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Hello everyone! My name is Caroline Mifsud and I am a student in PHR 7588: Toxic Substances. For my 4 topics, I chose to study Bacillus thuringiensis, arsenic, toluene, and poison ivy. I chose these four particular topics because not only were they specifically interesting to me, but they are all clinically relevant.

In the Bacillus thuringiensis blog, you’ll learn about the role that it plays as a pesticide. Interestingly, it is pretty safe to use in terms of toxicity. You’ll learn about the mechanism of action and how it works as an insecticide.

In the arsenic blog, you’ll learn about the differences between the three types of arsenic compounds: organic, inorganic, and arsine gas. In addition, you’ll discover the variety of places that arsenic can be found. Did you know it’s commonly found in rice and even drinking water? Later, you’ll read about a research study involving rats that suggests arsenic might be considered an essential metal.

In the toluene blog, you’ll explore the many ways that one could be exposed to toluene – and why you should avoid it! There is even some genetic differences in some people who have been exposed to toluene.

Finally, you’ll learn all about poison ivy, the plant that makes us all itchy. Did you know that over 85 percent of people are allergic to this pesky plant? You’ll get to see what a rash from poison ivy looks like, as well as learn about the different remedies to use if you do come into contact with it.

Thanks for taking the time to read my blog – I hope you enjoy!

Poison Ivy

Source

Poison ivy, also known as Toxicodendron radicans, is a poisonous plant that characteristically has three leaves – as the saying goes “leaves of three, let it be.”

The vast majority of people (>85%) are allergic to poison ivy. Poison ivy grows everywhere in the United States except Hawaii, Alaska and some deserts in Nevada. (American Skin Association, American Osteopathic College of Dermatology).

Image link.

The above chart is helpful in identifying poison ivy.

This map shows where Eastern Poison Ivy is found.

This map shows where Western Poison Ivy is found.

Biotransformation

N/A

Toxicokinetics

The causative agent in poison ivy, urushiol, is absorbed through the skin. From there, an allergic reaction ensues, and the immune system becomes activated. The rash is usually self-limiting, and the rash will eventually clear up, often without treatment.

Urushiol

Urushiol.svg

Image link. 

Carcinogenicity

Poison ivy is not known to be carcinogenic.

Mechanism of Action

The causative agent of poison ivy dermatitis is a substance found on the surface of the leaves called urushiol. After coming into contact with this substance, an allergic skin reaction typically ensues. (American Skin Association, American Osteopathic College of Dermatology).

The immune system produces a protein called interleukin 33 (IL-33), which is what triggers the itching associated with poison ivy dermatitis. In addition to causing inflammation, this protein is also capable of acting on nerves. (Researchers Identify Protein That Triggers Poison Ivy Itch).

Interleukin-33

2KLL.pdb.png

Image link. 

Target organ(s)

  • Skin
  • Poison ivy can also be inhaled in some cases if it is burned and enters the air, affecting the respiratory system.

Signs and symptoms of toxicity

  • Redness
  • Itchiness
  • Swelling
  • Blisters
  • If inhaled, can cause difficulty breathing
  • Anaphylaxis in extreme situations

(Mayo Clinic – Poison Ivy).

This image shows an example of poison ivy dermatitis. 

Genetic susceptibility or heritable traits

The vast majority of people are allergic to poison ivy (>85%), and it is unknown whether or not people are more susceptible as a result of genetics. (American Skin Association, American Osteopathic College of Dermatology).

Historical or unique exposures

  • Historically, it was thought that poison ivy could be used for medical purposes and healing.
  • André-Ignace-Joseph Dufresnoy, a physician in the 1700’s, was very interested in the effects of poison ivy and attempted to create medicines from poison ivy to heal skin wounds and even cure paralysis. He made a distilled extract using poison ivy and prescribed it to patients to attempt to “heal them.” He claimed to have positive results, but poison ivy is not used for these purposes today.
  • A Japanese chemist named Rikou Majima (pictured below) was the first to identify the causative agent in poison ivy as urushiol.

