The Science of Delay
Why we wait until millions are harmed by toxic chemicals before we act
On training fields and crash sites across the United States, Air Force firefighters once sprayed white foam to quench the flames. The foam smothered flames in seconds; it was hailed as a miracle. What no one saw was the invisible trail it left behind—PFAS, the “forever chemicals”—now detected in rivers, aquifers, drinking water, and human bloodstreams around the world.
Decades later, many of those same firefighters developed kidney or testicular cancers. Towns downstream found their drinking water contaminated. Mothers passed PFAS to their children through the placenta and breast milk. Their children produced fewer antibodies against measles and other vaccine preventable diseases.
By the time regulators acknowledged the harm, PFAS exposure had already become nearly universal; PFAS chemicals are now detected in nearly every human on the planet.
The First Signals
The warning signs weren’t subtle. Factory workers showed unusual liver abnormalities. Congenital eye defects were found in laboratory rodents and exposed workers’ children. Lab studies hinted at hormone disruption. Animals exposed to PFAS suffered reproductive damage. These early signals should have been enough.
But they weren’t. Epidemiologists, like me, who study poisons and pollutants knew better than to expect swift action. They had learned, often painfully, that regulators and industry rarely respond to evidence. They respond only to certainty.
How Delay Gets Built In
Here’s how the cycle plays out:
A researcher reports that pregnant women with higher PFAS levels give birth to babies prematurely.
Industry consultants’ step in: “Maybe it was diet, maybe smoking, maybe chance”.
Regulators nod, saying the study must be replicated—ideally in multiple populations, with confirmation of the mechanism in humans.
Years pass. More studies point in the same direction. Each is dismissed: too small, too large, not representative enough, not precise enough.
Even lawsuits become part of the delay. When DuPont settled claims over PFAS contamination, the public saw victory. But settlements are not admissions of guilt; they are simply another way of buying time, of delaying regulation. The message remains unchanged: until you prove beyond doubt that PFAS caused this disease in this person, the burden is yours to carry. Say that aloud, and it sounds absurd. Yet that’s how the system works.
Proof is always just out of reach. That’s not an accident; it’s the architecture of modern regulation.
The Myth of Definitive Proof
The standard of “definitive” is always just out of reach. That’s not an accident; it’s the architecture of modern regulation.
In the twentieth century, chemical companies successfully lobbied to minimize observational studies. In medicine, that’s reasonable—you can randomize patients to a drug or a placebo. In environmental health, it’s usually impossible. No one can assign families to drink PFAS-contaminated water for twenty years just to see what happens.
What we have are observational studies—tracking disease across populations, generations, and places. Observational studies aren’t weak substitutes; they are often the only, and the best, way to uncover harm from pollutants that never should have entered our environment.
The lesson should be clear: flip the burden. Don’t presume chemicals are safe until proven harmful; presume chemicals used in commerce are toxic until proven otherwise.
In 2009, the National Academies of Sciences warned that the EPA should assume that there is a safe level of exposure for noncarcinogens only if there is strong evidence for a threshold. Yet little has changed. The rules still dismiss observational studies as inadequate and keep alive the comforting misconception that every chemical has a threshold of safety—until proven otherwise.
The Human Cost
While the arguments play out in journals, community centers and court rooms, people remain exposed.
It’s not just factory workers or firefighters. It’s families near airports and military bases, where firefighting foam was used for decades. It’s farmers who discover their cows’ milk is contaminated. It’s suburban parents filling baby bottles with tap water. It’s city dwellers drinking from rivers polluted upstream. It’s Inuit families in the Arctic, where PFAS has traveled on the wind and settled into their food chain.
By the time the U.S. EPA proposed enforceable limits for PFAS in 2023, nearly the entire population was exposed. Those limits should have come years earlier. Under the Trump administration, PFAS regulation was delayed and weakened, giving industry more time while contamination spread. Every delay bought by politics translated into more children born with PFAS seeping into their blood and organs.
If this sounds familiar, it should. We saw the same script with lead in gasoline, asbestos fibers in talcum powder, pesticides in strawberries. The first signals were clear; the delays were deadly.
What the Public Thinks
Most people assume chemicals in commerce have been tested for safety. They imagine regulators standing guard, erring on the side of caution. The truth is closer to the opposite: chemicals are presumed safe until overwhelming evidence proves otherwise. And “overwhelming” usually means decades of exposure, multiple lines of evidence, and millions of preventable illnesses.
When people discover PFAS in their town’s water supply, they react with disbelief: How could this go on so long? The answer is both simple and unsettling. The system was built to protect industry from disruption, not people from harm.
