Environmental Risk Study
For
City of Chester, Pennsylvania
Conducted by the U.S.Environmental Protection Agency
Region III
in conjunction with the
Pennsylvania Department of Environmental Resources
May, 1995
Draft Report
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The U.S. Environmental Protection Agency wishes to
acknowledge the cooperation and support efforts of the
Pennsylvania Department of Environmental Resources(PADER), the
PADER Region I Office, the Pennsylvania Department of Health,
Bureau of Epidemiology, the Delaware County Commissioners,
Chester City Council, Mayor.Barbara Bohannon-Shepard, Chester
Citizens Concerned for Quality Living, Public Interest Law Center
of Philadelphia, Delaware Valley Toxics Coalition, and Pacific
Environmental Services Inc.
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CHESTER RISK PROJECT
TECHNICAL SUPPORT DOCUMENTS
EXTERNAL REVIEW DRAFT, VERSION 1.0
UNITED STATES ENVIRONMENTAL PROTECTION AGENCY, REGION III
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CHESTER RISK PROJECT
TECHNICAL SUPPORT DOCUMENT
EXTERNAL REVIEW DRAFT VERSION 1.0
TABLE OF CONTENTS
Executive Summary 1
1.0 Objective 3
2.0 Environmental Setting and Background Information 4
3.0 Principles of Risk Assessment and Basic Assumptions 5
3 .1 Introduction 5
3.2 Data Evaluation 6
3.2.1 Chemicals of Potential Concern 6
3.2.2 Exposure Point Concentrations 8
3 .3 Exposure Pathways 8
3.3.1 Receptors 8
3.3.2 Estimating Exposure 9
3.4 Risk Characterization 10
3.4.1 Toxicological Parameters 10
3.4.1.1 Noncarcinogenic Dose-Response Parameters 10
3.4.1.2 Carcinogenic Dose-Response Parameters 11
3.4.1.3 Other Parameters and Criteria 12
3.4.1.4 Adjustment of Dose-Response Parameters 13
3.5 Uncertainty Analysis 13
4.0 Specific Media and Data Sets Assessed 15
4.1 Groundwater and Drinking Water... 15
4.1.1 Data Sources 15
4.1.1.1 PADER Finished Water Data 15
4.1.1.2 USGS GWSI 16
4.1.1.3 Pennsylvania Bureau of Topographic and Geologic Survey.17
4.1.1.4 USGS Files of Well Driller Reports 17
4.1.1.5 1990 United States Census 17
4.1.1.6 Hazardous Waste CERCLIS and RCRA NCAPS 18
4.1.1.7 Geographic Information System 18
4.1.1.8 Federal Reporting Data System 18
4.1.2 Screening Data Analysis 19
4.1.3 Risk Assessment Data Analysis 19
4.1.4 Results and Discussion 20
4.1.4.1 Private Well Investigation 20
4.1.4.2 Groundwater Quality in the Study Area 21
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4.1.4.3 Public Water Supply 22
4.1.5 Uncertainty Analysis 29
4 .2 Lead 31
4.2.1 Introduction 31
,4.2.1.1 Lead in the Environment 31
4.2.1.2 Lead Exposure 32
4.2.1.3 Movement of Lead in the Body 33
4.2.1.4 Toxic Effects of Lead 33
4.2.1.5 The USEPA Three City Study 34
4.2.2 Data Source 34
4.2.3 Data Analysis 35
4.2.4 Results and Discussion ' 36
4.2.5 Uncertainty Analysis 38
4.3 RCRA TSDF Facilities 39
4.3.1 Data Source . 39
4.3.2 Data Analysis, Results and Discussion . 39
4.4 CERCLIS Facilities: Surface Soil and Leachate 41
4.4.1 Data Source 41
4.4.2 Screening Data Analysis 42
4.4.3 Risk Assessment Data Analysis 42
4.4.4 Results and Discussion 42
4.4.5 Uncertainty Analysis 43
4.5 Surface Water, Sediment, and Fish Tissue 43
4.5.1 Data Sources 44
4.5.1.1 STORET 44
4.5.1.2 CERCLIS 44
4.5.1.3 National Study of Chemical Residues 44
4.5.1.4 Data Quality . 45
4.5.2 Screening Data Analysis 46
4.5.3 Risk Assessment Analysis 46
4.5.4 Results and Discussion 47
4.5.5 Comparative Risks and Additional Information .....48
4.5.6 Uncertainty Analysis 50
4.6 Toxic Release Inventory (TRI) 51
4.6.1 Data Source 51
4.6.2 Data Analysis 51
4.6.3 Results and Discussion 52
4.6.3.1 Sun Refining and Marketing Co., Marcus Hook 52
4.6.3.2 Witco Corp., Trainer 53
4.6.3.3 Scott Paper, Chester 53
4.6.3.4 Foamex, L.P., Eddystone 54
4.6.3.5 Boeing Defense and Space Group, Ridley Park 54
4.6.3.6 Epsilon Products 54
4.7 Air 55
4.7.1 Modeled Air Concentrations 55
4.7.1.1 Data Source 55
4.7.1.2 Point Source Data Analysis 55
4.7.1.3 Point Source Results and Discussion 55
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4.7.1.4 Point Source Uncertainties Analysis 59
4.7.1.5 Mobile Source Data Analysis (Truck Route Modeling) 59
4.7.1.6 Results and Discussion 60
4.7.1.7 Mobile Source Uncertainty Analysis 61
4.7.2 Area Source Emissions 61
4.7.2.1 Definition of Area Sources 62
4.7.2.2 Data Source 62
4.7.2.3 Data Analysis 62
4.7.2.4 Results and Discussion 62
4.7.2.5 Uncertainty Analysis 63
4.7.2.6 Recommendations 63
4.8 Other Environmental Concerns ..63
4.8.1 Odors ' 63
4.8.1.1 Background Information 64
4.8.1.2 Long-Term Odor Investigation 65
4.8.1.3 ShortrTerm Odor investigation 65
4.8.2 Noise 66
4.8.2.1 Background Information 66
4.8.2.2 Noise Control Ordinance 68
4.8.2.3 Control of Environmental Noise 68
4.9 Epidemiological Issues 68
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EXECUTIVE SUMMARY
The Chester Risk Assessment Project was part of an
initiative by the United States Environmental Protection Agency
(USEPA) Region III and agencies of the Commonwealth of
Pennsylvania to study environmental risks, health, and regulatory
issues in the Chester, Pennsylvania area. Although the original
intent of the study was to provide a complete "cumulative risk
study," utilizing exposure data for all environmental media and
exposure pathways, the actual report is more of an aggregated
risk study due to the largely unknown nature of the interrelated
exposures.
The city of Chester is located approximately 15 miles
southwest of the city of Philadelphia along the Delaware River.
According to the 1990 United States Census, 41,856 persons reside
in Chester, which has an area of 4.8 square miles.- Surrounding
communities also examined in development of this report include
Eddystone, Trainer, Marcus Hook, and Linwood. The area contains
a mixture of commercial, residential, and industrial uses.
Often, industrial facilities and major highways are situated very
close to residences.
A key element in the project scope called for environmental
risks to be quantitated wherever possible, and supplemented with
qualitative information. Chemical data were gathered from
existing sources. The scope of this project did not include
collection of new data specifically designed for a Chester risk
assessment. Instead the workgroup performed an examination of
available data which yielded the following observations:
• The data had been collected for different programs and
different agencies. These data were not originally
designed to support a quantitative risk assessment of
the Chester area.
• The databases were of varying quality, and certain
chemicals and media had not been tested. However, even
with the limited data, many data sets were available to
be used to generate estimated risks.
• Modeling of air. data from point sources was performed
prior to the air risk assessment. Therefore, point
source air risks are based on projected data! rather
than data actually collected in the field. The lead
(Pb) data, area sources of volatile organic compound
(VOC) emissions, Resource Conservation and Recovery Act
(RCRA) site information, and Toxic Release Inventory
(TRI) data did not involve the types of environmental
data conducive to quantitative risk assessment.
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The findings of the report include:
• Over 60% of children's blood lead samples were above
the Center for Disease Control (CDC) recommended
threshold action level of 10 ug/dL.
• Both cancer and non-cancer risks from the pollution
sources at locations in the city of Chester exceed
levels which USEPA believes are acceptable. Air
emissions from facilities in and around Chester provide
a component of the cancer and non-cancer risk to the
citizens of Chester.
• The potential health risk from regularly eating
contaminated fish from streams in Chester and the
Delaware River is unacceptably high.
• Drinking water in Chester appears to be typical of
supplies in other cities through out the country.
In response to these findings, the USEPA Region III
recommends that:
• the lead paint education and abatement program in the
city of Chester should be aggressively enhanced,
• sources of air emissions which impact the areas of the
city with unacceptably high risk should be targeted for
compliance inspections and any necessary enforcement
action,
• a voluntary emission reduction program should be
instituted to obtain additional emissions reductions
from facilities which provide the most emissions in the
areas of highest risk,
• enhanced public education programs regarding the
reasons behind the existing state mandated fishing ban
should be implemented.
In addition, while fugitive dust emissions have not shown to
be a significant component of risk in the City, a program to
minimize fugitive emissions from dirt piles and streets should be
instituted to alleviate this nuisance.
There was limited ability to assess noise and odor
complaints for the city within the timeframe of the study. It is
recommended that follow-up continue in the form of a noise and.
odor monitoring program in areas most likely to suffer from these
nuisances. If significant levels are found, a noise and/or odor
reduction program should be implemented in those areas.
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1.0 OBJECTIVE
The Chester Risk Project was part of a larger initiative by
the United States Environmental Protection Agency (USEPA) Region
III and agencies of the Commonwealth of Pennsylvania to study
environmental risks, health, and regulatory issues in the
Chester, Pennsylvania area. This initiative was the result of
potential concerns from the perspective of environmental risk
because of factors such as a high concentration of industry and
the proximity of residences to industrial and high-traffic areas.
Members of the community contacted USEPA with concerns about
their health and environment. Additionally, factors such as the
economic status of the area and the presence of a significant
minority population raised potential concerns with respect to
environmental justice.
This report contains the technical findings and supporting
documentation for the environmental risk portion of the Chester
study. The USEPA Region III Toxicologists' Quality Circle was
tasked to perform a risk assessment of the Chester, Pennsylvania
area. The scope of the risk assessment was defined as follows:
• Environmental risks should be quantitated wherever
possible, and supplemented with qualitative
information.
• The study should be performed in 180 days. Within the
scope of the 180-day study, new environmental sampling
would not be conducted, and the study should rely on
existing data.
• The assessment should take into account multiple
sources and potential sources of environmental risk.
As far as possible, the sum of these risks should be
evaluated.
• Within the scope of the 180-day study, it was not
possible to perform a "control city" evaluation or a
comparative study. However, relevant data currently
available for the rest of the Region (Pennsylvania,
Maryland, Delaware, Virginia, West Virginia, District
of Columbia) or nation would be incorporated wherever
possible.
• As far as possible, the concerns of the Chester area
community should be considered in the study.
• Technical guidance for the performance of risk
3.ss©ssip.0nt should bs followed.
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2.0 ENVIRONMENTAL SETTING AND BACKGROUND INFORMATION
The city of Chester is located approximately 15 miles
southwest of the city of Philadelphia along the Delaware River
(see Fig. 2-1). According to the 1990 United States Census,
41,856 persons reside in Chester, which has an area of 4.8 square
miles. Approximately 75% of the population is reported to
consist of people of color (65% African-American). Surrounding
communities also examined in development of this report include
Eddystone, Trainer, Marcus Hook, and Linwood. Major, routes
transecting Chester include Interstate 95, which runs northeast
to southwest through the city, and US Route 13, which parallels
Interstate 95 to the east. US Route 322 bisects Chester from
northwest to southeast and leads to the Commodore Barry Bridge
over the Delaware River to New Jersey.
Drinking water for the City of Chester is supplied by the
Chester Water Authority (CWA) and Philadelphia Suburban Water
Company (PSWC). CWA is supplied with surface water from the
Octoraro Reservoir in Lancaster County and from the Susquehanna
River near the Peach Bottom nuclear plant. CWA's surface water
intakes are well outside the study area and do not receive
drainage from the city. The PSWC is supplied with surface water
and groundwater from six surface water sources and 39 wells. The
closest surface intake is located on Crum Creek about eight miles
north of the city of Chester. There are no PSWC wells in the
Chester City area.
Large sources of surface water in the city of Chester
include Chester Creek and the Delaware River. All streams in the
Chester vicinity ultimately drain into the Delaware River in a
dendritic pattern. The Delaware River is a protected waterway
for the maintenance and propagation of fish species that are
indigenous to a warm-water habitat. Additional uses for the
river include as a passageway for migratory fish, potable water
supply, livestock water supply, irrigation, water contact sports,
and navigation. Wetland areas front along the Delaware River in
the Chester city area. The short nose sturgeon (Ancipenser
brevirostrum) is a federally protected species with a habitat
that includes the Delaware River within the study area. In
addition, two federally listed endangered birds are expected to
be found as transient species in the project area. They are the
bald eagle (Haliaeetus leucocephalus) and the peregrine falcon
(Falco perearinusl. There are no listed critical habitats for
these species in the study area.
The hydrogeologic conditions beneath the study area are
highly dynamic in nature. Water levels are influenced by tides
and high rates of infiltration from storms. Shallow groundwater
will generally flow from topographic highs to lows and discharge
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into Chester Creek and the Delaware River. Groundwater flow in
the underlying crystalline bedrock is restricted to fractures and
joints.
The regional climate is moderate and humid due to the low
topographic relief and proximity to the Atlantic Coast. As a
result, the southeastern part of Pennsylvania is more humid and
has more precipitation than western Pennsylvania. The mean
annual temperature for Philadelphia, Pennsylvania, the closest
reporting station, is 54.3°F. Average monthly temperatures range
from 31.2°F in January to 76.5°F in July. The average annual
precipitation is 41.38 inches, which is evenly distributed
throughout the year.
3.0 PRINCIPLES OF RISK ASSESSMENT AND BASIC ASSUMPTIONS
Examination of available data yielded the following
observations: The data had been collected for different programs
and different agencies and were not originally designed to
support a quantitative risk assessment of the Chester area. The
databases were of varying quality, and certain chemicals and
media had not been tested. However, with the limited data
available, it was possible for many data sets to be used to
generate estimated risks.
The following principles and procedures were used for the
generation of quantitative risks. Modeling of air data from
point sources preceded the air risk assessment, such that point
source air risks are based on projected data rather than data
actually collected in the field. The lead data, area sources of
volatile organic compound (VOC) emissions, Resource Conservation
and Recovery Act (RCRA) site information, and Toxic Release
Inventory (TRI) data did not involve the types of environmental
data conducive to quantitative risk assessment, and they were
evaluated as described in Section 4.
3.1 INTRODUCTION
In a risk assessment, the hazards posed by chemicals
detected by chemical analysis are evaluated. Potential risks may
exist when there are chemicals present in media and receptors
which have access to the chemicals. This constitutes a complete
exposure pathway.
The following steps form a basic framework that the
quantitative assessments in this document followed wherever
possible. Special evaluations (i.e., lead, TRI data) were
performed for those data sets which did not lend themselves to
this type of analysis.
To evaluate risks, several steps are taken. First, the data
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are assessed for usability and comparability. Data may then
undergo statistical manipulations for use in the quantitative
risk assessment. An initial screening step occurs during data
evaluation for the purposes of narrowing down the list of
chemicals that are quantitatively assessed. Using conservative
assumptions, the chemical concentrations that would correspond to
the lower end of the target screening risk range are calculated.
These concentrations are called risk-based concentrations, or
RBCs, and are compared to the site data during the data
evaluation stage to rule out chemicals that will not contribute
significantly to risks at the site.
Exposure pathways are then determined. The receptors that
may be exposed are also chosen. Both current and future land
uses must be considered. Using site-specific or default
assumptions, estimated exposure doses are calculated for each
receptor.
Once the amount of exposure each receptor receives.has been
calculated, that amount or dose is compared with values designed
to assess the safety or toxicity of a chemical. This step, which
is called risk characterization, helps the risk assessor
determine the likelihood of adverse effects occurring for that
exposure scenario.
Finally, the uncertainty of the risk analysis is described,
either quantitatively, qualitatively, or both. This step helps
give a more complete picture of environmental risks, and helps
risk managers weigh their options in addressing potential
hazards.
The following sections give a detailed explanation of how
these steps were performed for the Chester area project.
3.2 DATA EVALUATION
Chemical data were gathered from existing sources. The
scope of this project did not include collection of new data
specifically designed for a Chester risk assessment. The data
sources and data quality are discussed in detail in Section 4.
3.2.1 Chemicals of Potential Concern
The data were examined in order to determine chemicals of
potential concern (COPCs). COPCs are defined as those substances
that are potentially related to the risk source being studied and
whose data are of sufficient quality for use in the risk
assessment. It is appropriate to select COPCs for each medium of
concern.
Data were often screened using RBCs. RBCs were used to
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determine whether, if included in the risk assessment, the
chemical would be likely to contribute significantly to the risk.
The screening concentrations were based on the following exposure
assumptions for soil and sediment:
For carcinogens, residential exposure was assumed to occur
during both childhood and adulthood for a total of 3 0 years, 350
days/year, divided into lifetime segments of 6 years at 15 kg
body weight, ingesting 200 mg/day of soil, and 24.years at 70 kg,
ingesting 100 mg/day.
For noncarcinogens, a six-year childhood exposure was
assumed, with a 15-kg child consuming 200 mg/day of soil, 350
days per year. For noncarcinogens, the child-only scenario is
more conservative than the adult scenario.
For leachate, the screening parameters included an exposure
frequency of 7 days/year for a 70-kilogram adult for 30 years.
The ingestion rate was 10 mL/event for liquid leachate and 100
mg/event for solid leachate samples.
Chemicals that are essential nutrients and common minerals
(calcium, iron, magnesium, potassium, and sodium) were not
selected as COPCs.
The RBCs for drinking water were derived as follows:
For carcinogens, residential exposure was assumed to occur
during both childhood and adulthood for a total of 30 years, 350
days/year, divided into lifetime segments of 6 years at 15 kg
body weight consuming 1 L/day and 24 years at 70 kg consuming 2
L/day. For noncarcinogens, the thirty-year adult-only scenario
was used. For volatile chemicals (those with a Henry's Law
constant greater than 1E-5 atm-m3/mol) , a volatilization factor
of 0.5 L/m3 and an inhalation rate of 20 m3/day were assumed.
' Several different types of surface water samples were
obtained. They included samples from constantly flowing streams,
large bodies of water such as the Delaware River, intermittent
streams, drainage ditches, and areas of ponded water.
Unfiltered inorganic results were used for surface water in
the assessment of human health effects, because any direct
contact would occur with the water in its unfiltered state,
including any suspended sediments.
Stream surface water COPCs were selected by comparing
results to RBCs. The surface water RBCs were derived using the
following assumptions: 30-year exposure (simplified as 6 years at
15 kg and 24 years at 70 kg) during swimming, with incidental
ingestion of 50 mL/hour of surface water, with each swimming
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event lasting 2.6 hours and occurring 7 times/year, based
primarily on suggested inputs from USEPA, 1989a.
Modeled air concentrations were compared to risk-based
concentrations (RBCs). The RBCs were based on the following
exposure assumptions: Residential exposure was assumed to occur
during both childhood and adulthood for a total of 30 years, 350
days/year, divided into lifetime segments of 6 years at 15 kg
body weight, inhaling 12 m3 of air per day, and 24 years at 70
kg, inhaling 20 m3/day (30 years of adulthood for
noncarcinogens). For air criteria pollutants, comparisons were
made to National Ambient Air Quality Standards (NAAQS) instead of
RfDs.
Fish tissue samples were compared with RBCs for fish tissue.
Consumption was assumed to occur by adults for a total of 30
years, 350 days/year, ingesting 54 g of fish per.day. This
corresponds to a fish consumption rate of approximately 3/4 lb.
of locally caught fish per week.
Using these assumptions, the RBCs were calculated at target
risks of Hazard Quotient (HQ) = 0.1 (one-tenth the expected no-
effects dose) and cancer risk = 1E-6 (probability of excess
cancer cases 1 in 1,000,000). Calculation of HQs and estimated
cancer risks is discussed in detail in Section 3.4.
3.2.2 Exposure Point Concentrations
Use of the 95% upper confidence limit (UCL) on the mean was
considered for exposure point concentrations. However, several
issues arose. Some data sets contained too few samples for the
derivation of a UCL. Some very large data sets were not
available in electronic format, making it doubtful that UCL
calculations could be performed within the time constraints of
the study. Some databases were clear in identifying positive
results and maximums, but interpretation of detection limits was
difficult. For other data sets, only averages were reported.
The detailed assessment of each data set (see Section 4)
includes a discussion of exposure point concentration and whether
maximum or average concentration was selected. The results for
each assessment must be placed in the context of whether it
represents estimated worst-case or average exposure.
3.3 EXPOSURE PATHWAYS
3.3.1 Receptors
Several factors determine what receptors may be exposed to
the COPCs. It is expected that adult and child residents could
be exposed to air, surface soil, sediment, and leachate. It is
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anticipated that local residents could be exposed to surface
water and sediment through recreational use. Public water supply
results were obtained, and adults and children served by these
supplies would be the potential receptors of concern for that
water. People were observed fishing in the Delaware River, and
it was assumed that the fish consumption pathway would also be
complete.
t
3.3.2 Estimating Exposure
Exposure estimations are calculated for each receptor and
each medium. Exposures from direct contact with soil and
sediment can occur via incidental ingestion and dermal contact.
Fugitive dust emissions and emissions of volatile organics from
surface soils may contribute to inhalation exposure, although
these pathways are usually much less significant than ingestion
and dermal exposure.
Incidental ingestion of soil and sediment is estimated as
shown in Table 3-1. Leachate risks were not quantitated because
the sample concentrations did not exceed the screening RBCs (see
Section 4.5).
Dermal exposure to soil and sediment is assessed as shown in
Table 3-2.
There are generally three routes of exposure to chemicals in
drinking water: ingestion, dermal exposure, and inhalation. The
greatest exposures are assumed to occur from the activities of
drinking and bathing or showering.
Ingestion exposure is estimated as shown in Table 3-3.
Dermal exposure to water is estimated as shown in Table 3-4.
Inhalation exposure through showering is generally assumed to
occur for adults only and is estimated as shown in Table 3-5.
For adults, the exposure from inhalation and ingestion comprises
the bulk of the risk, and these two routes were quantitated.
Because children are expected to bathe rather than shower,
ingestion and dermal exposure were quantitated for children.
The equations used for surface water exposure are the same
used to evaluate ingestion and dermal exposure to groundwater.
However, the inputs vary and are shown on Tables 3-3 and 3-4.
The equations used for exposure to air contaminants are
shown in Table 3-6.
The fish tissue ingestion equation was the same as that used
for soil ingestion. Some of the input parameters differ from
those of soil exposure and are shown on Table 3-1.
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3.4 RISK CHARACTERIZATION
3.4.1 Toxicological Parameters
Once exposure has been estimated in terms of a dose for each
receptor, further assessment must be done to determine the risk
associated with that dose. This is commonly done with the use of
dose-response parameters.
Dose-response parameters are based on scientific studies.
They attempt to correlate a given dose with its effect on a
receptor. Noncarcinogenic (non-cancer) effects are generally
assumed to have a threshold; that is, a level below which
exposure can occur without adverse effects. Carcinogenic
(cancer-causing) effects are assumed by USEPA to have no
threshold; that is, any exposure may potentially cause the
cellular changes that lead to uncontrolled celi proliferation.
Therefore, the two effects, carcinogenic and noncarcinogenic, are
evaluated differently.
The dose-response parameters for the COPCs in the Chester
area are shown on Tables 3-7 and 3-8. The following hierarchy
was followed in selecting these numbers: parameters from USEPA's
Integrated Risk Information System (IRIS), parameters from Health
Effects Assessment Summary Tables (HEAST), numbers withdrawn from
IRIS or HEAST but not yet substituted, numbers from USEPA's
Environmental Criteria and Assessment Office (ECAO), numbers from
other sources. Section 5.0 includes further discussion of the
sources of these numbers and the uncertainty associated with
them. Dose-response parameters used in the TRI assessment are
shown on Table 4-28.
This section addresses the quantitative toxicity of the
COPCs. Appendix I includes Toxicological Profiles for each COPC,
which contain descriptions of the properties and potential
effects of the COPCs.
3.4.1.1 Noncarcinogenic Dose-Response Parameters
Concentrations of chemicals at which no adverse effects have
been observed, or which were the lowest levels at which adverse
effects were observed, may be used to estimate a Reference Dose
(RfD) for human exposure. The No-Observed-Adverse-Effects-Levels
(NOAELs) or Lowest-Observed-Adverse-Effects-Levels (LOAELs) are
typically reported from animal data. Other experimental factors,
such as the route of administration of the chemical, may
contribute to difficulties comparing these data to human
exposures. Therefore, USEPA develops RfDs for human exposure by
multiplying the NOAEL or LOAEL by uncertainty factors and
modifying factors. The uncertainty factors are applied to
account for variation in the general population, extrapolation
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from animal data to humans, extrapolation from short-term studies
to assessing chronic exposure, differences between NOAELs vs.
LOAELs, and any other sources of uncertainty. RfDs are available
for ingestion and inhalation exposures. At this time, dermal
doses are assessed by comparison to adjusted oral RfDs (USEPA,
1989a).
To evaluate human noncarcinogenic risk, the exposure dose is
divided by the RfD. If the dose is less than the RfD, this
quotient, referred to as the Hazard Quotient (HQ), will be less
than 1, and adverse effects would not be anticipated. Because
RfDs are set below expected toxic doses, it is difficult to
determine at what dose toxicity would be expected to occur.
Therefore, although exceedance of RfDs does not necessarily mean
that toxic effects will be expected, it is prudent for exposures
to result in HQs less than 1.
When more than one chemical is present in the medium of
exposure, the combined effects of these chemicals must be
considered. Chemicals may act synergistically, where the
combined effect is much greater than would be expected when each
of their effects is considered individually. They may act
antagonistically, where the combined effect is less than would be
expected when considering the chemicals individually. Chemicals
may also act additively, where the combined effect is equal to
the sum of the individual effects. With the present state of
knowledge, chemicals in mixtures are assumed to act additively
unless there is evidence to the contrary. Therefore, HQs may be
added for a total Hazard Index (HI). When the chemicals act on
the same target organs via similar mechanisms, it is also
desirable for the HI to be less than 1. Therefore, for all His
greater than 1, an assessment of the mechanisms of toxicity will
be made to determine whether an unacceptable risk exists from a
combination of chemicals.
RfDs have not been developed for all chemicals. Where they
are unavailable, substitute values may be used. For example, a
provisional allowable daily intake (ADI) may be estimated using
the Layton method, which involves multiplying animal data
(usually an LD50, or dose lethal to 50 percent of an experimental
population) by a conservative factor (Layton, 1987). For
carcinogens, noncarcinogenic effects usually occur at much higher
levels than unacceptable carcinogenic risks. In such cases,
where the RfD is not available, only carcinogenic effects were
assessed.
3.4.1.2 Carcinogenic Dose-Response Parameters
USEPA assigns a "weight-of-evidence" to carcinogens to
evaluate the likelihood that the agent is a human carcinogen.
The weight-of-evidence classifications are defined below:
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Group A Human carcinogen
Group B Probable human carcinogen; B1 indicates that limited
human data are available; B2 indicates that there is
sufficient evidence in animals and inadequate or no
evidence in humans
Group C Possible human carcinogen
Group D Not classifiable as to human carcinogenicity
Group E Evidence of noncarcinogenicity for humans.
For the purposes of this risk assessment, carcinogenic
effects were assessed for Groups A, B, and C carcinogens.
The parameter that relates exposure dose to carcinogenic
response is the slope factor. The slope factor is used in risk
assessments to estimate an upper-bound lifetime probability of an
individual developing cancer as a result of exposure to a
carcinogen. Slope factors are derived from scientific study
data, to which a variety of mathematical models may be applied.
For each slope factor, the Integrated Risk Information System
(IRIS) database includes a summary of the information used to
derive that chemical's slope factor.
To estimate carcinogenic risk, the following equation is
used:
CR = 1 - exp(-CSF x D)
CR = Estimated cancer risk
CSF = Cancer slope factor (1/mg/kg/day)
D = Exposure dose (mg/kg/day)
3.4.1.3 Other Parameters and Criteria
For drinking water, in addition to estimations of risk as
described above, comparisons to drinking water criteria may be
made. Under the Safe Drinking Water Act, public water suppliers
are required to meet National Primary Drinking Water Regulations
(NPDWRs), which may take the form of Maximum Contaminant Levels
(MCLs) or Action Levels.
This is not a risk estimation method, since MCLs are based
on both human health information and available technology. In
some cases, MCLs may be well below levels expected to be
associated with significant human health risks. In other cases,
there may be evidence that MCLs may not be as protective as
desired, but the regulations have not been changed yet because of
the lengthy process involved in changing these numbers or because
no cost-effective technology currently exists for treatment of
the chemical in water. Some chemicals are unavoidable by-
products of the chlorination process necessary for the
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disinfection of public water supplies. Potential risks
associated with these unavoidable chemicals are balanced by the
benefits of removing pathogenic organisms from public water
supplies.
MCL Goals (MCLGs) are not required to be met by public water
supplies. They are health-based numbers, and MCLs are set as
close to MCLGs as possible. For known and suspected human
carcinogens, the MCLGs are set at zero.
Secondary MCLs (SMCLs) are not health-based. They are
designed to prevent unpleasant aesthetic effects in water such as
offensive taste or odor, corrosivity or staining of plumbing
fixtures.
3.4.1.4 Adjustment of Dose-Response Parameters
In accordance with USEPA, 1989a, Appendix A, the dose-
response parameters had to be adjusted when the estimated dose
was dermally absorbed,, but the original parameter was based on
oral intake. This was done by adjusting the orally administered
parameter by the oral absorption percentage (preferably for the
same route, vehicle, and species as the critical study on which
the parameter was based) to give an absorbed parameter. The
following absorption factors were obtained from USEPA IRIS and
ECAO:
Arsenic: 95%
1,2-Dichloroethene: 100%
Nickel: 4.3%
Tetrachloroethene: 100%
Vinyl chloride: 100%
Beryllium: 1%
Manganese: 3-4% from food, 100% from water
Cadmium: 5% from water, 2.5% from food
Copper: 60%
Zinc: 25%
Mercury: 15%
Polychlorinated biphenyls (PCBs): 89%
All other absorption factors for this adjustment were
assumed to be 100% if no other number was available. As can be
seen from the factors for other volatile compounds, this is
expected to be realistic for volatile compounds, and less so for
semi-volatiles, pesticides, and metals.
3.5 UNCERTAINTY ANALYSIS
Uncertainty will be discussed in Section 4 for each data set
and calculation, However, this section includes general
uncertainties common to all the data sets.
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Uncertainty associated with the assessment of risk may be
associated with exposure estimation, toxicity assessment, and in
risk characterization. The policy of the USEPA is to be
protective of human health and the environment. In accordance
with this policy, exposure estimates and the parameters used in
the characterization of the exposures are of a conservative
nature whenever possible. These conservative parameters are
designed to insure that all estimates are protective and that all
sensitive subpopulations are considered. Some of these exposure
parameters may -be overestimates of the actual exposures
experienced by receptors.
The use of default parameters may lead to an overestimation
of risk, since these values are conservative for the purpose of
protecting sensitive receptors in risk evaluation. There are
also uncertainties associated with chemical-specific input
parameters such as permeability constants.
Agency guidance assumes that the concentrations of
contaminants identified will remain the same over time. Since
the contaminant concentrations may decrease over time, the
exposures of receptors and subsequent risks calculated may be
overestimates for future exposure. This could also result in
underestimation if further releases were to occur.
Uncertainty associated with toxicity characterization may be
due to factors including extrapolation from subchronic to chronic
data, intraspecies extrapolation, interspecies variability, lack
of certain types of data, data limitations, and other relevant
modifying factors. All of these factors are taken into account
when evaluating the toxicity of the contaminants in question.
Toxicity factors may be based upon cases such as the
extrapolation of data obtained from animal studies in which
short-term exposure to very high concentrations of contaminants
produced some carcinogenic effects to possible human effects
produced by low-dose long-term exposures.
The evaluation of the uncertainty associated with toxicity
also includes an assessment of the certainty with respect to RfD
values and the safety factors built into the toxicity values used
for the evaluation of contaminants. It should be noted that in
applying the Agency's RfD methodology, arguments may be made for
various RfD values within a factor of 2 or 3 of the current RfD
value. Additionally, the RfD computation methodology derives, a
number with inherent uncertainty that may span an order of
magnitude. The IRIS database includes information related to the
uncertainty factors and the confidence in the RfD values for a
given contaminant.
Uncertainty associated with the characterization of risk is
related to the uncertainty of the exposure and toxicity
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characterizations. It is noted that risk is a function of the
intake of a contaminant as based on the exposure scenario and the
toxicity of the contaminant to which the receptor has beeri
exposed. It is acknowledged that the default exposure parameters
are conservative and therefore probably overestimate the actual
exposure. The uncertainty associated-with RfDs and other
toxicity data values is based upon the methodology used to derive
the data values, the quality of the data derived from the various
studies used to assess the toxicity of the contaminant, and the
margins of safety built into these values.
No special subpopulations (other than children, which are
considered to be part of almost every residential population)
were identified. While certain subpopulations such as
subsistence fishers, children with pica, and persons with
respiratory diseases may exist within the study area, there was
little or no available information that could be incorporated
within the framework of the 180-day study.
4.0 SPECIFIC MEDIA AND DATA SETS ASSESSED
This section consists of the results of the quantitative
risk assessments for specific data sets. Qualitative discussions
of risk and comparative information are also included, wherever
possible. Evaluation of environmental data sets (area sources,
blood lead, RCRA, and TRI data) that did not lend themselves to
standard quantitative risk assessment but contained information
relevant to the Chester area environment are also included.
4.1 GROUNDWATER AND DRINKING WATER
This study investigated the drinking water quality of both
private and public well users in the City of Chester and
surrounding municipalities including Marcus Hook Borough, Trainer
Borough, Chester City, Chester Township, Linwood, Upland Borough
and Eddystone Borough. The potability of the groundwater in the
study area and potential risk to private well users was evaluated
by qualitative assessment of the existing monitoring well data
from Comprehensive Environmental Response, Compensation, and
Liabilities Information System (CERCLIS) and Resource
Conservation and Recovery Act (RCRA) sites. Environmental equity
issues that would require further study were identified where
appropriate with respect to the data obtained to date.
4.1.1 Data Sources
4.1.1.1 PADER Finished Water Data
Hard copies of finished water data were obtained from the
Pennsylvania Department of Environmental Resources (PADER) for
the time period between 1980 and 1994. The monitoring data are
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collected for regulated contaminants as indicated by the Safe
Drinking Water Act (1986) (SDWA) and amendments thereafter
(USEPA, 1994d). Data for organics, inorganics, radionuclides and
other parameters (e.g., pH, hardness, etc.) were available.
Several limitations were noted including inconsistent reporting
of data parameters by the sampling laboratory (i.e., the use of
different names for the same parameter), the use of different
methods of reporting concentrations, errors in data recording,
errors in identification of sample type (raw vs. finished water),
and the use of different labels for similar sampling locations.
This database was used to assess the drinking water guality
of residents in the study area; their water is supplied by the
Chester Water Authority and Philadelphia Suburban Water Company.
The data from the Coatesville Water Authority and the
Philadelphia Water Department were used for comparative purposes.
All of the data were confirmed with the individual laboratories
serving each of the Water Companies to the fullest extent
possible.
When appropriate, the potential human health risks due to
contaminants in the drinking water were assessed. The data from
1989-1993 were used for risk purposes because this time period
appeared to be the most consistent regulatory period with respect
to the monitoring of currently regulated contaminants. The
monitoring data for 1994 were incomplete and were not used. Only
data from sampling points labelled as "distribution entry point,"
"distribution sample," "plant tap," and "finished water" were
assessed.
Note that all of the data used in assessing risk from
contaminants detected in the finished water distributed by the
Philadelphia Water Department (e.g., described as either high
service, gravity or effluent from the Baxter, Queen Lane and
Belmont Intakes) were from the Philadelphia Water Department,
Annual Report, Bureau of Laboratory Services, Fiscal Year 1993.
This Report was made available prior to receiving PADER's
finished water data. However, the data were cross-referenced
with the data from PADER received at a later date.
Note also that only the monitoring data for trihalomethanes
(THMs) from the Coatesville Water Authority were used for
comparative analysis of the THM levels with other water supplies
(discussed further in Section ,4.1.4, below). These data were
made available by the Coatesville Water Authority for 1993.
4.1.1.2 United States Geological Survey (USGS) Water Resources
Division, Groundwater Site Inventory (GWSI)
The data from the Groundwater Site Inventory (GWSI) database
are limited to sites visited during the conduct of a hydrologic
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investigation. At the time of entry into the database, the site
data are verified. Data in the GWSI are reviewed for correctness
arid revised where errors are detected. The geohydrologic unit
identifier may not conform to the latest geologic mapping,
although efforts are made to update this information
periodically. The database also contains chemical data for
private wells when made available through a hydrologic
investigation. However, no chemical data were available. This
database was used only to determine the number and location of
private wells in the study area.
4.1.1.3 Pennsylvania Bureau of Topographic and Geologic Survey
The data from the water well inventory for drillers include
many wells that do not have field location verification. No
records exist in the database for water wells that would have
been drilled previous to 1966. Drillers are currently required
by law to provide well records for all water wells that they
drill, but there is no field compliance monitoring system in
place. Therefore, information on all wells drilled since 1966
may not be available.
This database was used only to determine the number and
location of private wells in the study area. There are currently
no chemical dataxaccessible in this database.
4.1.1.4 USGS Files of Well Driller Reports
USGS files of well driller reports include well locations
that have been field verified. The information in the reports is
the same as that contained in the GWSI but presented in a hard
copy format. These reports may contain more information than the
GWSI database.
These reports were used as confirmation of the data reported
in the GWSI only to ascertain the number and location of private
wells in the study area. No chemical data were available.
4.1.1.5 1990 United States Census
The 1990 US Census of Population and Housing, United States
Department of Commerce, Economic and Statistics Administration,
Bureau of the Census STF 3A, File 29, Tables H22-H33, was another
source of groundwater data. The data in column H22-H33 "Source
of Water" were obtained from both occupied and vacant housing
units in the study area. A well that supplied greater than 5
housing units was assumed to be a public well and those that
supplied fewer than 5 housing units were assumed to be private
wells. Private wells were broken down into two categories,
drilled and dug wells. The category "other source" includes
water obtained from springs, creeks, rivers, lakes, cisterns,
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etc., but it is not clear whether these sources supply private or
public wells. Therefore, this data set was not used. The data
are estimates of the actual figures that would have been obtained
from a complete count if one had been made and, as such, are
subject to both sampling and non-sampling errors.
This database was used only to determine the number and
location of private wells in the study area. There are currently
no chemical data available in the database.
4.1.1.6 Hazardous Waste CERCLIS and RCRA National Corrective
Action Prioritization System (NCAPS)
These databases contain administrative information on
Superfund and RCRA sites in the Region. They are described
further in Sections 4.3 and 4.4.
These databases were used to determine the number of CERCLIS
and RCRA Corrective action sites in the study area with known or
suspected groundwater contamination. The data obtained from
CERCLIS and RCRA sites were also used to qualitatively assess the
potential risk of drinking groundwater in the study area by
private well users (if any).
4.1.1.7 Geographical Information Systems (GIS)
GIS allows for the mapping of data onto USGS maps. The GIS
was used to illustrate a number of data sets using a variety of
data layers. Several layers of data were overlain onto a map of
the study area as follows:
1. A map showing the number of estimated private wells by
census tract/block numbering.
2. A map showing the number of estimated private wells by
census tract/block numbering overlain with the location
of individual private wells retrieved from the USGS
database and the Pennsylvania Bureau of Topographic and
Geologic Survey database.
3. _ Same as above with an overlay of the Superfund sites
showing potential risk areas.
All other data sets were presented in a graphic format (see
text).
4.1.1.8 Federal Reporting Data System (FRDS)
The FRDS database maintains information on public water
supplies (PWSs) with MCL and monitoring violations for each state
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in the Region. The data may be retrieved by county and by zip
code.
This database was used to determine the number of MCL
violations and the parameters violated from 1989-1994 for the
Chester Water Authority, the Philadelphia Suburban Water Company,
and the Philadelphia Water Department.
4.1.2 Screening Data Analysis
The chemicals of potential concern (COPCs) in finished water
(regulated contaminants only) from the PWSs in the study area
were selected by comparison with RBCs for residential use of
drinking water, as described in Section 3.2.1. COPCs were
selected for each year from 1989-1993.
4.1.3 Risk Assessment Data Analysis
Exposure point concentrations were the average concentration
reported for each contaminant detected in the finished water for
the entire system for each year. The data sets were reported as
averages for each year for at least one of the systems under
investigation (e.g. the Philadelphia Water Department). A
Reasonable Maximum Exposure (RME) concentration, as recommended
in USEPA, 1989a was not calculated. Averages were used for
consistency's sake. The limitations of some of the data sets
included only averages being reported.
Exposure was estimated for use of the finished water. The
calculations and inputs presented in Tables 3-3, 3-4, and 3-5
were used for ingestion, inhalation and dermal contact with
contaminants in drinking water. Note that the monitoring well
data were assessed qualitatively for risk associated with the use
of private wells. There were no chemical data available for
private wells.
The Dermal Exposure Guidance document (USEPA, 1992d) was
used to assess dermal risk. Contaminant-specific dermal exposure
parameters [e.g., permeability constant (Kp) values] were
obtained from this guidance. Where appropriate, a Kp value was
calculated for some contaminants that lack a value based on the
contaminant-specific octanol-water partition coefficient (Kow)
and molecular weight. Contaminant-specific Kows were obtained
from USEPA, 1986a or Howard, 1989.
Risk was calculated using the exposure doses as described in
Section 3.4. The detailed calculations are included in Appendix
II. No toxicity criteria have been developed for total THMs;
therefore, the criteria for chloroform were used as a surrogate.
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This is a conservative assumption because chloroform has the
highest Cancer Slope Factor of the four regulated THMs. Toxicity
profiles for each COPC are provided in Appendix I.
Risks were characterized for two exposure scenarios. In the
first, a risk was calculated for an exposure duration of one year
for each year during 1989-1993. In the second, risks were
calculated for an exposure duration of 30 years based on the 1993
data only. This was done because of the uncertainty associated
with exposure duration to chemicals in finished water.
Typically, exposure point concentrations are assumed to remain
constant for the entire exposure duration. However, contaminants
may appear in the finished water at an unknown freguency, and
this variability was observed in the five-year data set.
Contamination varies over time and could vary significantly
within a time period of one year. Certainly, significant
variation in contaminant levels are expected to occur over a 30-
year, exposure period. Finished water is expected to be free of
contamination but may, in fact, contain contaminants at
concentrations below the MCL. These contaminant concentrations
may pose a certain amount of risk at levels that are
"permissible" in finished water.
4.1.4 Results and Discussion
4.1.4.1 Private Well Investigation
The census tract data obtained in 1990 involved a random
door-to-door survey of the housing units (both vacant and
occupied) in the study area (see Table 4-1). An assessment of
the data indicated that less than 1% of the housing units in the
study, area may obtain their drinking water source from private
wells. According to the local health department, the entire
population of Chester is connected to a PWS. However, the health
department had no data on which to base this conclusion (Gross, .
1994) . There are an estimated 61 private wells in the study
area, of which approximately 31 are believed to be dug wells and
approximately 3 0 are believed to be drilled wells. The data are
estimates of the actual figures that would have been obtained
from a complete count (USDOC, 1990). Therefore, the exact number
of private wells in the study area is largely unknown.
The location of these potential wells are indicated in
Figure 4-1 by the census tract/block numbering areas. Most of
these private wells may be concentrated in the City of Chester
area although there are wells apparently also situated in Trainer
Borough, Chester Township and Eddystone Borough (Figure 4-1).
Efforts to obtain locational information for any of the 61
private wells identified on the census tract have been hampered
primarily because of those regulations which protect individual
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rights to privacy. It should be noted that information retrieval
from the census tract is quite limited mostly because the quality
and quantity of the data input into the database are limited.
Data from other sources (e.g., the USGS GWSI and the
Pennsylvania Bureau of Topographic and Geological Survey
Databases) were retrieved in an effort to verify the existence
and to obtain locational and chemical data for the private wells
indicated in the census tract data of 1990. These databases were
found to contain very little in the form of locational
information and no chemical data. Locational information (e.g.,
in the form of longitudinal and latitudinal coordinates) was
found for three possible private wells (Figure 4-2), although
field verification has not been possible because no addresses
were associated with the locational data. Only names were
reported for those wells which are believed to be owned by '
private residents.
The addresses for the names of the people retrieved in the
databases (and confirmed in the USGS Well Driller Reports) were
cross-referenced with a telephone directory. None of the persons
contacted said that they were using the wells for potable sources
(Rundell, 1994). Some of the wells were in commercial
establishments, not private residences. This effort indicates
that there may be some private wells in the area (which may not
be currently used), and that further investigation may be
necessary. This is especially so in view of the fact that
groundwater in the study area is of poor quality (see below).
4.1.4.2 Groundwater Quality in the Study Area
Monitoring wells were installed as part of hazardous waste
site investigations in the study area. These wells are not used
for human consumption, but as indicators of groundwater quality.
Based on the monitoring data collected from several CERCLIS sites
in the study area, groundwater in the study area may be impacted
by a number of hazardous waste sources. Significant levels of
organic and inorganic contaminants were detected in monitoring
wells which are indicative of potential groundwater contamination
(Table 4-2). Contaminant-specific monitoring well data from RCRA
sites currently undergoing corrective action were not available
for analysis at the time of this study. The fact that the
existing groundwater in the study area appears to be highly
contaminated with anthropogenic sources of pollution is critical
for those who may be currently utilizing groundwater for their
drinking water sources (e.g., for private well users). Figure 4-
3 shows potentially affected groundwater areas from CERCLIS sites
in Chester City and Linwood, Marcus Hook and Trainer boroughs.
Until the quality of groundwater in private wells can be
ascertained, it may be prudent to avoid exposure to the
groundwater in the study area.
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It should be noted that this analysis is hampered by the
fact that the vertical and horizontal extent of contamination
(e.g., the groundwater flow of contaminants in the vertical and
horizontal planes) are not known.
4.1.4.3 Public Water Supply
Drinking water quality from public water sources in the
study area was investigated because greater than 99% of the
population is expected to obtain their drinking water from a
public supply. The study area is served by the Chester Water
Authority except for Eddystone, which is served by the
Philadelphia Suburban Water Company. It should be noted that
Philadelphia Suburban Water Company purchases water for Eddystone
from the Chester Water Authority. This water undergoes no
additional treatment; therefore, the actual source of drinking
water for Eddystone is the Chester Water Authority.
Finished water data obtained from PADER and in some cases
from the water company itself were analyzed and the potential
risk from reported contaminants were assessed as described above.
Contaminants were categorized as originating from water treatment
(i.e., those that occur as byproducts of chlorination,
fluoridation, or other intentional treatment) and non-treatment-
related (i.e., pollutant and naturally occurring chemicals). The
data indicate that both types of chemicals have existed and could
continue to exist in the finished water of citizens in the study
area. In all cases, however, reported contaminant levels for the
time period studied are lower than enforceable MCLs; therefore,
the PWS for the study area is in compliance with the National
Primary Drinking Water Regulations. The low levels of
contaminants that were measured were primarily by-products of the
disinfection process or treatment-related contamination.
Tables 4-3, 4-4, and 4-5 summarize risks for the 1-year and
30-year exposure scenarios for the PWSs. The supporting
information for these calculations was presented in Section 3;
the detailed calculations are shown in Appendix II.
Potential Risk from Treatment-Related Sources
Total Trihalomethanes
There were several THMs (chloroform, bromodichloromethane
and dibromochloromethane) detected in finished water in this
study at levels above their respective RBCs (Tables 4-6, 4-7, 4-
8). The data are consistent with Region-wide results.
Violations for the PWSs under study are shown in Tables 4-9, 4-
10, and 4-11. Note that these violations are primarily
associated with treatment performance techniques and/or late
reporting problems, and that no actual exceedances of MCLs were
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noted. Several MCL violations for THMs have been found in PWSs
across the Region. THMs were also found in most PWSs nationwide
(Olson, 1993).
THMs are degradation products of the disinfection process
which eliminates disease-causing microbial pathogens from
drinking water. THMs are formed in the drinking water during the
reaction between chlorine (an effective and widely used
disinfectant) and organic matter already in the water. Chronic
exposure to high levels of THMs in PWSs may result in an
increased risk of developing toxic effects from ingestion and/or
inhalation of these contaminants in the water. Chlorinated
drinking water has been associated with certain types of rectal,
colon and bladder cancers and with liver damage in studies
conducted in Louisiana and Wisconsin and in laboratory studies
(Amdur et al, 1993). Significant risks may exist even at levels
below the MCL for THMs of 100 ug/L. Risk estimates for THMs
range as high as 1E-4 (cancer risk) and 1 (non-cancer risk) for
the Chester study area PWSs. It may be noted that a lower MCL of
80 ug/L for total THMs (TTHM) has been recently proposed by USEPA
(USEPA, 1994e). The intent of this proposed rule is to reduce
TTHM levels and potential health risks in finished water without
increasing risks of health effects associated with microbial
pathogens. Many PWSs are preparing for the anticipated new rule
by replacing the chlorine in the disinfection process with other
disinfectants (e.g., chlorine dioxide, chlorite, chlorate, and
chloramine) (Calabrese et al, 1989). This change has generally
led to a decrease in the levels of TTHM.