Here is a picture of Rikou Majima with his students.

(No Ill Nature: The Surprising History and Science of Poison Ivy and Its Relatives).

Treatments

In most cases, the rash is self-limiting and will heal on its own within two to three weeks. Thus, treatment is not usually required. However, some treatments exist:

  • over the counter corticosteroid cream
  • calamine lotion
  • oatmeal baths
  • oral antihistamines (diphenhydramine)
  • soak in a cold water bath
  • apply a cool compress to the affected area
  • in some cases, your doctor may prescribe a steroid such as prednisone

Oatmeal baths can be helpful to get rid of itchiness. 

Image link.

(Mayo Clinic). 

Biomarkers

N/A

Disclaimer: I do not own any of these images or videos. They have been cited with their appropriate link. 

References

1. Poison ivy dermatitis—American Osteopathic College of Dermatology (AOCD). https://www.aocd.org/page/PoisonIvyDermatiti. Accessed July 21, 2019.

2. Poison ivy, sumac and oak  |  American Skin Association. http://www.americanskin.org/resource/poisonivy.php. Accessed July 21, 2019.

3. Poison ivy rash—Symptoms and causes. Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/poison-ivy/symptoms-causes/syc-20376485. Accessed July 21, 2019.

4. Poison ivy rash—Diagnosis and treatment—Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/poison-ivy/diagnosis-treatment/drc-20376490. Accessed July 21, 2019.

5. No ill nature: The surprising history and science of poison ivy and its relatives. Science History Institute. https://www.sciencehistory.org/distillations/no-ill-nature-the-surprising-history-and-science-of-poison-ivy-and-its-relatives. Published June 2, 2013. Accessed July 21, 2019.

6. Researchers identify protein that triggers poison ivy itch. National Institute of Environmental Health Sciences. https://www.niehs.nih.gov/research/supported/sep/2017/protein-poison-ivy-itch/index.cfm. Accessed July 21, 2019.

7. U.S. Food and Drug Administration. 4 Tips to Outsmarting Poisonous Plants. https://www.youtube.com/watch?v=CEBpYdgBALg&feature=youtu.be. Accessed July 21, 2019.

8. Centers for Disease Control and Prevention (CDC). How Poison Ivy Works. https://www.youtube.com/watch?v=dgwQ1DHepOw&feature=youtu.be. Accessed July 21, 2019.

9. Mayo Clinic. Mayo Clinic Minute: How to Treat Poison Ivy Rash. https://www.youtube.com/watch?v=G5mBkVdsoEE&feature=youtu.be. Accessed July 21, 2019.

Toluene

What is toluene? 

  • Toluene is also known as toluol, methylbenzene, and phenylmethane 
  • Organic compound 
  • Volatile liquid  
  • Non-polar solvent 
  • Cholinergic antagonist 
  • Neurotoxin 
  • Fuel additive 
  • Clear and colorless 

PubChem: Toluene.  

Chemical structure of toluene

Image link.

Watch this video to learn more about toluene. 

Sources of Toluene

  • Naturally found in crude oil and the tolu tree  
  • Can be produced as a byproduct of gasoline or other fuel production, or during the leather tanning process  
  • Also found in paints, nail polish, adhesives, rubber, and paint thinners 
  • People working in factories, workshops, and refineries are at risk for occupational exposure 
  • Voluntary exposure can be due to “huffing, sniffing, cuffing, or bagging” for recreational purposes 
  • Effects can last from 15-60 minutes 

PubChem: Toluene. Review of toluene action: clinical evidence, animal studies and molecular targets.

Image link.

Image link.

Image link.

Biotransformation 

Toluene undergoes biotransformation by the cytochrome P450 enzyme CYP2E1, which is a phase 1 enzyme. Interestingly, it has been found that increased exposure to toluene results in increased CYP2E1 mRNA expression.  

