Food Additives & Contaminants: Part A

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Cadmium body burden of the Swiss population Judith Jenny-Burri, Max Haldimann, Beat J. Brüschweiler, Murielle Bochud, Michel Burnier, Fred Paccaud & Vincent Dudler To cite this article: Judith Jenny-Burri, Max Haldimann, Beat J. Brüschweiler, Murielle Bochud, Michel Burnier, Fred Paccaud & Vincent Dudler (2015) Cadmium body burden of the Swiss population, Food Additives & Contaminants: Part A, 32:8, 1265-1272, DOI: 10.1080/19440049.2015.1051137 To link to this article: http://dx.doi.org/10.1080/19440049.2015.1051137

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Date: 25 October 2015, At: 23:57

Food Additives & Contaminants: Part A, 2015 Vol. 32, No. 8, 1265–1272, http://dx.doi.org/10.1080/19440049.2015.1051137

Cadmium body burden of the Swiss population Judith Jenny-Burria*, Max Haldimanna, Beat J. Brüschweilera, Murielle Bochudb, Michel Burnierc, Fred Paccaudb and Vincent Dudlera a Federal Food Safety and Veterinary Office, Risk Assessment Division, Bern, Switzerland; bInstitute of Social and Preventive Medicine, Lausanne University Hospital, Lausanne, Switzerland; cService of Nephrology and Hypertension, Lausanne University Hospital, Lausanne, Switzerland

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(Received 27 March 2015; accepted 10 May 2015) Urinary cadmium (Cd) excretion was measured within a representative Swiss collective. With a median of 0.23 µg/24 h (n = 1409) and the 95th percentile at 0.81 µg/24 h, no increased health risk for the general non-exposed population was identified. The independent variables Age, BMI and Smoking habit had a significant effect on urinary Cd excretion. No association was found with the region of residence and sex. A subsample comparison between 24-h and spot urines of the same subjects (n = 90) did not reveal an evident concentration difference for both creatinine-adjusted sample types. Dependencies on age and gender were observed for creatinine, which consequently impacts on the creatinine normalisation of urine samples. Keywords: urinary cadmium; excretion; Switzerland; 24-h urine; creatinine

Introduction The metallic element cadmium (Cd) is a contaminant released either by natural processes (volcanic emissions, weathering of rocks) or by anthropogenic activities (industry and agriculture) into the environment where it can enter the food chain. For the general non-smoking population, approximately 90% of Cd exposure comes from food, with cereal products, potatoes and vegetables as major sources. Inhalation and drinking water account for less than 10% (EFSA 2009, 2012). Other sources such as smoking or occupational exposure may prevail over food if present. The body burden of smokers is on average twice as high compared with non-smokers (EFSA 2009). Absorption of Cd is very efficient from the lung (up to 60%) compared with a maximum of 10% from the gastrointestinal tract. Nevertheless, long-term exposure may lead to systemic accumulation even at low absorption levels (EFSA 2009; Prozialeck & Edwards 2010). For the monitoring of exposure, whole blood or urine can be used as biomarkers. Blood-Cd indicates both recent and cumulative exposures, whereas urine-Cd reflects the body burden as well as the concentration in the kidney (Lauwerys et al. 1994; CDC 2009; EFSA 2009; Järup & Åkesson 2009). Absorbed Cd is eliminated very slowly and accumulates with age. The biological half-life is estimated to be 10–30 years (Järup et al. 1998; EFSA 2009). Once absorbed, this metal mimics other divalent essential elements such as calcium, zinc or iron within the human

