Position Document 1
       (U.S.) Envlronrental Protection Agency
       Arlington, VA
       18 Oct 78

j        PAGE   "

J. **efpi«nri Acc*taion Mo.

 «. Titlt ind Subtitle
     Pentachlorophenol:   Position  Document  1
             P.  Cirelli
                                                                         SL McpOft Oil*

                                                                          8L Pferformiftg Org*nix»tion Rvpt. No.
   Performing Organization Nam* and Addr**t
     Special  Pesticide  Review Division
     Environmental Protection Agency
     Crystal  Mall 12
     Arlington, VA
 12. lp-Jnionn(i Or(ini»tion Nlnw *nd

     Environmental Protection Agency
     401 M.  St.  S.W.
     Washington, D.C. 20460
10. Proi«ct/Tt»k/Work Unit No.

11. Cantr>ct!Q e» Grant(G) Mo.


13. Typt ot Report & Period Cov*rwd

 IS. SuOpl«n>«nt*ry Note*
 1L AbttrKt (limit: TOO
     Preliminary Risk  Assessment:   Examination of possible unreasonable
     risks associated  with uses  of pesticide and a gathering of  all  available
     information to determine whether or  not this or  any other risk  does
     exist.   Initiates literature  search  and evaluates  risk data.   Limited
     information on exposure to  forecast  extent of risk.
   b |fi«nt.ft«r%/Op»n tivje
   c. COSATI n»l«J/Creup
     Ur.1 imited
                                                          ». S«»rltT Cl»»» {TH*

                                                                                    21. No at >•«««
                                                                                         • WT1S-3S>

                                                                                          t ftt f fffr\f^*>rfm

 Daniel p. Cirelli, Project hanager
U.S. Btvironnental Protection Agency

       Pentachlorophanol (PC? or PEHTAJ  is a buff-colored crystal which

is produced.ia th« Doited State* by cbloriastion of molten phtool in the

presence of a catalyse.  Derivatives of PC? which are registered for us«
i                                                                .
as pesticides are the sodium, aod potassium salts (Na-PCP and K-PCP, re-

spectively), and the lauric acid ester (L-PCP).  The structures and physi-

cal properties of PCP and Na-PCP are given in Figure I.  K-PCP is pro-

duced cs in situ formulations by dissolving PCF in potassium hydroxide so-

lutions.  The physical and chemical properties of pure K-PCP are not avail-
              i       '                •
able from standard chemical references or froa EPA files.  L-PCP is pro-

duced by esterification of PCP with mixtures of alkyl carboxylic acids,

the most predominant of which is lauric acid.  Technically pure L-PCP is &

brown oil having a specific gravity of 1.28 at room temperature.  It ia

soluble in non-polar solvents, oils, fats, waxes and plaaticizers, and in-

soluble in water and alcohols.

       Incjstrial production of PCP is a two-stage process.  In Che first

•tags,  isomers of tri- and tatrachlorophenols are formed when the reaction
temperature is about 105 C.  In the second stage, the temperature is pro-
gressively increased to 130 C co keep the reaction mixture molten, and the

tri- and tatracblorophenols are further chlorinated to fom PCP.  This re-

action  is not quantitative; tetrachlorophenols persist during the reaction

and are carried wich PC? during subsequent processing.  The result is that
II  PCP will be used as an abbreviation for pentachlor(.phenol i» this

                            Figure I
Physical properties of pentacfalorophenol and sodium p«ntachlorochenate
Structural Formula


Molecular Weight


Specific Gravity


Vapor Pressure

    g/100 g, 25 C

 C Cl OB
  6  5


Buf^colored crystal


 0.00015 (25 C)
Sodium Pentacblorophenate
C a CNa-B 0
 65     2

Buff-colored crystal

water <
Disc tone
Bthanol (95%)
Ethylena glycol

technical grade PCP contains from 4 Co 122 tetrachlorophenols.  These

tetr&chlorophencls are lit Cad on the product label* aa active ingredients.

One of the three possible tetrachlorophenoi isomars, 2,3,4,6-tetrachloro-

phenol, was registered by the Dow Chemical Company as Dowicide 6, a fungi-

cide; this chemical is no linger produced as a separate product.  It is,
however, listed as an active ingredient in SON PC? products.

       The elevated temperatures required for the second stage of PC?

production favor condensation of the tri- and tetracbloropbenols to fora
                   \   .  - '•'
hexa-, hepta-, and octa-chlorodibenzo-jv-diojcins (dioxins) and various

chlorinated dibencofurans (furans).  These iapurities are also carried

forward with PC? and will be discussed in greater detail in Section I.C.
              . :• .        .     ' '  '•.-> ..
           2.  Environmental Residues

       The amount of PC? produced in the United States, approximately
                  .  ' •       . ' -   , '•  * /
50,000,000 pounds/year, and its widespread use aa a pesticide strongly

indicate its potential as an environmental pollutant.  Possible sources

of PCP in the environment are:  runoff from manufacturing or wood preserving

processes, leaching or vaporization from preserved wood, and from its use
                •     •   .          .1      •
as a teraiticide and herbicide.  Although there is evidence that PCP could

be found ia the environment, the ambient monitoring programs for air, water.,

and soils do not routinely test for PCP.

                a.  Air
       The vapor pressure of PCP, 0.00017 torr at 20 C and 0.0031 torr

«t 50 C, suggests that it can volatilize froa treated surface* (torr:
pressure required to support 1 n of aercury at 0 C).  Cebefugl et al.

(1976) eaasured PCP vapors ia a closed test area in which wall paneling

was covered according to label instructions with a wood-protecting agent
                                           ;                       o
containing PCP.  Air samples were taken every day for 9 days at 25 C,
                         o              ••...,
and then for 6 days at 28 C.  Samples were taken in the corning, and the sta-
      period was not specified.  Gas chroaatographic eeuurtmenca showed
                                         £    , i             3
PCP measurements ranging froa 1 aicrograa/cubic aeter (ug/a ) on the
                     3      "  '          :   . J   • .   .'
first day to 160 ug/a on the fourth day.  There were wide fluctuations

in PCP concentrations during the course of the experiment.  In a sepa-

rate experiment, an increase in the saount of water vapor in the test

area decreased the PCP levels in the air.

       Bevenue et al. (1972) measured PCP in rain  *atar in Hawaii [2-284

parts per trillion (ppt)], in snow samples taken froa Mauna tai Summit

(14 ppt), and in lake water fed by this snow (10 ppt).  The authors did

not determine whether this airborne PCP was in gaseous fora or adsorbed

on dust particles.  Because of the heavy use of PCP in Hawaii to protect

wooden surfaces against termites, both physical forms are likely to occur

in the air.

       There is indirect evidence that PCP vapors  can be toxic.  An ar-

ticle that appeared in California Health in 1970 (Anon. "Pentachlorophcnol

Poisoning in tha Hosa") described the effects on the inhabitants of painting

interior wood paneling with PCP-containing paint.   House plants within the

ham died is 3 or 4 days.  Orer a  3-*onth  period, the housewife becne

progressively weaker while losim-  20  pound*.  She recovered after hoipitali-

zation.  Her coodieioo w«* diaga.~..ed  as  PC? poisoning by 4 California Scate

Department toxicologist.

     Ferguson in 1959 showed  that  PC? vapors were toxic to conifer

seedlings grown is greenhouse* on  wood flats whose  sideboards had been

treated with PC?.  Leiching of PCP into  the.soils of the flats was not

implicated since transfer of  these,soils to untreated flats supported

normal seedling growth.  He observed  toxic effects, to a lesser extent,

on seedlings in untreated flats, which be  attributed to air acveaent

fron treated to the untreated flats.  PC?  has been  found in the blood

and mine of workers in wood-preserving  factories;  in one report this

was attributed, in part, to respiratory  exposure (Casarett et al., 1969).

       The Aaerican Conference of  Goveraeent Industrial Hygieniats has

established a PC? Threshold Limit  Value-Time Weighted Average of C.5
eg/a  for a normal 8-hour workday  or  40-hour workweek, and a Threshold
Liait Value-Short Term Exposure Liait of 1.5 ag/a   for a 15-minute period.

                b.  Water

       PC? can be released into water as an effluent froa eauufacturing
or wood-preserving plants, by leaching frost treated wood exposed to rain,

and by runoff froa its uses ait a herbicide, fungicide, and molluscicide.

In spite of its wide production and variety of uses, PC? is not routinely

Bonitored by the National Watitr Monitoring Program, which eaasures contaai-

nants in rivers and streams in the Gaited States.  This program reported

fifteen measurements of POP along the California Aqueduct between 1974 and

1976.  There waa no sampling previous to 1974. Valuea reported from five

• itea along the Aqueduct ranged from 0.01 to 16.0 ug/liter PC? in whole water


       Buhler et al. (1973) meaaured PC? in sewage treatment plant ef-

fluent collected simultanaoualy from three Oregon citiea.  He reported

PC? levela between 1 and 4 parts per billion (ppb).  The same workers

found POP concentrations between 0.10 and 0.70 ppb in water sampled

from Che Willamette River, and 0.6 ppb in drinking water from a wacer

treatment plant.  In unpublished data, the EPA Drinking Water Program

has found PCP in the water of 86 of the 108 cities sampled; the mean

concentration of the positives waa 0.07 ug/liter.  The emdian concen-

tration for all citiea waa 0.051 ug/liter (Kutz, 1977).

       In 1976 Fountmine et a1. analysed samples from a stream which

originated in an are* containing several manufacturing plants, including

a wood-preserving installation.  The highest measurement of POP, 5,450

parts per million (ppm), waa in surface oil slicks; water samples ranged

from 0.082 to 10.5 ppm.  The authors noted that  thjsse PCP levels are not

necessarily due to discharge from the wood-preserving factory outlet into

the strecm.  The factory had been in business for 20 years.  Crocs

spillage of PCP occurred in the factory area, particularly in the early

yearx of operation, and thia PCP seeped into the ground.  There is,

therefore, the possibility that the PCP levels in the stre&a were due

to runoff from FCP-cont«minated soil, rather thao direct discharge from

.the factory.   Measureaanta of PCP in the factory discharge were not re-


                 c.  Soil*

        Becauaa the National Suila Monitoring Progran does not routinely

 analyze  soil  samples for PC?, ambient level* in soils are not available.

