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                  <text>Alvin L. Young Collection on Agent Orange</text>
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              <description>An account of the resource</description>
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                  <text>&lt;p style="margin-top: -1em; line-height: 1.2em;"&gt;The Alvin L. Young Collection on Agent Orange comprises 120 linear feet and spans the late 1800s to 2005; however, the bulk of the coverage is from the 1960s to the 1980s and there are many undated items. The collection was donated to Special Collections of the National Agricultural Library in 1985 by Dr. Alvin L. Young (1942- ). Dr. Young developed the collection as he conducted extensive research on the military defoliant Agent Orange. The collection is in good condition and includes letters, memoranda, books, reports, press releases, journal and newspaper clippings, field logs and notebooks, newsletters, maps, booklets and pamphlets, photographs, memorabilia, and audiotapes of an interview with Dr. Young.&lt;/p&gt;&#13;
&lt;p&gt;For more about this collection, &lt;a href="/exhibits/speccoll/exhibits/show/alvin-l--young-collection-on-a"&gt;view the Agent Orange Exhibit.&lt;/a&gt;&lt;/p&gt;</text>
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              <text>1318</text>
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              <text>Series III Subseries II</text>
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                <text>Abstract: Agricultural Exposure to 2, 4 -D</text>
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              <elementText elementTextId="16247">
                <text>agricultural exposure</text>
              </elementText>
              <elementText elementTextId="16248">
                <text>herbicide toxicology</text>
              </elementText>
              <elementText elementTextId="16249">
                <text>human testing</text>
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                    <text>Item ID Number

01275

Author
Corporate Author

Office of the Federal Register

Report/Article Title
JOUrnal/BOOk TltlB

Federal Register

Year

1978

Month/Day

April 21

Color

n

Number of Imaues

8

DoSCTlptOn NOteS

Alvin L

- Young filed this item under the category
"DDT/Human Toxicology and Environmental Fate"
Missing initial page(s)

Thursday, April 26, 2001

Page 1275 of 1328

�17138

NQTIC1S

Kben and McKtaley (M0&gt; studied the
prenatal and postnatal effects of 2.4,6-T in
Wistar rats, using four raowlea containing
no TCDD (detection limit: O.S mg/fcg)
[Table 231. Twenty-five to one hundred
fifty mjf/fefj body weight per day were administered to the-dams, orally in gelatin or
corn oil, on days 6 to .15 of gestation. At 25
and 50 Big/kg, the differences between experimental and control values were minimal.
However, at 100 and 150 mg/feg, there were
significant &lt;p &lt;0,OS) effects on fetal weight,
number of dead fetuses, and percentage of
malformed fetuses per litter,'* The larger
proportion of malformed fetuses iti the
treated groups resulted from either an increased incidence of skeletal anomalies ate
seal in the controls or a low incidence of abnormalities not obaeped to the controls.
The former category Included wavy rites, retarded ossification, extra ribs, and a variety
of eternal defects; the latter included fused
rite, small-sized distorted scapula, malformed hnmerue shaft, and bent radius or
u]na. Abnormal kidneys were observed in 7
to 46% of the exanxtained fetuses, treated
with sample T-l, compared with a control
value of n to 38%.
- la the pestnasal portion of the study,
After normal delivery, survival rate, sex
ratio, and pup weight on days 1 and 31 were
compared. Although treated pups surviving
from day 2 to 21 were slightly mailer at
"Statistical significance was determined
using the average value per dose level. Data
from T-4 were not u&amp;d to this nnalyaia.

I
j
iDioiin I
|Cont«ntlDas«

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I
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IKortal-lpvr Llttarl Una*)

20 i 32.3 I
40 i TM !
80 i 94.* j

r.3
3.7
o.®

_Ljaft-J.Mft»9.-JL-.. JI-

9.1

0.5

40 t
80

10,«

i
i

80 I 8.5 I
40 i 4.0 t

«.«
1J.«

i

8.9

SO

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.

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Collins and Williams (124) tested seven
some dose levels, there were no significant
difference* from controls tot any variable. samples of 3,4,8-T from different sources for
In soraa experiments, Utters were standard- embryotoxie effects In golden Syrian hamteed at 8 pupa on day S, and the remaining sters (Mfsaerteatm aumtw) [Table 233, The
littermates examined for defects. The In- dioxin contents ranged from not detectable
creased incidences of malformations among (detection limit &lt;0.1 ppm) to 46 ppm. Daily
treated groups were comparable to those oral doses of 20 to 100 mg/kg body weight
found In the presiaW study. Assuming the were adminiitt«red
in
acetonexorn
same incidence for pups not examined, the j oi!:ciwrbo3symethyj cellulose (1:5.8:10) on
investigators concluded that there were no | daya 6 to 10 of gestation. 2,4,5-T with no dereal differences to survival rates among con- ! tectable dloxln significantly (p &lt;0.05) retrol and treated groups. The butyl eater of duced fetfll welffht and fetal viability per
2.4.5-T produced simitar toxic ef fecte,
litter at all levels tested.
Sokolifc ««&gt; or»Uy administered 100 and
Total fetaJ mortality
in400 mg/kg and §0 and 300 mg/k{r of 3,4,9-T creaued at all levels whenwas greatlywith
compared
and its butyl ester to r&amp;fcs of the Rappolovo
line on each of'days 1 to 14 or 1 to Ifl of controls and was dose-dependent, as was the
pregnancy. At 100 msf/kg, 2,4,8-T produced effect on fetal viability. The increased inciembryos with a combination ol deformities dence of gastrointestinal hemorrhage also
including absence of lower jaw, abnormal appeared to be dose related. At 100 mg/kg,
hind Hmbs, and exopnthtlmoa. At 400 me/ "pure" 3.4.W caused increased incidences
kg, the embryos of treated rate evidenced of malformations and reductions in the
cleft palate, hydrocephalus, hydronephro- number of live fetuses per Utter. One "pure"
sis, and ataonwajltisij of the upper limbs sample, F, at 100 mg/kg significantly rewhich Included trtdtictyly, webbed toes, and &lt; duced fetal weight from 1.8 to 1.6 grams, reabnormal shortness.
duced fetal viability from 86.7 to 71.4 perThe butyl ester of 2,4,8-T was more toxic cent, and increased abnormalities from 3.0
than the parent compound, causing more to 40 percent The anomalies associated
than 30 percent embryonic mortality at 300 with 2,4,5-T containing no dioxin were exenmg/fcg. The lower do«e, 50 mg/kA also cephaly, eye abnormalities, delayed head oscaused high mortality among the embryos. »lf ic&amp;tion, and hind limb deformities.
Cleft palate, hydronephrosia, hydrocephaIncreafllnt th« level of dioxin contaminalui, and extensive gastrointestinal hemorrhages were also observed within the treat- tion increased fetal mortality and the Incied groujw. From these results, the author dence of abnormalities per litter; fetal viaconcluded that. 3,4,6-T and its derivatives bility was reduced. A clear correlation was
have a high potential for teratogente sctiv- found between the level of dioxin and abnormalHiea per Utter. Although the InciIty.

