Per- and polyfluoroalkyl substances

  (Redirected from Fluorosurfactant)

Per- and polyfluoroalkyl substances (PFASs) are synthetic organofluorine chemical compounds that have multiple fluorine atoms attached to an alkyl chain. As such, they contain at least one perfluoroalkyl moiety, –CnF2n–.[1][2] According to the Organisation for Economic Co-operation and Development (OECD):[3]

PFASs are defined as fluorinated substances that contain at least one fully fluorinated methyl or methylene carbon atom (without any H/Cl/Br/I atom attached to it), i.e. with a few noted exceptions, any chemical with at least a perfluorinated methyl group (–CF3) or a perfluorinated methylene group (–CF2–) is a PFAS.

According to the OECD, there are at least 4730 different PFASs with at least three perfluorinated carbon atoms.[4] A U.S. Environmental Protection Agency (EPA) toxicity database, DSSTox, lists 8163 PFASs.[5] A subgroup, the fluorosurfactants or fluorinated surfactants, have a fluorinated “tail” and a hydrophilic “head” and are thus surfactants. They are more effective at reducing the surface tension of water than comparable hydrocarbon surfactants. They include the perfluorosulfonic acids such as the perfluorooctanesulfonic acid (PFOS) and the perfluorocarboxylic acids such as the perfluorooctanoic acid (PFOA).

PFOS, PFOA and other PFASs are known to persist in the environment and are commonly described as persistent organic pollutants, also known as “forever chemicals”. Residues have been detected in humans and wildlife,[6][7] with health concerns resulting in litigation. In 2021 Maine became the first US state to ban these compounds in all products by 2030, except in instances deemed “currently unavoidable”.[8][9]

Skeletal structure of PFOS, an effective, persistent and bioaccumulative fluorosurfactant
Space filling model of PFOS

Physical and chemical properties of fluorosurfactantsEdit

Fluorosurfactants can reduce the surface tension of water down to a value half of what is attainable by using hydrocarbon surfactants.[10] This ability is due to the lipophobic nature of fluorocarbons, as fluorosurfactants tend to concentrate at the liquid-air interface.[11] They are not as susceptible to the London dispersion force, a factor contributing to lipophilicity, because the electronegativity of fluorine reduces the polarizability of the surfactants' fluorinated molecular surface. Therefore, the attractive interactions resulting from the "fleeting dipoles" are reduced, in comparison to hydrocarbon surfactants. Fluorosurfactants are more stable and fit for harsh conditions than hydrocarbon surfactants because of the stability of the carbon–fluorine bond. Likewise, perfluorinated surfactants persist in the environment for that reason.[6]

Fluorine-containing durable water repellent makes a fabric water-resistant.

Economic roleEdit

PFASs play a key economic role for companies such as DuPont, 3M, and W. L. Gore & Associates because they are used in emulsion polymerization to produce fluoropolymers. They have two main markets: a $1 billion annual market for use in stain repellents, and a $100 million annual market for use in polishes, paints, and coatings.[12]

Health and environmental concernsEdit

Human health concerns associated with PFASsEdit

On their introduction in the 1940s, per- and polyfluoroalkyl substances (PFASs) were considered inert molecules since they lacked a chemically active group.[13][14] In fact, early occupational studies revealed elevated levels of fluorochemicals, including PFOS and PFOA, in the blood of exposed industrial workers but cited no ill health effects.[15][16] These results were consistent with the measured serum concentrations of PFOS and PFOA in 3M plant workers ranging from 0.04 to 10.06 ppm and 0.01-12.70 ppm respectively, well below toxic and carcinogenic levels cited in animal studies.[16] However, given the "forever chemical" property of PFASs (serum elimination half-life 4–5 years) and widespread environmental contamination, molecules have been shown to accumulate in humans to such a degree that adverse health outcomes have resulted.[13]

Effects of exposure to PFASs on human health[17][18][19][20][21][22]

In 2021, consumer advocate Erin Brockovich wrote about research by epidemiologist Shanna Swan, Icahn School of Medicine, linking hormone-disrupting chemicals, including PFAS, with rapid declines in human fertility.[23][24]

