CBD oil is growing in popularity and for a good reason. CBD, or cannabinoid, oil offers users a range of benefits, from relaxation to relieving pain and inflammation. The popularity of cbd oil isn’t restricted to just human use. Now there are a range of cbd oils for dogs as well.

If you are still unsure about whether CBD oil is safe for yourself or your pet, learn about some of its most popular side effects .

The Difference Between CBD and THC

Before getting into the CBD oil benefits, you should understand what cannabidiol oil is – and the difference between CBD vs. THC. There are multiple cannabinoids found in the cannabis plant (which also has THC), including CBD or cannabidiol. CBD does not have psychoactive properties, but it does interact with your endocannabinoid system. Those interactions let it provide a range of benefits for those who take the oil.

THC Is Psychoactive

THC, or tetrahydrocannabinol, is the cannabinoid in cannabis that is responsible for the plant’s psychoactive properties. This is the plant’s main psychoactive component. So if you consume THC, you will likely experience the “high” linked to marijuana. In contrast, taking CBD oil will not give you that high or any psychoactive effects.

CBD Oil Can Contain THC

The caveat here is that some CBD oils will contain small quantities of THC. This is intentional from a medical standpoint due to something called the entourage effect. The entourage effect is that CBD is more effective when taken in combination with THC.

For those who do not want to have any psychoactive effects from CBD oil, there are numerous options available without any THC at all. Those are a good choice if you have concerns about drug tests or operate heavy machinery.

If you do not have those types of restrictions in your life and want the best possible effects, then you may want to consider choosing a CBD oil that has small quantities of THC. Hemp oils, for example, always have 0.3 percent of THC or less. This is not normally enough to produce psychoactive effects, although it may show up on a drug test.

You can also try starting with a CBD oil that does not contain THC and then switch to one with this second cannabinoid if you do not notice strong enough results.

With a clearer idea of what cannabinoid oil is and why it is unlikely to produce psychoactive effects, it is time to look at some of the most notable benefits of taking CBD oil.

Pain Relief

One of the most popular uses for cannabidiol oil is pain relief. There is plenty of anecdotal evidence of those with chronic pain finally experiencing relief thanks to CBD oil.

Scientists believe that CBD’s ability to relieve pain comes from its interactions with the endocannabinoid system. This system is involved in regulating the immune system, pain, appetite, and sleep. Research indicates that CBD can affect the activity of the endocannabinoid receptors and that, in turn, interacts with neurotransmitters while reducing inflammation.

Other research indicates that CBD may reduce pain by affecting the body’s a3 glycine receptors in the brain and spinal cord. These receptors control our reactions to pain, so this interaction lets CBD oil reduce the pain sensation but without side effects.

Studies in rats have shown that CBD injections can reduce pain from surgical incisions as well as pain in the sciatic nerve. Human studies have found combinations of CBD with THC can help treat pain from arthritis and multiple sclerosis. In fact, several countries have approved the use of Sativex, an oral spray that combines CBD and THC, for treating multiple sclerosis pain.

Anti-inflammatory

The ability of CBD to reduce pain is closely linked to its anti-inflammatory properties. Those properties are due to its interactions with the endocannabinoid system. In many cases, pain comes from inflammation, so the reduction in pain from CBD oil is directly due to inflammation decreasing.

Reduces Anxiety and Depression

Numerous experts have also looked into CBD oil’s benefits on those who suffer from anxiety and depression. These are both common disorders affecting a person’s mental health with the ability to severely impact the overall well-being of those affected. The ability of CBD oil to reduce depression and anxiety is crucial as the World Health Organization reports that depression is the biggest factor contributing to disability in the world. Anxiety is also high on that list, ranking sixth.

Traditional treatments for anxiety and depression include pharmaceutical drugs, but those tend to come with side effects. Depending on the drug in question, side effects may include headaches, drowsiness, insomnia, sexual dysfunction, and agitation. Even worse, certain pharmaceutical drugs traditionally used to treat depression and anxiety can become addictive, potentially leading to substance abuse.

In contrast, CBD oil for anxiety and depression does not carry a risk of becoming addictive, nor does it potentially lead to substance abuse. It also tends to come with minimal side effects.

There is also research on the subject of CBD oil benefits for anxiety and depression in addition to anecdotal evidence. One study showed that CBD helps reduce anxiety before public speaking. It has also been used to safely treat anxiety and insomnia in kids suffering from post-traumatic stress disorder.

As with the other benefits of cannabidiol oil, its ability to reduce anxiety and depression comes from its interactions with the endocannabinoid system. In this case, CBD specifically interacts with serotonin receptors in the brain. Since this is the neurotransmitter that regulates social behavior and mood, that ability of CBD helps it relieve symptoms of those conditions.

Helps With Sleep

Many people have found that CBD oil can help them get a good night’s rest. Some research shows that the endocannabinoid system is likely connected to regulating sleep, so CBD’s interaction with that system helps with insomnia and other sleep disorders.

There has also been research and anecdotal evidence indicating the CBD oil can help relieve symptoms related to cancer. In particular, studies found it can help relieve symptoms like nausea, pain, and vomiting. One study found that CBD in addition to THC was able to relieve pain even among patients who did not get relief from traditional pain medications.

CBD oil can also help those undergoing cancer treatments overcome certain side effects of chemotherapy, specifically vomiting and nausea. Those are two of the most common side effects related to chemotherapy to treat cancer. CBD can also help patients increase their appetite, overcoming the common challenge of loss of appetite associated with cancer treatment. You can find traditional drugs for addressing those issues, but they are not always effective. On the other hand, a study found that a combination of CBD and THC got better results than the standard medical treatment.

The Potential to Reduce or Prevent Cancer

Although this is still in the very early stages, there is some evidence that CBD oil may have some anti-cancer properties. One study found that concentrated CBD caused human breast cancer cells to experience cell death. Another study in mice with aggressive breast cancer cells showed CBD prevented the spread of cancer.

Keep in mind, however, that more research on CBD and cancer is needed before being able to make any assumptions about cannabidiol’s ability to treat or prevent the spread of the disease. In the meantime, it does a great job at relieving other symptoms of cancer.

Overall, some studies show early indications that CBD might help deter cancer cell growth, weaken the cancer cells’ ability to attach onto structures, prevent migration of cancer cells, and shrink tumors.

Manages Appetite and Nausea

The cancer-related symptoms mentioned above, including loss of appetite and nausea, can also occur without cancer. Regardless of the cause, CBD oil can help treat those problems. Scientists have known that CBD has anti-emetic (anti-vomiting) properties for years, but other treatments arrived and took center stage. More recently, scientists have started looking at CBD for nausea once again. One study found that CBD and other cannabinoids may be better at treating appetite issues and vomiting that are hard to control compared to standard anti-emetics.

Prevents Infection

The CBD oil benefits also include its antibacterial properties. CBD and other specific cannabinoids have antiseptic properties. They show promise in countering drug-resistant bacteria when used topically or internally. In some cases, CBD seems to be more effective.

Reduces Acne

There is also some evidence that taking CBD oil can help patients reduce their acne. Acne is common, affecting over 9 percent of the population. The ability of CBD oil to treat acne stems from its anti-inflammatory properties. This is just one of several factors affecting the development of acne, with others, including sebum overproduction, bacteria, and genetics.

Scientific studies have shown that CBD not only has an anti-inflammatory effect, but it can also help reduce the production of sebum. One study found that with CBD oil present, sebaceous gland cells do not produce excessive sebum. That same study also indicated that the CBD oil was anti-inflammatory and stopped pro-acne agents such as cytokines (which are inflammatory) from activating.

This is one area where more research is necessary, but there seems to be great promise that CBD oil’s benefits extend to treating acne.

Heart Health Properties

Some research indicates that cannabidiol oil can also have a positive impact on your heart’s health as well as that of your circulatory system. These include its ability to potentially lower blood pressure. That is crucial since high blood pressure is connected to an increased risk of metabolic syndrome, heart attack, and stroke. Some studies have already shown that CBD may be able to control high blood pressure. This is likely due to the oil’s ability to reduce anxiety and stress.

Other studies have linked the anti-inflammatory properties of CBD to a reduction in cell death and inflammation from heart disease. This effect is also due to its ability to reduce stress and its antioxidant properties.

Treats Type 1 Diabetes

Type 1 diabetes is the type of diabetes that patients cannot control and is not based on lifestyle factors. This is an autoimmune system disorder, allowing CBD oil to help. That is because CBD oil can regulate body systems and promote balance. More research still needs to be done on the ability of CBD to treat type 1 diabetes, but some early research is optimistic.

It is important to note that this early research does not indicate that CBD would be able to cure or prevent type 1 diabetes. Instead, it would help treat it, reducing patients’ reliance on insulin to control their blood sugar levels.

Neuroprotective Properties

Going back to the interactions of cannabidiol with the endocannabinoid system, researchers mull that this could help treat certain neurologic disorders. There is particular promise in using CBD oil to treat multiple sclerosis and epilepsy, with promising results in multiple studies.

The Sativex oral spray, which contains THC and CBD, reduced muscle spasticity in people with multiple sclerosis. In fact, in muscle spasticity, which resisted medications, one study found a reduction in spasms of 75 percent. Other studies have found reductions of seizures by an average of 36.5 percent with a certain dosage of CBD oil and a significant reduction of seizures in kids with Dravet syndrome.

