Toxic exposure lethal dose

The LD50 may be either oral or dermal , depending on the method of exposure. Lethal doses with respect to inhalation of chemicals in the form of a gas or aerosol can also be tested. In this case, the concentration of gas or vapor that kills half the animals is known as the lethal concentration for 50%, or the LC50. The LD50 and LC50 are very widely used as indices of toxicity. The criteria shown in Table 8.1 are often used for purposes of classification of acute toxic effects in animals. In order to classify the acute toxicity of chemicals to humans, the scale shown in Table 8.2 can be used (see also IPGS 1996). 

The results from this type of study are coupled with the second, very limited, source of toxicity data from previous chemical exposure records of workers. Chemicals are then classified in terms of their inferred, relative toxicity. The two extremes being practically non-toxic (probable lethal dose for a 70 kg human 15g/kg) to super toxic (probable lethal dose for a 70 kg human < 5 mg/kg) . ... 

In summary, acute-toxicity testing in small mammals such as rats provides a range of valuable information on chemical toxicity, including lethal doses by different routes of exposure, mechanism(s) of lethal toxicity, the extent to which the lethal effect may be reversible in some members of the exposed population while others die, and the relative potencies of toxic chemicals as lethal agents. 

Environmental Impact of Ambient Ozone. Ozone can be toxic to plants, animals, and fish. The lethal dose, LD q, for albino mice is 3.8 ppmv for a 4-h exposure (156) the 96-h LC q for striped bass, channel catfish, and rainbow trout is 80, 30, and 9.3 ppb, respectively. Small, natural, and anthropogenic atmospheric ozone concentrations can increase the weathering and aging of materials such as plastics, paint, textiles, and mbber. For example, mbber is degraded by reaction of ozone with carbon—carbon double bonds of the mbber polymer, requiring the addition of aromatic amines as ozone scavengers (see Antioxidants Antiozonants). An ozone decomposing polymer (noXon) has been developed that destroys ozone in air or water (157). 

An acute lethal dose (LC q) for vapor exposure to 1,1,2-trichloroethane in the rat is 2000 ppm for a 4-h exposure. The same lethal effect occurs at 18,000 ppm vapor during 3 h exposure to 1,1,1-trichloroethane. The oral LD q for 1,1,2-trichloroethane in rats is 0.1—0.2 g/kg, classifying it as moderately toxic (109). Liver and kidney damage occurs at even lower dosages. Skin adsorption is a possible route of overexposure. 

Toxicity rating Commonly used term LDso Single oral dose for rats (g/kg) 4hr Vapour exposure causing 2 to 4 deaths in 6-rat group (ppm) LDso Skin for rabbits (g/kg) Probable lethal dose for humans... 

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. 

The acceptable limits for toxic exposure depend on whether the exposure is brief or prolonged. Lethal concentration for airborne materials and lethal dose for non-airbome materials are measured by tests on animals. The limits for brief exposure to toxic materials that are airborne are usually measured by the concentration of toxicant that is lethal to 50% of the test group over a given... 

Acute-Duration Exposure. Information is available regarding the effects of acute-duration inhalation exposure of humans to acrylonitrile and the effects are characteristic of cyanide-type toxicity. Quantitative data are limited but are sufficient to derive an acute inhalation MRL. Further studies of humans exposed to low levels of acrylonitrile in the workplace would increase the confidence of the acute MRL. Studies in animals support and confirm these findings. No studies are available on the effects of acute-duration oral exposure in humans however, exposure to acrylonitrile reveals neurological disturbances characteristic of cyanide-type toxicity and lethal effects in rats and mice. Rats also develop birth defects. Animal data are sufficient to derive an acute oral MRL. Additional studies employing other species and various dose levels would be useful in confirming target tissues and determining thresholds for these effects. In humans, acrylonitrile causes irritation of the skin and eyes. No data are available on acute dermal exposures in animals. 

LD50 values and the lowest lethal doses for acute- and intermediate-duration exposures classify hexachloroethane as slightly toxic (Hodge and Sterner 1949). It is unlikely that exposures to hexachloroethane at levels found at hazardous waste sites would cause death in humans. 

SYSTEMIC EFFECTS Occurs primarily through inhalation and ingestion. The T vapor or aerosol is less toxic to the skin or eyes than the liquid form. When inhaled, the upper respiratory tract (nose, throat, tracheae) is inflamed after a few hours latency period, accompanied by sneezing, coughing and bronchitis, loss of appetite, diarrhea, fever, and apathy. Exposure to nearly lethal doses of T can produce injury to bone marrow, lymph nodes, and spleen as indicated by a drop in white blood cell (WBC) count and, therefore, results in increased susceptibility to local and systemic infections. Ingestion of T will produce severe stomach pains, vomiting, and bloody stools after a 15-20 minute latency period. 

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... 

Neurological Effects. Depression, disorientation, and collapse have been reported in humans with acute exposure to toxic closes of 1,2-dibromoethane by oral (Saraswat et al. 1986) or dermal (Letz et al. 1984) routes. Residues of 1,2-dibromoethane were detected in the brain tissue of one fatality (Letz et al. 1984). The fact that the nervous system is at risk when humans are acutely exposed to lethal doses is supported by animal studies (Rowe et al. 1952). 

Death. Information regarding death in humans following exposure to 1,2-diphenylhydrazine by any route was not found. Some information is available on lethality of orally-administered 1,2-diphenylhydrazine in animals. This information, consisting of a gavage LDso value in fats (Marhold et al. 1968) and an unreliable 3-day dietary lethal dose in mice (Schafer and Bowles 1985), indicates that single or several oral doses of about 1000 mg/kg/day may be lethal for rodents. Based on these data, 1,2-diphenylhydrazine does not appear to be highly acutely toxic to humans he oral route. 

For oral exposures, different fuel oils have differing lethality profiles in rats. Acute lethal doses in rats were reported to be 12,000 mg/kg for kerosene (Muralidhara et al. 1982) and 47,300 mg/kg for JP-5 (Parker et al. 1981). However, an oral dose of 12,200 mg/kg of Deobase was not lethal in rats (Muralidhara et al. 1982). Although differences in the oral toxicity of fuel oils and differences in species thresholds of toxicity may exist, the oral toxicity of fuel oils is relatively low. The intestinal absorption of fuel oils is also relatively low, and aspiration, with its resultant pulmonary effects, is the primary risk from the ingestion of fuel oils. 

A minimum lethal dose of 30,000 mg/kg/day was reported for JP-5 from acute dermal exposure in mice, but this dose was decreased to 2,000 and 250 mg/kg/day following intermediate and chronic exposures, respectively (NTP/NIH 1986). A similar trend was also reported for dermal toxicity in mice exposed to marine diesel fuels (NTP/NIH 1986). Conclusions cannot be drawn from the available data regarding dermal exposure by humans to fuel oils near hazardous waste sites. 

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