In a recent study, adjustments for maternal characteristics mediated the association between maternal prenatal cannabis use and offspring autism spectrum disorder, indicating no statistically significant increase in risk.
There is no link between maternal cannabis use in early pregnancy and autism spectrum disorder (ASD) in offspring, according to a recent study published in JAMA Network Open.1
An increase in maternal cannabis use has been observed in the United States, with cannabis having a lower perceived risk compared to certain prescription medications among pregnant women.2 However, there may be a risk of disrupted fetal neurodevelopment from cannabinoids entering the fetal blood stream through the placenta.1
Data about the impacts of prenatal cannabis use on long-term child neurodevelopment remains lacking, and current data is conflicting. Sex-specific associations have also not been evaluated.
To evaluate the association between maternal cannabis use in early pregnant and ASD in children aged up to 12 years, investigators conducted a cohort study. Data was obtained from a health care system managed by Kaiser Permanente Northern California (KPNC).
There are over 4.6 million members in KPNC, receiving coverage through employer-sponsored insurance, the California insurance exchange, Medicare, and Medicaid. Electronic health records in the KPNC database include data about diagnoses, hospitalizations, outpatient visits, and prescribed medications.
Universal screening for prenatal substance use is included in KPNC care of pregnant patients, while universal autism screening is available for pediatric patients. Study participants included pregnant mothers and their singleton offspring born from January 1, 2011, to December 31, 2019.
Eligibility criteria included at least 1 year of continuous KPNC membership before pregnancy, maternal attendance at 1 or more KPNC prenatal care visit, and reporting cannabis use since pregnancy. Follow-up occurred until the end of the study period or the child reaching 12 years of age.
Cannabis use during early pregnancy was reported as the primary exposure of the analysis, with early pregnancy defined as approximately 8 to 10 weeks’ gestation. ASD was the primary outcome, determined by at least 1 diagnosis from a KPNC ASD center or at least 2 diagnoses on separate dates by a non-KPNC clinician.
Diagnoses were based on International Classification of Diseases, Ninth Revision (ICD-9) and ICD-10 codes. Covariates included age at pregnancy onset, race and ethnicity, parity, insurance type, education, Neighborhood Deprivation Index, other noncannabis prenatal substance use, prenatal care initiation, maternal comorbidities, and antidepressant use.
There were 178,948 singleton pregnancies included in the final analysis, 27.3% of which were of Asian or Pacific Islander mothers, 23.9% Hispanic, 5.4% non-Hispanic Black, and 39.5% non-Hispanic White. Mothers were aged a median 31 years at pregnancy onset. Medicaid insurance was reported in 4.6% of pregnancies and high school education or less in 14.2%.
A positive screening for cannabis was identified in 4.7% of pregnancies, with a self-reported frequency of use of monthly or less reported in 1.1%, weekly in 0.5%, daily in 0.4%, and unknown in 2.7%. Prenatal substance use screening occurred at a median gestational age of 8 weeks.
During the median follow-up period of 3.7 years, 3.6% of children were diagnosed with ASD. Diagnosis occurred at a median age of 3 years, with 22.5% of children with ASD being female and 77.5% male.
A hazard ratio (HR) of 1.25 was reported for ASD risk in children of mothers with cannabis use during early pregnancy, indicating an increase in risk. However, this effect was mediated by adjustments for maternal sociodemographic characteristics. With an HR of 1.10, this indicated a non-statistically significant increase in risk.
Prenatal cannabis use based on self-report was also not linked to child ASD in the sensitivity analysis, with an HR of 0.89. Similarly, an HR of 1.10 was reported during the toxicology test.
These results indicated no increase in child ASD following maternal prenatal cannabis use when adjusting for cofounders. Investigators recommended further research about sex-specific associations with patterns of maternal prenatal cannabis use.
References
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