CBD vs THC: What is the difference?
CBD is currently one of the most heated topics in the health industry. One might have heard about it while seeking medical advice from an allopathic practitioner, a holistic practitioner, a primary care physician, or a specialist. One might have also seen it from web platforms and is probably curious about the diversity of health benefits associated with it.
One thing that has left many people uncertain or confused about is whether or not a CBD product should have THC.
CBD was first isolated or purified for use outside of the whole marijuana plant in 1940, but THC would not be isolated for another 24 years. This took place in 1964 by way of scientist Raphael Mechoulam.
CBD and THC are only two of the isolated 113 cannabinoids to date. CBD and THC are the most vastly known and most thoroughly researched of the bunch. They are both compounds that occur naturally in plants that fall in the cannabis genus classification, and both are called phytocannabinoids. These two phytocannabinoid compounds are known to interact with two cannabinoid receptors, known as the CB1 receptors and CB2 receptors, which are part of the endocannabinoid system. The endocannabinoid system promotes homeostasis (or regularity) in the human body (and most mammalian species) by regulating numerous physiological and cognitive functions – such as sleep, appetite, mood, and pain.
While CBD oil has been legalized in many of the United States, the component tetrahydrocannabinol (or THC) does come at the cost of several additional and differing restrictions and prohibitions.
At its most basic, the main differences between cannabidiol (CBD) and tetrahydrocannabinol (THC) are the individuality of their physiological effects. CBD is a non-psychotropic compound of the marijuana plant, which means that (CBD) does not induce a psychoactive high or impart psychoactive effect, while THC is considered a psychotropic and does possess psychoactive properties. Additionally, THC is the only compound derived from cannabis that is known to produce the atypical “high” associated with marijuana to date.
Much like CBD, THC is a cannabinoid that can be extracted from the cannabis plant, and THC does offer many health benefits –but THC also contains intoxicating and psychoactive properties that are responsible for the “high” associated with marijuana and the recreational use of the cannabis plant.
For this reason, professional athletes should take precautionary care to ensure any high CBD supplements used are free of THC so as not to violate the USADA’s anti-doping regulations. Additionally, it would also be prudent for individuals who are subject to regular drug testing to check the ingredients of supplements.
The Chemical Breakdown
Chemically, the structures of CBD and THC are quite similar. They both share an identical molecular formula: 21 carbon atoms, 30 hydrogen atoms, and 2 oxygen atoms. Furthermore, the molecular mass of CBD and THC is also nearly identical, as THC has a mass of 314.469 g/mol, and CBD bears a mass of 314.464 g/mol.
THC and CBD are also biosynthesized in a very similar fashion. Cannabigerolic acid, or CBGA, is cycled into tetrahydrocannabinolic acid, or THCA and cannabinolic acid, or CBDA, by their own synthases. This is where the end products THC and CBD are produced by decarboxylation (or the chemical reaction that removes a carboxyl group, thus releasing carbon dioxide) of their acidic forms, THCA and CBDA.
While the processes are incredibly similar, there remains one vital structural difference: CBD is essentially a structural isomer of THC. This means that although CBD and THC have the same chemical composition, their atoms are arranged a bit differently. There is a ring that opens and closes in chemistry. If the ring is closed, it is THC, and if the ring is open, it is CBD. The molecular structure differences between these compounds are what differentiate the two, giving each their own unique pharmacological properties.
Similar to the majority of the other cannabinoids, CBD and THC have less than ideal solubility within the water. However, their solubility is greater than that of many organic solvents – especially alcohols and lipids.
Both CBD and THC are found in the cannabis plant in a melding of acidic forms that are readily decarboxylated and are altered chemically upon interaction with heat. This is an important detail considering the most popular form of cannabis consumption is smoking and vaporizing – as the heating of cannabis can ultimately cause damage to its medicinal components, such as the beneficial component, terpenes.
TCH is also notorious for binding to plastic and glass, so good quality THC products are generally stored in organic solvents (such as alcohol tinctures or carrier oils such as coconut oil and hemp oil). They may also be stored within glassware made of amber silicate to avoid the leaching of components and loss of medicinal value, especially during testing and analytical procedures.
