Calcium carbonate

100.08700

99.94730

615-782-4

H0G9379FGK

1193

DTXSID3036238|DTXSID9050486|DTXSID80163829

C332

White hexagonal crystals or powder (Calcite); white orthrombic crystals or powder (Argonite); colorless hexagonal crystals (vaterite)

A - Alimentary tract and metabolism

2836500000

63.19000

-2.44700

White-beige to slightly beige-gray random crystals

2.8 g/cm³

825 °C (decomp)

800 °C

197ºC

1.6583

H2O: Insoluble

Low temperature, ventilation, drying

0 mmHg (approx)

LD50 orally in Rabbit: 6450 mg/kg LD50 dermal Rat > 2000 mg/kg

Noncombustible Solid

Odorless

Chalky taste

pH = 8 to 9

Very flowable ... surface treated with fatty acids, hydrophobic|Enthalpy of Fusion: 36 kJ/mol at 800 °C (calcite)|Incompatibilities: acids, alum, ammonium salts.|White microcrystalline powder; mw: 100.09; mp: 825 °C (alpha), 1339 °C (beta) at 102.5 atm; density: 2.7-2.95. Odorless, tasteless powder or crystals. /Limestone/|Aragonite is metastable and irreversibly changes to calcite when heated in dry air to about 400 °C. Vaterite is metastable to calcite and aragonite under geological conditions but is found during high temperature precipitation of calcium carbonate.|MP: 1339 °C (102.5 atm); density: 2.7111 at 25.2 °C; formed at temperatures below 30 °C /Calcite/|White hexagonal crystals or powder. Decomposes at 700 to 900 °C. Density: 2.710 g/cu cm. Solubility: 6.6X10-4 g/100 g water at 20 °C; Soluble in dilute acid /Calcite/|Mohs hardness: 3.0 (Calcite); 3.5-4.0 (Argonite)|White orthorhombic crystals or powder; MP: trans calcite, 450 °C; density: 2.930 g/cu cm; solubility: 6.6X10-4 g/100 g water at 20 °C; soluble in dilute acid /Argonite/|MP: 825 °C (decomposes); Density: 2.83; Formed at temp above 30 °C /Aragonite/|Colorless hexagonal crystals; density: 2.653 g/cu cm; solubility: 1.1X10-3 g/100 g water at 20 °C; soluble in dilute acid /Vaterite/

No rapid reaction with air No rapid reaction with water

Carbonate Salts

CALCIUM CARBONATE is non-combustible. Decomposes at high temperature (825°C) to give gaseous carbon dioxide and calcium oxide (quicklime). Incompatible with acids, alum, ammonium salts, fluorine, magnesium. Reacts with acids and acidic salts to generate gaseous carbon dioxide with effervescence (bubbling). The reaction with concentrated solutions of acids is rapid and exothermic. The effervesence can create extensive foaming. Ignites on contact with fluorine.

Noncombustible Solid

Non-corrosive

NONH for all modes of transport

-

R36/37/38; R41

S26-S36/37/39-S37/39

FF9335000

Xi

Separated from acids, aluminium, ammonium salts, fluorine and magnesium.

Stable. Incompatible with acids, fluorine, ammonium salts, alum.

P201, P202, P260, P261, P264, P270, P271, P280, P281, P302+P352, P304+P340, P305+P351+P338, P308+P313, P310, P312, P314, P321, P332+P313, P337+P313, P362, P403+P233, P405, P501

H315

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure or environmental contamination. 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 soil or water; effects on animal, aquatic, and plant life; and conformance with environmental and public health regulations.

Calcium carbonate ... ignite and burn fiercely in contact with fluorine. /Fluorine: metal salts/|When a mixture of magnesium and calcium carbonate is heated in a current of hydrogen, a violent explosion occurs. /Magnesium: hydrogen and calcium carbonate/|Calcium carbonate reacts with acids with evolution of carbon dioxide and heat (reported to be about 19 kJ/mol in hydrochloric acid).|Acids, alum, ammonium salts, mercury & hydrogen, fluorine, magnesium.

