Sodium benzoate

144.10300

144.01900

208-534-8

OJ245FE5EU

1536

DTXSID1020140

White, granules or crystalline powder|Colorless crystalline powder

A - Alimentary tract and metabolism

4002191900

40.13000

log Kow = -2.27 (est)

White crystalline powder

1,44 g/cm3

>300 °C

249.3ºC at 760 mmHg

111.4ºC

Solubility in water, g/100ml at 20°C: 63

Low temperature, ventilation, drying

2.9X10-12 mm Hg at 25 deg C (est)

LD50 orally in rats: 4.07 g/kg (Smyth, Carpenter)

Odorless

Sweetish, astringent taste

Aqueous solution is slightly alkaline to litmus, pH about 8

Decomp by dil mineral acid liberating benzoic acid|Incompatibility: Acids, F

>500 °C

Dust explosion possible if in powder or granular form, mixed with air.

NONH for all modes of transport

1

R36/37/38

S24/25

DH6650000

Xi

Stable, but may be moisture senstive. Incompatible with strong oxidizing agents, alkalis, mineral acids.

P305 + P351 + P338

H319

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.|SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a permitted wastewater treatment facility is acceptable only after review by the governing authority and assurance that "pass through" violations will not occur. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must be evaluated in accordance with EPA 40 CFR Part 261, specifically Subpart B, in order to determine the appropriate local, state and federal requirements for disposal.|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.

Incompatible materials: Strong oxidizing agents

Substances classified as antimycotics, when migrating from food-packaging material shall include: ... sodium benzoate.|Substance added directly to human food affirmed as generally recognized as safe (GRAS). The ingredient is used in food at levels not to exceed good manufacturing practice. Current usage results in a maximum level of 0.1 percent in food.|Sodium benzoate used as a chemical preservative at a level not exceeding 1% in animal drugs, feeds, and related products is generally recognized as safe when used in accordance with good manufacturing or feeding practice.|Drug products containing certain active ingredients offered over-the-counter (OTC) for certain uses. A number of active ingredients have been present in OTC drug products for various uses, as described below. However, based on evidence currently available, there are inadequate data to establish general recognition of the safety and effectiveness of these ingredients for the specified uses: sodium benzoate is included in orally administered menstrual drug products.

Combustible under specific conditions. Gives off irritating or toxic fumes (or gases) in a fire. Finely dispersed particles form explosive mixtures in air.

|Warning|H319 (99.05%): Causes serious eye irritation [Warning Serious eye damage/eye irritation]|P264, P280, P305+P351+P338, and P337+P313|Aggregated GHS information provided by 2885 companies from 11 notifications to the ECHA C&L Inventory.|H319: Causes serious eye irritation [Warning Serious eye damage/eye irritation]

Eye/face protection: Safety glasses with side-shields conforming to EN166. Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU).|Skin protection: Handle with gloves.|Body Protection: Impervious clothing. The type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace.|Respiratory protection: For nuisance exposures use type P95 (US) or type P1 (EU EN 143) particle respirator. For higher level protection use type OV/AG/P99 (US) or type ABEK-P2 (EU EN 143) respirator cartridges. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU).|For more Personal Protective Equipment (PPE) (Complete) data for SODIUM BENZOATE (6 total), please visit the HSDB record page.

Combustible when exposed to heat or flame.|Sodium benzoate is combustible.

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.|Use dry chemical, carbon dioxide, water spray, or foam extinguishers. ... If material or contaminated runoff enters waterways, notify downstream users of potentially contaminated waters. Notify local health and fire officials and pollution control agencies. From a secure, explosion-proof location, use water spray to cool exposed containers. If cooling steams are ineffective (venting sound increases in volume and pitch, tank discolors, or shows any signs of deforming), withdraw immediately to a secure position.

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: Do not let product enter drains. 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.|Evacuate persons not wearing protective equipment from area of spill or leak until cleanup is complete. Remove all ignition sources. Collect powdered material in the most convenient and safe manner and deposit in sealed containers. Ventilate area after cleanup is complete. It may be necessary to contain and dispose of this chemical as a hazardous waste. If material or contaminated runoff enters waterways, notify downstream users of potentially contaminated waters.

