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Choloroform

Background of Chloroform

Chloroform is a colorless liquid that is not soluble in water and is very volatile, it has a pleasant non-irritating odor (has an odor threshold of 85 ppm). The Chemical formula of chloroform is CHCL3. Chloroform is nonflammable.

Where is chloroform found:

Low levels of chloroform can be found in the air and in costal waves, inland rives, lakes and groundwater. Levels can be noticeably higher in industrial areas as well as in the air above swimming pools containing chlorine.

Uses of Chloroform:

Chloroform can be used as a solvent to dissolve other substances. It can be used for the building, paper and board industries, and in pesticide and film production. Chloroform is used in making fluorocarbon-22 (a refrigerant).

Image result for fluorocarbon-22

Before the mid-1900’s, chloroform was used as an anesthetic to reduce any pain during a medical procedure. Eventually this was stopped due to the harmful effects of chloroform.

The EPA has classified chloroform as a Group B2, which means it is a probable human carcinogen.

How can people be exposed?

Most people are exposed to chloroform in food, drinking water, and indoor air. Some examples of chloroform being released into the environment are:Image result for swimming pools

  1. chlorination in drinking water
  2. wastewater
  3. swimming pools
  4. paper mills
  5. sanitary landfills
  6. tap water (chloroform is largely found in this)

Biotransformation:

Chloroform may undergo both oxidative and reductive biotransformation. The oxygenation of chloroform is catalyzed by cytochrome P450 and produces trichloromethanol. Elimination of HCL from trichlorometanol gives phosgene as a reactive intermediate.

Image result for uses of chloroform

Mechanism of action:

During the metabolism of chloroform, reactive intermediates, such as phosgene and dichloromethyl radicals are formed and cannot react with cellular components, such as fatty acids and phospholipids. The resulting lipid peroxidation account as least in part for the hepatoxic and nephrotoxic effects of chloroform.

Image result for chloroform mechanism of actionTarget Organs:

Chloroform is readily absorbed from the lungs, GI, and skin. The acute risks/organs affected are the CNS system (depression) and respiratory system (respiratory arrest). The late risks/organs affected are the liver and kidneys, resulting in overall damage.

Acute exposure to Chloroform:

Acute inhalation of chloroform can cause dizziness, ataxia and drowsiness. Convulsions, coma, and death may occur following substantial exposure. Delayed effects of chloroform exposure includes renal and hepatic damage (this is up to 48 hours post exposure). Local effects are observed following inhalation (irritation of the nose and throat), ingestion (burning sensation of the mouth and throat), ocular (stinging) and dermal exposure (irritation and redness).

Image result for chloroform poisoning

The OSHA permissible exposure limit (PEL) for chloroform is 50ppm, as a ceiling limit. The air odor threshold concentrations ranging from 85 to 307 ppm. The OSHA IDLH (immediately dangerous to life and health) limit is 500ppm.

Chronic exposure to Chloroform:

Chronic inhalation or ingestion of chloroform may cause hepatic damage. Again, the IARC classified chloroform as a category 2B carcinogen (possibly cancerous to humans). There is no data available regarding the reproductive and developmental effects of chloroform.

Testing for Chloroform exposure:

Chloroform can be detected in blood, urine, or body tissue tests. Although, these methods are not very reliable because chloroform is rapidly eliminated from the body and there are no tests specific for chloroform.

Image result for blood test

Treatment of Chloroform poisoning:

There is no exact treatment for chloroform poisoning. A study performed on a 19 year old man that tried to commit suicide with chloroform showed that an IV of N-acetylcysteine (NAC) was successful in treating the patient. There have been previous reports of survival with treatment after orally administered NAC.

Image result for n-acetylcysteine

Historical or unique exposures:

Chloroform is prepared through the chlorination of methane gas. It was prepared in 1831 by the American chemist Dr. Samuel Guthrie, who combined whiskey with chlorinated lime in attempt to produce a cheap pesticide. When administered by liquid onto a sponge or cloth (so that the patient inhaled the vapors) chloroform was seen to have narcotic effects on the CNS and happen very quickly. There were very high risks associated with chloroform and required physician skill. There were early reports of fatalities due to chloroform, beginning with a 15-year old girl in 1848. Still, chloroform use was still used and was actually used on Britain’s Queen Victoria during the birth of her 8th child.

