NDLI: Geotemporospatial and causal inferential epidemiological overview and survey of USA cannabis, cannabidiol and cannabinoid genotoxicity expressed in cancer incidence 2003–2017: part 1

Content Provider	Springer Nature : BioMed Central
Author	Reece, Albert Stuart Hulse, Gary Kenneth
Abstract	Background The genotoxic and cancerogenic impacts of population-wide cannabinoid exposure remains an open but highly salient question. The present report examines these issues from a continuous bivariate perspective with subsequent reports continuing categorical and detailed analyses. Methods Age-standardized state census incidence of 28 cancer types (including “All (non-skin) Cancer”) was sourced using SEER*Stat software from Centres for Disease Control and National Cancer Institute across US states 2001–2017. It was joined with drug exposure data from the nationally representative National Survey of Drug Use and Health conducted annually by the Substance Abuse and Mental Health Services Administration 2003–2017, response rate 74.1%. Cannabinoid data was from Federal seizure data. Income and ethnicity data sourced from the US Census Bureau. Data was processed in R. Results Nineteen thousand eight hundred seventy-seven age-standardized cancer rates were returned. Based on these rates and state populations this equated to 51,623,922 cancer cases over an aggregated population 2003–2017 of 124,896,418,350. Regression lines were charted for cancer-substance exposures for cigarettes, alcohol use disorder (AUD), cannabis, THC, cannabidiol, cannabichromene, cannabinol and cannabigerol. In this substance series positive trends were found for 14, 9, 6, 9, 12, 6, 9 and 7 cancers; with largest minimum E-Values (mEV) of 1.76 × 109, 4.67 × 108, 2.74 × 104, 4.72, 2.34 × 1018, 2.74 × 1017, 1.90 × 107, 5.05 × 109; and total sum of exponents of mEV of 34, 32, 13, 0, 103, 58, 25, 31 indicating that cannabidiol followed by cannabichromene are the most strongly implicated in environmental carcinogenesis. Breast cancer was associated with tobacco and all cannabinoids (from mEV = 3.53 × 109); “All Cancer” (non-skin) linked with cannabidiol (mEV = 1.43 × 1011); pediatric AML linked with cannabis (mEV = 19.61); testicular cancer linked with THC (mEV = 1.33). Cancers demonstrating elevated mEV in association with THC were: thyroid, liver, pancreas, AML, breast, oropharynx, CML, testis and kidney. Cancers demonstrating elevated mEV in relation to cannabidiol: prostate, bladder, ovary, all cancers, colorectum, Hodgkins, brain, Non-Hodgkins lymphoma, esophagus, breast and stomach. Conclusion Data suggest that cannabinoids including THC and cannabidiol are important community carcinogens exceeding the effects of tobacco or alcohol. Testicular, (prostatic) and ovarian tumours indicate mutagenic corruption of the germline in both sexes; pediatric tumourigenesis confirms transgenerational oncogenesis; quantitative criteria implying causality are fulfilled.
Related Links	https://archpublichealth.biomedcentral.com/counter/pdf/10.1186/s13690-022-00811-8.pdf
Ending Page	30
Page Count	30
Starting Page	1
File Format	HTM / HTML
ISSN	20493258
DOI	10.1186/s13690-022-00811-8
Journal	Archives of Public Health
Issue Number	1
Volume Number	80
Language	English
Publisher	BioMed Central
Publisher Date	2022-03-30
Access Restriction	Open
Subject Keyword	Public Health Medicine Health Policy Health Services Research Health Informatics Cannabis Cannabinoid Δ9-tetrahydrocannabinol Cannabigerol Cannabidiol Mechanisms Congenital anomalies Oncogenesis Genotoxicity Epigenotoxicity Chromosomal toxicity Multigenerational genotoxicity Transgenerational teratogenicity Dose–response relationship Supra-linear dose response Sigmoidal dose–response Medicine/Public Health
Content Type	Text
Resource Type	Article
Subject	Public Health, Environmental and Occupational Health
Journal Impact Factor	3.2/2023
5-Year Journal Impact Factor	3.3/2023

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