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Biomedical subjects

C G Elinder

Publications and source records attributed to C G Elinder.

At least 73 records · Page 4Linked to original sources
PubMed1988

Cumulative blood-cadmium and tubular proteinuria: a dose-response relationship.

Biological monitoring, i.e. using individual measures of exposure such as cadmium in blood, is supposed to reflect the real dose better than the more commonly used external measures such as air-cadmium. In order to investigate this, cumulative cadmium doses were estimated individually for 440 workers in a battery factory. Cumulative air-cadmium dose as well as two different cumulative blood-cadmium doses were computed for each study individual. Forty workers had evidence of tubular proteinuria and a clear dose-response relationship was found for each of the dose estimates. Our results suggest that cumulative blood-cadmium is a more sensitive indicator of cadmium-induced renal dysfunction than cumulative air-cadmium.

Air Pollutants, Occupational↗
PubMed1988

Uptake and urinary excretion of aluminum among welders.

The urinary excretion of aluminum was measured in 23 welders before and after an exposure-free interval of 16 to 37 days. In addition, the concentration of aluminum in the air was measured at the work site of 16 aluminum welders on the same workday as the first urine sample was taken. The concentration of aluminum in the urine depended on both the level and duration of exposure. The postshift urinary concentration of aluminum prior to an exposure-free interval was mainly related to the current air concentration, whereas the urinary concentration of aluminum determined after the exposure-free interval was related to total exposure duration (years). Among welders exposed for less than 1 year, the half-time for urinary concentration was about 9 days whereas welders exposed for more than 10 years had half-times calculated to be 6 months or longer. The results indicate that aluminum is retained and stored in at least two functional compartments of the body and is eliminated from these compartments at different rates.

Adult↗
PubMed1987

Cadmium, zinc, and copper in rabbit kidney metallothionein--relation to kidney toxicity.

Twenty-two rabbits were given repeated subcutaneous injection of cadmium chloride. The cumulative cadmium dose given ranged from 13 to 214 mumole/kg body weight. Five rabbits served as controls. The treatment resulted in cadmium concentrations in kidney cortex that ranged from 0.3 to 3.2 mmole Cd/kg and a subsequent production of metallothionein. The molar ratio of cadmium, zinc, and copper in metallothionein fractions from kidneys with different concentrations of cadmium was determined. At low concentrations of cadmium in rabbit kidneys, zinc was the dominating metal bound to metallothionein (70-90%). At high concentrations of cadmium in kidneys, cadmium was the dominating metal in metallothionein. Evidence of kidney toxicity, in the form of beta2-microglobulinuria, was seen when cadmium constituted 85% of the metal ions recovered from metallothionein fractions. The remaining 15% was zinc. This indicates that at most six of the seven metal-binding sites in mammalian metallothionein are occupied by cadmium and that the remaining site is occupied by zinc. Our data provide further support for the hypothesis that chronic cadmium nephrotoxicity develops when there is a lack of metal-binding sites available for cadmium in metallothionein.

Animals↗
PubMed1986

Distribution and concentration of cadmium in human kidney.

The left kidneys from twenty males, aged 30 to 59, were examined. On an average, the cortex, medulla, and the remainder (renal pelvis and adjacent fatty tissue) constituted 65, 27, and 8 percent of the whole kidney weight, respectively. The mean cadmium concentrations were 18.4, 6.9, and 3.2 micrograms Cd/g wet wt, respectively. The mean whole kidney cadmium concentration was 14.4 micrograms Cd/g wet wt. The kidney cortex concentration of cadmium can be approximated by multiplying the whole kidney concentration by a factor of 1.25, which is somewhat lower than the factor of 1.5 previously used. It may be necessary to recalculate previously reported estimates of critical concentrations for cadmium in kidney cortex based on neutron activation analyses in vivo of whole kidney.

Adipose Tissue↗
PubMed1986

Lung function in workers using cadmium containing solders.

The lung function of 57 male workers previously exposed to cadmium in connection with the use of cadmium containing solders was examined by spirometry (FVC, FEV1, FEV%, and MMF) and single breath nitrogen washout (CV, CV%, and phase III). A reference group (n = 31) from a nearby industry was examined at the same time. Despite the fact that the exposure in previous years had been relatively high, in the order of 0.05-0.5 mg Cd/m3, and that 24 (42%) of the workers had cadmium induced renal damage in the form of beta 2-microglobulinuria there was no evidence of pulmonary damage. There were no significant differences in lung function data from the exposed and reference group and there was no dose-response relation within the exposed group. It thus appears that signs of kidney toxicity in the form of low molecular weight proteinuria precede those that may be identified in the lung with commonly used lung function tests.

