Changes in the levels of anti-phospholipase A2 and hyaluronidase antibodies during bee venom immunotherapy.
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Biomedical subjects
Publications and source records attributed to M G Harries.
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Sulphur dioxide inhaled at low concentration had no detectable effect on forced expiratory volume in one second in non-asthmatic atopic controls, but it induced asthma and increased bronchial reactivity in nine symptomless atopic and non-atopic asthmatic patients. This increased reactivity was inhibited by sodium cromoglycate (SCG) and partly inhibited by atropine. This suggests that SCG, in addition to its ability to stabilise mast cells, may also act on bronchial irritant receptors or directly on smooth muscle in asthmatic patients.
Regardless of whether the stimulus to the airway is cold air, exercise, agents causing occupational asthma or sulphur dioxide the resulting bronchoconstriction is inhibited by prior treatment with cromolyn sodium, a drug thought to act only by preventing release of histamine from mast cells. Study of bronchial irritants, however, suggests that this drug may also act either directly on bronchial muscle or on irritant receptors.
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Dose-response curves for atropine and ipratropium bromide were made in nine asthmatics unresponsive to salbutamol. Conventional doses of ipratropium resulted in significantly less bronchodilatation than large doses of atropine, suggesting that larger doses of ipratropium should be used.
Flux cored solder commonly used in the electronics industry is a metal alloy, based on tin and lead, and a flux consisting of colophony with a small concentration of an activator. Thirty-four electronics workers with occupational asthma and seventeen with respiratory symptoms, probably from other causes, have been investigated by occupational type bronchial provocation testing. All the sensitized workers had a significant fall in FEV1 after exposure to colophony fumes for 15 min or less. The non-sensitized workers had no significant reactivity to this test. There was little correlation between the reaction to colophony fumes and the non specific reactivity to histamine, suggesting that colophony fumes were causing specific sensitization. In sensitized workers Portuguese Y colophony was found to cause slightly larger reactions than similar exposures to American WW colophony. In the six workers tested reactions followed exposure to abietic acid alone, the principal resin acid in colophony. Methylation of the carboxyl group of colophony was associated with decreased reactivity. Workers with non-specific bronchial hyperreactivity also sometimes reacted after exposure to fumes from the flux activators alone, but even this reaction could show specificity for the specific activator to which the workers was exposed. Finally two non-colophony substitute materials were evaluated.
The prevalence of work-related asthma, rhinitis and urticaria was measured in a scientific establishment working with locusts. Twenty-six percent of those handling the locust in the research centre had work-related wheeze or breathlessness, and one-third had work-related rhinitis and urticaria. Work-related symptoms were uncommon in scientists exposed to locusts in the field, and in other employees at the centre. Antigens were prepared from the locusts, Schistocerca gregaria and Locusta migratoria, as well as the moth, Chilo partellus, which was also bred at the centre. Skin prick testing with the locust antigens showed positive reactions in 55% of the atopic workers at the centre, but were also present in 43% of unexposed atopic workers. In this latter group there was a correlation between positive reaction to locust and dermatophagoides antigens. Atopic workers handling the locusts developed occupational asthma more often and more quickly than similarly exposed non-atopic workers. IgG and IgE antibodies to the locust antigens were found to correlate significantly with both the degree of exposure and the presence of disease.
A group of forty-two steroid-dependent perennial asthmatics was studied over a 13-week period incuding the 8 weeks of a double-blind controlled trial of oral sodium cromoglycate. Given at a dose of 200 mg four times per day the drug provided no significant benefit to the patients when compared with results for those on placebo. Blood from eleven patients consistently failed to release more than 25% of the total cellular histamine when challenged with a range of concentrations of antibody to IgE. All six of the cryptogenic (intrinsic) asthmatics in the trial fell within this group, together with 2/12 asthmatics with negative skin tests but suggestive clinical histories implicating common alergens, and 3/24 extrinsic asthmastics with positive skin prick tests. There was no correlation between drug usage and histamine release in response to challenge with antibody to IgE.
Thirty-seven patients with asthma or alveolitis thought to result from exposure to materials commonly encountered at their work were tested by inhalation of an aerosol of these materials. Twenty-four (65%) developed an immediate asthmatic reaction, which was followed by a non-immediate reaction in 10, of whom six developed the signs and symptoms of alveolitis. Eighteen (76%) patients with asthmatic reactions to test material were prick test positive to that material while only two our of 13 with a negative inhalation test were prick test positive (15%). Precipitating antibody to test material was measured in 23 and was present in nine (39%) of those with positive inhalation tests, and one (12%) of those with negative tests. It was present in five of the six with a reaction in the gas exchanging portions of the lung.
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A group of twenty four workers handling di-isocyanates and with respiratory disease were investigated by occupational-type bronchial provocation tests for sensitivity to toluene di-isocyanate (TDI), to which all were exposed, and to diphenylmethane di-isocyanate (MDI) and hexamethylene di-isocyanate (HDI). Sixteen gave asthmatic reactions to TDI and eight of these also reacted to MDI. Four of the eight TDI and MDI reactors had histories of exposure only to TDI, and of them two reacted also to HDI. Of nine subjects tested with HDI, three gave asthmatic reactions, and all three also reacted to TDI and MDI. Thus reactions to MDI and HDI were elicited only in the TDI reactors. The possibility of specific sensitivity to these and other di-isocyanates requires tests in subjects exposed to them and not to TDI.
In sixty-three workers exposed to toluene di-isocyanate (TDI), no overall differences in bronchial reactivity to histamine inhalation and to exercise testing were found between the total groups of positive and negative TDI reactors to provocation tests. A subgroup of TDI highly sensitive subjects reacting to very low concentrations (less than or equal to 0.001 p.p.m.) were more sensitive to both histamine and exercise than the group who were less sensitive to TDI, and who reacted to higher concentrations (0.002--0.02 p.p.m.) than the group of non-reactors. There were, however, in the last group a number of subjects with high degrees of histamine reactivity who did not react to the TDI. These findings suggest that, on the one hand, the asthmatic reactions to TDI cannot be attributed solely to non-specific mechanisms and, on the other, that in subjects with high degrees of specific sensitivity non-specific mechanisms may also be playing a part.