What Scientists Think
For young epidemiologists, the lesson arrives quickly. One study linking PFAS to disease is never enough. To be heard, findings must be replicated, triangulated, defended against attacks in journals, legal briefs, and expert panels too often stacked with industry scientists. By the time evidence is “undeniable,” millions have been exposed.
Many scientists outside environmental health don’t grasp this dynamic. A geneticist, for example, might see an epidemiologist’s cautious recommendations as scientific doubt—without realizing that the caution reflects a rule book written decades ago by industry to delay regulation.
The Larger Lesson
PFAS is not an exception. It is the pattern. We wait for certainty while the chemicals spread. We ask for proof while the harms multiply. We protect corporations while people remain unprotected.
And epidemiologists, often unknowingly, become part of the delay. Their hyper-skepticism does not come from protecting people—it comes from navigating a system that only listens when the evidence is definitive. But “definitive” is a trap. In environmental health, it means waiting until the damage is already done.
Waiting for Definitive Proof
The real question is not whether forever chemicals are harmful—we know they are. The question is how much longer we will let the demand for “definitive proof” justify inaction. Each year of delay adds to the tally of communities with poisoned water, children with disrupted hormones, and men with testicular cancer.
The lesson of PFAS is the same lesson we should have learned from lead, asbestos, and air pollution: if we wait until the evidence is definitive, we’ve waited too long. And when regulations are stalled—whether by industry lobbyists or political leaders like Donald Trump who weakened and delayed PFAS rules—we are reminded that science alone cannot protect us. Protection requires political will and community outrage. Without it, the cycle of delay will keep repeating, and the human cost will keep mounting.



I have watched FDA scientists for 15 years as they systematically dismiss epidemiology studies as unreliable. Only when the evidence is overwhelming (and adopted by other agencies) do they adopt it. It was not until 2018 that they adopted the findings on lead. They do the same for studies conducted by academics because they prefer industry studies conducted pursuant their "Redbook" standards. Those standards were written in the 1980s and do not reflect the subtle but critical health endpoints related to neurology, immunology, and endocrinology. I am concerned that folks are using the term "gold standard science" to refer to those industry studies and enable them to dismiss epidemiology and academic studies.
Your post on the systemic delays that have allowed these chemicals to harm entire populations is much appreciated. Your description of how regulatory frameworks demand “definitive proof” before acting - while contamination continues - was both accurate and important.
In the case of fluoride - both inorganic forms used in mass fluoridation programs and organic forms such as PFAS - the effects on thyroid hormone metabolism have been well documented since the 1930s and 1940s. Yet, these effects were denied for decades and continue to be denied by agencies meant to protect public health (WHO, EFSA, CDC, etc.). This continuing delay has undoubtedly caused substantial harm worldwide.
But there is another, often overlooked contributor to delay: scientific negligence. And in this case, it comes from within the very field seeking to raise the alarm.
In 2016, you co-authored a study showing that PFAS effects on thyroid hormones varied according to TPOAb and iodine status (Webster et al., 2016). In that paper, you and your co-authors explicitly wrote:
"Future research on PFASs and other thyroid-disrupting chemicals should consider effect modification by thyroid system stressors, including TPOAb, iodine deficiency, and pregnancy, among others."
Unfortunately, in that paper iodine status was only dichotomized as "deficient" versus "normal," with "normal" defined as >100 µg/L. This is certainly not adequate considering the well-established U-curve effects of iodine on health. Since then, numerous studies have confirmed that PFAS toxicity on thyroid hormones is modified by TPOAb status (thyroid autoimmunity), especially during pregnancy (e.g. Korevaar, 2018; Wang et al., 2023; Itoh et al., 2019).
Yet, when you later examined PFAS exposure in the MIREC cohort (Goodman et al., 2023), neither iodine status nor TPOAb was considered at all - despite the fact that nearly 90% of the women were taking iodine-containing supplements and had demonstrable elevated iodine levels and higher TPOAb titers - the classic result of more-than-adequate iodine intake. Why were iodine and TPOAb not considered in this study?
In all the papers published on the cohort, iodine has never been addressed properly. A persistent and fundamental misconception remains that risk exists only at the low end of iodine intake, while the dangers of more-than-adequate intake are ignored. Recent papers on iodine status in the MIREC cohort (Berghuis et al., 2025; Krzeczkowski et al., 2023) exemplify this failure. The studies relied on inappropriate reference ranges and methodology, and largely ignored the U-shaped relationship between iodine and thyroid outcomes.
