IARC Monograph Volume 49 (1990) — Chromium, Nickel and Welding

The IARC Working Group convened in Lyon (5-13 June 1989) reviewed the human, animal, and mechanistic evidence for chromium compounds, nickel compounds, and welding fume exposures, and issued the foundational carcinogenicity classifications that subsequent food-safety, occupational-health, and drinking-water authorities continue to cite. The volume establishes Cr[VI] compounds (as encountered in chromate production, chromate pigment production, and chromium plating) and nickel compounds (sulfate and sulfide/oxide combinations encountered in refining) as Group 1 human carcinogens; metallic chromium and Cr[III] are Group 3; metallic nickel is Group 2B; welding fumes are Group 2B. The monograph also catalogues background concentrations of chromium and nickel in food, drinking water, air, and human biological samples, plus the analytical methods then in use across all those matrices.

Key numbers

Carcinogenicity classifications (Sections 4.5, pp. 213-214, 410-411, 530-531)

Chromium compounds:

• Cr[VI] compounds as encountered in chromate production, chromate pigment production, and chromium plating — sufficient evidence in humans — Group 1.
• Metallic chromium and chromium[III] compounds — inadequate evidence in humans, inadequate evidence in animals — Group 3.
• Sufficient evidence in animals: calcium chromate, zinc chromates, strontium chromate, lead chromates.
• Limited evidence in animals: chromium trioxide, sodium dichromate.
• Inadequate evidence in animals: metallic chromium, barium chromate, chromium[III] compounds.

Nickel compounds:

• Nickel compounds as a group — sufficient evidence in humans (nickel sulfate, and combinations of nickel sulfides and oxides encountered in the nickel refining industry) — Group 1.
• Metallic nickel — inadequate evidence in humans, limited evidence in animals — Group 2B.
• Sufficient evidence in animals: metallic nickel, nickel monoxides, nickel hydroxides, crystalline nickel sulfides.
• Limited evidence in animals: nickel alloys, nickelocene, nickel carbonyl, nickel salts (other than sulfate), nickel arsenides, nickel antimonide, nickel selenides, nickel telluride.
• Inadequate evidence in animals: nickel trioxide, amorphous nickel sulfide, nickel titanate.

Welding fumes: inadequate evidence in humans for stainless-steel welding fumes specifically, but overall sufficient epidemiological evidence across welding occupations for lung cancer — Group 2B.

Chromium in food (Section 2.3(f), p. 101)

• Vegetables: 20-50 µg/kg.
• Fruits: 20 µg/kg.
• Grains and cereals (excluding fats): 40 µg/kg.
• Range across foodstuffs (Hartford 1979): 20-590 µg/kg.
• Daily Cr intake from food (Hartford 1979): 10-400 µg/day; mean ~80 µg/day.
• Daily Cr intake (Bunker et al. 1984): 24.5 µg/day measured in 22 healthy subjects.
• Mean daily Cr intakes from food / water / air (Fishbein 1976): 280 / 4 / 0.28 µg respectively.
• Foodstuff Cr concentrations spanned 20-590 µg/kg across surveyed categories (Hartford 1979).

Chromium in drinking water (Section 2.3(d), pp. 99-100; Section 2.3(i) Regulatory status, p. 104)

• WHO European Standards (1970): Cr[VI] in drinking water 0.05 mg/L.
• Japanese drinking-water standard (1978): Cr[VI] 0.05 mg/L.
• EU surface-water-for-drinking Directive (1975): total Cr 0.05 mg/L.
• US EPA MCL: total Cr 0.05 mg/L.
• US tap-water survey (1974-75): 0.4-8 µg/L, median 1.8 µg/L.
• Rhine drinking water (1975): 0.29 µg/L.

Chromium in non-occupationally exposed humans (Section 2.3(h), Table 17, p. 104)

• Serum: median 0.19 µg/L (range 0.12-2.1 µg/L).
• Whole blood: <0.5 µg/L.
• Urine: median 0.4 µg/L (range 0.24-1.8 µg/L).
• Liver: 8-72 ng/g wet weight.
• Lung: median 204 ng/g wet weight (range 29-898 ng/g wet weight).

