Perfluorooctanoic Acid (PFOA): A Global Water Contaminant
Brandon M. Montes, Ernesto M. Garcia and Antonio F. Machado
Department of Environmental and Occupational Health, California State University, Northridge
Perfluorooctanoic Acid (PFOA) is an anthropogenic perfluoroalkyl that was widely produced in the
second half of the 1900s. During that time, it was haphazardly introduced into the natural
environment through manufacturing processes and also exposed to humans through various
applications and products. What makes PFOA an attractive chemical for industrial use also gives it
low biodegradability properties. PFOA bioaccumulates in the food chain and will continue to do so
because of its persistence. This introduces a problem for humanity, and it must be studied in order
to understand the harm it has or will cause. The 3M company is responsible for much of the
contamination, and many epidemiological studies have been performed on their cohorts and
environments. Various toxicological studies have been performed, and the main endpoints seen are
at levels not found in the natural environment. The worst case are the workers exposed, whom have
the highest blood serum levels will have the most deleterious effects. PFOA is not a very toxic
chemical in the levels seen in the environment, and its effects are often times only produced at
levels not seen in nature. The regulations in place are only guidelines and not legally enforceable.
The most effective treatments and remediation include PFOA free products and carbon filters for
potable water. Many endpoints are unclear and need more research, but there is evidence
supporting PFOA as a liver, kidney, and testicular toxicant.
•Found in the blood of nearly all American citizens at an average level of .04 ppm.
•PFOA is very persistent with a half-life of 2.5-3.5 years in the human body
•Perfluoroalkyls are mobile in soil and leach into groundwater
•PFOA can now be traced in some foods, drinking water, and in dust found inside regular homes.
•PFOA is otherwise known as C8 because of its 8 carbon chain (C8HF15O2)
•Perfluoroalkyls are human-made substances that do not occur naturally in the environment.
•Manufacturing started in 1947 by 3M
•Used as part of the process of making products containing fluoropolymers
•Fluoropolymers contained the property of both being lipophilic and hydrophobic
•Used to make non-stick pans, water/stain resistant materials, and water repellant aerosolized
applicators.
•Although final products are not to contain PFOA, fluoropolymers decompose into sister products of
PFOA
•The EPA with 8 other companies created a Stewardship Program to reduce PFOA emissions
•Not until the 1990’s did the EPA start scrutinizing companies for the release of PFOA
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Carpeting and Carpet Care
Grease and Lubricant
Treated clothing, upholstery, textiles,
Medical and garments.(i.e. gortex applied
membranes or waterproofing sprays)
Food contact (i.e. popcorn bag liner)
PTFE Cookware
Sealants for stone, tile and wood.
Dental Floss
Studies would suggest that PFOA increases liver weight and size. They also found
that PFOA increased serum enzyme levels. The authors associated the leakage of
the serum enzymes with centrilobular necrosis, ballooning degeneration, and cellular
infiltration of liver. They found that PFOA increased the level of ROS, due to the
increase of oxidative stress indicators, but it was not concentration dependent. [4]
High levels of PFOA in studies have shown to activate p53 levels, while decreasing
both GRP78 and CTSD levels in liver cells. These changes in protein levels are
indicators of oxidative stress and may interfere with apoptosis.[5]
Not only did PFOA up regulate and promote cell invasiveness, it was proven using
JSH-23, which was a known inhibitor. JSH-23 treatment could possibly be used as
treatment in future studies to hinder the effects of PFOA. [6]
The chemical structure of PFOA is similar enough to fatty acid chains that it could
induce mitochondrial dysfunction. PFOA was essentially drawn to the area where
mitochondrial death was triggered and activated reactive oxygen species (ROS).
ROS creation was observed, which caused the mitochondria to depolarize, and in
turn flicked the switch (caspase-9 activation) of apoptosis. By adding antioxidants, it
slowed the effects of both caspase-9 and also showed some reversing actions.[7]
LD50 per 30 day time frame: 189 mg/kg in male Fischer rats. The rodents liver
showed slight growth compared to the controls [13]
Genotoxic at 50 to 400 µM: DNA Strands Break [15]
100 to 400 µM: HepG2 increased ROS and 8-OHdG [15]
Studies done by DuPont suggest that the most
effective method to treat water contaminated with
PFOA is with the use of granulated activated carbon
(GAC). GAC treatment methods are capable of
reducing levels to parts per trillion. Costs of this
method can range from $2.5-$3.5 million for the
initial installation in large water treatment facilities
(capable of 1mgd) with annual upkeep costs of
$100-$300K; similarly this can be done residentially
with initial installation costs of $5K and $1-$2K for
annual maintenance.[12]
1. Hu, C., Luo, Q. and Huang, Q. (2014), Ecotoxicological effects of perfluorooctanoic acid on freshwater microalgae Chlamydomonas reinhardtii and Scenedesmus obliquus.
