Cadmium in human lung tissue

Kollmeier, H.; Seemann, J.; Wittig, Peter; Rothe, G; Müller, Klaus

doi:10.1007/bf00381367

Cited by 22 publications

(5 citation statements)

References 10 publications

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“…Smokers in a cadmiumexposed workplace may contaminate their cigarettes with cadmium and increase their cadmium dose by up to 20 µg per cigarette 6 . Our patient was also a smoker and tobacco may have had a synergistic effect, either by increasing the cadmium burden on the lung as cadmium is a constituent of tobacco, or indirectly by reducing lung clearance of cadmium 7 .…”

Section: Discussionmentioning

confidence: 84%

Cadmium Poisoning in a Crematorium Worker

Nicholson

Fynn

Coroneos

1997

Anaesth Intensive Care

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Section: Discussionmentioning

confidence: 84%

Cadmium Poisoning in a Crematorium Worker

Nicholson

Fynn

Coroneos

1997

Anaesth Intensive Care

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“…Second, the Cd dose used in this study might not represent the ordinary exposure of human lung tissue. It is difficult to determine the appropriate dose because the reported cadmium levels in lung tissue were largely inconsistent (35)(36)(37). To solve this issue, we carried out preliminary experiments and determined suitable conditions that affected the biological behavior of cells significantly without decreasing cell viability.…”

Section: Discussionmentioning

confidence: 99%

Multiomics Landscape Uncovers the Molecular Mechanism of the Malignant Evolution of Lung Adenocarcinoma Cells to Chronic Low Dose Cadmium Exposure

et al. 2021

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Cadmium (Cd) from cigarette smoke and polluted air can lead to lung adenocarcinoma after long-term inhalation. However, most studies are based on short-term exposure to this toxic metal at high concentrations. Here, we investigate the effects of long-term exposure of A549 cells (lung adenocarcinoma) to cadmium at low concentrations using morphological and multiomics analyses. First, we treated A549 cells continuously with CdCl2 at 1μM for 8 months and found that CdCl2 promoted cellular migration and invasion. After that, we applied transmission electron and fluorescence microscopies and did not observe significant morphological changes in Golgi apparatus, endoplasmic reticulum, lysosomes, or mitochondria on Cd treated cells; microfilaments, in contrast, accumulated in lamellipodium and adhesion plaques, which suggested that Cd enhanced cellular activity. Second, by using whole-exome sequencing (WES) we detected 4222 unique SNPs in Cd-treated cells, which included 382 unique non-synonymous mutation sites. The corresponding mutated genes, after GO and KEGG enrichments, were involved mainly in cell adhesion, movement, and metabolic pathways. Third, by RNA-seq analysis, we showed that 1250 genes (784 up and 466 down), 1623 mRNAs (1023 up and 591 down), and 679 lncRNAs (375 up and 304 down) were expressed differently. Furthermore, GO enrichment of these RNA-seq results suggested that most differentially expressed genes were related to cell adhesion and organization of the extracellular matrix in biological process terms; KEGG enrichment revealed that the differentially expressed genes took part in 26 pathways, among which the metabolic pathway was the most significant. These findings could be important for unveiling mechanisms of Cd-related cancers and for developing cancer therapies in the future.

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“…4 Levels of cadmium and nickel in the lungs were also found to be significantly higher in smokers than nonsmokers in 17 autopsied urban dweller lungs, who were not occupationally exposed to dust or metal. 10 Although a large number of research studies [10][11][12][13][14][15][16][17][18][19][20] have reported the metal contents of autopsied lungs, most of them are on the urban or nonoccupational lungs, although some do include a few cases of occupationally exposed workers. Only a few papers have reported the metal content of the lungs exclusively from workers occupationally exposed to contaminants such as dusts and metal as reported in this Ontario study.…”

Section: Commentmentioning

confidence: 99%

Metals in the Lungs of Ontario Hardrock Miners

Verma

2013

Archives of Environmental & Occupational Health

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The objective of this study was to determine the concentration of nickel, cadmium, and lead in the autopsied lungs of 29 hardrock miners. It involved chemical analysis of the lungs, where each lung was divided horizontally into 3 sections and analyzed by an atomic absorption spectrophotometer equipped with a graphite furnace. The grand mean levels of nickel, cadmium, and lead were found to be 1.84, 1.74, and 2.75 μg/g of dry tissue, respectively. The effect of smoking was also examined. The ratios using the mean values between smoker and nonsmoker for nickel, cadmium, and lead were found to be 0.7, 5.4, and 1.4, respectively. The level of cadmium in smokers was significantly higher than nonsmokers. This study provides an estimate of retained metals in the lungs of the Ontario hardrock miners as a result of occupational exposure to hardrock mining environment.

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Cadmium in human lung tissue

Cited by 22 publications

References 10 publications

Cadmium Poisoning in a Crematorium Worker

Cadmium Poisoning in a Crematorium Worker

Multiomics Landscape Uncovers the Molecular Mechanism of the Malignant Evolution of Lung Adenocarcinoma Cells to Chronic Low Dose Cadmium Exposure

Metals in the Lungs of Ontario Hardrock Miners

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