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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

Stephen Savage

Rose Kyprianou

Tom Luminello

Office of General Counsel

Philip Ross
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TERMS, ABBREVIATIONS AND SYMBOLS

2,3,7,8 TCDD 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin

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 

CMA Chemical Manufacturers Association

CO2 carbon dioxide

cPAD chronic population adjusted dose 

DCI data call-in

EC50 median (or 50 percent) effect concentration

ECOTOX ECOTOXicology

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

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

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
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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

PDM Probabilistic Dilution Model

% percent

PC Code Pesticide Chemical Code

PCA pentachloroanisole

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

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

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.

WWTPs wastewater treatment plants
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Table of Contents

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

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

1.2 Updates to the Work Plan................................................................................................. 7

1.3 Case Overview ................................................................................................................. 8

1.4 Chemical Identification and Properties.......................................................................... 10

1.5 PCP and Contaminants................................................................................................... 11

1.6 Use/Usage Description................................................................................................... 12

1.6.1 Registrations ........................................................................................................... 12

1.6.2 Summary of Registered Uses.................................................................................. 13

1.6.3 Usage Information .................................................................................................. 13

1.7 Regulatory History ......................................................................................................... 13

1.7.1 Tolerance Information ............................................................................................ 14

1.8 Incidents......................................................................................................................... 14

1.8.1 Human Health ......................................................................................................... 14

1.8.2 Ecological ............................................................................................................... 14

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

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

3.1 Existing Toxicological Endpoints.................................................................................. 17

3.1.1 PCP ......................................................................................................................... 17

3.1.2 Contaminants.......................................................................................................... 19

3.2 Dietary Exposure............................................................................................................ 21

3.2.1 Food ........................................................................................................................ 21

3.2.2 Drinking Water ....................................................................................................... 21

3.3 Occupational and Residential Exposures....................................................................... 21

3.3.1 Occupational Exposure ........................................................................................... 22

3.3.2 Residential Handler Exposures............................................................................... 23

3.3.3 Residential Post-Application Exposures................................................................. 23

3.3.4 Aggregate Exposures.............................................................................................. 23

3.3.5 Cumulative Exposures............................................................................................ 23

4 Environmental Risk Assessment........................................................................................... 24

4.1 Environmental Fate Assessment .................................................................................... 25

4.1.1 Water Quality.......................................................................................................... 25

4.2 Environmental Exposure Pathways................................................................................ 26

4.3 Ecological Effects Analysis ........................................................................................... 27

4.3.1 Mechanism of Action.............................................................................................. 27

4.3.2 Measures of Effect (Ecotoxicology Endpoints)...................................................... 28

4.3.3 Ambient Water Quality Criteria for PCP................................................................ 29

4.3.4 Open literature ........................................................................................................ 30

4.4 Exposure Analysis Plan.................................................................................................. 30

4.4.1 Aquatic and Terrestrial Wildlife Exposure Estimates ............................................ 30

4.4.2 Screening Level Down-the-Drain Analysis............................................................ 30

5 Endocrine Disruptor Screening Program (EDSP)................................................................. 30

6 Optional Label Changes........................................................................................................ 31

7 Next Steps............................................................................................................................. 31

8 References............................................................................................................................. 33
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Appendix A Toxicology Profile............................................................................................... 34

Appendix B Environmental Fate ............................................................................................. 43

Appendix C Ecotoxicology Profile.......................................................................................... 50

Appendix D Product Chemistry............................................................................................... 63

Appendix E Comments Received Concerning the Preliminary Work Plan............................ 65

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 .................................................................................... 10

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................... 16

Table 10 – Toxicological Endpoints Selected for Risk Assessment of PCP (2008, RED) .......... 18

Table 11 – Toxicological Endpoints Selected for Risk Assessment of HCB (2008, RED) ......... 20

Table 12 – Occupational Exposure Scenarios for Workers Using PCP ....................................... 23

Table 13 – PCP Ecological Effects Endpoints for the Ecological Risk Assessment.................... 28
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1 Introduction

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

Agency”) Final Work Plan (FWP) for pentachlorophenol, herein referred to as PCP. This

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 registration 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.

