Docket Number EPA

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Page 2 of 71 Pentachlorophenol Registration Review Team

Human Health & Environmental Effects Jonatha n 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 RossDocket Number EPA

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Page 3 of 71 TERMS, ABBREVIATIONS AND SYMBOLS

2 ,3,7,8 TCDD 2, 3, 7, 8

- tetrachlorodibenzo

- p

- dioxin
A.I. or a.i. active ingredient aPAD a cute p opulation a djusted d ose ASRI a ctivated sludge r espiration i nhibition

atm

- m 3 /mole a tmospheric pressure

- cubic meter per mole BCF b ioconcentration f actor °C d egrees Celsius CAS Chemical Abstracts Service CDD chlorodioxin CDF chlorofuran CFR Code of Federal Regulations CMA Chem ical Manufacturers Association CO 2 c arbon dioxide cPAD c hronic p opulation a djusted d ose DCI data call

- in EC 50 m edian (or 50 percent) e ffect c oncentration ECOTOX ECOTOXicology EDSP E ndocrine 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 Feder al Food, Drug, and Cosmetic Act
FIFRA Federal Insecticide, Fungicide, and Rodenticide Act FQPA F ood Quality Protection Act
FWP Final Work Plan g/mol g rams per mole GLN guideline number HCB hexachlorobenzene
HPV h igh production v olume
HxCDD hexachlorodibenzo

- p

- dioxin
IDS Incident Data System
Koc o rganic carbon normalized soil

- water partition coefficient Kd s oil

- water partition coefficient
Kow o ctanol

- water partition coefficient LC 50 m edian (or 50 percent) l ethal c oncentration
LD 50 m edian (or 50 percent) l ethal d ose LOAEC l owest

- o bserved

- a dverse

- e ffect

- c oncentration LOEC l owest

- o bserved

- e ffect

- c oncentration LOAEL lowest

- observed

- adverse

- e ffect

- l evel Log K ow l ogarithm of the octanol

- water partition coefficient

μg m icrogram ml/g m illiliter p er g ram mg/kg m illigram p er k ilogram mg/kg/day m illigram p er k ilogram p er d ay mg/L m illigram p er l iter mm Hg m illimeter of mercury MOE m argin of e xposure MRID Master Record Identification NumberDocket Number EPA

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Page 4 of 71 MRL m aximum r esidue l imit N/A n ot a pplicable

nm n anometers NOAEC no

- observed

- adverse

- effect

- c oncentration NOAEL n o

- o bserved

- a dverse

- e ffect

- l evel OCSPP Office of Chemical Safety and Pollution Prevention OECD Organization for Economic Co

- operation and Development OPP Office of Pesticide Programs PCP Pentachlorophenol
PAD p opulation a djusted d ose PDM Probabilistic Dilution Model
% p ercent PC Code Pesticide Chemical Code PCA pentachloroanisole pH power of h ydrogen or power of the con centration of the hydrogen ion pKa p ower of the acid dissociation constant or negative base

- 10 logarithm of the acid

dissociation constant of a solution ppb p arts p er b illion

ppm p arts p er m illion
PWP Preliminary Work Plan QSAR q uantitative s tructure

- a ctivity r elationship
RED Rere gistration Eligibility Decision SAR s tructure a ctivity r elationship SF s afety f

actor TEP t ypical e nd

- u se p roduct TGAI t echnical grade active i ngredient
TMDL total maximum daily l oads
UF uncertainty factor UV/VIS ultraviolet/v isible light a bsorption
% w / w p ercent weight per weight.
WWTPs w astewater treatment plantsDocket Number EPA

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Page 5 of 71 

### 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 Toxicologi cal 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

................................ ................................ ................................ ............................. 33Docket Number EPA

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Page 6 of 71 Appendix A T oxicology 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 P lan

............................ 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

– Phy sical

- Chemical and Environmental Fate Properties for PCP

................................ .. 10 Table 5

– The Maximum Concentrations of C ontaminants 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, R ED)

.......... 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

.................... 28Docket Number EPA

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Page 7 of 71 

## 1 Introduction

This document is the United States Environmental Protection Agency ’s ( USEPA, EPA or “ the Agency ”) Final Work Plan ( F WP) for pentachlorophenol , herein referred to as PCP

. Th is 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 con ducting 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 m eet 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 reevalua tes 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 standa rd for registration. The regulations governing registration review begin at 40 CF R 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 eac h 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 publi shed 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 Ant icipated as Needed for the Registration Review of PCP” with the newly added neurotoxicity data and environmental fate data requirements.Docket Number EPA

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Page 8 of 71  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 a nd 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 response s 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 th e s e comment s

.

