Document ID: EPA-HQ-OPP-2006-0606-0004
Agency: epa
Document Type: Supporting & Related Material
Title: 
Posted Date: 2006-09-15T04:00Z

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

	WASHINGTON, D.C. 20460

OFFICE OF                  

PREVENTION, PESTICIDES AND 

TOXIC SUBSTANCES        

May 30, 2006

Memorandum

SUBJECT: 	Occupational and Residential Assessment of Individuals Exposed
to Hexavalent Chromium (Cr+6) in Acid Copper Chromate (ACC)
Pressure-Treated Wood.     DP Barcode 329700.

FROM: 	Tim Leighton, Environmental Scientist 

Tim McMahon, Ph.D., Toxicologist			

		Antimicrobials Division 

							

TO:		Mark Hartman, Branch Chief (RMBII)

Antimicrobials Division 

	Attached is an occupational and residential assessment of hexavalent
chromium (Cr+6 or Cr VI) exposures and risks associated with the current
registered ACC product (EPA Reg. No. 3008-60) and “me-too”
registration requests for a wood preservative containing ACC. 

 

EXECUTIVE SUMMARY

The following assessment outlines the potential occupational and
residential risks to hexavalent chromium (Cr+6) when used as a wood
preservative in Acid Copper Chromate (ACC).  The potential risk
estimates include exposure data submitted by Osmose, Inc., and Forest
Products Research Laboratory (FPRL).  

f 5 μg/m3.  Additional characterization of the inhalation risks can be
developed with better estimates of the volume of wood treated per day
per work shift.  At this point in time, the average volume of wood
assumed to be treated for unrestricted ACC use is 6,000 ft3 per day per
work shift and 1,454 ft3 for an industrial use only, as extrapolated
from statistics on volumes of wood treated with water-based
preservatives.

The concentrations of Cr+6 in the interior of wood range from 0.85 ppm
to 134 ppm 58 days after treatment (DAT) for Douglas-fir at a retention
of 0.25 pcf and Southern pine at a retention of 0.5 pcf, respectively. 
To estimate inhalation exposure and risks to wood dust, EPA has assumed
that the 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 wood dust MOEs 58 days after treatment range from 1 to 160
with an inhalation target MOE of 30.  The cancer risks using the same
assumptions range from 9.5E-4 to 6.0E-6.

.009 μg/cm2 at 36 to 197 days after treatment in cold weather (wood
temperature ranged from 31.6 to 54.7 F).  The various retentions and
wood species account for such a wide range.  These estimates could be
better characterized with a wipe study that is designed to sample
surface residues at a steady state (i.e., 20 passes of the wipe) and a
hand transfer reduction factor to better simulate dermal exposure. 
Finally, the non cancer risks from incidental ingestion of Cr+6 by
children playing on and/or around ACC-treated structures from soil and
hand-to-mouth activities do not trigger a risk of concern.

1.0	INTRODUCTION

	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 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).

	Two new exposure studies have been submitted to allow EPA to conduct a
risk assessment.  The two studies include a worker inhalation as well as
a study that provides the amount of Cr+6 residues available on the
surface of ACC treated wood.  

	The EPA’s concerns for Cr+6 risks and how those risks may be
mitigated are not without associated uncertainties.  Presented below are
the details of the risk assessment to inform the regulatory risk
managers in making a regulatory decision on the registration of ACC.

	This risk assessment relies in part on data from studies in which adult
human subjects were intentionally exposed to Cr+6.  The Nethercott
(1994) study was reviewed for its ethical conduct.  It was also reviewed
by the Human Studies Review Board and was found to be appropriate for
use.

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).  The proposed ACC
product by Forest Products Research Laboratory (FPRL), LLC is Treaters
Choice.  Both 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.

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

= ♂ 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,
bronchopneumonia), cardiovascular effects (cardiac arrest), and
gastrointestinal effects (hemorrhage, ulceration). 

	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. ppm females (week 3) were decreased.  

	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
resorptions, 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 resorption
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 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 can

be 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.   

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. 

(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 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)

 (All Durations)	The Antimicrobial Division, in consult with the FIFRA
SAP, agreed with the recommendation of the use of the 10% minimum
elicitation threshold (MET) of 0.088 μg/cm2 and with the EPA’s
Science Policy Council (SPC) uncertainty factor of 10x for intraspecies
variation (USEPA 2004).

