Bacillus Coagulans Toxicity

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 qualifications

IDENTIFICATION 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 formulas; acidulant in beverages; also 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 yeast; dehairing, 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 acid; therefore, 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 tube; the 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 died; dyspnea, 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 gestation; a 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)

The substance can be absorbed into the body by inhalation of its aerosol and by ingestion

Chronically high levels of Lactic acid are associated with at least a dozen inborn errors of metabolism including: 2-Methyl-3-hydroxybutyryl CoA dehydrogenase deficiency, Biotinidase deficiency, Fructose-1,6-diphosphatase deficiency, Glycogen Storage Disease Type 1A (GSD1A) or Von Gierke Disease, Glycogenosis, Type IB, Glycogenosis, Type IC, Glycogenosis, Type VI. Hers disease, Lactic Acidemia, Leigh Syndrome, Methylmalonate Semialdehyde Dehydrogenase Deficiency, Pyruvate Decarboxylase E1 Component Deficiency, Pyruvate dehydrogenase complex deficiency, Pyruvate dehydrogenase deficiency, Short Chain Acyl CoA Dehydrogenase Deficiency (SCAD Deficiency)

Burning sensation. Cough. Sore throat. Shortness of breath

Redness. Pain

Redness. Pain. Severe deep burns

Sore throat. Burning sensation. Abdominal pain. Abdominal cramps. Nausea. Vomiting

Dermatotoxin - Skin burns

Not listed by IARC

No indication can be given about the rate at which a harmful concentration of this substance in the air is reached on evaporation at 20 °C

The substance is corrosive to the eyes. The substance is irritating to the skin and respiratory tract. Corrosive on ingestion

Lactic acid (2-hydroxypropanoic acid) is exempted from the requirement of a tolerance when used as a plant growth regulator in or on all raw agricultural commodities

Residues of lactic acid are exempted from the requirement of a tolerance when used in accordance with good agricultural practice as inert (or occasionally active) ingredients in pesticide formulations applied to growing crops or to raw agricultural commodities after harvest. Use: solvent

Residues of lactic acid are exempted from the requirement of a tolerance when used in accordance with good agricultural practice as inert (or occasionally active) ingredients in pesticide formulations applied to animals. Use: solvent

Residues of the following chemical substances are exempted from the requirement of a tolerance when used in accordance with good manufacturing practice as ingredients in an antimicrobial pesticide formulation, provided that the substance is applied on a semi-permanent or permanent food-contact surface (other than being applied on food packaging) with adequate draining before contact with food. ... (b) The following chemical substances when used as ingredients in an antimicrobial pesticide formulation may be applied to: Dairy processing equipment, and food-processing equipment and utensils. Lactic acid is included on this list. Limit: When ready for use, the end-use concentration is not to exceed 138 ppm

Residues of the following chemical substances are exempted from the requirement of a tolerance when used in accordance with good manufacturing practice as ingredients in an antimicrobial pesticide formulation, provided that the substance is applied on a semi-permanent or permanent food-contact surface (other than being applied on food packaging) with adequate draining before contact with food. ... (c) The following chemical substances when used as ingredients in an antimicrobial pesticide formulation may be applied to: Food-processing equipment and utensils. Lactic acid is included on this list

Rubber gloves; goggles; self-contained breathing apparatus where high concentrations of mist are present

Eye/face protection: Tightly fitting safety goggles. Faceshield (8-inch minimum). Use equipment for eye protection tested and approved under appropriate government standards such as (US) or EN 166(EU)

Skin protection: Handle with gloves

Body Protection: Complete suit protecting against chemicals. The type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace

Respiratory protection: Where risk assessment shows air-purifying respirators are appropriate use a full-face respirator with multipurpose combination (US) or type ABEK (EN 14387) respirator cartridges as a backup to engineering controls. If the respirator is the sole means of protection, use a full-face supplied air respirator. Use respirators and components tested and approved under appropriate government standards such as (US) or CEN (EU)

Persons working with pure acid or concentrated solutions should wear protective clothing, eye and face protection, hand and arm protection and respiratory protective equipment

NO open flames

STRICT HYGIENE!

