Urinary Cd Levels Research Articles

Acute kidney injury following acute liver failure: potential role of systemic cadmium mobilization?

A significant fraction of patients with acute liver failure (ALF) suffer from a concomitant acute kidney injury (AKI), the mechanism of which is probably multifactorial. Cadmium (Cd) is a widespread environmental pollutant and a tubulotoxic metal that accumulates in the liver. We tested the hypothesis that a release of Cd during ALF may cause a redistribution of Cd from the liver to the kidneys and play a role in the occurrence of ALF-associated AKI. Twenty patients with ALF (ALF-patients), 20 patients from the ICU with no liver damage at admission (ICU-controls) and 20 healthy controls were recruited to compare the 24-h urinary excretion rate of Cd with that of lead (Pb), a nephrotoxic metal that does not accumulate in the liver, and zinc (Zn), a non-nephrotoxic element found in high amounts in the liver. The excretion rates of the low-molecular-weight proteins (LMWPs) were monitored. ALF-patients excreted markedly more Cd than the healthy controls and ICU-controls. In ALF-patients, the four urinary LMWPs (RBP, β2-MG, CC16 and α1-MG) increased as a function of Cd excretion, with high correlation coefficients. The prevalence of patients excreting a high amount of LMWPs also increased with increasing Cd excretion. No relationship was found between the other elements investigated and the LMWPs, with the exception of copper, which shares close toxicokinetic similarities with Cd. This study shows a strong association between urinary Cd levels and the excretion rates of LMWPs in patients with ALF. A causal relationship is possible but could not be fully demonstrated in this study.

THE RATE OF BONE DEMINERALIZATION WITH AGE DEPENDS ON THE URINARY CADMIUM CONCENTRATION

Purpose: Janghang Refinery which was built in 1936 and operated for 50 years had emitted great amount of pollutants including cadmium (Cd), a heavy metal which has been reported to be associated with decrease in bone mineral density (BMD). This study was aimed to evaluate the relationship between urinary cadmium concentration and decrement in bone mineral density in residents having lived in the vicinity of Janghang Refinery. Materials and Methods: The study subjects included 450 males and 619 females who were living within 20 km from Janghang Refinery. Bone mineral density was measured with ultrasonic method at the calcaneus area. Urinary cadmium concentration was evaluated using an atomic absorption spectrophotometer and adjusted with urinary creatinine concentration. The correlation between urinary Cd level and BMD was statistically tested according to age group (<50 yrs, 50 – 59 yrs, 60 – 69 yrs, >70 yrs) and sex, and the decreasing rate of BMD as age was estimated according to urinary Cd level (< 2, 2 – 5, 5 – 10, > 10 •g/g creatinine). Results: As the age increased, BMD decreased and urinary Cd concentration increased. Urinary Cd concentration was significantly correlated with BMD in young males aged less than 60 years, and in females aged less than 50 years after controlling effects of age and menopause using multiple regression models. Neither in males aged 60 years or more, nor in females aged 50 years or more, were those correlations found. BMD was more strongly correlated with age in females than in males and, it decreased more rapidly as the urine Cd increased in female subjects. Conclusion: These results suggest that cadmium exposure increases the rate of bone demineralization, especially in women.

Outdoor and indoor cadmium distributions near an abandoned smelting works and their relations to human exposure

The relationship of measured or modelled Cd concentrations in soil, house dust and available to plants with human urinary Cd concentrations were assessed in a population living around a Cd/Pb/Zn smelter in the UK. Modelled air concentrations explained 35% of soil Cd variation indicating the smelter contributed to soil Cd loads. Multi-variate analysis confirmed a significant role of biological and life-style factors in determining urinary Cd levels. Significant correlations of urinary Cd with soil, house dust and modelled plant available Cd concentrations were not, however, found. Potential reasons for the absence of clear relationships include limited environmental contact in urban populations; the role of undefined factors in determining exposure; and the limited spatial scope of the survey which did not sample from the full pollution gradient. Further, the absence of any significant relationship indicates that environmental measures provide limited advantage over atmospheric model outputs for first stage human exposure assessment.

