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Effects of dietary cadmium and copper on feeding and growth rates of adult Helix engaddensis snails were studied for a 1-month period. The concentrations of cadmium were 0, 50, 100, 200, 400, and 800 microg Cd/g dry food, while those of copper were 0, 4, 20, 100, 500, and 2500 microg Cu/g dry food. Both metals inhibited feeding and growth rates significantly after 1 week and 3 weeks of exposure to Cd and Cu, respectively. Inhibition caused by Cd was found to be irreversible, which indicates toxicity, while that of Cu was reversible, indicating starvation because snails identified and refused to consume contaminated food. After 4 weeks of exposure, the NOEC of Cd was 50 microg/g and the LOEC was 100 microg/g, while those for Cu were 20 and 100 microg/g, respectively. EC50,75,90,100 (growth and feeding) values were calculated, and indicated that H. engaddensis snails are suitable for short-term toxicity bioassays.

Bioaccumulation of cadmium (Cd) by oval squid, Sepioteuthis lessoniana, the relative contributions of Cd in water and food to bioaccumulation, and the distribution of cadmium among organs were studied. In a bioconcentration test, oval squid was exposed to 0.2 mg Cd/l seawater for 14 days, then was reared in Cd-free seawater for 14 days. After the exposure and elimination periods, the Cd concentrations in the whole body were 3.10 ± 0.18 and 1.90 ± 0.05 μg/g wet weight (ww), respectively. The bioconcentration factor (BCF) was 15.5 after exposure for 14 days. The liver exhibited the highest Cd concentration ( 49.3 μg / g ww), and had the highest proportion of organ Cd content (42.8%) to whole-body burden at the end of the exposure period. In a biomagnification test, oval squid was exposed to 0.12 mg Cd/l seawater for 15 days and was simultaneously fed mummichog, Fundulus heteroclitus, that were simultaneously exposed to the same Cd concentration. For a further eight days the squid was kept in Cd-free seawater and was fed mummichog that were also kept in Cd-free seawater. After the exposure and elimination periods, the Cd concentrations in the whole body were 4.18 ± 0.69 and 2.80 ± 0.44 μg/g ww, respectively. The concentration of whole-body Cd in the oval squid that was derived from water was estimated at 1.86 μg / g ww after calculation of a BCF from the bioconcentration test. The contribution of Cd derived from water to the whole-body Cd burden appeared similar to that of the Cd derived from food. In the biomagnification test, the liver Cd concentration ( 58.8 μg / g ww) and its proportion of the whole-body Cd concentration (40.6%) were the highest among those of all the organs after exposure for 15 days, regardless of the uptake route. Because wild squid seem to be exposed to much lower Cd concentrations in water and are subjected to similar Cd concentrations in their prey, compared with squid of the present study, the main Cd source for squid would appear to be dietary.

The influence of elevated dietary zinc and/or selenium on the suppressive effect of cadmium on egg production in hens has not been previously established. To address this question, two models of cadmium administration were used to differentiate protective effects of zinc or selenium that may result from a reduced absorption of cadmium from those resulting from an elevated nutritional status of these minerals. First, cadmium-induced suppression of egg production was produced in White Leghorn hens using intraperitoneal injections of Cd in order to determine protective effects that result from prefeeding diets supplemented with 803 ppm Zn, 0.91 ppm Se, or their combination relative to a basal diet (control). Feeding elevated dietary selenium throughout the experiment, including a 6-day prefeeding period before Cd administration, resulted in significant protection from the egg suppression produced by 2 injections of cadmium (0.27 mg/kg each) given 1 d apart. Feeding elevated dietary zinc alone or combined with +0.91 ppm Se for a similar period did not markedly protect against cadmium-induced egg suppression. After a 0.54-mg/kg dose of Cd was administered, for a cumulative dose of 1.08 mg/kg, no significant protection was observed from any of the supplemented diets. In a second experiment, the protective effect of the same dietary treatments on the egg-suppressive effect of dietary cadmium was determined. In contrast to cadmium injection, the suppressive effect of 153 ppm dietary cadmium was not mitigated by selenium supplementation, while supplemental zinc protected against this effect of dietary cadmium regardless of the amount of selenium in the diet. There was no significant change in plasma estrogen and vitellogenin levels as a result of cadmium administration in either model, with the exception of significant reduction in both these parameters in the dietary cadmium-exposed birds fed the basal diet. Together, the data suggest that the level of dietary zinc in food sources may be more important in influencing cadmium-induced egg suppression than the nutritional status of zinc in cadmium-exposed birds. In contrast, the nutritional status of selenium in cadmium-exposed birds may have the potential to mitigate this effect, but high exposures to dietary cadmium or zinc may preclude such protection.

The administration of cadmium, as food supplement, its bioaccumulation, and the effects on the development of tilapia Oreochromis niloticus were investigated. The average size and weight and its behavior compared with controls were investigated during the period January 31, 1997, until March 31, 1999. At intervals of 60 days the measurements of size and weight were performed, and the concentration of cadmium in feces, water, muscular tissue, and viscera were determined by atomic absorption spectroscopy. The initial average cadmium concentration in food was 5 mg small middle dotkg(-1) and only after 6 months a small effect on size and weight could be observed. With increases in cadmium concentration to 50 mg small middle dotkg(-1), beginning after the 7th month, and 100 mg small middle dotkg(-1) after the 16th month, a clear difference in size and weight and also in behavior could be observed. An LC(50) value of 40 mg small middle dotkg(-1) was observed after the 23rd month.

Cadmium levels were determined in 59 baby food samples, including milk-based, cereal and milk-based and soy-based formulas, recommended from 0 to 18 months of age. Determinations were performed by Zeeman graphite furnace atomic absorption spectrophotometry, after dry ashing, with parallel determinations of certified reference samples. Mean cadmium levels were found to range from 1.10 to 23.5 micrograms/kg fresh weight concentrated formulas. Levels were related to the composition of the diets. Formulas based on cow's milk had the lowest concentrations. Soy formulas contained approximately six times more cadmium than cow's milk formulas, and diets with a cereal content had 4-21 times higher mean levels. The mean weekly intakes of dietary cadmium were estimated to vary between 0.10 and 3.05 micrograms/kg body weight of the child, if the recommended amount of formula were to be consumed at the recommended age, and if the child were of average weight. This estimation however does not include the contribution of cadmium from drinking water. The highest intake on a body weight basis was found in 6-month-old children, consuming the recommended amount of wheat-, oat- and milk-based formulas. This intake is below the provisional tolerable weekly intake (PTWI) of 7 micrograms/kg body weight, established by a WHO/FAO expert group. However, the risk assessment is based on renal effects in adults. Furthermore, preparations of a formula by adding water with cadmium concentrations at the WHO guideline level could lead to intakes at the PTWI level. Compared to breast-fed children, the exposure of dietary cadmium from weaning diets can be up to 12 times higher in children fed infant formula.

In vitro and in situ findings suggest an impairment of digestive and absorptive functions in the small intestine by enteral cadmium salts. In the rat, diets with up to 1 mmol Cd/kg are well tolerated, however, so that the impairment might not be this drastic or compensated by adaptive changes. To elucidate whether small intestinal functions are altered, we studied the effect of dietary cadmium on the longitudinal pattern of mucosal enzymes and the in vitro uptake of methyl alpha-D-glucoside in the small intestine of female rats. Three groups of rats were employed, a control group and two groups receiving dietary CdCl2 either at 0.3 or 1.0 mmol Cd/kg of diet. Rats were killed after 1 week of feeding. The entire small intestine was removed, rinsed with ice-cold saline and divided into 12 segments of equal length. Mucosal scrapings from each segment were used to measure mucosal cadmium levels, sucrase, lactase, alkaline phosphatase, glycylleucine-hydrolase, and diamine oxidase activities. Sugar uptake was determined in vitro in all segments using everted rings tissue accumulation method. Although cadmium levels in the mucosa were high (100 ng Cd/mg protein or100 micromol Cd/kg WW) most enzyme activities were only slightly changed. When significant decreases in activity were detected, they were only observed in the proximal small intestine. Sugar uptake was also impaired only in proximal segments, the maximal transport capacity was reduced by approximately 20%. These findings suggest that cadmium even at dietary levels of 1 mmol/kg do not lead to a drastic impairment of digestive and absorptive functions in the small intestine and that in the rat presently observed, mostly proximal impairments are easily compensated by unaltered distal functions. Certainly, absorption of micronutrients, for which an impaired proximal function cannot be compensated, e.g. iron, might be critical in this respect.

