Introduction
Breast cancer (BC) is the commonest human cancer and its incidence (BCI) is rising worldwide. Whilst both tobacco and alcohol have been linked to BCI genotoxic cannabinoids have not been investigated.
Methods
Age-adjusted state-based BC incidence (BCI) 2003-2017 was taken from the Surveillance Epidemiology and End Results database of the Centers for Disease Control (CDC). Drug use from the National Survey of Drug Use and Health, response rate 74.1%. Median age, median household income and ethnicity were from US census. Inverse probability weighted (ipw) multivariable regression conducted in R.
Results
In bivariate analysis BCI was shown to be significantly linked with rising cannabis exposure (β-est.=3.93 (95%C.I. 2.99, 4.87), P=1.10x10-15). At 8-years lag cigarettes: cannabis (β-est.=2660 (2150.4, 3169.3), P=4.60x10-22) and cannabis: alcoholism (β-est.=7010 (5461.6, 8558.4), P=1.80x10-17) were significant in ipw-panel regression. Terms including cannabidiol (β-est.=16.16 (0.39, 31.93), P=0.446) and cannabigerol (β-est.=6.23 (2.06, 10.39), P=0.0034) were significant in spatiotemporal models lagged 1:2 years respectively. Cannabis-liberal paradigms had higher BCI (67.50±0.26 v. 65.19±0.21/100,000 (mean±S.E.M.), P=1.87x10-11; β-est.= 2.31 (1.65, 2.96), P = 9.09x10-12). 55/58 e-Values >1.25 and 13/58 >100. Abortion was independently and causally significant in space-time models.
Conclusion
Data show that exposure to cannabis and the cannabinoids THC, cannabidiol, cannabigerol, and alcoholism fulfill quantitative causal criteria for BCI across space and time. Findings are robust to adjustment for age and several known sociodemographic, socioeconomic and hormonal risk factors, and establish cannabinoids as an additional risk factor class for breast carcinogenesis. BCI is higher under cannabis-liberal legal paradigms.