Hydrogen sulphide

Endpoint summary

Description of key information

In two acute inhalation toxicity studies with rats the concentrations of H2S which led to the death of 50% of the animals (LC50) were 444 ppm (621 mg/m3) (Tansy et al., 1981) and 501 ppm (696 mg/m3) (Prior et al., 1988), respectively, after exposure for 4 hours.
The LC50 decreases with the exposure duration from 587 ppm (816 mg/m3) at 2 hours to 501 (696 mg/m3) and 335 ppm (466 mg/m3) at 4 and 6 hours, respectively. All rats that died had pulmonary oedema (Prior et al., 1988).
The same time-related toxicity was found with mice. The LC50 decreases with the exposure duration from 1160 ppm (1610 mg/m3) at 10 minutes to 800 ppm (1110 mg/m3) and 676 ppm (940 mg/m3) at 30 and 60 minutes, respectively (Zwart et al. 1990). These results can be compared with the effects seen after 60 min exposure to rats: LC50 712 ppm (990 mg/m³) (MacEwen and Vernot, 1972). With rats these authors found an LC50 of 712 ppm (990 mg/m³). So no relevant species specific effects were seen between rats and mice.
In aqueous environment H2S and its salt NaHS dissolves easily and are immediately hydrolyzed and an pH-dependent equilibrium is established between S2-, HS- and H2S. As there is no acute oral and dermal toxicity study available with H2S the results of the studies with NaHS are taken to derive an oral and dermal LD50.
An oral LD50 value has been calculated for H2S: 49 mg/kg bw. With NaHS no specific symptoms were observed. Fatalities occurred within one hour after administration.
A dermal LD50 value has been calculated for H2S: 124 mg/kg bw. With NaHS the animals showed reddenig at the application site and unbalancing. Fatalities occured until 2 hours after application.

Key value for chemical safety assessment

Acute toxicity: via oral route

Endpoint conclusion

Endpoint conclusion:

adverse effect observed

Dose descriptor:

LD50

Value:

49 mg/kg bw

Quality of whole database:

LD 50 derived from data of a study with NaHS, study well documented, meets generally accepted scientific principles (similar to OECD test guideline 403), acceptable for assessment

Acute toxicity: via inhalation route

Endpoint conclusion

Endpoint conclusion:

adverse effect observed

Dose descriptor:

LC50

Value:

621 mg/m³ air

Quality of whole database:

Study well documented, meets generally accepted scientific principles (similar to OECD test guideline 403), acceptable for assessment

Acute toxicity: via dermal route

Endpoint conclusion

Endpoint conclusion:

adverse effect observed

Dose descriptor:

LD50

Value:

124 mg/kg bw

Quality of whole database:

LD 50 derived from data of a study with NaHS, study well documented, meets generally accepted scientific principles (similar to OECD test guideline 403), acceptable for assessment

Additional information

Groups of male and female Long Evans, Sprague Dawley, and Fischer 344 rats were exposed to varying concentrations of hydrogen sulfide for 2, 4, or 6 hours, followed by a 14-day observation period. Exposure chambers were clear, acrylic horizontal flow chambers with two removable stainless steel cones with a total volume of 69 liters. Hydrogen sulfide concentrations were monitored by gas chromatography four times per hour. LC50 values of 587, 501, and 335 ppm were calculated for the 2, 4, and 6 hr time points, respectively. No strain differences were observed.

In a second study groups of five male and five female Sprague-Dawley rats were exposed to 0-600 ppm hydrogen sulfide for 4 hours, followed by a 14-day observation period. Animals were exposed simultaneously in a 75 liter glass chamber. A 4-hr LC50 of 444 ppm was calculated.

Up to a limit concentration H2S dissolves in water in a temperature dependent way. At 20 °C the limit is 3.98 g/l. H2S can stay present in water for several hours. In aqueous environments, H2S and the corresponding salt Na2S, are immediately hydrolyzed and, as a function of pH, an equilibrium is established between S2-, HS-, and H2S, with increasing H2S formation at decreasing pH. Temperature and salinity also affect this equilibrium but to a much lesser extent than pH.

