PFAS: exposure, negative health effects and 8 strategies to reduce their impact

Table of contents

Disclaimer: this article is intended for educational purposes only and is not intended as medical advice. Much of the information provided is based on in vitro and animal studies that may not translate to humans. Always seek the help of your doctor or other medical professional before making changes to your lifestyle.

Lately we’ve been seeing more and more stories in the news about PFAS contamination in drinking water supplies and their damaging effects on our health and the ecosystem. But what are PFAS, where do they come from and how do they affect our health? In this article I’m going to cover all of this as well as steps we can take to reduce our exposure and get rid of them quicker from our body.

What are PFAS?

PFAS (‘Per- and Polyfluoroalkyl Substances’) are a large family of nearly 15,000 chemicals used in industrial and consumer products that have gained the nickname ‘forever chemicals’ because they take a long time to break down and also accumulate in humans and animals and in ecosystems, especially in water supplies. They have found their way all over the planet and have even been found in polar bears in the Arctic far away from human activity. The reason they take so long to break down is because their covalent carbon-fluorine bonds are extremely strong and resist enzymatic and environmental breakdown. This same quality is the reason they have become so popular in industrial and consumer applications because they are very resistant to extreme heat, cold, water, acids, grease and stains, which means that their many uses range from water-repellent fabrics, food packaging, weapons manufacturing, firefighting foams, personal care and household products, dental floss, toilet paper and of course non-stick cookware such as Teflon®, or PTFE – the original member of the family.

These chemicals have been around for a while. PTFE was discovered by accident in 1938 by DuPont chemist Dr Roy Plunkett while trying to invent a better coolant gas. After leaving a new gas overnight, he came back in the morning and found that it had polymerised spontaneously into a slippery, resistant, resinous solid and PTFE was born. While it wasn’t used in food processing and cookware until the 50s it had many industrial applications in the meantime, including in industry and weapons manufacturing, with its first  appearance as part of the Manhattan project as an integral part of the first nuclear bomb. Later on it would be used in all sorts of consumer applications and joined by a host of other similar fluorinated compounds such as PFOA, PFOS, PFHxS, GenX chemicals and PFNA among the most well-known and well studied. TFA can also be added to the list as an extremely common and persistent breakdown product of other PFAS as well as a common component of pesticides that is turning up at alarming levels all throughout our ecosystem.

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What are the most common PFAS chemicals?

Although there are nearly 15,000 different PFAS according to CompTox, I’ve included some of the most common ones in the following list. Generally speaking, the longer the carbon chain, the longer they accumulate in the human body. The clue is in the name: the ‘O’ in PFOA and PFOS stands for ‘oct’ (like octane) meaning 8 carbons, whereas the ‘B’ in PFBS stands for ‘but’ (like butane) meaning 4 carbons. TFA is the shortest with only 2 carbons as a derivative of acetic acid.

• PFOA (Perfluorooctanic acid): used in the manufacture of PTFE, water-repellent fabrics and firefighting foams. It has been largely replaced due to toxicity concerns and was officially classified as a human carcinogen in 2023.
• PFOS (Perfluorooctanesulfonic Acid): used in Scotchgard, a stain-resistant fabric, firefighting foams and food packaging. Due to its toxicity it has largely been restricted. It was classified as a probable human carcinogen in 2023.
• PFBS (Perfluorobutanesulfonic acid): a shorter chain PFOS replacement used in paints, cleaning products, metal plating and firefighting foams.
• GenX /HFPO-DA (Hexafluoropropylene Oxide Dimer Acid, ): a newer shorter chain replacement for PFOA used in the production of other fluoropolymers. It has demonstrated many of the same toxicity concerns as PFOA.
• PFNA (Perfluorononanoic Acid): similarly to PFOA, it is used in the production of other fluoropolymers, and also in firefighing foams, metal plating, cleaning agents and waxes.
• PFHxS (Perfluorohexane Sulfonic Acid): used a lot in fire retardants, firefighting foams, water/oil resistant textiles and also cleaning agents. It has a half-life in humans between 5-8 years.
• PFDA (Perfluorodecanoic Acid): this is another common PFAS found in firefighting foams, cleaning agents and waxes.
• PFHxA (Perfluorohexanoic acid): also used in firefighting foams, cleaning agents and waxes.
• PFBA (Perfluorobutanoic acid): used in metal plating, firefighting foams, cleaning agents, waxes and energetic products.
• PVDF and FEVE: used as protective coatings on metal sheet roofs and shingles.
• TFA: a breakdown product from other PFAS and commonly used as a pesticide additive and also in other industrial applications. It is one of the most common environmental PFAS chemicals and has been found to exist at concentrations that are orders of magnitude greater than other PFAS. One study from Germany found that TFA made up 90% of the PFAS found in drinking water samples. It is an ultra short chain PFAS that gets taken up and accumulated in plants. It has been found to accumulate in pine needles, corn and several other crops and high levels have been found in tea and beer, although it only lasts a few days in the human body.

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How do we get exposed to these chemicals?

PFAS can get into our bodies via 3 main routes: oral ingestion, inhalation and passing through our skin. Exposure comes from both the PFAS rich products that we may use as well as from water and food that we consume and the air & dust that we breathe in, usually without us realizing it. Out of all the products we use in our daily lives, relatively few require the ingredients to be listed, and even these are far from transparent.

Here is a list of the most common sources:

• Tap water: given the pervasive nature of PFAS in the environment, high levels have found their way into municipal water supplies, but it is highly dependent on the area where you live. Check maps of your local area if they exist.
• Bottled water: the majority of bottled waters tested also contain detectable levels of PFAS such as TFA. Standard chemical and microbiological testing rarely includes any PFAS analysis.
• Foods: a common PFAS exposure from foods come from manufacturing and packaging – for example from pizza boxes, microwave popcorn bags, take-away containers or grease-proof materials used in production so fast foods and processed foods including baked goods and processed meats have been found to be the most contaminated. Fish and seafood from contaminated waters and some pork and dairy products can also be high in PFAS. Other sources included tea with plastic teabags, some sports drinks and some countries have also found high levels in wild animals such as wild boar in Poland.
• Cookware: any pans, pots or trays with an anti-stick coating are likely to contain PFAS. Many frying pans now say PFOA free, but this is just one chemical and its replacements may be just as toxic (and not on the label).
• In the kitchen: baking sheets, heat-proof packaging, fast-food packaging, cupcake containers and anything that advertises as grease-proof, non-stick or waxed should be suspected.
• Appliances: kitchen appliances such as breadmakers, yoghurt makers, waffle irons, air fryers and hair irons often contain a non-stick coating. PFAS are added to some light bulbs to make them shatterproof and easier to clean. PFAS have also been found in some smartwatch wristbands.
• Cleaning products: PFAS are commonly found in no streak glass and hard surface cleaners, fabric, upholstery and carpet cleaners, waxes and many types of polish for floors, furniture, cars and boats. Dishwasher rinse aids are also a common source.
• Personal care products: many personal care products contain PFAS including some shampoos, hairspray, dental floss, nail polish, lipsticks, eyeshadows, mascara, blushers, cleansers, sun cream, tampons, sanitary pads, period underwear and toilet paper. Suspect anything that has been formulated to be longer-lasting and water repellent, and check for any ingredients containing ‘fluoro’.
• Home improvement: Many paints, wood lacquers, caulks, sealants and adhesives contain PFAS as well as many types of tape including plumber’s tape, fiberglass and film tapes. Electrical cables are sometimes made of PFAS to make them more flexible and heat resistant. PFAS has been a common addition to carpets and rugs, although PFAS free alternatives are now becoming available.
• Dust: household dust can contain high levels of PFAS that come from other products that we may be using, especially during renovations when old paints, polishes and waxes are stripped.
• Clothing, fabrics and sports: any sports or outdoor clothing & fabrics (including camping & tents) marketed as breathable and water-repellent should be suspected as containing PFAS. Gore-tex was one of the original brands. This is less important as skin absorption is less of an issue compared to ingestion and inhalation – but could still be significant with regular use. Other fabrics include stain resistant sofa covers and soft furnishings and high PFAS levels have even been found in artificial turf covering sports pitches which ends up in athletes.

