Biomedical subjects
Publications and source records attributed to P S Burge.
Occupational asthma due to the pyrolysis products of polyvinyl chloride (PVC) produced by shrink wrapping processes has previously been reported. The first case of occupational asthma in a shrink wrap worker using a different plastic, polyethylene, is reported; the association was confirmed by specific bronchial provocation testing.
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.
Two patients are described with occupational asthma due to carmine, a natural dye extracted from the insect Coccus cactus. Both had dual asthmatic reactons after carmine inhalation. Oral challenge provoked gastrointestinal symptoms in one patient, and asthma in them both, perhaps accounting for their continuing symptoms. One patient worked extracting carmine from the insects and the other used carmine as a cosmetic colouring agent.
Histamine has been measured in whole blood and in the plasma of twenty-three subjects following exercise testing of seventeen asthmatics and six normal controls. Whole blood histamine rose in both asthmatics and controls and was associated with a concomitant rise in the basophil count. Plasma histamine in the peripheral venous blood only rose in one patient who developed urticaria after exercise.
Workers in a modern electronics factory were surveyed by questionnaire and lung function testing to see if there was evidence of widespread work-related respiratory symptoms. Of the responding workers exposed to solder flux fumes on the shop floor, 22% had work-related breathlessness or wheeze or both. Exposed workers had a lower FEV1 and FVC than unexposed workers. Work-related rhinitis was also present in 22% of exposed workers. The most likely cause for these results is sensitivity to colophony fumes, released from solder flux during soldering. Levels of solder flux fume were below the threshold limit value in this factory during the survey.
Examination of the records of employees leaving an electronics factory over three-and-a-half years showed that a significantly greater proportion left the shop floor (where soldering took place) because of ill health than left the stores and office areas. This difference was largely due to work-related respiratory disease in those whose job was soldering. Shop floor workers leaving for health reasons also had increased sickness certification due to respiratory illness compared to stores and office workers. These findings suggest that work-related respiratory illness is a significant cause of morbidity and loss of employment in solderers working at the factory and that this has been a longstanding problem with its onset before the first recorded cases of occupational asthma caused by solder flux containing colophony.
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Peak expiratory flow rate (PEFR) has been measured hourly from waking to sleeping in 29 workers with respiratory symptoms exposed to the fumes of soft soldering fluxes containing colophony (pine resin). Thirty-nine records of mean length 33 days have been analysed, and the results compared with the occupational history and bronchial provocation testing in the same workers. From plots of daily mean, maximum, and minimum PEFR, recurring physiological patterns of asthma emerge. The most common pattern is for asthma to increase with each successive working day. Some workers have an equivalent deterioration each working day. Regular recovery patterns taking one, two, and three days are described. The combination of a three-day recovery pattern and a late asthmatic reaction on Monday results in Monday being the best day of each week. Assessment of these records has shown them to be specific and sensitive, provided the worker was not taking corticosteroids or sodium cromoglycate during the period of the record and that bronchodilator usage was kept constant on days at home and at work. The results of the PEFR records correlate well with bronchial provocation testing, and provide a suitable alternative to this for the diagnosis of mild to moderate occupational asthma. The records are of particular use for screening symptomatic workers whose symptoms appear unlikely to be related to work.
Peak expiratory flow rate (PEFR) has been recorded hourly or two-hourly from waking to sleeping in workers with respiratory symptoms who were exposed to isocyanate fumes at work. Twenty-three recordings averaging 33 days duration were recorded in 20 workers. Each worker was also admitted for bronchial provocation testing to toluene di-isocyanate (TDI) or diphenylmethane di-isocyanate (MDI) fumes or both. A final assessment of work-related asthma made from subsequent work exposure was compared with the results of bronchial provocation testing and a subjective assessment of the peak flow records. Both techniques were specific and sensitive. Physiological patterns of occupational asthma were defined from the records of PEFR. The most striking finding was the slow recovery from work-induced asthma. This commonly took several days to start and in one worker took 70 days to complete after leaving work. Several workers developed a pattern resembling fixed airways obstruction after repeated exposure at work. The consequences of these findings for the recording of symptoms of occupational asthma are discussed and recommendations are made for the recording of PEFR in workers in general.
Occupationally related asthma developing in three patients due specifically to exposure to 1,5-naphthylene di-isocyanate (NDI), a hot curing agent used in manufacturing rubber, has been confirmed for the first time using bronchial provocation testing. This substance has been thought to be safer than toluene di-isocyanate (TDI) and diphenylmethane di-isocyanate (MDI) because of its relatively high melting point (120 degrees C). Each patient worked in the same factory and the circumstances of exposure were similar. Provocation testing was also performed with TDI in concentrations up to 0.018 parts per million (ppm) and MDI in concentrations up to 0.02 ppm, to which the patients had been exposed in the past, but no reactions were elicited. None of the patients had increased bronchial reactivity judged by histamine lability and exercise testing. Each patient was advised to give up his job, but two of the three could not find alternative employment and remained exposed. Three-year follow-up shows that airways narrowing has persisted in those who have remained exposed.
Twenty-one patients are described who developed asthma, or evidence of a peripheral airways reaction, while working in the electronics industry and exposed to solder flux fumes containing colophony (pine resin). This selected group contained five patients with pre-existing asthma. Fourteen patients had never smoked. Prick-testing with common environmental antigens gave one or more positive reactions in nine patients. The diagnosis was confirmed by occupational-type provocation tests in all workers with colophony-based cored solder, and reproduced by exposure to the fumes of heated colophony alone. Control subjects did not react to the test with colophony. The clinical findings and provocation test reactins have features of a hypersensitivity reaction, although so far specific antibodies have not been found.
Out of twenty patients with a history of asthma or urticaria attributed to food substances, ten reacted on oral challenge: seven with asthma, one with asthma and urticaria and two with urticaria alone. In five of the eight asthmatic reactors, the symptoms developed within a few sec and there was no associated rise in free venous plasma histamine. In those remaining, two with asthma, two with urticaria and one with both, the symptoms developed only after 20-30 min. A rise in free plasma histamine occurred only in the two subjects with urticaria alone. The third with urticaria and asthma did not have blood estimations performed. Sodium cromoglycate in a dosage of 800 mg a day for 1 week, or a single dose of 1.0 g by mouth, did not block any of the reactions. By inhalation it blocked the asthmatic reactions which developed within a few sec of challenge.
A teacher with breathlessness of insidious onset developed acute symptoms on return home following his discharge from hospital. His flat was found to have extensive dry rot (Merulius lacrymans). Precipitins and specific IgE and IgG antibody against M. lacrymans were present and intracutaneous testing gave a typical dual skin reaction. Pulmonary physiology demonstrated airflow obstruction with a low DLCO and KCO, and a chest X-ray showed diffuse micronodular shadowing, maximal in the mid-zones. Inhalation challenge testing provoked a combined asthmatic reaction without a change in DLCO. Rapid clinical recovery and more gradual radiographic and physiological improvement followed cessation of exposure to the antigen.
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A woman with an intracellular killing defect in the neutrophils had neutrophil pyruvate kinase deficiency. She had had recurrent staphylococcal infections throughout her life. The enzyme present was unstable and its kinetics were abnormal.