Cadmium (Cd)

This page draws on evidence from EFSA, OEHHA, JECFA, ATSDR, and Codex Alimentarius, together with 24 peer-reviewed studies and 7 other cited sources. The complete citation list is at the bottom of the page.

This page is the first cross-source synthesis on cadmium for Heavy Metal Index. It draws on the canonical Handbook on the Toxicology of Metals chapter 32 (Nordberg, Nogawa, Nordberg 2015, Nordberg 2015), the Casarett & Doull’s Essentials of Toxicology chapter 23 (Ufelle and Barchowsky 2021, Ufelle & Barchowsky 2021), Patty’s Toxicology chapter 7 (Jakubowski 2012, Jakubowski 2012), the EFSA 2009 scientific opinion (EFSA 2009 cadmium opinion), the paired California OEHHA Prop 65 documents (OEHHA 1996, OEHHA 2001), the JECFA 91st meeting 2022 dietary exposure assessment (JECFA 91st 2022), the ATSDR 2012 Toxicological Profile (ATSDR 2012), and the Codex CCCF17 session report (Codex CCCF17 2024). Codex CXS 193-1995 (the General Standard for Contaminants and Toxins in Food and Feed, matrix-level cadmium (Cd) MLs) and Codex CXC 81-2022 (Code of Practice for Cadmium in Cocoa Beans, the load-bearing source for cocoa-cadmium mitigation specifics) are also ingested. Operative 1985 EPA IRIS record, JECFA 73rd meeting derivation documents, and the EFSA 2011 reaffirming statement remain flagged as pending for later ingest waves. Open questions are tracked on synthesis.

Overview

Cadmium is a non-essential heavy metal and an environmental contaminant of the human food system. It enters the food supply through three pathways that compound over time: natural occurrence in soils at background concentrations of 0.1 to 1 mg/kg, accumulating anthropogenic loading from phosphate-fertilizer use and atmospheric deposition from non-ferrous metal refining, and biological concentration in filter-feeding marine invertebrates and in certain plant commodities (cereals, leafy vegetables, root vegetables, cocoa, tobacco) (Nordberg 2015, Jakubowski 2012). For non-smoking members of the general population, food is the dominant source of cadmium exposure; for smokers, tobacco contributes an internal exposure comparable in magnitude to diet (Nordberg 2015).

The metal is absorbed at low rates from the gastrointestinal tract (5 to 10 percent on average, with a 1 to 10 percent range that widens upward under iron deficiency and in pregnancy) and at substantially higher rates from the lung (10 to 50 percent of inhaled cadmium), and is then efficiently retained in the kidney and liver with a biological half-life measured in decades (Nordberg 2015, Jakubowski 2012). Cadmium body burden therefore accumulates across the human lifespan; the renal cortex concentration reaches its peak near age 55 under conditions of constant lifetime intake (ATSDR 2012). The primary toxic endpoint is renal tubular dysfunction, with skeletal demineralization a secondary endpoint that combines direct bone effects with calcium-handling consequences of the renal damage (Nordberg 2015, EFSA 2009). Cadmium is classified by the International Agency for Research on Cancer as a Group 1 human carcinogen on the basis of occupational inhalation studies, and dietary-exposure general-population epidemiology has produced statistical associations with cancers of the lung, endometrium, bladder, and breast (EFSA 2009, Nordberg 2015). No effective clinical treatment for cadmium intoxication exists; population-level dietary exposure reduction is the appropriate public-health response (Ufelle and Barchowsky 2021).

Four major regulatory and scientific bodies have issued dietary cadmium reference values. In order from tightest to most permissive when expressed on a daily per-body-weight basis: the US Agency for Toxic Substances and Disease Registry 2012 chronic oral Minimal Risk Level of 0.1 µg Cd/kg/day; the European Food Safety Authority 2009 tolerable weekly intake of 2.5 µg/kg b.w./week (daily equivalent approximately 0.36); the Joint FAO/WHO Expert Committee on Food Additives 2010 provisional tolerable monthly intake of 25 µg/kg b.w./month (daily equivalent approximately 0.83); and the US EPA Integrated Risk Information System oral reference dose, operative from 1985 and understood from secondary citations as approximately 1 × 10⁻³ mg/kg/day for food (the primary 1985 IRIS record is not yet in the library). All four values rest on overlapping primary literature but arrive at different numbers through different methodological choices. The factor of approximately 8 between the tightest and most permissive of the four is a live fact that any threshold-setting exercise must acknowledge rather than paper over; averaging across the four reference values without naming which one is being calibrated to obscures a methodological divergence the literature itself has not resolved.

At a glance

The three facts that matter most for a consumer trying to interpret cadmium in the food supply.

First, cadmium accumulates in the body over decades and is never meaningfully excreted; the kidney half-life is estimated at 20 years or more, and kidney-cadmium burden at middle age reflects dietary intake across essentially the whole of adult life, not recent consumption (Nordberg 2015, Jakubowski 2012). There is no clinical treatment that removes cadmium once it is accumulated (Ufelle and Barchowsky 2021). This is the medical basis for treating cadmium as a prevention problem rather than a treatment problem.

Second, the foods that contribute the most to population-level cadmium exposure do so because they are eaten in large volume, not because they are the most cadmium-contaminated foods. The population-level contributors are cereals (rice and wheat), potatoes and other starchy roots, leafy vegetables, nuts, oilseeds, pulses, and meat (EFSA 2009, JECFA 91st). The high-concentration foods, which matter most to consumers who eat them regularly, are bivalve molluscs (other than oysters), wild mushrooms, cocoa and chocolate products, seaweed, fungi, oilseeds, and edible organ meats (kidney and liver) (EFSA 2009). Regular consumers of bivalve molluscs show mean cadmium exposures above the EFSA tolerable weekly intake at 4.6 µg/kg body weight per week; regular consumers of wild mushrooms reach 4.3 µg/kg body weight per week (EFSA 2009).

Third, three groups are at materially higher risk than the general population and should pay more attention to cadmium than reference-value-for-adults summaries suggest. Children in the 0.5 to 12 year range have mean dietary cadmium exposure approximately 60 percent higher than adults because they eat more food relative to body weight (EFSA 2009); high-percentile child exposures in Australia and the United States reach 82 to 88 percent of the JECFA provisional tolerable monthly intake, and when cocoa-product contributions are added, the total for children aged 0.5 to 12 can reach 96 percent of that reference value (JECFA 91st). Women of reproductive age with low iron stores absorb cadmium more efficiently across multiple pregnancies (Nordberg 2015, Ufelle and Barchowsky 2021). Smokers receive an internal cadmium exposure from tobacco comparable in magnitude to their dietary exposure, which roughly doubles their body burden (Nordberg 2015).

Toxicology

Association of exposure to synthetic phenols and metal(loid)s with early puberty in Spanish girls: a multicentric case–control study reports urinary metal biomarkers and early-puberty associations in girls recruited across six Spanish hospitals during 2018–2022. The source keeps case and control summaries, detection frequencies and observational effect estimates separate. A single urine measurement and case–control sampling cannot establish exposure before puberty onset, causality, or a particular consumer-product source.

The primary target organ of cadmium toxicity is the kidney, specifically the proximal tubular cells of the renal cortex, where cadmium accumulates bound to metallothionein and gradually induces tubular dysfunction (Nordberg 2015, EFSA 2009). The kidney cortex concentration is approximately 1.25 times the whole-kidney concentration, reflecting the renal cortex’s role as the site of active reabsorption and therefore the tissue to which circulating cadmium-metallothionein complexes are preferentially delivered through glomerular filtration and tubular uptake (Nordberg 2015). The earliest detectable biological response is an increase in the urinary excretion of low molecular weight proteins, particularly beta-2-microglobulin, retinol binding protein, and protein HC, reflecting the loss of tubular reabsorption capacity (EFSA 2009, Nordberg 2015). Prolonged or high exposure progresses from tubular damage to decreased glomerular filtration rate and eventually to renal failure; in itai-itai disease patients, mean creatinine clearance of 42 mL/min and tubular reabsorption of phosphate of 51 percent have been observed alongside characteristic histopathology (tubular atrophy and dilatation with marked epithelial degeneration, in the absence of glomerular abnormalities at the light-microscopic level) (Nordberg 2015).