        In a aerie* of papers, Choi and Aoaune (1972, 1974a, 19745)  studied  the

 adsorption properties of POP on various soil types and under a variety

 of environmental conditions in the laboratory.  They found that PCP was

 adsorbed to some extent- on all soil types.  Soil acidity was a major fac-

 tor in determining the amount of PCP adsorbed; strongly acidic soils

 (pE 5) adsorbed more than less acid soils (pH 6).  There was less ad-

 sorption by weakly acidic or neutral soils.  However, increased organic

 matter or temperature or both increased PCP adsorption at the

 pH-vabies tested.  In a series of" experiments using different soil  types

 and ion  concentrations, the* author* demonstrated competition between

 inorganic ions and PCP for adsorption sites on soil colloids.  They con-

 cluded from their experiments that PCP is adsorbed on soil through  ion

 exchange reactions as well as molacular adsorption due to van dar Waals


       The fite of PCP in soils has been extensively studied.  The  pri-

 mary factor in the degradation of FCP in soils is microbiological ac-     "

 tivity;  other contributing factors include soil type, moisture content,

 and toaperature.   Kuwatsuka and Igaraahi (1975) demonstrated a positive

 correlation betveen the proportion of organic matter and the degradation

rat* of PCP in toils, observing that soils devoid of organic setter did

oof degrade PCP.  Idc et al. (1972) found that PCP did not degrade in steril-

ized soil saoples; Young and Carroll (1951) shoved Chat PCP decays most

rapidly in soil containing a large proportion of organic Better and at

temperatures which arc optimal for microbiological activity.  Kuvatsuka

and Igaraehi (1975) coopered the PCP degrading characteristics of upland

(i.e., eerated) soil with flooded (i.e.*, rice paddy) soil.  They found that

soil Bicroorgsnisms degraded PCP most rapidly when they were maintained in che

environment to which they ars adapted,  e.g. flooding upland soil and aerating

flooded soil decreased the rate of PCP  decay.  Using a gas chroatatograph

with an electron-capture detector the authors identified tri- and tetra-

chlorophenols as degradation prodacts of PCP end indicated that, at least

as a first step, PCP degrades by dachlorination.  Ide et al. (1972) found

cri- and tetrachloroanisoles as F-P degradation products.  Ibis indicated

that nethylation is also involvac in the degradation process.

       The persistence of PCP io soils  ranges between 21 days and 5 years,

depending primarily on the aicrobial population.  Uatanebe (1973) reported

complete degradation in paddy soil in 21 days*  Hetrick (1952) claimed

that PCP persisted for over 5 years in  an unspecified soil type.

                d.  Plants and A-nimals

                     i.  Plants

       There are no data svailab1^ on PCP residues in higher plants resulting

frora its use as a  pesticide.

                     ii. Anigala

       In 197'» Veroeer et al. reported  Che  death  of wildlife  caused

by application of Na-PCP to a rice  field  in Surinaa,  South America.

The Ha-PCP was applied at the rate  of 4 kg/hectare to control water

•nails which damaged young rice plants.   PCP residues were measured  in

auails (36.8 mean wet-weight ppa),  frog*  (8.1 nean wet-weight ppa),  fishes

(31.2, 41.6 and 59.4 a*an wet-vaight ppa  for three species),  and  snail kites,

a bird which feeds on water snails.  The  dead kites showed mean PCP  residues

of 11.25 _+_ 1.11 ppm in brain tissue, 45.56> 2.18 ppa in  liver, and  20.34 j^

1.25 ppa in the kidneys, all on a wet weight of tissue basis.   These PCP

levels were 53, 74, and 166 times greater,  respectively,  than those  in kites

collected frc-n an untreated man    The investigators attributed  the
                           ' ,  i          •      .
death of the kites from the trettea field to tteir feeding on water

snails containing PCP.  In addition, when other bird  species  which

frequented Che treated fields were  examined,  PCP  was  detected at  levels

ranging from 0.04 to 0.24 wet-weight ppa  in the liver and 0.08 to 0.49

wet-weight p?
•respectively.   As  a result of this incident,  the Aniaal and Plant Health

 Inspection Service of the Department of Agriculture (USDA)  instituted

 a nationwide survey of beef fat and liver for the presence  of the hesa-

 and octachlorodioxins found in PCP.  In the first group of  238 beef

 saaples collected  in seventeen States,  70 (29.42) shoved positive levels

 using Low resolution mass spectroaetry.  Of dies* 70 saaplea, 4 had  been

 confirmed using high resolution mass spectroaetry.  Detection levels
 were in fractional na nog rams/gram for both hexa- and octa-chlorodibenzo-£-

 dioxins.  The  determination of the signficance of these residues awaits

 the completion of  the survey and its subsequent statistical and aethodological


           e.   Humans

      PCP appears to be ubiquitous in human urine.  In 1970  Cranaer and

 Freal found PCP in urine at concentrations ranging from 2 to 11 ppb  in

 the general population.  In 1967 Bevenue et al. found PCP in the urine

 of 130 Hawaiians occupationally exposed to PCP at levels tanging from 0.03

 to 35.7 n»g/liter.   In the same study, PCP was found in the  urine of  all  but

 one of 117 unexpned subjects; these values varied from 0 to 0.44 mg/liter.

 In a recent study, preliminary data from a joint U.S. Public Health  Service -

 EPA effort disclosed that 86Z of the urine samples taken from subjects within

 the continental United States showed positive PCP values averaging 6.3 ppb,

 with a mxisua observed value of 193 ppb.  The limit of detection was 5  ppb

 (lutz et al.,  1978).

        Arsensult (1976) reported the mean blood serum level of PCP

 in twenty-one  workers in pressure treatment plants to be 1.05 ppn; there

war* about 0.1 ppa in Chi control* (unspecified).  Data for the general

popular ion arc not available.  In another study Shafick (1973) reported

PC? level* ranging fro* 12 Co 52 ppb in Che adipose tissue of eighteen

subjects who were not occupationally exposed to FCP.  Dougherty and Piotrovska

(1976) detected PC? in sesuinaJ. fluid frou seven sexually active san.

Levels detected averaged 50 ppb (range: 20-70 ppb).

       The source* and exposure route* of PC? residue* in toman tissues

have not been conclusively established.  Possible routes are inhalation

of vaporized PCP and ingestion of POP in water and food. In addition, PCP

forms as a metabolic product of hexachlorobenzene (HCB).  Lui and Sweeney

(1975) fed rat* 0.25Z HCB, which amounted to about 50 to 100 ag HCB daily.

Analysis of urine by gas-liquid chromatography showed a level of 12.5 ug/

ml PCP in a daily urine output of about 15 ml.  The analyses were con-

fined by gas-liquid chimatour*phy/«*ss spectroMtry.

       The Food and Drug Administration Market Basket Survey has esti-

mated the mount of pesticides in foodstuffs since 1965.  The estimates

are baaed on the average daily intake of an 18-year-old male, whose food

consumption is Che highest of any age group of either sex.   The stost recent

data fron this survey (Johnson and Hanske, 1977) are available froa food

saoples collected frosi August 1974 to July 1975.  PCP was assayed in twelve

food coccodities collected in twenty cities in the United States, so that

there were twenty •easuresienti for each commodity.  The results are

in Table 1.

TAILE 1. Psntac&loropbeaol la food coBBoditiec

Dairy Product*
Neat, Fi*h, aad Poultry
Grain aad Canal Product*

Leafy Vage tattle a
Laguae Vegetable*
Ro' t Vegetable*
Cardan Fruits
Oil*, fata, and Shortening
Sugar* and Adjunct*
Average, ppai Poaitive Coaooaitea Range , ppa
O.C-005 1 0.01
0.001 2 0.01-0.013
T .; 1 T
-..-.-• o
0.001 • 2 0.010
T i T
T ' , . 1 o.Oll
-''".,. • ' • • 0
0.006 5 0.01-0.04
, w : o
II  Data frost Johnson  and Kanaka (1977).
2j  Averages baaed on  twenty covpoaite »aaq>le*; trace residue* were  not included
    in calculating the average.  •
2_/  T - trace.
                             ,."... 1  ;••••••'.

       Tn«c« Low levels of Kf  in  food arc  «  eooscaac a»*fi» of

to boMM.  leawver, the connection  batmen tais mat* of esaosor* and

the presence of PCF la blood, urine,  aad  adipoaa cuaoa  is not claar.

    B.  Bataboliaa

         1.  Plant*

       As described aarliar, adcroorgaaissM ax* capable  of degrading

PCF ia soil*.  Certain bactarial atraiaa  bare been  iaolatad which are

capable of growing oa aadia contaiaiag Kf  (Itortoa  at ml., 1969) aad of

using PC? as tha «ole aoorca of caztoa (Chu aad Kirsch,  1972).  The
                                V •   ,-
•tcabolic Mchaaiau of  action  on PC? are, however, unknown.

Cartain speciea of funji, aoaw  of  which are present in wood, hare beea
                          . '• &
found to tolerate PCP.  Several of these  fungi depleted  PC? in treated
                            ^            ~
wood blocks, but loat their ability  to cause  wood decay  (Duncan and
                         .1      N  ' .
Dcverall, 1964).  As is the* ca*t with bacteria, awtabolic pathways
                     1 <-       •    •      t  .-- _ ~\  • '
of PC? degradation by fnagi b«v« not  beea identified.  There «re oo data

available oc the aetabolissi of  PCP fay higher  plants.

         2.  Animals

       There have been two studies on PC? •etabolisai in  aquatic anicals.

Each of these papers deaonatratied  the sasM  metabolic pathway.  In 1970

Eobnycshi ec al. reported that  the abort-necked clasi (Tapes ^hillippiaariua)

converts PC? to peatachloropheirrl  sulfate in  sea water.  The level of FCP -

in Che shellfish reached a plateau after  about 24 hours  of exposure.  After 50

hours, 802 of the PCP had been  converted  to tae sulfate  conjugate.  Th»

     detoxification eachaaisB wita  deawnetrated by Akitaka aad Kobayashi


(1975) in goldfiab calCured la fresa water g9"»*«ifliiif. *C*»  *n«tha

detoxification m*chaaia« 1« cosaon Co other aquatic anioals ia not
               an known to excreta Kf ia unchanged fora afcar exposure
by various routaa.  In  1974 Ahlborg at al. adaumstared   C-FCP orally

and intrapariroiaally to rata acd aica (10 to 25 mt/kf).  afsroximwtely
40Z vaa axcratad at PCP ia tba urina.    C-tetrachloroaydraauiaone vaa
also detected at levels equal to 52 of  the excreted radioactivity ia

rats, aed 242 of the activity ia mica. . The authors also  found PCP and

tetrachlorohydroquinone in  the urine of workers occupationally exposed
                                          :• ? : •     14
to FCP.  Larscn et al. (1972) orally administered   C-PCP to rats, and

found that 502 of the radioactivity waa excreted in the urine in 24 hours, 662

wss excreted in 10 days; between 9.2 and  13.22 waa excreted in the feces.  Tissue
analyses 40 hours after exposure showed small amounts of   C activity ia

the adrenal glaods, blood,  brain,  fat, heart, kidneys, liver, lungs, muscles,

ovaries, spleen, stomach and intestine, and taatea.  Highest levels were

found in liver (0.232 of administered radioactivity), kidney (0.182), and

blood (0.15Z).  In blood, 992 of the radioactivity detected was in the serum.