PubChem: Toluene.

Toxicokinetics 

  • Absorption: occurs primarily via the lungs, but can also occur through the skin (dermal) and through the gastrointestinal tract  
  • Distribution: occurs through organs that are primarily composed of lipids; it is important to note that toluene can readily cross the blood brain barrier and the placenta 
  • Metabolism: in the liver, where it is converted to benzyl alcohol and benzoic acid; metabolized by CYP2E1 
    • Ultimately forms hippuric acid 
    • This dissociates into anions and protons  
    • Excess hippuric acid formation can result in metabolic acidosis, or too much acid in the body, and hypokalemia, or very low potassium levels; this is extremely dangerous  
  • Excretion: urine  

Review of toluene action: clinical evidence, animal studies and molecular targets.

Watch this video to learn more about inhalants, including toluene. 

Carcinogenicity 

According to the EPA and IARC, toluene cannot be classified as a human carcinogen because of the insufficient evidence available. Therefore, more studies should be conducted to determine the carcinogenic potential of toluene in humans.  

PubChem: Toluene. Agency for Toxic Substances and Disease Registry: Toluene.

Mechanism of Action 

Toluene has a variety of effects on the central nervous system. Effects have been shown to be both reversible and irreversible.  

  • Impacts dopaminergic neurons in the basal ganglia 
    • This results in changes in sensory-motor functions 
  • Impacts glutamate and GABA receptor binding  

PubChem: Toluene.

Target organs 

Toluene impacts nearly every organ system, including the:  

  • immune system
  • nervous system
  • respiratory system
  • central nervous system
  • eyes
  • skin
  • liver
  • kidneys

PubChem: Toluene.

Signs and symptoms of toxicity 

  

Please click on the above image to read about the acute and chronic signs and symptoms of toluene exposure.

Review of toluene action: clinical evidence, animal studies, and molecular targets. Table 1: Effects of toluene exposure.

Genetic Susceptibility

Toluene diisocyanate (TDI) and Occupational Asthma (OA) 

  • Exposure to toluene diisocyanate is known to cause occupational asthma
    • OA is defined as “variable airflow limitation or airway hyperresponsiveness” that is a result of occupational exposure” (Christiani et al). 
    • Mechanism is unclear, but may be related to an IgE mechanism 
  • Studies have shown genetic differences in people with TDI-induced OA compared to normal subjects 
    • The results found a positive association between TDI-induced OA and the HLA-DQB1*0503 gene  
    • Interestingly, this demonstrates that genetic changes have occurred in people who have been exposed to TDI

 Genetic susceptibility to occupational exposures. 

Unique Exposures 

There have been many epidemiological studies conducted on the effects of toluene exposure. Here are some interesting examples: 

  • A study in Singapore found that women exposed to toluene while working in an audio speaker factory had higher rates of spontaneous abortion compared to the control group.  
  • A psychiatric study found that male workers who had over 12 years of toluene exposure were more likely to have intellectual impairments such as problems with concentration, learning, and memory when compared to the non-exposed control group.
  • A study in France examined those exposed to toluene while working in a printing plant found that many of the workers exhibited progressive changes in their color vision.

PubChem: Toluene.

Treatments 

  • Remove clothing and wash the exposed areas immediately  
  • Eyes can be flushed with saline  
  • Do not induce vomiting  
  • Activated charcoal may be helpful if the patient is alert and has a gag reflex  
  • Currently, there is no toluene antidote available 
  • Treatment should focus on respiratory and cardiovascular support  

Medical Management Guidelines for Toluene.

Biomarkers 

  • Levels of toluene in the blood are the most reliable indicator  
  • Levels of hippuric acid (see image below) in the urine can be used to determine acute toluene exposure 
    • This is not a reliable indicator of chronic exposure due to the short half-life of hippuric acid

PubChem: Toluene.

Hippuric Acid 

Image link.

