What are the primary sources of PFAS for dogs and cats?

Sources of PFAS exposure can be direct, or indirect, meaning that pets and people can be exposed to PFAS precursors or their degradation products. Within a typical household, PFAS exposure most likely occurs through a combination of contaminated water, food, and dust for both humans and animals.¹⁸ Children, especially toddlers, are thought to be exposed primarily through mouthing behaviors, such as crawling on carpets and furniture and then putting their hands or toys into their mouths.¹⁹ The proximity of small children and household pets to PFAS-treated carpets and floors where dust accumulates, in addition to their mouthing behaviors, potentially places children and pets at similar exposure risk.^15,20

Dust—In studying samples from > 2,500 sites around the world, Brusseau et al¹⁰ found that background levels of PFAS in soils ranged from 0.001 to 237 µg/kg in areas with no known contamination, whereas PFAS levels in soils from contaminated sites ranged from 0.4 to 460,000 µg/kg. Proximity to industrialized and urban areas factor into animal exposure to long-chain PFAS.^11,14 In a study of outdoor air within Korea, Kim et al²¹ found up to 500 times higher concentrations of volatile PFAS (fluorotelomer alcohols) compounds in urban and industrialized sites compared to their background site. A corresponding study²² investigating PFAS burdens in Oriental Magpies in Korea found that birds living in more urbanized areas had significantly higher PFAS in their livers compared to birds from suburban and rural locations.

Studies in Europe and North America have demonstrated that indoor air and dust have been a greater source of PFAS contamination than outdoor air. The companion Currents in One Health by Brake et al, JAVMA, July 2023, addresses the magnitude of differences between PFAS concentrations in indoor and outdoor air. Although PFAS can be detected outside, Shoeib et al²³ demonstrated PFAS concentrations inside could be 100 times greater. Similar findings were reported following a 2013 study of dust in homes across the United States, Canada, and the Czech Republic.

When considering dust exposure in pets or children, it may be better to measure whole house dust rather than vacuum individual pet beds or pieces of furniture. It would be challenging to correlate individual sample results with the many brands of furniture, carpets, or pet beds that are commercially available, much less the infinite combinations of fabric and flooring types. Trudel et al¹⁹ have developed an estimated daily intake (EDI) formula for children, which may be appropriate for application to pets.

Water—Drinking water and food are considered the primary routes of exposure in adults, particularly when living in an area with known water contamination. Analyzing data from EPA’s third Unregulated Contaminant Monitoring Rule (UCMR)⁷ conducted between 2013 and 2015, Hu et al⁵ estimated that the drinking water of approximately 6 million people serviced by public water systems within the United States was contaminated with PFAS above EPA’s 2016 health advisory recommendations of 70 ppt.²⁴ PFAS levels were highest in public water systems located near military sites and airports that used AFFF in fire-fighting training exercises, manufacturing facilities that produced or used PFAS, and wastewater treatment plants.⁵

Although most of the water systems denoted as having high PFAS concentrations during the third UCMR have been remediated, serum PFAS levels in the people living in those areas are still elevated. In 2022, ATSDR published the results^7,8 of an exposure assessment conducted in 10 sites with high levels of contamination as reported by the third UCMR. The 10 sites chosen were located near current or former US military bases with known use of AFFF in military training exercises. ATSDR reported maximum PFAS in drinking water as high as 3,100 ppt of PFOS in Moose Creek, AK; 2,900 ppt of PFOA in Lubbock County, TX; and 1,500 ppt of perfluorohexanoic acid (PFHxA) in Airway Heights, WA,⁸ which correlated with serum PFAS levels of residents.

We know PFAS in drinking water is a risk for animals. PFAS runoff from facilities using AFFF in Australia had contaminated the drinking water of nearby farms and resulted in increased serum PFAS levels of the livestock raised there.^11,25 Within the United States, at least 1 dairy farm has been depopulated due to exposure to PFAS-contaminated water²⁶ directly linked to a nearby military base. It is important to look at the drinking water sources, as well as PFAS use in nearby facilities when considering drinking water exposure.