body and affects their respective homeostasis (EFSA 2009). The kidney is particularly vulnerable to Cd toxicity under chronic low-level exposure (Lauwerys et al. 1994; EFSA 2009). Critical urinary Cd concentration associated with the onset of renal injury was estimated above 2 µg g–1 creatinine (µg gC–1) (Prozialeck & Edwards 2010); a reference point for risk evaluation was selected at 1 µg gC–1 (EFSA 2009). Besides the kidney, the liver, bone, lung and several other organs can be affected by Cd (Prozialeck & Edwards 2010). According to EFSA (2009, p. 7), ‘cadmium exposure has been associated with nephrotoxicity, osteoporosis, neurotoxicity, carcinogenicity and genotoxicity, teratogenicity, and endocrine and reproductive effects’. The risk related to the dietary exposure of Cd was reevaluated simultaneously by JECFA and EFSA. Both organisations discarded the former accepted PTWI of 7 µg kg–1 body weight (BW) but proposed a different health-based guidance value. EFSA established a TWI of 2.5 µg kg–1 BW (EFSA 2009, 2011b); while JECFA recommended a provisional tolerable monthly intake (PTMI) of 25 µg kg–1 BW corresponding to 5.8 µg kg–1 BW week–1 (JECFA 2011). Both assessments rely on the same epidemiological dataset; the disagreement on tolerable weekly intake is due to methodological differences (EFSA 2011a, 2011b). The aim of this study was to assess 24-h urinary Cd excretion in a representative non-exposed Swiss adult collective, its relationship with age, smoking status and

*Corresponding author. Email: [email protected] © 2015 The Author(s). Published by Taylor & Francis. This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License (http://creativecommons.org/licenses/ by-nc-nd/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way.

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body mass index (BMI), as well as the presence of potential regional differences. We also compared urinary Cd concentration in spot versus 24-h urine.

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Materials and methods Sampling As part of a nationwide survey on salt intake, which was approved by the regional ethical committees, a 24-h urine sample was collected in 2010–12 in 11 centres from nine Swiss cantons – Basle, Fribourg, Geneva, Lucerne, St. Gallen, Ticino (three centres), Valais, Vaud and Zurich – covering the three main linguistic regions of Switzerland (German, French and Italian). All participants gave a written informed consent before sampling. Inclusion criteria for the 1448 participants comprised: ≥ 15 years of age, permanent residents not living in institutions, and a sufficient knowledge of French, German or Italian to understand the study objectives. Each study centre aimed to recruit participants in eight predefined age and sex strata (15–29, 30–44, 45–59 and ≥ 60 years of age in men and women). Young participants were particularly difficult to recruit. Additional volunteers were recruited in universities and professional schools. A detailed description on recruitment and sampling strategy is given in the main report of the salt intake survey (Chappuis et al. 2011). At the end of the sampling period, 91 spot urine samples were additionally collected together with 24-h urine from participants in Fribourg. A frozen aliquot of 40 ml of each 24-h urine sample as well as the spot urines were brought to the laboratory of the Federal Food Safety and Veterinary Office and stored at −20°C until analysis. Plastic bottles used for urine collection and laboratory vials were beforehand checked for Cd contamination. Urinary albumin, calcium and creatinine as well as serum creatinine were analysed by the Laboratoire de Chimie Clinique, Centre Hospitalier Universitaire Vaudois (CHUV) (Lausanne, Switzerland). The types of assay used for the measurement of these parameters were immunoturbimetry (albumin), O-cresolphtalein (calcium) and Jaffé kinetic compensated method (creatinine) from Roche Diagnostics (Rotkreuz, Switzerland) (Chappuis et al. 2011).

Reagents and standards Spike solution was prepared at a concentration of 0.61 µg l–1 in 1% HNO3 Suprapure (Merck, Darmstadt, Germany) from an enriched isotopic reference material (11.28 mg kg–1, IRMM-621, Geel, Belgium) with certified isotope abundances (110Cd 0.43%, 111Cd 95.74%, 112Cd 2.08%, 113Cd 0.56%, 114Cd 1.04% and 116Cd 0.16%). A Cd standard stock solution (1000 mg l–1, Merck) in 1%

HNO3 Suprapure was used for mass discrimination adjustment and a molybdenum (Mo) standard stock solution (1000 mg l–1, Merck) for method validation. All solutions were diluted with high-purity water (18.3 MΩ cm, ELGA LabWater, Marlow, UK). Certified urine (NIST-2670a Urine Low Level, NIST, Gaithersburg, MD, USA) as well as a pooled urine sample were used for method validation and quality assurance throughout the entire measuring period (trending).

Sample preparation Prior to analysis, all samples were thawed overnight in a refrigerator at 4°C, equilibrated for 2 h to ambient temperature, and homogenised by manual panning before pipetting in order to ensure a suspension of the solid precipitates. Sample dilution comprised the addition of 2.6 ml of 1% HNO3 Suprapure as diluent and 0.1 ml of a spike solution to 0.3 ml of urine (1:10 v/v). Reference and quality control samples were prepared in the same way. The diluted sample solutions were kept overnight at 4°C and measured on the following day or in exceptional cases frozen at −20°C until the day of analysis.

