Lung edema

Lunar caustic Lundin process Lung cancer Lung edema Lung flukes Lungworms a-Lupilic acid b-Lupilic acid Lupin... 

Since diketene is a strong eye irritant even at low levels, it has a strong warning effect. Diketene becomes unbearable before acute toxic levels are reached. Due to the risk of delayed lung edema, a physician should be consulted and the patient monitored carefully after exposure. 

Intravenous administration of rTNF induces a disease state that closely resembles septic shock accompananied by tissue damage (M28, T12). TNF induces fever, leukocyte aggregation, hypotension, stress hormone release, lung edema, and hemorrhagic necrosis of various organs (T12). 

Severe Abrupt tremor, generalized convulsions, psychic disturbance, intensive cyanosis, lung edema, coma Respiratory or cardiac failure, death... 

Rat, Rattus sp. 27 mg/m3 air for 1-2 h Fatal death by asphyxiation lung edema necrosis of alveolar epithelium 7... 

Morphologic changes in medium-sized airways Threshold for lung edema formation with I-albumin test... 

ThreslK d for lung edema for- Rat matkm with albumin test... 

Symptoms of exposure Very irritating to eyes, nose and respiratory tract. An irritation concentration of 72.00 mg/m in air was reported by Ruth (1986). Exposure to 3,000 ppm for several min may result in serious blistering of skin, lung edema, and asphyxia leading to death (Patnaik, 1992). Ingestion may cause bronchospasm, difficulty in breathing, chest pain, and pulmonary edema. Contact with liquid ammonia or aqueous solutions may cause vesiculation or frostbite (IMIOSH, 1994). 

The 1-hour LCso in rats was 262 ppm, and the oral LDso was lOOmg/kg. In animal experiments lung edema and hydrothorax have occurred after inhalation exposure. Repeated oral administration causes necrosis of the liver, spleen, adrenal gland, and testis, as well as ulceration and perforation in the gastric area in rats. The dermal LDso in rabbits was 141 mg/ kg, indicating significant skin absorption. ... 

Humans can withstand exposures to 70mg/m (8.8 ppm) eye irritation begins at lOmg/m (1.3 ppm). Acute exposure to higher concentrations may cause coughing, dyspnea, lacrimation, nausea, cyanosis, convulsions, and death due to lung edema. ... 

All dead within 24 h with hemolysis and lung edema... 

Rat (Wistar) 4 hr Resp 15.3 (labored breathing) 37.6 (lung edema, pneumonia) Kimmerle 1976 HDI... 

Several experimental studies have described the respiratory effects of HDI after acute inhalation exposures in laboratory animals. The acute inhalation toxicity of the aerosols of HDI and various prepolymer products were tested on male and female Wistar rats exposed to 105, 143, 259, 341, 383, 443, 575, 589, or 719 mg HDI/m (15.3, 20.7, 37.6, 49.4, 55.5, 64.2, 83.4, 85.4, 104.3 ppm) in inhalation chambers for 4 hours. All HDI-exposed rats exhibited signs of labored breathing at all exposure concentrations. Lung edema and pneumonia were observed upon necropsy (Kimmerle 1976). 

An exception is perfluoro(2-methylpropene) (perfluoroisobutylene, PFIB), which is the most toxic fluorinated species known so far and is particularly dangerous due to delayed development of lethal lung edema, not starting until 1-2 days after the cessation of the exposure. 

Consequently, absorption enhancers were used in dry powder and liquid formulations to enhance the pulmonary absorption of SCT. Without absorption enhancers, SCT absorption from dry powder or solution was similar to that observed after intratracheal administration. However, the absorption was more improved from dry powder than from solution when absorption enhancers (oleic acid, lecithin, citric acid, taurocholic acid, dimethyl-[5-cyclodextrin, octyl-P-D-glu-coside) were co-administered intratracheally. Such improved absorption could be due to the fact that enhancers added to the dry powder dissolved at high concentration because only a trace volume of fluid lining the alveolar epithelium was available for their dissolution. However, the potential implications of such a mechanism on lung toxicity, especially in lung edema, is yet to be investigated in detail [68]. 

Fatal doses of phenol may be absorbed through the skin. Its acute toxicological effects are predominantly on the central nervous system. Death can occur as early as a half hour after exposure. Key organs damaged by chronic exposure to phenol include the spleen, pancreas, and kidneys. Lung edema can also occur. 

Factor, P., Dumasius, V., Saldias, F. and Sznajder, J. I. (1999). Adenoviral-mediated overexpression of the NA,K-ATPase betal subunit gene increases lung edema clearance and improves survival during acute hyperoxic lung injury in rats. Chest 116, 24S-25S. 

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