Specific Bronchial Responsiveness Research Articles

Treating the allergic patient: think globally, treat globally.

Treating the allergic patient: think globally, treat globally.

Persistence of airway responsiveness to occupational agents: what does it matter?

In the majority of workers with occupational asthma, the disease remains active even several years after removal from exposure or diminution of the levels of exposure to the causal agent. Only 25% or so normalize their lung function and their bronchial responsiveness to nonspecific agents. The aim of this review is to present recent findings illustrating the persistence of specific bronchial responsiveness and the associated factors in workers who apparently have recovered from occupational asthma. This subject is also examined from a socioeconomic perspective.

Outcome of specific bronchial responsiveness to occupational agents after removal from exposure.

A decrease in specific bronchial responsiveness (SBR) could occur after removal from exposure to an agent causing occupational asthma as a result of loss of immunologic and/or nonspecific bronchial reactivity (NSBR). We studied 15 subjects with occupational asthma (eight to a high- and seven to a low-molecular-weight agent, isocyanate in all instances), proved by specific inhalation challenges (SIC) done 2 yr or more before. Subjects were reexposed in the same way as in the initial SIC: for subjects who did not react, the exposure was increased until either an asthmatic reaction occurred or a maximum of 2 h was reached. NSBR was assessed before and after SIC. Subjects had a decrease in their SBR if the total dose of agent necessary to induce asthmatic reaction was greater by twofold compared with the initial SIC. There was a significant improvement in NSBR in seven of 15 subjects. Nine of 15 subjects (60%) had a decrease in their SBR. Only one had a complete loss of SBR. Changes in NSBR, molecular weight of the offending agent, decrease of antibody level against offending agents, or duration of exposure at work did not explain the decrease in SBR. We conclude that after removal from exposure to the offending agent a majority of subjects (60%) show a decrease but a persistence of SBR to high- and low-molecular-weight agents.

Absence of relationship between degree of nonspecific and specific bronchial responsiveness in occupational asthma due to platinum salts.

There is evidence that bronchial responsiveness to allergen is quantitatively correlated with bronchial responsiveness to nonspecific stimuli in subjects with allergic asthma. This association has been questioned in occupational asthma due to low molecular weight substances. It was the aim of this study to assess the quantitative association of bronchial responsiveness to methacholine (MCh) and platinum salts (Pt), in the form of hexachloroplatinic acid, in workers with occupational asthma due to platinum salts. Fifty seven subjects with exposure to Pt, work-related asthma, and a positive bronchial challenge with Pt, underwent skin prick tests with Pt and bronchial challenge with MCh. Using the provocation concentration causing a > or = 50% fall in specific airway conductance (PC50sGaw(Pt)) as dependent variable, anamnestic data (period from first symptoms to removal, period between removal from exposure and diagnosis, and smoking), season of the investigation, skin prick tests with environmental allergens, total immunoglobulin E (IgE), skin reactivity to Pt (Pt concentration causing a 2 mm wheal), and PC50sGaw(MCh) were included as independent variables for regression analysis. Fifty two subjects (91%) showed a PC50sGaw(MCh) < 8 mg.mL-1 (geometric mean for all subjects 1.6 mg.mL-1). Responsiveness to Pt varied widely between subjects (geometric mean of PC50sGaw 9 x 10-5 mol.L-1, range 2 x 10-7 to 10-2 mol.L-1). There was no univariate correlation between bronchial responsiveness to MCh and Pt, but there was a correlation between skin reactivity to Pt and PC50sGaw(Pt) (r = 0.6). This association could not be improved by considering PC50sGaw(MCh), the period from first symptoms to removal, or the period between removal from exposure and diagnosis. The parameters that showed the highest (negative) associations with PC50sGaw(Pt) were skin reactivity to Pt and the period between removal from exposure and diagnosis (r = 0.65). We conclude that there is a moderate association between bronchial responsiveness to platinum salts and skin reactivity to platinum salts. However, there is no association between methacholine responsiveness and bronchial responsiveness to allergen in occupational asthma due to platinum salts.

