DEQ-CFW_00002075

Health Consultation
3M CHEMOLITE
PERFLUOROCHEMICAL RELEASES AT THE
3M — COTTAGE GROVE FACILITY
CITY OF COTTAGE GROVE, WASHINGTON COUNTY, MINNESOTA
EPA FACILITY ID: MND006172969
FEBRUARY 18, 2005
U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES
Public Health Service
Agency for Toxic Substances and Disease Registry
Division of Health Assessment and Consultation
Atlanta, Georgia 30333
DEQ-CFW 00002075

Health Consultation: A Note of Explanation
An ATSDR health consultation is a verbal or written response from ATSDR to a specific
request for information about health risks related to a specific site, a chemical release, or
the presence of hazardous material. In order to prevent or mitigate exposures, a
consultation may lead to specific actions, such as restricting use of or replacing water
supplies; intensifying environmental sampling; restricting site access; or removing the
contaminated material.
In addition, consultations may recommend additional public health actions, such as
conducting health surveillance activities to evaluate exposure or trends in adverse health
outcomes; conducting biological indicators of exposure studies to assess exposure; and
providing health education for health care providers and community members. This
concludes the health consultation process for this site, unless additional information is
obtained by ATSDR which, in the Agency's opinion, indicates a need to revise or append
the conclusions previously issued.
You May Contact ATSDR TOLL FREE at
1-888-42ATSDR
or
Visit our Home Page at: http://www.atsdr.cdc.gov
DEQ-CFW 00002076

HEALTH CONSULTATION
3M CHEMOLITE
PEFFLUOROCHEMICAL RELEASES AT THE 3M — COTTAGE GROVE FACILITY
CITY OF COTTAGE GROVE, WASHINGTON COUNTY, MINNESOTA
EPA FACILITY ID: MND006172969
Prepared by:
Minnesota Department of Health
Under Cooperative Agreement with the
U.S. Department of Health and Human Services
Agency for Toxic Substances and Disease Registry
DEQ-CFW 00002077

U.S. Department of Health and Human Services
FOREWORD
This document summarizes public health concerns at a hazardous waste site in Minnesota. It is
based on a formal site evaluation prepared by the Minnesota Department of Health (MDH). For a
formal site evaluation, a number of steps are necessary:
• Evaluating exposure: MDH scientists begin by reviewing available information about
environmental conditions at the site. The first task is to find out how much contamination
is present, where it is found on the site, and how people might be exposed to it. Usually,
MDH does not collect its own environmental sampling data. Rather, MDH relies on
information provided by the Minnesota Pollution Control Agency (MPCA), the U.S.
Environmental Protection Agency (EPA), and other government agencies, private
businesses, and the general public.
• Evaluating health effects: If there is evidence that people are being exposed —or could be
exposed —to hazardous substances, MDH scientists will take steps to determine whether
that exposure could be harmful to human health. MDH's report focuses on public
health— that is, the health impact on the community as a whole. The report is based on
existing scientific information.
• Developing recommendations: In the evaluation report, MDH outlines its conclusions
regarding any potential health threat posed by a site and offers recommendations for
reducing or eliminating human exposure to contaminants. The role of MDH in dealing
with hazardous waste sites is primarily advisory. For that reason, the evaluation report
will typically recommend actions to be taken by other agencies —including EPA and
MPCA. If, however, an immediate health threat exists, MDH will issue a public health
advisory to warn people of the danger and will work to resolve the problem.
• Soliciting community input: The evaluation process is interactive. MDH starts by
soliciting and evaluating information from various government agencies, the individuals
or organizations responsible for cleaning up the site, and community members living near
the site. Any conclusions about the site are shared with the individuals, groups, and
organizations that provided the information. Once an evaluation report has been
prepared, MDH seeks feedback from the public. If you have questions or comments about
this report, we encourage you to contact us.
Please write to: Community Relations Coordinator
Site Assessment and Consultation Unit
Minnesota Department of Health
121 East Seventh Place / Suite 220 / Box 64975
St. Paul, MN 55164-0975
OR call us at. [phone] or 1-800-657-3908
(toll free call - press "4" on your touch tone phone)
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On the web: http://www.health.state.mn.us/divs/eh/hazardous/index.htmis
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Summary
3M produced perfluorochemicals (PFCs) at their Cottage Grove facility from the late 1940s until
2002 (on a pilot scale or in full production), using an electrofluorochemical process. PFC
products were produced, handled, used or packaged at several locations at the site. During
production, air emissions of PFCs occurred, and may have extended off the site property.
Wastes from the PFC production process were disposed in an on -site pit, and possibly in off -site
locations as well. Wastewater treatment plant effluent containing PFCs was discharged to the
adjacent Mississippi River for decades, and sludge from the wastewater treatment plant and
ponds that contained PFCs were also disposed on site. Fire -fighting foams containing PFCs
were also used at a fire -training area on the west side of the site.
The results of limited environmental monitoring to date indicate that groundwater beneath the
site is contaminated with perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA),
in some locations at levels significantly in excess of the MDH Health -Based Values (HBVs) for
groundwater. The full extent of the groundwater contamination has not been identified. Much
of the contaminated groundwater is contained and collected by an extensive system of
production wells, and is processed through the site wastewater treatment plant.- The plant has not
historically been able to remove the PFCs from the effluent. However, the recent (year) addition
of a large granular activated carbon treatment system has effectively eliminated PFC discharges
to the Mississippi River. An area of shallow groundwater contamination (in the D1 Area) is not
captured by the production wells, and likely discharges to the Mississippi River. The effects of
past discharges to the Mississippi River on surface water, sediments, or biota have not been
determined. Low levels of PFCs may also be discharged to the river by the adjacent Eagles
Point wastewater treatment plant.
Soil data for PFCs were not available for the site. Because of their physical properties, PFCs
may move easily with infiltrating water through some soil types, resulting in groundwater
contamination. The limited number of studies regarding PFC migration suggest that PFCs are
capable of entering groundwater from source areas (such as fire -training sites) and moving long
distances. Analysis of water samples for PFOS and PFOA from four private wells located just to
the east of the facility did not show the presence of either chemical. However, the wells are
completed a significant distance below ground, and are in a side -gradient direction in terms of
groundwater flow. The absence of PFCs in these wells does not rule out the possibility of PFC
contamination in groundwater on or off of the site as a result of aerial deposition of PFCs and
subsequent infiltration into groundwater, a transport mechanism that is thought to have occurred
at other PFC facilities in the US.
Workers at the site have been exposed to PFCs through their work activities and through the
facility's water supply. 3M has monitored workers at the facility for the presence of PFCs in
their blood since the 1970s. Studies of PFC concentrations in blood serum have shown
concentrations of PFOA of up to 115 parts per million (ppm). Epidemiological studies of
workers at Cottage Grove have shown little apparent impact of PFC exposure on worker
mortality. Epidemiological data for these chemicals is lacking for the general population.
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Studies of PFCs in blood samples from the general population have shown that PFCs are
ubiquitous in human blood, at concentrations much lower than seen in PFC production workers,
and are not age -dependent. The estimated half-lives of PFOS and PFOA in humans is on the
order of years. The source of exposure to PFCs in the general population is unclear, but is likely
through a number of pathways including food, water, use of consumer products, or other
environmental pathways. PFCs have also been found in the blood and tissues of various species
of wildlife from around the world. The highest concentrations have been observed in bald eagles
and mink in the Midwestern U.S. PFOS has been shown to bioconcentrate in fish.
Toxicological research on PFCs is ongoing. Animal exposure to PFCs at high concentrations
can have adverse effects on the liver and other organs, and has caused the death of test animals
(cynomolgus monkeys) for reasons that are not entirely clear. Exposure to high concentrations
of PFOA over long durations has been shown to cause cancer in some test animals, although
again the mechanisms are not clear. Developmental effects have also been observed in the
offspring of pregnant rats exposed to PFCs.
The potential impacts on public health from perfluorochemical releases from the 3M Cottage
Grove facility cannot be fully assessed by MDH at this time, because there are not sufficient
environmental data available regarding PFC impacts from the facility in soil, groundwater,
surface water, sediments, and biota. For this reason, MDH has recommended that additional
investigation take place. Understanding the contribution of individual sources of PFCs to the
environment is important, given the lack of information available about how the general
population is exposed to PFCs, the long half-life of PFCs in humans, and their potential for
toxicity based on animal studies. MDH will continue to work with the MPCA and 3M to
investigate and assess PFC releases from the 3M Cottage Grove facility.
1. Purpose
The manufacture and disposal of PFCs at the site has resulted in documented contamination of
groundwater at the site. Potential contamination of soil, and of surface water and sediments in
the adjacent Mississippi River remains to be investigated. Wastewaters containing PFCs were
discharged to the river. PFCs have been detected in multiple on -site monitoring and production
wells, and in the water supply system serving the facility. The Minnesota Pollution Control
Agency (MPCA) Superfund Program has been overseeing site investigation and cleanup
activities; because of other contamination issues the site was originally added to the Permanent
List of Priorities, the state Superfund List, in 1985. 3M has been conducting various
investigations and response actions under a consent order with the MPCA since that time. The
MPCA staff requested that MDH review site documents prepared to date, the results of
environmental monitoring conducted at the site, and information available on the toxicity of
PFCs and their behavior in the environment in order to develop conclusions and
recommendations regarding potential public health impacts from the site.
H. Background and History
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The 3M Company (formerly Minnesota Mining and Manufacturing Company) operates a facility
on approximately 865 acres in the city of Cottage Grove, Minnesota. The facility has been in
operation since 1947. The southeastern portion of the property has been used for a variety of
industrial operations such as the manufacture of adhesive products, industrial polymers, and
reflective road sign materials, and for research and development of similar products (Barr 1991).
The facility also includes a permitted hazardous waste incinerator used to treat wastes generated
at this and other 3M facilities. The remainder of the property has been for used recreation and
farming, or simply left in a natural state. The site has been known variously as the 3M Cottage
Grove Center and the 3M Chemolite Center. The location of the site is shown in Figure 1, and
the site layout is shown on a recent aerial photo in Figure 2. Note that 3M uses a numbering
system for the various buildings at the facility; the building numbers for the areas discussed in
this report are shown in Figure 2.
Perfluorochemicals (PFCs), primarily perfluorooctanoic acid (PFOA) and one of its salts,
ammonium perfluorooctanoate (APFO), as well as lesser amounts of related PFC products
derived from perfluorooctanesulfonyl fluoride (POSF) have been manufactured at the site since
approximately 1947 through an electrochemical flourination process known as the Simons
process (Abe and Nagase, 1982; Gilliland and Mandel 1993; Olsen et al 1998; 3M 1999a; -
Alexander 2001; OECD 2002). 3M voluntarily ceased production of PFCs at the site in 2002
(ERG 2004; 3M 2000a). Perfluorochemicals are a class of organic chemicals in which fluorine
atoms completely replace the hydrogen atoms that are typically attached to organic hydrocarbon
molecules (3M 2001a). Because of the very high strength of the carbon -fluorine bond, PFCs are
inherently stable, nonreactive, and resistant to degradation (3M 1999a). The PFCs manufactured
by 3M at the site were used in a variety of commercial and industrial products by 3M and other
companies, including stain repellents (such as Scotchgardrm), surfactants, fire retardants and
fire -fighting foams, and other chemical products.
The POSF production process through electrochemical flourination yields about 35%-40%
POSF, along with a mixture of byproducts and waste products of variable composition (3M
1999a; 3M 2000b). PFOA and its salts are typically produced in a similar fashion through a
batch process (3M 2000c; EPA 2002). Volatile wastes and byproducts were vented to the
atmosphere, and some byproducts were re -used in the manufacturing process. Waste tars from
the PFC production process were at times disposed in an on -site pit, or later incinerated.
Wastewaters containing PFCs from operations at the site have been discharged to the Mississippi
River. Although wastewater from the site is routed through an on -site wastewater treatment
plant prior to discharge to the river, many PFCs are resistant to treatment because of their
chemical stability. One of the byproducts of the production of POSF is perfluorooctane
sulfonate (PFOS), which is usually resistant to further degradation in the environment. It can
also be produced by the subsequent chemical or enzymatic hydrolysis of POSF. 3M estimated
that during POSF production at their Decatur, Alabama production plant, approximately 90% of
the wastes generated were in the form of solid wastes (incinerated or disposed in landfills), 9%
of the wastes were discharged as wastewater, and 1% in the form of air emissions (3M 2003b).
R
DEQ-CFW 00002082

