Triple the number of studies on toxins and autism are what the literature should presently hold given the current rate of autism at 1 in 36. Studies on genetics and autism should be closely examining the impact of toxins on various genes… or genetic susceptibility to various toxins, such as heavy metals.
Yet here we are, in the infancy state of a growing literature that seeks to provide us the solutions to this matter. Interesting and concerning are the findings of the following study within the air-pollution autism literature.
Kalkbrenner, A. E., Windham, G. C., Zheng, C., McConnell, R., Lee, N. L., Schauer, J. J., Thayer, B., Pandey, J., & Volk, H. E. (2018). Air Toxics in Relation to Autism Diagnosis, Phenotype, and Severity in a U.S. Family-Based Study. Environmental health perspectives, 126(3), 037004.
The authors examined over 155 pollutants in a single pollutant model, and then conducted analyses where they adjusted for another pollutant -this means, they wanted to determine if the first pollutant retained its impact even after controlling for co-exposure to another pollutant.
However, co-exposures to various pollutants often occur, which the authors recognize in the following statements:
“It would be ideal to identify the individual chemical species within the traffic pollution mixture responsible for increased ASD risk. This is difficult because these exposures occur together, confounding observational associations of a single pollutant, a problem of copollutant confounding that is common in environmental epidemiology. Disentangling the role of individual chemicals (i.e.,confounding) and whether combinations of chemicals may act in new ways (i.e.,interaction) are among the key questions of environmental mixtures currently being addressed.”
Co-exposures to multiple toxins is a bull the autism literature will have to wrestle, but we will get there.
Nevertheless, one pollutant that is noteworthy in this study is Propionaldehyde.
Propionaldehyde is formed from the combustion of gasoline, diesel, and waste/biomass burning, and also has industrial uses.
By itself, this study found prenatal exposure to Propionaldehyde resulted in an 1.92x increased odds of autism.
In two-pollutant models, the effect of Propionaldehyde remained significant when the effect of various other pollutants were adjusted for in the analyses:
adjusted for 2.2.4-Trimethylpentane– 2.76x Increased Odds of Autism
adjusted for Acrolein– 1.83x Increased Odds of Autism
adjusted for Diesel particulate matter– 1.93x Increased Odds of Autism adjusted for Xylenes– 2.01x Increased Odds of Autism
Finally, it is worth mentioning that the study utilized a family-based design where siblings with and without autism were compared to each other, as opposed to comparing a child with autism from one family to another child with autism from a different family. Although the authors did not analyze data on genes, this particular design of the study gives some degree of control over gene-environment interactions, as well as other confounds like urban vs. rural residences. Thus, the study provides very strong evidence regarding the impact of these various air pollutants and autism.
Interestingly, in 2008 the EPA published a Toxicological Review on Propionaldehyde. At the time, Propionaldehyde was primarily examined for carcinogenic effects, and they concluded the evidence at the time indicated that the data was insufficient to determine a carcinogenic effect.
Propionaldehyde was previously approved by both U.S. FDA in 2003 as well as the World Health Organization/Joint Expert Committee on Food Additives as a synthetic flavoring ingredient for direct addition to food. Its derivative Propionic acid was also approved.
Today, Propionic acid is a common food preservative generally recognized as safe by the US Food and Drug Administration with no limitation other than good manufacturing process. It is used as a mold inhibitor in breads, cheeses, tortillas, and cakes, as well as a mold inhibitor for various animal feeds. The human metabolic processes for its consumption are not well understood.
A recent randomized, placebo-controlled study in 28 healthy men and women found that exposure to propionic acid via oral consumption led to activation of the insulin-counterregulatory hormonal network [1]. However, this literature is also in its infancy and much more investigation is needed.
Searching for ‘propionaldehyde’ and ‘autism’ does not yield many results on PubMed. However, searching ‘propionic acid’ and ‘autism’ pulls up studies on animal-autism models whose ASD was induced by prenatal exposure to propionic acid. Thus, we have a growing literature that uses rat models whose autism is induced by propionic acid.
Please be reminded there also exists the Valproic Acid animal model of autism used for studying the condition. Valproic acid is a seizure medication contraindicated for use during pregnancy because of severe impacts to neurodevelopment of the child.
Given an apparently growing literature on propionic acid induced animal models of ASD, and further research pending regarding the metabolic consequences of its consumption, and finally, the aforementioned study Kalkbrenner et al. (2018) regarding prenatal exposure to Propionaldehyde and odds of autism, how concerned should we be regarding its presence in both our food and our air?
Hmm.
But what about our water?
Water is the icing on the cake. The EPA’s Toxicological review in 2008 states, “National Organics Reconnaissance Survey conducted in the 1970s, propionaldehyde was found to be one of the 18 organic chemicals detected most frequently in the drinking water of the 10 cities surveyed.”
Truly it seems, we live in a cocktail of chemicals.
Are we in a similar situation to fluoride? Is propionaldehyde’s safety assumed based upon the amount consumed?
Well, that’s exactly what the EPA’s 2008 Toxicological report states: “Propionaldehyde was determined to pose no safety concern since its expected oral intake (140 μg/day) is below the threshold for human intake (1800 μg/day, as defined by WHO) and it is oxidized to propionic acid, which is metabolized via the citric acid cycle (WHO, 1999; IPCS, 1998).”
Wonderful.
Make sure to not consume too much Propionaldehyde each day. 🙂
Oh…
that’s right…
we don’t know how much we’re consuming via our air, water, and food.
Have fun with that one.
1. Adler, G. K., Hornik, E. S., Murray, G., Bhandari, S., Yadav, Y., Heydarpour, M., Basu, R., Garg, R., & Tirosh, A. (2021). Acute effects of the food preservative propionic acid on glucose metabolism in humans. BMJ open diabetes research & care, 9(1), e002336.
The Causes of Autism 