A study claims that exposure to fine particulate matter pollution during pregnancy is associated with an increase in autism diagnoses

This paper shows a correlation between prenatal exposure to sulfate and ammonium components and childhood autism diagnoses. There is absolutely no evidence within the paper to suggest that the former caused the latter. It could potentially cause great worry to the general population if they thought this paper demonstrated a causal effect, having already been exposed to inaccurate claims around Tylenol and vaccines as causes of autism. Reports like this contribute to the very harmful myth that autism is increasing in prevalence: robust evidence from many studies indicates that this is not the case, but rather more autistic people, especially women and adults, are being recognised and diagnosed (which is an excellent thing, both on a personal level but also on a socioeconomic one, since late diagnosis is associated with poorer health and suicidality). The wording and framing of the article, talking about 'autism risk', also contributes to harmful narratives in which autism is presented such as a disease, something negative to be eradicated or avoided; we know that these kind of messages are felt as deeply detrimental by autistic people and their families, who feel they're living in a world where they're unwanted and unacceptable. It is deeply disappointing that authors continue to contribute to these harmful narratives rather than following responsible guidelines in the way they speak about autism - thus harming the community they're studying.

This study is showing correlation between air pollution exposure and potential cognitive development towards neurodivergence and autism.

This study is not confirming air pollution exposure causes autism in children. This is because we do not know the biological pathways where air pollution could change neuro-development in this way. We do know that negative impacts on cognitive function are associated with air pollution exposure but most of this research is for an older age category.

The study highlights important next steps around introducing socioeconomic variables alongside air pollution to suggest why an individual might be neurodiverse Vs neurotypical, another approach is called life course analysis where we model air pollution over different phases of life.

In this study, the authors observe a positive association between prenatal exposure to certain air pollutants (sulfate and ammonium anions) and the risk of autism spectrum disorders (ASD). The study analyzes more than 2 million births in the Ontario region (Canada) between 2002 and 2022.

Although there was previous epidemiological evidence on the relationship between air pollution and ASD, this is the largest study conducted to date, covering a long period of time. Therefore, the importance and significance of this study lies not only in the enormous size of the population sample analyzed, but also in its individual analysis of the effect of individual chemical components and specific periods during pregnancy and early childhood, establishing the last two trimesters of pregnancy as those of greatest susceptibility and risk to these pollutants. Furthermore, they also observe a positive association between postnatal exposure to ozone and an increased risk of ASD.

The study has several limitations:

1. Exposure estimates were assigned to residential zip codes, so they may not fully capture individual-level variability, especially in rural areas. They also did not account for temporal activity patterns, daily mobility, maternal physical activity, housing, or air filtration, which may influence personal exposure.
2. The study does not provide data on the mechanisms of action of pollutants that explain their association with ASD, based on the limited number of previous studies.
3. Potential interactions between air pollutants or factors such as race, ethnicity, lifestyle, differential access to medical care, and behavioral patterns, which may affect associations between prenatal exposure to pollutants and ASD risk, were not considered. Additional studies with more detailed individual-level data would be useful to clarify the observed patterns.