903R97035
PILOT MULTI-MEDIA ENVIRONMENTAL HEALTH
CHARACTERIZATION STUDY OF
SOUTH AND SOUTHWEST PHILADELPHIA
FINAL REPORT
APPENDICES
M U.S. EPA Region III
5 6 6 • ^ Regional Center for Environraenta
•p-* Information
B87 1650 Arch Street (3PM52)
,' Philadelphia, PA 19103
vol. 2 c ..-*%
-------
LIST OF APPENDICES
Appendix I Advisory Committee Recommendations 1-1
Appendix II Demographic Profile of Study Area Neighborhoods II-1
Appendix III Community Advisory Committee III-l
Appendix IV Toxics Release Inventory IV-1
Appendix V Air Pollution and Health V-l
Appendix VI Drinking Water Quality VI-1
Appendix VII Solid Waste Management VII-1
Appendix VIII SARA Covered Facilities VIM
Appendix IX Landview Comparisons IX-1
Appendix X Toxicological Data X-l
Appendix XI Details on Health Data XI-1
enter toi t-mininiTtfnt.il lnfnrm.il
I'SrP \Kccmn III
16MI \rchSt
Philadelphia, l'\ !<)KH
(; S. EPA Region III
Regional Center for Environmental
Infcrraation
'•' 50 Arch Street (3PM52)
: .iladelphia, PA 19103
------- OCR error (C:\Conversion\JobRoot\00000AMA\tiff\2000W2EN.tif): Saving image to "C:\Conversion\JobRoot\00000AMA\tiff\2000W2EN.T$F.T$F" failed.
-------
APPENDIX I
MEMBERSHIP OF ADVISORY COMMITTEES
Environmental Characterization Study of
South and Southwest Philadelphia
COMMUNITY ADVISORY COMMITTEE
wAivn?
iTtAiVIJli
Minister Yasin A. Bey
Reba Brown
Al Caporali
Myrtle Carter
Joanne Cavuto
Judy Cerrone
A. Charlie Chambers
Katie Cofey
Patricia Coyne
Jacqui Delario
Dennis Glancey
Andrea Hall
Gloria Inverse
••'••.'" ' : A1ll5TI"1rii^^^^''-r"':'Vlv-i5'M">:''c":'^:i
ArJP^JulJsLalMJfPI -_ ,.*2 »; ,,-. • ,;|
Moorish America Society
PACO-ACORN
Southwest Enlisted Against Toxics
Passyunk Homes Tenant Council
Eastwick Project Area Committee
Stadium Community Council
A. Charles Chambers & Associates
Southwest Community Enrichment Center
Southwest Community Services
Community Resident
Southwest Community Development Corp
PACO-ACORN
South Philadelphia Environmental
Action Coalition (SPEAC)
1-1
-------
NAME
Venard Johnson
Kay Sampson
Marlene Santore
Shirley Sellers
Dess Stokes
Connie Williams
Robert Wingert
AFFILIATION
Healthy Family /Healthy Life, Inc.
Guyer Resident's Association
Packard Park Civic Association
Passyunk Homes Tenant Council
Southwest Philadelphia Community
Taskforce (SWPCT)
South Philadelphia School Board
Advisor Family Resource Network
South Philadelphia Environmental
Action Coalition (SPEAC)
1-2
-------
Science Advisory Committee
South and Southwest Philadelphia
Environmental Characterization Study
Name
Sean Hennessy, Pharm.D.
Post Doctoral Fellow
Melvin A. Benarde, Ph.D.
Director
Asbestos and Lead Ctr.
Les Levin, CIH
Professor of Industrial
Hygiene
Bob Giegengack, Ph.D.
Professor of Geology
Richard J. Cohen, Ph.D.
Eddy A. Bresnitz
M.D..M.S.
Chair
Community and Preventive
Medicine
Martha Anderson
Director
Environmental Health & Safety
Katherine McGlynn, Ph.D.
Associate Member
Shelley A. Hearne, Ph.D.
Program Director
Conservation and
Environment
Rose Cheney, Ph.D.
Affiliation
University of Pennsylvania School of Medicine
Center for Clinical Epidemiology and Biostatistics
Princeton, NJ
Yardley, PA
University of Pennsylvania
Medical College of Pennsylvania and
Allegheny University of the Health Sciences
Thomas Jefferson University
Fox Chase Cancer Center
Division of Population Services
The PEW Charitable Trusts
Philadelphia Health Management Corporation
1-3
-------
ENVIRONMENTAL IMPLEMENTATION TEAM
The following agencies were represented on the BIT:
US EPA Region III (EPA)
Pennsylvania Department of Environmental Protection (PaDEP)
City of Philadelphia
Managing Director's Office
Department of Public Health
Law Department
Philadelphia Local Emergency Planning Commission (PLEPC)
Following are individuals who represented the agencies at meetings of the EIT:
Name
Martha Anderson
Carol Collier
John Domzalski
Ronald Drake
Ron Furlan
Rob Goldberg
Lou Guerra
John Hadalski
John Kennedy
Brigid Lowery
Leonard Mangiaracina
Robert Ostrowski
Patrick O'Neill
Lorna Rosenberg
William T. Wisniewski
Affiliation |
PLEPC
PaDEP
Philadelphia Department of Public Health
PaDEP
PaDEP
PaDEP
PaDEP
Philadelphia Managing Director's Office
PaDEP
EPA
EPA
Philadelphia Department of Public Health
Philadelphia Law Department
EPA
EPA 1
1-4
-------
APPENDIX II
DEMOGRAPHIC PROFILE OF STUDY AREA NEIGHBORHOODS
-------
-------
n-i
-------
-------
II-3
-------
TT-4
-------
II-5
-------
.2. o> S
I 2 I
II-6.
-------
TT-7
-------
II-8
-------
S R S"
o> o" CD" to" r»" in *-" cp" co" co"
-
SfeSSSSSS
CNCNCNCOCOOlCOCq
-q-" in" to" co" CN" r»-" CD" a>"
g£
o" »n"
CN ci N" c«i CNJ" co" V in V to" of
cnm
i^«o
CNO
cootinmcp'vtncDinoa)
T-" *-" W T-" T-" O| ClT CO" CN «-" •«-'
SK
COV*T^r-»40IDCD IO(M
3;:
8"
tj
8S5
CO* CO"
(N tp
SQS
COO>O>inCNt-CD
F
855
ss
88" 88
n ?
O n in
s'e
co r- o o> «-
Sco
i-
-------
m mo'-oof^r^h-ooiOT-cN
CM ^- T-T-CMCMCMCOCMfMCOCMT-
-
OUOfM^-OinCPO
CM in O CM *-
mintor-aorocncNiincMr-
tMeofOT^-r^mtDoor^1*
II
X ?
ii
minCDCOCDCOOr4U>i-r-
cMcoc*)'*^ir-incDcnh-^-
' S V
ifl ?
CM O tf> N
tn i- m 03
as
CMCMCMCOCOM^rintDinCN
X £
•V. *- o ^- T-
•N.f»<»o>cov»i-*-cMc»^«r
co^-*-*^-h-«)cof^incM
co o C
CM CM
>r^.miMOcocMh-rMco *rfMr-ocMini
>CMrM«-oocoro«OM- o> o T- tN CM o i
• T-" T-" r-* W W T-' *-" *-" W «-" ^-" *-" CM" '
§
X ^
0» C3 O O T-
(Dcor-acoroai-ni-h-
coro^^-inr^tncDi^i^in
•o
o
o
o
J3
J=
CO CO <
SR(
r^oi^iDocooov-coin
cococo^inotnintDinco
£
ra
in f
ss
ssssssssgf:
_a
o>
•o
ra
5 S
w
I
•v w>
in o"
CM 10
O
CO
•o
n
o
CO
x e
HI 3
•ffs'
* ?
-
800
^>
«DI^.K>CDCD«I>IMi-CMO>«-
S
a.
_o
a
SS
O)
o
i
o
to CM «-
"
Itland
KCO CDlOCa^-VO^-COCOCMfM COCMfDCMWr^^CMCOXCM
fo ^ inr>~cP2>"(^(^^r>*r^^ co^rvv^rN-^^cncpo
V » «-" CM" CM" CM CM V co" n" 10* CM *•* T-" «-" W W of W W W *-"
I
* s
a *
£ £
£8 |
oZ I
Alla
z S
-------
0
0)
0>
t-
•tf
0
0
•E
0
r.
0)
z
^^
m
ro
IE
Q.
Q)
•D
JS
!£
Q.
0)
0)
1
*-•
o
CO
•o
c
CO
£
"3
o
!i2
Jj>
•fc»
^.
Q.
0
a
ca
Demogr
^
O (jj Q
fl 5"
!i
o
yt
|| |
•) Q» *O
O.|
^
t4e to
C *o
S, ?-
•i 5 N
g"4
o
*
^? S
"2 2 .
» E tM
£ C
Total Population -
100Percent(1A)
g |gasfefc§?
a" ~E5g» " s
CM
*~^S?'~OOOco
O) ooco^i-ocncoo
2 tN CD l/l (M i- CO
^ "" m o>
CM *~
^0>^^ 000.0
CD i*-r--h-cocori^otD
fU o co in m ^J1 CD
•« CO ^ D)
.o^o-os
a ointntomrN^— to
- t- i- in
IT- o *-
-CDCNCNOOO.O
§ RS|S,NS£S
J^. of co" r-"
M
-SS"°°°S
2 CNQcocor^ocnm
3" *°" ° °
t«« *~ *~
£-.
ll I |fl| 1
*i t OH| i
§•« s |*^1 |
en w ^ T- CN
f^ oo_ ^ fw en_
t^ n oo" *•"
« o
O7 CO O •»— T-
CO i- •»—
o co co in co
I-- m CM r^
-------
B.I
s
tt to
04 W
f- CO ^
•W tO T-
* — "
" i- •*- en"
to co to T-
h- CD in r*-
^- co in to
at" CD"
CO *- *- «»
•*-•*- en in
co
-------
0
05
0>
•o
o
o
•£
o
0)
'3
z
m
.2
0.
0)
•D
IE
Q.
1
"3
o
CO
^
c
IB
JC
o
CO
•5
i":
0
Q.
o
Demographi
0) <0 r*» co o» w r-
«r "*!"**. -
5 ce" w g
e "
I (n ^- CO O O O OJ
.x ffco S00^
(Q £ o co r~- *~
PS ** *°*
• a
li
o
££ mr^ (oooo
•S S S " o
S.a *° *~ S
w|
s
•S M f^- OJ *—
•B S O) •»- CO
?** S o" CM" V
Q *~ "~
CO ^
25
i 01 (N CO O O> to O
1 1 ^. s a--
ti ""
I i
0
s
i e. 5 fe 5°°°
M £ CN
« •» ^-" CN* O>"
If '
^
*
t^ 4- in CN o o o
E o S r~.
5^ co" W co*
2,§
0
s
t »« O CO «- O O O
•le n CM o> m
•5 5 m fN
£ 0
•1 I
2 i i - H=
5 I | a £|=
IIP? fill
f l-lf 1 ll^s
o te i= I Q =-o-5f
a. «t " < o. in o.S£&
Sie ee
N O
»« ID
s
CM ^ CO
T- CO CO
CO
CO O ^
"C *°
m*
oV
Ol CN CO
jo r- r-
V
*"
CO CN O
CS CO CO
*"
ogg
CO*
ffi§t
in i-
OD
s^s
CM*
^"
Sewage Disposal
Public Sewer
Septic tank/Cesspool
Other
tnmcO(D
(N i- »- •«- T-
-r-" *-" fN CN T-" fN CN
t t^ CO CM CO CM
> CN CM (N *-
-" CM* *-* f-" *~" ^-"
CN CM *-" CN CN CO" CN CN *-" W
'^o-'-r
(Ooicoco
" "
^CN^O
oiint^-c
" ~
cnotooi^i-c
---•-
>*-COeO^1O)'-»-O,-<
03
m ^
Q o
e
Ll W
-------
^- tN (N i- *- «- ^
W *-~ W W CO" (N Of (N CO «-"
cot^r~-co*-ioou>o>o<
*-" W (N »-" W CM*
r--inrocoj-mo>;
01 »-" W W *-"
O)
•o
o
o
o
O)
1
X
m
.2
a
75
•o
re
tf)
i
i s
IS
||
"I
S*- CO I
a> *» i
*- co o i
» ao CD co n
coo(N(Nioi^oicDinioi
>ooirooinr*-^cDJocN
lOiCMincDor^-cDr^Tr^-
— CN CD m o>co
•--iftr*.2
. JN to »- o o Is- r^
: tft to v S « o> 01
" of of *- •»-" *-"
ir^cDtntncncM^-co^'
ifNOOJfM^-TtpCNW
>f*»(»N-COOO>TO^
) f^ •» CO O Is-
• O Ol ^ CD •-
c
i
i Igllllilllli i Isllillllili
I ?>?5as35sasS I -Efssassssss S
• z^ss&ss&ssss- g,
£ 5«?SSSS!SSSKS <
I
E
m S
JS -D
If
if
o g
I 6
s§
3 o:
o ^.
CO to
-------
CO
5
e
» o> o o o o
i!
OOOOOCOOOOOOO
^
!:
-
(N
•a"
0
o
_£
O)
'35
Z
m
.2
a
"25
•o
a.
17>
i
*••
0
.0
^
(0
£
•3
o
0)
•5
,2
a
a
(0
0)
o
0)
o
*S gSlllimSIS iB8B5|S3Si8E goooSRoS.ooo
!«
*
Is I sss^slsst128" RsStlssss s?5 oooooooooooo
|i
g •>
|
• g. r~-O5h~-(Ntnfh>-ocor<>»corocN -rocomcooorococoooo
5"§ S-v«)(*)- * To*J*s*i*-*-*'*'*'*!'' £. ^o*:*s*'*''*-*-*'<*-*'>^
w c«sOtf>OU)inioinininin 51 c+'oinomintninmtnin 5^ c^oinotninmintointn
o
0)
o>
(E
c
n>
y
-------
o
0>
at
•5
o
o
(/)
p
ii
a
I
OOOOOfMOOOOOO
Srviinr^^ro-i-f
•^coTcocnot
•«- i- CM »-»- CO •«
li
oooooooooooo
oooooooooooo
•D
O
O
o
£ s
oooco^-r-cocooooo
O)
CD
a
0)
•a
oootnoocoinoooo
Q.
"w
II
•o
re
ooo^moooooom
*-o
CO (*)
<0 (O
o
tt)
Q
S
s.gggggssggi
*$;*;;;;£;;£
»*??ss3asRS S
So.
|«oo55S£o55; „ ^^o5SSSfiooo^
i^g^SSSSSSlCS £ =£S£SSS!S:SSK£
-------
CO
-J
5
S
'????*"'
oo>^r
i- ^- in
o
morM<0O)O <
0.
E
CO
o
E
Q)
Q
ution
ll *-
$1 ZZ*.
s,§
1 U.
•S e 5 £ £ S S S S S S >
£+*OMou)inmuTu»*nu»
3to*-^e»jfs!f*»^u?«>r-ao
o *
T- O
=j o:
o ^^
CO (D
-------
s
Si
s"'
CM <*> fM O O O W
r*. O r-* r- v- o
0>
TJ
O
o
o
.0
JC
O)
m
(0
!E
"S
TJ
n
^ o T (
5eo in oo r-- <
^ * *- ^J- en
(O ^ «-
o *
2 fe
:= 9-
-------
2
2
g
SSSS588
to_ Is- r«- w f_ f»
eo n T- T-
01
Y-i
•V
•a
0
0
€
o
£
O)
'3
z
m*
.2
"23
•o
to
!£
a
a>
1
o
•a
c
10
1
o
»
•i
b.
Q.
O
*ir
a
re
o>
o
0)
a
i %
afi
I*
! 1
i
•)
°
tt
C •)
* 8
5!
n
H
»i
il
I
ih.
o
«
o
5:
SlOO1*- ^ CNCNOOO
fO O i/l IT) 0 O O O
CO O IO O *- ^» a)
^ co in co *~
S^-(NfN 00 Ot^-OOO
o 10 *- to m co
O) *- OJ «-
•-COO1'- ^o«oEo«
gg£gKgaSt^3££2g3g3£3=
CO ^ T- CN T~ CN ••-
eoeof-'»-cMcorM coinr'Joicoco'a'rM
^T*-i-mc0^f OF~-OO4*-O1^OJ
COCOCNCOCMCOO COtDlOf-'«-OinO
fNO) couico ^-r^r-^to^ co
in*- *-^- CNCNt-^- »-
•^ f^ O CO O Ol (NT-in
-------
-------
APPENDIX III
COMMUNITY ADVISORY COMMITTEE
JOB DESCRIPTION FOR
COMMUNITY ADVISORY COMMITTEE MEMBERS
Length of Commitment
Two years
Estimated Time Required
Quarterly meetings approximately 2 hours in length
Desired Attributes
• Commitment to improving the health of the community.
• Knowledgeable about the study area.
• Willingness to maintain a community-wide perspective.
• Ability to represent an important perspective, organization, or sector of the
community.
• Willingness and ability to provide the required time.
Overall roles
Advise, consult with, and make recommendations to the Project Team and the
Community Advisory Committee members.
Present the perspective you represent in discussions, balancing those views with
a community-wide perspective.
Specific Responsibilities
Provide input and diversity.
Provide guidance to the Project Team.
Liaison to the individuals hi the community.
Benefits
Opportunity to improve the health of area residents; community service; personal and
professional growth; and the opportunity to represent your organization or the
community hi which you live and/or are employed.
m-i
-------
MINUTES
South and Southwest Philadelphia Environmental
Characterization Study
COMMUNITY ADVISORY COMMITTEE
Passyunk Library
1935 Shunk
Philadelphia, PA
Monday, June 12, 1995
6:00 - 8:00 p.m.
Attendees: Lois Banks, Tom Burke, Abigail Bushley, Patricia Coyne, Andrea Hall, Leanne
Nurse, Nadia Shalauta, Dess Stokes, Bob Wingert, and RuthAnne Visnauskas
WELCOME AND INTRODUCTIONS
Tom Burke and Lois Banks welcomed and thanked meeting participants for their
presence and interest in this study.
PURPOSE OF THE STUDY
Nadia Shalauta gave a brief outline of the study. Ms. Shalauta explained that the study
is designed to develop a framework for characterizing the environmental health needs of South
and Southwest Philadelphia. Ultimately, the goal is to develop an improved capacity for
Region ffl to respond to community concerns about their health and environment.
THE WORKPLAN
The scope of work for this study was discussed by Tom Burke as he gave a slide
presentation of the study area. Dr. Burke explained that this two year study is made up of four
phases. In Year 1, problem(s) identification and environmental characterization will be the
primary focus. In Year 2, public health assessment and the reporting of results and
development of recommendations will be the primary focus. Dr. Burke went on further to
explain that this study will bring about information and will provide the community with new
tools (education) with which to fight for the improvement of environmental factors in their
community. He concluded by informing the CAC that this study will not answer the question,
"why do people die?".
m-2
-------
ACTIVITIES TO DATE
To date, the Project Team has visited many of the areas identified by both the
Environmental Protection Agency (EPA), as well as members of the study area community.
Since the beginning of this study, two committees/teams (in addition to the CAC) have
been implemented, the Science Advisory Committee (SAC) and the Environmental
Implementation Team (EIT). Each member in attendance was provided with a list of the
members on these Boards. Mr. Stokes desires that someone be appointed to the EIT that
would represent the community. He feels that Mr. Bishop is not that person because he is not
present nor is he involved in the South and Southwest Philadelphia community. In addition,
Mr. Stokes questioned EPA personnel being a part of the EIT and SAC. Dr. Burke informed
him that EPA personnel are not "formal" members of these two Boards. Mr. Stokes then
requested that we provide the CAC with a final list of Board members.
ROLES OF THE "PLAYERS"
The role of the CAC is to provide input and diversity; provide guidance to the Project
Team; and serve as liaison to the individuals hi the community. Meetings will be held
quarterly and meeting sites will alternate between South and Southwest Philadelphia.
Because of the extensive amount of work to be done, Ms. Hall (along with others in
attendance) would like for the CAC to grow in size. Recommendations for people to be
included on this Committee include: John Johnson and Joann Rossi. Ms. Banks will follow-up
with CAC members to obtain names and telephone numbers of prospective members of this
Committee.
FEEDBACK FROM THE COMMUNITY ADVISORY COMMITTEE
There are many environmental concerns in the South and Southwest Philadelphia study
area. The following are among those discussed at this meeting:
• Importance of community awareness. Community was not informed of MAB
paint fire in Summer of 1994. Many such incidents occur.
• Southwest Philadelphia has the highest infant mortality rate. Why?
• High amount of lead poisoning, asthma in children, and violence.
• Sun Oil produces 75% of fuel hi Philadelphia. Where is the city's evacuation
plan?
• Companies that can operate without having a permit.
• Things that are being stored at Bell Telephone site.
• There are problems not only in the ah", but also hi the soil.
• There are many BIG problems, but there are also many little ones that if they
m-3
-------
are not stopped, will grow into BIG ones. (Mr. Stokes offered to take the
Project Team on an informal "tour" showing some of these problems)
• There is a need for the community to validate the information/data given to them
by agencies/officials.
• There are many pipelines underground. Where are they and are they
dangerous?
• What are the City's zoning regulations for sites of concern?
• Dupont Labs
• Are there hazards at Marshall Labs?
• What authority will the Project Team have to "go behind the gates" of
environmentally hazardous companies? Will the CAC also be able to "go
behind the gates?"
• How will the Project Team design the incompetence factor into the final report
for this study?
• Can the community be assured of receiving information/feedback throughout the
entire Study?
• Proposed soil remediation facility on 61st Street
In addition to CAC environmental concerns, Mr. Wingert requested aerial maps of the
study area.
Each CAC member was asked to provide the Project Team with a list of environmental
and health concerns of their community, ranking them in order of most to least concern for the
individuals hi their communities. This information should be brought to the next meeting.
Pat Coyne mentioned a community health needs assessment that her organization has
already completed. The Project Team will request a copy for review. In addition, a John
Bartram Village lead poisoning study was mentioned. The Project Team will follow- up on
this also.
Ms. Banks will follow-up with each CAC member over the next week. She will
request names of prospective additions to the Committee as well as note any additional
concerns that were not mentioned at this meeting.
SCHEDULE NEXT MEETING
The next CAC meeting is scheduled for September (date TEA) at Southwest
Community Services, 6424 Woodland Avenue, Philadelphia, PA. As soon as a date is
determined, CAC members will be notified.
m-4
-------
MINUTES
South and Southwest Philadelphia Environmental
Characterization Study
COMMUNITY ADVISORY COMMITTEE
Southwest Community Services
6424 Woodland Avenue
Philadelphia, PA
Thursday, September 14, 1995
6:00 - 8:00 p.m.
Attendees: Lois Banks, Ron Bialek, Reba Brown, Tom Burke, Al Caporali, Joanne Cavuto,
Charlie Chambers, Patricia Coyne, Dennis Glancey, Andrea Hall, Brigid
Lowery, Kay Sampson, Shirley Sellers, Nadia Shalauta, Dess Stokes, Deborah
Wagner for (Evelyn Marcha-Hidalgo), and Bob Wingert
WELCOME AND INTRODUCTIONS
Lois Banks welcomed and thanked meeting participants for their presence and interest
in this study. Each attendee introduced him/herself stating their name and the organization or
community they represent,
COMMUNITY UPDATE
Lois Banks gave a brief overview and update of the CAC activities since the June 12th
meeting:
• New members have been contacted and added to the CAC including those
suggested by members in attendance at the first meeting
• JHU Project Team went on a tour of Southwest Philadelphia at the invitation
and leadership of Dess Stokes
• Site tour of the Southwest Philadelphia area was conducted with individuals of
the Philadelphia Health Department and the Air Management Services. The
JHU Project Team pointed out several sites where open dumping and
unpermitted trash transfer activities were occurring.
• Aerial photographs of the study area are available from the Delaware Valley
Regional Planning Commission located in the Bourse Building on South
Independence Mall. You may contact Sharon Smith at (215) 592-1800.
Photographs are available for the years 1959, 1965, 1970, 1975, 1980, 1985,
and 1990. The photos are $8.00 for 1 inch = 800 ft resolution^r $12.00 for 1
IH-5
-------
inch = 400 ft resolution. Older photos are available for viewing at the Free
Library of Philadelphia at 22nd and Vine Streets. Contact person is Richard
Boardman.
• There is an on-going task of compiling information on the issues and concerns
of the South and Southwest community.
CAC members were also asked if it would be helpful for EPA to provide updates on the
project progress to be included in their individual community newsletters. This was agreed
upon, and it was also requested that EPA put each CAC member's name on its mailing list to
receive information on ALL South and Southwest Philadelphia community activities.
EPA UPDATE
Brigid Lowery, an EPA employee from Headquarters hi Washington, D.C. working on
this study, introduced herself and her role in this project. She has been assigned to serve as
community relations representative on this study. She will develop a mailing list and will
ensure that each CAC member receives all EPA updates on this study, minutes from all BIT
meetings, zoning policy changes, and information regarding upcoming community activities
and programs. Ms. Lowery will also provide information to CAC members to include in their
organization/community newsletters.
It was announced that on September 26, 1995, a meeting is scheduled to discuss the
auto body repair shops hi both South and Southwest Philadelphia. All CAC members and
other community members are invited to attend.
Ms. Lowery reported the results of some "quick fixes" to short dumping. EPA is
discussing possibilities with City representatives. One of the problems identified is the slow
process by which illegal dumpers are prosecuted. Additionally, the small fines are ineffective
to serve as a deterrence.
Joanne Cavuto mentioned that her community has an environmental town watch
composed of individuals who are trained to use radios to report short dumping.
EPA is also working on a special initiative aimed at reviewing compliance status of
industries in Southwest Philadelphia.
DISCUSSION OF INTERIM FINDINGS
Each member in attendance received a Working Copy/DRAFT of the Interim Findings
of this study. Tom Burke and Nadia Shalauta prefaced the brief overview of the findings by
informing the CAC members that the report was hi no way complete or final. The findings
listed in the report are the results of the preliminary collection and analysis of data,
figures/tables must still be reviewed to ensure accuracy. This information should not be cited
until it is released hi its final version. In addition, Ron Bialek informed the CAC that there are
m-6
-------
limitations in the quantitative data, noting that it is only as good as the data available. These
sources are referenced hi the Interim Findings document.
OPEN DISCUSSION
Throughout the meeting, CAC members voiced their concerns/issues, anger, and fears
about this study. Some of those concerns are listed below:
• EPA, DER, Air Management, Planning Commission should be invited to a
future meeting to hear and discuss the concerns of the CAC, and provide
information as to how they are addressing these problems.
• There is a cumulative effect of environmental things going into our lungs
already. Why is the zoning board allowing existing companies to continue, and
new companies to come into the area?
• Would like to have a CAC member on the EIT to provide the community's
viewpoint (It was explained that the EIT addresses zoning and implementation.
Although community members are not on this team, the CAC is able to voice
then- concerns and they will be relayed to the EIT. It is important that CAC
members understand that the COMMUNITY HAS A SIGNIFICANT AND
CRITICAL ROLE IN THE PROCESS and then- concerns and issues are not
being taken lightly. Brigid Lowery will be sending EIT meeting minutes to all
CAC members.)
• Short dumping has turned into a monumental problem.
• The agencies are waiting for the results of this study before they take any
actions with existing problems.
• SEPTA asked DER and EPA for permission to discharge waste into the Victory
Creek. What can be done to stop this?
• There is a great concern with the refinery incinerating heavy metals.
• Air Monitoring Systems - What is the location of each system and what it is
designed to monitor?
• There is a need for ACTION. Too many studies have taken place, but the
community has seen no action.
Tom Burke commented on the importance of each CAC member and each issue that has
been brought up. Some issues are complicated and will not be changed with short-fixes.
Many things EPA can handle, others are not hi their jurisdiction (EPA has very little authority
over the trash issue). The greatest challenges are "ENFORCEMENT & INVOLVEMENT."
Lois Banks closed the discussion session by thanking all attendees for their interest and
support of this study. Although the discussion of the ranking of community environmental and
health issues did not occur, the rankings were collected and will be compiled.
SCHEDULE NEXT MEETING
m-7
-------
The next CAC meeting is scheduled for Tuesday, December 12, 1995, at the South
Philadelphia Older Adult Center, 1430 East Passyunk Avenue.
MINUTES
South and Southwest Philadelphia Environmental
Characterization Study
COMMUNITY ADVISORY COMMITTEE
South Philadelphia Older Adult Center
1430 East Passyunk Avenue
Philadelphia, PA
Tuesday, December 12, 1995
6:00 - 8:00 p.m.
Attendees: Lois Banks, Ron Bialek, Tom Burke, Al Caporali, Judy Cerrone, Rashid A.
Chotani, Gloria Inverse, Debbie Lee, Brigid Lowery, Len Mangiaracina, Kay
Sampson, Marlene Santore, Nadia Shalauta, Joe Warren, Bob Wingert, and
Wendy Yap
WELCOME AND INTRODUCTIONS
The meeting opened with individuals introducing themselves and the organization they
represented.
COMMUNITY UPDATE
Lois Banks gave a brief overview and update of the CAC activities since the September
14th meeting:
• Amendment to the minutes of the September 14, 1995 meeting. Joanne
Cavuto's name was mistakenly left off of the list of attendees.
• Johns Hopkins hosted two community-wide meetings on November 15, 1995,
where Interim Findings of the Study were presented and discussed.
• Four new members have been contacted and added to the CAC.
• The lists of environmental and health concerns and issues provided to the JHU
project team were compiled and handed out at this meeting. A request was
made that each member provide the specific issues/concerns next to the listed
sites. Additional sites that do not appear on the current list should be added.
This information should be brought to the next CAC meeting.
m-s
-------
THE STUDY UPDATE
Tom Burke and Nadia Shalauta attended a meeting today with the Assistant
Commissioner of Health and the Director of Air Management Services from the City of
Philadelphia Health Department (John Domzalski and Bob Ostrowski), and the Chairman of
the Epidemiology Department at Johns Hopkins University (Dr. Jonathan Samet). The
meeting addressed studies regarding particulates in the air and mortality. Because of the
concern raised in the community about these studies, the City requested a meeting with the
researchers who conducted them. The JHU project team will continue working with the City
to ensure that the questions of members of the community are answered.
Dr. Burke and Ms. Shalauta also informed the CAC of the recent meeting and tour of
the refinery. Information gained at this meeting and tour include the following:
• At the back fence of the refinery trucks are being filled with fuel. In its natural
form, this fuel is odorless, and therefore could be very dangerous in case of
spills. Mercaptons, which have a strong odor, are added so that leaks are
readily detected.
• The community has requested "sirens" for alarming the community when there
are releases.
The State DEP has assigned a multi-media inspector to serve in the Southern part of
Philadelphia. Paul Jardell has been temporarily assigned to serve in this position, and will
cover the area of Chester, South, and Southwest Philadelphia.
As we enter the second year of this study, our focus is shifting to health data, however,
your input of additional environmental issues of concern are always welcomed.
EPA UPDATE
Brigid J^owery and Len Mangiaracina commented on the many activities that are in
progress at sites identified by the community.
• The City has notified the owner of Keystone that asbestos clean-up is required.
The owner of this facility is a resident of New York. The City will pursue him
to take financial responsibility.
• There was a meeting with representatives of the owners of National Heat and
Power, the City, State, and EPA. The governments gave National Heat and
Power a list of priorities including securing the facility and leaving the tanks in
safer condition. National must submit a proposal to the City.
• The City of Philadelphia's Fleet Management Facility at 12th and Reed Streets
will no longer conduct any painting.
JJI-9
-------
Additional site updates are in the EPA Update Newsletter that was distributed at the
October 31st and November 15th meetings. Brigid Lowery will also send CAC members
copies of the minutes from the BIT meetings.
EPA is scheduled to put up 6 air monitors in the Study area for approximately 3 months
(April through June 1996). Locations have not been designated, and CAC input is welcomed
and needed. If you are interested in participating in this effort, please contact Brigid Lowery.
Gloria Inverse informed the CAC that Pam Dalton from the Monel Factory Research
Center is scheduled to meet with SPEAC on December 14, 1995, and offer to lend them
monitors. She will inform us of the outcome of this meeting.
South and Southwest Philadelphia is getting more attention than any other region in the
area. This Study is not only ABOUT the community, it IS the COMMUNITY. EPA is
willing and anxious to provide environmental education to community members and
organizations. Please telephone Brigid Lowery (597-6445) if this service is desired.
COMMENTS ON THE STUDY FROM INDIVIDUAL CAC MEMBERS
Each of the community members provided feedback on the work that had been done
since the onset of this study, and raised new issues of concern. Comments are as follows:
• the study has provided good background information on environmental status in
South and Southwest Philadelphia
• the proposed air monitoring study should extend into summer when pollution is
at its highest
• needs to be cooperation from the City
• what's going to happen if results from the air monitoring study shows that
pollution levels are dangerous to the community .
• there should be more frequent inspections of polluting facilities
• there should be warning systems to community when there are releases to the
environment from the refinery
• DEP should not issue permits to facilities that are environmentally unsafe
• the community does not want ChemNuclear (low-level nuclear waste site) in the
area
• each area should have at least one complete air monitoring station that is secured
from vandalism
• community would like to have access to the data obtained from the monitoring
stations
• there is a need for sufficient manpower to inspect current and future facilities in
the area
m-io
-------
• results of this study will not be filled with such hard data, but will be a
document for educating the public
• government departments should be brought to the table with the community so
that they (government departments) can assume the responsibilities that they
have been shunning (force accountability)
• community needs the support from City Council (political) and private
(agencies) people
• would like to have some in-door air quality monitoring at the school on Broad &
Vine
• the traffic at the Spectrum and the cumulative effect of it has to be checked
• enforcement is a major issue, and industry needs to be forced to comply with
rules and regulations
• regulators need to be re-educated and forced to completely fill out violation
forms (AMS Reports)
• when applying for permits, facilities must be required to operate on PA
definitions, not on definitions from other states
Members of the CAC unanimously agreed that they are pleased with the work of the
project team to date. They also realized that "fixes" to all problems are not the responsibility
of EPA, but are grateful for the help that has been given to reach other governmental agencies.
SCHEDULE NEXT MEETING
The next CAC meeting will be scheduled for March at a location hi Southwest
Philadelphia. We will inform you as soon as the meeting date and location are confirmed.
revised 1/30/96
m-n
-------
MINUTES
South and Southwest Philadelphia Environmental
Characterization Study
COMMUNITY ADVISORY COMMITTEE
Eastwick Library
2851 Island Avenue
Philadelphia, PA
Thursday, March 27, 1996
6:00 - 8:00 p.m.
Attendees: Ronald Abney, Jerome Avery, Lois Banks, Vaunrance Benjamin, Reba Brown,
Tom Burke, Al Caporali, Joanne Cavuto, Judy Cerrone, Charlie Chambers,
Rashid Chotani, Patricia Coyne, Pamela Dalton, Jacqui Delario, Dennis
Glancey, Sean Hennessy, Gloria Inverse, Venard Johnson, Debbie Lee, Lester
Levin, Jill Litt, Len Mangiaracina, Brenda McCoy, Mary Orr, Patrick Prosser,
Joanne Robinson, Kay Sampson, Marlene Santore, Shirley Sellers, Nadia
Shalauta, Ed Thomas, John Tissue, Bob Wingert, and Bill Wisniewski
WELCOME AND INTRODUCTIONS
The meeting opened with individuals introducing themselves and the organization they
represented. Bill Wisniewski, Assistant Regional Administrator of EPA - Region UJ,
expressed the interest and commitment of EPA in this Study.
COMMUNITY UPDATE
Lois Banks gave a brief overview and update of the C AC activities since the December
12, 1995 meeting:
• Those persons who have been identified and have agreed to serve on the CAC
and have never attended a meeting were polled to see if they wanted to continue
serving or if they could suggest the names of persons who could replace them
(by representing the views of the individual neighborhood or organization).
Due to the lack of response, their names have been deleted from the list of
members. No new members have been identified from these organizations.
• Dess Stokes and his family relocated to Dover, Delaware, but he promised to
keep in touch and assist in the writing of the final report.
• Tour of South Philadelphia community on February 9, 1996.
• Attended March 6, 1996 Supplemental Air Sampling Study Meeting.
JJI-12
-------
• Received and compiled information provided by members of the community.
Reminder: The purpose of this Study is to identify issues of concern; examine indicators
of community health; and provide a useful tool for the communities and
agencies involved, to collaborate your efforts to improve the environment
and health in South and Southwest Philadelphia.
The purpose of the C AC is to provide advice throughout the conduct of the
study, and to assist hi identifying short term measures which can be
implemented to improve the quality of the environment in the study area.
The CAC also assists Johns Hopkins in identifying pollution sources and
environmental health concerns in the community.
THE STUDY UPDATE
Tom Burke and Nadia Shalauta attended a meeting at the Navy Yard and obtained some
good information that will assist them in conducting this Study. JHU is also working with Sun
Oil Company and has invited Patrick Prosser (at the request of CAC members at the December
12, 1995 meeting) to attend this meeting and to provide input/answers to questions raised by
CAC members.
