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Pentachlorophenol Registration Review Team 

Human Health & Environmental Effects 

Jonathan Chen 

Nathan Mottl 

Bill Erickson 

Najm Shamim 

Siroos Mostaghimi 

Health Effects Division 

Jaclyn Pyne 

Risk Management 

Sandra O’Neill 

Rose Kyprianou 

Tom Luminello 

Office of General Counsel 

Philip Ross 
Docket Number EPA-HQ-OPP-2014-0653 

www.regulations.gov 

Page 3 of 63

TERMS, ABBREVIATIONS AND SYMBOLS 

X,3,7,8 TCDD 2, 3, 7, 8-tetrachlorodibenzo-p-dixoin

AD Antimicrobials Division 

A.I. or a.i. active ingredient 

aPAD acute population adjusted dose 

ASRI activated sludge respiration inhibition 

atm-m3

/mole atmospheric pressure-cubic meter per mole 

BCF bioconcentration factor 

°C degrees Celsius 

CAS Chemical Abstracts Service 

CDD chlorodioxin 

CDF chlorofuran 

CFR Code of Federal Regulations 

CHO Chinese hamster ovary 

CMA Chemical Manufacturers Association 

CO2 carbon dioxide 

COC concentration-of-concern 

cPAD chronic population adjusted dose 

DCI data call-in 

EC50 median (or 50 percent) effect concentration

EC05 5 percent effect concentration

ECOTOX ECOTOXicology 

EDI estimated daily intake 

EDSP Endocrine Disruptor Screening Program 

E-FAST Exposure and Fate Assessment Screening Tool 

EPI Suite Estimation Program Interface Suite 

EPA Environmental Protection Agency 

FDA Food and Drug Administration 

FFDCA Federal Food, Drug, and Cosmetic Act 

FGD flue-gas desulfurization 

FIFRA Federal Insecticide, Fungicide, and Rodenticide Act 

FQPA Food Quality Protection Act 

FWP Final Work Plan 

g/mol grams per mole 

GLN guideline number 

HCB hexachlorobenzene 

HPV high production volume 

HxCDD hexachlorodibenzo-p-dioxin

IDS Incident Data System 

Koc organic carbon normalized soil-water partition coefficient 

Kd soil-water partition coefficient 

Kow octanol-water partition coefficient 

LC50 median (or 50 percent) lethal concentration 

LD50 median (or 50 percent) lethal dose 

LOAEC lowest-observed-adverse-effect-concentration 

LOEC lowest-observed-effect-concentration 

LOAEL lowest-observed-adverse-effect-level 

Log Kow logarithm of the octanol-water partition coefficient

μg microgram 

ml/g milliliter per gram 
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mg/kg milligram per kilogram 

mg/kg/day milligram per kilogram per day 

mg/L milligram per liter 

mm Hg millimeter of mercury 

MOE margin of exposure 

MRID Master Record Identification Number 

MRL maximum residue limit 

N/A not applicable 

nm nanometers 

NOAEC no-observed-adverse-effect-concentration 

NOAEL no-observed-adverse-effect-level 

OCSPP Office of Chemical Safety and Pollution Prevention 

OECD Organization for Economic Co-operation and Development 

OPP Office of Pesticide Programs 

PCP Pentachlorophenol 

PAD population adjusted dose 

PAI pure active ingredient 

PDM Probabilistic Dilution Model 

% percent 

PC Code Pesticide Chemical Code 

PCA pentachloroanisole 

PCF pounds per cubic foot 

pH power of hydrogen or power of the concentration of the hydrogen ion 

PHED Pesticide Handler’s Exposure Data 

PIS primary irritation score 

pKa power of the acid dissociation constant or negative base-10 logarithm of the acid 

dissociation constant of a solution 

ppb parts per billion 

ppm parts per million 

PWP Preliminary Work Plan 

QSAR quantitative structure-activity relationship 

RED Reregistration Eligibility Decision 

SAR structure activity relationship 

SF safety factor 

SSTS Section Seven Tracking System 

TEP typical end-use product 

TGAI technical grade active ingredient 

TMDL total maximum daily loads 

UF uncertainty factor 

UV/VIS ultraviolet/visible light absorption 

% w/w percent weight per weight. 

WP wettable powder 

WWTPs wastewater treatment plants 

 
Page 5 of 63

Table of Contents 

1 Introduction ............................................................................................................................. 7

1.1 Statutory and Regulatory Authority ................................................................................. 7

1.2 Case Overview ................................................................................................................. 7

1.3 Chemical Identification and Properties ............................................................................ 9

1.4 PCP and Contaminants ................................................................................................... 11

1.5 Use/Usage Description ................................................................................................... 12

1.5.1 Registrations ........................................................................................................... 12

1.5.2 Summary of Registered Uses .................................................................................. 13

1.5.3 Usage Information .................................................................................................. 13

1.6 Regulatory History ......................................................................................................... 13

1.6.1 Tolerance Information ............................................................................................ 14

1.7 Incidents ......................................................................................................................... 14

1.7.1 Human Health ......................................................................................................... 14

1.7.2 Ecological ............................................................................................................... 14

2 Anticipated Data Needs ........................................................................................................ 15

3 Human Health Risk Assessment ........................................................................................... 16

3.1 Existing Toxicological Endpoints .................................................................................. 16

3.1.1 PCP ......................................................................................................................... 16

3.1.2 Contaminants .......................................................................................................... 18

3.2 Dietary Exposure ............................................................................................................ 19

3.2.1 Food ........................................................................................................................ 20

3.2.2 Drinking Water ....................................................................................................... 20

3.3 Occupational and Residential Exposures ....................................................................... 20

3.3.1 Occupational Exposure ........................................................................................... 21

3.3.2 Residential Handler Exposures ............................................................................... 21

3.3.3 Residential Post-Application Exposures ................................................................. 22

3.3.4 Aggregate Exposures .............................................................................................. 22

3.3.5 Cumulative Exposures ............................................................................................ 22

4 Environmental Risk Assessment........................................................................................... 22

4.1 Environmental Fate Assessment .................................................................................... 23

4.1.1 Water Quality .......................................................................................................... 24

4.2 Environmental Exposure Pathways ................................................................................ 24

4.3 Ecological Effects Analysis ........................................................................................... 25

4.3.1 Mechanism of Action .............................................................................................. 25

4.3.2 Measures of Effect (Ecotoxicology Endpoints) ...................................................... 26

4.3.3 Ambient Water Quality Criteria for PCP ................................................................ 27

4.3.4 Open literature ........................................................................................................ 28

4.4 Exposure Analysis Plan .................................................................................................. 28

4.4.1 Aquatic and Terrestrial Wildlife Exposure Estimates ............................................ 28

4.4.2 Screening Level Down-the-Drain Analysis ............................................................ 28

5 Endocrine Disruptor Screening Program (EDSP) ................................................................. 28

6 Optional Label Changes ........................................................................................................ 29

7 Guidance for Commenters .................................................................................................... 29

7.1 Preliminary Work Plan ................................................................................................... 29

7.1.1 Trade Irritants .......................................................................................................... 30
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7.1.2 Water Quality .......................................................................................................... 30

7.1.3 Environmental Justice ............................................................................................. 30

7.1.4 Additional Information ........................................................................................... 30

8 Next Steps ............................................................................................................................. 31

9 References ............................................................................................................................. 32

Appendix A Toxicology Profile ............................................................................................... 34

Appendix B Environmental Fate ............................................................................................. 42

Appendix C Ecotoxicology Profile .......................................................................................... 49

Appendix D Product Chemistry ............................................................................................... 62

List of Tables 

Table 1 – Summary of Anticipated Risk Assessments and Data Needs for Registration Review: 

PCP ................................................................................................................................................. 8

Table 2 – Anticipated Registration Review Schedule .................................................................... 9

Table 3 – Chemical Identification of PCP ...................................................................................... 9

Table 4 – Physical-Chemical and Environmental Fate Properties for PCP .................................. 10

Table 5 – The Maximum Concentrations of Contaminants in Technical PCP Detected in 2013 12

Table 6 – Characterization of Contaminants ................................................................................ 12

Table 7 – Summary of PCP Registered Uses ................................................................................ 13

Table 8 – Studies Anticipated as Needed for the Registration Review of PCP ............................ 15

Table 9 –Data Required by the September 21, 2011 Data Call-In for the PCP RED ................... 15

Table 10 – Toxicological Endpoints Selected for Risk Assessment of PCP (2008, RED) .......... 17

Table 11 – Toxicological Endpoints Selected for Risk Assessment of HCB (2008, RED) ......... 19

Table 12 – Occupational Exposure Scenarios for Workers Using PCP ....................................... 21

Table 13 – PCP Ecological Effects Endpoints for the Ecological Risk Assessment .................... 26

 
Page 7 of 63

1 Introduction 

This document is the United States Environmental Protection Agency’s (USEPA, EPA or “the 

Agency”) Preliminary Work Plan (PWP) for pentachlorophenol, herein referred to as PCP. The 

PWP document explains what EPA's Office of Pesticide Programs (OPP) knows about PCP, 

highlighting anticipated data and assessment needs, identifying the types of information that 

would be especially useful to the Agency in conducting the review, and providing an anticipated 

timeline for completing PCP’s review. 

The registration review process was designed to include a public participation component to 

solicit input from interested stakeholders. The Agency intends, by sharing this information in the 

docket, to inform the public of what it knows about PCP and what types of new data or other 

information would be helpful for the Agency to receive as it moves toward a decision on PCP. 

The Agency encourages all interested stakeholders to review the PWP and to provide comments 

and additional information that will help the Agency’s decision-making process for this 

chemical. 

1.1 Statutory and Regulatory Authority 

The Food Quality Protection Act (FQPA) of 1996 mandated a registration review program. All 

pesticides distributed or sold in the United States generally must be registered by EPA based on 

scientific data showing that they will not cause unreasonable risks to human health or the 

environment when used as directed on product labeling. The registration review program is 

intended to make sure that, as the ability to assess risk evolves and as policies and practices 

change, all registered pesticides continue to meet the statutory standard of no unreasonable 

adverse effects to human health or the environment. Changes in science, public policy, and 

pesticide use practices will occur over time. Through the registration review program, the 

Agency periodically reevaluates pesticides to make sure that as change occurs, products in the 

marketplace can be used safely. Information on this program is provided at 

http://www2.epa.gov/pesticide-reevaluation. 

The Agency is implementing the registration review program pursuant to Section 3(g) of the 

Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA) and will review each registered 

pesticide every 15 years to determine whether it continues to meet the FIFRA standard for 

registration. The regulations governing registration review begin at 40 CFR 155.40. The Agency 

will consider benefits information and data as required by FIFRA. The public phase of 

registration review begins when the initial docket is opened for each case. The docket is the 

Agency’s opportunity to state what it knows about the pesticide and what additional risk analyses 

and data or information it believes are needed to make a registration review decision. After 

reviewing and responding to comments and data received in the docket during this initial 

comment period, the Agency will develop and commit to a Final Work Plan (FWP) and 

anticipated schedule for the PCP case. 

1.2 Case Overview 

The docket for the PCP (case 2505) has been established at http://www.regulations.gov in docket 

number EPA-HQ-OPP-2014-0653. Documents associated with this registration review can be 
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viewed at this docket. Tables 1 and 2 below summarize the issues relevant to this registration 

review case and the anticipated registration review schedule. 

Table 1 – Summary of Anticipated Risk Assessments and Data Needs for Registration 

Review: PCP 

Risk Assessment 

Assessment 

Necessary to 

Support 

Registration 

Review 

Date of Most 

Recent 

Assessment 

Type of 

Assessment 

Required 

(New/Updated) 

*Data Anticipated as Needed 

(See Table 8 for details) 

Dietary (food) No1 9/25/2008 None None

Dietary (drinking water) No1 9/25/2008 None None

Occupational Handler Yes 9/8/2008 Updated None2

Residential Handler 

No (see 

Section 

3.3.2)

N/A None None

Residential Post 

Application - Incidental 

Oral and Dermal 

Yes1 9/8/2008 Updated None

Residential Post 

Application 

No (see 

Section 

3.3.3)

N/A None None

Aggregate Yes 9/25/2008 Updated None1

Cumulative 

No (see 

Section 

3.3.5)

N/A None None

Tolerance Review No (see 

Section 0) N/A None None

Ecological Yes 9/8/2008 Updated Aquatic invertebrates, semi-aquatic 

plants, benthic organisms

N/A = Not applicable 

* Table 1 is a summary of the anticipated risk assessments and data needs for Registration Review. For data called in through the postReregistration Eligibility Decision (RED) Data Call-In (DCI), see Table 9. 

1

Dietary (food and drinking water) and residential exposure are part of the general population biological monitoring data from NHANES and will 

be accounted for in the anticipated aggregate assessment. 2

 Data already required by the 2011 post-RED PCP DCI. 
Page 9 of 63

Table 2 – Anticipated Registration Review Schedule 

Anticipated Activity Target Date* Completion Date

Phase 1: Opening the Docket 

Open Docket and 60-Day Comment Period for Preliminary Work Plan 2014-12 2014-12 

Close Public Comment Period 2015-02 

Phase 2: Case Development 

Issue Final Work Plan 2015-06 

Issue Data Call-In (DCI) 2016-06 

Receive Data to be Considered in Risk Assessment 2018-06 

Open 30-Day Public Comment Period for Preliminary Risk Assessment(s) 2019-12 

Close Public Comment Period 2020-01 

Phase 3: Registration Review Decision and Implementation 

Open 60-Day Public Comment Period for Proposed Decision 2020-06 

Close Public Comment Period 2020-08 

Issue Final Decision 2020-12 

Begin Post-Decision Follow-up 2020 

Total (years) 6 

*The anticipated schedule will be revised as necessary (e.g., need arising under the Endocrine Disruptor Screening Program with 

respect to the active ingredient in this case).

1.3 Chemical Identification and Properties 

Table 3 presents the active ingredient to be assessed in case 2505: PCP (PC Code 063001). 

Table 3 – Chemical Identification of PCP

Chemical Name PCP 

Chemical 

Classification Chlorophenols

PC Code 063001 

CAS Number 87-86-5 

Molecular Formula C6HCl5O

Molecular Weight (grams/mole) 266.35 

Molecular Structure 
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The PCP product chemistry information relevant to risk assessment is summarized in Table 4, 

and the details of the product chemistry and environmental fate information are discussed in 

Appendix D and B, respectively. 

Table 4 – Physical-Chemical and Environmental Fate Properties for PCP 

Guideline No. Parameter PCP 

Physical/Chemical Properties

830.7000 pH 4.99 

830.7050 UV/Visible Absorption NA 

830.7200 Melting point ( 25 o C) 191 

830.7300 Density 1.987 g/ml 

830.7370 Dissociation constant (pKa) 4.74 

830.7550 Octanol-water partition coefficient 

at 25 o

C (Log Kow) 4.75 at pH 5, 5.27 at pH 7, and 5.1 at pH 9 

830.7840 Solubility in water (mg/L) 0.3g/L at pH 5; 20 mg/L at pH 7, and 2200 mg/L at pH 

9. 

830.7950 Vapor pressure (mmHg); 25 oC 1.1 x 10-4mm Hg 

Environmental Fate Properties

Mobility

835.1230 

Adsorption/desorption study 

Moderately mobile in sandy loam, immobile in clay 

loam, moderately mobile in silt loam at low pHs, and 

mobile at high pH (MRIDs: 42633709, and 43627000) 

Persistence in Water (half-life)

835.2120 Hydrolysis at 25 oC: pH 5, 7 &9 

(days) 

Hydrolytically stable at all three pHs in abiotic aqueous 

medium up to 30 days (MRID 42481101) 

835.2240 Aqueous photolysis at 25 oC 

(days) 

Degrades rapidly at all three pHs at half-life between 13-

30 minutes. (MRID 42885401) 

835.3100 Aerobic aquatic metabolism (days) Degrades in aqueous medium flooded with sandy loam 

soil; half-life of 14 days.(MRID 42288601) 

Persistence in Soil (half-life)

835.4100 Aerobic soil metabolism at 25 oC 

(days) 

Degrades with a half-life of 7-14 days in sandy loam soil 

(MRID 42594302) 

835.4200 Anaerobic soil metabolism (days) Degrades with an observed half-life of 1- 2 months 

(MRID 42436801) 

atm-m3/mol = atmosphere cubic meter per mole; oC = degrees Celsius; mg/L = milligrams per liter; mmHg = 

millimeters of mercury 

A potential degradate/metabolite of PCP and other compounds has been identified as 

pentachloroanisole (PCA), Mol For: C7H3Cl5O; Mol.wt: 280.37, CAS# 1825-21-4. PCA is a 

derivative of PCP and other chlorinated phenols found in the environmental media (such as 

pentachloronitrobenzene). 

The Agency has noted that the Stockholm Convention’s Persistent Organic Pollutants Review 

Committee (POPRC) decided in October 2014 to recommend to its Conference of Parties (COP) 

to list PCP and its salts and ester in Annex A to the Convention with specific exemptions for the 

production and use of PCP for utility poles and cross-arms. The POPRC considered PCA 

together with PCP in making this determination. The COP has not yet met to decide on this 

recommendation. 
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Pentachloroanisole (PCA) 

1.4 PCP and Contaminants 

There are three general types of contaminants in PCP. Two types are chlorinated dioxins 

(CDDs)/chlorofurans (CDFs) compounds: 2, 3, 7, 8-tetrachlorodibenzo-p-dixoin (2,3,7,8 TCDD) 

and generic HxCDD. The third type of contaminant is hexachlorobenzene (HCB). In the past, 

the Agency has referred to these as “microcontaminants.” For every pesticide product registered 

at EPA, a confidential statement of formula (CSF) is required to report all the components and 

their percentage by weight in the product. Contaminants below 0.1% are not reported on the 

CSF, hence the term microcontaminants - contaminants below the 0.1% reporting limit present at 

ppm levels (micro levels). These microcontaminants are herein referred to as contaminants. 