Diet—Untangling the potential exposures through diet is particularly challenging because of the variety of foods and sources of foods that are eaten by pets. In his assessment of the amount of PFAS produced and its disposition, Prevedouros et al² suggested that perfluorooctanoate accumulated in sediments and in the oceans, where currents transport PFAS around the world. Aquatic plants and animals near the bottom of the food chain absorb the substances and serve as sources of PFAS for higher trophic levels. Consequently, concentrations of PFAS have been found in both marine mammals and fish.^27,28 As addressed in the companion Currents in One Health by Brake et al, JAVMA, July 2023, PFAS was found in nearly 99% of commercial fishmeal with total concentrations ranging from 0.65 to 85.5 μg/kg.²⁹ Fish and fish byproducts, such as fishmeal, are frequently used in animal feeds, which could put both our large and small veterinary patients at risk.^30,31

Run-off from contaminated ground, rain, and the injection of biosolids into the ground as fertilizer are all sources of PFAS for terrestrial flora.¹⁷ The uptake of PFAS in plants differs by chain length and plant species, but there is a direct correlation between the amount of contamination and plant uptake.³ In reviewing studies related to PFAS exposure from agricultural plants, Ghisi¹⁷ and Felizeter³² surmised that small-chain PFAS accumulate in leaves and fruits, whereas the longer chain PFAS seemed to concentrate in the roots. Blaine et al³³ found this to be true when comparing PFAS distribution to various pant compartments of edible crops exposed to PFAS. The highest concentrations of long-chain PFAS were found in radish roots, celery shoots, and in pea fruit, respectively. Stahl et al³⁴ found that absorption of PFAS into plants decreased significantly with chain length and that PFAS tended to accumulate more in the stalks or “straw” of wheat, rye, barley, and canola rather than the kernels. Absorption of PFAS into plants is particularly important since these crops are critical components of silage fed to livestock and can make up a significant portion of commercial pet food ingredients.

The idea that animal feeds could be a contributor to PFAS exposure in cattle was demonstrated by Vestergren et al.³⁵ In his study of a Swedish dairy farm with no known sources of PFAS contamination, the researchers found that of all the food and water the cattle consumed, silage made from crops grown on the farm was the primary route of PFAS exposure. In 2016, a dairy farm in Maine, US, was depopulated due to PFAS-contaminated feed. Although the producer had installed a water treatment system and purchased new cows after discovering PFAS contamination on his farm, PFAS turned up again in the milk and manure of his animals. The recurring presence of PFAS was attributed to feeding hay grown on soil contaminated by years of fertilizing with sewage sludge (biosolids).²⁶ PFAS contamination of soil and crops is also responsible for shuttering a cattle company in Michigan. In January 2022, the Michigan Department of Agriculture and Rural Development issued a consumption advisory following discovery of PFOS in beef samples. The farm in question used biosolids from a waste treatment plant as fertilizer for their fields.³⁶

Fish, grains, meat, and dairy products are all important components of human and animal diets and may be a significant source of PFAS exposure.^28,35,37,38 Dietary studies^16,38 conducted within Europe, Canada, and the United States have determined that the amount of PFAS consumed through food was less than EPA’s reference dose for adults. In contrast, studies among Inuit people living in Nunavik, the northernmost region of Quebec, Canada, found long-chain PFAS levels at 4 to 7 times greater than the Canadian population.³⁹ This corresponds directly to the PFAS levels found in “natural foods” of the population, marine mammals, and seafood.

Just as with human diets,^24,38 the risks of PFAS exposure among pets consuming commercial pet foods are not well understood. An exploratory study⁴⁰ conducted by Chinthakindi et al using 11 different brands of popular dog and cat food sold within the United States demonstrated that nearly 30% of the samples contained PFCAs with total PFCA concentrations ranging from less than the limit of detection to 3.67 ng/g. Four of the 9 PFCAs were measurable: perfluorobutanoic acid (PFBA), PFHxA, perfluoroheptanoic acid (PFHpA), and PFOA. Of these, PFBA was found in the highest concentrations.

Chinthakindi et al⁴⁰ then conducted oxidation studies on the pet foods to determine whether the presence of fluorotelomer alcohols (which are PFAS pre-cursers and used in pet food packaging) could degrade into the PFCAs of interest. After subjecting the samples to the total oxidizable precursor assay, the laboratory found detectable levels for 8 of the 9 PFCAs analyzed.