1
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1.2

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i_L,,j^_J_u^.J™«^li.™.,^i.,.,.J
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-™.~,. «^,.,.^^^^™.3^..«jAfeJfli«»...A»j'«»r.^lK»^.r«'«™Jw»^.«*.H..«iA«(^-.-/'''iM'IV**^-«'^*.

few C»Ulnt» tnti Villlfla.t (124).
app-»rflntly norajal tiaifhta for stsplfli! A end 6 attc.lbu'cort to «i!sa«,V Hot dsteoted.
4/ p &lt; 0.05.
. . . : . . .

wmsm, vm. «, MO.

dence of hemorrhages also increased, no relationship between it and dioxin level could
be found. Bulging eyes (absence of eyelid)
and delayed ossification were the most
common anomalies seen among fetuses exposed to dkndn-contamlnated 2.4,5-T; exenceph&amp;ly, edema, cleft palate, ectopic heart,
and fused ribs were also observed.
Emerwm et al. U41) found no adverse effects of commercial 2,4,5-T, contataing 0.5
ppm TCDD, on fetid development in Spra- '
gue-Dawley derived rats and New Zealand
white rabbits, Daily oral doses of 2,4,6-T in
gelatin were administered to the rats at 1 to
34 mg/kg oa days 8 to 16 of gestation; to the
rabbits at 10 to 40 mg/kg on daya 6 to 18 of
KW.tation. The investigators found no maternal or embryonic toxic effect") to either
species, nor was 8,4,S-T considered teratogenie under the oonditions of these experiment®, Tho most frequently observed abnormalities were accessory ribs, hydronephrosts. and retardation in the development of
the stenicbrae, with the exception of par- |
tJirfJy ossified st«rn«bra® in both species and
bilateral acoeireory riba in the rabbit, the incidence of these anomalies was greater in
the control animals than in the examined
treated groups.
Sparselm et a!. U4G) orally administered
3,4,9-T, containing 0.8 ppm TCDD, to rats in
daily doses of SO and 100 nig/its on days 3 to
15 and 6 to 10 of gestation, respectively. Results are «!vro !,« Table 24. At SO ma/kg,
there were no slsmKtcant maternal or embryonic toxic effects attributable to a,4,6-T
except for an increased incidence of delayed
stcull osaiifleatic'ii, and a stogie fetus with iu-

, Mm n, nn

�17137
.te.....ftM-,4A^,L^«..i
5A —L-.iftft~.~
,i 'i
203

^

.
Viable
Total

252

-

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n' ri»lr ^ — "

\% Beaorptions
I Litters

. ;

I

60

- I

61

!

100

i&amp;. ttr^lB^-wiM^i .tW**#-lM»*^

i Fatal weight
! Halffl

.«1'

4.38 I
r Q^ww&amp;ifcttW4Mwfa«iMrii'

.

&amp;&amp;&amp;

Abnormalities
fetuses fl«sained)
Poorly os3ifi«d stertiobraaj
Fifth

Saoond and fifth
- Multiple
Malallgned at«rn«bra«
Delayed osaification
Interparletal

A/

i 22,1 !
i 4.2 I
I 12,6 5
! 8.1 !•

57

3.8
3.0

Data from Sparsohu et al,

fc./ All

&amp;/

15.a
3.0
8,3
0.®

p &lt;

?i*»i* f*t(I9«*

0.05

testiswl hemorrhaee. At 100 mg/kg. 8,4,8-T
WM toxic to both dams and fetuaea. '•
Kesorptlons were observed in till litters; 7s
percent were totally resorted Fetal weight
was significantly &lt;p &lt; 0.001) reduced In
both sexes and the sex ratio was shifted in
favor of females. Abnormalities observed
which hat! (significantly &lt;P &lt; 0,06) higher incidences than in the controls were poorly ossified and malaugncd sternebiiae and delayed skull ossification. The investigHtora
concluded that the delayed ossification observed in this study was a reversible manifestation, rather than &amp; tnte ti-ratcgenSc
effect.

(b) Advene Reproductive Efffxts in Otkar
MamnuMan Test Systems, Adverse reproductive effects of 3,4,6-T exposure have
been observed iu other tndmmalian test aysteiM. LJoyd et «L (173) reported on in vivo
enzymatic studies showing reduced uptake,
and metabolism of testosterone by the prostate gland in male mice treated orally with
doses of 2,4,8-T (8.38, 12.S, or 2B nig/kg, ten
times daily).

Yefimcnko USJf) reported on the effects
of acute aikd chronic exposure to th« bafcyJ
ester of 2,4,6-T on gonadal «snd swnatlc
tissue in an in vivo cytogenettc study to
"Tne high srato of »)itejr*al mortality
caused dosiug to be stopped on «toy 10, Instead of clay 15. SlgnUtcant reductions in
weight erain were also observed.

mate albino rats. Chronic ef/eete oa the
coords were otoserved sftcr exposure to O.I
up/kg for two and one h»U months. Adverse
affects (aeoii at seven mouths, when the experiment was terminivtcd}, which were considered persiatent effects, included testteular atrophy, decreased sperm count, desquamated ttttoules, a ad aberrant celte in the germinal epithelium. Chromosomal aberrations
were also.oteeirved during the chronic phase
of the oxpwiment. EJt"A evaiusation cf this
study found inadequacies in the methodolo$y which would prevent the drawing of firm
conditions from thia data Ud#),
Recent studies in rate by Sjoden and So'JSTbtfj-g [cited let HtS)J ftj'F9&gt;tr to show thst
prenatal exposure to 2,4.5-T leads to behavioral abnonualittes and chajigts in thyroid
activity and brain seritonin leve!a in the
progeny. Stogie oral doses of 100 ni«/lcg
were iHi&amp;iinJKtmd to th« AKW an days 7, 8,
or 9 of pregnancy,
(c) Adverse Kffeate in Avt&amp;n Species. Ktnbryotomic eflscte to avitin species due to
3,4.5-T exposure have been reported. Verrett U36) studied th« effects of 3.4,8-T, containing either 2'/ or 0.8 ppni TCDIJ, on
chicken egg«, The 2.4.S-T m-as injected
through the air cell of the sggs, either
prelncutetion or on the fourth day of incubatlou. The sample contaiataK VI ppm
TCDD was found to be mar* lethal (LD~
50«2S ug/egg) than the la® contaminated
sample &lt;UXM&gt;&lt;«100 wg/egg). Both aamples
produced teratogenle effects, including

chick edema, eye defects, beak defects &lt;ps1imrUy cleft palate), and short, twisted feet
restiltiBg from tendon slippage. Teratogenic
effects were observed at doaes as low an 1
ppm (50 us/e«g) with the sample containing
O.S pptn TCDD arKt as low as 0.125 ppm
«US us/egg) with the sample containing 27
ppm TCDD,
Lute and Lute-Osfeiiag U3S&gt; studied the
action of 3,4,5-T, in rufous solution at a
coiM«Kf.rali0n of 2 to 10 e/litcr, on the eiflbryoriic development of auull (Coiitrnfa; coturnix japontca), chicken (Qalhtt galim),
pheasant (Phtuianvt cclcMcwt), and two
partridge species iAlectoris nfa and Per&amp;rtx
penlrte). Tfe© 3,4,5-T was administered by
dipping, spraying, and organo-typic cultures. Abnorn»8l g«tital tracts were observed in all species, indicating abnormal
sexu&amp;l differentiation, i'urther, morphological change*; in the testes often gave the appearance of true testiculaj atrophy. In another study, 3,4.6-T affected fertility isi
bhxis of both sexes «M&gt;.
(d) Studies in Avian Species in Which Adverse SffecU Were Not Observed* lining 2,4,5T wntamimted with less than 0.1 ppm
dioxin, Stravige and Kerr (142} found no abnormal development in chicken embryos.
Doses of 12.5, ?S, 50, 78, 100, and 135 mg/kg
were injected into egga on days 0 and 5 of
incubation; observations were made 48
hours later. At this developmental stage,
kidneys were not sufficiently developed to
detect the tubule lesions reported by Bjorklund and Erne (.143),
&lt;e) Swnwj.n,. Studies ha?e «»UJ&gt;liah«:S
4hti 2,&lt;,C-T is fc-t«toxJc utd teiatogcnlc at
docca £J low as Sf-mt/kB (0.05 ± 0.03 ppm
TCDD) 49 Jmice (/2f); 4.6 mg/kg (approxla- .__
mately 30 ppm TCDD) to rats «M); and 20 3° f f1^
mg/kg &lt;O.S pput TCDD) to hamsters (12 i).
~rcc&gt;o
Cleft palate and kidney anomalies have
been observed in mice, rats, and hamsters.
Ho fetotoxic or ter&amp;togenic effects (nofy
effect levels) have been observed at doses of
SO mg/kg (0.05 ± 0.02 ppm TCDD) in mice
U25) and 25 to 150 ffifi/kg (0.05 ± 0.02 ppm
TCDD') in rats U25).
(3) ExuMSUTt Aii*ily.tts. In order to determine "whether a rebuttabie pretumptton
should be issued based on reproductive and
fetotoxic
effects.
pursuant
to
§ 162.1UaX3XiiXB&gt;, the Working Oroup
must deteroiine whether or not an ample
margin of safety exists between the levels of
3,4,8-T and/or TCDD which produce reproductive and fetotoxic effects, and the
SeveKs) to which hum&amp;no can reasonably be
anticipated to ba exposed.
The cmii'Cellatiton of u«s of 2,4,6-T on food
cropa intended for human consumption and
for ui$e around the home, recreation sites,
atnmtle srcM, and ditch banks in 1070 was
thought to have eliminated the potential
exposure to that portion of the population
at risk (women of child bearing age).
• Social eMR$!S# over th« taut few years,
however, have given wonsen the opportunity
for employment in areas that once were
considered open only to men. Since women
of child-bearing »gs are now employed In occupations such tie pestf.t'iile applicators, operators of highway construction and maintenance equipment, foresters, and chemical
forrnulstora, they have become part of the

