At a glance
| Chemical family | Heavy metal (Cd, atomic number 48); soft silvery-white metal; biological half-life 10-30 years in kidney — the longest of the major heavy metals |
| CAS number | 7440-43-9 (elemental); various CAS for cadmium compounds (cadmium chloride 10108-64-2, cadmium sulfide 1306-23-6, others) |
| Classification | IARC Group 1 (cadmium and cadmium compounds, carcinogenic to humans, Monograph Vol 100C, 2012); EFSA tolerable weekly intake 2.5 µg/kg body weight; EPA chronic oral RfD 0.5 µg/kg/day (water) and 1.0 µg/kg/day (food); ATSDR chronic oral MRL 0.1 µg/kg/day; California Prop 65 Maximum Allowable Dose Level 4.1 µg/day for cadmium |
| Where you encounter it | Tobacco smoke (largest single source for smokers; secondhand exposure for household non-smokers); cocoa and dark chocolate (origin-dependent — Latin American volcanic-soil cocoa typically higher); leafy greens, particularly spinach; rice and rice-based products; shellfish (especially crab and lobster hepatopancreas); some imported ceramics and pottery; nickel-cadmium battery damage; occupational welding, electroplating, and battery manufacturing; legacy contamination near smelters |
| Sleep micro environment relevance | Lower direct bedroom relevance than lead — cadmium is primarily a dietary and inhaled-smoke exposure rather than a settled-dust hazard at residential concentrations. Exception: bedrooms of smokers and households with current or recent indoor smoking carry elevated cadmium in dust from particulate deposition |
| Activated carbon capture | Not applicable for VOC-phase capture. For drinking water above EPA action levels, certified reverse osmosis (NSF/ANSI 58) and certain ion-exchange systems reduce cadmium. Inferred from general residential cadmium remediation engineering; activated carbon as designed for VOC capture is not the relevant technology |
What it is
Cadmium — chemical symbol Cd, CAS 7440-43-9, atomic number 48 — is a soft silvery-white heavy metal that occurs in nature primarily as a trace contaminant in zinc, lead, and copper ores. Industrial cadmium became widely available in the 20th century as a byproduct of zinc smelting and was used historically in pigments (cadmium yellow and cadmium red oil paints), nickel-cadmium rechargeable batteries, electroplating, and as a stabilizer in PVC plastics. Many of these applications have been substantially phased out in the EU and US over the past three decades; current US adult cadmium exposure is dominated by tobacco smoke (for smokers) and diet (for non-smokers).
The biological behavior that drives cadmium's regulatory framework is its extreme persistence in the kidney. Absorbed cadmium binds to metallothionein — a small cysteine-rich protein — in liver and kidney, and the metallothionein-bound cadmium accumulates in renal proximal tubule cells with a biological half-life estimated at 10 to 30 years. The slow elimination means dietary cadmium absorbed in childhood and young adulthood continues to contribute to kidney burden decades later, and chronic dietary exposure produces continuous accumulation throughout life. Tubular dysfunction develops when renal cadmium reaches a critical concentration threshold typically estimated around 100-200 µg/g cortex wet weight, though the threshold for early subclinical kidney effects appears to be lower based on more recent biomarker work.
Cadmium's gastrointestinal absorption is low (5-10%), but inhalation absorption (smokers, occupational) is substantially higher (30-50%) — which is why smoking is so disproportionately impactful for body burden compared to equivalent-mass dietary intake.
Where you encounter it
From tobacco smoke
Tobacco plants concentrate cadmium from soil, and smoking transfers that cadmium efficiently to the smoker through the lungs. Smokers typically carry approximately twice the blood and urine cadmium concentrations of non-smokers at population scale, and the smoker-versus-non-smoker cadmium contrast is one of the largest single environmental contrast effects in biomonitoring data. Secondhand smoke is a documented cadmium exposure route for household members. For the smoker, smoking cessation does not rapidly reduce body cadmium because of the long renal half-life — the accumulated burden persists, but ongoing exposure stops.