Three experiments were conducted with Atlantic salmon (Salmo salar) to assess the effects of dietary exposure to copper and cadmium. The results presented here provide an overview, details of each experiment will be published in full elsewhere. In the first experiment, salmon parr exposed for four weeks to 35 and 700 mg Cu kg−1 diet had significantly elevated intestinal copper concentrations, cell proliferation (PCNA) and apoptosis rates compared to control fish. No differences were observed in gill or plasma copper concentrations among the groups. In contrast to the controls, the Cu exposed groups did not grow significantly during the exposure period. The second experiment (three months exposure) was conducted to assess the effects of dietary copper (control, 35, 500, 700, 900 or 1750 mg Cu kg−1 diet) on growth and feed utilization in salmon fingerlings. Growth was significantly reduced after three months exposure to dietary Cu concentrations above 500 mg kg−1. Similarly, copper body burdens were significantly higher in fish exposed to elevated dietary copper concentrations (above 35 mg Cu kg−1 diet). In the third experiment, salmon parr were exposed to one of six dietary cadmium concentrations (0, 0.5, 5, 25, 125 or 250 mg Cd kg−1 diet) for four months. Cadmium accumulated in the liver>intestine>gills of exposed fish. Rates of apoptosis and cell proliferation in the intestine increased following exposure to dietary cadmium. Exposure to elevated concentrations of dietary cadmium had no effect on growth in salmon parr. Results from these studies indicate that cellular biomarkers have potential as early warning signs of negative effects on the overall fitness of an organism.

Metallothionein (MT) and cadmium (Cd) contents were determined in the subcellular fractions of the liver and kidneys of bank voles exposed for 6 weeks to elevated levels of dietary Cd-40 and 80 μg g-1 dry weight. Hepatic and renal MT was detected exclusively in the cytosol, while Cd was found in the cytosol (73–79% of the total content), nuclei (14–18%) and particulates (4–9%). The concentration of MT in the cytosol as well as Cd content in the particular subcellular fractions appeared to be a dose-dependent. The absence of MT in the nuclear and particulate fractions implied that Cd present in these compartments was not bound to the protein that is considered to provide protection against the toxic metal. Therefore, it is assumed that this component of intracellular Cd could be responsible for the histopathological changes that occurred in the liver (granuloma and focal hepatocyte swelling) and kidneys (focal degeneration of proximal tubules) of bank voles exposed to the higher level of dietary Cd.

The influence of dietary cadmium on the accumulation and effects of dietary lead, examined in chicken. This experiment was conducted to investigate the toxic effects of dietary Cd and Pb on chick's body weight and organ, content of the tissues of these two metals was also detected. One day age chicks of Gallus gallus domesticus fed diet supplemented with 25, 50, 100 ppm of Cd, second group exposure to 300, 500, 1000 ppm of Pb in feed daily during 4 weeks. The control groups were fed without supplementation of metals. The concentrations of Cd and Pb resulted in increased of Cd and Pb content in liver, gizzard and muscle. While Cd 100 ppm and Pb 1000 ppm were increased metals content in feather. Body weight of chicks was not influenced by Cd treatment. In contrary Pb treatment was significantly (p < 0.05) decreased body weight of chicks after dietary treatment. On the other hand, Liver weigh in chicks was significantly (p < 0.05) decreased after Cd and Pb treatments.

International audience; : Abstract To address the impact of cadmium sulphide nanoparticles (CdSNPs) of two different sizes (8 and 50 nm), Danio rerio zebrafish were dietary exposed to very low doses: 100 or 40 ng CdSNPs/day/g body weight for 36 or 60 days, respectively. The results obtained using RAPD-PCR genotoxicity test showed genomic alteration since the number of hybridisation sites of the RAPD probes was significantly modified after CdSNPs exposure. In addition, selected stress response genes were either repressed or upregulated in tissues of CdSNPs-exposed fish. Mitochondrial dysfunction was also caused by the presence of CdSNPs in food. Cadmium accumulation in fish tissues (brain and muscles) could only be observed after 60 days of exposure. CdSNPs toxicity was dependent on their size and concentration.

Because of inherent genetic and physiological characteristics, the natural concentration of cadmium in the kernels of sunflowers grown in uncontaminated soils of the northern Great Plains region of the United States is higher than in most other grains. We tested the hypothesis that a habitual consumption of sunflower kernels will increase the body burden and health effects of cadmium in humans. Sixty-six men and women who reported consuming various amounts of sunflower kernels were recruited and divided by sex and kernel consumption: those who consumed less than or equal to 1 ounce(oz)/week and those who consumed more than 1 oz/week. Cadmium intake was assessed by calculation from 7-day food diaries, cadmium burden by whole blood cadmium, red blood cell (RBC) cadmium and urine cadmium concentrations, and health effects by urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG) activity and beta2-microglobulin (beta2MG). The results showed that high intakes of sunflower kernels (>1 oz/day) significantly increased the intake of cadmium (p0.05). Because normal ranges for the excretion of these protein markers have not been established, it was not possible to determine if these elevated values were meaningful. However, given the knowledge that habitual consumption of sunflower kernels with natural cadmium concentrations higher than most other food products will increase the average intake of dietary cadmium, the potential exists for an increased body burden of cadmium. Controlled feeding studies in humans should be pursued in order to determine if the body burden does indeed increase and, if so, is it a cause for concern.

Summary The availability of dietary cadmium in the form of CdCl2 was compared with the availability of cadmium naturally incorporated in the feeding yeast. The effect of feeding yeast on the availability of supplemented CdCl2 was also assessed. Seventy-two weaned male Wistar rats were used in a randomized complete block design with six littermates per block. Animals within the block were randomly assigned to experimental groups and one animal was assigned to a group euthanized to establish the initial trace element status in the organs. The experimental groups included: 1. control, standard diet (Cd, 0 mg/kg); 2. diet with 10% yeast of low Cd concentration (Cd, 0.3 mg/kg); 3. diet with 10% yeast of high Cd concentration (Cd, 6 mg/kg); 4. diet with 10% yeast of low Cd concentration + CdCl2 (Cd, 6 mg/kg); 5. standard diet + CdCl2 (Cd, 6 mg/kg). Animals had ad libitum access to water and feed for the entire duration of the experiment (8 weeks). Body weight gain and feed consumption were recorded. At the end of the experiment, animals were euthanized and the duodenum, liver, and kidney were sampled. Cadmium concentrations in the tissue samples were determined using atomic absorption spectrophotometry after dry ashing of the samples. There was an obvious increase of cadmium concentration in the organs of animals that were fed diets with elevated cadmium concentrations (experimental groups 3, 4, 5). Among these groups, no significant differences were found in cadmium concentrations in the liver and kidney. However, cadmium concentrations in the duodenum differed significantly, with the highest cadmium concentration found in animals from group 5 (CdCl2 supplement, no yeast) which suggests a higher availability of dietary cadmium in the form of CdCl2 compared to cadmium incorporated in the feeding yeast. While zinc and copper concentrations in the organs examined remained unaffected by the experimental treatments, dietary cadmium reduced the iron concentrations in the duodenum and liver and this effect seemed to be alleviated by the presence of yeast in the diet. Different dietary treatments also caused differences in the liver concentrations of manganese. Zusammenfassung Der Einflus von organischem und anorganischem Diat-Cadmium auf die Verfugbarkeit von Cadmium, Zink, Kupfer, Eisen und Mangan bei Ratten Die Verfugbarkeit von Cd aus Nahrungsmitteln, die mit CdCl2 versetzt waren, wurde mit der Verfugbarkeit von naturlich aufgenommenem Cd aus Futtermittelhefe verglichen. Der Einflus von Futtermittelhefe mit zugesetztem CdCl2 wurde auch untersucht. Zweiundsiebzig entwohnte Wistar Ratten wurden zufallig durch ein vollstandiges Block-design mit jeweils 6 Wurfen pro Block ausgewahlt. Tiere innerhalb eines Blocks wurden zufallig den experimentellen Gruppen zugeordnet. Ein Tier wurde getotet, um die Ausgangskonzentrationen der Spurenelemente in den Organen zu bestimmen. Die Versuchsgruppen beinhalten: 1. Kontroll – Standardfutter mit (Cd, 0,0 mg/kg), 2. Futter mit 10% Hefe mit niedriger Cd-Konzentration Cd (Cd, 0,3 mg/kg); 3. Futter mit 10% Hefe mit hoher Cd-Konzentration Cd (Cd, 6,0 mg/kg); 4. Futter mit 10% Hefe mit niedriger Cd-Konzentration + CdCl2 (cD, 6,0 MG/KG); 5. sTANDARDNAHRUNG + cDcL2 (cD, 6,0 MG/KG). Die Tiere hatten Warend der ganzen Experimentdauer (8 Wochen) ad libitum Zugang zum Futter und Wasser. Zum Ende der Versuchsperiode wurdendie Tiere getotet und der Zwolffingerdarm, die Leber und die Nieren entnommen. Die Cd-Konzentration in den Gewebeproben wurde mit der Aas nach einer Trockenveraschung bestimmt. Es gab einen nennenswerten Anstieg der cd-Konzentration in den Organen der Tiere, die mit dem futter mit Erhohtem Cd-Gehalt gefuttert wurden (Gruppen 3, 4, 5). Zwischen diesen Gruppen wurden keine signifikanten Unterschiede der Cd-Konzentration in der leber und den Nieren gefunden. Dagegen unterschieden sich die Cd-Konzentration des Zwolffingerdarms signifikant, mit dem Hochsten Gehalt in der 5. Gruppe (Cdcl2 Zugabe ohne Hefe), was auf eine Hohere Verfugbarkeit des Gefutterten Cd in form von Cdcl2 im Vergleich zur Cd-Aufnahme aus futtermittelhefe Schliesen LasT. Wahrend die Zn-und Cu-Konzentration in den untersuchten Organen nicht durch die Rationen Beeinflust wurden, reduzierte das aufgenommene Cd den Fe-Gehalt im Zwoulffingerdarm und in der Leber. Dieser Effekt wird durch die Hefe in der Diat abgeschwacht. Unterschiedliche Futtermittelbehandlungen verursachten Auserdem Unterschiedliche Mn-Konzentration in der Leber.

