Chronic intoxication

Mercury-switch thermostats, 16 42 Mercury-thallium amalgam, 24 628 Mercury thermometers, 24 464, 465 Mercury vapor intoxication, chronic, 16 51 Mercury vapor lamps, vitreous silica in, 22 441... 

Use and exposure Styrene is a colorless liquid with a sweet smell. Styrene is primarily a synthetic chemical used extensively in the manufacture of plastics, rubber, and resins. It is also used as an intermediate in the synthesis of materials used for ion exchange resins and to produce copolymers. Toxicity and health effects Acute exposure to styrene causes respiratory effects, such as mucous membrane irritation, eye irritation, and gastrointestinal effects. Styrene causes subjective complaints of headache, fatigue, dizziness, confusion, drowsiness, malaise, difficulty in concentrating, and a feeling of intoxication. Chronic exposure to styrene affects CNS depression and dysfunction, hearing loss, and peripheral neuropathy. - ... 

In addition, other possible causes of dementia also need to be excluded, especially the treatable forms of cognitive impairment, such as that due to depression, chronic drug intoxication, chronic central nervous system infection, thyroid disease, vitamin deficiencies (i.e.. Bn and thiamine), central nervous system angitis, and normal-pressure hydrocephalus (Bird, 2008). Individuals who do not meet these criteria but have short-term memory loss and have only minimal impairment in other cognitive abilities and are not functionally impaired at work or at home are considered to have mild cognitive impairment (Petersen et al., 2001). 

Chronic ingestion of excessive amounts of ethyl bromide may produce a toxic syndrome known as bro-mism . The symptoms are behavioral changes, irritability, headache, confusion, anorexia, weight loss, lethargy, muscular weakness, and slurred speech. Incontinence may develop with chronic intoxication. Chronic intoxication usually develops over 2-4 weeks or longer and the condition is of long duration with symptoms disappearing slowly. 

Toxicology ACGIH TLV/TWA 2.5 mg(F)/m LCLo (inh., rat, 4 h) 128,000 ppm toxic by inh., ing., skin contact asphyxiant may cause frostbite on skin contact may cause skin/pulmonary irritation, dizziness, disorientation, narcosis, nausea, vomiting, headache, acute systemic intoxication, chronic bone changes, skeletal abnormalities, etc. neoplastigen experimental mutagen TSCA listed... 

Acute (occasional) overconsumption of alcohol results in intoxication. Chronically (over some period of time), this can lead to gradual damage of the brain and the nervous system. It is an obvious but rather debated question what effect moderate alcohol consumption may exert on the brain. Are the known risks overcompensated by the expected benefits The lifestyles of more than 1000 elderly people were monitored for at least 7 years in a related American study. Those who consumed moderate amounts of alcohol actually preserved their mental abilities better than those who opted for abstinence. But the authors of this study remarked that they would not recommend alcohol consumption for this purpose despite the positive results. The mechanism of the effect is still unknown, and another substance in the drinks rather than alcohol may very well turn out to be the cracial ingredient. It may be only speculated that the platelet aggregation inhibiting effect may lower the risk of microinfarctions in the brain, and this is why benefits for the brain arise. In observational studies, moderate alcohol consumption was also shown to decrease the risk of Alzheimer s disease. Mechanisms are not known here, either, but these results would warrant further studies about the effects on the central nervous system. 

The usual symptoms in human thaHotoxicosis resulting from acute, subacute, or chronic intoxication are generaHy the same. Common symptoms include nausea, vomiting, abdominal coHc, pain in legs, nervousness and irtitabHity, chest pain, gingivitis or stomatitis, and anorexia. Alopecia (hair loss) does not always occur, especiaHy in cases of mass intake of thallium and low resistance where the patient may die before the occurrence of hair loss. 

There are three common protocols for barbiturate detoxification. In all approaches, the goal is to prevent the occurrence of major symptoms and to minimize the development of intolerable minor symptoms. The first procedure is based on protocols described by several authors (Ewing and BakeweU 1967 Isbell 1950 Wilder 1968) (see Table 3 ). The first step is to determine the severity of tolerance. If the patient is intoxicated, no additional barbiturate should be given until the symptoms of intoxication have resolved. If there is substantial evidence or strong suspicion of chronic barbiturate use, it is not necessary or desirable to wait until withdrawal symptoms appear. A 200-mg oral dose of pentobarbital may be given on an empty stomach to a... 