Bi-linear dose–response relationship in general populations with low-level cadmium exposures in non-polluted areas in Japan

Previous findings suggest that the dose (e.g., cadmium in urine)-response (e.g., tubular dysfunction markers in urine) relationship after environmental exposure to cadmium (Cd) may be in a shape of a hockey stick with a steep slope when Cd exposure exceeds a certain level, i.e., the point of flexion. However, less attention has been paid to the relation below the flexion point whether it is linear or not. The present study was initiated to examine through epidemiological analyses whether the assumption of linearity holds true when Cd exposure is low. Data were cited from previous publications of this research group on Cd, α(1)-microglobulin (α(1)-MG), β(2)-microglobulin (β(2)-MG), N-acetyl-β-D: -glucosaminidase (NAG), and creatinine (CR) in urine from more than 17,000 adult Japanese women. The cases were selected for age (50-59 years), urine specific gravity (1.010-1.030) and CR (0.3-3.0 g/l), and 5,306 cases were available after selection (the group selected in terms of age and urine density, or the AD-selected group). Statistical analyses of the AD-selected group revealed that the relation was not linear. In case of β(2)-MG, the slope of the regression line between Cd as an independent variable and β(2)-MG a dependent variable was steeper at lower Cd level (i.e., <2.5 μg/l) and shallower when Cd was higher, showing a clear trend of leveling off. The same was also the case for α(1)-MG and NAG. When Cd was 2.0-2.1 μg/l or higher, α(1)-MG, β(2)-MG, and NAG were in excess of the 95%-tile values for the markers in more than 5% of the population. The significance of the observation was discussed in reference to existing criteria for Cd such as 2.5 or 5.2 μg/g cr or for β(2)-MG of 300 μg/g cr. When the present observation of bilinear relation at low Cd exposure levels was combined with the previous observation of very sharp increase in responses among heavily exposed cases, it appeared likely that the overall relationship is tri-phasic in Cd dose-response relationship in humans. A substantial fraction (>5%) of the populations had the marker levels in excess of the 95%-tile values when Cd was ≥2 μg/l. Comparison with findings in reported literature suggests that the presence of such cases by itself may not necessarily mean a risk of tubular dysfunction and that other factors including Cd levels in urine should be considered together.

Smoking status and urine cadmium above levels associated with subclinical renal effects in U.S. adults without chronic kidney disease

Tobacco smoke is a major source of adult exposure to cadmium (Cd). Urine Cd levels (CdU) above 1.0, 0.7, and 0.5 μgCd/g creatinine have been associated with increased rates of microproteinuria and reduction in glomerular filtration rate. The two study objectives were to determine the prevalence and relative risk (RR) by smoking status for CdU above 1.0, 0.7, and 0.5 μgCd/g creatinine in U.S. adults; and to describe geometric mean CdU by smoking status, age, and sex. NHANES 1999-2006 data for adults without chronic kidney disease were used to compute prevalence rates above the three CdU in current and former cigarette smokers, and non-smokers. RRs for smokers adjusted for age and sex were computed by logistic regression. Analysis of covariance was used to calculate geometric means of CdU adjusted for age, sex, smoking status, log urine creatinine, and interaction terms: age-smoking status and sex-smoking status. At selected ages, adjusted RR for exceeding each risk-associated CdU was highest for current smokers (3-13 times), followed by former smokers (2-3 times), compared to non-smokers. Adjusted RR for smokers increased with age and was higher in females than males. Adjusted geometric means of CdUs increased with age, were higher in females than in males regardless of smoking status, and were higher in current smokers than former smokers, who had higher levels than non-smokers at any age. Cigarette smoking greatly increases RR of exceeding renal risk-associated CdU. Former smokers retain significant risk of exceeding these levels compared to non-smokers. CdU increased with age, particularly in current smokers.