Little is known regarding the interactions between iron and cadmium during postnatal development. This study examined the effect of altered levels of dietary iron and cadmium loading on the distribution of cadmium and iron in developing rats ages 15, 21, and 63 days. The uptake of iron, transferrin, and cadmium into various organs was also examined using 59Fe, [125I]transferrin, and 109Cd. Dietary cadmium loading reduced packed cell volume and plasma iron and nonheme iron levels in the liver and kidneys, evidence of the inducement of an iron deficient state. Dietary iron loading was able to reverse these effects, suggesting that they were the result of impaired intestinal absorption of iron. Cadmium loading resulted in cadmium concentrations in the liver and kidneys up to 20 microg/g in rats age 63 days, while cadmium levels in the brain reached only 0.16 microg/g, indicating that the blood-brain barrier restricts the entry of cadmium into the brain. Iron loading had little effect on cadmium levels in the organs and cadmium feeding did not lower tissue iron levels in iron loaded animals. These results suggest that cadmium inhibits iron absorption only at low to normal levels of dietary iron and that at high levels of intake iron and cadmium are largely absorbed by other, noncompetitive mechanisms. It was shown that 109Cd is removed from the plasma extremely quickly irrespective of iron status and deposits mainly in the liver. One of the most striking effects of cadmium loading on iron metabolism was increased uptake of [125I]transferrin by the heart, possibly by disrupting the process of receptor-mediated endocytosis and recycling of transferrin by heart muscle.

The purpose of this investigation was to assess the impact of dietary cadmium on morphine-induced changes in locomotor activity. Adult male rats were exposed ad libitum to an adulterated food supply containing 100 ppm added cadmium chloride, or an identical diet containing no added cadmium, for 45 days prior to testing for the locomotor activating effects of successive daily morphine administration (0, 5, 10, or 20 mg/kg per session) on locomotor activity. On day 1 of testing, increasing doses of morphine produced a dose-related suppression of activity, and this sedative effect was greater in control than in cadmium-exposed animals. Repeated morphine administration resulted in tolerance to the sedative effects of the drug, and a systematic elevation of locomotor activity over the 14-day testing period was observed, with the augmentation (sensitization) effect more pronounced in control than cadmium-exposed animals. There was no indication that conditioning (context) events played a role in the effects observed here.

As a simulation of etiological factors known for Itai-Itai disease, female mice were subjected to the individual and combined stresses of dietary cadmium, nutrient-deficient diet, multiparity and ovariectomy. From age 68 days, female mice were maintained on either nutrient-sufficient (+) or -deficient (-), purified diets containing either 0.25 (environmental), 5, or 50 ppm Cd as CdCl(2); the nutritional composition of (-) diet simulated that of food consumed by Japanese women who contracted Itai-Itai disease. At age 70 days, half of the mice began a breeding regimen of six consecutive, 42-day rounds of pregnancy/lactation (PL mice); the remainder were maintained as virgin, non-pregnant controls (NP mice). Limited numbers of PL and NP mice were sacrificed at the end of each reproductive round. PL(+) mice taken in a given round had successively borne litters in that round and all preceding ones. PL(-) females taken at the end of round (R)-1, -2 and -3 had successively borne litters through those rounds; those taken at the end of R-5 or -6 had nonsuccessively borne litters in four of five or three of six rounds, respectively. At the end of the 252-day reproductive period, remaining females entered the 392-day, post-reproductive phase of the experiment. At age 546 days (mid-R-12), PL females having successfully borne at least three litters were ovariectomized (OV) to mimic human menopause, while NP females were either ovariectomized or sham-operated (SO). After surgery, all females were maintained to age 714 days (mid-R-16), then sacrificed. Food consumption, monitored on a weekly basis over the first nine rounds, was in general not significantly affected by dietary Cd level or nutrient deficiencies for females of the same reproductive status; consumption was increased about 2.5-fold in PL versus NP groups during the reproductive period and about 1.4-fold during the post-reproductive period. Over the reproductive period, small increases in liver concentrations of Zn and Cu were observed (ca. 3.1- and 2.5-fold, respectively) with far larger increases for Cd (ca. 22200-fold). Threshold hepatic Cd concentrations below which the concentrations of Zn and Cu were relatively constant and independent of Cd concentration were identified; they were 2.7 microg Cd/g liver for Zn and 3.3 microg Cd/g liver for Cu for females consuming (+) diet, and 4.9 microg Cd/g liver for Zn and 4.5 microg Cd/g liver for Cu for females consuming (-) diet. Regardless of Cd exposure level, round-by-round hepatic concentrations of Cd were generally 2- to 6-fold higher in PL than NP mice, while Zn or Cu levels were generally only 1.1- to 2.5-fold higher. For each reproductive round, hepatic concentrations of Cd in NP females were consistently about 10-fold greater in mice exposed to 50 than 5 ppm dietary Cd: corresponding Zn levels were essentially equivalent. For PL females. Cd levels were about 7-fold greater in 50 than 5 ppm Cd-exposed groups, however Zn concentrations were about 45% decreased. The pattern of Cd, Zn and Cu sequestration established during the reproductive period clearly differed from that of the post-reproductive period. Between R-6 and -16, hepatic concentrations of Cd, Zn and Cu appreciably decreased (14-69%) in 5 ppm Cd-exposed NPOV and PLOV females regardless of diet-type consumed. At the 50 ppm Cd level, Cd and Zn concencentrations dramatically rose with increases in Cd (37-129%) exceeding those of Zn (12-21%).

Glutathione S-transferases (GSTs) and carboxylesterases (CarEs) play important roles in the detoxification of endogenous and exogenous compounds. In this study, the biochemical effects of dietary cadmium (Cd) on the activities of GST and CarE in different developmental stages of the rice grasshopper Oxya chinensis Thunberg were studied. The results showed that the effects of the Cd concentration and developmental stage on GST activity were statistically significant. GST activity in O. chinensis increased at the highest Cd concentration in most nymphs, suggesting that GST is typically inducible by Cd. However, GST activity was inhibited in adults under Cd stress owing to life-stage-specific physiological characteristics. The results showed that the substrates, developmental stage, and Cd concentration had statistically significant effects on CarE activity. In most studies of CarE activity, the interaction between any two studied factors was statistically significant, although the interaction effects of the substrates, developmental stages, and Cd concentrations were not significant, which implied that the insect physiological condition and the external environmental may affect CarE activity. The results suggest that the insect's life stage and enzyme substrates should be considered when enzyme activity under Cd stress is studied.