PCP registrants provide monthly reports of analytical data which inform the levels of 

contaminants in the technical PCP. The samples of PCP are provided from a manufacturing plant 

currently in use. Table 5 lists measured value of concentrations in PCP products. The data are 

presented with written consent from the registrant for the PCP case to demonstrate the extent to 

which contaminants have decreased from 1986 to 2013. 
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Table 5 – The Maximum Concentrations of Contaminants in Technical PCP Detected in 

2013 

Substance 

Name 

1986 Maximum 

Concentrations in 

Technical PCP 

Levels Detected in 

2013 Samples 1 

Molecular Structure 

HCB 75 ppm 19.33 ppm 

2,3,7,8 TCDD Non-detect < 0. 001 mg/kg Non-detect < 0.001 

mg/kg 

HxCDD 2 ppm 0.554 ppm 

1 Registrant’s letter, dated Oct. 6, 2014 

Detailed product chemistry characteristics of all three contaminants were addressed in the 2008 

RED document. 

Some physical chemical characteristics are shown in Table 6. 

Table 6 – Characterization of Contaminants 

Substance Water solubility Vapor pressure Log Kow 

HCB 

(CAS# 118-74-1) 

6000 mg/L 1.1 x 10-5 mm Hg 6.18 

CDDs and CDFs (including 

HxCCD) 

Varies from 1.18 x 10-4

mg/L to 7.4 x 10-8 mg/L 

Varies from 1.4 x 10-8 mm Hg 

to 3.75 x 10-12 mm Hg 

Varies from 6.1 to 8.1 

1.5 Use/Usage Description 

1.5.1 Registrations 

There are four EPA-registered products that contain PCP as an active ingredient (a.i.). One of 

these products is a technical/formulation intermediate product, and the other three products are 

end-use products. The formulations include ready-to-use solutions and soluble concentrates. The 

technical/manufacturing use product contains a nominal concentration of 86 percent PCP (other 

chlorophenols listed as an additional 10 percent). The nominal concentrations of the three enduse products range from 4.3 percent (other chlorophenols listed as an additional 0.5 percent) to 

86 percent (other chlorophenols listed as an additional 10 percent). 
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PCP is classified as a restricted use pesticide (RUP) for sale and use by certified applicators only. 

Indoor applications of PCP are prohibited as well as application to wood intended for use in 

interiors (with certain exceptions) or for use in contact with food, feed, or drinking water. These 

restrictions were imposed on PCP registrations as part of the Agency’s Special Review process 

as indicated in the U.S.EPA Position Document 4 for Wood Preservative Pesticides: Creosote, 

Pentachlorophenol and Inorganic Arsenicals (1984, amended 1986). 

1.5.2 Summary of Registered Uses 

Table 7 presents a summary of the registered uses of PCP that will be assessed in this registration 

review case. PCP is applied using specialized high pressure treatment cylinders (also called 

“retorts”) by pressure and thermal treatment. The target rate of retention is not currently 

specified on labels because it varies with respect to the petroleum solvent used, species of wood 

treated, type of wood product and specific American Wood Protection Association (AWPA) 

standards. For specific retentions, refer to AWPA standards. 

Table 7 – Summary of PCP Registered Uses 

Use Application Method Application Rate

Wood or Wood Structure Protection Treatments 

Pressure Treatment to Forest Products Pressure Treatment NR

NR: Not reported on existing labels. 

1.5.3 Usage Information 

According to the Kline Biocides Report for 2004/2005, PCP is one of the leading wood 

preservatives for poles and is preferred by many utility companies. In 2004, U.S. consumption 

of PCP was estimated at 24.5 million pounds, and was forecasted to grow at an average volume 

rate of 1.6 percent. In 2004, there were only two major suppliers of PCP (Kline, 2005). 

1.6 Regulatory History 

PCP has been used as a wood preservative since 1936; however, the first pesticidal product 

containing PCP was registered by the United Sates Department of Agriculture (USDA) on 

December 1, 1950. In 1970, EPA was established and was charged with protecting human health 

and the environment, and assumed all pesticide registrations from USDA. 

In October 1978, an administrative review process was initiated to consider whether the pesticide 

registration of the three heavy duty wood preservative uses (including PCP) should be canceled 

or modified. The Federal Register (Vol.49, No.139) of July 13, 1984 concluded that process and 

announced that certain changes in the terms and conditions of registration were required if 

registrants and applicants wished to avoid cancellation. 
Page 14 of 63

After evaluating the risks to public health posed by these three heavy duty wood preservative 

chemicals (including PCP) along with the significant economic benefits resulting from their use, 

the Agency determined that the use of PCP as a wood preservative chemical in accordance with 

certain modifications to terms of registration would satisfy the statutory standard for registration. 

These modifications (classification as restricted use pesticide, worker protection/protective 

clothing and equipment label requirements, restricted to non-residential uses, etc.) are identified 

and described in the Federal Register of January 13, 1986 (Vol.51, No. 7). Additionally, all nonpressure treatment and non-thermal treatments for PCP products have been voluntarily deleted. 

The Agency completed a Reregistration Eligibility Decision (RED) for PCP in 2008. EPA 

determined that PCP products contribute benefits to society and are eligible for reregistration 

provided the mitigation measures and associated label changes identified in the 2008 RED are 

implemented and required data are submitted. A post-RED Generic-Data Call-In (GDCI) and 

Product-Specific-Data-Call-In (PDCI) were issued on September 21, 2011. 

1.6.1 Tolerance Information 

For the active ingredient PCP, EPA has not established tolerances or exemptions from tolerances 

in raw agricultural commodities or processed food and feed products under the Federal Food, 

Drug and Cosmetic Act (FFDCA) Section 408 for pentachlorophenol. PCP has been cleared as a 

food additive by the US Food and Drug Administration (US FDA) under FFDCA Section 409 

for use as a component in adhesives in 21 CFR 175.105 and is also a component in wood 

preservatives in 21 CFR 178.105. There are no existing food uses for the wood preservative use. 

1.7 Incidents 

1.7.1 Human Health 

Based on a search conducted on October 29, 2014, covering the period from January, 1905 to 

January, 2008, over 300 incident reports exist in the EPA’s Incident Data System (IDS) 

associated with human PCP exposures. No PCP incidents have been reported after this time 

period. In addition, the number of incidents and epidemiological studies published in scientific 

literature addressing possible associations between exposure to PCP and subsequent 

development of disease is large. The associated concerns include chloracne, tremors, allergies, 

insomnia, twitching, diarrhea, dizziness, soft tissue sarcoma, non-Hodgkin’s lymphoma and 

possibly abnormal births. Whether these deleterious health effects result from exposure to PCP 

specifically, or to one or more other chemicals typically found as contaminants, is not clear. 

1.7.2 Ecological 

No ecological incidents exist in the IDS as of August 12, 2014. 
Page 15 of 63

2 Anticipated Data Needs 

Several studies were required by the DCI following the assessment of PCP in the 2008 RED. In 

addition to the already-required post-RED DCI data, the following studies as listed in Table 8 are 

expected to be needed for the registration review of PCP. Table 9 outlines the data requirements 

required by the post-RED DCI issued on September 21, 2011. The Agency anticipates reviewing 

data received in response to the post-RED DCI as well as data requested for this registration 

review prior to conducting the registration review risk assessments for PCP. 

Table 8 – Studies Anticipated as Needed for the Registration Review of PCP 

GLN Study Name Test 

Substance

Time Frame 

(Measured in 

months from 

DCI Receipt)

Risk 

Assessment(s) 

Data Will 

Support

Use Site(s) 

Triggering 

Anticipated Data 

Requirement

Applicable 

Exposure 

Scenario

850.13001

Freshwater 

invertebrate, life 

cycle 

TGAI 12 Ecological Wood preservatives 

Aquatic 

environment – 

Aquatic 

invertebrates 

850.42252 Seedling 

emergence, rice TGAI 12 Ecological Wood preservatives 

Aquatic 

environment - 

Semi-aquatic 

plants 

 -No 

GLN3

Whole sediment, 

chronic, 

freshwater (2 

spp.) 

TGAI 24 Ecological Wood preservatives 

Aquatic 

environment - 

Benthic 

organisms 

No GLN3

Whole sediment, 

chronic, 

estuarine/marine

TGAI 24 Ecological Wood preservatives 

Aquatic 

environment - 

Benthic 

organisms 1 The anticipated DCI will require that testing be conducted with the most sensitive organism (either freshwater or 

estuarine/marine vertebrates, or freshwater or estuarine/marine invertebrates), as determined from the results of the existing acute 

toxicity tests. 

2 Data on only one plant species (rice, Oryza sativa) are anticipated to be required. 3 The anticipated DCI will require that a protocol must be approved by the Agency prior to the initiation of the study. 

Table 9 –Data Required by the September 21, 2011 Data Call-In for the PCP RED 

GLN Study Name Status of DCI 

835.6100 Terrestrial field dissipation Waiver request granted. 

875.1100 Dermal exposure – outdoor The 2011 DCI specified that the registrant is only required to perform 

two of the four exposure tests listed, one dermal and one inhalation. In 

place of these studies, the registrant submitted a biomonitoring protocol 

study for review (MRID 49278800). The Agency is reviewing the 

protocol for this observational study. If the protocol and results from the 

ensuing study are approved, this study would satisfy the exposure study 

requirements for the PCP case (GLNs 875.1100, 875.1200, 875.1300, 

875.1400, and 875.1600). 

875.1200 Dermal exposure – indoor 

875.1300 Inhalation exposure – outdoor 

875.1400 Inhalation exposure - indoor 

875.1600 Application exposure 

monitoring data reporting 

875.1700 Product use information No data have been submitted; this study is outstanding. 
Page 16 of 63

3 Human Health Risk Assessment 

The Agency anticipates the need to conduct an updated human health risk assessment for PCP 

based upon the updated exposure study data from the 2011 post-RED DCI. PCP contains CDDs, 

CDFs, and HCB as contaminants formed during the manufacturing process. Direct 

measurements of CDDs/CDFs and HCBs for the general population attributed to pressure treated 

wood are not available for this assessment. Therefore, to be inclusive of determining potential 

exposures to PCP contaminants, the amount of HCB and the toxicity equivalents (TEQ) of the 

CDDs/CDFs in the PCP during manufacturing will be used to extrapolate equivalent HCB and 

dioxin exposures for PCP in treated wood. The Agency will use the latest manufacturing 

reporting information about how much HCB and dioxin are present in PCP samples from the 

PCP task force, which was created to respond to data requirements and other reevaluation 

information for the PCP case. 

Population-based biological monitoring data from the National Health and Nutrition Surveys 

(NHANES) are available to assess the exposure of the general population to PCP. The NHANES 

data provides an encompassing review of all PCP exposures; the specific PCP treated wood 

contribution to total PCP exposure cannot be differentiated. The Agency used 2001–2002 

NHANES data to inform the 2008 RED and will update the registration review risk assessment 

with the latest available NHANES data from 2003-2004 or a more recent NHANES dataset 

should one become available at the time of risk assessment. Because NHANES does not include 

exposures to children under the age of 6 years old, the Children’s Total Exposure to Persistent 

Pesticides and Other Persistent Organic Pollutants (CTEPP) study (Wilson, et al. 2007) will be 

used to include estimates of exposures to children under 6 years old. 

3.1 Existing Toxicological Endpoints 

3.1.1 PCP 

In preparation for the reregistration risk assessment in 2008, the Agency selected a set of 

toxicological end-points (2008 RED). Subsequent to the RED, the Agency’s Integrated Risk 

Information System (IRIS) program released a PCP reassessment in 2010. The updated Cancer 

Potency Factor for PCP is 4 × 10-1 per mg/kg-day compared to the cancer slope factor (CSF) of 

7× 10-2 per mg/kg-day used in 2008 RED representing an almost 5.7-fold increase in cancer 

potency (IRIS, 2010, http://www.epa.gov/IRIS/subst/0086.htm). The revised hazard information 

will be used in the final risk assessment process. The existing database of studies is tabulated in 

Appendix A 
Page 17 of 63

Table 10 – Toxicological Endpoints Selected for Risk Assessment of PCP (2008, RED) 

Exposure 

Scenario 

Dose 

(mg/kg/day) 

Endpoint 

Study 

Acute Dietary Developmental NOAEL 

= 30 

Increased 

resorptions,reduced fetal 

weight, and skeletal 

malformations 

Developmental 

toxicity - rat 

MRID # 43091702 

UF = 100a

Acute RfD = 0.3 mg/kg/day

Chronic Dietary 

LOAEL = 1.5 

Incr. liver weight and alk. 

phos. activity; increased 

incidence of granular 

cytoplasmic pigment 

accumulation in the liver 

Chronic Toxicity - 

Dog 

MRID # 43982701 

UF = 300a Chronic RfD = 0.005 mg/kg/day

Carcinogenicity (dietary) Classified as a B2 (probable human carcinogen) carcinogen by the Health Effects 

Division Carcinogenicity Assessment Review Committee and EPA’s Science 

Advisory Board. An oral cancer risk estimate (q1*) of 7.0 x 10-2 per mg/kg-day was 

calculated based on the incidences of hepatocellular neoplasms, adrenal medullary 

neoplasms, and hemangiosarcomas that developed in female mice treated with 

technical grade PCP or Dowicide EC-7 (NTP, 1989). The slope factor was 

calculated as the geometric mean of the individual slope factors derived from two 

data sets: female mouse data for technical grade and Dowicide EC-7 PCP. This 

slope factor may change based on a more recent analysis of the NTP dataset by 

EPA’s National Center for Environmental Assessment (NCEA) pending peer review 

of the updated Toxicological profile for the IRIS database. 

Short and Intermediate -

term (Dermal)a

NOAEL = 30a

MOE = 100 

Increased resorptions, 

reduced fetal weight, skeletal 

malformations 

Developmental - Rat 

Long-term (Dermal) 

LOAEL = 1.5a

MOE = 300 

Incr. liver weight and alk. 

phos. activity; increased 

incidence of granular 

cytoplasmic pigment 

accumulation in the liver 

Chronic Toxicity - 

Dog 

Inhalation No inhalation data available for PCP. Inhalation risks for occupational exposure 

were not performed because most inhalation values derived from the biomonitoring 

study in workers were below the level of quantitation, thus implying that the 

majority of worker exposure is through dermal contact with PCP. a All exposure scenarios are based on absorbed dose from the biological monitoring studies (oral short- and 

intermediate-term NOAEL and oral long-term LOAEL are used to estimate risks with the Target MOEs of 100 

and 300, respectively). 

PCP also contains CDDs/CDFs and HCB as contaminants formed during the manufacturing 

process. HCB is present in PCP at a concentration of 19 ppm. TEQ dioxin is present in PCP at a 

concentration of 0.413 ng TEQ dioxin/mg PCP (Van den Berg et al, 2006). To estimate the TEQ 

dioxin lifetime average daily dose (LADD), the LADD for PCP is multiplied by the TEQ dioxin 

conversion factor (i.e., 1 mg/kg/day PCP x 0.413 ng TEQ dioxin/mg PCP x 1 mg/1,000,000 ng 

unit conversion = 4.13E-7).To estimate the HCB exposure dose, the exposure dose for PCP is 

multiplied by the HCB conversion factor (i.e., 1 mg/kg/day PCP x 19 ng HCB/mg PCP x 1 

mg/1,000,000 ng unit conversion = 0.000019). 
Page 18 of 63

3.1.2 Contaminants 

CDD and CDFs 

Acute and Chronic Toxicity 

The concept of toxic equivalency factors (TEFs) has been developed to facilitate risk assessment 

of exposure to chemical mixtures of CDDs and CDFs. In this procedure, individual TEFs are 

assigned to the various congeners of CDDs and CDFs. These values have been published by both 

the USEPA and the World Health Organization (Younes, 1998) and are based on assigning 

relative values in relation to 2,3,7,8-TCDD, which is assigned a TEF value of 1.0, it being the 

most potent congener. Multiplying the exposure concentration of individual congeners by their 

respective TEFs yields a toxic equivalency, which, when summed for all the components of the 

mixture, gives the TEQ for that mixture and is an indication of the additional exposure from the 

PCP contaminants. Recent developments in science policy in the Agency have resulted in a shift 

towards calculation of non-cancer risk from dioxins and furans using a body burden approach 

rather than a dose or intake approach. This is appropriate for dioxin/furan contaminants of PCP 

due to the long half-life of these chemicals. The Agency’s Office of Research and Development 

(ORD) has led the effort in characterizing hazards and risks from exposure to dioxins and dioxinlike compounds, and OPP, in its assessment of non-cancer risks posed by the dioxin/furan 

contaminants in PCP, is working with ORD to express these risks using the methodologies 

developed in ORD for calculation of body burdens from exposure to the contaminants in PCP 

treated wood. 

Carcinogenicity 

A carcinogenic endpoint related to absorbed doses of CDD and CDF contaminants 

has been identified. At this time, for purposes of cancer risk assessment, the Agency is using the 

currently published slope factor of 1.0 x 105 per mg/kg-day for the 2,3,7,8 congener. 

