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PROFESSIONAL VERSION

Halogenated Organic Pollutant Toxicosis in Animals

Full Review: Sept 2026 ByRobert W. Coppock, DVM, PhD, DABVT, DABT, Robert W. Coppock, DVM, Toxicologist and Associates Ltd. | Peer reviewed byWilson F Ramirez-Duarte, BScVM, PhD, DABVT, Concordia University of Edmonton
Last updated: Sept 2026
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Halogenated organic pollutants (HOPs) are considered persistent organic pollutants (POPs). These man-made chemicals include polybrominated diphenyl ethers (PBDEs), polybrominated biphenyls (PBBs), polychlorinated biphenyls (PCBs), the per- and poly-fluoroalkyl substances (PFAS), and some organophosphate flame retardants (OPFRs).

These halogen-containing organic molecules are resistant to biotransformation, and, except for OPFRs, biomagnify in the food chain (1, 2). POPs typically bioconcentrate in fat. However, studies in laboratory animals have shown that some OPFRs accumulate in the liver, brain, and placenta.

Polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans (PCDD/Fs) HOPs are unwanted by-products of industrial processes, such as incomplete combustion in the presence of chlorine/chloride, and incomplete combustion of medical and municipal wastes. Most governmental jurisdictions have banned HOPs because of their environmental persistence, especially in the food chain, and their chronic toxic effects, especially endocrine disruption (3). HOPs are dispersed worldwide via air, water, and the food chain.

Except for PCDD/Fs, HOPs have had multiple uses. PBDEs have been added to synthetic polymers to delay flame flash. PCBs were used as dielectrics and added to coatings. Newer HOPs include thousands of per- and polyfluoroalkyl substances (PFAS), also known as “forever chemicals” (4). PFAS are amphiphilic molecules, giving them unique mobility in environmental and biological compartments.

PFAS have been used for anti-sticking agents; oil-, water-, and stain-resistant coating for fabric and paper, including food and pet food packaging; and firefighting foams (5, 6, 7). PFAS are distributed worldwide in all environmental compartments and resist chemical degradation.

HOPs biomagnify and persist in the food web and have toxic effects on animals (1, 8, 9). It is important to view environmental and food-source exposures to HOPs as exposure to an anthropogenic chemical cocktail. The toxicological effects of a HOP mixture in the body can be different than the those of an individual HOP congener (ie, the parent molecular structure).

Micro- and nanoplastics (MNPs) are formed by degradation of plastics (through chemical, biological, or mechanical processes) into microscale (< 1000 mcm) or nanoscale (< 1 mcm) particles (10, 11, 12). Because nanoparticles can cross biological barriers, some nanoplastics have been suggested to act as particulate carriers, potentially facilitating entry of adsorbed environmental contaminants (such as HOPs, OPFRs, and heavy metals) into cells and tissues. However, the toxicological importance of MNP-mediated transport remains uncertain and likely depends on particle characteristics, contaminant properties, and species-specific factors.

Routes of Exposure of Halogenated Organic Pollutants

Halogenated organic pollutants are distributed worldwide in every environmental compartment. For terrestrial mammals, the primary routes of exposure to HOPs are oral and via transfer from the mother during fetal development and nursing. Large-scale contamination of feedstuffs for food-producing animals has resulted in secondary (indirect) exposure of humans and companion animals through the consumption of animal products (ie, relay toxicosis) (13).

In birds, offspring, prior to hatching, might be exposed to HOPs transferred to the egg. Ingestion of micro- and nanoplastics carrying adsorbed or embedded HOPs has been proposed as a potential additional exposure pathway; however, its importance relative to other environmental exposure routes remains uncertain (14).