However, scientists caution that some people involved in the studies were more sensitive to the rare side effects of CBD. Because of the existence of adverse reactions in these groups, those who want to use CBD oil for its neuroprotective properties should first consult with their doctor and keep a close eye on their condition.

Epilepsy and multiple sclerosis are not the only neurological disorders that CBD oil shows promise in treating. Other studies showed it could reduce inflammation while preventing the neurodegeneration linked to Alzheimer’s and can improve the sleep and quality of life of people with Parkinson’s.

May Treat Addiction

There is also some early research indicating that CBD oil shows promise in the treatment of addiction. Specifically, it may be therapeutic when overcoming addiction to psychostimulants, opioids, or cocaine. It can also help with treating tobacco addiction. Some evidence even indicates CBD might reduce the impact THC has on your mind.

Can Help Quit Smoking 

One of the specific CBD oil benefits related to addiction is its ability to help smokers overcome their addiction. This is particularly helpful given how hard it is to get over an addiction to smoking cigarettes.

One study found that those who wanted to stop smoking and took CBD had a 40 percent higher success rate in their first week. Even with a low dosage of CBD, those struggling to quit saw a reduction in intrusive thoughts, which made it easier to quit.

Experts are not sure why CBD oil can help people quit smoking, but think it is because of the interaction between nicotine and the endocannabinoid system. Scientists feel that addiction cues may reduce when the endocannabinoid system is in balance, which it is with CBD.

CBD, Multivitamins, and Herbal Medications

Aside from the numerous health benefits that CBD provides, the compound is also used as a supplement to help maintain good health or prevent common ailments.

Like CBD, multivitamins and herbal medications are finding their way into peoples’ households.

Many anecdotal reports promote the potentials of CBD oil and other herbal supplements in conjunction with a healthy diet and exercise.

Even U.S. Government Patent 1999/008769 claims that cannabinoids “act as free radical scavengers for use in prophylaxis (prevention) and treatment of disease.”

Riboflavin, or vitamin B2, is vital for skin health, reproduction, body growth, production of red blood cells, and development of normal vision.

The best way to obtain vitamin B2 is by consuming riboflavin-rich foods, such as hemp oil. Hemp (cannabis) oil is useful in balancing hormones, improving digestion, and promoting metabolism.

CBD is a potent antioxidant that is more powerful than vitamin C (ascorbic acid), the king of antioxidants.

Vitamin C helps produce collagen, which is a type of protein in the bones, skin, and connective tissues. Vitamin C also supports the body’s immune system in fighting viruses and bacteria.

Although no interactions have been found between cannabis and vitamin C, it does not necessarily mean that no interactions exist.

However, using CBD, along with other herbs and supplements that have sedative properties, might cause too much sleepiness. Some of these herbs and supplements include St. John’s wort, California poppy, catnip, Jamaican dogwood, and sage.

CBD may interact with specific substances. Thus, before trying CBD, it is crucial that one talks to a doctor first about all of the supplements, vitamins, and prescription and OTC medications that he or she is taking.

Take note that CBD is not advisable for pregnant women. The U.S. Food and Drug Administration (FDA) discourages “the use of CBD, THC, and marijuana in any form during pregnancy or while breastfeeding.”

Side Effects

Although there is a long list of CBD oil benefits, there are also some potential side effects to be aware of. The good news is that side effects tend to be very rare when taking CBD, especially if you take the proper dose. Even so, you should be aware of potential effects like:

  • Vomiting
  • Nausea
  • Dry mouth
  • Drowsiness
  • Dizziness
  • Diarrhea
  • Mood changes
  • Appetite changes
  • Anxiety

You should also consult your doctor or pharmacist before taking CBD oil if you are on any medications or over-the-counter supplements since these may cause interactions. This also applies if you are planning to use other forms of CBD such as gummies or capsules.

This is especially true if you plan to consume your cbd oil via vaping. Even if you have done all of your research and purchased the best cbd vape oil on the market, its prudent to check what impact it will have with your existing medication.

While CBD can supplement many other treatments, you need to ensure it will not make your pharmaceutical treatment less effective.

Finding Safe Products

It is also important to keep in mind that CBD oils are not regulated for the most part. This means that consumers must complete their own research to confirm that they choose a safe product. This is whether you are looking to find the best cbd oil for your personal use, or even if you are looking for the best cbd pet treats for your pet.

Do this by looking for products with third-party lab results available and strong reviews. This will help ensure that your CBD oil is as advertised does not contain any harmful ingredients.

Conclusion

There are a plethora of CBD oil benefits to help patients with everything ⁠—from pain relief and insomnia to seizures. We still need to conduct more research on CBD, but between early research and anecdotes, it is a very strong choice for those with certain conditions. This is especially true given its minimal side effects, particularly in comparison to pharmaceutical drugs.

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Folic Acid

  1. NAME

   1.1 Substance

   1.2 Group

   1.3 Synonyms

   1.4 Identification Numbers

      1.4.1 CAS number

      1.4.2 Other numbers

   1.5 Brand Names, Trade Names

   1.6 Manufacturers, Importers

   1.7 Presentation, Formulation

  1. SUMMARY

   2.1 Main risks and target organs

   2.2 Summary of clinical effects

   2.3 Diagnosis

   2.4 First aid and management principles

  1. PHYSICO-CHEMICAL PROPERTIES

   3.1 Origin of the substance

   3.2 Chemical structure

   3.3 Physical properties

      3.3.1 Properties of the substance

         3.3.1.1 Colour

         3.3.1.2 State/Form

         3.3.1.3 Description

      3.3.2 Properties of the locally available formulation(s)

   3.4 Other characteristics

      3.4.1 Shelf-life of the substance

      3.4.2 Shelf-life of the locally available formulation(s)

      3.4.3 Storage conditions

      3.4.4 Bioavailability

      3.4.5 Specific properties and composition

  1. USES

   4.1 Indications

      4.1.1 Indications

      4.1.2 Description

   4.2 Therapeutic dosage

      4.2.1 Adults

      4.2.2 Children

   4.3 Contraindications

  1. ROUTES OF ENTRY

   5.1 Oral

   5.2 Inhalation

   5.3 Dermal

   5.4 Eye

   5.5 Parenteral

   5.6 Other

  1. KINETICS

   6.1 Absorption by route of exposure

   6.2 Distribution by route of exposure

   6.3 Biological half-life by route of exposure

   6.4 Metabolism

   6.5 Elimination by route of exposure

  1. PHARMACOLOGY AND TOXICOLOGY

   7.1 Mode of action

      7.1.1 Toxicodynamics

      7.1.2 Pharmacodynamics

   7.2 Toxicity

      7.2.1 Human data

         7.2.1.1 Adults

         7.2.1.2 Children

      7.2.2 Relevant animal data

      7.2.3 Relevant in vitro data

   7.3 Carcinogenicity

   7.4 Teratogenicity

   7.5 Mutagenicity

   7.6 Interactions

   7.7 Main adverse effects

  1. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS

   8.1 Sample

      8.1.1 Collection

      8.1.2 Storage

      8.1.3 Transport

   8.2 Toxicological analytical methods

      8.2.1 Assay for folic acid may be found in the USP XXII, 1990.

      8.2.2 Test for biological sample

   8.3 Biochemical investigations

      8.3.1 Blood

      8.3.2 Urine

      8.3.3 Others

   8.4 Interpretation

   8.5 References

  1. CLINICAL EFFECTS

   9.1 Acute poisoning

      9.1.1 Ingestion

      9.1.2 Inhalation

      9.1.3 Skin exposure

      9.1.4 Eye contact

      9.1.5 Parenteral exposure

   9.2 Chronic Poisoning

      9.2.1 Ingestion

      9.2.2 Inhalation

      9.2.3 Skin exposure

      9.2.4 Eye contact

      9.2.5 Parenteral exposure

   9.3. Course, prognosis, cause of death

   9.4 Systematic description of clinical effects

      9.4.1 Cardiovascular

      9.4.2 Respiratory

      9.4.3 Neurological

         9.4.3.1 Central nervous system (CNS)

         9.4.3.2 Peripheral nervous system

         9.4.3.3 Autonomic nervous system

         9.4.3.4 Skeletal and smooth muscle

      9.4.4 Gastrointestinal

      9.4.5 Hepatic

      9.4.6 Urinary

         9.4.6.1 Renal

         9.4.6.2 Other

      9.4.7 Endocrine and reproductive systems

      9.4.8 Dermatological

      9.4.9 Ear, nose and throat: local effects

      9.4.10 Hematological

      9.4.11 Immunological

      9.4.12 Metabolic

         9.4.12.1 Acid-base disturbances

         9.4.12.2 Fluid and electrolyte disturbances

         9.4.12.3 Others

      9.4.13 Allergic reaction

      9.4.14 Other clinical effects

      9.4.15 Special risks

   9.5 Other

   9.6 Summary

  1. MANAGEMENT

   10.1 General principles

   10.2 Relevant laboratory analyses

      10.2.1 Sample collection

      10.2.2 Biomedical analysis

      10.2.3 Toxicological analysis

      10.2.4 Other investigations

   10.3 Life supportive procedures and symptomatic/specific treatment

   10.4 Decontamination

   10.5 Elimination

   10.6 Antidote treatment

      10.6.1 Adults

      10.6.2 Children

   10.7 Management discussion

  1. ILLUSTRATIVE CASES

   11.1 Case reports from literature

   11.2 Internally extracted data on cases

   11.3 Internal cases

  1. ADDITIONAL INFORMATION

   12.1 Availability of antidotes

   12.2 Specific preventive measures

   12.3 Other

  1. REFERENCES
  2. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE ADDRESS(ES)

 

  1. NAME

 

       1.1 Substance

 

           Folic Acid  (INN)

 

           (WHO, 1992)

 

       1.2 Group

 

           ATC classification index 

 

           Antianaemic preparations (B03)/Vitamin B12 and folic acid

           (B03B)/Folic acid and derivatives (B03BB).

