptomatic exposures, while symptomatic patients were more reactive to acetylcholine at diagnosis. For patients removed from isocyanate exposure and for those re-employed at the same work-place, quality of the new work site seems to play a role in the evolution of isocyanate-induced asthma. The aim of this study was to investigate the progression and long-term consequences of occupational asthma and to evaluate the effect of the pattern of response to specific bronchoprovocation test (SBPT) in the prognosis of occupational asthma among 40 subjects with asthma due to toluene diisocyanate (TDI). Nine subjects had immediate asthma, 25 subjects had late asthma and 6 subjects had dual asthma. Respiratory symptoms, persistence of exposure to TDI and lung function have been investigated both at diagnosis and at follow-up examination. At follow-up examination, 70.0% of the subjects were not exposed to TDI, and only 14.3% of "non-exposed" subjects were completely asymptomatic. At follow-up examination, 71.4% of "exposed" subjects and 55.6% of "non-exposed" subjects were regularly treated with medications because of their asthma (no statistical difference). No significant differences have been found in symptoms prevalence or lung function between "exposed" and "non-exposed" subjects. After comparing the results obtained at diagnosis and at follow-up examination, a significant decrease in FVC both in "exposed" and "non-exposed" groups (p < 0.005 and p < 0.0005, respectively) and a significant decrement in FEV1 (p < 0.05) and FVC (p < 0.0005) among the subjects with late asthma, was found. We can conclude that, despite the removal from TDI exposure, occupational asthma can lead to permanent disability with important socio-economic consequences, and late response to SBPT may be a negative prognostic factor in TDI asthma. We have compared the bronchial responsiveness (BR) of 12 aluminum potroom workers (index group) who were relocated due to work-related asthmatic symptoms (WASTH) and 26 subjects (reference group) with WASTH who continued to work in potrooms. The subjects were examined at regular intervals during a 2-year follow-up period. BR was expressed as the log-transformed dose-response slope [Ln(DRS 5)]. The monthly change in BR (delta BR) in the index group was -4.87 x 10(-2) compared with -1.58 x 10(-2) in the reference group. After adjustment for potential confounders, the difference between the index group and the reference group was -2.39 x 10(-2) (95% CI: -4.07 x 10(-2) to -0.71 x 10(-2)), i.e. 49% of the decrease in BR in the index group could be explained by the removal from exposure. No improvement in lung function was found in the index group compared with the reference group. The results indicate that the removal of potroom workers from exposure causes a decrease in BR. A follow-up study of 128 subjects with red cedar asthma was conducted to evaluate the clinical and socioeconomic impact of the disease in determining the working status of the subjects after the diagnosis was made. The results suggest that the severity of asthma is not the main determinant of working status. Comparing the data at diagnosis and at follow-up examination, we found that the persistence of exposure resulted in a deterioration in the asthma despite the use of more medications. Subjects who were working were younger and had a larger number of dependents than the subjects who were not working at the time of the follow-up examination. We conclude that the socioeconomic factors are important in determining the working status of subjects with red cedar asthma. To prevent severe impairment and disability, there should be more economic incentives for these subjects to choose other jobs. The clinical and socio-professional fate of subjects with occupational asthma is not univocal. We re-examined twenty-nine subjects diagnosed in our center as suffering from this disease an average 14 months, SE 1.54 after the diagnosis. At the follow-up examination each patient underwent interview, spirometry and methacholine challenge, 18 patients (group A) had ceased exposure to the sensitizing agent but among them only 7 had been relocated in another area of the plant, the others had resigned or retired. The other patients had not changed workplace, 7 (group B) having had intermittent exposure to the offending agent and 4 (group C) having continued to be exposed daily. At the follow-up examination only 9 patients were asymptomatic, each of them belonging to group A, whereas in the other 9 of the same group symptoms persisted, although reduced. In group B and C all patients were still symptomatic and required pharmacologic treatment. Within group A patients who became asymptomatic had shorter duration of symptoms before diagnosis (12.9 months, SE 6.4 vs 23.9, SE 9.7), higher FEV-1 (96.1, SE 6.7 vs 86.9, SE 5.6) and PD20FEV-1 (1773.4 micrograms, SE 590 vs 730.8, SE 295) at the time of the diagnosis and showed a significant (p < 0.01) increase in FEV-1 (from 96.1, SE 6.2 to 101.6, SE 5.5) and a tendency to decrease in bronchial reactivity to methacholine at the follow-up examination. At the time of the follow-up examination only 5 out of 29 patients (17.2%) had been contacted by the compensation board.