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. The PCP 

Preliminary Work Plan (PWP) was published on December 19, 2014 and the 60 day comment 

period ended on February 17, 2015.

1.2 Updates to the Work Plan

Since the publication of the PCP Preliminary Work Plan (PWP), the Agency has made the 

following updates:

 Updated Tables 1 and Table 8, “Studies Anticipated as Needed for the Registration 

Review of PCP” with the newly added neurotoxicity data and environmental fate data 

requirements.
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 Corrected the timeline in Table 2, the “Anticipated Registration Review Schedule.”

 Updated the Section 1.4 paragraph on the Stockholm Convention.

 Updated Section 3 Human Health Risk Assessment with inhalation exposure.

 Updated Section 3.3.4 on Aggregate Exposures

 Revised Section 4.1 and Appendix B with discussion of new data anticipated to be 

required.

 Deleted “Guidance for Commenters” and “Optional Label Changes” sections.

 Updated Section on “Next Steps.”

 Update Appendix A, the Agency‘s decision on neurotoxicity requirements.

 Added Appendix E, the Agency’s responses to comments submitted regarding the PWP.

The Agency received 20 submissions during the public comment period on the initial docket. See 

Appendix E for a synapse of these comments and the Agency’s responses to these comments.

The comments received resulted in additional modifications to the anticipated data needs detailed 

in the PCP Work Plan. This document makes final the work plan for the PCP registration review 

process.

1.3 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. Public comments received concerning the PWP and 

documents associated with this registration review can be 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 Environmental Fate

Residential Post 

Application

No (see 

Section 

3.3.3)

N/A None None

Aggregate Yes1 9/25/2008 Updated None
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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)

Cumulative

No (see 

Section

3.3.5)

N/A None None

Tolerance Review

No (see 

Section 

1.7.1)

N/A None None

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

plants, benthic organisms, 

Environmental Fate Yes N/A New Characterize all degradates of PCP 

including PCA

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.

1Dietary (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.

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 2014-12-19

Close Public Comment Period 2015-02 2015-2-17

Phase 2: Case Development 

Issue Final Work Plan 2015-06 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).
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1.4 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

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 oC (Log Kow)

4.75 at pH 5, 5.27 at pH 7, and 5.1 at pH 9 

830.7840 Solubility in water 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 with half-life between 

13-30 minutes. (MRID 42885401)
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Guideline No. Parameter PCP

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

Pentachloroanisole (PCA)

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 molecular structure of PCA is presented below.

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 esters 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 met in May 2015 and decided to list 

PCP, its salts and esters with a time-limited exemption.

1.5 PCP and Contaminants

There are three general types of contaminants in manufactured 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% reporting 

limit present at ppm levels (micro levels) are not reported on the CSF and are considered

microcontaminants. These microcontaminants are herein referred to as contaminants.
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PCP registrants provide monthly reports of analytical data which provide 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 concentrations of contaminants 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.

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

1.6 Use/Usage Description

1.6.1 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 
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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).

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). 

1.6.2 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. 

1.6.3 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).

1.7 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. 
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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. 

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.

1.7.1 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.

1.8 Incidents

1.8.1 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 birth abnormalities. Whether these deleterious health effects result from exposure to 

PCP specifically, or to one or more other chemicals typically found as contaminants of

manufactured PCP, is not clear.

1.8.2 Ecological

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

870.6200 Acute and subchronic 

neurotoxicity—rat TGAI 24 Human Health Wood preservatives

Occupational 

Handler

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

835.22404

Direct photolysis rate of 

parent and degradates in 

water

TGAI 12 Ecological Wood 

preservatives

Characterize 

all degradates 

of PCP 

including 

PCA

835.41004 Aerobic soil metabolism TGAI 24 Ecological Wood 

preservatives

Characterize 

all degradates 

of PCP 

including

PCA, if any

835.42004 Anaerobic soil metabolism TGAI 24 Ecological Wood 

preservatives

Characterize 

all degradates 

of PCP 

including 

PCA

850.17304 Fish BCF5 TGAI 12 Ecological Wood 

preservatives

Characterize 

all 

degradates, 

depuration 
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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

rates of PCP, 

including 

PCA

Non-GL

AWPA4

Leaching from PCP treated 

wood TEP 12 Ecological Wood preservatives

Characterize 

all leachates 

of PCP 

pressuretreated wood 

and 

characterize 

PCA

835.12304

Sediment and soil 

absorption/desorption for 

parent and degradates

TGAI 12 Ecological Wood 

preservatives

Binding with 

soils 

comparison 

with PCP

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.

