CAS number: 7440-43-9 — Elemental cadmium Empirical formula: Cd — Elemental cadmium RECOMMENDED BEI®
Cadmium in urine Cadmium in blood

Sampling Time
Not critical Not critical

5 µg/g creatinine 5 µg/L


Cadmium is a soft, silvery, and ductile metal with a melting point of 321°C and a boiling point of (1,2) 765°C. Solubility varies widely among the large (1) number of cadmium compounds.

cadmium or renal tubular dysfunction from other etiologies resulted in increased renal elimination of cadmium.

Distribution and Biochemical Interactions
Cadmium in plasma and tissues was bound to metallothionein, a small protein with a molecular weight of approximately 6500, and to certain high (1–4) molecular-weight proteins. In blood, cadmium was present mainly in erythrocytes, bound to metallothionein. At low exposure, 40% to 80% of retained cadmium was stored in the liver and kidneys and (2–5) 20% in muscle. In the kidney, the highest concentration of cadmium was in the cortex. With increasing exposure, cadmium retention decreased in the kidney and increased in the liver. Metallothionein production was stimulated by cadmium and other bivalent metals, such as zinc, copper, and mercury. When an insufficient amount of metallothionein is available to bind the cadmium, toxicity may occur, possibly as a result of cadmium (2) interference with zinc-dependent enzymes.

Cadmium is absorbed via the lungs and the gastrointestinal tract. In the workplace, the lungs are the major route of absorption of aerosols, dusts, and fumes. Gastrointestinal absorption, the major route of cadmium entry from environmental (nonoccupational) sources, can contribute significantly to exposure in the workplace if hands and food become (1,2) contaminated.

Pulmonary uptake ranged from 0.1% to 50% of (3,4) inhaled cadmium. The degree of absorption depended upon particle size and solubility of the cadmium compound.

No human data on dermal absorption of cadmium were found.

Possible Nonoccupational Exposure
Cadmium is widely spread in nature. It is closely related to zinc in its chemistry and is present in (1,2) nature wherever zinc is found. Cadmium content (2) in most foodstuffs is about 0.005 to 0.1 mg/kg. Oysters and beef kidney contain 0.1 to 0.5 mg of cadmium/kg. Rice in some areas of Japan may contain about 1 mg of cadmium/kg, a result of industrial contamination. Shellfish in Japan, the United Kingdom, and New Zealand are also rich in cadmium. In areas without industrial contamination, an adult ingests 10 to 60 µg of cadmium daily, from (2) which 0.5 to 1.5 µg is absorbed. In contaminated areas of Japan, the average daily intake is as high as 400 µg. Smoking is a significant source of cadmium exposure. Each cigarette contains about 1 to 2 µg cadmium, of which 25% to 50% is retained in the (2–4) lungs.
Cadmium & Compounds BEI – 1

Gastrointestinal absorption in healthy humans ranged between 3% and 7% of ingested cadmium. It increased with nutritional deficiencies of calcium, (1,4) iron, or protein to as high as 20%.

The estimated biological half-life of cadmium is (2–8) between 10 and 30 years. The main route of elimination in humans is renal. Cadmium in feces is mainly unabsorbed, ingested cadmium; fecal excretion of absorbed cadmium is a minor route of elimi(3) nation in humans. The total daily excretion represented only about 0.01% to 0.02% of the total body (2) burden of cadmium. Renal tubular damage from
2001 © ACGIH

