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.

This study examined data from three cross sectional surveys of 296 laboratory workers exposed to small mammals. Four indices of laboratory animal allergy were studied: symptoms suggestive of occupational asthma, symptoms suggestive of any occupational allergy, skin weals to animal urine extracts, and serum binding in radioallergosorbent tests with urine extracts. Pooled data from the three surveys showed an association between smoking and all indices except radioallergosorbent tests; the association was significant for symptoms of occupational asthma. One of the three surveys consistently showed a stronger association of allergy indices with smoking than with atopy (defined on skin tests with non-animal aeroallergens). Associations with smoking persisted after stratifying by atopic status, suggesting that smoking may be a risk factor for laboratory animal allergy.Smoking is associated with asthma caused by enzyme detergents' and snow crabs,2 with skin weals to Bacillus subtilis? and coffee bean,4 and with serum IgE antibody against ispaghula4 and tetrachlorophthalic anhydride (TCPA).5 This suggests that smoking is a risk factor for occupational allergy, possibly by increasing mucosal transport of antigen.56 The study of TCPA workers showed a statistically significant interaction between smoking and atopy (defined on skin tests with common aeroallergens): 16% of 31 atopic smokers had IgE antibody against TCPA, 12% of 111 non-atopic smokers, 8% of 36 atopic nonsmokers but none of 98 non-atopic non-smokers.5 In animal experiments inhalation of tobacco smoke and other bronchial irritants potentiates sensitisation by inhaled antigen. '-9 Laboratory animal allergy (LAA) is common in research workers, who may show prevalence rates of over 40%."' Atopy is associated with IgE antibody to animal allergens and with asthma caused by animals but less closely with nasal, eye, or skin symptoms when these are present without chest symptoms."1013 To date, no relation between smoking and LAA has been identified. The survey of laboratory workers described in a companion paper found a slight excess of current smokers in those with symptoms suggestive of occupational asthma.'0 We therefore examined data from this and two other populations to see if LAA is associated with smoking. Accepted 12 October 1987 MethodsWe have carried out cross sectional surveys of three populations occupationally exposed to animals. Survey A was ofpharmaceutical research workers and is described in a companion paper.'0 Survey B was of research workers at a tobacco company.'4 The laboratory had been open only a short time and all but three workers who had ever worked there were seen and the original survey record forms were available. Survey C was of pharmaceutical research workers. A study by company staff has been published" and our survey gave similar results.'5 The original forms were no longer available but some data were accessible on computer tape.The self completed questionnaire in survey A has been described and LAA symptoms were defined...

Occupational asthma after exposure to salbutamol in the pharmaceutical industry has not been previously reported. The occurrence of occupational asthma is described in two pharmaceutical process workers who were likely to have inhaled doses appreciably in excess of the therapeutic dose range. The findings do not lead to an unequivocal conclusion on the mechanism of the asthma but it was probably a pharmacological consequence of high exposure.ing samplers showed values ranging from 0 05 mg m-3 in the background of the finishing suite to an indeterminate value that exceeded 0-2 mg m-3 inside the milling cubicle. Two further airborne background environmental samples in 1982 taken in the finishing suite at a time of day when no work was in progress showed values of 0-015 mgMi3 of airborne "active" salbutamol dust. In 1981, 18 swab test samples were taken over areas of about 40 cm2 in the finishing suite and showed values ranging from nil to in excess of 6 (median 0. 1) mg salbutamol.