Study on the association between environmental cadmium exposure, cytochrome P450-mediated 20-HETE, heme-oxygenase-1 polymorphism and hypertension in Thai population residing in a malaria endemic areas with cadmium pollution

The aims of the study were to investigate (i) the effects of environmental cadmium (Cd) on hypertension, biological markers of renal dysfunction and renal cytochrome P450-mediated arachidonate metabolism; and (ii) the association between genetic polymorphism of heme oxygenase-1 (HO-1) and hypertension and Cd-induced renal injury in the exposed Thai population. The study was conducted in adult subjects residing in Cd-contaminated malaria endemic areas of Mae Sot District, Thailand. All subjects were randomly selected and consistently distributed for sex, age and residential areas. Blood and urinary Cd levels were not significantly different between the case (hypertensive) and control (matched-pair normotensive) groups. While other renal dysfunction biomarkers were comparable between the two groups, urinary microalbumin, urinary 20-hydroxy-5,8,11,14-eicosatetraenoic acid (20-HETE) and serum creatinine were siginificantly higher in the hypertensive group. Only N-acetyl-β-glucosaminidase (NAG) showed positive correlation with Cd in hypertensive and normotensive group. With respect to heme oxygenase-1 (HO-1) polymorphism, the frequencies of (GT) n alleles were similar in both case and control groups. The frequency of SL genotype was significantly higher in the control group, whereas the frequency of ML genotype was significantly higher in the case group. Although no significant difference between 20-HETE and NAG levels in various HO-1 genotypes was found, a trend of increase in 20-HETE and NAG levels was observed in subjects carrying longer (GT) n repeats. Results from the present study provide no clear evidence on the direct effects of environmental Cd on high blood pressure development in the non-occupational exposed Thai population. Furthermore, the indirect effect of Cd through HO-1 (genetic polymorphism and prevalence of long GT( n) repeats) and 20-HETE was inconclusive. Based on the data obtained in the present investigation further studies should be performed which use a larger sample size and effectively control for confounding. This should provide more definitive evidence of the relationship between Cd exposure and high blood pressure.

Evaluation of Associated Factors for Cadmium Exposure and Kidney Function in General Population

PP-29-159 Background/Aims: Cadmium (Cd) is a non-essential toxic metal which is widely distributed in the environment. General population is exposed to the low level Cd chronically and the kidney is the most sensitive target organ to Cd toxicity. Methods: We interviewed demographic characteristics, lifestyles, medical histories, and diet intakes during the last 24 hours. We estimated daily Cd intake through diet in 643 adults who had not been occupationally exposed to Cd. Whole blood and spot urine samples were collected from study subjects, we analyzed internal exposure level of Cd and affecting factors, also evaluated renal function and oxidative stress biomarkers. Results: The daily Cd intake from diet was 7.07 μg/day, the mean concentration of Cd was 1.21 μg/L in blood and 0.95 μg/g creatinine in urine. Blood Cd level was affected by age, sex, smoking habit, dietary Cd intakes. Urinary Cd level was affected by sex, age, and blood Cd level. Urinary Cd were positively correlated with MT, NAG activity, and MDA, but blood Cd only with MT. Increased NAG activity was observed at above 1.0 ug Cd/g creatinine in urine, which indicates that NAG responds to the urine Cd sensitively. However, NAG activity was also affected by age, hypertension, and diabetes histories. The urinary MT responded to the Cd in urine only, which finding suggests that MT is relatively specific to the chronic low level Cd exposure. Conclusion: In conclusion, general population have been exposed to low level Cd and exposure levels were affected by diet and smoking habits, sex, and age which might cause tubular damage in kidney through the oxidative stress mechanism. Urinary NAG and MT could be useful biomarkers under the environmental exposure to Cd.