Understanding How THC Induces a “High”
Some basic information for starters: CB1 is a cannabinoid receptor made of G proteins, which is located mostly in the peripheral and central nervous system and is particularly abundant in the brain. It makes up a portion of the body’s endocannabinoid system and is activated by endogenous neurotransmitters as well as compounds that are naturally occurring, such as the phytocannabinoids that are found in cannabis.
THC is a partial antagonist of CB1 (and potent, at that), thereby stimulating the CB1 receptors and leading to the hallucinatory effects that cannabis is known for. Meanwhile, CBD is considered to be a “negative allosteric modulator” of CB1, which means it changes the CB1 receptor’s shape. This makes it increasingly trying for CB1 agonists, such as THC, to offer any stimulation to the receptor. Furthermore, CBD is not capable of stimulating or binding to CB1, which may be another reason that it fails to bear the hallucinatory effects that are associated with marijuana use.
How CBD and THC interact with each other
By interacting with the CB1 receptors, CBD is assumed to inflect the psychoactive properties of THC by constraining tetrahydrocannabinol’s ability to connect to (and therefore its ability to stimulate) the CB1 receptors. CBD has also been shown to reduce a portion of the potential negative side effects of THC by minimizing paranoia, anxiety, and short-term impairment of memory that is commonly experienced when using cannabis or cannabis products that deliver THC above 0.3%. It is suggested that CBD-rich products with minimal THC (below the regulated 0.3%) can offer benefits that are therapeutic without the presence of dysphoric or euphoric reactions.
Medical Use of CBD and THC
Cannabis has been used medicinally for thousands of years, even dating back to China in the year 100 AD. It was recorded for being used as an anesthetic by mixing a powdered form of the plant with wine and being administered before surgery. Interestingly, the Chinese term for “anesthesia” literally means “cannabis intoxication.” It is also thought that Chinese pharmacists obtained Cannabis Indica rather than Cannabis sativa. Indica strains are generally believed to be physically sedating, whereas Sativa strains tend to illicit a more invigorating and uplifting effect – the terpenes in cannabis tend to play a large role in what its effects are, whether uplifting or sedating.
Due to modern restrictions and regulations, modern research on cannabis as a medicinal component, while vast, is still considered to be limited. As cannabis is legalized more and more, research potential for cannabis and its medical qualities and medical uses grows greater.
The World Health Organization published a 2017 pre-review report, providing a recent summary of the potential and current clinical use of CBD. The evidence unequivocally shows that CBD could be indicated for the treatment of some forms of epilepsy, including Dravet’s Syndrome, which is a complex disorder found in children and is associated with a high rate of mortality as well as high drug-resistant seizures.
CBD has also effectively been shown to be consistently beneficial for its neuroprotective, antipsychotic, anti-inflammatory, anxiolytic, analgesic, anti-tumor, and anti-asthmatic properties. This evidence is based on clinical, pre-clinical, and anecdotal evidence alike.
The World Health Organization also states that CBD may be of benefit to those who have Parkinson’s, Huntington’s, and Alzheimer’s disease in addition to Multiple Sclerosis anxiety, depression, psychosis, cancer, chronic pain, and many other conditions.
Medically, CBD and THC offer different benefits, largely due to their slightly different medicinal properties.
CBD tends to be better utilized as a calming supplement and offers benefits such as:
- Reducing pre-existing inflammation or anti-inflammatory
- Anti-tumor effects
- Treatment of inflammatory bowel disease
- Treatment of depression
THC tends to be useful for an array of conditions, such as:
- Use as an analgesic
- Treating, reducing and/or preventing nausea
- An appetite stimulant
- Reducing symptoms of glaucoma
- Aiding sleep and treating insomnia
- Treatment of Anxiety and anti-anxiety benefits
- Reducing muscle spasms and muscular spasticity
What are Terpenes?
People who are familiar with the concept of utilizing aromatherapy to relax or to invigorate (for mind and body) are then already familiar with terpenes on a basic level. Terpenes are aromatic compounds that are commonly produced by plants and fruit. They can be found in peppers, oranges, lavender flowers, hops, and cannabis, to name a few. The terpenes in Cannabis are secreted by the same glands that secrete CBD and THC, and they are what cause Cannabis to release scents reminiscent of citrus, pine, berries, fuel, and more.
Similar to diffusing essential oils in a vapor diffuser, the terpenes (or terpenoids) in cannabis can promote feelings of calmness, relaxation, and even drowsiness. They can also stimulate energetic and more euphoric reactions – it all comes down to what terpenes are being used. For example, the terpene pinene has an alerting effect, whilst linalool has more relaxing and sedating properties.