Image result for uses of chloroform

Chloroform became popular during the Civil War and Mexican-American War being used as a anesthetic. Chloroform became under attack in the 20th century, and was no longer used due to the fact it was shown to be carcinogenic by ingestion in lab mice and rats.

Genetic susceptibility or heritable traits:

There is no genetic susceptibility or heritable traits associated with chloroform.

 

Figure References:

  1. https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/chloroform. Accessed 6/23/19.
  2. https://infograph.venngage.com/p/198917/sullivan-wilke-chloroform. Accessed 6/23/19.
  3. https://www.amazon.com/Best-Naturals-NAC-N-Acetyl-Cysteine-Capsules/dp/B00TQ5NZ4I. Accessed 6/23/19.
  4. https://www.google.com/url?sa=i&rct=j&q=&esrc=s&source=images&cd=&ved=2ahUKEwjc54aykYLjAhWOK80KHRxJCxMQjxx6BAgBEAI&url=https%3A%2F%2Fwww.bbc.com%2Fnews%2Fuk-england-kent-45680970&psig=AOvVaw2ux4K9p7DTyK0RpuOA86Tw&ust=1561466294322244. Accessed 6/23/19.
  5. https://www.wisegeek.com/what-is-chloroform.htm. Accessed 6/23/19.
  6. https://en.wikipedia.org/wiki/Swimming_pool. Accessed 6/23/19.
  7. https://www.kullabs.com/classes/subjects/units/lessons/notes/note-detail/9385. Accessed 6/23/19.
  8. https://www.dhgate.com/product/new-available-500m-fluorocarbon-fishing-line/393097851.html. Accessed 6/24/19.

Information derived from:

  1. https://www.history.com/topics/inventions/ether-and-chloroform. Accessed 6/23/19.
  2. https://www.ncbi.nlm.nih.gov/pubmed/20552315. Accessed 6/23/19.
  3. https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/338535/Chloroform_Toxicological_Overview.pdf. Accessed 6/23/19.
  4. https://www.atsdr.cdc.gov/PHS/PHS.asp?id=51&tid=16. Accessed 6/23/19.
  5. https://dhss.delaware.gov/dhss/dph/files/chloroformfaq.pdf. Accessed 6/23/19.
  6. https://www.epa.gov/sites/production/files/2016-09/documents/chloroform.pdf. Accessed 6/23/19.

Nickel (Blog Post #2)

What is Nickel?

Figure 1:Nickel Elemental Symbol

Image result for Nickel element

Nickel is a hard, corrosive and resistant metal. Nickel can be divided and used for many products:

  • Nickel can be alloyed with steel to make amour plats, vaults and machine parts
  • ¬†Nickel can be alloyed with other metals to improve the strength and resistance to corrosion
  • Nickel can be used to manufacture coins and batteries
  • Nickel (finely divided) can be used as a catalyst for the hydrogenation of vegetable oil
  • Nickel can be added to glass to give it the green color

Figure 2: The element Nickel in pure form

Image result for Nickel metal

Nickel is a good conductor of electricity and heat. It is one of the four elements that are ferromagnetic (which means magnetized easily) at room temperature. Nickel is considered a transition metal, which means that is has valance electrons in two shells instead of just one (this allows it to form several different oxidation states). Nickel functions as a cofactor for metalloenzymes and helps with the GI absorption of iron and zinc.

Nickel can be considered a trace mineral nutrient. Nickel helps plants liberate nitrogen from the soil an absorb iron. Although the number is unknown, the typical American diet supplies an estimated 0.3 to 0.6mg of nickel daily.

Brief History of Nickel

Now that we know what Nickel is, lets understand the history of Nickel. Nickel comes from a German word, meaning “Old Nick”. Nickel was discovered by the Swedish chemist Axel Fredrik Cronstedt in 1751. A interesting face about Nickel is how it was discovered. An American astrophysicist had a theory that an asteroid that struck the earth contained so much nickel, that it was responsible for the mass extinction of dinosaurs. Nickel spread into the vegetation of plants and water and poisoned the herbivore dinosaurs. The herbivore dinosaurs became extinct, which led to the extinction of carnivore dinosaurs. Most of the worlds supply of Nickel is found in Sudbury region of Ontario, Canada.

Figure 3: Nickel Plating PlantImage result for history of nickel

Nickel is the fifth most abundant element on Earth and the second most abundant element in the Earth’s inner core. Nickel can be found in two types of deposits: laterite deposits (which is the result of intensive weathering of surface nickel-rich rocks) and magmatic sulfide deposits. The main mineral sources of nickel are limonite, garnierite, and pentlandite.