HCB 

As summarized in Table 11, the Agency selected a set of HCB toxicological end-points for the 

reregistration risk assessment in 2008 (2008 RED). No additional toxicological information was 

identified in the draft 2013 ATSDR Toxicological Profile for HCB which summarizes existing 

literature information for HCB. 

Acute and Chronic Toxicity 

The toxicology of HCB is discussed in detail within the 1991 “Drinking Water Criteria 

Document for Hexachlorobenzene,” prepared by the U.S. EPA’s Office of Health and 

Environmental Assessment (EPA, 1991) and the “ATSDR Toxicological Profile for 

Hexachlorobenzene” (ATSDR, 2002). Both assessments characterize the acute toxicity of HCB 

as low, with oral LD50 values in the range from 3500-10,000 mg/kg in rats, and other data citing 

1700 mg/kg in rats, 2600 mg/kg in rabbits, and 4000 mg/kg in mice. 
Page 19 of 63

Carcinogenicity 

The Agency has classified HCB as a B2 (probable human) carcinogen, based on data sets that 

showed induction of tumors of the thyroid, liver, and kidney in three rodent species (U.S.EPA, 

IRIS, 1996). In the IRIS database, the oral cancer slope factor was 1.7 (mg/kg/day)-1 based on 

hepatocellular carcinomas in female Sprague-Dawley rats using a 2/3's animal to human scaling 

factor. However, based on current agency policy, a 3/4's scaling factor is applied to adjust the 

slope factor. The cancer slope factor for HCB was modified by 0.6X to account for the newer 

factor. For this evaluation, carcinogenic risk was assessed for non-dietary exposure to HCB 

using the modified cancer slope factor of 1.02 per mg/kg-day. 

Table 11 – Toxicological Endpoints Selected for Risk Assessment of HCB (2008, RED) 

Exposure 

Scenario 

Dose 

(mg/kg/day) 

Endpoint 

Study 

Incidental Oral: 

Short-Term 

NOAEL = 40 

Target MOE = 100 

Body weight loss, 

hyperesthesia, tremors, 

convulsions in maternal 

rats at 60 mg/kg/day. 

Developmental 

toxicity – rat 

(Khera, 1974) 

Incidental Oral: 

Intermediate-Term 

LOAEL = 0.5 

Target MOE = 100 

Increased incidence of 

liver porphyrin levels in 

female rats at 2 mg/kg/day 

15 Week Oral 

Toxicity- Rat (KuiperGoodman et al, 1977) 

Dermal: 

Short-Term 

Oral NOAEL = 40 

mg/kg/day (a 

MOE = 100 

Body weight loss, 

hyperesthesia, tremors, 

convulsions in maternal 

rats at 60 mg/kg/day. 

Developmental 

toxicity – rat 

(Khera, 1974) 

Dermal: 

Intermediate-Term 

LOAEL = 0.5 

Target MOE = 100 

Increased incidence of 

liver porphyrin levels in 

female rats at 2 mg/kg/day 

15 Week Oral 

Toxicity- Rat (KuiperGoodman et al, 1977) 

Dermal: 

Long-Term 

Oral NOAEL 

=0.08 mg/kg/day 

Target Moe = 100 

Hepatic centrilobular 

basophilic chromogenesis at 

0.29 mg/kg/day 

Chronic Toxicity - 

Rat (Arnold et al., 

1985) 

Inhalation 

Short-, Intermediate, and 

Long-Term 

No route-specific endpoints are available for HCB. Therefore, in 

accordance with agency policy, oral endpoints and route extrapolation 

are employed to estimate inhalation risks as needed. 

Target MOE = 1000 

Carcinogenicity 

B2 (probable Human Carcinogen). Q*=1.02 per mg-kg/day. (Extrapolated using a 

Q*of 1.7(mg/kg/day)-1 derived from a linearized multistage model to which a 3⁄4 

scaling factor was applied: 1.7 x 0.6 =1.02) Sourced to EPA REDs for DCPA, 

November 1998, and Chlorothalonil, April 1999 and EPA’s IRIS Database. 

a). Since an oral endpoint was selected for HCB dermal risk assessments, a dermal absorption value of 26.0 % should 

be used in route-to-route extrapolations. 

3.2 Dietary Exposure 

The most recent dietary exposure assessment for PCP was done in support of the 2008 RED 

using dietary monitoring data assembled by the Food and Drug Administration (FDA) from 
Page 20 of 63

1991. The dietary monitoring data assembled by FDA for certain food items have been 

discontinued since 1992 based on a lack of detectable residues. The 2008 non-occupational 

exposure and risk assessment for the PCP RED was also based on the NHANES biological 

monitoring data from the 2001-2002 survey. The NHANES data account for both indirect 

dietary exposures and exposures through drinking water more effectively than the standard 

models normally used by the Agency to estimate exposures. Residues of PCP have been 

measured in urine by the NHANES data. Updated 2003-2004 data (or a more recent NHANES 

dataset) will be included in the aggregate assessment (see Section 3.3.4) as part of registration 

review. A separate dietary assessment is not anticipated to be required at this time since the 

NHANES data reflect any potential dietary exposure to PCP. 

3.2.1 Food 

Dietary exposure to PCP was previously evaluated as part of the U.S. EPA’s 2008 RED. Given 

the restrictions on use of this pesticide in place since 1984, a dietary risk assessment is not 

anticipated to be necessary. As part of the 2008 RED, the Agency conducted a dietary exposure 

assessment using FDA monitoring data from 1991 that showed levels of PCP in a few food items 

as well as NHANES data from 2001-2002. 

Since risks of concern were not identified at that time and no additional uses that would 

contribute additional exposure from food contact have been registered, the Agency does not 

anticipate the need for additional residue chemistry data. 

3.2.2 Drinking Water 

No separate human drinking water exposure assessment is expected for PCP. As discussed 

above, the NHANES biomonitoring data will include any human exposures from drinking water. 

3.3 Occupational and Residential Exposures 

The agency anticipates the need to revise the occupational and residential assessments conducted 

in support of the 2008 RED. This is needed to account for new exposure monitoring studies 

required in the 2011 post-RED DCI and the revised toxicological endpoints that are likely to be 

selected based on the new cancer slop factor for PCP. Since no residential handler uses are 

expected from the use of PCP, a risk assessment is not required. However, EPA will be assessing 

residential post-application exposures. 

As a result of the past RED mitigation, the Agency implemented mitigation measures to reduce 

exposure to workers in wood treatment facilities. In an effort to determine if those mitigation 

measures are effective in reducing exposure, the Agency issued a post-RED DCI notice requiring 

that new exposure monitoring studies be conducted at wood treatment facilities using the latest 

personal protective equipment (PPE) and engineering controls to mitigate exposures that were 

specified in the 2008 RED (e.g. ventilation systems, vacuums after treatment, and automated 

cylinder doors). These mitigation measures are reflected on the PCP product labels. The Agency 

received a protocol (MRID 49278801) for a wood pressure treatment biomonitoring study and 
Page 21 of 63

expects to receive a new study during registration review that should help the Agency to 

determine new exposures based on the new exposure control measures specified in the RED. 

To assess exposures to pole installers (electrical utility linemen), a chemical-specific biological 

monitoring post-application study was used by the Agency (Thind et al. 1991). The purpose of 

the study was to characterize chronic or long-term exposure of PCP to linemen by examining 

PCP levels in workers’ urine. 

3.3.1 Occupational Exposure 

The Agency conducted an occupational assessment for the RED for PCP on September 8, 2008 

(U.S. EPA, 2008e). The occupational assessment was based on absorbed doses for occupational 

workers using chemical-specific biological monitoring data submitted by the PCP Task Force 

(MRID 44813701) and the biological monitoring data for electrical utility linemen (Thind et al. 

1991). 

The Agency anticipates receiving new occupational studies for the wood preservative use 

(exposure studies to monitor work exposure at pressure treatment plant) in order to conduct new 

occupational risk assessments to assess the dermal and inhalation routes of exposure from 

pressure treatment exposure and pole lineman during registration review. The scenarios outlined 

in Table 12 are the typical worker exposure scenarios for a variety of exposures. Studies 

accounting for these exposure scenarios were required by the 2011 post-RED DCI (see Table 9). 

For example, for pressure treatment facilities, workers operate and monitor application system 

valves and controls, open and close cylinder doors (automated), and supervise the insertion and 

removal of charges (loads of dried or debarked poles) of timber from the treatment cylinders. 

Workers operate forklifts used to load untreated wood onto charge trams; move charges into and 

out of treatment cylinders; remove charge leads and bands from treated wood; distribute treated 

wood to load-out area, and load treated wood for shipment. Workers perform various labor and 

cleanup duties in treatment and drip pad area including: sweeping and pressure-washing drip pad 

and tracks; removing and shredding all bands from treated stacks of lumber; picking up and 

disposing treated wood waste; cleaning cylinders; and, handling hazardous waste. 

Table 12 – Occupational Exposure Scenarios for Workers Using PCP

Scenario Exposure Route(s) Duration

Occupational Exposures 

Pressure Treatment Workers Dermal and Inhalation * Short, Intermediate, and Long- Term 

Pole Installers Dermal and Inhalation* Short, Intermediate, and Long- Term 

*Biological monitoring data can be used in lieu of dermal and inhalation monitoring studies. 

3.3.2 Residential Handler Exposures 

Residential handler exposures are not expected based on the labeled use patterns; therefore, a 

residential assessment is not anticipated as needed for this registration review. 
Page 22 of 63

3.3.3 Residential Post-Application Exposures 

Population-based biological monitoring data from the NHANES data are available to assess the 

exposure of the general population to PCP. The NHANES data provides an encompassing 

review of all PCP exposures. Because NHANES does not include exposures to children under 

the age of 6 years old, the CTEPP study will also be used to include estimates of exposures to 

children under 6 years old. EPA will base the residential exposures based on NHANES and 

CTEPP data and calculate non-cancer and cancer risks. The amount of HCB and the toxicity 

equivalents (TEQ) of the CDDs/CDFs in the PCP during manufacturing are used to extrapolate 

equivalent HCB and dioxin exposures for PCP in treated wood. 

3.3.4 Aggregate Exposures 

EPA anticipates the need to revise the aggregate assessment conducted in support of the 2008 

RED using updated NHANES data. Upon a reevaluation and selection of toxicological 

endpoints, combined with the human health exposure assessments expected as a part of this 

registration review case, aggregate exposures will need to be assessed. 

This assessment will include dietary (food) exposures and residential exposures based on the 

latest NHANES data. EPA believes the NHANES dataset provides the most comprehensive data 

on exposure to PCP from all sources (dietary and non-dietary as well as both EPA- and FDAregistered uses) and is the best dataset for estimating aggregate risk to triclosan. Because 

NHANES does not include exposures to children under the age of 6 years old, the Children’s 

Total Exposure to Persistent Pesticides and Other Persistent Organic Pollutants (CTEPP) study 

(Wilson, et al. 2007) will be used to include estimates of exposures to children under 6 years old. 

3.3.5 Cumulative Exposures 

With respect to cumulative exposure, unlike other pesticides for which EPA has followed a 

cumulative risk approach based on a common mechanism of toxicity, EPA has not made a 

common mechanism of toxicity finding as to PCP. For the purposes of this registration review, 

therefore, EPA has not assumed that PCP has a common mechanism of toxicity with other 

substances. For information regarding EPA’s efforts to determine which chemicals have a 

common mechanism of toxicity and to evaluate the cumulative effects of such chemicals, see 

http://www.epa.gov/pesticides/cumulative/.

4 Environmental Risk Assessment 

The ecological risk assessment planned in registration review will allow the Agency to determine 

potential acute and chronic risks to non-target organisms and to aquatic organisms exposed to 

PCP and its degradates and impurities that may be transported from antimicrobial use sites into 

the terrestrial and aquatic environments (including in-service uses of PCP treated wood). The 

Agency has not yet conducted a risk assessment that supports a complete endangered species 

determination for PCP. The risk assessment will allow the Agency to determine whether its use 

has 'no effect' or 'may affect' federally listed threatened or endangered species (listed species) or 

their designated critical habitats. When an assessment concludes that a pesticide’s use 'may 

affect' a listed species or its designated critical habitat, the Agency will consult with the U.S. 
Page 23 of 63

Fish and Wildlife Service and/or National Marine Fisheries Services (the Services), as 

appropriate. 

The Agency conducted preliminary environmental risk assessments for the 2008 RED. 

Ecological risks were assessed separately for PCP (EPA 2008b), for the dioxin/furan 

(CDDs/CDFs) contaminants (EPA 2008c), and for the HCB contaminants (EPA 2008d). The 

only use assessed was the in-service use of treated utility poles. Risks from in-service uses of 

PCP-treated wood in other terrestrial situations (e.g., fences, timbers, railroad ties) and in the 

aquatic environment (e.g., pilings, wharves) were not assessed. Risk assumptions from the 

preliminary assessments are summarized below. Since the time of the RED, EPA has not 

received information that would alter the risk conclusions from 2008. However, in 2013, EPA 

released new data requirements for antimicrobial pesticides (Subpart W of 40 CFR Part 158) to 

update scientific framework for identifying and assessing risks. In registration review, the 

Agency anticipates the need to request ecotoxicity data to characterize the risks identified in the 

2008 RED. 

In the RED, based on the moderate toxicity of PCP to the laboratory rat and the low 

concentration of PCP expected in soil around utility poles, minimal acute risk was presumed for 

small wild mammals. Due to low estimated environmental concentration (EECs) modeled for 

surface waters, minimal acute risk also was presumed for birds feeding on aquatic organisms. 

The potential for chronic risk to birds and mammals, acute risk to beneficial insects, and acute 

risk to birds and mammals feeding on contaminated foods (e.g., soil invertebrates, seeds, small 

mammals) was not addressed. 

For PCP aquatic organism risk presumptions were based on RQ methodology. Aquatic EECs 

were modelled based on environmental fate parameters and resultant estimates of movement of 

leachate from utility poles. Based on comparing EECs to ecotoxicity values, minimal acute and 

chronic risks were presumed for exposure of freshwater fish and aquatic invertebrates. Minimal 

acute risk also was presumed for estuarine/marine fish and invertebrates, but chronic risk could 

not be assessed due to lack of chronic toxicity data for estuarine/marine organisms. Risk to 

freshwater and estuarine/marine benthic invertebrates was not addressed due to lack of sedimenttoxicity data. Risk to vascular aquatic plants and algae were below the Agency’s LOCs. 

The RED also examined risks from the contaminants and determined some potential risks. Since 

the amount of contaminant levels have been reduced since the time of the RED, these risks will 

be re-evaluated in registration review. 

4.1 Environmental Fate Assessment 

The environmental fate assessment is primarily for PCP and for the contaminants CDDs, CDF, 

and HCB. Previous analyses have not shown PCA as a major degradate of PCP. However, in 

light of the recent Stockholm Convention POPRC analysis of PCP, EPA is reviewing 

information and data available for PCA to determine if it is appropriate to include PCA in the 

risk assessment to be conducted in registration review. The Agency welcomes the submission of 

PCA information and data from the public and interested stakeholders to this PWP during the 

comment period. 
Page 24 of 63

PCP is hydrolytically stable at pH, 5, 7, and 9 under abiotic conditions. It degrades photolytically 

in aqueous medium with a half-life of between 13-20 minutes (MRID 42481101). Major and 

minor degradates have been identified as tetra and trichlorophenols which are discussed in more 

detail in Appendix B. 

PCP degrades in aerobic soils and aquatic systems with a half-life of 7-14 days, and under 

anaerobic conditions with a half-life of 1-2 months. 

PCP has a log Kow of 5.05 and may be bioaccumulative in aquatic animals. PCP adsorption to 

soils is pH dependent. At acidic pHs, PCP is tightly bound to the soil structure, but as pH 

increases, adsorption decreases resulting in greater mobility at neutral and higher pHs. 

Chlorinated dioxins, HCB, and PCA are relatively insoluble and stable in the environment. They 

all have characteristics which indicate the potential for bioaccumulation. 

4.1.1 Water Quality 

PCP is not identified as a cause of impairment for any water bodies listed as impaired under 

section 303(d) of the Clean Water Act.1

 In addition, no Total Maximum Daily Loads (TMDL) 

have been developed for PCP.2 However, PCP has two types of contaminants: CDDs, and CDFs 

(abbreviated as dioxins) and HCB. Dioxins are identified as a cause of impairment for 617 water 

bodies in the United States. Fish is consumed from these impaired water bodies. Source(s) of 

origin of these CDDs and CDFs in impaired water bodies and their presence in fish are not 

identified. HCB is identified as a cause of impairment for 44 water bodies in the United States. 

Fish is consumed from these impaired water bodies. Source(s) of origin of HCB in impaired 

water bodies and their presence in fish are not identified. It is stated that no TMDLs are needed 

for these impairments. More information on impaired water bodies and TMDLs can be found at 

EPA’s website.3 

4.2 Environmental Exposure Pathways 

Leachate from treated wood is likely to be the primary source of environmental exposure to 

nontarget organisms. PCP and its degradates and impurities may leach into the soil surrounding 

treated utility poles, fences, timbers, and other treated wood. PCP, CDDs/CFDs, and HCB might 

be transported into the aquatic environment via various environmental pathways, including 

runoff and leaching. PCP-treated wood used directly in the aquatic environment will leach PCP 

and its’ degradates and impurities directly into surface waters and sediments. Most material 

reaching the aquatic environments is expected to bind to organic matter and sediments and 

expose benthic invertebrates. A soluble fraction of the leachate also will be present in the water 

column and may expose fish, aquatic invertebrates, and aquatic plants. In the water column, 

exposure is expected to be acute, whereas chronic exposure is expected in aquatic sediments. 