It is important to note that trains of Indica or Sativa do not specifically determine the aromas and effects of the terpenes they produce, though some strains tend to offer more consistency than others.
Side Effects of THC and CBD
Some of the common adverse effects of cannabis as marijuana and cannabis with high concentrations of THC include:
- Changes in visual perception
- Decreased sperm count
- Slowed pupillary response to light
- Dry mouth
- Reduced coordination
- Altered sense of time
THC can cause temporary side effects, such as:
- Increased heart rate
- Dry mouth
- Red eyes
- Poor coordination
- Slowed reaction times
- Temporary memory loss
While neither compound is fatal, high THC may be contraindicated for long term use as it has been known to elicit negative psychiatric effects (with long term use). This is especially true for adolescents as the effect of high concentrations of THC is more profound in teens, increasing the risk for psychiatric disorders such as schizophrenia.
CBD, on the other hand, is well-tolerated, even in large doses. Research indicates that any side effects associated with CBD use are more likely the result of the drug to drug interactions between CBD and other medicines that an individual is taking. Always consult a primary physician or naturopath to ensure that CBD is compliant and not contraindicated with one’s current supplement and/or pharmaceutical regimen.
Hemp vs. Marijuana
Marijuana is defined, in the United States, as any Cannabis sativa plant that has a percentage of THC greater than 0.3%. THC, as addressed earlier, is the primary compound in cannabis that delivers psychoactive properties.
Hemp plants, on the other hand, are defined as any cannabis plant containing 0.3% or less of THC. This classification is strict, as a plant containing even 0.4% of THC is automatically classified as a marijuana plant – even despite the fact that the percentage would still be low enough to deliver little to no psychoactive effects.
Cannabis and Marijuana: Legality
Unfortunately, despite its revealed medicinal qualities, the use, sale and possession of cannabis and CBD products containing concentrations greater than 0.3% THC are illegal in the United States, under federal law (even despite individual state laws). As ruled by the Federal Controlled Substances Act of 1970, cannabis containing concentrations higher than 0.3% THC is considered to have “no accepted medical use” and is at risk of a higher potential for abuse, physical dependence, and psychological dependence. Some individual states have enacted legislation that permits exemptions for medicinal, industrial and recreational use.
Prior to the 1930s, no stigma or rules were inferred against cannabis and its use for any reason. It was commonly used for the production of cloth and products – such as clothing, paper, and rope – as well as herbal medicine and a recreational drug. Later in 1937, cannabis was placed under legal restriction and in 1970 found itself ruled illegal under the Controlled Substances Act of 1970.
In the Farm Bill of 2014, hemp was defined as plants with 0.3% or less of THC and was made legal for the purposes of industrial growth and research.
In 2018, under the Agriculture Improvement Act of 2018, hemp was made legal in all fifty states, and with that legality, the production and popularity of hemp-derived CBD oil accelerated rapidly.
The growth of cannabis for industrial use (specifically with hemp) was made illegal if grown without a permit under the Controlled Substances Act due to its relation to cannabis as a drug (marijuana), and thereby all imported products are required to adhere to a zero-tolerance policy abiding therewith. The Agricultural Act of 2014 allows for state-level departments and universities to cultivate cannabis for research purposes; to better determine its industrial potential.
All of that aside, cannabis continues to find extensive favor as a psychoactive drug amongst recreational and medical users in the United States. As of 2019, the recreational use of cannabis has been legalized in eleven U.S. states, two U.S. territories, as well as the District of Columbia. Meanwhile, the medicinal use of cannabis has been legalized in thirty-three U.S. states, four U.S. territories, and D.C.
There have been several failed efforts to reschedule cannabis under the Controlled Substances Act, and the United States Supreme Court even ruled that the federal government reserves the right to regulate and criminalize cannabis and its use – whether recreational or medicinal. As a result of this ruling, cannabis dispensaries are licensed individually by the state as well as any businesses that are state-licensed to sell products that have not been approved by the U.S. Food and Drug Administration.
Although the FDA has not approved cannabis due to legal risk, the FDA does recognize [cannabis and marijuana’s] potential benefits and has approved two drugs that contain components of marijuana.