Cadmium: a toxicant with paradoxical effects on reproduction. preliminary results

OBJECTIVE: Cadmium is one of the most important pollutants in industrialized countries, with potential mechanisms to affect steroidogenesis. This study aims to evaluate the correlation between cadmium levels in follicular fluid, semen and urine and the number of oocytes retrieved, metaphase II oocytes,embryos available, good quality embryos (≥ 8C G1/G2) and fertilization rate in couples undergoing ICSI cycles. DESIGN: Prospective cohort study. MATERIALS AND METHODS: From July to Dec 2009, 25 couples were enrolled after signing an informed consent. Women's age were ≤ 39.Follicular fluid (FF), semen and urine, were obtained on the day of retrieval. All samples were frozen at –20°C until being analyzed by electrothermal atomic absorption spectrometry. Standard occupational exposure Cd urine levels is ≥ 1.0 μg L−1. There are no reference values for FF and semen. RESULTS: The correlation between variables (Pearson's coefficient) in women presented a positive correlation between FF Cd levels (0.92 ± 0.19 μg L−1) and number of oocytes retrieved(r=0.42; p=0.0002); number of M II oocytes (r=0.51; p<0.0001) and the total number of embryos (r= 0.36; p=0.002). A negative correlation was observed between FF Cd and fertilization rate (r=-0.49; p< 0.0001). There was a positive correlation between urine Cd levels (0.28 ± 0.17 μg L−1) and the total number of good quality embryos (r= -0.32; p=0.008). A negative correlation was observed for semen Cd levels(0.21 ± 0.84 μg L−1) and the total number of embryos (r= - 0.46; p=0.001).No correlation was observed for urine Cd levels (0.28 ± 0.15 μg L−1) and the parameters analyzed. CONCLUSION: The intriguingly preliminary results of this ongoing study raise questions about paradoxical effects of cadmium concentrations that correlated positively with ovarian response (oocytes retrieved, MII oocytes and number of embryos obtained) and negatively with fertilization rate. Negative correlation between Cd semen and good quality embryos could be explained by DNA sperm fragmentation.

Cadmium induced renal dysfunction among residents of rice farming area downstream from a zinc-mineralized belt in Thailand

High levels of cadmium (Cd) in paddy soil and rice, and a concurrent increase in urinary Cd of inhabitants in the Mae Sot District, Tak Province, Thailand first emerged in 2003. Risk factors such as occupation, sources of staple food and drinking water as well as biomarkers of adverse renal effects of the increased body burden of Cd were investigated in 795 residents, 30 years or older, whose urinary Cd levels were between 0.02 and 106 μg/g creatinine. Farmers who consumed their own rice and residents who sourced drinking water from wells and/or the river demonstrated increased urinary Cd. Age-adjusted mean urinary cadmium for male and female subjects who consumed well water was 5.7 μg/g vs. 6.1 μg/g creatinine while the corresponding value for male and female subjects who did not consume well water was 3.7 μg/g vs. 4.8 μg/g creatinine, respectively. Increased urinary levels of β 2-microglobulin and N-acetyl-β- d-glucosaminidase were observed with the increase in urinary Cd, indicating tubular dysfunction and renal damage associated with increase in Cd body burden. Consumption of well water and rice grown in the contaminated area increase the body burden of Cd. Cessation of exposure is essential to prevent and possibly recover from Cd toxicity, especially among the residents whose kidney damage and malfunction may be reversible.

Estimation of Dietary Pb and Cd Intake from Pb and Cd in Blood or Urine

Successful trials were made to estimate the dietary daily intake of lead (Pb) and cadmium (Cd) via foods from the levels of the metals in blood or urine. In practice, 14 and 15 reports were available for Pb and Cd in blood (Pb-B and Cd-B), urine (Pb-U and Cd-U) and 24-h diet duplicates (Pb-D and Cd-D), respectively, from which 68 pairs each of Pb or Cd in blood and food duplicates [each being geometric mean (GM) values for the survey sites] were obtained. Regression analysis revealed that there was a significant correlation between Pb-B and Pb-D, and also between Cd-B and Cd-D, suggesting that it should be possible to estimate both Pb-D and Cd-D from Pb-B and Cd-B, respectively. For Cd-U, the number of available cases was limited (20 pairs), but a significant correlation was detected between Cd-U (as Cd-U(cr), or Cd levels in urine as corrected for creatinine concentration) and Cd-D. Care should be taken in estimating Pb-D from Pb-B, as the ratio of Pb-D over Pb-B may decrease as a function of increasing Pb-B levels. The Pb-D (μg/day) for typical Japanese women with Pb-B of 15 μg/l was best estimated to be 13.5 μg/day. No Cd-B- or Cd-U(cr)-dependent change was detected in case of Cd. The best estimate of Cd-D for Cd-B at 1.5 μg/l should be about 19.4 μg/day.