It may take more than a year of occupational exposure to increase the body burden to the extent that cadmium excretion rises above back(20–25) ground levels. Implementation of analytical quality assurance programs is recommended. including the United States. recommended in 1985. cadmium accumulated in the renal cortex.TLV–TWA The TLV –TWA for cadmium and its compounds 3 was reduced in 1993 to 0. cigarette smoking.5 and 1.02 to 4. Measurements of cadmium in blood are an indicator of recent exposure to cadmium. In most countries. binding to metallothionein. which was manifested by increased urinary excretion of cadmium and decreased concentration of cadmium in the kidney. and intake from a polluted (1–4) environment. medical. ® Summary Measurement of cadmium in urine is the most widely used biological measure of chronic exposure to cadmium. The second phase occurred when integrated exposure resulted in saturation of binding sites. Lauwerys described three phases of elimination. Correction for analytical background is needed due to high nonspecific absorption. The excretion reflected cadmium levels in the kidney and total body burden and was affected by past exposures and possibly by a recent high exposure. Other methods lack sensitivity or practicality. Interpretation of biological monitoring data. Creatinine measurement is required. however. During the first phase. was intended to protect against renal dysfunction in nearly all workers. The third phase occurred after the development of renal tubular dysfunction. Measurement of creatinine is required. Population Renal tubular dysfunction of any etiology may result in increased urinary excretion of cadmium.002 mg/m for its respirable fraction (both expressed as cadmium). makes a minor contribution to cadmium concentrations in urine of exposed workers. Biological Levels Without Occupational Exposure Cadmium concentration in urine is related to chronic cadmium exposure. Cadmium concentrations above 5 µg/g of creatinine may be a result of either long-term accumulation of cadmium or a very high recent exposure. Monitoring in blood should be preferred during the initial year of exposure and whenever changes in the degree of exposure are suspected. Justification The previous BEI of 10 µg/g of creatinine. Studies available at that time indicated a low ACGIH © 2001 Kinetics The estimated elimination half-life of cadmium in 2 – Cadmium & Compounds BEI . No saturation of binding sites occurred and cadmium was excreted in urine. probably bound to metallothionein. cadmium concentrations in urine were high and were no longer an indicator of the current exposure. or of both. particularly for individual workers. Sampling and Storage The sampling time is not critical because of the long elimination half-life. Measurements of cadmium in urine specimens obtained from workers with evidence of renal tubular dysfunction should not be used for evaluation of workplace exposure. Contact with colored plastic and rubber should be avoided. This (22) half-life reflects whole-body clearance. Samples stored frozen at –20°C must be mixed thoroughly (13) before an aliquot is taken for analysis. During this phase. CADMIUM IN URINE Analytical Methods The most widely used method for determination of cadmium in urine is atomic absorption spectrophotometry (AAS) with electrothermal atomization (10–18) (ETA). Renal tubular function tests should be performed in all workers with an elevated cadmium concentration in urine. human urine was between 10 and 30 years.5 µg/L. it may provide no information on integrated exposure during the first year of exposure. the average concentration of cadmium in urine was between 0. followed by an increase of cadmium concentration in urine. and environmental monitoring. Factors Affecting Interpretation of Measurements Analytical Procedure and Sampling The results of analysis depend on the method. Contamination of reagents and loss of cadmium due to volatilization during analysis are major sources of error. including cigarette smoking. Exposure Nonoccupational exposure to cadmium. (19–21) ranging from 0.01 mg/m for total dust 3 and to 0. The purpose of this action was to reduce the potential for lung cancer and preclinical signs of kidney dysfunction (β2-micro(9) globulin excretion above 290 µg/L). Risk of contamination is a (10) serious problem. Urine specimens should be collected outside the workplace in acidcleaned plastic or glass bottles. requires a program of periodic biological. However.0 µg/L. It increased with age.