Analysis All analyses were performed using an inductively coupled plasma mass spectrometer (ICP-MS) with a hexapole collision cell (X-Series II from Thermo Electron Corp., Winsford, UK). It was equipped with a SeaSpray nebuliser (Glass Expansion, West Melbourne, VIC, Australia), a Peltier cooled cyclonic spray-chamber (PC3 from ESI, Omaha, NE, USA) and an autosampler (ASX-510 from CETAC, Omaha, NE, USA). A mixture of He/O2 (9:1) was used as a collision cell gas, and 3% HNO3 Suprapure as a wash solution between samples. The instrument was tuned daily for maximum sensitivity and minimum oxide formation. Each Cd analysis comprised a survey scan between m/z 94–131 followed by four averaged peak jumps of 50 ms dwell time for the isotopes 111Cd, 114Cd and 118Sn. The isotope 95Mo as well as m/z 130 were additionally monitored for control purposes, m/z 130 representing 98Mo16O2.

Calibration and interference corrections Calibration by isotope dilution was performed by the addition of an enriched 111Cd spike to each sample and the subsequent measurement of the 114Cd/111Cd ratio. Element concentrations were calculated using the previously specified isotope dilution equation (Haldimann & Zimmerli 1994) adapted for Cd isotopes. Natural isotope abundances were considered as invariable at 12.80% for 111 Cd and at 28.73% for 114Cd according to the

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Food Additives & Contaminants: Part A International Union of Pure and Applied Chemistry (Berglund & Wieser 2011). The main interferences for the 111Cd and 114Cd isotopes were 95Mo16O as well as 98Mo16O and 114Sn respectively. Sn interference was corrected through the measurement of isotope 118Sn and subtraction of its corresponding portion on the 114Cd signal. The presence of MoO was minimised by means of the collision cell of the ICP-MS. MoO was brought to reaction with O2 to form MoO2 in order to remove the interfering signals at m/z 111 and 114. The optimum cell gas flow for maximal interference removal was determined experimentally. As a result of instrumental mass discrimination, the measured 114Cd/111Cd isotope ratio deviated from the isotope ratio based on natural abundance. A corrective factor was determined daily by means of pooled urine, with an additional 0.1 µg l–1 Cd to increase signal intensity. All measured isotope ratios of the urine samples were consistently corrected by the resulting factor.

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criteria of Reinivuo et al. (2006), were excluded from statistical analysis. A total of 1409 samples remained with complete data for multivariate analysis by means of a general linear model (GLM). Naturally log-transformed Cd excretion in urine (µg/24 h) was thereby the response variable, while Age, Gender, BMI, Smoking habit and Canton of sampling were included as independent explanatory variables. The model was complemented by the interactions of the categorical variables (Gender, Canton of sampling and Smoking habit). The relation of the log-transformed Cd excretion to explanatory variables was considered significant at p < 0.05. Residuals of the GLM were checked graphically for normal distribution. Representativity of a subgroup compared with the whole collective was tested by two-way cross-tabulation and all 95 percentiles were calculated with the weighted average 3 method. Results

Method validation Accuracy of the analysis method was verified in terms of multiple measurements of the certified urine NIST-2670a. Mean Cd concentration ± standard deviation (SD) of six independent analyses amounted to 0.052 ± 0.006 µg l–1 compared with the certified value of 0.0591 ± 0.0034 µg l– 1 . The recovery of urine samples was determined as 106% and 108% for added concentrations of 0.5 and 0.1 µg l–1 respectively. An RSD of 3.0% was obtained for repeatability and an RSD of 5.6% for between-run precision. Efficacy of MoO removal by the collision cell was tested with the pooled urine sample, enriched by up to 40 µg l–1 Mo, which would correspond to 400 µg l–1 Mo in real samples. Thereby, an RSD of 2.5% at a mean urinary Cd concentration of 0.11 µg l–1 was obtained for all spiked and unspiked samples combined. The analysis of the diluent as a blank solution resulted in an LOD of 0.01 µg l–1 (3 SD) and an LOQ of 0.03 µg l–1 (10 SD). Method performance during the whole measuring period was monitored by repeated analysis of the certified NIST-2670a urine and the pooled urine sample. Mean concentrations ± SD of 0.05 ± 0.01 µg l–1 (n = 43) and 0.11 ± 0.01 µg l–1 (n = 106) were obtained, respectively. Statistics and data treatment Systat (version 13.00.05, Systat Software Inc., San Jose, CA, USA) was used for statistical evaluation and Grapher (version 10.1.640, Golden Software Inc., Golden, CO, USA) for the creation of plots. All measured urinary Cd concentrations were normalised for 24-h Cd excretion before evaluation. Replicate samples from the same person as well as samples with incomplete 24-h urine, according to the