Exposure to Nickel

Nickel can enter the atmosphere and expose humans a variety of different ways including:

  • Refining Plants
  • Power Plants
  • Trash incinerators
  • (Once airborne) nickel can attach to the dust in the air, causing it to fall to the ground to mix with rain and snow. This eventually allows for Nickel to enter the soil.
  • Cigarette smoking
  • Skin to Skin contact through handling soil, water, or coils
  • Eating nickel contaminated food

Figures 4-6: Exposure to Nickel (power plant, trash incinerator, and cigarette smoking)

Image result for trash incineratorImage result for cigarette smokeImage result for nickel power plant

 

Nickel Poisoning

Larger amounts of nickel can be considered a carcinogen, and it increases the risk of lung, nose, and throat cancer. Nickel poisoning can also cause respiratory problems (asthma and bronchitis) if the nickel is inhaled. There are two sets of symptoms associated with nickel poisoning, initial symptoms and secondary symptoms. The initial symptoms of nickel poisoning occur within 16 hours of infection and progress rapidly, they are listed as:

Figure 7: Nickel Toxicity

  • headache
  • nausea
  • vomiting
  • dizziness
  • irritability
  • difficulty sleeping

The secondary symptoms are the ones that occur after the 16 hour mark. These symptoms can be similar to pneumonia and can be fatal, there are listed as:

  • chest pains
  • sweating
  • rapid heart beat
  • dry cough

Treatment of Nickel Poisoning

There is a good outcome for the treatment of nickel poisoning, as a long as it is started immediately. There are several treatments for nickel poisoning. These treatments are on a case-by-case basis and they include:

Figure 8: Chelation Therapy

Image result for chelation therapy

  • Giving oxygen
  • Chelation therapy – chelating agents will be used to rid the heavy metal from the body
  • Antibiotics
  • Corticosteroids
  • Bed Rest

Nickel Deficiency

Now that we have discussed nickel poisoning, we can move to nickel deficiency. Nickel deficiency in the body is rare due to the small needed quantity. The lack of nickel in the human body has not been sufficiently tested on humans. The lack of nickel has been studied in animals and the symptoms include slowed growth, reproductive changes, and altered fats/glucose levels in the body.

 

Text References

  1. https://education.jlab.org/itselemental/ele028.html. Retrieved 5/23/19.
  2. https://www.livescience.com/29327-nickel.html. Retrieved 5/23/19.
  3. https://safety.lovetoknow.com/Remedies_for_Food_Poisoning. Retrieved 5/24/19.
  4. https://www.mineravita.com/eng/nickel_disorders.php. Retrieved 5/24/19.
  5. https://www.dcnutrition.com/minerals/nickel-ni/. Retrieved 5/24/19.

Figure References:

  1. https://www.vectorstock.com/royalty-free-vectors/chemical-element-nickel-vectors. Accessed 6/2/19.
  2. https://en.wikipedia.org/wiki/Nickel. Accessed 6/2/19.
  3. https://blog.priorsrec.co.uk/nickel-and-chrome-plating-a-brief-history/. Accessed 6/2/19.
  4. http://www.civmats.com/news/news37/news37.HTML. Accessed 6/2/19.
  5. https://www.tampabay.com/news/localgovernment/pasco-extends-contract-with-operator-of-trash-incinerator/2157486. Accessed 6/3/19.
  6. https://www.modernmom.com/2c620212-051f-11e2-9d62-404062497d7e.html. Accessed 6/2/19.
  7. https://myersdetox.com/nickel-toxicity/. Accessed 6/2/19.
  8. https://www.hormonesmatter.com/chelation-therapy-medicine/. Accessed 6/2/19

 

DEET (Pesticide Blog #1)

What is DEET?

When we think about bug and insect bites, our first thought might not be to jump to DEET. So many people are using bug and insect spray but they don’t really understand the ingredients that go into the spray bottle. The main component in bug spray is DEET. DEET (chemical name N, N-diethyl-meta-toulamide) is used as the active ingredient in most insect repellents. A common misconception with bug spray is that the spray actually kills the insect, but in fact DEET is designed to¬† repel insects rather than kill them. [1] DEET is used for the direct application on to peoples skin in the forms of lotions, liquids, sprays, and more.

