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

1. Buck RC, Franklin J, Berger U, Conder JM, Cousins IT, de Voogt P, et al. Perfluoroalkyl and polyfluoroalkyl substances in the environment: Terminology, classification, and origins. Integrated Environmental Assessment and Management. 2011;7(4):513-41.
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.
5. Nomiyama K, Sato A, Tanoue R, Saeki K, Ikenaka Y, Mizukawa H. Widespread PFAS contamination in pet food: Dietary sources and health risks to companion animals. Environ Pollut. 2026;395:127779.
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.

Recent social media posts warn that “millions of dogs are in imminent danger” from copper in commercial pet food. Those posts are tapping into a real scientific debate, but they often miss critical nuance: copper is essential, some dogs are clearly being harmed by excess copper, and at the same time we genuinely do not know the optimal copper range for every dog.  Here we will walk through what we do know from peer‑reviewed research, where the uncertainty lies, and how pet owners can make informed decisions without the panic and fear‑mongering driven by social media.

1. Copper Is Essential and a “Goldilocks” Nutrient

Copper is an essential trace mineral involved in many everyday body functions: using iron to make healthy red blood cells, building strong bones and joints, keeping the immune system working, and protecting cells from damage. Dogs cannot synthesize copper on their own, so they must obtain it from food. Too little copper can lead to anemia, weak bones and connective tissue, poor growth, and changes in coat color or quality. A key point is that trying to avoid copper altogether is not a solution. Fortunately, true copper deficiency is rare in dogs eating “complete and balanced” diets that meet basic nutritional standards.

Copper works by enabling many enzymatic “worker proteins” to function properly. It acts like a key that turns certain enzymes “on,” supporting energy production, iron utilization, healthy connective tissues, normal pigmentation, and antioxidant protection. When copper is insufficient, these systems begin to struggle; when it is excessive, the liver can become overwhelmed by stored copper.

Copper is also a redox‑active metal, meaning that at high concentrations it can drive oxidative injury, inflammation, scarring (fibrosis), and eventually cirrhosis. In dogs, cirrhosis is an end‑stage liver change that can result from many chronic liver diseases; one important subset involves copper‑associated hepatopathy (CAH), also called copper‑associated chronic hepatitis.

Because too little is problematic and too much can be damaging, copper is best thought of as a “Goldilocks nutrient”: not too little, not too much, but a just‑right amount for that individual dog. Genetics, liver health, and the rest of the diet can all shift where that “just right” range falls. This factor is one of the many reasons nutrition is far more nuanced than “more is always better” or “less is always safer.” This complexity also explains why setting a single strict upper limit for copper that fits every breed and every dog is genuinely difficult. The fact is that some individuals may need more copper to support essential body processes, while others with copper‑handling defects can be harmed by amounts that are perfectly safe for most dogs.

2. What the Research Actually Shows

Rising Hepatic Copper Over Time

Over the past 30–40 years, multiple biopsy‑based studies have documented a clear upward trend in liver copper concentrations in dogs. Critically, this is not limited to breeds historically considered at risk for CAH; it is a broader, population‑level finding confirmed across several peer‑reviewed publications:

• In a 546‑dog archive spanning 1982–2015, median hepatic copper concentrations roughly doubled between the 1980s and the late 2000s. In the same study, the proportion of dogs with markedly increased copper (>1,000 μg/g dry weight) increased approximately threefold (1).
• A large pathology series of 4,559 dogs published in 2022 found that half of all liver samples had copper concentrations above 400 ppm (the upper end of many reference ranges), and 19% exceeded 1,000 ppm. Higher copper was associated with more severe inflammation and necrosis, and with certain breeds (Doberman Pinscher, Labrador Retriever, West Highland White Terrier) (2).
• A 2025 comparative review linking canine CAH to human Wilson disease highlighted that copper accumulation is now recognized across a broader range of breeds than the classic Bedlington Terrier — underscoring both genetic and environmental (dietary) contributors (3).

These are not fringe findings. They come from multiple institutions and journals and consistently show that more dogs have higher hepatic copper than in past decades.

