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Final report of the safety assessment of niacinamide and niacin.

Niacinamide (aka nicotinamide) and Niacin (aka nicotinic acid) are heterocyclic aromatic compounds which function in cosmetics primarily as hair and skin conditioning agents. Niacinamide is used in around 30 cosmetic formulations including shampoos, hair tonics, skin moisturizers, and cleansing formulations. Niacin is used in a few similar product types. The concentration of use of Niacinamide varies from a low of 0.0001% in night preparations to a high of 3% in body and hand creams, lotions, powders and sprays. Niacin concentrations of use range from 0.01% in body and hand creams, lotions, powders and sprays to 0.1% in paste masks (mud packs). Both ingredients are accepted for use in cosmetics in Japan and the European Union. Both are GRAS direct food additives and nutrient and/or dietary supplements. Niacinamide may be used in clinical treatment of hypercholesteremia and Niacin in prevention of pellegra and treatment of certain psychological disorders. Both ingredients are readily absorbed from skin, blood, and the intestines and widely distribute throughout the body. Metabolites include N1-methylnicotinamide and N1-methyl-4-pyridone-3-carboxamide. Excretion is primarily through the urinary tract. While Niacinamide is more toxic than Niacin in acute toxicity studies, both are relatively non-toxic. Short-term oral, parenteral, or dermal toxicity studies did not identify significant irreversible effects. Niacinamide, evaluated in an in vitro test to predict ocular irritation, was not an acute ocular hazard. Animal testing of Niacinamide in rabbits in actual formulations produced mostly non-irritant reactions, with only some marginally irritating responses. Skin irritation tests of up to 2.5% Niacinamide in rabbits produced only marginal irritation. Skin sensitization tests of Niacinamide at 5% during induction and 20% during challenge were negative in guinea pigs. Neither cosmetic ingredient was mutagenic in Ames tests, with or without metabolic activation. Niacinamide and Niacin at 2 mg/ml were negative in a chromosome aberration test in Chinese hamster ovary cells, but did produce large structural chromosome aberrations at 3 mg/ml. Niacinamide induced sister chromatid exchanges in Chinese hamster ovary cells, but Niacin did not. Under certain circumstances, Niacinamide can cause an increase in unscheduled DNA synthesis in human lymphocytes treated with UV or a nitrosoguanidine compound. Niacinamide itself was not carcinogenic when administered (1%) in the drinking water of mice. No data on the carcinogenic effect of Niacin were available. Niacinamide can moderate the induction of tumors by established carcinogens. Niacinamide in combination with streptozotocin (a nitrosourea compound) or with heliotrine (a pyrrolizidine alkaloid), produced pancreatic islet tumors. On the other hand, Niacinamide reduced the renal adenomas produced by streptozotocin; and intestinal and bladder tumors induced by a preparation of bracken fern. Niacinamide evaluated in in vitro test systems did affect development, but Niacinamide reduced the reproductive/developmental toxicity of 2-aminonicotinamide-amino-1,3,4-thiadiazole hydrochloride and urethane. Clinical testing of Niacinamide produced no stinging sensation at concentrations up to 10%, use tests produced no irritation at concentrations up to 5%, and a 21-day cumulative irritation test at concentrations up to 5% resulted in no irritancy. Niacinamide was not a sensitizer, nor was it a photosensitizer. The CIR Expert Panel considered that Niacinamide and Niacin are sufficiently similar from a toxicologic standpoint to combine the available data and reach a conclusion on the safety of both as cosmetic ingredients. Overall, these ingredients are non-toxic at levels considerably higher than would be experienced in cosmetic products. Clinical testing confirms that these ingredients are not significant skin irritants, sensitizers or photosensitizers. While certain formulations were marginal to slight ocular irritants, other formulations were not. Niacinamide, while not carcinogenic alone, can modulate the induction of tumors by certain established carcinogens. The Panel noted that the doses in these studies are high relative to the low concentrations at which Niacinamide is used in cosmetic formulations. In neither case (tumor protection or tumor promotion) are these findings considered relevant to the use of Niacinamide at its current low concentrations of use in cosmetics. Both ingredients were considered safe as used in cosmetics.

Animals↗

Niacinamide transport through the blood-brain barrier.