(34) Smith et al. Cadmium concentration in urine correlated better with beta-2-M concentration than with NAG concentration. Increased excretion of NAG may represent either functional enzymuria from accumulation of cadmium (isoenzyme A) or lesional enzymuria from damage to (29) tubular cells (isoenzyme B). Most studies were a cross section of a small number of workers.31) dysfunction. NAG and AAP concentrations in urine were significantly higher in workers with urinary cadmium concentrations above 2 µg/L than in those with concentrations below 2 µg/L. For more information. The cadmium concentration in urine of nine workers with tubular dysfunction ranged between 4. Cadmium concentrations in urine were below 10 µg/g of creatinine (geometric mean 1. only total NAG is measured. respectively. Probit analyses indicated that 10% of NAG values were elevated in urine of workers excreting cadmium at 6. β2M excretion was increased in all three groups. Workers were divided into three groups: group 1 — urine cadmium < 3 µg/g of creatinine (n = 22). studied workers (sex unreported) exposed to relatively low levels of cadmium pigment dust. A follow-up study of 19 workers showed decreasing cadmium excretion but unchanged renal function. Recent studies of the relationships between cadmium concentrations in urine and blood and the excretion of renal tubular function markers are summarized in Table 1. The studies are reviewed below. compared men exposed to cadmium at a pigment plant (n = 19) and in radiator welding (n = 7) to controls (n = 8). β2-microglobulin (β2M). see the reviews of clinical tests for early detection of renal (30. and group 3 — urine cadmium > 5 µg/g creatinine (n = 5). NAG exists as two isoenzymes. total protein. Jakubowski 2001 © ACGIH et al.27) quently. retinol binding protein (RBP). Relationship Between Cadmium Concentration in Urine and Renal Function A number of recently published studies indicate an increased excretion of markers of renal dysfunction in workers with cadmium concentrations in urine between 5 and 10 µg/g of creatinine.8% of cadmium smelter workers with an average cadmium concen-tration of 5 µg/g of creatinine (determined using a voltametric method). the incidences were 80% (mild) and 60% (marked). found that β2M and RBP were elevated in about 10% of alkaline battery factory workers excreting cadmium in concentration between 10 and (36) 15 µg/g of creatinine.8 µg/g of creatinine. increased urinary excretion of β2M is considered to be a sign of a proximal tubular defect. examined workers five years after cessation of exposure to cadmium solder. Alkaline phosphatase (AP). pooled cadmium smelter workers into four groups according to length of employment.5 µg/g of creatinine. but the measured values did not exceed the normal levels of β2M. GGT.8 µg/g of creatinine). reported a 38% incidence of mild β2M-uria in solderers excreting more than 10 µg/g of creatinine and a 10% incidence in those who excreted less than 10 µg/g of creatinine. observed that nickel cadmium battery workers (mean cadmium concentration in urine 5. Shaikh et al. but (35) Cadmium & Compounds BEI – 3 . Cadmium concentration in urine correlated better with NAG excretion than with β2M excretion. In workers excreting cadmium above 10 µg/g of creatinine. while 10% of AAP values were elevated in urine of workers excreting cadmium at 5 µg/g of creatinine. the incidences of "mild" and "marked" β2M-uria were 33% and 11%. (39) Mason et al. Two groups with a mean cadmium excretion above 14 µg/g of creatinine excreted significantly more beta-2-M than the two groups with mean cadmium concentrations of 3. The increase was statistically significant.1 µg/g of creatinine. The gender of the workers also varied and often was not specified. and albumin was significantly higher in exposed workers (40) than in controls.8 µg/g of creatinine). examined the dose–response relationships between urinary concentrations of cadmium. (32) Elinder et al.incidence of renal dysfunction in workers with cadmium concentrations in urine below 10 µg/g of creatinine. Urine protein electrophoresis showed that workers with cadmium concentrations above 5 µg/g of creatinine excreted more low-molecular-mass proteins and less high-molecular-mass proteins than controls and workers with cadmium concentrations (38) below 5 µg/g of creatinine. and a lysosomal enzyme N-acetyl-βD-glucosaminidase (NAG). In workers excreting cadmium of 5 to 10 µg/g of creatinine. The most commonly studied markers are the low-molecularmass proteins. AP. (37) Verschoor et al. Definition of normal renal function and dysfunction varied.0 and 5. almost all below 10 µg/g) with 75 matched controls (mean cadmium concentration 0.2 µg/g of creatinine).3 µg/g of creatinine. RBP. The data do not indicate a threshold. NAG excretion was increased only in group 3.9 and 13. NAG and AAP in cadmium smelter workers. compared 75 male copper cadmium alloy workers (mean cadmium concentration 7. the clinical significance of lowmolecular-weight proteinuria was uncertain. respectively. Moreover. The urinary excretion of β2M. (33) Liu et al. Mueller et al. which will likely be followed by a progressive loss of renal parenchyma if exposure to cadmium contin(28) ues. Data were not always analyzed to determine thresholds for renal effects and long-term follow-up of affected workers was limited. Christoffersson et al. In the absence of a reduced glomerular filtration rate. found tubular dysfunction in 13. group 2 — urine cadmium between 3 and 5 µg/g of creatinine (n = 7). (41) Kawada et al. alanine aminopeptidase (AAP) and γ-glutamyltransferase (GGT) have been examined less fre(26. Usually. NAG.4 µg/g of creatinine) excreted more β2M in urine than controls (mean cadmium concentration of 0.

