Chromium, Hexavalent

This page draws on evidence from UK Food Standards Agency, together with 12 peer-reviewed studies and 3 other cited sources. The complete citation list is at the bottom of the page.

Overview

Hexavalent chromium (Cr-VI, Cr(VI), or Cr6+) is the high-oxidation-state form of chromium found in chromate (CrO4^2-) and dichromate (Cr2O7^2-) anions. The species is operationally distinct from trivalent chromium (Cr3+), which is far less toxic and was historically (and contestedly) treated as an essential trace nutrient. The Heavy Metal Index maintains the Cr-VI / Cr(III) split throughout, treating hexavalent chromium as a separate analyte from total or trivalent chromium. Total chromium reported by a source is never substituted for Cr-VI on this wiki; sources that do not speciate are routed to chromium as total chromium and labeled as such. See also chromium for the parent element page.

Toxicology

Cr-VI crosses cell membranes through sulfate and phosphate transporters because the chromate and dichromate oxyanions resemble those nutrients structurally. Once inside the cell, Cr-VI is reduced to Cr(III) through reactive Cr-V and Cr-IV intermediates, generating reactive oxygen species and DNA damage along the way. The toxicology chapter Ufelle and Barchowsky 2021 characterizes Cr-VI as the high-concern carcinogenic chromium species and identifies its principal toxic endpoints as corrosive injury at high acute exposure, allergic contact dermatitis on chronic skin contact, acute renal injury after high-dose ingestion, and lung cancer and genotoxicity after inhalation exposure. The same chapter explicitly names chromium among the metals that can provoke immune reactions, alongside mercury, gold, platinum, beryllium, and nickel. Children and elderly individuals are highlighted as more susceptible than most adults at any given exposure level.

The carcinogenicity of Cr-VI is best characterized for inhalation exposure (occupational settings, chromate production, electroplating, leather tanning) where lung cancer is the canonical endpoint. Palazzo et al. 2026 report that IARC classifies Cr(VI) as a Group 1 human carcinogen, and characterise the epidemiological record as showing modest but significant increases in overall cancer incidence and mortality, particularly for respiratory and gastrointestinal cancers, while noting that cardiovascular disease evidence for Cr-VI specifically remains limited and inconsistent. The carcinogenicity of Cr-VI by ingestion is documented in animal studies and is the basis of the California OEHHA public-health goal for Cr-VI in drinking water and the related California maximum contaminant level. Ingested Cr-VI is partially reduced to Cr(III) in saliva and gastric fluid before systemic absorption, which complicates dose-response extrapolation from inhalation studies; the surviving systemic Cr-VI fraction is the toxicologically relevant dose for ingestion-route effects.

Immunotoxicity

Li et al. 2026 characterised Cr(VI)-induced disruption of macrophage function in vitro using RAW264.7 mouse macrophages exposed to 0.63 to 20.00 micromol/L Cr(VI) for 24 hours. Cr(VI) drove a shift toward M1-type (pro-inflammatory) macrophage polarization: markers TNF-alpha, CD36, and CD80 increased, while the M2-associated marker VEGFb decreased. At 2.50 micromol/L, cell viability was approximately 80%; at 5.00 micromol/L it fell to approximately 50%, marking the onset of frank cytotoxicity. Cr(VI) also reduced intracellular ATP production while simultaneously elevating glucose uptake and shifting metabolism toward glycolysis, a less efficient energy pathway; Slc2a1 (GLUT1) expression was approximately three times the control level in the 5.00 micromol/L group. Mitochondrial membrane potential collapsed and reactive oxygen species were elevated in a concentration-dependent pattern. Transcriptome-wide RNA-seq at 2.50 micromol/L identified 273 genes uniquely expressed after Cr(VI) exposure. These findings elaborate a coherent immunometabolic mechanism by which Cr(VI) perturbs innate immune defence: forced M1 polarization, bioenergetic failure, and mitochondrial injury occur together, suggesting that Cr(VI) effects on immune function arise from simultaneous disruption of inflammatory signalling and cellular energy supply.

Endocrine and reproductive toxicity

Savici et al. 2026a demonstrated endocrine pancreatic damage in Wistar rats given potassium dichromate at 75 mg/L in drinking water for three months (n = 6 per group). Histological examination revealed interlobular and intralobular edema, significant reductions in islet of Langerhans perimeter (p less than 0.0001 vs. controls), cytoplasmic vacuolisation, pycnotic nuclei, and endothelial cell swelling. Blood glucose was elevated in exposed animals relative to controls. Gene expression analysis showed elevated Bax/Bcl2 ratios, particularly in animals that stopped receiving chromium without recovery treatment, indicating ongoing apoptosis in endocrine cells even after chromium withdrawal. These findings establish the endocrine pancreas as a Cr(VI) target organ, adding to the documented organ range that includes the respiratory, cardiovascular, renal, and nervous systems.