The most comprehensive epidemiological studies linking[vague] adverse human health effects to PFASs, particularly PFOA, come from the C8 Science Panel.[25] The panel was formed as part of a contingency to a class action lawsuit brought by communities in the Ohio River Valley against DuPont in response to landfill and wastewater dumping of PFAS laden material from the West Virginia Washington Works Plant.[26] The panel measured PFOA (also known as C8) serum concentration in 69,000 individuals from around DuPont's Washington Works Plant and found a mean concentration of 83.0 ng/mL, compared to 4 ng/mL in a standard population of Americans.[27] From this panel, 35 studies investigating probable links[vague] between elevated C8 blood concentration and specific health outcomes were determined by measures of association and are summarized below.

Probable links[vague] to health issues as identified by the C8 Science Panel
Health outcome Reference
Ulcerative colitis
Thyroid disease
Testicular cancer
Kidney cancer
Pregnancy-induced hypertension and preeclampsia

Proposed mechanisms of PFAS-related adverse health outcomesEdit


Animal studies in the 1990s and early 2000s primarily aimed to investigate the effect of two widely used long-chain PFASs, perfluorooctane acid (PFOA, C8) and perfluorooctane sulphonic acid (PFOS, C8), on peroxisome proliferation in rat livers.[28] These studies determined that PFOA and PFOS acted as peroxisome proliferator-activated receptor (PPAR) agonists, increasing lipid metabolism.[28] A paradoxical response is observed in humans where elevated PFOS levels were significantly associated with[vague] elevated total cholesterol and LDL cholesterol, highlighting significantly reduced PPAR expression and alluding to PPAR independent pathways predominating over lipid metabolism in humans compared to rodents.[29]

Ulcerative colitisEdit

PFOA and PFOS have been shown to significantly alter immune and inflammatory responses in human and animal species. In particular, IgA, IgE (in females only) and C-reactive protein have been shown to decrease whereas antinuclear antibodies increase as PFOA serum concentrations increase.[30] These cytokine variations allude to immune response aberrations resulting in autoimmunity. One proposed mechanism is a shift towards anti-inflammatory M2 macrophages and/or T-helper (TH2) response in intestinal epithelial tissue which allows sulfate-reducing bacteria to flourish. Elevated levels of hydrogen sulfide result which reduce beta-oxidation and thus nutrient production leading to a breakdown of the colonic epithelial barrier.[31]

Thyroid diseaseEdit

Hypothyroidism is the most common thyroid abnormality associated with[vague] PFAS exposure.[32] PFASs have been shown to decrease thyroid peroxidase, resulting in decreased production and activation of thyroid hormones in vivo.[33] Other proposed mechanisms include alterations in thyroid hormone signaling, metabolism and excretion as well as function of nuclear hormone receptor.[32]


Rat studies investigating the carcinogenicity of PFASs reported significant correlation with liver adenomas, Leydig cell tumors of the testis and pancreatic acinar cell tumors and dietary PFOA consumption.[33] Naturally, The C8 Science Panel investigated the potential relationship between PFAS exposure and these three cancer types as well as 18 other cancer types in their epidemiological studies. Contrary to the animal studies, the C8 studies did not find a probable link[vague] between elevated C8 exposure and liver adenomas or pancreatic acinar cell tumors; however, a probable link[vague] was found with regards to testis and kidney cancer.[34] Two mechanisms have been proposed by which PFOA could cause Leydig cell tumors. Both mechanisms start by proposing that PROA exposure results in increased PPAR alpha activation in the liver which increases hepatic aromatase concentration and subsequent serum estrogen levels. The mechanisms now diverge, with one pathway suggesting elevated estradiol levels increase Tissue Growth Factor alpha (TGF alpha) which prompts Leydig cell proliferation. The other pathway suggests that aromatization of testosterone to estradiol reduces serum testosterone levels resulting in increased release of luteinizing hormone (LH) from the pituitary gland which directly results in Leydig Cell tumorgenesis.[35] A mechanism has not yet been proposed to explain how kidney cancer could be caused by C8 exposure as no in vivo animal studies have been able to model this epidemiological outcome.[36]