       L*r»en et al. (1972) postulated  a  two-component urinary excretion

pattern that has s 10-hour  half-life for  the first 2 days, followed by a

102-day half-life.  In 1969 Casarett «t al. me asurad FCP  concentrations

in the urine of two subjects after respiratory exposure And determined    -

chat after 24 hours, the half-life is approximately 10 hours.  They found

a blood-Co-urine FCP ratio  of between 1.5 and 2.5  in occupetionally ex-

posed individuals.  Ac about 10 ppa, PCP ia blood plasm reached a pla-

ted* while urine levels continued to increase.  They postulated that PCP

binds to plasaa proteia, aad in subsequently distributed to the tissues.

The work of Lanea et al. (1973) seem to confirn this.

       Taahiro at al. (1970) d
     6             4
      D1benzo-£-d1ox1n                           Dlbwzofuran
     FIGURE 2.  Structure of dfoxin and furan
the tetra-, penta-, hexa-, hepta-, and octa-dibenzofurans (Buser and
Bosshardt, 1976).  The amount of then chemicals 1n PCP varies with each
industrial batch produced, even when produced by the sane nnufacturer.
Analytical methods for wasuring Individual Isomers require sophisticated
and expensive analytical instrumentation, and standards for the isomers  are
not generally available.  Until recently, both the dioxins and furans in
PCP have been raaasured as 1someric groups.  Table 2 shows the composition
of typical commercial PCP.
       The physical, chemical, and toxicological properties of indi-
vidual dioxins and furans are, with one exception, relatively unknown.
The exception is 2,3,7,8-tetr3chlorod1benzo-j£-dioxin. (TCDD), which has
been stown to be one of the most toxic compounds knovn.  TCDD is not in PCP at a limit of detection less than 0.05 ppm (Johnson et al.,
1973).  However, the dioxins  in PCP have been shown by Johnson et al.

           tUSLL 2.  Composition of cooMrcial  pantachlorophgnol
It tradi loropbcnol
Cblorinatad Phcnoxyphcao I*
Dowieide 7
< 0.1Z
< 6.2Z
4 ppa
125 pp.
2500 ppa
30 ppm
80 ppa
80 pp*
Dowieide EC-?
89. 8 S
< 0.1%
1.0 ppa
6.5 ppa
15.0 ppa
< 1 PP»
1.8 ppa
< 1 ppa
II Data froo Dow Cheaical Coapitoy.
2/ Total gra«cw th«a lOOt bccicuse nusbcrs  ar«  rounded  off.

 (1973)  to cause cblorecne in rabbits and edeaa in chicks.   The only data

 available coap axing the toric effect* of individual diozia isoaers were

 reported by He Conn*1 tt ml. (1977),  and these are shown in Table 3.

 These data indicate thac the hexa- and hepta-dioxin isoaers tested vere

 less toxic than TCDD in sdce and (oinea pigs; haeerer, they would be

 classified as Category I poisons (oral IJ)-50 less than 50 ag/kg).
      TABLE 3.  Single oral LD-50-30 of dioxin isoaes





Guinea Pigs'


1,2,3,4,6,7,8-BeCDD          7180
TCDD                         2                    283.7
I/  Data froa HcCoanell et al. (1977).
2j  Estiaaced range represent* variability aaoog replicates.
3/  TCDD values are shown for coaparative purposes.
       Firestone (1977) detected PC?, individual bexa- and bepta-dioxin

isoosrs, aod octa-dioxin in asaples of coaatrcial gelatin procurrsd fzoa

supsraarbets and in bulk.  Gelatin is produced froa pork skioe and catcle

bones and bides, which My be preserved with PCP during processing both in

thia country aad abroad.  According  to Firestone, the annual consumption

of gelatin in the United State*  is 57 million pound* of doasstic production

and 13 million pounda of imports.

     Higheat level* of PCP aad total dioxina were found in bulk gelatin

that ma imported from Mexico and produced by a single company. Three

meaaurements of thia gelatin averaged 6.4 pom of PCP, and aix asaaurcments

averaged 26.8 ppb of total dioxina.  In contrast, bulk domestic porkskin

gelatin had no PCP and 0.1 ppb of total dioxina (octadioxins) in one of two

•ample •eaaurements.  Three  conauaer packages of unflavored gelatin purchased

in a supermarket showed 0.2, 0.8, and 3.6 ppb of total dioxins.

     0.   Regiatered Daea and Production

       Pentachlorophenol aad it* derivative* axe among the coat ver-

satile peetisidea now in uae in  the  Oaited States.  This versatility is

due first to their efficacy  against  a wide variety of pests (bac-

teria, yciac, slime molds, algra, fungi,  plants, insects, snails), and

second to their solubility in both organic solvents and water.  Thus,

PCP can be applied to a wide spectrun of  materials.  In various concentrations,

solvents, and formulationa,  pentachlorophenola are registered for use on

beans (for replanting purposes only), wood, leather, burlap, sasonry,

cordage, paints, patroleua,  pulp and paper mill systems, weeds on seed

crops (preharvost desiccant), secondary oil recovery injection waters, and

corasarcial and industrial water cooling towers and evaporation condensers


       Approximately 50,000,000 pound* of PC? is produced annually in the

Qaiccd States.  Ihf major use of PC? in the Obi ted States is an a wood

preservative.  This use COBSUMS approximately 802 of ail PC? produced.

About 111 of the PC? produced is formulated as Ma-PC? and used in the

produc?ioa of pressed and insulation board, and in cooling town.  Approxi-

mately 6Z is used in pulp and paper stills to control the growth of slime-

forming bacteria and fungi in paper production; 3Z is used for fan

treatment of fence posts, home .protection against termites, and as a

herbicide and pre-hazvest desiccant.     .    .       ,

       The number of federally-registered products coutainitg PC? and

the number of registrants is given in Table 4.  In addition, there are 75

State-registered products formulated by 60 registrants.
        TAJL£ 4.  Federal retiatration of pentactCorophenot"^

Ho. Products
No. Registrants
; .. • '

I/  Data  from computerized Eagistration Division  files.

E«  Regulatory History

       Technical PCP was  registered  for  us*  as  a wood  preservative in

1943 by Dow Cheaical Company and  Monsanto Agricultural Products Co«pany.

Subsequently, registrations were  granted for a  vide variety of uses,

including agricultural uses such .as  pre- or  postharvest weed  treatment

and prebarvest dessication of  seed crops.  Dhtil 1970, regulatory

actions against PCP were  confined to these kinds of uses.  For example,

in the "USDA Sunasary of Registered Agricultural Pesticide  Uses" issued

on August 31, 1968, PCP was registered as a  weed killer on alfalfa, cot-

ton, pineapples, and sugarcane.   These registrations were  car xlied by

Pesticide Regulation (PR) Notice* 69-4 (February 1, 1969) and 70-4

(February 26, 1970) when  the concept of  zero tolerance was abandoned by

tha Department of Agriculture.  Currently, PC?  is registered  for agri-

cultural u?e only as a seed treatment for nonfood uses on beans, alfalfa,

clover, lespcdeza, and vetch.

       On September 28, 1970,  US DA published PR Notice 70-22.  Although

PCP was oot eentioned by  name, the Hotice stated "Appropriate regulatory

action will be taken under the provisions of the Act (FXfBA)  if these

chlorodioxins are found in any economic  poison." The  notice was directed

toward tha presence of 2,3,7,8-tetrachlorodibenzo-jj-dioxin (TCDD) in the

herbicides 2,4,5-trichlorophenoxyacetic  acid and silvex; PC?  and ics

chlorodiozina wara not eectioeed.  The Dow Chenical Cctipacy, hcvaver,

interpreted the Hotice to apply to PCP and took action to reduce chlorodioxin

levels in its technical PCP.

      At the ti-«» 'die Notice was issued, Methodologies for the analysis

of diesiiia in PCP were not totally reliable.  Therefore, there was

disagreeaent within the industry on the actual level* of dioxins in

their products.  There were no tozicplogical studies on PCP dioxins, and

toxic effects vere inferred froa chloracne and chick edema effects of

conaercial PC?.  These same effects are caused by TCDD.  In the absence

of such evidence, regulatory action oc dioxin levels in PC? was not

possible.  This situation continued until 1974, when research

involving purified PCP (i.e., relatively  free of dioxins), in contrast

to commercial PC?, began to appear in the literature..

II. Suaaa.v of Scientific Evidence Relating to Reouttable Presumption

     A.   Reproductive and Fetotpxic Effects in Mammalian Species

       4C CFS 162.1lU)(3)(ii)(B) provides that "a.  rebuttable presump-

tion shall arise  if a pesticide's iagredient(s)...  Produces any other

chronic or delayed toxic effect in test animals at  any dosage up to  a

level, as dete rained by the Administrator, which  is substantially higher

than chat to which humans can reasonably  be anticipated  to b< exposed,

taking into account ample margins of safety."  This section reflects con-

cern thrtt chronic exposure to chemicals may result  in  injury  to the  re-

productive system and/or the fetus and provides that a  rebuttable pre-

sumption  .hall arise if chronic chemical  exposure  in test anima1* pro-

duces such results, and if human  exposure to the  chemicals exceed an

ample margin of  safety.

       In the studies summarized below, fatotoxic and  teracogenic effects

have be*n reported in rats exposed to purified and commercial grade

PCP.  These same effects were obsiirved in rats exposed  to a mixture

of two unspecified isomers of HCD1).  Specifically, exposure to PCP

and these HCDD isomers .resulted in statistically significant  increases

in the incidence of skeletal and noft tissue anomalies, growth-re:arded

fecuses and of embryonic resorption in the  lifters of  treated dams.

           1.  Fetotoxicity

                a.  Studies with TCP

       Schwetz et al. (1974) studied the effects of purified  and com-

mercial grade PC? on rat embryonal, and fetal development.  The Composi-

tions of the two types of PCP are given in table 5.  Dosages  of ;, 15,

30, and 50 mg/kg/day of both PCP types w«re administered by gavage on

gestation days 6 through 15 inclusive.  Their results,  shown  in  able 6,

may be summarized as follows:  both purified and commercial PCP caused

statistically significant increases in fetal resorptions at the two higher

doses, as veil as among litters exposed to  15 mg/kg/day of conmer-

cial PCP.  Specifically, the resorption rate ranged from 27.1* (64/235) to

lOOZ (229/229) in the two highest (commercial and purified) doie groups, com-

pared to A.22 (15/358) in the control group.  At 30 and 50 mg/Kj day,

purified PCP had a sore pronounced effect than commercial PCP.  .'-'or example,

at 50 Bg/kg/day, purified PCP caused 100Z fetal resorbtion, while commercial

TABLZ S.  Composition of pentachlorophenol material* used by Schweti et «1.  (1974)
                                   Coaaarcial Grade        Purified

identification                  Lot Ho. MW06210-9822A     fttf. Ho.  27-91-1

Phenolics, Z

   Pentacalorophenol                      88.4               98+

   Tecrachlorophanol                      4.4                (K27

   Tricblorophenol                        < 0.1              0.05

   Higher Chlorinated                     6.2                0.5
   Fbeooxy phenols
Moophenolics, ppn

   Di beozo -g^diat i as

      2,3,7,8-tetrachlorodibeozo-         < 0.05             < 0.05
      H«x«chlorodiben2o-2^-dioxin          -4                   < 0.5

      H«ptachlorodibenzo-j£-tiioxin          125                 < 0.5

      Octachlorodibanzo-£-ttioxin           2500                < 1^0


      Uexachlorodibenzofurmn               30                  < 0.5

      BeptAcblorodibenzofurui              80                  < 0.5

      Oct«chlorodibenzofur«n               80-                  <^ 0.5
JY  Deterainsd by gas-liquid  chromatography.
II  Determined by use of  an LK2  9000  gas  chrosuitograph-mass  spectrometer.

