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                    <text>Item D Number

02173

Author

Fecteau, Lois

Corporate Author
RODOrt/ArtiOlO TltlO P^B Experts Seek New Tests: No Conclusion on
Building

JOUmal/BOOk TRIO

Year
Month/Day

The

Saturday Press

1981
April 4
D

Number of Images

1

Thursday, September 20, 2001

Page 2173 of 2293

�FINAL EDITION

Saturday, Apr. 4,1981
Binghamtori, N.Y. 25 Cents

PGB experts
seek new tests
s

'

^™*i

; t.

' • . , ' •

^

No conclusion on building
ByLOISFECTEAU
NEW YORK — More testing needs to be done to
determine whether the contaminated Binghamton
State Office Building can be cleaned or will have to
be destroyed,.av panel of experts concluded yester-

cision may be that we^cannot make a decision,"
Haughie said.
"
'

Haughie and two members of the panel Will address the Brbome Cpunty Medical Society at 9.45
a.m. today on the health aspects of the contamination
at "PCB Information Day", at the Ramada Inn in
.Binghamton..:"
• ' ' ' ' ' ' ; , ' ? ; .
The state had asked the panel to determine the ac- .-'.
ceptable level of exposure to the chemicals polluting .
the state building. Panel members were reluctant tp
dp that, saying it is a sociolpgical and pplitical decision, i ;, i-V*''v,'r-f?''?' . - . • - . --'Sy4'^-i? ^rf?' •:
&gt;; ''I would think jt^would .not be appropriate for a
panel of scientists to decide this," Upton said. "This
,is a regulatory question, a societal question. What we
can perhaps do is define the levels Of risk." ' ' * » : "
Most panel members said they did not have enough
information on the state building contaminationi to
evaluate the rjsk^^s;v-&gt;.;.n;'";;'';V.'"':'-';;"/;&lt;;' '•'y.^?-'f "You do need some bioldgic data on the soot. Once
we hav,e that then we can begin talking about 'risky.',
said Major iAlvin L., Young, who has done extensivV,
research on dioxin, one of the toxic chemicals pollut-1
ing the^Uilding. ,
•&gt;,
. '
Ypung said he is frustrated the panel did npt come
;
"up with mbfe concrete suggestions.
• , • - : .','
....."I came prepared,to address the issues and we
didn't do that.?:There are; things;that could be done
right now','.. .'Ijwas going to suggest a cleaning re-"?
gime: I thjhk the^pught to-try a number of different
cleaning techniquesi-" Young said. • J
-;

day.
'
"I didn't think we've gotten past that point (of determining if the building can be cleaned). We're talking about dioxins and furans, compounds about
which there are a lot of gaps in pur knowledge," Dr.
Clark W. Heath Jr. said at a news conference after ;
the panel's meeting yesterday at LaGuardia Airport. •
"The toxicity of the soot has to be addressed before
you can answer the question of cleaning the building,-""said Heath, director of the federal Center for
Disease Control's Bureau of Chronic Disease, who
chaired one of the.panel's afternoon work sessions.
"W£agfee there needs to be much more comprehensive sampling of the building before this can be
dealt.wjth adequately,";said Dr. Arthur C. Upton,
chairman pf New York University Medical Center's
Department of Environmental Medicine, who
chaired the other work session!
Glenn E. Haughie, director,of the state Office of
Public Health, said he considers.the(.meeting a success even though no conclusions about the building
:
were reached." v
-;•••"'•
"It was successful in, that we got some of the best
.mindsAvailable on,this subject together,"'Haughie
said. v
'
Haughie said the state should not give up on the
problem despite the complexities it poses.
Young, an Air-Force troubleshooter, said he. will ,
"We cannot be paralyzed by problems of this sort. give the/state a plan,.to follo^ in:the absence of spe- t
1
The ainountr of''information needed will probably cific suggestions by the panel.
_
v ;.••••}• '
neve$jp,e availablevBut at some poinl we have to asN
semble what we'-kriow arid make a decision. That de- i . - ' :•' '
SeePCiB,4A . - , . . , ..•
'
::

�7

&lt;"Newv
question'number 1 (determining thevacceptable
level). We did spend a lot of time on it arid we
didri^t come up with 3 number/!Heath said.'/,;;; '
After the meeting Broome County Executive'
CarlS. Young said he was satisfied with the discussion. • • ' ' • '
'"-'•-•-'
"I'm satisfied that a process is under way, 1
that there seems to be a realeffort'tb address
everything," he said, adding that the conj;ami-'
nation has to be kept in perspective.
•
"When I hear, people talking abbut tearing
the.building down, I wonder where their heads '
are at," he added. "This has to be kept in the
realm of reality. We don't live in operating
rooms."
•••.",'••:•••••

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°2178
Young, Alvin L.

Corporate Author
Repert/ArtlClO TltlO Letter: from Alving L. Young to Glenn E. Haughie, May
7,1981

Journal/Book Title
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Month/Day
Color
Number of Images

D

6

DBscripton Notes

Thursday, September 20, 2001

Page 2178 of 2293

�*

�Alvin L. Young, Ph.D.
Environmental Scientist
520A Magnolia
Maxwell AFB AL 36113
7 May 1981
Dr. Glenn E. Haughie, MD
Director, Office of Public Health
New York Department of Health
Tower Building, Empire State Plaza
Albany NY 12237
Dear Dr. Haughie
I apologize for the tardiness of my correspondence! I did appreciate
the invitation to serve on the Expert Panel and to have had the opportunity of personally viewing the Binghamton State Office Building.
Let me formally share with you my observations and recommendations,
First, I commend you and your staff for the progress that has been made
on resolving this chemical contamination "episode". However, you are
faced with a monumental decontamination task which, unfortunately, has
the potential for becoming an albatrose around the neck of the NY
Department of Health for many years to come. It will likely produce
negative benefits for the State of New York in the press and with the
public unless the task is done carefully and tactfully. To this end,
I believe you must immediately initiate long-term plans. The most
important recommendation that I urge you to adopt is the formation of
an "Authority" or "Special Agency" to coordinate all activities and
functions associated with this episode. This "Authority" must be headquartered in Binghamton (preferably near the State Office Building so
that decontamination activities can be readily monitored, and so that
the "crisis" will be a daily reminder of the importance of its task).
The MBING-HAMTON AUTHORITY" should be composed of committee members or
advisors pMs a full-time, state-employed staff. The committee members
should represent the concerned public, appropriate labor unions or
employees of the State Office Building, and the city, county, state
and federal governments. The full-time staff should minimally consist
of a project director, staff scientist, public relations coordinator,
and a small support staff. The full-time staff should maintain a
facility where the Committee could hold weekly meetings, and where

1.

�letters could be typed, phone calls received, status reports prepared,
and interviews given to the news media. The current "Panel of Experts"
could periodically serve the Authority on difficult scientific questions
or sensitive public issues. The point that I am trying to make is that
the Binghamton Authority must have the responsibility and authority to
"get the job done". You desperately need a single focal point for this
episode. When I visited Binghamton I was appalled by the number of
"players" and the apparent lackoof coordination between them in collecting samples and giving interviews,and tours. Unless you can get this
facet of the program in hand,^, future accomplishments Mil be minimal.
A Binghamton Authority would provide the needed focal point. It is
important that every action that concerns this episode be coordinated
and appropriately documented. This includes proposals for research,
contractual arrangements and actions, sampling protocols, labor actions,
press releases, and the maintenance of a registry of visitors and tours
of the contaminated facility.
Although the cost of establishing a Binghamton Authority will be
significant, the dollars that will be saved, the knowledge that will be
documented, and favorable public relations that will be cultivated will
offset the investment.
The second issue I would like to address concerns exposure standards.
The Expert Panel meeting of 3 April was unable to establish permissible
expositae levels. In the absence of such data, I would recommend the
use of interim standards.
For example, for PCBs, an interim standard
of 2 micrograms/per square meter for public surfaces and 1 microgram
per cubic meter of air would be consistent with NIOSH actions. For
TCDD, I would recommend an interim standard of 0.01 microgram per square
meter and 0 0 6 microgram per cubic meter for similar surfaces and air,
.0
respectively. These latter interim standards are in keeping with actions
by the Italians and the US Air Force, respectively. I would also
recommend that different areas of the building have different interim
cleaning standards. For example, for TCDD, permissible levels of 5 micrograms per square meter should be adopted for inaccessible areas.
Obviously, until sufficient analytical and toxicological data are
2.

�available on the sample matrix, final exposure standards cannot be
decided. I believe that chemical binding within the soot has signifanctly decreased the toxicity of the samples (see ATCH 1, article fr©m
J, Agric. Food Ohem. 1981, 29:288-293). However , decontamination
efforts are pointless unless you have a goal-oriented program. Thus,
interim standards must be established concurrent with decontamination
actions, least you be faced with the delemma of when to stop cleaning.
In reference to toxicological testing, I was pleased to hear that you've
had state laboratories undertake the testing and evaluation of the soot
matrix. I feel very strongly that state and local laboratories should
play important roHes in this project. Nevertheless, testing protocols
should be prepared and evaluated on all projects, and all personnel
should be instructed in the safe handling of the chemicals associated
with the soot matrix. The entire project ooiald suffer if some laboratory personnel are contaminated due to poor testing and safety
procedures.
In reference to analytical determinations, I continue to support analyses
by Br O'Keefe and Br»Spalik. However, because of the complexity of
the analytical tasks, I believe it is important that confirmation of
selected samples be obtained from an independent laboratory. I
suggested to Br Schecter that the University of Nebraska has the necessary
capability to exam samples for 2,3,7,8-TCBB. A commercial laboratory
may also be of value in providing rapid turn-a-round time for selected
samples.
During my visit to Binghamton, I discussed with Br Schecter the need for
a standard sampling protocol. This should include a program where all
samples for all facets of the project (toxicology, characterization, and
decontamination) are collected by the same team with records established
on where, when, and how the samples were collected, I believe the
current procedure is not providing the adequate "economy of sample" nor
"maximum data per sample" that is so necessary in this project. For
example, I recommended to Br Schecter that:
A. The same location be wiped sampled on multiple floors.
I suggested that a site near the vent in the NE Mens
Room be sampled on Floors 3,7,11, 15, niid 18. This
will allow dispersion modelling from the source.
3.

�B. Wipe samples (from floor, wall, and ceiling) be collected from common areas (e.g., elevator lobbies)
associated with floors 4,8, 12, and 16. This will allow
comparisons between similar floors, walls, and ceilings
that are located at equal distance from each other.
C. Air samples be similarily collected from 2 locations
(heavy traffic areas) on 3 different floors. The
air samples should be 48-hr samples and should represent
both partic.ulate and vapor phases.
Detailed analyses of the above samples would provide a more complete
picture of the magnitude of chemical contamination of the State Office
Building,,They would also provide excellent baseline data prior to
extensive decontamination operations.
There are a few minor (but critical) items that I would bring to your
attention. It is essential that a registry be prepared of all personnel potentially exposed to the toxins. This should include fireman,
workers, visitors, etc. The more thorough the documentation of the
individuals (identification, job, age, address,etc.) and the exposure
(date, circumstances", located visited, etc.), the more valuable this
registry will become in the next few years, especially when legal
actions are taken and liability determinations are made. Another item
is the disposition of the contaminated office equipment and furniture.
I discussed an idea with Dr. Schecter concerning the equipment and
furniture; I believe that with appropriate safe guards (approved by
EPA), some enterprising firm may be willing to decontaminate, repair,
and repaint the equipment and furniture. The firm would be responsible
for safely removing the "bagged" equipment and furniture at no cost
to the state. It would in-turn recover costs through the sale of
the items. The county or state would profit by not ihaving to dispose
of the material in a sanitary landfill or through incineration. This
idea would be most feasible if it is shown that the soot reduces the
exposure potential of the toxic chemicals.
The parking garage was essentially decontaminated when I visited
Binghamton. I would hope that the latest wipe and air samples confirm
that the area is "essentially" decontaminated. Since this is an
important parking facility, and one that can be controlled, I believe
that the most stringent standards need not apply, I believe that the
4.

�benefits gained from opening this parking facitity as soon as possible
will outweigh the minimal risks associated with exposure to almost
negligible levels of soot-bound contamination. This brings me to my
last point. Because of the incidents associated with controlling the
fire, and the initial attempts at decontamination, the soot, and hence,
PCB, TCDD, and TCDP,;have spread from the building to other areas in
the community. I realize that some mapping of the surrounding contamination has been conducted. I would certainly recommend continuation
of a systematic (and periodic) mapping program. The public needs to
know that there is an environmental monitoring program. The public
needs to also hear "positive" information (the intent of my short
seminar to your medical association). The "Doom and Gloom" team
constantly maximizes any threat at the expense of perspectives and
probabilities. In truth, we have no information that the low levels
of PCBs, TCDDs, and TCDFs encountered in the environmental monitoring
programs or in the decontaminated areas pose a threat to man or his
environment. We must not let emotion dictate that the State Office
Building and all its contents be destroyed. The project that faces
you will be difficult but it ;is manageable?
I believe that my comments address the questions and concerns in your
letter of 15 April and Dr Schecter's letter of 10 April. It I can
be of further assistance or clarify any of my comments, please contact
me.
Sincerely yours,

AIVIN L. YOUNG, PhD

1 Atch
Journal Article
cc
Dr. Arnold Schecter

5.

