A study has been making the rounds on social media claiming an association between prenatal exposure to pesticides and the risk of autism and developmental delay. This means that I am getting asked by many people what the study actually shows. Spoiler alert – not much. But let’s break it down.

Autism spectrum disorder (ASD) is a neurological disorder involving brain development resulting in decreased communications among neurons in the brain and characterized by reduced social ability. Our current scientific understanding is that ASD is largely a genetic disorder. While environmental factors cannot be ruled out, it seems that genes are the primary factor. It’s reasonable to search for environmental risk factors, but so far none have been clearly established.

Those who feel there likely is an environmental factor also tend to believe that there is an autism epidemic – that the incidence of autism is increasing in a way that is not easily explained by genetics, and therefore suggests and environmental factor. While it is uncontroversial that the number of ASD diagnoses has been increasing over the last two decades, this does not necessarily mean that the true incidence of ASD has been increasing.

The evidence actually shows that diagnostic substitution, broadening of the definition of ASD, and increased surveillance account for much of the increased recorded incidence. It’s possible that changes in diagnostic behavior entirely accounts for the apparent increase. It’s also possible that a subset is due to a true increase, but that has not been clearly established.

This still leaves us with the conclusion that an environmental factor is possible in ASD, but not necessary.

What does this current study show? The study in question is a case-control study using data from the CHARGE study and data about pesticide use in California. A case-control study is a retrospective epidemiological study. It looks at two or more populations based upon whether or not they have a condition, in this study there are three groups – ASD, developmental delay (DD) and typical. The groups are then compared based on exposure to a potential risk factor to see if it is correlated with the condition.

In this study the authors looked at proximity to pesticide use prior to conception and during each trimester of pregnancy. They concluded:

“This study of ASD strengthens the evidence linking neurodevelopmental disorders with gestational pesticide exposures, and particularly, organophosphates and provides novel results of ASD and DD associations with, respectively, pyrethroids and carbamates.”

Orac has already reviewed this study and I agree with his assessment – this conclusion is not justified by the data presented.

First, there is a fatal flaw in the study design: the authors used proximity to pesticide use (either within 1.25, 1.5, or 1.75 km of the use) to estimate pesticide exposure. However, they made no attempt to justify their core assumption – that this proximity significantly affects pesticide exposure. There were no measurements of specific pesticides in the blood or urine of mothers, and no measurement of pesticides in the local environment where they lived. Proximity was the only measure.

If living 1.5 vs 3 km away from a farm using a certain pesticide has no significant affect on exposure, then the entire study evaporates.

Also, the data itself are far from convincing. The three groups in the study were relatively small for a case-controls study – ASD = 486, DD = 168, and typically developing referents = 316. Keep in mind these break down further into smaller and smaller groups based upon type of pesticide and distance from use.

If you look at table 3 in the study, you will see a summary of the data. This is not impressive – many of the confidence intervals overlap with 1, meaning the difference is not statistically significant. For those that are, there is no clear relationship to distance or to trimester of exposure. The authors claim there is a statistical distance relationship, but it is inconsistent. Overall effects sizes and statistical significant are also low.

My overall impression of the data is that we have a relatively small study with barely significant results, small effect sizes, and an inconsistent pattern of effects. This is all compatible with random noise, maybe with a little p-hacking thrown in. With such a complex data analysis, it is certainly possible to inadvertently extract apparently significant results by making numerous comparisons and using various methods and then choosing the one that “looks” the best.

I also noted that males overall had a higher pesticide exposure than females. The authors note:

“Overall, exposure to pesticides during gestation was slightly more common for male children than female children (31% vs. 26%, p=0.004).”

I couldn’t find anywhere else a note that this was accounted for in the data analysis. It’s possible I just missed it, but if not, it should be noted that male children have a higher incidence of ASD than female, and so this could be a confounding factor.

Conclusion

Overall this study is small and underwhelming. The data are not convincing, and in my opinion the authors overstate their conclusions. At best this is a preliminary study, of the kind that often does not pan with larger and more rigorous follow up studies.

Having said that, I would note that the default position is for pregnant women to minimize their exposure to any potential toxin. Pregnancy certainly is a vulnerable period, and I am not saying the there are no concerns with pesticide exposure during pregnancy.

This study does not establish, however, that living within 1.5 km of pesticide use contains any health risk.

It is unfortunately that such studies are often reported with a simplistic bottom line – pesticide exposure is associated with autism, sometimes with a “may” thrown in. This is a problem in general with reporting preliminary data in the lay media. Such reporting is much more likely to be misleading than useful. Most people will just remember the possible association, and either not read or remember the detailed analysis explaining why the study did not establish the association.