Forever Chemicals in Pet Food: What the Data Says

A federal class action against major pet food brands was certified in January 2026. A new peer-reviewed study on PFAS contamination in pet food in February of 2026. Seven states have new chemical restrictions taking effect this year. Your social feed is probably full of alarming headlines.

Before you overhaul your pet’s diet, read this.


You may have heard the term “forever chemicals”, referring to a broad family of synthetic compounds that don’t break down in the environment or in the body. The name likely sounds familiar because these chemicals are genuinely everywhere. Teflon, or PTFE, used in non-stick cookware. PFOS, the active compound in Scotchgard and firefighting foam. Fluorotelomer sulfonates in floor coatings, cleaning products, and waxes. Related compounds in stain-resistant rugs and fabrics, food packaging, clothing, makeup, dental floss. Because they are so pervasive in our homes and daily lives, they are also in our water supply, our food supply, and, as a growing body of research now confirms, in our pets. The concern is legitimate, the science is real and developing, and the media coverage is making it nearly impossible to respond to any of it proportionately. That’s what this piece is for.

What Are PFAS? A Brief, Precise Overview

PFAS stands for per- and polyfluoroalkyl substances (1). This is not one chemical, but a family of more than 12,000 synthetic compounds that share a common structural feature: a carbon-fluorine (C-F) bond (2). The C-F bond is one of the strongest in organic chemistry. That strength is exactly why PFAS were so commercially useful since it gives them the ability to resist heat, oil, water, and grease. However, this is also the reason why they are so environmentally persistent. They do not break down under ordinary environmental conditions. Hence being termed “forever chemicals.”

PFAS were first developed in the 1940s and found their way into an enormous range of applications: non-stick cookware coatings, waterproof fabrics, firefighting foam (AFFF), food packaging grease-proofing, carpet and furniture stain treatments, dental floss coatings, and industrial processes across dozens of sectors. Their ubiquity means that by now, detectable PFAS concentrations have been found in virtually every corner of the global environment including Arctic ice cores, remote mountain lakes, rainwater, topsoil, wildlife on every continent, and the blood of nearly every person tested.

Within the PFAS family, the most studied, and the most concerning, are two specific long-chain compounds:

  1. PFOA (perfluorooctanoic acid) was the primary ingredient in Teflon manufacturing for decades and was central to the 3M and DuPont contamination cases that shaped the modern regulatory landscape. It is classified as a Group 1 human carcinogen by the International Agency for Research on Cancer (IARC).
  2. PFOS (perfluorooctane sulfonic acid) was the active compound in Scotchgard and in AFFF firefighting foam. It is one of the most persistent PFAS known, has been detected in blood samples globally, and is regulated under the Stockholm Convention on persistent organic pollutants.

Both PFOA and PFOS have been phased out of production by U.S. manufacturers. PFOA largely by 2015, PFOS by 2002, however because they do not degrade, legacy contamination persists in soil, water, wildlife, and human and animal tissues. Many manufacturers replaced these long-chain compounds with shorter-chain variants or alternative fluorinated chemicals. Although, this may not negate risk of their predecessors since it’s possible they also carry their own concerns and are far less studied (2).

Where PFAS Come From: It’s Not Just the Food Bowl

This is the single most important context point to establish before any discussion of PFAS in pet food, and it is the one most consistently omitted from consumer-facing coverage.

Pets, particularly indoor dogs and cats, are exposed to PFAS from multiple simultaneous routes (3). Food is one of them. It is not the only one, and in many household environments it may not even be the primary one.

Indoor Environments

Stain-resistant carpeting and upholstered furniture treated with PFAS-based products shed these chemicals into household dust. Dogs are in close contact with flooring surfaces for most of their waking hours and ingest house dust at higher rates than humans through grooming and floor-sniffing behavior. Research published in the American Journal of Veterinary Research found that serum PFAS profiles in companion dogs closely mirror those of their human owners, suggesting shared indoor exposure routes including water, dust, and PFAS-treated textiles are primary contributors (3).

Drinking Water

PFAS contamination in municipal and private well water is widespread, particularly in areas near military bases, industrial sites, or locations where AFFF foam was historically used. The EPA established Maximum Contaminant Levels for six PFAS in drinking water in April 2024. Pets drink from the same water sources as their owners, often at higher volume relative to body weight.