Pregnancy-induced hypertension and pre-eclampsiaEdit

Pregnancy-induced hypertension is diagnosed when maternal systolic blood pressure (SBP) exceeds 140mmHg or diastolic blood pressure (DBP) exceeds 90mmHg after 20 weeks gestation.[37] Diagnostic criteria is the same for pre-eclampsia as pregnancy-induced hypertension; however, it also confers proteinuria. Mechanisms by which pregnancy-induced hypertension and preeclampsia could be caused by PFAS exposure have remained elusive and are largely speculative to date. One proposed mechanism highlights alterations in immune function leading to disruption of placentation, specifically as it pertains to natural killer (NK) cell infiltration of the placenta to facilitate trophoblastic integration with placental blood supply.[38] Another mechanism refers to agonism of PPARs contributing to alterations in cholesterol, triglyceride and uric acid levels which may lead to vascular inflammation and elevated blood pressure.[38]

Other adverse health outcomes that have been attributed to elevated PFAS exposure but were not found to be probable links[vague] in the C8 studies are decreased antibody response to vaccines, asthma, decreased mammary gland development, low birth weight (-0.7oz per 1 ng/mL increase in blood PFOA or PFOS level), decreased bone mineral density and neurodevelopmental abnormalities.[39][40][41]

The total annual health-related costs associated with human exposure to PFASs was found to be at least €52-€84 billion in the EEA countries.[42] Aggregated annual costs covering environmental screening, monitoring where contamination is found, water treatment, soil remediation and health assessment are totalling to €821 million-€170 billion in the EEA plus Switzerland.[42]

Environmental concernsEdit

Forever chemicalsEdit

Fluorosurfactants such as perfluorooctanesulfonic acid (PFOS), perfluorooctanoic acid (PFOA), and perfluorononanoic acid (PFNA) have caught the attention of regulatory agencies because of their persistence, toxicity, and widespread occurrence in the blood of general populations[43][44] and wildlife. In 2009, PFOS, its salts and perfluorooctanesulfonyl fluoride were listed as persistent organic pollutants under the Stockholm Convention, due to their ubiquitous, persistent, bioaccumulative, and toxic nature.[45][46] PFAS chemicals were dubbed the "Forever Chemicals" following a 2018 op-ed.[47] The nickname was derived by combining the two dominant attributes of this class of chemicals: 1) PFAS chemicals are characterized by a carbon-fluorine (C-F) backbone (the "F-C" in "Forever Chemicals"); and 2) the carbon fluorine bond is one of the strongest bonds in organic chemistry, which gives these chemicals an extremely long environmental half-life (the "Forever" in "Forever Chemicals"). The Forever Chemicals name is now commonly used in media outlets in addition to the more technical name of per- and polyfluorinated alkyl substances, or PFASs.[48][49][50][51] Their production has been regulated or phased out by manufacturers, such as 3M, DuPont, Daikin, and Miteni in the US, Japan, and Europe. In 2006 3M replaced PFOS and PFOA with short-chain PFASs, such as perfluorohexanoic acid (PFHxA), perfluorobutanesulfonic acid[12] and perfluorobutane sulfonate (PFBS). Shorter fluorosurfactants may be less prone to accumulating in mammals;[12] there is still concern that they may be harmful to both humans,[52][53][54] and the environment at large.[55] A majority of PFASs are either not covered by European legislation or are excluded from registration obligations under REACH (which is the European flagship chemical legislation).[56] Several PFASs have been detected in drinking water,[57] municipal wastewater[58] and landfill leachates,[59] worldwide.

Bioaccumulation and BiomagnificationEdit

PFAS from sediments and water can accumulate in marine organisms. Animals higher up the food chain accumulate more PFAS because they absorb the PFAS in their prey.

Bioaccumulation is the process by which PFASs are transferred into marine organisms. There are a variety of pathways by which PFASs can accumulate in a marine species. They can be absorbed from the environment, such as contaminated sediments or PFAS dissolved in water. PFASs can partition into the organs and tissues of marine organisms from these environmental compartments. They have been shown to bind to blood proteins and accumulate in the livers of marine animals.[60] Another pathway for bioaccumulation is predation. As larger marine animals feed on smaller organisms which have been exposed to PFAS, the larger animals absorb the PFAS contained in their prey.