Disclaimer: I do not own any of these images. Each image has been cited with its corresponding link. 

References 

  1. PubChem. Toluene. https://pubchem.ncbi.nlm.nih.gov/compound/1140. Accessed June 29, 2019.
  2. ATSDR – Toxic Substances – Toluene. https://www.atsdr.cdc.gov/substances/toxsubstance.asp?toxid=29. Accessed June 29, 2019.
  3. Cruz SL, Rivera-García MT, Woodward JJ. Review of toluene action: clinical evidence, animal studies and molecular targets. J Drug Alcohol Res. 2014;3. doi:10.4303/jdar/235840
  4. Filley CM, Halliday W, Kleinschmidt-Demasters BK. The Effects of Toluene on the Central Nervous System. J Neuropathol Exp Neurol. 2004;63(1):1-12. doi:10.1093/jnen/63.1.1
  5. Christiani DC, Mehta AJ, Yu C-L. Genetic susceptibility to occupational exposures. Occup Environ Med. 2008;65(6). doi:10.1136/oem.2007.033977
  6. ATSDR – Medical Management Guidelines (MMGs): Toluene. https://www.atsdr.cdc.gov/mmg/mmg.asp?id=157&tid=29. Accessed June 29, 2019.

Arsenic

Sources

Arsenic is found in a variety of places, including rocks, soil, water, plants, animals, and the food that we eat. It can be found in its pure form, but it’s most commonly seen in combination with other chemical compounds. These compounds can be organic or inorganic.  

Image link.

Watch the video below to learn more about arsenic.

Three significant groups of arsenic compounds  

  • Organic: Arsenic + carbon 
  • Inorganic: Arsenic + other elements (not carbon)  
  • Arsine gas  

Arsenic is found in the following foods: 

  • Rice 
  • Cereal 
  • Seafood 
  • Chicken 
  • Mushrooms  

Image link.

Watch the video below to learn more about arsenic in food.

Arsenic can be found in drinking water.   

  • Levels vary widely across countries 
  • Water in rural communities are more likely to have higher arsenic levels
  • Higher in groundwater sources than surface sources 

 Image link

Other sources of arsenic 

  • Industrial fumes 
  • Pressure-treated lumber (prior to 2004)  

(Arsenic and Cancer Risk; Arsenic and Arsenic Compounds)

Biotransformation 

Methylation

  • Inorganic arsenic (the toxic form) becomes methylated and turns into methylarsonic acid (MMA) and dimethylarsinic acid (DMA)
  • Diets low in methionine or protein can result in decreased methylation of arsenic
  • Age and pregnancy can impact arsenic methylation in humans

Reduction

  • Arsenic becomes reduced in the blood  
  • Glutathione serves as the reducing agent 

(Mechanisms of arsenic biotransformation).   

Toxicokinetics 

  • Absorption: primarily small intestine  
  • Distribution: kidneys, liver, heart, lungs, muscle, nervous system, gastrointestinal tract, spleen, and deposits in keratin-rich areas
  • Metabolism: hepatic  
  • Excretion: urine  

Carcinogenicity 

The International Agency for Research on Cancer (IARC) classifies arsenic and inorganic arsenic compounds as “carcinogenic to humans.” Cancer of the lung, bladder, skin, kidney, liver, and prostate is linked to arsenic exposure.

Organic arsenic compounds are less dangerous, as the IARC classifies them as “possibly carcinogenic to humans.” (Arsenic and Cancer Risk).  

Mechanism of Action

From a toxicological standpoint, the trivalent and pentavalent states of arsenic are of the most concern. Each will be discussed separately.  

Pentavalent arsenic MOA 

  • Inhibition of hexokinase in glycolysis 
  • Replacement of phosphate in the sodium pump of human erythrocytes 
  • Uncoupler of adenosine-5′-triphosphate (ATP) via arsenolysis and subsequent depletion of ATP 

Trivalent arsenic MOA 

  • Has the ability to bind strongly to thiol groups which could result in toxicity 
  • Inhibition of pyruvate dehydrogenase, which has downstream effects in the citric acid cycle  

(Arsenic toxicity and potential mechanisms of action).  

