| GHS-Einstufung | This chemical does not meet GHS hazard criteria for 97.6% (946 of 969) of all reports.Not ClassifiedAggregated GHS information provided per 969 reports by companies from 4 notifications to the ECHA C&L Inventory.This chemical does not meet GHS hazard criteria for 100% (3 of 3) of all reports.Aggregated GHS information provided per 3 reports by companies from 1 notifications to the ECHA C&L Inventory. |
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| Regulatorische Informationen | Chemical: D-GlucoseD-Glucose is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of D-Glucose are required to report information about their production and use of this chemical to the EPA under the Toxic Substances Control Act (TSCA). (40 eCFR Part 711)D-Glucose: Does not have an individual approval but may be used under an appropriate group standard |
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| Weitere Sicherheitsinformationen | IMAP assessments - D-Glucose: Environment tier I assessment |
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| Brandgefahren | Combustible. Finely dispersed particles form explosive mixtures in air. |
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| Gesundheitsgefahren | No toxicity (USCG, 1999) |
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| FDA-Anforderungen | Substance added directly to human food affirmed as generally recognized as safe (GRAS). |
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| Reaktive Gruppe | Alcohols and Polyols |
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| EPA Safer Chemical | Chemical: D-Glucose |
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| FIFRA-Anforderungen | Unless specifically excluded, residues resulting from the use of the following substance as either an inert or an active ingredient in a pesticide chemical formulation, including antimicrobial pesticide chemicals, is exempted from the requirement of a tolerance under FFDCA section 408, if such use is in accordance with good agricultural or manufacturing practices. Dextrose is included on this list. |
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| Reactivity Profile | A weak reducing agent. |
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| Chemical Dangers | Reacts violently with strong oxidants. |
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| Physical Dangers | Dust explosion possible if in powder or granular form, mixed with air. |
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| Air and Water Reactions | Water soluble. |
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| Brandbekämpfung | Use water spray, powder, foam, carbon dioxide. |
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| Erste-Hilfe-Maßnahmen | Fresh air, rest.First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.Rinse mouth. |
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| Erste Hilfe | None needed (USCG, 1999) |
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| Sichere Lagerung | Separated from strong oxidants. Well closed. |
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| Brandbekämpfungsverfahren | 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.For any fire, wear a self-contained breathing apparatus (SCBA) in pressure-demand, MHSA/NIOSH (approved or equivalent), and full protective gear. ... On fire use water spray, dry chemical, carbon dioxide, or appropriate foam. |
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| Lagerbedingungen | Keep container tightly closed in a dry and well-ventilated place. Hygroscopic. Keep in a dry place.General storage may be used. Store in a cool, dry, well-ventilated area away from strong oxidizers, strong acids. |
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| Reinigungsverfahren | ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Avoid dust formation. Avoid breathing vapors, mist or gasEnvironmental precautions: No special environmental precautions requiredMethods and materials for containment and cleaning up: Sweep up and shovel. Keep in suitable, closed containers for disposal.Provide adequate ventilation. Avoid generating dust. Vacuum or sweep up material and place into a suitable disposal container. Clean up spills immediately, using the appropriate protective equipment. |
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| Entsorgungsverfahren | SRP: Expired or waste pharmaceuticals shall carefully take into consideration applicable DEA, EPA, and FDA regulations. It is not appropriate to dispose by flushing the pharmaceutical down the toilet or discarding to trash. If possible return the pharmaceutical to the manufacturer for proper disposal being careful to properly label and securely package the material. Alternatively, the waste pharmaceutical shall be labeled, securely packaged and transported by a state licensed medical waste contractor to dispose by burial in a licensed hazardous or toxic waste landfill or incinerator.Product: Offer surplus and non-recyclable solutions to a licensed disposal companyContaminated packaging: Dispose of as unused product.SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices. |
