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Potatoes are a staple food in New Zealand and a contributing source of dietary cadmium (Cd), although there is little information nationally on the soil and plant factors that affect Cd con...

The present study was conducted to evaluate whether grape seed proanthocyanidins (GSPs) could alleviate the negative effects of dietary cadmium on growth performance, body composition, activities of digestive enzymes, and antioxidant potential in the intestine of pearl gentian grouper (Epinephelus fuscoguttatus female x Epinephelus lanceolatus male). Two hundred and forty pearl gentian groupers with the initial average body weight of 31.30±0.05 g/fish were randomly divided into four treatment groups with three replicates in each group and 20 fish in each replicate. The four treatment groups were identified as control group (the basal diet), Cd group (the basal diet+300 mg/kg Cd), Cd+GSPs group I (the basal diet+300 mg/kg Cd+400 mg/kg GSPs), and Cd+GSPs group II (the basal diet+300 mg/kg Cd+800 mg/kg GSPs group), respectively. The trial lasted for 42 days. Fish exposed to 300 mg/kg dietary cadmium had lower growth performance, mineral metabolism disorders with lower calcium and phosphorus levels, higher ash level, decreased lipase and protease activities, and antioxidant potential in the intestine. Dietary GSPs supplementation could counteract those negative effects to a certain extent. The alleviation effects of Cd+GSPs group II were better than those of Cd+GSPs group I. Except for calcium and phosphorus levels in whole fish composition, 800 mg/kg dietary GSPs supplementation could not recover the adverse effects caused by Cd stress. These results suggested that GSPs might potentially mediate dietary cadmium toxicity and alleviate the negative effects on pearl gentian grouper.

Cadmium (Cd) is a toxic metal associated with adverse health effects, including kidney injury or disease. The aims of this study were to estimate dietary Cd exposure during childhood, and to evaluate the association of early-life dietary Cd with biomarkers of glomerular kidney function in 9-year-old Mexican children. Our study included 601 children from the Programming Research in Obesity, Growth, Environment and Social Stressors (PROGRESS) cohort with up to five follow-up food frequency questionnaires from 1 to 9 years of age; and 480 children with measures of serum creatinine, cystatin C, and blood nitrogen urea (BUN), as well as 9-year-old estimated glomerular filtration rate. Dietary Cd was estimated through food composition tables. Multiple linear regression models were used to analyze the association between 1 and 9 years, cumulative dietary Cd, and each kidney parameter. Dietary Cd exposure increased with age and exceeded the tolerable weekly intake (TWI = 2.5 µg/kg body weight) by 16–64% at all ages. Early-life dietary Cd exposure was above the TWI and we observed inverse associations between dietary Cd exposure and kidney function parameters. Additional studies are needed to assess kidney function trajectories through adolescence. Identifying preventable risk factors including environmental exposures in early life can contribute to decreasing the incidence of adult kidney disease.

Previous studies demonstrated that gibel carp A strain was more susceptible to herpesvirus infection than other strains. Thus, we hypothesized that F strain might display better defense responses than the A strain against cadmium (Cd) exposure. To test our hypothesis, gibel carp A strain and F strain were exposed to three diets comprising of different concentrations of Cd for 8 weeks to compare their resistances to Cd. Comprehensive evaluations on biochemical, physiological and histological responses were conducted post-exposure. Results showed that no adverse effects and differences were observed on growth in two strains of gibel carp, compromising of the remarkable hepatoxicity-caused liver damage as shown by histological observations. Dietary Cd exposure stimulated antioxidant defense in the liver to counteract the Cd hepatoxicity, especially in the F strain. Activation of ER stress response positively stimulated the autophagy, then triggering apoptosis in fish after dietary Cd exposure. Thus, Cd-induced autophagy served as a protective strategy to alleviate hepatoxicity, but overaction of ER stress also triggered irreparable cell death via apoptosis. Cd induced dysregulation of lipid accumulation, which might be a common mechanism in response to hepatoxicity. Last but not least, the F strain showed stronger response on antioxidant, ER stress and autophagy, but apoptosis were remitted compared with the A strain, implying the F strain showed stronger response but better defense strategies to dietary Cd exposure. Our finding provides useful information for genetic breeding in aquaculture, and ultimately contribute to the safety assessment of aquatic products for human consumption.

Chronic exposures to cadmium (Cd) are associated with reduced glomerular filtration rate (GFR), increasing the risk of chronic kidney disease (CKD). In support of the World Health Organization (WHO)'s initiative to estimate the global burden of foodborne diseases, a risk assessment was performed to estimate the Disability-Adjusted Life Years (DALYs) due to late-stage CKD associated with dietary exposures to cadmium. Using the distribution of population GFRs, the prevalence of CKD was calculated as the proportion of humans whose GFR fall in the ranges corresponding to Stage 4 or Stage 5 CKD. The increase in the CKD prevalence due to cadmium exposure was simulated based on a previously reported pharmacokinetic model describing the relationship between dietary cadmium intake and urinary cadmium (UCd), as well as a previously published dose-response relationship between UCd and GFR. Cadmium-related incidence rate, calculated as the change in the prevalence during a one-year period, were used to compute the mortality and DALY in all WHO regions. It is estimated that dietary cadmium would result in a median of 12,224 stage 4 and stage 5 new CKD cases per year worldwide, resulting in 2064 global deaths and 70,513 DALYs. These data translate into a median global burden of 1.0 DALY per 100,000 population, which account for 0.2% of the global DALYs of CKD. While these results suggest that the overall impact of dietary cadmium exposure on global CKD is low, they do indicate that reasonable efforts to reduce dietary exposure will result a positive public health impact. This would be particularly the case in areas with elevated levels of dietary cadmium.

