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Pulmonary effects of combustion products from nickel‐coated polycarbonate
Author(s) -
Larsen James B.,
Williams Brian K.,
Nelson Gordon L.
Publication year - 1997
Publication title -
fire and materials
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.482
H-Index - 58
eISSN - 1099-1018
pISSN - 0308-0501
DOI - 10.1002/(sici)1099-1018(199709/10)21:5<213::aid-fam610>3.0.co;2-o
Subject(s) - lung , pulmonary toxicity , pathology , polycarbonate , alveolar epithelium , chemistry , toxicity , atelectasis , epithelium , medicine , organic chemistry
The pulmonary effects of acute (30 min) and chronic (7, 14, or 21 days; 30 min day −1 ) exposure to smoke from white polycarbonate structural foam, or a Ni‐urethane coated version of this plastic, were analyzed by exposing groups of 4 mice in a dome chamber apparatus. The lungs of test fatalities were consistently inflamed and hemorrhagic, and characterized histologically by areas of atelectasis and hyperinflation. The Ni‐coated material was more toxic than the uncoated material, and produced greater intrapulmonic hemorrhage. A histological method was developed for assessing the proliferation of type II pneumocytes as an index of damage to the alveolar epithelium. Examination of lungs from animals sacrificed at 2, 4, 8, 14, 21, or 28 days following acute exposure revealed that only the 8‐day animals in the Ni‐exposure group had significantly more type II pneumocytes than controls (P<0.01). Similar examination of lungs from chronically exposed animals sacrificed at 1 day following the last exposure revealed no significant differences between experimental animals and controls. The Ni content of coated samples and the ash following thermal decomposition was determined by atomic absorption spectrophotometry. The original samples were 2.5% Ni. Nickel lost during pyrolysis could account for the increased toxicity of the coated material through production of toxic Ni compounds. These results indicate that pulmonary irritants produced by these plastics affect the vascular elements of the lungs more than the alveolar epithelium, and that the pulmonary damage produced in mice under these conditions does not persist in survivors beyond 1 day post‐exposure. The acute combustion toxicity of Ni‐coated plastics may reflect the formation of toxic Ni compounds. © 1997 John Wiley & Sons, Ltd.