TABLE 6.  Effect  of pantachlorophenol on the incidence of fetal resorptions and

Test Material
sod Dose,
»S/ kg/day
Vehicle Control
> I/





the s«:x ratio of survivors






53. 1



; Fe tunes















Sex Ratio
M : F

50 50

50 50

52 48

60 40
79 21

48 52
50 50
83 17

_!_/  Adapted frwa Schwetz  et  al.  (1974)
y  2.0 nl/kjt body weight corn oil per  day.
_3_/  Doiages cdninistered  in  2.0 ml corn oil/kg body weight.
kj  Equivalent to 5.0 sig/kg/day ptwified PCP.
_5_/  Indicates values significantly different froa control
    values by the binomial expansion test,  p < 0.05.
_6_/  Equivalent to 30.0 ag/kg/day purified PCP.

KT canoed 5AZ resorptioa.  Ac 30 (purified) «ad 50 (couejsrcial)

ag/kg/day, there *«re statistically significant difference* ia the

sex ratio of surviving fetuses; Mica were heavily predonisMt,

Sebvau et al. fouad that adadoistration of FCP daring early

orgaoogeaesis (days 8 through 11 of geatation) had aon prooouacad

tfftetc oa fatal raorptioa than did its adaiaiatxatioa daring lata

orj«no|«n«iis (days 12 through IS) (Table 7).

       The no-effect dote for fatal rasorptioaa was 5.8 cosjuarcial

grade PCF/kg/day aod 15 ag purified PC?/kg/day.  ttaasurasjents were also

taken on  fetal body weight and crovn-rvp length, both of which decreased

with the  increase in dosage.  The no-effect dose for these parameters

was 15 *g conercial grade or purified KP/kg/day.
                                       1*       .

       Larsen et al.  (1975)  fed  60 Mg   C-PCP/kg body weight to pregnant

Charles River CD strain  rats on  day  15 of gestation;  They detected neg-

                    I*            .  .  t
ligible amounts of    C-PCP in  the placentas and fetuses up to 32 hours

•fter dosage.  This  indicated  that the aaount  of PC? that passes through

the placental barrier on day 15  is negligible.  la  a separate experiment that

used unlabeled KT?  and was reported  in the saaw paper, single oral doses

of 60 ag/kg adainistered to  separste groups of aniuls on days 6, 9,  10,

11, 12, or 13 of gestation had no statistically significant effect on

tha rate of reoorpcioa of the  teat anisuls as  cosiparttd to control*.

However, statistically significant reductions  in fetal weight were

reported in days 9  and 10.

TAIL! 7.  Effect of adaiaiatrai:ion of  peatachloropbanol auriaa. early or late

Teat Material
and Dose,
on the incidence of fetal resorptioea «
ratio of offspring

Aaoaii Fetuaes Avont Litters
t Bo. I Bo.
•d on the sax

Sex Batio
M : f
Vehicle Control
Coanercial 34.7

Purified 30.0
7.6 13/172 53.3 8/15

3/ 3/
45.3 105/232" 94.7 18/19"
3/ 3/
91il 163/179" 100.0 l6/lo"
53 47

55 45

62 38
Vehicle Control
Pent ach loropoenol
Coocrcial 34.7 ;
Purified 30.0
4.2 11/259 40.9 9/22

6.1 13/213 58.8 10/17
4.5 11/244 45.0 9/20
46 54

52 40
49 51
II  Adapted  from Scteratz *c al.  (1974).
2/  Equivalent  to  30.0 mf/kf/day purified PCP.
T/  Values significantly diffartat  fro* control values by tha
    binooial axpancion case, p < 0.05.

       •iakla (1973) reported ea the  fstotosic effecta ef PC?  ia cha

G»Um Syriaa baas* tar.  Afcar doaea of  1.25. 2.5. 5. 10, and 20  at/kg

war* c£ai&iLater«d by gavaga oa day* 6 through 10 of gestation, ha retorted

•a differoecaa bacvaen control end CMC aaiaala in cha«a aarsjaarers:

••canal barfy weight, fatal miffec, liccar aixa, aad Mater of laaorpciow.

Xaeraaaaa coxieicy vaa aocarf at cka fe*o aichaat aoaaa, tac tkaaa iacraaaas

«Jbra "miaiatl ia o«kar."  »a aataor aCacad that PC? vu foaad  la aacaccabla

aaooau (oaapacifiad) in eba oacraacad  aniaals a* wall as in chair diac.

       Fabric (1978), in a §ta4y Co ba  daacriaad in asra aacail  ia

Section III. B.. obaarrad oacraaaaa in  littar aixa afcar iajaccion

of SO aod 100 agna PCF/kg body vaifhc into cba paritonaal cavity of

prcgaaoc aica ac day can of gaacacioo.  Control mca, oa tba avaraga.

arodncad 6.4 fatuaac/doB.  Littar aixa  vaa radwcad at cha 50 at/kg

doeo to 3.67 fecaaM/daB, aad co 3.92 facvaaa/dav ac cha 100 ag/kg doaa.

PC? vac tdai.nistared in a 102 solution  of  diaathylforpaadda; a vaaicla

control vas not raportad.  Littar siza  calotlationa incladad daaa chat

had no litters.

       The Schwacs at al. study citad earlier eftablishea that iagettioo

of PCP by pregnant rats during organoganasis produces lethal and
                                               •"•  '\
toxic effects sach as fetal resorpcion  and reduced body sixe.  Coapereble  • **

effects were DOC observed when larger but  single doses were adadaistered

to rata during org&eeserasis (Larsen, 1975), nor whan single doses

vcrc ciaiaistored to hesators (Biakle.  1973).

Fable 8.    Effect of traatiaant with chlorinated iJibenco-p-J ioxin on  aatarnal  and fatal body aaasureaMBta ami  th«
incidence of fetal retorption—

M fatal body
2/ Ho. Maternal waijfhtja^in^s^ 4/
lost Compound littara Deya 6-11 Day a 13-21 Deyt 6-21 weight if
Control 30 36 *. 2 101 *_ 6 137^8 3.68 *. 0.05
dioxin (4)
0.1 ug/kg/day 19 28 * 2 102 + 5 130 + 5 5.73 + 0.04
1 ug/kg/day 19 27 * 3.. 99 7 5 126 * 6 3.93 * 0.16..
10 ug/kg/day 19 22 * 3y/ 97 + 3.. 119 +• 6,. 3.12 * 0.05-^
100 ug/kg/day 19 6*^2^ 13 _» 7-^ 19^9^ 3.65 7 0.28^
Oc t «ch 1 or od I ben«o-p_-
dioxin (5)
100 «£/kg/day 12 32 * 2 100 * 8 131 * 7 3.73 + 0.09
500 aig/kg/day 17 35 _* 3 115 ± 4 150 _» 5 5.69 7 0.05
I/ Adapted froa Schvets at al. (1973).
?/ Hexachlorodibenco-j^-diozin aaaipla: purity " >99X; two unapacifiad iaoaMra


~4/ Fatal Beaorptioa, t
runp length (M 5J
mm Populatioa
44.5 *.

43.8 *
45.7 7
42.6 7
35.2 *,

43.6 4
44.5 T

in ratio
0.1 7(22/337)

0.1 5(10/217)
0.3,, 9(20/218)

0.4 8(11/131)
0-2 5(9/199)




89:11. All scaplei adotiniatared on daya 6-15 of gestation aa a corn oil. -acetone
(9:1) aotution. Octachlorodibenio-j>-dioxin aaatplaa: purity • 98.862.
)/ Mean _*_ etandard error for various gaatation tinea.
£/ Mean of litter cs«n« • atkndard arror.
f/ % (number raaorptiona/nmbair implantation*).
?/ X (nuBber littara with at leaat one raaorption/nuaiber littera).
F/ Significantly different froa control by an analyaia of varianca and Tukey'a
or the 2x2 contingency tabla (reaoiptiona) , p < 0,05.



               b.   ltK*)M9 VJtk
       SctMts at «l. (1973) atdaiaia tared parifiad k*xacaloro-£-«ib«aco-

dioxiaa (ICSD) (two eaapecified iaoaars) cad oc tackier o-g-dioxia (OCSO)

by gawaga ^ •**•«*»* Sprajoe-Bawiey rat* OB 4ays 6 chroafB 13 of (••ca-

tion.  DCMMC were 0.1. 1, 10. or 100 eg/kg/day 1CDO aad 100 or 500 a*/

kg/day OCOD.

       The result* of taeae st»diaa en •hov» ia Ta*l« f.  For KCDO,

tb«r« were statistically sicaifieamt iacr*a*«a over eootrols ia fatal

r««orptiooa at th« 10 and 100 af/kg/das? doa«a. aa wtll aa oacr*aa«> ia

fetal body waighc cod fetal crowa-ruBp laagta.  Ia contract, OCDD at both

dose lava Is (100 azta 500 aig/ kg/day) prodocod ao fatal rcaorptioaa or othar

effaces accept for aa increase in  the iacideace of subcataneous edesu at

the hieh dose leval.

       The EO)D need ia this experiaeat vaa reported by the authors to

have a purity in excess of 99Z, aad to consist of two iaoaors ia the

ratio 89:11.  The presence of HCDD in PC? aad the low BCDD doses

producing fetotoxic effects in pregnant rats strongly suggests taat ex-

posure to HCDD via exposure to PC? caa cause chronic effects as defined

in 40 CPE 162.11(a)(3)(ii)(B).

          2.  Teratology

                *•  Studies with PC?