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PFAS contamination in the US and the EU

To give you an idea of the scale of the problem, the following maps show areas where PFAS contamination has been measured across the United States and Europe. These only include sites that have been tested, but it’s no surprise to see clusters in industrial areas. Click on the links below to see them in more detail.

The United States map comes from the Environmental Working Group. The European map comes from the Forever Pollution Project – a collaborative effort between several authorities and newspapers across Europe[⁸][⁹].

One of the worst-affected areas is Trissino in Veneto, Italy where the Miteni chemical plant has left around 600 square kilometers contaminated with PFAS affecting 350,000 people. After decades as one of the premier global PFAS producers, the company closed its doors in 2018 and started selling off its assets with the most dangerous equipment going to Indian company Viva Life Science who had 18 months to dismantle the site and ship everything to India, presumably to continue production. The decommissioning is a near-impossible task and doesn’t include the wider area, so the PFAS contamination lives on and will require an estimated €500 million in decontamination and remediation costs, not to mention the negative effects on the health of the local population.

This example shows what happens when companies chase profits with no care for people or the environment. Profits go to the shareholders while the costs are externalised with the environment and local population footing the bill. The PFAS remediation costs for Europe have been estimated at 100 billion euros a year while the costs to healthcare systems across the bloc have been estimated between 52 – 84 billion euros, and there is evidence of intense industry lobbying to slow the introduction of legislation that could curb the production and use of PFAS [¹⁰][¹¹].

What are government and local authorities doing?

Under increasing awareness and pressure, some local authorities and governments are taking action more decisively, but although there are some promising initiatives progress is slow. PFOS (2009), PFOA (2019) and PFHxS (2022) have all been added to the Stockholm convention list of persistent organic pollutants [¹²] and in 2024 PFOA and PFOS were designated as hazardous substances in the US [¹³]. Important steps forward have been made in replacing the longer-chain PFOA and PFOS and many companies have taken action, but so far this has been largely voluntary. Stricter regulations are also on the way in the European Union with bans in certain sectors being talked about. The US government has allocated $10 billion to deal with the PFAS and the EPA has a plan to reduce their spread and clean up contaminated sites, and some countries such as France have more widespread bans coming into force soon [¹⁴]. While these moves are encouraging and should help to reduce exposure from municipal water and certain products, they are slow in arriving and don’t do nearly enough to deal with the massive damage already been done. the choices we make every day still have a large bearing on exposure for most people, so we should still make an effort to identify and remediate any individual exposures.

How long do PFAS last in the environment?

In the environment they are very persistent: they are water soluble (and amphiphilic) so they get into rivers, lakes and groundwater as well as soil and sludge – especially around military bases, airports, landfill sites, wastewater treatment plants, chemical plants and firefighting training sites where they can persist for decades or even centuries [¹⁵]. In fact, one of the more recent cases in the news was on the island of Jersey [¹⁶] where the island’s private water supply was contaminated by firefighting exercises at the airport decades ago with residents kept in the dark and still finding high levels of PFAS in their blood today. There are many such cases of localised PFAS hotspots: two well-known European examples include Korsor in Denmark and Veneto in Italy, but there are thousands of other sites around the world and we are only just beginning to discover the true extent of the problem.

In terms of environmental decontamination, various solutions are being explored such as high temperature incineration, plasma treatment, electrochemical oxidation and supercritical water oxidation [¹⁷], although all of these are extremely energy intensive so local authorities tend to try to filter them out without breaking them down, if they do anything at all. There are some promising new technologies on the way though, such as using special LEDs as a catalyst [¹⁸].

Promising solutions are also coming in the form of bacterial and fungal breakdown. Some bacteria [¹⁹] and mushrooms [²⁰] [²¹] have been found to be capable of breaking apart the strong carbon-fluorine bonds and deactivating PFAS. Once again, we’re reminded that nature is the ultimate chemist – being able to carry out, at room temperature and normal atmospheric pressure, something which our best technologies are struggling with despite the high pressures and temperatures used exceeding 1000°C+.

How long do PFAS last in humans and how is acute exposure treated?

Despite the name, forever chemicals do not last forever in the human body even if they are extremely persistent. PFOA has a half-life of between 2.1-10.1 years, PFOS between 3.3-27 years, PFHxS between 4.7-35 years [²²] while the newer shorter-chain PFAS such as GenX last days to months [²³] and even shorter chain metabolites such as TFA lasting hours to days [²⁴]. In the blood they bind to plasma proteins such as albumin and slowly get excreted via the kidneys into the urine and the liver into the gut [²⁵]. The problem is that their tough carbon-fluorine bonds mean that they don’t get broken down by our phase I liver enzymes, and when they do make it into the gut or kidney filtrate, they often get reabsorbed back into circulation [²⁶].

For this reason, when high blood levels are discovered, doctors usually recommend bloodletting, which is where blood is taken periodically in order to remove the plasma proteins and the PFAS that are bound to them. Two drugs are also sometimes used: Cholestyramine and Probenecid. Cholestyramine (a cholesterol-lowering drug) helps bind bile salts up in the gut, reducing the reabsorption, and Probenecid (a uric acid-lowering drug) inhibits organic ion transporters in the kidney which may reduce kidney toxicity. These efforts, especially bloodletting, reduce levels and protect other tissues from higher exposure, for example the kidneys and the thyroid.

What are the effects of PFAS on human health?

Unfortunately when humans invent something new, our love for novelty and the potential financial opportunities that come with it often render us blind to any possible adverse effects on our health, which usually only become common knowledge decades later when the evidence is overwhelming. This was true for many inventions and discoveries of the last 100 years such as leaded petrol, DDT and any number of other industrial creations including forever chemicals. Teflon cookware was deemed harmless until people started noticing their pet birds suddenly dying when the pans got too hot, which happens when fluorinated gases are released into the air. For years DuPont maintained that this could only happen at temperatures that were well beyond normal cooking temperatures, but other studies have shown that this off-gassing starts much lower, and pans heat up quicker than expected, potentially leaving humans open to intoxication – albeit less so than their feathered friends. While acute exposure, known as Teflon flu (or more technically Polymer Fume fever) is more obvious and only comes with higher exposures, the long term effects of chronic low dose exposure to forever chemicals in general is still not understood well. But epidemiological studies have linked them to thyroid and immune dysfunction, cancer, liver disease, kidney disease and metabolic abnormalities, and some of these have now been backed up with experimental animal data [²⁷].

When looking at studies on PFAS and human health though, it is important to recognise that we don’t have strong human experimental data for these effects, because experimenting on people with potentially toxic substances is clearly unacceptable. In vitro studies and animal data combined with epidemiological and observational data can help to understand the situation better, but they are far from perfect. The main difference between these studies and real-life human exposures are the concentrations of PFAS, even if many studies try to replicate real-world concentrations in the lab. One re-occurring theme that I’ve seen is that lower concentrations seem to stimulate whereas higher concentrations inhibit. When comparing several studies, these variations can often look confusing, but it is probably due to differing doses.

With that said, here are several aspects of our health that suffer according to the available research:

Thyroid dysfunction

Good thyroid health is so important for good overall health: the thyroid hormones regulate our metabolism, energy, weight, bile flow, cholesterol levels, heart health, immune system and mood. But the thyroid is also sensitive to pollution, and PFAS have been found to disrupt thyroid function in several ways.