Dr. Burke reiterated the fact that although this current study is not an epidemiological one,
it will be a framework by which we will be able to learn about the health and sources of
environmental contamination of the community. He also solicited the aid of the CAC in
reviewing the report and providing input before it is finalized.
EPA UPDATE
Len Mangiaracina provided a brief update on the latest activities regarding the South
and Southwest Philadelphia study.
• Air Monitoring Meeting: A letter was sent out to community members regarding
the air monitoring initiative to be conducted by EPA. The letter identifies the
selected sites and schedules, and provides a brief background on the purpose of
the air monitoring initiative and program procedures. Furthermore, Point
Breeze was added to the list of sites to be monitored based on community
feedback. Carbon monoxide will be monitored in the Eastwick neighborhood
area, including the stadium complex.
• EPA hopes that additional monitoring may be conducted during the fall.
• Finally, Ted Erdman and Brigid Lowery will be visiting the designated sites
during the first and second week of April. These site visits will be open to
community representatives. Questions or comments should be forwarded to
Brigid Lowery at 597-6445.
m-13
-------
• Earth Day - In April, EPA will be sponsoring Earth Day hi Philadelphia. As
part of the festivities, EPA invited South and Southwest community members to
participate hi hands-on monitoring activities along the Schuylkill River. For
further information, please contact Pete Weber of EPA at 597-4238, by April
15th.
• Delaware Valley Recycling - The Delaware Valley Recycling Plant was shut
down by state officials. Mr. Mangiaracina commended the intense cooperation
between EPA, DEP, and community members and their influence in Delaware
Valley Recycling Plant's closure.
• Environmental Implementation Team (EIT) Meeting - At the most recent EIT
meeting officials from the State and City were present. The meeting provided
an opportunity for representatives to discuss long-term implementation strategies
and the future direction and role of the EIT.
• Scientific Advisory Committee (SAC) - This meeting was influential in the
progress of the Philadelphia study. The meeting was focused on strategies to
ensure long-term community involvement.
• South Philadelphia sites which were toured by the project team will be profiled
hi the next EPA Update (newsletter).
Mr. Mangiaracina commented on the fact that community involvement is essential to
this Study. Even after this Study is completed, it is the responsibility of EPA, the State, and
the Community to continue working together on a long-term relationship with open lines of
communication.
PENNSYLVANIA DEPARTMENT OF ENVIRONMENTAL PROTECTION
John Tissue of DEP introduced himself as the newly appointed liaison between the
communities and the State. He has worked during the past three years hi the Chester area and
has recently been assigned to the South and Southwest region of Philadelphia. His role will be
to respond to community concerns regarding the local industry - odors, leaks, noise and so
forth. Any questions or concerns should be directed to John at (610) 941-5108.
SUN COMPANY
Patrick Prosser of Sun Oil Company provided a brief update on community outreach
initiatives underway. Sun recently sent a letter to neighboring communities announcing a
Refinery Open House and Environmental Fair on June 1, 1996. More information regarding
this activity will be forthcoming.
The Sun Oil Refinery has also established a telephone information system to provide
more timely information in the event of an emergency or change hi operational procedures.
The telephone number is 1-800-786-5371. Though emergency response planning is still
m-14
-------
underway, the telephone information will serve as an interim step towards notification
procedures. Attached is copy of the letter stating this information.
In response to Mr. Prosser's comments, community members raised concerns regarding
the emergency response strategies and capabilities. Though no one present at the meeting was
prepared to answer questions from the community, the group agreed to identify key concerns
and questions and forward them to Mr. Prosser. In return, Mr. Prosser will deliver these
questions to the appropriate people at Sun. Venard Johnson agreed to coordinate the
community concerns and work with Mr. Prosser at Sun to ensure these concerns are addressed.
A copy of this letter/list will be forwarded by Mr. Johnson to Lois Banks, the community
liaison of this Study.
QUESTIONS AND ANSWERS
Community members present at this meeting were given the opportunity to submit
questions in writing. Questions and answers are as follows:
Q: From the study of the fuel under the Quartermaster, how far has it traveled, and
what is going to be done with it?
A: Dr. Burke has toured the Quartermaster and there are many unknowns. He offered the
expertise of JHU, and JHU will report on this as information is obtained. Dennis
Glancey (CAC member from the Housing Authority) stated that there is a plume under
Passyunk Homes and data has been given to the DEP. In addition, to looking at
housing, information about the sewers hi the area is also being looked at.
Q: Could you possibly provide a printed list naming all of the members of the
Environmental Implementation Team (EIT) and the Science Advisory Committee
(SAC) listing the person's name, agency affiliation, address, and telephone
number?
A: Yes, Brigid J^owery (EPA) will provide this information.
Q: The South and Southwest Study is funded as an Environmental Justice Project.
How is the Study addressing the Environmental Justice issue?
A: This Study is not specifically an environmental justice study.
Q: Will the data collected in South and Southwest Philadelphia be compared with a
less environmentally impacted area of the City to make a determination of whether
or not there is an injustice in South and Southwest Philadelphia's neighborhoods?
A: This study does not include the entire city, but findings will be compared to other cities
ffl-15
-------
nationally.
Q: How many violations have been reported from the Sports Complex area - south of
Oregon Avenue (re: burning, dumping, violations from L & I, DEP, and EPA)?
A: South Philadelphia sites toured by the project team will be profiled in the EPA Update.
This will also include areas south of Oregon Avenue.
Q: How can the community be assured that Delaware Valley Recycling will remove all
debris from their facility?
A: John Tissue will research this, however, the community should know that Delaware
Valley Recycling cannot reopen simply by paying the $350,000 hi fines.
Q: Can anything be done about traffic pollution and noise from 61st to 58th Streets?
Is there any law for cutting off traffic at a certain hour?
A: If AAA services a commercial customers, it has the right to operate 24 hours per day.
Q: Will the Study include recommendations for the City Planning Commission for a
re-distribution of existing land uses or for a moratorium of pollution sources in
highly impacted areas?
A: EPA met with Barbara Kaplan of the City Planning Commission to present the initial
findings regarding issues of decision making and zoning.
SCHEDULE NEXT MEETING
The next CAC meeting will be scheduled for June at a location hi South Philadelphia.
We will inform you as soon as the meeting date and location are confirmed.
ffl-16
-------
MINUTES
South and Southwest Philadelphia Environmental
Characterization Study
COMMUNITY ADVISORY COMMITTEE
Southern Home Services
3200 Broad Street
Philadelphia, PA
Wednesday, June 26,1996
6:00 - 8:00 p.m.
Attendees: John Baker, Lois Banks, Yasin Bey, Reba Brown, Tom Burke, Al Caporali,
Myrtle Carter, Joanne Cavuto, Judy Cerrone, Charlie Chambers, Katie Cofey,
Donna Drumm, Mary Fox, Regina Greaser, Gloria Inverse, Venard Johnson,
Debbie Lee, Len Mangiaracina, Virginia Moseley, Kay Sampson, Marlene
Santore, Nadia Shalauta, Connie Williams, Bob Wingert, and Wendy Yap.
WELCOME AND INTRODUCTIONS
The meeting opened with individuals introducing themselves and the organization they
represent.
COMMUNITY UPDATE
Lois Banks gave a brief overview and update of the CAC activities since the March 27
meeting:
• Many of the CAC members and the JHU project team attended the meeting of
the Restoration Advisory Board on May 21, 1996. Dr. Burke gave an overview
of the Study.
• The JHU project team went on a tour of the Passyunk Homes on June 26, 1996.
Myrtle Carter and members of this community facilitated the tour.
• The JHU project received and compiled information received from memebrs of
the community.
Members were asked to provide feedback on how information from this study is being
disseminated within the various communities. The following resources are currently being
used.
• local newspapers
• churches
ra-n
-------
• community organization meetings
• community block meetings
It was suggested that JHU create a one-page flyer about the study that is written in non-
technical language. This flyer can be distributed house-to-house and at upcoming community
events. The creation of a web-site on the Internet would also be beneficial to those with
computer network access.
Reminder: The purpose of this study is to identify issues of concern; examine indicators
of community health; and provide a useful tool for the communities and
agencies involved, to collaborate your efforts to improve the environment
and health in South and Southwest Philadelphia.
The purpose of the CAC is to provide advice throughout the conduct of the
study, and to assist in identifying short term measures which can be
implemented to improve the quality of the environment in the Study Area.
The CAC also assists Johns Hopkins hi identifying pollution sources and
environmental health concerns hi the community.
THE STUDY UPDATE
An updated interim report will soon be completed and distributed to the HIT, SAC, and
SAC.
The JHU study team has noticed some cleanup and securing of certain facilities in the
Study Area, such as Keystone, steps to Bartram Gardens Housing, and Orfa.
The Defense Personnel Supply Center (DPSC), Sun Oil, Department of the
Environment (DOE), and Pennsylvania Department of Environmental Protection (PaDEP) have
met to discuss the problem of the underground plumes. An analysis of the plumes must be
performed before removal plans can be made.
Preliminary health data will show the association between the day to day air quality and
increased mortality. Philadelphia is an unusually well-studied area and good data is available
from Air Management Services. The City has a new Asthma Task Force (6-8 months old) to
study the increased incidence of childhood asthma and determine intervention strategies. There
is an ongoing asthma epidemic nationwide to which more attention must be focused. At this
time however, there is no disease registry which requires reporting of asthma to health
authorities, so the extent of the problem is difficult to tally.
EPA UPDATE
Len Mangiaracina discussed the personnel transition of this study. Brigid Lowery has
m-18
-------
completed her course of study at Johns Hopkins School of Public Health and has currently
returned to her former position at EPA Headquarters in Washington, DC. RuthAnne
Visnaukas graduated from the University of Pennsylvania, and Mike D'Angelo is attending
Harvard University. We welcome Virginia Moseley, who will serve in the capacity of EPA
community liaison to the study.
Ms. Moseley informed the CAC that Asbury Park, NJ has a site hi the World Wide
Web, entitled "Gasping for Ah-." This is an asthma investigation that can be accessed via the
internet at app.com.
Al Caporali had spoken with Brigid Lowery (prior to her leaving the project) about
having a risk assessment performed in the Study Area. This responsibility has now been taken
on by Lorna Rosenberg.
DISCUSSION
Meeting participants were asked to provide comments on the Interim Report, and to
provide input to the design and content of proposed health education sessions. Comments
include the folio whig:
• demographics should be brought up to the year 1995 (this will be difficult to do
because census data is collected every 10 years, the last being collected in 1990
from the U.S. Census Bureau)
• provide more information on the treatment of lead levels in homes
• page 34 should provide a discussion of lead legislation and regulations
• include concerns about soil and soil remediation plants
• there is a concern about Philadelphia's non-compliance with national standards
for ozone (page 4)
• concern about the prioritizing of environmental concerns on page 11 (Joanne
Cavuto will provide us with a written copy of her suggested ranking order)
• a noise survey should be included (this would give a good index of other types
of industrial problems)
• provide air quality data that is specific to South and Southwest Philadelphia
• re-do chart of page 33 because it is not readable (there is little differentiation
between colors), and also provide the year that the information is from
• provide a better explanation of vehicle emissions (ie., where does the data come
from; how is it organized; what is included; and what is the significance)
• elaborate on the contacts that JHU and EPA have with the City (who was
present; what was discussed; when meetings were held; and where meetings
were held)
• report should provide awareness, enforcement procedures, and
recommendations for emergency response plans
IH-19
-------
• report should show the City's lack of following laws (ie., Planning Commission
not staying within their own rules regarding the re-zoning of the Snyder area)
(this information will not be part of the report, as this study is not a compliance
investigation)
• provide a list of City Council people that met with the project team and their
individual comments to the study
• include the Stadium Community Council and the Packer Park Civic Association
in the text and on the map
• include where Philadelphia falls hi the spectrum of auto body shops and
enforcement
• the report from air management (re: 6 monitoring sites during the Spring of this
year) should be included
• discuss the high incidence of asthma hi relation to the air quality
• there should be an educational partnership with community groups
• conduct workshops discussing topics such as quality of air in houses; effect of
heat and air quality on health; the effect of noise; and how to "live" in a lead
house
• since health education has been put into the curriculum of the City schools,
someone from that office should serve on the CAC (Connie Williams will
provide us with the contact person's name and phone number)
Overall, the report is stated to be comprehensive and in-depth.
In addition to comments on the Interim Report and health education, it was suggested
that "surprise" inspections of industrial facilities be made. This method would serve as a form
of quality control.
SCHEDULE NEXT MEETING
The next CAC meeting is scheduled for Wednesday, September 25, 1996, at St. James
Episcopal Church, 6800 Woodland Avenue (southeast corner of 68th Street).
m-20
-------
MINUTES
South and Southwest Philadelphia Environmental
Characterization Study
COMMUNITY ADVISORY COMMITTEE
Third District Police Station
llth and Wharton Streets
Philadelphia, PA
Wednesday, September 25, 1996
6:00 - 8:00 p.m.
Attendees: John Baker, Lois Banks, Yasin Bey, Harriet Brown, Reba Brown, Tom Burke,
Al Caporali, Myrtle Carter, Joanne Cavuto, Judy Cerrone, A. Charles
Chambers, Katie Cofey, Mary Fox, Dennis Glancey, Andrea Hall, Gloria
Inverse, Debbie Lee, Brigid Lowery, Virginia Moseley, Mary Orr, Shirley
Sellers, Nadia Shalauta, Bob Wingert
WELCOME AND INTRODUCTIONS
Those hi attendance introduced themselves and stated the organization/agency that they
represent.
COMMUNITY UPDATE
Lois Banks provided a brief overview of the activities since the June 26, 1996 meeting.
These activities included:
• The JHU project team received and compiled information sent to them from
members of the community.
• The JHU project team drafted and brought to this meeting (for distribution) the
one-page flyer that was requested by members of the CAC at our last meeting.
A copy of the flyer is enclosed.
• The CAC is commended for all of its hard work throughout this Study. Without
the CAC, this Study would not be.
Reminder: The purpose of this Study is to identify issues of concern; examine indicators
of community health; and provide a useful tool for the communities and
agencies involved, to collaborate your efforts to improve the environment
and health in South and Southwest Philadelphia.
m-2i
-------
The purpose of the CAC is to provide advice throughout the conduct of the
study, and to assist in identifying short term measures which can be
implemented to improve the quality of the environment in the study area.
The CAC also assists Johns Hopkins in identifying pollution sources and
environmental health concerns in the community.
THE STUDY UPDATE
Tom Burke and Nadia Shalauta presented a slide show outlining some of the findings
and details in the Interim Draft Report dated September 23, 1996. These reports were
distributed to CAC members by EPA. Each member is asked to review and provide comments
(if any) no later than November 1, 1996.
EPA UPDATE
Virginia Moseley provided CAC members with a brief overview of the EPA Open
House held on September 12, 1996. During the Open House, data from all the paniculate
samples ("valid" and "invalid") was requested. Gloria Inverse was promised that she would
receive the data during the week of October 1. CAC members in attendance at the Open
House stated that it was a very informative day.
Air data on metals for urban areas and eastern cities was requested by a member of the
CAC. The issues of traffic at stadiums, air quality, and noise pollution (from vehicles and the
Goodyear blimp) were raised.
Brigid Lowery was welcomed back to me Study by CAC members. Ms. Lowery asked
the CAC to mink about the future direction of the CAC once the Study is completed. She
asked members to provide her with their comments.
DISCUSSION
CAC members were asked to break out into 3 small groups. They were given the task
of developing a framework or strategic plan for the community after diis Study is completed.
After spending 15 minutes discussing this, the groups reconvened and provided a report to the
entire group. Reports are as follows:
Group A
• The CAC should remain together as a group, working together and making
decisions by consensus. The CAC has served as the vehicle for the sharing of
information between community groups
• Focus should be placed on politicians, zoning, and agencies
• The CAC should work widi all agencies especially PADEP and EPA
• Explore funding for independent technical advisor
m-22
-------
Grou B
Grou C
CAC should continue as a group after the Study is completed
Plan to work with agencies on enforcement and improvements to conditions with
the goal of having a moratorium on new toxic sites
The CAC needs to review the findings and support data from the Study
Study results should follow up with a priority list of health concerns to address,
and how best to begin an action plan
• The CAC should remain together
• There should be a community representative on the EIT and the Air Pollution
Control Board
• A moratorium is probably not practical
• An Emergency Response Plan MUST be implemented
• There should be a "mock" emergency procedures drill
• No permits should be issued unless the population density is considered by
PADEP
• Work to fill Air Pollution Control Board vacancies with good people
The groups were commended for then" action plans and encouraged to continue thinking
of steps that can be taken to maintain the CAC after this Study is completed.
SCHEDULE NEXT MEETING
The next CAC meeting will be held in early December. We will contact you as soon as
arrangements have been made.
m-23
-------
MINUTES
South and Southwest Philadelphia Environmental
Characterization Study
COMMUNITY ADVISORY COMMITTEE
Bartram Gardens
54th and Lindbergh Boulevard
Philadelphia, PA
Wednesday, December 4, 1996
6:00 - 8:00 p.m.
Attendees: Kelvin Anderson, Lois Banks, Reba Brown, Tom Burke, Al Caporali, Joanne
Cavuto, Katie Cofey, Marie Flake, Kenny Green, Andrea Hall, Gloria Inverse,
Venard Johnson, Debbie Lee, Brigid Lowery, Len Mangiaracina, Virginia
Moseley, Mary Orr, Carole Payne, Joanne Rossi, Marlene Santore, Shirley
Sellers, Nadia Shalauta, Connie Williams, Bob Wingert
WELCOME AND INTRODUCTIONS
Those in attendance introduced themselves and stated the organization/agency that they
represent.
COMMUNITY UPDATE
Lois Banks provided a brief overview of the activities since the September 25th
meeting. These activities included:
• The JHU project team received and compiled information sent to them from
members of the community.
• CAC members provided updates on how the information from this Study is
being disseminated in their community. Information is being shared at churches
and libraries, articles in community newspapers/newsletters, and at
neighborhood meetings.
• The CAC is commended for all of its hard work throughout this Study. Without
the CAC, this Study would not be.
Reminder: The purpose of this Study is to identify issues of concern; examine indicators
of community health; and provide a useful tool for the communities and
agencies involved, to collaborate your efforts to improve the environment
and health in South and Southwest Philadelphia.
m-24
-------
The purpose of the CAC is to provide advice throughout the conduct of the
study, and to assist in identifying short term measures which can be
implemented to improve the quality of the environment in the study area.
The CAC also assists Johns Hopkins in identifying pollution sources and
environmental health concerns in the community.
THE STUDY UPDATE
Tom Burke and Nadia Shalauta gave an update on the Study. In the month of
November, Brigid Lowery gave a presentation about this Study at the annual meeting of the
American Public Health Association (APHA) in New York City. In addition, Dr. Burke and
Ms. Shalauta exhibited during one of the poster sessions at the same meeting.
The current phase of the South and Southwest Philadelphia Environmental
Characterization Study is involved with analyzing health data. An example of the health data
that is being analyzed was handed out to those in attendance. Dr. Burke emphasized that it is
important that the health of the community becomes a part of the decision-making for the City
of Philadelphia.
EPA UPDATE
Virginia Moseley provided CAC members with a brief update of activities related to
this Study. The air monitoring at 61st Street is continuing. A sufficient number of samples
have been collected, and a second monitor has been placed in the area (further up 61st Street)
to test a theory about possible source(s) of emissions. By the end of the current week, 8
samples will be collected from the 10th and Reed location, and the monitor will be moved to
the stadium area for background samples. The filters will be sent to be analyzed when
sampling is concluded. The results will be shared with the community.
The new "state of the art" equipment (3 monitors) just arrived for the carbon monoxide
sampling at the Sports Complex. November through February is when carbon monoxide levels
are highest. Schedules for upcoming sporting events will be used to schedule the monitoring to
monitor maximum levels. Monitoring will be scheduled when there is the largest anticipated
attendance.
The contact person at the Pennsylvania Department of Environmental Protection
(PADEP) for solid waste permits is Tina Suarez-Murias (610) 832-6011. Ms. Suarez-Murias
stated that the Soil Remediation of Philadelphia (SRP) application was "accepted as
administratively complete" on November 19, 1996. Technical review has begun. A copy was
sent to the City (Rich Zipin), and a copy is being placed in the Eastwick Library on Island
Avenue. It should arrive late next week.
The permit application submitted for the old ORFA site will not be acted upon since
IH-25
-------
they did not supply PADEP with certification of publishing a public notice.
Ms. Moseley informed the CAC that Ms. Suarez-Murias has offered to set up a list of
"happenings" in the Study area on a regular basis. She also encourages calls from the
community and promises timely responses.
An Indoor Air Workshop will be presented by EPA Indoor Ah- expert, Francis
Dougherty, at Southwest Enrichment Center. Myrtle Carter (CAC member) has also requested
the workshop at Passyunk Homes. Ms. Moseley is facilitating bringing environmental
workshops on topics of concern to community groups throughout the Study area. Indoor air
sampling will also be done by Mr. Dougherty in the homes of residents who request it.
Len Mangiaracina reported that separate meetings were held at EPA with EIT members
and businesses named in the Study. The objective of this meeting was to foster a spirit of
cooperation with industry, and to obtain commitment hi addressing recommendations from
this Study.
Copies of Title VI were distributed with a cover letter from Ms. Moseley giving
sources for information at the U.S. Attorney's Office and the Department of Justice. In
addition, copies of an article that appeared in The Philadelphia Daily News on December 2,
1996, on Short Dumping in Southwest Philadelphia were distributed. The article contained
telephone numbers to report dumpers, to join a town watch, to ask for a clean-up, and to
dispose of items legally.
DISCUSSION
CAC members were given a list of facilities/environmental issues and concerns. Each
member was asked to rank theses issues and concerns in order of health concern. The rankings
will be tallied and will appear in the final report of this Study.
After completing the above task, CAC members were asked to break out into 3 small
groups. Each member was provided with a list of recommendations that were developed
throughout the Study (handout enclosed). Each group was given 23 minutes to discuss the list
of recommendations, rank, edit, and/or add to the existing list. Groups reported as follows:
Group 1
• All recommendations are viewed as good recommendations. Ordering should be
so that the following 2 recommendations are first:
• Develop a citizens guide to environmental health and protection in
Philadelphia. The purpose of the guide should be to de-mystify the
environmental decision-making process and provide the answers for the
question "who's in charge?" and accountability of the officials of the
regulatory agencies.
• Clearly define the roles of each level of government and agency in
licensing, permitting, and environmental enforcement. Explain the
m-26
-------
jurisdiction of each agency.
• Develop a plan as to how to implement recommendations, and develop
committees that work on specific issues.
• Determine a meeting schedule with BIT and all other Study players.
• Explore funding for a newsletter to alert community of what is going on.
Group B
• Although all of the recommendations are good ones, they should be ordered as
follows:
• Develop a concrete plan for continuing and strengthening the
communication links between the agencies, community members,
industry, and the academic community which have been developed
through the study. This should include specific plans and support for the
continuation of the BIT inter-agency group and the CAC community
advisors.
• Establish a method for the consideration of the cumulative impacts of
facilities when licensing, permitting, and citing new facilities.
• To evaluate the impact of the Study, and the BIT, develop and
"environmental report card" which tracks trends and uses the Study
results as a baseline to measure environmental progress.
• Provide the community with a clear explanation of zoning in the City of
Philadelphia, and examine the impact of historical zoning practices on
the environmental quality hi the communities of South and Southwest
Philadelphia. Examine opportunities for rezoning to improve
environmental quality.
• Establish a moratorium on citing of industrial facilities in areas already severely
impacted with industry.
Group C
This group also feels that the drafted recommendations are good ones.
However, rezoning should improve environmental quality and equity.
Therefore, the original recommendation should be revised to read:
• Provide the community with a clear explanation of zoning hi the City of
Philadelphia, and examine the impact of historical zoning practices on
the environmental quality hi the communities of South and Southwest
Philadelphia. Examine opportunities for rezoning to improve
environmental quality and equity.
Perform a study on the "living" vs. the dead. Report various respiratory
ailments, including asthma..
Grassroots people should be able to become members of various "Boards of
Action."
Put an end to Environmental Injustice.
The community should be involved with zoning and planning.
The community should be empowered to call for enforcement.
IH-27
-------
• EPA should continue their personal involvement in the Study area.
The groups were commended for their edits of the DRAFT Recommendations, and',
were asked to provide in writing to the JHU project team, any additional edits or additions NO
LATER THAN JANUARY 4. 1997.
CAC members were informed that even though this meeting is the last of the meetings
scheduled for the Study, the JHU project team will be holding one additional meeting at which
time each CAC member will be given a copy of the final report for this Study. We will
inform you of the date, time, and place of this upcoming meeting.
m-28
-------
Recommendations
In addition to the recommendations listed in the body of this Report, CAC members drafted
additional recommendations regarding this Study at their last meeting on December 4, 1996.
These recommendations are listed below.
• Develop a plan as to how to implement recommendations, and develop
committees that work on specific issues.
• Determine a meeting schedule with BIT and all other Study players.
• Explore funding for a newsletter to alert communities of what is going on.
• Establish a moratorium on citing of industrial facilities in areas already severely
impacted with industry.
• Provide the community with a clear explanation of zoning in the City of
Philadelphia, and examine the impact of historical zoning practices on the
environmental quality hi the communities of South and Southwest Philadelphia.
Examine opportunities for rezoning to improve environmental quality and
equity.
• Perform a study on the "living" vs. the dead. Report various respiratory
ailments, including asthma.
• Grassroots people should be able to become members of various "Boards of
Action."
• Put an end to Environmental Injustice.
• The community should be involved with zoning and planning.
• The community should be empowered to call for enforcement.
• EPA should continue their personal involvement in the Study area.
In addition to those recommendations drafted at the last CAC meeting, several CAC
members provided their individual recommendations. These recommendations are as follows:
• Current health problems amongst those living in the areas covered by the Study
should be addressed.
• All neighborhood polluting industries should be required to have fence-line
sensory monitoring systems along with warning systems, such as a siren to let
the surrounding residents know when an accident has occurred.
• Pennsylvania Department of Environmental Protection and the City's Air
Management Agency should not only conduct air monitoring hi our
neighborhoods, but also hi East Falls.
• The Asthma Task Force should address one of the main concerns of the CAC
Board and the community, to listen to the increased concerns surrounding the
increase in asthma both in juveniles and adults.
• There is a plume of petroleum products that has migrated underneath parts of
South Philadelphia, especially hi the Passyunk Homes Public Housing
Development, and those residents would appreciate a visit from the
Commissioner.
• Smaller sources such as small chemical companies that give off less than two
tons should be regulated.
m-29
-------
Considering the diversity, and self-interest of the various groups, consensus
building will be a necessary component in the months ahead.
Permit notification should be placed in local newspapers such as Southwest
Globe Times or South Philadelphia Review in addition to the Philadelphia
Enquirer and the Philadelphia Daily News.
There should be the correct number, type, and placement of air monitoring
stations to sufficiently protect residents.
Truck traffic must meet federal standard for noise, diesel exhaust, and soot, and
be routed away from residential areas.
Existing companies must be brought into compliance.
DEP should conduct more frequent unannounced inspections.
The Philadelphia Air Pollution Control Board (APCB) should live up to its
promise to address environmental justice issues in Philadelphia.
Existing vacancies on the APCB should be filled with environmentally
progressive individuals who are active hi community affairs, and if necessary,
to remove board members who are inactive or out of touch, in order to make
room for new members.
The Philadelphia Health Department should adhere to its duties outlined in the
Air Management Code that require it to make recommendations on zoning
permit applications involving air pollution sources as well as addressing the
location and concentration of pollution sources.
The Philadelphia Planning Commission should reform its Environmental
Planning Division to adopt a policy with an attitude to equitably protect the
environment, public health, and safety rather than simply trying to avoid
breaking environmental laws.
Health symptoms should be documented as part of Air Management Service's
response to environmental complaints.
Philadelphia City Council should respond to and heed requests for a public
hearing to allow Johns Hopkins University and others to review the findings and
recommendations of this Study with the City's policy makers.
Given that many of the recommendations contained here and elsewhere hi this
report are reiterations of concerns that have long been obfuscated and
stonewalled by the administrators and lawmakers of this City, I recommend that
this report be made as accessible as possible (via the Libertynet and other
information providers) and that it serve as a present day reference point by
which we can judge progressive or digressive movement on these
recommendations.
ffl-30
-------
U)
c
CD
U
O
o
o
o
O)
c
12
c
to
O
0
{Ranking of Community Concerns (N=17)
CM
in
1
JO
Q
1
in
.2
2
§
c
1
in
.2
«
o>
O
c
w
[Cumulative effects of pollutants from a variety of sources
(N
I Lax zoning regulations
in
T3
ra
p
b
'ra
ra
>,
I Emissions from traffic associated with stadiums, airports, expresswa
(N
K!
| Lack of information when spills/fires/other incidents occur at industri
o
[Soil Remediation of Philadelphia, particulate emissions
TT
[Auto Body and Repair Shops, emissions from industrial operations
-
t—
(Philadelphia Recycling and Transfer Station
m
|Dupont Marshall Labs, emissions from industrial operations
*-
ro
(Delaware Valley Recycling, particulate emissions
ro
| Noise from traffic and industrial operations
(Defense Personnel Supply Center, including underground oil plume
(N
I Evacuation plan for the City of Philadelphia
-
|C.R. Warner, proposed facility
CO
(SEPTA Building, asbestos
(inolex Chemical, emissions from industrial operations
[Ashland Chemical, emissions from industrial operations
s
W
rtj
•te
iFormer factory at 70th and Kingessing, short dumping and illegal tra
t_
[Woodland Oxygen Company, short dumping and illegal trash transfe
*-
CM
[Defense Personnel and Supply Center, re-use plans
in
c
ra
a.
1
o
"ra
n
•z.
IM.A. Bruder and Son, emissions from industrial operations
(N
|Bil Dry Corporation, emissions from industrial operations
-
o
<
a.
or
0
CN
I
or
O
01
c
o
1
-
10
(New stadiums
-
n
IUSN Philadelphia Naval Shipyard, re-use plans
I National Heat and Power
(Publicker Superfund Site
-
oo
in
J
Q.
0)
Is
'a
(N
in
o
|GE Skeats High Power Laboratory, emissions from industrial opeteti
CN
fM
I Former box assembly plant on Gray's Avenue
-
ID
CM
[Southwest Water Pollution Control Plant, odors and air emissions
-
(Southeast Water Pollution Control Plant, odors and air emissions
-
[Girard Point Transfer Station
fNI
[Atlantic Coast Demolition and Recycling
IBiosolids Recycling Center, odors and air emissions
8
o"
or
t-
[Old Barrett Building
[Dilworth Recycling and Transfer Station
fc
O
m
0)
•o
c
£
"o
to
8.
-------
-------
APPENDIX IV
TOXICS RELEASE INVENTORY
-------
-------
•o
c
I
0)
\
o
o
0
in
•^r
o
o
o
o
^r
o
o
o
m
CO
o
o
o
o
CO
i
0
o
o
in
CM
1
o
o
CN
I
0
o
0
m
i
o
0
o
o
1
o
o
o
m
1
o
spunod
-------
o
CO
•o
c
re
E ?
o T
«fc ^
oo
(A 0)
0) T-
tf)
(U
€
O
D.
O
o:
o
spunod
-------
i
C
(0
o
CO
2
o>
•o i
C 00
(D 0>
O W
*j 0)
0
o
m
»w
o
Q.
V
o:
spunod
-------
I
*J
o
CO
(0
o
CO
00
O)
o
tn ~
o -^
W m
CO W
o
Q.
s.
E
5
o
1
o
o
o
o
to
1
o
o
o
0
in
i
o
8
o
^r
i
o
o
0
o
CO
1
o
0
o
o
CM
1
o
o
o
0
1
o
spunod
-------
spunod
-------
I
4-1
o
CO
•O
c
OS
o
CO
c ^t
= o>
p o>
*- CO
£ 0>
in *™
0)
C
(0
0)
0> *0
5 LL
O
O
Q.
0
o:
(U
4-1
o
8
(D
spunod
-------
zinc
xylene (mixed
isomers)
toluene
phosphoric acid
molybdenum
trioxide
methyl ethyl ketone
diethanolamine
copper
aluminum oxide
acetone
Q.
O
L 000008
600000 4
400000 4
200000 4
000000 4
800000 4
600000 4
400000 4
200000 4
i
0
spunod
-------
S1
CO
a
o
o
15
o
(0
•o
€
O
a.
(D
en
CD
LU
X
X
X
X
X
X
X
X
spunoj
-------
0000000)0)0)0)0)
O)O)O)O)O)O5O)O)
o>
O)
00
o>
>*-
ro
a
O
O
O
E
a>
O
T3
C
o
c
(0
CO
£
O
•o
o
a
0)
CD
T3
C
CO
o
"ro
o
(0
^
"S
_E
">,
.C
"aJ
E
(O
in
to
o
o
_>,
O)
0)
C
Jl)
>,
0)
o
in
CM
O
O
O
o
o
o
o
o
o
o
m
oo
o
o
o
o
ro
o
o
o
m
CN
o
o
o
o
CM
o
o
o
o
o
o
o
o
o
o
m
spunod
-------
CM
spunod
-------
o
Q.
3
O
E
0
4-1
I
O
CO
.fc *!:
< o
(0 00
c o>
T-
s f
CO
_0>
0)
o:
o
Q.
i
o
o
o
I
o
o
o
CD
i
o
o
o
o
o
m
o
o
o
o
o
o
o
o
CO
8
o
o
o
o
spunod
-------
oo o> o T- CN co ^r
oo oo 05 en o CD en
ci en o o) o~) o~) o~>
Xylene (mixed
isomers)
Toluene
Styrene
Methyl Methacrylate
Methyl Ethyl Ketone
Methanol
Glycol Ethers
Butyl Acrylate
Acetone
-------
COCOCOO)CT)O)CT>O5
n n H
O>
O)
00
o>
.0
03
15
(0
O
Q.
3
Q
O
(0
c
2
O
•o
-------
.£ TJ fe C/3
i- ro C O !t
< ^ Jj 2 O
&
I
•u
1
o
o
o
o
CM
I
o
o
o
o
o
1
o
o
o
0
00
1
o
o
o
o
CO
I
o
0
o
o
T
!
o
o
8
CM
r
o
spunod
-------
o
N- oo en o T-
oo oo oo en en
en en CD en en
m
D m
1
o
o
o
o
ro
i
o
o
o
in
CM
i
o
0
o
o
CM
1
O
8
in
T—
1
O
o
o
o
T—
1
o
o
o
IT)
c
spunod
-------
GOGOCOO)O)G)O)O
0
.*
CO
2
DQ
(Q
Q.
E
o
o
o
fe
O o>
o c
«£ js
W Q-
o
tf)
(0
£
&
•a
*
o
Q.
0
spunod
-------
CO
O)
O>
00
O)
c
JS
Q.
L.
0)
^^
Cu
m
uj
O
E
V)
C
2
0)
*•»
1
O
•D
a>
r
O
a.
O
O
O
O
CM
O
O
0
O
O
O
O
O
0
00
O
O
O
O
CD
O
O
O
O
"3-
0
O
O
O
04
O
spunod
-------
O)
o>
N.
00
0)
T-
o
O
c
CO
O
O
c
.2
O
o>
(A
CG
oo
O)
C31
CN
en
CT)
O)
O
O)
or
O)
00
O5
<
•o
o
Q.
oo
00
O)
h-
00
CD
O
m
CM
o
o
CM
o
in
o
o
o
in
spunod
-------
05
o
u
c
^
o
c
(0
<+-!
0)
s
O 01
£ O>
o o
TO
st
o
T3
0)
r
o
Q.
o
00
CM
05
o
o
CO
o
10
CM
o
o
CN
o
in
o
o
o
IT)
o
o
o
o
o
in
O)
spunod
-------
o
3
I
Q.
TJ
O
O
u_
0
I
>» "aT
X n
II
(ft O
0) -
*
o
0
a:
o
Q.
Q)
a:
00 O>
00 00 CO
050)01
spunod
-------
X
0>
o
£
0
spunod
-------
00 CO CO G) O) O) O)
spunod
-------
O)
O
O
(Q
O
O
X
O
I
.5
'E
o
E
E
to
c
2
o
Q.
O
Of
E
O)
O3
co
o>
o>
en
(35
O
o
o
o
CO
o
o
o
o
o
o
o
o
co
o
o
o
o
10
o
o
o
o
o
o
o
o
CO
o
8
o
CM
O
O
O
O
spunod
-------
I
3
£
o
Q)
R
I
450000-1
400000-
350000 4
300000-
250000 4
200000 4
1 50000 4
1 00000 4
I
o
o
o
o
10
T
o
spunod
-------
o>
N.
CO
O)
c
JO
I
o
Q.
O
O
0)
o
c
2
u_
(Q
_J
O
(0
0)
en
cu
_0
0)
a:
0
t:
O
a.
