In a recent study, offspring of women with cannabis use in early pregnancy confirmed by self-report or toxicology test were not at an increased risk of childhood early developmental delay up to the age of 5.5 years.
There is not an association between maternal prenatal cannabis use and increased offspring childhood early developmental delay risk, according to a recent study published in JAMA Network Open.1
There has been an increase in cannabis use among US individuals, with states legalizing use and accessibility improving. This makes it vital to understand the impact of prenatal cannabis use on child developmental outcomes.
Data has indicated links between maternal prenatal cannabis use and adverse birth outcomes, but there is little data about how prenatal cannabis use impacts childhood developmental outcomes. This includes conflicting results about speech and language outcomes and motor skills.
In a recent analysis, no association was reported between prenatal cannabis use and offspring risk of autism spectrum disorder.2 Any initial association was mediated when adjusting for maternal sociodemographic characteristics, regardless of if cannabis use was determined by self-report or toxicology test.
To evaluate the association between maternal cannabis use in early pregnancy and childhood early developmental delay risk, investigators conducted a retrospective birth cohort study.1 Participants were selected from the Kaiser Permanente Northern California (KPNC) health care delivery system.
KPNC patients with a singleton pregnancy leading to birth from January 1, 2015, to December 31, 2019, were eligible for inclusion. KPNC health plan membership from at least 1 year before pregnancy through delivery was also required, alongside at least 1 prenatal care visit.
Exclusion criteria included teratogenic, antineoplastic, or antiepileptic drug prescription fill during pregnancy, missing parity or address data, and not enrolling infants in the health plan within 1 year of birth data. KPNC’s administrative databases were assessed alongside California State Birth Certificates for relevant data.
The primary exposure was maternal cannabis use during early pregnancy, defined as “maternal self-reported cannabis use since pregnancy and/or a positive urine toxicology test for cannabis.” This exposure was measured during entrance into prenatal care at a mean 8.2 weeks’ gestation.
The frequency of prenatal cannabis use was also measured based on self-reports. Categories of frequency included never, monthly or less, weekly, and daily. Patients with cannabis use based on urine toxicology test had an unknown frequency.
Developmental outcomes included speech and language disorders, motor delay, and global developmental delay. These outcomes were identified using International Statistical Classification of Diseases and Related Health Problems, Tenth Revision diagnosis codes and Common Procedure Terminology codes.
Covariates included age at pregnancy onset, parity, insurance type, Neighborhood Deprivation Index, race and ethnicity, and educational attainment. Other noncannabis prenatal substance exposure and maternal comorbidities were also reported.
There were 119,976 pregnancies included in the final analysis, 27.3% of whom were from Asian or Pacific Islander women, 24.6% Hispanic, 5.5% non-Hispanic Black, and 39% non-Hispanic White. Being aged no more than 24 years was reported in 21.3%, having 2 or more prior live births in 21.3%, and having Medicaid insurance in 8.6%
Of pregnancies, 5.6% were impacted by maternal prenatal cannabis exposure, with 26.3% of cannabis exposures being confirmed by both self-report and toxicity, 56.4% by toxicity alone, and 17.3% by self-report alone. Daily exposure was reported by 0.5%, weekly by 0.6%, and monthly or less by 1.3%.
During the median 29-month follow-up period, 11.1% of children aged up to 5.5 years were diagnosed with speech and language disorders, 0.5% with global developmental delay, and 2.2% with motor delay. These conditions were diagnosed at a mean 25 months, 23 months, and 13 months, respectively.
No association was reported between maternal prenatal cannabis use and speech and language disorders, with a hazard ratio (HR) of 1.01. In models adjusting for covariates, a similar HR of 0.93 was reported.
This lack of association remained in a sensitivity analysis determining cannabis use based on self-report only. When determining cannabis use based on toxicology test, a slight inverse association with speech and language disorders was reported, with an HR of 0.68.
For global developmental delay, the initial association with maternal prenatal cannabis use was mediated by adjustment for maternal demographic characteristics, reducing the HR from 1.38 to 1.08. No significant association was reported when determining cannabis use based on self-report or toxicology test.
Finally, the minor negative association between prenatal cannabis use and offspring motor delay was mediated when adjusting for all potential cofounders, from an HR of 0.84 to 0.86. There were also no associations reported during sensitivity analyses.
These results indicated no association between maternal cannabis use in early pregnancy and offspring developmental delays up to 5.5 years. Investigators recommended further research about cannabis use throughout pregnancy and potential factors that may mitigate adverse associations.
References
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