Lungs toxic effects

In rats, the administration of fullerene by inhalation, as nano- and microparticles generated by aerosol, does not lead to lesions and only a little increase of protein concentration in bronchoalveolar lavage fluid was obtained (Baker et al., 2007). Recently, Sayes et al. (2007) analyzed in vivo pulmonary toxicity of C60 and C60(OH)24, after intratracheal instillation in rats. They verified only transient inflammatory and cell injury effects, 1 day postexposure, without differences from water-instilled controls. No adverse lung tissue effects were measured, and the results demonstrated little or no differences in lung toxicity effects between the C60 and fiillerols, compared to controls. 

The toxic effect depends both on lipid and blood solubility. I his will be illustrated with an example of anesthetic gases. The solubility of dinitrous oxide (N2O) in blood is very small therefore, it very quickly saturates in the blood, and its effect on the central nervous system is quick, but because N,0 is not highly lipid soluble, it does not cause deep anesthesia. Halothane and diethyl ether, in contrast, are very lipid soluble, and their solubility in the blood is also high. Thus, their saturation in the blood takes place slowly. For the same reason, the increase of tissue concentration is a slow process. On the other hand, the depression of the central nervous system may become deep, and may even cause death. During the elimination phase, the same processes occur in reverse order. N2O is rapidly eliminated whereas the elimination of halothane and diethyl ether is slow. In addition, only a small part of halothane and diethyl ether are eliminated via the lungs. They require first biotransformation and then elimination of the metabolites through the kidneys into the... 

Several toxic effects of inorganic oxides become evident when oxides are inhaled in a finely powdered form. A high concn of powdered oxides can lead to asphyxiation on short exposure or lung cancer at somewhat lower concns if the exposure occurs over a prolonged period. 

Lefuma J, Chameaud J, Perraud R, et al. 1976. [An experimental study on a comparison between the toxic effects of radon-222 and its daughters on the lungs, and those exerted by alpha-emitters of the actinium series.] Occup Saf Health Ser 32 43-53. (French). 

Effects of Metabolism on Toxicity. Whether the toxic effects seen after exposure to diisopropyl methylphosphonate are caused by the parent compound or its metabolites is unknown. Studies of IMP A show that acute-duration exposure to IMPA results in reduced motor activity, prostration, and ataxia—effects also seen after exposure to diisopropyl methylphosphonate (EPA 1992). Other studies (Little et al. 1986, 1988) show that IMPA, the major metabolite of diisopropyl methylphosphonate, has an affinity for both lung and brain tissues and will bind to proteins in these tissues—effects that were not seen after exposure to diisopropyl methylphosphonate (EPA 1992 Little et al. 1988). These data and other data on the toxicity of IMPA neither support nor contradict the data found in the diisopropyl methylphosphonate studies, so it is not possible to attribute the effects after exposure to diisopropyl methylphosphonate to IMPA. Metabolites of IMPA other than MPA have not been identified. 

Lopez A, Prior MG, Reiffenstein RJ, et al. 1989. Peracute toxic effects of inhaled hydrogen sulfide and injected sodium hydrosulfide on the lungs of rats. Fundam Appl Toxicol 12 367-373. 

No information is available on the adverse health effects of hexachloroethane in humans. Animal studies revealed that hexachloroethane primarily causes liver and kidney toxicity. Effects on the nervous system and lungs have also been reported. The mechanism by which these effects are mediated is not well characterized. Reductive metabolism by cytochrome P-450 and production of a free radical intermediate have been suggested as factors in hexachloroethane-induced hepatotoxicity (Nastainczyk et al. 1982a Thompson et al. 1984 Town and Leibman 1984). Accordingly, one possible approach may be to reduce free radical injury. To that end, oral administration of N-acetylcysteine can be used as a means of reducing free radical injury. Also, oral administration of vitamin E and vitamin C may be of value since they are free radical scavengers. 

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