Cadmium uptake takes place mainly through food. Lymantria dispar larvae were exposed to dietary cadmium in concentrations of 10 and 30 mu g Cd/g dry food (NOEC, no-observed-effect and LOEC, lowest-observed-effect concentration, respectively) for acute and chronic treatment and recovery. We established that metal contamination decreased mass only during the chronic treatment at 30 mu g Cd/dry food with no recovery on removal of cadmium for 3 days. Significant reduction of protease activity was detected at LOEC after the acute and chronic treatments. Protease showed enhanced plasticity with regard to the fitness trait (mass) during environmental stress and the higher cadmium load, when it changed. The statistically significant higher index of phenotypic plasticity for protease correlated with lower variability. Protease isoforms at the same cadmium treatments differed between genotypes, while some protease isoforms from one egg-mass differed between cadmium treatments. Owing to the low sensitivity and plasticity of mass change during exposure to cadmium, as well as its small influence, we concluded that larval mass is not a good indicator of cadmium presence in food. We suggest that proteases, with further research, might be a suitable indicator of dietary cadmium contamination, as well as nutriment utilization during heavy metal stress. (C) 2013 Elsevier Inn All rights reserved. Serbian Ministry of Education, Science and Technological Development {[}173027]

Background Environmental exposure to cadmium causes renal dysfunction and bone damage. Cadmium contamination in food is regarded as the main environmental source of non-occupational exposure. The aim of this study was to assess the contribution of dietary cadmium exposure in environmental cadmium exposure and its health risk among adults in Shanghai, China. Methods A cross-sectional survey about food consumption was conducted in 2008 among 207 citizens aged over 40 years in Shanghai, China. The food frequency questionnaire was combined with food, tobacco and water cadmium exposure to estimate the daily environmental cadmium exposure in both point and probabilistic estimations. Urine and blood samples of the participants were analyzed for internal exposure to total cadmium. Correlation analysis was conducted between the internal cadmium exposure and environmental cadmium exposure. Results According to the point estimation, average daily environmental cadmium exposure of the participants was 16.7 μg/day and approached 33.8% of the provisional tolerable daily intake (PTDI). Dietary and tobacco cadmium exposure approached 25.8% and 7.9% of the PTDI, respectively. Males had higher levels of dietary cadmium exposure than females (p?=?0.002). The probabilistic model showed that 93.4% of the population did not have any health risks from dietary cadmium exposure. By sensitivity analysis, tobacco consumption, tobacco cadmium level, cadmium in vegetables and cadmium in rice accounted for 27.5%, 24.9%, 20.2% and 14.6% of the total cadmium exposure, respectively. The mean values of urinary and blood cadmium among the study population were 0.5 μg/L and 1.9 μg/L, respectively. Positive correlations were observed between environmental cadmium exposure and blood cadmium (R?=?0.52, P

Background: In vitro and animal data suggest that cadmium, a heavy metal that contaminates some foods and tobacco plants, is an estrogenic endocrine disruptor. Elevated estrogen exposure is associated with breast, endometrial, and ovarian cancer risk. Objectives: We examined the association between dietary cadmium intake and risk of these cancers in the large, well-characterized Women’s Health Initiative (WHI). Methods: A total of 155,069 postmenopausal women, 50–79 years of age, who were enrolled in the WHI clinical trials or observational study, participated in this study. We estimated dietary cadmium consumption by combining baseline food frequency questionnaire responses with U.S. Food and Drug Administration data on food cadmium content. Participants reported incident invasive breast, endometrial, or ovarian cancer, and WHI centrally adjudicated all cases through August 2009. We applied Cox regression to estimate adjusted hazard ratios (HRs) and 95% CIs for each cancer, comparing quintiles of energy-adjusted dietary cadmium intake. Results: Over an average of 10.5 years, 6,658 invasive breast cancers, 1,198 endometrial cancers, and 735 ovarian cancers were reported. We observed no statistically significant associations between dietary cadmium and risk of any of these cancers after adjustment for potential confounders including total dietary energy intake. Results did not differ in any subgroup of women examined. Conclusions: We found little evidence that dietary cadmium is a risk factor for breast, endometrial, or ovarian cancers in postmenopausal women. Misclassification in dietary cadmium assessment may have attenuated observed associations. Citation: Adams SV, Quraishi SM, Shafer MM, Passarelli MN, Freney EP, Chlebowski RT, Luo J, Meliker JR, Mu L, Neuhouser ML, Newcomb PA. 2014. Dietary cadmium exposure and risk of breast, endometrial, and ovarian cancer in the Women’s Health Initiative. Environ Health Perspect 122:594–600; http://dx.doi.org/10.1289/ehp.1307054

This study evaluated the effect of dietary cadmium (Cd) on atherosclerosis in the rabbit. Cholesterol was added to the diet to initiate and/or accelerate atherogenesis. Cd was added to the diet at two dose levels. Uptake of Cd was 55 micro gram/kg body weight (BW)/day at the low dose level and 1350 micrograms/ kg BW/day at the high dose level. Five groups of rabbits were fed five different diets for 9 months: (1) basal diet without additional constituents; (2) background diet, which was basal diet to which cholesterol had been added; (3) the low-dose level Cd diet, which was background diet to which 2 mg Cd/kg had been added; (4) high-dose level Cd diet, which was background diet to which 50 mg Cd/kg had been added; and (5) basal diet to which 50 mg Cd/kg had been added. Dietary cholesterol increased blood total leucocyte count, serum and liver total cholesterol concentrations, serum total bilirubin concentration, low-density lipoprotein vitamin E concentration and induction of atherosclerotic plaques in the aorta and coronary arteries. Cd in the diet increased liver and kidney Cd concentrations in a dose-dependent way, decreased prothrombin time and temporarily increased urea and creatinine clearances. Slight kidney damage was induced by Cd only in animals fed the high-dose level Cd diet (with or without cholesterol). Dietary Cd partly counteracted the dietary cholesterol-induced increases of serum and liver total cholesterol concentrations, and tended to reduce plaque formation in the aorta. Dietary Cd in rabbits fed cholesterol-containing diets influenced cholesterol metabolism and tended to decrease atherosclerosis in a dose-related fashion. This is in contrast with limited epidemiological human data. Dietary Cd also decreased serum ferritin concentration and increased serum transferrin concentration. Free iron concentration is associated with myocardial infarction in man and augments the development of atherosclerosis in rabbits. It is concluded that the observed reduction in atherogenesis is related to dietary Cd-induced changes in cholesterol metabolism, increased rheology of blood and/or, most likely, reduced free iron concentration.

Feeding diets with high zinc or cadmium concentrations to animals compromises their copper status. Previous work suggested that metallothionein (MT), induced in the intestinal mucosa by zinc or cadmium, binds copper and inhibits its absorption. More recent studies showed that this mechanism may not be operative for zinc and that intestinal MT adapts to long-term feeding of high-zinc diets. The present study was designed to determine the effects of feeding high-zinc and/or high-cadmium diets on the induction of intestinal MT and its subsequent effect on copper status. Six-week-old male rats were placed in a 2 × 2 × 3 factorial experiment with two concentrations of dietary zinc (60 and 350 mg/kg), two concentrations of dietary copper (3 and 9 mg/kg), and three concentrations of dietary cadmium (0, 1, and 5 mg/kg). After 3 weeks, the difference in the MT concentration between rats fed high- and normal-zinc diets was only 1.5 times. However, rats fed the highest amount of cadmium had MT concentrations about five time higher than those not fed cadmium. In both the zinc and cadmium groups, the concentration of intestinal zinc and cadmium followed that of MT; however, the copper concentrations were not changed. Although intestinal MT was not elevated appreciably in zinc-fed rats, the copper status of these rats fed 3 mg of copper/kg of diet was severely depressed. Rats fed 9 mg of copper/kg of diet were not affected. The copper status in rats fed high-cadmium and 3 mg of copper/kg of diet was depressed even more than with a high-zinc diet. This study suggests that the effects of high dietary zinc or cadmium on copper status are not the result of induced intestinal MT binding of copper thus preventing its passage into the circulation.