Geology/Hydrogeology
The 3M Cottage Grove facility is underlain by fill materials and unconsolidated glacial deposits
of sand, gravelly sand, and gravel terrace deposits associated with the adjacent Mississippi
River. The thickness of these deposits ranges from approximately 20 feet in the northwest to
more than 200 feet at the southern end of the site and in the stream -cut ravines along the eastern
and western borders of the property. In the ravines, the upper bedrock formations have been
partially or completely removed by erosion.
Beneath the glacial deposits, the first bedrock formation is the Prairie du Chien Formation,
composed of dolomite (a magnesium -rich form of limestone). The upper portion of the Prairie
du Chien has abundant solution cavities, but the lower portion tends to be more massive.
Beneath the site, the bedrock has been uplifted on a series of faults and only the lower, more
massive portion of the Prairie du Chien is present. The Prairie du Chien Formation overlies the
Jordan Sandstone. Groundwater generally does not flow readily from the more massive, basal
Prairie du Chien into the Jordan Sandstone, except where there are fractures or solution cavities.
Beneath the Jordan Sandstone, the shaley St. Lawrence formation acts as a "confining layer" that
inhibits the downward migration of groundwater to the underlying Franconia Sandstone. The
cross-section in Figure 3 illustrates the geology underlying the site.
Two deeply incised glacial river valleys run from north to south along the eastern and western
edges of the site. Intermittent streams run through the valleys. Erosion along these stream
channels has created steep ravines on the southeast and southwest sides of the facility. A recent
study by Mossler (2003) indicates the presence of a series of faults oriented northeast -southwest
in this portion of Washington County, with associated minor faults oriented northwest -southeast.
A pair of intersecting faults is reportedly present beneath the site (see Figure 4). Analysis of
these fault systems by Barr Engineering (Barr, 2003) suggests there may be up to 50 feet of
vertical off -set on the faults on the 3M property (see Figure 5). The northwest -southeast trending
fault on the site appears to control the location of the stream valley in the southeastern portion of
the site, where the ravine turns abruptly southeast before discharging to the Mississippi River.
The surface of the ground water, or water table, ranges from 60 to 100 feet below the ground
surface and generally follows the surface topography. The water table is found in the glacial
deposits near the river, in the Jordan Sandstone near the river bluffs, and in the Prairie du Chien
Formation further from the river. The groundwater in the various formations is interconnected
and is essentially one unit. The normal groundwater flow direction (i.e. when not influenced by
pumping wells on -site) is towards the Mississippi River. Groundwater modeling by Barr (2003)
suggests the faults and fractures in this area may have some influence on the pathways
groundwater follows as it migrates toward the river. The model did not specifically evaluate
faults on the 3M property, however it would be expected that once groundwater enters the faults,
it likely flows parallel to the fault trace.
However, groundwater flow beneath the site is heavily influenced by the pumping of the
facility's high -capacity production wells. Some of these wells reportedly have been in operation
since the 1940s. In 2002, 3M reported pumping just over one billion gallons of water from the
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production wells on the property (DNR 2003). In previous years, an even larger amount of water
was pumped from the aquifers beneath the site.
In fact, most of the groundwater from beneath the majority of the 865-acre site, and especially
from the developed portion of the site, appears to be captured by the action of the production
wells as shown in Figure 6 (ERG 2004). This figure is from a past groundwater model for the
site developed for 3M. The source of the model, and the data and assumptions upon which it
was created, were not available at the time this document was written. For example, it is not
known whether the model incorporated pumping effects from the numerous nearby residential
wells or included geologic features such as the intersecting faults recently identified in this area.
These factors may affect the pathway of groundwater flow, but it is likely that most ground
water that migrates beneath the site is captured by the facility production wells and only a small
portion may discharge to the Mississippi River. One exception appears to be the southeastern-
most portion of the site, where Sites D 1 and D2 are located (see below). This area does not
appear to be within the capture zone of the production wells and the groundwater beneath this
area likely discharges to the Mississippi River.
As shown on Figure 7, there are approximately 100 private water supply wells located within
one mile of the 3M property boundary. Most private and public wells in the area for which there
is geologic information available are completed in the Jordan Sandstone. Because groundwater
flows primarily to the south-southeast toward the Mississippi River, it appears that no private or
public water supply wells on the north side of the river are located in areas downgradient of
contaminant source areas.
Superfund Site History
The investigation and remediation activities conducted at the site under the MPCA Superfund
program have generally centered around ten waste disposal areas originally identified by the
MPCA and 3M (MPCA 1998). These activities, which were conducted under a consent order
signed between the MPCA and 3M in 1985, were not focused on PFCs. The MPCA and 3M are
currently negotiating an addendum to the existing consent order that will focus on the
investigation of PFCs in all media at the site (David Douglas, MPCA, personal communication,
2004). The existence of the waste disposal areas (not all of which were related to PFC
manufacture) was a primary reason the site was added to the state Superfund list. The locations
of the waste disposal areas are shown in Figure 8. They are as follows:
Site D1: Hydrofluoric Acid Neutralization Pit
This site was used to neutralize hydrofluoric acid tars (containing unspecified fluorochemical by-
products and hydrofluoric acid) with lime. Neutralization was thought to have been done in a
concrete pit or vault, but this has not been confirmed. The tar materials in the pit were never
directly sampled and analyzed for PFCs; instead hydrofluoric acid tars from the PFC production
process were analyzed to determine if they were a hazardous waste as defined under federal and
state regulations. Trace concentrations of metals were identified in the tars, but the neutralized
tar material itself was considered to be non -hazardous. Although PFCs were detected in the
N.
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groundwater in this area, site D1 has not been fully characterized as to the magnitude or extent of
PFC contamination.
Site D2: Sludge Disposal Site
This area was used for the disposal of sediments and sludge dredged from on -site wastewater
treatment ponds, and may be up to four acres in size. Laboratory analysis of samples of the
sludge material found elevated concentrations of numerous fluorinated compounds (including
likely by-products of the PFC production process). Samples of the sludge and soil beneath the
sludge showed lower levels of several volatile organic compounds (VOCs). This area has not
been characterized with respect to PFCs.
Site D3: Ash Disposal Area
The location of this site was investigated using ground -penetrating radar, and no evidence of
waste materials was found.
Site D4: Phenolic Waste Pit
This site was used for the disposal of a small process wastewater stream from Building 7 for a
period of three years. The wastewater stream contained phenol and possibly formaldehyde. Part
of Building 26 was built on top of this site, limiting infiltration of water through the former pit.
While it was never formally investigated, it was believed that some biodegradation of the wastes
would have occurred, and the construction of the building over the site would serve as an
effective cap preventing human contact or migration of any remaining contaminants.
Site D5: Solids Burn Pit Area
This area is a concrete pit approximately 10 feet deep and 350 feet in diameter. 3M used the pit
to burn off -spec products such as glass, tape, rubber, adhesives, rags, paper, wood, fiberglass,
oily sludge material, plastics, and resins. The burning was occasionally fueled with waste
solvents. The area has since been covered with several feet of fill. Soil borings drilled in this
area found the presence of wastes, sludge, ash and cinders. Low levels of VOCs, such as
toluene, ethylbenzene, trichloroethylene, and methylene chloride were detected in several soil
samples collected from the borings; the area was subsequently given regulatory closure by the
MPCA.
Site D6: Active Ash Disposal Area
This area is an inactive, MPCA-permitted waste disposal area for boiler ash and incinerator
residues. Due to its permitted status, it has not been investigated under the Superfund program.
Site D7: Pit Burning Area
The history of this area is unclear. Three borings advanced in this area did not encounter waste
materials, and soil sample analysis did not detect the presence of heavy metals or VOCs.
Site D8: Waste Disposal Area
This area is located along the bluff leading down to the Mississippi River. A variety of
construction debris and other waste materials, including numerous drums, were disposed here by
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dumping them over the edge of the bluff. An Interim Remedial Action (IRM) at Site D8
involved the removal of approximately 200 drums and drum carcasses (rotted drums). The
drums were disposed in the on -site 3M incinerator. A composite sample of the soil beneath the
drums showed no VOCs, but polychlorinated biphenyls (PCBs) were found at elevated levels. A
composite sample of the waste materials in the drums contained various VOCs and PCBs. It is
not known if samples were analyzed for fluorochemicals. Due to the extreme topography of Site
D8, not all of the wastes were removed, and the site was covered and replanted.
Boiler Ash Fill Area:
This area is located on the western edge of the facility, in an area that is used for training on -site
fire fighting personnel and for testing fire -fighting products (see Figure 8). Boiler ash from a
coal-fired boiler, used to produce steam for heat and various industrial processes, was used for
fill in this area (Barr 1991). Soil borings drilled in this area showed the boiler ash fill to be
approximately one foot in thickness, and the volume was estimated at 850 cubic yards. Some of
the boiler ash was exposed at the ground surface. Laboratory analysis of a sample of surface
water that had pooled in the area showed elevated levels of metals, including antimony, arsenic,
nickel, and vanadium. The ash was determined to be non -hazardous, and the area was covered
with clean fill and vegetated.
Acrylic Acid Release Area:
In October of 1973, 3M discovered that approximately 17,000 gallons of acrylic acid had been
released from an underground storage tank (UST) located adjacent to Building 7 (Barr 1991).
The UST that was the source of the release was abandoned in 1986. This area was investigated
by 3M, and no further action was required by the MPCA because the acrylic acid was thought to
have degraded naturally.
Areas of PFC Production and Use
As stated previously, PFC production began (on a pilot scale) at the site around 1947; full-scale
commercial PFOA production reportedly began in 1976. POSF-derived chemical production
began in the 1960s. The main area for PFC production, storage, and testing was centered around
Buildings 7, 15, 16, and 25, which are shown in Figure 2 (ERG 2004). The production of PFCs
was phased out at the end of 2002. Wastes from the PFC production process were disposed in
Site Dl and possibly Site D8. Wastewaters containing PFCs were routed through the on -site
wastewater treatment plant before discharge to the river. Sludge from the wastewater treatment
plant was disposed at one time in Site D2. PFC containing fire fighting chemicals were also
tested on the west side of the facility in the area of Building 43.
In 2001, the chemical sewer lines running from various chemical production areas of the site to
the wastewater treatment plant were upgraded and replaced (ERG 2003). Excavation of the old
sewer pipes at the northeast corner of Building 15 (the PFC production plant) revealed that the
pipes were corroded and had leaked. The soils in the base and sidewalls of the excavation had a
strong phenolic odor. A composite sample of the sidewall soil showed low levels of metals,
VOCs (trichloroethene (TCE) and 1,1-dichloroethane) and phenolic compounds. 3M also
removed a portion of the interior floor from the northeast corner of Building 15 in response to
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concerns over possible damage to the building foundation from releases of hydrofluoric acid.
Soil samples were collected from borings placed around the interior trench. Analysis of the soil
samples showed very low levels of metals, and one semi -volatile compound (butyl benzyl
phthalate). The activities related to the sewer replacement in and around Building 15 indicate
that releases to the soil (and possibly groundwater) of chemicals used in the PFC production
process did occur while the PFC production plant was in operation. No analyses for PFCs
themselves were conducted, however, so it is not clear if PFCs are present in soil and
groundwater at Building 15.
In 1991, an air dispersion model was developed for VOC and inorganic emissions at the 3M
Cottage Grove facility (Pace 1991). The emission points modeled included two 48-foot stacks at
Building 15, the PFC production plant, where hydrogen fluoride emissions occurred. The
emission rate used in the model was 0.38 pounds of hydrogen fluoride per hour of operation,
with a stack exit velocity of 1,440 feet per minute at ambient (70° F) temperature. The horizontal
extent and the estimated concentrations of hydrogen fluoride (both the 1986 annual average and
the second highest 24-hour average in micrograms per cubic meter) predicted by the model are
shown in Figures 9a and 9b. The results of the air dispersion model indicate that hydrogen
fluoride emissions extended off -site in 1986.
The PFC production process would also have resulted in the release of some PFCs to the
atmosphere, as mentioned previously. 3M estimated that 1,950 pounds of PFOA compounds
were released to the air from vent stacks at the Cottage Grove facility in 1997, and that the
releases occurred between 100 to 200 days per year (3M 2000c). Presumably, at least some of
the PFOA compound releases to the air were from Building 15, or nearby buildings where PFCs
were produced, handled, or used. Fugitive emissions of PFOA (both vapor and particulate) were
also likely from the various operations, such as drum loading, reactor sampling, and drying
operations (3M 2000c). The physical properties of PFOA and other PFCs are different from
hydrogen fluoride, and their behavior once released to the air are likely to differ as a result.
However, the air dispersion model results for hydrogen fluoride emissions shown in Figures 9a
and 9b suggest that PFOA emissions (both particulate and vapor phase) from the Building 15
area may also have extended off the site property. Deposition of PFOA to the soil from these
emissions may also have occurred.
On -Site Groundwater Monitoring and Use
Since investigation activities at the site began, at least 21 permanent monitoring wells have been
installed at and around the site to evaluate groundwater quality (Figure 10). The monitoring well
identifiers, unique well numbers, depth, and general locations are as follows:
Well ID
Unique Well Number
Dept) th
Monitoring Well General Location
MW-1
233567
200
Northern site boundary
MW-2
233568
192
East side of site
MW-3
233569
210
Center of site
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MW-4
233570
200
South-central area of site
MW-5
233571
210
Northwest corner of site
MW-6
233572
219
West -central area of site
MW-7
233573
146
Northeast corner of site
MW-8
233574
173
Southwest area of site
MW-9
233575
104
West -central area of site
MW-10
233554
237
Southeast area of site
MW-11
233950
200
Southeast area of site
MW-12
233951
126
Southern edge -of site
MW-13
233952
126
Southeast area of site, near ponds
MW-14
421705
60
D8 Area, southern edge of site, near PW-6
MW-15
431237
186
Southern edge of site
MW-16
431238
140
Southern edge of site
MW-17
570322
112
West -central area of site
MW-18
570323
91
West -central area of site
MW-19
612713
62
West -central area of site
MW-101
680685
100
D1 Area, southeast corner of site
MW-102
680686
96
Dl Area, southeast corner of site
Since the facility opened in 1947, 3M has installed eight production wells to serve the facility's
potable water supply and to provide water for various industrial operations (Figure 10). They are
as follows:
Well ID
Unique
Well Number
Date
Completed
Depth
(feet)
Casing Diameter
(inches)
PW-1
231867
1947
205
20
PW-2
231868
1948
202
20
PW-3
231869
1956
224
16
PW-4
231870
1958
275
16
PW-5
231871
c.1960s
113
24
PW-6
229117
1970
143
24
PW-7
233576
c.1980s
200
Unk.
PW-8
424131
1986
208
8
Four of the eight production wells (PW-2 to PW-5) serve the potable water distribution system,
while two wells are used on a periodic basis for fire suppression (PW-1) and to supply non -
contact cooling water to the 3M waste incinerator (PW-6; ERG 2004). Of the remaining two
wells, PW-7 is used occasionally at the 3M on -site trap range and PW-8 supplies the guard
shack.
In the past, low levels of VOCs including TCE, 1,1,2-trichloroethane, 1, 1 -dichloroethane,
ethylbenzene, toluene, and methylene chloride have been detected in various monitoring and
production wells at the southern end of the facility, specifically MW-4, MW-14, PW-5, and PW-
12
DEQ-CFW 00002088

