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Fatal dose

The smallest recorded fatal dose is 125 mg [10]. The action of vomiting has resulted in the recovery of a woman following the deliberate swallowing [Pg.385]

Arsenic is concentrated in the liver, spleen and kidney and is bound preferentially to sulphydryl groups in skin, hair and nails. Urine and gastric contents should also be obtained. The sequential analysis of hair sections has been shown to be of value in the examination of prolonged exposure to arsenic [8]. [Pg.386]


The effects of pollution can be direct, such as toxic emissions providing a fatal dose of toxicant to fish, animal life, and even human beings. The effects also can be indirect. Toxic materials which are nonbiodegradable, such as waste from the manufacture of insecticides and pesticides, if released to the environment, are absorbed by bacteria and enter the food chain. These compounds can remain in the environment for long periods of time, slowly being concentrated at each stage in the food chain until ultimately they prove fatal, generally to predators at the top of the food chain such as fish or birds. [Pg.273]

Arsenic(III) oxide is slightly soluble in water, giving a solution with a sweetish taste—but as little as 0.1 g can be a fatal dose (The antidote is freshly-precipitated iron(III) hydroxide.) The solution has an acid reaction to litmus, due to the formation of arsenic(III) acid ... [Pg.236]

It is very poisonous, 50 mg constituting an approximate fatal dose. Exposure to white phosphorus should not exceed 0.1 mg/ms (8-hour time-weighted average - 40-hour work week). White phosphorus should be kept under water, as it is dangerously reactive in air, and it should be handled with forceps, as contact with the skin may cause severe burns. [Pg.36]

The threshold of a toxic dose in adult humans is about 0.2—0.5 g Ba the lethal dose in untreated cases is 3—4 g Ba, LD q about 66 mg/kg (47). The fatal dose of barium chloride for humans is reported to be between 0.8 and 0.9 g (0.55—0.60 g of Ba) (50). However, for most of the acid-soluble salts of barium, doses greater than 1 g have been tolerated (51). Lethal doses are summarized in Table 5. Dusts of barium oxide are considered potential dermal and nasal irritants (52). [Pg.483]

The reader should note tliat since many risk assessments have been conducted on the basis of fatal effects, there are also uncertainties on precisely what constitutes a fatal dose of thennal radiation, blast effect, or a toxic chemical. Where it is desired to estimate injuries as well as fatalities, tlie consequence calculation can be repeated using lower intensities of exposure leading to injury rather titan dcatli. In addition, if the adverse healtli effect (e.g. associated with a chemical release) is delayed, the cause may not be obvious. Tliis applies to both chronic and acute emissions and exposures. [Pg.525]

NHi and benzene, and somewhat less soluble in numerous other organic solvents. The -form can be maintained as a solid up to 64.4°C under a pressure of 11 600 atm, whereas the or-form melts at 44.1°C. White phosphorus is highly toxic and ingestion, inhalation or even contact with skin must be avoided the fatal dose when taken internally is about 50mg. [Pg.480]

Todes-dosis, -gabe, /. fatal dose, lethal dose, -kampf, m. death struggle, agony, -stogg, m. [Pg.447]

The most important potential complication of phenol-based peels is cardiotoxicity. Phenol is directly toxic to myocardium. Studies in rats have shown a decrease in myocardial contraction and in electrical activity following systemic exposure to phenol [i6]. Since fatal doses ranged widely in these studies, it seems that individual sensitivity of myocardium to this chemical exists. In humans neither sex/age nor previous cardiac history/blood phenol levels are accurate predictors for cardiac arrhythmia susceptibility [17]. [Pg.85]

Very rapid death usually occurs within 15 min after absorption of fatal dose. [Pg.120]

FDS0 (average fatal dose) is a lethal (fatal) dose causing death in 50% of laboratory animals. [Pg.15]

Male Wistar rats were administered 330 or 660 mg/kg of ethanol intraperitoneally 30 minutes before being exposed to 800 ppm of hydrogen sulfide for a maximum of 20 minutes, which was a potentially fatal hydrogen sulfide exposure (Beck et al. 1979). Mean times to unconsciousness in animals that were exposed to hydrogen sulfide with ethanol pretreatment at either of these dose levels were approximately 35% less than times to unconsciousness without ethanol pretreatment (Beck et al. 1979). The clinical relevance of these findings, which used potentially fatal doses of both ethanol and hydrogen sulfide, is unclear. [Pg.116]

Ingestion — but not necessarily swallowing — of about 15 mL ( mouthful ) of a 20% solution 4->40 mg/kg BW Ingestion of 30 mg/kg BW Fatal dose (Kimbrough 1974) Acute oral LD50 (Manzo etal. 1979 Summers 1980) Associated with hepatic, cardiac, or renal failure, and sometimes death (Dasta 1978)... [Pg.1180]

Total ingested dose of 3-6 g Fatal dose (Haley 1979)... [Pg.1180]

The most extreme case of gamma radiation dose would arise from explosion of a nuclear weapon. Nuclear weapons release intense gamma radiation that can produce fatal doses miles from an explosion (see Chapter 5). A less extreme but more likely scenario involves radioactive materials dispersed via conventional explosives (dirty bombs), where only the immediate area is contaminated with gamma-emitting radionuclides. [Pg.62]

Figure 5.2 illustrates the effectiveness of an underground shelter to limit radiation dose. In the open, an individual will receive an unshielded radiation dose (D). If the individual is in a deep hole with only a thin overhead cover (e.g., plywood), the dose level drops by about a factor of ten (D/10). While this is better than being in an open area, fatal doses might still be received. If the cover is made of about one foot of concrete, the dose level drops by a factor of about 100 (D/100). Two feet or more of concrete will reduce dose levels by a factor of about 5000 (D/5000).2... [Pg.140]

An average fatal dose of 1.52 mg/kg cyanide for humans has been calculated from case report studies of intentional or accidental poisonings (EPA 1987a). The lowest fatal oral dose reported in humans is 0.56 mg/kg cyanide (Gettler and Baine 1938). [Pg.41]

It is difficult to estimate the lethal dose in man due to the many confounding factors that may be present, as well as the selective reporting of deaths following either unusually high or low dosage (both of which probably have more medical news value ). One authority has declared a surely fatal dose to be about 1200 mg. Most pharmacology texts, on the other hand, tend to give estimates at least ten times lower. [Pg.13]

The LDso in mice by intraperitoneal injection was 3 5 mg/kg lethal doses in animals also produced excitement, tremors, convulsions and tetany. Fatal doses were readily absorbed through the skin. A 0.2 M aqueous solution dropped in a rabbit s eye was only mildly irritating. ... [Pg.43]

Fentanyl transdermal patches are intended for transdermal use (on intact skin) only. Using damaged or cut fentanyl transdermal patches can lead to the rapid release of the contents of the fentanyl transdermal patch and absorption of a potentially fatal dose of fentanyl. [Pg.839]


See other pages where Fatal dose is mentioned: [Pg.478]    [Pg.479]    [Pg.462]    [Pg.352]    [Pg.521]    [Pg.414]    [Pg.280]    [Pg.721]    [Pg.68]    [Pg.36]    [Pg.46]    [Pg.15]    [Pg.135]    [Pg.350]    [Pg.58]    [Pg.100]    [Pg.1136]    [Pg.1136]    [Pg.1435]    [Pg.73]    [Pg.159]    [Pg.353]    [Pg.415]    [Pg.55]    [Pg.413]    [Pg.701]    [Pg.419]   
See also in sourсe #XX -- [ Pg.1107 ]




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