Cannabinoids, such as cannabidiol, were shown to have genotoxic properties, although their importance has not been thoroughly investigated across the teratological spectrum. In the United States, researchers investigated these challenges, which included contextual space-time linkages and formal causal inferential analysis. Data for the state congenital anomaly rate (CAR) was gathered from the National Birth Defects Prevention Network’s yearly reports from 2001 to 2015. The National Survey of Drug Use and Health, a nationally representative longitudinal survey of the non-institutionalized US population with a 74.1% response rate, provided substance addiction rates. Cigarettes, monthly and binge drinking, monthly cannabis, painkiller, and cocaine addiction were all investigated. The rates of early termination of pregnancy for abortion (ETOPFA) were culled from the literature. The Drug Enforcement Agency provided the cannabinoid concentrations. The US Census Bureau provided ethnicity and income data. For chosen CAs, inverse probability weighted (IPW) regressions and geotemporospatial regressions were done. For mid-year analyses, 2005–2013, data on 18,328,529 births from an aggregated population of 2,377,483,589 was compiled, with 12,611 CARs for 62 CAs, and ETOPFA-corrected (ETOPFACAR) when suitable. THC (40 CAs), cannabis (35 CAs), tobacco (11 CAs), cannabidiol (8 CAs), monthly alcohol (5 CAs), and binge alcohol (2 CAs) had higher E-Values for ETOPFACARs, with minimum E-Values dropping from 16.55, 1.55×107, 555.10, 7.53×1019, 9.30, and 32.98. CAs in the cardiovascular, gastrointestinal, chromosomal, limb reductions and urinary, facial, and body wall CAs were all affected. For tobacco, cannabis, and cannabidiol, the CAR prevalence ratios for highest vs lowest substance use quintiles were 2.84 (95% C.I. 2.44, 3.31), 4.85 (4.08, 5.77), and 1.92 (1.63, 2.27), respectively, and the attributable fraction in exposed was 0.28 (0.27, 0.28), 0.57 (0.51, 0.62), and 0.47 (0.38, 0.55). In lagged IPW pseudo-randomized causal regressions, small intestinal stenosis or atresia and obstructive genitourinary dysfunction were explored in detail, and spatiotemporal models verified the causal involvement of cannabis. Cannabidiol dose-response power-function correlations were substantially sigmoidal non-linear in spatiotemporal predictive modelling (P=2.83×10−60 and 1.61×10−71 respectively). Cannabinoids, especially cannabidiol, were linked to a wide range of heritable CAs. Non-linear sigmoidal dose-response relationships were a major source of worry. These putatively causal transgenerational genotoxic, epigenotoxic, and chromosomal-toxic teratogenic effects suggested that community cannabis penetration was severely limited.
Source:bmcpediatr.biomedcentral.com/articles/10.1186/s12887-021-02996-3