4 Data anticipated to be required on PCP and PCA

5 Bioconcentration Factor

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.

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 and the neurotoxicity 

data to be called in under registration review. PCP contains CDDs, CDFs, and HCB as 

contaminants formed during the manufacturing process. Direct exposure 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 in 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 
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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.

The Agency does not anticipate the need for inhalation toxicity data on PCP. Acute and 

subchronic inhalation toxicity studies for pentachlorophenol were waived by the Agency in the 

RED for pentachlorophenol. In granting the waiver for the acute inhalation toxicity study, the 

Agency assigned pentachlorophenol a Toxicity Category I for acute toxicity. This category 

includes concentrations up to and including 0.05 mg/L (50 mg/m3). For subchronic inhalation, a 

waiver was granted on the basis of information submitted by the registrant demonstrating an 

inability to generate a consistent concentration of test article for measurement of dose-response. 

Label instructions (based on EPA Position Document 4 for Wood Preservatives; USEPA, 1984) 

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

cylinders and other related equipment contaminated with wood treatment formulation also form 

the basis for the waiver of acute and subchronic inhalation toxicity studies. 

Inhalation exposure to PCP from wood preservative use is primarily in the occupational setting. 

Controls and labeling restrictions were established for PCP in EPA Position Document 4 for 

Wood Preservatives (US EPA, 1984) to minimize inhalation occupational exposure. Nonoccupational exposure to pentachlorophenol vapors from wood preservative use is minimal. 

Measurement of PCP concentrations in and around homes (Wilson et al., 2004; Wilson et al., 

2007) show that the range of PCP detected in these samples were at low levels, ranging from 0.2 

to 1.0 ng/m3. In comparison, the Threshold Limit Value-Time Weighted Average (TLV-TWA) 

of 0.5 mg/m3 established by the American Council of Government Industrial Hygienists, was 

established to minimize the potential for irritation, central nervous system and cardiac system 

impairment from long-term exposure to pentachlorophenol. Although the TLV-TWA is a value 

specifically for protection of occupational workers, the non-occupational measurement of PCP 

air concentrations stated above are 500,000-fold lower than this TLV-TWA. There is, therefore, 

likely no risk of concern for adverse effects from inhalation exposure to pentachlorophenol at a 

concentration of 0.2 to 1.0 ng/m3 in a residential setting.

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 
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Information System (IRIS) program released a PCP toxicological review in 2010. The updated 

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

(CSF) of 7× 10-2per 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 

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) 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

toxicity 

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 
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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).

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 

toward 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 and high lipid solubility (Kow). The Agency’s Office 

of Research and Development (ORD) has led the effort in characterizing hazards and risks from 

exposure to dioxins and dioxin-like 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 105per 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
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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.

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) 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 = 40a

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 levels of

liver porphyrin in

female rats at 2 mg/kg/day

15 Week Oral

Toxicity- Rat (KuiperGoodman et al, 1977)

Dermal: 

Long-Term

Oral NOAEL

=0.08

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.
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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 

1991. The dietary monitoring conducted by FDA for certain food items has 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. The reason the assessment is required is based on new 

exposure monitoring studies in the 2011 post-RED DCI, availability of new NHANES data, and 

the revised toxicological endpoints that are likely to be selected based on the new cancer slope

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.
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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 

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 

(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 at pressure treatment facilities were required by the 2011 postRED 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.
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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.

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 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. NHANES are a series of US national surveys of the health 

and nutrition status of the non-institutionalized civilian population conducted by the Centers for 

Disease Control and Prevention. As part of NHANES, urinary concentrations of specific 

chemicals (e.g. PCP) are measured a random sample of participants of ages 6 and over as part of 

a complex multi-stage, stratified survey that is nationally representative. 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 from PCP. 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 
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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. 

