Human toxicology最新文献

We reviewed available literature on the effects of inorganic arsenic on the skin to determine the potential hazards and to collate information regarding dosage and exposure to the incidence of skin cancer. Arsenic intake may result from occupational or medicinal exposure, or from drinking well water in areas with high arsenic levels in the soil. Arsenic causes a variety of benign skin lesions including hyperpigmentation and hyperkeratosis. Some hyperkeratotic lesions and squamous cell carcinomas in situ may progress to invasive carcinoma; other invasive squamous cell carcinomas will develop de novo. These cutaneous squamous cancers may metastasize; mortality is low, but has been reported. Locally invasive but non-metastasizing basal cell carcinomas may arise as well. These lesions occur in a characteristic pattern of distribution and are usually multiple. Observers reporting medicinally administered arsenic have described dose-response relationships between the amount of arsenic ingested and the frequency of various skin lesions. For arsenic found in drinking water, however, there is more controversy regarding the doses and exposure times necessary for cutaneous toxicity.

1. A retrospective epidemiological study was conducted to assess the hypothesis that sex differences exist with respect to selected lead-induced red blood cell parameters. The study utilized data previously collected in the Boston Childhood Lead Poisoning Prevention Program. 2. This study revealed no statistically significant difference between males and females (n = 1548) aged 1-6 years for blood FEP levels when blood lead levels were similar. 3. These findings are in contrast with previously published research with human adults, which has suggested that adult females display significantly greater FEP values at identical blood level values as similarly aged men.

1. The direct overall metabolic effects of calcium entry blockers on human platelets were evaluated using a sensitive microcalorimetric method. 2. The effect on platelet metabolism of four calcium entry blockers with different profiles of action was examined and compared with the relaxant response on human cerebral vessels in vitro. 3. Diltiazem (10(-8), 10(-4) M) and nifedipine (10(-10), 10(-6) M) were without effect on overall platelet metabolism. On the other hand flunarizine (10(-4) M) and verapamil (10(-4) M) significantly reduced metabolism, while lower concentrations of these agents did not change heat production. 4. The thermogenic response occurred at concentrations of the calcium entry blockers that were much higher than those observed during therapy and the concentrations which relax human cerebral arteries in vitro.

The activity of various inhibitors on several subcellular enzymes was studied. First we determined the inhibitory concentration required to reduce maximum enzymatic activity by 50%, then the effect of various hahnemannian dilutions of the same inhibitory agent was tested. Seven inhibitory agents were tested in this way on seven different enzymatic systems. No effects of these hahnemannian dilutions were shown.

In 10 adult patients acutely intoxicated with methanol, the base deficit and the total blood CO2 were highly correlated with blood formate level. No correlation was found between the same parameters and blood methanol level. Formate production is the main cause of acidosis in the early stages of methanol poisoning. The association of a latency period before treatment exceeding 10 hours and a blood formate level above 0.5 g/l (11.1 mmol/l) is predictive of severe methanol poisoning possibly leading to permanent sequelae.

For the purpose of sequestering paraquat in the plasma compartment and preventing it from accumulating in tissues the effects of intravenous administration of anti-paraquat antibodies to rats were studied. After an intravenous paraquat injection of 0.1 mg/kg, the plasma paraquat concentration from rats pretreated with anti-paraquat antibodies was significantly increased and the amount of paraquat excreted in urine was significantly decreased compared to the control group. The concentration of paraquat in bile and organs except liver, was not changed by the treatment, but the paraquat level in the liver was significantly increased. Although immunotherapy succeeded in sequestering paraquat in the plasma compartment, it could not prevent paraquat from accumulating in tissues.

Ranitidine was added in various concentrations (25-1600 ng/ml) to clonal assays of haemopoietic progenitors of normal human peripheral blood or bone marrow. Although a significant reduction in colonies forming from granulocyte-macrophage progenitors (CFU-GM) was demonstrated at the lowest drug concentration, no significant growth suppression was seen at higher concentrations. There was no evidence for growth inhibition of either erythroid progenitors (BFU-E) or pluripotent progenitors (CFU-mix) at any of the drug concentrations studied. A direct toxic effect of ranitidine on normal haemopoietic progenitors thus appears an unlikely cause of cytopenias observed during treatment.