(ABSTRACT TRUNCATED AT 250 WORDS) Isocyanates, particularly Toluene Diisocyanate (TDI), have been the most common cause of occupational asthma for decades. Fifty workers with a diagnosis of isocyanate-induced asthma were followed up for a mean period of 8.4 years. Pulmonary function testing for FVC and FEV1, allergological tests, nonspecific bronchial challenge to methacholine and specific bronchial challenge to isocyanates were performed at the time of diagnosis and during follow-up. Data on symptoms and drug response were rated on a scale. Patients were subdivided into two groups based on persistence of (A; 13 patients) or removal from (B; 37 patients) isocyanate exposure. There were no significant differences in any characteristic between the two groups at the time of diagnosis. At follow-up, group B subjects showed significant improvement in symptoms, consequent reduction in use of medications and increase in PD20. None worsened, sixteen (43.3%) remained stable, twelve (32.4%) improved and nine (24.3%) became asymptomatic. The latter subjects were generally younger, they had shorter duration of symptoms and exposure to the agents, and longer removal from exposure, although none of these differences was significant. In 67% of cases they had an immediate reaction to TDI challenge. By contrast, the condition of group A patients deteriorated significantly during the follow-up period in terms of symptoms, pulmonary function parameters, PD20 and use of medications. Overall, seven subjects (53.8%) worsened during follow-up and none improved. Group B subjects were further divided into subgroups B1 and B2 based on duration of removal from exposure: B1 < 10 years, B2 > or = 10 years. There were no significant differences between the two subgroups, even though PD20 was higher in B2. The present study confirms that early diagnosis and immediate removal from exposure are crucial, though not always sufficient, for a favourable evolution of the disease. Eighty-seven cases of occupational asthma induced by toluene diisocyanate (TDI) were diagnosed by an inhalation challenge with TDI and methacholine. After an average follow-up interval of 11 yrs, all subjects were re-examined. Of the 87 subjects examined, 13 (15%) had remained in the same job, 44 (50.5%) had been removed from exposure for <10 yrs and 30 (34.5%) had been removed for >10 yrs. The proportion of subjects who experienced symptoms of asthma and those who were hyperresponsive to methacholine was significantly lower. Of the patients, 59% used short-acting bronchodilators, 8% long-acting bronchodilators and 18% were on regular inhaled glucocorticoids. Thus, multiple regression analysis showed a positive correlation between forced vital capacity (FVC) and forced expiratory volume in one second (FEV1) at follow-up and FVC and FEV1 at diagnosis, and a negative correlation with smoking and with therapy with bronchodilators. Stepwise logistic regression showed that the follow-up provocative dose causing a 20% fall in the FEV1 (PD20) could be predicted from baseline PD20. These results indicate that respiratory symptoms and airway hyperresponsiveness to methacholine persist in subjects removed from exposure to TDI for >10 yrs. A more favourable prognosis was associated with a better lung function and a lower degree of airway hyperresponsiveness to methacholine at diagnosis. After an average follow-up interval of three and a half years (range one to nine years), 125 patients with occupational asthma due to red cedar exposure were re-examined. Fifty patients remained in the same job. All of them continued to have asthmatic attacks requiring regular medication for relief of symptoms. They had worse lung function and ther bronchial reactivity to methacholine increased. Seventy-five patients left the industry; half of them became asymptomatic, whereas the remaining half continued to have recurrent attacks of asthma. Several factors were of prognostic significance. Those with a shorter duration of exposure as well as a shorter duration of symptoms prior to diagnosis and removal from exposure showed improvement. Those who remained symptomatic tended to be older; they had longer duration of exposure and a longer duration of symptoms prior to diagnosis. They tended to have more abnormal results of lung function studied and more marked bronchial hyper-reactivity to methacholine at the time of diagnosis. They also tended to have dual asthmatic reaction rather than late asthmatic reaction to inhalation challenge with red cedar extract. Smoking, race and degree of peripheral blood eosinophilia did not play a role in determining the outcome. Since none of these patients had symptomatic asthma before employment and since they reacted to inhalation challenge of red cedar, it could be assumed that persistent asthma in those who failed to recover is the result of their previous occupational exposure. Early