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• W2916227984 abstract "The German Commission for the Investigation of Health Hazards of Chemical Compounds in the Work Area has re-evaluated cadmium and its inorganic compounds in 2010. The former BLW is withdrawn and Biological reference values (BAR) are established for cadmium in blood and urine. Available publications are described in detail.Studies of occupationally exposed persons show that tubular proteinuria can lead to glomerular damage and a reduced glomerular filtration rate, even after relatively low exposure levels of 4 μg cadmium/g creatinine (Järup et al. 1995). Moreover, studies of environmental exposure indicate that reduced glomerular filtration rates can occur at low cadmium concentrations similar to those at which tubular damage has been observed (Akesson et al. 2005; Suwazono et al. 2006). In a large study, the authors concluded that the probability of unusually high values for RBP, NAG, β2M, amino acids and calcium is 10% at cadmium concentrations of around 1–2 μg/g creatinine (Buchet et al. 1990). Considering the early tubular effects, the long half-life of more than 10 years and the accumulation of cadmium comparable to a permanent body burden and irreversibility, the former BLW of 7 μg cadmium/l urine is withdrawn.Using the database of the environmental survey from 1990/92 (Becker et al. 2002 b; Krause et al. 1996) and 1998 (Becker et al. 2002 a, b) the Human Biomonitoring Commission established a reference value for cadmium of 1.0 μg/l blood for adults (non-smokers, now 18–69 years old) (UBA 2003; Wilhelm et al. 2004). On this basis a BAR has been set for the non-smoking population of 1 μg cadmium/l blood* for adults. The sampling time is not fixed.On the basis of the environmental survey from 1998 (Becker et al. 2002 and 2003) a BAR of 0.8 μg cadmium/l urine* for adults was established. The sampling time is not fixed.Cadmium concentrations in the blood and urine of smokers are higher than in non-smokers. BLW (2010) Not established BAR (2010) 1 μg cadmium/l blood* 0.8 μg cadmium/l urine* Sampling time: not fixed MAK value Not established Absorption through the skin (2004) H Carcinogenicity (2004) Carcinogen Category 1 In 2004 cadmium was classified in carcinogen category 1 (MAK Value Documentation, Greim 2004). For cadmium there is comprehensive documentation available for the evaluation of a “Biologischer Leitwert” (BLW) (see Documentation 2008). In addition, there is a review of cadmium (“Stoffmonographie Cadmium”) from the Human Biomonitoring Commission of the Umweltbundesamt (Federal Environmental Agency) (UBA 1998). In 2007 a “Biologischer Leitwert” (BLW) was established for cadmium based on the nephrotoxicity of cadmium after occupational exposure to the substance (Documentation 2008). The BLW was established under the assumption that proteinuria was reversible at exposure levels below 5 µg/g creatinine or below 7 µg/l urine. The latter was the preferred unit of measurement as cadmium first of all damages the kidneys as the critical target organ, which can lead to the pathological elimination of creatinine. After the evaluation of the BLW, publications appeared which called into question the reversibility of the proteinuria (Järup and Akesson 2009) and described nephrotoxic effects in the range of environmental exposure levels (Thomas et al. 2009). This and the extensive data for the exposure to cadmium and effects in the general population make a re-evaluation of the BLW necessary and form the basis for the evaluation of a “Biologischer Arbeitsstoff-Referenzwert” (BAR). As a result of the long half-life of cadmium, it is not possible to establish a correlation between cadmium concentrations in the air and in urine. After long-term exposure, the kidneys are the main organ in which cadmium accumulates and are also the critical target organ and the organ where toxic symptoms can first be observed. The relationship between exposure to cadmium and the effects of this is best documented in the kidneys. There are also well validated biological monitoring methods and biomarkers available for kidney damage. Damage to the kidneys occurs even at relatively low