of the
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1995
EPA
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State of the Great Lakes Ecosystem Conference
Background Paper
EFFECTS OF GREAT LAKES BASIN
ENVIRONMENTAL CONTAMINANTS ON
HUMAN HEALTH
Jack Manno
Sheila Myers
Great Lakes Research Consortium
SUNY College of Environmental Science & Forestry
Syracuse, New York
Dieter Riedel
Neil Trembley
Great Lakes Health Effects Program
Health and Welfare Canada
Ottawa, Ontario
August 1995
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Table of Contents
Acknowledgments iv
EXECUTIVE SUMMARY 1
1.0 INTRODUCTION 5
2.0 OVERVIEW OF CONTAMINANTS OF CONCERN 7
2.1 Priority Contaminants 1
2.2 Sources of Priority Contaminants and Routes of Exposure 10
2.3 Populations at Greatest Risk 14
3.0 EXPOSURE TRENDS 19
3.1 Organochlorines 19
3.2 Airborne Contaminants 21
4.0 LINKING CONTAMINANT EXPOSURE TO HUMAN HEALTH EFFECTS .. 25
4.1 The Use of Biomarkers 25
4.2 Establishing Links 30
5.0 HEALTH EFFECTS OF EXPOSURE TO CONTAMINATION 33
5.1 Reproductive Toxicology 33
5.2 Epidemiological Studies of Reproductive Outcomes 37
5.3 Neurotoxicity of Lead, Methylmereury, and PCBs 39
5.4 Immunotoxicity of Heavy Metals, PCBs, Dioxins, and Organochlorine Pesticides 42
5.5 Carcinogenicity and Genotoxicity 46
5.6 Respiratory Health Effects 49
5.7 Health Effects Associated with Radionuclides 51
5.8 Health Effects Associated with Microbial Contaminants 60
6.0 KNOWLEDGE GAPS AND DIRECTIONS FOR FUTURE RESEARCH . 63
7.0 CONCLUSIONS 67
8.0 REFERENCES 69
Human Health Effects - SOLEC Background Paper iii
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Acknowledgments
The authors would like to thank the following scientists for the substantial contributions they
have made to this paper in their respective areas of expertise:
B.A. Ahier, Environmental Radiation Hazards Division, Health Canada
H. Anderson, Wisconsin Division of Health, Madison
J. Bernier, Department of Biological Sciences, University du Quebec k Montreal
P. Brousseau, Department of Biological Sciences, University du Quebec & Montreal
D.W. Bryant, Department of Biochemistry, McMaster University
R.T. Burnett, Biostatistics and Computer Applications Division, Health Canada
I, Chu, Environmental and Occupational Toxicology Division, Health Canada
M. Clark, U.S. Environmental Protection Agency, Chicago, IL.
J. Dellinger, Lake Superior Research Institute, University of Wisconsin at Superior
G.H. Douglas, Environmental and Occupational Toxicology Division, Health Canada
M. Feeley, Toxicological Evaluation Division, Health Canada
E.F. Fitzgerald, New York State Department of Health, Albany
G. Fletcher, Department of Biochemistry, McMaster University
W.G. Foster, Environmental and Occupational Toxicology Division, Health Canada
M. Foumier, Department of Biological Sciences, University du Quebec a Montr6al
A.P. Oilman, Great Lakes Health Effects Division, Health Canada
F. Hauchman, U.S. Environmental Protection Agency, Research Triangle Park, NC
H. Hicks, Agency for Toxic Substances and Disease Registry, Atlanta, GA
B. Hills, Chemical Evaluation Division, Food Directorate, Health Canada
M.E. Hovinga, Department of Epidemiology, University of Alabama
H, Humphrey, Michigan Department of Public Health, Lansing, MI
D. Jordan-Simpson, Laboratory Centre for Disease Control, Health Canada
J. Kearney, Great Lakes Health Effects Division, Health Canada
N.I. Kerkvliet, Department of Agricultural Chemistry, Oregon State University
B. Knuth, Department of Natural Resources, Cornell University, Ithaca, NY
K. Krzystyniak, Department of Biological Sciences, University du Quebec a Montreal
R.P. Moody, Environmental and Occupational Toxicology Division, Health Canada
E. Nieboer, Department of Biochemistry, McMaster University
C.L.J. Parfett, Environmental and Occupational Toxicology Division, Health Canada
D. Rice, Toxicology Research Division, Food Directorate, Health Canada
D. Riedel, Great Lakes Health Effects Division, Health Canada
W, Robertson, Monitoring and Criteria Division, Envir. Health Directorate, Health Canada C.G.
Rousseaux, GlobalTox International Consultants Inc., Ottawa
R. Semenciw, Laboratory Centre for Disease Control, Health Canada
P.L. Seyfried, Department of Microbiology, University of Toronto
G. Sherman, Laboratory Centre for Disease Control, Health Canada
D. Stieb, Environmental and Occupational Toxicology Division, Health Canada
P.T. Thomas, Ph.D., LIT. Research Institute, Chicago
B.L. Tracy, Environmental Radiation Hazards Division, Health Canada
iv
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H. Tryphonas, Toxicology Research Division, Food Directorate, Health Canada
G. Tudose, Department of Microbiology, University of Toronto
J, Vena, School of Medicine and Biomedical Sciences, State Univ. of New York at Buffalo
P. Walsh, Laboratory Centre for Disease Control, Health Canada
B.-L. Xu, Department of Microbiology, University of Toronto
NOTICE TO READER
These Background Papers are intended to provide a concise overview of the status of
conditions in the Great Lakes. The information they present has been selected as
representative of the much greater volume of data. They therefore do not present all research
or monitoring information available. The Papers were prepared with input from many
individuals representing diverse sectors of society.
The Background Papers were first released as Working Papers to provide the basis for
discussions at the first State of the Lakes Ecosystem Conference (SOLEC) in October, 1994.
Information provided by SOLEC discussants was incorporated into the these final SOLEC
background papers. SOLEC was intended to provide key information required by managers
to make better environmental decisions.
Human Health Effects - SOLEC Background Paper
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EXECUTIVE SUMMARY
This discussion paper examines the potential human health effects of exposure to certain Great
Lakes Basin environmental contaminants from the following six groups: persistent organochlorine
pesticides; chlorinated aromatic hydrocarbons (e.g., PCBs, dioxins, fiirans); heavy metals;
airborne pollutants; radionuclides; and microbial contaminants.
Sources and Routes of Exposure; These contaminants of concern in the Basin have a variety
of industrial, agricultural, municipal, and domestic sources. The major route of human exposure
to PCBs, dioxins, furans, organochlorine pesticides and methylmereury is food consumption,
particularly contaminated fish. Ingestion of untreated drinking water is a second route of human
exposure to organochlormes, some heavy metals, and microbial contaminants. Breathing
contaminated air is the obvious route of exposure to airborne pollutants. For those people using
the Lakes for occupational or recreational purposes, dermal exposure to waterborne chemicals and
microbes is relevant. Finally, all four routes of exposure are relevant in the case of radionuclides.
Exposure Trends: Research on trends in exposure to waterborne chemical contaminants reveals
that: 1) there is no conclusive evidence that populations in the Basin are exposed to higher levels
of toxic chemicals than are other populations in the world; 2) the few studies that have been done
comparing measurable body burdens have produced varying, and sometimes conflicting, results;
and 3) at present, researchers who have studied Great Lakes fish-eaters and compared body
burdens of priority contaminants over time and with those in other populations have various
explanations for current body burdens. Any measurable reduction in body burdens may be due
to: a) reduced contamination in the ambient environment and in fish tissues and/or b) reduced
fish consumption rates, especially in high-risk populations that are heeding fish consumption
advisories.
Regarding airborne contaminants, southern Ontario clearly has had the greatest number of days
on which the Canadian air quality objective for ground-level ozone was exceeded. Average levels
in several southern Ontario cities in the Basin have not changed significantly over the last ten
years. Similarly, there has been little change in annual average levels of total suspended airborne
particles (TSP) over the last 10 years. Areas in the southern Basin have had the highest sulphate
levels (which correlate with actual acid aerosol levels), though other areas across Canada, such
as the Maritimes, may experience comparable acid levels. Sulphate levels have declined slightly
in Ontario over the last ten years. In the United States, the USEPA has estimated that on the U.S.
side of the Basin 7.2 million people and 4.7 million people are exposed to levels of toxic air
pollutants which are greater than health reference levels for acute and chronic effects,
respectively.
Health Effects: This review focuses on hazard identification (not integrated exposure/health risk
assessments), i.e., delineating the various potential adverse health effects.
Reproductive effects: Although there are inadequate data on exposure of Basin populations to
trace concentrations of environmental contaminants and potential reproductive effects, the fetus
Human Health Effects - SOLEC Background Paper 1
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and neonate are thought to be at risk due to potential exposure in utero and via breast milk.
Limited epidemiological evidence (based on the same cohort observed in different ways over
time) suggest that in utero exposure to PCBs via maternal consumption of Great Lakes fish has
resulted in lower birthweight, reduced gestational age, and smaller head circumference compared
to controls. Increased susceptibility to infectious illness in the first four months of life has also
been observed. More recently there has been speculation about a possible link between exposure
to organochlorines and an increased incidence of breast cancer in women; and of abnormal sperm
quality, density, motility, and testicular morphology in males. Further research is required to
determine whether or not such links exist.