Cadmium↗
PubMed1986

Decreased blood lead levels in residents of Stockholm for the period 1980-1984.

A number of measures have been taken to decrease the spread of lead to ambient air and food. In a study of the effect of these and other preventive measures, blood samples from approximately 100 persons living in the inner city area of Stockholm were collected and analyzed for lead content on three different occasions, in 1980, 1983, and 1984. The same subjects were examined on at least two occasions and the analytical method, atomic absorption spectrophotometry, was carefully controlled by means of reference samples on each occasion. The blood lead levels decreased during the observation period. The average blood lead concentrations for all the examined persons were 0.37, 0.26, and 0.25 mumol/l for 1980, 1983, and 1984, respectively. The mean of the differences in individual blood lead levels for 1980 and 1984 was 0.12 mumol/l. This figure corresponds to an average decrease in blood lead of 34% for all the subjects examined in 1980. The decrease occurred mainly during the period 1980-1983 (mean 0.11 mumol/l) and, thereafter, was only slight for the period 1983-1984 (mean 0.01 mumol/l). Factors such as age, sex, and change of residence during the observation period did not influence the final results.

Adult↗
PubMed1985

beta 2-Microglobulinuria among workers previously exposed to cadmium: follow-up and dose-response analyses.

Sixty workers (58 males, 2 females) who had previously been exposed to cadmium in connection with the use of cadmium-containing solders were examined. Exposure times ranged from 4 to 24 years. For each worker a cumulative cadmium dose estimate was calculated. This ranged from 0.35 to 9.9 mg/m3 X year. The prevalence of slight (U-beta 2 greater than 0.034 mg/mmole creatinine) and more pronounced (U-beta 2 greater than 0.1 mg/mmole creatinine) beta 2-microglobulinuria in the whole group was 40% and 23%, respectively. The prevalence of beta 2-microglobulinuria was strongly related to the cumulative dose estimate and to urinary cadmium level. Among workers with a cumulative dose estimate below 1 mg/m3 X yr there were only a few cases with slight tubular proteinuria, whereas for workers who had a cumulative dose estimate exceeding 3 mg/m3 X yr the prevalence of slight and pronounced beta 2-microglobulinuria was 77% and 54%, respectively. There was no significant relationship between the concentration of beta 2-microglobulin in serum and urine. This indicates that the beta 2-microglobulinuria is due to tubular damage and is not secondary to an increased endogenous production. Repeated examinations of 19 workers between 1976 and 1983 revealed that in almost all cases the beta 2-microglobulinuria was irreversible.

Adult↗
PubMed1985

Cancer mortality of cadmium workers.

Several epidemiological studies of workers exposed to cadmium indicate an increased risk of lung and prostatic cancer. The increase is statistically significant in some of the studies but the SMR is greater than 100 in almost all. A cohort study of the mortality among 522 Swedish workers exposed to cadmium for at least one year in a nickel-cadmium battery plant support the earlier findings. The SMR for lung and prostatic cancer increased with increasing dose and latency but did not obtain statistical significance. A combination of all the available data from the most recent follow up of causes of death among cadmium workers in six different cohorts shows 28 cases of prostatic cancer (SMR = 162) and 195 cases of lung cancer (SMR = 121). This new analysis suggests that long term, high level exposure to cadmium is associated with an increased risk of cancer. The role of concomitant exposure to nickel needs further study.

Cadmium↗
PubMed1985

Assessment of renal function in workers previously exposed to cadmium.

Cadmium induced renal effects were examined in 60 workers (58 men, 2 women) previously exposed to cadmium. Tubular damage in the form of beta 2-microglobulinuria was found in 40%, and urinary albumin and orosomucoid increased significantly with increasing urinary cadmium and increasing relative clearance of beta 2-microglobulin. It is suggested that increased albumin excretion is secondary to the tubular damage. In no case was typical glomerular proteinuria found that could be related to cadmium. Histories of renal stones were more common among the workers with high urinary cadmium concentrations. The glomerular filtration rate was measured in 17 of the workers who had pronounced tubular dysfunction. The average glomerular filtration rate for these men was less than the age adjusted predicted value (mean = 84%). Furthermore, there was a significant (p less than 0.05) correlation (r = -0.47) between tubular reabsorption loss and a decreased glomerular filtration rate.

Adult↗
PubMed1984

A suggestion on how to use measurements of cadmium in blood as a cumulative dose estimate.