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: Do not let product enter drains.|Precautions for safe handling: Avoid contact with skin and eyes. Avoid formation of dust and aerosols. Provide appropriate exhaust ventilation at places where dust is formed.|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.|For more Preventive Measures (Complete) data for SODIUM BENZOATE (7 total), please visit the HSDB record page.

... Sodium benzoate was only slightly irritating to the eye ... .|The test substance is neither an irritant nor sensitizer when applied to guinea pigs.

Personal protection: particulate filter respirator adapted to the airborne concentration of the substance. Sweep spilled substance into covered containers.

A nuisance-causing concentration of airborne particles can be reached quickly when dispersed, especially if powdered.

The substance is mildly irritating to the eyes.

NO open flames. Closed system, dust explosion-proof electrical equipment and lighting. Prevent deposition of dust.

Avoid inhalation of dust.

Protective gloves. Protective clothing.

Wear safety goggles.

This action promulgates standards of performance for equipment leaks of Volatile Organic Compounds (VOC) in the Synthetic Organic Chemical Manufacturing Industry (SOCMI). The intended effect of these standards is to require all newly constructed, modified, and reconstructed SOCMI process units to use the best demonstrated system of continuous emission reduction for equipment leaks of VOC, considering costs, nonair quality health and environmental impact and energy requirements. Sodium benzoate is produced, as an intermediate or a final product, by process units covered under this subpart.

Sodium benzoate has been identified in tobacco collected from cigaretts(1).

IDENTIFICATION AND USE: Sodium benzoate is a colorless crystalline powder. It is used as food preservative, antiseptic, medicine, in tobacco, in pharmaceutical preparations, as an intermediate for manufacture of dyes, and as a rust and mildew inhibitor. HUMAN EXPOSURE AND TOXICITY: In a study with 2045 patients of dermatological clinics, only 5 persons (approximately 0.2%) showed a positive reaction in patch tests, while 34 of 5202 patients (approximately 0.7%) with contact urticaria reacted positively. Cases of urticaria, asthma, rhinitis, or anaphylactic shock have been reported following oral, dermal, or inhalation exposure to sodium benzoate. The symptoms appear shortly after exposure and disappear within a few hours. Chromosome aberration test was carried out on sodium benzoate using human embryonic lung culture cells. Sodium benzoate produced no significant increase in the aberration frequency in the anaphase chromosomes when tested at the dosage levels 0, 2.0 ug/mL, 20 ug/mL and 200 g/mL. In human embryonic lung cells (WI-38) treated with sodium benzoate both chromosome abnormalities and mitotic indices were within normal values. Sodium benzoate was mutagenic and cytotoxic in lymphocytes, where it caused micronucleus formation and chromosome break. ANIMAL STUDIES: An acute dermal irritation/corrosion study gave no indication for skin irritating effect in rabbits. Sodium benzoate was only slightly irritating to the eye. In a 90-day study with rats dosed with 0, 1, 2, 4, or 8% sodium benzoate via diet, the mortality in the highest dose group (approx. 6290 mg/kg body weight per day) was about 50%. Other effects in this group included a reduced weight gain, increased relative weights of liver and kidneys, and pathological changes in these organs. Sodium benzoate was given in drinking water to 50 female and 50 male mice from weeks 5 on for lifespan. The average daily intake of sodium benzoate was 119.2 mg for a female and 124.0 mg for a male (approx. 5.95 - 6.2 g/kg bw/d). There was no effect on the survival of the treated mice when compared with the untreated control. There were no significant differences between the tumor distribution in sodium benzoate-treated and untreated control mice. In a developmental study rats were injected intraperitoneally with 100, 315, or 1000 mg/kg sodium benzoate on gestation days 9 to 11 or 12 to 14. Reduced fetal body weight, increased in utero deaths (by 12%), and gross anomalies were noted at the highest dose. No evidence of teratogenicity was noted in rats administered 510 mg/kg of sodium benzoate by gavage on gestation days 9 to 11. Sodium benzoate (up to 3.0 mg/plate) was tested in the Salmonella/microsome test using S. typhimurium TA 92, TA 94, TA 98, TA 100, TA 1535 and TA 1537. No significant increases in the numbers of revertant colonies were detected in any S. typhimurium strains at the maximum dose. Sodium benzoate tested negative in a cytogenetic assay (bone marrow) in rats after single or multiple oral application of doses up to 5000 mg/kg body weight. In a study with mice, there was also no indication of mutagenic activity in a host-mediated assay.

