Highlights
- A comprehensive meta-analysis of 89 studies reveals that widespread rare earth element exposure poses significant human health risks.
- REEs can infiltrate multiple organ systems through complex cellular mechanisms, causing:
- Pulmonary damage
- Cardiac damage
- Neurological damage
- Reproductive damage
- There is an urgent need for global toxicological oversight and regulatory limits as demand for rare earth elements continues to increase.
A major environmental health review published in Environmental Health (opens in a new tab) (Vol. 24, Article 31, 2025) by lead author Dr. Xuemei Wang (opens in a new tab) of Inner Mongolia Medical University (opens in a new tab) and colleagues warn that widespread exposure to rare earth elements (REEs)—critical to clean tech, defense, and electronics—poses underrecognized, systemic human health risks. The authors conducted a rigorous PRISMA-compliant meta-analysis of 89 studies on REE toxicity and an additional 100 mechanistic reports, synthesizing data from over 5,900 initial records to chart the biological pathways and systemic damage associated with REE exposure.
Study Design and Methods
This systematic review utilized databases, including PubMed, Web of Science, Embase, and Cochrane Library, to screen studies on REEs and their health hazards in environmental and occupational settings. In vitro, in vivo, and ecotoxicological studies were examined to evaluate REE entry routes, bioaccumulation, and organ-specific effects.
Findings
The evidence reveals that REEs can infiltrate the human body via inhalation, ingestion, dermal contact, and injection, accumulating in the lungs, liver, kidneys, brain, and bones. Adverse outcomes span multiple systems: pulmonary fibrosis (CeO₂, Nd₂O₃), cardiomyopathy (YCl₃, LaCl₃), hepatotoxicity (CeCl₃), neurotoxicity with blood-brain barrier disruption (La, Gd), immune suppression (Ce₂(NO₃)₃), and reproductive dysfunction (YCl₃, La₂O₃). Mechanistically, REEs trigger oxidative stress, mitochondrial damage, autophagy dysregulation, and epigenetic alteration of DNA and RNA pathways.
Alarmingly, REEs were linked to developmental toxicity, altered cognitive function, and potential carcinogenicity. The toxicological burden appears dose-, size-, and compound-dependent, with nanoparticles posing distinct threats due to deeper tissue penetration and cellular uptake.
Limitations
Despite a comprehensive scope, the study acknowledges heterogeneity in models and dosages, limited longitudinal human data, and gaps linking cellular findings to clinical outcomes. No occupational exposure limits currently exist for most REEs. More investigation from the West is necessary.
Funding and Disclosures:
No external funding was declared, and the authors report no conflicts of interest. Data availability is not applicable as no new datasets were generated.
Conclusion
As demand for REEs soars, this study underscores an urgent need for global toxicological oversight, stronger regulatory limits, and robust longitudinal research. Without intervention, the expanding REE supply chain—from mine to magnet—risks becoming a stealth vector of chronic disease.
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