DSM-IV-TR (American Psychiatric Association 2000) criteria for hallucinogen intoxication are presented in Table 6-3. The normally used quantity of LSD ingested ranges from 30 to 400 pg, but doses as low as 20 pg may cause clinically detectable symptoms (Strassman 1984). However, tolerance to the effect of LSD develops relatively quickly, so that chronic users increase their dose over time. 

Barret MD, Garrel S, Danel V, et al. 1987. Chronic trichloroethylene intoxication A new approach by trigeminal-evoked potentials. Arch Environ Health 42 297-302. 

Effects in Laboratory Animals. As highlighted in other chapters, the central toxicities during and after repeated stimulant bingeing may be related to neuronal or terminal destruction and/or depletion of neurotransmitter in the brain. In monkeys and cats, the report by Duarte-Escalante and Ellinwood (1970) of neuronal chromatolysis associated with decreased catecholamine histofluorescence following chronic METH intoxication has been followed by extensive neurochemical demonstrations of damage to the monoamine pathways by chronic stimulants (Seiden and Ricaurte 1987). 

Duarte-Escalante, O., and Ellinwood, E.H., Jr. Central nervous system cytopathological changes in cat with chronic methedrine intoxication. 

Ellinwood, E.H., Jr., and Kilbey. M.M. Chronic stimulant intoxication models of psychosis. In Hanin, I., and Usdin, E., eds. Animal Models in Psychiatry and Neurology. New York Pergamon Press, 1977. pp. 61-74. 

Lerner, S.E., and Burns, R.S. Phencyclidine use among youth History, epidemiology and acute and chronic intoxication. In Peterson, R.C. and Stillman, R.C., eds. Phencyclidine (PCP) Abuse An Apprai sal. National Institute on Drug Abuse Research Monograph 21. DHEW Pub. No. (ADM) 78-728. Washington, D.C ... 

Seizure history ° Chronic benzodiazepine use ° Concomitant TCA intoxication... 

Initially, most prominent effect is elated mood, although depression may occur hypervigilance and anxiety that may progress to panic with high doses or chronic use, may see impairment of judgment, violence to others or self, paranoia or psychosis with delusions and hallucinations (hallucinations are generally tactile or auditory, rarely visual) an increase in motor activity is common compulsive or stereotyped behavior (e.g., skin picking) may be seen severe intoxication may result in a self-limited delirium... 

The involvement of the cerebellum in the psychoactive effects of marijuana and in changes in rCMR is consistent with the view that THC interacts with the high concentration of CB1 receptors in this brain area. Decreases in the cerebellar rCMR in habitual marijuana users may reflect the effects of chronic exposure to the drug. Functions known to be associated with the cerebellum, such as motor coordination, proprioception, and learning, are adversely affected both during acute marijuana intoxication and in habitual users. 

Volkow ND, Gillespie H, Mullani N, Tancredi L, Grant C, Valentine A, Hollister L. Brain glucose-metabolism in chronic marijuana users at baseline and during marijuana intoxication. Psychiatr Res Neuroimaging 1996 67 29-38. 

Renal Effects. The characteristics of early or acute lead-induced nephropathy in humans include nuclear inclusion bodies, mitochondrial changes, and cytomegaly of the proximal tubular epithelial cells dysfunction of the proximal tubules (Fanconi s syndrome) manifested as aminoaciduria, glucosuria, and phosphaturia with hypophosphatemia and increased sodium and decreased uric acid excretion. These effects appear to be reversible. Characteristics of chronic lead nephropathy include progressive interstitial fibrosis, dilation of tubules and atrophy or hyperplasia of the tubular epithelial cells, and few or no nuclear inclusion bodies, reduction in glomerular filtration rate, and azotemia. These effects are irreversible. The acute form is reported in lead-intoxicated children, whose primary exposure is via the oral route, and sometimes in lead workers. The chronic form is reported mainly in lead workers, whose primary exposure is via inhalation. Animal studies provide evidence of nephropathy similar to that which occurs in humans, particularly the acute form (see Section 2.2.3.2). 

A study of 55 adolescents who had been treated for lead intoxication in early childhood (11-17 years earlier) revealed no evidence of chronic nephropathy, as evidenced by endogenous creatinine clearance, BUN, serum uric acid, and routine urinalysis (Chisolm et al. 1976). PbB levels during the acute poisoning episode ranged from 100 to 650 pg/dL all patients received immediate chelation therapy. At the time of the study, their PbB levels had decreased to less than 40 pg/dL. 

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