Cadmium Pollution and Occupational Exposure

A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Human Toxicology and Epidemiology".

Deadline for manuscript submissions: 26 September 2025 | Viewed by 3324

Special Issue Editor


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Guest Editor
Department of Occupational and Environmental Medicine, Graduate School of Medicine, Chiba University, Chiba 260 8670, Japan
Interests: environmental medicine; occupational health; cadmium; epidemiplogy; exposure
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Special Issue Information

Dear Colleagues,

The renal and bone effects of cadmium exposure are well known, and there are also concerns about carcinogeneniety and life prognosis. The main sources of exposure to cadmium are in occupations, e.g., battery manufacturing, alloys, and plating industries, and in the general environment, e.g., food and smoking. The health effects of cadmium exposure are a global concern and remain an issue for many researchers.

This Special Issue is open to any subject area related to environmental and occupational exposure and the health effects of cadmium.

Prof. Dr. Yasushi Suwazono
Guest Editor

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Keywords

  • cadmium
  • environmental exposure
  • general population
  • occupational medicine
  • renal effect
  • mortality

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Published Papers (3 papers)

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Research

21 pages, 1307 KiB  
Article
Effects of Environmental Cadmium Exposure Sufficient to Induce Renal Tubular Dysfunction on Bone Mineral Density Among Female Farmers in Cadmium-Polluted Areas in Northern Japan
by Hyogo Horiguchi, Etsuko Oguma, Kayoko Miyamoto, Yoko Hosoi and Fujio Kayama
Toxics 2025, 13(8), 688; https://doi.org/10.3390/toxics13080688 - 18 Aug 2025
Abstract
In the Japanese Multi-Centered Environmental Toxicant Study (JMETS) conducted in five areas across Japan, we demonstrated that bone mineral density (BMD) in female farmers without renal tubular dysfunction was not adversely affected by exposure to low to moderate levels of cadmium (Cd). We [...] Read more.
In the Japanese Multi-Centered Environmental Toxicant Study (JMETS) conducted in five areas across Japan, we demonstrated that bone mineral density (BMD) in female farmers without renal tubular dysfunction was not adversely affected by exposure to low to moderate levels of cadmium (Cd). We then expanded JMETS to the most Cd-polluted area in northern Japan, Akita prefecture, with area A as the control and areas B and C as Cd-polluted areas (Cd exposure levels: B < C), which also covered more female farmers with a wider age range (20–82 years) and Cd exposure sufficient to induce renal tubular dysfunction. We selected 1267 eligible subjects in the three areas and classified them by age and menstrual status. The distribution of blood and urinary Cd levels over the areas was A < B < C (blood Cd: 2.10, 3.78, and 3.39 µg/L, and urinary Cd: 3.02, 4.29, and 6.15 µg/g cr., respectively; p < 0.05), with the steepest age-dependent increase in area C, particularly in older postmenopausal subjects with a urinary Cd level around the threshold for renal tubular dysfunction. Urinary α1-microglobulin (α1MG) and ß2-microglobulin (ß2MG) levels in the three areas also showed age-dependent increases, with higher levels being observed in areas B and C than in area A. Furthermore, ß2MG levels in older postmenopausal subjects were significantly higher in area C than in area A (273 and 157 μg/g cr., respectively, p < 0.05). Age-dependent decreases in BMD were noted in all areas, with rapid reductions from peri- to postmenopausal subjects; however, marked differences in each age class were not observed among the three areas. In multiple regression models of BMD in all subjects using age, body weight, grip, urinary creatinine, urinary α1MG or ß2MG, and blood or urinary Cd as independent variables, urinary α1MG and ß2MG levels correlated with BMD, whereas blood and urinary Cd levels did not. Moreover, age and body weight correlated more strongly with BMD than blood and urinary Cd levels. Therefore, Cd, not only at a low level but also at a level that was sufficient to deteriorate renal tubular function, did not affect bones. These results provide further support for Cd exposure itself not directly affecting bones. Full article
(This article belongs to the Special Issue Cadmium Pollution and Occupational Exposure)
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21 pages, 5031 KiB  
Article