Savici et al. 2026b conducted a three-generation study in Wistar rats receiving potassium dichromate at 25, 50, or 75 mg/L in drinking water continuously across F0, F1, and F2 generations (n = 7 males per group per generation). Effects were dose- and generation-dependent, with the most pronounced impairment in the F2 generation at 75 mg/L: sperm concentration decreased by approximately 31.35%, total motility by 66.79%, and progressive motility by 84.5% relative to F2 controls. Morphological abnormalities in sperm increased from 9.86% in F2 controls to 63.43% in F2 animals at 75 mg/L, involving the head, neck, and tail. Testicular injury score (modified Cosentino scale) increased from 0.64 in F2 controls to 3.71 in F2 animals at 75 mg/L; Johnsen score decreased from 9.65 to 6.54 over the same comparison. Lesions included seminiferous epithelium disorganisation, germ and Sertoli cell loss, germ cell detachment, Leydig cell degeneration, and defective spermiation. The cumulative multigenerational pattern is consistent with the reproductive toxicant and endocrine disruptor characterisations cited in prior literature and with chromium tissue accumulation data from related work by the same group showing that chromium concentrations in reproductive organs were higher in F1 animals than in directly exposed F0 animals.

The doses used in both animal studies (25 to 75 mg/L potassium dichromate) are substantially above typical human water exposure levels and are designed to produce detectable toxicity in short-duration animal models. These findings are mechanistic context for the ingestion-route hazard designation of Cr-VI, not direct dietary exposure estimates.

Genetic susceptibility

Palazzo et al. 2026 summarise evidence on how SNPs in DNA repair genes modulate individual susceptibility to Cr(VI)-induced genotoxicity. The XRCC1 Arg399Gln (rs25487) homozygous variant genotype (Gln/Gln) is associated with increased chromosomal aberrations in occupationally exposed workers, though a separate study reported reduced DNA damage in Cr(VI)-exposed individuals with this variant, a discrepancy the authors attribute to differences in endpoints, population characteristics, and exposure levels. XPD Lys751Gln (rs13181) and XPC Lys939Gln (rs2228000) are associated with increased lung cancer susceptibility in Cr(VI)-exposed individuals. The XRCC3 rs2295152 T allele is associated with increased micronuclei frequency with chromate exposure. The review notes that Cr(VI) is preferentially biomonitored in the erythrocytic fraction rather than serum or urine, reflecting its affinity for red blood cells after systemic distribution.

This genetic evidence is drawn from occupational cohorts at exposures far above dietary background and cannot be directly transposed to dietary risk assessment. The finding that substantially the same exposure produces different genotoxic outcomes in individuals with different DNA repair gene variants is relevant to understanding why population-level dose-response relationships for Cr(VI) carry uncertainty bands.

Typical exposure routes

Inhalation is the dominant occupational and environmental Cr-VI exposure route and is outside the dietary scope this wiki primarily tracks. The relevant Cr-VI exposure pathways for food and supply chain are drinking water used in food preparation, water and process water in the manufacturing chain, and contact with chromated stainless steel, chromated wood preservatives, or other chromate-bearing materials in equipment, packaging, or storage. Geogenic Cr-VI in groundwater is documented in regions with serpentinite or chromite-bearing geology and in some agricultural watersheds.

In finished food matrices, ambient chromium (Cr) is overwhelmingly trivalent chromium, both because Cr-VI is oxidatively unstable in many food matrices and because the analytical methods that resolve speciation are uncommon in routine occurrence surveys. The result is that nearly all chromium occurrence data this wiki has cataloged report total chromium, not Cr-VI; the corpus contains a single peer-reviewed Cr-VI food-occurrence study at present. See the speciation gap section below.

Food sources and occurrence

Soares et al. 2000 is, at the time of this writing, the only food-occurrence source loaded on the wiki that reports Cr-VI explicitly rather than total chromium. The study used an ion-exchange separation followed by electrothermal atomization atomic absorption spectrometry to measure Cr-VI selectively in 20 commercial powdered milk infant formulas from the Portuguese market. In the seven newborn-formula samples, the reported Cr-VI mean was 24 ng/g and the source-scope range was below 10 to 75 ng/g, which is equivalent to mass-basis 24 ppb mean and below 10 to 75 ppb range; the lower end is censored at the method limit. Group means for follow-up and dietetic milk subgroups were 12 to 33 ng/g.