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| Verschüttetes entsorgen | Sweep spilled substance into covered containers. Wash away remainder with plenty of water. |
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| Preventive Measures | Precautions for safe handling: 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: General industrial hygiene practice.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. |
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| Eye Prevention | Wear safety goggles. |
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| Fire Prevention | NO open flames. Closed system, dust explosion-proof electrical equipment and lighting. Prevent deposition of dust. |
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| Körperbelastung | Normal human blood contains 0.08-0.1% D(+)-glucose(1). |
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| Treatment | Treatment involves a healthy diet, physical exercise, not using tobacco, and being a normal body weight. Blood pressure control and proper foot care are also important for people with the disease. Type 1 diabetes must be managed with insulin injections. Type 2 diabetes may be treated with medications with or without insulin. |
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| Wechselwirkungen | Recent studies suggest that meat intake is associated with diabetes-related phenotypes. However, whether the associations of meat intake and glucose and insulin homeostasis are modified by genes related to glucose and insulin is unknown. We investigated the associations of meat intake and the interaction of meat with genotype on fasting glucose and insulin concentrations in Caucasians free of diabetes mellitus. Fourteen studies that are part of the Cohorts for Heart and Aging Research in Genomic Epidemiology consortium participated in the analysis. Data were provided for up to 50,345 participants. Using linear regression within studies and a fixed-effects meta-analysis across studies, we examined 1) the associations of processed meat and unprocessed red meat intake with fasting glucose and insulin concentrationsand 2) the interactions of processed meat and unprocessed red meat with genetic risk score related to fasting glucose or insulin resistance on fasting glucose and insulin concentrations. Processed meat was associated with higher fasting glucose, and unprocessed red meat was associated with both higher fasting glucose and fasting insulin concentrations after adjustment for potential confounders [not including body mass index (BMI)]. For every additional 50-g serving of processed meat per day, fasting glucose was 0.021 mmol/L (95% CI: 0.011, 0.030 mmol/L) higher. Every additional 100-g serving of unprocessed red meat per day was associated with a 0.037-mmol/L (95% CI: 0.023, 0.051-mmol/L) higher fasting glucose concentration and a 0.049-ln-pmol/L (95% CI: 0.035, 0.063-ln-pmol/L) higher fasting insulin concentration. After additional adjustment for BMI, observed associations were attenuated and no longer statistically significant. The association of processed meat and fasting insulin did not reach statistical significance after correction for multiple comparisons. Observed associations were not modified by genetic loci known to influence fasting glucose or insulin resistance. The association of higher fasting glucose and insulin concentrations with meat consumption was not modified by an index of glucose- and insulin-related single-nucleotide polymorphisms.Recent studies demonstrated an adverse effect of chronic exposure to air pollution (AP) on metabolic syndrome and its components. In a population-based study, we investigated the association between exposure to ambient AP and serum glucose (SG), among subjects with normal glucose, impaired fasting glucose (IFG), and diabetes mellitus (DM).We included 1,063,887 SG tests performed in 131,882 subjects (years 2001-2012). Exposure data included daily levels of SO2, NO2 and other pollutants of industrial, traffic, and nonanthropogenic sources. Demographical, clinical, and medications purchase data were assessed. Log-transformed SG levels were analyzed by linear mixed models adjusted for seasonal variables and personal characteristics.SG increases (%increase [95% CI]), among subjects with normal glucose, IFG, and DM, respectively, were associated with 6.36 ?ppb increase of NO2 measured 24 to 72? hours before the test (0.40% [0.31%0.50%], 0.56% [0.40%0.71%], and 1.08% [0.86%1.29%])and with 1.17?ppb increase of SO2 measured 24 ?hours before the test (0.29% [0.22%0.36%], 0.20% [0.10%0.31%], and 0.33% [0.14%0.52%]). Among DM population, weakest association was observed among patients treated with Metformin (0.56% increase in SG [0.18%0.95%]). In conclusion, NO2 and SO2 exposure is associated with small but significantly increased levels of SG. Although DM patients were found to be more susceptible to the AP induced SG variations, Metformin treatment seem to have a protective effect. Given the chronic lifetime exposure to AP and the broad coverage of the population, even small associations such as those found in our study can be associated with detrimental health effects and may have profound public health implications.Maternal diabetes-induced birth defects remain a significant health problem. Studying the effect of natural compounds with antioxidant properties and minimal toxicities on diabetic embryopathy may lead to the development of new and safe dietary supplements. Punicalagin is a primary polyphenol found in pomegranate juice, which possesses antioxidant, anti-inflammatory and anti-tumorigenic properties, suggesting a protective effect of punicalagin on diabetic embryopathy. Here, we examined whether punicalagin could reduce high glucose-induced neural tube defects (NTDs), and if this rescue occurs through blockage of cellular stress and caspase activation. Embryonic day 8.5 (E8.5) mouse embryos were cultured for 24 or 36 hr with normal (5 mM) glucose or high glucose (16.7 mM), in presence or absence of 10 or 20 uM punicalagin. 10 uM punicalagin slightly reduced NTD formation under high glucose conditionshowever, 20 uM punicalagin significantly inhibited high glucose-induced NTD formation. Punicalagin suppressed high glucose-induced lipid peroxidation marker 4-hydroxynonenal, nitrotyrosine-modified proteins, and lipid peroxides. Moreover, punicalagin abrogated endoplasmic reticulum stress by inhibiting phosphorylated protein kinase ribonucleic acid (RNA)-like ER kinase (p-PERK), phosphorylated inositol-requiring protein-1alpha (p-IRE1alpha), phosphorylated eukaryotic initiation factor 2alpha (p-eIF2alpha), C/EBP-homologous protein (CHOP), binding immunoglobulin protein (BiP) and x-box binding protein 1 (XBP1) mRNA splicing. Additionally, punicalagin suppressed high glucose-induced caspase 3 and caspase 8 cleavage. Punicalagin reduces high glucose-induced NTD formation by blocking cellular stress and caspase activation. These observations suggest punicalagin supplements could mitigate the teratogenic effects of hyperglycemia in the developing embryo, and possibly prevent diabetes-induced NTDs. |
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| Gesundheitliche Auswirkungen | High blood glucose (>7 mM) produces the symptoms of frequent urination, increased thirst, and increased hunger. Chronic exposure to high blood glucose (i.e. untreated diabetes) can cause many complications. Acute complications include diabetic ketoacidosis (characterized by nausea, vomiting and abdominal pain, the smell of acetone on the breath) and nonketotic hyperosmolar coma. Serious long-term complications include heart disease, stroke, kidney failure, foot ulcers and damage to the eyes. The major long-term complications relate to damage to blood vessels. Diabetes doubles the risk of cardiovascular disease and about 75% of deaths in diabetics are due to coronary artery disease. Other "macrovascular" diseases are stroke, and peripheral vascular disease. The primary microvascular complications of diabetes include damage to the eyes, kidneys, and nerves. Damage to the eyes, known as diabetic retinopathy, is caused by damage to the blood vessels in the retina of the eye, and can result in gradual vision loss and potentially blindness. Damage to the kidneys, known as diabetic nephropathy, can lead to tissue scarring, urine protein loss, and eventually chronic kidney disease, sometimes requiring dialysis or kidney transplant. Damage to the nerves of the body, known as diabetic neuropathy, is the most common complication of diabetes. The symptoms can include numbness, tingling, pain, and altered pain sensation, which can lead to damage to the skin. Diabetes-related foot problems (such as diabetic foot ulcers) may occur, and can be difficult to treat, occasionally requiring amputation. Gestational diabetes can damage the health of the fetus or mother. Risks to the baby include macrosomia (high birth weight), congenital cardiac and central nervous system anomalies, and skeletal muscle malformations. Increased fetal insulin may inhibit fetal surfactant production and cause respiratory distress syndrome. Hyperbilirubinemia may result from red blood cell destruction. |