Toxicological Effects of Combined Exposure of Cadmium and Enrofloxacin on Zebrafish
by Lingfei Ren, Yu He, Chao Hou, Chaoxuan Liao and Miao Chen
Toxics 2025, 13(5), 378; https://doi.org/10.3390/toxics13050378 - 7 May 2025
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Abstract
The combined pollution of cadmium (Cd) and enrofloxacin (ENR) in aquatic environments represents a critical issue in environmental toxicology. Using zebrafish as model organisms, we systematically investigated the combined toxicity of Cd and ENR through both acute (96-h) and chronic (20-d) exposure experiments. [...] Read more.
The combined pollution of cadmium (Cd) and enrofloxacin (ENR) in aquatic environments represents a critical issue in environmental toxicology. Using zebrafish as model organisms, we systematically investigated the combined toxicity of Cd and ENR through both acute (96-h) and chronic (20-d) exposure experiments. Our results demonstrated significant synergistic effects: co-exposure reduced the 96-h LC50 values from 89.12 mg/L (Cd alone) and 190.11 mg/L (ENR alone) to 46.35 mg/L and 99.39 mg/L, respectively (combined effect index = 0.96). Chronic exposure revealed that ENR enhanced Cd accumulation in the liver, intestine, and muscle tissues by 1.11–2.33-fold compared to single Cd exposure. Oxidative stress markers showed dynamic temporal changes, with superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) activities initially increasing by 1.34–7.06-fold, 0.98–3.28-fold, and 1.53–3.65-fold at 8 d, respectively, followed by 9.9–48.98% reductions after 20 d of exposure. Malondialdehyde (MDA) levels progressively accumulated, reaching up to 4.06-fold higher than controls. Notably, co-exposure elevated oxidative stress by 11.24–34.48% relative to single exposures. The 16S rDNA sequencing analysis indicated that Cd exposure significantly reduced the α-diversity of zebrafish gut microbiota (57–63% decrease in Shannon index), characterized by a 16–20% reduction in beneficial Cetobacterium and a 44–114% increase in pathogenic Aeromonas abundance. The combined exposure further exacerbated these gut microbiota dysbiosis patterns. These findings provide crucial evidence for ecological risk assessment, suggesting that current environmental standards based on single-pollutant evaluations may substantially underestimate the actual risks of heavy metal-antibiotic co-contamination in aquatic ecosystems. Full article
(This article belongs to the Special Issue Cadmium Pollution and Occupational Exposure)
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9 pages, 440 KiB  
Article
Benchmark Dose of Urinary Cadmium for Assessing Renal Tubular and Glomerular Function in a Cadmium-Polluted Area of Japan
by Takuya Hayashi, Kazuhiro Nogawa, Yuuka Watanabe, Teruhiko Kido, Masaru Sakurai, Hideaki Nakagawa and Yasushi Suwazono
Toxics 2024, 12(12), 836; https://doi.org/10.3390/toxics12120836 - 21 Nov 2024
Cited by 4 | Viewed by 1999
Abstract
The aim of the present study was to apply an updated benchmark dose (BMD) approach to estimate reference urinary cadmium (U-Cd) for renal tubular and glomerular effects. This cross-sectional survey was conducted 30 years ago in 30 men and 44 women living in [...] Read more.
The aim of the present study was to apply an updated benchmark dose (BMD) approach to estimate reference urinary cadmium (U-Cd) for renal tubular and glomerular effects. This cross-sectional survey was conducted 30 years ago in 30 men and 44 women living in a Cd-polluted area and in 18 men and 18 women living in a non-polluted area. We applied an updated hybrid approach to estimate the BMDs and 95% lower confidence limits (BMDLs) of U-Cd for creatinine (Cr) clearance (CrCl), estimated glomerular filtration rate (eGFR), β2-microglobulin (β2-MG), and β2-MG tubular reabsorption (%TRβ2-MG). Using a benchmark response (BMR) of 5%, we estimated the BMDLs of U-Cd for adverse renal effect markers to be 2.9 (eGFR), 1.8 (β2-MG), 1.8 (%TRβ2-MG < 95%), and 3.6 μg/g Cr (%TRβ2-MG < 90%) in men, and 3.5 (CrCl), 2.5 (β2-MG), 2.6 (%TRβ2-MG < 95%), and 3.9 μg/g Cr (%TRβ2-MG < 90%) in women. The obtained BMDLs for tubular effects were 1.8–3.6 µg/g Cr and for glomerular effects were 2.9–3.5 µg/g Cr; these are not very high compared to the exposure levels in the general population. The BMDLs calculated in this study provide important information for measures regarding protecting general inhabitants or workers from the adverse health effects of Cd exposure. Full article
(This article belongs to the Special Issue Cadmium Pollution and Occupational Exposure)
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