Spreading sewage sludge on agricultural lands is a source of HOPs in the human and animal food web (15, 16). Atmospheric deposition of HOPs in dust and precipitation on forage and soil is an important route of exposure for grazing animals (17, 18, 19, 20, 21). Ungulates are exposed to HOPs during feeding (22, 23). Cattle, sheep, and horses can consume from < 1% to 30% of their dry-matter intake as soil (18, 19, 20, 21, 24). Birds and other animals consume contaminated soil by geophagy (a type of pica in which animals intentionally ingest soil).

Bioaccumulated HOPs in animal fats and aquatic-source feed ingredients are important sources of HOPs in the diet of food-producing and companion animals. Dietary exposure to HOPs is highest from ingestion of ruminant-derived and aquatic-source foodstuffs (25, 26, 27, 28).

Pearls & Pitfalls

  • Human dietary exposure to halogenated organic pollutants is highest from ingestion of ruminant-derived and aquatic-source feedstuffs containing these ingredients.

For the organophosphate flame retardants and poly-fluoroalkyl substances, chewing seat cushions and forms used as padding or other synthetic materials and indoor dust are important pathways for exposure in dogs and cats. Contact exposure of fur and feathers to HOPs precedes oral exposure for preening animals and birds. Indoor companion animals, especially cats, are sentinels for exposure and adverse health effects of the indoor environment (29).

In contrast to most HOPs, which are highly influenced by environmentally linked concentrations in animal fat, the PFAS content in pet food is driven more by ingredient composition (especially aquatic sources) and food container contact (7).

Absorption, Biomagnification, Translocation, and Food Safety with Halogenated Organic Pollutants

Halogenated organic pollutants are readily absorbed via the GI tract and lungs and, in lesser amounts, through the skin. Preening is an important oral route of exposure to HOPs, with the pathway being translocation from fabrics to fur.

The bioaccumulation of HOPs in edible animal tissues presents a food and feed safety issue. The primary animal and human exposures are through food and feeds, respectively (30). For humans, dairy, fish, meat, and eggs account for > 90% of human exposure to polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans and polychlorinated biphenyls; however, limited data is available for companion animals (3). It can be assumed the same applies to pet foods, because abattoir and seafood processing by-products, including lipids, are ingredients in pet foods (31, 32).

Dry and wet atmospheric deposition of PCDD/Fs and PCBs on pasture lands is an important global pathway to terrestrial food-producing animals (33, 34). After atmospheric deposition, forage and soil are the primary pathways of exposure for forage-consuming animals.

There are forensic incidents of animal feed being directly contaminated with specific groups of HOPs (7, 13). In the US, polybrominated biphenyls, PCBs, and PCDD/Fs have been found contaminating dairy and other animal feedstuffs, and in Europe, PCBs (themselves containing PCDD/Fs) contaminated recycled animal fats that were added to animal feed. Both incidents resulted in large-scale human exposure from animal-derived foodstuff, demonstrating the importance of a one-health approach to animal feed vigilance.

HOPs are biomagnified in systemic lipids and translocated to the fetus, milk, and eggs. The bioconcentration of PCDD/Fs and PCBs in body fat, tissues, and milk is dependent on congener profile, species, breed, age, sex, lactation stage, milk yield, metabolic energy balance, and overall health (35, 36). Older studies often did not include the influence of these variables in toxicokinetics models. The congeners of TCDD/Fs, PCBs, have differing toxicokinetics within and among species, body organs, and edible tissues within species (37, 38, 39, 40). Residues of HOPs in cow butter can be used to estimate regional environmental contamination (41).

Transfer rates from diet to edible animal products vary with congener chemistry, species of animal, and the congener profile of the environmental HOP, nutritional metabolic balance, and parity (42). Models have been developed for feed-to-food transfer models (43).

Increased human exposure to organophosphate flame retardants is linked to their increasing usage as fire retardants in synthetic fabrics. The exposure of companion animals likely parallels that of humans living in the same household. OPFRs have a low bioconcentration factor, and some bind with blood proteins. They have also been observed in breast and dairy milk (44).