The individual cumulative cadmium dose was estimated for 44 smelter workers in a cadmium-copper alloy plant. Two different principles were used: cumulative respiratory dose and cumulative average annual blood-cadmium dose. Out of eight workers with a cumulative respiratory dose exceeding 500 mg Cd . h/m3, two of them (25%) had signs of a cadmium-induced renal dysfunction. These two men were the only workers that had a cumulative average annual blood cadmium dose exceeding 200 micrograms Cd . year/l. Our results suggest that measurements of cadmium in the blood can be used as an indicator of the cadmium exposure of each individual and that, in order to prevent renal dysfunction, the average blood-cadmium concentration should not exceed 10 micrograms Cd/l over periods of many years (decades).

Adult↗
PubMed1984

Conceptual problems in establishing the critical concentration of cadmium in human kidney cortex.

The definition of the "critical concentration" for cadmium is compared with the concepts used to establish this measure in some recent publications. The term has not been clearly defined on a population basis and this has given rise to certain confusion. Different groups of investigators therefore have arrived at different estimates of the "critical concentration" for cadmium in human kidney cortex. A new measure, the "population critical concentration" (PCC) with a clearly defined response rate, is suggested. A reanalysis of the published data indicates that the PCC-10 (10% response rate) for cadmium in kidney cortex is likely to be in the range 180-220 micrograms/g and the PCC-50 is likely to be about 25% higher.

Cadmium Poisoning↗
PubMed1984

Metallothionein in rabbit kidneys preserved for transplantation.

Thirteen rabbits were given repeated cadmium injections to achieve cadmium concentrations in kidney cortex ranging from 0.05 to 1 mmole Cd/kg wet weight. Another four animals served as controls. One kidney from each animal was frozen directly to -70 degrees C whereas the other kidney was kept for 24 hr at +4 degrees C in a preservative (Sachs' solution) to simulate conditions for preservation of human donor kidneys before transplantation. Protein binding of cadmium, zinc and copper in kidney homogenates and the concentration of metallothionein (MT) were measured in the kidney that was frozen directly and in the kidney that had been preserved. No gross differences in either the protein binding of cadmium, zinc and copper or in the MT content were seen between the directly frozen and preserved kidneys from the same animal. This indicates that MT is not rapidly broken down in rabbit kidneys which have been preserved similarly to human donor kidneys for 24 hr in a standard preservative solution prior to a transplantation.

Animals↗
PubMed1983

Lead and cadmium levels in blood samples from the general population of Sweden.

Lead and cadmium was determined in whole blood samples obtained from 473 nonoccupationally exposed adult persons in Sweden in 1980. Analyses were performed using atomic absorption spectrophotometry equipped with an electrothermal atomization unit. Accuracy of the analysis was confirmed by the analysis of quality control samples. Blood lead concentrations were shown to be significantly influenced by sex, smoking habits, and alcohol consumption. Current male smokers had a median blood lead level of 92 micrograms Pb/liter, as compared to 77 micrograms Pb/liter for nonsmokers. For females the corresponding values were 69 micrograms Pb/liter and 57 micrograms Pb/liter for current smokers and nonsmokers, respectively. Highly significant correlations were found between stated alcohol consumption and blood lead in most of the different sex and smoking categories. People living in apartments close to streets with heavy traffic in Stockholm had slightly, but not significantly, higher blood lead levels when compared to people living in areas of this city with low traffic density. Blood cadmium levels were very strongly affected by smoking habits. A significant correlation existed between the number of cigarettes consumed daily and blood cadmium concentration. The median blood cadmium level for nonsmoking males was 0.2 micrograms Cd/liter (less than or equal to 0.2, detection limit) and for females 0.3 micrograms Cd/liter. About 90% of all nonsmokers had cadmium concentrations in blood below 0.6 micrograms Cd/liter, whereas about 90% of the current male and female smokers had cadmium concentrations in blood of 0.6 micrograms Cd/liter or more.

Adult↗
PubMed1983

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↗
PubMed1983

Biological half-time of cadmium in the blood of workers after cessation of exposure.

The biological half-time of cadmium in the blood of previously exposed workers was estimated after the cessation of exposure. Five men were followed for a period of 10 to 13 years. One-compartment and two-compartment exponential elimination models were used to describe the decrease in blood cadmium levels over time. The best fit to the observed data was obtained with a two-compartment model. The half-times estimated from this model ranged from 75 to 128 d for the fast component and from 7.4 to 16.0 years for the slow component. The results confirm that there is a very long whole-body biological half-time for cadmium, and the estimated half-times are similar to those obtained with different methods.

Adult↗