Lead poisoning in cattle--transfer of lead to milk.

The transfer of lead to milk in cattle in relation to blood lead levels and the uptake of lead in edible tissues was studied for an accidental exposure over 1 or 2 days to lead in excessive amounts from the licking of burnt storage batteries. The degree of exposure was monitored by determination of blood lead levels. Milk and blood samples were taken from eight cows, without acute symptoms of lead poisoning, during a period of 18 weeks. Two weeks after the accidental exposure, lead levels (mean +/- SD) in milk were 0.08 +/- 0.04 mg kg-1 and in blood 0.36 +/- 0.04 mg kg-1 in six of the cows. The relationship between lead concentration in blood and those in milk was found to be exponential and could be expressed by the equation: log y = 3.19x - 2.36 (r = 0.85, p less than 0.001), where y and x are the lead concentrations in milk and blood, respectively. The lead level in milk was relatively constant up to a blood lead level of 0.2-0.3 mg kg-1, and increased sharply at higher blood levels. The biological half-life of lead in blood was shown to be approximately 9 weeks. In eight acutely sick cows, which were emergency slaughtered, the range of lead levels in edible muscle tissue was 0.23-0.50 mg kg-1 wet weight. Very high concentrations were found in the kidneys, with a range of 70-330 mg kg-1, and in the livers, with a range of 10-55 mg kg-1. Four of the cows were pregnant, in the first or second month of gestation, during the episode of exposure. The lead exposure was not found to disturb the gestation or development of the fetuses.

Mercury levels in hair from people eating large quantities of Swedish freshwater fish.

Mercury concentrations in hair were related to fish-eating habits in a group of 50 people reported to have a high consumption of freshwater fish. Mercury levels in hair ranged from 0.3 to 10.8 mg/kg with a mean +/- SD of 3.2 +/- 2.3 mg/kg. The average mercury level in hair from men was significantly higher than that in hair from women (3.8 +/- 2.6 mg/kg versus 2.4 +/- 1.8 mg/kg. Seven individuals (14%) had levels above 6 mg/kg. In people with equal fish consumption, significantly higher mercury levels were found in the hair of those eating fish from lakes Mälaren and Vättern than in those eating fish from Lake Hjälmaren. It has been reported that fish from the latter lake contains approximately 0.2 mg/kg mercury, whereas fish from the other two lakes contains approximately 0.4 mg/kg. The mean mercury level in hair was higher in the group eating freshwater fish more than three times a week (greater than or equal to 500 g fish flesh/week) than in the group eating less, although the difference was of borderline significance. Within couples (n = 16) eating equal numbers of fish meals per week, the men had significantly higher levels (mean 3.7 mg/kg) than the women (mean 2.5 mg/kg). The results from the present study show that people with a high consumption of Swedish freshwater fish have elevated levels of mercury in their hair, when compared with previously reported levels in the hair of Swedish pregnant women.

Di-(2-ethylhexyl)adipate: absorption, autoradiographic distribution and elimination in mice and rats.

Whole-body autoradiography was used to study the tissue distribution of the plasticizer di-(2-ethylhexyl) adipate (DEHA), labelled in the acid [carbonyl-14C] or alcohol [2-ethylhexyl-1-14C]moiety, after iv or ig administration to male mice and rats and pregnant mice. With both DEHA preparations, during the first 24 hr after administration high levels of radioactivity were observed particularly in the body fat, liver and kidneys (after iv and ig administration) and in the intestinal contents (after ig administration) of both species. After administration of [carbonyl-14C]DEHA, radioactivity was also registered in the adrenal cortex, corpora lutea of the ovary, bone marrow, forestomach mucosa, salivary glands and Harder's gland in both species. [2-ethylhexyl-1-14C]DEHA derived radioactivity was found in the bronchi in male mice. Radioactivity was observed in the foetal liver, intestine and bone marrow during the first 24 hr after iv or ig administration of [carbonyl-14C]DEHA to pregnant mice. There was very little accumulation of [2-ethylhexyl-1-14C]DEHA in the mouse foetus but some was found in the urinary bladder, liver and intestinal contents as well as in the amniotic fluid. In an absorption/elimination study in rats of doses of 25 microCi/kg body weight of [14C]DEHA administered ig, dissolved in corn oil or dimethylsulphoxide, blood levels of radioactivity increased somewhat faster and were two or three times higher when DMSO was the vehicle indicating poor absorption of DEHA from the corn oil solution which more accurately reflects human contact with DEHA. Little radioactivity from [carbonyl-14C]DEHA was recovered in the bile, whereas [2-ethylhexyl-1-14C]DEHA was excreted in the bile in significant amounts particularly when DMSO was the vehicle. There was evidence of enterohepatic circulation of DEHA. Radioactivity was also excreted in the urine. As shown by autoradiograms obtained 4 days after the administration of [14C]DEHA there was no retention of DEHA and/or its metabolites in the tissues of mice.