Use local exhaust or breathing protection

Protective gloves

Wear safety goggles or face shield

Do not eat, drink, or smoke during work

Excerpt from ERG Guide 153 [Substances - Toxic and/or Corrosive (Combustible)]:

ELIMINATE all ignition sources (no smoking, flares, sparks or flames) from immediate area. Do not touch damaged containers or spilled material unless wearing appropriate protective clothing. Stop leak if you can do it without risk. Prevent entry into waterways, sewers, basements or confined areas. Absorb or cover with dry earth, sand or other non-combustible material and transfer to containers. DO NOT GET WATER INSIDE CONTAINERS. (ERG, 2024)

Separated from strong bases

Keep container tightly closed in a dry and well-ventilated place. Containers which are opened must be carefully resealed and kept upright to prevent leakage. Hygroscopic

Separated from strong bases

When heated to decomposition it emits acrid smoke and irritating fumes

Fresh air, rest. Refer for medical attention

Remove contaminated clothes. Rinse skin with plenty of water or shower

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention

Rinse mouth. Do NOT induce vomiting. Give nothing to drink. Refer for medical attention

INHALATION: move to fresh air

INGESTION: give large amount of water

EYES: flush with water for at least 15 min

SKIN: flush with water; wash well with soap and water

Excerpt from ERG Guide 153 [Substances - Toxic and/or Corrosive (Combustible)]:

SMALL FIRE: Dry chemical, CO2 or water spray

LARGE FIRE: Dry chemical, CO2, alcohol-resistant foam or water spray. If it can be done safely, move undamaged containers away from the area around the fire. Dike runoff from fire control for later disposal

FIRE INVOLVING TANKS, RAIL TANK CARS OR HIGHWAY TANKS: Fight fire from maximum distance or use unmanned master stream devices or monitor nozzles. Do not get water inside containers. Cool containers with flooding quantities of water until well after fire is out. Withdraw immediately in case of rising sound from venting safety devices or discoloration of tank. ALWAYS stay away from tanks in direct contact with flames. (ERG, 2024)

Use water spray, powder, alcohol-resistant foam, carbon dioxide

Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide

Advice for firefighters: Wear self-contained breathing apparatus for firefighting if necessary

Excerpt from ERG Guide 153 [Substances - Toxic and/or Corrosive (Combustible)]:

IMMEDIATE PRECAUTIONARY MEASURE: Isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids

SPILL: Increase the immediate precautionary measure distance, in the downwind direction, as necessary

FIRE: If tank, rail tank car or highway tank is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions. (ERG, 2024)

Collect leaking and spilled liquid in sealable containers as far as possible. Cautiously neutralize spilled liquid with weak alkaline solution such as disodium carbonate. Then wash away with plenty of water

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas; Environmental precautions: Do not let product enter drains; Methods and materials for containment and cleaning up: Soak up with inert absorbent material and dispose of as hazardous waste. Keep in suitable, closed containers for disposal

Collect leaking liquid in sealable containers. Cautiously neutralize spilled liquid with weak alkaline solution, e.g. disodium carbonate. Then wash away with plenty of water

SRP: Expired or waste pharmaceuticals shall carefully take into consideration applicable DEA, EPA, and FDA regulations. It is not appropriate to dispose by flushing the pharmaceutical down the toilet or discarding to trash. If possible return the pharmaceutical to the manufacturer for proper disposal being careful to properly label and securely package the material. Alternatively, the waste pharmaceutical shall be labeled, securely packaged and transported by a state licensed medical waste contractor to dispose by burial in a licensed hazardous or toxic waste landfill or incinerator

Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material; Contaminated packaging: Dispose of as unused product

The following wastewater treatment technology has been investigated for lactic acid: Concentration process: Biological treatment

/HUMAN EXPOSURE STUDIES/ When 0.35% DL-lactic acid was administered to healthy babies from the tenth to the twentieth day of life, a threefold increase in the urinary excretion of the physiological L(+)-lactic acid and a twelvefold increase in the D(-)-lactic acid was observed. On withdrawing lactic acid from the diet the level of lactic acid excreted in the urine returned to normal. Since the racemic mixture used consisted of 80% of the L(+) and 20% of the D(-) forms it seems that the metabolism of the D(-) form by the young full-term baby is more difficult than the L(+) form. The increase in the urinary excretion of either form of lactic acid indicated that the young infant cannot utilize lactic acid at a rate which can keep up with 0.35% in the diet. A number of babies could not tolerate lactic acid. In such cases there was rapid loss of weight, frequent diarrhoea, reduction of plasma bicarbonate and increased excretion of organic acids in the urine. All these effects were reversed on withdrawing lactic acid from the diet

