Magnus Piscator

Cadmium exposure from smoking cigarettes: Variations with time and country where purchased

Cadmium has been determined in 26 brands of cigarettes purchased in eight different countries throughout the world and in 16 different samples of cigarettes produced in Sweden between 1918 and 1968. In addition the amount of cadmium released from smoking one cigarette to the particulate phase collected from a smoking simulation machine, corresponding to the amount actually inhaled by a smoker, has been determined. The cadmium concentration in different brands of cigarettes ranged from 0.19 to 3.0 micrograms Cd/g dry wt, with a general tendency toward lower values in cigarettes from developing countries. No systematic change in the cadmium concentration of cigarettes with time could be revealed. The amount of cadmium inhaled from smoking one cigarette containing about 1.7 microgram Cd was estimated to be 0.14 to 0.19 microgram, corresponding to about 10% of the total cadmium content in the cigarette.

Cadmium, zinc, copper, and lead in human renal cortex.

Analysis of cadmium and zinc in the renal cortex of 67 Swedish subjects disclosed the same dependence on age as in US subjects. In the 6–50 year age group, cadmium content and the cadmium-zinc ratio were correlated to age; thereafter, there was a decrease in cadmium and zinc and in the cadmium-zinc ratios. The increase in zinc paralleled the increase in cadmium. The difference between total zinc and the amount of zinc equivalent to the amount of cadmium provides a measure of the physiological zinc content of the cortex; this fraction, 160 ppm (based on dry weight of renal cortex), did not vary with age. In the age groups over 60, cadmium content was significantly lower in women than in men.

Cadmium in blood and urine related to present and past exposure. A study of workers in an alkaline battery factory.

Blood and urinary cadmium concentrations together with cadmium in air concentrations from the breathing zone of 18 male workers in an alkaline battery factory were determined at regular intervals for 11 consecutive weeks. Nine of the workers examined were smokers and nine non-smokers. Smokers and non-smokers did not differ in age or years of employment. Cadmium in air concentrations varied, but no definite trend was observed. The concentrations of cadmium in the blood and urine were found to be stable. Exposure to airborne cadmium was identical for smokers and non-smokers but average cadmium concentrations in the blood and urine of smokers were approximately twice as high as those in non-smokers. For the whole group, urinary cadmium was significantly correlated with years of employment, but no correlation was found between blood cadmium concentrations and exposure. For non-smokers, the correlation between cadmium in blood and years of employment was statistically significant (p less than 0.001). This finding indicated that blood concentrations of cadmium reflect body burden in non-smokers at current low exposure levels.

Histopathological changes in relation to cadmium concentration in horse kidneys

Abstract Histopathological changes in kidney cortex, as observed by light microscopy, are related to cadmium concentration in kidney cortex from 69 normal Swedish horses. Cadmium concentrations in kidney ranged from 11 to 186 μg Cd/g wet wt with an average of 60 μg Cd/g, which is considerably higher than those normally found in humans. The microscopical changes were rated and related to cadmium concentrations in kidneys by dose—response curves. A relationship existed between frequency of morphological changes and cadmium concentration in the renal cortex. There was no obvious relationship between age and frequency of histopathological changes. This indicates that in horse kidneys morphological changes occur at cadmium concentrations which are lower than the tentative critical level for humans of 200 μg Cd/g. It is concluded that horses constitute a population at risk for environmental cadmium contamination.

Serum proteins and kidney function after exposure to cadmium.

Six rabbits were examined seven months after exposure to cadmium for six months., Subcutaneous injections of cadmium chloride had been given five days a weekm One rabbit had nephrosis., The other five rabbits did not differ from a group of nine control rabbits in serum proteins, glomerular filtration rate, or glucose-reabsorption capacity. Hemoglobin was lower in the cadmium group, partly owing to hemolysis., There were large amounts of cadmium in the renal cortex., The alkaline phosphatase activity of the cortex was significantly lower than in the controls. Protein excretion was normal., Electrophoretic examination of urinary proteins revealed tubular patterns in some animalsm These results indicate that after exposure has ceased, a considerable regression of the tubular damage takes place and that large amounts of cadmium in the renal cortex can be tolerated without development of gross abnormalities.

