Registration Dossier

Administrative data

Workers - Hazard via inhalation route

Systemic effects

Long term exposure
Hazard assessment conclusion:
no hazard identified
Acute/short term exposure
Hazard assessment conclusion:
no hazard identified
DNEL related information

Local effects

Long term exposure
Hazard assessment conclusion:
hazard unknown (no further information necessary)
Acute/short term exposure
Hazard assessment conclusion:
no hazard identified
DNEL related information

Workers - Hazard via dermal route

Systemic effects

Long term exposure
Hazard assessment conclusion:
no hazard identified
Acute/short term exposure
Hazard assessment conclusion:
no hazard identified
DNEL related information

Local effects

Long term exposure
Hazard assessment conclusion:
hazard unknown (no further information necessary)
Acute/short term exposure
Hazard assessment conclusion:
no hazard identified

Workers - Hazard for the eyes

Local effects

Hazard assessment conclusion:
low hazard (no threshold derived)

Additional information - workers

Systemic toxicity:

Lactide is rapidly hydrolysed to lactic acid in water and in-vivo. Lactic acid is a ubiquitous and essential molecule of life. Both L- and D-lactic acid are common food ingredients and lactic acid (irrespective of stereochemistry) is an approved food additive. The hazard conclusion is thus valid for both enantiomers of lactic acid and, by read-across, for L-lactide. Lactate is non-toxic, any (local) effects are due to pH effects only; long-term DNELs are therefore considered not relevant.

In addition, in an oral toxicity (dose range finding) study, lactide (18:1 mixture of L-lactide and m-lactide) was administered to beagle dogs by capsule at dose levels of 10, 100, 400, 1.000 and 2.500 mg/kg bw/day for 2 weeks, and 0, 4, 20 and 100 mg/kg/d for 13 weeks. The primary toxic effect of lactide in dogs was irritation of the alimentary tract. As irritating effects occurred down to a daily dose of 400 mg/kg bw (for 2 wks), the sub-chronic study was run with a maximum dose of 100 mg/kg bw/d.

In the 14 days study, at 1.000 and 2.500 mg/kg/d effects on body weight, and absolute and relative organ weights were reported for thymus and spleen. These effects were considered to be related to the irritation of the alimentary tract. In addition, a mild to moderate renal tubular regeneration was reported in all animals of the 2.500 mg/kg/d dose. Regeneration of the renal tubular epithelium is frequently seen as a reparative or adaptive change following tubular epithelial necrosis, and is suggestive of prior damage to this tissue. Although the mechanism of this effect is unknown, lactide toxicity cannot be excluded. Based on the possible renal toxicity the (systemic) LOAEL is 2.500 mg/kg bw/day. The (systemic) NOAEL for orally administered lactide to dogs under the conditions of this study is 1.000 mg/kg/day.

Local toxicity:

Lactide is known to be unstable in aqueous solution and breaks down quickly to form the acidic compound lactoyl lactic acid (the open-ring lactic acid dimer), and subsequently to lactic acid. Lactate is non-toxic, any (local) effects are due to pH effects only.

Local effects after oral exposure to lactide have been reported in the gastric tract of dogs. In addition, L-lactide is an eye irritant (Eye Irrit 2, CLP), but not irritating to the skin. From available data no hazard can be concluded for local effects in the lung. 

General Population - Hazard via inhalation route

Systemic effects

Long term exposure
Hazard assessment conclusion:
no hazard identified
Acute/short term exposure
Hazard assessment conclusion:
no hazard identified
DNEL related information

Local effects

Long term exposure
Hazard assessment conclusion:
hazard unknown (no further information necessary)
Acute/short term exposure
Hazard assessment conclusion:
hazard unknown (no further information necessary)
DNEL related information

General Population - Hazard via dermal route

Systemic effects

Long term exposure
Hazard assessment conclusion:
no hazard identified
Acute/short term exposure
Hazard assessment conclusion:
no hazard identified
DNEL related information

Local effects

Long term exposure
Hazard assessment conclusion:
hazard unknown (no further information necessary)
Acute/short term exposure
Hazard assessment conclusion:
no hazard identified

General Population - Hazard via oral route

Systemic effects

Long term exposure
Hazard assessment conclusion:
no hazard identified
Acute/short term exposure
Hazard assessment conclusion:
no hazard identified
DNEL related information

General Population - Hazard for the eyes

Local effects

Hazard assessment conclusion:
low hazard (no threshold derived)

Additional information - General Population

Systemic toxicity:

Lactide is rapidly hydrolysed to lactic acid in water and in-vivo. Lactic acid is a ubiquitous and essential molecule of life. Both L- and D-lactic acid are common food ingredients and lactic acid (irrespective of stereochemistry) is an approved food additive. The hazard conclusion is thus valid for both enantiomers of lactic acid and, by read-across, for L-lactide.

Lactate is non-toxic, any (local) effects are due to pH effects only; long-term DNELs are therefore considered not relevant.

In addition, in an oral toxicity (dose range finding) study, lactide (18:1 mixture of L-lactide and m-lactide) was administered to beagle dogs by capsule at dose levels of 10, 100, 400, 1,000 and 2,500 mg/kg bw/day for 2 weeks, and 0, 4, 20 and 100 mg/kg/d for 13 weeks. The primary toxic effect of lactide in dogs was irritation of the alimentary tract. As irritating effects occurred down to a daily dose of 400 mg/kg bw (for 2 wks), the sub-chronic study was run with a maximum dose of 100 mg/kg bw/d. In the 14 days study, at 1,000 and 2,500 mg/kg/d effects on body weight, and absolute and relative organ weights were reported for thymus and spleen. These effects were considered to be related to the irritation of the alimentary tract. In addition, a mild to moderate renal tubular regeneration was reported in all animals of the 2.500 mg/kg/d dose. Regeneration of the renal tubular epithelium is frequently seen as a reparative or adaptive change following tubular epithelial necrosis, and is suggestive of prior damage to this tissue. Although the mechanism of this effect is unknown, lactide toxicity cannot be excluded. Based on the possible renal toxicity the (systemic) LOAEL is 2,500 mg/kg bw/day. The (systemic) NOAEL for orally administered lactide to dogs under the conditions of this study is 1,000 mg/kg/day.

Local toxicity:

Lactide is known to be unstable in aqueous solution and breaks down quickly to form the acidic compound lactoyl lactic acid (the open-ring lactic acid dimer), and subsequently to lactic acid. Lactate is non-toxic, any (local) effects are due to pH effects only.

Local effects after oral exposure to lactide have been reported in the gastric tract of dogs. In addition, L-lactide is an eye irritant (Eye Irrit 2, CLP), but not irritating to the skin. From available data no hazard can be concluded for local effects in the lung.