vet, m, NO.

h

�17188
at ttek wi&amp;h potential exposure
fe 8,4,»-T and/Of TCDD.
In order to tfeteraitna whether an atajrts
' i of safety extefej, the Waiting Group
first (Setenwta? hew much 8,4,5-T a
wtfld be exposed to through oral,
_ it, or Inhalation expesws. Ptar e*s*i of
these analyst, the Working Cftroup «,T«VMM
i to wei&amp;h SO fcs. lii? followfag adj a?« bfis«id SB an e%po£UTi sniays.%
W arsd TCDD Etorfonaed by I^A'a
m&amp; Evalutittoa Division CCmni

ity of oral expoacu* to MiS-T and/or TCCOE)
•sfattad, Treatment of rsaffl M&gt;&lt;5 Mature
laiM$ could mutt to oral exposure through
inf&lt;wttoi of neat wd mil* from asvfesusls
gnuing OR the t*««toS are*. 'Staee fteteat
date on w»Mte of M,fcT in satofe ew-sstec on fet«at^i migotatid Is HBRT&amp;J}6t»!«, for
mmposo) of fee S,4,*-T end «xposti» wudy«ii», t*-io Wwfsi^s Group «*i$ rcisW'Ji* l«fqrmatloft &lt;^3taln«a Sn » rtadJjtg study (37) in
whtoh cattte wete -fed co@»lde.t%I$1y .higJje•aKnintii cf t,4,R-T th*n they would norcwJly bs e?s&gt;ar*a to to gt'infns. OB treat«4 teid.
The Mlowing eaiculKtionn ate ?&gt;!,scd em tho
average aw*ntit3&amp;i of food eaten per day UJ
kg), as reported by LehWB (!&lt;!&lt;(, t9S).

Oral Exixisure, Fw ptitpoeeiS of tafj
the Woiktajf Oroap eooHd«red
air?enUy regieter«i VUCT where the poss31&gt;U-

-*f f «ot
I level for t«rafeo-»
jg^riicity in mioo
(Avarag* level of

IS of. food ifc« in
! total human &lt;U«t
J
•'
of
If 00*3 aatan par day

ag/kg

20

^ 0.2 ppffl*

Q»

K5 kg

1.5

0,0002
K-:iir . »
^

jt/ Animals wer« fed at 300 ppai 2,4,5"1 In th« diet for
to
3 weeks. This it «. 'worst o«se assumption fp»' oows
on frashly-tnsat'ad pasture without a withdrawal period;
silk and aeat wa» obtained froti auoh oous. Meat (b««f j
inoludea isuscle, fat, and liver tisauea Khioh eonttitut«the
sajor portion of *dibl« a««t»
To find tbg fevera,go a*!ty inM« of a
efeiS'te food item, m«3Uply tfce aveirti«« d&amp;tiy
food intftto by the percent of U?M ittsn in
the totRl diet: Per mills, U kgxlf .S%
kg; and for meat (beef), U
Tbt q«a««ty of 3,4,8'T ta th* average
equ»?A the »vera^« daily intaii; oil
food item multipUed by tho levoS of
to the food item; For mm,
mr, anfl for
.
The theoretical exposure of att
wot»»n OQiwto the wnouDt-ot 2,4.5-T ta the
daPy diet divided by the weight of tbe arersga weuwn: IPosr milk, 0.03 n*g/80 kg«0.000§
JSt/te; anc? to meat (beef), 0.914 rasr/SG
lK*»d.090S mg/kr. totsl wsposuy® from milk
MM! beef products could be 9.G007 t&amp;K/k^
t»er day,
data on TCBD ;-ft~(du«3 to fmJ.ta.'SJiig on treated misgi'lwvJi are too
to um for an nnttlyajls ol TCDP exto humoivs tJiroueh Ingeation of
The Worklnj[ Group coneiden that the*
difference between the np-adver.»e-offett
level of 2,4^5-T for toratogenlc eftete: (20
mjAs) and the calculated on-.l exiHWXv^
level for 3,4,6-T (0.0007 mg/k« r*r day) doc®

• e» twplQ marsta of nloty. Siiree
this rials crSterteu for otlier chwato advene

hsw not town met or exceeded, a
(to!^Dermal Sxposure, 'In order to conduct
tawMialyme.i th--) Worthing Group mu0t &lt;Serroto« the intount ef 3,4,15-T aj«&lt;J/or
TC0D wluteh would come ta contnct with
thftt would be «,b,(1) ^pnitf 4J9&gt;!fc»tofr S«c*-^««* Strove*.
Foir porpoeea of ttiis annlyala. the Working
OVQUP nssnnws th* applksKtor to b® a 60 kg
wowao of cliKd-beurtoii ««», and **» 8l** of
«U&gt;uHf«tlon either a right-of-wfty or spot
testtow'fflt *f petture or ransoland. The
cauiprnent J*i e baofc-pitck sprayer UW). The
f ollowint; ealetdecUoiu of exposure are tese&lt;?
on dttntten for wi-asrtng of three pinU of
forntuiatod SiWdact per as pints of water.
Typical SAW fermulatlon*. based OJB Intgtectioa of a larcc number of r««1s?«r*;d
tebeta &lt;!««!), ranp from 4 to 8 pounds active
(utriKOertt Cacid equivmlent) per gallon. The
product u««l' in thto exfiosuire Mialyslfl has
itn aaBURMd concentration of 4 pounds 2.4,8T per gfclte label njeomajeadattorw vary
from ft recommended (UMte) of. 0.004 to 4
poiindsj »cM equlvftlent pev S3 pinto of
w&amp;ter. A dtlutSoD rate of 1,6 potnufri per 88
plate has beion «e!ected as representative of
tt, typtoanjr-twed aprss' aalxlum
Wolfe et aL (IW&gt; studied dermal enpoituro
tofoTi&amp;hte»,durlne hiwd back-ptick graying
to mo&amp;JiuJtws for ten sttis«tlora, Etpoeure
Wt^ed from 0.1 to 6.8 Mg/tir, with a mean
value of S.6 tog/hr &lt;6 nil/to). Method of spp^ic*«sn »w &amp; hand pressure aprayer. using
a O.W percent aj&gt;ray. Work«r« wore shortsfeevK), opw-neckod shtita with no gloves
or hat. Bwed on Wolfe's Oat*, CED uei)
c«l«rtat«d a d«srsnal expoawrg__of approximately 0.1W ptata per day. CED &lt;f««!) nteo
jfeteiiiviPiM that apj&gt;roxiiaat«Bly 10 p-sro#»t
fif Ibfi. 44,6-T *nd TC0D ooinins in contect
With tlw skin of thtf applicators vould J&gt;e
evsn after washb^, based on »b~
oth«r peatleidos

JBjM^^iiaJCJUuutiAra^^
!