Heavy metals damage the structure, chemistry, and function of cells, including enzyme systems inside them. Variation in the profile of biochemical biomarkers in prevalent species should be used for assessing environmental contamination. The present study pays attention to the phosphatases present in the midgut of gypsy moth fourth instar caterpillars, which had been exposed to short- and long-term cadmium intake at 10 and 30 mu g Cd/g dry food. Chronic cadmium ingestion significantly inhibited the activity of all examined phosphatases, while only the activity of lysosomal phosphatase was acutely decreased. Total acid phosphatase activity recovered from both long-term cadmium treatments within 3 days. The low index of phenotypic plasticity was connected to high variability of plasticity. Dependence of phosphatase isoforms on genotype and duration of cadmium treatment was determined. We concluded that, with further investigations, profiling of total acid phosphatase activity, as well as the lysosomal fraction can be used as a biomarker for acute sublethal metal toxicity. Serbian Ministry of Education, Science and Technological Development [173027]

This survey was conducted in Seoul, Pusan, Chunan, and Haman in Korea to clarify cadmium and lead burden in the general Korean populations in terms of dietary intake of cadmium and lead and the concentrations of the two metals in blood. People who participated in the study were 141 healthy nonsmoking women aged 21-56 years. Determination of cadmium and lead in 24-hr food duplicates and blood samples was carried out by graphite furnace atomic absorption spectrophotometry. The geometric means for the four sites in combination were 21.2 micrograms/day for dietary cadmium, 20.5 micrograms/day for dietary lead, 1.27 ng/ml for blood cadmium, and 44.3 ng/ml for blood lead. Cadmium intake from boiled rice accounted for 23% of total daily cadmium intake. The counterpart value for lead intake from boiled rice was 12%. Blood cadmium levels and dietary cadmium intake were lower and blood lead level and dietary lead intake were higher in Korean women than in Japanese women. The values for dietary cadmium are similar to, and the values for dietary lead are somewhat lower than, the levels reported from Europe and the United States. Dietary intake was the main source of cadmium exposure, whereas lead exposure was from both ambient air and foods in the Korean population.

This study was undertaken in order to monitor the intake of lead, cadmium and mercury in different geographical areas of Spain. The intakes of four populations were estimated from their habitual diets and compared with the Provisional Tolerable Weekly Intake (PTWI) or the Acceptable Daily Intake (ADI) to estimate the health risk of toxicity. Representative market basket diets from four areas, Galicia, Valencia, Andalucía and Madrid, were collected and their contents of cadmium, lead and mercury determined. The number of different foodstuffs used in each area (64, 67, 71 and 73) was based on the number of foods providing 95% of the total energy intake. Data on the contribution of food groups to the total daily intake of heavy metals were also obtained. The daily amounts of lead in the diets were between 37 and 521 micrograms/day, the Madrid population having the highest average intake of this metal and exceeding the PTWI, because of the vegetables and cereals consumed. The average total dietary cadmium intakes--provided mainly by fish including crustacea and molluscs--were about 25-45% of the PTWI. The intake of mercury, which is mainly provided by the fish group (66-90%), was about 9-17% of the PTWI.

Background: Experimental data convincingly propose the toxic metal cadmium as a prostate carcinogen. Cadmium is widely dispersed into the environment and, consequently, food is contaminated. Methods: A population-based cohort of 41 089 Swedish men aged 45–79 years was followed prospectively from 1998 through 2009 to assess the association between food frequency questionnaire-based estimates of dietary cadmium exposure (at baseline, 1998) and incidence of prostate cancer (3085 cases, of which 894 were localised and 794 advanced) and through 2008 for prostate cancer mortality (326 fatal cases). Results: Mean dietary cadmium exposure was 19 μg per day±s.d. 3.7. Multivariable-adjusted dietary cadmium exposure was positively associated with overall prostate cancer, comparing extreme tertiles; rate ratio (RR) 1.13 (95% confidence interval (CI): 1.03–1.24). For subtypes of prostate cancer, the RR was 1.29 (95% CI: 1.08–1.53) for localised, 1.05 (95% CI: 0.87–1.25) for advanced, and 1.14 (95% CI: 0.86–1.51) for fatal cases. No statistically significant difference was observed in the multivariable-adjusted risk estimates between tumour subtypes (Pheterogeneity=0.27). For localised prostate cancer, RR was 1.55 (1.16–2.08) among men with a small waist circumference and RR 1.45 (1.15, 1.83) among ever smokers. Conclusion: Our findings provide support that dietary cadmium exposure may have a role in prostate cancer development.

Background: Cadmium (Cd) is a toxic metal associated with increased morbidity and mortality. Urinary Cd (U-Cd) concentration is considered a biomarker of long-term exposure. Objectives: Our objectives were to evaluate the within-person correlation among repeat samples and to identify predictors of U-Cd concentrations. Methods: U-Cd concentrations (micrograms per liter) were measured in 24-hr urine samples collected from 296 women enrolled in the California Teachers Study in 2000 and a second 24-hr sample collected 3–9 months later from 141 of the participants. Lifestyle and sociodemographic characteristics were obtained via questionnaires. The Total Diet Study database was used to quantify dietary cadmium intake based on a food frequency questionnaire. We estimated environmental cadmium emissions near participants’ residences using a geographic information system. Results: The geometric mean U-Cd concentration was 0.27 µg/L and the range was 0.1–3.6 µg/L. The intraclass correlation among repeat samples from an individual was 0.50. The use of a single 24-hr urine specimen to characterize Cd exposure in a case–control study would result in an observed odds ratio of 1.4 for a true odds ratio of 2.0. U-Cd concentration increased with creatinine, age, and lifetime pack-years of smoking among ever smokers or lifetime intensity-years of passive smoking among nonsmokers, whereas it decreased with greater alcohol consumption and number of previous pregnancies. These factors explained 42–44% of the variability in U-Cd concentrations. Conclusion: U-Cd levels varied with several individual characteristics, and a single measurement of U-Cd in a 24-hr sample did not accurately reflect medium- to long-term body burden.

The aim of the study was to estimate the association between dietary intake of cadmium, a carcinogenic heavy metal, and risk of invasive postmenopausal breast cancer.Study subjects were 30,543 postmenopausal women in the VITamins And Lifestyle (VITAL) cohort who completed a food frequency questionnaire (FFQ) at baseline (2000-2002). Dietary cadmium consumption was estimated by combining FFQ responses with US Food and Drug Administration data on food cadmium content. Incidence of invasive breast cancer was ascertained through linkage of the cohort to the western Washington Surveillance, Epidemiology, and End Results cancer registry through 31 December 2009. Cox regression was applied to estimate adjusted hazard ratios (aHRs) and 95 % confidence intervals (CIs) for breast cancer with increasing dietary cadmium intake, adjusted for total energy intake, smoking history, consumption of vegetables, potatoes, and whole grains, multivitamin use, education, race, body mass index, physical activity, age at first birth, postmenopausal hormone use, and mammography.Vegetables and grains together contributed an average of 66 % of estimated dietary cadmium. During a mean of 7.5 years of follow-up, 1,026 invasive postmenopausal breast cancers were identified. Among 899 cases with complete covariate information, no evidence of an association between dietary cadmium intake and breast cancer risk was observed (aHR (95 % CI), highest to lowest quartile cadmium: 1.00 (0.72-1.41), p (trend) = 0.95). No evidence was found for interactions between dietary cadmium and breast cancer risk factors, smoking habits, or total intake of calcium, iron, or zinc from diet, supplements, and multivitamins.This study does not support the hypothesis that dietary cadmium intake is a risk factor for breast cancer. However, non-differential measurement error in the estimate of cadmium intake is likely the most important factor that could have obscured an association.

The ubiquitous food contaminant cadmium has features of an estrogen mimetic that may promote the development of estrogen-dependent malignancies, such as breast cancer. However, no prospective studies of cadmium exposure and breast cancer risk have been reported. We examined the association between dietary cadmium exposure (at baseline, 1987) and the risk of overall and estrogen receptor (ER)–defined (ER+ or ER−) breast cancer within a population-based prospective cohort of 55,987 postmenopausal women. During an average of 12.2 years of follow-up, 2,112 incident cases of invasive breast cancer were ascertained (1,626 ER+ and 290 ER−). After adjusting for confounders, including consumption of whole grains and vegetables (which account for 40% of the dietary exposure, but also contain putative anticarcinogenic phytochemicals), dietary cadmium intake was positively associated with overall breast cancer tumors, comparing the highest tertile with the lowest [rate ratio (RR), 1.21; 95% confidence interval (CI), 1.07–1.36; Ptrend = 0.02]. Among lean and normal weight women, statistically significant associations were observed for all tumors (RR, 1.27; 95% CI, 1.07–1.50) and for ER+ tumors (RR, 1.25; 95% CI, 1.03–1.52) and similar, but not statistically significant associations were found for ER− tumors (RR, 1.22; 95% CI, 0.76–1.93). The risk of breast cancer increased with increasing cadmium exposure similarly within each tertile of whole grain/vegetable consumption and decreased with increasing consumption of whole grain/vegetables within each tertile of cadmium exposure (Pinteraction = 0.73). Overall, these results suggest a role for dietary cadmium in postmenopausal breast cancer development. Cancer Res; 72(6); 1459–66. ©2012 AACR.