The GRAS report cited studies in which ingestion of sodium benzoate reduced the glycine-dependent formation of creatine, glutamine, urea, and uric acid and increased the effects of procaine, lidocaine, cocaine, tetracaine, and dibucaine. Under conditions of severely restricted fluid and salt intake, benzoates increased and prolonged the concentration of serum penicillin.|The interaction between sodium benzoate (SB) and calf thymus DNA in simulated physiological buffer (pH 7.4) using acridine orange (AO) dye as a fluorescence probe, was investigated by UV-Vis absorption, fluorescence and circular dichroism (CD) spectroscopy along with DNA melting studies and viscosity measurements. An expanded UV-Vis spectral data matrix was resolved by multivariate curve resolution-alternating least squares (MCR-ALS) approach. The equilibrium concentration profiles and the pure spectra for SB, DNA and DNA-SB complex from the high overlapping composite response were simultaneously obtained. The results indicated that SB could bind to DNA, and hydrophobic interactions and hydrogen bonds played a vital role in the binding process. Moreover, SB was able to quench the fluorescence of DNA-AO complex through a static procedure. The quenching observed was indicative of an intercalative mode of interaction between SB and DNA, which was supported by melting studies, viscosity measurements and CD analysis.

LC50 Rat inhalation >12,200 mg/cu m air/4 hr|LD50 Rat oral 3450 mg/kg bw|LD50 Rabbit oral 2000 mg/kg|LD50 Mouse intramuscular 2306 mg/kg|For more Non-Human Toxicity Values (Complete) data for SODIUM BENZOATE (8 total), please visit the HSDB record page.

Low birthweight infants with immature livers may not be capable of metabolizing benzoate and hippurate. Sodium benzoate and sodium phenylacetate combination should not be administered to low birthweight infants unless the benefits of treatment outweight the risks.

Sodium benzoate's production and use as antimicrobial and preservative in foods, soft drinks, pharmaceuticals, tobacco and cosmetics and its use as a corrosion inhibitor and chemical intermediate(1-3) may result in its release to the environment through various waste streams(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of17(SRC), determined from a structure estimation method(2), indicates that sodium benzoate is expected to have very high mobility in soil(SRC). Volatilization of sodium benzoate from moist soil surfaces is not expected to be an important fate process(SRC) given sodium benzoate is expected to immediately dissociate and form the anion of benzoic acid in an aqueous environment(3), and ions do not volatilize(SRC). Sodium benzoate is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 2.9X10-12 mm Hg at 25 °C(SRC), determined from a fragment constant method(2). A variety of biodegradation screening tests have found sodium benzoate to be readily biodegradable(4,5). For example, CO2 evolution rates of 85-94% were reached after 28 days using an activated sludge inoculum(4).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 17(SRC), determined from a structure estimation method(2), indicates that sodium benzoate is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(SRC) given sodium benzoate is expected to immediately dissociate and form the anion of benzoic acid in an aqueous environment(3), and ions do not volatilize(SRC). According to a classification scheme(4), an estimated BCF of 3(SRC), from an estimated log Kow of -2.27(2) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is low(SRC). A variety of biodegradation screening tests have found sodium benzoate to be readily biodegradable(5,6). For example, CO2 evolution rates of 85-94% were reached after 28 days using an activated sludge inoculum(5). Hydrolysis is not expected to be an important environmental fate process since this compound lacks functional groups that hydrolyze under environmental conditions(7).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), sodium benzoate, which has an estimated vapor pressure of 2.9X10-12 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase sodium benzoate that is adsorbed to atmospheric aerosol 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 4.3 days(SRC), calculated from its rate constant of 3.7X10-12 cu cm/molecule-sec at 25 °C(3). Particulate-phase sodium benzoate may be removed from the air by wet and dry deposition(SRC).

