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...

A voluntary scheme for the surveillance of work related and occupational respiratory disease (SWORD) was established in January 1989

T Th he e e ep pi id de em mi io ol lo og gy y o of f m me es so ot th he el li io om ma a i in n h hi is st to or ri ic ca al l c co on nt te ex xt tThe epidemiology of mesothelioma in historical context. J.C. McDonald, A.D. McDonald. ©ERS Journals Ltd 1996. ABSTRACT: Primary malignant mesothelial tumours were recognized by pathologists before asbestiform minerals (chrysotile, crocidolite and amosite) were mined commercially. The discovery, 40 yrs ago, of a causal link with crocidolite and the wide-ranging epidemiological studies which followed are the subject of this review.Early case-control and descriptive surveys, supplemented by cohort studies in insulation workers and chrysotile miners, quickly demonstrated major occupational and geographical differences, with high risk in naval dockyard areas and in the heating trades. In the 1980s, reliable cohort surveys showed that in mining and in the manufacture of asbestos products the mesothelioma risk was much higher when exposure included crocidolite or amosite than chrysotile alone. However, qualitative and quantitative information on exposure was too often inadequate for this evidence to be conclusive. Well-controlled lung fibre analyses have reduced these deficiencies and demonstrated the probable implications of the greater biopersistence of amphibole fibres. Chrysotile for industrial use often contains low concentrations of fibrous tremolite, which may well explain the few cases of mesothelioma associated with this type of asbestos.Progress in this field has been much retarded by controversy, for which the 20 year gap between the availability of reliable estimates of risk for the mining of chrysotile and that for crocidolite or amosite may have been largely responsible.

Findings are presented from the initial cross sectional phase of a cohort study of employees exposed to flour in bakeries or mills. Of 401 eligible workers in seven sites 344 (86%) were surveyed; symptoms assessed by self completed questionnaire, and sensitisation measured by the response to skin prick tests, were related to intensity of exposure both to total dust and to flour aeroallergen. Among 264 subjects without previous occupational exposure to flour, work related symptoms which started after first employment at the site were related to exposure intensity, especially when exposure was expressed in terms of flour aeroallergen. The relations with eyelnose and skin symptoms were independent of atopic status and cigarette smoking. Positive skin test responses to mixed flour and to a amylase were also more frequent with increasing exposure intensity, although this was confounded by atopic status. There was only a weak association between symptoms and specific sensitisation.

Ascertainment, through 7,400 pathologists, of all fatal malignant mesothelial tumors in Canada (1960-75) and the U.S.A. (1972) gave a total of 668 cases (272 in 1972). In Canada, the annual number of male cases rose from about 17 in 1966 to 25 in 1972 but the number of female cases remained fairly steady at a much lower level. The annual incidence in North America in 1972 was estimated at 2.8 per million males and 0.7 per million females aged 15 years and over. Occupational histories were obtained "blind" for 480 of the 557 cases through 1972, and their matched controls; relative risks were as follows: insulation work, 46.0 asbestos production and manufacture, 6.1, heating trades (other than insulation) 4.4. For nearly half the male cases and for about 5% of female cases, the tumor could be attributed to occupational exposure to asbestos, of which a fifth were in shipyards. No indication was found of other possible causes (including man-made mineral fibers, tobacco smoking, or residence near zeolite deposits). Four subjects were men who had been employed in Quebec chrysotile mines and 3 were children of employees, but no other subject had lived in the mining area. The findings remain consistent with a much greater mesothelioma-producing potential for crocidolite and amosite than for chrysotile; however, further studies of factory workers exposed to chrysotile only are needed to confirm this. Mineral fiber analysis of lung tissue from patients and controls is in progress.

Findings are presented from the initial cross sectional phase of a cohort study of employees exposed to laboratory rats. Of 366 eligible workers at four sites 323 (88%) were surveyed; symptoms assessed by self completed questionnaire and sensitisation measured by the response to skin prick tests were related to intensity of exposure both to total dust and to rat urinary aeroallergen. Among 238 workers, without previous occupational expo--sure to rats, work related symptoms, which started after first employment at the site were related to exposure intensity (expressed either in terms of dust or of aeroallergen) at the time of onset of symptoms. These relations were stronger in atopic subjects but were unrelated to smoking. Positive skin tests to rat urinary extract were also more frequent with increased exposure, a relation found in both atopic subjects and in smokers. There was a strong association between work related symptoms and specific sensitisation. ( information; the current cohort study was designed to correct these deficiencies. We report findings of the initial phase. Subjects and methods SURVEY METHODSFour institutions specialising in small animal research in the United Kingdom were identified: three use a variety of animals including rats; the fourth uses almost exclusively mice and is not described in this paper. All full time employees in occupational groups where exposure to laboratory rats or mice was probable and a group of non-exposed office workers, who had started work at the site from 1 January 1986 onwards and had worked for at least one month, were invited to participate.Members of the cohort still employed at the sites have been surveyed at six-monthly intervals since 1990. We describe the findings from the initial survey. Two visits to each site were made, the second to collect information from those missed at the first visit. Of 366 eligible subjects 323 (88%) were surveyed, with no difference in response rates between the three workforces. Questionnaires were completed by 315 subjects (84%) and skin prick tests by 295

Objectives-To examine trends in estimated population based incidence of occupational asthma by age, sex, occupation, geographical region, and causal agents based on 9 years of the Surveillance of Work Related and Occupational Respiratory Disease (SWORD) data. Methods-In January 1989 the SWORD scheme for the surveillance of occupational respiratory disease was established in the United Kingdom to make good the lack of epidemiological information on the incidence of these diseases in the United Kingdom. Between 80% and 90% of chest and occupational physicians report voluntarily all new cases they see, on a monthly or random sampling basis. During the 9 years 1989-97, an estimated 25 674 new cases of occupational respiratory disease, including 7387 of occupational asthma, were reported. Suspected causal agents were classified into 44 categories and estimated annual incidences of asthma were calculated with denominators from the labour force survey. Results-Overall, a third of the suspected causes of asthma were organic, a third chemical, 6% metallic, and the rest miscellaneous, or in 8%, unknown. There was evidence of an increase since 1989 in cases due to latex, and possibly glutaraldehyde, and an apparent drop since 1991 in the proportion of cases attributed to isocyanates. Incidences were higher in men than women and the disparity was especially marked in the population aged 45 years or more in which rates for men were at least twice those for women. Average annual rates per million workers for 1992-7 ranged from 7 (95% confidence interval (95% CI) 5 to 9) for the lowest risk group of professional, clerical, and service workers to 1464 (95% CI 968 to 2173) for coach and other spray painters. Except for laboratory technicians, all other occupations with rates over 100 were concerned with manufacturing and processing that used chemicals, metals, and organic materials. Incidences were two to three times higher in the north and midlands than in East Anglia and the south. The introduction of a sampling scheme in 1992 doubled estimates of reported incidence of occupational asthma, but there was little evidence of other temporal changes. Conclusions-The SWORD scheme has produced consistent estimates of the causes and incidence of occupational asthma as seen by chest and occupational physicians. It has allowed the epidemiology of occupational asthma in the population to be studied and high risk occupations to be identified. There is certainly more occupational asthma in the population than that which reaches specialists in occupational and chest medicine; therefore the incidence rates presented here are underestimates, but by how much remains unknown. (Occup Environ Med 2000;57:823-829)

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