Skeletal toxicity is the second canonical endpoint. Cadmium causes bone demineralization through two mechanisms that operate in parallel: a direct effect on bone cells and mineralization, likely related to interference with calcium metabolism and with the enzyme lysyl oxidase (and therefore with bone collagen cross-linking), and an indirect effect secondary to renal dysfunction, through altered calcium and phosphate handling by the damaged kidney (Nordberg 2015). The bone effects manifest clinically as osteomalacia, osteoporosis, and increased fracture risk, with the heaviest burden falling on postmenopausal women and on populations with inadequate calcium, vitamin D, iron, zinc, or protein intake (Nordberg 2015). The combination of renal and skeletal damage in cadmium-polluted populations is what produces itai-itai disease in its severe form (see the itai-itai section below). At lower exposures, epidemiological studies have found associations between decreased bone mineral density, increased fracture risk, and urinary cadmium levels around 1 µg/g creatinine and higher (Nordberg 2015).

Cardiovascular effects are described differently by the two most current textbook sources. The Handbook on the Toxicology of Metals chapter 32 (Nordberg, Nogawa, Nordberg 2015) treats cardiovascular endpoints as contested in the literature: some human biomonitoring studies report associations between cadmium exposure and blood pressure, atherosclerosis, peripheral arterial disease, and cardiovascular mortality, while other studies do not reproduce these associations, with the chapter concluding that the evidence continues to be variable and that residual confounding, particularly by tobacco smoke, cannot be excluded in much of the positive literature. The Casarett & Doull’s Essentials of Toxicology chapter 23 (Ufelle and Barchowsky 2021), published six years later, uses notably less hedged language: it describes a “strong association” between cadmium exposure and peripheral vascular disease, and raises the possibility that cadmium partially mediates the negative effect of smoking on peripheral artery disease. Both positions are recorded here without resolution; the first synthesis pass has not completed a search of the 2015-to-present cardiovascular literature that would support reconciling them. See synthesis for tracking.

Cadmium does not interact directly with DNA. Its genotoxicity operates through induction of oxidative stress and inhibition of DNA repair mechanisms (Nordberg 2015). Cadmium causes lung cancer in rats after inhalation exposure (Nordberg 2015). In humans, IARC’s Group 1 classification rests on occupational inhalation studies; dietary cadmium’s carcinogenic potential at general-population exposure levels remains an area where the dose-response evidence is suggestive but not yet quantitative, with general-population epidemiology producing statistical associations for cancers of the lung, endometrium, bladder, and breast that the major regulatory bodies have not yet translated into quantitative dose-response reference values (EFSA 2009, Nordberg 2015).

Developmental and male reproductive toxicity are separate endpoints for which cadmium has been judged a sufficient hazard to warrant listing under California’s Proposition 65 (OEHHA 1996). The 1996 OEHHA hazard identification document compiled the human and animal evidence: reduced birthweight and pre-term labor correlated with maternal blood or infant hair cadmium in human epidemiology (with the acknowledgment that confounding by lead and tobacco smoking makes isolated cadmium effects difficult to establish), decreased pup birthweight and altered postnatal development in rodents exposed in utero via oral or inhalation routes, and effects on sperm counts, testes weight, and testicular histopathology in male experimental animals (OEHHA 1996). The California DART Identification Committee’s determination on the basis of this evidence produced the Prop 65 reproductive-toxicity listing effective May 1997; the 2001 MADL of 4.1 µg/day oral implements that listing (OEHHA 2001). The developmental endpoint (Ali et al. 1986 LOEL of 0.706 mg/kg/day in rats) was controlling because it was more sensitive than the male reproductive endpoint (Laskey et al. 1980 NOEL 1 ppm) (OEHHA 2001). Casarett & Doull’s Essentials 2021 adds the observation that pregnant women appear to accumulate more cadmium than nonpregnant women, a population-level exposure-biology fact that reinforces the reproductive-toxicity endpoint’s weight (Ufelle and Barchowsky 2021).

Central and peripheral nervous system effects are plausible but less well characterized. Animal data suggest that cadmium can alter brain development when exposure occurs before the blood-brain barrier is fully established, likely through interference with zinc metabolism and with metallothionein function in neural tissue (metallothionein-3 is a brain-expressed form rich in zinc and relevant to neurodegenerative disease; cadmium can displace zinc from metallothionein-1 and metallothionein-2 but does not induce metallothionein-3) (Nordberg 2015).

Clinical treatment

There is no effective clinical treatment for cadmium intoxication (Ufelle and Barchowsky 2021). Chelation therapy for cadmium generally produces significant adverse effects and is not an established standard of care. This is a durable clinical statement and it grounds the appropriate public-health response: population-level dietary exposure reduction is the intervention available to regulators, certification programs, and consumers, not pharmacological treatment after exposure.

Typical exposure routes

Dietary intake is the dominant route for the non-smoking general population (Nordberg 2015). Tobacco smoking contributes an internal exposure comparable in magnitude to dietary intake; uptake from smoking 20 cigarettes per day is approximately 2 µg of cadmium, and direct measurement in tissue shows that body burden in smokers is roughly double that of non-smokers (Nordberg 2015). House dust can be an important source of exposure for children (Nordberg 2015). Inhalation exposure in the non-smoking general population contributes only marginally to total body burden (Nordberg 2015). Dermal absorption of cadmium compounds is negligible (Jakubowski 2012).

Gastrointestinal absorption of ingested cadmium is 5 to 10 percent in humans on average, varying across a 1 to 10 percent range depending on individual factors, with low body iron stores common in women of reproductive age as the single largest upward variability factor; multiple pregnancies, preexisting health conditions, and nutritional deficiencies in zinc or calcium also raise absorption (Nordberg 2015). Pulmonary absorption of inhaled cadmium is higher, in the range of 10 to 50 percent (Nordberg 2015) or 10 to 60 percent (Ufelle and Barchowsky 2021), depending on particle size and solubility. These individual-level and route-level variability factors are incorporated into the EFSA TWI derivation through the toxicokinetic model, which is why the Panel applied no additional uncertainty factor for individual susceptibility; they are accounted for in ATSDR’s MRL derivation through the empirical environmental-exposure study base (EFSA 2009, ATSDR 2012).

Biological half-life and body burden accumulation

The biological half-life of cadmium in humans is long and has been estimated through multiple approaches. One-compartment models fit to empirical data on whole-body and renal cortex accumulation produce estimates of at least 20 years (Kjellström 1971, Tsuchiya and Sugita 1971, WHO/IPCS 1992), and this is the value most regulatory documents cite. Biopsy-based work (Akerstrom et al. 2013) has found that the half-life in the kidney depends on the cadmium burden itself: approximately 21 years at lower renal cortex concentrations (around 8 mg/kg) and approximately 43 years at higher concentrations (around 23 mg/kg). In urinary cadmium measurements from a Japanese cadmium-polluted region, half-lives of approximately 14 years and 24 years have been estimated for men and women respectively (Suwasono et al. 2009). Jakubowski 2012 gives the summary range as 10 to 30 years, consistent with the above.

Eight-compartment physiologically based toxicokinetic models (Kjellström and Nordberg 1978, Nordberg and Kjellström 1979) are used by ATSDR and by Thun et al. 1991 for quantitative risk assessment, with age-dependent amendments (Choudhury et al. 2001) that ATSDR explicitly adopted in the 2012 Toxicological Profile. These models take transfers between muscle, liver, and kidney into account, with short component half-lives (8 to 14 years for extra-renal tissues) and the dominant long-half-life component in the kidney. The practical consequence for wiki content is that cadmium body burden in a 50-year-old reflects dietary exposure over essentially the whole of adult life, not recent intake; population-level interventions to reduce exposure operate on timescales of decades, not months.

The renal cortex concentration typically reaches a peak near age 55 under conditions of lifetime constant intake. This is the anchor age for the ATSDR chronic oral MRL derivation and for the EFSA TWI’s kinetic back-translation, both of which calibrate their dietary-intake reference values against the kidney burden at this peak.