Coliforms
Coliforms represent a group of bacteria used as indicators
of fecal coliform. Coliform bacteria are normally fourid in the
intestinal flora of humans. Their presence may indicate that
water is contaminated with fecal matter that may contain other
disease-causing organisms from infected individuals. Some of
these disease-causing organisms may be enteric bacteria (bacteria
that live within the intestinal tract of mammals) that can cause
typhoid fever, cholera and dysentery; viruses, such as the
hepatitis virus; and protozoans, such as Giardia lamblia. which
can cause dysentery in exposed individuals (USEPA, 1993a). The
chlorination process is designed to eliminate these microbial
pathogens (see Figure 4-4). The recently proposed MCL for TTHM
of 80 ug/L is accompanied by other proposed risks that are
balanced against risks due to these pathogens (USEPA, 1994e).
Treatment system design failure may also lead to the
introduction of disease-causing organisms in drinking water. In
March, 1993, in Milwaukee, there was a surface water treatment
system failure when changing over to a new system design to
fulfill the surface water treatment rule promulgated by the SDWA
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in 1989. Apparently failure in the coagulation/sedimentation
process led to the introduction of a small parasite,
Cryptosporidium. in the distribution system, causing residents to
become ill, primarily with stomach and intestinal disorders
(Rice, 1993).
Several finished water samples from the Chester Water
Authority, Philadelphia Suburban Water Company and the
Philadelphia Water Department were found to have had positive
total coliform results in the time period between 1989 and 1993.
Results for fecal coliform were negative, and current data from
the FRDS database indicate that this MCL parameter has not been
recently violated. However, there have been reported monitoring
violations for the Surface Water Treatment Rule (SWTR) in FRDS
due to the failure of the PWSs to meet the proper treatment
performance required under the SWTR or due to the failure of the
PWSs to submit monitoring results as scheduled (Tables 4-9, 4-10,
and 4-11). These monitoring violations have resulted in
enforcement action within a reasonable time frame.
The new rule for surface water promulgated in June, 1989
requires that all surface water be filtered prior to distribution
and that all groundwater under the influence of surface water be
filtered as well (USEPA, I989d; USEPA, 1993a). Samples positive
for total coliforms are tested for fecal coliforms. This new
rule may lower the frequency of MCL violations for this
parameter.
Inorganics
Fluoride was detected in finished water from the Chester
Water Authority and the Philadelphia Water Department but was not
present at levels of concern. Fluoride is typically added to the
finished water of PWSs for the prevention of dental caries (Note:
the Philadelphia Suburban Water Company does not add fluoride to
their finished water). Therefore, fluoride was not considered in
the total risk estimate calculated. It should be noted that
fluoride has very low toxicity and at high levels is associated
with dental mottling (a cosmetic effect also known as dental
fluorosis). If the levels exceed 20 mg/day (far in excess of the
expected dose from the level allowed in finished public water)
and exposure is continuous (e.g., fdr a 20 year period), fluoride
may be associated with the development of crippling skeletal
fluorosis (USEPA, 1994c).
Potential Risk from Non-Treatment-Related Sources
Several contaminants in finished water may be attributed to
non-treatment-related sources. These contaminants include metals
and volatile organic compounds.
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Inorganics
Inorganics were detected infrequently in the Chester Water
Authority, the Philadelphia Suburban Water Company and the
Philadelphia Water Department finished water. No metals were
present at levels of concern. The only inorganics detected that
were of potential concern to human health based on their
respective RBCs are fluoride and nitrite. Nitrite was detected
only in the Chester Water Authority in 1989 and 1993 does not
represent a significant noncancer risk to those exposed (HI < 1).
Fluoride was discussed under treatment-related issues.
Metals such as lead have just begun to be monitored at the
tap (USEPA, 1991b). Therefore, there are limited monitoring data
on lead to determine if the lead levels in drinking water of PWSs
in Chester are safe. The low lead levels reported in the PWSs
serving the Chester study area were not of concern based on the
Action Level for lead of 15 ug/L. However, a periodic assessment
of the monitoring data is recommended before a final assessment
is made. Note that there were some monitoring violations
reported for the Chester Water Authority and the Philadelphia
Water Department (Tables 4-9, 4-10 and 4-11), which resulted in
enforcement action.
In other parts of Region III, which includes Pennsylvania,
Maryland, Delaware, Virginia, West Virginia, and the District of
Columbia, the following chemicals were found at levels that
exceeded MCLs in PWSs: barium, cadmium, chromium, fluoride, lead,
mercury, selenium and the inorganic compound nitrate.
Overall, nitrate appears to be a Regional concern, with
Lancaster County having the greatest number of MCL violations for
that parameter in Pennsylvania. Currently, the PWSs serving the
Chester study area do not appear to be impacted with high levels
of nitrate at this time, although low levels of nitrate that did
not exceed the RBC were detected in finished water.
Metals are common in metal plating facilities, foundries,
smelters, etc. They tend to leach into groundwater with changes
in the physical and chemical characteristics of soils. Most
metals, e.g., lead compounds, however, are expected to come from
corrosion of plumbing materials in the water distribution system
(e.g., corrosion by-products) (USEPA, 1991b).
Metals and other inorganics (e.g., nitrite and nitrate) have
varying degrees of toxicity as indicated in the toxicity profiles
found for each metal and/or inorganic compound detected in
finished water in the Region (Appendix I). Most exposure to
metals (e.g., arsenic and beryllium) is associated with lung
disease and lung cancer mostly in occupational settings from
inhalation. Other metals like fluoride are associated with
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erosion of tooth enamel, skin cancer (e.g., arsenic) and central
nervous system failure (e.g., thallium).
Volatile Organic Compounds
Volatile organic compounds (VOCs) were detected at trace
levels in PWSs serving the Chester area. Those that exceeded
their respective RBCs were carbon tetrachloride and
tetrachloroethene.
Trace levels of carbon tetrachloride were also detected in
finished water from the Philadelphia Water Department, not used
as a drinking water source in the Chester study area.
Overall significant increased cancer risk and noncancer risk
are not expected from exposure to VOCs in finished water in the
study area at the levels reported between 1989-1993 (see Tables
4-3, 4-4, and 4-5).
In the Region in general, a significant number of MCL
violations for VOCs such as trichioroethene (TCE) anci TCE
derivatives such as vinyl chloride were detected, in PWSs in
Pennsylvania. These were limited primarily to Berks and
Montgomery Counties. In the State's Water Quality Report
submitted by Pennsylvania in 1992, other organics (e.g.,
unregulated contaminants at levels of potential concern such as
cis-l,3-dichloropropene) are noted in PWSs [305(b) Reports] that
may be of concern. Data from the Chester Water Authority and the
Philadelphia Water Department also indicate the presence of
unregulated contaminants such as cis-l,3-dichloropropene. The
data may be biased towards Pennsylvania showing the greatest
number of violations in the Region, however. Pennsylvania has
the largest number of PWSs of all the States and better reporting
systems in FRDS. The reporting schedules for MCL violations of
VOCs for large and small PWSs differ. Although they both have to
report at the same frequency, their starting monitoring dates
difffer. Large systems started monitoring by 1/88, while small
systems started monitoring by 1/91.
Sources of VOCs include dry cleaners, underground storage
tanks, landfills, etc., all of which were ranked as the major
sources of drinking water contamination in Region III [305(b)
Reports].
VOCs have varying degrees of toxicity ranging from non-
cancer effects such as neurological disorders and kidney failure
to cancer effects such as liver cancer. VOCs in drinking water
and their toxic effects are summarized in ENR, 1988. The
toxicity profiles for those VOCs of concern in this study are
summarized in Appendix I.
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Pesticides
There were no pesticides detected in finished water in the
study area during the time period investigated.
It is still questionable whether pesticides pose' a risk'to
drinking water supplies (USEPA, 1986b). Over 250 pesticides have
been detected in the groundwater of at least 42 States in the
nation, of which only 24% of the wells tested had detections
(Weber, 1993). Ongoing studies conducted in Region III of the
Delmarva Peninsula (USGS 1989, 1992 and 1993) measured only trace
levels of pesticides: atrazine, cyanazine, simazine, alachlor,
metolachlor, and dicamba. Most detections correlated with the
intensive use of these herbicides in three widely distributed and
commonly rotated crops—corn, soybean, and small grain—
particularly if grown in well-drained soils. Most pesticides,
were detected in the upper aquifer (10 m) above the water table.
The presence of trace levels of pesticides in groundwater suggest
that pesticides can leach into groundwater and affect drinking
water, especially in shallow aquifers, suggesting that the levels
of pesticides should be monitored.
The need for continued monitoring of pesticides in
groundwater has also been indicated when studying the Region as a
whole. The detection of highly toxic pesticides 2,4,5-
trichlorophenoxyacetic acid, endrin, ethylene dibromide, lindane,
methoxychlor and toxaphene were reported to be found in PWSs in
Pennsylvania at levels above the MCL. Upcoming Regional studies
in Jefferson and Lancaster Counties in Pennsylvania will
demonstrate to states how GIS can be used for the development of
their Pesticide in Groundwater State Management Plans to protect
their groundwater from pesticides (Weber, 1993).
Radionuclides
Radon monitoring finished water data were not available for
the PWSs serving the Chester study area. It is not known if
radon in drinking water is a concern for residents in the study
area at this time.
An MCL for radon of 300 pCi/L has been proposed by USEPA.
The chief hazard of radon exposure is caused by the action of
alpha-emitting short-lived daughters of radon (e.g., 218Po and
2UPo) , which are isolids and deposit on the bronchial airways
during inhalation and exhalation, resulting in lung cancer.
Although risks from exposure through the ingestion route are
possible, there are currently no studies available for review.
Radon ingested in water is absorbed into the bloodstream from the
small intestine and circulates to the lungs, from which it is
exhaled. Radon is also distributed to other body organs such as
the stomach, intestine, liver, muscle, body fat and other
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tissues. Therefore, the approach to assessing the risk of
ingested radon is to determine the individual organ doses of
radiation based on radon (USDWSD, 1991).
Radionuclides (gross alpha, gross beta particles and radium
226/228) detected in finished water in PWSs serving the Chester
study area did not represent a significant concern based on the
RBCs of these contaminants.
Regional studies on the levels of radionuclides in drinking
water supplies are not available or accessible for the most part.
Radionuclides (e.g., gross alpha and beta; combined radium
226/228) have been detected infrequently in the Region. Both
Pennsylvania and Virginia had greater MCL violations for this
parameter than Delaware, Maryland, West Virginia, suggesting that
radionuclides in drinking water in Region III should continue to
be monitored.
According to a nationwide study done in 1993 (Olson, 1993),
about 49 million people drink water containing significant levels
of radioactive radon, and millions more drink water contaminated
with radium, uranium, and other radioactive substances. Yet most
of these contaminants still are not regulated in drinking water,
although some have proposed MCLs.
Comparison of Risk Levels of Finished Water Supplies
In order to compare the potential risk from contaminants in
finished water of Chester residents with other communities, a
comparative analysis was done of the risk levels from
contaminants in finished water from the Chester Water Authority,
the Philadelphia Suburban Water Company, and the Philadelphia
Water Department. Figures 4-5 and 4-6 show a comparison of
cancer and non-cancer risk levels for the finished water
supplies. In this analysis the risk levels (for all sources of
contamination including treatment-related sources) for the
Chester Water Authority (serving the study area) were compared
with those of the Philadelphia Suburban Water Company and the
Philadelphia Water Department. An exposure duration of 30 years
(90th percentile of time spent at one residence) was assumed.
All risk levels were either at or below a Hazard Index of 1 and a
cancer risk level of 1E-4). It is apparent from this figure that
most of the risk (>90%) is due to "treatment process" residuals,
i.e., THMs.
A comparative analysis of the risk levels from THMs for the
Chester Water Authority, Coatesville Water Authority,
Philadelphia Suburban Water Company and the Philadelphia Water
Department during 1993 (Figures 4-7 and 4-8) indicates that the
risk levels for THMs are largely within the acceptable risk
ranges. Although the cancer risk levels are approaching 1E-4,
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the risk levels are below the risk levels for THMs at the MCL of
100 ug/L.
A comparative analysis of the annual risk levels from all of
the reported contaminants during 1989-1993 for the Chester Water
Authority, the Philadelphia Suburban Water Company and the
Philadelphia Water Department indicates cancer risk levels (<1E-
4) and hazard indices (<1) generally lower than the risks based
on 30-year exposure (Figures 4-9 and 4-10). It should be noted
that these risk levels were calculated assuming an exposure
duration of 1 year only. The actual risk levels could be higher
if the contaminants remain in finished water over a lifetime.
Risk estimates could be as high as or higher than those risks
calculated using an exposure duration of 30 years.
4.1.5 Uncertainty Analysis
Uncertainty associated with the analytical data used to
assess risk for the Chester Project may be characterized as being
associated with exposure estimation, toxicity assessment, and
risk characterization. General uncertainties common to all
quantitative assessments were summarized in Section 3.5.
There are uncertainties associated with the exposure
parameters used in this study. The exposure duration used in
calculating the risk may have overestimated the actual exposures
experienced by the receptors at their residences. It is
difficult to determine the frequency at which contaminants appear
for each system and their duration over a lifetime since these
data are not available. Therefore, it was assumed that the type
and concentrations of contaminants will remain the same over time
(i.e., are static). Since the contaminant concentrations may
vary over time, the potential risk to receptors may also vary.
Consequently, averaging risks over a 30-year lifetime may not be
appropriate. This was taken into consideration by assuming a
minimum exposure duration of one year and a maximum exposure
duration of 3 0 years (for 1993 data only).
On the other hand, the actual risk levels for the
contaminants detected in finished water from the PWSs may be
underestimated because only average values were considered in the
risk assessment. This was necessary in order to be consistent in
the risk methodologies used for comparative purposes, since some
of the finished water data were available as averages only.
Therefore, the actual risk may be higher if the maximum
concentrations or the 95% UCL of the mean were used.
There are other uncertainties inherent in the risk estimates
related to data quality. There were variations seen in the
manner in which the data were reported from one PWS to another
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and from one laboratory to another. In addition, there were a
few errors in data recording on the state compliance forms.
While attempts were made to verify all suspect data, the
possibility of additional undetected errors cannot be ruled out.
Data assessment is further complicated by the fact that PWSs
typically receive water from different sources and from different
locations at different times. TTHM levels, for example, are
generally higher in water derived from surface sources. For
example, the Chester Water Authority uses two surface sources,
the Octorara Reservoir and the Susquehanna River. It is
difficult to determine which sources of water were mixed. This
makes it difficult to establish trends in contaminant levels from
the different contributing sources.
Some contaminants were detected infrequently (e.g.,
tetrachloroethene and carbon tetrachloride) and thus may be
considered to be outliers. However, because of the small
database' and the different monitoring times for each of the
regulated contaminants, it is possible that those contaminants
designated as outliers appear at a higher frequency over a
resident's exposure duration (estimated to be 30 years by the
USEPA)1
There are significant data gaps associated with the private
well data. The current data are equivocal with regard to the
number of wells in the area. The census tract data of 1990
report that approximately 61 private wells may be found in the
City of Chester area. Other data sources from USGS GWSI and the
Pennsylvania Bureau of Topographic and Geologic Survey indicate
that there are only about 3 potential private wells in the study
area. Conversation with some of the users indicates that the
wells are not being used for potable sources and/or are owned by
private businesses and not residences. This has not been
verified.
There are currently no chemical data available from which to
assess risk for potential private well users. Hence, it is not
known whether residents that may be on private wells are drinking
contaminated water. The state and municipal health departments
are not aware of any private wells in the area. The USEPA has no
jurisdiction over private wells and has only limited if any data
on private wells from Superfund sites.
The qualitative risk for contaminants in monitoring wells
emanating from CERCLIS sites in the study area and assumed to be
in private wells in the study area are probably overestimated by
virtue of the fact that the vertical and horizontal extent of
contamination are largely unknown. It is not known if residents
that may be on private wells are receiving the contamination that
was detected at these monitoring points.
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In some cases, toxicity information for some contaminants
were not available. In these cases, conservative default values
were used. For example, there are currently no toxicity criteria
available for TTHM. The toxicity criteria for the most toxic
THM, chloroform, was used to be conservative.
Dermal toxicity criteria are not readily available. Oral
toxicity criteria were used. No adjustments were deemed
necessary because this route represents a minor percentage of the
total risk and the appropriate absorption factors needed to make
the adjustments are not consistently available. It is expected
that the potential risks from the inhalation and the oral routes
will significantly outweigh the potential risks from the dermal
route. For VOCs, the absorption is very close to 100% in any
case.
There are uncertainties associated with the level of
protectiveness of the MCLs. While most MCLs are protective of
human health, many are based on the technical and economic
feasibility of treating down to health-based levels in addition
to human health consideration. This is the apparent case with
TTHM. This poses a question as to whether drinking contaminated
finished water is an environmental equity issue or an economic
issue. When considering TTHM in finished water, one must weigh
the risk of potential cancer and non-cancer effects due to
ingestion of TTHM with that of drinking water with high levels of
coliform and potentially deadly disease-causing microorganisms
which can pose a more immediate health threat.
As stated previously, the duration of the exposurie to
contaminants in finished water may vary over time. It is
difficult to determine the frequency at which COPCs will occur in
finished water in the future. Since contaminants may appear at
levels below their respective MCLs and no further treatment is
deemed necessary, there is potential for significant risk if the
MCLs are not protective.
4.2 LEAD
4.2.1 Introduction
4.2.1.1 Lead in the Environment
Inorganic lead is an ingredient in solder, paints and
ceramic glazes, glass, storage batteries, plastics, and
electronic devices. Processes such as mining, smelting,
combustion (of coal, oil, or municipal waste), battery
manufacture, welding, and spray coating emit lead to the air.
Automobiles once produced 90% of all US lead emissions, but this
source has been largely eliminated by the removal of tetraethyl
lead from gasoline. Human activity has distributed lead widely
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in the environment. Workers and the general population have many
opportunities for significant exposure.
Lead is volatile only at high temperatures, so most
emissions take the form of lead dust rather than gas. Dispersal
depends on wind speed and direction. The dust particles tend to
deposit quickly, usually within ten miles of the source. Over
time, lead accumulates in soil near sources of air emissions.
Once in soil lead tends to stay there, attached to organic
molecules or in the form of insoluble salts.
4.2.1.2 Lead Exposure
People can be exposed to lead by five important routes: from
air, food, drinking water (and beverages), soil and dust, and
across the placenta before birth. Lead absorption through the
skin is not significant.
• People may inhale lead-bearing dust before it is deposited.
Small dust particles (less than 4 ten-thousandths of an inch
in diameter) are deposited in the lungs and absorbed into
the body.
• Lead can be ingested with food. Food gets contaminated by
lead particles deposited onto crops, lead-bearing
pesticides, or cans made with leaded spider. Garden
vegetables grown in lead-bearing soils may have high lead
levels.
• Drinking water may contain substantial amounts of lead.
Some US water supplies have high lead levels at the source,
especially if the water is naturally acidic. More-often,
lead leaches from pipes and solder at a rate which depends
on the acidity, hardness, and temperature of the water.
Absorption of lead in food and water ranges from about 15%
in adults to over 50% in small children. Unabsorbed lead is
excreted in feces.
• People may be exposed to lead by incidental ingestion of
soil and house dust. Lead in house dust comes from outdoor
soil, deposition from air, and small particles of
deteriorated lead paint. Adults pick up small amounts of
soil and dust on the hands, and ingest it when they eat or
smoke. Children get higher lead doses from soil and dust
than adults do, for two reasons. First, children ingest a
larger amount of soil and dust as part of their normal
mouthing behavior. Second, ingested lead reaches a higher
concentration in tissues because the small size of the
child's body allows for less dilution.
Absorption of lead ingested with soil and dust depends on
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particle size, chemical species of lead, and concentration.
Lead which is dissolved in the gastrointestinal tract is
more easily taken into the body. Larger soil particles
dissolve more slowly, and less lead is absorbed. Lead
sulfides are less soluble than lead oxides or acetates, so
absorption of sulfides is thought to be less. Where lead
levels in soil and dust are very high, a smaller percentage
of lead appears to be absorbed. Lead at mining sites, where
lead sulfide is found in large particles at high
concentrations, tends to be less readily absorbed. Lead
absorption in areas contaminated by more soluble lead
species in smaller particles tends to be higher.
• Lead readily crosses the placenta, and distributes into the
tissues of the growing fetus.
4.2.1.3 Movement of Lead in the Body
Once lead is absorbed into the body, half is eliminated in
bile or urine within a few weeks. Of the remaining half, 95%
goes into bone and the rest into soft tissues (internal organs,
blood, etc.). Soft-tissue lead has an elimination half-life of a
few weeks, but lead in bone persists for many years. Slow
leaching of bone lead can keep soft-tissue lead levels high, even
after exposure stops. Accelerated bone loss caused by aging or
pregnancy may lead to even higher soft-tissue levels for short
periods, placing pregnant women, fetuses, and older people at
high risk. Lead levels in soft tissue are important, because it
is soft tissue that sustains the most damage from lead. USEPA
uses blood lead concentrations as a measure of internal lead
dose.
4.2.1.4 Toxic Effects of Lead
Lead affects several organ systems, including the nervous,
hematopoietic (blood-forming), circulatory, urinary, and
reproductive systems. Nervous effects include irritability,
short attention span, muscular tremors, memory loss, and tingling
in the extremities. In addition to these overt symptoms,
children suffer significant losses in motor skills and cognitive
ability. Children with blood lead levels at or above 10
micrograms per deciliter (ug/dL) have significantly lower
Intelligence Quotient (IQ) scores. The IQ loss increases in
proportion to blood lead.
Lead blocks an important step in the synthesis of heme, a
critical part of hemoglobin (the oxygen-carrying molecule in red
blood cells). At high blood lead levels, this effect results in
anemia. Inhibition of heme synthesis is detected early by the
buildup of erythrocyte protoporphyrin (EP, a partially assembled
heme molecule), or decreased activity of ALA-D (the enzyme that
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controls the blocked step) in the blood. Lead causes lesions in
the proximal tubules of the kidney, resulting in impaired kidney
function. In animal studies, lead also creates kidney tumors.,
USEPA has classified it as a probable human carcinogen on the
basis of this evidence. Evidence for lead-induced cancer in
humans is inconclusive.
Other toxic effects of lead include increased blood pressure
and decreased sperm production in adult males, decreased serum
vitamin D in children, decreased birth weights in newborns,
increased spontaneous abortion rates in women.
The toxic effect which USEPA uses as the basis of regulatory
actions for lead is decreased IQ in children. USEPA uses this
effect because it occurs at lower blood lead concentrations than
do other toxic effects.
4.2.1.5 The USEPA Three City Study
The Superfund Amendments and Reauthorization Act of 1986
(SARA) authorized USEPA to conduct a detailed study (the "Three
City Study") of environmental lead levels and blood lead
concentrations in children in three urban areas. The purpose of
the study was to determine whether abatement of lead in soil
could reduce blood lead levels in inner city children. In 1987,
USEPA established criteria for site selection, and selected
Boston, Baltimore, and Cincinnati as the study sites. In order
to determine the effects of intervention, it was first necessary
to establish baseline environmental and blood lead levels for
these urban areas, before intervention took place.
This baseline information is also useful for comparison with
other urban areas in which no abatement has occurred. It is
important to note that the study was designed to assess the
effects of reducing soil lead levels; identifying sources of
environmental lead was not a study objective. Before abatement,
average surface soil lead levels ranged from 505 mg/kg in
Cincinnati to 2620 mg/kg in Boston. In Baltimore, of these three
cities the nearest and perhaps most similar to Chester, the
average surface soil lead was 571 mg/kg. Pre-abatement geometric
mean blood lead levels were 12.6 ug/dL in Boston, 12.5 ug/dL in
Baltimore, and 11.7 ug/dL in Cincinnati. Seventy-one percent of
children exceeded the Centers for Disease Control's criterion of
10 ug/dL in Boston, versus 59% in Baltimore and 52% in
Cincinnati.
4.2.2 Data Source
Paper records of over 10,000 blood lead measurements for
children in the Chester area, taken between 1989 and 1992, were
obtained from the City of Chester. Names, addresses, and blood
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lead measurements were entered into a computer database. Age and
sex were not reported, nor was information available about how
the children were chosen for blood lead sampling. Some children
were sampled 10 times or more during the 5-year period covered by
the data, and some were sampled only once. Also, many of the
children lived at more than one address during this period.
Lead concentration data for the media to which children are
exposed—air, tap water, soil, dust, and food—were extremely
scarce. Although water data from the city's water treatment
plant were analyzed as part of this study, water supplies
typically have very low lead levels at the source. Lead solder
and lead pipes in the distribution system, especially in private
homes, contribute most of the lead found at the tap.
Measurements of lead levels at taps in private homes were not
available.
Lead measurements in soil on residential lots and in dust in
the interiors of homes were also unavailable. It is believed
that most cases of childhood lead poisoning are caused by
elevated lead levels in interior dust which children ingest as
part of normal mouthing behavior. Thus, the lack of these
concentration data makes it very difficult to determine whether
high blood lead levels resulted from exterior soils or
contributions of paint to interior dust.
Quantitative information about lead concentrations in air,
tap water, residential soil, interior dust, and food were for the
most part unavailable. Municipal water supply data were
examined, but were considered unrepresentative of lead
concentrations at the tap because they did not include the
contribution of the water distribution system. Residential soil
and dust data were not found. Site investigation reports for
nine sites in Chester which USEPA evaluated for potential
inclusion on the Superfund list were examined. Lead
concentration data in these reports were limited, and it could
not be determined whether significant off-site releases could
have occurred.
4.2.3 Data Analysis
To enhance the analysis of trends and improve the
reliability of the database, analysis was restricted to children
whose blood lead was measured two times or more. . Data were
separated by year to analyze for temporal trends. Spatial trends
were analyzed by averaging blood lead measurements for each
residence, including multiple measurements of the same child and
measurements of siblings. Summary statistics and graphs were
prepared using a desktop personal computer running Lotus 123
version 4. Maps were prepared by the USEPA Information Resources
Management Branch, using their minicomputer-based GIS.
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USEPA's Integrated Exposure/Uptake/Biokinetic (IEUBK) model
(USEPA, 1994f) was used to predict blood lead levels for a
population of children aged 1 through 6 exposed to national
average lead concentrations in air, tap water, soil, dust, and
food. This prediction was compared to the blood lead data for
Chester. The IEUBK model was then run iteratively, with
different additional amounts of lead exposure, until a close
match was found between the modeled results and the Chester data.
This amount of additional lead intake needed for the model's
predictions to match the observations serves to estimate whether
mean lead intake in Chester exceeded national averages.
This lack of concentration data in environmental media
forced the lead analysis to concentrate on a description of
children's blood lead. The blood lead data served as: (1) as a
surrogate for exposure, (2) as a basis of comparison with other
intensively studied urban areas, and (3) as a basis for
estimating total lead intake by Chester children, compared with
national averages. However, it must be emphasized that this
analysis cannot estimate the relative contributions of potential
lead sources, or even identify these potential sources (except
for those generic to urban areas, such as auto emissions, paint,
etc.).
4.2.4 Results and Discussion
Results of USEPA's ambient air modeling exercise (Section
4.7 and Appendix III) suggest that ambient levels of lead are in
compliance with national standards. Since these standards were
developed with the IEUBK model, it is unlikely that lead levels
in air had a substantial impact of children's blood lead.
Site investigation reports for Chester area properties
investigated as potential Superfund sites (see Section 4.4) were
examined to determine if substantial lead releases could have
occurred. Of these, three (Delaware County Incinerator, ABM
Wade, and East 10th Street) appeared to have high on-site lead
levels in one or more media. One site (Delaware County
Incinerator) may have released significant quantities of lead
off-site during the past operation of the incinerator. However,
it is important to note that this evaluation was completely
qualitative, and was based on extremely limited data. These data
cannot be extrapolated to predict lead content of soils in
surrounding areas.
Blood lead levels over the five years for which data were
available (Table 4-12) showed a geometric mean concentration of
14.2 ug/dL, which is between 1.4 and 2.5 ug/dL higher than the
blood lead levels observed in USEPA's Three City Study. Sixty-
eight percent of the children in Chester exceeded 10 ug/dL,
similar to Boston (71%) but substantially worse than Baltimore or
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Cincinnati (59% and 51%, respectively). There are several
significant uncertainties about the Chester blood statistics.
First, the process by which the Chester children were selected
for blood lead measurement was not recorded. However, the sample
was unlikely to be random, and the degree to which the sampled
individuals represent the entire population in Chester is
unknown. Second, the ages of the children were not provided, so
direct comparison with data from the Three City Study (which
included only children of specific ages) may be misleading.
To analyze temporal trends, the blood data were separated
into years (Table 4-13). Geometric mean blood lead concentration
declined from a high of 18.0 ug/dL in 1990 to 11.9 ug/dL in 1993.
The percentage of children exceeding 10 ug/dL declined from 79%
in 1990 to 61% in 1992; the percentage above 50 ug/dL declined
even more dramatically, from 6.2% in 1989 to 0.22% in 1993.
Frequency distributions by year (Fig. 4-11) show a
substantial decrease in the number of observations above 20
ug/dL, and a trend for most of the population to be concentrated
in the range 5 and 30 ug/dL in the later years. Fig. 4-12 shows
substantial decreases in the percentage of children exceeding 10,
15, 25, and 50 ug/dL. Little change occurred between 1989 and
1991, but later data show significant declines in incidence of
high blood lead levels. The decreases in observations above 25
and 50 ug/dL are especially large. Fig. 4-13 shows that the
decrease in geometric mean blood lead levels between 1991 and
1992 was statistically significant. Fig. 4-13 also indicates
that the 10th percentile of blood lead remained fairly stable
during the five-year period, but the 90th percentile blood lead
level decreased from 50 to 25 ug/dL.
Fig. 4-14 shows the prediction of blood lead distribution
for a population of children exposed to national default lead
levels, plus typical urban soil and dust lead concentrations of
500 mg/kg. The predicted geometric mean blood lead level was
6.6, with 25.7% of the population above 10 ug/dL. Postulating
130 ug/day additional lead intake produced the closest fit with
the blood lead distribution observed in Chester children. This
suggests that the lead intake among area children may exceed
national averages, by about 130 ug/day. This should be used as a
rough estimate only. It is important to note that the IEUBK .
model's predictions would be appropriate for a randomly selected
population of children 6 years of age and less (see Fig. 4-15).
The Chester children were probably not randomly selected, and the
data may have included children of other ages.
Two maps of mean blood lead were prepared. Fig. 4-16 shows
the location of each address at which a child resided at the time
of a blood lead measurement. All blood lead values for each
address were averaged. Points are color-coded by range of blood
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lead. Fig. 4-17 shows the average blood lead level observed at
homes within areas 100 meters square. The areas are color-coded
for range of blood lead. These maps fail to reveal any
geographic trends in blood lead levels, which appear to be
randomly distributed through the city. This inability to find
trends can be interpreted two ways: (1) blood lead levels tend to
be similar throughout Chester, or (2) geograpihic trends do exist,
but could not be detected with the limited, non-random database
available.
4.2.5 Uncertainty Analysis
Several major sources of uncertainty have influenced the
interpretation of the blood lead data.
The paper records of blood lead from the city of Chester did
not include age or sex of the children or information on how they
were selected for sampling. Because of these uncertainties, it
is possible that these data may not be truly representative of
blood lead levels among small children in Chester. USEPA cannot
predict whether the actual blood lead levels in the community
would have been over- or underestimated due to this effect.
Different children were sampled different numbers of times.
Children with very high blood lead levels may have been sampled
more often than those with lower levels. Restricting the data
analysis to children measured more than once may have reduced
potential errors from this effect, but it is still possible that
community blood lead levels were overestimated.
Maps showing area distribution of blood lead were prepared
by averaging all blood lead readings obtained at each residence.
Because blood lead does not change immediately upon changed
exposure, showing blood lead by residence may have obscured real
geographical differences.
Lead concentration data for air, tap water, soil, dust, and
food were essentially unavailable. This lack of information made
it impossible to draw even tentative conclusions about sources of
lead exposure to children.
USEPA's IEUBK model is most effective when used in
combination with a large database of measured blood lead and lead
concentrations in residential soil, dust, and tap water. The
model was not intended to be used in the way described in this
chapter. Accordingly, the estimate of an excess 130 ug/day lead
intake in Chester children, when compared with national averages,
should be considered a range-finding exercise only.
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4.3 RCRA TSDF FACILITIES
4.3.1 Data Source
In USEPA Region III, 605 Resource Conservation and Recovery
Act (RCRA) Treatment, Storage and Disposal facilities (TSDFs)
were ranked by the RCRA National Prioritization System. USEPA
has established this ranking system to ensure that
corrective actions are initiated in a timely manner at RCRA
facilities with the highest priority. It is an internal USEPA
management tool. Facilities are scored and ranked based on
the information about toxicant releases to environmental media,
toxicities of contaminants, proximity to residents and sensitive
environments, waste quantity, etc. As a result of the
prioritization system, the facilities are categorized as "High",
"Medium", and "Low" as indicated below. Corrective action will
be required under the authority of the 1984 Hazardous and Solid
Waste Amendments (HSWA). The HSWA corrective action applies to
releases to any media from any waste management units. Subpart F
in HSWA requires groundwater remediation at a regulated unit. A
regulated unit is defined as any surface impoundment, waste pile,
and land treatment unit or landfill that receives hazardous waste
after July 26, 1982.
The corrective action program is incorporated into a
facility permit or enforcement actions with consent or unilateral
orders. The TSDF facilities were screened for inclusion in the
Chester risk study.
4.3.2 Data Analysis, Results and Discussion .
In the State of Pennsylvania, there are 378 TSDFs. Eight
facilities are identified in the Chester study area. They are
listed below, with their priority rankings.
1. Sun Refining Company (High).
2. PECO, also known as Chem Clear (High).
3. BP Oil Company (High).
4. Congoleum Corporation (High).
5. Scott Paper (Medium).
6. Enviro Safe, also known as Marcus Hook
Processing (Medium).
7. Witco Corporation (Low).
8. East Coast Chemical Disposal (Low).
Four facilities (Sun Refining Co., BP Oil Co., PECO, and
Congoleum Corp.) were given a high Agency priority. Sun
Refinery Co. stabilized its wastes on site, and BP Oil Co.
excavated contaminated media and disposed of it off site.
Additionally, both facilities currently conduct groundwater
monitoring and evaluation to determine whether hazardous waste is
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actually entering groundwater. The data available so far are for
groundwater quality evaluation such as total organic carbon
(TOC), TOX, pH, salinity, etc. For long-term corrective actions,
these facilities are subject to USEPA's HSWA permit requirements
for complete site investigation to define the nature and extent
of contamination. Based on the investigation results, cleanup
activities will be implemented. The draft permits for these
facilities will be prepared in Fiscal Year 1995 (FY 95).
For Congoleum Corp., it is anticipated that this facility
will be subject to initial corrective action activities during FY
95.
The PECO facility is inactive. The facility is currently
engaged in corrective action activities in the early sampling
stage of a RCRA Facility Investigation (RFI), pursuant to a USEPA
Enforcement Consent Order. In a response to USEPA's request for
information concerning all releases of hazardous wastes at or
from the facility, dated April 27, 1992, PECO reported that there
were 54 individual incidents of releases at the facility that
occurred from 1981 to 1983. The total quantity of released
hazardous wastes and/or hazardous constituents was reported to be
approximately 57,000-62,000 gallons. These releases consisted of
treated, semi-treated, and untreated waste water, sludge
material, oil, and water mixtures, polymer, hexavalent chromium
mixtures, or unknown contents from hazardous waste storage tanks
and hazardous waste receiving pits. Analysis of spilled
materials listed in the September 16, 1983 Hazardous Spill Report
revealed that these spilled materials contained cadmium,
chromium, copper, nickel, lead and zinc. In addition, arsenic
and mercury were detected in soil where the spill occurred.
Enviro Safe, ranked as Medium, has completed an RFI. Based
on the findings of the RFI, USEPA concluded that the site poses
no adverse risk to human health and environment. Therefore, no
further action is warranted at Enviro Safe.
Based on a file search, the potential compounds of concern
in the study area for all sites are:
In groundwater: trichloroethene, phenanthrene, lead, and
other metals
In surface water: phenanthrene, methyl chloride, chromium,
and lead
In soil: phenanthrene, toluene, arsenic and other
metals
In air: asbestos, naphthalene, and toluene
In addition to the above, benzene, toluene, ethylbenzene,
and xylene would generally be considered chemicals of potential
concern at refineries such as Sun Refining Co. and BP Oil.
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There are no completed quantitative data available for the
above RCRA facilities, with the exception of Enviro Safe. Only
qualitative descriptions of waste types and impacted media are
available at this time. Therefore, the RCRA facilities could not
be quantitatively assessed and were handled qualitatively in this
report.
4.4 CERCLIS FACILITIES: SURFACE SOIL AND LEACHATE
4.4.1 Data Source
Under CERCLA/SARA (Comprehensive Environmental Response,
Compensation, and Liabilities Act/Superfund Reauthorization and
Amendments Act), potential hazardous waste sites undergo
preliminary investigations to determine whether they are
candidates for the National Priorities List'(NPL) ("Superfund"
list). The data from these site assessments are kept on file at
the Regional office of USEPA. Information for sites that undergo
preliminary investigations, removal actions, and NPL listing is
compiled on the Comprehensive Environmental Response,
Compensation, and Liability Information System (CERCLIS)
database.
The CERCLIS database was reviewed to identify sites located
in the Chester Risk Project study area (Chester City, Chester
Township, Eddystone, Linwood, Lower Chichester Township, Marcus
Hook, and Trainer). Based upon this review, a total of 36 sites,
with various levels of USEPA involvement, were identified. The
files for each of these sites were evaluated, and potentially
usable analytical data were available for eight sites, as
indicated below:
Chester City:
Chester Township:
Eddystone:
Marcus Hook:
Trainer:
Scott Paper Company (PAD002274991)
ABM Wade (PAD980539407)
Delaware Incinerator Fill #1 (PAD982367542)
Monroe Chemical (PAD049630502)
Air Products & Chemical Inc. (PAD002346732)
East Tenth Street Site, a.k.a. FMC Site
(PAD987323458)
Vermiculite Dump (PAD980509020)
Metro Container Corp. (PAD04454895)
For these sites, all relevant information from the files,
including analytical results, sample location maps, sample
descriptions and site histories, were copied. For the remaining
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28 sites without potentially usable data, either (1) analytical
data were not generated, (2) samples were collected from sealed
drums or from the interior of buildings, (3) the data were of
questionable quality, (4) sample media or locations could not be
determined, (5) the data were reported in obviously incorrect
units, or (6) the file (for two sites) was unavailable.
For the facilities evaluated during this study (i.e., those
with usable analytical data), site-specific information is
presented in Table 4-14.
4.4.2 Screening Data Analysis
Analytical results for the eight sites in the study area
with usable data were screened for the purpose of identifying
chemicals of potential concern (COPCs). To accomplish this task,
RBCs were used, as described in Section 3.2.1.
Unlike the soil exposure pathway, for aqueous and solid
leachate, default screening values for determining COPCs are not
provided in Region III technical guidance. Therefore, risk-based
screening equations for aqueous and solid leachate were derived
as described in Section 3.2.1.
Based upon the application of Region III technical guidance
for selecting COPCs, seven of the eight sites with usable
analytical data were retained for further evaluation, as
presented in Table 4-15.
4.4.3 Risk Assessment Data Analysis
None of the leachate samples assessed contained chemicals in
excess of screening RBCs. However, in several instances, soil
constituents were observed at concentrations of potential
concern. To quantify the doses associated with residential
exposure (child and adult) to contaminants in surface soil,
standard equations and default exposure parameters were applied,
as presented in Tables 3-1 and 3-2. With regard to routes of
exposure, inadvertent soil ingestion was considered for all
COPCs, while dermal exposure was quantified for PCBs only. For
the sake of simplicity and protectiveness, and due to the general
lack of high-quality data, the maximum reported concentration of
each COPC at each site was used in the dose calculations.
Estimated doses for the COPCs at each site are presented in
Tables 4-16 and 4-17.
4.4.4 Results and Discussion
To predict the risks associated with exposure to surface
soil under a residential scenario, toxicity criteria for the
COPCs must be considered. Quantitative risks (Hazard Indices and
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cancer risks) were estimated as described in Sections 3.3 and
3.4.
Generally, the Superfund program defines unacceptable risk
as follows:
• individual or cumulative carcinogenic risks that exceed
the upper bound (1E-4) of the established range (1E-6
to 1E-4) for acceptable cancer risk
• HQs in excess of 1.0, or cumulative HQs — referred to
as the Hazard Index (HI) — in excess of 1.0 for
similar target organs
Individual risk estimates are presented in Tables 4-18 and
4-19, while cumulative risk for each receptor at each site is
presented in Table 4-20. As demonstrated in Tables 4-18 through
4-20, unacceptable risks (carcinogenic and non-carcinogenic) may
exist at the following sites in the study area: Vermiculite
Dump, ABM Wade, Air Products & Chemicals, Inc., and East Tenth
Street Site, a.k.a. FMC Site. The risks are also displayed on
Figures 4-18, 4-19, 4-20, and 4-21. The ABM Wade soil risks
represent historical conditions. Records indicate that remedial
action, including soil removal, has since been performed.
The percent contribution to overall risk from each COPC is
provided in Table 4-21.
4.4.5 Uncertainty Analysis
In addition to the generic uncertainties, including the use
of conservative exposure assumptions that accompany most
quantitative risk assessments (discussed in Section 3.5), a few
issues related specifically to this evaluation are presented
below:
• A possible weakness in the data relates to those sites
where removal actions were conducted, but sampling
results represent pre-removal conditions.
• Some data may be antiquated; in these instances,
current environmental conditions may not be accurately
characterized by the reported analytical results. Such
data are identified with qualifying statements where
this is known.
• Many of the CERCLIS sites evaluated for this study are
located in industrial or commercial areas, making
residential exposure improbable.
4.5 SURFACE WATER, SEDIMENT, AND FISH TISSUE
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4.5.1 Data Sources
Three main data sources were used for surface water,
sediment, and fish tissue data: the STORET database, CERCLIS
files, and the National Study of Chemical Residues in Fish.
4.5.1.1 STORET
Surface water, sediment, and fish tissue data from areas
sampled in Region III are stored on the STORET database. STORET
is a computerized management information system residing on
USEPA's computer at Research Triangle Park, NC. States, federal,
and local governments supply and retrieve the information. The
information is used to detect changes in pollution levels,
demonstrate effects of pollution abatement programs, aid in basin
planning and management, prepare data for permit processing, meet
reporting requirements, and monitor water quality and toxic
substances. Over 130,000,000 parametric observations for over
700,000 sampling sites throughout the United States are contained
within STORET. Data quality varies between reporting agencies
and is indicated by self-reported "remark codes." The remark
codes indicate whether the sample is a composite, whether the
reported result is believed to be biased high or low, whether the
value is believed to be estimated, etc.
The Region III Toxicologists' Quality Circle agreed to use
only ambient, not effluent, data from this source. A summary of
all STORET data for Delaware County was examined. The STORET
locations were mapped (Fig. 4-22). The map showed that all
county stations except three were in or near the study area, with
approximately four locations appearing to be in Chester city.
All except the three remote stations (422094, WQN0159, and
332052) were retained on the assumption that Chester or general
study area residents could have access to and come in contact
with these stations for recreational or fishing purposes.
4.5.1.2 CERCLIS
The CERCLIS database was described in Section 4.4. Five
.CERCLIS sites in the Chester study area had surface water and/or
sediment data. These sites underwent data quality review in
accordance with the Quality Assurance Plans under which the work
was authorized.
4.5.1.3 National Study of Chemical Residues
The National Study of Chemical Residues in Fish was
performed by USEPA to study fish tissue contamination nationwide
(USEPA, 1992b). This study began as an outgrowth of the National
Dioxin Study, which found notable concentrations of dioxins in
fish tissue. It involved the collection of fish tissue from over
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300 stations nationwide.
One station from this study was located within the Chester
study area, and these fish tissue results were used for the
Chester risk assessment. Analytical data were obtained in
accordance with the analytical procedures and quality assurance
plans cited in the national study.
4.5.1.4 Data Quality
None of these data were originally collected for the
purposes of conducting a cumulative risk assessment of the
Chester area. The STORET data are basically generated to monitor
certain chemicals in certain water bodies, often in relation to
state discharge permits or evaluation of water quality. Water
quality can include health and diversity of aquatic organisms,
presence of harmful bacteria and microorganisms, etc., and is
often not targeted to toxic chemicals. However, several toxic
chemicals are regularly monitored, and these results were
retrieved.
The site assessment and removal data are collected in likely
"worst-case" spots on hazardous waste sites in order to determine
whether chemical contamination exists at the site in harmful
amounts and whether it is attributable to the site. The data are
used to characterize a small area and provided the only source of
sediment data available, except for one STORET sediment result.
The National Chemical Residue study was designed to identify
chemicals that accumulate in fish tissue in areas most likely to
be contaminated (i.e., urban and industrial areas, areas
downstream of facilities that commonly use bioconcentrating
chemicals).
All three of these data sets are biased toward detecting
contamination; the sampling designs involved targeting areas
where pollution is suspected or expected. The sampling designs
were not random. Some "background" or "upstream" samples were
obtained for site assessments. Such samples are designed to be
unaffected by the site in question but may be affected by other
environmental sources.
The STORET fish tissue samples were all composites. They
were identified as fillet of white perch with skin, channel
catfish fillet, American eel (no viscera, head, or skin), edible
portion of blue claw crab, or fillet with skin of the white
sucker. The fish tissue sample from the National Chemical
Residue study was the fillet of a brown bullhead (bottom feeder).
Since all samples were considered to represent edible portions of
edible fish, they were used as such in the dose estimations.
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Fish tissue concentrations reported for wet weight were
used. Where dry weight concentrations were available, these were
only used if percent moisture was also available and the
concentration could be converted. When both dry and wet weight
concentrations were available for the same chemical, the wet
weight was used preferentially.
Data gaps include chejnicals not analyzed for (such as most
organics in surface water), locations not sampled, and media not
sampled (such as sediment in most locations). Area-specific
exposure parameters (such as consumption rates of locally-caught
fish) were also unknown. People were observed fishing in the
Delaware River during a study area visit in September, indicating
that at least occasional and perhaps subsistence fishing are
possible exposure pathways.
4.5.2 Screening Data Analysis
The goal of this assessment was to estimate a risk for each
station location. Therefore, a preliminary screening was
performed to rule out chemicals that would not contribute
significantly to the risk, and to focus on chemicals that would
comprise the bulk of the risk. Data were screened using RBCs as
described in Section 3.2.1. Inorganic data less than 10 ug/1
from STORET, rejected, non-detect, "B" CERCLIS data (attributed
to blank contamination), and "K" STORET data (less than detection
limit), were not used. This screening was used to select COPCs
at each location. Thallium in water was screened using the
Maximum Contaminant Level (MCL) because no RfD is available.
This screening approach is consistent with Region Ill's method of
performing risk assessments at hazardous waste sites.
One assessment of the ABM Wade site involved groundwater-to-
surface water modeling to predict Delaware River concentrations
based on groundwater samples. The predicted concentrations were
less than 0.1 ug/1 for each chemical, and none of the modeled
results exceeded the human health-based screening RBCs for
surface water.
4.5.3 Risk Assessment Data Analysis
The maximum positive concentration for each chemical of
concern was used in risk assessment. This results in a "high-
end" exposure scenario. Because of the limitations on time and
available data, only this estimate was performed. Ideally,
"central tendency" and "reasonable maximum exposures" might also
be used. However, it would be recommended that if such effort
were undertaken, the data should be derived from a sampling
program designed specifically for a cumulative risk assessment of
Chester.
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Five stations had no COPCs. In order to derive risks for
these stations, estimated risks for all positively detected
chemicals at these locations were derived.
For surface water, risks to potential swimmers via ingestion
and dermal contact were estimated. For fish tissue, risks to
people potentially consuming fish tissue were estimated. For
sediment, risks to potential swimmers via ingestion and dermal .
contact were estimated. For all routes, both adults and children
were considered. Exposure estimations are calculated for each
receptor and each medium. The equations and input parameters
were presented in Tables 3-1 through 3-4. Quantitative risks
(Hazard Indices and cancer risks) were estimated as discussed in
Sections 3.3 and 3.4.
Risk addresses the quantitative toxicity of the chemicals.
Appendix I includes Toxicological Profiles for each chemical,
which contain descriptions of their properties and potential
effects.
No RfD or cancer slope factor (CSF) has been established for
lead. Lead was assessed separately under this project (see
Section 4.2).
4.5.4 Results and Discussion
Table 4-22 presents the COPCs and their maximum
concentrations at each station'.
