Inhalational injury clinical effects

TOXIC INHALATIONAL INJURY Physical Aspects Clinical Effects Physiology Evaluation of Injury... 

Hepatic Effects. Carbon tetrachloride has been known for many years to be a powerful hepatotoxic agent in humans and in animals. The principal clinical signs of liver injury in humans who inhale carbon tetrachloride are a swollen and tender liver, elevated levels of hepatic enzyme (aspartate aminotransferase) in the serum, elevated serum bilirubin levels and the appearance of jaundice, and decreased serum levels of proteins such as albumin and fibrinogen (Ashe and Sailer 1942 McGuire 1932 New et al. 1962 Norwood et al. 1950 Straus 1954). In cases of acute lethal exposures, autopsy generally reveals marked liver necrosis with pronounced steatosis (Jennings 1955 Markham 1967 Smetana 1939), and repeated or chronic exposures leads in some cases to fibrosis or cirrhosis (McDermott and Hardy 1963). 

Immunotoxicity. There are numerous studies of the immune system in workers (active or retired) exposed to asbestos in workplace air (deShazo et al. 1988 Froom et al. 2000 Kagan et al. 1977 Pemis et al. 1965 Sprince et al. 1991, 1992 Warwick et al. 1973). These studies indicate that the immune system may be depressed in individuals who have developed clinical signs of injury, such as asbestosis or cancer. However, the cause-effect relationship between the immunological changes and the asbestos-related diseases is not certain. Also, it is not known if similar effects occur after oral exposure, or if the effects are inhalation specific. Prospective studies on this subject may be useful, both in discerning the importance of... 

In animal and in vitro studies, inhaled nitric oxide has led to surfactant inactivation and promotion of oxidative and nitrosylative lung injury (2). These effects have not been reported during clinical use of inhaled nitric oxide at concentrations less than 80 ppm. In a review of two articles it was noted that nitric oxide does not increase the risk of chronic lung disease of the newborn, despite speculation that it may increase chronic lung disease of prematurity due to the formation of nitrogen dioxide and peroxynitrite, in addition to membrane lipid peroxidation and increased unbound plasma iron in preterm infants (7). 

Historically, injuries and fatalities have been reported from acute methanol overexposure via ingestion, inhalation, as well as prolonged or repeated skin contact. Inhalation toxicity can occur in occupational settings or as a result of inhalant abuse (huffing). Clinical studies of individuals acutely poisoned by methanol ingestion have identified visual disturbances and possibly blindness as the most notable toxic effects in humans. Methanol is also a CNS depressant, although less potent than ethanol, and has also been shown to produce liver damage upon overexposure. 

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