Introduction
This topic covers occupational poisoning with nickel and chromium and their compounds: where exposure happens, how the metals act in the body, the clinical picture of acute and chronic toxicity, diagnosis, treatment and the medical expertise (fitness-for-work) assessment of exposed workers.
Nickel: sources and etiology
Nickel is used widely in industry, and most occupational harm comes from soluble nickel salts and fine dusts or fumes. Typical exposure settings include:
- Metallurgy: production of stainless steel and nickel alloys, smelting and refining, welding and grinding of alloys.
- Electroplating (nickel plating) and galvanic baths.
- Manufacture of glass and ceramic pigments and enamels.
- Production of nickel-cadmium batteries, where nickel and cadmium exposure often coincide.
- Catalysts (hydrogenation), and exhaust and fumes from vehicles and industrial processes as an additional source of airborne nickel.
- Nickel carbonyl Ni(CO)4, formed in some refining processes, is a volatile and exceptionally toxic gas and the most dangerous acute form.
Nickel: pathogenesis
- Absorption: inhalation of dust, fume or vapour is the main route in workers; gastrointestinal absorption of soluble salts is low, but higher than for many metals in susceptible individuals.
- Distribution: Ni2+ binds mainly to albumin and other plasma proteins and is distributed to the lungs, kidneys and liver, where it accumulates. It also crosses the blood-brain barrier and the placenta.
- Allergic contact dermatitis: nickel ions act as haptens, binding to skin proteins and triggering a delayed-type (type IV) hypersensitivity reaction. Nickel is the most common contact allergen.
- Respiratory injury: irritation and inflammation of the airways, with chemical pneumonitis after heavy acute exposure and sensitisation leading to asthma.
- Carcinogenicity: nickel compounds are established human carcinogens (IARC group 1), mainly causing cancers of the lung, nasal cavity and paranasal sinuses. Proposed mechanisms include oxidative stress, impaired DNA repair and epigenetic changes.