Limitations of the Biopsy Data

That said, (warning, this is a little technical, but important) the biopsy data we have come primarily from referral hospitals and pathology archives. This means samples are biased toward dogs sick enough to be biopsied and not a random sampling of the general pet dog population. 

Additional technical factors matter too. For example, copper distribution across the liver tissue is often uneven (e.g., centrilobular vs. periportal). This means that the site and size of the biopsy can affect the measured concentration. The method of which the copper is measured can also give varied results. For example, histologic stains such as rhodanine are useful for semi‑quantitative (not exact measurements) screening but can under‑ or over‑estimate copper compared with other methods with true quantitative assays (AAS/ICP‑MS). 

Together, these factors show just how complicated this problem is, but that investigating it is also complicated, and nuance. We do know that the documented rise in hepatic copper is a real signal, but it does not directly tell us the true prevalence of copper‑associated disease in the general dog population.

3. Breed‑Specific and Individual Risk

Breeds with Inherited Copper‑Handling Defects

Several breeds carry a markedly increased risk of CAH due to inherited defects in hepatocellular (liver) copper handling and biliary excretion. Bedlington Terriers are the classic example: an autosomal recessive deletion in the COMMD1 gene impairs copper excretion, leading to extreme hepatic copper accumulation (often >10,000 μg/g dry weight) and progressive hepatitis and cirrhosis if untreated. Even within this breed, genetic testing and selective breeding have reduced but not eliminated disease prevalence, and additional ATP7B variants have been described in some affected dogs.

Other breeds showing a strong association with abnormally high hepatic copper and copper‑associated chronic hepatitis include:

• Labrador Retrievers
• Doberman Pinschers
• West Highland White Terriers
• Dalmatians
• Welsh Corgis
• Cavalier King Charles Spaniels

In Labradors and Dobermans, familial clustering and centrilobular copper accumulation patterns support a heritable defect in copper metabolism, likely involving variants in copper transporters such as ATP7A/ATP7B or related regulators which interact with environmental (dietary) copper exposure. Notably, some breeds such as Bloodhounds may have lower‑than‑expected hepatic copper, emphasizing that both genetic susceptibility and diet shape individual risk (5)

Why One Cutoff Doesn’t Fit All Breeds

Historical and more recent data both show that median “normal” hepatic copper is not identical across breeds. Studies have reported significantly different mean liver copper concentrations in Doberman Pinschers, Cocker Spaniels, Keeshonds, and West Highland White Terriers compared with mixed‑breed dogs; West Highland White Terriers in particular show a very wide, continuous range of values. This has led investigators to question whether a single numeric upper limit of normal (e.g., 400 ppm or 1,000 ppm dry weight) is appropriate for all breeds, versus moving toward risk‑stratified thresholds that consider breed, age, lesion pattern, and clinical context. Current cutoffs are pragmatic rather than biologically universal.

4. Primary vs. Secondary Copper Accumulation

Copper‑associated hepatopathy is classically described as a primary storage disease in which copper itself is the main driver of hepatocellular injury, inflammation, and fibrosis. However, excess hepatic copper can also accumulate secondarily in many chronic liver diseases that impair bile flow or hepatocellular function, including cholestatic disorders and chronic hepatitis of other causes. In such cases, copper may exacerbate damage but is not necessarily the initiating cause.

Distinguishing primary CAH from secondary copper accumulation based on a single biopsy can be challenging. This is why most hepatologists emphasize integrating quantitative copper measurements, lesion pattern and distribution, clinical history, and when available genetic information before labeling a case as “primary copper‑associated hepatopathy.”

5. Diagnosis Requires More Than a Blood Panel

Serum ALT, ALP, bile acids, and ultrasound can suggest liver disease, but they cannot reliably distinguish copper‑associated hepatopathy from other hepatopathies, nor can they quantify hepatic copper burden. The current diagnostic gold standard for CAH is histopathologic evaluation of a liver biopsy combined with quantitative measurement of hepatic copper on a separate sample from the same liver.