Table 4-23 presents the risks associated with direct contact
with surface water at each location. It can be seen that the
Hazard Indices for each location are less than 1, indicating that
significant adverse noncancer health effects due to contact with
surface water at the reported concentrations are not expected.
Estimated cancer risks are at or below 1E-6 for all locations
except the Delaware County Incinerator Landfill #1 (3.9E-5). The
cancer risk at this site was based on arsenic and beryllium in a
drainage ditch water sample taken adjacent to the landfills. The
water sample was reported as "greenish brown" and is likely to
have contained high amounts of suspended solids. The feasibility
of people actually swimming in a drainage ditch depends upon its
depth and width, seasons of flow, and may also depend upon its
aesthetic appeal.
Table 4-24 presents the risks associated with direct contact
with sediment at each location. It can be seen that the Hazard
Indices for each location are less than 1, indicating that
significant adverse noncancer health effects due to contact with
sediment at the reported concentrations are not expected.
Estimated cancer risks were all below 1E-5. Risks were between
1E-6 and 1E-5 at the Monroe Chemical site (stream sediment
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upstream of the site, due to arsenic), East 10th Street site
[polycyclic aromatic hydrocarbons (PAHs) in sediment taken at
outfalls to Marcus Hook Creek], Delaware County Incinerator
Landfill #1 (due to arsenic and beryllium in drainage pipe inlets
and drainage ditch sediment), and ABM Wade (due to arsenic in
Delaware River sediment). The drainage pipe inlets and outfalls
are probably not likely to be used for recreation such as
swimming. It can be seen that arsenic contributes the majority
of the cancer risk. Beryllium and PAHs also contribute notably
to cancer risk. Arsenic and beryllium are metals that are found
both naturally occurring in the environment and as the result of
anthropogenic activities. PAHs result from the incomplete
combustion of organic material and are also found from both
natural and anthropogenic sources.
Table 4-25 presents the risks associated with fish
consumption at each station. It can be seen that the HI at every
station exceeds 1, except for the adult receptor at station 3096.
This is due to chlordane and dieldrin at WQF00511-000.6;
chlordane at WQN0182; chlordane, DDT, arsenic, copper, cadmium,
and oxychlordane at WQF00002-084.9; chlordane, DDT> and
oxychlordane at WQF00002-81.8; mercury and alpha-chlordane at
DELFISH-07; and a combination of chlordane, dieldrin, and mercury
at 3096. The cancer risks at every station exceed 1E-4. This is
due to dieldrin at WQF00511-000.6; PCBs and chlordane at WQN0182;
chlordane, arsenic, and PCBs at WQF00002-084.9; chlordane, DDE,
and PCBs at WQF00002-81.8; PCBs, DDE, and alpha-chlordane at
DELFISH-07; and PCBs and dioxins at 3096. It is currently
unknown whether locally-caught fish is a regular part of the diet
of citizens of Chester and the surrounding area. Therefore, this
exposure pathway may or may not be complete.
Table 4-26 summarizes the total risks at each location and
the chemicals that contribute the greatest portion to the total
risk.
Figures 4-23, 4-24, and 4-25 also display this information.
4.5.5 Comparative Risks and Additional Information
An analysis of the National Study of Chemical Residues in
Fish shows that the PCB concentrations at station 3096 are not
atypical for southeastern Pennsylvania/northern Delaware. Of 15
fish samples in that area, all but one showed comparable or
higher concentrations of PCBs. However, fish tissue samples from
other areas in Region III, notably central Pennsylvania and
central and western Virginia, had lower PCBs than southeastern
Pennsylvania. A similar pattern was observed for dioxins,
mercury, and dieldrin. It seems that station 3096 was typical of
southeastern Pennsylvania. In general, southeastern Pennsylvania
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had chemical concentrations comparable to or higher than the rest
of the Region, although certain other areas of Region III
reported high concentrations of particular chemicals (i.e., PCBs
and dioxins in West Virginia, DDE in eastern Pennsylvania).
Nationally, station 3096 was in the lowest category for
dioxins (concentration from 0 to 1 pg/g), along with 29 other
sites in the nation. Seventy sites in the nation had dioxin and
furan, concentrations higher than station 3096.
Nationwide, 362 sites were tested for organic compounds in
fish tissue and 374 were tested for mercury. The Chester area
fish tissue sample concentrations were greater than the national
mean and median for 3 locations for DDE (with 2 more exceeding
the median only); 3 locations for PCBs; one location for dieldrin
(with 2 more exceeding the median only); and 2 locations for
oxychlordane. One Chester area mercury sample exceeded the
national median concentration. (National means were calculated
using 1/2 the detection limit for non-detects).
The Commonwealth of Pennsylvania conducts water quality
assesments [called "305(b) Reports"] of surface water. The
Chester study area is in Subbasin 3 of. the Lower Delaware Basin.
This subbasin includes all of Philadelphia and Delaware Counties.
The subbasin consists of the Schuylkill River basin as well as
other tributaries to the lower Delaware, including Brandywine,
Chester, Ridley, Crum, and Darby Creeks. The 1994 305(b) report
included an assessment of 1182.5 of the 2825.6 stream miles in
this subbasin. The assessment examines whether the water quality
is such that the stream supports its use as designated by the
Commonwealth of Pennsylvania (i.e., drinking water, swimming and
other recreation, propagation of aquatic species, etc.).
Approximately 59% of the assessed stream miles fully supported
their designated uses. Approximately 29% partially supported
designated uses, leaving 12% not capable of supporting their
designated, uses. The four major sources of this degradation were
considered by the state to be agriculture, resource extraction
(i.e., mining), industrial point sources, and municipal point
sources. Industrial point sources were particularly mentioned
with respect to the Schuylkill River. Municipal point source
impacts were reported to be concentrated in the heavily populated
areas of the subbasin, including Chester Creek.
Other sources of degradation include unknown sources, other
nonpoint sources, other point sources, natural sources,
hydromodification, urban runoff, atmospheric deposition, combined
sewer overflows, and onsite wastewater systems.
Fish consumption advisories are in place for the Delaware
River and estuary from Yardley, Pennsylvania, to the
Pennsylvania/Delaware state line for white perch, channel
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catfish, and American eel, due to PCBs and chlordane.
4.5.6 Uncertainty Analysis
Along with the sources of uncertainty discussed in Section
3.5, the following uncertainty is important in evaluation of this
data set.
Aluminum (oral RfD), mirex (oral CSF), t-nonachlor (oral RfD
and CSF), and pentachloroanisole (oral RfD and CSF) have no
toxicity values listed for them in IRIS or the Health Effects
Assessment Summary Tables (HEAST). Interim toxicity values have
been used for these constituents [either withdrawn IRIS or HEAST
values, numbers from the Environmental Criteria and Assessment
Office (ECAO), or, in the case of aluminum, a 1987 OHEA
document]. The oral CSF for arsenic was based on exposure to
water, and the application of this number to exposure via soil
may not be strictly appropriate. t-Nonachlor was addressed using
parameters for heptachlor. The CSFs for PAHs were derived
relative to that of benzo[a]pyrene.
Chromium was assumed to be hexavalent, since the analytical
techniques did not differentiate between trivalent and hexavalent
chromium and hexavalent is generally more toxic. However, this
in all probability results in overestimate of risks from
chromium.
Some exposures could not be assessed at all because of lack
of any sort of toxicity criteria (dermal exposure to sediment
PAHs). USEPA ECAO determined that it is not appropriate to apply
the oral CSF to dermal effects from PAHs since they may act
locally. Therefore, dermal carcinogenic risk from these PAHs may
only be addressed qualitatively at this time.
There was additional uncertainty associated with the
adjustment of oral dose-response parameters for dermally absorbed
doses. As noted, when absorption factors were not available, the
chemical was assumed to be 100% absorbed during the RfD or CSF
study. While this is likely to be realistic for volatile
compounds, the assumption could be underprotective for chemicals
absorbed less than 100%.
As noted earlier, surface water and sediment risks are
likely to be overestimated where the samples were obtained from
outfalls and drainage ditches.
It is likely that most of the general population of Chester
does not consume locally-caught fish. However, subpopulations
may exist consisting of occasional fishers or possibly even
subsistence fishers. Subsistence fishers could have risks higher
than those quantitated herein.
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This risk assessment, which utilized existing data that were
targeted at likely areas of contamination, can only be used to
identify where risks are "high" or "of potential concern," but
cannot necessarily identify "low-risk" locations because of data
gaps. Data gaps include chemicals not analyzed for, chemicals
whose detection limits exceeded RBCs, chemicals without dose-
response parameters or other properties necessary for risk
quantitation, and locations and media not sampled.
4.6 TOXIC RELEASE INVENTORY (TRI)
4.6.1 Data Source
The TRI database contains information about chemical
releases from industrial manufacturers and processors (primary
Standard Industrial Classification (SIC) codes 20-39) to
environmental media. Since 1987, facilities meeting established
thresholds have been required to report release data according to
section 313 of the Emergency Planning and Community Right-to-Know
Act of 1986 (EPCRA).
4.6.2 Data Analysis
Region III has developed a method for evaluating these
releases in terms of their relative toxicity. This method is
documented in the Chemical Indexing System for the Toxic Chemical
Release Inventory Part I: Chronic Index (USEPA,.1993d). The
Chemical Indexing analysis provided in the present report
displays the 1992 TRI data in terms of the Chronic Index
(toxicity-weighted releases) and Residual Mass (non-weighted
releases) for Region III, highlighting TRI facilities in Delaware
County, Pennsylvania. •
The Regional maps (Figures 4-26, 4-27, and 4-28) show TRI
releases.in terms of the Chronic Index, including non-
carcinogenic and/or carcinogenic index dose. Those releases
which do not have an associated toxicity factor are combined
according to the amount of the release and are termed Residual
Mass. The resultant Chronic Indices and Residual Mass values are
summed for each facility and for each 8x8 mile geographic grid
area in Region III. Combining the facility Chronic Indices
within a geographic grid gives an indication of the potential for
cumulative hazard from TRI facilities within a given geographic
area.
After aggregation, the grids are ranked from lowest to
highest, and represented by the 10 percentiles indicated in the
map keys. The green coded maps represent a combination of the
highest ranking Chronic Index grids and the-highest ranking
Residual Mass grids.
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For the reporting year 1992, the calculated Chronic Indices
account for more than 85% of the total TRI mass released in
Region III.
Table 4-27 shows the top six TRI facilities in the Chronic
Index and Residual Mass ranking. In addition, a summary and
complete tabular output of the chemical releases reported for
each TRI category is provided (see Tables 4-28 and 4-29).
It is important to point out that it is not the purpose of
this analysis to formulate comparisons of potential risk due to
exposure to various chemicals. An assessment of these parameters
may be performed during Phase II of this process, using site
specific exposure data and demographic information. The intent
of this analysis is to provide an estimate of relative hazard for
screening purposes. In addition, since this analysis focuses
only on release data obtained from the TRI database, it is
subject to the requirements under which this reporting occurs.
In this respect, both the quantitative ranking as well as
qualitative evaluation contained in this report must be
considered equally.
4.6.3 Results and Discussion
In Delaware County, 28 facilities were subject to TRI
reporting under EPCRA for the reporting year (RY) 1992. A-
summarized priority listing of these facilities is included in
Table 4-27 and a complete listing is provided in Tables 4-28 and
4-29. Table 4-27 shows a quantitative summary of the facilities
which ranked in the top 90th percentile - 95% confidence of the
28 facilities subject to reporting under EPCRA. This analysis
should be viewed in conjunction with the qualitative evaluation
included in this report.
It has not been determined whether these releases were
continuous for the entire year or if they reflect one-time
accidental releases or spills. In addition, the proximity of
these releases relative to potentially exposed populations has
not been established. The determination of a potential health
threat of the volumes released depends on the proximity of the
stack to residential areas, the surrounding terrain and the
meteorological conditions. Furthermore, should it be determined
that additional analysis is required at any site listed in this
report, documentation which identifies these release as
continuous or intermittent should be obtained prior to the
analysis.
4.6.3.1 Sun Refining & Marketing Co., Marcus Hook
According to the TRI database, Sun Refining & Marketing
filed 21 Form R's for the RY1992. Ethylene oxide, benzene and
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methyl tert-butyl ether (MTBE) pose the greatest potential
threat. These compounds are reported to be released from
fugitive and point sources to the air medium. The reader is
referred to pages 3, 6 and 9 of Table 4-28 for more complete
information regarding the amounts and relative toxicity of these
releases.
The toxicity factors for both ethylene oxide and MTBE were
obtained from secondary sources (USEPA, 1993b; USEPA, 1990b).
While these toxicity factors have received some form of peer
review within individual USEPA programs, the data are not
recognized as Agency-wide consensus information. -Ethylene oxide
is considered to be a Group B1 carcinogen causing point-of-entry
tumors (stomach) after chronic gavage in rats. MTBE has been
documented by the Office of Drinking Water to possess non-
carcinogenic effects. The noncarcinogenic toxicity factor (oral
RfD) is derived from laboratory rat inhalation experiments which
documented a slight reduction in lung weights and increasing
depth of anesthesia with increasing dose. The carcinogenic and
noncarcinogenic toxicity factors for benzene, whose effects
include carcinogenicity (Group A) and leukemia, are derived from
USEPA-approved oral toxicity data (USEPA, 1994c) and possess
Agency-wide agreement.
Inhalation data for these chemicals are available from
secondary USEPA sources. The relative toxicity rank using
inhalation data is similar to that provided for the oral
assessment. The target organ effects from inhalation exposure
include central nervous system impairment (MTBE) and leukemia
(benzene and ethylene oxide).
4.6.3.2 Witco Corp, Trainer
This facility filed three Form R reports during the RY1992
indicating releases of 2-methoxyethanol and methanol from
fugitive and point sources to the air medium. The reader is
referred to pages 3, 6 and 9 of Table 4-28 for more detail. Of
greatest concern for potential health effects are the fugitive
and stack releases of 2-methoxyethanol to the air medium. This
compound has been determined to cause testicular effects in
inhalation studies in laboratory rabbits.
4.6.3.3 Scott Paper, Chester
Scott Paper has filed 4 Form R reports for RY1992. Three of
the four chemicals—chloroform, hydrochloric acid and sulfuric
acid—are of concern from a health perspective. The relatively
high volume of stack emissions of these compounds may be
significant due to the acute irritating effects of these
compounds via the inhalation route (see pages 3,6 and 9 of Table
4-28). Effects.of acids and chloroform include irritation of the
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mucous membranes including eyes and respiratory tract, persistent
cough, degeneration and ulceration of the nasal epithelium
(Sittig, 1985). The proximity of this facility to the Sun
Refining and Marketing Co. in Marcus Hook should be considered to
determine potential contributory risks to exposed populations.
4.6.3.4 Foamex, L.P., Eddystone
While this company submitted three Form R reports for
RY1992, only one compound is of concern from a health
perspective. Dichloromethane (DCM; also known as methylene
chloride) was reported to be released from fugitive sources to
the air medium. Detailed TRI release information may be found on
pages 3, 6 and 9 of Table 4-28. This compound possesses both
carcinogenic and non-carcinogenic effects. The USEPA-approved
toxicity factors are derived from IRIS (USEPA, 1994c), and the
compound has been shown to produce liver toxicity in laboratory
rats exposed to DCM in drinking water. DCM is also classified by
the USEPA as a Group B2 carcinogen, and inhalation exposure of
mice to DCM has been shown to produce tumors.
4.6.3.5 Boeing Defense and Space Group, Ridley Park
Boeing Defense and Space Group filed six Form R reports for
the RY1992. The chemicals included methyl isobutyl ketone,
acetone, trichloroethylene, toluene, methyl ethyl ketone and
sulfuric acid, (see pages 2, 5, and 8 of Table 4-28. While most
of these chemicals (except trichloroethylene) are less toxic than
some of the others mentioned above, the volumes and combination
of these chemicals released from stacks to the air may contribute
to a significant health risk. As mentioned previously, however,
the determination of a potential health threat of the volumes
released depends on the proximity of the stack to residential
areas, the surrounding terrain and the meteorological conditions.
4.6.3.6 Epsilon Prods.
Three facilities released chemicals for which oral toxicity
values were unavailable. Of these, Epsilon Prods, released the
largest volumes of chemicals. The company filed 2 Form R reports
for the RY1992. Ethylene and propylene were released from
fugitive and stack sources. Most significant is the release of
53,000 lbs./year of propylene from fugitive sources. The
National Toxicology Program (NTP) has tested the carcinogenicity
of propylene by the inhalation route and found no evidence of
carcinogenicity in rats or mice (NTP). Sittig, 1985, reports
that propylene is a mild toxicant, producing narcosis and
irregular heartbeat during acute exposure. Sun Oil also reported
similar releases to air of ethylene and propylene at 46,000 and
45,000 lbs./year, respectively.
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4.7 AIR
4.7.1 Modeled Air Concentrations
4.7.1.1 Data Source
Estimated air concentrations for 699 chemicals were provided
for approximately 1400 locations in Chester City. Of the
pollutants assessed, 640 are gaseous in nature, while 59 exist as
particulate matter. A detailed description of the air modeling
process for this project is presented in Appendix III of this
report.
4.7.1.2 Point Source Data Analysis
Although emission contributions from many sources were
modeled, only the total concentration of each pollutant at each
location was considered in risk calculations. The general VOC
source category included an assumption about the presence of
creosote/coal tar. There were indications that this assumption
was not valid for the industries concerned (see discussion of
Prime Sources, below), and creosote was therefore not included in
the quantitative risk assessment. Of the 699 chemicals
evaluated, 122 have toxicity values in the form of RfDs or CSFs.
Five of the modeled chemicals are criteria pollutants, and are
regulated under the authority of the Clean Air Act via the
National Ambient Air Quality Standards (NAAQS).
For chemicals with RfDs or CSFs, modeling results were
screened using RBCs as described in Section 3.2.1. to identify
chemicals of potential concern (COPCs). Accordingly, inhalation
under a standard residential exposure scenario was considered.
In instances where both an RfD and a CSF exist for a given COPC,
only the most sensitive endpoint (cancer or non-cancer) was
evaluated. Based upon the application of Region III technical
Guidance, 15 COPCs were identified in Chester City air. COPCs
and their associated toxicity criteria are presented in Tables 4-
30 and 3-8.
Estimated criteria pollutant concentrations were compared to
the NAAQS. (This approach for evaluating potential threats is
similar to the methodology employed for "assessing non-cancer
threats posed by chemicals with RfDs.) For the purpose of this
report, all criteria pollutants were retained for evaluation.
The criteria pollutants assessed for this project, and their
associated NAAQS, are presented in Table 4-31.
4.7.1.3 Point Source Results and Discussion
To evaluate the carcinogenic risks or the non-cancer threats
associated with exposure, the ratio between the screening RBC and
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the predicted air concentration was calculated for each COPC
possessing a CSF or an RfD. These risks are representative of
the calculation shown in Table 3-6.
For gasoline and diesel, carcinogenic risks were assessed
based upon respective unit risks for these compounds, as
determined by a recent USEPA investigation (USEPA, 1993c).
For the criteria pollutants, predicted concentrations at
each grid location were compared to NAAQSs. (Note that the
concentrations of lead predicted by the model represent annual
average levels, rather than quarterly concentrations. Although
annual average levels of lead were compared to the quarterly
standard, inaccuracies related to such a comparison are
insignificant in the context of this study.)
Individual Risks
At various locations in Chester, several chemicals were
predicted to exist in air at concentrations of potential concern.
Chromium VI was determined to contribute the most to carcinogenic
risk at any given location, while hydrogen chloride presents the
greatest non-cancer threat. A summary of the highest individual
risks in Chester City is presented in Table 4-32 for carcinogenic
COPCs, and in Table 4-33 for COPCs with non-cancer endpoints.
None of the predicted concentrations of criteria pollutants
in Chester exceeded NAAQSs, as illustrated in Table 4-34.
Cumulative Risks
Cumulative carcinogenic risks and non-cancer threats are
predicted to exceed benchmarks at several locations in Chester
City. The range of aggregate carcinogenic risks in Chester as a
result of inhalation is estimated to be 1.IE-5 to 6.6E-5. For
non-cancer endpoints, the range of His is predicted to be 1.0 to
3.8. The risks are also displayed on Figures 4-29, 4-30, 4-31,
4-32, 4-33, and 4-34.
To evaluate the cumulative impacts related to the criteria
pollutants, the ratios between the modeled concentrations at each
location to the NAAQS were calculated. Then; for each grid point
in Chester City, ratio values for individual criteria pollutants
were summed. (This approach for evaluating potential threats is
similar to the methodology employed for assessing non-cancer
threats posed by chemicals with RfDs.) Cumulative values for the
criteria pollutants were estimated to range from 0.6 to 1.6.
This is illustrated on Fig. 4-35.
It is possible to discuss the culpability of various sources
of air pollution to these risks. As outlined in the section on
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air qual-ity modeling, a large number of sources was modeled, the
sources vary dramatically in their contribution to both
carcinogenic risk and noncarcinogenic hazards.
In order to compare the contributions of the various sources
to air pollution in Chester, it was first necessary to develop a
means of comparison. The examination of risks at the location of
the most exposed individual, MEI, (a common practice in Superfund
and other programs) is not appropriate in the case of Chester for
a number of reasons.
First, the air quality analysis is inadequate to support
such comparisons. For many types of sources, emission rates were
calculated by estimating the emission rate of total respirable
particulate or total volatile organic compounds (VOC) and
multiplying this emission rate by the weight fractions of the
various constituent chemicals. The weight fractions were
generally derived from source profiles found in USEPA's SPECIATE
database which is used for emissions inventory development for
ozone modeling. The difficulty in applying these source profiles
to Chester is that, while the profiles are meant to be
representative of the average source of a given type, they are
not representative of many typical sources.
For example, Prime Sources, Incorporated, was initially
predicted to be the primary cause of increased cancer risk due to
air pollution at the location of the MEI. This original
interpretation was corrected upon discovery of the following
information. Prime's VOC-related emission rates were calculated
by'multiplying the state-identified classification ("organic
solvent evaporation— miscellaneous") profile to the State's
estimate of Prime's VOC emissions. In an initial step of the
analysis, this profile reflected estimates that 12.5% of
emissions from such activities are creosote. Prime, however, was
a manufacturer of cocoa products, and may not have used creosote
at all. (Additionally, this company is reported to have ceased
operations.) Risks related to creosote exposure have been
deleted from the analysis because the 12.5% assumption may not
apply to specific individual facilities.
Second, risk at the location of the MEI is probably not the
best way of identifying the most important sources. A source may
have highly localized impacts, yet not have a large effect on the
city as a whole.
The sources that pose the greatest risk or hazard to the
greatest number of people are probably those that are most
important to identify. Pursuant to this philosophy, sources were
identified that caused the greatest risk or hazard averaged over
the city as a whole. As noted in the discussion on air quality
modeling, estimates of air toxic concentrations and total risk
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were accomplished at 1392 receptors (locations) in and near the
city of Chester. [Some of these receptors were just outside of
the city (within 200 meters of the boundary). This does not
substantively affect the results of the analysis.] The risks
posed by the fifteen chemicals of potential concern were
calculated and averaged over the entire city.
I
Point sources accounted for roughly 40 percent of
environmental carcinogenic risk in Chester and more than half of
the sub-chronic risk. PQ, Delcora, and Sun each contribute
roughly one quarter of the long-term cancer risk. PQ emits
chromium and arsenic, Delcora emits those and other heavy metals,
and Sun emits many organic species. DuPont and Westinghouse
account for approximately 80 percent of the non-cancer risk. The
culpability of major point sources to long-term and short-term
risk throughout the city is listed in Table 4-35. The
contribution of each pollutant of concern to carcinogenic risk is
shown in the pie chart below.
Cancer Risk Contribution
»BTll I
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4.7.1.4 Point Source Uncertainties Analysis
In addition to the generic uncertainties discussed in
Section 3.5, including the use of conservative exposure
assumptions, that accompany most quantitative risk assessments, a
few issues related specifically to this evaluation are presented
below:
• For pollutants with RfDs and CSFs, either carcinogenic
risks or non-cancer endpoints were evaluated, but not
both. In instances where a chemical has both
carcinogenic and non-cancer potential, because of the
exclusion of the less sensitive endpoint, systemic
effects may be slightly under-estimated.
• When totaling HQs to arrive at an HI for each location,
target organs were not considered. Therefore, the
assumption of additivity for non-cancer endpoints may
be overly conservative for pollutants with differing
target organs.
• The unit risks used in calculations involving gasoline
and diesel are based on investigations and literature
searches performed by the USEPA in USEPA, 1993c. These
values have not been verified by the Science Advisory
Board, and should be considered provisional.
Although this analysis has certain limitations (especially
the use of SPECIATE and the generalization of some modeling
inputs), it is useful in identifying facilities for further study
and enhanced focus (enforcement, emissions control). See
Appendix III of this report and Section 5 of the Air Toxic
Emissions Inventory and Dispersion Modeling for Chester.
Pennsylvania for a description of emissions/modeling uncertainty.
4.7.1.5 Mobile Source Data Analysis (Truck Route Modeling)
/
Systems Applications International (SAI), working as a
subcontractor to Pacific Environmental Services (PES), analyzed
particulate matter (PM-10) and hydrocarbon (expressed as total
organic gases or TOG) impacts of the heavy duty diesel truck
traffic associated with the Delaware County Resource Recovery
Facility (DCRRF) for a portion of the truck route along Second
Street between Thurlow and Montgomery Streets. SAI's analysis is
summarized below; SAI's final report is included in the PES
report as Appendix J.
Emission estimates were accomplished for TOG and PM-10 using
the MOBILE5a and PART5 emission estimation models, respectively.
The models were driven by roadway geometry and signalization data
for obtained from the Pennsylvania Department of Transportation
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(PENNDOT). Estimates of 1991 average daily traffic volumes for
Second and Flower Streets were obtained from projections included
in the application for the solid waste permit for the DCRRF
(Valley Forge Laboratories, 1985). The traffic volume for
Jeffrey Street was obtained from traffic count data provided by
PENNDOT.
After they estimated emissions rates, the contractor applied
the CAL3QHC and ISCST2 dispersion models. The CAL3QHC model was
used to estimate maximum hourly concentrations under the worst
case microscale modeling conditions, and the ISCST2 model was
used to estimate the annual average hourly concentrations for
distances up to 500 meters from Second Street. Conditions for
1991 were modeled since this was the most recent year for which
traffic data along the corridor could be obtained. Hourly
surface meteorology data for Philadelphia International Airport
for 1991 were used as inputs to the ISCST2 modeling. The
methodology used with each model is discussed in detail in
Appendix J of the PES report.
4.7.1.6 Results and Discussion
Hourly Averages
The results of CAL3QHC modeling are presented in Table 4-36.
CAL3QHC was used to model the worst-case hourly average
conditions with and without the DCRRF truck traffic. As
evidenced by Table 4-36, the truck contribution to the predicted
emission levels is more significant for PM-10 than for TOG. This
can be attributed to the fact that truck PM-10 emission factors
are significantly larger than the fleet average, whereas TOG
emission factors of the trucks are similar or below the fleet
average. For the intersection of Jeffrey and Second Streets, the
truck contribution to transportation-caused ambient PM-10 near
the intersections is estimated at 50 percent, and at Flower and
Second Streets is over 60 percent.
Table 4-37 shows the location of the receptors with the 10
highest concentrations for the modeling that included the DCRRF
trucks. The highest concentrations occur at the receptors
located at the corners of the intersection. This indicates below
capacity roadway operation (i.e., the queue is being cleared in
each signal cycle).
Annual Averages
The annual average concentrations predicted by ISCST2 are
presented in Table 4-38. The results for the two cases (with and
without the DCRRF trucks) are shown for the two cross sections
perpendicular to Second Street. The cross sections illustrate
the concentration of emissions as a function of distance from
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Second Street. The concentration data in Table 4-38 are
presented in Figures 4-39 through 4-42. As was seen with
CAL3QHC, the truck contribution to PM-10 emissions is more
significant than the contribution to TOG emissions. The annual
average concentrations are significantly below the worst-case
concentrations predicted by CAL3QHC.
Table 4-39 shows the location of the receptors measuring the
six highest concentrations for the modeling that included the
DCRRF trucks. The highest annual average concentrations occur at
the receptors located nearest Second Street.
Note that the ISCST2 results are best, used for obtaining the
annual contribution to ambient pollutant concentrations from
trucks associated with the DCRRF. These concentrations do not
reflect the additional emissions from traffic on cross streets to
Second Street in the section modeled.
These emissions contribute to overall exposure. However,
since dose-response parameters are usually chemical-specific, it
is difficult to relate total PM-10 or total gases to a
quantitative risk. Therefore, it is merely noted here that
vehicles pose an additional source of exposure to particulate and
gaseous pollutants. The short-term PM-10 concentrations are
below the 24-hour NAAQS for PM-10 of 150 ug/m3.
4.7.1.7 Mobile Source Uncertainty Analysis
Factors contributing to uncertainty in the truck route
modeling include:
• potential unrepresentativeness of the traffic data;
• potential dissimilarities between the Chester fleet and
"typical" fleets described in the emissions estimation
tools;
• uncertainties in the dispersion model algorithms; and
• representativeness of the meteorological data.
4.7.2 Area Source Emissions
County-wide estimated emissions were available for area
sources of air contaminants. These data were not conducive to
the performance of a quantitative risk assessment because of the
difficulty in identifying individual chemicals and separating the
Chester area out from the county. However, a qualitative/semi-
quantitative assessment follows.
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4.7.2..1 Definition of Area Sources
Sources of toxic air releases which are small when evaluated
individually, but are significant when combined with other
facilities of similar type, may be identified in a given
geographic area. Volatile organic compounds (VOCs) are of
particular concern because some are classified by USEPA as
probable or possible human carcinogens. Also, they
photochemically combine with oxides of nitrogen (N0x) and carbon
monoxide (CO) in the presence of sunlight to form ozone, which
causes respiratory problems and plant damage.
4.7.2.2 Data Source
Information about area sources comes from two sources of
data. Information about the location, industry type, and number
of employees is available through Dun and Bradstreet.
Information about the amount of VOCs released per employee per
year is available in USEPA, 199Id. Combining these two databases
gives an estimate of VOC emissions per facility per year.
4.7.2.3 Data Analysis
A' list of facilities with Standard Industrial Classification
(SIC) codes between 4000 and 9999 (which include businesses such
as transportation services, gasoline service stations, automobile
repair shops, and dry cleaners), and within the study area was
retrieved from the Dun and Bradstreet (D&B) data base.
[Facilities with SIC codes between 2000 and 3999 (manufacturing)
are reported in the TRI data base and are evaluated in the Air
Toxics Modeling portion of the study]. The information for each
facility included the name of the facility, address, DUNS number,
and SIC code. For each facility, the VOC emissions estimate, in
lbs./year per employee, was determined, based on the SIC code.
248 facilities were found to have an SIC code with a
corresponding VOC emissions estimate. The number of employees for
each facility was then multiplied by the VOC estimate to arrive
at a value for total emissions for that facility per year.
A grid system was established for the study area, with each
grid square approximately one square kilometer (or about 1/2 mile
by 1/2 mile), and the sum of the estimated emissions for each
facility within a given grid square was calculated. The.values
for the grid system were assigned colors from red to blue, with
grey indicating no facilities.
4.7.2.4 Results and Discussion
Fig. 4-36 shows the estimated emissions for all the grid
squares in the study area.
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Fig. 4-37 highlights the top 9 (15%) grid squares, which
represent estimated annual releases of VOCs of over 40,000
pounds.
Fig. 4-38 shows the minority distribution of the study area
with the 9 high squares indicated in cross-hatching. This
indicates that grid squares 6, 7, and 8 are in an area with a
very high percentage of minority population, indicating that the
potential for impact to the minority community is greatest in
these areas.
4.7.2.5 Uncertainty Analysis
There are several limitations to the approach used to
estimate the VOC emissions for the area sources. First, the D&B
data base does not contain every facility in the study area that
releases VOCs. New businesses that have started since the last
update of the data, and facilities which are not large enough to
be included would be omitted. This is not likely to contribute
significantly to the overall total of emissions, but could have
an effect on the evaluation of a particular grid.
The estimates of VOC releases are based on studies of
"typical" facilities and are not actual measures of' the releases
from the facilities in the study area. The actual type and
amount of VOC releases is not available. The estimates are not
identified for the specific SIC codes that were identified in the
D&B database, so that approximate values were used instead of SIC
code-specific ones.
4.7.2.6 Recommendations
Further investigation should be conducted to determine if
actual releases are occurring, and which VOCs are from the
facilities within grid squares 6, 7, and 8. This could be done
through surveying the facilities listed in the D&B data base
and/or conducting air monitoring for the specific VOCs that would
be expected to be released from these facilities.
4.8 OTHER ENVIRONMENTAL CONCERNS
One of the study objectives was to be responsive to
environmental concerns raised by the citizens in the study area.
Some of these were issues for which USEPA had no available
database and could therefore not assess with quantitative risk
assessment. These issues included odors and noise and are
addressed below.
4.8,1 Odors
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4.8.1.1 Background Information
Odor is a very difficult sensory phenomenon to describe
objectively. Many attempts and subsequently many descriptors
have been, utilized in trying to describe the human olfactory
system and especially its variability, thresholds and the time
duration aspect of the sensation.
At least three different odor thresholds have been
identified: (1) the absolute perception threshold, (2) the
recognition threshold, (3) the objectionability threshold
(Verschueren, 1983). For our purposes in this discussion, the
Threshold Odor Concentration will be considered to be 50% of the
recognition threshold. This is the concentration at which 50% of
odor receptors defined the odor as being representative of the
chemical being studied.
It is key to understand that many odors may be perceived at
concentrations as low as 1 part per billion (e.g. ammonia
ethylacrylate, isopropylmercaptan), while still others can be
detected as low as 1 part per trillion (e.g. n-butyric acid).
The mere ability to sense an odor does not necessarily mean that
it is harmful at threshold levels. On the other hand, some
chemicals which are potentially harmful at lpw concentrations may
not be perceived by most humans at levels which are significantly
harmful. This certainly exacerbates individual fears and adds to
stress associated with the perceived odors which people
encounter.
Another physiologic process which adds to the confusion with
odors is the fact that short-term perception of even low-
concentration odors taxes the olfactory system in such a manner
that it seems to adapt to or "shut down" the perception of the
odor. This often leads to odor complaint data of reported short
duration. The actual phenomenon may be an adaptation response
where the odor is no longer perceptible although it still exists
at a similar concentration. A typical investigator might record
an event of short duration.
Instrumentation utilized for such an investigation would not
be affected by the adaptation response but may have threshold
sensitivities several orders of magnitude higher than the human
sense of smell.
A major source of concern in the Chester neighborhoods are
the odors which seem to emanate from the industries along the
Delaware River coastline. It may be that individual small
industrial or commercial operations could be sources of these
emissions.
Although the incidence of odor complaints has been one of
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the greatest concerns in Chester, the pervasiveness of odor could
not be addressed quantitatively in the environmental risk
assessment. This does not diminish the importance of odors to
residents, nor is it meant to ignore or screen them out of the
assessment. There were virtually no data available at the onset
of the study related to odors. During the study, several
meetings were held among the participating agencies and a
workgroup was formed in order to define a monitoring effort to
identify and quantify the perceived odors.
It was the conclusion of the workgroup that a short-term
surveillance and analysis effort would not adequately identify
odors, could not be used for quantification purposes, and would
offer no assistance to identifying sources of the odors.
For purposes of this report, odors are being considered only
as a source of further investigation. They are a nuisance which
may add to the overall stress of residing in an urbanized
environment. It is much like intrusive noise, unsightly vacant
lots, and unwanted traffic through a neighborhood.
As of the date of this report, little data exist regarding
odors in the city of Chester. The best sources of information
related to odors is the Commonwealth of Pennsylvania's Department
of Environmental Resources (PADER) log of odor complaints for the
past few years. As part of the data log, complainants are asked
to provide location and possible source of the odor. This time,
date, location and possible source could be used to identify
neighborhoods at risk from this obtrusive environmental concern.
However, since the data provided to PADER are kept confidential,
it is inappropriate to attempt to use GIS to map the complaint
information in such a way as to infer sources of odors in
neighborhoods.
The data do clearly show that the vast majority of
complaints derive from the residential area contiguous to the
industrialized river front in the western portion of Chester.
Waste management facilities located in this area handle solid
waste (trash), medical wastes, and sewage wastes.
4.8.1.2 Long-Term Odor Investigation
During the Chester study, it was decided that in order to
provide an adequate depiction of the air emissions, pollutants
and possibly odors, a long-term study was necessary. The USEPA
Environmental Service Division, in conjunction with the PADER
Bureau of Laboratories, began a year long study utilizing Summa
canisters in December 1994. The field protocol for the study is
presented in Appendix IV.
4.8.1.3 Short-Term Odor Investigation
EXTERNAL REVIEW DRAFT V. 1.0
65
-------
It was decided that although a short-duration odor
investigation could not be used for risk assessment purposes, it
would be a useful tool in determining what chemicals are present
during certain time periods and what evidence is present to
identify emission sources.
During November 1994, for a continuous 120-hour time period,
investigators patrolled the areas where significant complaint
data had been compiled. The investigators logged odor/location
information and were prepared to investigate odor complaints as
they were received. In addition, during the evening and night-
time hours, PADER's Mobile Analytic Unit was on site
concentrating on the waste facility complex along the riverfront
that is bordered by residential neighborhoods in the western side
of the city. The investigation plan for this surveillance is
included in Appendix V. The results of this study will be
published at a future date by PADER.
4.8.2 Noise
4.8.2.1 Background Information
Many residents of Chester have complained that environmental
noise diminishes the quality of life they experience in a home
setting. They cite numerous sources of the noise and have
requested help from the industrial community and the
environmental agencies in reducing noise to acceptable, non-
intrusive levels. Some of the sources identified include:
• truck traffic passing through residential areas
• industrial operating equipment
• aircraft over-flights
• music sources, such as car radios, home hi-fi
• train pass-by
Transportation noise sources are often cited as leading
disruptions in residential neighborhoods. In the case of large
trucks, the inherent low frequency engine and drive train noise
are "felt" (pressure waves) as low frequency sounds often
"exciting" structures or even individuals' body frames. These
vibrations may be unsettling to sensitive individuals. In
addition, any vehicle which has not been properly maintained can
produce sound far in excess of the original equipment
manufacturer levels, and may be in violation of state or local
noise regulations.
Other transportation noise sources in Chester can include
trains and aircraft over-flights. These are typically short in
duration but high in amplitude, usually causing a temporary
intrusive event.
EXTERNAL REVIEW DRAFT V. 1.0
66
-------
Industrial noise sounds can have single or multiple sources
and can be short or long in duration. Depending on the sound
level (amplitude) and/or the quality (frequency or tone), the
sound may. vary from imperceptible to annoying or intrusive.
Residential sounds such as radios, televisions, hi-fi
systems, barking dogs and even children playing may be sources of
unwanted sound. There is great variability regarding the
intrusiveness of these sounds.
As part of the Chester Risk Project, USEPA staff reviewed
applicable environmental noise studies performed in the Chester
area and performed a literature search for any applicable
mitigation measures. This limited search found a Pre-Operational
Noise Monitoring Study (Westinghouse, 1991) and a subsequent
Noise Report Summary (Westinghouse, 1993).
In the study, environmental noise monitoring was performed
at seven locations. This was considered to be background noise
monitoring, at facility site locations, prior to final
construction and operation of the Delaware County Resource
Recovery facility. A total of three continuous 24-hour time
periods were sampled including one weekend day and two weekdays.
An additional four locations were sampled in the residential
community in February 1991 in areas adjacent to the Resource
Recovery facility.
Although there was some variability in the measured noise
data due to short-duration transient events, the levels measured
in and around the facility and in the residential neighborhoods
are typical of urban residential settings and would be considered
generally acceptable.
Comparing the 1990 data with a follow-up 1993 similar noise
evaluation after the Resource Recovery facility was in operation,
indicates that at several locations, sound levels (Energy
Equivalent Sound Level) are similar to pre-operational levels.
It is also noted in the 1993 report that reports of short-term
intrusive sounds were logged by facility staff and follow-up
investigations were attempted. These tests were designed to
establish a time history of sound amplitude in order to discover
plant operations possibly responsible for the noise disturbance.
Additional, discrete narrow-band frequency analysis was also
attempted in order to identify the offending sound. One-third
octave band analysis as well as very narrow (0.5H3) spectral
measurements were taken. Suspected sources were coo-ling tower
fans, roof ventilation fans, air compressors, and a vacuum truck.
No definitive source was identified in the report.
EXTERNAL REVIEW DRAFT V. 1.0
67
-------
4.8.2.2 Noise Control Ordinance
A noise control ordinance for the City of Chester,
Pennsylvania was passed on January 14, 1993. This ordinance
applies to vehicles, appliances and equipment, and includes many
of the "nuisance" type of unwanted sounds. The ordinance
includes subjective aspects of noise as well as objective
criteria limits for motorized vehicles and property line limit
depending on land use zoning.
4.8.2.3 Control of Environmental Noise
Urbanization typically brings together the key ingredients
of sustaining life in a city. Industry means jobs and a tax
base, residents supply homes and workers for industry, and
commercial businesses provide support to industry and residents.
When these key elements are condensed into a tight geographical
area, intrusions begin to occur. A workable plan of action to
enable the synergism of community to function must be based on
communication and cooperation. Where these attributes do not
exist, intervention must then occur. In the case of noise,
reasonable people can usually agree on action plans (or
compromise actions) which satisfy all parties. When an impasse
arises, local and in some cases state intervention must decide
the course of action. This can occur by utilization of a noise
control ordinance, civil litigation, or some other type of
objective third-party dispute resolution.
4.9 EPIDEMIOLOGICAL ISSUES
A study.of the existing public health status of the
community and a specific epidemiological study to try to
establish cause-and-effect links between environmental risks and
health effects were beyond the scope of the environmental risk
project. However, the state health department, as a preliminary
exercise, looked at the mortality rate for certain diseases in
the city as compared to the state and county. This exercise may
be found in Appendix VI. This may give useful information
regarding the existing health of the community, although it
cannot be used to establish causes of the health conditions.