       Schwetz at al. (1974*) also investigated the teratoganic effects

of PC? oa rats.  In this study they observed fetal anoswlies produced by

oral adnioistratioa (gssrege) of 5.8, 15, 34.7, and 50 ag/kg/day of c cause r-

cial grade PCP, and 5, 15, and 30  Bg/kg/day of purified PC?.  In one

experiment, they administered these amounts of PCP during days 6 through

ef pantacfeloropfeaool on tba
of fetal accBalies
Peatachloropbeaol (sx/ki/day)
Ka. of kitten 33
Stabcata»eou« Idea* 18
Dilated Ureter* 0
Bo. of Litters 31
Skull (delayed ossification) 19
> - *
Laa&ar Sr-'ars • 13
Elba (sap«CTs&Qtrary, 1 tartar, 0
or ftued)
Vertebrss (saparaosMrary, 19
* b sorea! shape, delayed
ossification, sussing or
uafiuad canters of ossi-
Stsmsbre* ( tcps rawer ary , 16
delayed or unrusad centers
of ossification, fused or
Cooaercial Grade
5.8 15 34.7 50
18 16 19 13
Fercant of Litters
27 27 27
11 5


axa on cna utciaanca 01 zacai sjaoMiu
Days 8-11 of Cantatioo Days
12-15 of

86. of Lit tar*
Subcutsnaous cdeaa
80. of Litters
ffthicl* Coamrcial Purifiad fahiela O
34.7 30
Coatrol •kykx/dar •ir/kc/day CoaCrol at/kayday
15 17 4 22 17
Parcaat of Littara Affactad
2/ 2/
7 82" 100~ 59
15 18 6 22,
Parcaat of. Lit tars
                                         27       2/
                                      1QO      100

                                         2/       37
                                      100~     100


Skull (dalcyad             33         33        17        36          4.         70~

Ribs (saptrauaarary         0
or fuaad)

Vertebraa (superauaarary,  27
abnoraal shape, dalayad
oaeif icacioo, fucad,
•iwing or ua fused
cantata of ossification)

Slaroabraa (dalayad or     47         VT     100~       50
ua fuaad caatars of
ossification, fuasd
or stages r«l)
JY /^riiaietarssd po  in  corn oil during aarly or laca organo(aa«
15 of gescatioa; statistically  nigaificaat iacr*es«*  in skeletal defects

of til* rib*, steraebree cad vertebrae war* observed ia tetla  treacaaat group*

(Table 9).  Xa a aeceai experieunt,  they gevo  30.0 (purified) aad 34.7

(conBareial grada) Kg/kg/day rC?  oo  day* 8 through 11 of gestation to one

group of eaisMla, *ad oa day* 11  through 15 to • second group; statistically

significant iaer*a**s ia abaorsttl staraebrae sed skulls were observed ia

eaiaals treated with purified Kf and abooraal steraebrae ia aaiaals

treated with eosiBMreial r<7 (Table 10).

       These results establish  that  the higher doses  of PC? produce

fetal aaoMlies ia the rat.  At the  30 «g/kg/day dose the effects

of purified PC? were sore pronounced than  tbose of the equivalsnt of coaaer-

cial grade POP.

                b.  Stuaiea with  Dio«ias

       Ia the 1973 paper cited  above, Scbwetx  et al.  reported tsrato-

geaic effects fooa the dioxins  found ia PCP.   they adxiaistercd doses of

0*1, 1, 10, and 100 ug HGDD/kg/day to pregnant Sprague-Dawley rat* oa days

6 through 15 of gestation.  Thfy  found statistically  sigsificaac increases over

the controls ia all of the terstogenic parameter* observed at 100 ug/kg.

For «aae?l«, cleft pelete wee observed in  471  (6/17)  of tht fetuses

exposed to HCDD, coopered to none (0/156)  io the coot roll; 121 (2/17) of

rhe treeted fetoseo had dilated renal pelvis compared to 0.6Z (1/56) in

tbe ccntrols; and J1Z (5/16) oi: the  treated fetuses had abnorxal verte-

brae cospar*d to 6X (9/158) in  the controls.   Subcutaneous cios* was

o6aorvcd &t all doeas except 0..1  ug/kg/dey, which was coasidered tfae no-

effect dose.  In contrast, OCD1) did  not cease  teratogenicity at 100

c$/kg/day; doses of 500 ns/kg/ciay caused stibcutaneous cdeea, trat no other



       Table 11 MaatriMi the reeults of treacsjeat vick ICDO.

       3«  fcnoeure Analysis

       In order to attenine whether • »res«ption sboald b« issued

based oa reproductive and fatotoxic effects, pursuant to Section

162.11(a)(3)(ii)(B). the Agency suet dctersdae whether or not aa

anpla margin of aafeey exists between Cke level* of Kf which produce

reproductive and fetotoxic efface*, aod the laral(«) to •bica cfae popole-

^ioa at tick (woveo of chile-beari>| age) eaa reasonably be amticipetad

to be expoaed.

       This section orescats eacisutes of dietary, inhalatioa aod derail

exposure to PCP eod HCDD oo a "worst case" basis.  These estimate* art o»»«a

oa the exposure of a pregnant woaan in the BOB* and at work at aiajor PCP and

IU-PCP use work sites, i.e., wood preaerring plants, cooling towers, tanneries,

and construction sites,  this approach to PCP exposure analysis is taken because

of the fetotoxic end taratogenic effects of PC? described in Section II.A.I and

II.A.2 and because of the continued •oveneoc of woawn into all areas of the labor

force.  Estimates are coopuced on Che basis of 60 kg prignaoc wooan, 100* absorp-

tion via dietary and inhalation exposure, and 102 adsorption via deraal contact

for both PCP and tts-PCP.  lharr Is no data available on denutl absorption of pregnant woven; the 10Z estimate is baaed oo the penetration v*lu«

of 7-151 of several chlorinated hydrocarbons, reported by Hcibach and
Folds*n (1974).  A noraal breathing rate is defined as 1.8 n /hour at work,
and 1.0 u /hour in the bone*

       Isnalat^en of water vapor cootailing He-PC? ic an exposure route

for workers in industrial cooling towers, paper palp Bills end tanneries.

Appendix I shews the calculations used to derive estimate? of PCP in

water vapors at these sites.

TAUI£ 11.  Hffect of treatment with hexachlorodibenzo-p-dioain on the incidence
of fetal flncnu
Incidence of Annual ies After Treatment on Days 6-15 of Gestation
Cleft Palate
Dilated Renal Pelvis
Subcutaneous Bdesa
Split Vertebral
Sp 1 i t S temebrae
Delayed Ossification
of Sternebrae

L -.

0.1 uj/ky/day
1 (1/104)
5 (1/19)
0 (0/104)
0 (0/19)
6 (6/104)
12 (6/19)
2 (2/101)
5 (1/19)
1 (1/103)
5 (1/19)
28 (29/103)
74 (14/19)
1 ugAq/day
0 (0/99)
0 (0/19)
2 (2/99) >-
5 (1/19)
35 (54/99)
100 (19/19)
1 (1/99)
6 (1/18)
2 (2/99)
11 (2/18)
12 (12/99)
50 (9/18)
10 u^/kq/day
0 (0/86)
0 (0/18)
6 (5/86)
17 (3/18)
100 (86/86)
100 (18/18)
7 (6/86)
29 (5/17)
2 (2/86)
12 (2/17)
34 (29/86)
71 (12/17)
100 uq/kq/day
47 (8/17)
73 (8/11)
12 (2/17)
18 (2/11)
100 (17/17)
100 (11/11)
31 (5/16)
56 J5/9)
31 (5/16)
56 (5/9)
56 (9/16)
56 (5/9)
j/  Adapted frcro Sclwatz et al. (1973).
2/  Incidence anony fetal population: * (rxsiix>r of affected  fetuses/mniier
    fetuses examined).             *
3/  Incidence cnvong litters: % (ntf^«r of affected iittbrs/nurber litters
    S iyn if leant ly different (van control by 2 x 2 contingency  table,  p < 0.05.


       Exposure to BCDD is developed using the same base* as for PCP.  In

addition these assumptions are made:  that the HCDD content of most technical

PC? and Na-PCP in the market place is 4 ppm (Table 2) and that assimilation

of HCDD is identical to that of PCP and Ha-PCP.  Using these assumptions,
exposure -3 BCDD is equal to the exposure to PCP times the factor 4 X  10

(4 ppm).

            a.  Dietary Exposure

       Although PCP has no registered uses on any food commodity,

PCP residues have been measured in foodstuffs (Table 1), and therefore

there is exposure to PCP in the diet. Using the data in Table 1 and the

average daily intake of the commodities which have been found to contain

PCP, it is possible to obtain an estimate of PCP exposure from foodstuffs.

Table 12 displays these results,' computed for average and •«••»•?««• PCP  intake

per day.  For a 60 kg pregnant woman, the intake would be:

     0.0015 mg/day/60 " O.C2S ug/kg/day average,

     or 0.0181 mg/kg/day/£G » 0.302 ug/kg/day maximum.

For HCDD, intake would be:

        -6                                -6
0.1 X 10   ug/kg/day average, or 1.21 X 10   ug/kg/day maximum.

             b.  Dermal Exposure

                i. Homeowners

       PCP is sold in retail stores for treatment of wood to prevent

rot and decay in boats, masonry, fences, and other sites.'  Common directions

call for tvo coats of 52 PCP in mineral oil or a 3 to 30 minute soak.

Assuming that a 60 kg applicator spills enough of the solution to cover

one hand (10 ml or about 10 grams), the exposure would be:

     (10 gms x 0.05 x O.D/60 - 0.833 mg/kg/day.
For ECDD, exposure would be 3.33 X 10   og/kg/day.

Table 12.  Estimated Average and Maximum Daily Intake of PCP in the Diet

                          I/         2/
Dairy Products
Grains and
Root Vegetables
Sugars and
kg /day
PCP Residue
Max iraura
PCP Residue
wg /kg
PCP Intake
f~~ ' ,
PCP Intake
  1  From Agricultural Handbook No.  62, August 1961, p. 42

  2  From Table 1 (Johnson and Manske, 1977)

               ii. Construction Barken

       PCF-treated wood i» used Co construct platforms, fences, porches,

aad other structures.  It is estimated that 6 months after treatment, PC?

will be present on the wood surface at about 0.5 mg/ square foot (Koppers

Chemical Company, 1978).  Denial exposure occurs if workers handle wood

without wearing gloves.  Assuming that die worker actually handles wood

40 times during an 8-hour period, aad that the ana of the hands averages

0.23 sq. ft., then exposure would be:

     (40 x 0.5 mg/sq.ft. x 0.25 sq.ft./operation x O.D/60 - 8.3 ug/kg/aay.
       For HCDD, exposure would be 33.2 X 10   ug/kg/day.

              iii.  Cooling Tower Workers

       Na-PCP is used to control the growth of algae, bacteria and

fungi in water cooling systems.  Formulations typically contain SOX

Na-PCP, and are added to the system at concentrations of 60 ppm for

initial cleaning, then reduced to 30 ppa to maintain control.  A worker

could be exposed dermally to 100 al of cooling water containing

80* x 60 ppn formulation, or 48 ppm (48 mg/liter), of Na-?CP.  (Shamaiengar,

1978).  Exposure would then be:

     (48 mg/1 x 0.1 liter x O.D/60 kg - 0.008 mg/kg/aay.

       During routine maintenance, this would drop to 0.004 ng
Na-PCP/kg/day.  For HCDD, exposure would be 0.032 I 10   «g/kg/day for
initial cleaning, and 0.016 X 10   lag/kg/day during routine maintenance.

          iv.  Paper/Pulp Mill Workers

       To control slime, algae and bacteria, Na-PCP is added to the

paper-pulp slurry during the manufacturing process.  A typical product

contains 452 active ingredients of which 252 is Na-PCP.  The concentration

of the product used is 450 ppa, of which 113 ppa (113 mg/1) is Na-PCP.