/HUMAN EXPOSURE STUDIES/ A skin test was performed using 49 a topic and 56 nonatopic patients to determine whether application of 2.5% lactic acid in water produces an urticarial reaction. Finn chambers containing 20 uL of test solution were fixed on the skin using porous tape for 20 min. Lactic acid produced no immediate reactions

/HUMAN EXPOSURE STUDIES/ The ability of lactic acid to induce hyperkeratosis was evaluated. Lactic acid, 3 and 8%, pH 3, was applied to the outer aspect of the calf to induce scaling. When visible scaling and irritation occurred, the skin desquamation profile was altered. Control values were 5.7% for cell renewal and 1 for irritation, clinical scaling, desquamation amount, and desquame size. After 3 weeks of application of 3% lactic acid, the values increased to 27.8% for cell renewal, 1.9 for irritation, 1.5 for scaling and the desquamation amount, and 1.6 for desquame size. With 8% lactic acid, these values increased to 44.2% for cell renewal, 4.2 for irritation, 3.5 for scaling, 1.8 for desquamation amount, and 3.8 for desquame size

/SIGNS AND SYMPTOMS/ In general, on the basis of animal studies and human use, the most significant effects caused by exposure to lactate esters are respiratory, dermal, and ocular irritation. Irritation may be associated with the formation of lactic acid, a product of hydrolysis of lactate esters. /Hydroxyal esters: lactates/

/LABORATORY ANIMALS: Acute Exposure/ Groups of male Fischer 344 rats, five per group, were dosed with 0.5 mL of 130, 650, or 1300 mg/2000 kg body wt lactic acid via stomach tube; the 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 concentrations of lactic acid in the blood were 0.43 and 0.47 mg/mL for rats of the control and 1300-mg groups, respectively, one day after dosing. The rats were dosed with the same amounts of lactic acid after 8 days. Two rats of the 1300 mg readministration group died; dyspnea, snivel, vomiting, and abdominal inflation were observed in these animals immediately after dosing

/LABORATORY ANIMALS: Acute Exposure/ A 5% aqueous solution of Lactic Acid, 0.2 mL, was "very slightly irritant" after repeated application to shaved rat skin (number of animals not stated). One-half milliliter of 5 and 10% aq. Lactic Acid was applied for 4 hr to the clipped dorsum of rabbits (number and sex not stated) using occlusive patches; the treatment sites had been prehydrated for 60 min immediately prior to dosing. The 5% solution was "virtually nonirritant," and the 10% solution was "only slightly irritant, causing similar effects to those of marketed skin care creams."

/LABORATORY ANIMALS: Acute Exposure/ A maximization study was performed using guinea pigs (number of animals not stated) in which induction consisted of intradermal injection of 0.2% and topical application of 50% Lactic Acid; challenge consisted of intradermal injection of 0.2% and application of 10%. Lactic Acid was not a sensitizer

/LABORATORY ANIMALS: Acute Exposure/ Five phototoxicity assays were performed on a face cream containing 0.25% of 85% aq. lactic acid using six New Zealand White rabbits per test. The undiluted test materials and the positive control, 8-methoxypsoralen (1/128% in ethanol), were applied to the shaved left side of the back and allowed to penetrate for 30 min; one application/animal was made in all tests except one (test 3) in which two applications/animal were made. The backs of the animals were irradiated with a UV light source (FL40-BL, >320 nm) placed 8 inches above the midline. In tests 1 and 4, there was one 1-hr irradiation period; in test 2, there was one 1-hr and one 2-hr irradiation period; and in tests 3 and 5, there was one 2-hr irradiation period. Following irradiation, the test materials were applied to the shaved right side of the back in the same manner. Test sites were scored using the Draize scale for erythema and edema at 24, 48, 72, and 96 hr after application. Upon examination of all results, it was concluded that the face cream containing 0.25% of 85% aq. lactic acid was a "weak phototoxin."