Certification of this color additive when used as a color additive in drugs is not necessary for the protection of the public health, and therefore batches thereof are exempt from the certification pursuant to section 721(c) of the act.|An ingredient whose use in food or food packaging is subject to a prior sanction or approval within the meaning of section 201(s)(4) of the Act is exempt from classification as a food additive. ... Substances classified as stabilizers, when migrating from food-packaging material shall include: ... calcium carbonate.|Substance added directly to human food affirmed as generally recognized as safe (GRAS).|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: calcium carbonate is included in antidiarrheal drug products.|For more FDA Requirements (Complete) data for CALCIUM CARBONATE (8 total), please visit the HSDB record page.

Optimal Calcium Uptake. Current Bibliographies in Medicine 94-4. Public Services Division/National Library of Medicine. 775 citations from January, 1990-April, 1994.[Available from, as of April 4, 2003: http://www.nlm.nih.gov/pubs/cbm/calcium.html]

Not combustible.

|Danger|H315 (94.64%): Causes skin irritation [Warning Skin corrosion/irritation]|P261, P264, P271, P280, P302+P352, P304+P340, P305+P351+P338, P310, P312, P321, P332+P313, P337+P313, P362, P403+P233, P405, and P501|Aggregated GHS information provided by 3269 companies from 25 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.|Not Classified

Skin: No recommendation is made specifying the need for personal protective equipment for the body. Eyes: No recommendation is made specifying the need for eye protection. Wash skin: No recommendation is made specifying the need for washing the substance from the skin (either immediately or at the end of the work shift). Remove: No recommendation is made specifying the need for removing clothing that becomes wet or contaminated. Change: No recommendation is made specifying the need for the worker to change clothing after the work shift. (NIOSH, 2016)|Use local exhaust.|Protective gloves. Wear safety spectacles.|(See protection codes)

Not combustible.

In case of fire in the surroundings, use appropriate extinguishing media.

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

SRP: The scientific literature for the use of contact lenses by industrial workers is inconsistent. The benefits or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.|Do not eat, drink, or smoke during work.

Permissible Exposure Limit: Table Z-1 8-Hr Time Weighted Avg: 15 mg/cu m, total dust. /Calcium carbonate, RN 1317-65-3/|Permissible Exposure Limit: Table Z-1 8-Hr Time Weighted Avg: 5 mg/cu m, respirable fraction. /Calcium carbonate, RN 1317-65-3/

Recommended Exposure Limit: 10 Hour Time-Weighted Average: 10 mg/cu m (total); 5 mg/cu m (respirable fraction).

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

Separated from acids, aluminium, ammonium salts, fluorine and magnesium.

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

May cause mechanical irritation to the respiratory tract and eyes.

Health effects of the substance have been investigated but none have been found

Avoid inhalation of dust. Use local exhaust.

Protective gloves.

Wear safety goggles.

SEDIMENT: Calcium carbonate concentrations in core samples from the Southern California Bight(1).[Table#2467]|SEDIMENT: Calcium carbonate range concentrations were reported as 4.9-85.2, 67.5-90.7, and 67.2-94.3 mg/kg in the sediments of Geothermal Springs, Mangrove Lagoon and the Santispac Bight, Baha Concepcion, Baja California Peninsula, respectively(1).

The PM2.5 samples of dust collected 1 and 2 days following the World Trade Center collapse on September 11, 2001 were alkaline and composed primarily of calcium-based compounds such as calcium sulfate (gypsum) calcium carbonate (calcite), which were attributed to crushed building materials such as cement, concrete aggregate, ceiling tiles, and wallboard(1).

