Nervous system inhalant effects

Most cases of intoxication from industrial exposure have been mild, with rapid onset of eye irritation, headache, sneezing, and nausea weakness, light-headedness, and vomiting may also occur. Acute exposure to high concentrations may produce profound weakness, asphyxia, and death. Acrylonitrile is metabolized to cyanide by hepatic microsomal reactions. Deaths from acute poisoning result from inhibition of mitochondrial cytochrome oxidase activity by metabolically liberated cyanide. Inhalation of more moderate concentrations for a longer period of time leads to damage to the liver tissues in addition to central nervous system (CNS) effects. ... 

The principal effects of carbon tetrachloride in humans are on the liver, the kidneys and the central nervous system. These effects are apparent following either oral or inhalation exposure, and limited data indicate they can occur after dermal exposure as well. All of the effects seen in humans except renal injury are demonstrable at roughly comparable exposure levels in animals, although there are some variations in susceptibility between species that are likely to be related to differences in metabolism. No studies were located regarding reproductive and developmental effects in humans after exposure to carbon tetrachloride. In rats, carbon tetrachloride was not shown to adversely affect reproduction or development. Studies with both mice and rats suggest that sufficiently high doses of carbon tetrachloride may increase the risk of liver tumors in exposed humans. 

HUMAN TOXICITY DATA oral-human TDLo 130 mg/kg toxic effect central nervous system inhalation - human LCLo 20,000 ppm/5 months inhalation-human TCLo 210 ppm toxic effect blood inhalation-human TCLo 100 ppm/10 years - intermittent toxic effect carcinogenic EPA Cancer Risk Level (1 in a million excess lifetime risk) 1.0 x 10 mg/m. ... 

HEALTH SYMPTOMS inhalation (dizziness, drowsiness, headache, nausea, lung edema, effects on central nervous system, blood effects, lowering of consciousness) skin contact (dry skin, redness, dermatitis) eye contact (redness) ingestion (effects on the liver and kidney). 

HUMAN TOXICITY DATA inhalation-human TCLo 4000 ppm/H toxic effect central nervous system, peripheral nervous system, gastrointestinal tract oral-human LDLo 286 mg/kg toxic effect gastrointestinal tract oral-human TDLo 428 mg/kg toxic effect gastrointestinal tract, central nervous system, pulmonary system oral-man TDLo 892mg/kg toxic effect central nervous system, cardiovascular effects, pulmonary system msc-human lymphocyte lOOmg/L. 

HUMAN TOXICITY DATA inhalation-human TCLo 920 ppnV70M toxic effect eye, central nervous system inhalation-man TCLo 200 ppm/4H toxic effect central nervous system inhalation man TCLo 350 ppm toxic effect central nervous system inhalation-man LCLo 27 mg/mVlOM oral-human TDLo 670 mg/kg toxic effect gastrointestinal tract eye-man 450 ppm/8H. 

HUMAN TOXICITY DATA inhalation-human TCLo 125 ppm toxic effect central nervous system inhalation-human TCLo 60mg/m toxic effect central nervous system, cardiovascular system. 

HUMAN TOXICITY DATA oral-human LDLo 50mg/kg inhalation-human TCLo 200 ppm toxic effect central nervous system, blood effects, brain inhalation-man TCLo 100 ppm toxic effect central nervous system eye-human 300 ppm. 

Absorption routs Can enter the body by Inhalation or ingestion or through the skin. Harmful atmospheric concentrations build up fairly slowly on evaporation, but much more rapidly In aerosol form. Immediate effects Irritates the eyes, skin and respiratory tract. Liquid destroys the skin s natural oils. Affects the nervous system. Inhalation can cause severe breathing difficulties (asthma). In serious oases risk of seizures and unconsciousness. Effeota of prolonged/repeated exposure Prolonged or repeated contact can cause skin disorders. Can cause kidney damage. ... 

Absorption route Can enter the body by inhalation or ingestion. immediate afleeta Irritates the eyes, skin and respiratory tract. Affects the nervous system (narcotic effect). ... 

In humans, acute intoxieation by PAHs is related with expositions to concentrations around 100 to 200 ppm. These eoneentrations promote nonspeeifie elinic signs and symptoms such as dizziness, nausea, headaches and difficulties in the motor coordination, by the action of these substanees in the nervous system. Chronis effects can lead to toxic manifestations in several organs and systems, mainly, hematopoietic, renal, hepatic and nervous (Pedrozo et al., 2002). The effeets of the B[a]P inhalation by humans result in patch opacities, prominent bronchiovascular markings and pleural effusions, besides vomits with blood, problems in the respiration, pain and irritation on the chest, irritation in the throat and cough (Gupta et al. 1993). 

Health and Safety Factors. Carbonyl sulfide is dangerously poisonous, more so because it is practically odorless when pure. It is lethal to rats at 2900 ppm. Studies show an LD q (rat, ip) of 22.5 mg/kg. The mechanism of toxic action appears to iavolve breakdowa to hydrogea sulfide (36). It acts principally on the central nervous system with death resulting mainly from respiratory paralysis. Little is known regarding the health effects of subacute or chronic exposure to carbonyl sulfide a 400-p.g/m max level has been suggested until more data are available (37). Carbon oxysulfide has a reported inhalation toxicity in mice LD q (mouse) = 2900 ppm (37). 

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