Excerpt from ERG Guide 153 [Substances - Toxic and/or Corrosive (Combustible)]:

Combustible material: may burn but does not ignite readily. When heated, vapors may form explosive mixtures with air: indoors, outdoors and sewers explosion hazards. Those substances designated with a (P) may polymerize explosively when heated or involved in a fire. Corrosives in contact with metals may evolve flammable hydrogen gas. Containers may explode when heated. Runoff may pollute waterways. Substance may be transported in a molten form. (ERG, 2024)

Combustible

The substance is a medium strong acid

Soluble in water

Acids, Carboxylic

Alcohols and Polyols

LACTIC ACID is a carboxylic acid. Carboxylic acids donate hydrogen ions if a base is present to accept them. They react in this way with all bases, both organic (for example, the amines) and inorganic. Their reactions with bases, called "neutralizations", are accompanied by the evolution of substantial amounts of heat. Neutralization between an acid and a base produces water plus a salt. Carboxylic acids with six or fewer carbon atoms are freely or moderately soluble in water; those with more than six carbons are slightly soluble in water. Soluble carboxylic acid dissociate to an extent in water to yield hydrogen ions. The pH of solutions of carboxylic acids is therefore less than 7.0. Many insoluble carboxylic acids react rapidly with aqueous solutions containing a chemical base and dissolve as the neutralization generates a soluble salt. Carboxylic acids in aqueous solution and liquid or molten carboxylic acids can react with active metals to form gaseous hydrogen and a metal salt. Such reactions occur in principle for solid carboxylic acids as well, but are slow if the solid acid remains dry. Even "insoluble" carboxylic acids may absorb enough water from the air and dissolve sufficiently in it to corrode or dissolve iron, steel, and aluminum parts and containers. Carboxylic acids, like other acids, react with cyanide salts to generate gaseous hydrogen cyanide. The reaction is slower for dry, solid carboxylic acids. Insoluble carboxylic acids react with solutions of cyanides to cause the release of gaseous hydrogen cyanide. Flammable and/or toxic gases and heat are generated by the reaction of carboxylic acids with diazo compounds, dithiocarbamates, isocyanates, mercaptans, nitrides, and sulfides. Carboxylic acids, especially in aqueous solution, also react with sulfites, nitrites, thiosulfates (to give H2S and SO3), dithionites (SO2), to generate flammable and/or toxic gases and heat. Their reaction with carbonates and bicarbonates generates a harmless gas (carbon dioxide) but still heat. Like other organic compounds, carboxylic acids can be oxidized by strong oxidizing agents and reduced by strong reducing agents. These reactions generate heat. A wide variety of products is possible. Like other acids, carboxylic acids may initiate polymerization reactions; like other acids, they often catalyze (increase the rate of) chemical reactions. Slowly corrodes most metals

Incompatible materials: Bases, Oxidizing agents, Reducing agents

Mixtures with nitric acid + hydrofluoric acid may react vigorously and are storage hazards

Volatile with superheated steam

A mixture of 5 parts lactic acid, 5 parts nitric acid, 2 parts water, and 1 part hydrofluoric acid being stored in a plastic bottle ruptured with explosive force

Mixtures of /lactic acid, hydrofluoric acid and nitric acid/, used as metal polishing solutions, are unstable and should not be stored. Lactic acid and nitric acid react autocatalytically after a quiescent period, attaining a temperature of about 90 °C with vigorous gas evolution after about 12 hr. Prepare freshly, discard after use and handle carefully. /Nitric acid/

Special hazards arising from the substance or mixture: Carbon oxides

Immediate First Aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand-valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention

Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist respirations if necessary. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport. ... Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool. Activated charcoal is not effective ... . Do not attempt to neutralize, because of exothermic reaction. Cover skin burns with dry, sterile dressings after decontamination ... . /Organic acids and related compounds/

Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Early intubation, at the first sign of upper airway obstruction, may be necessary. Positive-pressure ventilation techniques with a bag-valve-mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W TKO /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's (LR) if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Consider vasopressors if patient is hypotensive with a normal fluid volume. Watch for signs of fluid overload... . Use proparacaine hydrochloride to assist eye irrigation ... . /Organic acids and related compounds/