 

           (WHO, 1992)

 

       1.3 Synonyms

 

           Acidum Folicum; Folacin; PGA; Pteroylglutamic Acid;

           Pteroylmonoglutamic Acid; Wills’ factor; Vitamin M;

           liver Lactobacillus casei factor; Folsaure. 

 

           (Reynolds, 1993; Budavari, 1989)

 

           (To be completed by each Centre using local data) 

 

       1.4 Identification Numbers

 

           1.4.1 CAS number

 

                 Folic acid 59-30-3

 

                 Sodium folate 6484-89-5

 

           1.4.2 Other numbers

 

                 RTECS

 

                 LP5425000

 

       1.5 Brand Names, Trade Names

 

           Acfol (Torlan, Spain), Folacid (Netherlands), Folaemin 

           (Netherlands), Folasic (Nelson, Australia), Foldine (France), 

           Folettes (Australia), Folicid (USV, Australia), Folico 

           (Ecobi, Italy), Folina (Tosi, Italy), Folsan (Kali-Chemie, 

           Germany), Folvite (Lederle, Canada)(Lederle, 

           Switzerland)(Lederle, USA), Lexpec (R.P. Drugs, United 

           Kingdom), Nifolin (Denmark), Nivofolacid (Novopharm, Canada), 

           Speciafoldine (Specia, France) 

 

           Combination Preparations; Fefol-Ferrous sulfate USP and folic 

           acid (SKF, Philippines), Ferro-Folsan-Ferrous sulfate, 

           succinic acid, folic acid (Phil.), Iberet-Folic-500-Iron, 

 

           Vitamin C, Vitamin B Complex, Folic Acid (Philippines). 

 

           (To be completed by each Centre using local data)

 

       1.6 Manufacturers, Importers

 

           To be completed by each Centre using local data.

 

       1.7 Presentation, Formulation

 

           Oral 

 

           Folic acid tablets (monocomponent) or in combination with 

           other vitamins and minerals. Strengths usually available are 

           100 mcg, 250 mcg, 400 mcg, 800 mcg, 1 mg and 5 mg. 

 

           Syrup 2.5 mg/5 mL

 

           Parenteral 

 

           Folate sodium injection; strength usually available is 

           equivalent of folic acid 5 mg/mL 

 

           (To be completed by each Centre using local data)

 

  1. SUMMARY

 

       2.1 Main risks and target organs

 

           Folic acid is relatively non-toxic. However, there have been 

           reports of reactions to parenteral injections. Allergic 

           reactions to folic acid have been rarely reported. 

 

       2.2 Summary of clinical effects

 

           Severe allergic reactions are characterized by hypotension, 

           shock, bronchospasm, nausea, vomiting, rash, erythema. 

           Itching may also occur. 

 

           Adverse gastrointestinal and central nervous system effects 

           have been reported. 

 

           Treatment with folic acid is usually well tolerated except 

           for rare reports of allergic reactions. 

 

       2.3 Diagnosis 

 

           Clinical, haematological and analytical aspects to be 

           addressed. No clinical signs and symptoms are typical for 

           folic acid overdose. Diagnosis should be based on listing and 

           circumstantial evidence. 

 

       2.4 First aid and management principles

 

           In case of massive overdose, gastric lavage or induced 

           vomiting could be considered, if seen within 1 to 2 hours 

           after ingestion. Repeat dose activated charcoal to be given, 

           followed by supportive treatment. In case of anaphylaxis, 

           treatment with epinephrine (adrenaline) and support of vital 

           functions should be provided. 

 

           For adverse reactions not related to overdose, withdraw drug 

           and provide symptomatic and supportive therapy. 

 

  1. PHYSICO-CHEMICAL PROPERTIES

 

       3.1 Origin of the substance

 

           Folic acid was isolated in 1941 by Mitchell and co-workers 

           from green leafy vegetables, liver, yeast and fruits. 

           Synthetic folic acid is commercially available. 

 

       3.2 Chemical structure

 

           Structural formula

 

             

 

           Molecular formula

 

           C19H19O6 

 

           Molecular weight 

 

           441.4

 

           Chemical names

 

           N-[4(2-Amino-4-hydroxypteridin-6-ylmethylamino)benzoyl]-L(+)-

           glutamic acid. 

 

           N-{4-[[(2-Amino-1,4-dihihydro-4-oxo-6-

           pteridinyl)methyl]amino]benzoyl}-L-glutamic acid. 

 

           N-{p-[[2-amino-4-hydroxy-6-pteridinyl)methyl]amino]benzoyl}-

           glutamic acid. 

 

           (Reynolds, 1993; Budavari, 1989)

 

       3.3 Physical properties

 

           3.3.1 Properties of the substance

 

                 3.3.1.1 Colour

 

                         Yellow to orange brown

 

                 3.3.1.2 State/Form

 

                         Crystalline powder

 

                 3.3.1.3 Description

 

                         Odourless 

 

                         Readily soluble in alkali, hydroxides and 

                         carbonates. Insoluble in alcohol, acetone, 

                         chloroform and ether. Solutions are inactivated 

                         by ultraviolet light. Alkaline solutions are 

                         sensitive to oxidation and acid solutions are 

                         sensitive to heat. Dissociation constant – pKa 

                         4.7, 6.8, 9.0 (30°) (Moffat, 1986). 

 

           3.3.2 Properties of the locally available formulation(s) 

 

                 To be completed by each Centre using local data

 

       3.4 Other characteristics

 

           3.4.1 Shelf-life of the substance

 

                 No data available.

 

           3.4.2 Shelf-life of the locally available formulation(s) 

 

                 To be completed by each Centre using local data.

 

           3.4.3 Storage conditions

 

                 Preserve in well closed, light resistant containers. 

                 For injection-preserve in single dose or in multiple 

                 dose containers, preferably of type 1 glass (USP, 

                 1990). 

                  

                 Store between 15 to 30 °C

                 

                 Protect from freezing

 

                 (To be completed by each Centre using local data)

 

           3.4.4 Bioavailability

 

                 Folic acid is rapidly absorbed from gastrointestinal 

                 tract following oral administration. Peak folate 

                 activity in blood is 30 to 60 minutes after oral 

                 administration. 

 

                 (To be completed by each Centre using local data)

 

           3.4.5 Specific properties and composition

 

                 Commercially available folic acid is prepared 

 

                 synthetically as yellowish orange crystalline powder. 

 

                 Folic acid injection is a sterile solution of folic 

                 acid in water, prepared with the aid of sodium 

                 hydroxide or sodium carbonate which results in 

                 formation of sodium folate which is the soluble sodium 

                 salt of folic acid. Commercially available folic acid 

                 injection has a pH of 8 to 11 and the aqueous solutions 

                 are heat sensitive and decompose rapidly in the 

                 presence of light and/or riboflavin, so solutions 

                 should be protected from light. 

 

                 Folic acid is incompatible with oxidizing and reducing 

                 agents and with heavy metal ions (McEvoy, 1990). 

 

                 (To be completed by each Centre using local data)

 

  1. USES

 

       4.1 Indications

 

           4.1.1 Indications

 

                 For the prevention and treatment of vitamin B 

                 deficiency, 

 

                 For the treatment of megaloblastic anaemia and 

                 macrocytic anaemia due to folic acid deficiency. 

 

                 Folic acid supplements may be required in low birth 

                 weight infants, infants breastfed by folic acid 

                 deficient mothers, or those with prolonged diarrhoea 

                 and infection. 

 

                 Other conditions which may increase folic acid 

                 requirements include alcoholism, hepatic disease, 

                 haemolytic anaemia, lactation, oral contraceptive use 

                 and pregnancy. 

 

                 It has been given to pregnant mothers to reduce the 

                 risk of birth defects (Klaassen et al., 1986). 

 

                 Folic acid has been suggested in the management of 

                 methanol poisoning, but its efficacy has not been 

                 proven (Ellenhorn & Barceloux, 1988). 

 

           4.1.2 Description

 

                 Not applicable.

 

       4.2 Therapeutic dosage

 

           4.2.1 Adults

                         

                 Folate deficient megoblastic anaemia 

 

                  Therapeutic dose

 

                 5 mg daily orally for 4 months; up to 15 mg daily may 

                 be required in malabsorption states.(UK) 

 

                 250 mcg to 1.0 mg orally daily (USA)

                         

                  Prophylactic dose

 

                 200 to 500 mcg orally daily (UK)

                 400 mcg orally daily (USA)

                         

                 Other indications

 

                  Prophylactic dose

 

                 5 mg daily or weekly by mouth in thalassaemia or 

                 sickle-cell anaemia (and sometimes in patients 

                 receiving renal dialysis)  

                         

                 Note: Folic acid may also be administered by 

                 intramuscular, intravenous or subcutaneous injection as 

                 the sodium salt. 

