Nickel-based particulates, including nickel nanoparticles and nickel oxide nanoparticles, are increasingly utilized in industrial and medical applications. However, there are significant concerns regarding their systemic toxicity. Due to their small size and high reactivity, these particles can deposit in the respiratory tract particularly the lungs and subsequently translocate into the bloodstream following inhalation, and ingestion. Evidence indicates that smaller particles exhibit broader biodistribution, with nanoparticles accumulating in organs such as the liver, kidneys, spleen, brain, and heart. Nickel particulates elicit robust immune responses, resulting in the release of inflammatory mediators, induction of oxidative stress, and genotoxic effects. Documented toxicities in the liver, kidneys, spleen, heart, blood, and brain are primarily attributed to particle dissolution, nickel ion release, and reactive oxygen species generation. In summary, nickel-based particulates induce complex, multi-organ toxicity influenced by particle size, solubility, and exposure route. This review outlines the principal mechanisms of nickel toxicity and underscores the necessity for improved risk assessment and longitudinal studies to inform occupational and environmental health policies.
Ugwu et al. (Wed,) studied this question.