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This study investigated the dietary structure, Cadmium (Cd) contents in foods and exposure to Cd through diets of the residents in the mining-affected areas of Nandan County in summer 2013 (July to August) and winter 2014 (November to December). The weighing of foods and the chemical analysis of foods were applied to determine the dietary structure, and the concentration of trace element Cd in the diets, respectively, of the residents in the mining-affected areas (Chehe town, Dachang town, and Zhanglao town) and a control area (Liuzhai town), and subsequently the Cd exposure from the diets was estimated. In the mining-affected areas, the geometric mean of Cd in rice and rice products was the highest (0.29 μg/g) among all food types, and it exceeds the value of 0.2ug/g from the China Food Safety National Standard for Maximum Levels of Contaminants in Foods (GB2762-2017). The Cd contents in rice and rice products, vegetables, and beans in the mining-affected areas were significantly higher than those in the control area. The estimated daily food intakes of Cd in the mining-affected areas were higher than the intake in the control area. The THQ in the mining-affected areas of Chehe town, Dachang town, and Zhanglao town was 3.03, 2.31, and 3.27, respectively. All of which were higher than the value of 1.44 in the control area. Thus, the high level of dietary cadmium intakes of residents in this area deserves our attention.

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.

Soil contamination in some areas of southern China has resulted in elevated dietary intake of cadmium (Cd), posing a potential risk to human health. A survey of paired soil-rice (n = 200) and soil-vegetable (n = 142) samples was conducted in Xiangtan county of Hunan province, southern China. The concentrations of Cd in all the samples were determined by inductively coupled plasma mass spectrometry. Dietary intakes of Cd from the consumption of locally produced rice and vegetables were estimated for different age groups. Among the 342 crop samples collected in the survey, 88% and 29% of rice grain and vegetable samples, respectively, exceeded the Chinese maximum permissible limit for Cd (0.2 mg dry weight kg−1, 0.2 mg fresh weight kg−1 and 0.1 mg fresh weight kg−1 for rice, leafy vegetables and for rootstalk and legume vegetables, respectively). The median dietary Cd intake varied from 66.5 to 116 μg Cd kg−1 body weight (BW) month−1, with children (4–11 years) exhibiting the highest intake. These values are 2.7–4.6 times the tolerable dietary intake of 25 μg kg−1 BW month−1 recommended by the Joint FAO/WHO Expert Committee on Food Additives. For the general population in Xiangtan county, rice contributed the majority (81%) of the Cd intake with vegetables contributing only 19%. The median hazard quotient calculated from dietary Cd intake was 2.4 times the permissible level, indicating a high risk to the local residents. This study highlights an urgent need to reduce the transfer of Cd from soil to the food chain in the investigated region.

The tolerable dietary intake of cadmium was recommended at provisional tolerable monthly intake of 25 μg kg-1 body weight. However, several studies indicated that this tolerable level should be re-evaluated for sufficient health protection. In this study, we show the reference levels of dietary cadmium intake for renal dysfunction by using a benchmark dose (BMD) approach. A total of 790 subjects (302 men and 488 women) living in control and cadmium-polluted areas were included. The dietary cadmium intake was estimated by a food survey. Blood cadmium, urinary cadmium and renal function markers (microalbuminuria, N-acetyl-β-d-glucosaminidase [NAG] and its isoform B [NAGB], β2 -microglobulin and retinol binding protein) in urine were measured. We calculated the 95% lower confidence bounds of BMD (BMDLs) of cumulative cadmium intake. In control and two polluted areas, the median cumulative cadmium intake was 0.5, 2.1 and 11.1 g. The odds ratio of the intermediate (1.0-3.0 g), second highest (3.0-11.0 g) and the highest cumulative cadmium intake (>11.0 g) compared with the lowest cumulative cadmium intake (

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.