Rhodanine staining on biopsy or cytology can screen for increased copper and correlates moderately with quantitative values, but it does not replace a true numerical copper concentration when treatment decisions (such as chelation therapy and strict dietary restriction) are being made. Repeat biopsies with quantitative copper can be useful to monitor treatment response in severely affected dogs, because serum liver enzymes alone may lag or incompletely reflect changes in hepatic copper stores.

6. Is Diet to Blame? What We Know and Don’t Know

Evidence Supporting a Dietary Contribution

Several lines of evidence implicate diet as a contributing factor. The temporal increase in hepatic copper coincides with regulatory and formulation changes that increased dietary copper and its bioavailability (for example, greater use of highly bioavailable copper chelates and supplements, and reduction of dietary antagonists such as certain fibers and minerals) (4). In dogs with copper‑associated liver disease, low‑copper diets and copper chelation can reduce hepatic copper and improve clinical outcomes, implying that ongoing dietary intake is driving the accumulation. A 2021 JAVMA viewpoint by Center et al. argued that copper content in many commercial dog foods appears to exceed biological requirements for some dogs and may surpass tolerance in copper‑sensitive individuals, and called for AAFCO to re‑establish a maximum copper concentration in its nutrient profiles (4).

What We Still Don’t Know

These data are not “smoking gun” controlled trials in which normal dogs are fed different copper levels for years and prospectively tracked for liver disease. This is because those studies do not exist. Other variables influence risk: genetics, nutrient interactions, copper in the water source, environmental exposures, chronic hepatitis of other causes, and overall liver health. In many dogs, copper accumulation may be one important piece of a multifactorial puzzle rather than the sole cause of disease. It is more accurate to say that diet is a plausible and likely contributor, but not the only one. Focusing on a single cause risks oversimplifying a genuinely complex disease process.

Image retrieved February 25, 2026 via @happytrailswagntails Instagram feed. It should be noted that this account has paid partnerships and/or affiliate links with multiple pet food brands that do not third‑party test for copper prior to releasing each lot into the marketplace, and do not provide those reports publicly.

7. AAFCO, Copper, and the Limits of Minimum Standards

As we emphasize consistently at NorthPoint, AAFCO nutrient profiles are designed to define minimum levels to prevent overt deficiency. These profiles are not designed to define optimal intake for every nutrient, breed, or life stage. Copper is a textbook example of that gap.

AAFCO’s Dog Food Nutrient Profiles currently specify minimum copper requirements but do not include a numeric maximum for adult maintenance diets. In their 2021 paper, Center et al. proposed a range of 0.9–1.1 mg Cu per 1,000 kcal and urged AAFCO to re‑establish a maximum and restrict supplemental sources to copper oxide (4). In response, AAFCO convened an expert panel to review the literature; the panel acknowledged the rising hepatic copper data but concluded there were insufficient controlled toxicity data to set a scientifically defensible maximum that would apply to all dogs.

The panel’s review of older toxicity studies suggested that the no‑observed‑adverse‑effect level could fall somewhere between roughly 28–31 mg and 112–124 mg Cu per 1,000 kcal. It’s important to emphasize that this is an extremely wide range reflecting limited data. The panel argued that selecting a single number would be somewhat arbitrary and might falsely reassure consumers that any diet below that value is “safe” for all dogs.

In parallel, the AAFCO Copper Claim Workgroup reviewed whether to allow label claims about copper content and concluded that “low copper” wording could easily mislead consumers into thinking a food is below minimum requirements or inherently safer for all dogs. The workgroup explored a voluntary “controlled copper” claim tied to specific upper limits (e.g., 15 mg/kg dry matter and 3.75 mg/1,000 kcal), but even this was contentious. Some members and industry groups argued these values are not proven to benefit dogs with or at risk for CAH, and raised concerns that manufacturers might cluster around the new target range in ways that are not ideal for all life stages.

For comparison, the European body FEDIAF does set a maximum of approximately 28 mg/kg dry matter. However, notably this limit is driven largely by environmental concerns about copper excretion rather than canine health endpoints.

These regulatory decisions highlight how much of the nutritional conversation is built on incomplete evidence and differing priorities. Copper illustrates why “AAFCO‑compliant” should be viewed as a baseline, not a guarantee of optimal or ideal nutrition for every individual dog.

