Evaluation of Contaminants in Fish from Lake Washington, 2004 Report

Final Report

Evaluation of Contaminants in Fish from Lake Washington

King County, Washington

DOH 333-061 September 2004

Table of Contents

Acknowledgements 2

Foreword 3

Glossary 4

Executive Summary 6

Introduction 8

Results 11

Discussion 14

References 26

Appendix A 28

Appendix B 33

Appendix C 45

Appendix D 67

Appendix E 73

Acknowledgements

We would like to thank the King County Department of Natural Resources and Parks (King

County DNRP) for funding this research and providing the data for this study. Jen McIntyre and

Dave Beauchamp, University of Washington School of Aquatic and Fishery Sciences, designed

the study, collected and analyzed fish tissue, and assisted with data and report review. Jonathan

Frodge, Randy Shuman, and Deb Lester (King County DNRP) provided valuable comments and

information for the report. We wish to thank Eric Warner and Glen St. Amant (Muckleshoot

Indian Tribe), Sandie O’Neill (Washington State Department of Fish and Wildlife), Dale Norton

and Maggie Dutch (Washington State Department of Ecology), and Lon Kissinger (US

Environmental Protection Agency) for their comments and review. We also want to thank Liz

Carr, Rob Duff, and Gary Palcisko, Washington State Department of Health, for their input and

review. Finally, we would like to thank Public Health Seattle and King County for their

partnership in issuing fish consumption guidance based on this report.

Foreword

The Washington State Department of Health (DOH) prepared this technical support document as

a basis for evaluating the necessity of public advisories on fish consumption. This document is

not intended to provide advice to the public. It represents a scientific analysis of fish tissue

sampling data that serves as a necessary precursor to any decisions made regarding the need for

a fish consumption advisory.

The toxicologists who prepared this report were Joan Hardy, Ph.D. and Dave McBride, MS.

For additional information or questions contact us at:

Washington State Departme

nt of Health

Office of Environmental Health, Safety, and Toxicology

P.O. Box 47825

Olympia, WA 98504-7846

1-877-485-7316

Website: www.doh.wa.gov/etoxcontact

For people with disabilities, this document is available on request in other formats, to submit

a requ

est, please call 1-800-525-0127 (TDD/TTY call 711).

Glossary

Acute Occurring over a short time (compare with chronic).

Agency for Toxic

Substances and Disease

Registry (ATSDR)

The principal federal public health agency involved with

hazardous waste issues, responsible for preventing or reducing

the harmful effects of exposure to hazardous substances on

human health and quality of life. ATSDR is part of the U.S.

Department of Health and Human Services.

Cancer Slope Factor

A number assigned to a cancer causing chemical that is used to

estimate its ability to cause cancer in humans.

Carcinogen Any substance that causes cancer.

Chronic

Occurring over a long time (more than 1 year) (compare with

acute).

Comparison value

Calculated concentration of a substance in air, water, food, or

soil that is unlikely to cause harmful (adverse) health effects in

exposed people. The CV is used as a screening level during

the public health assessment process. Substances found in

amounts greater than their CVs might be selected for further

evaluation in the public health assessment process.

Contaminant

A substance that is either present in an environment where it

does not belong or is present at levels that might cause harmful

(adverse) health effects.

Dose

(for chemicals that are

not radioactive)

The amount of a substance to which a person is exposed over

some time period. Dose is a measurement of exposure. Dose

is often expressed as milligram (amount) per kilogram (a

measure of body weight) per day (a measure of time) when

people eat or drink contaminated water, food, or soil. In

general, the greater the dose, the greater the likelihood of an

effect. An “exposure dose” is how much of a substance is

encountered in the environment. An “absorbed dose” is the

amount of a substance that actually gets into the body through

the eyes, skin, stomach, intestines, or lungs.

Environmental

Protection Agency

(EPA)

The federal agency that develops and enforces environmental

laws to protect the environment and the public's health.

Epidemiology

The study of the occurrence and causes of health effects in

human populations. An epidemiological study often compares

two groups of people who are alike except for one factor, such

as exposure to a chemical or the presence of a health effect.

The investigators try to determine if any factor (i.e., age, sex,

occupation, economic status) is associated with the health

effect.

Exposure

Contact with a substance by swallowing, breathing, or

touching the skin or eyes. Exposure may be short-term (acute

exposure), of intermediate duration, or long-term (chronic

exposure).

Hazardous substance

Any material that poses a threat to public health and/or the

environment. Typical hazardous substances are materials that

are toxic, corrosive, ignitable, explosive, or chemically

reactive.

Ingestion

The act of swallowing something through eating, drinking, or

mouthing objects. A hazardous substance can enter the body

this way (see route of exposure).

Ingestion rate

The amount of an environmental medium that could be

ingested, typically on a daily basis. Units for IR are usually

liter/day for water, and mg/day for soil.

Inorganic

Compounds composed of mineral materials, including

elemental salts and metals such as iron, aluminum, mercury,

and zinc.

Lowest Observed

Adverse Effect Level

(LOAEL)

The lowest tested dose of a substance that has been reported to

cause harmful (adverse) health effects in people or animals.

Media

Soil, water, air, plants, animals, or any other part of the

environment that can contain contaminants.

Minimal Risk Level

(MRL)

An ATSDR estimate of daily human exposure to a hazardous

substance at or below which that substance is unlikely to pose

a measurable risk of harmful (adverse), non-cancerous effects.

MRLs are calculated for a route of exposure (inhalation or

oral) over a specified time period (acute, intermediate, or

chronic). MRLs should not be used as predictors of harmful

(adverse) health effects (see reference dose).

No Observed Adverse

Effect Level (NOAEL)

The highest tested dose of a substance that has been reported

to have no harmful (adverse) health effects on people or

animals.

Oral Reference Dose

(RfD)

An amount of chemical ingested into the body (i.e., dose)

below which health effects are not expected. RfDs are

published by EPA.

Organic

Compounds composed of carbon, including materials such as

solvents, oils, and pesticides that are not easily dissolved in

water.

Parts per billion

(ppb)/Parts per million

(ppm)

Units commonly used to express low concentrations of

contaminants. For example, 1 ounce of trichloroethylene

(TCE) in 1 million ounces of water is 1 ppm. 1 ounce of TCE

in 1 billion ounces of water is 1 ppb. If one drop of TCE is

mixed in a railroad tank car (13,200 gallons), the water will

contain about 1 ppb of TCE.

Route of exposure

The way people come into contact with a hazardous substance.

Three routes of exposure are breathing (inhalation), eating or

drinking (ingestion), or contact with the skin (dermal contact).

Executive Summary

The Washington State Department of Health (DOH) works to protect and improve the health of

people in Washington State. Part of this mission is to reduce or eliminate exposures to health

hazards in the environment, including contaminants found in fish. Recently, King County

Department of Natural Resources and Parks (King County DNRP) provided DOH with fish

tissue data collected by the University of Washington, School of Aquatic and Fishery Sciences

(UW) as part of an ecological risk assessment to evaluate bioaccumulation of contaminants

through the Lake Washington food web. Whole body fish tissue from cutthroat trout

(Oncorhynchus clarki), northern pikeminnow (Ptychocheilus oregonensis), yellow perch (Perca

flavescens), smallmouth bass (Micropterus dolomieui), and adult sockeye salmon (Oncorhychus

nerka) was collected and analyzed for contaminants that bioaccumulate, including chlordane,

p,p’-dichlorodiphenyltrichloroethane (DDT), mercury, and polychlorinated biphenyls (PCBs).

Data from Lake Washington analyzed in this report are limited due to the small sample size for

most size classes of fish (n =10) and the use of whole body fish tissue rather than edible muscle

tissue (fillets). Regardless of these data limitations, high PCB concentrations in some species

warranted a health assessment for consumers of Lake Washington fish. Findings include:

• Highest mean concentrations of PCBs and mercury in Lake Washington fish were

observed in large northern pikeminnow (>300mm) (1071.4 ppb total PCBs, 387.1 ppb

mercury).

• Large yellow perch (>271 mm) also had elevated mean levels of total PCBs and mercury

(191.1 ppb and 183 ppb, respectively).

• Large cutthroat trout (> 300 mm) had the second highest mean concentrations of total

PCBs (377.4 ppb) and relatively high concentrations of mercury (175.6 ppb).

• Only three smallmouth bass were sampled. Mean concentrations of mercury and total

PCBs were 244.3 ppb and 371.2 ppb, respectively.

• Sockeye salmon had the lowest mean levels of all chemicals of concern.

Based on estimates of consumption for Lake Washington anglers and concentrations of

contaminants in fish, DOH determined that the average angler may be exposed to contaminants

of concern above recommended levels. In order to protect consumers of Lake Washington fish,

DOH provides the following recommendations. These recommendations are emphasized for

women of childbearing age and young children because of potential adverse impacts on the

developing child.

• Eat a variety of fish as part of a balanced diet. Health benefits of eating fish are:

o Fish is an excellent low-fat food, a great source of protein, vitamins, and minerals.

o The oils in fish are important for unborn and breastfed babies.

o Eating a variety of fish helps to reduce your chances of stroke or heart attack.

• Northern pikeminnow should not be consumed.

• Yellow perch greater than 270 mm (10½ inches) may be consumed as an eight-ounce

meal once per month. Yellow perch smaller than 270 mm (10½ inches) may be

consumed as an eight-ounce meal four times per month.

• Consumers of large cutthroat trout greater than 300 mm (12 inches) from Lake

Washington should eat no more than one eight-ounce meal per month. For small

cutthroat trout greater than 300 mm (12 inches), no more than 3 eight-ounce meals per

month are recommended.

• No meal restrictions on sockeye salmon from Lake Washington. Consumers are

encouraged to choose sockeye when consuming local fish.

• Prior to the issuance of this interim advisory, a statewide fish consumption advisory for

large and smallmouth bass due to mercury was in place throughout water bodies in

Washington State, including Lake Washington. Women of childbearing age and children

six years of age or younger should eat no more than two meals per month of any bass

caught in Washington state freshwaters.

The recommendations given above are based on a 60 kg (132 lbs) adult eating eight-ounce

meals. In general, children should eat proportionally smaller meal sizes. Calculations for

multiple chemical exposures do not change the above advice.

Since the above recommendations are based on a small sample size, DOH recommends

additional sampling of northern pikeminnow, yellow perch, and cutthroat trout, to confirm initial

findings of high contaminant concentrations in fish tissue. We recommend that future sampling

include fillet samples for better estimation of human exposure. Other species of fish consumed

by anglers such as rainbow trout, crappie, and bluegill should also be sampled.

Introduction

The Washington State Department of Health (DOH) works to protect and improve the health of

people in Washington State. Part of this mission is to reduce or eliminate exposures to health

hazards in the environment. DOH’s Office of Environmental Health Assessments (OEHA)

conducts environmental health assessments, develops strategies, and provides education and

outreach to communities in order to minimize health impacts from exposure to environmental

contaminants. One focus of OEHA is on contaminants found in fish.

Recently, the King County Department of Natural Resources and Parks (King County DNRP)

provided DOH with fish tissue data collected by the University of Washington, School of

Aquatic and Fishery Sciences (UW) (J. McIntyre, personal communication, 2004). These data

were analyzed as part of an ecological risk assessment to evaluate bioaccumulation of

contaminants through the Lake Washington food web. Tissue from cutthroat trout

(Oncorhynchus clarki), northern pikeminnow (Ptychocheilus oregonensis), yellow perch (Perca

flavescens), smallmouth bass (Micropterus dolomieui), and adult sockeye salmon (Oncorhychus

nerka) was collected and analyzed for four contaminants (chlordane, p,p’-

Dichlorodiphenyltrichloroethane (DDT), mercury, and polychlorinated biphenyls (PCBs))

(hexachlorocyclohexane was measured but not detected). Because this study was designed to

investigate accumulation of toxicants in the food web, whole body fish were used in the analysis.

When DOH conducts a human health evaluation of contaminants in fish, analysis is generally

conducted on fillet tissue because the use of whole body fish tissue is likely to overestimate

potential risks to humans. Nevertheless, DOH decided that data from the King County

DNRP/UW study is useful in making a preliminary human health evaluation for these

contaminants in Lake Washington fish.

The purpose of this report is to review and evaluate potential health risks that may result from

exposure to bioaccumulative contaminants through the consumption of five Lake Washington

fish species. Four chemicals are assessed for cancer and non-cancer endpoints. Consideration is

given to data quality issues (i.e., use of whole body fish tissue vs. fillets and small sample size),

toxicity of the chemicals, potential exposure of fish consumers, consumer body weight,

comparison of contaminant levels with fish in other lakes, and the benefits of eating fish. DOH

provides interim guidance for consuming Lake Washington fish and makes recommendations for

future sampling.

Background

Lake Washington

Lake Washington is a large (87.6 km

) lake located directly east of Seattle, Washington. It is

approximately 28 km long and 65 m deep (Edmondson 1991). Lake Washington is usually

stratified from April through November, with average epilimnetic (the upper thermally-stratified

layer of the lake) temperatures of 6° to 8°

C in winter and 21° to 23° C in summer (Bartoo 1972,

Brocksmith 1999;

http://dnr.metrokc.gov/wlr/waterres/lakes/monitor.htm). Thirty native fish species and

23 introduced fish species have been documented in the Lake Washington basin (E. Warner,

personal communication, 2004; Nowak 2000).

Fish Species

Cutthroat trout, northern pikeminnow, yellow perch, smallmouth bass, and sockeye salmon were

collected from Lake Washington as part of the food web study funded by King County DNRP.

Cutthroat trout were collected from Lake Sammamish for comparison with Lake Washington

fish. Descriptions of the five species including information on their distributions, feeding

patterns, and life histories can be found in Appendix A. Other native and introduced fish species

live in Lake Washington but were not collected for this study (Appendix A). For the species

sampled, northern pikeminnow live the longest (up to 19 years), followed by smallmouth bass

(greater than 10 years), cutthroat trout (6 – 7 years), yellow perch (less than 7 years), and

sockeye salmon (S. O’Neill, personal communication, 2004). For the resident fish, northern

pikeminnow feed higher in the food web than cutthroat trout, followed by smallmouth bass and

yellow perch. Contaminants such as PCBs and mercury may be higher in older and larger fish

because these metabolically resistant contaminants can bioaccumulate over time (i.e., exposure

time is greater) and because they biomagnify as fish grow and feed at a higher trophic level.

Chemicals of Concern

Chemicals that were analyzed and detected in whole fish tissue include chlordane, DDT, PCBs,

and mercury. Hexachlorocyclohexane (lindane and other isomers) was analyzed but not detected

in any samples. These chemicals were chosen since they are frequently observed in aquatic

organisms due to their persistence, toxicity, and ability to bioaccumulate and/or biomagnify. A

description of chemicals that were analyzed and detected in fish tissue samples from Lake

Washington can be found in Appendix B.

Methods

Sampling

Fish were collected to obtain as large of a sample of different predator and prey fish as possible

given the logistical constraints of the project. Whole fish were tested to provide data for toxic

accumulation in the food web of Lake Washington as part of an ecological risk assessment being

conducted by King County DNRP. Fishes were collected by a variety of methods including

gillnetting, angling, mid-water trawl, electroshocking, snorkeling, minnow traps, and submerged

emergent traps. Northern pikeminnow (squawfish), cutthroat trout, and yellow perch were

captured opportunistically throughout the lake between October 2001 and April 2003. Four

cutthroat trout (>300 mm) were sampled from Lake Sammamish. Sample sizes are given below

(Table 1).

Table 1. Number of samples collected per fish species from Lake Washington, Seattle,

Washington between October 2001 and April 2003.

Species Size Class

Number of samples

collected from Lake

Washington

Species Size Class

Number of samples

collected from Lake

Washington

Northern pikeminnow <300 mm 10

>300 mm 10

Cutthroat trout <300 mm 10

>300 mm 10

Yellow perch < 200 mm 10

201 – 271 mm 10

> 271 9

Smallmouth bass NA 3

Sockeye salmon NA 10

Fishes were euthanized in tricane methanosulfonate before they were measured in length to the

nearest millimeter and weighed to the nearest 0.01 gram (McIntyre, 2004). Otoliths and scales

were removed for aging. Individual fish were wrapped in aluminum foil and stored in plastic

bags at –20°

C until they were analyzed for contaminants.

Samples were processed at the King County Environmental Laboratory (KCEL) located in

Seattle, Washington. Large fish were cut into pieces while partially frozen then homogenized

with liquid nitrogen in a Hobart™ buffalo chopper. Equipment was cleaned with methanol

before each sample was homogenized.

Homogenized wet samples were ground with diatomaceous earth to absorb excess water. High

molecular weight (DBC) and low molecular weight (TCX) surrogates were added along with a

50:50 methylenechloride-acetone solvent. The sample was cleaned first by gel permeation

chromatography (GPC) then further cleaned by Alumina. A small aliquot was set aside for

analysis of pesticides (DDT, chlordane, hexachlorocyclohexane). The remainder was digested

with sulphuric acid and reduced in volume. Quality assurance and control measures included

method blanks (diatomaceous earth + surrogates + solvents), spike blanks (method blank +

analytes), two matrix spikes (spike blank + tissue), and a laboratory duplicate (method blank +

tissue). Accepted variability was 100% between duplicates and ± 50% for all recoveries. One

small northern pikeminnow had too little volume of sample for analysis.

Analytical Methods

All fish tissue was analyzed (in 6 batches) as individual whole fish. With the exception of

sockeye salmon and smallmouth bass, fishes were collected and assessed by size (small and large

cutthroat trout and northern pikeminnow, or small, medium and large yellow perch). Total

mercury was analyzed by cold vapor atomic absorption (CVAA) using a modified EPA Method

245.6. Methylmercury was analyzed by Frontier Geosciences using a KOH-methanol digestion

followed by gas chromatography and measurement by cold vapor atomic fluorescence

spectroscopy (CVAFS). Organochlorine analyses followed standard protocols used by KCEL

(gas chromatography with electron capture detection (GC-ECD)) and were reported as

chlordane, DDT, and PCBs.