The unidirectional influx of niacinamide across cerebral capillaries, the anatomical locus of the blood-brain barrier, was measured with an in situ rat brain perfusion technique employing [14C]niacinamide. Niacinamide was transported rapidly across the blood-brain barrier by a system that was not saturable with 10 mM niacinamide in the perfusate. However, with periods of perfusion longer than 30 seconds, there was substantial backflow of [14C]niacinamide into the perfusate. Niacinamide (1.7 microM) transport through the blood-brain barrier was not significantly inhibited by 3-acetylpyridine. Thus, niacinamide is transported rapidly and bidirectionally through the blood-brain barrier by a high capacity transport system. Although involved in the transfer of niacinamide between blood and brain, this transport system does not play an important regulatory role in the synthesis of NMN, NAD, and NADP from niacinamide in brain.

Animals↗

The effect of niacinamide on osteoarthritis: a pilot study.

OBJECTIVE: To evaluate the effect of niacinamide, on selected parameters of osteoarthritis using a double-blind, placebo controlled study design. METHODS: Seventy two patients with osteoarthritis were randomized for treatment with niacinamide or an identical placebo for 12 weeks. Outcome measures included global arthritis impact and pain, joint range of motion and flexibility, erythrocyte sedimentation rate, complete blood count, liver function tests, cholesterol, uric acid, and fasting blood sugar. Compliance was monitored with a pill record sheet and interview. RESULTS: Global arthritis impact improved by 29% (95% confidence interval [CI] 6, 46) in subjects on niacinamide and worsened by 10% in placebo subjects (p = 0.04). Pain levels did not change but those on niacinamide reduced their anti-inflammatory medications by 13% (95% CI 9, 94; p = 0.01). Niacinamide reduced erythrocyte sedimentation rate by 22% (95% CI 6, 51; p < 0.005) and increased joint mobility by 4.5 degrees over controls (8 degrees vs 3.5 degrees; p = 0.04). Side effects were mild but higher in the niacinamide group (40% vs 27%, p = 0.003). CONCLUSION: This study indicates that niacinamide may have a role in the treatment of osteoarthritis. Niacinamide improved the global impact of osteoarthritis, improved joint flexibility, reduced inflammation, and allowed for reduction in standard anti-inflammatory medications when compared to placebo. More extensive evaluation of niacinamide in arthritis is warranted.

Aged↗

Niacinamide pretreatment reduces microvesicle formation in hairless guinea pigs cutaneously exposed to sulfur mustard.

It has been proposed that sulfur mustard (HD) may indirectly activate poly(ADP-ribose) polymerase (PADPRP) by alkylating cellular DNA (Papirmeister et al., 1985). Activation of PADPRP results in the depletion of cellular NAD+, which initiates a series of biochemical processes that have been proposed to culminate in blister formation. Preventing PADPRP activation and NAD+ depletion should inhibit blister formation. Niacinamide is both an inhibitor of PADPRP and a precursor for NAD+ synthesis. The present study was undertaken to determine whether niacinamide can protect against HD-induced microvesication in cutaneously exposed hairless guinea pigs. Each site was exposed to HD for 8 min by means of a vapor cup. Niacinamide (750 mg/kg, ip) given as a 30-min pretreatment inhibited microvesicle formation by 50% after HD application. However, niacinamide given 2 hr after HD application did not reduce microvesicle formation. There was no benefit when niacinamide was given as both a pretreatment and treatment when compared to niacinamide given only as a pretreatment. The reduction in microvesication 24 hr after HD did not correlate with skin NAD+ content. Niacinamide did not reduce the degree of erythema or edema. Ballooning degeneration of basal epidermal cells was present in some niacinamide pretreated HD exposure sites. These results suggest that niacinamide may only be effective as a pretreatment compound to reduce the incidence of HD-induced microvesicle formation. Maintenance of skin NAD+ content may not be solely responsible for inhibiting microvesicle formation and inhibition of PADPRP may be of greater importance.

Animals↗

The effect of niacinamide on reducing cutaneous pigmentation and suppression of melanosome transfer.