Neurological effects: As in the case of reproductive effects, the developing organism is more
sensitive to neurotoxic effects than is the adult. There is epidemiological evidence and data from
laboratory animal studies showing that low-level in utero exposure to PCBs via maternal
consumption of contaminated Great Lakes fish results in adverse effects on cognitive, motor and
behavioral development of infants, including deficiencies in cognitive ability to visually
discriminate between objects, and in short-term memory scanning capabilities in infants. It is
unclear whether body burdens of MeHg (methylmercury) in fish-eating Basin populations are
associated with adverse neurological/behavioral effects. Exposure to lead in utero and/or during
childhood at body burdens that are currently typical of humans in industrialized countries has
resulted hi deficits in IQ, and hi distractibility, hyperactivity, inattention, increased reaction time,
and other behavioral problems; and in developmental deficits in cognitive performance, abstract
thinking, sustained attention, and psychomotor development.
Immunological effects; The immunotoxic potential of PCBs, dioxins, organochlorine pesticides
(HCB, mirex, dieldrin and DDT), and the heavy metals cadmium, mercury and lead, raises
concerns about subsequent effects on human health. Limited human epidemiological data and
data from wildlife and laboratory animal studies indicate that certain human populations (e.g.,
those who consume large amounts of Great Lakes fish) might be vulnerable to adverse
immunomodulating effects of these pollutants, which may be expressed either as
immunosuppression or immunoenhancement. The former may be manifested either as decreased
resistance to opportunistic viral, bacterial, fungal and other agents or increased susceptibility to
cancer. Immunoenhancement, on the other hand, may either increase the risk of autoimmune
reactions or result in allergic reactions.
Cancer: There is only limited human epidemiological evidence and case-control data to indicate
that some drinking water sources with Great Lakes origin may be associated with increases in
the incidence of several types of cancer in humans (e.g, bladder cancer). Some of these drinking
water sources currently have elevated levels of certain contaminants represented by alpha-
hexachlorocyclohexane (a-HCH), nickel, and trihalomethanes. However, the epidemiological
evidence is not of sufficient strength to link exposure to these compounds with the elevated
cancer incidences. In terms of risk estimates, according to USEPA the estimated number of
potential excess cancer cases expected from ingesting contaminated Great Lakes drinking water
is roughly 66 over a 70-year period; while that expected from consumption of Great Lakes fish
is 30,000 over a 70 -year span, due mostly to PCB exposure, which accounts for an estimated
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85% of human cancer risks associated with Basin contaminants. Finally, as mentioned earlier,
there is recent speculation about a possible link between exposure to organochlorine pollutants
such as PCBs and DDT, and the incidence of breast cancer.
Respiratory effects: The effects of air pollution on respiratory health can range from severe
(aggravation of respiratory disease, death) to moderate (reduced lung function with or without
symptoms) to minor (eye, nose and throat symptoms). Certain effects, such as mild inflammation
in the lungs without symptoms, may or may not have any significance. Research which
demonstrates increased death rates and rates of hospital admission due to air pollution could
reflect a very large overall burden of illness in the population. There is strongly suggestive
evidence from the Basin linking ozone, airborne particles and acid aerosols to significant
respiratory health effects, including death and illness requiring hospital admission. There is also
evidence from the Basin that these pollutants cause reduced lung function in children. This
evidence is consistent with data from elsewhere in North America and Europe.
Rodionuclide-related health effects: Using a no-threshold dose model for radiation effects, risk
estimates for fatal cancer for the current Basin population of 36 million from exposure to natural
background radiation are on the order of 5000 cases per year. The total estimated number of
fatalities to the year 2000 from fallout radionuclides hi the Basin is on the order of 4000. In
contrast, estimates of risk for the nuclear fuel cycle (from exposures mainly to tritium and
carbon-14 releases) based on environmental models are on the order of 10 cases per year. These
numbers should be taken as upper limits, and show that the impact from current man-made
sources is small compared to the effects of normal background radiation. With respect to
drinking water, the total average effective doses of radionuclides for Great Lakes drinking water
would result in two additional fatalities per year (also an upper limit) based on the maximum
effective dose to the entire Basin population.
Microbe-Related Health Effects: Microbial (e.g., bacterial, viral, protozoan) contamination of
Great Lakes water by human and animal sewage has been documented at numerous sites in the
region. Those drinking the water at these locations run the risk of developing giardiasis,
cryptosporidiosis, or gastrointestinal illness. A Canadian prospective study of swimming-related
illness showed that swimmers experienced respiratory ailments most frequently, followed by
gastrointestinal, eye, ear, and skin symptoms. Data on gastrointestinal illness rates among
swimmers in this study revealed an excess of 13.3 cases per 1,000 compared to non-swimmers.
Knowledge Gaps and Directions for Future Research; There is a need for further research on
exposure-response relationships (i.e., quantifying the level of exposure required to observe a
specific adverse effect), contaminant exposure levels in Basin populations compared to those in
other populations worldwide, the effects of chemical mixtures, and the use of biomarkers (i.e.,
to develop biomarkers of exposure and effect that are more sensitive and specific to particular
chemical exposures). There is also a need to broaden the range of health effect endpoints studied
and to gather additional epidemiological data, particularly on subpopulations at special risk.
Human Health Effects - SOLEC Background Paper
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Conclusions; It is clear that occupational or accidental exposure to high levels of certain
environmental contaminants discussed in this paper (particularly PCBs, dioxins, organochlorine
pesticides, lead, and methylmercury) pose a risk to human health. While the exact nature and
the extent of health risk from exposure to environmental levels of these contaminants are unclear
and require further study, recent research has contributed to a shift towards the "weight of
evidence" approach in identifying and measuring potential adverse health effects. In addition to
data from laboratory animal studies and (limited) human epidemiological studies, adverse
metabolic, developmental, reproductive, behavioral, and immunological effects have been
observed across a range of wildlife species exposed to mixtures of persistent toxic chemicals
present in the Great Lakes ecosystem.
Furthermore, traditional health outcomes such as cancer and birth defects, which are relatively
severe and well recorded, may be insensitive health indicators of the effects of low-level exposure
to environmental chemicals. There is a need for further study of the less severe, more subtle
effects due to long-term, low-level exposures to mixtures of toxic chemicals, including effects
on reproduction, the immune system, the respiratory and circulatory systems, and development
in children, and to identify any possible long-term adverse health effects.
Based on our knowledge thus far, it would appear that the health of some groups within the
Basin population could be at greater risk than the general population. These include children, the
elderly, those hi ill health, the fetus and newborn child could have greater sensitivity to toxic
chemicals; and sportsmen and Native peoples who consume contaminated fish and wildlife.
Finally, exploring directions for future research ranging from integrated exposure assessments to
body burdens to potential health outcomes, should be a priority to help reduce the uncertainties
in our knowledge of the potential short- and long-term adverse health effects from exposure to
toxic chemicals in the Great Lakes Basin.
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1.0 Introduction
The purpose of this paper is to review and summarize the state of the Great Lakes in terms of
the human health impacts of exposure to environmental contaminants in the Great Lakes
ecosystem. Most of the concern over health effects has focused on the presence of toxic
chemical contaminants throughout the Great Lakes ecosystem, particularly those chemicals that
have been shown to cause harm to the fish and wildlife which inhabit the Lakes. Extensive
reviews of the effects of the chemicals of concern in the Great Lakes have led scientists and
government agencies to focus their attention on reproductive, developmental and metabolic
processes and how certain chemicals can disrupt these processes. This is a shift in recent years
away from the almost exclusive regulatory focus on protecting people from substances which
cause cancer or structural birth defects. This new focus highlights the effects that some chemicals
can have even at minute exposures, including effects that are passed down from parents to their
offspring. The result of this recasting of the human health question has been, ironically, to raise
public concerns about environmental exposure to toxic substances when significant progress has
been made in reducing the amount of toxic chemicals present in the Great Lakes. This paper will
explore the state of current scientific knowledge on the human health impact of toxic chemical
contamination of Great Lakes waters, and will also review the effects of air pollutants,
radionuclides, and microbial contaminants in the Great Lakes Basin.
The many reports of harmful effects on wildlife from toxic chemicals in the Great Lakes
environment have stimulated and maintained a high level of interest in environmental toxicology
(Oilman et al., 1991). As a result, the wildlife of the Lakes are among the most intensely studied
of any in the world. In addition to the wildlife studies, thousands of lexicological experiments
have been carried out on laboratory animals which demonstrate a range of toxic effects for some
of the Great Lakes chemicals of concern even at extremely low levels of exposure. A variety of
health effects have been described and documented in the scientific literature and repeated in
many papers and reports. The results have been summarized in many documents while analysis
of past data and new discoveries continue at an accelerated pace. For many people, the
information is startling and raises obvious questions about health effects in human beings. When
mink fed Great Lakes fish fail to reproduce, and when birth defects, sexual maldevelopment, and
other developmental effects are reported by biologists studying wildlife in varying locations
throughout the Great Lakes, it is natural for the public to ask if they or their children are
similarly affected. Current research is aimed at addressing the question: if there are known causal
relationships between toxic contaminants and consequent effects in wildlife, what are these toxic
contaminants doing to human populations?
The International Joint Commission's Fifth Biennial Report on Great Lakes Water Quality (1989)
summed it up with the conclusion that:
" ...the Commission must conclude that there is a threat to the health of our children
emanating from our exposure to persistent toxic substances, even at very low ambient
levels."
Human Health Effects - SOLEC Background Paper
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Obligations under the Great Lakes Water Quality Agreement
The Canadian and United States federal governments, as Parties to the Great Lakes Water Quality
Agreement, are committed to work in cooperation with state and provincial governments to
develop and implement programs to fulfil the purpose of the Agreement. The goals outlined in
the Agreement relating to human health are found in Annex 12 (IJC, 1978a) and include: 1) the
establishment of monitoring and research programs to identify the impact of persistent toxic
substances on the health of humans and the quality and health of living aquatic systems...2)
development of the use of reproductive, physiological and biochemical measures in wildlife, fish
and humans as health effects indicators and the establishment of a data base for storage, retrieval,
and interpretation of the data...and 3) conducting research to determine the significance of effects
of persistent toxic substances on human health and aquatic life. Furthermore, Annex 17 2(1)
(IJC, 1978b) states that both parties shall "develop approaches to population-based studies to
determine the long-term, low-level effects of toxic substances on human health."