'

'lUAnJIsI

Dilution. .jrat'4

3 pints

:
i

! Amount of diiutod
Imatofiel gotten
ton skin dally
J
i* Diluted eaterial
1 absorbed

JAftft

3 pint*

(1.6 powads
•

\0,00000016

Sr^S^f) par
| pints
2

pounds TCDD)
par 32 pints
0»18 pint

10*

0.0*09 ug
O.OOOT ug/kg

I
20

f level for t«rato-

msmm, vou 4% HO.

, AP» si,

0.03

ug/kg

�H130
Th« foltowias CAkuteUons (see .TAblo 31
''at mathematics) will give th« "daily derma)
KWosure tor both 3.4,8-T ar\d TCDDi (1)
Convert the dilution rate to grama; (8) mulsiply this figure 3&gt;y 1,000 &lt;f&lt;» 3,4,8-T) to concert to minieranM awl toy 1,000,000 &lt;tor
ICDD) to convert to mtorogrwas: (8) muttl*
9ly thte fiwu€ by the *My d&lt;sn»«l dose of
United material; (4) multiply tbls figure by
!;he percent absorbed; and (6) divide this
flswj* by the weighs of the applicator for
'ihc daily exposure to 3,4,8-T or TCDD per
8-hour working day. •
The Working Group considers that the
difference between the np-adyerse-effect
level of 3,4,6-T for teratogenie eftecto &lt;20
rnjf/kg) and this calculated dcrnml exposure
Jevel for 2,4,5-T (6.8 rflg/kg), as well as the
difference between the nc-advene-effect
level Q| TCDD lor tcrntogenic effects (6.03
.-jig/kfjt) find thfa calculated exposure tevel
tor TCDD &lt;0,OC07 pg/kg), do not constitute
ui ample margin o£ safety. The Working
Group therefore recommends issuance of a
rebuttable presumption asatost pesticide
products containing 2,4,8-T and/or TCDD
pursuant
to
40
CFB
Section '
iea.ll(aX3)(ilXB).
• '
(11) S'praj/ Applicator:
Low-boom Spnv jSquiptnent. For the purpose of this analysts, the Working Oroup assumes the applicator to be a 60-kg feraato of
childbcaring &amp;«e «l»arSng broah on either
jranselwuS or righte-of-way. The same product cited above &lt;a,4,5-T ttt 4 poimds/gfil) !»
being used, and the dilution rate 'fe l.fl
pounds of formulation to S3 pints of water
(equal to 4 pauncte of 2,4,5-T per 10 galtons
of water). Based on exposure studies uatag
sijtnilar equipment but a different herbicide
(147), the Working Group determined that,
during an eight-hour working day, the applicator would (;et 6.048 pints of diluted material on her skta, Th&amp; Working Group detenaineiJ iltsA IQ percent oTSIe pesticide on
the skJn woxjid bo absorbed (.14$, m, IK).
The following calculation* (see Table SS
for mathematics) will give tbe daily dermal
sxposure for both 8,4,6-T and TCDD: (i)
Convert the dilution late to grams; (S) multiply this figure by 1,000 (for 2.4,5-T) to convert to milligrams and by 1,000,000 (for
TCDD) to convert to mlerograms; (3) multiply this figure by the daily dermal dose of
diluted material; (4) multiply ttoiM figure by
the percent absorbed; and (S) divide thte
figure by the weight of the appMcator tear
the dally exposure to 3,4,3-T or TCDD per
8-hour working day.

ID .1.6 'pound.s/32 pi X
\ pound « 22.70
.

'-' Si.) 6.00000016 pouhds/I
32 pt X 454 g/pound »
t
0.00000227 g/pt;

12) 22.70 g/pt X UOOO ag/« i
I
22,?00 ag/ptj" i
: •
I
13) 22, TOO Bg/pt- X 0,18 pt &gt;
1
4,086 *tei
4,086 iii« X 10* »; 408.6 » 5

i
155 408. .6 rag / 60 kg V

12) 0,00000227 g/pt X

S
i
13)
i
!4)
f
IS)

1,000,000 ug/g s
2.27 ug/pfcj
2*27 ug/pt X 0.18 pt s
0*41 ug;
3.41 ug X 10? a
0,041 ug;
0,041 wg / 60 kg e

,U.«jiMJiAJl..Jfl.ttJiauftan.U
B.tlution

3 pint*
(1.6 pounds
2,4,5-T) per
32 pints

3 pints
(0,00000016
pounds TCDD)
par 32 pints

I Amount of dllutad
(material gotten
Ion skin daily

0.048 pint

0.048 pint

1%

10$

level
l«vel
1 8o-Adver8«-S'f f eoi"
jl«val for t«r«to«

109. sag

0.0109 ug

1,8 tag/kg

0*00018 ug/kg

20 Kg/kg

0,03 ug/kg

,,. — ^
^
1) 1,6 pounds/32 pt X '.45* g/- ID 0.00000016 pounds/pt X 454 g/pound
pound a 22.70 g/pt;
2) 22.70 g/pt X 1,000 Bg/« *
. 22,700 «g/ptj
3) 22,700 mg/pt X 0.048 pt •
1,089.6 agj
4) 1,085.6 rag X 10J *
108,96 ng;
5) 108.96 ng / 60 kg «

VOL 43, MO.

i
!2)
I
I
!3)
!
!4)
I .
15)

, A?lSi M, 1W8

0.00000227 g/Pt;
0.0000022? g/pt X
1,000,000 ug/g *
2.2? ug/pt}
2.27 'ue/pt X 0.048 pt •
0.109 ug;
0.109 «g X 10$ a
0.011 ug;
'
I
0.011 ug / 60 kg =
I

�17140
The Working Group consfcton that the
difference between the no-ftdveise-effcet
level of 8,4.8-T for t«ratogcnte effects (30
rag/kg) and this calculated dermal exposure
level for 3.4,6-T (1.8 mg/kg&gt;. as well as the
difference between the no-adverso-cttOTt
level of TCDD for teratogenie effects
«.03fte/fc8&gt; and. this .calculated exposure
level for TCOD (0.00018 j*s/fcg&gt;, do not con-

an ample nuurgtu of tsfety. The
Working Croup therefore recciaMveads fastifusee of a rebattable pmumptlon against
peetiddi» products containing 14,8-T wid/or
TCDD
pursuant
to
40
CFE
163.U(aX3XltXB&gt;.
&lt;U1) 4ertel Application:
tion Directly Beneath Spray fi«.n&amp;. Caplan
et al. &lt;i«7), working with aet'JaMy applied

(Dermal exposure to
laorially applied
.|nal«thion
Dilution rate

matothlon SB oil wraps applied at 0,40
pounds per 0.76 gallons water/aero, determined &amp; dermal exposure to persona directly
beneath the spray irtwie for bare akin (head,
necls, shoulders, forearms, hand;:, and
ffafghsT of 3.856 mg/d&amp;y. With these data.
an equivalent dermal exposure for 2,4.5-T
and TCDD, aerially &lt;*.ppl!«xl at 4 pounds acid
equivalent 2.4,6-T per 10 gallons watev/acre,
eajj ?»e detonnlned.