In atmospheric hydroxyl radical reactivity tests of compounds adsorbed on aerosol materials, sodium benzoate had an OH rate constant of approximately 3.7X10-12 cu cm/molecule-sec at 25 °C(1). This corresponds to an atmospheric half-life of about 4.3 days at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(2). Sodium benzoate is expected to immediately dissociate and form the anion of benzoic acid in an aqueous environment(3). Sodium benzoate is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(4).

An estimated BCF of 3 was calculated in fish for sodium benzoate(SRC), using an estimated log Kow of -2.27(1) and a regression-derived equation(1). According to a classification scheme(2), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

Using a structure estimation method based on molecular connectivity indices(1), the Koc of sodium benzoate can be estimated to be 17(SRC). According to a classification scheme(2), this estimated Koc value suggests that sodium benzoate is expected to have very high mobility in soil.

Sodium benzoate dissociates in aqueous solution to the sodium cation and the benzoic acid anion and ions do not volatilize; therefore, volatilization from water surfaces or moist soil is not expected to be an important fate process(SRC). Sodium benzoate is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 2.9X10-12 mm Hg(SRC), determined from a fragment constant method(1).

Sodium benzoate is added directly to human food(1). It is used as a preservative in such foods as sauces, pickles, cider, fruit juices, wine coolers, syrups and concentrates, mincemeat and other acidic pie fillings, margarine, egg powder, fish (as a brine dip component), bottled carbonated beverages, and fruit preserves, jams, and jellies(1). The popularity of diet soft drinks has led to an increased demand(1).

According to the 2012 TSCA Inventory Update Reporting data, 17 reporting facilities estimate the number of persons reasonably likely to be exposed during the manufacturing, processing, or use of sodium benzoate (CAS 532-32-1) in the United States may be as low as <10 workers and as high as 100-499 workers per plant; the data may be greatly underestimated due to confidential business information (CBI) or unknown values(1).|Occupational exposure to sodium benzoate may occur through inhalation and dermal contact with this compound at workplaces where sodium benzoate is produced or used. Use data indicate that the general population may be exposed to sodium benzoate via ingestion of food and beverages and dermal contact with consumer products containing sodium benzoate. (SRC)