2 2/13 > 200 0/15 3/24 5/13 107 (11.40) 0.2 44.1) 0.2 47.6 52 56.5 11.7 34. C Average (range) or category.11 15% > 3.3 (4.0) 20. Average (number) or minimum (<).2–10.2 5. NAG con4 – Cadmium & Compounds BEI centrations rose continuously with the cadmium concentration in urine.1) 2±2 10.3–18.5 43.8 33.23 (0.000) 0.8 (IU/g) 6.21 2.TABLE 1.3 2.79 (± 0.1 37.0 (0.89) <3 3–5 5–10 >10 6. Urinary excretion of β2M also rose with increasing cadmium concenACGIH © 2001 .1) 1.4 6/13 > 139 9/15 > 139 15/24 > 139 11/13 > 139 1.1–25) 14.76) 0.73 (± 3.9–4.71 1.11 2.2 ± 5.44) 245 249 300 197 95.3 14.1 41.68) 0.8 0–5 >5 0 >5 1.4) 13.46–8.86 (± 2. or other) Elinder (1985)(32) 60 58 M >5 48 2 2–5 5–10 10–15 Liu (1985)(33) Smith (1986)(34) Jakubowski (1987)(35) Shaikh (1987)(36) 65 47 M 7.29) 2.7–136.1) < 2.8 7.0 (9.66 (0.89 (0.0 (1 ± 1) > 2.6–51) 213. reported similar results in female nickel cadmium battery workers.4 0 43. Chia et al.8 (1.0 (1.2–4.7 29.4 (± 0.1 (8 > 420) 2/21 > 220 12/32 > 220 59 (9–380) 20% > 380 82 (5–122) 86 (28–263) 586 (145–2354) 523 (170–1607) 100 (63–155) 172 (88–339) 258 (97–689) 125 (29–605) 59 (13–525) 935 (± 12) 156 (± 10) 21 ? 32 ? 85 45 M 102 45 M M 20 M 13 M 13 M 7 M Verschoor 22 M (1987)(37) 7 M 5 Christoffersson 20 M (1987)(38) 20 M Mason 75 M (1988)(39) 75 M Mueller 36 M (1989)(40) 40 M ? Kawada 53 ? (1990)(42) 9 ? 8 ? 9 F Chia 9 (1989)(43) F 65 13 15 24 13 Bernard 58 M (1990)(44) 58 M 61 25 15 15 A B 0.3 45.5) 0.8 (± 1. Studies of Relationships Between Cadmium in Urine and Blood and â2M and NAG in Urine Exposure (yrs) B Author N SexA Avg.84) M = male.3 28 42 41 41 27.9–42.18–2.7 4. Age (yrs) Urine CadmiumC (ì g/g creat.1 (± 1.0 56.87–165) 6.3 (7.00 (± 3.14–2.3 3.7 41 (Mì /L) 38 68 >1 0 0 ? 0 10.9 30. rather a continuous response of NAG excretion to increasing cadmium concentrations.4 11.7–255) <2 0>300 2–55 0>300 5–10 0>300 > 10 26% > 300 9.8 (3.8) 5.6) < 10 (20/21) > 10 (31/32) 1.2 1.3 46 7.3 35.54 (1.96 (0.6 8.8 (± 0.6) > 10 (57/102) 3.5 18. the increase becoming statistically significant when cadmium excretion exceeded 3 µg/g of creatinine.2 95% < 3.0) > 10 (66/102) 1/14 > 300 3/12 > 300 (0/12 > 900) 6/18 > 300 (2/18 > 900) 4/5 > 300 (3/5 > 900) 224.3 45 39 41 5.7 55 55 48.6 0 3.2 10.96 (± 1.4 32.3 (0.3 < 10 (18/21) > 10 (28/32) 4.9) 53.6 32. F = female.0 (10 ± 7) 0.5–13) 0. This finding was confirmed in a follow-up study of the same work(42) (43) ers.7 10.6 (nmol/h/mg Cr) 218.4 0.57 (± 5.1 108.9–20) <3 3–5 >5 5.27 0.03 (0.44 0.) Blood CadmiumC (ì g/L) Urine â2M (ì g/g creatinine) C Urine NAGC (ì /g creat.4 (2.3–2.4 0 8.09 1.87 (± 167) 0.

