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Heavy Metal Index

Nickel exposure induces gut microbiome disorder and serum uric acid elevation

Source

This Environmental Pollution paper from Lanzhou University investigates the mechanism linking long-term occupational nickel exposure to elevated serum uric acid by combining biomarker measurements with gut-microbiome 16S rRNA sequencing in a 109-participant cohort of Ni-exposed workers and ...

Page snapshot
Cited by8 pages
Metals measured1
Evidence tierA
Year2023

Overview

This Environmental Pollution paper from Lanzhou University investigates the mechanism linking long-term occupational nickel exposure to elevated serum uric acid by combining biomarker measurements with gut-microbiome 16S rRNA sequencing in a 109-participant cohort of Ni-exposed workers and matched controls. Serum Ni was significantly elevated in the exposure group (5.70 ± 3.21 µg/L versus controls), serum uric acid was significantly elevated (355.95 ± 67.87 µmol/L), and the abundances of uric-acid-lowering bacteria were significantly diminished in the exposure group. The authors propose that intestinal degradation of purine to uric acid is disturbed by nickel-driven gut microbiome perturbation, producing the observed serum uric acid elevation.

Key numbers

CohortSerum Ni (µg/L)Serum uric acid (µmol/L)
Ni-exposed workers5.70 ± 3.21355.95 ± 67.87
Controlsreferencereference (significantly lower)

The mechanism proposed in the paper: excessive nickel disrupts gut microbiota composition; uric-acid-lowering bacteria (Lactobacillus and related taxa) are diminished; intestinal purine-to-uric-acid degradation is impaired; serum uric acid rises. The paper is the first cohort-level human evidence linking dietary or occupational Ni body burden to a microbiome-mediated metabolic endpoint.

Methods (brief)

109-participant cohort with Ni-exposed and control groups. Serum Ni quantified by ICP-MS. Gut microbiota characterized by 16S rRNA sequencing. Statistical comparisons used standard cohort-comparison tests for serum Ni, uric acid, and microbial taxon abundances.

Implications

  • Certification: Mechanistic support for the EFSA 2020 dietary Ni TDI by demonstrating a microbiome-mediated metabolic pathway from elevated body Ni to a clinically meaningful endpoint (serum uric acid elevation, a hyperuricemia / gout risk factor). Useful when contextualizing why dietary Ni at chronic exposure matters even at sub-acute levels.
  • Microbiome: The first wiki source establishing the Ni-microbiome-metabolic axis with direct human cohort evidence. Crosswalks to WikiBiome as a Ni-specific microbial-axis topic. Lactobacillus and uric-acid-lowering Bacteroidota taxa flagged as Ni-sensitive.
  • Courses: Useful for teaching the metals-to-microbiome-to-metabolic-disease chain.

Wiki pages updated on ingest

Update history

The five most recent substantive edits to this page, classified major (evidence or structure moved), correction (a published value or statement was wrong and has been fixed), or minor (narrative rewritten without changing the underlying evidence). Each description is derived from what the edit did to this page; the linked commit is the authoritative record, routine regeneration passes are excluded, and 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.

CommitDateChangeDescription
a8052bb2026-08-09major6 sections added; narrative text revised