Ultimately, it is strongly recommended that any individual considering usage of CBD, THC medical marijuana, and similar products should look into the laws in their state of residence before acquiring, using and consuming products that contain CBD or THC, regardless of whether the product is for medical purposes or for recreational use. Furthermore, any individual considering incorporating cannabis into their healthcare or recreational routine should consult with a healthcare provider to ensure that it does not interact poorly with any pre-existing medical conditions.
All in all, THC and CBD both have been shown to offer health benefits, and both have been used for centuries, and research continues to unveil their benefits and any associated risks further.
Physical properties of 2-Aminophenol:
- Melting point (decomposes): 170-174°C
- Density: 1.3 g/cm³
- Solubility in water, g/100 ml at 20°C: 1.7
- Vapor pressure, Pa at °C: negligible
- Relative vapor density (air = 1): 3.77
- Flash point: >175°C c.c.
- Auto-ignition temperature: 190°C
- Octanol/water partition coefficient as log Pow: 0.62
2-Aminophenol comes in the form of colorless to white crystals that turn dark on exposure to air or light. The substance decomposes on heating, producing toxic fumes (nitrogen oxides). 2-Aminophenol reacts violently with oxidants causing fire and explosion hazard.
The substance can be absorbed into the body by ingestion, through the skin, and by inhalation of its aerosol. A harmful concentration of airborne particles can be reached quickly when dispersed, especially if powdered. The substance may cause effects on the blood, resulting in the formation of methemoglobin. The effects may be delayed. Medical observation is indicated. Meanwhile, repeated or prolonged contact may cause skin sensitization.
2-Aminophenol may be hazardous in the environment; special attention should be given to aquatic organisms. Depending on the degree of exposure, periodic medical examination is suggested. Specific treatment is necessary in case of poisoning with this substance; the appropriate means with instructions must be available. 2-Aminophenol is combustible. It gives off irritating or toxic fumes (or gases) in a fire. Avoid exposure to open flames. As first aid treatment, use an alcohol-resistant foam, carbon dioxide, water spray or powder.
To prevent 2-Aminophenol ingestion, do not eat, drink, or smoke during work. Symptoms of 2-Aminophenol ingestion are blue lips or finger nails, blue skin, confusion, convulsions, cough, dizziness, headache, labored breathing, nausea, and unconsciousness. Symptoms may be delayed. For first-aid treatment, rinse the mouth and give a slurry of activated charcoal in water to drink. Refer for medical attention. To prevent 2-Aminophenol inhalation, employ the use of a local exhaust or breathing protection. Let the person get fresh air and rest, and then refer for medical attention.
Store 2-Aminophenol in an area without drain or sewer access. Keep the container well-closed. Separate 2-Aminophenol from oxidants, food and feedstuffs. Personal protection to use in 2-Aminophenol spillage disposal is the P3 filter respirator for toxic particles. Chemical protection suit is also required. Do NOT let this chemical enter the environment. Sweep spilled substance into sealable containers; if appropriate, moisten first to prevent dusting. Carefully collect remainder, then remove to a safe place. Packaging and labelling guideline: Do not transport 2-Aminophenol with food and feedstuffs.
2-Aminopyridine is colorless or white powder or crystals, with characteristic odor. Dust explosion possible if in powder or granular form, mixed with air.
2-Aminopyridine decomposes on burning producing nitrogen oxides and reacts with strong oxidants causing fire and explosion hazard. The solution in water is a strong base, it reacts violently with acid and is corrosive. 2-Aminopyridine can be absorbed into the body by inhalation of its aerosol, through the skin and by ingestion. A harmful contamination of the air can be reached very quickly on evaporation of this substance at 20°C.
2-Aminopyridine is combustible, and it gives off irritating or toxic fumes (or gases) in a fire. Avoid open flames. First aid treatment includes powder, alcohol-resistant foam, water spray, carbon dioxide. In cases of explosion, finely dispersed particles form explosive mixtures in air. Prevent deposition of dust; closed system, dust explosion-proof electrical equipment and lighting.
Symptoms of 2-Aminopyridine inhalation are convulsions, dizziness, headache, nausea, shortness of breath, and weakness. Use local exhaust or breathing protection. Fresh air and rest are recommended. Artificial respiration may be needed. Refer for medical attention.