• Hypothalamus-pituitary-thyroid axis disruption: as endocrine disrupters, PFAS have been shown to change brain-thyroid communication, interfering with thyroid hormone production and use. PFAS seems to interfere with the thyroid hormone substrate thyroglobulin as well as TSH. One of TSH’s actions is to stimulate thyroid iodine uptake, and some studies have found that PFAS interfere with the TSH receptor differently depending on the PFAS dose. Low concentrations stimulate iodine uptake but high concentrations inhibit it [²⁸][²⁹] which is probably the reason why some studies find increases in thyroid hormones while others find reductions. Some researchers have also speculated that if this happens during pregnancy, it might lead to increased risk of developmental disorders and autism [³⁰].
• Hormone receptor changes: PFAS also likely change the way thyroid hormones are used in the body by binding to thyroid receptors THRα and THRβ [³¹][³²] and inhibiting their function.
• Transthyretin changes: Transthyretin helps transport thyroid hormones into tissues including the brain, and initial studies have suggested that PFAS also bind to this thyroid transport protein. Computer studies have found that longer-chain PFAS and sulphur containing PFAS show the strongest interactions, even though the shorter chain PFAS are not far behind [³³][³⁴]. PFAS may also interfere with the deiodinase enzymes whihc convert T4 to T3.
• Increased oxidative stress: PFAS increase oxidative stress which damages the thyroid and potentially increase cancer risk [³⁵] although newer PFAS may not have this effect [³⁶].

Metabolic disruption and mitochondrial dysfunction

• Mitochondrial dysfunction: mitochondria make most of our cellular energy, but in vitro studies suggest that PFOS can suppress mitochondrial respiration and decrease ATP production [³⁷]. Although these types of studies use higher concentrations, some of the effects were seen at very low levels. The same study found that mitochondrial genes related to biogenesis, fusion and fission genes were also inhibited, some as low as 0.1μM, or about 50ppb. These three processes are essential to having healthy, numerous mitochondria in our cells. Another study looking at PFOA found cytotoxocity, increased oxidative stress and decreases in ATP synthase at higher concentrations with decreases in mitochondrial membrane potential at lower concentrations in the range of 10μM or 5ppm [³⁸]. More studies are needed to see if this translates to real world exposures in humans.
• Insulin resistance: Studies on insulin function and PFAS have been mixed, and this is probably due to the different types of PFAS, concentrations and different exposures over time. Shorter exposures probably lead to greater insulin secretion [³⁹] whereas chronic exposure likely lead to beta cell burnout [⁴⁰]. Other studies have found a decrease in insulin sensitivity[⁴¹].
• PPAR activation: PPARs (Peroxisome Proliferator-Activated Receptors) are involved in regulating many different metabolic pathways. Their physiological activation has many metabolic benefits, but when chronically activated, they can lead to detrimental effects. For example, one study links PFAS induced PPARγ activation with reduced bone quality and increased adipogenesis, or fat deposition [⁴²] while other studies have suggested detrimental effects on mitochondria, oxidative stress, fat beta oxidation and liver health via PPARα interference [⁴³].

Immune dysregulation and immunotoxicity

PFAS have also been found to impact the immune system in many different ways:

• B cell suppression: perhaps the best studied immune response to PFAS is a reduced antibody response to antigens such as vaccination [⁴⁴]. This might be particularly relevant for the developing immune system.
• Increase in allergies and asthma:  one of the first studies to show increased asthma rates was from Taiwan [⁴⁵] and further in vivo studies found lower Th1 cytokines and higher Th2 cytokines, which is a hallmark of an immune shift towards an allergic response. Subsequent studies have found changes in the Th17/Treg balance which also suggest a shift towards autoimmune skin diseases and intestinal issues and away from immune tolerance [⁴⁶]. Further studies have noted associations with higher PFAS and higher food allergies [⁴⁷] although not for all PFAS.
• T cell suppression: researchers from Milan & Leipzig universities found that in vitro a mixture of PFAS reduced the activation of several types of T cell, including T helper cells, cytotoxic T cells and Natural killer T cells. These cells are critical for fighting off infections and keeping cancer and latent viruses at bay [⁴⁸]. Although this study was in vitro, the concentrations used of 0.02ng/ml – 2ng/ml (or 0.02ppb – 2ppb) were within the range of environmental exposures and far below acute exposures related to drinking contaminated water.
• Innate immune changes: another study found an association with PFAS exposure and a greater number of childhood colds [⁴⁹]. This may be due to natural killer suppression [⁵⁰], but other studies have found an increase [⁵¹]. This initial stimulation response followed by chronic inhibition is probably downt o different concentrations as mentioned before.
• Macrophage polarisation: the pro-inflammatory M1 phenotype helps us fight off bacteria and viruses while the anti-inflammatory M2 phenotype is involved with tissue repair. PFAS have been found to shift the balance from M1 to M2 which may weaken our bacterial and viral defenses and at the same time cause excessive M2 activity which can lead to fibrosis. M2 dominance can also favour tumour progression [⁵²].
• Mast cell activation: in a mouse allergy model, PFOA made the allergic response worse by increasing histamine and inflammatory cytokine release from mast cells [⁵³]. In vitro studies have found similar results with PFOS [⁵⁴]. This also fits with a potential TH2 shift mentioned above.
• Changes in Toll-like receptors: toll-like receptors are the alarm system of the innate immune system: they recognise molecular patterns of pathogens and toxins and activate the innate immune system. Some in vitro studies suggest that PFAS activate TLR4 and TLR2 [⁵⁵]. This could lead to the increase in NF-kB and inflammatory cytokines seen in other studies.

Increased cancer risk

Although probably not directly mutagenic, some PFAS have been classified as carcinogens and epidemiological studies have found strong associations between increases in PFAS exposure and certain cancers [⁵⁶]. But what could be drigin this?

• Endocrine disruption: PFAS may increase hormone related cancer risk by increasing estrogenic activity while also inhibiting androgens. They have been found to bind to estrogen receptors ERα and GPER. Some researchers have suggested that this could increase cancer risk by stimulating the MAPK and PI3K/AKT pathways. These are pathways related to growth and energy metabolism and are usually stimulated by insulin and growth factors, but chronic stimulation has been implicated in many different types of cancer [⁵⁷].
• Epigenetic regulation: many cancer promoting substances change the way our DNA expresses – and dozens of human and animal studies have found these types of changes relating to PFAS. Firefighters have been studied due to their very high exposures and higher cancer rates, and some studies have found epigenetic changes [⁵⁸]. Another recent study in Michigan looked at PFAS exposure and reduced birth weights in 141 mother-infant pairs and found that epigenetic changes were the cause [⁵⁹].
• Metabolic disruption: it is now widely accepted that many cancers have a strong metabolic component, and chronic PPAR activation could lead to detrimental metabolic changes.
• DNA damage and genotoxicity: Most studies do not find evidence of genotoxicity, but PFAS do increase oxidative stress [⁶⁰] which might lead to DNA breaks at high enough concentrations. PFHxS has been found to suppresses p53 in vitro [⁶¹] which is a critical DNA repair protein. Still, human studies are needed to see if this also applies to real-world exposures.
• Immune dysfunction: as well as potentially causing cancer directly, we also need to consider the immune system. One of its main jobs is to destroy cells that turn cancerous, and it does this every day of our lives. When the immune system is compromised, cancers have a better chance of establishing themselves and proliferating.

Liver disease

The liver is a primary target for PFAS accumulation, and when they’re there, they can cause problems:

• Steatosis & NAFLD: PFAS accumulate in hepatocytes and have been found to induce non-alcoholic fatty liver and eventually cirrhosis [⁶²]. One concern is that this may also lead to liver cancer, although other studies have found no association.
• Increased liver enzymes: PFAS have also been associated with increases in liver enzymes, an effect which seems to be more pronounced in men. An Italian study [⁶³] found moderate increases while a study from Korea found more pronounced increases [⁶⁴].
• CYP450 changes: although PFAS are not metabolised by our CYP450 enzymes, they have been found to interfere with other CYP enzymes. One study found inhibition of CYP3A7 [⁶⁵] which may be why PFAS exposure is linked with lower birth weights and poor fetal development. Another study found inhibition of CYP2E1 [⁶⁶], one of the most common CYP enzymes and important for the metabolism of retinoids and prostaglandins as well as many xenobiotics such as drugs and alcohols. Although these two studies mentioned were in vitro and more studies are needed, the idea that PFAS could make our already high toxic burden worse is concerning.