Environmental Toxicology and Chemistry, 33: 1129–1134. doi: 10.1002/etc.2532
2. Steenland, K., & Woskie, S. (2012). Cohort mortality study of workers exposed to perfluorooctanoic acid. American Journal of Epidemiology, 176(10), 909-917.
doi:http://dx.doi.org/10.1093/aje/kws171
3. Savitz, David A. et al. “Relationship of Perfluorooctanoic Acid Exposure to Pregnancy Outcome Based on Birth Records in the Mid-Ohio Valley.”Environmental Health
Perspectives 120.8 (2012): 1201–1207. PMC. Web. 12 Dec. 2014.
4. Yang, Bei et al. “Involvement of Oxidative Stress and Inflammation in Liver Injury Caused by Perfluorooctanoic Acid Exposure in Mice.” BioMed Research International 2014 (2014):
409837. PMC. Web. 12 Dec. 2014.
5. Qingyu Huang, Jie Zhang, Francis L. Martin, Siyuan Peng, Meiping Tian, Xiaoli Mu, Heqing Shen, Perfluorooctanoic acid induces apoptosis through the p53-dependent mitochondrial
pathway in human hepatic cells: A proteomic study, Toxicology Letters, Volume 223, Issue 2, 25 November 2013, Pages 211-220, ISSN 0378-4274,
http://dx.doi.org/10.1016/j.toxlet.2013.09.002.
6. Weidong Zhang, Fengliang Wang, Pengfei Xu, Chen Miao, Xin Zeng, Xianwei Cui, Cheng Lu, Hui Xie, Hong Yin, Fei Chen, Jingjing Ma, Sheng Gao, Ziyi Fu, Perfluorooctanoic acid
stimulates breast cancer cells invasion and up-regulates matrix metalloproteinase-2/-9 expression mediated by activating NF-κB, Toxicology Letters, Volume 229, Issue 1, 17 August 2014,
Pages 118-125, ISSN 0378-4274, http://dx.doi.org/10.1016/j.toxlet.2014.06.004.
7. Theoharis Panaretakis, Irina G. Shabalina, Dan Grandér, Maria C. Shoshan, Joseph W. DePierre, Reactive Oxygen Species and Mitochondria Mediate the Induction of Apoptosis in
Human Hepatoma HepG2 Cells by the Rodent Peroxisome Proliferator and Hepatocarcinogen, Perfluorooctanoic Acid, Toxicology and Applied Pharmacology, Volume 173, Issue 1, 15
May 2001, Pages 56-64, ISSN 0041-008X, http://dx.doi.org/10.1006/taap.2001.9159. (http://www.sciencedirect.com/science/article/pii/S0041008X01991598)
8. Gloria B. Post, Perry D. Cohn, Keith R. Cooper, Perfluorooctanoic acid (PFOA), an emerging drinking water contaminant: A critical review of recent literature, Environmental Research,
Volume 116, July 2012, Pages 93-117, ISSN 0013-9351, http://dx.doi.org/10.1016/j.envres.2012.03.007. (http://www.sciencedirect.com/science/article/pii/S0013935112000904)
9. United States. Environmental Protection Agency .Perfluorooctanoic Acid (PFOA) and Fluorinated Telomers. 2012. Print. <http://www.epa.gov/oppt/pfoa/pubs/pfoainfo.html>.
10. United States. Agency for Toxic Substances and Disease Registry. Toxicological Profile for Perfluoroalkyls. Atlanta, GA : Agency for Toxic Substances and Disease Registry Division of
Toxicology and Human Health Sciences, 2009. Web. <http://www.atsdr.cdc.gov/toxprofiles/tp.asp?id=1117&tid=237>.
The Carbon Fluorine Bond is what gives PFOA it’s strong polarized
characteristics that also make it extremely persistent in the environment
and in humans.
•PFOA bioaccumulates in the natural environment. [1]
•Studies done on algae have shown that certain species of algae can readily absorb
the chemical. [1]
•Studied algae species showed an increase in proline and MDA levels and decrease
in cell density. [1]
•Fish are more susceptible to
PFOA as compared to
invertebrates, and it can
fully saturate water
(as compared to other PFCs),
which increases potency. [11]
•The chart to the right shows
the levels found of PFOA
hotspots in the environment,
measured in pg/L -1. [16]
PFOA exhibits poor biodegradability in the environment, which is also true for excretion
from organisms alike. PFOA shows no metabolism due to its strong carbon fluorine bonds.