There were no differences from controls in spite of the fact that 24 workers (42%) (49) had β2M-uria. This study is not suitable for determination of a threshold for lung cancer because the majority of workers rapidly achieved cadmium concentrations above 10 µg/g of creatinine. compared urinary excretion of cadmium and β2M in 3178 individuals in the 50-plus age group residing in cadmium-polluted areas and 294 residents of similar age in nonpolluted areas. but not RBP. in urine were significantly increased in the exposed group compared to controls. The prevalences of increased concentrations of β2M. predictive of exacerbation of the agerelated decline in glomerular filtration rate. RBP. which may have persisted after cessation of exposure.73 m . however. Mean concentrations of β2M and NAG. were increased in some workers with cadmium excretion below 10 µg/g of creatinine. compared carbon monoxide transfer coefficient factors and chest radiographs of 101 male copper cadmium alloy workers to matched controls.) Cadmium concentration in urine has been measured periodically since 1948. The BEI is intended to prevent the potential for renal dysfunction in workers.23 µg/g) and 58 matched control workers (mean cadmium concentration 0.66 µg/g). but the correlation was insignificant. Cadmium & Compounds BEI – 5 ® Relationship Between Cadmium Excretion and Lung Function Edling et al. Therefore. Significance of Low-Molecular-Weight Proteinuria Roels et al. Recommendation ACGIH recommends monitoring of cadmium in urine as a specific test for chronic exposure to cadmium. Huang (47) and Liu followed up 17 workers removed from cadmium exposure for 0. it was above 20 µg/L.5-year follow-up period. the data suggested that the changes might progress and become clinically significant when combined with effects associated with aging. only two samples were taken per person (range 0 to 79). Relationship Between Cadmium Excretion and Lung Cancer Thun et al. (45) Ishizaki et al. median cadmium concentration was above 10 µg/L. The recommended BEI is equivalent in International System of Units (SI) to 5 µmol/mol of creatinine. but on an average. (44) Bernard et al. which is five times that accounted for by aging). The difference was. Although these changes were subclinical and often within the range of normal values. The measurements indicate a high exposure: in 90% of the measurements.000) were higher in cadmium workers than in controls. there was evidence that they may have been followed by deterioration of renal function. it is prudent to maintain cadmium concentration in urine below 5 µg/g of creatinine. updated the cohort study on mortality among U. (This study was one of the bases for lowering the TLV–TWA for cadmium. The BEI of 5 µg/g of creatinine is supported by studies indicating altered excretion of markers of renal dysfunction at cadmium excretion above 5 µg/g of creatinine. they reported evidence 2001 © ACGIH (48) . Proteinuria persisted.7 years. There is no evidence for adjusting the cadmium (51. Probit regression lines determined that the cadmium threshold for increasing β2M-uria is between 3. NAG.1 µg/g of creatinine for women. studied 58 cadmium smelter workers (mean cadmium concentrations 6. The authors concluded that early. the mean β2M concentration more than doubled. Urinary albumin and transferrin.8 and 4. and protein 1 (an α-microglobulin of molecular weight 20. and five workers with normal β2M values at time of removal developed abnormal values. (46) Current Database Available The amount of information on the relationship between cadmium concentration in urine and renal function is adequate to support the BEI. conducted a follow-up study of 23 workers removed from cadmium exposure for at least 5 years because of increased excretion of lowmolecular-mass proteins. cadmium production workers with an increased risk for lung cancer.S. Although this effect of cadmium on the kidney may not be pathological. of emphysema in workers after five or more years of exposure to cadmium. The authors concluded that subtle defects in glomerular function in some cadmium-exposed subjects may precede the onset of tubular impairment. (50) Summary Most studies indicated an increase of either NAG or β2M excretion when the cadmium excretion exceeded 5 µg/g of creatinine. Sampling time is not critical. Cadmium concentration of 5 µg/g of creatinine is recommended as a BEI. subclinical renal changes should be regarded as an adverse effect.52) concentration for urine density. markers of glomerular dysfunction.5 to 3. When the data were grouped according to cadmium excretion. used spirometry to assess the lung function of 57 male workers previously exposed to cadmium solder. but precautions must be taken to avoid contamination. the prevalences of increased values for the four tubular markers were increased only if cadmium excretion exceeded 10 µg/g of creatinine.8 and 4. statistically insignificant. and in 81%. as did an increase in serum creatinine and progressive decrease in glomerular filtration rate (average 31 2 ml/min/1.trations in urine. During the 2.0 µg/g of creatinine for men and between 3. Davison et al.

