Estimation of health risks associated with dietary cadmium exposure

Satarug, Soisungwan; Vesey, David A.; Gobé, Glenda C.; Phelps, Kenneth R.

doi:10.1007/s00204-022-03432-w

Cited by 33 publications

(37 citation statements)

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“…Cadmium (Cd) is an environmental contaminant of continuing public health concern worldwide because it is detectable in most food types; as such, diet forms the main source of exposure in non-occupationally exposed and non-smoking populations [1,2]. Multiple organ systems, including kidneys [1,2], bone [3], liver [4,5] and the central nervous system [6], are susceptible to the toxicity of Cd, even at low body burdens. The cytotoxicity of Cd has been demonstrated in nearly all cell types, such as erythrocytes and the tubular epithelial cells of kidneys, which are known to actively accumulate Cd [1,2,7].…”

Section: Introductionmentioning

confidence: 99%

“…Multiple organ systems, including kidneys [1,2], bone [3], liver [4,5] and the central nervous system [6], are susceptible to the toxicity of Cd, even at low body burdens. The cytotoxicity of Cd has been demonstrated in nearly all cell types, such as erythrocytes and the tubular epithelial cells of kidneys, which are known to actively accumulate Cd [1,2,7].…”

Section: Introductionmentioning

confidence: 99%

“…An elevated excretion of low-molecular-weight proteins, namely, retinol binding protein, β 2 -microglobulin (β 2 M), and α1-microglobulin (α 1 M), has been the most frequently investigated [1,2]. The protein β 2 M, with a molecular weight of 11,800 Da, is synthesized and shed by all nucleated cells in the body [21].…”

Section: Introductionmentioning

confidence: 99%

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Cadmium-Induced Proteinuria: Mechanistic Insights from Dose–Effect Analyses

Satarug

Vesey

Gobé

2023

IJMS

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Cadmium (Cd) is a toxic metal that accumulates in kidneys, especially in the proximal tubular epithelial cells, where virtually all proteins in the glomerular ultrafiltrate are reabsorbed. Here, we analyzed archived data on the estimated glomerular filtration rate (eGFR) and excretion rates of Cd (ECd), total protein (EProt), albumin (Ealb), β2-microglobulin (Eβ2M), and α1-microglobulin (Eα1M), which were recorded for residents of a Cd contamination area and a low-exposure control area of Thailand. Excretion of Cd and all proteins were normalized to creatinine clearance (Ccr) as ECd/Ccr and EProt/Ccr to correct for differences among subjects in the number of surviving nephrons. Low eGFR was defined as eGFR ≤ 60 mL/min/1.73 m2, while proteinuria was indicted by EPro/Ccr ≥ 20 mg/L of filtrate. EProt/Ccr varied directly with ECd/Ccr (β = 0.263, p < 0.001) and age (β = 0.252, p < 0.001). In contrast, eGFR values were inversely associated with ECd/Ccr (β = −0.266, p < 0.001) and age (β = −0.558, p < 0.001). At ECd/Ccr > 8.28 ng/L of filtrate, the prevalence odds ratios for proteinuria and low eGFR were increased 4.6- and 5.1-fold, respectively (p < 0.001 for both parameters). Thus, the eGFR and tubular protein retrieval were both simultaneously diminished by Cd exposure. Of interest, ECd/Ccr was more closely correlated with EProt/Ccr (r = 0.507), Eβ2M (r = 0.430), and Eα1M/Ccr (r = 0.364) than with EAlb/Ccr (r = 0.152). These data suggest that Cd may differentially reduce the ability of tubular epithelial cells to reclaim proteins, resulting in preferential reabsorption of albumin.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Cadmium-Induced Proteinuria: Mechanistic Insights from Dose–Effect Analyses

Satarug

Vesey

Gobé

2023

IJMS

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“…Additionally, according to other studies, Pb-poisoned cattle exhibit ataxia, paresis of the hypoglossal nerve, severe depression, muscle twitching, convulsions, coma, death, and respiratory failure ( 83 , 100 ). Pb is a tissue toxin that accumulates over time and is stored throughout the body but especially in the bones, the liver, the kidney, and the brain ( 101 , 102 ). A primary component of ingested blood Pb burden that raises blood Pb levels is stored Pb in the body ( 61 ).…”

Section: Heavy Metals: Their Toxicity Mechanism and Effectsmentioning

confidence: 99%

A review of important heavy metals toxicity with special emphasis on nephrotoxicity and its management in cattle

Tahir

Alkheraije

2023

Front. Vet. Sci.

