SEQ CHAPTER \h \r 1 	UNITED STATES ENVIRONMENTAL PROTECTION AGENCY

	WASHINGTON, D.C. 20460

OFFICE OF

PREVENTION, PESTICIDES AND

TOXIC SUBSTANCES

January 8, 2007

Memorandum

SUBJECT: 	Revised:  Occupational and Residential Assessment of
Individuals Exposed to Hexavalent Chromium (Cr+6) in Acid Copper
Chromate (ACC) Pressure-Treated Wood.  DP Barcode 335008.

FROM: 	Tim Leighton, Environmental Scientist

Tim McMahon, Ph.D., Toxicologist

		Antimicrobials Division

TO:		Mark Hartman, Branch Chief (RMBII)

Antimicrobials Division

	This memorandum represents a revision of the May 30, 2006, (USEPA
2006a) occupational and residential assessment of hexavalent chromium
(Cr+6 or Cr VI) in acid copper chromate (ACC).  This revision to the
original assessment has been developed to respond to a registration
application under the Pesticide Registration Improvement Act (PRIA) from
Forest Products Research Laboratory (FPRL), LLC, for a wood preservative
containing ACC.  The application seeks to register ACC as a general wood
preservative to include residential uses.

EXECUTIVE SUMMARY

Acid Copper Chromate (ACC) is a wood preservative product that contains
hexavalent chromium (Cr+6).  ACC was registered by EPA as a general use
wood preservative to Osmose Inc. (EPA Reg. No. 3008-60) on September 27,
1994.  Although ACC was registered as a general use wood preservative,
Osmose limited its use to the treatment of wood for cooling towers.  In
response to new applications for ACC, EPA issued an occupational and
residential risk assessment on May 30, 2006 (USEPA 2006a) and
subsequently registered an ACC product to FPRL for treatment of wood
only to be used in commercial and industrial applications.  At the same
time, EPA did not grant the residential uses sought as part of the
general use application.  In August 2006, FPRL submitted a repeat open
application test (ROAT) to refine the uncertainties in the dermal
sensitization toxicity data identified by the EPA’s Science Advisory
Panel (SAP).  EPA reviewed and presented the ROAT study to the Human
Studies Review Board (HSRB) and found it to be both scientifically and
ethically sound.  The risk assessment provided herein is based largely
on the refinement to the dermal toxicity endpoint based on the newly
submitted ROAT study.  The scope of this risk assessment is to identify
the potential exposure and risks from the use of ACC-treated wood and to
identify and discuss the uncertainties and limitations in the
development of the risks presented.  Any mitigation options that might
reduce the risks identified, and the feasibility of such mitigation
measures are beyond the scope of this document and will be addressed
during the regulatory decision making process.

In summary, potential risk estimates have been developed for both
occupational and residential exposures.  For occupational populations,
the assessment looks at inhalation exposures for industrial workers at
pressure treatment facilities and wood workers breathing wood dust
during fabrication of articles out of ACC-treated wood.  The potential
for dermal contact with Cr+6 residues is also discussed for workers at
the treatment facility and in retail/construction.  Residential dermal
exposure for adults and dermal/incidental oral ingestion for children
were evaluated from contact with ACC-treated wood structures in
residential settings.

The cancer and non cancer risk estimates presented are based on
toxicological endpoints derived from the oral, dermal, and inhalation
routes.  Section 3.3 Table 2 provides a summary of the toxicological
endpoints used to estimate risk for each of the three routes of
exposure.  Cr+6 is classified as a known human carcinogen, by the
inhalation route of exposure.  Carcinogenicity by the oral route of
exposure has not been determined and is classified as Group D (i.e., not
classifiable as to human carcinogenicity).  Note:  The National
Toxicology Program (NTP) is currently conducting an oral cancer study
for Cr+6.  However, the results of this study are not expected until at
least the spring of 2007.

Inhalation Risks:

The cancer and non cancer Cr+6 ACC inhalation risk assessment for
workers at pressure treatment facilities rely on Cr+6 air concentrations
collected during CCA treatments.  The air concentrations collected for
CCA are proportionally increased for ACC estimates to account for the
increased chromium content of ACC.  The Cr+6 inhalation assessment
includes four scenarios:  (1) risks from CCA in the study; (2)
extrapolated risks to ACC for the volume of wood treated in the CCA
study; (3) extrapolated risks to ACC for an estimated volume of wood for
industrial only uses; and (4) extrapolated risks to ACC for an estimated
volume of wood for residential uses.  The risks have been estimated for
the ground contact retention for ACC of 0.5 pounds per cubic foot (pcf)
to represent the high end of exposure.  Treatments at the above ground
contact retention of 0.25 pcf would result in risks that are half of
those presented.  It was necessary to extrapolate the ACC risks from an
existing product such as CCA because ACC is not currently used in this
manner.  The inhalation risk assessment for wood workers breathing wood
dust during fabrication of articles using ACC-treated wood is based on
both a residue study conducted by Osmose coupled with the assumption
that workers would be breathing wood dust at the rate at which OSHA has
set the PEL for wood dust (i.e., untreated total wood dust and
respirable wood dust).   Uncertainties associated with this assessment
are discussed in Section 5.0.

The results of the cancer and non cancer inhalation risks at pressure
treatment facilities are summarized individually in Tables 10 and 11 and
as ranges in Table 20.  The inhalation cancer risks for the volume of
wood presumed to be treated for residential use of ACC, at the ground
retention of 0.5 pcf (i.e., scenario 4 discussed above), range from
2.1E-3 to 6.9E-5.  The non cancer risks, expressed as the margin of
exposure (MOE), for scenario 4 ranges from 2 to 20 with a target MOE of
30.

The results of the cancer and non cancer inhalation risks due to wood
dust exposure from ACC-treated wood have been presented for the last
sampling interval (i.e., 58 days after treatment (DAT)) for two wood
species at both the above ground and ground contact retentions of 0.25
pcf and 0.5 pcf.  From these four combinations of wood
species/retentions, the concentrations of Cr+6 in the interior of wood
is the highest for Southern pine at a retention of 0.5 pcf at the last
day sampled (i.e., 58 DAT).  See Table 12 for a complete review of the
residue levels monitored.  To estimate inhalation exposure and risks
from exposure to ACC-treated wood dust, EPA has assumed that the upper
bound inhalation exposure is equal to the PEL for wood dust adjusted for
the concentration of Cr+6 in the wood.  Based on these assumptions,
inhalation cancer risks for those individuals exposed to ACC-treated
wood dust 58 days after treatment range from 9.5E-4 to 6.0E-6.  The MOEs
for the same assumptions range from 1 to 160 with an inhalation target
MOE of 30.  Again, risks from wood treated at a retention of 0.25 pcf
would be half these estimates.  Based on the Osmose data, it is
predicted that the Cr+6 concentrations in Southern pine would reduce to
15 ppm at 94 DAT, resulting in a cancer risk of 1.1E-4 and a MOE of 9.

Dermal Risks:

μg/cm2 with an uncertainty factor of 1x.  Once the surface residues of
Cr+6 on ACC-treated wood decline below the level of concern (LOC) of
0.092 μg/cm2, dermal contact is no longer expected to elicit
sensitization in already sensitized individuals or to cause dermal
irritation.  This LOC is also protective for individuals that are not
currently sensitized to chromium as the concentration required for
induction is greater than that selected to protect against elicitation.

μg/cm2  of Cr+6 would be left.  A surface residue study for ACC has
been submitted by Osmose.  However, the design of the study has several
limitations (see Section 5.0).  It is evident from the wipe study data
that the surface residue reduction of chromium is highly variable in the
area of interest (i.e., the time frame where Cr+6 reduces enough to be
below the LOC).  Therefore, this assessment includes the predicted daily
average, the predicted 95th% upper confidence interval on the mean, and
the actual sampling intervals from the study.  Of concern is the fact
that the average predicted surface concentration of Cr+6 is less than
the measured mean values for 3 of 4 of the experiments or wood
species/retentions (i.e., Southern Pine 0.25 and 0.5 pcf and Douglas fir
0.5 pcf).  For example, the surface concentration of Cr+6 in Southern
Pine (0.25 pcf) did not reduce to below the LOC in the actual field
samples at the 23 DAT sampling interval, yet the daily mean predicted
timeframe is 4 days.  These dermal risk estimates could be more
accurately characterized with a wipe study that is designed to correlate
the cloth wipe samples to actual wet hand wipe samples to simulate
dermal exposure.  Additionally, more sampling intervals and controlled
cold and warm weather conditions would also more accurately characterize
the Cr+6 reduction rate.  The reliability of the surface wipe data in
the area of interest (i.e., the time frame where Cr+6 reduces enough to
be below the LOC) needs to be considered during the regulatory decision
making process.

Incidental Ingestion:

There is the possibility that incidental ingestion of Cr+6 may occur for
children coming in contact with ACC-treated wood or soil around
ACC-treated wood structures such as play sets and/or decks.  Data
specific to ACC were not available for the soil ingestion estimates but
can be estimated from the data available for CCA.  To assess the soil
ingestion potential, the Cr+6 soil concentration was taken from the CCA
Stochastic Human Exposure and Dose Simulation (SHEDS).  The CCA soil
estimate from SHEDS was adjusted to account for the increased
concentration of Cr+6 in ACC.  To be protective of children, a bounding
input for the soil ingestion was the assumption that a child’s entire
soil ingestion rate comes from a source of soil contaminated by
ACC-treated wood.  For the child’s hand-to-mouth exposure resulting
from directly contacting an ACC-treated structure, the CCA SHEDS
probabilistic estimate of the 99th percentile of the average daily dose
for total chromium was adjusted by 1.5x to account for the increase in
Cr+6 in ACC.  The SHEDS assessment was based on total chromium and no
downward adjustment was made to estimate the amount of Cr+6 that were
attributable to total chromium.  Because the SHEDS assessment was used
as the basis for the hand-to-mouth estimates, the assessment is
predicated that the Cr+6 in ACC-treated wood has the opportunity to
become fixed (i.e., reduced).

The non cancer risk estimates from incidental ingestion of Cr+6 from
soil around ACC-treated wood or from hand-to-mouth exposure from
children playing on ACC-treated wood that has been given the proper time
for fixation result in MOEs of 6,000 and 200, respectively, with a
target MOE of 100.  Cr+6 is not classifiable as to human
carcinogenicity, and therefore, there are no cancer risk estimates for
the children’s incidental ingestion route of exposure.  The NTP oral
cancer study is ongoing and not available at this time.

1.0	INTRODUCTION

	EPA is currently reviewing a request for the expansion of the use of
ACC to residential applications.  Currently, ACC products are limited to
industrial/commercial applications.  EPA is currently reviewing the
existing ACC product (EPA Reg. No. 3008-60) along with several
applications for a “me-too” registration for ACC.  EPA initiated a
risk assessment for the ACC registration because (1) Cr+6 non cancer and
cancer risks are of concern for CCA using the limited data in ACC (2002)
(MRID No. 455021-01); (2) ACC-treatments use nominally 50 percent more
Cr+6 in the treatment process than CCA for equivalent retentions; (3)
preliminary data indicate that the fixation/reduction process for Cr+6
(i.e., reduction to Cr+3) in ACC is much longer than that of CCA; and
(4) substitution of ACC for CCA would significantly change the market
share of the product (i.e., ACC is not currently marketed and was
previously only sold for treating cooling tower wood and it may become
an alternative for CCA-treated lumber in the residential setting).

	EPA has revised its initial ACC risk assessment (USEPA 2006a) because
of a request for the expansion for ACC into residential applications
based on a revision to the dermal toxicological endpoint.  The dermal
endpoint has been revised based on the submission of new data (i.e., a
repeat open application test (ROAT)) submitted by FPRL.  Therefore, this
risk assessment relies in part on data from studies in which adult human
subjects were intentionally exposed to Cr+6.  The ROAT study was
reviewed for its scientific and ethical conduct both by EPA and the
Human Studies Review Board (HSRB) and was found to be appropriate for
use.

The EPA’s estimates of Cr+6 risks are not without associated
uncertainties.  The details of the risk assessment are provided below to
inform the regulatory risk managers in making a regulatory decision on
the registration of ACC.  The document is organized as follows:

Section	Content/Description

1.0	Introduction

2.0	Product Chemistry

3.0	Hazard Characterization

4.0	Exposure Assessment and Risk Characterization

5.0	Uncertainties and Data Limitations

6.0	Summary of Results

7.0	References

1.1	Population Potentially at Risk

	The population potentially at risk to Cr+6 exposures from ACC pressure
treated wood is a function of the route of exposure and the potential
for contact with the treated wood.  The routes of exposure include
inhalation during the treatment process; inhalation to wood dust
containing Cr+6 at indoor wood working facilities; dermal contact
resulting from deposition of mist at the treatment facility (e.g.,
opening pressure treatment cylinder); dermal contact with treated wood;
and incidental oral contact by children via incidental soil ingestion.
EPA has identified the following potential exposure scenarios:

Pressure Treatment Facilities - inhalation cancer and non cancer
effects; dermal contact occurring from exposure to mists and direct
contact with the treated wood;

Retail - dermal contact occurring from handling treated wood;

Construction workers – dermal contact with handling treated wood
(e.g., deck builders) and inhalation exposure at indoor wood working
facilities;

General Public - potential for exposure (dermal and oral) from contact
with treated wood with Cr+6 residue levels above the threshold
concentration selected for the risk assessment, and from contacting
contaminated soils.

Identification of Products

Acid Copper Chromate (ACC) is currently registered as ACC 50% Wood
Preservative by Osmose, Inc (EPA Reg. No. 3008-60) and as Treaters
Choice by Forest Products Research Laboratory (FPRL), LLC (EPA Reg. No.
75832-3).  Both products are for industrial uses.  The proposed
residential ACC product by FPRL is Copper Shield (EPA Reg. No. 75832-E).
 The products contain 14.07% copper oxide and 35.46% chromic acid.  Both
products claim to be protective against decay and termites.  The Osmose
label also claims to protect against marine borers.

2.0	PRODUCT CHEMISTRY

	Chromium, a transition metal and like other transition metals, can
exist in various oxidation states and in each oxidation state chromium
will have a unique chemistry. Most common and stable oxidation states of
chromium are + 3 and + 6. Chromic oxide sometimes is also known as
chromic acid or chromic anhydride, although chromic acid (H2CrO4) is
formed when chromic oxide or sodium or potassium dichromate is dissolved
in a strong acid. As chromic acid, chromium retains its +6 oxidation
state.

Name:			Chromic Acid

Formula:		H2CrO4

CAS#:			7738-94-5

Molecular Wt:		118.0

If the pH of chromic acid is less than 1, it exists as H2CrO4. However,
if the pH of the solution lies between 2 and 6 chromic acid exists
mainly as HCrO4 (chromic acid ion) and

Cr2O7-2 (dichromate ion) in labile equilibrium with each other.

The pressure treatment of wood to inject wood preservatives into the
wood results in a series of chemical reactions within the wood and is
called “fixation”.  Due to the fixation process, Cr (VI) converts to
Cr (III) which is a dominant species leaching out from inside the wood
to the wood surface.  The fixation process may also change the rate of
release of metal species leaching out.  It has been observed that Cr
(III) is oxidizable to the more water soluble Cr (VI) with prolonged
exposure to UV light.