EXTERNAL REVIEW DRAFT V. 1.0
68
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CHESTER RISK PROJECT
EXTERNAL REVIEW DRAFT VERSION 1.0
LIST OF TABLES
3-1 Ingestion of Chemicals in Soil, Sediment, and Fish Tissue:
Dose Equation for Residential Exposure
3-2 Dermal Absorption of Chemicals in Soil and Sediment: Dose
Equation for Residential Exposure
3-3 Ingestion of Drinking Water and Surface Water: Dose Equation
for Residential Exposure
3-4 Dermal Exposure to Drinking Water and Surface Water: Dose
Equation for Residential Exposure
3-5 Inhalation Exposure to Drinking Water: Dose Equation for
Residential Exposure
3-6 Inhalation of Chemicals in Air: Dose Equation for
Residential Exposure
3-7 Oral Dose-Response Parameters for Chemicals of Potential
Concern
3-8 Inhalation Dose-Response Parameters for Chemicals of
Potential Concern
4-1 US Census of Population and Housing—STF—3A Sample Count
Data (1990) Summary
4-2 CERCLIS Sites Ground Water Monitoring Data Summary
4-3 Summary Risk Table: Chester Water Authority
4-4 Summary Risk Table: Philadelphia Suburban Water Authority
4-5 Summary Risk Table: Philadelphia Water Department
4-6 Chester Water Authority: Chester High/Low Water Supply Data,
1989 to Present: Contaminants of Concern—Sorted by Year
4-7 Philadelphia Suburban Water Company: Chester High/Low Water
Supply Data, 1989 to Present: Contaminants of Concern—
Sorted by Year
4-8 Philadelphia Water Department: Chester High/Low Water Supply
Data, 1989 to Present: Contaminants of Concern—Sorted by
Year
4-9 Chester Water Authority Violation Summary
4-10 Philadelphia Suburban Water Company Violation Summary
4-11 Philadelphia Water Department Violation Summary
4-12 Comparison of Children's Blood Lead in Chester, PA with
Results of USEPA's Three-City Study
4-13 Temporal Trends in Children's Blood Lead: Chester, PA
4-14 Site-Specific Information (CERCLIS Sites)
4-15 Summary of Findings at CERCLIS Sites
4-16 Soil Ingestion Dose Calculations
4-17 Dermal Absorption Dose Calculations
4-18 Soil Ingestion Risk Calculations
4-19 Dermal Absorption Risk Calculations (Soil)
4-20 Hazard Index and Cumulative Carcinongenic Risk, Per Site
(CERCLIS Sites)
4-21 Percent Contribution to Hazard Index and Cumulative
Carcinogenic Risk, Per Site (CERCLIS Sites)
4-22 Surface Water, Sediment, and Fish Tissue Chemicals of
Concern
4-23 Surface Water Risks
-------
4-24 Sediment Risks
4-25 Fish Tissue Risks
4-26 Surface Water, Sediment, and Fish Tissue Risks
4-27 Delaware County, PA TRI Facilities Chronic Index and
Residual Mass Ranking
4-28 1992 TRI for Region III: Delaware County, PA
4-29 Delaware County, PA Summary Ranking for Total Onsite
Releases
4-30 Chemicals of Potential Concern in Air
4-31 Criteria Pollutants and National Ambient Air Quality
Standards
4-32 Maximum Carcinogenic Risks in Air
4-33 Maximum Non-Cancer Threats in Air
4-34 Maximum Ratio of Predicted Concentrations of Criteria
Pollutants to National Ambient Air Quality Standards
4-35 Relative Contributions of Point Sources to Long and Short-
Term Risk from Environmental Air Pollution
4-36 CAL3QHC Predicted Emissions Concentrations Under the Worst-
Case Modeling Conditions
4-37 Ten Highest Concentrations by Receptor Location from the
CAL3QHC Model for the Emissions of the Existing Traffic with
the DCRRF Trucks
4-38 ISCST2 Predicted Annual Average Hourly Emissions
Concentrations for 1991
4-39 Six Highest Concentrations by Receptor Location from the
ISCST2 Model for the Emissions of the Existing Traffic with
the DCRRF Trucks
-------
CHESTER RISK PROJECT
TABLE 3-1
INGESTIOM 07 CHEMICALS IN SOIL, SEDIXEHT, AHD FISH TISSUE
DOSE EQUATION FOR RESIDENTIAL EXPOSURE
C x IR x CF x EF x ED
DOSE (mg/kg/d) =
BW x AT
Where: C = chemical concentration in soil,
sediment, solid leachate, or fish tissue
(mg/kg)
IR = ingestion rate
s 200 mg/d. soil or sediment
» 100 mg/d soil or sediment
years old)*
¦= 54 g/d fish tissue*
CF = conversion factor
= 1E-6 kg/mg soil or sediment
» IE-3 kg/g fish tissue
EF a exposure frequency
¦ 350 d/yr*
ED » exposure duration
= 6 years for children*
= 24 years for adults*
BW - body weight
• 15 leg for children*
- 70 kg for adults*
AT = averaging time
- ED x 365 d/yr for non-carcinogens
¦ 70 yr x 365 d/yr for carcinogens,
for children*
for adults (>6
"Standard default exposure factors from USEPA, 1991a
-------
CHESTER RISK PROJECT
TABLE 3-2
DERMAL ABSORPTION 07 CHEMICALS IN SOIL AMD SEDIMEMT
DOSE EQUATION FOR RESIDENTIAL EXPOSURE
C X CF X SA x AF X ABS X EF X ED
DOSE (mg/kg/d) =
BW x AT
Where: C = chemical concentration in soil,
sediment, or leachate (mg/kg)
CF* = conversion factor
= 1E-6 kg/mg for soil and sediment
SA = skin surface area available for contact
= 860 cm2/event for children (hands and
feet)**"
= 1800 cm2/event for adults (hands and
feet)a,d
AF = soil-to-skin adherence factor
= 1 mg/cm2 b
ABS = absorption factor
= 6% for PCBsb
= 1% for cadmiumb
EF « exposure frequency
= 350 events/yr for soilb
= 7 events/yr for sedimentd
ED = exposure duration
=» 6 years for children6
- 24 years for adults6
BW = body weight
* 15 kg for children0
= 70 kg for adultsc
AT » averaging time
= ED x 365 d/yr for non-carcinogens
» 70 yr x 365 d/yr for carcinogens
*USEPA, 1989b
huSEPA, 1992a
CUSEPA, 1991a
^USEPA, 1989a
-------
CHESTER RISK PROJECT
TABLE 3-3
INGESTION OF DRINKING WATER AND SURFACE HATER
DOSE EQUATION TOR RESIDENTIAL EXPOSURE
C X IR X EF X ED
DOSE (mg/kg/d) = ,
BW X AT
Where: C = chemical concentration in water (mg/L)
IR = ingestion rate of water
= 2 L/day for adults, drinking water*
= 1 L/day for children, drinking waterb
» 0.05 L/hour x 2.6 hrs/d for surface
water, recreational usec
EF = exposure frequency
=» 350 d/yr for drinking water*
= 7 events/yr for surface water'
ED « exposure duration
= 6 years for children"
= 24 years for adults"
BW = body weight
= 15 kg for children*
a 70 kg for adults"
AT ™ averaging time
¦ ED x 365 d/yr for non-carcinogens
= 70 yr x 365 d/yr for carcinogens
"USEPA, 1991a
"USEPA, 1989b
CUSEPA, 1989a
-------
CHESTER RISK PROJECT
TABLE 3-4
DERMAL EXPOSURE TO DRINKING HATER AND SURFACE WATER
DOSE EQUATION FOR RESIDENTIAL EXPOSURE
DOSE (mg/kg/d)
Kp X C x t X CF X A X EF X ED
BW x AT
Where:
C = chemical concentration in water (mg/L)
Kp = permeability coefficient from water
(cm/hr) (chemical-specific)*
t = duration of exposure event
= 0.33 hrs/d for child bathb
= 2.6 hrs/d for surface water, recreation0
CF = Conversion factor (L/cm3: 1E-3)
A = Skin surface area available for contact
= 18000 cm2 for adultc
= 7200 cm2 for child6
EF
ED
BW
AT
exposure frequency
350 d/yr for drinking water*
7 events/yr for surface water6
exposure duration
6 years for children*
24 years for adults*
body weight
15 kg for children*
70 kg for adults*
averaging time
ED x 365 d/yr for non-carcinogens
70 yr x 365 d/yr for carcinogens
*USEPA, 1992a
bProfessional judgment
CUSEPA, 1989a
*USEPA, 1991a
-------
CHESTER RISK PROJECT
TABLE 3-5
INHALATION EXPOSURE TO DRINKING WATER
DOSE EQUATION FOR RESIDENTIAL EXPOSURE
D X EF x ED
DOSE (mg/kg/d) =
BW x AT
D = [(VR x S)/(BW x Ra x CF1)] x [Ds - 1/Ra + exp(-Ra
x Ds)/Ra]
S = Cwd x FR/SV
Cwd = C x CF2 x (l-exp[(-KaL x ts)/60d)])
KaL = KL/SQRT [(T1 x uS)/(Ts x ul)]
KL - 1/[(1/kl) + ((R x T)/(H x kg))
kg = kH X SQRT(MWH/MW)
kl = kC X SQRT(HWC/MW)
Where: D = Inhalation dose (mg/kg/shower)
VR = Inhalation rate
= 14 L/min (20 m3/d)a
S = Indoor VOC generation rate (ug/m3/min)
(calculated)
Ra = Rate of air exchange
= 0.01667/minb
CFl = Conversion factor
= 1E+6 ug L /mg/mc
Cwd = Concentration leaving water droplet
(ug/L) (calculated)
FR = Shower flow rate
= 20 L/minc
SV = Shower stall air volume
= 2.9 m3 c
C = Concentration in water (mg/L)
-------
TABLE 3-5
PAGE 2/3
CF2 = Conversion factor
- 1000 ug/mg
KaL = Adjusted overall mass transfer
coefficient (cm/hr) (calculated)
ts = shower droplet tine
= 2 secb
d = Shower droplet diameter
= 1 mmb
KL = Mass transfer coefficient (cm/hr)
(calculated)
T1 = Calibration water temperature of KL
- 293 K**
Ts = Shower water temperature
= 318 K*
ul - Water viscosity at T1
= 1.002 centipoiseb
us ® Water viscosity at Ts
= 0.596 centipoiseb
R = Gas constant
= 8.2E-5 atm a^/mol/K
T = Absolute temperature
= 293 K
H = Henry's Lav constant (atm m*/mol)
(chemical-specific)
leg ¦ Gas-film mass transfer coefficient
(cm/hr) (calculated)
Jcl = Liquid-film mass transfer coefficient
(cm/hr) (calculated)
kH = kg for water
= 3000 cm/hr
kc = kl for carbon dioxide
= 20 cm/hr
MWH «* Molecular weight of water
= 18 g/mol
-------
TABLE 3-5
PAGE 3/3
MWC = Molecular weight of carbon dioxide
= 44 g/mol
MW = Molecular weight of contaminant (g/mol)
(chemical-specific)
Ds = duration of shower
¦ 12 minc
EF = exposure frequency
« 350 showers/yr*
ED 8 exposure duration
= 24 years for adults"
BW = body weight
= 70 kg for adults*
AT = averaging time
= ED x 365 d/yr for non-carcinogens
= 70 yr x 365 d/yr for carcinogens
•USEPA, 1991a
Foster and Chrostowski, 1987
cProfessional judgment
-------
CHESTER RISK PROJECT
TABLE 3-6
INHALATION OF CHEMICALS IN AIR
DOSE EQUATION TOR RESIDENTIAL EXPOSURE
C x IR x, EF x ED
DOSE (mg/kg/d) = —
BW x AT
Where: C = chemical concentration in air (mg/m3)
(modeled)
IR = inhalation rate
- 20 m3/day for adults*
=12 m3/day for childrenb
EF = exposure frequency
= 350 d/yr*
ED » exposure duration
= 6 years for children (carcinogenic)*
= 24 years for adults (carcinogenic)*
= 30 years for adults (noncarcinogenic)*
BW = body weight
- 15 kg for children*
= 70 kg for adults*
AT ¦ averaging time
= ED x 365 d/yr for non-carcinogens
¦ 70 yr x 365 d/yr for carcinogens
*USEPA, 1991a
''Professional judgment
-------
CHE8TER RISK PROJECT
TABLE 3-7
ORAL D08E-R88P0N8E PARAMETERS FOR CHEMICALS 07 POTENTIAL CONCERN
CHEMICAL
ORAL RFD
(mg/kg/day)
ORAL CSF
(l/mg/kg/day)
MANGANESE
5E-3 (WATER)
1.4E-1 (FOOD)
N/A
CHLORDANE COMPOUNDS
6E-5
1.3
p,p'-DDE
N/A
3.4E-1
DIELDRIN
5E-5
16
PCBs
N/A
7.7
CADMIUM
5E-4 (HATER)
IE-3 (FOOD)
N/A
p,p'-DDD
N/A
to
•
<*>
w
1
l-»
MERCURY
3E-4 (HEAST)
N/A
BENZO[B]FLUORANTHENE
N/A
7.3E-1 (ECAO)
ARSENIC
3E-4
1,75 1
BERYLLIUM
5E-3
4.3 1
VANADIUM
7E-3 (HEAST)
N/A
ANTIMONY
4E-4
N/A
CHROMIUM VI
5E-3
N/A
NICKEL
2E-2
N/A
SILVER
5E-3
N/A
BENZO[K]FLUORANTHENE
N/A
7.3E-2 (ECAO)
CHRYSENE
N/A
7.3E-3 (ECAO)
BENZ[A]ANTHRACENE
N/A
7.3E-1 (ECAO)
BENZO[A]PYRENE
N/A
7.3
DIBENZ[A,H]ANTHRACENE
N/A
7.3 (ECAO)
INDENO[1,2,3-
C,D]PYRENE
N/A
7.3E-1 (ECAO)
p,p'-DDT
5E-4
3.4E-1
t-NONACHLOR
5E-4 (heptachlor)
4.5 (heptachlor)
COPPER
3.71E-2 (HEAST)
N/A
-------
CHEMICAL
ORAL RFD
(mg/kg/day)
ORAL CSF
(1/mg/kg/day)
ZINC
3E-1
N/A
SELENIUM
5E-3
N/A
ALUMINUM
2.9 (RBCo)
H/A
BARIUM
7E-2
N/A
MIREX
2E-4
*
CO
9
H
PENTACHLOROANISOLE
3E-2 (HEAST 1989)
1.2E-1 (HEAST
1990)
TETRACHLOROETHENE
1E-2
5.2E-2 (ECAO)
TOTAL THMs
1E-2 (CHLOROFORM)
6.1E-3 1
(CHLOROFORM) 1
CARBON TETRACHLORIDE
7E-4
1.3E-1 1
FLUORIDE
6E-2
N/A
NITRITE
1E-1
N/A
DIOXINS
N/A
1.5E5
The - following hierarchy was used in selecting these numbers:
parameters from USEPA's Integrated Risk Information System
(IRIS), parameters from Health Effects Assessment Summary Tables
(HEAST), numbers withdrawn from IRIS or HEAST but not yet
substituted (W), numbers from USEPA's Environmental Criteria and
Assessment Office (ECAO), numbers from other sources (RBCo).
USEPA, 1989c
USEPA, 1990a
USEPA, 1994a
USEPA, 1994b
USEPA, 1994c
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CHESTER RISK PROJECT
TABLE 3-8
INHALATION DOSE-RESPONSE PARAMETERS FOR CHEMICALS OF POTENTIAL
CONCERN
CHEMICAL
INHALATION RFD
(mg/kg/day)
INHALATION CSF
(1/mg/kg/day)
BENZENE
1.7E-3 (ECAO)
2.9E-2
FORMALDEHYDE
N/A
4.5E-2
2-METHOXYETHANOL
5.7E-3
N/A
ACROLEIN
5.7E-6
N/A
VINYL CHLORIDE
N/A
3E-1 (HEAST)
CADMIUM
N/A
6.3
ACRYLONITRILE
5.7E-4
2.4E-1 (HEAST)
MERCURY
8.6E-5 (HEAST)
N/A
ETHYLENE GLYCOL
.5. 7E=3 (HEAST)
N/A
ARSENIC
N/A
15.1
1,3-BUTADIENE
N/A
9.8E-1
CROTONALDEHYDE
N/A
1.9 (W)
HYDROGEN CHLORIDE
2E-3
N/A
TETRACHLOROETHENE
N/A
2.03E-3 (ECAO)
TOTAL THMs
N/A
8.05E-2
(CHLOROFORM)
CARBON TETRACHLORIDE
N/A
5.3E-2
DIESEL
N/A
l^E-S/ug/m5 *
GASOLINE
N/A
S.lE-5/ug/m5 *
CHROMIUM VI
N/A
4.2E1 (HEAST)
The following hierarchy was used in selecting these numbers:
parameters from USEPA's Integrated Risk Information System
(IRIS), parameters from Health Effects Assessment Summary Tables
(HEAST), numbers withdrawn from IRIS or HEAST but not yet
substituted (W) , numbers from USEPA's Environmental Criteria and
Assessment Office (ECAO), numbers from other sources (RBCo).
~unit risk USEPA, 1994a USEPA, 1994c
-------
CHESTER RISK PROJECT
TABLE 4-1
U.S. CENSUS Or POPULATION AND HOUSING - 8TF- 3A SAMPLE COUNT DATA (1990)*
SUMMARY
Are*
Total
Housing
Uttit»; '
dottipita
Housing
Vacant
Housing
units ...
Public*
Drilled wall
Dug wall
Other
Marcus Hook Borough
1055
990
65
1055
0
0
0
Trainer Borough
912
871
41
902
7
3
0
Chester City
16,512
14,538
1,975
16,445
18
22
26
Chester Township CDP
1,879
1,778
101
1,868
5
6
0
Linwood
1,190
1,123
67
1,190
0
0
0
Upland Borough
1,224
1,187
37
1,224
0
0
0
Eddystone Borough
1,071
993
78
1,065
0
0
6
* Data obtained from. STF 3A, Pile 29, Tables H22-H33
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CHESTER RISK PROJECT
TABLE 4-2
CERCLlS SITES GROUND WATER MONITORING DATA*
SUMMARY
Site Name :
G* Contamination
organise*
GW Contamination
Inorganics*
No GW
Contamination*
Comments
Air Products
Benzene (16)
Carbon Tetrachloride (1400)
Chloroform (57)
Tetrachloroethene (720)
1,1,1-Trichloroethane (l)
Trichloroethene (1700)
Vinyl Chloride (4)
Barium (700)
Zinc (230)
Residents (547)
-2 miles NW
known to rely
on homewells
Delaware Co
Incinerator
Landfill
Chlorobenzene (1)
Manganese (932)
ABM Wade
Acetone (11)
Benzene (110%)
Carbon Disulfide (5)
Chlorobenzene (113%)
Chloroethane (17)
1.1-Dichloroethane (15)
1.2-Dichloroethane (93)
1.1-Dichloroethene (107%)
1.2-Dichloroethene (690)
1,2-Dichloropropane (49)
Ethylbenzene (3)
Methylene Chloride (5)
Toluene (111%)
Xylene (1)
Vinyl Chloride (270)
CERCLIS Data:
Data units
appear to be
incorrect; no
filter metal
data presented
for metals
Data presented
are from 5-Year
Review in 1993.
No metals data
were provided.
-------
site Nana
GW Contamination
organioa*
GW Contamination
inorganics*
Ho aw
Contamination*
comments
Monroe
Chemical
No recent
monitoring
data PADER
results in
1984 showed no
contaminat ion
Mn and
methaclor were
detected above
or at EPA
regulatory -
levels in 1981
only; Locals
residents are
served by the
Chester Water
Authority
Scott Paper
Benzene (26)
1,1-Dichloroethane (5)
Ethylbenzene (6)
Fluorotrichloromethane (7)
Methylene Chloride (280)
Phenanthrene (149)
Pyrene (23)
Metro
Container
Corporation
Cresols (30)
Carbon Disulfide (unknown)
Carbon Tetrachloride (9)
Methylene Chloride (14)
Phenols (9670)
Nitrate (1200000)
Arsenic (8)
Cadmium (70)
Total Chromium (500)
Lead (140)
Total Cyanide (2700)
Sulfate (1250000000)
Detection
limits are
quite high for
volatiles;
Local residents
supplied by a
municipal water
source
-------
site Mane
-------
site Han©
GW Contamination
organics*
-------
CHESTER RISK PROJECT
TABLE 4-3
RISK SUMMARY
CHESTER WATER AUTHORITY
DRINKING WATER ADULT
CANCER RISK NON-CANCER RISK
TOTAL RISK FROM ALL SOURCES
TOTAL RISK FROM ALL SOURCES
TOTAL RISK WITHOUT FLUORIDE
TOTAL RISK FROM ALL SOURCES
TOTAL RISK WITHOUT FLUORIDE
TOTAL RISK WITHOUT FLUORIDE
DRINKING WATER CHILD
TOTAL RISK FROM ALL SOURCES
TOTAL RISK FROM ALL SOURCES
TOTAL RISK WITHOUT FLUORIDE
TOTAL RISK FROM ALL SOURCES
TOTAL RISK WITHOUT FLUORIDE
TOTAL RISK WITHOUT FLUORIDE
INHALATION ADULT
(1989-ED-
(1990-ED-
(1991-ED-
(1992-ED-
(1993—ED-
(1993—ED-
(1989-ED-
(1990—ED-
(1991-ED-
(1992-ED-
(1993—ED-
(1993-ED-
1 YEAR)
1 YEAR)
1 YEAR)
1 YEAR)
1 YEAR)
30 YEARS)
1 YEAR)
1 YEAR)
1 YEAR)
1 YEAR)
1 YEAR)
30 YEARS)
1.34E-07
2.13E—07
1.86E-07
1.98E-07
1.78E-07
4.27E-06
3.12E-07
4.96E-07
4.35E-07
4.62E-07
4.15E-07
2.49E—06
3.95E-01
2.29E-01
2.14E-01
2.27E-01
2.39E—01
2.39E-01
9.21 E-01
5.33E-01
4.99E-01
5.31 E-01
557E-01
5.57E-01
TOTAL RISK FROM
TOTAL RISK FROM
TOTAL RISK FROM
TOTAL RISK FROM
TOTAL RISK FROM
TOTAL RISK FROM
DERMAL CH1U)
ALL SOURCES
ALL SOURCES
ALL SOURCES
ALL SOURCES
ALL SOURCES
ALL SOURCES
(1989-ED-
(1990—ED-
(1991—ED-
(1992—ED-
(1993—ED-
(1993—ED-
1 YEAR)
1 YEAR)
1 YEAR)
1 YEAR)
1 YEAR)
30 YEARS)
2.24E—06
2.90E-06
3.12E-06
3.3^-06
2.64E-06
6.33E-05
O.OOE+OO
4.47E-02
0.00E+00
O.OOE+OO
0.00E+00
O.OOE+OO
TOTAL RISK FROM
TOTAL RISK FROM
TOTAL RISK FROM
TOTAL RISK FROM
TOTAL RISK FROM
TOTAL RISK FROM
TOTAL RISK*
ALL SOURCES
ALL SOURCES
ALL SOURCES
ALL SOURCES
ALL SOURCES
ALL SOURCES
(1989-ED-
(1990—ED-
(1991—ED-
(1992—ED-
(1993—ED-
(1993—ED-
1 YEAR)
1 YEAR)
1 YEAR)
1 YEAR)
1 YEAR)
30 YEARS)
7.41 E-08
1.00E-07
1.03E—07
1.10E-07
1.32E-07
755E-07
8.51E-02
1.13E-01
1.18E-01
126E-01
1.06E-01
1.06E-01
1989(1
1990(1
1991 (1
1992(1
1993(1
1989(1
1990(1
1991 (1
1992 (1
1993(1
YEAR)
YEAR)
YEAR)
YEAR)
YEAR)
YEAR)
YEAR)
YEAR)
YEAR)
YEAR)
ADULT
ADULT
ADULT
ADULT
ADULT
CHILD
CHILD
CHILD
CHILD
CHILD
2.37E-06
3.11E-06
3.30E-06
351E-06
2.82E-06
3.86E-07
5.96E-07
5.38E-07
5.72E—07
5.48E—07
3.95E-01
2.74E-01
2.14E-01
227E-01
2.39E-01
1.01E+00
6.46E-01
6.17E-01
657E-01
6.63E-01
*Total Risk without Fluoride
1993 (30 YEARS)
7.09E—05
9.02E-01
-------
CHESTER RISK PROJECT
TABLE 4-4
RISK SUMMARY
PHILADELPHIA SUBURBAN WATER COMPANY
DRINKING WATER ADULT
CANCER RISK NON-CANC® RJSK
TOTAL RISK FROM ALL SOURCES (1989-ED- 1 YEAR)
TOTAL RISK FROM ALL SOURCES (1990-ED- 1 YEAR)
TOTAL RISK FROM ALL SOURCES (1991 -ED- 1 YEAR)
TOTAL RISK FROM ALL SOURCES (1992-ED- 1 YEAR)
TOTAL RISK FROM ALL SOURCES (1993-ED- 1 YEAR)
TOTAL RISK FROM ALL SOURCES (1993-ED- 30 YEARS)
1.13E-07
1.51E-07
9.72E-08
8.69E-08
2.34E-07
5.62E-06
1.30E-01
1.73E—01
1.12E-01
9.97E-02
2.68 E-01
2.60E-O1
DRINKING WATER CHILD
TOTAL RISK FROM ALL SOURCES (1989-ED- 1 YEAR)
2.65E-07
3.04E-01
TOTAL RISK FROM ALL SOURCES (1990-ED- 1 YEAR)
3.52E-07
4.03E-01
TOTAL RISK FROM ALL SOURCES (1991 -ED- 1 YEAR)
2.27E-07
2.60E-01
TOTAL RISK FROM ALL SOURCES (1992-ED- 1 YEAR)
2.03E-07
2.33E-01
TOTAL RISK FROM ALL SOURCES (1993-ED- 1 YEAR)
5.46E-07
626E-01
TOTAL RISK FROM ALL SOURCES (1993-ED- 30 YEARS)
3.28E—06
6.26E-01
INHALATION ADULT
TOTAL RISK FROM ALL SOURCES (1989-ED- 1 YEAR)
1.90E-06
O.OOE+OO
TOTAL RISK FROM ALL SOURCES (1990-ED- 1 YEAR)
2.52E-06
O.OOE+OO
TOTAL RISK FROM ALL SOURCES (1991 -ED- 1 YEAR)
1.63E—06
O.OOE+OO
TOTAL RISK FROM ALL SOURCES (1992-ED- 1 YEAR)
1.46E-06
O.OOE+OO
TOTAL RISK FROM ALL SOURCES (1993-ED- 1 YEAR)
3.92E—06
O.OOE+OO
TOTAL RISK FROM ALL SOURCES (1993-ED- 30 YEARS)
9.41E-05
O.OOE+OO
DERMAL CHILD
TOTAL RISK FROM ALL SOURCES (1989-ED- 1 YEAR)
6.29E-08
7.21 E-02
TOTAL RISK FROM ALL SOURCES (1990-ED- 1 YEAR)
8.35E—08
9.58E-02
TOTAL RISK FROM ALL SOURCES (1991 -ED- 1 YEAR)
5.39E-08
6.18E—02
TOTAL RISK FROM ALL SOURCES (1992-ED- 1 YEAR)
4.82E-08
5.53E-02
TOTAL RISK FROM ALL SOURCES (1993-ED- 1 YEAR)
1.30E—07
1.49E-01
TOTAL RISK FROM ALL SOURCES (1993-ED- 30 YEARS)
7.78E—07
1.49E—01
TOTAL RISK*
1989 (1 YEAR) ADULT
2.01 E-06
1.30E-01
1990 (1 YEAR) ADULT
2.67E—06
1.73E-01
1991 (1 YEAR) ADULT
1.73E-06
1.12E-01
1992(1 YEAR) ADULT
154E-06
9.97E-02
1993(1 YEAR) ADULT
4.15E—06
2.68E-01
1989 (1 YEAR) CHILD
3.28E—07
3.76E-01
1990(1 YEAR) CHILD
4.35E—07
4.99E-01
1991 (1 YEAR) CHILD
2.31 E-07
3.22E-0i
1992(1 YEAR) CHILD
251E—07
2.88E-01
1993 (1 YEAR) CHILD
6.76E-07
7.75E-01
1993 (30 YEARS)
*Note fluoride is not added to the finished water
1.04E-04
1.04E+00
-------
CHESTER RISK PROJECT
TABLE 4-5
RISK SUMMARY
PHILADELPHIA WATER DEPARTMENT
DRINKING WATER ADULT
CANCER RISK NON- CANCER RISK
Total Risk without Fluoride (1989-ED-
Total Risk without Fluoride (1990-ED-
Total Risk without Fluoride (1991 -ED-
Total Risk without Fluoride (1992-ED-
Total Risk without Fluoride (1993-ED-
Total Risk without Fluoride (1993-ED-
DFBNWNG WATERCHILD
Total Risk without Fluoride (1989-ED-
Totai Risk without Fluoride (1990-ED-
Total Risk without Fluoride (1991 -ED-
Total Risk without Fluoride (1992-ED-
Total Risk without Fluoride (1993-ED-
Total Risk without Fluoride (1993-ED-
INHAliAtfON ADULT
1 YEAR)
1 YEAR)
1 YEAR)
1 YEAR)
1 YEAR)
30 YEARS)
1 YEAR)
1 YEAR)
1 YEAR)
1 YEAR)
1 YEAR)
30 YEARS)
1.63E—07
1.96E-07
1.97E—07
1.41E—07
2.14E—07
5.14E-06
3.80E-07
4.58E—07
4.60E-07
328E—07
5.00E—07
3.006-06
1.87E-01
2.15E-01
2.20E-01
1.61E—01
2.406-01
2.406-01
4.37E-01
5.03E-01
S.14E-01
3.77E—01
5.606-01
5.606-01
Total Risk from All
Total Risk from All
Total Risk from All
Total Risk from All
Total Risk from All
Total Risk from All
Soivces (1989—ED— 1 Year)
Sources (1990-ED- 1 Year)
Sotrces (1991 -ED- 1 Year)
Sources (1992-ED- 1 Year)
Sources (1993-ED- 1 Year)
Sources (1993-ED- 30 Year)
2.736-06
2.87E—06
3.05E—06
2.356-06
3.34E—06
8.006—05
0.006+00
2.92E—02
1.75E—02
0.006+00
1.75E—02
1.756-02
DERm CHILD
Total Risk from
Total Risk from
Total Risk from
Total Risk from
Total Risk from
Total Risk from
TOTAL RISK*
All Sotrces (1989-ED- 1 Year)
All Sources (1990-ED- 1 Year)
All Sources (1991 -ED-1Year)
All Sources (1992-ED- 1 Year)
All Sources (1993-ED- 1 Year)
All Sources (1993-ED- 30 Year)
9.046-08
9.77E—08
1.03E—07
7.806-08
1.12E-07
6.73E—07
1.04E-01
1.11E—01
1.17E-01
8556-02
1286-01
1286-01
1989(1
1990(1
1991 (1
1992(1
1993(1
1989 (1
1990 (1
1991 (1
1992(1
1993(1
YEAR)
YEAR)
YEAR)
YEAR)
YEAR)
YEAR)
YEAR)
YEAR)
YEAR)
YEAR)
ADULT
ADULT
ADULT
ADULT
ADULT
CHILD
CHILD
CHILD
CHILD
CHILD
2.89E—06
3.06E—06
3246-06
2.49E—06
3.556—06
4.71E—07
5.556-07
5.62E —07
4.06E—07
6.12E—07
1.87E-01
2.45E—01
2.38E-01
1.61E—01
2.57E-01
5.406-01
6.14E—01
6.31E-01
4.66E—01
6.88E-01
•Total Risk without Fluoride
1993 (30 YEARS)
8.896-05
9.45E-01
-------
CHESTER RISK PROJECT
TABLE 4-fl
CHESTER WATER AUTHORITY
CHEMICALS OF POTENTIAL CONCERN (COPC)
sse* ¦"
PPM
«m«s~oflcwics
HiGH-PPM
LOW-PPM
' . "-'irttJ..
HldH-^PM
COPC
LOW-PPM
1991
hioh-Ppm
COPC
LCJW-PPM
OJ00017
bromodchlarom e^iana
0005
y?8
0008
0003 yes
001
0004 yes
000015
chloroform
0033
0019 y«fe
0044
0017 ye*
0046
0021 ye*
00061
cfibromom ethane
0O08
yea
000015
total frlhalomatiane"
0056
0022 ya«
0072
0024 Wt
0078
0023 yes
000013
dltranochlcram ethane
00011
00009 yes
00011
entfrln
0000052
llnctone
000018
methoxychlcr
00029
silvex P.4J5—TP S)
0000061
tonaphene
00061
2.4—0
000016
carbon telrachlarlda
00008
yes
00011
tetach tor oe then e
INORGANICS
1969
1990
1991
00015
antimony
OJ000038
arsenic
0000016
beryllium
00018
cadnliffn
000029
thallium
000022
ftirolde
092
ye»
10
nltata
59
TO
08
ho
5.1
no
000037
nirltB
0A8
jree
0015
lead
15
0-oss alpha (pCIA.)
2
no
*RBCs-FSsk Based OoncanTalcns from tie Screening Guidance, EP^aa/R-B3-00l
"Average ooncentratlana (cr the system are rapartad; minimum and maximum average are reported (or each year.
Note: Sana contaminants such as cls-1 ,3-dfchlcrop-openerapcrted during 1B93 at 3.2 ppb by the Chester WatBr Authority In November, 1904 were not Included
Note Oorrtd. - because tiey are not regulated. See Uncartelnty Suction" In the risk assessment.
-------
CHESTER RI8K PROJECT
TABLE 4-6 (CONTINUED)
CHE8TER WATER AUTHORITY
CHEMICALS OF POTENTIAL CONCERN (COPC)
RBC»
PPM
CHB»ICAW-9RaAMC8
1992 ' OOPC
A-f: -iv
: 1993 00 PC
HQH~PPM •.-. lOVV-PPM ...
1994 00PC
HOH~PPM ujw-ppm
0.00017
bromodlchlorometiane
0.0111 0.009 yes
, 0.012 0.0066 yes
0.00015
chloroform
0.075 0.0548 yas
0.069 0.026 yes
0.0061
dibono methane
0.00016
total trtiabmethane**
0.083 0.055 yot
0.066 0.061 yM
0.0568 0.0546 yea
0.00013
dlbDmoehkNometune
0.0028 0.001 y
-------
CHESTER RISK PROJECT
TABLE 4-7
PHILADELPHIA 8UBURBAN WATER COMPANY
CHEMICALS OF POTENTIAL CONCERN (COPC)
HBO*
CONTAMINANTS-ORQANICS
'W.r'
LGv\M>PMcopo: •
:: 1990 • .
1991
PPM
HIGH-PPM LOW-PPM COPC
HIQHt-PPM LOW-PPM COPC
0.000044
1,1- dlchloroethene
0.00012
1,2-dlchloroothane
0.000087
benzene
0.00017
bromodichtoromethsne
0.0129 0.014 yes
0.00016
carbop tetrachloride
0.00015
chloroform
0.0417 0.0096 yes
0.00013
dlbromoohloromethane
0.0017 0.0014 yes
0.0061
dlbromoiTiethane
0.00044
1,4—dlchlorobenzene
0.0016
trlchlorocithene
0.000019
vhyl chloride
0.00015
total trlhetomethanes**
0.0475 0.0127 yes
0.0631 0.0154 ye*
INORGANICS-;
1989
1990
1991
0.000038
arsenic
0.015
lead
0.0031 no
0.002 no
15
gross alpha
11/94 Data obtained frpm PADER-June 1994
•RBCa-Rlsk Based Concentration• from ths Screening Guidance, EPA/903/R-93- 001
"Average concentrations for the system are reported; minimum and maximum average are reported for each year.
-------
CHESTER RISK PROJECT
TABLE 4-7 (CONTINUED)
CHESTER WATER AUTHORITY
CHEMICAL8 OF POTENTIAL CONCERN (COPC)
tec* -''
PPM :
tt^AMINA
i^oridANilidV.
HloM** tomr-PPM COPC
:: 1993
Ww-IPiPM : LdWr*PPM coPc
1994
HIGH-PPM ! LOW-PPM COPC
0.000044
0.00012
0.000087
0.00017
0.00016
0.0001 S
0.00013
0.0061
0.00044
0.0016
0.000019
0.0001 S
0.000038
0.015
15
1.1—dlohloioethene
1.2- dlchloroethane
banzena
bromodlchlaromethane
carbon tetrachloride
chloroform
dlbromochloromathane
dlbromometfiane
1,4- dlohloiobenzene
trlchloroethane
vinyl chloride
total tlhatomeftanes**
INORGANIC#
arsenlo
lead
groaa alpha
0.0182 0.0046 yes
0.0414 0.0088 y*9
0.0023 0.0007 fiM
0.0291 0.0035
0.00245 |K>
3pCI/l rio
0.0125 0.005yB$
0.0259 0.0092 yM
0.0033 0.0012 ypa
0.0007 no
0.098 0.0173 yes
1993
0.022 0.0151 y*&
1994
11/94 Data obtained from PADER-June 1984 ! '
*RBCe-Rlsk Based Concentration* from the 8oreenlng Guidance, EPA/903/R-93-001
••Awraga concenratlons for the system are reported; minimum and maximum average ere reported far eech year.
-------
CHESTER RISK PROJECT
TABLE 4-8
PHILADELPHIA WATEH DEPARTMENT
CHEMICALS OF POTENTIAL CONCERN (COPC)
we*-.- .
• • .
1WB-,
. ' .1090
1931
PPM
CO^AMNAmS-OflmNCS
HlGH~PPM ;-:v ¦I LOW^MOOPCT :.
HlGH-PPM LOW-PPMOOPC
UGH-PPM LCW-PPMCOPC
0.000044
1,1 -dchkroethena
0.00012
12-dchlcroethane
0.000087
benzene
0.00017
bronodchla unuUane
0.00016
carbon tatacNcrlda**
0.0005 yas .
o.oooa yes
0.00015
chtardcrm
0.00013
dlhromochloromethana
0.0061
dltromomathana
0.00044
1,4-dchlarabenzene
0.0016
rictilcraetienB
o.ooooie
vinyl chlarldB
0.00016
total 111 haleim ethanes"
0.0683 yas
0.0715 yas
0.0781 ye£
IN0RQANt3$
19BB
1B90
1961
0.000038
arsenic
0.015
lead
0.22
fluoride**
i yss
1.01 yea
i .01 yas
16
g-oss alpha
11/94
Data obtained ram PWD-Nwember lB04-(Annuel Repcrt RsobI 1083)
•RBOs-Flsk Based Cmcenfraflans (ram the Screening Guidance. EPA®03fl-93-001
**HtfwstaveragB conoentatlons fcr the system are reported
***Tha 1B04 dafi were not avaQaUa for analysis
Note: Same contaminants such as ethylene dlbromlde detected up to 0.14 ppb cluing 19GB were not Included because they are not regulated See "Uncertainty Section- In the risk assessment.
-------
CHESTER RISK PROJECT
TAELE 4-8 (CONTINUED)
PHILADB.PHIA WATER DEPARTMENT
CHEMCALS OF POTENTIAL C ONCE FN (COPC)
RBC* ¦: •
PPM .
mmu \ cow-ppmocm^c
1003
HCSH^PPM LGM/~PPMOCM=t:
•< .. 1894***
rt<3H-PPM , : LCfW-PPMCOPC
0.000044
1,1 -dchlaraethene
0.00012
1 ,2-dchlaroethBne
0.000087
benzene
0.00017
bran odchUxam ethane
0.00016
carbon tefachlolde**
o.ooos yss
0.00015
chluufu hi
0.00013
dlbromochlcram ethane
0.0061
dlbromomelhBne
0.00044
1,4-dchlorabenzBne
0.0016
ftchlcraelhene
0.000019
vinyl chlarldB
0.00015
total trl ha torn ethanes**
0.0589 yes
0.0833 yes-
INORQVJC3
1BB2
1983
1994
0.000038
arsenic
0.015
lead
0.22
flucrWe**
1 yw
I —11 m ¦- rnj 1 lit""'
o.98 ya$
15
4 4
u u&s alpha
*R80s-Rsk Based Concentraflcns from the Saeenlng Guidance, EP>VBoa/R-93-001
"Hlgfiast average concentatlons fa* tie system are reported
***Tha 1BB4 data ware not mailable tar analysts
Naffl: Same ccnfimtnerrts such as ethylene tfflromlda detectBd up to 0.14 ppb dulng 1889 were not Included because they are not regulated
See "Uncertainty Section" in the risk assessment
-------
CHESTER RISK PROJECT
TABLE 4-9
CHESTER WATER AUTHORITY
VIOLATION SUMMARY
Violation
Parameter
Compliance Achieved
January 1994
Treatment Technique
Not meeting
Treatment
Performance
requirement*
January 1994
June 1993
Treatment Technique
Not meeting
Treatment
Performance
requirement*
June 1993
June, July ,
October 1992
Treatment Technique
Not meeting
Treatment
Performance
requirement*
November 1992
January 1992
Late submitting
monitoring results
Required
samples under
the Lead Rule
January 1992
December 1991
Treatment Technique
Not meeting
Treatment
Performance
requirement*
January 1992
* Under the Surface Hater Treatment Rule (SWTR)
Data from the Federal Reporting Data System (FRDS)
-------
CHESTER RISK PROJECT
TABLE 4-10
PHILADELPHIA SUBURBAN WATER COMPANY
VIOLATION SUMMARY
pate
Vidlatipti
Parameter
ComplianceAohieVed
May 1994
Late submitting
monitoring
results
Volatile
Organics under
Phase II
May 1994
March 1992
Treatment
Technique
L- ¦
Not meeting
Treatment
Performance
requ i rement*
March 1992
* Under the Surface Water Treatment Rule (SWTR)
Data from the Federal Reporting Data System (FRDS)
-------
CHESTER RISK PROJECT
TABLE 4-11
PHILADELPHIA WATER DEPARTMENT
VIOLATION SUMMARY
Data
Violation
parameter
Compliance Achieved
March 1992
Treatment
Technique
Not meeting
Treatment
Performance
requirement*
March 1992
February 1992
Treatment
Technique
Not meeting
Treatment
Performance
requirement*
March 1992
January 1992
Late
submitting
initial
monitoring
results for
lead
Required
samples under
the Lead Rule
September 1992
December 1991
Treatment
Technique
Not meeting
Treatment
Performance
requirement*
December 1991
December 1991
Late
submitting
monitoring
results
Required
samples under
the SWTR
January 1992
November 1991
Treatment
Technique
Not meeting
Treatment
Performance
requirement*
November 1991
Data from the Federal Reporting Data System (FRDS)
-------
CHESTER RISK PROJECT
TABLE 4-12
COMPARISON OF CHILDREN'8 BLOOD LEAD III CHESTER, PA
WITH R88ULT8 07 USEPA'S THRU-CITY STUDY
1
city
Geometric Mean
(ug/dL)
Children Above 1
10 ug/dL |
Chester (all years combined)
14.2
m
Baltimore
12.5
59%
Boston
12.6
71%
Cincinnati
11.7
52%
-------
CHESTER RISK PROJECT
TABLE 4-13
TEMPORAL TREHD8 ZH CHILDREN'S BLOOD LEAD
CHESTER, PA
Year
Geosetric
Ktart (ug/dL)
Children Above
io ug/dL
Children Above 50
ug/dL
1989
16.6
72%
6.2%
1990
H
OS
•
o
79*
3.8%
1991'
17.1
78%
2.8%
1992
12.1
61%
0.27%
1993
11.9
62%
0.22%
-------
CHESTER RISK PROJECT
TABLE 4-14
SITE-SPECIFIC INFORMATION
SITE
OPERATIONAL
HISTORY
LOCATION
SIZE
DE County
Incinerator
Landfill No. 1
incinerator ash
disposal,
municipal waste
disposal
Chester
Township
30 acres
Vermiculite Dump
rayon production
disposal
Marcus Hook
4 acres
ABM Wade
rubber recycling
debris disposal
Chester City
3 acres
Monroe Chemicals
production of
benzaldehydes and
benzyl alcohol
Eddystone
2.3 acres
Scott Paper
paper mill waste
discharge
Chester City
?
Air Products &
Chemicals, Inc.
catalyst and
petroleum cracking
waste disposal
Marcus Hook
?
Metro Container
RCRA drum
recycling, sludge
and incinerator
ash production
Trainer
?
East Tenth
Street Site, .
a.k.a. FMC Site
rayon production
Marcus Hook
35 acres
-------
CHESTER RISK PROJECT
TABLE 4-15
SUMMARY OF FINDINGS AT CERCLIS SITES1
SITE
COMMENTS
DE County Incinerator
Landfill No. 1
Exceedances of risk-based screening
levels for soil, under a residential
exposure scenario, for arsenic and
beryllium.
Vermiculite Dump
Exceedances of risk-based screening
levels for soil, under a residential
exposure scenario, for copper, mercury,
benz[a]anthracene and benzo[a]pyrene.
ABM Wade
Exceedances of risk-based screening
levels for soil, under a residential
exposure scenario, for antimony,
arsenic, beryllium and manganese.
Monroe Chemicals
Exceedances of risk-based screening
levels for soil, under a residential
exposure scenario, for arsenic,
beryllium and silver.
Scott Paper
Exceedances of risk-based screening,
levels for soil, under a residential
exposure scenario, for benz[a]pyrene.
Air Products &
Chemicals, Inc.
Exceedances of risk-based screening
levels for soil, under a residential
exposure scenario, for arsenic and
mercury.
Metro Container
Based on usable data, no exceedances of
risk-based screening levels for soil,
under a residential exposure scenario.
East Tenth Street
Site, a.k.a. FMC Site
Exceedances of risk-based screening
levels for soil, under a residential
exposure scenario, for antimony,
arsenic, beryllium, copper, mercury,
vanadium, benz[a]anthracene, benzo[b]-
fluoranthene, benzo[k]fluoranthene,
benzo[a]pyrene, chrysene, dibenz[a,h]-
anthracene, indeno[1,2,3-c,d]pyrene,
Aroclor-1254 and Aroclor-1260.
^ased on available historical, data
-------
CHESTER RISK PROJECT
TABLE 4-16
SOIL INGESTION OOSE CALCULATIONS
SITE
CHEMICAL
MAXIMUM
CONCENTRATION
(mgftg)
CHILD
NONCARCINOGENIC
DOSE
(mgAg/day)
CHILD
CARCINOGENIC
DOSE
(mgftg/tfay)
ADULT
NONCARCINOGENIC
DOSE
(mgAg/day)
sasessBheDBnn
ADULT
CARCINOGENIC
DOSE
(mgftg/day)
DECO. INC NO.1
VERMICUUTE DUMP
ABM WADE®
MONROE CHEMICAL
SCOTT PAPER
AIR PROD A CHEM
EAST TENTH STREET
SE SOIL
MIDDLE SOIL
WELL #10
WELL #6
WELL #14
WAREHOUSE
88-1
FH—3GSOIL
8-3
8 — 1
8-4A
S-3
8-4A
8-3
At
Be
Cu
Hfl
BENZ(A]ANTHRACENE
BENZO[AJPYRENE
8b
At
Mn
Be
At
Be
BENZO(A]PYRENE
At
Hfl*
8b
At
Be
•Cu
Hfl
V
BENZ(A)ANTHRACENE
BENZO(B]FLUORANTHENE
BENZO(K]FLUORANTHENE
BENZO[A]PYRENE
ruovnc IJC
DIBENZ[A,H]ANTHRACENE
INDENO[1,2,3-C.DJPYRENE
AROCLOR 1254
AROCLOR 1260
IS
2.3
6410
81.3
3.6
2.4
6
20
21000
1 6
07
04
100
10.1
201
29
664
74
2720
32
316
61
66
3.3
42
62
0 97
16
8.2
6.2
1.60E-O4
2.766-05
6 406-02
0 74E-04
5ME-05
2.40E-04
2 52E-01
1.806-05
6 396-06
4 796- 06
1 206-03
1.21E-04
2.41E-03
3.46E-04
7.006-04
6 67E-05
3 266 - 02
3 646-05
3 61E-03
1.646-05
2.306-06
3 006-06
2.476-06
2.05E—05
1 546-06
7.196-07
4 11E-07
6.166-07
1.046-05
6.0C6-0S
7.606-06
6 276-05
6646-05
3 386-06
4 326-05
6 346-05
5 646-07
1 6SE-05
8.42E-06
6.42E-06
2.0SE-0S
3.16E-06
7.41E-03
1 11E-04
6.656-06
2.74E-05
2.666-02
2 096-06
9 586-07
5.466-07
1.37E-04
1.366-05
2.7S6-04
3 976-05
6006-05
1.01E-05
3.73E-03
4.366-06
4.366-04
7.0SE-06
1.066-06
1 76E-06
1.136-06
9.386-08
7.05E-07
3 286- 07
1 666-07
2 62E-07
4.74E-06
2.74E-05
3466-06
2 666 -05
4.04E-05
1.556-06
1.97E-0S
2.44E-05
2 666-07
6.4S6-06
3.856-06
3 65E-06
aaesaesa
Beted on available historical data.
'Because the maximum concentration ol Hg reported at thto tbe was tuspect (tcreentng method of analyeis with retuftt that could not be verified), the htghost level ol Hg detected by a
feed laboratory was used.
©Remedial action, including toil removal, hat occurred at thto sfte.
-------
CHESTER RISK PROJECT
TABLE 4-17
DERMAL ABSORPTION D08E CALCULATIONS
| SITE
SOURCE
| EAST TENTH STREET
3-3
S-4A
D8B3BSB
BBSsssssaa
MAXIMUM
CONCENTRATION
(mgftg)
AROCLOR 1254
AROCLOR1260
82
82
Based on available historical data.
CHILO
NONCARCINOGENIC
D08E
CHILO
CARCINOGENIC
DOSE
(mgAg/day)
ADULT
NONCARCINOGENIC
DOSE
(mgAg/day)
ADULT |
CARCINOGENIC j
DOSE j
(mg/kg/day) j
,
2 17E-0Q
2.17E-06
4.16E-06 |
4 16E-06 |
I
-------
CHESTER RISK PROJECT
TABLE 4-16
80IL INGESTION RISK CALCULATIONS
s seesnsBsanaanon
SITE
SOURCE
SOBBSSSBC G3BBDBBBBB6BaaaaaaBBB88DBBVBaBSB8&8838SSOBB8Ba33S
MAXIMUM
CONCENTRATION
CHEMICAL (mg*g)
SaSBBBBBBBaBaB
CHILD
HO*
IBBBBBBBBBBgBSaaaO
•CHILD
CARCINOGENIC RISK
8BBBB8BB&BBBB83BBB3BBBB
ADULT
HQ*
ADULT
CARCINOGENIC RISK
DECO. INC. NO.1
810
At
16
06
2.7E-05
0.1
1 2E-05
Be
2.3
0.0
1.flE-05
0.0
4.6E-06
VERMICUUTE DUMP
NW SOIL
Cu
9410
.1.7
0.2
Hg
61 3
3.2
0.4
8E8OIL
BENZ[A)ANTHRACENE
3.6
2.66-06
1.3E-06
MIDDLE 80IL
BENZO (A)PYRENE
2.4
1 0E-OS
6.2E-06
ABM WADE®
WELL #10
Sb
5
0.1
0.0
WELL #6
As
20
0.6
3.6E-05
0.1
1 flE-05
Mn
21000
60.3
6.6
WELL #14
Be
1.6
00
6 6E-06
0.0
3 OE-06
MONROE CHEMICAL
WAREHOUSE
As
0.7
00
1.3E-06
00
6 8E-07
Be
04
00
1.6E-06
00
61E-07
*g
100
0.2
00
SCOTT PAPER
80IL PILES
BENZO (A)PYRENE
06
4.5E-06
2.1E-06
AIR PROD&CHEM
6S— 1
As
101
04
1.6E-05
0.0
8 3E-06
FH-3QSOIL
Hg"
201
SO
00
EAST TENTH STREET
S-3
8b
29
00
0.1
s-s
AS
56.4
23
1.0E-04
0.3
4.flE-05
Be
7.4
0.0
3.3E-05
0.0
1.SE-05
8-3
Cu
2720
OB
0 1
8-1
Hg
3.2
01
00
8-4A
V
316
05
0.1
8-3
BENZfAJANTHRACENE
61
4 flE-05
2 1E-05
BENZO {B]PLUORANTHENE
66
6 4E-05
2.flE-05
8-4A
BENZO [KjFLUORANTHENE
3.3
2 5E-07
1 1E-07
8-3
BENZO [AJPYRENE
42
3 2E-04
1.4E-04
CHRYSENE
82
3 96-07
1.0E—07
DIBENZ(A.H)ANTHRACENE
0.57
4 3E-06
2.QE-06
INDENO|l.2,3-C,0|PyflENE
16
1 3E-0S
6.2E-06
AROCLOR 1254
62
6.6E-05
3 06-05
8-4A
AROCLOR 1260
62
6.5E-05
3 OE-05
Based on available historical data.
•A value of zero tn this column Indicates an HQ ol < 0.1.
(^Remedial action, Including soO removal, has occurred at this site.
"Boeause the maximum concentration of Hg reported at this site was suspect (screening method ol analysis with resufts that could not be verified), the highest level of Hg detected by a
fixed laboratory was used.
-------
CHESTER RISK PROJECT
TABLE 4-t9
DERMAL ABSORPTION RISK CALCULATIONS
MAXIMUM
CONCENTRATION
SITE SOURCE CHEMICAL (mg/kg)
EAST TENTH 8TREET 8-3 AROCLOR1254 8 2
S-4A AROCLOR1260 8 2
Baaed on avallabto historical data
CHILD
HQ
CHILD
CARCINOGENIC RISK
AOULT
HO
AOULT|
CARCINOGENIC RISK
1 67E-0S
1 87E-05
3 20E-05 j
3 20E-05 j
-------
CHESTER RISK PROJECT
TABLE 4-20
HAZARD INDEX* AND CUMULATIVE CARCINOGENIC RISK, PER SITE
| CHILD CHILD
I SITE HI** CARCINOGENIC RISK
DE CO. INC. NO.1
0.6
3.7E-05
VERMICULITE DUMP
5.0
2.1E-05
ABM WADE®
51.3
4.3E-05
MONROE CHEMICAL
0.3
3.0E-06
SCOTT PAPER
4.5E-06
AIR PROD & CHEM
8.4
1.8E-05
EAST TENTH STREET
4.8
7.4E-04
Based on available historical data.
*ln summing Hazard Quotients to calculate Hazard Indices, target organs were not considered.
(©Remedial action, including soil removed, has occurred at this site.
**A value of zero in this column Indicates an HI of < 0.1.
ADULT ADULT
HI** CARCINOGENIC RISK
0.1
1.7E-05
0.6
9.5E-06
5.9
1.9E-05
0.0
1.4E-06
2.1E-06
1.0
8.3E-06
0.5
3.9E-04
-------
CHESTER RISK PROJECT
TABLE 4-21
PERCENT CONTRIBUTION TO HAZARD INDEX AND CUMULATIVE CARCINOGENIC RISK. PER SITE
| SITE
PERCENT CONTRIBUTION
CHEMICAL
CHILD
HI
CHILD
CARCINOGENIC RISK
ADULT
HI
ADULT |
CARCINOGENIC RISK j
| DECO. INC. NO.1
As
99
73
99
73 |
Be
1
27
1
27 j
| VERMICUUTE DUMP
Cu
35
35
Hg
65
65
BENZ[A]ANTHRACENE
14
14 |
BENZO[A]PYRENE
86
86 j
| ABMWADE@
Sb
<1
<1
As
2
84
2
84 |
Mn
98
98
Be
<1
16
<1
16 |
| MONROE CHEMICAL
As
10
42
10
42 |
Be
<1
58
<1
58 j
Ag
89
89
| SCOTT PAPER
BENZO[A]PYRENE
100
100 |
| AIR PROD &CHEM
As
5
100
5
100 |
Hg
95
95
| EAST TENTH STREET
Sb
18
18
As
49
14
49
12 |
Be
<1
4
<1
4 I
Cu
18
18
Hg
3
3
V
11
11
BENZJAJANTHRACENE
6
5 I
BENZO[B|FLUORANTHENE
9
8 j
BENZO[K|FLUORANTHENE
<1
<1 I
BENZO[A|PYRENE
42
37 j
CHRYSENE
<1
<1 I
DIBENZ[A,H]ANTHRACENE
1
1 j
INDENO[1.2.3-C.DJPYRENE
2
2 I
AROCLOR 1254
11
16 j
AROCLOR 1260
11
16 j
Based on available historical data.