Data Analysis

Summary statistics were calculated for compounds measured in each fish species and size class

within a given species. Statistics included the mean and median values, standard deviation and

error, minimum and maximum values, 95% confidence interval, sample size, and detection

frequency.

All chemical concentrations were expressed in parts per billion (ppb) wet weight, unless stated

otherwise. Chlordane concentrations were expressed as the sum of alpha and gamma chlordane.

DDT concentrations were expressed as the sum of p,p' congeners of DDT, DDE, and DDD.

PCBs were expressed as the sum of Aroclors 1254 and 1260 (Aroclors 1016, 1221, 1232, 1242,

and 1248 were analyzed but not detected). Mercury was expressed as total mercury (organic and

inorganic forms). Non-detected samples were assigned the value of ½ the corresponding

detection limit. If samples were below a 10% detection frequency, they were not evaluated.

High detection frequencies were observed for each of the four contaminants detected. Arranging

the samples into functional groups, ΣDDT and ΣPCB were detected in all predatory fish samples,

and chlordanes were detected in 96% of predatory fish samples. In forage fishes, ΣDDT was

detected in 86% of samples, ΣPCB in 96%, and chlordanes in 82%.

Metabolites of DDT (DDD and DDE) were detected more frequently than was DDT itself.

Aroclor 1254 was detected more frequently than was Aroclor 1260. All predatory fish samples

contained Aroclor 1254. Alpha-chlordane was more frequently detected than was gamma-

chlordane. For all chemicals, detection frequencies were greater in predatory fish than in forage

fish.

Relative magnitudes of the three organochlorine groups (ΣDDT, ΣPCB, Σchlordanes) were

similar among species, indicating that organochlorines behaved similarly relative to each other in

terms of bioaccumulation. The most concentrated organochlorine was ΣPCB followed by ΣDDT

and Σchlordanes, in the average order of 13:3:1 across species.

Results

Mean contaminant concentrations of chlordane, DDT, mercury, and PCBs were determined for

five fish species by size class (Table 2, Figure 1). Highest mean concentrations of DDT,

mercury, and PCBs were observed in large northern pikeminnow. Highest mean concentration

of chlordane was observed in large cutthroat trout. Lowest mean concentrations for all

chemicals were observed in sockeye salmon. For cutthroat trout, yellow perch, and northern

pikeminnow, the highest mean concentrations for all chemicals were observed in the largest size

class of each species. Mean fish length and mean contaminant concentrations with

corresponding summary statistics were calculated for individual fish species by size class and are

included in Appendix C, Tables C1 - C5.

Figure 1.

Mean contaminant concentrations in whole fish tissue samples from Lake Washington, King

County (2001-2003)

0.0

200.0

400.0

600.0

800.0

1000.0

1200.0

Smallmouth

Bas s

< 300 mm > 300 mm < 200 mm 201 - 270 mm > 270 mm < 300 mm > 300 mm Sockeye

Salmon

Fish Species

Concentration (ppb

)

Chlordane

DDT

Mercury

PCBs

Bars indicate Standard Error (SE)

Cutthroat Trout

Yellow Perch

orthern Pikeminnow

While fish age is generally a better predictor than length in estimating contaminant levels in fish,

fish age is not easily available or known to anglers. Therefore, fish length was used to establish

size categories for assessment purposes. Contaminant concentrations for each chemical were

Table 2. Summary information for fish sampled in 2001 - 2003 from Lake Washington, King County, Washington.

Size

Sample

Class

Chlordane DDT Mercury PCBs size

Smallmouth Bass all 11.0 62.9 244.3 371.2 3

S (< 300mm) 15.0 47.4 42.8 79.2 10

L (> 300mm) 44.3 168.0 175.6 377.4 10

S (< 200mm) 5.0 13.9 32.9 46.6 10

M (201-271 mm) 9.6 48.5 86.8 66.4 10

L (> 271 mm) 16.3 58.7 183.0 191.1 9

S (< 300mm) 7.1 44.5 53.1 140.0 10

L (> 300mm) 40.1 257.7 387.1 1071.4 10

Sockeye Salmon all ND 5.4 37.0 7.8 10

* ppb = parts per billion (wet weight)

S = small, M = medium, L = large

Chlordane concentration is the sum of alpha and gamma chlordanes

DDT concentration is the sum of DDT, DDE, and DDD congeners

Mercury concentration is for total mercury (organic and inorganic)

PCB concentration is the sum of Aroclors 1254 and 1260

All nondetects were reported as 1/2 detection level (except where nondetected below 10%)

ND = nondetected value (below 10% detection frequency)

Northern Pikeminnow

Species

Mean Concentration in Whole Fish (ppb)*

Cutthroat Trout

Yellow Perch

plotted in ppb (wet weight) versus fish length in millimeters (mm) for each species except

smallmouth bass, which were excluded due to their small sample size (see Appendix C). For

cutthroat trout, contaminants increased with greater fish length (p < 0.05). For yellow perch,

mercury and chlordane also increased with increased fish length (p < 0.05). All contaminants

increased with greater fish length for northern pikeminnow (p < 0.05). Fish length was not

correlated with contaminant levels in sockeye salmon.

Chlordane

All species except sockeye had detectable levels of chlordane in whole body samples (Table 2,

Figure 1, and Appendix C). For those species with detectable levels, alpha chlordane was the

predominant form. Higher concentrations of chlordane were associated with increased fish size.

Larger cutthroat trout and northern pikeminnow had the highest concentrations of total

chlordane, with levels of 44.3 and 40.1 ppb, respectively.

Dichlorodiphenyltrichloroethane (DDT)

Total DDT was detected in all fish species. Detection frequencies were high, nearly 100% for all

species except for sockeye, which had a 60% detection frequency. A trend of increased total

DDT concentration was observed with increased fish length (Table 2, Figure 1, and Appendix

C). For all fish species, p,p'-DDE concentrations were greatest, followed by p,p'-DDD, and then

p,p'-DDT. The larger size class of northern pikeminnow and cutthroat trout had the highest

concentrations of total DDT at 257.7 and 168.0 ppb, respectively. Sockeye salmon had the

lowest average concentration of total DDT at 5.4 ppb.

Mercury

All fish species collected from Lake Washington had detectable levels of mercury in whole body

samples. With the exception of sockeye salmon, an increase in mercury concentration was seen

with increased fish length (Table 2, Figure 1, and Appendix C). Highest concentrations of total

mercury were observed in smallmouth bass and large northern pikeminnow at 244.3 and 387.1

ppb, respectively. Small yellow perch, sockeye salmon, and small cutthroat trout all had total

mercury concentrations below 50 ppb.

Polychlorinated biphenyls (PCBs)

Total PCBs were based on Aroclors 1254 and 1260; other Aroclors were analyzed but not

detected. Detection frequencies for total PCBs were greater than 90% for all species except for

sockeye salmon (detection frequency of approximately 25%). With the exception of sockeye,

total PCB concentrations tracked well with increased fish length (Table 2, Figure 1, Appendix

C). A possible explanation for the lower association in sockeye may be due to their more

uniform fish size relative to other species. As with the other contaminants, concentrations of

total PCBs were lowest in sockeye salmon (7.9 ppb). Large northern pikeminnow exceeded

1000 ppb total PCBs. The next highest concentration of total PCBs was observed in large

cutthroat trout at 377.4 ppb.

Discussion

The following is a discussion of the possible human health risks associated with eating fish from

Lake Washington. Estimates of current exposure are made based on assumptions about how

much fish people eat from the lake. These estimates indicate that some Lake Washington fish

eaters may be exposed to contaminants above a level of concern; therefore, allowable

consumption rates are calculated below.

Also considered in the discussion are data limitations, including sample size and the use of whole

body tissue (instead of fillets). Finally, other factors important to the process of providing advice

to fish consumers regarding exposure to contaminants are discussed, such as multiple chemical

exposure, background levels of contaminants, and benefits of eating fish.

Estimating Exposure

To determine whether a contaminant in fish is a health risk, we must estimate the dose to which a

person may be exposed. Dose is defined as the amount of a substance to which a person is

exposed over some time period, usually expressed as milligrams per kilogram per day. A basic

premise of toxicology is that the “dose makes the poison,” meaning that health risks usually

increase with dose. In addition to our dose estimate, we also need information regarding what

dose is toxic. The most sensitive endpoints of PCB toxicity include the immune system for the

general population and developmental effects for the fetus and young children. For mercury,

impacts on the developing fetus are of primary concern, leading to guidance for consumption of

mercury-contaminated fish that is focused on women of childbearing age. This toxicity

information is used to set allowable daily intakes, also known as oral reference doses (RfDs).

RfDs are doses below which adverse health effects are not expected. Specific toxicity

information on PCBs, mercury, DDT, and chlordane is presented in Appendix B.

The amount of fish consumed is a key parameter when estimating exposure to contaminants in

fish. One way to establish this parameter is to conduct a consumption survey, asking how much

fish is being eaten, how often, and which species is being consumed. Information on

consumption is used to determine if consumers are exposed to a chemical above the RfD and

focus risk communication on those populations.

King County DNRP recently released results of a human use survey for shoreline areas in Lake

Union, Lake Washington, and Lake Sammamish (King County DNRP 2004). The study

included information on areas of highest recreational use for Lake Washington (Gene Coulon

Park, Magnuson Park, Seward Park, and Kennydale Park) and areas with the highest average

number of anglers per visit (Clarke Beach, Stan Sayers Park, Gene Coulon Beach Park, and

Mount Baker Park). One of three goals of the survey was to provide exposure information for

use in human health risk assessment for Lake Washington, Lake Sammamish, and Lake Union.

The survey focused on identifying fishing frequency and consumption patterns of anglers who

used these lakes.

Anglers from Lake Washington fished from either the shoreline or from a boat at relatively equal

rates. Approximately 98% of all anglers sought finfish rather than other aquatic organisms.

Oral Reference Dose (RfD)

Oral reference doses (RfDs) are levels

of exposure to chemicals below which

non-cancer effects are not expected.

EPA sets RfDs based on chronic

exposure only. An RfD is derived by

dividing a toxic effect level determined

in animals or humans by “safety

factors” to account for uncertainty and

provide added health protection.

Most anglers fished only at the site where they were interviewed. The race of anglers in Lake

Washington was predominately Caucasian (62%), Asian (14%), or African American (10%).

The overall mean fish consumption rate for anglers in Lake Washington was 10.8 grams/day

(95

percentile = 30.2 grams/day) and for children of Lake Washington anglers was 9.5

grams/day (95

percentile reported as 86.2grams /day). Major fish species preferred by anglers

in the three lakes included perch, trout, bass, and salmon. Anglers from Lake Washington, Lake

Union, and Lake Sammamish consumed their catch an average of 1.3 times per month.

Consumption patterns from this study suggest that the surveyed population does not rely on self-

caught fish as a large portion of their diet (King County DNRP 2004).

Comparison with Oral Reference Dose

To determine if consumers of Lake Roosevelt fish are

exposed above the RfDs for each contaminant of concern,

a dose was calculated for each contaminant using the

overall mean fish consumption rate of 10.8 grams/day for

Lake Washington anglers (converted to 11.6 ounces/month

or 1.5 eight-ounce fish meals per month). This

consumption rate was then used to estimate a dose for each

contaminant, which was divided by its respective RfD to

yield a ratio known as a hazard quotient. A ratio less than

1.0 would indicate no expected adverse health effects. If a

dose exceeds its RfD, this indicates only the potential for

adverse health effects. The magnitude of this potential can be inferred from the degree to which

this value is exceeded. If the estimated exposure dose is only slightly above the RfD, then that

dose will fall well below the toxic effect level. The higher the estimated dose is above the RfD,

the closer it will be to the toxic effect level.

People who eat this amount or more of large cutthroat trout (> 300 mm), large yellow perch

(>271 mm), and small (<300 mm) and large (>300 mm) northern pikeminnow would exceed the

RfDs for both mercury and PCBs (Appendix D, Tables D1 – D5). Adults who eat small

cutthroat trout, small and medium yellow perch, and sockeye salmon at the overall mean level of

consumption do not exceed this protective level of exposure. Estimated exposures based on the

percentile consumption rate (King County DNRP 2004) were also determined and compared

with the protective level of exposure. Adults who consume fish at the 95

percentile rate would

exceed the RfD for all fish except sockeye salmon (Appendix D, Tables D6 – D10).

For all respondents, the ratio of mean estimated exposure to allowable daily dose (RfD) for PCBs

ranged from 0.1 (sockeye salmon) to 9.6 (northern pikeminnow) (Table 3). For children, the

ratio of mean estimated exposure to allowable daily dose (RfD) for PCBs ranged from 0.1

(sockeye salmon) to 8.5 (northern pikeminnow). Ratios calculated using the 95

percentile

consumption rate for all consumers ranged from 0.2 (sockeye salmon) to 27 (northern

pikeminnow). For children, ratios using the 95

percentile consumption rate ranged from 0.6

(sockeye salmon) to 77 (northern pikeminnow).

Table 3. Ratio of estimated total polychlorinated biphenyl (PCB) dose to EPA’s oral reference dose

(RfD).

Sockeye salmon was the only species where the ratio was less than one if consumed at average

or 95

percentile rates. Bass, large cutthroat trout, large yellow perch, and large northern

pikeminnow exceeded a ratio of 1.0 using both consumption rates. Thus, anglers who consume

fish from Lake Washington at or above average rates as estimated by King County DNRP are

exposed to contaminants at levels that may have a negative effect on human health.

Lake Washington is within the Muckleshoot Indian Tribe’s Usual and Accustomed fishing area.

Tribal members most likely consume fish at a higher rate than the mean shown in the King

County study. Native Americans from the Tulalip, Squaxin Island, and Suquamish Indian

Nations have been shown to consume marine fish species from Puget Sound at much higher rates

than the national average (6.5 grams/day) (Toy et al. 1996, Suquamish 2000). Surveys of Asian

Pacific Islanders from King County also showed fish consumption rates higher than the national

average (EPA 2000). Thus, the exposure estimates based on results from the recent King County

survey may underestimate potential exposure to these populations.

Determination of Allowable Consumption Rates

DOH used an approach similar to EPA’s risk-based method to characterize and evaluate risks

from exposure to chemicals (EPA 2000). The DOH approach calculates an allowable monthly

consumption rate based on the RfD, the body weight of an individual, and the known

contaminant concentration in fish. Current weight-of-evidence suggests that non-cancer

endpoints are more sensitive and, therefore, sufficiently protective for possible cancer effects.

By using the known concentration of a contaminant in a fish species, it is possible to calculate an

allowable amount that can be consumed for that species without exceeding the RfD for that

contaminant. In this approach, the RfD is used to calculate the quantity of fish a person of a

given weight can safely consume given varying contaminant concentrations found in fish tissue.

The equation used to calculate a safe consumption rate is shown below (EPA 2000). Note that

the equation is solved for “grams of fish per day” which can then be converted into meals per

month.

()()

FishinionConcentratFactorConversionUnitWeightBodyRfD

Day

FishofGrams

÷××=

Total PCB Concentration Mean 95th percentil

Mean 95th percentil

Fish Specie

(ppb) (10.8 gm/day) (30.2 gm/day) (9.5 gm/day) (86.7 gm/day)

Smallmouth Bas

371.2 3.3 9.3 2.9 26.7

Large Cutthroat Trout 377.4 3.4 9.5 3 27.1

Large Yellow Perch 191.1 1.7 4.8 1.5 13.7

Large Northern Pikeminnow 1071.4 9.

27 8.5 77

Sockeye Salmon 7.8 0.1 0.2 0.1 0.

Estimated dose = (consumption rate x body weight)/fish tissue PCB concentration.

Body weight of 60 kg used to calculate dose.

All Respondents Children (ages (0-18 yrs

)

Consumption Rate Ratio

Where:

Parameter Value Units Source

Reference Dose (RfD) Chemical specific mg/kg-day EPA IRIS

Unit Conversion

Factor

1000 g/kg

Body Weight 60 (adult female) kg EPA Exposure

Factors Handbook

Concentration in fish Mean contaminant

concentration.

Specific to water

body and fish species.

mg/kg Current Study

Based on this equation, there are two variables that affect the amount of fish a person can

consume and stay below the RfD. These variables include the concentration of a contaminant in

fish and an individual’s body weight. Both the RfD and the unit conversion factors are constant;

thus, reducing the consumption rate will reduce exposure. The consumption rate is expressed as

grams of fish per day, which can be converted to allowable meals per month. The RfD is

expressed on a microgram per kilogram per day basis. For general advice, an assumed body

weight of 70 kg is commonly used in EPA risk assessments (EPA 1997, EPA 1999). For this

assessment, DOH used an assumed body weight of an average woman of 60 kg (approximately

132 lbs). This weight was chosen to ensure that women of childbearing age are appropriately

considered and protected when determining a consumption rate so as to be protective of

neurological and developmental endpoints in the developing fetus.

Allowable Consumption Rates for Lake Washington Fish

Allowable consumption rates were calculated for various size classes of northern pikeminnow,

yellow perch, cutthroat trout, and sockeye salmon (Appendix C, Tables C6 – C9). Highlighted

in each table is the most restrictive consumption rate for a given species. Based on whole fish

analysis for each fish species, total PCB concentrations resulted in the lowest allowable

consumption rates. Thus, if fish consumers follow consumption recommendations as determined

by PCB concentrations, they would be protected from possible adverse health effects due to

other contaminants.