BACKGROUND: Cutaneous hyperpigmentation occurs in multiple conditions. In addition, many Asian women desire a lighter skin colour. Thus, there is a need for the development of skin lightening agents. Niacinamide is a possible candidate. OBJECTIVES: To investigate the effects of niacinamide on melanogenesis in vitro and on facial hyperpigmentation and skin colour in vivo in Japanese women. METHODS: Melanin production was measured in a purified mushroom tyrosinase assay, cultured melanocytes, a keratinocyte/melanocyte coculture model, and a pigmented reconstructed epidermis (PREP) model. The clinical trials included 18 subjects with hyperpigmentation who used 5% niacinamide moisturizer and vehicle moisturizer in a paired design, and 120 subjects with facial tanning who were assigned to two of three treatments: vehicle, sunscreen and 2% niacinamide + sunscreen. Changes in facial hyperpigmentation and skin colour were objectively quantified by computer analysis and visual grading of high-resolution digital images of the face. RESULTS: Niacinamide had no effect on the catalytic activity of mushroom tyrosinase or on melanogenesis in cultured melanocytes. However, niacinamide gave 35-68% inhibition of melanosome transfer in the coculture model and reduced cutaneous pigmentation in the PREP model. In the clinical studies, niacinamide significantly decreased hyperpigmentation and increased skin lightness compared with vehicle alone after 4 weeks of use. CONCLUSIONS: The data suggest niacinamide is an effective skin lightening compound that works by inhibiting melanosome transfer from melanocytes to keratinocytes.

Adolescent↗

Protective effects of niacinamide in staphylococcal enterotoxin-B-induced toxicity.

Staphylococcal enterotoxins (SE) interact with major histocompatibility complex (MHC) class II cell-surface receptors, eliciting signal transduction in antigen-presenting cells (APC). Subsequent toxin-class II complex interaction with specific T-cell receptors induces T-cell activation. We investigated the effect of niacinamide and interleukin (IL)-10 on SEB-induced responses. In a macrophage cell line, niacinamide (ED50--2mM) and IL-10 (ED50--7U/ml) inhibited interferon (IFN)-gamma-induced MHC class II expression in a dose-dependent manner. Also, niacinamide was a potent inhibitor of T-cell proliferation induced by SEB (ED50-- 1 mM) while IL-10 has minimal effects. In mice, the temporal responses of IL-1alpha, tumor necrosis factor (TNF)-alpha, IL-2, and IFN-gamma evoked by SEB were synergistically potentiated by lipopolysaccharide (LPS). Lethality occurred only when SEB was potentiated by LPS. Niacinamide or IL-10 improved survival of mice after lethal SEB challenge. Niacinamide reduced cytokine serum levels, although the pattern differed from that of IL-10. Niacinamide primarily reduced IL-2 and IFN-gamma, while IL-10 predominantly reduced IL-1alpha and TNF-alpha. The immunomodulatory effects of niacinamide observed on SEB-induced activation of APC and T-cells in vitro and in the LPS potentiated murine model for SEB-induced toxicity suggest it may have therapeutic value.

Animals↗

Effective inhibition of melanosome transfer to keratinocytes by lectins and niacinamide is reversible.

Skin pigmentation results in part from the transfer of melanized melanosomes synthesized by melanocytes to neighboring keratinocytes. Plasma membrane lectins and their glycoconjugates expressed by these epidermal cells are critical molecules involved in this transfer process. In addition, the derivative of vitamin B(3), niacinamide, can inhibit melanosome transfer and induce skin lightening. We investigated the effects of these molecules on the viability of melanocytes and keratinocytes and on the reversibility of melanosome-transfer inhibition induced by these agents using an in vitro melanocyte-keratinocyte coculture model system. While lectins and neoglycoproteins could induce apoptosis in a dose-dependent manner to melanocytes or keratinocytes in monoculture, similar dosages of the lectins, as opposed to neoglycoproteins, did not induce apoptosis to either cell type when treated in coculture. The dosages of lectins and niacinamide not affecting cell viability produced an inhibitory effect on melanosome transfer, when used either alone or together in cocultures of melanocytes-keratinocytes. Cocultures treated with lectins or niacinamide resumed normal melanosome transfer in 3 days after removal of the inhibitor, while cocultures treated with a combination of lectins and niacinamide demonstrated a lag in this recovery. Subsequently, we assessed the effect of niacinamide on facial hyperpigmented spots using a vehicle-controlled, split-faced design human clinical trial. Topical application of niacinamide resulted in a dose-dependent and reversible reduction in hyperpigmented lesions. These results suggest that lectins and niacinamide at concentrations that do not affect cell viability are reversible inhibitors of melanosome transfer.

Administration, Topical↗

Response of male poults to high levels of dietary niacinamide.