The c omment s received result ed in a dditional modification s to the anticipated dat a 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 ( c ase 2505 ) has been established at http://www.regulatio ns.gov in docket number EPA

- HQ

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- 2014

- 0653. Public comments received concerning the PWP and d ocuments associated with this registration review can be viewed at this docket. Tables 1 and 2 b elow summar ize 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 Nece ssary to Support Registration Review Date of Most

Recent Assessment Type of

Assessment Required (New/Updated) * Data Anticipated as Needed (See T able 8 for detail s)

Dietary (food) No 1 9/25/ 20 08 None None
Dietary (drinking water) No 1 9/25/ 20 08 None None
Occupational Handler Yes 9/ 8 / 20 0 8 Updated None 2

Residential Handler No (see Section 3.3.2 ) N/A None None

Resident i al Post Application

- Incidental Oral and Dermal Yes 1 9/ 8 / 20 0 8 Updated Environmental Fate

Resident i al Post Application No (see Section 3.3.3 ) N/A None None

Aggregate Yes 1 9/25/ 20 08 Updated NoneDocket Number EPA

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Page 9 of 71 Risk Assessment Assessment Nece ssary to Support Registration Review Date of Most

Recent Assessment Type of

Assessment Required (New/Updated) * Data Anticipated as Needed (See T able 8 for detail s)

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 post

Reregistration Eligibility Decision ( RED ) Data Call

- In ( DCI ) , see Table 9

. 1 Dietary (food and drinking water) and residential exposure are part of the general population biological monitoring data from NHANES and will be accounted for in the anticipated aggregate assessment.

2 Data already required by the 2011 post

- RED PCP DCI

.

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 Preli minary Work Plan 201 4

- 12 2014

- 1 2

- 19
Close Public Comment Period 201 5

- 02 2015

- 2

- 17 Phase 2: Case Development
Issue Final Work Plan 201 5

- 06 2015

- 06

Issue Data Call

- In (DCI) 201 6

- 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).Docket Number EPA

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Page 10 of 71 

## 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 Chlorophenol s

PC Code 063001

CAS N umber 87

- 86

- 5
Molecular Formula C 6 HCl 5 O 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. P arameter 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 c onstant (pKa) 4.74

830.7550 Octanol

- water partition coefficient

at 25 o C (Log K ow ) 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 o C 1.1 x 10

- 4 mm Hg Environmental Fate Properties

Mobility

835.1230 Adsorption/desorption study Moderately mobile in sandy loam, im mobile 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 o C: 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 o C

(days) Degrades rapidly at all three pHs with half

- life between 13

- 30 minutes. (MRID 42885401)Docket Number EPA

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Page 11 of 71 Guideline No. P arameter PCP

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

- life of 14 days.(M RID 42288601) Persistence in Soil (half

- life)

835.4100 Aerobic soil metabolism at 25 o C

(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

- m 3 /mol = atmosphere cubic meter per mole; o C = degrees Celsius; mg/L = milligrams per liter; mmHg = millimeters of mercury

Pentachloroanisole (PCA) A potential degradate/metabolite of PCP and other compounds has been identifi ed as pentachloroanisole (PCA), Mol For: C 7 H 3 Cl 5 O; 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 belo w.

The Agency has noted that the Stockholm Convention’s Persistent Organic Pollutants Review Committee (POPRC) decided in October 2014 to recommend to its Conference of Parties (COP) to list PCP and its salts and ester s 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 a nd esters with a time

- limited exemption

.



## 1.5 PCP and C ontaminants

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 repor t all the components and their percentage by weight in the product. C ontam inants below 0.1% reporting limit present at ppm levels (micro levels) are not report ed on the CSF and are considered microcontaminants

. These microcontaminants are herein referred to as contaminants.Docket Number EPA

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Page 12 of 71 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 h ave decreased from 1986 to 2013.

Table 5

– The Maximum Concentrations of C ontaminants 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 .0 01 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

– Characteri zation of C ontaminants

Substance Water solubility Vapor pressure Log K ow

HCB (CAS# 118

- 74

- 1) 6000 m g/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 areDocket Number EPA

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Page 13 of 71 end

- use products. The formulations include ready

- to

- use solutions and soluble concentrate s

. 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 end

use products range from 4.3 percent (other chloro phenols 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 wit h 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 Re gistered 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 perc ent . In 2004

, there w ere only two major suppliers of PCP (Kline, 2005)

.