Household Products

Non-stick cookware, waterproof outerwear stored in the home, treated textiles, certain dental floss products, and some cleaning agents contribute to the ambient PFAS load in indoor environments. Dogs exposed to homes with high levels of treated textiles or flooring show correspondingly higher serum PFAS concentrations than dogs in less-treated environments.

Food Packaging

Grease-resistant food packaging which has historically been a major dietary PFAS exposure route for humans has been a focus of both regulatory action and litigation. The FDA announced in February 2024 that PFAS-based grease-proofing agents for paper and paperboard food packaging are no longer being sold for food-contact use in the United States and reaffirmed this again in January 2025 (4). This action was intended to eliminate the primary authorized dietary exposure source from food contact surfaces. The key word is “authorized” legacy packaging, imported products, and non-paper packaging materials operate under different frameworks.

The relevance to pet food: the active litigation is about packaging migration is a contested scientific question about whether PFAS from bag coatings migrates into the kibble or wet food inside. It is not about PFAS inherently present in the ingredients themselves. That distinction matters enormously and will be revisited in the litigation section below.

Why Fish-Based Diets Test Higher And What The Headline Is Missing

Breeds with Inherited Copper‑Handling Defects

In February 2026, a peer-reviewed study from Ehime University’s Center for Marine Environmental Studies was published in Environmental Pollution (5). Researchers analyzed 100 commercial pet foods sold in Japan. The study included 48 dog foods, and 52 cat foods, measuring concentrations of 34 PFAS compounds. The study found PFAS were detectable across many products, with fish-based pet foods consistently showing higher concentrations of long-chain PFAS, particularly PFOS, perfluoroundecanoic acid (PFUnDA), and perfluorotridecanoic acid (PFTrDA).

This result is not surprising to anyone with a working knowledge of environmental contaminant chemistry. It is a direct consequence of biomagnification.

How PFAS Accumulate in Aquatic Food Chains

PFAS are proteinophilic. This just simply means they bind to proteins, particularly albumin and fatty acid-binding proteins. Unlike many lipophilic environmental contaminants that concentrate in fat tissue, PFAS concentrate in blood and protein-rich tissues. In aquatic environments, PFAS enter the food chain through contaminated water and sediment, are taken up by plankton and small invertebrates, and increase in concentration at each successive trophic level. This process is called biomagnification. By the time a predatory fish like tuna or salmon has accumulated PFAS across its lifespan, it carries substantially higher concentrations than the water it swims in.

“The ocean often acts as a final sink for many synthetic chemicals,” the lead researcher Kei Nomiyama noted in commentary accompanying the study (5). “PFAS can move and concentrate in aquatic food webs.” Fish used as ingredients are a significant source of PFAS exposure, and this pattern is consistent with what has been observed in human seafood consumption studies as well.

The Critical Caveat: Human Reference Values Applied to Pets

This is where the coverage loses the thread, and where the science requires precision.

The Nomiyama study calculated hazard quotients (HQs) for dogs and cats using the European Food Safety Authority’s (EFSA) tolerable weekly intake thresholds established for humans (5). Several products showed average HQs exceeding 1, which is the threshold that signals potential concern. This is the number the headlines ran with.

What the headlines omitted: EFSA itself, when asked to comment on the study, explicitly stated that its human reference values should not be applied as-is to risk assessments in other species. The researchers agree, and the authors state clearly that “due to the lack of species-specific toxicokinetic information for dogs and cats, the EFSA-based risk characterization presented here should be interpreted as a preliminary assessment.”

No reference doses for PFAS have been established for dogs or cats. The HQ calculations in this study are the best available approximation given current data. This is genuinely useful as a signal that the topic warrants further investigation and species-specific toxicological work. What they are not is a confirmed finding of harm. 

The study also found that while dry foods had higher PFAS concentrations per gram, estimated daily exposure was greater from wet foods due to higher serving volumes. Meat-based products generally showed lower PFAS than fish-based products. Some brands tested at or near non-detectable levels.