 

                 (Reynolds, 1993)

 

           4.2.2 Children

 

                  Dietary supplements

 

                 100 mcg/day may be increased to 500 mcg to 1 mg/day 

                 when conditions causing increased requirements are 

                 present. 

 

                  Deficiency states

 

                 250 mcg to 1 mg/day until haematological response 

                 occurs. 

 

                  Maintenance

 

                 Infants                  100 mcg/day.

                 Children up to 4 years   up to 300 mcg/day. 

                 Children above 4 years   400 mcg/day.

 

                 (Reynolds, 1993)

 

       4.3 Contraindications

 

           It should be given with caution to patients with abnormal 

           renal function. 

 

           It is also contra-indicated in patients who show 

           hypersensitivity reactions to folic acid. 

 

           Caution is advised in patients who may have folate dependent 

           tumours (Reynolds, 1989). 

 

           Folic acid should never be given alone or in conjunction with 

           inadequate amounts of Vitamin B12 for the treatment of 

           undiagnosed megaloblastic anaemia. Although folic acid may 

           produce a haematopoietic response in patients with 

           megaloblastic anaemia due to Vitamin B12, it fails to prevent 

           the onset of subacute combined degeneration of the cord 

           (Reynolds, 1989). 

 

  1. ROUTES OF ENTRY

 

       5.1 Oral

 

           Tablets

 

       5.2 Inhalation

 

           Not applicable.

 

       5.3 Dermal

 

           Not applicable.

 

       5.4 Eye

 

           Not applicable.

 

       5.5 Parenteral

 

           Aqueous solution.

 

       5.6 Other

 

           Not relevant.

 

  1. KINETICS

 

       6.1 Absorption by route of exposure

 

           Oral

 

           Folic acid is rapidly absorbed from the proximal part of the 

           gastrointestinal tract following oral administration. It is 

           mainly absorbed in the proximal portion of the small 

           intestine. The naturally occurring folate polyglutamate is 

           enzymatically hydrolyzed to monoglutamate forms in the 

           gastrointestinal tract prior to absorption. The peak folate 

           activity in blood after oral administration is within 30 to 

           60 minutes (McEvoy, 1990). Enterohepatic circulation of 

           folate has been demonstrated. 

 

       6.2 Distribution by route of exposure

 

           Tetrahydrofolic acid and its derivatives are distributed in 

           all body tissues. Folate is actively concentrated in the CSF 

           at about 0.016 to 0.021 mg/ml while the normal erythrocyte 

           level is about 0.175 to 0.316 mg/ml. The liver contains half 

           of the total body stores of folate and is the principal 

           storage site (McEvoy, 1990). 

 

       6.3 Biological half-life by route of exposure

 

           No data available.

 

       6.4 Metabolism

 

           Folic acid once absorbed is acted upon by hepatic 

           dihydrofolate reductase to convert to its metabolically 

           active form which is tetrahydrofolic acid. 

 

           Following absorption of 1 mg or less, folic acid is largely 

           reduced and methylated in the liver to N-5 

           methyltetrahydrofolic acid, which is the main transporting 

           and storage form of folate in the body. Larger doses may 

           escape metabolism by the liver and appear in the blood mainly 

           as folic acid. 

 

       6.5 Elimination by route of exposure

 

           Oral

           

           Following oral administration of single 0.1 to 0.2 mg doses 

           of folic acid in health adults, only a trace amount of the 

           drug appears in urine . Following administration of large 

           doses, the renal tubular reabsorption maximum is exceeded and 

           excess folate is excreted unchanged in urine. Small amounts 

           of orally administered folic acid have been recovered from 

           faeces. About 0.05 mg/day of normal body folate stores is 

           lost by a combination of urinary and faecal excretion and 

           oxidative cleavage of the molecule. 

 

           Folic acid is also excreted in the breastmilk.

 

  1. PHARMACOLOGY AND TOXICOLOGY

 

       7.1 Mode of action

 

           7.1.1 Toxicodynamics

 

                 Folic acid is relatively non-toxic. Toxicity studies in 

                 mice showed that folic acid could cause convulsions, 

                 ataxia and weakness. Histopathological studies in some 

                 strains of mice showed that toxic doses may also cause 

                 acute renal tubular necrosis. A possible relationship 

                 between folic acid neurotoxicity and cholinergic 

                 receptors in the pyriform cortex and amygdala has been 

 

                 shown (McGeer et al, 1983). 

 

           7.1.2 Pharmacodynamics

 

                 Folic acid is transformed into different coenzymes that 

                 are responsible for various reactions of intracellular 

                 metabolism mainly conversion of homocysteine to 

                 methionine, conversion of serine to glycine, synthesis 

                 of thymidylate, histidine metabolism, synthesis of 

                 purines and utilization or generation of formate. 

 

                 In man, nucleoprotein synthesis and the maintenance of 

                 normal erythropoiesis requires exogenous folate. Folic 

                 acid is the precursor of tetrahydrofolic acid which is 

                 active and acts as a co-factor for 1-carbon transfer 

                 reactions in the biosynthesis of purines and 

                 thymidylates of nucleic acids. 

 

       7.2 Toxicity

 

           7.2.1 Human data

 

                 7.2.1.1 Adults

 

                         There is little data available on folic acid 

                         toxicity in humans. A case of 2 patients who 

                         showed exacerbation of psychotic behaviour 

                         during treatment with folic acid has been 

                         reported (Prakash et al., 1982). The 

                         significance of this finding is uncertain since 

                         other authors have suggested that folic acid 

                         has antipsychotic properties. 

 

                         Adverse gastrointestinal and central nervous 

                         system effects have been reported rarely in 

                         patients receiving 15 mg of folic acid daily 

                         for one month. However, other studies have 

                         failed to confirm these findings (McEvoy, 

                         1990). 

 

                 7.2.1.2 Children

 

                         No data available.

 

           7.2.2 Relevant animal data

 

                 Toxicity in different strains of mice showed that toxic 

                 doses of folic acid may lead to convulsions, ataxia and 

                 weakness (Parchure et al., 1985). Histopathological 

                 studies in some strains of mice showed acute renal 

                 tubular necrosis. 

 

           7.2.3 Relevant in vitro data

 

                 Cytomorphological effects of folic acid were studied 

 

                 using in-vitro establishment human oral epithelium. A 

                 concentration twice that used clinically (200 mcg/ml of 

                 folic acid) did not induce marked cytotoxic reaction in 

                 cultured cells. The most pronounced changes were 

                 cultures which showed degenerating cells showing 

                 oedema, increased translucency of the cytoplasm, 

                 flattened cells and atypical filaments (Jainkittivong  

                 et al., 1989). 

 

       7.3 Carcinogenicity

 

           No data available.

 

       7.4 Teratogenicity

 

           No data available.

 

       7.5 Mutagenicity

 

           No data available.

 

       7.6 Interactions

 

           Folic acid therapy may increase phenytoin metabolism in 

           folate deficient patients resulting in decreased phenytoin 

           serum concentration. It has also been reported that 

           concurrent administration of folic acid and chloramphenicol 

           in folate deficient patients may result in antagonism of the 

           haematopoietic response to folic acid. 

 

           The use of ethotoin or mephenytoin concurrently with folic 

           acid may decrease the effects of hydantoins by increasing 

           hydantoin metabolism. 

 

           Trimethoprim acts as a folate antagonist by inhibiting 

           dihydrofolate reductase, so in patients receiving this drug 

           leucovorin calcium must be given instead of folic acid. Folic 

           acid may also interfere with the effects of pyrimethamine. 

 

           Aminopterin (4 aminofolic acid) and methotrexate (4 amino- 10 

           methylfolic acid) antagonizes reduction of folic acid to 

           tetrahydrofolic acid. Methotrexate continues to be used as an 

           antineoplastic drug whose activity may be dependent on 

           blocking certain syntheses, e.g., of purines, in which folic 

           acid is required, thereby depriving neoplastic cells of 

           compounds essential for their proliferation. Calcium 

           leucovorin is used therapeutically as a potent antidote for 

           the toxic effects of folic acid antagonists used as 

           antineoplastic agents. Methotrexate or pyrimethamine or 

           triamterene also acts as folate antagonist by inhibiting 

           dihydrofolic reductase (USP DI, 1983). 

 

           Analgesics, anticonvulsants, antimalarials and 

           corticosteroids may cause folic acid deficiency (USP DI, 

           1983). 

 

           Folic acid precipitates in some proprietary amino acid 

           solutions and in the presence of high concentration of 

           calcium ions, but it appears to be stable and remains in 

           solution provided the pH remains above 5. There have also 

           been reports of folic acid being absorbed by the polyvinyl 

           chloride containers and administration set, however, other 

           studies have not substantiated such observations. 

 

           Regarding intravenous incompatibilities, calcium gluconate 

           and folic acid injections have been shown to interact even 

           though a precipitate is not present. The recoverable amount 

           of folic acid from a 10 mg/ml solution declined with 

           increasing concentrations (0.5 to 10 mg/ml) of calcium 

           gluconate. This interaction was reversed by the addition of 

           edetic acid (Trissel, 1986). 