Low Cadmium Levels in Urine of Residents in two Prefectures where Cadmium Levels in Locally Harvested Brown Rice are Higher than in other Prefectures in Japan

Recent publications in Japan suggest that Cd in river beds and locally harvested rice tend to be higher in seven prefectures in the north-eastern part on the coast of the Sea of Japan (the high-Cd zone). The present study was initiated to investigate the current level of exposure to Cd and possible health effects among local populations in the zone. Thus, levels of Cd and three tubular dysfunction markers [i.e., α(1)-MG, β(2)-MG, and N-acetyl-β-D-glucosaminidase (NAG)] were examined in urine of local residents (700 and 704 adult women, respectively) in two prefectures (prefecture 1 and prefecture 7), which were located in the north-east (prefecture 1) and south-west ends (prefecture 7) of the high-Cd zone. Urinary Cd levels [e.g., 0.99 and 0.78 μg/l as geometric mean (GM) for observed (non-corrected) values, respectively] in prefecture 1 and prefecture 7 were comparable to the levels in other parts of Japan (All Japan-A; 0.99 μg/l). Correspondingly, GM values for α(1)-MG (2.29 and 1.99 mg/l vs. 2.17 mg/l for All Japan-A) and for β(2)-MG (87 and 80 μg/l vs. 99 μg/l for All Japan-A) were not elevated, and NAG also stayed unchanged (2.89 and 2.87 units/l for prefecture 1 and prefecture 7, respectively). Evaluation in combination with the findings in other five prefectures in the zone suggests that Cd exposure is equal to the national average both in prefecture 1 and in prefecture 7, whereas Cd exposure appeared to be elevated in the central part of the zone. The observation appears to be on line with geographical location of the two prefectures that they are on the two ends of the zone of high natural Cd background.

Cadmium and tubular dysfunction marker levels in urine of residents in non-polluted areas with natural abundance of cadmium in Japan

Literature survey has suggested that cadmium (Cd) in the general environment is more abundant in the northern part of the coast on the sea of Japan. The present survey was initiated to examine if the exposure to Cd in the area has been higher than other parts of Japan, and if so, the higher exposure has been associated with tubular dysfunction among the local residents. In three prefectures of Akita, Yamagata and Ishikawa in the region, adult women (about 700 subjects per prefecture) were invited to participate in the survey. Each of the participants provided informed consents, offered spot urine samples and filled questionnaires (on age etc.). The urine samples were analyzed for Cd, alpha(1)-microglobulin (alpha(1)-MG), beta(2)-microglobulin (beta(2)-MG) and N-acetyl-beta-D: -glucosaminidase, together with creatinine and specific gravity. The results were combined with published data on two other prefectures of Niigata and Toyama (both in the area), as well as Japan as a whole (all Japan-A excluding Niigata prefecture, which was studied separately in the present study), and subjected to analysis for possible difference from all Japan-A in terms of the levels of internal Cd burden, and prevalence of beta(2)-MG-uria. Geometric means (GMs) for urinary Cd in the five prefectures were in a range from a low of 1.20 to a high of 2.65 microg/l, being higher than the GM (0.99 microg/l) for all Japan-A. GMs for alpha(1)-MG (2.15-2.80 mg/l) and beta(2)-MG (99-107 microg/l) were only slightly higher or even lower than all Japan-A values depending on the prefectures. Elevation in the prevalence of beta(2)-MG-uria was significant in Akita prefecture, but the elevation in beta(2)-MG was not associated with elevation in Cd in urine. Literature survey on general population Cd epidemiology showed that Cd, alpha(1)-MG and beta(2)-MG levels in urine of the residents in the five prefectures were within the levels reported for non-polluted areas, and such was also the case for prevalence of beta(2)-MG-uria. In an over-all evaluation, no clear-cut evidence was available for increased prevalence of Cd exposure-associated renal tubular dysfunction among general populations in the five prefectures in the northern part on the coast of Sea of Japan than in other prefectures in Japan, despite moderate elevation in urinary Cd levels.