Antifungal Agents; Food Preservatives|Sodium phenylacetate and sodium benzoate is used as adjunctive therapy for the treatment of acute hyperammonemia and associated encephalopathy in patients with disorders (i.e., deficiencies in enzymes) of the urea cycle. Sodium phenylacetate and sodium benzoate is designated an orphan drug by the US Food and Drug Administration (FDA) for this use.|/EXPL THER/ In addition to dopaminergic hyperactivity, hypofunction of the N-methyl-d-aspartate receptor (NMDAR) has an important role in the pathophysiology of schizophrenia. Enhancing NMDAR-mediated neurotransmission is considered a novel treatment approach. To date, several trials on adjuvant NMDA-enhancing agents have revealed beneficial, but limited, efficacy for positive and negative symptoms and cognition. Another method to enhance NMDA function is to raise the levels of d-amino acids by blocking their metabolism. Sodium benzoate is a d-amino acid oxidase inhibitor. /The objective of this study was/ to examine the clinical and cognitive efficacy and safety of add-on treatment of sodium benzoate for schizophrenia. /The study consisted of/ a randomized, double-blind, placebo-controlled trial in 2 major medical centers in Taiwan composed of 52 patients with chronic schizophrenia who had been stabilized with antipsychotic medications for 3 months or longer. /Interventions included/ six weeks of add-on treatment of 1 g/d of sodium benzoate or placebo. The primary outcome measure was the Positive and Negative Syndrome Scale (PANSS) total score. Clinical efficacy and adverse effects were assessed biweekly. Cognitive functions were measured before and after the add-on treatment. Benzoate produced a 21% improvement in PANSS total score and large effect sizes (range, 1.16-1.69) in the PANSS total and subscales, Scales for the Assessment of Negative Symptoms-20 items, Global Assessment of Function, Quality of Life Scale and Clinical Global Impression and improvement in the neurocognition subtests as recommended by the National Institute of Mental Health's Measurement and Treatment Research to Improve Cognition in Schizophrenia initiative, including the domains of processing speed and visual learning. Benzoate was well tolerated without significant adverse effects. Benzoate adjunctive therapy significantly improved a variety of symptom domains and neurocognition in patients with chronic schizophrenia. The preliminary results show promise for d-amino acid oxidase inhibition as a novel approach for new drug development for schizophrenia.|/EXPL THER/ N-methyl-D-aspartate receptor (NMDAR)-mediated neurotransmission is vital for learning and memory. Hypofunction of NMDAR has been reported to play a role in the pathophysiology of Alzheimer disease (AD), particularly in the early phase. Enhancing NMDAR activation might be a novel treatment approach. One of the methods to enhance NMDAR activity is to raise the levels of NMDA coagonists by blocking their metabolism. This study examined the efficacy and safety of sodium benzoate, a D-amino acid oxidase inhibitor, for the treatment of amnestic mild cognitive impairment and mild AD. We conducted a randomized, double-blind, placebo-controlled trial in four major medical centers in Taiwan. Sixty patients with amnestic mild cognitive impairment or mild AD were treated with 250-750 mg/day of sodium benzoate or placebo for 24 weeks. Alzheimer's Disease Assessment Scale-cognitive subscale (the primary outcome) and global function (assessed by Clinician Interview Based Impression of Change plus Caregiver Input) were measured every 8 weeks. Additional cognition composite was measured at baseline and endpoint. Sodium benzoate produced a better improvement than placebo in Alzheimer's Disease Assessment Scale-cognitive subscale (p = .0021, .0116, and .0031 at week 16, week 24, and endpoint, respectively), additional cognition composite (p = .007 at endpoint) and Clinician Interview Based Impression of Change plus Caregiver Input (p = .015, .016, and .012 at week 16, week 24, and endpoint, respectively). Sodium benzoate was well-tolerated without evident side-effects. Sodium benzoate substantially improved cognitive and overall functions in patients with early-phase AD. The preliminary results show promise for D-amino acid oxidase inhibition as a novel approach for early dementing processes.|/EXPL THER/ A recent clinical study demonstrated that sodium benzoate (SB), a prototype competitive d-amino acid oxidase inhibitor, was effective in the treatment of several symptoms, such as positive and negative symptoms, and cognitive impairment in medicated patients with schizophrenia. The objective of the study was to examine the effects of SB on behavioral abnormalities such as pre-pulse inhibition (PPI) deficits and hyperlocomotion in mice after a single administration of the N-methyl-D-aspartate (NMDA) receptor antagonist, phencyclidine (PCP). The effects of SB on behavioral abnormalities (PPI deficits and hyperlocomotion) in mice after PCP administration were examined. Furthermore, effects of SB on tissue levels of amino acids were also examined. A single oral dose of SB (100, 300, or 1000 mg/kg) attenuated PPI deficits in mice after administration of PCP (3.0 mg/kg, s.c.) in a dose-dependent manner. In contrast, L-701,324 (10 mg/kg), an antagonist at the glycine site of the NMDA receptor, did not affect the effect of SB (1000 mg/kg) on PCP-induced PPI deficits. Furthermore, a single oral dose of SB (1000 mg/kg) significantly attenuated the hyperlocomotion in mice after administration of PCP (3.0 mg/kg, s.c.). However, a single oral dose of SB (1000 mg/kg) caused no changes to D-serine levels in plasma or in the frontal cortex, hippocampus, and striatum of these animals. This study suggests that SB induced antipsychotic effects in the PCP model of schizophrenia, although it did not increase D-serine levels in the brain.

At /the therapeutic/ dose level, clinical signs of toxicity are rare and in most cases limited to anorexia and vomiting, especially after intravenous bolus infusions.

Substances that destroy fungi by suppressing their ability to grow or reproduce. They differ from FUNGICIDES, INDUSTRIAL because they defend against fungi present in human or animal tissues. (See all compounds classified as Antifungal Agents.)|Substances capable of inhibiting, retarding or arresting the process of fermentation, acidification or other deterioration of foods. (See all compounds classified as Food Preservatives.)