Bioconcentration in fish and aquatic invertebrates may result in exposure and bioaccumulation in 

predators, such as fish-eating birds and mammals, larger fish, and reptiles. 

 

1 http://iaspub.epa.gov/tmdl_waters10/attains_nation_cy.cause_detail_303d?p_cause_group_id=885

2

http://iaspub.epa.gov/tmdl_waters10/attains_nation.tmdl_pollutant_detail?p_pollutant_group_id=885&p_pollutant_

group_name=PESTICIDES

3 http://www.epa.gov/owow/tmdl/
Page 25 of 63

Terrestrial organisms also may be exposed via various environmental pathways. Invertebrates in 

and around treated wood structures may be exposed from contaminated soil. Contaminated 

invertebrates may be eaten by other terrestrial animals, including small mammals, birds, and 

reptiles. Bioaccumulation may lead to higher trophic levels being exposed as PCP, CDDs/CDFs, 

and/or HCB move through the food chain. 

Likely pathways for exposure of nontarget organisms are summarized below. All relevant routes 

of environmental exposure will be considered in the risk assessment. 

Terrestrial Organisms 

 • Dietary exposure of small mammals and birds to leachate in soil and food sources (e.g., 

invertebrates, seeds) on and in the soil surrounding treated wood structures. 

 • Dermal contact of beneficial insects, birds, and small mammals with treated wood surfaces. 

 • Dietary exposure of predatory mammals, birds, and reptiles to contaminated prey; 

bioaccumulation may lead to exposure at higher trophic levels in the food chain. 

 • Ingestion of residues through drinking water sources such as puddles or roadside ditches at 

the use site. 

Aquatic or Semi Aquatic Organisms 

 • Exposure via contaminated surface waters. 

 • Exposure via contaminated aquatic sediments. 

 • Dietary exposure of predatory and herbivorous fish and reptiles to contaminated prey and 

aquatic plants; bioaccumulation may lead to exposure at higher trophic levels in the food 

chain. 

 • Uptake of residue in surface waters by aquatic plants. 

 • Uptake of residue in surface waters and sediments by rooted semi-aquatic plants. 

A conceptual model diagram (CMD) also is available for wood preservative uses. Based on 

antimicrobial use patterns, the Agency developed conceptual models for potential routes of 

environmental exposure to terrestrial and aquatic receptor groups. The “Conceptual Models for 

Environmental Exposure Pathways of Antimicrobial Pesticides” are located in the docket at 

www.regulations.gov (EPA-HQ-OPP-2014-0638-0002). For In‐Use Service of Wood Treated 

Wood Products, see page 29 in that document. 

4.3 Ecological Effects Analysis 

4.3.1 Mechanism of Action 

The toxicity of PCP to animals is due to the uncoupling of oxidative phosphorylation in the 

mitochondria. This results in reduced production of adenosine triphosphate (ATP), accompanied 

by weight loss due to acce1eration of metabolic rate and utilization of tissue energy reserves 

(EPA 1986). Activities of various enzymes also are affected. 
Page 26 of 63

4.3.2 Measures of Effect (Ecotoxicology Endpoints) 

4.3.2.1 Available Ecotoxicity Endpoints 

Acute and chronic ecotoxicity endpoints are currently available for PCP from several sources. 

Registrants have submitted ecotoxicity studies conducted in accordance with the 850 OCSPP 

Harmonized Test Guidelines to address the data requirements for pesticide registration. 

Additional data are available in EPA’s Office of Water Ambient Water Quality Criteria for 

Pentachlorophenol – 1986 (EPA 1986) and the OPP Pesticide Ecotoxicity Database. These 

acute and chronic data will be used to evaluate the potential effects of PCP to terrestrial and 

aquatic animals and plants. For the CDDs/CDFs and HCB contaminants, which are not 

registered pesticides, 850 guideline studies are not available, but some data were previously 

compiled from the open literature. See Appendix C for additional information on the ecotoxicity 

data EPA has for the PCP case.

4.3.2.2 PCP 

All data requirements (existing database of studies and studies anticipated to be required) and 

available ecotoxicity endpoints for PCP are tabulated in Appendix C . The most sensitive of 

those endpoints will be used for assessing risk to each receptor group. The endpoints currently 

available for the risk assessment for PCP are provided in Table 13. Endpoints for mammals are 

found in section 3.1 (Human Health Risk Assessment – Existing Toxicological Endpoints). 

Table 13 – PCP Ecological Effects Endpoints for the Ecological Risk Assessment

Receptor 

Group 

Test 

Material

Risk 

Scenario Toxicity Endpoint Reference 

Freshwater fish TGAI Acute LC50 = 15 μg ai/L 43485104 

Chronic NOAEC = 11 μg ai/L EPA 1986 

Freshwater invertebrates TGAI Acute EC50 = 92 μg ai/L EPA 1986 

Chronic NOAEC <4.1 μg ai/L 1EPA 1986 

Freshwater benthic 

invertebrates TGAI Chronic Data gap -- 

Estuarine/marine fish TGAI Acute LC50 = 31 μg ai/L 40228401 

Chronic NOAEC = 6.6 μg ai/L See Appendix C 

Estuarine/marine 

invertebrates TGAI Acute EC50 = 34 μg ai/L USFWS 1980 

Chronic Not required -- 

Estuarine/marine benthic 

invertebrates TGAI Chronic Data gap -- 

Algae TGAI 

EC50

NOAEC 

EC50 = 27 μg ai/L 

NOAEC = 9 μg ai/L 42633704 

Aquatic vascular plants TGAI EC50

NOAEC 

EC50 = 250 μg ai/L 

NOAEC = 32 μg ai/L 42633708 

Semi-aquatic plants TGAI EC50

NOAEC Data gap -- 

Birds TGAI Acute LD50 = 380 mg ai/kg 160000 
Page 27 of 63

Dietary LC50 = 3400 ppm 22923 

Chronic Not required -- 

Amphibians TGAI Acute LC50 = 207 μg ai/L OPP database 

Nontarget insects TGAI Acute LD50 >48.3 μg ai/bee 36935 

1 This chronic endpoint is from the Ambient Water Quality Criteria for PCP; however, based on concerns with the 

study, the Agency anticipates the need to require a new chronic freshwater invertebrate study. See Appendix C for 

additional detail. 

4.3.2.3 Contaminants 

Ecotoxicity studies conducted in accordance with the 850 OCSPP Harmonized Test Guidelines 

are not available. Available ecotoxicity information from the open literature and EPA/OW’s 

Ambient Water Quality Criteria for 2,3,7,8-tetrachlorodibenzo-p-dioxin (EPA 1984) was 

compiled for the 2008 PCP RED (EPA 2008b). Some selected endpoints are presented in 

Appendix C and summarized below along with the risk conclusions.

CDDs/CDFs 

Data on the ecological effects of CDDs and CDFs are relatively limited. Most effects data are 

for the 2,3,7,8-chlorinated CDD/CDFs, especially 2,3,7,8-TCDD, which is very highly toxic to 

birds (LD50 = 15 μg/kg bw), small mammals (LD50=114-284 μg/kg), and aquatic organisms. 

CDFs are moderately toxic to fish (LC50 = 1140 μg/L) and aquatic invertebrates (LC50 = 1310 

μg/L), but TCDD’s are very highly toxic to fish (e.g., coho salmon 96-h LC50 = 0.005 μg/L). 

However, TCDD-induced mortality often occurs up to 30 to 80 days after exposure, even from 

durations as short as 6 h. Exposure of coho salmon (Oncorhynchus kisutch) to an initial 

concentration of 0.0056 μg/L resulted in 55% mortality within 60 days. Sublethal effects have 

also been reported for polychlorinated dioxins and furans, including: reduced growth; weight 

loss; abnormal hatching; cellular alterations; numerous types of lesions in numerous organs; and 

behavioral effects on swimming, reduced feeding, and loss of response to external stimuli. 

Despite the reported toxicity of the CDDs/CDFs to aquatic organisms, acute and chronic risks to 

aquatic organisms were deemed to be low due to low aquatic exposure expected from runoff of 

leachate from PCP-treated utility poles. However, the assessment also concluded that 

CDDs/CDFs might eventually reach toxic levels and pose risks to benthic organisms due to 

accumulation of these compounds in sediments. 

HCB 

The available information indicates that HCB is less toxic than PCP or the CDDs/CDFs. 

However, it has shown high toxicity to some fish (LC50s = 140 and 200 μg/L for sole and 

flounder, respectively) and is moderately toxic to birds. Toxicity to freshwater and saltwater 

benthic invertebrates ranged from 42 to 60 mg/kg sediment. 

4.3.3 Ambient Water Quality Criteria for PCP 

The AWQC document contains a review of public literature on acute and chronic effects of PCP 

on freshwater and saltwater organisms (EPA 1986). Some of the more sensitive endpoints 
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provided in that document are include in the Ecotoxicity Profile (Appendix C) and will be used 

for the risk assessment. The AWQC document also derived water quality criteria values. 

Because the toxicity of PCP varies with pH (i. e., toxicity decreases as pH increases), values 

were adjusted to pH 6.5 for developing the criteria. EPA/OW’s current ambient water quality 

criteria for PCP are as follows: 

Freshwater:

 Acute: 10.97 μg ai/L

 Chronic: 3.46 μg ai/L 

Saltwater:

 Acute: 25.05 μg ai/L 

 Chronic: 7.91 μg ai/L 

4.3.4 Open literature 

Additional open literature studies also will be identified through EPA’s ECOTOXicology 

(ECOTOX) database. The ECOTOX database will be searched when the risk assessment is 

prepared. Any acute or chronic endpoints more sensitive than what is currently available will be 

used in the risk assessment and risk characterization. Additional information on the Agency’s 

use of open literature is found on the Agency’s website: 

http://www.epa.gov/pesticides/science/efed/policy_guidance/team_authors/endangered_species_

reregistration_workgroup/esa_evaluation_open_literature.htm.

4.4 Exposure Analysis Plan 

4.4.1 Aquatic and Terrestrial Wildlife Exposure Estimates 

Available OPP models will be used to determine the estimated environmental concentration 

(EECs) in the aquatic environment. Resulting exposure estimates will be compared to the 

toxicity endpoints to determine if levels of concern are exceeded for each receptor group. 

4.4.2 Screening Level Down-the-Drain Analysis 

The Agency does not anticipate the need for a Down-the-Drain (DtD) assessment because the 

PCP treated wood at the site of the treatment is dried with a drain pad underneath and any leaked 

chemical is recycled for use. Remaining chemical in the pad (if any) must be treated as a 

hazardous waste and disposal (if any) must be conducted according to a state pesticide or 

environmental control agency, or by guidance from a hazardous waste representative. 

5 Endocrine Disruptor Screening Program (EDSP) 

As required by FIFRA and FFDCA, EPA reviews numerous studies to assess potential adverse 

outcomes from exposure to chemicals. Collectively, these studies include acute, subchronic and 

chronic toxicity, including assessments of carcinogenicity, neurotoxicity, developmental, 

reproductive, and general or systemic toxicity. These studies include endpoints which may be 

susceptible to endocrine influence, including effects on endocrine target organ histopathology, 

organ weights, estrus cyclicity, sexual maturation, fertility, pregnancy rates, reproductive loss, 

and sex ratios in offspring. For ecological hazard assessments, EPA evaluates acute tests and 
Page 29 of 63

chronic studies that assess growth, developmental and reproductive effects in different 

taxonomic groups. As part of the 2008 RED, for PCP, EPA reviewed these data and selected the 

most sensitive endpoints for relevant risk assessment scenarios from the existing hazard 

database. However, as required by FFDCA section 408(p), PCP is subject to the endocrine 

screening part of the Endocrine Disruptor Screening Program (EDSP). 

EPA has developed the EDSP to determine whether certain substances (including pesticide 

active and other ingredients) may have an effect in humans or wildlife similar to an effect 

produced by a “naturally occurring estrogen, or other such endocrine effects as the Administrator 

may designate.” The EDSP employs a two-tiered approach to making the statutorily required 

determinations. Tier 1 consists of a battery of 11 screening assays to identify the potential of a 

chemical substance to interact with the estrogen, androgen, or thyroid (E, A, or T) hormonal 

systems. Chemicals that go through Tier 1 screening and are found to have the potential to 

interact with E, A, or T hormonal systems will proceed to the next stage of the EDSP where EPA 

will determine which, if any, of the Tier 2 tests are necessary based on the available data. Tier 2 

testing is designed to identify any adverse endocrine-related effects caused by the substance, and 

establish a dose-response relationship between the dose and the E, A, or T effect. 

Under FFDCA section 408(p), the Agency must screen all pesticide chemicals. Between October 

2009 and February 2010, EPA issued test orders/data call-ins for the first group of 67 chemicals, 

which contains 58 pesticide active ingredients and 9 inert ingredients. A second list of chemicals 

identified for EDSP screening was published on June 14, 20134

 and includes some pesticides 

scheduled for registration review and chemicals found in water. Neither of these lists should be 

construed as a list of known or likely endocrine disruptors. 

PCP is on List 2. List 2 represents the next set of chemicals for which EPA intends to issue test 

orders/data call-ins in the near future. For further information on the status of the EDSP, the 

policies and procedures, the lists of chemicals, future lists, the test guidelines and the Tier 1 

screening battery, please visit our website.5

6 Optional Label Changes 

The Agency invites comment on any label amendments that could be considered to eliminate the 

anticipated need for EPA to require certain data, reduce the possibility that EPA’s planned risk 

assessments overestimate risk due to reliance on conservative assumptions, and/or improve label 

clarity. 

7 Guidance for Commenters 

7.1 Preliminary Work Plan 

 

4

 See http://www.regulations.gov/#!documentDetail;D=EPA-HQ-OPPT-2009-0477-0074 for the final second list of 

chemicals. 5

 http://www.epa.gov/endo/ 
Page 30 of 63

The public is invited to comment on EPA’s Preliminary Work Plan and rationale. The Agency 

will carefully consider all comments as well as any additional information or data provided in a 

timely manner prior to issuing a Final Work Plan for the PCP registration review case. 

7.1.1 Trade Irritants 

Through the registration review process, the Agency intends to solicit information on trade 

irritants and, to the extent feasible, take steps toward facilitating irritant resolution. The Agency 

will work to harmonize tolerances and international maximum residue limits (MRLs) and may 

modify tolerance levels to do so, when possible. Stakeholders are asked to comment on any 

trade irritant issues resulting from lack of MRLs or disparities between U.S. tolerances and 

MRLs in key export markets, providing as much specificity as possible regarding the nature of 

the concern. 

7.1.2 Water Quality 

The Agency invites submission of water quality data for this pesticide. To the extent 

possible, data should conform to the quality standards in Appendix A of the OPP Standard 

Operating Procedure: Inclusion of Impaired Water Body and Other Water Quality Data in 

OPP’s Registration Review Risk Assessment and Management Process6 in order to ensure they 

can be used quantitatively or qualitatively in pesticide risk assessments. 

7.1.3 Environmental Justice 

EPA seeks to achieve environmental justice, the fair treatment and meaningful involvement of all 

people, regardless of race, color, national origin, or income, in the development, implementation, 

and enforcement of environmental laws, regulations, and policies. To help address potential 

environmental justice issues, the Agency seeks information on any groups or segments of the 

population who, as a result of their location, cultural practices, or other factors, may have 

atypical, unusually high exposure to PCP compared to the general population. Please comment 

if you are aware of any sub-populations that may have atypical, unusually high exposure 

compared to the general population.

7.1.4 Additional Information 

Stakeholders are also specifically asked to provide available information and data that will assist 

the Agency in refining its risk assessments, including any species-specific ecological effects 

determinations. 

As mentioned in Section 1.6, the Agency determined in the 2008 RED that PCP products 

contribute benefits to society and were eligible for reregistration. In registration review, EPA 

plans to update the benefits and alternatives assessments for PCP. Stakeholders are encouraged 

to provide updated information on benefits and alternatives during the PWP comment period. 

EPA is seeking additional information on PCA, particularly any pertinent monitoring data. 

 

6 http://www.epa.gov/oppsrrd1/registration_review/water_quality_sop.htm
Page 31 of 63

Additionally, the Agency is interested in receiving the following information: 

1. Confirmation on the following label information: 

A. Sites of application 

B. Geographic limitations on use 

2. Use or potential use distribution 

3. State or local use restrictions 

4. Ecological incidents (non-target plant damage and avian, fish, reptilian, amphibian and 

mammalian mortalities) not already reported to the Agency 

5. Monitoring data 

8 Next Steps 

After the 60-day comment period closes in February 2015, the Agency will review and respond 

to any comments received in a timely manner, and then issue a Final Work Plan for the PCP 

case. 
Page 32 of 63

9 References 

ATSDR, 2002. Toxicological Profile for Hexachlorobenzene. September, 2002. 

EPA, 1986. Ambient Water Quality Criteria for Pentachlorophenol – 1986. USEPA Office of 

Water, Regulations and Standards Criteria and Standards Division, Washington DC. 

EPA, 1991. Drinking Water Criteria Document for Hexachlorobenzene. Prepared for Office of 

Water by Environmental Criteria and Assessment Office, Office of Health and Environmental 

Assessment, USEPA, Cincinnati, OH. 

