Urinary beta2-microglobulin excretion among people exposed to cadmium in the general environment: an epidemiological study in cooperation between Japan and Sweden.

In a cadmium-exposed area, 138 farming women between 51 and 60 years of age and 40 reference women in the same age group were studied. Cadmium exposure was estimated from data on cadmium concentration in the individual farm's rice production, and on individual residence times. Possible cadmium exposure from the consumption of river water was also taken into account. The average urinary cadmium concentration was about twice as high in the exposed group as in the reference group. Cadmium levels in the blood among the exposed persons were also considerably elevated. Urinary β₂-microglobulin excretion was measured quantitatively as an indicator of renal tubular changes. Increased excretion was strongly related to residence time in the exposed area as well as to the use of contaminated river water in the household. Among the 35 women who had lived only at one place within the exposed area and who had not consumed river water, there was a tendency toward increased β₂-microglobulin excretion with an increased cadmium level in rice and increased residence time. There was also a correlation between cadmium levels in the blood and β₂-microglobulin excretion.     

Dose-response analysis of cadmium-induced tubular proteinuria: a study of urinary beta2-microglobulin excretion among workers in a battery factory.

The study covered 240 male and female workers exposed to cadmium oxide and nickel hydroxide dust in a Swedish battery factory. The control group comprised 87 unexposed males. Air samples from the plant showed the present exposure level to be about 50 μg Cd/m³ air. Cadmium-induced effects were studied by measuring urinary β₂-microglobulin excretion. Urinary β₂-microglobulin concentration followed a log-normal distribution in the reference group with a geometric mean of 84 μg/liter (adjusted to a specific gravity of 1.023). In the group of 185 persons continuously exposed to cadmium dust in the work environment, the prevalence of increased urinary β₂-microglobulin excretion increased with employment time. The prevalence was 19% for the workers with 6–12 years of exposure to about 50 μg Cd/m₃ as compared to 3% for those in the reference group. Smokers had about three times higher prevalence than nonsmokers.     

Dose-response relations between urinary cadmium and tubular proteinuria in cadmium-exposed workers

Cadmium in urine reflects the body burden in cadmium-exposed individuals. Urinary β2-microglobulin is frequently used as a marker of tubular proteinuria with an arbitrarily chosen value (34 μg/mmole creatinine) as the cut-off limit. Both this cut-off level and a lower limit (25 μg/mmole creatinine) were used in a study of the relationship between urinary cadmium and β₂-microglobulin in 561 cadmium-exposed battery workers. There was a clear dose-response relation between the urinary cadmium level and the prevalence of tubular proteinuria ranging from 0.8% in the lowest exposure group, excreting less than 1 nmole cadmium/mmole creatinine, to 46.4% (50.0 for the lower cut-off level) in the highest exposure group with a mean urinary cadmium of 15 nmole/mmole creatinine. The relation between urinary cadmium and tubular proteinuria was also assessed using probit analysis. There was a 10% response at a urinary cadmium of 3 nmole/mmole creatinine. The impact of age on the dose-response relation was explored in two age groups with the cut-off point at 60 years of age, showing a 10% prevalence of tubular proteinuria at urinary cadmium levels of 1.5 nmole/mmole creatinine in this older age group and 5.0 nmole/mmole creatinine in the category under 60 years of age. The study thus indicates that the present health-based limit (10 nmole/mmole creatinine) proposed by the World Health Organization (WHO) is too high and it is suggested that a new limit should be set to 3 nmole/mmole creatinine.     

Low level exposure to cadmium and early kidney damage: the OSCAR study

OBJECTIVES—To study the dose-response relation between cadmium dose and renal tubular damage in a population of workers and people environmentally or occupationally exposed to low concentrations of cadmium.
METHODS—Early kidney damage in 1021 people, occupationally or environmentally exposed to cadmium, was assessed from cadmium in urine to estimate dose, and protein HC (α₁-microglobulin) in urine to assess tubular proteinuria.
RESULTS—There was an age and sex adjusted correlation between cadmium in urine and urinary protein HC. The prevalence of tubular proteinuria ranged from 5% among unexposed people to 50% in the most exposed group. The corresponding prevalence odds ratio was 6.0 (95% confidence interval (95% CI) 1.6 to 22) for the highest exposure group, adjusted for age and sex. Multiple logistic regression analysis showed an increasing prevalence of tubular proteinuria with urinary cadmium as well as with age. After adjustment to the mean age of the study population (53 years), the results show an increased prevalence of 10% tubular proteinuria (taking into account a background prevalence of 5%) at a urinary cadmium concentration of 1.0 nmol/mmol creatinine.
CONCLUSION—Renal tubular damage due to exposure to cadmium develops at lower levels of cadmium body burden than previously anticipated.