... A mixture of 2 parts magnesium oxide and 1 part calcium carbonate produces relatively normal stool for many patients.|Milk-alkali syndrome may occur after prolonged admin of calcium carbonate with concomitant use of sodium bicarbonate and/or homogenized milk containing Vit D.|Certain anions in antacids (carbonate and hydroxide) ... are thought to form insoluble complexes when combined with iron. A study evaluating the effect of antacids and iron absorption used patients with mild iron deficiency and found that when Mylanta II (5 mL) was given with 10 mg of iron, the increase in plasma iron seen two hours after the dose was not significantly different from the iron level seen two hours after a control dose. ... calcium carbonate 500 mg also decreased the two-hour plasma levels, with serum iron levels attaining only one-third of the control dose.|Concurrent use of excessive amounts of /alcohol, caffeine (usually more than 8 cups of coffee a day), or tobacco/ has been reported to decrease calcium absorption.|For more Interactions (Complete) data for CALCIUM CARBONATE (45 total), please visit the HSDB record page.

LD50 Mouse oral 6450 mg/kg bw|LD50 Rat oral 6450 mg/kg

/AQUATIC SPECIES/ This study was undertaken to determine whether calcium could render any protection against copper (Cu) toxicity in Nile tilapia with emphasis on histopathological and histochemical analysis. The copper LC50 values for 24, 48, 72, and 96 hr to tilapia in the laboratory were 210.27, 213.34, 193.30, and 185. 75 mg/L, respectively. Prior to Cu exposure, fish were exposed to 0 (G1 and G3) and 30 mg/L calcium carbonate (G2 and G4) for 4 days. After that, fish were exposed to 46 mg/L copper, which corresponds to 25% of the 96 hr LC50 (G3 and G4) for 96 hr and 7 days. In the gills of the copper treatment group, primary filament cell hyperplasia, epithelial lifting, or edema, secondary lamellar fusion, and aneurysm were observed. Swollen hepatocytes showing vacuoles and congestion in sinusoids were observed. Necrosis was observed in some areas. In the kidney, glomerulus's atrophy, tubular swelling, and also necrosis were seen. Fish that were pre-exposed to calcium showed slight alteration when compared to copper alone-treatment groups. Histochemical staining for calcium and copper by alizarin red S and rhodanine staining, respectively, indicated no accumulation of calcium and copper in kidney, liver, gills, and muscle. In conclusion, calcium appears to be beneficial in reducing the effects of heavy metal contaminations in aquatic organisms.|/AQUATIC SPECIES/ To determine the effects of water hardness on the toxicities of cobalt (Co) and nickel (Ni) to a freshwater fish, Capoeta fusca. Toxicity was investigated by static bioassay. Fish were exposed to cobalt (as CoCl2) and nickel (as NiCl2) for 96 hr in waters with two levels of hardness ("hard" and "very hard", nominally 130 mg/L and 350 mg/L as CaCO3, respectively). Water hardness had a significant effect on the acute toxicity of both elements. The 96 hr LC50 values for Co were 91.7 mg/L and 204.8 mg/L in hard and very hard waters, respectively, and for Ni the 96 hr LC50 values were 78.0 mg/L and 127.2 mg/L, respectively. The fish were more sensitive to Co and Ni toxicity in hard water than in very hard water; very hard water protects C. fusca against the toxicity of Co and Ni.|/AQUATIC SPECIES/ The potential modifying effects of certain water quality parameters (e.g., hardness, alkalinity, pH) on the acute toxicity of boron were tested using a freshwater cladoceran, Ceriodaphnia dubia. By comparison, boron acute toxicity was less affected by water quality characteristics than some metals (e.g., copper and silver). Increases in alkalinity over the range tested did not alter toxicity. Increases in water hardness appeared to have an effect with very hard waters (>500 mg/L as CaCO3)...|/AQUATIC SPECIES/ In this study, the toxicity of mercuric chloride (HgCl2), an important pollutant threatening water resources for many years, and the effects of water temperature and hardness on the toxicity in cultured rainbow trout Oncorhynchus mykiss (4.79 +/- 0.16 g; 7.38 +/- 0.24 cm; mean +/- SD) were investigated at different temperatures (12 and 17 °C) and hardness concentrations (35, 70 and 120 mg/ L as calcium carbonate, CaCO3). For this purpose, the acute toxicity tests were performed by 96-hr static tests in different water temperatures and water hardness concentrations. For acute toxicity tests, solutions ranging from 0.4 to 1.2 mg/L were used at 12 °C and solutions ranging from 0.4 to 1.0 mg/L at 17 °C. The LC50 values of HgCl2 that killed 50% of rainbow trout within 96 hr in the hardness concentrations of 35, 70 and 120 mg/L CaCO3 were calculated using probit analysis, and were found to be 0.725, 0.788, 0.855 mg/L at 12 °C and 0.670, 0.741, 0.787 mg/L at 17 °C, respectively. Consequently, the toxicity of HgCl2 on rainbow trout decreased when the temperature decreased from 17 to 12 °C. Toxicity increased when the hardness decreased from 120 to 35 mg/L CaCO3. In contrast to temperature, water hardness presents a negative effect on the toxicity of HgCl2.|For more Ecotoxicity Excerpts (Complete) data for CALCIUM CARBONATE (9 total), please visit the HSDB record page.