levels of exposure and is therefore regarded as the basis for preventive measures. For this reason, the re-evaluation of the BLW for cadmium focusses on the nephrotoxic effects. Threshold values for cadmium-induced kidney damage after occupational exposure to the substance are described in the Documentation 2008. From the data available at the time (Bernard et al. 1990; Järup and Elinder 1994; Roels et al. 1991, 1993; van Sittert et al. 1993; Toffoletto et al. 1992), it was decided that damage to the kidney tubules can occur above a concentration of 5 µg cadmium/g creatinine (corresponding to 7.5 µg cadmium/l urine); it was still unclear whether this is reversible. Publication Area of industry n Tubular effects Glomerular effects Threshold value [µg cadmium/g creatinine] Bernard et al. 1990 NF metal smelters 58 ß2M, RBP, protein-1, NAG albumin, serum ß2M, transferrin 10 Roels et al. 1991 Zn-Cd smelters 108 decreased GFR 10 Toffoletto et al. 1992 Cd mixture factory 105 ß2M 10 Roels et al. 1993 Zn-Cd smelters 37 ß2M, RBP and other markers albumin, transferrin 4 (G) 10 (T) van Sittert et al. 1993 Zn-Cd refinery 14 ß2M, RBP, NAG albumin 7 Järup and Elinder 1994 battery factory 561 ß2M 1.5 (> 60 y) 5 (< 60 y) In addition, several studies have been published which describe functional disturbances in the kidneys in the general population even after the elimination of concentrations of 5 µg cadmium/g creatinine or less: Buchet et al. 1990 1991 investigated as part of the large Cadmibel study 1 699 persons from Belgium aged between 20 and 80 years with high or low levels of exposure to cadmium. They found a significant relationship between the concentration of cadmium in urine and the elimination of the retinol-binding protein (RBP), N-acetyl-β-D-glucosaminase (NAG), ß2-microglobulin (ß2M), amino acids and calcium. The authors calculated the probability of the occurrence of noticeably increased values of RPB, NAG and ß2M after the elimination of cadmium levels of 2.87 µg/24 hours, 2.74 µg/24 hours and 3.05 µg/24 hours to be 10%. After conversion assuming urinary elimination to be 1.7 l/24 hours (van Haarst et al. 2004; Müller et al. 2005; Parsons et al. 2007) and the median creatinine concentration in urine to be 1.2 g/l (Barr et al. 2005), the values correspond to ˜ 1–2 µg cadmium/g creatinine. For the biomarkers NAG and ß2M, there was also a relationship between the exposure to cadmium and diabetes. In the PheeCad study, Hotz et al. 1999 investigated the further development of the renal effects determined during the Cadmibel study. Around five years on average after the first study, the levels of cadmium in blood and urine were again determined in some of the participants (208 men and 385 women) and functional disturbances in the kidneys were investigated. The cadmium concentrations in urine and blood were reduced in men by 16% and 35%, respectively, compared with the levels in the first study, and in women by 14% and 28%. The authors found no evidence of functional disturbances of the glomeruli or progressive kidney damage as a result of the exposure to cadmium and came to the conclusion that the observed effects were weak, stable or even reversible and that tubular effects are not necessarily associated with subsequent impairment of glomerular function. Järup et al. 2000 2002 investigated the relationship between exposure to cadmium and tubular damage in persons with low-level occupational or environmental exposure to the substance in Sweden. Tubular proteinuria was analysed in urine by means of protein HC (α1 microglobulin: α1M). After taking the average age of 53 years into consideration, the results showed there to be an increase of 10% in the prevalence of proteinuria at cadmium concentrations of 1.0 nmol/mmol creatinine (˜ 1.0 µg cadmium/g creatinine). Akesson et al. 2005 found there to be a positive relationship between the increased elimination of NAG and the concentration of cadmium in urine in Swedish women with relatively low-level background exposure to cadmium (median 0.67 µg/g creatinine). They observed also changes in glomerular function (glomerular filtration rate, creatinine clearance) at mean cadmium concentrations of 0.8 