From cocoa and dark chocolate
Cocoa plants accumulate cadmium from soil at rates that depend on the growing region's geology and soil chemistry. Volcanic-origin soils in parts of Latin America — Ecuador, Peru, the Dominican Republic, Nicaragua, and Venezuela in particular — produce higher-cadmium cocoa than West African (Côte d'Ivoire, Ghana) origins. Dark chocolate has higher per-serving cadmium than milk chocolate because of the higher cocoa solids content. Multiple industry investigations have documented dark chocolate brands exceeding the California Proposition 65 Maximum Allowable Dose Level of 4.1 µg/day per labeled serving. Industry investigation — Consumer Reports and similar consumer-product testing The pragmatic interpretation is moderation rather than elimination: the flavonoid and magnesium benefits of dark chocolate are real, and the cadmium concern scales with consumption volume.
From leafy greens and other vegetables
Spinach is the highest-cadmium leafy green in typical US diets, accumulating cadmium from soil at higher rates than most other vegetables. Other leafy greens (kale, chard, lettuce) carry lower but non-zero cadmium loads. Root vegetables grown in contaminated soils (notably near former smelters and certain industrial-legacy areas) can accumulate elevated cadmium. The dietary mitigation is variety: rotating spinach with other greens (and other greens with each other) reduces the single-food contribution to total dietary cadmium.
From rice and rice products
Rice plants accumulate cadmium and arsenic from soil and water more efficiently than other major grains, due to the anaerobic flooded paddy growing conditions that mobilize both metals. Rice cadmium varies by region of origin and variety; rice from certain Asian and US growing regions carries higher cadmium than others. Rinsing rice before cooking and cooking with excess water (5:1 water-to-rice) followed by draining reduces both cadmium and inorganic arsenic loads. The same mitigation strategy works for both metals because they share the rice-accumulation pathway.
From shellfish, batteries, and legacy industrial sources
Crab and lobster hepatopancreas (the brown or green tomalley) concentrates cadmium at substantially higher levels than the muscle meat — the FDA has recommended limiting tomalley consumption for this reason. Nickel-cadmium batteries (largely phased out for consumer products in favor of lithium-ion) release cadmium when damaged or improperly disposed. Legacy soil contamination near former zinc and lead smelters produces elevated background cadmium in some communities; the most famous such case is the Tar Creek Superfund site in Oklahoma but multiple similar sites exist nationally.
What the research says
Carcinogenicity — the IARC Group 1 classification
The IARC Monograph Volume 100C (2012) classified cadmium and cadmium compounds as Group 1 (carcinogenic to humans) based on sufficient evidence in humans for lung cancer from inhalation exposure in occupationally exposed workers, with additional evidence for kidney cancer and prostate cancer. Regulatory The classification covers cadmium and cadmium compounds collectively rather than separating inhaled from ingested forms; the dose-response for dietary cadmium and cancer in general populations is less clearly established than the occupational inhalation dose-response.
Kidney effects — the critical chronic endpoint
The kidney is the critical target organ for chronic cadmium toxicity. Renal proximal tubular dysfunction is the earliest functional change documented in cadmium-exposed populations, detectable through urinary biomarkers (beta-2-microglobulin, retinol-binding protein, N-acetyl-beta-D-glucosaminidase). At higher cumulative doses, glomerular filtration declines, renal stones develop, and chronic kidney disease can result. Järup and Åkesson 2009 in Toxicology and Applied Pharmacology reviewed the cadmium environmental health picture with particular attention to the renal endpoint dose-response. Peer-reviewed
Bone effects and the Itai-itai context
Cadmium interferes with calcium metabolism and contributes to osteomalacia and osteoporosis at high chronic exposures. The historical reference case is Itai-itai disease — Japanese for "it hurts, it hurts" — a severe combination of renal failure and osteomalacia documented in postwar Japanese populations consuming rice grown in cadmium-contaminated paddy fields in the Toyama Prefecture, downstream from zinc-mining operations. Itai-itai represents the extreme end of the chronic-cadmium toxicity spectrum; the more clinically relevant question for contemporary populations is the dose-response for early renal and skeletal effects at the much lower exposures that characterize typical US diets.