@Remedlal action, Including soil removal, has occurred at this site.
-------
CHESTER RISK PROJECT
TABLE 4-22
SURFACE WATER. SEDIMENT. AND FISH TISSUE CHEMICALS OF CONCERN
STATION
MEDIUM
CHEMICAL OF CONCERN
MAXIMUM |
CONCENTRATION J
WQF00511-000.6
fish
Technical chlordane
0.09 mg/kg
Dieidrin
0.03 mg/kg
VERMICUUTE DUMP
i
SW (DS)
Aluminum
2290 ufl/1
Chromium
9.1 ug/l
Barium
99.7.ug/l
Cadmium
0.4 ug/l
Nickel
15.9 ug/l
Manganese
391 ug/1
Zinc
260 ug/l
Arsenic
4 ug/l
Selenium
20 ug/l
Mercury
5.7 ug/l
SW(US)
Aluminum
2130 ug/l
Chromium
10.4 ug/l
Barium
93.6 ug/l
Cadmium
0.35 ug/l
Copper
17.8 ug/l
Nickel
15.5 ug/l
Manganese
373 ug/l
Zinc
175 ug/l
Vanadium
12.9 ug/l
Arsenic
9 ug/l
Selenium
19 ug/l
Mercury
13 ug/l
WQN0182
SW
Manganese
17700 ug/l
FISH
Technical chlcrdane
0.33 mg/kg
p.p'-DDE
0.2B mg/kg
Dieldrin
0.01 mg/kg
PCBs
0.43 mg/Vg
Cadmium
0.003 mg/kg
MONROE CHEMICAL
POND SW
Arsenic
22 ug/l
POND SED
Antimony
36.8 mg/kg
Arsenic
1.5 mg/kg
Beryllium
0.3 mg/kg
Cadmium
12.6 mg/kg .
Chromium
44 mg/kg
Silver
73 mg/kg
SED(US)
Benzofblfluoranthene
200 ug/kg
Arsenic
21.7 mg/kg
Beryllium
0.9 mg/kg
Vanadium
142 mg/kg
SH)(DS)
Arsenic
8 mg/kg
Antimony
21.4 mg/kg
Beryllium
0.7 mg/kg
Chromium
243 mg/kg
Manganese
6076 mg/kg
Nickel
201 mg/kg
Vanadium
89 mg/kg
EAST 10TH STREET
SB)
Benzfalanthracene
5800 ug/kg
Benzolblfluoranthene
8700 ug/kg
Benzofa]pyrene
3400 ug/kg
lndeno[1,2,3-c,d]pyrene
3500 ug/kg
Dibenz[a,h]anttvacene
1100 ug/kg
WQF00002-084.9
RSH
Technical chlordane
0.14 mg/kg
cis-Chlordane
0.027 mg/kg
t-Nonachlcr
0.033 mg/kg
p.p'-DDT
0.26 mg/kg
p.p'-DDD
0.23 mg/kg
p,p'-DDE
0.52 mg/kg
PCBs
2 mg/kg
Arsenic (converted from dry)
0.45 mg/kg
Copper
18.4 mg/kg
Cadmium
0.22 mg/kg
Cadmium (converted from dry)
0.78 mg/kg
Copper (converted from dry)
41.4 mg/kg
Oxychlordane
0.034 mg/kg
-------
CHESTER RISK PROJECT
TABLE 4-22
SURFACE WATER. SEDIMENT. AND RSH TISSUE CHEMICALS OP CONCERN
STATION
MEDIUM
CHEMICAL OF CONCERN
| MAXIMUM I
CONCENTRATION
WQF00002-081.8
PISH
Technical chlordane
1.6 mg/kg
c-Chlordane
0.024 mg/kg
t-Nonachlor
0.033 mg/kg
p.p'-DDT
0.24 mg/kg
£,p' -DDD
0.5 mg/kg
p.p'-DDE
2.1 mg/kg
PCBs
1.9 mg/kg
Oxy chlordane
0.027 mg/kg
DELF1SH-07
FISH
PCB1260
1.54 mg/kg
PCB 1254
1.46 mg/kg
p.p'-DDD
0.58 mg/kg
p.p'-DDE
2.77 mg/kg
Mercury
0.19 mg/kg
alpha-Chlordane
150 ug/kg
DELAWARE COUNTY
INCINERATOR LAND-
FILL #1
SW
Arsenic
69 ug/1
Beryllium
12 ug/l
Manganese
7260 ug/1
SED
Arsenic
12 mg/kg
Beryllium
1.8 mg/kg
Cadmium
9.4 mg/kg
Chromium
110 mg/kg
Vanadium
67 mg/kg
Benzfalanttvacene
1700 ug/kg
Benzofblfluoranthene
2200 ug/kg
Benzo[a]pyrene
2700 ug/kg
~ibenzfa.h]anthracene
230 ug/kg
ABM WADE
SED
Arsenic
164 mg/kg
422120
SW
Free cyanide
42 uo/l
Total cyanide
0.046 mg/l
Cadmium
39 ug/l
Chromium
88 ug/l
Copper
65 ug/l
Zinc
96 ug/l
3096
RSH
Chlordane
0.01711 mg/kg
p.p'-DDE
0.03438 mg/kg
Dietdrin
0.00689 mg/kg
Mirex
0.00301 ma/kg
Pentachloroanisole
0.00215 mg/kg
Dioxjns
0.000001 mg/kg
PCBs
0.15309 mg/kg
Mercury
0.06 mq/kg
422088
SW
Cadmium
55 ug/1
Chromium
130 ug/l
Copper
82 ug/l
Zinc
888 ug/l
Mercury
2 ug/l
422115
SED
Antimony
10 mg/kg
WQN0172
SW
Chromium
5 ug/l
Copper
80 ug/l
Manganese
130 ug/l
Nickel
50 ug/l
Zinc
60 ug/l
Aluminum
1090 ug/l
WQN0158
SW
Chromium
5 ug/l
Manganese
60 ug/l
Nickel
50 ug/l
Zinc
50 ug/l
Aluminum
1000 ug/1
-------
CHESTER RISK PROJECT
TABLE 4-23
SURFACE WATER RISKS
CHILD
ADULT
STATION .
CHEMICAL OF CONCERN
HAZARD
HAZARD
CANCER
INDEX
INDEX
RISK
VERMICUUTE DUMP (DS)
Aluminum
0.00015
0.000036
N/A
Chromium
0.00038
0.00011
N/A
Barium
0.00027
0.000068
N/A
Cadmium
0.00051
0.00023
N/A
Nickel
0.00013
0.00003
N/A
Manganese
0.015
0.0038
N/A
Zinc
0.00019
0.000056
N/A
Arsenic
0.0025
0.00065
2.3E-07
Selenium
0.00075
0.00019
N/A
Mercury
0.0061
0.0023
N/A 1
TOTAL
0.026
0.0075
2.3E-07
VERMICUUTE DUMP (US)
Aluminum
0.00014
0.000035
N/A
Chromium
0.00044
0.00012
N/A
Barium
0.00025
0.000064
N/A
Cadmium
0.00045
0.0002
N/A
Copper
0.000098
0.000027
N/A
Nickel
0.00013
0.000029
N/A
Manganese
0.014
0.0036
N/A
Zinc
0.00013
0.000037
N/A
Vanadium
0.00035
0.000088
N/A
Arsenic
0.0057
0.0015
5.2E-07
Selenium
0.00072
0.00017
N/A
Mercurv
0.014
0.0052
N/A
TOTAL
0.036
0.011
5.2E-07
WQN0182
Manganese
0.6727
0.17
N/A
II TOTAL
0.67
0.17
N/A
MONROE CHEMICAL
Arsenic
0.014
0.0036
1.3E-06
TOTAL
0.014
0.0036
1.3E-06
DELAWARE COUNTY
Arsenic
0.044
0.011
4.0E-06
INCINERATOR LAND-
Beryllium
0.0061
0.0032
3.5E-05
FILL #1
Manganese
0.28
0.0703
N/A
TOTAL
0.33
0.085
3.9E-05
422120
Free cyanide
0.0004
0.0001
N/A
Total cyanide
0.00044
0.00011
N/A
Cadmium
0.05
0.023
N/A
Chromium
0.0038
0.0011
N/A
Copper
0.00036
0.0001
N/A
Zinc
0.000071
0.00002
N/A
TOTAL*
0.055
0.024
N/A
422088
Cadmium
0.07
0.032
N/A
Chromium
0.0055
0.0016
N/A
Copper
0.00044
0.00012
N/A
Zinc
0.00066
0.0001»
N/A
Mercurv
0.0022
0.00079
N/A
TOTAL
0.079
0.035
N/A
WQN0172
Chromium
0.0002
0.00006
N/A
Copper'
0.00043
0.00012
N/A
Manganese
0.0049
0.0012
N/A
Nickel
0.00042
0.000095
N/A
Zinc
0.000044
0.000013
N/A
Aluminum
0.00007
0.000017
N/A
TOTAL
0.0061
0.0015
N/A
WQN0158
Chromium
0.00021
0.00006
N/A
Manganese
0.0023
0.00058
N/A
Nickel
0.00043
0.000095
N/A
Zinc
0.0028
0.0006
N/A
Aluminum
0.000065
0.000016
N/A
-
TOTAL
0.0058
0.0014
N/A
•INCLUDES TOTAL NOT FREE. CYANIDE
-------
CHESTER RISK PROJECT
TABLE 4-24
SEDIMENT RISKS
CHILD
ADULT
STATION
CHEMICAL OF CONCERN
HAZARD
HAZARD
CANCER
INDEX
INDEX
RISK
MONROE CHEMICAL-POND SED
Antimony
0.024
0.0025
N/A
Arsenic
0.0013
0.00014
8.2E-08
Beryllium
0.000015
0.000001
4.0E-08
Cadmium
0.0087
0.0028
N/A
Chromium
0.0022
0.00024
N/A
Silver
0.0037
0.0004
N/A
TOTAL
0.040
0.0061
1.2E-07I
MONROE CHEMICAL-US SED
Benzo[b]fluoranthene
N/A
N/A
4.6E-09
Arsenic
0.0185
0.002
1.2E-06
Beryllium
0.000046
0.000004
1.2E-07
Vanadium
0.0052
0.00056
N/A
TOTAL
0.024
0.0026
1.3E-06
MONROE CHEMICAL-DS SED
Arsenic
0.0068
0.00073
4.4E-07
Antimony
0.014
0.0015
N/A
Beryllium
0.000035
0.000003
9.4E-08
Chromium
0.012
0.0013
N/A
Manganese
0.011
0.0012
N/A
Nickel
0.0026
0.00028
N/A
Vanadium
0.0032
0.00035
N/A
TOTAL
0.050
0.0054
5.3E-07I
EAST 10TH STREET
Benzfa]anthracene
N/A
N/A
1.3E-07
Benzo[b]fluoranthene
N/A
N/A
2.0E-07
Benzo[a]pyrene
N/A
N/A
7.8E-07
lndeno[1,2,3-c,d]pyrene
N/A
N/A
8.0E-08
Dibenzfa.hlanthracene
N/A
N/A
2.5E-07
TOTAL
N/A
N/A
1.4E-06I
DELAWARE COUNTY
Arsenic
0.01
0.0011
6.6E-07
INCINERATOR LAND-
Beryllium
0.00009
0.000009
2.4E-07
FILL #1
Cadmium
0.0065
0.0021
N/A
Chromium
0.0056
0.0006
N/A
Vanadium
0.0024
0.00026
N/A
Benz[a]anthracene
N/A
N/A
3.9E-08
Benzo[b]fluoranthene
N/A
N/A
5.0E-08
Benzo(a]pyrane
N/A
N/A
6.2E-07
Dibenzfa.hlanthracene
N/A
N/A
5.3E-08
TOTAL
0:025
0.0041
1.7E-06I
ABM WADE
Arsenic
0.14
0.015
9.0E-06
TOTAL
0.14
0.015
9.0E-06
422115
Antimony
0.0064
0.00068
N/A
TOTAL
0.0064
0.00068
N/A I
-------
CHESTER RISK PROJECT
TABLE 4-25
FISH TISSUE RISKS
STATION
CHEMICAL OF CONCERN
j
CHILD ADULT
HAZARD HAZARD CANCER
INDEX INDEX RISK.
WQF00511-000.6
Technical chlordane
5.2 1.1 6.4E-05
Dieldrin
2.1 % 0.44 2.6E-04
TOTAL
7.3 1.5 3.3E-04
WQN0182
Technical chlordane
19 4.07 2.4E-04
p.p'-DDE
N/A N/A 5.2E-05
Dieldrin
0.69 0.15 8.8E-05
PCBs
N/A N/A 1.8E-03
Cadmium
0.01 0.002 N/A
TOTAL
20 4.2 2.2E-03
WQF00002-084.9
Technical chlordane
8 1.7 1.0E-04
cis-Chlordane
1.6 0.33 1.9E-05
t-Nonachlor
0.23 0.05 8.2E-05
p.p'-DDT
1.8 0.38 4.9E-05
p,p'—DDD
N/A N/A 3.0E-05
p.p'-DDE
N/A N/A 9.7E-05
PCBs
N/A N/A 8.5E-03
Arsenic (converted from dry)
5.2 1.1 4.3E-04
Copper
1.7 0.37 N/A
Cadmium
0.76 0.16 N/A
Cadmium (converted from dry)
2.7 0.58 N/A
Copper (converted from dry)
3.8 0.83 N/A
Oxvchlordane
2 0.42 2.4E-05
I TOTAL 1*
16 3.4 8.9E-03
TOTALS*
12 2.5 4.3E-04I
WQF00002-081.8
Technical chlordane
92 19.7 1.1E-03"
c-Chlordane
1.38 0.3 1.7E-05
t-Nonachlor
0.23 0.05 8.2E-05
p,p'-DDT
1.7 0.36 4.5E-05
p,p'-DDD
N/A N/A 6.6E-05
p.p'-DDE
N/A N/A 3.9E-04
PCBs
N/A N/A 8.0E-03
Oxvchlordane
1.6 0.33 1.9E-05
TOTAL
97 21 9.8E-03
DELFISH—07
PCB 1260
N/A N/A 6.5E-03
PCB 1254
N/A N/A 6.2E-03
p.p'-DDD
N/A N/A 7.7E-05
p.p'-DDE
N/A N/A 5.2E-04
Mercury
2.2 0.47 N/A
alpha-Chlordane
8.6 1.8 1.1E-04
TOTAL
11 2.3 1.3E-02
3096
Chlordane
0.98 0.21 1.2E-05
p,p'—DDE
N/A N/A 6.4E-06
Dieldrin
0.48 0.1 6.1E-05
Mirex
0.05 0.01 3.0E-06
Pentachloroanisole
0.00025 0.000053 1.4E-07
Dioxins
N/A N/A 9.8E-05
PCBs
N/A N/A 6.5E-04
Mercurv
0.69 0.15 N/A
TOTAL
2.2 0.47 8.3E-04
•TOTAL 1 includes wet weight metals, TOTAL 2 includes dry weight metals only
-------
CHESTER RISK PROJECT
TABLE 4-26
SURFACE WATER, SEDIMENT, AND ASH TISSUE RISKS
STATION ID
SOURCE
CHILD HI
ADULT-24 HI
DRIVER
CANCER
RISK
DRIVER
WQN0182
SW
0.673
0.171
Mn
N/A
FISH
19.687
4.219
chlordane
2.20E—03
PCBs
DELFISH07
FISH
10.816
2.318
chlordane, Hg
1.30E-02
PCBs
WQF00002—081.8
FISH
96.874
20.759
chlordane
9.80E-03
PCBs
WQF00002—084.9
DRY FISH
11.698
2.507
As
4.30E—04
As
WET FISH
16.036
3.441
chlordane
8.90E—03
PCBs
WQF00511-000.6
FISH
7.249
1.553
chlordane
3.30E-04
dieldrin
422068
SW
0.080
0.035
Cd
N/A
422115
SED
0.006
0.001
Sb
N/A
422120
SW
0.055
0.024
Cd
N/A
3096
FISH
2.203
0.472
chlordane
8.30E—04
PCBs
WQN0158
SW
0.006
0.001
ZaMn '
N/A
WQN0172
SW
0.006
0.002
Mn
N/A
ABM WADE
SED
0.140
0.015
As
9.00E-06
As
MONROE
POND SW
0.014
0.004
As
1.30E-06
As
POND SED
0.040
0.006
Sb
1.20E-07
As
US SED
0.024
0.003
As
1.30E-06
As
DS SED
0.050
0.006
Cr.Sb.Mn
5.30E-07
As
DELCO INCINERATOR LF-1
SW
0.326
0.085
Mn .
3.90E-05
Be
SED
0.025
0.004
As
1.70E-06
As, benzo[a]pyrene
EAST 10TH STREET
SED
N/A
N/A
1.406-06
benzofa]pyrene
VERMICUUTE DUMP
SWUS
0.037
0.011
Mn
5.20E—07
As
SW DS
0.026
0.007
Mn
2.30E-07
As
-------
CHESTER RISK PROJECT
TABLE 4-27
Delaware County, PA TRI Facilities
Chronic Index and Residual Mass Ranking
Rank
Company Name
City
TRI Category
Chemical and Issue of Concern
6
Epsilon Prods.
Marcus
Hook
Air fugitive, Air
stack
Ethylene, Propylene: volume
5
Boeing Defense & Space
Group
Ridley
Park
Air stack
VolaHles mixture: volume
4
Foamex LP.
Eddystone
Air fugitive
Dichloromethane: toxicity
3
Scott Paper
Chester
Air fugitive, Air
stack
Chloroform: toxicity
Acids: volume, acute toxicity
2
Wrtco Corp.
Trainer
Air fugitive, Air
stack
2-Methoxyethanol: volume and
toxicity
1
Sun Refining & Marketing
Marcus
Hook
Air fugitive, Air
stack
Ethylene Oxide: volume, toxicity
Benzene and MTBE: volume,
toxicity
This analysis does not represent relative risk. The rank provides a rough estimate of potential hazard for screening purposes and must
be evaluated with the qualitative information contained in this report
-------
CHESTER RISK PROJECT
TABLE 4-28
1S92 TRI FOR REGION III
DELAWARE CO., PA
Chamlcal Nam* fffglllfr IPff
Facility Nam*
Sir—tAddr—a
CHROMIUM
NICKEL
SULFURIC ACID
AMMONIA
PHOSPHORIC ACID
AMMONIA
10013PNNSY100BE PENNSYLVANIA MACHINE WORKS 100 BETHEL RD.
19013PNNSY1008E PENNSYLVANIA MACHINE WORKS 100 BETHEL RD.
19013NRTHM1200W NORTH AMERICA SILICA
19013NRTHM1200W NORTH AMERICA SILICA
10331CNCROCONOCONCORD BEVERAGE CO.
1933) CNCRDCONCt-CONCORD BEVERAGE CO.
1200 W. FRONT ST.
1200 W. FRONT 8T.
CONCHE8TER RO. & ALDAN AVE.
CON CHESTER RO. ft ALDAN AVE.
ETHYLENE
PROPYLENE
CHROMIUM COMPOUNDS
FORMALDEHYDE
19061P8LNPBLUEB EPSILON PRODS. CO.
10061PSLNPBLUEB EPSILON PROOS. CO.
19013THPQCFRONT PQ CORP.
100S0HYDRL520CO HYDROL CHEMICAL CO.
BLUE BALL AVE. & POST RD.
BLUE BALL AVE. ft POST RD.
1201 W. FRONT ST.
620 COMMERCE DR.
NAPHTHALENE
BUTYL BENZYL PHTHALATE
FREON 113
1.1,1-TRICHLOROETHANE
COPPER COMPOUNDS
1.1,1 -TRICHLOROETHANE
ACETONE
10061CNGLMRIDGE CGNQOLEUM CORP.
10061CNQLMRIDQE CONQOLEUM CORP.
19014MCQND0CRO2MCQEE INDUSTRIES INC.
1O014MCQND0CRO2MCQEE INDUSTRIES INC.
10013HRCST6S1EO HARCAST CO. INC.
1001GRBND82RACE ORB IND. INC.
19016RBNDS2RACE ORB IND. INC.
RIDQE RD. ft YATES AVE
RIDQE RD. ft YATES AVE.
0 CROZERVILLE RO.
0 CROZERVILLE RD.
661 E. 0TH 8T.
2 RACE ST.
2 RACE ST.
XYLENE (MIXED ISOMERS)
TOLUENE
100238NTRY237MI SENTRY PAINT TECH.
100238NTRY237MI SENTRY PAINT TECH.
237 MILL 8T.
237 MIU 8T.
METHANOL
DIBUTYL PHTHALATE
METHYL METHACRYLATE
TOLUENE
1,1.1 -TRICHLOROETHANE
NICKEL
TOLUENE
1.1,1 -TRICHLOROETHANE
19014CSTVC6CROZCUSTOM COMPOUNDING INC.
10O2OS8CHM48POWE66CHEM CO.
190298SCHM48POWE88CHEM CO.
10014NTRNT11CRO INTERNATIONAL ENVELOPE CO.
10018LTTNSMARPL CLIFTON PRECISION - N.
10018BCHNNPENN J BUCHAN IND.
100188CHNNPENNJ BUCHAN IND.
100168CHNNPENNJ BUCHAN IND.
8 CROZERVILLE RD.
48 POWHATTAN AVE.
48 POWHATTAN AVE.
11 CROZERVILLE RD.
MARPLE AT BROADWAY AVE.
PENN ft JEFFERSON ST
PENN ft JEFFERSON ST.
PENN ft JEFFERSON ST.
N-BUTYL ALCOHOL
10014ZNTHP200CO ZENITH PROOUCTS CORP.
200 COMMERCE DR.
SIC
ifll? £itt County Latllud* Lonoltuda Coda
100133486
190133485
10013
10013
10331
10331
10061
10061
10013
10060
10061
19061
10014
19014
10013
10015
10016
10023
10023
10014
100200056
100200068
<0014
100162405
100182604
100162604
100162604
19014
ASTON
ASTON
CHESTER
CHESTER
CONCORDV1LLE
CONCORDVIUE
MARCUS HOOK
MARCUS HOOK
CHESTER
YEADON
MARCUS HOOK
MARCUS HOOK
ASTON
ASTON
CHESTER
UPLAND
UPLAND
DARBY
DARBY
ASTON
ESSINQTON
ESSINQTON
ASTON
CLIFTON HEIGHTS
CLIFTON HEIGHTS
CLIFTON HEIGHTS
CLIFTON HEIGHTS
ASTON
OELAWARE
DELAWARE
DELAWARE
DELAWARE
DELAWARE
DELAWARE
DELAWARE
DELAWARE
DELAWARE
DELAWARE
DELAWARE
DELAWARE
DELAWARE
DELAWARE
DELAWARE
DELAWARE
DELAWARE
DELAWARE
DELAWARE
DELAWARE
DELAWARE
DELAWARE
DELAWARE
DELAWARE
DELAWARE
762600
762600
305005
3S500S
305326
305326
304856
304856
304002
304002
305244
305244
DELAWARE 305118
305104
305104
305450
306450
305244
305168
395168
306242
304610
305620
306820
305820
305216
-395000 3498
-395000 3408
-752221 2610
-762221 2610
-763150 2086
-763160 2086
-752548 2821
-762548 2621
DELAWARE 305008 -752230 2810
DELAWARE 305030 -761600 2860
-762405 3006
-752405 3006
-762725 2899
-752725 2890
-762108 3324
-752303 2851
-752303 2851
-751538 2851
-761536 2861
-762736 2821
-751806 2821
-761606 2821
-762746 2677
-761713 3621
-760104 2782
-760104 2782
-760104 2782
-760015
-------
CHESTER RISK PROJECT
TABLE 4-28
1992 TRI FOR REGION III
DELAWARE CO., PA SIC
Chemical Nam* Facility ID# FMilltY Nim* gfrttt ftMfW flP COtff £1& Counlv latllud. Lonaltud. Coda
XYLENE (MIXED ISOMERS)
19014ZNTHP200CO ZENITH PRODUCTS CORP.
200 COMMERCE DR.
10014
ASTON
DELAWARE
385215
-760015 2514
TOLUENE
19014ZNTHP200CO ZENITH PRODUCT8 CORP.
200 COMMERCE OR.
18014
ASTON
DELAWARE
305216
-750015 2514
ETHYLENE GLYCOL
10032MZRCH1830C PPG IND. INC.
1630 COLUMBIA AVE.
18032
FOLCROFT
DELAWARE
385319
-751637 2643
DIETHANOLAMINE
19032MZRCH1B30C PPG IND. INC.
1630 COLUMBIA AVE.
18032
FOLCROFT
DELAWARE
395310
-761637 2643
DIETHYL SULFATE
10032MZRCH1830C PPG IND. INC.
1830 COLUMBIA AVE.
18032
FOLCROFT
DELAWARE
395318
-761637 2843
GLYCOL ETHERS
19032MZRCH1630C PPG IND. INC.
1830 COLUMBIA AVE.
18032
FOLCROFT
DELAWARE
395318
-751637 2843
CHLOROMETHANE
18032MZRCH1830C PPG IND. INC.
1830 COLUMBIA AVE.
18032
FOLCROFT
DB-AWARE
395318
-761637 2843
BENZYL CHLORIDE
19032MZRCH1830C PPG IND. INC.
1830 COLUMBIA AVE.
18032
FOLCROFT
DELAWARE
385318
-751637 2843
DECABROMOOIPHENYL OXIDE
18013TR8CQ800WF TRS ACQUISITION CORP.
800 W. FRONT ST.
18013
CHESTER
DELAWARE
385000
-752230 2862
XYLENE (MIXED ISOMERS)
18060JLNBS300EB JULIAN B. SLEVIN CO. INC.
300 E. BALTIMORE AVE.
18050
LANSDOWNE
DELAWARE
385600
-761800 2688
TOLUENE
1B0S0JLNBS300EB JULIAN B. SLEVIN CO. INC.
300 E. BALTIMORE AVE.
19060
LANSOOWNE
DELAWARE
385600
-761800 2699
HYDROCHLORIC ACID
10O32THBLL16400 BULLEN COMPANIES
1640 DELMAR DR.
18032
FOLCROFT
DELAWARE
395343
-761640 2842
HYDROGEN FLUORIDE
19032THBLL1640D BULLEN COMPANIES
1640DELMAR OR.
18032
FOLCROFT
DELAWARE
395343
-761640 2642
PHOSPHORIC ACID
te032THBLL16400 BULLEN COMPANIES
1640 DELMAR DR.
18032
FOLCROFT
DELAWARE
385343
-761640 2842
GLYCOL ETHERS
19032THBLL1640D BULLEN COMPANIES
1640 DELMAR DR.
18032
FOLCROFT
DELAWARE
395343
-751640 2642
1,1,1 -TRICHLOROETHANE
18016TLDYN4THTO TELEDYNE PACKAGING
4TH A TOWNSEND 8T6.
18016
CHE8TER
DELAWARE
395030
-762150 3409
DIETHANOLAMINE
19061BPLCMPO8TRBP EXPLORATION A OIL INC.
POSTRD.
18061
TRAINER
DELAWARE
394000
-752400 2911
NICKEL
18061BPLCMPOSTRBP EXPLORATION & OIL INC.
POSTRD.
18061
TRAINER
DELAWARE
394900
•762400 2011
PHOSPHORIC ACID
18081BPLCMPO8TRBP EXPLORATION A OIL INC.
P08T RD.
18061
TRAINER
DELAWARE
394800
-762400 2011
SULFURIC ACID
18061BPLCMPO8TRBP EXPLORATION 5 OIL INC.
POST RD.
10061
TRAINER
DELAWARE
394000
-762400 2011
1,2,4-TRIMETH YLBENZENE
19061BPLCMPO8TRBP EXPLORATION A OIL INC.
P08T RD.
10061
TRAINER
DELAWARE
394900
-762400 2011
CYCLOHEXANE
19061BPLCMPOSTRBP EXPLORATION A OIL INC.
P08TRD.
19061
TRAINER
DELAWARE
384000
-752400 2011
HYDROGEN FLUORIDE
19061BPLCMPOSTRBP EXPLORATION A OIL INC.
POST RD.
10061
TRAINER
DELAWARE
394000
-752400 2011
ETHYLENE
10061BPLCMP08TRBP EXPLORATION A OIL INC.
POST RD.
10061
TRAINER
DELAWARE
394900
-752400 2011
PROPYLENE
19061BPLCMPOSTRBP EXPLORATION A OIL INC.
POST RD.
10061
TRAINER
DELAWARE
394900
-762400 2011
AMMONIA
10061BPLCMPOSTRBP EXPLORATION A OIL INC.
POST RD.
18061
TRAINER
DELAWARE
394900
-752400 2011
METHANOL
ie061BPLCMPOSTRBP EXPLORATION A OIL INC.
POSTRD.
10061
TRAINER
DELAWARE
394900
-762400 2011
XYLENE (MIXED ISOMERS)
19O01BPLCMPO8TRBP EXPLORATION A OIL INC.
POST RD.
10061
TRAINER
DELAWARE
304900
-762400 2011
ETHYLBENZENE
1S061BPLCMPOSTRBP EXPLORATION A OIL INC.
P08T RD.
10061
TRAINER
DELAWARE
304000
-752400 2011
TETRACHLOflOETHYLENE
1M61BPLCMPOSTRBP EXPLORATION A OIL INC.
POST RD.
10061
TRAINER
DELAWARE
384800
-762400 2011
TOLUENE
19061BPLCMPO8TRBP EXPLORATION A OIL INC.
P08T RD.
18061
TRAINER
DELAWARE
394900
-762400 2011
1 ,2-DICHLOROETHANE
19061BPLCMPOSTR BP EXPLORATION A OIL INC.
POST RD.
18061
TRAINER
DELAWARE
394900
-762400 2011
NAPHTHALENE
10061BPLCMPOSTRBP EXPLORATION A OIL INC.
POSTRD.
10061
TRAINER
DELAWARE
394900
-762400 2011
METHYL TERT-BUTYL ETHER
ie06IBPLCMPO8TRBP EXPLORATION A OIL INC.
P08T RD.
10061
TRAINER
DELAWARE
394900
-762400 2011
BENZENE
18061 BPLCMPOSTR BP EXPLORATION A OIL INC.
POST RD.
18061
TRAINER
DELAWARE
394900
-762400 2011
SULFURIC ACID
10013BNGHLINDUS BOEING DEFEN8E A SPACE GROUP STEWART AVE. A INDUSTRIAL HWY.
18103
RIDLEY PARK
DELAWARE
395261
-761032 3721 .
METHYL ETHYL KETONE
19013BNGHLIN0US BOEING DEFENSE A SPACE GROUP STEWART AVE. & INDUSTRIAL HWY.
10103
RIDLEY PARK
DELAWARE
386261
-761032 3721
TOLUENE
10013BNGHLINDUS BOEING DEFENSE A SPACE GROUP STEWART AVE. A INDUSTRIAL HWY.
10103
RIDLEY PARK
DELAWARE
395251
-761032 3721
-------
CHESTER RISK PROJECT
TABLE 4-28
1092 TRI FOR REGION III
DELAWARE CO., PA
ChamlcalNama
Facility IO»
Facility Nam*
Straat Addraaa
TRICHLOROETHYLENE
ACETONE
METHYL ISOBUTYL KETONE
19013BNQHLINDUS BOEING DEFENSE & SPACE GROUP STEWART AVE. A INDUSTRIAL HWY.
I9013BNGHLINDUS BOEING DEFENSE & SPACE GROUP STEWART AVE. A INDUSTRIAL HWY.
10013BNGHLINDUS BOEING DEFENSE A 8PACE GROUP 8TEWART AVE. A INDUSTRIAL HWY.
SULFURIC ACID 19013SCTFM1600E FOAMEX L.P.
TOLUENEDIISOCYANATE (MIXED ISCI9013SCTFM1600E FOAMEX L.P.
DIOILOROMETHANE
HYDROCHLORIC ACID
SULFURIC ACID
BUTYL BENZYL PHTHALATE
CHLOROFORM
te0138CTFM1600E FOAMEX L P.
19013SCTTPFRONT SCOTT PAPER CO.
19013SCTTPFRONT SCOTT PAPER CO.
10013SCTTPFHONT SCOTT PAPER CO.
190138CTTPFRONT SCOTT PAPER CO.
1SOOE. 2ND ST.
1600 E. 2ND ST.
1600 E. 2ND ST.
FRONT & AVE. OF THE STATES
FRONT A AVE. OF THE STATES
FRONT A AVE. OF THE STATES
FRONT A AVE. OF THE 8TATE8
SULFURIC ACID
METHANOL
2-METHOXYETHANOL
CHLORINE
CRESOL (MIXED ISOMERS)
ETHYLENE GLYCOL
PHENOL
SULFURIC ACID
1.&BUTAD1ENE
CYCLOHEXANE
1,2,4-TRIMETHYLBENZENE
AMMONIA
PROPYLENE
ETHYLENE
ZINC COMPOUNDS
METHANOL
XYLENE (MIXED ISOMERS)
ETHYLBENZENE
TOLUENE
CHROMIUM COMPOUNDS
ANTIMONY COMPOUNDS
METHYL TERT-BUTYL ETHER
BENZENE
ETHYLENE OXIDE
19013WTCCR3300W WITCO CORP.
16013WTCCR3300WWITCO CORP.
19013WTCCR3300W WITCO CORP.
3300 W. 4TH ST.
3300 W. 4TH8T.
3300 W. 4TH 8T.
19061SNRFNGREENSUN
19061SNRFNQREENSUN
19061SNRFNGREENSUN
19061 SNRFNQREENSUN
19061SNRFNGREENSUN
190618NRFNGREENSUN
19061 SNRFNQREENSUN
19061 SNRFNQREENSUN
190618NRFNGREEN8UN
19061SNRFNGREEN8UN
190618NRFNGREENSUN
19061 SNRFNQREENSUN
190618NRFNGREEN SUN
190618NRFNQREEN8UN
190616NRFNQREEN8UN
19061 SNRFNQREENSUN
19061SNRFNQREEN8UN
19061SNRFNQREENSUN
19061SNRFNGREENSUN
190618NRFNGREENSUN
19061SNRFNQHEENSUN
REFINING A MARKETING CO.
REFINING A MARKETING CO.
REFINING A MARKETING CO.
REFINING & MARKETING CO.
REFINING A MARKETING CO.
REFINING A MARKETING CO.
REFINING A MARKETING CO.
REFINING A MARKETING CO.
REFINING A MARKETING CO.
REFINING A MARKETING CO.
REFINING A MARKETING CO.
REFINING A MARKETING CO.
REFINING A MARKETING CO.
REFINING A MARKETING CO.
REFINING A MARKETING CO.
REFINING A MARKETING CO.
REFINING A MARKETING CO.
REFINING A MARKETING CO.
REFINING A MARKETING CO.
REFINING A MARKETING CO.
REFINING A MARKETING CO.
GREEN 8T.
GREEN 8T.
GREEN 8T.
GREEN ST.
GREEN 8T.
GREEN 8T.
GREEN 8T.
GREEN 8T.
GREEN 8T.
GREEN 8T.
GREEN ST.
GREEN ST.
GREEN 8T.
GREEN 8T.
GREEN ST.
GREEN 8T.
GREEN ST.
GREEN 8T.
GREEN 6T.
GREEN 8T.
GREEN ST.
A DELAWARE AVE.
A DELAWARE AVE.
A DELAWARE AVE.
A OELAWARE AVE.
A DELAWARE AVE.
A DELAWARE AVE.
A DELAWARE AVE.
A DELAWARE AVE.
A DELAWARE AVE.
A DELAWARE AVE.
A DELAWARE AVE.
A DELAWARE AVE.
A DELAWARE AVE.
A DELAWARE AVE.
A DELAWARE AVE.
A DELAWARE AVE.
A DELAWARE AVE.
A DELAWARE AVE.
A DELAWARE AVE.
A DELAWARE AVE.
A DELAWARE AVE.
SIC
Coda £lft County Latitude Lonaltuda Coda
19103
RIDLEY PARK
DELAWARE
395251
-751932
3721
19103
RIDLEY^ PARK
DELAWARE
395251
-751932
3721
19103
RIDLEY* PARK
DELAWARE
395251
-751932
3721
19022
EDDY8TONE
DELAWARE
395119
-717006
3086
19022
EDDYSTONE
DELAWARE
395119
-717006
3086
19022
EDOY8TONE
DELAWARE
395119
-7.17006
3086
19013
CHESTER
DELAWARE
395042
•752124
2621
19013
CHESTER
DELAWARE
395042
-752124
2621
19013
CHESTER
DELAWARE
395042
-762124
2621
19013
CHESTER
DELAWARE
395042
-762124
2621
19061
TRAINER
DELAWARE
394946
-752400
2843
19061
TRAINER
DELAWARE
394948
-752400
2843
19061 .
TRAINER
DELAWARE
394948
-752400
2843
190610426
MARCUS HOOK
DELAWARE
394800
-752600
2911
190610426
MARCUS HOOK
DELAWARE
394800
-752600
2911
190610426
MARCUS HOOK
DELAWARE
394800
-752600
2911
190610426
MARCUS HOOK
DELAWARE
394800
-752600
2911
190610426
MARCUS HOOK
DELAWARE
394800
-752600
2911
190610426
MARCUS HOOK
DELAWARE
394800
-752600
2911
190610426
MARCUS HOOK
DELAWARE
394800
-752600
2911
190610426
MARCUS HOOK
DELAWARE
394800
-752600
2911
190610426
MARCUS HOOK
DELAWARE
394800
-752600
2911
190610426
MARCUS HOOK
DELAWARE
394800
-752600
2911
190610426
MARCUS HOOK
DELAWARE
394800
-752600
2911
190610426
MARCUS HOOK
DELAWARE
394800
-762600
2911
190610426
MARCUS HOOK
DELAWARE
394800
-752600
2911
190610426
MARCUS HOOK
DELAWARE
394800
-752600
2911
190610426
MARCU8 HOOK
DELAWARE
394800
-752600
2911
190610426
MARCUS HOOK
DELAWARE
394800
-752600
2911
190610426
MARCUS HOOK
DELAWARE
394800
-752600
2911
190610426
MARCUS HOOK
DELAWARE
394800
-762600
2911
190610426
MARCUS HOOK
DELAWARE
394800
-752600
2911
190610426
MARCUS HOOK
DELAWARE
394800
-762600
2911
190610426
MARCUS HOOK
DELAWARE
394800
•752600
2911
pages
-------
CHESTER RISK PROJECT
TABLE 4-28
1092 TRI FOR REGION III
DELAWARE CO., PA
Chemical Nam* Facility IP*
TOXICITY DATA:
Reference Confidence
Dose Statement
;
Reference
Dos*
s"»tua
CHROMIUM
NICKEL
6ULFURIC ACID
AMMONIA
PHOSPHORIC ACID
AMMONIA
ETHYLENE
PROPYLENE
CHROMIUM COMPOUNDS
FORMALDEHYDE
NAPHTHALENE
BUTYL BENZYL PHTHALATE
FREON 113
1,1.1 -TRICHLOROETHANE
COPPER COMPOUNDS
1.1.1-TRICHLOROETHANE
ACETONE
XYLENE (MIXED ISOMERS)
TOLUENE
METHANOL
DIBUTYL PHTHALATE
METHYL METHACRYLATE
TOLUENE
1,1,1 -TRICHLOROETHANE
NICKEL
TOLUENfe
1,1,1 -TRICHLOROETHANE
N-BUTYL ALCOHOL
19013PNNSY100BE
19013PNNSY100BE
10013NRTHM1200W
10013NRTHM1200W
19331 CNCRDCONCt
19331CNCRD CON Ct
19061PSLNPBLUEB
19061PSLNPBLUEB
19013THPQCFRON1
19060H YDRL620CO
10061CNQLMRIDQE
19081 CNQLMRIDQE
19014MCQND9CRO
19014MCGND9CRO;
19013HRCST651E9
19016RBNDS?RACE
19016RBNDS2RACE
19Q23SNTRY237MI
19023SNTRY237MI
19014CSTMC8CRO2
19029SSCHM4BPOV
19O29SSCHM40POV
19014NTRNT11CRO
19018LTTN6MARPL
190188CHNNPENNJ
19018BCHNNPENNJ
190188CHNNPENNJ
19014ZNTHP200CO
0.02 medium
0
0
0
0
0
0
0.005 low
0.2 medium
0.004 na
0.2 km
30 low
0.09 na
0.006 medium
0.09 na
0.1 low
2 medium
0.2 medium
0.5 medium
0.1 low
0.06 na
0.2 medium
0.09 na
0.02 medium
0.2 medium
0.09 na
0.1 low
Iris
Iris
Iris
ECAO: Risk Assessment 2/92
Iris
Iris
w/d from Ms and heast
Iris
w/d Irom Iris and heast
Iris
Iris
Iris
Iris
Iris
HEAST
Iris
w/d Irom Iris and heast
Iris
Iris
w/d Irom Iris and heast
Iris
Cancar Weight RfD CPF
Potency. of Index Index
(CPF) Evidence Poae Poa*
0 0 0
0 1.4 0
0 0 0
0 0 0
0 0 0
0 0 0
0 0 0
0 0 0
0 0.35- 0
0 14 0
0 0.28 0
0 C 14 0
0 2100 0
0 6.3 0
0 0.35 0
0 6.3 0
0 7 0
0 140 0
0 14 0
0 36 0
0 7 0
0 6.6 0
0 14 0
0 6.3 0
0 1.4 0
0 14 0
0 63 0
0 7 0
page4
-------
CHESTER RISK PROJECT
TABLE 4-28 toxicity data:
1992 TRI FOR REGION III
Reference Confidence
Reference
Cancer Weight
RfD
CPF
DELAWARE CO., PA
Doss Statement
Doae
Potency of
Index
Index
Chemical Name
Facility ID*
fflfm
Status
-------
CHESTER RISK PROJECT
TABLE 4-28 toxicity data:
1992 TRI FOR REGION III
Reference Confidence
Refaranca
Canear Weight
RfD
CPF
DELAWARE CO., PA
Ooaa Statemant
Doaa
Potency of
Indax
Indax
Chemical Nam*
Facility ID*
(RfD)
Status
(CPF» Evidence
Doaa
Doaa
TRICHLOROETHYLENE
160138NQHLINDUS
0
0.011 c-b2
0
1.2477725
ACETONE
19013BNQHLINDUS
0.1 low
Iris
0
7
0
METHYL ISOBUTYL KETONE
19013BNQHLINDUS
0.06
HEAST
0
3.5
0
SULFURIC ACID
190138CTFM1500E
0
0
0
0
TOLUENEDIISOCYANATE (MIXED I8C190138CTEM1600E
0
0
0
0
DICHLOROMETHANE
19013SCTFM1500E
0.06 medium
Iris
0.0076 B2
4.2
1 3930355
HYDROCHLORIC ACID
190138CTTPFR0NT
0
0
0
0
6ULRJRIC ACID
19013SCTTPFR0MT
0
0
0
0
BUTYL BENZYL PHTHALATE
19013SCTTPFRONT
0.2 low
Iris
0 C
14
0
CHLOROFORM
190138CTTPFRONT
0.01 medium
Iris
0.0061 B2
0.7
1.7127486
SULFURIC ACID
19013WTCCR3300W
0
0
0
0
METHANOL
19013WTCCR3300W
0.6 medium
Iris
0
35
0
2-METHOXYETHANOL
19013WTCCR3300W
0.001 na ~
HEAST
0
0.07
0
CHLORINE
19061SNRFNQREEN
0
0
0
0
CRESOL (MIXED I80MERS)
19061 SNRFNGREEf
0
0
0
0
ETHYLENE GLYCOL
190618NR FNGREEI*
2 high
Iris
0
140
0
PHENOL
19061 SNRFNQREEf
0.6 low
Iris
0
42
0
SULFURIC ACID
19061 SNRFNQREEh
0
0
0
0
1.3-8UTADIENE
igoeiSNRFNQREEPi
0
0
0
0
CYCLOHEXANE
190618NRFNQREE>
0
0
0
0
1,2,4-TRIMETH YLBENZENE
19081SNRFNGREEf>
0
0
0
0
AMMONIA
19061 SNRFNGREEf
0
0
0
0
PROPYLENE
19061SNRFNGREEh
0
0
0
0
ETHYLENE
19061 SNRFNQREEf
0
0
0
0
ZINC COMPOUND8
190616NRFNGREEf>
0.3 medium
Iris
0
21
0
METHANOL
19061 SNHFNGREEh
0.6 medium
Iris
0
36
0
XYLENE (MIXED ISOMERS)
190618NRFNGREEfi
2 medium
Iris
0
140
0
ETHYLBENZENE
19061SNRFNGREEf>
O.I low
Iris
0
7
0
TOLUENE
190616NRFNGREEfi
0.2 medium
Iris
0
14
0
CHROMIUM COMPOUNDS
190618NRFNQREEf>
0.005 low
Iris
0
0.35
0
ANTIMONY COMPOUNDS
19061 SNRFNGREEh
0.0004 low
Iris
0
0.028
0
METHYL TERT-BUTYL ETHER
. 190618NRFNGREE^
0.005 na
0
0.35
0
BENZENE
19061SNRFNQREEf>
O
0.029 A
0
0.2413794
ETHYLENE OXIDE
19061SNRFNGREEf>
0
1.02 B1
0
0.0081699
-------
CHESTER RISK PROJECT
TA BLE 4-28 tri releases:
1992 TRI FOR REGION III
Air Nan point Air NonPoint
Air Point
Air Point
Water
Water
Land Land
Onalte Total Onsito Total
Onelto Total
Onsita Total
DELAWARE CO., PA
RllM8M
Chronic
Releasee
Chronic
Releasee
Chronic
Ralaaaaa Chronic
a
1
!
m
Chronic
Roleaseo
Chronic Index
Chemical Nam*
Facility ID*
(IbAii)
Index
(Ib/wrl
Index
(Ihfrrt
Index
Index
flb/vrt
Index
Sums
Sums
CHROMIUM
19013PNNSY100BE
0
0
0
0
0
0 0
0
0
NICKEL
19013PNNSY100BE
0
0
0
0
0
a o
0
0
0
0
SULFURIC ACID
19013NHTHM1200W
0
0
0
0
0
0 0
0
0
AMMONIA
19013NRTHM1200W
0
0
1700
0
0
0 0
1700
0
1700
0
PHOSPHORIC ACID
19331CNCRDCONC)
0
0
0
0
0
0 0
0
0
AMMONIA
19331CNCRDCONCI
sou
0
0
0
0
0 0
8048
0
5045
0
ETHYLENE
19061P8LNPBLUEB
IT00
0
2400
0
0
0 0
0100
0
PROPYLENE
19061PSLNPBLUEB
0
0100
0
0
0 0
01100
0
70200
0
CHROMIUM COMPOUNDS
19013THPQCFRONT
0
0
8
17730
0
0 0
8
17730
6
17730
FORMALDEHYDE
190G0H YDRL520CO
70
6018
841
47980
0
0 0
010
84074
619
54874
NAPHTHALENE
19061CNQLMRIDQE
8
231*2
S
22102
0
0 0
10
44325
BUTYL BENZYL PHTHALATE
19061CNGLMRIDQE
ISO
22102
>80
22102
443
0 0
808
44788
515
80093
FREON113
19014MCGND9CRO.