When exposed to 2-Aminopyridine, eyes may manifest redness. Use face shield or eye protection in combination with breathing protection. For first treatment, first rinse with plenty of water for several minutes (remove contact lenses if easily possible), then take to a doctor.
2-Aminopyridine may be absorbed through the skin. Redness is an indication. Use protective gloves and protective clothing. Remove contaminated clothes. Rinse skin with plenty of water or shower.
Effects of Short-Term Exposure
The substance is irritating to the eyes and the skin. The substance may cause effects on the central nervous system, resulting in convulsions, respiratory depression. The substance may cause an increase in blood pressure. Exposure far above the OEL may result in death. The substance is toxic to aquatic organisms.
There is no odor warning even when toxic concentrations are present. The relation between odor and the occupational exposure limit cannot be indicated. Card has been partly updated in October 2005. See section Occupational Exposure Limits.
Store 2-Aminopyridine separated from food and feedstuffs, strong oxidants, and strong acids. Personal protection to use in 2-Aminophenol spillage disposal is the P3 filter respirator for toxic particles. Chemical protection suit is also required. Do NOT let this chemical enter the environment. Sweep spilled substance into sealable containers; if appropriate, moisten first to prevent dusting. Carefully collect remainder, then remove to a safe place.
The physical state or appearance of 1,5-Naphthalenediol is described as orange powder. Melting point (decomposes): 250°C. Solubility in water, g/100 ml at 20°C: 0.06. Flash point: 252°C c.c. Octanol/water partition coefficient as log Pow: 1.82
Chemical dangers of this substance include the formation of toxic fumes on combustion. 1,5-Naphthalenediol reacts with strong oxidants. The substance can be absorbed into the body by ingestion.
Effects of Short-Term Exposure: The substance is mildly irritating to the eyes.
1,5-Naphthalenediol is combustible. Avoid open flames. Use water spray or powder in case of fire. Use local exhaust or breathing protection to prevent 1,5-Naphthalenediol inhalation. Fresh air and rest. Use protective gloves to avoid skin exposure to 1,5-Naphthalenediol. Rinse affected area and then wash skin with water and soap.
Eyes exposed to 1,5-Naphthalenediol may manifest redness. Use safety goggles. As first aid treatment, first rinse with plenty of water for several minutes (remove contact lenses if easily possible), then take to a doctor. Do not eat, drink, or smoke during work to avoid 1,5-Naphthalenediol ingestion. Rinse mouth in case of ingestion.
Store 1,5-Naphthalenediol separated from strong oxidants. When disposing of 1,5-Naphthalenediol spillage, use personal protection like P1 filter respirator for inert particles. Sweep spilled substance into containers; if appropriate, moisten first to prevent dusting.
1,2,4-Trimethylbenzene is flammable. Avoid open flames, sparks, and smoking. Use alcohol-resistant foam, dry powder, or carbon dioxide in case of fire. For temperatures above 44°C, explosive vapor/air mixtures may be formed during explosions. For temperatures above 44°C, use a closed system, ventilation, and explosion-proof electrical equipment. Prevent build-up of electrostatic charges (e.g., by grounding). In case of fire, keep drums cool by spraying with water.
Prevent generation of mists to avoid exposure to 1,2,4-Trimethylbenzene. Symptoms of 1,2,4-Trimethylbenzene inhalation include confusion, cough, dizziness, drowsiness, headache, sore throat, and vomiting. A harmful contamination of the air will be reached rather slowly on evaporation of this substance at 20°C; on spraying or dispersing, however, much faster. Use ventilation, local exhaust, or breathing protection in case of 1,2,4-Trimethylbenzene inhalation. Fresh air and rest are recommended. Refer for medical attention.
Symptoms of 1,2,4-Trimethylbenzene skin exposure include redness and dry skin. Use protective gloves. Rinse skin with plenty of water or shower. Eyes exposed to 1,2,4-Trimethylbenzene may manifest redness and pain. Use safety spectacles. As first aid treatment, first rinse with plenty of water for several minutes (remove contact lenses if easily possible), then take to a doctor. To avoid 1,2,4-Trimethylbenzene ingestion, do not eat, drink, or smoke during work. As first aid treatment, rinse mouth, but do not induce vomiting. Refer for medical attention.