EPA, 2008a. Reregistration Eligibility Decision for Pentachlorophenol. September 25, 2008, 

Antimicrobials Division, Office of Pesticide Programs, Washington, DC. 

EPA, 2008b. Ecological Hazard and Environmental Risk Assessment Chapter – 

Pentachlorophenol, PC Code: 63001, Case No.: 2505, R. C. Petrie, August 25 2008, 

Antimicrobials Division, Office of Pesticide Programs, Washington, DC. 

EPA, 2008c. Chlorinated Dibenzo Dioxins (CDDs) and Chlorinated Dibenzo Furans (CDFs) as 

Contaminants of Pentachlorophenol. Ecological Hazard and Environmental Risk Assessment for 

the Pentachlorophenol Reregistration Eligibility Decision (RED), PC Code: 63001, Case No.: 

2505, R. C. Petrie, September 18 2008, Antimicrobials Division, Office of Pesticide Programs, 

Washington, DC. 

EPA, 2008d. Hexachlorobenzene (HCB) as a Contaminant of Pentachlorophenol. Ecological 

Hazard and Risk Assessment – Supplement to the Pentachlorophenol Reregistration Eligibility 

Decision (RED) Document, PC Code: 63001, Case No.: 2505, R. C. Petrie, August 25 2008, 

Antimicrobials Division, Office of Pesticide Programs, Washington, DC. 

EPA, 2008e. Occupational Exposure and Risk Assessment of Dioxins and Furans (CDD/CDFs) 

in Pentachlorophenol, August 19, 2008, Antimicrobials Division, Office of Pesticide Programs, 

Washington, DC. 

Kline, 2005. Specialty Biocides North America 2004-2005, Volume II: United States, Kline and 

Company, Inc. 

NTP (National Toxicology Program). (1989) NTP toxicology and carcinogenesis studies of two 

pentachlorophenol technical-grade mixtures (CAS No. 87-86-5) in B6C3F1 mice (feed 

studies). Public Health Service, U.S. Department of Health and Human Services; NTP TR 349. 

Available from the National Institute of Environmental Health Sciences, Research Triangle Park, 

NC. 

Thind, K.S., Karmali, S., and House, R.A., 1991. Occupational Exposure of Electrical Utility 

Linemen to Pentachlorophenol. American Industrial Hygiene Association Journal 52:547-552. 
Page 33 of 63

Wilson et al., 2007. An observational study of the potential exposures of preschool children to 

pentachlorophenol, bisphenol-A, and nonylphenol at home and daycare. Environmental Research 

103 (2007) 9-20. 

Younes, M., 1998. WHO toxic equivalency factors (TEFs)for dioxin-like compounds for human 

and wildlife of WHO meeting held in Stockholm, Seden on June 15-18. World Health 

Organization, International Programme on Chemical Safty. 
Page 34 of 63

Appendix A Toxicology Profile 

Toxicology Profile for PCP 

The Agency does not anticipate the need to require additional toxicology data for PCP. 

Acute Toxicity for Product Labeling 

Acute toxicity studies available for labeling purposes have been summarized in Table A1. The 

acute toxicity database for PCP is considered complete. The acute toxicity of PCP is low for 

dermal toxicity (Toxicity Category IV) and primary dermal irritation (Toxicity Category III) but 

shows higher toxicity for acute oral toxicity and primary eye irritation (Toxicity Category II). No 

dermal sensitization was observed with the technical test material. Acceptable acute inhalation 

toxicity data for PCP were not available, but waivers were granted for these data. No additional 

data are anticipated to be required. 

Table A1 – Acute Toxicity Studies for PCP 

Guideline No./ Study 

Type MRID No. Results Toxicity Category

870.1100/ 

Acute oral toxicity 00101715 LD50 = 155 mg/kg (M); and 

LD50 = 137 mg/kg (F) II

870.1200/ 

Acute dermal toxicity 00101715 LD50 > 3980 mg/kg IV

870.1300/ 

Acute inhalation toxicity N/A Waiver granted (a) I 

870.2400/ 

Primary eye irritation 00101715 Corneal involvement at day 7 postinstillation II 

870.2500/ 

Acute dermal irritation 46616602 Moderate irritation at 72 hours postapplication III 

870.2600/ 

Skin sensitization 42594301 No sensitization observed using Buehler method N/A 

Note: N/A=Not available 

 (a) The PCP Task Force previously submitted data to the Agency on efforts to develop methods to conduct inhalation 

studies. This effort was without success, based on an inability to generate consistent chamber concentrations of 

PCP. The Task Force also cited label instructions (based on EPA Position Document 4 for Wood Preservatives) 

requiring the use of respirators and protective clothing for applicators entering pressure treatment cylinders and 

other related equipment contaminated with wood treatment formulation. On this basis, waivers were requested by 

the Task Force for inhalation toxicity data. The Agency granted these waiver requests and a Toxicity Category I 

for inhalation hazard will be assigned. 
Page 35 of 63

Subchronic Toxicity 

There is one 90-day dermal toxicity study (MRID # 43182301). In the study, PCP (88.9% a.i.) 

was administered by dermal occlusion to groups of 10 male and female Sprague-Dawley rats for 

6 hours/day, 5 days/week, at doses of 0, 100, 500, or 1000 mg/kg/day. No statistically significant 

differences in group mean body weight or weight gain were observed at any treatment level, nor 

were there any treatment related mortalities or clinical signs of toxicity. Dermal irritation 

consisting of erythema (grade 1-2) at 100 mg/kg/day and erythema (grade 1-4) at 500 and 1000 

mg/kg/day was observed during weeks 2-5 of the study. The magnitude of the dermal irritation 

decreased after week 5. There was no dermal irritation observed in control rats. At the 500 and 

1000 mg/kg/day dose levels, increased total white blood cell counts and absolute lymphocyte 

counts were observed in female rats. Decreased platelet count was observed at all dose levels in 

female rats. The hematological effects were ascribed to dermal irritation and not to systemic 

effects of the test chemical. Significant increases in alanine and aspartate aminotransferase 

activities were observed in male and female rats at the 500 and 1000 mg/kg/day dose levels, 

while increased cholesterol was observed at these dose levels in females only. Significant 

increases in absolute liver weight were observed at the 1000 mg/kg/day dose level for both males 

and females. The increase in liver weight was thought to be the result of enzyme induction. 

Kidney weights were increased at the 1000 mg/kg/day dose in males, and at the 500 and 1000 

mg/kg/day dose levels in females. At necropsy, tan crusty areas, acanthosis of the epidermis, and 

chronic inflammation of the dermis was noted at the treatment site in all treatment groups of both 

sexes. An increased incidence of hepatocellular degeneration accompanied by chronic 

inflammation was observed at 500 and 1000 mg/kg/day in both males and females. Based on the 

results of this study, the Systemic LOAEL = 500 mg/kg/day (enzyme induction and minimal to 

mild hepatocellular degeneration and chronic inflammation in males and females), and the 

Systemic NOAEL = 100 mg/kg/day. This study is classified as acceptable and satisfies the 

guideline requirement ('82-3) for a subchronic dermal toxicity study in rats. No additional data 

are anticipated to be required. 

Developmental Toxicity 

In a developmental toxicity study (MRID # 43091702), pregnant Crl: CD BR VAF/plus rats 

(25/dose) received oral administration of PCP (88.9%) at doses of 0, 10, 30 or 80 mg/kg/day 

during gestation days 6 through 15. Developmental toxicity observed at 80 mg/kg/day included: 

significant increase in the number of resorptions (mainly early) with a corroborative decrease in 

litter size; reduced mean fetal weights; significant increase in the number of fetuses with 

external, visceral and/or skeletal malformation/variations (hydrocephaly, diaphragmatic hernia, 

and dilation of the renal pelvis); and significant increase in the number of litters (22 of 23) that 

contained fetuses (6 of 22) with skeletal anomalies. The most common were vertebral structural 

variations and incomplete ossification. For developmental toxicity, the NOAEL was 30 mg/kg 

and the LOAEL was 80 mg/kg/day based on increased resorptions, reduced fetal weight and 

skeletal malformations/variations. 
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In a study conducted by Schwetz et al. (Toxicol. Appl. Pharmacol 28: 151-161, 1974), doses of 

0, 5, 15, 30, and 50 mg/kg/day commercial grade (88.4% a.i.) or purified (>98% a.i.) PCP 

prepared in corn oil were administered to groups of pregnant Sprague-Dawley rats on gestation 

days 6-15 inclusive. For purified PCP, the number of rats per group was as follows: control, 33 

rats; 5 mg/kg, 15 rats; 15 mg/kg, 18 rats; 30 mg/kg/, 20 rats; 50 mg/kg, 19 rats. For the 

commercial grade of PCP: 5 mg/kg, 18 rats; 15 mg/kg, 17 rats; 30 mg/kg, 19 rats; 50 mg/kg, 15 

rats. Additional groups of rats were administered 0 or 30 mg/kg/day PCP (type of a.i. not 

specified) on days 8-11 or 12-15 of gestation. Maternal toxicity from purified PCP was 

evidenced by decreased maternal weight gain at the 30 and 50 mg/kg dose groups for days 6-21 

of gestation (74% decrease vs. control). For the commercial grade, weight gain was decreased 

43% at the 50 mg/kg dose, and by 22% at the 30 mg/kg dose. Weight gain appeared more 

significantly affected by purified PCP. No other significant signs of maternal toxicity were 

observed. Fetal incidence of resorption was significantly increased at 30 and 50 mg/kg purified 

and commercial grade PCP. The report stated that the fetal and litter incidence was also 

significantly increased at 15 mg/kg commercial grade PCP, but the fetal incidence (7 and 8% at 

control and 15 mg/kg/day) as well as the litter incidence (55 and 64% at control and 15 

mg/kg/day) did not appear biologically meaningful. Fetal body weight was reported significantly 

decreased for commercial grade PCP at 30 and 50 mg/kg/day and at 30 mg/kg/day for purified 

PCP, but actual values were not reported. Crown-rump length was significantly decreased at 30 

mg/kg/day purified PCP. The litter incidence of subcutaneous edema, lumber spurs, and 

supernumerary, lumber or fused ribs was significantly increased at 30 and 50 mg/kg commercial 

grade PCP, but the data did not indicate a dose-response, i.e. the number of litters affected with 

subcutaneous edema, rib and vertebral abnormalities were greater at 30 mg/kg than at 50 mg/kg 

for the commercial grade of PCP and for the purified PCP. The number of litters at the high dose 

of purified PCP was also severely limited (only 2 litters at this dose). Resorptions were 

significantly increased when PCP (both grades) was administered on gestation days 8-11, but not 

on gestation days 12-15. Based on the results of this study, the Maternal NOAEL can be 

considered as 15 mg/kg/day, based on body weight effects, for both grades of PCP. The 

Developmental NOAEL would appear to differ according to grade of PCP used. Limited data for 

purified PCP at the 50 mg/kg/dose hampers evaluation of a NOAEL and LOAEL for this grade. 

For the commercial grade of PCP, the NOAEL can be considered as 15 mg/kg/day, and the 

LOAEL as 30 mg/kg/day, based on decreased fetal body weight and crown-rump length. The 

responses observed at the low dose of commercial grade PCP for fetal anomalies (i.e. lumber 

spurs, anomalous ribs, subcutaneous edema) do not show a dose-response pattern at the higher 

doses of PCP, and are also limited by reduced number of litters at the high dose. 

In a study conducted by Welsh et al. (Fd. Chem. Toxic. 25(2): 163-172, 1987), groups of male 

and female Sprague-Dawley rats (20/group) were placed on diets containing purified PCP at 

dose levels of 0, 60, 200, or 600 ppm (0, 4, 13, and 43 mg/kg/day reported for females; no actual 

intake data for males). These test diets were administered for 181 days. At the end of the 

subchronic phase, male and female rats were mated for teratological evaluation following 

subchronic exposure to PCP. Body weight gain in maternal rats exposed to PCP was 

significantly decreased at the high dose (76% from control). Pregnancy rates were low in all dose 

groups (77.5, 55, 84.2, and 85 for the 0, 60, 200, and 600ppm dose groups, respectively) but, 
Page 37 of 63

according to the report, there was no effect on fertility. Decreased number of viable fetuses (due 

to early death) was observed at the 600 ppm dose level of PCP, as well as an increase in total 

litter resorptions. Body weight of fetuses appeared decreased at the 200 ppm dose level; analysis 

at the 600 ppm dose level was not complete, due to an alteration in the sex ratio at this dose 

(100% male sex ratio at this dose as reported). There were no reported alterations in external or 

sternebral observations at any dose level tested in this study. Increased incidence of misshapen 

centra was reported at 200 ppm PCP, but the high dose could not be analyzed due to inadequate 

numbers of fetuses. The incidence of total skeletal variations was reported increased at the 200 

ppm dose level for PCP. The results of this study demonstrate toxicity of PCP at 200 ppm (13 

mg/kg/day) in the form of increased percentage of female rats with 2 or more resorptions. 

However, this study is hampered by a lack of fetal data at the high dose, and inconsistent and low 

percentages of pregnancy at each dose level of PCP tested. The data appear to point to a 

definitive toxic effect of PCP at the 43 mg/kg/day dose level on both maternal and fetal rats, with 

decreased weight gain in maternal rats, and decreased viable fetuses, increased early deaths, and 

increased resorptions at the high dose. 

In a developmental toxicity study (MRID # 43091701), inseminated New Zealand White rabbits 

(20 rabbits/dose) were administered PCP by gavage at doses of 0, 7.5, 15, and 30 mg/kg/day on 

gestation days 6-18 inclusive. Cesarean section examinations were performed on all surviving 

does on gestation day 29, followed by external, visceral, and skeletal examination of all fetuses. 

There were no maternal deaths or signs of maternal toxicity at any dose level. Significantly 

reduced weight gain was observed in the high dose group on gestation days 6-9 (loss of 40g vs. 

gain of 20 g in controls), and in the mid and high dose groups for gestation days 9-12 (gain of 20 

g at the mid and high dose vs. gain of 50 g in controls). These changes were considered minimal 

as the differences in weight gain were equivalent to only 0.5-1% of mean body weight. A 

consistent reduction in mean food consumption (71-90% of control value on gestation days 9-12) 

was observed at the high dose. Weight gain was comparable for treated and control rabbits 

following the treatment interval. A slight but non-significant dose-related decrease in litter size 

was observed, corresponding to a decrease in implantations/litter for the treated does. There were 

no statistical differences in the number of treated litters vs. control when the incidences for all 

observations of external, visceral, and skeletal effects were combined. Although the incidence of 

affected litters was not statistically significant, a significantly greater (p < 0.01) number of 

individual fetuses in the 15 mg/kg litters contained interfrontal ossification sites compared to 

controls. Based on the results of this study, the Maternal toxicity NOAEL = 15 mg/kg/day, and 

the Maternal toxicity LOAEL = 30 mg/kg/day, based on minimally reduced body weight gain 

and consistent reductions in food consumption during treatment. The Developmental toxicity 

NOAEL = 30 mg/kg/day; a Developmental toxicity LOAEL was not identified. This study is 

classified as acceptable and satisfies the guideline requirement (83-3b) for a developmental 

toxicity study in non-rodents. No additional data are anticipated to be required. 

Reproductive Toxicity 

In a 2-generation reproduction study (MRID 44464101), PCP (88.9% a.i.; lot no. EL-604) in 

corn oil was administered to 30 male and female Sprague-Dawley rats/sex/dose by gavage at 
Page 38 of 63

dose levels of 0, 10, 30, and 60 mg/kg/day. P1 male and female rats were given the test material 

once daily at least 70 days prior to cohabitation and continuing through the day before sacrifice. 

F1 generation rats may have been exposed in utero during gestation and via maternal milk during 

the postpartum period. The day after weaning, F1 generation rats were administered the test 

material by gavage at the same dose levels as P1 rats and were continued until one day prior to 

sacrifice. F2 pups were exposed possibly indirectly during maternal gestation or via maternal 

milk. In addition to standard parameters, estrous cycling and sperm morphology and function 

were measured. At 60 mg/kg/day PCP, body weight and body weight gain of P1 and F1 parental 

rats was significantly decreased from control over the period of treatment pre-mating. 

Gestational and lactational body weights of P1 and F1 female rats were also significantly 

decreased. Fertility index and number of litters were decreased in both generations at 60 

mg/kg/day PCP. Days to vaginal patency were significantly increased in P1 female pups, as was 

days to preputial separation in P1 male pups. Estrous cycling was not significantly affected in 

either P1 or F1 females, but in F1 males, the number of sperm observed with a broken flagellum 

was significantly increased at 60 mg/kg/day, and the average testicular spermatid count was 

significantly decreased at 60 mg/kg/day. Testis weight in F1 generation males was also 

decreased. Decreased brain weight (4-8%) and increased liver weight (20-33%) were observed in 

both P1 and F1 male and female rats at 60 mg/kg/day. Macroscopic pathology (enlarged liver) 

and microscopic pathology (centrilobular hypertrophy, subacute inflammation, single cell 

necrosis, pigment deposition) were observed in increased incidence at 60 mg/kg/day. The single 

cell necrosis and pigment deposition were considered related to treatment. Mean litter size, 

number of live pups, and viability index were significantly reduced in the P1 and F1 pups. 

