PULMONARY RESPONSE OF FISCHER-344 RATS TO ACUTE NOSE-ONLY INHALATION OF INDIUM TRICHLORIDE

被引:16
作者
BLAZKA, ME
TEPPER, JS
DIXON, D
WINSETT, DW
OCONNOR, RW
LUSTER, MI
机构
[1] MANTECH ENVIRONM TECHNOL INC,RES TRIANGLE PK,NC 27709
[2] NIEHS,EXPTL PATHOL LAB,RES TRIANGLE PK,NC 27709
关键词
D O I
10.1006/enrs.1994.1065
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
We have previously shown that rats dosed intratracheally with indium trichloride (InCl3) develop severe lung damage and fibrosis. However, it is not clear what pulmonary effects would result following accidental occupational exposure to low concentrations of indium by inhalation. The present study uses a model of acute lung injury based on single 1-hr nose-only exposures to 0.2, 2.0, or 20 mg InCl3/m(3). Exposure to 0.2 mg InCl3/m(3) was capable of initiating an inflammatory response. Seven days following inhalation of 20 mg InCl3/m(3) the total cell number, fibronectin, and TNF alpha levels in the bronchial alveolar lavage fluid were 8, 40, and 5 times higher than the control, respectively. Commensurate with the level of lung injury 7 days after exposure, an acute restrictive lung lesion and increased airway responsiveness to acetylcholine were observed. Forty-two days after exposure a compensatory increase in lung Volume and carbon monoxide diffusing capacity in the 20 mg InCl3/m(3) group suggested recovery from the lung injury. Lung collagen levels were increased in a concentration-dependent manner 42 days postexposure. These data indicate that inhalation of InCl3/m(3) causes acute inflammatory changes in the lung. (C) 1994 Academic Press, Inc.
引用
收藏
页码:68 / 83
页数:16
相关论文
共 39 条
[1]   PULMONARY TOXICITY TO INTRATRACHEALLY ADMINISTERED INDIUM TRICHLORIDE IN FISCHER-344 RATS [J].
BLAZKA, ME ;
DIXON, D ;
HASKINS, E ;
ROSENTHAL, GJ .
FUNDAMENTAL AND APPLIED TOXICOLOGY, 1994, 22 (02) :231-239
[2]  
CASTRONO.FP, 1973, J NUCL MED, V14, P677
[3]  
CHVAPIL M, 1979, ARCH ENVIRON HEALTH, V34, P402
[4]  
Costa DL, 1992, COMP BIOL NORMAL LUN, V1, P367
[5]  
DOWNS WL, 1959, UR558 U ROCH AT EN P
[6]   STIMULATION OF RAT ALVEOLAR MACROPHAGE FIBRONECTIN RELEASE IN A CADMIUM CHLORIDE MODEL OF LUNG INJURY AND FIBROSIS [J].
DRISCOLL, KE ;
MAURER, JK ;
POYNTER, J ;
HIGGINS, J ;
ASQUITH, T ;
MILLER, NS .
TOXICOLOGY AND APPLIED PHARMACOLOGY, 1992, 116 (01) :30-37
[7]   PULMONARY RESPONSE TO SILICA OR TITANIUM-DIOXIDE - INFLAMMATORY CELLS, ALVEOLAR MACROPHAGE-DERIVED CYTOKINES, AND HISTOPATHOLOGY [J].
DRISCOLL, KE ;
LINDENSCHMIDT, RC ;
MAURER, JK ;
HIGGINS, JM ;
RIDDER, G .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 1990, 2 (04) :381-390
[8]   RESPIRATORY-TRACT RESPONSES TO DUST - RELATIONSHIPS BETWEEN DUST BURDEN, LUNG INJURY, ALVEOLAR MACROPHAGE FIBRONECTIN RELEASE, AND THE DEVELOPMENT OF PULMONARY FIBROSIS [J].
DRISCOLL, KE ;
MAURER, JK ;
LINDENSCHMIDT, RC ;
ROMBERGER, D ;
RENNARD, SI ;
CROSBY, L .
TOXICOLOGY AND APPLIED PHARMACOLOGY, 1990, 106 (01) :88-101
[9]   CYTOKINE AND GROWTH-FACTOR RELEASE BY ALVEOLAR MACROPHAGES - POTENTIAL BIOMARKERS OF PULMONARY TOXICITY [J].
DRISCOLL, KE ;
MAURER, JK .
TOXICOLOGIC PATHOLOGY, 1991, 19 (04) :398-405
[10]   METALORGANIC CHEMICAL VAPOR-DEPOSITION OF III-V-SEMICONDUCTORS [J].
DUPUIS, RD .
SCIENCE, 1984, 226 (4675) :623-629