## 1.7 Regulatory Histor y

PCP has been used as a wood preservative since 1936; however, the first pesticidal product containing PCP was registered b y 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.Docket Number EPA

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Page 14 of 71 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

- du ty 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 registratio n 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 d escribed in the Federal Register of January 13, 1986 (Vol.51, No. 7). Additionally, all non

pressure 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 comm odities 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 t he period from January 1905 to January 2008, over 300 incident reports exist in the EPA’s Incident Data System (IDS) associated wit h 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 includ e chloracne, tremors, allergies, insomnia, twitching, dia rrhea, 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.Docket Number EPA

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Page 15 of 71 

## 2 A nticipated Data Needs

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

- require d post

- RED DCI data, the following studies as listed in T able 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 reques ted for this registration review prior to conducting the registration review risk assessments for PCP

.

T able 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

850.13 00 1 Freshwater invertebrate,

life cycle TGAI 12 Ecological Wood preservatives Aquatic

environment

– Aquatic invertebrates

850.4225 2 Seedling emergence, rice TGAI 12 Ecological Wood preservatives Aquatic

environment

- Semi

- aquatic plants

No GLN 3 Whole sediment, chronic,

freshwater (2 spp.) TGAI 24 Ecological Wood preservatives Aquatic

environment

- Benthic organisms

No GLN 3 Who le sediment, chronic,

estuarine/marine TGAI 24 Ecological Wood preservatives Aquatic

environment

- Benthic organisms

835.2240 4 Direct photolysis rate of

parent and degradates in

water TGAI 12 Ecological Wood preservatives Characterize

all degradates of PCP including PCA

835.4100 4 Aerobic soil metabolism TGAI 24 Ecological Wood preservatives Characterize

all degradates of PCP including PCA, if any

835.4200 4 Anaerobic soil metabolism TGAI 24 Ecological Wood preservatives Characterize

all degradates of PCP including PCA

850.1730 4 Fish BCF 5 TGAI 12 Ecological Wood preservatives Characterize

all degradates, depurationDocket Number EPA

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Page 16 of 71 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 AWPA 4 Leaching from PCP treated

wood TEP 12 Ecological Wood preservatives Characterize

all leachates of PCP

pressure

treated wood and characterize PCA

835.1230 4 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 t esting 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 p rotocol 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 F actor

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 f

ield d issipation 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 875.1 1 00, 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 ha ve been submitted ; this s tudy is outstanding

. 

## 3 Human Health Risk Assessment

The Agency anticipates the need to conduct a n 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 reg istration review

. PCP contains CDDs

, CDFs

, and HCB as contaminants formed during the manufactur ing process. Direct exposure measurements of CDDs/CDFs and HCBs for the general population attributed to pre ssure

- 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 informationDocket Number EPA

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Page 17 of 71 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

.

P opulation

- 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

. T he 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 th e 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 T otal 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 toxici ty 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 Toxic ity 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 generat e 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 press ure 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. Non

occupational 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 T hreshold 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 f

r om l ong

- 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, therefo re, 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

I n 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 RiskDocket Number EPA

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Page 18 of 71 Information System ( IRIS ) program released a PCP toxicological review in 2010

. The updated C an cer Potency Factor for PCP is 4 × 10

- 1 per mg/kg

- day co mpared to the cancer slope factor ( CSF ) of 7 × 10

- 2 per mg/kg

- day used in 2008 RED representing an almost 5.7

- fold increase in cancer potency (IRIS

, 2010, http://www.epa.gov/IRIS/subst/0086.htm )

. The revised hazard information will be used in the final risk assessment process. The existing database of studies is tabulated in Appendix A

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 I ncreased resorptions, reduced fetal weight, and skeletal malformations Developmental toxicity

- rat

MRID # 43091702

UF = 100 a 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 Tox i city

- Dog

MRID # 43982701

UF = 3 00 a 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 hema ngiosarcomas that developed in female mice treated with technical grade PCP or Dowicide EC

- 7 (N TP, 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 grad e 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 t oxicological profile for the IRIS database

.
Short and Intermediate

- term (Dermal) a NOAEL = 30 a MOE = 100 I ncreased resorptions, reduced fetal weight, skeletal malformations Developmental

– r at toxicity

Long

- term (Dermal) LOAEL = 1.5 a MOE = 3 00 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 contac t 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 manufactur ing

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 estima te the TEQDocket Number EPA

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Page 19 of 71 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, t he 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 = 0.0000 19 ).



### 3.1.2 C ontaminants

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 the ir 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 ch emicals and high lipid solubility (K ow )

. 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 r elated 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 10 5 per mg/kg

- day for the 2,3,7,8 congener.