diagnosis and removal from exposure were found to be associated with recovery. Thirty-nine electronics workers were investigated by bronchial provocation testing to soldering fluxes containing colophony and were followed up one to four years later. At presentation and on follow-up each worker had nonspecific bronchial reactivity measured with inhaled histamine, and also had detailed measurements of lung function and estimation of total immunoglobulin levels. They completed a questionnaire designed to detect residual disability. The workers were divided into three groups. Twenty had left work after their initial diagnosis, eight had been moved to alternative work within their original factories, and 11 were thought to have asthma unrelated to colophony exposure as they failed to react to colophony at presentation. Histamine reactivity had returned to normal in half the workers who had left their original factories, but in only one worker who had moved within her original factory. This suggested that the nonspecific bronchial reactivity to histamine was the result rather than the cause of the occupational asthma, and that indirect exposure at work was sufficient to delay recovery of histamine reactivity. However, only two of the 20 affected workers who had left their original factories were symptom free on follow-up, and most had a considerable reduction in their quality of life by continuing asthma, which was particularly provoked by exercise, respiratory infections, and nonspecific irritants. Continuing symptoms may have been caused by domestic sources of colophony, or possibly the failure to eliminate colophony from the lungs. Persulfate salts are among the most frequently implicated causes of occupational asthma. The aim of this study was to describe the course of bronchial hyperresponsiveness and immunologic test results in patients with occupational asthma due to persulfate salts.
                Ten patients with occupational asthma due to persulfate salts were studied. Diagnosis was based on specific bronchial challenge tests performed at least 3 years before enrollment. An exhaustive medical and work history was taken during interviews with all patients, and all underwent spirometry and nonspecific bronchial challenge testing. Total immunoglobulin E levels were determined and skin prick tests to several persulfate salts were performed.
                At the time of evaluation, 7 patients had avoided workplace exposure to persulfate salts. The bronchial hyperresponsiveness of 3 of those 7 patients had improved significantly. No improvement was observed in patients who continued to be exposed. Specific skin prick tests became negative in 3 patients who were no longer exposed at the time of the follow-up evaluation. Most of the patients continued to report symptoms, although improvements were noted. One patient, however, reported worsening of symptoms in spite of avoidance of exposure.
                Although asthma symptoms and bronchial hyperresponsiveness may persist for patients with occupational asthma due to persulfate salts, their condition seems to improve if they avoid exposure. This course does not seem to differ from that reported for other cases of occupational asthma. Thirty-five subjects with occupational asthma due to toluene diisocyanate (TDI) exposure were examined. All the subjects were studied with inhalation challenges with TDI and with methacholine. TDI asthma was documented by a positive inhalation challenge to low levels of TDI. Airway responsiveness to methacholine was in the range of asthmatic patients at the time of diagnosis. After an average follow-up interval of 10 months, all the subjects were re-examined. Of the 35 subjects examined, 30 subjects (85.7%) left the workplace, and 5 remained in the same job. Twenty-seven subjects (77.1%) continued to have asthmatic attacks requiring medication for relief of symptoms. At follow-up examination, TDI asthma was documented by a positive inhalation challenge to TDI in 27 subjects. Of these 27 TDI reactors, 22 subjects were removed from occupational exposure to TDI. The TDI reactors had persistent respiratory symptoms and airway hyperresponsiveness to methacholine. At follow-up visit, 8 subjects (22.9%) lost sensitization to TDI; 5 subjects (62.5%) in this group had also normal airway responsiveness to methacholine after removal from exposure. Only 1 subject among the TDI nonreactors complained of mild respiratory symptoms. At diagnosis, there were no significant differences between subjects who recovered and those who did not with regard to age, smoking habits, atopy, duration of exposure to isocyanates, duration of symptoms, baseline FEV1 (% pred), and baseline airway responsiveness to methacholine.(ABSTRACT TRUNCATED AT 250 WORDS) There are few reports about longitudinal changes in lung function in asthmatic patients. Patients with asthma had a greater loss of lung function than normal healthy adults. To date, there have been no studies about the longitudinal changes in lung function in patients with occupational asthma.
