Synopsis

Under the Canadian Environmental Protection Act, 1999 (CEPA 1999), the Ministers of the Environment and of Health have conducted a screening assessment of perfluorooctanoic acid (PFOA), Chemical Abstracts Service Registry Number 335-67-1, its salts and its precursors under sections 68 and 74 of CEPA 1999. Some of these substances were categorized in under section 73 of CEPA 1999. PFOA was also assessed due to its persistent nature, widespread occurrence in biota, presence in the Canadian Arctic due to long range transport, and international interest in emerging science indicating a potential concern for the environment and human health from PFOA and its salts. In addition, precursors to PFOA were considered in this assessment on the basis of their contribution to the total presence of PFOA and its salts in the environment.

PFOA is an anthropogenic substance belonging to a class of chemicals known as perfluorocarboxylic acids (PFCAs). PFCAs, in turn, belong to the broader class of chemicals known as perfluoroalkyls (PFAs). The term “PFOA” may refer to the acid, its conjugate base or its principal salt forms. Historical uses of PFOA include applications in industrial processes and in commercial and consumer products. It continues to be used as a reactive intermediate, with its salts used as processing aids in the production of fluoropolymers and fluoroelastomers. PFOA is not manufactured in Canada; however, quantities of the ammonium salt are imported.

PFOA may be found in the environment due to releases from fluoropolymer manufacturing or processing facilities, effluent releases from wastewater treatment plants, landfill leachates and due to degradation/transformation of PFOA precursors. Such precursors may include parent compounds, chemical products containing PFOA (either as part of formulations or as unintended residuals) and substances transforming to intermediates that ultimately degrade to PFOA. Potential precursors also include related fluorochemicals (e.g., fluorotelomer alcohols [FTOHs], fluorotelomer iodides and fluorotelomer olefins), some of which are currently used and detectable in the atmosphere and can degrade or transform to PFOA through biotic or abiotic pathways.

Once in the environment, PFOA is persistent and not known to undergo any further abiotic or biotic degradation under relevant environmental conditions. PFOA is highly water soluble and typically present as an anion (conjugate base) in solution. It has low vapour pressure; therefore, the aquatic environment is expected to be its primary sink, with some additional partitioning to sediment. The presence of PFOA in the Canadian Arctic indicates the long-range transport of PFOA (e.g., via ocean currents) or of volatile precursors to PFOA (e.g., via atmospheric transport).

PFOA has been detected at trace levels in the northern hemisphere. In North America, higher levels were measured in surface waters in the vicinity of US fluoropolymer manufacturing facilities (<0.025–1900 µg/L) and in groundwater near US military bases (not detected [ND] to 6570 µg/L). PFOA was detected in effluent from Canadian wastewater treatment facilities at concentrations ranging from 0.007 to 0.055 µg/L. PFOA was also detected in the influent at US wastewater treatment facilities at concentrations ranging from 0.0074––0.089 µg/L.

Trace levels of PFOA have been measured in Canadian fresh water (ND–11.3 µg/L) and freshwater sediments (0.3–7.5µg/kg). PFOA has also been detected in a variety of Canadian biota (ND–90 µg/kg wet weight [kg-ww] tissue) in southern Ontario and the Canadian Arctic. The highest concentration of PFOA in Canadian organisms was found in the benthic invertebrate Diporeia hoyi at 90 µg/kg-ww, followed by burbot liver at 26.5 µg/kg-ww, polar bear liver at 13 µg/kg-ww, caribou liver at 12.2 µg/kg-ww, ringed seal liver at 8.7 µg/kg-ww and walrus liver at 5.8 µg/kg-ww. Following a spill of fire-fighting foam in Etobicoke Creek (Ontario), PFOA was measured in common shiner liver at a maximum of 91 µg/kg-ww. However, current PFOA concentrations in Canadian biota (tissue specific and whole body) are below the highest concentration found in US biota (up to 1934.5 µg/kg-wwin gar liver).

Temporal or spatial trends in PFOA concentrations in guillemot eggs, lake trout, thick-billed murres, northern fulmars or ringed seals could not be determined. However, temporal trends were found for PFOA concentrations in polar bears and sea otters. PFOA doubling time in liver tissue was calculated to be 7.3 ± 2.8 years for Baffin Island polar bears and 13.9 ± 14.2 years for Barrow, Alaska, polar bears; central East Greenland polar bears showed an annual increase of 2.3% in PFOA concentrations. Concentrations of PFOA also increased significantly over a 10-year period for adult female sea otters.