Likely scenarios for the fate of metals like Cr (III) when leached from
treated wood include migration into the soil or transfer to water
through various environmental processes (migration or soil erosions).
Depending on the nature of the soils, Cr (III) may undergo oxidation if
manganese oxides are present in soil. This process may result in Cr
(III) conversion into Cr (VI), which is a more mobile and toxic
chemical.  Since Cr (VI) can easily move through wet soils and water, it
is also more likely to be bioavailable.  Cr (VI), however, can be
converted into Cr (III) in soils where anoxic conditions prevail. Cr
(III), which is less soluble in water than Cr (VI), also has a tendency
to speciate in environmental media like soil and water. Depending on the
presence of anions it can form chromium halides and hydroxyl species in
soil and water. The presence of humid acids in soils and soil/water
mixtures facilitate the formation of Cr (III) complexes.  All this may
lead to making Cr (III) less bioavailable as well as lowering the degree
of conversion of Cr (III) to Cr (VI).

If Cr(III) ends up in freshwater systems, at pH 6 some of the commonly
detected species are: HCrO4- , Cr(OH)+2 , Cr(OH)2+ , CrO4-2 , Cr(III),
and Cr(OH)3.  Some prominent and common Cr(III) species detected in
seawater at pH 8 are: CrO4-2 ,  Cr(OH)2+ , Cr(OH)3, NaCrO4-, KCrO4- ,
HCrO4- , Cr(OH)+2 ,and Cr(OH)4- .

In water systems, Cr (III) can under go a series of speciation, again
depending on the pH, and the redox conditions of the water system.
Cr(III) in water can speciate into: (1) free metal ions with a known
number of  water molecules around the cation (hydration), (2) simple
inorganic species like oxo, hydroxy Cr(III) species as indicated above
or halides, or carbonates, or (3) it can complex with inorganic or
organic ligands (humic acids) etc.  Cr (III) hydroxyl species are many
and hydroxyl Cr (III) can be simple Cr (III) hydroxide or it could form
complex polymeric Cr (III) hydroxides.

It has been shown recently (Cooper 2002) that cleaning solutions
containing oxidizing agents like sodium hypochlorite can convert Cr
(III) to the more water soluble Cr (VI) in a short time frame.  A more
recent study (Awan 2003) has shown that pure analytical solutions of
Cr(III) as well as Cr(III) present in wastewater streams as a waste from
the tanning industry  were converted within a short time frame to the
more water soluble Cr(VI) in the presence of oxidizing agents like
sodium hypochlorite, hydrogen peroxide etc.

3.0	HAZARD CHARACTERIZATION

3.1	Acute Toxicity

	Table 1 provides a summary of the acute toxicity for Cr+6 (USEPA 2002).

  SEQ CHAPTER \h \r 1 Table 1: Acute Toxicity Summary of Chromium (VI)

Guideline

Study Type

[Substance]

MRID/Literature

Results

	Toxicity

Category

81-1

(OPPTS 870.1100)	Acute Oral/Rat

[Chromic Acid, 100% a.i.]	434294-01

= ♂ 56 mg/kg

        = ♀ 48 mg/kg

M+F = 52 mg/kg 	I

81-2

(OPPTS 870.1200)	Acute Dermal/Rabbit

[Chromic Acid, 100% a.i.]	434294-02	LD50  = ♂ >48 mg/kg

          =  ♀ 48 mg/kg

M+F = 57 mg/kg	I

81-3

(OPPTS 870.1300)	Acute Inhalation/Rat

[Chromic Acid, 100% a.i.]	434294-03	LC50 = ♂ 0.263 mg/L

        =  ♀ 0.167 mg/L

      M+F = 0.217 mg/L

I

81-4

(OPPTS 870.2400)	Primary Eye Irritation

[Various Cr(VI) compounds]

	Literature

Corrosive

(data waiver)	I

81-5

(OPPTS 870.2500)	Primary Dermal Irritation

[Various Cr(VI) compounds]	Literature

Corrosive

(data waiver)	I

81-6

(OPPTS 870.2600)

	Dermal Sensitization

/Guinea Pig

[Various Cr(VI) compounds]	Literature	Strong sensitizer

Not Applicable

3.2	Hazard Profile

	Acute Toxicity

	The measured oral LD50 in rats was reported as 52 mg/kg, the dermal
LD50 as 57 mg/kg, and the inhalation LC50 as 0.217 mg/L, placing
chromium (VI) in Toxicity Category I for acute lethality by the oral,
dermal, and inhalation routes.  Human reports of death after ingestion
of chromium show lethality at similar dose levels (ATSDR, 1998).
Chromium (VI) is a significant eye and skin irritant, and severe
allergic reactions consisting of redness and swelling of the skin have
also been noted in exposed animals and humans. Case reports of humans
who have intentionally or accidentally ingested chromium have also shown
severe respiratory effects (pulmonary edema, bronchitis, and
bronchopneumonia), cardiovascular effects (cardiac arrest), and
gastrointestinal effects (hemorrhage, ulceration).

Chromium VI is one of the most common and potent dermal sensitizing
chemicals (USEPA, 1998).  Sensitization reactions consisting of
erythema, edema, papule formation, and vesicles are observed in both
experimental animals and in humans in studies designed to investigate
dermal sensitization potential of chromium VI (USEPA, 1998; Nethercott
et al., 1994; Basketter et al., 2001; Hansen et al., 2003).  For the
purposes of the current risk assessment, the Agency has reviewed a
recently conducted dermal sensitization study conducted in human test
subjects using the Repeat Open Application Test (ROAT) protocol (Proctor
et al., 2006) that is relevant for the types of exposure expected from
dermal contact with wood treated with the ACC wood treatment solution.

	Dermal absorption of hexavalent chromium is low (absorption of 1.3% of
an applied dose through the skin of guinea pigs).  Relative
bioavailability of hexavalent chromium through ingestion of soil and
water is also low.

	Non-Acute Toxicity:

	Subchronic toxicity studies in experimental animals have demonstrated
hematologic and hepatic effects from repeated oral exposure to chromium
(VI).   In a 9 week study in which male and female Sprague-Dawley rats
were fed diets containing potassium dichromate at dose levels of 0, 15,
50, 100, or 400 ppm potassium dichromate [NTP, 1996], there were no
treatment related findings noted in mean body weights, water and feed
consumption, organ weights or microscopic pathology of the liver,
kidneys and ovaries. Hematology findings effects consisted of decreases
in mean corpuscular volume (MCV) and mean corpuscular hemoglobin (MCH)
at the high dose (8.4 and 9.8 mg/kg/day in male and female rats
respectively).  There were no reported hepatic effects in this study.
However, Kumar and Rana (1992) reported increased accumulation of
hepatic lipids after gavage treatment of rats with 13.5 mg/kg chromium
(VI) (as potassium chromate) after 20 days of treatment.

	In a 9-week feeding study in mice conducted by the National Toxicology
Program (1996) in which mice were fed diets containing 1.1, 3.5, 7.4,
and 32 mg/kg/day chromium (males) or 1.8, 5.6, 12, and 48 mg/kg/day
chromium (females), hepatic cytoplasmic vacuolization was observed to be
slightly increased at the high dose in males and females, and the
appearance of the vacuoles was suggestive of lipid accumulation.
Additional endpoints examined in this study included body weights, feed
and water consumption, organ weights, microscopic evaluation of the
liver, kidney and ovaries, hematology, histology of the testis and
epididymis for Sertoli nuclei,  and preleptotene spermatocyte counts in
Stage X or XI tubules and chromatin analysis.  Slight decreases in body
weight were observed during this study, but there was no significant
effect of treatment on clinical signs, necropsy findings, or microscopic
histology.  Hematologic effects were observed and consisted of a 2-4%
decrease in MCV at weeks 3, 6, and 9 in high dose males and females and
at week 6 in the 100 ppm females.

	Animal studies have consistently shown that chromium, particularly
chromium (VI), is a developmental toxicant.  Oral ingestion of chromium
(VI) compounds in experimental animals results in significant
developmental toxicity. Studies describing the effects observed have
been published in the IRIS Toxicological Reviews for both chromium (VI)
and chromium (III) as well as from submitted studies to the Agency and
are summarized here.

	Trivedi et al. (1989) exposed mice to 250, 500, and 1,000 ppm potassium
dichromate daily through drinking water during the entire gestational
period. The authors reported decreased fetal weight, increased
resumptions, and increased abnormalities (tail kinking, delayed
ossification of the cranium) in exposed mice. The medium- and high-dose
groups registered significant reductions in body weight gain when
compared to controls. The most significant finding of the study was the
complete absence of uterine implantation in the high-dose group. The 250
and 500 ppm dose groups also showed significant incidences of resumption
as compared to controls. The authors observed significant increases in
preimplantation and postimplantation losses and dose-dependent
reductions in total weight and crown-rump length in the lower dose
groups.  Additional effects included treatment-related increases in
abnormalities in the tail, wrist

forelimbs and subdermal hemorrhagic patches in the offspring.  Junaid et
al. (1996) exposed female Swiss albino mice to 250, 500, or 750 ppm
potassium dichromate in drinking water to determine the potential
embryotoxicity of hexavalent chromium during days 6-14 of gestation. No
notable changes in behavior or clinical signs were observed in the
control or treated dams. Chromium levels in blood, placenta, and fetus
increased in a dose-dependent fashion over the course of the study. The
authors reported retarded fetal development and embryo- and fetotoxic
effects including reduced fetal weight, reduced number of fetuses (live
and dead) per dam, and higher incidences of stillbirths and
postimplantation loss in the 500 and 750 ppm dosed mothers.
Significantly reduced ossification in nasal, frontal, parietal,
interparietal, caudal, and tarsal bones was observed in the high-dose
group, while reduced ossification in only the caudal bones was observed
in the 500 ppm dose group. Based on the body weight of the animals (30
+/- 5 g) and the drinking water ingested by the animals in the 250 ppm
dose group (8.0 ml/mouse/day), the dose level in the 250 ppm group can
be identified as 67 mg/kg-day. The maternal NOAEL was 63 [22.3]
mg/kg/day while the LOAEL was 42.1 mg/kg/day and was based on a
decreased gestational body weight. At the lowest dose tested, the
incidence of resorptions was increased and a developmental NOAEL was,
therefore, not determined.

	Kanojia et al. (1996) exposed female Swiss albino rats to 250, 500, or
750 ppm potassium

dichromate in drinking water for 20 days to 3 months prior to gestation
to determine the potential teratogenicity of hexavalent chromium. No
notable changes in behavior or clinical signs were observed in the
control or treated dams. Chromium levels in blood, placenta, and fetus
were significantly increased in the dams of the 500 and 750 ppm dose
groups. The authors reported a reduced number of corpora lutea and
implantations, retarded fetal development, and embryo- and

fetotoxic effects including reduced number of fetuses (live and dead)
per dam and higher

incidences of stillbirths and post implantation loss in the 500 and 750
ppm dosed mothers.

Significantly reduced parietal and interparietal ossification was
observed in the high-dose group.

Based on the body weight of the animals (175 +/- 25 g) and the drinking
water ingested by the

animals in the 250 ppm dose group (26 ml/mouse/day), the dose level in
the 250 ppm group is identified as 37 mg/kg-day.

	Tyl (1991) examined the developmental and maternal effects of daily
administration of chromic acid (55.0% a.i.) at dosages of 0, 0.1, 0.5,
2.0 or 5.0 mg/kg/day by gavage in rabbits. Clinical signs of toxicity,
including diarrhea, and slow, audible or labored breathing were observed
in predominately in the 2.0 and 5.0 mg/kg/day groups.  However, these
signs did not show a dose-response and were observed in lesser incidence
at 5.0 mg/kg/day vs. 2.0 mg/kg/day. However, the incidence of mortality
(at 2.0 mg/kg/day, one doe died on gestation day (GD) 28; at 5.0
mg/kg/day, 5 does died (one each on GD 10, 14, and two on GD 15) and the
magnitude of decreased body weight gain during the dosing period
(average weight loss of 48 grams at 2.0 mg/kg/day, and average weight
loss of 140 grams at 5.0 mg/kg/day during gestation days 7-19) were
observed to occur in a dose-related fashion at 2.0 and 5.0 mg/kg/day.
Food efficiency was also observed to be significantly lower during the
dosing period in the 5.0 mg/kg/day dose group.  Cesarean section
observations were unremarkable in this study at any dose level.  No
treatment related effects on either fetal malformations or variations
were observed.

	The National Toxicology Program conducted a three-part study to
investigate oral ingestion of hexavalent chromium in experimental
animals (NTP, 1996a, b, 1997). The study included a determination of the
potential reproductive toxicity of potassium dichromate in
Sprague-Dawley rats, a repeat of the study of Zahid et al. (1990) using
BALB/C mice, and a Reproductive Assessment by Continuous Breeding study
in BALB/C mice. The study in the Sprague-Dawley rat (NTP, 1996a) was
conducted in order to generate data in a species commonly used for
regulatory studies. Groups of 24 males and 48 females were exposed to 0,
15, 50, 100, or 400 ppm potassium dichromate daily in the diet for 9
weeks followed by a recovery period of 8 weeks. Six male and 12 female
rats were sacrificed after 3, 6 or 9 full weeks of treatment or after
the full recovery period. Animals were examined for body weights; feed
and water consumption; organ weights; microscopic evaluation of the
liver, kidney, and ovaries; hematology; histology of the testis and
epididymus for Sertoli nuclei and preleptotene spermatocyte counts in
Stage X or XI tubules; and chromatin analysis. No treatment-related
hematology findings were reported except for slight decreases in MCV and
MCH values in the male and female treatment groups receiving 400 ppm
potassium dichromate (24 mg/kg-day). While the trends in MCV and MCH
were not large and were within the reference ranges, they are consistent
with the findings of the companion studies in BALB/C mice and were
characterized by the authors as suggestive of a potential bone
marrow/erythroid response. The authors considered the 100 ppm (6
mg/kg-day) dose group to be representative of the NOAEL for the study.

	The reproductive study in BALB/C mice (NTP, 1996b) was conducted to
reproduce the

conditions utilized by Zahid et al. (1990) in their examination of
comparative effects of trivalent

and hexavalent chromium on spermatogenesis of the mouse. Groups of 24
male and 48 female BALB/C mice were exposed to 0, 15, 50, 100, or 400
ppm potassium dichromate in the diet for 9 weeks followed by a recovery
period of 8 weeks. Six male and 12 female mice were sacrificed after 3,
6, or 9 full weeks of treatment or after the full recovery period.
Animals were examined for body weights; feed and water consumption;
organ weights; microscopic evaluation of the liver, kidney, and ovaries;
hematology; histology of the testis and epididymus for Sertoli nuclei
and preleptotene spermatocyte counts in Stage X or XI tubules; and
chromatin analysis.  Treatment-related effects included a slight
reduction in the mean body weights in the 400 ppm males and the 100 ppm
females, a slight increase in food consumption at all dose levels, a
slight decrease in MCV and MCH at 400 ppm, and cytoplasmic vacuolization
of the hepatocyte at 50, 100 and 400 ppm. None of the effects on
spermatogenesis reported by Zahid et al. (1990) were

observed in this study. On the basis of the cytoplasmic vacuolization of
the hepatocyte in the 50, 100, and 400 ppm dose groups, the authors
selected 15 ppm (4 mg/kg-day) as the NOAEL.

