ニコチン酸

Fires involving this material can be controlled with a dry chemical, carbon dioxide or Halon extinguisher. A water spray may also be used. (NTP, 1992)

Use water spray, foam, powder, carbon dioxide.

Fresh air, rest.

Rinse skin with plenty of water or shower.

Rinse with plenty of water (remove contact lenses if easily possible).

Rinse mouth. Give one or two glasses of water to drink.

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.

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.

Keep container tightly closed in a dry and well-ventilated place. Light sensitive.

Niacin should be stored in well-closed, light-resistant containers at 20-25 °C. When stored under these conditions, Niaspan extended-release and Niacor immediate-release tablets are stable for 3 and 2 years, respectively, after the date of manufacture. The fixed-combination preparation containing extended-release niacin and lovastatin (Advicor) should be stored at room temperature (20-25 °C).

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Avoid breathing dust. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided. Methods and materials for containment and cleaning up: Pick up and arrange disposal without creating dust. Sweep up and shovel. Keep in suitable, closed containers for disposal.

SMALL SPILLS AND LEAKAGE: If you spill this chemical, you should dampen the solid spill material with water, then transfer the dampened material to a suitable container. Use absorbent paper dampened with water to pick up any remaining material. Seal your contaminated clothing and the absorbent paper in a vapor-tight plastic bag for eventual disposal. Wash all contaminated surfaces with a soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned.

SRP: Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in air, soil or water; effects on animal, aquatic and plant life; and conformance with environmental and public health regulations. If it is possible or reasonable use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination.

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.

Personal protection: particulate filter respirator adapted to the airborne concentration of the substance. Do NOT let this chemical enter the environment. Sweep spilled substance into covered containers. If appropriate, moisten first to prevent dusting. Carefully collect remainder. Then store and dispose of according to local regulations.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Avoid breathing dust. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided.

Precautions for safe handling: Avoid contact with skin and eyes. Avoid formation of dust and aerosols. Further processing of solid materials may result in the formation of combustible dusts. The potential for combustible dust formation should be taken into consideration before additional processing occurs. Provide appropriate exhaust ventilation at places where dust is formed.

Appropriate engineering controls: Handle in accordance with good industrial hygiene and safety practice. Wash hands before breaks and at the end of workday.

Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands.

SRP: Local exhaust ventilation should be applied wherever there is an incidence of point source emissions or dispersion of regulated contaminants in the work area. Ventilation control of the contaminant as close to its point of generation is both the most economical and safest method to minimize personnel exposure to airborne contaminants. Ensure that the local ventilation moves the contaminant away from the worker.

Nicotinic acid is widely distributed in nature and is the precursor to coenzymes NAD (nicotinamide adenine dinucleotide) and NADP (nicotinamide adenine dinucleotide phosphate)(1). An antipellagra vitamin, it is essential to many animals for growth and health. In humans, niacin is believed necessary, along with other vitamins, for the prevention and cure of pellagra. It functions in protein and carbohydrate metabolism. As a component of two important enzymes, coenzymes I and II, it functions in glycolysis and tissue respiration(2). Nicotinic acid has been reported in humans at 1.47 mg/L(3).

Chronic kidney disease (CKD) in patients is strongly associated with cardiovascular morbidity and mortality, and prevalent abnormal lipid metabolism. The AIM-HIGH trial examined the benefits of adding extended-release niacin (ERN) to simvastatin in patients with established coronary heart disease. Here we conducted a post hoc analysis of the AIM-HIGH trial examining whether participants derived cardiovascular or renal benefits when stratified by renal function. Of 3414 participants, 505 had stage 3 CKD at baseline. Among the CKD subset, demographics and cardiovascular disease (CVD) risk factors were well balanced in the ERN and placebo arms. Compared with placebo, CKD participants receiving ERN had a significant decrease in triglycerides by a median of 59.0 mg/dL, and high-density lipoprotein cholesterol significantly increased by a mean of 11.3 mg/dL over a mean follow-up of 3 years. CVD events were similar between CKD participants in both arms. However, all-cause mortality was significantly higher in the ERN group (hazard ratio of 1.73). Mean change in eGFR among ERN-treated CKD participants was not significantly different between study arms. Thus, among AIM-HIGH participants with CKD, the addition of ERN to simvastatin for secondary prevention of CVD improved triglyceride and high-density lipoprotein-cholesterol concentrations but did not improve cardiovascular outcomes or kidney function, and was associated with higher all-cause mortality.