Association of environmental cadmium exposure with periodontal disease in U.S. adults.

BackgroundPeriodontal disease is a complex, multifactorial, chronic inflammatory disease that involves degradation of periodontal structures, including alveolar bone. Cadmium adversely affects bone remodeling, and it is therefore possible that environmental Cd exposure may be a risk factor for periodontal-disease–related bone loss.ObjectiveWe examined the relationship between environmental Cd exposure and periodontal disease in U.S. adults.MethodsWe analyzed cross-sectional data from the third National Health and Nutrition Examination Survey (NHANES III). We defined periodontal disease as clinical attachment loss of at least 4 mm in > 10% of sites examined. We used multivariable-adjusted logistic regression analyses to estimate the association between creatinine-corrected urinary Cd levels and periodontal disease.ResultsOf the 11,412 participants included in this study, 15.4% had periodontal disease. The age-adjusted geometric mean urine Cd concentration (micrograms per gram creatinine) was significantly higher among participants with periodontal disease [0.50; 95% confidence interval (CI), 0.45–0.56] than among those without periodontal disease (0.30; 95% CI, 0.28–0.31). Multivariable-adjusted analyses, which included extensive adjustments for tobacco exposure, showed that a 3-fold increase in creatinine-corrected urinary Cd concentrations [corresponding to an increment from the 25th (0.18 μg/g) to the 75th (0.63 μg/g) percentile] was associated with 54% greater odds of prevalent periodontal disease (odds ratio = 1.54; 95% CI, 1.26–1.87). We observed similar results among the subset of participants who had limited exposure to tobacco, but only after removing six influential observations.ConclusionEnvironmental Cd exposure was associated with higher odds of periodontal disease.

Biomonitoring of urinary metals in a population living in the vicinity of industrial sources: A comparison with the general population of Andalusia, Spain

The Ria of Huelva (south-west Spain) is one of the most polluted fluvial-estuarine systems in the world. Industrial activity delivers huge amounts of pollutants to the local environment, particularly heavy metals and arsenic. Here we aimed to determine urinary levels of As, Cd, Cr, Cu and Ni in a representative sample ( n = 857) of adults living in the Ria of Huelva. Levels were compared to those from a representative sample of 861 adults of the general urban population of Andalusia (southern Spain) and multiple regression models were developed to identify individual factors associated with urinary levels of these elements. Arsenic levels were significantly higher in the Ria of Huelva as compared to other Andalusian cities, whereas Cd and Ni levels were significantly lower. Despite these differences, levels in both groups were similar to the reference values reported in previous studies for general population. Age, gender, diet and lifestyle were the major factors contributing to the interindividual variation in urinary metals. In conclusion, despite living in a highly polluted area, the population of the Ria of Huelva failed to show higher urinary levels of the studied metals as compared to a reference urban population of the same region.

Uptake of cadmium from Pacific oysters ( Crassostrea gigas) in British Columbia oyster growers

Background Pacific oysters along the North American coast from Washington to Alaska contain concentrations of cadmium (Cd) that are high by comparison with Atlantic oysters, frequently exceeding 2 μg/g wet weight, but it is unclear whether this Cd is absorbed by consumers. Objectives To determine the effect of oyster consumption on Cd in blood and urine among a group with high oyster consumption. Methods Sixty-one non-smoking oyster growers and family members with a mean age of 47.3±7.6 years (range 33–64) were interviewed by telephone to assess their oyster consumption and other sources of Cd exposure at present and 5 years prior to the start of oyster farming. Their blood and urine Cd concentrations were measured. Results The geometric mean Cd concentration in blood was 0.83 μg/L and in urine was 0.76 μg/g creatinine. Thirty-six percent of participants had urinary Cd levels above 1 μg/g creatinine and 5% were above 2 μg/g creatinine. Recent (last 12 months) and long-term oyster consumptions were positive predictors of blood Cd but did not directly predict urinary Cd. The optimal model for predicting the variance in blood Cd included recent intake of oyster-derived Cd, serum iron concentration and recent ketchup consumption ( R 2=0.34, p=0.00004), with the latter two variables showing a protective effect. The factors found to predict urinary Cd were blood Cd concentration and duration of oyster farming. A rise in blood Cd was observed after 12 years of farming oysters, likely caused by higher consumption of oysters during this period. Conclusions Oyster-derived Cd is bioavailable and affects body stores of the metal.