Food sources

Major dietary contributors to population cadmium exposure, identified by EFSA’s analysis of approximately 140,000 European occurrence samples collected 2003 to 2007 and consumption data from EFSA’s Concise European Food Consumption database, are cereals and cereal products, vegetables, nuts and pulses, starchy roots and potatoes, and meat and meat products. These categories dominate because of high consumption volumes rather than because they carry the highest cadmium concentrations. The JECFA 91st meeting 2022 reanalysis using the GEMS/Food database (277,292 cleaned records covering 10 of 17 GEMS/Food cluster diets) confirms the same commodity list across the international regional diets, with rice, wheat, root vegetables, tuber vegetables, leafy vegetables, other vegetables, and molluscs collectively accounting for 40 to 85 percent of total mean dietary cadmium exposure depending on regional diet.

The foods with the highest cadmium concentrations, rather than the highest contribution to exposure, are seaweed, fish and seafood (particularly bivalve molluscs other than oysters), chocolate and cocoa, foods for special dietary uses, fungi, oilseeds, and edible offal (especially kidney and liver). These food categories produce substantial per-serving exposure even at moderate consumption levels; regular consumers of bivalve molluscs showed a mean cadmium exposure of 4.6 µg/kg b.w./week and regular consumers of wild mushrooms 4.3 µg/kg b.w./week, both well above the EFSA mean of 2.3.

The 91st meeting of JECFA, convened in November 2020 at the request of the Codex Committee on Contaminants in Foods, substantially updated the evidence base for cocoa and cocoa-derived products. Occurrence data submitted to the Committee in 2019 showed higher mean cadmium concentrations in cocoa products than had been recognized in the JECFA 77th meeting 2013 cocoa-specific assessment. The updated analysis estimated that cocoa-product contributions push total dietary cadmium exposure in children aged 0.5 to 12 years to as high as 96 percent of the JECFA provisional tolerable monthly intake, essentially saturating the international reference value from dietary sources alone. Cocoa powder specifically drove a high-percentile (P97.5) exposure of 12 µg/kg b.w./month in European children aged 7 to 11. Cocoa, cocoa powder, and chocolate are therefore priority ingredient-page targets when the ingredient wave begins.

Cadmium accumulates in plants through root uptake from soil. The use of phosphate fertilizers, which contain cadmium as a trace contaminant of the phosphate rock, has progressively elevated agricultural soil cadmium levels across much of Europe (Nordberg 2015, Jakubowski 2012). Local contamination from mining, smelting, and sewage-sludge application can produce substantially higher soil concentrations in hotspot areas, with corresponding elevation in locally produced food (Nordberg 2015).

For rice specifically, irrigation regime is an emerging cadmium-risk driver that interacts with the established arsenic story. Soil redox conditions controlled by water management drive opposite accumulation dynamics: flooded paddies suppress Cd and favor inorganic arsenic (iAs); aerobic or alternate-wetting-and-drying (AWD) paddies suppress iAs and favor Cd. Two companion field studies from the University of Delaware RICE facility quantify the trade-off. Limmer and Seyfferth 2024 reports Cd ranges of approximately 10 to 150 µg/kg dw in polished grain across six irrigation treatments, with continuously flooded plots at the low end and aerobic management at the high end. Seyfferth et al. 2025 found that the driest paddy conditions exceeded the Codex Cd maximum level of 0.4 mg/kg in polished grain in both years of the study. arsenic (As) AWD adoption scales globally in response to climate adaptation pressure, the cadmium dimension of rice contamination may grow relative to the arsenic dimension that has historically defined regulatory attention. See Climate adaptation creates new heavy-metal trade-offs for the full synthesis and Rice (irrigation-management cadmium risk section).

Industrial cadmium production and use is itself a major upstream driver of environmental cadmium loading. Global cadmium production declined from approximately 22,000 metric tons per year at the early-2000s peak to approximately 16,000 metric tons per year by the 2012 period (Jakubowski 2012). The dominant uses are electrode material in nickel-cadmium batteries (77 percent), pigments (11 percent), protective plating on steel (8 percent), and alloys (4 percent). Ambient air cadmium concentrations reflect this industrial footprint: remote areas at 0.1 to 1 ng/m³, rural areas at 0.1 to 5, urban areas at 1 to 20, with higher concentrations in proximity to cadmium-emitting industrial sources.

What this means for food choice

The population-level dietary contributors to cadmium exposure are foods most people cannot and should not avoid. Rice, wheat, potatoes, leafy vegetables, nuts, and meat are nutritional staples, and the cadmium they deliver to an average adult diet is at or slightly above the European tolerable weekly intake of 2.5 µg/kg body weight per week (EFSA 2009). The appropriate consumer response to this baseline is not avoidance of staples but attention to the high-concentration foods and high-exposure behaviors that push a person above the population average.

The foods and behaviors that materially raise an individual’s cadmium exposure above the population average:

• Regular consumption of bivalve molluscs other than oysters (clams, mussels, scallops, cockles) at mean levels that place regular consumers at approximately twice the EFSA mean dietary exposure (EFSA 2009).
• Regular consumption of wild mushrooms, which can concentrate cadmium from their substrate at levels that place regular consumers similarly elevated (EFSA 2009).
• Regular consumption of organ meats (kidney and liver of cattle, pigs, horses), which are the tissues where cadmium accumulates most in food animals (EFSA 2009, Nordberg 2015).
• Cocoa powder and chocolate products consumed frequently, particularly by children in the 0.5 to 12 year range, for whom cocoa alone can drive a 97.5th-percentile exposure of 12 µg/kg body weight per month on top of dietary intake from other sources (JECFA 91st).
• Tobacco smoking, which contributes an internal cadmium exposure comparable in magnitude to dietary intake (approximately 2 µg of cadmium per 20 cigarettes), roughly doubling body burden in smokers (Nordberg 2015).
• Locally-produced food from areas with historic mining, smelting, or sewage-sludge-amended agriculture (Nordberg 2015).

The framing for consumer choice is not “safe versus dangerous” but “your total weekly exposure, summed across diet, environment, and smoking, relative to the reference values you find most credible.” Consumers who would like to benchmark their own exposure to the tighter reference values (ATSDR chronic oral MRL of 0.1 µg/kg/day, which is approximately 0.7 µg/kg b.w. per week) should treat the population-level dietary staples as their baseline exposure and actively manage the high-concentration items above (ATSDR 2012).

Regulatory limits

Reference values and maximum levels established to date, with more to populate as ingests complete:

The four dietary-reference values on the daily per-body-weight scale that are comparable to one another: ATSDR chronic oral MRL 0.1 µg/kg/day (tightest, anchored on a UCDL10 of 0.5 µg/g creatinine with a toxicokinetic translation to 0.33 µg/kg/day in females at age 55 and an uncertainty factor of 3 for human variability); EFSA TWI 2.5 µg/kg b.w./week (daily equivalent 0.36, anchored on a BMDL5 of 4 µg U-Cd/g creatinine with a chemical-specific adjustment factor of 3.9 and a kinetic back-translation); JECFA PTMI 25 µg/kg b.w./month (daily equivalent 0.83, established at the 73rd meeting in 2010 with a monthly averaging window reflecting cadmium’s long half-life); EPA IRIS oral RfD 1 × 10⁻³ mg/kg/day for food (1.0 µg/kg/day, from the 1989 IRIS record verified directly from the EPA IRIS database). The factor-of-10 range across the four values reflects different methodological choices on overlapping primary literature, not disagreements on underlying toxicology; the ordering tightest-to-most-permissive is ATSDR → EFSA → JECFA → EPA IRIS.

ATSDR itself notes (p. 43 of the 2012 profile) that its chronic oral MRL is below the estimated age-weighted US dietary cadmium intake of approximately 0.3 µg/kg/day, and that the UCDL10 point of departure is approximately twofold above the CDC 2011 US adult geometric mean urinary cadmium of 0.247 µg/g creatinine. The tightest regulatory reference value is below typical US exposure. This is a load-bearing fact for interpreting the reference values: at least one major regulatory body has set a chronic oral limit beneath the level at which the general US population is already exposed through diet.

What the reference values mean in practice

A consumer reading the table above and wondering which number to use as a benchmark for personal decision-making is asking the right question, and it does not have a single answer. Each of the four major dietary cadmium reference values is defensible within its own methodological frame, and a consumer should choose among them based on the level of precaution that matches their own situation.