Data for different subgroups are presented in Table 1 together with the corresponding concentrations in µg l–1 as well as creatinine-adjusted values. The latter are only of an informative nature as creatinine dependencies on age and gender are observed. Figure 1 shows the overlaid histograms of the 24-h urine-Cd excretions of never-smokers versus smokers separately. Both histograms approximate a log-normal distribution. An overall Cd excretion mean ± SD of 0.30 ± 0.25 µg/ 24 h and a median of 0.23 µg/24 h were obtained (n = 1409), with the 95th percentile at 0.81 µg/24 h. The median 24-h urine volume was 1880 ml (range between 305 and 7500 ml). No sample was below the LOD (measured range between 0.01 and 1.93 µg l–1). In order to analyse the association between the independent explanatory variables and urinary Cd excretion, GLM analysis was performed (Table 2). The overall fit of the resulting model was assessed by a squared multiple correlation (R2) of 0.434. Age, BMI and Smoking habit (smokers, ex-smokers or never-smokers) showed p < 0.001, while p = 0.004 resulted from the interaction Smoking habit*Canton of sampling. No significant association was found for the variables Canton of sampling (p = 0.244) and Gender (p = 0.399), nor for the remaining two interactions (Smoking habit*Gender with p = 0.262 and Canton of sampling*Gender with p = 0.946). Age stratification of the collective into 10-year periods revealed maximum urinary Cd for women between 71 and 80 years of age (median = 0.35 µg/24 h) and for men between 61 and 70 years of age (median = 0.36 µg/24 h), respectively. The Cd excretion of the different age strata is shown in Figure 2.

0.11 0.12 0.15 0.13 0.12 0.15 0.14 0.13 0.12 0.07 0.11 0.16 0.19 0.09 0.10 0.15 0.17 0.19 0.15 0.11

186 85 113 185 154 163 98 165 260

334 323 347 405

44 700

464 201

247 386 776

Note: aClassification according to WHO (2000).

0.13

Median (µg l–1)

1409

n

0.25 0.20 0.14

0.19 0.21

0.13 0.15

0.08 0.14 0.22 0.28

0.15 0.17 0.16 0.18 0.19 0.15 0.16 0.16 0.16

0.16

Median (µg gC–1)

All

0.32 0.28 0.19

0.27 0.32

0.15 0.18

0.12 0.20 0.31 0.33

0.20 0.24 0.23 0.24 0.26 0.21 0.23 0.22 0.23

0.23

Median (µg/24 h)

132 220 346

277 116

12 293

157 145 178 218

93 36 56 92 67 84 51 84 135

698

n

0.20 0.17 0.11

0.17 0.18

0.10 0.10

0.07 0.11 0.17 0.20

0.12 0.13 0.14 0.12 0.14 0.16 0.16 0.14 0.13

0.14

Median (µg l–1)

Urinary cadmium (Cd) levels (24-h sampling) of subgroups of the collective under study.

Whole collective Canton of sampling Basle Fribourg Geneva Lucerne St. Gallen Ticino Valais Vaud Zurich Age strata from recruitment (years) 15–29 30–44 45–59 ≥ 60 BMIa < 18.5 (underweight) 18.5–24.9 (normal range) 25.0–29.9 (pre-obese) ≥ 30 (obese) Smoking habit Smokers Ex-smokers Never-smokers

Table 1.