	Increased resorptions and increased post-implantation loss as well as
gross fetal abnormalities were observed in offspring of pregnant mice
exposed to potassium dichromate at 57 mg/kg/day in drinking water during
gestation (ATSDR, 2000b). At a higher dose of 234 mg/kg/day, no
implantations were observed in maternal mice. In a second study in mice,
potassium dichromate was administered in the diet for 7 weeks at dose
levels of 15.1 and 28 mg/kg/day. Reduced sperm counts and degeneration
of the outer layer of the seminiferous tubules was observed at the 15.1
mg/kg/day dose, and morphologically altered sperm was observed at the 28
mg/kg/day dose.

	In male rats administered 20 mg/kg/day chromium trioxide for 90 days by
gavage, reduced testicular weight, decreased testicular testosterone,
and reduced Leydig cell number was observed (Chowdhury and Mitra, 1995).

	Despite the wealth of animal studies on the developmental and
reproductive toxicity of chromium VI, there are too few human data with
which to make any reliable conclusion regarding the susceptibility of
the developing fetus, infants, or children to the toxic effects of
chromium VI. The evidence available suggests similar toxic effects in
adults and children from ingestion of chromium VI (ATSDR, 2000b).

	Chronic Toxicity:

	In chronic toxicity studies, groups of eight male and eight female
Sprague-Dawley rats [MacKenzie 1958] were supplied with drinking water
containing 0.45-11.2 ppm (0, 0.45, 2.2, 4.5, 7.7, and 11.2 mg/L)
hexavalent chromium (as K2CrO4) for 1 year. The control group received
(10/sex) received distilled water. No significant toxic effects were
observed in this study despite the accumulation of chromium residues in
tissues. The authors stated that “apparently tissues can accumulate
considerable quantities of chromium before pathological changes
result.” In a chronic toxicity study in dogs, dogs were orally exposed
to potassium chromate in drinking water for 4 years at 0, 0.45, 2.25,
4.5, 6.75 and 11.2 ppm [Anwar et al. (1961)]. No effects were observed
with regard to gross and microscopic analysis of all major organs,
urinanalysis and the weights of the spleen, liver and kidney

	Carcinogenicity:

	In long-term inhalation studies, Glaser (1986, 1988) exposed groups of
20 male Wistar rats to aerosols of sodium dichromate (Na2Cr2O7) at
measured concentrations of 0.025, 0.05, and 0.1 mg Cr(VI)/m3, 22 hr/day,
7 days/ week for 18 months in horizontal flow inhalation chambers. Three
lung tumors, (one adenocarcinoma and two adenomas), were reported in the
high-concentration group, although, it is not clear whether the
adenocarcinoma and adenomas occurred in the same animal or in different
animals (U.S. EPA 1998).  A squamous cell carcinoma in the
pharynx/larynx region was also observed in the high-concentration group.
 One primary lung adenoma was observed in the chromium oxide (CrO3)
exposed group.  No tumors were reported in the lungs or pharynx of
control rats.  All other tumors in other tissues were not considered to
be related to treatment by the study authors.

	The results of this study indicate that exposure to sodium dichromate
or chromium oxide aerosols at levels of 100 μg Cr/m3 result in a weak
carcinogenic effect.  However, the authors recommended that additional
studies involving larger populations of animals and longer observation
periods be conducted.

	Hexavalent chromium (Cr VI) is known to be carcinogenic in humans by
the inhalation route of exposure.  Results of occupational epidemiologic
studies of chromium-exposed workers are consistent across investigators
and study populations. Dose-response relationships have been established
for chromium exposure and lung cancer. Chromium-exposed workers are
exposed to both Cr(III) and Cr(VI) compounds. Because only Cr(VI) has
been found to be carcinogenic in animal studies, however, it was
concluded that only Cr(VI) should be classified as a human carcinogen.
The carcinogenicity of orally administered hexavalent chromium is
currently under study by the National Toxicology Program.

	Under the current guidelines, Cr(VI) is classified as Group A - known
human carcinogen by the inhalation route of exposure.  The cancer
classification, listed in the EPA’s IRIS document for Cr+6, is based
upon the studies of Mancuso.  Mancuso (1975) followed 332 chromate
workers employed from 1931-1951 until 1974.  By 1974, > 50% of this
cohort had died. Of these men, 63.6%, 62.5%, and 58.3% of the cancer
deaths for men employed from 1931-1932, 1933-1934, and 1935-1937,
respectively, were due to lung cancer. Lung cancer death rates increased
by gradient of exposure to total chromium, and significant deposition of
chromium was found in the lungs of workers long after the exposure
ceased.  Mancuso (1975) reported that these lung cancer deaths were
related to insoluble (trivalent), soluble (hexavalent), and total
chromium exposure, but the small numbers involved make identification of
the specific form of chromium responsible for the lung cancer uncertain.
 However, studies of chrome plating workers in the United States (Hayes
et al. 1989), England (Davies 1984, 1979, 1978), Norway (Langard and
Vigander 1983; Langard and Norseth 1975), and in the Netherlands and
Germany (Frentzel-Beyme 1983) have consistently demonstrated an
association between occupational chromium exposure (predominantly to
Cr+6) and lung cancer. In addition, animal data are consistent with the
findings of human epidemiological studies of hexavalent chromium in that
hexavalent chromium compounds have been found to produce lung tumors
following inhalation of aerosols of sodium chromate and pyrolized
Cr+6/Cr+3 oxide mixtures in rats (Glaser et al., 1986). On the basis of
these and other data, Cr+6 is classified as group A (known human
carcinogen) with a continuous 24-hour 7-day lifetime inhalation unit
risk of 1.16E-2 (μg/m3)-1 or 11.6 (mg/m3)-1.

	Carcinogenicity by the oral route of exposure cannot be determined and
is classified as Group D.   Mutagenicity studies revealed that Cr(VI) is
a potent mutagen in virtually all mutagenicity tests performed so far.

Non Cancer Inhalation Endpoint:

A non cancer inhalation endpoint has also been identified for Cr+6.  As
stated in EPA’s CCA risk assessment:

“…consistent with Agency practice, the endpoint for the inhalation
risk assessment is taken from the 1998 IRIS updates for chromium VI and
applies to all durations of inhalation exposure.  The epidemiological
study of workers in the chrome plating industry by Linberg and
Hedenstierna, 1983 was selected for the LOAEL.  The authors concluded
that 8 hour exposure to chromic acid above the LOAEL value of 0.002
mg/m3 can be identified for incidence of nasal septum atrophy following
exposure to chromic acid mists in chrome plating facilities.  No one
exposed to levels below 0.001 mg/m3 complained of subjective
symptoms.”

EPA has selected the LOAEL of 0.002 mg/m3 for use in the risk assessment
along with an uncertainty factor (UF) of 30 (i.e., 10x intraspecies
human variability and 3x for lack of a NOAEL).  In simplistic terms,
EPA’s risk-based allowable exposure limit for Cr+6 is 0.00007 mg/m3 or
0.07 μg/m3 (i.e., 0.002 mg/m3 / 30x UF).

3.3	Dose-Response Assessment  tc "3.3 Dose-Response Assessment " \l 2

	Table 2 summarizes the endpoint selection for hexavalent chromium
(USEPA 2002 and USEPA 2004).

Table 2.  Toxicological Endpoints for Assessing Exposures/Risks to
Chromium (VI)

EXPOSURE

SCENARIO	DOSE

(mg/kg/day)	ENDPOINT	STUDY

Acute Dietary	This risk assessment is not required.

Chronic Dietary	This risk assessment is not required.

Incidental Short- and Intermediate- Term Oral 	(a) NOAEL= 0.5 mg/kg/day
of chromic acid

[0.12 mg/kg/day of Cr(VI)](d)

Target MOE = 100

(10x intraspecies and 10x interspecies)	based on the increased incidence
of maternal mortality and decreased body weight gain at LOAEL of 2.0
[0.48](d)	Developmental/Rabbit (Tyl, 1991)

Dermal Exposure (b)

μg/cm2 from the Repeat Open Application Test conducted by Proctor et
al. (2006). An uncertainty factor of 1x is applied to this endpoint.

Inhalation Exposure

(All Durations)

	(a) LOAEL= 0.002 mg/m3

Target MOE = 30

(10x intraspecies and 3x for lack of NOAEL)	 nose and throat symptoms
observed at the LOAEL	Industrial survey on chrome plating workers

(Linberg  and Hedenstierna, 1983)

Carcinogenicity - Inhalation

(Inhalation Unit Risk)	Inhalation unit risk (IUR) 11.6 (mg/m3)-1 (c)
Lung tumors	IRIS

Note:

	(a)	MOE = Margin of Exposure; NOAEL = No observed adverse effect level;
and   LOAEL = Lowest observed adverse effect level.  Cr+6 target MOE
represents 10x for intra variability for human study and 3x for lack of
a NOAEL.

	(b) 	Although not needed in this assessment, the dermal absorption
factor for Cr(VI) = 1.3%.

	(c) 	Inhalation unit risk of 1.16 x 10-2 (μg/m3)-1. (EPA, 1998).

	(d)   The NOAEL/LOAEL values are denoted as the weight of the Cr(VI)
compound actually used in the study in mg/kg/day. The molar equivalents
of Cr(VI) in mg/kg/day is also included and this value is denoted in
brackets "[ ]".  The 0.12 mg/kg/day is used in the risk assessment.

4.0	EXPOSURE ASSESSMENT AND RISK CHARACTERIZATION

	The exposure and risk characterization section presents a range of
exposure and risk estimates for various uses of ACC.

4.1	Inhalation Exposure and Risks

	There is the potential for inhalation exposure of particulates to
occupational handlers at pressure treatment facilities.  In addition,
potential inhalation exposure and risks to wood dust containing Cr+6 is
presented.

Pressure Treatment Facilities

Inhalation Exposure Study (FPRL 2005):

One of the pieces of data that EPA has cited as needed in order to make
the necessary finding to support the ACC registration is a worker
inhalation study at pressure treatment facilities to determine
inhalation exposures of hexavalent chromium (Cr+6).  EPA provided FPRL
with two options in selecting the test substance for such a study:  (1)
the study could be conducted with CCA and extrapolated to approximate
the conditions of actual ACC-treatments, or (2) EPA could issue an
Experimental Use Permit (EUP) for ACC.  FPRL selected the first option
and submitted an inhalation exposure study conducted with CCA to be used
as a surrogate to assess inhalation exposures to Cr+6 for ACC (FPRL
2005, MRID 467208-01, and USEPA 2006b).

The CCA study used as a surrogate for ACC was conducted to estimate the
potential worker inhalation exposure to Cr+6 at three treatment
facilities in the United States treating dimensional lumber, plywood,
and poles.  The commercial facilities were located in Rainier, OR;
Savannah, GA; and Tampa, FL.  Each site had a unique layout, but all
sites used similar CCA pressure treatment processes.  The wood at each
facility was treated at nominal retention rates of 0.25 to 2.5 pounds
per cubic foot (pcf).  Specific information for each site is provided in
Table 3.

Table 3.  Study Site Parameters

Parameter	Rainier, OR	Savannah, GA	Tampa, FL

Treatment-related Parameters

Number and type of cylinders	3 cylinders:

1 @ 6½’ x 82’

1 @ 6’ x 80’

1 @ 6’ x 62’

(used exclusively for CCA)	3 cylinders:

1 out of service

2 @ 6’ x 60’

newer one used exclusively for borate

other one used exclusively for CCA	4 cylinders

1 @ 6’ x 86’ (utilize copper azole preservative)

2 @ 6’ x 82’ (one dedicated to CCA

1 @ 6’ x 80’ (utilize copper azole preservative)

CCA articles treated during study	Plywood and 6 x 6 lumber	Mostly 0.25
pcf retention plywood

0.4 pcf cross arms (for utility poles)

10’ x 12’ beams	0.4 pcf retention fence posts

2.5 pcf poles for marine applications (primary articles treated)

0.6 pcf poles for near salt water application

0.25 pcf plywood

Type of plant (i.e. pressure treatment capacity)	Automateda	Manualb
Automatica

Rail bridge (connects track on pad with tracks into cylinder)	Pneumatic
rail bridge with expanded metal walking surface lowered in place	2
single rails put in place by worker; glove use inconsistent	2 single
rails put in place by worker; glove use inconsistent

Cylinder door	Closed/opened manually, sealed pneumatically	Left open
from last charge

Closed/opened/sealed  manually	Left open from last charge

Closed/opened manually, sealed pneumatically

Due to sump/door configuration, worker must open door in front of him
and cross through the mist escaping from cylinder

Ventilation system	Local exhaust canopy above all 3 cylinder doors	None
mentioned	None mentioned

Relative wind direction	Workers generally upwind of cylinders	Not
specified in relationship to workers	Workers generally upwind of
cylinders

Removal of debris from cylinder	After completion of cycle:  worker uses
hose to spray off excess solution and debris from bottom of cylinder
After completion of cycle:  worker uses hose to spray off excess
solution and debris from bottom of cylinder	Before cycle:  worker uses
piece of wood or metal to scrape out debris at bottom of cylinder and in
lower lip of door

Sampling/study-related Parameters

Sampling dates	September 12 - 16	October 10 - 14	November 7 - 11

Number of test days c	5c	5	5

No. of charges monitored	16	17	32

Total cubic feet of wood treated over study duration	5,414	6,870	18,790

Total pounds of Chromic acid absorbed over study durationd	1,339	1,455
8,065

Average lbs of   CrO3 absorbed during a monitoring period	117	280	877

Mean charge duration	3.7 hours	0.75 hourse	1 hour

Mean retention (pcf)	0.58	0.48	0.95

Automatic = duration of the treatment cycles and the concentration of
the preservative to be pumped into the cylinders are determined by
operations software from input parameters.  The treatment cycles advance
automatically and operations can be monitored from an enclosed
operations area above the cylinders.

Manual = Treatment operation valves are opened and closed by the
Treatment Operator

At the Rainier site, three shifts were monitored: day, swing, and
overnight.  The study team members left workers unattended from midnight
to 7:00 AM.

Report lists this as total pounds of chromic acid absorbed, but states
that the form of chromium in chromic acid is hexavalent.  Chromic acid
is 47.5% of CCA by weight.

Study report states that this value is estimated because not all charge
durations were reported.

 A variety of tasks were monitored at each site.  Even though many of
the tasks overlapped job functions, the worker replicates were assigned
as follows: treatment operator (TO), treatment assistant (TA), forklift
operator (FO), packer (PK), tagger (TG), supervisor (SU), and test borer
(TB).  The number of replicates for each job function monitored included
18 treatment operators, 22 treatment assistants, 8 packers, 15
supervisors, 12 forklift operators, 10 taggers, and 7 test borers.  The
duration of inhalation monitoring was approximately 6 working hours per
replicate. Table 4 provides the responsibilities performed for each job
function monitored.

Table 4.  Job functions And Responsibilities At Each Of The Facilities

Job function	Responsibilities at each site

	Rainier, OR	Savannah, GA	Tampa, FL

Treatment Operator

(TO)	Responsible for monitoring treatment cycle of wood, mixing
treatment chemicals, and loading and unloading charges of work from
treatment cylinder

	Workers performed tasks largely on the drip pad, including chaining and
unchaining charges, opening and closing cylinder door, and moving wood
to and from the tracks with a forklift.