The tightest reference, ATSDR’s chronic oral MRL at 0.1 µg Cd per kilogram body weight per day, is the appropriate benchmark for a consumer who prioritizes margin of safety, who is a member of a vulnerable subpopulation (pregnancy, childhood, smokers, high-seafood or high-cocoa consumption), or who is accumulating cadmium body burden that will continue to compound over decades (ATSDR 2012). For a 70 kilogram adult, this reference corresponds to approximately 7 µg of cadmium per day. Typical US dietary cadmium intake is estimated at approximately 0.3 µg per kilogram body weight per day, or 21 µg per day for the same adult (ATSDR 2012). The ATSDR reference value is approximately one-third of typical US intake.

The EFSA tolerable weekly intake at 2.5 µg/kg body weight per week, which is the operative reference value across the European Union, corresponds to approximately 175 µg per week for the 70 kg adult, or approximately 25 µg per day. Typical European dietary cadmium intake sits close to or slightly above this reference value at the population mean (2.3 µg/kg b.w./week); the European Panel’s risk characterization states that population-level cadmium exposure should be reduced (EFSA 2009).

The JECFA provisional tolerable monthly intake of 25 µg/kg b.w./month, which is the international reference value Codex standards are aligned to, corresponds to approximately 1,750 µg per month for the 70 kg adult, or approximately 58 µg per day (JECFA 91st). This value is the most permissive of the four daily-equivalent dietary references on the wiki.

A consumer’s practical choice: if your dietary pattern is high in seafood (particularly bivalve molluscs), wild mushrooms, organ meats, or cocoa, or if you are pregnant or a frequent smoker, calibrate your attention to the ATSDR value and consider the EFSA value as a secondary reference. If your dietary pattern is European and typical of a Member State average, the EFSA TWI is the operative regulatory reference in your jurisdiction and the benchmark that informs national-level exposure-reduction policy. The JECFA value is more appropriate as a benchmark for regulators considering trade-standard harmonization than for individual dietary decisions.

Testing

Analytical methods in use across the occurrence and biomonitoring literature span flame atomic absorption spectrometry (FAAS, detection limits 0.8 to 12.5 µg/L), inductively coupled plasma optical emission spectrometry (ICP-OES, detection limits 0.1 to 1 µg/L), graphite furnace atomic absorption spectrometry (GFAAS, detection limits 0.002 to 0.02 µg/L), and inductively coupled plasma mass spectrometry (ICP-MS, detection limits 0.00001 to 0.001 µg/L). The four-order-of-magnitude range in detection limits across methods is material for what wiki claims about cadmium occurrence can actually be supported by individual data points: FAAS data at 20 µg/L and ICP-MS data at 0.1 µg/L both encode “non-detect” by different thresholds, and pooled datasets must be handled carefully to avoid false precision. FDA’s Toxic Elements Program uses an ICP-MS method; the ATSDR 2012 profile uses an ICP-MS protocol for biomonitoring; the NIOSH Method 7048 for occupational air cadmium uses flame AAS at 228.8 nm with deuterium background correction, producing a working range of 0.1 to 2 mg/m³ at 25 L air-sample volume.

Biomonitoring for exposure assessment typically measures cadmium in whole blood (reflecting recent exposure with a few-month memory) or urine (reflecting body burden and cumulative exposure over years, normalized to urinary creatinine). The EFSA TWI derivation, the ATSDR chronic oral MRL derivation, and the JECFA PTMI all use urinary cadmium normalized to creatinine as the exposure metric. Reference intervals and clinical action levels for urinary β2-microglobulin as a tubular-dysfunction biomarker use an upper limit of 300 µg/g creatinine (Jakubowski 2012). See Jakubowski 2012 for the occupational sampling-procedure detail (NIOSH Method 7048, urine sample handling requirements, matrix-modifier protocols for GFAAS urinary cadmium).

A dedicated wiki/testing/ section with detailed method-specific pages will be stood up in a later wave.

Gut microbiome and cadmium

Cadmium changes gut community composition in mice and rats under the exposures the sources state, and a 30-day rat study reports lower intestinal barrier protein with higher inflammatory cytokines. Human evidence in the systematic review read here is one infant study, and that review says a general conclusion is not available. A review mentions a probiotic strain in connection with cadmium toxicity. That is not a measured change in cadmium absorption from a food.

Cadmium and gut communities

Zhang and colleagues (Zhang et al. 2015) exposed mice to 10 mg/L cadmium in drinking water for 10 weeks. Per WikiBiome source summary, DOI 10.1021/acs.chemrestox.5b00237, and the abstract on the source record, Firmicutes and gamma-proteobacteria decreased in feces after 4 weeks, Firmicutes decreased in cecum contents after 10 weeks, and 16S rRNA gene sequencing showed a perturbed community structure and richness at family and genus level. The abstract says the microbiome change might raise serum lipopolysaccharide and hepatic inflammation, and might indirectly perturb energy homeostasis. The animal count is not stated in the summary used here. The word “might” is the abstract’s. This is not a cadmium absorption result.

Liu and colleagues (Liu et al. 2023) exposed Sprague-Dawley rats to cadmium chloride for 30 days. Per WikiBiome source summary, DOI 10.3389/fvets.2023.1219729, intestinal ZO-1 was reduced (p below 0.05), and tumor necrosis factor alpha and interleukin-6 increased in intestine and blood (p below 0.05). A second summary of the same DOI conflicts on metabolite direction and on the name of a translocated phylum. Those conflicting items are omitted. The milligram dose and the number of rats are not in the summary used here.

Richardson and colleagues (Richardson et al. 2018) gavaged Sprague-Dawley rats for 5 days, 5 rats per cohort, with cadmium chloride among five metals. Per WikiBiome source summary, DOI 10.1038/s41598-018-24931-w, cadmium produced a dose-dependent compositional shift on PERMANOVA. Differential abundance affected 5 genera for cadmium, 37 for nickel, 17 for arsenic, 10 for chromium, and 1 for cobalt (47 genera across the metals). The summary does not print the milligram doses. It states that Proteobacteria increased across most metals except cadmium, and that lower Shannon diversity and observed operational taxonomic units were reported for arsenic, chromium, and nickel, not for cadmium.

People, and microbes that are reported to change cadmium toxicity

Rezazadegan and colleagues (DOI 10.1186/s41043-025-00750-4) systematically reviewed human observational studies searched through October 2023. The article included 12 studies on arsenic, lead, mercury, and cadmium. For cadmium it reports one United States cross-sectional study of 179 infants, using toenail cadmium, with a positive association between the review’s moderate cadmium category and Bifidobacterium. The discussion states that a general conclusion on mercury and cadmium cannot be made because the data are too inconclusive. The article’s Collinsella increase is described for high arsenic, lead, and mercury, and the discussion excepts cadmium.

Ghosh and colleagues (Ghosh et al. 2024) is a review. Per WikiBiome source summary, DOI 10.1530/MAH-23-0015, cadmium reduces ZO-1, ZO-2, JAM-A, occludin, and claudin-1. The summary states that lower cadmium doses decrease Akkermansia muciniphila, without restating the dose, and that Lactobacillus plantarum CCFM8610 reduces cadmium-induced toxicity. The summary does not give a host, a food matrix, or a percent change in cadmium absorption.

Studies of cadmium and the gut microbiome

Brands, suppliers, and testing

A rat barrier marker or a probiotic strain report does not change the cadmium result on a certificate of analysis. Brands, suppliers, and quality teams still assay cadmium in the ingredient or finished product by the method the specification names. A Lactobacillus plantarum finding is evidence about that experiment only when the study measured cadmium. It is not evidence that a supplier’s lot concentration moved.

What remains uncertain

Human cadmium evidence in the review read here is a single infant toenail study, and the review withholds a general conclusion. Zhang does not state an animal count, and the lipopolysaccharide sentence is conditional. Liu and Richardson do not state milligram doses in the summaries used here. Metabolite directions in the duplicate Liu summaries conflict, so they are left out. No study in this section reports a percent change in cadmium absorption from a food.