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| Umweltverhalten | TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 10(SRC), determined from a structure estimation method(2), indicates that D(+)-glucose is expected to have very high mobility in soil(SRC). Volatilization of D(+)-glucose from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 3.5X10-20 atm-cu m/mole(SRC), derived from its vapor pressure, 8X10-14 mm Hg(3), and water solubility, 5.46X10+5 mg/L(4). D(+)-Glucose is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(3). D(+)-Gglucose absorbs at wavelengths >290 nm(5) and, therefore, may be susceptible to direct photolysis by sunlight on soil surfaces(SRC). The dominant fate process in soil is expected to be biodegradation(SRC). Various screening studies have found D(+)-glucose to be readily biodegrade(6-10). Soil half-lives on the order of 1 day are reported(7), but a range of 0.25-19 days has also been observed(11).AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 10(SRC), determined from a structure estimation method(2), indicates that D(+)-glucose is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 3.5X10-20 atm-cu m/mole(SRC), derived from its vapor pressure, 8X10-14 mm Hg(4), and water solubility, 5.46X10+5 mg/L(5). According to a classification scheme(6), an estimated BCF of 3(SRC), from its log Kow of -3.00(6) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Various screening studies have found D(+)-glucose to be readily biodegrade(8-12). A biodegradation half-life of about one day was reported for aquifer material(9). Hydrolysis is not expected to be an important environmental fate process since this compound lacks functional groups that hydrolyze under environmental conditions(3).ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), D(+)-glucose, which has a vapor pressure of 8X10-14 mm Hg at 25 °C(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase D(+)-glucose may be removed from the air by wet and dry deposition(SRC). D(+)-Glucose absorbs at wavelengths >290 nm(3) and, therefore, may be susceptible to direct photolysis by sunlight(SRC). |
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| Lebensmitteluntersuchungswerte | The D(+)-glucose concentration in varietal grape juices from 56 Canadian cultivars pressed in the 1988-1989 season ranged from 4.91 to 9.99 g/100 mL(1). The D(+)-glucose concentration in five prunes juices obtained from markets in Davis, CA ranged from 4.35 to 11.60 g/100 mL juice(2). The D(+)-glucose concentration in fresh apple, cherry, grape, nectarine, peach, pear, plum, kiwi fruit and strawberry juices (California-grown) were 2.14, 7.50, 9.59, 0.85, 0.67, 1.68, 4.28, 6.94 and 1.80 g/100 mL juice, respectively(2). |
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| Expositionspfade | The substance can be absorbed into the body by ingestion. |
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| Milk Concentrations | ENVIRONMENTAL: Glucose levels in 188 quarter for milks from different cows were determined by an enzymic procedure. Mean glucose content was 0.22 mM (standard error +/- 0.009) and results ranged from 0.02-0.57 mM. Abnormal quarters had lower glucose levels (P less than 0.01) than normal quarters but variability within each classification was large. Glucose content was negatively correlated with both somatic cell count (r = 0.49) and N-acetyl-beta-D-glucosaminidase level (r = -0.61). Milk glucose was considered to be of limited value as a diagnostic test for mastitis. |
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| Toxizitätsübersicht | 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.orgIDENTIFICATION AND USE: Glucose forms colorless crystals or white granular powder. It is used in confectionary, infant foods, medicine, brewing and wine making, caramel coloring, baking and canning, source of methane by anaerobic fermentation, source of certain amino acids by fermentation. A principal industrial fermentation use of glucose is for the production of fuel ethanol as an oxygenate or octane enhancer. Glucose is hydrogenated to sorbitol for use in various food and nonfood applications. Liquid glucose is an ingredient of Cocoa Syrup, It is used as a tablet binder and coating agent, and as a diluent in pilular extractsit has replaced glycerin in many pharmaceutical preparations. It is sometimes given per rectum as a food in cases when feeding by stomach is impossible. It should not be used in the place of dextrose for intravenous injection. HUMAN EXPOSURE AND TOXICITY: Normal fasting blood-sugar values for adults are 80 to 120 mg/dLtrue glucose is 65 to 100 mg/dL. When the blood-sugar values exceed 120 (hyperglycemia), diabetes mellitus should be suspected and can be confirmed by evidence of diminished carbohydrate tolerance. Hyperglycemia