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

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. Although analyses have not shown PCA as a major degradate of PCP, EPA has 

decided to include PCA in the risk assessment to be conducted in registration review. There are

no existing registrations for PCA but PCA is a degradation product of pentachlorophenol (and 

other chlorinated aromatics). The physical chemistry and fate characteristics of PCP and PCA are 

summarized below, and data requirements have been added to Table 8. The Agency anticipates 

calling in additional environmental fate studies to help determine the persistence and mobility of 

PCP in water and soil. Studies are to examine the rate that PCP leaches from treated poles into 

soil and water to help inform the risk assessment and determine the risk of PCA entering the 

environment. Further, soil adsorption data will clarify the potential for PCP and PCA to move 

through soil. There are multiple potential degradation pathways of PCA formation from PCP: 

hydrolytic degradation of PCP at pH 5, 7, 9 and aquatic photolytic degradation of PCP at similar 

pHs can result in the formation of PCA along with other degradates. In addition, aerobic and 

anaerobic soil metabolism of PCP also could form degradates along with PCA. PCP leachates 

from PCP-treated wood may result in PCA formation. Additional fate studies on 

bioaccumulation will determine the bioaccumulative characteristics of PCP and PCA in aqueous

environments and the extent to which PCA forms in aquatic environments.

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

in aqueous medium with a half-life of 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 was shown to be slightly mobile in an acceptable batch equilibrium study, but mobility did 

not correlate with pH, organic matter, or soil texture. Further, historically, PCP has been 

assumed to be highly absorbed to soils. To confirm the potential for mobility, EPA anticipates 

requiring mobility data for PCP and PCA during registration review.

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

 

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

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

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

bodies and their presence in fish are not known. 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, its degradates, and contaminants 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 may 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.

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.

 

2http://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/
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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.
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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
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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 (e.g., 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 concentrations

(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 
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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, 20134and 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 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 Next Steps

A DCI will be developed regarding the anticipated data needs listed under the “Risk 

Assessments and Anticipated Data Needs” section of this document. The Agency expects to 

issue the DCI by June of 2016.

 

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/
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8 References 

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

EPA (1984): Wood Preservative Pesticides: Creosote, Pentachlorophenol, Inorganic 

Arsenicals: Position Document 4.

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
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Linemen to Pentachlorophenol. American Industrial Hygiene Association Journal 52:547-552.

Wilson et al. 2004. Design and sampling methodology for a large study of preschool children’s 

aggregate exposures to persistent organic pollutants in their everyday environments. Journal of 

Exposure Analysis and Environmental Epidemiology (2004) 14, 260-274

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 Safety.

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); andLD50 = 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
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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.

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

weight and skeletal malformations/variations.

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 
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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, 

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 
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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 

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 
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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 

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.
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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

Agency reviewed available scientific literature and concluded PCP has neurotoxic concern 

(McMahon, 2008. Pentachlorophenol-Toxicology Chapter for the Reregistration Eligibility 

Decision Document). The data on PCP indicate the potential for nervous system effects in vitro 

(decrease in neuromuscular and ganglionic conduction, inhibition of human red cell 

cholinesterase) and in vivo animal data. Clinical signs associated with PCP exposure, including 

depression, chronic fatigue, dizziness, sleep disturbances, aggressive behavior, loss of appetite, 

headache, nausea, diarrhea, fear, thirst, and hyperthermia are suggestive of neurotoxicity. 

Pentachlorophenol is structurally related to known neurotoxicants such as hexachlorobenzene 

and hexachlorophene, which have been demonstrated to cause swelling of the myelin sheath 

and/or convulsions after stimulation with auditory or physical stimuli. 

Based on these considerations, an acute neurotoxicity study and a 90-day rat neurotoxicity study 

(OPPTS 870.6200) are identified as data gaps.

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
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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) 

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.], 
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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.
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Appendix B Environmental Fate

Environmental Fate and Transport Properties of PCP

The Agency anticipates the need to require environmental fate studies for registration review.