HCB

As summarized in Table 11

, the Agency selected a set of HCB toxicological end

- points for the reregistration risk assessment in 2008 (2008 RED)

. No additional toxicolog ical information was identified in the draft 2013 ATSDR Toxicological Profile for HCB which summariz es existing literature information for HCB.

Acute and Chronic ToxicityDocket Number EPA

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Page 20 of 71 The toxicology of HCB is discussed in detail within the 1991 “Drinking Water Criter ia 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 ra ts 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 evaluatio n, carcinogenic risk was assessed for non

- dietary exposure to HCB using the modified cancer slope factor of 1.02 p er 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 B ody 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 I ncreased incidence of liver porphyrin levels in female rats at 2 mg/kg/day 15 Week Oral Toxicity

- Rat (Kuiper

Goodman e t al , 1977)

Dermal: Short

- Term Oral NOAEL = 40 a

MOE = 100 B ody 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 I ncreased levels of liver porphyrin in female rats at 2 mg/kg/day 1 5 Week Oral Toxicity

- Rat (Kuiper

Goodman e t al , 1977)

Dermal: Long

- Term Oral NOAEL =0.08

Target Moe = 100 H epatic 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.Docket Number EPA

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Page 21 of 71 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 d ietary monitoring data assembled by the Food and Drug Administration (FDA) from
1991. The dietary monitoring conducted by FDA for certain food items has been dis continued since 1992 based on a lack of detectable residues. The 2008 non

- occupational exposure and risk
assessment for the P CP RED was also based on the NHANES biolo gical 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 A gency 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 r egistration r eview. 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 restricti ons 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 f ew 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 200 8 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 slop e factor for PCP

. Since no residential handler uses are expected from the use of PCP, a risk

assessme nt is not required. However, EPA will be assessing residential post

- application

exposures.Docket Number EPA

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Page 22 of 71 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 deter mine 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 proto col (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.

T o 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 PC P to linem e n 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, 2008 e ). The occupational assessment w as 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 anticipa tes receiv ing 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 t reatment exposure and pole lineman during registration review. The scenarios outlined in Table 12 are the typical worker exposure scenarios for a variety of exposures

. S tudies

a ccounting for these exposure at pressure treatment facilities were required by the 2011 post

RED DCI (see Table 9 ).

For example, for pressure treatment facilities

, workers operate and monitor application system valves and controls, open and close cylinder doors (automated) , and supervise the insertion and removal of charges ( loads of dried or debarked poles) of timber from the treatment cylinders. Workers operate forklifts used to load untreated wood onto charge trams; move charges into and out of treatment cylinders; remove charge leads and bands from treated wood; distribute treated wood to load

- out area, and load treated wood for shipment. Workers perform various labor and cleanup duties in treatment and drip pad area including: sweeping and pressure

- washing drip pad and tracks; removing and shredding all bands from treated stacks of lumber; picking up and disposing treated wood waste; cleaning cylinders; and, handling hazardous waste.Docket Number EPA

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Page 23 of 71 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 label ed 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. T he NHANES data provides an encompassing review of all PCP exposures

. Because NHANES does not include exposure s 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. Th e 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 as sessment 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 Prevent ion. As part of NHANES, urinary concentrati ons 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 FDA

registered uses) and is th e 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 P C P. For the purposes of this registration review, therefore, EPA has not assumed that P C P has a common mechanism of toxicity with otherDocket Number EPA

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Page 24 of 71 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. Th e 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 u se ‘ 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 ri sk assessments for the 2008 RED. Ecological risks were assessed separately for PCP (EPA 2008 b ), for the dioxin/furan (CDDs/CDFs) contaminants (EPA 2008 c ), and for the HCB contaminants (EPA 2008 d ). The only use assessed was the in

- service use of treated uti lity 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 scien tific framework for identifying and assessing risks. In registration review, the Agency anticipates th e need to request ecotoxicity data to characterize the risk s identified in the 2008 RED.

In the RED, b ased on the moderate toxicity of PCP to the laborato ry 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 addres sed.

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 sediment

toxicity data. Risk to vascular aquatic plants and algae were below the Agency ’s LOCs

.Docket Number EPA

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Page 25 of 71 The RED also exam ined 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 assess ment 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 h as decided to include PCA in the risk assessment to be conducted in registration review . T here are no existing reg istrations 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 an ticipates 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 th at 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 fr om PCP: hydrolytic degradatio n of PCP at pH 5, 7, 9 and aquatic photolytic degradation of PCP at similar pH s can result in the formation of PCA along with other degradates. In addition, aerobic and

an aerobic soil metabolism of PCP also could form degradate s along w ith PCA. PCP leachates from PCP

- treated wood may result in PCA formation. Additional fate studies on b ioaccumulation will determine the bioac c umulative characteristics of PCP and PCA in aqueous environments and the extent to which PCA forms in aqu atic 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 trichl orophenols 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 u nder anaerobic conditions w ith 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 mobi lity 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 in dicate the potential for bioaccumulation.



