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Follow‐up study of patients with respiratory disease due to toluene diisocyanate (TDI)
Author(s) -
PAGGIARO P. L.,
LOI A. M.,
ROSSI O.,
FERRANTE B.,
PARDI F.,
ROSELLI M. G.,
BASCHIERI L
Publication year - 1984
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1111/j.1365-2222.1984.tb02230.x
Subject(s) - toluene diisocyanate , medicine , bronchial hyperresponsiveness , pulmonary function testing , asthma , respiratory system , occupational asthma , respiratory disease , chronic bronchitis , physical examination , bronchitis , occupational disease , gastroenterology , pathology , lung , materials science , composite material , polyurethane
Summary The outcome of the respiratory symptoms, pulmonary function tests and bronchial hyperresponsiveness was studied in forty‐seven workers with respiratory disease due to toluene diisocyanate (TDI) (twenty‐seven asthmatic and twenty non‐asthmatic subjects) after about 2 years from the first examination. Eight of twelve asthmatic subjects who left the industry after the first examination complained at the follow‐up of dyspnoea and wheezing, but pulmonary function tests were unchanged; bronchial hyperresponsiveness decreased in three, but most were still positive to challenge test with bethanechol at the follow‐up. Fifteen subjects who continued their exposure to TDI showed at the follow‐up a significant decrease of the spirometric parameters and an increase of the bronchial hyperresponsiveness, and symptoms of chronic bronchitis were more frequent at the second examination. Non‐asthmatic subjects, both exposed and non‐exposed to TDI at the second examination, showed a significant decrease of the pulmonary function tests but no relevant changes in bronchial hyperresponsiveness. Our data suggest that stopping occupational exposure to TDI frequently did not produce an improvement of the TDI bronchial asthma, and persistence of the occupational exposure causes a more rapid decline in the respiratory function.