8. How Serious Is the Risk for the Average Dog?

The social media claim that “millions of dogs are in imminent danger” goes beyond what the available evidence supports. Pathology archives do show more dogs with higher hepatic copper, but CAH represents a subset of all liver disease cases. Importantly, not every dog with elevated liver copper develops clinical disease.

As one large study suggested, roughly one‑third of dogs with chronic hepatitis have copper‑associated disease. While this is significant, it not universal (2). The remaining two‑thirds have other variables at play that appear to be larger drivers in that subset. This underscores the need for more research to understand those factors and how to mitigate individual risks. Many dogs with high hepatic copper are clinically normal at the time of biopsy; some may never progress, while others may decompensate later.

The concern is real, especially for at‑risk breeds and dogs with unexplained liver enzyme elevations. However, this is more accurately described as a growing, under‑recognized chronic liver disease problem rather than an acute poisoning crisis for every dog eating commercial food. Individual assessment and management are far more valuable than mass alarm.

9. Practical Take‑Home Points

Copper is essential, but a “Goldilocks” nutrient. Too little is harmful; too much over time can damage the liver in susceptible dogs.

Liver copper levels in dogs have increased over recent decades. Histopathology archives document higher median hepatic copper and more dogs with very high levels compared with the 1980s.

Diet is likely one contributor, but not the only one. Genetics, overall liver health, nutrient interactions, and copper bioavailability all play roles.

AAFCO profiles protect against overt deficiency, not necessarily against long‑term, low‑grade excess in every dog. There is currently no AAFCO maximum for copper in dog food, and experts disagree on where that maximum should be.

We still lack high‑quality data on optimal copper levels for different dogs and life stages. That uncertainty is exactly why some specialists are calling for more conservative targets and greater transparency about copper content and sources in commercial diets.

What Pet Parents Can Do Right Now

• Work with a veterinarian to monitor liver enzymes in at‑risk breeds (e.g., Labs, Dobermans, Westies) or dogs with chronic GI or hepatic signs.
• If copper‑associated disease is diagnosed or strongly suspected, use diets formulated to be lower in copper alongside appropriate medical management — or work with a Board‑Certified Veterinary Nutritionist to formulate a homemade diet tailored to individual needs.
• Avoid assuming that “more copper” or “more of any trace mineral” is better simply because a label exceeds AAFCO minimums.

For us at NorthPoint, this topic is a powerful illustration of why “complete and balanced” based on AAFCO minimums is the bare minimum benchmark and not the finish line. We simply do not have definitive, long‑term data defining optimal levels for many nutrients across diverse dog populations living modern lifestyles and eating a wide variety of commercial diets. This means nutrition must be approached individually rather than by seeking the “perfect” or “best” product. Individual needs change over time, and as pet parents, acknowledging our pets’ unique risks and needs helps us avoid the many fear‑based marketing tactics that exist in today’s marketplace.

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

1. Strickland JM, Buchweitz JP, Smedley RC, Olstad KJ, Schultz RS, Oliver NB, et al. Hepatic copper concentrations in 546 dogs (1982–2015). J Vet Intern Med. 2018;32(6):1943–50.
2. Ullal TV, Lakin S, Gallagher B, Sbardellati N, Abdo Z, Twedt DC. Demographic and histopathologic features of dogs with abnormally high concentrations of hepatic copper. Journal of Veterinary Internal Medicine. 2022;36(6):2016–27.
3. Ullal T, Choi EA, Gui D, Medici V. Comparative review of copper‑associated chronic hepatitis in dogs and Wilson disease in humans. Frontiers in Veterinary Science. 2025;Volume 12.
4. Center SA, Richter KP, Twedt DC, Wakshlag JJ, Watson PJ, Webster CRL. Is it time to reconsider current guidelines for copper content in commercial dog foods? J Am Vet Med Assoc. 2021;258(4):357–64.
5. Dirksen K, Fieten H. Canine Copper‑Associated Hepatitis. Vet Clin North Am Small Anim Pract. 2017;47(3):631–44.