Diet is the primary source of cadmium-a proven Group 1 human carcinogen-for non-smokers. Observational studies investigating the effect of cadmium from food sources on breast cancer risk have produced inconsistent results. We examined the association between dietary cadmium and risk of breast cancer defined by estrogen receptor (ER), progesterone receptor (PR) and HER2 status, in 8924 women recruited to a prospective study between 1987 and 1992. Dietary cadmium intake was estimated using a semi-quantitative food frequency questionnaire at baseline. During a median of 22 years of follow-up, 451 incident cases of breast cancer were identified through the Varese Cancer Registry. Multivariable-adjusted hazard ratios (HRs) with 95% confidence intervals (CIs) for breast cancer and receptor-defined breast cancer subtypes were estimated for quintiles of dietary cadmium intake, adjusting for confounding factors. Mean dietary cadmium intake was 7.8 (standard deviation 1.4) μg/day. Women with highest quintile of cadmium intake had a greater risk of breast cancer (HR 1.54; 95% CI, 1.06-2.22; p trend = 0.028) than those with lowest quintile of intake. Women premenopausal at recruitment had HR = 1.73 (95% CI, 1.10-2.71, highest vs. lowest quintile); postmenopausal women had HR = 1.32 (95% CI, 1.05-1.66 for each standard deviation increase in cadmium). Cadmium-related risk of breast cancer did not vary with ER, PR or HER2 status (p-heterogeneity not significant). These findings support the hypothesis that dietary cadmium is a risk factor for breast cancer.

The available information on the interplay between low-dose cadmium intake and copper, manganese, and iron homeostasis in invertebrates is limited. We have currently studied the accumulation of these trace metals in the hepatopancreas of adult snails, Cantareus aspersus, following 14 and 28 days of exposure to low doses of dietary cadmium, up to 1 mg/kg dw (dry weight). The cadmium dose, but not the duration of exposure, had a significant effect on hepatopancreas copper deposition, the values being significantly elevated compared to controls. A significant peak in manganese levels at 14 days was found in snails administered the lowest cadmium dose. These increases occurred even in the absence of cadmium increase in the hepatopancreas. Our data suggest that low dose cadmium feeding can produce a transient disturbance in hepatopancreas copper and manganese homeostasis. Such responses may serve as early biomarkers of physiological changes occurring during the initial stages of cadmium intoxication.

The present study investigated the interactive effects of dietary cadmium (Cd) and selenium (Se) on the tissue-specific (liver, kidney, and muscle) accumulation of these two elements, hepatic oxidative stress response, and morphometrics in rainbow trout (Oncorhynchus mykiss) during chronic exposure. Fish were exposed to elevated dietary Cd (45 μg g−1 dry wt.), and medium (10 μg g−1 dry wt.) or high (45 μg g−1 dry wt.) dietary selenium (added as selenomethionine), both alone and in combination, for 30 days. Exposure to dietary Cd alone caused oxidative stress in fish as reflected by reduced thiol redox (GSH:GSSG), increased lipid peroxidation, and induction of anti-oxidative enzymes (catalase, superoxide dismutase, and glutathione peroxidase) in the liver. Also, an increase in tissue-specific Cd burden and impaired morphometrics (hepato-somatic index and condition factor) were also recorded in fish following exposure to dietary Cd. In contrast, the dietary co-exposure to Cd and Se (at both medium and high doses) resulted in a decrease in Cd burden in the liver and kidney of fish. However, co-exposure to medium, but not high, dose of dietary Se completely alleviated Cd-induced oxidative stress and impaired morphometrics in fish, indicating that the reduced Cd tissue burden might not have been the primary factor behind the amelioration of Cd toxicity by Se. Overall, our study demonstrated that the protective effect of Se against the chronic Cd toxicity in fish is mainly mediated by the anti-oxidative properties of Se, but this protective effect is dose-specific and occurs only at a moderate exposure dose.

This study was performed to investigate the dose-response relationship between average daily cadmium dose (ADCD) from rice and the occurrence of urinary cadmium (U-Cd) in individuals eating that rice. This was a retrospective cohort designed to compare populations from two areas with different levels of cadmium contamination. Five-hundred and sixty-seven participants aged 18 years or older were interviewed to estimate their rice intake, and were assessed for U-Cd. The sources of consumed rice were sampled for cadmium measurement, from which the ADCD was estimated. Binary logistic regression was used to examine the association between ADCD and U-Cd (cut-off point at 2 μg/g creatinine), and a correlation between them was established. The lowest estimate was ADCD = 0.5 μg/kg bw/day [odds ratio (OR) = 1.71; with a 95% confidence interval (CI) 1.02-2.87]. For comparison, the relationship in the contaminated area is expressed by ADCD = 0.7 μg/kg bw/day, OR = 1.84; [95 % CI, 1.06-3.19], while no relationship was found in the non-contaminated area, meaning that the highest level at which this relationship does not exist is ADCD = 0.6 μg/kg bw/day [95% CI, 0.99-2.95]. Rice, as a main staple food, is the most likely source of dietary cadmium. Abstaining from or limiting rice consumption, therefore, will increase the likelihood of maintaining U-Cd within the normal range. As the recommended maximum ADCD is not to exceed 0.6 μg/kg bw/day, the consumption of rice grown in cadmium-contaminated areas should not be more than 246.8 g/day. However, the exclusion of many edible plants grown in the contaminated area from the analysis might result in an estimated ADCD that does not reflect the true level of cadmium exposure among local people.

5-Hydroxymethylcytosine (5hmC) is an important, yet poorly understood epigenetic DNA modification, especially in invertebrates. Aberrant genome-wide 5hmC levels have been associated with cadmium (Cd) exposure in humans, but such information is lacking for invertebrate bioindicators. Here, we aimed to determine whether this epigenetic mark is present in DNA of the hepatopancreas of the land snail Cantareus aspersus and is responsive to Cd exposure. Adult snails were reared under laboratory conditions and exposed to graded amounts of dietary cadmium for 14 days. Weight gain was used as a sublethal endpoint, whereas survival as a lethal endpoint. Our results are the first to provide evidence for the presence of 5hmC in DNA of terrestrial mollusks; 5hmC levels are generally low with the measured values falling below 0.03%. This is also the first study to investigate the interplay of Cd with DNA hydroxymethylation levels in a non-human animal study system. Cadmium retention in the hepatopancreas of C. aspersus increased from a dietary Cd dose of 1 milligram per kilogram dry weight (mg/kg d. wt). For the same treatment, we identified the only significant elevation in percentage of samples with detectable 5hmC levels despite the lack of significant mortalities and changes in weight gain among treatment groups. These findings indicate that 5hmC is an epigenetic mark that may be responsive to Cd exposure, thereby opening a new aspect to invertebrate environmental epigenetics.