Decreased weight of the liver, brain, spleen, and thymus were observed in F2 pups at 60 

mg/kg/day. At 30 mg/kg/day, body weight and weight gain decreases of approximately 11% 

were observed in F1 female parental rats. Significant decreases in average testicular spermatid 

count and testis weight were observed in F1 male parental rats. Based on the data in this study, 

the Systemic NOAEL = 10 mg/kg/day for male and female parental rats. The Systemic LOAEL 

= 30 mg/kg/day for male and female rats, based on decreased body weight and weight gain in F1 

generation parental rats, and adverse testicular effects in F1 male rats (decreased testis weight, 

decreased spermatid count). The reproductive NOAEL = 10 mg/kg/day in this study. The 

reproductive LOAEL = 30 mg/kg/day, based on decreased group mean litter weight. This 

reproductive study in the rat is classified acceptable and satisfies the guideline requirement for a 

2-generation reproductive study (OPPTS 870.3800) in rats. No additional data are anticipated to 

be required. 

Chronic Toxicity 

In a chronic toxicity study, (MRID 43982701) PCP (90.9% a.i.) was fed (gelatin capsules) to 

four beagle dogs/sex/dose at dose levels of 0, 1.5, 3.5, or 6.5 mg/kg/day for 52 weeks. At 6.5 

mg/kg/day, one male and one female dog were sacrificed in extremis on days 247 and 305, 

respectively, due to significant clinical toxicity (significant weight loss, lethargy, marked 

dehydration, vomiting, icterus). The LOAEL was 1.5 mg/kg-day (lowest dose tested), based on 

liver pathology consisting of dose-related increases in incidence and severity of hepatocellular 
Page 39 of 63

pigmentation, cytoplasmic vacuolation, and chronic inflammation, and significant increases in 

relative liver weight and increases in absolute liver weight (significant in females), and increased 

serum enzyme activity. The NOAEL could not be established. This study is considered 

acceptable and satisfies the guideline requirement ('83-1; OPPTS 870.4100) for a chronic 

toxicity study in non-rodents. No additional data are anticipated to be required. 

Carcinogenicity 

The Agency’s IRIS program (2010, http://www.epa.gov/IRIS/subst/0086.htm) classified PCP as 

“likely to be carcinogenic to humans.” This cancer weight of evidence determination is based 

on: (1) evidence of carcinogenicity from oral studies in male mice exhibiting hepatocellular 

adenomas and carcinomas, and pheochromocytomas and malignant pheochromocytomas, and in 

female mice exhibiting hepatocellular adenomas and carcinomas, pheochromocytomas and 

malignant pheochromocytomas, and hemangiomas and hemangiosarcomas (NTP, 1989); (2) 

some evidence of carcinogenicity from oral studies in male rats exhibiting malignant 

mesotheliomas and nasal squamous cell carcinomas (Chhabra et al., 1999; NTP, 1999); (3) 

strong evidence from human epidemiologic studies showing increased risks of non-Hodgkin’s 

lymphoma and multiple myeloma, some evidence of soft tissue sarcoma, and limited evidence of 

liver cancer associated with PCP exposure (Demers et al., 2006; Hardell et al., 1995, 1994; 

Kogevinas et al., 1995); and (4) positive evidence of hepatocellular tumor-promoting activity 

(Umemura et al., 2003a, b, 1999) and lymphoma and skin-adenoma promoting activity in mice 

(Chang et al., 2003). For more detail on Characterization of Hazard and Dose Response, see the 

toxicological review, Section 6 (PDF). No additional data are anticipated to be required. 

Mutagenicity 

The available evidence for gene mutations in bacterial systems suggests that PCP is largely 

devoid of positive effects with the exception of one published report, in which a positive 

response was noted. PCP is also observed to be weakly clastogenic, with chromosomal 

aberrations observed using Chinese hamster ovary cells in the presence of rat liver S9. In contrast 

to the data for PCP, data for the metabolite tetrahyhdroquinone (THQ) show positive effects on 

Chinese hamster V79 cells (increase in frequency of thioguanine-resistant mutants; Jansson and 

Jansson, Mutation Res. 260: 83-87), increase in micronuclei using V79 cells (Jansson and 

Jansson, Mutation Res. 279: 205-208), covalent binding to DNA (Witte et al., Mutation Res. 

145: 71-75), and induction of DNA single-strand breaks (Witte et al., Mutation Res. 145: 71-75; 

Ehrlich, W.: Mutation Res. 244: 299-302). THQ has been thought to be involved in some or all 

of the mutagenic and carcinogenic effects of PCP. No additional data are anticipated to be 

required. 

Neurotoxicity 

Although a vailable data on PCP indicate the potential for nervous system effects in vitro 

(decrease in neuromuscular and ganglionic conduction, inhibition of human red cell 
Page 40 of 63

cholinesterase) and in vivo animal data Clinical signs associated with PCP exposure are 

suggestive of neurotoxicity, based on the available data, there is no evidence of frank, 

unequivocal neurotoxicity in the database, including changes in brain weight or incidence of 

neuropathology in the central nervous system tissues (nonperfused). Therefore, nervous system 

has not been generally considered as a target tissue from PCP exposure. No additional data are 

anticipated to be required. 

Immunotoxicity 

The immunotoxic effects of PCP have been studied by the U.S. Department of Health and 

Human Services’ National Toxicology Program (NTP) and others. The data appear to indicate 

that the immunotoxic effects of PCP are largely mediated by the chlorinated dioxin 

contaminants. Although data from human studies are limited, it is likely that the immune effects 

observed are also due in part to the contaminants present within PCP. No additional data are 

anticipated to be required. 

Dermal Absorption 

For PCP, a dermal absorption factor of 40% is used for correction of oral to dermal 

dosing. This value is based on a dermal absorption study (MRID # 00259257) in which 

radiolabelled PCP (5% solution in P-9 oil) was applied to the skin of young adult 

Sprague-Dawley rats for 0.25, 1, 4, 8, and 24 hours. At 8 hours post-application, the calculated 

absorption was 40%. At 24 hours post-application, the calculated absorption was 60%. This risk 

assessment is required for PCP, all of the human exposures are measured with biological 

monitoring data, and therefore no additional dermal absorption data are anticipated to be 

required. 

Metabolism 

PCP has been shown to be readily absorbed by oral, inhalation, and dermal routes of exposure 

(Reigner et al., Pharmaceut. Res. 9: 1053-1057, 1992; Yuan, JH et al., Xenobiotica 24(6): 553-

560, 1994; Hoben, Bull. Environ.Contam. Toxicol 15: 466-474, 1976). Peak plasma levels have 

been shown to occur in the range of 1.3-6 hours in experimental animals in an oral dose range of 

0.1-15 mg/kg, while in humans, maximum plasma concentration of PCP occurred at 4 hours 

following a single 0.1 mg/kg oral dose. Absorption from dermal exposure has been shown to 

range from 24% in rhesus monkeys (Wester et al., Fundam. Appl. Toxicol. 20: 68-71, 1993) to 

40% in rats (EPA MRID # 00259257). 

Biotransformation of PCP has also been examined in several studies published in the scientific 

literature. Reigner et al. (Xenobiotica 21(12): 1547-1558, 1991) observed a 60% recovery in 

urine from i.v. or oral administration of 2.5 mg/kg PCP, mainly as conjugated PCP and 

conjugated tetrahydroquinone. In two earlier studies by Ahlborg (Arch. Toxicol 40: 45-53, 1978) 
Page 41 of 63

and Braun (Toxicol. Appl. Pharmacol. 41: 395-406, 1977), glucuronides of PCP were the major 

urinary metabolites observed after oral doses of 10 mg/kg and 100 mg/kg respectively. 

Pretreatment with phenobarbital in the study by Ahlborg et al. enhanced the formation of 

tetrahydroquinone. In other work by Rener and Hopfer (Renner, G. And Hopfer, C.: Xenobiotica 

20: 573-582, 1990), 24 female Sprague-Dawley rats were treated with PCP at 53 mg/kg/day for 

28 days. The results of this study indicated that PCP leads to tetrahydroquinone via 2,3,5,6-

tetrachlrophenol as a main degradative pathway, and to trichlorohydroquinone via 2,3,4,6-

tetrachlorophenol and 2,3,4,5-tetrachlorophenol via a minor pathway. PCP, tetrachlrophenol, and 

trichlorophenol can become conjugated with glucuronic acid or sulfate. While previous work in 

humans has shown the absence of formation of the tetrahydroquinone metabolite, newer 

published literature indicates formation of this metabolite both in vitro (Mehmood et al., 

Chemosphere 33(4): 759-769, 1996) as well as in vivo. The kinetics of elimination of PCP have 

been published, with half-lives of elimination ranging from 5-6 hours in mice ( Reigner et al., 

Pharmaceut. Res. 9: 1053-1057, 1992), 2-11 hours in rats (Reigner et al., Xenobiotica 21(12): 

1547-1558, 1991; Braun et al., Toxicol. Appl. Pharmacol. 41: 395-406, 1977) and 72-84 hours in 

monkeys (Braun and Sauerhoff, Toxicol. Appl. Pharmacol. 38: 525-533, 1976). In humans, mean 

plasma half-life was calculated to be 30.2 ± 4.0 hours following a 0.1 mg/kg oral dose to four 

male volunteers (Braun et al., in Toxicology and Occupational Medicine [W.B. Diechmann, ed.], 

pp. 289-296). Limited data on the volume of distribution of PCP indicate that in contrast to rats, 

where the volume of distribution ranges from 116-268 ml/kg, humans show a higher volume of 

distribution (348 ml/kg). One study was available with human data on volume of distribution. No 

additional data are anticipated to be required. 

 
Page 42 of 63

Appendix B Environmental Fate 

Environmental Fate and Transport Properties of PCP 

The Agency does not anticipate the need to require environmental fate studies for registration 

review. 

Water and Sediment 

Hydrolysis (MRID 42481101) 

PCP was hydrolytically stable in sterile aqueous pH 5, 7 and 9 buffer solutions incubated at 25°C 

for up to 30 days. 

Photodegradation in Water (MRID 42855401) 

PCP photodegraded rapidly with half-lives of 13-20 minutes in sterile aqueous pH 5, 7 and 9 

buffer solutions irradiated with natural sunlight at 42°N (in MA) on different days and at 

different times of the day in August/September, and was stable in dark controls under similar 

conditions; air temperatures during the studies ranged from approximately 8 to 36°C. 

Dichloromaleic anhydride (more likely present as dichloromaleic acid) was reported to be the 

major degradate at all pHs, and reached respective maximums of 64.5-67.5% (80 minutes posttreatment), 100% (110 minutes), and 98.9% (90 minutes) of the applied radioactivity at pH 5, pH 

7 and pH 9. Tetrachlororesorcinol was a major degradate at pH 5 (maximum of 34.8-36.1%) and 

pH 7 (maximum of 15.7%) and was a minor degradate at pH 9. Tetrachlorohydroquinone and 

tetrachlorocatechol were minor degradates at pH 5 and pH 7, but were not detected at pH 9. 

Aerobic Aquatic Metabolism (MRID 42288601) 

PCP degraded in a flooded sandy loam soil with an observed half- life of approximately 14 days 

(calculated first-order half-life of 4.9 days) in flooded sandy loam soil incubated aerobically 

(under continuous airflow) at 25°C for up to 30 days. Initial PCP degradation was less rapid 

(52% of the applied radioactivity remained as parent at 14 days) than that observed after an 

apparent acclimation period; only 7% of the applied was present as parent compound at 21 days. 

The major degradate 3,4-dichlorophenol was 0.30% of the applied prior to 30 days and was 

36.6% at day 30. Various isomers of tetrachlorophenol (maximum of 10%) and trichlorophenol 

(maximum of 82.2%) were also formed as major degradates; individual isomers were not 

identified. Volatiles were negligible (0.9%), and nonextractable [14C] residues were 41% of the 

applied at 30 days. The soil:water distribution ratio for PCP was approximately 1:32 initially, 

then changed to approximately 1:1 by 14 days, and was 2.5:1 at 30 days. 
Page 43 of 63

Anaerobic Aquatic Metabolism (MRID 42436801) 

PCP degraded with an observed half-life of 1-2 months (calculated first-order half-life of 34 

days) in flooded sandy loam soil incubated anaerobically (nitrogen atmosphere) at 25C for up to 

one year. Initial PCP degradation was relatively slow (84% and 72% of the applied remained as 

parent at 14 days and 1 month, respectively), then accelerated after an apparent acclimation 

period; only 5% of the applied was present as parent compound at 2 months. Various isomers of 

tetrachlorophenol (maximum of 9.7%) and trichlorophenol (maximum of 82.7%) were formed as 

major degradates; individual isomers were not identified. Volatiles were negligible (1.4%), and 

nonextractable [14C] residues were 7.8% of the applied at 12 months. The soil:water 

distribution ratio for PCP was approximately 1:13 initially, then changed to 1:1 by 7 days, and 

was 4:1 at 1-12 months. 

Soil 

Soil Leaching/Adsorption/Desorption Batch Equilibrium (MRID 42633709 and 43627000) 

Based on batch equilibrium studies, PCP, at approximately 1-14 ppm, was determined to be 

moderately mobile in one sandy loam soil and slightly mobile in two sandy loam soils, and was 

immobile in a clay loam soil. In silt loam soils designated as “high” organic matter soils, PCP 

was moderately mobile in the lower pH soil and mobile in the higher pH soil. In silt loam soils 

designated as “low” organic matter soils, PCP was slightly mobile in the lower pH soil and 

mobile in the higher pH soil. The soil properties and the Freundlich adsorption coefficients 

(Kads) and associated exponents are listed in the following table. Desorption coefficients were 

not reported for the sandy loam or clay loam soils. Data were not provided for a coarse-textured 

soil such as loamy sand or sand. 

Table B1: Soil-water Partition Coefficient (Kds) in Various Soils 

 

 

Soil Series or Origin Texture % OM pH Kads 1/N (ads)

Georgia Sandy loam 0.4 5.9 5.72 0.81 

Nebraska1 Sandy loam 1.2 6.9 9.96 0.86 

California Sandy loam 2.6 7.9 10.8 0.87 

Ohio 

Clay loam 3.7 5.3 74.6 0.88 

Silt loam High 5.8 8.3 - 

Silt loam High 7.5 2.0 - 

Silt loam Low 4.2 18 - 

Silt loam Low 6.6 1.3 - 

1

Indicates the same “blue sandy loam” soil utilized in all other guideline laboratory studies. 
Page 44 of 63

Kd values were also obtained in a second acceptable study on the major PCP degradates 2,3,4-

trichlorophenol and 2,3,4,5-tetrachlorophenol in a sandy loam soil (pH 6.3, 1.6% organic). 

Based on batch equilibrium studies, the PCP degradates 2,3,4-trichlorophenol and 2,3,4,5-

tetrachlorophenol were both determined to be slightly mobile in one sandy loam soil. No data 

were submitted for the PCP degradates dichloromaleic acid, tetrachlororesorcinol, or other 

isomers of tri- and tetrachlorophenol. 

Table B2: Kds for the PCP Degradates 

Kds 2,3,4-trichlorophenol 2,3,4,5-tetrachlorophenol 

Kads 10.2 14.6 

Koc 1080 1550 

1/N 0.78 0.78 

Aerobic Soil Metabolism (MRID 42594302) 

PCP degraded with an observed half-life of 7-14 days (calculated first-order half-life of 63 days) 

in sandy loam soil maintained at 75% of 0.33 bar moisture and incubated at 25C for up to one 

year. An acclimation period for the microbial degradation was not observed. The degradation 

rate was observed to decrease with time; at 7 days, 54.7% of the applied radioactivity remained 

present as parent, while 23.5% was present as parent at 61 days (the interval closest to the 

calculated first-order half-life). No major degradates were observed. The minor degradates were 

various isomers of tetrachlorophenol (maximum of 2.3-2.4% of the applied) and trichlorophenol 

(maximum of 4.4%); individual isomers were not identified. By 12 months post-treatment, 

25.7% of the applied radioactivity had volatilized as CO2 and 1.3% had volatilized as a 

trichlorophenol. Nonextractable [14C] residues increased throughout the study and were a 

maximum of 64.0% of the applied at 12 months, with the majority (76%) associated with the 

humic fraction of the soil organic matter. 

Bioaccumulation in Fish (165-4) 42633710, 42855402 

PCP residues bioaccumulated in bluegill sunfish exposed to PCP, at a nominal concentration of 

2.5 ug/L in a flow-through system (pH 6.7-7.2) for 28 days, with bioconcentration factors (BCF) 

of 190x for the edible tissue, 790x for the nonedible tissue and 490x for the whole fish. 

Maximum mean concentrations of [14C] residues were 640 ppb, 2800 ppb and 1500 ppb in 

edible, nonedible and whole fish tissues, respectively. Total [14C] residues at exposure day 28 

were 170 ppb in edible tissues, 930 ppb in nonedible tissues and 500 ppb in whole fish tissues. 

At day 28, all of the residues in the edible tissues were identified as PCP; in the nonedible 

tissues, 87-94% of the accumulated [14C] residues were identified as PCP and 6-13% as 

glucoronide conjugates of PCP. Depuration was rapid, with over 97% of the accumulated 

residues eliminated from all tissues by day 14. The exposure to the parent may not have been 
Page 45 of 63

constant. [14C]Residues in the water were not adequately characterized; approximately 24% of 

the [14C] residues in the water at days 26 and 28 (the only water samples characterized) were not 

present as the parent compound. 