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02179

Author
Corporate Author
Approves PCS Destruction Process

JOUmal/BOOk TltlB

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Chemical &amp; Engineering News

1981

Month/Day
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D

1

Dosorlpton Notes

Thursday, September 20, 2001

Page 2179 of 2293

�News of the Week

EPA APPROVES PGB DESTRUCTION PROCESS
The Environmental Protection
Agency last week approved the first
chemical process for destroying toxic
polychlorinated biphenyls, which
have been widely used in electrical
transformer and capacitor insulating
fluids. The process, developed by
Sunohio of Canton, Ohio, and called
PCBX (C&amp;EN, Sept. 22,1980, page
6), becomes the only approved alternative to incineration or burial for
PCB-contaminated oils.
EPA's acting assistant administrator for pesticides and toxic substances, Edwin H. Clark, says the
process is "of significant value in
solving the nationwide PCB problem." Contamination of the environment by PCB's has become ubiquitous since their introduction in 1929.
Animal tests have shown that PCB
exposure can lead to reproductive
failures, birth defects, skin lesions,
and tumors.
Clark says the process has been
approved for limited use in EPA Region IV (based in Atlanta) and for
more widespread use in Region VII
(headquartered in Kansas City, Mo.),
tinder current rules, each regional
administrator determines what PCB
disposal practices are used in that
region. And the process will be limited
to decontamination of mineral oils
used as coolants and dielectrics in
large electrical transformers. About
750 million Ib of PCB's are still in use
or in storage, much of which could be
eliminated by PCBX.

The PCBX process uses a proprietary reagent that strips the chlorine
atoms from the compounds, converting them to chloride. The biphenyl moiety is polymerized to a
polyphenylene and precipitated from
the oil with calcium chloride, into a
holding tank. The cleaned oil can be
returned to the transformer for reuse.
Excess reagent in the oil is destroyed
or removed before going back to the
transformer. The waste polyphenylene from the process is not soluble in
water, is only slightly soluble in alcohol or other hydrocarbon solvents,
and is considered environmentally
safe.
The prototype setup used by
Sunohio for the EPA tests can decontaminate oil at a rate of about 10 gal
per minute, but future setups are expected to do better. The system's size
and efficiency permit it to be built
into a truck trailer, which can go to
the transformers, rather than having
to transport the oil from the transformers to a plant. It can take PCB
levels from any concentration down
to less than 2 ppm, the detection limit
for these compounds.
At this time Sunohio has only one
unit ready for commercial use, but
two more are under construction and
a total of five mobile units are
planned. The technology also is
available for licensing. Sunohio officials estimate the price of decontamination to be competitive with other
systems, figuring about $3.00 per gal

Mobile Sunohio unit cleans PCB-contamlnated transformer oil on site
4

C&amp;EN June 1,1981

vs. up to more than $5.00 per gal for
incineration.
Preliminary testing indicates that
with modifications the process can be
used to destroy chlorinated pesticides
as well. Although Sunohio officials are
reluctant to speculate, this also could
save companies with stores of now illegal pesticides considerable expense
in disposing of the materials.
D

Senate okays funds for
binary weapons facility
After only a 40-minute debate on the
floor, the Senate last week approved
$20 million to equip the Pine Bluff,
Ark., facility which is being built to
produce binary nerve-gas shells.
The money, sought by the Reagan
Administration in its fiscal 1981 defense supplemental request, already
was approved by the House. It is,
however, only a pittance of the estimated $2 billion to $4 billion required
to bring binary chemical weapons into
full production.
The Senate's decision to accede to
the Administration's request was
reached without value of Appropriations Committee hearings. Opponents
of a resumption of a chemical arms
race argue that the decision was,
therefore, reached inappropriately.
Sen. Mark 0. Hatfield (R.-Ore.),
chairman of the Appropriations
Committee, last year successfully
blocked insertion of $19 million in the
defense appropriations bill for the
weapons facility. This time around, in
an emotional outburst, he asked: "My
God, is there no limit to the voracious
appetite of the military machine that
wants to suck up every dollar that we
have?" Again he cited lack of public
hearings, and lack of consultation
with NATO allies on whose soil these
weapons will have to be stockpiled.
Sen. David H. Pryor (D.-Ark.), in
whose state the facility will be built,
and who opposes a chemical weapons
program, argued that such a program
"repeals the spirit of what the civilized world has been working toward
since the Geneva agreements of
1925." He noted that the action taken
by the Senate would "reverse the
position of the past three Administrations" and begin "a race that has
no finish line."

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                    <text>Item D Number

021 si

Author
Corporate Author
RBDOrt/ArtlClB HtlB Typescript: Proposed Worker Surveillance, BSOB,
Draft June, 19,1981

Journal/Book Title
Year

000

°

Month/Day
Color
Number of Images

D

9

DBSGPlpton Notes

Thursday, September 20, 2001

Page 2181 of 2293

�PROPOSED WORKER SURVEILLANCE, BSOB
J

DATA BASE

Ba&amp;ed on data in the possession of the NYS Ueoartment of Health at this
tine, partial or complete records exist on 479 persons working for 20
different firms not including a small miscellaneous category.

They are

shown by employer and leve 1 of exposure categories in Appendix I. It should
be pointed out that information on both employer and exposure was obtained
from the individuals themselves , either at the time of the blood drawing
when a Binqhamton General Hospital medical record questionnaire was completed,
or during a personal interview with a nurse.

Based on place of exoosure, the 208 persons actually in the BSOB would be
the most likely to have sustained genuine exposure.

In addition, the

qroup in the basement or subbasement (unknown if this was the garage or
building) and the 65 with unknown exposure are considered suspect for
f

building exposure until further information can be obtained on them.

The

other exposure categories would appear to represent minimal non-exposures
to BSOB soot.

V
,T u\
1 4*^ U
k \ S.
**' tt*
^

wide variation in duration of exposure was indicated as well. At one end
of the spectrum, the 33 NEPCO employees worked a minimum of 100 hours in
, with many in excess of 700 hours.

the

The OGS clean-up crew

soent between 50 and 100 hours in the building.

A few OGS
_--.—--•employees have

sDent more than, 100 hours in the building.

——

The Miske Electric electricians

------

—

appear to have spent less than 100 hours in the building. Virtually all

other oersons seem to have spent no more than a few minutes to a few hours
,
in the

�Department to their private physicians.

Most of the remaining individuals

either have no private physician or failed to indicate one at the time of
evaluation.

«• /""

�on an as needed basis.

A telephone answering service is on line to refer

health inquiries from individuals in this group to the NYSDH.

If the

inquiry is in response to a health problem that might reasonably be related to exposure to the BSOB, arrangements will be made, at no expense to
the individual, to be seen by a local internist with referral to a dermatolo
gist if deemed appropriate.

Both of these evaluations are offered for

general health screening without regard to etiology and, as such, no
attempt will be made to summarize or analyze the data from the group as a
whole.

SUBSET EVALUATIONS
The most intensive surveillance monitoring and analytical efforts will be
focused on a small subset of individuals with we11-documented high exposure.
High exposure can be defined by both place and duration of exposure.

Since

contamination is largely an intra-building problem, those persons who have
entered the building since the fire are the most likely to have encountered
i
f
significant exposure.

Of the groups who have been in the building, duration

apparently was greatest for NEPCO cleaners, followed in decreasing order of
duration by the OGS clean-up crews, Miske electricians, and National Insulation cleaners.

Other groups in the building tended to be small and spend

only limited time in the building though individual exceptions exist.
guably the most fvp^'if^ riingili

n

ir V-MS I Ti" • NFP1"" "TtMH"i"rr

Unar-

Howvftri thn

fact that they are more or less continuously involved in toxic 'clean-ups of
one sort or another renders any information gleaned fr
^
—
^ ^ *
m ^
i i.
if not impossible to interpret. While data will be collected on this group,
no analysis will be attempted on this information.

�*. U

V _ •&gt; c

-4-

The general surveillance scheme is shown graphically in Appendix III.

The

general health screening which will be provided to persons whose exposure
was limited to outside the building has already been described. Persons
who have been inside the BSOB but for only a short time will have a similar
blood screen with an additional tube of blood saved for potential future
reference.

Those persons determined to have spent a long time in the BSOB

will have a similar blood screen.with sera being saved.

A portion of the

saved sera will be used to determine a serum PCB level.

The long duration

BSOB exposures group will also be offered a physical examination.

. Because of what is known to occur in animals and humans exposed to PCBs and
other compounds in this group, certain a priori hypotheses can be advanced
as to health effects one might see amongst the population exposed to the soot
from the BSOB.

Conclusions on the human health effects of exposure to BSOB
»
soot wi^l be limited to analytical results which are biologically plausible
and have been generated in response to these prestated hypotheses.
organ systems of most concern are the liver and integument.

The

Since a diag-

nosis of liver disease is often arrived at only late in the natural course
of an illness, we will focus on liver function test abnormalities under the
presumption that they are surrogate markers of potential or real future
disease,

ajj p&lt;=»-gQng '"fr"'"0 v^"" •»p +-v&gt;p Vm-iirHng j=p,pqethe fire for a

minimum of 25 hours will be included in t-hir, n m l y n i n i
subset may also be analyzed separately.

Subsets among this

The mean values for several liver

function tests drawn while in the building will be compared to the mean
values obtained after having terminated exposure for a period of time.

The

hypothesis, succinctly stated, is that there is an association between exposure to the building and an alteration (either up or down) in liver function
tests.

The hypothesis must be two-tailed because initial bloods were not

�timing then, follc.w-up liver tests might be expected to show a rise or a
fall.

The liver function tests which will be analyzed include SCOT and

GGTP.

The physical examinations will give special attention to the skin.

Chlor-

acne, a condition essentially pathognomonic for exposure to PCBs and related compounds, will be looked for.
period before its appearance.

Chlgracn_e_.is known to require, a latent

It is jalsg^.verv persistent.

As such. a single

examination approximately six months after initial contact seems a reasonable
time to look for such a condition.

Since no cases of chloracne are expected,

/observation of even a single documented case will be presumptive evidence
of an adverse health effect.

Skin biopsy of suspect lesions will be required to document chloracne.
Dr. Kimbrough of CDC in Atlanta, GA, has agreed to review slides from any

biopsied lesions to determine if the changes characteristic of chloracne
are present.

In an attempt to quantitate exposure to PCBs in the building, a comparison
will be made between the initial serum PCS values obtained either before or
shortly after entering the building, and the value obtained at follow-up.
This evaluation will be performed on values from all persons who were in
the BSOB a long time and for, whom an initial sera for PCBs is available.

To make data as comparable as possible, several things will be done whenever
possible.

First, the same laboratory will be used for both initial and

follow-up general blood screening. Second, a limited number of physicians
familiar with chloracne and other PCB effects will be utilized for physical
exams. Finally, serum for PCB levels will be sent to a reputable laboratory

�well experienced in PCB analysis.

They will be sent both initial and

follow-up sera at the same time and asked to analyze them blind as to the
time that they were drawn.

SUMMARY
In summary, the surveillance of persons potentially exposed to contaminants
in the BSOB will involve a 3 tiered approach.

Those whose only exposure was

outside the BSOB will receive a follow-up blood screen while those exposed
inside the BSOB may have sera saved for future^ testing, serum PCB determinations and/or a physical examination depending on duration of time spent
in the building.

Analysis of

infnr-mal-irm

o n h a a H - h e f f e t e w i l l ho '. in)j,-

to selected liver function tests and a search for chloracne.

An attempt to

quantitate exposure to PCBs will be made by comparing initial and follow-up
serum PCB levels.

If no health effect or exposure is demonstrated/ no

further investigation is expected.

Should significant effects or exposure

be found, additional investigative steps might be indicated.

�APPENDIX I
Place of Exposure

Total
N

Firm or Group

1.
2.

New York Telephone
Press

3.

Firemen

4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.

Police
AJ Cerasaro

Talent Search
NIOSH

Broome County
City of Binghamton
Bldg. Services Aides
BGH Staff
NEPCO

New York Gas &amp; Electric
Valley Welding

Fanta Sea
Central Steel
OGS
Miske Electric S
NYS, Miscellaneous
Security

Miscellaneous
TOTALS

In SOB
Bldg.

3

In
Garage
Only

0
1
0
4
0
0
0
9
0

In City or In Cars
County
From
Bldg.
Garage

1

6
6
32
39
14
4
1
60
54
3
4
48
21
1
2
6
66
33
39
20
20

6
2
0
0
34
19
0
0
4
48
29
22
1
2

0
0
0
0
0
2
0
0
0
1
0
0

0
0
17
0
0
0
19
48
0
4
0
0
0
0
0
8
0
1
0
1

479

208

17

99

4
27
4
2

0
I

0
0
0
7
0
0
0
14
0

Exposed to
Bldg. Materials
In B
Outside of
or SB
Bldg. or
Definite
Bldg. or
Near
NonGarage
Bldg .
Exposure

0
0
1
0

0
0
0
0
0
0
0
0
0
0
0
0

12
0
0
7
0
0
0
0
0
0
0
0
2
0
2
2
0

0
0
1
0
0
4
0
0
0
0
0
0
0
1
0
0
2
0
4
13
3

21

26

28

0
0
0
0
0
0
0

1
0
3
0
8
0
0
0
0
0

0

i

i
Unknown i

2
1
3

:

7

.
F

0
0
0

4
4
0
0
6
2
0
0
2
6

2
0

4
8
2
14

15

65

1

;•
;

,
!

