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Airborne metals and malignant pleural effusions: the role of oxidative stress

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This review examined the association between airborne metals and malignant pleural effusions (MPE, defined as the presence of neoplastic cells in pleural fluid), which are present in 15% of lung cancer patients at diagnosis. The review searched PubMed, Science Direct, and the Cochrane Library through January 2026 for original scientific articles. It compiles Table 1, a comprehensive summary of metals associated with lung pathogenesis disorders, covering arsenic, cadmium, lead, nickel, chromium, hexavalent chromium, aluminum, iron, tin, vanadium, cobalt, copper, manganese, silver, molybdenum, and zinc.

Key numbers

  • For arsenic (IARC Group 1): lung pathogenesis disorders listed in Table 1 include irritation of nasal mucosa, larynx, bronchi, and later perforation of nasal septum; rhino-pharyngolaryngitis; trachea bronchitis; pulmonary insufficiency; chronic cough; bronchopulmonary disease; arsenic bronchitis; asthma; dyspnea; chest pain; non-cardiogenic pulmonary edema; increased capillary permeability; lung cancer.
  • Arsenic toxicity mechanisms (Table 1): ROS production and oxidative stress damage; inhibit mitochondrial respiration and uncouple mitochondrial oxidative phosphorylation; regulate glycolysis; deplete ATP; dysregulate and inhibit proteins/enzymes.
  • In MPE-associated studies: higher zinc concentration in malignant versus benign pleural effusions (statistically significant difference). Elevated copper, chromium, lead, selenium, and iron were documented in MPE, but without statistical significance.
  • Superoxide dismutase activity was increased in MPE compared to benign pleural effusions. Lactate dehydrogenase, malondialdehyde, and reactive oxygen species modulator 1 (ROMO1) were also elevated in MPE.
  • PM2.5 aerodynamic diameter less than 2.5 µm can reach the alveolar region; PM0.1 less than 0.1 µm can reach the alveoli and enter the bloodstream.
  • Epidemiological studies cited: correlation between PM2.5 levels and lung cancer (LC) risk (OR 4.1 versus 1.8 in non-COPD patients); 1 µg/m3 increase in 3-year PM2.5 exposure associated with 10% increased risk of LC in 36 Chinese cities.

Methods (brief)

Review of original scientific articles published through January 2026; databases PubMed, Science Direct, and Cochrane Library. Search terms included: trace elements, heavy metals, metalloids, particulate matter, air pollution, pleural effusion, oxidative stress, antioxidant enzymes, and lung cancer. Table 1 compiled from multiple review and primary sources; not a systematic review with PRISMA methodology.

Evidence fitness

Supports: contextual inhalation toxicology of arsenic and other airborne metals; Table 1 provides a synthesized listing of arsenic lung pathogenesis disorders drawn from IARC and other authoritative sources. Provides oxidative stress mechanism context linking airborne metal exposure to pleural pathology. Limitation: narrative review; pleural effusion data are for mixed metal exposures, not arsenic-specific; arsenic-specific pleural effusion data are limited in the literature.

Limitations

Narrative review (not systematic); most pleural fluid metal data are for multi-metal exposures; small sample sizes in referenced pleural fluid studies; attribution of MPE to specific metals confounded by co-exposures; some tables derived from other reviews rather than primary studies.

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