µg/g creatinine. In addition, cadmium amplified the nephrotoxic effects of diabetes. The LOEL (lowest observed effect level) in the study was lower than in other studies (Buchet et al. 1990 1991; Järup et al. 2000 2002; Noonan et al. 2002); the authors attributed this to the homogeneity of the population investigated, the lack of healthy worker effects and the precision of the biomarker analysis. Thomas et al. 2009 determined the exposure to cadmium of 180 adults (74 men, 106 women) who lived near a zinc smelting plant in Avonmouth (southwest England).The concentrations of NAG, RBP and α1M in urine were determined as markers for early renal damage. In the ranges of 0.3–0.5 nmol cadmium/mmol creatinine (˜ 0.3–0.5 µg cadmium/g creatinine) and ≥ 0.5 nmol cadmium/mmol creatinine (˜ ≥ 0.5 µg cadmium/g creatinine) the authors found a significant dose-response relationship between the cadmium concentration in urine and the level of NAG eliminated. The exclusion of former and current smokers did not alter the trend of the dose-response relationship. Trzcinka-Ochocka et al. 2004 investigated the influence of age during the exposure to cadmium with regard to the effects on kidney function. In 136 children and young adults who grew up in the vicinity of a zinc smelting plant in Poland and 172 adults not exposed as children, ß2M, RBP and NAG were determined in urine as markers for tubular damage, and albumin in urine and β2M in serum as markers for glomerular effects. The levels of RBP, β2M and NAG in the urine were increased in persons with cadmium values above 2 µg/g creatinine. Overall, the observed effects on tubular absorption were more pronounced in those persons who were exposed to cadmium as children. Järup et al. 1995 investigated the relationship between exposure to cadmium and the glomerular filtration rate in 42 welders with at least 5 years occupational exposure to cadmium. 24 workers were found to have tubular proteinuria with β2M levels of > 34 µg/mmol creatinine (˜ > 304 µg β2M/g creatinine) and 17 workers with > 60 µg/mmol creatinine (˜ > 536 µg β2M/g creatinine). The workers were divided into three groups according to tubular function; a relative β2M clearance of less than 0.1% was regarded as normal, and 0.1–2.5% and ≥ 2.5% as slightly and greatly reduced tubular reabsorption. The corresponding mean cadmium levels in urine were 2.2 ± 1.1 µg/g creatinine, 4.0 ± 1.7 µg/g creatinine and 7.1 ± 4.4 µg/g creatinine. The glomerular filtration rate in the group with slight disturbances in tubular function was significantly decreased compared with that in the group with normal β2M clearance. In 12 workers whose glomerular filtration rate was determined three times during the study (1984, 1989 and 1993), no improvement in the glomerular filtration rate was observed even years after the occupational exposure had ended. The cadmium-induced reduction of the glomerular filtration rate thus seems to be irreversible. Suwazono et al. 2006 calculated BMDL5 values (Benchmark Dose (95% below the confidence limit, comparable to NOAEL)) for cadmium-induced effects in the kidneys in 820 Swedish women with low-level environmental exposure to the substance. They found significant relationships between the cadmium concentration in urine and the levels of NAG and protein HC (α1M) and also decreased glomerular filtration rates. The BMDL5 values for the tubular effects (NAG and α1M) were 0.5–0.8 µg cadmium/g creatinine and for the glomerular filtration rate 0.7–1.2 µg cadmium/g creatinine. The observed critical value for glomerular damage is lower and closer to the critical value for tubular damage than the values given earlier. Studies from the USA and Asia yielded similar results. Noonan et al. 2002 investigated 361 persons aged 6–74 years, 64% of whom were exposed to higher environmental concentrations of cadmium resulting from the proximity of a zinc smelting plant. As the cadmium concentrations in the urine of the two groups were, however, of a similar low level (mean cadmium concentration 0.26 µg/g creatinine), the groups were combined for further analysis. After adjustment for creatinine, age, sex, smoking status, diabetes and thyroid diseases, the