780
443
0
0
0
0 0
780
443
1,1,1-TRICHLOROETHANE
19014MCQND9CRO:
780
147780
280
40280
0
0 0
1000
198099
1750
197443
COPPERCOMPOUNDS
19013HRCST661E9
0
0
101
308287
0
0 0
10*
383237
103
365237
1,1,1-TRICHLOROETHANE
19016RBNDS2RACE
1100
216699
0
0
0
0 0
1400
216699
ACETONE
19016RBNDS2RACE
1700
801400
0
0
0
0 0
1700
301409
2800
618108
XYLENE (MIXED ISOMERS)
19023SNTR Y237M1
0
0
4100
38340
0
0 0
4100
38346
TOLUENE
190238NTRY237MI
0
0
8100
840703
0
0 0
0100
840763
10200
577110
METHANOL
19014CSTMC8CRO2
034
20874
18004
880507
0
0 0
10820
886001
16528
586081
DIBUTYL PHTHALATE
19029SSCHM48POV
0
0
0
0
0
0 0
0
0
METHYL METHACRYLATE
19029S8CHM48POVI
nco
896000
0
1100
0
0 0
2008
687116
2965
657116
TOLUENE
19014NTRNT11CRO
11870
1020380
0
0
0
0 0
11870
1026388
11678
1026386
1,1,1-TRICHLOROETHANE
19018LTTNSMARPL
nso
482040
3800
080400
0
0 0
8850
1182446
6850
1152446
NICKEL
1901BBCHNNPENNJ
0
0
0
0
0
0 0
0
0
TOLUENE
190168CHNNPENN J
0
0
1002
88827
0
0 0
1002
88827
1
1.1,1-TRICHLOROETHANE
190168CHNNPENNJ
0
0
8204
1820003
0
0 0
0284
1828003
9266
1716830]
N-BUTYL ALCOHOL
19014ZNTHP200CO
0
0
0
0
0
0
0 0
0
0
page 7
-------
CHESTER RISK PROJECT
TABLE 4-28
TRI RELEASES:
1992 TRI FOR REGION III
Air Nonpoint Air NonPoInt
Air Point
Air Point
DELAWARE CO., PA
Raiaasaa
.Chronic
Raiaasaa
Chronic
Chamlcal Nam*
Facility ID*
(IhArr)
Index
(IhArrt
Indax
XYLENE (MIXED ISOMERS)
19014ZNTHP200CO
280
2216
25500
226057
TOLUENE
10014ZNTHP200CO
MO
22162
20000
1772004
ETHYLENE GLYCOL
10032MZRCH1630C
0
0
0
0
DIETHANOLAMINE
19032MZRCH1830C
17
0
0
0
DIETHYL SULFATE
10032MZRCH1630C
134
0
0
0
GLYCOL ETHERS
19032MZRCH1830C
28
300030
0
0
CHLOROMETHANE
10032MZRCH1B30C
S
MIS
578
452057
BENZYL CHLORIDE
1003ZMZRCH1830C
*11
4261020
0
0
DECABROMODIPHENYL OXIDE
10013TR8CQ800WF
aooa
U10082
0
0
XYLENE (MIXED ISOMER8)
190S0JLN8S300EB
i otto
166478
3487
30012
TOLUENE
10060JLNBS300EB
730*7
•470276
13555
1201647
HYDROCHLORIC ACID
1B032THBLL164QO
aso
0
tM
0
HYDROGEN FLUORIDE
1B032THBLL16400
260
0
250
0
PHOSPHORIC ACID
19032THBLL16400
aso
0
250
0
GLYCOL ETHERS
I9032THBLL16400
tso
44324M
HO
4432485
1,1,1 -TRICHLOROETHANE
10016TLDYN4THTO
tost
4389432
88004
17533730
DIETHANOLAMINE
10061BPLCMP08TF
0
0
•
0
NICKEL
10061BPLCMP08TF
•
0
0
0
PH08PH0RIC ACID
19061BPL CM P08TF
e
0
0
SULFURIC ACID
10061BPLCMP08TF
6
0
0
0
1,2,4-TRIMETH YLBENZENE
10061BPLCMP08TF
0
0
5
0
CYCLOHEXANE
10061BPLCMPOSTF
S82
0
33
0
HYDROGEN FLUORIDE
10061BPLCMP08TF
•45
0
0
0
ETHYLENE
10061 BPLCMPOSTF
114
0
1193
0
PROPYLENE
10061BPLCMP08TF
1187
0
32M
0
AMMONIA
10061BPLCMPOSTR
TO
0
174M
0
METHANOL
19061BPLCMPO8TR
0
0
100
10263
XYLENE (MIXED ISOMERS)
10061BPLCMP08TF
4406
30050
483
4282
ETHYLBENZENE
10061 BPLCMPOSTF
Ml
103011
12
2128
TETRACHLOROETHYLENE
1006IBPLCMP06TF
4S
201374
0
0
TOLUENE
10061 BPLCMPOSTF
4406
100591
483
42818
U-DICHLOROETHANE
10061 BPLCMPOSTF
in
1437722
0
0
NAPHTHALENE
10061 BPLCMPOSTF
m
2060000
0
0
METHYL TERT-BUTYL ETHER
10061 BPLCMPOSTF
M
127696
2840
10446481
BENZENE
10061BPLCMP08TF
M44
13M480S
414
21286M
SULFURIC ACID
100136NQHLINDU8
0
0
2M
0
METHYL ETHYL KETONE
10013BNGHLINDUS
tso
7307
24000
700188
TOLUENE
10013BNGW. INDUS
1000
88650
57000
5053013
Water
Release*
(IMrrl
Water
Land
Land
Onaite Total Onaite Total
Onaite Total
Onaite Total
Chronic
Releases
Chronic
RetaMea
Chronic
Releaaea
Chronic Indax
Indax
(Ibfrrt
Index
(IbArrl
Index
Suma
Suma
0
0
0
25750
228273
0
0
0
20250
1795157
40000
2023430
0
0
0
0
0
0
0
0
57
0
0
0
0
234
0
0
0
0
22
390050
0
0
0
583
456876
0
0
0
211
4261020
1107
610795S
0
0
0
3000
5318082
3000
5318982
0
0
0
222M
197367
0
0
0
8(542
7671023
108808
7869310
0
250
0
750
0
0
250
0
750
0
0
250
0
750
0
0
2M
4432485
750
13287456
3000
13297456
0
0
0
111255
21017162
111256
21917162
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
«
0
0
0
0
415
0
0
0
0
645
0
0
0
0
1267
0
0
0
0
4483
0
0
0
0
84M1
0
0
0
0
290
10203
0
0
0
4888
43341
0
0
0
503
105139
0
0
0
45
201374
0
0
0
4889
433408
0
0
0
133
1437722
0
0
0
6M
2060000
0
0
2082
10574137
0
0
0
SON
15723261
108893
31579565
0
0
2M
0
0
0
0
24250
716565
0
0
oj
68000
5141683
pagae
-------
CHESTER RISK PROJECT
TABLE 4-28 tri releases:
1802 TRI FOR REGION III
Ah N on point Air NonPoInt
Air Point
Air Point
Water
Water
Land
Land
Onalte Total Onsite Total
Onolte Total
Onaite Total
DELAWARE CO., PA
Releasee
Chronic
Roloaooo
Chronic
RoImsoo Chronic
Raieasos Chronic
Releasee
Chronic
Roleaaeo
Chronic Index
Chemical Nam*
Facilltv ID#
(Ih/Wr)
Index
(Ibfrrl
Index
(Ib/Vrl
Index
(Ihfor)
lnd«
(Ib/vr)
Index
Sums
Sums
TRICHLOROETHYLENE
19013BNQHLINDU8
MO
246662
0400
0388083
0
0
0080
8603718
ACETONE
1S013GNGHLINDUS
12000
2127893
40000
7001977
0
0
82000
0219S69
METHYL ISOBUTYL KETONE
1 SOI 3BNQHLINDUS
200
80880
41000
14838882
0
0
41280
14027202
184400
38300755
SULFURIC ACID
19013SCTFM1600E
0
0
0
0
0
0
0
0
TOLUENEDIISOCYANATE (MIXED ISC19013SCTFM1600E
8
0
181
0
0
0
180
0
DICHLOROMETHANE
19013SCTFM1600E
33832
39783300
10
11884
0
0
33842
39703173
33698
30705173
HYDROCHLORIC ACID
190138CTTPFRONT
0
0
83000
0
0
0
83000
0
SULFURIC ACID
1S013SCTTPFRONT
•
0
110000
0
0
0
110000
0
BUTYL BENZYL PHTHALATE
19013SCTTPFRONT
7300
047143
80000
8230333
0
0
88300
8877476
CHLOROFORM
19013SCTTPFRONT
0800
10003702
7800
18732123
0
0
14300
>8718918
243600
41503391
SULFURIC ACID
19013WTCCR3300W
0
0
0
0
0
0
0
0
METHANOL
19013WTCCR3300W
207100
7301436
40707
1720001
0
0
290300
9091417
2-METHOXYETHANOL
19013WTCCR3300W
382004
0242808040
138888 2480740318
0
0
490080
889038S284
747045
8708446682
CHLORNE
190618NRFNGREET
0
0
0
0
0
0
0
0
CRESOL (MIXED I80MERS)
1006l8NRFNGREEf
0
0
0
0
0
0
0
0
ETHYLENE GLYCOL
190618NRFNGREB
0
0
0
0
0
0
0
0
I
PHENOL
1S0618NRFNGREB
•
0
0
0
0
0
0
0
|
SULFURIC ACID
190618NRFNGREEf
0
0
0
0
0
0
0
0
[
1.S-BUTAOIENE
190618NRFNGREEf
'120
0
0
0
0
0
120
0
|
CYCLOHEXANE
190618NRFNQREEf
1(00
0
080
0
0
0
2880
0
1,2,4-TRIMETHYLBENZENE
190618NRFNGREEf
4(00
0
00
0
0
0
4000
0
AMMONIA
190618NRFNQREEf
0100
0
0
0
0
0
0300
0
PROPYLENE
190618NRFNGREEh
>3000
0
12000
0
0
0
48000
0
ETHYLENE
190618NRFNQREB
40000
0
0
0
0
0
40000
0
ZINC COMPOUKD8
190618NRFNQREEh
0
0
270
18987
0
0
270
1S957
METHANOL
190618NRFNGREEI*
8700
202121
1100
30008
0
0
8000
241127
|
XYLENE (MIXED ISOMER8)
19061 SNRFNGREEd
20000
287084
1700
18070
0
0
30700
27218S
I
ETHYLBENZENE
190618NRFNQREEt
3000
831898
220
18008
0
0
3220
870904
J
TOLUENE
190618NRFNGREEfi
31000
2740141
7000
881468
0
0
30000
3439609
0
CHROMIUM COMPOUNDS
19061SNRFNGREEf
0
0
1300
4809788
0
0
1300
4609783
ANTIMONY COMPOUNDS
19061 SNRFNGREEf
0
0
400
17720941
0
0
400
17729941
METHYL TERT-BUTYL ETHER
190618NRFNGREEH
4000
17020744
0400
33332200
0
0
14200
80383033
BENZENE
190618NRFNQREEh
81000
202228734
1900
200S2SS6
0
0
84000
292279290
ETHYLENE OXIDE
190618NRFNGREEf
110000
18710188820
400
80764312
0
ol
110400
187709S0232
388966
17130461033
pages
-------
CHESTER RISK PROJECT
TABLE 4-28
TRI TRANSFERS:
TRI TOTALS:
1QB2 TRIFOR REGION III
POTW
POTW
Offalte
Offaita
Total Roleaaoa
Total
Total Releasee
Total
DELAWARE CO., PA
Tranafere
Chronic
Tranafars
Chronic
and Tranafera
Chronic
and Tranalere
Chronic Index
Chemical Nam*
Facility ID*
(IbArr)
Index
(IbArr)
Index
(Ihfrrt
Index
Sums
Sum#
CHROMIUM
19013PNNSY1008E
0
16160
0
1(160
0
NICKEL
19013PNNSY100BE
0
11660
10239041
11660
10239041
29700
10239041
SULFURIC ACID
19013NRTHM1200W
0
0
0
0
0
AMMONIA
10013NRTHM1200W
#
0
0
1700
0
1700
0
PHOSPHORIC ACID
19331 CNCRDCONCf
0
0
0
0
0
AMMONIA
19331CNCRDCONO
0
0
0
6046
0
6045
0
ETHYLENE
19061PSLNPBLUEB
0
0
0
•100
0
PROPYLENE
19061PSLNPBLUEB
0
0
0
81100
0
70200
0
CHROMIUM COMPOUNDS '
190I3THPQCFRONT
0
147M0
623139640
147638
623167379
147535
523167378
FORMALDEHYDE
190S0HYDRLS20CO
0
0
0
610
64874
019
54874
NAPHTHALENE
19061 CNGU.MRIDGE
6
7400
32000391
7410
32844716
BUTYL BENZYL PHTHALATE
19061CNQLMRIDQE
443
62100
4618660
62610
4663861
60020
37508577
FREON 113
190HMCGND0CRO,
0
0
0
760
443
1,1.1-TRICHLOROETHANE
19014MCQND9CRO;
0
•too
1201696
7100
1308696
7950
1399139
COPPER COMPOUNDS
19013HRC6T661E9
0
0
0
101
366237
103
365237
1,1.1-TRICHLOROETHANE
1901GRBNDS2 RACE
0
0
0
1100
216699
ACETONE
18016RBND82RACE
0
196Sa
1490671
SIMS
3792080
22488
4008779
XYLENE (MIXED ISOMERS)
190238NTR Y237MI
0
16435
138831
10618
173177
TOLUENE
190238NTRY237MI
0
•897
762122
14697
1302886
34232
1476062
METHANOL
19014CSTMC8CR02
0
•
0
18628
688081
18828
686081
OIBUTYL PHTHALATE
190298SCHM48POV
0
600
108380
600
106380
METHYL METHACRYLATE
19029SSCHM48POV
0
*200
709198
0168
1366314
6765
1472693
TOLUENE
190MNTRNT11CRO
0
4201
372417
16779
1398804
1577#
1398804
1.1,1 -TRICHLOROETH ANE
1901BLTTNSMARPL
0
0060
1685846
11980
2738201
13900
2738291
NICKEL
1901B8CHNNPENNJ
4412
0
0
6
4432
TOLUENE
1901BBCHNNPENNJ
0
0
0
1002
•6827
1,1,1 -TRICHLOROETHANE
19018BCHNNPENNJ
0
>118
817790
11400
2246793
12407
2339052
N-BUTYL ALCOHOL
19014ZNTHP200CO
0
0
0
0
0
0
-------
CHESTER RISK PROJECT
TABLE 4-28
TRI TRANSFERS:
TRI TOTALS:
1992 TRI FOR REGION III
POTW
POTW
Offalte
Offal ta
Total Ralaaaea
Total
Total Releases
Total
DELAWARE CO., PA
Tranafara
Chronic
|
•
s
to
Chronic
and Tranafara
Chronic
and Tranafara
Chronic Index
Chemical Nam*
FaeilltvIM
flb/vrt
Index
flbfrrt
Index
flhfrrl
Index
Suma
Suma
XYLENE (MIXED ISOMERS)
19014ZNTHP200CO
0
800
4432
29299
232705
TOLUENE
19014ZNTHP200CO
0
too
44325
30750
1830481
47000
2072187
ETHYLENE GLYCOL
19032MZRCH1830C
d
1000
177 SO
2000
17730
OIETHANOLAMINE
19032MZRCH1830C
0
727
0
791
0
DIETHYL SULFATE
19032MZRCH1830C
0
0
0
234
0
GLYCOL ETHERS
19032MZRCH1830C
im
120191272
9779
120191272
13500
240772803
CHLOROMETHANE
19032MZRCH1830C
0
0
0
593
456879
BENZYL CHLORIDE
1903ZMZRCH1830C
0
0
0
211
4261020
173M
246608229
DECABROMODIPHENYL OXIDE
19013TR8CQ600VYF
0
MOO
5319982
0090
10637965
eooo
10637985
XYLENE (MIXED ISOMERS)
1M50JLNB8300EB
0
4000
38490
29299
232047
TOLUENE
19060JLNB8300EB
0
12192
1092342
99994
9764265
125130
8997112
HYDROCHLORIC ACID
19032THBLL16400
0
0
0
780
0
HYDROGEN FLUORIDE
19032THBLL16400
0
0
0
780
0
PHOSPHORIC ACID
19032TH8LL1640D
0
0
0
780
0
GLYCOL ETHERS
19032THBLL16400
Hi
11U1IB
9
0
1099
17729941
3250
17729941
1.1.1-TRICHLOROETHANE
19016TLDYN4THTO
0
9
0
111295
21917162
11125S
21917182
OIETHANOLAMINE
19061BPLCMPOSTF
0
9
9
9
0
NICKEL
10O61BPLCMPO8TR
0
0
0
9
0
PHOSPHORIC ACID
19061BPLCMPO8TR
0
9
0
9
0
SULFURIC ACID
19061BPLCMPOSTP
0
0
0
9
0
1,2,4-TRIMETHYLBENZENE
19061BPLCMPO8TF
0
0
0
5
0
CYCLOHEXANE
19061BPLCMPOSTF
0
0
0
415
0
HYDROGEN FLUORIDE
10O61BPLCMPO8TR
0
0
0
945
0
ETHYLENE
19061BPLCMPOSTF
0
0
0
1297
0
PROPYLENE
1906IBPLCMPO8TR
0
0
0
446)
0
AMMONIA
19061BPLCMPO8TF
0
0
0
94531
0
METHANOL
19061BPLCMPO8TF
0
9
0
290
10293
XYLENE (MIXED ISOMER8)
19061BPLCMPOSTF
0
0
0
4999
43341
ETHYLBENZENE
19061BPLCMPO6TF
0
0
0
883
105139
TETRACHLOROETHYLENE
1S061BPLCMPO8TP
0
9
0
45
291374
TOLUENE
19061BPLCMPO8TF
0
9
0
4989
433408
1,2-DICHLOROETHANE
19061BPLCMPOSTP
0
9
0
133
1437722
NAPHTHALENE
19061BPLCMPO8TF
0
0
0
sea
2060900
METHYL TERT-BUTYL ETHER
19061BPLCMPOSTF
0
0
0
2992
10574137
BENZENE
19061BPLCMPO8TF
0
9
0
3989
15723261
108893
31570565
SULFURIC ACID
18013BNGHLINDUS
0
710
0
1900
0
METHYL ETHYL KETONE
19013BNQHLINDUS
It
16S50
499051
40000
1205636
TOLUENE
1 SOI 3BNGHLINDU8
0
12980
1112554
70580
6254237
-------
CHESTER RISK PROJECT
TABLE 4-28
TRI TRANSFERS:
In?/ TOTALS:
1992 TRI FOR REGION III
POTW
POTW
Off sit*
Oifslte
Total Releases
Total
Total Releases
Total
DELAWARE CO., PA
Transfers
Chronic
Transfer*
Chronic
and Transfers
Chronic
and Transfers
Chronic Index
Chemical Nam*
Facility ID*
(IbSvr)
Index
(IMrrt
Index
(IbArr)
Index
8ums
Sums
TRICHLOROETHYLENE
190138NGHLINDUS
0
0
15850
I58846S4
24(00
24468170
ACETONE
190t3BNQHLINDUS
0
0
29000
5141683
81000
14361252
METHYL ISOBUTYL KETONE
19013BNQHLINDUS
0
0
2550
804227
43800
15531428
261750
61820*24
SULFURIC ACID
19013SCTFM1600E
0
0
0
0
0
0
TOLUENEDIISOCYANATE (MIXED ISC19013SCTFM1600E
0
0
750
0
80S
0
DICHLOROMETHANE
190I38CTFM1600E
0
0
0.
0
>3542
39795173
34448
39795173
HYDROCHLORIC ACID
190138CTTPFRONT
0
0
0
0
53000
0
SULFURIC ACID
19013SCTTPFRONT
0
0
770
0
110770
0
BUTYL BENZYL PHTHALATE
19013SCTTPFRONT
1MM
9884*7
10
886
78310
878485*
CHLOROFORM
19013SCTTPFRONT
800
1248808
0
0
14800
38*64724
264880
43729583
SULFURIC ACID
19013WTCCR3300W
4
0
0
0
4
0
METHANOL
1B013WTCCR3300W
(700
237581
0
0
24*086
9328*99
2-METHOXYETHANOL
19013WTCCR3300W
20110 356726419
0
0
510778
9056081583
773889
906S410682
CHLORINE
19061 SNRFNQREEH
•
0
0
0
0
0
CRESOL (MIXED ISOMERS)
190618NRFNQREEfi
0
0
0
0
0
0
ETHYLENE QLYCOL
1906l8NRFNQREEh
0
0
0
0
0
0
PHENOL
190818NRFNQREEh
44000
1300196
0
0
44000
1300188
SULFURIC ACID
19061 SNRFNQREEh
0
0
0
0
0
8
1.3-BUTADIENE
lOOeiSNRFNQREEf
0
0
0
0
120
0
CYCLOHEXANE
19061 SNRFNQREEh
0
0
0
0
2550
0
1,2.4-TRIMETH YLBENZENE
19061 SNRFNQREEh
•
0
0
0
4896
0
AMMONIA
19061 SNRFNQREEh
*20000
0
0
0
*28300
0
PROPYLENE
190618NRFNQREEK
0
0
0
0
45000
0
ETHYLENE
19061 SNRFNQREEh
0
0
0
0
46000
0
ZINC COMPOUND8
19061 SNRFNQREEh
7100
4*1429
710
43143
8300
4*0528
METHANOL
19061SNRFNQREEh
75000
2984951
0
0
82800
2938078
XYLENE (MIXED ISOMER8)
10061 SNRFNQREEh
20000
257084
0
0
80700
52921*
ETH YLBENZENE
190618NRFNQREEH
2800
496418
0
0
8020
1087342
TOLUENE
1906l6NRFNQREEf
•MOO
5584932
0
0
101000
9024540
CHROMIUM COMPOUNDS
19061 SNRFNQREEh
9400
33332290
480
1737534
11180
3867*60*
ANTIMONY COMPOUNDS
19061 SNRFNQREEh
460
20389432
10880
482697652
11750
520817025
METHYL TERT-BUTYL ETHER
190618NRFNQREEI*
eseO
24487319
0
0
21100
74820352
BENZENE
19061 SNRFNQREEh
29000 1491087S1
0
0
03800
431387041
ETHYLENE OXIDE
19061 SNRFNQREEh
0
0
0
0
110400
1 •770990232
968920
17853002183H
page 12
-------
CHESTER COUNTY RISK PROJECT
TABLE 4-29
SUMMARY RANKING FOR
TOTAL ONSITE RELEASES
Facility Name
City
Total Onsita
Total Onaite
Total Onsita
Raaidual Maes
Chronic Index
Chronic Index and Reaidual Masa
Sums
Relative Hazard
Relative Hazard
28
PENNSYLVANIA MACHINE WORK
ASTON
0
0
0
27
PQCORP.
CHESTER
S
17730
17730
26
HYDRO. CHEMICAL CO.
YEADON
•10
54874
54874
25
CONGOLEUM CORP.
MARCUS HOOK
815
89003
89093
24
MCGEE INDUSTRIES INC.
ASTON
1780
197443
197443
23
HARCAST CO. NC.
CHESTER
103
365237
365237
22
ORB IND. INC.
UPLAND
2800
518108
518108
21
SENTRY PAINT TECH.
DARBY
10200
S77110
677110
20
CUSTOM COMPOUNDING INC.
ASTON
16528
586081
586081
19
ESSCHEM CO.
ESSJNGTON
2985
657116
657116
18
NORTH AMERICA SILICA
CHESTER
1700
0
865414
17
INTERNATIONAL ENVELOPE CO.
ASTON
11S78
1026386
1026386
16
CLIFTON PRECISION - N.
CLIFTON HEIGHTS
5880
1152446
1152446
15
BUCHAN IND.
CLIFTON HEIGHTS
•286
1716830
1716830
14
ZENITH PRODUCTS CORP.
ASTON
46000
2023430
2023430
13
CONCORD BEVERAGE CO.
CONCORDVtLLE
8045
0
2568245
12
PPG IND. INC.
FOLCROFT
1107
5107955
5107955
11
TRS ACQUISITION CORP.
CHESTER
3000
5318982
5318982
10
JULIAN B. SLEVIN CO. INC.
LANSOOWNE
108808
7869310
7869310
9
BULLEN COMPANIES
FOLCROFT
3000
13297456
13297456
8
TELEDYNE PACKAGING ¦
CHESTER
111288
21917162
21917162
7
BP EXPLORATION & OIL INC.
TRAINER
108883
31579565
31579565
6
EPSILON PRODS. CO.
MARCUS HOOK
70200
0
35736527
5
BOEING DEFENSE & SPACE GRC
RIDLEY PARK
184400
38308755
38308755
4
FOAM EX LP.
EDDYSTONE
33998
39795173
39795173
3
SCOTT PAPER CO.
CHESTER
243800
41593391
41593391
2
wrrco corp.
trainer
747045
8708446682
8708446682
1
SUN REFMNG & MAfWETNG CC
MARCUS HOOK
388858
17130461033
17130461033
KEY
(Mr MWfe
pmtmiUb
aonfitbne* limit
Ibooi vmtnurn an eantu»m»
>
6
-------
CHESTER RI8K PROJECT
TABLE 4-30
CHEMICALS OF POTENTIAL CONCERN IN AIR
CHEMICAL
VOLATILE
PARTICULATE
MATTER
CARCINOGEN
ENDPOINT
EVALUATED
NON-
CANCER
ENDPOINT
EVALUATED
arsenic
X
X
cadmium
X
X
chromium
X
X
hydrogen
chloride
¦
X
X
mercury
X
X
acrolein
X
X
acrylonitrile
X
X
benzene
X
X
'
1,3-butadiene
X
X
crotonaldehyde
X
/
X
diesel
X
X
formaldehyde
X
X
gasoline
X
X
2-
methoxyethano1
X
' ¦
X
vinyl chloride
X
X
-------
CUSTER RISK PROJECT
TABLE 4-31
CRITERIA POLLUTANTS AMD
HATXOHAL AMBIENT AIR QUALITY STANDARDS
CHEMICAL
NATIONAL AMBIENT AIR QUALITY
STANDARD (uq/m3)*
carbon monoxide
40,000 (l hour)**
carbon monoxide
10,000 (8 hours)**
lead
1.5 (quarter)***
nitrogen dioxide
100 (annual)***
ozone
235 (1 hour)****
PM-10
150 (24 hours)****
PM-10
50 (annual)*****
sulfur dioxide
1300 (3 hours)**
sulfur dioxide
365 (24 hours)**
sulfur dioxide
80 (annual)***
~Values represent primary standards — except for sulfur dioxide
(3 hours), which is a secondary standard.
**Standard is not to be exceeded more than once per year.
***Standard is never to be exceeded.
~~~•Standard is attained when the expected number of exceedances
is less than or equal to 1.
*****Standard is attained when the expected annual arithmetic
mean is less than or equal to SO uqfw.
-------
CHESTER RISK PROJECT
TABLE 4-32
MAXIMUM CARCINOGENIC RISKS IN AIR
CHEMICAL
MAXIMUM
PREDICTED
CONCENTRATION
(ug/m3)
RISK-BASED
LEVEL
(ug/m3)
CARCINOGENIC
RISK*
chromium VI
0.0047
0.00015
3E-05
benzene
2.8
0.22
1E-05
gasoline
0.19
5.10E-05
(ug/m3)-1**
9E-06
1,3-butadiene
0.044
0.0064
7E-06
cadmium
0.0067
0.00099
7E-06
arsenic
0.0022
0.00041
5E-06
diesel
0.24
1.70E-05
(ug/m3)'1**
4E-06
crotonaldehyde
0.012
0.0033
3E-06
acrylonitrile
0.042
0.026
2E-06
formaldehyde
0.30
0.14
2E-06
vinyl chloride
0.025
0.021
1E-06
~Value represents the maximum carcinogenic risk posed by an
individual chemical at a specific location.
**Value represents the unit risk for this compound.
-------
CHUTES SZ8X PROJECT
TABLE 4-33
MAXIMUM MOM-CAHCCR THREATS ZV AIR
CHEMICAL
MAXIMUM
PREDICTED
CONCENTRATION
(ug/a5)
RISK-BASED
LEVEL
(ug/n5)
HAZARD
QUOTIENT*
hydrogan chlorida
17
7.3
2.4
acrolein
0.33
0.021
1.6
2-methoxyathano1
19
21
0.9
mercury (inorganic)
0.061
0.31
0.2
~Value rapraaants the maximum non-cancer threat, aa pradictad by
the Hazard Quotient, poaad by an individual chemical at a
specific location.
-------
CHUTES RISK PROJECT
TABLE 4-34
MAXIMUM RATIO Of PREDICTED CONCENTRATIONS
07 CRITERIA POLLUTANTS TO
NATIONAL RUBIEST AIR QUALITY STANDARDS
CHEMICAL
MAXIMUM
PREDICTED
CONCENTRATION
(ug/m5)
NATIONAL
AMBIENT AIR
QUALITY
STANDARD
(ug/m3) *
RATIO**
carbon monoxide (l hour)
1960
40,000
0.05
carbon monoxide (8 hours)
675
10,000
0.07
lead (quarter)
0.11***
1.5
0.08
nitrogen dioxide (annual)
32
100
0.3
ozone (1 hour)
****
235
-
PM-10 (24 hours)
70
150
0.5
PM-10 (annual)
14
50
0.3
sulfur dioxide (3 hours)
372
1300
0.3
sulfur dioxide (24 hours)
170
365
0.5
sulfur dioxide (annual)
41
80
0.5
~Please refer to Table 4-31 for a detailed explanation of each
standard.
"Value represents the ratio between the maximum predicted
concentration and the National Ambient Air Quality Standard.
***The modeled concentration for lead represents an annual
average level, rather than a quarterly concentration. Although
the annual average level was compared to the quarterly standard
for lead, inaccuracies related to such a comparison are
insignificant in the context of this study.
****Ozone was not evaluated in the air modeling exercise.
-------
CHESTER RISK PROJECT
TABLE 4-35
RELATIVE CONTRIBUTIONS OF POINT SOURCES
TO L0N6 AND SHORT-TERM RISK
FROM ENVIRONMENTAL AIR POLLUTION
Source
Pollutants
Risk
PQ
28%
chromium, arsenic
Delcora
26%
metals
Sun
22%
organics
DuPont
10%
organics
Westinghouse
7%
metals
Other
8%
i
Itiak
es crita
rift pollutants*
DuPont
51%
2-Methoxyethanol, Acrolein
Westinghouse
31%
HC1
Crozer-Chester
7%
Mercury, HC1
Other
11%
1 / :
-------
TABLE 4-36. CAL3QHC predicted emissions concentrations under
the worst-case modeling conditions with and without the DCRRF
trucks. The concentration difference indicates the contribution due to
the trucks.
Intersection
Pollutant
Concentration (/ug/m3)
With Without
Trucks Trucks
Concentratio
- n Difference
(/ig/m3)
Second and
TOG
326
314
12
Jeffrey Streets
PM-10
9.6
3.6
6.0
Second and
TOG
265
253
12
Flower Streets
PM-10
7.2
3.6
3.6
-------
TABLE 4-37. Ten highest concentrations by receptor location from the
CAL3QHC model for the emissions of the existing traffic with the
DCRRF trucks.
TOG
PM-10
Cone.
Cone.
Location
(/ig/m3)
Location
(/ig/m3)
Second and Flower Streets
NW block at corner
326
NE block at corner
9.6
SE block at corner
289
NW block at corner
9.6
NE block at corner
241
SW block at corner
8.4
SW block at corner
229
SE block at corner
6.0
NE block 25 m E of corner
205
NE block 25 m E of corner
6.0
SW block 25m W of corner
193
NW block 25 m W of
6.0
corner
SE block 25 m E of corner
181
SW block 25 m W of
6.0
corner
NW block 25 m W of corner
181
SE block 25 m E of corner
6.0
NW block 50 m W of corner
145
NE block 50 m E of corner
6.0
SE block 50 m E of corner
145
NW block 50 m W of
6.0
corner
Second and Jeffrey Streets
SE block at corner
265
SW block at corner
7.2
NE block at corner
265
NE block at corner
7.2
NW block at corner
265
SE block at corner
6.0
SW block at corner
253
NW block at corner
6.0
NE block 25 m E of corner
253
SW block 25 m W of
6.0
corner
SW block 25 m W of corner
253
NE block 25 m E of corner
6.0
SE block 25 m E of corner
217
SE block 25 m E of corner
6.0
NW block 25 m W of corner
217
NW block 25 m W of
6.0
corner
, NW block 50 m W of corner
145
SW block 50 m W of
6.0
corner
-------
SE block 50 m E of corner 145 NE block 50 m E of corner 6.0
TABLE 4-38. ISCST2 predicted annual average hourly emissions
concentrations for 1991 with and without DCRRF trucks. The
concentration difference indicates the contribution due to the trucks.
Concentrations are reported for two cross sections showing the
concentration versus distance from Second Street.
Cross
Meters
Section with
Second
Street
North of
Second
Street
TOG Concentration (|ig/m3)
PM-10 Concentration (jig/m3)
With
Without
With
Without
Trucks
Trucks
Difference
Trucks
Trucks
Difference
600 m east
500
0.084
0.078
0.006
0.0089
0.0038
0.0051
, of Thurlow
Street
300
0.171
0.158
0.013
0.0187
0.0077
0.0109
100
0.560
0.514
,0.046
0.0638
0.0252
0.0386
11.5
1.517
1.386
0.131
0.1783
0.0678
0.1104
-11.5
1.411
1.286
0.124
0.1678
0.0630
0.1048
-100
0.473
0.432
0.041
0.0554
0.0212
0.0342
-300
0.138
0.127
0.011
0.0158
0.0062
0.0096
-500
0.067
0.062
0.005
0.0076
0.0030
0.0046
1,200 m east
500
0.116
0.109
0.007
0.0111
0.0053
0.0058
of Thurlow
Street
300
0.224
0.211
0.013
0.0213
0.0104
0.0109
100
0.734
0.692
0.042
0.0693
0.0339
0.0354
11.5
2.476
2.327
0.148
0.2403
0.1140
.0.1262
-11.5
2.236
2.102
0.134
0.2170
0.1030
0.1140
-100
0.599
0.563
0.037
0.0586
0.0276
0.0311
-300
0.173
0.162
0.011
0.0175
0.0079
0.0096
-500
0.090
0.083
0.006
0.0093
0.0041
0.0052
-------
TABLE 4-39. Six highest concentrations by receptor location from the
ISCST2 model for the emissions of the existing traffic with the DCRRF
trucks.
TOG
PM-10
Location
Concentration
(jig/m3)
Location
Concentration
(ng/m3)
I,400 m east of Thurlow,
II.5 m north of Second
2.57
I,200 m east of Thurlow,
II.5 m north of Second
0.24
I,200 m east of Thurlow,
II.5 m north of Second
2.48
400 m east of Thurlow, 11.5
m north of Second
0.22
I,400 m east of Thurlow,
II.5 m south of Second
2.30
I,000 m east of Thurlow,
II.5 m north of Second
0.22
I,200 m east of Thurlow,
II.5 m south of Second
2.24
I,200 m east of Thurlow,
II.5 m south of Second
0.22
I,000 m east of Thurlow,
II.5 m north of Second
2.15
400 m east of Thurlow, 11.5
m south of Second
0.20
I,600 m east of Thurlow,
II.5 m north of Second
2.04
I,000 m east of Thurlow,
II.5 m south of Second
0.20
-------
CHESTER RISK PROJECT
TECHNICAL SUPPORT DOCUMENT
EXTERNAL REVIEW DRAFT VERSION 1.0
LIST OF FIGURES
2-1 Map of the Study Area
4-1 Private Wells
4-2 Number of Private Wells
4-3 Sensitive Ground Water Areas in Relationship to Private
Wells
4-4 Risk Trade-Offs: Disinfection Byproducts vs. Microbial
Growth
4-5 Comparison of Risk Levels for Finished Water Supplies:
Lifetime Cancer Risks Based on Average Contaminant Levels
4-6 Comparison of Risk Levels for Finished Water Supplies:
Lifetime Non-Cancer Risk Estimates Based on Average
Contaminant Levels
4-7 Comparison of Risk Levels for Finished Water Supplies:
Lifetime Cancer Risk Estimates for THMs Based on Average
Levels Detected in 1993
4-8 Comparison of Risk Levels for Finished Water Supplies:
Lifetime Non-Cancer Risk Estimates for THMs Based on Average
Levels Detected in 1993
4-9 Comparison of Risk Levels for Finished Water Supplies:
Annual Cancer Risk Estimates Based on Average Contaminant
Levels
4-10 Comparison of Risk Levels for Finished Water Supplies:
Annual Non-Cancer Risk Estimates Based on Average
Contaminant Levels
4-11 Blood Lead in Children
4-12 Blood Lead in Children by Year
4-13 Trends in Children's Blood Lead
4-14 Distribution of Children's Blood Lead Predicted by the IEUBK
Model, Assuming That Residential Soil and Interior Dust
Contain 500 mg Pb/kg.
4-15 Distribution of Children's Blood Lead Predicted by the IEUBK
Model, Assuming That Residential Soil and Interior Dust
Contain 500 mg Pb/kg, Plus 130 ug Pb/day Intake.
4-16 Map of Children's Residence at Time of Blood Lead
Measurement
4-17 Average Blood lead Levels Plotted on 100 m2 Grid
4-18 Site-Related Hazard Index for Soil: Child Receptor
4-19 Site-Related Hazard Index for Soil: Adult Receptor
4-20 Site-Related Carcingenic Risk for Soil: Child Receptor
4-21 Site-Related Carcinogenic Risk for Soil: Adult Receptor
4-22 STORET Locations: Delaware County, PA
4-23 Cancer Risks: Surface Water, Sediment, and Fish Tissue
4-24 Noncancer Risks to Children: Surface Water, Sediment, and
Fish Tissue
4-25 Noncancer Risks to Adults: Surface Waer, Sediment, and Fish
Tissue
4-26 Chronic Index: EPA Region III On-Site Releases
4-27 Residual Mass: EPA Region III On-Site Releases
-------
4-28 Chronic Index and Residual Mass On-Site Releases
4-29 Upper Bound Lifetime Cancer Risk by Inhalation for VOCs
4-30 Upper Bound Lifetime Cancer Risk by Inhalation for Pip
4-31 Upper Bound Lifetime Cancer Risk by Inhalation for VOC and
PM
4-32 Non-Carcinogenic Hazard Index by Inhalation for VOCs
4-33 Non-Carcinogenic Hazard Index by Inhalation for PM
4-34 Non-Carcinogenic Hazard Index by Inhalation for VOC and PM
4-35 Criteria Air Pollutants
4-36 Estimated Area Emissions
4-37 Top Nine Area Emissions Blocks
4-38 Minority Distribution Overlay with Area Emissions
4-39 Annual Average HC Concentrations, Second Street 1200 m East
of Thurlow Street
4-40 Annual Average HC Concentrations, Second Street 600 m East
of Thurlow Street
4-41 Annual Average PM10 Concentrations, Second Street 1200 m
East of Thurlow Street
4-42 Annual Average PM10 Concentrations, Second Street 600 m East
of Thurlow Street
-------
15%
10%
15%
10%
15%
10%
5%
0%
15%
10%
5%
0%
15%
10%
5%
0%
Fig. 4-11. Chester Risk Project. Blood Lead in Children
1989
10 20 30 40 50 60 70 80 90 100
10 20 30 40 50 60 70 80 90 100
1992
10 20 30 40 50 60 70 80 90 100
1993 |
10 20 30 40 50 60
Blood Lead (pg/dL)
70 80 90 100
-------
Fig. 4-12. Chester Risk Project. Blood Lead in Children by Year j
100%
O)
iS
c
a>
o
2 40%
05
Q_
>10Mg/dL >15 pg/dL >25 (jg/dL >50 pg/dL
Children Above Blood Lead Level
60
[Fig. 4-13. Chester Risk Project. Trends in Children's Blood Lead]
50 ilr-
40
O)
to 30
m 20
10
1989
-A 90tn Percentile
— 95% Upper Conf. Limit
9 Geometric Mean
— 95% Lower Conf. Limit
~ 10th Percentile
1990
1991
Year
1992
1993
-------
Figure 4-14. Chester Risk Project. Distribution of children's blood lead predicted by the
IEUBK model, assuming that residential soil and interior dust contain 500 mg Pb/kg.
Figure 4-15. Chester Risk Project. Distribution of children's blood lead predicted by the
IEUBK model, assuming that residential soil and interior dust contain 500 mg Pb/kg,
plus 130 fig Pb/d additional intake. '
i £
m
i!
£
i £
m
= 5
tea
LCRD 0.99d
BLOOD LERD CONCENTRATION
0 to 84 Month*
-------
Annual Average HC Concentration
Second St 1,200 m East of Thurlow
-500
-400
-300
-200
-100 0 100
Distance North of Second St (meters)
200
300
400
500
With Trucks -E3- Without Trucks
FIGURE 4-39 . Annual average HC concentrations, Second Street 1,200 m east of Thurlow Street.
-------
Annual Average HC Concentration
Second St 600 m East of Thurlow
Distance North of Second St (meters)
With Trucks -E3- Without Trucks
figure 4-40 Annual average HC concentrations, Second Street 600 m east of Thurlow Street.
-------
Annual Average PM10 Concentration
Second St 1,200 m East of Thurlow
0.25-
r
\
/
\
/ 171
A
Yv
_ 0.2-
w.
a>
©
E
o
5
3
O
E
ca
w
O)
0
b
1
c
o
to
S
03
O
s
o
0.15
0.1
0.05-
-500 -400 -300 -200 -100 0 100 200
Distance North of Second St (meters)
300
400
500
With Trucks
Without Trucks
figure 4-41 Annual average PM10 concentrations, Second Street 1,200 m east of Thurlow Street.
-------
Annual Average PM10 Concentration
Second St 600 m East of Thurlow
0.25
m
-------
CHESTER RISK PROJECT
TECHNICAL SUPPORT DOCUMENT
EXTERNAL REVIEW DRAFT VERSION 1.0
LIST OF REFERENCES
Amdur, M.O., Doull, J. and Klaassen, C.D., Editors, 1993.
Casarett and Doull's Toxicology, The Basic Science of Poisons.
Fourth Edition. McGraw-Hill, Inc., NY.
BP Oil Groundwater Quality Data. February 1994.
Calabrese, E.J., Gilbert, C.E., and H. Pastides, (Editors),
•1989. Safe Drinking Water Act: Amendments, Regulations and
Standards. Lewis Publishers, Chelsea.
Doull, J., C.D. Klaassen, and M.O. Amdur, 1986. Casarett and
Doull's Toxicology: The Basic Science of Poisons. Third Edition.
MacMillan Publishing Company, New York.
Energy and Natural Resources (ENR), 1988. A Total Exposure and
Risk Assessment for Drinking Water Contaminated with Volatile
Organic Compounds. ILENR/RE-AQ-87/22. November.
Foster, S.A. and P.c. Chrostowski, 1987. Inhalation Exposures to
Volatile Organic Contaminants in the Shower. ICF Clement
Associates, Washington, D.C. For Presentation at the 80th Annual
Meeting of APCA (The Association Dedicated to Air Pollution
Control and Hazardous Waste Management), New York, June 21-26.
Gross, 1994. Personal Communication: June 1994. Carol Ann
Gross. U.S. EPA. Region 3. Water Division.
Hall, G.M, 1934. 3rd printing, 1973. Ground Water in
Southeastern Pennsylvania. 255p., 7 pis., geol. map, scale
1:380,160.
Hawley, Gessner G. 1981. The Condensed Chemical Dictionary.
Tenth Edition. Van Nostrand Reinhold Co., New York.
Howard, P.H., 1989. Handbook of Environmental Fate and Exposure
Data for Organic Chemicals. Volume 1. Lewis Publishers,
Chelsea.
Layton, D.W., et al, 1987. Deriving allowable daily intakes for
systemic toxicants lacking chronic toxicity data. Regulatory
Toxicology and Pharmacology 7:96-112.
Lewis, Richard J., Sr., 1992. Sax's Dangerous Properties of
Industrial Materials. Eighth Edition. Van Nostrand Reinhold
Co., New York.
National Toxicology Program (NTP) Report #TR-267.
-------
Olson, E.D., 1993. Natural Resources Defense Council. Think
Before You Drink. The Failure of the Nation's Drinking Water
System to Protect Public Health. September.
Pennsylvania Department of Environmental Resources (PADER), April
1994. Commonwealth of Pennsylvania 1994 Water Quality
Assessment; 305(b) Report. Bureau of Water Quality Management.
PECO RCRA Facility Investigation Work Plan. April 1994.
Rice, 1993. Personal communication: March 1993. Eugene Rice,
Ph.D. USEPA Headquarters. Microbiological Treatment Branch.-
Rundell, 1994. Personal Communication: October 1994. Bruce
Rundell. U.S. EPA. Region 3. Hydrogeologist, Superfund Branch,
Technical Support Section.
Sax, N.I. and R.J. Lewis, Sr., 1989. Dangerous Properties of
Industrial Materials. Seventh Edition. Van Nostrand Reinhold
Co., New York.
Sittig, M., 1985. Handbook of Toxic and Hazardous Chemicals and
Carcinogens. Second Edition. Noyes Publications, Park Ridge,
New Jersey.
Sittig, Marshall, 1991. Handbook of Toxic and Hazardous
Chemicals and Carcinogens. Third Edition. Noyes Publications,
Park Ridge, New Jersey.
States 305(b) Water Quality Reports. 1989-1991. Delaware,
District of Columbia, Maryland, Pennsylvania, Virginia and West
Virginia.
Sun Oil Refinery Work Plan. September 1993.
Traffic Planning and Design, 1991. Delaware County Resource
Recovery Facility Chester, Delaware County Traffic Generation
Study. Memorandum from Kevin L. Johnson to Fred N. Stefany,
Westinghouse Electric Corporation, January 28, 1991.
United States Department of Commerce (USDOC), 1990. Economic and
Statistics Administration. Bureau of the Census. Summary Tape
File 3 on CD-ROM.
United States Drinking Water Standards Division (USDWD), 1991.
Final Draft for the Drinking Water Criteria Document on Radon.
Office of Ground Water and Drinking Water. Office of Water.
ICAIR Program No. 1524. June 14, 1991.
United States Environmental Protection Agency (USEPA), 1986a.
Superfund Public Health Evaluation Manual * EPA 540/1-86/060.
Office of Emergency and Remedial Response, Washington, D.C.
USEPA, 1986b. Pesticides in Ground Water: Background Document.
-------
EPA 440/6-86-002. May.
USEPA, 1989a. Risk Assessment Guidance for Superfund. Volume I:
Human Health Evaluation Manual. Interim Final. Office of
Emergency and Remedial Response, Washington, D.C. December.
USEPA, 1989b. Exposure Factors Handbook.. Office of Health and
Environmental Assessment, Washington, D.C. EPA/600/8-89/043.
May.
USEPA, 1989c. Health Effects Assessment Summary Tables (HEAST).
Office of Emergency and Remedial Response, Washington, D.C.
USEPA, 1989d. Surface Water Treatment Rule. 54 Federal
Register. June 29.
USEPA, 1990a. Health Effects Assessment Summary Tables (HEAST).
Office of Emergency and Remedial Response, Washington, D.C.
USEPA, 1990b. Drinking Water Quantification of Toxicologic
Effects for Methyl Tertiary-Butyl Ether (MTBE). Environmental
Criteria and Assessment Office, Cincinnati, OH, prepared for
Office of Drinking Water, ECAO-CIN-D023.
USEPA, 1990c. RCRA Orientation Manual. EPA 530-SW-90-036.
USEPA, 1991a. Human Health Evaluation Manual, Supplemental
Guidance: Standard Default Exposure Factors. Office of Emergency
and Remedial Response, Washington, D.C. OSWER Directive 9285.6-
03. March.
USEPA, 1991b. Lead and Copper Rule. 56 Federal Register 26460-
26564. June 7.
USEPA, 1991c. National Primary Drinking Water Regulations;
Radionuclides; Proposed Rule. Part II. 56 Federal Register
33050-33127. July 18.
USEPA, 1991d. Procedures for the Preparation of Emission
Inventories for Carbon Monoxide and Precursors of Ozone. Volume
I: General Guidance for Stationary Sources. EPA 450/4-91-016.
May 1991.
USEPA, 1991e. RCRA Prioritization System Scoring Summary. July.
USEPA, 1992a. Dermal Exposure Assessment: Principles and
Applications. Interim Report. Office of Health and
Environmental Assesment, Washington, D.C. EPA/600/8-91/011/B.
January.
USEPA, 1992b. National Study of Chemical Residues in Fish.
Office of Science and Technology, Washington, D.C. EPA 823-R-92-
008. September.
-------
USEPA, 1993a. Total Coliform Rule. Learner's Guide for Public
Water Supply System Regulatory and Health Officials.
USEPA, 1993b. Health Effects Assessment Summary Tables (HEAST),
Annual Update. Office of Emergency and Remedial Response,
Washington, D.C. EPA/540-9-93/058. March.
USEPA, 1993c. Motor Vehicle-Related Air Toxics Study. EPA 420-
R-93-005. April.
USEPA, 1993d. Chemical Indexing System for the Toxic Chemical
Release Inventory Part I: Chronic Index. EPA/903/R-93/002.
USEPA, 1994a. Health Effects Assessment Summary Tables (HEAST).
Office of Emergency and Remedial Response, Washington, D.C.
USEPA, 1994b. Region III Risk-Based Concentration Table, First
Quarter 1994.
USEPA, 1994c. Integrated Risk Information System (IRIS)
Database.
USEPA, 1994d. Drinking Water Regulations and Health Advisories.
Office of Water. May.
USEPA, 1994e. National Primary Drinking Water Regulations;
Disinfectants and Disinfection Byproducts. 59 Federal Register
34320-34325. July 29.
USEPA, 1994f. Integrated Exposure Uptake Biokinetic Model for
Lead in Children. Office of Emergency and Remedial Response,
Washington, D.C.
USEPA, 1994g. Comprehensive Environmental Response,
Compensation, and Liability Information System (CERCLIS)
Database.
USEPA, 1994h. STORET Database, Retrievals 4/13/94, 5/10/94, and
5/25/94. Research Triangle Park, N.C.
United States Geological Survey (USGS), 1989. Selected Ground-
Water Data, Chester County, PA. Open-file Report 87-217.
USGS, 1992. Are Fertilizers and Pesticides in the Ground Water?
A Case Study of the Delmarva Peninsula, Delaware, Maryland, and
Virginia. Circular 1080.
USGS, 1993. Pesticides in Shallow Ground Water in the Delmarva
Peninsula. Unpublished Draft Report, March.
Valley Forge Laboratories, 1985. Traffic Impact Study. Exhibit
1 of Solid Waste Permit Application submitted to Pennsylvania
Department of Environmental Resources, June 1985.
-------
Versar, Inc. for United States Environmental Protection Agency.
1979. Water-Related Fate of 129 Priority Pollutants. Monitoring
and Data Support Division, Washington, D.C. EPA 440/4-79-029.