Historical context: itai-itai disease

Itai-itai disease is the most severe clinical presentation of chronic dietary cadmium poisoning documented in the human record, and the historical event that established cadmium’s renal and skeletal toxicity as a paired public-health concern rather than two separate endpoints (Nordberg 2015). It occurred in the Jinzu River basin of Toyama Prefecture, Japan, from the 1950s onward, in a population exposed to cadmium primarily through the consumption of rice and other produce grown in paddies and fields irrigated with water contaminated by effluent from a zinc mine upstream (Nordberg 2015). The clinical picture combines renal injury (both tubular and glomerular dysfunction, with urinary excretion of low molecular weight proteins elevated several-thousand-fold above normal, together with glucosuria and general aminoaciduria) and skeletal injury (osteomalacia and osteoporosis severe enough to produce spontaneous bone fractures, with the associated moderate-to-severe anemia and elevated serum alkaline phosphatase characteristic of active bone disease) (Nordberg 2015).

Through 2011, 196 cadmium-exposure cases had been officially recognized as itai-itai disease (3 men and 193 women), with an additional 255 subjects (46 men and 209 women) requiring observation for the condition (Nordberg 2015). The overwhelming sex-skew toward postmenopausal women reflects the combined vulnerability of calcium-depleted skeletons and iron-deficiency-enhanced cadmium absorption across multiple pregnancies and lactations, against a dietary pattern with limited zinc and calcium (Nordberg 2015). Renal tubular injury is highly prevalent across the broader Jinzu basin population beyond the diagnosed cases: urinary B2M concentrations exceeded 4 mg/L in 71 to 74 percent of residents aged 50 to 59 in the most heavily polluted district, and in 91 to 100 percent of residents 70 years of age or older (Nordberg 2015). At least 16 itai-itai-like cases have been reported from other cadmium-polluted regions outside the Jinzu basin (Nordberg 2015).

The disease is the historical anchor for every regulatory cadmium reference value derived since the 1970s. The Kjellström-Nordberg toxicokinetic model was developed in the same period in direct response to the Jinzu epidemic (Nordberg 2015). The EFSA, JECFA, ATSDR, and EPA IRIS derivations all operate against the Jinzu cohort and the subsequent environmental-exposure epidemiology that extended the observations to less-polluted populations (EFSA 2009, ATSDR 2012, JECFA 91st). The modern wiki content on cadmium’s renal and skeletal endpoints descends, through those regulatory derivations, from this clinical cohort.

Vulnerable populations

Populations for which cadmium exposure warrants particular attention, synthesized across the ingested sources:

If you are in one of these groups

The vulnerable-populations framing is not advice to avoid food; it is a framing to help a reader understand whether reference values derived for the general population apply to them or whether their own exposure profile calls for more attention. Three practical implications for consumers who recognize themselves on the list above.

For pregnant and potentially-pregnant women, two facts matter. First, iron deficiency (common in women of reproductive age) raises cadmium absorption from the gut, so correcting iron status through diet or supplementation is itself a cadmium exposure reduction. Second, the California OEHHA Maximum Allowable Daily Level of 4.1 µg per day oral is derived specifically from a developmental-toxicity endpoint and is therefore the most directly relevant regulatory reference for this population; products carrying a California Proposition 65 warning for cadmium are products that, at typical use, would exceed this level.

For parents of children under 12, frequent cocoa-product consumption is the single most consequential dietary variable under parental control. The JECFA 91st meeting 2022 assessment finds that cocoa powder and chocolate products can drive a high-percentile exposure that, combined with whole-diet cadmium, reaches 96 percent of the international tolerable monthly intake in this age group. Moderating cocoa-product frequency is a higher-leverage intervention than modifying any other single food category.

For people who regularly eat bivalve molluscs, wild mushrooms, or organ meats, the population-level mean exposure exceeds the EFSA tolerable weekly intake by approximately twofold, and the ATSDR chronic oral Minimal Risk Level by a larger factor. If these foods are cultural or nutritional staples rather than occasional choices, calibrating attention to the ATSDR reference value rather than to the more permissive EFSA or JECFA values is the more protective posture.

App-layer integration

Machine-readable takeaways from this synthesis for the Heavy Metal Index consumer app pipeline.

Population-level contamination-profile confidence is high for cereals (rice, wheat), potatoes and other starchy roots, leafy vegetables, nuts, oilseeds, pulses, meat, and offal, on the basis of the 140,000-sample EFSA occurrence dataset (2003 to 2007) and the 277,292-record JECFA GEMS/Food dataset (2011 onward). For these commodities, contamination-profile populated states with confidence: high and n_studies: many are appropriate once ingredient pages are stood up. Cocoa powder, cocoa products, and chocolate carry high-confidence occurrence data from the JECFA 91st meeting 2022 but require specific handling because the 2019 occurrence data showed higher concentrations than the 77th meeting 2013 values; ingredient pages should cite the 2022 values.

For app exposure estimation, the 90th percentile consumption values from EFSA (adults) and the JECFA GEMS/Food cluster diets provide default per-commodity serving sizes, but pediatric multipliers are required: children aged 0.5 to 12 should use approximately 1.6x adult per-kg intake by default, with the toddler-specific multiplier approximately 2.65x (UK FSA 2009 finding that toddlers 1.5 to 4.5 years had exposure 165 percent higher than adults) (EFSA 2009).

For app risk-scoring against reference values, the four reference values in order of increasing daily-equivalent permissiveness are:

The app should allow a user to choose which reference value they want to benchmark against, default to the ATSDR value for conservative estimation, and never silently average across reference values. For the vulnerable-population flag layer, flag users in pregnancy, childhood (0.5 to 12), frequent-smoker, and high-seafood/high-cocoa categories against the ATSDR value specifically, and render the OEHHA Prop 65 MADL of 4.1 µg/day as a product-labeling cross-reference for California-market products.

Structured outputs the app can consume directly, in addition to the reference-value table:

• Absorption fractions: GI 5 to 10 percent (general population, with 1 to 10 percent individual range), pulmonary 10 to 50 to 60 percent; use midpoint of 7.5 percent GI for default dose estimation, 10 percent for low-iron or pregnancy flags.
• Biological half-life default: 20 years (regulatory convention); use 21 to 43 year range for high-exposure percentiles when kidney-concentration-dependent kinetics matter.
• Peak renal cortex concentration age: 55 years; use this as the reference age for lifetime-cumulative exposure estimates.
• Smoking cadmium contribution: approximately 2 µg per 20 cigarettes absorbed internally; treat as additive to dietary intake for smoker users.

Open questions

Five load-bearing open questions tracked on synthesis, surfaced during ingest of the initial cadmium batch:

First, the four major dietary reference values (ATSDR chronic oral MRL, EFSA TWI, JECFA PTMI, EPA IRIS oral RfD) differ by up to approximately a factor of 8 on overlapping primary literature. The synthesis page tracks the methodological choices that drive the differences. Any threshold-setting exercise drawing on these reference values cannot silently average across the four; it must name which reference it calibrates to and why, because the divergence reflects unresolved methodological choices rather than measurement noise. The EFSA 2011 reaffirming statement, which articulates the EU-side explanation for the divergence from JECFA, is not yet in the corpus and is flagged for future ingest.

Second, dietary cadmium carcinogenicity dose-response remains unresolved. IARC maintains the Group 1 classification on the basis of occupational inhalation studies; general-population epidemiology produces statistical associations for cancers of the lung, endometrium, bladder, and breast; EFSA 2009 judged the data insufficient for quantitative dose-response modeling. The synthesis needs to surface the uncertainty without under- or over-claiming on cancer risk.

Third, the cardiovascular endpoint has shifted in framing between the 2015 Handbook chapter (“variable” evidence) and the 2021 Casarett Essentials chapter (“strong association”). The wiki records both positions without resolution pending a 2015-to-present literature search.

Fourth, the EPA IRIS cadmium assessment provenance gap: the raw PDF labeled “EPA_IRIS_Cadmium_ToxicologicalReview.pdf” is a 1999 external review draft that was never adopted; the operative 1985 IRIS record remains the canonical US EPA reference, but is not in the corpus. The 1999 draft is flagged for a future historical ingest wave.

Fifth, the Codex standards landscape is now substantially covered. Matrix-level Codex cadmium MLs are captured in CXS 193-1995, and the cocoa-cadmium Code of Practice is captured in CXC 81-2022 (the precedent document that anchors the broader CoP work initiated at CCCF17 2024).

