E-waste-the aftermath of large amount of electrical and electronic equipment ferried into Africa from which Nigeria receives a significant chunk, is composed of components known to be hazardous to health. Composition of series of heavy metals (HMs) in e-waste is traceable to many health conditions including cancer which is hitherto incompletely understood. This study harmonizes primary data on HMs from e-waste in different Nigerian environmental media including the air, soil, surface dust, water and plant. We estimated the possible health implications, single and aggregative soil and water pollution indices both in adult and children categories, carcinogenic and non-carcinogenic risks secondary to HM exposure and mapped out the possible mechanism of carcinogenesis. Analysis showed that s oil, water, surface dust and plant matrices in Nigerian environment are variedly but considerably contaminated with combination of HMs. The significantly high values of the hazard quotient and hazard index of both water and surface dust matrices are indicative of adverse health effect of the non-carcinogenic risk. The highest HQ is generated by Pb and Cr through dermal exposure to soil and surface dust with mean values of 1718.48, 1146.14, 1362.10 and 1794.61 respectively among Nigerian children followed by the oral exposure. This pattern of observation is similar to that obtained for adult category. HI due to Pb and Cr in soil constitutes the highest HI (2.05E+03 +03 and 1.18E+03 +03 respectively) followed by surface dust. However, this study precipitates the observation that children are more at health risk than adults in contaminated environment. Carcinogenic risk also follows the same pattern of expression in the Nigerian environment. We conclude that exposure to e-waste poses significant carcinogenic and non-carcinogenic health risks and the induction of toxicity may be mediated via DNA damage, oxidative stress and inflammatory/immune cells dysfunction in Nigerian environment.

Cadmium (Cd) is a malleable element with odorless, tasteless characteristics that occurs naturally in the earth's crust, underground water, and soil. The most common reasons for the anthropological release of Cd to the environment include industrial metal mining, smelting, battery manufacturing, fertilizer production, and cigarette smoking. Cadmium-containing products may enter the environment as soluble salts, vapor, or particle forms that accumulate in food, soil, water, and air. Several epidemiological studies have highlighted the association between Cd exposure and adverse health outcomes, especially renal toxicity, and the impact of Cd exposure on the development and progression of carcinogenesis. Also highlighted is the evidence for early-life and even maternal exposure to Cd leading to devastating health outcomes, especially the risk of cancer development in adulthood. Several mechanisms have been proposed to explain how Cd mediates carcinogenic transformation, including epigenetic alteration, DNA methylation, histone posttranslational modification, dysregulated noncoding RNA, DNA damage in the form of DNA mutation, strand breaks, and chromosomal abnormalities with double-strand break representing the most common DNA form of damage. Cd induces an indirect genotoxic effect by reducing p53 ' s DNA binding activity, eventually impairing DNA repair, inducing downregulation in the expression of DNA repair genes, which might result in carcinogenic transformation, enhancing lipid peroxidation or evasion of antioxidant interference such as catalase, superoxide dismutase, and glutathione. Moreover, Cd mediates apoptosis evasion, autophagy activation, and survival mechanisms. In this review, we decipher the role of Cd mediating carcinogenic transformation in different models and highlight the interaction between various mechanisms. We also discuss diagnostic markers, therapeutic interventions, and future perspectives.