Chinthakindi et al⁴⁰ used data before and after oxidation to calculate the EDI of PFAS that can be attributed to pet foods. Before oxidation, the EDI was 14.2 ng/kg body weight/day for cats and 14.1 ng/kg body weight/day for dogs.⁴⁰ This value is lower than the EPA’s reference dose in humans (20 ng/kg body weight/day).²⁴ However, when inputting the oxidized sample into the equation, the EDI of cats and dogs is 95.2 ng/kg body weight/day and 125 ng/kg body weight/day, respectively, which exceeds the human reference dose. There is no reference dose for PFAS in dogs and cats. Chinthakindi et al⁴⁰ concluded that pet food itself may not be a significant risk in pets but that pet food packaging, which includes precursors to several PFCAs, may be a larger problem.

As addressed in the companion Currents in One Health by Brake et al, JAVMA, July 2023, PFAS has been authorized by FDA for use in food contact surfaces since the 1960s. It is a well-known coating for the inside of microwave popcorn bags, pizza boxes, and fast-food wrappers. Small amounts of PFAS do leak from coated food-contact surfaces into human-grade food, particularly into oils or emulsified foods like butter,⁴¹ and it is likely that coatings on pet food packaging do the same.

Maternal transfer—Evidence of maternal transfer of PFAS to the fetus and through lactation has been documented in humans and animals. Kim et al⁴² collected maternal blood, umbilical cord serum, and breast milk from 20 volunteers in Seoul, Korea in 2007. Six PFCAs were detected in all maternal and cord serum samples, while 3 were found in breast milk. Of all the PFCAs, PFOS was found in highest concentration across the 3 tissues sampled—making up 94% of the total PFCA concentration in breast milk. Kim et al concluded that the transfer of PFCAs between maternal serum and umbilical cord depended on the length of the carbon chain and the type of PFAS. Regardless of which type of PFAS was found, breast milk concentrations were several orders of magnitude less than maternal serum. Hinderliter et al⁴³ discovered a similar phenomenon when conducting pharmacokinetic studies of PFOA on pregnant rats. After dividing the rats into subgroups, Hinderliter et al administered a daily dose of 3, 10, or 30 mg/kg/day starting on gestation day 4. PFOA was found in the amniotic fluid, placentas, fetuses, and milk of the rats at rates proportional to the dose. The concentration of PFAS in milk was steady state throughout the lactation period and represented about 10% of the concentration found in maternal plasma. Maternal transfer of PFAS has been documented in multiple other species including birds, fish, cattle,^30,37 and marine mammals.^11,30,44,45 Based on these observations, maternal transfer likely occurs in pets as well and could be an area of future study.

Dermal exposure—Dermal exposure in pets has not been well described. Besides contact with floors and furniture treated with PFAS-containing products, dogs and cats may also be at risk from popular flea and tick prevention. The environmental watchdog, Public Employees for Environmental Responsibility (PEER), commissioned laboratory analysis of a flea and tick collar and a topical flea and tick preventative.⁴⁶ Four types of PFAS, PFHxA, PFHpA, perfluoroheptane sulfonate (PFHpS), and hexafluoropropylene oxide dimer acid (GenX), were measured in the topical product for a total of 2,390 ng/L. The collar contained 0.25 ng/g perfluorododecane sulfonate.⁴⁷

In addition to the flea and tick products mentioned, researchers have found that when increasing concentrations of PFOA are applied to the skin of mice, there was a corresponding increase in serum PFOA levels.⁴⁸ Whitehead et al⁴⁹ evaluated 231 human cosmetic products purchased in the United States and Canada and found that foundations, mascaras, and lip products had the highest proportion of total fluorine. PFAS concentrations ranged from 22 to 10,500 ng/g product weight with the highest amounts of PFAS found in foundation and lip products. Investigators are still working out the risks of using PFAS-containing cosmetics. In the same way, more work should be done to investigate the risk of topical flea and tick preventatives in animals.

Are serum PFAS levels in dogs and cats comparable to humans?

In at least 2 studies, researchers have found that serum PFAS levels in cats were similar to levels found in humans. Bost et al²⁰ collected serum from cats in clinics and shelters in Raleigh, NC, and analyzed samples for 9 different PFAS. The team found at least 1 species of measured PFAS in all but 1 of their samples (98.6%). The most frequently found analytes were PFOS (in 97% of the samples), perfluorononanoic acid (PFNA; 93%), and PFOA (82%) with the largest concentrations being PFOS and PFHxS, respectively. The research team found similar PFAS profiles between cats and humans when they compared their findings with those reported by human data in the 2007–2009 National Health and Nutrition Examination Survey (NHANES).

