A survey of dust exposure, respiratory symptoms, lung function, and response to skin prick tests was conducted in a modern British bakery. Of the 318 bakery employees, 279 (88%) took part. Jobs were ranked from 0 to 10 by perceived dustiness and this ranking correlated well with total dust concentration measured in 79 personal dust samples. Nine samples had concentrations greater than 10 mg/m3, the exposure limit for nuisance dust. All participants completed a self administered questionnaire on symptoms and their relation to work. FEVy and FVC were measured by a dry wedge spirometer and bronchial reactivity to methacholine was estimated. Skin prick tests were performed with three common allergens and with 11 allergens likely to be found in bakery dust, including mites and moulds. Of the participants in the main exposure group, 35% reported chest symptoms which in 13% were work related. The corresponding figures for nasal symptoms were 38% and 19%. Symptoms, lung function, bronchial reactivity, and response to skin prick tests were related to current or past exposure to dust using logistic or linear regression analysis as appropriate. Exposure rank was significantly associated with most of the response variables studied. The study shows that respiratory symptoms and sensitisation are common, even in a modern bakery.Occupational asthma and rhinitis occur in bakers' and the environmental agents responsible appear to be components of the grain itself" or grain contaminants, such as mites, weevils, and moulds"7 The relative importance of these potential allergens may vary according to the source of the flour, conditions of storage, and intensity of exposure. Recent papers describing grain components as important allergens have come from Australia,24 where grain has a low moisture content. A higher moisture content, or storage ofgrain or flour for long periods, may promote the growth of contaminant micro-organisms, mites, and insects. Materials added to flour before baking, such as yeast and amylase, derived from Aspergillus species,' may also be allergenic. As many as a third ofbakers and grain workers may show evidence of sensitisation,9" which appears to be related to intensity and duration of exposure in the industry as well as to host factors, such as atopy." 12 Mechanisms involving IgE and the mast cell have been implicated,'2 13 but precipitins to components of flour have also been identified' and non-immunological processes, such as direct activation of complement pathways, may be involved.'4Apart from case reports, there is little information about asthma and sensitisation in British bakers. This study was designed to (a) describe the levels of exposure to bakery dust in a modern British bakery, (b) estimate the prevalence of symptoms and sensitisation in the workforce of the bakery, and (c) explore relations between indices of exposure and response. Methods STUDY DESIGN AND SUBJECTSThe study was a cross sectional survey of current employees conducted over six consecutive days and nights. All current...

A survey was carried out of a population of workers exposed to tetrachlorophthalic anhydride, an acid anhydride epoxy resin curing agent known to cause asthma. Using a radioallergosorbent test with a tetrachlorophthalic anhydride human serum albumin conjugate, specific IgE antibody was detected in serum from 24 out of 300 factory floor workers exposed to tetrachlorophthalic anhydride. Of these 24, 20 (83-3%) were current smokers compared with 133 (48 2%) of 276 without antibody (p <0 01), and there was a weaker association with atopy, defined by skin tests with common allergens. Smoking and atopy interacted, the prevalence of antibody being 16 1% in atopic smokers, 11-7% in non-atopic smokers, 8-3% in atopic non-smokers, and nil in non-atopic non-smokers (p <0 025). Smoking may predispose to, and interact with atopy in, the production of specific IgE antibody to this hapten protein conjugate.