:3»5S6 fflg/0.^6 pounds a«lathion

Ifi&amp;fi

O.OOOQ'004
pounds TCDD
p«r 10 gallons of water

pounds
2 , « , 5 - T p«r
10 gallon.^ of
water/aor-a

©or®

% Diluted material
absorbed
**

10*

0 , 0 0 6 3 ug

Esposure level
0.051 s&gt;6/kg

5 X 1(J~6

10 sjj/kg

0,03

ug/kg
ug/kg

llevel for t«rato~
The following cialeuiattoaB («sa Table 31 _..
for
will give the daily dermal^
exposure for both 2,4,8-T and TCDD: (l&gt;
Divide th« dwmal exposure to malathion toy

the matathton application rate 6»&lt;J multiply
by the application rate of 3,4.0-T and TCDD
to obtain the desinal exposure; for TCDD,
multiply tbto flgturo by 1,000 to convert to

i
i

micrognxrm; (2) Multiply this figure by the
percent absorbed; and (3) divide this figure
by the weight of the applicator tor the daily
to 3,4,5-T or TCDD p«r 8-hour
!day.

.iuwuS,-——

10* » 3.1 ««;
3.1 B«/ 60 kg »

0.051 Kg/kg per day
Working Oroun coiusideni that the
difference between the 'ivt&amp;tssas-SSfi&amp;t
level of TCDD for ter&amp;togottic effecte (0.03
)*g/kg) and this calculated &amp;;rniat e^osure
level for TCDjgJS_x i*-"#5/Itg&gt; does coasti.^teltfi an ample marpn of safety. The WorteIns Oroup also ooiistdsra, iK-wever, that the
difference between the iM?-ac!v«sa-effecfc
level of 2,4,5 T for teratcgenie effectfl (26
me/kg) aad thii calculated dermal exposure
level for 8,4,8-T (0.051 mg/ky) dw^s not con-

ID
I
!
I
12)
I
S3&gt;

3.556 rag/0. «»6 pounds X
0«0000004 pounds 3
0,000003 atg X 1,000 «
9*003 ug;
0,003 ug X 10? »
0,0003 ug;
0,0003 ug / 60 kg *

aMUiU; au ftmpiis masictn of safe'.-s, Tbo
Working Group tlwrefors reconuiwnda touasi«) of a rebwtt'sbie prestuffipttoi
peatldde products contal'fiing 8,4,*-T:
ant to 40 CF» W3»il&lt;aX3XliXB).
(c) InluOatttm tx^omre: Aei~M Ap&amp;licntion. There «r« no studies jwailable on inhalifinon exnoBure of: 3,4,5-T, There are, however, several studies on inh^Micn expoatu^ to
Bialathion (1«7, 168) which CSJ0 «sed as a

43, MO.

iK6M tor this 2,4,8-T exposute
CJW). Caplan et al, (18") determ$j\ed asi air
eoncentintion, for unprotected persom directly beneath the apray plane during application rad for two hours afterward, of 0.067
mg malathton/m* from aerial api&gt;lU»tSon of
®M uoun«te AJ/gallon per acre. The collection period spanned the course of the actual
application time plus two hours thereafter.
The authors considered the sampling technique to be equivalent to average liuprlra-

81, lf?8

�17141
tten throwgSs the nostrils. Thla tohrt&amp;tto
unt ftvftJIaWn to- Ual&amp;tioii.)
n pcrceBt of tlie applied stwtothkm.
]. furtlwr report«d thajt ihe a«M_*l« Median dtemeteJ1 .£"-volume mediait di«meter, or vmd u) f as 1@ micrsflfi. Baj)od oa
work by Akeanon and Yates (f CtTCBD (/Srf)
e3tim&amp;i*4 SMt tHe ste of the malathiora
diQpteta which could t&gt;e inhaled mui imder
«0 niicrons. 81n.ee J.4.6-T is typically applied
"Th« nod to tl»t droplot size which divide* the total volume ol drops to tnlf, !«.,
60 tioreeut «f the volume Ss to dUop«
the vied .1)7^; and &amp;9 ixscent, telow it.

!*ir concentration of
iaerially appliad

as &amp; meiliura o? warse spi-*y, whils malatbion ta wvpisod ai a fine cuw, tl&gt;e percent of
2,4,6-T dro&amp;lets smalt ca/jugh to be inhaled
(under 60 microns) would be lea* than the
i»ercent of malftthiott droplet* amali enough
to be Inhaled, Aocor&lt;!ing to Akesson and
Yfetes U88\ 3 percent of 2,4.8-T spray droplets would be available for Inhalation (or H
th* amount of imlathion dropleto avaJlable
for Inhalation), on a "wojrst «ae" baste.
Tiu followsiig calcnlatSoiis (sea Table 33
for mattam&amp;Mcg) will $iw&gt; the dally l»h*lation espoaure for both $,4,S-T and TCIDD:
(1) MultiiiSj- the Btr o»ncentr»ti!&lt;m of ma..lltSlJJISt.l
..ItlL.^'MLlM.

0,067 »g/»3 with application
rat* of 0.46 pounds
gallon par

I
S
H'ae Dilution rut«

IfiAB

pound .1

0.0000004
pound* TCDD

I
10 gaiiOKS Of

lons of wat«r
p«r&gt;

100$

lev«l

par! "10 gal-

water/tore
iLung

100?

0.31

0.000032

2 hr

2 hr

2 I. 10*"5«g/kg

0,023 sg/kg
8 hr . .

level

!

8 hr
0.03 tg/kg

fop t«rato
w^^

&lt;Wi'.-

l

1CP.K

w«i

t) 0.067 rag/on s p«r 0.46
pounds 1 4 pounds «• 0»
HS/OU n 1 1/6 •&gt; O.OST

1) O.QS? ssg/ou H per 0.46
pounds y. 0.0006004
jjoanda o O.OOOOOOOS8

Klg/OU fi&amp;J

Bg/C»J SS 1 1/6

i

1 2 ) 0.097 »«/ou w X 1,
I
hr a 0 . 1 7 Kg/hi*}

«/«.

L -°*°^

a

0.000000009 mjs/au n 1
1,000 » 0*000009 MS/CU si j
2) 0,008009 ug/o«fflX

1«8 o« m/hr •

1 3 ) 0.17 mg/hr'x 8 * 1.36 mgj
i 1 4 } 1 . 3 6 tag / 60 kg •

lathion by the amount of 3,4,5-T and TCOD
applied, then multiply this figure by &gt;A for
the inhalation exposure to 2,4,8 -T nn&lt;i
TCOD; for TCDD, multiply this figure by
1,000 to convert to aiierogra»ts; (3) multiply
this Harare by the breathing rate; (3) multiply this figure by eight 18} fro get the 8-hour
exposure toM end &lt;*)' divide this figure by
the weight at the applicator for the inhalation exposure to 2,4,B~T or TCDD p«r 8hoiTO exposure.
The Working Group considers that the
diffeience between the no-adverse-effect
level of TCDD for teratogenlc effccte (0.03
»ig/kg) aiKl this ealcBlsted dermal espoflure
level for TCDI» (2 x 10 ••^e/kg) doe?s constitute «n ample margin of safety. The
Worfctag Group also considers, however,
that the difference between the no-adverse)effect leve&gt;] of 3,4,5-T for teratogenic effeefa
&lt;30 ffifi/ks) and thii calculated dermc! expoBUTO level tar 3,4.9-7 (0.0:99 mgA«lr&gt; does
sot oamtttate en ample margin of aafaty.
The Workkv Oroup therefore reoomMf;7i{s»
bniftnce ®f a rcbuttable pre8tt*aptlc&gt;&amp;
ipfaflt tnatiekto predicts containing; 2,4,9-T
I&lt;82.1i(aX8XUXB}.
XstpattUTt. The
Oroup has also considered the possibility of
a single individim! beiny esiposed througti
two 02- store of th# ebove i«utes. Tba result*
(derived fraa taMos 37, 80, and 31) are
sfeowti to 'l^blo £4. The Workin® Group felw
tlmt po»Me cumulative exposure to
dIo»J!t~&amp;ijiitaM5XS pesticides could
the totet tody burden and liicr«*eo
total rkt frora dlttxln exp^usB.
Workims Crnnp eomlfeta that the
f,we«m the no-adverse-effect
levd of fCim M t«ratogeiitc effect* (0.03
its/kg) »fid the oeleulaMt ewaiulatlw expol«7el« for TCDD in Situatioiu 3 «ud 8
T*bJ« 34) do constitute an ample
of safety. The WoftUSng Group oiao
, however, thst i^ie diffcraicoo bothe :i)-i&gt;-*&lt;Jv8«-3f-e«ecJ. levels of 3.4.&amp;-T
and TC£»D for teratccenlc ciffecte (20 mc/k*
«nd Q&lt;G3 ^ff/fes;, ia5j&gt;a:'t5vcly) und tho calculated Cumulative expowM levels for 2,4,8,-T
to feitufitiorjs l, 8, and 8 ai*d TCDD in 81f,u»tloffi 1 (see Table H) do not coiwtitute an
ample margin of safety. The Working
Group therefore «t»ai!infeiM'j issuance of a
rebuttab^ praumj'tiairi agfttet peaUotda
products eont«iAf!i$ rj,4,8-T pursuant to 40