The Soares 2000 dataset is small, market-specific, and reports group means and ranges rather than sample-level values, so it provides direct Cr-VI occurrence context for the dairy-based powdered formula row but cannot, on its own, support a percentile calculation for Cr-VI. The occurrence row is retained as direct dairy / non-soy powdered formula context per the Cr-VI species discipline. The result is also useful as a Cr-VI method reference: it documents an analytical pathway for routine selective Cr-VI quantification in a complex food matrix.

Regulatory limits

No regulation in the current wiki corpus carries a Cr-VI maximum level for a food matrix. The regulatory instruments that do address hexavalent chromium specifically sit in adjacent domains, principally drinking water and consumer-product labeling, and two of them are now cited here.

California sets an enforceable drinking-water Maximum Contaminant Level for hexavalent chromium of 10 µg/L (0.010 mg/L), adopted by the State Water Resources Control Board on April 17, 2024 and effective October 1, 2024 (California — Maximum Contaminant Level for Hexavalent Chromium in Drinking Water). This MCL is species-specific to Cr-VI and is tighter than the total-chromium MCL of 50 µg/L it supplements; an earlier California Cr-VI MCL at the same value took effect in 2014 and was invalidated in 2017 for an inadequate economic-feasibility record before the present re-adoption. Hexavalent chromium is also listed under California Proposition 65, as a carcinogen since February 27, 1987 and as a developmental and reproductive toxicant since December 19, 2008, with a cancer No Significant Risk Level of 0.001 µg/day by inhalation and a reproductive Maximum Allowable Dose Level of 8.2 µg/day by the oral route (California Proposition 65 — Hexavalent Chromium Listing and Safe-Harbor Levels).

Both instruments are drinking-water or product-labeling measures, not food maximum levels. The MCL governs the concentration of Cr-VI permitted in public-water-system water, and the Proposition 65 listing governs consumer-product warning obligations; neither sets a permitted concentration in a food. The other frameworks that touch hexavalent chromium remain un-ingested: the US EPA national primary drinking-water regulation sets a total-chromium MCL (100 µg/L) that is not Cr-VI-specific, occupational exposure limits (OSHA, NIOSH, ACGIH) are inhalation values, and Codex Alimentarius general standards do not separately specify Cr-VI for food. The practical consequence is unchanged: there is at present no food-specific regulatory benchmark for Cr-VI, so any concentration of toxicological concern for a food matrix is derived from drinking-water-derived toxicology and a thin food-occurrence base, not from a food-specific regulatory limit.

Testing methods

Selective Cr-VI quantification in food matrices is non-trivial because total digestion methods (microwave-assisted nitric acid digestion typical of ICP-MS occurrence surveys) reduce Cr-VI to Cr(III) and report only total chromium. Speciation-preserving methods route the chromium-bearing analyte through an ion-exchange or chromatographic step before quantification. Soares 2000 used Chromabond NH2 anion-exchange retention of chromate followed by nitric-acid elution and electrothermal atomic absorption at 357.9 nm; modern speciation work more typically uses ion chromatography coupled to ICP-MS with isotope-dilution standards or post-column hydride generation. Drinking-water Cr-VI is most commonly measured by EPA Method 218.7 (ion chromatography with post-column reaction).

A dedicated chromium-speciation testing page in testing is a near-term addition; the current testing index does not yet carry a Cr-VI-specific entry.

Microbiome effects

The current wiki corpus does not carry a microbiome-Cr-VI mechanism page. Cr-VI’s documented intracellular reduction by gastric and intestinal contents implies a real interaction with the gut microbial environment, but the metals/microbiome literature within this corpus is silent on Cr-VI specifically. Cr-VI microbiome content should be drafted when peer-reviewed mechanism or taxon-level evidence is added; it would crosswalk to WikiBiome as a Cr-VI-specific microbial-axis page.

Vulnerable populations

Infants and young children fed reconstituted powdered formula are the principal Cr-VI dietary vulnerable group identifiable from the loaded corpus. Cr-VI exposure assessment for this population would draw from formula Cr-VI concentration (Soares 2000 type data), water Cr-VI concentration (jurisdiction-specific drinking-water surveys not yet ingested), and reconstitution volume per serving. Body-weight-normalized Cr-VI intake is a more stringent test of exposure adequacy than absolute concentration because infant intake per kilogram body weight far exceeds adult intake per kilogram body weight. Children and elderly individuals are flagged in Ufelle and Barchowsky 2021 as more susceptible than most adults at any given exposure level.

