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. 2022 Mar 30;80(1):100.
doi: 10.1186/s13690-022-00812-7.

Geotemporospatial and causal inferential epidemiological overview and survey of USA cannabis, cannabidiol and cannabinoid genotoxicity expressed in cancer incidence 2003-2017: part 2 - categorical bivariate analysis and attributable fractions

Albert Stuart Reece  1   2   3 , Gary Kenneth Hulse  4   5
Affiliations

Geotemporospatial and causal inferential epidemiological overview and survey of USA cannabis, cannabidiol and cannabinoid genotoxicity expressed in cancer incidence 2003-2017: part 2 - categorical bivariate analysis and attributable fractions

Albert Stuart Reece et al. Arch Public Health. .

Abstract

Background: As the cannabis-cancer relationship remains an important open question epidemiological investigation is warranted to calculate key metrics including Rate Ratios (RR), Attributable Fractions in the Exposed (AFE) and Population Attributable Risks (PAR) to directly compare the implicated case burden between emerging cannabinoids and the established carcinogen tobacco.

Methods: SEER*Stat software from Centres for Disease Control was used to access age-standardized state census incidence of 28 cancer types (including "All (non-skin) Cancer") from National Cancer Institute in US states 2001-2017. Drug exposures taken from the National Survey of Drug Use and Health 2003-2017, response rate 74.1%. Federal seizure data provided cannabinoid exposure. US Census Bureau furnished income and ethnicity. Exposure dichotomized as highest v. lowest exposure quintiles. Data 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. Fifteen cancers displayed elevated E-Values in the highest compared to the lowest quintiles of cannabidiol exposure, namely (in order): prostate, melanoma, Kaposi sarcoma, ovarian, bladder, colorectal, stomach, Hodgkins, esophagus, Non-Hodgkins lymphoma, All cancer, brain, lung, CLL and breast. Eleven cancers were elevated in the highest THC exposure quintile: melanoma, thyroid, liver, AML, ALL, pancreas, myeloma, CML, breast, oropharynx and stomach. Twelve cancers were elevated in the highest tobacco quintile confirming extant knowledge and study methodology. For cannabidiol RR declined from 1.397 (95%C.I. 1.392, 1.402), AFE declined from 28.40% (28.14, 28.66%), PAR declined from 15.3% (15.1, 15.5%) and minimum E-Values declined from 2.13. For THC RR declined from 2.166 (95%C.I. 2.153, 2.180), AFE declined from 53.8% (53.5, 54.1%); PAR declined from 36.1% (35.9, 36.4%) and minimum E-Values declined from 3.72. For tobacco, THC and cannabidiol based on AFE this implies an excess of 93,860, 91,677 and 48,510 cases; based on PAR data imply an excess of 36,450, 55,780 and 14,819 cases.

Conclusion: Data implicate 23/28 cancers as being linked with THC or cannabidiol exposure with epidemiologically-causal relationships comparable to those for tobacco. AFE-attributable cases for cannabinoids (91,677 and 48,510) compare with PAR-attributable cases for tobacco (36,450). Cannabinoids constitute an important multivalent community carcinogen.

Keywords: Cannabidiol; Cannabigerol; Cannabinoid; Chromosomal toxicity; Congenital anomalies; Dose-response relationship; Epigenotoxicity; Genotoxicity; Mechanisms; Multigenerational genotoxicity; Oncogenesis; Sigmoidal dose-response; Supra-linear dose response; Transgenerational teratogenicity; cannabis; Δ9-tetrahydrocannabinol.

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Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Fig. 1
Fig. 1
Relationship of selected cancer incidence to tobacco exposure rates by tobacco quintiles
Fig. 2
Fig. 2
Relationship of selected cancer incidence to AUD exposure rates by AUD quintiles
Fig. 3
Fig. 3
Relationship of selected cancer incidence to THC exposure rates by THC quintiles
Fig. 4
Fig. 4
Relationship of selected cancer incidence to cannabidiol exposure rates by cannabidiol quintiles
Fig. 5
Fig. 5
Comparison of lowest and highest quintiles of tobacco exposure on various cancer rates
Fig. 6
Fig. 6
Comparison of lowest and highest quintiles of AUD exposure on various cancer rates
Fig. 7
Fig. 7
Comparison of lowest and highest quintiles of cannabidiol exposure on various cancer rates
Fig. 8
Fig. 8
Rate ratios of highest v lowest cannabidiol exposure quintiles calculated from age adjusted rates
Fig. 9
Fig. 9
Attributable fractions in the exposed of highest v lowest cannabidiol exposure quintiles calculated from age adjusted rates
Fig. 10
Fig. 10
Population attributable risks of highest v lowest cannabidiol exposure quintiles calculated from age adjusted rates
Fig. 11
Fig. 11
Log P-values ratios of highest v lowest cannabidiol exposure quintiles calculated from age adjusted rates
Fig. 12
Fig. 12
Log E-values ratios of highest v lowest cannabidiol exposure quintiles calculated from age adjusted rates
See this image and copyright information in PMC

References

    1. Callaghan RC, Allebeck P, Akre O, McGlynn KA, Sidorchuk A. Cannabis use and incidence of testicular Cancer: a 42-year follow-up of Swedish men between 1970 and 2011. Cancer Epidemiol Biomark Prev. 2017;26(11):1644–1652. - PMC - PubMed
    1. Daling JR, Doody DR, Sun X, Trabert BL, Weiss NS, Chen C, Biggs ML, Starr JR, Dey SK, Schwartz SM. Association of marijuana use and the incidence of testicular germ cell tumors. Cancer. 2009;115(6):1215–1223. - PMC - PubMed
    1. Lacson JC, Carroll JD, Tuazon E, Castelao EJ, Bernstein L, Cortessis VK. Population-based case-control study of recreational drug use and testis cancer risk confirms an association between marijuana use and nonseminoma risk. Cancer. 2012;118(21):5374–5383. - PMC - PubMed
    1. Trabert B, Sigurdson AJ, Sweeney AM, Strom SS, McGlynn KA. Marijuana use and testicular germ cell tumors. Cancer. 2011;117(4):848–853. - PMC - PubMed
    1. Song A, Myung NK, Bogumil D, Ihenacho U, Burg ML, Cortessis VK. Incident testicular cancer in relation to using marijuana and smoking tobacco: a systematic review and meta-analysis of epidemiologic studies. Urol Oncol. 2020;38(7):642.e641–642.e649. - PubMed