### 4.1.1 Water Quality

PCP i s 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, n o Total Maximum Daily Load s (TMDL)

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

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Page 26 of 71 have been develope d 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 U nited S tates

. 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 c an 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

treate d 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 lea chate 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 aq uatic 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 treate d 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 exp osure 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.

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

3 http://www.epa.gov/owow/tmdl/Docket Number EPA

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Page 27 of 71 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 (CM D) also is available for wood preservative uses. Based on antimicrobial use pattern s , the Agency develop ed 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

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- 0002). For In

‐ Use Service of Wood Treated Wood Products

, see page 29 in that document

.



## 4.3 Ecological Effects A nalysis

4.3.1 Mechanism of Action

T he 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.Docket Number EPA

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Page 28 of 71 

### 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 C riteria 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 contamin ants , 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 assessmen t 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 LC 50 = 15 μ g ai/L 43485104

Chronic NOAEC = 11 μ g ai/L EPA 1986

Freshwater invertebrates TGAI Acute EC 50 = 92 μ g ai/L EPA 1986

Chronic NOAEC <4.1 μg ai/L 1 EPA 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 EC 50 = 34 μ g ai/L USFWS 1980

Chronic Not required

--
Estuarine/marine benthic invertebrates TGAI Chronic Data gap

--

Algae TGAI EC 50 NOAE C EC50 = 27 μ g ai/L

NOAEC = 9 μ g ai/L 42633704

Aquatic vascular plants TGAI EC 50 NOAE C EC50 = 250 μ g ai/L

NOAEC = 32 μ g ai/L 42633708

Semi

- aquatic plants TGAI EC 50 NOAE C Data gap

--

Birds TGAI Acute LD50 = 380 mg ai/kg 160000Docket Number EPA

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Page 29 of 71 Dietary LC50 = 3400 ppm 22923

Chronic Not required

-- Amphibians TGAI Acute LC50 = 207 μ g 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, b ased 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 C ontaminants

E cotoxicity studies conducted in accordance wit h 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 concen tration 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, a cute 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 s ediments.

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 li terature on acute and chronic effects of PCP on freshwater and saltwater organis ms (EPA 198 6 )

. Some of the more sensitive endpointsDocket Number EPA

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Page 30 of 71 provided in that document are include in the Ecotoxicity Profile (Appendix C) and will be used for the risk assessment. The AWQC document also derive d water quality criteria values

. Because the toxicity o f 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 c urrent 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 o pen literature studies also will be identified through EPA’s ECOTOXicology (ECOTOX) database. The ECOTOX database will be searched when the risk assessment is prepared. A ny 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_ reregi stration_workgroup/esa_evaluation_open_literature.htm

.



## 4.4 Exposure Analysis Plan

4.4.1 Aquatic and Terrestrial Wildlife Exposure Estimates

Available OPP models will be used to determine the estimated environmental concentration s (EECs) in the aquatic environment. R esulting 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) asses sment because the PCP treated wood at the site of the treatment is dried with a d rain pad underneath and any leaked chemical is recycled for use. R emaining chemical in the pad (if any) must be treated as a hazardous waste and disposal (if any) must be cond ucted 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, neurotoxicit y, 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 maturatio n, fertility, pregnancy rates, reproductive loss, and sex ratios in offspring. For ecological hazard assessments, EPA evaluates acute tests andDocket Number EPA

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Page 31 of 71 chronic studies that assess growth, developmental and reproductive effects in different taxonomic groups. As par t 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 “na turally 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 p otential 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

- res ponse 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 ident ified for EDSP screening was published on June 14, 2013 4 and includes some pesticides scheduled for registration review and chemicals found in water

. Neither of these lists should be construed as a list of known or likely endocrine disruptors.

PCP is on L ist 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 g uidelines 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 EP A’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

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- 2009

- 0477

- 0074 for the final second list of chemicals.

5 http://www.epa.gov/endo/Docket Number EPA

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Page 32 of 71Docket Number EPA

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Page 33 of 71 

## 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 Do cument 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. Septemb er 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. Chlor i nated Dibenzo Dioxins (CDDs) and Chlorinated Dibenzo Furans (CDFs) as Contaminants of Pentachlorophenol. Ecological Hazard and Environmental Risk Assessment for the Pentachloropheno l 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, 2008 e

. 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

- 20 05, 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 Serv ice, 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 UtilityDocket Number EPA

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Page 34 of 71 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 e t 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 d ioxin

- 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 T oxicology 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 purpose s 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 sensi tization was observed with the technical test material. Acceptable acute inhalation toxicity data for PCP were not available, but waivers were granted for these data. No additional data are anticipated to be required.