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Toxicity with heavy metals has proven to be a significant hazard with several health problems linked to it. Heavy metals bioaccumulate in living organisms, pollute the food chain, and possibly threaten the health of animals. Many industries, fertilizers, traffic, automobile, paint, groundwater, and animal feed are sources of contamination of heavy metals. Few metals, such as aluminum (Al), may be eliminated by the elimination processes, but other metals like lead (Pb), arsenic (As), and cadmium (Ca) accumulate in the body and food chain, leading to chronic toxicity in animals. Even if these metals have no biological purpose, their toxic effects are still present in some form that is damaging to the animal body and its appropriate functioning. Cadmium (Cd) and Pb have negative impacts on a number of physiological and biochemical processes when exposed to sub-lethal doses. The nephrotoxic effects of Pb, As, and Cd are well known, and high amounts of naturally occurring environmental metals as well as occupational populations with high exposures have an adverse relationship between kidney damage and toxic metal exposure. Metal toxicity is determined by the absorbed dosage, the route of exposure, and the duration of exposure, whether acute or chronic. This can lead to numerous disorders and can also result in excessive damage due to oxidative stress generated by free radical production. Heavy metals concentration can be decreased through various procedures including bioremediation, pyrolysis, phytoremediation, rhizofiltration, biochar, and thermal process. This review discusses few heavy metals, their toxicity mechanisms, and their health impacts on cattle with special emphasis on the kidneys.

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Satarug et al (2023) described the upper limit of tolerable cadmium (Cd) intake from dietary materials, which is about 58.1 µg/day for subjects with 70 kg body weight. Kidney is a critical organ of Cd body burden, and the limitation was set by β2-microglobulin (β2MG) excretion in urine under 300 μg/g creatinine.

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confidence: 99%

Health risks associated with dietary cadmium exposure

Kawada

2023

Arch Toxicol

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Satarug et al. (2023) described the upper limit of tolerable cadmium (Cd) intake from dietary materials, which is about 58.1 µg/day for subjects with 70 kg body weight. Kidney is a critical organ of Cd body burden, and the limitation was set by β2-microglobulin (β2MG) excretion in urine under 300 μg/g creatinine. If the period of survival is set as 80 years, a total amount of Cd intake from dietary materials is about 1.7 g in this subjects. The same author summarized dietary Cd intake with special reference to kidney damage (Satarug 2018), which was based on FAO/WHO safe intake guideline (1993).There had been a report that the total Cd intake resulting in both metallothioneinuria and beta 2-microglobulinuria was calculated to be approximately 2 g for both sexes (Nogawa et al. 1992), which was also accepted in the criteria of FAO/WHO safe intake guideline (1993). I also discussed minimum health risk by Cd body burden (Kawada 2022), and there is an ethnic difference in Cd intake and smoking should also be considered for Cd body burden. Anyway, protection or keeping function from chronic kidney disease may also be important in aging population.Funding There is no financial disclosure in this study.Data availability There are no data available in this study. DeclarationsConflict of interest No.

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Estimation of health risks associated with dietary cadmium exposure

Cited by 33 publications

References 289 publications

Cadmium-Induced Proteinuria: Mechanistic Insights from Dose–Effect Analyses

Cadmium-Induced Proteinuria: Mechanistic Insights from Dose–Effect Analyses

A review of important heavy metals toxicity with special emphasis on nephrotoxicity and its management in cattle

Health risks associated with dietary cadmium exposure

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