:

�Bjochem is try 5c reen
Glucose

BUN
Creatim'ne
Total bflirubin
Direct bilirubin
Total protein
Albumin
Uric acid
Alkaline phosphatase

SCOT
LDH

SGPT
GGPT

Cholesterol'
Triglycerides
Calcium
Phosphorus

Acid phosphatase
Serum iron
Total iron binding capacity

ootainea,

�APPKNDiX III

Possible Exposure

Initial Blood Screen
(CBC, SMAC 20, Saved Sera)

Exposure Outside BSOB

Exposure Inside BSOB

Short Duration

Follow-up Blood Screen
(CBC, SMAC 20)

Follow-up Blood Screen
(CBC, SMAC 20, Saved
Sera)

Long Duration

Follow-up Blood Screen
(CBC, SMAC 20, Serum
PCB, Saved Sera)

Physical Exam

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            <name>Title</name>
            <description>A name given to the resource</description>
            <elementTextContainer>
              <elementText elementTextId="22743">
                <text>Typescript: Proposed Worker Surveillance, BSOB, Draft June, 19, 1981</text>
              </elementText>
            </elementTextContainer>
          </element>
          <element elementId="49">
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            <description>The topic of the resource</description>
            <elementTextContainer>
              <elementText elementTextId="22745">
                <text>exposure assessment</text>
              </elementText>
              <elementText elementTextId="22746">
                <text>PCBs</text>
              </elementText>
              <elementText elementTextId="22747">
                <text>health monitoring</text>
              </elementText>
            </elementTextContainer>
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  <item itemId="3113" public="1" featured="0">
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        <src>https://www.nal.usda.gov/exhibits/speccoll/files/original/853b047330bd474a0bc02eb0ee2e5c84.pdf</src>
        <authentication>73689b98be00e93815db3d804a567c57</authentication>
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                  <elementText elementTextId="63559">
                    <text>Item D Number

02133

Author

Smith, P.M.

Corporate Author
ROport/APtlClO HUB Typescript: Analysis of a Binghamton Soot Sample for
Tetrachlorodibenzofurans and Tetrachlorodibenzo-pdioxins, October 1, 1981

Journal/Book Title
Year
Month/Day
Color
Number of Images

D

21

Descrfyton Notes

Thursday, September 20, 2001

Page 2183 of 2293

�Analysis of a Binghamtcm Soot Sample for Tetrachlorodibetizafurans and
;" --Tetrachlorodibenzo-p-dloxins

R.M. Smith., D.L. Hilker, P.W. O'Keefe, S. Kumar, J. O'Brien,
B.L. Jelus-Tyror, K. Aldous

October 1, 1981

�INTRODUCTION

A fire caused by a malfunctioning PCB-filled transformer in the
Binghamton state office building on February 6, 1981 released an unknown
amount of incomplete combustion products into the 18-story building.

A

sample of soot (Tox. No. 811711965) was collected from an unspecified area
*

u

of the building using a vacuum cleaner.

"

A portion of the homogenized soot,

intended to be used for animal toxicology studies, was soxhlet extracted
for 16 hrs in benzene and analyzed for TCDF's and TCDD's by capillary GC/High
resolution mass spectrometry (HUMS).
PROCEDURE
Fifty yl of the benzene extract (corresponding to 46 mg soot) was
spiked with 6 ng of

13

C labelled 2,3,7,8-TCDD and cleaned-up prior to GC/HRMS

injection using sequential liquid chromatographic columns containing PX-21
adsorptive carbon, 2% deactivated silica gel, and activated Florisil. An
.-.-!. ;.

aliquot of the concentrated sample was then injected onto a 40 m x 3 mm OV275
coated soda glass GC capillary which is interfaced to the MS-50 HRMS through
a jet separator.

The temperature was appropriately programmed and mass profile

data was accumulated for the m/e 306 CTCDF), 322,320 (TCDD) and 334 (13C TCDD)
ions.

13
Standards ( C 2,3,78-TCDD and unlabelled 2S3,7,8-TCDF) were run. prior

to sample injection.

A control sample of Fisher activated coconut charcoal

was similarly spiked and analyzed.

RESULTS AND DISCUSSION
The sample was found to contain a complex mixture of TCDFs as shown
in the chromatogram in Figure 1.
present.

At lea'st twelve distinct TCDF peaks are

2,3,7,8-TCDF eluted as peak No. 12 as determined by comparison

with an injection of authentic 2,3,7,8-TCDF.

Trie presence of amounts of

tetrachloroclibenzo-p-dioxicis in the sample are indicated by the M3 chroma tog ram

�—3-

in. Figure 2.

Closer inspection of the data revealed the presence of an

interferent.

However the data system allowed consideration of -the intensity

due to tetrachlorodioxin ions which were partially resolved from the interferents (Figure 3 .
)

The interferent appears at an m/e value very similar to

that of the [M ~C1] fragment of heptachlorobiphenyl.

Signal detected in

the dioxin ion position in the m/e 321.8936 mass region, which occurred at
the same time in the chromatogram as the
being due to native 2,3,7,8-TCDD.

C-2,3,7,8-TCDD were taken as

This implies a relative retention tine

of 1.00 for native 2,3,7,8-TCDD.
The quantitative results of the analysis of the. samples are summarized
in Table I.
and TCDD.

The figures given in the table denote only "detectable" TCDF
The sample cleati-up procedure that was used requires the use of

isotypically labelled standards to correct for low recovery.

Presently, no

labelled TCDF is available and the assumption was made that the recovery
of all TCDF and TCDD isomers was the same as that of the

13

C labelled 2,3,7,8-

TCDD internal standard based on preliminary TCDF recovery experiments.
Although the capillary GC column gives a high degree of isomer separation,
the analysis should not be considered completely 2,3,7,8-TCDD or TCDF isomer
specific as other isomers may co-elute.

The unexpectedly large amounts of

TCDFs found in the sample exceeded the linear range of the HEMS, making a
second injection using less sample necessary (Fig. 4) for proper quantitation
(All calculations and several important mass profiles are included in the
appendix).

No TCDDs or TCDFs were found in the control carbon.

The results show that concentrations of TCDDs and TCDFs in this
soot appear to be similar to those found in soot

TOX No. 811710280 and

air particulate sample Tox No. 811710977 previously taken from the Binghamton
state office building.

�u

TIME:

Ml

166

�B-S55 HIGH RESOLUTION MPM
.» • RUNNRME FDHM3
DOTE 7/10/81

TT-H
TIME

G9:30

L

05:30

1

1

10:30

1

TIME 21 :11

20:30

1

,* ?5:30

ric

Ml

12

13

14

. 105

1

209

313

41?

*DL *
DRTE 7/10/81
TIME 21:11
RUNHRME FDHM8
SWEEP
300 (PPM)
SCRNTIME 0.3 (SECS)
MRSS 305.8936
SCflNS 194-205 100'-S INTENSITY 143676
100

75

305.8527

305,8986

395.9445

�R U N N f l M E FTJHM9
•MBSS 321.893B
SC.RNS 149-433

IIRTE 7/1D/81
TlM'E 21 i l l
SWEEP
389 ( P P M )
S C f l N T I M E 0.3
I N T E N S I T Y 442547

CSECS)

109

25

321.8452
*BL HOU KRNY RRERS73*

321.8935
DSSS HIGH RESOLUTION MP«
PERK SUtlilRTION REPORT

RUNNflJIE FBHM8

DOTE

7/10/81

TIME 21 i l l

MOSS
321.8935
389 PPM
SCflN WIDTH
SCRN TIME
6.3 SECS
SCRN NUMBERS 149- 438

STRNDflRD
FflCTOR

0.6899
0

KflMINSKY'S BING. SOOT 2.S5 OF 9.0UL
MPSS
ITEM
CENTROID '
321.8789 TOTRL
321.8733
1
321.9021
2
321.9331
3

RREfl - 'BRSELIHE
BRSELINE
SUBTRflCTED SKIMflED
32772100.
YES
NO
27343790.
YES
NO
5367326.
YES
NO
61077.
YES
NO

•&lt;TOTfiL RELATIVE
RRER TO STflNBRRB
95.17
0.00
79.41
0.00
IS.59
0.G0
Q.18
0.00

�bfcC0JUft

• 720 SCITSS6A HIGH RESOLUTION MPM
•„• RUNNflJlE TDHM4
DflTE
7/16x81

"I

vit

-*- *&gt;/ **

TINE 12i28

RETN
TltlE
,60:39 ,

,03:39

^16:39 n-

.* 2 : 3 a .

f

t20130

TIC

305.8986

'^l 060255

Ml

M2

?=Ty^y2^?"

1

•

~T

r-

105

1

1

209

*DL *
DS55 HIGH RESOLUTION MPM
RUNNflJIE TDHM4
DfiTE 7/16/81

RETN
TIME

69:39

rw

r"' •™""r"—r*

313

r

417

TIME 12:28

04 ;39

20! 38

.

313
*DL *

180'-S» 1869255

'4 1 ?

�Table I.

Results for Sample 811711965*

TotalVpuran Concentration - 597 ppm (Detection Limit = 2.3 ppm)
2,3,7,8-Furan Concentration - 48 ppm (D.L. - .45 ppm)
Total Dioxin - 1.8 ppm (D.L. = .04 ppm) Ratio 320/322 = 0»87
2,3,7,8-Dioxin - 1.2 ppm (D.L. =.008 ppm.) Ratio 320/322 = 0.86
Recovery - 4%
Amt. of

13

C-2,3,7,8-TCDD spike - 6000 pg

Weight of Sample - 46 ing
Cone, of Spike - .13 ppm
Relative Retention Times:
2,3,7,8-tetrachlorofuran - Standard: .1.264

Sample:

1.269

2,3,7,8-tetrachlorodioxin -

Sample:

1.00

No TCDF or TCDD was found in the control carbon sample

�_APPENDIX:

Supplementary Data

1.

Carbon blank

2.

External standards

3.

Mass profiles 1st injection-Runname FDHM8

4.

Second injection data-Runnarae TDHM4

5.

Calculations

�DS55 HIGH RESOLUTION MPM
RUNNRME: FBHM?
DRTE
RFTH
TIME

60; 30

t

•

85; 39

r1""

TINE 20»26

15i39

.

f

25:38

'TIC

Ml

M2

«3

N4

101

**&gt;

201

301

T"

�BS55 HIGH RESOLUTION MPM
•RUMNRME FBHMb
DOTE 7/18/81
RETt)
TIME

03:39

J

TIC

M2

M3

M4

03:39
j
i

06:30

J

TIME 19:43

L

89:38
j
L.

12:39

15

�-T&lt;rr&gt;1L
linear ravine m » sT
RUNNflME FDHN8
DflTE 7/10/81
TIME 21jll
MflSS 395.8986
SUEEP
300 (PPM)
SCRNTIME 8.3 CSECS)
SCRNS 149-438 188'&lt; INTENSITY ?9?1778

108

305.8986

395.8527
*SK OREO IBt2

DS55 HIGH RESOLUTION MPtt
PERK SUMMRTION REPORT
RUNNflUE FDHM8

DflTE

7/10/81

TIME 21 ill

MOSS
3D5.8987
SCRN UIDTH
300 PPM
SCflH TIME
0.3 SECS
SCflN NUMBERS 149- 438
STflNDflRD
6.0000
FRCTOR
0

KRMIHSKY'S BING. SOOT 2.55 OF 9.8UL
MRSS
CEHTROID
305.9972
3Q5.8716
385.9972
305 .9333

ITEM
TOTRL
1
2
3

RREfl
585240398.
1871699.
551408180.
1415924.

BRSELINE
BRSELINE
SUBTRRCTED SKIMMED
YES
HO
YES
NO
YES
YES
YES
NO

'•iTOTRL RELRTIVE
RRER TO STflNDRRD
98.97
6.00
0.32
0.0Q
93.25
0.60
0.24
0.C0

�FHHK§

DATE! 7/10/81

TIME: 21111

MOSS 333.9335
SUEEP
399 (PPM)
SCRNS 279-307 10ET-S INTENSITY 4589

SCRHTIME 0.3 CSECS)

333.9335

333V8835

333.983^

BS55 HIGH RESOLUTIOH MPJ1
PEflK SUMMflTION REPORT

RUNNfiME FDHM8

DflTE '7/10/81

TIME 2It'll

MflSS
333.9336
SCflH U1TJTH
309 PPM
SCflN TIME
8.3 SECS
SCRN NUMBERS 279- 307
STRNBflRD
0.0000
FflCTOR
0

KflMIHSKY'S BIHG. SOOT 2.SS OF 9.0UL
MfiSS
CENTROID
333.9351
333.8982
333 .9402
333.9746

ITEM
TOTOL
1
2

RREfl
319029.
44037.
223488.
17729.

BRSELINE
BflSELINE
SLIBTRRCTED SKItlMED
HO
YES
NO
YES
YES
YES
NO
YES

•&lt;TOTPL RELRTIVE
RRER TO STRHDRRB
66.S4
e.ea
9.19
0.00
46.61
0.08
3.70
0.08

�U.3 ISECS)
•SCRNS

279-397 188** INTENSITY 83676

109

25

321.8935

321.84S2

321.9418

DSB5 HIGH RESOLUTION MPW
PEflK SUMMRTIOH REPORT

RUNHRME: FDHMS DRTE

TIME

MflSS
321.8935
SCflN WIDTH
308 PPM
SCffN TIME
8.3 SECS
SCflN NUMBERS 279- 307
STBMDflRD
0.8008
FflCTOR
0

KRMINSKY'S BIHG. SOOT 2.55 OF 9.8UL
MflSS
CEHTROID
321 .8323
321 .8748
321 .9023
321 .9319

ITEM
TOTflL
1
2

7275879.
5220057.
2050417.
5485.

BRSELINE
BRSELINE
SUBTRfiCTEET S K I M M E D
HO
YES
YES
YES
YES

HO
NO

NO

RELfiTIVE
flREfl TO STRNBflRD
97.33
8.00
69.83
0.QO
27.43
0.08
0.07
0.00

v.TOTOL

�•RUNNRME FDHMB

J3RTE 7x10x81
TIME 21 11
MRSS 319.8964
SUEEP
300 (PPM)
SCflNTIME 0.3 (SECS)
SCflNS 149-438 1.00*4 INTENSITY 89622

180

25

319.8483
*SK RREfl JD:2

319.94?S

~3T9.89~S"4"
DSB5 HIGH RESOLUTION MPM
PERK SUMMATION REPORT
RUNNRtlE FDHM8

BflTE

7/10x81

TIMESltll

HflSS
319.8965
SCflN UIBTH
300 PPM
SCRN TIME
0.3 SECS
SCON NUMBERS 149- 438
STflNDflRB
0.8009
FfiCTOR
8

KflMINSKY'S BING. SOOT 2.55 OF 9.0UL
MflSS
CENTROID
319.8972
319.8596
319.8930
319.9319

ITEM
TOTRL
1
2

E364537.
79597.
46853S7.
66501 .

