In 1949, 3M began producing PFOS-based compounds by electrochemical fluorination.[5] In 1968, organofluorine compounds were detected in the blood serum of consumers, and in 1976, perfluorooctanoic acid (PFOA) or a related compound such as PFOS were suggested as components.[6][7][8] In 1997, 3M detected PFOS in blood from global blood banks,[9] although the company's internal documents indicate knowledge of this decades earlier, dating from the 1970s.[10] In 1999, the U.S. Environmental Protection Agency began investigating perfluorinated compounds after receiving data on the global distribution and toxicity of PFOS, the key ingredient in Scotchgard.[11] For these reasons, and USEPA pressure,[12] the primary American producer of PFOS, 3M, announced, in May 2000, the phaseout of the production of PFOS, PFOA, and PFOS-related products.[13][10] Most other manufacturers (particularly, those in Europe) phased out the production of PFOS and perfluorooctanoic acid (PFOA) in 2000 and 2006, respectively. A shorter-chain PFOS (perfluorohexanesulfonic acid, PFHxS), was included in Annex A to the Stockholm Convention in 2022.[14]
Currently, most of PFOS and PFOS-related chemicals are produced in China.[15]
The main method used for the industrial scale production of PFOS is electrochemical fluorination (ECF).[16] ECF is an electrolysis method whereby the precursor of octanesulfonyl fluoride is electrolyzed in a solution of hydrogen fluoride to give perfluorooctanesulfonyl fluoride. This production method also results in shorter chain perfluoroalkyl substances being formed.[citation needed] PFOS predominates in the resultant mixture. A distinct isomer ratio has been observed in PFOS produced by ECF, in the order of 70% linear PFOS, 25% branched and 5% terminal; this is not a function of the production process but rather that the precursor also exhibits this isomer ratio. ECF was the means by which 3M produced PFOS up until May 2000 when the company announced a phaseout of fluorosurfactants.
Although 89 constitutional isomers of PFOS are possible,[17] environmental samples usually consist of a mixture of the linear isomer and 10 branched isomers.[18]
Telomerisation involves constructing the PFOS molecule using short chain (often 2-carbon) precursors and adding a sulfonate group as a final step. This production process results in 100% linear PFOS. This production method, whilst cleaner and resulting in a much purer product than ECF, is not known to have been widely used except for the production of reagent grade PFOS and analytical standards.[citation needed]
PFOS virtually does not degrade under environmental conditions and is thus highly persistent. Waste water treatment plants are also unable to degrade PFOS.[23] On the other hand, precursors are transformed to PFOS in waste water treatment plants.[24]
PFOS compounds can also be found in some impregnation agents for textiles, paper, and leather; in wax, polishes, paints, varnishes, and cleaning products for general use; in metal surfaces, and carpets.
In the semiconductor industry, PFOS is used in multiple photolithographic chemicals including: photoacid generators (PAGs) and anti-reflective coatings (ARCs). It has been phased out in the European Union semiconductor industry due to health concerns.
The most important emission sources of PFOS are metal plating and fire-fighting foams.[25] Because of concerns about PFOS, F-53B has been used as a replacement for mist suppression in metal plating.[26]
Levels in humans
Because of its chemical nature, PFOS will remain in the body for several years. It is estimated that it takes 4 years for half of this substance to be eliminated from the body.[27]
PFOS is detected in the blood serum of almost all people in the U.S., but concentrations have been decreasing over time. In contrast, PFOS blood levels appear to be rising in China[28] where PFOS production continues. A study of ca. 2000 teenagers from 9 European countries with most samples collected in years 2016-2018 found higher blood concentrations of several PFOS’s in those, who consumed more seafood, eggs or offal, as well as in those from North and West (versus the South and East) Europe. Within the same country, boys had a higher PFOS concentrations than girls. A typical PFOS blood concentration range in this study was 1,500-2,500 ppb.