Kidney disease

Together with the liver, the kidneys are another PFAS target because during PFAS elimination they re-absorb and accumulate them which have been linked with a number of kidney conditions:

• Kidney cancer: strong associations have been made between PFAS exposure and increased kidney cancer rates, especially in heavily exposed areas such as Veneto in Italy. This is likely due to their bioaccumulation in kidney tissue after being reabsorbed (particularly the older, longer chain PFAS such as PFOA and PFOS), causing oxidative stress and DNA damage and potentially decreased p53 function [⁶⁷][⁶⁸].
• Reduced kidney function & nephrotoxicity: the oxidative stress and PPAR dysfunction could also be responsible for the declining kidney function that has been associated with PFAS [⁶⁹]. Some researchers have also found a link with the gut microbiome, suggesting that up to half of the losses in kidney function could be down to the effect of PFAS on gut microbes [⁷⁰].

Neurotoxicity

• Brain accumulation: PFAS are able to cross the blood brain barrier and accumulate in the brain. The newer shorter-chain PFAS have been found to accumulate more than legacy, long-chain PFAS [⁷¹].
• Blood brain barrier disruption: PFAS have been found not only to cross the blood-brain barrier, but to disrupt it as well by damaging the tight junctions [⁷²]. The breakdown of the blood brain barrier has been implicated in many neurodegenerative diseases.
• Neurotransmitter disruption: PFAS neurotoxicity has been linked to changes in neurotransmitters, particularly the dopamine and glutamate systems. Studies have found increased glutamate in the hippocampus and decreased dopamine signalling in the rest of the brain. Glutamate is important for wakefulness and cognition, but too much leads to excitotoxicity and neuronal death. Dopamine is important for motivation, reward and spacial orientation and changes in these neurotransmitters have also been linked with many neurodegenerative diseases [⁷³].
• Calcium dysregulation: PFOS has been found to cause increases in intracellular calcium which can lead to excitotoxicity and induction of the calpain enzymes. In one study this effect was blocked by NMDA antagonists, suggesting that PFOS is either acting directly on the NMDA receptor, or indirectly by liberating glutamate. Calcium dysregulation is central to many neurodegenerative diseases [⁷⁴].
• Mitochondrial dysfunction & oxidative stress: mitochondrial dysfunction and oxidative stress are two common features of neurodegeneration and have been strongly implicated in neurodegenerative diseases such as Alzheimer’s where the presence of oxidative stress favours the aggregation of beta amyloid peptides into plaques. It is still not clear whether the real-world PFAS exposures can cause this kind of effect in humans though, so more studies are urgently needed [⁷⁵].
• Neuroinflammation: animal models have found that the microglia may be activated by PFAS via increases in calcium and NF-kB [⁷⁶].

Testing for PFAS

Testing yourself for overall PFAS exposure would be near impossible given the nearly 15,000 different chemicals in this family. Blood tests also don’t give any idea about accumulation in certain organs. But there are blood tests available for around 40 of the most common PFAS, and this is definitely a good idea in cases of specific exposures such as drinking water risk from nearby PFAS contamination. In this case, local authorities usually make specific PFAS tests available.

If you are considering blood testing for PFAS with regards to litigation, consult a lawyer first as running a blood test may start the clock and limit the time available for a legal case.

Can you detox PFAS out of your body?

So the million dollar question is how to get rid of this stuff? Even though PFAS are persistent, they do gradually leave the body, and there are also things we can do to speed up the process. In this section we’re going to look at how.

To do this, we’re going to focus on the liver and the kidneys, because they’re the main ways we excrete PFAS [⁷⁷]. We have other way to get rid of toxins such as sweating, breathing out toxins and growing them out in hair and nails, but these don’t seem to play a significant role in PFAS removal. Menstruation may contribute a little, as well as unfortunately pregnancy and breast feeding.

Liver detoxification of PFAS

Toxic substances are usually transformed in the liver by phase I enzymes or phase II conjugation or both. The phase I CYP450 enzymes oxidise drugs, environmental toxins and metabolic wastes so that in phase II they can be conjugated for easier excretion via the intestine or the kidneys. Conjugation reactions involve attaching another molecule to the toxin such as methyl, acetyl or sulfur group, glucuronic acid, glutathione or glycine.

But PFAS don’t get metabolised by our phase I enzymes and evidence for phase II conjugation is low. Instead, they bind directly to bile after being liberated from albumin in the liver. Bile leaves the liver, collects in the gallbladder and is excreted into the gut via the bile duct when stimulated. It then travels down the intestine helping us to digest fats, neutralise stomach acid, kill microbes and further bind up toxins. In the ileum around 95% of the bile is re-absorbed and travels back to the liver so it can be used again, and while many of the conjugated toxins part ways at this point to be excreted in the stool, PFAS hangs on and also gets re-absorbed. Decreasing this re-absorption is a promising approach, and the drug cholestyramine works in this way by binding up bile salts in the intestine so they can be excreted in the stool. One study of residents near a contaminated site in Denmark demonstrated a reduction in blood PFAS by around 60% in 12 weeks [⁷⁸], but it is not without side effects. Some specific herbs and foods may also help to stimulate bile and reduce re-absorption which I’ll explore below.

Kidney detoxification of PFAS

The kidneys filter an impressive 180 litres of blood every day, removing many toxic substances and re-absorbing useful minerals, nutrients and water. This all happens in nephrons, of which there are about a million in each kidney. First, blood is filtered by the glomerulus – a ball of capillaries. This removes about 20% of the plasma which travels down the proximal tubule, the loop of Henle, the distal tubule and then on to the collecting duct and the bladder. During this path, blood capillaries run next to these tubes and exchange molecules so that essential nutrients and water are re-absorbed back into the blood and wastes and toxins are excreted into the urine.

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The first consideration for PFAS removal is that people with a high filtration rate through the glomerulus remove more PFAS, so the younger and healthier the person, the more PFAS is removed whereas those with reduced kidney function remove less at this first stage. (This is estimated on lab tests as eGFR). There is one exception to this: in renal failure albumin is not filtered out and is excreted in large amounts into the urine together with the PFAS.

Next, PFAS are also removed at the proximal tubule. A single epithelial cell separates the blood supply from the tubule lumen which takes filtrate to the collecting duct and onto the bladder. Substances are transported in two steps: firstly from the blood supply into the cell, and then from the cell into the tubule lumen. This happens both by passive diffusion and via active transport via membrane proteins, which are the subject of a lot of ongoing research – not only to better understand PFAS but also because many other drugs, toxins and metabolic wastes leave the body this way.

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Research suggests that the ion transporters OAT1 and OAT3 transport PFAS from the blood into the tubular epithelial cell. Then, different transporters such as OAT4 and URAT1 excrete PFAS into the filtrate in the tubular lumen which ends up travelling to the collecting duct and forming the urine in the bladder. These transporters are antiporters, meaning that they exchange molecules: as one molecule comes in, another must leave. Some also work on concentration gradients. And when high levels of a substance such as a mineral are in the filtrate, these transporters pull it back into the cell so it can be re-used.