3RSELINE
BRSELINE
SUBTRflCTED SKIMMED
HO
YES
NO
YES
YES
YES
NO
YES

"sTOTflL RELPT1VE
RRER TO STRNDflRD
72.82
6.00
1.98
C.B0
63.60
0.B8
8.99
0.0B

�.MOSS 305.8936
SWEEP
390 (PPMl
SCPHS 338-406 109'-: INTENSITY 31138

SCFWTINE 0.3 (SECS)

1,39

305.852?

305.8986'
DS55 HIGH RESOLUTION MPM
PERK SUMMflTION REPORT
RUHNflME TDHM4

BRTE

TIME 12»28

MOSS
305.8987
SCOH UIDTH
309 PPM
SCON TIME
0.3 SECS
SCflH HUMBERS 388- 406
STflNBPRD
0.0009
FflCTOR
0

l.PUL D-ILUTIOH OF KflMINSKY'S SOOT

MPSS

ITEM

CEHTROID
395.8933
305 .8613
305.8938
335.9392

TOTflL
1
2
3

flRER
2859185.
14863,
1917649.
11737.

BflSELIHE
BRSELIHE
•SUBTRflCTED SKIMMED
HO
YES
HO
YES
YES
YES
NO
YES

VTOTflL RELfiTIVE
RREfl TO STRHDP.RB
6.00
95.36
0.00
0.69
89.20
0.00
0.55
0.00

�I 1 1 t n I I !_

i JJ I 1 1 &gt; I

•MOSS
305.8986
SUEEP
300 (PPtli
SCRHS 214-478 189V: INTENSITY 379262

SCflNTIME 8.3

(SECS)

TcD'f

Joe

306.8527

30'6.8986

80S. 9445

DS65 HIGH RESOLUTION MPtt
PERK SUMMflTION REPORT
RUNNflME TBHM4

DflTE

.7/16x81

T I M E 12$28

MflSS
385.8987
SCflN W I D T H
300 PPM
SCPH TIME
8.3 SECS
SCflN NUMBERS 214- 478
STflHDBRB
8.0080
FflCTOR
8

1.0UL B'lLUTIOH OF KRMIHSKY'S SOOT

MRSS
CENTROID
305.8948
305.8611
305.8948
385.9309

ITEM
TQTflL
1
2
3

flREfl

25127260.
64216.
24077639.
73307.

BRSELINE
EflSELINE
'SUBTRflCTED SKI TIMED
YES
NO
YES
HO
YES
YES
YES
HO

'-iJOTRL RELRTIVE
RRER TO STRNDR.RB
92.56
0.08
0.24
0.08
88.70
8.08
0.27
8.00

�Calculation of Response Factor of Furau to Dioxia

Asit of TCDF injected = 1.2 yL of 150 pg/uL
Int of TCDF con = 677482
Sensitivity = 677482/180 = 3764 counts/pg
Amt of

13

C TCDD injected ~ 1.0 uL of 600 pg/^L

Int. of TCDD ion = 1949179
Sensitivity = 1949179/600 = 3249 counts/pg.
Response Factor of Furan is 3764/3249 « 1.16
For equal amounts of material, the response of TCDF is 1.16 times

13
C TCDD,

�Calculation, of Furan in peak number 1 (this peak was used as internal furan
standard for the second injection)

Amt

Furan = X305 x &lt;Amt

13c I

/ 334&gt; *R -F-

1305 = intensity of m/z 305 ion for peak no. 1 (the small peak delimited
which has not saturated the amplifier)
= 8596844
Anit|, = Amt of
1J
C
= 6 ng

C-TCDD spike (internal std.) added to sample

I334 = intensity of m/z 334 ion (int. std.) = 223480
R.F. = response of 2,3,7,8-TCDF compared to 13C 2,3,7,8-TCDD =1.16
Amt

Furan = 8'597x ^6 ng/.223480) x 1.15

- 268 ng

�Calculation of 2 , 3 , 7 , 8-TCDF

^ 3 8 = J2378X
2 7
Amt2378 = amt of 2, 3 ,7, 8-TCDF
I

2378 = intensity of 2,3,7,8-TCDF ions = 1917649
, « amt of furan in peak 1 = 268 ng

I

= intensity of furan in peak 1 = 235188
= 1.918 x (268/235)

- 2187 ng
Conc2378 = 2187 ng/46 mg
«= 48 ppm

Calculation of Total TCDF

- ITOT
= 24. -78 x (268/.23S)
*= 27459 ng
Cone

= (27459 ng/46 mg)

= 597 ppm

�Calculation, of 2,3,7,8-TCDD (scans 279-307)

1

2378 X

-^Vj

» 2.050417 x (6/.223480)
=* 55.04 ng
Conc___ — 55.0 ng/46 mg
Z3/O
=1.2 ppm

CalcualtiQn of Total TCDD (scans 149-438)

Ant

TOT

=1

x (Ant

13

C/Io )

= 5.367 x (6/. 395528)
= 80.4 ng

ac23
-

= 80.4 ng/46 mg
— 1 . 8 pptn

�</text>
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                  <text>Alvin L. Young Collection on Agent Orange</text>
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                <elementText elementTextId="49809">
                  <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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        <element elementId="52">
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                <text>Smith, R.M.</text>
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                <text>D.L. Hilker</text>
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                <text>P.W. O'Keefe</text>
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                <text>S. Kumar</text>
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                <text>B.L. Jelus-Tyror</text>
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                    <text>Item D Number

0219

Author

Turner, J.N.

°

Corporate Author
RepOrt/ArtlOlB TltlB Typescript: Binghamton State Office Building SootInduced Morphologic Alterations in the Liver of Guinea
Pigs, Preliminary Report Submitted to Dr. D.O.
Carpenter, Januarys, 1982

Journal/Book Title
Year

000

°

Month/Day
Color
Number of Images

D

31

Thursday, September 20, 2001

Page 2190 of 2293

�BINGHAMTON STATE OFFICE BUILDING SOOT-INDUCED
MORPHOLOGIC ALTERATIONS IN THE LIVERS OF
GUINEA PIGS

Preliminary Report submitted to
Dr. D«0« Carpenter
on 1/6/82
by

J«,N. Turner, PtuD,, and D«&gt;Ne Collins, M.D.
Division of Laboratories and Research
New York State Department of Health
Albany, New York

�ABSTRACT

A fire in an office building transformer cooled with Pyranol
which is composed of 65% Aroclor 1254 (containing tri, tetra, penta
and hexachlorobiphenyls) and 35% chlorinated benzenes, resulted in contamination of the building with a fine sooto

Due to the pyrolysis of the

fluid mixture, the soot contains a number of polychlorinated organics,
including biphenyls, dioxins, and dibenzofurans. As part of the evaluation
of the soot's toxicity, it was dispersed in 0.75% methyl cellulose and administered by gavage to Hartley guinea pigs in a single dose* Animals were
sacrificed after forty-two days and liver tissue was examined by light and
electron microscopy.
Hypertrophy of hepatocytes, fat infiltration, focal piecemeal necrosis,
bile duct proliferation with fibrosclerosis, and hyaline-like bodies were
observed by light microscopy.

Proliferation of the smooth endoplasmic

reticulum (SER), concentric membrane arrays (CMA), mitochondrial alterations,
decreased rough endoplasmic reticulum (RER), and autophagolysosomes were
observed by electron microscopy,, The CMAs frequently surrounded lipid
droplets, but also encircled areas of the cytoplasm including mitochondria
and degenerating organelles.

These CMAs corresponded to the hyaline-like

bodies observed by light microscopy.

�On February 5, 1981 a fire occurred in the electric service transformer of the New York State Office Building in Binghamton, New York
(henceforth referred to as the BSOB)0

The transformer was cooled and in-

sulated with Pyranol-65% Aroclor 1254 (a mixture of polychlorinated biphenyls-PCBs) and 357= chlorinated benzenes. The building was contaminated
with a fine soot subsequently shown to contain a number of PCB, dioxin,
and dibenzofuran isomers including the highly toxic 2, 3, 7, 8 - tetrachlorodibenzo-p-dioxin (Schwetz, et al., 1973)»

Chemical analysis was done and

will be reported elsexvfhere by P. O'Keeffe and co-workers, Division of
Laboratories and Researchj New York State Department of Health,

The dioxin

and dibenzofuran isomers x?ere formed by pyroloysis of the Pyranol (Butnb, et al.,
1980;

Buser, et al., 1978).
A series of animal tests were designed and performed by Dr« L» Kaminsky

and co-workers of the Division of Laboratories and Research, New York State
Department of Health, to test the soot's toxicity. In one of these experiments, guinea pigs were fed a single dose of BSOB soot, and the morphologic
alterations of their livers are reported here. Other experimental data and
results will be presented elsewhere by Kaminsky and co-workers. Guinea pigs
were selected as the experimental animal because they are more sensitive to
dioxin and dibenzofuran intoxication than other laboratory animals including
rats, mice, Rhesus monkeys, rabbits, and dogs (Gupta, et al», 1973; Harris,
et al., 1973; Schwetz, et al., 1973; McConnell, et al., 1978; Moore, et al.,
1979). The liver was of particular interest because it is a target organ for
PCBs, dioxin, and dibenzofuran (Litterst, et al., 1972; Harris, et al,, 1973;
Piper, et al,, 1973; Rose, et al., 1976; Gasiewicz and Neal, 1979)0
PCBs, and chlorinated dioxins and dibenzofurans all produce similar morphological alterations in the liver (Kimbrough, 1974), At the light microscopic

�level the changes are: liver necrosis, fat infiltration, hypertrophy of
hepatocytes, proliferation of bile ducts, and hyaline bodies in the cytoplasm of the hepatocytes.

These observations have been reported in a

number of species - rats (Bennett, et al., 1938; Miller, 1944; Jones and
Butler, 1974; Gupta, et al., 1973; Greig and Osborne, 1978; Norback and Allen,
1973; Kasza, et al., 1976; Jonsson, et al., 1981), mice (Nishizumi, 1970;
Gupta, et al., 1973), monkeys (Nishizumi, 1970; Norback and Allen, 1973;
McConnell, et al., 1978), rabbits (Miller, 1944; Vos and Beems, 1971), and
guinea pigs (Miller, 1944; Gupta, et al., 1973).

The presence of a yellow-

brown or brown pigment sometimes weakly staining for hemosiderin is reported
for PCB intoxication, but not for purified dioxins or dibenzofurans (Nishizumi,
1970; Vos and Beems, 1971; Kimbrough, et al., 1972; Buse, et al., 1974;
Jonsson, et al., 1981). The pigment is not, however, a consistent finding,
and Kimbrough, et al., 1972, reported its presence in rats fed Aroclor 1242,
but not in those fed Aroclor 1016. The presence of necrosis is frequently reported as single cell, focal, or piecemeal (Vos and Beems, 1971; Gupta, et al.,
1973; Jones and Butler, 1974; McConnell, et al., 1978; Jonsson, et al., 1 8 )
91,
and altered hepatocytes were predominantly in the centrilobular region.
Bile duct proliferation has been reported as a result of feeding both
purified dioxin (Norback and Allen, 1973) and PCBs (Kimbrough, et al., 1972;
Norback and Allen, 1972; Kasza, et al., 1976; Jonsson, et al., 1981). Adenofibrosis, generally taken to be the result of bile duct proliferation, has also
been reported (Kimbrough, et al., 1972, and 1973; Kimbrough and Linder, 1974;
Wassermann, et al., 1978).

Kimbrough, et al., 1972, reported a higher in-

cidence of adenofibrosis in female rats than in males.

Kimbrough, 1973, re-

ported extensive adenofibrosis and the development of pancreatic-type cells
in rats chronically fed high levels of Aroclor 1254.

�Animals fed purified dioxin have been frequently reported to have
multinucleated hepatocytes (Jones and Butler, 1974; Gupta, et -al., 1973;
Norback and Allen, 1973; Greig and Osborne, 1978; McConnell, et al., 1978).
Jones and Butler claim these cells arise by cell fusion as opposed to mitosis.
This is supported by the fact that none of the other authors report mitosis of
bi or multinucleated cells. Similar cells have not been reported in PCB fed
animals*
Ultrastructurally, the livers of animals fed PCS or purified chlorinated
dioxins and dibenzenofurans have similar alterations. These changes include
proliferation of SER, decreased RER, large numbers of lipid droplets, concentric membrane arrays (CMAs), and mitochondrial alterations. For a review
of these changes, see Kimbrough, 1974. Most workers report large numbers of
lipid droplets,proliferated SER,and decreased RER (Nishizumi, 1970; Norback
and Allen, 1972; Kimbrough, et al., 1972; Allen and Abrahamson, 1973;
Jones and Butler, 1974; Kasza, et al., 1976; Jonsson, et alc, 1981). CMAs are
also frequently reported in hepatocytes (Norback and Allen, 1972 and 1973;
Kimbrough, et al., 1973; Allen and Abrahamson, 1973; Jonsson, et al., 1981).
Mitochondrial alterations are occasionally reported and range from shape
changes,to parallel arranged cristae,to severe deterioration and dense
granulation in the matrix (Burse, et al., 1974; Jonsson, et al,, 1981). Jones
and Butler, 1974 demonstrated multinucleated cells,and Greig and Osborne, 1978
demonstrated areas of lateral plasma membrane fusion.
The morphological alterations of the liver of a wide variety of species
fed PCBs,and chlorinated dioxins and dibeiizofurans are usually reported as
similar to each other and a number of other toxic organic molecules (Kimbrough,
1974). The reports are not, however, completely consistent and may vary with
respect to the mixture of compounds, dose,or method of administration.