Zinc Fume or Dust
Toluene
Sulfuric Acid
Styrene
Sodium Hydroxide
Nitric Acid
Nickel
Hydrochloric Acid
Cyanide Compounds
Copper Compounds
I Chromium Compounds
spunod
-------
COCOOOO)OG)G)O>
O)O>O>G)O)O)O)O)
T—T-T-T-T— T— T— T—
mmnmmmmm
zinc compounds
sulfuric acid
sodium hydroxide
nickel
cyanide cpds.
copper
chromium cpds.
o
o
o
o
o
o
o
o
o
o
o
o
o
m
co
o
o
o
o
o
co
o
o
o
o
ir>
CNJ
o
o
o
o
o
CM
o
o
o
o
in
o
o
o
o
o
o
o
o
o
m
spunod
-------
spunod
-------
D II
D;
spunod
-------
OOOOOOO)OC7)O)O)
o>
0>
00
o>
o
3
•o
2
Q_
2
O
0
(0
CO
_fl)
0
or
t:
o
Q.
0)
o:
E
o o o o o
o in o m o
in -sj- -sf co co
CM
o
o
CM
o
m
o
o
o
in
spunod
-------
D H
S
o>
00
O)
o
3
•o
2
a.
2
o>
o
(0
(0
0)
(0
(0
.22
o>
O
a
0)
o:
spunod
-------
o
o
o
o
o
o
o
o
O
o
o
o
o
o
o
o
o
CO
o
o
o
o
CD
o
o
o
o
o
o
o
o
CM
spunod
-------
Ea BI n PI n
ea B LJ t£j H
Zinc Compounds
Xylene (mixed isomers)
Toluene
Phthalic Anhydride
N-Butyl Alcohol
Methyl Isobutyl Ketone
Methyl Ethyl Ketone
Lead Compounds
Ethylene Glycol
Chromium Compounds
Barium Compounds
spunod
-------
B D
E
O
Q.
i_
O
o
V)
O
-------
•o
o
o
03
O
Ss
E?
u. c
•- oo
o o>
II
•55
I*
(0 ^
"0
o:
•o
^
o
Q.
0
(0
'E
o
I
1
o
o
o
CM
1
O
o
8
1
o
o
o
00
1
o
o
o
CD
1
o
o
o
^r
1
o
o
o
CM
1
c
spunod
-------
spunod
-------
COOOOOO>O)O)G)(7>
• •DHIffllS
it
0>
O)
00
o>
O
c
3
CO
I
(ft
Q)
(0
"3
O
Q.
o:
nickel
naphthalene
ethylene glycol
diethanolamine
Q)
O
-2
O
O
ir
c
TO
C
O
0)
^
O
fc_
0)
£
T3
"o
biphenyl
1,3-butadiene
1 I
D O
3 O
D O
J> CO
O
O
O
r-
o
o
o
CO
o
o
o
If)
o
o
o
^r
o
0
0
eo
o
o
o
CM
o
o
o
T—
o
spunod
-------
0>
O)
00
0>
C
CO
V)
Q)
(A
(0
•o
€
O
Q.
methyl tert butyl
ether
hydrogen fluoride
ethylene
ethyl benzene
CO
0)
O
45
O
O
or
CD
|
0)
x:
O
CD
L_
£
in
T3
15
cyclohexane
chromrum cpds.
O
0
o
o
00
1
o
o
o
o
r^
o
o
0
0
CD
o
o
o
0
in
o
o
0
o
•
-------
N-COOOT-CMOOM-
COCOOOO)O)O)O)O>
O)O>O)O)O)O)O)O>
o>
0>
CO
o>
CO
2
M-
(/}
(/>
(0
"3
£
•o
o:
EE
xylene (mixed
isomers)
toluene
propylehe
dichlorodifluoromet
hane
cumene
benzene
aluminum oxide
1,2,4
trimethylbenzene
o
£
O
O
OL
ro
cu
6
0)
0)
spunod
-------
OOOOGOO)O>G)G)O>
zinc compounds
o>
o>
sodium hydroxide
oo
o>
phenol
3
(0
o
lead
o
•Si
O
O
T>
t=
CO
0
carbon
tetrachloride
•o
o
t:
o
Q.
O
o:
E
0)
.c
O
QJ
(O
o>
Tl
T5
c:
1,2-dichloroethane
1,1,1-
trichloroethane
o
o
o
CO
o
o
o
o
o
o
o
o
o
CO
o
o
o
CM
o
o
o
spunod
-------
OOCOCOO)O)O)O5Ob
• •nSiiiii
0>
O)
00
o>
0
c
M=
0)
a:
(0
E
0
(Q
_0)
O
o
Q.
0)
o
o
CO
o
o
o
o
CM
o
o
o
o
o
CO
o
o
CD
o
o
I
o
o
CN
spunod
-------
0)
a:
6
c
3
CO
E
0
+*
i
CO °>
E
E
a:
•o
-------
OOOOOOO)O)O)G)<7>
0>
o>
00
o>
0
8.
3
CO
o
«t-
73
C
(U
(A
0
(0
(0
o
Q.
nickel
lead
ethylbenzene
cumene
benzene
1,2,4-trimethylbenzene
1,1,1-trichloroethane
8 8
CD
O
O
CO
\
O
o
o o o
o o o
co 10 <^-
i
o
o
CO
o
o
CM
I
o
o
spunod
-------
cococoa>0>a>a)cn
m n n
o>
O)
CO
o>
cr:
E
O
O
O
o
CO
I
o
o
o
o
o
o
o
o
o
CO
o
o
o
CM
o
o
o
spunod
-------
0>
.£ I
o
eg
0
CO
E
•o
C'
01
.
Eh-
^ °o
o o>
O
«*-
o
0
{/)
(0
o
Q.
&
spunod
-------
o
ro
c
3
CO
I
.2
Q) O>
i
o co
(u o>
LU T-
o
4-1
tf)
CO
^0)
0
a:
o
D.
&
E
o
o
o
o
o
o
O
O
O
O
o
m
CO
o
o
o
o
o
o
CO
o
o
o
o
o
If)
CM
o
o
o
o
o
o
CM
o
o
o
o
o
in
o
o
o
o
o
o
o
o
o
o
o
10
spunod
-------
COCOCOO)O)CT)O)O)
spunod
-------
cocooocr>cr>cr>
oooooooo
cccccccc
DDDDDDDZJ
COCOC/3COWC/3O3C/5
xylene (mixed
isomers)
toluene
sodium hydroxide
lead
ethyl benzene
cyclohexane
cumene
chlorine
benzene
ammonia
1,2,4
trimethylbenzene
CD
O
CO
O
O
•a
c
03
CD
.C
O
i_
CD
CD
TJ
"o
c
*
spunod
-------
n
O)
o>
00
0>
3
CO
O
c
(0
o
•o
0
r
o
a.
o
a:
zinc compounds
su If uric acid
phosphoric acid
phenol
nickel
naphthalene
molybdenum
trioxide
manganese
diethanolamine
chromium cpds.
aluminum oxide
V)
0)
o
£
O
O
CL
•o
ro
.
O
L_
0)
(A
0)
TD
T5
spunod
-------
o>
0>
00
O)
O
c
3
CO
E
D
spunod
-------
-------
APPENDIX V
AIR POLLUTION AND HEALTH
Over the last several decades, the ambient concentrations of all criteria pollutants
except nitrogen dioxide (NO2) have declined substantially in the United States. Between 1970
and 1994, VOCs (which are largely responsible for ozone formation) decreased by 24 percent,
paniculate matter (PM10) decreased by 78 percent, carbon monoxide (CO) decreased by 23
percent, sulfur oxides (SOX) decreased by 32 percent, lead (Pb) decreased by 98 percent, and
NO2 increased by 14 percent.1'2 Despite these improvements, there is evidence that current
levels of air pollution, e.g., ozone and particle pollution, contribute to adverse health effects.
It has been suggested that fine and ultrafine particles are the subtractions of the paniculate
matter component of air pollution that has a significant role in this association.
While pollutants such as NO2, ozone, PM10, CO, and SO2 are regulated under the
CAA, a standard for fine and ultrafine particles (PM2 5), including acid aerosols, has only
recently been considered by the EPA. This is due, in part, to new epidemiologic information
suggesting that adverse health outcomes such as premature mortality, aggravation of
respiratory and cardiovascular illness in children and other sensitive populations, reduced lung
function, and changes to lung structure and defense mechanisms attributed to PM10 could be
equally attributed to fine particles. These effects are evidenced by increased hospitalization
rates, physician and emergency room visits, school absences, restricted activity and work loss
days.3
A separate standard for PM25 would entail a shift in air pollution control measures to
target combustion sources such as chemical processes and motor vehicles hi addition to coarse
particle sources such as construction and demolition-related activities and wood burning stoves.
Particulate Matter
Paniculate air pollution refers to solid and liquid particles suspended in the air, which
vary in size (ranging from .005 to 500 microns (10*) in aerodynamic diameter), geometry,
chemical composition and other physical properties (e.g., density). These particles are
pervasive throughout our environment in various forms such as dusts, fog, fumes, mists,
'U.S. EPA, Notional Air Quality Emissions Trends Report, 1994.
2The increase in NO2 is attributed to increased production and processing by industry and greater fuel
combustion by electric utilities (EPA, 1994, pp. 1-3).
3Committee of the Environment and Occupational Health Assembly of the American Thoracic Society,
"State of the Art: Health Effects of Outdoor Air Pollution," American Journal Respiratory and Critical Care
Medicine (AJRCCM), vol. 153, 1996, pp. 29-31.
V-l
-------
smog, and smoke (see Box I).4
Paniculate matter is generated
from fuel combustion sources such as
motor vehicles, power generation,
industrial plants, solid waste
incineration, and residential fireplaces.
Additionally, particulates can be formed
in the atmosphere from gaseous
precursors produced from fuel
combustion, construction and
demolition activities, wind blown dust,
and road dust.
Based on particle size and
method of formation, particles are
classified as 'coarse' and 'fine'
particles.
Coarse Particles
Coarse particles (greater than 3
microns in diameter) are emitted
directly into the atmosphere and are
generated from mechanical processes
through crushing, grinding,
construction and agricultural operations.
Coarse particles represent a mixture of
various sizes and chemical
compositions, depending on location
and season.5'6 They are composed of
soil particles, fly ash, road and
construction dust, wood ashes, soot,
and pollen.
Box 1: Characterization of Particulate Matter
Fumes consist of tiny particles, less than one .micron
in diameter. They are formed when material from a
volatilized solid condenses in cool air. Fumes are a
byproduct of welding, metalizing, and other
operations that involve molten metals.
Smoke particles refer to fine particles less than one-
tenth of a micron. They are the by-product of
incomplete combustion of carbonaceous materials
such as coal or oil.
Aerosols are liquid droplets or small particles that
remain suspended in the air for extended periods of
time.
Dusts are solid particles generated by mechanical
processes such as handling, crushing, and grinding
of materials (rock, coal, wood, grain, and metal).
Mists are finely divided liquid droplets suspended in
the atmosphere. Examples include oil mist
generated during cutting and grinding operations,
acid mists from electroplating, paint spray mist from
painting operations, and the condensation of water
vapor to form a fog or rain.
Gases are formless fluids that expand to occupy the
space or enclosure in which they are confined.
Vapors are defined as the volatile form of
substances normally in the solid or liquid state at
room temperature and pressure. Evaporation is the
process by which a liquid is changed into the vapor
state and mixed with the surrounding atmosphere.
4Definitions were adapted from: Plog, B., ed, Fundamentals of Industrial Hygiene, 4th Ed., 1996,
Chapter 1.
5Moolgavkar, S.H., Luebeck, E.G., "Particulate Air Pollution and Mortality: A Critical Review of the
Evidence." Epidemiology (In Press). Draft Copy: February 2, 1996.
Measurements of course particles include PM(10.2 5), PM(15.2 5)) and TSP-PM10.
V-2
-------
In Philadelphia, it was demonstrated that sources of coarse particles were dependent
upon local conditions. The concentration of these particles was highest during the week,
largely due to the high volume of commuter traffic.7
Fine Particles
Fine particles are defined as particles 2.5 microns in diameter and smaller.8 They are
formed from gases through chemical reactions, nucleation (formation of new particles),
condensation of gases onto existing particles, and coagulation of smaller particles. Particles
that form secondarily as a result of atmospheric chemical reactions, e.g., sulfur dioxide
converted to particulate sulfate, dominate the fine fraction of particulate matter.
Fine particles contain high concentrations of sulfate, ammonium nitrate, nitric acids,
elemental carbon, and condensed organic compounds. On the east coast, sulfate constitutes 40
to 50 percent of the composition of fine particles.
Sources of fine particles include combustion of coal, oil, gasoline, diesel, and wood;
atmospheric chemical reactions involving gaseous precursors such as nitrogen oxides and
sulfur dioxide; and smelters and steel mills.
A study by Burton, et al. recently completed in Philadelphia found that local factors
(e.g., day of the week, population density, and location) did not affect fine particle
concentrations and that local sources of pollution did not contribute significantly to the ambient
concentrations of fine particles.9 Rather, sources of fine particles tended to be regional in
nature and located to the west and south of the city (e.g., the Ohio River Valley). The study
also found that the levels of fine particles were uniform throughout the Philadelphia
Metropolitan area.10
Particulate Air Pollution and Health Outcomes
Several epidemiological studies have evaluated the association between particulate
matter and adverse health outcomes, such as acute morbidity and mortality, hospital admissions
7Burton, Robert, Helen Suh, and Peter Koutrakis, "Spatial Variation in Particulate Concentrations within
Metropolitan Philadelphia," Environmental Science and Technology, in press.
8This is an approximation for fine particles. The cutpoint between fine and coarse particles is typically
•given in a range of Ijrni to 3 /mi (U.S. EPA, 1996, p. IV-3).
9Burton, Robert, Helen Suh, and Peter Koutrakis, "Spatial Variation in Particulate Concentrations within
Metropolitan Philadelphia," Environmental Science and Technology, in press.
"Ibid.
V-3
-------
and emergency room visits, respiratory symptoms (reduced lung function), and chronic disease
conditions (asthma, COPD, and reduced pulmonary function).11'12 A brief review of these
findings is discussed below.
Risk Factors
Exposure to particulate matter places certain subpopulations at greater risk for mortality
and excess morbidity. Children, elderly, those with COPD, asthma, and other respiratory
conditions, and those who have cardiovascular disease are at greatest risk.13
Children have been observed to experience morbidity including decreased lung function
and increased respiratory symptoms and infections. This is attributed, in part, to the fact that
most children spend more tune outdoors. Increased activity results in increased ventilation
rates thus allowing for increased particle deposition in the deeper recesses of the lung. Infants
also may be at risk. PM exposure may increase the incidence and severity of acute respiratory
infection among infants, including bronchitis and pneumonia.14
Elderly populations are more sensitive to respiratory insult from PM, which compounds
existing decrements hi pulmonary and respiratory function that are associated with increased
age. Also, cardiorespiratory disease and infection (pneumonia and influenza) are more
prevalent in the elderly and thus may predispose such individuals to the effects of PM
exposure.15
Asthmatics' heightened responsiveness of airways to pollutants may be exacerbated by
PM exposures. Finally, individuals with cardiovascular disease and respiratory symptoms and
infections are at increased risk.
Fine Particulate Matter and Health Outcomes
nU.S. Environmental Protection Agency, "Review of the National Ambient Air Quality Standards for
Particulate Matter: Policy Assessment of Scientific and Technical Information," Office of Air Quality Planning
and Standards (OAQPS) Staff Paper, July 19%, Section V.
12 Committee of the Environment and Occupational Health Assembly of the American Thoracic Society,
"State of the Art: Health Effects of Outdoor Air Pollution," American Journal Respiratory and Critical Care
Medicine (AJRCCM), vol. 153, 1996, pp. 3-50.
13U.S. Environmental Protection Agency, "Review of the National Ambient Air Quality Standards for
Particulate Matter: Policy Assessment of Scientific and Technical Information," Office of Air Quality Planning
and Standards (OAQPS) Staff Paper, July 1996, pp. V-31-35.
"ibid, p. V-35.
I5lbid, p. V-34.
V-4
-------
Environmental and health consequences associated with airborne particles are
dependent upon their size and composition, which influence the degree of particle penetration,
deposition, and clearance in the upper and lower airways of the respiratory system.
"Respirable" particles 2.5 microns or smaller are capable of penetrating and depositing
in the deeper recesses of the lung, specifically the alveoli (lung tissue) and thus present a
different set of health consequences. Clearance (removal) of fine particles hi the alveolar
region of the lung (lower respiratory tract) can take weeks to months and thus enable fine
particles to remain in contact with sensitive tissue for extended periods of tune, causing
irritation and inflammation of lung tissue. Continuous exposure compromises the elasticity of
the lung and gas exchange capabilities with the circulatory system (i.e., supply of oxygen to
the bloodstream and removal of carbon dioxide from the bloodstream). Furthermore, soluble
particles (e.g., lead and other metals such chromium and mercury) may be transported to other
parts of the body that may cause systemic, neurologic, immunologic, developmental,
reproductive, and carcinogenic effects.16
Health effects associated with short-term exposure to fine particles include acute
mortality, increased hospital admissions, increased respiratory symptoms, and decreased lung
function.17'18'19 For long-term exposures, studies have shown that adults exposed to fine
particles suffer from increased chronic mortality and exposed children suffer from increased
bronchitis. Also, decreased lung function has been observed among children.20
Acid Aerosols and Associated Health Effects
Over the last decade, air pollution research has focused on how the chemical
composition of particles plays a role hi adverse health outcomes. One subset of fine particles
that has received attention is acid aerosols.
16Agency for Toxic Substances and Disease Registry, Toxicological Profile for Lead, October, 1991,
Chapter Two.
17Schwartz, J., "Air Pollution and Hospital Admissions for Respiratory Disease," Epidemiology, vol 7,
1996, pp. 20-28.
I8U.S. Environmental Protection Agency, "Review of the National Ambient Air Quality Standards for
Particulate Matter: Policy Assessment of Scientific and Technical Information," Office of Air Quality Planning
and Standards (OAQPS) Staff Paper, July 1996, p. V-61.
19Neas, L.M., D.W. Dockery, P. Koutrakis, D.J. Tollerud, and F.E. Speizer, "The Association of .
Ambient Air Pollution with Twice Daily Peak Expiratory Flow Rate Measurements in Children," American
Journal of Epidemiology, vol. 141, 1995, pp. 111-122.
20Dockery, D.W., C.A. Pope, X. Xu, J.D. Spengler,-J.H. Ware, M.E. Fay, E.G. Ferris, and F.E.
Speizer, "An Association Between Air Pollution and Mortality in Six U.S. Cities," New England Journal of
Medicine, vol. 329, 1993, pp. 1753-1759.
V-5
-------
Acid aerosols are defined as acidic liquid droplets or small particles that remain
suspended in the air for extended periods of time. Acid aerosol formation depends on the
concentration and mix of pollutants as well as physical factors such as wind speed and
direction, sunlight intensity, temperature, and humidity (See Box 2).21
Acid aerosols (referred to as "secondary" pollutants) are responsible for most of the
smog, haze, eye irritation, and for plant and material damage attributed to ah" pollution. In
order to control secondary pollutants, efforts
must be directed at controlling emissions of
their precursors (referred to as "primary"
pollutants). These precursors include SO2,
NOX, CO, ammonia (NH3), hydrogen sulfide
(H2S), and hydrogen chloride (HC1).
Box 2: Factors which Influence Acid Aerosol
Formation
Acid Sulfates
Acidic sulfate, an example of an acid
aerosol, constitutes an important fraction of
the total mass of fine particles. It is formed
through the reaction of sulfur oxides,
generated by combustion of coal and high-
sulfur content oils and metallic ore smelting,
with atmospheric water vapor. Once
formed, acidic sulfates are transported by
prevailing winds and are brought to ground
level by atmospheric mixing processes.
Near the surface, acid sulfates may be
Winds
Winds affect the transport and dilution of
ah- pollutants so that a shift in wind
direction enables the dispersion of air
pollutants over a larger area and thus
reduces the concentration of ah" pollutants
hi a given exposed area.
Sunlight Intensity
Sunlight intensity influences the extent of
photochemical reactions that oxidize acid
precursors such as SO2 and nitric oxide
(NO) to form sulfates and NO2,
respectively.
Temperature
Temperature affects the mixing of
atmospheric pollutants by changing the
density of ah". Warm ah" (lower density)
near the earth's surface will rise while cool
ah" (high density) high hi the atmosphere
will suik.
Humidity
Increased humidity signifies increased
water hi the air that can lead to increased
acidic aerosol concentrations.
21Committee of the Environment and Occupational Health Assembly of the American Thoracic Society,
"State of the Art: Health Effects of Outdoor Air Pollution," American Journal Respiratory and Critical Care
Medicine (AJRCCM), vol. 153, 1996, pp. 27-37.
V-6
-------
neutralized by ambient ammonia.22
Ambient concentrations of acidic sulfates have been linked to adverse health outcomes.
Epidemiological data have shown an association between daily mortality and concentration of
acid aerosols (e.g., sulfate).23 Controlled human exposure studies have shown that asthmatic
subjects have greater sensitivity to the effects of acid sulfates on lung function. Also,
adolescent asthmatics may be more sensitive than adult asthmatics and may experience small
decrements in lung function at exposure levels less than 100 jiig/m3.24 Under experimental
conditions, acidic sulfate has been shown to cause bronchoconstriction.25 Other studies have
shown altered defense mechanisms in the upper airways, which may affect mucus clearance of
infectious and noninfectious particles.
Acid Rain
Another example of acidic aerosols is acid rain. In the northeastern region of the
United States, ambient sulfuric and nitric acids create acid aerosols and contribute to acid rain.
Acid rain causes acidification of lakes and streams and can damage trees, crops, as well as
building materials such as marble and mortar, metals, and fabrics. It is a complex and variable
mixture of water droplets and dissolved gaseous pollutants. The major sources of acid
precursors that contribute to the formation of acid rain include emissions from coal-fired power
plants, industrial boilers, metal smelters, and motor vehicles. Emission sources with tall
stacks (ranging from 200-400 feet) disperse emissions at higher altitudes and consequently
provide longer residence times during which acid precursors can form acidic aerosols.
Subsequently, these aerosols are removed from the atmosphere through dry (acidic gases) and
wet deposition (acidic rain).26
22Sources of ammonia include soil, animal wastes, automobiles, humans, and agricultural processes. The
largest non-agricultural sources of ammonia in the northeastern part of the United States include humans and
traffic (Suh et al, June 1995).
23U.S. Environmental Protection Agency, "Review of the National Ambient Ah" Quality Standards for
Paniculate Matter: Policy Assessment of Scientific and Technical Information," Office of Air Quality Planning
and Standards (OAQPS) Staff Paper, July 1996, pp. V-58-78.
24U.S. Environmental Protection Agency, Air Quality Criteria for Paniculate Matter; Research Triangle
Park, NC: National Center for Environmental Assessment, Office of Research and Development, Final Draft,
April 12, 1996, pp. 11-31.
25Committee of the Environment and Occupational Health Assembly of the American Thoracic Society,
"State of the Art: Health Effects of Outdoor Air Pollution," American Journal Respiratory and Critical Care
Medicine (AJRCCM), vol. 153, 1996, p. 33.
26Prior to the 1970 CAA, acid precursors such as SOX were released from smoke stacks at relatively low
heights. As a result, there precursors deposited on the ground, vegetation, and other surfaces. In response to
limits placed on emissions of SO2, tall stacks were installed to reduce the local ambient air concentrations of SO2
Thus; higher elevations, higher wind speed and greater air volume air pollutants are diluted by increasing
dispersion of particles over a wider area.
V-7
-------
Health Effects
Recent studies suggest that acid aerosols may decrease the ability of the upper and
lower respiratory tracts to remove harmful particles. Additional studies have shown that
increased incidence of chronic bronchitis is linked to ambient acidic concentrations, yet the
mechanisms responsible for this remains unclear.27 Though some epidemiological studies have
implicated acid aerosols as an important toxic component of PM10, other studies do not support
this hypothesis.
Animal toxicology studies have shown that exposure to acid aerosols reduces the ability
of the respiratory system to remove potentially harmful particles inhaled into the lungs. There
also is limited toxicological evidence suggesting that fine particles play a role in inflammatory
lung damage and other conditions that may increase the risk of hospitalization or death for
sensitive individuals, such as those with chronic lung disease.28
In addition, human exposure studies of the effects of acid aerosols have shown that
individuals with asthma may be more sensitive to the effects of acid aerosols on lung
function.29 Furthermore, adolescent asthmatics may experience increased sensitivity and
decrements in lung function when exposed to acidic aerosols.30'31 These findings are supported
by animal and clinical studies.
27Committee of the Environment and Occupational Health Assembly of the American Thoracic Society,
"State of the Art: Health Effects of Outdoor Air Pollution," American Journal Respiratory and Critical Care
Medicine (AJRCCM), vol. 153, 1996, pp. 30-31.
28Schwartz, Joel, Douglas Dockery, and Lucas Neas, "Is Daily Mortality Associated Specifically with
Fine Particles?," Journal of Air and Waste Management, in press.
29Sensitivity is an acquired reaction whereby an individual develops an immune response after initial
exposure to a substance. Subsequent exposures to this substance 'trigger' a physiological response (e.g.,
asthmatic attack).
30U.S. Environmental Protection Agency, "Review of the National Ambient Air Quality Standards for
Paniculate Matter: Policy Assessment of Scientific and Technical Information," Office of Air Quality Planning
and Standards (OAQPS) Staff Paper, July 1996, pp. V-25.
3'Committee of the Environment and Occupational Health Assembly of the American Thoracic Society,
"State of the Art: Health Effects of Outdoor Air Pollution," American Journal Respiratory and Critical Care
Medicine (AJRCCM), vol. 153, 1996, p. 6.
V-8
-------
o
U-*
CD
•*-•
CO
0)
c
c
o
0
CO
T3
CO
2
CD
13
O
CO
o
o
CD
0
0
CD
o
tr
CO
CL
o>
o>
co
o>
O5
CM
05
O5
05
05
O
O5
O5
(C
T3
C
CD
.^
CO
o
CD
O
OJ
o
o
o
00
o
CD
O
CM
o
<
O3
O)
O)
o
o
o>
O3
I
0)
O)
E
0)
ro
CM
O)
CO
0)
CD
£iu/6n
£
i s
c E
ro .9
03
^ to
£ 0)
0)
r w
TO T3
<2 C
£ JS
c J2
^ g
oj g
' c *;
0) ™
(0 C
2 QJ
0-5
S -2
3 -a
§
-------
.0
"•+-•
CO
•+-•
V)
D)
c
c
o
0
CO
•O
CD
E
00
O
CO
o
o
IO
0
•a
-
CO
0
C/)
T3
'x
g
b
CO
a>
oo
O3
O)
CM
O)
O)
O)
•o
•§
0)
2
Q.
O
O5
a>
O)
o
o
a>
03
I
0)
O)
03
a>
(D
CM
0)
(0
0)
_2
ro
E
3
'x
TO
o
a>
o
05
a>
(0
•o
*S
55
0)
2
Q) Q.
I I
C Q.
SP. E
a 8
II
10 w
0) -g
£ CD
*- TJ
C C
V CO
QJ W
Q. "CD
0 c
S: o
II
O 0}
w £
J= ai
CO CD
> Q.
-------
c
o
"CD
•+-•
co
-I—•
0
o>
0>
OJ
03
O
OJ
O)
CO
T3
C
CO
•#-»
CO
O)
.c
3
I
•4-*>
O
O>
I
O)
(D
CO
TJ
C
(C
0)
£
(O
2 a>
CD O)
> CD
I 5
| CD
I O
CD O
|i
§i
8 2
0) ^
£ oo
"D QJ
CO
o to
•*: T3
0) C
E JS
J^ OT
=
CD
_
CD
IT)
CO
O
CO
CM
o
CM
If)
-
*- CD
S 0)
Q) (D
t §
CD CO
.C 'C
O CD
•»- o
•- "
w o
d) H-
3 T3
lAIdd
5 O
H fe.
-------
.g
"-*-•
CO
O)
c
O
CD
C/)
(0
2
00
o
V)
o
o
CO
•o
§
(/>
CO
0)
-------
CO
•4-*
CO
*•*
0)
2
-»—•
CO
T3
O
O
E
LLJ
O
O
CO
CO
CO
CD
0)
_J
CD
c
O
N
O
O)
oo
o>
O5
(0
TJ
*s
55
co
c>
in
CN
CM
O
in
T—
C)
lAIdd
10
O
(C
g
'•«-'
03
C
0)
T3
0
0)
O
X
0
"55
3
TO
TO
C
ro
o
c
TO
_
E
o
o
o
0)
_Q
(U
D)
ro
o3
ro
.2
0}
TO
I co
E 03
•o ^
C (D
O 0)
o *—
0) £
!f! a)
O
0)
-------
CO
0)
c
o
^
'c
o
s
-*-^
0
55
2
CD
O
CO
O
O
O3
o
T—
O
co
O)
C35
00
o
CM
0>
05
O
CD
O)
O)
00
o
o
a>
o>
CO
T3
C
CO
•*-*
CO
CO
00
O
CO
o
-------
APPENDIX VI
WATER QUALITY
-------
E
.o
c
u.
«
-------
s
o»
fcj
.£ "3
E
.o
$-™ ^
S,gff y
•« "• —•
0)-T C
' 3 S
= ^§
P S
U in
^o
~° tt
S|
Sg
SOc
O —
2 la
0)
O
€ S3
"8
»w
I
III
5
I?
0)
Q
i. . ..1 .1 1 - - -I . -A
ill
3=13
-------
o>
o>
I
0>
00
o>
0
0)
05
^-i
0
E
o
£
o
.Q
o
u
a
*j
c
(0
X
(0
m
-------
o>
o>
I
0)
00
o>
V)
0
0
0>
c
re
*j
0)
E
o
u
o
E
o
.Q
O
•*->
J5
Q_
X
re
CD
IE 11/10/94
E i 8/4/94
j i 6/16/94
i \ 3/24/94
I i 2/3/94
12/15/93
g
w
u_
O
0)
+•>
re
Q
1/6n
-------
c
CO
S>
O
Is
o
H
^j
C
(U
Q.
LB
fl^
jj
X
CO
CD
11/10/94
8/4/94
6/16/94 c
CD
N
3/24/94 g
2/3/94 |
o
12/15/93 -Q
•a
c
10/20/93 B
oT
9/8/93 §
E
7/21/93 g
CD"
4/14/93 g
9/16/92 IT
3/25/92 5
•e
2/5/92 J
12/26/91 -|
0) X
11/13/91Q- x;
& TO
t t_
CO en
9/25/91 .
X
9/18/90 oj-
c
m
8/8/90 N
CD
6/19/90 f.
JC
5/2/90 »_
CD"
3/21/90 S
2/7/90 °
-------
1/6n
-------
O)
0>
I
o>
oo
o>
0)
0
E
£
O
J>
O
4-1
(0
c
O
E
0
CD
H/Bn
-------
O)
0>
I
O)
CO
o>
JW
$
(0
Q
CN
1/6n
-------
o>
0)
1
o>
00
O)
1
0)
E
£
o
E
o
m
c
(U
QL
*•»
O
__
m
4.
^
f
§
^^^^^^BSSS
^^^^^E^^^wZ
*SF=
A
V— ~^™
•
1
~4—
•
I =
=^
4"
-=*
*-=*
*— •==
4~^
»
«-^
*.
4c
•>•
»•==
i^VM^BB^^I^H^H
=^
4
^
4*=
4
4
WVHWHMK-^
=^=t
— >
^^
-^.^^
^
^^•B—^k.
^^^
'
4<
«^— •"•^"^^
r „.
* j
—
,
^J^
!!>>
t3^ E
4<
S
E2%^
•^^:
• —
•
: 12/15/94
! 9/15/94
; 7/7/94
; 4/14/94
; 2/24/94
i 1/6/94
11/10/93
9/29/93
D 1 A /AO
B/4/93
4/28/93
10/21/92
7/8/92
3/11/92
0)
1/16/92 a
11/97/Q1 .5
I I /^- / IS I (/)
10/18/91 °
8/21/91 g
3/19/91
1/13/91
10/21/90
8/22/90
7/1 5/90
6/4/90
4/11/90
2/21/90
1/10/90
11/29/89
10/11/89
8/30/89
•1 M/PQ
00
CD
CO
CNJ
n/6n
-------
0>
1
o>
00
0)
(A
03
D)
!_
O
Is
t5
^j
c
(0
Q.
^^
O
E
o>
CD
0
c
D h
3 C
0
3 C
D U
3 C
4
4
•> T
3 C
<
MMHHH^M
4
••^^•^•H
<
t C
3 C
— ^0^^
^^^^••B
•E=^^
•^^^^•^^^
^^^^^•^^M
— ^^^«B
0 C
3 C
••^W^I^^BB
^^^^^^^"^™
'ii.
^^••^^•^••^iH
M T
3 C
.......•.•.•.•
•^^••^••^•^
••••••••••••••«
•^^•^^••^M*
C
3
12/15/94
9/15/94
7/7/94
4/14/94
2/24/94
1/6/94
11/10/93
9/29/93
8/4/93
4/28/93
10/21/92
7/8/92 |
N
c:
3/11/92 ^
o
1/16/92 ® |
a £
11/27/91 | -g
w ro
10/18/91 *- g
° 0)
8/21/91 £ |
Q
3/19/91 g
£
1/13/91 t
Vt
10/21/90 S"
CO
CL
8/22/90 «-
"S3
7/15/90 E
w"
6/4/90 |
^/1 *i /on ^
*f/ i i /yu CD
=
2/21/90 >>
1/10/90 |
N
• 11/29/89 S
: 3^,
10/11/89 £
CD
i 8/30/89 « g
: (/) CO
F 1/4/89 ^ s
^ Ol **
o 1
__ CD
1/Bn
o a>
t- J3
-------
en
O)
i
o>
00
O)
0>
2
_o
O
4-1
JS
Q_
0)
c
(0
_l
c
0>
0)
3
O
i 10/18/91 w
re
6/13/91 °
1/6n
-------
o>
O)
00
o>
0
I
0
C
-------
O)
0>
I
o>
00
o>
0
0
0)
c
03
E
O
O
O
E
.O
Q
-------
*
s
1
O)
00
Or
^
0)
-J
E
2
m
0)
c
_l
0)
0
0
O_^_>^M.
'«— i
^
•
r I
i
4-
-------
Disposal facilities listed in the City's Municipal Waste Management Plan include the
following:
• Commonwealth Environmental
Landfill
• Conestoga Landfill
• Cumberland County Landfill
• Delaware County R.R. Facility
• Grand Central Landfill
• GROWS Landfill
• Harrisburg M.F.R. and R.F.
• Keystone Landfill
• Modern Landfill
• Montenay R.R. Facility
• Pine Grove Landfill
• Pioneer Crossing Landfill
• Pottstown Landfill
• R and A Bender Landfill
• Tullytown Landfill
• York Country R.R. Facility
• Wheelabrator Falls Twp.R.R.
The Streets Department's Sanitation Division also collects 40,000 to 50,000 tons of
source separated recyclables from residents each year including commingled glass beverage
containers, tin and bimetal cans, steel cans (including empty paint and aerosol cans), aluminum
cans, and newspapers tied separately. In addition, the curbside collection of mixed paper
began in November, 1996. The Sanitation Division also collects approximately 3,000 to 4,000
tons per year of leaf wastes for composting in addition to separate Christmas tree collections.
In June 1994, the City adopted commercial recycling regulations mandating that all
commercial establishments with private collections submit a recycling plan to the Streets
Department. Haulers are required to report recycling quantities once every six months. In the
fiscal year 1996, it was reported that commercial recycling produced 130,000 tons of
recyclables with over 9,000 businesses submitting recycling plans.
In June 1995, the City of Philadelphia Streets Department released its updated
Municipal Waste Management Plan. The report contained recommendations and plans for
reducing solid waste generation.2 Following are the plan recommendations and a summary of
the City's 10 year plan for solid waste disposal.
2Department of Streets, Sanitation Division. City of Philadelphia Municipal Waste Management Plan, Plan
Update. Vol. 1. June, 1995. Philadelphia, PA.
VII-2
-------
Plan recommendations:
Reduce waste by aggressively counteracting the expected increase in waste
regeneration (an increase of 7-8% per person is expected by the year 2000).
Increase recycling and composting by expanding current curbside programs, drop-
off sites, buy back, processing, composting and private sector collection.
Divert from disposal by promoting innovative and alternative technologies and
recovery of resources from waste.
Re-evaluate and amend plans when necessary.
Provide public education to reduce waste generation.
Emphasize environmental quality and flexibility hi tackling issues at hand.
City of Philadelphia 10-year plan for solid waste disposal3
[ Goals
Innovative technology4
Landfill
Resource recovery (waste to
energy)
Landfill and/or resource
recovery
Combined recycling,
composting, and reduction
Quantity of waste generated
Year 1991 to 2000
22%
(100,000 tons per year)
over 30%
over 30%
18%
increase from 15% to
56% of quantity
same, or reduced
Year 2001 to 2010
22%
(100,000 tons per year)
78%
increase from 15% to 56%
of quantity
same, or reduced
City agencies involved in solid waste management:
• Department of Streets Sanitation Division (Recycling Office if part of the Division)
• Department of Public Health
• Water Department
• Department of Licenses and Inspection
• Air Pollution Control Board
• Recycling Advisory Committee (RAC)
• Interagency Task Force on Recycling (LATF)
• City of Philadelphia SWAC
3Ibid.
