Sulphur trioxide

Endpoint summary

Description of key information

No acute toxicity studies are available for sulphur trioxide.  A study of acute oral toxicity is available for sulphuric acid.  A number of non-standard acute inhalation studies are available; studies were performed in various species and using various exposure times.  In three of the studies, sulphuric acid aerosols were generated by mixing sulphur trioxide and humid air.  Studies performed using sulphuric acid are therefore relevant to sulphur trioxide.

Key value for chemical safety assessment

Acute toxicity: via oral route

Link to relevant study records

Reference

Endpoint:

acute toxicity: oral

Data waiving:

study scientifically not necessary / other information available

Justification for data waiving:

the study does not need to be conducted because the substance is classified as corrosive to the skin

Endpoint conclusion

Dose descriptor:

LD50

Value:

2 140 mg/kg bw

Acute toxicity: via inhalation route

Endpoint conclusion

Dose descriptor:

LC50

Value:

375 mg/m³ air

Additional information

Acute oral toxicity

A single acute oral toxicity study is available for sulphuric acid. Sulphur trioxide reacts rapidly with moisture in the gastrointestinal tract to form sulphuric acid, therefore the results of this study are relevant to sulphur trioxide.

The acute oral toxicity study (Smyth et al, 1969) performed with sulphuric acid reports an LD50 value of 2140 (1540 -2990) mg/kg bw. The study is reported in summary form only but the protocol design is comparable to OECD 401. The results of this study indicate that sulphuric acid is of low acute systemic toxicity when administered by gastric intubation. However it should be noted that the route of administration used in this study eliminates the potential for local corrosive effects of the test material on the upper gastrointestinal tract (mouth, pharynx and oesophagus). Following accidental/intentional oral ingestion of sulphuric acid by humans, the local effects on the upper gastrointestinal tract are likely to dominate the clinical presentation and the potential for systemic toxicity is likely to be low. Further testing of sulphuric acid for acute oral toxicity in animals (i.e. in a guideline- and GLP-compliant study) is not proposed for acute oral toxicity and for reasons of animal welfare, due to the corrosivity of the substance.

Acute dermal toxicity

No data on acute dermal toxicity in animals are available. Although this is a potential route of exposure for workers, testing is not justified for scientific reasons and on animal welfare grounds. Sulphur trioxide will react rapidly with moisture in the skin to produce sulphuric acid and is not likely to be absorbed systemically. The effects of acute dermal exposure to sulphuric acid on animals can be readily predicted (local irritation and corrosivity), and the data from human exposure are sufficient to characterise the effects.

Acute inhalation toxicity

A large number of acute inhalation toxicity studies have been performed with sulphuric acid, using various species and exposure times. In a number of these studies, sulphuric acid aerosols were generated by mixing sulphur trioxide gas and humid air. Due to the rapid reaction of sulphur trioxide with water, either in the air or in the respiratory tract, the studies performed with sulphuric acid are considered to be relevant to sulphur trioxide.

In all tested species (rats, mice, rabbits and guinea pigs) the concentration of acid aerosol, the length of exposure and particle size are important factors in determining lethality by inhalation.  Among the different species tested, the guinea pig appears to be the most sensitive to the acute inhalation toxicity of sulphuric acid mist/aerosols.  In the guinea pig, the apparent LC50 for an 8 hour-exposure period to sulphuric acid mist/aerosol with a particle size of approximately 1 um ranges from 0.018-0.050 mg/l depending on the age of the animals, with younger guinea pigs apparently more sensitive to than older animals. In the more reliable studies performed in other species, LC50 values vary with exposure duration and are in the range 0.375-0.425 mg/l in the rat, 0.600-0.850 mg/l in the mouse and 1.47-1.61 mg/l in the rabbit. The sensitivity of the guinea pig may be caused by its tendency to bronchoconstriction and laryngeal spasm compared with the other tested species.  The main macroscopic and or microscopic alterations observed in respiratory tract following acute inhalation exposure were haemorrhage, oedema, atelectasis and thickening of the alveolar wall in the guinea pig lung; haemorrhage and oedema of the lungs, ulceration of the nasal turbinates, trachea and larynx in rats and mice. These lesions are directly related to the corrosive/irritant effects of sulphuric acid and there is no indication of systemic toxicity following acute inhalation exposure.

Justification for classification or non-classification

No classification for acute oral or dermal toxicity is proposed according to current EU criteria.