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Occupational asthma caused by allergy to pigs' urine We report a case of asthma due to occupational exposure to pigs. The cause of the symptoms was exposure to the urine of the animals. This was proved by provoking acute asthma with an inhalation challenge of an extract of pigs' urine at a concentration of 1 g/l. On a second occasion this asthmatic response was blocked by prior treatment with 40 mg sodium cromoglycate (Intal). The patient's serum contained specific IgE antibody to the urine extract which was not found in unexposed controls. Case report The patient, a 21-year-old eczematous woman who enjoyed a vigorous sporting life, playing squash and hockey to a high standard, had not suffered respiratory symptoms since the age of 3. During her second year at university studying agricultural sciences her class visited a pig house. Within two to three minutes she had to leave because she felt as if she was being "stifled with a plastic bag." She took about an hour to recover her breath and within a few minutes her eczema had begun to itch, and this took a further two hours to settle. One year later, within five minutes after starting to watch a laparo-tomy on a pig, she again became short of breath. Her only other exposure to these animals had been during a visit to the pig house in her first year, when she remained symptomless. Skin-prick tests yielded positive reactions to grass, house-dust mite, horse, cat, dog, and pork extract. Pigs' urine (50 ml) was filtered, sterilised, and freeze dried as described1 and reconstituted in Coca's solution at 01 and 1 0 g/l. Skin testing produced a 3 mm weal with the solution at 1 0 g/l. After inhaling a nebulised dose (0-0015 g) for one minute her forced expiratory volume in one second (Vitalograph) fell by 70 % from 2-3 to 0-7 1. The same test was conducted one week later after 40 mg of sodium cromoglycate had been given by inhalation 10 minutes before the challenge. On this occasion her forced expiratory volume in one second fell by nearly 28 %0 from 2-5 to 1-8 1. In each case recordings were made for a further five hours throughout-Chcallenge 3 eDSCG (40 mg). Oi beeNo trestment 0 c 2-E '-1 0 w2 0 102030 40 5060 2 3 4 5 6 Time (minutes) Time (hours) Results of two inhalation tests performed one week apart. On each occasion subject inhaled nebulised pigs' urine 1 g/l for 60 seconds. Asthmatic response was inhibited with sodium cromoglycate (DSCG) 40 mg given 10 minutes before test. the day. No non-immediate reaction developed (figure). A radioallergo-sorbent test performed with the same urine extract showed her blood to contain specific IgE antibody, 23-9 % of the counts added in the assay being bound, as compared with 0-73 , with cord blood and a mean of 0-69 %o with six blood-bank controls. Comment Asthma has resulted from inhaling certain proteins in the urine of mice, rats, guinea-pigs, and rabbits in sensitised subjects but not from inhaling the animal serum.' 2 Our patient's sensitivity to pigs' urine raises the possibility that urine of other mammals may also cause...

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The prevalence of work-related wheeze and breathlessness was measured in factory employees manufacturing flux-cored solder. The flux contained colophony which was heated in the production process, exposing the workers to colophony fumes. Measurement of colophony in the breathing zone defined three grades of exposure with median levels of 1-92 mg/i3 (six subjects), 0-02 mg/m3 (14 subjects), and less than 0O01 mg/m3 (68 subjects). All but two workers in the first two groups, and 90 % of a random sample of the last group, were studied. Occupational asthma was present in 21 % of the higher two exposure groups and 40% of the lowest exposure group. Mean values of FEV1 and FVC fell with increasing exposure. The prevalence of upper and lower respiratory symptoms was only one-third to a half that found in a previous study of shop floor electronics workers, whose work raised the flux to a higher temperature and produced higher concentrations of colophony fume. Total IgM levels were higher in the solder manufacturers than in unexposed controls, and were higher still in the electronics workers. The solder manufacturers were exposed to colophony fumes at 140°C, below the temperature at which the resin acids decompose, supporting the hypothesis that it is the whole resin acids rather than decomposition products which cause occupational asthma. The threshold limit value should be based on the resin acid content of the fume, and not the aldehyde content as at present. The survey suggests that sensitisation will not be prevented unless exposure is kept well below the present threshold limit value.Colophony (rosin, pine resin), the principal constituent of non-corrosive soft soldering fluxes, has been shown to be the sensitising agent in a group of electronics workers with occupational asthma.'-3 A prevalence study of respiratory symptoms in a factory making consumer electronics by mass production techniques showed that 22% of the shop floor workforce had work-related wheeze or breathlessness or both. It was thought that the level and duration of exposure to fume were the most important factors leading to sensitisation.5 6 Resin acids are broken down on heating above 200°C to form a large number of compounds, some of which are aldehydes,7 so the composition of the fume depends on the temperature at which it is heated.8 Bronchial provocation studies have shown that reactions to colophony in sensitised workers are reduced by methylation of the resin acid carboxyl groups. The whole resin acids are likely to be the cause of the asthma as the thermal degradation products should be similar with methylated and unmodified resin acids. The factory processWe were asked to investigate workers in a factory making flux-cored solder containing American WW and Portuguese Y colophonies (in future called solder manufacturers) to investigate the effects of colophony fumes produced by heating at a temperature lower than the 350-450°C common in electronics factories. The factory was in two separated buildings. Four men were employed in a sm...

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