Keywords: cadmium; environmental; tubular damage     

Urine analysis for detection of cadmium-induced renal changes, with special reference to beta2-microglobulin. A cooperative study between Japan and Sweden.

An analysis of total protein, β₂-microglobulin, glucose, and cadmium was performed on urine samples from people with Itai-itai disease and glomerular kidney disease, as well as on samples from a reference group. Blind analyses of creatinine, protein, and cadmium performed in Japanese and Swedish laboratories correlated well, but there was a tendency toward systematic differences between the laboratories' analyses of creatinine and protein. Within the range of the samples analyzed the difference was never larger than 30%. The use of three different methods of electrophoresis of urine proteins verified that the proteinuria in Itai-itai disease is tubular. On an average, urinary β₂-microglobulin excretion among Itai-itai disease patients was 100–300 times higher than among the reference group, whereas total protein excretion was only 7–17 times higher. In a group of women with different degrees of cadmium exposure urinary excretion of proteins was evaluated with qualitative determination of protein, electrophoresis, and radioimmunoassay of β₂-microglobulin. At slightly elevated β₂-microglobulin excretion the first two methods gave negative results and it was concluded that radioimmunoassay of β₂-microglobulin in urine is a sensitive indicator of cadmium-induced proteinuria.     

Statistical observations of the dose-response relationships of cadmium based on epidemiological studies in the Kakehashi River basin.

Statistical analysis was performed on the results of the epidemiological study for Itai-itai disease carried out in 1974 and 1975 by Ishikawa Prefecture Health Authorities in the cadmium-polluted Kakehashi River basin.As indices of the effects of cadmium on health, we used the urinary excretion of retinol binding protein, of suspected patients, and of tubular dysfunction. As indices of cadmium exposure, village average cadmium concentration in rice and urine were employed. Close dose-response relationships between cadmium exposure and health effects were found to exist and the curves obtained indicated sigmoid lines when the inhabitants were stratified according to their village average rice or urinary cadmium concentrations. When retinol binding protein was employed as the index of the effect on health, significant differences, compared with the control, in inhabitants ages 60 to 69 were observed at the levels of 0.50–0.59 μg/g in rice or 9.0–10.9 μg/liter in urine as village averages and 0.60–0.69 μg/g in rice eaten by inhabitants ages 50 to 59. However, in the inhabitants more than 70 yr of age significant differences in the prevalence of tubular proteinuria were observed between the lowest polluted village and the control ones. This fact indicated that the prevalence of tubular proteinuria in these inhabitants increased continuously from the nonpolluted levels of cadmium.Probit analysis of urinary cadmium concentration and renal effects was performed on 262 inhabitants selected for close examination. Probit linear regression lines were obtained when the inhabitants were arranged according to their urinary cadmium concentrations expressed as micrograms per gram creatinine.     

Reversibility of microproteinuria in cadmium workers with incipient tubular dysfunction after reduction of exposure

The study aimed at assessing the evolution of cadmium (Cd)-induced renal tubular dysfunction in Cd workers according to the severity of the microproteinuria observed at the time the exposure was substantially decreased. Male workers employed in the Cd production industry for whom formerly high exposure had markedly decreased by 1984 and for whom standardized medical data were available during two observation periods (1980–1984 and 1990–1992) were eligible for the study. A total of 32 Cd workers fulfilling this profile were divided into two groups on the basis of historical records of urinary Cd concentration (Cd-U) covering the period until 1984. The workers with Cd-U values of > 10 μg Cd/g creatinine were subdivided further on the basis of the urinary concentration of β₂-microglobulin (β₂MG-U) measured during the first observation period (1980–1984). In each group, the tubular microproteinuria as reflected β₂MG-U and the concentration of retinol-binding protein in urine as well as the internal Cd dose as reflected by the concentration of Cd in blood and urine were compared between the first and second (1990–1992) observation periods. Increased microproteinuria was often diagnosed in cases with Cd-U values of > 10 μg Cd/g creatinine. The evolution of tubular renal function has been found to depend on the extent of the body burden of Cd (as reflected by Cd-U) and the severity of the initial microproteinuria at time high Cd exposure was reduced or ceased. When reduction of Cd exposure took place while β₂MG-U did not exceed the upper reference limit of 300 μg/g creatinine, the risk of developing tubular dysfunction at a later stage was likely to be low, even in cases with historical Cd-U values occasionally > 10 but always <20 μg Cd/g creatinine. When the microproteinuria was mild (β₂MG-U > 300 and ≤1,500 μg/g creatinine) at the time exposure was reduced, and the historical Cd-U values had never exceeded 20 μg Cd/g creatinine, there was indication of a reversible tubulotoxic effect of Cd. When severe microproteinuria (β₂MG-U > 1,500 μg/g creatinine) was diagnosed in combination with historical Cd-U values exceeding 20 μg Cd/g creatinine, Cd-induced tubular dysfunction was progressive in spite of reduction or cessation of Cd exposure. Am. J. Ind. Med. 31:645–652, 1997. © 1997 Wiley-Liss, Inc.     