The additional environmental fate studies on PCP and PCA will help determine the persistence 

PCP in water and soil. Additional fate studies on bioaccumulation will help determine the 

bioacummulative characteristics of PCP and PCA. The fate of leachate from pressure treated 

woods using PCP is also being added as a special study. 

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 a with half-life 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% 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 
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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.

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 and one clay 

loam soil. The soil properties and the Freundlich adsorption coefficients (Kads), Koc, 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 (Kads and Koc) in Various Soils

Soil Series or Origin Texture % OM pH Kads 1/N (ads) Koc

Georgia Sandy loam 0.4 5.9 5.72 0.81 2430

Nebraska1 Sandy loam 1.2 6.9 9.96 0.86 1410

California Sandy loam 2.6 7.9 10.8 0.87 706

Ohio

Clay loam 3.7 5.3 74.6 0.88 3420

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.
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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 
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residues eliminated from all tissues by day 14. The exposure to the parent may not have been 

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/ft3are 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

Condition1 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

1

Final Concentration mg/L

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
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Isomers of tetrachloro and trichloro formed also as major degradates.

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
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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] 

Pentachlorophenol on the Surface of Soil: Final Report: Lab Project Number: 38440.

Unpublished study prepared by ABC Laboratories, Inc. 32 p.

41969201 Schmidt, J. (1991) Determination of the Photolysis Rate of [carbon 14] on the Surface 

of Soil: Final Report: Lab Project Number: 38440. Unpublished study prepared by

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 Coefficients: 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 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 
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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 formigration into groundwater. 

41995201 Schmidt, J. (1991) Anaerobic Soil Metabolism of [Carbon 14] Pentachlorophenol: 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.
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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.
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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.
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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
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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 40924115Supplemental

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
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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 1986Supplemental

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. 
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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 1986

Supplemental

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
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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.
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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
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(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
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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)
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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)
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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.
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00160000 Hudson, R.H. et al. 1984. Handbook of Toxicity of Pesticides to Wildlife (2nd

edition). U.S. Fish and Wildlife Service, 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.
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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
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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

A Confidential business information
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Appendix E Comments Received 

Concerning the Preliminary Work Plan

On December 19, 2014, EPA opened a 60-day public comment period on the PWP for the 

registration review of PCP. The comment period ended on February 17, 2015. During the public 

comment period, the Agency received 20 comments.

As a result of public comments, AD has revised sections of the work plan for pentachlorophenol. 

The main revision includes:

 The addition of anticipated data needs to explore the relationship between PCP and PCA

as noted in Section 4.1 and Table 8.

The Antimicrobials Division (AD) generally uses an outline format to address the comments 

(with name of submitter, comment and Agency response, in that order). The comments are often 

written verbatim while other times they are summarized. Similar comments from one or more 

respondents are combined and paraphrased.

Appendix E is divided in two parts to address comments (Table E1). Part I includes comments 

that were similar in nature or shared in common by two or more submitters and the Agency’s 

responses to these. Part II offers all remaining individual comments, not included in Part I, and 

the Agency’s responses. 

Table E1. Organization of the Agency’s Response to Comments to the “Pentachlorophenol 

Preliminary Workplan”

Part Name Page No.

I Common Comments from Multiple Submitters 66

II Individual Comments by Submitter 68

Many commenters provided copies of letters previously sent to government officials, supporting 

documents, and various scientific data and assessments. The Agency thanks commenters for 

providing these and will consider relevant information from these letters, articles, and studies 

when conducting the risk assessment for PCP.
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Part I. Common Comments from Multiple Submitters

1. Submitters: 3 Anonymous Commenters, Chuck Idol, Dina De Giorgio (North 

Hempstead Town Councilwoman), Helen Forst (Chairperson of Long Island Businesses 

for Responsible Energy (LIBFRE)), Manhasset Civic Association for Town of North 

Hempstead, Michael Forst, Rebecca Singer (Co-chair of LIBFRE)

Comment: Please ban PCP. Submitters stated that many countries have banned PCP and 

suggested that EPA’s continued registration of PCP products is influenced by large 

businesses. Submitters expressed concern that the current timeframe for completing 

registration review of PCP (five years) is too long, especially in sole-source aquifer areas and 

there are no hazardous waste regulations for the chemical. Submitters believe that PCP 

should be banned for the same reasons that it is listed as a deadly contaminant in Brownfield 

cleanup.