This is not a minor oversight. It directly biases risk estimates and obscures true PFAS toxicity. More-than-adequate iodine intake, at the levels seen in MIREC, has been shown to increase the toxicity of lead, cadmium, and other pollutants (e.g., Mergetaki et al., 2021) - in addition to causing significant harm on its own. While little can be done now about the historic delay in PFAS regulation and the widespread contamination, the public - and especially pregnant women and young children - could at least be alerted to monitor iodine intake, as this strongly influences how these toxic substances affect thyroid hormone metabolism. Failure to do so risks damage that can be passed on to future generations.
Negligence and scientific ignorance can delay action just as effectively as industry lobbying, and often longer, because they masquerade as science. By ignoring well-known effect modifiers and failing to properly assess iodine effects, your group’s work risks providing false reassurance and faulty conclusions, which in turn lead to continued exposure and preventable harm.
If the toxicity of lead, PFAS, cadmium, fluoride, and similar substances is misrepresented because it is studied without adequately accounting for high iodine intake, then the public is not protected. They are being misled.
The system’s failures are not only political - they are also scientific. And acknowledging that is essential if we are to break the cycle of delay.
References
Berghuis SA, Hall M, Krzeczkowski JE, Goodman CV, Chevrier J, Ayotte P, Lanphear B, Till C - "Urinary Iodine Concentration and Thyroid Hormone Metabolism in Pregnant Women and Neurodevelopment in Their Children: A Longitudinal Canadian Birth Cohort" Nutrients 17(5):830 (2025) d
https://www.mdpi.com/2072-6643/17/5/830
Goodman CV, Till C, Green R, El-Sabbagh J, Arbuckle TE, Hornung R, Lanphear B, Seguin JR, Booij L, Fisher M, Muckle G, Bouchard MF, Ashley-Martin J - "Prenatal exposure to legacy PFAS and neurodevelopment in preschool-aged Canadian children: The MIREC cohort" Neurotoxicol Teratol 98:107181 (2023)
https://www.sciencedirect.com/science/article/pii/S0892036223000314
Itoh S, Araki A, Miyashita C, Yamazaki K, Goudarzi H, Minatoya M, Ait Bamai Y, Kobayashi S, Okada E, Kashino I, Yuasa M, Baba T, Kishi R - "Association between perfluoroalkyl substance exposure and thyroid hormone/thyroid antibody levels in maternal and cord blood: The Hokkaido Study" Environ Int. 133(Pt A):105139 (2019)
https://www.sciencedirect.com/science/article/pii/S0160412019301199
Korevaar TIM - "Exposure to Per- and Polyfluoroalkyl Substances Is Associated with Lower Thyroid Hormone Availability during Pregnancy" Clin Thyroidol 30(4):190-192 (2018)
https://www.liebertpub.com/doi/abs/10.1089/ct.2018%3B30.190-192
Krzeczkowski JE, Hall M, McGuckin T, Lanphear B, Bertinato J, Ayotte P, Chevrier J, Goodman C, Green R, Till C - "Iodine status in a large Canadian pregnancy cohort" Am J Obstet Gynecol MFM 5(1):100784 (2023)
https://linkinghub.elsevier.com/retrieve/pii/S2589-9333%2822%2900214-2
Margetaki K, Vafeiadi M, Kampouri M, Roumeliotaki T, Karakosta P, Daraki V, Kogevinas M, Hu H, Kippler M, Chatzi L - "Associations of exposure to cadmium, antimony, lead and their mixture with gestational thyroid homeostasis" Environ Pollut 289:117905 (2021)
https://pmc.ncbi.nlm.nih.gov/articles/PMC11808336/
Wang X, Yang L, Wang Z, Feng X, Ji H, Liang H, Song X, Miao M - "Association between perfluoroalkyl and polyfluoroalkyl substances and maternal thyroid-related hormones in pregnant women" J Environ Occup Med 40(12):661-666 (2023)
https://www.jeom.org/cn/article/doi/10.11836/JEOM22314
https://pesquisa.bvsalud.org/gim/resource/pt/wpr-976511
Webster GM, Rauch SA, Marie NS, Mattman A, Lanphear BP, Venners SA - "Cross-Sectional Associations of Serum Perfluoroalkyl Acids and Thyroid Hormones in U.S. Adults: Variation According to TPOAb and Iodine Status (NHANES 2007-2008)" Environ Health Perspect 124(7):935-42 (2016)
https://ehp.niehs.nih.gov/doi/10.1289/ehp.1409589