This re-absorption doesn’t just happen with useful minerals though, it also happens with PFAS and other unwanted substances – and together with the bile re-absorption is the reason why PFAS persist for such a long time in our bodies. The re-absorption and subsequent accumulation in these kidney cells is bad news for many reasons: it inhibits the basolateral transporters which elevates blood levels, and it also causes pathological changes in these cells such as oxidative stress and PPAR dysreguation which is probably the reason why PFAS are associated with reduced kidney function.

The Uric acid / gout connection

This picture has many parallels with uric acid. Uric acid gets dumped into the urine in the same way and via the same transporters, but under certain conditions it also gets re-absorbed leading to higher levels in these epithelial cells which can also lead to kidney damage. High re-absorption (together with increased production) causes blood levels to rise and uric acid crystals form and deposit around the body causing gout – a painful, inflammatory condition of the joints.

With high uric acid levels, metabolic dysfunction is a key driver because it increases production and decreases excretion. High insulin levels stimulate URAT1 transporter re-absorption which increases blood levels. Lactate is also a substrate for URAT1, so if there is mitochondrial dysfunction and/or a lack of NAD+ in the tubular cells leading to increased lactate, this can also stimulate the re-uptake of uric acid from the filtrate as the tubule cell gets rid of lactate [⁸¹]. And given the transporter affinities, it’s likely to happen to PFAS too. But it’s not only metabolic issues that change how these transporter proteins work – there are many things that speed them up or slow them down including certain drugs, herbs and supplements as well as hormones that we produce. PTH for example increases uric acid (and possibly PFAS) retention via inhibition of the ABCG2 transporter [⁸²].

Which transporters affect renal excretion and re-absorption of PFAS?

Finding out exactly which transporters do what and when is a difficult task for researchers. This is made harder because there are major differences between animals and humans. For example, rats are able to get rid of PFAS in a matter of hours or days probably because their apical transporters work much better at excreting PFAS. For the basolateral membrane (the side of the blood supply) OAT1 and OAT3 have been identified as important for a number of PFAS without much difference between rodents and humans [⁸³]. They transport all sorts of different negatively charged substances including many drugs and xenobiotics from the blood supply into the kidney tubule cells.

On the apical membrane (next to the tubular lumen), things are less clear although URAT1 and OAT4 are thought to be important for excretion and also re-absorption. ABC transporters have also been found to pay a role [⁸⁴]. One ABC transporter that has drawn some interest is ABCG2. It is an important way that cells get rid of drugs and environmental toxins including PFAS, and researchers have found that a genetic variant of this transporter that reduces transport leads to PFAS accumulation in the placenta [⁸⁵]. The Q141K variant is present in 15%-35% of individuals[⁸⁶] and might lead to PFAS accumulation in other tissues too. Interestingly, this slower variant also predisposes people to gout and kidney stones by increasing uric acid retention [⁸⁷][⁸⁸] and potentially also to cadmium accumulation in the kidney [⁸⁹]. Metabolic dysfunction is again involved in uric acid retention as high insulin levels also reduce ABCG2 activity [⁹⁰], which potentially means that metabolic dysfunction will also impede PFAS detoxification.

ABCG2 and NRF2 in cellular detoxification

It turns out that one of the main ways ABCG2 is increased is via NRF2. When our cells get stressed, NRF2 turns on and activates many different protective mechanisms including anti-oxidants, cell repair and detoxification. These include direct protein effects, epigenetic changes and gene expression, which includes ABCG2 upregulation. And the more ABCG2 we have, the better our cells get rid of a litany of different toxic substances. One of the reasons olive oil and broccoli are healthy is because the plant chemicals they contain are seen by the body as weak poisons which activate NRF2 and have an overall positive effect, and it turns out that this effect could also extend to increasing PFAS excretion by increasing ABCG2 expression, as well as many other toxic substances such as pesticides & heavy metals. ABCG2 is also present in the blood brain barrier and helps to protect the brain by keeping toxic substances out.

In one rat study, researchers found that sulforaphane (from broccoli and broccoli sprouts) increased ABCG2 excretion of uric acid from the kidney via NRF2 upregulation in the intestine. It also reduced uric acid production, reduced inflammation levels, improved liver enzymes and protected the kidneys and liver from damage and the effect was more pronounced than allopurinol, a traditional uric acid drug [⁹¹]. Could this do the same for PFAS? We don’t know yet, but it represents a promising possibility.

Conversely, some other contaminants such as BPA, BPS, BPF, mercury and cadmium have been found to inhibit the ABCG2 transport, potentially leading to retention of all the things that ABCG2 usually gets rid of, including PFAS. While these studies are preliminary, they demonstrate the importance of considering the synergy of all of these novel chemical substances. Reducing exposure to BPA and heavy metals is important for everyone, but it may be especially important for those with high PFAS exposure.

ABCG2 in cancer treatment

Although ABCG2’s ability to remove toxic substances from the cell is important, there are times when we don’t want this. In cancer research this transporter is also known as breast cancer resistance protein (BCRP) because it gets rid of chemotherapy drugs from cancer cells, making them more resistant to treatment. It is also hyper-expressed in some cancer cells which helps them survive and is the subject of studies looking for inhibitors to make chemotherapy drugs more effective. In nature many plant chemicals such as flavonoids have been found to inhibit ABCG2 in vitro such as curcumin (from turmeric), chrysin (in propolis) and silymarin (from milk thistle) [⁹²][⁹³], but these same substances have also been found to activate NRF2 – so why the paradox? It seems likely that some of these compounds are able to inhibit ABCG2 at high concentrations which could help sensitise cancer cells to chemotherapy. But with low, chronic doses such as those found in foods these flavonoids probably don’t reach high enough concentrations to inhibit ABCG2, but they do act indirectly – for example, by activating NRF2 in the gut which can lead to body-wide benefits and paradoxically, an increase in ABCG2 expression which can last several days. There are also many other mechanisms besides ABCG2 inhibition, and Sulforaphane for example is a well studied chemosensitiser with many anti-cancer effects [⁹⁴]. This effect needs to be studied in much more detail, but in the meantime these plants substances like sulforaphane and silymarin at levels typically found in foods are very safe and have a good chance of helping rid the body of PFAS and many other toxicants.

Many of these substances have also been found to mildly inhibit OAT1 and OAT3. This may seem detrimental because we want OAT1 and OAT3 to be transporting toxins into the kidney cells so they can be excreted into the urine, but kidney cells also get damaged in the process and many of these plant chemicals have been found to protect the kidneys, probably for this reason. Silymarin from milk thistle for example, mildly inhibits OAT1 and OAT3, but it also decreases inflammatory cytokines and MMP9 while increasing bile production and flow, which potentially redirects some of these toxic substances away from the kidneys, towards the liver and out into the stool, which is a much safer exit path because the liver is less delicate than the kidneys and can regenerate much more readily.

This example shows that we always need to consider the context: herbs act on many different pathways in the body so although focusing on one may suggest negative effects, the sum total is often beneficial.

8 strategies to reduce the impact of PFAS on your body

Based on the mechanisms above, I have listed 8 strategies that support kidney health, liver health and bile flow which will likely help in reducing the impact of PFAS on your body. While these strategies are very safe and healthy for most people, keep in mind that there have been very few human studies on PFAS removal in general. Use caution when using herbs & supplements or indeed making any changes to your lifestyle and always seek professional advice where necessary.

Furthermore, if you suspect an acute PFAS exposure, talk to your doctor who will organise testing and may suggest pharmaceutical or medical options such as cholestyramine or blood letting. As mentioned both of these may be useful in acute situations as they reduce the amount of PFAS passing through the kidneys and other organs, but they should always be done under doctor supervision.

1) Reduce exposure

The first consideration should always be to reduce your exposure. It is the chronic, daily exposure that accumulates silently. This involves removing or reducing as many of the sources listed above as possible – for example, to remove all non-stick cookware from your kitchen and find suitable replacements. This can be a challenge for frying pans because non-stick pans work very well at not sticking! But most foods can still be prepared in properly seasoned stainless steel or black carbon pans. Other suggestions for the house include regular dusting and hoovering to minimise dust exposure.