As there are no acute oral and dermal toxicity studies with H2S available the acute and dermal oral toxicity is taken from studies with NaHS.

A LD50 range >46.4 and >215 mg/kg bw. was seen with sodium hydrogensuldide (70%) in the oral study. An estimated LD50 value can be calculated as 115 mg/kg bw..Lethal effects started with dosages of 68.1 mg/kg bw and reached 100% after dosages of 215 mg/kg bw.

The lethal effects emerged within one hour, at later timepoints no further fatalities were observed.

From these data the LD50 of 100% NaHS can be calculated: 80.5 mg/kg bw.; further on a LD50 value for H2S can be derived:

molecular weight of NaHS: 56.06;

molecular weight of H2S: 34.08;

oral LD50 of H2S: 49 mg/kg bw.

As there is no acute dermal toxicity study with H2S available an acute dermal toxicity study with 31 -32% NaHS is taken to evaluate the acute dermal toxicity of H2S. A LD50 of 632 mg/kg bw. with a 95% range from 458 to 872 mg/kg bw. was found.

The lethal effects emerged within 2 hours after application. No later fatalities were observed. The application was done in an occlusive way. After 24 hours the skin at the application site showed mild reddening and eschar. Beside this local effect all dosed animals showed symptoms of unbalancing (lowest dosage: 100 mg/kg bw.).

Calculation to 100% NaHS: LD50 204 mg/kg bw.

Calculation of the acute dermal LD50 of H2S:

molecular weight of NaHS: 56.06;

molecular weight of H2S: 34.08;

dermal LD50 of H2S with rats: 124 mg/kg bw.

Justification for selection of acute toxicity – oral endpoint
In aqueous environment H2S and its salt NaHS dissolves easily and are immediately hydrolyzed and an pH-dependent equilibrium is established between S2-, HS- and H2S. As there is no acute oral toxicity study available with H2S the result of the study with NaHS is taken to derive a LD50 for the rat.

Justification for selection of acute toxicity – inhalation endpoint
Key study

Justification for selection of acute toxicity – dermal endpoint
In aqueous environment H2S and its salt NaHS dissolves easily and are immediately hydrolyzed and an pH-dependent equilibrium is established between S2-, HS- and H2S. As there is no acute oral toxicity study available with H2S the result of the study with NaHS is taken to derive a LD50.

Justification for classification or non-classification

Acute inhalation toxicity:

The LC₅₀of H₂S was 444 ppm equivalent to 0.621 mg/L. On the basis of this study and in accordance with Regulation (EC) No 1272/2008 H₂S shall be classified as Acute Tox. 2 (Hazard statement: H330; Fatal if inhaled) and in accordance with Annex VI of Commission Directive 2001/59/EC/ Council Directive 67/548/EEC, H₂S shall be classified as being Toxic by inhalation (R23).

Harmonised classification:

- according to annex VI Table 3.1 of regulation Regulation (EC) No 1272/2008 index 016-001-00-4: Acute Tox 2 H330, fatal if inhaled)

- according to annex I of Council Directive 67/548/EEC: R26 Very toxic by inhalation.

Acute oral toxicity:

The LD₅₀of H₂S was 49 mg/kg bw. On the basis of this study and in accordance with Regulation (EC) No 1272/2008 H₂S shall be classified as Acute Tox. 2 (Hazard statement: H300; Fatal if swallowed) and in accordance with Annex VI of Commission Directive 2001/59/EC/ directive 67/548/EEC, H₂S shall be classified as being Toxic when swallowed. (T; R25). Relevant only for oral intake of aqueous solutions of H₂S.

Acute dermal toxicity:

The LD₅₀of H₂S was 124 mg/kg bw. On the basis of this study and in accordance with Regulation (EC) No 1272/2008 H₂S shall be classified as Acute Tox. 2 (Hazard statement: H310; Fatal in contact with skin) and in accordance with Annex VI of Commission Directive 2001/59/EC/ directive 67/548/EEC

, H₂S shall be classified as being Toxic in contact with skin (R24).

Relevant only for dermal application of aqueous solutions of H₂S.