Table A1

– Acute Toxicity Studies for PCP

Guideline No./ Study Type MRID No. Results Toxicity Category

870.1100/ Acute oral toxicity 00101715 LD50 = 155 mg/kg (M); and LD50 = 137 mg/kg (F) II

870.1200/ Acute dermal toxicity 00101715 LD50 > 3980 mg/kg IV

870.1300/ Acute inhalation toxicity N/A Waiver granted (a) I

870.2400/ Primary eye irritation 00101715 Corneal involvement at day 7 postinstillation IIDocket Number EPA

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Page 35 of 71 870.2500/ Acute dermal irritation 46616602 Moderate irritation at 72 hours postapplication III

870.2600/ Skin sensitization 42594301 N o 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 applica tors 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 Toxici ty 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 rat s 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 wa s 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 fem ale 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 t hought 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 o f 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

res ults 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 sati sfies the guideline requirement ('82

- 3) for a subchronic dermal toxicity study in rats. No additional data are anticipated to be required.Docket Number EPA

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Page 36 of 71 

## 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 numbe r 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 toxic ity, 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, 1 5, 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 follo ws: 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 3 0 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). F or 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 o f 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 3 0 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 administere d 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 . TheDocket Number EPA

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Page 37 of 71 Developmental NOAEL would appear to differ accord ing 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 decre ased 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 w as 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 lac k 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 decrease d 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 gestat ion 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 rabbitsDocket Number EPA

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Page 38 of 71 following the treatment interval. A slight but non

- significant dose

- related decrease in litter size was observed, cor responding 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. Al though 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 To xicity

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 a fter 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 an d 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

ce ll 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 spermatidDocket Number EPA

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Page 39 of 71 count and testis weight were observed in F1 male parental r ats. 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 advers e 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 t he 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 (9 0.9% 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). T he 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 pigme ntation, 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 st udy 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 studie s 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 hemangioma s 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 st udies 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, 1 999) 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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Page 40 of 71 

## 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 con cluded 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 ganglio nic 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, nause a, 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 shea th 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 effec ts of PCP have been studied by the U.S. Department of Health and Human Services’ N ational T oxicology P rogram (NTP) and others . The data appear to i ndicate 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 AbsorptionDocket Number EPA

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Page 41 of 71 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 Sprag ue

- 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 measur ed 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 or al 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 uri nary 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.: Xen obiotica 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 trichlo rohydroquinone 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 formati on 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 Medi cine [W.B. Diechmann, ed.],Docket Number EPA

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Page 42 of 71 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). O ne study wa s available with human data on volume of distribution. No additional data are anticipated to be required.Docket Number EPA

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Page 43 of 71 

# Appendix B Environmental Fate

Environmental Fate and Transport Properties of PCP

The Agency anticipate s the need to require environmental fate studies for re gistration 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 3 0 days.

Photodegradation in Water (MRID 42855401)

PCP photodegraded rapidly a with half

- li fe 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 post

treatment), 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 le ss 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 3 0 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. VolatilesDocket Number EPA

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Page 44 of 71 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.

A n a erobic 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 appl ied 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 trichlorophen ol (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 approxim ately 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 (K ads ), K oc , 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: S oil

- water P artition C oefficient ( K ads and K oc ) in V arious Soils

Soil Series or Origin Texture % OM pH K ads 1/N (ads) K oc

Georgia Sandy loam 0.4 5.9 5.72 0.81 2430

Nebraska 1 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 L ow 4.2 18

- -- Silt loam L ow 6.6 1.3

- --

1 Indicates the same “blue sandy loam” soil utilized in all other guideline laboratory studies.Docket Number EPA

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Page 45 of 71 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

- trichlorophe nol 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

K ads 10.2 14.6

K oc 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 tetrachloropheno l (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 CO 2 and 1.3% had volatilized as a trichlorophenol. Nonextractable [ 14 C] 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 4 90x for the whole fish. Maximum mean concentrations of [ 14 C] residues were 640 ppb, 2800 ppb and 1500 ppb in edible, nonedible and whole fish tissues, respectively. Total [ 14 C] residues at exposure day 28 were 170 ppb in edible tissues, 930 ppb in nonedibl e 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 [ 14 C] residues were identified as PCP and 6

- 13% as glucoronide conjugates of PCP

. Depuration was rapid, with over 97% of the accumulatedDocket Number EPA

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Page 46 of 71 residues eliminated from all tissues by day 14. The exposure to the parent may not have been

constant. [ 14 C]Residues in the water were not adequately characterized; approximately 24% of the [ 14 C] resid ues 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 i n diameter) treated with PCP at 0.50 lbs/ft 3 are reported in the following table. Reported data indicated that the average leaching rate and the maximum leaching rate of PCP increased with increased pH.