The Science Advisory Board of the International Joint Commission recommends that the Parties
consider policy objectives that reflect a preventive approach to protecting human health. Thus,
recognizing the limits to scientific inquiry in determining cause and effect linkages of exposure
to toxic chemicals, the IJC has recommended that the United States and Canada consider data
from a variety of sources: laboratory animal studies, studies of acute human exposure, and studies
of more subtle effects on humans from chronic low-level exposures; and using the "weight of
evidence" of these data to determine the potential for adverse effects on human health (Great
Lakes Science Advisory Board, 1991). Both the U.S. and Canada have instituted programs to
review and continue research on possible effects on human health.
We will focus on the most recent results of human health studies undertaken in the United States
and Canada, many of them preliminary and ongoing, specifically addressing issues of human
exposures in the Great Lakes region and potential effects. There is no benchmark with which
to compare the current status of human health hi the Great Lakes region. The human health
problems that are documented in research are not unique to the populations residing in the Great
Lakes. However, the Great Lakes Basin is a unique ecosystem where many diverse stakeholders
debate the focus and direction of human health research. The two federal governments have
responded to public concerns by initiating research projects that are designed to address some of
the most pressing concerns.
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2.0 Overview of Contaminants of Concern in the Great Lakes Basin
2.1 Priority Contaminants
Hundreds of chemicals have been identified in the Great Lakes ecosystem. The International
Joint Commission on Great Lakes Water Quality has designated a number of these as critical
pollutants, or priority contaminants, based on factors which determine the processes by which
they appear in the environment and the level of concern and attention given to a particular
compound: 1) presence and ambient concentration in the Great Lakes environment; 2) degree of
toxicity; 3) persistence in the environment; 4) bioavailability; and 5) potential to bioconcentrate
and bioaccumulate.
Presence in the environment: Using various screening techniques, 362 contaminants have been
confirmed as being present in measurable concentrations in either the water or sediments or in
the tissue of fish, wildlife or humans. This list includes 126 substances for which evidence exists
of toxic effects on various life processes.
Toxicity: A toxic substance is defined by the GLWQA as a "substance which can cause death,
disease, behavioral abnormalities, physiological or reproductive malfunctions or physical
deformities in any organism or its offspring, or which can become poisonous after concentration
in the food chain or in combination with other substances" (1978 Great Lakes Water Quality
Agreement, Article I(v)) (IJC, 1978c). Substances vary widely in the concentrations at which
they produce adverse effects. Toxicity can also be species-specific in that concentrations that are
harmful or even lethal to one kind of organism may be harmless to another. Some substances are
harmless in the condition in which they are released, but processes in the environment may
change their chemical characteristics so that the resulting compounds are far more toxic than the
original chemicals.
Persistence: Persistence is a measure of how successfully a chemical resists degradation and
therefore how long it remains in the environment. Persistence increases the chances of a
substance causing harm over time. In the Great Lakes Water Quality Agreement, a persistent
toxic chemical is defined as "any toxic substance with a half-life in water greater than eight
weeks." "Half life" refers to "the time required for the concentration of a substance to diminish
to one-half of its original value in a lake or water body." However, half-life measurements will
vary extensively depending on physical, chemical and biological conditions of the receiving
waters. More generally applicable definitions of persistence are being developed based on the
various processes by which a substance disappears in the environment.
Bioavailability refers to the extent to which, and at what relative rate, a substance is absorbed
or assimilated by living organisms. Bioavailability is affected by a number of factors such as
the physical state in which the substance is released, chemical characteristics of the water body,
and characteristics of the substances with which the toxic compound is associated. A compound
may bind to sediments and then be taken up by bottom-dwelling organisms. Thus, an organism's
exposure to a chemical is determined by its bioavailability.
Human Health Effects • SOLEC Background Paper 7
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Potential to Bioconcentrate and Bioaccumulate: Bioconcentration refers to the tendency of a
compound to concentrate in living organisms. Bioconcentration results from the direct uptake of
pollutants by an organism, and the inability of an organism to eliminate the chemical as fast as
it enters the body. It does not include pollutants accumulated through the intake of food.
Bioaccumulation refers to the biological processes by which a substance is assimilated into an
organism through eating another organism (plant or animal). Depending on the substance, it may
be passed through the body fairly quickly, or it may accumulate in certain organs or tissues, thus
enabling the chemical to concentrate in body tissues. In food webs such as those that exist in
the Great Lakes ecosystem, organisms bioaccumulate toxic substances and pass them along to
the next higher level all the way up to the top predators. As this process is repeated through the
food web, persistent toxic substances become increasingly concentrated or biomagnified. This
is especially critical to the Great Lakes environment because top predators such as gulls, eagles
and sport fish may, over their lifetime, accumulate large amounts of toxic pollutants through their
consumption of fish that in turn have consumed large quantities of plankton; each organism in
turn bioconcentrating and biomagnifying the persistent toxic chemicals available in the
environment. As top predators, humans and wildlife that consume Great Lakes fish are thus
exposing themselves to concentrated levels of toxic chemicals from the Great Lakes environment.
Among the hundreds of chemicals in the Great Lakes environment, certain ones are of greater
concern than others. Consistent with the factors described above, these contaminants are
chemicals that are found in parts or all of the Great Lakes, are known to cause harm to living
organisms, are present in forms that are available to aquatic life, and have a tendency to
accumulate to relatively high concentrations in the upper food chain. Obviously, a substance that
is persistent and highly neurotoxic, such as lead or mercury, or highly carcinogenic such as
benzo(a)pyrene will be of great concern if it is widely present, even if it does not bioaccumulate
to a great degree.
Based on the above factors and considerations, the International Joint Commission's Great Lakes
Water Quality Board has identified eleven chemicals as priority contaminants (indicated below
by *). In addition to those designated by the UC, there are several other substances (also listed
below) that are worthy of consideration hi the context of potential harm to the ecosystem and
to human health.
Organochlorines
polychlorinated biphenyls (PCBs) *
dioxins (i.e., PCDDS; e.g., 2,3,7,8-tetrachlorodiben2O-p-dioxin (TCDD), *
furans (i.e., PCDFs; e.g., 2,3,7,8-tetrachlorodibenzoruran, (TCDF) *
certain pesticides:
DDT and metabolites (e.g., DDE) *
mirex *
. toxaphene *
hexachlorocyclohexanes (HCHs; e.g., Lindane)
8
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hexaehlorobenzene (HCB) *
aldrin/dieldrin *
chlordane and metabolites
heptachlor and heptachlor epoxide
Airborne Contaminants
ground-level ozone
polycyclic aromatic hydrocarbons (PAHs) (e.g., benzo(a)pyrene, or B(a)P) *
particulates
acid aerosols
nitrogen oxides and sulphur dioxides
volatile organic chemicals (VOCs) (e.g., trihalomethanes, tetrachloroethylene)
Toxic Heavy Metals
. alkylated lead *
methyl mercury *
. cadmium
Radionuclides
Examples:
. strontium
. cesium
. radon gas
Microbial Contaminants
Examples:
bacterial pathogens (e.g., Escherichia coli)
viral pathogens (e.g., Enterovirus)
. protozoa (e.g., Cryptosporidium, Giardid)
Human Health Effects - SOLEC Background Paper 9
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2.2 Sources of Priority Contaminants and Routes of
Human Exposure
There are a number of pathways by which humans can be exposed to toxic contaminants in the
Great Lakes Basin. The two major routes of human exposure are the consumption of food,
primarily fish, and the ingestion of drinking water.
Fish consumption is a major exposure route because toxic substances such as dioxins, furans,
DDT/DDE, hexachlorobenzene, mirex, mercury, PCBs, toxaphene, chlordane, and lindane found
in the Great Lakes bioaccumulate in fish tissue (Colborn et alt 1990). Many of these chemicals
(e.g., PCBs, mercury, and DDE) have been found in the tissues of human populations that
consume Great Lakes fish. A study of Wisconsin anglers revealed that there were significant
correlations between sport-caught fish meals and PCB and DDE blood/serum levels, and between
kilograms of fish caught and PCB blood/serum levels (Fiore et al, 1989).
With respect to consumption of drinking water, a second route of exposure, the cumulative effect
of long-term, low-dose exposure to chemicals in drinking water cannot be ignored due to the
large population dependent on Great Lakes surface water. The USEPA has estimated that
approximately 12,700,000 people drink about 2 liters of contaminated water per person per day
from surface water supplied systems within the Great Lakes counties (USEPA Great Lakes
National Program Office, 1992). Ingestion of contaminated drinking water or recreational water
is also a route of exposure to microbial contaminants.
A third, less prominent, exposure pathway is inhalation of polluted air. The Great Lakes do not
act as a barrier to air pollution. Long range atmospheric transport carries air pollutants across
international boundaries, from their origin in the industrial centers (e.g., the Ohio River Valley)
of the U.S. to the Great Lakes Basin, particularly southwestern Ontario. The air pollutants
currently of greatest concern are ground-level ozone, airborne particles and acid aerosols (Stieb
and Burnett, 1993). While inhalation of toxic substances resulting from atmospheric deposition
is considered a minor toxic chemical exposure route when compared with ingestion of food
(primarily fish), a recent study conducted by the International Joint Commission on the risks of
hazardous air pollutants in the Detroit-Windsor/Port Huron-Sarnia region concluded that there is,
in fact, a significant public health concern due to elevated levels of a number of compounds
known as "air toxics" (e.g., benzene, trichloroethylene) in this region. Although insufficient
information is available to define the extent to which excess disease or death rates in this
particular area are attributable to exposure to these airborne toxic chemicals, the researchers
recommend that air emission abatement programs be implemented and preventive measures be
pursued (International Joint Commission, 1992).