Biomagnification is the process by which the amount of PFAS contamination increases with increasing trophic level, due to predation by the species at the higher trophic level. Top predators have higher levels of PFAS than species lower down the food chain. Seabirds that feed on fish have among the highest levels of PFAS contamination.[60] Perfluorosulfonic acids, which have a sulfonic acid functional group attached to the fluorinated “tail”, have a greater tendency to bioaccumulate than perfluorocarboxylic acids, which contain a carboxylic acid function group. Longer chain PFAS compounds, which have 6, 7, or more fluorinated carbons, bioaccumulate in greater quantities than shorter chain PFASs. The concentration of PFOS, a long chain sulfonic acid, was found at the highest concentrations relative to other PFAS compounds measured in fish and birds in Northern seas such as the Barents Sea and the Canadian Arctic.[61]


In 2017, the ABC's current affairs programme Four Corners reported that the storage and use of firefighting foams containing perfluorinated surfactants at Australian Defence Force facilities around Australia had contaminated nearby water resources.[62] In 2019, remediation efforts at RAAF Base Tindal and the adjacent town of Katherine were ongoing.[63]


Although PFASs are not manufactured in Canada, they may be present in imported goods and products. In 2008, Canada prohibited the import, sale, or use of PFOS or PFOS-containing products, with some exceptions for products used in firefighting, in the military, and in some forms of ink and photo media.[64]

Health Canada has published drinking water guidelines for maximum concentrations of PFOS and PFOA. The guidelines were established to protect the health of Canadians, including children, over a lifetime's exposure to these substances. The maximum allowable concentration for PFOS under the guidelines is 0.0002 milligrams per litre. The maximum allowable concentration for PFOA is 0.0006 milligrams per litre.[65]

United KingdomEdit

Although it is recognized that they may also cause disease, for example through absorption via drinking water, water companies in the United Kingdom do not test for PFASs.[66]

United StatesEdit

In productsEdit

Certain PFASs are no longer manufactured in the United States, as a result of phase-outs including the PFOA Stewardship Program, in which eight major chemical manufacturers agreed to eliminate the use of PFOA and PFOA-related chemicals in their products and as emissions from their facilities.[67] Although PFOA and PFOS are no longer manufactured in the United States, they are still produced internationally and are imported into the United States in consumer goods such as carpet, leather and apparel, textiles, paper and packaging, coatings, rubber and plastics.[68]

In 2020, manufacturers and the Food and Drug Administration (FDA) announced an agreement to phase out some types of PFAS which are used in food packaging by 2024.[69]

PFAS are also used by major companies of the cosmetics industry in a wide range of cosmetics, including lipstick, eye liner, mascara, foundation, concealer, lip balm, blush, nail polish and other such products. A 2021 study tested 231 makeup and personal care products and found organic fluorine, an indicator of PFAS, in more than half of the samples. High levels of fluorine were most commonly identified in waterproof mascara (82% of brands tested), foundations (63%), and liquid lipstick (62%).[70][71] As many as 13 types of individual PFAS compounds were found in each product.[70] Since PFAS compounds are highly mobile, they are readily absorbed through human skin and through tear ducts, and such products on lips are often unwittingly ingested. Manufacturers often fail to label their products as containing PFAS, which makes it difficult for cosmetics consumers to avoid products containing PFAS.[72] In response, Senators Susan Collins of Maine and Richard Blumenthal of Connecticut proposed the No PFAS in Cosmetics Act in the United States Senate.[73] It was also introduced in the United States House of Representatives by Michigan Representative Debbie Dingell.[74]

Contaminated sites, drinking water and wastewaterEdit

There are an estimated 26,000 PFAS-contaminated sites across the United States, and scientists have estimated that at least six million Americans have PFAS-contaminated drinking water above the existing safe limits recommended by EPA.[75][76]