and decreased glucose tolerance are seen in diabetes mettilus (to 500 mg/dL) and hyperactivity of the adrenal, pituitary, and thyroid glands. Hypoglycemia, with a blood-sugar value of <60 mg/dL and increased glucose tolerance, is encountered in insulin overdose, glucagon deficiencies, and hypoactivity of various endocrine glands. Injection of 5% soln into superficial temporal artery caused edema of eyelids, protrusion of eye, inability to move eye, necrosis of soft tissues and opacification of cornea. In one of the eyes, extensive atrophy of temporal half of choroid was observed. Maternal hyperglycemia may lead to an increased fetal lactate production resulting in metabolic acidosis. Fetal glucose excess may stimulates fetal oxidative metabolism with increases in fetal glucose and lactate entry and stimulation of fetal oxygen consumption. ANIMAL STUDIES: Calves fed with a mixture of glucose and milk substitute in the ratio of 2:1 instead of the recommended 1:1 showed depression and diarrhea, with four animals dying overnight. The post-mortem findings included dehydration, sunken eyes, congested abomasal mucosa, and distended intestines. The lungs were congested and the urinary bladder distended, the urine having a glucose content of over 0.5 g/dL. It was found that hyperglycemia increases the threshold for shivering, whereas hypoglycemia lowers the threshold on rabbits. In developmental studies in mice it was found that maternal diabetes and high glucose in vitro induce DNA damage and activates DNA damage response through oxidative stress, which may contribute to the pathogenesis of diabetes-associated embryopathy.Very high serum levels of glucose are found in untreated diabetic (type I or type II) patients. Glucose in chronic excess causes toxic effects on the structure and function of many cells and organs, including the pancreas and pancreatic islet cells. Multiple biochemical pathways and mechanisms of action for glucose toxicity have been suggested. These include glyceraldehyde auto-oxidation, protein kinase C activation, methylglyoxal formation and glycation, hexosamine metabolism, sorbitol formation, and oxidative phosphorylation. All these pathways have in common the formation of reactive oxygen species that, in excess and over time, cause chronic oxidative stress, which in turn causes defective insulin gene expression and insulin secretion as well as increased apoptosis. Exposure of endothelial cells to high glucose causes GAPDH inhibition through reactive oxygen species-activated poly(ADP-ribosyl)ation of GAPDH by poly(ADP-ribose) polymerase. Three products from glucose metabolism (glyoxal, methylglyoxal, and 3-deoxyglucosone) form advanced glycation end products (AGEs) by reacting with amino groups on intracellular and extracellular proteins. AGEs play important roles in the pathogenesis of secondary complications of diabetes, especially with regard to microvascular disease in the retina, nerves, and kidney and likely islets. Glycated hemoglobin is a particularly important AGE. A 1% increase in absolute concentrations of glycated hemoglobin is associated with about 10-20% increase in cardiovascular disease risk. |
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| Plant Concentrations | D(+)-Glucose levels in some plants(1).d-Glucose has been identified in 37 plants. Levels in some plants are as follows(1): /d-Glucose/[Table#1353] |
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| Ongoing Test Status | EPA has released the Interactive Chemical Safety for Sustainability (iCSS) Dashboard. The iCSS Dashboard provides an interactive tool to explore rapid, automated (or in vitro high-throughput) chemical screening data generated by the Toxicity Forecaster (ToxCast) project and the federal Toxicity Testing in the 21st century (Tox21) collaboration. /The title compound was tested by ToxCast and/or Tox21 assays/[USEPAICSS Dashboard ApplicationAvailable from, as of December 17, 2015: http://actor.epa.gov/dashboard/] |
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| Effluent Concentrations | D(+)-Glucose as alpha- and beta-form was present in open burn smoke particulate matter at 7.9, 12.4 and 48.4 ng/mg smoke particles from open-burning of plastic shopping bags, roadside trash and landfill garbage, respectively, in Concon Chile. It was not detected in particulate matter smoke from burning new plastic shopping bags from the United States. It was not detected in any of the plastic surface extracts prior to burning(1). |
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| Alarmwort | Warnung |
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| Gefahrenhinweise | Code Gefahrenhinweise Gefahrenklasse Abteilung Alarmwort Symbol P-Code H302 |
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