0*000016 ug/hr;
3&gt; 0,000016 ug/hr X
8 * 0.000128 tsg;
4) 0,000126 / 60 kg a

-6
A.-' aefiimtmr* .KMrtunt: »&lt;Bfll».r ! ' i « ( * i M . 5 *MilRiS«J6lW.*«ftMrSiiCi-"MJ4JwUS.,-,» »lu»
W*«»«««*i!

"Johnson («8) (sea fJeetlon I.O.(8)&gt;, in a
review article, calculated a daDy iali*l»tilou
exrxwure to ptosnoxy hcrblddes of O.S26 pg/
kg for a 70-ks adult. Tbo m.i.valM'Cum wei«
based or&gt; wtel air mon!torto£ &lt;itjta of sir
8ft&lt;upl«fi collw.t«d fc» two wheftt-sro'tflBjg
»r*5B to the stats of Washiwii during
«piisi{T end suttiiMt' and eum'ijmad for pheuoxy herbicide. ?%« author did not specify
how soon aflter tp^tetlon the ttmples was'c
taken.

�Nona*

17142

\^^A^^I^mmK^.^J^*^^m^JU^M^^
lOral0,000? mg/Kg
I Dental- 6,8 ag/kg
'0.2.8*/kg*'

I
I Oral-'""" 0,0007 sg/kg
|D«r0al- 1.8 Big/kf
flnhel.- 0,05 A/
« 1.85

t Oral
I Dermal- 0,0007 ug/Icg
ilnhal.'jCuss. « 0.000? ,«f/kg
iOra),-

,
0.00016 ug/fcg
ilnhal.- negligible*'
0,00018 ug/kg

I Oral!Dermal- 5 I 10~6 ug/kg
Ilnhal.- 2 X 10"6 ug/kg
6
-J.
A/ Calculations ware sead« on a worst-oase basis as 3f
of da'real «poaur« basod ort Wolf* (1?9) who states, "orar
972 of th« p«3tields feo which the body la- subjected during
most axposure altuatlona, an&lt;J espwaially to applicators of
liquid apraya, is depoaited on the akin." TCDD inhalation
exposure values uoro negligible: Situation 4H, 21 X 10"
Situation #2, 5M JE tO"? us/kg,
I Oral0.000? rog/kg
IDapmal- 0.051 sag/kg
ilnhal.- 0,0^6 ing/kg

iv.

ws-ixw
ThJs section wl«ir«««ss other types of adverse effwte of 3. 4, 5-T for which the
Working Group tuts detewntaK? that Iraufficienf. &lt;jvt(.!«nca eitfcits to Initiate a wbutteble i»res«tnj?t10n. TIic Agency eaiidta coram«its from isgistrc )iis and other interested
parties on the evi(J*n«? list ad below, and r«^uetrfd (sabmlssSisn of m,y gdtiitiorai studies
or relevant inforafctioii on St, 4, 8-T »Jid/or
TCOD relative to these potential fidvatsc effects,
A.
M't(.t&lt;iffmteitt?.
- Secttoa
U3.1KAX8XUXA) providea fctet a rebuttable presumption shall R-rtee If a pesticide's
tngfedieKt(e), Met»&amp;oyte&lt;s&gt;, or dosraclatlon
produces) Induce m^temte effecie. as determtocd fey iaultit«8t STOWCC.
(1) «, 4, 5-T-&lt;a&gt; AMitive «tu^. Majumdar
anrt Oolte &lt;f 75) fed raftJo Dmtashtta, meHanogaxter either 290 or 1,OM ppm dioxto f rea
'8, 4, 5-T. (obtsinwl £ram wtessn

for IB days. They WCM then mated to sets of
virstn females to generate three 4'rtfl.y
breiods of offspidng. R flies were altowed to
mate, 1 F. flies were scored for X-llnk«d
and
access! /* lethals. Mo difference among
broods wort} notsd, and sals from &amp;J1 broods
we^a pooled. The percent lethala in coutixjte,
250 and 1,000 ppm croupe wsir*: dose-reMed
aanfl were 0.05, 0.026, and 0.88 percent, respectively. The control vs. 1,000 ppm lethal
rate mtra sJgoJ/tejnay different from ono
moth«? &lt;u &lt; 0.01). Kthyl methano saUonats &lt;3SO ppm) wes included »a a positiva control; it- yielded 13,70 percent tethals.- The
totej &amp;uatb«7 of flies te w-ch rapertacstol
group was no larger than 3,000.
&lt;b) Negative Stttdita, lite Rmtagercldty of
3, 4, 6-T was evaluated by Urcegovlch et el.
(14S), ejiiployiHsr the procedurd of Amos,
using five strains.of Sotoumdlti imhimurivm without activation. They concluded
WiM- 3,4, S-T to not HiBtsgesSc,
Fujita e* 81. (W9) reported chromosomal
L v(*9•cytogenetlc studies

U9 tffft, VOL 48, MO.

of human lymphocytes exposed to 1
10-' M of 2, 4. 5-T, which contalne
ppm TCDD, Breaks, deletions, and
were observed. Chromatld breako inc;
with increasing ixtwientratiorwi of 2, &lt;
It wua not t»*;!b!e to dfetinguUh ?;)
thin was «tosic effect or a. potential g
effect USO).
Maijuwdar arid Hall (JA9) reported •
oytogenetic effects of 2,4,6-T" on b
tone-marrow eelte of MougoUan gc-rlfil
aniniais wera injet»te4 with total amou
3.4.S-T at the rate of SO, 150, 350, 3SO,
me/kg body weight over the 5-d»y p«
the study. Increasing numbers of chrc
gaps, breaks, and fragments were obi
at 3£0, 950, eud $00 wg/fc.-j dose,-.. F
change fteui«a or teochromosome g*
breate were observed. This Us not a (
tlv@ exjxrriment for Indicating the p«&gt;t
of 3,4,5-T for causing heritable chrouv
damage &lt;11Q\ Toxiclty effects of the c
cal could give sinxfiar results (17t)\
Davring »md Hultg-ren (.171) report
«n in vivo study on the cytogeratic t
on boKe-itwsrrow cells of JViu mia
&lt;m*le ml«i) induced by a Swedish cw
ciaJ 2.4.S-T ester formulation '• and itt
pont'ttts. l"he study 8howe,3 that '»
cc&lt;mmercial products can affect chro
mal and repvoducUve mech«nisnis. Tw
ferent strains of mice were used with *
results for both. These results com
with effects seen In Drcaophfla. Th
thws stated that chromatid intsr- i
traexcbanses were never observed,
study was not carried out sufficient)
the demoratratlon of chromosomal e
sweh iis roaj-rangrment-i in future i«
tioswi of somatic, cells U70).
O^vdiig and Suruvn* U72) denwrvst
eytogenettc effects of B Swedish comm
3,4,8-T formulation • on oogenesia and
embryogenesis In Drosoykifa inela.nct&gt;
A BO percent decrease in fertility fo
flies wgvs detenaimd to be 350 ppui.
level is 40 to 60 times lotto thm field uw
f eatration levels. Reproductive and ela
sompi affects were observed.
""The 2,4,8-T used in this study wap,
chnsed from JEJtwtoian Kodak Co., He
ter, K.Y., ar'd contotued no measu
amount of TCDD. The authors do not
cste the limit, of sensitivity.
"The concentration of TCDD was gu
toed to fe« 1»3 than 0,1 ppta In the pro
"TCDD concentration was less thv
ppm in this formuJatiora which «»3 test
praftMca.' field uae concetitratioiut or lo%