6, which are located in the vicinity of D8. Levels of these VOCs have only occasionally
exceeded health -based drinking water criteria in the individual monitoring wells, and the
distribution of the contaminants suggests that the sources of the VOC contamination are
localized and not extensive (ERG 2001a, ERG 2001b). The concentrations of individual VOCs
in PW-5, one of the wells that are used for the drinking water supply, have recently been less
than approximately one microgram per liter (µg/L). Such concentrations do not exceed
applicable regulatory or health -based standards for a'water supply system. The system is
regulated and monitored by MDH as a public water supply. Exposure to VOCs in groundwater
at the site does not appear to be a human health concern at this time.
PFC Monitoring at the Site
3M has been monitoring groundwater, production wells, the water distribution system, and
wastewater treatment plant effluent for PFCs (primarily PFOS and PFOA) for a number of years.
Data from monitoring wells, production wells, and the water distribution system are shown in
Table 1, while effluent data from the wastewater treatment plant are presented in Table 2. The
majority of the data is for PFOA alone, because it has been the focus of investigation activities at
the site being conducted by 3M under a voluntary agreement with EPA (3M 2001b). Some
samples were analyzed for PFOS, PFOA, and the 4-, 6-, and 7-carbon perfluorosulfonates and
other acids. The 4-, 5-, and 6- carbon PFCs were likely found in the groundwater because they
present in the PFC wastes that were disposed in several areas of the site. Much of the data were
collected only in 2001, so information on long-term trends in the PFC concentrations in
groundwater is not yet available.
The well monitoring results indicate that PFOS and PFOA are present in groundwater at the site
in the D1 area (MW-101 and MW-102) and the D8 area (MW-14, PW-5 and PW-6). Levels of
PFOS and/or PFOA exceed the MDH Health Based Values (HBVs) for PFOS and PFOA in
these wells, sometimes by a factor of 100 or more. The HBVs represent a level of a contaminant
in drinking water that MDH considers to be safe for human consumption over a lifetime. The
HBVs were developed by MDH based on review of available toxicological information as of
November 2002; neither the values themselves nor the toxicological inputs were derived by the
EPA. The HBV for PFOS is 1 µg/L; the HBV for PFOA is 7 µg/L. The derivation of the MDH
HBVs for these two compounds and their toxicological basis can be found in Appendix 1. MDH
has not developed HBVs for the other perfluorosulfonates and acids, mainly because of a lack of
available toxicological information.
Detectable levels of PFCs (in some cases slightly above the HBVs) were also found in: MW-4 at
the southern end of the facility on top of the bluff; PW-2 at the northern end of the facility; PW-4
northwest of the main facility; and in the water distribution system itself. The sample from the
distribution system was collected from the cafeteria in Building 116. A very low level of PFOA
(less than one µg/L) was also found in MW-7 northeast (and upgradient hydrogeologically) from
the main facility. Note that PFC data are not available for all of the monitoring and production
wells at the site. 3M has proposed to collect a coordinated round of groundwater sampling from
all of the available monitoring and production wells at the site. This would be very helpful in
characterizing PFC contamination in groundwater across the facility. The available data
13
DEQ-CFW 00002089

indicate, however, that groundwater in several areas of the site has been affected by past PFC
production or disposal practices. This in turn is affecting the water wells serving the facility.
A groundwater model found in the site files suggests that much of the contaminated groundwater
is likely captured by the pumping action of the production wells at the site, as shown in Figure 6,
with the exception of the D1 and D2 areas, located just southeast of the area shown in the figure.
The PFCs detected in the water distribution system lends support to this conclusion, although it
is not possible to evaluate the validity of this model because the underlying data and assumptions
used in its construction were not available at the time this document was written. Contaminated
groundwater in the D1 Area most likely discharges to the Mississippi River, either directly or
possibly via the intermittent stream in the ravine immediately north of the D1 Area.
The facility's water distribution system is used for potable water, and for various industrial
processes. Bottled water has been provided to employees for drinking water for some time,
however, and a GAC treatment system has been installed in the main cafeteria in building 116 to
treat water used in food preparation and cleanup. Wastewater from these uses is collected in
various sewer systems (see below) for treatment in the on -site wastewater treatment plant. The
wastewater therefore contains PFCs from the groundwater contamination, and any PFCs picked
up during the use of the water for production or other purposes throughout the plant.
Under its federal National Pollutant Discharge Elimination System (NPDES) permit
(MN000149) the effluent from the wastewater treatment plant is monitored before discharge to
the Mississippi River. Since 2000, 3M has regularly collected 24-hour composite samples of the
treated effluent for analysis for PFOA. Limited data is available back to 1996 (see Table 2).
Levels of PFOA have generally declined since 1996, with an overall high of 1,991 µg/L detected
in early 2000. With the phase out of PFOA production in late 2002, effluent concentrations of
PFOA and PFOS should continue to drop. 3M also installed a large granular activated carbon
(GAC) treatment plant at the site to remove organic contaminants (including PFCs) from the
wastewater treatment plant effluent before discharge to the Mississippi River. It should also be
noted that the effluent from a regional wastewater treatment plant (the Eagles Point plant,
operated by the Metropolitan Council) located essentially within the grounds of the 3M Cottage
Grove facility (see Figure 2) may also contain low levels of PFCs as has been found in limited
studies at other wastewater treatment plants in the U.S. (see page 23).
For most chemicals, aerial deposition of a contaminant is not typically a pathway for
groundwater contamination. However, given the physical properties and environmental behavior
of PFOA and other PFCs it is possible. Air emissions of PFOA and/or other PFCs at production
facilities in West Virginia and Alabama are suspected to have contributed to PFOA/PFC
contamination of soil and groundwater from those facilities, in addition to other releases (West
Virginia Dept. of Environment Protection 2003; Daikin 2004).
Because of the potential for past air emissions (and deposition) of PFOA to have extended off
site, in December 2003 MDH staff collected water samples from four private residential wells
located just east of the 3M Cottage Grove Facility for analysis for PFOA and PFOS by the MDH
14
DEQ-CFW 00002090

laboratory. The locations of the four residential wells are shown in Figure 11, along with the
approximate extent of air emissions of hydrofluoric acid predicted by the 1991 air model. All
four wells are relatively deep (approximately 220 feet below grade). The results of the
PFOA/PFOS analysis showed no detections of PFOA or PFOS above the laboratory detection
limits of 1.0 µg/L and 0.5 µg/L, respectively, in any of the four wells. However, the absence of
detectable PFOA or PFOS in the four deep wells sampled does not resolve the question of
whether surface deposition and subsequent infiltration has occurred. The MDH laboratory does
not have the ability to analyze for the 4-, 5-, or 6- carbon PFCs at this time.
Site Visit
On October 14, 2003 MDH staff visited the 3M Cottage Grove facility, along with
representatives of the MPCA Superfund program. MPCA staff arranged the site visit for the
purpose of becoming acquainted with the facility layout and areas of the facility where
perfluorochemicals (PFCs) were manufactured and used, and where PFC wastes were disposed.
3M facility and corporate staff conducted the site visit, along with their lead environmental
consultant for the facility (ERG).
The 865-acre site is located just south of the intersection of -US Highway 61 and Washington
County Road 19 in Cottage Grove, Minnesota, on the Mississippi River. Because the site is a
chemical plant, it is a secure facility with a full perimeter fence and controlled entry. The
facility is used for chemical manufacture, testing, product development, and for the incineration
of hazardous chemical wastes. To the east of the facility are a golf course and residential
development (River Oaks). To the south are the Burlington Northern Santa Fe Railroad main
line and the Mississippi River. To the west are a regional wastewater treatment plant (the Eagles
Point plant, operated by the Metropolitan Council), agricultural and rural residential land. To the
north are US 61, scattered homes, and a regional park.
The site visit focused on the following areas: the fire training area, production wells PW-5 and
PW-6, the PFC production area, the D 1 land disposal area, the wastewater treatment plant outfall
at the Mississippi River, and the wastewater treatment plant area.
Fire Training Area:
The fire training area is located below the main facility, near Building 43 (Figure 2). Facility
employees are trained here in fire fighting through various mock situations, such as a chemical
spill, a fire in a laboratory vent hood, or a leaking pipeline. Part of this area is underlain by a
gravel -covered concrete pad with drains leading to a lined holding pond. The area appears to
have been upgraded relatively recently. 3M staff indicated that the area was used for facility
staff training purposes and to test fire suppressants containing PFCs (ERG 2004).
Production Wells PW-5 and PW-6:
These two production wells are located on the southern edge of the facility, close to the
Mississippi River (see Figure 10). PW-5 feeds into the facility water distribution system, while
PW-6 is only used for non -potable cooling water for the incinerator. Both PW-5 and PW-6 have
detectable levels of PFCs, and a monitoring well located adjacent to PW-6 (MW-14) has
15
DEQ-CFW 00002091