During tfce process, copies of pulp •lurry are  taken periodically.   If

• worker Cakes samples hourly (8  i:iaes/day) and wees one hand with  10 ml

of the slurry (International Paper Company, 1978), the exposure voula be:

       (8 z 0.01 liter x  113  mg/JL z O.D/60 kg •

                     0.015 mg PCP/kg/day

For HCDO, exposure would  be 0.060 Z 10   af/kg/day.

           v.  Tannery Workers

       A typical product  used to  control growth of sliae and fungi  contains

12.92 PCP.  With a use concentration of 1:4,000, the solution would contain

1 gin/4,000 gn 'rater or 250 ppn of product.  If  a worker were exposed during

normal operations, she'could demally receive about 1400 ml of solution daily

on her exposed arms and neck (Shasiaiengar, 1978). Exposure here would be:

       (1.4 liter x 250 otg/1 x 0.129 z O.D/61  kg -

                0.075 mg  Na-PCP/kg/day

                       !             -6
For HCDD, exposure would  be 0.3 X 10   «g/kg/day.

          vi.  Workers ia Pressure-Treatment Planes

       Although data id not available on dermal exposure at these sices,

it can be assuaed that this exposure is at least equal to exposure  at

construction sites.  Freshly treated wood can be expected to contain

teore PC? on its surface than wood used at construction sites, the latter

having been subjected to weathering, i.e., leaching, vaporization, etc.,

in the interval between pressure  treatment at the plant and use at

construction tites.  Therefore,  dermal exposure at pressure treatment

plants is taken to be at  least the saae as that at construction sites.


Table 13.    Pentnchlorophenol  Concentrations  in Air  et  a  Pressure Treatment
             Kcppert  Company,  Incorporated
             North Little Rock,  Arkansas
             February 24, 1976

                                                               **Concentrut ions
Sample No
. Operation Period (oin)
Hand Nix Oper.
Hand Nix Oper.
Sampling Nan
Asst. Treater
Treating Oper.
Locoootive Oper.
Hand Nixer
Hand Mix Oper.
Conference on Governmental


Industrie I

*Type of

(*K/M )

       Table  11  itwimnriirtu  t«e results  of treatment with 1CDD.

       3.  Exposure Analysis

       In order  to detenus* whether a  prestsaption should  be  issued

based on reproductive  «ad fetotoxii:  effects,  pursuant  to S«ctioa

162.11(a)(3)(ii)(B), the Agency mast determine  whether or  Dot aa

••pi* margin  of  safety exist*  betwiea the levels  of PCP which produce

reproductive  end fetotozic  effects,  end the  level(s) to which the popula-

fion at risk  (women of child-bearing age) can reasonably be «iticipatad

to be exposed.

       This section presents estisuttes  of dietary, inhalation and denul

exposure to PCP  and HCDO on a  "voruc case" basis.  These estiaates art basea

on the exposure  of a pregnant  woven  in  the hoae and at work at major PCP and

Ha-PCP use work  sites, i.e., wood preserving  plants, cooling  towers, tanneries,

and construction sites.  This  approach  to PCP exposure analysis is taken beceuse

of the fetctoxic and taratogeaic effects of PC? described  in  Section II.A.1 and

II. A. 2 and because of  the continued  snvesttnt  of woven  into all areas of the I sis or

force.  Estimates are  computed on iihe b*si»'of  60 kg pregnant wooan, 10U« absorp-

tion via dietary a?d inhalation exposure, and 101  adsorption  via der&al contact

for both PCP  and Ha-PCP.  There is no data available on deraal absorption of pregnant  woaen; the  10Z estimate is based  on the peaetration value

of 7-151 of several chloriuated hydrocarbons, reported by  Haibach cod
Feldnsn (1974).   A noraal breathing  rate is defined as  1.8 n  /hour at work,
         3                •
and 1.0 01 /hour  in the hoe*.

       Inhalation of water vapor containing Ma-PC? is  an exposure route

for workers in industrial coo ling towers, paper pulp mills and tanneries.

Appendix I shows  the calculations used  to derive  ettisatcs of PC? in

water vapors  at  these  sites.

the daily exposure of a 60 kg worker at • Moderate breathing race (1.8 • /hr)

would be:

            3        3
     (8 ug/»  z 1.8 • /hr s 8 hours)760 • 1.92 ug/kg/day.

For HCDD, exposure would be 7.68 X  10   ug/kg/day.

       la the abeeace of data on PC? cooceatraciona in the air at

construction sites, these values for PC? and HCDO are taken as

worst case estimate* at the** sites.

                iii.  Cooling Towers

       Son persons working near cooling towers can be exposed by

inhalation of vapors and drift containing Ma- PC?.  The relative

amounts of Ma-PC? aad water evaporating from the cooling water is a

function of their Molecular weights and vapor pressures, and is esti-
aaccd to be 0.02 ug PC?/«  (Appendix 1).  Exposure therefore would be:

                 3        3
       (0.02 ug/n  x 1.8 • /hr x 8  hr)/60 - 0.004 ug Ha-PCP/kg/day.
For BCDD, exposure would be 0.016 X 10   ug Ea-PCP/kg/day.

       Drift is the entrained water carried from the tower by the exhaust

air. In an average cooling tower, approximately 12 of the cooling fluid is

lost to drift.  For a properly fv.-.ctioning cooling tower, the ratio of vatec.

to air voight should be unity in order to insure y^in""** heat exchange.  At  an
average cooling rcte of 300 gallons/minute,  this weight of water is equivalent
£0 tha veight of 880 •  of air.  The drift (3 gallons or 11.355 liters), distri-

buted in this volust- of air, gives an Ha-PCP concentration of:

                                  3                  3
        (11.355 1 X 45 mg/l)/880 m  - 0.6 eg Ha-PCP/m .

       * would than b«:

                3        3
       (0.6 ag/a  x 1.8 •  /hr x 8 hrs)/60 - 0.15 &g Na-iCP/kg/day
For QCDD, exposure would be 0.60 X 10   nrj/kg/day.

          iv.  Papgr/Pulp Mills

       Inhalation «posure in based on a concentration of 0.047 ug Na-PCP/
a  (se« Appendix 1), vhidi cc«put*s to:

                  3       .3
       (0.047 ug/ta  x 1.8 m /hr x 8 hrs)/60 » 0.01 ug Na-PC?/tog/day.
For HCDD, exposure would be 0.04 X 1U   ug/tog/day.

           v.  Tanneries
Inhalation exposure is based -on a concentration of 0.013 ug/m  (see

Appendix 1} so that exposure is:      "

                   3        3
        (0.013 ug/to  x l.fc m /hr x 8 hr3)/60 leg » 0.003 ug m-PCP/)cg/d<^
For HCDD, exposure would be 0,012 X 10   ug/kg/day.

     4.  Conclusions      ;  •       ;   ;   ,

     Table 14 sunnarizes the exposure estimates for PCP and HCDD deve-

loped in Section II.A.3.  Table 15 gives the ratios of the no effect

dose level to total PCJP and HCDD of the major use sites.

     Cie foregoing discussion establishes that PCP and possibly its HCDD

contaminants cause teratcgenic and fetotoxic effects in test animals.  The

adverse effects observed among the injured fetuses include distorted sax

ratios, increased incidences of. resorbed embryos, steletal anomalies arid

subcutaneous edsna.  The no-effect levels are 5.8 mg/kg/day for PCP ard

1 ug/kg/day for HCDD.  In addition, PCP contains other dioxin contaminants

which have not been fully characterized toxicologically, and which vary

quantitatively fron batch to batch.

TABLE 14.  Estimates of Huatn Exposure to PC? >nd  liCDD
ug x 10 /kg/day




Psper Pulp

0.025 av
0.302 max
0.025 av
0.302 max

0.025 av
0.302 max

0.025 av
0.302 MX
0.025 av
0.302 max
Pressure Treat-0.025 av
mcnt Plants
0.302 MX










0.1 av
1.21 MX
0.1 av
1.21 MX
0.1 av
f 1.21 MX
O.I av
1.21 MX
0.1 av
1.21 MX
0.1 *t
1.21 MX










\j  Based on a 60 kg pregnant woman
27  Initial Treatment
_3/  Routine Treatment
4/  Cooling Tower Drift
2/  Inhalation of cooling tower drift
    f PCP vapors + dermal and dietary

     Data available to  the Agency indicate that the physical and rhaaical

properties of PCP,  and  its ccaaercia.1 uses and distributions lead to

substantial hsan and erwironeental 'exposure to this pesticide.  In this

regard, several factors arc significant;

        - Currant KP production  apprcads*tes  50,000,000 pounds
          per year  and  production is expected  to  inciease to
          80.000,000 pounds par ytsr in tti« naar  future (Josephson,
          1977).  If PCP is squally distributed asoog the total
          U.S. population, ssauairq 60 kg  body might for each
          individual exposed, the theoretical  exposure potential
          for each  parson  in the  general population is 5 ng/kg/day.

        - Although  PCP  is  registered! seunly for non-agri culture!
          uses, the cbeaical is widely distributed  in the environ-
          ment and  in huean tissues.  It is present in the blood
          and urine of  persons not Jmown to be exposed to the
          pesticide.  It has been found in the drinking water of
          80% of  108 cities sespled,, in rainwater in Hawaii, and
          at low  levels in food coeiDdities such  as sugars, root
          vegetables, and  grain and c-ireal products (Table 1).

        - PCP is  registered for hosn and industrial uses.  As a
          result, hoaieoMnara, workaacs using PCP in  leather, wood,
          and paper processing plants, and others using products
          containing PCP are exposed to the chemical,  toe Agency
          estimates that user exposure levels  range from appratioately
          0.9 ng/kg/day for hone  uses to less  than  0.01 ag/kg/day at
          construction  sites (Table 14).
        - Bcsss, tanneries, wood pressure treatment plants,
          pulp mills, and cooling towers are major use sites presen-
          ting significant exposure potential, particularly since
          PCP bea been shown to be absorbed through the skin.  These
          uses cay involve denial as well as inhalation contact with
          the pesticide.  Further, since 80% of the annual PCP pre-
          diction is used for wood preservatives, substantial numbers
          of. people who spray, dip, and pressure-treat wood at plants
          Eay bs exposed to the pesticide.  In addition, workers
          using PCP-traated wood at: construction sites can be exposed.