You can also check to see if your local area has any factories known for PFAS use as well as airports or firefighting drill areas and check with local authorities who manage the water supply. Find a PFAS map for your area like the ones listed above and see if there have been any reported high levels near you.

Water filters can also reduce exposure. Reverse osmosis filters remove almost all PFAS together with microplastics and many other contaminants, but they also remove some beneficial minerals and waste a lot of water in the process. Carbon filters also remove PFAS and many other toxicants, but are less efficient and remove an estimated 60-80% of PFAS in tests. They also need to be changed regularly because when they become saturated, PFAS levels increase.

2) Drink more clean water

Once you’ve got a source of clean water, make sure you drink it regularly. Ensuring proper hydration helps to remove PFAS from the body because it dilutes the PFAS concentration in the kidney filtrate and reduces their re-absorption through the organic ion and SLC transporters. But don’t overdo it – drinking excessive pure water can reduce the minerals in our body and stress the kidneys.

Increasing water intake with herbal teas is also a great idea, especially if using some of the herbs listed below – but be careful of plastic teabags, as they have also been found to contain PFAS. Some herbs such as dandelion leaf and green tea also act as mild diuretics, which can also be helpful in lowering the PFAS concentration.

3) Improve bile production & flow

Bile is essential for absorbing fats and fat-soluble vitamins, as well as maintaining a balanced gut by killing microbes and neutralising stomach acid – but it is also important for removing toxins from the body including PFAS that bind to it. Good bile production and release requires a healthy liver and thyroid. Thyroid hormone stimulates the first step of bile production in the liver (CYP7A1) from cholesterol and its release is stimulated by dietary fats. Adequate stomach acid levels also stimulate bile, and taurine and glycine are also necessary for its production.

So a well balanced diet with plenty of healthy fats and adequate protein is a good start and good thyroid health is essential, but stress also plays an important role: parasympathetic nervous system activation increases bile production and excretion via the vagus nerve, so stress reduction and eating in a relaxed environment are also important considerations. Breathing exercises such as 4-7-8 breathing are great to help reduce stress and increase parasympathetic nervous system activity, together with good lifestyle habits like regular exercise and good sleep – which promote good liver and gallbladder health in many different ways.

Finally, a number of herbs are helpful for bile. Green tea and milk thistle support bile production and flow and many cultures include bitter herbs before or after meals to stimulate bile flow and digestion in general. Good bitter herbs for bile flow include dandelion (root & leaves), artichoke (leaves), coffee (fruit) and gentian (root). Avoid green tea supplements though, as excessive EGCG (>800mg) content has been linked with an increase in liver damage. Turmeric has also proven beneficial for many different aspects of liver health including bile flow, but check with a professional if it is suitable for you.

A note on herb safety: Herbs (especially coming from outside Europe) are also often contaminated with heavy metals and pesticides, so use local herbs where possible and make sure you use trustworthy suppliers who regularly test their products. Organic herbs are a good start, but they still might suffer from contamination which may also include PFAS.

4) Decrease bile re-absorption

As mentioned, nearly all bile salts get re-absorbed in the ilium together with the PFAS, and one of the main medical interventions is the drug cholestyramine which binds bile salts so they can be excreted instead. While research is at an early stage, there are many natural approaches that have been researched with a view to lowering cholesterol which may have a similar effect. Fibre, especially soluble fibres in the diet have been found to bind bile salts and increase fecal excretion. Pectin binds strongly to bile salts [⁹⁵] and can be found in many fruits and vegetables with some of the highest being apples, carrots and blackberries. Lemon, oranges and grapefruits also have high amounts in the skins. Apricots and plums are also quite high. Stewed apples or citrus marmalade have good amounts of pectin, and it can also be used as a supplement or gelling agent in food preparations. Another source of soluble fibres are mucilages such as those found in chia seeds. A Spanish Simgi® study (a machine which simulates the digestive tract) found a marked decrease in bile salt bioavailability using chia seed mucilage [⁹⁶]. Finally, beta-glucans from barley or oats are another soluble fibre that may help reduce bile re-absorption [⁹⁷]. And together with fibre, good thyroid and liver health are also key areas to improve transit time as slow transit time increases re-absorption and dysbiosis. If slow transit time or constipation are frequent, it is important to find out why and take steps to remedy it.

Other potential bile binders include cranberry, zeolite and activated charcoal. The anthocyanins in cranberry have demonstrated an increase in bile fecal excretion in animal studies [⁹⁸][⁹⁹]. Zeolite and activated charcoal have also shown promise as a powerful bile binder both in vitro and in vivo [¹⁰⁰][¹⁰¹][¹⁰²][¹⁰³], although they should always be taken away from food, medications and other supplements and activated charcoal use should be avoided long term as it may reduce fat soluble vitamins. Combining activated charcoal with some bitter herbs could be advantageous as bile is released then adsorbed by the charcoal.

Another approach to reducing bile re-absorption is to inhibit the ASBT transporter which pulls bile from the intestine back into the circulation. Green tea [¹⁰⁴] and Poria Cocos, a popular asian medicinal mushroom [¹⁰⁵] have shown potential benefit here.

5) Decrease kidney re-absorption

Although human PFAS studies are lacking, it seems that many things that increase uric acid excretion and reduce re-absorption may also do the same for PFAS. Plant chemicals that can increase NRF2 have been found to do this and will likely improve PFAS kidney excretion by increasing ABCG2 transport. Some of the most powerful NRF2 inducers include sulforaphane found in broccoli and broccoli sprouts and hydroxytirosol & oleuropein found in olive leaf & olive oil [¹⁰⁶][¹⁰⁷]. These substances have also been found to improve URAT transport and to decrease oxidative stress and inflammation in kidneys and the liver.

Another substance found in pre-clinical studies to significantly reduce URAT1 while increasing ABCG2 is Astaxanthin [¹⁰⁸], the pink colouring in salmon also available as a supplement. Animal studies have also demonstrated that astaxanthin protects kidneys from oxidative damage from lithium, mercury and BPA [¹⁰⁹][¹¹⁰][¹¹¹] and have been found to protect yeast cells from PFOA in vitro [¹¹²].

Metabolic health is also important for several reasons, and good metabolic health is protective against both uric acid accumulation (and by extension likely PFAS too) as well as kidney and liver health in general. High insulin increases URAT1 re-absorption of uric acid as well as decreasing ABCG2 activity, so it is important to avoid excessive refined carbohydrates and to be proactive in improving your metabolic health through good lifestyle habits like getting enough sun during the day and darkness at night, getting good sleep and plenty of exercise and avoiding junk food, refined food and excess calories. Insulin is good for us when raised for short periods, but chronically high levels have been linked with almost every chronic disease. Although insulin resistance can be adaptive, it can also be pathological, so it is one of those markers that has a huge bearing on our longevity and healthy aging. As of now, sedentary lifestyles, modern, refined diets, poor circadian rhythms and chronic stress have lead to an epidemic of metabolic dysfunction in many developed countries, but it is something that can be measured and improved with correct lifestyle choices.

Finally, reducing other contaminants where necessary will also likely help including mercury and cadmium which have been shown experimentally to reduce ABCG2 function.

6) Protect kidneys and your liver

NRF2 activation goes beyond increasing ABCG2 and also upregulates a host of antioxidant defenses and repair mechanisms which help to protect our detox organs from damage associated from toxin accumulation. Liver and kidney disease are often not mentioned, but are some of our most common killers in the modern world and are increasing rapidly, so strategies to protect them are essential if we want to live a long and healthy life in the modern world.

We’ve seen how sulforaphane and olive leaf can increase NRF2 and how astaxanthin can also reduce kidney damage from various toxic insults in animal studies, but other important herbs to mention here include green tea [¹¹³], milk thistle [¹¹⁴] [¹¹⁵], dandelion root and leaf, phyllanthus niruri [¹¹⁶] as well as berries and cruciferous vegetables.