elevated levels of PFCs. A disposal site (D8) was located on the hillside just above PW-6 and
MW-14. Apparently, construction debris and drums of waste materials were removed from this
location during the mid-1980s. The wastes had reportedly been dumped over the edge of the
hillside and buried sometime in the past. The main wastes identified at D8 were volatile organic
compounds (VOCs); it is not known if PFC wastes were present as well. 3M has agreed to
complete additional PFC monitoring in the area of PW-5 and PW-6.
PFC Production Area:
PFCs were produced in Building 15 for many years; the plant has now been shut down and is to
be decommissioned. PFCs were used in the production of other compounds in Buildings 7, 16,
and 25. These buildings are shown in Figure 2. Wastes from these processes were discharged to
buried sewer lines that ran to the on -site wastewater treatment plant. These buried sewer lines
have since been replaced with an upgraded system that is contained within a concrete trench
open to the ground surface. There are numerous stacks and vents in the PFC production and use
areas, and 3M staff confirmed that there were air emissions of chemicals (permitted by the
MPCA) from these stacks.
D 1 Area:
This area was used in the past for the disposal of PFC production wastes. It is located on the top
of a narrow peninsula of land that extends southeast from the rest of the facility (Figure 8). From
the top of the peninsula, the land drops off sharply to the south towards the railroad and
Mississippi River. To the north the land drops towards a ravine, through which the wastewater
treatment plant outfall stream runs. Another disposal site, D2, is located just west of D 1. Two
monitoring wells (MW-101 and MW-102) flank the D1 disposal site. These wells have shown
the highest levels of PFOS so far detected at the site, and are located slightly downhill from the
D1 area. According to 3M's consultant, no seeps or springs have been observed around the base
of the peninsula or in the stream.
Wastewater Treatment Plant Outfall:
The output of the wastewater treatment plant is piped to an intermittent stream that runs through
a ravine along the eastern edge of the facility. The output enters the stream through a pipe after
exiting the smallest (and last) treatment pond just west of the D2 and D 1 land disposal areas.
There is a permanent effluent monitoring point there as well. Stormwater is also discharged at
this point when necessary. The stream enters a small pond just north of the railroad tracks,
passes under the railroad track bridge, and enters the Mississippi River, as shown in Figure 2.
The stream is very clear, and vegetation and small fish could be readily observed in it.
Wastewater Treatment Plant:
The current wastewater treatment plant consists of various settling basins, biologic treatment
vessels, and filters to handle four of the five waste streams at the facility (sanitary, organic
wastes, inorganic wastes, and the incinerator process wastewater). Stormwater is not usually
routed through the treatment plant, but can be in the event of a spill or accidental release. At the
end of the treatment process the wastewater is piped into a series of holding ponds before
discharge to the river, as described above.
16
DEQ-CFW 00002092

3M has constructed a large granular activated carbon (GAC) treatment plant to augment its
wastewater treatment operations and remove PFCs from the wastewater treatment plant effluent.
The efficiency of the GAC for removing the PFCs from the waste stream has so far been in
excess of 99%. The GAC treatment plant consists of 18 large GAC treatment vessels that are the
final treatment step for the combined waste streams from the sanitary sewer, organic wastes, and
inorganic wastes. A subset of the treatment vessels will be used specifically for treating the
incinerator wastewater stream. The existing treatment ponds are to be abandoned and filled,
with the exception of the largest one, which has been refurbished with a synthetic liner and will
be used as a backup storage pond when needed.
Off -site Water Use and Samling
As noted in the "Geology/Hydrology" section, there are approximately 100 private and
commercial wells located within one mile of the 3M property boundary. In addition, the well
field for the City of Cottage Grove is located approximately 1.5 miles northwest of the 3M
property, and the well field for the City of Hastings is located approximately the same distance
to the southeast, across the Mississippi River. Water samples from four residential wells located
immediately east -of the site were analyzed for PFOS and PFOA by the MDH lab (see Figure 11).
Neither compound was detected in the sampled wells.
Public Comments
On June 24, 2004 a draft version of this document was released for public comment. Comments
were received from EPA, MPCA, Washington County, the City of Cottage Grove, and 3M. The
comments are attached as Appendix 2.
EPA provided several general comments, as well as suggestions as to specific language to
describe EPA's ongoing work with the perfluorochemical industry to investigate the sources,
fate, and transport of PFCs in the environment. EPA did not review the document for
toxicological accuracy, in part because a draft risk assessment for PFOA is not due until late
2004. The specific comments and suggestions made by EPA were incorporated into the
document. The MPCA comments were mostly general in nature; MDH staff have addressed
them by clarifying the text in several places described in the comments, including the description
of past investigations at the site and the status of the consent order between the MPCA and 3M.
Washington County's comments generally were in the form of recommendations to 3M for
further investigation or disclosure of information relative to releases of PFCs and VOCs at the
site. As the county's comments appeared to reinforce MDHs own recommendations and
statements made in the text of the document, no further changes were made to the document
itself as a result. The City of Cottage Grove comment letter simply expressed support for the
recommendations made in the draft Health Consultation, including the need for continued
monitoring.
3M submitted extensive comments on each section of the document. General comments from
3M on the conclusions and recommendations did not result in significant changes by MDH.
17
DEQ-CFW 00002093

Specific comments regarding the text of the document were helpful in that they clarified certain
historical facts regarding PFC production and disposal at the site; changes were made to reflect
these comments. 3M provided missing information relative to certain monitoring and production
wells at the site. 3M also provided several useful toxicological references that were not
available at the time the document was first written, and these references have been included.
Specific comments on toxicological issues were addressed with the major exception of the
comments on the potential for developmental effects from exposure to PFOS (see 3M comments,
page 12 in Appendix 2). This comment was apparently in response to MDH's statement on page
20 of this document that MDH may consider developmental effects when reviewing the current
HBV for PFOS. Because MDH is not currently reviewing the PFOS HBV, this comment was
not addressed.
III. Discussion
Perfluorochemicals (PFCs), primarily perfluorooctanoic acid (PFOA; C81715O211) and one of its
salts, ammonium perfluorooctanoate (APFO; C8F15O2NH4), as well as lesser amounts of other
PFCs such as perfluorooctanesulfonyl fluoride (POSF; C$F17SO2F) have been manufactured or
used at the site since 1947. One of the byproducts of the production of POSF is perfluorooctane
sulfonate (PFOS; C8F17SO3 ), which can also be produced by the subsequent chemical or
enzymatic hydrolysis of POSF. These chemicals are used by 3M and other companies around
the world in the production of stain repellents, lubricants, fire retardants and suppressants, and
pesticides, and as industrial surfactants and emulsifiers.
The chemical structures of PFOA and PFOS make them extremely resistant to breakdown. As a
result, they are persistent once released to the environment. On the basis of its physical
properties, PFOS is essentially non-volatile, and would not be expected to evaporate from water
(OECD 2002). If discharged to air (such as during production of POSF) it will rapidly deposit to
soil and due to its low sorption tendency, once in soil it tends to remain there with the major loss
due to run-off to surface water (DMER 1999). Infiltration of water could also carry it into the
subsurface or into groundwater, however. In soil -water mixtures, PFOS has a strong tendency to
remain in water due to its solubility (typically 80% in water and 20% in soil). PFOS does not
easily adsorb to sediments, and is expected to be mobile in water at equilibrium (3M 2003b).
PFOA is slightly more volatile than PFOS, although it still has a very low volatility and vapor
pressure (EPA 2002). PFOA is very soluble and completely disassociates in water; in aqueous
solution it may loosely collect at the air/water interface and partition between them (3M 2003a).
In limited studies, PFOA has shown a high mobility in some soil types (EPA 2002). In an
attempt to estimate the potential for long-range transport of PFOA released to the air, Franklin
(2002; unpublished report on EPA's PFOA web site) stated that PFOA emitted to the air is likely
to undergo dry or wet deposition within a few days, but could under certain conditions travel a
distance of up to 800 kilometers from the source.
In a study of PFCs in groundwater at a former military fire -training site in Michigan, Moody et
18
DEQ-CFW 00002094

al (2003) found PFOS concentrations up to 120 µg/L and PFOA as high as 105 µg/L near the
original concrete pad used for the training. Concentrations of PFOS and PFOA in excess of the
MDH HBVs were found in groundwater as far away as 500 meters from the pad. The facility
was used for fire -training from 1952 until the early 1990s, and fire fighting foams containing
PFCs were routinely used in training exercises. The results of the study indicate that PFCs in
aqueous solution are easily capable of migrating into groundwater. They can travel extended
distances with little or no retardation of the contaminants through adsorption to the aquifer
substrate, and can persist for years after they were used at the ground surface. The 3M site
contains a similar fire -training area where fire fighting foams containing PFCs were reported to
have been used (ERG 2004). While the site studied by Moody et. al. has some similarities to the
3M fire -training site, actual site characteristics will determine the potential for PFCs to enter the
groundwater and migrate away from the site. This has not yet been evaluated at the 3M fire -
training site.
Because of the recent widespread interest in PFC compounds such as PFOS and PFOA, a great
deal of toxicological, epidemiological, and environmental monitoring information has been
published in government and industry reports and in peer -reviewed literature. Much of this
research has been funded or conducted by 3M. Most recently, an analysis of the potential risk to
the general population from exposure PFOA was published by Butenhoff et al (2004), and 3M
has produced an updated environmental and health assessment of PFOS (3M 2003b). The
following represents a brief summary of available information.
Summary of Toxicological Information
Animal studies have shown that PFOA and APFO (its ammonium salt) are easily absorbed
through ingestion, inhalation, and dermal contact (EPA 2002; Kennedy 1985; Kennedy et al
1986; Kudo and Kawashima 2003). PFOS is also well absorbed orally, but is not absorbed well
through inhalation or dermal contact (OECD 2002). In the past, workers at the 3M Cottage
Grove facility were occupationally exposed to PFOA, and it is believed that dermal absorption of
PFOA was significant (EPA 2002). Once absorbed, APFO disassociates to the PFOA anion.
Both PFOA and PFOS are distributed and found mainly in the blood serum, liver and kidney
(EPA 2002; Kudo and Kawashima 2003; OECD 2002). PFOA and PFOS are not metabolized,
and are excreted in the urine and feces at different rates in various test animal species and
humans. There also appear to be significant gender differences in excretion rates for PFOA in
rats, but these differences have not generally been observed in higher animals and humans. The
estimated half-life of PFOA in animals ranges from four hours in female rats and nine days in
male rats to hundreds of hours in dogs (Kudo and Kawahima 2003). Half-lives of PFOS have
been estimated at over 100 days in rats in a single -dose study, and 200 days in a sub -chronic
dosing study in cynomolgus monkeys (OECD 2002). In a limited study of retired 3M workers,
the mean serum half-life of PFOA was estimated to be 4.37 years, and the mean half-life of
PFOS was estimated at 8.67 years (EPA 2002; OECD 2002).
Exposure to high levels of PFOA and PFOS is acutely toxic in test animals (Kudo and
Kawashima 2003; OECD 2002). Chronic or sub -chronic exposure to lower doses of PFOA in
rats typically results in reductions in body weight and weight gain, and in liver effects such as an
19
DEQ-CFW 00002095