Environmental exposure to cadmium and renal function of aged women in three areas of Belgium

The relationship between environmental cadmium pollution and prevalence of signs of renal disturbance was investigated. Women over 60 years of age who had spent the major part of their life in a cadmium-polluted area in Belgium (Liège, n = 60) and who had never been occupationally exposed to cadmium constituted the “exposed” group. Women living in two areas less polluted by cadmium (Charleroi, n = 70, and Brussels, n = 45) served as “control” groups. The group of aged women from the Liège area has on the average a higher cadmium body burden, as reflected by an increased excretion of cadmium in urine, than the groups of aged women in the two other areas. The parameters selected for evaluating renal function (urinary excretion rates of total protein, amino acids, β₂-microglobulin, albumin) follow the same trend. Furthermore, a statistically significant correlation was found between the urinary excretion rate of cadmium and that of total protein, amino acids, β₂-microglobulin, and albumin. The results suggest that environmental pollution by cadmium as found in some industrialized areas in Europe may exacerbate the age-related decline of renal function in population groups nonoccupationally exposed to heavy metals.     

The relationship between the renal effects of cadmium and cadmium concentration in urine among the inhabitants of cadmium-polluted areas.

The relationship between urinary cadmium concentration and the effects of cadmium on the kidney was studied in inhabitants of cadmium-polluted areas. As the indexes of the effects of cadmium on the kidney, total protein, retinol-binding protein, glucose, α-amino N, and proline in urine were employed. The prevalence of proteinuria, glucosuria, proteinuria with glucosuria, tubular proteinuria, and aminoaciduria increased distinctly with increasing cadmium in urine when the inhabitants were sorted according to their urinary cadmium concentrations expressed as micrograms per gram of creatinine. Probit analysis of urinary cadmium concentration (micrograms per gram of creatinine) and prevalence of renal effects showed linear regression lines. Therefore, cadmium concentration in urine expressed as micrograms per gram of creatinine seems to be useful in estimating the renal effects of cadmium exposure in the environment.     

Dose-response analysis of cadmium in man: Body burden vs kidney dysfunction

The primary objective of this study was to develop dose-response relationships of cadmium in human beings. In vivo measurements of kidney, liver, urine, and blood cadmium, and urinary levels of β₂-microglobulin and total protein were obtained in 82 industrially exposed workers and 30 control subjects. The values of 200 μg/g creatinine for urinary β₂-microglobulin and 250 mg/g creatinine for urinary total protein were used to define the upper limit for normal kidney function. Forty-one of the cadmium workers (18 active, 23 retired) were classified as having abnormal kidney function; all control subjects had normal kidney function. Most workers with Cd above 70 ppm in the liver were judged to have some evidence of kidney abnormalities. The dose-response relationship for liver cadmium for the actively employed workers could be described by a linear logistic regression model:

$\text{ln}\text{p}\text{1?p}\text{0.118 ×}\text{liver cadmium (ppm)}\text{? 5.00}$

where p is the individual's probability of having kidney dysfunction. The loss of cadmium from the kidney following dysfunction prohibited a direct logistic analysis of the kidney cadmium data. However, when the linear relationship between kidney and liver cadmium for the subjects with normal kidney function was combined with the logistic equation for the liver, a predicted-response curve was obtained for the kidney. The logistic models predict a 50% probability of having kidney dysfunction at 38.4 mg for the kidney and 42.3 ppm for the liver, respectively.     