Chronic exposure to cadmium, which primarily occurs through diet and smoking, damages the kidneys, weakens bones, and may increase cancer risk. The metal is also an endocrine disrupter and may adversely affect reproduction and child development. Animal studies indicate cadmium induces multiple defects in developing embryos, but it is unknown whether similar effects occur in humans. However, a new study shows that maternal cadmium exposure is associated with reduced head circumference and birth weight in newborn girls [EHP 120(2):284–289; Kippler et al.]. The study used data collected from more than 1,600 pregnant women participating in the Maternal and Infant Nutrition Interventions, a food and micronutrient supplementation trial in Matlab, Bangladesh. The women provided urine samples and completed clinical examinations in early pregnancy. Information on demographics and tobacco and betel use during pregnancy also was collected, along with newborns’ sex and physical measurements. Average adult daily intakes of cadmium were estimated on the basis of rice consumption to be 25–35 µg, similar to those in other Asian countries where rice is a staple but higher than levels reported in U.S. and European women. Statistical analyses, controlled for confounding by maternal, birth, and newborn factors, suggested that for each 1-µg/L increase in maternal urinary cadmium, head circumference decreased by 0.26 cm and weight dropped by 45 g on average among newborn girls. Far smaller associations were seen for boys. Cadmium may affect fetal growth by several mechanisms, including impaired nutrient transport and endocrine disruption. Sex-based differences in specific hormone levels as well as in cadmium uptake and mechanisms of action—which have been reported in experimental studies—may have played a role in the current findings. The authors say the estimated average reductions in head circumference and weight are unlikely to be clinically significant for individual children but could have public health implications given widespread dietary cadmium exposure and adverse effects associated with reduced birth size. The main strengths of the study are its prospective design, large number of participants, wide range of exposure, and consideration of numerous confounding factors. However, the potential for unmeasured or residual confounding remained, as in all observational studies, and infants’ cadmium exposure was not directly assessed (for instance, by measuring cadmium levels in cord blood). Continuing research should follow the children to determine if growth effects are sustained through childhood and whether other health changes appear later in childhood. Asian diets high in rice consumption may lead to elevated cadmium intake, which has been linked to reduced birth size in girls.

The retention of cadmium and selenium influence on Cd retention in the muscle, liver and kidneys of hens, chickens and in eggs was studied. Cadmium (Cd) as cadmium chloride (CdCl(2)) and selenium (Se) as sodium selenite (Na(2)SeO(3)) were added to feed at dosages: group 0-control, group 1-20 mg/kg Cd, group 2-30 mg/kg Cd + 4 mg/kg Se. The birds were exposed to Cd for 8 weeks. Cadmium level in hens and cocks was found highest in the kidneys, followed by the liver and muscle. Se supplementation resulted in Cd increase in the muscle tissue and in the reduction of Cd content in the liver and in significant decrease in the kidneys (p0.05). A higher Cd level in the yolk and lower in the white was noted in both experimental groups. Nonsignificant increase of Cd in eggs was noted in experimental groups with Se supplementation. Level of cadmium in organs of 7-day-old chicks hatched from Cd-treated hens in both experimental groups was low but the tendency to accumulate preferentially the Cd in the liver and kidneys was recorded. Supplementation of selenium in hens and cocks was not reflected in the decrease of Cd in these two organs of F(1) chickens but was reflected in increase in the muscle. In spite of relatively high Cd levels in the organs of layers no layer-egg-chickens transfer was observed. It was confirm that kidneys and liver are organs more attacked by dietary cadmium than muscle. Supplementation of low dose of Se resulted in decrease of cadmium deposition in analyzed organs.

To investigate the toxicity of cadmium (Cd) on female reproduction in birds, this study was conducted to determine the changes in biochemical parameters of serum and ovary tissue caused by dietary cadmium in hens. Ninety 50-day-old hyline white hens were randomly divided into three groups (30 hens per group): a control group was fed with basal diet, a low dose group was fed with basal diet containing 140 mg/kg CdCl2 and a high dose group was fed with basal diet containing 210 mg/kg CdCl2. After being treated with Cd for 20, 40 and 60 days, ovary and serum samples were collected and examined for Cd content, histological evaluations, malondialdehyde (MDA) content, glutathione peroxidase (GPx) content, activities of superoxide dismutase (SOD), nitric oxide (NO) content, nitric oxide synthase (NOS) activity, and serum estradiol and progestogen levels. The results showed that the content of Cd, MDA, NO and the activity of NOS in ovary and serum were increased (P

Interactions of Cu, Cd and Zn were studied at the subcellular level in juvenile rainbow trout ( Oncorhynchus mykiss ) fed diets containing (μg/g) 500 Cu, 1000 Zn and 500 Cd singly and as a ternary mixture for 28 days. Livers were harvested and submitted to differential centrifugation to isolate components of metabolically active metal pool (MAP: heat-denaturable proteins (HDP), organelles, nuclei) and metabolically detoxified metal pool (MDP: heat stable proteins (HSP), NaOH-resistant granules). Results indicated that Cd accumulation was enhanced in all the subcellular compartments, albeit at different time points, in fish exposed to the metals mixture relative to those exposed to Cd alone, whereas Cu alone exposure increased Cd partitioning. Exposure to the metals mixture reduced (HDP) and enhanced (HSP, nuclei and granules) Cu accumulation while exposure to Zn alone enhanced Cu concentration in all the fractions analyzed without altering proportional distribution in MAP and MDP. Although subcellular Zn accumulation was less pronounced than that of either Cu or Cd, concentrations of Zn were enhanced in HDP, nuclei and granules from fish exposed to the metals mixture relative to those exposed to Zn alone. Cadmium alone exposure mobilized Zn and Cu from the nuclei and increased Zn accumulation in organelles and Cu in granules, while Cu alone exposure stimulated Zn accumulation in HSP, HDP and organelles. Interestingly, Cd alone exposure increased the partitioning of the three metals in MDP indicative of enhanced detoxification. Generally the accumulated metals were predominantly metabolically active: Cd, 67–83%; Cu, 68–79% and Zn, 60–76%. Taken together these results show both competitive and cooperative interactions dependent on the subcellular fraction, metal, exposure duration and relative metal exposure concentrations. Competitive interactions likely result from ionic mimicry with the metals displacing each other from common binding sites, whereas cooperative interactions suggest increased abundance of metal binding sites and/or existence of metal-specific non-interacting binding sites in some of the fractions. Moreover, the changes in subcellular distribution of the biometals Cu and Zn due to Cd exposure together with the shifts of the metals between MAP and MDP observed may have toxicological consequences.