AMtt «, 1W«

�17146
•118. KeJtermftn, O., M, Luyten-KeU«rmsm and C. R. Shaw. 1073. Genetic variation of aryl hydrocarbon hydroxylaiw in
human lymphocytes. Amor. J. Hum. Genet.
28:327-331.
•114. Kouri, R. E., R. A. Salerno, and C. B,
Whltmire. 1873. Relationships between asryl
hydrocarbon hydroxylswa fedticibllity and
sensitivity to chemically induced oubcutoneoua saroomw in various strains of mice. S.
Natl. Ceacer tot. 80&lt;a):S6S-383.
•118. Poland, A., and E. Olover. 1973.
Studies on the mechanism of toxieity of the
chlorinated dibenao-jMlioxlna. EnvJroa.
Health Perspec. 8:348-251.
•118. Poland. A., and S, Glover. 1974.
Comparison of 2, 3. 7, 8-tetrMhlorodibenmjHSioxin, A potent inducer of aryl hydrocarbon hydroxylase, with 8-methyleholanthrene. Molcc. Phsrmacol. 10:340-389.
•117. Poland, A., E., GIovw, and A. S.
Kende. 1978. Stereospecific, high, affinity
btadtog of 2, 3. 7, a4etmchloroditoeoao-jjdioxte by hepatic cystosol. J. Bio. Chen*.
2SlU®):4930-4948,
•118. Allen, J. R., D, A, Barsottl. J, P. Van
Miller, L. J, Abrahamson, and J. J. LaJieh.
Undated. Morphological changes in mon~
keys consuming a diet containing low-levels
of 2, 8, 7, 8-tetrachIorodlbeiKO-jMlJoxin. (In
Press, W. Cosmet. Toxicol.)
•119. Green, B. 1975. Cytogentte evaluation of several dioxins In the wt, (DRAFTunpublished.)
•ISO, Tung, T, T. 1073. Primary cancer of
the liver in Vietnam. (Transl. from French.)
Chirargie &amp;S: 427-438.
131. U.8. Department of Health, Education, end Welfare, I960. Report of the Secretary's Commission on pesticides, and their
relationship to environmental health.
Washington, D.C.
•122. Clew. I&gt;. J. 1671. Itobryotodcity at
chemicals contaminants of foods, Fd.
Coraiet. ToKlcol. 9:198-208.
•18S. Courtney. K. D.. D. W. Gaylor, U. D.
Hogan, H. L, Ps*, R. R. Bates, and I. Mitchell. 1970. Teratogenic evaluation of 3, 4, 9-T.
Siteice 108:864-864.
*134. CoMteB, T. F. X., »nd C. H. Wffitenw.
1871. Teratogwde studies with 3, 4. 6-T and
3, 4, 843 in the hamstw. Bull, Environ.
Oontom. Toxieol. e«J):8B»-W7.
*1S8. Roil, R. 1971. Steadies of th« teratofenic effect of a, 4, 8-T in mice. (Tram form
L Cornet. Toxicol. 9:8?HJT8.
Ron, R. 1973. Toxicologlcal evahiaof aj»eial orsBnoohlorfimtcd own?
pounds. SMvirom. Qus.1. Safety 3:117-124.
*137. Nwbert, B., sad I. DHlmaiw. 1973.
, natteyofoMdo effect* to asioe tn;%te4 with 3,
4, 64rtetolo?optoenoxyaoetic add and 3, 8, 7,
.

*183. Bwe, O., S. Cekouova, and K. S.
taKsoa. 1973, Teratogenic and e?»laryotosic
effects of tho berbteidei di- and
trlcblorophenoxyacctic adds (S, 4-D and 3,
4. 5-T). Aeta Phsnnacol. Toxicol. SS&lt;6&gt;:4684ie.
*133. Courtney, K. 0. !S7fl. MOWB« teratology studies with chlorodibCTOO-jMMojttra.
Bull, Knvirois, Contam. Toxlook i6:&lt;6)874881.
" • ' - . . • '.',
•184. Courtney, K. D, Undated, Premtai
effects of Jierbicides: evaluation by the prenatel developraeist to&lt;tex, &lt;1« Prea», Arch,
Environ, Contain. Toxicol.)
•138. Smith, F. A.. B. 2, Schwets, and K.
D. Nitschke, 1S76. Tewtogsniclty of 2,3,7,8tetrachloK»dlbeiKsy.|»-diosin In CF-1 mice,
Toxicol. Appl. PhunMCoL 88:017-833.
138. Ven-ett, J. 1970. Statement of Dr. Jacqueline Verrett, Food and Drug Administration, Department of HKW. P«f@s 100-203 in
Effects of 3,4,8-T on man and the environment: hearings before the Subcommittee on
Energy, Natural Resources, and the Environment of the Committee OJB Commerce,
Unites' States Senate, Ninety .First Coweas,
Second Session on Effects of 2,4,S-T on M*n
and tiie SnYironitt^nt: April 7 and 18, 1&amp;70.
U^S. Government Printing Offiw, Wagnington, D.C.
'
'
-•
•137..Bowca, O. W., B, B. Simoneit, A, L.
Burlingame, B. W. de Lappe, and R. W. Higebrough. 1973. TS»e wwrcfe for chlorinated
dibengofurans and ohlorinated ditenssodioxira to wildlife population sliowing elevated
kvels of embryonk death. Environ. Health
FersjOCC. 8,191-198.
*138. Lute, H,. and Y. lAiteOatertae. 1972.
Tlie action of different pesticides on the development of bird embryos. Adv. E?.p, Mcd.
Blol. 37:127-150.
189. Bal. H. S. 1977. Validation report.
tT.8. Environmental Protection Agency,
WaRfiingU&gt;n, D.C, (unpublished.)
•140. Sp*reehu, O. I*, F. L. Dunn, E. W.
Uaowe, and V. 1C. Rowe. 1671. Study of the
effects
of high
levels of 2,4,6trtetilorophertoxyacetic aoM on foetal development in the rat, F&lt;1, Comet. Toxicol.
®:527 830.
•141. Erawon, J. L,, D. J. Thoaijwm, B, J,
Streging, C. G. Gerbig, and V. B. BoWwon.
1971, Te»t«|r«nSo stvidte on M,6tdcMofaphenoayaefltSc «;Jd fa the rat stnd
»bWt. W. Cosroet, Ttostoift. e:3fl5-i04.
*143. Strp»«e, J. B., and W. SB. Kan. HW. '
Teratogenlc and tosicoloetea! cxftrntoM-toK
of 3,4,S-triehloropheBo»acetic acid in deveSaptog chicfe embryo*. Toxtel. 6:35-40.
•143. Bjorklwnd, k, and K. Brae. iWa.
Ftaeaoxy-ocid-iiKluc$4 renal c4i»!)g0s ta tine
cfeleken, I. uHrastaJcture. Acts Vet.