Verschueren, K. 1983. Handbook of Environmental Data on Organic
Chemicals. Second Edition. Van Nostrand Reinhold Co., New York.
Weber, 1993. Personal Communication: March 1993. Pete Weber.
U.S. EPA. Region 3. Maryland Program Manager for Ground Water
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Resource Recovery Facility, Pre-dperational Noise Monitoring
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February.
Westinghouse Electric Corporation, 1993. Delaware County
Resource Recovery Facility, Noise Report Summary. October.
-------
APPENDIX I
TOXICOLOGICAL PROFILES
-------
ACIDS
Acids- (pH < 7) are generally noted for their ability to burn skin
and mucous membranes. Effects are more severe at very low pH;
near the neutral 7, effects are typically negligible. Strong
acids can burn and corrode the skin. When present in the air,
acids can irritate the respiratory tract.
ACROLEIN
Acrolein is used as an herbicide and slimicide, and in the
synthesis of many chemicals (Sittig, 1991)'. Acrolein is a highly
toxic irritant to the skin, eyes, and respiratory tract, and can
cause pulmonary edema after high-level inhalation exposure
(Sittig, 1991; Lewis, 1992). Acrolein is classified as a Group C
(possible) human carcinogen by USEPA.
ACRYLONITRILE
Acrylonitrile, also known as vinyl cyanide, is used in the
manufacture of synthetic materials and as a pesticide (Sittig,
1991).
Acrylonitrile may be absorbed through the skin as well as via the
oral and inhalation routes. -Toxic effects are similar to those
of cyanide poisoning. Reddening and blistering of the skin,
dizziness, cyanosis, and convulsions may occur. Target organs
include th§ central nervous system, cardiovascular system, liver,
kidneys, and skin (Sittig, 1991).
Acrylonitrile is classified as a Group B1 (probable) human
carcinogen by USEPA, based on lung cancer in industrial workers
and brain cancer in rats.
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ALUMINUM
Aluminum is a common, virtually ubiquitous element. This metal
has been used in smelting,,refining, electrical, aircraft,
automotive, jewelry, petroleum processing, and rubber industries
(Sittig, 1985). Aluminum foil is widely used in packaging.
Aluminum is not generally noted for toxicity. Some aluminum
salts have been associated with skin and respiratory irritation.
Inhalation of aluminum powder has been reported to cause
pulmonary fibrosis. Some studies have suggested a link between
aluminum exposure and Alzheimer's disease. (Sax, 1989; Sittig,
1985)
Aluminum has not been classified as a carcinogen by USEPA.
ANTIMONY
Antimony has been used in mining, smelting, refining, and alloy
abrasive manufacture. Antimony has also been used in ammunition,
batteries, pigments, plasticizers, glass, enamels, pottery,
pharmaceuticals, and explosives (Sittig, 1985).
Antimony compounds can cause skin irritation. Acute oral
ingestion of antimony can produce extreme irritation of the
gastrointestinal tract, and in extreme cases, circulatory or
respiratory, failure. Chronic oral toxicity may be associated
with dry throat, nausea, and anorexia. Other target organs
include the liver and kidney. Antimony has not been classified as
a carcinogen.
ARSENIC
Arsenic has been used by the agricultural, pigment, glass, and
metal smelting industries. Arsenic is a ubiquitous metalloid
element. Acute ingestion of arsenic can be associated with
damage to mucous membranes including irritation, vesicle
formation, and sloughing. Arsenic can also be associated with
sensory loss in the peripheral nervous system and anemia. Liver
injury is characteristic of chronic exposure. Effects of arsenic
on the skin can include hyperpigmentation, hyperkeratosis, and
skin cancer. (Doull et al, 1986)
USEPA classifies arsenic in drinking water as a Group A known
oral human carcinogen.
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BARIUM
Barium has been used in metal alloys. Barium compounds have also
been used in the manufacture of rubber, paints, glass, paper, and
linoleum. Barium compounds can be found in valves, X-ray
diagnostics, and rodenticides (Sittig, 1985). Barium is
relatively abundant in nature (Doull et al, 1986).
Some barium compounds are insoluble and are not absorbed by the
gastrointestinal tract. However, ingestion of soluble barium
compounds can affect the muscles, especially smooth muscles.
Symptoms of such toxixity include gastroenteritis, muscle
paralysis, and central nervous system effects. In severe
toxicity, cardiac arrest can result. Barium is not classified as
a carcinogen by USEPA.
BENZENE
Benzene is an aromatic hydrocarbon. It is associated with
gasoline and has been used as a solvent in many industries,
including the printing, plastics, and rubber industries.
Exposure to benzene may be associated with effects on the central
nervous system (headache, dizziness), respiratory system
(irritation), blood (aplastic anemia, anemia, leukemia), and skin
(dermatitis) (Sittig, 1985). Gastrointestinal irritation has
also been reported.
EPA has classified benzene as a Group A known human carcinogen.
This is based on an increased incidence of leukemia in exposed
workers and neoplasia in rats.
BERYLLIUM
Beryllium is used in alloys as well as X-ray and nuclear
applications. The major source of beryllium exposure of the
general population is from the combustion of coal and oil. (Doull
et al, 1986)
Adverse effects can include respiratory effects (after inhalation
exposure) or contact dermatitis. Other target organs include the
liver, spleen, and heart (Sittig, 1985). Beryllium is classified
by USEPA as a Group B2 probable human carcinogen via the oral and
inhalation routes.
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1,3-BUTADIENE
1,3-Butadiene has been most widely used in rubber manufacturing,
but its uses in other industries such as plastics and resins are
growing (Sittig, 1991). 1,3-Butadiene may act as a central
nervous system depressant (causing narcotic effects)., an
asphyxiant (causing suffocation), and as an irritant (causing
skin burns). It is classified as a Group B2 (probable) human
carcinogen by the USEPA.
CADMIUM
Major sources of environmental cadmium contamination include
sewage sludge and emissions from smelting. Cadmium has also been
used in plating, pigments, and batteries. As an environmental
contaminant, it is virtually ubiquitous.
Acute cadmium toxicity can be associated with gastrointestinal
distress. Inhalation of cadmium can produce chemical pneumonitis
and pulmonary edema. The principal effects of chronic exposure
include kidney disease and effects on the cardiovascular and
skeletal systems. (Doull et al, 1986)
USEPA classifies cadmium compounds as Group B1 probable human
carcinogens via inhalation exposure.
CARBON TETRACHLORIDE
Carbon.tetrachloride is a common solvent that has been used
extensively in the dry cleaning industry (Sittig, 1985).
Carbon tetrachloride can be irritating to the skin and eyes.
Carbon tetrachloride also depresses the central nervous system,
and symptoms such as dizziness, headache, and loss of
coordination may occur. Other symptoms may include nausea and
vomiting (Sittig, 1985). Chronic exposures have been shown to
cause liver and kidney damage. Alcohol is reported to act
synergistically with carbon tetrachloride.
EPA has classified carbon tetrachloride as a Group B2 probable
human carcinogen.
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CHLORDANE
Chlordane is an insecticide that has been extensively used for
termite control, but it has been banned in the United States.
Chlordane affects the nervous system, and toxic effects can
include ataxia, tremors, and'convulsions. Liver toxicity may
also be associated with chronic exposure. Chlordane is a
lipophilic, persistent compound that, like DDT, can
bioconcentrate significantly. Chlordane is often detected in
conjunction with heptachlor; heptachlor can be a component of
technical grade chlordane. Chlordane is classified by USEPA as a
Group B2 probable human carcinogen (Sittig, 1985; Sax, 1989).
CHLOROFORM
Chloroform has been used as an anesthetic, although this use has
been discontinued. Chloroform has been used as a solvent by a
variety of industries. Chloroform is a common contaminant of
public water supplies where it is formed by the interaction of
chlorine and naturally occurring organic compounds (Sittig,
1985) .
Chloroform can affect the liver, heart, and nervous system. The
gastrointestinal system can also be affected.. Symptoms of
exposure can include dizziness, nausea, and skin irritation.
Chloroform is classified a Group B2 probable human carcinogen by
EPA.
CHROMIUM
Two forms of chromium, the hexavalent (Cr6+) and trivalent (Cr3+)
forms, are considered to have the greatest biological
significance. Trivalent is the more common form, but hexavalent
compounds have greater industrial importance. Chromium compounds
are associated "with the chrome plating and metal finishing
industries, textile plants, tanneries, and wood preservatives.
Hexavalent chromium is more toxic and mobile than trivalent
chromium. Effects of chromium exposure include dermatitis and
acute renal tubular necrosis, skin irritation and dermatitis.
Trivalent compounds are considerably less toxic and are neither
irritating nor corrosive. Inhalation exposure to chromium has
been associated with respiratory carcinomas. (Doull et al, 1986)
Hexavalent chromium is considered to be a Group A known human
carcinogen by inhalation, according to USEPA.
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COAL TAR (CREOSOTE)
Coal tar compounds are derived from the carbonization of
bituminous coal. Such emissions can occur from coke ovens,
foundries, metal industries, etc. (Sittig, 1991). In studying
the toxic effects of these chemicals, attention has primarily
been focused on their cancer-causing potential. USEPA classifies
coke oven emissions as a Group A (known) human carcinogen, and
creosote as a Group B1 (probable, includes some evidence in
humans) human carcinogen.
COPPER
Copper is a common and essential element. It has been used in
the electrical industry and in piping, alloys, pesticides,
catalysts, paints, and electroplating (Sittig, 1985).
Copper sulfate has been used as an emetic, and ingestion of
excessive amounts of copper salts can produce gastorintestinal
distress. Copper poisoning can produce hemolytic anemia. Dermal
contact with copper may be associated with dermatitis. (Doull et
al, 1986)
Copper has not been classified as a carcinogen by USEPA.
CROTONALDEHYDE
Crotonaldehyde has been used in resin and rubber manufacturing
and has varied uses as a solvent; It is similar to acrolein
(q.v.), though slightly .less toxic. Irritant effects,
gastrointestinal distress, and respiratory effects have been
noted (Sittig, 1991). Crotonaldehyde is classified as a Group C
(possible) human carcinogen by USEPA.
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DDT, DDD AND DDE
4,4'-DDT is an insecticide that has been banned in the United
States since 1972. 4,4'-DDT and its metabolites, 4,4'-DDD and
4,4'-DDE, are toxicants with long-term persistence in soil and
water. Their high lipophilicity and low water solubility result
in concentrated accumulation in the fat of wildlife and humans
(Sittig, 1985) . Thinning of eagle and osprey eggshells led to
population declines for those birds (Doull et al, 1986).
Because of the persistence and dispersion of DDT compounds, they
are therefore widespread environmental contaminants. Toxic
effects to humans include convulsions, vomiting, and skin
irritation. The target organs are the central nervous system,
liver, kidneys, skin, and peripheral nervous system (Sittig,
1985). Experimental ingestion of 1.5 g of 4,4'-DDT resulted in
discomfort, moderate neurological changes, and vomiting (Sax,
1989) .
4, 4'-DDT, 4", 4'-DDD, and 4 , 4 '-DDE are classified as oral Group B2
probable human carcinogens. 4,4'-DDT is also classified as an
inhalation Group B2 carcinogen.
DIELDRIN
Dieldrin is a chlorinated hydrocarbon insecticide that is
currently banned in the United States. It was used to control
corn and citrus pests (Sittig, 1985).
Dieldrin has low volatility and low water solubility, which
contribute to its persistence, and has a high affinity for fat,
which results in a tendency to bioaccumulate. Dieldrin can
affect the central nervous system, liver, kidneys, and skin.
Symptoms can include dizziness, nausea, convulsions, and coma
(Sittig, 1985) .
Dieldrin is classified by USEPA as a Group B2 probable human
carcinogen via the oral and inhalation routes.
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2,3,7,8-TCDD, DIOXINS, AND FURANS
/
Chlorinated dioxins and furans are typically evaluated in terms
of their congeners that are chlorinated in the 2,3,7,8-
positions. 2,3,7,8-Tetrachloro-p-dibenzodioxin (2,3,7,8-TCDD) is
the best known. These chemicals are inadvertent contaminants in
the manufacturing process of chlorinated phenols, and may be
found in trace amounts in pesticides. For this reason, trace
amounts of dioxins are widespread in the environment (Sittig,
1991) .
Chlorinated dioxins and furans can affect the skin (notably with
a distinctive rash called chloracne), nervous system, liver,
pancreas, and reproductive system. These compounds are extremely
persistent, difficult to break down, and tend to bioaccumulate in
living organisms (Sittig, 1991).
USEPA classifies 2,3,7,8-TCDD as a Group B2 (probable human)
carcinogen.
ETHYLENE
Ethylene has many industrial uses in manufacturing. It has been
used as a fruit ripener, and as an anesthetic (Sittig, 1991).
Toxic effects of ethylene include "freezing burns" of the skin,
depression of the central nervous system, and inflammation of the
kidney. The liver is also reported to be a target organ (Sittig,
1991).
ETHYLENE GLYCOL
Ethylene glycol is used as a solvent and a chemical intermediate.
It is also used in heat exchangers, and perhaps its best-known
use is as an antifreeze (Sittig, 1991).
Ethylene glycol is a mild irritant. Ingestion of this chemical
has produced nausea and vomiting, depression of the central
nervous system, and kidney failure as a delayed effect (Sittig,
1991). '
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ETHYLENE OXIDE
Ethylene oxide is used in the plastics industry, as a fumigant,
and as a sterilizing agent. High-level exposure can produce
respiratory system effects such as dyspnea, pneumonia, and
pulmonary edema. Other target organs include the central nervous
system and liver. Nausea, vomiting, cardiac arrhythmias, and
irritant effects have also been reported (Sittig, 1991).
HEPTACHLOR, HEPTACHLOR EPOXIDE
Heptachlor is an insecticide closely related to chlordane. It
has been banned in the United States except for external,
subsurface application to dwellings for termite control (Sax,
1992). Heptachlor epoxide is a degradation product of heptachlor
that also acts as a pesticide (Hawley, 1981).
Heptachlor is a persistent organochlorine pesticide, like DDT.
Acute symptoms of toxicity can involve tremors, convulsions,
kidney damate, and respiratory collapse. In man, a dose of 1 to
3 g can cause serious symptoms (Sax, 1992).
Both heptachlor and heptachlor epoxide are classified as Group B2
(probable human) carcinogens by USEPA via the oral and inhalation
routes.
FLUORIDES
Fluorides are used in many industries, including the chemical
industry. Uses range from fluoridation of drinking water to
application as a pesticide (Sittig, 1991).
Fluoride toxicity typically manifests itself through nausea,
vomiting, and effects on the bones and teeth. Such effects are
not expected from the low levels used in drinking water. When
inhaled, fluorides can irritate the respiratory tract (Sittig,
1991).
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FORMALDEHYDE
Formaldehyde has been used in many industries. Its uses include
as a fungicide, disinfectant, and preservative (Sittig, 1991).
Formaldehyde can cause respiratory irritation, pneumonia, and
pulmonary edema at high levels. Nausea, vomiting and diarrhea,
nephritis, and liver toxicity have also been reported. It is
possible for allergies to formaldehyde to develop (Sittig, 1991).
Formaldehyde is classified by USEPA as a Group B1 (probable)
human carcinogen.
GASOLINE
Gasoline is a highly flammable solvent. It is commonly used as a
fuel. The composition may vary, but common components include
benzene compounds (q.v.) and alkanes (Sittig, 1991).
Gasoline may cuase respiratory irritation, drowsiness, nausea,
and numbness following inhalation. The component hexane has been
associated with nerve damage, and benzene has been associated
with hematopoietic effects such as anemia. Tetraethyl lead
(q.v.) has also been a component of some gasoline formulas. The
liver is another target organ for gasoline (Sittig, 1991).
HYDROGEN CHLORIDE
This chemical has a wide variety of uses, both as hydrogen
chloride and in the form of aqueQus solutions (hydrochloric or
muriatic acid). Hydrochloric acid is also found as a digestive
agent in the gastrointestinal tract. The most notable toxic
effect is its ability to burn and corrode tissue. In the air,
hydrogen chloride can cause respiratory irritation and pulmonary
edema. Via the oral route, effects such as nausea and kidney
inflammation are possible (Sittig, 1991).
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MANGANESE
Manganese is used in the manufacture of dry cell batteries,
paints, dyes, and in the chemical and glass and ceramics
industries. Manganese is an essential nutrient in in food; the
average human intake is reported to be approximately 10 mg/day
(Sittig, 1985).
Previous reports of neurotoxicity from manganese were generally
reported from high-level occupational exposure to dust and fumes.
More recent studies have focused on exposures to drinking water,
with subtle neurologic effects being reported after chronic
consumption of high concentrations of manganese in water (Sittig,
1985; USEPA, 1994c).
Manganese is not classified as a carcinogen by USEPA.
MERCURY
Mercury has historically been linked to, mining, smelting, paper
pulp, electrical, chemical, pharmaceutical, and pesticide
industries. Inorganic mercury is used in metal plating, tanning,
feltmaking, taxidermy, and photography. Mercury may also be
emitted from burning coal and natural gas and refining petroleum
products.
Inhalation of mercury vapor can cause excitability, tremors, and
gingivitis; upon acute exposure, corrosive bronchitis may occur.
Ingestion of inorganic mercury compounds has resulted in
corrosion of the gastrointestinal tract and renal failure (severe
acute exposure, often seen with accidental or suicidal ingestioon
of mercuric salts) . Vasodilation and rashes have been associated
with exposure to mercurous compounds. The major clinical
features of organic mercury poisoning are paresthesia, ataxia,
dysarthria, and deafness, resulting from neurologic damage.
(Doull et al, 1986)
USEPA classifies mercury and its compounds as Group D, not
classifiable as to carcinogenicity.
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2-METHOXYETHANOL
2-Methoxyethanol is an ethylene glycol ether. It is used as a
solvent in resin and paint manufacturing and as a constituent of
soaps and cleaners (Sittig, 1991).
2-Mehtoxyethanol is a mild irritant both to the skin and
respiratory tract, Ingestion of this chemical can affect the
brain, liver, and kidney. Anemia is another reported effect
(Sittig, 1991).
METHYLENE CHLORIDE (DICHLOROMETHANE)
Methylene chloride, also known as dichloromethane, is a volatile
solvent and common laboratory contaminant. Like many volatile
solvents, methylene chloride can affect the nervous system,
especially after inhalation exposure. Potential effects include
dizziness, numbness, eye and skin irritation, and cardiac
effects.
Methylene chloride is classified by the EPA as a Group B2
(probable human) carcinogen via the oral and inhalation routes of
exposure.
MIREX
Mirex is an organochlorine insecticide that is especially .
effective against fire ants. It has also been used as a fire
retardant in plastics (Sittig, 1991).
Like other organochlorine pesticides, mirex can affect the skin
(irritation), gastrointestinal system, nervous system, liver, and
reproductive system. Organochlorine pesticides are persistent in
the environment, tending to accumulate in fatty tissues (Sittig,
1991).
USEPA has classified mirex as a Group B2 (probable human)
carcinogen.
NICKEL
Nickel is a metal that has been associated with ore refining,
stainless, steel, electroplating, jewelry, plastics, batteries,
enamels, coal oils, and a variety of other industries.
Nickel, a skin sensitizer, can cause dermatitis. The kidney and
circulatory system may also be potential target organs. Nickel
has not been classified as a carcinogen by USEPA.
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t-NONACHLOR
t-Nonachlor is the major constituent of technical chlordane and
technical heptachlor (q.v.).
PENTACHLOROANISOLE
Pentachloroanisole is a*chlorinated hydrocarbon pesticide. It
also occurs as a metabolite of the pesticides pentachlorophenol,
pentachloronitrobenzene, and hexachlorobenzene. Reproductive
effects have been reported in experimental studies (Lewis, 1992).
POLYCHLORINATED. BIPHENYLS (AROCLORS)
Polychlorinated biphenyls (PCBs) have been.used widely as
insulators in transformers and capacitors. Other uses have
included carbonless duplicating paper, plasticizers, adhesives,
and hydraulic fluids. PCBs may be contaminants of waste oils.
Dermal contact with PCBs can result in chloracne, a form of
severe dermatitis. Effects upon the liver can also be
significant, involving jaundice, edema, and nausea. Target
organs include the skin, eyes, and liver (Sittig, 1985). PCBs
are also noted for their extreme tendency to bioaccumulate in fat
tissue (Versar, 1979).
USEPA classifies PCBs as Group B2 (probable human) carcinogens,
. based on hepatocellular carcinomas in rats and mice (Aroclor
1260) and limited evidence of liver cancer in humans.
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POLYCYLIC AROMATIC HYDROCARBONS
Polycyclic aromatic hydrocarbons (PAHs), also called polynuclear
aromatic hydrocarbons, are compounds that consist of annelated
aromatic rings. They are found in coal, tar, tobacco smoke, and
petroleum, and occur as products of the combustion of organic
material (Doull et al, 1986). PAHs can be formed in any
hydrocarbon combustion process and may be released from oil
spills (Sittig, 1985). This group of compounds includes
phenanthrene, fluoranthene, pyrene, benz[a]anthracene, chrysene,
benzo[b] f luoranthene, behzo[a]pyrene (q.v-.), indeno[ 1, 2 , 3-
c,d]pyrene, dibenz[a,h]anthracene, benzo[g,h,i]perylene,
naphthalene, acenaphthylene, acenaphthene, dibenzofuran,
fluorene, anthracene, benzo[k]fluoranthene, and carbazole.
Naphthalene is an irritant that can cause dermatitis, toxic
effects on the red blood cells, liver, kidneys, and central
nervous system. Damage to the lenses of the eyes has also been
reported.
Benzo[a]pyrene, benz[a]anthracene, benzo[b]fluoranthene,
indeno[1,2,3-c,d]pyrene, dibenz[a,h]anthracene,
benzo[g,h,i]perylene, benzo[k]fluoranthene, and carbazole have
been classified by USEPA as Group B2 probable human carcinogens.
BENZO[A]PYRENE
Benzo[a]pyrene is a polycyclic aromatic hydrocarbon (PAH) that is
found in coal tar, oil, asphalt, and other petroleum products.
It can also form from the incomplete combustion of organic
material.
Dermal.irritation upon contact with high concentrations of PAHs
has been reported. Benzo[a]pyrene has produced tumors in all
species tested by both the oral and dermal route of application
(Sittig-, 1985) . USEPA classifies benzo [a] pyrene as a Group B2
probable human carcinogen. The toxicity of PAHs is often
expressed in terms of equivalents to benzo[a]pyrene.
PROPYLENE
Propylene is a component of gasoline and is used in resin and
alcohol manufacturing, among other industrial uses. Its primary
effect in the air is as an asphyxiant, causing displacement of
oxygen. Contact with the pure liquid can produce a "frostbite"
effect. Target organs also include the heart and liver (Sittig,
1991) .
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SELENIUM
Selenium is used as a pigment in paints, dyes; and glass. It is
also used in the rubber, insecticide, and photographic
industries, and is an additive in anti-dandruff shampoos.
Elemental selenium is relatively nontoxic. However, compounds
such as selenium dioxide and selenium oxychloride can be
irritating to the eyes, mucous membranes, and respiratory tract.
Symptoms of selenium exposure include gastrointestinal and
central nervous system effects. Target organs include the upper
respiratory system, eyes, skin, liver, kidneys, and blood
(Sittig, 1985).
Selenium is classified as USEPA's Group D, not classifiable as to
carcinogenicity.
SILVER
Silver is used in the manufacture of silverware, jewelry,
scientific instruments, photographic films, plates, and paper,
and mirrors. The main adverse effect of silver exposure derives
from the deposition of silver particles in the skin, which causes
a pigmentation called argyria. Silver nitrate can be an
irritant. Silver tends to accumulate in the body and is not
readily excreted (Sittig, 1985).
TETRACHLOROETHENE
Tetrachloroethene (PCE), also known as perchloroethylene, is a
commonly used solvent in the dry cleaning, degreasing, and
textile industries. It is also used as an intermediate in the
manufacture of organic chemicals (Sittig, 1985).
Irritation of the skin can occur after dermal exposure. High-
level inhalation exposure can cause respiratory and eye
irritation. Other effects include CNS depression and liver
damage (Sax, 1989).
EPA ECAO classifies PCE as a Group B2 probable human carcinogen,
although this is not considered Agency-wide consensus at this
time.
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VANADIUM
Vanadium is a ubiquitous element. It has been associated with
petroleum refining, steel industries, pigments, glass
manufacturing, photography, and insecticides.
Toxicity is usually reported after industrial inhalation
exposure, which can be associated with bronchitis,
bronchopneumonia, irritation, gastrointestinal distress, heart
palpitations, and kidney damage. Ingestion of vanadium has been
associated with gastrointestinal disturbances and renal and
nervous system effects. Experimental studies suggest the liver,
adrenals, and bone marrow as target organs. (Doull et al, 1986)
Vanadium has not been classified as a carcinogen by USEPA..
VINYL CHLORIDE
Vinyl chloride is a volatile organic compound used in the
manufacture of polyvinyl chloride and other resins. It is also
used as a chemical intermediate and a- solvent (Sittig, 1985).
Vinyl chloride can be found environmentally as a breakdown
product of tetrachloroethene, trichloroethene, 1,1-
dichloroethene, and 1,2-dichloroethene.
Vinyl chloride can cause skin irritation and CNS depression.
Chronic exposure may cause hepatic damage (Doull, 1986). Vinyl
chloride is classified by EPA as a Group A (known) human
carcinogen, and has been specifically associated with
hemangiosarcoma of the liver.
ZINC
Zinc is a common element and an essential metal not usually noted
for toxicity. intake occurs mainly from the diet, and the
average American daily intake is reported to be approximately 12
to 15 g. About 2 0 to 3 0 percent of ingested zinc is absorbed
(Doull et al, 1986).
Some zinc salts can be irritants. Gastrointestinal symptoms have
sometimes been reported after ingestion of high zinc
concentrations. Metal fume fever can result from inhalation of
zinc fumes (Doull et al, 1986). Zinc is not classified as a
carcinogen by USEPA.
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APPENDIX II
CALCULATIONS
-------
Chaster Water Authority
Reference doses and carcinogenic potency slope factors.
Contaminant
TETRACHLOROETHENE
TOTAL TRIHALOMETHANES
CARBON TETRACHLORIDE
FLUORIDE
NITRITE
Oral RfD
mgfk&d
1.00E-02
1.00E-02
7.00E-04
6.00E-02
1 .OOE-01
Inhaled
RfD
mg/kg/d
5.71 E-04
Oral;
Slope:
Factor
kg*ctfmg
5.20E-02
6.10E-03
1.30E-01
Inhaled
Slope
Factor
kg*tfmg
2.03E-03
8.05E-02
5.25E-02
Note: The toxicity criteria for chloroform were used to estimate risk from trihaiomelhanes
-------
Chester Water Authority
Adui reaidert (tfrttig water Ingestion
Concentration
mgl.
CW
Ingestion rate
Ud
2IR
E^osure frequency
cvy
350 BF
E^osure titration
y
24 ED
Body weltf*
kg
70 BW
Awraglng time care.
d
2S550 AT
Averaging tfrne ncarc.
d
8760 AT
Intake (m(j4
-------
Cheater Water AuBwty
CMkl residert drtrtdng water Ingestion.
Concertraikn
mgiL
CW
Ingestion rate
Ud
1 IR
E^KMure tea*ncy
tW
350 EF
E^poaure dLradon
y
6 ED
Body weK/t
Kg
15 BW
Averaging tfrne care.
d
25550 AT
Averaging tkne ncarc.
d
2190 AT
Wate (motto-day)»
CWx RxExE)
BWxAT
Ufettae
AMraQft Ctaxfc
RfwE Da* Daly Ufottne Systemic
Cane. Dote Dose Cancer Hazard
Contaminait mgiL mQfcgrtJ mgfcQ/d Rfsfc Quotient
TETRACHLOROETVENE
TOTAL TRHALOfcCTHANES 5.60G-02 5.11E-05 3.586-03 3.12E-07 3.58E-01
CARBON TETRACHLORDE
FUJORDE
NTHRrTE 8.80E-01 8.04E-04 5.63E-02 — 5.63E-01
TOTAL M8K FROM All. SOURCES (1969-ED-1 YEAJ? 3,126-07 9.21E-01
TETHACHLOfiOETV^NF —— —— «.
TOTAL TRHALOfdHANES 7.2DG-02 6.58E-06 4.606-03 4.01E-07 4.606-01
CARBON TETRACHLORDE 8.00E-04 7.31E-07 5.11E-05 9.506-08 7.31E-02
FUJORDE
NTTRUE — — — —
TOTAL RtSK FROM ALL30URCE3 (1990-ED-1 YEAF& 4J6E-07 5J3E-01
TETRACHLOROETVCNE
TOTAL TRHALOMETHANES 7.806-02 7.12E-05 4.996-03 4.35E-07 4.996-01
CARBON TETRACHLORDE
FLUORDE 9.206-01 8.406-04 5.88E-02 — 9.806-01
MTRfTE
TOTAL RIBK FROM ALL 80URCE8 -ED-1 YEABJ A3BE-& 1.486+00
TOTAL RMK WITHOUT FUUORDE 436E-G7 4.99E-01
TETRACHLOROETHENE
TOTAL TRHALOfcCTHANES 8.30E-02 7.586-05 5.31E-03 4.626-07 5.31E-01
CARBON TETRACHLORDE
FUJORDE
MTRfTE
TOTAL RI6K FfttM ALL SOURCES (1908—ED~ 1 YEAR} 4 626-07 5.31E-01
TETRACH.OROETWNE 1.006-03 9.136-07 6.39E-06 4.75E-08 6.396-03
TOTAL TRHALOfcCTHANES 6.60E-02 6.036-06 4.22E-03 3.686-07 4.22E-01
CARBON TETRACHLORDE
FUJORDE 1.006+00 9.136-04 6.396-02 — 1.07E+00
MTRITE 2.01E-01 1.846-04 1.286-02 — 1.286-01
TOTAL RtflKFAOM ALL SOURCES (1983—EDM iYEAfQ 4A9E<-QT T.62E+00
TOTAL RtflKWflHOUTFLUORDE 4.15E-07 5576-Ot
1.006-03 S.48E-06 6.396-06 1856-07 6.396-03
6.606-02 3.62E-04 4.22E-03 221E-06 4.22E-01
TETRACHLOROETHENE
TOTAL TRHALO*ETHA»CS
CARBON TETRACHLORDE
FLUORDE 1.006+00 5.48E-03 6.396-02 — 1.07E+00
NTTRITE 2.01 E-01 1.106-03 1.28E-02 — 1.286-01
TOTAL FltSK FROM ALL SOURCES (1993-ED- 30YEAR8) 2.486-06 1.62E+00
TOTAL RISK WITHOUT R.UOWDE 1486-06 5J57E-01
-------
Oin— Wmr Authoity
Adut rmtdtrt tfcomrtnfl ttpmtm onnnUBIuw.
L-p>aaic. CC2
Q-PM« te. HZO
WMrvke.ataDC
Wovvac. «49C
ShowartMip
Orapto Jnulr
Orep vrm
Show flow fa
3howw ml votum#
3hu»> dn(M
Mrsxctunga m
CootemiMnt
TETHACHLOflOETHENE
TOTAL THHALOfcETHANEB
GAA0ON TE1BACHLOROE
FUXMOE
MTWTE
I9M ED-1WIW
TETRACHLOICETHS4E
TOTAL TRHALOkEmAMEB
CAflBON TETHACHLOfME
FLUOflOE
NTWTE
IMO-eVtYEffi
TETRACHLOfOETMS4E
TOTAL THHALOkETHANEB
CARBON TETR&CHLO(«OE
RJJORDE
NITTOTE
tati-e^vem
TETmCHLOmETHB4E
TOTAL TWHALOMETMANeB
CM BON TETWOiMBC
FljUORDE
MTHTE
tW-BJ-tlTHR
TETRACHLOnOCTHENE
TOTAL TKHALOftCTHANB
OA BOM TFTRAOLOACE
FLIJOflDE
NITWTE
tMS-ED^tVEm
TETTMCHLOROETHBtt
TOTAL TftHALOfcETHAMEB
OWBON TETRACHOBBE
FUJOfllOE
NITHTE
HB-BB-tttBW
Cfflftl
20
emyh
3000
CO
1.003
cp
OJSS .
K
319
mm
1
•
2
umn
S
nO
2J06+00
mti
1.20E+01
flih-i
00199907 (F
Onra*
T«w-^
Gooo.
VOC
' «r
Tram.
fan.
bwtov
9mt.
Cans.
Avg. Air
ME
Hnfi
CMC
CML •
HK>
M9
9t»W
Coro.
dm
MOtWl.
Oi—1
10
*9.
KL
KM.
CM
9
EfO
KtStJWB
¦tfL
grtwf
ntx-mOHmt
amih
cm*
amjH
•0*
mq/MX
1J0E+O2
2JSE-02
1.036+01
9J9E+02
1.026+01
1J7E+01
»
--
--
S.90E-02
1.19E+Q2
2J1E-03
123S+01
1.17E+03
1.12E+01
1 JOE+01
isde-os
1JSE-01
1.9BE+00
9J3E-01
1J4E+02
2.416-08
1.076+01
' 103E+03
1.09E+O1
1.42E+01
9J0E-01
1.99E+Q2
ZJ9E-02
1.036+01
9J9E+02
UHE+01
1J7E+01
__
„
7 JOE-02
1.19E+0B
2J1E-03
1.226+01
1.17E+03
1.12E+01
1 JOE+01
2J3E-02
1J0E-O1
2.12E+00
1106+00
9.006-04
1J4E+Q2
2.41 E-02
1.07E+01
1.036+03
1.09E+01
1.42E+01
3.01E-O4
2J9E-0S
2J9E-02
1,17E-02
1J9E+02 2J9E -02 1 £36+01
7J0E-O2 1.196+02 2J1E-03 1.226+01
1-34E+oa 2.41E-02 t.OJE+01
9.20E-01
3ME+03 1.026*01
1.17E+03 1.I2E+01
103E+03 UJ9E+01
1376 *01
uoe+oi
1.4aE+01
&09E-02 2.116-01 2JOE+00 1.186 *00
1.99E+02 2J8E-02 1.036+01
a JOE-02 1.19E+02 U1E-49 1.226+01
1J4E+0B 2.41E-02 107E+01
9JBE+03 1.0SE+01 1.J7E+01
1.17E+03 1.12E+01 1 JOE+01 3J
iobe+03 io«Etoi i.4se+oi ,
E-02 2.296-01 2.44E+00 1.26E+00
1.00E-00
uoE-oa
1.00E+00
2J51E—01
1*
1.1*
:+02 2J96-02
1+02 2J1E-03
1.54C+0B 2.41E—OS
1.03E+01
1 mf+en
1.07E+01
9J9E+02 1O2E+01
1.17E+09 1.12E+01
1.03E+03 1096+01
1J7E+01
1 JOE+01
1.426+01
-04 2J2E-03
1.796-01
2.74E-02 1 42E-02
1.94E+00 i.ooe+oo
1.006-03 IJOE+OS 2J9E-02 1.036+01
9 JOE-02 1.186+02 2J1E-03 1.22E+01
9496+02 1O2E+01
1.17E+0S 1.12E+01
100E+00
2J1E-01
1J4E+0B 2-416-02 1.07E+01 1.036+03 1O9E+01
IJ7E+01
1 JOE+01
I.42E+01
3.996-0* U2E-03
2J9E-02 1.79E-01
S. 746-02
I.ME+00
1 42E-02
1 006+00
-------
Cheater Water Authority
Aduft residert showertig Inhalation.
Concentration
Inhalation rate
E*>osure freojency
E^xaure duration
Bodywettft
Averaging ttne carc.
Averaging ttne ncarc.
Shower duration
Intake $mafca-day)
m^rna
CA
rrtVmn
0.0138889 IR
cW
350 5=
y
24 ED
kg
70 BW
d
25550 AT
d
8760 AT
mh/d
12 ET
CAxIRxETxEFxEO
BWxAT
rac
Cane.
mo/mi
Lfeftne
Average
Oaty
Dose
mgifc^d
Contamtioft
TETRACHLOROETHENE
TOTAL TRIHALOKCTHANES
CARBON TETRACHLORIDE
FLUORDE NA
NrmrTE na
TOTAL N8K FROM ALL SOURCES fl«»-ED- 1 VEAfl}
Cfrorib
Dafly
Oose
mgfcQfd
Ufetfcne
Career
RWc
Systemic
Hazard
Quotient
8.52E-01 2.786-05 1.95E-03 2.24E-06
2246-06
TETRACHLOROETHENE
TOTAL TRHALOHCTHANES 1.10E+00 3.57E-05
CARBON TETRACHLORDE 1.17E-02 3.81E-07
FLUORDE NA
NTTRITE NA
TOTAL RISK FROM ALL SOURCES (19Q0-ED-1 YEARS
2.506-03
2.666-OS
2.886-06
2.00E-08
4.67E-02
2SOE-OS 4.S7E-02
TETRACHLOROETHENE
TOTAL TRMALOHCTHANES
CARBON TETRACHLORDE
FLUORDE NA
NrmrTE na
TOTAL RISK FROM ALL 80URCES 0991 -ED-1 YEAR)
1.19E+00 3.87E—06 2.71 E-03 3.12E-06
3.12E-06
TETRACHLOROETHENE
TOTAL TRWALOfcCTHANES
CARBON TETRACHLORDE
FLUORDE
NTTRITE NA
TOTAL RISK FROM ALL SOURCES (1902-ED-1 YEAR)
1.2B6+00 4.12E-05 2.88E-03 3.32E-06
NA
TETRACHLOROETHENE 1.42E-02 4.62E-07 3.24E-05
TOTAL TRHALOMiTHANES 1.006+00 3.28E-05 £296-03
CARBON TETRACHLORDE
FLUORDE NA
NTTRITE NA
TOTALRSKFROMALL SOURCES (19M-ED-1 YEAH>
TETRACHLOROETHENE 1.42E-02 1.11E-05 3.24E-06
TOTAL TRHALOfcCTHANES 1.006+00 7.866-04 2.296-03
CARBON TETRACHLORDE
FLUORDE NA
NrmrTE na
TOTAL RWC FROM ALL SOURCES (tStt-ED-tti YEARS)
USE—08 —
9.386-10
2.64E-06
2.646-06 —
2.256-08
6.336-06
&33E-06
NA—Not AppicaMe
-------
Chester Water Authority
Cttid reakJert drinking water denrtai contact
Concentration mgt. CW
Surface area cm3 7200 SA
Ejqioaure tequercy d/y 350 EF
Exposure duration y 6 ED
Bodyweitf* ¦ kg 15 BW
Averaging tine carc. d 25550 AT
Averaging tfrne ncaic. d 2190 AT
Bath deration rvd 0.33 FT
Conversion Factor fcrrx3 1.006-03 CF
Dermal Peimeablltty Constant crTvtv PC
(chemical specfffc)
Absorbed Dose tmgrfcg-day) » CWx SA x PC x ETn EF x ED x CF
BW x AT
Ufettne
Average Chrortc Dermal
RME OaBy Dally Ufettne Systemic Permeao,
Cone. Dose Dose Cancer Hazard Coef.
Cortfamfrart mot mgikg/d maficQ/6 Rbk Quotient crrvfi
TETRACHLOROETHENE — — — — 4.006-01
TOTAL TWHALOWETHANES 5.606-02 1.22E-05 8.51E-04 7.41E-08 8.51E-02 1.006-01
CAflBON TETRACHLORIDE — — — — 2.20E-02
FLUORIDE NA
NITRITE MA
TOTALRKK FROM ALL SOURCES (1989-ED • 1 YEAR} 7.41E-08 8.51E-02
TETRACHLOROETHENE -- — — — 4.00E-01 .
TOTAL TRHALOACTHANES 7.206-02 1.566-05 1.096-03 9.536-08 1.096-01 1.006-01
CARBON TETRACHLORIDE 8.0Q6-O4 3.826-08 2.67E-06 4.96E-09 3.82E-C3 Z20E-Q2
FLUORIDE NA
NITRITE NA
TOTfiLOtSK FROM ALL SOURCES {ISM-ED-1 YEAR 1.006-07 1.136-01
TETRACHLOROEWENE — — — — 4.006-01
TOTAL TRtt-iALONSTTHANES 7.806-02 1.696-05 1.18E-03 1.03E-07 1.18E-01 1.006-01
CARBON TETHACH.OP IDE — — — — 2.206 -02
FLUOR BDE NA
NrmrTE na
TOTAL RISK FROM AJ. SOURCES (1 fl»1 -ED-1 YEAR) 1.03E-07 1.18E-01
TETRACHLOROETHENE — — — — 4.006 -01
TOTAL TRM-MLOfcCTVMNES 8.306-02 1.806-05 1.266-03 1.106-07 1.266-01 1.006-01
CARBON TETOACHLOROE — — — — £206-02
FLUORCE NA
NTTRITE NA
TOTALRtSK FROM ALL SOURCES (IMC-EDo-l YEAR) 1.10E-07 1.266-01
TETRACHLOROETHENE 1.006-03 8.68E-07 6.086-05 4.51E-08 6.08E-03 4.006-01
TOTAL TRHALOMETHANES 6.606-02 1.43E-0S 1.006-03 8.746-08 1.006 -01 1.006-01
CAflBON TETRACHLORDE — — — — 2.206-02
FLUORDE NA
hrmrTE na
TOTAL RISK FROM ALL SOURCES pass-ED-1 VEAR) 1.32E-07 1.06E-01
TETRACHLOROETHENE 1.006-03 5.21E-06 6.08E-05 2.71 E-07 6.086- 03 4.006-01
TOTAL TRHALOMETHANES 6.606-02 8.596-05 1.006-03 5.24E-07 1.006-01 1.006-01
CARBON TETRACHLORCE — — — — 2.206 -02
FLUOR OE NA
NrmtTE NA
TOTAL RISK FROM ALL SOURCE S<196»-£D- 30 YEARS) 7.356-07 1.066-01
NA-Not AppNcabie
-------
Philadelphia Suburban Water Company
Reference doses and carcinogenic potency slope factors.
Oral Inhaled
Inhaled Slope Slope
OrafR© RID Factor Factor
Contaminant mg/kg/d mg/kg/d kg*d/mg kg*d/mg
6.10E-03 8.05E-02
TOTAL TRIHALOMETHANES 1.00E-02
Note: The toocity criteria for chloroform were used to estimate risk from trihalomethanes
-------
Philadelphia Suburban Water Company
Adult resident drinking water ingestion.
Concentration
mg/L
CW
Ingestion rate
L/d
2IR
Exposure frequency
d/y
350 EF
Exposure duration
y
24 ED
Body weight
kg
70 BW
Averaging time carc.
d
25550 AT
Averaging time ncarc.
d
8760 AT
Intake (mg/kg-day) =
CWxIRxEFxED
BWxAT
Lifetime
Average Chronic
HUE DailyDaily Lifetime Systemic
Cone. Dose Dose Cancer Hazard
Contaminant mg/L mg/kg/d mg/kg/d Risk Quotient
TOTALTRIHALOMETHANES 4.75E-02 1.86E-05 1.30E-03 1.13E-07 1.30E-01
TOTAL RISK FROM ALL SOURCES {1989-ED= 1 YEAR) U3E-07 1.30E-01
TOTALTRIHALOMETHANES 6.31 E-02 2.47E-05 1.73E-03 1.51 E-07 1.73E-01
TOTALRISK FROM ALL SOURCES {1990-ED»1 YEAR) 151 E-07 1.73E-01
TOTALTRIHALOMETHANES 4.07E-02 1.59E-05 1.12E-03 9.72E-08 1.12E-01
TOTAL RISK FROM ALL SOURCES (1991-ED= 1 YEAR) 9.72E-08 1.12E-01
TOTALTRIHALOMETHANES 3.64E-02 1.42E-05 9.97E-04 8.69E-08 9.97E-02
TOTAL RISK FROM ALL SOURCES {1992—ED= 1 YEAR) 8.69E-08 957E-02
TOTALTRIHALOMETHANES 9.80E-02 3.B4E-05 2.68E-03 2.34E-07 2.68E-01
TOTAL RISK FROM ALL SOURCES (1393-ED=1 YEARJ 2J34E-07 2.68E-01
TOTALTRIHALOMETHANES 9.80E-02 9.21 E-04 2.68E-03 5.62E-06 2.68E-01
TOTAL RISK FROM ALL SOURCES (1993-ED= 30 YEARS) 5.62E-06 2.68E-01
-------
Philadelphia Suburban Water Company
Child resident drinking water ingestion.
Concentration
mg/L
CW
Ingestion rate
L/d
11R
Exposure frequency
d/y
350 EF
Exposure duration
y
6 ED
Body weight
kg
15 BW
Averaging time care.
d
25550AT
Averaging time ncarc.
d
2190 AT
intake (mg/kg-day) = CW x IR x EF x ED
BWxAT
Lifetime
Average Qirordc
FWE! OaSy Daily Lifetime Systemic
ConC. Dose Dose Cancer Hazard
Contaminant mg/t , mg/kg/d mg/kg/d Rsk Quotient
TOTALTRIHALOMETHANES 4.75E-02 4.34E-05 3.04E-03 2.65E-07 3.04E-01
TOTAL RISK FROM ALL SOURCES (1S89-ED= 1YEAR) 2.65E-07 3.04E-01
TOTALTRIHALOMETHANES 6.31 E-02 5.76E-05 4.03E-03 3.52E-07 4.03E-01
TOTAL FflSK FROM ALL SOURCES (1990-ED= 1 YEAR) 3.52E-07 4.03E-01
TOTALTRIHALOMETHANES 4.07E-02 3.72E-05 Z60E-03 2^7E-07 2.60E-01
TOTALF8SK FROM ALL SOURCES (f 991-ED= T YEAR* 2£7E-07 2.60E-01
TOTALTRIHALOMETHANES 3.64 E-02 3.32E-05 2.33E-03 2.03E-07 2.33E-01
TOTAL RISC FROM ALL SOURCES(1992-ED= 1 YEAR) 2.03E-07 2.33E-01
TOTALTRIHALOMETHANES 9.80E-02 8.95E-05 6.26E-03 5.46E-07 6.26E-01
TOTAL RE5K FROM ALL SOURCES (1993-ED= 1 YEAR) 5.48E-07 6.26E-01
TOTALTRIHALOMETHANES 9.80 E-02 5.37E-04 6.26E-03 3.28E-06
TOTAL RISK FROM ALL SOURCES (t993-ED= 30 YEARS) 3.28E-06
S.26E-01
6.26E-01
-------
AOfcfti
L-promccoe
0-pOMtU.HJO
W«rvac. «2DC
WUvvhc.«40C
3ho—ramp
Orapwutoiaia
Orgptma
IMim
9MUH
Air mangtmii
TOTAL THHflLOMETMANES
»-1l
TOTAL mhALOMETHMCS
1W0-H>-i>&W
TOTAL TWHALOMETHANEB
TOTAL TWHALOMETHANEB
WM3-1YW
TOTAL HWALOMETMAMEB
IW-HJ-ITEAfl
TOTAL mHALOMETHANEB
UMMWMni.
emit)
aMt
cp ¦
op
K
mm
«
urm
m3
rrtfi
mti-1
mic
Core
4.79£-09
131 e-oa
4.07E-02
X04C-02
aaoe-02
ft.aoc-oa
20
3000
1 002
0.9M
318
1
2
20
2.B0E+00
1.206*01
0.0188887 pANGE: .9 TO 1.9 PER HOUR
QmrnI
TMm
Cm VOC
Mot Wi Cnm
itm-maftnpl enWfc
«o
sinA
1.106+02 2.876-03 1.226+01 1.17E+03
1.186+02 2.B7E-OJ 1.22E+01 1.176+03
1.106+02 2.S7E-03 1.226+01 1.176+03
1.106+02 2.876-03 1.226+01 1.176*03
8.306+01 1186-02 1.87E+01 1.806+03
1.186+00 2.I7E-03 1.226+01 1.176+03
cmM
1.126+01
1.1JE+01
1.126+01
1.126+01
1.876+01
1.126+01
ca/K
1.S06+01
1.S06+01
1.S06+01
1.806+01
3J3E+01
1.306+01
tOO Ra»
Cad 3
¦Q/l
1.87E-02 1.286-01
ZOE-OB 1.71E-01
1.806-02 1.106-01
1.436-01 ».«7E-0a
1146-08 1586-01
&886-02 2.006—01
«»
Com.
Eno
mo/"*
1.406+00
A*?.A*
Cenc
HWw«r
7.246-01
1.M6+00
1.206+00
1.076+00
3.886+00
&asE+oo
8.B1E-01
0.206—01
isae-oi
1.9(6+00
1 486+00
-------
PhBadelphia Suburban Water Company
Adult resident showering inhalation.