The risk of developing myopathy and rhabdomyolysis is increased in patients receiving niacin (particularly at antilipemic dosages [exceeding 1 g daily]) concomitantly with statins. ... Myopathy or rhabdomyolysis has occurred in some patients receiving certain statins concomitantly with antilipemic dosages of niacin. However, some manufacturers state that no cases of rhabdomyolysis were reported in 124 patients receiving extended-release niacin (Niaspan) concomitantly with various statins; rhabdomyolysis also was not reported in 1079 patients receiving extended-release niacin in fixed combination with lovastatin (Advicor) for up to 2 years. Other severe adverse effects, including disturbances in glycemic control requiring hospitalization, development of diabetes mellitus, adverse GI effects, myopathy, gout, rash, skin ulceration, infection, and bleeding, have been reported in patients with established cardiovascular disease following concomitant use of extended-release niacin with statin-based therapy. ... Therefore, the potential benefits (e.g., further alterations in lipid concentrations) of concomitant use of antilipemic dosages of niacin with statins should be weighed carefully against the possible risks of severe adverse effects, and caution is advised if such concomitant therapy is employed. The manufacturer of atorvastatin states that lower initial and maintenance dosages of this statin should be considered during concomitant therapy with antilipemic dosages of niacin, and patients should be carefully monitored for manifestations of muscle pain, tenderness, or weakness, particularly during the initial months of therapy and following an increase in dosage of either drug. The manufacturers of fluvastatin, pitavastatin, and pravastatin state that dosage reduction of these statins should be considered when used concomitantly with antilipemic dosages of niacin.

Concomitant use of aspirin may decrease the metabolic clearance of niacin; the clinical relevance of this interaction has not been fully elucidated.

Niacin reportedly potentiates the hypotensive effects of ganglionic blocking and vasoactive drugs, resulting in postural hypotension.

For more Interactions (Complete) data for Nicotinic acid (25 total), please visit the HSDB record page.

Niacin at extremely high doses can have life-threatening acute toxic reactions. Extremely high doses of niacin can also cause niacin maculopathy, a thickening of the macula and retina which leads to blurred vision and blindness. This maculopathy is reversible after stopping niacin intake. Side effects of hyperglycemia, cardiac arrhythmias and birth defects have also been reported. (A729)

Niacin in doses above 500 mg daily causes transient, asymptomatic elevations in serum aminotransferase levels in up to 20% of people. The elevations are rarely greater than 3 times the upper limit of the normal range and usually resolve spontaneously even with continuation of the drug. The effect is partially dose related and is more common with doses above 3 g/day. In some patients, there is an overall decrease in serum proteins synthesized by the liver and, in some instances, coagulopathy with an increase in prothrombin time and decline in serum albumin, coagulation factors and apolipoproteins. These changes resolve rapidly upon stopping therapy and may not recur with lower doses.

LD50; Species: Coturnix coturnix (Quail) oral > 1000 mg/kg

EC50; Species: Daphnia magna (Water flea); Concentration: 77 mg/L for 48 hr; Effect: immobilization /Conditions of bioassay not specified in source examined/

EC50; Species: Scenedesmus subspicatus (Green algae); Concentration: 89.93 mg/L for 72 hr; Effect: Growth inhibition /Conditions of bioassay not specified in source examined/

LC50; Species: Salmo trutta (Brown trout); Conditions: static; Concentration: 520 mg/L for 96 hr /Technical material, 99.8%/

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 8(SRC), determined from a structure estimation method(2), indicates that nicotinic acid is expected to have very high mobility in soil(SRC). The pKa of nicotinic acid is 4.75(3), indicating that this compound will exist almost entirely in the anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4). Nicotinic acid is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 9.4X10-5 mm Hg at 25 °C(SRC), determined from a fragment constant method(2). In aqueous, aerobic soil suspensions, nicotinic acid was completely degraded after 2 to 4 days of incubation(5), suggesting that biodegradation may be an important environmental fate process in soil(SRC).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 8(SRC), determined from a structure estimation method(2), indicates that nicotinic acid is not expected to adsorb to suspended solids and sediment(SRC). A pKa of 4.75(3) indicates nicotinic acid will exist almost entirely in the anion form at pH values of 5 to 9 and, therefore, volatilization from water surfaces is not expected to be an important fate process(SRC). According to a classification scheme(4), an estimated BCF of 3(SRC), from its log Kow of 0.36(5) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is low(SRC). In aqueous, aerobic soil suspensions, nicotinic acid was completely degraded after 2 to 4 days of incubation(6), suggesting that biodegradation may be an important environmental fate process in water(SRC).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), nicotinic acid, which has an estimated vapor pressure of 9.4X10-5 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase nicotinic acid is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 22 days(SRC), calculated from its rate constant of 1.72X10-13 cu cm/molecule-sec at 25 °C(3). Particulate-phase nicotinic acid may be removed from the air by wet and dry deposition(SRC). Nicotinic acid absorbs UV light at wavelength 263 nm(4) and, therefore, is not expected to be susceptible to direct photolysis since sunlight consists of wavelengths above 290 nm(SRC).