Regulatory reference values
The ATSDR Toxicological Profile for Cadmium sets a chronic oral Minimal Risk Level of 0.1 µg/kg/day based on early renal effects. Regulatory The European Food Safety Authority Scientific Opinion on cadmium in food set a tolerable weekly intake of 2.5 µg/kg body weight, also based on early renal effects detected via urinary biomarkers in general-population biomonitoring studies. Regulatory The US EPA IRIS chronic oral reference dose for cadmium is 0.5 µg/kg/day (water) and 1.0 µg/kg/day (food). Regulatory The differences across agencies reflect different uncertainty-factor frameworks and different weighting of recent biomarker evidence; the EFSA TWI is the most conservative of the major reference values in current use.
Biomonitoring and population body burden
CDC NHANES biomonitoring measures urinary and blood cadmium in nationally representative US population samples. Regulatory — population-scale biomonitoring The data consistently shows the smoker/non-smoker contrast, age-related increases (reflecting lifetime accumulation), and modest sex differences with higher cadmium in women (partly attributable to iron-deficiency-mediated absorption enhancement during menstruation and pregnancy). The CDC biomonitoring data underpins much of the dose-response work characterizing the US population's relationship to the EFSA TWI and other regulatory thresholds.
What helps reduce exposure
Don't smoke; minimize secondhand smoke exposure. The single highest-leverage intervention for cadmium body burden. The cessation benefit is real even though accumulated body cadmium persists — stopping smoking stops further accumulation, and the population-scale cadmium contrast between smokers and never-smokers is among the largest in environmental biomonitoring data.
Moderate dark chocolate consumption rather than eliminating it. Vary chocolate sources and brands. For children, where exposure per body weight is higher, the moderation framing applies more strongly. The flavonoid and magnesium benefits of dark chocolate are real and the optimal intake balance depends on baseline cadmium body burden and overall dietary context.
Rotate leafy greens; don't rely on spinach daily. Spinach is the highest-cadmium common leafy green. Rotating spinach with kale, chard, lettuces, and other greens reduces the single-food contribution to total cadmium intake without sacrificing the broader nutritional benefits of leafy-green consumption.
Rinse rice thoroughly; cook in excess water and drain. A 5:1 water-to-rice ratio with draining of excess water reduces inorganic arsenic by 40-60% and reduces cadmium meaningfully as well. The same technique works for both metals. Variety across grains (oats, quinoa, barley, millet) reduces over-reliance on rice as the dietary staple.
For shellfish: limit consumption of crab and lobster tomalley (the brown or green hepatopancreas). The muscle meat is substantially lower in cadmium and remains a reasonable dietary protein source.
Avoid imported low-end ceramics for food use. Some imported ceramics contain cadmium pigments and stabilizers that can leach into food. Certified domestic and EU-compliant ceramics are the safer default for daily food service.
Recycle nickel-cadmium batteries through proper hazardous-waste channels. Most municipal recycling programs accept rechargeable batteries; the disposal pathway prevents long-term environmental cadmium release.
What does NOT help
- Avoiding all chocolate. Consumer-product testing recommends moderation rather than elimination. The chocolate-flavonoid benefit literature is well-established; the cadmium concern scales with intake, not with the presence of any consumption.
- Avoiding all leafy greens. The nutritional trade-off favors continued consumption with rotation across green types. Spinach is the highest-cadmium individual green, not all greens.
- Generic "non-toxic" labels on imported ceramics. The terms are unregulated. Third-party certification (NSF, Prop 65 compliance documentation) is the actionable verification.