Arch. Pharaa»co).
•144. ielsmea,:, A/J, 1MI. The annitsi jsaf
«*|Sita oonsvaaptioa of Mtectal itenss of ioo^
•1318. Courtney, K. D., and J. A. Moore. to tl$e United St&amp;tf g, Qt]y. Bull, Acsoe. Food
1»71. Teratology studies with 3, 4, SOffte. 2«(8):U8-181.
trScliterophenosyH-OBtic acid and 3, 9, 7, 8^e«, H. a., K, c, w«ak«r, jr. w. mtracMojwS!o8D.TO-3J-di«J55to. ToxicoL Ai&gt;pl.
W. F. Dm-Jwm, 1999. Evaluation of
FhRrouwl. 20:^06-403,
the health htmurdt tavoSved In house -opray •
*JS8. %ftrschw, O. L., F. t&gt;. Diura, »nd V, tog with DOT. Bull. World Health Org.
K. Rwe. 167L Study of the terftiogenieity 4a*i lrT4%i
of a, 8, 7, 8-iatrad»10ro4tt»ni!o jj-dloxte In f 14O%Jerml Working Group on Pest Manthe rat. PdL Cosmet, Toxkoi. 8:403:41 a.
a^eitieut. 1974.. Oceapattea «x:ooaure to
*1SC. Kher*, E. S,, and W. l», McEinley. p^ritlcldw report to the Fadera) Working
1972. Fi«-»n4 posfoiRtel studies on 3, 4, 8- Group on Pest Hnms^m^nt from the Tank.
trlcWorophe»oxya«etlc
acid,
2,
4- Group on Oceupfttio'tt&amp;l Exposure to Pest-idichlcrophen0xy«bcetic acid and their d&lt;i- eides. Waahtagton, ».C.
iia »ta. Toxtcoi. Appl, PhannoooL
•147. St&amp;tf f, D. C., 8. W. Comer, J. B. Armstrong; and H. E. Wolfe. 1670. Bxpos'sre to
1. Sofeolik, I. Yu. 1973. Effect of S, 4, 8- the herbidda, pestwjaivi. Bull. Stwiron,
tttstiloroptenoxyacetic aei&lt;S «md its butyl Contara. TodcoL 14(8 ):834 -340,
ester on eeibryogenests of tftts. Bull
•148. Brcsgorfch, C. D., and K. A. R&amp;shid.
Biol. Med. 7«m:831-833.
1977. Muta$«rnis in muteat stnUm of

vot

montlla tvt&gt;Mmurtum by pesticides. Presented at 174th Amer. Chem, Soc. NU. Meettag, AupiiBt 80, 1977. (TJnpubltehed.)
•149. Fujita, K., H. Fujita. and Z. Funa•&amp;&amp;(. 1978. Chromospheric abnormalities
brought about by the use of 3,4,8-T. (Transl.
from Japanese.) J. Jap. Assoc. Rural Med.
24(8):77-79.
180. Memo: TCDI&gt;-d)oxin: mutageniclty,
dftted August 28, 1977. From Ruth Pertel,
O8PE, to Mary Ileece and Harvey Warnick
I'Project Manwesrs, OSPRJ.
*151. Yefknenlto, L. P. 1974. Data for assessing the gonadotropic and mutagenic
effect of the herbicide butyl ether 2.4,6-T.
(Trannl. from Russian.) Gig. TV. Prof. Zabol.
l8(4):24-27.
182. ConununicAtion presented at the
. HKW seminar on Environmental Mutagenidty, October 12, 1976,
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and chloracne. Trans. St. John's Hosp.
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•184. Kleu, O,, and R. GoMz. 1971. Late
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Oerawun.) Med. Klin. (Munich) 8fX2):63-58.
"138. ter Beek, F,, R. Bokhorst, M. v.d.
Fisa, K. Olsthoorti, P. Vergragt. and O. v.d.
Zwan. 1973 Dioxine, a dangerous pollutant
Us a widely u*ed herbicide. (Transl. from
Dutch.) Chernlflch Wwkblad 69(23):8-4.
'168, XeMkov, A. Kit., and L. N. Danilov.
1974. Oxiupattonal dermatitis (acne) in
workers engaged in the production of 2,4,8trichlorophenol. (Trwsl. from Russian.) So•157. Oliver. R. M. 1975, Toxic effects of
2,3,7,8 tetrachlorodibensso 1,4 dlox^n In laboratory worfcer*. Br. J. todust. Med. 82:49-83.
*1S8. Dugois, P., and L Colomb. 1087. ReniarSw OB halogen acne (as rega.rds an outbreak of CM'SS reBulting from the preparation of 2,4,S-tdchlorophiinol&gt;. [Transl. from
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ohlorinje acne.' (Trmtsl. from Oenuan).
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•160. Woods, J. S. 1973. Studies of the effects of 3,8,7,8-tetj'RChlorodibenTO-jMiioxin
on mamaite hepatic 8-aminol&lt;evilinlc acid
syjtthftaas, Knviron. Health Perspec. 5:221Wb,
•191. Ooidstelu, J. A., P. Hictoian, H.
Bertnoan, and J. 0. Vos. 1973. Hepatic porphyria induced by 3,8,7,8-tetrftchlorodibeiuo~jj-dioa!n. Res. Comm, Chem. Path.
PhftCTftWOi. S&lt;3):9J9-S28,
*193, ConiwoTOS1, B., and H. E. Scott. 1973.
Accidental oontatnin&amp;tion of soil with dloxin
in Mteouri: effects and countenneaaures.
CBNB, Watshtngton Univ., 6t Louin, MlusouW. F., and H. R. Wolfe,
issswrornent of the exposure of workera to pesticides. Bull. World Health Org.
Exposure analysis, 3,4,8-T,
'February 1878. From Chief, Chemistry Branch, Criteria, and Kv&amp;luation Division, to Project Manager, Office of Special
Pesticide Reviews.
188. Association of Food &amp; Drug Officials
of the United States. 1985, Appraisal of the
safety of chemicals in foods, drugs and cosmetics, Topeloi, Ksm
•160. Wolfe, H. R., J. F. Armstrong, and
W. F. Durham, 1974. Exposure of mosquito
control workers to feoihkm, Mo-iKjuito News

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&lt;p&gt;For more about this collection, &lt;a href="/exhibits/speccoll/exhibits/show/alvin-l--young-collection-on-a"&gt;view the Agent Orange Exhibit.&lt;/a&gt;&lt;/p&gt;</text>
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&lt;p&gt;For more about this collection, &lt;a href="/exhibits/speccoll/exhibits/show/alvin-l--young-collection-on-a"&gt;view the Agent Orange Exhibit.&lt;/a&gt;&lt;/p&gt;</text>
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                  <text>&lt;p style="margin-top: -1em; line-height: 1.2em;"&gt;The Alvin L. Young Collection on Agent Orange comprises 120 linear feet and spans the late 1800s to 2005; however, the bulk of the coverage is from the 1960s to the 1980s and there are many undated items. The collection was donated to Special Collections of the National Agricultural Library in 1985 by Dr. Alvin L. Young (1942- ). Dr. Young developed the collection as he conducted extensive research on the military defoliant Agent Orange. The collection is in good condition and includes letters, memoranda, books, reports, press releases, journal and newspaper clippings, field logs and notebooks, newsletters, maps, booklets and pamphlets, photographs, memorabilia, and audiotapes of an interview with Dr. Young.&lt;/p&gt;&#13;
&lt;p&gt;For more about this collection, &lt;a href="/exhibits/speccoll/exhibits/show/alvin-l--young-collection-on-a"&gt;view the Agent Orange Exhibit.&lt;/a&gt;&lt;/p&gt;</text>
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&lt;p&gt;For more about this collection, &lt;a href="/exhibits/speccoll/exhibits/show/alvin-l--young-collection-on-a"&gt;view the Agent Orange Exhibit.&lt;/a&gt;&lt;/p&gt;</text>
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&lt;p&gt;For more about this collection, &lt;a href="/exhibits/speccoll/exhibits/show/alvin-l--young-collection-on-a"&gt;view the Agent Orange Exhibit.&lt;/a&gt;&lt;/p&gt;</text>
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