When news broke about the Swedish study questioning a link between prenatal Tylenol use and autism or ADHD, headlines buzzed with urgency.
Was a drug many consider “safe” during pregnancy now implicated in neurodevelopmental disorders? Within days, professional bodies rushed to reassure the public: “no causal link, nothing to see here.”
It’s a familiar pattern. Regulators use the same line with glyphosate — that it’s “safe if used as instructed.” But reassurance is not the same as proof, and safety claims often rest on narrow definitions that ignore what matters most: how real-world exposures stack up during pregnancy.
Tylenol may or may not play a role in neurodevelopmental disorders, but glyphosate — present in bread, cereals, oats, and even water — has been only lightly studied in this context, with a handful of troubling human findings largely ignored by regulators.
And that’s the bigger problem: it’s rarely just one pill, or one drug, or one chemical. It’s the entire cocktail of exposures that babies now encounter before they’ve taken their first breath. And among those exposures, pesticides — especially glyphosate — deserve far more scrutiny than they’ve ever received.
Prenatal Exposures: More Than One Smoking Gun
Decades of research have shown that multiple prenatal exposures — from alcohol to anticonvulsants, antidepressants, opioids, nicotine, and environmental chemicals — can alter brain development. Some act directly on neural pathways. Others trigger inflammation, oxidative stress, or endocrine disruption that reshapes the developmental landscape.
When scientists look for “the” cause of autism, ADHD, or other neurodevelopmental disorders, they often run into the same statistical problem: confounding. Was it the drug? Or the underlying condition that led the mother to take it? Was it socioeconomic factors, genetics, or something else entirely?
The Tylenol debate shows how confounding complicates the picture. Some studies report higher risks of autism or ADHD, while others see those signals weaken once parental health history or family environment are factored in. But even then, uncertainty is not the same as safety — and what often gets lost is that real-life exposures rarely happen in isolation.
This should have been the take-home message: single-exposure studies can mislead. The real risk may come not from one chemical but from the combination — and glyphosate shows us why this lesson matters.
Enter Glyphosate: The Ubiquitous Passenger in Pregnancy
Unlike Tylenol, which a mother can choose to take or not, glyphosate is an involuntary exposure. It’s not prescribed — it’s consumed daily through residues in bread, cereals, oats, honey, pulses, fruit, and even drinking water. Independent testing (including here in New Zealand) shows glyphosate is quietly present in the foods that fill our pantries.
Emerging evidence paints a troubling picture:
- Animal studies show prenatal glyphosate exposure can lead to altered social behaviors, anxiety-like traits, and learning or memory deficits in offspring.
- Human studies have linked maternal glyphosate biomarkers with shorter gestation, smaller head circumference, and other adverse birth outcomes.
- Multigenerational research (2025) has shown that even dietary-level exposure can disrupt immune, metabolic, and behavioral markers across several generations in mice.
These are not isolated effects. They intersect with other exposures — from plasticizers like BPA, to air pollutants, to prescription medications. Together, they may push developing systems past tipping points.
The Cocktail Effect: When Exposures Stack
Think of it this way: one exposure might weaken the placenta’s protective barrier. Another primes inflammatory pathways. A third alters the fetal microbiome. Individually, none might look catastrophic. Together, they create conditions where a child’s neurological development is more vulnerable.
Glyphosate is especially concerning because it doesn’t act in isolation:
- It disrupts gut bacteria, many of which rely on the shikimate pathway — a pathway humans don’t have, but our microbiome does.
- It induces oxidative stress and mitochondrial dysfunction, sapping the very energy cells need for growth.
- It alters hormone signaling, interfering with endocrine pathways critical in brain development.
Now imagine those effects layered on top of maternal stress, prescription drug use, air pollution, or nutritional deficiencies. The “confounded associations” we see in studies may not be noise at all — they may be signals of interaction.
Why Acetaminophen Gets a Pass — and Glyphosate Doesn’t Even Get Asked
When the Tylenol controversy flared, at least seven major medical societies rushed to reassure the public, declaring acetaminophen safe in pregnancy. Whatever the true risks of acetaminophen, it has at least been studied intensively, debated openly, and defended — while glyphosate slips past without even being asked the question.
Glyphosate is widely present in food and water, yet only a handful of studies have examined its impact in pregnant populations — and those that exist raise troubling signals regulators prefer to downplay.
Why does one exposure face endless scrutiny, while another — far less voluntary — is ignored?