 

       7.7 Main adverse effects

 

           Allergic reactions to folic acid have been rarely reported 

           including erythema, rash, itching, general malaise and 

           bronchospasm. Adverse gastrointestinal and central nervous 

           system effects have been reported in patients receiving 15 mg 

           of folic acid daily for one month. 

 

  1. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS

 

       8.1 Sample

 

           8.1.1 Collection

 

           8.1.2 Storage

 

                 Pharmaceutical product, should be preserved in well 

                 closed, light resistant containers, preferably type 1 

                 glass. 

 

           8.1.3 Transport

 

       8.2 Toxicological analytical methods

 

           8.2.1 Assay for folic acid may be found in the USP XXII, 

 

                 Identification: 

                 Folic acid injection: to a volume of the injection 

                 equivalent to about 100 mg of folic acid add water to 

                 make about 25 mL. Adjust with hydrochloric acid to a pH 

                 of 3.0 cool to 5, then filter, and wash the precipitate 

                 of folic acid with cold water until the last washing 

                 shows an absence of chloride. Then wash with acetone, 

                 and dry at 80 for 1 hour: the ultraviolet absorption 

                 spectrum of a 1 in 100,000 solution of the folic acid 

                 so obtained in sodium hydroxide solution (1 in 250) 

                 exhibits maxima and minima at the same wavelengths as 

                 that of a similar solution of USP Folic Acid RS, 

 

                 concomitantly measured. The ratio A256/A365 is between 

                 2.80 and 3.00. 

 

                 Folic acid tablet-digest a quantity of powdered 

                 tablets, equivalent to about 100 mg of folic acid, with 

                 100 mL of sodium hydroxide solution (1 in 250), and 

                 filter. Proceed as directed in the identification test 

                 under Folic Acid Injection (USP, 1985). 

 

           8.2.2 Test for biological sample

 

                 Blood may be used for microbiological assay or 

                 competitive binding technique to determine the plasma 

                 and red cell folate levels (USP XX11, 1990). 

 

       8.3 Biochemical investigations

 

           8.3.1 Blood

 

                 BUN, Creatinine-to test for renal function AST, ALT, 

                 Alkaline Phosphatase-to test for liver status 

 

           8.3.2 Urine

 

                 No data available.

 

           8.3.3 Others

 

                 No data available.

 

       8.4 Interpretation

 

           Normal serum total folate concentration have been reported to 

           range from 0.005 to 0.015 mg/mL (AHFS Drug Information, 

           1990). Use of antibiotics may interfere with microbiological 

           assay for serum and erythrocyte folic acid concentration and 

           cause falsely low levels (US XX11, 1990). 

 

       8.5 References

       

    Position   Radical Congener

 

       N       -CH   CH H PteGlu        Methyltetrahydrofolate 

       N       -CHO   5-CHOH PteGlu      Folinic acid (Citrovorum 

                                              factor) 

       N       -CHO   10-CHOH PteGlu     10 Formyltetrahydrofolate 

       N       -CH-   5, 10-CHH PteGlu   5, 10-Methenyltetrahydro-

                                              folate

       N       -CH-   5, 10-CH H PteGlu  5, 10 Methylenetetrahydro-

                                              folate

       N       -CHNH   CH OHH PteGlu      Forminiotetrahydrofolate

       N       -CH OH   CH OHH PteGlu      Hydroxymethyltetrahydro-

                                              folate

 

    Structures and Nomenclature of Folic Acid and Congeners (Goodman & 

    Gillman, 1990). 

       

  1. CLINICAL EFFECTS

 

       9.1 Acute poisoning 

 

           9.1.1 Ingestion

 

                 No data available.

 

           9.1.2 Inhalation

 

                 Not known.

 

           9.1.3 Skin exposure

 

                 No data available.

 

           9.1.4 Eye contact

 

                 No data available.

 

           9.1.5 Parenteral exposure

 

                 Therapeutic doses may cause anaphylaxis.

 

       9.2 Chronic Poisoning

 

           9.2.1 Ingestion

 

                 Unconfirmed reports of gastrointestinal and central 

                 nervous system effects have been reported rarely in 

                 patients receiving 15 mg of folic acid daily for one 

                 month (McEvoy, 1990). 

                 

           9.2.2 Inhalation

 

                 Not known.

 

           9.2.3 Skin exposure

 

                 No data available.

 

           9.2.4 Eye contact

 

                 No data available.

 

           9.2.5 Parenteral exposure

                         

                 No data available.

 

       9.3. Course, prognosis, cause of death

 

           No data available.

 

       9.4 Systematic description of clinical effects

 

           9.4.1 Cardiovascular

 

                 Hypertension and shock may be seen as a manifestation 

                 of allergic reaction. 

 

           9.4.2 Respiratory

 

                 Bronchospasm may be seen as a manifestation of allergic 

                 reaction. 

 

           9.4.3 Neurological

                                   

                 9.4.3.1 Central nervous system (CNS)

 

                         No data available.

                                   

                 9.4.3.2 Peripheral nervous system

 

                         No data available.

 

                 9.4.3.3 Autonomic nervous system 

 

                         No data available.

                         

                 9.4.3.4 Skeletal and smooth muscle

 

                         Unconfirmed reports of general malaise and 

                         ataxia have been received following therapeutic 

                         doses. 

 

           9.4.4 Gastrointestinal

 

                 Nausea and vomiting as an adverse reaction has been 

                 reported. 

 

           9.4.5 Hepatic

 

                 No data available.

 

           9.4.6 Urinary

 

                 9.4.6.1 Renal

 

                         No data available.

 

                 9.4.6.2 Other

 

                         No data available.

 

           9.4.7 Endocrine and reproductive systems

 

                 No data available.

 

           9.4.8 Dermatological

 

                 No data available.

 

           9.4.9 Ear, nose and throat: local effects

 

                 No data available.

 

           9.4.10 Hematological

 

                  No data available.

 

           9.4.11 Immunological

 

                  No data available.

 

           9.4.12 Metabolic

 

                  9.4.12.1 Acid-base disturbances

 

                           No data available.

 

                  9.4.12.2 Fluid and electrolyte disturbances

 

                           No data available.

 

                  9.4.12.3 Others

                                   

                           No data available.

 

           9.4.13 Allergic reaction

 

                  Rash, erythema and itching.

 

           9.4.14 Other clinical effects

 

                  No data available.

 

           9.4.15 Special risks

 

                  No data available.

 

       9.5 Other

 

           Unknown

 

       9.6 Summary

 

           Not relevant

 

  1. MANAGEMENT

 

        10.1 General principles

 

             In cases of overdose, treatment is symptomatic and 

 

             supportive and is guided by the clinical features. 

 

             In case of anaphylactic reaction standard treatment should 

             be given. (See Treatment Guide on Anaphylaxis). 

 

             In case of massive ingestion gastric lavage or induced 

             vomiting could be considered if seen within 1 to 2 hours 

             after ingestion. Activated charcoal should be given 

             repeatedly in view of the enterohepatic circulation of 

             folic acid. 

 

        10.2 Relevant laboratory analyses

 

             10.2.1 Sample collection

 

                    Collect blood for plasma and red cell folate levels. 

 

             10.2.2 Biomedical  analysis

 

                    Request for other test would depend on patient 

                    presentation. 

 

                    There are no confirmed reports of folic acid 

                    overdose in humans. In case of an overdose, 

                    determination of blood urea nitrogen and creatinine 

                    level would be appropriate because of the 

                    possibility of renal toxicity which has been 

                    reported in experimental mice. Determination of 

                    liver function (AST, ALT, Alkaline phosphatase) 

                    should also be done due to the possibility of 

                    hepatotoxicity, (the liver being the primary storage 

                    site of folic acid). 

 

             10.2.3 Toxicological analysis

 

                    Not relevant

 

             10.2.4 Other investigations

 

                    Not relevant

 

        10.3 Life supportive procedures and symptomatic/specific treatment

 

             Treatment is largely supportive. In case of anaphylactic 

             reaction, epinephrine (adrenaline) should be given. 

             Maintain a clear airway and aspirate secretions from 

             airway. Administer oxygen and perform endotracheal 

             intubation when necessary. Support ventilation using 

             appropriate mechanical device. Control convulsions with 

             appropriate drug regimen. Perform cardio-respiratory 

             resuscitation when necessary. Correct hypotension with 

             isotonic fluids and  inotropic agents. 

 

        10.4 Decontamination

 

             In case of massive ingestion induce vomiting or gastric 

             lavage,  if seen within 1 to 2 hours after ingestion. 

             Repeat dose activated charcoal. 

 

        10.5 Elimination

             

             Adequate hydration would be sufficient to eliminate the 

             drug through the kidneys. 

 

        10.6 Antidote treatment

 

             10.6.1 Adults

 

                    No antidote.

 

             10.6.2 Children

 

                    No antidote.

 

        10.7 Management discussion

 

             Folic acid is relatively non-toxic and management is 

             directed toward symptomatic and supportive therapy. 

 

             The only allergic reaction to folic acid, which is life 

             threatening, is anaphylaxis. For anaphylaxis one should 

             give epinephrine (adrenaline) and (if considered necessary) 

             corticosteroids and fluids. 

 

             For hypotension unresponsive to volume expansion, one may 

             give dopamine. 

 

             Repeated doses of activated charcoal are necessary to 

             remove excess folic acid from the enterohepatic 

             recirculation. 