Substantial amounts of nicotinic acid are found in fish, yeast and ceral grains(1). The compound is especially concentrated in brewer's yeast, wheat germ and liver(2). The average cup of coffee contains between 1-2 mg nicotinic acid, depending on roasting conditions(2). The nicotinic acid content of several nuts has been reported (in mg/kg) as follows: chestnut, 200; hazel nut, 600; almond, 1600; and sunflower seed, 5000(3).

Nicotinic Acid and Nicotinamide (Vitamin B3) Foodstuff Content(1). [Table#4461]

Nicotinic Acid and Nicotinamide (Vitamin B3) in Coffee(1). [Table#4462]

Occupational hepatotoxin - Secondary hepatotoxins: the potential for toxic effect in the occupational setting is based on cases of poisoning by human ingestion or animal experimentation.

Hepatotoxicity: The most severe adverse effect is niacin hepatotoxicity. Mild elevation of hepatic transaminase levels, up to double the upper limit of the normal range, is common.

Safe in the present practices of use and concentration. Ingredient, concentration, and use information are available in documents discoverable at https://cir-reports.cir-safety.org

IDENTIFICATION AND USE: Nicotinic acid (Niacin) is a solid. It is a part of the vitamin B complex. Niacin and niacinamide (also known as nicotinamide) are similarly effective as a vitamin because they can be converted into each other within the organism. The blanket term vitamin B(3) is used for both. Niacinamide is a component of important coenzymes involved in hydrogen transfer. Niacin is used in medicine as a cholesterol-lowering agent, nutrition, feeds, enriched flours, and as a dietary supplement. It is also an electroplating bath ingredient. HUMAN STUDIES: A deficiency of this vitamin causes pellagra, a disease characterized by dermatitis, diarrhea, and dementia that is endemic today in parts of India and China, and may result in death in severe cases. Niacin deficiency is rare in the United States but may still be seen in alcoholics, dietary cultists, and patients with malabsorption syndrome. In single doses of 50 mg niacin, intense flushing and pruritus have been reported. When the practice of giving niacin in doses ranging upward to 30 g or more a day was advocated, more serious toxicity was noted. These effects included intense flushing and unbearable pruritus, skin rash, heartburn, nausea and vomiting, diarrhea, ulcer activation, abnormal liver function, hypotension, tachycardia, fainting, hyperglycemia, hyperbilirubinemia and jaundice, dermatoses, hyperuricemia, elevated serum enzymes, and hyperkeratosis of the skin. A greater incidence of atrial fibrillation and other cardiac arrhythmias is seen in persons taking niacin. One of the most significant adverse reactions of niacin is the hepatotoxicity seen in dosages exceeding 3 g/day. Sensitivity to the skin flush effect of niacin is reduced in a portion of patients with schizophrenia. As a precursor of pyridine nucleotides (nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP), niacin participates in the function of numerous enzymatic pathways, which are critical for normal cell metabolism, involving, for example redox reactions and those that consume NAD. ANIMAL STUDIES: Niacin administered to mice for a lifetime as a 1% solution in drinking water was not carcinogenic. A decreased growth rate in male rats fed diets containing 10% casein and large amounts of niacin daily was reported. A slight decrease in growth rate was noted at the 2% level with niacin, but not at 1%. Fatty liver formation was noted at both niacin feeding levels. Niacin administration to pregnant rats during the period of organogenesis at oral doses up to 200 mg/kg/day was without adverse effects. At 1000 mg/kg/day maternal body weight gain, placental and fetal weights were slightly depressed. Niacin deficiency causes dramatic genomic instability in bone marrow cells in an in vivo rat model. The end result is seen in the increased incidence of sister chromatid exchanges, micronuclei, chromosomal aberrations and the eventual development of nitrosourea-induced leukemias. Pigs deficient in niacin have inflammatory lesions of the digestive tract and exhibit diarrhea, weight loss, rough skin and coat, and dermatitis on the ears. Niacin deficiency in poultry is characterized by severe metabolic disorders in the skin and digestive organs. An Ames test using Salmonella typhimurium strains TA92, TA1535, TA100, TA1537, TA94 and TA98, with and without metabolic activation, and a chromosome aberration test using a Chinese hamster fibroblast cell line were carried out on niacin. Niacin tested negative at maximum concentrations of 10 mg/plate and 2 mg/mL, respectively.