About 15% of orally admin Ca+2 is absorbed, causing a transient hypercalcemia. Although not a problem in normal patients, the hypercalcemia from as little as 3 to 4 g per day can be problematic in patients with uremia ... /Antacids/|Ingestion of large quantities of a Ca+2 salt does not generally by itself cause hypercalcemia, an exception being patients with hypothyroidism, who absorb Ca+2 with increased efficiency. Also the uncommon hypercalcemic disorder called milk-alkali syndrome is caused by concurrent ingestion of large quantities of milk and alkalinizing powders, in which setting renal Ca+2 excretion is impaired. /Hypercalcemic States/|Concurrent use /of other calcium-containing medications or oral magnesium-containing medications/ with calcium supplements may increase serum calcium or magnesium concentration in susceptible patients, mainly patients with impaired renal function, leading to hypercalcemia or hypermagnesemia, respectively. /Calcium supplements/

Calcium acts as a co-factor to numerous enzymes.

EGG SHELLS ARE 94% CALCIUM CARBONATE. LIMESTONE...IS NATURAL SOURCE OF TECHNICAL OR AGRICULTURAL GRADES.|Calcium carbonate ... occurs naturally as the principal constituent of limestone, marble and chalk|Calcium carbonate /is present in/ ... oyster shells and dolomite|Exists in nature as minerals aragonite, calcite and vaterite. Two crystal forms are of commercial importance: aragonite, orthorhombic...calcite hexagonal-rhombohedral...|The solubility of calcium carbonate in water containing carbon dioxide causes the formation of caves with stalactites and stalagmites and is responsible for hardness in water

NIOSH (NOES Survey 1981-1983) has statistically estimated that 2,341,639 workers (392,183 of these were female) were potentially exposed to calcium carbonate in the US(1). The survey statistically estimated that 20,008 workers (656 of these were female) were potentially exposed to marble dust in the US(1). The survey statistically estimated that 6,239 workers (2,955 of these were female) were potentially exposed to calcium carbonate powder in the US(1). The NOES Survey does not include farm workers. Occupational exposure to calcium carbonate may occur through inhalation and dermal contact with this compound at workplaces where calcium carbonate is produced or used. Use data indicate that the general population may be exposed to calcium carbonate via ingestion of certain foods and pharmaceuticals and dermal contact with this consumer containing calcium carbonate(SRC).