The speciation gap

This is the most important short-term finding for the Cr-VI page. The wiki currently has total-chromium occurrence data from at least seven peer-reviewed and government sources that explicitly disclaim Cr-VI measurement: Chuchu et al. 2013, UK FSA 2016, Milani et al. 2023, Chekri et al. 2019, Chung et al. 2021, Meli et al. 2024, and the broader survey ecosystem. Each of these sources reports total chromium with an explicit note that the chromium quantity is not speciated. None of them can be substituted for Cr-VI under the species-discipline rule that total chromium is never reported as Cr-VI.

The result is that the loaded corpus has many total-chromium values and exactly one Cr-VI dataset (Soares 2000, n=20, Portugal, 2000). For any application that requires category-representative Cr-VI occurrence data, this is a structurally weak evidence base: a single small market-specific dataset cannot characterize a food-matrix Cr-VI distribution, and the literature does not at present support a food-specific Cr-VI concentration of toxicological concern. Closing the gap requires either commissioning Cr-VI speciation work for category-representative samples, or surfacing additional Cr-VI-specific peer-reviewed studies from the broader ingest corpus that have not yet been promoted to source pages.

Open questions

How does Cr-VI in finished powdered formula relate to Cr-VI in the reconstitution water? Soares 2000 used doubly deionized water for reconstitution, isolating the dry-product Cr-VI signal. A real-feeding Cr-VI exposure depends on both the powder and the tap or bottled water used to prepare it. The two-component exposure model is missing from the loaded corpus.

What is the rate at which dietary Cr-VI is reduced to Cr(III) in saliva and gastric fluid before absorption, and how does that rate vary with infant gastric pH? Infant gastric pH is higher (less acidic) than adult gastric pH, which would reduce the Cr-VI to Cr(III) conversion efficiency before systemic absorption and elevate the systemic Cr-VI dose per unit of ingested Cr-VI. This is a quantitative gap with direct consequences for infant Cr-VI exposure assessment and is not currently characterized in the corpus.

What Cr-VI speciation evidence exists outside the infant-formula matrix? Drinking water and produce grown on chromite-bearing or chromated-irrigation soils are the obvious candidate matrices. The current ingest is silent on these.

How do supply-chain Cr-VI exposures (chromated wood pallets, chromate-containing process equipment, chromated leather and gelatin) propagate into finished food? This is a manufacturing and packaging question, not a primary-agriculture question, and the loaded sources do not address it.

Chromium research: qualified source context

In a laboratory electrokinetic trial, the authors attributed 44.58% removal to Cr(VI), but the denominator includes native bulk chromium and the reported mass balance is incomplete. Acid digestion followed by UV–visible analysis was described without demonstrated preservation of oxidation state, so the result cannot establish validated species-specific recovery (Tables 2 and 4). LABORATORY SCALE ELECTROKINETIC REMEDIATION OF HEXAVALENT CHROMIUM FROM CONTAMINATED SOIL

Saha et al.’s editorial attributes Senegal fish measurements to Cr(VI) in its summary of Ndiaye et al. It does not establish extraction chemistry, measurement basis, sample N or species validation. These are secondary leads, not a new verified fish occurrence cohort (p1780). Special Issue: Hexavalent Chromium: Sources, Toxicity, and Remediation

Diphenylcarbazide measurements in a synthetic-water nanotube experiment quantify residual Cr(VI) signal. The study does not establish total-chromium mass balance, so signal loss alone does not distinguish adsorption from reduction. Conflicting efficiencies, kinetic units and test conditions are preserved alongside the supplementary duplicate measurements (Methods; Supplement A.1–A.5). Removal of hexavalent chromium from contaminated synthetic groundwater via functionalized carbon nanomaterials modified with zinc and potassium

Jacaranda-derived carbon: laboratory chromium treatment

Ghimire’s 2026 MSc thesis reports 97.75% apparent loss of aqueous Cr(VI) after 90 minutes at pH 2 using a Jacaranda-derived cobalt/carbon composite prepared at 900 °C (Table 2). The experiment used synthetic solution and measured the remaining diphenylcarbazide colorimetric response. It did not measure Cr(III), total chromium after treatment or cobalt leaching, so the result does not establish chromium reduction, complete removal or treated-water safety. Replicate counts and numerical detection limits were not reported. MOF-Derived Carbon Composites from Jacaranda Seed Pods for Selective Removal of Hexavalent Chromium [Cr(VI)]