Workers also performed tasks of Test Borer, taking core samples from
treated wood	Worker remained within the enclosed treatment office
overlooking drip pad, with occasional visits to the drip pad to
communicate with workers and perform wood counts

Treatment Assistant

(TA)	Workers performed tasks largely on the drip pad, including chaining
and unchaining charges, opening and closing cylinder door, and moving
wood to and from the tracks with a forklift.

	Workers were also observed performing post-treatment tasks such as
packaging, banding and tagging wood	No additional details provided

Forklift Operator

(FO)	Workers in several job functions were observed operating forklifts,
however, at the Savannah and Tampa sites, some individuals spent more
time than others so that a separate job function was created.  Workers
loaded/unloaded trams before and after treatment, stacked wood in
storage, and loaded/unloaded wood on trucks for shipping/receiving

	Forklifts capable of having an enclosed cab, but side doors were always
observed open	Open air cabs	Open air cabs

Packager

(PK)	Workers observed performing post-treatment tasks, such as tagging,
banding, packaging treated wood, moving stacks of wood with a forklift.
Activities took place on treatment floor, adjacent to cylinder tracks.
Workers performed other tasks such as sweeping/cleaning cylinder tracks.

	Had workers dedicated to packager job function	No additional details
provided	No additional details provided

Tagger

(TG)	Workers applied plastic tags with manual or pneumatic staplers to
ends of treated wood

	No additional details provided	Temporary workers hired to fill 5
full-time shifts	One workers performed full-time for the monitoring week

Supervisor

(SU)	Workers spent a portion of time on treatment floor supervising
workers.

	Supervisor also performed forklift duties all over the plant	Members of
study team acted as supervisor; spent time in main office and in
treatment area	Supervisor spent considerable amount of time away from
treatment area and when in area, was typically in treatment office
overlooking drip pad

Test Borer

(TB)	Workers collected all test boring samples, performed analyses and
collected CCA work tank samples

	No additional details provided	No additional details provided	Has
workers dedicated to this job function

Inhalation exposure was monitored using two sampling train
configurations: (1) cassettes containing a PVC filter used to collect
total or inhalable particles (>10 um diameter cut point) and (2) a
personal environmental monitor (PEM) containing a PTFE filter used to
collect thoracic-sized particles (10 um diameter cut point or PM10).
For the ACC inhalation risk assessment, the data collected in the
cassettes are used in the non cancer risk estimates and the PM10 data
are used in the cancer risk assessment because it represents the high
end of the particles that may reach the lungs.  Several method
validation experiments and storage stability experiments were conducted
prior to the initiation of the study to verify recovery efficiency and
storage stability under the conditions to be used in the study.  These
experiments validated the limit of quantitation (LOQ) at 100 ng/sample
for the flow rates of both 7 and 10 liters per minute.

	Pre-field recovery testing was performed using only PVC filters and
resulted in recoveries which ranged from 92-100%.  The average recovery
was reported to be 97.3 ± 3.1%.  Field fortification samples were also
taken during the study at each of the three test sites for both the PVC
filters and PTFE filters.  Spike levels ranged from 100 to 1000 ng at
the Rainier site and from 100 to 2000 ng at the Savannah and Tampa
sites.  For the Rainier site, the average recovery was 86.9 ± 14.4% for
the PVC filters and 90.0 ± 15% for the PTFE filters.  For the Savannah
site, the average recovery was 97.6 ± 5.8% for the PVC filters and 97.4
± 9.5% for the PTFE filters.  For the Tampa site, the average recovery
was 102.0% ± 7.3% for the PVC filters and 102.2 ± 3.6% for the PTFE
filters.

To use the Cr+6 air concentration data collected for CCA as a surrogate
to represent ACC exposure, the air concentration data need to be
adjusted for the amount of Cr+6 to be used for ACC treatments.  In the
CCA study, a range of 71 to 1,189 pounds of chromic acid was absorbed by
all charges during each work shift.  The average amount of chromic acid
absorbed by all charges during each work shift/monitoring period was 117
pounds at the Rainier site, 280 pounds at the Savannah site, and 877
pounds at the Tampa site.  When normalized by the average amount of
chromic acid absorbed by charges (i.e., each air sample was normalized
for the amount of chromic acid in the particular monitoring period), the
cassette (i.e., total particulates) and PM10 (i.e., thoracic-sized
particles) air concentrations (ng Cr+6/m3/lb chromic acid) for all job
functions combined were highest at the Rainier treatment facility.
Total particulate Cr+6 air concentrations averaged 0.17, 0.21, and 0.42
ng/m3/lb chromic acid at the Tampa, Savannah, and Rainier site,
respectively.  PM10 Cr+6 particulates averaged 0.068, 0.23, and 0.39
ng/m3/lb chromic acid at the Tampa, Savannah, and Rainier site,
respectively.

μg/m3 (or the previously proposed OSHA PEL of 1 μg/m3).

Table 5.  Arithmetic Mean Air Concentrations Measured using

Cassettes (total) for each Site and Job Function for CCA (ng/m3)

Site	Average CrO3 handled (lbs)	TO	TA	PK	SU	FL	TG	TB

Rainier	117	59	63	29	17	N/A	N/A	N/A

Savannah	280	148	64	N/A	18	22	16	N/A

Tampa	877	107	114	N/A	85	296	41	149

Table 6.  Normalized Arithmetic Mean Air Concentrations Measured using

Cassettes (total) for each Site and Job Function for CCA (ng/m3/lb CrO3)

Site	Average CrO3 handled (lbs)	TO	TA	PK	SU	FL	TG	TB

Rainier	117	0.62	0.54	0.29	0.19	N/A	N/A	N/A

Savannah	280	0.60	0.25	N/A	0.074	0.087	0.054	N/A

Tampa	877	0.12	0.13	N/A	0.12	0.36	0.047	0.17

Table 7.  Arithmetic Mean Air Concentrations Measured using

PEM (PM10) for each Site and Job Function for CCA (ng/m3)

Site	Average CrO3 handled (lbs)	TO	TA	PK	SU	FL	TG	TB

Rainier	117	50	67	21	17	N/A	N/A	N/A

Savannah	280	150	78	N/A	37	18	12	N/A

Tampa	877	42	34	N/A	33	141	20	44

Table 8.  Normalized Arithmetic Mean Air Concentrations Measured using

PEM (PM10) for each Site and Job Function for CCA (ng/m3/lb CrO3)

Site	Average CrO3 handled (lbs)	TO	TA	PK	SU	FL	TG	TB

Rainier	117	0.49	0.70	0.18	0.17	N/A	N/A	N/A

Savannah	280	0.58	0.31	N/A	0.176	0.063	0.040	N/A

Tampa	877	0.047	0.041	N/A	0.052	0.17	0.023	0.053

Potential ACC Inhalation Exposure and Risk Estimates:

The amount of Cr+6 in the CCA formulations used in the submitted study
are less than that in the proposed ACC formulation.  Therefore, to
estimate the potential Cr+6 inhalation exposure from similar ACC uses,
the air concentrations need to be extrapolated to the amount of Cr+6
expected to be handled daily in ACC treatment facilities.  Table 9
illustrates the differences in the Cr+6 concentrations for CCA and ACC.
The CCA-C 50% and 60% formulations contain 23.75% and 28.5% chromic acid
(respectively) while the proposed ACC 50% formulation contains 35.46%
chromic acid.

Table 9.  Information on Active Ingredients in CCA

Used in Test Formulations and Proposed ACC

Parameter	Chromic Acid	Copper Oxide	Arsenic Acid	Arsenic Pentoxide

CAS Reg. No.	1333-82-0	1317-38-0	7778-39-4	1303-28-2

Formula	CrO3	CuO	H3ASO4	As2O5

Wolmanac Concentrate 50% (CCA)	23.75%a	9.0%a	17.4%a	N/Ab

60% Wood Preservative (CCA)	28.5%	11.1%	20.4%	N/Ab

ACCc	35.46%	14.07%	N/Ab	N/Ab

According to the label (EPA Reg# 62190-2), the percent active
ingredients are as follows: chromic acid, 23.7%; cupric oxide, 9.3%;
arsenic acid, 21%.

N/A = not applicable

c.	ACC label (EPA Reg. No. 075832-3 and 75832-E).

	ACC has not been used for industrial and/or residential treatments
except for the treatment of wood used in cooling towers.  Therefore, it
is difficult to estimate the amount of chromic acid that could
potentially be used at ACC treatment plants for industrial and/or
residential uses.  The potential ACC inhalation exposure and risk
estimates presented below have been based on a range of potential wood
volumes treated.  The following inhalation risk scenarios are presented:

Air concentrations as monitored in the CCA study are used to estimate
CCA risks;

Air concentrations assuming the same volume of wood treated in the CCA
study but extrapolated to the amount of chromic acid to represent ACC
risks;

Air concentrations from the CCA study extrapolated to represent an
assumed average volume of wood for ACC industrial uses;

Air concentrations from the CCA study extrapolated to represent an
assumed average volume of wood for an unrestricted ACC use, including
residential; and

Note:  Air concentrations from the CCA study are used to back-calculate
the volume of wood that represent the cancer risk threshold (i.e., 1E-4
cancer risks).

	The amount of wood treated in the first two scenarios is based on the
actual treatment volume from the inhalation exposure study.  The
estimate of the amount of wood treated for the industrial uses is based
Vlosky’s (2006) water-based treatments and CCA estimates.  Vlosky
(2006) reports that the annual volume of round wood treated with
waterborne treatments is 85,600,000 ft3 and that there are a total of
452 treatment plants of which 82% use waterborne preservatives.  Of the
plants using waterborne preservatives, 35% use CCA.  From these data an
average estimate of the volume of wood treated with CCA is 450,769 ft3.
Assuming that treatment plants operate ~6 days per week the average
daily industrial production of round wood is 1454 ft3/day.  The round
wood (e.g., poles and piles) have longer treatment charge times and may
underestimate the volume of southern pine lumber treated daily.
Nonetheless, at this time these data are the only data available for
this risk assessment and are subject to variation.

Similarly, the volume of wood treated for industrial and residential has
been estimated from Micklewright (1998).  A total of 200 water-based
treatment plants responded to this survey.  According to this report,
372,100,000 ft3 of wood is treated via water-based preservatives
annually with 98% of those plants using CCA.  Based on these data, it is
estimated that 6,000 ft3 of wood on average are treated daily per
facility (i.e., (372,100,000 ft3 / 200 plants) / 310 days of operation
per year).  Note:  The Tampa Site in general treated more wood than the
average assumed 6,000 ft3 per day.  Finally, because of the lack of
information on the daily volume of wood treated, the volume of wood
treated per day per work shift has been back-calculated to represent an
inhalation risk of 1E-4.

	In summary, the volumes of wood treated are used to estimate the amount
of chromic acid used per work shift to extrapolate the air concentration
for an assumed industrial use and an unrestricted use (i.e., including
residential).  The average volumes of wood represent the following
amount of chromic acid used per work shift:

Industrial Use = 1,454 ft3 wood x 0.5 pcf ACC x 71.8% chromic acid = 518
lbs chromic acid; and

Unrestricted Use = 6,000 ft3 wood x 0.5 pcf ACC x 71.8% chromic acid =
2,139 lbs chromic acid.

Inhalation Cancer Risks

	The summary of the inhalation cancer risks derived from the PM10 air
concentrations of Cr+6 are presented in Table 10.  Appendix A presents
the calculation of these inhalation risks.  The inhalation cancer risks
for the multiple job functions range up to 2.1E-4 for the CCA uses
monitored in the study.  Extrapolating the volume of wood treated in the
CCA study submitted as a surrogate for ACC (i.e., multiplying the air
concentrations by a factor of 1.5 to account for a 50% higher chromic
acid concentration) the risks range up to 3.2E-4.  Using the average
industrial use (round poles) per day, the inhalation cancer risks for an
industrial use of ACC range up to 5.1E-4.  Finally, assuming a similar
market share for residential uses as the average CCA plant production
prior to the voluntary cancellation of CCA, the inhalation cancer risks
are estimated to range up to 2.1E-3.  For the extrapolated industrial
use and the “all” or unrestricted use, the inhalation risks are only
presented for the ground contact retention of 0.5 pcf.  The inhalation
risks for the above ground retention of 0.25 pcf would be half of that
reported for the ground retention.

Table 10.  Summary of Inhalation Cancer Risk Estimates for Various ACC
Scenarios.

Job Function	Inhalation (PM10) Cancer Risks (a)

	(1) CCA Study	(2) ACC (CCA Study)	(3) Industrial ACC	(4) All ACC

Rainier Site

TO	7.1E-5	1.1E-4	3.6E-4	1.5E-3

TA	9.5E-5	1.4E-4	5.1E-4	2.1E-3

PK	3.0E-5	4.4E-5	1.3E-4	5.4E-4

SU	2.4E-5	3.6E-5	1.2E-4	5.1E-4

Savannah Site

TO	2.1E-4	3.2E-4	4.2E-4	1.8E-3

TA	1.1E-4	1.7E-4	2.3E-4	9.4E-4

SU	5E-5	8E-5	1.3E-4	5.3E-4

FL	3E-5	4E-5	5E-5	1.9E-4

TG	2E-5	3E-5	3E-5	1.2E-4

Tampa Site

TO	5.9E-5	8.9E-5	3.4E-5	1.4E-4

TA	4.8E-5	7.2E-5	3.0E-5	1.2E-4

SU	4.7E-5	7.0E-5	3.8E-5	1.6E-4

FL	2.0E-4	3.0E-4	1.2E-4	5.1E-4

TG	2.8E-5	4.2E-5	1.7E-5	6.9E-5

TB	6.2E-5	9.3E-5	3.9E-5	1.6E-4

(a) Inhalation Risk = LADC (ng/m3) x Inhalation unit risk 0.0000116
(ng/m3)-1

Where:  Lifetime Average Daily Concentration (LADC, ng/m3) = PM10 air
conc (TWA ng/m3/lb Cr+6) x lbs CrO3          x (8hrs/24hrs) x (250
days/365 days) x (40 yrs/75 yrs)

Air concentrations as monitored in the CCA study are used to estimate
CCA risks;

Air concentrations assuming the same volume of wood treated in the CCA
study but extrapolated to the amount of chromic acid to represent ACC
risks;

Air concentrations from the CCA study extrapolated to represent an
assumed average volume of wood for ACC industrial uses; and

Air concentrations from the CCA study extrapolated to represent an
assumed average volume of wood for an unrestricted ACC use, including
residential.

Because of the uncertainty in the average production volume of
industrial and/or residential uses of ACC, the average volume of treated
wood has been back-calculated at a cancer risk of 1E-4.  The highest air
concentration measured at the 3 sites was for the TA at the Rainier
Site.  Based on that test subject’s exposure, treating 280 ft3 of wood
at the retention of 0.5 pcf would be equivalent to a cancer risk of
1E-4.  Other back-calculated estimates could be developed if they prove
useful to the risk managers.  At this time, only the job function at the
site with the highest air concentration has been presented.

Inhalation Non Cancer Risks

	The summary of the inhalation air concentrations and margins of
exposures (MOEs) for each job function at each of the 3 sites are
presented in Table 11.  The MOE is calculated as the ratio of the LOAEL
divided by the air concentration of the total portion of the Cr+6
collected in the worker’s breathing zone.  The inhalation
route-specific LOAEL is based on an 8-hour time weighted average (TWA)
air concentration from the epidemiology study of 8-hour work shifts in
chrome plating facilities.  The TWA air concentration to represent the
worker’s exposure is based on 6-hour TWA measurements from the CCA
pressure treatment facility study.  The 6-hour TWA from the study is
believed to be representative of the 8-hour TWA (i.e., the exposure for
the 2 hours that the sampling pumps were not run are not believed to be
higher or lower then the average over the 6-hours sampled).