If you saw the recent headlines about “toxins in dog food” and felt your stomach drop, you’re not alone. The coverage is designed to sound urgent. But like most things in media, it’s also missing critical context.

Here’s what we know, what we don’t, and what we recommend at NorthPoint Pets, without panic, without tribalism, and without pretending one report rewrites everything.

What this report did

The nonprofit Clean Label Project (CLP) purchased 79 top-selling dog foods across formats (dry kibble, air-/freeze-dried, fresh/frozen). Foods were subjected to a total of 11,376 tests through a lab they identify in their report as an ISO 17025 accredited laboratory operated by Ellipse Analytics.

Testing screened foods for several contaminant categories, including heavy metals (lead, arsenic, cadmium, mercury), acrylamide (a heat-formed process contaminant), and certain packaging/industrial chemicals like bisphenols and phthalates, along with other categories such as pesticides.

The headline-level findings in both the coverage and CLP’s summary are consistent:

• Dry kibble tested highest across many contaminants.
• Fresh/frozen tested lowest on average.
• Air-/freeze-dried often fell in between.  

The group also compared dog food results to a database of human-consumable products they’ve tested and reported higher heavy metal levels in dog foods (especially dry) using their comparison approach.

Two important points for accuracy (because details matter):

1. “No brand results were released” is only half true.
   CLP did publish a list of the products tested and also published a “Clean 16” list. What’s still missing is the piece that would allow true independent interpretation: the full product-by-product contaminant data (the actual numbers for each product).

2. The coverage cites a 2021 Scientific Reports paper about heavy metals in pet foods, but some summaries appear to have misstated the percentages. In that paper’s dataset, the authors reported that all dog food samples exceeded the mercury maximum tolerable level used in that study, and ~80.55% exceeded the lead maximum tolerable level (in their sampled market).

That’s not “proof of harm.” It is, however, a reminder that contaminant exposure in pet food is a real topic—not a conspiracy theory.

What the report does not prove

Detecting a chemical is not the same thing as demonstrating a health outcome. Toxicology is dose + time + the individual dog. A screening report can tell us what’s present and how it varies, but it cannot, on its own, prove that a given food is “poisoning” dogs or causing cancer. This is where influencers and fear mongers will have you feeling uneasy.

Even the Cornell research often referenced in this news cycle found that dogs can have higher heavy metal intake per calorie than humans, while also concluding that chronic toxic exposure levels were “highly unlikely” in their sample set. Although it is important to note that they expressed concern about occasional outliers and the lack of long-term dog-specific data.

We should take contaminants seriously. But “serious” does not mean we need to “panic.”

Why kibble tends to look worse in testing

CLP and the media coverage emphasize that kibble tested highest and fresh/frozen tested lowest. Why? Said simply: water.

Fresh and frozen diets are high-moisture, while kibble is highly concentrated and low-moisture. A veterinary nutrition researcher quoted in coverage cautioned that you cannot interpret raw concentration numbers correctly without considering caloric density and how much food a dog actually eats to meet energy needs.

That said, even when reports attempt adjustments (per serving size or energy), the pattern does demonstrate higher values in dry foods, particularly for acrylamide, which is a heat-processing byproduct strongly tied to high-heat processing.

Acrylamide: what it is, and what we know about it

Acrylamide is a chemical that can form when carbohydrate-rich foods are cooked at high temperatures (typically above ~120°C / 248°F) under low moisture conditions. Think baking/roasting/frying and industrial high-heat processing.

In rodent models, acrylamide exposure has been associated with increased cancer risk, while human dietary studies have been mixed and not definitive. It’s also recognized for neurotoxicity and reproductive toxicity at sufficient exposures.

What does that mean for dogs?

We have far less long-term outcome data than we should. That’s exactly why we advocate for better research and better transparency.

Processing is not “good” or “bad”—but it does change food

This part gets oversimplified online.

High-heat processing can create Maillard reaction products (including advanced glycation end-products, or AGEs), alter amino acid bioavailability (notably reactive lysine), and contribute to other chemical changes in food that impact nutrient availability. (This is one reason we see most pet foods supplemented with synthetic nutrients.) In fact, there is a solid body of pet food processing research showing that these reactions occur and can change nutrient characteristics.