Aqueous Availability from Treated Wood (MRID 43205001) 

Maximum and average leaching rates for southern pine wood (11-inch length and 1-inch in 

diameter) treated with PCP at 0.50 lbs/ft3

 are reported in the following table. Reported data 

indicated that the average leaching rate and the maximum leaching rate of PCP increased with 

increased pH. 

Table B3: Leaching Rates at Various Conditions 

Final Concentration 

mg/L 

Max. Leaching Rate x 10-2

mg/kg leachate/in2

/day 

Average Leaching Rate x 10-3

mg/kg leachate/in2

/day 

pH 5 5.73 1.04 0.51 

pH 7 36.2 2.28 3.27 

pH 9 65.5 3.32 6.33 

0.1N HCl 1.73 0.6 0.17 

Seawater 22.7 3.11 2.21 

Purified water 6.57 0.66 0.61 

Degradates of PCP in Environmental media 

Environmental fate studies on PCP have shown that a number of degradates are formed in 

aquatic and soil metabolism studies as shown below. 

Table B4: Degradates of PCP in Environmental media 

Study Type Degradates Characterized 

Hydrolysis No degradate formed in pHs 5, 7, and 9 under abiotic conditions 

Aqueous Photolysis Dichloromaleic anhydride (formed at pHs 5, 7, and 9 

Tetrachlororescorcinol, major at pH5 

Minor at pHs 7, and 9 

Tetrachlorohydroquinone and tetra chlorocatchechol: minor at pH 5, and 7. None at pH 9 

Aerobic Aquatic metabolism 3,4-dichlorophenol: < 30% up to 30 days; 36.6% at day 30 Major degradate 

Isomers of tetrachloro and trichloro formed also as major degradates. 
Page 46 of 63

Anaerobic aquatic metabolism Tetrachlorophenol (9.7%) and trichlorophenol (82.7%). Isomers were not identified 

Aerobic soil metabolism Tetrachorophenol (2.3-2.4%); trichlorophenol (4.4%) as minor degradates. No isomers 

were identified 

Adsorption/ Desorption/ batch 

equilibrium study 

2,3,4 trichlorophenol, and 2,3,4,5-tetrachlorophenol were identified in sandy loam soil 

(pH 6.3, 1.6 organic matter). These degradates were slightly mobile in the sandy loam 

soil 

 
Page 47 of 63

Environmental Fate References for Appendix B 

42481101 Blumhorst, M. (1993) Aqueous Hydrolysis of Pentachlorophenol 

 Project ID 156001 EPL Bio Analytical Services, Inc. 

42855401 Connor, S. (1993) Pentachlorophenol-Determination of Aqueous 

 Photolysis Rate Constant and Half-Life: Final Report: Lab 

 Project Number: 12836.0692.6112.720: 93-1-4568. Unpublished 

 study prepared by Springborn Labs, Inc. 68 p. 

41969201 Schmidt, J. (1991) Determination of the Photolysis Rate of [carbon 

 14]-Pentachloro-phenol on the Surface of Soil: Final Report: Lab 

 Project Number: 38440. Unpublished study prepared by ABC Labor- 

 atories, Inc. 32 p. 

41969201 Schmidt, J. (1991) Determination of the Photolysis Rate of [carbon 

 14]-Pentachloro-phenol on the Surface of Soil: Final Report: Lab 

 Project Number: 38440. Unpublished study prepared by ABC Laboratories, Inc. 32 p. 0 42594302 Schmidt, J. (1992) Aerobic Soil Metabolism of 

(carbon 14)-Pentachlorophenol: Lab Project Number: 38353. 

Unpublished study prepared by ABC Labs, Inc. 41 p. 

42288601 Schmidt, J. (1992) Aerobic Aquatic Metabolism of [carbon 14] 

 Pentachlorophenol: Lab Project Number: 38354. Unpublished 

 study prepared by ABC Labs, Inc. 38 p. 

42436801 Schmidt, J. (1992) Anaerobic Aquatic Metabolism of 

 14C-Pentachlorophenol: Lab Project Number: 38355. Unpublished 

 study prepared by ABC Laboratories, Inc. 37 p. 

42633709 Weeden, D. (1993) Pentachlorophenol: Determination of the 

 Sorption and Desorption Properties: Lab Project Number: 

 92-12-4536: 12836.0692.6113.710. Unpublished study prepared by 

 Springborn Laboratories, Inc. 69 p. 

43627001 Christensen, K. (1995) Metabolites of Pentachlorophenol- 

 Determination of Adsorption/Desorption Coeffecients: Final 

 Report: Lab Project Number: 95-3-5756: 12836.0195.6117.710. 

 Unpublished study prepared by Springborn Labs, Inc. 68 p. 

42633710 Dionne, E. (1993) Pentachlorophenol: Bioconcentration and 

 Elimination of (carbon 14)-residues by Bluegill Sunfish: Lab 
Page 48 of 63

 Project Number: 92-12-4532: 12836.0692.6114.140. Unpublished 

 study prepared by Springborn Laboratories, Inc. 90 p. 

42855402 Dionne, E. (1993) Pentachlorophenol-Bioconcentration and 

 Elimination of (carbon 14)--Residues by Bluegill Sunfish 

 (Lepomis macrochirus): Amended Final Report: Lab Project 

 Number: 12836.0692.6114.140: 92-12-4532. Unpublished study 

 prepared by Springborn Labs, Inc. 83 p. 

43205001 Connor, S. (1994) Pentachlorophenol-Leaching from Utility 

 Poles Exposed to the Aquatic Environment: Final Report: Lab 

 Project Number: 12836.1293.6116.795: 94-3-5201. Unpublished 

 study prepared by Springborn Labs., Inc. 66 p. 

43214601 Schocken, M. (1994) Pentachlorophenol: Determination of 

 Photodegradation in Air: Amended Final Report: Lab Project 

 Number: 12836/0692/6115/722: 94/4/5226. Unpublished study 

 prepared by Springborn Lab., Inc. 90 p. 

40924102 Banerji, S.; Piontek, K.; O'connor, J. (1986) (Pentachlorophenol)- 

 pentachlorophenol adsorption on soils and its potential for 

 migration into groundwater. 

41995201 Schmidt, J. (1991) Anaerobic Soil Metabolism of [Carbon 14]-Penta- 

 chlorophenol: Lab Project Number: 38437. Unpublished study 

 prepared by ABC Laboratories, Inc. 46 p. 

Unacceptable studies submitted to OPP to satisfy guideline requirements: 

43214601 Schocken, M. (1994) Pentachlorophenol: Determination of 

 Photodegradation in Air: Amended Final Report: Lab Project 

 Number: 12836/0692/6115/722: 94/4/5226. Unpublished study 

 prepared by Springborn Lab., Inc. 90 p.
Page 49 of 63

Appendix C Ecotoxicology Profile 

Ecotoxicity data for PCP are available from several sources. In addition to the guideline studies 

submitted by registrants, data also are available in the EPA Office of Water’s Ambient Water 

Quality Criteria for Pentachlorophenol – 1986 (EPA 1986), and the EPA/OPP Pesticide 

Ecotoxicity Database. The ecotoxicity database is compiled from actual studies reviewed by 

EPA in conjunction with pesticide registration or reregistration and studies performed by 

USEPA, USDA and USFWS laboratories which have been reviewed by agency biologists and 

judged acceptable for use in the ecological risk assessment process. Some ecotoxicity data also 

are available for the PCP contaminants (dioxins/furans and HCB). The data for these 

contaminants is from the OPP/AD risk assessments conducted in conjunction with the 2008 PCP 

RED as compiled by Petrie (EPA 2008a,b). 

PCP Ecotoxicity Profile 

 Terrestrial Organisms 

Birds, acute oral 

Three available acute-oral (LD50) studies categorize PCP as being slightly to moderately toxic to 

birds. The guideline (850.2100) is satisfied. No additional acute oral toxicity data are 

anticipated to be needed. 

Table C1: Avian Acute-oral Toxicity

Test Species Test Material 

(% ai)

LD50 

(mg ai/kg bw) 

Toxicity 

Category

EPA Study 

ID

Northern bobwhite 

(Colinus virginianus) 88.9 627 Slightly toxic 42633701 

Acceptable 

Mallard 

(Anas platyrhynchos) 99.6 380 Moderately toxic 160000 

Supplemental 

Ring-necked pheasant 

(Phasianus colchicus) 99.6 504 Moderately toxic 160000 

Supplemental 

Birds, dietary 

Six available studies categorize PCP as being slightly to practically nontoxic to birds when 

provided in their diet. The guideline (850.2200) is satisfied. No additional dietary toxicity data 

are anticipated to be needed. 
Page 50 of 63

Table C2: Avian Dietary Toxicity

Test Species Test Material 

(% ai)

LC50 

(ppm) 

Toxicity 

Category

EPA Study 

ID

Northern bobwhite 

(Colinus virginianus) 

88.9 5581 Practically nontoxic 42633702 

Acceptable 

40 3400 Slightly toxic 22923 

Supplemental 

Mallard 

(Anas platyrhynchos)

88.9 3763 Slightly toxic 42633703 

Acceptable 

40 4500 Slightly toxic 22923 

Supplemental 

Ring-necked pheasant 

(Phasianus colchicus) 40 5204 Practically nontoxic 22923 

Supplemental 

Japanese quail 

(Coturnix japonica) 40 22923 Practically nontoxic 22923 

Supplemental 

Nontarget Insects 

Additional toxicity data are not anticipated to be needed for beneficial insects. One acceptable 

study is available. The guideline for an acute toxicity test (850.3020) is satisfied. For PCP, the 

Agency does not anticipates needing a honeybee study for toxicity of residues on wood 

(850.3030) to support wood preservative uses. 

Table C3: Honeybee Toxicity

Test Species Test Material 

(% ai)

LD50 

(μg ai/bee) 

Toxicity 

Category

EPA Study 

ID

Honeybee 

(Apis mellifera) Tech. > 48.3 Not determined - 

slightly toxic at most 

36935 

Acceptable 

 Aquatic Organisms 

Freshwater Fish, acute 

The 21 acute toxicity studies tabulated below categorize PCP as being highly to very highly toxic 

to a variety of freshwater fish. The guideline (850.1075) for acute toxicity testing is satisfied. 

No additional acute toxicity data are anticipated to be needed. 
Page 51 of 63

Table C4: Freshwater Fish Acute Toxicity

Test Species Test Material 

(% ai) 

LC50 

(μg ai/L) 

Toxicity 

Category 

EPA Study 

ID 

Rainbow Trout 

(Oncorhynchus mykiss)

100 15 Very highly toxic 43485104 

Acceptable 

100 75 Very highly toxic Bionomics 19771

Acceptable 

96 34 Very highly toxic 40098001 

Acceptable 

37 76 Very highly toxic TN0918 

Supplemental 

88 86 Very highly toxic 63572 

Acceptable 

15.7 370 Very highly toxic 00090429 

Acceptable 

96 115 Highly toxic 40098001 

Acceptable 

Bluegill 

(Lepomis macrochirus) 

96 32 Very highly toxic 40098001 

Acceptable 

100 60 Very highly toxic Bionomics NR1 

Acceptable 

37 150 Highly toxic TN0943 

Supplemental 

96 215 Highly toxic 40098001 

Acceptable 

15.7 345 Highly toxic 00033067 

Acceptable 

Fathead minnow 

(Pimephales promelas) 

96 205 Highly toxic 40098001 

Acceptable 

100 600 Highly toxic 00033067 

Acceptable 

Chinook salmon 

(Oncorhynchus tshawytscha) 96 31 Very highly toxic 40098001 

Acceptable 

Channel catfish 

(Ictalurus punctatus) 88 <53 Very highly toxic EPA 1986

Supplemental 

96 66 Very highly toxic 40098001 

Acceptable 

White sucker 

(Catostomus commersoni) Tech 85 Very highly toxic USFWS2 

Supplemental 

Largemouth Bass 

(Micropterus salmoides) Tech 136 Highly toxic USFWS2 

Supplemental 

Brook trout 

(Salvelinus fontinalis) 99 138 Highly toxic EPA 1986 

Supplemental 

Atlantic salmon 

(Salmo salar) Tech 500 Highly toxic USFWS2 

Supplemental 
Page 52 of 63

1

 OPP reviewed data cited in the OPP Pesticide Ecotoxicity Database 

2

 US Fish and Wildlife Service reviewed data cited in the OPP Pesticide Ecotoxicity Database 

Freshwater Fish, chronic 

Two early life-stage studies are available. The guideline (850.1400) for a fish early life-stage 

toxicity test is satisfied. No additional acute toxicity data are anticipated to be needed. 

Table C5: Freshwater Fish Early Life-Stage Toxicity

Test Species Test Material 

(% ai) 

NOAEC and LOAEC 

(μg ai/L) 

Endpoints 

Affected 

EPA Study 

ID 

Rainbow Trout 

(Oncorhynchus mykiss) 99 NOAEC = 11 

LOAEC = 19 

Survival and 

Growth (length, 

weight) 

EPA 1986 

Acceptable 

Fathead minnow 

(Pimephales promelas) 88 NOAEC = 16 

LOAEC = 34 Survival 40924115 Supplemental 

Freshwater Invertebrates, acute 

The 12 acute toxicity studies tabulated below categorize PCP as being moderately to very highly 

toxic to freshwater invertebrates. The guideline (850.1010) for acute toxicity testing is satisfied. 

No additional acute toxicity data are anticipated to be needed. 

Table C6: Freshwater Invertebrate Acute Toxicity

Test Species Test Material 

(% ai) 

EC50 

(μg ai/L) 

Toxicity 

Category 

EPA Study 

ID 

Waterflea 

(Daphnia magna) 

93.7 134 Highly toxic EPA 1986 

Supplemental 

99 145 Highly toxic EPA 1986 

Supplemental 

96 240 Highly toxic 40098001 

Supplemental 

86 410 Highly toxic 40098001 

Supplemental 

88 450 Highly toxic 00063572 

Acceptable 

88 480 Highly toxic 00085230 

Acceptable 

37 1350 Moderately toxic TN0952 

Acceptable 

Cladoceran 

(Simocephalus 

vetulus) 

93.7 160 Moderately toxic EPA 1986 

Supplemental 
Page 53 of 63

Amphipod 

(Hyalella azteca) 99 239 Highly toxic EPA 1986 

Supplemental 

Amphipod 

(Gammarus 

pseudolimnaeus) 

88 92 Very highly toxic EPA 1986 

Supplemental 

Bladder snail 

(Aplexa hypnorum) 88 142 Highly toxic EPA 1986 

Supplemental 

Snail 

(Gillia altilis) 99 300 Highly toxic EPA 1986 

Supplemental 

Freshwater Invertebrates, chronic 

Four supplemental life cycle tests are available. However, an NOAEC for the most sensitive 

species (Ceriodaphnia reticulata) was not determined. Although an NOAEC was reported for 

Daphnia magna, the invertebrate species most commonly tested, the test material for that study 

is unknown. Therefore, an additional study using a daphnid species is anticipated to be needed 

for the TGAI. The guideline (850.1300) for a freshwater invertebrate life cycle is not satisfied. 

Table C7: Freshwater Invertebrate Life Cycle Toxicity

Test Species Test Material 

(% ai) 

NOAEC and LOAEC 

(μg ai/L) 

Endpoints 

Affected 

EPA Study 

ID 

Cladoceran 

(Ceriodaphnia 

reticulata) 

93.7 NOAEC <4.1 

LOAEC = 4.1 

Reduction in 

offspring 

EPA 1986 

Supplemental 

Snail 

(Physa gyrina) 93.7 NOAEC <26 LOAEC = 26 

Embryo 

production 

EPA 1986 

Supplemental 

Waterflea 

(Daphnia magna) NR NOAEC = 180 

LOAEC = 320 

Survival EPA 1986 

Supplemental 

Cladoceran 

(Simocephalus 

vetulus) 

93.7 NOAEC = 119 

LOAEC = 264 Survival EPA 1986 Supplemental 

Estuarine/Marine Fish and Invertebrates, acute 

The available acute toxicity studies categorize PCP as being highly toxic to estuarine/marine fish 

and moderately to very highly toxic to estuarine/marine invertebrates. No additional acute 

toxicity data are needed. The guidelines for fish (850.1075), bivalve (850.1025 or 850.1055), 

and one additional invertebrate sp. (850.1035) are satisfied. 
Page 54 of 63

Table C8: Estuarine/Marine Fish and Invertebrate Acute Toxicity

Test Species Test Material 

(% ai) 

EC50 

(μg ai/L) 

Toxicity 

Category 

EPA Study 

ID 

Sheepshead minnow 

(Cyprinodon variegatus) 

100 240 Highly toxic 43485104 

Acceptable 

96 220 Highly toxic 40228401 

Acceptable 

96 330 Highly toxic 40228401 

Acceptable 

Pinfish 

(Lagodon rhomboides) 96 31 Very highly toxic 40228401 Acceptable 

Mysid shrimp 

(Americamysis bahia) 96 320 Highly toxic 40228401 

Acceptable 

Pacific oyster 

(Crassostrea gigas) 100 48 Very highly toxic 43485104 Acceptable 

Eastern oyster 

(Crassostrea virginica) 98 49 Very highly toxic EPA 1986Supplemental 

Tech. 34 Very highly toxic USFWS2

Supplemental 

Shrimp 

(Palaemon elegans) 100 84 Very highly toxic 43485104 Acceptable 

Grass shrimp 

(Palaemonetes pugio) 96 2500 (LC50) Moderately toxic 40228401 Acceptable 

1

 Office of Water reviewed data cited in the OPP Pesticide Ecotoxicity Database 2

 US Fish and Wildlife Service reviewed data cited in the OPP Pesticide Ecotoxicity Database 

Estuarine/Marine Fish and Invertebrates, chronic 

One supplemental life cycle test is available for fish. However, because the NOAEC of 47 μg 

ai/L for the sheepshead minnow is a higher value than the LC50 for the pinfish (31 μg ai/L), an 

acute-to-chronic ratio (ACR) is used to estimate an NOAEC for the more sensitive pinfish. 

