Between 1980 and 1987 a total of 166 patients were diagnosed as having occupational (mostly allergic) rhinitis at the Institute of Occupational Health. This is about 20% of all the diagnosed cases in Finland. The most common causes were: flour (50 cases), wood dust (30 cases), animal epithelia (19 cases), and natural fibers, mainly cotton (19 cases). Between 1981 and 1987 the number of cases of occupational rhinitis in all of Finland more than doubled (from 61 to 128 cases per year), and in 1991 a total of 319 cases were detected. This was mainly due to the increase in rhinitis caused by animal epithelium and flour dust, which were then the most common causes of occupational rhinitis in Finland. This increase, in turn, was based on changes in the Finnish legislation, which in 1982 was extended to cover farmers. Other causes of the increase were probably the increased awareness of the public and health personnel, but a true increase in occupational rhinitis cannot be excluded.
Summary
Three cases of allergic rhinitis from a vegetable gum, guar gum, have been detected. Two subjects were exposed to fine guar gum powder (Emco Gum 563, Meyhall Chemical AG, Switzerland), an insulator in rubber cables, when opening cables in a power cable laboratory. After 1–2 years’ exposure the patients developed rhinitis. Scratch‐chamber tests, nasal provocation tests, nasal eosinophilia and a RAST test proved their allergy. A third subject developed allergic rhinitis from another guar gum product (Meyproid 5306, Meyhall Chemical AG) after 2 years’ exposure in a paper factory. A positive skin test and nasal provocation test confirmed the diagnosis. A fourth case of possible allergy to guar gum after exposure to Meyproid 5306 in a paper factory is also presented. No final diagnosis was reached in this case (in 1974). The present subjects, only one of whom was atopic, developed allergy within 2 years, although their exposure to guar gum was not especially heavy. Therefore, when handling guar, adequate ventilation facilities should be provided and protective clothing, including a respiratory mask, should be worn.
Forty-eight persons (age 44, SD 9 years) exposed to paint solvents and 40 nonexposed referents (age 45, SD 9 years) were examined. The duration of exposure was 4 to 30 (mean 20) years and the life-time exposure level was estimated to have been 10 to 330 (mean 60%) of the hygienic standard. The methods used were a neurological examination, electroencephalography, brainstem auditory-evoked potentials, electronystagmography, and posturography. Life-time exposure was estimated on the basis of a detailed occupational history and environmental measurements made at the work places over several years. The average weekly alcohol consumption was established in a detailed interview. Due to the small number of subjects examined, the study was inconclusive. The findings classified as abnormal were slightly more common in the exposed than in the referents, and in the persons who used alcohol than in the non-users. The differences were not statistically significant, and no exposure-response relationships were found.
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