Table B3: Leaching Rates at Various Conditions

Condition 1 Max. Leaching Rate x 10

- 2 mg/kg leachate/in 2 /day Average Leaching Rate x 10

- 3 mg/kg leachate/in 2 /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

0.1 N 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

Mino r 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 degradateDocket Number EPA

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Page 47 of 71 Isomers of tetrachloro and trichloro formed also a s 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 soilDocket Number EPA

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Page 48 of 71 Environmental Fate Refe rences 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 Rep ort: Lab Project Number: 38440. Unpublished study prepared by ABC Labor atories, Inc. 32 p.

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

of Soil: Final Report: Lab Project Number: 38440. Unpublished study prepared by Labor a tories, 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 Metaboli sm 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) M etabolites 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 Dion ne, 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: LabDocket Number EPA

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Page 49 of 71

Project Number: 12836.0692.6114.140: 92

- 12

- 4532. Unpublished study prepared by Springborn Labs, Inc. 83 p.

43 205001 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.Docket Number EPA

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Page 50 of 71 

# 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 data base 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.Docket Number EPA

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Page 51 of 71 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 t oxicity 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 no t anticipates needing a honeybee study for toxicity of res idues 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.Docket Number EPA

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Page 52 of 71 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 1977 1 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 NR 1 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 USFWS 2 Supplemental Largemouth Bass ( Micropterus salmoides ) Tech 136 Highly toxic USFWS 2 Supplemental

Brook trout ( Salvelinus fontinalis ) 99 138 Highly toxic EPA 1986 Supplemental

Atlantic salmon ( Salmo salar ) Tech 500 Highly toxic USFWS 2 SupplementalDocket Number EPA

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Page 53 of 71 1 OPP reviewed data cited in the OPP Pesticide Ecotoxicity Database

2 US Fish and Wildlife Service reviewed data cited in the OPP Pesticide Ecotoxicity Database

Freshwater Fish, chronic

Two early life

- stage studies are available. The guideline (850.1400) for a fish early life

- stage toxicity test is satisfied. No additional acute toxicity data are anticipated to be needed.

Table C5: Freshwater Fish Early Life

- Stage Toxicity

Test Species Test Material (% ai) NOAEC and LOAEC

(μg ai/L) Endpoints Affected EPA Study
ID

Rainbow Trout ( Oncorhynchus mykiss) 99 NOAEC = 11
LOAEC = 19 Survival and Growth (length, weight) EPA 1986

Acceptable

Fathead minnow ( Pimephales promelas ) 88 NOAEC = 16
LOAEC = 34 Survival 40924115 Supplemental

Freshwater Invertebrates, acute

The 12 acute toxicity studies tabulated below categorize PCP as being moderately to very highly
toxic to freshwater invertebrates. The guideline (850.1010) for acute toxicity testing is satisfied. No additional acute toxicity data are anticipated to be nee ded.

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 SupplementalDocket Number EPA

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Page 54 of 71 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. T he g uideline (850.1300) for a freshwater invertebrate life cycle is not satisfied.

Table C7: Freshwater Invertebrate Life Cycle Toxicity

Test Species Test Material (% ai) NOAEC and LOAEC

(μg ai/L) Endpoints
Affected EPA Study

ID

Cladoceran ( Ceriodaphnia
reticulata ) 93.7 NOAEC <4.1
LOAEC = 4.1 Reduction in offspring EPA 1986

Supplemental

Snail ( Physa gyrina ) 93.7 NOAEC <26
LOAEC = 26 Embryo production EPA 1986

Supplemental

Waterflea ( Daphnia magna ) NR NOAEC = 180
LOAEC = 320 Survival EPA 1986 Supplemental

Cladoceran ( Simocephalus
vetulus ) 93.7 NOAEC = 119
LOAEC = 264 Survival EPA 1986 Supplemental

Estuarine/Marine Fish and Invertebrates, acute

The available acute toxicity studies categorize PCP as being highly toxic to estuarine/marine fish and moderately to very highly toxic to estuarine/marine invertebrates. No additional acute toxicity data are needed. The guidelines for fish (850.1075), bivalve (850.1025 or 850.1055), and one additional invertebrate sp. (850.1035) are satisfied.Docket Number EPA