correlation between NAG and alanine aminopeptidase (AAP) and cadmium in urine was statistically significant in adults. When the adults were divided into five groups, a statistically significant increase in the activity of the enzymes NAG and AAP of 53% and 43%, respectively, was determined in the group with the highest cadmium values (≥ 1.0 µg cadmium/g creatinine) compared with the enzyme activities in the group with the lowest exposure levels (< 0.25 µg cadmium/g creatinine). Jin et al. 2002 compared the levels of β2M, RBP, albumin and cadmium in the urine of persons from three regions of China with different levels of exposure. Altogether 790 persons were investigated, who lived in regions with no exposure to cadmium (mean cadmium concentration in urine 1.83 µg/g creatinine; n = 253), moderate exposure to cadmium (mean cadmium concentration 3.55 µg/g creatinine; n = 243) and high exposure to cadmium (mean cadmium concentration 11.18 µg/g creatinine; n = 294). The dose-response relationship was pronounced and statistically significant for all biomarkers. Uno et al. 2005 investigated the levels of total protein, β2M, NAG and cadmium in the urine of 410 men and 418 women aged 40–59 years. They found a relationship between the levels of cadmium and increased biomarker values for β2M and NAG, with BMDL10 values of 0.7 (♂)/1.3 (♀) µg cadmium/g creatinine and 0.6 (♂)/1.2 (♀) µg cadmium/g creatinine, respectively. The significance of tubular damage (frequently the result of low long-term exposure to cadmium) for the health of the individual has long been the subject of discussion. The irreversibility of “severe” tubular proteinuria (elimination of > 1 000 µg β2M/g creatinine) is unquestionable (Bernard 2008; Kobayashi et al. 2008), but some studies have indicated that “mild” proteinuria (elimination of 300–1 000 µg β2M/g creatinine) may be reversible (Bernard 2008; Hotz et al. 1999; Roels et al. 1997). The irreversibility of cadmium-induced proteinuria, however, is still the subject of much discussion (Järup and Akessson 2009). For cadmium there are numerous publications available in which the background exposure of the population not occupationally exposed to the substance is objectified by means of determining cadmium in blood and/or urine. As a basis for the evaluation of BAR, only those studies are included that were published in 1998 or later and in which the 95th percentiles (if possible with the 95% confidence intervals) from representative collectives of persons fit for work are given. These data are listed in Table 2. Other studies are not taken into account and will not be cited. The German Environmental Survey from 1998 (Becker et al. 2002 a, 2002 b, 2003) provides a well-founded basis for the evaluation of BAR, and is compared below with in some cases more recent data from other countries. The cadmium concentration in blood reflects the exposure to cadmium during the previous days and weeks and is thus the most suitable parameter for determining the current exposure to cadmium (UBA 1998). All the studies listed in Table 2 show that the most important influence on the cadmium concentration in the blood of adults not occupationally exposed to chemical substances is their smoking habits. Smokers always have higher systemic levels than non-smokers; this level of internal exposure is found to correlate directly with the number of cigarettes consumed, if investigated (Becker et al. 2002 a, 2002 b). In ex-smokers the concentration of cadmium in blood decreases with the duration of abstinence in a statistically significant manner. A study in South Korea showed that the differences between smokers and non-smokers become smaller at overall higher levels of environmental exposure, but remain significant (Son et al. 2009). Sex-specific differences in the concentrations of cadmium in blood in total collectives are not apparent. The German Environmental Survey from 1998 showed, however, that women who have never smoked have higher values than men who have never smoked and the difference is statistically significant. The situation is similar with age-related differences: while age plays no role if smoking habits are not taken into consideration, the