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Depressants, central nervous system

Full eye protection should be worn whenever handling acryhc monomers contact lenses must never be worn. Prolonged exposure to Hquid or vapor can result in permanent eye damage or blindness. Excessive exposure to vapors causes nose and throat irritation, headaches, nausea, vomiting, and dizziness or drowsiness (solvent narcosis). Overexposure may cause central nervous system depression. Both proper respiratory protection and good ventilation are necessary wherever the possibiHty of high vapor concentration arises. [Pg.157]

Paraffins. Methane and ethane are simple asphyxiants, whereas the higher homologues are central nervous system depressants. Liquid paraffins can remove oil from exposed skin and cause dermatitis or pneumonia in lung tissue. Generally, paraffins are the least toxic class of hydrocarbons. [Pg.370]

Sahcylamide [65-45-2] is prepared by the reaction of methyl sahcylate with ammonia. Sahcylamide has mild analgesic, antiinflammatory, and antipyretic properties. Sahcylamide is unlike other sahcylates in that it causes sedation and central nervous system depression. Sahcylamide is not hydroly2ed to sahcylate and its action depends on the entire molecule. Sahcylamide has been useful for protection against mil dew and fungus in a variety of soaps, salves, lotions, and oils. The May 1996 price was 8.00/kg (18). [Pg.290]

AH four butanols are thought to have a generaHy low order of human toxicity (32). However, large dosages of the butanols generaHy serve as central nervous system depressants and mucous membrane irritants. Animal toxicity and irritancy data (32) are given in Table 4. [Pg.358]

AH volatile organic solvents are toxic to some degree. Excessive vapor inhalation of the volatile chloriaated solveats, and the central nervous system depression that results, is the greatest hazard for iadustrial use of these solvents. Proper protective equipment and operating procedures permit safe use of solvents such as methylene chloride, 1,1,1-trichloroethane, trichloroethylene, and tetrachloroethylene ia both cold and hot metal-cleaning operations. The toxicity of a solvent cannot be predicted from its chlorine content or chemical stmcture. For example, 1,1,1-trichloroethane is one of the least toxic metal-cleaning solvents and has a recommended threshold limit value (TLV) of 350 ppm. However, the 1,1,2-trichloroethane isomer is one of the more toxic chloriaated hydrocarboas, with a TLV of only 10 ppm. [Pg.507]

Inhalation of high concentrations of monochlorotoluenes will cause symptoms of central nervous system depression. Inhalation studies produced an LC q (rat, 4 h) of 7119 ppm for o-chlorotoluene (68). o- and Chlorotoluene are both considered moderately toxic by ingestion (Table 2). A study of the relationship between the electronic stmcture and toxicity parameters for a series of mono-, di-, and tri-chlorotoluenes has been reviewed (72). A thin-layer chromatographic method has been developed to assess the degree of occupational exposure of workers to chlorotoluenes by determining j -cblorobippuric... [Pg.54]

Inhalation is the most common means by which ethers enter the body. The effects of various ethers may include narcosis, irritation of the nose, throat, and mucous membranes, and chronic or acute poisoning. In general, ethers are central nervous system depressants, eg, ethyl ether and vinyl ether are used as general anesthetics. [Pg.427]

Solvents acetone, methyl ethyl ketone (MEK), toluene, xylene, glycol, ethers, alcohol defats and dries skin some may be absorbed may carry other components through skin high volatility, exposure possible irritation central nervous system depression (e.g. dizziness, loss of coordination) low to high toxicity, longterm effects... [Pg.145]

Health Hazards Information - Recommended Personal Protective EquipmetU Goggles or face shield Symptoms Following Exposure Low toxicity. Excessive exposure produces some central nervous system depression. Prolonged contact produces skin irritation General Treatment for Exposure INHALATION if necessary, support respiration. INGESTION induce vomiting and call a doctor. SKIN AND EYES wash with copious amounts of water Toxicity by Inhalation (Threshold Limit Value) Data not available Short-Term Inhalation Limits Data not available Toxicity by Ingestion Data not available Late Toxicity Data not available Vapor (Gas) Irritant Characteristics Data not available Liquid or Solid Irritant Characteristics Data not available Odor Threshold Data not available. [Pg.307]

Pyridine may cause central nervous system depression, irritation of skin and respiratory tract Large doses may produce gastro-intestinal disturbances, kidney and liver damage (Refs 3 4)... [Pg.974]

Levels greater than 150 mcg mL may result in symptoms of mild salicylism, namely tinnitus (ringing sound in the ear), difficulty in hearing, dizziness, nausea, vomiting, diarrhea, mental confusion, central nervous system depression, headache, sweating, and hyperventilation (rapid, deep breathing). [Pg.155]

Respiratory and central nervous system depression, nausea, vomiting, constipation, diarrhea, bradycardia, hypotension, syncope, hypersensitivity reactions, headache Same as amobarbital sodium... [Pg.238]

There is an increase in anticholinergic effects when antihistamines are administered with the monamine oxidase inhibitors (MAOIs) and additive sedative effects if administered with central nervous system depressants (eg, narcotic analgesics or alcohol). When cimetidine and loratadine are administered together there is a risk for increased loratadine levels. [Pg.328]

Oral poisoning after accidental phenol ingestion has caused fulminant central nervous system depression, hepatorenal and cardiopulmonary failure [20]. No hepatorenal or central nervous system toxicities with properly performed chemical peels have been reported in the literature [21]. [Pg.85]

Animal experimentation has revealed inhaled concentrations that result in death following acute, intermediate, and chronic exposure. An LC50 value for acute exposure in rats was reported as 12,500 ppm for a 4-hour exposure (Siegel et al. 1971). Two out of 10 mice died after a 4-hour exposure to 6,400 ppm trichloroethylene (Kylin et al. 1962). Death was often caused by the central nervous system depression that... [Pg.24]

In the past, trichloroethylene was used as a human anesthetic. Trichloroethylene has also been used by individuals who intentionally inhale it for its narcotic properties. Therefore, most of the information regarding the effects of trichloroethylene in humans comes from case studies and experiments describing effects of trichloroethylene after inhalation exposure. These studies indicate that the primary effect of exposure to trichloroethylene is on the central nervous system. Effects include headache, vertigo, fatigue, short-term memory loss, decreased word associations, central nervous system depression, and anesthesia. [Pg.139]

Attempts to diminish the overall metabolism of trichloroethylene might be useful (e.g., hypothermia, mixed-function oxidase inhibitors, competitive inhibitors of trichloroethylene metabolism [i.e., P-450 substrates]), if instituted soon enough after trichloroethylene exposure. Catecholamines (especially beta agonists) act in concert with trichloroethylene, increasing the risk of cardiac arrhythmias. Hence, catecholamines should be administered to patients only in the lowest efficacious doses and for certain limited presentations of trichloroethylene poisoning. Ethanol should also be avoided because concurrent exposure to trichloroethylene and ethanol can cause vasodilation and malaise and may potentiate central nervous system depression at high dosage levels of either compound. [Pg.177]


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