 

  1. ILLUSTRATIVE CASES

 

        11.1 Case reports from literature

 

             There is little data available on folic acid toxicity in 

             humans. A case of 2 patients who showed exacerbation of 

             psychotic behaviour during treatment with folic acid has 

             been reported (Prakash et al., 1982). The significance of 

             this finding is uncertain since other authors have 

             suggested that folic acid has antipsychotic properties. 

 

        11.2 Internally extracted data on cases

                         

             Unknown

 

        11.3 Internal cases

 

             To be completed by each Centre using local data

             

  1. ADDITIONAL INFORMATION

 

        12.1 Availability of antidotes

 

             Not relevant

 

        12.2 Specific preventive measures

 

             Not relevant

 

        12.3 Other

 

             Not relevant

 

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        eds. (1987) Harrison’s principles of internal medicine, 11 th 

        ed., New York, McGraw-Hill Book Company. 

 

        Budavari S ed. (1989) The Merck Index: an encyclopedia of 

        chemicals, drugs, and biologicals, 11th ed. Rahway, New Jersey, 

        Merck and Co., Inc.  p 660 

             

        Ellenhorn MJ & Barceloux DG (1988) Medical toxicology, diagnosis 

        and treatment of human poisoning, New York, Elsevier, pp 30, 79. 

 

        Gilman AG, Rall TW, Nies AS & Taylor P eds.(1990) Goodman and  

        Gilman’s the pharmacological basis of therapeutics, 8th ed. New 

        York, Pergamon Press, pp 1294-1296, 1302-1306. 

 

        Goldfrank LR, Flomenbaum NE, Lewin NA, Weisman RS, Howland MA, & 

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        Edition, C.V. Mosby Company, Maruzen Company Limited 1980. 

 

        Haddad LM & Winchester JF eds. (1983) Clinical management of 

        poisoning and drug overdose. Philadelphia, Saunders. 

 

        Jainkittivong A, Arenholt-Bindsler D, Jepsen A, & Philipsen HP 

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        Dent Assoc Thai, 39: 121-127. 

 

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        toxicology: the basic science of poisons. New York, Macmillan 

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        and treatment. Lange Medical Company. 

 

        McEvoy GK ed. (1990) American hospital formulary service, drug 

        information. Bethesda, American Society of Hospital Pharmacists. 

        

        McGeer PL, McGeer EG, Nagai T, & Wong PT, A possible 

        relationship between folic acid neurotoxicity and cholinergic 

        receptors in the pyriform cortex and amygdala, J. Neural Transm 

        Suppl, 1983, 18: 327-344. 

 

        Moffat AC ed.  (1986) Clarke’s isolation and identification of 

        drugs in pharmaceuticals, body fluids, and post-mortem material. 

        2nd ed. London, The Pharmaceutical Press. 

 

        Osola, Pratt R (1973) The US Dispensary, 27th ed. J.B. 

        Lippincott Company, 

        

        Parchure M, Ambaye RV, Lalitha VS, & Gokhale SV( 1985) Acute 

        toxicity of folic acid in mice. Experientia, 41(1): 72-73. 

 

        Prakash R & Petrie WM (1982) Psychiatric changes associated with 

        an excess of folic acid. Am  J Psychiatry, 139(9):1192-1193 

 

        Reynolds JEF ed. (1989) Martindale: the extra pharmacopoeia, 

        29th ed. London, The Pharmaceutical Press. pp 1262-1263 

 

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        30th ed. London, The Pharmaceutical Press. pp 1039-1040 

 

        Trissel LA (1986)  Handbook on injectable drugs. Bethesda, 

        American Society of Hospital Pharmacists. 

 

        USP DI Drug Information for the Health Care Provider, Vol. 1, 

 

        United States Pharmacopeia, 21st rev. The National formulary 

        16th ed. (1985)  Rockville MD, United States Pharmacopeial 

        Convention. 

 

        United States Pharmacopeia, 22nd rev. The National formulary 

        17th ed. (1990)  Rockville MD, United States Pharmacopeial 

        Convention. 

 

        US Pharmacopeia, National Formulary, 22nd ed., 1990. 

 

        White, Handler and Smith Principles of Biochemistry, 4th ed., 

        McGraw-Hill Book Company, 1970. 

 

        WHO (1992) Anatomical Therapeutic Chemical (ATC) classification 

        index. Oslo, WHO Collaborating Centre for Drug Statistics 

        Methodology, p19. 

 

        WHO (1992) International nonproprietary names (INN) for 

        pharmaceutical substances. Geneva, World Health Organisation, 

        p 13. 

 

  1. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE 

        ADDRESS(ES) 

 

        Author         Dr E.S. Castillo

                       National Poison Control & Information Service 

                       Department of Pharmacology

                 UP College of Medicine

                 Manila

                       Philippines

 

        Date           August 1991.

 

        Reviewer       –

 

        Peer Review    Drs Pronczuk, Tempowski, Hartigan-Go, Ten-Ham. 

                       Newcastle-upon-Tyne, United Kingdom, February 

                       1992Newcastle-upon-Tyne, United Kingdom, February 

                       1992          

       

    

 

SECTION 1. CHEMICAL IDENTIFICATION

 

CHEMINFO Record Number: 604

CCOHS Chemical Name: Citric acid

Synonyms:

beta-Hydroxy-tricarboxylic acid

beta-Hydroxytricarballylic acid

2-Hydroxy-1,2,3-propanetricarboxylic acid

Acide citrique

Chemical Name French: Acide citrique

Chemical Name Spanish: Acido cítrico

CAS Registry Number: 77-92-9

Other CAS Registry Number(s): 5949-29-1

RTECS Number(s): GE7350000

EU EINECS/ELINCS Number: 201-069-1

Chemical Family: Saturated aliphatic carboxylic acid / saturated aliphatic tricarboxylic acid / saturated aliphatic hydroxycarboxylic acid / hydroxyalkanoic acid

Molecular Formula: C6-H8-O7

Structural Formula: HOOC-CH2-C(OH)(COOH)-CH2-COOH

 

SECTION 2. DESCRIPTION

 

Appearance and Odour:

Colourless crystals, or white, granular to fine crystalline powder (2,10); deliquescent (absorbs moisture from the air and forms wet solid or solution) in moist air.(2)

Odour Threshold:

Odourless (11)

Warning Properties:

Insufficient information available for evaluation.

Composition/Purity:

Citric acid exists and is available commercially as the anhydrous form (CAS 77-92-9) and as the monohydrate (CAS 5949-29-1). It is also available as an aqueous solution, mainly as a 50% w/w solution.

Uses and Occurrences:

Used widely as an acidulant, pH regulator, flavour enhancer, preservative and antioxidant synergist in many food and beverage products; in pharmaceutical preparations; in metal cleaning, polishing and finishing; as a scale remover in boiler and heat exchanger cleaning; as a hard surface cleaner; as a builder in both liquid and powder laundry detergents; in shampoos and cosmetics; as mordant to brighten colours; as a chelating agent in liquid fertilizers; in animal feeds; in enhanced oil recovery; in removal of hydrogen sulfide from natural and refinery gas; in flue gas desulfurization; as a dispersing agent in mineral and pigment slurries; in electroplating; in concrete, mortar and plaster formulations; in textile manufacturing; in the manufacture of alkyd resins and plastics; as a chemical intermediate for esters used as plasticizers in PVC film; in effervescent type denture cleansers; in shampoos and cosmetics; chemical cleaning; in refractories and moulds; and in analytical chemistry.(2,10,11)

Citric acid is found naturally in plants and animals. It is found in greatest amounts in many citrus fruits, but is also present as the free acid or as a salt in the fruit, seeds or juices of a wide variety of flowers and plants. In the body, citric acid is an essential component of the citric acid cycle which releases energy for physiological functions.(2)

 

SECTION 3. HAZARDS IDENTIFICATION

 

EMERGENCY OVERVIEW:

Colourless crystals, or white, granular to fine crystalline powder. Deliquescent. May burn if strongly heated. POTENTIAL COMBUSTIBLE DUST HAZARD. Dry powdered material may form explosive dust-air mixtures. CORROSIVE to the eyes and skin. Can cause permanent eye damage, including blindness, or permanent scarring of the skin.

 

POTENTIAL HEALTH EFFECTS

 

Effects of Short-Term (Acute) Exposure

 

Inhalation:

Dusts and mists from solutions can probably cause temporary irritation of the nose and throat, based on acidity. The severity of these effects would depend on the airborne concentration, concentration of the solution and the duration of exposure. There is no human or animal information available.

Skin Contact:

Dusts probably cause mild to severe irritation depending upon the duration of exposure. Concentrated solutions are probably corrosive, based on their acidity. Corrosive materials can cause severe skin damage, possibly with permanent scarring. There is no human information and only unconfirmed animal information available.

Eye Contact:

Dusts and solutions can cause severe irritation and corrosive injury (destruction of eye tissue), based on animal information. Depending on the concentration of the solution and the degree of exposure, corrosive materials can cause permanent eye damage, including blindness.

A severe reaction and injury to the cornea (dense white opacity) was reported following an incident in which a large quantity of saturated citric acid solution was splashed into the eyes of one individual.(1)

Ingestion:

Citric acid is present in citrus fruits (lemons contain 4-8% citric acid) and is present in many other foods at lower concentrations.(2) It is also used as a food additive.(3) Ingestion of large amounts may cause stomach pain and vomiting. Ingestion is not a typical route of occupational exposure.