EPA published non-enforceable drinking water health advisories for PFOA and PFOS in 2016.[77][78] In March 2021 EPA announced that it will develop national drinking water standards for PFOA and PFOS.[79] EPA also proposed that drinking water utilities begin to conduct monitoring for 29 PFAS compounds. The agency would use the monitoring data to possibly develop additional regulations.[80][81]

In mid-2021 EPA announced plans to revise federal wastewater regulations (effluent guidelines) for several industries that manufacture PFAS or use PFAS in fabricating various products.[82][83]


In 2021 California banned PFAS for use in food packaging and from infant and children’s products and also required PFAS cookware in the state to carry a warning label.[84]


Launched in 2017, the Michigan PFAS Action Response Team (MPART) is the first multi-agency action team of its kind in the nation. Agencies representing health, environment and other branches of state government have joined together to investigate sources and locations of PFAS contamination in the state, take action to protect people's drinking water, and keep the public informed.[85]

Groundwater is tested at locations throughout the state by various parties to ensure safety, compliance with regulations, and to proactively detect and remedy potential problems. In 2010, the Michigan Department of Environmental Quality (MDEQ) discovered levels of PFASs in groundwater monitoring wells at the former Wurtsmith Air Force Base. As additional information became available from other national testing, Michigan expanded its investigations into other locations where PFAS compounds were potentially used.[85]

In 2018, the MDEQ's Remediation and Redevelopment Division (RRD) established cleanup criteria for groundwater used as drinking water of 70 ppt of PFOA and PFOS, individually or combined. The RRD staff are responsible for implementing these criteria as part of their ongoing efforts to clean-up sites of environmental contamination. The RRD staff are the lead investigators at most of the PFAS sites on the MPART website and also conduct interim response activities, such as coordinating bottled water or filter installations with local health departments at sites under investigation or with known PFAS concerns. Most of the groundwater sampling at PFAS sites under RRD's lead is conducted by contractors familiar with PFAS sampling techniques. The RRD also has a Geologic Services Unit, with staff who install monitoring wells and are also well versed with PFAS sampling techniques.[85]

The MDEQ has been conducting environmental clean-up of regulated contaminants for decades. Due to the evolving nature of PFAS regulations as new science becomes available, the RRD is evaluating the need for regular PFAS sampling at Superfund sites and is including an evaluation of PFAS sampling needs as part of a Baseline Environmental Assessment review.[85]

Earlier this year, the RRD purchased lab equipment that will allow the MDEQ Environmental Lab to conduct analyses of certain PFAS samples. (Currently, most samples are shipped to one of the few labs in the country that conduct PFAS analysis, in California, although private labs in other parts of the country, including Michigan, are starting to offer these services.) As of August 2018, RRD has hired additional staff to work on developing the methodology and conducting PFAS analyses.[85]


In February 2018, 3M settled a lawsuit for $850 million related to contaminated drinking water in Minnesota.[86]

New JerseyEdit

In 2018 the New Jersey Department of Environmental Protection (NJDEP) published a drinking water standard for PFNA. Public water systems in New Jersey are required to meet a maximum contaminant level (MCL) standard of 13 ppt.[87][88] In 2020 the state set a PFOA standard at 14 ppt and a PFOS standard at 13 ppt.[89]

In 2019 NJDEP filed lawsuits against the owners of two plants that had manufactured PFASs, and two plants that were cited for water pollution from other chemicals. The companies cited are DuPont, Chemours and 3M.[90] NJDEP also declared five companies to be financially responsible for statewide remediation of the chemicals. Among the companies accused were Arkema and Solvay in regard to a West Deptford Facility in Gloucester County, where Arkema manufactured PFASs, but Solvay claims to have never manufactured but only handled PFASs.[91] The companies denied liability, and contested the directive.[92]

Class action lawsuitsEdit

In October 2018, a class action suit was filed by an Ohio firefighter against several producers of fluorosurfactants, including the 3M and DuPont corporations, on behalf of all US residents who may have adverse health effects from exposure to PFASs.[93] Five New Jersey companies were declared to be financially responsible for statewide remediation of the chemicals in a directive from the New Jersey Department of Environmental Protection in March 2019.[92]