Lactic acidosis occurs in a number of clinical conditions, e.g. in surgeries, orthotopic liver transplant, and anesthetic agent administration, which has deleterious effects on the patient's survival. The most rational therapy for these patients, the sodium bicarbonate administration, cannot prevent those accompanying deficiencies and may actually be harmful. In addition, tromethamine adjusts the blood pH, it does not affect the lactate accumulation. Therefore, discovery of a therapeutic agent is still a major unsolved problem. In this study, the rats were divided into different groups and lactic acidosis type B was induced in them. Then, the effect of different injection doses of spermidine (0-20 nmol) on lactic acidosis was analyzed by measuring the lactate level and pH in the rat blood samples. The results showed that spermidine effectively and simultaneously inhibited the lactate and pyruvate accumulations, and also adjusted the pH of bloodstream. On the other hand, it has been shown that spermidine increases the activity of phosphatase, leading to prevention of lactate accumulation. The results indicate that administration of only nanomole level of spermidine may be the best treatment in the liver transplant and other patients suffering from lactic acidosis type B

The effects of local myocardial administration of lactic acid and low-dose edaravone were investigated to determine if this combination provides benefits similar to mechanical postconditioning. We randomly divided 108 rats into 6 groups: sham, reperfusion injury, postconditioning (Post), lacticacid (Lac), low-dose edaravone (Eda), and lactic acid + low-dose edaravone (Lac+Eda). The left coronary arteries of the rats were occluded for 45 minutes, before the administration of the treatments. The rats were euthanized at different time points to examine the infarct size and serum markers of myocardial injury and apoptosis and measure the expression of signal pathway markers. We found that the infarct areas caused by ischemic-reperfusion injury were reduced largely by postconditioning and Lac+Eda injection; a similar trend was observed for serum markers of myocardial injury, apoptosis, and hemodynamic parameters. Compared with the Post group, the Lac+Eda group had similar blood pH values, levels of reactive oxygen species, mitochondrial absorbance, and levels of signal pathway marker. The Lac and Eda groups partly mimicked the protective role. These data suggest that local myocardial administration of lactic acid and low dose of edaravone initiates protective signal pathways of mechanical postconditioning and replicates the myocardial protection

Excretion of carbon dioxide and L-lactic acid through exhalation and perspiration provides olfactory signals to mosquitoes which allow them to find and bite humans; however, mosquito species differ in this regard. This study investigated upwind responses of Anopheles stephensi, mysorensis form, an important malaria vector in Asia, to carbon dioxide and L-lactic acid under laboratory conditions. While a minimal dose of carbon dioxide (90 ppm) activated the mosquitoes, 10 times this amount suppressed them. L-lactic acid alone did not produce a significant effect by itself, but addition of 6 ug/min of L-lactic acid to a range of 90 to 410 ppm carbon dioxide resulted in attraction. The results provide further support for the hypothesis that CO2 plays an important role in the host-seeking behavior of zoophilic mosquitoes, and suggests that L-lactic acid might play a more critical role than CO2 in the attraction of An. stephensi

During the pulmonary edema stage ... metabolic acidosis may occur because of increased lactic acid production in response to hypoxemia. /NO2-induced acute lung injury/

Burning and/or stinging is one of the most common concerns expressed by patients using topical therapies for treatment of dermatologic disorders. Topical lactic acid preparations often are used to treat dry scaly skin. In this study, we compared the level of burning/stinging reported by participants with application of lactic acid cream 10% containing strontium versus ammonium lactate lotion 12% and cetearyl alcohol lotion. The mean rating of burning/stinging reported for lactic acid cream 10% with strontium and cetearyl alcohol lotion was lower than ammonium lactate lotion 12% (P<.0001). Based on the study results, lactic acid cream 10% with strontium causes less burning/stinging than ammonium lactate lotion 12%

EPA has released the Interactive Chemical Safety for Sustainability (iCSS) Dashboard. The iCSS Dashboard provides an interactive tool to explore rapid, automated (or in vitro high-throughput) chemical screening data generated by the Toxicity Forecaster (ToxCast) project and the federal Toxicity Testing in the 21st century (Tox21) collaboration. /The title compound was tested by ToxCast and/or Tox21 assays/

Corrosive