increase in liver weight and alterations in lipid metabolism (Kudo and Kawashima 2003). The
liver appears to be the primary target organ of PFOA toxicity in rats, although effects on the
kidneys, pancreas, testes, and ovaries have also been observed (EPA 2002). The effects on the
liver may be more severe in aged rats (Badr and Birnbaum, 2004). Exposure to PFOA in rats
results in a phenomenon in the liver known as peroxisome proliferation. This phenomenon is
limited to rats and similar test animals, and is not observed in primates (or humans). Some of the
adverse liver effects observed in rats (such,as an increase in liver weight) that are in part
attributed to peroxisome proliferation may not be seen in higher animals. Adverse liver effects
in higher animals are likely the result of a different mode of action.
A 90-day study of relatively high -dose oral PFOA exposure in rhesus monkeys resulted in
adverse effects on the adrenal glands, bone marrow, spleen, lymphatic system, and death in some
animals (EPA 2002). A six-month study of oral PFOA exposure in male cynomolgus monkeys
exposed to different doses of APFO showed toxicity (primarily to the liver) at even the lowest
doses studied. Extreme toxicity was observed at the highest exposure level, prompting a
modification of the dosage to prevent the death of the test animals (Butenhoff et al 2002). Even
with the dosage adjustment, one test animal at the highest dose became extremely ill and had to
be sacrificed. A similar condition developed in one of the lowest dose group animals. The
toxicological mechanism for the apparent extreme adverse reaction in these two animals is
unknown. A steady-state concentration of PFOA in the serum was reached within four to six
weeks after dosing began; mean serum PFOA concentrations ranged from 77 parts per million
(ppm) in the low dose group to 158 ppm in the high dose group (Butenhoff et al 2002). This
study did demonstrate that the dose -response characteristics of APFO in this species of monkey
are very steep — indicating that a small increase in dose can be associated with a significant
increase in the number or severity of adverse effects.
Exposure studies of PFOS in rats have also demonstrated effects on the liver, weight loss, and
death, with a steep dose -response curve for mortality observed (OECD 2002). In studies of
PFOS exposure in rhesus monkeys, adverse effects included anorexia, convulsions, a marked
decrease in serum cholesterol, and adrenal effects. Similar effects were observed in studies of
cynomolgus monkeys. The adverse effects were no longer observed after a 52-week recovery
period, and in fact some recovery was noted much earlier.
Some long-term animal studies suggest that exposure to PFOA (and possibly PFOS) could
increase the risk of cancer of the liver, pancreas, and testes (Kudo and Kawashima 2003, EPA
2002, OECD 2002). The mechanism of potential carcinogenesis is unclear, but evidence
suggests that the cancers are the result of tumor promotion (via oxidative stress, cell death, or
hormone -mediated mechanisms) and not from direct damage to the genetic material within cells
(genotoxicity). The tumors observed in rats may be a result of peroxisome proliferation, and
may not be seen in higher animals or be of relevance in humans (Kennedy et al 2004).
Various reproductive studies of rats followed for two generations showed postnatal deaths and
various developmental effects in offspring of female rats exposed to relatively low doses of
PFOS and APFO (EPA 2002, OECD 2002). These studies demonstrate that exposure to
20
DEQ-CFW 00002096

APFO/PFOA and PFOS can result in adverse effects on the offspring of rats exposed while
pregnant.
At the request of the MPCA, in November 2002 MDH developed Health -Based Values (HBVs)
for drinking water for PFOS and PFOA of 1 ppb and 7 ppb, respectively, based on existing
toxicological information (liver toxicity; see Appendix 1). The HBVs represent a level of a
contaminant in drinking water that MDH considers to be safe for human consumption over a
lifetime. The HBV documentation in Appendix 1 states that reproductive and developmental
effects occur at levels higher than doses associated with liver toxicity. However, recent studies
on PFOS (Thibodeaux et al 2003; Lau et a12003) suggest that developmental effects may also be
of concern. These recent studies may lead MDH to examine developmental toxicity as a
possible basis for the PFOS HBV, which could result in a different HBV for PFOS. MDH is
awaiting further information or guidance from EPA before initiating a review of the HBVs for
PFOS and PFOA. Note that MDH is also in the process of revising all HRLs to more directly
account for childhood exposures, and this change could result in the lowering of all HBVs by a
factor of three or four (see Appendix 1).
Also at the request of the MPCA, MDH staff developed interim Soil Reference Values (SRVs)
for both PFOS and PFOA of 40 ppm and 200 ppm, respectively. The SRVs are soil evaluation
criteria for protection of people from direct contact with contaminated soil through ingestion,
skin contact, and inhalation of vapors and/or contaminated soil particles. Soil concentrations at
or below the SRV are considered to be safe.
Summar�of Epidemiological Data
The 3M Company has conducted a medical monitoring program of employees engaged in the
manufacture of perfluorochemicals since at least the 1970s. The company initially measured
total serum organic fluorine. In the mid-1990s, the company began measuring serum PFOA and
PFOS when such analyses became available (Olsen et al 1998; Olsen et a12003a; Olsen et al
2003b). A study of 3M employees at its Decatur, Alabama PFC manufacturing facilities showed
a mean serum PFOS concentration of 1.32 parts per million (range 0.06 to 10.06 ppm) and a
mean serum PFOA concentration of 1.78 ppm (range 0.04 to 12.70 ppm) in 263 employees. The
mean concentrations in employees at 3M's Antwerp, Belgium facility were approximately 50%
less (Olsen et al 2003b). There was no association between serum PFOS and PFOA
concentrations and decreased serum cholesterol (or other common biological parameters)
observed in this group of employees such as has been observed in animal studies. Exposure to
PFOS and PFOA has been shown in test animals (including primates) to interfere with
cholesterol metabolism and alter (usually lower) serum lipid and cholesterol concentrations.
A separate study of reproductive hormones in male 3M employees occupationally exposed to
PFOA at the Cottage Grove facility showed no significant linear association between serum
PFOA concentration and the measured hormones, although mean concentrations of one hormone
(estradiol) were 10% higher in those employees (five in all) with a serum PFOA concentration
above 30 ppm (Olsen et al 1998). This association was confounded by a high body mass index
in the five employees, however. Serum PFOA concentrations in this study ranged from 0 to 115
21
DEQ-CFW 00002097

ppm for the Cottage Grove workers. The higher serum PFOA concentrations observed in some
workers in this study suggests that occupational exposures to PFOA at the Cottage Grove facility
were higher than at the Decatur and Antwerp facilities, and/or that the exposures were of a
longer duration. No association between serum estradiol and serum PFOA levels was observed
for workers in 3Ms Decatur and Antwerp facilities.
Mortality of employees at the Cottage Grove facility has also been the subject of several
epidemiological studies (Gilliland and Mandel 1993; Alexander 2001). In the earlier study,
Gilliland and Mandel (1993) reported that the overall standardized mortality ratios (SMR) for
2,788 male and 749 female employees who worked at the facility for at least six months between
1947 and 1983 were 0.77 and 0.75, respectively (a value significantly below the expected rates).
The SMR represents the ratio of the observed deaths in a study population over the expected
deaths in a study population based on death rates in a non -exposed population of similar
characteristics. This phenomenon, where the overall SMR is significantly below the expected
rate for a similar, non -exposed population, is sometimes referred to as the "healthy -worker
effect" in occupational studies. The study findings did show that male employees who worked
in the PFOA production area for greater than 10 years had a 3.3-fold increase in mortality from
prostate cancer. However, the low number of prostate cancers (four) in this group makes the
findings tentative, and a later study by the same lead author (Olsen et al 1998) reported that only
one of the four cases of prostate cancer occurred in a worker directly engaged in PFOA
production. A separate study of workers at the 3M Decatur, Alabama facility who were
primarily exposed to POSF/PFOS also showed an overall low SMR for all causes of death, but a
higher than average risk of death from bladder cancer. This was due to three cases observed,
again meaning that the findings may not be repeatable (Alexander et al 2003). There is no
current toxicological evidence that suggests that the bladder is a critical target organ of PFOS
(3M 2003b).
In a later study at Cottage Grove, Alexander (2001) looked at the mortality of 3,992 workers
employed at the facility for at least one year prior to the end of 1997. The cohort was divided
into three exposure groups based on their work history: definite PFOA exposure, probable PFOA
exposure, and no PFOA exposure. It should be noted that, given the past exposure by workers to
PFC contamination in the facility water supply, there may have been some exposure to PFOA
even in the "no PFOA exposure" group. The results of this study showed that the overall SMR
for all causes of death (0.85) for the workers was again well below the expected rate. No
increase in prostate cancer was observed in this later study, but deaths from cerebrovascular
disease were elevated in the definite PFOA exposure group. Once again, the low number of
cases of cerebrovascular disease in this group (five) makes the findings tentative and difficult to
interpret. Taken together, the results of these studies (three different findings of slightly elevated
disease -different in each study - based on small numbers of cases) do not represent
epidemiological findings of significance.
PFOS, PFOA, and other perfluorochemicals have been detected in human blood serum from
adults and children in the general population at levels from 1/100 to 1/1000 of those seen in
workers (Olsen et al 2003c, Olsen et al 2003d, 3M 2001c). In a study of 645 adult donor serum
22
DEQ-CFW 00002098

samples from six Red Cross donation centers across the U.S., PFOS concentrations ranged from
<4.1 ppb (the limit of detection) to 1,656 ppb. No substantial differences in PFOS
concentrations in serum were observed with age of the donor. Serum PFOA concentrations
ranged from <1.9 ppb to 52.3 ppb. A preliminary study of sera from 599 children ages 2-12
years from 23 different states showed PFOS concentrations ranging from 6.7 to 515 ppb, and
PFOA concentrations ranging from <1.92 to 56.1 ppb. A study of elderly people in the Seattle
area showed similar PFOS and PFOA serum concentrations compared to the rest of the
population that has been studied so far (Olsen et al 2004). The source(s) of exposure to PFOS,
PFOA, and other perfluorochemicals in the general population is unclear, but could include
consumer products, environmental exposures, or other occupational exposures (3M 1999c).
Analysis of blood samples collected in the early 1950s from army recruits show no PFOS (3M
1999c). Both PFOS and PFOA have been detected in samples of dust collected from household
vacuum cleaner bags in Japan, indicating the indoor environment is a potential source of
exposure (Moriwaki 6t al 2003).
Based on animal studies and available human epidemiological data for PFOA concentrations in
blood serum, in a preliminary report in 2003 the EPA calculated a margin of exposure (MOE)
range for PFOA for women of childbearing age and children of between 66 and 9,125 (EPA
2003). The MOE describes the relative difference between current measured human PFOA
serum levels and serum levels determined in animal studies to be associated with adverse
developmental effects. There are numerous uncertainties in such calculations as a result of intra-
and interspecies differences, dose metrics used, and the choice of the animal model; EPA advises
that they must be interpreted cautiously. The preliminary EPA report also may have seriously
underestimated the serum PFOA concentrations in the rat study used to derive the MOE, making
the low end, of the MOE range too low. In a recent evaluation of the risk of PFOA exposure to
the general population, Butenhoff et al (2004) calculated a MOE of between 1600 and 8900 for
various toxicological endpoints, with a mean of 2100 based on the mean serum PFOA
concentration in general population data. For PFOS, 3M has calculated a MOE range for non -
occupationally exposed people of 310 to 1550 based on PFOS serum levels measured in the
human population (3M 2003b).
Sumrnary of Environmental Data
PFOS has been detected in the plasma and tissues of wildlife from across the globe, including
seals, otters, dolphins, aquatic birds, bald eagles, polar bears, freshwater and saltwater fish, and
reptiles (Giesy and Kannan 2001). The results of this study show that PFOS is widely
distributed in the global environment. Levels of PFOS were higher in fish -eating and predatory
animals than in their typical prey, indicating that PFOS may bioaccumulate as it moves up the
food chain. Bald eagles from the Midwestern U.S. showed the highest levels of PFOS in plasma
(up to 2,570 nanograms per milliliter), and mink from the Midwestern U.S. showed the highest
levels in tissue (in liver; up to 3,680 nanograms per gram). Concentrations of other PFCs in
wildlife samples, such as PFOA, are typically approximately ten times lower and are much less
widely distributed (Giesy et a12001).
Broader studies have found detectable levels of PFOS in surface waters, fish and bird blood and
23
DEQ-CFW 00002099