For relief of heartburn and acid indigestion. May also be used as a nutritional supplement or to treat hypocalcemia.|Prevention of skeletal related events in patients with advanced malignancies involving bone|Combination treatment of osteoporosis

Mesh Heading: Antacids|/EXPL THER/ The aim of the present study was to test the hypothesis that a fibrin matrix enhances the osteogenic differentiation and expression of vascular endothelial growth factor (VEGF) by human bone marrow stromal cells (hBMSCs) seeded into mineralised scaffolds. Porous calcium carbonate scaffolds were droplet seeded with hBMSCs using a matrix containing 3 % fibrinogen and cultured for 3 weeks. Seeded scaffolds without the fibrin matrix served as controls. The scaffolds were evaluated, using undecalcified thick sections, for fluorescence staining for nuclei, osteocalcin (OC) and VEGF. The sections were systematically scanned using optical sectioning and three dimensional distributions of cells and positive staining indicating expression of OC and VEGF were reconstructed from the z-stacks. The fibrin matrix maintained a significantly higher level of cell numbers after 2 d and 1 week and delayed the onset of osteogenic differentiation while sustaining a significantly higher level of OC and VEGF expression after 2 and 3 weeks, starting from the periphery of the scaffolds. There was a decrease in cell density from the periphery to the centre of the scaffolds in both groups. The percentage of cells expressing OC and VEGF was significantly different between the centre and the periphery of the scaffolds in the fibrin(+) group but not in the controls. It is concluded that the fibrin matrix used appears to be a useful adjunct for supporting and sustaining osteogenic and angiogenic activity of hBMSCs in tissue engineered constructs. This could help to improve their performance in a clinical setting.|/EXPL THER/ Thirty coral-derived calcium carbonate-based macroporous constructs with limited hydrothermal conversion to hydroxyapatite (7% HA/CC) were implanted in the rectus abdominis of three adult non-human primate Papio ursinus to investigate the intrinsic induction of bone formation. Macroporous constructs with 125 ug human recombinant osteogenic protein-1 (hOP-1) or 125 ug human recombinant transforming growth factor-beta(3) (hTGF-beta(3)) were also implanted. The potential synergistic interaction between morphogens was tested by implanting binary applications of hOP-1 and hTGF-beta(3) 5:1 by weight, respectively. To evaluate the role of osteoclastic activity on the implanted macroporous surfaces, coral-derived constructs were pre-loaded with 0.24 mg of bisphosphonate zoledronate (Zometa). To correlate the morphology of tissue induction with osteogenic gene expression and activation, harvested specimens on day 90 were analyzed for changes in OP-1 and TGF-beta(3) mRNA synthesis by quantitative real-time polymerase chain reaction (qRT-PCR). The induction of bone formation in 7% HA/CC solo correlated with OP-1 expression. Massive bone induction formed by binary applications of the recombinant morphogens. Single applications of hOP-1 and hTGF-beta(3) also resulted in substantial bone formation, not comparable however to synergistic binary applications. Zoledronate-treated macroporous constructs showed limited bone formation and in two specimens bone formation was altogether absent; qRT-PCR showed a prominent reduction of OP-1 gene expression whilst TGF-beta(3) expression was far greater than OP-1. The lack of bone formation by zoledronate-treated specimens indicates that osteoclastic activity on the implanted coral-derived constructs is critical for the spontaneous induction of bone formation. Indirectly, zoledronate-treated samples showing lack of OP-1 gene expression and absent or very limited bone formation by induction confirm that the spontaneous induction of bone formation by coral-derived macroporous constructs is initiated by secreted BMPs/OPs, in context the OP-1 isoform.|/EXPL THER/ Calcium is an essential cotherapy in osteoporosis treatment. The relative effectiveness of various calcium salts for this purpose is uncertain. Many older women with osteoporosis have phosphorus intakes of <70% of the Recommended Dietary Allowance. /The study's/ objective was to test the hypothesis that calcium phosphate would better support anabolic bone building than would calcium carbonate. This study was a 12-mo, randomized, positive-comparator, 2-arm, single-blind clinical trial in 211 patients treated with teriparatide who consumed <1000 mg phosphorus/d. Participants were randomly assigned to receive, in addition to teriparatide and 1000 IU cholecalciferol, 1800 mg calcium/d as either tricalcium phosphate or calcium carbonate. The primary endpoints were changes in lumbar spine and total hip bone mineral densities (BMDs); secondary endpoints were changes in bone resorption biomarkers and serum and urine calcium and phosphorus concentrations. In the combined group, the lumbar spine BMD increased by 7.2%, and total hip BMD increased by 2.1% (P < 0.01 for both). However, there was no significant difference between calcium-treatment groups, and there were no significant between-group differences in serum calcium and phosphorus concentrations or in urine calcium concentrations. Bone resorption biomarkers increased in both groups, as expected with teriparatide, but the increases in the 2 calcium groups did not differ significantly.Tricalcium phosphate and calcium carbonate appear to be approximately equally effective in supporting bone building with a potent anabolic agent; phosphate salt may be preferable in patients with restricted phosphorus intakes.|For more Therapeutic Uses (Complete) data for CALCIUM CARBONATE (20 total), please visit the HSDB record page.