In a separate study, Wang et al⁵⁰ sampled cats within the San Francisco Bay region of California during 2 different time periods, 2008–2010 and 2012–2013, and compared serum PFAS levels to that of human sera collected in 2009 from the same region. Of the 12 PFAS which were analyzed during the time periods, Wang et al⁵⁰ found that cats and people had similar PFAS profiles, with PFAS and PFOA being the dominant species. When feline serum PFAS levels across the 5-year time span were compared with human data from NHANES during the same time periods, researchers again noted that PFAS profiles were similar between cats and humans and that PFOA and PFOS in both data sets declined similarly over time. These cross-sectional studies demonstrate that at any given time, PFAS levels among cats are similar to their human counterparts. Although extremely important, we do not know the half-life of PFAS in cats nor do these studies take into consideration the magnitude or route of exposure. More information is needed to determine whether or not cats could be good sentinel species for human exposure.

To date, there has not been a study comparing serum PFAS levels between dogs and humans. However, work has been done examining the amount and types of PFAS in dog sera. A study⁵¹ conducted with laboratory beagles and police dogs in China found a number of PFAS species in all of the sera tested. The average concentration of PFAS was 3.553 ng/ml with PFOA the most common PFAS found, followed by PFBA and PFOS. Since the half-lives of PFAS are so short in dogs compared to humans, comparing serum PFAS levels following a single exposure or an exposure that has been mitigated may not be appropriate if a long time has elapsed. Overall, pets could be accurate sentinels for human health, particularly for sustained exposures in the home due to contaminated dust or drinking water.

Can dog and cat exposure to PFAS be diagnosed from blood chemistry or clinical signs?

Human epidemiological and laboratory animal studies have demonstrated that PFAS exposure can impact the health of individuals. The C8 study,⁵² conducted among people working in and around a Teflon manufacturing facility in West Virginia, found probable associations between exposure to high levels of PFOA and kidney cancer, testicular cancer, pregnancy-induced hypertension, thyroid disease, high cholesterol, and ulcerative colitis. Though the geometric mean of serum PFOA concentrations found in the C8 was an order of magnitude higher than documented in the dog and cat studies cited here. There is mounting evidence that animals experience similar adverse events following exposure to PFAS. PFAS exposure in companion animals may impact body condition scores, blood chemistry levels, fetal development, as well as multiple body systems (hepatic, respiratory, immunological, amongst others).^{18,50,51,53,54} To date, PFAS has been significantly linked to changes in kidney and liver function in both dogs⁵¹ and cats^20,54 and has been positivily associated with obesity,²⁰ pleural effusion,²⁰ and altered thyroid function^20,50,54 in cats (Figure 3).

View Full Size

Major organs affected by PFAS can differ depending on species and sex. To date, PFAS has been linked to developmental delays, liver damage, immune suppression, some cancers, and disruption of the endocrine system in humans. Limited research indicates that cats may be subject to respiratory effusion, liver damage, and hyperthyroidism. PFAS appears to impact liver and kidney function in dogs.

Citation: American Journal of Veterinary Research 84, 7; 10.2460/ajvr.22.12.0221

• Download Figure
• Download figure as PowerPoint slide

Liver enzymes and cholesterol—In human and laboratory animal studies, PFAS exposure is associated with liver changes. As covered in the companion Currents in One Health by Brake et al, JAVMA, July 2023, article, PFAS activates the peroxisome proliferator-activated receptor-α in hepatocytes, which ultimately leads to liver enlargement due to accumulation of cholesterol in the liver and hypertrophy of hepatocytes. In reviewing data from the general population gathered by the NHANES studies in 1999–2000, 2003–2004, and 2007–2010, researchers found consistent associations between serum PFAS levels and increased liver enzymes (aspartate aminotransferase [AST], alanine aminotransferase [ALT], and gamma-glutamyl transferase [GGT]).^55,56 Laboratory rodent and nonhuman primate studies also demonstrated links between exposure to certain types of PFAS and increases in liver weight,^57,58 altered serum lipid levels, and elevated liver enzymes.^42,57,59