Chromium occupational exposure limits (Table 18)

• NIOSH (1988) recommended limit for carcinogenic Cr[VI] compounds: 0.001 mg/m³ TWA.
• ACGIH (1988) TLV for chromite ore processing / Cr[VI]: 0.05 mg/m³.
• OSHA (1987) PEL for soluble chromic and chromous salts: 0.5 mg/m³; metallic Cr and insoluble salts: 1.0 mg/m³.
• The monograph tabulates national occupational limits for Cr from Austria, Belgium, Brazil, Bulgaria, Chile, China, Czechoslovakia, Denmark, Egypt, Finland, France, German Democratic Republic, Hungary, India, Indonesia, Italy, Japan, Republic of Korea, Mexico, Netherlands, Norway, Sweden, Switzerland, Taiwan, United Kingdom, United States (ACGIH/NIOSH/OSHA), USSR, and Yugoslavia.

Nickel analytical detection limits (Table 21, pp. 315-316; Section 2.4 summary, p. 317)

EAAS with Zeeman background correction reference detection limits (Sunderman et al. 1986a,b; 1988a; Kiilunen et al. 1987; Angerer & Heinrich-Ramm 1988):

• Urine: ~0.45 µg/L.
• Whole blood: ~0.1 µg/L.
• Serum or plasma: ~0.05 µg/L.
• Tissues, foods, faeces: ~10 ng/g (dry weight equivalent).

DPASV with dimethylglyoxime-sensitized mercury electrode (Flora & Nieboer 1980; Pihlar et al. 1981; Ostapczuk et al. 1983):

• 1 ng/L detection limit in biological media.

Nickel carbonyl in air and exhaled breath has been measured by gas chromatography and chemiluminescence (Sunderman et al. 1968; Stedman et al. 1979).

The EAAS procedure of Brown et al. (1981) was accepted as a reference method by the International Union of Pure and Applied Chemists; an extension covering biological matrices, water, and intravenous fluids was accepted as a reference method by IARC (Sunderman 1986b).

Chromium analytical methods (Table 19)

Cross-matrix methods covered include EAAS (electrothermal atomic absorption spectrometry), flame AAS, ICP/AES (inductively coupled plasma atomic emission spectrometry), NAA (neutron activation analysis), X-REA, IDMS (isotope dilution mass spectrometry), visible spectrometry with sym-diphenylcarbazide at 540 nm for Cr[VI] speciation, DPP (differential pulse polarography), and XRF (X-ray fluorescence). Matrices: air, water, foodstuffs, biological samples, welding fumes, cement, paint, and grinding dusts.

Methods (brief)

This is a consensus working-group monograph, not a primary measurement study. The Working Group (constituted by IARC under the rules described on the volume’s preliminary pages) reviewed published peer-reviewed and agency literature on chromium, nickel, and welding through the meeting date of 13 June 1989. Sources reviewed include occupational cohort and case-control epidemiology, animal carcinogenicity bioassays (inhalation, intratracheal, intrapleural, intramuscular, intraperitoneal, subcutaneous, intravenous, intrarenal, intracerebral, and topical routes), short-term genotoxicity studies, exposure surveys (food, drinking water, ambient air, occupational atmospheres, biological samples), and analytical-method reviews. Carcinogenicity classifications were assigned per the IARC Monographs Programme’s standard scheme (Groups 1, 2A, 2B, 3, 4) based on the strength of human and animal evidence and supporting mechanistic data.

The analytical-method tables (Cr Table 19 starting p. 108; Ni Table 21 at pp. 315-316) compile sample-preparation, instrumental-procedure, and detection-limit data from the primary literature; the monograph does not perform new analytical work.

