[Occupational poisoning; arsenic poisoning; benzene poisoning].
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Arsenic poisoning continues to be a serious medical problem that may easily be overlooked or misdiagnosed. The broad constellation of symptoms and signs in arsenic poisoning, along with changing sources of this toxin, contributes to misdiagnosis. A re-examination of current potential sources was carried out. Sources were determined in 17 of 20 documented cases of arsenic poisoning. Fourteen cases resulted from ingestion of a single, commonly available, arsenic-containing ant killer. In contrast to earlier reports, this survey found that agricultural and industrial sources were relatively uncommon. A peculiar posturing of the hand is commonly seen in the early stages of arsenic poisoning prior to the development of Mee's lines or palmar hyperkeratosis. An illustrative case is reported that resulted from intermittent self-administration of an arsenic-containing ant killer in order to maintain a state of chronic invalidism.
Arsenic poisonings are still important in the field of toxicology, though they are not as frequent as about 20-30 years ago. In this paper, the arsenic concentrations in ante- and post-mortem materials, and also forensic and anatomo-pathological aspects in three cases of massive acute poisoning with arsenic(III) oxide (two of them with unexplained criminalistic background, in which arsenic was taken for amphetamine and one suicide), are presented. Ante-mortem blood and urine arsenic concentrations ranged from 2.3 to 6.7 microg/ml, respectively. Post-mortem tissue total arsenic concentrations were also detected in large concentrations. In case 3, the contents of the duodenum contained as much as 30.1% arsenic(III) oxide. The high concentrations of arsenic detected in blood and tissues in all presented cases are particularly noteworthy in that they are very rarely detected at these concentrations in fatal arsenic poisonings.
Arsenic poisoning continues to require awareness of its diverse clinical manifestations. Industry is the major source of arsenic exposure. Although epidemiologic studies strongly contend that arsenic is carcinogenic, there are little supportive research data. Arsenic poisoning, both acute and chronic, is often overlooked initially in the evaluation of the patient with multisystem disease, but once it is suspected, many accurate methods are available to quantitate the amount and duration of exposure. Treatment with dimercaprol remains the mainstay of therapy, and early treatment is necessary to prevent irreversible complications.
Arsenic intoxication is a common form of heavy metal poisoning. Although arsenic-induced circulatory collapse, seizures, and syncope are well known, the potential for serious ventricular arrhythmias is less well recognized. Reported in this study are two cases of arsenic poisoning causing torsade de pointes. Furthermore, marked prolongation of the QT-U interval and the rarely observed phenomenon of T-U wave alternans are demonstrated. Thus, arsenic intoxication may be complicated by prolongation of the QT-U interval and torsade de pointes. T-U wave alternans occurs in the presence of a long QT-U interval and may be an electrocardiographic warning sign of torsade de pointes.
Arsenic (As2O3)-poisoned rats were treated with either 2,3-dimercaptosuccinic acid (DMS) or dimercaptopropanol (BAL) at doses of 30 mg/kg/day. A control group received no treatment. The total quantity of arsenic excreted was not significantly different in response to 4 days of treatment with either DMS or BAL. In addition, there was no difference between the two drug treatment groups in the residual arsenic content of brain, liver, kidney and spleen after treatment. Both drugs reduced the arsenic content of each tissue to approximately 40% of that of untreated controls. Previous studies have shown that DMS is orally effective for the treatment of lead poisoning. The LD50 of DMS was determined to be in excess of 3 g/kg in rats and mice, approximately 30 times the LD50 of BAL. No gross, histopathological or biochemical evidence of toxicity was observed in mice, rats or dogs which received DMS 5 days per week for 6 months. DMS did not affect the excretion of zinc, iron, calcium or magnesium. Urinary copper excretion was significantly elevated in response to 30 mg/kg of DMS, suggesting that the drug might also be useful for the treatment of Wilson's disease.
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Chronic arsenic poisoning has serious and extensive impact on human health, which attracts wide attention worldwide. Bases on vast public survey, this article introduces recent field studies on chronic arsenic poisoning from three aspects: exposure history, clinical symptoms and laboratory evidences, and also explains the meaning of each index to the determination of chronic arsenic poisoning, then bring forward some considerations on further epidemiological studies on chronic arsenic poisoning.