Inhalation Exposure

(All Durations)

	(a) LOAEL= 0.002 mg/m3; (or 2.3 x 10-4 mg/kg/day using 1m3/workday and
70kg body weight)

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%.

 (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 "[ ]".

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 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, USEPA 2006a). 

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 Unites 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	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	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	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	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	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	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	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
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).  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
at 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
for ACC, the air concentration needs to be adjusted for the amount of
Cr+6 to be used for ACC.  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 inhalable and respirable
air concentrations (ng Cr+6/m3/lb chromic acid) for all job functions
combined were highest at the Rainier treatment facility.  Inhalable Cr+6
air concentrations averaged 0.17, 0.21, and 0.42 ng/m3/lb chromic acid
at the Tampa, Savannah, and Rainier sites, respectively.  Respirable
Cr+6 particles averaged 0.068, 0.23, and 0.39 ng/m3/lb chromic acid at
the Tampa, Savannah, and Rainier sites, respectively.  

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

Table 5.  Arithmetic Mean Air Concentrations Measured using

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

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

Rainier	117	43	59	63	29	17	N/A	N/A	N/A

Savannah	280	54	148	64	N/A	18	22	16	N/A

Tampa	877	140	107	114	N/A	85	296	41	149

Table 6.  Normalized Arithmetic Mean Air Concentrations Measured using

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

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

Rainier	117	0.42	0.62	0.54	0.29	0.19	N/A	N/A	N/A

Savannah	280	0.21	0.60	0.25	N/A	0.074	0.087	0.054	N/A

Tampa	877	0.17	0.12	0.13	N/A	0.12	0.36	0.047	0.17

Table 7.  Arithmetic Mean Air Concentrations Measured using 

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

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

Rainier	117	39	50	67	21	17	N/A	N/A	N/A

Savannah	280	58	150	78	N/A	37	18	12	N/A

Tampa	877	55	42	34	N/A	33	141	20	44

Table 8.  Normalized Arithmetic Mean Air Concentrations Measured using 

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

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

Rainier	117	0.39	0.49	0.70	0.18	0.17	N/A	N/A	N/A

Savannah	280	0.23	0.58	0.31	N/A	0.176	0.063	0.040	N/A

Tampa	877	0.068	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

Treaters Choice (ACC)c	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.	Proposed ACC label (EPA Reg. No. 075832-x).

	

	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

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
these 371 plants using waterborne preservatives (i.e., 452 total plants
x 82% waterborne), 35% use CCA or 130 CCA treatment plants (i.e., 371
waterborne treatment plants x 35% 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 (and 3 additional
holidays) the average daily industrial production of round wood is 1454
ft3/day (i.e., 450,769 ft3 / 310 days per year).  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.  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 for each job function at
each of the 3 sites 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.  Assuming an 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 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

Overall	5E-5	8.3E-5	2.9E-4	1.2E-3

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

Overall	8E-5	1.2E-4	1.7E-4	6.9E-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

Overall	7.8E-5	1.2E-4	5E-5	2.1E-4

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

Where:  Lifetime Average Daily Concentration (LADC, ng/m3) = 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 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 13 to 170 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 concentration,
the MOEs range from 9 to 110.  Assuming an average industrial use (i.e.,
third scenario), the inhalation MOEs for an industrial use of ACC range
from 6 to 170.  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 1 to 41.  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.

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

Job Function	Air Conc	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	0.49	50	75	254	1048	40	27	8	2