Image link: Arsenic Exposure and Toxicology: A Historical Perspective. Figure 2.

Target organs 

Arsenic impacts nearly all organ systems, including the skin, gastrointestinal, cardiovascular, neurological, genitourinary, respiratory, endocrine, and hematological systems (Acute and chronic arsenic toxicity).  

Signs and symptoms of toxicity 

Acute poisoning signs and symptoms 

  • Vomiting 
  • Diarrhea (dominant feature) 
  • Abdominal pain 
  • Hypersalivation 
  • Psychosis 
  • Diffuse skin rash 
  • Seizures  
  • Hemoglobinuria 
  • Pancytopenia  
  • Anemia 
  • Respiratory failure 
  • Pulmonary edema 
  • Peripheral neuropathy 

Chronic signs and symptoms  

  • Abdominal pain 
  • Diarrhea  
  • Sore throat 
  • Cancer and other malignancies  

(Acute and chronic arsenic toxicity)

How is arsenic poisoning diagnosed? 

If arsenic poisoning is suspected, samples should be taken from hair, urine, and blood. 

  • Acute poisoning: 1.0-3.0 mg/kg in a hair sample.
  • Chronic poisoning0.1-0.5 mg/kg in a hair sample  

(Acute and chronic arsenic toxicity)

How is arsenic poisoning treated?

If arsenic poisoning is suspected, contaminated clothes should be removed immediately. The skin should be rinsed to remove leftover arsenic that may be present. Treatment for acute arsenic poisoning includes gastric lavage, hemodialysis, and dimercaprol (British anti-Lewisite; pictured below) (Acute and chronic arsenic toxicity).

Image link.

Genetic susceptibility or heritable traits 

Studies have shown there is variability in genetic susceptibility to arsenic toxicity. Some genetic polymorphisms in enzymes responsible for arsenic metabolism include: 

  • Arsenic (III) methyltransferase 
  • Glutathione S-transferase  
  • Methylenetetrahydrofolate reductase  

Please click here to see more on the genetic polymorphisms involved in arsenic toxicity by going to page 1533, Table 2.  

Some individuals possess single nucleotide polymorphisms which render them less likely to repair oxidative damage. This includes the following genes:  

  • HOGG1 
  • APE1 
  • XRCC1 
  • XRCC3 

In simpler terms, individuals who have variation in these enzymes or genes can be more susceptible to arsenic toxicity if and when they encounter it.

Historical or unique exposures 

  • Arsenic has been commonly used as a homicidal and suicidal poison 
  • It has been used for these reasons since the Middle Ages 
  • It is sometimes called the “poison of kings” as it was used to remove members of the ruling class; it was used to kill Napoleon Bonaparte in 1851 
  • Arsenic was used as a pigment in the 1800s and caused many accidental arsenic poisonings  

Please click here and go to page 307, Table 2 to learn more about historical events related to arsenic toxicity.  

Arsenic Exposure and Toxicology: A Historical Perspective.

Biomarkers of Exposure

Arsenic can be quantified using samples from hair, nails, blood, or urine.  

  • Arsenic levels in keratin-rich areas such as nails may indicate chronic or past exposure 
  • Arsenic levels in blood or urine may indicate recent or acute exposures  
  • Urine levels typically range from 5-20 µg/L 

(Arsenic and Arsenic Compounds)

Essentiality

Although it is up for debate, some studies suggest that arsenic is an essential nutrient that plays a role in methionine metabolism. Methionine (pictured below) metabolism is vital during pregnancy, lactation, and vitamin B6 deprivation (Evidence for arsenic essentiality). 

Image link.