Recommended meal consumption rates based on PCB concentrations ranged from 0.2 eight-

ounce fish meals per month for northern pikeminnow

to over twenty meals per month for

sockeye salmon. For species with different size classes, more restrictive meal limits are

observed in the larger fish class. Calculated meal limits based on contaminant concentrations

measured in cutthroat trout, yellow perch, northern pikeminnow, and sockeye salmon collected

from Lake Washington are given below.

Northern Pikeminnow. Northern pikeminnow recorded the highest concentrations for three of

the four detected contaminants (DDT, mercury, and PCBs) (Appendix C, Tables C6a and C6b).

Calculated meal limits are the most restrictive for any species due to the high chemical levels

observed. The highest mean concentration of mercury was observed in large northern

pikeminnow resulting in a calculated meal limit of 2.1 meals per month. Concentrations of

PCBs in both small and large northern pikeminnow resulted in allowable meal limits of 1.2 and

0.2 meals per month, respectively.

Yellow Perch. Three size classes of yellow perch were analyzed for contaminants. Since

concentrations for all contaminants increased as yellow perch size increased, calculated meal

limits decreased with increased fish size (Appendix C, Tables C7a, C7b, and C7c). The most

restrictive meal limits were based on PCB concentrations (3.5 meals per month for small yellow

perch, 2.4 for medium yellow perch, and 0.8 meals per month for large yellow perch). Mercury

levels in small, medium, and large yellow perch resulted in meal limits of 24.4, 9.3 and 4.4 meals

per month, respectively.

Cutthroat Trout. Calculated consumption rates decreased with increasing size of cutthroat

trout (Appendix C, Tables C8a and C8b). In both size classes of cutthroat, PCBs levels gave the

most restrictive meal limits at 2.0 meals per month for small cutthroat trout and 0.4 meals per

month for large cutthroat trout.

Sockeye Salmon. Sockeye salmon had the lowest levels for all contaminants tested in this

study. All calculated meal limits were above EPA’s unrestricted level of 16 meals per month for

a 60 kg person (Appendix C, Table C9). Consumption rates were not calculated for chlordane

because of the low detection frequency (no samples were above the detection limit).

Estimated consumption rates calculated above were based on an average woman’s body weight

(60 kg or 132 lbs) (EPA 1997). The amount of a contaminant that a person can safely consume

varies with body weight. For example, the greater a person’s weight, the greater amount of fish

the consumer may safely ingest. Conversely, the lower a person’s weight, the fewer fish he/she

may safely consume. An illustration of how meal limit calculations vary using differing body

weights is given for chlordane, DDT, mercury, and total PCBs in Appendix C (Figs. C16 – C23).

These graphs provide allowable meals per month for each contaminant with the understanding

that DOH used meal limits based on PCB exposure as these were the most restrictive and,

therefore, the most protective.

Data Uncertainty

Sample Size. The sample size for each fish species in this assessment is small for a lake as large

as Lake Washington and limited relative to assessments conducted by DOH in other state

waterbodies. For example, 21 – 176 fish per species were collected for a health assessment in

Lake Roosevelt (Munn et al 1995, DOH 2001a) and 13 - 95 fish per species were collected in

Lake Whatcom, near Bellingham (DOH 2001b). In particular, the number of smallmouth bass

sampled (n = 3) is inadequate to evaluate possible health concerns associated with consumption

of this species. The sample size was also small for other species; numbers for most size classes

of fish included 10 individuals. Determination of appropriate sample size is dependent on

several factors, including variability of contaminant data. Sufficient sample size should increase

with increasing variability of chemical concentrations in fish. Lake Washington is a fairly large

lake (87.6 km

and 35 km long), which might affect variability within a species. Given the lack

of previous contaminant data from Lake Washington, the degree of variability to adequately

determine an appropriate sample size was unknown prior to this study.

In a related study, the UW obtained a much larger sample size of aquatic organisms for diet and

stable isotope investigations. Results showed a great deal of homogeneity in food habits for a

given size of fish for each species, lending additional support for conclusions based on low

sample sizes for contaminants. Further, Lake Washington piscivores, particularly cutthroat trout

and northern pikeminnow, are very mobile, which would integrate potential regional differences

in contaminants. Nevertheless, DOH recommends further sampling of cutthroat trout, northern

pikeminnow, and yellow perch based on the small number of samples and the large size of the

lake.

Whole Fish Analysis. All fish tissue samples in the Lake Washington data set were analyzed

using whole body measurements. Fish tissue data for this project were originally collected by

the UW as part of a collaborative project to investigate bioaccumulation of contaminants through

the Lake Washington food web, not for the purpose of evaluating human health. Typically,

edible muscle tissue (fillet) is used to estimate potential human health risks from consuming fish.

While some individuals or groups use whole fish in various cooking methods, fillet contaminant

data provides more useful information on potential contaminant exposure levels to the general

population.

Using whole fish tissue data would likely overestimate potential risks to the consumer since most

lipophilic contaminants (those that concentrate in fat) concentrate in areas such as head, liver,

and fat near the skin. Whole body-to-fillet ratios are generally less than one for lipophilic

compounds such as chlordane, DDT, and PCBs. The reverse is seen for mercury, which

concentrates in muscle tissue rather than fat. Using whole body samples would likely

overestimate the amount of PCBs, chlordane, and DDT for fillets (the part of the fish usually

consumed) while underestimating the amount of mercury. Whole body-to-fillet contaminant

concentration ratios are often used to correct for this potential bias.

Although the current study did not measure whole body-to-fillet ratios, several studies have

compared whole body-to-fillet data (Appendix C, Table C10). Whole body-to-fillet ratios

ranged from a low of approximately 0.1 in walleye to 1.0 in brown trout. The average ratio for

salmonid species is 0.68. Information was more limited for whole body-to-fillet ratios for bass,

cyprinid, and percid species and, in general, averaged about 0.5. Ratios were not available in the

literature for fish species collected from Lake Washington.

For comparative purposes, DOH estimated whole body-to-fillet average tissue concentrations

based on ratios found in the literature for related fish species (Table 4). Estimated concentrations

were then used to calculate meal limits for northern pikeminnow, yellow perch, and cutthroat

trout (by size class). Smallmouth bass consumption guidelines fall under the statewide bass

advisory mentioned earlier, and sockeye salmon from Lake Washington do not require an

advisory. As expected, meal limits for all species based on estimated PCB concentrations in

fillets (range: 0.3 – 6.9 meals per month) were higher than those based on whole body samples

(range: 0.2 – 3.5 meals per month). However, advice based on adjusted meal limits would not

change appreciably. DOH recommends future sampling and analyses of fish fillets from Lake

Washington species to determine more precise measurements of contaminant levels in tissue

generally ingested by fish consumers.

Table 4. Comparison of meal limits based on measured total PCBs in whole body fish tissue from Lake

Washington, Seattle, Washington, with estimated concentrations in fillets.

Fish Species/Size Class Whole Fish Fillet*

Cutthroat Trout < 300 mm** 2.0 3.0

Cutthroat Trout < 300 mm** 0.4 0.6

Yellow Perch < 200 mm*** 3.5 6.9

Yellow Perch 200 - 271 mm*** 2.4 4.9

Yellow Perch > 271 mm*** 0.8 1.7

Northern Pikeminnow < 300 mm *** 1.2 2.3

Northern Pikeminnow < 300 mm *** 0.2 0.3

* Estimated allowable meals per month of fillet base on the following whole:fillet ratios

** Fillet concentrations estimated using a whole body:fillet ratio of 0.68

*** Fillet concentrations estimated using a whole body:fillet ratio of 0.50

Allowable 8 oz. meals per month

based on PCB concentrations in:

Other Health Assessment Considerations

Background Comparison. Another consideration in this study is the magnitude of contaminant

concentrations relative to known or estimated background concentrations. PCB concentrations

are elevated in Lake Washington cutthroat trout and northern pikeminnow compared to fish from

other Washington lakes and rivers. The current study also collected four cutthroat trout from

Lake Sammamish > 300 mm, similar in size to large cutthroat trout collected from Lake

Washington. The mean total PCB concentration of these fish was 60 ppb compared to 377.4 ppb

for large cutthroat trout from Lake Washington. The large difference in concentrations in the

same size fish from a neighboring waterbody suggests a localized rather than regional problem

for total PCBs. A further explanation is the longer food chain in Lake Washington (compared

with the food chain in Lake Sammamish) that could increase bioaccumulation in the lake through

increased predation on predatory fishes (J. McIntyre, personal communication, 2004).

Studies are available with which to compare total PCB (Aroclor) levels in Lake Washington fish

with fish from other fresh water bodies in Washington. Such comparisons are often complicated

by differences in study design, such as analytical methods, detection limits, fish species, size,

and tissue type (i.e., whole body versus fillet sample preparations). Despite these confounding

factors, it is useful to consider PCB levels observed in various fish throughout the state.

Concentrations of ΣPCB in Lake Washington fish were many times higher than levels found in

fish from many Washington State lakes and rivers, including Lake Sammamish (McIntyre 2004)

(Figure 2). Levels of ΣPCB in Lake Washington fishes were comparable to those in fishes near

PCB Superfund sites along the Lower Duwamish waterway and the Spokane River in

Washington State. Levels of ΣPCB from fillets of fish previously sampled in Lake Union, a

highly industrial site downstream of Lake Washington, were also assessed for comparison:

yellow perch (~20 µg/kg), smallmouth bass (~50 µg/kg), and northern pikeminnow (~500 µg/kg)

(McIntyre 2004).

Figure 2. PCB concentrations in large fishes from Washington State systems (Lake Whatcom, Palouse

River, Crab Creek, Lake Chelan, Vancouver Lake, Yakima River, Lake Sammamish, Lake Washington,

Lower Duwamish River, and Spokane River).

Crab

Creek

L.Whatcom Lake Washington Spokane R.Lake Chelan Yakima R.

L.Sammamish Duwamish R.Palouse R. Vancouver L.

KOK SMB NP MWF SMB RT KOK LMB SMB Carp CT SMB CT NP E.Sole MWF RT

[PCB] ppb fillet

200

400

600

800

Hatched bars highlight data from the current study. L.Washington PCB values were multiplied

by 0.68 to estimate fillet concentrations. KOK=kokanee, SMB=smallmouth bass, NP=northern

pikeminnow, MWF=mountain whitefish, RT=rainbow trout, CT=cutthroat trout. Excluded from

the comparison were sites undergoing ongoing assessment by the Washington State Department

of Ecology for high levels of PCB and DDT under the Toxics Cleanup Program, including Walla

Walla R., Chehalis R., and Okanogan R. PCBs at these sites ranged from 45 – 300 ppb.

Sources: (Davis et al. 1998; Serdar et al. 1999; Johnson 2001; EPA 2003b)

Figure provided by McIntyre, 2004.

Multiple Chemical Exposure. Different chemicals may interact in the body and increase or

decrease the potential for adverse health effects. Since there are many chemicals in the

environment, it is not possible to measure all interactions. However, the toxicity of contaminants

with similar health endpoints should be considered additive unless information is available to

suggest otherwise (ATSDR 2001a, ATSDR 2001b). In the case of contaminants measured in

Lake Washington fish, mercury, PCBs and DDT impact childhood development following in

utero exposure. Therefore, exposure doses were calculated assuming that the toxicity of PCBs,

mercury, DDT and chlordane are additive by summing individual hazard quotients yielding a

hazard index. This approach, however, did not significantly change estimated doses, or meal

limits, calculated for PCB exposure alone demonstrating that efforts to reduce PCB exposure

below its respective RfD will be protective with respect to each detected contaminant of concern.

Similarly, most cancer risk is attributed to PCBs. Using the mean consumption rate for Lake

Washington anglers (10.8 g/day), estimated upper bound cancer risks for multiple chemicals

ranged from 1.4 in one million (sockeye salmon) to 1.8 in ten thousand (large northern

pikeminnow). These risks are within or close to the acceptable range of EPA’s Superfund

Program, which considers risks to be acceptable if within 1 x 10

–4

to 1 x 10

–6

. Our calculated

cancer risks are upper bound estimates while actual risks are likely to be much less, possibly

zero. Appendix D provides hazard indices and total cancer risk estimated for the combined

exposures of each contaminant of concern.

Sources of Contaminants. The source of contaminants in Lake Washington fish is largely

unknown. However, DDT was sprayed for mosquito control in the past, PCBs were widely used

in industry prior to the 1970’s, and mercury continues to be deposited aerially. King County

DNRP recently collected sediment samples from 29 locations in Lake Washington. Although

concentrations of most analytes were relatively low, there were some areas that exhibited

sediment toxicity and an impaired benthic community. In addition, freshwater sediment

guidelines were exceeded for PCBs, DDTs, mercury, and chlordane at some locations (D. Lester,

personal communication, 2004). While 62% of the sites sampled (n = 29) had non-detected

levels of PCBs (detection limits around 60 ppb dry weight; based on sum of Aroclors 1248,

1254, and 1260), the remaining sites where PCBs were detected had an average PCB

concentration of > 200 ppb (dry weight) (range: 60 – 577 ppb dw). Sites with highest sediment

concentrations were associated with combined sewage overflows (CSOs), storm drains, urban

runoff, and past industrial spill locations adjacent to urban areas around the lake.

Sediment concentrations reported by King County DNRP agree well with those for areas of the

Spokane River that had PCB concentrations in fish similar to those in Lake Washington (S.

O’Neill, personal communication, 2004). But average total PCB sediment concentrations in

Puget Sound urban bays like Elliott Bay and Sinclair Inlet (372 ppb dry weight (n = 496) and

148 ppb dry weight (n = 267), respectively) and in a known contaminated area, the Lower

Duwamish (439 ppb dry weight, n = 1,079) are higher than in Lake Washington (M. Dutch,

personal communication, 2004) (Puget Sound summaries were calculated on detected and

undetected values). Thus, sediment levels in 40% of sampled sites in Lake Washington are

elevated, but not to the highest level observed in state waterbodies. Nevertheless, these levels

have resulted in demonstrable bioaccumulation in fish from the lake.

Estimates of cancer risk. The toxicological endpoint, or point of impact, is an important factor

in determining potential effects from exposure to a chemical. Health effects that are transient,

reversible, or have low severity are treated differently in a health assessment than those that

produce long lasting, severe, or irreversible effects, such as those caused by PCBs and mercury.

PCBs have been associated with impaired neurological development and with adverse effects on

the immune system.

Another consideration in health assessments is the relative importance of cancer versus non-

cancer endpoints. Current weight-of-evidence based on scientific studies that evaluated possible

adverse human health effects from exposure to chlordane, DDT, mercury, and/or PCBs supports

the use of non-cancer endpoints over the use of cancer endpoints in calculation of meal limit

recommendations. The use of non-cancer endpoints does not disregard possible cancer

endpoints but rather places greater weight to observed and measured adverse effects rather than

high dose extrapolation to probabilistic cancer endpoints. The most compelling argument

against the use of cancer endpoints is in the lack of significant evidence of cancer in occupational

exposure settings where exposure to contaminants is likely to be greatest both in terms of

magnitude and duration. While evidence of cancer in occupational settings may not be

significant, this may be due to confounding factors rather than true lack of significance. A

summary of cancer classifications for chlordane, DDT, mercury, and PCBs is in Appendix E.

Recommendations based on a chronic dose, the RfD, also protect against possible cancer

endpoints at risks typically used in a regulatory framework. To check this assertion, we used

calculated meal limits from this study’s results based on the RfD to determine potential cancer

risks for each fish species (by size category). Estimated cancer risks ranged from 1.6 – 8.2 X 10

–5

. These cancer risk estimates fall within EPA’s risk range for Superfund of 1 x 10

-4

to 1 x 10

-6

In short, protecting against known non-cancer will protect consumers from cancer endpoints as

well.

Benefits of fish consumption. Recent studies have attempted to quantify risks of eating

contaminated fish with benefits associated with their ingestion (Rembold 2004, Tuomisto et al.

2004, Lund et al. 2004, Sakamoto 2004). Further work is expected on this subject as more

reports on fish contaminant levels and human health become available. At present, we know that

fish is an excellent source of protein that is low in saturated fats, rich in vitamin D and omega-3

fatty acids as well as other nutrients. Health benefits of eating fish have been associated with

low levels of saturated versus unsaturated fats. Saturated fats are linked with increased

cholesterol levels and risk of heart disease while unsaturated fats (e.g., omega-3 polyunsaturated

fatty acid) are an essential nutrient.

Fish also provide a good source of vitamins and minerals. Health benefits of eating fish are well

documented and linked to the reduction of cardiovascular disease, osteoporosis, and partial

reduction of certain types of cancer. These major chronic diseases afflict much of the U.S.

population. Replacing fish in the diet with other sources of protein such as red meat brings other

considerations such as the link between saturated fat intake and cardiovascular disease.

Advisories can be protective yet acknowledge benefits of eating fish, by recommending

decreased consumption of fish known to have high concentrations of contaminants in favor of

fish that are lower in contaminants. The American Heart Association and the U.S. Food and

Drug Administration recommend two servings (12 oz.) of fish per week as part of a healthy diet.

Health benefits of eating fish deserve particular consideration when dealing with groups that

consume fish for subsistence. Removal of fish from the diet of subsistence consumers may have

serious health, social and economic consequences. Such populations are encouraged to consume

a variety of fish species, to fish from locations with low contamination, and to follow

recommended preparation and cooking methods. Further, consuming fillets rather than whole

fish may reduce potential risks by another 50% (Appendix C, Table C10).

Conclusions and Recommendations

Data from Lake Washington analyzed in this report are limited. Specifically, the sample size is

small and the use of whole body fish tissue may overestimate exposure to contaminants.