TA	0.7	67	101	363	1497	30	20	6	1

PK	0.18	21	32	93	385	95	63	21	5

SU	0.17	17	26	88	364	120	78	23	6

Overall	0.39	39	59	202	834	51	34	10	2

Savannah, GA Site

TO	0.58	150	225	300	1241	13	9	7	2

TA	0.31	78	117	161	663	26	17	12	3

SU	0.176	37	56	91	376	54	36	22	5

FL	0.063	18	27	33	135	110	74	61	15

TG	0.04	12	18	21	86	170	110	97	23

Overall	0.23	58	87	119	492	34	23	17	4

Tampa, FL Site

TO	0.047	42	63	24	101	48	32	82	20

TA	0.041	34	51	21	88	59	39	94	23

SU	0.052	33	49.5	27	111	61	40	74	18

FL	0.17	141	212	88	364	14	9	23	6

TG	0.023	20	30	12	49	100	67	170	41

TB	0.053	44	66	27	113	45	30	73	18

Overall	0.068	55	82.5	35	145	36	24	57	14

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 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 2006b.  The levels of
hexavalent chromium in the interior of the ACC-treated wood were
assessed by analyzing expressate of the wood.  The study report states
that the initial levels on 0 days after treatment (DAT) are of similar
magnitude to the treating solution levels. As the number of days after
treatment increases, the levels in the expressate decrease.  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.  

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 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 exposure estimate.  It is believed that any
wood dust concentrations in the air exceeding these PELs will be
mitigated by the industry.  The PELs for wood dust are for the wood dust
itself, not chemical treatments.  Inhalation non cancer and cancer
exposure estimates to Cr+6 in ACC-treated wood are estimated using 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.

	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	15	5	15	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.  It is
this subpopulation that 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.”

	If equilibrium is achieved using this method, then the sample results
could be used to determine what concentration of Cr+6 transfers from the
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 equilibrium between the wood
surface and hand.

Cloth Wipe Residue Study (Osmose 2005):

	A second data requirement that EPA has cited as needed in order to make
the necessary finding to support the ACC registration is a wood wipe
study to determine the concentration of Cr+6 on the surface of
ACC-treated wood.  In response, Osmose, Inc., has submitted MRID No.
466447-01 (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.  For each retention and
each wood species, 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 refine the analysis if warranted.

	The predicted DAT for residue levels to reach the Cr+6 level-of-concern
of 0.009 μg/cm2 for Southern Pine at a retention of 0.25 pcf is 45 days
and 100 days at a retention of 0.5 pcf.  For Douglas Fir, Cr+6 reduces
to 0.009 μg/cm2 at 36 DAT at a retention of 0.25 pcf and not until 197
DAT at a retention of 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 equilibrium or 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 necessary to accurately determine the amount of Cr+6
available for human exposure.

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

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

4.3	Incidental Oral Exposure and Risks

	The potential for ingestion of Cr+6 contaminated soil 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 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 17.

Table 17.  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 be 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
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 (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. 
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.  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 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/DATA LIMITATIONS

	The uncertainties and limitations of this risk assessment are provided
to inform the regulatory decision making process.  The uncertainties and
limitations of the toxicity data, worker inhalation exposure study,
surface wipe residue study, and the risk assessment are provided below.

Uncertainties and Limitations Associated with the Toxicity Data:

The Nethercott study used to select the dermal endpoint is based on a
single dose whereas dermal exposure will result in repeated exposures. 
This introduces some uncertainty in that the threshold for elicitation
of dermal sensitization can be lower from repeated exposure than from a
single dose.

The Nethercott study used an occluded patch in the application of Cr+6. 
 An occluded patch may elicit a response at a lower dose then an open
test.   

Limited data were presented in the Nethercott study for exposure to
larger skin areas.  However, based on the limited data available, it
appears that the dose response is to a localized skin area.  

The 10% minimum elicitation threshold (MET) value of 0.088 μg/cm2  from
the study of Nethercott et al (1994) was selected as a value intended to
be protective against elicitation of dermal sensitization in humans. 
This value is considered conservative based on the use of occlusive
patch test conditions used in the Nethercott et al study. However, EPA
is not in possession of non –occluded patch test data in humans for a
direct comparison.

Limited data suggest that by the oral route, Cr+6 may be a more potent
dermal sensitizer than by the dermal route.  Oral administration of 50
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.

The National Toxicology Program (NTP) is currently conducting an oral
cancer study for Cr+6.  The timing of the availability of the results is
unknown.  

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 were less than the guideline
recommended number of 15.

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

The inhalation exposure study monitored Cr+6 resulting from CCA
applications to be used as a surrogate for ACC.  Therefore, the air
concentrations are normalized by the amount of Cr+6 used during the
monitoring period.