�Cockerham, et al,, 1980, for example, reported no liver alterations
in beach mice exposed to dioxin.

�METHOD
Soot collected from the BSOB was suspended in 0.75% aqueous methyl
cellulose, and administered in a single gavage at 1, 10, 100, and SOOmgm
soot/kgm body weight to Hartley guinea pigs.
of six males and six females.

Each dose group was composed

A fifth group was fed SOOmgm activated

carbon/kgm body v/eight in 0.75% methyl cellulose as a control.

An additional

control group of six males was fed 0.75% methyl cellulose, while a second
group of six males served as an untreated control.

Female animals were

eleven weeks old at the start of the test and the males were eight weeks old.
All animals were sacrificed by suffocation in CC^ 42 days after administration of the single dose, and complete necropsy performed.
free access to food and water during the test.

Animals had

This animal experiment was

designed and carried out by L.S. Kamlnsky, J. Silkworth and D. McMartin of the
Toxicology Institute, Division of Laboratories and Research, New York State
Department of Health, and results, other than the liver morphology presented
here, will be reported elsewhere.
Two other untreated control groups, both composed of ten animals - five
males and five females - were used for comparison to the experimental groups.
One group was randomly selected from the New York State Department of Health's
guinea pig colony.
(Charles Rivers).

The other group was from an outside commercial supplier
These animals were sacrificed and necropsied in the same

way as the experimental animals.
Specimens from the liver of 91 guinea pigs (one female in the SOOmgm
soot/kgm group died during the test) were processed for light microscopy.
Samples from all livers were fixed in buffered formalin and embedded in
paraffin.

Sections were stained with hematoxylin and eosin ( &amp; ) periodic
HE,

acid - Schiff (PAS), PAS after diastase,and phosphotungstic acid hematoxylin

�;:t V- r&gt; 'j _...:. i .•;;-! I.:1-.-1 • ' • L ^ ' . n i l r;:..;; J,

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i b y a.t;.''iu- ' f ". r.ir.ricim na::be': '&lt;•.•'•&gt; ] -) ,':-!Laci'A p &gt; . 23 t r&gt; - each doaa f.;roup, to a
ace Lvct^u';! c'irbon C') p i::rc'i ,u : ;T'.p T aiid •'t'hfr ^ ^ i r r e a t ^ d c o n t r o l grc".sp»

I~-."^

males r.ud t ;.;.-» f r f p ^ l . i s :-;er3 os'!dcc- o 'i fr-om o^oh losa l e v e l "nd iron tT"i«
Two ^ - - ' ' - - ^ ?" ; -o 3 w^"^ d-lecced From i;'&gt;.a ::a-

acti vaf'eti c a r b o n eoi'crol...
(.""Gti-ed n i l ma' 1 ^ 3 r o u p &gt;

^?.i?.nl-3 ;/^re a]';o caken. _\'om one fenale pig f r o n

tbs 'rrv^Vib-jt d w s ^ j j'.rox.p -/b'.ch wan ;.:or '.'r)'.".id ;.nd sacrificed aC Jay 17 into
the I:-?:-.1:-,

'"'tie l l v ^ ^ - j "-''" 2'3 ^ u i n ^ n ? ' - g a v?ra e--c -.nla-d by e l * c t r - &gt; n aicr:\-;^

A cb ',:•&gt;. ol t-.'e &gt;~&gt;'~ I ' , . ' - : - : :MJ r^-inov^d f-utn ca^ •jai-i.di-; ay so&gt;;n a f c e r deacn .-.13

-i i un

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hydr\i"prl

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ucaivyi. a c ^ f t c i

�RESULTS
Gross Observations and Light Microscopy
At necropsy, single and occasionally multiple focal pale areas were
observed on the surface of the livers of guinea pigs from all groups0
Microscopically, morphologic alterations in the hepatocytes were
observed in the experimental .guinea pigs and in one guinea pig in the
activated carbon control group (guinea pig No. 37),

These alterations were:

hypertrophy of hepatocytes, fat infiltration, focal piecemeal necrosis, bile
duct proliferation with fibrosclerosis, and hyaline-like cytoplasmic inclusion bodies.
Figo 1 is representative of the widespread fat infiltration
It is a micrograph of a frozen section stained with oil red 0,

observed.
The fat

droplets vary from cytoplasmic microdroplets to confluent globules larger
than the nucleus. With the exception of No. 37, the control guinea pigs
exhibited fat droplets of normal size, number and distribution.
Fig. 2
sclerosis.

illustrates proliferation of bile ductulea and fibroSeveral small duct-like structures intermingled with collagenous

proliferation are evident.

This alteration was observed in six female guinea

pigs, two in the 1 mgm soot/kgm group, three in the 100 mgm soot/kgm group
and one in the 500 mgm soot/kgm group, as well as in one male in the 500 mgm/kgm
group,
Fig. 3 shows a paraffin section stained with PTAH.

Cytoplasmic alteration

is reflected in the numerous discrete spherical hyaline-like bodies which stain
an intense dark blue. These hyaline-like bodies shoxtf greater contrast and detail
in PTAH stained than in H&amp;E stained sections.
of these hyaline-like bodies.

Fig. 4 is a higher magnification

They exhibit a wide range of sizes and shapes -

some minute, others as large or larger than the nucleus„

Single round bodies

ranging in size from 1.9 to 5.7/im are observed, some with clear centers (small

�arrows), others of solid density (large arrows)0

Individual cells may

contain several bodies or &amp; confluent group. These groups may'be as large
as lOum (double arrows).
Figo 5 illustrates a l^im toludine blue stained plastic section.

Hexa-

gonally shaped hepatocytes appear enlarged and contain round appearing nuclei
with prominant nucleoli. Binucleated cells, such as the one in the center
of the field, are not uncommon. The hyaline-like bodies present in the
cytoplasm display a wide range of sizes, and most have a light center with a
dark peripheral annulus consisting of as much as 2/3's the diameter of the
body. Multiple bodies are frequently seen in a single cell, and confluent
groups as large as 14um are present. Many small bodies appear uniformly
dense«
The PAS and PAS/diastase stained sections showed normal amounts of
glycogen in all animals.
Electron Microscopy
Electron microscopic examination of ultrathin sections show the following
hepatocyte alterations: proliferated SER, CMAs, mitochondrial degeneration,
decreased RER,and margination of organelles. All experimental anJmals and
No« 37 show proliferated SER, frequently causing margination of mitochondria
by increasing the cytoplasmic matrix.

CMAs were most frequently observed

surrounding fat droplets, and occasionally encompassing volumes of cytoplasm,
mitochondria and degenerating organelles0

CMAs were, on occasion, found in

the sinusoidal lumen. The mitochondrial alterations appeared to be of two
types, changes in shape and lamination of cristae. All experimental animals
and No. 37 showed variations in shape but variations in cristae were observed
only in the two highest dose groups.
Fig. 6 is a low magnification electron micrograph of 5 hepatocytes showing
nuclei, lipid droplets, proliferated SER and margination of mitochondria.

�Two large CMAs surround lipid droplets.
Figo 7 shows details of two CMAs in which regularly spaced smooth
membranes are arranged concentrically about lipid droplets*

The outer

membranes appear to be continuous with portions of the SER, Fig« 8 more
clearly demonstrates this association of the membranes to a large lipid
droplet^

The membrane layers nearest the lipid droplet are regularly and

closely spaced, appearing to continuously surround the droplet. The outer
layers are less evenly spaced and are irregularly organized with large
protruding areas. The outermost membranes are continuous with portions of
the SER as indicated by the arrows, and are present as discrete leaflets
that appear to cover only part of the circumference of the CMA«,
The sinusoid and associated perisinusoidal space of Disse occasionally
contained cellular debris and CMAs as in Fig0 9.
Fig* 10 shows three lipid droplets which are confluent and contain
internal membrane fragments. The droplets are membrane bound, but lack
concentric arrays as illustrated in Figs« 6, 7,and 8. Fig. 11 shows two
lipid droplets with fragmented membranes internally, with concentric membranes
associated with part of their circumference.
Random condensations of SER associated with islands of proliferated SER
are illustrated in Fig. 12.
Alterations in the shape of mitochondria were occasionally noted. Fig» 13
shows many normal mitochondria, and one irregularly shaped one0

A pseudo-inclusioi

composed of cytoplasmic components is evident in the large central mitochondria.
The two highest dose groups show motochondria with parallel cristae. Fig. 14
is an illustration of this alteration.

10

�DISCUSSION

The pale areas on the liver surface observed at necropsy in all groups
have been shown to be manifested microscopically as coagulative necrosis,
and to be present in otherwise normal guinea pig populations (Wagner and
Manning, 1976).
All of the control animals with the exception of guinea pig No, 37 in the
activated carbon group showed morphologically normal livers at both the light
and electron microscopic levels. The experimental animals in all dose groups
exhibited alterations at both microscopic levels, demonstrating a toxic reaction
to the ingestion of BSOB soot. Since guinea pig No» 37 was only one of fortyfour control animals and only one of twelve in the activated carbon group, the
observation of morphologic alterations in its liver was not taken to be significant. An adequate control is., therefore, established and differences between control and experimental guinea pigs have been demonstrated. Comparison
of the four dose groups did not produce differences, and to date the only
alteration that is a function of the dose level is the parallel raitochondrial
cristae observed in the 100 and 500 mgm soot/kgm groups. The morphologic
alterations observed are consistent with those found by other workers in the
liver of animals fed either PCBs or purified chlorinated dioxins (see Kimbrough,
1974 for a review).
However, the current experiment did not exhibit the multinucleated hepatocytes observed by workers who fed purified dioxins (Gupta, et al,, 1973;
Norback and Allen, 1973; Jones and Butler, 1974; Greig and Osborne, 1978), nor
did other studies of PCB fed animals (Nishizumi, 1970; Kimbrough, et al., 1972;
Norback and Allen, 1972; Allen and Abrahamson, 1973; Kasza, et al,, 1976;
Jonsson, et al., 1981), Since PCBs, dioxins and dibenzofurans are present in
the BSOB soot and the PCBs of the other studies were probably contaminated with

11

�dioxins, it appears that multinucleated cells are not formed when a mixture
is present.
The observation of bile duct proliferation with fibrosclerosis in seven
of forty-seven experimental animals is consistent with a number of other
reports in which animals were fed PCBs or dioxins (see introduction for references). It is difficult, however, to compare the various studies since
the dose levels, number of doses, and time course of the experiments are
different, Kimbrough, et al0, 1972 and 1973 report a large percentage of
animals with this alteration, but their experiment involved multiple doses
over longer time periods. Differences in toxicity of the particular compounds used may also be a variable as Kimbrough, et al», 1972 reported a
difference between Aroclor 1254 and 1260»

The possibility and extent of

dioxin contamination in various PCB mixtures is also an unknown parameter.
Kimbrough, et ale, 1972 reported an increased incidence in females as opposed
to males, and six of the seven animals exhibiting the alteration in this study
were females .
Hyaline-like bodies in the cytoplasm of the hepatocytes have been observed
in a number of studies for a variety of toxic organic molecules including PCBs,
dioxins, and dibenzofurans (Kimbrough, 1974)D

The CMAs at the ultrastructural

level undoubtedly correspond to these bodies at the light microscopic level*
This is also suggested by Kimbrough, 1974. The observation of the CMAs is consistent with many other studies in which a variety of species were fed PCBs or
dioxins (Kimbrough, 1974, Jonsson, et al., 1981)0

Jonsson, et al0, 1981 suggested

that the ejection of CMAs into the sinusoids and bile canaliculi was a mechanism
to rid the hepatocyte of toxic materials. The ejection of CMAs and other cell
debris into the sinusoids was also observed in this study.
The ultrastructural alterations reported here are in general consistent with
other reports, but some variation is also observed.

For example, Jonsson, et al«,

1981 reported severe degeneration of mitochondria, but we observed few de12

�generated mitochondria,, The observation of parallel cristae in a small
number of mitochondria in the two highest dose groups is in agreement with
the results of Burse, et al,, 19740

The increased SER and decreased RER is in

agreement with all previous studies of PCB, dioxin and dibenzofuran intoxication except Fowler, et al., 1973 who reported an increase in RER in
rat hepatocytes following a single oral dose of dioxin. The condensed,
laminated SER of Fig. 12 has not been previously reported, but was occasionally
observed in some experimental animals,
The morphological differences between control and treated guinea pigs
demonstrate a toxic effect due to the ingestion of BSOB soot, but dose level
related effects have not been documentede

The alterations reported here

and in the literature vary in some details, but are generally consistent. The
explanation of the variation in morphological alterations cannot be determined
at this time, but is probably a complex function of sampling, ingested
moleculeSjdose level, number of doses, time course of the experiment, and
animal species.

1,3

�REFERENCES

l e "Allen, J.R., Abrahamson, L.J, Morphological and biochemical changes
in the liver of rats fed polychlorinated biphenyls0 Arch, Environ,
Contam. Tox. 1., 265-280, 1973.
2. Bumb, R.R., Cruramett, W.B., Gutie, S.Se, Gledhill, J0R0, Hummel, R,H.,
Kagel, R.O., Lamparski, L.L., Luoma, E0V., Miller, D0Le, Nestrick, T.J.,
Shadoff, L.A., Stehl, R.H., Woods, J.S. Trace chemistries of fire:
a source of chlorinated 'dioxins. Science 210, 385-390, 1980,
3. Burse, V.W., Kimbrough, R.D., Villanueva, E.G., Jennings, R.W., Linder,
R.E., Sovocool, G»W» Polychlorinated biphenyls. Arch. Environ,
Health 29., 301-307, 1974.
4»

Buser, H.R., Bosshardt, H.P«, Rappe, C» Formation of polychlorinated
dibenzofurans (PCDFs) from the pyrolysis of PCBs, Cheraosphere !_,
109-119, 1978.