Deficiency

Arsenic deprivation studies have demonstrated that rats deprived of arsenic had changes in their coats and growth rate compared to the control group. Some studies show that arsenic deprivation manifests similarly to vitamin B6 deficiency (Evidence for arsenic essentiality).  

Disclaimer: I do not own any of these images. Each image has been cited with its corresponding link. 

References 

  1. Arsenic and Cancer Risk. https://www.cancer.org/cancer/cancer-causes/arsenic.html. Accessed June 7, 2019.
  2. Ng J, Gomez-Caminero A, International Programme on Chemical Safety, eds. Arsenic and Arsenic Compounds. 2. ed. Geneva: World Health Organization; 2001.
  3. Hughes MF, Beck BD, Chen Y, Lewis AS, Thomas DJ. Arsenic Exposure and Toxicology: A Historical Perspective. Toxicological Sciences. 2011;123(2):305-332. doi:10.1093/toxsci/kfr184
  4. Ratnaike RN. Acute and chronic arsenic toxicity. Postgraduate Medical Journal. 2003;79(933):391-396. doi:10.1136/pmj.79.933.391
  5. Uthus EO. Evidence for arsenic essentiality. Environmental Geochemistry and Health. 1992;14(2):55-58. doi:10.1007/BF01783629
  6. Vahter M. Mechanisms of arsenic biotransformation. Toxicology. 2002;181-182:211-217. doi:10.1016/S0300-483X(02)00285-8
  7. Arsenic poisoning: Causes, symptoms, and treatment. Medical News Today. https://www.medicalnewstoday.com/articles/241860.php. Accessed June 7, 2019.
  8. Hughes MF. Arsenic toxicity and potential mechanisms of action. Toxicology Letters. 2002;133(1):1-16. doi:10.1016/S0378-4274(02)00084-X
  9. Faita F, Cori L, Bianchi F, Andreassi M. Arsenic-Induced Genotoxicity and Genetic Susceptibility to Arsenic-Related Pathologies. International Journal of Environmental Research and Public Health. 2013;10(4):1527-1546. doi:10.3390/ijerph10041527
  10. Hughes MF, Beck BD, Chen Y, Lewis AS, Thomas DJ. Arsenic Exposure and Toxicology: A Historical Perspective. Toxicological Sciences. 2011;123(2):305-332. doi:10.1093/toxsci/kfr184

Bacillus Thuringiensis

What is Bacillus Thuringiensis (Bt)?

Bacillus Thuringiensis (Bt) is a microbial pesticide that acts as an insecticide (Casarett & Doull). 

Watch this video to learn more about Bt.

 

 

The bacterial structure of Bt. Image link.

The microscopic structure of Bt. Image link. 

Bt is commonly sprayed on plants. Image link.

 

 

 

 

 

 

 

 

 

Bt is a commonly used insecticide, as seen here. Image link.

Where is Bt found?

  • Since Bt is a commonly used insecticide, it is commonly found in the soil where plants are treated.

Image link.

Biotransformation 

When Bt enters the body, it remains confined to the gut. While in the gut, it is broken down normally and excreted within 2-3 days. However, if Bt is absorbed through inhalation, it enters the respiratory system and is attacked via an immune response. After this immune response, it only takes about 1 day for Bt levels to markedly decrease. (Bacillus Thuringiensis General Fact Sheet). 

Toxicokinetics 

If Bt is consumed:

  • When it enters the body, it is broken down similarly to the way proteins in our diet are broken down.
  • When consumed, it remains confined to the gut.
  • Bt is excreted within 2 to 3 days (Bacillus Thuringiensis General Fact Sheet). 

If Bt is inhaled:

  • Bt can move to other areas of the body including the lungs, blood, lymph, and kidneys.
  • The immune system can mount a response against Bt and eliminate it.
  • This process usually takes 1 day (Bacillus Thuringiensis General Fact Sheet).

Carcinogenicity 

Bt has not been demonstrated to possess carcinogenic effects (Bacillus Thuringiensis General Fact Sheet).