More recently, controlled work in dogs has linked diet processing differences with measurable changes in AGE-related markers in the body. While this is indeed useful mechanistic information, it is still not the same as “this food causes disease.” It is just NOT that simple.

Bottom line: processing level is a legitimate variable to care about, but we need not turn it into a moral verdict.

Regulation and safety context

This is context consumers deserve to understand: In the U.S., pet food is regulated (federal + state), and the FDA’s Center for Veterinary Medicine (CVM) monitors contaminants in animal food, including chemical contaminants such as heavy metals.

At the same time, it’s also true that there is not a single, simple “dog/cat lifetime contaminant standard” that covers every chemical discussed in viral headlines. Reference points often involve a mix of FDA action levels/guidance, NRC maximum tolerable levels, and AAFCO model guidance. Much of this information is built from broader animal feed frameworks, not decades-long feeding trials in pet dogs/cats. In other words, we have a substantial gap in dog/cat nutrition where we don’t know enough about contaminants (and even in some cases specific nutrients) to make broad sweeping claims.

That gap is exactly why better dog & cat-specific research and better manufacturer transparency matter.

What NorthPoint Pets is concluding

Here’s our stance:

We agree with the core signal: contaminants exist in pet food and levels vary by format and manufacturer. That aligns with multiple lines of evidence, including academic research showing measurable heavy metals in commercial diets and variability by ingredient category.

We do not agree with the social-media leap to:

• “All kibble is poison,”
• “Fresh is toxin-free,” or
• “This proves your dog’s food is causing cancer.”

That’s not what this type of screening can legitimately prove.

Instead, we are choosing to focus on practical guidance you can use today.

For most healthy dogs, this is not an emergency. But it can be taken as a prompt to feed more intentionally.

If you want to reduce long-term risk without chaos, do this:

1. Don’t abruptly switch diets out of fear.

   Take a breath and look at the dog/cat in front of you. Are they doing well on their current diet? Coat thick and shiny? Overweight? GI issues? Are they generally healthy? Asking these questions can help you assess how your individual pet is managing their current diet. If any concerns are noted, then a diet change or adjustment could be explored.

2. Reduce “single-food lifetime exposure.”

   This is one of my favorite pieces of advice in any situation. Rotating between transparent brands, different proteins, and feeding different formats is a reasonable risk-management strategy when done carefully and appropriately for your dog.

3. If budget/logistics allow, include some less intensively processed options.

   Similar to the last suggestion, rotating in fresh, frozen, gently cooked, or thoughtfully selected toppers provides benefits through various fresh nutrients, antioxidants, essential fatty acids, and lean proteins. However, the type and quality of these formats can carry their own risks when sourced or handled inappropriately. Ensure you always follow good food safety handling practices, microbial controls, and proper storage.

4. For dogs with kidney disease, liver disease, cancer, or complex medical needs, simply stop guessing or trying to find a product or diet to ‘cure’ the disease.

   Use your veterinarian or contact us to schedule an appointment with a board-certified veterinary nutritionist to make targeted changes.

5. Ask brands better questions than “Is it safe?”
   
   Ask what matters:
   

   • Do you test for heavy metals and key process contaminants?
   • How often, what methods, what benchmarks?
   • Will you share summary results or a COA-style overview?

We’re happy to help NorthPoint customers think through options based on your dog, your constraints, and what you’re trying to optimize.

What we want to see next (and what we’re doing)

This report should push the industry and the research community toward:

• More transparency; this means brands include meaningful product-level data, not just marketing lists on their website.
• Dog-specific chronic exposure research that links measured contaminants and processing byproducts to real health outcomes, not just one-time screens.
• Better consumer education around risk vs. detection.

At NorthPoint Pets, we will:

• Continue pressing partner brands for real quality-system answers (e.g., testing, sourcing controls, traceability).
• Keep educating on processing, ingredients, and nutrient adequacy without fear marketing.
• Update guidance as higher-quality data emerges.