Regardless of data limitations, PCB concentrations in northern pikeminnow are some of the

highest recorded in Washington, and concentrations in large yellow perch and large cutthroat

trout are elevated relative to many areas throughout the state and a cause for concern.

Based on estimates of consumption for Lake Washington anglers and the concentrations of

contaminants in fish discussed above, DOH estimates that the average angler is exposed to

contaminants of concern above recommended levels. In order to protect consumers of Lake

Washington fish, DOH provides the following recommendations.

• Eat a variety of fish as part of a balanced diet. Health benefits of eating fish are:

o Fish is an excellent low-fat food, a great source of protein, vitamins, and minerals.

o The oils in fish are important for unborn and breastfed babies.

o Eating a variety of fish helps to reduce your chances of stroke or heart attack.

• Northern pikeminnow should not be consumed.

• Yellow perch greater than 270 mm (10½ inches) may be consumed as an eight-ounce

meal once per month. Yellow perch smaller than 270 mm (10½ inches) may be

consumed as an eight-ounce meal four times per month.

• Consumers of large cutthroat trout (>300 mm) (12 inches) from Lake Washington should

eat no more than one eight-ounce meal per month. For small cutthroat trout (< 300 mm)

(12 inches), no more than 3 eight-ounce meals per month are recommended.

• No meal restrictions on sockeye salmon from Lake Washington. Consumers are

encouraged to choose sockeye when consuming local fish.

• Prior to the issuance of this interim advisory, a statewide fish consumption advisory for

large and smallmouth bass due to mercury was in place throughout water bodies in

Washington State, including Lake Washington. Women of childbearing age and children

six years of age or younger should eat no more than two meals per month of any bass

caught in Washington state freshwaters.

The recommendations given above are based on a 60 kg (132 lbs) adult eating an eight-ounce

meal. In general, children should eat proportionally smaller meal sizes. Calculations for multiple

chemical exposures do not change the above advice.

Since the above recommendations are based on a small sample size, DOH recommends

additional sampling of northern pikeminnow, yellow perch, and cutthroat trout to confirm initial

findings of high contaminant concentrations in fish tissue. We recommend sampling whole body

fish and fillet samples with skin off for comparison with initial data. Other species of fish

consumed by anglers such as rainbow trout, crappie, and bluegill should also be sampled.

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Thesis. University of Washington. Seattle, WA. 204 pgs.

McIntyre J. 2004. Personal communication. University of Washington.

Munn M, Cox S, and Dean C. 1995. Concentrations of mercury and other trace elements in

walleye, smallmouth bass, and rainbow trout in Franklin D. Roosevelt Lake and the upper

Columbia River, Washington, 1994. U.S. Geological Survey, Tacoma, WA. 95-195.

Nowak, G. 2000. Movement patterns and feeding ecology of cutthroat trout (Oncorhynchus

clarki clarki) in Lake Washington. MS thesis. University of Washington. Seattle, WA 75 pgs.

O’Neill S. 2004. Personal communication. Washington State Department of Fish and Wildlife.

Rembold 2004. Health benefits of eating salmon. Science. July 23, 2004;305(5683):475.

Sakamoto M, Kubota M, Liu XJ, Murata K, Nakai K, and Satoh H. 2004. Maternal and Fetal

Mercury and n-3 Polyunsaturated Fatty Acids as a Risk and Benefit of Fish Consumption to

Fetus. Environ. Sci. Technol. 2004. 38:3860-3863.

Suquamish 2000. Fish Consumption Survey of the Suquamish Indian Tribe of the Port Madison

Indian Reservation, Puget Sound Region. The Suquamish Tribe, Port Madison Indian

Reservation, Fisheries Department, Suquamish, WA. August 2000.

Tabor R. and Chan J. 1997. Predation on sockeye salmon fry by piscivorous fishes in southern

Lake Washington , 1996. US Fish & Wildlife Service. Western Washington Fishery Resource

Office. Olympia, WA.

Toy KA, Polissar NL, Liao S, and Gawne-Mittelstaedt GD. 1996. A Fish Consumption Survey

of the Tulalip and Squaxin Island Tribes of the Puget Sound Region. Tulalip Tribes, Natural

Resources Department, Marysville, WA. October 1996.

Tuomisto JT, Tuomisto J, Tainio M, Niittynen M, Verkasalo P, Vartiainen T, Kiviranta H, and

Pekkanen J. Risk-benefit analysis of eating farmed salmon. Science. July 23,

2004;305(5683):476-7.

Warner E. 2004. Personal communication. Muckleshoot Indian Tribes.

APPENDIX A

Description of Lake Washington Fish Species

Cutthroat Trout (Oncorhynchus clarki)

The cutthroat population in Lake Washington is thought to be wild, self-sustaining and mostly

non-anadromous (anadromous means migrating up rivers from the ocean to spawn in fresh

water) (Nowak 2000). A recent study showed that cutthroat trout generally live below the

thermocline when the lake is stratified (the thermocline is the region of rapid decrease in

temperature in a lake separating the upper warmer layer from the cooler lower layer) (Nowak

2000). Large cutthroat trout spend most of their time offshore to minimize contact with the

warmer near-surface water, while in winter and spring they move near to shore, perhaps to prey

on juvenile sockeye and Chinook salmon that migrate from streams. Cutthroat in Lake

Washington do not inhabit localized areas within the lake but tend to move to various locations,

most likely following prey, searching for food, or moving to more favorable conditions.

Cutthroat trout consume a large number of Chinook fry and fingerlings, and predation by

cutthroat trout appears to be responsible for substantial losses of juvenile sockeye salmon in

Lake Washington. Average fork length of cutthroat in the littoral zone is 195.0 mm and in the

limnetic zone is 366.4 mm (Nowak 2000).

Northern Pikeminnow (Ptychocheilus oregonensis)

The northern pikeminnow is long-lived (up to age 19 in Montana) and reaches a large size (up to

25 inches) (Wydoski and Whitney 1979). Between 1996-1997, the mean length of northern

pikeminnow in Lake Washington was 382.8 mm (15.07 inches). Sexual maturity is attained in

about 6 years at a length of about 12 inches. The fish is edible, but the flesh is very bony. The

most recent estimate of population numbers in Lake Washington ranged from 148,000 to

183,000 fish (Brocksmith 1999).

Northern pikeminnow prefer warm water. Fish appear to congregate near the mouth of the Cedar

River in relatively high densities and near the mouth of the Lake Washington Ship Canal

(Brocksmith 1999). The diet of northern pikeminnow varies with season, with salmon pre-

smolts, smolts, and longfin smelt comprising a large part of the diet (smolts are young salmon at

the life stage when they migrate from freshwater to the sea). In Lake Washington, the northern

pikeminnow plays an important role as a sockeye salmon predator (Brocksmith 1999).

Yellow Perch (Perca flavescens)

Historically, yellow perch was an important percentage of overall fish harvest from lakes in King

County. This fish was first released into Lake Washington in the early 1900s (E. Warner,

personal communication, 2004). The flesh of perch is firm, white, and mild in flavor (Wydoski

and Whitney 1979). Young perch feed in the pelagic zone on zooplankton, and as they grow,

they shift to shallower areas and feed on immature insects and mysid shrimp. Larger perch feed

on forage fish when they are available. Yellow perch are often found in water 15 to 25 feet deep,

making them easy to catch from shore. In Lake Washington, yellow perch range from

approximately 3.8 inches at one year of age to 13.1 inches at 7 years of age. Males become

mature between 1 and 2 years of age while females mature between 2 and 3 years of age.

Smallmouth Bass (Micropterus dolomieui)

Smallmouth bass were first introduced to the western U.S. in 1874 (Wydoski and Whitney

1979). Smallmouth bass usually have a defined home range and do not travel over long

distances. They prefer water temperatures of 70° – 80° F. Smallmouth bass fry eat crustaceans

such as copepods and cladocerans and, when still small (between one and two inches), change to

a diet of insects and begin to eat fishes. Smallmouth bass usually mature when 3 or 4 years old

and, as adults, feed on insects, crayfish, and fishes.

Sockeye Salmon (Oncorhynchus nerka)

Sockeye salmon are the second most abundant salmon on the Pacific coast and account for about

25 percent of the commercial salmon catch (Wydoski and Whitney 1979). Opportunities to fish

recreationally for sockeye salmon in Lake Washington are limited because in most years the

numbers returning to the lake are too low to permit a fishery (generally once every three to four

years).

Sockeye differ from other species of salmon because they require a lake environment for part of

their life cycle. Lake Washington sockeye return to spawn after 1 to 3 years of ocean life.

About 90 percent of the fish that return have spent 1 year in fresh water and 2 - 3 years in the

ocean. Although adult sockeye salmon may reach a length of 33 inches and a weight of 15.5

pounds, most adult fish weigh 3.5 to 8 pounds. Adult sockeye arrive in Lake Washington

starting in early June, peaking in early July, and declining rapidly in early August. Fish remain

in the lake for several months before migrating up streams and rivers to spawn. In the Cedar

River, the first spawners may arrive by mid-August with the main spawning period lasting from

September to early December, peaking in mid-October. The Cedar River is the largest sockeye

spawning area in the basin, but over a third of the sockeye can spawn elsewhere (e.g.,

Bear/Cottage Creek system, Issaquah, and Lake Washington). Spawning occurs on Lake

Washington beaches between early November and mid-January, peaking in mid-November.

Most young fry migrate from the Cedar River into Lake Washington between January and June

(peak migration from mid-February through April) and stay in the lake for 12 to 15 months until

the majority become smolts and migrate to sea (D. Beauchamp, personal communication, 2004).

Many smolts leave a year “early” as young-of-the-year smolts and a small percentage leaves the

lake a year late as two-year-old smolts. Most sockeye smolts are from 110 – 150 mm (4.3 – 5.9

inches) long, with a maximum length of 190 mm (7.5 inches) (E. Warner, personal

communication, 2004).

During their fresh-water life, juvenile sockeye salmon feed largely on zooplankton, especially

crustaceans. While at sea, sockeye feed mainly on planktonic foods such as crustaceans,

especially euphausid (mysid) shrimp.

Other Species

Piscivorous fish found in Lake Washington but not collected in this study include rainbow

trout/steelhead (Oncorhynchus mykiss), coho salmon (Oncorhynchus kisutch), Chinook salmon

(Oncorhynchus tshawytscha), Pacific lamprey (Lampetra tridentata), river lamprey (Lampetra

ayresi), largemouth bass (Micropterus salmoides), brown bullhead (Ameiurus nebulosus), prickly

sculpin (Cottus asper), coast range sculpin (Cottus aleuticus), black crappie (Pomoxis

nigromaculatus), warmouth (Chaenobryttus gulosus), bull trout (Salvelinus confluentus), and

Dolly Varden (Salvelinus malma) (Tabor and Chan 1997). Some of the above species may have

a much higher proportion of fish in their diet than others. The following are much less

piscivorous or non-piscivorous fish found in the lake that were not included in the study:

Western brook lamprey (Lampetra richardsoni), mountain whitefish (Prosopium williamsoni),

peamouth (Mylocheilus caurinus), largescale sucker (Catostomus macrocheilus), longfin smelt

(Spirinchhus thaleichtys), three-spine stickleback (Gasterosteus aculeatus), pumpkinseed

(Lepomis gibbosus), bluegill (Lepomis macrocheilus), weather loach (Misgurnus

angillicaudatus), common carp (Cyprinus carpio), and tench (Tinca tinca) (E. Warner, personal

communication, 2004).

References

Beauchamp, D. 2004. Personal communication. University of Washington, Seattle.

Brocksmith, R. 1999. Abundance, feeding ecology, and behavior of a native piscivore northern

pikeminnow (Ptychocheilus oregonensis) in Lake Washington. MS Thesis. University of

Washington, Seattle, WA. 104 pgs.

Nowak, G. 2000. Movement patterns and feeding ecology of cutthroat trout (Oncorhynchus

clarki clarki) in Lake Washington. MS thesis. University of Washington. Seattle, WA. 75 pgs.

Tabor R. and Chan J. 1997. Predation on sockeye salmon fry by piscivorous fishes in southern

Lake Washington , 1996. US Fish & Wildlife Service. Western Washington Fishery Resource

Office. Olympia, WA.

Warner, E. 2004. Personal communication. Muckleshoot Indian Tribes. Auburn, Washington.

Wydoski R. and Whitney R. 1974. Inland fishes of Washington. University of Washington

Press. Seattle and London. 220 pgs.

APPENDIX B

Contaminants of Concern

Introduction

The following is a summary of information on the background, exposure, and toxicity of four

detected contaminants (∑chlordane, ∑DDT, mercury, and total PCBs) in five fish species

(northern pikeminnow (Ptychocheilus oregonensis), yellow perch (Perca flavescens), cutthroat

trout (Oncorhynchus clarki), smallmouth bass (Micropterus dolomieui), and sockeye salmon

(Oncorhychus nerka)) collected from Lake Washington. This section represents a synopsis of

information from ATSDR documents, EPA IRIS, and journal articles.

Chlordane

Background

Chlordane is a man-made chemical that was used as a pesticide in the United States from 1948 to

1988. Chlordane is not a single chemical but is a mixture of many related chemicals, of which

about 10 are major components. Some major components are trans-chlordane, cis-chlordane,

β-chlordane, heptachlor, and trans-nonachlor. For the first thirty years of its production,

chlordane was used as a pesticide on agricultural crops, lawns, and gardens and as a fumigating

agent. Mounting evidence of potential human exposure, persistence in the environment,

detriments to wildlife, and knowledge of toxicity caused the U.S. Environmental Protection

Agency (EPA) to phase out chlordane’s use. For the last five years of its production, chlordane

was approved for use only to control termites in and around homes. All approved uses within the

U.S. for chlordane ended in 1988, although manufacture continues for export where it may be

used in other countries (ATSDR 1994).

Chlordane enters the environment when used as a pesticide on crops, on lawns and gardens, and

to control termites in houses. In soil, it attaches strongly to particles in the upper layers of soil

and is unlikely to enter into groundwater. It is not known whether chlordane breaks down in

most soils. However, if breakdown occurs, it is very slow and the chemical is known to remain

in some soils for over 20 years. Most chlordane is lost from soil by evaporation. In water, some

chlordane attaches strongly to sediment and particles in the water column and some is lost by

evaporation. It is not known whether much breakdown of chlordane occurs in water or in

sediment. Although chlordane breaks down in the atmosphere by reacting with light and with

some chemicals in the atmosphere, it is sufficiently long-lived that it may travel long distances

and be deposited on land or in water far from its source. Chlordane and its breakdown products

accumulate in some form in the fat of fish, birds, mammals, and almost all humans.

Exposure

Today, people receive the highest (but not the most common) exposure to chlordane from living

in homes that were treated with chlordane for termites. Although houses built since 1988 have

not been treated with chlordane for termite control, over 50 million persons have lived in

chlordane-treated homes. Chlordane may be present in the air of these homes for many years

after treatment. Indoor air in the living spaces of treated homes has been found to contain

average levels of between 0.00003 and 0.002 milligram (mg) of chlordane in a cubic meter of air

(mg/m

). Levels as high as 0.06 mg/m

have been measured in the living areas of treated homes,

and even higher levels have been found in basements and crawl spaces (ATSDR 1994).

The most common (but not the highest) source of chlordane exposure is from ingesting

chlordane-contaminated food. Due to its high affinity from lipids, chlordane is almost never

detected in drinking water. A survey conducted by the Food and Drug Administration (FDA)

determined daily intake of chlordane from food to be 0.0013 microgram per kilogram of body

weight (µg/kg) for infants and 0.0005 - 0.0015 µg/kg for teenagers and adults (a microgram is

one thousandth of a milligram). The average adult would, therefore, consume about 0.11 µg of

chlordane per day.

The amount of chlordane that enters the body depends on the amount in air, food, or water, and

the length of time a person is exposed. Most chlordane that enters the body leaves in a few days,

mostly in feces, and a much smaller amount leaves in urine. Chlordane and its breakdown

products (metabolites) may be stored in body fat, where they cause no adverse effects unless

released from body fat. It may take months or years before chlordane and its metabolites stored

in fat are able to leave the body.

Chlordane and its breakdown products can be measured in human blood, urine, feces, and breast

milk and measurements have shown that most Americans have low levels of chlordane

metabolites in their body fat. The breakdown products can stay in body fat for very long periods,

so finding them in body fat or breast milk does not tell how much or how long ago exposure to

chlordane occurred.

Toxicity

Most health effects in humans linked to chlordane exposure are on the nervous system, the

digestive system, and the liver. These effects have been observed mostly in people who

swallowed chlordane mixtures. No harmful effects on health have been confirmed in studies of

workers who produced chlordane. One study found minor changes in liver function in workers

in Japan who used chlordane as a pesticide. There are indications that chlordane may cause

anemia and other changes in blood cells, but the evidence is not very strong.

The EPA guidelines for drinking water suggest that no more than 60 ppb chlordane should be

present for longer than 10 days in drinking water that children consume. Drinking water should

contain no more than 0.5 ppb for children or 2 ppb for adults if they drink the water for longer

periods. FDA has established that levels of chlordane and its breakdown products in most fruits

and vegetables should not be greater than 300 ppb, while animal fat and fish should not exceed

100 ppb.

EPA’s Fish Advisory Guidance Manual (2000) states that, “Multiple neurological effects have

been reported in humans exposed both acutely and chronically to chlordane.” Adults (n = 109

women and n = 97 men) exposed to uncertain levels of chlordane from air and ingestion showed

significant (p< 0.05) differences in neurophysiological and neuropsychological function tests.

Profiles of mood states such as tension, depression, anger, vigor, fatigue and confusion were

affected significantly (p< 0.0005) compared to “a referent population.” The RfD listed in IRIS

for chlordane is 5.0 X 10

–4

mg/kg-d based on a NOAEL of 0.15 mg/kg-d for hepatic necrosis in

a 2-yr feeding study in mice (EPA IRIS 1999). FDA action level for chlordane in fish tissue is

300 ppb.