264 Outcome of specific bronchial responsiveness to occupational agents after removal from exposure

264 Outcome of specific bronchial responsiveness to occupational agents after removal from exposure

Nonspecific and specific bronchial responsiveness in occupational asthma caused by platinum salts after allergen avoidance.

Most data about the course of occupational asthma after removal from exposure are based upon the longitudinal assessment of employees exposed to substances inducing late asthmatic reactions in bronchial provocation tests. It was the aim of this study to describe the course of immediate-type occupational asthma after allergen avoidance. Twenty-four platinum refinery workers were examined on two occasions. All subjects reported work-related asthma while they worked in the refinery department. The diagnosis of platinum salt asthma was established by a positive bronchial challenge test with hexachloroplatinic acid in each case. Eleven of the 24 subjects were still exposed to platinum salts at the time of the first investigation, but all had been removed from exposure for 19 mo (1 to 77) on the second investigation. Asthma was still reported by 17 subjects, and all but two showed bronchial hyperresponsiveness (PC50SGaw < 8 mg/ml) on the second investigation. Bronchial responsiveness to methacholine, skin reactivity, and bronchial responsiveness to platinum salt, as well as FEV1, did not change between assessments. Total serum IgE decreased from 126 to 103 U/ml (p < 0.005). Analysis of variance showed no association of the individual differences in PC50 (methacholine) between both investigations with smoking, time from the onset of symptoms to removal, time from removal to the first or second investigation, skin sensitization to environmental allergens, or total IgE. We conclude that both nonspecific and specific bronchial responsiveness do not decrease after removal from exposure in immediate-type asthma caused by platinum salts.

98 Effects of hyperosmolar saline challenge on non specific bronchial responsiveness to methacholine

98 Effects of hyperosmolar saline challenge on non specific bronchial responsiveness to methacholine

Bronchial responsiveness to histamine or methacholine in asthma: measurement and clinical significance

Bronchial responsiveness is the term used to describe the tendency of the airways to bronchoconstrict to specific stimuli such as allergens and isocyanates, which select a limited population of apparently sensitized subjects, and to nonspecific (nonallergic) stimuli, which affect most asthmatic persons. Specific bronchial responsiveness to allergic stimuli is difficult to quantitate because commonly available allergen extracts are not well standardized for the number and concentration of components. Nonspecific responsiveness can be quantitated by inhalation tests with histamine or methacholine, by exercise, or by isocapnic hyperventilation of cold air, and may be increased in asthma and other conditions such as chronic obstructive bronchitis and cystic fibrosis. In this article we will discuss the measurement of nonspecific bronchial responsiveness by inhalation tests with histamine or methacholine and its relationship to the occurrence and severity of asthma.

Asthma caused by occupational exposure to a furan-based binder system

A 50-yr-old mold maker developed severe asthma a few weeks after commencing work with a furan binder. Asthma recurred within hours of subsequent exposure and was confirmed by measurements every 2 hr of peak flow rate. The molds were prepared by mixing sand with a resin (containing furfuryl alcohol, paraformaldehyde, and xylene) and a catalyst (containing sulfuric acid, phosphoric acid, and butyl alcohol). Occupation-type exposure in the laboratory to the resin mixed with catalyst, and to pure furfuryl alcohol mixed with sulfuric acid or butyl alcohol, provoked late asthmatic responses and heightened nonallergic bronchial responsiveness to inhaled histamine. No changes were produced by the same exposures in an asthmatic volunteer with a similar degree of histamine bronchial responsiveness, or in the worker after exposure to resin alone and catalyst alone. Avoidance of exposure was followed by clearing of symptoms and return of histamine bronchial responsiveness towards normal. The findings identify the occurrence of specific bronchial responsiveness to volatile reaction product(s) of furfuryl alcohol following reaction with sulfuric acid or with butyl alcohol. The incidence of this problem needs investigation, especially since furan-based binder systems are replacing traditional methods.