Outside of the laboratory the findings are different. You et al⁵¹ explored PFAS’s influence on liver enzymes in police dogs and laboratory beagles by analyzing individual blood chemistry components with several different types of PFAS. The results indicated that different species of PFAS could significantly alter blood chemistry parameters in different ways. For example, PFNA and perfluorodecanoic acid (PFDA) were both significantly associated with an increase in cholesterol while PFOA and PFOS were significantly associated with a decrease in cholesterol.⁵¹ Only 2 of the species measured, 6:2 chlorinated polyfluorinated ether sulfonate and PFDA, were associated with significant differences in alkaline phosphatase in their study. In analyzing sera of cats in Swedish households, Weiss et al⁵⁴ could not find a significant association between cholesterol levels and PFOA or PFOS but did find a significant increase in cholesterol associated with total PFAS levels. In the C8 project participants, there were also discrepancies in the biochemistry results. Some researchers¹⁸ found associations between serum PFOA levels and ALT and bilirubin while others did not.

Thyroid hormones—In their 2021 PFAS Toxicological Profile,¹⁸ ATSDR concluded that there is a relationship between PFAS exposure and altered thyroid function but cautions that results are not consistent across human or animal studies. As with liver enzymes, the findings on PFAS and thyroid hormone seem to differ based on the type of PFAS and the study conducted. As Winquist et al⁵² found, sometimes a single study reveals different results. In their retrospective cohort study of C8 participants, they found positive associations between PFOA exposures and both hypothyroidism and hyperthyroidism among women participants in the C8 study,⁶⁰ whereas only hypothyroidism was seen in men.

No data have been reported for thyroid function disruption in dogs, although studies conducted by Wang et al,⁵⁰ Bost et al,²⁰ and Weiss et al⁵⁴ have pointed to some disruption in cats. In a study of 72 cats in North Carolina, Bost et al²⁰ discovered that PFAS was detectable in all but 1 of their cat samples with PFOS and PFHxS being the most common compounds measured. Bost reported a significant association between hyperthyroidism and serum PFOA levels and a weaker association between hyperthyroidism and total PFAS.²⁰ These findings correspond with a similar study conducted by Wang et al⁵⁰ in California. In studying hyperthyroidism in cats living in the San Francisco Bay area, Wang et al⁵⁰ found that PFOA and PFHxS levels were significantly higher in hyperthyroid cats compared to nonhyperthyroid cats. Swedish researchers found that all of their feline samples tested for PFAS contained PFOA, PFDA, PFOS, and perfluoroundecanoic acid (PFUnDA).⁵⁴ The team reported a significant positive increase in serum total T4 levels with increasing PFNA levels but did not see a correlation between serum PFAS and thyroxine (T4), TSH thyroid-stimulating hormone (TSH), or the T4/TSH ratio.

The question of how PFAS disrupts thyroid function remains unsolved. After finding that high serum PFOA and PFOS levels were associated with hypothyroidism among participants in the C8 study, Knox et al⁶¹ hypothesized that PFAS-induced production of thyroid-binding globulin in the presence of PFAS was to blame. Hamers et al⁶² tested binding affinities of several compounds found in household dust to an important thyroid hormone carrier protein, transthyretin (TTR). They found that while PFAS does bind to transthyretin, its affinity was not as strong as that of the actual target protein thyroxine. This indicates that while PFAS species may compete for TTR in the signaling pathway they cannot completely competitively inhibit the binding of T4 and thus prevent normal thyroid functions on this pathway. Still, ATSDR and others have found that there is a significant correlation between PFAS exposure, disruption of free T4 and thyroid function. While there is no clear relationship between PFAS binding to TTR compounds and circulating T4, there appears to be some relationship between thyroid function and exposure to PFAS compounds in house dust.

Body mass—The question of whether PFAS exposure contributes to obesity largely remains unanswered. In a systematic review of 19 maternal studies evaluating the association between prenatal persistent organic pollutants exposure and childhood obesity, Stratakis et al⁶³ found no associations between PFAS exposure in utero and childhood obesity. In a retrospective cohort study of nearly 9,000 adults living in the Mid-Ohio Valley region, Barry et al⁶⁴ also could not find significant correlations between PFAS exposure in early childhood and body mass. Alternatively, in a study of 803 children enrolled in a National Institute of Child Health and Human Development Fetal Growth Study, Bloom et al⁶⁵ found gestational exposure to PFUnDA in some women was positively associated with childhood adiposity. Similarly, in a study of 940 adolescents, Averina et al¹⁸ reported that PFHxS and PFHpS concentrations were positively associated with obesity.