Osteoporosis and its main health outcome, fragility fractures, are large and escalating public health problems. Cadmium, a widespread food contaminant, is a proposed risk factor; still the association between estimated dietary cadmium exposure and bone mineral density (BMD) has never been assessed. Within a sub-cohort of the Swedish Mammography Cohort, we assessed dietary cadmium exposure based on a food frequency questionnaire (1997) and urinary cadmium (2004-2008) in relation to total-body BMD and risk of osteoporosis and fractures (1997-2009) among 2676 women (aged 56-69 years). In multivariable-adjusted linear regression, dietary cadmium was inversely associated with BMD at the total body and lumbar spine. After further adjustment for dietary factors important for bone health and cadmium bioavailability--calcium, magnesium, iron and fiber, the associations became more pronounced. A 32% increased risk of osteoporosis (95% CI: 2-71%) and 31% increased risk for any first incident fracture (95% CI: 2-69%) were observed comparing high dietary cadmium exposure (≥13 μg/day, median) with lower exposures (

A model previously developed in the laboratory to predict chronic bioaccumulation and toxicity of cadmium to Hyalella azteca from a diet of periphyton was validated by comparing predictions with measurements of Cd in two exposure scenarios: laboratory-cultured H. azteca exposed for 28 d to field-contaminated water and periphyton, and Cd measured in field-collected H. azteca. In both exposure scenarios, model predictions of bioaccumulation were shown to be robust; however, effects on Cd bioaccumulation from complexation with dissolved organic carbon (DOC) and inhibition of Cd bioaccumulation by Ca2+ must be incorporated into the model to permit its wider application. The model predicted that 80 to 84% of Cd in H. azteca came from periphyton when H. azteca were chronically exposed to dissolved Cd in lake water at 2.63 to 3.01 nmol/L and periphyton at 1,880 to 2,630 nmol/g ash-free dry mass. Dietary Cd contributed markedly to the model-predicted decrease in 28-d survival to 74% at environmental Cd concentrations in food and water. In reality, survival decreased to 10%. The lower than predicted survival likely was due to the higher nutritional quality of periphyton used to develop the model in the laboratory compared with the field-collected periphyton. Overall, this research demonstrated that Cd in a periphyton diet at environmental concentrations can contribute to chronic toxicity in H. azteca. Environ. Toxicol. Chem. 2011;30:2628–2638. © 2011 SETAC

The effect of various dietary cadmium levels on iron metabolism in growing male Wistar rats was studied in a 6-week experiment. The diets contained 0, 6, 11 and 24 μg Cd/g diet and equal iron concentrations (approx. 33 μg/g). The increase in dietary cadmium from 6 to 24 μg/g resulted in its higher concentration in liver, kidney and duodenum. The highest level of cadmium in the diet decreased significantly diet consumption. All cadmium doses caused inhibition in rat growth, decrease in liver weight and ceruloplasmin concentration in plasma. Hematocrit, liver and duodenum iron concentrations were statistically lower in all cadmium-treated groups, while the transferrin concentration in plasma was higher and the saturation of transferrin with iron was markedly lower when compared to the control group. Two higher doses of cadmium (11 and 24 μg/g) caused a marked reduction of the apparent absorption of iron, hemoglobin concentration as well as iron storage in kidney.

A prospective follow-up study was carried out to assess the prognosis of renal tubular function after reduction of environmental cadmium exposure. Time-related changes in urinary beta 2-microglobulin and cadmium excretion were followed from 1979 to 1989 in 102 residents of a cadmium-polluted area in Nagasaki, Japan. The average dietary cadmium intake among the study population was more than 200 micrograms/d in 1969, which decreased to approximately half that amount in 1983 because cadmium-polluted paddy fields were replaced with new soil in 1981. The geometric mean urinary beta 2-microglobulin concentration for 28 subjects aged 40 y or older in 1979 increased from 1,135.8 micrograms/g creatinine in 1979 to 1,999.7 micrograms/g creatinine in 1989. A similar tendency was also observed in 16 subjects with urinary beta 2-microglobulin concentrations greater than 1,000 micrograms/g creatinine in 1979, although the statistical significance of the difference did not reach the 5% level, probably because of the small sample size. In 48 persons examined in 1982, 1986, and 1989, the geometric mean of urinary cadmium concentration decreased from 8.49 micrograms/g creatinine in 1982 to 6.03 micrograms/g creatinine in 1989. The tendency for increasing beta 2-microglobulin excretion observed in the present study could not be explained by aging alone. Thus, it was concluded that renal tubular dysfunction caused by environmental cadmium was irreversible and slowly progressive, even after reduction of exposure. Six of 8 subjects who had severe renal dysfunction and who were included in the study died before 1986 and could not be followed. The implication of loss of subjects because of death is also discussed.

Blood samples and 24-h duplicates of food were collected in the years around 1980 and then in 1990's from inhabitants of nonpolluted regions in Japan. The 1990 study is still in progress with 286 blood samples and 125 food duplicates already collected from 7 regions. A preliminary analysis is made in the present study with the data obtained from the 7 study regions where the survey was conducted in 1980 and then in 1990, to examine possible changes in dietary cadmium intake (Cd-D) and consequently cadmium levels in blood (Cd-B) during this 10 year period. The food duplicate analysis showed that Cd-D in 1980 was 47.1 μg/day (1.74):65 [GM (GSD):N] for men and 27.7 μg/day (1.75):65 for women. The counterpart values in 1990 were 29.5 μg/day (1.66):40 for men and 23.8 μg/day (1.73):85 for women; the difference between the two values for the same sex is significant (P

The effects of cadmium on the enzyme activity of the Mixed Function Oxidase (MFO) system was studied in female and male starlings (Sturnus vulgaris) fed with diets containing 10 and 50 ppm CdCl2. Inhibition of cytochrome P‐450 was observed only in females. Increases in the activity of NADPH‐cytochrome‐c reductase (in both sexes), and NADH‐cytochrome‐c reductase (only in males) were significant in Cd‐fed groups. Cytochrome P‐450 levels and NADH‐cytochrome‐c reductase activity showed significant differences between sexes, the control females having higher levels than the control males. The results of the present study suggest that exposure to cadmium at doses comparable to those observed in polluted areas could exert an adverse effect on the MFO enzyme system. Constitutional differences between sexes in MFO enzyme levels suggest caution in the interpretation of field monitoring data.

International audience; The aim of this study was to estimate the dietary cadmium (Cd) intake of the Belgian adult population, to compare this dietary Cd exposure to the tolerable weekly intake (TWI) recently established by the European Food Safety Authority (EFSA) and to determine the major food groups that contribute to dietary Cd exposure in Belgium. Food consumption data were derived from the 2004 Belgian food consumption survey (two 24h recalls, 3,083 participants). Cadmium concentrations in food items (n= 4,000) were gathered from the control program of the Belgian Federal Agency for the Safety of the Food Chain for the period 2006-2008. Dietary intake per individual was calculated from consumption data and median Cd concentrations. The population mean, median and 95th percentile of the dietary intake values were 0.98, 0.85 and 2.02 µg kg-1 body weight per week respectively. Two percent of the Belgian adult population has a dietary Cd intake above the recent TWI of 2.5 µg kg-1 body weight established by EFSA. Cereal products and potatoes contribute for more than 60% to Cd intake.

Recent evidences suggest that dietary cadmium (Cd) uptake likely occurs via the dietary iron (Fe) uptake pathway in freshwater fish, at least in part. The present study investigated the interactive effects of dietary Cd and Fe in juvenile rainbow trout ( Oncorhynchus mykiss ). Fish were treated for four weeks with four different diets: normal Fe, high Fe, normal Fe plus Cd, and high Fe plus Cd. Physiological parameters, tissue-specific Fe and Cd level, plasma Fe status, and tissue-specific mRNA expression of transferrin, metallothioneins (MT-A and MT-B) and heat shock proteins 70 (HSP70a and HSP70b) were analyzed. Exposure to dietary Cd increased Cd burden in the following order: intestine > kidney > stomach > liver > gill > carcass. Interestingly, high dietary Fe reduced Cd accumulation in the stomach and intestine as well as in the wholebody of fish. Dietary Cd increased hepatic transferrin mRNA expression and total Fe binding capacity in the plasma, indicating the effect of Cd on Fe handling in fish. The mRNA expression of MTs and HSP70s was also increased in various tissues following dietary Cd exposure, however the response profile of different MT and HSP70 genes was not consistent among different tissues. In general, MT-A was more responsive to Cd exposure in the intestine and liver, whereas MT-B was more responsive in the kidney. Similarly, HSP70a expression was more sensitive to Cd exposure than HSP70b, particularly in the intestine. Interestingly, high Fe diet suppressed Cd-induced induction of transferrin, MT and HSP70 genes in various tissues. Overall, our study suggests that elevated dietary Fe can reduce Cd accumulation and ameliorate Cd-induced stress responses in freshwater fish.