0.16 0.17 0.11

0.16 0.17

0.07 0.11

0.07 0.11 0.17 0.22

0.13 0.15 0.13 0.14 0.16 0.12 0.14 0.13 0.15

0.14

Median (µg gC–1)

Men

0.32 0.30 0.18

0.28 0.32

0.12 0.17

0.11 0.19 0.31 0.33

0.20 0.28 0.22 0.26 0.26 0.25 0.23 0.22 0.24

0.23

Median (µg/24 h)

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115 166 430

187 85

32 407

177 178 169 187

93 49 57 93 87 79 47 81 125

711

n

0.18 0.13 0.10

0.13 0.17

0.09 0.10

0.07 0.11 0.14 0.19

0.11 0.11 0.15 0.13 0.11 0.13 0.13 0.13 0.09

0.12

Median (µg l–1)

0.31 0.24 0.17

0.24 0.28

0.15 0.18

0.10 0.17 0.27 0.36

0.17 0.21 0.26 0.23 0.22 0.18 0.19 0.23 0.20

0.21

Median (µg gC–1)

Women

0.32 0.27 0.19

0.26 0.32

0.15 0.19

0.12 0.20 0.31 0.33

0.19 0.22 0.27 0.22 0.25 0.20 0.22 0.22 0.22

0.22

Median (µg/24 h)

1268 J. Jenny-Burri et al.

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Figure 1. Histograms of the urinary cadmium (Cd) excretion of never-smokers and smokers. Figure 2. Twenty-four-hour urinary cadmium (Cd) for men and women depending on age.

Table 2. Independent explanatory variables of the general linear model (GLM) influencing the response variable naturally logtransformed cadmium (Cd) excretion in urine (µg/24 h). Analysis of variance (ANOVA) GLM model predictors Gender Female Male Canton of sampling Basle Fribourg Geneva Lucerne St. Gallen Ticino Valais Vaud Zurich Age BMI Smoking habit Smokers Ex-smokers Never-smokers Gender × Canton of sampling Smoking habit × Canton of sampling Smoking habit × Gender

Estimates of effects (βi)

d.f.

F-ratio

p-value

1

0.710

0.399

8

1.290

0.244

0.015 0 −0.048 0.044 0.015 −0.016 −0.064 0.089 0.072 −0.070 0 0.020 0.023

Comparison of creatinine-adjusted 24-h urine and spot samples from a subsample of the collective (n = 90) showed, after elimination of one outlier value (identified with the Grubbs’ test for outliers), median concentrations of 0.17 µg gC–1 (24-h urine) and 0.15 µg gC–1 (spot urine), respectively. The paired t-test revealed a p-value of 0.100 for the two types of urine, both naturally logtransformed.

Discussion

1 1 2

537.8 43.77 86.51

0.000 0.000 0.000

0.287 −0.025 0 8

0.349

0.946

16

2.180

0.004

2

1.340

0.262

Analysis Cd is a challenging element to analyse by ICP-MS because of numerous interferences on each isotope. Furthermore, the composition of urine represents a very variable sample matrix with Cd only present at low concentrations. The measures taken during this study, namely He/O2 as the collision cell gas, the mathematical 114Sn correction on isotope 114Cd, as well as the calibration by isotope dilution nonetheless allowed direct determination of Cd in diluted urine.

Urinary Cd excretion Overall Cd excretion is for the adult Swiss population at a low level. Nevertheless, some influencing variables have been identified. Significant relations between age and smoking habit to urinary Cd excretion have been confirmed. Figure 2 depicts Cd accumulation until the age

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of 60 years, which is in line with the long biological halflife of this element as well as the already specified 45–60 years of exposure needed in order to achieve a steady state (JECFA 2011). Higher Cd levels through the additional source of smoking also agreed with the general notion of an elevated body burden for smokers. Median Cd excretion from current smokers was in this study 1.7 times higher than from never-smokers. Whether the association between urinary Cd and BMI is explained solely by dietary intake or whether other biochemical processes play a role needs further investigation. The uniform distribution of Cd excretion observed for the whole population indicated the absence of regional differences. Median Cd excretions of 0.23 µg/24 h for men (n = 698) and 0.22 µg/24 h for women (n = 711) revealed no significant difference between the sexes. This finding was rather unusual as most other studies reported higher Cd concentrations for women compared with men (Olsson et al. 2002; Levy et al. 2007; EFSA 2009).

2012). To corroborate a potential difference between spot and 24-h samples, a larger subgroup sample size would be necessary, together with a standardised sampling time of the spot urines, as Cd excretion follows the circadian rhythm (Akerstrom et al. 2014).

