Registration Dossier

Administrative data

Link to relevant study record(s)

Description of key information

Key value for chemical safety assessment

Bioaccumulation potential:
no bioaccumulation potential

Additional information


Two inhalation studies in rats (Benson et al. 1988, NTP 1996) indicate that lung nickel burdens increase with increasing concentrations of nickel sulphate (at least up to around 0.8 mg Ni/m3) in the inhaled air as well as with duration of exposure. The study by Benson et al. (1988) indicates that the lung nickel burden may rise to a steady state level as the lung nickel burdens were almost similar in rats exposed to 15 or 30 mg/m3. A third study (Dunnick et al. 1989) found similar concentrations of nickel in the lungs of rats and mice after 4, 9, and 13 weeks of inhalation to nickel sulphate (0.02 to 0.4 mg Ni/m3). Of nickel remaining in the body after 96 hours following a single dose of nickel sulphate administered by intratracheal administration, over 50% was in the lungs. The deposition of nickel in the lungs of rats is apparently greater than in the lungs of mice. No human data have been located.

Generally, nickel tends to deposit in the lungs of workers occupationally exposed to nickel compounds and in experimental animals following inhalation or intratracheal instillation of nickel compounds. The tissue distribution of nickel in experimental animals does not appear to depend significantly on the route of exposure (inhalation/intratracheal instillation or oral administration) although some differences have been observed. Low levels of accumulation in tissues are observed (generally below 1 ppm). A primary site of elevated tissue levels is the kidney. In addition, elevated concentrations of nickel are often found in the lung, also after oral dosing, and in the liver. Elevated nickel levels are less often found in other tissues. Limited information exists on tissue distribution in humans.

Absorbed nickel is excreted in the urine, regardless of the route of exposure. Most ingested nickel is excreted via faeces due to the relatively low gastrointestinal absorption. In humans, nickel excreted in the urine following oral intake of nickel sulphate accounts for 20-30% of the dose administered in drinking water to fasting subjects compared with 1-5% when administered together with food or in close proximity to a meal. From biological monitoring in small groups of electroplaters exposed to nickel sulphate and nickel chloride, the half-life for urinary elimination of nickel has been estimated to range from 17 to 39 hours.

Inhaled nickel particles can be eliminated from the respiratory tract either by exhalation, by absorption from the respiratory tract, or by removal due to mucociliary elimination.

In addition to this summary from the EU Risk Assessment, data on the bioaccessibility of Ni sulfate in biological fluids as a surrogate for bioavailability are reported within Section 7.1.1 of this IUCLID file.