Store 1,2,4-Trimethylbenzene in fireproof containers separated from strong oxidants. Keep the containers well-closed and keep them in a well-ventilated room. For spillage disposal, collect leaking and spilled liquid in sealable containers as far as possible. Absorb remaining liquid in sand or inert absorbent and remove to safe place. Do not wash away 1,2,4-Trimethylbenzene into a sewer. Do not let this chemical enter the environment. Use a filter respirator for organic gases and vapours for personal protection.
Effects of Short-Term Exposure:
The substance is irritating to the eyes the skin and the respiratory tract. If this liquid is swallowed, aspiration into the lungs may result in chemical pneumonitis. The substance may cause effects on the central nervous system.
Effects of Long-Term or Repeated Exposure:
The liquid defats the skin. Lungs may be affected by repeated or prolonged exposure, resulting in chronic bronchitis. The substance may have effects on the central nervous system and blood.
1,2,4-Trimethylbenzene is toxic to aquatic organisms. Bioaccumulation of this chemical may occur in fish. Use of alcoholic beverages enhances the harmful effect. Depending on the degree of exposure, periodic medical examination is suggested.
Avoid all contact with 1,3-Bis(aminomethyl)benzene. In all cases, consult a doctor. 1,3-Bis(aminomethyl)benzene is combustible. Avoid open flames. Fire may be extinguished by using powder, AFFF, foam, carbon dioxide.
Exposure to 1,3-Bis(aminomethyl)benzene through inhalation causes a burning sensation, cough, sore throat, labored breathing, and shortness of breath. However, symptoms may be delayed. Employ ventilation, local exhaust, or breathing protection to alleviate symptoms of exposure. Fresh air, rest, and sitting in half-upright position are recommended. Artificial respiration may be needed in some cases. Always refer for medical attention.
Skin exposure to 1,3-Bis(aminomethyl)benzene may cause redness, pain, or burns. Use protective gloves and protective clothing as precautionary measure. Upon skin exposure, remove contaminated clothes and rinse skin with plenty of water or shower. Refer for medical attention.
Eye exposure to 1,3-Bis(aminomethyl)benzene may cause pain, redness, or severe deep burns. Use a face shield or eye protection in combination with breathing protection. Upon eye exposure, first rinse with plenty of water for several minutes (remove contact lenses if easily possible), then take to a doctor.
Symptoms of 1,3-Bis(aminomethyl)benzene ingestion may result to abdominal pain, burning sensation, shock or collapse. To prevent ingestion of this substance, do not eat, drink, or smoke during work. Upon ingestion, rinse mouth, and give plenty of water to drink. However, do not induce vomiting. Refer for medical attention.
1,3-Bis(aminomethyl)benzene is a colorless liquid and it decomposes on burning, producing toxic fumes including nitrogen oxides. The substance can be absorbed into the body by inhalation, through the skin and by ingestion. A harmful contamination of the air can be reached rather quickly on evaporation of this substance at 20°C; on spraying or dispersing, however, much faster.
1,3-Bis(aminomethyl)benzene is corrosive to the eyes, the skin and the respiratory tract. Inhalation of high concentration of the fume of this substance may cause lung edema. 1,3-Bis(aminomethyl)benzene is also corrosive on ingestion. Repeated or prolonged contact with 1,3-Bis(aminomethyl)benzene may cause skin sensitization.
The symptoms of lung edema often do not become manifest until a few hours have passed, and they are aggravated by physical effort. Rest and medical observation are therefore essential. The occupational exposure limit value should not be exceeded during any part of the working exposure.
Do not transport 1,3-Bis(aminomethyl)benzene with food and feedstuffs. In case of spills, consult an expert in large spills. Collect leaking and spilled liquid in sealable containers as far as possible. Absorb remaining liquid in sand or inert absorbent and remove to safe place. Carefully collect remainder. Extra personal protection: filter respirator for organic gases and vapors. Do not let this chemical enter the environment. 1,3-Bis(aminomethyl)benzene is harmful to aquatic organisms.
What is Cyanogen?
Cyanogen is a colorless gas, with an almond-like odor, which is acrid and pungent at high concentrations. The vapor irritates the eyes and causes tears. Odor threshold level detection tests on humans indicate that cyanogen cannot be detected at concentrations as high as 250 ppm. Eye and nasal irritations were observed at 16 ppm. Cyanogen is available with a minimum purity of 98.5%. Impurities present may include nitrogen, oxygen, nitric oxide, carbon dioxide and cyanogen chloride.
