Sulphuric acid

Endpoint summary

Description of key information

Short description of key information on bioaccumulation potential result: 
Primary information is limited to a study of the absorption and kinetics of radiolabelled sulphate following the inhalation of sulphuric acid aerosols.  Sulphuric acid immediately dissociates to the hydrogen and sulphate ions, with the hydrogen ion being responsible for the local toxicity (irritation and corrosivity) of sulphuric acid.
Short description of key information on absorption rate: 
No studies are proposed for scientific reasons and (given the corrosive nature of the substance), also reasons of animal welfare.  No dermal absorption is predicted under normal conditions of use, based on the physicochemical properties of the substance.

Key value for chemical safety assessment

Bioaccumulation potential:

no bioaccumulation potential

Additional information

The effects of sulphuric acid are essentially the result of the hydrogen ion (local deposition of H+, pH change) rather than an effect of the sulphate ion. Sulphuric acid (as such) is not expected to be absorbed or distributed throughout the body as the acid will rapidly dissociate; the hydrogen ion will form water. The sulphate anion will enter the body electrolyte pool, its kinetics will be governed by sulphate homeostatic mechanisms, and is therefore not predicted play a specific toxicological role. This supposition is supported by experiments which have studied the active component in inorganic acids on various endpoints, using different acids or salts. The results of these studies lead to the conclusion that the observed effects are due to the hydrogen ion, while the anion appeared to have no effect. In a study of the clearance of radiolabeled sulphuric acid aerosol in different species, the authors observed that the sulphur from sulphuric acid was rapidly cleared (from 2 -9 minutes) from the lungs of animals into the blood following inhalation exposure (Dahl, 1983). Sulphate is a normal constituent of the blood (present at 0.8 -1.2 mg/dl) and is a normal metabolite of sulphur-containing amino acids. The body has efficient sulphate homeostatic mechanisms and excess sulphate is excreted in the urine (capacity-limited proximal tubular absorption); urinary sulphate concentrations of up to 500 umol/dl/kg bw have been reported. The body pool of this anion is large, and it is therefore unlikely that occupational exposure will significantly add to the normal body burden.

Systemic absorption of the hydrogen ion following dermal or inhalation exposure to sulphuric acid is not predicted to be significant, and the low level of hydrogen ions absorbed will be effectively controlled by the homeostatic mechanisms governing pH including the action of the enzyme carbonic anhydrase and NA+/H+ exchange in the proximal renal tubule. Although acidaemia and metabolic acidosis have been noted following cases of ingestion exposure, similar effects are not predicted following occupational inhalation exposure (which will be much lower and effectively limited by respiratory tract irritation) or following dermal exposure (due to low dermal absorption and local dermal irritation).

The deposition of sulphuric particles in the human lung has been studied extensively. Deposition is influenced by subject age, particle size and breathing rate. Sulphuric acid particles are hygroscopic and therefore will absorb moisture present in the airways, thereby increasing particle size and potentially increasing particle retention. Respiratory mucus has a limited buffering capacity and may reduce tissue contact.

The absence of systemic effects in the large number of toxicity studies performed with sulphuric acid is consistent with this assessment of its toxicokinetics.

Discussion on absorption rate:

No dermal absorption is predicted under normal conditions of use, based on the physicochemical properties of the substance. However dermal absorption may occur when the integrity of the skin is lost (i.e. in accidental exposures resulting in burns).