Chromium research: qualified source context

Cadmium was reported as not detected in a Nilore, Islamabad soil characterization (Table 2). No numerical detection limit was supplied; this result is retained as a nondetect and cannot be replaced with zero. LABORATORY SCALE ELECTROKINETIC REMEDIATION OF HEXAVALENT CHROMIUM FROM CONTAMINATED SOIL

Nahavand farm study: evidence limitations

Sharafi et al. reported total cadmium in farm soil, irrigation water and whole above-ground crop biomass. The soil prose first states less than 1.6 mg/kg and then gives a sugar-beet-system maximum of 20.3 mg/kg. Both statements are retained as conflicting source reports. Whole biomass is not an edible grain/root sample, and the inconsistent risk models do not establish clinical effects (pp10–21). Soil–water–crop pathways of heavy metal contamination and human health risks in intensive smallholder farms of the Nahavand Plain, Iran

Arzew surface-soil survey

The Arzew survey reports cadmium below 0.01 mg/kg in all 84 study soils. This is an upper-bound report; the authors do not identify it as a formal detection or quantitation limit. It cannot be replaced with zero or treated as a measured food concentration (Boudia et al. 2019, Results 3.1). Spatial contamination and health risks of heavy metal(loid)s in surface soils from a petrochemical complex in the north-eastern region of Algeria

Sea-bass dietary exposure abstract

A SETAC 2025 abstract reports behavioral changes in juvenile sea bass after 21 days of experimentally contaminated diets, with nominal cadmium levels of 10 and 100 mg/kg. It supplies no fish counts, tissue concentrations or numerical effect sizes. These treatment levels are not measurements of cadmium in market fish, and the separate antibiotic findings do not establish a cadmium interaction effect (Bedrossiantz et al., abstract 1.01.P-Tu004). Neurobehavioral Impairments in the Sea Bass (Dicentrarchus labrax) Chronically Exposed to Cadmium and Ciprofloxacin Contaminated Diets

Zebrafish short-exposure abstract

Gawra et al. report decreased catalase and cholinesterase activities after a 24-hour cadmium exposure in zebrafish larvae, without numerical effect sizes or sample counts. Their nominal cadmium range is 0.24–24 µg/L in the official abstract record, which resolves a corrupted unit in the printed book. Antibiotic-associated swimming changes remain separate, and the study does not measure food contamination (SETAC 2025, abstract 1.01.P-Tu009). Linking Molecular and Phenotypic Endpoints in Zebrafish Larvae Exposed to Ciprofloxacin and Cadmium

China imported pet foods: preprint evidence

Du et al.’s pet-food preprint reports 29 Cd-positive products out of 93, a positive-only mean 0.138 mg/kg and range 0.0200–0.279 mg/kg (2024,Table 3). These values conflict with the paper’s stated CdLOD 0.08 andLOQ 0.20 mg/kg and definition of positivity aboveLOQ. The reported facts remain qualified and cannot support an assumed corrected decimal or a validated detection rate. Individual and Combined Contamination of the Heavy Metals in Commercial Cat and Dog Food

Dry dog-food formulation comparison

In 51 US retail dry dog foods, Kim et al.(2018) report cadmium medians 0.027 mg/Mcal for fish formulations,0.015 for poultry and 0.013 for red meat(N=17/group;Table 1). The fish-group range was 0.014–0.215 mg/Mcal. These are author-normalized energy-basis summaries; individual energy-density data are absent for conversion to mass basis. Evaluation of Arsenic, Cadmium, Lead and Mercury Contamination in Over-the-Counter Available Dry Dog Foods With Different Animal Ingredients (Red Meat, Poultry, and Fish)

Texas animal-feed survey

Dai et al. report cadmium mean 0.54 mg/kg, SD 1.04 and median zero in 36 Texas premixes from fiscal years 2012–2015 (2016, Table 3). Below-quantitation results were replaced with zero; the median is not proof of absence. The 2011 narrative uses cadmium units and extrema that conflict with Table 2. Premixes require their inclusion rates before characterizing complete rations. Heavy Metal Contamination of Animal Feed in Texas

Banat soil–nettle–snail study

In Nica et al.’s Romanian field study, nettle cadmium correlated with shell height at −0.80 (P<0.05) and whorl number at 0.84 (P<0.01). These are site-level associations from selected shells, with unclear statistical aggregation and no causal exposure experiment. Figure 3 shows strong tissue and site differences; the concentration bars are graphical estimates rather than exact tabulated sample values (2012, pp9–10 and Figure 3). Bioaccumulative and conchological assessment of heavy metal transfer in a soil-plant-snail food chain

Ganga freshwater-fish study: qualified evidence

In the Ganga survey, Table 4 reports C. mrigala liver cadmium of 2.64 ± 0.33 µg/g; narrative values of 2.54 do not match that cell (Maurya et al. 2019). Muscle and organ summaries are retained separately with the source’s unresolved wet/dry basis. The exposure table mixes tissue averages and contains apparent decimal anomalies, so its risk outputs are retained only as unvalidated source-model context. Bioaccumulation and potential sources of heavy metal contamination in fish species in River Ganga basin: Possible human health risks evaluation

Foamed hydrogels: synthetic-water experiments

Pille’s 2021 hydrogel thesis reports 92.3 ± 9.3 mg/g dry gel operational Cd(II) removal for the foamed and foam-stabilized material after 24 hours in a 109 ppm single-metal solution (three replicates; Results 2.4.7). The corresponding mixed-solution bar is approximately 34 mg/g, with initial Cd labeled 42 ppm versus 35 ppm each for Cu and nickel (Ni). The mixed-solution mass-removal ranking therefore does not establish intrinsic cadmium selectivity. Direct measurement of metal bound to the gel was unsuccessful. The use of foaming agents and foam stabilizers to improve heavy metal removal properties of acrylic acid/acrylamide hydrogels for use in wastewater remediation

Frequently asked questions

References

Works cited in this page’s text, in first-appearance order. See Sources for this page’s source inventory. Each title links to a source record with bibliographic details, reported findings, and document provenance.

