Human health hazard profile

• Author: Clemm, Christan; Löw, Clara; Baron, Yifaat; Moch, Katja; Möller, Martin; Köhler, Andreas R; Gensch, Carl-Otto; Deubzer, Otmar
• Pages: 21-23

RoHS Annex II Dossier, final

Nickel sulphate a nd nickel sulfamate

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3. HUMAN HEALTH HAZARD PROFILE

The toxicological summary in the registration dossier provided in the ECHA database35 show the

same results for nickel sulphate and nickel sulfamate (the guidance values are given in terms of

mg nickel and not as mg substance). It is therefore assumed that the nickel ion is the entity being

mostly relevant for the human health hazards. In the regulatory context, it is commonly referred to

a group “nickel and its compounds”.36

The Nickel Institute in its contribution 2019 pointed out that it should be noted here that nickel

metal has a different and lower hazard classification than inorganic nickel compounds.

Nickel metal as nickel (CAS 7440-02-0) has a lower carcinogenic classification of category 2 by

inhalation (Carc. 2 – H351 Suspected of causing cancer) compared to the inorganic compounds

such as nickel sulphate and nickel sulfamate being harmonised classified for Carc. 1A (H350 May

cause cancer) by inhalation; however, nickel is also classified for specific organ toxicity STOT RE 1

(H372 Causes damage to organs through prolonged or repeated exposure) and skin sensitation

(Skin Sens. 1: H317 May cause an allergic skin reaction). Critical endpoint

The opinion of ECHA RAC (ECHA RAC 2018) is the most recent evaluation of the critical

endpoints of nickel and its compounds. The following conclusions are relevant for the human

health hazard of nickel sulphate and nickel sulfamate:

•The main hazard of nickel compounds is their carcinogenicity in the respiratory tract. Exposures

to mixed nickel compounds have resulted in increased lung cancer risk. In some studies, cancer

risk has correlated best with the exposure to soluble nickel. In addition, an increased risk for

nasal cancer has been demonstrated.

•Differences in lung clearance and local cellular uptake between different nickel species are

assumed to explain the variability in their carcinogenic potency.

•In humans, exposure to nickel is often via a mixture of soluble and poorly soluble nickel

compounds.

•Nickel compounds are not directly mutagenic but have been shown to induce genotoxic effects

via different indirect mechanisms.

•Chronic inflammation in the respiratory tract is also likely to play a significant role in nickel-

induced carcinogenicity together with indirect genotoxicity.

•The available information on the mechanisms of genotoxicity and cancer support a mode-of-

action based threshold for carcinogenic effects.

•The proposed OEL therefore relies on a mode of action-based threshold for the carcinogenicity

of nickel compounds. In addition to the mechanistic data reviewed by RAC, data on the lack of

genotoxicity in animals at inhalation doses below the levels causing inflammation and

cytotoxicity support this conclusion.

•At exposures below the proposed limit value, no significant residual cancer risk is expected for

workers.

35 Op. cit. ECHA Registered Substance Database: Entries for Nickel sulphate and Nickel bis(sulphamidate)

36 https://echa.europa.eu/de/substance-information/-/substanceinfo/100.239.198