Chlordane is classified as B2 (probable human carcinogen) using the Guidelines for Carcinogen

Risk Assessment (EPA 1986). The oral cancer slope factor is 0.35 ug/kg/day. Under the 1996

Proposed Guidelines, it would be characterized as a likely carcinogen by all routes of exposure.

These characterizations are based on the following summaries of the evidence available: (1)

human epidemiology studies showing non-Hodgkin's lymphoma in farmers exposed to chlordane

and case reports of aplastic anemia (chlordane data associated with home use are inadequate to

demonstrate carcinogenicity); (2) animal studies in which benign and malignant liver tumors

were induced in both sexes of four strains of mice and liver toxicity but no tumors in rats of two

strains; and (3) structural similarity to other rodent liver carcinogens.

Dichlorodiphenyltrichloroethane (DDT)

Background

DDT is a pesticide that was once used to control insects on agricultural crops. It was also used to

control insects that carry diseases like malaria and typhus, but it is now used in only a few

countries to control malaria (ATSDR 2002). Technical grade DDT is a mixture of three forms,

p,p’-DDT, o,p’-DDT, and o,o’-DDT. All of these are white, crystalline, tasteless, and almost

odorless solids. DDT may also contain p,p’-Dichlorodiphenyldichloroethylene (DDE) and p,p’-

Dichlorodiphenyldichloroethane (DDD) as contaminants. DDD was used to a lesser extent than

DDT to kill pests, and one form of DDD was used medically to treat cancer of the adrenal gland.

DDE and DDD are breakdown products of DDT.

DDT does not occur naturally in the environment. The use of DDT was no longer permitted in

the United States after 1972 except in the case of a public health emergency, but it is still used in

some areas of the world for controlling malaria. Most DDT in the environment is a result of past

use, but current use in other countries is still introducing DDT into the environment. DDE is

only found in the environment as a result of contamination or breakdown of DDT. DDD also

enters the environment during the breakdown of DDT.

DDT enters the atmosphere when it evaporates from contaminated water and soil and is then

deposited on land or surface water. This cycle may be repeated many times, with the result that

DDT, DDE, and DDD are carried long distances in the atmosphere, including Arctic and

Antarctic regions.

DDT, DDE, and DDD persist in the soil for a very long time (decades), depending on many

factors such as temperature, type of soil, and whether the soil is wet. In surface water, DDT

binds to particles, settles, and is deposited in the sediment. It can accumulate to high levels in

fish and marine mammals, with the highest levels found in adipose tissue. DDT in soil can also

be absorbed by some plants and by animals or people who eat those crops.

Exposure

Since the ban on DDT in the US and other parts of the world, environmental concentrations of

DDT and metabolites have decreased. Average adult intakes of DDT have fallen over the years,

as levels in food items have decreased. However, there are still measurable quantities of DDT,

DDE, and DDD in many food groups. Mean concentrations of DDT in fish as measured by FDA

between 1991 and 1999 range from 0.2-9.2 ppb (ATSDR 2002). People who eat fish caught in

the Great Lakes consume larger amounts of DDT in their diets than average; however, as levels

of DDT in the environment decline this exposure route is also expected to decline. At this time,

low levels of DDT, DDE, and DDD are expected to be present in the diet for several more

decades (ATSDR 2002).

DDT and its metabolites accumulate in adipose tissue. Indigenous peoples of the arctic are

considered at risk to DDT exposure since their diets are particularly high in fatty tissues from

marine mammals. Another route of potential exposure of DDT to children is through breast-

feeding.

Toxicity

Most information on health effects in humans comes from studies of workers in plants that

manufacture DDT or applicators who spray DDT over an extended period (ATSDR 2002). DDT

impairs nerve impulse conduction. Observed effects vary from mild altered sensations to

tremors and convulsions. DDT is also capable of inducing alterations on reproduction and

development in animals, an effect attributed to the alteration of hormones. The o,p’-DDT isomer

has the strongest estrogen-like properties. The p,p’-DDE isomer has anti-androgenic properties

and can alter development of reproductive organs in rats (ATSDR 2002). An RfD of 5.4 X 10 –4

mg/kg/d was established based on liver effects in rats.

Animal studies have shown that DDT, DDE, and DDD can cause cancer in the liver. There is no

conclusive evidence to link DDT to cancer in humans, although possible genotoxic effects have

been reported. EPA assigned DDT, DDE, and DDD a weight-of-evidence classification of B2,

probable human carcinogens (EPA IRIS 2001). An oral slope factor of 0.34 (mg/kg-day)

-1

was

derived for DDT. IARC assigned a weight-of-evidence classification of B2 to DDT, possibly

carcinogenic to humans (IARC 2002).

Mercury

Background

Mercury is widespread in the environment as a result of natural and anthropogenic releases.

Everyone is exposed to small amounts of mercury (Clarkson 1993, and Clarkson 1997, in

Goldman and Shannon, 2001). Most mercury in the atmosphere is elemental mercury vapor and

inorganic mercury, and mercury in water, soil, plants, and animals is in organic or inorganic

forms. Organic mercury is primarily in the form of methylmercury.

Mercury is released into surface waters from natural weathering of rocks and soils from volcanic

activity. Mercury is also released from human action such as industrial activities, fossil fuel

burning, and disposal of consumer products. Global cycling of mercury via air deposition occurs

when mercury evaporates from soils and surface waters to the atmosphere. From the

atmosphere, mercury is redistributed on land and surface water then absorbed by soil or

sediments. Once inorganic mercury is released into the environment, bacteria convert it into

organic mercury, the primary form that accumulates in fish and shellfish (ATSDR 1999).

Exposure

In the aquatic food chain, methylmercury biomagnifies as it is passed from lower to higher

trophic levels through consumption of prey organisms. Fish at the top of the food chain can

biomagnify methylmercury approximately 1 to 10 million times greater than concentrations in

the surrounding waters. Nearly all of the mercury found in fish is in the methylmercury form.

Predatory ocean fish that live for a long time may have increased methylmercury content because

of exposure to natural and industrial sources of mercury (Goldman and Shannon 2001).

Methylmercury content of fish varies by species and size of the fish as well as harvest location.

The top ten commercial fish species represent about 85% of the seafood market and contain a

mean mercury level of approximately 0.1 µg/g.

Some states have issued advisories about consumption of fish containing mercury. DOH issued

a statewide fish consumption advisory for women of childbearing age and young children based

on elevated levels of mercury in various commercially bought fish as well as freshwater bass

caught for recreation (DOH 2003). http://www.doh.wa.gov/fish/FishAdvMercury.htm

Toxicity

Most organic mercury compounds are readily absorbed by ingestion and appear in the lipid

fraction of blood and brain tissue. Organic mercury readily crosses the blood-brain barrier and

also crosses the placenta. Fetal blood mercury levels are equal to or higher than maternal levels

(Goldman and Shannon 2001). Methylmercury also appears in human milk. Organic mercury

compounds are most toxic in the central nervous system and may also affect the kidneys and

immune system (Clarkson 1993, and Clarkson 1997, in Goldman and Shannon, 2001).

Methylmercury is toxic to the cerebral and cerebellar cortex in the developing brain and is a

known teratogen. In Minamata Bay, Japan, mothers who were exposed to high amounts of

mercury but were asymptomatic gave birth to severely affected infants. The infants often

appeared normal at birth but developed psychomotor retardation, blindness, deafness, and

seizures over time. Since the fetus is susceptible to neurotoxic effects of methylmercury, several

studies have focused on subclinical effects among children whose mothers were exposed to high

levels of methylmercury. A study in Iraqi children exposed to high levels of methylmercury in

contaminated seeds demonstrated motor retardation in children whose mothers had hair mercury

levels ranging from 10-20 ppm. Two prospective epidemiologic studies were conducted in the

Seychelles and the Faroe Islands. Results from the Faroe Islands suggest that exposure in utero

to mercury at lower levels is associated with subtle adverse effects on the developing brain

(maximum level in hair was 39.1 ppm and in blood was 351 ppb). Memory, attention, and

language tests were inversely associated with higher methylmercury exposures in children up to

7 years of age (Grandjean et al. 1997, Goldman and Shannon 2001). In the Seychelles study,

adverse effects on development or IQ have not been found up to 66 months of age. The Faroe

Islands and Seychelles studies are continuing, in order to provide a long-term developmental

evaluation of exposed children. Further support for the developmental effects seen in Faroese

children is demonstrated in a study of New Zealand children exposed in utero to methylmercury

consumed in fish by their mothers.

In 1998, the National Academy of Sciences (NAS) was directed by the United States Congress to

evaluate methylmercury toxicity and provide recommendations on exposure limits (NRC 2000).

The study established a reference dose for mercury of 0.1 µg/kg-day. The EPA has recently re-

confirmed 0.1 µg/kg-day as its Reference Dose (RfD) (EPA IRIS, 2003). This RfD is based on

health effects data specific to the protection of the developing fetus. As the developing fetus

represents the population of greatest concern, the RfD is considered protective of all other

populations that are less exposed and/or less sensitive. The current action level of FDA for

mercury in fish tissue is 1 ppm (1000 ppb).

Polychlorinated Biphenyls (PCBs)

Background

PCBs are persistent environmental contaminants that are ubiquitous in the global environment

due to intensive industrial use. PCBs were used as commercial mixtures (Aroclors) that contain

up to 209 different chlorinated biphenyl congeners, which are structurally similar compounds

that vary in toxicity. Each congener has a biphenyl ring structure but differs in the number and

arrangement of chlorine atoms substituted around the biphenyl ring. PCBs are lipid soluble and

are stable; their stability depends on the number of chlorine atoms and the position of the

chlorine atoms on the biphenyl molecule. Their lipophilic character and resistance to

metabolism enhances concentration in the food web and exposure to humans and wildlife.

PCBs were produced commercially in the U.S. from the 1930’s to 1977 and sold primarily as

mixtures under the trade name Aroclor. The name Aroclor 1254, for example, means that the

molecule contains 12 carbon atoms (the first 2 digits) and approximately 54% chlorine by weight

(second 2 digits) (ATSDR 2000). Each mixture (1016,1242,1254, and 1260) contained many

different PCB congeners. In 1971, the sole US producer of PCBs (Monsanto Chemical

Company) voluntarily stopped open-ended uses of PCBs and in 1977 ceased their production.

Because PCBs do not burn easily and are good insulators, they were commonly used as

lubricants and coolants in capacitors, transformers, and other electrical equipment. Old

capacitors and transformers that contain PCBs are still in operation. Over the years, PCBs have

been spilled, illegally disposed, and leaked into the environment from transformers and other

electrical equipment. PCBs in the environment have decreased since the 1970’s but are still

detectable in our air, water, soil, food, and in our own bodies.

The breakdown of PCBs in water and soil occurs over many years. The lower chlorinated PCBs

are more easily broken down in the environment, while adsorption of PCBs generally increases

as chlorination of the compound increases. The highly chlorinated Aroclors (1248, 1254, and

1260) resist both chemical and biological degradation in the environment. Microbial degradation

of highly chlorinated Aroclors to lower chlorinated biphenyls has been reported under anaerobic

conditions, as has the mineralization of biphenyl and lower chlorinated biphenyls by aerobic

microorganisms. Although they are slow processes, volatilization and biodegradation are the

major pathways of removal of PCBs from water and soil (ATSDR 2000). In water, photolysis

appears to be the only viable chemical degradation process. The chemical composition of the

original Aroclor mixtures released to the environment changes over time since the individual

congeners degrade and partition at different rates (ATSDR 2000).

Many PCB congeners persist in ambient air, water, marine sediments, and soil at low levels

throughout the world. The half-life of PCBs (the time it takes for one-half of the PCBs to

breakdown) in the air is 10 days or more, depending on the type of PCB. PCBs in the air can be

carried long distances and may be deposited onto land or water. Once in water, most PCBs tend

to stick to organic particles and sediments.

In Lake Washington and other waterbodies, PCBs in sediments are taken up in the bodies of

aquatic organisms, which are in turn consumed by creatures higher in the food web. Fish, birds,

and mammals tend to accumulate certain congeners over time in their fatty tissue.

Concentrations of PCBs can reach levels thousands of times higher than the levels in water.

Bioconcentration is the uptake of a chemical from water alone, while bioaccumulation is the

result of combined uptake via food, sediment, and water. These processes can lead to high levels

in the fat of predatory animals (ATSDR 2000). Also, PCBs can biomagnify in fresh and

saltwater ecosystems. Humans may be exposed to PCBs when they eat fish, use fish oils in

cooking, or consume meat, milk or cheese.

Exposure

The general population is exposed to PCBs through inhalation and ingestion of contaminated

water and food. The dominant source of PCBs to humans is through consumption of seafood,

meat, and poultry. Of particular concern is exposure through consumption of fish. Some groups

may consume greater amounts of fish than others; for example, Native Americans, Asian

immigrant populations and sport anglers are three groups with high rates of seafood ingestion in

the Puget Sound area (Landolt et al. 1985, Landolt et al. 1987, Toy et al. 1996, EPA 1999,

Suquamish 2000). Several studies have found PCBs in local seafood (Landolt et al. 1987,

PSAMP 1997, O’Neill et al. 1998, West and O’Neill 1998, PSAMP 2000, O’Neill and West

2001, West et al. 2001).

Toxicity

Toxic responses to PCBs include dermal toxicity, immunotoxicity, carcinogenicity, and adverse

effects on reproduction, development, and endocrine functions. Some epidemiological studies

indicate that consumption of fish containing PCBs may cause slight but measurable impairments

in physical growth and learning behavior in children. Some PCB congeners have a structure and

biological activity that is similar to dioxin. EPA has determined that PCBs are probable human

carcinogens and assigned them the cancer weight-of evidence classification B2 based on animal

studies. Human studies are being updated; current available evidence is inadequate, but

suggestive regarding cancer to humans. The upper-bound cancer slope factor for PCBs is 2.0 per

(mg/kg)/day.

Part of the uncertainty in assessing PCB effects from consuming fish is that PCB congeners

selectively bioaccumulate in fish in different patterns than found in commercial mixtures of

PCBs (Schwartz et al 1987). The congener mix that a fetus would encounter during pregnancy

and via nursing may be quite different than congener patterns initially released into the

environment. Since PCB congeners differ in their potency and in the specific ways they interact

with biological systems, health criteria based on data from Aroclor mixtures fed to animals (e.g.,

the EPA RfD) may not account for the effects of biodegradation that result in differing initial and

final congener patterns. While some information on pattern changes is available in studies in the

Great Lakes (Kostyniak et al., 1999 and Humphrey et al., 2000), data from Lake Washington did

not include enough information to account for this occurrence (i.e., no congener data). This

issue is one that is being investigated at a national and international level.

DOH recently conducted a thorough review of recent scientific literature in an attempt to set a

state standard for exposure to PCBs through consumption of fish and shellfish. DOH concluded

that ATSDR’s minimal risk level (MRL) of 0.02 µg/kg-day for chronic-duration oral exposure to

PCBs would be protective of the most sensitive population (fetus) for the most sensitive

endpoints reviewed (immune and developmental). The chronic oral MRL is based on a lowest-

observed adverse effect level (LOAEL) of 0.005 mg/kg-day for immunological effects seen in

adult monkeys exposed to Aroclor 1254 (ATSDR 2000). EPA verified an oral reference dose

(RfD) of 0.02 µg/kg-day for Aroclor 1254 (EPA IRIS 2000), based on dermal/ocular and

immunological effects in monkeys. For comparison, FDA set residue levels in fish and edible

shellfish as 2 mg/kg.

References

ATSDR 1994. Toxicological Profile for Chlordane. U.S. Department of Health and Human

Services, Public Health Service. Agency for Toxic Substances and Disease Registry. May 1994.

ATSDR 1999. Toxicological Profile for Mercury. U.S. Department of Health and Human

Services, Public Health Service. Agency for Toxic Substances and Disease Registry. March

1999.

ATSDR 2000. Toxicological Profile for Polychlorinated Biphenyls (PCBs). U.S. Department of

Health and Human Services, Public Health Service. Agency for Toxic Substances and Disease

Registry. November 2000.

ATSDR 2002. Toxicological Profile for DDT, DDE and DDD. U.S. Department of Health and

Human Services, Public Health Service. Agency for Toxic Substances and Disease Registry.

September 2002.

Clarkson TW. 1993. Mercury: major issues in environmental health.

Environ Health Perspect. 1993 Apr;100:31-8.

Clarkson TW. 1997. The Toxicology of Mercury. Crit Rev Clin Lab Sci. 1997 Aug;34(4):369-

403.

DOH 2003. Statewide Bass Advisory. September 2003.

http://www.doh.wa.gov/ehp/oehas/publications%20pdf/statewide_%20bass_%20advisory-

2003.pdf.

EPA IRIS – Integrated Risk Information System

http://www.epa.gov/iris/index.html.

EPA 1986. Guidelines for Carcinogen Risk Assessment. U.S. Environmental Protection

Agency, Office of Research and Development. 1986. 51 Federal Register 33992 (September 24,

1986).

EPA 1996. Proposed Guidelines for Carcinogen Risk Assessment. U.S. Environmental

Protection Agency, Office of Research and Development. April 1996. EPA/600/P-92/003C.

EPA 1999. Asian and Pacific Islander Seafood Consumption Study in King County, WA. U.S.

Environmental Protection Agency, Office of Environmental Assessment. May 1999. EPA

910/R-99-003.

Goldman LR and Shannon MW. 2001. Technical Report: Mercury in the Environment:

Implications for Pediatricians. Pediatrics 108:197-205, 2001.