After normalizing to dry weight, wet pet foods have increased exposure to poly-fluoroalkyl substances compared to dry pet foods (7). Biomagnified HOPs are important contaminants in animal-source human foodstuffs and animal-source ingredients that are used in companion-animal and food-animal feedstuffs. By-products used in animal feedstuffs include meat, bonemeal, fish meals, and recycled animal fats, including fish oil.

Chronic Toxicology of Halogenated Organic Pollutants

Halogenated organic pollutants, by all routes of exposure, bioaccumulate in body lipids. Dose response to HOPs is from the external exposure to environmental HOPs and the internal exposure to HOPs stored in body lipids. Catabolism of lipids stored in adipose tissues releases dormant HOPs into general circulation (45).

Across animal species, HOPs can cause endocrine disruption, altered signaling pathways, reproductive dysfunction, altered metabolism, and neurotoxicity. HOPs also cause up-regulation and down-regulation of xenobiotic-metabolizing enzyme systems, especially in the hepatic and adrenal cytochrome P450 enzymes (CYPs) (46, 47).

Immune dysregulation and altered vaccine responses have also been reported after exposure to some HOPs (48, 49).

HOPs can have epigenetic effects. The toxic effects of exposure to HOPs are dependent on the life stage when exposure occurred, with prenatal and postnatal exposures being particularly consequential (50, 51). Endocrine disruption targets for HOPs include thyroid, reproductive, and adrenocortical hormones (10, 47, 50).

Underappreciated are the interactive toxicological effects of bioaccumulated complex HOP mixtures that occur over a lifetime of exposure. There is some evidence that exposure to HOPs can be associated with hyperthyroidism in cats (50, 52). Naturally occurring hydroxyl forms of polybrominated diphenyl ethers in aquatic-source foods target thyroid endocrinology. These can be present in pet foods, and there is evidence that cats have increased risk.

Dogs have a strong capacity to metabolize polychlorinated biphenyls and form hydroxy-PCBs (OH-PCBs). Some OH-PCBs mimic thyroid hormones and bind with transthyretin. PCB exposure induces the up-regulation of thyroid transporters and conjugation enzymes. Excretion and transport of thyroid hormones to tissues can be increased. Increase in blood concentrations of total T4 can have negative feedback on release of thyroid-stimulating hormone and decrease blood concentrations of thyroid hormones (40). This model, although likely incomplete, shows that dogs exposed to PCBs can be euthyroid or show hyper- or hypothyroidism. Polybrominated diphenyl ethers disrupt thyroid function in American kestrels, and there is an association between feline acromegaly and total serum concentrations of HOPs (53, 54).

Some HOPs can be steroid hormonal agonists and antagonists and can disrupt endocrine homeostasis. Exposure to PCBs and polybrominated biphenyls can delay onset of parturition in cattle. There is increasing concern that some HOPs can alter hormonal function in utero (55).

Cats can have higher intake of HOPs than dogs because of the ingredients used in formulating cat foods. They also metabolize and bioconcentrate HOPs differently than dogs and other species. There is a negative relationship between HOPs and thyroid function in cats (56). Cats concentrate HOPs in their kidneys; however, the relationship with feline renal disease is unknown (57).

Prenatal and early postnatal exposure to HOPs through direct and epigenetic mechanisms disrupts endocrine mechanisms and can alter mammary gland development and function and increase the risk of mammary diseases. Some evidence suggests that OPFRs can alter prolactin concentrations, especially in males. HOPs are mobilized from lipid stores during lactation and contribute to HOPs excreted in milk (58).

There is a growing consensus that the increased diagnosis of obesity in humans and companion animals cannot be completely explained by genetics, lifestyle, and energy balance. Evidence suggests that HOPs and other persistent nonhalogenated chemicals can have highly interactive pathophysiological effects on metabolomics (the study of the metabolism of small molecules such as sugars, fats, and amino acids) (5, 6, 59, 60). An emerging opinion is that obesity in humans and companion animals is caused by multiple factors that include exposure to HOPs (5, 6).