     The Agency's pre-KPAR review of pesticide exposure is based on

data about the chenical under reviisw, other pesticides, general

assumptions, end other relevant information.  The Agency recognizes

that the exposure data available is sketchy and incomplete.  The Agency

suppleaoented this data with reasonable worst case assumptions, which by

                                  /I                           /2
Tattle 15.  Ratio of No Effect DOM  to Stood Exposure Estimates
                            for PCP ted BCDD
     Site                             PCP           BCDD
     Bane                             6.55          282
     Construction Sites               557           24073
     Cooling Towers                   37.2          1602
     Paper Pulp Mills                 382           16477
     Tanneries                        77.2   :      3327
     Pressure Treatment                        -
     Plants                           557           24073
1)  No Effect Doses are 5.8 ng/ug/day for PCP and
    1 ug/fcg/day for BCDD.
2}  Averages of Total Exposures from Table 14.
their nature are conservative.  Nevertheless, uncertainty remains as to
the validity of the preliminary exposure estimates derived froc the data
and the assumptions.  Therefore, in determining whether an adequate
Bargin of safety exists, the Agency considers it prudent public policy
to utilize greater safety factors for PCP than it would in situations
where it had greater confider-s in the underlying exposure data and

     40 CHI 162.11(a)(3)(ii}(B) provides that a rebuttable presurption
shall arise if a pesticide produces ery "chronic or delayed toxic effect
in test znimals at any dosage up to a level. . . which is substantially
higher than that to which nunans can reasonably be anticipated to be


cqposed,  taking into account acple xargins of safety .  .  .  .• KP
produces  teratoganic and fetotcxic effects in test enianls,  and workers
using KP in connection with tannery, hcae, pressure treatment, paper
pulp processing, cooling fewer and all other uses Kay be  esgposad to PQ>,
with levels at Major use sites ranging from 0.01 to 0.9 Kg/kg/day,  B>e
Agency has concluded that the difference between these  huun exposure
levels and the no-effect level in test aniaal* eay not  constitute an aspic
amrgin of safety. Accordingly, the Agency has concluded  that all POP
registrations exceed this risk criterion.
      The  Agency invites registrants to provide data and infatuation
to confirm,  refine,  or rebut the information upon which the  exposure
                  ;  .  '      '.?.-.
estimates are based.  The Agency will use the new data  to determine
whether or not the presvapticn has been rebutted and in asse&sirsg the
risks which FCP uses nay present to health and the envircnaent.
ni.   Studies Relating  to Possible Adverse Effects
       ISnis section  describes stiadies on PCP ,v*iich do not meet  the cri-
teria outlined in 40 CFR Section 162.11.   It is  intended  to  provide
information on other toxic effects of FCP,  including those resulting
from misuse,   with the exception of the discussion of oncogenicity
and inategenicity, the studies prisented were chosen as  exaoplcs of these
effects;  other r^xjrts  are availiible  in the scientific  literature.
      A-    Oncogfenic  Effects in T^st Aninals
       In 19©,  Irrses et al.  adoijustered FCP  (Dowicide 7) by gavsge to
slice  at doses  of 46.4 eg/kg on days 7-28 of age  and at  130 ppn  (17 mg/
kg/day) in the diet  for the following 17 months.   'Say  report ad that
this  reginss  erased no significant  increase  in  bznor incidence in test
aninals es oxtpared  to  the control  eniraals.  In  1976 Schwetz et si. in en


unpublished •tody submitted Co EPA, reported that dietary regimes of

Dowicide EC-7 at 1, 3, 10, and 30 mg/kg/day for 22 and 24 Months for

male and female rate, respectively, did not increase tumor incidence

over control animals.  The cosmosition of toe PCP products used in

these studies was similar to those shown in Table 2.

       Boutvell and Bosch (1959) tested a series of phenolic chemicals

for their ability to induce skin tumors in mice.  In these experiments

a simple application of 6.3* dimethylbenzanthracene (CUBA) in benzene was

first applied to shaved back skin as an initiator.  Subsequently, 202

PCP, the promoter, was applied in benzene to the back skin of each test

animal twice weekly for IS weeks.  In this short-term study the investi-

gators reported a survival rate of 82.9Z (29/35) in the test animals and

a r».te of 752 (15/20) in control animals treated with benzene only after

the initial exposure to "DHBA.  The average number of papillomas per sur-

vivor in the test group vac 0.04, slightly less than the 0.07 observed

in the controls; the percent of survivors with papillonas was fc.02 as

compared to 72 in the control group.
       These papers hove been reviewed by the EPA Carcinogen Assessment

Croup and were found to be negative with respect to oncogenie effects

of PCP (Albert, 1978).

     B.   Mutagenic Effect*

       Fahrif (1974) induced mi totic gene conversion at

the ade 8 and trp 5 loci of Saccharomyces cerevisiae.  Using a con-

centration of 0.19 millimoles (50 ppm) PCP in 12 dimethyl sulfoxide
for 6 hours, he found 6.62 ade 2 convertant* per 10   survivor*


                     5                .                             5
(control: 0.45 per 10  survivors) and 4.31 trp 5 convert ants per 10
survivors (control: 0.36 per 10  survivors).  Fahrig did not report on

the statistical reliability of thtse data.

       In a later report, Fahrig  (1978) studied the mutagenic

properties of certain chlorophenols, including PCP, in yeast and mice

("mammalian spot test").  He used £. cerevisiae MP-1, a diploid multipurpose

strain for screening intergenie recombination (mitotic crossing over),

intragenic recombination (mitotic gene conversion) and forward mutation.
He incubated cell suspensions at 25 C with 400 Kg/liter PCP foi 3.5 hours.
He spread aliquots of the suspensions, approximately 3x10  cell;, on solid

nutrient-deficient (intragenic recombinants and mutants) or complete
(intergenic recombinants) 'media and incubated at 25 C for 4 and 8 days

respectively.  Fahrig reported statistically significant (p<0.001)

increase* is fovard mutation and mitotic gene conversion.  Table 16 contains

the results of this experiment.

       In the mammalian spot test, he mated females of inbred C57£L/6JHan

strain mice to males of rotation bred 7-stock.  The progeny of this combination

are susceptible to color spots in the adult coat if a mutagenic agent is

injected into the peritoneal cavity of the dam during the tenth day of

fetal development.  The incidence of color spots in untreated mice bred

as described was 0.1Z.  A dosage of 50 mg/kg PCP to pregnant mice produced

color spots in 0.6* of the progeny; a dosage with 100 mg/kg resulted in a

1.32 incidence of spots.  Fahrig did not give the statistical significance

of these data.

TABLE 16. Induction of forward mutation, intragenic and intergenic recombination  in
          S. cereviaiae HP-1 in vitro with pentachlorophenol at » treatnmnt time  of
          3.5 hours
            t of    Concen-
  Genetic   Experi- tration
                 Colonies  of
                 Genet ica 1 ly
         Colonies  of,
I of     Genet ically
                 Altered Cells     Experi-  Altered Cells
Alteration  ments   (mg/1)  Survival   Per Survivor

Mutation       4
400   59 ± 8   2.00 _* 0.22 (216)

               0.47 + 0.14 (50)
ments	Per Survivor  '   Significance

  4     0.61 _f 0.07 (113)    < 0.001

        0.49 + 0.08 (91)     > 0.8
In ^agen.
               ?.64 + 0.45 (*
        2.93 + 0.10 C542)    < 0.001
1.  Adapted from Fahrig et al.. (1977>

2.  Control Survival - IOOX

3.  Miitants, Convertants  (Intragenic Recombination)/10  surviviors,
    Hecombinanta (Intergenic Recombination)/10  survivors

The numbers in parenthesis give the actual numbers of colonies counted.

       A geneticist and statistician assigned to EPA have reviewed the Fahzig

et al. paper (1978).  In the opinion of the geneticis*-    is study does not

provide evidence of the mutagenicity of PCF.  This op:    . was based on the face

that the experiment has certain shortcomings.  Among these are absence of

information on the controls as well as on maternal toxicity (Mauer, 1978).  Only

two animals were affected at each dose level; the EPA statistician has found that

this response is not statistically significant at the 0.05 level (Rossi, 1978)

using the chi-square test.       -.     :     -

       For these reasons, the reviewers did not consider the mammalian spot

test to be sufficient evidence of matiigenicity, and the criteria of multitesc

evidence of 40 CFR Section 162.11 (a) (3)(ii')(A) are not met.

       It should be noted that outagenicity tests on PCP were negative with

the Aiaes test (Andersen et al.' 1971) , the host-mediated assay (buselmaier

et al. 1973), and the sex-linked recessive"lethal test on Drosophila

(Vogel and Chandler, 1974). -'"••'         '

     C.  Chloracne

       Chloracne ("chlorine acne") is a human skiri disorder characterized

by distention of hair follicles by horny cutaneous tissue, and by a de-

crease or absence of the sebaceous glands in the area of infection.

This condition has been observed 'in workers in" PCP manufacturing plants

and wood preserving operations (Baader and Bauer, 1951).  Chloracne can

arise in these workers weeks or months after exposure, and a!: first was

 thought  to be due to PCP itself.   However,  using the rabbit eat  test,

 Jones et ml.  showed in 1962 that  the acnegenic agent in the herbicide

 2,4,5-T  was its contaminant TCDD.  Further  study of the acnegenic effects

 of pare  and coraercial grade PCP  identified its dioxin contaminants as

 the causative agent (Johnson et al., 1973).

      D.    Hepatic Effects

       Goldstein et al. (1976) fed pure and technical grade PCP  to female

 Sherman  rats for 8 months at dosages of 20, 10ft, and 500 ppn. Technical

 PCP produced hepatic porphyria at 100 and 500 ppn, and all doses caused

.increased hepatic aryl hydrocarbon hydroxylaje activity, glucuronyl trans-

 ferase activity, liver weight, cytochrome P-450-, and aicrosoaal  hene.

 N-deaethylase activity was not affected.   In contrast, pure PCP  had no

 significant effect on these parameters, except for .increasing glucuronyl

 transferase at 500 ppsn.  Both PCP types decreased the rate of body weight

 gain at  500 ppn.  The technical PCP used  contained 8 ppm hexa-,  520 ppm

 hepta-,  and 1380 ppm octachlotodibenzodioxin.  Pure PCP contained less

 than C.I ppm each of these contaminants.

       Kimbrough and Linder (1975) fed 1000 ppm "relatively pure" PCP  and

 technical PCP to male rats for 3  months.   All of, the animals were reported to

 have statistically significant enlargement  of the liver when compared  to the

 controls.  Histological examination of the  liver using the light microscope

 showed that the rats fed technical PCP had  foany cytoplasm or pronounced vaciro-

 lation of the hepatocytes, inclusions, single hepatocellular necrosis, inter-

 stitial  fibresis, and a brown pigment in  macrophages and Kupffer cells.

Examination with  the  electron microscope  (bowed  an  increase  in (Booth

endoplasmic reticulum, many  lipid vacuoles,  and  atypical  mitochondria.

Livers of rats  fed  the relatively  pure  PCP showed enlarged hepatocytes,

and many cells  contained  inclusion*  in  their cytoplasm.   Electron micro-

scope studies showed  a slight increase  in smooth endoplasmic reticulua,

atypical mitochondria, and some  lipid vacuoles.  Livers of control  rats

were normal.  Kimbrough and  Linder did  not report the amount of dioxin

contaminants in the pure  and technical  PCP which was used in the study.

       In 1976, Schwetz et *1. observed discoloration of  the liver  in

fenale rats fed 10  or 30  ng/kg/day PCP*  Histological examioacicn re-

vealed pigmented  material in the hepatocytes-.surrounding  the central

veins with smaller  amounts present in the reticuloendothelial cells.