Creatinine adjustment In this study, urinary Cd was assessed as the amount excreted over 24 h. An adjustment with creatinine was therefore not necessary for data evaluation. In most other studies, spot urines were the samples of choice, with the results given as µg gC–1. For purposes of comparison, our 24-h urines were alternatively considered as single-spot samples and creatinine adjustment was performed as well. Age and gender dependency of creatinine thereby became obvious. Our data suggest that any gender difference in urinary Cd is introduced through creatinine adjustment (Figure 2). Previous studies already specified this dilemma of creatinine adjustments on collectives with both sexes and with a wide age range (Moriguchi et al. 2003; Suwazono et al. 2005; Chaumont et al. 2013).

Comparison with other Western European countries Given the lack of data with 24-h urine, studies from other countries using spot samples were selected. Although two types of urine are thus compared, it still allows an approximate comparison at the population level. Our results of the creatinine-adjusted spot versus 24-h samples affirm this assumption, as concentrations in the same order of magnitude were obtained. However, only similar stratified population groups regarding gender and age were compared. For Cd, Smoking habit is another important influencing factor. As a consequence, only the never-smoking sub-collectives were considered here. From the current 24-h samples, a median Cd concentration of 0.11 µg l–1 or 0.14 µg gC–1 resulted, respectively (15–91 years of age, n = 776, 430/ 346 women/men). Becker et al. (2003) reported a median concentration of 0.18 µg l–1 or 0.14 µg gC–1 for a representative sample of the German population (18–69 years, n = 2106). In Belgium, Hoet et al. (2013) assessed a median concentration of 0.22 µg l–1 or 0.22 µg gC–1 (18–80 years, n = 620, 340/280 women/men). A median concentration of 0.29 µg l–1 or 0.27 µg gC–1 (18–74 years, n = 913, 655/258 women/men) was measured by Fréry et al. (2011) for France. For the Swedish Mammography Cohort, which was used by EFSA for TWI determination (EFSA 2009), and which represents upper-middle-age Swedish women, a median concentration of 0.31 µg gC–1 was measured (Amzal et al. 2009). The equally stratified group of women from our collective (56– 70 years) also showed a median of 0.31 µg gC–1 (n = 98).

Spot versus 24-h urine samples For a subgroup of 90 participants, both spot and 24-h urine samples were analysed. The latter samples showed a median excretion of 0.24 µg/24 h, similar to the 24-h excretion of the whole collective. Further statistical tests (two-way cross-tabulation) demonstrated the representativity of the subgroup for the whole study collective regarding the factors Age (grouped by 10-year periods, p = 0.237), Gender (p = 0.121) and Smoking habit (p = 0.461). When both urine types of the subgroup were creatinine-adjusted, a difference of 0.02 µg gC–1 resulted in the medians. This difference is less evident than in former studies, where significantly lower Cd concentrations for spot urines compared with the corresponding 24-h samples were found (Trevisan et al. 1994; Akerstrom et al.

Urinary Cd in relation to TWI and intake The CONTAM Panel selected a reference point of 1 µg gC–1 for risk evaluation, ‘in order to remain below 1 µg/gC in urine in 95% of the population by age 50 years’ (EFSA 2009, p. 3). The age and gender stratified 95th percentiles of urinary Cd are listed in Table 3. With the highest 95th percentile at 1.09 µg gC–1 (women between 51 and 60 years of age), the reference point of 1 µg gC–1 is only marginally exceeded. In the absence of recent intake data, this finding gives an indication of the weekly Cd intake of the Swiss population. When comparing the percentiles of Cd excretion in µg/24 h with concentration in µg gC–1, the age and gender bias due to creatinine adjustment was again obvious. Our data on Cd excretion show higher values for the 95th percentiles in men between 41 and 80 years of age.

