16. Occupational intoxications with cadmium compounds - etiology, pathogenesis, clinical manifestations, diagnosis, treatment, medical expertise.

Introduction

Occupational cadmium intoxication is caused by cadmium and its compounds, which accumulate in the kidney and lung over decades. This note covers the sources and forms of exposure, the pathogenesis of acute and chronic poisoning, clinical features, diagnosis, treatment, prevention and medical expertise.

Etiology and sources of exposure

Cadmium is a by-product of zinc, lead and copper ore processing, so exposure is common in metallurgy. The most acutely dangerous form is cadmium oxide fume, produced when cadmium-containing materials are heated, melted or welded. Other forms include cadmium chloride, sulfate and sulfide (used in pigments), and metallic dust.

• Smelting and refining of zinc, lead and copper ores
• Manufacture of nickel-cadmium (Ni-Cd) batteries
• Pigments and heat stabilisers in paints, glass, ceramics and plastics (PVC)
• Welding, cutting and burning of cadmium-coated or cadmium-containing metals
• Non-occupational sources: phosphate fertilisers, some pesticides and, importantly, tobacco smoke, which roughly doubles the body burden in smokers

Pathogenesis

The main occupational route is inhalation of fine fume particles, which are deposited in the alveoli and absorbed rapidly. Gastrointestinal absorption is low, only a few percent, but it rises when iron or calcium stores are deficient. In blood, cadmium binds mainly to erythrocytes and haemoglobin. In the liver and kidney it is bound to metallothionein, a small cysteine-rich protein. Cadmium has a very long biological half-life, roughly 10 to 30 years, mostly stored in the kidney cortex.

The main toxic mechanisms are:

1. Renal tubular damage: cadmium-metallothionein is filtered and reabsorbed by proximal tubular cells, where it accumulates and causes cell injury, leading to tubular dysfunction
2. Vitamin D disturbance: damaged tubules fail to hydroxylate vitamin D to its active form, so calcium absorption falls and bone is demineralised
3. Alpha1-antitrypsin inhibition: cadmium inactivates this protease inhibitor in the lung, so elastase activity is unopposed, which favours emphysema
4. Oxidative stress and DNA damage: impaired DNA repair underlies the carcinogenic effect