| 毒性の概要 | Based on the available information included in this report, the CIR Expert Panel concludes that Glycolic and Lactic Acid, their common salts and their simple esters, are safe for use in cosmetic products at concentrations less than or equal to 10%, at final formulation pH greater than or equal to 3.5, when formulated to avoid increasing sun sensitivity or when directions for use include the daily use of sun protection. These ingredients are safe for use in salon products at concentrations less than or equal to 30%, at final formulation pH greater than or equal to 3.0, in products designed for brief, discontinuous use followed by thorough rinsing from the skin, when applied by trained professionals, and when application is accompanied by directions for the daily use of sun protection...Lactic Acid...Safe for use in cosmetics, with qualificationsIDENTIFICATION AND USE: Lactic acid forms yellow to colorless crystals or syrupy 50% liquid. It has multiple uses in dyeing baths, as mordant in printing woolen goods, solvent for water-insoluble dyes. It is also used for reducing chromates in mordanting wool, in manufacture of cheese, confectionery. Lactic acid is a component of babies' milk formulasacidulant in beveragesalso used for acidulating worts in brewing. It is used in prepn of sodium lactate injections, and as ingredient of cosmetics, component of spermatocidal jellies. Other uses: for removing Clostridium butyricum in manufacture of yeastdehairing, plumping, and decalcifying hides, solvent for cellulose formate, flux for soft solder. Lactic acid is used to manufacture lactates which are used in food products, in medicine, and as solvents. It is also a plasticizer, catalyst in the casting of phenolaldehyde resins. HUMAN EXPOSURE AND TOXICITY: Its effect on eye is similar to that of other acid of moderate strength, causing initial epithelial coagulation on cornea and conjunctiva, but having good prognosis if promptly washed off with water. In man, accidental intraduodenal administration of 100 mL 33% lactic acid was fatal within 12 hours. Hyperlactatemia and lactic acidosis are among the most dangerous and life-threatening side effect that occurs during therapy with some nucleoside reverse transcriptase inhibitors. Lactic acidosis is associated with both inherited and acquired metabolic diseases. Lactic acid metabolism in the presence of altered gluconeogenesis, anaerobic glycolysis, and acid-base balance is a major factor in many disorders. Lactic acid can be formed only from pyruvic acidtherefore, disorders that increase pyruvate concentration, enhance lactic acid formation, or reduce lactic acid degradation cause lactic acidosis. Inborn metabolic errors that are accompanied by derangement of metabolic pathways of glucose, pyruvate, amino acids, and organic acids as well as toxic and systemic conditions that promote tissue hypoxia or mitochondrial injury result in lactic acidosis. ANIMAL STUDIES: Applied to rabbit eyes in a standard manner, the reaction at twenty-four hours has been graded 8 on scale of 1 to 10. If allowed to remain on rabbit eyes, both the full strength acid and a 50% solution in water have caused corneal necrosis and persistent stromal scarring. Groups of male rats, five per group, were dosed with 0.5 mL of 130, 650, or 1300 mg/2000 kg body wt lactic acid via stomach tubethe control group received the same volume of water. Two rats of the 650-mg group and one rat of the 1300-mg group died within 24 hr of dosing. The rats were dosed with the same amounts of lactic acid after 8 days. Two rats of the 1300 mg group dieddyspnea, snivel, vomiting, and abdominal inflation were observed in these animals immediately after dosing. No overt toxic effects were observed in pigs given approximately 3.6-18 g/kg lactic acid in feed or water for up to 5 months. Drunken lamb syndrome has been described as lamb D-lactic acidosis syndrome. In developmental study, twelve mice were dosed daily with 570 mg/kg lactic acid by gavage on days 6 to 15 of gestationa control group of 13 mice received distilled water. All dams were killed on day 18 of gestation. No significant difference was observed in gestational body weight gain between test and control animals, but feed consumption was significantly decreased as compared to control values. Also, relative maternal liver weight was significantly decreased as compared to controls. The only observed effect on the fetus was a statistically significant increase in delayed ossification of the parietal bones. Female rabbits were dosed orally with 0.1 - 0.2 g/kg lactic acid in 100 -150 mL water twice daily for 5 months, and five female rabbits were dosed orally with 0.1 - 0.7 g/kg lactic acid in 50 - 100 mL water twice daily for 16 months (13 months actual treatment). No tumors were reported after 5 or 16 months, respectively. Negative results were obtained when the mutagenic potential of lactic acid, 90.5% pure, in phosphate buffer was assayed in an Ames test using S. typhimurium strains TA92, TA1535, TA100, TA1537, TA94, and TA98 with metabolic activation. Negative results were obtained in an Ames test for 1000 ug/mL 11 mM lactic acid using a clonal subline of Chinese hamster fibroblasts derived from lung tissue in the absence of metabolic activation. Lactic acid was negative for chromosomal aberrations. ECOTOXICITY STUDIES: Feeding of 10% lactic acid to birds has been blamed for the development of polyneuritic crises resembling B1 deficiency on diets rich in carbohydrates, proteins or fats.Accumulation of L-lactic acid in the body has been shown to be toxic. At times of lactic acidosis, when excess intracellular lactate is released into the blood, maintenance of electroneutrality of the blood requires that a cation be released into the blood, as well. This can reduce blood pH. Lactate may exert a strong action over GABAergic networks in the developing brain, making them more inhibitory than it was previously assumed, acting either through better support of metabolites, or alterations in base intracellular pH levels, or both. (Wikipedia) |
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