How does cadmium chloride cause toxicity in humans and animals?

1. How cadmium chloride gets into the body and where it goes

The highly water‑soluble nature of cadmium chloride makes it more readily absorbed than less soluble cadmium compounds, with inhalation and ingestion being common routes and percutaneous uptake possible through binding to cysteine sulfhydryl groups or induction of metallothionein in skin ^{[1] [5] [6]}; once absorbed, cadmium is inefficiently excreted and accumulates in liver, kidney and other organs with a biological half‑life measured in decades, so low chronic exposures concentrate into long‑term body burdens ^{[2] [7]}.

2. The central molecular assault: oxidative stress and disrupted metal homeostasis

A persistent theme across animal and cell studies is that Cd2+ provokes reactive oxygen species (ROS) formation, overwhelms antioxidant defenses (SOD, CAT, glutathione systems) and causes lipid peroxidation, protein oxidation and mitochondrial dysfunction—events that underlie cell membrane damage, apoptosis or necrosis and set the stage for organ injury ^{[8] [9] [2]}; simultaneously, cadmium competes with and displaces essential metals (zinc, iron, calcium) in metalloproteins, deranging enzyme function and signaling pathways ^{[2] [7]}.

3. Protein binding, metallothionein, and paradoxical protection

Cadmium binds avidly to cellular proteins, notably inducing metallothioneins which sequester Cd and can temporarily protect cells, but metallothionein‑bound cadmium alters tissue distribution (favoring kidney accumulation) and can still mediate toxicity when released, making metallothionein both a biomarker and a double‑edged player in cadmium toxicokinetics ^{[10] [1]}.

4. DNA damage, cell‑cycle disruption and carcinogenic potential

Multiple in vitro and animal studies link CdCl2 exposure to DNA strand breaks, chromosomal aberrations, p53 activation, and cell‑cycle irregularities consistent with genotoxic stress; those mechanistic data support cadmium’s carcinogenicity in animals and form part of epidemiologic associations with lung, prostate, kidney and other cancers in humans, although complexities of dose, co‑exposures and mechanism mean human evidence is sometimes less definitive than animal models ^{[11] [9] [4]}.

5. Organ targets and clinical patterns

Clinically and experimentally, the kidney (proximal tubule) and lungs are the primary targets—chronic cadmium causes proteinuria, reduced renal function and bone demineralization secondary to renal tubular dysfunction, while inhaled cadmium can provoke pulmonary inflammation, reduced vital capacity and emphysematous changes; other systems (liver, reproductive, cardiovascular, immune, nervous) show effects in animals and in occupational studies, reflecting broad systemic toxicity ^{[3] [2] [7] [4]}.

6. Dose, form and susceptibility: why some exposures are worse

Toxicity depends on dose, exposure route and chemical form—soluble salts like CdCl2 deliver higher bioavailable Cd2+ than insoluble pigments—while life stage, nutritional status (low Zn, Fe or Ca increases Cd uptake), smoking and occupational settings raise susceptibility; experimental doses are often higher than typical environmental exposures, which complicates translating animal findings straight to human risk, a caveat noted across reviews ^{[5] [8] [2]}.

7. Treatment, prevention and unresolved questions

Acute management relies on supportive care and has explored chelators (dithiocarbamates and others) in animals, with limited human data and a need for documentation of efficacy; prevention through source control, occupational limits, reducing environmental emissions and maintaining adequate dietary micronutrients (Zn, Fe, Ca) is emphasized by public‑health agencies, while mechanistic gaps—exact pathways linking low‑dose epigenetic changes to human cancer—remain active research questions ^{[3] [8] [7]}.