Overall there are signs of systemic absorption via oral and dermal exposures, no evidence of target organs or of excretion. After oral ingestion and dermal absorption, the test substance will be metabolised to hippuric acid. Despite the low log Pow value, results of the 28-day study in rats and the predicted metabolism do not indicate a potential for the substance to bioaccumulate.|After oral ingestion of benzoic acid and sodium benzoate, there is a rapid absorption (of undissociated benzoic acid) from the gastrointestinal tract in experimental animals or humans. ... 100% absorption can be assumed. In humans, the peak plasma concentration is reached within 1-2 hr.|Hippuric acid is rapidly excreted in urine. In humans, after oral doses of up to 160 mg/kg body weight, 75-100% of the applied dose is excreted as hippuric acid within 6 hr after administration, and the rest within 2-3 days.|Experiments on the distribution and elimination of (14)C-benzoate in the rat have shown no accumulation of sodium benzoate or benzoic acid in the body.|For more Absorption, Distribution and Excretion (Complete) data for SODIUM BENZOATE (6 total), please visit the HSDB record page.

After oral and dermal uptake, benzoate is metabolized in the liver by conjugation with glycine, resulting in the formation of hippuric acid. The rate of biotransformation in humans is high: after oral doses of 40, 80 or 160 mg sodium benzoate/kg body weight, the transformation to hippuric acid was independent of the dose - about 17-29 mg/kg body weight per hour, corresponding to about 500 mg/kg body weight per day. Other /studies/ obtained higher values of 0.8-2 g/kg body weight per day.|Another metabolite of benzoate is the benzoyl glucuronide.|The metabolism of the benzoates depletes glycine concentrations and can therefore alter the glycine-dependent metabolism of other compounds. /A study/ demonstrated that ... sodium benzoate successfully competed with aspirin for glycine, resulting in increased concentration and persistence of salicyclic acid in the body.|This study underlines the importance of cinnamon, a widely-used food spice and flavoring material, and its metabolite sodium benzoate (NaB), a widely-used food preservative and a FDA-approved drug against urea cycle disorders in humans, in increasing the levels of neurotrophic factors [e.g., brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3)] in the CNS. NaB, but not sodium formate (NaFO), dose-dependently induced the expression of BDNF and NT-3 in primary human neurons and astrocytes. Interestingly, oral administration of ground cinnamon increased the level of NaB in serum and brain and upregulated the levels of these neurotrophic factors in vivo in mouse CNS. Accordingly, oral feeding of NaB, but not NaFO, also increased the level of these neurotrophic factors in vivo in the CNS of mice. NaB induced the activation of protein kinase A (PKA), but not protein kinase C (PKC), and H-89, an inhibitor of PKA, abrogated NaB-induced increase in neurotrophic factors. Furthermore, activation of cAMP response element binding (CREB) protein, but not NF-kappaB, by NaB, abrogation of NaB-induced expression of neurotrophic factors by siRNA knockdown of CREB and the recruitment of CREB and CREB-binding protein to the BDNF promoter by NaB suggest that NaB exerts its neurotrophic effect through the activation of CREB. Accordingly, cinnamon feeding also increased the activity of PKA and the level of phospho-CREB in vivo in the CNS. These results highlight a novel neutrophic property of cinnamon and its metabolite NaB via PKA - CREB pathway, which may be of benefit for various neurodegenerative disorders.