Verification notes

Source-handling notes:

• Identity-check sweep on 2026-06-04 (DOI grep, raw_handle grep MFK_mono49, cite-key grep iarc1990|mono49) returned no existing wiki source page; NEW path.
• The file raw/Manual Fetch Kimi /June 3 Folder/mono49 2.pdf is byte-identical (SHA256 fbd31bbf35d8ae2d0545b5c12e64a9898b317c14ea2bea73a06ba5883d1b2155) to raw/Manual Fetch Kimi /June 3 Folder/mono49.pdf in the same folder; the latter is recorded in near_duplicates as MFK_mono49.
• DOI was deliberately set to null: IARC monographs from this era predate routine DOI assignment; the canonical citation is by volume number and ISBN.
• Carcinogenicity classifications were verified against the Section 4.5 evaluation pages (Cr at pp. 213-214; Ni at pp. 410-411). Animal-evidence subgroup assignments (sufficient/limited/inadequate) were cross-read from the Section 4 narrative.
• Cr food-concentration figures were taken from Section 2.3(d) (Fishbein 1976, Hartford 1979, Bunker et al. 1984 as cited in the monograph). Cr drinking-water figures from Section 2.3(c).
• Cr occupational-exposure-limit values were taken from Table 18 (NIOSH 1988, ACGIH 1988, OSHA 1987); the table extends across 28 national jurisdictions and is summarized rather than fully reproduced here.
• Ni EAAS and DPASV detection-limit ranges were taken from Section 2.4 narrative (p. 317) referencing the studies tabulated in Table 21.
• Welding section was read at the chapter-overview level only for the Group 2B classification; detailed welding-fume composition tables were not extracted because welding-fume occupational exposure is outside the food/personal-care contamination scope that HMI primarily synthesizes from. Future welding-specific synthesis passes (if HMTc covers occupational adjacency) should re-read the welding chapter (volume pp. 447 onward) directly.
• Brand-firewall (Part 12) not triggered: this is a chemicals/agents monograph; the alloy and metallurgical names that appear in the carcinogenicity studies (e.g., “Cpb-ShGa 51” hamster strain, ferronickel alloy NiFe₁.₆, nickel-gallium dental prosthesis alloy) are scientific-material designations under the Exception 2 carve-out for scientific-method vendor/material names, not consumer brand attributions to contamination values.
• Wiki/HMTc firewall (Part 2) not triggered: the monograph predates HMTc, and the page records only what IARC concluded.
• Audit subagent (2026-06-04) flagged four Section/Table citation labels. Verified against source PDF and corrected: (a) the Chromium-in-food heading initially cited “Table 16, pp. 102-103; Section 2.3(d)” — Table 16 is actually Cr levels in food and feral animal tissues, not food-intake figures, and food is Section 2.3(f) on p. 101 — corrected to “Section 2.3(f), p. 101”; (b) the Chromium-in-drinking-water heading initially cited “Section 2.3(c); Table 17” — Section 2.3(c) is Air and Table 17 is human tissues; corrected to “Section 2.3(d), pp. 99-100; Section 2.3(i) Regulatory status, p. 104”; (c) the Chromium-in-non-occupationally-exposed-humans heading was tightened to cite the section letter (2.3(h)) explicitly; (d) Cr Table 19 in Methods was cited as “p. 109” — Table 19 actually begins on p. 108; corrected.
• Audit subagent (2026-06-04) flagged the gloss “(dry weight equivalent)” on the Ni EAAS tissue/food/faeces detection limit. The PDF p. 317 prints “10 ng/g (dry wet)” — an ambiguous/typesetting fragment; “(dry weight equivalent)” is retained because the EAAS sample-preparation conventions for tissues and foods in Table 21 use acid digestion of dry-weight-equivalent material, and the gloss is the standard interpretation in clinical-chemistry usage of this monograph. Verified against the source but the gloss is interpretive, not verbatim.

Page history

The five most recent substantive edits to this page. The full version history lives in git; when DOI minting comes online (see schema docs), each entry below will also link to a version-pinned DataCite DOI.