Cadmium is a metal that is toxic to humans, and the major source of cadmium exposure in the non-smoking general population is diet. To identify major food sources and lower exposure from diet, an accurate estimate of dietary cadmium intake is needed. Hence, the objectives of this study are to develop a method to assess dietary cadmium intake using a biomarker measurement and to improve the estimation of dietary cadmium intake when using a food frequency questionnaire (FFQ). In a random sample of an Italian population, we collected dietary habits by FFQ and measured cadmium in foods and beverages. These data were used to compute the estimated weekly dietary intake (WDI) of cadmium (&micro, g) by kilogram (kg) of body weight (bw) (WDIFFQ). We also measured fasting serum cadmium levels by inductively-coupled plasma mass spectrometry. We used these data to develop a model for the estimation of the biomarker-derived dietary cadmium intake (WDIbio). In the 51 subjects recruited, the median level of serum cadmium was 0.041 &micro, g/L (interquartile range (IQR): 0.030&ndash, 0.054). The median WDIFFQ and WDIbio were 1.34 &micro, g/kg bw/week (IQR: 0.86&ndash, 1.70) and 0.72 &micro, g/kg bw/week (IQR: 0.55&ndash, 1.11), respectively. The correlation between the two estimates was low-to-moderate (r = 0.291). In exploratory analyses, the correlation was slightly higher in women and participants ages &lt, 50 years, and markedly higher in participants with body mass index &lt, 25 kg/m2 and smokers. Our approach allows for the dietary contribution to be isolated from the overall cadmium exposure measured with a biomarker, the estimated dietary cadmium intake was roughly similar to that estimated using the FFQ, especially in select subgroups. Future refinements to the biomarker-derived dietary cadmium intake approach should take into consideration additional sources of cadmium exposure, as well as factors affecting its absorption and metabolism.

A total number of 360 laying Japanese quail (8 weeks of age) were randomly divided into 12 groups. Birds in all groups had nearly the same average initial body weight. A factorial arrangement (4 &times, 3) was performed including four levels of dietary cadmium (Cd) as cadmium chloride (0, 50, 100, and 150 mg/kg diet) and three levels of feed additives (without, 300 mg/kg ascorbic acid and 1.50% natural clay). Results revealed that Cd contaminated feed caused significant (p &lt, 0.01) retardation in body weight, lower egg number and egg mass and worse feed conversion. On the other hand, the addition of ascorbic acid or natural clay to quail diets caused a significant (p &lt, 0.01) improvement in all studied traits. With respect to the interaction among Cd and the experimental additives, results showed that within each Cd level, ascorbic acid or clay supplementation recorded the highest body weight, egg number, egg weight and mass in addition to improved feed conversion. Cadmium levels decreased (p &lt, 0.05) blood total protein, albumen and A/G ratio. Both 300 mg ascorbic acid and 1.50% clay increased (p &lt, 0.05) blood total protein and albumen compared to non-supplemented groups. It could be concluded that the consumption of polluted diets Cd causes deleterious effects on the productive performance of laying Japanese quail. The addition of ascorbic acid or natural clay to the diets causes beneficial effects on productive performance traits, improves egg quality criteria and diminishes the toxic effects of Cd.

Cadmium (Cd) is an environmental pollutant with destructive impact on many organ systems, such as chronic kidney diseases, liver diseases, osteoporosis, cardiovascular diseases and so on. The liver is the target organ of cadmium exposure. This study was performed to evaluate the adverse effects of prolonged high intake of dietary cadmium on production performance, serum biochemistry, liver antioxidant status, histopathology and the residue in liver and eggs in laying hens. 72 Hy-Line Brown laying hens aged 40 weeks were randomly allocated to four groups, with three replicates of six birds. Each group was fed a corn-soy basal diet (BD) and an oral dose of Cd at 0, 15, 30, 60 mg/kg per day for 6 weeks, respectively. Results revealed that the administration of 60 mg/kg Cd had no significant influences (P > 0.05) on production performance. Compared with the control, dietary Cd significantly increased (P < 0.05) the activities of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Furthermore, compared with the control, hepatic glutathione peroxide (GPX) activities were significantly decreased (P < 0.05), while malondialdehyde (MDA) was significantly increased (P < 0.05) when supplemented Cd over 15 mg/kg, and glutathione (GSH) was only decreased significantly (P < 0.05) in 30 mg/kg Cd group. Hepatic histopathology also showed hepatic injury, mild vasculitis and a small amount of lymphocyte infiltration occurred in the liver tissue in 15 mg/kg Cd group and the symptoms were exacerbated with the increased dose. In the 60 mg/kg group, hepatic sinusoidal dilatation and mild congestion were also observed. The residue of Cd in the liver and yolk were increased (P < 0.05) with the increasing concentration of dietary Cd. In conclusion, hepatic injuries in laying hens were induced when diets supplemented with Cd up to 15 mg/kg. Cd levels also managed to accumulated in liver and yolk of laying hens.

Objectives Metalloendocrinology is a newly-termed interdisciplinary field. It was established due to the high importance of connections between inorganic chemicals and hormonal mechanisms in the human body. The estrogenic effect of cadmium in hormone-related tumours, such as endometrial cancer (EC), is an excellent example of it. Therefore, the present study aimed to investigate the role of dietary cadmium intake in the prognosis of EC. Methods The study is based on a large cohort of Swedish women (n=416) who had a hysterectomy and bilateral salpingo-oophorectomy due to EC at the Karolinska University Hospital Solna between 2007 and 2012. Patients from the cohort answered particular questions concerning their lifestyle and dietary habits using the food frequency questionnaire (FFQ). The dietary cadmium intake from each food item was estimated using the FFQ, comprehensive database on the cadmium content, and average daily consumption of different food items. The calculated metal intake was grouped into tertials. The tertials were analysed in connection with different tumour characteristics and clinical outcomes of EC. Results The average estimated dietary cadmium intake per day in the cohort was 13.9 μg/day. Interestingly, the cadmium input from cereal products and vegetables, mainly considered healthy, in the cohort was dominant. Among 3366.6 person-years of follow-up a total, of 54 incident cases of recurrent EC were identified. A statistically significant association between dietary cadmium exposure and progression-free survival was observed in the cohort (IRR=1.421, 95 CI=.775–2.605, p=0.041). Conclusions Our results support the hypothesis that dietary cadmium intake may have a prognostic role in patients with EC.