livers, and human blood collected in Japan, with the highest levels observed in the waters and
fish from heavily industrialized Tokyo Bay (Taniyasu et al 2003). A decreasing gradient of
PFOS levels in aquatic invertebrates and two species of fish in an estuary and the North Sea was
observed with distance from the port of Antwerp, Belgium (Van de Vijver et al 2003; Hoff et al.
2003). 3M operated a PFC manufacturing plant in Antwerp.
Estimated bioconcentration factors for PFOS in fish range from 200 to 1,124 in bluegills and
carp (OECD 2002). Studies of APFO and PFOA have estimated that bioconcentration factors
are quite low (1.8 in fathead minnows). Therefore, in contrast to PFOS, PFOA does not
bioconcentrate through the food chain (EPA 2002).
In the United States, 3M researchers _conducted a study of PFOA and PFOS levels in the
Tennessee River both upstream and downstream of its facility in Decatur, Alabama (Hansen et al
2002). Analysis of 40 water samples showed that low levels of PFOS were present throughout
the 80-mile section of the river studied. Concentrations increased from an average of 32 +/- 11
parts per trillion (ppt) upstream of the PFC manufacturing facility in Decatur to an average of
114 +/- 19 ppt downstream. Concentrations of PFOA were below the laboratory detection limits
(25 ppt) upstream of the Decatur facility, but averaged 394 +/- 128 ppt downstream of the
facility. The relatively consistent concentrations of PFOS and PFOA found in the Tennessee
River suggest that there are no significant removal mechanisms (such as volatilization or
adsorption to sediment) affecting their presence in the water. Boulanger et. al. (2004) studied
PFOS and PFOA concentrations in sixteen water samples collected from Lake Erie and Lake
Ontario. PFOS concentrations ranged from 21— 70 ppt (mean 43 +/- 18 ppt) in the two lakes,
while PFOA concentrations ranged from 27 — 50 ppt (mean 39 +/- 9 ppt). These concentrations
were higher than those observed in the Tennessee River upstream of the 3M facility in Decatur
Ongoing studies (coordinated mainly by 3M) are designed to determine PFC concentrations in
drinking water, food products, sediments, wastewater treatment plant effluent, sewage sludge,
and landfill leachate in a number of cities across the U.S. (Battelle 2000; OECD 2002, EPA
2002). Four cities where PFCs are manufactured or used (supply cities), and two control cities
were initially targeted. PFOS concentrations in wastewater treatment plant effluent ranged from
0.041 to 5.29 ppb while PFOA concentrations ranged from 0.040 ppb to 2.42 ppb. In dried
treatment plant sludge the PFOS concentrations ranged from 0.2 ppb to 3,120 ppb and PFOA
concentrations were from non -detect to 244 ppb. Drinking water samples showed maximum
PFOS and PFOA concentrations of 0.063 ppb and 0.029 ppb, respectively; landfill leachate
ranged from non -detect to 53.1 ppb for PFOS and non -detect to 48.1 ppb for PFOA. Surface
waters ranged from non -detect to 0.138 ppb for PFOS and from non -detect to 0.083 ppb for
PFOA; sediments ranged from non -detect to 1.13 ppb for PFOS and from non -detect to 1.75 ppb
for PFOA. Data from the control cities were generally at the lower end of these ranges, with a
few exceptions. More than 200 food product samples (green beans, apples, pork, milk, chicken,
eggs, bread, fish, and ground beef) were also collected. PFOS was only detected in five samples,
(one ground beef and four milk samples), at a maximum concentration of 0.852 nanograms per
gram (ng/g). Only one of the four milk samples was from a control city, with the remainder from
supply cities. PFOA was detected at concentrations up to 2.35 ng/g in two ground beef samples
from control cities, two bread samples (from one control and supply cities), two apple samples
24
DEQ-CFW 00002100

(supply cities), and one green bean sample from a supply city.
ERG, on behalf of 3M, has proposed a workplan conducting a facility -wide investigation of PFC
releases at the site (ERG 2004). The purpose of the workplan is to:
• Define the extent and magnitude of on -site contamination resulting from the past site
waste disposal practices of PFCs;
• Define the hydrology and geology of the site and the potential routes of exposure; and
• Provide information and data needed for consideration of response actions.
The workplan involves the collection of historical information on PFC production, use, and
disposal, including releases to the environment, summarizing all available information regarding
groundwater monitoring and production wells on the site. It also involves preparation of a
groundwater flow model, and collection of groundwater samples for PFC analysis from all wells
on the site. A further step will be to collect groundwater samples near the Mississippi River
using push -probes in locations where PFCs were used or disposed, and finally preparation of a
summary report.
EPA's Office of Pollution Prevention and Toxics, through an enforceable consent agreement
(ECA) process undertaken with various manufacturers and users of PFCs (including 3M) and
other interested parties, has been studying the extent, distribution, and fate of PFCs (primarily
PFOA) in the environment associated with the manufacture, use, or disposal of PFCs or PFC
containing products. All documents related to this undertaking are posted and available on. an
EPA web site (www.epa.gov/edocket/) under docket number OPPT-2003-0012.
In this ECA process, EPA identified several needs for monitoring information, including
monitoring in the vicinity of facilities currently manufacturing, processing, and using various
PFCs. Three companies — 3M, Dyneon (a 3M company), and DuPont — participating in this
process have indicated a willingness to enter into Memoranda of Understanding (MOU) with the
EPA for monitoring on and around their respective fluoropolymer manufacturing facilities
located in Decatur, Alabama and Washington, West Virginia. These MOUs are currently being
negotiated. A fourth company, Daikin America, is undertaking an independent, voluntary
monitoring program at its fluoropolymer manufacturing facility, which is co -located with the
3M/Dyneon plant in Decatur, Alabama. The 3M Cottage Grove facility has not been included in
this effort to date because it is no longer producing PFOA on a commercial basis (M.F.
Dominiak, EPA, personal communication, 2004). The phased -approach monitoring plan
proposed by 3M for the 3M/Dyneon plant in Decatur, Alabama involves the following (in no
particular order; Weston 2004):
• Monitoring of groundwater wells and plant effluent (on and off -site);
• Monitoring of surface water, sediments, aquatic organisms and fish in the adjacent
Tennessee River;
• Air dispersion modeling of PFC emissions;
• Soil sampling (on and off -site);
25
DEQ-CFW 00002101

• Sampling of terrestrial vegetation and vertebrates (on and off -site); and
• Monitoring of aquatic avian biota (on and off -site).
Some of the proposed monitoring has already been conducted, with other work proposed for
2004 and 2005. The results of the studies will be provided to EPA when completed. Similar
monitoring (including air monitoring for PFCs) has been proposed for other PFC manufacturing
sites. The proposed scope of this monitoring plan is broader than the scope proposed by ERG
for the 3M Cottage Grove facility. Due to business data privacy concerns, the relative sizes of
the two facilities in terms of the production quantities of PFCs are not available from 3M.
However, there are many apparent similarities in terms of overall PFC production, site layout,
past on -site waste disposal, discharge of PFC containing wastes to a major waterway (the
Tennessee River in Decatur and the Mississippi River in Cottage Grove), and the length of time
PFCs were produced (40+ years at Decatur and as many as 50 years at Cottage Grove). Based
on these factors, a similar, phased scope of investigative work for the 3M Cottage Grove site
may be needed to properly assess the potential impact of decades of PFC production and waste
disposal. Some aspects of the Decatur workplan may not be applicable to the Cottage Grove
facility. The MPCA has also stated that PFC production wastes from the Cottage Grove facility
may have been disposed at other known 3M waste disposal sites in the Twin Cities area (MPCA
2004). If so, there is a potential for PFCs to have affected various media (soil, groundwater, or
surface water) in these locations as well.
Child Health Considerations
ATSDR and MDH recognize that the unique vulnerabilities of infants and children make them of
special concern to communities faced with contamination of their water, soil, air, or food.
Children are at greater risk than adults from certain kinds of exposures to hazardous substances
at waste disposal sites. They are more likely to be exposed because they play outdoors and they
often bring food into contaminated areas. They are smaller than adults, which means they
breathe dust, soil, and heavy vapors close to the ground. Children also weigh less, resulting in
higher doses of chemical exposure per body weight. The developing body systems of children
can sustain permanent damage if toxic exposures occur during critical growth stages. Most
importantly, children depend completely on adults for risk identification and management
decisions, housing decisions, and access to medical care.
Because the site is a secure chemical production and waste disposal facility, children are very
unlikely to have been exposed to PFCs at the site itself. There are currently no data available to
determine if children could have been exposed to PFCs off of the site property. If air emissions
of PFCs extended off the site property, children who may have been living in areas beyond the
site boundaries could have been exposed while production was occurring, or could be exposed
through other environmental media. PFCs have been detected in blood samples of children from
at least 23 different states.
IV. Conclusions
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DEQ-CFW 00002102

The potential impacts on public health from perfluorochemical releases at the 3M Cottage Grove
facility cannot be fully assessed by MDH at this time, because there are not sufficient
environmental data available regarding PFC impacts from the facility in soil, groundwater,
surface water, sediments, and biota. At this time perfluorochemical releases from the site
represent an indeterminate public health hazard. There is a lack of information about how the
general population is exposed to PFCs. PFCs have a long half-life in humans and animal studies
indicate a potential for toxicity to the liver and effects on reproduction and development.
V. Recommendations
1. Consideration should be given to developing and implementing a scope of investigation
work that is generally similar to that developed by 3M for the Decatur, Alabama facility
under their proposed voluntary agreement with the EPA (see pages 23-24). Some aspects
of the Decatur workplan may not be applicable to the Cottage Grove facility, so a phased
approach is recommended. The data from such an investigation are needed to understand
the extent of PFC contamination from the facility in all media, and to assess its potential
impact on public health.
2. 3M should continue to take action to ensure that workers at the Cottage Grove facility are
not exposed to PFCs through the facility water supply at concentrations in excess of the
MDH HBVs (currently being implemented by 3M).
3. While releases of PFCs to the Mississippi River are now being generally prevented by the
installation of GAC treatment, 3M should continue to identify and reduce (or eliminate
where possible) any other potential ongoing discharges of PFOS and PFOA to the
environment from the facility.
4. Information should be gathered by 3M regarding any off -site locations where PFC
processing wastes from the site were disposed in the past, and appropriate steps should be
taken to investigate possible PFC releases from those locations.
VI. Public Health Action Plan
MDH's Public Health Action Plan for the site consists of continued consultation with MPCA
staff on the investigation of PFC releases at the site, distribution of this report, possible
additional private well sampling, and participation in any planned public outreach activities.
Preparers of Report:
James Kelly, M.S.
Health Assessor
Site Assessment and Consultation Unit
Minnesota Department of Health
tel: [phone]
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DEQ-CFW 00002103

Virginia Yingling
Hydrogeologist
Site Assessment and Consultation Unit
Minnesota Department of Health
tel: [phone]
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DEQ-CFW 00002104