[29]
Much higher levels of blood PFOS (12,830 ppb) have been reported in people with occupational exposure [30]—or possibly 1,656 parts per billion[31]—in a consumer. Occupationally exposed individuals may have an average level of PFOS over 1000 parts per billion, and a small segment of individuals in the upper range of the general population may be over the 91.5 parts per billion level.[32]
PFOS exposure has been demonstrated as early as fetal development during pregnancy since PFOS can easily pass through the placenta.[33] It has been shown that fetal exposure to PFOS is quite prevalent and has been shown to be detected in greater than 99% of umbilical cord serum samples.[34]
PFOS has been detected in U.S. freshwater fish,[35][36] as well as in municipal wastewater[37] and drinking water samples,[38] worldwide, at concentrations ranging between few ng/L and some μg/L.
Levels in wildlife
A variety of wildlife species have had PFOS levels measured in egg, liver, kidney, serum, and plasma samples and some of the highest recorded values as of January 2006 are listed below.[39]
Despite the global wide-ranging restriction, PFOS concentrations in air continued to increase at many monitoring stations between 2009 and 2017.[41]
Health effects in humans and wildlife
There is a growing body of research investigating the health effects of PFOS in humans and animals, including the reproductive, developmental, liver, kidney, thyroid, and immunological effects.[42] According to a 2002 report by the Environmental Directorate of the OECD, "PFOS is persistent, bioaccumulative, and toxic to mammalian species."[43]
Pregnancy outcomes
Several studies have focused on pregnancy outcomes in infants and mothers who are exposed to PFOS during pregnancy. For developing offspring, exposure to PFOS occurs through the placenta.[33] While the impact of PFOS compounds on fetal development continues to be an ongoing investigation, findings have demonstrated a relationship between PFOS exposure in pregnant mothers and negative birth outcomes.[44]
There has been some evidence to suggest that PFOS levels in pregnant women have been associated with preeclampsia, preterm labor, low birth weight and gestational diabetes.[45][46] Although, the strongest association is between PFOS levels with preterm birth and preeclampsia.[46][47] There has been some evidence to suggest that PFOS impairs fetal growth during pregnancy, although findings have been inconsistent.[46]
The specific physiological mechanisms behind adverse pregnancy outcomes with PFOS exposure remain unclear. One proposed cause has to do with PFOS impairment on placental blood flow.[42] This mechanism could help explain several of the pregnancy-related outcomes from PFOS exposure including such as intrauterine growth development, low birth weight, preterm birth labor, and preeclampsia. Additional physiological mechanisms may include disruption in inflammatory signals during pregnancy, decreased trophoblast signaling and trophoblast migration.[48] Additionally, PFOS exposure has been shown to be related to the downregulation genes corresponding to growth factors, pregnancy-related signal transducers, and maternal hormones.[49] PFOS impact on thyroid hormone regulation also has the potential to impact several birth outcomes.[50][51]
Breastfeeding and lactation
PFOS has been measured in breastmilk and is estimated to contribute the greatest level of PFOS exposure in infants. Specifically, the duration of breastfeeding has been shown to be associated with increases in PFOS in infants.[52] Some evidence has shown that breastmilk provides more than 94% of the PFOS exposure in infants up to six months old.[53] The Agency for Toxic Substances and Disease Registry (ATSDR) concluded that breastfeeding benefits continue to outweigh potential risks associated with PFOS in breastmilk.[54]
Thyroid disease
Increased levels of PFOS have been shown to accumulate in thyroid gland cells and have been associated with altered thyroid hormone levels in adults.[55][56] Appropriate levels of thyroid hormone during pregnancy are critical for a developing fetus as this hormone is involved with brain development and body growth.[57] Studies have demonstrated a relationship between PFOS exposure and thyroid dysfunction during pregnancy resulting in altered thyroid hormone levels in both the mother and the fetus.[58][59]
Serum levels of PFOS were found to be associated with increased risk of chronic kidney disease in the general US population.[64] "This association was independent of confounders such as age, sex, race/ethnicity, body mass index, diabetes, hypertension, and serum cholesterol level."[64]
Cancer
