Toxicity, general lethal dose

In general, lethal doses,of NDMA and causes of death are similar among animal species. Human fatalities due to ingestion or inhalation of NDMA were also attributed to liver toxicity but adequate dose information is not available. 

Health Hazards Information - Recommended Personal Protective Equipment Eye protection Symptoms Following Eiqzosure Dust irritates eyes in same way as any foreign material. Penetration of skin by fragments of metal is likely to produce local irritation, blisters, and ulcers which may become infected General Treatment for Exposure EYES flush with water to remove dust. SKIN treat as any puncture Toxicity by Inhalation (Threshold Limit Value) Data not available Short-Term Inhalation Limits Not pertinent Toxicity by Ingestion Oral LDLo (lowest lethal dose) = 230 mg/kg (dog) Late Toxicity Data not available Vtqtor (Gas) Irritant Characteristics Not pertinent Liquid or Solid Irritant Characteristics Data not available Odor Threshold Not pertinent. 

Witkin (1956) reported intravenous (i.v.), i.p., and oral LD50 (lethal dose for 50% of the animals) values for mice and rats, and i.v. LD50 values for dogs. Similar to hydrazine, the route of administration had minimal effect on the LD50 within species. Generally, monomethylhydrazine and 1,2-dimethylhydrazine appeared to be somewhat more potent in mice and rats than was hydrazine. Results of this study showed that the 1,1-dimethylhydrazine was less acutely toxic than hydrazine or the other hydrazine derivatives. 

Organic cyanide compounds, or nitriles, have been implicated in numerous human fatalities and signs of poisoning — especially acetonitrile, acrylonitrile, acetone cyanohydrin, malonitrile, and succinonitrile. Nitriles hydrolyze to carboxylic acid and ammonia in either basic or acidic solutions. Mice (Mus sp.) given lethal doses of various nitriles had elevated cyanide concentrations in liver and brain the major acute toxicity of nitriles is CN release by liver processes (Willhite and Smith 1981). In general, alkylnitriles release CN much less readily than aryl alkylnitriles, and this may account for their comparatively low toxicity (Davis 1981). 

Death. Clinical reports in humans and studies in animals demonstrate that death due to central nervous system toxicity is the primary acute lethal effect associated with endrin exposure. A lethal dose of endrin in humans has not been identified, but 0.2-0.25 mg endrin/kg body weight is sufficient to cause convulsions (Davies and Lewis 1956). Liver, kidney, heart, and brain damage were reported following oral and inhalation exposures. Since endrin is no longer used commercially, the general public is not... 

The more classical approach to assess the presence of marine biotoxins in seafood is the in vivo mouse bioassay. It is based on the administration of suspicious extracted shellfish samples to mice, the evaluation of the lethal dose and the toxicity calculation according to reference dose response curves, established with reference material. It provides an indication about the overall toxicity of the sample, as it is not able to differentiate among individual toxins. This is a laborious and time-consuming procedure the accuracy is poor, it is nonspecific and generally not acceptably robust. Moreover, the mouse bioassay suffers from ethical implications and it is in conflict with the EU Directive 86/609 on the Protection of Laboratory Animals. Despite the drawbacks, this bioassay is still the method of reference for almost all types of marine toxins, and is the official method for PSP toxins. 

Barium ion is a muscle poison causing stimulation and then paralysis. Initial symptoms are gastrointestinal, including nausea, vomiting, colic, and diarrhea, followed by myocardial and general muscular stimulation with tingling in the extremities. Severe cases continue to loss of tendon reflexes, general muscular paralysis, and death from respiratory arrest or ventricular fibrillation. Threshold of a toxic dose in humans is reported to be about 0.2-0.5 g Ba absorbed from the gut the lethal dose is 3 g Ba. 

The general approach in generating toxic potency data from chemical analysis is to assume additive behavior of individual toxicants, and to express the concentration of each toxicant as its fraction of the lethal concentration for 50% of the population for a 30 min exposure (LC50). Thus an fractional effective dose (FED) equal to one indicates that the sum of concentrations of individual species will be lethal to 50% of the population over a 30 min exposure. Two equations have been developed for the estimation of the FED for lethality from the chemical composition of the environment in the physical fire model. Each begins with the precept that the fractional lethal doses of most gases are additive, as developed by Tsuchiya and Sumi.32... 

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