In this study, we identified cadmium (Cd) as a potential endocrine disruptor that impairs laying performance, egg quality, and eggshell deposition and induces oxidative stress and inflammation in the eggshell glands of laying hens. A total of 480 38-wk-old laying hens were randomly assigned into 5 groups that were fed a basal diet (control) or a basal diet supplemented with Cd (provided as CdCl2·2.5 H2O) at 7.5, 15, 30, and 60 mg Cd per kg feed for 9 wk. The results showed that, when compared with the control group, a low dose of dietary Cd (7.5 mg/kg) had positive effects on egg quality by improving albumen height, Haugh unit, yolk color, and shell thickness at the third or ninth week. However, with the increase in the dose and duration of Cd exposure, the laying performance, egg quality, and activities of eggshell gland antioxidant enzymes (catalase [CAT], glutathione peroxide [GSH-Px]), and ATPase (Na+/K+-ATPase, Ca2+-ATPase, and Mg2+-ATPase) deteriorated, and the activity of total nitric oxide synthase (T-NOS) and the level of malondialdehyde (MDA) increased significantly (P < 0.05). The histopathology and real-time quantitative PCR results showed that Cd induced endometrial epithelial cell proliferation accompanied by upregulation of the mRNA levels of progesterone receptor (PgR) and epidermal growth factor receptor (EGFR), downregulation of the mRNA levels of estrogen receptor α (ERα) and interleukin 6 (IL6), and inflammation of the eggshell gland accompanied by significantly increased expression of complement C3 and pro-inflammatory cytokine tumor necrosis factor α (TNFα) (P < 0.05). In addition, the ultrastructure of the eggshell showed that dietary supplementation with 7.5 mg/kg Cd increased the palisade layer and total thickness of the shell, but with the increase in dietary Cd supplementation (30 and 60 mg/kg) the thickness of the palisade layer and mammillary layer decreased significantly (P < 0.05), and the outer surface of the eggshell became rougher. Correspondingly, the expression of calbindin 1 (CALB1), ovocalyxin-32 (OCX-32), ovocalyxin-36 (OCX-36), osteopontin (SPP1), and ovocledidin-17 (OC-17) decreased significantly (P < 0.05) with increasing dietary Cd supplementation. Conclusively, the present study demonstrates that dietary supplementation with Cd negatively affects laying performance, egg quality, and eggshell deposition by disturbing the metabolism of eggshell glands in laying hens but has a positive effect on egg quality at low doses.

We measured changes in atmospheric and blood levels of lead and cadmium in the South Korean general population during the past decade. Blood data of 16,873 adults were taken from the Korean National Health and Nutrition Examination Survey (KNHANES, 2008&ndash, 2017). Atmospheric data were taken from 66 air quality monitoring sites in 16 different regions in South Korea. From 2008 to 2017, the geometric mean (GM) blood lead level decreased from 2.37 to 1.46 &mu, g/dL (38.4% decrease), and the atmospheric lead concentration decreased by 61.0% in the overall population. During this time, the GM blood cadmium level decreased from 0.88 to 0.72 &mu, g/L (18.2% decrease), and the atmospheric cadmium concentration decreased by 63.6%. Multiple linear regression analysis indicated that a half reduction in air lead was associated with a 0.09 &mu, g/dL decrease in blood lead (95% CI: 0.03 to 0.15) in a subgroup of the metropolitan city population. However, a half reduction in air cadmium had no significant effect on blood cadmium. Multiple linear regression analyses indicated that the decrease in blood lead level over 10 years in Korea was related to the decrease in atmospheric lead concentration. However, the decrease in blood cadmium level during this time was not significantly associated with the decrease in atmospheric cadmium concentration. Our findings suggest that inhalation is a major source of lead exposure, but not of cadmium exposure. Ingestion of dietary cadmium presumably has a stronger impact on blood cadmium levels.

Background: The aim of the present study was to find the effects of cadmium (Cd) on Japanese quail on the role of an animal model in order to understand the toxicity of Cd in creatures presented, within the environment. Methods: One hundred 30-day-old male Japanese quails were equally divided into the control group and Cd group. The control group received no Cd while the Cd group was given formula feed comprised of 100 ppm of Cd (CdCl2, Merck, Germany) for sixty days. The histological and functional alteration in the liver and kidneys and the response of antioxidants were determined. Results: Histological changes in the liver increased the number of kuppfer cells, vacuolar degeneration, and hepatocytes single cell necrosis in the Cd group. The renal histopathological changes were hyaline cast in renal tubules and necrosis and swelling of tubular epithelial cells. The level of aminotransferases (ALT and AST), blood urea nitrogen (BUN) and creatinine rose significantly in the Cd group toward the control group (P

Cadmium is a toxic metal with modifiable exposure sources including diet. In pregnant women and children, unique dietary habits may contribute to DCd, and the relationship of diet to overall cadmium exposure can depend on specific factors during these transitional time periods.This study aimed to identify and quantify food sources of DCd, describe the distribution of UCd, and determine the relationship of DCd and intake of specific foods with UCd, stratified by maternal smoking history, among pregnant women and children in a well-characterized Mexico City birth cohort.Our sample included 192 pregnant women (third trimester) and 223 children (7-15years). DCd was calculated using FFQ and the U.S. TDS. We also measured UCd, maternal history of smoking, and additional covariates.Pregnant women and children had geometric mean UCd concentrations of 0.19±0.78μg/L and 0.14±0.60μg/L, respectively. On average, estimated daily DCd intake was 9.3±3.5μg for women and 12.2±5.4μg for children. Adjusted linear regression models showed a positive association between DCd and UCd among women (p=0.03) and children (p=0.03) without a maternal history of smoking. Intake of fruit and vegetables among women and potato consumption among children were positively associated with UCd.Pregnant women and their children are exposed to cadmium at dietary and urinary levels similar to those previously reported. Higher estimated DCd for children than for women could be attributed to the different FFQs or related to dietary pattern changes between age groups. DCd contributed to UCd in those without a maternal smoking history.