Research demonstrating the association between PFOS and cancer is still ongoing. A few studies have demonstrated an elevated risk for prostate and bladder cancer, however, there were notable limitations in the design and analysis of these studies.[46] As of November 2023, the International Agency for Research on Cancer (IARC) has classified PFOS as possibly carcinogenic to humans (Group 2b) based on “strong” mechanistic evidence.[65] The Division of Cancer Epidemiology & Genetics (DCEG) is currently investigating the association of several PFAS compounds and cancers including kidney cancer, testicular cancer, prostate cancer, ovarian and endometrial cancer, thyroid cancer, non-hodgkins lymphoma, and childhood leukemia.[66]
In wildlife
The levels observed in wild animals are considered sufficient to "alter health parameters".[67][68]
PFOS affects the immune system of male mice at a blood serum concentration of 91.5 parts per billion, raising the possibility that highly exposed people and wildlife are immunocompromised.[32] Chicken eggs dosed at 1 milligram per kilogram (or 1 part per million) of egg weight developed into juvenile chickens with an average of ~150 parts per billion in blood serum—and showed brain asymmetry and decreased immunoglobulin levels.[69]
Regulation
Globally
It was added to Annex B of the Stockholm Convention on Persistent Organic Pollutants in May 2009.[4] Originally, parties agreed on acceptable proposes (time-unlimited exemptions) for the following uses—in addition to a range of specific exemptions (time-limited):[70]
Photo-imaging
Photo-resist and anti-reflective coatings for semi-conductors
Etching agent for compound semi-conductors and ceramic filters
Aviation hydraulic fluids
Metal plating (hard metal plating) only in closed-loop systems
Certain medical devices (such as ethylene tetrafluoroethylene copolymer (ETFE) layers and radio-opaque ETFE production, in-vitro diagnostic medical devices, and CCD colour filters)
Insect baits for control of leaf-cutting ants from Atta spp. and Acromyrmex spp.
In 2019, it was decided to only keep one acceptable purpose:[71]
Insect baits with sulfluramid (CAS No. 4151-50-2) as an active ingredient for control of leaf-cutting ants from Atta spp. and Acromyrmex spp. for agricultural use only
Canada
In 2023, the Government of Canada is considering addressing PFAS as a class rather than as individual substances or in smaller groups. A report to conclude that PFAS as a class are harmful to human health and the environment, and to define risk management aspects and alternatives to PFAs, is under development."Per-and polyfluoroalkyl substances (PFAS)"
Europe
Based on an OECD study on PFOS[43] and a risk assessment by Europe's Scientific Committee on Health and Environmental Risks[72] the European Union practically banned the use of PFOS in finished and semi-finished products in 2006 (maximum content of PFOS: 0.005% by weight).[73] However, PFOS use for industrial applications (e.g. photolithography, mist suppressants for hard chromium plating, hydraulic fluids for aviation) was exempted.
In 2009 this directive was incorporated into the REACH regulation.[74] In the summer of 2010 PFOS was added to the regulation on persistent organic pollutants and the threshold was lowered to max. 0.001% by weight (10 mg/kg).[75]
United States
In 2018 the State of Michigan established a legally enforceable groundwater cleanup level of 70 ppt for both PFOA and PFOS.[76]
In 2020, a California bill was passed banning PFOS and the following salts as an intentionally added ingredient from cosmetics: ammonium perfluorooctane sulfonate, diethanolamine perfluorooctane sulfonate, lithium perfluorooctane sulfonate and potassium perfluorooctane sulfonate.[79]
In March 2021 the U.S. EPA announced that it will develop national drinking water standards for PFOA and PFOS.[80]
In October 2021 the EPA proposed to designate PFOA and PFOS as hazardous substances in its PFAS Strategic Roadmap.[81][82] In September 2022 the EPA proposed to designate as hazardous substances under the Superfund Comprehensive Environmental Response, Compensation, and Liability Act of 1980 (CERCLA).
^Paul AG, Jones KC, Sweetman AJ (January 2009). "A first global production, emission, and environmental inventory for perfluorooctane sulfonate". Environ. Sci. Technol. 43 (2): 386–92. Bibcode:2009EnST...43..386P. doi:10.1021/es802216n. PMID19238969.
^Rayne, Sierra; Forest, Kaya; Friesen, Ken J. (2008). "Congener-specific numbering systems for the environmentally relevant C4 through C8 perfluorinated homologue groups of alkyl sulfonates, carboxylates, telomer alcohols, olefins, and acids, and their derivatives". Journal of Environmental Science and Health, Part A. 43 (12): 1391–1401. doi:10.1080/10934520802232030.