- Activated carbon water filters for cadmium removal. Activated carbon as designed for VOC capture is not validated for cadmium. NSF/ANSI 58 (reverse osmosis) is the relevant water-filter standard for cadmium reduction.
- Chelation therapy for general cadmium body burden. No validated clinical chelation protocol exists for cadmium. Some experimental chelators have shown limited animal efficacy but have not translated to clinical practice. Cadmium body burden management is fundamentally a prevention story, not a remediation story.
Open research questions
- Long-term health effects of chronic low-dose dietary cadmium below current regulatory thresholds — the EFSA TWI was set based on early subclinical renal effects, but the dose-response for cardiovascular, neurological, and cancer endpoints at typical US dietary intake is less precisely characterized. Speculation re: shape of low-dose dose-response; established at higher chronic exposures
- Cadmium-zinc and cadmium-iron interactions — nutritional zinc and iron status modulate cadmium absorption and toxicity in animal studies; the population-level relevance for protective dietary strategies is an active area. Speculation
- Bedroom-specific cadmium exposure pathways — settled-dust cadmium data is sparse compared to lead, and the household-dust contribution to total daily cadmium exposure in non-smoking households has not been quantitatively characterized. Speculation
- Cadmium during pregnancy and breastfeeding — placental transfer of cadmium is limited (metallothionein-mediated barrier), but exposure during specific developmental windows for endpoints other than birth weight is less well characterized. Inferred from established placental cadmium toxicokinetics; developmental-window-specific endpoint data is sparse
Citations
- International Agency for Research on Cancer (2012). IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Volume 100C: Arsenic, Metals, Fibres and Dusts — Cadmium and cadmium compounds Group 1. Lyon: IARC. NCBI Bookshelf — Cadmium Monograph Regulatory
- Agency for Toxic Substances and Disease Registry. Toxicological Profile for Cadmium. atsdr.cdc.gov/ToxProfiles/tp5.pdf Regulatory
- US Environmental Protection Agency. Cadmium — Integrated Risk Information System chemical assessment. RfD 0.5 µg/kg/day (water), 1.0 µg/kg/day (food). iris.epa.gov Regulatory
- European Food Safety Authority Panel on Contaminants in the Food Chain (2009). Scientific Opinion on cadmium in food. EFSA Journal, 980:1-139. DOI 10.2903/j.efsa.2009.980 Regulatory — TWI 2.5 µg/kg body weight
- Järup L, Åkesson A (2009). Current status of cadmium as an environmental health problem. Toxicology and Applied Pharmacology, 238(3):201-208. DOI 10.1016/j.taap.2009.04.020 Peer-reviewed
- Bernhoft RA (2013). Cadmium toxicity and treatment. The Scientific World Journal, 2013:394652. DOI 10.1155/2013/394652 Peer-reviewed
- Satarug S, Garrett SH, Sens MA, Sens DA (2010). Cadmium, environmental exposure, and health outcomes. Environmental Health Perspectives, 118(2):182-190. DOI 10.1289/ehp.0901234 Peer-reviewed
- Nordberg GF (2009). Historical perspectives on cadmium toxicology. Toxicology and Applied Pharmacology, 238(3):192-200. DOI 10.1016/j.taap.2009.03.015 Peer-reviewed
- US Centers for Disease Control and Prevention. National Report on Human Exposure to Environmental Chemicals — NHANES cadmium biomonitoring. cdc.gov/exposurereport Regulatory — population-scale biomonitoring
- California Office of Environmental Health Hazard Assessment. Proposition 65 — No Significant Risk Levels and Maximum Allowable Dose Levels for cadmium (oral MADL 4.1 µg/day). oehha.ca.gov Regulatory
Frequently asked questions
How much cadmium is in dark chocolate?