Substance added directly to human food affirmed as generally recognized as safe (GRAS).

Niacin used as a nutrient and/or dietary supplement in animal drugs, feeds, and related products is generally recognized as safe when used in accordance with good manufacturing or feeding practice.

The Approved Drug Products with Therapeutic Equivalence Evaluations identifies currently marketed prescription drug products, including niacin, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act.

CIR ingredient: Niacin

Occurs naturally especially in liver, fish, yeast, and cereal grains; Used as a drug (antilipemic and vitamin); [Merck Index] Used in the chemical, agricultural, animal feed, and food industries, in cosmetics, pharmaceuticals, as a food additive, intermediate, and laboratory chemical; [IUCLID] Used as a medication, nutrient, in animal feeds, enriched flours, as a chemical intermediate, and in electroplating bathes; [HSDB] Used as a nutritional supplement; [FDA] Permitted for use as an inert ingredient in non-food pesticide products; [EPA]

Electroplating [Category: Plate]

Hypolipidemic Agents, Vasodilator Agents, Vitamin B Complex

For nicotinic acid (USEPA/OPP Pesticide Code: 056701) there are 0 labels match. /SRP: Not registered for current use in the U.S., but approved pesticide uses may change periodically and so federal, state and local authorities must be consulted for currently approved uses./

Medicine (cholesterol-lowering agent), nutrition, feeds, enriched flours, dietary supplement

2023: 235,012 lb

(1972) 2.49X10+9 GRAMS /NIACIN & NICOTINAMIDE/

(1975) 2.5X10+9 GRAMS /NIACIN & NICOTINAMIDE/

Non-confidential 2016 Chemical Data Reporting (CDR) information on the production and use of chemicals manufactured or imported into the United States. Chemical: Nicotinic acid:

In an aqueous solution 5-ethyl-2-methylpyridine is oxidized to nicotinic acid in a single-tube reactor by using an excess of nitric acid. The continuous process takes place at 230-270 °C and 6-8 MPa. Pyridine-2,5-dicarboxylic acid is formed as an intermediate, but is not stable under the reaction conditions, undergoing decarboxylation to nicotinic acid nitrate. Neutralization of the nitrate with 5-ethyl-2-methylpyridine yields nicotinic acid. Water and carbon dioxide formed in the reaction are separated from the product. The nitrogen oxide formed is oxidized with air to nitrogen dioxide and then absorbed in water to yield nitric acid, which is recycled into the process.

Preparation by oxidation of alkyl beta-substituted pyridines

Preparation by oxidation of nicotine

Commercial sources: Synthetic nicotinic acid is made by oxidation of nicotine, quinoline, or 2-methyl-5-ethylpyridine (from ammonia and formaldehyde or acetaldehyde).

Table: Niacin Preparations [Table#4463]

Table: Niacin Combination Preparations [Table#4464]

Table: Niacin Preparations [Table#4465]

Grades: National Formulary; Food Chemical Codex; blended with soy flour (animal feeds)

Niacin is commercially available as conventional (immediate-release) and extended-release preparations and in fixed combination with lovastatin. Niacin also is available as a dietary supplement; these preparations are not FDA-labeled for management of dyslipidemias and should not be used as substitutes for prescription-only niacin preparations.

Pharmaceutical and Medicine Manufacturing

3-Pyridinecarboxylic acid: ACTIVE

Niacin is a naturally occurring substance. Nicotinic acid is the form present in food of plant origin, whereas nicotinamide occurs in animal products.

The terms niacin, Vitamin B3, and Vitamin PP have been used to refer to both nicotinamide and nicotinic acid.

NIACIN, MOST STABLE OF VIT, IS NOT DESTROYED BY HEATING IN ACID OR ALKALINE SOLN. IT WITHSTANDS MILD OXIDATION, & RETAINS ITS BIOLOGICAL ACTIVITY DURING PROCESSING OF FOOD & PREPN & STORAGE OF PHARMACEUTICALS.

RECOMMENDED ALLOWANCE OF THE DIETARY ALLOWANCES COMMITTEE OF THE NATIONAL RESEARCH COUNCIL, EXPRESSED IN NICOTINIC ACID EQUIVALENTS, IS 6.6 MG/1000 KCAL.