^Trojanowicz, Marek; Bojanowska-Czajka, Anna; Bartosiewicz, Iwona; Kulisa, Krzysztof (2018). "Advanced Oxidation/Reduction Processes treatment for aqueous perfluorooctanoate (PFOA) and perfluorooctanesulfonate (PFOS) – A review of recent advances". Chemical Engineering Journal. 336: 170–199. Bibcode:2018ChEnJ.336..170T. doi:10.1016/j.cej.2017.10.153.
^Eriksson, Ulrika; Haglund, Peter; Kärrman, Anna (2017). "Contribution of precursor compounds to the release of per- and polyfluoroalkyl substances (PFASs) from waste water treatment plants (WWTPs)". Journal of Environmental Sciences (China). 61: 80–90. Bibcode:2017JEnvS..61...80E. doi:10.1016/j.jes.2017.05.004. PMID29191318.
^PFAS levels and determinants of variability in exposure in European teenagers – Results from the HBM4EU aligned studies (2014–2021). 2023. Int J Hyg Environ Health. 247/. D. Richterová, E. Govarts, L. Fábelová, K. Rausová, L. Rodriguez Martin, L. Gilles, et al. doi: 10.1016/j.ijheh.2022.114057.
^Fromme H, Tittlemier SA, Völkel W, Wilhelm M, Twardella D (May 2009). "Perfluorinated compounds—exposure assessment for the general population in Western countries". Int. J. Hyg. Environ. Health. 212 (3): 239–70. Bibcode:2009IJHEH.212..239F. doi:10.1016/j.ijheh.2008.04.007. PMID18565792.
^Arvaniti, Olga S.; Stasinakis, Athanasios S. (15 August 2015). "Review on the occurrence, fate and removal of perfluorinated compounds during wastewater treatment". Science of the Total Environment. 524–525: 81–92. Bibcode:2015ScTEn.524...81A. doi:10.1016/j.scitotenv.2015.04.023. PMID25889547.
^Dauwe, Tom; Van de Vijver, Kristin; De Coen, Wim; Eens, Marcel (April 2007). "PFOS levels in the blood and liver of a small insectivorous songbird near a fluorochemical plant". Environment International. 33 (3): 357–361. Bibcode:2007EnInt..33..357D. doi:10.1016/j.envint.2006.11.014. PMID17188355.
^Peden-Adams, M. M.; Keil, D. E.; Romano, T.; Mollenhauer, M. A. M.; Fort, D. J.; Guiney, P. D.; Houde, M.; Kannan, K.; Muir, D. C.; Rice, C. D.; Stuckey, J.; Segars, A. L.; Scott, T.; Talent, L.; Bossart, G. D.; Fair, P. A.; Keller, J. M. (2009). "Health effects of perfluorinated compounds—What are the wildlife telling us?". Reproductive Toxicology. 27 (3–4): 414–415. Bibcode:2009RepTx..27..414P. doi:10.1016/j.reprotox.2008.11.016.
^Peden-Adams, M.; Stuckey, J.; Gaworecki, K.; Berger-Ritchie, J.; Bryant, K.; Jodice, P.; Scott, T.; Ferrario, J.; Guan, B.; Vigo, C.; Boone, J. S.; McGuinn, W. D.; Dewitt, J. C.; Keil, D. E. (2009). "Developmental toxicity in white leghorn chickens following in ovo exposure to perfluorooctane sulfonate (PFOS)". Reproductive Toxicology (Elmsford, N.Y.). 27 (3–4): 307–318. Bibcode:2009RepTx..27..307P. doi:10.1016/j.reprotox.2008.10.009. PMID19071210.
^SCHER (2005). "RPA's report "Perfluorooctane Sulphonates Risk reduction strategy and analysis of advantages and drawbacks"". Scientific Committee on Health and Environmental Risks, European Commission.
^EPA (2021-03-03). "Announcement of Final Regulatory Determinations for Contaminants on the Fourth Drinking Water Contaminant Candidate List." Federal Register, 86 FR12272
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