Sodium hypochlorite

Endpoint summary

Description of key information

The Kaestner data is considered of higher reliability, and it is based on the rat, the standard animal, contrary to the Momma study which used mice. The LD50 and LD0 values were calculated as follows:
LD50= 12.5% (% of available Cl2 in sol.) x 8.83 (g/kg BW LD50 of the sol. to male rat) = 1.1 g/kg BW (LD50 as available Cl2) = 1100 mg/kg BW NaClO as av. Cl2
LD0= 12.5% (% of available Cl2 in sol.) x 5.01 (g/kg LD50 of the sol. to male rat) 0.626 g/kg BW (LD50 as available Cl2) = 626 mg/kg BW NaClO as av. Cl2
In a acute dermal toxicity study, animals showed signs of moderate to severe skin irritation. The dermal LD50 was determined to be greater than 20 g/kg bw.
In the acute inhalation toxicity study, generalised inactivity and lacrimation were evident at the dose of 10.5 mg av Cl/L. The LC50 was determined to be greater than 10.5 mg av Cl/L.

Key value for chemical safety assessment

Acute toxicity: via oral route

Endpoint conclusion

Dose descriptor:

LD50

Value:

1 100 mg/kg bw

Acute toxicity: via inhalation route

Endpoint conclusion

Dose descriptor:

LC50

Value:

10 500 mg/m³ air

Acute toxicity: via dermal route

Endpoint conclusion

Dose descriptor:

LD50

Value:

20 000 mg/kg bw

Additional information

Oral route

Several acute toxicity studies, the majority in rats, have been reported. The LD0 value for a 3.6 % solution (as available chlorine) was reported to be greater than 10.5 g/kg (corresponding to 0.378 g/kg as available chlorine). No deaths and no alteration of the gastric mucosae of the exposed animals were reported (CERB 1985). Similarly, the LD0 of 3.6% solution of sodium hypochlorite was reported to be > 11.8 g/kg (>0.425 g/kg as available chlorine) (AISE, 1997). The LD50 of a solution of 12.5 % sodium hypochlorite was reported to be approximately 5.23 g/kg, corresponding to 0.653 g/kg as available chlorine (Griffiths, Chlorine Institute 1980).

A solution of sodium hypochlorite at a concentration of 12.5% (available chlorine) caused no mortality up to the level of 5.8 g/kg. Gastric lesions were found in all animals exposed and sacrificed after 14 days of observation (CERB, 1985).

An oral LD50 of 8.8 g/kg in rats was quoted for a 12.5% bleach solution (based on available chlorine). Five groups of 10 male Wistar rats each were given 20 ml/kg bw of a dilution of chlorine bleach containing 12.5% available chlorine. During the observation period of 14 days, the following symptoms of toxicity were recorded: ungroomed fur, light to moderate sedation, diarrhea, ataxia, and increased breathing of differing severity. The deaths observed occurred in most cases within 24 hours after application. Pathology upon dissection showed strong gas accumulation in the stomach and intestines, swelling of the liver, bleeding gastritis and enteritis. There were no symptoms noted in the animals that survived. The LD50 was determined to be 8.83 (8.2 – 9.51) g/kg bw, and the NOAEL was found to be 5.01 g/kg bw, all based on the 12.5% available chlorine solution (or 626 mg/kg bw of sodium hypochlorite expressed as available chlorine) (Kaestner, 1981).

Osterberg (1977) reported an LD50 > 5.0 g/kg for commercial bleach containing 4.74% of available chlorine, corresponding to a value > 0.237g/kg available chlorine. Using an unspecified commercial solution of sodium hypochlorite an LD50 value of 8.91 g/kg (6.83-11.68g/kg) was reported for the the Male Albino rat. Signs of intoxication reported were hypoactivity, muscular weakness, hemorragic rhinitis, emaciation and death. No significant findings were observed following examination of both survivors and decedents (Industrial Bio-Test Laboratories Inc., 1970).

In the mouse the LD50 was reported as 5.8 ml/kg and 6.8 ml/kg for females and males respectively for a commercial solution of sodium hypochlorite of 10% as available chlorine diluted 50% v/v with water, leading to 0.36 and 0.42 g/kg available chlorine respectively. Signs of toxicity consisted of depression of spontaneous activity and irritation of the gastrointestinal tract (Momma, 1986).

A LD50 of 0.88 g/kg sodium hypochlorite solution in the mouse is also reported in the literature (Klimm, 1989). The concentration of sodium hypochlorite was not reported and the methodology used was not fully explained. Therefore the value was not considered to be relevant for the risk assessment.

Conclusion on oral toxicity:

The acute toxicity of marketed hypochlorite solutions by the oral route is low. The LD50 values for solutions containing active chlorine concentrations up to 12.5 % are greater than 5.8 g/kg. The data for dermal acute toxicity as well as inhalation toxicity indicate a low level of toxicity even for these routes of administration.

