When “Risk” Means We Shouldn’t Exist: A Critique of the BPA–Autism Study in *Scientific Reports
Another week, another study claiming to trace autism back to a molecule.
On July 17, 2025, Scientific Reports published a paper titled “Prenatal exposure to bisphenol A disrupts RNA splicing in the prefrontal cortex and promotes behaviors related to autism in offspring.” The authors exposed pregnant rats to bisphenol A (BPA), observed behavioral changes in their pups, and concluded that BPA may contribute to autism “pathophysiology.”
It’s a polished paper. Densely cited. Methodologically tidy. And narratively devastating.
Because despite the jargon, this isn’t science in search of understanding. It’s science rehearsing an old story: that autism is a chemical mistake, a tragic misfire of development — one we should detect, prevent and eventually eliminate.
Let’s name the pattern. Then let’s answer back.
The Premise: Autism as Pollution Outcome
The study’s logic is familiar:
- BPA is an endocrine disruptor used in plastics.
- When pregnant rats ingest it at EPA-approved levels, their offspring behave differently.
- Those differences include hyperactivity, anxiety and aggression — traits the authors call “autism-associated.”
- In the brain, thousands of RNA splicing events are altered, including genes linked to autism in humans.
- Conclusion: BPA “disrupts” developmental biology in ways that may help explain autism.
Sounds compelling, right?
But here’s the catch: not once does the paper consider what these traits mean in context. Not once does it acknowledge that “autism-associated” is not the same as autism. Not once does it pause to reflect on the consequences of framing autism as something chemically preventable.
Instead, it speaks the language of certainty: disruption, promotion of behaviors, underlying pathophysiology. That’s not interpretation. That’s ideology — wrapped in peer-reviewed packaging.
Of Rats and Reductionism
Let’s be clear:
There is no autistic rat. There are rats who stim, who startle, who retreat. But there are no rats who mask. No rats who navigate school IEPs or survive diagnostic gauntlets. No rats who lose services when they stop meeting someone else’s criteria for being “disabled enough.”
Autism isn’t a checklist of behaviors. It’s a lived neurotype — shaped not just by biology, but by systems, stigma and survival.
So when researchers label rodent hyperactivity or social withdrawal as “autism-associated,” they’re not studying autism. They’re studying stress. And they’re projecting human narratives onto animals that can’t consent, can’t contextualize and certainly can’t reflect back the complexity of autistic life.
The moment we map a neurotype onto a lab rat, we collapse difference into deficit. And that flattening — not the science, but the frame — is what turns curiosity into harm.
A Brain Without a Person
The study focuses heavily on gene expression, particularly splicing events in the prefrontal cortex. The findings are extensive. And they may, in isolation, be worth studying.
But the interpretation is what matters. And here, the interpretation says:
- These molecular shifts contribute to autism.
- These behavioral traits mirror autistic symptomology.
- Therefore, BPA exposure may help explain autism causation.
That leap is enormous. And it erases the most important variable of all: the person.
There are no autistic co-authors. No mention of lived experience. No attempt to contextualize what makes life difficult for autistic people — or what makes it valuable.
It’s autism without people. Genes without joy. Behavior without meaning.
The Real-World Consequences
Studies like this don’t stay in labs. They travel. They enter headlines. They shape policy, parenting, and public health fear/misinformation (RFK Jr., anyone?).
They tell pregnant people: “Don’t eat that. It might make your child autistic.”
They tell funders: “Support prevention, not inclusion.”
They tell autistic people: “Your existence is the result of contamination. And we’re working on that.”
Even when no one says it outright, that’s the subtext. That autism is a developmental derailment — and the solution is to intervene before we arrive.
That’s not public health. That’s erasure by another name.
What This Study Doesn’t Ask
- What makes autism hard — the traits, or the environment?
- Are hyperactivity and aggression signs of damage, or responses to overwhelming stimuli?
- Are there protective genes or social factors that mediate BPA’s effects?
- Why frame difference as dysfunction when the outcome is not suffering, but variation?
And most importantly: Why aren’t autistic people part of this conversation?
The answer is structural. Because inclusion complicates the clean narrative. And clean narratives are easier to fund, easier to publish and easier to sell.
A Better Compass
Let’s be clear: studying environmental effects on development isn’t wrong. BPA should be scrutinized. Endocrine disruptors matter.
But the question isn’t just what does this chemical do?
It’s: What kind of story does this research tell? And what does that story cost the people being named?
If you’re studying autism causation without autistic collaborators, you are not telling the whole story.
If your study results in shame, fear or blame — even unintentionally — you are accountable for that outcome.
And if your definition of “prevention” includes the absence of people like me, you’re not protecting the future. You’re deciding who gets to be in it.
Final Thought
Autism isn’t a molecular error. It’s a way of being — one that comes with needs, yes, but also meaning. One shaped not just by genes or chemicals, but by community, experience, and dignity.
This study may offer insights into splicing. But it offers nothing to autistic people. Except the message — once again — that the world would rather engineer our absence than make room for our presence.
We’re not the error. But this framing? This silence? This flattening of difference into danger?
That’s the mistake.
And we’re here to answer back.