Cadmium dietary intake and biomarker data in French high seafood consumers

Seafood and especially mollusks are known to be a rich source of cadmium (Cd), but little data are available concerning French seafood contamination and Cd exposure of French populations. The objective was then to assess food intake and biological level of Cd in high consumers of seafood, and to determine the impact of the consumption of self-fished mollusks on urinary Cd. Seafood consumption levels of 80 products were assessed for 1011 high consumers aged 18 and over in four French coastal areas, thanks to a validated food frequency questionnaire (FFQ). According to a total diet study approach, seafood samples were collected taking into account preservation methods and supply habits. Food samples were analyzed for Cd. Exposure was assessed by crossing consumption data with contamination data. Total blood and urine samples were collected from 380 subjects of the cohort and analyzed for Cd. The impact of the self-collected mollusks consumption on the Cd biological level adjusted for creatinine was assessed by a multivariate linear regression model. The mean dietary intake of Cd is 2.44+/-3.34 microg/kg bw/wk and the mean urinary Cd (U-Cd) level is 0.65+/-0.45 microg/g creatinine, and is significantly higher in women than in men (P<0.05). The consumption of self-fished mollusks is significantly negatively associated with U-Cd (r=-0.11 [-0.185, -0.009], P=0.03). The results of this study indicate that the biological Cd levels remain below the standards, and also suggest a protective effect of self-fishing, which inspires confidence about the high consumer health safety in terms of Cd exposure.

Urinary Cadmium and Age-related Macular Degeneration

To evaluate the association between urinary and blood cadmium (Cd) levels with age-related macular degeneration (AMD). Prospective case-control study. In 53 participants older than 60 years with AMD in both eyes and in 53 age-matched (+/- 3 years) controls without AMD, Cd levels were measured in blood and urine specimens (with and without creatinine adjustment) by using inductively coupled plasma-mass spectrometry. Data on age, gender, smoking status, and family history were obtained. By using color stereoscopic fundus photographs, the degree of AMD was graded using the Age-Related Eye Disease Study's 4-stage AMD severity scale. The inclusion criterion for AMD cases was a photographic severity level of two to four in both eyes. Median blood and urine Cd and median urine Cd/creatinine concentrations in cases and controls were compared by using the rank-sum test, stratifying for smoking status. Current and former smokers with AMD had median urine Cd/creatinine levels (1.18 microg/g; range, 0.84 to 1.44 microg/g) that were 97% higher than smokers without AMD (0.60 microg/g; range, 0.49 to 0.90 microg/g; P = .02), 111% higher than never smokers with AMD (0.56 microg/g; range, 0.40 to 0.80 microg/g; P < .001) and 107% higher than never smokers without AMD (0.57 microg/g; 0.40 to 0.65 microg/g; P < .001). Blood Cd levels, indicative of short-term exposure levels, were not associated with AMD (P >/= .06). A higher urinary Cd level, which reflects the total body burden of Cd, was associated with AMD in smokers. Accumulated Cd exposure may be important in the development of smoking-related AMD.

