Metal ions affecting the skin and eyes.

The skin and eyes remain in constant exposure to the surrounding environment and are subject to accidental, occupational, and biological risks at all times, Normal development, homeostasis, and repair following injury depend upon appropriate levels of calcium, zinc, magnesium, copper, iron, and minute amounts of other trace metals. Both tissues exist in a permanent state of dynamic equilibrium with the environment whereby cells lost through natural wear and tear are replaced through genetically regulated mitotic patterns. Normal functional requirements of the constituent tissues depend on critical balances between trace metals, metal ion gradients, and specific carrier proteins which are modulated by upregulation of growth factors, cytokines, hormones, and subcellular regulators acting by autocrine, paracrine, and endocrine mechanisms. Metal ion gradients in epidermal tissues serve critical functions in basal cell proliferation, post-mitotic migration, and functional differentiation in normal homeostasis and in repair following injury. Toxic mechanisms reflect imbalances in trace metals or interaction between xenobiotic and trace metals through competitive binding key carrier proteins and metabolic pathways leading to trace metal imbalances and functional impairment. Alternatively, toxic injuries result through direct cytotoxic action of metal ions on cell membranes, intercellular communication, RNA and DNA damage, and mutagenic change. Arsenic is the only primary carcinogen in the skin following ingestion or topical exposure; beryllium, aluminum, and zirconium are a cause of granuloma. Aluminum as a cause for breast cancer is equivocal. Metal toxicities in the eye result from direct accidental or occupational exposure and systemic uptake of neurotoxic metals and their action on the retina and optic nerve. Calcium, zinc, magnesium, and iron are essential trace elements in eye development and physiology but silver, gold, lead, and mercury are absorbed through optic membranes or from the circulation to accumulate in the vitreous leading to local or systemic action. Lead, mercury, cadmium, aluminum, and other xenobiotic metals are implicated in structural and physiological damage in the mammalian eye. Thallium shows an affinity for melanin.