Human health hazard profile

• Author: Clemm, Christan; Löw, Clara; Baron, Yifaat; Moch, Katja; Möller, Martin; Köhler, Andreas R; Gensch, Carl-Otto; Deubzer, Otmar
• Pages: 27-29

RoHS Annex II Dossier, final

Diantimony trioxide (flame retardant)

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3 HUMAN HEALTH HAZARD PROFILE

Endpoints of concern

Diantimony trioxide is classified for carcinogenicity Category 2 (H351 - Suspected of causing cancer)

according to Annex VI of the CLP Regulation.

The Swedish Chemicals Agency KEMI (2015) summarised in its assessment of the risk reduction

potential of hazardous substances in electrical and electronic equipment on the EU market: “It has

been agreed [this refers to e.g. the opinion of SCHER]52 that the carcinogenic effects are most likely

caused by particle overload and impaired lung clearance which leads to the formation of tumours

(particle effect, no substance specific effect). ATO is considered a threshold carcinogen with an

NOEL of 0.5 mg/m³ (with the critical concentration expected to be 10 times higher). The carcinogenic

hazard by inhalation does not apply via dermal or oral exposure.”

This hazard based on particle effect is also described by Campine:53 “Fine dust inhalation leads to

lung overload and lung toxicity, which has triggered a carcinogenic response in certain test animals

through inflammation and hypoxia (NTP)”

The Canadian Ministers of the Environment and of Health have conducted a screening assessment

of diantimony trioxide in 2010 concluding that there is no evidence available to suggest carcinogenic

potential for antimony trioxide via the oral route.

In the EU RAR54, it was concluded that diantimony trioxide is of low acute toxicity via oral and dermal

route. As for the repeated dose toxicity; the EU RAR stated that the studies “indicate that repeated

inhalation exposure to diantimony trioxide may cause pulmonary inflammation, lung emphysema

and pneumoconiosis.”

As for mutagenicity, in the EU RAR it is explained that “diantimony trioxide does not cause systemic

mutagenicity in vivo after oral administration. However, it is not possible to conclude on mutagenicity

in specific site of contact tissues (local mutagenicity) and thus, whether the result is relevant for the

situation in the lung after inhalation exposure, which is the site where tumours have been found in

the carcinogenicity studies. However, the in vivo data might suggest that a possible mutagenic

potency of diantimony trioxide would be low and it is believed that a possible local genotoxic effect

of diantimony trioxide would only be biologically relevant at concentration levels that also cause

particle overload.”

Collective evidence from genotoxicity studies suggests that antimony trioxide is not likely to be

mutagenic but may exert some clastogenic effects in vitro. (Canada 2010) noted the clastogenic

effect in vitro and independently decided that no conclusive in vivo evidence of genotoxicity was

available for antimony trioxide.

52 Scientific Committee on Health and Environmental Risks SCHER (2010/2011): Opinion on the Risk from the Use of

Diantimony Trioxide in Toys;

https://ec.europa.eu/health/scientific_committees/environmental_risks/docs/scher_o_125.pdf (last viewed 24.07.2019)

53 Op. cit. Campine (2018) and Annex 1 of the contribution submitted by Campine (2018);

http://rohs.exemptions.oeko.info/fileadmin/user_upload/RoHS_Pack_15/1st_Consultation_Contributions/Contribution

_Campine_diantimony_Annex_1.pdf, last viewed 28.06.2018

54 Op. cit. EU RAR European Union Risk Assessment Report (2008): Diantimony trioxide, November 2008