4The city has not been successful in implementing an Innovative and Technology Project for 1991-2000.
VII-3
-------
Participants in the Municipal Waste Management Plan Project:
• City of Philadelphia SWAC
• Recycling Advisory Committee
• City of Philadelphia Streets Department
• Citizen organizations
• Industry
• Private solid waste industry
• City recycling coordinator (member of SWAC)
• Academia
• Labor
• Government
• Local public and private institutions.
Special wastes:
• Biosolids fWastewater Treatment Sludgel: 252,000 tons/yr (57,600 dry tons/yr) from
drinking water treatment plants (for 1.8 million people) and wastewater treatment
plants (for 2.3 million people). A large proportion is recycled into a compost
material and soil amendment.
• household hazardous waste (HH\\0: existing collection program established, > 2
collections/yr
• litter : street and parking lot sweepings
II. Illegal Waste Disposal5
There is an illegal waste disposal city crew and volunteer groups who regularly remove
trash dumped illegally hi the city streets.
•^
Magnitude of the problem
• 44,730 tons at 362 active sites hi 1994 (18,000 tons of trash litter the city at any
given time).
• Crew spends 90% of the tune removing illegally dumped material. The Streets
Department has enough manpower to remove about 60% of illegally dumped debris,
but this is a recurrent problem.
5Pennsylvania Economy League, Inc., Eastern Division. Survey of the Costs Associated with Illegal
Dumping in Philadelphia, 1995, Philadelphia, PA.
VIM
-------
Costs
• Direct cost: over $5 million per year is spent on waste removal (40% of costs),
disposal (50%), law enforcement by the Environmental Response Unit (6%),
prosecution (2%); and processing of hazardous materials (1%).
• Direct cost to taxpayers: $90 per ton of waste, which is largely household and
construction debris.
• Indirect costs: minimum $2 million/year costs of private removal/disposal, volunteer
time, property devaluation, lost tax revenues.
Control
The City of Philadelphia police department has an Environmental Response Unit (4
officers and 1 supervisor).
Arrests: about 60 per year (no trends in data). In 1994, 31 offenders were convicted
and fined a total of $4000.
The Pennsylvania Economy League recommends the following:
• Focus should be on making illegal dumping financially infeasible (raise penalties,
increase enforcement and prosecution).
• Create economic incentives for reporting illegal dumping (e.g., offer a bounty).
Applicable Regulations: Pennsylvania Municipal Waste Planning, Recycling and
Waste Reduction Act (Act 101), legislated 9-26-88.
New law enacted 7-31-90 to enhance enforcement/prosecution of illegal dumpers.
VII-5
-------
-------
APPENDIX VIII
SARA COVERED FACILITIES
SARA Covered Facilities - 1995 (1/30/96)
Census Tracts 0012 - 0052 and 0054 - 0075
Census
Tract
0012
0013
0019
0024
0027
0033
0034
Name
AT&T
Bell of PA, PennyPacker Co
Broad and Pine, Inc.
Philadelphia Facility,
Philadelphia Newspaper
The Graduate Hospital
Peco Christian St Service
Bldg
Schuylkill Generating Station,
Peco
Trigen, Philadelphia Energy
Corp, Schuylkill PI
Economy Asphalt Co.
Lerro Products, Inc.
Webb Manufacturing
Wricley Nut Products, Inc.
Asco Fuel Inc.
F.C. Haab (Schuylkill
Terminal)
B & L Propane
Consolidated Freightways,
Inc.
M.G. Industries
Philadelphia Transfer &
Recycling Center
Ryder Commercial Leasing &
Services
Chemical Report for SARA
500 S. 27th Street
423 S. 17th Street
400 S. Broad Street
400 S. Broad Street
NEC 19th and South Sts.
830 Schuylkill Ave
2800 Christian St
2600 Christian St
1920 Washington Ave
1727 Carpenter St
1241 Carpenter St
110 Tasker St
1056 S. 31st St
Morris & Schuylkill Strs.
3420 Grays Ferry Ave
1600 S. Warfield St
36th & Moore Sts., E. Side Yard,
Schuylkill
3605 Grays Ferry Ave
1450 South Warfield St
Extremely
Hazardous
Substances
YES
YES
NO
YES
NO
NO
YES
YES
NO
NO
NO
NO
NO
NO
NO
NO
NO
NO
NO
VIII-1
-------
SARA Covered Facilities - 1995 (1/30/96)
Census Tracts 0012 - 0052 and 0054 - 0075
Census
Tract
0035
0039
0040
0042
0043
0044
0046
Name
E.I. Dupont, Marshall
Research and Development
Lab
Degussa Corporation
TDSI/BIDS (CSX)
Bell of PA
Buckley Co Inc
CSXT Philadelphia PA Shops
Philadelphia Gas Works
Bell of PA, DeweyCo
Peco, Shunk Service Bldg
Inolex
United Parcel Service, Inc.
Ashland Chemical Co.
Delaware Ave Distribution
Center
Dubin Paper Co
Peco Oregon Shop
Peco Southwark Substation
TRC, Inc.
Conrail - Flex-Flo Terminal
Dockside Refrigerated
Warehouse, Inc.
Defense Personnel Support
Center
SPC Corp
Sun Refining & Marketing
Co.
Chemical Report for SARA
3401 Grays Ferry Ave
36th & Moore St
36th & Moore St
1851 S. 34th St
1800 S. 34th St
38th St & Jackson St
3100 Passyunk Ave
2000 S. Broad St
1316 Shunk St
Jackson & Swanson Sts
15 Oregon Ave
2801 Christopher Columbus Blvd
2204 S. Delaware Ave
1910 S. Delaware Ave
2610 S. Delaware Ave
2501 S. Delaware Ave
2904 S. Delaware Ave
52 E. Oregon Ave
#8 East Oregon
2800 S. 20th St
2600 Penrose Ave
3144 Passyunk Ave
Extremely
Hazardous
Substances
YES
YES
NO
NO
NO
NO
YES
YES
NO
YES
NO
YES
YES
NO
NO
YES
NO
NO
YES
NO
NO
YES
vm-2
-------
SARA Covered Facilities - 1995 (1/30/96)
Census Tracts 0012 - 0052 and 0054 - 0075
Census
Tract
0049
0049
0050
0052
Name
Sun Refining & Marketing-
Belmont Terminal
Acme Markets, Inc. DC #3
Arrow Terminals -
Philadelphia
Blue Star Lines Ltd.
Colonial Beef Co.
Holt Cargo System - Packer
Ave Terminal
Kansas Beef Industries of
Philadelphia Inc
Mario Maggio Co.
Philadelphia Water Dept, SE
Water Pollution
Procacci Bros. Sales Corp.
Procacci Bros. Sales Corp.,
Bldg. 1
Procacci Bros. Sales Corp.,
Bldg. 5
Refrigerated Distrib. Center
(Packer Ave. M)
Tartan Sysco Food Services
Triple Seven Ice
Naval Station (Shipyard),
Philadelphia
Aircraft Service Inter., Inc.
Alamo Rent A Car Inc
American Airlines
AMR Services
Chemical Report for SARA
2700 Passyunk Ave
700 Pattison Ave
3609 S. Darien St
3301 S. Columbus Blvd
3333 S. 3rd St
3301 S. Columbus Blvd
3101 S. 3rd St
3300 S. 7th St
25 E. Pattison Ave
3333 S. Front St
3655 S. Lawrence St
201 Pattison Ave
3301 S. Columbus Blvd.
666 Packer Ave
777 Pattison Ave
Building 75/2
Unit 5A S. Island Ave (4875)
P.I.A.
Philadelphia International Airport
Philadelphia International
Airport, A-6
Extremely
Hazardous
Substances
NO
YES
NO
NO
NO
NO
YES
YES
YES
YES
NO
YES
NO
YES
YES
YES
NO
NO
NO
NO
vm-3
-------
SARA Covered Facilities - 1995 (1/30/96)
Census Tracts 0012 - 0052 and 0054 - 0075
Census
Tract
Name
Chemical Report for SARA
Extremely
Hazardous
Substances
Caterair International
8401 Escort Ave
Delta Air Lines, Inc.
P.I.A.
Dobbs International Services,
Inc.
P.I.A., Cargo City, Bldg. Cl
Hertz Corp
P.I.A., Cargo City
Hertz Corporation
P.I.A.
La France Corp
8425 Executive Ave
National Car Rental Systems
Inc.
P.I.A.
Trans World Airlines, Inc.
P.I.A., Terminal B
United Airlines - PHLGQ
P.I.A.
United Parcel Service
1 Hog Island Rd
US Air Philadelphia
P.I.A.
NO
NO
NO
NO
NO
YES
NO
YES
NO
NO
NO
0052
Van Waters & Rogers Inc,
Univar Corp
8335 Enterprise Ave
Water Dept, SW Water
Pollution Control
8200 Enterprise Ave
YES
YES
0054
Hygrade Food Products
8400 Executive Ave
YES
0055
Hachik Distributors, Inc.
2300 Island Ave
NO
0057
Bell of PA, Eastwick Co
3400 Island Ave
YES
0058
Amoco Oil Co, Philadelphia
63rd St & Passyunk Ave
C.R.Warner, Inc.
61st & W. Passyunk Ave
Chevron, USA
70th St & Essington Ave
Exxon Philadelphia Terminal
6850 Essington Ave
Glenco/Star Corp.
8000 Penrose Ave
Maritank Philadelphia Inc.
6700 Essington Ave (67th St &
Schuylkffl)
NO
NO
NO
NO
NO
NO
vm-4
-------
SARA Covered Facilities - 1995 (1/30/96)
Census Tracts 0012 - 0052 and 0054 - 0075
Census
Tract
0061
0062
0067
0068
0069
0070
0072
0074
0075
Name
•
National Car Rental System,
Inc.
Carbonator Rental Service
Inc
General Electric Breaker
Plant
Angelica Healthcare Serv.
Group, Inc.
Delaware Valley Recycling
Joseph T Ryerson & Son
Louis Dreyfus Energy -
Philadelphia
M.A. Bruder & Sons, Inc.
Bell of PA, Saratoga Co
Amoroso's Baking Company
Septa - Woodland Shop
Amerada Hess Corp
Chemical Report for SARA
6950 Norwitch Dr
6500 Eastwick Ave
6901 Elmwood Ave
58th St & Lindbergh Blvd
3107 S. 61st St
5200 Grays Ave
58th St & Schuylkill River
5213 Grays Ave
5400 Woodland Ave
845 S. 55th St
49th & Woodland Ave
1630 S. 51st St
Extremely
Hazardous
Substances
NO
NO
NO
NO
NO
NO
NO
NO
YES
NO
NO
NO
vm-s
-------
-------
APPENDIX IX
LANDVIEW COMPARISONS
-------
-------
*
%
C0
i
o
s
O O
'•& *"
« 5 .
3 &'
O, «5
«£-
a
o
3
1
£
s
sr
t/i
$
«n
> «
o o
2 S
-------
*
«5
eu
•e
*
cu
«
s
I
M
O
§
o 'C
s 'S
o a,
£4
W CL O ^-*
- * 6 S -52
*-' tM O u^ »-J
o\ o o g *"*
»—i en .y w -^
^ *-> r^ u^
en" CX 5 O .g
I M
G 'Zl
° S
60 §
.S ^*
y o
O en
DO'S §
•S .S >
.i-< w •*- «] —
« « « g g
« 'S ?*
Ja fe °-
-------
Table 2: Number of toxic
City
Albany, NY
Allentown, PA
Altoona, PA
Baltimore, MD
Boston, MA
Dover, DE
Hagerstown, MD
Harrisburg, PA
Jersey City, NJ
Lancaster, PA
New Haven, CT
New York, NY
Newark, NJ
Philadelphia, PA
Pittsburgh, PA
Pittsfield, MA
Portland, ME
Providence, RI
Reading, PA
Rochester, NY
Scranton, PA
Trenton, NY
Wilmington, DE
compounds or chemical categories released to
cities in the Northeast U.S., 1992*
Number of compounds
Total
15
23
12
72
7
7
14
10
9
32
13
47
58
78
64
11
7
31
49
79
20
27
23
York, PA 37
An-
il
21
7
68
6
6
11
9
8
29
6
46
58
74
63
11
6
26
47
73
14
24
22
32
or chemical
Water Underground
injection
7
4
0
28
0
0
0
0
0
1
2
4
0
20
20
2
1
5
14
57
2
2
0
11
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
1
0
0
different media,
selected
categories released by medium
Land
5
0
0
4
0
0
1
0
0
0
0
4
8
15
0
0
0
2
5
4
0
1
2
10
Publicly-owned
treatment
works
8
0
7
42
1
4
1
1
4
18
1
23
41
41
21
2
3
12
26
33 v
5
9
8
15
Off-site
transfer
9
14
9
53
5
0
12
4
6
27
12
32
39
49
51
10
5
24
48
59
12
23
17
24
*Data from Toxics Release Inventory. No facilities were listed for Atlantic City, NJ, or Washington, DC, in
1992.
IX-3
-------
Table 4: Number of facilities
City
Albany, NY
Allentown, PA
Altoona, PA
Atlantic City, NJ
Baltimore, MD
Boston, MA
Dover, DE
Hagerstown, MD
Harrisburg, PA
Jersey City, NJ
Lancaster, PA
New Haven, CT
New York, NY
Newark, NJ
Philadelphia, PA
Pittsburgh, PA
Pittsfield, MA
Portland, ME
Providence, RI
Reading, PA
Rochester, NY
Scranton, PA
Trenton, NJ
Washington, DC
Wilmington, DE
York, PA
CO
8
5
1
7
56
15
10
9
3
5
6
27
266
24
43
33
4
11
18
12
25
3
6
10
21
12
emitting criteria
NOj
9
10
1
8
70
19
11
8
3
6
12
27
284
25
45
33
4
12
18
18
28
5
6
10
23
16
air pollutants, selected
Number
PM,a
0
6
1
0
0
0
7
0
4
0
9
27
0
0
36
28
0
14
0
15
0
3
0
0
15
13
cities in the Northeast U.S., 1982-1994*
of facilities emitting pollutant
SO2
0
8
1
0
50
18
10
9
3
0
5
27
0
0
3
25
4
13
16
15
0
2
0
10
23
12
Volatile
Organic
Compounds
15
11
10
8
95
21
13
10
15
3
22
34
445
44
66
42
4
12
29
21
49
6
6
12
23
28
Total
particulates
0
0
0
0
53
14
9
9
0
0
0
1
0
0
41
31
4
13
16
1
0
0
0
10
22
0
Lead
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
4
0
0
0
0
0
0
o 1
o 1
o 1
o 1
*Data from the Aerometric Information Retrieval System:4804 (79%) of the records are from 1990; 5970 (98%) are
from 1990-1993.
IX-4
-------
Table 3: Number of facilities reporting the
media, selected cities
City
Albany, NY
Allentown, PA
Altoona, PA
Baltimore, MD
Boston, MA
Dover, DE
Hagerstown, MD
Harrisburg, PA
Jersey City, NJ
Lancaster, PA
New Haven, CT
New York, NY
Newark, NJ
Philadelphia, PA ,
Pittsburgh, PA
Pittsfield, MA
Portland, ME
Providence, RI
Reading, PA
Rochester, NY
Scranton, PA
Trenton, NJ
Wilmington, DE
York, PA
Total
5
9
6
76
4
4
7
6
6
32
9
87
42
64
40
3
3
41
19
43
7
17
8
34
release or transfer of toxic compounds to different
in the Northeast U.S., 1992*
Number of facilities reporting
Air
4
8
3
70
3
4
6
6
6
28
7
77
40
57
37
3
3
34
17
41
7
15
7
30
Water
2
2
0
17
0
0
0
0
0
1
1
3
0
6
5
1
1
2
5
2
1
2
0
7
Underground
injection
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
1
0
0
release of toxic compounds
Land Publicly-owned
treatment works
2
0
0
3
0
0
1
0
0
0
0
1
1
6
0
0
0
2
2
3
0
1
1
6
3
0
3
22
1
2
1
1
2
8
1
20
27
25
8
1
2
15
11
20
3
5
2
12
Off-site
transfer
3
5
5
45
3
0
7
3
3
26
9
43
26
38
32
3
2
34
14
33
5
14
7
20
*Data from the Toxics Release Inventory. No facilities were listed for Atlantic City, NJ, or Washington,
DC, in 1992.
IX-5
-------
Table 5: Summary counts of point-source discharges
Discharge Elimination System, selected cities
City
Albany, NY
Allentown, PA
Atlantic City, NJ
Baltimore, MD
Boston, MA
Hagerstown, MD
Harrisburg, PA
Jersey City, NJ
Lancaster, PA
New Haven, CT
New York, NY
Newark, NJ
Philadelphia, PA
Pittsburgh, PA
Pittsfield, MA
Portland, ME
Providence, RI
Reading, PA
Rochester, NY
Scranton, PA
Trenton, NJ
Washington, DC
Wilmington, DE
Total number**
Permits Parameters
6
. 4
1
29
1
2
1
4
2
2
56
18
8
23
2
1
5
1
21
1
13
4
3
18
76
4
39
4
19
6
11
14
7
42
43
92
106
13
21
23
10
72
12
18
19
24
to water under the National Pollution
in the Northeast U.S., 1993*
Releases
35
91
4
134
4
20
6
17
23
8
425
113
177
257
16
21
30
10
170
12
51
24
34
Average number
of parameters
per permit
5.8
22.8
4.0
4.6
4.0
10.0
6.0
4.2
11.5
4.0
7.6
6.3
22.1
11.2
8.0
21.0
6.0
10.0
8.1
12.0
3.9
6.0
11.3
*No facilities were listed for Altoona, PA, Dover, DE, or York, PA in 1993.
**"Parameters" include all chemical, biological, and physical parameters, with die exception of flow
parameters. A "release" represents one parameter discharged under one permit, e.g. if Permit A allows the
discharge of 5 parameters and Permit B allows 10 parameters, then the total number of "releases" is 15.
IX-6
-------
Table 6: Top 25 toxic chemicals ranked by pounds released to air, 26 cities, 1992*
Chemical
Dichloromethane
Toluene
Methanol
Acetone
1,1, 1-trichloroethane
Hydrochloric acid
Xylene (Mixed Isomers)
Ammonia
Methyl ethyl ketone
Cumene
Carbonyl sulfide
Methyl isobutyl ketone
Trichloroethylene
Glycol ethers
N-butyl alcohol
Freon 113
1 ,2-dichloropropane
Tetrachloroethylene
Cyclohexane
Benzene
Dichlorodifluoromethane
Sulfiiric acid
Di(2-ethylhexyl) phthalate
Hydrogen fluoride
Phenol
Pounds released to air
4,627,191
4,405,274
3,913,186
3,095,418
2,986,359
2,784,630
1,777,179
1,454,897
1,392,284
1,366,975
868,107
696,601
689,596-
606,907
586,155
553,595
367,250
287,293
265,239
244,714
205,074
140,904
136,476
123,874
113,710
IX-7
-------
Point-source Emissions of
Criteria Air Pollutants, 1982-1993.*
0 40 80 120 Miles
[•Source: the Aerometric Information Retrieval System, as recorded in Landview II.]
US EPA
Region III
CIS Team
EPA RS QIC Project SO QIS.14S [D. MwDonaM] 12/4/98 map 73
-------
Point-source Discharges of
Industrial and Municipal Wastewater, 1993*
0 40 80 120 Miles
["Source: the Permit Compliance System, as recorded in Landview II.]
oo
N
US EPA
Region III
CIS Team
EPA R3 QIC Project SK3 QIS.143 [D, MwDorwM] 12/4/98 rap 75
-------
Facilities Reporting Releases or
Off-site Transfers of Toxic Compounds
to the Toxics Release Inventory, 1992.*
0 40 80 120 Miles
N
pSource: the Toxics Release Information System, as recorded in Landview II.]
US EPA
Region III
GIS Team
EPA RS QIC Prate* 8KS QI9.14S [D. MwDoraUd] 1Z/4AB map 78
-------
National Priority List (Superfund) Sites, 1993
N
0 40 80 120 Miles
US EPA
_ Region III
[•Source: the Comprehensive Environmental Response, Compensation, and Liability Information System, XNl/Z CIS Team
as recorded In Landview II.]
EPA RS QIC Project SK3 QI8.143 [D, MaoDonald] 12/4/BB map 74
-------
-------
APPENDIX X
TOXICOLOGIC DATA
-------
-------
Printed From:
Common Name: Ammonia
Common Name: Ammonia
CAS Number: 7664-41-7
DOT Number: UN 2672/UN 2073/UN 1005
Date: January, 1989
HAZARD SUMMARY
* Ammonia can affect you when breathed in.
* Breathing Ammonia may irritate the lungs, causing coughing
and/or shortness of breath. Higher exposures can cause a
buildup of fluid in the lungs (pulmonary edema), which can
cause death.
* Ammonia is a CORROSIVE CHEMICAL and can severely burn the
eyes, leading to permanent damage. Contact with Ammonia liquid
can severely burn the skin.
* Long term exposure to Ammonia can cause chronic irritation of
the eyes, nose, mouth, and throat.
IDENTIFICATION
Ammonia is found as a colorless gas and in water solution with a
strong and suffocating odor. It is used in making fertilizer,
plastics, dyes and textiles.
REASON FOR CITATION
* Ammonia is on the Hazardous Substance List because it is
regulated by OSHA and cited by ACGIH, DOT, NIOSH, NFPA and
EPA.
* This chemical is also on the Special Health Hazard Substance
List because it is CORROSIVE.
* Definitions are attached.
HOW TO DETERMINE IF YOU ARE BEING EXPOSED
* Exposure to hazardous substances should be routinely
evaluated. This may include collecting personal and area air
samples. You can obtain copies of sampling results from your
employer. You have a legal right to this information under
OSHA 1910.20.
* If you think you are experiencing any work related health
problems, see a doctor trained to recognize occupational
diseases. Take this Fact Sheet with you.
WORKPLACE EXPOSURE LIMITS
OSHA: The legal airborne permissible exposure limit (PEL) is 50
ppm averaged over an 8 hour workshift.
NIOSH: The recommended airborne exposure limit is 50 ppm, which
should not be exceeded during any 5 minute work period.
ACGIH: The recommended airborne exposure limit is 25 ppm
averaged over an 8 hour workshift•and 35 ppm as a STEL
(short term exposure limit).
WAYS OF REDUCING EXPOSURE
* Where possible, enclose operations and use local exhaust
ventilation at the site of chemical release. If local exhaust
ventilation or enclosure is not used, respirators should be
worn.
* Wear protective work clothing.
* Wash thoroughly immediately after exposure to Ammonia.
-------
* Post hazard and warning information in the work area. In
addition, as part of an ongoing education and training effort,
communicate all information on the health and safety hazards
of Ammonia to potentially exposed workers.
This Fact Sheet is a summary source of information of all potential
and most severe health hazards that may result from exposure.
Duration of exposure, concentration of the substance and other
factors will affect your susceptibility to any of the potential
effects described below.
HEALTH HAZARD INFORMATION
Acute Health Effects
The following acute (short term) health effects may occur
immediately or shortly after exposure to Ammonia:
* Contact can cause severe skin burns.
* It can cause severe burns of the eyes, leading to permanent
damage.
* Breathing Ammonia can irritate the mouth, nose, and throat.
Higher levels may irritate the lungs, causing coughing and/or
shortness of breath. Very high exposures can cause a buildup
of fluid in the lungs (pulmonary edema), which can result in
death.
* Exposure can cause headaches and loss of sense of smell.
* Ammonia may make you feel sick to your stomach and cause
vomiting.
Chronic Health Effects
The following chronic (long term) health effects can occur at some
time after exposure to Ammonia and can last for months or years:
* According to the information presently available to the New
Jersey Department of Health, Ammonia has not been tested for
its ability to adversely affect reproduction.
Cancer Hazard
* According to the information presently available to the New
Jersey Department of Health, Ammonia has not been tested for
its ability to cause cancer in animals.
Other Long Term Effects
* Repeated exposure can cause chronic irritation of the eyes,
nose, throat, and airways.
* Very irritating substances may affect the lungs. It is .not
known whether Ammonia causes lung damage.
Medical Testing
Before beginning employment and at regular times after that, the
following are recommended:
* Lung function tests.
If symptoms develop or overexposure is suspected, the following may
be useful:
* Consider chest x ray after acute overexposure.
-------
Printed From:
Common Name: Benzene
Common Name: Benzene
CAS Number: 71-43-2
DOT Number: UN 1114
Date: January, 1988
HAZARD SUMMARY
* Benzene can affect you when breathed in and by passing through
your skin.
* Benzene is a CARCINOGEN HANDLE WITH EXTREME CAUTION.
* Exposure can cause you to become dizzy and lightheaded. Higher
levels can cause convulsions and death.
* Exposure can irritate the nose and throat and may cause an
upset stomach and vomiting.
* Benzene can cause an irregular heart beat that can lead to
death.
* Prolonged exposure can cause fatal damage to the blood
(aplastic anemia).
* Benzene is a FLAMMABLE LIQUID and a FIRE HAZARD.
IDENTIFICATION
Benzene is a colorless liquid with a pleasant odor. It is used
mainly in making other chemicals, as a solvent, and is found in
gasoline.
REASON FOR CITATION
* Benzene is on the Hazardous Substance List because it is
regulated by OSHA and cited by ACGIH, DOT, NIOSH, IARC, NTP,
CAG, DEP, NFPA and EPA.
* It is on the Special Health Hazard Substance List because it
is a CARCINOGEN, a MUTAGEN and is FLAMMABLE.
* Definitions are attached.
HOW TO DETERMINE IF YOU ARE BEING EXPOSED
* Exposure to hazardous substances should be routinely
evaluated. This may include collecting air samples. Under OSHA
1910.20, you have a legal right to obtain copies of sampling
results from your employer. If you think you are experiencing
any work related health problems, see a doctor trained to
recognize occupational diseases. Take this Fact Sheet with
you.
* ODOR THRESHOLD = 12.0 ppm.
* The odor threshold only serves as a warning of exposure. Not
smelling it does not mean you are not being exposed.
WORKPLACE EXPOSURE LIMITS
OSHA: The legal airborne permissible exposure limit (PEL) is
1 ppm averaged over an 8 hour workshift, and 5 ppm which
should not be exceeded in any 10 minute period.
ACGIH: The recommended airborne exposure limit is 10 ppm
averaged over an 8 hour workshift.
NIOSH: The recommended airborne exposure limit is 1.0 ppm,
which should not be exceeded during any 60 minute
•*"__ period.
* Benzene is a CANCER CAUSING AGENT in humans. There may be no
safe level of exposure to a carcinogen, so all contact should
-------
be reduced to the lowest possible level.
* The above exposure limits are for air levels only. Skin
contact may also cause overexposure.
WAYS OF REDUCING EXPOSURE
* A regulated, marked area should be established where Benzene
is handled, used, or stored.
* Wear protective work clothing.
* Wash thoroughly immediately after exposure to Benzene and at
the end of the workshift.
* Post hazard and warning information in the work area. In
addition, as part of an ongoing education and training effort,
communicate all information on the health and safety hazards
of Benzene to potentially exposed workers.
This Fact Sheet is a summary source -of information of all potential
and most severe health hazards that may result from exposure.
Duration of exposure, concentration of the substance and other
factors will affect your susceptibility to any of the potential
effects described below.
HEALTH HAZARD INFORMATION
Acute Health Effects
The following acute (short term) health effects may occur
immediately or shortly after exposure to Benzene:
* Exposure can cause symptoms of dizziness, lightheadedness,
headaches, and vomiting. Convulsions and coma, or sudden death
from irregular heart beat, may follow high exposures.
* Exposure can also irritate the eyes, nose, and throat.
Chronic Health Effects
The following chronic (long term) health effects can occur at some
time after exposure to Benzene and can last for months or years:
Cancer Hazard
* Benzene is a CARCINOGEN in humans. It has been shown to cause
leukemia.
* Many scientists believe there is no safe level of exposure to
a carcinogen.
Reproductive Hazard
* There is limited evidence that Benzene is a teratogen in
animals. Until further testing has been done, it should be
treated as a possible teratogen in humans.
Other Long Term Effects
* Repeated exposure can damage the blood forming organs causing
a condition called aplastic anemia. This can cause death.
* Long term exposure may cause drying and scaling of the skin.
MEDICAL TESTING
Before beginning employment and at regular times after that, the
following are recommended:
* Complete blood count.
* Urinary Phenol (a test to see if Benz.ene is in the body) .
-------
Printed From:
Common Name: Chlorine
Common Name: Chlorine
CAS Number: 7782-50-5
DOT Number: UN 1017
Date: January, 1989
HAZARD SUMMARY
* Chlorine can affect you when breathed in.
* Exposure can cause irritation of the eyes, nose, and throat,
and also tearing, coughing and chest pain. Higher levels burn
the lungs and can cause a buildup of fluid in the lungs
(pulmonary edema) and death.
* Contact can severely burn the eyes and skin.
* Repeated exposures or a single high exposure may permanently
damage the lungs. It can also damage the teeth and cause a
skin rash.
IDENTIFICATION
Chlorine is a greenish yellow gas with an irritating odor, or
present in liquid solutions. It is used in making solvents, many
chemicals, disinfectants, and chlorine bleach cleaners.
REASON FOR CITATION
* Chlorine is on the Hazardous Substance List because it is
regulated by OSHA and cited by ACGIH, NIOSH, EPA, DOT, DEP and
NFPA.
* Definitions are attached.
HOW TO DETERMINE IF YOU ARE BEING EXPOSED
* Exposure to hazardous substances should be routinely
evaluated. This may include collecting air samples> Under OSHA
1910.20, you have a legal right to obtain copies of sampling
results from you employer. If you think you are experiencing
any work related health problems, see a doctor trained to
recognize occupational diseases. Take this Fact Sheet with
you.
* ODOR THRESHOLD = 0.31 ppm.
* The odor threshold only serves as a warning of exposure. Not
smelling it does not mean you are not being exposed.
WORKPLACE EXPOSURE LIMITS
OSHA: The legal airborne permissible exposure limit (PEL) is 1
ppm, not to be exceeded at any time.
NIOSH: The recommended airborne exposure limit is 0.5 ppm., which
should not be exceeded during any 15 minute period.
ACGIH: The recommended airborne exposure limit is 1 ppm averaged
over an 8 hour workshift and 3 ppm as a STEL (short term
exposure limit).
WAYS OF REDUCING EXPOSURE
* Where possible, enclose operations and use local exhaust
ventilation at the site of chemical release. If local exhaust
ventilation or enclosure is not used, respirators should be
worn.
* Wear protective work clothing.
* Wash thoroughly immediately after exposure to liquid Chlorine
or Chlorine solutions.
-------
* Post hazard and warning information in the work area. In
addition, as part of an ongoing education and training effort,
communicate all information on the health and safety hazards
of Chlorine to potentially exposed workers.
This Fact Sheet is a summary source of information of all potential
and most severe health hazards that may result from exposure.
Duration of exposure, concentration of the substance and other
factors will affect your susceptibility to any of the potential
effects described below.
HEALTH HAZARD INFORMATION
Acute Health Effects
The following acute (short term) health effects may occur
immediately or shortly after exposure to Chlorine:
* Exposure causes irritation of the eyes, nose, and throat. It
can include tearing, coughing, sputum, bloody nose, and chest
pain. Higher levels cause a buildup of fluid in the lungs
(pulmonary edema) and death.
* Contact can severely burn the eyes and skin, causing permanent
damage.
Chronic Health Effects
The following chronic (long term) health effects can occur at some
time after exposure to Chlorine and can last for months or years:
Cancer Hazard
* According to the information presently available to the New
Jersey Department of Health, Chlorine has not been tested for
its ability to cause cancer in animals.
Reproductive Hazard
* According to the information presently available to the New
Jersey Department of Health, Chlorine has not been tested for
its ability to adversely affect reproduction.
Other Long Term Effects
* Chlorine can irritate the lungs. Repeated exposure may cause
bronchitis to develop with cough, phlegm, and/or shortness of
breath.
* Long term exposure can damage the teeth.
MEDICAL TESTING
Before beginning employment and at regular times after that, the
following are recommended:
* Check teeth for signs of erosion.
* Lung function tests.
If symptoms develop or overexposure is suspected, the following may
be useful:
* Lung function tests.
* Consider chest xray after acute overexposure.
Any evaluation should include a careful history of past and present
-------
Printed From:
Common Name: Cumene
Common Name: Cumene
CAS Number: 98-82-8
DOT Number: UN 1918
Date: January, 1989
HAZARD SUMMARY
* Cumene can affect you when breathed in and by passing through
your skin.
* Exposure can cause you to become dizzy, lightheaded, and to
pass out.
* Contact can irritate the eyes. It may also cause a skin rash.
* Exposure may irritate the eyes, nose, mouth, and throat.
IDENTIFICATION
Cumene is a colorless liquid with a sharp, penetrating odor. It is
used as an industrial solvent and occurs in petroleum.
REASON FOR CITATION
* Cumene is on the Hazardous Substance List because it is
regulated by OSHA and cited by ACGIH, DOT, DEP, NFPA and EPA.
HOW TO DETERMINE IF YOU ARE BEING EXPOSED
* Exposure to hazardous substances should be routinely
evaluated. This may include collecting air samples. Under OSHA
1910.20, you have a legal right to obtain copies of sampling
results from your employer. If you think you are experiencing
any work related health problems, see a doctor trained to
recognize occupational diseases. Take this Fact Sheet with
you.
* ODOR THRESHOLD = 0.088 ppm.
* The odor threshold only serves as a warning of exposure. Not
smelling it does not mean you are not being exposed.
WORKPLACE EXPOSURE LIMITS
OSHA: The legal airborne permissible exposure limit (PEL) is
50 ppm averaged over an 8 hour workshift.
ACGIH: The recommended airborne exposure limit is 50 ppm
averaged over an 8 hour workshift.
* The above exposure limits are for air levels only. When skin
contact also occurs, you may be overexposed, even though air
levels are less than the limits listed above.
WAYS OF REDUCING EXPOSURE
* Where possible, enclose operations and use local exhaust
ventilation at the site of chemical release. If local exhaust
ventilation or enclosure is not used, respirators should be
worn.
* Wear protective work clothing.
* Wash thoroughly immediately after exposure to Cumene.
* Post hazard and warning information in the work area. In
addition, as part of an ongoing education and training effort,
communicate all information on the health and safety hazards
of Cumene to potentially exposed workers.
This Fact Sheet is a summary source of information of all potential
-------
and most severe health hazards that may result from exposure.
Duration of exposure, concentration of the substance and other
factors will affect your susceptibility to any of the potential
effects described below.
*
*
HEALTH HAZARD INFORMATION
Acute Health Effects
The following acute (short term) health effects may occur
immediately or shortly after exposure to Cumene:
* The liquid may irritate- the skin, causing a rash or burning
feeling on contact.
Contact can irritate the eyes.
Exposure can irritate the eyes, nose, mouth, and throat.
Higher levels can cause you to become dizzy, lightheaded, and
to pass out.
Chronic Health ^Effects
The following chronic (long term) health effects can occur at some
time after exposure to Cumene and can last for months or years:
Cancer Hazard
* According to the information presently available to the New
Jersey Department of Health, Cumene has not been tested for
its ability to cause cancer in animals.
Reproductive Hazard
* According to the information presently available to the New
Jersey Department of Health, Cumene has not been tested for
its ability to adversely affect reproduction.
Other Long Term Effects
* Long term exposure can cause drying and cracking of the skin.
* Exposure may damage the lungs, liver, and kidneys.
* This chemical has not been adequately evaluated to determine
whether brain or other nerve damage could occur with repeated
exposure. However, many solvents and other petroleum based
chemicals have been shown to cause such damage. Effects may
include reduced memory and concentration, personality changes
(withdrawal, irritability), fatigue, sleep disturbances,
reduced coordination, and/or effects on nerves supplying
internal organs (autonomic nerves) and/or nerves to the arms
and legs (weakness, "pins and needles").
MEDICAL
Medical Testing
If symptoms develop or overexposure is suspected, the following may
be useful:
* Interview for brain effects, including recent memory, mood
(irritability, withdrawal), concentration, headaches, malaise
and altered sleep patterns. Consider cerebellar, autonomic and
peripheral nervous system evaluation. Positive and borderline
individuals should be referred for neuropsychological testing.
Any evaluation should include a careful history of past and present
symptoms with an exam. Medical tests that look for damage already
done are not a substitute for controlling exposure.
-------
Printed From:
Common Name: Cyclohexane
Common Name: Cyclohexane
CAS Number: 110-82-7
DOT Number: UN 1145
Date: March, 1986
HAZARD SUMMARY
* Cyclohexane can affect you when breathed in.
* Exposure may cause nausea, dizziness, lightheadedness and
drowsiness. Unconsciousness and death may occur at high
exposures.