cadmium concentration in the blood of persons who have never smoked increases with age in a statistically significant manner (Becker et al. 2002 a, 2002 b). In Table 2, the geographical and temporal influences on the cadmium concentrations in blood become evident. The following order is apparent from the geometric mean values given in the studies for the representative total population of the various countries: Germany 1990–1992 (Becker et al. 2002 b; Krause et al. 1996)<Germany 1998 (Becker et al. 2002 a, 2002 b)˜USA 1999–2000 (CDC 2005)<Czech Republic 2001–2003 (Batáriová et al. 2006)<South Korea 2007–2008 (Son et al. 2009). Consideration of the 95th percentile changes this order to USA<Germany<South Korea<Czech Republic. It is clear from the German Environmental Survey 1998 that the cadmium concentrations in blood are also dependent on geographical provenance: persons living in Germany who have never smoked and were born in Central, Northern or Western Europe have lower values than those born in other countries. The difference in the cadmium levels is statistically significant (Becker et al. 2002 b). The elimination of cadmium with the urine is statistically related to the internal exposure to cadmium, in particular the cadmium concentration in the kidneys (main storage organ), and can therefore be regarded as an indicator of cumulative long-term exposure (UBA 1998). Correspondingly, all the studies that take age into account show there to be a statistically significant increase in the cadmium concentrations in urine with increasing age (Batáriová et al. 2006; Becker et al. 2002 b; CDC 2005). This applies both for the total collectives and sub-collectives of smokers and persons who have never smoked (Becker et al. 2002 b, 2003). The age-dependency of the cadmium concentrations in urine is, therefore, much more pronounced than that of the values in blood. Smoking habits are also an important influence on the concentration of cadmium in urine in adults not occupationally exposed to chemical substances. Smokers have higher values than non-smokers of the same age; the differences are statistically significant but not quite so pronounced as in the blood values (Batáriová et al. 2006; Becker et al. 2002 b, 2003). The influence of smoking habits on the cadmium concentrations in urine is, however, smaller than that of age. Young smokers have lower urinary levels than older persons who have never smoked (Becker et al. 2002 b, 2003). Sex-specific differences in the concentrations of cadmium are clearer in urine than in blood. Women have higher urinary values than men, and this difference is statistically significant. This applies both for total collectives (Batáriová et al. 2006; Becker et al. 2002 b, 2003) and also for persons who have never smoked (Becker et al. 2002 b, 2003). The differences are greater after adjustment for creatinine than when the values are related to volume (Becker et al. 2002 b, 2003). Geographic influences on the cadmium concentrations in urine tend to be slight. On the basis of the creatinine-adjusted1 geometric mean values and the 95th percentiles, the countries investigated in the available studies can be ranked in the following order: Germany (Becker et al. 2002 b, 2003)<USA (CDC 2005)<Czech Republic (Batáriová et al. 2006). Also here, the differences are smaller than those in the blood values. In the German Environmental Survey, the dependency of the urinary values on geographical provenance, unlike the cadmium concentrations in blood, was not statistically significant (Becker et al. 2002 b, 2003). For two countries there are in both cases two environmental surveys available for the evaluation of the temporal course of the cadmium concentrations: these are the USA with studies from 1999–2000 and 2001–2002 (CDC 2005) and Germany with studies from 1990–1992 and 1998 (Becker et al. 2002 a, 2002 b, 2003; Krause et al. 1996). In both countries a decrease in exposure was determined, although the differences in the USA are less pronounced, as a result of the shorter interval between the studies. In the Documentation 2008, a BLW of 7 µg cadmium/l urine was established on the basis of the data available at the time. It