This study aimed to examine the relationship between exposure to rat urinary allergens, atopic status, smoking and the development of allergic symptoms and specific sensitization.It is a case-referent analysis of a cohort of 342 newly employed laboratory animal workers. Cases comprised persons developing symptoms of laboratory animal allergy or a positive skin prick test to rat urinary allergens; each was matched with up to two asymptomatic referents. Subjects were assigned to categories of exposure based on measurements of airborne rat urinary allergens.Of the cases, 80% reported that their symptoms started within 2 yrs of employment. The odds ratio (OR) for development of each symptom type (respiratory, eye or nose and skin) and of an immediate skin test reaction was increased in those with direct contact with rats. A gradient of increasing OR for the development of any such symptom across exposure categories was found; for respiratory symptoms and skin test reactions the OR for subjects in the highest exposure category were lower than those in intermediate categories, a pattern attenuated when the analysis was confined to outcomes developing within 2 yrs of first exposure. Atopy increased the OR of most outcomes as did cigarette smoking, although there was no evidence of a relationship between smoking and the development of a specific skin test reaction.In conclusion, allergen exposure was confirmed as the most important determinant of laboratory animal allergy; by implication, measures to reduce exposure may be the most effective means to reduce its incidence. Eur Respir J 1999; 13: 1139±1143. Allergy to inhalable, animal-derived proteins is a common occupational health problem among employees working with small laboratory animals. In a prospective study of new staff at a large toxicological laboratory with several animal species, the incidence of clinically-diagnosed laboratory-animal allergy in the first year was 9% and that of specific immunoglobulin (Ig)E development~22% [1].Figures from the surveillance of work-related and occupational respiratory disease (SWORD) national surveillance scheme indicate that laboratory animal proteins are the commonest high molecular weight cause of occupational asthma seen by chest and occupational physicians in the UK [2]; the annual incidence of new cases of laboratory animal asthma in the UK, estimated from the same source, is at least 188 per million exposed employees [3].With the development of immunoassays [4] it has become possible to measure directly the relationship between intensity of exposure to airborne animal allergens and sensitization and allergic disease. This relationship has been studied in a cohort with occupational exposure to laboratory rats; in a previous report of the initial, cross-sectional phase [5] weak associations between allergic symptoms and rat urinary aeroallergen exposure, modified by atopic status were described. The present study describes the findings of a full longitudinal study, analysed using a nested case-referent approa...

This study supports the view that patients with specific IgE to grass pollen are at risk of thunderstorm-related asthma. The details of the causal pathway from storm to asthma attack are not clear. Case-control and time series studies are being carried out.

A cross sectional survey was carried out on 138 workers exposed to laboratory animals. Sixty (44%) had symptoms in a self completed questionnaire that were consistent with laboratory animal allergy (LAA) of whom 15 (11%) had chest symptoms. There was a positive skin prick test to one or more animal urine extracts (rat, mouse, guinea pig, rabbit) in 13% and 38% had a positive radioallergosorbent test to urine extract. LAA chest symptoms were almost five times more common in atopic than non-atopic subjects (who were distinguished by skin test response to common, non-animal aeroallergens). A positive skin test to animal urine was associated with LAA chest symptoms and with atopy. Nose, eye, or skin symptoms without chest symptoms were not associated with atopy. There was an inverse relation between duration of employment at the firm and LAA chest symptoms, suggesting selection of affected people out of employment with animals.

After identification of a case of extrinsic allergic alveolitis due to exposure to wood dust at a sawmill, all employees at the sawmill where he worked were studied with an occupational, environmental, and symptom questionnaire, spirometry, skin prick tests, and serum specific IgG measurements. Ninety five of current and 14 of 17 ex-sawmill workers were studied. As a basis for comparison, a group of 58 workers from a nearby light engineering factory were also studied. Few women (6) were employed and they were excluded from the analysis. Workers at the sawmill were stratified into high and low exposure groups depending on their place of work. This division was supported both by their subjective assessment of the dustiness of their environment and the results of personal dust samples. There were no significant differences between the three groups in age, height, smoking habits, exposure to other causes of extrinsic allergic alveolitis, forced expiratory volume in one second, forced vital capacity, atopic state, or cutaneous reactivity to moulds. In the high exposure group the prevalence of work related cough and nasal and eye symptoms was higher than in the low exposure and comparison groups. The prevalence of work related wheeze was similar in both the high exposure and comparison groups, but was lower in the low exposure group. The prevalences of chronic bronchitis and symptomatic bronchial hyper-reactivity were similar in the high and low exposure groups but were lower in the comparison group. Serum concentrations of specific IgG against extracts of sawdust and Trichoderma koningii were significantly higher in the high exposure group than in the other two groups. The prevalence of symptoms suggestive of extrinsic allergic alveolitis was 4 4% in the high exposure group, greater than in the low exposure group (0%), and the comparison group

This study supports the view that patients with specific IgE to grass pollen are at risk of thunderstorm-related asthma. The details of the causal pathway from storm to asthma attack are not clear. Case-control and time series studies are being carried out.

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This study supports the view that this epidemic was larger than previously reported epidemics and the hypothesis that "thunderstorm associated asthma' is related to aeroallergens. Demands on resources were considerable; a larger proportion of patients needing intensive care would have caused greater problems.

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