Health consequences of an intravenous injection of metallic mercury.

BACKGROUND: Mercury poisoning presents a variety of clinical pictures depending on chemical structure, the route of exposure, amount absorbed and individual factors. Thus, an injection of metallic mercury can be considered relatively harmless in contrast to inhalation of mercury vapor. Injection of elemental mercury is rare, and a total of only 78 cases have been reported in the literature over the period 1923-2000. CASE REPORT: We report a suicide attempt by intravenous injection of approximately 8 g metallic mercury. By X-ray examination widespread multiple mercury shadows were visible in the whole lung and also in the subcutaneous region of the cubital fossa, the small pelvis and the right hypogastrium. Mercury excretion after treatment with 2,3-dimercaptopropane-1-sulfonate (DMPS) was significantly higher than in occupationally exposed workers. CLINICAL SYMPTOMS: The patient showed symptoms typical of acute mercury intoxication, including gastroenteritis, ulceromembranous colitis and stomatitis mercuralis. No biochemical abnormalities in hepatic or renal function occurred, despite the persistence of metallic densities in the body. The patient's lung function was normal. The patient transitionally developed erethismus and tremor mercuralis. After 1 month of DMPS treatment, the mercury levels in blood were still high and the tremor was persistent. Three years after the suicide attempt the surgical removal of residual mercury in the left fossa cubitalis was performed. The extirpation of residual mercury was successful in cutting the mercury levels to almost half. After the operation the patient showed no symptoms of chronic mercury intoxication. CONCLUSIONS: Since only 1 mg of mercury per day could be removed with DMPS treatment, it can be calculated, that it would take about 8,000 daily treatments to remove a total of 8 g solely by DMPS. Although DMPS itself does not dissolve the metallic deposits, it may considerably reduce the blood level of mercury and may therefore mitigate clinical symptoms, albeit transitorily. We therefore recommend that in cases of symptomatic metallic mercury injections, where the mercury cannot be removed by surgery, the patient's condition should be managed by repeated long-term DMPS treatment in order to control blood mercury levels.

Neurobehavioral effects of vanadium.

It was our aim to study whether chronic exposure to vanadium reduces cognitive abilities. We investigated effects on attention, visuospatial and visuomotor functioning, reaction time, short-term memory, and prefrontal functioning. Forty-nine vanadium exposed subjects with a mean vanadium level in urine (VanU) of 14.4 micro/L and 49 controls (VanU: 0.8 microg/L) with the same socioeconomic background were investigated. Neuropsychological tests were done using a modified Wisconsin Card Sorting Test (WCST), Block Design Test (BDT), Visual Recognition Test (VRT), Simple Reaction Time (SRT), Choice Reaction (CR), Digit Symbol Substitution (DSS), and Digit Span (DS). Exposure was assessed by using the vanadium level in urine and serum. While there were significant differences in BDT and DSS, no differences were found in WCST, SRT, CR, and DS. Significant correlations existed between the vanadium levels in urine and serum and the cognitive deficits. Vanadium concentrations around 14.2 microg/L in urine reduce neurobehavioral abilities, particularly visuospatial abilities and attention.

[Chronic anemia and abdominal pain as a sequela of lead poisoning]. / Chronische Anämie und abdominelle Schmerzen als Folge einer Bleiintoxikation.

HISTORY AND ADMISSION FINDINGS: 3 years ago, a 63-year-old man underwent laparotomia due to clinical signs of acute abdominal pain. The anemia was treated with erythrocyte concentrates. Several weeks before the current admission to our outpatient department, the patient was again hospitalized because of acute abdominal pain and anemia. The patient was then transferred to the University clinic for further medical tests. INVESTIGATIONS: In addition to a normocytic anemia, a secondary porphyria was found. Further medical tests demonstrated lead poisoning. DIAGNOSIS, TREATMENT AND COURSE: Initially, the cause of the lead poisoning remained unclear because the patient had reported neither an occuppational nor an environmental exposure to lead. Finally, a prescription-prepared ointment was evaluated, which the patient had applied to his feet and lips over the past 3 years. CONCLUSION: Lead poisoning can be found outside the realm of occupational exposure; therefore, the knowledge of lead poisoning is still important.