BACKGROUND: Arsenic poisoning has been discussed frequently in Norway during the past year on the background of a suspected crime case. There seem to be several uncertainties regarding this issue, also in the medical profession. MATERIAL AND METHODS: We have searched the literature and made a review based upon the present knowledge about arsenic and arsenic poisoning. RESULTS: Arsenic can be found in numerous chemical compounds with different properties. Inorganic arsenic compounds, like arsenic trioxide, are reactive and can cause damage to the body. Organic arsenic compounds, which are found in high concentrations in fish and shellfish, are not considered toxic. Ingestion of inorganic arsenic affects cellular energy production; lethal poisonings can occur. Common clinical features after acute intoxication with arsenic are dysphagia, nausea, vomiting, abdominal pain, diarrhoea, intense thirst, and muscle cramps. Clinical features of chronic poisoning are hyperkeratosis in the palms and foot soles, pigmentation and conjunctivitis. INTERPRETATION: Arsenic poisoning is a rare condition; its clinical features are uncharacteristic and the diagnosis must be confirmed by analysis of blood, urine and hair.
A case of arsenic poisoning in cattle is reported, in which six out of fifteen animals died. The source of poisoning was traced to a substance in the loft of the hay-barn, which probably consisted of the remains of a pesticide which had been there for several years. This had become liquefied as the result of a leak in the roof and had found its way into the hay. The arsenic content of the substance ranged from 17 to 37 per cent, that of the hay being up to 0.3 per cent. The concentration of arsenic in the organs, blood, faeces and urine of the animals were indicative of poisoning. The main clinical findings consisted in profuse diarrhoea, loss of appetite, muscular weakness and an ataxic gait. Dehydration set in later and the animals became deeply soporous. Symptomatic treatment was mainly directed against dehydration, hypoglycaemia and hypocalcaemia. The greater part of the animals gradually recovered. Marked hyperaemia of the abomasal mucosa and, to a less extent, hyperaemia of the small and large intestines was observed on post-mortem examination.
This article reports the results of an investigation on environmental arsenic pollution and chronic arsenic poisoning in a rural area. Exploitation of high arsenic coal caused drinking and irrigating water to be polluted by arsenic and burning of this coal caused severe environmental arsenic pollution including air, food, soil and drinking well water. 1548 villagers in 47 villages suffered from chronic arsenic poisoning who used this coal in daily life. The polluted air and food were mainly responsible, while the polluted drinking water and skin absorption played some part in poisoning. When arsenic level in coal is as high as 100mg/kg, we should consider the possibility of environmental arsenic pollution and chronic arsenic poisoning in exposed population. The high arsenic coal's distribution is very uneven. When controlling the disease, it is important to remember monitoring the quantity of arsenic coal outside the arsenic coal mining area.
Symptomatic arsenic poisoning is not often seen in occupational exposure settings. Attempted homicide and deliberate long-term poisoning have resulted in chronic toxicity. Skin pigmentation changes, palmar and plantar hyperkeratoses, gastrointestinal symptoms, anemia, and liver disease are common. Noncirrhotic portal hypertension with bleeding esophageal varices, splenomegaly, and hypersplenism may occur. A metallic taste, gastrointestinal disturbances, and Mee's lines may be seen. Bone marrow depression is common. 'Blackfoot disease' has been associated with arsenic-contaminated drinking water in Taiwan; Raynaud's phenomenon and acrocyanosis also may occur. Large numbers of persons in areas of India, Pakistan, and several other countries have been chronically poisoned from naturally occurring arsenic in ground water. Toxic delirium and encephalopathy can be present. CCA-treated wood (chromated copper arsenate) is not a health risk unless burned in fireplaces or woodstoves. Peripheral neuropathy may also occur. Workplace exposure or chronic ingestion of arsenic-contaminated water or arsenical medications is associated with development of skin, lung, and other cancers. Treatment may incklude the use of chelating agents such as dimercaprol (BAL), dimercaptosuccinic acid (DMSA), and dimercaptopanesulfonic acid (DMPS).
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The population in an arsenic polluted area of Hungary was studied in respect of dermatological signs. Melanosis was observed in 23,75 per cent and keratosis in 10,83 per cent. Vitiligo has been present in 3 per cent of the population being partly associated to melanosis and partly independent. The observations suggest that arsenic does not only induce malignant neoplasms but also enhances development of benign skin tumours.
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