Agency Response: EPA is aware of PCP’s status in other countries, including the Stockholm 

Convention decision in May 2015 to list PCP for elimination.

Registration review is a multiyear process as outlined at http://www2.epa.gov/pesticidereevaluation/registration-review-process. It involves developing a plan, allowing for public 

input, and includes time to develop data for use in the risk assessment, including data that the 

Agency requires to be generated by pesticidal manufacturers and data voluntarily submitted 

or available in the open literature. If at any time EPA receives information warranting more 

immediate attention, the Agency will determine whether it should take appropriate regulatory 

action, regardless of the registration review status of the pesticide.

EPA notes that the Office of Pesticide Programs regulates pesticidal use of PCP for utility 

pole preservation. The Office of Solid Waste and Emergency Response (OSWER) handles 

remediation of Brownfield and Superfund sites. For Superfund information, please see 

http://www.epa.gov/superfund/.

2. Submitters: Anonymous Commenter, Chuck Idol, Dina De Giorgio (North Hempstead 

Town Councilwoman), Helen Forst (Chairperson of LIBFRE), Judi Bosworth (North 

Hempstead Town Supervisor), Laurence Penny (Environmental Consultant), Michael 

Forst, Nichelle Harriott (Science and Regulatory Director, Beyond Pesticides), Rebecca 

Singer (Co-chair of LIBFRE)

Comment: PCP contaminates groundwater and aquifers. Submitters expressed concerns 

that PCP may be leaching into beach bathing water, local groundwater, and aquifers. 

Submitters requested that Section 4.1.1 of the work plan include a discussion of the impacts 

to surface water and groundwater from PCP and its microcontaminants.

Agency Response: Although EPA does not expect PCP to contaminate groundwater or 

aquifers, the Agency has decided to require additional data to further assess the possibility of 

leaching and water contamination due to PCP or its degradates from registered uses. This 
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information will be incorporated into the risk assessment planned for registration review. See 

Section 4, Environmental Risk Assessment, of the FWP for more detailed information. EPA 

welcomes submission of any data supporting/indicating concern.

3. Submitters: Chuck Idol, Helen Forst (Chairperson of LIBFRE), Judi Bosworth (North 

Hempstead Town Supervisor), Manhasset Civic Association for Town of North 

Hempstead, Nichelle Harriott (Science and Regulatory Director, Beyond Pesticides), 

Rebecca Singer (Co-chair of LIBFRE), 

Comment: EPA’s assessments do not address residential risk/exposure to communities 

and children. Submitters expressed concern regarding the potential for adverse effects of 

PCP in local communities on humans, animals and the environment and notes that the 

Stockholm Convention provides scientific evidence of PCP toxicity. Submitters requested

that the Agency examine the risks and impacts from concentrated pockets of soil 

contamination by PCP, from its associated micro-contaminants, and the carrier oils used to 

apply it which result from the accepted treatment of the poles and the surrounding soils 

through ‘slumping.’ Commenters also expressed concern that PCP has many contaminants 

including dioxins, furans and HCB, all of which are on the EPA’s National Waste 

Minimization Program.

Agency Response: During the Registration Review process, the Agency anticipates the need 

to revise the occupational and residential exposure and risk assessments conducted in support 

of the 2008 RED. EPA will be assessing residential post-application exposures by examining 

biomonitoring data as well as biological monitoring (see Section 3.3). The NHANES and 

CTEPP data for PCP represent a reasonable appreciation of behaviors occurring in the U.S. 

population and will be used to estimate potential residential risk. These data are expected to 

be representative of the general population, both adults and children, and the infrequent 

contact with utility poles and soil directly adjacent would not substantially impact one’s 

average daily exposure to PCP over a 75 year lifetime. In addition to assessing residential 

exposure to PCP, the Agency has and will assess the exposure to HCB and dioxin as 

contaminants from PCP.