5. Cockerham, L.G., Young, A.L., Thalken, C.E. Histopathological and
ultrastructural studies of liver tissue from TCDD-exposed beach mice
FJSRL. Technical Report 80-0008, United States Air Force, 1980.
6»

Fowler, B,A«, Lucien, GeW«, Brown, H.W., McDaniel, 0 S
, . Ultrastructural
changes in rat liver cells following a single oral dose of TCDD»
Environ. Health Perspectives 5_, 141-148, 1973,

7. Gasiewicz, T.A., Neal, R,A« 2,3,7,8-tetrachlorodibenzo-p-dioxin tissue
distribution, excretion and effects on clinical chemical parameters in
guinea pigs. Tox. Appl. Pharmacol. 51, 329-339, 1979.
8. Greig, J.B., Osborne, G. Changes in rat hepatic cell membranes during
2,3,7,8 tetrachlorodibenzo-p-dioxin intoxication. In: Dioxin (edc
F, Cattabeni, A. Cavallaro and G« Galli), SP Medical, and Sci3ntific
Books, a division of John Wiley, New York, 1978.
9. Gupta, B.N., Vos, J.G., Moore, J.A», Zinkl, JaG., Bullock, B.C,
Pathologic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin in laboratory
animals. Enriron. Health Perspectives 5_, 125-140, 1973.
10. Harris, M.W., Moore, J.A., Vos, J.G», Gupta, BeN, General biological
effects of TCDD in laboratory animals. Environ. Health Perspectives
5_, 101, 1973.
11. Jones, G., Butler, W0H. A morphological study of the liver lesion induced
by 2,3,7,8-tetrachlorodibenzo-p-dioxin in rats. J. Pathol0 112, 93-97,
1974.

14

�12. Kasza, L., Weinberger, M.A., Carter, C0, Hinton, D.E., Trump, B.F.,
Brouwer, EoA. Acute,subacute and residual effects of polychlorinated
biphenyl (PCB) in rats II Pathology and electron microscopy of liver
. and serum enzyme study. J 0 Tox» and Environ, Health !_, 689-703, 1976.
13.

Kimbrough, R.D. The toxicity of polychlorinated polycyclic compounds and related chemicalsdn: Critical Reviews in Toxicology (ed.
L. Goldberg). The Chemical Rubber Co,, West Palm Beach, Fla., 1974.

14.

Kimbrough, R.D., Linder, R.E., Gaines, T.B. Morphological changes in
livers of rats fed polychlorinated biphenyls. Arch, Environ» Health
25., 354-364, 1972.

15. Kimbrough, R.D., Linder, R.E., Burse, V.W., Jennings, R0W. Adenofibrosis in the rat liver. Arch. Environ. Health 27, 390-395, 1973.
16.

Kimbrough, R.D., Linder, R.E, Induction of adenofibrosis and hepatomas
of the liver in Balb/cJ mice by polychlorinated biphenyls (Aroclor 1254)»
J. Nat. Cancer Inst. 53., 547-552, 1974.

17. Litterst, C.L., Farber, T.M., Baken, A.M. van Loon, E»JC Effect of
polychlorinated biphenyls on hepatic microsomal enzymes in the rate
Tox. Appl. Pharmacol. 23, 112-122, 1972.
18. McConnell, E.E., Moore, J«A0, Dalgard, D.W. Toxicity of 2,3,7,8tetrachlorodibenzo-p-dioxin in Rhesus monkeys (Macaca mulatta) following
a single oral dose. Tox* Appl* Pharmacol. 43, 175-187, 1978a,
19. McConnell, E0E., Moore, J 0 A 0 , Hoseman, J.K», Harris, M.W» The comparative toxicity of chlorinated dibenzo-p-dioxins in mice and guinea
pigs. Tox. Appl, Pharmacolc 44, 335-356, 1978b.
20.

Miller, J.W. Pathologic changes in animals exposed to a commercial
chlorinated biphenyl. Public Health Rep. 59., 1085-1093, 1944.

21m

Moore, J.A., McConnell, EeE., Dalgard, D.W., Harris, M»W. Comparative
toxicity of three halogenated dibenzofurans in guinea pigs, mice, and
Rhesus monkeys. Ann. N.Y. Acad. Sci. 320. 151-163, 1979.

22.

Nishizumi, M., Fukuoka, M.D. Light and electron microscope study of
chlorobiphenyl poisoning. Arch. Environ, Health 27, 16-21, 19700

23»

Norback, D.H., Allen, J.R, Chlorinated aromatic hydrocarbon induced
modifications of the hepatic endoplasmic reticulum: concentric membrane
arrays. Environ. Health Perspectives 1., 137-143, 1972,

24.

Norback, D»H., Allen, J,Ri&gt; Biological responses of the nonhuman primate,
chicken, and rat to chlorinated dibenzo-p-dioxin ingestions Environ,
Health Perspectives 5_, 233-240, 1973.

15

�25. Piper, W.N., Rose, J.G., Gehring, P.J. Excretion and tissue
distribution of 2,3,7,8~tetrachlorodibenzo-p-dloxin in the rat.
Environ. Health Perspectives 5_, 241-244, 1973.
26. Rose, J.Q., Ramsey, J.C., Wentzler, T.H., Hummel, R.A., Gehring, P.J.
The fate of 2,3,7,8-tetrachlorodibenzo-p-dioxin following single and
repeated oral doses to the rat. Tox. Appl. Pharmacol. 36, 209-226,
1976.
27. Schwetz, B.A., Norris, J.M., Sparschu, G.K., Rowe, V.K., Gehring, P.J.,
Emerson, J.L., Gerbig, G.C, Toxicology of chlorinated dibenzo-p-dioxins,
Environ. Health Perspectives 5_, 87-99, 1973.
28. Vos, J. G., Beems, R.B. Dermal toxicity studies of technical polychlorinated biphenyls and fractions thereof in rabbits. Tox. Appl. Pharmacol.
19., 617, 1971.
29. Wagner, J.E., Manning, P.J.
Press, New York, 1976.

Biology of the Guinea Pig. Academic

30. Wassermann, D», Miller, H.J., Wassermann, M. Polychlorinated biphenyls induced rat liver adenomas. Tox. European Res. 1^, 159-172,
1978.

16

�FIGURE LEGENDS
Fig. 1 is a photomicrograph of a frozen liver section stained with
oil red 0 Magnification is 500X,
.

Figo 2 is a photomicrograph of an H&amp;E stained paraffin section of
liver from an area of bile duct proliferation with fibrosclerosis.
Magnification is 800X.
Fig. 3 is a photomicrograph of a PTAH stained paraffin section of the
liver.

The magnification is 320X.

Fig, 4 is a photomicrograph of a PTAH stained paraffin section of the
liver. The hyaline-like bodies are indicated by the arrows: clear centers
by the small arrows, dense bodies by the large arrows, and a confluent group
by the double arrow.

The magnification is 800X.

Fig. 5 is a photomicrograph of a lura plastic section of the liver
stained with toludine blue.

The magnification is 800X.

Fig, 6 is an electron micrograph of an ultrathin section at 5,100 times
magnification.

The nuclei (N), lipid droplets (Li), concentric membrane

arrays (CMA), and mitochondria (Mi) are readily observed.
Fig, 7 is an electron micrograph of three CMAs viewed at 26,192X
magnification.
Fig, 8 is an electron micrograph of a portion of a CMA around a lipid
droplet (Li).

The arrows indicate areas of continuity between the outer CMA

membrane and the SER.

Magnification is 18,OOOX»

Fig. 9 is an electron micrograph of a CMA in a liver sinus. A red blood
cell (RBC) and Disse space (DS) are seen. Magnification is 18,OOOX.
Fig. 10 is an electron micrograph of three lipid droplets and their
associated membrane systems in a hepatocyte. Magnification is 18,OOOX.
Fig. 11 is an electron micrograph of two lipid droplets x^ith associated

17

�membrane systems, and some areas of parallel aligned SER in a hepatocyte.
Magnification is 18,OOOX.
Fig« 1.2 is an electron micrograph of areas of condensed SER in a
hepatocyte. Magnification is 18,OOOX0
Fig, 13 is an electron micrograph of several mitochondria in a
hepatocyte. Magnification is 18,OOOX.
Fige 14 is an electron micrograph of several mitochondria, two of
which have parallel arranged cristae. Magnification is 51,000x.

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°2193

Author

Eadon G

&gt; -

Center for Laboratories and Research, New York State

Report/Article TltlB Comparisons of Chemical and Biological Data on Soot
Samples From the Binghamton State Office Building

Journal/Book Title
Year

1982

Month/Day

March

Color
Number of Images

D

24

Dascrlpton Notes

Thursday, September 20, 2001

Page 2193 of 2293

�Comparisons Of Chemical and Biological Data
on Soot Samples From the Binghamton State
Office Building

G. Eadon, K. Aldous, G. Frenkel, J. Gierthy, D. Hilkerr L.
Kaminsky, P. O'Keefe, J. Silkworth and R. Smith

Center for Laboratories and Research
(
New York\State Department of Health
Albany, N^ 12201

March, 1982

�Soot samples from two separate samplings of the Binghamton
State Office Building (BSOB) have been the objects of a
coordinated interdisciplinary study at the New York State Health
Department. On May 26, 1981, replicate soot samples were
collected from above the ceiling panels of 16 of the 17 floors of
the BSOB.

Each sample was subjected to exhaustive soxhlet

extraction (benzene).

One portion of each extract was analyzed

for polychlorinated biphenyls (PCBs), another for polychlorinated
dibenzofurans (PCDFs) and related compounds.

A third portion of

all extracts not spiked with PCDDs and PCDFs as part of the
chemical analysis procedure was examined using the cell
keratinization assay.
Another set of experiments utilized a much larger soot
sample collected by a vacuum cleaner on the 3rd and 4th floors of
the BSOB shortly after the fire occurred.

The bulk of this

sample has been used in animal toxicology studies.

However/

portions of this soot were extracted and analyzed for PCBs,
PCDFs, 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) and
2,3,7,8-tetrachlorodibenzofuran (2,3,7,8-TCDF).

The cell

keratinization assay was also applied to an extract of this
sample.
The results of each of these studies have been described in
detail in separate reports (Smith et al. , 1981a, 1981b, 1982;
Silkworth et al., 1982; Gierthy et al., 1982).

This

paper will seek comparisons among the various chemical and
biological data sets generated with these samples, and will
attempt to determine whether the results are mutually consistent.

�Chemical Data
The number of samples which could be analyzed for PCDFs and
related trace contaminants is severely limited by the difficulty
of the analytical procedure.

In contrast, the quantitation of

the much more abundant PCBs is a fairly straightforward process;
more than 800 PCB analyses have already been reported on
BSOB-related samples.

If the ratios of PCB to PCDF are

approximately constant then the results of the PCB analyses can
be used to estimate PCDF levels, with a considerable savings in
time and manpower.

Table I contains analytical data relevant to

the PCB and PCDF (tetra through octa chlorinated)

concentrations

on soot samples collected from 16 of 17 floors of the BSOB, and
on the soot sample used in animal toxicology experiments.

The

PCB concentrations vary by nearly 3 orders of magnitude, while
total PCDF levels vary from not detected
approximately 1200 ppm.

«1.0 ppm) to

For the 11 samples in which the ratio of

total PCDFs to total PCBs has been determined, the total PCDFs
measured ranges from 51 ppm to 1200 ppm, and the ratio of PCDF to
PCB averages .066 * .024 (error limits represent one standard
deviation). t Thus, the total PCDF levels correlate with PCB
levels.
More detailed consideration of the data in Table I indicates
that the total concentrations of tetra CDFs, penta CDFs and hexa
CDFs (groupings which include the isomers predicted (see later)
to be most active with respect to acute oral toxicity and
keratinization) relative to the total PCDF concentration is
relatively constant (Table II).

In the 11 samples for which

these ratios have been determined, tetra CDFs constitute 33 + 5%

�of the total PCDF mixture, while penta CDFs constitute 40 + 3%,
and the hexa CDFs constitute 18 ± 7% of the total mixture.

Thus,

the PCB concentration can be used to predict approximate
concentrations of each family of chlorinated dibenzofurans in
these samples.

For illustrative purposes, Table III contains the

measured and predicted concentrations.
Further studies will be required to rigorously validate the
use of PCB analysis as a surrogate for the more elaborate
analytical procedures.

Since concentrations of dibenzodioxins

and biphenylenes (Stalling, 1981) have not yet been determined in
these samples, it cannot be demonstrated that the concentrations
of these compounds correlate with PCB concentrations.

Further,

the samples analyzed to date have all been collected before May,
1981 and have been predominantly obtained from the same location
on the 17 floors.

The validity of the observed correlation must

be tested with more recent samples and with samples taken at
other locations; the similarity of the ceiling panel samples and
vacuum cleaner sample is encouraging in the latter regard.
Finally, the validity of the observed correlation in the very
slightly contaminated samples likely to be generated during the
!

final phases of the clean-up should also be tested.

�Biological Data
Evaluation of the consistency of the chemical data and the
biological data requires knowledge of the concentrations and
toxicities of particular congeners believed to be especially
active.

Because of the very few reference standards available,

the laboratories of the Health Department have produced little
congener-by-congener

analytical data.

Therefore, in the

following discussions it will be necessary to assume that within
a particular isomeric series the relative concentration of a
given isomer is comparable to its concentration in a sample
earlier subjected to congener by congener analysis (Stalling,
1981; Rappe, 1981).
Among the tetra CDFs, the isomer believed to be most toxic
is 2,3,7,8-Tetra CDF (Poland et al., 1977).

Stalling and

Rappe report that this isomer constitutes 68% and 41% of the
tetra CDFs.