Effect of dietary trans fatty acids on microsomal enzymes and membranes.

Three groups of rats were maintained on diets containing different proportions of trans fatty acids (0, 18.3 or 36.6% of the total fatty acids) for eight weeks. No differences in body weight were observed among the three groups, but the fat cell size, determined in epididymal fat, differed significantly between the controls and the rats fed diets containing trans fatty acids. The supernatant obtained by centrifuging homogenates of liver from the rats at 9000 X g (S-9 fraction) was used as an activator in a bacterial test for mutagenicity of 2-aminofluorene and aflatoxin B1 using Salmonella typhimurium strains TA 98 and TA 100, respectively. The mutagenicities of 2-aminofluorene in strain TA 98 and of aflatoxin B1 in strain TA 100 were significantly lower with the liver S-9 fraction from rats fed a diet containing 36.6% trans fatty acids than with the liver S-9 fraction from rats fed a control diet with no trans fatty acids.

Inhibition of protein pyrolysate mutagenicity by retinol (vitamin A).

The mutagenicity in the Ames Salmonella-microsome test of four protein pyrolysate products, formed during the cooking of meat, (Trp-P-1, Trp-P-2, Glu-P-1 and Glu-P-2) was found to be inhibited by the addition of vitamin A in vitro in the form of retinol. The effect is interpreted as an inhibition of the metabolic activation of the mutagens to their respective ultimate mutagenic forms since retinol has been shown to have no effect on the survival of the Salmonella cells, no effect on directly acting mutagens and no effect on the formation of NADPH in the test system. The results demonstrate the need for an increased understanding of the interaction of dietary components in evaluating mutagenic/carcinogenic risks from processed food.

Toxicity of 29 plasticizers to HeLa cells in the MIT-24 system.

The toxicity to HeLa cells of 29 plasticizers was determined in the MIT-24 test system. The 7-day IC50 for HeLa cells varied from 260 to 1.5 g/l. Phthalates, adipates, sebacates, azelates and phosphates with long carbon chain alcohols were very non-toxic to the cells, probably due to insolubility in water of the compounds, while the citrates, some phosphates and the 2 polymer plasticizers had a higher toxicity to the cells. A comparison of the HeLa cytotoxicity with the toxicity in vitro to other cells for 7 plasticizers showed a similarity of the cytotoxicity to all cell types. A comparison of the HeLa cytotoxicity for 20 plasticizers with i.p. lethal dosage in rodents demonstrated a rough similarity of values, suggesting a toxicity in rodents of the compounds by toxic interference of the agents with basal functions and structures of tissues (basal cytotoxicity). Tissue culture studies of the cytotoxic mechanisms of the plasticizers therefore could reveal modes of toxic action in vivo.

Multiple oral doses of diazepam, oxazepam and phenobarbital to dogs--behavioural effects and correlation with antipyrine half-life.

The effects of prolonged treatment with phenobarbital, diazepam, and oxazepam on behaviour and on the plasma half-life of antipyrine have been studied in the dog. In this species the biotransformation of diazepam and oxazepam is known to be very similar to man. After equipotent doses of phenobarbital (25 mg/kg) and diazepam (35 mg/kg), antipyrine half-life was found to decrease 80 and 40%, respectively, while after treatment with oxazepam (150 mg/kg) there was an increase of 20%. The behavioural effects declined in the dogs during the course of treatment with diazepam but were rather constant during treatment with oxazepam.