Grandjean P, Weihe P, White R, Debes F, Araki S, Yokoyama K, Murata K, Sorensen N, Dahl

R, and Jorgensen P. 1997. Cognitive deficit in 7-year-old children with prenatal exposure to

methylmercury. Neurotoxicol. Teratol. 19(6):417-428.

Humphrey H, Gardiner J, Pandya J, Sweeney A, Gasior D, McCaffrey R, and Schantz S. 2000.

PCB congener profile in the serum of humans consuming Great Lakes fish. Environ. Health

Perspect. 2000 Feb.;108(2):167-72.

IARC 2002. http://193.51.164.11/htdocs/monographs/vol53/04-ddt.htm

Kostyniak P, Stinson C, Greizerstein H, Vena J, Buck G, and Mendola P. 1999. Relation of

Lake Ontario fish consumption, lifetime lactation, an dparity to breast milk polychlorobiphenyl

and pesticide concentrations. Environ. Res. 1999 Feb;80(2):S166-S174.

Landolt M, Hafer F, Nevissi A, van Belle G, Van Ness K, and Rockwell C. 1985. Potential

toxicant exposure among consumers of recreationally caught fish from urban embayments of

Puget Sound. NOAA Technical Memorandum NOS OMA 23. Rockville, MD.

Landolt M, Kalman D, Nevissi A, van Belle G, Van Ness K, and Hafer F. 1987. Potential

toxicant exposure among consumers of recreationally caught fish from urban embayments of

Puget Sound: Final Report. NOAA Technical Memorandum NOS OMA 33. Rockville, MD.

NRC 2000. Toxicological Effects of Methylmercury. Committee on the Toxicological Effects

of Methylmercury, Board on Environmental Studies and Toxicology, Commission on Life

Sciences. National Academy of Science National Research Council. National Academy Press.

2000.

O’Neill S, West J, and Hoeman J. 1998. Spatial trends in the concentration of polychlorinated

biphenyls (PCBs) in Chinook (Oncorhynchus tshawytscha) and coho salmon (O. kisutch) in

Puget Sound and factors affecting PCB accumulation: results from the Puget Sound Ambient

Monitoring Program. In R.Strickland (ed.). Proceedings of the 1998 Puget Sound Research

Conference. Puget Sound Water Quality Action Team, Olympia, WA.

O’Neill S, and West J. 2001. Exposure of Pacific Herring (Clupea pallasi) to persistent organic

pollutants in the Puget Sound and the Georgia Basin. Puget Sound Research ’01 Proceedings.

Puget Sound Water Quality Action Team, Seattle, WA.

PSAMP 1997. Draft. Summary report of contaminants in Puget Sound fishes and factors

affecting contaminant uptake and accumulation. Puget Sound Ambient Monitoring Program, Fis

Monitoring Component, Marine Resources Division, Washington Dept. of Fish and Wildlife,

Olympia, WA.

PSAMP 2000. Toxic Contaminants in Fish. In 2000 Puget Sound Update: Seventh Report of the

Puget Sound Ambient Monitoring Program. Puget Sound Water Quality Action Team.

Olympia, WA.

Schwartz P, Jacobson W, Fein G, Jacobson J, and Price H. 1983. Lake Michigan fish

consumption as a source of polychlorinated biphenyls in human cord serum, maternal serum, and

milk. Am. J. Public Health. 1983 Mar;73(3):293-6.

Suquamish 2000. Fish Consumption Survey of the Suquamish Indian Tribe of the Port Madison

Indian Reservation, Puget Sound Region. The Suquamish Tribe, Port Madison Indian

Reservation, Fisheries Department, Suquamish, WA. August 2000.

Toy KA, Polissar NL, Liao S, and Gawne-Mittelstaedt GD. 1996. A Fish Consumption Survey

of the Tulalip and Squaxin Island Tribes of the Puget Sound Region. Tulalip Tribes, Natural

Resources Department, Marysville, WA. October 1996.

West J, and O’Neill S. 1998. Persistent Pollutants and Factors Affecting their Accumulation in

Rockfishes (Sebastes spp.) from Puget Sound, Washington. In E. R. Strickland, editor. Puget

Sound Research ’98 Proceedings. Puget Sound Water Quality Action Team, Seattle, WA.

West J, O’Neill S, Lippert G, and Quinnell S. 2001. Toxic contaminants in marine and

anadromous fishes from Puget Sound, Washington: Results of the Puget Sound Ambient

Monitoring Program fish component, 1989-1999. Technical Report FTP01-14, Washington

Dept. of Fish and Wildlife, Olympia, WA.

APPENDIX C

Lake Washington Fish

Contaminant Data and Analysis

Length

(mm) Chlordan

Mercur

PCBs

Mean 418.9 11.0 62.9 244.3 371.2

Standard Error 24.1 2.6 10.7 12.6 35.7

Median 405.8 10.9 69.7 251.0 385.0

Standard Deviation 41.8 4.5 18.5 21.8 61.9

Minimum 385.2 6.5 41.9 220.0 303.6

Maximum 465.7 15.5 77.1 262.0 425.0

Confidence Level (95.0%) 103.9 11.2 46.1 54.1 153.7

Sample Size 3 3333

Detection Frequency - 50% 100% 100% 100%

* ppb = parts per billion (wet weight)

Chlordane conc. is the sum of alpha and gamma chlordanes

DDT conc. is the sum of DDT, DDE, and DDD congeners

Mercury conc. is for total mercury (organic and inorganic)

PCB conc. is the sum of Aroclors 1254 and 1260

All nondetects were reported as 1/2 detection level

Smallmouth Bass

Concentration in Whole Fish (ppb)*

Table C1. Summary statistics for length and contaminant concentrations

in smallmouth bass.

Cutthroat Trout Length

< 300 mm (mm) Chlordan

Mercur

PCBs

Mean 247.8 15.0 47.4 42.8 79.2

Standard Error 12.2 6.3 19.3 7.1 21.2

Median 239.7 9.1 22.9 37.0 52.7

Standard Deviation 38.5 20.0 60.9 22.6 67.2

Minimum 188.5 1.0 10.2 21.7 21.4

Maximum 294.6 68.3 210.6 98.4 239.5

Confidence Level (95.0%) 27.5 14.3 43.6 16.1 48.1

Sample Size 10 10 10 10 10

Detection Frequency - 70% 100% 100% 95%

Cutthroat Trout Length

> 300 mm (mm) Chlordan

Mercur

PCBs

Mean 429.1 44.3 168.0 175.6 377.4

Standard Error 14.0 7.9 21.5 26.3 49.4

Median 431.7 37.5 181.6 159.5 359.0

Standard Deviation 44.3 25.1 68.0 83.1 156.1

Minimum 350.0 2.3 14.6 35.0 38.8

Maximum 500.0 73.7 238.0 299.0 563.3

Confidence Level (95.0%) 31.7 17.9 48.7 59.5 111.6

Sample Size 10 10 10 10 10

Detection Frequency - 70% 100% 100% 100%

* ppb = parts per billion (wet weight)

Chlordane conc. is the sum of alpha and gamma chlordanes

DDT conc. is the sum of DDT, DDE, and DDD congeners

Mercury conc. is for total mercury (organic and inorganic)

PCB conc. is the sum of Aroclors 1254 and 1260

All nondetects were reported as 1/2 detection level

Concentration in Whole Fish (ppb)*

Table C2a. Summary statistics for length and contaminant

concentrations in cutthroat trout <300 mm.

Table C2b. Summary statistics for length and contaminant

concentrations in cutthroat trout >300 mm.

Yellow Perch Length

< 200 mm (mm) Chlordane DD

Mercury PCBs

Mean 136.0 5.0 13.9 32.9 46.6

Standard Error 4.0 0.6 0.9 1.9 5.2

Median 134.5 4.4 13.6 33.3 37.9

Standard Deviation 12.7 1.8 2.9 5.9 16.3

Minimum 116.0 2.6 10.7 22.5 29.2

Maximum 158.0 8.3 18.9 41.3 74.9

Confidence Level (95.0%) 9.1 1.3 2.1 4.2 11.7

Sample Size 10 10 10 10 10

Detection Frequency - 50% 93% 100% 90%

Yellow Perch Length

201 - 271 mm (mm) Chlordane DD

Mercury PCBs

Mean 243.5 9.6 48.5 86.8 66.4

Standard Error 4.2 1.3 6.6 16.9 14.1

Median 238.0 9.2 48.4 65.6 50.7

Standard Deviation 13.3 4.2 20.7 53.4 44.7

Minimum 231.0 4.5 21.8 40.3 24.0

Maximum 271.0 18.9 87.5 207.0 166.9

Confidence Level (95.0%) 9.5 3.0 14.8 38.2 32.0

Sample Size 10 10 10 10 10

Detection Frequency - 100% 100% 100% 95%

Yellow Perch Length

> 271 mm (mm) Chlordane DD

Mercury PCBs

Mean 303.7 16.3 58.7 183.0 191.1

Standard Error 6.7 2.8 6.8 17.4 18.3

Median 302.0 13.4 64.9 180.0 184.5

Standard Deviation 20.2 8.4 20.4 52.3 55.0

Minimum 273.0 8.0 26.0 121.0 119.2

Maximum 332.8 34.8 84.3 293.0 286.6

Confidence Level (95.0%) 15.6 6.5 15.6 40.2 42.3

Sample Size 9 9 9 9 9

Detection Frequency - 50% 100% 100% 100%

* ppb = parts per billion (wet weight)

Chlordane conc. is the sum of alpha and gamma chlordanes

DDT conc. is the sum of DDT, DDE, and DDD congeners

Mercury conc. is for total mercury (organic and inorganic)

PCB conc. is the sum of Aroclors 1254 and 1260

All nondetects were reported as 1/2 detection level

Concentration in Whole Fish (ppb)*

Table C3a. Summary statistics for length and contaminant concentrations

in yellow perch <200 mm.

Table C3b.

Summary statistics for length and contaminant concentrations

in yellow perch 201 - 271 mm.

Table C3c. Summary statistics for length and contaminant concentrations

in yellow perch >271 mm.

Northern Pikeminnow Length

< 300 mm (mm) Chlordan

Mercur

PCBs

Mean 234.3 7.1 44.5 53.1 140.0

Standard Error 13.9 1.2 8.6 11.1 29.2

Median 234.5 7.0 38.2 35.1 118.0

Standard Deviation 43.9 3.6 25.7 35.2 87.7

Minimum 145.6 2.3 14.6 18.6 57.9

Maximum 297.3 13.8 90.3 106.0 325.0

Confidence Level (95.0%) 31.4 2.8 19.8 25.2 67.4

Sample Size 10 9 9 10 9

Detection Frequency - 50% 96% 100% 100%

Northern Pikeminnow Length

> 300 mm (mm) Chlordan

Mercur

PCBs

Mean 458.7 40.1 257.7 387.1 1071.4

Standard Error 16.8 5.3 29.9 42.4 171.0

Median 444.3 37.3 274.7 334.0 998.0

Standard Deviation 53.0 16.7 94.5 134.0 540.8

Minimum 401.9 15.1 72.7 212.0 210.1

Maximum 568.0 68.3 436.4 598.0 2289.0

Confidence Level (95.0%) 37.9 11.9 67.6 95.8 386.8

Sample Size 10 10 10 10 10

Detection Frequency - 50% 100% 100% 100%

* ppb = parts per billion (wet weight)

Chlordane conc. is the sum of alpha and gamma chlordanes

DDT conc. is the sum of DDT, DDE, and DDD congeners

Mercury conc. is for total mercury (organic and inorganic)

PCB conc. is the sum of Aroclors 1254 and 1260

All nondetects were reported as 1/2 detection level

Concentration in Whole Fish (ppb)*

Table C4a. Summary statistics for length and contaminant concentrations

in northern pikeminnow <300 mm.

Table C4b. Summary statistics for length and contaminant concentrations

in northern pikeminnow >300 mm.

Length

(mm) Chlordan

DDT Mercury PCBs

Mean 606.2 1.0 5.4 37.0 6.3

Standard Error 12.5 0.0 0.7 1.4 1.4

Median 603.5 1.0 4.6 36.5 5.2

Standard Deviation 39.7 0.0 2.3 4.4 4.4

Minimum 553.0 1.0 3.2 30.2 2.5

Maximum 660.0 1.0 10.9 44.8 14.3

Confidence Level (95.0%) 28.4 0.0 1.7 3.2 3.1

Sample Size 10 10 10 10 10

Detection Frequency - 0% 60% 100% 25%

* ppb = parts per billion (wet weight)

Chlordane conc. is the sum of alpha and gamma chlordanes

DDT conc. is the sum of DDT, DDE, and DDD congeners

Mercury conc. is for total mercury (organic and inorganic)

PCB conc. is the sum of Aroclors 1254 and 1260

All nondetects were reported as 1/2 detection level

Sockeye Salmon

Concentration in Whole Fish (ppb)*

Table C5.

Summary statistics for length and contaminant concentrations

in sockeye salmon.

Contaminant

RfD

(ug/kg day)

Concentration in

Whole Fish ppb

(ug/kg)*

Consumption rate

(ounces of fish per

month)**

Consumption rate

(number of 8 oz. meals

per month)***

Chlordane

0.5 7.1

4536.9

567.1

DDT

0.5 44.5

723.9

90.5

Mercury

0.1 53.1

121.3

15.2

PCBs

0.02 140.0

9.2

1.2

Contaminant

RfD

(ug/kg day)

Concentration in

Whole Fish ppb

(ug/kg)*

Consumption rate

(ounces of fish per

month)**

Consumption rate

(number of 8 oz. meals

per month)***

Chlordane

0.5 40.1

803.3

100.4

DDT

0.5 257.7

125.0

15.6

Mercury

0.1 387.1

16.6

2.1

PCBs

0.02 1071.4

1.2

0.2

* ppb = parts per billion (wet weight)

** Consumption rate = (RfD x body weight)/(conc. in fish) x (30.4 days/month)

*** Number of 8 oz. meals per month that would put a 60 kg person at the RfD

RfD - EPA's chemical specific reference dose

Chlordane conc. is the sum of alpha and gamma chlordanes

DDT conc. is the sum of DDT, DDE, and DDD congeners

Mercury conc. is for total mercury (organic and inorganic)

PCB conc. is the sum of Aroclors 1254 and 1260

Highlighted value indicates most restrictive meal limit for each size class

Northern Pikeminnow < 300 mm

Northern Pikeminnow > 300 mm

Table C6a. Calculated consumption rates of northern pikeminnow <300 mm for a 132 lb (60 kg) woman

based on contaminant concentration.

Table C6b. Calculated consumption rates of northern pikeminnow >300 mm for a 132 lb (60 kg) woman

based on contaminant concentration.

Contaminant

RfD

(ug/kg day)

Concentration in

Whole Fish ppb

(ug/kg)*

Consumption rate

(ounces of fish per

month)**

Consumption rate

(number of 8 oz. meals

per month)***

Chlordane

0.5 5

6442.3

805.3

DDT

0.5 13.9

2317.4

289.7

Mercury

0.1 32.9

195.2

24.4

PCBs

0.02 46.6

27.6

3.5

Contaminant

RfD

(ug/kg day)

Concentration in

Whole Fish ppb

(ug/kg)*

Consumption rate

(ounces of fish per

month)**

Consumption rate

(number of 8 oz. meals

per month)***

Chlordane

0.5 9.6

3355.4

419.4

DDT

0.5 48.5

664.2

83.0

Mercury

0.1 86.8

74.2

9.3

PCBs

0.02 66.4

19.4

2.4

Contaminant

RfD

(ug/kg day)

Concentration in

Whole Fish ppb

(ug/kg)*

Consumption rate

(ounces of fish per

month)**

Consumption rate

(number of 8 oz. meals

per month)***

Chlordane

0.5 16.3

1976.2

247.0

DDT

0.5 58.7

548.8

68.6

Mercury

0.1 183.0

35.2

4.4

PCBs

0.02 191.1

6.7

0.8

* ppb = parts per billion (wet weight)

** Consumption rate = (RfD x body weight)/(conc. in fish) x (30.4 days/month)

*** Number of 8 oz. meals per month that would put a 60 kg person at the RfD

RfD - EPA's chemical specific reference dose

Chlordane conc. is the sum of alpha and gamma chlordanes

DDT conc. is the sum of DDT, DDE, and DDD congeners

Mercury conc. is for total mercury (organic and inorganic)

PCB conc. is the sum of Aroclors 1254 and 1260

Highlighted value indicates most restrictive meal limit for each size class

Yellow Perch < 200 mm

Yellow Perch 201 - 271 mm

Yellow Perch > 271 mm

Table C7a.

Calculated consumption rates of yellow perch < 200 mm for a 132 lb (60 kg) woman based

on contamiant concentration.

Table C7b.

Calculated consumption rates of yellow perch 201 - 270 mm for a 132 lb (60 kg) woman

based on contaminant concentration.

Table C7c.

Calculated consumption rates of yellow perch > 271 mm for a 132 lb (60 kg) woman based

on contaminant concentration.