The response was determined of male poults to high levels of dietary niacinamide, when maintained in a stressful environment of high stocking density and high litter moisture induced by excess dietary NaCl. The experiment was designed as a factorial (2 by 2 by 2) with 70 versus 140 mg of niacinamide per kg; .3 versus 1% NaCl; 7 versus 14 birds per m2. Each treatment was assigned to 6 pens, with either 20 or 40 males per pen depending on stocking density. The calculated niacin content of the basal diet was 22 mg per kg; the experimental diets contained 92 and 162 mg of total niacin per kg. Added niacinamide at 140 mg per kg increased the body weight at 8 wk of age (3,095 versus 3,198) at .3% dietary NaCl. The response to 140 mg per kg of niacinamide was 4.6% at .3% NaCl and only 1.9% at 1% NaCl. The high level of niacinamide was ineffective in terms of alleviating the growth depression induced by a high stocking density. Treatment effects were not detected in relation to feed efficiency. The incidence of leg abnormalities was not influenced by dietary niacinamide or by litter moisture, but was aggravated by a high stocking density. The treatments did not induce ascites or macroscopic lesions in the heart or kidney. These findings demonstrated that supplemental niacinamide at 140 mg per kg, in a basal diet calculated to contain 22 mg of niacin per kg of feed, will produce a significant increase in the weight gain of male poults at 8 wk of age under praxis conditions when dietary salt is at .3%, but not at 1%.

Animals↗

Sulfur mustard-induced microvesication in hairless guinea pigs: effect of short-term niacinamide administration.

It has been postulated that sulfur mustard (HD) damage may activate poly(ADP-ribose) polymerase (PADPRP), resulting in depletion of cellular NAD+. This biochemical alteration is postulated to result in blister (vesicle) formation. It has been previously demonstrated that niacinamide (NAM), an inhibitor of PADPRP and a precursor for NAD+ synthesis, may be useful as a pretreatment compound to reduce HD-induced microvesication. The present study was undertaken to determine whether niacinamide's protective action could be extended beyond 24 hr and if the degree of microvesication is related to changes in skin NAD+ content. HD exposures were made by vapor cup to hairless guinea pigs. Niacinamide (750 mg/kg, ip) given as a 30-min pretreatment did not reduce the degree of microvesication 72 hr after HD compared to saline controls. However, niacinamide given as a 30-min pretreatment and at 6-, 24-, and 48-hr after HD, exhibited a 28% reduction in microvesication 72 hr after HD. Skin NAD+ content at 72 hr after HD was depleted by approximately 53% in the saline and NAM-treated groups. Skin NAD+ content was depleted despite NAM administration. Niacinamide did not reduce the degree of erythema at 48 or 72 hr. These results suggest that niacinamide's protective effect against HD-induced microvesication may be extended for at least 72 hr, but NAM levels must be sustained during the post-HD period. The link between maintenance of skin NAD+ and reductions in microvesication is still uncertain.

Animals↗

The effect of 2% niacinamide on facial sebum production.

BACKGROUND: The presence of sebum on the face is responsible for both facial shine and the formation of comedonal and inflammatory acne lesions. Sebum control is a goal of many OTC skin care products; however, most currently available products function by absorbing sebum from the face rather than modulating its production. OBJECTIVE: To demonstrate the effect of topical 2% niacinamide on sebum excretion rates and casual sebum production in Oriental and Caucasian populations. METHODS: Separate clinical trials were conducted in both Japan and the USA to evaluate the effect of topical 2% niacinamide in different ethnic groups. A total of 100 Japanese subjects were enrolled in a double-blind, placebo-controlled comparison between two independent balanced groups. Fifty subjects applied the 2% niacinamide moisturizer to the face for 4 weeks and 50 subjects used a placebo moisturizer for 4 weeks, with sebum excretion rate (SER) measurements taken at baseline, week 2, and week 4. In addition, 30 Caucasian subjects were enrolled in a randomized split-face study for 6 weeks with SER and casual sebum levels (CSL) measured at baseline, week 3, and week 6. RESULTS: The results of the Japanese study demonstrated that the SER of the two groups was not significantly different at baseline, but the 2% niacinamide treated group demonstrated significantly lowered SER after 2 and 4 weeks of application. The results were somewhat different in the Caucasian study. After 6 weeks of treatment, the CSL was significantly reduced, but the SER was not significantly reduced. CONCLUSIONS: Topical 2% niacinamide may be effective in lowering the SER in Japanese individuals and CSL in Caucasian individuals.

Administration, Topical↗

The influence of excipients on the stability of the moisture sensitive drugs aspirin and niacinamide: comparison of tablets containing lactose monohydrate with tablets containing anhydrous lactose.

