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Objective: The aim of the study was to evaluate the metabolic disturbances in ethanol dependent patients acutely poisoned with ethanol. This paper presents time profiles of ethanol, methanol, acetaldehyde, acetone, isopropanol and n-propanol and quantitative relationship between their concentrations and elimination rates. Methods: 171 patients acutely poisoned with ethanol (22 women, 149 men), aged 16-75 years (mean 41 [+ or -] 11.6), with a history of alcohol use ranging from one year to more then ten years, participated in the study. The clinical diagnosis was done based on a patient interview, and physical, psychological and psychiatric examination. The liver state was examined based on biochemical tests. Blood samples for toxicological study were taken just after admission to the Department of Clinical Toxicology and after 6, 18 and 24 hours. Concentration of ethanol and other compounds in a series samples were measured using headspace gas chromatography. Chromatograms were recorded and calculations were done using the Turbochrom computer programme. Results: In all patients the addiction was confirmed. The biochemical markers of liver impairment were changed-ALT activity was raised in 62.1% of patients, ALT in 53.1%, in 40.3% of patients bilirubin concentration was elevated, GGT activity was normal only in 36.8% of the studied group, albumin concentration was decreased in 32.1% of patients. At the time of admission average ethanol concentration in blood was 3.06 [+ or -] 1.15 g/L and ranged from 0.76 to 6.6 g/L. Except for a few cases other volatile compounds were found in the blood of these patients. The elimination rate constant (zero order) of ethanol ranged from 0.09 to 0.54 g/h/kg (mean 0.262 [+ or -] 0.077, n = 122). For patients with a higher ethanol concentration at the beginning, faster ethanol elimination was observed. Average methanol concentration at admission was 28.6 [+ or -] 38.7 mg/L, ranged from 0.4 to 324.4 mg/L. The concentration of methanol decreased very slowly when ethanol concentration was high. After 6 hours, while the mean ethanol concentration was around 1.5 g/L, the rate of methanol elimination increased. The calculated elimination rate between 6 and 18 hour was around 0.2 [h.sup.-1]. The [T.sub.1/2] of methanol was 3.36 [+ or -] 1.94 h (n = 79) and was independent of ethanol concentration at 6 hour. The mean concentration for other studied compounds was: acetaldehyde 5.56 [+ or -] 3.68 mg/L, acetone 10.74 [+ or -] 25.5 mg/L, isopropanol 4.56 [+ or -] 8.9 mg/L and n-propanol 1.09 [+ or -] 1.3 mg/L. The elimination rate constants for these compounds ranged from 0.137 [h.sup.-1] for n-propanol (n = 70), 0.144 [h.sup.-1] for isopropanol (n = 57) to 0.246 [h.sup.-1] for acetaldehyde (n = 73). During the whole study period (24 hours), the acetone concentration was elevated and stayed at the same level-around 10 mg/L. Conclusion: The presence of other alcohols and volatile compounds in the blood of ethanol addicted patients is common. There is not significant correlation between the ethanol concentration and other determined compounds. The elimination of methanol in addicted patients can start when the concentration of ethanol is still high., Zuba D, Piekoszewski W, Pach J, Groszek B, Parczewski A. Department of Clinical Toxicology College of Medicine Jagiellonian University, Department of Analytical Chemistry Jagiellonian University, Institute of Forensic Research, Krakow, [...]

Objective: We present 3 cases of acute, occupational poisonings in workers exposed to lead during cutting and smelting discarded automobile storage batteries in a 'backyard' plant. Neuropsychological, neurological, examinations as well as EEG, CT scan and MRI were performed to assess the CNS lead neurotoxicity. Case Series: In the last days of October 2000, 3 patients were admitted to the Department of Clinical Toxicology with signs and symptoms of acute lead poisoning. Case 1: In a 36-year-old man, exposed to lead for 5 months, clinical examination revealed a severe encephalopathy (coma, brain edema, seizures), moderate anemia and slight liver dysfunction. Lead concentration in blood was 3100 [micro]g/L, excretion with urine 17.6 mg/24h, delta aminolevulinic acid (ALA) in urine-21.0 mg/L. CT scan performed in the first day confirmed diffuse cerebral edema. Chelating therapy with BAL and Ca[Na.sub.2]DTA was started immediately together with symptomatic and supportive treatment. MRI performed two weeks later revealed cortical and subcortical atrophy of the brain. In neuropsychological examination massive disorders of memory, thought processes, attention and learning ability were stated. In EEG epileptiform waves were observed. The last neurological examination showed proximal paresis in the upper extremities. Case 2: A 34-year-old man was exposed to lead for 5 weeks. At admission generalized weakness, dizziness, headache, abdominal pain and vomiting were observed. Laboratory findings revealed anemia and increased activity of the liver enzymes. Lead blood concentration was 1200 [micro]g/L, lead urinary excretion-16.8 mg/24h, ALA in urine-52 mg/L. Neuropsychological examination showed disorders in non-verbal functions. The CT scan and MRI of the brain showed slight cortical and subcortical atrophy. EEG was normal. Neurological examination revealed tremor of upper extremities and nystagmus. Chelating therapy with BAL and Ca[Na.sub.2]DTA was started. Case 3: A 21-year-old man was exposed to lead for 1 week. He presented only abdominal pain and weakness. Blood lead concentration was 1200 [micro]g/L, lead urinary excretion-3.8 mg/24h, ALA in urine-55.1 mg/L. Laboratory results: insignificant anemia and increased activity of the liver enzymes were observed. Moderate impairment of memory was stated in neuropsychological tests. CT scan, MRI and EEG did not reveal significant changes. Neurological examination: nystagmus and dysesthesia were observed. The treatment was started with DMPS and then continuing with Ca[Na.sub.2]DTA. Peripheral nervous system evaluation will be performed and further dynamic investigations are planed. Conclusion: In all patients exposed to lead by inhalation at the workplace, the blood lead concentration was in the range that causes severe neurotoxicity. The severity of the CNS manifestations was related to the blood lead concentration and the time of exposure. Groszek B, Pach J, Hydzik P, Szczepanska L. Department of Clinical Toxicology College of Medicine, Jagiellonian University, Krakow, Poland