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Table 3. Urinary cadmium (Cd) 95th percentiles of the age- and gender-stratified collective. Men Age (years)

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≤ 20 21–30 31–40 41–50 51–60 61–70 71–80 81–90

Women

n

(µg/24 h)

(µg gC–1)

n

(µg/24 h)

(µg gC–1)

49 118 90 116 118 123 64 19

0.19 0.28 0.48 0.85 1.07 1.00 0.98 0.68

0.12 0.16 0.22 0.40 0.65 0.63 0.76 0.48

46 141 125 106 124 98 57 14

0.20 0.28 0.55 0.81 0.93 0.86 0.72 1.09

0.19 0.25 0.45 0.60 1.09 0.92 0.93 1.74

Thus, women within our collective are not at a higher risk of adverse effects due to Cd compared with men when excretion data are considered. Furthermore, the very low percentiles in excretion and creatinine-adjusted concentrations of the age group below 20 years of age together with the assessments of higher daily Cd exposure of younger people (EFSA 2009; BfR 2010) underline the long half-life of Cd and affirm the notyet-achieved steady state in the kidneys of young people (JECFA 2011).

Acknowledgements

Conclusions

References

The measured urinary Cd excretions do not imply an increased health risk for the general non-exposed Swiss population. Comparable levels of Cd burden were found in populations from other Western European countries. Whether or not an association between Cd excretion and renal dysfunction might already occur at these low Cd concentrations will be subject of additional investigations. Moreover, further work needs to focus on potential highrisk consumers in order to estimate their Cd body burden compared with the general population. There is only a slight concentration difference between creatinine-adjusted 24-h and spot urine in a subsample of participants. A larger sample size as well as a consideration of the circadian rhythm influencing Cd concentration in spot samples could corroborate these results. Unexpectedly, no difference in Cd excretion was found between men and women and, therefore, women within this collective are not at a higher risk for adverse effects. Further studies with 24-h urine of other populations are needed to get a better understanding of the Cd excretion of both sexes as well as the influence of creatinine adjustment on Cd concentration. A corresponding TWI estimation based on Cd 24-h excretion data instead of creatinine-adjusted spot urines would, as a second step, be advisable if gender bias, exclusively introduced through creatinine adjustment, is further confirmed.

Akerstrom M, Barregard L, Lundh T, Sallsten G. 2014. Variability of urinary cadmium excretion in spot urine samples, first morning voids, and 24 h urine in a healthy nonsmoking population: implications for study design. J Expo Sci Environ Epidemiol. 24:171–179. Akerstrom M, Lundh T, Barregard L, Sallsten G. 2012. Sampling of urinary cadmium: differences between 24-h urine and overnight spot urine sampling, and impact of adjustment for dilution. Int Arch Occup Environ Health. 85:189–196. Amzal B, Julin B, Vahter M, Wolk A, Johanson G, Åkesson A. 2009. Population toxicokinetic modeling of cadmium for health risk assessment. Environ Health Perspect. 117:1293– 1301. Becker K, Schulz C, Kaus S, Seiwert M, Seifert B. 2003. German Environmental Survey 1998 (GerES III): environmental pollutants in the urine of the German population. Int J Hyg Environ Health. 206:15–24. Berglund M, Wieser E. 2011. Isotopic compositions of the elements 2009 (IUPAC technical report). Pure Appl Chem. 83:397–410. [BfR] Bundesinstitut für Risikobewertung. 2010. Aufnahme von Umweltkontaminanten über Lebensmittel [Internet]. [cited 2015 Feb 25]. Available from: http://www.bfr.bund.de/cm/ 350/aufnahme_von_umweltkontaminanten_ueber_lebensmit tel.pdf [CDC] Centers for Disease Control and Prevention. 2009. Fourth report on human exposure to environmental chemicals [Internet]. [cited 2014 Jun 12]. Available from: http://www. cdc.gov/exposurereport Chappuis A, Bochud M, Glatz N, Vuistiner P, Paccaud F, Burnier M. 2011. Swiss survey on salt intake: main results [Internet]. [cited 2013 Jul 30]. Available from: http://www.blv.admin.

The authors express their sincere gratitude to the Swiss Survey on Salt Group, namely E. Battegay, I. Binet, A. Chappuis, D. Conen, P. Erne, L. Gabutti, A. Gallino, N. Glatz, P. Greminger, I. Guessous, D. Hayoz, P. Meier, F. Muggli, A. Péchère-Bertschi, P. M. Suter and A. von Eckardstein, for their key participation in data collection.

Disclosure statement No potential conflict of interest was reported by the authors.

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Cadmium body burden of the Swiss population.

Urinary cadmium (Cd) excretion was measured within a representative Swiss collective. With a median of 0.23 µg/24 h (n = 1409) and the 95th percentile...
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