The Agency will take into consideration PCP and contaminants, as well as PCA, in the risk 

assessment process and will examine the possibility for soil transport. The environmental fate 

assessment will be for PCP, PCA, and for the contaminants CDDs, CDF, and HCB. Previous 

analyses have not shown PCA as a major degradate of PCP, and the Agency anticipates 

calling in additional data on PCA to explore this relationship further. See Section 4.1 of this 

FWP for more information.

4. Submitters: Anonymous Commenter, Chuck Idol 

Comment: PCP should be regulated by local officials. This chemical violates NY state 

law (N.Y. PBH. LAW 3380: NY Code - Section 3380) and is listed as a major source of 

hazardous air pollution in the Clean Air Act. Submitters suggested that EPA should 

consult with municipalities on health issues and alternative solutions. Current action by the 

Agency could be considered a form of Criminal Negligent Battery (introducing a substance 
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that is known for its capability of causing death should be accompanied by special care and 

restraint).

Agency Response: EPA is conducting this review of registered pesticidal uses of PCP to 

determine whether it continues to meet the FIFRA standard for registration. Labelled use 

instructions and restrictions are intended to ensure that PCP can be applied and will not result 

in unreasonable risks to human health or the environment when used in commerce. The 

Agency assessment is conducted for labeled uses, and state or local governments may impose 

further restrictions as needed to assess site specific protocols in addition to the federal 

standard.

5. Submitters: Helen Forst (Chairperson of LIBFRE), Nichelle Harriott (Science and 

Regulatory Director, Beyond Pesticides), Rebecca Singer (Co-chair of LIBFRE) 

Comment: The Agency should consider the long term costs of all utility poles and 

consider the alternatives available for PCP-treated wood poles. Submitters suggested that 

long term costs of the utility poles should be considered, including: installing a hazardous 

waste clean-up program, damage from major storms, transportation costs for poles, liability 

insurance costs for chemicals, and disability costs for workers. Submitters stated that 

alternative technologies for PCP-treated wood include undergrounding, recycled plastics, 

composites, recycled steel, concrete, and a number of new wood preserving chemicals that 

contain neither arsenic, chromium nor PCP including: Alkaline Copper Quaternary (ACQ), 

Copper Azole, Copper-8-quinolinate, and borate-based wood preservatives. 

Agency Response: As part of its registration review decision, EPA will evaluate the 

available alternatives to PCP and the benefits to society of continued registration of PCP. 

Part II. Individual Comments by Submitter

1. Submitter: Chuck Idol

Comment: The Agency’s work plan for registration review of PCP is incomplete. The 

submitter suggested that the work plan must have a breakdown of state by state issues and a 

state by state financial impact statement (including impact on property values and taxes that 

support a local community). The submitter also proposed that the work plan should document 

and list all of the links to the existing Superfund and Minifund sites that currently exist from 

PCP use.

Agency Response: EPA conducts human health and ecological risk assessments for 

pesticides at a national level based on labeled uses. When potential risks of concern are 

identified, the Agency will refine the risk assessment including assessments for smaller 

geographic areas. The benefits and alternatives analysis planned for registration review will 

allow EPA to make an appropriate risk/benefit finding as part of the registration review 

decision. Information on Superfund sites is available on EPA’s website at

http://www.epa.gov/superfund/.
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2. Submitter: Anonymous

Comment: DOT needs warning signs for PCP. This chemical should not be allowed to be 

placed on Utility Poles that are then placed in the direct path of citizens on sidewalks without 

clear warning signs about the hazards of the chemical. The warning signs need to be placed 

on the poles no different than the waning signs placed on and near gas station pumping 

stations.

Agency Response: Although residential contact with PCP-treated poles is expected to be 

negligible, EPA anticipates conducting a revised residential assessment as part of this 

registration review. In the event that EPA identifies risks of concern for the general public 

based on potential exposure, EPA will explore practical ways to mitigate those risks. The 

Agency notes that state or local governments may impose further restrictions as needed to 

assess site specific protocols in addition to the federal standard.

3. Submitter: Judi Bosworth (North Hempstead Town Supervisor)

Comment: EPA should consider local legislations during registration review and adjust 

the environmental risk assessment estimates using updated soil sampling data. 