Based on these results it will be assummed that

2,3,7,8-TCDF constitutes 50% of the total tetra CDF concentration
in these samples.
Given the greater toxicity of 2,3,7,8-chlorinated isomers
(Poland et al., 1977) the most toxic penta CDF isomers are
predicted to be 1,2,3,7,8- and 2,3,4,7,8-penta CDF.

Stalling and

Rappe report that these congeners comprise together 47% and 53%
of the penta CDF mixture.

A value of 50% will be assumed in

subsequent discussions.
Given the greater toxicity of 2,3,7,8-chlorinated isomers
(Poland et al., 1977), the most toxic hexa CDF isomers are
predicted to be 1,2,3,4,7,8-, 1,2,3,6,7,8-, 1,2,3,7,8,9- and
2,3,4,6,7,8-hexa CDF.

Rappe reports that the total concentration

�of three of these isomers in a BSOB sample was 49% of the total
hexa CDF concentration.

A value of 50% will be assumed here for

the four isomers.
Knowledge of the relative concentrations of dibenzodioxins
and dibenzofurans will also be required for these discussions.
In the soot sample used in animal toxicology experiments, the
2,3,7,8-TCDD/2,3,7,8-TCDF ratio was determined to be .025 (Smith
et al., 1981b).
this sample.

This ratio will be used in connection with

However, since analytical data on the dioxin levels

in the remaining samples is not yet available, an estimate of
these concentrations must be made.

In a sample analyzed by Rappe

and Stalling, Rappe concluded that the tetra through octa
PCDD/PCDF ratio was about .01, and Stalling concluded that it was
less than .02.

In a heavily contaminated soot sample, Smith et

al (1981a) concluded that the 2,3,7,8-TCDD/2,3,7,8-TCDF ratio
averaged .015.

The average ratio observed in the three samples

was .017; this value will be assumed for the ceiling panel
derived soot samples.
Based on Stalling's report (1981), the biphenylene/dibenzofuran ratio in a sample was less than .067.

This value will of

i

necessity be used in subsequent discussions.

Efforts are

presently underway to obtain experimental data on the soot
samples currently under discussion to place these estimates on a
firmer basis.
a.

Animal Toxicology Experiments
It is difficult to rigorously demonstrate consistency

between results obtained via chemical analysis and acute toxicity
data for a number of reasons.

The chemical data is incomplete;

�7
not all classes of toxicants have been quantified,and the
concentrations of individual congeners have not been established.
More important, however, very limited data is available on the
acute oral toxicities of individual PCDFs, PCDDs or
Polychlorinated Biphenylenes.

Nevertheless, despite these and

other difficulties, crude comparison of this data will be
attempted.
A useful first step is to express the observed acute oral
toxicity of the soot in terms of "2,3,7,8-TCDD equivalents",
i.e., the concentrations of 2,3,7,8-TCDD, that, in an inert
matrix, would produce the observed LDgQ. An extract of soot
when administered to guinea pigs in aqueous suspension exhibited
an LD5Q equivalent to 327 mg soot/kg.

When 2,3,7,8-TCDD was

administered under identical conditions, it exhibited an LD50
of 19 ug/kg.

If the soot in fact had contained only 2,3,7,8-TCDD

at 58 ug/g, its extract would be predicted to exhibit an LD,-n
of 327 mg soot equivalents/kg.

Therefore, the "2,3,7,8-TCDD

equivalent" contamination of the soot is 58 ug/g.
The chemical data can then be used to "predict" the
"2,3,7,8-TCDD equivalent" concentration of the soot, based on
known toxicities of the components.

This is a complicated task,

since no data is available on the LDcris of dibenzofurans in
bu
guinea pigs other than 2,3,7,8-tetra CDF, and since very limited
data is available on the PCDDs.

The following assumptions will

therefore be made about the I&lt;DCQS of these compounds:

(1)

The

ratio of the LDcQs of a particular PCDF congener and
2,3,7,8-tetra CDF will be the same as the ratio of the LD5Qs oE
the correspondingly substituted PCDD congener and 2,3,7,8-TCDD.

�8
There is no direct experimental data to support this assumption.
(2)

The LD50s of PCDFs and PCDDs lacking chlorines on all four

lateral positions will be sufficiently high that their influence
can be ignored in this calculation.

This assumption is based on

the LD5Qs in guinea pigs of 2,8-diCDD, 2,3,7-triCDD, and
1,2,4,7,8-penta-CDD.

All have LE&gt;

s more than 450 times

higher than that of 2,3,7,8-Tetra CDD itself (Table IV).

(3)

Introduction of a single additional chlorine substituent on a
2,3,1,8-substituted congener has essentially no effect on the
congener's guinea pig LD

. This assumption is based on

comparison of the LD5Qs of 2,3,7,8-TCDD and 1,2,3,7,8~tetra-CDD
(Table IV).

(4)

Introduction of two additional chlorine

substituents on a 2,3,7,8-chlorinated congener raises its LD,-0
by a factor of at least 29. The assumption is based on comparison
of the LD5Qs of 1,2,3,4,7,8-, 1,2,3,6,7,8-, and
1,2,3,7,8,9-hexa CDD and 2,3,7,8-tetra CDD (Table IV).

(5)

The

LDf-QS of compounds with more than 6 chlorines will be
sufficiently large that their influence can be ignored in this
calculation.

This assumption is based on comparison of the

LD5Qs of 1,2,3,4,6,7,8-hepta CDD and 2,3,7,8-tetra CDD (Table

IV).
These assumptions require that attention be focussed only on
the tetra, penta, and hexasubstituted PCDDs and PCDFs.

The

concentration of 2,3,7,8-TCDF in the sample used in animal
toxicology experiments was measured at 48 ppm; since the data in
Table IV indicates that the LD5Q of 2,3,7,8-tetraCDF is about
three times that of 2,3,7,8-TCDD, this is equivalent in terms of
acute toxicity to a 2,3,7,8-TCDD concentration of ca. 16 ug/g.

�Based on assumption (2), other tetra CDFs can be neglected in
this calculation.

The penta CDFs were measured at 120 ug/g.

If

1,2,3,7,8- and 2,3,4,7,8-penta CDF together constitute 50% of the
penta CDFs, and if their LDcQS are equal to that of
2,3,7,8-TCDF, this is equivalent in terms of acute toxicity to a
2,3,7,8-TCDD concentration of ca. 20 ug/g.

Based on assumption

(2), other penta CDFs can be neglected in this calculation.
hexa CDFs have been measured at 70 ug/g.

The

The isomers believed to

have the lowest LD5Qs (1,2,3,4,7,8-, 1,2,3,6,7,8-, and
2,3,4,6,7,8-hexa CDF) are expected to comprise 50% of the total
hexa CDF mixture.

Since, based on assumption (4), their LD^s

are 29 times higher than that of 2,3,7,8-TCDF, this is equivalent
to a 2,3,7,8-TCDD concentration of 0.4 ug/g.
calculated

Thus, the PCDFs are

to constitute a "2,3,7,8-TCDD equivalent"

concentration of 36 ug/g.
The concentration of 2,3,7,8-TCDD itself has been measured
at 1.2 ppm in this sample.

Other tetrachlorinated dibenzodioxins

are predicted to have much higher LD,-QS and can be ignored.
The concentration of other PCDDs in this sample are unknown, but
are likely to be comparable to the TCDDs.

Thus, the dioxins as a

whole probably have a negligible influence on the soot's
"2,3,7,8-TCDD equivalent" concentration.
Stalling (1981) has reported on the presence of
polychlorinated biphenylenes in a soot sample from BSOB; he cites
unpublished results by Dr. Alan Poland that suggests that the
toxicity of the 2,3,6,7 congener is comparable to that of
2,3,7,8-tetra CDD.

If Stalling's ratio of biphenylene to

dibenzofuran is (.067) is assummed to hold for all of these

�10

compounds, and if it is assummed that the biphenylenes have
acute oral toxicities three times that of the corresponding
dibenzofurans, it can be calculated that the biphenylenes will
contribute about 0.2 times as much "2,3,7,8-TCDD equivalent"
activity as the dibenzofurans. Thus, to a very crude
approximation, the polychlorinated biphenylenes account for a
"2,3,7,8-TCDD equivalent" concentration of 7 ppm.
In summary, the dibenzofurans and the tetra CDDs are
estimated to constitute a "2,3,7,8-TCDD equivalent" activity of
37 ug/g.

Together, the remaining dibenzodioxins and the

biphenylenes probably provide a significant but smaller
"2,3,7,8-TCDD equivalent" activity.

This calculation is in good,

probably somewhat fortuitous agreement with the observed activity
in the soot-equivalent to a 2,3,7,8-TCDD concentration of 58

ug/g.
Since considerable effort has been devoted to animal
toxicology experiments on a single large sample of soot, it is
important to assess whether this sample is reasonably typical.
The data in Table I indicates that the average PCB concentration
in 16 samples collected above the ceiling panels at the BSOB is
(

7200; the PCB concentration in this sample is 5,000 ppm. " The
average total PCDF concentration on 14 such samples was ppm; the
total PCDF concentration in this sample is 320 ppm.

The average

ratio of total PCDF to PCB in the 12 samples for which this is
well defined is .066; the ratio for this sample was .063.

The

proportions of tetra- penta-, and hexa CDFs in this sample are
similar to those in the ceiling panel samples (Table II).
the sample used in animal toxicology experiments appears

Thus,

�11
comparable to the samples collected from above the ceiling
panels, based on presently available data.
b.

Cell Keratinization Assay
Development of the cell keratinization assay based on an in

vitro keratinization model (Knutson et al., 1981) has been
pursued because of its potential use as an alternative or
supplement to chemical analysis.

Both applications demand that

the biological and chemical methods generate mutually consistent
results.

One question can be answered fairly readily.

Do the

two methodologies agree which samples fall into particular broad
categories of contamination?

The samples and blanks run as part

of this program exhibit four broad categories of contamination.
Blanks did not exhibit positive responses in this assay.

A

single sample (floor 1) exhibited activity equivalent to 0.01 0.10 ppm 2,3,7,8-TCDD; chemical analysis detected only 0.2 ppm
Tetra-CDF.

Three samples (floors 4,6, and 14) exhibited

activities near 0.10 - 1.0 ppm; chemical analysis confirmed low
levels of PCDFs in these samples (total PCDFs of 51, 76, and 87
ppm).

The remaining samples in which PCDFs were detected

chemically exhibited activities ranging from 1.1 - 11 ppm to 5.3
!

- 53 ppm.

Chemical analysis confirmed that these samples were

more heavily contaminated (total PCDFs of 410 , 200, 320, 1200,
400, 750, and 670 ppm).
Table V.

These results are collected together in

They suggest that the keratinization assay results

correlate with chemical data.
It is markedly more difficult to determine whether the
activity observed in the cell keratinization assay is
quantitatively consistent with chemical analysis.

Little

�12

published information exists to relate the keratiniation
activities of the various compounds present in the soot to one
another.

However, the following assumptions will be made to

permit a crude calculation:

(1)

The ratios of the activity of a

particular dibenzofuran congener to 2,3,7,8-TCDF is equal to that
of the ratio of the activity of the corresponding dibenzodioxin
congener to 2,3,1,8-TCDD.
assumption.

(2)

There is no direct support for this

2,3,7,8-Tetra CDF is 1/20 as active as

2,3,7,8-TCDD (Knutson et al., 1980).

(3)

Congeners not

substituted at all four lateral positions are sufficiently
inactive to be neglected.

This assumption is based on comparison

of the activities of 2,3-, 2,7-, 1,6-, 1,3,6,8-, 1,3,7,8-, and
2,3,7- chlorodibenzodioxins to 2,3,7,8-tetra CDD.
al., 1980) (Table VI).

(4)

(Knutson et

Introduction of a single

additional chlorine on a 2,3,7,8 chlorinated nucleus decreases
activity by a factor of 2.

This assumption is based on a

comparison of the activities of 1,2,3,7,8-Penta CDD and
2,3,7,8-tetra CDD (Knutson et al., 1980) (Table VI).

(5)

Introduction of two or more chlorines depresses activity
sufficiently to make the activity of such compounds negligible.
This assumption is based on comparison of the activities of
1,2,3,7,8,9-hexa CDD and 2,3,7,8-tetra CDD (Knutson et al.,
1980) (Table VI).

(6)

Polychlorinated biphenylenes are 1/2 as

active as the corresponding dibenzodioxin.

This generalization

is based on comparison of the activities of 2,3,6,7-tetra CB and
2,3,7,8-tetra CDD (Knutson et al., 1980) (Table VI).
As a direct result of assumptions (3) and (5), the bulk of
keratinization activity will reside in tetra- and penta-

�13

chlorinated compounds.

As already discussed, 2,3,7,8-tetra CDF

is predicted to be by far the most active tetra CDF, and expected
to constitute 50% of the tetra CDF mixture.

Since 2,3,7,8-tetra

CDF is 1/20 as active as 2,3,7,8-TCDD, the "2,3,7,8-TCDD
equivalent" activity due to this compound can be obtained by
dividing the total tetra CDF concentration by 40.

Similarly, the

"TCDD equivalent" activity of the two most active penta CDFs can
be estimated by dividing the total penta CDF concentration by 80.
The calculated

"2,3,7,8-TCDD equivalent" activity due to PCDFs is

compared to the experimentally observed value for a number of
samples in Table VII.
The PCDDs will make a significant contribution to the cell
keratinizing activity of these samples; although they are
estimated to be 1/50 to 1/100 as abundant as the PCDFs, they may
be 20 times as potent in the assay.

The polychlorinated

biphenylenes may be even more important factors in this analysis.
Stalling's data suggests that they may be 1/10 to 1/20 as
abundant as the PCDFs.
as active.