Prenatal and neonatal exposure to some HOPs and other chemicals is linked to obesity in the offspring. Feline obesity is potentially associated with poly-fluoroalkyl substances exposure and living indoors (61). When an animal is in negative energy balance, the blood concentrations of bioconcentrated HOPs increase, because these persistent chemicals are liberated during catabolism of fatty tissues. Thus, blood concentrations of HOPs can be dynamic with weight loss, and this phenomenon is considered internal dosing of HOPs and is a factor in dietary management (45).

In humans, substantial weight loss has been associated with increased concentrations of bioaccumulated HOPs (45, 62). Stores of HOPs in adipose tissue should be considered in managing the rate of weight loss in obese patients. The relationship between maladies observed in patients with rapidly decreasing lean-to-fat ratios and HOPs is not known.

Clinical Findings, Lesions, and Diagnosis of Halogenated Organic Pollutant Toxicosis

Acute exposure of chickens to polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans has been shown to cause a sudden drop in egg production followed by decreased egg hatchability. Ascites, edema, and ataxia can be evident. Lesions include degenerative changes in skeletal and cardiac muscle (63, 64, 65).

Altered thyroid function is associated with anomalous development in birds and mammals, and altered thyroid function is linked to dietary halogenated organic pollutants. Histopathological changes might not be observed.

Chewing and ingesting foam impregnated with organophosphate flame retardants can be fatal to dogs. Seizures can occur, and pieces of OPFR-impregnated foam have been identified in GI contents.

HOPs can upregulate and downregulate the activities of cytochrome P450 enzymes and other enzymes. Unpredictable changes in drug pharmacokinetics and pharmacodynamics can occur. Cats diagnosed with liver disease, hyperthyroidism, respiratory disease, or kidney disease, compared to controls, had increased poly-fluoroalkyl substances, specifically perfluorooctane sulfonic acid, perfluorooctanoic acid, and perfluorohexane sulfonic acid (7, 61, 66). However, the interactions of these PFAS with existing HOPs in the body is not known.

Serum and body fat can be used to assay for HOPs. However, serum/plasma, liver, and whole blood are often more informative for PFAS. It is important to consult with the analytical laboratory before collecting samples for assay. Canine saliva can be used to diagnose exposure to PFAS, and perfluorononanoic acid is the predominate PFAS in saliva (67). Saliva concentrations of these PFAS do not correlate with total PFAS in serum.

Prevention and Treatment of Halogenated Organic Pollutant Toxicosis

There is no known specific treatment for acute toxicosis from halogenated organic pollutants. Supportive care is recommended.

Pearls & Pitfalls

  • There is no known specific treatment for acute toxicosis from halogenated organic pollutants.

For chronic exposure to HOPs, attention should be given to preventing exposure to known sources of HOPs. Using natural bio-sourced materials in home finishing and furniture generally decreases the overall indoor exposure to HOPs. Using stainless-steel feed and water bowls also decreases exposure to toxic substances that leach out of synthetic materials.

HOPs are ubiquitous environmental contaminants, and many biomagnify in body fat and body organs. A lifetime of exposure to HOPs starts at conception and epigenetic effects can reprogram life history.

Animal feed, human foodstuffs, and the indoor environment are the most important exposure pathways for exposing indoor companion animals and humans to HOPs. Environmental chemicals are complex mixtures, and most bioaccumulate and biomagnify in the food web. The complex toxicological interactions of HOPs in biological systems is underappreciated.

Key Points

  • HOPs are distributed worldwide, and most HOPs biomagnify in the body fat of animals and persist in the food chain.

  • HOPs can disrupt thyroid, adrenal, and reproductive endocrinology.

  • The health effects of HOPs in domestic animals are likely underappreciated.

For More Information

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