DJ-1 (PARK7) is a neuroprotective protein that protects cells from oxidative stress. Accordingly, loss-of-function DJ-1 mutations have been linked with a familial form of early onset Parkinson disease. Mechanisms by which DJ-1 level could be enriched in the CNS are poorly understood. Recently we have discovered anti-inflammatory activity of sodium benzoate (NaB), a metabolite of cinnamon and a widely-used food additive. Here we delineate that NaB is also capable of increasing the level of DJ-1 in primary mouse and human astrocytes and human neurons highlighting another novel neuroprotective effect of this compound. Reversal of DJ-1-inducing effect of NaB by mevalonate, farnesyl phosphate, but not cholesterol and ubiquinone, suggests that depletion of intermediates, but not end products, of the mevalonate pathway is involved in the induction of DJ-1 by NaB. Accordingly, either an inhibitor of p21(ras) farnesyl protein transferase (FPTI) or a dominant-negative mutant of p21(ras) alone was also able to increase the expression of DJ-1 in astrocytes suggesting an involvement of p21(ras) in DJ-1 expression. However, an inhibitor of geranyl geranyl transferase (GGTI) and a dominant-negative mutant of p21(rac) had no effect on the expression of DJ-1, indicating the specificity of the effect. Similarly lipopolysaccharide (LPS), an activator of small G proteins, also inhibited the expression of DJ-1, and NaB and FPTI, but not GGTI, abrogated LPS-mediated inhibition. Together, these results suggest that NaB upregulates DJ-1 via modulation of mevalonate metabolites and that p21(ras), but not p21(rac), is involved in the regulation of DJ-1.|This study underlines the importance of cinnamon, a widely-used food spice and flavoring material, and its metabolite sodium benzoate (NaB), a widely-used food preservative and a FDA-approved drug against urea cycle disorders in humans, in increasing the levels of neurotrophic factors [e.g., brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3)] in the CNS. NaB, but not sodium formate (NaFO), dose-dependently induced the expression of BDNF and NT-3 in primary human neurons and astrocytes. Interestingly, oral administration of ground cinnamon increased the level of NaB in serum and brain and upregulated the levels of these neurotrophic factors in vivo in mouse CNS. Accordingly, oral feeding of NaB, but not NaFO, also increased the level of these neurotrophic factors in vivo in the CNS of mice. NaB induced the activation of protein kinase A (PKA), but not protein kinase C (PKC), and H-89, an inhibitor of PKA, abrogated NaB-induced increase in neurotrophic factors. Furthermore, activation of cAMP response element binding (CREB) protein, but not NF-kappaB, by NaB, abrogation of NaB-induced expression of neurotrophic factors by siRNA knockdown of CREB and the recruitment of CREB and CREB-binding protein to the BDNF promoter by NaB suggest that NaB exerts its neurotrophic effect through the activation of CREB. Accordingly, cinnamon feeding also increased the activity of PKA and the level of phospho-CREB in vivo in the CNS. These results highlight a novel neutrophic property of cinnamon and its metabolite NaB via PKA - CREB pathway, which may be of benefit for various neurodegenerative disorders.

Fresh air, rest.

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.

If this chemical gets into the eyes, remove any contact lenses at once and irrigate immediately for at least 15 min, occasionally lifting upper and lower lids. Seek medical attention immediately. If this chemical contacts the skin, remove contaminated clothing and wash immediately with soap and water. Seek medical attention immediately. If this chemical has been inhaled, remove from exposure, begin rescue breathing (using universal precautions, including resuscitation mask) if breathing has stopped and CPR if heart action has stopped. Transfer promptly to a medical facility. When this chemical has been swallowed, get medical attention. Give large quantities of water and induce vomiting. Do not make an unconscious person vomit.

/HUMAN EXPOSURE STUDIES/ The information concerning skin reactions caused by benzoic acid or sodium benzoate in the general population is limited. In a study with 2045 patients of dermatological clinics, only 5 persons (approximately 0.2%) showed a positive reaction in patch tests, while 34 of 5202 patients (approximately 0.7%) with contact urticaria reacted positively. From these data, it can be concluded that skin reactions caused by benzoic acid or sodium benzoate in the healthy general population are rare.|/HUMAN EXPOSURE STUDIES/ In Europe amoxicillin plus clavulanic acid is the most commonly prescribed antibiotic and sodium benzoate is contained in the suspension formulation as a preservative. We studied the relevance of sodium benzoate as the culprit agent in a group of children with a history of adverse reactions to amoxicillin plus clavulanic acid suspension. A total of 89 children were enrolled over a period of 3 years (2006-2009). Single blind oral provocation tests (OPTs) with amoxicillin plus clavulanic acid, sodium benzoate and placebo were performed. 20 children with recurrent idiopathic urticaria were investigated as a control group. According to personal history: 70% of reactions were late in developing while 23% of reactions were immediate and for 5% of the cases it was not possible to define the timing. 8 children (8/89=9%) resulted positive to the provocation tests with amoxicillin plus clavulanic acid; ten children (10/89=11%) had positive results with sodium benzoate; 3% had a double positivity (i.e. excipient and active drug). The timing of reactions significantly differs between the Amoxicillin plus clavulanic acid and sodium benzoate groups (p=0.002). Sodium benzoate probably acts through a non-immunologic mechanism and care should be given to children allergic to sodium benzoate containing pharmaceutical formulations.|/SIGNS AND SYMPTOMS/ Cases of urticaria, asthma, rhinitis, or anaphylactic shock have been reported following oral, dermal, or inhalation exposure to benzoic acid and sodium benzoate. The symptoms appear shortly after exposure and disappear within a few hours, even at low doses.|/GENOTOXICITY/ Chromosome aberration test was carried out on sodium benzoate using human embryonic lung culture cells. Sodium benzoate produced no significant increase in the aberration frequency in the anaphase chromosomes when tested at the dosage levels 0, 2.0 ug/mL, 20 ug/mL and 200 g/mL.|For more Human Toxicity Excerpts (Complete) data for SODIUM BENZOATE (10 total), please visit the HSDB record page.