1. Scientific Opinion of the Panel on Contaminants in the Food Chain on a request from the European Commission on cadmium in foodEFSA Panel on Contaminants in the Food Chain (CONTAM) · The EFSA Journal · 2009 · doi.org/10.2903/j.efsa.2009.980Government
2. Evidence on the Developmental and Reproductive Toxicity of CadmiumCalifornia Office of Environmental Health Hazard Assessment, Reproductive and Cancer Hazard Assessment Section · California Environmental Protection Agency, Office of Environmental Health Hazard Assessment · 1996 · doi.org/10.1016/0890-6238(96)00019-6Government
3. Cadmium: dietary exposure assessmentJoint FAO/WHO Expert Committee on Food Additives · WHO Food Additives Series, No. 82 (Safety evaluation of certain contaminants in food, prepared by the 91st meeting of JECFA) · 2022 · www.who.intGovernment
4. Toxicological Profile for CadmiumAgency for Toxic Substances and Disease Registry · 2012 · www.atsdr.cdc.govGovernment
5. Report of the 17th Session of the Codex Committee on Contaminants in Foods (REP24/CF17)Codex Alimentarius Commission, Codex Committee on Contaminants in Foods · Joint FAO/WHO Food Standards Programme, Codex Alimentarius Commission · 2024 · www.fao.orgGovernment
6. Cadmium (Chapter 32), in Handbook on the Toxicology of Metals, Fourth Edition, Volume II: Specific MetalsNordberg GF, Nogawa K, and Nordberg M · Academic Press / Elsevier, Amsterdam · 2015 · doi.org/10.1016/B978-0-444-59453-2.00032-9Textbook
7. Toxic Effects of Metals (Chapter 23), in Casarett & Doull’s Essentials of Toxicology, Fourth EditionUfelle AC and Barchowsky A · Casarett & Doull’s Essentials of Toxicology, Fourth Edition. McGraw Hill Education · 2021 · www.mhprofessional.comTextbook
8. Zinc and Cadmium Compounds (Chapter Seven), in Patty’s Toxicology, Sixth EditionJakubowski M · John Wiley & Sons, Inc · 2012 · doi.org/10.1002/0471435139.tox029.pub2Textbook
9. Proposition 65 Maximum Allowable Daily Level (MADL) for Reproductive Toxicity for Cadmium (Oral Route)California Office of Environmental Health Hazard Assessment, Reproductive and Cancer Hazard Assessment Section · California Environmental Protection Agency, Office of Environmental Health Hazard Assessment · 2001 · oehha.ca.govGovernment
10. General Standard for Contaminants and Toxins in Food and Feed (CXS 193-1995)Codex Alimentarius Commission · Codex Alimentarius (Joint FAO/WHO Food Standards Programme) · 1995 · www.fao.orgGovernment
11. Code of Practice for the Prevention and Reduction of Cadmium Contamination in Cocoa Beans (CXC 81-2022)Codex Alimentarius Commission · FAO and WHO, 2023. Codex Alimentarius Code of Practice No. CXC 81-2022. Joint FAO/WHO Food Standards Programme. Rome · 2022 · doi.org/10.4060/cc5333enGovernment
12. Association of exposure to synthetic phenols and metal(loid)s with early puberty in Spanish girls: a multicentric case–control studyOlivas-Martinez A, Escribano A, Riaño-Galán I, Torrebias M, Olmedo P, Gil F, et al. · European Journal of Pediatrics 185:295 · 2026 · doi.org/10.1007/s00431-026-06919-1Peer-reviewed
13. Controlling exposure to As and Cd from rice via irrigation managementLimmer MA and Seyfferth AL · Environmental Geochemistry and Health · 2024 · doi.org/10.1007/s10653-024-02116-xPeer-reviewed
14. Concentrations and Health Implications of As, Hg, and Cd and Micronutrients in Rice and Emissions of CH4 From Variably Flooded PaddiesSeyfferth AL, Limmer MA, Jackson BP, and Runkle BRK · GeoHealth · 2025 · doi.org/10.1029/2025GH001410Peer-reviewed
15. Subchronic Exposure of Mice to Cadmium Perturbs Their Hepatic Energy Metabolism and Gut MicrobiomeSongbin Zhang, Yuanxiang Jin, Zhaoyang Zeng, Zhenzhen Liu, and Zhengwei Fu · Chemical Research in Toxicology · 2015 · doi.org/10.1021/acs.chemrestox.5b00237Peer-reviewed
16. Environmental cadmium exposure alters the internal microbiota and metabolome of Sprague-Dawley ratsLiu S, Deng X, Li Z, Zhou W, Wang G, Zhan J, et al. · Frontiers in Veterinary Science · 2023 · doi.org/10.3389/fvets.2023.1219729Peer-reviewed
17. Exposure to toxic metals triggers unique responses from the rat gut microbiotaRichardson JB, Dancy BCR, Horton CL, Lee YS, Madejczyk MS, Xu Z, et al. · Scientific Reports · 2018 · doi.org/10.1038/s41598-018-24931-wPeer-reviewed
18. Effects of heavy metals on gut barrier integrity and gut microbiotaSweta Ghosh, Syam P. Nukavarapu, and Venkatakrishna Rao Jala · Microbiota and Host 2(1):e230015 · 2024 · doi.org/10.1530/MAH-23-0015Peer-reviewed
19. LABORATORY SCALE ELECTROKINETIC REMEDIATION OF HEXAVALENT CHROMIUM FROM CONTAMINATED SOILM. Khalid, N. Ahmed, and R. M. Qureshi · The Nucleus 45(1–2):55–61 · 2008 · doi.org/10.71330/nucleus.45.01-2.998Peer-reviewed
20. Soil–water–crop pathways of heavy metal contamination and human health risks in intensive smallholder farms of the Nahavand Plain, IranSaeed Sharafi, Maryam Sharafi, and Maryam Lorvand · Scientific Reports 16:9947 · 2026 · doi.org/10.1038/s41598-026-38637-xPeer-reviewed
21. Spatial contamination and health risks of heavy metal(loid)s in surface soils from a petrochemical complex in the north-eastern region of AlgeriaHayat Boudia, Laurent Vassalo, Mohammed Hadjel, Pascale Prudent, and Jean-Luc Boudenne · International Journal of Environmental Science and Technology 16:4707–4718; HAL author-manuscript version read · 2019 · doi.org/10.1007/s13762-018-02195-1Peer-reviewed
22. Neurobehavioral Impairments in the Sea Bass (Dicentrarchus labrax) Chronically Exposed to Cadmium and Ciprofloxacin Contaminated DietsJuliette Bedrossiantz, Janan Gawra, Nerea Sanchis, Paula Medina, Demetrio Raldua, Joana Luisa Pereira, et al. · SETAC Europe35th Annual Meeting Abstract Book, Vienna,11–15May2025; 1.01.P-Tu004 · 2025 · digital.csic.esConference
23. Linking Molecular and Phenotypic Endpoints in Zebrafish Larvae Exposed to Ciprofloxacin and CadmiumJanan Gawra, Énia Correia, Bruna Vieira, Joana Luisa Pereira, Inês Domingues, and Laia Navarro-Martin · SETAC Europe35th Annual Meeting Abstract Book, Vienna,11–15May2025; 1.01.P-Tu009 · 2025 · digital.csic.esConference
24. Individual and Combined Contamination of the Heavy Metals in Commercial Cat and Dog FoodJiaying Du, Kerui Zhou, Han Jiang, Shen Hu, Wei Zhang, Qiang Zheng, et al. · Research Square, version1, posted8September2024 · 2024 · doi.org/10.21203/rs.3.rs-4838876/v1Preprint
25. Evaluation of Arsenic, Cadmium, Lead and Mercury Contamination in Over-the-Counter Available Dry Dog Foods With Different Animal Ingredients (Red Meat, Poultry, and Fish)Hyun-Tae Kim, John P. Loftus, Sabine Mann, and Joseph J. Wakshlag · Frontiers in Veterinary Science5:264 · 2018 · doi.org/10.3389/fvets.2018.00264Peer-reviewed
26. Heavy Metal Contamination of Animal Feed in TexasSusie Y. Dai, Ben Jones, Kyung-Min Lee, Wei Li, Lynn Post, and Timothy J. Herrman · Journal of Regulatory Science4(1):21–32 · 2016 · doi.org/10.21423/jrs-v04n01p021Peer-reviewed
27. Bioaccumulative and conchological assessment of heavy metal transfer in a soil-plant-snail food chainDragos V Nica, Marian Bura, Iosif Gergen, Monica Harmanescu, and Despina-Maria Bordean · Chemistry Central Journal 6:55 · 2012 · doi.org/10.1186/1752-153X-6-55Peer-reviewed
28. Bioaccumulation and potential sources of heavy metal contamination in fish species in River Ganga basin: Possible human health risks evaluationPradip Kumar Maurya, D. S. Malik, Krishna Kumar Yadav, Amit Kumar, Sandeep Kumar, and Hesam Kamyab · Toxicology Reports 6:472–481 · 2019 · doi.org/10.1016/j.toxrep.2019.05.012Peer-reviewed
29. The use of foaming agents and foam stabilizers to improve heavy metal removal properties of acrylic acid/acrylamide hydrogels for use in wastewater remediationAnn Pille · MSc thesis, Bioresource Engineering, McGill University, Macdonald Campus; December2021 · 2021 · mcgill.scholaris.caThesis
30. Wastewater Irrigation and Accumulation of Heavy Metals in Vegetable Crops (Broccoli and Cauliflower)Bayan Rashid Rahim · Tikrit Journal for Agricultural Sciences 23(2):162–170 · 2023 · doi.org/10.25130/tjas.23.2.13Peer-reviewed
31. Effects of sewage water irrigation on heavy metals accumulation in vegetables in peri-urban areas of Faisalabad, PakistanMuhammad Abubakar, Basit Haider, Hadeeqa Arshad, Tufail Shah, Ameer Khan, Hummera Nawaz, et al. · Agricultural Research Reports 3(1):46–57 · 2025 · doi.org/10.54219/arr.03.1.2025.418Peer-reviewed
32. Assessment of the Level of Heavy Metals in Irrigation Water, Farm Soil, and Vegetables Grown in Gobbiya Dam, Bogoro Local Government Area Bauchi State, NigeriaJohn Joseph, Toma Buba, Jalo Enoch, and Ayuba Kaluri · Journal of Energy Technology and Environment 7(4):79–92 · 2025 · doi.org/10.37933/jete/7.4.2025.2568Peer-reviewed
33. Occurrence and Risk Assessment of Pesticides, Phthalates, and Heavy Metal Residues in Vegetables from Hydroponic and Conventional CultivationShanshan Chen, Chunxia Yao, Jiaxin Zhou, Haiyao Ma, Jing Jin, Weiguo Song, et al. · Foods 13, 1151 · 2024 · doi.org/10.3390/foods13081151Peer-reviewed
34. Study of Peculiarities of Accumulation of Heavy Metals and Arsenic in Medicinal Plant Raw Materials of Synanthropic Flora of Voronezh RegionNina Alekseevna Dyakova · Khimiya Rastitel’nogo Syr’ya 2:163–170 · 2023 · doi.org/10.14258/jcprm.20230211725Peer-reviewed
35. Removal of Heavy Metals from Industrial Sludge Using Soil Washing TechniqueJ. Sumalatha, B. P. Naveen, and R. K. Malik · Asian Journal of Water, Environment and Pollution 16(3):83–89 · 2019 · doi.org/10.3233/ajw190036Peer-reviewed
36. Bioaccessibility of Heavy Metals in Raw and Processed Alternanthera sessilis and Centella asiatica: An In vitro StudyThilini Kananke, Jagath Wansapala, and Anil Gunarathne · Nature Environment and Pollution Technology25(1):D1830 · 2026 · doi.org/10.46488/nept.2026.v25i01.d1830Peer-reviewed
37. HEAVY METALS ACCUMULATION IN SOIL AND CELERY ROOT (APIUM GRAVEOLENS L.) HARVESTED FROM THE POLLUTED AREAS IN SIBIU COUNTY, CENTRAL ROMANIABogdan Ștefan Oprea, Nicoleta Olimpia Vrînceanu, Dumitru-Marian Motelică, Georgiana Iuliana Plopeanu, Vera Carabulea, and Mihaela Costea · Annals of the University of Craiova—Agriculture,Montanology,Cadastre52(1):422–429 · 2022 · doi.org/10.52846/aamc.v52i1.1370Peer-reviewed
38. Assessment of the Risk of Heavy Metals Accumulation in Vegetable CropsVladimir N. Bashkin and Rosa A. Galiulina · Issues of Risk Analysis 18(4): 48-65 · 2021 · doi.org/10.32686/1812-5220-2021-18-4-48-65Peer-reviewed
39. Application of principal component analysis in the pollution assessment with heavy metals of vegetable food chain in the old mining areasIosif Gergen and Monica Harmanescu · Chemistry Central Journal6:156 · 2012 · doi.org/10.1186/1752-153x-6-156Peer-reviewed