Large doses of calcium carbonate (above 2 g) increase gastric secretion for a period of time that considerably outlasts elevation of pH. ... With single doses below 2 g, this effect is negligible.|After ingestion /of CaCO3 tablets/, it is converted to sol calcium salts in bowel, and calcium is thereby made available for absorption. Patients with achlorhydria may not solubilize calcium from ... preparation.|Gastric hypersecretory action is counter productive and may possibly account for various reports that calcium carbonate is less efficacious than other antacids. Calcium carbonate has been known to cause fecal concretions.|Constipating effects and chalky taste of calcium carbonate are clinically disadvantageous.|For more Drug Warnings (Complete) data for CALCIUM CARBONATE (23 total), please visit the HSDB record page.

Gastric-peptic disease occurs as a result of an imbalance between protective factors, such as mucus, bicarbonate, and prostaglandin secretion, and aggressive factors, such as hydrochloric acid, pepsin, and Helicobacter pylori (H. pylori). Antacids work by restoring acid-base balance, attenuating the pepsin activity and increasing bicarbonate and prostaglandin secretion. The acid-neutralizing capacity of calcium carbonate is 58 mEq/15 ml. When used as a nutritional supplement, calcium carbonate acts by directly increasing calcium stores within the body.

Substances that counteract or neutralize acidity of the GASTROINTESTINAL TRACT. (See all compounds classified as Antacids.)

Maximal absorption occurs at doses of 500 mg or less taken with food. Oral bioavailability depends on intestinal pH, the presence of food and dosage.|Excreted mainly in the feces. The majority of renally filtered calcium is reabsorbed in the ascending limb of the loop of Henle and the proximal and distal convoluted tubules. Also secreted by sweat glands.|Calcium is rapidly distributed taken up by skeletal tissues following absorption and distribution into extracellular fluids. Bone contains 99% of the body's calcium and the remaining 1% is approximately equally distributed between intracellular and extracellular fluids.|Calcium absorption is best when a person consumes no more than 500 mg at one time. So a person who takes 1,000 mg/day of calcium from supplements, for example, should split the dose rather than take it all at once.|Amount of calcium absorbed from calcium carbonate is usually stated to be 10%, but ... depends upon amount of gastric acid; in 1 study, 0-2% of single 2 g dose was ... absorbed in achlorhydric persons, 9-16% in normal subjects, and 11-37% in patients with peptic ulcer ...|Fraction absorbed seems to be nearly the same when CaCO3 is given chronically in daily doses of 20 g /as when it is given in single 2 g dose/. ... Amount absorbed probably reaches a plateau at a dose of about 20 g.|... Increased calcium excretion almost always follows admin of antacid doses of calcium carbonate ...|For more Absorption, Distribution and Excretion (Complete) data for CALCIUM CARBONATE (15 total), please visit the HSDB record page.