Benzoate, Sodium

Cough.

Rash.

Redness.

Grade: USP, FCC /Food Chemicals Codex/, technical.|National Formulary, Food Chemicals Codex dense powder, flake, low dusting dense beverage, granular and technical grades available.|It is then milled and classified into two product forms; dense granular and dense powder. Sodium Benzoate is also available in extruded form.

All other basic organic chemical manufacturing|Benzoic acid, sodium salt (1:1): ACTIVE

A rapid and sensitive fluorescence polarization immunoassay (FPIA), based on a polyclonal antibody, has been developed for the detection of sodium benzoate in spiked samples. The immunogen and fluorescein-labeled analyte conjugate were successfully synthesized, and the tracer was purified by TLC. Under the optimal assay conditions, the FPIA shows a detection range of 0.3-20.0 ug/mL for sodium benzoate with a detection limit of 0.26 ug/mL in the borate buffer. In addition, the IC50 value was 2.48 ug/mL, and the cross-reactivity of the antibodies with ten structurally and functionally related analogs were detected respectively. Four kinds of food samples (energy drink, candy, ice sucker, RIO(TM) cocktail) were selected to evaluate the application of FPIA in real systems. The recoveries were 96.68-106.55% in energy drink; 95.78-100.80% in candy, 86.97-102.70% in ice sucker, and 103.58-109.87% in benzoate contained sample RIO(TM) cocktail, and coefficients of variation of this method were all lower than 11.25%. Comparing with the detection results of HPLC, the developed FPIA has comparative performance in the real sample determination. The results suggest that the FPIA developed in this study is a rapid, convenient and simple method, which is suitable to be used as a screening tool for homogeneous detection of sodium benzoate in food products.|Potassium sorbate and sodium benzoate are food additives that are generally employed for prevention of food spoilage originating from bacteria, molds or yeasts. Although these compounds were generally recognized as safe due to their low risk of acute and chronic toxicity, they have limitations of usage to protect human health. Development and validation of a novel RP-HPLC method, in which a C18-bonded monolithic silica column was used as stationary phase to assay these compounds, is described for the first time. Aliquots of 10 uL of samples were injected into chromatograph and eluted using phosphate buffer (0.025 M, pH 2.0)-water-acetonitrile (50:45:5, v/v/v) solution, which was pumped at the rate of 3.0 mL/min. To sharpen the peaks, 10 mM octylamine was added to the mobile phase. Potassium sorbate and sodium benzoate were detected at about 12th and 14th min, respectively, and quantified at 230 nm using photodiode array detector. A total of 41 samples were prepared by simply filtering through 0.45 um filters after sonication, and injected into the system without any pre-treatment steps. Applicability of the method was demonstrated by performing total procedure on samples of different brands and types, and their compliance to official regulations was assessed.|Sodium benzoate in soda beverages using liquid chromatographic method.

EPA Safer Chemical Functional Use Classes -> Preservatives and Antioxidants|Safer Chemical Classes -> Green circle - The chemical has been verified to be of low concern|Food additives|Human drugs -> Rare disease (orphan)|Human Drugs -> FDA Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) -> Active Ingredients|Food Additives -> PRESERVATIVE; -> JECFA Functional Classes|Cosmetics -> Preservative

Food Additives -> PRESERVATIVE;