Figure 1: Show a commonly used bug spray that contains DEET. [2]

Image result for bug spray

Now that we have a better understanding of what DEET is, lets look into the mechanism of action, toxicity, and target organs associated with DEET.

Figure 2: Chemical Structure of DEET [3]

Image result for chemical structure of DEET

The mechanism(s) of action by which the insects are repelled and how humans are affects by DEET is still unknown and being continuously studied. The suggested mechanism of action in how DEET repels insects is that the chemical in DEET blocks the olfactory receptors of insects to the “smell” of human sweat and breath [4].The mechanism of action associated with human exposure is poorly understood. A recent study suggested that DEET is capable of blocking the human Na+ and K+ channels in the rat animal model [5]. This blocking of the channels leads to neuro-sensory adverse effects experienced (ex: numbness or tingling of extremities).

DEET is commonly employed as a liquid that is applied to the human skin. DEET is absorbed quickly through the skin and 48% of the applied dose is absorbed within 6 hours [6]. The toxicity of DEET is related to concentration levels of the applied chemical. Once DEET is in the body, it is broken down by the liver and eliminated from the body, mainly through urine. Nearly all of DEET that is taken in from the skin is eliminated by the body within 24 hours of applying it [7].

There has been research performed on the incidence of cancer development while using DEET and the increased risk of birth defects. Studies have shown there is no relation to cancer development or birth defects with the use of DEET. There has been information that has shown that children are more sensitive to DEET than adults.

Another way that DEET can be exposed to humans and wildlife is through the soil. DEET can be released into the soil during administration. Once in the soil, DEET is broken down by man microbes. DEET found in the soil can spread to waste water and into other bodies of water [6]. There have been studies to show this does not lead to any dangerous levels of toxicity in humans and wildlife.

Figure 2: DEET spreading to soil [7].

Exposure of DEET has been associated with a variety of health effects that include neurological, respiratory, cardiovascular, GI, dermal, and ocular [8]. There have been limited reports of serious health effects associated with DEET, even though there are millions of applications a year. Some adverse effects of DEET reported are seizures, restlessness, impaired cognitive function, and hyperextension of muscles [8]. More common adverse effects reported are skin irritation and watering of the eyes.

Figure 3: Spraying of bug spray [9].

Image result for bug spray adverse effects

Treatment of DEET poisoning must be performed immediately after exposure. Ocular exposure of DEET should be irrigated with water for~15 minutes and any skin exposure should be washed with soap and water. Most serious DEET poisoning will be treated with supportive therapies, including but not limited to seizure medication, anti-emetics, IV’s, and antihistamines. There is no specific treatment for DEET poison at the this time.

Now that we have a full understanding of DEET, lets look at a brief history of it. DEET was actually developed by the U.S army in 1946 for protection of the soldiers in infect infected areas. This was due to the lack of medical treatment for insect based diseases, such as malaria. Another interesting fact about DEET is that the EPA classifies DEET as “Group D”. This means that DEET is not classified as a human carcinogen.

I believe that DEET is a good pesticide to use, as long as we are using it carefully. Even with all the information and data available, there are still ongoing studies to examine the effects of DEET. I assume this is because it is a commonly used pesticide in every day life. Hopefully this blog allows you to take a closer look into DEET.

References

[1] https://www.cdc.gov/malaria/toolkit/DEET.pdf

[2] https://www.amazon.com/Repel-Insect-Repellent-Single-Bottle/dp/B004H89KFC

[3] https://www.researchgate.net/figure/DEET-chemical-structure_fig1_326381078

[4]Ditzen M, Pellegrino M, Vosshall LB: Insect odorant receptors are molecular targets of the insect repellent DEET. Science. 2008 Mar 28;319(5871):1838-42. doi: 10.1126/science.1153121. Epub 2008 Mar 13. [PubMed:18339904]

[5]Swale DR, Sun B, Tong F, Bloomquist JR: Neurotoxicity and mode of action of N, N-diethyl-meta-toluamide (DEET). PLoS One. 2014 Aug 7;9(8):e103713. doi: 10.1371/journal.pone.0103713. eCollection 2014. [PubMed:25101788]

[6]IPCS INCHEM: DEET Profile [Link]

[7]http://npic.orst.edu/factsheets/DEETgen.html

[8] https://www.atsdr.cdc.gov/toxprofiles/tp185-c2.pdf

[9] https://www.menshealth.com/trending-news/a19513661/what-is-kd-drug-bug-spray/