* It can irritate the eyes, nose and throat.
* Prolonged or repeated skin contact will cause cracking, drying
and chapping of exposed areas.
* Cyclohexane is a FLAMMABLE LIQUID and a FIRE HAZARD.
IDENTIFICATION
Cyclohexane is a colorless liquid with a sweet odor. It is used as
a paint remover, a solvent for lacquers and resins, and in making
organic materials like nylon.
REASON FOR CITATION
* Cyclohexane is on the Hazardous Substance List because it is
regulated by OSHA and cited by ACGIH, DOT and NFPA.
* This chemical is also on the Special Health Hazard Substance
List because it is FLAMMABLE.
HOW TO DETERMINE IF YOU ARE BEING EXPOSED
* Exposure to hazardous substances should be routinely
evaluated. This may include collecting personal and area air
samples. You can obtain copies of sampling results from your
employer. You have a legal right to this information under
OSHA 1910.20.
* ODOR THRESHOLD =25 ppm.
* The odor threshold only serves as a warning of exposure. Not
smelling it does not mean you are not being exposed.
* If you think you are experiencing any work-related health
problems, see a doctor trained to recognize occupational
diseases. Take this Fact Sheet with you.
WORKPLACE EXPOSURE LIMITS
OSHA: The legal airborne permissible exposure limit (PEL) is
300 ppm averaged over an 8-hour workshift. (Final Rule,
January 1989) .
ACGIH: The recommended airborne exposure limit is 300 ppm
averaged over an 8-hour workshift.
WAYS OF REDUCING EXPOSURE
* Where possible, enclose operations and use local exhaust
ventilation at the site of chemical release. If local exhaust
ventilation or enclosure is not used, respirators should be
worn.
* Wear protective work clothing.
* Wash thoroughly immediately after exposure to Cyclohexane.
-------
* Post hazard and warning information in the work area. In
addition, as part of an ongoing education and training effort,
communicate all information on the health and safety hazards
of Cyclohexane to potentially exposed workers.
This Fact Sheet is a summary source of information of all potential
and most severe health hazards that may result from exposure.
Duration of exposure, concentration of the substance and other
factors will affect your susceptibility to any of the potential
effects described below.
HEALTH HAZARD INFORMATION
Acute Health Effects
The following acute (short term) health effects may occur
immediately or shortly after exposure to Cyclohexane:
* Exposure can irritate the eyes, nose and throat.
* Exposure to high levels can cause nausea, dizziness,
lightheadedness and drowsiness. Unconsciousness and death may
occur at higher exposures.
Chronic Health Effects
The following chronic (long term) health effects can occur at some
time after exposure to Cyclohexane and can last for months or
years:
Cancer Hazard
* According to the information presently available to the New
Jersey Department of Health, Cyclohexane has not been tested
for its ability to cause cancer in animals.
Reproductive Hazard
* According to the information presently available to the New
Jersey Department of Health, Cyclohexane has not been tested
for its ability to affect reproduction.
Other Long Term Effects
* Prolonged or repeated skin contact can cause drying, cracking
and chapping of the exposed areas.
* Cyclohexane may affect the liver and kidneys.
MEDICAL
Medical Testing
If symptom
be useful:
* Liver and kidney function tests.
Medical Testing
If symptoms develop or overexposure is suspected, the following may
be useful:
Any evaluation should include a careful history of past and present
symptoms with an exam. Medical tests that look for damage already
done are not a substitute for controlling exposure.
'Request copies of your medical testing. You have a legal right to
this information under OSHA 1910.20.
-------
Common Name: Ethyl Benzene
CAS Number: 100-41-4
DOT Number: UN 1175
Date: July, 1988
HAZARD SUMMARY
* Ethyl Benzene can affect you when breathed in and by passing
through your skin.
* Exposure can irritate the eyes, nose and throat.
* High concentration can cause you to become dizzy, lightheaded,
or to pass out. Very high levels can cause paralysis, trouble
breathing and death.
* Contact can irritate the skin. Prolonged exposure can cause
drying, scaling and even blistering.
* High exposure may damage the liver.
* Ethyl Benzene is a FLAMMABLE LIQUID and a FIRE HAZARD.
IDENTIFICATION
Ethyl Benzene is a colorless liquid with an aromatic odor. It is
used in the production of styrene and synthetic polymers, as a
solvent and as a component of automotive and aviation fuels.
REASON FOR CITATION
* Ethyl Benzene is on the Hazardous Substance List because it is
regulated by OSHA and cited by ACGIH, DOT, DEP, NFPA and EPA.
* This chemical is on the Special Health Hazard Substance List
because it is FLAMMABLE.
* Definitions are attached.
HOW TO DETERMINE IF YOU ARE BEING EXPOSED
* Exposure to hazardous substances should be routinely
evaluated. This may include collecting air samples. Under OSHA
1910.20, you have a legal right to obtain copies of sampling
results from your employer. If you think you are experiencing
any work related health problems, see a doctor trained to
recognize occupational diseases. Take this Fact Sheet with
you.
* ODOR THRESHOLD =2.3 ppm.
* The odor threshold only serves as a warning of exposure. Not
smelling it does not mean you are not being exposed.
WORKPLACE EXPOSURE LIMITS
OSHA: The legal airborne permissible exposure limit (PEL) is
100 ppm averaged over an 8 hour workshift.
ACGIH: The recommended airborne exposure limit is 100 ppm
averaged over an 8 hour workshift and 125 ppm as a STEL
(short term exposure limit).
* The above exposure limits are for air levels only. When skin
contact also occurs, you may be overexposed, even though air
levels are less than the limits listed above.
WAYS OF REDUCING EXPOSURE
* Where possible, enclose operations and use local exhaust
ventilation at the site of chemical release. If local exhaust
ventilation or enclosure is not used, respirators should be
worn.
-------
* Wear protective work clothing.
* Wash thoroughly immediately after exposure to Ethyl Benzene
and at the end of the workshift.
* Post hazard and warning information in the work area. In
addition, as part of an ongoing education and training effort,
communicate all information on the health and safety hazards
'of Ethyl Benzene to potentially exposed workers.
This Fact Sheet is a summary source of information of all potential
and most severe health hazards that may result from exposure.
Duration of exposure, concentration of the substance and other
factors will affect your susceptibility to any of the potential
effects described below.
HEALTH HAZARD INFORMATION
Acute Health Effects
The following acute (short term) health effects may occur
immediately or shortly after exposure to Ethyl Benzene:
* Ethyl Benzene can irritate the eyes, nose and throat.
* Exposure to high concentrations can cause you to become dizzy,
lightheaded and to pass out. Very high levels can cause
trouble breathing, paralysis and death.
* Contact with Ethyl Benzene can irritate the skin.
Chronic Health Effects
The following chronic (long term) health effects can occur at some
time after exposure to Ethyl Benzene and can last for months or
years:
Cancer Hazard
* According to the information presently available to the New
Jersey Department of Health, Ethyl Benzene has not been tested
for its ability to cause cancer in animals.
Reproductive Hazard
* There is limited evidence that Ethyl Benzene may damage the
developing fetus.
Other Long Term Effects
* Repeated contact can cause drying and scaling of the skin.
Prolonged contact can cause blistering.
* High exposure may cause liver damage.
* This chemical has not been adequately evaluated to determine
whether brain or other nerve damage could occur with repeated
exposure. However, many solvents and other petroleum based
chemicals have been shown to.cause such damage. Effects may
include reduced memory and concentration, personality changes
(withdrawal, irritability), fatigue, sleep disturbances,
reduced coordination, and/or effects on nerves supplying
internal organs '(autonomic nerves) and/or nerves to the arms
and legs (weakness, "pins and needles").
MEDICAL TESTING
If symptoms develop or overexposure is suspected, the following may
be useful:
-------
* Liver function tests.
* Interview for brain effects, including recent memory, mood
(irritability, withdrawal), concentration, headaches, malaise
and altered sleep patterns. Consider cerebellar, autonomic and
peripheral nervous system evaluation. Positive and borderline
individuals should be referred for neuropsychological testing.
Any evaluation should include a careful history of past and present
symptoms with an exam. Medical tests that look for damage already
done are not a substitute for controlling exposure.
Request copies of your medical testing. You have a legal right to
this information under OSHA 1910.20.
-------
Printed From:
Common Name: Ethylene
Common Name: Ethylene
CAS Number: 74-85-1
DOT Number: UN 1962/UN 1038
Date: . January, 1989
HAZARD SUMMARY
* Ethylene gas can affect you when breathed in.
* Ethylene gas is HIGHLY FLAMMABLE and EXPLOSIVE. This is the
major hazard of Ethylene exposure.
* Exposure to the gas can cause you to feel dizzy, lightheaded,
and to pass out.
* Contact with liquid Ethylene could cause frostbite.
* Ethylene may cause suffocation. Excessive amounts in the air
in an enclosed space will decrease the amount of oxygen.
* The health effects caused by exposure to Ethylene are much
less serious than its FIRE and EXPLOSION RISK.
IDENTIFICATION
Ethylene is a colorless gas at room temperatures. At very low
temperatures it is a liquid. It is used as a refrigerant and in
welding and cutting metals.
REASON FOR CITATION
* Ethylene is on the Hazardous Substance List because it is
cited by ACGIH, DOT, NFPA and EPA.
* This chemical is on the Special Health Hazard Substance List
because it is FLAMMABLE and REACTIVE.
* Definitions are attached.
HOW TO DETERMINE IF YOU ARE BEING EXPOSED
* Exposure to hazardous substances should be routinely
evaluated. This may include collecting air-samples. Under OSHA
1910.20, you have a legal right to obtain copies of sampling
results from you employer. If you think you are experiencing
any work related health problems, see a doctor trained to
recognize occupational diseases. Take this Fact Sheet with
you.
* ODOR THRESHOLD = 290 ppm.
* The odor threshold only serves as a warning of exposure. Not
smelling it does not mean you are not being exposed.
WORKPLACE EXPOSURE LIMITS
* No exposure limits have been determined.
* Large amounts of Ethylene will decrease the amount of
available oxygen. Before entering an enclosed space, oxygen
content should be tested to ensure that it is at least 19.5%
by volume.
WAYS OF REDUCING EXPOSURE
* Where possible, enclose operations and use local exhaust
ventilation at the site of chemical release. If local exhaust
ventilation or enclosure is not used, respirators should be
worn.
* Wear specially designed protective clothing where exposure to
cold equipment, vapors, or liquid can occur.
* Permanently installed analyzers should be used to monitor for
-------
a dangerous release of Ethylene gas.
* Post hazard and warning information in the work area. In
addition, as part of an ongoing education and training effort,
communicate all information on the health and safety hazards
of Ethylene to potentially exposed workers.
This Fact Sheet is a summary source of information of all potential
and most severe health hazards that may result from exposure.
Duration of exposure, concentration of the substance and other
factors will affect your susceptibility to any of the potential
effects described below.
HEALTH HAZARD INFORMATION
Acute Health Effects
The following acute (short term) health effects may occur
immediately or shortly after exposure to Ethylene:
* Exposure can cause you to feel dizzy, lightheaded, and to pass
out.
* Contact with liquid Ethylene can cause frostbite.
Chronic Health Effects
The following chronic (long term) health effects can occur at some
time after exposure to Ethylene and can last for months or years:
Cancer Hazard
* There is insufficient evidence available to evaluate Ethylene
for its ability to cause cancer in animals.
Reproductive Hazard
* According to the information presently available to the New
Jersey Department of Health, Ethylene has not been tested for
its ability to adversely affect reproduction.
Other Long Term Effects
* Ethylene has not been tested for other chronic (long term)
health effects.
MEDICAL
Medical Testing
* There is no special test for this chemical. However, if
illness occurs or overexposure is suspected, medical attention
is recommended.
Any evaluation should include a careful history of past and present
symptoms with an exam. Medical tests that look for damage already
done are not a substitute for controlling exposure.
-------
Printed From:
Common Name: Lead
Common Name: Lead
CAS Number: 7439-92-1
DOT Number: None
Date: October 1986
HAZARD SUMMARY
* Lead can affect you when breathed in and if swallowed from
food, drinks, or cigarettes.
* Lead is a TERATOGEN--HANDLE WITH EXTREME CAUTION.
* Repeated exposure causes Lead build-up in the body. Low levels
may cause tiredness, mood changes, headaches, stomach problems
and trouble sleeping.
* Higher levels may cause aching, weakness, and concentration or
memory problems.
* Lead can also cause serious permanent kidney or brain damage
at high levels.
* Lead exposure increases risk of high blood pressure.
IDENTIFICATION
Lead is a heavy, soft gray metal. It has wide industrial use due
to its properties of high density, softness, low melting point,
resistance to corrosion and ability to stop gamma and x-rays.
REASON FOR CITATION
* Lead is on the RTK Hazardous Substance List because it is
regulated by OSHA and cited by ACGIH and NIOSH.
* This chemical is on the Special Health Hazard Substance List
because it is a TERATOGEN.
HOW TO DETERMINE IF YOU ARE BEING EXPOSED
* Exposure to hazardous substances should be routinely
evaluated. This may include collecting personal and area air
samples. You can obtain copies of sampling results from your
employer. You have a legal right to this information under
OSHA 1910.20.
* If you think you are experiencing any work-related health
problems, see a doctor trained to recognize occupational
diseases. Take this Fact Sheet with you.
WORKPLACE EXPOSURE LIMITS
* These exposure limits are recommended for inorganic Lead dusts
and fumes measured as Lead.
OSHA: The legal airborne permissible exposure limit (PEL) is
0.05 mg/m3 averaged over an 8-hour workshift.
NIOSH: The recommended airborne exposure limit is less than 0.10
mg/m3 averaged over an 10-hour workshift.
ACGIH: The recommended airborne exposure limit is 0.15 mg/m3
averaged over an 8-hour workshift.
* Lead is a TERATOGEN. All contact with this chemical should be
reduced to the lowest possible level.
WAYS OF REDUCING EXPOSURE
* Where possible, enclose operations and use local exhaust
ventilation at the site of chemical release. If local exhaust
-------
ventilation or enclosure is not used, respirators should be
worn.
* Wear protective work clothing.
* Wash thoroughly at the end of the work-shift.
* Post hazard and warning information in the work area. In
addition, as part of an ongoing education and training effort,
communicate all information on the health and safety hazards
of Lead to potentially exposed workers.
This Fact Sheet is a summary source of information of all potential
and most severe health hazards that may result from exposure.
Duration of exposure, concentration of the substance and other
factors will affect your susceptibility to any of the potential
effects described below.
HEALTH HAZARD INFORMATION
Acute Health Effects
The following acute (short-term) health effects may occur
immediately or shortly after exposure to Lead:
* Extremely high exposures could cause seizures, but usually
symptoms from Lead occur after weeks to months of exposure.
Chronic Health Effects
The following chronic (long-term) health effects can occur at some
time after exposure to Lead and can last for months or years:
Cancer Hazard
* According to the information presently available to the New
Jersey Department of Health, Lead has not been tested for its
ability to cause cancer in animals.
Reproductive Hazard
* Lead is a PROBABLE TERATOGEN in humans.
* Lead may decrease fertility in males and females.
Other Long-Term Effects
* Repeated exposure to Lead causes Lead to build up in the body.
The earliest symptoms may be tiredness, trouble sleeping,
stomach problems, constipation, headaches and moodiness
(mostly irritability and depression).
* Higher levels may cause aching and weakness in your arms and
legs, trouble concentrating and remembering things, and may
cause a low blood count (anemia).
* Lead can cause serious, permanent kidney and brain damage at
high enough levels.
* Lead exposure increases risk of high blood pressure.
MEDICAL
Medical Testing
Before first exposure and every six months thereafter, OSHA
(1910.1025) requires your employer to provide:
* Blood Lead test.
* ZPP test (a special test for the effect of Lead on blood
cells).
-------
Before first exposure, and yearly for exposed person with blood
Lead over 40 micrograms per 100 g of whole blood, OSHA also
requires a complete medical history and exam with the above tests,
and:
* Complete blood count.
* Kidney function tests.
OSHA defines "exposure" for these tests as air levels averages 30
micrograms of Lead or more in a cubic meter of air. OSHA requires
your employer to send the doctor a copy of the Lead standard and
provide one for you.
Any evaluation should include a careful history of past and present
symptoms with an exam. Medical tests that look for damage already
done are not a substitute for controlling exposure.
Request copies of your medical testing. You have a legal right to
this information under OSHA 1910.20.
Mixed Exposures
Body exposures to Lead from hobbies using Lead solder or pigments;
target practice; and drinking moonshine made in Leaded containers
will increase Lead levels. Repeated breathing or handling Leaded
gasoline may also add somewhat to body Lead levels.
-------
Printed From:
Common Name: Methyl Methacrylate
Common Name: Methyl Methacrylate
CAS Number: 80-62-6
DOT Number: UN 1247
Date: May, 1989
HAZARD SUMMARY
* Methyl Methacrylate can affect you when breathed in.
* It may damage the developing fetus.
* Exposure can irritate the eyes, skin, nose, and throat.
* High exposures can cause you to feel dizzy, lightheaded, and
to pass out.
* Methyl Methacrylate can cause a skin allergy.
* Exposure could damage the nervous system. Symptoms may include
"pins and needles", numbness, weakness, and changes in the
ability to remember and concentrate.
* Methyl Methacrylate is a FLAMMABLE and REACTIVE CHEMICAL and
a FIRE and EXPLOSION HAZARD.
IDENTIFICATION
Methyl Methacrylate is a colorless liquid with a sharp, fruity
odor. It is used to make resins, plastics, and specifically plastic
dentures.
REASON FOR CITATION
* Methyl Methacrylate is on the Hazardous Substance List because
it is cited by OSHA, ACGIH, DEP, EPA and other authorities.
* This chemical is on the Special Health Hazard Substance List
because it is FLAMMABLE and REACTIVE.
HOW TO DETERMINE IF YOU ARE BEING EXPOSED
* Exposure to hazardous substances should be routinely
evaluated. This may include collecting personal and area air
samples. You can obtain copies of sampling results from your
employer. You have a legal right to this information under
OSHA 1910.20.
* If you think you are experiencing any work related health
problems, see a doctor trained to recognize occupational
diseases. Take this Fact Sheet with you.
* ODOR THRESHOLD = 0.083 ppm.
* The odor threshold only serves as a warning of exposure. Not
smelling it does not mean you are not being exposed.
. WORKPLACE EXPOSURE LIMITS
OSHA: The legal airborne permissible exposure limit (PEL) is
100 ppm averaged over an 8 hour workshift.
ACGIH: The recommended airborne exposure limit is 100 ppm
averaged over an 8 hour workshift.
WAYS OF REDUCING EXPOSURE
* Where possible, enclose operations and use local exhaust
ventilation at the site of chemical release. If local exhaust
ventilation or enclosure is not used, respirators should be
worn.
* Wear protective work clothing.
* Wash thoroughly immediately after exposure to Methyl
Methacrylate and at the end of the workshift.
-------
* Post hazard and warning information in the work area. In
addition, as part of an ongoing education and training effort,
communicate all information on the health and safety hazards
of Methyl Methacrylate to potentially exposed workers.
This Fact Sheet is a summary source of information of all potential
and most severe health hazards that may result from exposure.
Duration of exposure, concentration of the substance and other
factors will affect your susceptibility to any of the potential
effects described below.
HEALTH HAZARD INFORMATION
Acute Health Effects
The following acute (short term) health effects may occur
immediately or shortly after exposure to Methyl Methacrylate:
* Exposure can irritate the nose and throat. High levels could
cause lung irritation, and may cause you to feel dizzy,
lightheaded, and to pass out.
* Methyl Methacrylate can irritate the eyes on contact, causing
damage.
Chronic Health Effects
The following chronic (long term) health effects can occur at some
time after exposure to Methyl Methacrylate and can last for months
or years':
Cancer Hazard
* There is limited evidence that Methyl Methacrylate causes
mutations (genetic changes) in living cells.
* Methyl Methacrylate has been tested in animals and there is
insufficient data to assess its ability to cause cancer.
Reproductive Hazard
* Methyl Methacrylate may damage the developing fetus.
Other Long Term Effects
* Methyl Methacrylate may cause a skin allergy. If allergy
develops, very low future exposures can cause itching and a
skin rash.
* Repeated exposure may affect the nervous system.
* Symptoms could include a feeling of "pins and needles",
numbness, weakness, changes in function of nerves to internal
body organs (autonomic nervous system) and reduced ability to
concentrate and remember.
* Very irritating substance may affect the lungs. It is not
known whether Methyl Methacrylate causes lung damage.
MEDICAL
Medical Testing
For those with frequent or potentially high exposure (half the TLV
or greater), the following are recommended before beginning work
and at regular times after that:
* Lung function tests.
* Interview for brain effects, including recent memory, mood
(irritability, withdrawal), concentration, headaches, malaise
and altered sleep patterns. Consider cerebellar, autonomic and
peripheral nervous system evaluation. Positive and borderline
individuals should be referred for neuropsychological testing.
-------
If symptoms develop or overexposure is suspected, the following may
be useful:
* Exam of the nervous system.
* Evaluation by a qualified allergist, including careful
exposure history and special testing, may help diagnose skin
allergy.
Any evaluation should include a careful history of past and present
symptoms with an exam. Medical tests that look for damage already
done are not' a substitute for controlling exposure.
-------
Printed From:
Common Name: Propylene
Common Name: Propylene
CAS Number: 115-07-1
DOT Number: UN 1077
Date: October 30, 1986
HAZARD SUMMARY
* Propylene can affect you when breathed in.
* Exposure to high levels can cause you to feel dizzy and
lightheaded. Very high levels can cause you to pass out from
lack of oxygen. Death can result.
* Contact with liquefied Propylene can cause frostbite.
* Exposure may cause an irregular the heart beat. It may also
damage the liver.
* Propylene is a HIGHLY FLAMMABLE GAS and is a DANGEROUS FIRE
HAZARD.
IDENTIFICATION
Propylene is a colorless gas with a slight odor or a liquid under
pressure. It is used in the production of many organic chemicals
including resins, plastics, synthetic rubber and gasoline.
REASON FOR CITATION
* Propylene is on the Hazardous Substance List because it is
cited by ACGIH, DOT and NFPA.
* This chemical is on the Special Health Hazard Substance List
because it is FLAMMABLE.
* Definitions are attached.
HOW TO DETERMINE IF YOU ARE BEING EXPOSED
* Exposure to hazardous substances should be routinely
evaluated. This may include collecting personal and area air
samples. You can obtain copies of sampling results from your
employer. You have a legal right to this information under
OSHA 1910.20.
* If you think you are experiencing any work related health
problems, see a doctor trained to recognize occupational
diseases. Take this Fact Sheet with you.
WORKPLACE EXPOSURE LIMITS
No occupational exposure limits have been established for
Propylene. This does not mean that this substance is not harmful.
Safe work practices should always be followed.
* Large amounts of Propylene will decrease the amount of
available oxygen. Oxygen content should be tested to ensure
that it is 19% by volume.
WAYS OF REDUCING EXPOSURE
* Where possible, enclose operations and use local exhaust
ventilation at the site of chemical release. If local exhaust
ventilation or enclosure is not used, respirators should be
worn.
* Wear protective gloves and clothing to avoid contact with
liquid Propylene.
* Permanently installed detectors can be used to monitor any
dangerous release of Propylene gas.
-------
* Post hazard and warning information in the work area. In
addition, as part of an ongoing education and training effort,
communicate all information on the health and safety hazards
of Propylene to potentially exposed workers.
This Fact Sheet is a summary source of information of all potential
and most severe health hazards that may result from exposure.
Duration of exposure, concentration of the substance and other
factors will affect your susceptibility to any of the potential
effects described below.
HEALTH HAZARD INFORMATION
Acute Health Effects
The following acute (short term) health effects may occur
immediately or shortly after exposure to Propylene:
* Exposure to high levels can cause you to feel dizzy and
lightheaded. Very high levels can make you pass out and even
die from lack of oxygen.
* Contact with liquefied Propylene can cause frostbite.
* Exposure may cause an irregular heart beat. This can cause
death.
Chronic Health Effects
The following chronic (long term) health effects can occur at some
time after exposure to Propylene and can last for months or years:
Cancer Hazard
* According to the information presently available to the New
Jersey Department of Health, Propylene has been tested and has
not been shown to cause cancer in animals.
Reproductive Hazard
* According to the information presently available to the New
Jersey Department of Health, Propylene has not been tested for
its ability to adversely affect reproduction.
Other Long Term Effects
* Propylene may damage the liver.
Medical Testing
If symptoms develop or overexposure is suspected, the following may
be useful:
* Liver function tests.
* Holter monitor (a special 24 hour EKG to look for irregular
heart beat).
Any evaluation should include a careful history of past and present
symptoms with an exam. Medical tests that look for damage already
done are not a substitute for controlling exposure.
-------
Printed From:
Common Name: Styrene Monomer
Common Name: Styrene Monomer
CAS Number: 100-42-5
DOT Number: UN 2055
Date: May, 1989
HAZARD SUMMARY
* Styrene Monomer can affect you when breathed and by passing
through skin.
* Because this is a MUTAGEN, handle it as a possible cancer
causing substance WITH EXTREME CAUTION.
* It may also damage the fetus.
* Exposure can irritate the eyes, nose, and throat. Higher
levels can cause you to feel dizzy, lightheaded, and to pass
out. Very high levels could cause brain and liver damage, and
death.
* Repeated exposure to lower levels can cause trouble
concentrating, memory problems, and affect learning ability.
* It is a FLAMMABLE and REACTIVE CHEMICAL and a FIRE and
EXPLOSION HAZARD.
IDENTIFICATION
Styrene Monomer is a colorless oily liquid with an aromatic odor.
It is used in making polystyrene plastics, protective coatings,
polyesters, resins, and as a chemical intermediate.
REASON FOR CITATION
* Styrene Monomer is on the Hazardous Substance List because it
is regulated by OSHA and cited by ACGIH, NIOSH, DOT, DEP, NFPA
and EPA.
* This chemical is also on the Special Health Hazard Substance
List because it is a MUTAGEN, FLAMMABLE, and REACTIVE.
* Definitions are attached.
HOW TO DETERMINE IF YOU ARE BEING EXPOSED
* Exposure to hazardous substances should be routinely
evaluated. This may include collecting air samples. Under OSHA
1910.20, you have a legal right to obtain copies of sampling
results from your employer. If you think you are experiencing
any work related health problems, see a doctor trained to
recognize occupational diseases. Take this Fact Sheet with
you.
* ODOR THRESHOLD = 0.08 ppm.
* The odor threshold only serves as a warning of exposure. Not
smelling it does not mean you are not being exposed.
WORKPLACE EXPOSURE LIMITS
OSHA: The legal airborne permissible exposure limit (PEL) is 50
ppm averaged over an 8 hour workshift and 100 ppm not to
be exceeded during any (15 minute) work period.
NIOSH: The recommended airborne exposure limit is 50 ppm
averaged over a 10 hour workshift and 100 ppm, not to be
exceeded during any 15 minute work period.
* Styrene Monomer is a MUTAGEN. Mutagens may have a cancer risk.
All contact with this chemical should be reduced to the lowest
possible level.
-------
* The above exposure limits are for air levels only.
WAYS OF REDUCING EXPOSURE
* Where possible, enclose operations and use local exhaust
ventilation at the site of chemical release. If local exhaust
ventilation or enclosure is not used, respirators should be
worn.
* Wear protective work clothing.
* Wash thoroughly immediately after exposure to Styrene Monomer
and at the end of the workshift.
* Post hazard and warning information in the work area. In
addition, as part of an ongoing education and training effort,
communicate all information on the health and safety hazards
of Styrene Monomer to potentially exposed workers.
This Fact Sheet is a summary source of information of all potential
and most severe health hazards that may result from exposure.
Duration of exposure, concentration of the substance and other
factors will affect your susceptibility to any of the potential
effects described below.
HEALTH HAZARD INFORMATION
Acute Health Effects
The following acute (short term) health effects may occur
immediately or shortly after exposure to Styrene Monomer:
* Exposure can irritate the eyes, nose, throat and skin. Higher
levels can cause you to feel dizzy, lightheaded, and to pass
out. Very high levels could cause brain and liver damage and
death.
* Contact can irritate the skin and eyes.
Chronic Health Effects
The following chronic (long term) health effects can occur at some
time after exposure to Styrene Monomer and can last for months or
years:
Cancer Hazard
* Styrene Monomer causes MUTATIONS (genetic changes). Such
chemicals may have a cancer risk, and in fact, there is
limited evidence that it causes cancer of the lung in animals.
* Many scientists believe there is no safe level of exposure to
a cancer causing agent. Such substances may also have the
potential for causing reproductive damage in humans.
Reproductive Hazard
* Styrene Monomer may damage the developing fetus.
* There is limited evidence that it may decrease fertility in
females.
Other Long Term Effects
* Repeated exposure can cause memory and concentration problems,
difficulty in learning, slowed reflexes, and trouble with
balancing.
* Styrene Monomer can cause headaches, drowsiness, numbness and
stomach upset.
Medical Testing
-------
For those with frequent or potentially high exposure (half the TLV
or greater, or significant skin contact), the following is
recommended before beginning work and at regular times after that:
* Exam of the nervous system.
If symptoms develop or overexposure is suspected, the following may
be useful:
* EEG (brain wave study) ..
* Interview for brain effects, including recent memory, mood
(irritability, withdrawal), concentration, headaches, malaise
and altered sleep patterns. Consider cerebellar, autonomic and
peripheral nervous system evaluation. Positive and borderline
individuals should be referred for neuropsychological testing.
-------
Printed From:
Common Name: Styrene Oxide
Common Name: Styrene Oxide
CAS Number: 96-09-3
DOT Number: None
DATE: December, 1989
HAZARD SUMMARY
* Styrene Oxide can affect you when breathed in and may be
absorbed through the skin.
* Styrene Oxide should be handled as a CARCINOGEN and a
TERATOGEN--HANDLE WITH EXTREME CAUTION.
* Styrene Oxide can irritate the skin and eyes. Long term
exposure may cause dermatitis.
* Breathing Styrene Oxide can irritate the nose and throat.
* Styrene Oxide can cause headache, nausea, vomiting,
dizziness, drowsiness and to pass out.
* Very high levels could cause nervous system depression, liver
damage, anemia and may cause death.
IDENTIFICATION
Styrene Oxide is a colorless to straw-colored liquid. It is used
as a chemical intermediate in cosmetics and in making other
chemicals, and as a catalyst and cross-linking agent for epoxy
resins.
REASON FOR CITATION
* Styrene Oxide is on the Hazardous Substance List because it is
cited by DEP, IARC, NFPA and EPA.
* This chemical is on the Special Health Hazard Substance List
because it is a CARCINOGEN and a TERATOGEN.
* Definitions are attached.
HOW TO DETERMINE IF YOU ARE BEING EXPOSED
* Exposure to hazardous substance should be routinely evaluated.
This may include collecting personal and area air samples.
You can obtain copies of sampling results from your employer.
You have a legal right to this information, under OSHA 1910.20.
* If you think you are experiencing any work-related health
problems, see a doctor trained to recognize occupational
diseases. Take this Fact Sheet with you.
WORKPLACE EXPOSURE LIMITS
No occupational exposure limits have been established for Styrene
Oxide. This does not mean that this substance is not harmful.
Safe work practices should always be followed.
It should be recognized that Styrene Oxide can be absorbed through
your skin, thereby increasing your exposure.
* Styrene Oxide may be a PROBABLE CARCINOGEN in humans. There
may be no safe level of exposure to a carcinogen, so all
contact should be reduced to the lowest possible level.
* Styrene Oxide is a Teratogen in humans. All contact with this
chemical should be reduced to the lowest possible level.
WAYS OF REDUCING EXPOSURE
* Where possible, enclose operations and use local exhaust
-------
ventilation at the site of chemical release. If local exhaust
ventilation or enclosure is not used, respirators should be
worn.
* A regulated, marked area should be established where Styrene
Oxide is handled, used, or stored.
* Wear protective work clothing.
* Wash thoroughly immediately after exposure to Styrene Oxide
and the end of the workshift.
* Post hazard and warning information in the work area. In
addition, as part of an ongoing education and training effort,
communicate all information on the health and safety hazards
of Styrene Oxide to potentially exposed workers.
This Fact Sheet is a summary source of information of all potential
and most severe health hazards that may result from exposure.
Duration of exposure, concentration of the substance and other
factors will affect your susceptibility to any of the potential
effects described below.
HEALTH HAZARD INFORMATION
Acute Health Effects
The following acute (short-term) health effects may occur
immediately or shortly after exposure to Styrene Oxide:
* Contact can irritate the skin and eyes.
* Breathing Styrene Oxide can irritate the nose and throat'.
* Exposure to high concentrations can cause headache, nausea,
vomiting, dizziness, drowsiness and to pass out.
Chronic Health Effects
The following chronic (long-term) health effects can occur at some
time after exposure to Styrene Oxide and can last for months or
years:
Cancer Hazard
* Styrene Oxide causes MUTATIONS (genetic changes). Such
chemicals may have a cancer or reproductive risk.
* Styrene a closely related chemical, is a PROBABLE CARCINOGEN
in humans. There is. some evidence that Styrene causes
leukemia and lymphoma in humans and Styrene has been shown to
cause lung and stomach cancer in animals.
* Many scientists believe there is no safe level of exposure to
a carcinogen.
Reproductive Hazard
* Styrene Oxide may be a TERATOGEN in humans since it has been
shown to be a teratogen in animals.
* Styrene Oxide has caused CANCER in the offspring of animals
exposed during pregnancy.
Other Long-Term Effects
* Repeated overexposure may cause drying, cracking, and rash
(dermatitis) of the skin.
* This chemical has not been adequately evaluated to determine
whether brain or other nerve damage could occur with repeated
exposure. However, many solvents and other petroleum-based
chemicals have been shown to cause such damage. Effects may
include reduced memory and concentration, personality changes
(withdrawal, irritability), fatigue, sleep disturbances,
-------
reduced coordination, and/or effects on nerves supplying
internal organs (autonomic nerves) and/or nerves to the arms
and legs (weakness, "pins and needles").
* Styrene Oxide may damage the liver, and may cause anemia.
MEDICAL
Medical Testing
For those with frequent or potentially high exposure (half the TLV
or greater), the following are recommended before beginning work
and at regular times after that:
* Liver and function tests.
* Complete blood count.
* Interview for brain symptoms, including recent memory, mood
(irritability, withdrawal), concentration, headaches, malaise
and altered sleep patterns. Consider 'cerebellar, autonomic
and peripheral nervous system evaluation. Positive and
borderline individuals should be referred for
neuropsychological testing.
Any evaluation should include a careful history of past and present
symptoms with an exam. Medical test that look for damage already
done are not a substitute for controlling exposure.
-------
Printed From:
Common Name: Toluene
Common Name: Toluene
CAS Number: 108-88-3
DOT Number: UN 1294
Date: November 3, 1986
HAZARD SUMMARY
* Toluene can affect you when breathed in and by passing through
your skin.
* Toluene may cause mutations. Handle with extreme caution.
* It may damage the developing fetus.
* Toluene is a FLAMMABLE LIQUID and a FIRE HAZARD.
* Exposure can irritate the nose, throat, and eyes. Higher
levels can cause you to feel dizzy, lightheaded, and to pass
out. Death can occur.
* Repeated exposures can damage bone marrow causing low blood
cell count. It can also damage the liver and kidneys.
* Toluene can cause slowed reflexes, trouble concentrating, and
headaches.
* Prolonged contact can cause a skin rash.
IDENTIFICATION
Toluene is a colorless liquid with a sweet pungent odor. It is used
as a solvent and in aviation gasoline, making other chemicals,
perfumes, medicines, dyes, explosives, and detergents.
REASON FOR CITATION
* Toluene is on the Workplace Substance List because it is
regulated by OSHA and cited by ACGIH, DOT, NIOSH, NFPA and
other authorities. .
* This chemical is on the Special Health Hazard Substance List
because it is FLAMMABLE.
* Definitions are attached.
HOW TO DETERMINE IF YOU ARE BEING EXPOSED
* Exposure to hazardous substances should be routinely
evaluated. This may include collecting air samples. Under OSHA
1910.20, you have a legal right to obtain copies of sampling
results from your employer. If you think you are experiencing
any work related health problems, see a doctor trained to
recognize occupational diseases. Take this Fact Sheet with
you.
* ODOR THRESHOLD =2.9 ppm.
* The odor threshold only serves as a warning of exposure.. Not
smelling it does not mean you are not being exposed.
WORKPLACE EXPOSURE LIMITS
OSHA: The legal airborne permissible exposure limit (PEL) is
200 ppm averaged over an 8 hour workshift and 300 ppm,
not to be exceeded during any 15 minute work period and
a maximum peak concentration of 500 ppm.
NIOSH: The recommended airborne exposure limit is 100 ppm
averaged over an 8 hour workshift and 200 ppm, not to be
exceeded during any 10 minute work period.
* The above exposure limits are for air levels only.
* Toluene may cause mutations. All contact with this chemical
-------
should be reduced to the lowest possible level.