Effects of Long-Term (Chronic) Exposure

 

INGESTION: Ingestion of citric acid continuously and in large amounts can cause tooth erosion, based on animal information. There is no human information available.

Carcinogenicity:

Citric acid is probably not carcinogenic. There is no specific information available, but citric acid is a normal part of body metabolism and of the human diet.

The International Agency for Research on Cancer (IARC) has not evaluated the carcinogenicity of this chemical.

The American Conference of Governmental Industrial Hygienists (ACGIH) has no listing for this chemical.

The US National Toxicology Program (NTP) has not listed this chemical in its report on carcinogens.

Teratogenicity and Embryotoxicity:

There is no human or animal information available.

Reproductive Toxicity:

Citric acid was not harmful to reproduction in two animal studies. There is no human information available.

Mutagenicity:

Negative results were obtained in three in vitro tests, one using mammalian cells. There is no human or animal in vivo information available.

Toxicologically Synergistic Materials:

There is no information available.

Potential for Accumulation:

Citric acid does not accumulate in the body. It is an essential component of the body’s processes for producing energy. It is continually produced and broken down. Even high doses would be rapidly cleared from the body.

 

SECTION 4. FIRST AID MEASURES

 

Inhalation:

If symptoms are experienced, remove source of contamination or have victim move to fresh air. If symptoms persist, obtain medical advice immediately.

Skin Contact:

Quickly and gently blot or brush away excess chemical. Remove contaminated clothing, shoes and leather goods (e.g. watchbands, belts). Flush contaminated area with lukewarm, gently flowing water for at least 20-30 minutes, by the clock. If irritation persists, repeat flushing. DO NOT INTERRUPT FLUSHING. If necessary, keep emergency vehicle waiting. Transport victim to an emergency care facility immediately. Completely decontaminate clothing, shoes and leather goods before re-use.

Eye Contact:

Quickly and gently blot or brush away excess chemical. Immediately flush the contaminated eye(s) with lukewarm, gently flowing water for at least 20-30 minutes, by the clock, while holding the eyelid(s) open. Neutral saline solution may be used as soon as it is available. DO NOT INTERRUPT FLUSHING. If necessary, keep emergency vehicle waiting. Take care not to rinse contaminated water into the non-affected eye or onto the face. If irritation persists, repeat flushing. Quickly transport victim to an emergency care facility.

Ingestion:

NEVER give anything by mouth if victim is rapidly losing consciousness, is unconscious or is convulsing. Have victim rinse mouth thoroughly with water. DO NOT INDUCE VOMITING. Have victim drink 240-300 mL (8 to 10 oz.) of water to dilute material in stomach. If milk is available, it may be administered AFTER the water has been given. If vomiting occurs naturally, repeat administration of water. Quickly transport victim to an emergency care facility.

First Aid Comments:

Provide general supportive measures (comfort, warmth, rest).

Consult a doctor and/or the nearest Poison Control Centre for all exposures except minor instances of inhalation or skin contact.

All first aid procedures should be periodically reviewed by a doctor familiar with the material and its conditions of use in the workplace.

 

SECTION 5. FIRE FIGHTING MEASURES

 

Flash Point:

Not applicable.

Lower Flammable (Explosive) Limit (LFL/LEL):

Not applicable

Upper Flammable (Explosive) Limit (UFL/UEL):

Not applicable

Autoignition (Ignition) Temperature:

1010 deg C (1850 deg F) (10)

Sensitivity to Mechanical Impact:

Probably not sensitive. Stable material.

Combustion and Thermal Decomposition Products:

Carbon monoxide and carbon dioxide are normal products of combustion.(12) Incomplete combustion may produce irritating fumes and acrid smoke.

Flammable Properties:

Specific Hazards Arising from the Chemical:

During a fire, irritating/toxic gases and fumes may be generated.

Extinguishing Media:

Carbon dioxide, dry chemical powder, alcohol foam, polymer foam, water spray or fog.(12)

 

Fire Fighting Instructions:

Evacuate area and fight fire from a safe distance or a protected location. Approach fire from upwind to avoid toxic decomposition products.

Water or foam may cause frothing. The frothing may be violent and could endanger personnel close to the fire. However, a water spray or fog that is carefully applied to the surface of the burning material, preferably with a fine spray or fog nozzle, will cause frothing that will blanket and extinguish the fire. In addition, water spray or fog can be used to prevent dust formation, absorb heat, keep containers cool and protect exposed material. If a leak or spill has not ignited, use water spray to disperse the vapours and protect personnel attempting to stop a leak. Water spray may be used to flush spills away from ignition sources. Solid streams of water may be ineffective and spread material.

The decomposition products of citric acid may be hazardous to health.

Do not enter without wearing specialized protective equipment suitable for the situation. Firefighter’s normal protective clothing (Bunker Gear) will not provide adequate protection. Chemical resistant clothing (e.g., chemical splash suit) and positive pressure self-contained breathing apparatus (MSHA/NIOSH approved or equivalent) may be necessary.

 

NATIONAL FIRE PROTECTION ASSOCIATION (NFPA) HAZARD IDENTIFICATION

 

NFPA – Comments:

NFPA has no listing for this chemical in Codes 49 or 325.

 

SECTION 9. PHYSICAL AND CHEMICAL PROPERTIES

 

Molecular Weight: 192.13 (anhydrous); 210.14 (monohydrate)

Conversion Factor:

Not applicable

Physical State: Solid

Melting Point: 153-154 deg C (307.4-309.5 deg F) (anhydrous) (2,16,17)

Boiling Point: Decomposes at 175 deg C (347 deg F) (2)

Relative Density (Specific Gravity): 1.665 at 20 deg C (anhydrous) (water = 1) (17)

Solubility in Water: Very soluble (59.2 g/100 g at 20 deg C) (2,16)

Solubility in Other Liquids: Anhydrous citric acid is very soluble in absolute ethanol and moderately soluble in amyl acetate and diethyl ether at 25 deg C.(2,11) The monohydrate is very soluble in methanol and propanol, soluble in amyl alcohol, moderately soluble in amyl acetate, ethyl acetate and diethyl ether and practically insoluble in chloroform at 25 deg C.(10,11)

Coefficient of Oil/Water Distribution (Partition Coefficient): Log P(oct) = -1.72 (measured); -1.25 to -1.80 (calculated) (18)

pH Value: 2.2 (1% solution); 1.7 (10%); 1.2 (30%); 0.8 (50%) (2)

Vapour Density: Not applicable

Vapour Pressure: Practically zero at normal temperatures.

Saturation Vapour Concentration: Not applicable

Evaporation Rate: Probably very low at normal temperatures.

Critical Temperature: Not available

Other Physical Properties:

ACIDITY: Moderately strong acid: pKa1 = 3.14; pKa2 = 4.77; pKa3 = 6.39 at 20 deg C.(2)

VISCOSITY-DYNAMIC: 6.5 mPa.s (6.5 centipoises) at 25 deg C (50% aqueous solution) (10)

NOTE: When gently heated, the monohydrate loses water of hydration at 70-75 deg C (158-167 deg F) and melts in the range 135-152 deg C (275-306 deg F).

Rapid heating causes dehydration at 100 deg C (212 deg F) to form crystals that melt at 153-154 deg C.(2)

 

SECTION 10. STABILITY AND REACTIVITY

 

Stability:

Normally stable. Decomposes (loses carbon dioxide and water) at 175 deg C.(2,11)

Hazardous Polymerization:

Does not occur

Incompatibility – Materials to Avoid:

NOTE: Chemical reactions that could result in a hazardous situation (e.g. generation of flammable or toxic chemicals, fire or detonation) are listed here. Many of these reactions can be done safely if specific control measures (e.g. cooling of the reaction) are in place. Although not intended to be complete, an overview of important reactions involving common chemicals is provided to assist in the development of safe work practices.

 

STRONG OXIDIZING AGENTS (e.g. perchloric acid, peroxides, chromates, nitric acid) – mixtures may react violently if heated. Increased risk of fire.(12)

STRONG REDUCING AGENTS (e.g. phosphorus, tin (II) chloride, metal hydrides) – may react vigorously or violently.(12)

STRONG BASES (including alkalis such as sodium hydroxide) – mixtures may generate heat and pressure. Increased risk of fire.(12)

METAL NITRATES – a mixture exploded during a vacuum evaporation procedure.(19)

Hazardous Decomposition Products:

Not available

Conditions to Avoid:

Generation of dust, heat, flames, sparks, build-up of static electricity and other ignition sources

Corrosivity to Metals:

Mildly corrosive to carbon steel, gray and nickel cast iron, copper, brass, aluminum and lead.(2,20) Not corrosive to type 316 stainless steel, copper- nickel, nickel-molybdenum, nickel-chromium-molybdenum and nickel-chromium-iron- molybdenum alloys.(20,21) High acid concentrations may severely corrode 304 stainless steels, which are also not recommended for use at elevated temperatures. 316 stainless steel is the recommended material for handling citric acid.(2,21)

Stability and Reactivity Comments:

Citric acid is corrosive to normal concrete and should not be used with nylon, polycarbonates, polyamides, polyimides and acrylics. It may be used with fibre glass-reinforced polyester, polyethylene, polypropylene and polyvinyl chloride.(2O)