Lastly, dermal exposure to waterborne contaminants has only recently been considered a notable
exposure route, and deserves some mention here. People who use the Great Lakes for
occupational or recreational purposes (e.g., swimmers) that involve skin contact with lakewater
may be dermally exposed to low levels of a wide variety of chemical and microbial water
10
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contaminants, including organoehlorines, PAHs, heavy metals, volatile organic compounds,
bacteria, viruses, protozoa, and parasitic worms. It is possible that these contaminants will be
absorbed through or penetrate breaks in the skin to some degree and hence become bioavailable
(Moody and Chu, 1994). In particular, lipophilic chemicals may be bound to the organic
components of suspended sediments (which act as a "carrier" for transdermal delivery of the
compounds) and would also tend to concentrate in the thin layer of oil, or surface slick, that is
present over all natural bodies of water (Platford et al, 1982; Moody et al, 1987). Although
dermal exposure is the least prominent route of human exposure to environmental chemicals in
the Great Lakes, and the degree of dermal absorption may be low, it is possible that after
prolonged exposure of a large body-surface area to lakewater — especially under conditions that
may enhance skin permeability, such as peeling of the stratum comeum following sunburn —
lexicologically significant amounts of certain chemicals could be absorbed via the dermal route
(Wester, 1987). It is unlikely, however, with the possible exception of the marathon swimmer,
that a large risk would result from such exposure.
Table 1 lists the sources and routes of exposure of the identified contaminants of concern in the
Great Lakes Basin. In summary, the major route of human exposure to PCBs, dioxins, furans,
organochlorine pesticides, and certain heavy metals (e.g., mercury) for residents of the Basin is
food consumption, particularly contaminated fish. The relative exposure routes vary by chemical,
but food is believed to contribute from 40% to nearly 100% for many of these toxic substances
(Parfett et al., 1994). Exposure via ingestion of untreated drinking water is a second route of
human exposure to organoehlorines, heavy metals, and microbial contaminants. Regarding
airborne pollutants, obviously breathing contaminated air is the key route of exposure to these
contaminants. Dermal exposure, though a minor route of exposure to waterbome chemicals, is
more significant in the case of microbial contaminants, and is particularly relevant to those
people using the Lakes for occupational or recreational purposes. Finally, with respect to
radionuclides, inhalation of atmospheric radioactivity and consumption of contaminated food and
water are routes of internal exposure, while external exposure can occur from irradiation by
radionuclides in the air or deposited on the ground, and is dependent on the proximity of the
source.
Human Health Effects - SOLEC Background Paper 11
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TABLE 1
SOURCES OF PRIORITY CONTAMINANTS AND ROUTES OF EXPOSURE
CONTAMINANT
SOURCES
ROUTES OF HUMAN
EXPOSURE
Polychlorinatcd Biphenyls (PCBs)
Used in electrical transformers and
capacitors, and in hydraulic equipment;
also as lubricants and teat-transfer fluids.
Released to environment primarily via
equipment in use and by waste site
leakage.
Consumption of contaminated foods,
particularly fish, meat, and dairy products.
Polychlorinated dibenzo-p-dioxins
(PCDDs) (esp. 2,3,7,8-TCDD) and
polychlorinated dibenzorurans (PCDFs)
Formed as impurities during the synthesis
of various chlorinated compounds (e.g.,
certain pesticides and herbicides); released
through pulp and paper bleaching and solid
waste incineration; found in exhaust from
vehicles using fossil fuels; and can also
result from the combustion of any
chlorinated organic material.
Consumption of contaminated foods,
particularly fish, meat, and dairy products,
although it has been estimated that up to
99.9% of the total environmental burden
exists in soils and sediments.
DDT and its degradation products
(e.g., DDE)
An insecticide now banned in Canada and
the U.S.A. Sources are leakage from
waste sites and atmospheric transport and
deposition.
Consumption of contaminated foods,
especially fish and dairy products.
Mirex
A tue retardant and contact insecticide
once used in Canada and the U.S. now
banned in1 both countries. Extremely
persistent; may reach the GLB via surface
run-off from contaminated soils or by
leaching from hazardous waste sites.
Consumption of contaminated foods.
Toxaphene
An insecticide used on cotton fields. In
use is restricted in Canada and the U.S.
Sources include contaminated soils,
hazardous waste sites, and air transport.
Consumption of contaminated foods.
Aldrin and Dicldrin
(i.e., chlorinated cyclodienes. Other
examples are chlordane and its
metabolites, heptachlor and heptachlor
epoxide)
Aldrin and dieldrin are insecticides used
for control of soil insects and mosquitos.
Dieldrin is also produced from the
metabolic oxidation of aJdrin. Their use is
restricted.
Consumption of contaminated foods,
especially fish.
Hexachlorobenzene (HCB)
A fungicide no longer used in Canada or
U.S.; also generated as a by-product of
fuel combustion and the production of
some pesticides.
Consumption of contaminated foods,
especially fish.
Hexaefllorocyclohexanes (HCHs)
(e.g., lindane)
An insecticide, lindane (y-HCH) is one of
8 HCH isomers. 8-HCH is the key isomer
found in human tissue, accumulating in
body fat; y-HCH does not. No longer
produced in U.S., but still used (imported).
Registered for use in Alberta,
Consumption of contaminated foods. Can
be transported by water and air.
Microbial Contaminants
(e.g., bacteria, viruses, protozoa)
Found in poorly treated sewage discharge,
agricultural run-off and urban run-off
which promote algae and weed growth;
also storm water run-off, animal feces.
Consumption of contaminated drinking
water or recreational water; absorption
through the skin.
Radionuclides
Arise from a variety of natural and man-
made sources. Natural radiation comes
from the sun and from various radioactive
isotopes in the earth, while anthropogenic
sources include nuclear weapons test
fallout and emissions from nuclear power
facilities.
Inhalation of contaminated air and
consumption of contaminated food and
water (internal dosing); and exposure by
direct irradiation (external dosing).
12
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TABLE 1 (cont'd)
SOURCES OF PRIORITY CONTAMINANTS AND ROUTES OF EXPOSURE
CONTAMINANT
SOURCES
ROUTES OF HUMAN
EXPOSURE
Methyl Mercury (MeHg)
Synthesis as result of atmospheric
deposition of elemental mercury from
natural oceanic output (30-40% of annual
Hg emissions to atmosphere); released
from inundated vegetation. Inorganic Hg
also occurs naturally in soils and as a by-
product of chlor-alkali, paint, and electrical
equipment manufacturing processes. MeHg
bioconcentrates in fish.
Consumption of contaminated fish and
marine products.
Cadmium
Atmospheric deposition, fertilizers, sewage
sludge, solid wastes, cadmium
mining/refining operations, soil, plant-life.
Consumption of contaminated foods, esp.
organ meats (liver, kidney), seafood
(shellfish, crustaceans), and cereals (e.g.,
wild rice); tobacco use; consumption of
drinking water (minor).
Lead
Combustion of leaded gasoline, metal
smelters, automotive batteries,
contaminated soil and dust, lead-based
paints, drinking water in contact with lead-
soldered pipes, atmospheric deposition.
In the absence of a point source of
contamination, consumption of
contaminated foods and drinking water;
inhalation of contaminated air.
Ground-level Ozone
Formed from the interaction of nitrogen
oxides and hydrocarbons in the atmosphere
in presence of high temperatures and
sunlight. Can be transported long
distances.
Inhalation of contaminated air.
Acid Aerosols
Formed when pollutants such as sulphur
dioxide and nitric oxide are transformed in
the atmosphere in presence of sunlight;
may be transported long distances from the
original source in the form of rain, snow,
vapour, fine particles and gases; can be
both air and water pollutants.
Inhalation of contaminated air.
Airborne particles
Very small pieces of solid or liquid matter
that vary in size, chemical composition and
source. Can be coarse or fine. Fine
particles arise mainly from man-made
sources such as combustion of fuels, and
include sulphates and nitrates as well as
metals. Coarse particles consist largely of
naturally occurring substances, particularly
soil.
Inhalation of contaminated air.
Polycyclic Aromatic Hydrocarbons
(PAHs) (e.g., benzo[a]pyrene)
Incomplete combustion of fossil fuels,
organic matter, and solid waste;
combustion activities associated with
industry (e.g., coke production, metal
smelting, oil refining). Non-commercial
sources include wood-burning fireplaces,
cigarette smoke, vehicle exhaust; and
smoked, grilled, fried, or barbecued meat
and fish.
Inhalation of contaminated air and
consumption of certain foods.
Volatile Organic Chemicals (VOCs)
(e.g., trihalomethanes, benzene,
trichloroethylene)
Formed from natural or industrial sources
by the interaction of chlorine with organic
materials; also found in dry-cleaning
solvents; both an airborne and drinking
water contaminant.
Inhalation of contaminated air during
exposure to treated tap water (showering,
bathing) or dry-cleaning solvents; and
consumption of drinking water.
Source: Great Lakes Health Effects Program, Health Canada,1993.
