Perinatal Impacts of Cannabis and Nicotine: An Analysis of the Cannabis Use During Development and Early Life Study

OBJECTIVEEvaluate associations between prenatal cannabis use (PCU) and perinatal outcomes. METHODSWe performed an interval analysis of a prospective cohort study of pregnant individuals with pre-pregnancy cannabis use and negative self-report of nicotine use, comparing those who continued cannabis through pregnancy with those who stopped. Patients underwent interviews and urine drug screening for cannabis and cotinine, a nicotine metabolite, in each trimester. The primary outcome was small for gestational age (SGA) at delivery. Secondary outcomes included antenatal and postpartum complications, mode of delivery, and neonatal outcomes. Secondary analyses included stratification by intensity of cannabis use and urinary cotinine positivity. RESULTSBirthing persons with PCU differed in age (25.5 vs 27.8 years, p=0.001), body mass index (BMI; 27.4 vs 30.9, p=0.001), area deprivation index percentiles (92% PCU vs 88%, p=0.013), cotinine positivity (42.8% vs 10.8%, p<0.001), Hispanic ethnicity (2% vs 7.2%, p=0.009), and education attainment beyond high school (29.4% vs 50%, p<0.001) compared to controls. Birthing person outcomes did not differ. Risks of SGA and other neonatal outcomes did not differ when adjusted for confounders on initial analysis, or with stratification by intensity of cannabis use. Despite negative self-report for nicotine, 42.8% of PCU patients tested positive for cotinine (PCU+c). PCU+c was associated with increased risk of SGA and birthweight less than the 5th percentile, compared to PCU cases without nicotine exposure (17.4% vs 8.3%, aRR 2.7 [1.21-5.38], 35.8% vs 18.6%, aRR 2.4 [1.51-3.48]), and controls (35.8% vs 12.9%, aRR 2.75 [1.64-4.13]). Cotinine-negative PCU patients and controls did not differ. CONCLUSIONPCU was not independently associated with adverse birthing person outcomes. Many patients demonstrated nicotine exposure, either via inadvertent exposure or undisclosed use. While neonates exposed to cannabis alone did not differ from unexposed neonates, those exposed to both cannabis and nicotine were at increased risk of SGA.