The adverse impact of cadmium on immune function and lung host defense

Abstract

Cadmium (Cd) is a transition metal, also referred to as a heavy metal, that is naturally abundant in the earth’s crust. It has no known benefit to humans. It is primarily released into our environment through mining and smelting in industrial processes and enters the food chain through uptake by plants from contaminated soil and water. In humans, Cd primarily enters the body through ingestion of foods and cigarette smoke and has an extremely long resident half-life in the body compared to other transition metals. Environmental workplace exposure is also a source through inhalation, although much less common. The principal organs adversely affected by Cd following acute and chronic exposure are the kidneys, bone, vasculature and lung. Cd adversely impacts cell function through changes in gene expression and signal transduction and is recognized as a carcinogen. Despite a substantial body of mechanistic studies in cells and animal models, the overall impact of Cd on innate immune function in humans remains poorly understood. The best evidence is perhaps alteration of reactive oxygen species balance and signaling in cells that regulate innate immunity causing alteration of the inflammatory response that is postulated to contribute to chronic diseases. Epidemiologic studies support this possibility since increased tissue levels in humans are strongly associated with leading chronic diseases including chronic obstructive pulmonary disease (COPD), which will be discussed in depth. Additional studies are required to understand how chronic exposure and accumulation of this leading environmental toxicant in vital organs negatively impact innate immune function and host defense leading to chronic disease in humans.