Many of the plant chemicals mentioned help protect the kidney cells, but some may also reduce OAT1 and OAT3 activity, including green tea and milk thistle. Theoretically this reduces the kidney cell’s ability to get rid of toxic substances as these transporters are on the basolateral membrane as mentioned above, and some animal studies suggest that this reduced kidney excretion could lead to kidney toxicity by increasing serum toxins [¹¹⁷]. But the study mentioned used very large doses on rats, and real world human doses are much smaller especially when coming from tea consumption or foods like milk thistle seeds and whole herb powders. At lower doses, this mild inhibition of OAT1 and OAT3 likely protects the kidneys from excessive toxic exposure without blocking their action completely, and help to steer some of the toxic burden away from the kidneys and towards liver-intestinal excretion instead which is preferred because the liver regenerates much more readily and so can handle a higher toxic load, especially from toxic metals. Detrimental inhibition of the OAT transports likely only becomes a problem with highly concentrated herb extracts and drugs, if at all.

7) Increase folate (natural B9)

Several studies have found an inverse relationship between folate levels and PFAS in the blood, leading some researchers to suggest that folate may be helping to eliminate PFAS [¹¹⁸]. It might be competing for the same series of receptors: the OAT transporters, and adequate folate might reduce bio-accumulation and help with PFAS excretion into the bile as well as reducing its re-absorption in the kidneys. Lead researcher on the studies in question Carmen Messerlian, Ph.D also believes that this could protect unborn babies from the risks associated with early PFAS exposure. The research also looked at the antibody-lowering response of PFAS and found that this association only existed for those with low folate levels.

Folic acid has long been given to expecting mothers because folate is essential for proper spinal chord and brain formation and prevents neural tube defects. It’s also essential for growth, red blood cell formation and reducing homocysteine. Folic acid is a synthetic form and natural folate forms are superior as they don’t need to be converted first. The best sources of folate are green leafy vegetables, salad leaves such as rocket and romaine lettuce, legumes, eggs and liver.

8) Manage stress effectively

The state of your nervous system has a big impact on your ability to detox. When we are stressed, the sympathetic nervous system is more active: stress hormones are higher and our body’s resources are focused on surviving and getting things done. This means that important bodily functions such as digestion, detoxification and sleep are low priority and blood flow to these organs is also reduced, which is particularly problematic for the kidneys.

When we are relaxed, the parasympathetic nervous system is more active. This means that the vagus nerve is more active and digestion, bile flow, detoxification, recovery, cell repair and blood flow to our organs all increase – all of which help rid the body of metabolic and xenobiotic wastes.

Modern life often favours the stressed-out, sympathetic mode as we rush around and try to get everything done – but this has all sorts of negative long-term consequences for our health, so it has never been more important to find time to switch off, relax, spend time in nature, with friends and family and actively encourage parasympathetic activity with gentle exercise, breathing techniques, sleep, meditation, saunas, Epsom salt baths or other relaxing activities. All of these activities improve vagal tone and blood flow to the organs, so they have direct effects on improving kidney filtering, kidney health, liver health and bile flow.

Conclusion

Although research into PFAS and health is at an early stage, it is clear that they can cause significant negative health effects – and even though some of the older PFAS are being reduced and phased out, many of the newer short-chain PFAS seem to be just as bad. Even though much more research is needed, there are some clear mechanisms that I have outlined and some approaches that are likely to help based on these which are also well-researched for safety in other areas and well known to be beneficial for many different toxic insults that we deal with. While their complete removal would be impossible at this point, focusing on reducing the largest exposure sources as well as employing some of these generally healthy strategies to support our innate detox systems is likely to reduce our PFAS load and the health problems that come with them.

