Cadmium exposure and its role in joint disease: A brief review of experimental and population-based evidence

Abstract

Cadmium is a toxic metal released into the environment mainly by mining and industrial activities, posing health risks through inhalation and ingestion. Smoking is a major source of exposure, followed by consuming contaminated foods such as vegetables and offal. Due to its long half-life, Cadmium accumulates in the body and contributes to chronic diseases, including rheumatic and metabolic disorders such as osteoporosis, osteoarthritis, rheumatoid arthritis, systemic lupus erythematosus, gout, and hyperuricemia. The impact of Cadmium on bone health was first documented in Japan in 1955 when contaminated rice consumption caused significant bone mineral loss and severe pain. Recent studies suggest that Cadmium concentrations above 1 µg/L have osteotoxic effects, likely due to impaired Calcio absorption or its replacement in bone tissue. Cadmium accumulation also disrupts joint homeostasis, promoting cartilage degradation, osteophyte formation, and synovitis. This may result from its interference with essential metals such as Zinc, Iron, Manganese, and Chromium, which are critical for the extracellular matrix. Cadmium has also been linked to rheumatoid arthritis by disrupting immune function, promoting oxidative stress, and increasing inflammatory mediators like TNF-α, IL-6, and COX-2. It may contribute to systemic lupus erythematosus by increasing antinuclear antibodies and altering cytokine profiles. Additionally, Cadmium exposure raises the risk of hyperuricemia and gout by interfering with urate metabolism, renal transport, and inducing oxidative stress. This article highlights Cadmium’s toxic effects and underscores the need for public health strategies to monitor and reduce exposure, ultimately preventing musculoskeletal, rheumatic, and metabolic diseases while improving quality of life.