Condition
Cadmium Poisoning
Editors: Ahmed Mian MD, HonBSc, BEd, CCFP-EM, CAC; Dan Randall MD, MPH, FACP
Background Information
Description
- cadmium is a soft, silvery-white metal that is a naturally occurring, toxic, nonessential heavy metal used in batteries, color pigments, and corrosive reagents (as a stabilizer in polyvinyl chloride [PVC] products), and in the electroplating protective layer for steel to prevent corrosion
- cadmium poisoning typically results from chronic low-level environmental or occupational exposure but acute poisonings from massive exposure have been reported in Japan, Thailand, and Sri Lanka,,,
- cadmium exposure can result in complications involving almost all organ systems leading to respiratory disease, renal tubular disease, bone disease, cancer, cardiovascular disease, diabetes, and adverse pregnancy and early life outcomes, and is associated with increased mortality,
Also Called
- itai-itai disease
Epidemiology
Who Is Most Affected
- most cases are reported in people working in occupations with exposure to cadmium, including,,
- nickel-cadmium battery manufacturing
- polyvinyl chloride manufacturing (plastic stabilizer)
- metallurgy (silver polishing)
- zinc mining
- young children and female patients of childbearing age may have increased cadmium absorption and higher body cadmium burden than male adults,,
- residents of Asia (China and Japan) have greater exposure than residents of Europe and United States due to rapid evolution of polluting industries and high intake of rice locally grown on contaminated soil
- cadmium-contaminated water from upstream zinc mining and smelting operations leading to outbreaks of renal and bone disease have been reported in
- Kakehashi River basin and Toyama Prefecture (site of renal tubular osteomalacia outbreak, also known as itai-itai disease), Japan
- Mae Sot District in Tak Province, Thailand
- North Central Province, Sri Lanka
- PubMed31686724Indian journal of clinical biochemistry : IJCBIndian J Clin Biochem20191001344371-378371Reference - Indian J Clin Biochem 2019 Oct;34(4):371
Incidence/Prevalence
- STUDY SUMMARY< 1% of heavy metal poisonings in the United States due to cadmium in 2020POPULATION-BASED SURVEILLANCE: Clin Toxicol (Phila) 2021 Dec;59(12):1282
Risk Factors
- occupational exposure, including,,
- metallurgy (silver polishing)
- nickel-cadmium battery manufacturing
- polyvinyl chloride manufacturing (plastic stabilizer)
- zinc mining
- smoking,,
- cadmium present in cigarettes
- 1-2 mcg cadmium per cigarette (varies depending on type and brand)
- if smoking 20 cigarettes per day, about 1 mcg cadmium absorbed
- exposure to cadmium-polluted air,
- may occur near some metal industry sites
- house dust is potential route of exposure even after elimination of emitting source
Associated Conditions
- concurrent heavy metal exposure, such as lead, is common and may result in synergistic toxicity
- zinc, iron, or calcium deficiency may increase cadmium absorption
- PubMed31494513Environmental toxicology and pharmacologyEnviron Toxicol Pharmacol2019110172103219103219anemia may be present in patients with deficiencies of essential metals, such as copper, iron, zinc, and calcium, which promotes cadmium absorption (Environ Toxicol Pharmacol 2019 Nov;72:103219)
- pulmonary emphysema can occur in patients who are exposed to cadmium via cigarette smoking (Environ Toxicol Pharmacol 2019 Nov;72:103219)
Etiology and Pathogenesis
Causes
- cadmium poisoning most often due to inhalation of cadmium (Cd) fumes or dust; major sources include,,,
- occupational exposure during smelting and refining metals
- tobacco use (tobacco is highly efficient in absorbing cadmium from the soil)
- house dust in areas with contaminated soils
- Cd exposure can also occur through ingestion of food contaminated with Cd,,,
- > 80% of Cd exposure from foods reported to come from cereals, vegetables, and potatoes
- Cd present in almost all foods, with highest concentration in
- food from plants (higher concentrations than in meat, egg, milk and dairy products, and fish muscle)
- rice
- wheat
- green leafy vegetables
- potato and root vegetables (for example carrots and celery)
- mollusks and crustaceans
- oysters and other bivalve molluscs
- cephalopods and crabs (especially parts with brown meat)
- offal products such as liver and kidney, especially from older animals
- oil seeds, cocoa beans, and certain wild mushrooms
- food from plants (higher concentrations than in meat, egg, milk and dairy products, and fish muscle)
- mean Cd intake from food 8-25 mcg per day, which may be higher in persons who consume high amounts of shellfish, vegetarians, and Asian populations
- soil in which crops and vegetables grown may be contaminated by
- atmospheric deposition of airborne Cd
- mining activities leading to Cd-contaminated irrigation water, which was the cause of itai-itai disease outbreak in early-20th-century Toyama Prefecture, Japan
- application of Cd-containing fertilizers and sewage sludge on farm land
- other sources of Cd exposure include
- Cd contaminated drinking water near factories or mines
- paints with Cd pigments, which may be used for yellow, red, and orange hues
- Cd dyes in industrial coloring of plastic
Pathogenesis
- cadmium (Cd) is primarily absorbed and retained in the kidneys and liver and accumulates throughout life,,
- cadmium absorption varies by route and patient factors
- 40%-50% of inhaled cadmium is reported to be absorbed
- 3%-5% of ingested cadmium is reported to be absorbed
- young children and female patients of childbearing age may have increased cadmium absorption
- zinc, iron, or calcium deficiency may increase cadmium absorption
- estimated half-life 10-33 years
- PubMed28932363Caspian journal of internal medicineCaspian J Intern Med2017070183135-145135half-life in blood is 3-4 months and may indicate recent exposure
- cadmium absorption varies by route and patient factors
- pathogenesis of Cd-related renal damage
- inhaled Cd deposited in alveoli and/or ingested Cd absorbed into blood
- Cd transported into erythrocytes or bound to large-molecular-weight albumin proteins
- hepatic Cd uptake induces synthesis of metallothionein (MT) (low-molecular-weight protein) which binds with Cd to form nontoxic Cd-MT complexes
- Cd-MT complex slowly released back into blood
- in kidney, Cd-MT complex filtered through glomeruli and taken up by renal proximal tubule cells
- Cd-MT complex degradation releases free Cd, which recombines with MT newly synthesized by tubular cells
- if MT binding sites saturated, free Cd in tubular cells remains and combines to form nephrotoxic Cd-fluoride and Cd-nitrate compounds
- pathogenesis of Cd-associated bone disease
- excess Cd in kidney deposited in renal cortex and inhibits 1,25-dihydroxycalciferol
- secondary alteration in vitamin D metabolism leads to
- calcium deficiency
- osteoporosis
- osteomalacia
- pseudofractures
- pathogenesis of placental and fetal development disorders related to Cd exposure
- low-dose exposure to Cd may cause changes to embryonic gene expression
- Cd can bind to thiols with depletion of methyl donor S-adenosyl methionine and resulting methylome alterations can lead to changes in DNA methyltransferase activity
- Cd may be considered an endocrine disruptor and may bind to estrogen receptor alpha affecting the signaling transduction, estrogen, and MAPK pathways
- pathogenesis of zinc deficiency related to Cd exposure
- Cd competes with zinc for absorption and at enzyme binding sites
- MT binds preferentially with Cd, limiting zinc transport to tissues
- zinc-dependent enzyme activity is subsequently depleted
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