However, they are reported to be 10 times

Thus, the calculated values in Table VII are likely

to be below the values that would be calculated if more complete
t

analytical data were available.

However, in view of the large

uncertainties present in these calculations and the data upon
which they are based, the calculated and experimental data are in
fair agreement.
It should be noted that the soot sample used in the animal
toxicology experiments exhibited a cell keratinizing activity of
2-20 ppm "2,3,7,8-TCDD Equivalents", and a calculated activity of
4 ppm due to PCDFs.

This differs from the "2,3,7,8-TCDD

�14

equivalents" calculated and observed in the animal toxicology
experiments

This does not represent a discrepancy in the data.

Rather, it is due primarily to the large difference between the
ratios of the guinea pig LD5Qs for 2,3,7,8-TCDF and
2,3,7,8-TCDD, and the corresponding ratios of cell keratinization
activity.
Conclusions
(1) Available chemical data indicate that the relative
concentrations of PCBs, tetra-, penta-, and hexa-CDFs, and total
PCDF are similar in soot samples taken from above the ceiling
panels of the BSOB, and in a sample collected by vacuum cleaner
during the early stages of the clean-up.

If this relationshiip

is valid for samples collected at other times and from other
locations, the PCB analysis can serve as a useful surrogate for
the more difficult analytical procedures.

(2)

A soot sample

exhibited an LDcQ in guinea pigs equivalent to 58 ppm
2,3,7,8-Tetra CDD.

If certain assumptions are made about the

chemical composition of this sample and the LD

s of the

compounds therein, it can be calculated that the PCDFs, tetra
CDDs, and the biphenylenes should account for ca. 45 ppm
"2,3,7,8-TCDD equivalent" activity.

Since this calculation

ignores other chlorinated dioxins, it is in good (probably
fortuitous) agreement with the observed value.

Based on these

results, there appears to be no basis for proposing unusual
synergistic or antagonistic effects among the components in this
mixture.

(3)

The cell keratinization assay can reliably

distinguish among samples containing widely differing
concentrations of PCDFs.

If certain assumptions are made about

�15

the chemical composition of compounds therein, it can be
calculated that the observed keratinizing activity in these
extracts is generally plausible.

(4)

Chemical analysis and the

cell keratinization assay suggest that the soot used in animal
toxicology studies is fairly typical of the soot samples
collected from above the ceiling pannels of the BSOB.

�TABLE I
Concentrations (ppm) of Polychlorinated Biphenyls and Polychlorinated Dibenzofurans in. Soot Samples Taken From the Binghamton State Office Building
Floor #
PCBsa
PCDFsb
Tetra CDF

2

28

3

4

1300

1

6

5

840

7

8

9

2800

6600

1800

23000

10

11

12

9600 21000 11000

13

3400

14

15

930 10000

16

9200

17

Ave

3-4*

6500 7200

5000

0.2

&lt;8g

16

220

23

190

70

320

140

250

d

d

32

300

h

220

145

100

Penta CDF

&lt;0.2g

&lt;9g

21

280

36

180

79

440

170

360

d

d

31

310

150h

260

165

120

Hexa CDF

&lt;0.3g

&lt;llg

13

180

14

35

32

290

84

260

d

d

e

56

89h

140

86

70

Hepta CDF

&lt;0.3g

&lt;12g

1.2

62

3

3.7

14

100

6.5

97

d

d

5.8

71

33h

32

31

20

Octa CDF

&lt;0.3g

&lt;14g

1.2

21

0.5

--

3

35

2

31

d

d

2.8

17

llh

15

11

4

51

760

76

410

200

1200

400

1000

—

87

750

670

438

310

.027

.062

.11

.052

.042

.048

.094

.075

.103

.066

.062

Total PCDF
Ratio Total PCDF cone.
PCB c
o
n
e

.

.

0

6

1

(a) quantitated as Arochlor 1254; data uncorrected for recovery
(b) correction for recovery incorporated
( ) not sampled because of dissimilar ceiling construction
c
(d) data not used because of poor recovery of internal

37

C1-Tetra CDF standard (&lt;10%)

(e) data lost because of instrumental malfunction; for purposes of calculation of total PCDF, it is assummed that hexa CDF is % the concentration of penta
( f Table 2)
c.
(f) soot collected by vacuum cleaner and used in animal toxicology studies
(g) detection limits are per congener, not per chlorination number
data not corrected for recovery.

Instrument malfunction caused loss of data on 37C1-Tetra CDF recovery

�Table II

Relative Proportions of Tetra-, Penta-, Hexa-, Hepta- and Octachlorodihenzofurans in Soot Samples
Taken from the Binghamton State Office Buildinga
Floor #

4

5

6

7

8

9

10

11

14

15

17

Aveb

Tetra CDF

31

29

30

46

35

27

35

25

37

39

33

33 ± 5

32

Penta CDF

41

37

47

44

40

37

41

36

36

41

39

40 ± 3

38

Hexa CDF

25

24

18

9

16

24

21

26

--

7

21

18 ± 7

22

2

8

4

1

7

8

2

10

7

10

5

6 ± 3

6

Hepta CDF

3-4°

_

Octa CDF

&lt;1

3

1

&lt;1

1

3

&lt;!

3

(a) Expressed as percent of total PCDF in sample.'
(b) Error limits represent one standard deviation.
(c)

Soot sample used in animal toxicology studies.

3

2

2

_-—

1

�CO

Table III
Comparison of Predicted3 (and Observed) Concentrations (ppm) of PCDFs in BSOB Soot Samples
Floor #

1

3

4

9

6

10

11

14

15

17

3-4

Jetra CDF

0.6(0.2) 26( 8)

17(16)

56(23)

133(190)

39(70)

60(320)

190(140)

420(250)

19(32)

200(300) 130(220) 100(100)

Penta CDF

0.9(&lt;.2) 30(&lt;9)

19(21)

64(36)

151(180)

45(79)

130(440)

220(170)

480(360)

21(31)

230(310) 150(260) 115(120)

Hexa CDF

0.3(&lt;.3) 16(&lt;11)

10(13)

33(14)

79(35)

23(32)

70(290)

115(84)

250(260)

11C")

120(56)

78(140)

60(70)

Hepta CDF

0.1(&lt;.3) 5.6(&lt;12)

3.6(1.2)
.6(1.2)

12(3)

28(3.7) 8.4(14)

99(100)

41(6.5)

90(97)

5(5.8)

43(71)

28(32)

22(20)

Octa CDF

.04(&lt;.3)

1.3(&lt;1.2) 4.2(0.5)

10(--)

35(35)

15(2)

32(31)

1.4(2.8

15(17)

10(15)

84
()

Total PCDF

1.9

2(&lt;13)
80

51(51)

3(3)

.400(1200)

(a) Prediction based on PCB levels and average ratio calculated in Table I and II

580(400)

1300(1000)

57(87)

610(754) 400(670) 300(310)

�19

Table IV
Influence of Structure and Chlorination Pattern on Guinea Pig
Oral LD5Qs (Male, Hartley, 200-250g)
Compound

LD3 U • &lt;f «—
cn(ug/kg)

2,3,7,8-Tetra CDD

2.5a

2,3,7,8-Penta CDF

5-10b

1,2,3,7,8-Penta CDD

3.1°

1,2,3 ,4,7,8-Hexa CDD

73C

1,2,3,7,8,9-Hexa CDD

60-100°

1,2,3,6,7,8-Hexa CDD

70-100°

1,2,3,4,6,7,8-Hepta CDD

&gt;600°

1,2,4,7,8-Penta CDD

1,125°

2,3,7-Tri CDD

29,444°

2,8-Di CDD

730,000°

a

J.B. Silkworth, D. McMartin, A.P. DeCaprio, R. Rej, S. Kumar
and L. Kaminsky (1981). Acute toxicity in guinea pigs and
rabbits of soot from a polychlorinated biphenyl-containing
transformer fire, N.Y. State Dept. of Health Report, January 6,
1982.
J.A. Moore, E.E. McConnell, D.W. Dalgard, and M.W. Harris
(1979). Comparative toxicity of three halogenated dibenzofurans
in guinea pigs, mice and thesus monkeys. NY Acad. Sci. 320,
151-163.
°E.E. McConnell, J.A. Moore, J.K. Baseman, and M.W. Harris
(1978). The comparative toxicity of chlorinated
dibenzo-p-dioxins in mice and guinea pigs. Toxi co 1.
Pharmacol. 44, 335-356.
0

�Table V
o
CSl

Comparison of the Observed Keratinization Activities with Total PCDF Concentrations
Observed
Floor I

"2,3,7,8-TCDD Equivalents(ppm)

Total
PCDF Concentrations

1

. 1 1
0 -

6

0.1-1.0

76

4

.11-1.1

51

14

.12-1.2

87

3

1.2-12

b

9

1.1-11

1200

8

1.6-16

200

3-4a

2-20

310

10

3.2-32

400

15

4.0-40

750

17

4.0-40

670

7

5.3-53

410

a

Soot used in animal toxicology experiments

•L^

Total concentration not defined, (cf. Table I)

b

(ppm)

�21

Table VI
Influence of Structure and Chlorination Pattern on Relative
Activity in the Cell Keratinization Assay3.
Compound

Relative Activity

2,3,7,8-Tetra CDD

1

2,3,7,8-Tetra CDF

0.05

2,3/6,7-Tetrachlorobiphenylene

0.5

1,2,3,7,8-Penta CDD

0.5

2,3,7-Tri CDD

0.01

1,3,7,8-Tetra CDD

0.01

1,2,3,7,8,9-Hexa CDD

0.005

1,3,6,8-Tetra CDD

&lt; .003

1,6,-DiCDD

&lt; .001
i

2.7-DiCDD

&lt; .001

2.3-DiCDD

&lt; .001

(a) Data adapted from J.C. Knutson and A. Poland (1980).
Keratinization of mouse teratoma cell line XB produced by
2,3,7,8-tetrachlorodibenzo-p-dioxin: an in vitro model of
toxicity, Cell 22, 27-36.

�Table VII
Comparison of the Observed Keratinization Activity in BSOB Soot Samples with Value
Predicted based on PCDF Concentrations

« Floor #

Observed
"2,3,7,8-TCDD equi

Lents" (ppm)

Calculated
"2,3,7,8-TCDD equivalents" (ppm)
PCDFs only

1

.Ol-.l

(b)

6

0.1-1.0

1

4

.11-1.1

1

14

.12-1.2

1

3

1.2-12

(b)

9

1.1-11

10

8

1.6-16

3

3-4a

2-20

4

10

3.2-32

6

15

4.0-40

10

17

4.0-40

9

7

5.3-53

7

(a)
-(b)

Sample used for animal toxicology studies,
PCDFs not detected in chemical analysis.

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23
REFERENCES

Gierthy, J.P. and Prenkel, G.D. (1982).

A preliminary report on

the c.,-aluation of an In Vitro assay for the detection of
"dioxin-like" activity using extracts of soot from the Binghamton
State Office Building.

New York State Department of Health

Report, January, 1982.

Knutson, J.C. and Poland, A. (1980).

Keratinization of mouse

cell line XB produced by 2,3,7,8-tetrachlorodibenzodioxin:

an in

vitro model of toxicity. Cell, 22, 27-36.

Poland, A., and Glover, E. (1977).

Chlorinated biphenyl

induction of aryl hydrocarbon hyudroxylase activity:
the structure-activity relationship.

a study of

Mol. Pharmacol., 13,

924-38.

Rappe, C. (1981) Report on the analysis of Binghamton soot.
Report, University of Umea, Sweden, 1981.

Silkworth, J. , McMartin, D., DeCaprio, A., Re j, R. , O'Keefe, P.,
and Kaminsky, L. (1982).

Acute toxicity in guinea pigs and

rabbits of soot from a polychlorinated biphenyl-containing
transformer fire.
January 6, 1982.

New York State Department of Health Report,

�'&gt; •

I

A

'i

24

i

Smith, R.M., O'Keefe, P.W. , Hilker, D.L., Jelus-Tyror, B.L., and
Aldous, K. (1981a).

Analysis of 2,3,7,8-tetrachlorodibenzofuran

and 2,3,7,8-tetrachlorodibenzo-p-dioxin in a soot sample from a
transformer explosion in Binghamton, New York.

New York State

Department of Health Report, February 20, 1981.

Smith, R.M., Hilker, D.L., O'Keefe, P.W., Kumar, S., O'Brien, J.,
Jelus-Tyror, B.L., and Aldous, K. (1981b)

Analysis of a

Binghamton soot sample for tetrachlorodibenzofurans and
tetrachlorodibenzo-p-dioxins.

New York State Department of

Health Report, October 1, 1981.

Smith, R.M., Hilker, D., O'Keefe, P.W., Kumar, S., Aldous, K.,
and Jelus-Tyror, B. (1982).

Determination of polychlorinated

dibenzofurans and polychlorinated dibenzodioxins in soot samples
from a contaminated office building.

New York State Department

of Health Report, March, 1982.

Stalling, D.L., (1981) Chlorinated dibenzofurans and related
compounds in soot formed in a transformer fire in Binghamton,
(

N.Y., Preliminary Report, Columbia National Fisheries REsearch
Laboratory, U.S. Fish and Wildlife Service.

�</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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                <text>R. Smith</text>
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          <element elementId="41">
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              <elementText elementTextId="22914">
                <text>&lt;strong&gt;Corporate Author: &lt;/strong&gt;Center for Laboratories and Research, New York State Department of Health, Albany, New York</text>
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          <element elementId="40">
            <name>Date</name>
            <description>A point or period of time associated with an event in the lifecycle of the resource</description>
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                <text>1982-03-01</text>
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                <text>Comparisons of Chemical and Biological Data on Soot Samples From the Binghamton State Office Building</text>
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                <text>BSOB</text>
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                <text>PCBs</text>
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              <elementText elementTextId="22921">
                <text>analytical studies</text>
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