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15. Chemotyping of ∆8-THC-Containing e-Liquids Analyzed during the 2019–2020 New York State EVALI Investigation.

Author

Duffy, Bryan C, Li, Lingyun, Lu, Shijun, Dittmar, Mark A, Delaney-Baldwin, Em, Durocher, Lorie A, and Spink, David C

Subjects
CANNABIS (Genus), CANNABIDIOL, ELECTRONIC cigarettes, PRINCIPAL components analysis, E-cigarette or vaping product use-associated lung injuries
Abstract

The investigation of the 2019–2020 E-cigarette or Vaping Product Use-Associated Lung Injury (EVALI) outbreak in New York State provided a unique opportunity to examine the formulations and chemical components found in clandestine cannabis-containing e-liquids. In this EVALI investigation, it was determined that an unusually high proportion (16%) of the cannabis e-liquids analyzed contained significant levels of ∆8-tetrahydrocannabinol (∆8-THC). Although not thought to be the causative agent in the outbreak, the manufacturing origin of vaping e-liquids containing large concentrations of ∆8-THC was of great interest, since high ∆8-THC concentrations are not observed in the extracts of common cannabis strains. A principal component analysis of multiple cannabinoid concentrations revealed clusters of similar or identical ∆8-THC-containing products. This technique may be useful in identifying common manufacturing sources in this and future investigations. Several possible manufacturing methods to enrich ∆8-THC appear in literature and are discussed based on their likelihood as sources of this cannabinoid in these samples from the EVALI investigation. The presence of high levels of ∆8-THC in numerous illicit vaping products may implicate cannabidiol, which is readily available at low cost, as its synthetic precursor. [ABSTRACT FROM AUTHOR]

Published
2022
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32. Expression of the aryl hydrocarbon receptor is not required for the proliferation, migration, invasion, or estrogen-dependent tumorigenesis of MCF-7 breast cancer cells

Author

Spink, Barbara C., Bennett, James A., Lostritto, Nicole, Cole, Jacquelyn R., and Spink, David C.

Subjects
Neovascularization, Pathologic, Blotting, Western, Cell Cycle, Apoptosis, Breast Neoplasms, Estrogens, Mice, SCID, respiratory system, Article, respiratory tract diseases, Immunoenzyme Techniques, Mice, Cell Transformation, Neoplastic, Receptors, Aryl Hydrocarbon, Receptors, Estrogen, Cell Movement, Cytochrome P-450 CYP1B1, Cell Adhesion, Cytochrome P-450 CYP1A1, Tumor Cells, Cultured, Animals, Humans, Female, Aryl Hydrocarbon Hydroxylases, Cell Proliferation
Abstract

The AhR was initially identified as a ligand-activated transcription factor mediating effects of chlorinated dioxins and polycyclic aromatic hydrocarbons on cytochrome P450 1 (CYP1) expression. Recently, evidence supporting involvement of the AhR in cell-cycle regulation and tumorigenesis has been presented. To further define the roles of the AhR in cancer, we investigated the effects of AhR expression on cell proliferation, migration, invasion, and tumorigenesis of MCF-7 human breast cancer cells. In these studies, the properties of MCF-7 cells were compared with those of two MCF-7-derived sublines: AH(R100) , which express minimal AhR, and AhR(exp) , which overexpress AhR. Quantitative PCR, Western immunoblots, 17β-estradiol (E2 ) metabolism assays, and ethoxyresorufin O-deethylase assays showed the lack of AhR expression and AhR-regulated CYP1 expression in AH(R100) cells, and enhanced AhR and CYP1 expression in AhR(exp) cells. In the presence of 1 nM E2 , rates of cell proliferation of the three cell lines showed an inverse correlation with the levels of AhR mRNA. In comparison with MCF-7 and AhR(exp) cells, AH(R100) cells produced more colonies in soft agar and showed enhanced migration and invasion in chamber assays with E2 as the chemoattractant. Despite the lack of significant AhR expression, AH(R100) cells retained the ability to form tumors in severe combined immunodeficient mice when supplemented with E2 , producing mean tumor volumes comparable to those observed with MCF-7 cells. These studies indicate that, while CYP1 expression and inducibility are highly dependent on AhR expression, the proliferation, invasion, migration, anchorage-independent growth, and estrogen-stimulated tumor formation of MCF-7 cells do not require the AhR.

Published
2012

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