WAYS OF REDUCING EXPOSURE
* Where possible, enclose operations and use local exhaust
ventilation at the site of chemical release. If local exhaust
ventilation or enclosure is not used, respirators should be
worn.
* Wear protective work clothing.
* Wash thoroughly immediately after exposure to Toluene and at
the end of the workshift.
* Post hazard and warning information in the work area. In
addition, as part of an ongoing education and training effort,
communicate all information on the health and safety hazards
of Toluene to potentially exposed workers.
This Fact Sheet is a summary source of information of all potential
and most severe health hazards that may result from exposure.
Duration of exposure, concentration of the substance and other
factors will affect your susceptibility to any of the potential
effects described below.
HEALTH HAZARD INFORMATION
Acute Health Effects
The following acute (short term) health effects may occur
immediately or shortly after exposure to Toluene:
* Exposure can irritate the nose, throat, and eyes. Higher
levels can cause you to feel dizzy, lightheaded, and to pass
out. Death can occur.
* Lower levels may cause trouble concentrating, headaches, and
slowed reflexes.
Chronic Health Effects
The following chronic (long term) health effects can occur at some
time after exposure to Toluene and can last for months or years:
Cancer Hazard
* Toluene may cause mutations (genetic changes) in living cells.
Whether or not it poses a cancer hazard needs further study.
Reproductive Hazard
* Toluene may damage the developing fetus.
Other Long Term Effects
* Repeated exposure may damage bone marrow, causing low blood
cell count.
* Prolonged contact can cause drying and cracking of the skin,
and a rash.
* Repeated Toluene exposure can cause headaches, loss of
appetite, nausea, and liver and kidney damage, and may cause
brain damage.
MEDICAL TESTING
For those with frequent or potentially high exposure (half the TLV
or greater, or significant skin contact), the following
is recommended before beginning work and at regular times after
that:
-------
* Urinary Hippuric acid excretion (at the end of shift) as an
index of overexposure.
If symptoms develop or overexposure is suspected, the following may
be useful:
* Exam of the nervous system.
* Liver and kidney function tests, and evaluation for renal
tubular acidosis.
* Complete blood count.
Any evaluation should include a careful history of past and present
symptoms with an exam. Medical tests that look for damage already
done are not a substitute for controlling exposure.
-------
APPENDIX XI
HEALTH DATA: BACKGROUND INFORMATION ON MAJOR CAUSES OF
MORBIDITY AND MORTALITY
CARDIOVASCULAR DISEASES1
Since 1900, cardiovascular diseases have been the number one killer in the United
States (except for 1918). Of the current U.S. population (258 million), more than 60 million
people have some form of these diseases. Cardiovascular disease is the general term for
diseases of the heart, blood vessels, and the circulatory system. The following sections
describe some of the more common cardiovascular diseases.
Atherosclerosis
Atherosclerosis is a major cause of cardiovascular disease, and is the leading cause of
death from heart attack and stroke. Atherosclerosis affects large and medium-sized arteries,
and is characterized by deposits of fatty substances, cholesterol, cellular waste products,
calcium and fibrin (a clotting material in the blood) in the inner lining of an artery. The
resulting build up is called plaque. As the interior walls of arteries become lined with layers
of these deposits, the arteries narrow, and the flow of blood through them is reduced. This
decreases oxygen supply to the heart (leading to heart attacks), brain (leading to strokes) or the
arms and legs (leading to gangrene).
Atherosclerosis is a slow, progressive disease, which may be evidenced in childhood.
In some individuals, this disease progresses rapidly in their third decade; hi others it does not
become threatening until they are in their 50s or 60s. Among the causes of damage to arterial
walls leading to atherosclerosis are: 1) elevated levels of cholesterol and triglyceride hi the
blood, 2) high blood pressure, 3) cigarette smoke, and 4) diabetes.
High blood pressure
Blood pressure is the result of forces created by the heart pumping blood into the .
arteries, while the arterial blood vessels exert resistance to the blood flow from the heart.
Blood pressure is measured using an instrument called a sphygmomanometer and is measured
in millimeters of mercury (mmHg). Two measurements are recorded: 1) systolic pressure is
the pressure of the blood flow when the heart beats, and 2) diastolic pressure is the pressure
between heartbeats. For example, a blood pressure reading for an adult might be 122/72
mmHg, the first number is the systolic pressure and the second is diastolic pressure. For most
adults, a blood pressure reading that is less than 140/90 mmHg indicates that there is no cause
for worry. However, in adults high blood pressure (hypertension) exists when systolic
1 American Heart Association. "Heart and Stroke Facts." http://www.amhrt.org/1996/list.html (November,
1996).
XI-1
-------
pressure is equal to or greater than 140 mmHg and/or diastolic pressure is equal to or greater
than 90 mmHg for extended periods of time.
High blood pressure means that the heart is working harder than normal, putting both
the heart and the arteries under a greater strain. This may contribute to heart attacks, strokes,
kidney failures and atherosclerosis. If high blood pressure is not treated, the heart works
progressively harder to pump enough blood and oxygen to meet the body's organs and tissues.
When the heart is forced to work harder than normal for an extended tune, it tends to enlarge.
A slightly enlarged heart may function well, but one that is significantly enlarged may have
difficulty providing sufficient flow of blood to the body's organs and tissues.
Arteries and arterioles also suffer from the effects of high blood pressure. Over time
they become scarred, hardened and less elastic. This may occur as people age, but high blood
pressure accelerates this process, probably because hypertension speeds atherosclerosis.
Coronary Heart Diseases (heart attacks) and Angina (chest pain)
Heart attacks result from blood vessel disease hi the heart. Coronary heart disease or
coronary artery disease are general names for heart attack which occurs when the blood supply
to part of the heart muscle itself is severely reduced or stopped. This occurs when one of the
coronary arteries (arteries that supply blood to the heart muscle) is blocked by an obstruction,
such as a blood clot that has formed due to atherosclerosis. If the blood supply is cut off
drastically or for an extended time, muscle cells suffer irreversible injury and die. Disability
or death can result, depending on how much heart muscle is damaged.
Angina — Chest pain called angina pectoris is another result of coronary artery disease.
Angina is a symptom of a condition called myocardial ischemia, which occurs when the heart
muscle (myocardium) does not get as much blood (hence oxygen) as it needs for a given level
of work. Lack of blood supply is called ischemia.
Angina can occur when blood circulation to the heart is enough for normal needs but
not sufficient when the heart's needs increase, such as during physical exertion or emotional
excitement. Angina can be a warning sign that someone is at risk of heart attack.
Arrhythmias and Sudden Cardiac Death
Normal cardiac rhythm results from electrical impulses that start hi the sinoatrial (SA
or sinus) node. They spread through the atria to the atrioventricular (AV) node. These
impulses travel over the many specialized fibers of the His-Purkinje system, distributing the
electrical "ignition signal" to the ventricular muscle cells. The transmission of impulses is
delayed a fraction within the AV node. This allows time for the atrial contraction which helps
fill the ventricles with blood.
XI-2
-------
The term arrhythmia refers to any change from the normal sequence of beginning and
conducting impulses. Some arrhythmias are so brief that the overall heart rate is not greatly
affected. However, if arrhythmias last for extended periods the heart rate may be too slow or
too fast. Arrhythmias can produce a broad range of symptoms, from barely perceptible to
cardiovascular collapse and death. The term bradycardia is used to describe a rate of less than
60 beats per minute. Tachycardia usually refers to a heart rate of more than 100 beats per
minute.
The prevalence of atrial and ventricular arrhythmias tends to increase with age, even
when there is no overt sign of heart disease. Certain congenital conditions may also make a
person prone to arrhythmias. For example, an incompletely developed conduction system can
cause chronic heart block and bradycardia. Additionally, individuals with extra conduction
pathways, either near the AV node or bridging the atria and ventricles, are prone to reentrant
supraventricular tachycardias.
Acquired heart disease is the most important factor predisposing a person to
arrhythmias. The main causes are atherosclerosis, hypertension, and inflammatory or
degenerative conditions. The scarring or abnormal tissues found with these diseases can cause
bradycardias. Many chemical agents may provoke arrhythmias, sometimes with serious
consequences. Known factors include high or low blood and tissue concentrations of a variety
of minerals, such as potassium, magnesium and calcium.
Sudden Cardiac Death (SCD) is the sudden, abrupt loss of heart function (i.e., cardiac
arrest) in a person who may or may not have diagnosed heart disease, but in whom the time
and mode of death occur unexpectedly. The unexpected nature of the event is the key point in
the definition. About half of all deaths from heart disease are sudden and unexpected,
regardless of the underlying disease. Thus 50% of all deaths due to atherosclerosis of the
coronary arteries are sudden, as are 50% of deaths due to degeneration of the heart muscle, or
to cardiac enlargement in patients with high blood pressure. SCD is the result of an
unresuscitated cardiac arrest, which may be caused by almost all known heart diseases. Most
cardiac arrests are due to rapid and/or chaotic activity of the heart (ventricular tachycardia or
fibrillation); some are due to extreme slowing of the heart. These events are called life-
threatening arrhythmias and are responsible for sudden death.
Congestive Heart Failure
Congestive heart failure is a condition that occurs because the heart muscle is damaged
or overworked. This damage can result from high blood pressure, a heart attack,
atherosclerosis, a congenital heart defect, heart muscle disease, heart valve disease, infection
of the heart valves or heart muscle itself, or high blood pressure in the lungs resulting from
lung disease. When the heart it is damaged, it lacks the strength to keep blood circulating
normally throughout the body. As blood flow out of the heart slows, blood returning to the
heart through veins backs up, causing congestion in the tissues. Swelling often results, most
XI-3
-------
commonly in the legs and ankles, but can occur in the lungs which interferes with breathing,
causing shortness of breath, especially when a person is lying down. Heart failure also affects
the ability of the kidneys to dispose of sodium and water and, the retained water increases
swelling.
Congenital Heart Defects
A congenital heart defect occurs when the heart or blood vessels near the heart do not
develop normally before birth. Congenital heart defects are present in about 1 % of live births
and are the most frequent congenital malformations in newborns. In most cases, there is no
scientific explanation as to why they occur.
Most heart defects either 1) obstruct blood flow in the heart or vessels near it or 2)
cause blood to flow through the heart hi an abnormal pattern. An obstruction (stenosis) is a
narrowing that partially or completely blocks the flow of blood. Obstructions can occur in
heart valves, arteries or veins. The three most common forms of obstructed blood flow are
pulmonary valve stenosis, aortic valve stenosis, and coarctation of the aorta. In pulmonary
stenosis, the pulmonary valve (which lets blood flow from the right ventricle to the lungs) is
narrowed. As a result, the right ventricle must pump harder to overcome the obstruction. In
aortic stenosis, the aortic valve (between the left ventricle and the aorta) is narrowed. This
makes it hard for the heart to pump blood to the body. In coarctation of the aorta, the aorta is
pinched or constricted. This obstructs blood flow to the lower part of the body and increases
blood pressure above the constriction.
Some congenital heart defects allow blood to flow between the right and left chambers
of the heart. This happens when a baby is born with an opening between the wall (septum)
that separates the right and left sides of the heart. The two most common types of such
openings are atrial septal defect and ventricular septal defect. In atrial septal defect, some
blood from the left atrium is allowed to return to the right atrium instead of flowing through
the left ventricle to the aorta and to the rest of the body. In ventricular septal defect, some
blood in the left ventricle flows to the right ventricle through the opening instead of being
pumped into the aorta.
Another defect, patent ductus arteriosus, allows blood to mix between the pulmonary
artery and the aorta. Before birth, there is an open passageway (the ductus arteriosus) between
these two blood vessels. Normally this closes within a few hours after birth. When this does
not happen, some oxygen-rich blood that should flow through the aorta to the body is returned
to the lungs. This defect is common hi premature babies but rare hi full term babies.
Another classification of heart abnormalities is congenital cyanotic heart defects. In
these defects, blood pumped to the body contains less-than-normal amounts of oxygen. This
results hi a condition called cyanosis or "blue babies". Two examples of cyanotic defects are
tetralogy ofFallot and transposition of the great arteries. Tetralogy of Fallot has four
XI-4
-------
components: 1) ventricular septal defect, 2) a narrowing at or just beneath the pulmonary
valve, 3) the right ventricle is more muscular than normal, and 4) the aorta lies directly over
the ventricular septal defect.
In transposition of the great arteries, the position of the pulmonary artery and the aorta
are reversed. The aorta is connected to the right ventricle, so most of the blood returning to
the heart from the body is pumped back out to the body without first going to the lungs. The
pulmonary artery is connected to the left ventricle so that most of the oxygen-rich blood
returning from the lungs goes back to the lungs again. In this type of a defect, some type of
opening, such as an atrial septal defect or ventricular septal defect, also exists.
Rheumatic Heart Disease
Rheumatic heart disease is a condition in which the heart valves are damaged by a
disease process that begins with a strep throat. If it is not treated, the streptococcal infection
can develop into acute rheumatic fever. It is an inflammatory disease that can affect many
connective tissues in the body, especially those of the heart, the joints, the brain or the skin.
When rheumatic fever permanently damages the heart, the damage is called rheumatic heart
disease.
A damaged heart valve is one that does not completely close or does not completely
open. When a heart valve does not completely close, blood is allowed to leak back into the
chamber from which it was pumped. This is called regurgitation or leakage. With the next
heartbeat, regurgitated blood flows through the valve and mixes with blood that flows
normally. This extra volume of blood passing through the heart puts added strain on the heart
muscle. When a valve does not open enough, the heart must pump harder than normal to
force blood through the narrowed opening. Usually there are no symptoms of this until the
valve opening becomes very narrow.
The symptoms vary greatly from person to person. Often the damage to heart valves is
not immediately noticeable. Some people have no problem for years; others feel only mild
discomfort for years. Eventually damaged heart valves can cause serious, even disabling
problems. These problems depend on the severity of the damage and on which heart valve is
affected.
Kawasaki disease
Kawasaki disease is a children's illness and tends to strike most often under the age of
8. Boys are almost twice as likely to get it as girls. The disease also tends to appear more
often among those of Asian ancestry. Fever, rash, swollen hands and feet, redness of the
whi;es of the eyes, swollen lymph glands in the neck, and irritation and inflammation of the
mouth, lips and throat all characterize Kawasaki disease. The cause of Kawasaki is unknown;
it is not hereditary or contagious.
XI-5
-------
In as many as 20% of the children with Kawasaki disease, the heart is affected. The
coronary arteries are most often affected. Often, part of a coronary wall can be weakened and
will balloon in an aneurysm. A blood clot can form in this weakened area and block the
artery, sometimes leading to a heart attack. In rare instances, the aneurysm can burst. Other
cardiac changes include inflammation of the heart muscle (myocarditis) or of the sac
surrounding the heart (pericarditis). Arrhythmias or abnormal functioning of some heart
valves also can occur. Usually, the cardiac problems recede in 5 to 6 weeks, and there is no
lasting damage; however, sometimes coronary artery damage persists.
Prevalence
According to current estimates, 60,340,000 Americans have one or more types of
cardiovascular disease. About 1 in 5 males and females have some form of major
cardiovascular disease.2>3
Hypertension - About 50 million Americans age 6 and older have high blood pressure.4
Coronary heart disease — Approximately 13,490,000 people alive today have a history of
heart attack, angina pectoris (chest pain), or both.5
Arrhythmias - Approximately 4,154,000 Americans had arrhythmias in 1993.
Atherosclerosis - An estimated 1,789,000 Americans had "hardening of the arteries" in 1993.
Rheumatic heart disease - An estimated 1,360,000 Americans have rheumatic heart disease.
Many of the 66,000 annual operations on valves are due to rheumatic heart disease.6
2 American Heart Association. Heart and Stroke Facts, http://www.amhrt.org/1996/list.html (November,
1996).
(Note: This data was originally reported by the National Center for Health Statistics, Phase I, National Health and
Nutrition Examination Survey HI (NHANES III), 1988-91.)
3 American Heart Association. Heart and Stroke Facts. http://www.amhrt.org/1996Aist.html (November,
1996).
(Note: This data was originally reported by the National Center for Health Statistics, National Health and Nutrition
Examination Survey (NHANES II), 1976-80.)
4 American Heart Association. Heart and Stroke Facts. http://www.amhrt.org/1996Aist.html (November,
1996).
(Note: This data was originally reported by the National Center for Health Statistics, Phase I, National Health and
Nutrition Examination Survey III (NHANES III), 1988-91.)
5 Ibid.
6 American Heart Association. Heart and Stroke Facts. http://www.amhrt.org/1996Aist.html (November,
1996).
(Note: This data was originally reported by the National Center for Health Statistics, National Health and Nutrition
Examination Survey (NHANES II), 1976-80.)
XI-6
-------
Mortality7
Cardiovascular diseases claimed 954,138 lives in the United States in 1993. This is
42.1 % of all deaths or 1 of every 2.4 deaths. The 1992 U.S. mortality data show that
cardiovascular diseases account for 48.1% of all male and 51.9% of all female deaths.
From 1983 to 1993 death rates from cardiovascular diseases declined 23.1%. Despite
this decline in the death rates, hi the same period the actual number of deaths declined only
3.8%. However, in 1993 total deaths from these diseases increased significantly. One reason
is that the population of middle-aged and older people is increasing. Another reason is that
advances in medical treatment have allowed more people to survive previously fatal
cardiovascular events, but now these people are dying of subsequent cardiovascular illnesses.
For example, heart attack victims whose lives were saved by better emergency care may now
be dying of congestive heart failure.
Coronary heart diseases - Heart attack is the single largest killer of American males and
females. About every minute someone will die from a heart attack. 489,970 people died
from heart attacks in the U.S. hi 1993.
Arrhythmias -- Arrhythmias caused 40,843 deaths hi the U.S. hi 1992.
Hypertension - High blood pressure killed 37,520 Americans hi 1993 and contributed to the
deaths of thousands more through stroke, heart attack and heart failure. One hi four American
adults has high blood pressure.
Congestive heart failure - Congestive heart failure killed 36,387 Americans in 1992. It is a
contributing cause hi an estimated 250,000 deaths a year.
Atherosclerosis -- Atherosclerosis killed approximately 17,090 Americans hi 1993. It is also a
leading cause of many deaths from heart attack and stroke.
Major Risk Factors
Heredity - Heart disease and atherosclerosis appear to have a large hereditary component.
That means that children of parents with cardiovascular disease are more likely to develop it
themselves.
Race — African-Americans have moderate high blood pressure twice as often as white and
severe hypertension three tunes as often. Consequently, their risk of heart disease is greater.
Gender — Males have a greater risk of heart attack than females earlier hi life. After
menopause, the death rate from heart disease increases among females.
Age - About four out of five people who die of heart attack are age 65 or older. At older
ages, women who have heart attacks are twicQ as likely as men to die within a few weeks of
the attack.
7American Heart Association. Heart and Stroke Facts: 1996 Statistical Supplement.
http://www.amhrt.org/1996/list.html (November, 1996).
XI-7
-------
Hypertension — High blood pressure usually has no specific symptoms and no early warning
signs. It is truly a "silent killer." High blood pressure increases the heart's workload,
causing the heart to enlarge and weaken over time. It also increases the risk of stroke, heart
attack, kidney failure and congestive heart failure. When high blood pressure exists with
obesity, smoking, high blood cholesterol levels or diabetes, the risk of heart attack or stroke
increases several times.
As a rule, blood pressure tends to increase with age. Men are at greater risk for high
blood pressure than women until age 55. From age 55 to 74 the risks for men and women are
about equal; after that, women are at greater risk than men.
Blacks, Puerto Ricans, and Cuban- and Mexican Americans are more likely to suffer
from high blood pressure than Anglo-Americans. Black and whites in the Southeastern US
have a greater prevalence of high blood pressure and higher death rate from stroke than those
from other regions of the country.
Cigarette/Tobacco Smoke — In recent years, studies have shown cigarette smoking to be an
important risk factor. The risks of heart attack in smokers are more than twice that of
nonsmokers. In fact, cigarette smoking is the greatest risk factor for sudden cardiac death;
smokers have two to four times the risk of nonsmokers. Evidence also indicates that chronic
exposure to environmental tobacco smoke increases the risk of heart disease. The risk of death
due to heart disease is increased about 30% among those exposed to environmental tobacco
smoke at home and could be much higher hi those exposed hi the workplace, where higher
levels of environmental tobacco smoke may be present.
Nearly one-fifth of deaths from cardiovascular diseases are attributable to smoking. It
is also estimated that about 37,000 to 40,000 nonsmokers die each year from cardiovascular
diseases as a result of exposure to environmental tobacco smoke.
Cholesterol — High blood cholesterol increases the risk of coronary heart disease. When
other risk factors, such as high blood pressure and cigarette/tobacco smoke are present, this
risk increases even more. A person's cholesterol level is also affected by age, sex, heredity
and diet.
A certain amount of cholesterol in the body is necessary to build cell membranes.
However, the liver produces enough cholesterol to meet these needs. A diet high hi saturated
fat and cholesterol tends to raise blood cholesterol; a diet low hi saturated fat and cholesterol
usually means lower levels of blood cholesterol.
Physical Inactivity — Physical inactivity or sedentary lifestyle is a risk factor for coronary
heart disease. Physical inactivity can lead to several changes that are risk factors for heart
disease. When lack of exercise is combined with overeating and excess weight, increased
blood cholesterol levels can result - and these unquestionably contribute to the risk of heart
disease.
XI-8
-------
The relative risk of coronary heart disease associated with physical inactivity ranges
from 1.5 to 2.4, an increased risk comparable with that observed for high cholesterol, high
blood pressure and cigarette smoking. Less active, less fit persons have a 30-50 % greater risk
of developing high blood pressure.
Chemical Agents — Many chemical agents may provoke arrhythmias, sometimes with serious
consequences. Known factors include high or low blood and tissue concentrations of a variety
of minerals, such as potassium, magnesium, and calcium. These minerals play a vital role hi
starting and conducting normal impulses in the heart. Substances such as alcohol, cigarettes,
and recreational drugs, can provoke arrhythmias, as can various cardiac medications.
Contributing Risk Factors
Obesity — People who are overweight or obese are more likely to develop heart disease and
stroke even if they have no other risk factors. Excess weight is unhealthy because it increases
the strain on the heart. It is linked with coronary heart disease mainly because it influences
blood pressure and blood cholesterol and can lead to diabetes.
Recent evidence indicates that how fat is distributed in the body may affect the risk of
coronary heart disease. A waist/hip ratio greater than 1.0 for men indicates a significantly
increased risk. For women it is 0.8. This means that a man's waist measurement should not
exceed his hip measurement, and a woman's waist measurement should not be more than 80%
of her hip measurement.
Based upon NHANES III (1988-91) data, an estimated 61 million American adults are
20% or more above their desirable weight.
Diabetes — Diabetes is the inability of the body to produce or respond properly to insulin.
Insulin is needed for the body to metabolize or use glucose (sugar). Diabetes appears most
often hi middle age and among overweight people. In a mild form, it can go undetected for
many years. Besides increasing the risks of kidney disease, blindness, nerve and blood vessel
damage, diabetes also seriously increases the risk of developing cardiovascular disease. In
fact, more than 80% of people with diabetes die of some form of heart or blood vessel disease.
Part of the reason for this is that diabetes affects cholesterol and triglyceride levels. Many
times, diabetics also have hypertension, increasing their risk of stroke.
Stress - Some scientists have noted a relationship between coronary heart disease risk and a
person's life stress, behavioral habits and socioeconomic status. These factors may affect
established risk factors. For example, people under stress may start smoking or smoke more
than they otherwise would.
XI-9
-------
CEREBROVASCULAR DISEASE (STROKE)
Stroke is a form of cardiovascular disease that affects the arteries of the central nervous
system. A stroke occurs when a blood vessel bringing oxygen and nutrients to the brain bursts
or is clogged by a blood clot or some other particle. Because of this rupture or blockage, part
of the brain does not get the flow of blood it needs. Deprived of oxygen, nerve cells hi the
affected area of the brain cannot function and die within minutes. When nerve cells do not
function, the part of the body controlled by these cells does not function. The devastating
effects of stroke are often permanent since dead brain cells cannot be replaced.
There are four types of stroke: two caused by clots (ischemic strokes), and two by
hemorrhage. Cerebral thrombosis and cerebral embolism are by far the most common,
accounting for 70-80% of all strokes. They are caused by clots that plug an artery. Cerebral
and subarachnoid hemorrhages are caused by ruptured blood vessels. They have a much
higher fatality rate than strokes caused by clots.
Strokes affect different people in different ways, depending on the type of stroke and
the area of the brain affected. Brain injury from a stroke can affect the senses, speech, and the
ability to understand speech, behavioral patterns, thought patterns and memory. Paralysis on
one side of the body is common. Stroke also can cause depression, as survivors think they are
now less than "whole."
Prevalence — Approximately 3,820,000 stroke victims are alive today. Of this number, 45%
are male; 52% female.8
Mortality - Stroke killed 149,740 people in 1993 and accounted for about one of every 15
U.S. deaths. According to the National Center for Health Statistics, stroke is the third largest
cause of death, ranking behind diseases of the heart and cancer.
Major Risk Factors
Hypertension—High blood pressure is the most important risk factor for stroke. Stroke risk
varies directly with blood pressure.
Cigarette Smoking-ln recent years, studies have shown cigarette smoking to be an important
risk factor for stroke. Inhaling cigarette smoke produces a number of effects damaging to the
cardiovascular system. Nicotine in tobacco smoke increases a person's blood pressure.
Cigarette smoke also causes platelets hi the blood to become sticky and cluster, shortens
platelet survival, decreases clotting tune and increases blood thickness.
8American Heart Association. Heart and Stroke Facts, http://www.amhrt.org/1996/list.html (November,
1996).
Note: This data was originally reported by the National Center for Health Statistics, Phase I, National Health and
Nutrition Examination Survey III (NHANES III), 1988-91.
XI-10
-------
Heart diseases - A diseased heart increases the risk of stroke. Atrial fibrillation is particularly
problematic. Independent of blood pressure, people with heart problems have more than twice
the risk of stroke than people with normally functioning hearts.
Transient Ischemic Attacks (TIAs) -- Only about 10% of strokes are preceded by TIAs.
Nevertheless, TIAs are extremely important; they are strong predictors of stroke. TIAs are
usually treated with drugs that inhibit clots from forming.
High Red Blood Cell Count — A marked, or even moderate increase in the red blood cell
count is a risk factor for stroke. The reason is that increases in red blood cells thicken the
blood and make clots more likely.
Prior Stroke - The risk of stroke for someone who has already had one is many times that of
someone who has not.
Asymptomatic Carotid Bruit - a bruit is an abnormal sound heard when a stethoscope is
placed over an artery, in this case the carotid artery. Carotid bruit clearly indicates increased
stroke risk. However, a bruit mainly indicates atherosclerosis; it does not necessarily mean
the carotid artery will become clogged and a stroke will result.
Race—African-Americans have more than 60% greater risk of death and disability from stroke
than whites. Asian-Pacific Islanders and Hispanics also have a higher risk of stroke.
Gender—The incidence of stroke is about 19 percent higher for men than for women. For men
under age 65, the difference is even greater.
Age~The incidence of stroke is also strongly related to age. According to the American Heart
Association, only 28% of those who suffer a stroke in a given year are under the age of 65.
This means that 72% of stroke victims each year are over the age of 65. The stroke incidence
rate for those in the age group of 65-74 is about 1 % in a given year.9
Heredity-Stroke risk is greater for people who have a family history of stroke.
'American Heart Association. Heart and Stroke Facts:1996 Statistical Supplement.
http://www.amhrt.org/1996/list.html (November, 1996).
XI-11
-------
ASTHMA
Asthma is a respiratory condition that is characterized by 1) airway obstruction
(blocking) that is reversible or partly reversible; 2) airway inflammation (swelling); and 3)
increased airway responsiveness to a variety of stimuli that cause breathing difficulty such as
allergens, airborne irritants, exercise, viral infections, weather, and sometimes emotion.10
Episodes of wheezing, cough, shortness of breath, or chest tightness are common to
asthmatics. However, these symptoms can be conditions of other respiratory illnesses.
Presently, there is no universal definition of asthma. This is attributed to 1) a lack of
understanding of the underlying disease process, and 2) a lack of consensus among clinicians
and researchers on a definition specific to asthma that excludes conditions with characteristics
similar to asthma.
Why is Asthma a Concern?
Asthma effects over 14 million Americans, including 4.8 million children under the age
of 18.11 Over the past several decades, asthma has become more prevalent and severe, with
increased morbidity and mortality across all age groups. An overall increase in the.incidence
of asthma and health care utilization for asthma-related symptoms also has been observed. In
addition, the economic impact of asthma poses a tremendous burden on society, families, and
the poor. The estimated cost to manage asthma is 6.2 billion dollars per year with
hospitalizations and emergency room visits accounting for 50 percent of the costs.12 Asthma
exacts an indirect cost as well. It is the number one cause of absenteeism for schoolchildren
and a common reason for adult absenteeism from work. Among children 5 to 17 years of age,
asthma accounted for a loss of more than 10 million school days, at a cost of $726 million in
caretakers' time lost from work (including outside and domestic work). In 1985, adults 18
years or older lost nearly 3 million work days due to asthma-related illness, at a cost of $285
million.13
10U.S. Department of Health and Human Services, Guidelines for the Diagnosis and Management of
Asthma, Publication No. 91-3042, August 1991.
"American Lung Association, Childhood Asthma Fact Sheet, 1996, p. 2.
12Silbergeld, Ellen, "Investing in Prevention: Opportunities to Reduce Health Care Costs Through
Identifying and Reducing Environmental Contributions to Preventable Disease," New Solutions, Fall 1993,
pp. 37-51.
nWeiss, K.B., Gergen, P.J., and Hodgson, T.A., "An Economic Evaluation of Asthma in the United
States," The New England Journal of Medicine, vol. 326, March 26, 1992, pp. 862-866.
XI-12
-------
Prevalence
During the 1980s, the number of cases of reported asthma in the United States
increased by 42 percent.14 Prevalence increased 33 percent from 1970 to 1986, and 29 percent
from 1980 to 1987.15 From 1981 to 1988, asthma prevalence rates increased among children
under-18 years of age by 39 percent. Based on data collected from the National Health
Interview Study, prevalence of asthma has increased during the past decade with the largest
increase among younger age groups. The study found that 4.3 percent of all children less than
17 years of age have asthma. Prevalence of asthma is 20 percent higher among black children
than white children.
Hospitalizations and Emergency Room Visits
Hospitalizations and emergency room visits for asthma have increased substantially in
the United States. From 1980 through 1987, the hospital discharge rate for asthma as the first-
listed discharge diagnosis increased 4.5 percent per year.16 From 1965 through 1983, asthma-
related hospitalization rates increased by 50 percent hi adults and over 200 percent in
children.17 For children, asthma is the most frequent cause of hospital admissions and
pediatric emergency room visits. Among children aged 0 to 4, black children had 1.8 times
the increase of white children.18
• A recent study using data from the National Center for Health Statistics (NCHS)
compared asthma-related hospitalization rates to all other hospitalization rates and found that
asthma-related hospitalization rates remained relatively constant. This is in sharp contrast to
overall hospitalization rates, which have declined dramatically over the last decade.19
MFriebele, Elaine, "The Attack of Asthma," Environmental Health Perspectives, vol. 104 (1), January
1996, pp. 22-25.
15Buist, A. and Vollmer, W., "Reflections on the Rise of Asthma Morbidity and Mortality," Journal of
the American Medical Association, vol. 264 (13), October 3, 1990, pp. 1719-1720.
16Gergen, P. and Weiss, K., "Changing Patterns of Asthma Hospitalization Among Children: 1979 to
1987," Journal of the American Medical Association, vol. 264 (13), October 3, 1990, pp. 1688-1692.
17Friebele, Elaine, "The Attack of Asthma," Environmental Health Perspectives, vol. 104 (1), January
1996, p. 23.
18Gergen, P. and Weiss, K., "Changing Patterns of Asthma Hospitalization Among Children: 1979 to
1987," Journal of the American Medical Association, vol. 264 (13), October 3, 1990, pp. 1688-1692.
l9Weiss, K.B., Gergen, P.J., and Wagener, O.K., " Breathing Better or Wheezing Worse? The Changing
Epidemiology of Asthma Morbidity and Mortality," Annual Review Public Health, vol. 14, 1993, pp. 491-513.
XI-13
-------
Between 1975 and 1990, rates of ambulatory care visits for asthma among persons aged
15 through 44 and over 65 increased from 2.7 to 2.85 visits per 100 population.20 Acute
asthma exacerbations have been estimated to account for 1.8 million emergency room visits
annually, 48 percent of which involved children under 18 years old.21
Mortality
The number of asthma deaths in the United States increased by 58 percent from 1979
and 1992.22 Though the majority of asthma-related deaths were among asthmatics 50 years or
older, the rise in the mortality rate has been observed for all age groups.23 Geographically,
studies have shown that deaths from asthma occur primarily in large cities. This observation
suggests that higher mortality may be associated with the urban environment.24 The increase
in mortality rates is not specific to the US, as similar trends in mortality rates have been
observed in other industrialized nations.
Effects of ICD Revisions and Diagnostic Recognition
In 1979, the ninth revision of the International Classification of Disease (ICD)
reclassified asthma. The 8th revision of the ICD classified "bronchitis with mention of
asthma" as bronchitis. Under the ninth revision, "asthma coexisting with bronchitis ".was
classified as asthma. As a result of the change in the definition, deaths ascribed to asthma
increased 35 percent based on reviews of death certificates. Additionally, deaths ascribed to
asthma as the underlying cause of death (not primary cause of death) increased by 39 percent
from 1978 to 1979.25 Nevertheless, the change in classification is not perceived to account for
20Ibid.,p. 495.
2IWeiss, K.B., Gergen, P.J., and Hodgson, T.A., "An Economic Evaluation of Asthma in the United
States," The New England Journal of Medicine, vol. 326, March 26, 1992, pp. 862-866.
22Friebele, Elaine, "The Attack of Asthma," Environmental Health Perspectives, vol. 104 (1), January
1996, p. 22.
23Sly, Michael, "Mortality from Asthma in Children 1979-1984," Journal of the Air Pollution Control
Association, vol. 60, May 1988, pp. 433-443.
24Lang, David and Polansky, Marcia. "Patterns of Asthma Mortality in Philadelphia From 1969,to 1991.'
The New England Journal of Medicine. December 8, 1994. 331:1542-1546.
25Sly, Michael, "Mortality from Asthma in Children 1979-1984," Journal of the Air Pollution Control
Association, vol. 60, May 1988, p. 433.
XI-14
-------
subsequent increases observed in the 1980s and the early part of this decade.26'27 Though
greater awareness of asthma among physicians contributes to the rising number of cases of
asthma, it does not completely explain the rise in asthma-related morbidity and mortality
rates.28
Populations At Risk
Children, Hispanics, blacks and the urban poor are at greatest risk for developing
asthma.29 Asthma has been found to occur more frequently among black children than white
children, and more often among urban populations than among rural populations.30
Children and Infants
Asthma is one of the most common chronic diseases of childhood. The American Lung
Association estimates that 4.8 million children under 18 years of age have asthma and many
others have undiagnosed asthma. Childhood asthma is a chronic disease with genetic
predispositions and a strong allergic component. It can be triggered by exercise, infections,
allergy, airborne irritants, weather, and sometimes emotions. Approximately 75 to 80 percent
of children with asthma also have allergies to various materials such as pollen, mold, animal
dander, and food.31
Despite these statistics, asthma is a dynamic disease that affects people of all racial and
ethnic groups and across all age groups. Signs and symptoms vary in severity from one
individual to the next as well as within one individual over time.
Risk Factors
There are a number of risk factors that trigger asthmatic attacks or exacerbate asthmatic
symptoms.32 However, it is not clear how these risk factors act independently or interact to
26Ibid., p. 437.
27,
7Weiss, K.B., Gergen, P.J., and Wagener, O.K., " Breathing Better or Wheezing Worse? The Changing
Epidemiology of Asthma Morbidity and Mortality," Annual Review Public Health, vol. 14, 1993, p. 501.
2&Ibid.,p. 500.
29Friebele, Elaine, "The Attack of Asthma," Environmental Health Perspectives, vol. 104 (1), January
1996, p. 23.
30Ibid.
31 American Lung Association, Childhood Asthma Fact Sheet, 1996, p. 2.
32"Triggers" such as airborne particles set off a reaction in the lungs and other parts of the body.
XI-15
-------
cause asthma or whether they induce episodes of asthmatic responses in persons already
sensitized.33 This section briefly discusses environmental exposures, genetic factors, and
lifestyle, which are recognized to contribute to the development and/or exacerbation of
asthma.
Among environmental risk factors, exposure to environmental tobacco smoke and
combustion by-products of gas and wood stoves and fireplaces are recognized to exacerbate
asthma. Environmental allergens inhaled in the air such as pollen, mold spores, animal
dander, or dust also can provoke asthmatic attacks. Household dust mites are the one of the
major triggers for people with allergic asthma.34 It is known that mite fecal particles are
responsible for releasing large amounts of allergens, which are inhalable. These allergens
penetrate the epithelial surfaces of the airways and lead to sensitization.35 Asthmatic attacks
also can be caused by food allergies to eggs, shellfish, or chocolate, as well as drug-related
allergies to medications such as aspirin. Finally, atopy (an allergy for which there is a genetic
predisposition) is recognized as a strong risk factor for the development of asthma.36
Ambient air pollution has been linked to asthma and other respiratory illnesses.