The inhalation MOEs range from 7 to 130 for the CCA uses monitored in
the study.  In the second scenario, the volume of wood treated in the
CCA study was used to extrapolate to ACC (i.e., multiplying the air
concentrations by a factor of 1.5 to account for a 50% higher chromic
acid concentration).  Once extrapolated to the ACC Cr+6 concentrations,
the MOEs range from 5 to 83.  Assuming an average industrial use (i.e.,
third scenario), the inhalation MOEs for an industrial use of ACC range
from 6 to 82.  Finally, assuming a similar market share for residential
uses as the average CCA plant production prior to the voluntary
cancellation of CCA (scenario 4), the inhalation MOEs are estimated to
range from 2 to 20.  The inhalation target MOE is 30.  For the
extrapolated industrial use and the “all” or unrestricted use, the
inhalation MOEs are only presented for the ground contact retention of
0.5 pcf.  The inhalation risks for the above ground retention of 0.25
pcf would be half of that reported for the ground retention (i.e.,
double the MOEs).

Table 11.  Worker Total Particulate Air Concentrations and Non Cancer
Inhalation MOEs.

Job Function	Air Conc.

(from Table 6)	Air Concentration (ng/m3)

	Inhalation MOEs

(Target MOE = 30)

	(ng/m3/lb CrO3)	(1) CCA	(2) ACC	(3) ACC Industrial	(4) ACC All	(1) CCA
(2) ACC	(3) ACC Industrial	(4) ACC All

Rainier, OR Site

TO	0.62	59	89	321	1326	34	23	6	2

TA	0.54	63	95	280	1155	32	21	7	2

PK	0.29	29	44	150	620	69	46	13	3

SU	0.19	17	26	98	406	120	78	20	5

Savannah, GA Site

TO	0.60	148	222	311	1283	14	9	6	2

TA	0.25	64	96	130	535	31	21	15	4

SU	0.074	18	27	38	158	110	74	52	13

FL	0.087	22	33	45	186	91	61	44	11

TG	0.054	16	24	28	116	130	83	72	17

Tampa, FL Site

TO	0.12	107	161	62	257	19	12	32	8

TA	0.13	114	171	67	278	18	12	30	7

SU	0.12	85	128	62	257	24	16	32	8

FL	0.36	296	444	186	770	7	5	11	3

TG	0.047	41	62	24	101	49	33	82	20

TB	0.17	149	224	88	364	13	9	23	6

Air concentrations as monitored in the CCA study are used to estimate
CCA risks (see Table 5);

Air concentrations assuming the same volume of wood treated in the CCA
study but extrapolated to the amount of chromic acid to represent ACC
risks;

Air concentrations from the CCA study extrapolated to represent an
assumed average volume of wood for ACC industrial uses;

(4) Air conc from the CCA study extrapolated to represent an assumed
average volume of wood for an unrestricted ACC use, including
residential.4.1.2	Wood Dust Exposure and Risk Estimates

	Osmose, Inc., has submitted an ACC-treated wood combined surface wipe
and internal wood expressate study (i.e., MRID No. 466447-01).  The
“expressate” sample is the liquid within the wood that was pressed
from a 1 x 1 x 1.5 inch piece of treated wood.  A summary of the study
is presented below in Section 4.2.3 and USEPA 2006c.  The levels of
hexavalent chromium in the interior of the ACC-treated wood were
assessed by analyzing expressate of the wood.  The percent reduction in
hexavalent chromium on each sampling day after treatment was determined
using the initial levels of treating solution.  Table 12 provides a
summary of the levels of hexavalent chromium and the average percent
reduction over time.  Although the percent reduction appears to be
fairly rapid, the absolute value of Cr+6 remains high throughout the
study (up to 58 days after treatment).  At the end of the study, Cr+6
was still present in the Douglas fir wood at 0.85 ppm and 16 ppm at
retention rates of 0.25 pcf and 0.50 pcf, respectively.  In the Southern
pine wood, Cr+6 was still present at 73 ppm and 134 ppm at retention
rates of 0.25 pcf and 0.50 pcf, respectively.  Note:  The 0.5 pcf is for
ground contact ACC-treated wood and it is also the highest retention
level proposed for ACC.

Table 12.  Levels of Hexavalent Chromium in the Interior of the Wood

(as determined by expressate samples)

Retention (pcf)	Initial Treatment Solution (ug/g)	Average Hexavalent
Chromium found in Expressate Liquid (µg/g, ppm)

DAT 0	DAT 3	DAT 9	DAT 23	DAT 36	DAT 58

Douglas fir

0.25	3417.98	859.6	74.62	46.43	0.41	0.17	0.85

Average Percent Reduction	74.85%	97.82%	98.64%	99.99%	100.00%	99.98%

0.50	7403.96	1292.59	699.32	44.41	39.81	21.23	15.78

Average Percent Reduction	82.54%	90.55%	99.40%	99.46%	99.71%	99.79%

Southern pine

0.25	3230.73	1792.73	1005.83	682.64	258.76	178.71	72.83

Average Percent Reduction	44.51%	68.87%	78.87%	91.99%	94.47%	97.75%

0.50	6882.42	4708.51	1854.91	1320.28	630.38	359.88	134.33

Average Percent Reduction	31.59%	73.05%	80.82%	90.84%	94.77%	98.05%

	Based on the internal concentrations of Cr+6 in the wood, inhalation
exposure and risk estimates for occupational workers exposed to wood
dust from ACC-treated wood indoors have been estimated (e.g.,
manufacturing outdoor furniture with ACC-treated wood).  The OSHA PEL of
15 mg/m3 for total wood dust and the PEL of 5 mg/m3 for respirable wood
dust have been used as the upper bound exposure estimates.  It is
believed that any wood dust concentrations in the air exceeding these
PELs will be mitigated by the industry.  If it was deemed necessary to
characterize the upper bound exposure estimate, EPA could review the
monitoring data for wood dust in OSHA’s Integrated Management
Information System (IMIS).  The two PELs cited for wood dust are for the
wood dust itself, not chemical treatments within the wood dust.
Inhalation non cancer and cancer exposure estimates to Cr+6 in
ACC-treated wood are based on the following equations:

Non Cancer:  Total wood dust (OSHA PEL 15 mg/m3) x expressate (ng/mg or
ppm) = air concentration (ng/m3).  Where the target MOE = 30.

Cancer:  Respirable wood dust (OSHA PEL 5 mg/m3) x expressate (ng/mg or
ppm) = air concentration (ng/m3).

	Table 13 presents the potential for non cancer (i.e., MOEs) and cancer
risk estimates for occupational workers breathing wood dust from cutting
and/or sanding wood treated with Cr+6.  Using the last day of
measurements from the Osmose study (i.e., 58 DAT) the MOEs are of
concern for the Southern pine treated at the retention of 0.25 and 0.5
pcf and for the Douglas-fir at the retention of 0.5 pcf.  The expressate
for the highest risk (i.e., SP at 0.5 pcf) is an order of magnitude
higher at 9 DAT as presented in Table 12 above.  The MOE is also
presented in Table 13 at the expressate concentration of 15 ppm to
simulate “fixation”.  The MOE at fixation is 9.  The cancer risks
achieve the value of 1E-4 at an expressate concentration of 15 ppm.  The
Cr+6 expressate in the Southern pine did not reduce to 15 ppm after 58
days but reached this level at or before 58 days for Douglas-fir.  Using
a first-order exponential decay for the expressate data reported in
Table 12 for SP @ 0.5 pcf, the predicted mean of the expressate reaches
15 ppm 94 DAT.

	Residential inhalation risks to wood dust are believed to be less than
that for occupational workers because of the intermittent residential
use and most residential uses would be in ambient conditions.

Table 13.  Inhalation Cancer and Non Cancer Risks To Workers Exposed to
Cr+6 At The OSHA PEL For Wood Dust (Ground Retention 0.5 pcf).

Wood Species

and Retention (pcf)	OSHA PEL for Wood Dust (mg/m3)	Expressate at 58 DAT

(ppm or ng/mg)	Estimated Cr+6 Air Concentration (ng/m3)	Total Dust

MOE

(Target = 30)	Respirable

LADC

(ng/m3)	Respirable

Cancer Risk

	Total Dust	Respirable

Total Dust	Respirable

	DF @ 0.25	15	5	0.85	12.75	4.25	160	0.518	6.0E-06

DF @ 0.5	15	5	16	240	80	8	9.74	1.1E-04

SP @ 0.25	15	5	73	1095	365	2	44.4	5.2E-04

SP @ 0.5	15	5	134	2010	670	1	81.6	9.5E-04

Fixation for SP@ 0.5	15	5	15 ppm at 94 DAT	225	75	9	9.1	1.1E-04

4.2	Dermal Exposure and Risks

	There is the potential for dermal exposure to occupational handlers at
pressure treatment facilities, at the retail stores, construction
workers, and the general public.  EPA has expressed concern for dermal
risk from exposure to ACC treated wood, as there are higher levels of
Cr+6

in ACC treated wood than CCA treated wood.

Pressure Treatment Facilities

The majority of lumber/wood that is treated at a pressure treatment
facility is moved mechanically (e.g., forklifts).  However, there is the
potential for dermal contact with this wood or surfaces that have Cr+6
residues (e.g., equipment near the pressure treatment cylinder door).
It is EPA’s policy to require personal protective equipment (PPE) such
as gloves, long pants, long sleeved shirts, or coveralls for chemicals
that are either dermal irritants or dermal sensitizers to mitigate the
localized skin effects.  It is recommended that ACC labels require this
PPE.

Retail/Construction Workers

Pressure-treated wood such as ACC is considered by EPA to be a treated
article and as such there are no pesticide labels transported with the
lumber/wood.  The Cr+6 residues on the surface of treated wood are
reduced to the less toxic Cr+3 over time.  The shorter the duration from
treatment to the retail chain and/or construction uses the more likely
Cr+6 residues will be available for dermal contact.  The reduction of
Cr+6 to Cr+3 is temperature and time dependant.  Cold temperatures slow
the reduction process and warmer temperatures speed the process.  The
retail/construction workers will most likely handle freshly treated wood
on a daily basis.  The time it takes Cr+6 to reduce to below the EPA’s
level of concern of 0.009 ug/cm2 is presented in Section 4.2.3 below.

General Public

The opportunities for the general public to come in contact with treated
wood include do-it-yourself (DIY) builders (e.g., building a deck) and
children and/or adults contacting play sets and/or decks.  The potential
for DIY and/or children to come in contact with Cr+6 on ACC-treated wood
is dependant upon how long the wood has been treated prior to dermal
contact and at what temperatures it was stored.  EPA has selected a
level-of-concern (LOC) for Cr+6 for dermal contact of 0.009 ug/cm2 (10%
MET and an uncertainty factor of 10x).  Note:  Cleaners such as bleach
that raise the pH will convert the wood surface residues of Cr+3 back to
Cr+6 (Taylor et al 2001).  However, there is insufficient information on
this phenomenon to determine if there are any risks of concern.

	To determine the potential for dermal exposure to Cr+6, a surface
residue dislodgeability study over time has been submitted by Osmose,
Inc., to the EPA.  EPA has required and accepted wood wipe studies to
determine the amount of residue on the surface of the wood for potential
exposure.  The initial wipe study protocol was developed by the Consumer
Product Safety Commission (CPSC) in response to arsenic on CCA-treated
wood (CPSC 2001).  EPA provided comments in the development of this
cloth wipe protocol.  The CCA registrants further refined this cloth
wipe protocol to establish a relationship between skin contact and cloth
contact for wiping.  The wiping with a test subject’s hand has been
used in a CCA wipe study to develop a hand transfer reduction factor
(TRF) to more accurately mimic human exposure (Gradient 2002 and RTI
2003).  The hand sampling method consisted of passes of the hand over a
given area of treated wood.  In summary:

“Results from both the RTI Pilot Study and the recent CPSC study
(CPSC, 2003) indicate that the amount of dislodgeable arsenic collected
on a block wipe or a hand does not increase after about 10 to 15 passes
on a test board, and that increasing the weight of the block or the
weight on the hand does not significantly increase the amount collected.
 Also, based on experiments in the CPSC (2003) study, once equilibrium
is achieved, even sampling a larger surface area of treated wood does
not significantly increase levels of dislodgeable arsenic on a sampling
device.  If equilibrium is achieved, then it is appropriate to divide
the mass of dislodged metal by the surface area of the sampling
device.”

	EPA’s current methodology for assessing the residues available for
transfer from treated wood is to sample wood as described in the studies
above with a wet hand and then determine the relative relationship
between the residues collected by a hand wipe and a cloth wipe.  Based
on work done by CPSC with CCA, roughly 18% of what is collected on a
cloth wipe is collected on a wet hand (i.e., residues from cloth wipes
are about 5x higher than residues from wet hand wipes).  Results from
this type of sampling methodology could be used to determine what
concentration of Cr+6 transfers from the ACC-treated wood to human skin
(i.e., on the palm of the hand).  Hand sampling of ACC-treated wood
could, in theory, be used as the maximum “exposure” (in ug/cm2) one
could receive from contact with the wood.  This assumption is based on
achieving a near steady state between the wood surface and hand.
However, the only data available to assess the ACC-treated wood is the
cloth wipe study results submitted by Osmose, Inc.  This study did not
provide data for the hand wipe portion of the methodology.  The results
of the cloth wipe study and the associated uncertainties and study
design limitations are discussed in detail throughout the remainder of
this risk assessment.

Cloth Wipe Residue Study (Osmose 2005):

Osmose, Inc., has submitted a wipe study where the wood was pressure
treated with ACC in Buffalo, NY (Osmose 2005, USEPA 2006b).  The purpose
of this study was to examine the potential dermal exposures to treated
wood associated with use of ACC as a wood preservative through pressure
treatment application methods.  In particular, the goals of the study
were to examine the changes in dislodgeable hexavalent chromium residues
and expressate and the extent of reduction of hexavalent chromium over
time.  The registered product examined in this study, Osmose ACC 50%
Wood Preservative, is not currently produced or available.  An
equivalent test material was prepared using the following products:  (1)
cupric oxide (EPA Reg. No. 65345-1; 98.6% ai) and (2) Osmose chromic
acid (EPA Reg. No. 3008-78; 99.7% ai).  The treatment solution was
reported to be identical to a diluted version of the Osmose ACC 50%
registered product and was formulated according to Standard P5-05 of the
American Wood-Preservers’ Association (AWPA).  The analysis of the
test material indicated 33.4% chromic acid and 13.5% cupric oxide.

This study was conducted under normal commercial practices at a reduced
scale treatment plant. In commercial settings, the lumber to be treated
(typically 2 x 6 x 8 pieces) is dead stacked (i.e., no space between
layers) and metal banded into units, which are 8 pieces wide and 16
pieces high.  Each unit is treated once and maintained as a unit through
the drying, storage and shipment processes.  The lumber chosen for this
study included southern pine and Douglas-fir.   The charge (or treatment
batch) consisted of one full unit of dead stacked 2” x 6” x 8”
lumber.  The ACC concentrate was added to water to achieve the required
concentration for the treating solution (about 1 or 2%) to reach a
desired retention of 0.25 to 0.50 pounds per cubic feet (pcf).  The
treating solutions were analyzed for pH, the active ingredients (CrO3
and CuO), and hexavalent chromium (Cr+6).  Table 14 provides the results
of the pH and active ingredient analysis.