Unlike other organic pollutants that are persistent and found in biota, certain perfluorinated substances, such as PFOA, are present mainly as ions in environmental media. Due to the perfluorination, the hydrocarbon chains are oleophilic and hydrophobic and the perfluorinated chains are both oleophobic and hydrophobic. PFOA primarily binds to proteins in biota and preferentially partitions to liver, blood and kidney rather than to lipid tissue. The numeric criteria for bioaccumulation, outlined in the Persistence and Bioaccumulation Regulations of CEPA 1999, are based on bioaccumulation data for aquatic species (fish) only and for substances that preferentially partition to lipids. As a result, the criteria do not account for the bioaccumulation of PFOA that is preferentially partitioning in the proteins of liver, blood and kidney in terrestrial and marine mammals.There is experimental evidence indicating that PFOA is not highly bioaccumulative in fish. Reported laboratory bioconcentration factors for fish species (primarily rainbow trout) ranged from 3.1–27. In the pelagic aquatic food web of Lake Ontario, two studies indicate that PFOA concentrations do not biomagnify with increasing trophic level. However, these results should not be extrapolated to other species, since gills provide an additional mode of elimination for PFOA that air-breathing organisms, such as terrestrial and marine mammals, do not possess. Field studies indicating biomagnification factors greater than 1 for Arctic and other mammals (such as narwhal, beluga, polar bear, walrus, bottlenose dolphins, and harbour seals) suggest that PFOA may bioaccumulate and biomagnify in terrestrial and marine mammals. Reported field biomagnification factors for terrestrial and marine mammals ranged from 0.03–31. Polar bears, as the apex predator in the Arctic marine food web, have been shown to be the most contaminated with PFOA relative to other Arctic terrestrial organisms.

In traditional toxicity studies, PFOA exhibits moderate to low acute toxicities in pelagic organisms, including fish (70–2470 mg/L). PFOA exhibits low chronic toxicities in benthic organisms (>100 mg/L). There is one study on the toxicity of PFOA and its salts in avian wildlife. In this study, PFOA was found to have no effect on embryonic pipping success for white leghorn chickens at concentrations up to 10 µg/g. However, PFOA accumulated in the liver of these embryos to concentrations greater than the initial whole-egg concentration

There are studies showing the potential for PFOA to affect endocrine function where visible effects may not be apparent until the organisms reach adulthood. In female and male rare minnows, 3–30 mg/L PFOA elicited inhibition of the thyroid hormone biosynthesis genes, induced vitellogenin expression in males, developed oocytes in the testes of male fish and caused ovary degeneration in females.

There are other studies showing hepatotoxicity, immunotoxicity, and chemosensitivity. For example, a PFOA concentration of 0.02 µg/L increased the chemosensitivity in marine mussels. PFOA at 25.9 mg/L, activated the mammalian peroxisome proliferator–activated receptor a (PPARa) in the livers of Baikal seals--PPARa plays a critical physiological role as a lipid sensor and a regulator of lipid metabolism. Field data also reveal that there may be increases in indicators of inflammation and immunity in bottlenose dolphins related to PFOA concentrations, suggesting possible autoimmune effects. Another field study has also suggested that low levels of PFOA may alter biomarkers of health in loggerhead sea turtles.

PFOA is persistent in all media in the environment and can bioaccumulate and biomagnify in terrestrial and marine mammals. Given these inherent properties of PFOA, together with environmental concentrations that may approach effect levels affecting endocrine function (including vitellogenin induction, feminization in male fish, ovary degeneration in female fish and hepatotoxicity), current temporal trends of PFOA in polar bears, the widespread occurrence of PFOA in biota, including in remote areas, and the fact that other PFCAs and precursors to PFOA may contribute to the overall additive or synergistic impact of PFOA in biota, it is proposed that PFOA, its salts and its precursors are entering the environment in a quantity or concentration or under conditions that have or may have an immediate or long-term harmful effect on the environment or its biological diversity.

