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Description of key information

A (limited) acute oral toxicity study determined an LD50 as >2000 mg/kg bw. This low toxicity is supported by a number of other studies discussed under Section 5.2.3.

Key value for chemical safety assessment

Acute toxicity: via oral route

Endpoint conclusion
Endpoint conclusion:
no adverse effect observed

Acute toxicity: via inhalation route

Endpoint conclusion
Endpoint conclusion:
no study available

Acute toxicity: via dermal route

Endpoint conclusion
Endpoint conclusion:
no study available

Additional information

During preparation for a one-week dose range finding study of ammonium perrhenate by oral gavage to rats it was found that corn oil did not appear to be a satisfactory vehicle, and thus some question as to the validity of the 1978 acute oral toxicity study (in which "plant oil" was the stated vehicle) was raised.

A low oral acute toxicity for ammonium perrhenate is supported by additional data on ammonium perrhenate itself, and the related material dirhenium heptaoxide, as described below.

In a one-week dose range finding study for ammonium perrhenate [~69% Re], using a 40% PEG400 in Milli-Q water vehicle, by oral gavage in rats, treatment up to 1000 mg/kg bw/day for 7 days was not associated with any mortality, clinical signs, changes in body weight gain or food consumption, or gross pathology. [An LD50 at this level would still have placed it in only the lowest GHS Cat 4].

Data are available on dirhenium heptaoxide. Dirhenium heptaoxide [~85% Re] was found to have an oral LD50 of >500 mg/kg bw, but <2000 mg/kg bw, placing it in GHS Acute Tox Cat 4. In this study, no mortality occurred at 500 mg/kg bw, whilst 4/6 animals given 2000 mg/kg bw died (between 1 and 3 days). Dirhenium heptaoxide is corrosive, and there were pathological signs of corrosion on necropsy of the animals that died - black erosions/ulcers of the glandular stomach and a red, diffuse discolouration of the small and large intestine. Amongst surviving animals, a severe thickening of the wall of the glandular stomach was found. Even so, mortality results suggest that the LD50, even for this substance, is towards the upper end of this acute toxic class, and support the view that the acute oral toxicity for ammonium perrhenate is low.

An acute inhalation toxicity study for dirhenium heptaoxide is also available. This indicated a GHS classification Cat 4, with LC50s determined as approximately 3.87 mg/l for female rats and >3.87 mg/l for male and females taken together. Higher concentrations were not tested due to the corrosive nature of the substance.

Irritation data indicate that ammonium perrhenate is not irritating to the skin or eyes.

Taken together, the available data suggest that acute oral toxicity for ammonium perrhenate is low and no classification is justified.


Justification for selection of acute toxicity – oral endpoint
Only one (albeit limited) study available.

Justification for classification or non-classification

A weight-of-evidence approach for ammonium perrhenate has been taken, as outlined under Discussion, above. A (limited) acute oral toxicity study is available on ammonium perrhenate and an LD50 value of >2000 mg/kg bw was determined. Although some question as to the validity of this study resulted from more recent work in preparation for a one-week dose range finding study, additional data supports justification for non-classification.

The inhalation and dermal routes are not considered to be significant routes of exposure for acute toxicity.