Screening Assessment Perfluorooctanoic cheap nfl jerseys Acid

Information identified as archived on the Web is for reference, research or recordkeeping purposes. It has not been altered or updated after the date of archiving. Web pages that are archived on the Web are not subject to the Government of Canada Web Standards. As per the , you can request alternate formats on the page.Table of ContentsSynopsisIntroductionSubstance IdentityPhysical and Chemical PropertiesSourcesUsesReleases to the EnvironmentEnvironmental FatePersistence and Bioaccumulation PotentialPotential to Cause Ecological HarmPotential to Cause Harm to Human HealthConclusionReferencesAppendix 1: Summary of health effects information for PFOASynopsisUnder 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[1] 335 67 1, its salts and its precursors under sections 68 and 74 of CEPA 1999. The ammonium salt of PFOA and some precursors to PFOA, present on Canada Domestic Substances List (DSL), were categorized under section 73 of CEPA 1999. While PFOA itself is not on the DSL, PFOA can be formed in the environment through transformation or degradation from a variety of other perfluorinated chemicals. PFOA was identified for assessment based on 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). In this assessment, 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. PFOA and its salts are used as polymerization aids in the production of fluoropolymers and fluoroelastomers. PFOA, itself, is not manufactured in Canada; however, quantities of the ammonium salt are imported.EnvironmentPFOA 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. This assessment defines precursors as substances where the perfluorinated alkyl moiety has the formula CnF2n+1 (where n= 7 or and is directly bonded to any chemical moiety other than a fluorine, chlorine or bromine atom. 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.Once in the environment, PFOA is extremely persistent and not known to undergo significant further abiotic or biotic degradation under relevant environmental conditions. PFOA is highly soluble in water 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.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 (PFOA was detected in effluent from Canadian wastewater treatment facilities at concentrations ranging from 0.007 to 0.055 g/L. PFOA was also detected in the influent at US wastewater treatment facilities at concentrations ranging from 0.0074 g/L.Trace levels of PFOA have been measured in Canadian freshwater (ND g/L) and freshwater sediments (0.3 g/kg). PFOA has also been detected in a variety of Canadian biota (ND g/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 g/kg ww, followed by turbot liver at 26.5 g/kg ww, polar bear liver at 13 g/kg ww, caribou liver at 12.2 g/kg ww, ringed seal liver at 8.7 g/kg ww and walrus liver at 5.8 g/kg ww. Following an accidental release of fire fighting foam in Etobicoke Creek (Ontario), PFOA was measured in common shiner liver at a maximum concentration of 91 g/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 g/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 (1972 2002 and 1984 2006) and sea otters (1992 2002). 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, PFOA is present mainly in its ionic form in environmental media. Due to the perfluorination, the perfluorinated chains are both oleophobic and hydrophobic. PFOA primarily binds to albumin proteins in the blood of biota and, as a result, is present in blood and highly perfused tissues such as liver and kidney, rather than lipid tissue. The numeric criteria for bioaccumulation, outlined in the Persistence and Bioaccumulation Regulations of CEPA 1999, are based on bioaccumulation data for freshwater aquatic species (fish) only and for substances that preferentially partition to lipids. As a result, the criteria may not completely reflect the bioaccumulation potential 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 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 non aquatic 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 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 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 g/g of embryos. However, PFOA accumulated in the liver of these embryos to concentrations 2.9 4.5 times 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 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 20 mg/L increased the chemosensitivity in marine mussels. PFOA at 25.9 mg/L activated the mammalian peroxisome proliferator receptor (PPAR in the livers of Baikal seals PPAR 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. In 2 year carcinogenicity bioassays in rats, males administered a high dose of PFOA ammonium salt (APFO) in the diet had significantly higher incidences of adenomas of the liver hepatocytes, Leydig cells in the testes and pancreatic acinar cells. 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. There is some evidence to suggest that PFOA may be capable of causing indirect oxidative DNA damage.Human HealthIn humans, PFOA is well absorbed by all routes of exposure; it has not been demonstrated cheap jerseysto 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 or plasma) 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 g/mL) with the serum or plasma levels found in non occupationally exposed adults, infants, and children (0.00162 g/mL) results in margins of exposure greater than 660. These margins are considered to be adequately protective to account for uncertainties in the hazard and exposure databases. Based on the available information, it is concluded that PFOA, its salts and its precursors are entering or may be 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 addition, it is concluded that PFOA and its salts meet the criteria for persistence as set out in the Persistence and Bioaccumulation Regulations. PFOA and its salts do not meet the criteria for bioaccumulation as set out in the Persistence and Bioaccumulation Regulations. Nevertheless, the weight of evidence is sufficient to conclude that PFOA and its salts accumulate and biomagnify in terrestrial and marine mammals.Based on the available information on the potential to cause Wholesale NFL Jerseys harm to human health and the resulting margins of exposure, it is concluded 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.Therefore, based on available information for environmental and human health considerations, it is concluded that PFOA, its salts and its precursors meet one or more of the criteria set out in section 64 of CEPA 1999.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.Top of PageIntroductionThis screening assessment was conducted pursuant to sections 68 and 74 of the Canadian Environmental Protection Act, 1999 (CEPA 1999) (Canada 1999).A screening assessment was undertaken on perfluorooctanoic acid (PFOA) (Chemical Abstracts Service Registry Number 335 67 1) and its salts. In addition, precursors to PFOA were considered on the basis of their contribution to the total presence of PFOA and its salts. This assessment defines precursors as substances where the perfluorinated alkyl moiety has the formula CnF2n+1 (where n= 7 or and is directly bonded to any chemical moiety other than a fluorine, chlorine or bromine atom.The ammonium salt, CAS RN 3825 26 1, and the precursors, CAS RN 53515 73 4, CAS RN 678 39 7, CAS RN 65530 61 2, and CAS RN 70969 47 0 are on the Domestic Substances List (DSL) and were found to meet the ecological categorization criteria for persistence and/or bioaccumulation potential and/or inherent toxicity to non human organisms. However, none of these substances were considered to be a high priority for assessment of potential risks to human health, based upon application of the simple exposure and hazard tools developed by for categorization of substances on the Domestic Substances List.