Cadmium, zinc, and copper in horse liver and in horse liver metallothionein: comparisons with kidney cortex

Cadmium, zinc, and copper were determined in liver and in kidney cortex samples obtained from 33 normal Swedish horses. Cadmium concentrations in liver ranged from 0.002 to 0.165 mmole/kg and in kidney from 0.01 to 2.15 mmole/kg. There was a significant correlation between liver and kidney concentrations of cadmium. The average kidney concentration of cadmium was about 15 times that of liver. Zinc concentrations increased with increasing cadmium concentrations in both liver and kidney. The relative increase of zinc with cadmium was more pronounced in liver than in kidney. However, the absolute increase of zinc was larger in kidney due to the much higher concentration of cadmium in kidney compared to liver. Any significant correlation between copper and cadmium, or copper and zinc, could not be revealed. Sephadex gel filtration was performed on supernatants from homogenates of kidney and liver from 19 of the horses. In both organs the major part of cadmium was recovered in protein fractions corresponding to metallothionein (MT), in which the increase of zinc also took place. The molar ratio between zinc and cadmium was higher in MT fractions obtained from liver than in MT fractions obtained from kidney.

Health hazards from inhalation of metal fumes

Hazards to the health of workers exposed to metal fumes in high-temperature industrial operations (such as in shipyards) are detailed. After oxidation, the metals appear as submicron particles which are deposited in various parts of the respiratory system. Mixed exposures and a wide variety of symptoms may occur, depending on the type of metal and the intensity and duration of exposure. The major metal may not always be the most dangerous. Two of the most hazardous metals are lead and cadmium, the former being well recognized but still a problem, the latter often unrecognized but capable of causing severe, acute or chronic disease. (RFC)

Some Views on Metabolism, Toxicity and Carcinogenicity of Cadmium

A few selected topics deemed to be of interest are briefly discussed. In the model for uptake and distribution of cadmium after ingestion the role of metallothionein-bound cadmium should be included. Renal effects are discussed with regard to the question if cadmium causes primary glomerular damage. The usefulness of horses for studies on cadmium is pointed out. The carcinogenicity of cadmium for human beings is put in relation to possible mechanisms, actual exposure and some problems in epidemiological studies.

Lead, zinc, and copper levels in intraocular brain tissue grafts, brain, and blood of lead-exposed rats

Adult female Sprague-Dawley rats were exposed to various concentrations of lead acetate for different lengths of time. Six weeks exposure to lead acetate at concentrations of 0, 0.125, 0.25, 0.5, 1, and 2% in the drinking water, gave rise to brain and blood lead levels that were highly correlated with the lead concentration in the drinking water. When animals were exposed to 1% lead acetate for different lengths of time, an apparent delay in the rate of lead transport into the brain was seen during the first day. However, if animals were exposed for longer time periods, brain lead levels increased faster than did the blood levels. Pieces of fetal cortex cerebri were grafted to the anterior eye chamber of host animals exposed to either 1% lead acetate or to sodium acetate. Six weeks after grafting, the lead concentration in the lead-exposed grafts were 31.6 mg/kg dry wt, as compared to 6.4 mg/kg dry wt in sodium acetate control grafts. However, grafts from both groups had lead levels that were approximately five times higher than in cerebral cortex “punches” from corresponding areas of the host brains. Furthermore, zinc and copper levels were also higher in the grafts as compared to punches of in situ cortex. Taken together with previous reports on animal and human lead exposure, these data indicate that oral lead intake in adult rats bearing intraocular brain grafts yields blood and brain levels which are physiologically relevant to problems of clinical lead toxicity.

CADMIUM AND HYPERTENSION

SIR,-A 38-year-old woman with puerperal depression was admitted having swallowed, 1 hour previously, 40 ml of ’Verdone’ (I.C.I. selective weedkiller containing potassium salts of 2,4-dichlorophenoxyacetic and proprionic acids). She was fully conscious when washed out and there was no evidence of inhalation. Shortly afterwards she developed repeated haematemesis necessitating a two unit blood-transfusion. Nervous-system involvement consisted of drowsiness and