References

1. https://www.niehs.nih.gov/health/topics/agents/pfc ↩︎
2. https://pubs.rsc.org/en/content/articlelanding/2020/em/d0em00291g ↩︎
3. https://www.aps.org/archives/publications/apsnews/202104/history.cfm ↩︎
4. https://www.federalregister.gov/documents/2024/02/08/2024-02324/listing-of-specific-pfas-as-hazardous-constituents ↩︎
5. https://www.sciencedirect.com/science/article/abs/pii/S1385894721002308 ↩︎
6. https://pubs.acs.org/doi/10.1021/acs.est.4c06189 ↩︎
7. https://pmc.ncbi.nlm.nih.gov/articles/PMC6380916/ ↩︎
8. https://www.ewg.org/interactive-maps/pfas_contamination/map/ ↩︎
9. https://foreverpollution.eu/map/ ↩︎
10. https://www.osservatoriodiritti.it/2025/02/18/pfas-2/ ↩︎
11. https://lavialibera.it/it-schede-1229-vicenza_miteni_smantellata_la_sua_contaminazione_rimane ↩︎
12. https://chm.pops.int/Implementation/IndustrialPOPs/PFAS/Overview/tabid/5221/Default.aspx ↩︎
13. https://www.epa.gov/pfas/key-epa-actions-address-pfas ↩︎
14. https://www.safefoodadvocacy.eu/france-bans-pfas-in-cosmetics-and-consumer-textiles ↩︎
15. https://www.nature.com/articles/s41538-024-00319-1 ↩︎
16. https://www.theguardian.com/uk-news/2025/jan/16/bloodletting-recommended-for-jersey-residents-after-pfas-contamination ↩︎
17. https://www.ivl.se/english/ivl/our-offer/our-focus-areas/pfas/questions-and-answers-on-pfas.html ↩︎
18. https://www.nature.com/articles/s41586-024-08327-7 ↩︎
19. https://www.buffalo.edu/ubnow/stories/2025/01/forever-chemicals-bacteria.html ↩︎
20. https://factor.niehs.nih.gov/2022/9/science-highlights/pfas-remediation ↩︎
21. https://www.michiganpublic.org/environment-climate-change/2024-05-29/research-funded-to-see-whether-mushrooms-can-remediate-pfas ↩︎
22. https://www.atsdr.cdc.gov/toxguides/toxguide-200.pdf ↩︎
23. https://pmc.ncbi.nlm.nih.gov/articles/PMC10790670/ ↩︎
24. https://pubs.acs.org/doi/10.1021/acs.est.4c06189 ↩︎
25. https://pmc.ncbi.nlm.nih.gov/articles/PMC10328216 ↩︎
26. https://pmc.ncbi.nlm.nih.gov/articles/PMC7118038/ ↩︎
27. https://pmc.ncbi.nlm.nih.gov/articles/PMC7906952/ ↩︎
28. https://www.sciencedirect.com/science/article/abs/pii/S001393512302176X ↩︎
29. https://www.endocrine-abstracts.org/ea/0081/ea0081oc9.2 ↩︎
30. https://pmc.ncbi.nlm.nih.gov/articles/PMC9816503/ ↩︎
31. https://www.sciencedirect.com/science/article/abs/pii/S004896972406114X ↩︎
32. https://www.sciencedirect.com/science/article/pii/S0160412023005299 ↩︎
33. https://pubmed.ncbi.nlm.nih.gov/36566436/ ↩︎
34. https://www.sciencedirect.com/science/article/abs/pii/S0890623818305549 ↩︎
35. https://www.thelancet.com/journals/ebiom/article/PIIS2352-3964(23)00397-3/fulltext ↩︎
36. https://pubmed.ncbi.nlm.nih.gov/33315184/ ↩︎
37. https://pmc.ncbi.nlm.nih.gov/articles/PMC10621633/ ↩︎
38. https://www.sciencedirect.com/science/article/abs/pii/S0161813X21000541 ↩︎
39. https://pubs.acs.org/doi/10.1021/acs.est.9b07295 ↩︎
40. https://pmc.ncbi.nlm.nih.gov/articles/PMC10656111 ↩︎
41. https://www.sciencedirect.com/science/article/abs/pii/S0013935123003924 ↩︎
42. https://academic.oup.com/endo/article/162/12/bqab194/6364127 ↩︎
43. https://www.sciencedirect.com/science/article/pii/S0160412023004117 ↩︎
44. https://pmc.ncbi.nlm.nih.gov/articles/PMC11081924/ ↩︎
45. https://pmc.ncbi.nlm.nih.gov/articles/PMC3620752/ ↩︎
46. https://www.sciencedirect.com/science/article/abs/pii/S0048969724070153 ↩︎
47. https://www.sciencedirect.com/science/article/abs/pii/S0160412015301227?via%3Dihub ↩︎
48. https://www.sciencedirect.com/science/article/pii/S0045653523014716?via%3Dihub ↩︎
49. https://www.tandfonline.com/doi/full/10.3109/1547691X.2012.755580#d1e1707 ↩︎
50. https://pmc.ncbi.nlm.nih.gov/articles/PMC8577040/ ↩︎
51. https://linkinghub.elsevier.com/retrieve/pii/S0013-9351(24)01126-5 ↩︎
52. https://www.sciencedirect.com/science/article/abs/pii/S0045653524016527 ↩︎
53. https://pubmed.ncbi.nlm.nih.gov/22322153/ ↩︎
54. https://www.sciencedirect.com/science/article/pii/S0278691521005111 ↩︎
55. https://www.tandfonline.com/doi/full/10.1080/1547691X.2024.2343362#d1e1959 ↩︎
56. https://www.nature.com/articles/s41370-024-00742-2 ↩︎
57. https://www.sciencedirect.com/science/article/pii/S0147651323004840 ↩︎
58. https://pmc.ncbi.nlm.nih.gov/articles/PMC8549684 ↩︎
59. https://clinicalepigeneticsjournal.biomedcentral.com/articles/10.1186/s13148-023-01461-5 ↩︎
60. https://pubmed.ncbi.nlm.nih.gov/25455676/ ↩︎
61. https://www.sciencedirect.com/science/article/pii/S0048969721070212 ↩︎
62. https://www.sciencedirect.com/science/article/pii/S0160412023005081 ↩︎
63. https://www.sciencedirect.com/science/article/pii/S0013935124019893 ↩︎
64. https://www.sciencedirect.com/science/article/abs/pii/S0045653523004757 ↩︎
65. https://www.sciencedirect.com/science/article/abs/pii/S0162013423000028 ↩︎
66. https://www.sciencedirect.com/science/article/pii/S2666027X23000142 ↩︎
67. https://pmc.ncbi.nlm.nih.gov/articles/PMC8096365/ ↩︎
68. https://pmc.ncbi.nlm.nih.gov/articles/PMC10627102/ ↩︎
69. https://www.sciencedirect.com/science/article/pii/S0160412020323291 ↩︎
70. https://keck.usc.edu/news/usc-study-finds-link-between-pfas-kidney-function-and-gut-health ↩︎
71. https://www.sciencedirect.com/science/article/pii/S0160412024003052 ↩︎
72. https://pubs.rsc.org/en/content/articlelanding/2021/em/d1em00228g ↩︎
73. https://pubs.acs.org/doi/abs/10.1021/acs.chemrestox.2c00072 ↩︎
74. https://www.sciencedirect.com/science/article/pii/S0300483X20302493?via%3Dihub ↩︎
75. https://www.sciencedirect.com/science/article/abs/pii/S0048969724070980 ↩︎
76. https://www.tandfonline.com/doi/full/10.1080/1547691X.2024.2343362#d1e1959 ↩︎
77. https://pmc.ncbi.nlm.nih.gov/articles/PMC10886393 ↩︎
78. https://www.sciencedirect.com/science/article/pii/S0160412024000837 ↩︎
79. https://www.sciencedirect.com/science/article/abs/pii/S1063582322000011 ↩︎
80. https://link.springer.com/article/10.1007/s00204-024-03797-0 ↩︎
81. https://www.sciencedirect.com/science/article/pii/S2211124724009781 ↩︎
82. https://linkinghub.elsevier.com/retrieve/pii/S0085-2538(16)30597-X ↩︎
83. https://ehp.niehs.nih.gov/doi/10.1289/EHP11885 ↩︎
84. https://www.sciencedirect.com/science/article/abs/pii/S0300483X24001823 ↩︎
85. https://pmc.ncbi.nlm.nih.gov/articles/PMC8242356/ ↩︎
86. https://pubmed.ncbi.nlm.nih.gov/34855903/ ↩︎
87. https://academic.oup.com/rheumatology/article-abstract/49/8/1461/1789767 ↩︎
88. https://pmc.ncbi.nlm.nih.gov/articles/PMC10036833/ ↩︎
89. https://pmc.ncbi.nlm.nih.gov/articles/PMC8382159/ ↩︎
90. https://journals.physiology.org/doi/full/10.1152/ajprenal.00012.2017 ↩︎
91. https://www.sciencedirect.com/science/article/pii/S209012322200251X ↩︎
92. https://pmc.ncbi.nlm.nih.gov/articles/PMC3337630/ ↩︎
93. https://pubmed.ncbi.nlm.nih.gov/15102949/ ↩︎
94. https://pmc.ncbi.nlm.nih.gov/articles/PMC10814109/ ↩︎
95. https://applbiolchem.springeropen.com/articles/10.1007/s13765-016-0184-5 ↩︎
96. https://www.sciencedirect.com/science/article/abs/pii/S0963996920303896 ↩︎
97. https://www.cambridge.org/core/journals/british-journal-of-nutrition/article/barley-glucan-reduces-blood-cholesterol-levels-via-interrupting-bile-acid-metabolism/F48053467893E28DF785656521C79D83 ↩︎
98. https://www.sciencedirect.com/science/article/abs/pii/S0944711317301691 ↩︎
99. https://www.sciencedirect.com/science/article/abs/pii/S095528631830175X ↩︎
100. https://pubmed.ncbi.nlm.nih.gov/7392829/ ↩︎
101. https://pubmed.ncbi.nlm.nih.gov/28605233/ ↩︎
102. https://pubmed.ncbi.nlm.nih.gov/26439642/ ↩︎
103. https://www.sciencedirect.com/science/article/pii/S0928493108001550 ↩︎
104. https://pmc.ncbi.nlm.nih.gov/articles/PMC2838517/ ↩︎
105. https://www.sciencedirect.com/science/article/abs/pii/S0090955624078048 ↩︎
106. https://www.sciencedirect.com/science/article/pii/S209012322200251X ↩︎
107. https://www.sciencedirect.com/science/article/abs/pii/S1756464618300094 ↩︎
108. https://pmc.ncbi.nlm.nih.gov/articles/PMC7759838/ ↩︎
109. https://www.sciencedirect.com/science/article/abs/pii/S0041010124002368 ↩︎
110. https://www.sciencedirect.com/science/article/abs/pii/S0278691507002785?via%3Dihub ↩︎
111. https://www.frontiersin.org/journals/pharmacology/articles/10.3389/fphar.2023.1142001/full ↩︎
112. https://pmc.ncbi.nlm.nih.gov/articles/PMC7478099/ ↩︎
113. https://www.sciencedirect.com/science/article/pii/S2161831322012923 ↩︎
114. https://pmc.ncbi.nlm.nih.gov/articles/PMC4205984/ ↩︎
115. https://www.sciencedirect.com/science/article/abs/pii/S0891584917306421 ↩︎
116. https://www.sciencedirect.com/science/article/abs/pii/S037887411630993X ↩︎
117. https://www.nature.com/articles/srep16226 ↩︎
118. https://factor.niehs.nih.gov/2023/7/science-highlights/folate-and-pfas ↩︎