was assumed that tubular damage to the kidneys can occur above a concentration of 5 µg cadmium/g creatinine in urine (corresponding to 7.5 µg cadmium/l urine). In the meantime, much discussion has taken place as to whether these effects occur also below these concentrations (Järup and Akesson 2009), in particular as glomerular damage has also grown in importance. The increased elimination of low molecular proteins is a widely accepted indicator of kidney damage, which should be regarded as an adverse effect independent of its progression to severe or clinically relevant kidney disease. Studies of occupationally exposed persons show that tubular proteinuria, even after relatively low exposure levels of 4 µg cadmium/g creatinine, can lead to glomerular damage and a reduced glomerular filtration rate (Järup et al. 1995). More recent studies of environmental exposure indicate moreover that reduced glomerular filtration rates can occur at low cadmium concentrations similar to those at which tubular damage has been observed (Akesson et al. 2005; Suwazono et al. 2006). In a large study, the authors concluded that the probability of unusually high values for RBP, NAG, ß2M, amino acids and calcium is 10% at cadmium concentrations of around 1–2 µg/g creatinine (Buchet et al. 1990 1991). In view of this, the former BLW of 7 µg cadmium/l urine is withdrawn. In accordance with the BAR concept, the evaluation uses the results for the non-smoking population of working age not occupationally exposed to chemical substances. The 95th percentile of this sub-collective (in the case of sufficient data if possible the upper limit of the 95% confidence interval) serves as the basis for the BAR. The Human Biomonitoring Commission evaluated a reference value for cadmium of 1.0 µg/l blood for adults (non-smokers, 25–69 years old) using the database of the environmental survey from 1990/92 (Becker et al. 2002 b; Krause et al. 1996) (UBA 1998). In the re-evaluation of this value using the database of the environmental survey from 1998 (Becker et al. 2002 a, 2002 b) noticeable changes in the cadmium levels in blood compared with in the environmental survey from 1990–1992 were not found, so that the reference value of the Human Biomonitoring Commission for cadmium of 1.0 µg/l blood for adults (non-smokers, now 18–69 years old) has been retained (UBA 2003; Wilhelm et al. 2004). 1 µg cadmium/l blood for adults This value covers also the slightly higher concentrations of cadmium in blood, compared with the concentrations found in men, of women who have never smoked. The sampling time is not fixed. As described above, the cadmium concentrations in the blood of smokers are markedly higher than in non-smokers. In the environmental survey from 1998 (Becker et al. 2002 a, 2002 b) a median cadmium concentration of 1.17 µg/l blood and a 95th percentile of 3.32 µg/l blood were found in smokers. In heavy smokers (> 20 cigarettes/day) these values are increased to 1.68 µg and 4.09 µg cadmium/l blood. In accordance with the conditions described in Section 2.2.2 that also apply for the BAR concept, the Human Biomonitoring Commission evaluated an initial reference value for cadmium of 1.5 µg/l urine for adults (non-smokers, 25–69 years old) (UBA 1998) using the database of the environmental survey from 1990/92 (Becker et al. 2002 b; Krause et al. 1996). In the re-evaluation of this value using the database of the environmental survey from 1998 (Becker et al. 2002 b, 2003) the reference value was lowered to 0.8 µg/l urine for adults (non-smokers, now 18–69 years old) as a result of the above-mentioned decrease in exposure (UBA 2003; Wilhelm et al. 2004). The data available from the two German Environmental Surveys from 1990–1992 and 1998 (Becker et al. 2002 b, 2003; Krause et al. 1996) suggest that when the first reference value was set, much greater analytical uncertainties were assumed and taken into consideration than in the re-evaluation. It cannot, therefore, be deduced from the data with certainty that the background exposure in the period of time covered was really reduced by almost half. Whether and to what extent the reduction in the levels of cadmium in urine visible between 1990–1992 and 1998 continued after 1998 cannot be answered as there are insufficient data. There is, however, no reason to doubt a dramatic reduction, as the exposure in 1998 in Germany, compared with that in the USA in 2001–2002, had already reached a very low level. 