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.  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 treated wood.  The
CPSC wood wipe protocol recommends a total of 20 passes.  The effect of
only 10 passes is that an equilibrium or maximum residue 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 coefficient of determination (R2) for the predicted daily
dislodgeable residues are 0.67 and 0.80 for the retention of 0.25 pcf. 
However, the R2 at the retention of 0.5 pcf is low (i.e., 0.36 and
0.02).  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.

Uncertainties and Limitations Associated with the Risk Assessment:

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

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 at the work place will be traceable to Cr+6 and
appropriate correction measures taken to reduce exposure.  However, if
overexposed workers 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 products are not labeled. 
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 with the cloth wipes to establish
equilibrium or 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 necessary to 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 concentration on the wood at a faster rate.  

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 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 produced.  Note:  Four of the top 10 producers
did not allow the volume of wood treated to be published.  Appendix B
provides the data from the top 25 pressure treatment companies as
presented in the April 2006 issue.  These data were converted by EPA to
(1) cubic feet per day assuming all of the wood is treated in one shift
(average 20,000 ft3), and (2) cubic feet per day assuming each plant has
3 work shifts (6,600 ft3). 

 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.  The risk estimates are based on inhalation
exposure potential to wood dust at the PEL level for wood dust.  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	CONCLUSIONS

Based on the results of the inhalation worker exposure study and wood
residue wipe study, risk estimates have been provided for the use of ACC
as a general wood preservative (i.e., residential market) and for
industrial uses only.  Table 18 summarizes the risks presented in this
document.  Using the volume of wood treated in FPRL’s inhalation
exposure study extrapolated to ACC (i.e., scenario #2 in Table 18) the
inhalation cancer risks at treatment facilities range from 3.2E-4 to
3E-5.  The inhalation MOEs for the same scenario range from 9 to 110
with a target MOE of 30 (5 of 15 MOEs are below the target MOE of 30). 
See Table 18 for the range of inhalation risk estimates at treatment
facilities for the 3 other scenarios.  

None of the air concentrations estimated at treatment facilities exceed
the new OSHA PEL of 5 μg/m3.  A better characterization of the
inhalation risks can be developed with better data on the volume of wood
treated per day per work shift.  At this point in time, the average
volume of wood that may be treated with ACC for an unlimited
registration is assumed to be 6,000 ft3 per day per work shift and for
an industrial-only registration the volume of wood treated is assumed to
be 1,454 ft3.

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 to wood dust, EPA has assumed the
air concentration of wood dust is equal to the PEL of total dust and
respirable dust.  The inhalation MOEs for Cr+6 from wood dust exposure
occurring 58 days after treatment range from 1 to 160.  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.

	

The wipe study indicates that the surface concentration of Cr+6 on
ACC-treated lumber will reduce to the level-of-concern (i.e., 0.009
μg/cm2) at 36 to 197 days after treatment in cold weather.  The wide
range in days is based on the various retentions and wood species. 
These estimates could be better characterized with a wipe study that is
designed to sample surface residues at a steady state (i.e., 20 passes
of the wipe) and a hand transfer reduction factor to better simulate
dermal exposure.  Additionally, warm weather conditions would also
better characterize the Cr+6 reduction rate.  Finally, the non cancer
risks from incidental ingestion of Cr+6 from soil around treated wood or
from hand-to-mouth exposure from children playing on treated wood do not
trigger a risk of concern.



μg/cm2)

Retention	SP @ 0.25 pcf	SP @ 0.5 pcf	DF @ 0.25 pcf	DF @ 0.5 pcf

Time To Reach LOC	45 days	100 days	36 days	197 days

Inhalation Risks To Wood Dust (Ground Retention of 0.5 pcf)

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

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.

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

7.0	REFERENCES

American Chemistry Council (ACC). 2002.  Assessment of Potential
Inhalation and Dermal Exposure Associated With Pressure Treatment of
Wood with Arsenical Wood Products.  MRID 455021-01.

Anwar RA, Langham RF, Hoppert CA, et al. 1961. Chronic toxicity studies
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ATSDR (2000): Toxicological Profile for Chromium.  U.S. Department of
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Chowdhury AR, Mitra C. 1995. Spermatogenic and steroidogenic impairment
after chromium

treatment in rats. Indian J Exp Biol 33:480-484.

CPSC.  2001.  Consumer Product Safety Commission.  Sampling Chromated
Copper Arsenate (CCA) Pressure Treated Wood Playground Equipment For
Dislodgeable Residues of Arsenic, Chromium, and Copper.