μg/gm)

CrO3	CuO

	Southern pine	0.25	71.4	28.6	0.99	3.23	3231

	0.50	71.8	28.2	2.12	2.83	6882

Douglas fir	0.25	71.6	28.4	0.99	3.27d	3418

	0.50	71.8	28.2	2.14	2.80	7404

According to standard:  CuO = 28.0 – 31.8%; CrO3 = 63.3 – 68.2%.

According to study report:  1% or 2%.

According to standard:  2.0-3.9.

pH of solution after treatment

	After treatment, the wood units were stored outdoors.  Temperature on
the surface of the wood units and in the interior of the wood units was
monitored every 30 minutes over the 58 day monitoring period.  The 30
minute temperatures ranged from 8 to 85oF (-13 to 29.4oC) on the outside
of the unit and from 23 to 77oF (-5 to 25oC) in the interior of the
unit.  Average daily temperatures in the interior of the stacked wood
ranged from 31.6 to 54.7oF.  Over the course of the sampling intervals,
temperatures appeared to decrease at first, with a gradual warming trend
up until the end of the study.  Ambient conditions were recorded at a
nearby NOAA reporting station and indicated that the temperatures
recorded at the test site during the monitoring period were slightly
below normal.  Precipitation over the two months of the study period
totaled 5.88 inches and was reported to be normal.

Three types of samples were taken post-treatment:  (1) wipe samples were
taken from the surface of boards in each unit immediately after
treatment and at predetermined intervals after treatment,  (2) liquid
samples were expressed from cross sections cut from interior pieces of
lumber to determine the reduction of chromium in the interior of the
board, and (3) borings were taken for confirmation of penetration and
retention immediately after treatment and for qualitative determination
of the presence of hexavalent chromium at certain sampling intervals
post-treatment.  Wipe, wood expressate and boring samples were taken on
0, 3, 9, 23, 36, and 58 days after treatment.

Wood Surface Concentrations (Wipe Samples):

The following procedure was followed to conduct the wipe sampling:

Personnel wore powder free latex gloves which were changed as necessary.

A polyester cloth wipe (4.5 in2) was weighed and moistened with
deionized water to double its weight.  It was squeezed and worked to
uniformly distribute the water throughout the wipe.

The wipe was attached to a 1.1 kg steel block (covered in Parafilm®)
using heavy duty rubber bands and pulled across a 75.4 in2 area of the
wood five times, rotated 90o, and pulled across another five times.
Note:  Existing protocols for hand wipe studies recommend a total of 20
passes, not the 10 passes used in this study.

The wipe was removed and placed in a labeled four ounce glass jar and
immediately given to Analytical Services for extraction and analysis for
hexavalent chromium.

Before the next wipe sample was taken, the Parafilm® and rubber bands
were replaced.

	Field and concurrent laboratory fortification samples and blank samples
were not reported in the study report or in the raw data table in the
Appendix.  The SOP for the wipe samples indicated a blank and fortified
wipe sample should be analyzed along with the study samples, but no
further information was provided.

	Table 15 provides a summary of the wipe sample residues as measured on
the sampling days of 0, 3, 9, 23, 36, and 58.  A first order exponential
decay function was fit to the surface residue values measured on 3, 9,
23, 36, and 58 DAT.  The residues for DAT 0 were excluded because of the
unabsorbed treatment solution and the fact that the wood would remain on
the drip pad at the facility while wet.  Table 16 provides the daily
predicted residues over time based on the fitted regression function.
The coefficient of determination (R2) for the 0.25 pcf ACC retention was
higher than the R2 for the 0.5 pcf retention rate indicating that the
first order exponential decay function explains more of the variation
for the lower retention data set than the higher retention data set.
The R2 for the 0.25 pcf retention is 0.67 for Southern Pine and 0.80 for
Douglas Fir.  The R2 for the 0.5 pcf retention is 0.36 for Southern Pine
(SP) and 0.02 for Douglas Fir (DF).  The analysis used by the EPA is a
relatively simple regression approach in which each wood species and
retention rate data set was analyzed separately.  The regression model
used by the EPA assumes Cr+6 surface residues decline as a function of
time (i.e., first-order exponential decay).  The default assumption is
that residues decline at a constant rate at a give temperature (or fixed
half-life at a given temperature).  A more complex regression that
incorporates categorical variables from the wood species and/or
retention rates could be used to further analyze the data.  However,
based on the limitations of the wipe study as described in Section 5
below (e.g., the study did not control for temperature of wood during
chromium reduction, the study included limited sampling intervals, the
study used cloth wipes only and did not correlated these wipes to
residue levels from hand wipes, etc.), further statistical refinements
are not recommended.

 μg/cm2 was presented.  USEPA (2006a) reported that the level of Cr+6
in Southern Pine at the retention of 0.25 pcf was reduced to 0.009
μg/cm2 at 45 days and 100 days at the retention of 0.5 pcf.  For
Douglas Fir, Cr+6 was reduced to 0.009 μg/cm2 at 36 DAT at retention of
0.25 pcf and 197 DAT at retention of 0.5 pcf.

μg/cm2 yet the average measured value at 23 DAT is 0.1338 μg/cm2 and
0.0809 μg/cm2 at 36 DAT.  Similar variability in the data is evident
for the Southern Pine treated at the retention of 0.25 pcf.  The average
residue predicted at 4 DAT is 0.090 μg/cm2 yet the average measured
value is 0.1104 μg/cm2 at 3 DAT and 0.0477 μg/cm2 at 9 DAT.  For
Douglas Fir (0.5 pcf), the average residue predicted at 1 DAT at the
retention of 0.5 pcf is 0.040 μg/cm2 yet the average measured value at
23 DAT is 0.1193 μg/cm2 and 0.1050 μg/cm2 at 36 DAT.  Note:  The
average measured residue values for the Douglas Fir (0.25 pcf) are below
those predicted at the sampling intervals in the study (except for 0
DAT).

	The variability of the measured values is illustrated in Table 17 for
Southern Pine at retentions of 0.25 and 0.5 pcf.  As illustrated in
Table 17 and Appendix B  the average predicted residue level of 0.090
μg/cm2 at 4 DAT for Southern Pine (0.25 pcf) is exceeded by the average
measured residue level on 23 DAT (i.e., average of 0.0964 μg/cm2).
Similarly, as illustrated in Table 17 and Appendix B, the average
predicted residue level of 0.091 μg/cm2 at 21 DAT for Southern Pine
(0.5 pcf) is exceeded by the average measured residue level on 23 DAT
(i.e., average of 0.1338 μg/cm2) but not by the average measured
residue level on 36 DAT (i.e., average of 0.0809 μg/cm2).  The lower
and upper 95th% confidence limits on the mean predicted residue levels
for both wood species are presented in Appendix B.  The 95th% upper
confidence limit on the predicted mean reduces to below the level of
concern (i.e., 0.092 μg/cm2) at 10 DAT for the 0.25 pcf and 30 DAT for
0.5 pcf.

	The variability of the measured values is illustrated in Table 18 for
Douglas Fir at the retention of 0.5 pcf.  As illustrated in Table 18 and
in Appendix B, the average predicted residue level of 0.040 μg/cm2 at 1
DAT for Douglas Fir (0.5 pcf) is exceeded by the average measured
residue levels on 23 DAT (i.e., average of 0.1193 μg/cm2) and 36 DAT
(i.e., average of 0.1050 μg/cm2).  However, the measured values on 3
DAT and 9 DAT are below the level of concern.  The 95th% upper
confidence limit on the predicted mean reduces to the level of concern
(i.e., 0.092 μg/cm2) at 1 DAT for the 0.5 pcf.

Several limitations have been noted in this study.  The limitations of
this study that would tend to underestimate the residues of Cr+6 include
no recovery samples were reported and there were insufficient number of
passes with the cloth wipes to establish maximum residues to mimic human
exposure from contacting treated wood.   On the other hand, the cloth
wipe methodology without a hand transfer reduction factor tends to
overestimate the amount of residues available for human exposure.  These
data provided in this report are useful as a range finder to determine
dermal exposure to ACC-treated wood.  A more refined study would be more
appropriate to accurately determine the amount of Cr+6 available for
human exposure.

Table 15.  Levels of Hexavalent Chromium on the Surface of the Wood

(as determined by wipe samples)

Retention (pcf)	Hexavalent Chromium found in Wipe Samples (average
µg/cm2 ± standard error) (a)

	DAT 0	DAT 3	DAT 9	DAT 23	DAT 36	DAT 58

Douglas fir

0.25	14.028 ± 0.800	0.0681 ± 0.0089	0.0809 ± 0.0353	0.0193 ± 0.0069
0.0105 ± 0.0017	0.0029 ± 0.0008

0.50	16.198 ± 3.532	0.0352 ± 0.0012	0.0108 ± 0.0018	0.1193 ± 0.0153
0.1050 ± 0.0253	0.0111 ± 0.0038

Southern pine

0.25	10.164 ± 2.684	0.1104 ± 0.0278	0.0477 ± 0.0108	0.0964 ± 0.0306
0.0123 ± 0.0042	0.0048 ± 0.0005

0.50	30.173 ± 7.527	0.1361 ± 0.0435	0.1699 ± 0.0105	0.1338 ± 0.0190
0.0809 ± 0.0332	0.0305 ± 0.0076

(a)  Four wipe samplers were taken at each sampling interval.

μg/cm2).

DAT	Southern pine (SP)	Douglas-Fir

	0.25 pcf	0.5 pcf	0.25 pcf	0.5 pcf

1	0.106	0.161	0.075	0.040

2	0.100	0.157	0.071	0.039

3	0.095	0.152	0.066	0.039

4	0.090	0.148	0.063	0.039

5	0.085	0.144	0.059	0.038

6	0.080	0.140	0.056	0.038

7	0.076	0.136	0.052	0.038

8	0.072	0.132	0.049	0.038

9	0.068	0.128	0.047	0.037

10	0.064	0.125	0.044	0.037

11	0.061	0.121	0.041	0.037

12	0.058	0.118	0.039	0.037

13	0.055	0.114	0.037	0.036

14	0.052	0.111	0.035	0.036

15	0.049	0.108	0.033	0.036

16	0.046	0.105	0.031	0.035

17	0.044	0.102	0.029	0.035

18	0.042	0.099	0.027	0.035

19	0.039	0.096	0.026	0.035

20	0.037	0.094	0.024	0.034

21	0.035	0.091	0.023	0.034

22	0.033	0.088	0.022	0.034

23	0.032	0.086	0.020	0.034

24	0.030	0.083	0.019	0.033

25	0.028	0.081	0.018	0.033

26	0.027	0.079	0.017	0.033

27	0.025	0.077	0.016	0.033

28	0.024	0.074	0.015	0.032

29	0.023	0.072	0.014	0.032

30	0.022	0.070	0.013	0.032

31	0.020	0.068	0.013	0.032

32	0.019	0.066	0.012	0.032

33	0.018	0.065	0.011	0.031

34	0.017	0.063	0.011	0.031

35	0.016	0.061	0.010	0.031

36	0.015	0.059	0.009	0.031

37	0.015	0.058	NA	0.030

38	0.014	0.056	NA	0.030

39	0.013	0.054	NA	0.030

40	0.012	0.053	NA	0.030

41	0.012	0.051	NA	0.030

42	0.011	0.050	NA	0.029

43	0.011	0.048	NA	0.029

44	0.010	0.047	NA	0.029

45	0.009	0.046	NA	0.029

46	NA	0.044	NA	0.028

47	NA	0.043	NA	0.028

48	NA	0.042	NA	0.028

49	NA	0.041	NA	0.028

50	NA	0.040	NA	0.028

51	NA	0.039	NA	0.027

52	NA	0.037	NA	0.027

53	NA	0.036	NA	0.027

54	NA	0.035	NA	0.027

55	NA	0.034	NA	0.027

56	NA	0.033	NA	0.026

57	NA	0.032	NA	0.026

58	NA	0.032	NA	0.026

100	NA	0.009	NA	0.019

197	NA	NA	NA	0.009

NA – not applicable, predicted values below the level of concern.

Predicted Residue = exp(intercept + slope * Day)

Where:

Wood @ retention (pcf)	intercept	Slope	coefficient of determination (R2)

Southern Pine @ 0.25 pcf	-2.19	-0.05	0.67

Southern Pine @ 0.5 pcf	-1.80	-0.03	0.36

Douglas-Fir @ 0.25 pcf	-2.53	-0.06	0.80

Douglas-Fir @ 0.5 pcf	-3.22	-0.01	0.02

Table 17.  Individual Wipe Sample Results For Southern Pine On Sampling
Days 3, 9, and 23 DAT For 0.25 pcf and 23 and 36 DAT For 0.5 pcf.

Wood Species	Retention (pcf)	DAT	Replicate	Surface Wipe (ug/cm2)

S. pine	0.25	3	1	0.0709

S. pine	0.25	3	2	0.1537

S. pine	0.25	3	3	0.0544

S. pine	0.25	3	4	0.1626

3 DAT:  Average Southern Pine (0.25 pcf retention) 0.1104 ± 0.0278
μg/cm2

S. pine	0.25	9	1	0.0571

S. pine	0.25	9	2	0.0453

S. pine	0.25	9	3	0.0189

S. pine	0.25	9	4	0.0693

9 DAT: Average Southern Pine (0.25 pcf retention) 0.0477 ± 0.0108
μg/cm2

S. pine	0.25	23	1	0.0828

S. pine	0.25	23	2	0.0204

S. pine	0.25	23	3	0.1664

S. pine	0.25	23	4	0.116

23 DAT:  Average Southern Pine (0.25 pcf retention) 0.0964 ± 0.0306
μg/cm2

S. pine	0.5	23	1	0.1404

S. pine	0.5	23	2	0.1218

S. pine	0.5	23	3	0.091

S. pine	0.5	23	4	0.1819

23 DAT: Average Southern Pine (0.5 pcf retention) 0.1338 ± 0.0190
μg/cm2

S. pine	0.5	36	1	0.152

S. pine	0.5	36	2	0.0205

S. pine	0.5	36	3	0.0284

S. pine	0.5	36	4	0.1226

36 DAT: Average Southern Pine (0.5 pcf retention) 0.0809 ± 0.0332
μg/cm2

DAT = Days after treatment; pcf = pounds cubic foot

Table 18.  Individual Wipe Sample Results For Douglas Fir On Sampling
Intervals 23 and 36 DAT For 0.5 pcf.