Contaminant

RfD

(ug/kg day)

Concentration in

Whole Fish ppb

(ug/kg)*

Consumption rate

(ounces of fish per

month)**

Consumption rate

(number of 8 oz. meals

per month)***

Chlordane

0.5 15.0

2147.4 268.4

DDT

0.5 47.4

679.6 84.9

Mercury

0.1 42.8

150.5 18.8

PCBs

0.02 79.2

16.3 2.0

Contaminant

RfD

(ug/kg day)

Concentration in

Whole Fish ppb

(ug/kg)*

Consumption rate

(ounces of fish per

month)**

Consumption rate

(number of 8 oz. meals

per month)***

Chlordane

0.5 44.3

727.1 90.9

DDT

0.5 168.0

191.7 24.0

Mercury

0.1 175.6

36.7 4.6

PCBs

0.02 377.4

3.4 0.4

* ppb = parts per billion (wet weight)

** Consumption rate = (RfD x body weight)/(conc. in fish) x (30.4 days/month)

*** Number of 8 oz. meals per month that would put a 60 kg person at the RfD

RfD - EPA's chemical specific reference dose

Chlordane conc. is the sum of alpha and gamma chlordanes

DDT conc. is the sum of DDT, DDE, and DDD congeners

Mercury conc. is for total mercury (organic and inorganic)

PCB conc. is the sum of Aroclors 1254 and 1260

Highlighted value indicates most restrictive meal limit for each size class

Cutthroat Trout < 300 mm

Cutthroat Trout > 300 mm

Table C8a.

Calculated consumption rates of cutthroat trout <300 mm for a 132 lb (60 kg) woman based

on contaminant concentration.

Table C8b.

Calculated consumption rates of cutthroat trout >300 mm for a 132 lb (60 kg) woman based

on contaminant concentration.

Contaminant

RfD

(ug/kg day)

Concentration in

Whole Fish ppb

(ug/kg)*

Consumption rate

(ounces of fish per

month)**

Consumption rate

(number of 8 oz. meals

per month)***

DDT

0.5 5.4

5965.1

745.6

Mercury

0.1 37.0

174.1

21.8

PCBs

0.02 7.9

163.1

20.4

* ppb = parts per billion (wet weight)

** Consumption rate = (RfD x body weight)/(conc. in fish) x (30.4 days/month)

** Number of 8 oz. meals per month that would put a 60 kg person at the RfD

RfD - EPA's chemical specific reference dose

DDT conc. is the sum of DDT, DDE, and DDD congeners

Mercury conc. is for total mercury (organic and inorganic)

PCB conc. is the sum of Aroclors 1254 and 1260

Highlighted value indicates most restrictive meal limit for each size class

Sockeye Salmon

Table C9.

Calculated consumption rates of sockeye salmon for a 132 lb (60 kg) woman based on

contaminant concentration.

Species Group Fillet:Whole Body Ratio Reference

Black Bass Bass 0.43 Bevelheimer et al. 1997

White Bass Bass 0.44 Thompson et al. 2002

Carp Cyprinid 0.53 Thompson et al. 2002

White sucker Cyprinid 0.48 Thompson et al. 2002

Walleye Percid 0.17 Thompson et al. 2002

Walleye Percid 0.1 Parkerton 1993

Walleye Percid 0.09 Connolly et al. 1992

Brown trout Salmoid 1.0 Connolly et al. 1992

Brown trout Salmoid 0.88 Connolly et al. 1992

Brown trout Salmoid 0.57 Connolly et al. 1992

Coho Salmoid 0.59 Amrhein et al. 1999

Coho Salmoid 0.89 Connolly et al. 1992

Rainbow trout Salmoid 0.68 Amrhein et al. 1999

Rainbow trout Salmoid 0.34 Niimi and Oliver 1983

Rainbow trout Salmoid 0.43 Carline et al. 2001

Table courtesy of Jan McIntrye

Data presented for discussion only, and where not used in determining consumption rates.

Fillet-to-Whole Body Ratios for PCBs

Table C10.

Fillet-to-whole body PCB ratios for various fish species.

y = 0.1969x - 37.009

= 0.559

0 100 200 300 400 500 600

Cutthroat trout length (mm)

Chlordane conc. (ppb) wet weight

Coefficient P-value

Intercept -37.009 0.020

Length 0.1969 0.0002

Figure C1.

Correlation between cutthroat trout length (mm) and associated chlordane concentration (ppb)

measured in whole body tissue samples on wet weight basis. Data represents the sum of alpha and gamma

chlordanes. N = 20.

y = 0.7312x - 139.78

= 0.7061

100

150

200

250

0 100 200 300 400 500 600

Cutthroat trout length (mm)

DDT conc. (ppb) wet weight

Coefficient P-value

Intercept -139.78 0.002

Length 0.7312 0.000004

Figure C2. Correlation between cutthroat trout length (mm) and associated DDT concentration (ppb)

measured in whole body tissue samples on wet weight basis. Data represents represents the sum of

DDT, DDE, and DDE. N=20.

y = 0.0007x - 0.1123

= 0.5398

0.05

0.1

0.15

0.2

0.25

0.3

0.35

0 100 200 300 400 500 600

Cutthroat trout length (mm)

Mercury conc. (ppm) wet weight

Figure C3. Correlation between cutthroat trout length (mm) and associated mercury

concentration (ppb) measured in whole body tissue samples on wet weight basis. Data

represents the sum of organic and inorganic mercury. N=20.

Coefficient P-value

Intercept -0.1123 0.038

Length 0.0007 0.0002

y = 1.5804x - 306.56

= 0.692

100

200

300

400

500

600

0 100 200 300 400 500 600

Cutthroat trout length (mm)

PCB conc. (ppb) wet weigth

Figure C4. Correlation between cutthroat trout length (mm) and associated PCB concentration (ppb)

measured in whole body tissue samples on wet weight basis. Data represent sum of PCB aroclors

1254 and 1260. N=20.

Coefficient P-value

Intercept -306.56 0.003

Length 1.5804 0.00001

y = 0.0545x - 2.1883

= 0.3143

0 50 100 150 200 250 300 350

Yellow perch length (mm)

Chlordane conc. (ppb) wet weight

Coefficient P-value

Intercept -2.1883 0.554

Length 0.0545 0.002

Figure C5. Correlation between yellow perch length (mm) and associated chlordane concentration

(ppb) measured in whole body tissue samples on a wet weight basis. Data represents the sum of

alpha

and gamma chlordanes. N=29.

y = 0.2601x - 18.786

= 0.5464

100

0 50 100 150 200 250 300 350

Yellow perch length (mm)

DDT conc. (ppb) wet weight

Coefficient P-value

Intercept -18.7863 0.092

Length 0.2601 0.000005

Figure C6. Correlation between yellow perch length (mm) and DDT concentrations (ppb)

measured in whole body tissues samples on wet weight basis. Data represent the sum of

DDT, DDE, and DDD. N=29.

y = 0.0008x - 0.0868

= 0.6233

0.05

0.1

0.15

0.2

0.25

0.3

0.35

0 50 100 150 200 250 300 350

Yellow perch length (mm)

Mercury conc. (ppm) wet weight

Coefficient P-value

Intercept -0.0868 0.006

Length 0.0008 4e-7

Figure C7. Correlation between yellow perch length (mm) and associated mercury

concentration (ppb) measured in whole body tissue samples on wet weight basis. Data

represent the sum of

organic and inorganic mercury. N=29.

y = 0.7104x - 61.657

= 0.4592

100

150

200

250

300

350

0 50 100 150 200 250 300 350

Yellow perch length (mm)

PCB conc. (ppb) wet weight

Coefficient P-value

Intercept -61.657 0.09

Length 0.7104 0.00005

Figure C8. Correlation between yellow perch length (mm) and associated PCB

concentration (ppb) measured in whole body tissue samples on wet weight basis. Data

represent the sum of PCB aroclors 1254 and 1260. N=29.

y = 0.1513x - 30.087

= 0.7416

0 100 200 300 400 500 600

Northern pikeminnow length (mm)

Chlordane conc. (ppb) wet weight

Coefficient P-value

Intercept -30.087 0.002

Length 0.1513 2.2E-06

Figure C9.

Correlation between northern pikeminnow length (mm) and chlordane concentration (ppb)

meaured in whole body tissue samples on wet weight basis. Data represent the sum of alpha and

gamma chlordanes. N=20.

y = 0.9715x - 190.12

= 0.7901

100

150

200

250

300

350

400

450

500

0 100 200 300 400 500 600

Northern pikeminnow length (mm)

DDT conc. (ppb) wet weight

Coefficient P-value

Intercept -190.12 6.4E-04

Length 0.9715 4E-07

Figure C10. Correlation between northern pikeminnow length and associated DDT concentration

(ppb) meaured in whole body tissue samples on wet weight basis. Data represent the sum of DDT,

DDE, and DDE. N=20.

y = 0.0014x - 0.2751

= 0.8235

0.1

0.2

0.3

0.4

0.5

0.6

0.7

0 100 200 300 400 500 600

Northern pikeminnow length (mm)

Mercury conc. (ppm) wet weight

Coefficient P-value

Intercept -0.2751 0.001

Length 0.0014 3E-08

Figure C11. Correlation between northern pikeminnow length (mm) and associated mercury concentration

(ppb) meaured in whole body tissue samples on wet weight basis. Data represents the sum of organic and

inorganic mercury. N=20.

y = 4.3379x - 918.62

= 0.697

500

1000

1500

2000

2500

0 100 200 300 400 500 600

Northern pikeminnow length (mm)

PCB conc. (ppb) wet weight

Coefficient P-value

Intercept -918.62 0.003

Length 4.3379 1E-05

Figure C12. Correlation between northern pikeminnow length (mm) and PCB concentration (ppb)

meaured in whole body tissue samples on wet weight basis. Data represent the sum of PCB aroclors

1254 and 1260. N=20.

y = 0.0112x - 1.4044

= 0.0364

540 560 580 600 620 640 660 680

Sockeye salmon length (mm)

DDT conc. (ppb) wet weight

Figure C13. Correlation between sockeye salmon length (mm) and associated DDT concentration

(ppb) measured in whole body tissue samples on wet weight basis. Data represent the sum of DDT,

DDE, and DDT. N=10.

Coefficient P-value

Intercept -1.404 0.912

Length 0.0112 0.597

y = -3E-05x + 0.0556

= 0.0747

0.005

0.01

0.015

0.02

0.025

0.03

0.035

0.04

0.045

0.05

540 560 580 600 620 640 660 680

Sockeye salmon length (mm)

Mercury conc. (ppm) wet weight

Coefficient P-value

Intercept 0.00556 0.043

Length -3E-05 0.695

Figure C14. Correlation between sockeye salmon length (mm) and assoicated mercury concentration

(ppb) meaured in whole body tissue samples on wet weight basis. Data represents the sum of organic

and inorganic mercury. N=10.

y = 0.0156x - 3.6418

= 0.0202

540 560 580 600 620 640 660 680

Sockeye salmon length (mm)

PCB conc. (ppb) wet weight

Coefficient P-value

Intercept -3.6418 0.880

Length 0.0156 0.695

Figure C15. Correlation between sockeye salmon length (mm) and associated PCB concentration (ppb)

measured in whole body tissue samples on wet weight basis. Data represents the sum of PCB aroclors

1254 and 1260. N=10.

0.1

100

1000

25 50 75 100 125 150 175 200 225 250 275 300 325 350

Person's Body Weight (lbs)

Number of 8 oz. Meals per Month

15.0 ppb Chlordane

47.4 ppb DDT

42.8 ppb Mercury

79.2 ppb PCBs

Figure C16.

Allowable number of 8 oz. meals per month of cutthroat trout < 12 inches (300 mm)

from Lake Washington for varying body weights based on contaminant concentration.

Measured contaminant

concentrations in whole

body fish tissue.

0.01

0.1

100

1000

25 50 75 100 125 150 175 200 225 250 275 300 325 350

Person's Body Weight (lbs)

Number of 8 oz. Meals per Month

44.3 ppb Chlordane

168.0 ppb DDT

175.6 ppb Mercury

377.4 ppb PCBs

Figure C17.

Allowable number of 8 oz. meals per month of cutthroat trout > 12 inches (300 mm)

from Lake Washington for varying body weights based on contaminant concentration.

Measured contaminant

concentrations in whole

body fish tissue.

0.1

100

1000

10000

25 50 75 100 125 150 175 200 225 250 275 300 325 350

Person' Body Weight (lbs)

Number of 8 oz. Meals per Month

5.0 ppb Chlordane

13.9 ppb DDT

32.9 ppb Mercury

46.6 ppb PCBs

Measured contaminant

concentrations in whole

body fish tissue.

Figure C18.

Allowable number of 8 oz. meals per month of yellow perch <8 inches (200

mm) from Lake Washington for varying body weights based on contaminant concentration.

0.1

100

1000

10000

25 50 75 100 125 150 175 200 225 250 275 300 325 350

Person's Body Weight (lbs)

Number of 8 oz. Meals per Month

9.6 ppb Chlordane

48.5 ppb DDT

86.6 ppb Mercury

66.4 ppb PCBs

Measured contaminant

concentrations in whole

body fish tissue.

Figure C19.

Allowable number of 8 oz. meals per month of yellow perch 8 -10.5 inches

(201 - 270 mm) from Lake Washington for varying body weights based on contaminant

concentration.

0.1

100

1000

25 50 75 100 125 150 175 200 225 250 275 300 325 350

Person's Body Weight (lbs)

Number of 8 oz. Meals per Month

16.3 ppb Chlordane

58.7 ppb DDT

183.0 ppb Mercury

191.1 ppb PCBs

Measured contaminant

concentrations in whole

body fish tissue.

Figure C20.

Allowable number of 8 oz. meals per month of yellow perch >10.5 inches

(270 mm) from Lake Washington for varying body weights based on contaminant

concentration.

0.1

100

1000

10000

25 50 75 100 125 150 175 200 225 250 275 300 325 350

Person's Body Weight (lbs)

Number of 8 oz. Meals per Month

6.6 ppb Chlordane

44.5 ppb DDT

53.1 ppb Mercury

140.0 ppb PCBs

Measured contaminant

concentrations in whole

body fish tissue.

Figure C21.

Allowable number of 8 oz. meals per month of northern pikeminnow <12

inches (300 mm) from Lake Washington for varying body weights based on contaminant

concentration.

0.01

0.1

100

1000

25 50 75 100 125 150 175 200 225 250 275 300 325 350

Person's Body Weight (lbs)

Number of 8 oz. Meals per Month

40.1 ppb Chlordane

257.7 ppb DDT

387.1 ppb Mercury

1071.4 ppb PCB

Measured contaminant

concentrations in whole

body fish tissue.

Figure C22.

Allowable number of 8 oz. meals per month of northern pikeminnow >12

inches (300 mm) from Lake Washington for varying body weights based on contaminant

concentration.

100

1000

10000

25 50 75 100 125 150 175 200 225 250 275 300 325 350

Person's Body Weight (lbs)

Number of 8 oz. Meals per Month

5.4 ppb Chlordane

37.0 ppb Mercury

7.8 ppb PCBs

Measured contaminant

concentrations in whole

body fish tissue.

Figure C23.

Allowable number of 8 oz. meals per month of sockeye salmon from Lake

Washington for varying body weights based on contaminant concentration.

APPENDIX D

Multiple Chemical Exposure Calculations

Table D1. Cancer and non-cancer calculations for multiple chemicals for large northern

pikeminnow using the mean consumption rate (i.e., 1.5 eight-ounce meals per month).

Large Pikeminnow PCB Hg DDT Chlordane

Exposure parameters

alue

alue Units

30.4 30.4 30.4 30.4 Days/month

BW body weight 60 60 60 60 kg

MS meal size 0.227 0.227 0.227 0.227 kg/meal

C conc. 1071.4 387.1 257.7 40.1 ug/kg

ED exposure duration - cancer 30 na 30 30 years

AT averaging time - cance

70 na 70 70 years

meals/month* 1.5

* based on King County DNRP consumption study (ave. consumption rate)

PCB Hg DDT Chlordane

Dose (ug/kg/day) 0.200 0.072 0.048 0.007

Noncancer

RfD (ug/kg/day) 0.02 0.10 0.50 0.50

Hazard Index

Hazard Quotient (HQ) 10.00 0.72 0.10 0.01 10.8

intake = (conc x Ingestion freq x exp freq x exp duration) / (bw x ave time)

PCB Hg DDT Chlordane

Dose cancer (ug/kg/day) 0.0857 na 0.0206 0.0032

Potential Cancer

Slope Factor (kg-day/ug) 2.0E-03 na 3.4E-04 3.5E-04

Risk

Risk 1.7E-04 na 7.0E-06 1.1E-06 1.8E-04

Noncancer Endpoints

Cancer Endpoints

Table D2. Cancer and non-cancer calculations for multiple chemicals for large cutthroat trout

using the mean consumption rate (i.e., 1.5 eight-ounce meals per month).

Large Cutthroat trout PCB Hg DDT Chlordane

Exposure parameters

alue

alue Units

30.4 30.4 30.4 30.4 Days/month

BW body weight 60 60 60 60 kg

MS meal size 0.227 0.227 0.227 0.227 kg/meal

C conc. 377.4 175.6 168 44.3 ug/kg

ED exposure duration - cancer 30 na 30 30 years

AT averaging time - cance

70 na 70 70 years

meals/month* 1.5

* based on King County DNRP consumption study (ave. consumption rate)

PCB Hg DDT Chlordane

Dose (ug/kg/day) 0.070 0.033 0.031 0.008

Noncaner

RfD (ug/kg/day) 0.02 0.10 0.50 0.50 Hazard Index

Hazard Quotient (HQ) 3.52 0.33 0.06 0.02 3.9

intake = (conc x Ingestion freq x exp freq x exp duration) / (bw x ave time)

PCB Hg DDT Chlordane

Dose cancer (ug/kg/day) 0.0302 na 0.0134 0.0035 Cancer

Slope Factor (kg-day/ug) 2.0E-03 na 3.4E-04 3.5E-04

Risk

Risk 6.0E-05 na 4.6E-06 1.2E-06 6.6E-05

Noncancer Endpoints

Cancer Endpoints

Table D3. Cancer and non-cancer calculations for multiple chemicals for large yellow perch

using the mean consumption rate (i.e., 1.5 eight-ounce meals per month).