None.|After ingestion /of CaCO3 tablets/, it is converted to sol calcium salts in stomach, and calcium is thereby made available for absorption.

Calcium carbonate is a basic inorganic salt that acts by neutralizing hydrochloric acid in gastric secretions. It also inhibits the action of pepsin by increasing the pH and via adsorption. Cytoprotective effects may occur through increases in bicarbonate ion (HCO₃^-) and prostaglandins. Neutralization of hydrochloric acid results in the formation of calcium chloride, carbon dioxide and water. Approximately 90% of calcium chloride is converted to insoluble calcium salts (e.g. calcium carbonate and calcium phosphate).

Major contaminants: magnesium carbonate and silica|Both natural ground and precipitated calcium carbonate can contain low levels of impurities that are regulated. The impurities depend on the source of material, processing, and the final grade. Impurities are typically trace metals and naturally occurring minerals.

Exposure Routes: inhalation, skin and/or eye contact Symptoms: Irritation eyes, skin, respiratory system; cough Target Organs: Eyes, skin, respiratory system (NIOSH, 2016)

Eye: If this chemical contacts the eyes, immediately wash the eyes with large amounts of water, occasionally lifting the lower and upper lids. Get medical attention immediately. Contact lenses should not be worn when working with this chemical. Skin: If this chemical contacts the skin, wash the contaminated skin with soap and water. Breathing: If a person breathes large amounts of this chemical, move the exposed person to fresh air at once. Other measures are usually unnecessary. (NIOSH, 2016)|(See procedures)

Fresh air.

Rinse skin with plenty of water or shower.

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

A serum calcium concentration exceeding 2.6 mmol per liter (10.5 mg per 100 mL) is considered a hypercalcemic condition. Withholding additional administration of calcium and any other medications that may cause hypercalcemia usually resolves mild hypercalcemia in asymptomatic patients, when patient renal function is adequate. /Calcium supplements/|When serum calcium concentration are greater than 2.9 mmol per liter (12 mg per 100 mL), immediate measures may be required with possible use of the following: Hydrating with intravenous 0.9% sodium chloride injection. Forcing diuresis with furosemide or ethacrynic acid may be used to rapidly increase calcium and sodium excretion when saline overload occurs. Monitoring of potassium and magnesium serum concentrations and starting replacement early to prevent complications of therapy. ECG monitoring and the possible use of beta-adrenergic blocking agents to protect the heart against serious arrhythmias. Possibly including hemodialysis, calcitonin, and adrenocorticoids in the treatment. Determining serum calcium concentration at frequent intervals to guide therapy adjustments. /Calcium supplements/|/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/|/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

/HUMAN EXPOSURE STUDIES/ Thirty-two healthy volunteers were exposed to 0 (control), 500, 1000, and 5000 ug/cu m calcium carbonate dust for 3 hours and nasal saccharin transport time (STT), rhinomanometry, and visual analog scales (VAS) on nasal discomfort were obtained. A dose dependent decrease of STT (P = 0.02) and nasal patency (P = 0.04), and increased sensation of nasal obstruction (P = 0.002) and dryness (P = 0.03) was observed. The results indicate that acute exposure to low-toxicity particulate matter in concentrations frequently encountered in western agglomeration areas may affect nasal functions and cause nasal symptoms.|/SIGNS AND SYMPTOMS/ Admin of calcium carbonate promotes positive phosphate balance; plasma phosphate concn may or may not be incr, but hyperphosphatemia is usual finding in patients with milk-alkali syndrome.|/SIGNS AND SYMPTOMS/ ... Enough is absorbed to cause systemic and renal effects ... a slight-to-moderate metabolic alkalosis occurs during treatment with CaCO3, but it is slow to develop.|/SIGNS AND SYMPTOMS/ When phosphate intake is low /during chronic calcium carbonate admin/, hypophosphatemia may occur. Hypercalciuria and alkaluria predispose to nephrolithiasis.|For more Human Toxicity Excerpts (Complete) data for CALCIUM CARBONATE (27 total), please visit the HSDB record page.