Almost one in ten Chinese adults has chronic kidney disease (CKD). However, the link between dietary patterns, dietary cadmium intake and CKD has not been studied in China.Adults (n = 8429) in the China Health and Nutrition Survey who had at least one 3-day 24 h food record in combination with household food inventory in 1991, 1993, 1997, 2000, 2004, 2006, and 2009 and estimated glomerular filtration rate (eGFR) measured in 2009. Dietary pattern was identified using factor analysis. CKD was defined as eGFR60 mL/min/1.73 mThere were 641 (7.6%) cases of CKD in the sample. After adjustment for demographic, lifestyle factors (i.e. smoking, alcohol drinking, physical activity) and chronic conditions, the odds ratio (OR) for CKD was 4.05 (95%CI 2.91-5.63, p for trend0.001) for extreme quartiles of estimated cumulative cadmium intake. A traditional southern dietary pattern (high intake of rice, pork, and vegetables, and low intake of wheat) was associated with more than four times increased prevalence of CKD (comparing extreme quartiles, OR 4.56, 95%CI 3.18-6.56). A modern dietary pattern (high intake of fruit, soy milk, egg, milk and deep fried products) was inversely associated with CKD (for extreme quartiles, OR 0.5, 95%CI 0.36-0.71). The association between dietary patterns and CKD were attenuated by cadmium intake.Traditional southern dietary pattern is positively associated, and modern dietary pattern is inversely associated, with CKD among Chinese adults. However, these associations can be partly attributed to cadmium contamination in parts of the food supply.

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.

The decline of cadmium pollution in fish farms is needed by any adequate method. The present study was designed to explore the effect of dietary cadmium contamination and its amelioration by using dietary clay, probiotic (Bactocell®), vitamin C, and vitamin E supplementation in Nile tilapia fish diet on growth rate, feed efficiency, blood components, and cadmium residues. Fish were separated into 15 groups, each group of fish was stocked into three aquaria and each contains 20 fishes. The fish of the first five groups were fed the basal diet, the second five groups were fed the basal diet contaminated with 25 mg cadmium/kg, and the third five groups were fed the same diet contaminated with 50 mg cadmium/kg. Within each dietary cadmium level, the first group was fed the diet without any supplementation, the second was fed the diet supplemented with natural clay (bentonite) at level 3%, the third group was fed the diet supplemented with 1 g Bactocell®/kg, the fourth group was fed the diet supplemented 50 mg vitamin E/kg, and the fifth group was fed the diet supplemented with 100 mg vitamin C/kg. Live body weight, daily body weight gain, and feed intake of Nile tilapia decreased significantly (P

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 (Cd) is a widely distributed toxic metal, which is mainly exposed to humans through diet. The impact of dietary guidelines on the Chinese diet structure has indirectly led to changes in dietary Cd exposure. The Chinese Dietary Guidelines were issued in 1997 and revised in 2007. Based on the time between issuance and revision, this study examined the Cd contamination levels in Shanghai foods from 1988 to 2018 and evaluated cancer risk and disease burden of dietary Cd exposure accordingly. Over the time periods of 1988-1997, 1998-2007, and 2008-2018, it was found that Cd dietary exposure of Shanghai residents showed a trend of increasing and then decreasing (39.7, 44.7, and 36.4 μg/day, respectively). In contrast to cereals, the contribution rates of meat and vegetables to Cd exposure have gradually increased over time, and aquatic foods have become the main source of Cd exposure (40.6%). Although the non-cancer risk hazard quotients of dietary Cd exposure and the excess lifetime cancer risks (ELCR) are relatively low (HQ 1, ELCR 10

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.

This study was conducted to investigate the adverse effects of cadmium (Cd) on the production performance, serum biochemistry, liver antioxidant status, histopathology, and egg residue in laying hens. A total of 72 healthy Hy-Line brown laying hens at 40-week-old were randomly assigned to four diets containing 0 (control diet), 15, 30, or 60 mg/kg Cd for 6 weeks. Laying hens exposed to 60 mg/kg Cd had lower egg production rate and worse feed to egg ratio (P < 0.05). Dietary Cd exposure (≥ 15 mg/kg) significantly decreased hepatic glutathione peroxide (GPX) activities, while increasing malondialdehyde (MDA) (P < 0.05). Hepatic histopathology and ultrastructure also showed damage and the symptoms were exacerbated in a dose-dependent manner. The residue of Cd in the yolk was increased with increasing dietary Cd concentration. The mRNA expression levels of mt4L, mt3, sod1, sod2, gpx1, gpx3, and gpx4 in the liver of laying hens exposed to 60 mg Cd/kg feed were significantly decreased (P < 0.05). In conclusion, dietary Cd exposure at ≥ 15 mg/kg induced hepatic damage in laying hens, indicating that the content of Cd in feed must be critically controlled.

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

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