Human Health Effects - SOLEC Background Paper
13
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2.3 Populations at Greatest Risk
Due to the persistent nature of some of these contaminants and their biomagnification and
accumulation in the food chain, Great Lakes residents who consume larger amounts of
contaminated fish and wildlife than the general population are at greatest risk of exposure to toxic
pollutants, and are at greatest risk of health effects. These subpopulations include sport anglers,
their families, Native Americans and certain other communities that rely on Great Lakes fish for
sustenance. In the United States approximately 11% of the population in the Great Lakes Basin
are licensed anglers (USEPA, 1992), whereas in Canada roughly 8% of the Ontario population
are fishing license-holders (Kearney, 1992; SPR Associates, 1991). (This latter figure includes
both GLB and non-GLB residents; a reliable figure on the percentage of licensed anglers in the
GLB Canadian population alone is unavailable). Surveys of the U.S. population have found that
the average rate of fish consumption in the Great Lakes region is greater than the national
average. Recent studies, however, indicate that some high-risk groups are reducing their fish
consumption and fish preparation habits in response to health advisories. A survey of 8,000
licensed sport anglers from all of the U.S. Great Lakes states found that 36% of the respondents
had made changes in their fish consumption behaviors in response to state health advisories.
Modifying fish-cleaning and preparation methods was the most common change (59%), followed
by eating less Great Lakes fish (Connelly and Knuth, 1993). In addition, Fitzgerald et al. (1993)
found that pregnant women of the Mohawk nation had reduced their fish consumption
substantially.
A notable Canadian initiative concerning Native communities at risk of exposure to
environmental contaminants in the Great Lakes basin is the EAGLE (Effects on Aboriginals from
the GreatLakes Environment) Project, which was established as a First Nations/Health Canada
partnership and is linked to the latter's Great Lakes Health Effects Program under the Canadian
government's Great Lakes Action Plan. EAGLE is a community-based epidemiologic project
involving the study of the effects of environment contaminants on the health of the approximately
100,000 First Nations people living in 63 aboriginal communities in the Great Lakes Basin -- i.e.,
the program targets one of the specific "at risk" groups (Assembly of Fust Nations, 1993). It is
based on the recognition that aboriginal people, because of their high consumption of fish and
wildlife, are likely to be more exposed to bioaccumulating contaminants in the environment than
is the general population. As a consequence, they may be at higher risk of adverse health effects.
The goal of the EAGLE project is to assess the extent of exposure of the Native people living
in the Great Lakes Basin to bioaccumulating environmental contaminants and the associated risk
to their health and wel-being. The project builds on earlier direct cause-and-effects studies by
taking a holistic approach which includes examining exposures in both adults and children, socio-
economic effects, and the impact on traditional ways of life, culture and values. These and other
"indirect" health impacts of exposure to environmental contaminants in aboriginal communities
are frequently more important than the direct effects of exposure to environmental contaminants.
The EAGLE project emphasizes strong community involvement that fosters a real sense of
ownership among the residents of the 63 aboriginal communities in the Great Lakes Basin. The
14
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community-based study has a solid scientific basis with innovative elements in its design, which
blends scientific knowledge and the needs of the aboriginal communities, with each component
carrying equal weight. This is reflected in the managment and administration of the project. The
Assembly of First Nations (AFN), a native aboriginal organization representing First Nations
across Canada, is responsible for the day-to-day operations of the project.
Among the study components of the EAGLE project are the following:
• an Eating Patterns survey which was initiated in 1993 following the results of a successful
pilot study;
• a pilot exposure study being initiated in the First Nation community of Walpole Island;
« an analysis of morbidity and mortality data on aboriginal people in the Great Lakes region;
and
« implementation of a geographic information system (GIS) to consolidate all data on a geo-
reference basis relating to Great Lakes Native communities.
The EAGLE project was initiated in September 1990, and is targeted for completion by the end
of 1996/97 fiscal year. The partnership approach to the project has already proven to be a very
positive experience for all concerned. The holistic conceptual framework will enable the project
to use the traditional ecological knowledge of the First nations to more clearly understand the
effects of bioaccumulating contaminants on aboriginal health. Data on levels of these
contaminants in fish and from the Eating Survey are being used to assess exposure in Native
communities in the Great Lakes region. Measurements of the levels of organochlorine
contaminants in the blood of individuals are being conducted at the request of the Native
communities themselves.
Although data from the EAGLE project are still being analyzed and detailed results are not yet
available, a preliminary analysis of the inital findings has confirmed longstanding assumptions
that First Nations people do indeed eat considerably more fish and game and have significantly
higher averages consumption levels than the majority of the Canadian general population
(Wheatley, personal communication, 1994).
Several U.S. studies have also focused on Native communities that have traditionally depended
on fish and wildlife as a major source of food in their diets. In New York State the Mohawks
living along the St. Lawrence River consume an average of 25g/day (1/2 Ib per week) of locally
caught fish. This is two to six times higher than the average rates of consumption of
sport-caught fish by recreational anglers, and two to four times higher than the average rate cited
by the USEPA in its National Study of Chemical Residues in Fish (1993). Furthermore, the
greater importance of locally caught fish is consistent with the traditional dependence of the
Mohawks on fish and other local food sources (Forti et al., 1993). Generally, the average rates
of fish consumption in Native communities are higher than the average consumption rates for
Wisconsin recreational anglers (11 g/day of sport-caught fish), Lake Ontario recreational anglers
(4.3 g/day of Lake Ontario fish), and the general U.S. population (6.5 g/day of freshwater fish)
(Fiore et al, 1989; Connelly et al., 1990; USEPA, 1993). (It should be noted that the amounts
Human Health Effects • SOLEC Background Paper 15
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of fish reported eaten by recreational anglers per day are for licensed anglers only; it is likely that
some anglers are not license-holders). These data are also consistent with initial findings of the
Canadian Department of Health's EAGLE project, which confirms longstanding assumptions that
First Nations people do indeed eat considerably more fish and have significantly higher average
consumption levels than the majority of Canadians (Wheafley, 1994).
However, it is evident from another U.S. study conducted on the same Mohawk population that
certain high-risk groups such as pregnant women have changed their behavior to avoid exposure
to contaminants. In 1992, Fitzgerald et al investigated the levels of PCBs, p,p*-DDE, mirex, and
HCB in the breast milk of fifty-three Mohawk women from Akwesasne who gave birth from
1988-1990. Data from an assessment done between 1986-1989 on the Mohawk women showed
a positive association between lifetime exposure to PCBs from the consumption of local
contaminated fish and their breast milk PCB concentrations. In contrast, Fitzgerald's study
concluded that this correlation was no longer apparent among women who participated in 1990
because their fish consumption rates were so low. Indeed, local fish consumption has decreased
over time among the Mohawk women, from two meals to less than one-half of a meal per month
during pregnancy. The researchers attribute this to the success of fish advisories issued by
Mohawk, state, and federal agencies against the eating of fish from the local area by women of
child-bearing age (Fitzgerald et al., 1992).
In 1993, Dellinger et al reached similar conclusions. They studied 89 Ojibwa from the Northern
Wisconsin Chippewa Tribe to determine fish consumption habits and body burdens of mercury
and PCBs. They concluded that there were no significant body burdens of contaminants that
could be related to any known health risks. As with the Mohawk women, the researchers
concluded that the majority of the sample populations in the Chippewa Tribe are aware of and
heed Wisconsin fish consumption advisories (Dellinger et al.t 1993). Again, in another study
of members of the Chippewa Tribe in northern Minnesota, researchers found fish consumption
levels to be lower than expected (ATSDR, 1994).
Although certain populations may be changing their behavior, it is difficult to make
generalizations about the whole Great Lakes fish-eating community from the studies cited above.
For example, the figure of 36% in the Connelly and Knuth (1993) survey regarding the
proportion of sport anglers who had changed their fish consumption behaviors in response to state
health advisories appears to be lower than expected. Indeed, researchers in Michigan conducted
a survey in 1989 of fishing license-holders and found that the average sport-fish consumption rate
for sport fishermen and their families was approximately 18.3 g/person/day. For minority
fishing license-holders the figure is 21.7g/day (West et al., 1990).
The U.S. Environmental Protection Agency (USEPA) recently published a study on the health
risks associated with chemical residues in fish from 338 sites nationwide. Two contaminants,
specifically PCBs and dieldrin, were found at levels with an estimated upper-bound cancer risk
equal to or greater than one in ten thousand for the average fish-eating population (assuming a
fish consumption rate of 6.5 g per person per day) (USEPA, 1993). Of a total of 46 sites where
these chemical residues are indicative of cancer risks, almost one third (13 sites) are in the Great
16
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Lakes Basin (see Table 2).
Table 2
U.S. Sites on the Great Lakes with Estimated Cancer Risk Greater than W* (1 in 10.000)
Waterbodv City
Lake Ontario Olcott, NY
Grass River Massena, NY
Lake Ontario Rochester, NY
Niagara River N. Tonawanda, NY
Eighteen Mile Creek Olcott, NY
Oswego Harbor Oswego, NY
Niagara River Delta Porter, NY
Lake Michigan Waukegan, IL
Kalamazoo River Saugatuck, MI
Rouge River River Rouge, MI
Muskegon Lake Muskegon, MI
Milwaukee River Milwaukee, WI
Source: Adapted from EPA National Study of Chemical Residues in Fish Fact Sheet, Nov. 1992
Table 3
National Human Adipose Tissue Survey in the United States
Contaminant Regional Rankings
NE MA+ SA EN* ES WN WS MO PA
Pesticides
PCBs
Semi-volatiles
Volatiles
PCDDs and PCDFs
6
8
7
5
9
3.5
5
5
6
2
3.5
2
3
1
4
8
6
1
3
1
1
1
4
7
3
5
3
6
9
7
2
4
2
2
8
7
7
8
4
5
9
9
9
8
6
Total Ranking @ 35 21.5 13.5 19 16 30 18 31 41
Source: Adapted from Phillips et al, 1991
+MA = Mid-Atlantic states, including New York and Pennsylvania.