The purpose of this study is to test the hypothesis that in tablet formulations, moisture-sensitive drugs formulated with lactose monohydrate have the same stability as formulations containing anhydrous lactose, and to characterize the kinetics of niacinamide degradation in the solid state. Aspirin and niacinamide decomposition were used as indicators of stability. Aspirin and niacinamide tablets containing either lactose monohydrate or anhydrous lactose were separately investigated at different temperatures and relative humidities; the stability tests were done at 25 degrees C--60% RH, 40 degrees C--80% RH, 60 degrees C--60% RH, 60 degrees C--80% RH, and 80 degrees C--80% RH. Official U.S. Pharmacopeia methods were used for the aspirin and niacinamide assays. Statistical analysis showed that tablets containing lactose monohydrate have the same stability as tablets containing anhydrous lactose, which means that even though water is present in the crystal structure, the bound water does not influence the reaction rate. In addition, niacinamide degradation in the solid-state can be described by a third order rate equation.

Aspirin↗

Niacinamide: A B vitamin that improves aging facial skin appearance.

BACKGROUND: In multiple chronic clinical studies, topical niacinamide (vitamin B3) has been observed to be well tolerated by skin and to provide a broad array of improvements in the appearance of aging facial skin (eg, reduction in the appearance of hyperpigmentated spots and red blotchiness). OBJECTIVE: To clinically determine the effect of topical niacinamide on additional skin appearance and property end points (wrinkles, yellowing, and elasticity). METHODS: Female white subjects (N = 50) with clinical signs of facial photoaging (fine lines and wrinkles, poor texture, and hyperpigmented spots) applied 5% niacinamide to half of the face and its vehicle control to the other half twice daily for 12 weeks (double blind, left-right randomized). Facial images and instrumental measures were obtained at baseline and at 4-week intervals. RESULTS: Analyses of the data revealed a variety of significant skin appearance improvement effects for topical niacinamide: reductions in fine lines and wrinkles, hyperpigmented spots, red blotchiness, and skin sallowness (yellowing). In addition, elasticity (as measured via cutometry) was improved. Corresponding mechanistic information is presented. CONCLUSION: In addition to previously observed benefits for topical niacinamide, additional effects were identified (improved appearance of skin wrinkles and yellowing and improved elasticity).

Administration, Topical↗

Effect of supplemental niacin or niacinamide and soybean source on ruminal bacterial fermentation in continuous culture.

Effects of niacin or niacinamide in diets containing either soybean meal, raw whole soybeans or whole soybeans extruded at 132 and 149 C on ruminal bacterial fermentation were examined with a dual-flow continuous culture system. In Exp. 1, soybean sources each provided 50% of total crude protein in diets comprised of 52% concentrate mix, 36% corn silage and 12% alfalfa hay (dry-matter basis). Each diet was supplemented with 0 or 100 mg/kg niacin. Niacin supplementation increased (P less than .05) total nonstructural carbohydrate digestibility and lowered (P less than .05) butyrate concentration. There was also an increase (P less than .10) in amino acid effluent flow from 8,413.3 to 8,665.3 mg/d with addition of niacin to the diet. In Exp. 2, diets were supplemented with 0 or 100 mg/kg of niacin or niacinamide. The total mixed diet was comprised of 60% concentrate mix, 20% corn silage and 20% alfalfa hay (dry matter basis). Acid detergent fiber and cellulose digestibilities and total amino acid effluent flow were higher (P less than .10) with niacinamide supplementation. Niacin or niacinamide had no effect on dry matter and organic matter digestibilities, ammonia-N, total VFA concentration or crude protein degradation. Contrary to results found in other studies, niacin or niacinamide supplementation had no effect on bacterial protein synthesis.

Animals↗

Ultrastructural correlates of the protection afforded by niacinamide against sulfur mustard-induced cytotoxicity of human lymphocytes in vitro.

Sulfur mustard (HD) has been shown to cause a concentration-dependent decrease in viability of human lymphocytes in vitro as measured by dye exclusion; this decrease is preventable by inhibitors of poly(adenosine diphosphatase ribose) polymerase such as niacinamide. The present study investigates the morphologic correlates of the protection afforded by niacinamide through scanning and transmission electron microscopic analysis of human lymphocytes incubated in the presence or absence of 10(3) M niacinamide for 24 h at 37 degrees C and exposed in vitro to 10(-3) M HD. Lymphocytes exposed to HD alone demonstrated 30% to 40% viability and loss of microvilli, large cytoplasmic vacuoles, extensive blebbing of the perinuclear envelope, loss of cytoplasmic organelles, condensation of nuclear chromatin, and multiple perforations of the plasmalemma. In the presence of niacinamide HD-treated lymphocytes had a viability of 87% and, except for blunting of the microvilli, essentially normal ultrastructure. Although the sequence of observed ultrastructural changes was not established, results of this morphologic study suggest that, in addition to the prevention of plasmalemmal defects and dye infusion, the mechanism of niacinamide protection appears to include preservation of the morphologic and functional integrity of cellular organelles.