Hepatocytes in  the  centrilobular region alsq  contained pigmented mater-

ial but were not  necrotic.   The  PCP  used  in  this study was representa-

tive of Cow's product and contained  approximately 30 ppm  total dioxins.

     E.  Toxicity to  Humans      t,      ...-•-,

       There are  reports  of  deaths caused by  industrial or accidental

exposure to PCP.  In  most cases  exposure  occurred by dermal contact,

either to PCP in  solution or to  materials treated with PCP.  Bergner

et al. (1965) described five cases ofrPCP intoxication in Winnipeg  in

1963.  The one  fatality involved a worker in  a wood treating

plant who, using  his  bare hands, dipped wood  into a vat containing  a so-

lution of &.1J  PCP  in petroleum  solvent.  A similar incident had pre-

viously been reported in  1952 in France by Truhaut et al.  IE  this case

two workers were  immersing wooden planks  in  a 32 aqueous  solution of a

mixture of 802 Na-PCP and 202 •odium tetrachlorophenate.  The worker*

plunged their hands and forearms into Che liquid bath to remove the

planks.  After 6 days of this work, both Men becane ill and ultimately

died.  In all three cases, the initial symptoms cf intoxication were

profuse sweating and elevated temperatures.

       These saw symptoms were observed in an incident involving nine

neonates in a nursery for newbora infants in St. Louis.  Kobson et al.

(1969) reported these and other symptom* in these infants, two of whom

died.  Other symptoms reported were increased pulse rate ( > 150/minute),

hepatomegaly, and respiratory distress*  "Of the seven survivors, six

received exchange blood transfusions, and one received only supportive

therapy.  Exposure was proven to be via percutaneous absorption

of Na-PCP which had been mistakenly used to launder'the infants'

diapers and bed linsns.           -

       In a followup paper, Armstrong et al. (1969) measured PCP levels

in samples of these diapers and linens, in autopsy tissues, and in the

serum of a surviving infant.  They detected the following PCP residues:

six diapers, 2.64 to 17.20 ing/100 g; two shirts, 7.38 and 7.90 mg/100 g;

two shirt backs, 22.40 and 195 mg/100 g; two crib pads, 4.89 and 17b.70

ag/100 g; one mattress pad, 14 mg/100 g; one pillow case, 6.25 mg/100 g;

and two muslins, 1.15 and 2.80 mg/100 g.  In autopsy tissues, PCP measure-

ments were:  kidney, 2.8 mg/100 g; adrenal, 2.7 mg/100 g; heart and blood

vessel, 2.1 mg/100 g; fat, 3.4 mg/100 g; and connective tissue, 2.7 mg/100 g.

An infant who survived through exchange transfusion, had PCP levels of 11.8

mg/100 ml before, 6.5 mg/100 ml curing, and 0.2 eg/mi after the transfusion.

     F.   Toxicity  to  Aniatals

       Toxicological data oc  PCP are complicated by the presence of vary-

ing quantities  of tetrachlorophencls,  dioxins, and furan* in the technical

material.  Table 17 suaaarizes  the  available toxicity data for PC? on var-

ious mamalian  species.

       There  are reports  of  fatalities to far* animals following exposure

to PCP.  Spencer, in 1957, described the deaths of two Hereford cows within

24 hours after  drinking a 52  solution of PCP in kerosene.  Blevins (1965)

reported on the death  of  a litter of ten pigs kept in a farrowing house
whose floor had been overly  treated with PCP dissolved in used crankcase

oil.  They theorized that the pigs;  were triply exposed by direct adsorp-

tion through  the skin, frost  the silk of the gilt,  and through inhalation

of PCP "aerosol."   The gilt recovered  when it was  Moved outside the far-

rowing house.

       Adelman  et al.  (1976)  established the LC-50's  for Ma-PCP as 0.21

ng/liter for  fathead minnows, and 0.22 Big/liter for goldfish.   Holnberg

et al. (1972) found that  the.eel  [Anguilla anguilla.L) did not survive

5 days of exposure  to  0.1 ppm Na-?CP in fresh water.   Eanec et al.  (1968)

found that the  LC-50 for  coho salmon. (Onchorynchus  kisutch) is 0.15 ng/

liter of K-PCP.

       The Public Health  Service  of DHEW has  reportt  on  numerous fish

kills from 1964 to  1970 that  were caused by effluents  froa wood  treatment

plant washing into  fresh  water.   Since  1970,  the Pesticide Episode  Review  Systess

(PEES) fans recorded only  four incidents  involving  fish kills.   This  indicate*

either that wood preserving practices with effluents  hitve becooe  no re stringent,

or that incidents are  not being reported to PEES.

TABLE 17.  Toxicity of pentachlorophenol to memmala"
(Sen, Strain)
Route of
 Dose or
Wiatar Rats
Albino Rats (H)

Albino Spraguc-
Davley Rats (M,F)
Albino Wistar
Rat* (F)
Sherman Rata (H,F)
Oral (0.5* in
Stanoflex fuel oil)

SubcutaneouR (2Z
in water)

Oral (IX in olive oil)
Oral (21 in water)

Intraperitoneal  8 C.
Intrapcritoneal 26 C
Intraperitoneal 36 C

Percutaneous (dermal)
/iOX w/v in glycerol

Oral (in peanut oil)
Oral       "
Dermal     "
Dermal     "
 27.3 mg/kg

 66.3 mg/kg

 77.9 mg/kg
210.6 mg/kg

   56 mg/k| /

  620 otf/kg (LD-100)

  420 Big/kg (LD-100)

  120 mg/kg (LD-100)

  149 mg/kg
  146  mg/kg
  175  mg/kg
  320  mg/kg
  330  mg/kg
Uclchmann et al. (1942)

Deichmann et al. (1942)

Deichmann tt al. (1942)
Deichmann et •!. (1942)

Furquharaon et •!. (1942)

Keplinger et «1. (1969)

Keplinger et •!. (1969)

Keplinger et al. (1969)

Noaket and Sanderson (1969)
Caiuea (1969)
Uaittea (1969)
Gainea (1969)
Cainea (1969)

                                                   * I
TABLE 17.  Toxicity of pentachlorophenol to mamma Ia  (Continued)
(Sex. Strain)
Route of
 Dose or
Rata (H)

White Mice


Inhalation 80 ml/mtn


Orii (5% PCP in

Oral (5X PCP in
 11.7 mg/kg
   29 »g/kf,
   63 Big/kg
  130 mg/kg
  261 mg/kg

512.5 «g/kg (LB-100)
275.0 mg/kg (LB-100)
135.5 mg/kg (LD-100)
550.0 mg/kg (LD-100)
Hoben et at (1976)
Pleskova and Benct« (1959)
Pleskova and B«ncte (1959)
Pleskova and Bencie (1959)
Pleskova and Bencce (1959)

HcCavack et al. (1941)
HcCavack et al. (1941)
McUavack et al. (1941)
HcCavack et al. (1941)
  120 ng/kg (LD-100)   Harrison (1959)!
  140 mg/kg (LD-100)   Harrinon (1959)
\J All values represent the LD   unless otherwise noted.

     C.  Effects of Tetrachlorophenol

       As stated previously, th* presence of tetrachlorophenols in «11

PCf products raises the possibility that adverse effects of PC? could

be attributed to these compounds.  The toxicological properties of tetra-

chloroDheaols have not been studied extensively.  The "Registry of Toxic

Effects of Substances,"  published by th* Rational Institute of

Occupational Safety aad Health, DHEW, lists the oral LD   for the rat as
  i                                            '        50
140 eg/kg, both for tetrachlorophenol (presiaubly mixed isomers) and for


       Schwetz et al. (1974*) evaluated toe effects of purified and com-

mercial grade tetrachlorophenol on rat embryonal and fetal development.

They fed pregnant Sprague-Dawley rats 10 and 30 mg/kg/day on days 6-15

inclusive of gestation.  These doses hid no effect on resorptions, fetal

body weight, or fetal crown-rump length.  At 30 mg/kg/day, there were

stati tic ally significant increases in delayed ossification' of the skull

boner for both tetrachlorophenol types.  Schvetz'et al. observed subcu-

taneous edena at 10 mg/kg/day with both compounds, but not with the 30

ng/'kg/day doses.  Since this effect was not dose-related, the authors

speculate thai it may have been due to chance.

                               Appendix  1

Ha-PC? Content in Uat«r Vapor

Ha-PCP is registered for use as a slinicide  in cooling cowers, paper pulp

mills and canneries.  In these uses, Na-PCP  is normally  found in water

aC concentrations of 48, 113 and 32 mg/liter respeccively.  The huaidity

in the work areas at these sices can approach 1002, due  to vaporiza-

tion froa Che large volumes of water required.  Na-PCP can also vaporize
froa solution, and Che amounts of Ha-PCP in  Che vapor can be estimated.
  1                                 '  ,T< •   -  .  -
In Che following calculations, ic is assumed that  Che Na-PCF/water solution
is an ideal binary system.  The following constants will be required:

At 1002 humidity and 20*C,
   weight of water vapor • 17.3 gms/m

   vapor pressure of water »*17.54 mm

   Vapor pressure of Na-PCP                    -4
   (assosing same volatility as PCI1),* 4.7 X 10  mm

Molecular weight of water » 18

Molecular weight of Na-PCP - 269  '

In 1 liter of solution, at 48 mg/1 Na-PCP, there are approximately
.048/289 - 1.7 X 10  moles Na-PCP Jind 1000 gms/18  - 55.5 moles

water. According to Raoult's Lav, the partial pressure (p*) of each

component in a binary system equali; Che mole fraction M  (moles of component/
                             - *     ' '   ,  .    '                              -*<
total moles present) multiplied by the Vapor pressure of Che component (VP ):
                                 •.       -  -                               c
p* - K  X VP                  ..,:...•
      f     C

                       -4                -4-9
  f Ha-PCP • (1.7 X 10  755.5) (4.7 X 10  ) - 1.4 X 10

  P* Watar - (55.5/55.5) (17.54) - 17.54 •*
The mole fraction of Na-PCP vapor in the air can be calculated using the
f oral a:

           mole fraction Ha-PCP » p* Ha-PCP	
                                  p*^ Water * p* Ma-PCP

                                - 1.4 X 10
                                        '  '	-9
                                  17.54, t 1.4 X 10
or aoles Na-PCP in v*r^             -11
   noles water in vajs. r      • 8 X  10
The aoles of water on the vapor is
                                       3                     3
                             17.3 gas/a  - 0.96 Holes water'n

                                      3         -11
     moles Na-PCP " 0.96 noles water/a  X 8 X 10

               -11        3
     - 7.7 X 10    noles/m
                            -11        3
     Crams Na-PCP - 7.7 X  10    noles/m.  X 298

                  - 0.02 ug/m

These same calculations apply  for vapors in pulp mills ana  .anneries,

and using the concentrations of Na-PCP specified earlier, tnese

calculate to:

           Pulp mills:   Na-PCP - 0.047 ug/m
           Tanneries:    Na-PCP - 0.013 ug/m

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