Toxicity route

When sulfonic acids are neutralized to sulfonic acid salts, the materials become relatively innocuous and low in toxicity, as compared to the parent sulfonic acid (see Table 4). The neutralized materials cause considerably less eye and skin irritation. The most toxic route of entry for sulfonic acid salts is ingestion (39). The toxicity of neutralized sulfonic acids, especially detergent sulfonates, has been directiy related to the foaming capabiUty of the material. 

N-methyl carbamates are absorbed by inhalation and ingestion, and somewhat by skin penetration, although the last tends to be a less toxic route. 

Local (intralesional, intra-arterial, or intraperitoneal) administration of tumor necrosis factor alfa may well prove to be a more promising and less toxic route of administration. Although mild adverse effects, namely fever, hypotension, and fatigue, were similar to those reported after intravenous administration, coagulation disorders, pulmonary, central nervous system, liver, and renal forms of toxicity were usually not observed (17). 

Symptomatic and supportive measures are the mainstay of management of this highly toxic route of exposure. There is some evidence that the intravenous administration of anti-ricin antibody shortly (within 1-2 h) after ricin exposure may improve survival (Houston, 1982) although this has to be confirmed and probably has no utility in a civilian population where there would be no near real-time detection of ricin exposure. 

Fig. 10. Trade-offs between cost and the use of toxic intermediates in the chemical industry. Point A is the lowest-toxicity route currently feasible, but it comes at a greater cost than the most economical approach (Point C). Point B (low cost, low toxicity) is not currently technologically feasible. Point D is the closest feasible technology mix to Point B (Fathi-Afshar and Yang. 1985).

Target organs skin, eyes, gastrointestinal tracts, and respiratory system. Toxic routes ingestion, inhalation, and skin contact. 

Causes anemia, reticulocytosis, and cyanosis on chronic exposure absorbed through skin other toxic routes are ingestion and inhalation of its vapors, and symptoms are headache and dizziness ... 

The cyanide antidote 4-dimethylamino-phenol plus sodium thiosulfate showed some protective action only after oral intake. However, against inhalation and other toxic routes, the antidote above was ineffective (Appel et al. 1981). Buchter and Peter (1984) reported the effectiveness of cysteine [52-... 

The toxic routes are inhalation, ingestion, and absorption through skin. The target organs are kidney, liver, central nervous system, lungs, and eyes. Inhalation of 500 ppm for 4 hours was lethal to rats. When administered intraperitoneally to mice, it caused corneal damage, ataxia, and dyspnea. The acute oral toxicity of this compound was found to be moderately high in rodents. 

Methylacrylonitrile is a moderate to severe acute toxicant. The degree of toxicity varied with toxic routes and species. Inhalation, ingestion, and skin application on test subjects produced convulsion. Exposure to high concentrations can result in asphyxia and death. The lethal concentrations varied among species from 50 to 400 ppm over a 4-hour exposure period. The clinical symptoms observed in rats suggested a toxic activity of metabolically formed cyanide (Peter and Bolt 1985). This finding was in contrast with acrylonitrile toxicity in the same species, where formation of metabolic cyanide played a minor role. 

Malononitrile is a highly toxic compound by all toxic routes. Its acute toxicity is somewhat greater than that of the aliphatic mononitriles, propionitrile, and butyronitrile. The increased toxicity may be attributed to the greater degree of reactivity in the molecule arising from two —CN functional groups. The acute toxic symptoms in test animals have not been well documented. An intraperitoneal dose of 10 mg/kg was lethal to rats. 

Hydrogen cyanide is a dangerous acute poison by all toxic routes. Acute inhalation may cause death in seconds. Lethal effects due to inhalation of its vapor depend on its concentration in air and time of exposure. Inhalation of 270 ppm HCN in air can be fatal to humans instantly, while 135 ppm can cause death after 30 minutes (Patty 1963 ACGIH... 

The lethal effect from cyanide poisoning varied with species. Investigating the acute oral toxicity of sodium cyanide in birds, Wiemeyer et al. (1986) observed that the LDso values for the flesh-eating birds were lower than that for the birds that fed on plant material vulture 4.8 mg/kg versus chicken 21 mg/kg. In a study on marine species, Pavicic and Pihlar (1983) found that at 10 ppm concentration of NaCN, invertebrates were more sensitive than Ashes. In animals, the lethal dose of NaCN were in the same range by different toxic routes. A dose of 8 mg NaCN/kg resulted in ataxia, immobilization, and death in coyotes (Sterner 1979) however, the lethal time was longer, at 18 minutes. 