It is primary excreted through urine in female mice, but for male mice, it is found in both
urine and feces. The renal clearance (CLR) is increased in female mice. When a male
mouse is castrated, the CLR increases. Treatment with testosterone lowered the CLR,
while the opposite occurred in the group treated with estrogen. It was found that organic
anion transporter 2 (OAT2) and OAT3 caused PFOA to be excreted, and these levels are
affected by testosterone and estrogen. Males in turn have a longer half life of PFOA in
their blood serum. [14]
•The EPA has established a provisional drinking water advisory for PFOA and PFOS of 0.4
and 0.2 µg/L.[9]
•ATSDR has not yet developed any Minimal Risk Level (MRL) values.[10]
•EPA has not developed a Reference Dose (RfD) or Reference Concentration (RfC)
•The EPA has not classified it as a carcinogen.[9]
•In 2006, EPA and the eight major companies in the industry launched the 2010/15 PFOA
Stewardship Program, in which companies committed to reduce global facility emissions and
product content of PFOA and related chemicals by 95 percent by 2010, and to work toward
eliminating emissions and product content by 2015. [9]
• PFOA can enter the water table
through a contamination plume.
• Air releases from industrial facilities
can deposit PFOA into the soil and
eventually groundwater.
• Some releases into well water have
occurred over 20 miles away from a
facilities’ smoke stocks.
• Other releases come from the
treatment of wastewater discharge and
storm water runoff. [8]
Studies on the effects during pregnancy have had no strong association between background
levels of PFOA and stillbirths, preterm births, and low birth weights.[2]
Some studies have suggested a probable relationship for the development of high cholesterol,
kidney cancer, and testicular cancer. [3]
Most epidemiological studies focus on the cohort of the workers in the DuPont facility and
prospective studies are in progress for the prognosis of the cohorts.
PFOA is a very persistent chemical that has become a part of our background. Its
effects are not entirely understood, but some scientific research has pointed to certain
toxic endpoints. Studies from the field suggest that PFOA likely targets the liver and
kidneys, and it may possibly induce testicular cancer. Other effects such as higher levels
of cholesterol have been reported. The good news is that PFOA is slowly being phased
out by major manufacturers, but more research will need to be done on the long term
effects. Some perfluorinated compounds (PFC’s) should be expected to have similar
effects in humans. Some of these chemicals include; perfluorooctane sulfonate (PFOS),
Perfluorooctanesulfonamide (PFOSA), Perfluorononanoic acid (PFNA), and
Perfluorooctanesulfonyl fluoride (POSF). There are currently no standards enforceable
that protect the workers or the environment. More awareness should be made so that in
the future we may have PEL’s and MCL’s.
11. Kyunghee Ji et al. Toxicity of Perfluorooctane Sulfonic Acid (PFOS) and Perfluorooctanoic Acid (PFOA) On Freshwater Macroinvertebrates and Fish Environmental Toxicology and Chemistry
Vol. 27, No. 102159-2168, 2008
12. Hartten, Andrew. "Water Treatment for PFOA and PFOS."Http://www.epa.gov/oppt/pfoa/pubs/Water Treatment Methods Hartten Oct16-09.pdf. DuPont, 16 Oct. 2009. Web. 13 Dec. 2014.
<http://www.epa.gov/oppt/pfoa/pubs/Water Treatment Methods Hartten Oct16-09.pdf>
13. Olson CT, Andersen ME; Toxicology Applied Pharmacology 70 (3):362-72 (1983)
14. USEPA, OPPT; Draft Risk Assessment of the Potential Human Health Effects Associated with Exposure to PFOA and Its Salts p.39-40 (Jan 4, 2005) (http://www.epa.gov/opptintr/pfoa/pfoarisk.pdf)
15. Yao, X, Zhong, L; Mutat Res 587 (1-2): 38-44 (2005)
16.Ahrens*, Lutz. "Polyfluoroalkyl Compounds in the Aquatic Environment: A Review of Their Occurrence and Fate." Journal of Environmental Monitoring (2010). J. Environ. Monit., 2011, 13, 20. Web. 15 Dec. 2014.
<file:///C:/Users/Brandon/Downloads/Ahrens - Review - PFASs aquatic environment - 2011 (1).pdf>.