0.8 µg cadmium/l urine for adults The sampling time is not fixed. As described above, the cadmium concentrations in the urine of smokers are higher than in non-smokers. In the environmental survey from 1998 (Becker et al. 2002 b, 2003) generally a 95th percentile of 1.2 µg cadmium/l urine was found in smokers. In heavy smokers (> 20 cigarettes/day) the 95th percentile is as high as 1.39 µg cadmium/l. In order to be able to recognize and control additional occupational exposure, biological monitoring of cadmium should be carried out as part of occupational-medical health surveillance. In view of the described effects, occupational exposure to cadmium must be minimized as far as possible. The BAT value relates to normally concentrated urine, in which the creatinine concentration should be in the range of 0.3–3.0 g/l. In addition, the Commission considers selecting a more restricted target range of 0.5–2.5 g/l for urine samples to be useful, as this further improves the validity of the analyses undertaken. As a rule, in urine samples outside the limits cited above, a repetition of the analysis in normally hydrated test persons is recommended (see Documentation 2010, translated). 2 References Comments (Sub)collective Cd in blood [µg/l] Cd in urine [µg/l] Cd in urine [µg/g creatinine] n GM P95 + CI n GM P95 + CI n GM P95 + CI Becker et al. 2002 a, 2002 b, 2003; Wilhelm et al. 2004 Germany 1998 18–69 y total 4 645 0.44 2.34 4 740 0.23 0.96 4 728 0.18 0.73 ♂ 2 342 0.43 2.53 2 391 0.22 1.00 2 384 0.15 0.66 ♀ 2 303 0.44 2.10 2 349 0.23 0.91 2 345 0.21 0.81 smokers 1 584 1.06 3.32 1 611 0.29 1.20 1 606 0.21 0.91 ex-smokers 999 0.33 0.88 1 022 0.25 0.90 1 018 0.21 0.71 never smoked 2 062 0.25 0.71 2 106 0.18 0.65 2 102 0.15 0.61 non-smokers 3 061 0.78 0.90 3 128 0.76 0.80 never smoked ♂ 825 0.20 0.52 842 0.15 0.45 841 0.10 0.30 never smoked ♀ 1 237 0.29 0.78 1 264 0.20 0.77 1 261 0.20 0.71 Becker et al. 2002 b Germany 1998 25–69 y sub-collective from above studies for comparison with the study from 1990–1992 below total 3 973 0.43 2.2 4 052 0.24 0.99 4 043 0.20 0.75 smokers 1 277 1.05 3.2 1 293 0.33 1.30 1 288 0.25 0.94 ex-smokers 945 0.33 0.9 968 0.25 0.91 964 0.21 0.71 never smoked 1 750 0.26 0.7 1 791 0.19 0.70 1 790 0.17 0.64 Becker et al. 2002 b; Krause et al. 1996 Germany 1990–1992 25–69 y total 3 965 0.37 2.6 4 002 0.29 1.27 4 002 0.21 0.92 smokers 1 255 1.04 3.8 1 257 0.42 1.66 1 257 0.28 1.14 ex-smokers 1 069 0.26 1.0 1 085 0.28 1.08 1 085 0.21 0.75 never smoked 1 640 0.21 0.7 1 660 0.23 0.90 1 660 0.18 0.73 Wilhelm et al. 2005 North Rhine-Westphalia, Germany 2000 Mothers, 23–48 y (smokers and non-smokers) ♀ 213 0.35 1.77 129 0.27 1.16 130 0.26 0.94 Batáriová et al. 2006 Czech Republic 2001–2003 (blood), 2002–2003 (urine) 18–58 y total 1 188 0.6 3.0 3.3 657 0.29 1,29 1.45 ♂ 863 0.6 3.2 3.6 497 0.27 1,24 1.43 ♀ 325 0.5 2.7 3.4 160 0.33 1.48 1.46 smokers 375 1.3 4.3 5.4 204 0.30 1.78 2.36 non-smokers 813 0.4 1.1 1.3 453 0.28 1.20 1.38 dell'Omo et al. 1999 Umbria, Italy 1992–1993 18–65 y smokers 163 2.3 ♂ 96 2.4 ♀ 67 2.3 non-smokers 271 1.4 ♂ 130 1.3 ♀ 141 1.5 CDC 2005 USA 2001–2002/1999–2000 ≥ 20 y (smokers and non-smokers) 2001–2002 4 772 – 1.6 1.8 1 560 0.27 1.28 1.43 1 559 0.26 0.98 1.12 1999–2000 4 207 0.47 1.5 1.6 1 299 0.28 1.31 1.57 1 299 0.27 1.07 1.17 McKelvey et al. 2007 New York City, USA 2004 ≥ 20 y total 1 811 0.77 1.88 2.07 ♂ 762 0.76 1.95 2.32 ♀ 1 049 0.79 1.83 2.01 smokers 449 1.22 3.00 3.49 ex-smokers 310 0.71 1.32 1.58 never smoked 1 036 0.66 1.28 1.34 Son et al. 2009 South Korea 2007–2008 ≥ 18 y total 2 266 1.02 2.62 ♂ 776 0.92 2.29 ♀ 1 486 1.08 2.74 smokers 338 1.23 2.83 ex-smokers 239 0.95 2.28 never smoked 1 665 1.00 2.62" @default.
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• W2916227984 title "Addendum to Cadmium and its inorganic compounds [BAT Value Documentation, 2011]" @default.
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