Wood Species	Retention (pcf)	DAT	Replicate	Surface Wipe (ug/cm2)

DF	0.5	23	1	0.112

DF	0.5	23	2	0.0796

DF	0.5	23	3	0.1495

DF	0.5	23	4	0.1361

23 DAT:  Average Douglas Fir (0.5 pcf retention) 0.1193 ± 0.0153
μg/cm2

DF	0.5	36	1	0.0652

DF	0.5	36	2	0.0716

DF	0.5	36	3	0.1076

DF	0.5	36	4	0.1755

36 DAT: Average Douglas Fir (0.5 pcf retention) 0.1050 ± 0.0253 μg/cm2

DAT = Days after treatment; pcf = pounds cubic foot

4.3	Incidental Oral Exposure and Risks

	The potential for ingestion of Cr+6 contaminated soils resulting from
ACC-treated wood can not be measured directly as there are no sources of
ACC-treated decks.  Therefore, estimates of soil ingestion are derived
from the available soil concentration data in the CCA Stochastic Human
Exposure and Dose Simulation (SHEDS) assessment (i.e., soil sampled
around CCA-treated structures).  Table 10 of the 2005 SHEDS document
summarizes the soil data used in the probabilistic assessment and
reports a mean concentration of total Cr of 39.5 ± 27.7 mg/kg
(75th%tile = 49.6 mg/kg)  in warm climates (Solo-Gabriele et al. 2001)
and 16.9 ± 39.2 mg/kg (75th%tile = 16.8 mg/kg) in cold climates (Doyle
and Malaiyandi 1992).  In addition, the SHEDS assessment provides
additional support data of total Cr from 42 samples taken at Fort Fun
Park, Newport News, VA.  Note: The Fort Fun Park data were not used in
determining the exposures in the probabilistic estimates but are within
the range of the data reported by Solo-Gabriele and Doyle and
Malaiyandi.  Of the 42 samples taken at Fort Fun Park, 8 are below the
LOD (LOD range <3.6 to <1.7 mg/kg) and the range of data are from <1.7
to 60.6 mg/kg.  To extrapolate the CCA data used in the SHEDS assessment
into potential Cr+6 soil estimates for ACC, the soil concentration is
adjusted by 1.51x to account for the increased concentration of Cr+6 in
ACC, and then multiplied by 10 percent to estimate the portion of total
Cr that maybe Cr+6 (USEPA 2001).  The soil concentration estimates are
provided in Table 19.

Table 19.  Potential Cr+6 Soil Concentrations Assigned to ACC-Treated
Decks.

Statistic	CCA Total Cr  (mg/kg or ppm)a	ACC Cr+6 (mg/kg or ppm)b

Mean ± std	Warm:  39.5 ± 27.7	Warm: 6.0 ± 4.2

	Cold:  16.9  ±39.2	Cold: 2.6 ± 5.9

75th%tile	Warm: 49.6	Warm: 7.5

	Cold: 16.8	Cold: 2.5

Note:  Soil concentrations are on a dry weight basis.

a 	Warm climates Solo-Gabriele et al. 2001 and cold climates Doyle and
Malaiyandi 1992.

b	Cr+6 soil conc (mg/kg) = total Cr (mg/kg) x 1.51 conversion from CCA
to ACC x 0.1 (portion of total Cr that may be present as Cr+6).

	The potential occurrence of Cr+6 soil concentrations around ACC-treated
decks are used to provide estimates for the soil ingestion exposure
pathway.  The daily soil intake reported in the CCA SHEDS assessment is
31 mg/day (geometric mean), 61 mg/day (arithmetic mean), and 74 mg/day
(75th%tile).  There are no data available to indicate what portion of a
daily intake of soil ingestion would actually occur from soil
contaminated from a treated structure.  Therefore, a conservative
bounding estimate using the daily intake (i.e., assuming a child
receives the daily intake from an ACC-source contaminated soil) is
estimated from the following equation:

soil ingestion (mg/kg/day) = soil conc (mg/kg) x (1 kg/1E6 mg) x 61 mg
daily intake rate x (1/15 kg BW)

The daily Cr+6 soil ingestion using the mean soil concentration in a
warm climate and assuming 100 percent of the intake rate is from
contaminated soil is 0.00002 mg/kg/day.  A margin of exposure (MOE)
approach is used to estimate the potential risk to ingesting soil around
ACC-treated decks.  The target MOE is 100.  The daily Cr+6 soil
ingestion is 0.00002 mg/kg/day using the mean soil concentration in a
warm climate and assuming 100 percent of the intake rate is from
contaminated soil.  The MOE equation is:

MOE = incidental oral NOAEL of 0.12 mg/kg/day / soil ingestion of
0.00002 mg/kg/day

The estimated MOE is 6000, and therefore, not of concern.

In addition to the potential incidental oral ingestion of chromium from
contaminated soil there is the potential for incidental oral ingestion
of chromium from hand-to-mouth exposure from children playing on
ACC-treated structures over time (e.g., decks and play sets).  As with
the soil ingestion route of exposure, the incidental oral route for
children playing on treated structures is expected to be minor for
chromium when the proper time has been allotted for the chromium to be
fixed.  However, to indicate that the risks are not of concern for the
non cancer oral endpoint, a screening-level assessment using bounding
inputs is provided.  The average daily dose (ADD) for total chromium
residue ingestion from play sets from the SHEDS (2005) report was used
to screen the potential risks for hand-to-mouth exposure from
ACC-treated wood.  As a bounding input, the 99th percentile from the ADD
for total chromium was selected for a screening-level assessment.  The
99th percentile ADD is 4.0E-4 mg/kg/day for total chromium residue
ingestion from play sets treated with CCA (Table 20 of the SHEDS report,
warm climate).  The CCA ADD was multiplied by 1.5x to adjust for the
amount of chromium in ACC-treated wood.  Because the SHEDS assessment
was used as the basis for the hand-to-mouth estimates, the assessment is
predicated that the Cr+6 in ACC-treated wood has the opportunity to
become fixed (i.e., reduced).

The MOE equation is:

MOE = incidental oral NOAEL of 0.12 mg/kg/day / (residue ingestion of
0.0004 mg/kg/day x 1.5x)

The estimated MOE is 200, and therefore, not of concern.

Note:  This screening-level assessment used total chromium residues for
the hand-to-mouth exposures and the toxicological endpoint used is for
Cr+6 (worst-case assumptions to indicate no concerns).  If necessary,
this risk can be further refined at a later date.

5.0	UNCERTAINTIES AND DATA LIMITATIONS

	The uncertainties and limitations associated with the toxicity data,
inhalation exposure study, cloth wipe residue study, and the risk
assessment are provided in the subsections below.  The uncertainties and
limitations in the data used to develop the risk assessment, as well as
the assumptions used in estimating the risks, are highlighted to provide
additional characterization of the risks presented and to inform the
regulatory decision making process.

5.1	Uncertainties and Limitations Associated with the Toxicity Data

g potassium dichromate [which is equivalent to 18 g Cr(VI)] to
five chromium sensitive individuals caused acute reaction on the hands
of all test subjects and one developed generalized eruptions (Fregert,
1965).  Assuming that each of the subjects weighed 70 kg, the dose per
kg body weight was 0.26 g (18 g Cr(VI/70 kg) .  This was the
lowest oral dose that elicited ACD in 100% of the tested subjects.  The
10% MET will probably be much lower than 0.26 g Cr(VI)/kg body
weight. This value is lower than the RfD which is 5 ug/kg/day suggesting
that the Cr(VI) reference dose based on other systemic endpoints may not
be protective of Cr(VI)-induced ACD in the sensitized population.
However, the EPA workgroup concluded that these data were not adequate
to support the conclusion of greater dermal potency by the oral route.
Only 5 individuals were studied, these individuals were already
sensitized to chromium, and the data are not recent.  A selected value
of 0.12 mg/kg/day as an incidental oral endpoint already exists for Cr+6
and is from an acceptable study reviewed by EPA (with an uncertainty
factor of 100). Therefore, this value will continue to be used for
incidental oral risk assessments.

As noted in both the EPA’s Toxicological Review of Hexavalent Chromium
(USEPA, 1998) and in the Occupational Health and Safety
Administration’s proposed hexavalent chromium rule (Federal Register
69: 59360-59388, October 1994), carcinogenic risk from exposure to
hexavalent chromium was estimated on the basis of total chromium
obtained from all of the soluble and insoluble chromium to which workers
in the Mancuso (1975) study were exposed.  Because the total chromium
air concentration may include a contribution from the non-carcinogenic
chromium (III), and based on recent dose-response assessments discussed
in OSHA’s proposed hexavalent chromium rule, the unit risk for
hexavalent chromium derived from Mancuso (1975) may underestimate the
actual risk anywhere from two to five-fold.

The National Toxicology Program (NTP) is currently conducting an oral
cancer study for Cr+6.  The availability of the results is expected to
be in April or May of 2007 at the earliest.

5.2	Uncertainties and Limitations Associated with the Inhalation
Exposure Study

The number of replicates monitored per job function (a minimum of 5 per
site) for some of the job functions was less than the guideline
recommended number of 15.

Breakthrough/retention testing was only performed on PVC filters, not
PTFE filters.

As approved in the EPA protocol review, the inhalation exposure study
submitted in support of ACC is based on CCA applications.  The CCA air
concentrations are used in this risk assessment as a surrogate for ACC.
Therefore, the air concentrations collected for CCA have been normalized
by the amount of Cr+6 used during the study monitoring period.  Once the
CCA air concentrations are normalized, the ACC air concentrations are
estimated by proportionally adjusting them to the amount of Cr+6 in ACC.

5.3	Uncertainties and Limitations Associated with the Cloth Wipe Residue
Study

The protocol was not submitted to the EPA prior to the initiation of the
study.  If it had been reviewed, modifications would have been
recommended (as noted below).

The study did not control the temperature of the wood while in storage.
Instead, the study was conducted in late winter/early spring in Buffalo,
NY.  The reduction of Cr+6 to Cr+3 is temperature and time dependant.
Reduction is slower at colder temperatures.  Once frozen, reduction is
thought to cease.  Average daily temperatures for some days were at or
below 32 F (for 24 of 57 days).  The effect of below freezing
temperatures would be to stop reduction of Cr+6 on those days.

The study only monitored residues determined by cloth wipes.  The wipe
studies conducted previously to support CCA treated wood also included
hand wipes to determine the relationship between the amounts of residues
dislodged by a moistened hand versus a moistened cloth wipe.  It is the
residues collected on a wet hand that are meant to represent the
exposure one receives when contacting treated wood.  The cloth wipe is
only an intermediate step in the sampling process to obtain estimates
for dermal contact exposure.  However, based on the CCA data, the hand
dislodges less than the cloth wipe.  A hand transfer reduction factor
(TRF) of ~18% was determined for CCA.  The TRF for CCA is not believed
to be identical for ACC treated wood because of the differences in the
amount of Cr+6 in the wood.  The effect of only having cloth wipe
samples overestimates the amount of Cr+6 available for human exposure.

The cloth wipes included a total of 10 passes on the ACC-treated wood.
The CPSC wood wipe protocol recommends a total of 20 passes.  The effect
of only 10 passes is that maximum residue transfer was not achieved.
The effect of an insufficient number of passes/wipes per sample would
underestimate the amount of Cr+6 available for human exposure.

The coefficients of determination (R2) for the predicted daily
dislodgeable residues are 0.67 and 0.80 for the retention of 0.25 pcf
for SP and DF, respectively.  However, the R2 at the retention of 0.5
pcf is low (i.e., 0.36 for SP and 0.02 for DF).  A study with more
sampling intervals and controlled temperature would be needed to
determine if the reduction to Cr+3 is more predictable.

The study report stated that the wipe samples were turned in immediately
to Analytical Services.  The study report did not mention the storage
time of the expressate samples or the borings.  However, in the raw data
table provided in the Appendix, the expressate samples collected on day
36 from the southern pine treated wood at a retention rate of 0.50 were
reported to have been sealed in a freezer bag in a freezer for 5 days
prior to analysis.  It is not clear how the other samples were kept
prior to analysis or for how long.  A storage stability study was not
provided.

Method validation information was not provided for AWPA methods followed
in the analysis of the samples.  The SOPs followed for determination of
the levels of hexavalent chromium in wood expressate and wipe samples
also did not provide information on method efficiency nor the limit of
quantification.

Field and concurrent laboratory fortification samples and blank samples
were not reported in the study report or in the raw data table in the
Appendix.  The SOP for the wipe samples indicated a blank and fortified
wipe sample should be analyzed along with the study samples, but no
further information was provided.

5.4	Uncertainties and Limitations Associated with the Risk Assessment

The dermal endpoint selected for Cr+6 is based on both irritation and
elicitation of sensitization which is a more conservative approach (and
thus more protective) than an endpoint based on induction of
sensitization.

As noted in the HSRB's review of the ROAT study, it was not clear from
the data in the study that differences in irritant responses and
allergic responses were clear cut, as the study dermatologist was not
blinded to the status of the sensitized and control groups.  The
adjustment of dermal responses by use of the NACDG database was also
considered inappropriate by the HSRB.  As noted in the report, it was
not clear from the information provided that the database is a
representative sample of the U.S. population. Second, it was not clear
that the classification of irritant vs. allergic response was consistent
across all dermatologists who contributed data to the database. Third,
it was not clear whether some of the patients who participated in the
study were also included in the database.  Therefore, the Agency
followed the HSRB's recommendation to treat all responses classified as
irritant or allergic as allergic responses, and to use the unadjusted
data for selection of the dermal endpoint. This resulted in a more
conservative selection of the dermal endpoint.

EPA assumes that treatment facility dermal exposures will be mitigated
with the use of PPE and the PPE would be worn by the workers.  EPA also
believes that any deviations or improper PPE will be self limiting as
dermal sensitization/irritation at the work place will be traceable to
Cr+6 and appropriate correction measures taken to reduce exposure.
However, if overexposed, workers may have the potential to become
sensitized to Cr+6.  The same PPE policy does not apply to the treated
article (i.e., pressure treated wood) because these wood products do not
include an EPA label.  Moreover, the effects from dermal sensitization
are not immediate and the exposure to treated wood may not be identified
as causing the effect.

The limitations of the wipe study that would tend to under estimate the
residues of Cr+6 include no recovery samples were reported and there
were insufficient number of passes (i.e., 10 passes) with the cloth wipe
to establish maximum residue transfer to mimic human exposure from
contacting treated wood.   On the other hand, the cloth wipe methodology
without a hand transfer reduction factor tends to overestimate the
amount of residues available for human exposure by approximately 5x for
20 passes of a cloth wipe.  These data provided in this report are
useful as a range finder to determine dermal exposure to ACC treated
wood.  A more refined study would be needed to more accurately determine
the amount of Cr+6 available for human exposure.

The dermal risk assessment is based on cold weather data.  Warm weather
will reduce the Cr+6 concentrations within and on the surface wood at a
faster rate.  These data, however, do represent a realistic swing in
temperatures that occur during the spring in an area such as Buffalo,
NY.

The inhalation exposure study monitored CCA as a surrogate for ACC.  The
use of a surrogate requires the extrapolation of air concentrations to
the amount of Cr+6 that would be used by ACC treatment plants.  Because
of the uncertainty in extrapolation, risk estimates for the actual CCA
study results are presented along with the various extrapolations.
There is insufficient data available at this time to get an accurate
survey of the volume of wood treated per work shift per day.  An
estimate of 6,000 ft3 is provided in this assessment but it is
recommended that additional information on volumes of wood treated for
water-based preservatives be collected.  Even then, ACC is not currently
on the market so any estimates will be theoretical.  Additional
information to put the 6,000 ft3 estimate into perspective, a key
parameter used to estimate worker inhalation cancer risks, can be found
in the April 2006 copy of the Building Products Digest.  This journal
has an article listing the top 25 wood producers and the volumes of wood
they treated.  Note:  Four of the top 10 producers did not allow the
volume of wood treated to be published.  Appendix C provides the data
from the top 25 pressure treatment companies as presented in the April
2006 issue.  The data presented in Appendix C were also converted by EPA
to include estimates of (1) cubic feet per day assuming all of the wood
is treated in one shift (results indicate an average of 20,000 ft3), and
(2) cubic feet per day assuming each plant has 3 work shifts (results
indicate an average of 6,600 ft3).  The estimate of the volume of wood
potentially treated with ACC if EPA granted an unrestricted use (i.e.,
6,000 ft3 per work shift), is in close agreement with the average of
6,600 ft3 per work shift presented for the top 25 wood producers
(excluding 4 of the top 10 producers).