VH. References
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February 5, 1999.
3M 1999b. Fluorochemical Use, Distribution, and Release Overview. 3M Company, St. Paul,
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3M 1999c. Perfluorooctane Sulfonate: Current Summary of Human Sera, Health, and
Toxicology Data. 3M Company, St. Paul, Minnesota. January 21, 1999.
3M 2000a. Correspondence from William A. Weppner, 3M Company, to Charles Auer, US
Environmental Protection Agency. June 16, 2000.
3M 2000b. Voluntary Use and Exposure Information Profile — Perfluorooctane Sulfonic Acid
and Various Salt Forms. 3M, St. Paul, Minnesota. April 27, 2000.
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Pollution Prevention and Toxics. August 1, 2003.
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report, 3M Company Medical Department, St. Paul, Minnesota. June 25, 2001.
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Office of Pollution Prevention and Toxics. August 1, 2003.
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Salts. 3M Company, St. Paul, Minnesota. August 20, 2003.
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perfluorinated organic compounds of industrial interest. In: Banks, R.E., editor. Preparation,
properties, and industrial applications of organofluorine compounds. New York: John Wiley &
Sons; 1982. p. 19-43.
Alexander, B.H. 2001. Mortality Study of Workers Employed at the 3M Cottage Grove Facility.
(unpublished).
Alexander, B.H., Olsen, G.W., Burris, J.M., Mandel, J.H., and Mandel, J.H. 2003. Mortality of
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employees of a perfluorooctanesulphonyl fluoride manufacturing plant. Occupational and
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senescent rats by the peroxisome proliferator-activated receptor alpha agonist perfluorooctanoic
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Areas, 3M Chemolite Center. Barr Engineering Company, August 1991.
Barr 2003. Cottage Grove Nitrate Study Report. Prepared Barr Engineering for Washington
County, October 2003.
Battelle 2000. Design and Structure of Multi -City Study. Battelle Memorial Institute,
Columbus, Ohio. May 1, 2000.
Boulanger, B., Vargo, J., Schnoor, J.L., and Hornbuckle, K.C. 2004. Detection of
perfluorooctane surfactants in Great Lakes water. Environmental Science and Technology 38:
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Butenhoff, J., Costa, G., Elcombe, C., Farrar, D., Hansen, K., Iwai, H., Jung, R., Kennedy, G.,
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L.R. 2004. Characterization of risk for general population exposure to perfluorooctanoate.
Regulatory Toxicology and Pharmacology 39: 363-380.
Daikin 2004. Letter to Charles M. Auer, U.S. EPA, from Satoshi Doi, Daikin America, Inc.
January 28, 2004.
DMER 1999. Letter to Dr. Rich Purdy, 3M and Dr. Joyce Cooper, Battelle. D. Mackay
Environmental Research, Ltd., Peterborough, Ontario, Canada. April, 1999.
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http://www.dnr.state.mn.us/waters/watenngmt section/appropriations/wateruse.html. Minnesota
Department of Natural Resources, St. Paul, Minnesota.
ERG 2001a. Correspondence from Paul Book, Environmental Resource Group, LLC, to Mark
Rys, MPCA. January 30, 2001.
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Douglas, MPCA. July 17, 2001.
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ERG 2003. 3M Cottage Grove Chemical Sewer Replacement Environmental Oversight Report.
Environmental Resource Group, LLC. September 9, 2003.
ERG 2004. Facility -wide Fluorocarbon Investigation Work Plan — 3M Cottage Grove.
Environmental Resource Group, LLC. January 27, 2004.
EPA 2002. Revised Draft Hazard Assessment of Perflourooctanoic Acid and its Salts. U.S.
Environmental Protection Agency, Office of Pollution Prevention and Toxics. November 4,
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EPA 2003. Preliminary Risk Assessment of the Developmental Toxicity Associated with
Exposure to Perflourooctanoic Acid and its Salts. U.S. Environmental Protection Agency,
Office of Pollution Prevention and Toxics. April 10, 2003.
Franklin, J. 2002. Screening Assessment of the Potential for Long -Range Atmospheric
Transport of Perfluorooctanoic Acid. James Franklin, Solvay Research & Technology. March
24, 2002. Accessed at www.0a.gov/edocket/. OPPT-2003-0012-0183.
Giesy, J.P., and Kannan, K. 2001. Global distribution of perfluorooctane sulfonate in wildlife.
Environmental Science and Technology 35: 1339-1342.
Giesy, J.P., Kannan, K., and Jones, P.D. 2001. Global biomonitoring of perflourinated organics.
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production plant. Journal of Occupational Medicine 35: 950-954.
Hansen, K.J., Johnson, H.O., Eldridge, J.S., Butenhoff, J.L., and Dick, L.A. 2002. Quantitative
characterization of trace levels of PFOS and PFOA in the Tennessee River. Environmental
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perfluorooctanoic acid (PFOA), perfluorooctane sulphonic acid (PFOSA) and clofibric acid.
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Hoff, P.T., Van de Vijver, K., Van Dongen, W., Esmans, E.L., Blust, R., and De Coen, W.M.
2003. Perfluorooctane sulfonic acid in bib (Trisopterus luscus) and plaice (Pleuronectes
platessa) from the western scheldt and the Belgian North Sea: distribution and biochemical
effects. Environmental Toxicology and Chemistry 22: 608-614.
Kennedy, G.L. 1985. Dermal toxicity of ammonium perfluorooctanoate. Toxicology and
Applied Pharmacology 81: 348-355.
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Kennedy, G.L., Hall, G.T., Britelli, M.R., Barnes, J.R., and Chen, H.C. 1986. Inhalation
toxicity of ammonium perfluorooctanoate. Food Chemistry and Toxicology 24: 1325-1329.
Kennedy, G.L., Butenhoff, J.L., Olsen, G.W., O'Connor, J.C., Seacat, A.M., Perkins, R.G.,
Biegel, L.B., Murphy, S.R>, and Farrar, D.G. 2004. The toxicology of perfluorooctanoate.
Critical Reviews in Toxicology 34: 351-384.
Kudo, N. and Kawashima, Y. 2003. Toxicity and toxicokinetics of perfluorooctanoic acid in
humans and animals. The Journal of Toxicological Sciences 28: 49-57.
Lau, C., Thibodeaux, J.R., Hanson, R.G., Rogers, J.M., Grey, B.E., Stanton, M.E., Butenhoff,
J.L., and Stevenson, L.A. 2003. Exposure to perfluorooctane sulfonate during pregnancy in rat
and mouse. H: postnatal evaluation. Toxicological Sciences 74: 382-392.
MPCA 1998. Site Evaluation Checklist & Summary. Eric Porcher, Minnesota Pollution Control
Agency, St. Paul, Minnesota. February 9, 1998.
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Memorandum from David Douglas to Bruce Brott. Minnesota Pollution Control Agency, St.
Paul, Minnesota. February 5, 2004.
Moody, C.A., Hebert, G.N., Strauss, S.H., and Field, J.A. 2003. Occurrence and persistence of
perfluorooctanesulfonate and other perflourinated surfactants in groundwater at a fire -training
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341-345.
Moriwaki, H., Takata, Y., and Arakawa, R. 2003. Concentrations of perlfuorooctane sulfonate
(PFOS) and perfluorooctanoic acid (PFOA) in vacuum cleaner dust collected in Japanese homes.
Journal of Environmental Monitoring 5: 753-757.
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Organization for Economic Cooperation and Development. November 21, 2002.
Olsen, G.W., Gilliland, F.D., Burlew, M.M., Burris, J.M., Mandel, J.S., and Mandel, J.H. 1998.
An epidemiologic investigation of reproductive hormones in men with occupational exposure to
perfluorooctanoic acid. Journal of Occupation Environmental Medicine 40: 614-622.
Olsen, G.W., Logan, P.W., Hansen, K.J., Simpson, C.A., Burris, J.M, Burlew, M.M., Vorarath,
P.P., Venkateswarlu, P., Schumpert, J.C., and Mandel, J.H. 2003a. An occupational exposure
assessment of a perfluorooctanesulfonyl fluoride production site: biomonitoring. Journal of the
American Industrial Hygiene Association 64: 651-659.
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Olsen, G.W., Burris, J.M., Burlew, M.M., and Mandel, J.H. 2003b. Epidemiologic assessment
of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA)
concentrations and medical surveillance examinations. Journal of Occupation Environmental
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Olsen, G.W., Hansen, K.J., Stevenson, L.A., Burris, J.M., and Mandel, J.H. 2003c. Human
donor liver and serum concentrations of perfluorooctanesulfonate and other perfluorochemicals.
Environmental Science and Technology 37: 888-891.
Olsen, G.W., Church, T.R., Miller, J.P., Burris, J.M., Hansen, K.J., Lundberg, J.K., Armitage,
J.B., Herron, R.M., Medhdizadehkashi, Z., Nobiletti, J.B., O'Neill, E.M., Mandel, J.H., and
Zobel, L.R. 2003d. Perfluorooctanesulfonate and other fluorochemicals in the serum of
American Red Cross adult blood donors. Environmental Health Perspectives 111: 1892-1901.
Olsen, G.W., Church, T.R., Larson, E.B., van Belle, G., Lundberg, J.K., Hansen, K.J., Burris,
J.M., Mandel, J.H., and Zobel, L.R. 2004. Serum concentrations of perfluorooctanesulfonate and
other fluorochemicals in an elderly population from Seattle, Washington. Chemosphere 54:
1599-1611.
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Inorganic Emissions. Pace, Incorporated. May, 1991.
Taniyasu, S., Kannan, K., Horii, Y., Hanari, N., and Yamashita, N. 2003. A survey of
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humans from Japan. Environmental Science and Technology 37: 2634-2639.
Thibodeaux, J.R., Hanson, R.G., Rogers, J.M., Grey, B.E., Barbee, B.D., Richards, J.H.,
Butenhoff, J.L., Stevenson, L.A., and Lau, C. 2003. Exposure to perfluorooctane sulfonate
during pregnancy in rat and mouse. I: maternal and prenatal evaluations. Toxicological Sciences
74: 382-392.
Van de Vijver, K.I., Hoff, P.T., Van Dongen, W., Esmans, E.L., Blust, R., and De Coen, W.M.
2003. Exposure patterns of perfluorooctane sulfonate in aquatic invertebrates from the western
scheldt estuary and the southern North Sea. Environmental Toxicology and Chemistry 22: 2037-
2041.
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Groundwater Investigation Steering Team Report. August, 2003.
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Plant for PFOA. Weston Solutions, Inc., West Chester, PA. February 2004.
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CERTIFICATION
This 3M Cottage Grove Health Consultation was prepared by the Minnesota Department of
Health under a cooperative agreement with the Agency for Toxic Substances and Disease
Registry (ATSDR). It is in accordance with approved methodology and procedures existing at
the time the health consultation was begun.
Jeff Kellam
Technical Project Officer, CAT, SSAB, DHAC
ATSDR
The Division of Health Assessment and Consultation, ATSDR, has reviewed this public health
consultation and concurs with the findings.
Roberta Erlwein
Chief, Cooperative Agreement Team, SSAB, DHAC, ATSDR
DEQ-CFW 00002110

Appendix 1
Derivation of MDH Health -Based Values and
Soil Reference Values for PFOS and PFOA
DEQ-CFW 00002111

m
Date: November 20, 2002
To: Douglas Wetzstein
Dave Douglas
From: Helen Goeden, Health Risk Assessment Unit
Phone: [phone]
Subject: Response to Request for Health Based Values and interim Soil Reference Values
This memorandum is in response to a request by the Minnesota Pollution Control Agency (08/21/02)
for Health Based Values (HBVs) and interim Soil Reference Values (SRVs) for perfluorooctanoic
acid (PFOA) and perfluorooctane sulfonate (PFOS).
There is limited published information on the toxicity of PFOA and PFOS. The MDH relied heavily
on readily available toxicity summary information provided by 3M, EPA and the West Virginia
Department of Environmental Protection. After reviewing this information the MDH modified the
RfD and RfC values proposed by 3M.
Health Based Values (HBVs)
Chemical CAS # Endpoint
PFOA 3825-26-1 Liver
PFOS 2795-39-3/ Liver
1763-23-1
Soil Reference Values (SRVs)
Chemical CAS# Endpoint
PFOA 3825-26-1 Liver
PFOS 2795-39-3/ Liver
1763-23-1
Toxicity Value Sources: See Attachment H.
RfD
(mg/kg/d)
0.001
0.0002
MW
µPS
RfD
RfC
Residential
Industrial
(mg/kg/d)
(mg/m3)
SRV (ma/kg)
SRV (mg/kg)
0.001
2E-5
30
200
0.0002
2E-5
6
40
Based on information currently available we feel that the above values will provide an adequate level of protection
from exposure to PFOA and PFOS in drinking water and direct exposure to PFOA or PFOS in soil; however, there is
a degree of uncertainty associated with the HBVs and SRVs, and they should be considered provisional. The above
criteria do not address impacts to groundwater as a result of soil leaching, food chain impacts or ecological impacts.
Please note that carcinogenicity studies in the rat have shown PFOA and PFOS to be potentially carcinogenic. However,
at this time the available data are not sufficient to determine relevance to humans or for development of cancer potency
values.
Environmental Health Division - 121 E. 7'b Place, P.O. Box 64975, St. Paul, MN, 55164-0975 - [phone]
http://www.healtb.state.mn.us
DEQ-CFW 00002112