Accidental human data are reported for ingestion and parenteral route: it can be concluded that the effects of accidental ingestion of domestic sodium hypochlorite bleaches are not expected to lead to severe or permanent damage of the gastrointestinal tract as recovery is rapid and without any permanent health consequences. This is also expected for small quantities of solutions accidentally injected in blood system or in the tissues.

Although the overall lowest LD50 available is from the Momma study, it is preferred to use the value of the Kaestner study as the key reference study. The Osterberg study is poorly reported and the LD50 value is not exactly defined but indicated just as higher than 5000 mg/kg. The Momma study is poorly reported as well. Therefore the Kaestner data is considered of higher reliability, and it is based on the rat, the standard animal, contrary to the Momma study which used mice. The LD50 and LD0 values were calculated as follows:

LD50= 12.5% (% of available Cl2 in sol.) x 8.83 (g/kg BW LD50 of the sol. to male rat) = 1.1 g/kg BW (LD50 as available Cl2) = 1100 mg/kg BW NaClO as av. Cl2

LD0= 12.5% (% of available Cl2 in sol.) x 5.01 (g/kg LD50 of the sol. to male rat) 0.626 g/kg BW (LD50 as available Cl2) = 626 mg/kg BW NaClO as av. Cl2

Dermal route

In the acute dermal toxicity study (key, Griffith, 1978), groups of adult albino rabbits (4/sex) were dermally exposed to sodium hypochlorite (% 12.5) in water at doses of 7.5, 10.4; 14.42 and 20.0 g/kg bw. Animals then were observed for 14 days.

Dermal LD50 > 20 g/kg bw

No mortality in dose levels 7.5, 10.4, and 14.42 g/kg bw. 2 of 8 animals died on day 1 and 2 after application in the high dose group (20 g/kg bw). Sodium hypochlorite is of low toxicity based on males and females.

Major clinical signs observed: Decreased activity, backs badly burned and swollen, nasal discharge, ataxia, urinary incontinence, sores on mouth, bloody nasal discharge, bloody salivation

Major pathological findings observed: Lungs: pale, Liver: dark and mottled, Spleen: dark and granular, Kidneys: pale, Intestines: pale, Bladder: full, Stomach: full, Chest Cavity: contained bloody liquid

An LD0 value > 10.0 g/kg in rabbits was reported for a sodium hypochlorite solution of unspecified concentration. The animals showed no signs of intoxication, however moderate to severe erythema was observed at the site of the application. No adverse effects were found at necropsy at the end of the observation period (Industrial Bio- Test Laboratories Inc., 1970).

Acute dermal toxicity is reported to be > 2.0g/kg body weight for a 5.25% available chlorine solution, corresponding to a value greater than 0.105 g/kg available chlorine (Chlorox unpublished data, in AISE, 1997).

Inhalation route

The LC0 value by inhalation in rat was found to be greater than 10.5 mg/l for 1 hour exposure, using an unspecified commercial solution. The test was carried out at room temperature with a total air flow of 10 litres per minute. No death occurred and there was no sign of inactivity or lacrimation and no significant gross pathological changes reported (Industrial Bio-Test Laboratories Inc., 1970). This study is considered of limited interest since inhalation exposure of sodium hypochlorite is only possible if aerosols are formed.

Other routes

The only information available is a very old study (Taylor et al 1918), where sodium hypochlorite was administrated subcutaneously and intraperitoneally in mice and guinea pigs. The results demonstrated the low toxicity of sodium hypochlorite. However, these routes of administration are not relevant for the direct human exposure and therefore the studies are not considered for the risk assessment.

Justification for classification or non-classification

Because the acute toxicity of corrosive substances is more related to concentration then to dose, extrapolation from data obtained from using a hypochlorite solution to a fictive 100% sodium hypochlorite is not possible. As the highest concentrations of hypochlorite solutions as industrially produced and marketed are about 15%, and solutions marketed for consumer use are typically 5% or less, it can be concluded from the data presented that hypochlorite solutions are of low acute oral toxicity. This is confirmed by the available data from human accidents, where the few deaths that have occurred after hypochlorite ingestion are mostly attributable to aspiration pneumonia.

The information available shows that sodium hypochlorite has a very low dermal acute toxicity.

The study on inhalation acute toxicity available did not show an effect on rat. This confirms that inhalation is not a route of exposure for sodium hypochlorite,

except in case of aerosol formation.

Based on the results obtained in the acute toxicity studies and taking into account the provisions laid down in Council Directive 67/548/EEC and 1272/2008/EC (CLP), sodium hypochlorite does not have to be classified with respect to acute oral, dermal and inhalation toxicity.