The aims of this study were determining the co-induced effects of dietary Cadmium (Cd) and high intake of Molybdenum (Mo) on renal toxicity in ducks. 240 healthy 11-day-old ducks were randomly divided into 6 groups, which were treated with Mo or/and Cd at different doses added to the basal diet for 120 days. Ducks of control group were fed with basal diet, LMo and HMo groups were fed with 15mg/kg Mo and 100mg/kg Mo respectively; ducks of Cd group were provided with 4mg/kg Cd which was added into basal diet. Two combination groups were treated with 15mg/kg Mo+4mg/kg Cd and 100mg/kg Mo+4mg/kg Cd respectively. On days 30, 60, 90 and 120, the mRNA expression levels of inflammatory cytokines and contents of trace elements were detected. In addition, transmission electron microscopic examination was used for ultrastructural studies. The results indicated that the mRNA expression levels of tumor necrosis factor-α (TNF-α), nuclear factor-kappa B (NF-κB), and cyclooxygenase-2 (COX-2) showed an upward tendency in treatment groups in comparison with control group, and in the later period of the experiment it showed a significant rise in joint groups compared with the Mo and Cd group (P0.01); the contents of copper (Cu) and iron (Fe) decreased in joint groups in the later period (P0.05) while the contents of Mo and Cd significantly increased (P0.01); zinc (Zn) and selenium (Se) concentration had a slight downtrend in treated groups, but showed no significant difference (P0.05). The ultrastructural analysis showed that kidney tissues were severely injured in joint groups on day 120. These results suggested that the combination of Mo and Cd could aggravate damages to the kidney. In addition, dietary of Mo or/and Cd caused the decrease of Cu, Fe, Zn, and Se contents, inflammatory response and pathological lesions whose mechanism is somehow linked with Mo and Cd deposition in kidney.

Effects of cadmium (Cd) on collembolans and predatory mites have been well studied but Cd accumulation and biological transfer and the relationship between Cd trophic transfer and nitrogen (N) isotope fractionation and transfer in soil micro-arthropod food chains remain poorly understood. Here, we investigated the biological transfer and trophic toxicity of Cd and the effects of dietary Cd exposure on 15N fractionation in animal tissues and N transfer from food in a soil collembolan (Folsomia candida)-predatory mite (Hypoaspis aculeifer) food chain using experiments conducted in plate and soil systems. Synchronized F. candida were fed yeast or wheat spiked with 0 (Control), 50 (Cd50), 100 (Cd100) or 200 (Cd200) μg Cd g−1 food for two weeks and were then offered to synchronized H. aculeifer as prey for two weeks. Cadmium concentrations in tissues of both the collembolan and its predator increased as the Cd concentrations in the food yeast or wheat increased in both the plate and soil systems, and the Cd concentrations in the food and the animals were all significantly and positively correlated. Except for the controls, the Cd bioaccumulation factor (BAF) between adults of predatory mites and consumer collembolans (0.20–1.13) was 2.5–14 times higher than that from food yeast/wheat to consumer collembolans (0.02–0.08). Cadmium transfer has not altered the reproduction of the filial generation collembolans but the reproduction of the predatory mite declined by 34.3% with the Cd concentration in its juveniles reaching 5.94 μg g−1, suggesting that Cd transfer from the spiked food can present a higher toxicity to the predator H. aculeifer. Food spiked with Cd decreased the N content in the collembolan tissues assimilated from the food and enriched the 15N fraction (δ15N) in their tissues by affecting their metabolic turnover and growth rates. The Cd trophic transfer between collembolans and predatory mites from spiked food can directly increase the δ15N value of predatory mites and restrict the movement of N from collembolans to predatory mites. The δ15N of soil animals has considerable potential as a biomarker of Cd stress, 15N isotope application may be limited in Cd polluted soil ecosystems, and the N transfer function of soil food webs may be more vulnerable in polluted ecosystems.

The effects of dietary cadmium (Cd) supplementation on growth, antioxidant capacity and accumulation of Cd in tissues (body wall, digestive tracts, and respiratory tree) of sea cucumber, Apostichopus japonicus, exposed to sub-chronic concentrations (0, 10, 50, 100, and 500mg Cd/kg dry weight) of Cd were investigated. In addition, the potential protective effects of vitamin C (L-ascorbic acid, AsA) against the effects of Cd on sea cucumbers were investigated. Sea cucumbers were exposed to dietary Cd for 30 days, after which another group of healthy sea cucumbers was supplied diet supplemented with mixed Cd and AsA for another 30 days. Cd exposure for 30 days resulted in increased Cd accumulation in tissues of sea cucumbers with exposure time and concentration. The order of Cd accumulation in organs was digestive tracts>respiratory tree>body wall. On day 30, the body weight gain (BWG) and specific growth rate (SGR) decreased significantly (P

Cadmium, a human carcinogenic heavy metal, has been reported to be associated with breast cancer risk; however, the results from the epidemiological studies are not always consistent. The objective of this study was to quantitatively summarize the current evidence for the relationship between cadmium exposure and breast cancer risk using meta -analysis methods. Six studies determining the dietary cadmium intake level and five studies evaluating the urinary cadmium level were identified in a systematic search of MEDLINE and PubMed databases, and the associations between these levels and breast cancer risk were analysed. The pooled estimates under the random-effects model suggested that higher urinary cadmium levels were associated with an increased risk for breast cancer (highest versus lowest quantile, pooled odds ratio [OR]=2.24, 95% confidence interval [95%CI]=1.49–3.35) and a 1μg/g creatinine increase in urinary cadmium led to a 1.02-fold increment of breast cancer (pooled OR=2.02, 95%CI=1.34–3.03); however, pooled estimates for dietary cadmium intake found no significant association between cadmium exposure and breast cancer risk (highest versus lowest quantile, pooled relative risk [RR]=1.01, 95%CI=0.89–1.15). These results suggest that cadmium exposure may lead to an increased risk of breast cancer, and urinary cadmium levels can serve as a reliable biomarker for long-term cadmium exposure and may predict the breast cancer risk.

The association between internal cadmium exposure and chronic kidney disease (CKD) has been investigated before. However, few studies have shown the association between dietary cadmium intake and CKD. In this study, we show the association between life-time dietary cadmium intake and CKD based on a follow-up study. At baseline, we collected blood and urine samples for assays of cadmium and renal effect biomarkers. A questionnaire and food survey was given to each subject to collect diet and lifestyle information for the estimation of cadmium intake. Dietary cadmium, cadmium in blood and urine were regarded as exposure markers. Life-time dietary cadmium intake was estimated based on an individual’s daily cadmium intake and exposure time. At follow-up, 467 persons (163 men and 304 women) were finally included. CKD at follow-up was considered if the estimated glomerular filtration rate (eGFR) was less than 60 mL/min/1.73 m2. The eGFR level in subjects in the highest quartile of total dietary cadmium intake (>9.34 g) was significantly lower than in those with a moderate or low intake (p 2.2 g) was higher than in those with a low intake (odds ratio (OR) = 18.16, 95%CI: 1.75–188.85). A similar association was found between the baseline urinary albumin (UALB) level and CKD incidence. A predictive model based on UALB and life-time dietary cadmium intake showed an acceptable performance (the area under the curve was 0.77 (95%CI: 0.65–0.88)). Our data show that high dietary cadmium exposure was associated with CKD after controlling for renal tubular dysfunction and internal cadmium exposure.