Long-term monitoring of sister chromatid exchanges and micronucleus frequencies in pharmacy personnel occupationally exposed to cytostatic drugs.

OBJECTIVES: Many antineoplastic drugs were found to have carcinogenic, mutagenic and teratogenic potential. The aim of this study was to carry out cytogenetic and internal dose monitoring of hospital pharmacy personnel regularly involved in the preparation of cytostatic agents, in order to test possible cytostatics-induced genotoxic effects due to occupational exposure under routine working conditions, and in cases of accidental contamination. METHODS: Platinum in whole blood and anthracyclines in plasma were measured to assess internal exposure to cytostatics. The level of cytogenetic damage was determined in peripheral blood lymphocytes with the micronucleus test and the sister chromatid exchange assay. Five series of monitoring were performed over a period of 2 years. RESULTS: No significant differences in the mean frequencies of sister chromatid exchanges (SCE) and micronuclei (MN) were found between occupationally exposed probands and controls (9.9 +/- 1.4 vs 10.1 +/- 1.2 SCEs/cell and 21.2 +/- 7.2 vs 23.3 +/- 7.5 MN/2000 binucleated (BN) cells, n = 16). Significant elevations of SCE or MN were detected in seven out of 12 cases of accidental contamination at the workplace, whereas no increase in platinum in blood and anthracyclines in plasma was observed in these probands. Two cases of non-reported contamination were identified by measurement of epirubicin in plasma. Smoking was found to increase the SCE significantly. No correlation between individual SCE scores and MN scores was observed. CONCLUSIONS: Our findings support a transient increase in SCE or MN after relevant exposure to cytostatic drugs in cases of accidental contamination. The lack of significant differences in SCE and MN between hospital pharmacy personnel and unexposed controls, points to high standards of safety at the corresponding workplaces.

[Pseudostenocardia due to exposure to "electrosmog"]. / Pseudostenokardie bei Belastung durch "Elektrosmog".

HISTORY AND REASON FOR ADMISSION: A 44-year-old man had anginal-like complaints. He was convinced that cardiac problems had been caused by electromagnetic fields. INVESTIGATIONS: Apart from hypertension and hyperlipidaemia there were no other significant findings. ECG, ergometry Holter-ECG were normal. EXPERIMENT: We tried to verify with a double-blind provocation test if the patient's complaints had been caused by electromagnetic fields. The patient was exposed to an electric instrument without being aware whether it was switched on or off. He was questioned about his perception of the presence of an electric current. CONCLUSION: The results of the test showed that there was no causal relation between the patient's angina-like-symptoms and electromagnetic fields. The phenomenon of electrosensitivity was probably caused by psychological mechanisms.

Acquired dyschromatopsia in combined exposure to solvents and alcohol.

HYPOTHESIS: Does occupational exposure to solvents in combination with alcohol intake give rise to acquired color vision defects? METHOD: A total of 138 individuals exposed to solvents (toluene, xylene, trichloroethylene, tetrachloroethylene) were examined using Lanthony's D-15 test and compared with 100 nonexposed controls. The extent of color vision loss was quantitatively assessed based on Bowman's color confusion index (CCI). A cumulative exposure index was calculated from the hours of exposure per day and the years of exposure. In 30 persons who were exposed to trichloroethylene and tetrachloroethylene, urinary trichloroacetic acid was assessed as a parameter of exposure. Alcohol intake was calculated as based on interviews of patients in grams of ethyl alcohol per week. RESULTS: Individuals who consumed more than 250 g alcohol/week and were simultaneously exposed to solvents showed a significantly elevated CCI (P = 0.0044). No significant correlation emerged between trichloroacetic acid excretion in the urine or the cumulative exposure index and the CCI. CONCLUSION: The combination of alcohol intake and occupational exposure to solvents discloses the risk of acquired subclinical color vision defects.