Despite evidence that air quality has improved over the past several decades, over a million
Americans still reside in areas where ambient concentrations of pollutants exceed the national
ambient air quality standards. Extensive air pollution studies have focused on individual air
pollutants such as paniculate matter, ozone, NO2, and S02 to explain observed associations
between asthma incidence and air pollution. However, some researchers argue that it is
difficult to implicate any one pollutant since air pollution represents a mixture of various
pollutants. Thus, the role of air pollution in the development of asthma remains unclear and
requires further investigation.
Other explanations for the rise in asthma-related morbidity and mortality rates include
increased rates of premature births, decreased rates of breastfeeding, low socioeconomic
status, more limited patient access to timely and appropriate health and preventive care, as
well as increased use of medications to control asthma symptoms.37
33Sensitization is an acquired reaction whereby an individual develops an immune response after initial
exposure to a substance. Subsequent exposures to this substance "trigger" a physiological response (e.g., allergic
reaction such as skin irritation, asthmatic attack and so forth).
34Household dust mites are tiny, microscopic spiders usually found hi house dust (several thousand mites
can be found in a pinch of dust).
35Holgate, S.T. "Asthma: Past, Present, and Future." European Respiratory Journal. 1993. 6:1509-1510.
36Ibid.,p. 1512.
37Weiss, K.B., Gergen, P.J., and Wagener, D.K., " Breathing Better or Wheezing Worse? The Changing
Epidemiology of Asthma Morbidity and Mortality," Annual Review Public Health, vol. 14, 1993, pp. 502-506.
XI-16
-------
Children and Infants
Among infants, risk factors for developing asthma include early exposure to allergens
(dust, pollen, animal dander, cockroach antigens)38 and maternal smoking and nutrition. In
infants, viral respiratory infections are the principal trigger of asthma. Allergens play a lesser
role in this age group because it takes time for allergic sensitivity to develop.
Lifestyle factors such as smoking and poor nutritional habits of a pregnant woman may
increase the risk of asthma in her child. Maternal smoking adversely affects maternal nutrition
which subsequently influences fetal growth and immune system development and response.
Additionally, infants have been shown to be at increased risk of wheezing and other respiratory
illnesses as a result of maternal smoking during pregnancy.39 For children, exposure to
second-hand cigarette smoke plays a role in the exacerbation and provocation of respiratory
illnesses.40
Public Health Implications
Asthma is a disease that affects both adults and children. Understanding the
mechanisms and risk factors for asthma is essential to combat and control the disease that
afflicts millions of Americans. Studies have shown that the prevalence and incidence of
asthma are on the rise. Morbidity among children, as measured by hospitalization rates and
doctors visits, has increased.
Prevention of early childhood asthma (wheezing) can occur through avoidance of
certain foods by infants and lactating mothers and the removal of house dust mite antigen from
bedrooms and living rooms. Research also suggests that breastfeeding acts as a protective
mechanism against wheezing, especially for children who are not genetically predisposed to
have allergies.
To better understand the development and exacerbation of asthma, research should
continue to look at the role of certain risk factors such as viral infections, indoor and ambient
air pollution, allergens, and behavior.
38An antigen is a substance that causes the formation of an antibody and reacts specifically with that
antibody. For example, animal dander is an antigen.
39"Early Childhood Asthma: What are the Questions?," American Journal of Respiratory and Critical Care
Medicine, vol. 15 (2) Supplement, February 1995, p. S5.
"Ibid.
XI-17
-------
INFANT MORTALITY
Infant mortality rate is the number of infants under 1 year of age dying in 1 year, per
1000 live births. It is one of the clearest indication of the overall public health and well
being. The leading causes of infant mortality include low birthweight and disorders relating to
short gestation, birth defects, and Sudden Infant Death Syndrome (SIDS). Risk factors for
SIDS include maternal smoking and drug use, births to teens, and infections late hi pregnancy.
The National Commission to Prevent Infant Mortality estimates that as many as 25 percent of
infant deaths could be prevented if the mothers received adequate prenatal care.41 According to
the National Institute of Health low birthweight contributes to 60% of deaths in the first year
of life (Nffl, 1989).
The infant mortality rate hi the U.S. has been steadily declining from 20.0 per 1000
live births hi 1970 to 8.0 per 1000 live births hi 1994.42 The preliminary infant mortality rate
hi 1995 is 7.5 per 1000 livebirths. Declines between 1994 and 1995 occurred among neonates
(infant deaths under 28 days of age) as well as among postneonates (age 28 days to 11
months).43 In 1990 the infant mortality rate for males was 10.3 per 1000 live births, slightly
decreasing from a rate of 10.8 in 1989. In comparison, the 1990 infant mortality rate for
females was 8.1 per 1000 live births, dropping from a rate of 8.8 hi 1989.44
Despite the steady decline in infant mortality rate in the US, the gap between black and
white remains quite large. Since 1980 infant mortality rate for black infants has been more
than double that for white infants. In 1980, the mortality rate was 10.9 per 1000 live births
for white infants and 22.2 for black infants. In 1994 while the mortality rate for white infant
declined to 6.6 per 1000 live births, rate for black infants remained very high at 15.8 per 1000
live births.45'46
A 1990 estimate of 7.8 per 1,000 live births for the Latino population was derived
from 45 of the 50 states and the District of Columbia, a slight decrease from the 1989 rate of
8.5 based on data from 43 states and the District of Columbia.47
41Child Welfare League of America, The Child Welfare Statistic Book 1993, Washington, DC, 1993.
42National Center for Health Statistics, Health, United States, 1995; Hyattsville, Maryland: Public Health
Service, 1996, p. 102.
43CDC, Monthly Vital Statistics Report, vol 45(3), Supplement 2, 1996
""Child Welfare League of America, The Child Welfare Statistic Book 1993, Washington, DC, 1993.
45National Center for Health Statistics, Health, United States, 1995; Hyattsville, Maryland: Public Health
Service, 1996, p. 102.
, Monthly Vital Statistics Report, vol 45(3), Supplement 2, 1996
47Child Welfare League of America, The Child Welfare Statistic Book 1993, Washington, DC, 1993.
XI-18
-------
LOW BIRTHWEIGHT
Birthweight of less than 5 pounds, 8 ounces is classified as low birthweight. Incidence
of low birthweight is presented as percent of live births. Low-birthweight infants may be
preterm (short gestational age) or term babies small for gestational age. Maternal malnutrition,
close child spacing, and low socioeconomic status are risk factors commonly associated with
low birthweight. Insufficient weight gain by the mother during pregnancy is a primary cause
of low birthweight. Women who gain less than 20 pounds during pregnancy are twice as
likely to bear a baby of low birthweight as women who gain over 20 pounds.48 Improper
prenatal care and exposure to alcohol and other drugs are also important factors in low-weight
births. The incidence of low birthweight for mothers who are smokers almost double the
incidence for mothers who are non-smokers. In 1993 the incidence of low birthweight for
smoking mothers was 11.84 percent of live births, and only 6.56 percent for non-smoking
mothers.49
The incidence of low birthweight in the US had risen from 6.8 percent of live births
in 1986 to 7.3 percent in 1994. In 1995, the incidence of low birthweight remained at the
1994 level, at 7.3 percent. Between 1994 and 1995, levels of low birth weight increased for
white births (from 6.1 to 6.2 percent) and for Hispanic births (from 6.2 to 6.3 percent), while
the rate for black births fell from 13.2 to 13.0 percent.50
48
;Child Welfare League of America, The Child Welfare Statistic Book 1993, Washington, DC, 1993.
49National Center for Health Statistics, Health, United States, 1995; Hyattsville, Maryland: Public Health
Service, 1996, p. 90, Table 11.
50lbid.
XI-19
-------
CANCER SUMMARIES
Introduction
The following section describes the epidemiology of various cancer endpoints,
including breast, colorectal, liver, kidney, bladder, prostate, and lung cancers, as well as
leukemia. The summaries for this report include mortality and incidence statistics, discussion
of risk factors, symptoms, methods of early detection, and an overview of racial, ethnic, age,
and gender trends.
For each type of cancer, a general review of United States data is provided. Where
available, specific information regarding Pennsylvania, Philadelphia, and study area data is
presented. The majority of the United States incidence and mortality data comes from the
"SEER Cancer Statistics Review, 1973-1991" report from the National Institutes of Health of
the US Department of Health and Human Services. The SEER Program routinely collects
cancer incidence, mortality, and patient survival data from designated cancer registries in
various regions of the country. The geographic areas represented by the registries cover rural,
suburban and metropolitan areas and "with respect to selected demographic and
epidemiological factors, they are reasonably representative subsets of the United States
Population".51
The Pennsylvania and Philadelphia incidence and mortality data is from the
Pennsylvania Department of Health Report "Pennsylvania Cancer Incidence and Mortality
1988-1992". The study area data was provided by the Pennsylvania Department of Health.
Lung Cancer
Clinical Description/Summary
The term "lung cancer" includes cancer of the lung, bronchus, trachea, and pleura.
Signs and symptoms of lung cancer include persistent cough, sputum streaked with blood,
chest pain, recurring pneumonia or bronchitis. Symptoms often do not appear until advanced
stages of disease, which makes early detection difficult. Among smokers who quit smoking
when precancerous changes have been detected, the damaged lung tissue often returns to
normal.52 Lung cancer is a severely debilitating disease, with the 5-year relative survival rate
from time of diagnosis of only 13%.
5llbid,pg. l.
52American Cancer Society, Cancer Facts and Figures 1996, 1996
XI-20
-------
General Background- Public Health Importance
Lung cancer is the leading cause of cancer death in the United States, among both men
(1 in 13) and women (1 in 24).53 In 1996, it is estimated that there will be 177,000 new cases
of lung cancer and 158,700 deaths from lung cancer.54 The 1991 incidence rate of invasive
lung and bronchus cancer in the United States (new cases) for males was 79.7 per 100,000 and
for females was 42.0 per 100,000. The 1991 age-adjusted mortality rates were 74.5 per
100,000 for males and 32.1 per 100,000 for females. The five-year survival rate for lung
cancer is 13% for all stages.
Risk Factors
More than 90% of cases of lung cancer among men are attributable to cigarette
smoking. People who smoke 20 cigarettes per day increase then" risk of developing lung
cancer 10-fold. Use of other tobacco products such as cigar smoking and pipe smoking also
play a role hi the development of cancer. Other risk factors include exposure to radon gas,
asbestos, a risk which is exacerbated by cigarette smoking, and alcohol consumption hi
conjunction with smoking.55 Environmental and occupational risk factors include exposure to
ionizing radiation such as uranium ores, vinyl chloride, mustard gas, nickel chromates,
polycyclic aromatic hydrocarbons (PAHs) from coal production, chromium, inorganic arsenic
and chloromethyl ethers. In addition, second-hand smoke increases the risk of lung cancer to
non-smokers. Air pollution may slightly increase the risk of lung cancer; however, it is
difficult to differentiate the effects of smoking.56
Effects of Race and Gender
In the United States, lung cancer rates are higher among males than females. Several
factors may contribute to this difference, including higher proportion of male cigarette smokers
and higher proportion of males occupationally exposed to materials which cause lung cancer.
53American Cancer Society, Lung Cancer, Document 004470.
54Estimates are based on 1979-1992 SEER incidence and mortality rates, as quoted in American Cancer
Society, Cancer Facts and Figures 1996, 1996.
55The risk of developing lung cancer with exposure to radon levels of 4 pCi/1 (the EPA Action Level) is 2 in
1000 exposed individuals. For individuals who smoke, the risk of lung cancer when exposed to radon at 4 pCi/1
increases almost 15-fold to 29 in 1000 exposed individuals. (USEPA, USDHHS, USPHS, A Citizen's Guide to
Radon, 2nd edition, May 1992, 402-K92-001).
The risk of developing lung cancer for workers exposed to asbestos is seven times higher than the general
population. Smokers who have exposure to asbestos fibers increase their risk of lung cancer 50-fold. (American
Cancer Society, Cancer Facts and Figures 1996, 1996.)
56American Cancer Society, Lung Cancer, document #004470.
XI-21
-------
The differences in lung cancer rates between blacks and whites are greatest between
males. In 1991, the incidence of lung cancer among white males was 77.9 per 100,000 and
among black males was 122 per 100,000. A smaller difference is seen between black and
white females: the 1991 incidence rates for white females was 42.8 per 100,000 and for black
females was 49.0 per 100,000. Differences in incidence rates may be due to differential
susceptibility and differences in behavioral factors (such as cigarette smoking) or other risk
factors. Mortality rates are different in rates, but only between black and white males. The
mortality rate from lung cancer in 1991 was 72.5 per 100,000 for white males and 104.7 per
100,000 for black males. The discrepancies in mortality and survival rates may be due to
differences hi access to health care.
Changes in Trends
Beginning hi 1987, lung cancer incidence has declined among both black and white
men. From 1987 through 1991, the incidence rates have shown an overall decline of 4.7%
among white men and 3.9% among black men. Incidence rates for women, however, have
increased approximately 5% per year from 1973 through 1991. Among white women, the
increase hi incidence has slowed hi recent years (from 1987 through 1991). The same pattern
is present hi mortality rates among women. 1991 was the sixth consecutive year hi which lung
cancer mortality was higher than breast cancer mortality.
There is an overall decline hi lung cancer mortality rate for men under age 55 and
women under age 45, largely due to reductions hi cigarette smoking since the 1964 Surgeon
General's report on smoking and health.57
Pennsylvania- and Philadelphia-Specific Information
The following table provides lung cancer incidence and mortality rates for Philadelphia
County, Pennsylvania and the United States.
57Ries, et al., SEER Cancer Statistics Review, 1973-1991: Tables and Graphs, National Cancer Institute,
NIH Pub. No. 94-2789.
XI-22
-------
Comparison of Average Annual Age-Adjusted Lung Cancer Rates per 100,000 for
Philadelphia County, Pennsylvania, and the United States
Rate Philadelphia County58
(1988-1992)
Overall Incidence
Overall Mortality
Male Mortality- All races
Female Mortality - All races
White Mortality: male/female
Black Mortality: male/female
Male Incidence - all races
Female Incidence - all races
White Incidence- male/female
Black Incidence - male/female
not available
not available
100.0
41.0
not available
not available
111.2
51.2
not available
not available
Pennsylvania*9
(1988-1992)
56.6
48.6
74.5
30.0
71.6/29.1
117.4/41.4
84.2
36.3
81.2/35.3
122.2/47.9
United States60
(1987-1991)
58.2
49.3
74.9
30.5
73.0/30.9
105.5/30.4
82.1
40.4
80.7/41.3
122.4/44.5
1
1
•
Breast Cancer
General Background
Breast cancer is cancer that has developed in the external or internal structures of the
breast, including the nipple. It is the second leading cause of cancer mortality among women,
surpassed only by lung cancer. The 1991 SEER data report states that the age-adjusted
incidence rate of female breast cancer hi the United States for 1987 through 1991 was 109.5
per 100,000 population. The age-adjusted mortality rate for the same time period was 27.3
per 100,000. It is estimated that hi 1996 there will be 184,300 new cases of breast cancer
diagnosed in women, and 1,400 new cases among men.
Clinical Description/Summary
Some pre-clinical radiographic signs of breast cancer can be seen on a mammogram.
Clinical symptoms include, breast changes, including thickening of tissues, lumps, skin
irritation, dimpling, retraction, scaliness, pain, tenderness of the nipple, distortion, or nipple
discharge.61
58Pennsylvania Department of Health, Pennsylvania Cancer Incidence and Mortality 1988-1992,
Pennsylvania Center for Health Statistics and Research, 1995.
59Ibid.,p. 84.
^Ries, et al., SEER Cancer Statistics Review, 1973-1991: Tables and Graphs, National Cancer Institute,
NIH Pub. No. 94-2789.
6'American Cancer Society, Cancer Facts and Figures 1996, 1996.
XI-23
-------
After diagnosis of localized breast cancer, the relative 5 year survival rate is 96%. The
5 year relative survival rates for those with regional spread and distant metastases are 75 % and
20%, respectively.62
Risk Factors and Early Detection
Several risk factors for breast cancer have been established and include late onset of
menopause, nulligravidity (never pregnant), first full term pregnancy after age 30, obesity,
high fat diet, early onset of menarche, family history of breast cancer in mother or sister,
personal history of fibrocystic disease, and personal history of ovarian or endometrial cancer.
Researchers have recently identified a series of genes associated with increased risk of breast
cancer, which may aid in early detection of those at high risk of developing disease.63
However, known risk factors and genetic susceptibility explain only approximately 40% of
breast cancer cases.64 Unknown risks and uncharacterized environmental exposures may
contribute to breast cancer risk.
The American Cancer Society recommends that asymptomatic women aged 40-49
should have a screening mammogram every 1-2 years; and women aged 50 every year. In
addition, a clinical breast exam is recommended every three years for women 20-24, and every
year for women over 40.65 These methods enhance a clinician's ability to detect lumps at an
early stage and thus improve a patient's' prognosis. Self breast exam is also effective at early
detection when taught and practiced correctly.
Effects of Race, Gender, and Age
After a steady increase in female breast cancer rates hi the United States through the
early and mid - 1980s, incidence rates appear to have leveled off, beginning hi 1987. Much of
the recent increase in breast cancer rates is believed to be due to increased mammography
utilization and subsequent increased diagnosis of clinically inapparent breast cancer.66 From
1973 to 1991, there was an overall 8.5% increase in incidence rates for white women less than
50 years old, and 31.8% increase among white women age 50 years and older. The estimated
62lbid.
"ibid.
64 U.S. Department of Health and Human Services, SEER Cancer Statistics Review 1973-1991, National
Institutes of Health, Pub. No. 93-2789.
"American Cancer Society, Cancer Facts and Figures 1996, 1996, pg. 12.
"Ibid.
XI-24
-------
annual percent increases were 0.8% and 2.2% for women under 50 years old and 50 years of
age or older, respectively. The incidence increase was much more dramatic among black
women under 50 years old, who demonstrated a 26.1 % overall rate increase. Black women
over 50 years old showed an overall increase in incidence of 32% over the same time period.
The estimated annual percent changes among black women were 1.2 % for those under 50
years old and 2.2 for those 50 years of age or older.
Although breast cancer mortality decreased by 14% among white women under 50
years old, from 1973-1991, mortality increased by 4% among white women 50 and older, by
2% for black women under 50 and by 26.3% for black women 50 and older.
The 1994 SEER report supports the evidence that the dramatic increase in breast cancer
incidence during the early 1980s was due primarily to an increase in screening, especially
among those women age 50 and older.67 However, the long-term increase hi breast cancer
incidence over the last few decades is largely unexplained.
Pennsylvania- and Philadelphia- Specific Information
For the tune period of 1988-1992, the age adjusted incidence rate for breast cancer in
Pennsylvania was 118.3 per 100,000 population. The incidence rates among whites was
10.5% higher than among blacks. Rates for both blacks and whites have increased since 1985.
In contrast to incidence rates, however, mortality rates were higher for black women than
among white women. The mortality rate in 1992 among Pennsylvania resident black women
was 35.3 per 100,000 while the rate for white women was 28.1 per 100,000. This
discrepancy may indicate differences in access to screening, post-diagnosis care, or differences
hi susceptibility. This trend hi Pennsylvania mimics that seen hi the U.S. population.
The Standardized Incidence Ratio (SIR) for breast cancer in Philadelphia County
compared to SEER national data is 95.7, demonstrating a significantly lower incidence of
breast cancer cases among Philadelphia county resident women when compared to the national
rate.
The table below lists incidence and mortality data for the U.S., Pennsylvania, and
Philadelphia County.
"U.S. Department of Health and Human Services, SEER Cancer Statistics Review 1973-1991, National
Institutes of Health, Pub. No. 93-2789.
XI-25
-------
Comparison of Average Annual Age-Adjusted Female Breast Cancer Rates per 100,000
for Philadelphia County, Pennsylvania, and the United States
Rate6" Philadelphia
County® (1988-
1992)
Overall Incidence
Overall Mortality
White Incidence
Black Incidence
White Mortality
Black Mortality
5 year relative survival*
120.8
34.5
not available
not available
not available
not available
not available
Pennsylvania70
(1988-1992)
118.3
29.4
118.9
107.6
29.1
34.5
not available
United States71
(1987-1991)
109.5
27.3
113.2
94.0
27.2
31.2
78.0 (under 50)
81.3(50+)
*1983-1990
Prostate Cancer
Clinical Description/Summary
Prostate cancer is a disease that originates in the prostate, a gland found only in men
which is located behind the base of the penis. The symptoms of prostate cancer include
inability to urinate, difficulty starting or stopping the flow of urine, weak or interrupted urine
flow, frequent need to urinate (especially at night), burning or pain upon urination, blood in
the urine, and pain in the lower back, pelvis, or upper thighs. These symptoms are similar to
those caused by benign prostate enlargement or infection.72 Digital rectal exam and prostate-
specific antigen blood tests are used as early detection methods.
The five-year survival rate for patients whose tumors are diagnosed early is 98%. 61 %
of men diagnosed with prostate cancer survive 10 years, and 49% survive 15 years.73
68Rates are per 100,000 unless otherwise indicated
69Pennsylvania Health Department, Pennsylvania Cancer Incidence and Mortality 1988-1992, State Center
for Health Statistics and Research, 1995.
70Ibid., p. 100.
71U.S. Department of Health and Human Services, SEER Cancer Statistics Review 1973-1991, National
Institutes of Health, Pub. No. 93-2789.
72American Cancer Society, Cancer Facts and Figures 1996, 1996.
73American Cancer Society, Prostate Cancer, Document 004625.
XI-26
-------
Public Health Importance
Prostate cancer is the leading site of new cancer cases and the second leading cause of
cancer death among men in the United States. Only lung cancer surpasses prostate cancer in
cancer deaths among men.74 It is estimated that hi the US there will be 317,100 new cases of
prostate cancer in 1996, and 41,400 deaths due to prostate cancer.75
Risk Factors and Effects of Race, Age, and Secular Trends
The risk of prostate cancer increases with age: over 80% of all prostate cancers are
diagnosed hi men over age 65.76 The mortality rate from prostate cancer among black males is
over two times higher than that for white males. The age-adjusted mortality rate for 1987-
1991 for men 65 and over was 215.6 per 100,000 population for whites and 462.4 per 100,000
population for blacks.77 In fact, black Americans have the highest incidence of prostate cancer
hi the world.78 Prostate cancer is common hi North America and Northwestern Europe, while
it is rare in Africa, the Near East and South America. Some international studies suggest a
link between dietary fat and prostate cancer.79
The incidence of prostate cancer increased 65% between 1980 and 1990, a trend largely
due to unproved detection.
Pennsylvania- and Philadelphia-Specific Information
The trend hi prostate cancer incidence hi the United States is also reflected hi
Pennsylvania incidence rates. The number of new cases diagnosed among Pennsylvania
residents hi 1991 was 23.4 % higher than that diagnosed in 1991, and 142.4% higher than the
number of cases diagnosed hi 1985.*° Again, this increase is ascribed to increased surveillance
and early detection. The table below presents incidence and mortality rates for Philadelphia
County, Pennsylvania, and the United States.
75Ibid., p. 13.
76'Ibid., p. 13.
77Ries et al., SEER Cancer Statistics Review. 1973-1991.
78American Cancer Society, Cancer Facts and Figures 1996: Tables and Graphs, National Cancer
Institute, NIH Pub. No. 94-2789.
19Ibid.,p. 13.
80Pennsylvania Department of Health, Cancer Incidence and Mortality 1988-1992.
XI-27
-------
Comparison of Annual Average Age-Adjusted Prostate Cancer Rates per 100,000
population for Philadelphia County, Pennsylvania, and the United States
Rate Philadelphia County81
(1988-1992)
Overall Incidence
Overall Mortality
White Mortality
Black Mortality
White Incidence
Black Incidence
127.8
31.4
not available
not available
not available
not available
Pennsylvania82
(1988-1992)
111.4
25.0
23.4
54.2
107.3
166.5
United States83
(1987-1991)
123.0
25.6
23.6
52.0
121.2
163.1
L
Colorectal Cancer
Clinical Description/Early Detection
Colorectal cancer originates in the colon or rectum, and results from the abnormal
growth of cells in the large bowel.84 Symptoms of colon and rectum cancer include rectal
bleeding, obstruction or diarrhea, and tenesmus. Tenesmus is a painful spasm of the anal
sphincter (anal muscle) that is often the result of very advanced disease. The American Cancer
Society recommends digital rectal exam, fecal occult blood tests, and sigmoidoscopy as
methods for early detection of colorectal cancer.85 The American Cancer Society recommends
digital rectal exam annually after the age of 40, fecal occult blood testing yearly after age 50,
and sigmoidoscopy every 3 to 5 years after age 50.
The 5 year relative survival rate for patients with localized, early stage colorectal
cancer is as high as 91 %. The 5 year relative survival rate drops to 63% among patients with
regional spread of the disease to adjacent organs or lymph nodes. This rate drops even
further, to below 7% among those with distant metastases (spreading to distant organs).86
81
Ibid.
83Ries et al., SEER Cancer Statistics Review, 1973-1991.
84American Cancer Society, Colorectal Cancer, document 004095, 1996.
85
'Ibid.
"Ibid.
XI-28
-------
General Background - Public Health Importance
Colon and rectum cancer (often termed together as "colorectal") is the third leading
cause of cancer death in the United States, behind lung and prostate cancer among men, and
lung and breast cancer among women. It is estimated that there will be 133,500 new cases in
1996, including 94,500 cases of colon cancer and 39,000 cases of rectal cancer.87 It is
estimated that in 1996 colon cancer will be responsible for 46,400 deaths and rectal cancer will
be responsible for 8,500 deaths. The mortality rate for colorectal cancer hi the United States
has fallen 9% among men hi the United States and 31 % among women over the last 30
years.88 For the purposes of the initial discussion, "colorectal" refers to colon and rectum
cancer together. Later in this profile, the two cancers are considered separately for clarity.
Risk Factors
Inflammatory bowel disease and personal or family history of colorectal cancer or
polyps have been associated with increased risk of colon cancer. Physical inactivity and high-
fat and/or low-fiber diet are other possible risk factors. Some studies have shown that workers
exposed to certain chemicals seen to be at increased risk for developing cancer of the large
bowel.89
Effects of Race, Gender, and Age
The incidence rates of colorectal cancer are higher for males than for females, among
both blacks and whites. The age-adjusted incidence rates from 1987-1991 was 58.7 per
100,000 population for white males and 39.9 per 100,000 population for white females. For
black males, the incidence rate for this time period was 60.9 per 100,000 population and for
black females was 46.7 per 100,000 population.90 The incidence of colorectal cancer is
dramatically higher among those age 65 and older compared to those under age 65: The 1987-
1991 incidence rates for white men and white women age 65 and older was 324.7 per 100,000
population and for black men and black women was 324.4, white the incidence rates for that
same time period for those under 65 were 17.5 for whites and 22.6 for blacks.91
87American Cancer Society, Cancer Facts and Figures 1996, document 004095, 1996.
™Ibid., p. 10.
"Ibid.
90Riesetal., SEER Cancer Statistics Review, 1973-1991: Tables and Graphs, National Cancer Institute,
NIH Pub. No. 94-2789.
91W, p. 147.
XI-29
-------
Incidence rates for colorectal cancer among blacks and whites are relatively similar.
The mortality rates are slightly higher, however, among blacks, which is a trend seen for both
men and women and people of different ages. The 1987-1991 death rate from colon and
rectum cancer for whites was 18.8 per 100,000 and for blacks was 23.5.92
Colon vs. Rectum Cancer
The symptoms, methods of early detection and risk factors are the same for both colon
and rectum cancer. The incidence rate of colon cancer is much higher than that for rectum
cancer. The age-adjusted incidence rate of colon cancer from 1987-1991 was 12.1 per
100,000 for those under age 65 and 238.8 per 100,000 for those age 65 and older. The
incidence rates during that same time period for rectum cancer were much lower: 6.1 per
100,000 under age 65, and 84.3 per 100,000 for those age 65 and older. The SEER report
does not list the mortality rates for the two cancers separately. The 5 year relative survival
rates of colon cancer and rectum cancer are similar. For those diagnosed with colon cancer
between 1983 and 1990, the 5 year relative survival rate was 59.9%, and for those diagnosed
during the same tune period with rectum cancer, the 5 year relative survival was 57.7%.93
Pennsylvania- and Philadelphia- Specific Information
A comparison of United States, Pennsylvania, and Philadelphia County colon and
rectum cancer incidence data is provided in the table below. Among Pennsylvania residents,
colon cancer was the second most common cancer site diagnosed among women, and the third
most common among men.94
93
'Ibid., pp. 150-151.
94Pennsylvania Department of Health, Pennsylvania Cancer Incidence and Mortality 1988-1992, State
Center for Health Statistics and Research, 1995.
XI-30
-------
Comparison of Annual Age-Adjusted Colon and Rectum Cancer Incidence Rates95 per
100,000 population for Philadelphia County, Pennsylvania, and the United States
Rate
COLON - Overall Incidence
Male Incidence - all races
Female Incidence - all races
White Incidence- male/female
Black Incidence - male/female
RECTUM - Overall Incidence
Male Incidence - all races
Female Incidence - all races
White Incidence- male/female
Black Incidence - male/female
Philadelphia County*6
(1988-1992)
not available
49.6
35.7
not available
not available
not available
22.7
12.9
not available
not available
Pennsylvania*7
(1988-1992)
39.7
47.1
34.4
47.0/34.2
47.4/36.6
16.5
21.6
12.7
21.9/12.9
17.1/10.3
United States"*
(1987-1991)
34.5
40.7
29.9
40.4/29.5-
46.2/36.8
13.8
18.2
10.4
18.3/10.4
14.7/9.9
L
Bladder Cancer
Clinical Description
The bladder is a muscular organ which stores and empties urine carried down from the
kidneys. Urine is emptied from the bladder through the ureter and emptied through the
urethra. Bladder cancer can be characterized as tiny mushroom-like growths which are
attached to the inner lining of the bladder (papillary tumors), or as solid tumors which grow
directly on the lining of the bladder. Bladder cancer may result in bloody urine and increased
frequency of urination." To determine whether an individual has bladder cancer, a cytoscope
is used to examine the bladder internally.
General Background- Public Health Importance
Bladder cancer is the fourth leading cause of cancer among men, behind prostate, lung
95The Pennsylvania information is separated into Colon Cancer and Cancer of the Rectum, Anus and
Rectosigmoid. The United States data does not provide mortality data for the two cancers separately, therefore,
mortality rates are not compared here.
96Pennsylvania Department of Health, Pennsylvania Cancer Incidence and Mortality 1988-1992, State
Center for Health Statistics and Research, 1995.
"ibid.
98Ries et al., SEER Cancer Statistics Review, 1973-1991: Tables and Graphs, National Cancer Institute,
NIH Pub. No. 94-2789.
99
American Cancer Society, Bladder Cancer, Document 004050.
XI-31
-------
and colorectal cancer. Among women, bladder cancer is the ninth leading cause of cancer.
An estimated 52,900 new cases and 11,700 deaths from bladder cancer occurred hi 1996 hi the
United States.100 Since the early 1970s, both the male and female mortality rates of bladder
cancer has decreased among both black and white populations.
Risk Factors
Smoking is the greatest risk factor for bladder cancer. It is estimated that smoking
accounts for 47% of bladder cancer deaths among men and 37% among women. Occupational
exposures during the manufacture or processing of rubber, leather, and benzidine and
2-naphthlamine used hi dye manufacture are also associated with increased risk, as is living in
urban areas, or being exposed to ionizing radiation. Use of the alkylating agent
cyclophosphamide hi the treatment of cancer or abuse of phenacetin-containing analgesic
compounds increases the risk of developing bladder cancer.101 Ingestion of chlorinated
drinking water has also been associated with slight increases hi bladder cancer risk, due to the
carcinogenicity of water chlorination by-products.
Effects of Race, Gender and Age
The incidence rate of bladder cancer is more than three tunes higher among men than
among women. The national age-adjusted incidence rate for the period from 1987 to 1991 for
both sexes was 16.9 per 100,000 but was 29.9 per 100,000 for males compared to 7.4 per
100,000 for females. Some suggested reasons for the excess male bladder cancer are gender
differences in urination habits, unidentified environmental risk factors or hormonal and
metabolic determinants of risk.102
A pronounced difference between bladder cancer incidence rates exists for persons
under 65 years of age and those over 65 years of age. The 1987-1991 incidence rate for
bladder cancer among those under 65 was 10.9 per 100,000 for males and 3.0 per 100,000 for
females, while the rates for those 65 years of age and older was 203.5 per 100,000 for males
and 47.4 for females.103
The incidence of bladder cancer is higher for whites than for blacks. The age-adjusted
total incidence rate for 1987-1991 was 18.2 per 100,000 for whites compared to 9.7 per
""American Cancer Society, Cancer Facts and Figures 1996, 1996.
101U.S. Department of Health and Human Services, SEER Cancer Statistics Review 1973-1990, National
Institutes of Health, Pub. No. 93-2789.
]02Ibid.
XI-32
-------
100,000 for blacks, a trend seen among both males and females. However, the age-adjusted
total mortality rate for both whites and blacks was 3.3 per 100,000, indicating a higher
case-fatality rate among blacks than whites.
Pennsylvania- and Philadelphia- Specific Information
The age adjusted incidence rate for bladder cancer among white males living hi
Pennsylvania for 1988-1992 was 34.5, compared to 15.4 for black males and 8.3 for all
females.104 Annual incidence rates for males have been higher in recent years, while annual
incidence rates for females have remained stable.105
The following table provides a comparison of U.S., Pennsylvania and Philadelphia
County bladder cancer data.
Comparison of Average Annual Age-Adjusted Bladder Cancer Rates per 100,000
population for Philadelphia County, Pennsylvania, the United States
Rate Philadelphia
Countyio6
(1988-1992)
Overall Incidence
Overall Mortality
Male Mortality- All races
Female Mortality - All races
White Mortality: male/female
Black Mortality: male/female
Male Incidence - all races
Female Incidence - all races
White Incidence- male/female
not available
not available
6.4
2.5
not available
not available
31.0
8.6
not available
Black Incidence - male/female 1 not available
Pennsylvania1"
7 (1988-1992)
18.7
3.4
6.0
1.8
6.1/1.7
5.2/3.0
33.3
8.3
34.5/8.4
15.4/6.8
United States'"8
(1987-1991)
16.9
3.2
5.7
1.7
5.8/1.6
4.8/2.4
29.9
7.4
32.3/7.8
15.0/5.9
I04T
Pennsylvania Department of Health, Pennsylvania Cancer Incidence and Mortality 1988-1992, State
Center for Health Statistics and Research, Pennsylvania Cancer Registry, Pennsylvania Cancer Control Program,
Harrisburg, PA, February, 1995.
105
106
'Ibid., p. 148.
'Ibid.,pg. 149.
}07Ibid., pg. 150-151.
I08U.S. Department of Health and Human Services, SEER Cancer Statistics Review 1973-1990, National
Institutes of Health, Pub. No. 93-2789.
XI-33
-------
Leukemia
Clinical Description/Summary
Leukemia is a progressive disease of the blood-forming organs, which is marked by
distorted proliferation and development of leukocytes and their precursors in the blood and
bone marrow. Leukemia is accompanied by a reduced number of red blood cells and platelets,
resulting in anemia and increased susceptibility to infection and bleeding.109 There are several
types of leukemia, depending on cell type affected, the duration and character of the disease,
and the increase in or maintenance of the number of abnormal cells in the blood.
The symptoms of leukemia are often vague and can resemble less serious conditions,
making early diagnosis difficult. Symptoms of acute leukemia include fatigue, weight loss,
nosebleeds or other hemorrhages, paleness, bruising easily and repeated infections. These
acute symptoms may appear suddenly in cases of childhood leukemia and over a period of a
few months in adult acute leukemia, while cases of chronic leukemia occur slowly (duration of
symptom development is longer than one year) and with few detectable symptoms, including
marked enlargement of spleen, liver or lymph nodes.110
Public Health Importance
In 1996, it is estimated that 27,600 new cases of leukemia will occur in the United
States, divided between acute leukemia and chronic leukemia. Of these cases, 2,600 will
occur in children. In children, acute lymphocytic leukemia makes up the majority of cases
(1600 cases), while in adults approximately 6,800 cases are acute myelocytic and 7,200 are
chronic lymphocytic leukemia. It is estimated that there will be 21,000 deaths due to leukemia
in the United States in 1996.m
Risk Factors
Exposure to ionizing radiation and certain chemicals including benzene is linked to an
increased risk of leukemia. Persons with Down's Syndrome, Bloom Syndrome, Klinefelter
Syndrome, Fanconi's Syndrome, and Wiskott-Aldrich Syndrome are also at higher risk of
developing leukemia.112 The retrovirus HTLV-1, human T-cell leukemia/lymphoma virus-1,
has been associated with increased risk of leukemia.