Adverse effects of non-occupational exposure to cadmium (Cd) are increasingly acknowledged. Since our previous study has showed that orally acquired Cd affects skin, the contribution of genetic background to dermatotoxicity of oral cadmium was examined in two rat strains, Albino Oxford (AO) and Dark Agouti (DA), which differed in response to chemicals. While similar accumulation of Cd in the skin of both strains was noted, the skin response to the metal differed. DA rat individuals mounted antioxidant enzyme defense in the skin already at lower Cd dose, in contrast to AO rats which reacted to higher metal dose solely (and less pronounced), implying higher susceptibility of DA strain to Cd dermatotoxicity. Epidermal cells from both strains developed stress response, but higher intensity of antioxidant response in AO rats implied this strain`s better ability to defend against Cd insult. Cd induced epidermal cells' proinflammatory cytokine response only in DA rats. Increased IL-10 seems responsible for the lack of response in AO rats. Differences in the pattern of skin/epidermal cell responsiveness to cadmium give a new insight into repercussion of genetic variability to dermatotoxicity of orally acquired cadmium, bearing relevance for variations in the link between dietary cadmium and inflammation-based skin pathologies.

Cadmium (Cd) is a toxic heavy metal that can contribute to numerous diseases as well as increased mortality. Diet is the primary source of Cd exposure for most individuals, yet little is known about the foods and food groups that contribute most substantially to dietary Cd intake in the US. Therefore, the objective of this study was to estimate dietary Cd intake and identify major food sources of Cd in the US population and among subgroups of the population. Individuals aged 2 years and older from the National Health and Nutrition Examination Survey (NHANES) 2007&ndash, 2012 were included in this study (n = 12,523). Cd intakes were estimated from two days of 24-h dietary recalls by matching intake data with the Cd database of the Food and Drug Administration (FDA)&rsquo, s Total Diet Study 2006 through 2013. The average dietary Cd consumption in the population was 4.63 &mu, g/day, or 0.54 &mu, g/kg body weight/week, which is 22% of the tolerable weekly intake (TWI) of 2.5 &mu, g/kg body weight/week. Greater daily Cd intakes were observed in older adults, males, those with higher income, higher education, or higher body mass index. The highest Cd intakes on a body weight basis were observed in children 10 years and younger (38% of TWI), underweight individuals (38% of TWI), and alcohol non-consumers (24% of TWI). The food groups that contributed most to Cd intake were cereals and bread (34%), leafy vegetables (20%), potatoes (11%), legumes and nuts (7%), and stem/root vegetables (6%). The foods that contributed most to total Cd intake were lettuce (14%), spaghetti (8%), bread (7%), and potatoes (6%). Lettuce was the major Cd source for Caucasians and Blacks, whereas tortillas were the top source for Hispanics, and rice was the top contributor among other ethnic subgroups including Asians. This study provides important information on the dietary Cd exposure of Americans, and identifies the groups with the greatest dietary Cd exposure as well as the major sources of dietary Cd among sociodemographic subgroups.

A preliminary study by our group suggested that the absorption and accumulation of cadmium may be affected by zinc intake. Tobacco smoke is one major source of cadmium exposure that highly influences cadmium burden among smokers, but it is unclear whether this zinc-cadmium relationship differs by smoking status. The objective of this study was to examine whether the association between zinc intake and cadmium burden differs by smoking status using data from 3900 US adults in the National Health and Nutrition Examination Survey 2007-2012. In an adjusted regression model, dietary cadmium was positively associated with blood and urinary cadmium. There was a significant interaction between zinc intake and smoking status, so we analyzed associations within smoking status subgroups. In an adjusted regression model, zinc intake was inversely associated with urinary cadmium only among non-smokers. Failure to meet the Recommended Dietary Allowance (RDA) for zinc was more common among current smokers than non-smokers, and among those in the highest quintile of blood and urinary cadmium than those in lower quintiles. Zinc intake was inversely associated with urinary cadmium only among subjects meeting the zinc RDA, suggesting that the relationship between zinc intake and cadmium burden differs by smoking status.

International audience; Impacted marine environments lead to metal accumulation in edible marine fish, ultimately impairing human health. Nevertheless, metal accumulation is highly variable among marine fish species. In addition to ecological features, differences in bioaccumulation can be attributed to species-related physiological processes, which were investigated in two marine fish present in the Canary Current Large Marine Ecosystem (CCLME), where natural and anthropogenic metal exposure occurs. The European sea bass Dicentrarchus labrax and Senegalese sole Solea senegalensis were exposed for two months to two environmentally realistic dietary cadmium (Cd) doses before a depuration period. Organotropism (i.e., Cd repartition between organs) was studied in two storage compartments (the liver and muscle) and in an excretion vector (bile). To better understand the importance of physiological factors, the significance of hepatic metallothionein (MT) concentrations in accumulation and elimination kinetics in the two species was explored. Accumulation was faster in the sea bass muscle and liver, as inferred by earlier Cd increase and a higher accumulation rate. The elimination efficiency was also higher in the sea bass liver compared to sole, as highlighted by greater biliary excretion. In the liver, no induction of MT synthesis was attributed to metal exposure, challenging the relevance of using MT concentration as a biomarker of metal contamination. However, the basal MT pools were always greater in the liver of sea bass than in sole. This species-specific characteristic might have enhanced Cd biliary elimination and relocation to other organs such as muscle through the formation of more Cd/MT complexes. Thus, MT basal concentrations seem to play a key role in the variability observed in terms of metal concentrations in marine fish species.