The data utilized in the derivation of the HBVs is provided in Attachment I. Standard assumptions of a 70 kilogram
person with a drinldng water ingestion rate of 2 liters per day, and a relative source contribution of 20 percent were used
to calculate these values.
MDH is in the process of revising its Health Risk Limits for groundwater rule. The MDH is likely to recommend that
the standard assumptions of 70 kilograms and 2 liters/day be replaced by a body weight and an intake rate more
appropriate for children. If this recommendation is accepted and promulgated as rule, HBVs would likely decrease by
a factor of 3 to 4.
The data utilized in the derivation of the SRVs is provided in Attachment II. The default exposure scenarios and target
risk values presented in the MPCA's Draft Guidelines for the Soil -Human Health Pathway, Technical Support Document
(Working Draft, January 1999) were utilized to calculate these values.
The MDH's authority to promulgate health risk limits under the Groundwater Protection Act is limited to situations
where degradation has already occurred. Similarly, the HBVs and SRVs provided are intended to serve as interim advice
issued for specific sites where a contaminant has been detected. As such, neither the HBVs nor SRVs are developed for
the purpose of providing an upper limit for degradation.
cc: Larry Gust, MDH
Anne Kukowski, MDH
Jim Kelly, MDH
Gerry Smith, MDH
Shelley Burman, MPCA
Luke Charpentier, MPCA
Mary Dymond, MPCA
Laura Solem, MPCA
Michael Santoro, 3M
John Butenhoff, 3M
Environmental Health Division • 121 E. 7' Place, P.O. Box 64975, St. Paul, MN, 55164-0975 • [phone]
httv://www.health.state.mn.us
DEQ-CFW 00002113

DATA FOR DERIVATION OF GROUND WATER HEALTH BASED VALUE (HBV)
Compound Name: Pertluorooctanoate (PFOA)
CAS #: 3825-26-1 (Oct. 16, 2002 personal communication with Dr. John Butenhoff, 3M)
LOAEL (ingestion): 3 mg/kg/day
Uncertainty Factor: 3000 (3 - interspecies; 10 - intraspecies; 10 subchronic-to-chronic; 10
LOAEL-to-NOAEL)
Modifying Factor: 1
RfD*: 0.001 mg/kg/day
Health effect: Liver
Relative Source Contribution (RSC): 20%
Oral Slope Factor: NA
Applied Risk Level: NA
HBV = (Rff), mg/kQ/d) (RSC) (1000 ma/ma)
Intake Rate (2 L per day/70 kg)
_ (0.001 mg/kg/d) (0.2) (1000 mg/In = 7 µg/L
0.029 L/kg/d
Data Sources:
1. EPA Revised Draft Hazard Assessment of Perfluorooctanoic Acid and Its Salts (Nov 4, 2002);
2. EPA Draft Hazard Assessment of Perfluorooctanoic Acid and Its Salts (Feb 2002);
3. 3M Lifetime Drinking Water Health Advisory for Perfluorooctane sulfonate (April 2002);
4. 3M Soil Screening Guidelines for PFOS (May 2002);
5. Subchronic Toxicity Studies on Perfluorooctanesulfonate Potassium Salt in Cynomolgus Monkeys.
Seacat et al., Toxciological Sciences 68:249-264, 2002; and
6. 3M Soil Screening Guidelines for PFOA (March 2002).
* Carcinogenicity studies in the rat have shown PFOA to be carcinogenic. However, at this time the available data are
not sufficient for a quantitative assessment. Reproductive and developmental effects, based on studies in rats and rabbits,
occur at levels higher than doses causing liver toxicity. However, due to rapid elimination in female rats (serum half-life
of 1 day) it is unclear to what degree the fetuses and neonates were exposed. Ovarian tubular hyperplasia has also been
observed in female rats at doses as low as 1.6 mg/kg/d (note: a NOAEL was not determined for this effect since effects
were observed at the lowest dose evaluated). Women do not appear to have the same active secretory mechanism that
exists in the female rat.
Environmental Health Division • 121 E. 7°i Place, P.O. Box 64975, St. Paul, MN, 55164-0975 • [phone]
http://www.health.state.mn.us 3
DEQ-CFW 00002114

Compound Name: Pertluorooctanesulfonate (PFOS)
CAS #: 2795-39-3 (potassium salt)
1763-23-1 (free salt)
(Oct. 16, 2002 personal communication with Dr. John Butenhoff, 3M)
LOAEL (ingestion): 0.15 mg/kg/day
Uncertainty Factor: 1000 (3 - inteaspecies; 10 - intraspecies; 10 subchronic-to-chronic; 3 LOAEL-to-
NOAEL)
Modifying Factor: I
RfD*: 0.0002 mg/kg/day
Health effect: Liver
Relative Source Contribution (RSC): 20%
Oral Slope Factor: NA
Applied Risk Level: NA
HBV = (RfD, mpJka(d) (RSC) (1000 u¢1mg)
Intake Rate (2 L per day/70 kg)
_ (0.0002 ma/kg(d) (0.2) (1000 mg/mg) = 1 µg/L
0.029 L/kg/d
Data Sources:
1) EPA Hazard Assessment and Biomonitoring Data on Perfluorooctane Sulfonate — PFOS (July 2000);
2) 3M Lifetime Drinking Water Health Advisory for Perfluorooctane sulfonate (April 2002);
3) 3M Soil Screening Guidelines for PFOS (May 2002);
4) Subcbronic Toxicity Studies on Perfluorooctanesulfonate Potassium Salt in Cynomolgus Monkeys. Seacat et
al., Toxciological Sciences 68:249-264, 2002; and
5) 3M Comments on Inteaspecies Uncertainty in Risk Assessment for PFOS.
*Carcinogenicity studies in the rat have shown PFOS to be carcinogenic. However, at this time the available data are
not sufficient for a quantitative assessment. Reproductive and developmental effects, based on studies in rats and rabbits,
occur at levels higher than doses causing liver toxicity.
Date (Prepared or Modified): November 14, 2002
Prepared by: H. Goeden
Environmental Health Division • 121 E. 7' Place, P.O. Box 64975, St. Paul, MN, 55164-0975 • [phone]
http://www.health.state.mn.us 4
DEQ-CFW 00002115

ATTACHMENT II
DATA FOR DERIVATION OF SOIL REFERENCE VALUE (SRV)
Compound Name: Perfluorooctanoate (PFOA)
CAS #: 3825-26-1 (Oct. 16, 2002 personal communication with Dr. John Butenhoff, 3M)
LOAEL (ingestion): 3 mg/kg/day
Uncertainty Factor: 3000 (3 - interspecies; 10 - intraspecies; 10 subchronic-to-chronic; 10
LOAEL-to-NOAEL)
Modifying Factor: 1
RfD*: 0.001 mg/kg/day
RfC**: 2E-5 mg/m3
Dermal Absorption: 10% (MPCA Default for organic compounds)
Health effect: Liver
Hazard Quotient: 0.2 (MPCA target risk value)
Oral Slope Factor: NA
Inhalation Unit Risk: NA
Residential SRV: 30 mg/kg
Industrial SRV: 200 mg/kg
Data Sources:
1) EPA Revised Draft Hazard Assessment of Perfluorooctanoic Acid and Its Salts (Nov 4, 2002);
2) EPA Draft Hazard Assessment of Perfluorooctanoic Acid and Its Salts (Feb 2002);
3) 3M Lifetime Drinking Water Health Advisory for Perfluorooctane sulfonate (April 2002);
4) 3M Soil Screening Guidelines for PFOS (May 2002);
5) Subchronic Toxicity Studies on Perfluorooctanesulfonate Potassium Salt in Cynomolgus Monkeys.
Seacat et al., Toxciological Sciences 68:249-264, 2002; and
6) 3M Soil Screening Guidelines for PFOA (March 2002).
* Carcinogenicity studies in the rat have shown PFOA to be carcinogenic. However, at this time the available data
are not sufficient for a quantitative assessment. Reproductive and developmental effects, based on studies in rats and
rabbits, occur at levels higher than doses causing liver toxicity. However, due to rapid elimination in female rats
(serum half-life of 1 day) it is unclear to what degree the fetuses and neonates were exposed. Ovarian tubular
hyperplasia has also been observed in female rats at doses as low as 1.6 mg/kg/d (note: a NOAEL was not
determined for this effect since effects were observed at the lowest dose evaluated). Women do not appear to have
the same active secretory mechanism that exists in the female rat.
** There is insufficient information on the toxicological effects of PFOA following inhalation exposure. PFOA is
not considered to be a volatile chemical and therefore the inhalation exposure pathway is anticipated to be a minor
pathway. 3M has suggested a RfC of 2E-5 mg& based on a generic exposure guideline for chemicals found to be
carcinogenic in animals but with unknown relevance to humans. The CATT report generated a RfC of 1.1 E-3
mg&. In the absence of information the provisional RfC suggested by 3M will be utilized for the development of
an interim Soil Reference Value.
5
DEQ-CFW 00002116

Compound Name: Perfluorooctanesulfonate (PFOS)
CAS #: 2795-39-3 (potassium salt)
1763-23-1(free salt)
(Oct. 16, 2002 personal communication with Dr. John Butenhoff, 3M)
LOAEL (ingestion): 0.15 mg/kg/day
Uncertainty Factor: 1000 (3 - interspecies; 10 - inteaspecies; 10 subchronic-to-chronic; 3 LOAEL-to-NOAEL)
Modifying Factor: 1
RfD*: 0.0002 mg/kg/day
RfC**: 2E-5 mg/m3
Dermal Absorption: 10% (MPCA Default for organic compounds)
Health effect: Liver
Hazard Quotient: 0.2 (MPCA target risk value)
Oral Slope Factor: NA
Inhalation Unit Risk: NA
Residential SRV: 6 mg/kg
Industrial SRV: 40 mg/kg
Data Sources:
Data Sources:
1) EPA Hazard Assessment and Biomonitoring Data on Perfluorooctane Sulfonate — PFOS (July 2000);
2) 3M Lifetime Drinking Water Health Advisory for Perfluorooctane sulfonate (April 2002);
3) 3M Soil Screening Guidelines for PFOS (May 2002);
4) Subchronic Toxicity Studies on Perfluorooctanesulfonate Potassium Salt in Cynomolgus Monkeys. Seacat et
al., Toxciological Sciences 68:249-264, 2002; and
5) 3M Comments on Interspecies Uncertainty in Risk Assessment for PFOS. -
*Carcinogenicity studies in the rat have shown PFOS to be carcinogenic. However, at this time the available data are
not sufficient for a quantitative assessment. Reproductive and developmental effects, based on studies in rats and rabbits,
occur at levels higher than doses causing liver toxicity.
**There is insufficient information on the toxicological effects of PFOS following inhalation exposure. PFOS is not
considered to be a volatile chemical and therefore the inhalation exposure pathway is anticipated to be a minor pathway.
3M suggested a RfCs of 2E-4 and 2E-5 mg/m3 for PFOS and PFOA, respectively. The value for PFOA was based on
a generic exposure guideline for chemicals found to be carcinogenic in animals but with unknown relevance to humans.
PFOS appears to be carcinogenic in rats but it is not clear whether suggested mechanism of action is relevant to humans.
In the absence of information the provisional RfC for PFOA (2E-5 mgW) suggested by 3M will be utilized for the
development of an interim Soil Reference Value for PFOS as well.
Date (Prepared or Modified): November 14, 2002
Prepared by: H. Goeden
DEQ-CFW 00002117