A biomarker-based study of prenatal smoking exposure and autism in a Finnish national birth cohort.
Keely Cheslack-Postava, Andre Sourander, Susanna Hinkka-Yli-Salomäki and 3 others
PMID 34505741WHAT IT FOUND
Biomarker levels of maternal smoking and secondhand smoke exposure were not associated with childhood autism in this large Finnish cohort.
This suggests early to mid-pregnancy tobacco exposure is not a risk factor for autism, though a possible link with autism co-occurring with ADHD remains unclear.
Key findings
01Prenatal maternal serum cotinine levels, a biomarker for smoking and secondhand smoke exposure, showed no association with childhood autism in either unadjusted or adjusted models.
02Self-reported maternal smoking during pregnancy was also not associated with autism in this sample.
03There was a borderline significant association between heavy cotinine exposure and autism specifically when the child also had an ADHD diagnosis, though this finding is limited by small sample size.
STILL TO COME
How it was doneWhat they found
Read the rest of this summary
You get three full summaries a month, free, and we do not ask for a card. Search, the TL;DRs and your library stay unlimited either way.
What it does not show
Exposure was assessed at only one time point (first to early second trimester), so intermittent smoking later in pregnancy may have been missed. The study examined only childhood autism (ICD-10/9 F84.0/299.0), excluding broader ASD diagnoses like Asperger's or PDD-NOS, which limits generalizability to the full spectrum. The subgroup analysis linking heavy smoking exposure to autism with ADHD was underpowered and the confidence intervals were very wide. As an observational study, it cannot rule out confounding by unmeasured factors.
Declared interests
The study was supported by the National Institute of Mental Health (N.I.H., Extramural). The authors declared no competing financial interests.
The easy way to misread this
Do not interpret the borderline finding regarding heavy smoking and autism with ADHD as evidence of a causal link. The authors state this should be interpreted cautiously due to the limited size of the subgroup, and the primary outcome for autism overall was null.