Mechanism of Action  

After an insect ingests Bt, the spores that Bt forms are solubilized and turned into active toxins in the midgut of the insect. They subsequently bind to epithelial cell receptors and insert into the cellular membrane. Next, pores are formed, and the potassium flux across the epithelial cells changes. This leads to changes in pH, causing it to become alkaline. The high pH destroys the epithelial cells of the midgut in the insect. Eventually, they die as a result of gut paralysis and feeding inhibition. Bt is selective because the alkaline conditions under which it operates is much different than the acidic environment of the human stomach (Casarett & Doull).  

This video below helps visualize how the Bt toxin works.

Target organs

  • In insects:
    • midgut, located in the alimentary canal, of the insect.  
  • In humans:

Signs and symptoms of toxicity 

In humans and other mammals, there are little to no side effects from Bt as it has relatively low toxicity in species other than insects. Because of the low toxicity of Bt, this makes it a relatively safe insecticide to use. In some cases, Bt has been shown to cause the following symptoms (associated with acute and chronic exposure) in mammals:

  • skin irritation
  • eye irritation
  • allergic skin reactions
  • weight loss
  • sleep difficulties
  • stomach discomfort
  • nose irritation
  • throat irritation

Chronic exposure can further result in adverse immune responses.

(Bacillus Thuringiensis General Fact Sheet).

Image link. 

Image link. 

Genetic susceptibility or heritable traits 

So far, there are no known genes that render humans more susceptible to the effects of Bt. This is unsurprising as Bt is relatively nontoxic and safe for humans.

Interestingly, the genes of certain crops have been altered to make them resistant to insects by incorporating Bt genes into their genomes (Ibrahim et al). Adding the Bt genes to certain crops makes them insect-resistant and helps ensure their survival.

Historical or unique exposures 

One of the most controversial historical issues associated with Bt is some people have claimed that Bt is killing monarch butterflies via pollen from transgenic crops. Many people are against the use of genetically modified crops and food products, for example, crops that are genetically altered to possess Bt genes, giving them resistance against insects. However, entomologists and other researchers have claimed that the effects on the monarch butterflies are “negligible” and the transgenic pollen does not negatively impact them (Clark et al).

Treatments 

In humans, there is no treatment for Bt as the digestive and/or immune system is able to handle the elimination of the toxin. Although side effects such as skin or eye irritation are limited and uncommon, they are easily managed.

Biomarkers 

  • There is a biomarker for Bt spore germination called calcium dipicolinate (CaDPA).  
  • The paper can be found here (Shu-shi Huang et al). 
  • CaDPA is used to characterize the spore germination process.  
  • This biomarker is of use in food safety. 

Disclaimer: I do not own any of these images. Each image has been cited with its corresponding link. 

References 

  1. Klaassen CD, Casarett LJ, Doull J, eds. Casarett and Doull’s Toxicology: The Basic Science of Poisons. 8th ed. New York: McGraw-Hill Education; 2013.  
  2. Bacillus thuringiensis (Bt) General Fact Sheet. http://npic.orst.edu/factsheets/btgen.html. Accessed May 18, 2019.
  3. Ibrahim MA, Griko N, Junker M, Bulla LA. Bacillus thuringiensis: A genomics and proteomics perspective. Bioengineered Bugs. 2010;1(1):31-50. doi:10.4161/bbug.1.1.10519
  4. Clarke T. Monarchs safe from Bt. Nature. September 2001. doi:10.1038/news010913-12
  5. PubChem. Calcium dipicolinate. https://pubchem.ncbi.nlm.nih.gov/compound/9900462. Accessed May 18, 2019.
  6. Shu-shi Huang, De Chen, Yong-qing Li. Detection of bacillus thuringiensis spore germination via CaDPA biomarker using laser tweezers raman spectroscopy. In: 2007 Quantum Electronics and Laser Science Conference. ; 2007:1-2. doi:10.1109/QELS.2007.4431273