Toxicity and bioaccumulation of cadmium in Chlorella.

Chlorella pyrenoidosa cultures grown at pH 7 in the presence of 0, 0.25, 0.50, and 1.00 mg of Cd/liter had doubling times of 11, 21, 22, and 35 hours, respectively, whereas similarly exposed cultures grown at pH 8 had doubling times of 11, 16, 17, and 25 hours, respectively. C. pyrenoidosa is capable of concentrating cadmium, and the amount accumulated is directly proportional to the concentration of metal present initially and is dependent upon the pH of the medium. No accumulation occurs in the dark, at 4°C, or in dead cells. Cadmium accumulation is not affected by the concentration of calcium, magnesium, molybdenum, copper, zinc, or cobalt in the growth medium, whereas a level of manganese equal to 0.20 mg/liter completely blocks cadmium accumulation; iron may also play a role in regulating cadmium accumulation. Cells which had accumulated cadmium could still fix atmospheric CO₂, albeit at reduced rates; O₂ evolution was also inhibited, but to a lesser extent. The ability of C. pyrenoidosa to accumulate large concentrations of cadmium before showing adverse effects may be related to the presence of cadmium-sequestering agent(s) within the cell. The concentration of cadmium by C. pyrenoidosa could pose a hazard to the freshwater food chain.     

Significance of cadmium concentration in blood and in urine in workers exposed to cadmium.

All the workers (n = 11) occupied in a small factory producing cadmium salts were followed up during several months. Four of them were newly employed workers. At regular time intervals the workers were equipped with a personal air sampler and cadmium concentrations in blood and in urine were measured. The total airborne concentration of cadmium at the different work places was very high. The median values ranged from 110 to 2125 μg/m³. In view of the hygiene practice of the workers, ingestion of cadmium may also have played a role in the overall exposure. After the start of the exposure, cadmium concentration in blood increases linearly up to 120 days and then levels off. This suggests that when equilibrium is reached cadmium level in blood is a good indicator of the average intake during recent months. The interpretation of the cadmium levels in urine is more complex. In seven workers exposed for more than 250 days cadmium level in urine seemed to reflect mainly current exposure. Our results suggest also the existence of three phases in the evolution of the Cd levels in urine after the onset of high exposure. A first phase of very short duration (0–15 days) is observed during which cadmium level in urine increases rapidly to reach a value of about 15 μg/g creatinine. This is followed by a second phase (15–120 days) during which cadmium level in urine increases more slowly. After 120 days there is apparently a rapid increase of the cadmium level in urine (third phase). The results obtained during this study as well as our previous clinical observations on workers exposed to cadmium lead us to propose a tentative biological threshold of 10 μg Cd/g urinary creatinine. It should be stressed that this proposal applies only to adult males occupationally exposed to cadmium and not necessarily to other groups of the general population.     

Determination of carbonic anhydrase C and beta 2-microglobulin by radioimmunoassay in urine of heavy-metal-exposed subjects and patients with renal tubular acidosis.

Carbonic anhydrase C (CA-C) was measured by the radioimmunoassay in urine specimens from normal individuals, residents in mercury-polluted area, cadmium-exposed workers, lead-exposed workers, and patients with primary or secondary renal tubular acidosis. None of the urine in the normal subjects demonstrated CA-C levels above 40 μg/g creatinine. Some of the cadmium-exposed workers, residents in mercury-polluted area, and patients with renal tubular acidosis excreted large amounts of CA-C that were 10–250 times higher than the normal. Urinary β₂-microglobulin (BMG) was also determined in relation to the CA-C levels. Most of the subjects exposed to heavy metals had high levels of urine CA-C or BMG or both. Some individuals had high levels of urine CA-C although BMG levels were within normal values. These findings seem to suggest that the mechanisms of urinary excretion of these two proteins were different and the quantitative determination of urinary CA-C by radioimmunoassay appears to be also a useful and sensitive test for detecting the renal tubular disorders in environmental exposure of heavy metals or those in renal tubular acidosis.     