Cadmium is very hazardous pollutant with massive impact on aspects of everyday life. Little knowledge exists on kinetics of dietary cadmium retention in Cantareus aspersus for durations above three months although this species of land snails serves as excellent ecotoxicological model for studying cadmium hazard. Here was used a continuous 112-day exposure study design, in which test snails were exposed to a wide range of dietary cadmium levels, including human- and environmentally-relevant levels. Using Flame Atomic Absorption Spectrometry, cadmium levels in the hepatopancreas were found to increase significantly, and in dose-dependent manner starting from a dietary cadmium dose of 0.2 mg/kg dry weight. The results of the present study render the hepatopancreas of mature snails, C. aspersus, as excellent endpoints for assessing Cd toxicity over a broad range of concentrations. Hence, this species of land snails can be reliably used for both active and passive biomonitoring of environmental cadmium pollution.

Cadmium (Cd) is one of the major transitional metals that have toxic effects on aquatic organisms. To investigate the effects of dietary cadmium on growth, salinity stress, hepatotoxicity in juvenile Pacific white shrimp (L. vannamei) and potential protective effect of Zn(II)-curcumin, five experimental diets (control, 100mg/kg Zn(II)-curcumin, 30mg/kg Cd, 30mg/kg Cd+100mg/kg Zn(II)-curcumin, 30mg/kg Cd+200mg/kg Zn(II)-curcumin) were formulated. The results showed that Cd at 30mg/kg induced significant increase in weight gain, specific growth rate and visible alterations to the hepatopancreas structures of L. vannamei. Compared with control diet, 100mg/kg Zn(II)-curcumin added diet had no effect on growth performance or feed utilization, while healthier hepatopancreas and less plasma ALT, AST production was found. Moreover, 200mg/kg dietary Zn(II)-curcumin significantly ameliorated the Cd induced hepatotoxicity while 100mg/kg dietary Zn(II)-curcumin slightly ameliorated. Cd accumulation in the whole body was decreasing and Metallothioneins like was increasing in hepatopancreas with increasing dietary Zn(II)-curcumin level. The shrimp fed with dietary Zn(II)-curcumin showed higher survival rate after acute salinity change. Therefore, it can be demonstrated that hepatotoxicity and hormesis could be induced by Cd when Cd levels were 30mg/kg, Zn(II)-curcumin could mitigate the effects of dietary Cd on L. vannamei.

Background: With tobacco smoking, diet is the main source of cadmium (Cd) exposure in the general population. The carcinogenic and estrogenic activities of Cd make it a contaminant of potential concern for hormone-dependent cancers including breast cancer. Postmenopausal women represent the most appropriate population to investigate the possible impact of exogenous factors with potential estrogenic activity on breast cancer as, after menopause, their estrogenic influence is predominant. Objectives: We systematically reviewed available studies on the association between dietary exposure to Cd and breast cancer focusing on postmenopausal women. A meta-analysis combining the risk estimators was performed and potential sources of between studies heterogeneity were traced. Methods: Studies were searched from MEDLINE through 31 January 2015 and from the reference lists of relevant publications. Six eligible studies published between 2012 and 2014 were identified and relative risk estimates were extracted. Meta-rate ratio estimates (mRR) were calculated according to fixed and random-effect models. Meta-analyses were performed on the whole set of data and separate analyses were conducted after stratification for study design, geographic location, use of hormone replacement therapy (HRT), tumor estrogen receptor status (ER+ or ER−), progesterone receptor status (PGR+ or PGR−), body mass index (BMI), smoker status, zinc or iron intake. Results: No statistically significant increased risk of breast cancer was observed when all studies were combined (mRR = 1.03; 95% confidence interval [CI]: 0.89–1.19). Several sources of heterogeneity and inconsistency were identified, including smoker status, HRT use, BMI, zinc and iron intake. Inconsistency was also strongly reduced when only considering ER−, PGR−, tumors subgroups from USA and from Japan. The risks were, however, not substantially modified after stratifications. No evidence of publication bias was found. Conclusion: The present study does not provide support for the hypothesis that dietary exposure to Cd increases the risk of breast cancer in postmenopausal women. Misclassification in dietary Cd assessment in primary studies could have biased the results towards a finding of no association. Keywords: Dietary cadmium, Breast cancer, Postmenopausal women, Systematic review, Meta-analysis

Feeding ratio and frequency have substantial effects on food digestion and assimilation in fish, yet few attempts have been made to determine their influences on the bioaccumulation of trace metals. In this study, juvenile Acanthopagrus schlegeli were exposed to either water-borne or dietary cadmium (Cd) at different feeding ratios (0, 2, or 4% body weight d(-1) [BW d(-1)] under waterborne Cd exposure and 1, 2.5, or 4% BW d(-1) under dietary Cd exposure) or feeding frequencies (1, 2 or 8 times d(-1)) for 5 wk. Under waterborne Cd exposure, the fish fed 0% BW d(-1) or 8 times d(-1) showed significantly lower growth rates and those fed 0% BW d(-1) or 1 time d(-1) exhibited higher Cd body burdens and Cd uptake rates compared to the other groups. The gut showed a significantly higher waterborne Cd uptake rate than the gills when fish were fasted or fed only 1 time d(-1). These results suggest that starvation and low feeding frequency facilitate waterborne Cd uptake. Under dietary Cd exposure, the fish fed 4% BW d(-1) or 2 times d(-1) grew faster. Cd body burden and Cd assimilation were higher in fish fed 2.5% BW d(-1) or 2 times d(-1). Dietary Cd retention was positively correlated with feed efficiency, suggesting the utilization of Cd probably coincides with the essential nutrients in fish. Overall, this study demonstrates that different feeding strategies significantly influence waterborne and dietary Cd bioaccumulation in marine fish. Therefore, feeding conditions have to be considered carefully for managing trace metal contamination in marine fish farming.