Cyanogen is used primarily in organic synthesis. It is also used as a fuel gas for welding and cutting heat-resistant metals; as a rocket and missile propellant (with an oxidizing agent such as ozone or fluorine); and as a fumigant. Cyanogen production and use may result in its release to the environment through various waste streams. It may be encountered as a decomposition product of chemicals with a carbon-nitrogen bond (e.g. metal cyanides, such as mercury and silver cyanides, and cyanogen iodide) and in blast-furnace gases and automobile exhausts.
Effects of Short-Term (Acute) Exposure Through Inhalation:
Cyanogen is an extremely toxic gas at room temperature and poses a very serious inhalation hazard. The toxicity of cyanogen is similar to hydrogen cyanide, but cyanogen is also severely irritating. Cyanogen caused nose irritation in 5 volunteers exposed to 16 ppm for 6 or 8 minutes, but no irritation at 8 ppm. Exposure to high concentrations may cause a potentially fatal accumulation of fluid in the lungs (pulmonary edema), based on the severe irritancy of cyanogen. Symptoms of pulmonary edema (chest pain and shortness of breath) can be delayed for up to 24 or 48 hours after exposure.
Cyanogen is broken down in the body to release cyanide. It is unlikely that anyone would voluntarily remain in a highly irritating cyanogen contaminated environment long enough to experience cyanide toxicity. However, cyanide toxicity is possible if the victim is unable to escape from a contaminated environment.
The early symptoms of cyanide poisoning may include anxiety and excitement, weakness, headache, nausea, vomiting, metallic taste, chest tightness, facial flushing, drowsiness, dizziness, irritation of the eyes, nose and throat, rapid breathing, a rise in blood pressure and a decrease in pulse. Labored breathing, falling blood pressure, rapid, weak irregular heartbeat, unconsciousness, and convulsions follow these symptoms. In severe cases, cardiovascular collapse, shock, and fluid accumulation in the lungs (pulmonary edema) are followed by death.(4,6,7,13) With massive doses, many of the signs and symptoms may not be seen, and there is rapid onset of poisoning with convulsions, collapse, and death. A characteristic sign of cyanide poisoning is the bright red color of the blood, which may result in red skin color.
The majority of people who survive acute cyanide poisoning do not have long-lasting effects. However, depending on the degree of exposure, there may be enduring effects from low oxygen, including impaired memory and mathematical abilities, personality changes, and altered control and coordination of movement.
Effects of Short-Term (Acute) Exposure Through Skin Contact:
Direct contact with liquefied cyanogen gas escaping from its high-pressure cylinder may cause frostbite. Symptoms of mild frostbite include numbness, prickling and itching in the affected area. Symptoms of more severe frostbite include a burning sensation and stiffness of the affected area. The skin may become waxy white or yellow. Blistering, tissue death and gangrene may also develop in severe cases. Cyanogen does not appear to be absorbed through the skin, based on a limited animal study.
Effects of Short-Term (Acute) Exposure Through Eye Contact:
Cyanogen gas caused eye irritation in 5 volunteers exposed to 16 ppm for 6 or 8 minutes, but no irritation occurred at 8 ppm. Higher concentrations are expected to produce severe eye irritation. Direct contact with liquefied gas escaping from its high-pressure cylinder may cause frostbite.
Effects of Long-Term (Chronic) Exposure
Cyanogen is broken down in the body to cyanide. Several human population studies have evaluated the potential health effects of long-term exposure to cyanide compounds. In general, these studies are limited by factors such as the small number of employees evaluated and the possibility of concurrent exposure to other potentially harmful chemicals (particularly in the electroplating industry). In addition, few studies report reliable measurements of cyanide exposures and even when airborne concentrations are reported, exposure may also have occurred by skin absorption. Despite these limitations, the available evidence suggests that long-term occupational cyanide exposure may be associated with harmful effects on the thyroid gland and the nervous system. Less consistently, there have been reports of effects on the respiratory and gastrointestinal systems, blood chemistry and the skin and eyes. For more information on the available studies, refer to the CHEMINFO reviews of hydrogen cyanide, sodium cyanide and potassium cyanide.