Dark chocolate cadmium content varies substantially by brand and cocoa origin, ranging from below detection limits to concentrations several times the California Proposition 65 Maximum Allowable Dose Level of 4.1 µg/day. Cocoa from certain volcanic-soil growing regions (notably parts of Latin America) accumulates more cadmium than cocoa from other regions. Multiple industry investigations have documented dark chocolate brands exceeding the Prop 65 threshold per serving. The pragmatic interpretation is moderation rather than elimination: dark chocolate's flavonoid and magnesium benefits are real, and the cadmium concern scales with intake.
Is rice safe to eat given cadmium levels?
Rice accumulates cadmium from soil and water more efficiently than most grains, but rice cadmium is generally below the regulatory thresholds set by EFSA and the FDA. Variety matters — basmati and jasmine rice typically carry lower cadmium than US-grown long-grain white. The practical mitigation is grain rotation rather than rice elimination: substitute oats, quinoa, barley, and millet for some rice meals. Rinsing rice before cooking and cooking in excess water with draining (5:1 water-to-rice ratio) reduces both cadmium and inorganic arsenic loads.
How long does cadmium stay in the body?
Cadmium has the longest biological half-life of any of the major heavy metals — 10 to 30 years in the kidney, where the majority of absorbed cadmium accumulates and binds to metallothionein. The slow elimination means that cadmium absorbed in childhood and young adulthood continues to contribute to body burden decades later, and chronic dietary exposure produces continuous accumulation throughout life. There is no clinical chelation protocol for cadmium analogous to lead chelation; once absorbed, cadmium is essentially a permanent body-burden contributor.
Does smoking really increase cadmium exposure?
Yes — substantially. Tobacco plants concentrate cadmium from soil, and smoking transfers a meaningful fraction of that cadmium into the smoker through highly efficient inhalation absorption (estimated 30-50% pulmonary absorption, compared to 5-10% gastrointestinal absorption from dietary cadmium). Smokers carry approximately twice the blood and urine cadmium of non-smokers on average. Secondhand smoke is also a documented cadmium exposure route for non-smoking household members.
Is cadmium dangerous in low doses?
The kidney effects of cadmium (tubular dysfunction, renal stones, eventual decreased glomerular filtration) develop slowly over decades of cumulative exposure. The EFSA tolerable weekly intake of 2.5 µg/kg body weight reflects this slow-accumulation framework: the goal is to prevent the kidney from reaching the critical concentration threshold over a lifetime, not to avoid acute toxicity from any single exposure. Many people in the general population approach or exceed the EFSA TWI through routine dietary intake, particularly heavy consumers of cadmium-accumulating foods (cocoa, leafy greens, certain shellfish).
What organs does cadmium affect?
The kidney is the critical target organ — proximal tubule cells accumulate cadmium and develop dysfunction at the highest cumulative doses. Bone is the second major target, with cadmium interfering with calcium metabolism and contributing to osteomalacia and osteoporosis at high chronic exposures (the historical Itai-itai disease in Japan was the most severe documented example). The lung is the target organ for inhalation exposure, with IARC's lung-cancer classification driven by cadmium worker cohorts. Cardiovascular and reproductive effects are documented but less central to the regulatory framework.
Can cadmium be removed from the body?
There is no validated clinical chelation protocol for cadmium analogous to lead chelation. Some experimental chelators have shown limited effectiveness in animal studies but have not translated to clinical practice. The practical implication: cadmium body burden management is fundamentally a prevention story — minimizing absorption through dietary and behavioral choices — rather than a remediation story. Stopping smoking is the highest-leverage individual intervention for cadmium body burden; dietary moderation is the next.
Related compounds
Embr Sleep is a sleep environment company researching the chemistry of the bedroom. See the methodology page for how this Atlas tags claims by evidence strength. For broader context on dietary and dust-mediated contamination, see non-toxic bedroom.
Last reviewed 2026-05-25. If you find a factual error, contact us.