A Public Health Blind Spot
Regulators argue that glyphosate residues in food are “within safe limits.” But those limits are based on outdated toxicology — focused on high-dose animal testing and tumor formation, not subtle developmental impacts or combined exposures.
In real life, no pregnant person is exposed to glyphosate alone. It almost always comes as part of a chemical mix in Roundup formulations with added surfactants. And beyond that, glyphosate is just one of many exposures converging during pregnancy — alongside Tylenol, SSRIs, plastics, air pollution, and ultra-processed food chemicals — each separate on its own, but collectively adding to the chemical burden within the same gestational window.
The regulatory framework isn’t built to handle this reality. Instead, it treats each exposure as if it exists in a vacuum.
Where This Leaves Us
The Tylenol story may not be settled at all. Advocates like RFK Jr. and MAHA argue that acetaminophen during pregnancy carries real risks — and the scientific literature does show troubling signals, even if medical societies are quick to downplay them. The danger is not just in whether Tylenol is guilty or innocent, but in framing the issue so narrowly. By focusing public debate on one pill, we miss the bigger picture: the chemical cocktail that includes pesticides like glyphosate, which no pregnant woman can opt out of.
If we truly care about the health of future generations, we need to move beyond the narrow hunt for one “bad actor” drug or chemical. We need to confront the uncomfortable truth: it’s the cocktail that counts — and glyphosate remains one of its most overlooked ingredients.
Call to Action
- Support independent testing — without it, we’d never know how much glyphosate is ending up in bread, cereals, or infant foods.
- Question outdated safety limits — are they based on what we now know about low-dose, long-term, multigenerational effects?
- Think holistically — pregnancy safety is not about one pill or one weedkiller. It’s about the total burden of exposures.
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Critical thinking starts with asking better questions. And perhaps the most urgent one is this: how many more children must be born into a chemical soup before we admit that the recipe itself is the problem?
Resources & References
When it comes to pregnancy and chemical exposures, the evidence is often buried in technical journals, fragmented across animal studies, human biomonitoring, and multigenerational experiments. Each study is a piece of a larger puzzle. Together, they raise a critical question: are we underestimating the risks by looking at chemicals one by one, rather than as part of the cocktail we actually live with?
Acetaminophen Use During Pregnancy and Children’s Risk of Autism, ADHD, and Intellectual Disability.
Ahlqvist VH et al. (2024).
JAMA.
Large Swedish population study (2.4 million children) showing crude associations between acetaminophen and autism/ADHD, but no independent link once sibling controls were applied.
Glyphosate-based herbicide disrupts energy metabolism and activates inflammatory response through oxidative stress in mice liver.
Qi X et al. (2023).
Food and Chemical Toxicology.
Demonstrates how glyphosate formulations impair mitochondrial function and trigger oxidative stress — key pathways in fetal development.
Effects of glyphosate exposure on western diet-induced non-alcoholic fatty liver disease in mice.
Romualdo GR et al. (2023).
Environmental Toxicology & Pharmacology.
Shows glyphosate worsens liver inflammation and metabolic disruption when combined with an unhealthy diet, highlighting synergy effects.
The Ramazzini Institute 13-week pilot study on glyphosate and Roundup.
Manservisi F et al. (2019).
Environmental Health.
Independent pilot study reporting developmental and endocrine effects at doses regulators considered “safe.”
Carcinogenic effects of long-term exposure from prenatal life to glyphosate and glyphosate-based herbicides in Sprague–Dawley rats.
Panzacchi S et al. (2025).
Environmental Health.
Long-term animal study showing glyphosate and GBHs increased rates of multiple tumors when exposure began prenatally, raising concerns about lifelong risk.
Glyphosate exposure in pregnancy and shortened gestational length.
Parvez S et al. (2018).
Environmental Health.
Human biomonitoring study in Indiana: >90% of pregnant women had detectable glyphosate, with higher levels linked to shorter pregnancies.
Glyphosate exposure in early pregnancy and reduced fetal growth.
Gerona RR et al. (2022).
Environmental Research.
Human study showing glyphosate detected in nearly all participants, with higher levels associated with lower birth weight percentiles.
The weight of evidence may not always point in a single direction, but it is shifting. From shortened gestation to altered metabolism across generations, the signals around glyphosate and pregnancy are too consistent to dismiss as coincidence. The real challenge now is not whether one chemical or one pill is “guilty,” but whether our regulatory and public health systems are ready to grapple with the complexity of combined exposures.
Image Source & Attribution
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