Limited information suggests that long-term exposure to cyanide compounds may be associated with harmful effects on the nervous system. Some of the symptoms observed are non-specific (e.g. headaches) and could be associated with many causes. Nevertheless, there does seem to be an association between some nervous system symptoms and cyanide exposure. The types of nervous system symptoms observed in the available studies include: headaches, dizziness, weakness, and nervous instability.
It is not possible to conclude that cyanogen is an occupational sensitizer based on the available information. In a study of 1939 farmers in Saskatchewan, the incidence of self-reported, medically diagnosed allergic “hay-fever” type reactions (allergic rhinitis) was compared with the use of specific pesticides, fertilizers, and the raising of different livestock. Data was adjusted for age and current smoking behavior, but not for family history of allergies. There was a statistically significant association between the incidence of allergic rhinitis and the use of certain herbicides, including cyanogen, and with the raising of horses.(16) It is not possible to draw specific conclusions about the sensitizing capability of cyanogen based on this study due to limitations such as self-reporting bias and the non-specific nature of the study.
Evidence from human and animal studies indicate that long-term exposure to cyanide compounds can result in impaired thyroid function and enlargement of the thyroid (goiter). Thiocyanate, the main metabolite of cyanide, is believed to cause these effects by inhibiting the uptake of iodine by the thyroid. In the only animal study available, long-term (6 months) exposure to relatively low concentrations (up to 25 ppm) of cyanogen did not produce significant harmful effects.
What is Cyanuric Acid?
Cyanuric acid is a white, odorless, crystalline solid, granule or powder. Cyanuric acid is hygroscopic, meaning it absorbs moisture from the air.
Cyanuric acid exists as an equilibrium mixture of two chemical forms (tautomers), the keto or oxo form and the enol or trihydroxy form. The keto or oxo form is called isocyanuric acid, while the enol or trihydroxy form is called cyanuric acid. In solution and in the solid state, the keto form is the main form. In alkaline solution, the enol form predominates. Cyanuric acid (or isocyanuric acid) is available as the anhydrous material and as a dihydrate. The anhydrous form is the main commercial compound. Cyanuric acid is sold mainly in coarse granular form. It is also available as a powder. Typical commercial products contain 98.5% and greater cyanuric acid. Impurities present include ammelide and ammeline.(1) Crude cyanuric acid contains up to 30% impurities consisting of melamine and its precursors, biuret, triuret, ammelide and ammeline.
Cyanuric acid is widely used to produce chlorinated isocyanurates, which are used as swimming pool, and spa and hot tub disinfectants, scouring powders, household bleaches, institutional and industrial cleansers, automatic dishwasher compounds and general sanitizers; as a stabilizer to inhibit ultraviolet destruction of chlorine and hypochlorous acid in swimming pools. It is also used as a laboratory source of isocyanic acid gas; and in the preparation of melamine, sponge rubber, selective herbicides, dyes, resins and antimicrobial agents. Cyanuric acid is used on a small scale for reducing nitrogen oxides in stationary diesel engine exhaust gases and coal, oil or gas fired boilers.
Effects of Short-Term (Acute) Exposure Through Inhalation:
Cyanuric acid is a solid, which absorbs moisture from the air, and does not form a vapour at normal temperatures. It is not irritating and is not expected to pose an inhalation hazard. In general, high airborne concentrations of dusts or mists formed from solutions can cause irritation of the nose and throat and coughing. However, there is no human or animal information available for cyanuric acid.
Effects of Short-Term (Acute) Exposure Through Skin Contact:
Cyanuric acid is not expected to be irritating to the skin, based on animal information. In a review of pesticide injuries in California from 1949-1988, there is a single report of skin injury from exposure to cyanuric acid as a pesticide. No other details are available for evaluation. Cyanuric acid is not expected to be absorbed through the skin in harmful amounts, based on limited animal toxicity information.
Effects of Short-Term (Acute) Exposure Through Eye Contact:
Cyanuric acid is expected to cause no to very mild eye irritation, based on animal information. The dust may cause mechanical or abrasive injury to the eye and tearing as it is rinsed from the eye. In a review of pesticide injuries in California from 1949-1988, there is a report of 4 cases of eye injury from exposure to cyanuric acid as a pesticide. No other details are available for evaluation.
Effects of Short-Term (Acute) Exposure Through Ingestion:
Cyanuric acid is not expected to be toxic, based on limited animal information. There is no human information available. Ingestion is not a typical route for occupational exposure