苏中地区农村普通人群尿镉水平及参考值研究

目的分析苏中地区农村普通人群尿镉(Cd)含量,探讨其参考值范围,为我国制定尿镉参考值范围提供依据。方法在江苏中部地区某市,按东西南北中5个方位抽取5个乡镇,共调查1 000人;在每个乡镇采集3份农田土壤和当年产大米6份,共45份环境样品,进行镉含量测定。结果土壤、大米中镉的平均含量分别为0.16、0.05mg/kg,均低于国家标准限值(0.20mg/kg)。总人群尿镉(肌酐校正值)的中位数为0.19μg/g,参考值上限为0.98μg/g。尿镉含量在性别组间差异无统计学意义。吸烟组尿镉含量明显高于非吸烟组(P0.01)。尿镉含量随着年龄和烟龄的增加而呈不同程度的增高趋势。尿镉与NAG、RBP有弱相关性,与β2-MG无相关性。结论苏中地区农村普通人群尿镉含量处于正常浓度水平,尿镉含量可能受吸烟因素的影响。     

尿β_2-微球蛋白对判定环境性镉致肾病的指标意义

根据镉污染区和对照区抽样人群的555名病例对照调查，尿β_2-微球蛋白的正常值为464μg／g肌酐，其镉致肾病早期的判定值为1000μg／g肌酐。此指标的特异度为91％，在配对病例对照中镉接触者肾小管损害的危险性为无接触者的40倍，说明尿β_2-微球蛋白对判定环境性镉致肾病早期具有良好的指标意义。     

Relations between liver cadmium, cumulative exposure, and renal function in cadmium alloy workers.

Detailed biochemical investigations of renal function were made on 75 male workers exposed to cadmium and an equal number of referents matched for age, sex, and employment status. The exposed group consisted of current and retired workers who had been employed in the manufacture of copper-cadmium alloy at a single factory in the United Kingdom for periods of up to 39 years and for whom cumulative cadmium exposure indices could be calculated. In vivo measurements of liver and kidney cadmium burden were made on exposed and referent workers using a transportable neutron activation analysis facility. Significant increases in the urinary excretion of albumin, retinol binding protein, beta 2 microglobulin, N-acetylglucosaminidase (NAG), alkaline phosphatase, gamma-glutamyl transferase and significant decreases in the renal reabsorption of calcium, urate, and phosphate were found in the exposed group compared with the referent group. Measures of glomerular filtration rate (GFR) (creatinine clearance, serum creatinine, and beta 2 microglobulin) indicated a reduction in GFR in the exposed population. Many of these tubular and glomerular function indicators were significantly correlated with both cumulative exposure index and liver cadmium burden. Using cumulative exposure index and liver cadmium as estimates of dose, a two phase linear regression model was applied to identify an inflection point signifying a threshold level above which changes in renal function occur. Many biochemical variables fitted this model; urinary total protein, retinol binding protein, albumin, and beta 2 microglobulin gave similar inflection points at cumulative exposure levels of about 1100 y.micrograms/m3 whereas changes in the tubular reabsorption of urate and phosphate occurred at higher cumulative exposure indices. Measures of GFR, although fitting the threshold model did not give well defined inflection points. Fewer variables fitted the two phase model using liver cadmium; those that did gave threshold levels in the range 20.3-55.1 ppm. When cadmium workers with cumulative exposure indices of less than 1100 y.micrograms/m3 were compared with their respective referents only serum beta 2 microglobulin and urinary NAG were significantly increased in the exposed group and these differences were not related to the degree of cadmium exposure.(ABSTRACT TRUNCATED AT 400 WORDS)     

含镉粉尘治理前后工人尿镉与血镉水平分析

目的 分析某锌粉加工厂含镉粉尘治理前后作业工人尿镉、血镉和尿β2-微球蛋白的变化.方法 对锌粉加工厂粉尘进行治理,对粉尘治理前后84名镉作业工人尿镉、血镉、β2-微球蛋白水平进行自身对照分析.结果 治理后,作业场所锌尘几何均数由3.38mg/m3降至2.22mg/m3,差异有统计学意义(P＜0.01).治理前调查对象的血镉、尿镉几何均数浓度[血镉(2.19±1.19)μg/L,尿镉(1.96±0.74)μg/gCr]明显高于治理后1年[(1.63±0.83)μg/L,(1.25±0.83)μg/g Cr]和治理后2年[(1.36±0.95)μg/L,(0.94±0.72)μg/g Cr],差异有统计学意义(P＜0.01).治理前及治理后1年、2年接触工人尿镉与血镉浓度作相关分析,r=0.466,差异有统计学意义(P＜0.01).结论 粉尘治理能降低低浓度镉作业工人的血镉、尿镉水平,对防止镉中毒效果明显.     

