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A comprehensive examination of the impact of environmental pollution on lung cancer: A review

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This narrative review comprehensively examined the impact of environmental pollution on lung cancer, covering heavy metals (arsenic, cadmium, lead, nickel, hexavalent chromium), particulate matter, polycyclic aromatic hydrocarbons (PAHs), and radon. It synthesizes epidemiological and mechanistic evidence. The review highlights lung cancer as the most diagnosed and most lethal cancer worldwide (nearly 2.5 million new cases and 1.8 million deaths in 2022), with an increasingly recognized multi-factorial etiology beyond cigarette smoking.

Key numbers

For cadmium (most quantitatively detailed in the reviewed first pages):

  • Historical mortality analysis of cadmium production facility workers: a marked elevation in lung cancer fatalities among exposed workers.
  • Case-control study: top versus bottom quartile cadmium occupational exposure category OR = 4.41 (95% CI: 2.01-9.67) for lung cancer.
  • Prospective study: cadmium exposure associated with 25% significant increase in lung cancer incidence; OR 4.41 times greater in top quartile than bottom quartile.
  • Each 1 µg/L increment in urinary cadmium was associated with 1.25 times higher risk of lung cancer (prospective study).

For arsenic:

  • IARC Group 1 carcinogen for lung cancer; arsenic inhalation and ingestion both documented as carcinogenic routes.
  • Arsenic promotes lung adenocarcinoma cells invasion and metastasis capability by inhibiting ACSS2/atg5-mediated autophagy.
  • Hexavalent chromium can induce apoptosis in hepatocytes through the ASK1/NK signaling pathway.

For nickel:

  • IARC classified nickel compounds as human carcinogens as early as 1991.

Methods (brief)

Narrative review; no systematic search strategy or PRISMA flow reported. Covers epidemiological cohort, case-control, and meta-analytic studies alongside mechanistic evidence.

Evidence fitness

Supports: contextual evidence for heavy metal-induced lung cancer, particularly for cadmium (most quantitatively documented) and arsenic. Provides mechanistic pathway context for PAH-arsenic-cadmium co-exposure in lung carcinogenesis. Not a source for food arsenic concentrations or dietary exposure estimates.

Limitations

Narrative review (not systematic); quantitative data cited from primary studies; cadmium data are most extensively quantified in the accessible pages; arsenic effects are described mechanistically and epidemiologically without specific effect size extraction in this review section.

Update history

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