In February 2017, DuPont and Chemours (a DuPont spin-off) agreed to pay $671 million to settle lawsuits arising from 3,550 personal injury claims related to releasing of PFASs from their Parkersburg, West Virginia plant, into the drinking water of several thousand residents.[94] This was after a court-created independent scientific panel, "The C8 Science Panel", found a 'probable link' between C8 exposure and six illnesses: kidney and testicular cancer, ulcerative colitis, thyroid disease, pregnancy-induced hypertension and high cholesterol.[26]

This story is told in the film Dark Waters, released in November 2019, produced by the actor Mark Ruffalo and directed by Todd Haynes.[95]

Corporate and federal government suppression of informationEdit

Starting in the 1970s, 3M scientists learned that PFOS and PFOA were toxic to humans, documenting damage to the human immune system. Also in the 1970s, 3M scientists found that these substances accumulate over time in the human body. However, 3M suppressed revelation of these facts to the public or to regulators.[96]

In 2018 White House staff and EPA pressured the U.S. Agency for Toxic Substances and Disease Registry to suppress a study that showed PFASs to be even more dangerous than previously thought.[97][98]

Water contamination by U.S. military basesEdit

The water in and around at least 126 U.S. military bases has been contaminated by high levels of PFASs, according to a study by the U.S. Department of Defense. Of these, 90 bases reported PFAS contamination that had spread to drinking water or ground water off the base. The chemical is correlated with cancer and birth defects.[99]

Occupational exposureEdit

Occupational exposure to PFASs occurs in numerous industries due to the widespread use of PFASs in products and as an element of industrial process streams.[18] PFASs are used in more than 200 different ways in industries as diverse as electronics and equipment manufacturing, plastic and rubber production, food and textile production, and building and construction.[100] Occupational exposure to PFASs can occur at fluorochemical facilities that produce PFASs and other manufacturing facilities that use PFASs for industrial processing like the chrome plating industry.[18] Workers who handle PFAS-containing products can also be exposed during their work. Examples include people who install PFAS-containing carpets and leather furniture with PFAS coatings, professional ski-waxers using PFAS-based waxes, and fire-fighters who use PFAS-containing foam and wear flame-resistant protective gear impregnated with PFASs.[18][101][102][103][104]

People who are exposed to PFASs through their jobs typically have higher levels of PFASs in their blood than the general population.[18][102][103][105][106] Additionally, while the general population is exposed to PFASs through ingested food and water, occupational exposure includes both accidental ingestion and inhalation exposure in settings where a PFAS becomes volatilized.[107] There has been increased attention to the health risks associated with exposure to PFASs, which can affect the immune system, increase cholesterol, and increase the risk of cancer.[39] The severity of PFAS-associated health effects can vary based on the length of exposure, level of exposure, and health status.[18] In 2009, under decision SC-4/17, certain PFASs (perfluorooctane sulfonic acid, its salts and perfluorooctane sulfonyl fluoride) were listed in Annex B of the 2009 Stockholm Convention on Persistent Organic Pollutants, dictating acceptable purposes and specific exemptions to the chemical usage. Among these exemptions are numerous uses in manufacturing as well as firefighting foams.

Professional ski wax techniciansEdit

Professional ski wax technicians are disproportionately exposed to PFASs from the glide wax used to coat the bottom of skis to reduce the friction between the skis and snow. During this process, the wax is heated to 130-220 °C, which releases fumes and airborne fluorinated compounds. Exposure to aerosolized PFASs is associated with alveolic edema, polymer fume fever, severe dyspnea, decreased pulmonary function, and respiratory distress syndrome in those chronically exposed.[102] In a 2010 study, blood serum levels of PFOA were significantly higher in ski wax technicians compared to levels of the general Swedish population. Serum levels of PFOA in ski wax technicians was positively correlated with years spent working, suggesting bioaccumulation of PFOA over time.[102]

Manufacturing workersEdit

People who work at fluorochemical production plants and in manufacturing industries that use PFASs in the industrial process can be exposed to PFASs in the workplace. Much of what we know about PFASs exposure and health effects began with medical surveillance studies of workers exposed to PFASs at fluorochemical production facilities. These studies began in the 1940s and were conducted primarily at U.S. and European manufacturing sites. Between the 1940s and 2000s, thousands of workers exposed to PFASs participated in research studies that advanced scientific understanding of exposure pathways, toxicokinetic properties, and adverse health effects associated with exposure.[15][108][109][16][110][111][112][113][114][115][116][117][118]