Based on the sheepshead LC50 (220 μg ai/L) and NOAEC, an ACR of 4.68 (220 μg ai/L /47 μg 

ai/L) is derived. The extrapolated NOAEC for the pinfish is then calculated as 31 μg ai/L/4.68 = 

6.6 μg ai/L. That value will be used for the risk assessment. No additional data are anticipated 

to be needed. The guideline (850.1400) for an estuarine/marine fish early life-stage toxicity test 

is satisfied. 

Table C9: Estuarine/Marine Fish Early Life-Stage Toxicity

Test Species Test Material 

(% ai) 

NOAEC and LOAEC 

(μg ai/L) 

Endpoints 

Affected 

EPA Study 

ID 

Sheepshead minnow 

(Cyprinodon variegatus) 100 NOAEC = 47 

LOAEC = 88 

Survival of 1st

generation fish 

EPA 1986 

Supplemental 

Pinfish -- NOAEC = 6.61 -- -- 

1

 extrapolated value based on the ACR as described above 
Page 55 of 63

Aquatic and Semi-aquatic Plants 

Five acceptable studies are available for aquatic plants, but none are available for semi-aquatic 

plants. The guidelines for testing with duckweed, a vascular sp. (850.4400), three algal spp. 

(850.4500), and cyanobacteria (850.4550) are satisfied. No additional aquatic plant data are 

needed. A seedling emergence toxicity test with rice is anticipated to be needed; the guideline 

(850.4225) is not satisfied. 

Table C10: Aquatic and Semi-aquatic Plant Toxicity

Test Species Test Material 

(% ai) 

EC50 

(μg ai/L) 

NOAEC 

(μg ai/L) 

EPA Study 

ID 

Aquatic species: 

Duckweed 

(Lemna gibba) 88.9 250 32 42633708 

Acceptable 

Green algae 

(Selanastrum capricornutum) 88.9 50 9 42633706 

Acceptable 

Marine diatom 

(Skeletonema costatum) 88.9 27 9 42633704 

Acceptable 

Freshwater diatom 

(Navicula pelliculosa) 88.9 124 28 42633705 

Acceptable 

Cyanobacteria 

(Anabaena flos-aquae) 88.9 50 6 42633707 

Acceptable 

Semi-aquatic species: 

Rice 

(Oryza sativa) Data gap -- 

Sediment-dwelling Invertebrates 

Sediment toxicity data are not available. Based on its environmental fate properties (e.g., log 

Kow = 4.7 at pH 5), PCP is expected to accumulate in aquatic sediments. Because PCP persists 

in sediments (half-life > 10 days), chronic testing is anticipated to be needed for freshwater (2 

spp.) and estuarine/marine (1 sp.) benthic invertebrates. There currently is no guideline number 

for this test. 

Amphibians 

Amphibian data are not required, but acute toxicity endpoints are available for two species in the 

OPP Pesticide Ecotoxicity Database. These studies demonstrate that PCP is highly toxic to 

amphibians. 
Page 56 of 63

Table C11: Amphibian Acute Toxicity

Test Species Test Material 

(% ai) 

LC50 

(μg ai/L) 

Toxicity 

Category 

EPA Study 

ID 

Bullfrog 

(Rana catesbeiana) 99 207 Highly toxic OPP1 

Supplemental 

Salamander 

(Ambyystoma 

mexicanum)

Tech. 300 Highly toxic OPP1 

Supplemental 

1

 OPP Pesticide Ecotoxicity Database 

Ecotoxicity Profile - Dioxins/Furans 

The data tabulated below are from the 2008 Chlorinated Dibenzo Dioxins (CDDs) and 

Chlorinated Dibenzo Furans (CDFs) as Contaminants of Pentachlorophenol – Ecological 

Hazard and Risk Assessment for the Pentachlorophenol Reregistration Eligibility Decision 

(RED) Document, R.C. Petrie, Antimicrobials Division, USEPA Office of Pesticide Programs, 

Washington, DC. These data were selected for use in that risk assessment. Additional 

ecotoxicity data are available in the appendices of that document. Additional ecotoxicity data for 

dioxins and furans are not anticipated to be required. 

Table C12: Selected Avian and Mammalian Toxicity Values for Dioxins (2,3,7,8-TCDD) 

Species Test Toxicity Toxicity Category 

Northern bobwhite

Acute oral LD50 = 15 μg/kg Very highly toxic

8-day dietary LC50 = 167 ppt Very highly toxic

Ringneck pheasant Reproduction 

(10 week)

NOAEL= 0.014 μg/kg-day 

(fertility, embryo mortality) NA

Mouse acute oral LD50=114-284 μg/kg Very highly toxic

Rat

Reproduction 

(exposed days 6-15 of 

gestation)

NOAEL = 0.125 μg/kg-day 

(litter size and pup weight) NA

Table C13: Selected Aquatic Toxicity Values for Dioxins (CDDs/CDFs)

Compound/ 

Test species Test Toxicity Toxicity Category 

2,3,7,8-TCDD: 

Coho salmon 96-h acute LC50=5.60 ppt very highly toxic 

Rainbow trout 

(sac fry) 96-h acute LC50=1.83 ppt very highly toxic 

Rainbow trout 28-day early life-stage LC50=0.046 ppt very highly toxic 
Page 57 of 63

(swim-up fry) NOEC=0.0011 ppt 

fathead minnow 28-day LC50=1.7 ppt very highly toxic 

Daphnia magna 48-h acute EC50>1020 ppt very highly toxic 

Annelid worm 55 days NOEC = 200 ppt NA 

Snail 12 days NOEC = 200 ppt NA 

Dibenzofuran: 

Sheepshead minnow 96-h acute LC50=1800 ppb moderately toxic 

fathead minnow 96-h acute LC50=1140 ppb moderately toxic 

Daphnia magna 48-h acute LC50=1340 ppb moderately toxic 

Mysid 96-h acute LC50=1310 ppb moderately toxic 

Diatom, Skeletonema 

costatum

96-h acute EC50=1500 ppb NA 

2,3,7,8-TDCF: 

Medaka 13-day LC50=16 ppb very highly toxic 

Ecotoxicity Profile HCB

The data tabulated below are from the 2008 Hexachlorobenzene (HCB) as a Contaminant of

Pentachlorophenol – Ecological Hazard and Risk Assessment for the Pentachlorophenol 

Reregistration Eligibility Decision (RED) Document, R.C. Petrie, Antimicrobials Division, 

USEPA Office of Pesticide Programs, Washington, DC. Additional ecotoxicity data for HCB are 

not anticipated to be required. 

Table C14: Selected Aquatic Toxicity Values - HCB 

Species Test Endpoint/Effect Toxicity Category 

Acute and Subchronic Toxicity: 

Flounder 

(Platichthys flesus) 96 h LC50 – 200 μg/L Highly toxic 

Sole 

(Solea solea) 96 h LC50 – 140 μg/L Highly toxic 

Channel catfish 

(Ictalurus punctatus) Static – 24 h LC50 – 6400 μg/L Moderately toxic 

Bluegill (Lepomis 

macrochirus) 

Static – duration 

not reported LC50 – 12,000 μg/L Slightly toxic 

Largemouth bass 

(Micropterus salmoides) Static – 96 h LC50 – 12,000 μg/L Slightly toxic 
Page 58 of 63

Coho salmon Static – 96 h. LC50 – 50,000 μg/L Slightly toxic 

Largemouth bass 10 days 3.5 μg/L 

(liver and kidney damage) NA 

Diatom 

(Cyclotella meneghiniana) Static - 48 h EC50 - 2 μg/L 

(genetic effect) NA 

Freshwater green algae 

(Selanastrum capricornutum) Static - 96 h EC50 > 30 μg/L NA 

Chronic Toxicity: 

Water flea 

(Daphnia magna) 14 days EC50 – 16 μg/L 

(50% reduction in fertility) 

NA 

Cladoceran, 

(Ceriodaphnia dubia) 

Life cycle/partial 

life cycle – 7 days NOEC > 7 μg/L NA 

Rainbow trout 

(Salmo gairdneri)

Early life stage – 90 

days NOEC > 3.68 μg/L NA 

Fathead minnow 

(Pimephales promelas) Early life stage – 32 

days 

NOEC > 4.8 μg/L NA 

Snail 

(Lymnaea palustris) 10-12 weeks 

0.5 μg/L, 5 μg/L 

(significantly reduced growth 

rate) 

NA 

Crab 

(Portunus pelagicus) 6 weeks 5 μg/L (reduction in carapace 

growth rate) NA 

Table C15: Whole Sediment Acute Toxicity - HCB

Species NOAEC 

(mg/kg) 

Test duration/ 

type 

Freshwater amphipod 

(Hyalella azteca)

42 14-day test (spiked sediment) 

60 10-day test (spiked sediment) 

Midge 

(Chironomus tentans)

42 14-day test (spiked sediment) 

60 10-day test (spiked sediment) 

Estuarine amphipod 

(Leptochirus plumulosus) 

60 10-day test (spiked sediment) 
Page 59 of 63

Table C16: Selected Avian Toxicity Values for HCB 

Species Test Method/Duration Endpoint 

Ring-necked Pheasant 

 (Phasianus colchicus) 5 days LC50 – 617 ppm 

Japanese Quail 5-day LC50 – 568 ppm 

Bobwhite Quail NR LD50 -- 575 mg/kg 

Mallard NR LD50 -- 1450 mg/kg 

Mallard Duck 

(Anas platyrhynchos) 8 days LC50 > 5000 ppm 

Herring gull 

(Larus argentatus) Egg injection study LD50 – 4300 μg/kg (embryo mortality) 

Herring gull Egg injection study 1500 μg/kg – significant reduction in 

embryonic weight 

Japanese Quail 

(Coturnix japonica) 90 days 

NOEL – 5 ppm 

LOEL – 20 ppm 

(egg volume) 

NOEL – 1 ppm 

LOEL – 5 ppm 

(morphology, organ weight) 

 
Page 60 of 63

Ecotoxicity References for Appendix C 

42633701 Campbell, S.; Jaber, M. (1993) Pentachlorophenol: An Acute Oral Toxicity Study 

with the Northern Bobwhite: Lab Project Numbner: 345-103. Unpublished study 

prepared by Wildlife International Ltd. 18 p. 

42633702 Campbell, S.; Jaber, M. (1993) Pentachlorophenol: A Dietary LC50 Study with the 

Northern Bobwhite: Lab Project Number: 345-101. Unpublished study prepared by 

Wildlife International Ltd. 37 p. 

42633703 Campbell, S.; Jaber, M. (1993) Pentachlorophenol: A Dietary LC50 Study with the 

Mallard: Lab Project Number: 345-102. Unpublished study prepared by Wildlife 

International Ltd. 36 p. 

00033067 Mattson, V.R.; Arthur, J.W.; Walbridge, C.T. (1976) Acute Toxicity of Selected 

Organic Compounds to Fathead Minnows: EPA-600/3-76- 097. (Unpublished study 

received May 2, 1980 under 32240-2; prepared by U.S. Environmental Protection 

Agency, Office of Re- search and Development, Environmental Research 

Laboratory, sub- mitted by Domain Industries, Inc., New Richmond, Wis.; CDL: 

099418-G) 

00063572 McCarty, W.M.; Alexander, H.C. (1977) Toxicity of Dowicide EC-7 to Freshwater 

Organisms. (Unpublished study received May 16, 1978 under 464-431; submitted 

by Dow Chemical U.S.A., Midland, Mich.; CDL:234322-A) 

42633704 Hoberg, J. (1992) Pentachlorophenol Technical: Toxicity to the Marine Diatom: 

Lab Project Number: 92-12-4540: 12836.0692.6109.450. Unpublished study 

prepared by Springborn Laboratories, Inc. 61 p. 

42633705 Hoberg, J. (1993) Pentachlorophenol Technical: Toxicity to the Freshwater Diatom: 

Lab Project Number: 92-12-4521: 12836.0692.6108.440. Unpublished study 

prepared by Springborn Laboratories, Inc. 62 p. 

42633706 Hoberg, J. (1993) Pentachlorophenol Technical: Toxicity to the Freshwater Green 

Alga: Lab Project Number: 92-10-4481: 12836.0692.6107.430. Unpublished study 

prepared by Springborn Laboratories, Inc. 62 p. 

42633707 Hoberg, J. (1993) Pentachlorophenol Technical: Toxicity to the Freshwater Bluegreen Alga: Lab Project Number: 92-11-4502: 12836.0692.6110.420. Unpublished 

study prepared by Springborn Laboratories, Inc. 61 p. 

42633708 Hoberg, J. (1993) Pentachlorophenol Technical: Toxicity to the Duckweed: Lab 

Project Number: 93-1-4560: 12836.0692.6111.410. Unpublished study prepared by 

Springborn Laboratories, Inc. 66 p. 

00022923 Hill, E.F. et al. 1975. Lethal Dietary Toxicities of Environmental Pollutants to 

Birds. U.S. Fish and Wildl. Serv., Special Scientific Report – Wildlife No. 191. 

Washington, DC. 
Page 61 of 63

00160000 Hudson, R.H. et al. 1984. Handbook of Toxicity of Pesticides to Wildlife (2nd

edition). U.S. Fish and Wildl. Serv., Resource Publ. 153. Washington, DC. 

00085230 McCarty, W.M. (1977) Toxicity of Dowicide^(TM)I EC-7 to Daphnids. 

(Unpublished study received Oct 28, 1977 under 464-31; submit- ted by Dow 

Chemical U.S.A., Midland, Mich.; CDL:232112-A) 

40098001 Mayer, F.L., Jr. and M.R. Ellersieck. 1986. Manual of Acute Toxicity: 

Interpretational Data Base for 410 Chemicals and 66 Species of Freshwater Animals. 

US Fish and Wildlife Service, Res. Publ. 160, Washington, DC 

40924115 Spehar, R.; Nelson, H.; Swanson, M.; et al (1985) Pentachlorophenol toxicity to 

amphipods and fathead minnows at different test pH values. Environmental 

Toxicology and Chemistry 4:389-397. 

40228401 Mayer, F.L., Jr. 1986. Acute Toxicity Handbook of Chemicals to Estuarine 

Organisms. EPA/600/X-86/231. Environ. Res. Lab., Gulf Breeze, FL 

EPA 1986 Stephen, C. 1986. Ambient Aquatic Life Water Quality Criteria for 

Pentachlorophenol. USEPA/ORD. EPA-440/5-86-009. 

TN0918 Report of Analysis: Certox P-40 Wood Preserver. Rainbow trout. EPA Animal 

Biology Lab., Washington, D.C. January 19, 1976. 

TN0952 Report of Analysis: Certox P-40 Wood Preserver. Daphnia magna. EPA Animal 

Biology Lab., Washington, D.C. March 1, 1976. 

 
Page 62 of 63

Appendix D Product Chemistry 

The PCP product chemistry information is summarized in Table D1 (source: EPA RED, 2008). 

Table D1 – Product Chemistry of PCP. 

Guideline 

Numbers PCP Source 

830.1550 

Product identity and composition Refer to Table 4 

830.1600 

Description of materials used to 

produce the product 

CBIA

830.1620 

Description of production process CBI 

830.1650 

Description of Formulation Process CBI 

830.1670 

Description of Formulation Process CBI 

830.1700 

Preliminary analysis CBI 

830.1750 

Certified limits CBI 

830.1800 

Enforcement 

analytical method 

MRID 41002702 

830.1900 

Submittal of samples CBI 

830.6302 

Color 

Light brown/tan 

TGAI: White 

needle-like crystals

EPA RED, 2008 

830.6303 

Physical State Solid EPA RED, 2008 

830.6304 

Odor Phenolic EPA RED, 2008 

830.6313 

Stability Stable for a year EPA RED, 2008 

830.6314 

Oxidation/Reduction Not applicable 

830.6315 

Flammability Not applicable 

830.6316 

Explodability Not applicable 

830.7000 

pH at25 °C 4.99 EPA RED, 2008 

830.7050 

UV/Visible Absorption Not applicable 

830.7200 

Melting point (°C) 190-191 o

 C EPA RED, 2008 
Page 63 of 63

Guideline 

Numbers PCP Source 

830.7220 

Boiling point (°C) Not applicable 

830.7300 

Density (g/cm3) 1.979 g/ml EPA RED, 2008 

830.7370 

Dissociation Constant pKa(s) 4.74 EPA RED, 2008 

830.7520 

 Particle size, fiber length, & 

diameter distribution 

Not applicable 

830.7550 

Log Kow 5.05 at pH 5 EPA RED, 2008 

830.7840 

Solubility in water (mg/L) at 25 oC 

0.3 g/L at pH 5 

20 ppm at pH 7 

2200 ppm at pH 9 

EPA RED, 2008 

830.7860 

Solubility in organic solvents Not applicable 

830.7950 

Vapor pressure (mm Hg) at 25 °C 

1.1 x 10-4mm Hg at 

25 o C EPA RED, 2008 

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