Physiology of PFAS Accumulation: How These Chemicals Behave in the Body

PFAS do not behave like most toxicants. They do not accumulate in fat. They bind to albumin and liver fatty acid-binding proteins, concentrating in blood, liver, and kidneys. This protein affinity has several important physiological consequences:

Half-life differences between species. In humans, some PFAS persist in serum for years. For instance, PFOS has an estimated half-life in humans of roughly 4 years; PFOA approximately 3.5 years. In dogs, data we do have suggests that PFAS are cleared far more quickly. Research presented at the 2023 AVMA Convention by Dr. Heather Brake of Michigan State University found that exposed dogs may clear PFAS from the body within eight days to a couple of months, compared to years in humans (3). This species difference is critical when interpreting studies that measure serum PFAS levels in pets as proxies for cumulative dietary or environmental exposure.

Hepatic effects. PFAS exposure is associated with increased liver weight and elevated liver enzymes, including ALT, AST, and GGT, in both rodent models and companion animals. A study by You et al. (2022) analyzed PFAS levels and blood chemistry in police dogs and beagles, finding that specific PFAS compounds were significantly associated with changes in hepatic biomarkers, though the directionality and magnitude varied by PFAS type (6).

Thyroid disruption. Among the most consistent findings in companion animal research is a possible association between long-chain PFAS, particularly PFOS and PFNA, and thyroid function, especially in cats. A 2018 study by Wang et al. examining serum PFAS in Northern California cats found significantly higher concentrations of long-chain perfluorinated carboxylic acids in hyperthyroid cats compared to euthyroid controls, and elevated PFOS levels in hyperthyroid animals specifically (7). Feline hyperthyroidism is among the most common endocrine disorders in older cats. Whether PFAS exposure is a contributor, a correlate, or unrelated to the disease’s prevalence increase over recent decades remains an open research question, certainly not a settled one.

Kidney function. Significant associations between PFAS exposure and kidney function markers have been documented in both dogs and cats. Given that the kidneys are a primary excretion route for PFAS, this is biologically plausible. Causation has not been established.

Maternal transfer. PFAS cross the placenta and are present in milk in both humans and animals. This means developmental and neonatal exposure occurs before any direct dietary exposure, and cumulative lifetime burden begins at conception. For breeding animals, this is a particularly important consideration.

Immunological effects. Decreased vaccine response is among the more consistently documented effects of PFAS in human research, including in children. Whether this translates to clinically meaningful immune suppression in companion animals at typical exposure levels has not been adequately studied.

What the Litigation Actually Found

The legal landscape around PFAS in pet food has moved fast. Understanding what the lawsuits claim, and what courts have and have not established, is essential context.

Jeruchim v. The J.M. Smucker Co. (N.D. Cal., No. 22-cv-6913)

This is the case that generated most of the headlines. In January 2026, U.S. District Judge William H. Orrick certified a class action against J.M. Smucker, covering California consumers who purchased 9Lives, Kibbles ‘n Bits, or Meow Mix between November 2018 and December 2022, over allegations that PFAS in the packaging were not disclosed despite health-based marketing claims like “100% healthy” (8).

Certification is a procedural threshold, not a verdict. It means the case can proceed as a class rather than as individual suits. It is not a finding that PFAS migrated into the food, that any pet was harmed, or that Smucker violated the law. Those questions go to trial, currently scheduled for October 27, 2026 in San Francisco, with summary judgment motions this summer that could narrow or end the case before it gets there.

What the court did find is narrower: that consumers plausibly alleged economic harm, overpayment based on an omission. A reasonable consumer, the court concluded, would not expect a product labeled “100% healthy” to contain packaging with PFAS. That is a consumer protection theory. It is a meaningful legal development. It is not proof of harm.

The plaintiffs’ operative theory that “any prolonged exposure to PFAS is harmful to animals” is a litigation posture designed to establish a class wide common question. It is not a scientific consensus statement, and it cannot be, because the data doesn’t exist to support one. There are no established reference doses for PFAS in dogs or cats. There are no regulatory limits for PFAS in pet food. The same evidentiary gap that makes this a legitimate scientific concern also makes it nearly impossible to prove, or disprove, specific harm in a courtroom. That tension is exactly what the merits trial will have to navigate.

Judge Orrick has been here before. He drew explicitly on his 2021 ruling in Zeiger v. WellPet, where he certified a class over arsenic, lead, and bisphenol in dog food on the same logic: that “any exposure could be harmful” functions as a class wide question even without individualized exposure data. The PFAS case rests on the same legal scaffold. A parallel class action against Nestle Purina over Cat Chow packaging is pending in the same court.