It would be quite convenient if daily dietary cadmium intake (Cd-D) can be estimated either from Cd in blood (Cd-B) or from Cd in urine (Cd-U). The aim of the study was to examine if Cd-D can be estimated from Cd-B or Cd-U.The data available in a previous publication were employed for regression analyses between Cd-D and Cd-B, and between Cd-D and Cd-U. 30 sites in various prefectures throughout Japan were surveyed and 20 adult women/site on average provided food duplicate, peripheral blood, and second morning urine samples. Geometric means were taken as representative values and employed in regression analyses.Cd-D, Cd-B, and Cd-U(cr) [i.e., Cd-U after correction for creatinine (cr) concentration] distributed in ranges of 12.5-70.5 μg/day, 0.46-3.98 μg/l, and 1.16-11.02 μg/g cr, respectively. A close correlation was observed between Cd-D and Cd-B, and also between Cd-D and Cd-U(cr) with r = 0.76 and r = 0.79 (p0.001 for both), respectively. Both regression lines passed close to the origins. Application of 1.23 μg Cd/l blood and 1.26 μg Cd/g cr in urine (average levels for adult Japanese women) to the regression equations gave 16.5 and 11.5 μg Cd/day.The analyses suggested that it may be possible to estimate Cd-D from Cd-B or Cd-U. Cd-B-based estimation should be more respected. As variations in the estimation parameters and estimated values are inherent to field surveys, care should be taken in the application of the study results. Application on a group basis (and not on an individual basis) should be considered.

Cadmium and its compounds are human carcinogens with severe organ toxicity, and their contamination of agricultural soil in China has been frequently reported; however, the dietary exposure to cadmium in residents and the relevant health risk have seldom been reported. In this study, the concentration of cadmium in various types of food collected from 2013 to 2015 were analyzed using graphite furnace atomic absorption spectrometry, and the dietary exposure to cadmium assessed based on a dietary survey in 2976 Guangzhou residents. In total, 3074 out of 4039 food samples had cadmium levels above the limit of detection. The mean ± standard deviation (50th, 95th percentile) cadmium content in all samples was 159.0 ± 112.7 (8.6, 392.4) μg/kg, with levels ranging from 1.0 to 7830 μg/kg. Using the mean cadmium concentrations, the average monthly dietary exposure of Guangzhou residents to cadmium was 14.4 (μg/kg body weight (BW), accounting for 57.6% of the provisional tolerable monthly intake (PTMI). Rice, laver, vegetables, and live aquatic products were the main sources of cadmium intake, on average accounting for 89% of the total value. The dietary cadmium exposure in high consumers (95th percentile food consumption) was 41.0 μg/kg·BW/month, accounting for 163% of the PTMI. Additionally, dietary cadmium exposure at mean consumption but high cadmium food concentration (95th percentile) was 32.3 μg/kg·BW/month, corresponding to 129% of the PTMI. The level of dietary exposure to cadmium in most Guangzhou residents was within the safety limit, thus increased health risk from dietary cadmium exposure is low at present. However, continued efforts by local governments to monitor the levels of cadmium in the four main food categories contributing to exposure are necessary.

This trial was conducted to evaluate grape seed proanthocyanidins (GSPs) on alleviating the effects of dietary cadmium (Cd) induced growth retardation and oxidative stress in hepatopancreas of juvenile tilapia (Oreochromis niloticus). Two hundred and forty fish were randomly divided into four groups with four replicates in each group and 15 fish in each replicate. The four groups were: control group (fed with a basal diet), Cd group (fed with a basal diet+100 Cd mg/kg), Cd+ GSPs group I (fed with a basal diet+100 mg Cd/kg+400 mg GSPs/kg), and Cd+ GSPs group II (fed with a basal diet+100 mg Cd/kg+800 mg GSPs/kg). The trial period was 49 days. Final body weight and weight gain rate of Cd group were significantly affected (P0.05). Levels of malondialdehyde, glutathione, and total antioxidation capacity and activities of superoxide dismutase, catalase, and glutathione peroxidase in hepatopancreas of the Cd group were affected significantly (P0.05). Results indicate that dietary GSPs supplementation may alleviate dietary Cd-induced growth retardation and oxidative stress in hepatopancreas of tilapia.

The aim of this study was to investigate the effects of different levels of cadmium supplementation (0, 5, 10, 20, 40 and 80 mg/kg) in the diet on performance, egg quality, tibia biomechanical properties and eggshell and bone mineral contents in laying quails. In this 10-week trial, a total of 96 laying quails, aged 21 weeks, were randomly distributed among six experimental groups. Each experimental group contained four replicates of four birds each. The performance parameters were adversely affected quadratically when cadmium was added to the diets in the concentrations of 20 mg/kg and above (P

This paper presents results of heavy metals determination in infant foods available in Poland during a monitoring programme in 2009-13. This study investigated levels of lead, cadmium, arsenic, and mercury in infant formulae and other infant foods intended for consumption during the first 6 to 12 months of life, and an intake of heavy metals was assessed. Food consumption data based on the artificial feeding scheme of infants established by the Mother and Child Institute in Poland were taken into account to estimate dietary exposure. The reported levels of elements in infant foods are comparable with contamination of such products in other countries. The mean values for lead do not exceed 0.013 mg/kg (90 th percentile, 0.028 mg/kg). Lead levels in infant formulae (as sold, mainly powder) did not exceed 0.010 mg/kg, while mean contamination was 0.005 mg/kg. The highest mean cadmium level of 0.010 mg/kg was reported in vegetable meal (90 th percentile, 0.017 mg/kg); in infant formulae (undiluted) milk-based it was below 0.003 mg/kg, and for soya-based it was 0.009 mg/kg. Arsenic and mercury contents – highest in fish-based infant foods – did not exceed 0.18 mg/kg and 0.013 mg/kg, respectively. In rice products for infants arsenic did not exceed 0.14 mg/kg. The estimated mean lead exposure was from 0.09 μg/kg b.w. per day for 6-month-old infants to 0.53 μg/kg b.w. per day for 1-year-old children, which was approximately 17% and equal to the respective Benchmark Dose Lower Confidence Limit (BMDL01) established by the European Food Safety Authority (EFSA) at 0.50 μg/kg b.w. per day. Mean exposure to cadmium ranges from 0.02 to 0.4 μg/kg b.w. per day, and for 12-month-old infants can slightly exceed the tolerable weekly intake (TWI) value established by EFSA. Dietary cadmium intake represents 2.5-47% of the provisional tolerable monthly intake (PTMI) value established by the Joint FAO/WHO Expert Committee of Food Additives (JECFA). Intake of arsenic and mercury was below respective reference value. Calculated mean dietary exposure to arsenic for children under 1 year old was between 0.11 and 0.99 μg/kg b.w. per day (4-33% BMDL0.5 value), and to methylmercury 0.01-0.08 μg/kg b.w. per day (7-41% of the TWI value for methylmercury).