Sources

Source records associated with this topic. Inclusion does not establish that every finding applies to this product or ingredient. References above identify works cited in the text. Additional records await source or bibliographic review and are excluded from this list.

Recent source records are shown below. Browse the complete evidence table for all source records and their reported findings.

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Additional geographic and remediation evidence

Bayan Rashid Rahim, 2023. Rahim measured lead, cadmium, iron and copper in dried edible broccoli and cauliflower heads grown under three irrigation regimes in Sulaymaniyah, Iraq. The tables preserve crop-specific differences: wastewater-irrigated broccoli had the largest listed values for the four metals, whereas cauliflower cadmium was greatest under alternating irrigation. The paired treatment summaries contribute source-native vegetable occurrence and irrigation-pathway evidence. The dried basis is not interchangeable with fresh vegetables. The experiment is site- and season-specific and does not characterize all river water, all Iraqi produce or long-term dietary exposure.

Muhammad Abubakar, 2025. Abubakar and colleagues measured seven metals in sewage water, soil, spinach and cauliflower at two peri-urban sites in Faisalabad, Pakistan. The paper reports substantial differences between the two crop/site combinations, but its design does not separate plant-species effects from location. Concentrations are retained with the source’s measurement and tissue limitations. These are localized paired environmental and crop measurements, with plant results routed as leafy-tissue evidence. They do not establish a cauliflower-head concentration, a fresh-weight concentration, or a causal reduction in biomass from metal exposure. Industrial source attribution is proposed by the authors, rather than measured by a source-apportionment experiment.

John Joseph, 2025. Joseph and colleagues measured seven metals in kenaf, chili pepper, tomato and spinach plant parts, with associated soil and irrigation water from Gobbiya Dam in Nigeria. The paper separates edible leaves or fruits from roots and stems. Its concentration tables are preserved independently of several inconsistent safety comparisons and a soil-index calculation that uses water standards. The organ-resolved dry-weight values support local occurrence and irrigation-pathway analysis. Roots, stems and non-edible leaves are retained as pathway context rather than assigned to edible-product distributions. Broad leafy-vegetable and herb/spice ingredient routes retain kenaf and chili identity in the structured record without substituting a named cultivar.

Shanshan Chen, 2024. Shanghai farm samples had lower reported lead and cadmium concentrations under hydroponic cultivation than conventional soil cultivation. The element-specific summaries combine four vegetables, while commodity-specific means combine lead with cadmium; neither split can be reconstructed into commodity-by-element concentrations from the preserved main paper. Supports a local cultivation-system comparison and the soil/irrigation pathway. It does not establish commodity-specific lead (Pb) or Cd distributions or universal hydroponic safety. Mixed-contaminant hazard indices include pesticides and phthalates; their interpretation remains source-reported.

Nina Alekseevna Dyakova, 2023. Dyakova compares nine elements in medicinal plant materials collected in disturbed and control environments in Russia’s Voronezh region during 2015–2020. The reported ranges preserve tissue and environmental setting; the paper also proposes regional background means across species. Supports geographic and tissue-specific contamination evidence for botanical raw materials and environmental attribution hypotheses. It does not measure finished supplements or isolate an individual polluter’s causal contribution.

J. Sumalatha, 2019. Column washing of Bangalore-area industrial sludge removed substantially more metals with hydrochloric acid plus EDTA than with distilled water. This is a remediation experiment relevant to sludge contamination pathways, with no measurements in food or a demonstrated safe land-application endpoint. Supports laboratory washing and contaminant-transport comparisons. Metal-rich leachate still requires management; the study does not establish agricultural reuse or field-scale safety.

Thilini Kananke, 2026. This Sri Lankan study compares elemental concentrations and simulated digestive release in two leafy vegetables across five growing areas. Raw, coconut-milk-cooked and coconut-oil-stir-fried portions were tested separately; lower in-vitro release does not establish lower human absorption or safe consumption. Supports region-specific leafy-vegetable occurrence and cooking/bioaccessibility comparisons. Processing effects are not uniform: for example Wellampitiya A. sessilis gastric Pb is 15.3% raw and 20.7% cooked. Coconut additions can change the matrix; an in-vitro endpoint is not in-vivo absorption.

Bogdan Ștefan Oprea, 2022. Celery roots and garden soils from 26 households in a historically polluted Romanian area showed wide cadmium and lead variation in 2021–2022. Soil results use dry weight, while edible celeriac results use fresh weight; these paired measurements preserve a legacy-contamination pathway without assigning sole liability to any facility. Supports historical industrial-burden and present edible-root occurrence evidence. Celery here is celeriac, not stalk celery; the product category is root/tuber vegetables. Geographic sampling is targeted to a polluted area and is not a national market sample.

Vladimir N. Bashkin, 2021. Bashkin and Galiulina review vegetable-associated metal exposure assessment and microbial/agronomic risk-management approaches. Chinese and Russian case-study values are secondary reports; they remain traceable to the cited studies and are not counted as new independent occurrence samples. Supports exposure-method and remediation literature discovery. Bacterial effects can increase as well as decrease uptake depending on organism, metal and plant; the review does not establish a universal inoculant intervention. Secondary model outputs are not contemporary health or certification thresholds.

Iosif Gergen, 2012. Gergen and Harmanescu analyze metal contamination patterns across two historic Romanian mining areas and a reference area. Their PCA study reproduces vegetable concentrations and male hazard quotients from the earlier Harmanescu 2011 study; these remain linked secondary observations rather than additional independent samples. Supports legacy mining and tissue/region differences. Parsley root and leaf remain distinct, as do carrot root and leaf. The fresh-matter food table is retained with cohort linkage so that a reanalysis cannot inflate the evidence pool. Source THQ rankings are model results, not clinical outcomes.