Broader PFAS Packaging Litigation

The Smucker case is part of a broader wave. Nestle Purina faces a similar class action alleging PFAS in Cat Chow packaging, also filed in the Northern District of California. Similar suits have been filed against fast food packaging, microwave popcorn manufacturers, and other food brands. Many of these cases have struggled or been dismissed due to standing challenges, lack of product-specific testing, and the difficulty of proving migration. The Smucker certification is notable precisely because most comparable cases failed at this stage.

The litigation’s central premise, that PFAS in packaging poses a risk through migration into food, is scientifically plausible but unproven. FDA’s January 2025 determination that grease-proofing PFAS are no longer being sold for food contact uses eliminates the primary authorized source going forward. It does not retroactively address legacy packaging or clarify what concentrations, if any, historically migrated into packaged food.

The Regulatory Gap

Federal oversight of PFAS in pet food is essentially nonexistent, and this is not unlike many other contaminants found in commercial pet food. The FDA regulates PFAS in food contact materials for human food, but there are no established maximum contaminant levels for PFAS in pet food ingredients or finished products. AAFCO nutrient profiles, the standard framework for pet food nutritional adequacy, do not address contaminants at all. They are designed to define minimum nutrient requirements, not to set toxicological limits for environmental contaminants. As always, AAFCO compliance is a floor, not a ceiling, and in this case the floor says nothing about PFAS.

At the state level, as of 2026, seven states have new consumer product PFAS restrictions taking effect, covering food packaging, cookware, cosmetics, and other product categories (9). Fourteen states have enacted food packaging PFAS laws of varying scope. Minnesota’s Amara’s Law is among the most comprehensive, with reporting requirements that took effect in 2025 and a phased ban on all consumer products with intentionally added PFAS by 2032. Connecticut, where NorthPoint Pets operates, banned intentionally added PFAS in packaging beginning in 2023. These are meaningful steps, but their reach is narrower than the headlines suggest. They target deliberate use of PFAS in packaging materials. They do not address PFAS entering the food supply through contaminated ingredients, environmental bioaccumulation, or imported products. And without systematic independent testing for compliance, these laws create legal accountability on paper without consistently delivering it in practice. The regulatory infrastructure is catching up to the science, but slowly and unevenly.

Internationally, EFSA has established tolerable weekly intakes for PFAS in humans. Japan’s Pet Food Safety Act, enacted in 2008, does not currently regulate PFAS in pet food. No national regulatory body has established species-specific PFAS reference doses for companion animals.

Where Does This Leave Us? Practical Guidance Without Panic

The honest answer to “what should I do?” is: apply proportionate concern and make targeted adjustments where the evidence is strong enough to act on.

What the evidence supports

Reducing fish-heavy diets as a primary protein source is a reasonable precautionary step given what is known about PFAS bioaccumulation in aquatic food chains, especially for cats consuming fish-based wet food as the bulk of their diet. This does not mean fish is never appropriate or that a fish topper ruins an otherwise varied diet. It means fish-centric feeding patterns carry a higher PFAS load than meat-based alternatives, and that is consistent with the literature.

Addressing water quality matters. If your municipal water supply or well water has known PFAS contamination, this is a significant exposure route for your pet. Filtered water, using activated carbon or reverse osmosis, meaningfully reduces PFAS in drinking water. This is one of the highest-leverage interventions available.

Consider indoor exposure. PFAS-treated carpeting, upholstered furniture, and stain-resistant products are meaningful contributors to household PFAS burden for indoor animals. When replacing flooring or furniture, PFAS-free alternatives exist. Regular wet mopping (which removes dust more effectively than dry vacuuming) reduces the settled dust load.

Monitor routine blood work. Given the association between PFAS exposure and hepatic and thyroid biomarkers, routine monitoring of liver enzymes, kidney values, and thyroid function in older cats and dogs is sound preventive medicine regardless of PFAS concerns. If values are trending in the wrong direction, PFAS exposure is one factor worth investigating alongside others.

What the evidence does not support

Complete elimination of all fish from the diet based on current data is disproportionate. A varied diet with occasional fish-based components does not create the same exposure profile as daily fish-centric feeding.