Recent studies suggested the probable involvement of an apical iron (Fe(2+)) transporter, the divalent metal transporter-1 (DMT1), in the uptake of several divalent metals in fish. The present study examined the gastrointestinal expression of the DMT1 gene, and investigated the kinetics of Fe(2+) uptake and its interactions with cadmium and lead in isolated enterocytes of freshwater rainbow trout (Oncorhynchus mykiss). The expressions of two DMT1 isoforms (Nramp-beta and -gamma) were recorded along the entire gastrointestinal tract of fish as well as in the enterocytes. Fe(2+) uptake in isolated enterocytes was saturable and sensitive to the proton gradient and membrane potential, suggesting DMT1-mediated transport. Both cadmium and lead inhibited Fe(2+) uptake in isolated enterocytes in a concentration-dependent manner, and lead appeared to be a stronger inhibitor than cadmium. The kinetic characterization of Fe(2+) uptake revealed that the apparent affinity of uptake was significantly decreased (increased K(m)) in the presence of either cadmium or lead, whereas the maximum uptake rate (J(max)) remained unchanged-indicating that the interaction between Fe(2+) and cadmium or lead is competitive in nature. Overall, our study suggests that the uptake of dietary cadmium and lead may occur via the iron-transporting pathway in fish.

To examine possible reduction in dietary cadmium (Cd) intake, 24-h duplicates of diet were collected twice in the same village in north-eastern Japan, once in 1976-1977 (71 samples) and then in 1989 (198 samples) and analyzed for Cd contents. The statistical analysis by sex and age decade showed that there has been a significant (P less than 0.01-0.05, depending on sex and age) reduction in Cd intake during this 12-year period. The intake by men at 30-59 years was 28.8 micrograms/day (as a geometric mean of 41 samples) in 1976-1977 and 20.8 micrograms/day in 1989, indicating some 28% reduction, whereas the value for women of the same age range was 24.9 micrograms/day in 1976-1977 and 15.7 micrograms/day in 1989, with a reduction by 37%. A similar reduction in Cd contents was observed in cooked rice samples collected in 1980 and 1990 in the vicinity of the study field. Probable reasons for the improvement are discussed.

Thirty-five pigs were randomly allocated at 8 kg liveweight to seven dietary treatments consisting of no supplemental cadmium, either 0.44, 0.89, 2.21 or 4.43 mg Cd kg−1 supplied in the form of Cd Cl2, 2 1/2 H2O or either 0.60 or 1.20 mg Cd kg−1 supplied by rock phosphate. Pigs were fed protein-adequate diets on a restricted basis and were slaughtered at 90 kg liveweight. The growth rate and feed efficiency of pigs between 8 and 90 kg liveweight were unaffected by dietary cadmium level. Samples of meat, fat, liver, kidney, hair and blood collected at slaughter were analysed for cadmium and expressed on a wet tissue basis. Cadmium could not be detected in meat and fat samples (

1. Fish stressed by restrainment displayed elevated serum cortisol, copper and zinc levels; dietary cadmium had no effect. 2. Stress/dietary cadmium increased liver copper levels in a metal pool containing metallothionein and non-metallothionein proteins but decreased intestinal zinc bound as low molecular weight forms. 3. After restrainment, zinc losses occurred in dorsal skeletal muscle, ovary and spleen: copper decreased in intestine and pyloric caecum. 4. Dietary cadmium altered intestinal zinc distribution and raised hepatic Cu-binding protein levels but did not alter plasma zinc, copper or cortisol levels. 5. Alterations in zinc and copper concentrations during stress contrast with mammalian models.

Some residents of the Mae Sot district in Thailand have suffered long-term exposure to elevated dietary levels of cadmium. To test the hypothesis that chronic dietary cadmium exposure can cause imbalance in calcium dynamics and accelerate bone resorption, a group of these residents (156 men and 256 women aged ≥ 50) were selected on the basis of previous records of elevated urinary cadmium and tested for urinary and blood cadmium, bone formation and resorption markers, and the renal tubular dysfunction markers. Both genders had high levels of blood and urinary cadmium and high urinary levels of the markers for renal dysfunction and bone resorption in a dose–response relationship to urinary cadmium. The excretion of bone resorption markers was positively correlated to the ratio of excreted calcium and urinary cadmium. The results of a multivariate regression analysis indicated that bone resorption was accelerated by impaired calcium reabsorption in renal tubules.

The present study was conducted to investigate the effect of dietary cadmium (Cd) level on the growth, body composition and several enzymatic activities of juvenile yellow catfish, Pelteobagrus fulvidraco. The experimental diets were formulated with CdCl2·2.5H2O at levels of 0, 0.01, 0.1 and 1.0 g kg−1 diet, resulting in four dietary Cd levels of 0.25 (control), 4.92, 48.57 and 474.7 mg Cd kg−1 diet respectively. They were fed to juvenile yellow catfish (mean initial weight: 3.26±0.07 g, mean±SD) for 4 weeks. Weight gain, specific growth rate, feed intake and protein efficiency ratio tended to decline with increasing dietary Cd levels (P 0.05). Hepatic alkaline phosphatase, glutathione peroxidase and lactate dehydrogenase activities increased (P 0.05). The present study provided for the first time the toxic assessment of dietborne Cd in yellow catfish, based on growth performance and the changes in hepatic enzymatic activities for the fish species.

International audience; This study aimed to assess the effect of two dietary cadmium (Cd) levels (C1: 1 mg kg−1; C10: 10 mg kg−1) on bird Anas platyrhynchos exposed for 10, 20 and 40 days (5 animals per experimental condition). Ducks were able to accumulate high amounts of Cd, especially in kidneys (after 40 days: C1 8.1±1 mg kg−1, C10 37.7±4.3 mg kg−1). After 40 days, the lowest Cd level triggered oxidative stress and stimulated mitochondrial metabolism. At the same time, highest amounts of Cd (C10 group) only triggered repression of genes encoding for catalase and acetyl-CoA carboxylase, with repression factors of 1/50 and 1/5, respectively. High dose exposures were then associated with the repression of genes encoding for antioxidant, whereas low dose exposure triggered their induction. In contrast, the onset of MT gene expression appeared quickly for the C10 group even if a time delay was observed between gene expression and protein accumulation. Through the comparison of A. platyrhynchos and Cairina moschata, the response to Cd toxicity appeared species-dependent. Discrepancies between species could be explained by differential utilization of MT. This pathway of detoxification seemed sufficient to counter Cd toxicity.

Cadmium is a ubiquitous hazardous element with nephro-toxicity after long-term exposure. The present study was initiated to examine possible effects of dietary cadmium (Cd) intake on health of local residents across Japan. For this purpose, Cd in locally harvested brown rice (Cd-BR) was taken as the parameter of Cd exposure, and two measures of mortality, i.e., standardized mortality ratio (SMR) and age-adjusted renal insufficiency mortality rate (AARIMR) were employed as parameters of over-all health effects including effects on kidney. Japan consists of 47 prefectures. Data on Cd in 37,250 brown rice samples harvested in 1997–1998 in the 47 prefectures were made available from the Ministry of Agriculture, Forestry and Fisheries, Japan. SMR and AARIMR data (for the year 2000) by two genders in the 47 prefectures were cited from publications of the Ministry of Health, Labour and Welfare, Japan. Possible correlation of Cd in brown rice (Cd-BR) with SMR and AARIMR was examined by Poisson regression analysis. The geometric mean (GM) Cd-BR for Japan as a whole was 0.040 mg/kg with a geometric standard deviation (GSD) of 2.72. Prefectural GM values varied from a low of

Cadmium in soil poses a risk for human health, due to its accumulation in food and feed crops. The extent of accumulation depends strongly on soil type and the degree of pollution. The objective of the present study was to develop a predictive model to estimate human dietary cadmium exposure from soil characteristics. This chain model consists of three basic steps: (i) calculation of plant cadmium levels from soil contamination levels and soil characteristics, (ii) calculation of animal transfer from consumption and contamination levels, and (iii) human exposure from both plant and animal products. Six soil scenarios were assessed, reflecting a specific contaminated region and ranging from 0.5 mg/kg of Cd (pH 4.5) to 2.5 mg/kg of Cd (pH 5.5). Cadmium levels in feed crops and vegetables were estimated with regression and mathematical models. Animal exposure and transfer to cattle kidneys, livers, and meat were calculated using a consumption database and a parameterized linear simulation model. Human exposure was estimated by Monte Carlo simulation, using a consumption database. The median human exposure for the different scenarios ranged from 0.24 to 0.98 microg/kg of body weight per day, which is comparable to results obtained from exposure levels based on observed field contamination data. The study shows that a chain model approach from soil contamination to human exposure, including animal exposure and transfer to animal products, can successfully be applied. The model can be used for fast evaluation of dietary cadmium exposure and the identification of risk areas based on soil conditions.