CPSC.  2003.  Consumer Product Safety Commission.  Experimental
Methodology for the Collection and Analysis of Surrogate and Hand Wipes
on CCA-Treated Wood,  in Briefing Package, Part 5, Re Petition HP 01-3. 
February.

Davies, JM. (1979) Lung cancer mortality of workers in chromate pigment
manufacture: An epidemiological survey. J Oil Chem Assoc 62:157-163. 

Davies, JM. (1984) Lung cancer mortality among workers making lead
chromate and zinc chromate pigments at three English factories. Br J Ind
Med 41:158-169.

Doyle, E. and Malaiyandi, M.  1992.  Field Study to Investigate the
Leaching and Dislogeability of Copper, Chromium, and Arsenic from CCA-C
Treated Lumber and to Evaluate Means for Reducing Environmental
Contamination and User Exposure.  Health and Welfare Canada, Ontario,
Canada.

FPRL.  2005.  Assessment of Potential Inhalation Exposure to Hexavalent
Chromium At Wood Treatment Facilities Using CCA.  Final Report. 
Prepared for Forest Products Research Laboratory (FPRL), LLC by
Intertox, Inc.  Dated December 20, 2005.  MRID No. 467208-01.

Frentzel-Beyme, R. (1983) Lung cancer mortality of workers employed in
chromate pigment factories. A multicentric European epidemiological
study. J Cancer Res Clin Oncol 105:183-188.

Glaser U, Hochrainer D, Klopper H, et al. 1986. Carcinogenicity of
sodium dichromate and chromium (VI/III) oxide aerosols inhaled by male
Wistar rats. Toxicology 42:219-232. 

Glaser U, Hochrainer D and Oldiges H. 1988. Investigations of the lung
carcinogenic potentials of sodium dichromate and Cr (VI/III) oxide
aerosols in Wistar rats. Envir Hyg 1:111-116. 

Gradient.  2002.  Protocol for Hand and Wipe Sampling of CCA-Preserved
Wood (Draft Report).  Prepared for American Chemistry Council (ACC) by
Gradient Corporation.  Dated April 11, 2002.

Hayes, RB; Sheffet, A; Spirtas, R. (1989) Cancer mortality among a
cohort of chromium pigment workers. Am J Ind Med 16:127-133.

Ivankovic, S; Preussman, R. (1975) Absence of toxic and carcinogenic
effects after

administrations of high doses of chronic oxide pigment in subacute and
long term

feeding experiments in rats. Food Cosmet Toxicol 13:347-351.

 ADVANCE \d4 

Langard, S; Norseth, T. (1975) A cohort study of bronchial carcinomas in
workers producing chromate pigments. Br J Ind Med 32:62-65.

Langard, S; Vigander, T. (1983) Occurrence of lung cancer in workers in
producing chromium pigments. Br J Ind Med 40:71-74.

 ADVANCE \d4 

Lindberg, E; and Hedenstierna, G. (1983) Chrome plating: Symptoms,
finding in the upper airways, and effects on lung functions. Arch
Environ Health 38(6):367-374.

MacKenzie RD, Byerrum RU, Decker CF, et al. 1958. Chronic toxicity
studies II. Hexavalent and trivalent chromium administered in drinking
water to rats. A.M.A. Arch Industrial  Health 18:232-234.

Mancuso, TF. (1975) Consideration of chromium as an industrial
carcinogen.International Conference on Heavy Metals in the Environment,
Toronto, Ontario, Canada, October 27-31. pp. 343-356.

Micklewright 1998.  A Report to the Wood Preserving Industry in the
United States.  Wood Preservation Statistics 1997.  August, 1998.

National Toxicology Program (NTP). 1996. Final report on the
reproductive toxicity of potassium dichromate (hexavalent)(CAS No.
7778-50-9) administered in diet to SD rats. Dec. 16, 1996. U.S.
Department of Commerce, National Technical Information Service,
PB97125355.

National Toxicology Program (NTP). 1997a. Final report on the
reproductive toxicity of potassium dichromate (hexavalent) (CAS No.
7778-50-9) administered in diet to BALB/C mice. Jan 10, 1997. U.S.
Department of Commerce, National Technical Information Service,
PB97125363.