109American Cancer Society, Leukemia, Document 004400.
1 '''"Leukemia", Stedman 's Medical Dictionary, 25th edition; Baltimore: Williams and Wilkins, 1990.
1' 'American Cancer Society, Cancer Facts and Figures 1996, 1996.
"2Harrison, Principles of Internal Medicine, 13th edition; New York: McGraw-Hill, 1995.
XI-34
-------
Effects of Race, Gender, and Age
Males have higher incidence and mortality rates for leukemia than females. The United
States incidence of all leukemias from 1987 to 1991 was 13.1 per 100,000 population for
males and 7.7 per 100,000 population for females.113 Incidence and mortality rates are also
generally higher among whites than among blacks.
The effects of age on leukemia incidence vary for each type of leukemia. Figure 1
shows the age-specific incidence rates for all leukemias. There is an initial high incidence rate
among young children, followed by a decline and a gradual rise into the older ages. Acute
lymphocytic leukemia, the predominant form of leukemia among children, demonstrates a high
incidence among children and very low incidence among the adult population until age 75 and
older. Chronic lymphocytic leukemia, however, shows almost no incident cases (0.0 to 0.8
cases per 100,000 population) until age 45 (still quite low, with only 1.4 cases per 100,000),
increasing to 34.5 cases per 100,000 population among those 85 and older.114
Pennsylvania- and Philadelphia-Specific Information
From 1988 through 1992, the age-adjusted incidence rate for leukemia was higher for
males than for females, and the incidence rates for both sexes has been increasing each year.
As with the data from the United States, incidence rates are lower among blacks than whites.
Mortality trends among black males and females in Pennsylvania are difficult to interpret due
to small numbers.115 The table below provides a comparison of incidence and mortality rates
for males, females, whites and blacks in Philadelphia County, Pennsylvania, and the United
States.
"3Ries et al., SEER Cancer Statistics Review, 1973-1991: Tables and Graphs, National Cancer Institute,
NIH Pub. No. 94-2789.
"'Ibid., p. 232.
"'Philadelphia Department of Health, Pennsylvania Cancer Incidence and Mortality 1988-1992, 1995.
XI-35
-------
Comparison of 1991 Leukemia Rates (all leukemias) per 100,000 population for
Philadelphia County, Pennsylvania, the United States
Rate Philadelphia
County* (1988-
1992, age-adjusted)
Overall Incidence
Overall Mortality
Male Mortality- All races
Female Mortality - All races
White Mortality: male/female
Black Mortality: male/female
Male Incidence - all races
Female Incidence - all races
White Incidence- male/female
Black Incidence - male/female
not available
not available
9.1
4.9
not available
not available
9.1
5.8
not available
not available
Pennsylvania*
(1988-1992,
age-adjusted)
8.3
6.5
8.4
5.1
8.5/5.1
8.3/4.8
10.4
6.8
10.7/6.8
7.4/5.8
United States**
(1987-1991, age-
adjusted)
10.0
6.3
8.3
4.9
8.5/5.0
8.0/4.7
13.1
7.7
13.4/7.8
11.5/6.9
L
* Philadelphia Department of Health, Pennsylvania Cancer Incidence and Mortality 1988-1992, 1995.
**Riesetal., SEER Cancer Statistics Review, 1973-1991: Tables and Graphs, National Cancer Institute, NIH
Pub. No. 94-2789.1
Kidney Cancer (Renal Cell Carcinoma)
General Background - Public Health Importance
Kidney cancer116 is the 8th leading cause of cancer among men in the United States,
and the 10th leading cause of cancer among women.117 From 1973 to 1991, the estimated
annual percent increase in kidney cancer incidence was 2.1%. There was also a gradual rise in
mortality from kidney cancer, indicated by an estimated annual percent change in mortality of
0.9%.118
Clinical Description/Early Detection
The classic symptom of kidney cancer is actually a "triad" of three symptoms: flank
pain, abdominal mass, and blood in the urine. However, this triad only occurs in
M6both data sources (Pennsylvania Health Department and SEER) term kidney cancer as cancer of kidney
and renal pelvis.
"'American Cancer Society, Cancer Facts and Figures 1996, 1996.
"8Ries et al., SEER Cancer Statistics Review 1973-1991: Tables and Graphs. National Cancer Institute,
NIH Pub. No. 94-2789.
XI-36
-------
approximately 10% of patients. Most patients (60%) with kidney cancer will experience blood
in the urine. Many symptoms are more general, including weight loss, intermittent fever, and
anemia.119
Risk Factors
There are few identified risk factors for kidney cancer. Cigarette smoking, however, is
an established and significant risk factor, accounting for approximately 25% of all kidney
cancer cases.120 Excessive exposure to cadmium (primarily occupational exposure) and history
of von Hippel-Landau Syndrome are also risk factors for kidney cancer.121
Effects of Race, Gender, and Age
The incidence rates and mortality rates of kidney cancer are approximately twice as
high for males than for females, a trend seen among both blacks and whites. The average
annual age-adjusted incidence rates hi the United States from 1987-1991 for males was 12.1
per 100,000 population and for females was 5.9 per 100,000 population.122 The average age-
adjusted mortality rates for that same tune period hi the United States were 5.0 per 100,000
for males and 2.3 per 100,000 for females.123 There is a substantial effect of age on the
incidence and mortality of kidney cancer. The average age-adjusted incidence rates from
1987-1991 for those less than 65 years of age in the U.S. was 4.9 per 100,000 population and
for those age 65 and older in the U.S. was 42.5 per 100,000. The same trend is seen for
mortality rates: the average age-adjusted mortality rates from 1987-1991 hi the U.S. was 1.6
per 100,000 among those less than age 65, and 20.0 per 100,000 for those age 65 and older.124
Philadelphia- and Pennsylvania- Specific Information
A comparison of the average annual age-adjusted incidence and mortality rates for the United
States, Pennsylvania and Philadelphia County is provide hi the table below.
'"Harrison, Principles of Internal Medicine, 13th Edition; New York: McGraw-Hill, 1995, pp. 1336-8.
'^Pennsylvania Department of Health, Pennsylvania Cancer Incidence and Mortality 1988-1992,
Pennsylvania Center of Health Statistics and Research, 1995.
12lHarrison, Principles of Internal Medicine, 13th Edition; New York: McGraw-Hill, 1995, pp. 1336-8.
122Ries et al., SEER Cancer Statistics Review 1973-1991: Tables and Graphs, National Cancer Institute,
NIH Pub. No. 94-2789.
mlbid., p. 205.
I24lbid.
XI-37
-------
Comparison of Average Annual Age-Adjusted Kidney Cancer Rates per 100,000
population for Philadelphia County, Pennsylvania, the United States
Rate Philadelphia
County125 (1988-1992)
Overall Incidence
Overall Mortality
Male Mortality- All races
Female Mortality - All races
White Mortality: male/female
Black Mortality: male/female
Male Incidence - all races
Female Incidence - all races
White Incidence- male/female
not available
not available
6.0
2.2
not available
not available
14.1
5.9
not available
Black Incidence - male/female not available
Pennsylvania"0
(1988-1992)
8.8
3.5
5.0
2.3-
4.9/2.3
6.2/2.4
12.1
6.2
12.0/6.2
14.0/6.2
United States"7
(1987-1991)
8.6
3.4
5.0
2.3
5.0/2.3
5.0/2.2
12.1
5.9
12.2/6.1
13.7/6.5
L
Liver Cancer
General Background- Public Health Importance
Tumors which originate is the liver are uncommon in the United States, and account
for only 1 % of all cancers.128 There are several types of liver cancer, the most common being
hepatocellular carcinoma.
Liver cancer is the 8th leading cause of cancer deaths in the United States among both
males and females. From 1973 to 1991, the estimated annual percent increase in liver cancer
incidence was 2.3%.129 There was also an increase in mortality over the same time period,
demonstrated by an estimated annual percent increase of 1.4%.m
125
126
'Ibid., p. 149.
'Ibid., p. 150-151.
127U.S. Department of Health and Human Services, SEER Cancer Statistics Review, 1973-1990, National
Institutes of Health, Pub. No. 93-2789.
I28American Cancer Society, Liver Cancer: Adult Primary, Document 004456.
I29Ries et al., SEER Cancer Statistics Review 1973-1991: Tables and Graphs, National Cancer Institute,
NIH Pub. No. 94-2789.
130,,..
Ibid., p. 250.
XI-38
-------
Clinical Description/Early Detection
Liver cancer may be difficult to detect early. Most patients with liver cancer present
with abdominal pain or an abdominal mass. Jaundice (yellowing of the skin and whites of the
eyes) occurs with certain liver disorders.131
Risk Factors
Liver cancer usually occurs in a "cirrhotic" liver (a liver with extensive cellular
damage and progressive fibrosis). Cirrhosis can result from alcoholism, alpha-1 trypsin
deficiency, hemochromatosis (excessive iron in the blood), and chronic hepatitis B and/or C
infection. Environmental toxins including vinyl chloride (a chemical used in the manufacture
of plastics) have been linked to angiosarcoma. Exposure to aflatoxin, a chemical produced by
a mold which grows on peanuts and other grains, is also linked to increased risk of liver
cancer. Thorium dioxide and long-term administration of androgenic steroids also lead to
cirrhosis and subsequently, liver cancer.132
Effects of Race, (fender, and Age
Liver cancer is more common among men than women: the average annual age-
adjusted incidence rate from 1987-1991 in the United States was 4.7 per 100,000 population
for males and 1.8 per 100,000 for females. This increased incidence of liver cancer among
males is seen among both whites and blacks and for all age groups. The age-adjusted
incidence of liver cancer was higher among blacks (4.7 per 100,000 population) than among
whites (2.4 per 100,000) in the United States from 1987-1991.133 The following table
provides a comparison of average annual age-adjusted incidence and mortality rates for males
and females, blacks and whites for the period 1987 to 1991 in the U.S.
Age also has considerable effect on both the incidence and mortality of liver cancer.
The average annual age-adjusted incidence rate of liver cancer among those less than age 65
from 1987-1991 was 1.6 per 100,000 population in the U.S. compared to 16.7 per 100,000
population among those age 65 and older.134 The average annual age-adjusted mortality rates
for the same time period was 1.2 per 100,000 for those less than age 65 and 17.4 per 100,000
for those age 65 and older.135
l31Harrison, Principles of Internal Medicine, 13th edition; New York: McGraw-Hill, 1995, pp. 1496-7.
mlbid.
133Ries et ah, SEER Cancer Statistics Review 1973-1991: Tables and Graphs, National Cancer Institute,
NIH Pub. No. 94-2789.
"4Ibid.,p. 251.
XI-39
-------
Pennsylvania- and Philadelphia- Specific Information
Liver cancer data was not available for Philadelphia County or Pennsylvania.
Average Annual Age-Adjusted Bladder Cancer Rates per 100,000 population for the
United States
Rate United States"6
(1987-1991)
Overall Incidence
Overall Mortality
Male Mortality- All races
Female Mortality - All races
White Mortality: male/female
Black Mortality: male/female
Male Incidence - all races
Female Incidence - all races
White Incidence- male/female
Black Incidence - male/female
3.0
2.8
4.1
1.8
3.6/1.7
6.3/2.6
4.7
1.8
3.6/1.5
7.8/2.4
I36U.S. Department of Health and Human Services, SEER Cancer Statistics Review, 1973-1990. National
Institutes of Health, Pub. No. 93-2789.
XI-40
-------
1993
CO
O)
0)
•4
N.
O)
T- .*
.. c
re
8
0)
O
(0
O
0
Q.
O
OS
ro
OOO'OOl-
-------
1993
CO
O)
0)
0>
= 2
5 i
O D)
S .E
*s ^
O _L
85
Q.
O
-------
-------
OOO'OOL
»paisnfpe-a6v
-------
CO
0>
0>
4
h-
o>
f s
W
0)
O
-------
1993
CO
o>
0>
8
o> ,2
*~ -2
w
UJ
ffi-g
o £
CD
0 O
> CO
Q.
O
1978
- 1977
- 1976
- 1975
1974
000'001- Jsd ajej ¥paisnfpe-a6v
-------
1993
CO
o>
o>
o>
4S
£ JS
0
« o
o
0
CL
O
OOO'OOL
¥pajsnfpB-aBv
-------
-------
O
O
O
.Q
O)
*«
£
w
w
«
u
CO
O
in
Q.
O
£
*«B
"ro
4«
o
•D
S
I
a
a>
I8
Is
*^ IN.
gR
IS
"R
IS
Is
"s
gg
II
lfe
ii
Is
? o>
il
0 cv
58
O CM
Si
S3
» CM
0 ^-
55
N, tO
fe8
<2 co
•a cn
£a
R?
|l
|<3
l!
a.
3
s
a
5
a
s
N
S?
a
n
K
fN.
O)
CM
S
in
CO
s
to
m
00
CD
CO
s
a
ID
a
?
a
[Colon Cancer
S
ft
o>
S
S
CO
N.
N
00
8
CM
R
5
8
0)
CM
a
CO
8
CO
CO
s
a
to
o
in
O
a
K
a
CM
s?
CM
in
o
a
I Breast Cancer
i
IN.
O
cn
m
8
CO
a
1
R
o
CM
*<*
^
g
fN.
O
IN,
CM
8
8
D
8
a
s
8
s
5
00
3
s
8
CM
8
CM
[prostate Cancer
to
IN.'
in
in
f1-.
to
CO
3
CO
a
CO
8
&
cn
fN.
CO
O
CM
g
O
CM
cn
m
cn
tn
CD
3
cn
g
CO
CO
Ipancreas Cancer
R
a
O
CM
tn
fN.
to
CO
CM
fN.
CM
8
fc
g
cn
fN.'
to
R
CO
to
*-
cn
CO
CM
CO
3
3
fN.
3
8
R
ro
3
•N.
£
S
s
§
s
I
m
cn
i
!
i
i
i
i
Dn
I
I
g
i
i
i
CM
i
i
£
i
s
s
i
i
J
I
3
3
g
cn
CM
7)
CO
00
N.
D
S
N
a
9
GO
&
K
in
m
in
R
5
8
S
8
8
00
8
cn
IN.
§
1
g
R
°
3
|Lung Cancer
n
D
3
to
N
CO
CM
S
tn
CD
a
s
in
cn
s
8
m
s
[O
8
CM
S
CO
o
CM
CO
CM
9
O
8
CO
to
o>
CO
8
CD
CM
O>
K
CN
I Co Ion Cancer
f".
CO
CN)
8
a
cn
CM
10
CM
8
CD
CD
a
CM
8
tn
s
s
in
CD
a
CM
8
1
3
O
CM
IN.
CM
CM
00
3
CO
fN.
m
s
8
00
a
00
8
1 Breast Cancer
in
S
in
o>
CO
o
CM
R
O
cn
s
i
00
CO
to
i
8
CD
r*-
CM
a
s
o
IN.
a
m
O
CL
K
(N
CO
r
S
O
CD
00
CO
CO
R
a
m
cn
CM
s
0>
cn
o
-
CM
S
CD
CN
CO
K
CN
(pancreas Cancer
DO
8
S
i
s
I
a
R
s
I
i
CD
8
g
3
i
1
a
CO
3
CO
a
8
m
to
CM
cn
CM
m
to
i
s
IAII sites
f
i
i
i
1
I
i
i
i
I
3
fO
to
on
M
3
en
o
i
i
£
R
S
S
t
S
|
U
1
8
(O
IN.
S
8
I
S
o
Cn
si
3
S
at
IO
S
3
8
n
s
00
CO
00
s
o
CO
ti
s
a
Icolon Cancer
a
a
m
to
to
CM
3
m
s
8
CM
m
cn
a
g
in
CO
s
CM
m
CO
3
a
8
s
§
CD
a
CO
8
8
m
a
8
m
00
h-
0>
(Breast Cancer
"
n
O
r>
cn
00
n
S
n
8
JJ
N
3
N
CO
(D
J
30
8
CO
»
T
CM
8
o>
cn
^
8
o
00
(prostate Cancer
CO
in
00
s
CD
S
O
0
CO
o
CM
fN.
8
0
&
3
O)
fN.
00
in
5
CD
8
CM
8
CO
GO
CM
R
3
CN
m
CM
CM
m
CO
m
O
1
CM
CO
O*
i
s
s
3
\
3
CM
8
S
3
i
R
"
D
CM
0
O
CM
D
O
i
;
R
8
N
g
m
o
CM
Z
S
en
!
n
cn
on
i
cn
n
i
§
i
3
3
i
3
i
3
I
i
z
to
i
6
i
i
u
CO
!S
8
3
S
§
K'
•N,
to
to
3
8
O
V
m
m
D
3
8
g
0
cn
CO
M
3
O
O
N.
8
8
8
g
D
8
3
3
8
n
8
s?
n
N.
CO
CM
CO
8
8
in
8
in
CM
8
8
S
CO
3
(prostate Cancer
CO
CM
CM
00
00
R
O
s
fN.
g
8
CM
3
O
CD
m
CM
3
00
s
CO
8
5
r—
01
s
CD
8
CN
O
CM
(pancreas Cancer
I
0
CM
in
CO
CM
i
3
a
CM
CO
K
cn
a
cn
°
CM
CO
8
CM
fN.
i
CM
8
i
1
S
•a
o
n
o
i
R
i
i
CM
0
n
D
n
3
n
10
i
ID
•a
K
£
i
V)
IN.
tn
N
in
§
g
CD
O
R
5
8
D
O
CD
R
8
N
m
m
8
R
8
a
N
3
m
m
8
S
S
R
in
00
CO
3
8
O
CO
8
8
a
u
D
8
a
fe
a
00
CO
D
N.
cn
N
S
5
"
§
a
1
§
3
N
O
CM
00
in
to
ro
8
8
a
CD
CO
m
00
CM
CO
a
(colon Cancer
a
8
CM
71
tM
8
3
in
cn
CO
§
m
8
§
8
M
8
O
N.
O
m
GO
8
3
a
3
K
IN.
m
D
N
D
3
00
N
a
m
in
CM
CN
00
CN
CD
CM
(Breast Cancer
m
CD
N
5
5
m
D
CO
CM
CO
M
8
CO
CD
O
3
N
8
a
M
8
S
a
§
2
s
cn
8
CO
CM
S
00
CO
g
CO
CM
a
1 Prostate Cancer
o
3
to
CM
to
to
CO
8
CO
to
i
to
CD
tn
IN.
8
CO
cn
CO
3
00
CO
to
CD
3
m
8
CO
in
m
CM
£
Ipancreas Cancer
«
S
to
o
CM
8
8
8
O
CM
cn
CM
CM
N.
cn
CD
8
g
S
1C
CO
CM
CM
CO
m
CM
CM
in
fN.
DO
in
CM
%
to
8
8
g
g
S
8
8
tc
(All Sites
s,
s
1
i
CO
cn
i
i
i
s
s
IO
00
on
S
n
00
on
i
on
i
§
1
(N.
R
S
i
u
cn
3
8
Si
8
CM
in
o
to
co'
g
CO
•a-
00
i
CM
§
3
3
9
3
g
CM
a
IN-
CO
3
tf>
5?
IN.
cn
to
in
a
s
i
i
\
c
1
£
ID
S
CM
O
£
i
&
in
CM
o>
CM
CM
CM
CM
8
to
&
o
CO
CO
ft
8
CO
g
s
a
s
3
1
3
m
s
3
a
s
in
»-
CM
m
00
CO
o
tn
s
a
3
CM
CD
in
fN.
CD
8
in
CO
S
(colon Cancer
O
cn
to
in
CM
8
CD
CM
O
3
00
a
3
CM
8
8
cn
in
CM
CO
8
m
IN
(Breast Cancer
CM
m
CD
O)
g
f
3
cn
8
a
cn
K
8
n
;o
5
5*
00
s
to
s
in
CD
0>
CN
to
m
CM
to
00
CM
IN.
o
a
in
ID
fN.
cn
cn
in
CM
00
S
8
SJK
r
co!
5
a
a
SIS
tel?
00
in
to
fN
fN
ID
fN.
O
*-
CO n
*- eo
cn i01
8|
S
a
alfejs
8
8
•^
*— O)
CM
CN
0
cn
•H
Ipancreas Cancer
s
CN
fN-
i
g
si
a
8
Ol
i
IAII sites "" _7*
8
§
g
s
s
(O
cn
tM
(0
0
CO
glRIS
i
1
cn
5
R
»
R
°
o
CO
R
CO
R
3
CN
CO
s
8
g
I
OD
00
2
fN.
8
CO
00
to
8
CO
o
(O
CM
CN
8
m
CM
s
R
CO
CM
S
2
00
to
8
CO
U)
R
co fN-jin co jco
to JOQ !tn (^ 1^
loo mien iN>icn
*- *- ice
1 Colon Cancer
Breast Cancer
(prostate Cancer
Ipancreas Cancer
1
=
K
-------
CO
o>
o>
• •
0)
•- .a
o
O HI
*
•o
D)
OOO'OOl- -13d 9JBJ pajsnfpe-sBv
c
o
I
3
Q.
O
O.
CO
D
o
OJ
ID
.C
_o
T3
tn
o>
ro
£
CD
_
"CO
o:
-------
1993
CO
o>
o>
4
1^
O)
(0
£
(0
t- 0)
gu.
c £
re re
O 2
* O
•o
To
0
U)
OOO'OOl- -lad eiej pajsnfpe-aBv
c
O
Q.
O
Q.
D
o
a>
o>
f
o
7
i
05
CO
u>
Si
"CD
o:
-------
1993
- 1992
1991
1990
1989
- 1988
§•52
O DO Q- CL
OOO'OtH J9d ajej pajsnfpe-aBv
o
15
Q.
O
Q.
D
o
Tf
o>
1—
03
T3
0}
to
^
TO
i>
D>
CD
CO
(O
^5
"5
o:
-------
OOO'OOl-
o
1
O.
O
O.
CO
o
•*
01
0)
_o
•o
O)
CO
0)
co
-------
_0
a.
o
o.
CO
Z)
o
TT
o>
T—
0)
T3
0)
"S5
3
TT
TO
i
o>
0)
OOO'OOL
OJ
ro
tr
-------
1993
CO
o>
o>
4
1^
o>
CO
a
CO
?
i- 0)
§ o 2 2 g
O m a. Q.
o
Jo
.Q.
O
o.
CO
0)
•o
0)
I/)
^
CO
O)
CD
cc
OOO'OCH J3d ajBJ paisnfpB-aBv
0)
"55
-------
1993
OOO'OOL
c
o
*-»
CO
3
Q.
O
O.
O)
=)
O
i
0)
S
T3
(C
0)
O)
TO
TO
tr
-------
1993
CO
o>
o>
4
o>
• •
CO
£-9
Q: .12
o
O o
* CO
"O
0>
O)
000 '00 1-
pajsnfpe-sBv
Q.
O
Q.
o
•««•
O)
CD
T3
CD
T3
CD
CD
O)
CO
£
CD
10
0)
"CD
o:
-------
*
.2
"E
cc
c
c
CO
r-
05
o>
Di
w
1_
0)
o
c
CD
O
OL
UJ
UJ
(0
en
oo
en
oo
oo
en
oo
en
CO
oo
en
LO
CO
en
OOO'OOL
a.
o
a.
CO
n'
o>
at
cp
i
O)
cc
CO
I/)
.2
to
a:
CM
a>
CO
oo
en
CO
•e
o
73
CO
CD
O
C
a>
0)
o
CO
O
CO
a>
c
CD
E
•c
CO
a.
a>
Q
c
CO
~>*
(A
C
c
CD
a.
a>
2
3
O
CO
CO
*-•
CO
Q
-------
W V) < <
S . fe
<5 CD a)
u. u- u- u.
m
m
">»
(0
o 5
o *
V)
0
O)
o>
O)
o
O5
O)
O)
oo
OJ
oo
00
O)
oo
O)
oo
O5
m
oo
05
o
CO
o
CM
OOO'OOl-J9d
g
*-•
JS
3
Q.
a
O)
o
1^.
CO
0)
x:
T3
O
c
O)
03
ro
U)
S
03
a:
-------
•o
c
(U
*
CO
'E
«J
I
c
Q)
Q.
co < <
0)
0)
o>
0>
o
0)
0)
CD
O
O5
O5
O)
00
CO
CO
O)
00
O)
CD
CO
CD
CO
Q.
o
o
Q.
CO
0>
a>
T3
0)
•55
(D
05
CO
CD
CM
to "
i «
-------
Crude Cancer Incidence Rates for All Sites: 1985-1993
By Neighborhood "
1000
900
BOO
700
- Eastwick-Elmwood
- Grays-Ferry/Passyunk
- Paschall-Kingsessing
- Pennsport-Queen Village
-Schuy!kill-Pt Breeze
- Snyber-Whitman
- South Broad-Girard Estates
-Southwark-Bella Vista
1985
1986
1987
1988
1989
1990
1991
1992
1993
Age-Adjusted Cancer Incidence Rates for All Sites: 1985-1993
By Neighborhood
1000
900
800
700
600
500
•400
300
200
100
_L
J_
- Eastwfck-Bmwood
- Grays-Ferry/Passyunk
- Paschall-Kingsessing
- Pennsport-Queen Village
-SchuylkiB-Pt Breeze
- Snyder-Whitman
- South Broad-Girard Estates
- SouthwarK-Beiia Vista
1985
1986
1987
1988
1989
1990
1991
1992
1993
Incidence rates are age-adjusted to the 1970 U.S. population.
-------
Crude Incidence Rates for Top Five Cancer Sites: 1985-1993
Eastwick-Elmwood
250
1985 1986 1987 1988 1989 1990 1991 1992 1993
Age-Adjusted Incidence Rates for Top Five Cancer Sites: 1985-1993
Eastwick-Elmwood
250
1985 1986 1987 1968 1989 1990 1991 1992 1993
Incidence rates are age-adjusted to the 1970 U.S. population.
-------
Crude Incidence Rates For Top Five Cancer Sites: 1985-1993
Grays Ferry-Passyunk
§
g
250
200
_L
-Lung Cancer
-Colon Cancer
-Bladder Cancer
-Breast Cancer
-Prostate Cancer
1985 1966 1987 1988 1989 1990 1991 1992 1993
Age-Adjusted Incidence Rates for Top Five Cancer Sites: 1985-1993
Grays Ferry-Passyunk
250
1985 1986 1987 1988 1989 1990 1991 1992 1993
Incidence rates are age-adjusted to the 1970 U.S. population.
-------
Crude Incidence Rates for Top Five Cancer Sites: 1985-1993
Paschall-Kingsessing
1985 1986 1987 1988 1989 1990 1991 1992 1993
Age-Adjusted Incidence Rates for Top Five Cancer Sites:1985-1993
Paschall-Kingsessing
250
1985 1986 1987 1988
1990 1991 1992 1993
Incidence rates are age-adjusted to the 1970 U.S. population.
-------
Crude Incidence Rates for Top Five Cancer Sites: 1985-1993
Pennsport-Queens Village
1985 1966 1967 1988 1989 1990 1991 1992 1993
Age-Adjusted Incidence Rates for Top Five Cancer Sites: 1985-1993
Pennsport-Queens Village
250
I
1985 1986 1987 1988 1989 1990 1991 1992 1993
Incidence rates are age-adjusted to the 1970 U.S. population.
-------
350
Crude Incidence Rates for Top Five Cancer Sites: 1985-1993
Schuylkill-Point Breeze
1985 1986
1987
1988 1989 1990 1991
1992 1993
350
1985
Age-Adjusted Incidence Rates for Top Five Cancer Sites: 1985-1993
Schuylkill-Point Breeze
1986
1987
1988
1989
1990
1991
1992
1993
Incidence rates are age-adjusted to the 1970 U.S. population.
-------
200
§
I
S
3.
8
Crude Incidence Rates for Top Five Cancer Sites: 1985-1993
Snyder-Whitman
1985
1966
1987
1988
1990 1991 1992 1993
Age-Adjusted Incidence Rates for Top Five Cancer Sites: 1985-1993
Snyder-Whitman
I
-Lung Cancer
- Colon Cancer
- Bladder Cancer
-Breast Cancer
-Prostate Cancer
1985 1986 1987 1988 1989 1990 1991
1992 1993
Incidence rates are age-adjusted to the 1970 U.S. population.
-------
Crude Incidence Rates for Top Five Cancer Sites: 1985-1993
South Broad-Girard Estates
1985 1966 1967 1988 1989 1990 1991 1992 1993
Age-Adjusted Incidence Rates for Top Five Cancer Sites: 1985-1993
South Broad-Girard Estates
300
250
200
150
§
§
£
I
3 100
Lung Cancer •
•_ Colon Cancer
Bladder Cancer
Breast Cancer
Prostate Cancer
1985 1986 1987 1988 1989 1990 1991 1992
1993
Incidence rates are age-adjusted to the 1970 U.S. population.
-------
§
i-
I
Crude Incidence Rates for Top Five Cancer Sites: 1985-1993
Southwark-Bella Vista
1985 1986 1967 1988 1989 1990 1991 1992
1993
350
Age-Adjusted Incidence For Top Five Cancer Sites: 1985-1993
Southwark-Bella Vista
__Lung Cancer
-•-Colon Cancer
_*_ Bladder Cancer
_._ Breast Cancer
-.-Prostate Cancer
1985 1986
1987
1988
1989 1990 1991 1992
1993
Incidence rates are age-adjusted to the 1970 U.S. population.
-------
•O
|
O
£
S
o>
u
n
U
fi
w
S5
a
o
n
O
in
a
£
w
'o
i
o
8.8
e »
-ft
|5
I"
*" CO
§in
-i
i"
il
n
I"
*"*
U
to
'
S
R
8
in
3
CM
S
S
g
3
«
En
00
T
$
a
s
«
CM
5
O
S
to
2
s
«?
R
S
S
a
CD
to
n
s
i
s
CO
I
g
a
in
co
^_
S
S
in
8
i
CM
CD
i
i
cn
CO
CO
CD
CM
ft
CO
s
to
i
s
s
a
in
CO
CN
S
CM
to
S*~
i
CD
"
a
s
a
1
j
g,
$
i
s
s
i
cn
i
i
i
s
r«~
ID
8
S
CM
I
8
S
r*.
CD
m
r*-
i
i
CD
CO
CM
in
ft
£
S
CO
8
CD
8
1
S
CO
CM
O>
£
o>
I
s
R
g
8
O
R
CD
^
CD
8
in
m'
CO
s
CD
1
CO
R
8
f-.
CM
8
Ol
R
S
CO
m
8
S
CO
CO
i
CM
CO
00
i
j
S
O
§ cold
a
g
$
CM
ft
CO
g
i
g
1
ft.
«
h-
CO
8
CM
ft
S
a
; j
i
CO
\ \ ' ! i
j ' '
•e
IEtstwIck-eimwoo
Lung Cancer
[Colon Cancer
(Bladder Cancer
(Breast Cancer
(Prostate Cancer
i
i
|
(Lung Cancer
(Colon Cancer
R
g
|
(Bladder Cancer
i
(Breast Cancer
(Prostate Cancer
g,
i
^
1
1
i
1
i
i
a
i
§
i
s
CM
O)
i
«
co
8
s
CM
CM
S
S
to
Cb
h-
in
^
CO
ft
§
8
8
n
1
CM
S
o
1
•fl.
]
cn
cn
S
(O
y
£
CM
ft
S
a
a
CO
CO
1
1
*-|CD
CD [CO
a^1
CM
Z
a
£18
?fe
s
CJ
Ico
CO
1 *~
CB
i
4
tn
CM
CM
8
1
s.
<0
CM
S
cn
i
8
eo
CO
t
1
1
I j 1
S
(O
cn
cn
,_
•*
r-
co
CD
11
CO CO
CO CO
S1CO
If-
«,
e
*
**1
cn
Ol
CO
cn
(O
ft
a
5
Co
CM
CO
5
in
S
1
CO
in
&i"
i
"
!
tn
s
i
tn
to
CO
sis
ts
i
^
S
in
CO »~ *- CMICD 'f •**• |CO «-
' 1 i I ' i ' ' i '
i 1 !
R
R
3
$
8
CO
in
m
1
m
CO
s
U)
s
lAII Sttes
I
CM
5
in
i
$
g
CO
in
cO
S
s
tn
g
CD
r«.
CM
8
CD
O
8
CO
CD
i
CO
(5
tn
CO
i
m
in
CO
CD
Q
K
CM
t
i
Of
Ol
i
i
1
;
to
CD
8
CD
S
S
$
s
1
1
>
1
8
a
s
s
m
CM
in
CM
?
cn
CM
S
i
g
m
tn
in
s
m
S
a
to
CO
s
i
g
r-
m
CO
eo
8
3
ft
S
CM
S
a
R
CM
1
1
1
(Lung Cancer
1
I Colon Cancer
(Bladder Cancer
1
m
in
g
CD
3
S?
i
s
a
;
S
CO
CM
i
1
CO
i
§
s
s
^_
1
CO
s
o
8
§
m
CO
to
m
I
.
2
m~
r*.
8l5f
O) *-
s
i ;
1
| Breast Cancer
(Prostate Cancer
lAII Sttes
i
i
ID
•0
o»
1
1
g
00
8
m
CD
^_
S
a
fe
I
u
1
3)
8
sjs
in
i
I
a
CM
CM
00
8
3
a
CO
rt
K
eo
O
00
00
8
O
to
i *-
; ,
1 i
i i *
&
tn
to
s
eo
r-
s
i
in
CO
CO
K
m
S
in
in
00
v
in
CO
CO
CO
r-
CD
8
F
i
s
m
i
i
i
i
! ! i
1
s
s
CO
m
CD
s
s
CD
i
s
i
s
s
s
r-
o
m
to
s
o
CO
|
i
i
3
g
S
f-
s
00
r-
m
s
m
CM
CM
a>
CO
CM
o
i
'
10
«0
cn
i
tn
R
I ' i
I
(prostate Cancer
1
I
rrfEsfa
1
S
41
O
1
u
Icolon Cancer
s
§
CD
00
CM
(Bladder Cancer
,
O
Ol
s
1
o>
a
CN
CO
fS
m
Ol
s
CM
i
i
S
2
CD
in
CO
;
1
SIS
g|R
to
1
CO
CM
CO
to
CM
tn
S
eo
CO
g
i
in
S
!
I
1 ' ,
s
|
i
s
i
i
CO
i i
in
1
1
CO
g
]
i
g
^
CM
CM
«-
8
j
i
to
S "
r^
CO
r--
co
o
1
m
(O
Ol
CD
: 1
(Breast Cancer
(Prostate Cancer
1
IAII Sites
Souihwark-B
-------
O)
*5
UJ
CO
^
o
u
c
n
U
u>
Q.
,2
a
o
u
I
•o
S
a
a
8E5
1°
*
i|
g "!
M
85
" s
§ °
1
1
iss
s?
II
§10
,2
1
i
i
1
IEistwlck-Elm
Lung Cancer
3
V
8
S
R
co
«O
8
K
S
?
S
•n
| Col on Cancer
§
s
0(
0
in
n
to
n
to
o
a
(M
«
~
S
(Bladder Canci
8
§
i
S
8
8
O»
2
I
S
•0
1
s
8
(Breast Cancel
1
•0
§
s
n
i
s
i
s
K
S
S
__
8
S
•
S
|prostate Cane
i
I
3
8
i
i
*
s
g
5
s
3
8
sO
j
g,
i
<
n
8
I
S
S
•
8
*
40
|
S
!
i
8
S
S
r»-
K
8
S
S
8
S
5
"
•*>
•p
2
S
r?
(Lung Cancer
a
in
S
i
s
§
*
s
a
at
a
s
8
3
S
R
(V
g
H
O
1
~
s
m
s
in
s
m
s
§
s
0
8
§
i
8
§
(All Sites
1
*
s
8
8
i
O>
8
g
8
8
.
*
^
IP
1
i
1
10
i
2
8
3
8
R
r»
8
S
9
2
at)
*O
1 Lung Cancer
S
3
S
«
3
I
*O
S
a
2
m
(colon Cancer
I
s
S!
o>
o»
3
a
«D
S
2
^
1 Bladder Cane
«
2
=
2
s
i
m
i
s
i
v
(Breast Cance
S S
K S
m rv
s s
^ *
53
|
O N
8 .
"3
8 3
S X
s a
'
I
SIS
s s
s i
«
1 Prostate Cane
Aillites
1
ll«j»
**
** 1- w
: '
i
CM (0 »-
at n N
i « s
,
= ss
; ,
ss s
*~ m M
fsl?
i ;
tstss
* s ^
S SIS
S 8 S
-S3
5
1
Southwtrk'Bt
Lung Cancer
Colon Cancer
S
«D
0
O)
«
g
BO
e
o
i
s
^
._
laiadderCanc
s
S
R
~
«*>
O
g
m
0)
!
•o
01
R
I
S!
ID
1 Brent Cance
S
to
1
Of
n
z
a
s
3
5
S
S
J
(prostate Cane
1
1
in
3
i
«*)
i
S
1
i
n
in
n
JAN Sites
-------
------- |