Submitter informs that the Town of North Hempstead has enacted legislation requiring that 

PCP-treated utility poles be labeled with standard language identifying the presence of a 

hazardous material. In addition, New York State Senators Thiele and Lavalle have introduced 

a State-level ban of PCP in the New York State Senate. Regarding the environmental risk 

assessment, submitter notes that the 2008 PCP RED assumed minimal acute risk for small 

wild mammals, however local soil testing data may exceed estimates used in 2008. 

Agency Response: State or local governments may impose further restrictions as needed to 

assess site specific protocols in addition to the federal standard. Commenters are welcome to 

submit data as part of the review process to assist in EPA making a determination. As 

discussed in the FWP, the Agency anticipates calling in additional data, and the possibility of 

leaching will be re-examined as part of the risk assessment during registration review (see 

Section 4). 

4. Submitter: Nichelle Harriott (Science and Regulatory Director, Beyond Pesticides)

Comment: PCP poses unacceptable risks to workers, residential bystanders, and the 

environment from unintended dermal, inhalation and dietary exposures under Section 

3(c)(7)(A) of FIFRA. PCP is a persistent organic pollutant whose use as a wood preservative 

is not necessary and risks unreasonable under FIFRA. This substance, by nature of its 

contamination with hazardous toxicants like hexachlorobenzene, dioxins and furans, has risks 

that far outweigh any perceived benefit given the availability of alternatives. PCP is 

associated with numerous adverse health outcomes and environmental impacts and has been 

targeted for global elimination on the international stage.

Agency Response: In the 2008 reregistration eligibility decision (RED), EPA determined 

that pentachlorophenol-containing products were eligible for reregistration. The RED 
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identified potential risks of concern for workers exposed to pentachlorophenol at wood 

treatment plants but determined that, provided that risk mitigation measures (e.g., changes to 

treatment facilities designed to reduce worker exposure) were adopted and labels amended 

accordingly, the benefits of pentachlorophenol to society outweighed the remaining risks. 

EPA will review this finding through the registration review process as outlined in this FWP.

Registration review of PCP will also look at the risks to contaminants of PCP (see Section 

1.5 of this FWP).

5. Submitter: Anonymous Commenter

Comment: The EPA must consider the impacts of PCP-treated utility poles, where 

there can be exposure to children. Executive order # 13045 states that children may suffer 

disproportionately from environmental health risks and safety risks. The risks of PCP to 

children include: proximity to vapor released from the pole and liquid in volumes greater 

than 50 Mg leaching off the pole in clear and present danger of being touched and ingested.

Agency Response: EPA will consider exposure to children during registration review. As 

stated in Section 3.3.3 of the FWP, 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. The review process accounts for 

vulnerable subpopulations and exposure rates in the risk assessment in accordance with the 

law.

EPA considered the need to evaluate inhalation exposure during the 2008 reregistration 

process. Because most inhalation values derived from the biomonitoring study in workers at 

wood treatment plants were too low to measure and residential exposure is much lower than 

treatment plant workers, EPA determined inhalation exposure was therefore not of concern at 

that time. Potential inhalation and other exposures to the general population, including 

children, will be reexamined based on updated applicator exposure data as PCP undergoes 

registration review.

6. Submitter: Herb Estreicher, Keller and Heckman LLP on behalf of Pentachlorophenol 

Task Force

Comment: In response to the Agency’s request in the PWP, the PCP Taskforce 

submitted information on pentachloroanisole (PCA), a microcontaminant of PCP. 

Submitter cited The Stockholm Convention's Persistent Organic Pollutants Review 

Committee (POPRC) deliberations regarding PCP and PCA, and included information on 

PCA’s potential for bioaccumulation and PCP's potential to bio-transform in soil into PCA. 

Submitter expressed that based on the information presented, PCA is not a microcontaminant 

of concern.

Agency Response: The Agency has reviewed information from the POPRC and other 

information submitted and determined that additional data are needed to examine the 

relationship between PCA and PCP. EPA anticipates calling in environmental fate data for 
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both PCP and PCA and will include PCA in the risk assessment to be conducted in 

registration review.

7. Late comments submitted: Submissions received after the open comment period have been

posted to the docket. EPA will consider this information, as appropriate, when conducting the 

risk assessment for PCP.