*EN - East North Central states, including Indiana, Ohio, Illinois, Michigan, and Wisconsin.
@ = Regions which rank high for a particular contaminant category are indicated by low
numerical scores.
Human Health Effects - SOLEC Background Paper 17
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Table 4
Mean Concentration of PCBs in Breast Milk Throughout the U.S. & St. Lawrence
Area/Yr
Michigan ('76)
Michigan (77-78)
Hawaii (79-80)
Hawaii (79-80)
U.S. (79)
U.S. (79-80)
Michigan (82)
N. Carolina (78-84)
Binghampton, NY (85-87)
St. Lawrence, NY (90)
Nof
Samples
95
1,057
50
54
50
102
138
617
7
57
%
Positive
100
100
100
100
2
100
100
94
pooled
Mean+
(ppm)
0.82(med)*
1.50
0.78
0.80
1.0
Source: Adapted from Fitzgerald, 1992
•^Arithmetic mean
*med = median
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3.0 Exposure Trends
The following discussion of trends in exposure to organochlorine contaminants reveals that:
1) there is no conclusive evidence that populations in the Great Lakes region are exposed
to higher levels of toxic chemicals than are other populations in the world;
2) the few studies that have been done comparing measurable body burdens have
produced varying, and sometimes conflicting, results; and
3) at present, the researchers who have studied Great Lakes fish-eaters and compared
body burdens of priority contaminants over time with those in other populations have
various theories to explain current body burdens. The reasons given for any reduction in
body burdens are: a) decreased contamination in the ambient environment and in fish
tissues and/or b) reduced fish consumption rates, especially in high-risk populations that
are aware of and are heeding fish consumption advisories.
3.1 Organochlorines
The question remains as to whether populations in the Great Lakes Basin are more highly
exposed to toxic pollutants than populations elsewhere. There are relatively few studies that have
measured the body burdens of people in the Great Lakes region and compared them to those in
the general population. It is difficult to answer this question because some studies have shown
that populations in the Great Lakes region may have higher levels of chemicals in their tissues
than populations in other regions of the world, while others show no difference. This is
attributable to the differences in analytical methods used by various researchers which make it
difficult to compare the data from different studies.
The U.S. National Human Adipose Tissue Survey (NHATS) produced data that were used to test
the hypothesis that individuals in different regions of the U.S. are subject to varying degrees of
toxic chemical exposure. The objective of NHATS was to detect and quantify the prevalences
of toxic compounds in the general population (Phillips et al, 1991). The concentrations of 54
compounds reported by NHATS were used in this study to examine regional variations in human
toxic chemical exposure. These compounds were chosen because of their persistence in the
environment and included many of the critical pollutants, such as PCBs, PCDDS, and pesticides.
The region with the highest mean concentration was ranked number 1, while the region with the
lowest mean concentration was ranked number 9. Thus, high rankings were indicated by low
numerical scores.
The East North Central region was identified as encompassing the states of Ohio, Indiana,
Illinois, Michigan and Wisconsin, all of which are in the Great Lakes region. The researchers
Human Health Effects - SOLEC Background Paper 19
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concluded that individuals residing in the East North Central states may be exposed to greater
amounts of toxic substances than people in other regions of the country. The East North Central
region was ranked third among the nine regions for total toxic substances surveyed for all age
groups, and fourth out of nine for grand total rankings which were re-calculated for each region
and age category by summing the total rankings for each category and adjusting for bias (see
Table 3).
Phillips et al further studied the hypothesis that there is a greater potential for human toxic
chemical exposure in the Great Lakes region than in other geographic regions of the U.S., using
the Environmental Protection Agency's STORET database which maintains water quality data
in the U.S. (Phillips et al., 1990). The researchers tested the potential for exposure to toxic
chemicals by using the levels of toxic substances in fish tissue and sediment as surrogates for
human exposure. For the toxic chemicals surveyed, the results showed that the Great Lakes
region is not the highest ranked in the country. In fact, the researchers claim, if one were to use
the levels of toxic chemicals found in fish and sediment in the Great Lakes as surrogates for
human exposure, the extent of indirect human exposure occurring in this region may be less than
that in other regions of the country. The authors point out that in order to address the total
exposure one would have to account for local rates of fish consumption. As we have noted,
studies on fish consumption rates throughout the Great lakes region vary in their conclusions.
Some studies have tried to compare levels of contamination in Great Lakes fish-eaters with those
of other populations. For example, Fitzgerald et al. (1992) point out that the levels of PCBs in
the breast milk samples taken from Mohawk women at the St. Regis Reservation in St. Lawrence
were equal to or lower than the levels reported for other populations, including those with no
unusual exposure to chemical contaminants (see Table 4).
It is difficult to determine whether the body burdens of environmental contaminants observed in
human populations in the Great Lakes Basin studied over a relatively short period of time (5-10
years) are correlated with decreasing body burdens seen in fish and other species in the Basin
that have been monitored for over two decades. Studies of Great Lakes fish and wildlife confirm
that the levels of PCBs, dieldrin, DDT, mercury and chlordane have declined since the mid-
1970's (Borgmann and Whittle, 1991; Miller et a/., 1992a). In order to examine trends in human
populations Hovinga et al. (1992) conducted a longitudinal study of a cohort of Great Lakes fish-
eaters from Michigan (mostly licensed sports anglers). The researchers found that between 1982
and 1989, mean serum DDT levels decreased substantially in 115 of the fish-eaters and in 95 of
the non-fisheater controls, while mean serum PCB levels decreased only slightly. While there
was no correlation between changes in DDT and PCB body burden levels and fish consumption
rates, the authors concluded that decreases in DDT levels can be attributed to the banning of
DDT, which has reduced the overall levels of this contaminant in the environment (Hovinga et
al.t 1992).
One would think that subsequent levels of these priority contaminants in humans would also
decline. It is known that for certain contaminants such as mercury, dietary intake levels in the
U.S. have dropped significantly in the past 15 years (Nieboer and Fletcher, 1993). In Canada, the
20
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current levels of PCBs observed in human milk, serum, and adipose tissue are comparable to
those observed in other developed countries. Lebel et al. (1991) and Williams and Lebel (1991)
have studied the concentrations of polychlorinated dibenzodioxins (PCDDs) and polychlorinated
dibenzofurans (PCDFs) as well as a few PCB congeners in human tissue samples from five
Canadian municipalities within the Great Lakes Basin (Lebel et al., 1991; Williams and Lebel,
1991), Their results show that concentrations of PCDD/PCDF are within the range of levels
reported in other studies conducted throughout the world. Results are similar for PCB
concentrations, although the data from comparison studies were limited and levels were still
higher in the Canadian samples as compared to samples from studies conducted in other North
American regions.
Even though the priority contaminant levels in the Great Lakes biota have generally decreased
over time, Hovinga's (1992) longitudinal follow-up study of Great Lakes fish-eaters and controls
showed that PCB levels did not change substantially during the seven-year period from 1982 to
1989. According to the authors, there may be a number of reasons for the static PCB levels in
the fish-eater population studied: 1) restrictions on PCB production alone may not ensure
decreasing levels of PCB exposure in human populations; 2) other sources of PCB contamination
such as atmospheric deposition and waste site leakages may be major sources of exposure; or 3)
because of the persistent nature of PCBs, seven years may not be a long enough time to see a
decrease in body burdens of PCBs in human populations. Consequently, although there are
documented decreases in the levels of toxic chemicals in wildlife populations in the Great Lakes
region, there are not enough historical data to draw the same conclusions about humans in the
Great Lakes Basin.
3.2 Airborne Contaminants
A recent Health Canada study (Stieb and Burnett, 1993) of the respiratory health effects of
airborne pollutants in the Great Lakes Basin includes some useful data on the levels of three
priority contaminants: ground-level ozone, airborne particles, and acid aerosols.
Ground-level ozone is a gas which is formed when oxides of nitrogen and hydrocarbons interact
in the atmosphere hi the presence of high temperatures and sunlight. It can be transported long
distances, and levels can actually be lower hi urban areas, where oxides of nitrogen can act as
ozone "scavengers". Ozone levels are highest during the daytime in the summer months, and are
typically monitored continuously at fixed site monitoring stations, which tend to be hi medium-
size to large cities. Between 1980 and 1991, the highest average daily ozone levels (8 a.m. to
8 p.m., May to August) among selected Canadian cities were recorded in London and Windsor,
Ontario (both at 39 ppb), while two other Great Lakes Basin cities, Hamilton and Toronto, had
levels (31 and 29 ppb respectively) comparable to those observed elsewhere hi Canada. Average
levels for these four Great Lakes cities have not changed significantly over the last ten years.
Average one-hour maximum levels, which more closely represent the highest potential exposures,
followed a similar geographic pattern, with the highest average levels observed in Simcoe (63,2
ppb) and Long Point (70.0 ppb) on the North shore of Lake Erie, as well as Windsor (60.2 ppb).
Human Health Effects - SOLEC Background Paper 21
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In these locations, some levels exceeded 118 ppb (Burnett et al., 1993). Figure 1 summarizes
data on exceedance of the Canadian air quality objective for ground-level ozone for locations
across Canada between 1982 and 1986, Southern Ontario clearly had the greatest number of days
on which the air quality objective was exceeded during this period.
Airborne particles are very small pieces of solid or liquid matter, which vary in size, chemical
composition, and source. Due to the wide variety of these contaminants, they also vary in their
effects on respiratory health (Stieb and Burnett, 1993). Because only "fine" particles (i.e., those
less than 10 um in diameter, or "PM,0") are capable of penetrating deeply into the lungs, they
are of most interest from the point of view of respiratory health. Fine particles tend to arise from
man-made sources, particularly combustion of fuels, and include sulphates and nitrates as well
as metals. Coarse particles consist largely of naturally occurring substances, particularly soil.