The first research study to report elevated organic fluorine levels in the blood of fluorochemical workers was published in 1980.[15] This study established inhalation as a potential route of occupational PFAS exposure by reporting measurable levels of organic fluorine in air samples at the facility.[15] Workers at fluorochemical production facilities have higher levels of PFOA and PFOS in their blood than the general population. Serum PFOA levels in fluorochemical workers are generally below 20,000 ng/mL but have been reported as high as 100,000 ng/mL whereas the mean PFOA concentration among non-occupationally exposed cohorts in the same time frame was 4.9 ng/mL.[115][16][119][120][121][122][123][124][125][126] Among fluorochemical workers, those with direct contact with PFASs have higher PFASs concentrations in their blood than those with intermittent contact and those with no direct PFAS contact.[15][108][115] Further, blood PFAS levels decline when direct contact ceases.[115][110][112] Levels of PFOA and PFOS have declined in US and European fluorochemical workers due to improved facilities, increased usage of personal protective equipment, and the phase out of these chemicals from production.[108][116][118] However, occupational exposure to PFASs in manufacturing continues to be an active area of study in China with numerous investigations linking worker exposure to various PFASs.[127][128][129][130][131]


PFASs are commonly used in Class B firefighting foams due to their hydrophobic and lipophobic properties as well as the stability of the chemicals when exposed to high heat.[132] Due to firefighters’ potential for exposure to PFASs through these aqueous film forming foams (AFFF), studies raise concerns that there are high levels of bioaccumulation of PFASs in firefighters who work and train with these substances.

Research into occupational exposure for firefighters is emergent, though frequently limited by underpowered study designs. A 2011 cross-sectional analysis of the C8 Health Studies found higher levels of PFHxS in firefighters compared to the sample group of the region, with other PFASs at elevated levels, without reaching statistical significance.[133] A 2014 study in Finland studying eight firefighters over three training sessions observed select PFASs (PFHxS and PFNA) increase in blood samples following each training event.[132] Due to this small sample size, a test of significance was not conducted. A 2015 cross-sectional study conducted in Australia found  that accumulation of PFOS and PFHxS was positively associated with years of occupational AFFF exposure through firefighting.[103]

Due to their use in training and testing, recent studies indicate occupational risk for military members and firefighters, as higher levels of PFASs in exposure were indicated in military members and firefighters when compared to the general population.[134] Further, exposure to PFASs is prevalent among firefighters not only due to its use in emergencies but because it is also used in personal protective equipment.  In support of these findings, states like Washington and Colorado have moved to restrict and penalize the use of Class B firefighting foam which contains PFAS for firefighter training and testing.[135]

Exposure after World Trade Center terrorist attacksEdit

The September 11, 2001 collapse of the World Trade Center buildings in New York City resulted in the release of chemicals from the destruction of construction and electrical material and long-term chemical fires. This collapse caused the release of several toxic chemicals, including fluorinated surfactants used as soil- and stain-resistant coatings on various materials.[136] First responders to this incident were exposed to PFOA, PFNA, and PFHxS, through inhalation of dust and smoke released during and after the collapse of the World Trade Center.[136]

Fire responders who were working at or near ground zero were assessed for respiratory and other health effects from exposure to emissions at the World Trade Center.  Early clinical testing showed high prevalence of respiratory health effects. Early symptoms of exposure often presented with persistent coughing and wheezing. PFOA and PFHxS levels were present in both smoke and dust exposure. Yet, first responders with smoke exposures had higher concentrations of PFOA and PFHxS than those with dust exposures.[136]

Remediation solutionsEdit

Liquids treatmentEdit

Several technologies are currently available for remediating PFASs in liquids. These technologies can be applied to drinking water supplies, groundwater, industrial wastewater, surface water, and other miscellaneous applications (such as landfill leachate). Influent concentrations of PFASs can vary by orders of magnitude for specific media or applications. These influent values, along with other general water quality parameters (for example, pH) can influence the performance and operating costs for the treatment technologies. The technologies are:

Private and public sector applications of one or more of these methodologies above is being applied to remediation sites throughout the United States and other international locations.[138] Most solutions involve on-site treatment systems, while others are leveraging off-site infrastructure and facilities, such as a centralized industrial wastewater treatment facility, to treat and dispose of the PFAS pool of compounds.