Large perch PCB Hg DDT Chlordane

Exposure parameters

alue

alue Units

30.4 30.4 30.4 30.4 Days/month

BW body weight 60 60 60 60 kg

MS meal size 0.227 0.227 0.227 0.227 kg/meal

C conc. 191.1 183 58.7 16.3 ug/kg

ED exposure duration - cancer 30 na 30 30 years

AT averaging time - cance

70 na 70 70 years

meals/month* 1.5

* based on King County DNRP consumption study (ave. consumption rate)

PCB Hg DDT Chlordane

Dose (ug/kg/day) 0.036 0.034 0.011 0.003 Noncancer

RfD (ug/kg/day) 0.02 0.10 0.50 0.50 Hazard Index

Hazard Quotient (HQ) 1.78 0.34 0.02 0.01 2.2

intake = (conc x Ingestion freq x exp freq x exp duration) / (bw x ave time)

PCB Hg DDT Chlordane

Dose cancer (ug/kg/day) 0.0153 na 0.0047 0.0013 Cancer

Slope Factor (kg-day/ug) 2.0E-03 na 3.4E-04 3.5E-04

Risk

Risk 3.1E-05 na 1.6E-06 4.6E-07 3.3E-05

Noncancer Endpoints

Cancer Endpoints

Table D4. Cancer and non-cancer calculations for multiple chemicals for large yellow perch

using the mean consumption rate (i.e., 1.5 eight-ounce meals per month).

Smallmouth bass PCB Hg DDT Chlordane

Exposure parameters

alue

alue Units

30.4 30.4 30.4 30.4 Days/month

BW body weight 60 60 60 60 kg

MS meal size 0.227 0.227 0.227 0.227 kg/meal

C conc. 371.2 244.3 62.9 11 ug/kg

ED exposure duration - cancer 30 na 30 30 years

AT averaging time - cance

70 na 70 70 years

meals/month* 1.5

* based on King County DNRP consumption study (ave. consumption rate)

PCB Hg DDT Chlordane

Dose (ug/kg/day) 0.069 0.046 0.012 0.002 Noncancer

RfD (ug/kg/day) 0.02 0.10 0.50 0.50 Hazard Index

Hazard Quotient (HQ) 3.46 0.46 0.02 0.004 3.9

intake = (conc x Ingestion freq x exp freq x exp duration) / (bw x ave time)

PCB Hg DDT Chlordane

Dose cancer (ug/kg/day) 0.0297 na 0.0050 0.0009

Cancer

Slope Factor (kg-day/ug) 2.0E-03 na 3.4E-04 3.5E-04

Risk

Risk 5.9E-05 na 1.7E-06 3.1E-07 6.1E-05

Noncancer Endpoints

Cancer Endpoints

Table D5. Cancer and non-cancer calculations for multiple chemicals for large yellow perch

using the mean consumption rate (i.e., 1.5 eight-ounce meals per month).

Sockeye PCB Hg DDT Chlordane

Exposure parameters

alue

alue Units

30.4 30.4 30.4 30.4 30.4 Days/month

BW body weight 60 60 60 60 kg

MS meal size 0.227 0.227 0.227 0.227 kg/meal

C conc. 7.8 37 5.4 1 ug/kg

ED exposure duration - cancer 30 na 30 30 years

AT averaging time - cance

70 na 70 70 years

meals/month* 1.5

* based on King County DNRP consumption study (ave. consumption rate)

PCB Hg DDT Chlordane

Dose (ug/kg/day) 0.001 0.007 0.001 0.0002

Noncancer

RfD (ug/kg/day) 0.02 0.10 0.50 0.50 Hazard Index

Hazard Quotient (HQ) 0.07 0.07 0.002 0.0004 0.1

intake = (conc x Ingestion freq x exp freq x exp duration) / (bw x ave time)

PCB Hg DDT Chlordane

Dose cancer (ug/kg/day) 0.0006 na 0.0004 0.0001 Cancer

Slope Factor (kg-day/ug) 2.0E-03 na 3.4E-04 3.5E-04

Risk

Risk 1.2E-06 na 1.5E-07 2.8E-08 1.4E-06

Noncancer Endpoints

Cancer Endpoints

Table D6. Cancer and non-cancer calculations for multiple chemicals for large northern

pikeminnow using the 95

percentile consumption rate (i.e., four eight-ounce meals per month).

Large Pikeminnow PCB Hg DDT Chlordane

Exposure parameters

alue

alue Units

3 30.4 30.4 30.4 30.4 Days/month

BW body weight 60 60 60 60 kg

MS meal size 0.227 0.227 0.227 0.227 kg/meal

C conc. 1071.4 387.1 257.7 40.1 ug/kg

ED exposure duration - cancer 30 na 30 30 years

AT averaging time - cance

70 na 70 70 years

meals/month* 4

* based on King County DNRP consumption study (95 percentile consumption rate)

PCB Hg DDT Chlordane

Dose (ug/kg/day) 0.533 0.193 0.128 0.020

Noncancer

RfD (ug/kg/day) 0.02 0.10 0.50 0.50

Hazard Index

Hazard Quotient (HQ) 26.67 1.93 0.26 0.04 28.9

intake = (conc x Ingestion freq x exp freq x exp duration) / (bw x ave time)

PCB Hg DDT Chlordane

Dose cancer (ug/kg/day) 0.2286 na 0.0550 0.0086

Potential Cancer

Slope Factor (kg-day/ug) 2.0E-03 na 3.4E-04 3.5E-04

Risk

Risk 4.6E-04 na 1.9E-05 3.0E-06 4.8E-04

Noncancer Endpoints

Cancer Endpoints

Table D7. Cancer and non-cancer calculations for multiple chemicals for large cutthroat trout

using the 95

percentile consumption rate (i.e., four eight-ounce meals per month).

Large Cutthroat trout PCB Hg DDT Chlordane

Exposure parameters

alue

alue Units

30.4 30.4 30.4 30.4 Days/month

BW body weight 60 60 60 60 kg

MS meal size 0.227 0.227 0.227 0.227 kg/meal

C conc. 377.4 175.6 168 44.3 ug/kg

ED exposure duration - cancer 30 na 30 30 years

AT averaging time - cance

70 na 70 70 years

meals/month* 4

* based on King County DNRP consumption study (95 percentile consumption rate)

PCB Hg DDT Chlordane

Dose (ug/kg/day) 0.188 0.087 0.084 0.022

Noncaner

RfD (ug/kg/day) 0.02 0.10 0.50 0.50 Hazard Index

Hazard Quotient (HQ) 9.39 0.87 0.17 0.04 10.5

intake = (conc x Ingestion freq x exp freq x exp duration) / (bw x ave time)

PCB Hg DDT Chlordane

Dose cancer (ug/kg/day) 0.0805 na 0.0358 0.0095 Cancer

Slope Factor (kg-day/ug) 2.0E-03 na 3.4E-04 3.5E-04

Risk

Risk 1.6E-04 na 1.2E-05 3.3E-06 1.8E-04

Noncancer Endpoints

Cancer Endpoints

Table D8. Cancer and non-cancer calculations for multiple chemicals for large yellow perch

using the 95

percentile consumption rate (i.e., four eight-ounce meals per month).

Large perch PCB Hg DDT Chlordane

Exposure parameters

alue

alue Units

30.4 30.4 30.4 30.4 Days/month

BW body weight 60 60 60 60 kg

MS meal size 0.227 0.227 0.227 0.227 kg/meal

C conc. 191.1 183 58.7 16.3 ug/kg

ED exposure duration - cancer 30 na 30 30 years

AT averaging time - cance

70 na 70 70 years

meals/month* 4

* based on King County DNRP consumption study (95 percentile consumption rate)

PCB Hg DDT Chlordane

Dose (ug/kg/day) 0.095 0.091 0.029 0.008

Noncancer

RfD (ug/kg/day) 0.02 0.10 0.50 0.50 Hazard Index

Hazard Quotient (HQ) 4.76 0.91 0.06 0.02 5.7

intake = (conc x Ingestion freq x exp freq x exp duration) / (bw x ave time)

PCB Hg DDT Chlordane

Dose cancer (ug/kg/day) 0.0408 na 0.0125 0.0035 Cancer

Slope Factor (kg-day/ug) 2.0E-03 na 3.4E-04 3.5E-04

Risk

Risk 8.2E-05 na 4.3E-06 1.2E-06 8.7E-05

Noncancer Endpoints

Cancer Endpoints

Table D9. Cancer and non-cancer calculations for multiple chemicals for smallmouth bass using

the 95

percentile consumption rate (i.e., four eight-ounce meals per month).

Smallmouth bass PCB Hg DDT Chlordane

Exposure parameters

alue

alue Units

30.4 30.4 30.4 30.4 Days/month

BW body weight 60 60 60 60 kg

MS meal size 0.227 0.227 0.227 0.227 kg/meal

C conc. 371.2 244.3 62.9 11 ug/kg

ED exposure duration - cancer 30 na 30 30 years

AT averaging time - cance

70 na 70 70 years

meals/month* 4

* based on King County DNRP consumption study (95 percentile consumption rate)

PCB Hg DDT Chlordane

Dose (ug/kg/day) 0.185 0.122 0.031 0.005 Noncancer

RfD (ug/kg/day) 0.02 0.10 0.50 0.50 Hazard Index

Hazard Quotient (HQ) 9.24 1.22 0.06 0.011 10.5

intake = (conc x Ingestion freq x exp freq x exp duration) / (bw x ave time)

PCB Hg DDT Chlordane

Dose cancer (ug/kg/day) 0.0792 na 0.0134 0.0023

Cancer

Slope Factor (kg-day/ug) 2.0E-03 na 3.4E-04 3.5E-04

Risk

Risk 1.6E-04 na 4.6E-06 8.2E-07 1.6E-04

Noncancer Endpoints

Cancer Endpoints

Table D10. Cancer and non-cancer calculations for multiple chemicals for sockeye salmon

using the 95

percentile consumption rate (i.e., four eight-ounce meals per month).

Sockeye PCB Hg DDT Chlordane

Exposure parameters

alue

alue Units

30.4 30.4 30.4 30.4 30.4 Days/month

BW body weight 60 60 60 60 kg

MS meal size 0.227 0.227 0.227 0.227 kg/meal

C conc. 7.8 37 5.4 1 ug/kg

ED exposure duration - cancer 30 na 30 30 years

AT averaging time - cance

70 na 70 70 years

meals/month* 4

* based on King County DNRP consumption study (95 percentile consumption rate)

PCB Hg DDT Chlordane

Dose (ug/kg/day) 0.004 0.018 0.003 0.0005

Noncancer

RfD (ug/kg/day) 0.02 0.10 0.50 0.50 Hazard Index

Hazard Quotient (HQ) 0.19 0.18 0.005 0.0010 0.4

intake = (conc x Ingestion freq x exp freq x exp duration) / (bw x ave time)

PCB Hg DDT Chlordane

Dose cancer (ug/kg/day) 0.0017 na 0.0012 0.0002 Cancer

Slope Factor (kg-day/ug) 2.0E-03 na 3.4E-04 3.5E-04

Risk

Risk 3.3E-06 na 3.9E-07 7.5E-08 3.8E-06

Noncancer Endpoints

Cancer Endpoints

APPENDIX E

Cancer Evaluation

Introduction

Some chemicals detected in Lake Washington fish have the ability to cause cancer. In order to

quantify a fish consumer's increased cancer risk, a cancer slope factor describing the potency of a

chemical's carcingenicity must be determined through scientific study. Some cancer slope factors

are derived from human population data. Others are derived from laboratory animal studies

involving doses much higher than those encountered in the environment. Use of animal data

requires extrapolation of the cancer potency obtained from these high dose studies down to real-

world exposures. This process involves much uncertainty. Despite uncertainties associated with

cancer slope factors for each contaminant, it is possible to calculate the potential cancer risk by

applying the following equation (EPA 1986):

Risk of cancer = (Chronic Daily Intake) x (Cancer Slope Factor).

In this equation, the chronic daily intake is replaced with the chemical-specific reference dose

(RfD) with units of mg/kg-day. The cancer slope factor is also chemical specific with units of

(mg/kg-day)

-1

. CSFs for each chemical are listed above. The product of the RfD and CSF

results in a unitless value that represents the population risk, expressed as the probability of

developing cancer over a lifetime. The resulting calculated cancer risks ranged from 2 in 10,000

for chlordane and DDT, to 4 in 100,000 for PCBs. These risks are upper bound estimates, while

true risks may be as low as zero. These calculated values fall under current typical regulatory

guidelines used by EPA for acceptable risk levels and range from 1 in one million to one in ten

thousand.

The following summaries provide an overview of available cancer data and assessment for each

contaminant of concern in Lake Washington fish.

Chlordane

Chlordane is classified by EPA as B2 (probable human carcinogen) using the 1986 Guidelines

for Carcinogen Risk Assessment. These characterizations are based on the following summaries

of the evidence available: (1) human epidemiology studies showing non-Hodgkin's lymphoma in

farmers exposed to chlordane and case reports of aplastic anemia (chlordane data associated with

home use are inadequate to demonstrate carcinogenicity); (2) animal studies in which benign and

malignant liver tumors were induced in both sexes of four strains of mice and occurred with an

elevated, but not statistically significant, incidence in a fifth strain, as well as liver toxicity but no

tumors in rats of two strains; and (3) structural similarity to other rodent liver carcinogens.

EPA’s IRIS has assigned a cancer slope factor (CSF) for chlordane of 0.35 (mg/kg-day)

-1

Dichlorodiphenyltrichloroethane (DDT)

DDT is classified also as B2 (probable human carcinogen). The basis for this classification is

from observations of tumors (generally of the liver) in seven studies in various mouse strains and

three studies in rats. DDT is structurally similar to other probable carcinogens, DDE and DDD.

The existing human epidemiological data are inadequate and autopsy studies relating tissue

levels of DDT to cancer incidence have yielded conflicting results. Three studies reported that

tissue levels of DDT and DDE were higher in cancer victims than in those dying of other

diseases (Casarett et al.1968, Dacre and Jennings 1970, Wasserman et al.1976). In other studies,

no such relationship was seen (Robinson et al.1965, Hoffman et al.1967). Studies of

occupationally exposed workers and volunteers have been of insufficient duration to be useful in

assessment of the carcinogenicity of DDT to humans. EPA’s IRIS database shows a CSF for

DDT of 0.34 (mg/kg-day)

-1

Mercury

Mercury has been classified as C (possible human carcinogen). This is based on inadequate data

in humans and limited evidence of carcinogenicity in animals. Three studies were identified that

examined the relationship between methylmercury exposure and cancer in humans. No

persuasive evidence of increased carcinogenicity attributable to methylmercury exposure was

observed in any of the studies. In animal studies, male mice exposed to methylmercuric chloride

in the diet had an increased incidence of renal adenomas, adenocarcinomas, and carcinomas.

The tumors were observed at a single site and in a single species and single sex. Renal epithelial

cell hyperplasia and tumors were observed only in the presence of profound nephrotoxicity and

were suggested to be a consequence of reparative changes in the cells. A CSF has not been

calculated for mercury in the IRIS database.

Polychlorinated biphenyls (PCBs)

PCBs are also classified as a B2 (probable carcinogen) and the following studies showed

possible associations between PCBs and occupational exposure. A cohort study by Bertazzi et

al. (1987) analyzed cancer mortality among 2,100 workers at a capacitor manufacturing plant in

Italy. Male workers showed a statistically significant increase in death from gastrointestinal tract

cancer compared with national and local rates. In females, a statistically significant excess risk

of death from hematologic cancer was reported. Analyses by exposure duration, latency, and

year of first exposure revealed no trend; however, the numbers were small. A cohort study by

Brown (1987) analyzed cancer mortality among workers at two capacitor manufacturing plants

in New York and Massachusetts. The cohort included 2,588 workers employed at least three

months in areas of the plants considered to have potential for heavy exposure to PCBs. Cancer

rates of workers were compared with national rates. Analyses by time since first employment or

length of employment revealed no trend; again, the numbers were considered small. A third

study involving 3,588 workers at a capacitor manufacturing plant in Indiana by Sinks et al.

(1992) analyzed cancer mortality. Workers were classified into five exposure zones based on

distance from the impregnation ovens. Compared with national rates, a statistically significant

excess risk of death from skin cancer was reported. A proportional hazards analysis revealed no

pattern of association with exposure zone; however, the numbers are small.

Other occupational studies by NIOSH (1977), Gustavsson et al. (1986) and Shalat et al. (1989)

looked for an association between occupational PCB exposure and cancer mortality. The studies

examining the cancer causing effect of PCBs often have methodological limitations. However,

the evidence, taken in totality, indicates a potential cancer causing effect for PCBs. EPA

determined that the human data are inadequate, but suggestive of carcinogenicity (EPA IRIS

2000), and IARC (1998) concluded that the evidence for carcinogenicity to humans is limited.

Cancer studies in animals are more conclusive in demonstrating a link with PCB exposure. A

1996 study found liver tumors in female rats exposed to Aroclors 1260, 1254, 1242, and 1016,

and in male rats exposed to 1260. These mixtures contain overlapping groups of congeners that,

together, span the range of congeners most often found in environmental mixtures. Earlier

studies found high, statistically significant incidences of liver tumors in rats ingesting Aroclor

1260 or Clophen A 60 (Kimbrough et al., 1975; Norback and Weltman, 1985; Schaeffer et al.,

1984). Mechanistic studies are beginning to identify several congeners that have dioxin-like

activity and may promote tumors by different modes of action. PCBs are absorbed through

ingestion, inhalation, and dermal exposure, after which they are transported similarly through the

circulation. This provides a reasonable basis for expecting similar internal effects from different

routes of environmental exposure. The current CSF for PCBs is 2 (mg/kg-day)

-1

References

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