Whilst cannabis is known to be toxic to brain development, it is unknown if it is
driving rising US autism rates (ASMR). A longitudinal epidemiological study was conducted
using national autism census data from the US Department of Education Individuals
with Disabilities Act (IDEA) 1991-2011 and nationally representative drug exposure
(cigarettes, alcohol, analgesic, and cocaine abuse, and cannabis use monthly, daily,
and in pregnancy) datasets from National Survey of Drug Use and Health and US Census
(income and ethnicity) and CDC Wonder population and birth data. Analysis was conducted
in R. 266,950 were autistic of a population of 40,119,464 8-year-olds in 1994-2011.
At national level after adjustment, daily cannabis use was significantly related to
ASMR (beta estimate =4.37 (95%C.I. 4.06, 4.68), P < 2.2 x10(-16)) as was first pregnancy
trimester cannabis exposure (beta estimate= 0.12 (0.08, 0.16), P = 1 .7 x 10(-)(12)).
At state level following adjustment for cannabis, cannabigerol (from beta estimate
= -13.77 (-19.41, 8.13), P = 1.8 x 10(-6)) and Delta 9-tetrahydrocannabinol (from
beta estimate =1.96 (0.88-3.04), P=4 x 10(-4)) were significant. Geospatial state-level
modelling showed exponential relationship between ASMR and 09-tetrahydrocannabinol
and cannabigerol exposure. Exponential coefficients for the relationship between modelled
ASMR and Delta 9-tetrahydrocannabinol and cannabigerol exposure were 7.053 (6.39-7.71)
and 185.334 (167.88-202.79; both P < 2.0 x 10(-7)). E-values are an instrument related
to the evidence for causality in observational studies. High E-values were noted.
Dichotomized legal status was linked with elevated ASMR. Data show cannabis use is
associated with ASMR, is powerful enough to affect overall trends, and persists after
controlling for other major covariates. Cannabinoids are exponentially associated
with ASMR. The cannabis-autism relationship satisfies criteria of causal inference.