nonsmokers have a median cadmium concentration in blood between 0. total protein.9.4 and 4. probably metallothionein and albumin. Chia et al. and then rose sharply.5 µg/L. Sampling and Storage Samples should be collected in acid-cleaned heparinized glass or plastic tubes free from heavy (10) metal contamination. Contamination of reagents and loss of cadmium due to volatilization during analysis are major sources of error. (39) Mason et al. AP. these studies were not conclusive. ACGIH © 2001 Kinetics At least 70% to 80% of the cadmium in blood is present in erythrocytes. cigarette smoking. and smokers have median concentration between 1.4 to 16 years (11–16 years without renal dysfunction). and 7. Relationship Between Cadmium Concentration in Blood and Renal Function Several studies indicated higher incidence of renal dysfunction in workers with cumulative cadmium concentration in blood below 10 µg/L than previously estimated (Table 1). Justification The previously recommended BEI of 10 µg/L for cadmium in blood was based on a number of studies suggesting a low incidence of renal dysfunction in workers whose cadmium concentration in blood (25–27. A similar (24) observation was made by Kjellstrom in 17 new employees exposed at a cadmium concentration of 3 50 µg/m . studied female workers exposed to cadmium. GGT. In one study of subacute intoxication in jewelry workers. Biological Levels Without Occupational Exposure Cadmium concentrations in blood increase with age. β2M did not start to rise until cadmium concentrations in blood exceeded 10 µg/L. Regular monitoring of cadmium in blood was suggested for (53–57) the estimation of cumulative dose of cadmium. Exposure The contribution of tobacco smoking to cadmium concentrations in blood may be significant. The influence of sex and age on cadmium concentration in blood appears to be overshadowed by the impact of smoking. from which approximately (2–4) 60% is bound to metallothionein. (53) Jarup et al. observed a linear increase of cadmium concentration up to 120 days of exposure. However. Dose–response relation(35) ship reported by Jakubowski et al. particularly at low occupational exposure when the cadmium concentration in blood is below 5 µg/L. and albumin) in workers with a mean cadmium concentration in blood equal to 8. in countries where dietary intake is between 10 and 20 µg/day. Factors Affecting Interpretation of Measurements Analytical Procedure and Sampling The results of analysis depend on the analytical method. Population No population characteristics influencing cadmium concentrations in blood have been identified. Although no certified reference standards are available. partly to the recent exposure. leveled off at cadmium concentrations between 3 and 10 µg/L. In the blood of four new employees exposed to 3 (25) 110 at 2125 µg Cd/m .58. indicates an increase of low-molecular-mass protein excretion in about 10% of workers having cadmium concentration in blood equal to 10 µg/L for 30 to 40 years. Samples should be analyzed on the same day as collected or kept refrigerated if analyzed on the next day. freeze-dried blood reference samples are (10. Cadmium in plasma is bound to at least two different proteins.55.CADMIUM IN BLOOD Analytical Methods The most widely used method for determination of cadmium in blood is atomic absorption spectrophotometry (AAS) with an electrothermal atomization (4. Elinder reviewed a number of studies measuring cadmium concentration in blood of nonoccupationally exposed persons and concluded that. and intake from environ(19) (19) mental pollution. observed changes in markers of renal function (urinary β2M. There is a dose-related increase in cadmium concentration in blood and number of cigarettes smoked per day. followed by a plateau. Procedures for preparation of quality control samples of bovine blood spiked with cadmium nitrate and reference analysis by isotope (17) dilution mass spectrometry has been described. Lauwerys et al. Two studies have examined the rise in cadmium concentration in blood during occupational exposure.16) commercially available in Germany.8 µg/L (43) (mostly below 10 µg/L). an estimated threshold concentration of (57) cadmium in blood was between 5 and 10 µg/L.10) detector (ETA).0 µg/L.59) consistently remained below 10 µg/L. Mean urinary NAG excretion started to rise when cadmium in blood reached a concentration of 1 µg/L.4 and 1. Analytical quality assurance programs should be implemented. Cadmium concentration in blood is partly related to body burden. studied five workers for 15 years after cessation of cadmium exposure. The elimination was biphasic with half-lives of 75 to 130 days 6 – Cadmium & Compounds BEI . NAG. RBP.