In companion animals, the data on obesity and exposure are scarce. Bost et al²⁰ found a significant relationship between PFAS concentration and body weight among cats in North Carolina, US. Statistical analysis revealed a strong association with body weight in PFOS and PFHxS but not PFOA or C9. Laboratory animal findings are the opposite. The 2021 PFAS Toxicological Profile reports that exposures to PFAS “have consistently shown decreases in body weight or decreases in body weight gain.”¹⁸

Respiratory effusion—To date, there have been very few studies evaluating respiratory endpoints in humans exposed to PFAS. Epidemiological studies of humans with known exposure to PFOA have mixed results. Workers at the Washington Works Plant, who presumably would have high levels of exposure, did not seem to be affected. Conversely, residents living near the plant reported a significant increase in chronic bronchitis and shortness of breath.¹⁸ Respiratory disease has been documented in both laboratory animals and cats for PFOA, PFOS, and PFHxS. Bost et al²⁰ divided cats into 4 distinct quartiles according to their serum PFAS concentrations in their study. Three of the cats in their study suffered respiratory effusion, and significantly greater PFHxS levels were demonstrated in all 3 cats with respiratory disease. The authors hypothesized that since PFAS is known to embed in lipid bilayers, it may disrupt the surface tension of a particular lung surfactant common in cats, dipalmitoylphosphatidylcholene. A similar finding was reported in laboratory animals. Inhalation exposure of very high concentrations of PFOS and PFOA dust induced wheezing and nasal discharge.¹⁸ Prolonged exposure to the sodium salt of PFHxA resulted in a reversible degeneration of the nasal olfactory epithelium in rats.⁶⁶

Pharmacokinetics of PFAS

Although exposure and absorption of PFAS across species are comparable, there are still some unique differences between humans and companion animals, which may prevent a direct comparison. To address the question of whether PFAS levels in pets can be compared to that of their owners, we first need to learn whether or not proteins that bind and transport PFAS throughout the body are different between animal species and humans; differences may affect how long and where PFAS can circulate.

Distribution—During exposure, PFAS is rapidly absorbed into the bloodstream and binds quickly to transport proteins. High concentrations of both PFOS and PFOA have been found in serum, liver, and kidneys of laboratory animals exposed to the chemicals with smaller amounts found in the skin, spleen, and reproductive orgins (Figure 3).⁶⁷ Distribution of PFAS is related to the dose: at smaller doses, a larger proportion of PFAS concentrates in the liver compared to larger doses where concentrations are more evenly distributed between organs.⁶⁸

The protein-binding properties and level of resorption (ie, enterohepatic recirculation) of PFAS in the body increases with the number of carbon atoms. In the same way, transporter proteins and carbon-chain length also influence how PFAS are eliminated from the body.⁵³ PFAS can be eliminated via urine or feces, lactation, pregnancy, and menstruation. However, depending on the specific chemical, sex, and animal species-specific properties, elimination rates differ and influence the half-lives of PFAS.^14,18,22,53 For example, the half-life of PFOS in mice ranges from days to weeks, while in pigs it is almost 2 years (634 days).^14,69 For PFOA, the half-life could be as short as 2 hours in mice, while in pigs the half-life of the same compound was 236 days.⁶⁹ In dogs, the half-life of PFOA ranged between 8 and 30 days.⁷⁰ At the time of this writing, there was no report for half-lives in cats. When analyzing data from retired fluorochemical production workers, Olsen et al⁷¹ recorded mean half-lives of PFOS, PFHS, and PFOA as 5.4 years (95% CI, 3.9 to 6.9), 8.5 years (95% CI, 6.4 to 10.6), and 3.8 years (95% CI, 3.1 to 4.4), respectively.

Sex and species differences—In oral and inhalation studies, researchers found a difference in the absorption and excretion of PFAS by species and sex. When a single oral dose of radiolabeled ammonium perfluorooctanate was administered to male and female mice, rats, hamsters, and rabbits, Hundley et al⁶⁷ found that the male and female rabbits, the female rat, and the male hamsters all excreted more than 99% of the original dosing within 120 hours, while the male rat and the female hamster excreted 39% and 60% of the dose within the same time frame. When exposing rats to aerosolized PFOA, Hinderliter et al⁷² found the time to maximum plasma concentrations took much longer in male rats than in female rats. A similar trend occurred when the plasma PFOA concentrations returned to baseline. Species and sex differences found in inhalation and gastrointestinal studies may also apply to dermal absorption.