The assumption that “your pet’s food is making them sick right now.” The research establishes that PFAS are detectable in pet food, that some products show levels that would exceed human reference thresholds, and that PFAS are associated with certain health markers in companion animals. It does not establish that typical commercial pet food, at typical feeding volumes, is causing clinical disease in otherwise healthy animals eating a varied diet.

Switching to homemade or raw diets based on PFAS concerns alone. This introduces a separate set of nutritional risks that are far better documented than the PFAS risks being avoided. Ingredient sourcing matters in homemade diets too, meat from animals raised in contaminated areas carries its own PFAS burden.

The NorthPoint Pets Position

PFAS are a legitimate environmental health concern that deserves serious scientific attention. The coverage they are currently receiving is not serious scientific attention but rather fear-based content that strips away context, misapplies human reference thresholds to animals without noting the species limitation, and buries the packaging-versus-ingredient distinction that is central to the entire legal and scientific debate.

Companion animals are, in the words of PFAS researchers, “sentinels”, as they share our environments, eat from the same ingredient supply chains, and are exposed to the same indoor contamination sources we are (10). That makes them valuable early-warning systems. It also means that PFAS in a pet’s body is usually a reflection of the household environment broadly, not just the food bowl.

There are no PFAS-free diet options for pets. There are no PFAS-free environments. The goal is not zero exposure, that is not achievable. The goal is proportionate reduction of avoidable exposures while keeping nutritional adequacy, digestibility, and overall health optimization at the center of every feeding decision.

AAFCO compliance tells you a diet meets minimum nutrient thresholds. It tells you nothing about contaminant load, ingredient quality, bioavailability, or how a specific animal with specific genetics and history will respond. Individual assessment, actual health monitoring, diet diversity, and relationship with a veterinarian who knows your animal remains the most protective intervention available regardless of what the next alarming headline says.

We will continue tracking this research as it develops. The 2026 Nomiyama study is the first of what will be many. Nonetheless, species-specific toxicokinetic data are urgently needed, regulatory frameworks are lagging, and the litigation will push disclosure requirements forward. When the science moves, we will move with it.

Not sure what’s right for your dog? Our team at NorthPoint Pets specializes in personalized nutrition guidance based on your dog’s unique needs—not trends or fear-based marketing. Stop in or talk with us today.


REFERENCES

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  2. Kwiatkowski CF, Andrews DQ, Birnbaum LS, Bruton TA, DeWitt JC, Knappe DRU, et al. Scientific Basis for Managing PFAS as a Chemical Class. Environ Sci Technol Lett. 2020;7(8):532-43.
  3. Brake HD, Wilkins MJ, Kaneene JB. Per- and polyfluoroalkyl substances: using comparative medicine to understand exposure and adverse health outcomes in people and their pets. Am J Vet Res. 2023;84(7).
  4. Administration USFaD. Per- and Polyfluoroalkyl Substances (PFAS) 19 December 2025 [Available from: https://www.fda.gov/food/environmental-contaminants-food/and-polyfluoroalkyl-substances-pfas.
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  6. You D, Chang X, Guo L, Xie W, Huang S, Li X, et al. Per- and polyfluoroalkyl substances (PFASs) in the blood of police and Beagle dogs from Harbin, China: Concentrations and associations with hematological parameters. Chemosphere. 2022;299:134367.
  7. Wang M, Guo W, Gardner S, Petreas M, Park JS. Per- and polyfluoroalkyl substances in Northern California cats: Temporal comparison and a possible link to cat hyperthyroidism. Environ Toxicol Chem. 2018;37(10):2523-9.
  8. Atkins D. Smucker Pet Food Buyers Win Cert. In PFAS Disclosure Fight. Law360. 2026 January 22.
  9. Tomlinson H, Giambrone B. States Continue to Address PFAS in U.S. Food and Water Supply 2025 [updated July 25, 2025. Available from: https://www.astho.org/communications/blog/2025/states-continue-addressing-pfas-in-food-and-water/.
  10. Rock KD, Polera ME, Guillette TC, Starnes HM, Dean K, Watters M, et al. Domestic Dogs and Horses as Sentinels of Per- and Polyfluoroalkyl Substance Exposure and Associated Health Biomarkers in Gray’s Creek North Carolina. Environ Sci Technol. 2023;57(26):9567-79.