Control measures should be applied if a measurement exceeds 5 µg/g of creatinine or 5 µg/L of blood.8. there is evidence that they persist and may be followed by deterioration of renal function. Cumulative cadmium concentrations in blood were calculated from an average of seven measurements per worker taken over 15 years. the U. The recommended BEI is equivalent in SI units to 0. (56) Jarup et al. examined 440 workers (326 men and 114 women) exposed to cadmium oxide dust in battery manufacturing. and 10 µg/L. reported the absence of tubular effects and the presence of subtle glomerular dysfunction (increased albumin excretion measured by a very sensitive assay) in workers with a cadmium concentration below 10 µg/L. The BEI is intended to prevent the potential for renal dysfunction in workers. Occupational Safety and Health Administration proposed annual monitoring of cadmium in blood and urine and of protein in urine of all workers (61) exposed to cadmium. A (69) transportable unit has been developed. The BEI Committee does not recommend monitoring for cadmium in hair because the concentration correlates poorly with body burden. (60) Current Database Available The information on blood cadmium is scant compared with the information available on urinary cadmium. It is. adequate to recommend a BEI of 5 µg/L. A dose–response relationship between the prevalence of tubular proteinuria and cumulative cadmium concentration in blood predicted that the 5%. (44) reflect chronic exposure. The measure of tubular proteinuria was β2M excretion exceeding a concentration of 35 µg/mmol (311 µg/g) of creatinine. Although the observed changes were subclinical. Precautions must be taken to avoid contamination. 10%. which primarily Historical BEIs Date 1986 1987 1988 1991 1993 Action Proposed Proposed Adopted Proposed Adopted Determinant Cadmium in urine Cadmium in blood Cadmium in urine Cadmium in blood Cadmium in urine Cadmium in blood Cadmium in urine Cadmium in blood Cadmium in urine Cadmium in blood Sampling Time Not critical Not critical Not critical Not critical Not critical Not critical Not critical Not critical Not critical Not critical BEI 10 µg/g creatinine 10 µg/L 10 µg/g creatinine 10 µg/L 10 µg/g creatinine 10 µg/L 5 µg/g creatinine 5 µg/L 5 µg/g creatinine 5 µg/L Notation † † B B B B B B B B 2001 © ACGIH Cadmium & Compounds BEI – 7 . Cadmium concentration in blood primarily reflects recent exposure and is complementary to the cadmium measurements in urine. Reviews of a metallothionein test revealed that the data were inadequate to (62–66) recommend a BEI.68) in vivo by neutron activation analysis (NAA). Therefore. Cadmium concentration of 5 µg/L is recommended as a BEI for the monitoring of cadmium exposure. it is prudent to maintain an average cadmium concentration in blood below 5 µg/L. The sampling time is discretionary. nevertheless. The BEI of 5 µg/L is supported by recent studies indicating altered excretion of markers of renal dysfunction at concentrations below 10 µg/L. even after the cessation of the exposure.Bernard et al. respectively. The German Commission for the Investigation of Health Hazards of Chemical Compounds in the Work Area recommends the following Biological Tolerance (54) Values (BATs): 15 µg Cd/L blood and 15 µg Cd/L urine. Due to limitations in the availability of equipment.6. and 16% prevalence of tubular proteinuria appeared at concentrations of 2. Other Reference Values The World Health Organization in 1980 recommended that cadmium concentrations should not be allowed to exceed 10 µg/g of creatinine or 10 µg/L of blood.S. In 1990. Recommendation ACGIH recommends monitoring of cadmium in blood as a specific indicator of the recent exposure to cadmium. 5. These BAT values are strictly for nephrotoxic effects. When cadmium concentrations exceeded 5 µg/g of creatinine.044 µmol/L. the BEI Committee does not recommend monitoring cadmium in liver or kidney. This thorough study indicates that the prevalence of tubular proteinuria may become significant even if cadmium concentrations in blood remain for many years at 5 µg/L. Other Indicators of Exposure Metallothionein in urine appears to correlate with cadmium concentration in urine. offering the advantage of a specific assay without interference by contamination. exposure and work practices should be reassessed and appropriate measures taken to reduce the exposure. Cadmium in liver and kidney can be determined (67.

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