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Lungs absorption

Absorption lung, skin, stomach (poor), intestine (better), (poor absorption in the stomach because nicotine is a strong base)... [Pg.63]

Metabolism. Absorption, distribution, metaboHsm, and excretion of thioglycolic acid have been reviewed (20). In summary,. -thioglycolic acid was absorbed significantly after appHcation to the skin of rabbits. After intravenous injection, the greatest counts of radioactivity were found in the kidneys, lungs, and spleen of monkey and in the small intestine and kidneys of rat. Most of the radioactivity was rapidly excreted in the urine in the form of inorganic sulfate and neutral sulfur. [Pg.4]

The GI absorption of the dmg after po adrninistration is slow and variable with estimates ranging from 20—55%. Once absorbed, 96% of the dmg is bound to plasma proteins and other tissues on the body. Whereas peak plasma concentrations may be achieved in 3—7 h, the onset of antiarrhythmic action may occur in 2—3 days or more. This may result, in part, from distribution to and concentration of the dmg in adipose tissue, Hver, spleen, and lungs. Therapeutic plasma concentrations are 1—2 p.g/mL, although there appears to be no correlation between plasma concentration and antiarrhythmic activity. The plasma half-life after discontinuation of the dmg varies from 13—103 days. The dmg is metabolized in the Hver and the principal metaboHte is desethylamiodarone. The primary route of elimination is through the bile. Less than 1% of the unchanged dmg is excreted in the urine. The dmg can also be eliminated in breast milk and through the skin (1,2). [Pg.121]

Exposure occurs almost exclusively by vapor inhalation, which is followed by rapid absorption into the bloodstream. At concentrations of 150—186 ppm, 51—70% of the trichloroethylene inhaled is absorbed. MetaboHc breakdown occurs by oxidation to chloral hydrate [302-17-OJ, followed by reduction to trichloroethanol [115-20-8] part of which is further oxidized to trichloroacetic acid [76-03-9] (35—37). Absorbed trichloroethylene that is not metabolized is eventually eliminated through the lungs (38). The OSHA permissible exposure limit (PEL) eight-hour TWA concentration has been set at 50 ppm for eight-hour exposure (33). [Pg.25]

Exposure to tetrachloroethylene as a result of vapor inhalation is foUowed by absorption into the bloodstream. It is partly excreted unchanged by the lungs (17,18). Approximately 20% of the absorbed material is subsequently metabolized and eliminated through the kidneys (27—29). MetaboHc breakdown occurs by oxidation to trichloroacetic acid and oxaHc acid. [Pg.30]

Other important determinants of the effects of compounds, especially solvents, are their partition coefficients, e.g., blood-tissue partition coefficients, which determine the distribution of the compound in the body. The air-blood partition coefficient is also important for the absorption of a compound because it determines how quickly the compound can be absorbed from the airspace of the lungs into the circulation. An example of a compound that has a high air-blood partition coefficient is trichloroethane (low blood solubility) whereas most organic solvents (e.g., benzene analogues) have low air-blood partition coefficients (high blood solubility). [Pg.260]

Volatile solvents are fluids or gases contained in a wide variety of products (e.g., gasoline, paint thinner, butane gas) that have significant concentrations of aliphatic, aromatic, or halogenated hydrocarbons, which vaporize at room temperature. Because of their rapid absorption in the lungs, volatile solvents exert a rapid intoxicating effect. [Pg.272]

This product is also only available by prescription. The recommended treatment period is up to 24 weeks (McNeil Consumer Products 1997). Using the inhaler by puffing 80 deep inhalations over 20 minutes results in a systemic absorption through the buccal mucosa of 2 mg of nicotine, with maximal nicotine concentrations occurring 15 minutes after the end of inhalation. When the product is used as directed, the patient will likely use 6-16 inhalers per day. This form of NRT is relatively contraindicated in patients with asthma because, although most of the nicotine is absorbed through the buccal mucosa and it is not delivered to the lungs (McNeil Consumer Products 1997), nicotine by inhalation may produce bronchial constriction. [Pg.320]

The major routes of uptake of xenobiotics by animals and plants are discussed in Chapter 4, Section 4.1. With animals, there is an important distinction between terrestrial species, on the one hand, and aquatic invertebrates and fish on the other. The latter readily absorb many xenobiotics directly from ambient water or sediment across permeable respiratory surfaces (e.g., gills). Some amphibia (e.g., frogs) readily absorb such compounds across permeable skin. By contrast, many aquatic vertebrates, such as whales and seabirds, absorb little by this route. In lung-breathing organisms, direct absorption from water across exposed respiratory membranes is not an important route of uptake. [Pg.21]

Absorption of trichloroethylene in humans is very rapid upon inhalation exposure. Trichloroethylene has a blood/gas partition coefficient that is comparable to some other anesthetic gases (i.e., chloroform, diethylether, and methoxyfluorene), but it is much more lipophilic than these gases. As a consequence of these properties, the initial rate of uptake of inhaled trichloroethylene in humans is quite high, with the rate leveling off after a few hours of exposure (Fernandez et al. 1977). The absorbed dose is proportional to the inhaled trichloroethylene concentration, duration of exposure, and alveolar ventilation rate at a given inhaled air concentration (Astrand and Ovrum 1976). Several studies indicate that 37-64% of inhaled trichloroethylene is taken up from the lungs (Astrand and Ovrum 1976 Bartonicek 1962 Monster et al. 1976). [Pg.110]


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See also in sourсe #XX -- [ Pg.45 ]




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