 

SECTION 11. TOXICOLOGICAL INFORMATION

 

LD50 (oral, rat): 3000 mg/kg (4, unconfirmed); 11700 mg/kg (5, unconfirmed)

LD50 (oral, mouse): 5000 mg/kg (3, unconfirmed); 5040 mg/kg (5, unconfirmed)

Eye Irritation:

Little or no injury was observed in rabbits following application of a single drop of 2-5% citric acid solution in water. However, irreversible injury (permanent cloudiness of the cornea to severe dense opacification) was observed following 30-minute continuous contact with 0.5-2% solutions.(1) Severe irritation was observed in rabbits following application of citric acid in another study (details not available in English).(4, unconfirmed)

Skin Irritation:

Mild irritation was observed in rabbits following application of citric acid in one study (details not available in English).(4, unconfirmed) Irritation (degree unspecified), but not corrosive effects, were observed in other animal studies. Details of the procedures used and citric acid concentrations tested are not available.(2, unconfirmed)

Effects of Short-Term (Acute) Exposure:

Ingestion:

No symptoms of kidney damage or other toxic effects were observed in dogs fed a daily dose of 1380 mg/kg for 112 to 120 days.(5)

Effects of Long-Term (Chronic) Exposure:

Ingestion:

No harmful effects except a slight increase in wearing away of the teeth were observed in rats fed 1.2% citric acid for 90 weeks.(5) A loss in body weight gain and reduced survival time were observed in mice fed a high concentration (5%) in the diet for an unspecified period of time.(6) Blood in the urine was observed in 4/5 rats fed a high concentration (4.8%) in the diet for 6 weeks. Decreased food intake and body weight gain was observed in animals fed 1.2-4.8%. No other harmful effects were observed.(7)

Carcinogenicity:

An increased rate of bladder cancer was observed in rats given citric acid (route of administration unspecified) following pre-treatment with oral doses of known bladder carcinogens (compared to those receiving only the known bladder carcinogens). However, these effects were judged to be a secondary effect of increased water consumption and not a direct effect of citric acid exposure.(5)

Reproductive Toxicity:

No harmful effects on reproduction were observed in rats fed 1.2% citric acid over 2 successive generations (90 weeks).(5) No effect on reproduction (litter size, still births, survival of young) was observed following feeding of female rats or mice with 5% citric acid in the diet prior to, during and subsequent to mating (duration unspecified).(8)

 

SECTION 16. OTHER INFORMATION

 

Selected Bibliography:

(1) Grant, W.M., et al. Toxicology of the eye. 4th edition. Charles C. Thomas, 1993. p. 411

(2) Blair, G., et al. Citric acid. In: Kirk-Othmer encyclopedia of chemical technology. 4th edition. Volume 6. John Wiley and Sons, 1993. p. 354-380

(3) Gosselin, R.E., et al. Clinical toxicology of commercial products. 5th edition. Williams and Wilkins, 1984. p. II-225

(4) RTECS record for citric acid. Last updated: 9704

(5) Katz, G.V., et al. Aliphatic carboxylic acids. In: Patty’s industrial hygiene and toxicology. 4th edition. Edited by G.D. Clayton et al. Volume II. Toxicology. Part E. John Wiley and Sons, 1994. p. 3572, 3574, 3587-3589

(6) Wright, E., et al. Some effects of dietary citric acid in small animals. Food and Cosmetics Toxicology. Vol. 14 (1976). p. 561-564

(7) Yokotani, H., et al. Acute and subacute toxicological studies of TAKEDA- citric acid in mice and rats. Journal of the Takeda Research Laboratories. Vol. 30, no. 1 (1971). p. 25-31

(8) Wright, E., et al. The influence of a dietary citric acid supplement on the reproduction and survival time of mice and rats. Nutrition Reports International. Vol. 13, no. 6 (June, 1976). p. 563-566

(9) Ishidate, Jr., M., et al. Primary mutagenicity screening of food additives currently used in Japan. Food and Chemical Toxicology. Vol. 22, no. 8. (1984). p. 623-636

(10) HSDB record for citric acid. Last revision date: 97/04/07

(11) Verhoff, F.H. Citric acid. In: Ullmann’s encyclopedia of industrial chemistry. 5th revised edition. Vol. A 7. VCH Verlagsgesellschaft, 1985. p. 103-108

(12) The Sigma-Aldrich library of chemical safety data. Edition II. Volume 1. Sigma-Aldrich Corporation, 1988. p. 892B,D

(13) Her Majesty’s Factory Inspectorate. Dust explosions in factories. Her Majesty’s Stationary Office, [nd]

(14) Grossel, S.S. Safety considerations in conveying of bulk solids and powders. Journal of Loss Prevention in the Process Industries. Vol. 1 (April, 1988). p. 62-74

(15) Schwab, R.F. Dusts. In: Fire protection handbook. Edited by A.E. Cote. 18th edition. National Fire Protection Association, 1997. p. 4-174 to 4-181

(16) Dean, J.A. Lange’s handbook of chemistry. 14th edition. McGraw-Hill, Inc., 1992. p. 1.146, 8.32

(17) Weast, R.C., ed. Handbook of chemistry and physics. 66th edition. CRC Press, 1985-1986. p. C-213, D-146, D-161

(18) Leo, A., et al. Partition coefficients and their uses. Chemical Reviews. Vol. 71, no. 6 (December, 1971). p. 573

(19) Urben, P.G., ed. Bretherick’s handbook of reactive chemical hazards. 5th edition. Volume 2. Butterworth-Heinemann Ltd., 1995. p. 210-211

(20) Corrosion data survey: metals section. 6th edition. National Association of Corrosion Engineers, 1985. p. 40-9 to 41-9

(21) Elder, G.B. Materials of construction for organic acids. In: Process industries corrosion: the theory and practice. Edited by B.J. Moniz, et al. National Association of Corrosion Engineers, 1986. p. 287-296

(22) Forsberg, K., et al. Quick selection guide to chemical protective clothing. 4th ed. Van Nostrand Reinhold, 2002

(23) Schliemann-Willers, S., et al. Fruit acids do not enhance sodium lauryl sulphate-induced cumulative irritant contact dermatitis in vivo. Acta Dermato-Venereologica. Vol. 85 (2005). p. 206-210

(24) European Commission. Citric acid. IUCLID Dataset. European Chemicals Bureau, Feb. 2000. Available at: <ecb.jrc.it/esis>

Information on chemicals reviewed in the CHEMINFO database is drawn from a number of publicly available sources. A list of general references used to compile CHEMINFO records is available in the database Help.

 

Review/Preparation Date: 1997-12-24

 

Revision Indicators:

Resistance of materials for PPE 2004-04-06

Bibliography 2006-04-05

LFL/LEL 2006-10-05

UFL/UEL 2006-10-05

 

RIBOFLAVINICSC: 1454
Date of Peer Review: October 2002

Lactoflavine

Vitamin B2

CAS #83-88-5C17H20N4O6
RTECS #VJ1400000Molecular mass: 376.4
UN #
EC #

 

TYPES OF HAZARD / EXPOSUREACUTE HAZARDS / SYMPTOMSPREVENTIONFIRST AID / FIRE FIGHTING
FIRECombustible. Gives off irritating or toxic fumes (or gases) in a fire.NO open flames.Coarse water spray, carbon dioxide.
EXPLOSIONFinely dispersed particles form explosive mixtures in air.Prevent deposition of dust; closed system, dust explosion-proof electrical equipment and lighting.

 

EXPOSUREPREVENT DISPERSION OF DUST!
InhalationCough. Sore throat.Local exhaust or breathing protection.Fresh air, rest.
SkinProtective gloves.Rinse and then wash skin with water and soap.
EyesRedness. Pain.Safety spectacles.First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then take to a doctor.
IngestionDo not eat, drink, or smoke during work.

 

SPILLAGE DISPOSALPACKAGING & LABELLING
Sweep spilled substance into covered containers; if appropriate, moisten first to prevent dusting.EU Classification

UN Classification

EMERGENCY RESPONSESTORAGE
NFPA Code: H0; F3; R0;Well closed.
IPCS

International

Programme on

Chemical Safety

Prepared in the context of cooperation between the International Programme on Chemical Safety and the Commission of the European Communities © IPCS, CEC 1999

SEE IMPORTANT INFORMATION ON BACK

 

RIBOFLAVINICSC: 1454

 

IMPORTANT DATA
PHYSICAL STATE; APPEARANCE:

ORANGE-YELLOW CRYSTALS

PHYSICAL DANGERS:

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

CHEMICAL DANGERS:

The substance decomposes on heating producing toxic fumes.

OCCUPATIONAL EXPOSURE LIMITS:

TLV not established.

ROUTES OF EXPOSURE:

The substance can be absorbed into the body by ingestion.

INHALATION RISK:

A nuisance-causing concentration of airborne particles can be reached quickly when dispersed.

PHYSICAL PROPERTIES
Melting point (decomposes): 280°C

Solubility in water, g/100 ml at 25°C: 0.01

Octanol/water partition coefficient as log Pow: -1.46
ENVIRONMENTAL DATA
NOTES
ADDITIONAL INFORMATION
LEGAL NOTICENeither the CEC nor the IPCS nor any person acting on behalf of the CEC or the IPCS is responsible for the use which might be made of this information
© IPCS, CEC 1999

 

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