Mitochondrial Mechanisms in the Potential Male Reproductive Toxicity of E‐Cigarette‐Derived Metal‐Containing Nanoparticles

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Abstract
E‐cigarette devices emit ultrafine metal‐containing particles from heating coils, solder joints, and other wetted components, but their reproductive toxicology remains poorly defined. This review integrates evidence from aerosol chemistry, nanoparticle toxicology, and male reproductive biology to evaluate whether these particles may contribute to male reproductive dysfunction through mitochondrial injury. E‐cigarette aerosols can contain nanoscale and ultrafine particles bearing chromium, nickel, iron, copper, zinc, tin, and lead. These particles may deposit in the distal lung and, based on broader nanoparticle toxicokinetics, could enter the systemic circulation. However, direct particle‐resolved evidence of their accumulation in testicular tissue is currently absent. Mechanistic evidence therefore derives mainly from engineered nanoparticle and soluble‐metal models. These studies indicate that metal exposure can disrupt blood–testis barrier integrity, impair Sertoli‐ and Leydig‐cell function, alter steroidogenesis, damage germ cells, and reduce sperm quality. Mitochondria represent a plausible point of convergence because particle‐ and ion‐mediated mechanisms can promote mitochondrial reactive oxygen species generation, lipid peroxidation, respiratory dysfunction, mitochondrial DNA damage, altered fusion–fission balance, defective mitophagy, apoptosis, and inflammatory signaling. These pathways provide a biologically plausible framework linking inhaled metal‐containing particles to impaired spermatogenesis and steroidogenesis, without establishing causality under realistic vaping conditions. Future studies should combine inhalation‐relevant exposure models with particle‐resolved biodistribution, dosimetry, and mechanistic reproductive endpoints to determine whether these pathways operate following e‐cigarette exposure.

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