Urinary calcium as a biomarker of renal dysfunction in a general population exposed to cadmium

Urinary beta 2-microglobulin and N-acetyl-beta-D-glucosaminidase have been recommended as sensitive indicators of renal dysfunction induced by cadmium. However, an increase in urinary calcium in early renal damage induced by cadmium has been reported both in humans and in animal experiments. To investigate the feasibility of using urinary calcium as a biomarker of renal dysfunction induced by cadmium, two areas were selected in this study, namely, a polluted area with a 3.71 mg/kg cadmium concentration in rice and a control area with a 0.07 mg/kg cadmium concentration. The total number of participants was 499, made up of 252 in the control group and 247 from the cadmium-polluted area. Urinary cadmium, urinary calcium, and zinc concentrations were measured by atomic absorption spectrometry, and beta 2-microglobulin and N-acetyl-beta-D-glucosaminidase in urine were analyzed. The levels of urinary cadmium and urinary calcium in persons from the exposed area were significantly higher (P < 0.05) than those in the control area for both men and women, but there was no significant difference regarding urinary zinc between the two areas. A significant dose-response relationship between the prevalence of hypercalciuria and the excretion of urinary cadmium was observed, and a significantly increased prevalence of calciuria was found when excretion of urinary cadmium exceeded 2 micrograms/g creatinine. The findings were similar to those for excess urinary secretion of beta 2-microglobulin and N-acetyl-beta-D-glucosaminidase. Because cadmium can affect Ca2+ uptake by tubular cells, with decreased renal Ca2+ reabsorption, calciuria may reflect tubular cell damage caused by cadmium. It was concluded that cadmium exposure can result in increased excretion of urinary calcium in a general population and that there is a significant dose-response relationship. Urinary calcium can therefore be used as a biomarker of renal dysfunction induced by cadmium.     

Relations between liver cadmium, cumulative exposure, and renal function in cadmium alloy workers

Detailed biochemical investigations of renal function were made on 75 male workers exposed to cadmium and an equal number of referents matched for age, sex, and employment status. The exposed group consisted of current and retired workers who had been employed in the manufacture of copper-cadmium alloy at a single factory in the United Kingdom for periods of up to 39 years and for whom cumulative cadmium exposure indices could be calculated. In vivo measurements of liver and kidney cadmium burden were made on exposed and referent workers using a transportable neutron activation analysis facility. Significant increases in the urinary excretion of albumin, retinol binding protein, beta 2 microglobulin, N-acetylglucosaminidase (NAG), alkaline phosphatase, gamma-glutamyl transferase and significant decreases in the renal reabsorption of calcium, urate, and phosphate were found in the exposed group compared with the referent group. Measures of glomerular filtration rate (GFR) (creatinine clearance, serum creatinine, and beta 2 microglobulin) indicated a reduction in GFR in the exposed population. Many of these tubular and glomerular function indicators were significantly correlated with both cumulative exposure index and liver cadmium burden. Using cumulative exposure index and liver cadmium as estimates of dose, a two phase linear regression model was applied to identify an inflection point signifying a threshold level above which changes in renal function occur. Many biochemical variables fitted this model; urinary total protein, retinol binding protein, albumin, and beta 2 microglobulin gave similar inflection points at cumulative exposure levels of about 1100 y.micrograms/m3 whereas changes in the tubular reabsorption of urate and phosphate occurred at higher cumulative exposure indices. Measures of GFR, although fitting the threshold model did not give well defined inflection points. Fewer variables fitted the two phase model using liver cadmium; those that did gave threshold levels in the range 20.3-55.1 ppm. When cadmium workers with cumulative exposure indices of less than 1100 y.micrograms/m3 were compared with their respective referents only serum beta 2 microglobulin and urinary NAG were significantly increased in the exposed group and these differences were not related to the degree of cadmium exposure.(ABSTRACT TRUNCATED AT 400 WORDS)     

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 μg Pb/liter, as compared to 77 μg Pb/liter for nonsmokers. For females the corresponding values were 69 μg Pb/liter and 57 μg 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 μg Cd/liter (?0.2, detection limit) and for females 0.3 μg Cd/liter. About 90% of all nonsmokers had cadmium concentrations in blood below 0.6 μg Cd/liter, whereas about 90% of the current male and female smokers had cadmium concentrations in blood of 0.6 μg Cd/liter or more.