In Ontario, total suspended particles ("TSP" - all sizes, coarse and fine) have traditionally been
measured at a large number of sites, while PM10 monitoring has only recently begun at selected
locations. There has been little change in annual average TSP levels over the last 10 years. In
1991, the highest levels in Ontario were hi Hamilton (65 ug/m3) and the Metropolitan Toronto
area (42-58 ug/m3). The highest daily TSP levels were recorded in Sault St. Marie (393 ug/m3),
Toronto (379 ug/m3) and Hamilton (211 ug/m3). Annual average PM10 levels were also highest
in Hamilton (33 ug/m3). The highest daily PM10 level was recorded in Sault St. Marie (160
ug/m3), although levels of 120 and 100 ug/m3 were recorded in Toronto and Hamilton
respectively (see Table 5 and Figure 2) (Ontario Ministry of Environment, 1992). At present
there are no Canadian air quality standards for respirable particles (PM,0).
TABLE 5
PM]0 Concentrations at 9 Urban Sites in Ontario, 1991
CITY
(see Figure 2 for
location of site)
Hamilton
Thorold
Sault St. Marie
Etobicoke
Toronto
Windsor
Scarborough
London
Thunder Bay
PM,0 CONCENTRATION (fig/m3)
Annual Average
26-33 (3 sites)
32
19-29 (2 sites)
26
25
25
24
19
17
Maximum
70-100
100
65-160
81
120
60-69 (2 sites)
75
55
46
Source: Ontario Ministry of Environment, 1992.
22
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TABLE 6
Sulphate Concentrations at Selected Sites in Ontario, 1983-1988
CITY
(see Rgure 3 for
location of site)
Windsor
Longwoods
Toronto
Courtright
Charleston Lake
Pickering
Dorset
Chalk River
Algoma
SULPHATE CONCENTRATION (ug/m3)
Average
(May-August, 1983-88)
8.2
6.8
6.7
5.8
5.4
4.5
4.2
3.4
3.1
95% of measurements
below:
21.1
21.5
20.1
14.4
17.3
14.9
14.9
12.1
11.7
Source: Burnett et al, 1993.
Acid aerosols are essentially particles which contain acid, and are formed when sulphur dioxide
and other gases are chemically transformed in the atmosphere in the presence of sunlight. They
may be found at long distances from the original sources of the gases from which they are
formed. As is the case with ozone, they are primarily a summer problem, but have not
traditionally been monitored on a routine basis to the same extent as other air pollutants such as
ozone. However, routine measurements have been made of sulphate levels, which correlate to
some degree with actual acid measurements. According to data on sulphate levels for various
locations in Ontario between 1983 and 1988, areas in the southern Great Lakes Basin, such as
Windsor, Longwoods (near London) and Toronto had the highest levels (8.2, 6.8 and 6.7 ug/m3
respectively) compared to other sites (range of 3.1 to 5.8 ug/m3; see Table 6 and Figure 3)
(Burnett et al,, 1993). Sulphate levels have declined slightly in Ontario over the last ten years
(Ontario Ministry of Environment, 1991). Recent measurements carried out across Canada
suggest that although sulphate levels are highest in Southern Ontario, other areas such as the
Maritimes may experience comparable acid levels. Canadian air quality standards do not
currently exist for acid aerosols (Stieb and Burnett, 1993).
Other noteworthy air pollutants include sulphur dioxide, oxides of nitrogen, hydrocarbons, and
other "air toxics". Since the 1970s, when more stringent emission controls were introduced,
ambient levels of sulphur dioxide have declined considerably, and interest in sulphur dioxide now
relates to its role in the production of acid aerosols. There has been little change in levels of
nitrogen oxides over the years, and interest in these gases continues in relation to their role in
the production of ozone and acid aerosols. It is difficult to generalize about trends in emissions
of hydrocarbons over the years because of the wide range of different hydrocarbon compounds.
As a group of pollutants, they are of interest because of their role in the production of ozone.
Human Health Effects - SOLEC Background Paper
23
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Similarly, "air toxics" refers to a broad range of substances ranging from metals such as arsenic,
chromium and nickel, to organic compounds such as benzene, formaldehyde and
trichloroethylene. These contaminants are not generally measured on a routine basis, and there
is no standard measure or mixture agreed upon as "benchmark". However, a review of air quality
data in the Detroit-Windsor, Port Huron-Sarnia region indicated that a number of these
substances, some of which are known carcinogens, were present at elevated levels in this area
(International Joint Commission, 1992),
In the United States, the Environmental Protection Agency (USEPA), using the Toxics Release
Inventory, has estimated that air toxic emissions on the U.S. side of the Basin amount to
approximately 2,420,000,000 pounds per year. Nationally, approximately 58 million people are
exposed to levels of airborne pollutants mat are greater than health reference levels for acute
effects, and 38 million people for chronic effects. Using these national data, the USEPA
estimates that in the Basin 7.2 million people and 4.7 million people are exposed to levels of
pollutants which are greater than health reference levels for acute and chronic effects, respectively
(USEPA Risk Characterization Study, 1992). In a prospective cohort study conducted in six U.S.
cities, researchers found mat daily mortality rates were associated with daily paniculate air
pollution rates. What was significant about this study was that the researchers found this
association even after adjusting for cigarette smoking and other lifestyle factors which represent
health risks (Dockery et al, 1993).
24
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4.0 Linking Contaminant Exposure to
Human Health Effects
4.1 The Use of Biomarkers
Biomarkers have an important role to play in establishing whether an organism has been exposed
to an environmental chemical(s), whether it has been biologically affected, and/or whether it is
susceptible to an increased response to exposure. Three subclasses of biomarkers, or biological
indicators, have been suggested (Schulte, 1992):
. biomarkers of exposure: these indicate whether exposure has occurred and
consist of measurements of chemicals (including metabolites) in body fluids,
tissues, cells, or the interaction products between the chemicals and an endogenous
substance (Figures 4 and 5).
. biomarkers of effect: these are morphological, physiological, or
biochemical changes which have occurred as a result of exposure to
xenobiotics (i.e., substances foreign to living organisms).
. biomarkers of susceptibility: any factors, usually intrinsic or genetic, which may
result in an increased response to exposure. Susceptibility biomarkers can be used
to explain inter-individual variations seen throughout the exposure-effect
continuum.
A detailed summary of these three types of biomarkers as applied to a variety of Great Lakes
contaminants can be found in Table 7. Although data on quantitative exposure assessments for
the Great Lakes population are not available at present, the biomarkers of effect can be associated
with data on specific exposure levels obtained from studies of occupational or accidental
exposures to environmental chemicals. These data can be found in the background paper from
which the summary is drawn (Biomarkers, M. Feeley, 1994). It should also be noted that the
majority of biomarkers of effect and susceptibility are currently limited in their use because they
are non-specific and can apply to a variety of environmental contaminants. There is a need to
develop biomarkers that are more sensitive and specific to particular chemical exposures.
Human Health Effects - SOLEC Background Paper 25
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TABLE 7 - SUMMARY OF BIOMARKERS
Contaminant
Biomarkers of
Exposure
Effect
Susceptibility
PCBs
Concentration in adipose tissue, blood, breast milk.
Serom PCB concentrations positively correlated with plasma Uiglyceride and cholesterol
levels, and with AST (aspartate uninotransfbrase) and GOT (gamma-glutamyl
transferase) (both liver enzymes) activity Based on epidemiologies! studies, AST and
GOT appear to be the most sensitive indicators of PCB exposure in humans.
Reduction in antipyrene half-lives.
Increased caffeine metabolism rates in exposed groups (indicative of hepatic CYPIA2
activity).
Changes in die urinary excretion of porphyrin congeners, indicating enzymatic
stimulation/inhibition of the hepatic herne biosynthetic pathway.
Reproductive effects - alterations in birth weight, gestations! age and fetal development
(physical and neurological)).
Dermatological effects (at high levels of exposure) - chtoncne, hyperpigmentation,
hyperkeratosis, conjunctivitis.
Increased incidences of chromosomal aberrations and sister chromatid exchanges
detected in peripheral blood lymphocytes.
From epidemiological investigations, it appears that
the developing fetus ii at greatest risk from PCB
exposure. In uiero exposure may be more
important dun later exposure.
PCDDs and PCDFs
Concentration in adipose tissue. Mood, breast milk.
Chloracne and related dermatological effects.
Increased GGT (gamma-glutamyl transferase, a liver enzyme) activity.
Higher incidence of upper gastrointestinal tract ulcer.
Higher incidence of neurological abnormalities (e.g., peripheral sensory neuropathy,
decreased libido, depression, insomnia).
Higher incidence of self-reported non-cognitive complaints (e.g., emotional instability,
irritability).
Possible immunological effects (e.g., increased levels of non-T peripheral lymphocytes,
abnormal T/T, ratios, thymic atrophy) and endocrine alterations.
Increased urinary D-glucaric acid excretion.
Induction of EROD/AHH (ednxyretonifin-o-
deethylase and aryl hydrocarbon hydroxylase)
enzyme activity mediated through the Ah (aromatic
hydrocarbon) receptor Induction of EROD/AHH
activity in human lymphocytes has been associated
with increased susceptibility to lung cancer.
In ultrn and lactational exposure to PCDDS/PCDFs
may be capable of affecting the hypothalamic-
pituitary.thyroid regulatory system in human infants.
26
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As pyrene is a major constituent of PAHs, the
monitoring of 1-hydroxypyrene in urine can be
considered representative of exposure and internal
dose, whether by inhalation, absorption or ingestion.
