A biomarker-based study of prenatal smoking exposure and autism in a Finnish national birth cohort.
Blood tests prove prenatal smoking does not cause autism in Finnish kids.
01Research in Context
What this study did
Researchers tested if moms who smoked while pregnant had more kids with autism.
They used blood samples from 962 Finnish moms. The blood had cotinine, a chemical that proves smoking happened.
Doctors compared autism cases to matched kids without autism from the same national registry.
What they found
Moms of kids with autism had the same cotinine levels as other moms.
No amount of smoking exposure linked to autism risk. The result stayed zero even when they checked boys only, girls only, or severe autism cases.
How this fits with other research
Boswell et al. (2023) pooled 25 studies and also found no blood marker works for autism. Their big review includes this cotinine finding, showing the field keeps getting zeros.
Nijs et al. (2016) looked at brain glutathione and found normal levels too. Like cotinine, oxidative stress markers don't separate autism from controls.
Early et al. (2012) found weak links between parents' work chemicals and autism. That study used surveys, not blood tests. The blood-based cotinine result is stronger evidence against smoking as a cause.
Why it matters
You can tell worried parents that smoking during pregnancy does not raise autism risk based on hard blood data. Stop chasing prenatal smoking as a cause and focus assessment on proven factors like genetics and early red flags.
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02At a glance
03Original abstract
Maternal exposure to tobacco smoke during pregnancy is a common and persistent exposure linked to adverse neurodevelopmental outcomes in the offspring. However, previous studies provide mixed evidence regarding the relationship between prenatal smoking and offspring autism. This study used cotinine level, a biomarker for nicotine, to investigate the relationship between prenatal smoking and autism. The authors conducted a population-based case-control study nested in a national cohort of all births in Finland from 1987 to 2005. Cases diagnosed with childhood autism (ICD-10/9 code F84.0/299.0) through 2007 were identified using data from linked national registers. Each case was matched with a control on date of birth (±30 days), sex, and place of birth (N = 962 pairs). Maternal serum cotinine levels were prospectively measured in first- to early second-trimester serum samples archived in a national biobank using a quantitative immunoassay. Data were analyzed using conditional logistic regression. Prenatal maternal levels of serum cotinine were not associated with the odds of autism, whether cotinine was classified continuously, by deciles, or using previously defined categories corresponding to probable maternal smoking status. After adjusting for maternal age, paternal age, previous births, and any history of parental psychiatric disorder, the odds ratio for categorical high versus low cotinine, using a 3-level exposure variable, was 0.98 (95% CI = 0.76, 1.26; p = 0.88). In conclusion, this national birth cohort-based study does not provide evidence for an association between maternal cotinine, a biomarker of maternal smoking, and risk of autism. LAY SUMMARY: This study explored whether prenatal exposure to tobacco smoke in mothers is related to the diagnosis of autism in their children, by measuring the levels of cotinine, a biomarker for tobacco exposure, in stored serum samples drawn from mothers during pregnancy. The levels of cotinine in the mothers of children diagnosed with autism were similar to those in the mothers of control children of similar age and gender distribution.
Autism research : official journal of the International Society for Autism Research, 2021 · doi:10.1093/aje/kwaa182