                280 male patients with red cedar asthma (RCA) who were followed up for at least one year were the study group. The exposed controls consisted of 399 male sawmill workers. Forced expiratory volume in one second (FEV1) was measured with a Collins water spirometer. Changes in FEV1 over time (FEV1 slope) were calculated by a two point method for each subject. Atopy was considered to be present if the subjects showed at least one positive response to three allergens by skin prick test.
                Multiple regression analysis was carried out to examine factors that might affect longitudinal decline in FEV1. Patients with RCA who were still exposed had a greater decline in FEV1 slope (-26 ml/y) than sawmill workers. Smokers also showed a greater rate of decline in FEV1 (-43 ml/y) than non-smokers.
                Patients with RCA who continued to be exposed had a greater rate of decline in FEV1 than sawmill workers. Early diagnosis of occupational asthma and removal of these patients from a specific sensitiser is important in the prevention of further deterioration of lung function and respiratory symptoms. The outcome of the respiratory symptoms, pulmonary function tests and bronchial hyperresponsiveness was studied in forty-seven workers with respiratory disease due to toluene diisocyanate (TDI) (twenty-seven asthmatic and twenty non-asthmatic subjects) after about 2 years from the first examination. Eight of twelve asthmatic subjects who left the industry after the first examination complained at the follow-up of dyspnoea and wheezing, but pulmonary function tests were unchanged; bronchial hyperresponsiveness decreased in three, but most were still positive to challenge test with bethanechol at the follow-up. Fifteen subjects who continued their exposure to TDI showed at the follow-up a significant decrease of the spirometric parameters and an increase of the bronchial hyperresponsiveness, and symptoms of chronic bronchitis were more frequent at the second examination. Non-asthmatic subjects, both exposed and non-exposed to TDI at the second examination, showed a significant decrease of the pulmonary function tests but no relevant changes in bronchial hyperresponsiveness. Our data suggest that stopping occupational exposure to TDI frequently did not produce an improvement of the TDI bronchial asthma, and persistence of the occupational exposure causes a more rapid decline in the respiratory function. We performed a follow-up study on nine subjects with occupational asthma due to cobalt hypersensitivity confirmed by a specific bronchial provocation test. Both at diagnosis and at the two follow-up visits (1 and 3 years after the diagnosis, respectively), we graded the severity of asthmatic symptoms and the need for antiasthma treatment and performed lung function tests, measurement of airways responsiveness to methacholine (PD15) and skin tests. The evolution of the disease was established on the basis of the increase or decrease in asthmatic symptoms and the requirements for medication, FEV1 and PD15. After cessation of exposure, two subjects recovered, five improved and one remained stable; the subject who carried on working in the same environment deteriorated. The improvement in symptoms, medication need and lung function occurred earlier and in a larger number of patients than the improvement in methacholine hyperreactivity. At follow-up, the inhalation test with cobalt was repeated on three subjects who had stopped exposure and were asymptomatic and again they had bronchoconstriction. Our data show that early diagnosis and early removal from exposure after the onset of asthma are important factors for a favourable evolution of the disease and that specific and non-specific bronchial hyperresponsiveness can persist even in asymptomatic subjects no longer exposed to the sensitizing agent.
There is very low-quality evidence that removal from exposure improves asthma symptoms and lung function compared with continued exposure.
Reducing exposure also improves symptoms, but seems not as effective as complete removal.
However, removal from exposure is associated with an increased risk of unemployment, whereas reduction of exposure is not. The clinical benefit of removal from exposure or exposure reduction should be balanced against the increased risk of unemployment. We need better studies to identify which interventions intended to reduce exposure give most benefit.