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Occupational asthma and rhinitis due to Western red cedar (Thuja plicate), with special reference to bronchial reactivity
  1. Bryan Gandevia,
  2. James Milne
  1. University of New South Wales Department of Medicine, Prince Henry Hospital, Little Bay, New South Wales, Australia
  2. Department of Health, Melbourne, Victoria, Australia


    Gandevia, B., and Milne, J. (1970).Brit. J. industr. Med.,27, 235-244. Occupational asthma and rhinitis due to Western red cedar (Thuja plicata), with special reference to bronchial reactivity. With the increasing use of Western, or Canadian, red cedar (Thuja plicata) in the timber industry, a distinctive respiratory syndrome of rhinitis and asthma has been observed with increasing frequency in clinical and industrial practice. Six cases of asthma and four of rhinitis are described in some detail; the onset of symptoms some hours after exposure, the nocturnal predominance of symptoms, especially of cough, and their persistence for days or weeks after cessation of exposure may conspire to make diagnosis difficult if the occupational hazard is not appreciated.

    Both immediate and late skin reactions to extracts of Western red cedar were mild or absent, and serum precipitins were absent in the two cases in which they were sought. Positive bronchial reactions, reflected in serial estimations of ventilatory capacity, occurred in response to provocative inhalations of extracts of the cedar dust, commonly at four to six hours and at night, rarely within the first hour. In some instances, a single provocative exposure to the nebulized extract over 90 seconds was shown to produce exacerbations of asthma for two or three successive nights, with normal or reduced ventilatory capacity during the intervening days. Regularly recurring asthma after an isolated exposure has not previously been documented, and is perhaps of fundamental importance to the understanding of non-occupational asthma. Bronchial reactions were not observed to house dust extract, to which patients consistently showed dermal sensitivity. Symptoms subsided gradually when exposure was avoided, but there was considerable individual variation as to how much exposure could be tolerated without relapse; symptomatic therapy, with or without specific hyposensitization, did not adequately control the symptoms.

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