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The facts are about how they cause lung damage

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2,807 cases of e-cigarette or vaping product use associated with lung injury (EVALI) have been reported up to February 2020. EVALI, or VAPI (Vaping Associated Pulmonary Injury), is an illness related to THC (and nicotine) portable vaporizer devices that have killed at least 68 vapers. (1) But, what is the science behind vapes, surfactants (such as vitamin E acetate), as well as THC that causes massive lung damage?

It began almost suddenly and caused a lot of hysteria since few explanations were initially drawn. Black market THC and CBD carts (and counterfeit e-cigs) were to blame at first, but our previous report detailed the problems with overall vape regulations in Canada.

Lung collapse by tocopherols (vitamin E acetate) is far easier to explain than the tissue damage caused by these THC vape pens. To be frank, though, we cannot yet explain what happens to THC in a vape pen—let alone other additives.

Photo courtesy of Gentlemen’s CBD.

How do vape pens collapse a lung?

The consensus has been that tocopherols (Vitamin E acetate) are partly responsible for lung damage caused by THC vapes. Vitamin E acetate is not water-soluble but also replaces the natural surfactant that lines the inside of your lungs.

There is a fluid in your lungs that allows the little sacs known as alveoli to expand with air. A lung will collapse if it loses this fluid. Therefore, it is highly problematic that tocopherols can replace this fluid since this will potentially collapse the lung. But, Vaping Associated Lung Injury also comes with large amounts of tissue damage—which has come with little explanation.

2021 research with new answers

A century-old cancer mystery was just uncovered in January 2021 – and cancer is on the other side of lung damage. (2) This detailed the importance of a messenger known as PI3K. Cell-division in the immune system, as well as cancerous tissue, is driven by this special messenger. The surfactants, Vitamin E acetate and Polysorbate 80, block this messenger and potentially slow down cell division. This might ramp lung damage if the surrounding tissues are not fed enough oxygen (Warburg Effect).

New tissue will still need to form via cell division if lung tissue is attacked by a toxin and killed in any condition. Otherwise, the result might be catastrophic lung damage.

Photo courtesy of VaporDNA.

What toxin is emitted from vape pens?

Vape pens increase carbon monoxide and ultimately induce an anaerobic condition. In an anaerobic environment, cell division is driven by the messenger, PIK3. In symmetry, the messenger helps cancer, but also healthy tissues to grow in replace of dead cells. But, the tocopherols found in lethal THC vapes block this messenger.

Constant repair is crucial under the constant attack of a small toxin, such as oxygen but especially carbon monoxide. Unfortunately, however, that repair cannot happen if you were to outright inhibit PIK3 with tocopherols in carbon monoxide’s anaerobic state.

Vape pen additives and cannabinoid receptor function

In greater detail, the full function of the messenger (PIK3) is not black and white. (3) In contrast, THC can inhibit but also activate the messenger for different reasons. Unlike vaporized Vitamin E acetate, however, oral doses of cannabinoids maintain homeostasis.

On the other end, Huntington’s disease causes brain cells to die by specifically shutting down cannabinoid 1 (CB1) receptors. A study published in Springer Nature in 2019 detailed the importance of PI3K in neuron cell death in Huntington’s Disease. (4)

Cannabis‘s natural polypharmacy works on a highly balanced rhythm that does not cause the same risk of cancer or lung damage as THC vapes. So, it is typically ill-advised to alter this balance unnaturally. And, can we not agree that successful vape pens only need a simple formulation of pure live resin, without any added surfactants?

Testing vaping pen emissions in 2021

In reality, the concept of tocopherols is all but a hypothesis. Unfortunately, we still don’t know how THC itself reacts in a red hot vape cartridge. This is what I was told by CLN’s resident scientist Dr. Markus Roggen. His experience in this matter rests in the hands of the Health Canada licensed cannabis research lab he founded, CBDV (Delic Labs). This lab can do full quantitative analyses on vape emissions.

Photo courtesy of Cambustion.

What happens to the cannabis oil itself in a vape pen?

Heat influences THC to turn into Delta-8, CBN, or degrade. So, heat is an issue in the identity of the molecule. When you put THC in a vape cartridge, it is Delta-9 THC in the beginning. But, does anything happen to the THC when you heat it for vaporization?

That question hasn’t really been answered, yet. Everyone tests if the material that is in the cartridge is safe. But, no one tests if the material that comes out of the cartridge is safe. 

It is like testing the grape juice that goes in a wine bottle to ensure there is no alcohol in it after you get the bottle out of the cellar 80 years later. You missed a step. Therefore, it would be good to test the vapour that comes out of a cartridge to know if there is any risk factor.

Dr. Markus Roggen

Thank you for your time, Dr. Roggen. End of the phone call.

We will explore other potential toxins and degradation products in a future installment. For now, stay tuned to learn how Vitamin E Acetate found its way into THC vapes and before the first case of lung damage.

Sources

  1. Michael T Colesar, MC, USA, Daniel J McCollum, MD, E-Cigarette or Vaping Product Use-Associated Lung Injury (EVALI) in an Active Duty Service Member, Military Medicine, Volume 186, Issue 1-2, January-February 2021, Pages e250–e253, https://doi.org/10.1093/milmed/usaa349
  2. Xu, K., Yin, N., Peng, M., Stamatiades, E. G., Shyu, A., Li, P., Zhang, X., Do, M. H., Wang, Z., Capistrano, K. J., Chou, C., Levine, A. G., Rudensky, A. Y., & Li, M. O. (2021). Glycolysis fuels phosphoinositide 3-kinase signaling to bolster T cell immunity. Science (New York, N.Y.)371(6527), 405–410. doi/10.1126/science.abb2683
  3. Wang, H., Hong, J., & Yang, C. S. (2016). δ-Tocopherol inhibits receptor tyrosine kinase-induced AKT activation in prostate cancer cells. Molecular carcinogenesis55(11), 1728–1738. https://doi.org/10.1002/mc.22422
  4. Rai, S.N., Dilnashin, H., Birla, H. et al. The Role of PI3K/Akt and ERK in Neurodegenerative Disorders. Neurotox Res 35, 775–795 (2019). https://doi.org/10.1007/s12640-019-0003-y





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