Theoretical and early stage solutionsEdit

The Michigan State University-Fraunhofer team has a viable solution to treat PFAS-contaminated wastewater that, in 2018, was reported to be ready for a pilot-scale investigation. The electrochemical oxidation system used boron-doped diamond electrodes, in a process breaking down the contaminants’ formidable molecular bonds and cleaning the water while systematically destroying the hazardous compounds.[139]

"EO, or electrochemical oxidation, is a simple, clean and effective method for destruction of PFAS and other co-contaminants as a complementary procedure to other wastewater treatment processes," said Cory Rusinek, electrochemist at MSU-Fraunhofer. "If we can remove it from wastewater, we can reduce its occurrence in surface waters."[139]

In September 2019 it was reported Acidimicrobium sp. strain A6 could be a potential remediator.[140]

Example chemicalsEdit

Some common per- and polyfluoroalkyl substances:[141][142]

Perfluorinated carboxylic acidsEdit

Name Abbreviation Structural formula Molecular weight (g/mol) CAS No.
Pentafluoropropionic acid [de] - C2F5COOH 164.03 422-64-0
Perfluorobutanoic acid PFBA C3F7COOH 214.04 375-22-4
Perfluoropentanoic acid [de] PFPeA C4F9COOH 264.05 2706-90-3
Perfluorohexanoic acid [de] PFHxA C5F11COOH 314.05 307-24-4
Perfluoroheptanoic acid [de] PFHpA C6F13COOH 364.06 375-85-9
Perfluorooctanoic acid PFOA C7F15COOH 414.07 335-67-1
Perfluorononanoic acid PFNA C8F17COOH 464.08 375-95-1
Perfluorodecanoic acid PFDA C9F19COOH 514.08 335-76-2
Perfluoroundecanoic acid [de] PFUDA C10F21COOH 564.09 2058-94-8
Perfluorododecanoic acid [de] PFDoDA C11F23COOH 614.10 307-55-1
Perfluorotridecanoic acid [de] PFTrDA C12F25COOH 664.10 72629-94-8
Perfluorotetradecanoic acid [de] PFTeDA C13F27COOH 714.11 376-06-7


Name Abbreviation Structural formula Molecular weight (g/mol) CAS No.
Perfluorobutanesulfonic acid PFBS C4F9SO3H 300.10 375-73-5
Perfluoropentanesulfonic acid PFPS C5F11SO3H 350.11 2706-91-4
Perfluorohexanesulfonic acid PFHxS C6F13SO3H 400.12 355-46-4
Perfluoroheptanesulfonic acid PFHpS C7F15SO3H 450.12 375-92-8
Perfluorooctanesulfonic acid PFOS C8F17SO3H 500.13 1763-23-1
Perfluorononanesulfonic acid PFNS C9F19SO3H 550.14 68259-12-1
Perfluorodecanesulfonic acid PFDS C10F21SO3H 600.15 335-77-3
Perfluorobutane sulfonamide H-FBSA C4F9SO2NH2 299.12 30334-69-1
Perfluoropentanesulfonamide PFPSA C5F11SO2NH2 349.12 82765-76-2
Perfluorohexanesulfonamide PFHxSA C6F13SO2NH2 399.13 41997-13-1
Perfluoroheptanesulfonamide PFHpSA C7F15SO2NH2 449.14 82765-77-3
Perfluorooctanesulfonamide PFOSA C8F17SO2NH2 499.14 754-91-6
Perfluorobutanesulfonyl fluoride PFBSF C4F9SO2F 302.09 375-72-4
Perfluorooctanesulfonyl fluoride PFOSF C8F17SO2F 502.12 307-35-7


See alsoEdit


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