In humans, PFOA is well absorbed by all routes of exposure; it has not been demonstrated to be metabolized and has a relatively long half-life. Salts of PFOA are expected to dissociate in biological media to produce the perfluorooctanoate (PFO) moiety, and are therefore considered toxicologically equivalent to PFOA. Low concentrations of PFOA have been identified in blood samples from non-occupationally exposed Canadians, including newborns, indicating environmental exposure to PFOA and/or compounds that can degrade to PFOA. The available data indicate that Canadians are exposed to PFOA and its precursors in the environment, including via air, drinking water and food; and from the use of consumer products, such as new non-stick cookware and perfluorinated compound (PFC)-treated apparel and household materials such as carpets and upholstery. Canadians are also potentially exposed to PFOA in utero and through lactational transfer. The relative contributions of PFOA and its salts and precursors to total PFOA exposure were not characterized; rather the focus was on aggregate exposure to the moiety of toxicological concern, PFOA.

Epidemiological studies have not identified a causal relationship between PFOA exposure and adverse health effects in humans. Therefore, toxicity studies in laboratory animals were used to determine the critical effects and associated serum levels of PFOA. Following oral dosing of PFOA ammonium salt (APFO), increased liver weight in mice and altered lipid parameters in rats were observed in short-term (14-day) toxicity studies; increased liver weight was noted in a 26-week toxicity study in monkeys; and increased liver weight in dams, alterations in fetal ossification and early puberty in male pups were found in a developmental toxicity study in mice.

In 2-year carcinogenicity bioassays in rats, males administered a high dose of APFO in the diet had significantly higher incidences of adenomas of the liver hepatocytes, Leydig cells in the testes and pancreatic acinar cells. No evidence of carcinogenic activity was seen in the female rats. Liver tumours in male rats may be induced via liver toxicity resulting from PFOA-induced peroxisome proliferation, and additional pathways secondary to peroxisome proliferation may be involved in the generation of tumours at other sites. As primates are much less suspectible than rodents to peroxisome proliferation, the PFOA-induced tumours in male rats are considered to have little or no relevance for humans. Although blood levels of PFOA were not determined in the chronic studies, the oral dose of APFO was several times higher than those in the critical short-term and subchronic studies. Although there is some evidence to suggest that PFOA may be capable of causing indirect oxidative DNA damage, the genotoxicity database indicates that PFOA is not mutagenic. Thus, as the tumours observed in male rats are not considered to have resulted from direct interaction with genetic material, a threshold approach is used to assess risk to human health.

The assessment of PFOA is based on a comparison of the margin between the levels of PFOA in the blood (serum) of humans and serum levels that are associated with the development of adverse effects in laboratory animals. This approach aggregates exposure to PFOA from all sources, including those resulting from releases from fluoropolymer manufacturing or processing facilities, effluent releases from sewage treatment plants, landfill effluents, or degradation/transformation of PFOA precursors.

Comparison of the PFOA serum levels associated with adverse effects in laboratory animals (13–77 µg/mL) with the serum levels found in non-occupationally exposed adults and in children (0.0034–0.010 µg/mL) results in margins of exposure of =1300. These margins are considered to be adequately protective to account for uncertainties in the hazard and exposure databases.

Based on the available information on the potential to cause harm to human health and the resulting margins of exposure, it is proposed that PFOA and its salts are not entering the environment in a quantity or concentration or under conditions that constitute or may constitute a danger in Canada to human life or health. Precursors of PFOA were not individually assessed, but were considered in terms of their contribution to total PFOA exposure because they can degrade to PFOA in the environment.

Based on available information for environmental and human health considerations, it is proposed to conclude that PFOA, its salts and its precursors meet one or more of the criteria set out in section 64 of CEPA 1999.

PFOA is highly persistent in the environment and meets the criteria for persistence as defined in the Persistence and Bioaccumulation Regulations. While there is scientific evidence that PFOA and its salts can accumulate and biomagnify in terrestrial and marine mammals, PFOA and its salts do not meet the criteria for bioaccumulation as defined in the Persistence and Bioaccumulation Regulations.

Where relevant, research and monitoring will support verification of assumptions used during the screening assessment and, where appropriate, the performance of potential control measures identified during the risk management phase.