Central nervous system acute 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. ... 

Ingestion of 5-12 g of hydroquinone has been reported to be fatal. In one nonfatal case of hydroquinone ingestion of approximately 1 g, tinnitus, dyspnea, cyanosis, and extreme sleepiness were observed. Although acute, high-dose oral ingestion produces noticeable central nervous system (CNS) effects in humans, no effects have been observed in workers exposed to lower concentrations in actual industrial situations. No signs of toxicity were found in subjects who ingested 3 00-500 mg hydroquinone daily for 3-5 months. ... 

Adverse effects that are not unequivocally related to inhibition of prostaglandin synthesis include hepatic effects (hepatitis, hepatic necrosis, cholestatic jaundice, increased serum aminotransferases), dermal effects (photosensitivities, Stevens-Johnson syndrome, toxic epidermal necrolysis, onycholysis), central nervous system (CNS) effects (headaches, dizziness, tinnitus, deafness, drowsiness, confusion, nervousness, increased sweating, aseptic meningitis), ocular effects (toxic amblyopia, retinal disturbances), and certain renal effects (acute interstitial nephritis, acute papillary necrosis). 

Neurological effects. Case reports of humans demonstrated that chlorobenzene caused disturbances of the central nervous system, but there were no reports of changes in the structure of the brain and other parts of the nervous system. Effects were observed in humans who inhaled vapors of chlorobenzene in the workplace for up to 2 years (Rozenbaum et al. 1947). Effects included headaches, dizziness, and Sleepiness. Unconsciousness, lack of response to skin stimuli, and muscle spasms were noted following accidental ingestion. While there is qualitative evidence for central nervous system effects in humans, a quantitative assessment can not be made since exposure levels were not reported. Because work practices have changed significantly since these studies, it is reasonable to assume that exposure levels in this study were higher than current permissible federal exposure levels. Acute studies in animals confirm that chlorobenzene is potentially neurotoxic. These effects appear to be the result of narcotic effects of chlorobenzene on the central nervous system. Acute inhalation exposure produced narcosis preceded by muscle spasms in rabbits at 1,090 ppm (Rozenbaum et al. 1947). 

Sodium borate decomposes into borate and peroxide and is less toxic than potassium bromate. From 3 to 6g and from 15 to 30 g boric acid is potentially fatal to children and adults, respectively. Cutaneous manifestations include desquamating, erythematous rash commonly over palms, soles, buttocks, and scrotum. The lesion may progress to exfoliation. Central nervous system (CNS) effects range from irritability, restlessness, and headache to coma and convulsions in severe cases. Gastrointestinal symptoms include anorexia, nausea, vomiting, and diarrhea. Acute renal tubular necrosis may lead to renal failure in moderate to severe cases. 

Acute toxicity induced by pentazocine is primarily associated with central nervous system (CNS) effects that include dizziness, anxiety, hallucinations, mood alterations, and seizures. Respiratory depression, increased PaCOi levels, pulmonary edema, and apnea may occur. Tachycardia, increased systolic and diastolic blood pressure, pinpoint pupils, nausea, vomiting, and abdominal pain have also been reported. In a recently published case series, 40% of acute pentazocine overdose patients did not have the classic opioid toxidrome of CNS and respiratory depression with miosis. 

The acute toxicity from overexposure to petroleum ether is manifested primarily in central nervous system (CNS) effects. The mechanism of toxicity is unknown however, the general anoxia observed is most likely due to oxygen deprivation. The mechanism of toxicity from long-term overexposure to petroleum ether is dependent on the chemical makeup of the distillate. For example, if peripheral neuropathy is observed, it is most likely due to a high concentration of -hexane in the petroleum ether. -Hexane is known to cause axonal damage in peripheral nerves. 

Acute overdosage can result in both cardiovascular and neurologic effects. Ventricular dysrhythmias and hypotension are the most serious toxicities. Cardiac effects occur as a result of myocardial depression and depression of atrial, atrioventricular, and ventricular conduction. EKG changes will be evident. These EKG changes include a widening of the QT, PR, and QRS complexes ST depression and T inversion. Myocardial depression and vasodilation can cause hypotension to develop. Syncope can result from transient Torsade de Pointes (i.e., bursts of atypical ventricular tachycardia). Ventricular tachycardia and ventricular fibrillation may develop. Possible central nervous system (CNS) effects include lethargy, seizures, and coma. Other acute effects can include apnea. Signs of toxicity are expected to occur in... 

Although small, single doses of acrylamide to experimental animals (the acute oral LD50 for rodents is approximately 200mg/kg) are not particularly hazardous, the product possesses a high degree of cumulative toxicity. Repeated and prolonged intake of small quantities by experimental animals results in disturbance of certain functions of the central nervous system. The effect is manifested by muscular weakness and disorders of equilibrium and locomotion. 

Parkinson-like effects and acute dystonias may be seen. Central nervous system (CNS) effects include somnolence and seizure activity, as well as a lack of core temperature regulation due to hypothalamic effects. Autonomic effects include dry mouth, blurred vision, and urinary retention, coupled with cardiovascular effects such as tachycardia, cardiac arrhythmias, and hypotension. 

ACUTE HEALTH RISKS irritation of eyes, nose and throat irritation to respiratory tract coughing shortness of breath headache nausea vomiting diarrhea may affect the central nervous system narcotic effects in high concentrations may cause dermatitis possible comeal bums eye damage pulmonary changes. 

ACUTE HEALTH RISKS headache, dizziness nausea vomiting convulsions unconsciousness effects on central nervous system gastrointestinal effects coma death at high concentrations. 

B. Pharmacokinetics. Lithium is completely absorbed within 6-8 hours of ingestion. The initial volume of distribution (Vd) is about 0.5 L/kg, with slow entry into tissues and a final Vd of 0.7-0.9 L/kg. Entry into the brain is slow, which explains the delay between peak blood levels and central nervous system (ONS) effects after an acute overdose. Elimination is virtually entirely by the kidney, with a half-life of 14-30 hours. 

The adverse side effects of bisphosphonates are renal toxicity, acute-phase reactions, gastrointestinal toxicity, hypocalcemia, ocular complications, asthma erythema, phlebitis, altered taste, and central nervous system side effects. The osteonecrosis of the jaw is the emerging one (Diel et ah, 2007 Tanvetyanon and Stiff, 2006). To overcome this kind of problem, researchers are now turning toward nature-based drugs. 

Trichloroethylene is acutely toxic, primarily because of its anesthetic effect on the central nervous system. Exposure to high vapor concentrations is likely to cause headache, vertigo, tremors, nausea and vomiting, fatigue, intoxication, unconsciousness, and even death. Because it is widely used, its physiological effects have been extensively studied. 

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. 

Lotti M, Becker CE. 1982. Treatment of acute organophosphate poisoning Evidence of a direct effect on central nervous system by 2-PAM (pyridine-2-aldoxime methyl chloride). J Toxicol Clin Toxicol 19 121-127. 

---