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. Survey of metals in commercial infant foods, infant formula and non-infant specific foodsFood Standards Agency / Fera Science Ltd · UK Food Standards Agency report FS102048 · 2016 · www.food.gov.ukGovernment
2. 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
3. Genetic Polymorphisms as Modifiers of Health Risks from Exposure to Toxic Elements: A Traditional Literature ReviewPalazzo M, Borghini A, Bustaffa E, Baldacci S, Gorini F, and Minichilli F · Toxics 14(5): 375 · 2026 · doi.org/10.3390/toxics14050375Peer-reviewed
4. Chromium(VI) Modulates Macrophage Polarization and Metabolic Reprogramming to Impair Immune FunctionLi C, Zhang R, Zhang Y, Yu H, Zheng Y, Du Y, et al. · Toxics 14(2): 160 · 2026 · doi.org/10.3390/toxics14020160Peer-reviewed
5. Hexavalent Chromium Toxicity in the Pancreas: A Study on the Protective Effects of Hypericum perforatum ExtractSavici J, Marc S, Boldura OM, Grigorescu CC, Paul C, Vaduva C, et al. · International Journal of Molecular Sciences 27(8): 3706 · 2026 · doi.org/10.3390/ijms27083706Peer-reviewed
6. Potassium Dichromate Exposure and Sperm Quality in Rats: A Multi-Generational StudySavici J, Marc S, Boldura OM, Shalaby S, Oprescu M, Brezovan D, et al. · Toxics 14(10): 870 · 2026 · doi.org/10.3390/toxics14100870Peer-reviewed
7. Selective Determination of Chromium (VI) in Powdered Milk Infant Formulas by Electrothermal Atomization Atomic Absorption Spectrometry after Ion ExchangeMaria E Soares, Maria L Bastos, and Margarida Ferreira · Journal of AOAC International 83(1):220-223 · 2000 · doi.org/10.1093/jaoac/83.1.220Peer-reviewed
8. The aluminium content of infant formulas remains too highNancy Chuchu, Bhavini Patel, Blaise Sebastian, and Christopher Exley · BMC Pediatrics · 2013 · doi.org/10.1186/1471-2431-13-162Peer-reviewed
9. Trace Elements in Soy-Based Beverages: A Comprehensive Study of Total Content and In Vitro BioaccessibilityMilani RF, Mauri AA, Sanches VL, Morgano MA, and Cadore S · International Journal of Environmental Research and Public Health · 2023 · doi.org/10.3390/ijerph20064986Peer-reviewed
10. Trace element contents in foods from the first French Total Diet Study on infants and toddlersRachida Chekri, Emilie Le Calvez, Julie Zinck, Jean-Charles Leblanc, Veronique Sirot, Marion Hulin, et al. · Journal of Food Composition and Analysis · 2019 · doi.org/10.1016/j.jfca.2019.02.002Peer-reviewed
11. Content and Dietary Exposure Assessment of Toxic Elements in Infant Formulas from the Chinese MarketSu C, Zheng N, Gao Y, Huang S, Yang X, Wang Z, et al. · Foods 9(12):1839 · 2020 · doi.org/10.3390/foods9121839Peer-reviewed
12. Chemical characterization of baby food consumed in ItalyMeli MA, Desideri D, Sisti D, Fagiolino I, and Roselli C · PLOS ONE · 2024 · doi.org/10.1371/journal.pone.0297158Peer-reviewed
13. 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
14. Special Issue: Hexavalent Chromium: Sources, Toxicity, and RemediationBidyut Saha, Aziz Amine, and Francis Verpoort · Chemistry Africa5:1779–1780 · 2022 · doi.org/10.1007/s42250-022-00443-zEditorial
15. Removal of hexavalent chromium from contaminated synthetic groundwater via functionalized carbon nanomaterials modified with zinc and potassiumPeter D. Ibikunle, Olugbenga O. Elemile, Praise O. Ejigboye, David O. Bala, Ayodeji P. Olawolu, Asegun A. Adebayo, et al. · Scientific Reports 15:33823 · 2025 · doi.org/10.1038/s41598-025-01025-yPeer-reviewed
16. MOF-Derived Carbon Composites from Jacaranda Seed Pods for Selective Removal of Hexavalent Chromium Cr(VI)Bibek Ghimire · MSc thesis, Materials Science and Engineering, Tribhuvan University, Institute of Engineering, Pulchowk Campus; May 2026 · 2026 · elibrary.tucl.edu.npThesis

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.

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

Total-chromium sources that explicitly do not speciate Cr-VI

These are useful as total-chromium occurrence context only and should not be cited as Cr-VI evidence.

• Chuchu et al. 2013
• UK FSA 2016
• Chekri et al. 2019
• Chung et al. 2021
• Milani et al. 2023
• Meli et al. 2024

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