Worker inhalation exposure presumably is influenced by the activity
related job functions of the workers (e.g., the proximity of treatment
operator to the pressure treatment cylinder door) and the use of
engineering controls to reduce exposure (e.g., local exhaust fans above
cylinder doors).  Therefore, the inhalation risks are reported
separately for each job function (e.g., treatment operator) and for each
site.  These data were not combined because the various configurations
at the treatment plant presumably influence worker exposure.  It is
important to review the study site parameters presented in Table 3
(e.g., use of local exhaust fans) and the responsibilities of each job
function presented in Table 4 when reviewing the estimated inhalation
worker risks.

 The inhalation cancer risks are based on the standard 250 days worked
per year and 40 years worked per 75 year lifetime.  The work activities
at pressure treatment facilities other than the treatment operator
and/or treatment assistant are not expected to be lifetime occupations.

Concentration of Cr+6 in wood dust were estimated from the expressate
residues reported by Osmose (2005).  The inhalation risk estimates are
based on the upper bound inhalation exposures being equal to the PEL for
wood dust.  If necessary, EPA could review the monitoring data for wood
dust in OSHA’s Integrated Management Information System (IMIS) for
additional characterization (e.g., what percentages of the samples
exceed the PEL?).  Risk estimates are provided only for indoor use in
occupational settings.  Residential inhalation exposure to wood dust is
expected to be lower because of the intermittent nature of exposure and
the ambient conditions.

6.0		SUMMARY OF RESULTS

	This risk assessment presents the occupational and residential risks
associated with exposure to Cr+6 in ACC-treated wood and the
corresponding uncertainties and limitations of those risk estimates.
The document does not attempt to recommend various mitigation measures
to reduce the risks identified such as the use of local exhaust fans,
respiratory protection, wood holding times after treatment, or the
feasibility of such measures.  Potential mitigation measures are out of
the scope of this document and will be considered during the regulatory
decision process.  Table 20 provides a summary of the risk estimates
developed for this risk assessment.  As discussed in Section 5.0, there
were several uncertainties and limitations identified in conducting the
risk estimates provided.  Therefore, Table 20 also highlights some of
the uncertainties and limitations highlighted in Section 5.0 to inform
the regulatory decision making process.

	Risk estimates have been provided for (1) inhalation exposure at
treatment facilities; (2) dermal exposure at treatment facilities as
well as for contacting treated wood; (3) inhalation exposure to wood
dust generated from ACC-treated wood; and (4) incidental ingestion by
children of Cr+6 from the use of ACC-treated wood.  These risks are
presented below and summarized in Table 20.

Inhalation Risk (Treatment Facilities):

Inhalation risk estimates have been provided for the use of ACC for a
limited industrial only use as well as a general wood preservative use
(i.e., residential market).  Table 20 summarizes the risks presented in
this document.  Four scenarios are assessed for the worker inhalation
exposure at the treatment facilities.  The inhalation risks presented
for scenario 1 are representative of CCA, not ACC.  The CCA inhalation
risks are included in this assessment of ACC because the actual air
samples collected were for CCA treatments.  Thus the data in scenario 1
do not include uncertainties associated with extrapolation.  Scenario 2
represents the actual air monitoring data collected for CCA treatments
extrapolated to the amount of  Cr+6 in ACC.  Although scenario 2
extrapolates the air concentrations monitored for CCA to account for the
~50% higher concentration of Cr+6in ACC, it does not extrapolate the air
concentrations to a higher volume of wood expected to be treated.
Scenarios 3 and 4, on the other hand, extrapolate the air concentrations
from scenario 1 (i.e., actual air concentrations for CCA in the study)
not only to account for the increased amount of Cr+6 in ACC-treated
wood, but also to account for the predicted average volume of ACC
treated wood for industrial only uses in scenario 3 and for scenario 4
the predicted volume of ACC treated wood for a general use (i.e.,
residential).

The summary in Table 20 only presents ranges of risks.  The reader is
referred to Tables 10 (cancer) and 11 (non cancer) to review the risks
to workers involved in the various job functions (e.g., Treatment
Operator (TO)) at each of the three treatment facilities.  For example,
the various job functions and site locations have cancer risk estimates
ranging from 2.1E-3 to 6.9E-5 for scenario 4.  Within this range of
cancer risks, Table 10 indicates that the cancer risk of 2.1E-3
corresponds to the Treatment Assistants (TA) at the Rainier Site and
that the 6.9E-5 cancer risk corresponds to the Taggers (TG) at the Tampa
Site.

It is also noteworthy that none of the air concentrations measured at
treatment facilities during the study exceeds the new OSHA PEL of 5
μg/m3 for Cr+6.

The uncertainties and limitations of note in the inhalation risk
assessment include (1) Cr+6 air concentrations were measured in a study
using CCA as a surrogate for ACC and thus the inhalation risks provided
for scenarios 2, 3, and 4 are based on extrapolated volumes of wood
presumably to be treated with ACC; and (2) the unit risk for Cr+6
derived from Mancuso (1975) may underestimate the actual risk anywhere
from two to five-fold.  The reader is referred to Section 5.0 for a
complete discussion of the uncertainties and limitations for the
inhalation risk estimates.

Dermal Risks:

	A quantitative risk assessment was not performed for occupationally
exposed individuals potentially contacting ACC-treated wood.  Instead,
the use of personal protective equipment (PPE) is mandated on the
pesticide label when the dermal toxicological endpoint of concern is
based solely on either irritation or sensitization.  However, for
individuals exposed to treated articles such as ACC-treated wood, the
dermal exposures are quantified.  Based on previous CPSC and EPA work on
CCA, surface residue wipes studies that include wet hand wipes are used
to estimate the residues on the surface of wood that are available for
dermal contact.  A limited cloth wipe study was submitted to EPA by
Osmose for ACC-treated wood.

The Osmose wipe study indicates that the surface concentration of Cr+6
on ACC-treated lumber during the time frame of interest is highly
variable.  In the initial assessment (USEPA 2006a) the time required to
reduce the surface concentration of Cr+6 to below the level-of-concern
(LOC) was well beyond the last sampling interval in the study.  For
example, SP @ 0.5 pcf required 100 days and DF @ 0.5 pcf required 197
days for the surface residues to reduce to below the LOC.  Therefore,
the limitations of the wipe study identified as uncertainties in the
risk assessment still allowed EPA to make a decision with these data.
However, a new dermal endpoint has been developed for the dermal
assessment and now the LOC occurs in the area of the curve for the
surface residues where the limitations of the study impact the selection
of a time frame of interest.  The reliability of the data as described
within this document will need to be considered during the regulatory
decision making process.

Table 20 summarizes the time necessary to reduce surface concentrations
of Cr+6 to below EPA’s LOC.  Because of the variability in the data,
the summary includes the predicted average, the predicted 95th% upper
confidence interval on the mean, and the actual sampling intervals from
the study.  Of concern is the fact that the average predicted surface
concentrations of Cr+6 are less then the measured mean values for 3 of 4
of the experiments/wood species/retentions (i.e., Southern Pine 0.25 and
0.5 pcf and Douglas Fir 0.5 pcf).  The surface concentration of Cr+6 in
Southern Pine (0.25 and 0.5 pcf) did not reduce to below the LOC in the
actual field samples at the 23 DAT sampling interval.  But these
residues are reduced to below the LOC at the 36 DAT sampling interval.
For Douglas Fir (0.25 pcf) all field sampling interval means are below
the LOC (except for 0 DAT).  For Douglas Fir (0.5 pcf) at the 36 DAT
sampling interval, the surface residues are still greater than the LOC.
The residues do reduce to below the LOC at the 58 DAT sampling interval.
 These estimates could be more accurately characterized with a wipe
study that is designed to correlate the cloth wipe samples to actual wet
hand wipe samples to simulate exposure.  Additionally, more sampling
intervals and controlled cold and warm weather conditions would also
more accurately characterize the Cr+6 reduction rate.

Inhalation Risk (Wood Dust):

	Occupational inhalation risk to workers breathing wood dust at
manufacturing settings during fabrication of articles out of ACC-treated
wood have been estimated.  Residential inhalation exposure to wood dust
is expected to be lower than that for occupational estimates because of
the intermittent nature of exposure for residents and because of the
ambient conditions in which they work.  The concentrations of Cr+6 in
the interior of wood range from 0.85 ppm to 134 ppm 58 days after
treatment (DAT) for DF at a retention of 0.25 pcf and Southern pine at a
retention of 0.5 pcf, respectively.  To estimate inhalation exposure and
risks due to exposure to ACC-treated wood dust, EPA has assumed the air
concentration of wood dust itself is equal to the PELs for both total
dust and respirable dust.  The PEL concentrations were then adjusted for
the concentration of Cr+6 in the interior of wood.  The inhalation MOEs
for Cr+6 from ACC-treated wood dust exposure occurring 58 days after
treatment range from 1 to 160 with a target MOE of 30.  The cancer risks
using the same assumptions range from 6E-6 to 9.5E-4.  The interior
concentration of Cr+6 in the wood at 9 DAT are an order of magnitude
higher then sampled at 58 DAT.  Thus the inhalation MOEs and cancer
risks are proportionally affected (i.e., risks are also greater by one
order of magnitude).  “Fixation”, defined as 15 ppm Cr+6 in the
interior of the wood, is predicted for Southern Pine (0.5 pcf) at 94
DAT.  At fixation, the MOE for wood dust inhalation exposure is 9 and
the cancer risk is 1.1E-4.

Incidental Ingestion:

There is the possibility that incidental ingestion of Cr+6 may occur for
children coming in contact with ACC-treated wood or soil around
ACC-treated wood structures such as play sets and/or decks.  Data
specific to ACC were not available for the soil ingestion estimates but
can be estimated from the data available for CCA.  To assess the soil
ingestion potential, the  Cr+6 soil concentration was taken from the CCA
Stochastic Human Exposure and Dose Simulation (SHEDS).  The CCA soil
estimate from SHEDS was adjusted to account for the increased
concentration of Cr+6 in ACC.  To be protective of children, a bounding
input for the soil ingestion was the assumption that the entire
child’s soil ingestion rate comes from a source of soil contaminated
by ACC-treated wood.  For the child’s hand-to-mouth exposure resulting
from directly contacting an ACC-treated structure, the probabilistic CCA
SHEDS model’s 99th percentile of the average daily dose for total
chromium was adjusted by 1.5x to account for the increase in Cr+6 in
ACC.  The SHEDS assessment was based on total chromium and no downward
adjustments were made to estimate the amount of Cr+6 that was
attributable to total chromium.  Because the SHEDS assessment was used
as the basis for the hand-to-mouth estimates, the assessment is
predicated that the Cr+6 in ACC-treated wood has the opportunity to
become fixed (i.e., reduced).

The non cancer risk estimates from incidental ingestion of Cr+6 from
soil around ACC-treated wood or from hand-to-mouth exposure from
children playing on ACC-treated wood that has been given the proper time
for fixation result in MOEs of 6,000 and 200, respectively, with a
target MOE of 100.  Cr+6 is not classifiable as to human
carcinogenicity, and therefore, there are no cancer risk estimates for
the children’s incidental ingestion route of exposure.  The NTP oral
cancer study is ongoing and not available at this time.

Table 20.  Summary of the ACC Inhalation, Dermal, and Incidental Oral
Cr+6 Risks to ACC-Treated Wood.

Inhalation Risks at Treatment Facilities (Ground Retention of 0.5 pcf)

Scenario of Concern	(1) CCA Study	(2) ACC	(3) Industrial ACC	(4) All ACC

Cancer Risks 	2.1E-4 to 2.4E-5	3.2E-4 to 3E-5	5.1E-4 to 1.7E-5	2.1E-3 to
6.9E-5

MOEs

(Target MOE = 30)

7 to 130

5 to 83

6 to 82

μg/cm2)

Estimate	SP @ 0.25 pcf	SP @ 0.5 pcf	DF @ 0.25 pcf	DF @ 0.5 pcf

Predicted Average	4 days (R2 = 0.67)	21 days (R2 = 0.36)	 1 day (R2 =
0.80)	1 day (R2 = 0.02)

95th% Upper CI	10 days	30 days	3 days	1 day

Measured in Study

(average surface residue from stated DAT)	Greater than 23 days

(0.0964 ±0.0306 µg/cm2 @ 23 DAT)	Greater than 23 days

(0.1338 ± 0.0190 µg/cm2 @ 23 DAT)	All sample days less then LOC

(except 0 DAT)	Greater than 36 days

(0.1050 ± 0.0253  µg/cm2 @ 36 DAT)

Uncertainties & Limitations	The dermal worker risks are mitigated via
personal protective equipment (PPE) and assume that label PPE will be
properly worn and maintained.  The wipe study available for the
assessment did not control for temperature during the study; minimal
time intervals were sampled; no relationship was established between
hand exposure and cloth wipe residues; QA/QC samples were not reported;
and the predicted average residues are an underestimate of the actual
data collected for the sampling intervals of concern.  A better designed
wipe study would be needed to more accurately predict dermal exposures.

Inhalation Risks To Cr+6 in Wood Dust (Ground Retention of 0.5 pcf at 58
DAT)

Risk	SP @ 0.25 pcf	SP @ 0.5 pcf	DF @ 0.25	DF @ 0.5 pcf

MOEs

(Target MOE = 30)	2	1	160	8

Cancer	5.2E-4	9.5E-4	6E-6	1.1E-4

Uncertainties & Limitations	The wipe study available for the assessment
did not control for temperature during the study and QA/QC samples were
not reported.  The inhalation exposure estimate for workers is assumed
to be at the OSHA PEL(s) for wood dust.  The above ground retention of
0.25 pcf would result in half the risks.  It is assumed that outdoor
wood dust exposure would be less than that estimated for manufacturing.

Incidental Ingestion Risks (Ground Retention of 0.5 pcf)

Soil Ingestion MOE	6,000

Hand-to-Mouth	Screening-level assessment indicates this pathway is not
of concern (see Section 4.3).

Uncertainties & Limitations	The Cr+6 soil concentration used to develop
risk estimates for ACC is based on adjusting the total chromium soil
concentration from a CCA source by multiplying by 1.5x to account for
the higher concentration of Cr+6 in ACC and multiplying by 10% to
estimate the amount of chromium that may be Cr+6.  Additionally, 100% of
the mean daily soil intake is assumed to be attributable to soil
contaminated from ACC.

Scenarios used in the inhalation risk assessment:

Air concentrations as monitored in the CCA study are used to estimate
CCA risks;

Air concentrations assuming the same volume of wood treated in the CCA
study but extrapolated to the amount of chromic acid to represent ACC
risks;

Air concentrations from the CCA study extrapolated to represent an
assumed average volume of wood for ACC industrial uses;

(4)  Air concentrations from the CCA study extrapolated to represent an
assumed average    volume of wood for an unrestricted ACC use, including
residential

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