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Acute toxicity lethal doses

Skin absorption and administration by intraperitoneal and intravenous routes exhibited high acute toxicity lethal dose in mice intraperitoneally was 4 mg/kg... [Pg.1086]

According to Hodge and Sterner (1943) the REE are only slightly toxic and the extensive review by Haley (1979) similarly concluded that REE have a very low acute toxicity . Lethal dose rates for various species and routes of administration have been reported by Haley (1965). [Pg.433]

Oligonucleotide therapeutics have a relatively low order of acute toxicity, with the notable exception of the polyanionic PS ODNs, which have been known to activate complement through the alternative pathway in monkeys. Because these compounds do not cross the blood-brain barrier nor accumulate in cardiac muscle, and because the uptake of these compounds is dependent on saturable processes, very high doses of oligonucleotides tend not to produce central effects or acute organ failure, thus lowering the potential for acute lethality. [Pg.554]

How close do the above estimates relate to the actual LD50 Studies have shown that the approximate lethal dose for 86% of those chemicals tested in this manner were within 30% of the known LD50 values determined by the classical approach. The method is not infallible for example, some 14% of chemicals were outside this range and no dose-response or slope information can be obtained. International agreement has been reached that the up-and-down procedure could replace the conventional acute toxicity test for the purposes of hazard classification and label (including color-coding) production. [Pg.2725]

The classification as very toxic, toxic, or harmful is based on the median lethal dose (LD50, see Section 2.3). Most often the LD50 value (oral, rat) is used for the classification, because oral investigations are most often carried out to determine the acute toxicity. In contrast to the oral toxicity, the dermal and inhalative toxici-ties are much more important for the workplace assessment, the oral toxicity being of little relevance to the workplace. Howevei the oral, dermal, and inhalative toxicities do not usually differ significantly. [Pg.38]

The acute oral LDjo in guinea pigs and rabbits for kerosene has been reported to be 16,320 mg/kg and 22,720 mg/kg, respectively (Deichmann et al. 1944). These data suggest that guinea pigs may be more sensitive to kerosene than rabbits. Similarly, a lethal dose of kerosene of 6,400 mg/kg has been reported in calves (Rowe et al. 1973), but the lethal dose for rats is 12,000 mg/kg (Muralidhara et al. 1982). Comparison of these data is problematic however, they do suggest that species differences and age sensitivity may exist for oral kerosene toxicity, although such differences have not been established. [Pg.83]

Stark JD. 2005. How closely do acute lethal concentration estimates predict effects of toxicants on populations Integr Environ Assess Manage 1 109-113. [Pg.144]

While these treatment regimens have been the standard for many years, they are not ideal and suffer from a number of disadvantages. The major drawback of current approaches is that, while they can be effective in preventing lethality, they do not prevent performance deficits, behavioral incapacitation, loss of consciousness, or permanent brain damage, all of which can result from acute OP toxicity. "... [Pg.228]

Acute intoxication due to short-chain alkylmercury derivatives such as methyl- or ethylmercury produces signs and symptoms that differ significantly from intoxications with other mercury compounds. Usually, several weeks are required before the symptoms of poisoning become manifest. Even high lethal doses of methylmercury normally do not cause death before 4-7 weeks (Harada 1995). Clarkson (2002) stated that ethylmercury (a component of thiomersal in stabilizers of vaccines) is less stable, and consequently less toxic than methylmercury. Acute intoxication with short-chain alkylmercury compounds causes symptoms which are no different from those seen with chronic intoxication (see Section 17.6.5) (WHO 1990). [Pg.972]

Flowers and Haji bagheii (2001) reported that the effect of ion on the growth of leaves is determined by the ability of plants to accommodate the ions within compartments of the leaves cells where they will not do damage. If the ions are accommodated in the vacuole and concentration rises in the leaf apoplast then there will be osmotic effect on the leaf growth. Okoloko and Bewley (1982) reported the enhancement of protein synthesis in moss (Torhila ruralis) gametophytes exposed to 5mM aqueous SO2. Higher levels were toxic. Some components, particularly compoxmds, are toxic to aquatic animals and plants (Odiete, 1999). They are acutely lethal and chronically lethal in sublethal concentration of part per billion (ppb). However, plants and animals vary widely in their sensitivity (Clark, 1982). [Pg.175]


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Acute Toxicants

Acute lethal

Acute toxicity

Lethal toxicity

Lethality

Lethality acute

Toxic Acute

Toxic doses

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