Aragonite

inhalation, skin and/or eye contact

irritation eyes, skin, respiratory system; cough|irritation eyes, skin, mucous membrane; cough, sneezing, rhinorrhea (discharge of thin nasal mucus); lacrimation (discharge of tears)|irritation eyes, skin, mucous membrane, upper respiratory system; cough, sneezing, rhinorrhea (discharge of thin nasal mucus); lacrimation (discharge of tears)

Cough.

Redness.

Eyes, skin, respiratory system

(Pigment grade) (est.) 17% in paint; 17% in plastics; 17% in carpet backing; 17% in putty; 13% in rubber; 19% in other applications, including precipitated calcium carbonate used principally for coating paper (1969)|Derivative: Construction, 72%; Raw Material, 19%; Filler & Extender, 1%; and others, 8% (1982)|The use of calcium carbonate in paint, paper, and plastics make up the principal part of the market.

Formulations: dispersible, nonwettable.|/Available in/ Filler grades; USP grades; technical grades; high-purity grades; and specialty grades|Found in: Tums, 500 mg; Tums-Extra strength, 750 mg|Both natural ground or precipitated calcium carbonate are available as dry products. Calcium carbonate slurry, primarily used in the paper industry, is typically >70% solids by weight for ground products and 20-50% solids by weight for precipitated. Some grades are surface coated to improve handling and dispersibility in plastics. Agents used for surface treatment used are fatty acids, resins, and wetting agents.|MAALOX QUICK DISSOLVE: 600 mg CaCO3/tablet; CALCIUM RICH ROLAIDS: 80 mg Mg(OH)2 and 412 mg CaCO3/tablet; TUMS EX 750 mg CaCO3 ... /From table/

336111 - automobile manufacturing|Carbonic acid calcium salt (1:1): ACTIVE|The principal U.S. producers of ground calcium carbonate are Columbia River Carbonates, ECC International, Franklin Limestone Co., Genstar Stone Products, Georgia Marble, J.M. Huber Corp., Calcium Carbonate Division, James River Limestone Co., Inc., OMYA Inc. (Pluess-Staufer), and Pfizer Inc. The principal U.S. producers of precipitated products are Mississippi Lime Co., and Pfizer Inc.

Method: OSHA ID-121; Procedure: atomic absorption; Analyte: calcium; Matrix: air, wipes, or bulks; Detection Limit: 0.03 ug/mL. /Calcium/|Method: NIOSH 7020, Issue 2; Procedure: flame atomic absorption; Analyte: calcium; Matrix: air; Detection Limit: 0.001 mg/sample. /Calcium and compounds/|Method: NIOSH 7300, Issue 3; Procedure: inductively coupled argon plasma, atomic emission spectroscopy (nitric/perchloric acid ashing); Analyte: calcium; Matrix: air; Detection Limit: 36.3 ng/mL. /Calcium/|Method: NIOSH 7303, Issue 2; Procedure: inductively coupled argon plasma, atomic emission spectroscopy (hot block/HCl/HNo3 digestion; Analyte: calcium; Matrix: air; Detection Limit: 0.009 ug/ml. /Calcium/|For more Analytic Laboratory Methods (Complete) data for CALCIUM CARBONATE (20 total), please visit the HSDB record page.

EPA Safer Chemical Functional Use Classes -> Processing Aids and Additives|Safer Chemical Classes -> Green circle - The chemical has been verified to be of low concern|Food additives|Human Drugs -> EU pediatric investigation plans|Human Drugs -> FDA Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) -> Active Ingredients|Food Additives -> ANTICAKING_AGENT; -> JECFA Functional Classes|Cosmetics -> Abrasive; Absorbent; Buffering; Bulking; Cosmetic colorant; Opacifying; Oral care; Viscosity controlling

Food Additives -> ANTICAKING_AGENT;