National Toxicology Program (NTP). 1997b. Final report on the
reproductive toxicity of potassium dichromate (hexavalent) (CAS No.
7778-50-9) administered in diet to BALB/C mice. Feb 25, 1997. RACB94014.
U.S. Department of Commerce, National Technical Information Service,
PB97-144919.

Nethercott, J., Paustenbach, D., Adams, R., Fowler, J., Marks, J.,
Morton, C., Taylor, J., Horowitz, S., Finley, B. (1994): A Study of
Chromium induced allergic contact dermatitis with 54 volunteers:
implications for environmental risk assessment. Occup. Environ. Med. 51:
371-380.

Osmose.  2005.  Osmose ACC 50% Wood Preservative:  Determination of
Hexavalent Chromium Residues In and On Wood Following Treatment with
Acid Copper Chromate.  Dated September 13, 2005.  MRID No. 466447-01.

RTI.  2003.  Assessment of Exposure To Metals In CCA-Preserved Wood: 
Full Study.  Prepared for American Chemistry Council (ACC) by RTI
International.  Dated June 20, 2003.

Solo-Gabriele et al.  2001.  New Lines of CCA-Treated Wood Research: 
In-service and Disposal Issues.  State University System of Florida,
Florida Center for Solid Hazardous Waste Management.  Gainesville, FL.

Taylor A, Cooper PA, Ung YT.  2001.  Effects of Deck Washes and
Brighteners on the Leaching of CCA Components.  February 2001.  Forest
Products Journal.  Vol. 51, No. 2.

 

 

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萎Z萏ː萑ﴰ葝Z葞ː葠ﴰ摧₮ÞᄀTyl RW, Marr M, Meyers CB.
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gavage to New Zealand White rabbits. Research Triangle Institute,
Research Triangle Park, NC 27709. Study No. 60C-4808-30/40. December 13,
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Exposure to Hexavalent Chromium At Wood Treatment Facilities Using
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(USEPA).  Dated May 2006.

USEPA.  2006b.  Review of the, “Osmose ACC 50% Wood Preservative: 
Determination of Hexavalent Chromium Residues In and On Wood Following
Treatment with Acid Copper Chromate. Memorandum from Tim Leighton
(USEPA) to Mark Hartman (USEPA).  Dated May 2006.

Vlosky, R.P., and T.S. Shupe. 2006. Statistical Overview of the U.S.
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Appendix A.  Inhalation Cancer Risks (Treatment Facilities).

Job Function

 	Air Conc

(ng/m3/lb CrO3)	Lifetime Average Daily Concentration (LADC)	Inhalation
Risk

CCA (study)	ACC (CCA study)	ACC Industrial	ACC All	CCA (study)	ACC (CCA
study)	ACC Industrial	ACC All