Cell Membrane↗

Liquid chromatographic determination of free and added niacin and niacinamide in beef and pork.

A simple liquid chromatographic (LC) method is described for the determination of free and added niacin and niacinamide in meats. A sample is homogenized and extracted with water, and the water extract is centrifuged, deproteinized with zinc hydroxide, and filtered first through a fluted paper and then through a microporous filter. The filtrate is subjected to liquid chromatography with UV detection at 263 nm. Different ion-pair systems are needed for the measurement of niacin and niacinamide on a reverse phase column. Methanol-water (1 + 9) containing 5mM tetrabutyl ammonium ion is used to separate niacin. Water containing 10mM heptane sulfonic acid is recommended for niacinamide. Recoveries (CV,%) are 104.8% (2.9%) for niacin and 96.3% (2.7%) for niacinamide at a 10 mg/100 g fortification level. Detection limit is 1 mg/100 g sample for niacin and niacinamide.

Animals↗

Reduction of erythema in hairless guinea pigs after cutaneous sulfur mustard vapor exposure by pretreatment with niacinamide, promethazine and indomethacin.

Erythema is the initial symptom that occurs after sulfur mustard (HD) cutaneous exposure. The time course of HD-induced erythema is similar to that observed after UV irradiation, which can be reduced by indomethacin. Sulfur mustard lethality is decreased by using promethazine, which is an antihistamine. Niacinamide can reduce microvesication after HD vapor exposure in hairless guinea pig (HGP) skin. The present study examines the effect of the combined administration of niacinamide, indomethacin and promethazine used alone or in all possible combinations on the degree of erythema and histopathologic skin damage after HD exposure in HGP. Niacinamide (750 mg kg-1, i.p.), promethazine (12.5 mg kg-1, i.m.) or indomethacin (4 mg kg-1, p.o.) used singly or in combination was given as a 30-min pretreatment before an 8-min HD vapor cup skin exposure. Using a combination pretreatment of niacinamide, promethazine and indomethacin, erythema was reduced at 4 (91%) and 6 (55%) h, but not 24 h after HD. The incidence of histopathological skin changes (microvesicles, follicular involvement, epidermal necrosis, intracellular edema and pustular epidermatitis) 24 h after HD was not reduced. This study indicates that HD-induced erythema may result from several different mechanisms, including inflammation, histamine release and DNA damage. It is suggested that two phases of inflammation may occur: an early phase sensitive to antihistamines and non-steroidal antiinflammatory drugs and a late phase of extensive cell damage that was not sensitive to these drug pretreatments.

Animals↗

Use of column switching for the determination of niacinamide in compound feed.

A high-performance liquid chromatographic method is described for the determination of niacinamide in compound feed. The niacinamide is extracted with 0.2 M hydrochloric acid in order to suppress the hydrolysis of the niacinamide to nicotinic acid. The chromatography is carried out with the aid of column switching. An RP-18 column is used for the preseparation, and the analytical separation takes place in a cation-exchange column. With the proposed method, the limit of determination is about 2 ppm of niacinamide.

Animal Feed↗

Ion-selective piezoelectric sensor for niacinamide assay in serum and urine.

An ion-selective piezoelectric (ISP) sensor was successfully applied for the determination of niacinamide in serum and urine. By coating a polyvinylchloride membrane containing niacinamide-silicotungstate on one electrode of a thickness-shear mode piezoelectric quartz crystal, the ISP device can adsorb niacinamide selectively. The amount of coating applied to the crystal was calculated from the Sauerbrey equation by monitoring the frequency change. The logarithm of the frequency shift was linear with the logarithm of niacinamide concentration over the range from 1.0 x 10(-9) to 1.0 x 10(-3) M with a detection limit of 1.0 x 10(-9) M at pH 7.0. Influencing factors were investigated and optimized. The results for real samples obtained by the proposed method were in good agreement with those obtained by the conventional methods.

Electrodes↗