Nervous toxicity

Central nervous toxicity has been seen with efavirenz (Clifford et al., 2005). Manifestadons of this process include... 

Symptoms of central nervous toxicity, such as fatigue and agitation, have been experienced by people occupationally exposed to 2,4-DNP (Gisclard and Woodward 1946 Perkins 1919). 

Aveline C, Cognet F, Bonnet F. Ineffectiveness of intralipid infusion for central nervous toxicity following ultrasound-guided sciatic nerve block with lidocaine-ropivacaine solution interaction between carbamazepine, local anaesthetic and intralipid Eur J Anaesthesiol 2010 27 1070-2. 

The authors postulate bupivacaine- or opioid-induced central nervous toxicity, vestibular pressure effects of the injected drug or partly subdural injection as potential causes. 

Effects of repeated ethylene glycol peroral overexposure in treated rats and mice can result in kidney, Hver, and nervous system damage. The most sensitive indicators of ethylene glycol toxicity are disturbances in acid—base balance and nephrotoxic (kidney) effects. Effects of repeated chronic peroral overexposure of diethylene glycol in treated rats result in kidney and Hver damage (48). 

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. 

The toxicity of 2,4-pentanedione is shown in Tables 3 and 11 to be similar to mesityl oxide, and greater than most other 1,2- or 1,4-diketones or monoketones. Inhalation of low levels of 2,4-pentanedione can cause nausea, eye contact can induce stinging, and recurrent exposure to high concentrations (300—400 ppm) can adversely affect the central nervous system and immune system (325). 

Lead is toxic to the kidney, cardiovascular system, developiag red blood cells, and the nervous system. The toxicity of lead to the kidney is manifested by chronic nephropathy and appears to result from long-term, relatively high dose exposure to lead. It appears that the toxicity of lead to the kidney results from effects on the cells lining the proximal tubules. Lead inhibits the metaboHc activation of vitamin D in these cells, and induces the formation of dense lead—protein complexes, causing a progressive destmction of the proximal tubules (13). Lead has been impHcated in causing hypertension as a result of a direct action on vascular smooth muscle as well as the toxic effects on the kidneys (12,13). 

Phenol. Phenol monomer is highly toxic and absorption by the skin can cause severe blistering. Large quantities can cause paralysis of the central nervous system and death. Ingestion of minor amounts may damage kidneys, Hver, and pancreas. Inhalation can cause headaches, dizziness, vomiting, and heart failure. The threshold limit value (TLV) for phenol is 5 ppm. The health and environmental risks of phenol and alkylated phenols, such as cresols and butylphenols, have been reviewed (66). 

Side Effects and Toxicity. Adverse effects to the tricycHc antidepressants, primarily the result of the actions of these compounds on either the autonomic, cardiovascular, or central nervous systems, are summarized in Table 3. The most serious side effects of the tricycHcs concern the cardiovascular system. Arrhythmias, which are dose-dependent and rarely occur at therapeutic plasma levels, can be life-threatening. In order to prevent adverse effects, as weU as to be certain that the patient has taken enough dmg to be effective, the steady-state semm levels of tricycHc antidepressant dmgs are monitored as a matter of good practice. A comprehensive review of stmcture—activity relationships among the tricycHc antidepressants is available (42). 

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). 

Health nd SMety Factors. The lowest pubhshed human oral toxic dose is 430 mg/kg, causing nervous system disturbances and gastrointestinal symptoms. The LD q (rat, oral) is 750 mg/kg (183). Thiocyanates are destroyed readily by soil bacteria and by biological treatment systems in which the organisms become acclimatized to thiocyanate. Pyrolysis products and combustion products can include toxic hydrogen cyanide, hydrogen sulfide, sulfur oxides, and nitrogen oxides. 

Bromothiophenes are toxic materials by aU routes. Inhalation toxicity of 2-bromothiophene is significant. Ecotoxicity is also noted for these materials, particularly for 2-bromo-3-methylthiophene. 2-Thiophenecarboxaldehyde and the 3-methyl derivative can cause minor irritation to the skin and eyes of rabbits. The former is a sensitizer to guinea pig skin, the latter is not. 2-Acetylthiophene is toxic in aU modes of contact. Severe exposure causes serious inflammation of the lung, damage to many organs, and depression of the central nervous system. 

Arsenic compounds must be considered extremely poisonous. Dust or fumes irritate mucous membranes and lead to arsenical poisoning. When swallowed they irritate the stomach and affect the heart, Hver, and kidneys. Nervousness, thirst, vomiting, diarrhea, cyanosis, and coUapse are among the symptoms of arsenical poisoning (3). In spite of the toxicity of arsenic compounds, there is evidence that arsenic is an essential nutrient for several animal species (4). 

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. 

The Class I agents have many similar side effects and toxicities. The anticholinergic side effects include dry mouth, constipation, and urinary hesitancy and retention. Common gastrointestinal (GI) side effects include nausea, vomiting, diarrhea, and anorexia. Cardiovascular adverse effects are hypotension, tachycardia, arrhythmias, and myocardial depression, especially in patients with congestive heart failure. Common central nervous system (CNS) side effects are headache, dizziness, mental confusion, hallucinations, CNS stimulation, paraesthesias, and convulsions. 

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