TY - JOUR
T1 - Acute and subacute inhalation toxicity of diborane in male ICR mice
AU - Uemura, Takamoto
AU - Omae, Kazuyuki
AU - Nakashima, Hiroshi
AU - Sakurai, Haruhiko
AU - Yamazaki, Kazuto
AU - Shibata, Toshikatsu
AU - Mori, Koji
AU - Kudo, Mitsuhiro
AU - Kanoh, Hirokazu
AU - Tati, Masatomo
PY - 1995/5
Y1 - 1995/5
N2 - To clarify the toxicity of diborane, we conducted acute (15 ppm for 1, 2, 4 or 8h) and subacute (5 ppm for 2 or 4 weeks) inhalation studies on ICR mice. The concentration resulting in a 50% kill after 4 h exposure was 31.5 ppm. body weight gain was suppressed and the lung weight was increased in diborane-exposed mice in both acute and subacute studies. In the acute study, diffuse pan bronchiolitis-like lesions developed in the lung in various degrees depending on exposure time, which can be pathologically characterized as infiltration of inflammatory cells into the terminal bronchioles and surrounding alveoli, pulmonary congestion and bleeding and/or edema. In the subacute study, we observed lymphoid hyperplasia in the perivascular and peribronchial areas, and infiltration of macrophage and plasma cells into the alveoli. In the mice exposed for 4 weeks, the lesions were more severe than in those exposed for 2 weeks, consisting of hyperplasia and desquamation of Clara cells. In the nasal cavity, we saw mucous exudate and inflammatory cells, suggesting irritation caused by diborane. The histopathological findings, except for the respiratory organs, did not reveal any exposure-related changes. No significant changes were seen in hematological and serum biochemical examinations either. In conclusion, the target organ of diborane inhalation is the respiratory organs, particularly the lung. Further inhalation experiments are essential to investigate the safety exposure levels of diborane.
AB - To clarify the toxicity of diborane, we conducted acute (15 ppm for 1, 2, 4 or 8h) and subacute (5 ppm for 2 or 4 weeks) inhalation studies on ICR mice. The concentration resulting in a 50% kill after 4 h exposure was 31.5 ppm. body weight gain was suppressed and the lung weight was increased in diborane-exposed mice in both acute and subacute studies. In the acute study, diffuse pan bronchiolitis-like lesions developed in the lung in various degrees depending on exposure time, which can be pathologically characterized as infiltration of inflammatory cells into the terminal bronchioles and surrounding alveoli, pulmonary congestion and bleeding and/or edema. In the subacute study, we observed lymphoid hyperplasia in the perivascular and peribronchial areas, and infiltration of macrophage and plasma cells into the alveoli. In the mice exposed for 4 weeks, the lesions were more severe than in those exposed for 2 weeks, consisting of hyperplasia and desquamation of Clara cells. In the nasal cavity, we saw mucous exudate and inflammatory cells, suggesting irritation caused by diborane. The histopathological findings, except for the respiratory organs, did not reveal any exposure-related changes. No significant changes were seen in hematological and serum biochemical examinations either. In conclusion, the target organ of diborane inhalation is the respiratory organs, particularly the lung. Further inhalation experiments are essential to investigate the safety exposure levels of diborane.
KW - Diborane
KW - Inhalation
KW - Mice
KW - Toxicity
UR - http://www.scopus.com/inward/record.url?scp=0029016690&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0029016690&partnerID=8YFLogxK
U2 - 10.1007/s002040050190
DO - 10.1007/s002040050190
M3 - Article
C2 - 7495378
AN - SCOPUS:0029016690
SN - 0340-5761
VL - 69
SP - 397
EP - 404
JO - Archives of Toxicology
JF - Archives of Toxicology
IS - 6
ER -