Concentration mg/m3 CA
Inhalation rate m3/min 0.0138889 IR
Exposure frequency d/y 350 EF
Exposure duration y 6 ED
Body weight kg 70 BW
Averaging time care. d 25550 AT
Averaging time ncarc. d 2190 AT
Shower duration min/d 12ET
intake (mg/kg-day)« CA x IR x ET x EF x ED
BW x AT
Lifetime
Average Chronic
RME Daily Daily Lifetime Systemic
Cow. Dose Dose Cancer Hazard
Contamfoffitt mg/m3 mg/kgWT mg/kg/d Risk Quotient
TOTAL TRI HALO METHANES 7.24E-01 2.36E-05 1.65E-03 1.90E-06
TOTAL RISK FROM: ALL SOURCES (1989»-ED= 1 YEARJf 1.90E-06
TOTAL TRIHALOMETHANES 9.61E-01 3.14E-0S 2.19E-03 2.52E-06
TOTAL FtiSKFROtt ALL SOlftCES (1990-ED« i YEAFj.: Z52E-06
TOTAL TRIHALOMETHANES 6.20E-01 2.02E-05 1.42E-03 1.63E-06
TOTALTOSKFROM ALL SOURCES (1991-ED« 1 YEAR) : ^ 1.63E-G6
TOTAL TRIHALOMETHANES 5.55E-01 1.81E-05 1.27E-03 1.46E-06
TOTAL RISKmttW SOURCES (1982-ED- 1 YEAR} 1.46E-06
TOTAL TRIHALOMETHANES 1.49E+00 4.87E-05 3.41 E-03 3.92E-06
TOTALRtSKfROMAy;SOl^CES (1993-ED« 1 YEAH} ^ 3.92E-06
TOTAL TRIHALOMETHANES 1.49E+00 1.17E-03 3.41E-03 9.41E-05
TOTAL RISK FROM ALL SOURCES (1993-ED- 30 YEARS) 9.41 E-05
-------
Philadelphia Suburban Water Company
CWW resident drinking water dermai contact
Concentration mg/L
Surface area cm3
Exposure frequency d/y
Exposure duration y
Body weight kg
Averaging time carc. d
Averaging time ncarc. d
Bath duration h/d
Conversion Factor l/cm3
Dermal Permeability Constant cm/hr
(chemical specific)
Absorbed Dose (mtfkg-day) =
CW
7200 SA
350 EF
6 ED
15 BW
25550 AT
2190 AT
0.33 ET
1.00E-03 CF
PC
CW x SA x PC x ET x EF x ED x CF
BW x AT
Contaminant
TOTAL TRIHALOMETHANES
RME
Cone.
mj^L
4.75E—02
Lifetime
Average
Daily
Don
mg/kg/d
1.03E-05
TOTAL RISK FROM AIL SOURCES (19B9-ED= 1 YEAR}
TOTAL TRIHALOMETHANES 6.31E-02 1.37E-0S
TOTAL RISK FROM ALL SOURCES (1900-ED= 1 YEAR)
TOTAL TRIHALOMETHANES 4.07E-02 8.83E-06
TOTAL RISK FROM ALL SOURCES (1981-ED«* 1 YEAR)
TOTAL TRIHALOMETHANES 3.64E-02 7.90E-06
TOTAL RISK FROM ALL SOURCES (1982- ED= 1 YEAR)
TOTAL TRIHALOMETHANES 9.80E-02 213E-05
TOTAL RISK FROM AU. SOURCES {1903- ED= 1 YEAR)
TOTAL TRIHALOMETHANES 9.80E-02 1.28E-04
TOTAL RISK FROM ALL SOURCES 30 YEARS)
Chronic
DaSy
Dow
mj^kgte
7.21 E-04
9.58E-04
6.18E-04
5.53E-04
1.49E-03
1.49E-03
Utet&ne
Cancer
Risk
6.29E-08
6.29E-0S
1.3OE-07
1.30E-Q7
7.78E-07
7.78E-07
Systemic
Hazard
Quotient
7.21 E-02
7.21E-02
8.35E-08 9.58E-02
&35E-06 ' 9.586-02
5.39E-08 6.18E-02
5.3SE-0S 5.18E-02
4.82E-08 5.53E-02
4.82E-08 5.53E-02
1.49E-01
1.4SE-01
1.49E-01
1.4SE-01
Dermai
Permeab.
Coeff.
cm/h
1.00E-01
1.00E—01
1.00E-01
1.00E-01
1.00E-01
1.00E-01
-------
Philadelphia Water Department
Reference doses and carcinogenic potency slope factors.
Contaminant
CARBON TETRACHLORIDE
TOTAL TRIHALOMETHANES
FLUORIDE
Oral Inhaled
Inhaled Slope Slope
OrafRfD RID Factor Factor
mg/kgfd mg/kgfd kg*dftng kg*cVmg
7.00 E-04 5.71 E-04 1.30E-01 5.25E-02
1.00E-02 6.10E-03 0.O5E-O2
6.00 E-02
Note: The toxicity criteria for chloroform were used to estimate risk from trihalomelhanes
-------
PftHadetptfa Waer Department
Adidt resident drinking water ingestion.
Concentration
mg/L
CW
Ingestion rate
Lid
2
IR
Exposure frequency
d/y
350
EF
Exposure duration
y
24
ED
Body weight
•<9
70
BW
Averaging time carc.
d
25550
AT
Averaging time ncarc.
d
8760
AT
intake (mg/kg-day) =
CW x IR x EF x ED
BWxAT
RME
Cone.
mg/L
Contaminant
CARBON TETRACHLORIDE
TOTAL TRIHALOMETHANES
FLUORIDE
Tom Rsk from AR Sources (1989)-ED- 1 Year
Totat Risk wtftout Fluoride
LJetime
Average
Daily
Doee
mg/kQ/tt
Chronic
Daiy
Doee
mgftcgftj
LSetime
Cancer
Rtek
6.83E-02
1.Q0E+Q0
2.67E-05
3.91E-04
CARBON TETRACHLORIDE 5.00E-04 1.96E-07
TOTAL TRIHALOMETHANES 7.15E-02 2.80E-05
FLUORIDE 1.01E+00 3.95E-04
Totstf Rfekfirom AS Sources-1980 (ED ¦ 1 Year)
Totstf Rfakwflhottf Fluoride
CARBON TETRACHLORIDE 3.00E-04 1.17E-07
TOTAL TRIHALOMETHANES 7.61 E-02 2.98E-05
FLUORIDE 1.01E+00 3.9SE-04
Total Ftefc from Ai Sot*ces-1991 (ED -1 Year)
Total Risk wtttoulFfuorid*
CARBON TETRACHLORIDE
TOTAL TRIHALOMETHANES 5.89E-02 2.31 E-06
FLUORIDE 1.00E+00 3.91 E-04
Total Ri»kiro^ A» Sourcae-1982 (ED »t Yaai)
lom Risk wtf|^:fiorfd»;"/::':r^''.
CARBON TETRACHLORIDE 3.00E-04 1.17E-07
TOTAL TRIHALOMETHANES 8.33E-02 3.26E-05
FLUORIDE 9.80E-01 3.84E-04
Total Hsk ftora AlSources-1993 (ED «1 Yea#
Total Risk wfthoul Fluoride
CARBON TETRACHLORIDE 3.00E-04 2.82E-06
TOTAL TRIHALOMETHANES 8.33E-02 7.82E-04
FLUORIDE 9.80E-01 9.21 E-03
Total Risk from AB Sourcae-1993 (ED « 30 Yeai}
Totti RWc wfihotA Fluoride
1.87E-03
2.74E-02
1.37E-05
1.96E-03
2.77E—02
8.22E-06
2.Q8E-Q3
Z77E-02
Systemic
Hazard
Quotient
1.61E-03
2.74E-02
8.22E-06
2.28E-03
2.68E-02
8.22E-06
2.28E-03
2.68E-02
1.63E-07
1.63E-07
t.fflE-07
2.54E-08
1.71E-07
1.96E-07
1.96E-07
1.53E-08
1.82E-07
1.97E-07
1A7E-07
1.87E—01
4.57E-01
8.44E—01
1.B7E-01
1.96E-02
1.96E-01
4.61E-01
8.77E-01
2.15E-01
1.17E—02
2.08E-01
4.61E-01
M1E-G1
2^0E-01
1.41E-07 1.61E-01
4.57E—01
1.41E-07 8.18E-01
1.41E-07 t.rfE-01
1.53E-08
1.996—07
2.14E-0T
2.t4E-07
3.56E—07
4.77E-06
S.14E-06
&14E-08
1.17E-02
2.28E-01
4.47E—01
6JWE-01
2.40E-01
1.17E-02
2.28E-01
4.47E—01
8J7E-01
2.40E-01
-------
PftBadeipWa Water Department
CtiHd resident drinking water Ingesttoa
Concentration
mg/L
CW
Ingestion rate
ua
1 IR
Exposure frequency
d/y
350 EF
Exposure duration
y
8 ED
Body weight
Kg
15 BW
Averaging time carc.
d
25550 AT
Averaging time ncarc.
d
2190 AT
intake (mg/kg-day) =* CW x IR x EF x ED
BW x AT
RME
Cone.
mg/L
Contaminant
CARBON TETRACHLORIDE
TOTAL TRIHALOMETHANES 6.B3E-02
FLUORIDE 1.00E+00
Total Risk from Afi Sources- t9S9 (ED-1year)
Total Risk wtttoutFluorid*
Uetime
Average
Dafty
Dose
Chronfc
DaSjr
mgflcgftf
Uetime Systemic
Cancer Haz»d
FWt Quotient
6.24E-05 4.37E—03 3.80E-07 4.37E-01
9.13E-04 6.39E-02 — 1.07E+00
3J8E-0? iJSBEiUl
3.806-07 4.376-01
CARBON TETRACHLORIDE 5.00E-04 4.57E-07 3.20E-05 5.94E-08 4.57E-02
TOTAL TRIHALOMETHANES 7.15E-02 8.53E-05 4.57E-03 3.98E-07 4.S7E-01
FLUORIDE 1.01E+00 9.22E-04 6.46E-02 -- 1.08E+00
Total Riak from Aff3ot*ees-I990 (ED * 1 Yeei) 4.58E-07 1.885+00
T6HI Risk w«»ur Fluoride 43SE-07 5.03E-01
CARBON TETRACHLORIDE 3.00E-04 Z74E-07 1.92E-05 3.56E-08
TOTAL TRIHALOMETHANES 7.61 E-02 6.95E-05 4.86E-03 4.24E-07
FLUORIDE 1.01E+00 9.22E-04 6.46E-02
Total Risk from All CD Ytori 4JCE-07
Total Ettsk wktewtFtuorfcf* 4.60E-07
CARBON TETRACHLORIDE
TOTAL TRIHALOMETHANES S.89E-02 5.38E-05 3.77E-03 3.28E-07
FLUORIDE 1.00E+00 9.13E-04 0.39E-O2
Total FBsk (Ml foiieat-1^ (ED - tYsai) &28E-07
TotaiR^wiiteFluoftte &2BE-07
CARBON TETRACHLORIDE 3.00E-04 2.74E-07 1.92E-05 3.56E-08
TOTAL TRIHALOMETHANES 8.33E-02 7.61E-05 5.33E-03 4.64E-07
FLUORIDE 9.80E-01 8.95E-04 6.2SE-02
Tottl Risk front Afi 8ource*-1993 (ED- t Yes#
Tfataf Kb* without Fluoride SJJ06-07
CARBON TETRACHLORIDE 3.00E-04 1.84E-06 1.92E-05 2.14E-07
TOTAL TRIHALOMETHANES 8.33E-02 4.56E-04 5.33E-03 Z78E-06
FLUORIDE 9.80E-01 5.37E-03 6.26E-02
Total Risk from AH Sources—1fl93 {EI} • 30Yaai) 1006-08
Tottl Risk wSftout Fluoride &00E-06
2.7.4E-02
4.86E-01
1.08E+00
1J9E+00
5.14E-01
3.77E-01
1.07E+00
1.44E+00
8J7E-01
2.74E—02
5.33E-01
1.04E+00
1.80E+0O
SJOE-01
2.74E-02
5.33E-01
1.04E+00
. 1 JQE-fOO
Ot
-------
a-ptMB U. HM
Vft«rvtc.«40C
itantMt
Oraptt da/Mar
0«M
cm*
oivwti
a
9000
«o
',.<300
C9
OJSO
K
319
mm
1
•
a
Utim
»
i*d
2J06+00
mm
1-»E*01
mm* t
O01OT7
Mfe
CM&-''
Mot Wl
-
JUrwAaigi a
OMNf OMK VOC J*
M| tar, Cms. to»J»
wo- Ms matomm.,
CM • M to
^ _ .. _ . :
1 TEiTwcHLonac — i.M>*aa 2^ic-at utc+oi ijac-i-a im*oi i.«e«oi
TOTAL 11II ItLIJMi11IAMU IDC-OI l.ltf+OB 2416-41 1^3E*01 1.l7E*Oa 1.1JS«01 1 J0£ ~CI 2JK-4B 1JBE-41 101E«-Oi 1JXC+00
aUOHOE . 14K+40M
iinn
«tetwchlonoc um t.lS«01 1J0S*O1 2J1C-0* IMC-01 1 aaC*00
FUJORCE 1.016+00 «•
CMKN TETIMCMjOROC lOOK-M IMtfl 1416-48 1A(*41 1.nK«6a 1JNE«et 1.13P-0* 7.JW-4* L47{-a OK-<30
TUIM.TD»M.OMETMANEa 7J16-4B I.HE+flt UlC-41 1J*+01 1.17E«4> 1.1S«41 1 JOE *41 LMC-4I UK-41 IME*40 1.1K+00
aUORCE 1.01E«O0w
WB»l im)
CNVON TCTMCHLOMOC — 1M«4B 1416-48 1J7E+01 l««« 1«4
-------
Philadelphia Water Department
Adult resident showering inhalation.
Concentration
mg/m3
CA
Inhalation rate
m3/min
0.0138889 IR
Exposure frequency
d/y
350 EF
Exposure duration
y
24 ED
Body weight
Kg
70 BW
Averaging time carc.
d
P55S0 AT
Averaging time ncarc.
d
8760 AT
Shower duration
min/d
12 ET
intake (mo/kg-day) =
Contaminant
CARBON TETRACHLORIDE
TOTAL TRIHALOMETHANES
FLUORIDE
CAxIRxETxEFxED
BWxAT
Lifetime
Average
Daily
Cone. Doe*
mg/ta3 mg/kgfc
Systemic
Hazard
1.04E+00 3.39E—05
na
Totai FB^frwn ABS
-------
Phfladeiphfe Vttttr Department
CMd resfcfer* drirftftg water dermal contact.
Concentration
mg/L
CW
Surface area
cm3
7200 SA
Exposure frequency
d/y
350 EF
Exposure durakm
y
6 ED
Body weight
*g
15 BW
Averaging time care.
d
25550 AT
Averaging time ncarc.
d
2190 AT
Bath duration
h/d
0.33 ET
Conversion Factor
l/cm3
1.00E-03 CF
Dermal Permeatafity Constant
cm/tir
PC
(chemical specific)
Absorbed Doee (mg/fcg-
-------
CoatesvHIe Water Authority
Reference doses and carcinogenic potency slope factors.
Oral Inhaled
Inhaled Stop* Slope
OraiRfD WD Factor Factor
Contaminant mg/koAf m
-------
Coatesvie Water Authority
Child resident drinking water ingestion.
Concentration
mg/L
CW
Ingestion rate
L/d
11R
Exposure frequency
d/y
350 EF
Exposure duration
y
6 ED
Body weight
kg
15 BW
Averaging time carc.
d
25550 AT
Averaging time ncarc.
d
2190 AT
fntake(mg/kg-day} »
CWxIRxEFxED
BWxAT
Contaminant
TOTAL TRIHALOMETHANES
RME
Cone.
moft*
Lifetime
Amngi
Dafly
Chronic
0*i
lifetime
mgfl^ mg/fcg/3 Rtak
Systemic
Hazard
Quotient
8.62E-02 4.72E-04 S.S1E-03 2.88E-06 5.51 E-01
Total
2J8E-08 5.51 E-Ot
-------
TOTM. THHWjggTHmCB
im-ca ijg-»oi i.i7g+o» M2g»oi i.ang*oi i**-" »t-ot ime*ob i.«ae*oe
-------
Coatesvilte Water Authority
Adult resident showering inhalation.
Concentration
mg/m3
CA
Inhalation rate
mS/min
0.0138889
IR
Exposure frequency
d/y
350
EF
Exposure duration
y
24
ED
Body weight
Kg
70
BW
Averaging time care.
d
25550
AT
Averaging time ncarc.
d
8760
AT
Shower duration
min/d
12
ET
Intake {mglcg-day} — CA x IR x ET x EF x ED
BW x AT
dyatamlc
Hazard,
Quotient
unim
Average Qvonfe
RME . Dail?;. '"•••'•: Dafly IMm
Cone. ."•¦¦¦ DoaeOoee . Cancar
Contaminant mofetS mg/ktfl mgflitfel FWt
TOTAL TRIHAL0METHANE3 1.49E+00 1.17E-03 3.41E-03 9.41E-05
M1E*H «"¦=•
Totat
-------
CoatBSvtiie Water Authority
Adult resident showering Inhalation.
Concentration
m^m3
CA
Inhalation rate
m3/min
0.0138889 IR
Exposure frequency
d/y
350 EF
Exposure duration
y
24 EO
Body weight
Kg
70 BW
Averaging time carc.
d
25550 AT
Averaging time ncarc.
d
8760 AT
Shower duration
min/d
12 ET
intake (mg/kg-day) m CA x IR x ET x EF x ED
BW x AT
Contaminant
TOTAL TRIHALOMETHANES
mir
Cane;
mgfctS
UCrtfme
Awigi
Daily
Oos*
mgffgtf
Qwunfc
v w&-;:
mgfcQtt
UMnw
RWt
Systemic
Hazard
Quotient
1.496+00 1.17E-03 3.41E-03 9.41E-08
Total
9.41E-QS
-------
Coatastfle Water Aulhorty
CNtd reafdem drinking water dwmai contact
Concentration
Surface irn
Expoaure fnquancy
Expoaure duration
Body weight
AvaragJng time carc.
Averaging time ncarc.
Bath duration
Conversion Factor
Dermal Permeability Constant
(chemical specific)
AbaotMtf Com (jntfJtQ-dqfl"
Cbofimtnant
mg/L CW
cm3 7200 SA
d/y 350 EF
y BED
kg IS BW
d 25550 AT
d 2190 AT
h/d 0.33 ET
l/cma 1.006-03 CF
cm/hr PC
CWxSAxPCxETxEFxEDxCF
BWxAT
UMme
. . Avenge Ctwxite
.fUlgv;' 01^ DoBjf. ; UMm« ; Syrttfrtc PwmMfc.
Cooc Qom Ooea ¦ ¦ ' Cine«rt" Hax«rd ' ' - Coeft
mg& ^ng/kgfd fMc' Quotient xmfit
TOTAL TRIHALOMETHANES
Ttitat;
&62E-02 1.12E-04 1.31E-03 6.856-07 1.31E-01 1.006-01
trn-tt i3E=& ~—
-------
RisJc Estimates for TotafTrthalomatfiarwa at th« MCL
Rafsrsnes doses wd csrdnogsnte potency stop# factors.
• • ; mtairt
" Muted : Sbpr ' flop*
Oral no HO--; VFacw- •: Niiicr;
Comamknnt tng/kgftf rng/fcgft? kg«d|fmg Irg'^rttg
TOTAL TRIHALOMETHANES 1.00E-02 6.10E-Q3 g.QSE-02
Not#: The toxicity criteria for chloroform wars used to estimate risk from tritaiomethanes at the MCL at 100 pptx
-------
Risk Estimates forTotaiTrBialometliaies at tfte MCL
Aduft resident drinking water Ingestion,
Concentration
Ingestion rate
Exposure frequency
Exposure duration
Body weight
Averaging time carc.
Averaging time ncarc.
mg/L
cw
Ud
2IR
d/y
350 EF
y
24 ED
kg
70 BW
d
25550AT
d
8760 AT
irtfrfce (mg/fcg-day) <
Contaminant
TOTAL TRIHALOKdHANES
CWxiRxEFxED
BWxAT
RME
Cone.
tngIL
1.00E-01
uraome
Average
Daay
. Dose
mg/kgfd
Chronic
ko«ay
?:do»-
mQ/kgft
Lifetime
Cancer
nitnltr
. rw
Systemic
Hazard
Quotient
9.39 E-04 2.74E-03 5.73E-06 2.74E-01
-------
Rak &6nates tor Total Trflialomethanes at the MCL
CWM resident drinking water fngestioa
Concentration mg/L CW
Ingestion rate Ud 11R
Exposure frequency d/y 350 EF
Exposure duration y 6 ED
Body weight kg 15BW
Averaging time carc. d 2S550AT
Averaging time ncarc. d 2190 AT
Intake (mg/kg-
-------
WerBwi*HdrTwiWetomf***iBWX
nimiliai g»fi y hiim itmnaiw.
TOTOL THmUMETHOWB
ioee-
-------
Risk Estimates for Total TrtiaJomethanes at the MCL
Mutt resident showering inhalation.
Concentration
mg/m3
CA
Inhalation rate
m3/min
0.0138889 IR
Exposure frequency
d/y
350 EF
Exposure duration
y
24 ED
Body weight
Kg
70 BW
Averaging time carc.
d
25550 AT
Averaging time ncarc.
d
8760 AT
Shower duration
min/d
12 ET
Intake(mo/fco-day) a» CAxlRxETxEFxED
BW x AT
tortile
Avenge Chronic
RUE OaBy .. ,DeBy-/:
Cone. Dees Dess
ComMrHnant mg/m3 mgftgfd mgfr gfd
TOTAL TRIHALOMETHANES 1.52E+00 1.19E-03 3.48E-03
lifetime Systemic
Cancer Htaerd
Risk Quotient
9.606-05
?.80EH»
-------
Male Estimate for Total Trtiafomeffiane* at the MCL
CWJtf resident df&iktag water darmai contact
Concentration m^L
Surface area cm3
Exposure frequency d/y
Exposure duration y
Body weight kg
Averaging Urns care. d
Averaging time ncarc. d
Bath duration h/d
Convaraion Factor l/cm3
Oarmal Permeability Constant cm/hr
(chemical specific)
CW
7200 SA
350 EF
6 ED
15 BW
25550 AT
2190 AT
0.33 ET
1.00E-03 CP
PC
CWx SAx PCx ETx EFx ED x CF
BWxAT
Contaminant
TOTAL THIHALOMETHANES
RM6
Cone
Utotfmi
Average;
•-"Oa»y.
Ooac
Chronic
' B**
OOf
mgflctfd
UVSRIV
Csicar
v Rttt '
Syitfemte
Hazard
Quottant
Deanat
Permeate
Coefil
cm/ft
1.00E-01 " 1.306-04 1.52E-03 7.946-07 1.52E-01 1.006-01
EttE-CT 1-S2E-Q1
-------
APPENDIX III
AIR MODELING SUMMARY
-------
Air Pollution
An important component of environmental risk in the City of
Chester is air pollution. Air pollutants are airborne
contaminants that can be particulate (including smoke or dust
particles and fine liquid mists) or gaseous in form. The primary
route of exposure to these pollutants is through inhalation.
AIR QUALITY MONITORING
Pursuant to federal regulations (40 CFR 58), the
Pennsylvania Department of Environmental Resources (PADER)
maintains a statewide network of air quality monitors in order to
determine compliance with health-based National Ambient Air
Quality Standards (NAAQS). NAAQS exist for the six criteria
pollutants: carbon monoxide (CO), lead, nitrogen dioxide (N02) ,
ozone1, particulate matter (expressed as particulate smaller
than 10 micrometers in diameter, PM-10), and sulfur dioxide
(S02) .
In Chester, PADER samples the air for five of these
pollutants (all except CO) at its monitoring station on
Philadelphia Gas Works (PGW) property at Front & Norris Streets.
Table 1 summarizes air quality with respect to the five
pollutants monitored at the PGW site.
Note that monitored concentrations for ozone exceed national
standards. More than the other pollutants for which NAAQS exist,
ozone exceedances are caused by the release of other substances
(especially volatile organic compounds, nitrogen oxides, and
carbon monoxide) that cause the formation of ozone downwind,
sometimes after travel distances of hundreds of miles. Tens of
million of Americans, including most citizens of the northeast
corridor in a contiguous area that stretches from Virginia to
Maine, live in areas that violate the ozone NAAQS. The Clean Air
Act, as amended in 1990, has established a number of requirements
for areas exceeding the ozone NAAQS in an effort to reduce
emissions of ozone precursors and meet the NAAQS. See EPA's
Ozone— Good Up High. Bad Nearby (EPA-451/F-93-010) and Smog; Its
Nature and Effects. (Inside EPA, October 1987)j_ for more
information.
Although enforceable ambient standards exist for only six
criteria pollutants, many other contaminants threaten human
health. Because routine monitoring is limited to the criteria
1In this context, we are discussing ground-level
(tropospheric) ozone, which can irritate and damage the lungs and
other sensitive tissue. Ozone in the upper atmosphere (the
stratosphere) helps shield the earth from certain ultra-violet
radiation emitted by the sun. This "good" ozone is formed
naturally and independently from ground-level ozone pollution.
-------
pollutants and this monitoring may not be representative of the
entire City of Chester, air quality modeling has been used to
estimate potential inhalation risks to Chester residents. This
modeling is described below.
MODELING OF POINT AND AREA SOURCES
Air quality models are mathematical representations of the
way contaminants move in the atmosphere. Models are useful in
characterizing air pollution in the City of Chester for a number
of reasons. First, the number of monitors and the location of
suitable monitoring sites in the city are finite, while a model
can accomplish estimates of air quality impacts at any location.
Second, while it is impractical to monitor for every conceivable
contaminant that may be in the air, modeling can be used to
estimate concentrations of most non-reactive contaminants for
which an emission rate can be estimated. Finally, monitoring can
only provide information regarding the pollutants being
monitored, at the time and location the monitoring is performed.
The information gathered during short-term monitoring studies is
not always representative of typical conditions or long-term
averages, nor can it generally be used to predict the
effectiveness of control strategies.
In order to estimate ambient concentrations, air quality
models require data that describes the emissions, the
meteorology, and the terrain of the area to be modeled. For the
Chester Study, meteorological data collected at Philadelphia
International Airport and terrain data from the United States
Geological Survey were used. The emissions inventory was
developed by using inventories of criteria air pollutants and
ozone precursors, maintained by the states of Pennsylvania, New
Jersey, and Delaware (pursuant to Title I of the Clean Air), and
limited air toxics inventories (Toxics Release Inventory)
maintained by EPA (pursuant to Title III of the Clean Air Act) to
identify as many potential sources of air pollution as possible.
Then, emissions of specific air contaminants were estimated using
information found in a variety of references. All of the
emission sources and methods used to estimate the emission rates
are found in the report Air Toxic Emission Inventory and
Dispersion Modeling for Chester. Pennsylvania, prepared by
Pacific Environmental Services (PES) under contract to EPA.
Figure 1 summarizes the emissions inventories in terms of
emissions of volatile organic compounds (VOCs) and particulate
(PM) from point and area sources. Point sources are emissions
from stacks and vents that are handled as discrete sources in the
modeling. Area sources are emissions such as consumer solvent
use that occur reasonably uniformly over some geographical area.
Point, area, and mobile source inventories are discussed in
detail in the report Air Toxic Emission Inventory and Dispersion
Modeling for Chester. Pennsylvania.
-------
Once emission rates were estimated for the 700-odd
pollutants that were identified, the. model was run once for each
pollutant to generate estimates of annual average concentrations
at locations throughout the City of Chester. Shorter-term
averages were estimated for some of the criteria pollutants. The
results of this modeling are found in the report Air Toxic
Emission Inventory and Dispersion Modeling for Chester.
Pennsylvania.*
MODELING OF MOBILE SOURCES
While emissions from mobile sources were included with the
area source inventory, a special modeling study was made of
emissions from vehicular traffic on Second Street, between
Thurlow and Montgomery Streets. Pennsylvania Department of
Transportation traffic counts and estimates from the Delaware
County Resource Recovery Facility solid waste permit application
were used, along with the MOBILE and PART5 emissions of VOCs and
particulate, respectively. Then, the CAL3QHC model, which is
specifically designed to accomplish estimates of short-term
average pollutant concentrations from roadway emissions, and the
ISC model were used to estimate ambient concentrations of VOC and
particulate. Speciation profiles were applied to the particulate
and VOC concentrations to produce contaminant-specific
concentration estimates, the methodology and results*of this
modeling are documented in Appendix J of the report Air Toxic
Emission Inventory and Dispersion Modeling for Chester.
Pennsylvania~
UNCERTAINTY
While the air quality analysis provides a reasonable
estimate of airborne the contaminant levels in Chester, there are
a variety of sources of uncertainty associated with the study,
most notably:
• Incompleteness of the emissions inventory;
• Unrepresentative and/or inaccurate the toxic profiles;
• Errors in the source emission estimates;
• Errors/omissions in the emissions source characteristics
2The modeling of ozone, which requires emissions and
meteorological data representing many thousands of square miles,
was beyond the scope of this study. Because ozone is formed and
transported over large distances, ground-level concentrations
tend not to vary substantially from location to location. For
the purpose of the current study, the monitored ozone
concentrations will suffice to characterize current conditions.
-------
(e.g., stack exit velocity, building heights);
• Uncertainties in the dispersion model algorithms; and
• Representativeness of the meteorological data.
The problem of the incompleteness of the source inventory is
troubling as it is impossible to account for non-reported
emissions in a rigorous, representative way.
The problem of unrepresentative or inaccurate toxic profiles
results, in part, from the use of very broad source categories.
For many of the VOC sources, especially those related to solvent
use and chemical and petrochemical manufacture, the existing
inventories are not specific in describing the industrial
activities that are producing emissions. (For example, "chemical
manufacturing— average" and "organic solvent use— general" were
not uncommon).
Reliance on the SPECIATE database for many of the profiles
of VOC emissions is also an important source of uncertainty.
SPECIATE was developed for use in ozone modeling and,
consequently, has drawbacks for use in the Chester emissions
inventory.
First, because ozone is a secondary pollutant (formed by the
photo-oxidation of VOCs and other precursor emissions), the ozone
domains are quite large and concentration gradients are
correspondingly small. Correctly estimating the constituent
chemical species of VOC emissions from any single emission point <
(even a large one) is much less important than the correctness of
large geographical portions of the inventory as a whole. For
these types of inventories, the speciation of source categories
only needs to be accurate on average for a fairly broad region.
(In statistical terms, the estimate of the average that is
important, but the deviation of any given source from the average
is inconsequential.) In contrast, the modeling for Chester, did
was quite local, and if a large emission points source's profile
deviates greatly from the estimate from the SPECIATE database,
then estimates of local pollutant concentrations will be
effected.
Also, in the development of the SPECIATE database, emphasis
was placed on reactivity with respect to the potential ozone
formation— toxicity was a secondary concern at best. There may
be instances were chemical is in a SPECIATE profile is used to
represent a class of compounds of similar reactivity. While the
compounds may have similar reactivity, they may not have similar
toxicities.
Uncertainty is discussed in more detail in Section 5 of Air
Toxic Emission Inventory and Dispersion Modeling for Chester.
Pennsylvania.
-------
Table 1
Pollutant
NAAQS
(|lg/m3 unless indicated)
1993 Monitored
Concentration
Oj, l-hr(a)
120 ppb
123 ppb
PM-10, annual(b)
50
27
PM-10, 24-hr(a)
150
60
Pb, cal. quarter(c)
1.5
0.04
SO* annual(c)
80
24
SO* 24-hour(d)
365
69
SOa 3-hour(d)
1300
121
NOz, annual(c)
100
39
CO, 8-hour(d)
10
not monitored
CO, l-hour(d)
40
not monitored
Data shown are from 1993, the most recent year for which complete data are available.
(a) Standard is attained when the expected number of exceedances per year is less
than or equal to 1. (Reported monitored concentration is the second-high.)
(b) Standard is attained when the expected annual arithmetic mean is less than or
equal to 50.
(c) Never to be exceeded. (Reported monitored concentration is the average of one
quarter of available data from 1994.)
(d) Not to be exceeded more than once per year. (Reported monitored concentration
is the second-high.)
-------
Refinery Fugitives
Misc. Production
Figure 1: Modeling Emissions Inventory
VOC Point Sources VOC Area Sources
67,258 tons/year 17,408 tons/year
Chemical Processes Lawnmowers/Tractors
Surface Coating
Coating Oven
Paper ^oatip,|(ro|eum jap^g Petro. 1 ransfer
Automobile Painting Gravure Printing
PM Point Sources
5,001 tons/year
Industrial Boilers
Utility Boilers
Consumer Solvents A
A/ft
Industrial Boilers
Other
Airport Operations
Gasoline Dist.
Other
PM Area Sources
29,234 tons/year
Unpaved Roads
Mineral Products
Other
Petroleum Refining
Paved Roads
Off-Road Diesel
Stationary Combu
Other
Clonstuction Erosion
Figure 1 displays the major emission sources from the point and area source modeling
inventories. (Mobile sources are excluded.) It should be noted that, as a modeling
inventory, this inventory is biased toward larger sources (especially sources outside
of Chester) because only those sources which were believed to have the potential to
significantly impact Chester were included. For example, a 1,000 ton/year source in
Wilmington would be included in the inventory while a 10 ton/year source may not.
-------
APPENDIX IV
FIELD PROTOCOL FOR AIR MONITORING STUDY
-------
CHESTER MONITORING STUDY
A Ion? term (1-year), canister based air monitoring study is
proposed for the Chester, PA area to assist in the identification
of air pollutants impacting the study area.
t The Study will be a cooperative effort involving EPA, PA DER
and MD Division of Monitoring (DAM).
& Air analysis will be conducted by MD DAM focusing on T014 and
an Ozone precursor scan for air, toxics ( approximately 80
volatile organic compounds).
& Plans are for 3 stations in the Chester area located at the
Chester COPAMS, Center City Chester, PA and Marcus Hook,PA
PADER will operate the air toxic monitoring stations and MD DAM
will provide the analytical support.
& Three sampling units ($15,000/site) will be set up at each
station to enable uninterupted monitoring. PADER will be
responsible for the monitoring, receipt and shipment of canisters
to and from MD DAM for analysis. ( Note that the $15,000/site is
only the cost of the sampling units - the canisters, operator and
analytical costs are not included. Analytical costs would exceed
$250,000 if a contractor were to be utilized).
£> Current action items include:
- Preparation of Work Plan / QA Plan by ESD.
- PADER conducting a site surveillance investigation for
possible locations for the Center City Chester site.
- PADER to meet with MD DAM and certify/leak check/clean
samplers that are currently available for use.
- ESD to procure the loan/use of 5 samplers
and 30 canisters for the study.
The current plans are for the first station to commence
sampling in mid-December/ 1994 at the Chester COPAMS.
Victor Guide 215-597-1602
Patrick Anderson 215-597-8177
Ted Erdman 215-597-1193
EPA Contacts:
PADER Contacts:
Ben Brodovicz
Michael zuvich
Dick Ruhl
Gary La Belle
717-787-6548
717-787-6546
610-832-6133
717-787-9480
410-631-3280
410-631-3288
MD DAM Contacts: Dick Weis
Walt Cooney
-------
APPENDIX V
INVESTIGATION PLAN FOR MOBILE ODOR SURVEILLANCE
-------
Chester City Odor Investigation
The project began on Friday, Nov 25th at 4:00 PM and ran
continuously until Wednesday Nov 30th at midnight.
The major activities we planned to do were:
1. Respond to citizen complaints
2. Conduct general surveillance
3. Conduct off-hour inspections at DELCORA, Thermal-Pure
and Westinghouse
4. Conduct air monitoring for organics using the mobile
analytical unit. This would involve monitoring the
ambient air in the general vicinity and comparing those
results with grab samples taken from suspected sources
of odor.
During the study period we did not receive complaints form the
community. The surveillance logs indicate that odors from
DELCORA and Westinghouse could be detected by DER staff from
time-to-time. These odors did not constitute violations however,
because the public component was missing.
The MAU was in operation each night of the study. The hours of
operation were 6:00 PM to 6:00 AM.
The following off-hour inspections were conducted during the
study:
Westinghouse 11/26
11/30
11/30
Thermal-Pure 11/28
11/30
DELCORA 11/29
11/30
No odor violations were documented during the study. An NOV was
sent to Thermal-Pure for storage and manifest violations
documented during the 11/30 inspection.
The absence of complaints could be due to the following:
1. Thermal-Pure was not operating until 11/20
2. DELCORA had low flow into the facility. The
incinerator was down for a period of time due to no
sludge feed.
3. The winds were generally blowing away from the
community.
-------
Private Wells
66 Wells
1 1 Walk
10 Wells
6 Wells
No Welle
i
Chester, PA - Study Area
Site Locations
Chester
Trainer'
TC3 ..vaMj*CU#
\ ~net v<
i
Tf
u
5,
-------
> 16
11-15
6-1 O
no wells
Additional Well*
Number of Private
Wells
Chester, PA - Study Area
Site Locations
fS
i
u
.1
-------
Number of Private
Wells
Additional Wells
Eddv«twi« S*
Wi h(M WADE
|/ChMer
DUMP
MILES
Ground Water Contamination
No Ground Water Contamination
Unknown
Sensitive Ground Water Areas
in Relationship to Private Wells
rn
I
Tf
4J
a
fa
-------
CHESTER RISK PROJECT
FIGURE 4-4 - RISK TRADE-OFFS
DISINFECTION BYPRODUCTS VS. MICROBIAL GROWTH
-------
1.00E-05
1.00E-03
CHESTER RISK PROJECT
FIGURE 4-5 - COMPARISON OF RISK LEVELS FOR FINISHED WATER SUPPLIES
LIFETIME CANCER RISK ESTIMATES BASED ON AVERAGE CONTAMINANT LEVELS IN 1993
1.00E-06
1.00E-07
SOURCES
CHESTER WATER AUTHORITY
PHILADELPHIA WATER DEPARTMENT
1.00E-04
Treatment Process
OF CONTAMINATION
PHILADELPHIA SUBURBAN WATER AUTHORITY
EPA'S CANCER RISK LEVEL POINT OF DEPARTURE
V.
- ONE ADDITIONAL CANCER IN 10,000
-------
CHESTER RISK PROJECT
FIGURE 4-6 - COMPARISON OF RISK LEVELS FOR FINISHED WATER SUPPLIES
, ^ LIFETIME NON-CANCER RISK ESTIMATES BASED ON AVERAGE CONTAMINANT LEVELS IN 1993
1 .ou
EPA'S NON-CANCER RISK LEVEL POINT OF DEPARTURE-INTAKE DOSE EQUALS BENCHMARK DOSE
All Sources Treatment Process
SOURCES OF CONTAMINATION
CHESTER WATER AUTHORITY
PHILADELPHIA SUBURBAN WATER AUTHORITY
PHILADELPHIA WATER DEPARTMENT
-------
CHESTER RISK PROJECT
FIGURE 4-7 - COMPARISON OF RISK LEVELS FOR FINISHED WATER SUPPLIES
LIFETIME CANCER RISK ESTIMATES FOR THMS BASED ON AVERAGE LEVELS DETECTED IN 1993
1.00E-03 r—
1.00E-04
1.00E-05
1.00E-06
PUBLIC WATER SUPPLY
CHESTER WATER AUTHORITY
ill
PHILADELPHIA SUBURBAN WATER COMPANY
ill COATESVILLE WATER AUTHORITY
III PHILADELPHIA WATER DEPARTMENT
iSiiSi
¦¦ ¦ 0$m
iiiiiaiii
THMS-TRIHALOMETHANES ARE PRODUCED DURING THE CHLORINATION PROCESS
MCL-MAXIMUM CONTAMINANT LEVEL; PP8-PARTS PER BILLION
-------
1.50
1.00
0.50
0.00
PUBLIC WATER SUPPLY
CHESTER WATER AUTHORITY
I , 3 PHILADELPHIA SUBURBAN WATER COMPANY
, COATESVILLE WATER AUTHORITY
% /i: PHILADELPHIA WATER DEPARTMENT
CHESTER RISK PROJECT
FIGURE 4-8 - COMPARISON OF RISK LEVELS FOR FINISHED WATER SUPPLIES
LIFETIME NON-CANCER RISK ESTIMATES FOR THMS IN 1993 BASED ON AVERAGE LEVELS
RISK LEVEL FOR THMS AT THE MCL OF 100 PPB - INTAKE DOSE EQUALS BENCHMARK DOSE
X
-------
1.00E-05
CHESTER RISK PROJECT
FIGURE 4-9 - COMPARISON OF RISK LEVELS FOR FINISHED WATER SUPPLIES
ANNUAL CANCER RISK ESTIMATES BASED ON AVERAGE CONTAMINANT LEVELS
CO
cc
oc
LU
o
z
<
o
1.00E-06 -
1.00E-07
1989
1990
1991
YEAR
1992
1993
-B- CWA-ADULT
CWA-CHILD
PSWC-ADULT
+- PWD-ADULT
PWD-CHILD
PSWC-CHILD
CWA-CHESl ER WATER AUTHORITY
PSWC-PHILADELPHIA SUBURBAN WATER COMPANY
PWO-PHILADELPHIA WATER DEPARTMENT NOTE' RISK ESTIMATES BASED ON AN EXPOSURE DURATION OF ONE YEAR ONLY
-------
CHESTER RISK PROJECT
FIGURE 4-10 - COMPARISON OF RISK LEVELS FOR FINISHED WATER SUPPLIES
YEAR
-e- CWA-ADULT -
-------
Blood Lead Levels
in Children
Upland
Chester, PA - Study Area
Site Locations
Chester
0*11 MM
•TU &=! 10th tin
Train,
Mar cub
vo
iH
i
OJ
u
3)
-------
-------
Upl#rtd
Eddyttone
Chester
IADE
Tr«inor
iMICULI'
E DUMP
;\Mareu*
MILES
Chester, PA - Study Area
Site-Related Hazard Index For Soil:
Child Receptor
HI < 1
HI >= 1
No Data
HI = Hazard Index
ao
fH
i
g
.1
£
-------
Upland
Eddv«ten«
Chester
tADE
Tr«ini
iMtCULltE DUMP
\M»rcu«
Chester, PA - Study Area
Site-Related Hazard Index for Soil
Adult Receptor
HI < 1
HI >= 1
No Data
IH = Hazard Index
c
OS
CP
u
a
-------
-------
Upland
Ettdy«te>ne
DE CuV INCINERATOR LF #1
Chester
fADE r
Tr«ini
fMICULitE DUMP
MILES
Wi
\ «
>A\
SrVSX
0\f TJjL
r
,M»reu«
W <¦
\ N
V.
\ x*
\//
Chester, PA - Study Area
Site-Related Carcinogenic Risk for Soil:
Adult Receptor
Cancer Risk < 1.0E-06 $
Cancer Risk >= 1.0E-06
but
Cancer Risk < 1.0E-04
Cancer Risk >= 1.0E-04 ®
No Data
mum
i
Tt
4)
U
.1
-------
STORET Locations
Delaware County, PA
Chester Study Area
9 STORET Stations
^22094
0/QNO172
477O50 |gELFISH-07
£p/QN016B
tf0|||0aG49HB
'QN01 62
-------
Chester, PA - Study Area
Cancer Risks:
Surface Water, Sediment and Fish Tissue
CR >= 1E-6
CR < 1E-6 and CR >= 1E-4
CR < 1E-4
Surface Water A M, ' A
Sediment ~ ~ ~
Fish Tissue # ig? V
CR = Cancer Risk
-------
iA
-------
Chester, PA - Study Area
HI = Hazard Index
Surface Water
Sediment
Fish Tissue
HI < 1
HI >=
A
~
~
~
•
m
Noncamcer Risks To Adults
Surface Water, Sediment, and Fish Tissue
•n
ri
4)
U
-------
Chronic Index: EPA Region
On-Site Releases
¦L
-------
Residual Mass: EPA Region III
On-Site Releases
o
< 10th Percentile
10th Percentile
20th Percentile
30th Percentile
40th Percentile
50th Percentile
ISIlfll 60th Percentile
70th Percentile
80th Percentile
90th Percentile
MILE6
Scale 1 : 3308410
Aggregated Grid:
S x 8 Mile Blocks
Sewcs. Toxic R* It as a Inventory Dusia for 1997
1:2,000,000 USGS DLG3 Film
Prqjr.Tion. ARxtrs Equal Area Projection
Preptzrsd by; Ltiht S. Rickordj
EPA JUgiom El Geographic fafomumoa Csnltrr
Dose: April It, 1994
EpA Region UI
S
Air, Radiation, A Toxics Division
£ Dr. Debra L Forman
-------
Chronic Index & Residual Mass
On-Site Releases
< 10th Percentile
10th Percenti
20th Percenti
30th Percenti
40th Percenti
50th Percenti
60th Percenti
70th Percenti
80th Percenti
90th Percenti
No 1992 Releases or
Transfers Reported
EPA HI
%
& Air. Radiation. A Toxics Division
o
Dr. Debra L Forman
0 10 20 30 40 60 60 70 80 80 1QO
MILES
Scale 1 : 3308410
Aggregated Grid:
8X8 Mile Blocks
Samrce Toxic Release lnvmlory Data for 1992
1 2,000,000 USGS DI.G3 Files
Projection Album Et/nal Area Projection
Prqtared iy: Leslie S. Richards
EPA Jiegiom JJ3 Geographic btformantm Cmuer
Date: April 11, 1&4
-------
Chester, PA - Study Area
Upper Bound Lifetime Cancer Risk
by Inhalation for VOCs (Without Coal Tar)
Cancer
Risk
< le-6
Cancer
Risk
>= le-6
&
<
3e-6
Cancer
Risk
>= 3e-6
&
<
le-5
# Cancer
Risk
>= le-5
&
<
3e-5
Cancer
Risk
>= 3e-5
&
<
le-4
• Cancer
Risk
>= le-4
i
<0
Sh
• I"*
-------
/ V Y S
yyV/
\yy ,s
/5x\
V AA -
¦•^7/1
/V
l—X^ / //s\ ,i ^sJ(i M // (XXX7\Y( *T
yx J t M
i /^LcV'3^>/>tK^rX' 11/
\ ... ttll
<< \V /\ /•/• Vc' \
r\\\ \v>/y A>s
\ x \ < \ / V> v /i
\XW //\i5 v
S<>:.,
> ;v>.,'
Y a-I •' • *•> > ¦''
^Ssl-OSN
l-: < > ? ' v ^ '
Jr
'-.Hi $ Uptand
£$hp J#
.r^ #| # w
- ,• '
us
} '
. C !&* v < -v *"v > * '
¦ * ,-- * -':
< ; > vr '
^ v v V" •-•
?vU
Eddy«ton«
\4*
"T^ V S t ^ -
" V v\A^TxS= 3e-6
&
<
le-5
Cancer Risk
>= le-5
&
<
3e-5
Cancer Risk
>= 3e-5
&
<
le-4
->
Cancer Risk
>= le-4
0.26
0.6
MJLf S
a 75
-------
Chester, PA - Study Area
* VOCs Without Coal Tar
Upper Bound Lifetime Cancer Risk
by Inhalation for VOCs* and PM
Cancer
Risk
< le-6
Cancer
Risk
>= le-6
&
<
3e-6
Cancer
Risk
>= 3e-6
&
<
le-S
# Cancer
Risk
>= le-S
&
<
3e-5
Cancer
Risk
>= 3e-5
&
<
le-4
• Cancer
Risk
>= le-4
¦
CD
u
a
-------
Non-Carcinogenic Hazard Index
by Inhalation for VOCs
Risk
< 1.0
Risk
>= 1.0
& < 1.5
Risk
>= 1.5
& < 2.0
Risk
>= 2.0
& < 2.5
Risk
>= 2.5
i
Chester, PA - Study Area
n
rn
Tf"
-------
* vr'rf'-yrl*-
-iV •••?' si*"* >' ¥
0- •>:•' ;"
. ', ir..i.-; .«• i A V- v -
:.A j.<.; •«- f -.-4
i&4»''
Upinml
Eddy*ton«
hester
Tr«in.
\ \V\\
MILE6
Chester, PA - Study Area
Non-Carcinogenic Hazard Index
by Inhalation for PM
t&s
m
Risk
< 1.0
Risk
>= 1.0
&
<
1.5
Risk
II
A
&
<
2.0
Risk
>= 2.0
&
<
2.5
Risk
>= 2.5
m
¦*t
a>
u
.§>
-------
Chester, PA - Study Area
Non-Carcinogenic Hazard Index
by Inhalation for PM and VOCs
Risk
< 1.0
Risk
>= 1.0
&
<
1.5
Risk
>= 1.5
&
<
2.0
Risk
V
II
K>
O
&
<
2.5
Risk
>= 2.5
Tf
OJ
u
a
-------
-------
* VOC Locations
Chester, PA - Study Area
Site Locations
Chester
rt<*;
TCI M>Wn>4a Contrarlt
Tti TK«frrwl 4r*ti
TC1Q h! RamaAtflv (a
TC11 WntlftfhaUM lr»«fc>.
TCI 3
TCT4 Dm
VOC Emiiuinn Volumes
70,001
- ao.ooo
60,001
" 70,000
60,001
- 60,000
40,001
- 49,998
30,001
- 40,000
20,00 1
- 30,000
10,001
¦ 20,000
6,001
- 10,000
1 -
B,o5o
~
~
~
~
VO
m
i
oj
u
a
-------
VOC Emission Volumes
80,000
70,000
60,000
49.998
40,000
* JOC Locations
TCI«
Chester
Chester, PA - Study Area
Site Locations
TC3AM»«u.
TCI.
y'. ' \
\ ~ rci V'
r-
i
Tf
4J
fc.
S
-------
------- |