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Page 55 of 71 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 USFWS 2 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 r atio (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 1 st generation fish EPA 1986

Supplemental

Pinfish

-- NOAEC = 6.6 1

-- --

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Page 56 of 71 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 K ow = 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, bu t 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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Page 57 of 71 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 OPP 1 Supplemental

Salamander ( Ambyystoma

mexicanum ) Tech. 300 Highly toxic OPP 1 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 ecot oxicity 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 toxicDocket Number EPA

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Page 58 of 71 (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 Divis ion, 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 toxicDocket Number EPA

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Page 59 of 71

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

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Page 60 of 71 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

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Page 61 of 71 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 Toxic ity 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 Hob erg, 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 Blue

green 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

Bir ds. U.S. Fish and Wildl. Serv., Special Scientific Report

– Wildlife No. 191. Washington, DC.Docket Number EPA

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Page 62 of 71 00160000 Hudson, R.H. et al. 1984. Handbook of Toxicity of Pesticides to Wildlife (2 nd

edition). U.S. Fish and Wildl ife Serv ice , 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) Pentachlo rophenol 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. Ra inbow 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.Docket Number EPA

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Page 63 of 71 

# Appendix D Product Chemistry

The PCP product chemistry information is summarized in Table D 1 (source: EPA RED, 2008 ).

Table D 1

– 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 CBI A

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

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Guideline Numbers PCP Source

830.7220 Boiling point (°C) Not applicable

830.7300 Density ( g/cm 3 ) 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 o C 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

- 4 mm Hg at 25 o C EPA RED, 2008

A Confidential business informationDocket Number EPA

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Page 65 of 71 

# Appendix E Comments Received Concerning the Preliminary Work Plan

On December 19, 201 4

, EPA opened a 60

- day public comment period on the PWP for the registration review of PCP

. The comment period ended on February 17, 201 5

. During the public comment period

, the Agency received 20 comments. As a res ult 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 T able 8

.
The Antimicrobials Division (AD) generally uses an outline format to address the commen ts (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 tw o 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 th e 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.Docket Number EPA

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Page 66 of 71

Part I. Common Comments from Multiple Submitters

1. Submitters: 3 Anonymous Commenters, Chu ck 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 registr ation 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/pesticide

reevaluation/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, th e A gency will determine whether it should take appropriate regulatory action, regardless of the registration review status of the pesticide.

EPA notes that t he 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 Regul atory 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 reques t ed 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 decid ed to requir e additional data to further assess the possibility of leaching and water contamination due to PCP or its degradates from registered uses. ThisDocket Number EPA

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Page 67 of 71 information will be incorporated into the risk assessment planned for registration review. See Secti on 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 (C o - 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 environme nt and notes that the Stockholm Convention provides scientific evidence of PCP toxicity. Submitters request ed 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 P CP has many contaminants including dioxins, furans and HCB, all of which are on th e 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 b e 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 w ill be used to estimate potential residential risk

. These data are expected to be representative of the general population, both adults and children, and t he infrequent contact with utility poles and soil directly adjacent would not substantially impact on e’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 contam inants , 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 substanceDocket Number EPA

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Page 68 of 71 that is known for its capability of causing death should be accompanied by special care and restraint).

Agency Respo nse : EPA is conducting this review of registered pesticidal uses of PCP to determine whether it continues to meet the FIFRA standard for registratio n . 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 gover nments may impose further restrictions a s needed to assess site specific protocols in additi on 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

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- quinolinate, and borate

- based wood preservatives.

Age ncy 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

s ubmitter 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 s ubmitter 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 an d 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 alternat ives analysis planned for registration review will allow EPA to make an appropriate risk / benefit finding as part of the registration review decision

. I nformation on Superfund sites is available on EPA’s website at http://www.epa.gov/superfund/

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Page 69 of 71 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 mit igate those risks. The Agency notes that s tate or local gover nments 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
P CP

- 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 enviro nmental 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 gover nments may impose further restrictio ns 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 addi tional 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 unr easonable 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 nume rous 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 produc ts were eligible for reregistration. The REDDocket Number EPA

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Page 70 of 71 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 acco unts 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 biomon itoring 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 expo sures 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. Su bmitter 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 exam ine the relationship between PCA and PCP. EPA anticipates calling in environmental fate data forDocket Number EPA

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Page 71 of 71 both PCP and PCA and will include PCA in the risk assessment to be conducted in registration review.

7. Late comments submitted: S ubmission s received after the o pen comment period ha ve been posted to the docket. EPA will consider this information, as appropriate, when conducting the risk assessment for PCP.