Calcium cyanide is a highly poisonous compound to humans, animals, and fish. The toxic routes are ingestion, skin contact, and inhalation of the dust. It forms HCN readily when it reacts with CO2 or water. This makes it highly hazardous, more so than the alkali-metal cyanides, although the LD50 value of Ca(CN)2 is greater than the sodium or potassium cyanides. 

Acute exposure can result in death by asphyxia. The toxic routes are inhalation and percutaneous absorption. At sublethal concentrations the symptoms of acute toxicity are nausea, vomiting, headache, confusion, and weakness. 

Cyanogen bromide is a highly poisonous substance. Toxic routes are oral intake and skin absorption. Acute toxic symptoms on test animals were convulsion, paralysis, and respiratory failure. Ingestion of a 5-g amount could be fatal to humans. 

Cuprous cyanide is a highly toxic substance. The toxic routes are inhalation of dust, ingestion, and skin contact. Toxicology and LD50 values for this compound are not reported. Because it is slightly soluble in water, its dissociation to cuprous and cyanide ions in the body may not be significant. The role of cyanide ion in the toxicity of cuprous cyanide is not established. The inhalation hazard, however, is attributable to copper. It is a skin irritant. 

Methylene chloride is a low to moderately toxic compound, the toxicity varying with the animal species. It is less toxic in small animals than in humans. The toxic routes of exposure are inhalation of its vapors, ingestion, and absorption through the skin. It may be detected from its odor at a concentration of 300 ppm. Acute toxic symptoms include fatigue, weakness, headache, lightheadedness, euphoria, nausea, and sleep. High concentrations may produce narcosis. Rabbits exposed to 10,000 ppm for 7 hours died from exposure. The LC50 value in mice is 14,400 ppm/7 h (NIOSH 1986). Mild effects may be felt in humans from an 8-hour exposure to 500 ppm of methylene chloride vapors. Oral intake of 15-20 mL of the liquid may be lethal to humans. Chronic exposure to this compound can lead to liver injury. Contact of the liquid with skin or eyes can cause irritation. 

The toxic route is primarily inhalation. The vapor pressure of this compound at ambient temperature is very low, 0.00014 torr at 25°C. However, when heated to about 75°C, the acute health hazard is greatly enhanced (Hadengue and Philbert 1983). The acute toxic symptoms were found to be similar to those of toluene-2,4-diisocyanate and other aromatic isocyanates. Inhalation of its vapors or particulates can cause bronchitis, coughing, fever, and an asthma-like syndrome. Other symptoms were nausea, shortness of breath, chest pain, insomnia, and irritation of the eyes, nose, and throat. The immunologic response, however, varied among humans. Exposure to 0.1-0.2 ppm for 30 minutes is likely to manifest the acute toxic effects in humans. 

Toxic routes of exposure to lead are food, water, and air. It is an acute as well as a chronic toxicant. The toxic effects depend on the dose and the nature of the lead salt. Ingestion of lead paint chips is a common cause of lead poisoning among children. Chronic toxic effects may arise from occupational exposure. 

Its toxicity is comparable to that of tert-butyl hydroperoxide. The toxic routes are ingestion and inhalation. The acute toxicity symptoms in rats and mice were muscle weakness, shivering, and prostration. Oral administration of 400 mg/kg resulted in excessive urinary bleeding in rats. 

White phosphorus is a highly poisonous substance. The toxic routes are ingestion, skin contact, and inhalation. 

Godin, S. C., and P. A. Crooks. 1989. V-Methy-lation as a toxicant route for xenobiotics. n. In vivo formation of Af,Af-dimethyl-4,48-bipyridyl ion (Paraquat) from 4,4-bipyridyl in the guinea pig. Drug Metab. Dispos. 77(2) 180-85. 

Moderate to high toxicity toxic routes inhalation, ingestion, and skin absorption target organs lungs, central nervous system, and peripheral nerve symptoms observed in test animals were respiratory stimulation, dyspnea, ataxia, convulsion, lowering of body temperature, and spastic paralysis LD50 oral (rats) ... 

Low toxicity in test animals toxic routes inhalation and ingestion symptoms somnolence, muscle weakness and excitement ... 

Acute toxicity low to moderate in test animals toxic routes — inhalation and ingestion an oral dose of 1000 mg/kg was fatal to guinea pigs exposure limits TLV-TWA in air 0.5 mg/m (OSHA)... 

Moderate to high toxicity toxic route—inhalation LD50 data not available in humans, acute toxic symptoms can be bronchitis, wheezing, congestion in chest, and pulmonary edema—similar to other aromatic diisocyanates low oral toxicity LD50 intravenous (mice) 5.6 mg/kg exposure limits TLV-TWA (relative to diisocyanate) 0.0327 mg/m ... 

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