Estimation of Benchmark Dose for Pancreatic Damage in Cadmium-Exposed Smelters

The aim of this study was to estimate the benchmark dose (BMD) for pancreas dysfunction caused by cadmium (Cd) exposure in smelters. Smelter workers who had been exposed to Cd for more than 1 year and matching nonoccupationally exposed subjects were asked to participate in this study. Urinary cadmium (UCd) was used as a biomarker for exposure, serum insulin and amylase were used as biomarkers for pancreatic effects. In this study, serum insulin and amylase were lower in the smelter workers than in the nonoccupationally exposed subjects. A significant dose-response relationship with UCd was displayed. BMDs in terms of urinary Cd corrected for creatinine were calculated by use of BMDS (version 1.3.2). The benchmark dose lower limit of a one-sided 95% confidence interval (BMDL) for 10% excess risk was also determined. It was found that the BMDL10 for serum insulin and serum amylase was 3.7 and 5.3 microg/g Cr, respectively. Compared to the BMDL for renal damage caused by Cd exposure, identified by the effect biomarkers urinary beta2-microglobulin, urinary N-acetyl-beta-glucosaminidase, and urinary albumin (UALB), it was shown that BMDL10 for serum insulin is the lowest among all values and UALB gave the highest value (5.8 microg/g Cr). This study indicates that Cd exposure can result in pancreatic dysfunction and the effect appears at lower urinary Cd level than renal dysfunction. The endocrine function of the pancreas was affected at lower urinary levels of Cd, compared to the exocrine function, which was seen at higher urinary levels of Cd than those giving rise to renal tubular dysfunction.

Chronic exposure of mice to environmentally relevant, low doses of cadmium leads to early renal damage, not predicted by blood or urine cadmium levels

Mice were exposed to cadmium (Cd) concentrations ranging from 0 to 100mg CdCl2/l in the drinking water for 1, 4, 8, 16 and 23 weeks. Urine samples were taken regularly, Cd content was determined in blood, liver, kidney and urine and histological analyses of the kidney were performed.Kidney cortex Cd content increased linearly with time and dose, while blood levels reached a plateau at 8 weeks and liver at 16 weeks in mice exposed to 100mg CdCl2/l after which both started to decrease. Urinary Cd levels were not correlated with the kidney Cd content.A multivariate regression model taking into account the actual Cd intake, calculated from the volume of water taken in by each animal and the exposure concentration, confirmed that blood is an indicator of acute exposure, while kidney Cd content is a reliable indicator of chronic exposure. The urinary protein content was significantly increased from 16 weeks on in mice exposed to 100mg CdCl2/l (p<0.05), while other signs of proximal tubular damage (glucosuria, enzymuria) were not detected. Histologically more vacuoles and lysosomes were present in the proximal tubule cells with increasing time and dose.The results indicate that chronic exposure to low doses of Cd induced functional and histological signs of early damage at concentrations in or below the ones generally accepted as safe. Our study does not corroborate the statement that urine Cd levels are a reliable indicator of total Cd body burden, at least when the body burden is low.

Plasma lipid peroxidation and erythrocyte antioxidant enzymes status in workers exposed to cadmium

Cadmium (Cd) is a corrosion-resistant metal, used extensively for electroplating in the automobile, electronic and aerospace industry. Only a few studies are available regarding Cd-induced oxidative stress in animals, but no reports are available regarding the effects of Cd on oxidative stress during occupational exposure. The present study was carried out to determine the plasma lipid peroxidation and erythrocyte antioxidant enzymes status in workers exposed to Cd during electroplating. 50 subjects exposed to Cd during electroplating formed the study group. An equal number of age-sex matched subjects, working in the administrative section, formed the control group. Urinary Cd levels were determined using the flameless atomic absorption spectrophotometer. Plasma lipid peroxidation and erythrocyte antioxidant enzymes were determined using spectrophotometric methods. A significant increase of plasma lipid peroxidation and a significant decrease of superoxide dismutase and glutathione peroxidase levels were noted in the study group compared with the control group. The level of plasma lipid peroxidation was positively and erythrocyte antioxidant enzymes were negatively and significantly associated with Cd levels in urine. Multiple regression analysis assessed the oxidative stress associated with Cd and other lifestyle confounding factors, such as age, body mass index, the consumption of vegetables, coffee, tea, smoking and alcohol. Analysis showed that the lifestyle confounding factors viz; smoking, body mass index and urinary Cd levels > 5 microg/g of creatinine, were significantly associated with oxidative stress. The results of the present study suggest that increased plasma lipid peroxidation and decreased superoxide dismutase levels could be used as biomarkers of oxidative stress in cadmium-exposed workers.