Rainier, OR Site

TO	0.49	6.1	9.1	30.9	127.6	7.1E-05	1.1E-04	3.6E-04	1.5E-03

TA	0.7	8.2	12.2	44.2	182.3	9.5E-05	1.4E-04	5.1E-04	2.1E-03

PK	0.18	2.6	3.8	11.4	46.9	3.0E-05	4.4E-05	1.3E-04	5.4E-04

SU	0.17	2.1	3.1	10.7	44.3	2.4E-05	3.6E-05	1.2E-04	5.1E-04

Overall	0.39	4.7	7.1	24.6	101.6	5.5E-05	8.3E-05	2.9E-04	1.2E-03

Savannah, GA Site

TO	0.58	18.3	27.4	36.6	151.1	0.00021	0.00032	0.00042	0.00175

TA	0.31	9.5	14.2	19.6	80.7	0.00011	0.00017	0.00023	0.00094

SU	0.176	4.5	6.8	11.1	45.8	0.00005	0.00008	0.00013	0.00053

FL	0.063	2.2	3.3	4.0	16.4	0.00003	0.00004	0.00005	0.00019

TG	0.04	1.5	2.2	2.5	10.4	0.00002	0.00003	0.00003	0.00012

Overall	0.23	7.1	10.6	14.5	59.9	0.00008	0.00012	0.00017	0.00069

Tampa, FL Site

TO	0.047	5.1	7.7	3.0	12.2	5.9E-05	8.9E-05	3.4E-05	1.4E-04

TA	0.041	4.1	6.2	2.6	10.7	4.8E-05	7.2E-05	3.0E-05	1.2E-04

SU	0.052	4.0	6.0	3.3	13.5	4.7E-05	7.0E-05	3.8E-05	1.6E-04

FL	0.17	17.2	25.8	10.7	44.3	2.0E-04	3.0E-04	1.2E-04	5.1E-04

TG	0.023	2.4	3.7	1.5	6.0	2.8E-05	4.2E-05	1.7E-05	6.9E-05

TB	0.053	5.4	8.0	3.3	13.8	6.2E-05	9.3E-05	3.9E-05	1.6E-04

Overall	0.068	6.7	10.0	4.3	17.7	7.8E-05	1.2E-04	5.0E-05	2.1E-04

Lifetime Average Daily Concentration (LADC, ng/m3) = air conc (TWA
ng/m3/lb Cr+6) x lbs CrO3 x (8hrs/24hrs) x (250 days/365 days) x (40
yrs/75 yrs).  Where lbs CrO3 = (1) amount handled per replicate in CCA
study; (2) CCA study amount x 1.5 (i.e., 50% more Cr+6); (3) industrial
use assumes 518 lbs CrO3 (i.e., 1454 ft3 x 0.5 pcf ACC x 71.3% CrO3);
(4) general use assumes 2139 lbs CrO3 (i.e., 6,000 ft3 wood).

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

Top 25 Pressure Treatment Facilities

Rank

 	Company

 	Production 2005

(millions bd ft)	Cubic Ft

(million)	Number

Plants	Cubic Ft 

per plant	Ft3/plant

per day	Ft3/plant/day

per shift

1	Great Southern Wood Preserving	NA	#VALUE!	7	#VALUE!	#VALUE!	#VALUE!

2	Universal Forest Products	1112	92.66667	24	3861111	12455	4152

3	Georgia-Pacific Corp	850	70.83333	12	5902778	19041	6347

4	Culpeper Wood Preservers	497	41.41667	4	10354167	33401	11134

5	Robbins Manufacturing Co. 	NA	#VALUE!	6	#VALUE!	#VALUE!	#VALUE!

6	Rocky Top Building Products	NA	#VALUE!	3	#VALUE!	#VALUE!	#VALUE!

7	Cox Industries	220	18.33333	8	2291667	7392	2464

8	McFarland Cascade	NA	#VALUE!	5	#VALUE!	#VALUE!	#VALUE!

9	John A. Biewer Lumber Co.	190	15.83333	3	5277778	17025	5675

10	C.M. Tucker Lumber	185	15.41667	1	15416667	49731	16577

11	Allweather Wood Treaters	177	14.75	4	3687500	11895	3965

12	Pacific Wood Preserving Co.	176	14.66667	4	3666667	11828	3943

13	Eastex Forest Products	141	11.75	1	11750000	37903	12634

14	Bestway Enterprises	128	10.66667	5	2133333	6882	2294

15	New South Inc.	128	10.66667	2	5333333	17204	5735

16	Curt Bean Lumber Co.	127	10.58333	3	3527778	11380	3793

17	BB&S Treated Lumber	122	10.16667	1	10166667	32796	10932

18	Madison Wood Preservers	116	9.666667	1	9666667	31183	10394

19	California Cascade Industries	115	9.583333	2	4791667	15457	5152

20	Coastal Lumber Co.	113	9.416667	5	1883333	6075	2025

21	Commonwealth Wood	103	8.583333	1	8583333	27688	9229

22	Exterior Wood Inc.	100	8.333333	1	8333333	26882	8961

23	Durawood Treating	95	7.916667	1	7916667	25538	8513

24	Fortress Wood Inc.	90	7.5	3	2500000	8065	2688

25	Conrad Wood Preservers	80	6.666667	3	2222222	7168	2389

Average	6155556	19857	6619

Cubic feet = board feet / 12

	Std	3760783	12132	4044

Cubic feet/day = cubic feet / 310 days per year

median	5277778	17025	5675

Cubic Ft/day/shift = Ft3/day / 3 shifts per day

75%tile	8583333	27688	9229

90%tile	10354167	33401	11134

max	15416667	49731	16577

count	21	21	21