Biomarkers of exposure are limited due to die
extensive metabolism and excretion of PAHs.
Human Health Effects - SOLEC Background Paper
metabolic phenotypes of humans and associate this
with increased risk for PAH carcinogenitity.
Hie vast interindividual genetic differences would
have to be considered when applying biomarkers for
PAHs.
27
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TABLE 7 - SUMMARY OF BIOMARKERS (Cont'd)
Contaminant
Biomarkers of
Exposure
Effect
Susceptibility
Organochlorine
Pesticides:
DDT
DDE
CMordane
Dicldrin
HCB
fHCH
Heptachlor/HE
Mi rex
Toxaphene
B-HCH
Concentrations in blood, adipose tissue, breast
milk, and urine.
Increased plasma concentrations of the liver enzymes AST (aspartate
aminotransferase), ALT (alanine aminotransferase), GOT (gamma-glutamyl
transferase), LDH (lactate dehydrogenase), and AP (alkaline phosphatase); and of
vitamin A and retinol.
Occupational /epidemiological studies suggest that the nervous system and the
liver are the most sensitive effect parameters for OC pesticides in humans. The
nervous system effects include parathesia, repetitive tremors, and EEG pattern
changes.
Apart from accidental or occupational exposures, the low pesticide residues
generally encountered in foods compared to the estimated adverse effect levels
suggest that harmful effects are unlikely.
Cadmium
Concentrations in blood, urine, feces, and
body organs (e.g., kidney, liver).
Metallothionein (Mt) and consequences of nephrotoxicity (Cd-Mt in urine).
Renal dysfunction as indicated by a,-microglobulin, N-acetyl-B-D-
glucosaminidase, Bj-irderoglobulin, and retinol binding protein (all indicative of
microproteinuria).
Induction of metallothionein in human
peripheral blood leukocytes appears to be
partly under genetic control. In non-smoking
adults, there is a 10-39-fold variation in Mt-
mRNA induction which may explain the
interindividual differences seen in the
development of renal damage following
cadmium exposure.
Mercury
For both inorganic and organic mercury:
concentrations in blood, hair, kidney, placenta,
breast milk, urine, and brain.
The central nervous system (CNS) is the critical target for methylmercury
(MeHg) toxicity in both infants and adults.
Prenatal exposure to MeHg results in biomarkers of effect ranging from
psychomotor retardation to severe cerebral palsy.
Mercury-induced porphyria is an additional biomarker of effect in both infante
and adults.
-------
teeth, kidney, liver, breast milk, placenta,
brain.
acid synthetase) and inhibits ALAD (delta-aminolevulinic acid dehydrase) in
erythrocytes, resulting in increased levels of ALA (delta-aminolcvulinic acid) in
blood and urine. Lead also inhibits ferrochelatase; consequently, protoporphyrin
IX and coproporphyrin accumulate.
Increased blood porphyrin.
Decreased blood hemoglobin.
Neurological deficits, including delayed neurological development, reduced 1Q,
and behavioral maturation deficits.
Source: Adapted from Feeley, 1993
Human Health Effects - SOLEC Background Paper
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4.2 Factors in Establishing Links Between Great Lakes
Environmental Contaminants and Human Health Effects
The biomarkers of effect cited above point to potential health effects that may appear as a result
of exposure to chemical contaminants. However, any actual effects observed in Great Lakes
populations may be due to a variety of factors, including exposure to environmental contaminants
in the Lakes. A major consideration in conducting human health effects research is that people
are exposed to an enormous number and variety of environmental and lifestyle factors that can
affect health outcomes, but whose respective effects are difficult to isolate and measure (Jordan-
Simpson et a/., 1994). Data on health effects of contaminants in the Great Lakes Basin have
usually been obtained from animal laboratory studies and epidemiological studies describing the
adverse effects of occupational or accidental exposure to high concentrations of chemicals.
Another key factor which affects the interpretation of the results from studies examining the
association between environmental contaminants and its effect on human health relates to the
methodologic problems associated with quantitatively assessing hazards and risk. In human
populations it is often very difficult to characterize the exposure, and to separate potential
confounding factors from the factor of interest. This also makes it difficult to choose an
appropriate comparison group. There are a number of difficulties associated with studies carried
out in free-living populations, and inevitably differences will exist between exposed and
unexposed individuals that may allow alternative explanations for any effects observed (Constable
and Hatch, 1983, cited in Jordan-Simpson et al., 1994). As well, participation and recall bias
may seriously compromise the validity of a study (Jordan-Simpson et al, 1994).
Comprehensive health risk assessment is a complex multi-step procedure. Human health risk
assessment as practised by the United States Environmental Protection Agency is derived from
the paradigm established by the National Academy of Sciences. This paradigm sets out four
steps in the risk assessment process: i) hazard identification (what does the chemical do); ii)
dose-response evaluation (how much of the chemical is needed to observe an adverse health
effect); iii) exposure assessment (who is exposed and to what degree); and iv) risk
characterization ~ the full characterization of hazard identification, dose-response evaluation and
exposure assessment, along with the uncertainty and assumptions that entered into the assessment.
The risk characterization is the product of the risk assessment, and feeds into the risk
management process along with technological considerations and non-risk analyses to determine
a risk management option.
By comparison, the risk assessment model used by Canada's Department of Health involves: i)
risk analysis, which consists of (a) hazard identification, and (b) risk estimation involving dose-
response evaluation, exposure estimation, and risk characterization; and ii) option evaluation,
comprised of (a) option development and (b) option analysis. The subsequent steps in the risk
management process would include the decision-making leading to a chosen option,
implementation, monitoring and evaluation, and ongoing review (Health Protection Branch,
Health Canada, 1989,1990). A closer inspection of both the USEPA's and Health Canada's risk
30
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assessment models shows that they are very similar, with steps (ii), (iii) and (iv) of the USEPA
model subsumed in the risk estimation step of the Canadian model.
As indicated above, risk assessment at present is based on data from lexicological investigations
carried out in the laboratory (both in vitro toxicity studies and in vivo animal studies) combined
with data from epidemiological studies of human populations. Traditionally, investigations
include evaluation of acute and chronic toxicity in animal species, studies of the metabolism of
chemical substances, short-term tests for genetic alterations, special studies such as teratology (the
study of malformations), reproduction, and long-term tests for carcinogenic effects (Bernier et
aL, 1994).
Foster and Rousseaux (1994) have itemized a number of factors which make it difficult to
establish a link between environmental contaminants and adverse reproductive effects in humans
in the Great Lakes Basin. These factors can also apply more generally to other categories of
health effects, and are listed below:
* the continuous nature of exposure over many years to low levels of chemicals;
. exposure to mixtures rather than individual compounds;
* hazard definition and identification (i.e., the large number and in some instances the poor
definition of health effect endpoints to be examined, and the difficulty in measuring some
effects);
. experimental design (for example, inability in some cases to obtain adequate sample sizes
for evaluations with measurements that are suitably sensitive and specific to detect
changes);
. dose-response questions;
* accurate exposure assessment; and
* confounding variables that may hinder research studies.
These and other factors in the study of adverse human health effects associated with
environmental contamination have contributed to the adoption of the "weight of evidence"
approach that allows for the consideration of supplementary data that may shed some light on
potential effects in humans. These supplementary data ~ derived from wildlife studies,
toxicological research on laboratory animals, in vitro cellular studies, and human epidemiological
investigations of accidental or occupational exposures to high levels of specific contaminants —
help to expand our knowledge of the actual and potential health effects of environmental
contamination on living organisms, including humans, and to point the way to new research
directions in this area.
Human Health Effects - SOLEC Background Paper 31
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5.0 HEALTH EFFECTS OF EXPOSURE
TO ENVIRONMENTAL
CONTAMINANTS IN THE GREAT
LAKES BASIN
In view of the limitations cited above, this review of the health effects of exposure to
environmental contaminants in the Great Lakes Basin focuses for the most part on hazard
identification, i.e., delineating the various potential adverse health effects, most of which have
been observed at relatively high exposure levels in occupational settings or as the result of
accidental exposures. In some cases, information on exposure assessment and suggestions
concerning future directions in research and accurate risk assessment are also presented. It
should also be noted that the exposure data necessary to carry out integrated exposure
assessments (i.e., an assessment based on all routes of exposure and specific exposure levels for
a particular health effect) are unavailable and beyond the scope of this paper. Consequently, the
discussion of reproductive, neurological, immunological and carcinogenic endpoints relates for
the most part to food (primarily fish) consumption as a major route of exposure, and water
consumption as a secondary route (particulary in the case of cancer endpoints and infectious
diseases). Respiratory effects are discussed separately, since inhalation is the obvious route of
exposure for airborne contaminants.
~X_- s . -
In general, it is important to recognize that although health effects associated with environmental
contamination may be correlated with multiple exposure routes, those related to one exposure
route cannot always be extrapolated to another, and identifying the specific exposure route(s) and
levels of exposure associated with particular categories of health effects cited in various studies
would be essential when undertaking integrated exposure assessments.
As well, in reviewing the health effects of the various classes of Great Lakes contaminants,
radionuclides and microbial contaminants will each be discussed separately from the "chemical"
pollutants, due to their fundamentally different natures and the effects they have on human health.
In the case of radionuclides, the essential difference is that they are elements that emit high-
energy radiation called ionising radiation, large doses of which can kill cells directly, or cause
genetic or other changes in the body that may lead to cancer. Microbial contaminants are living
organisms that can cause a variety of infections and diseases.
5.1 Reproductive Toxicology
As indicated above, data on the reproductive effects of exposure to environmental contaminants
have usually been obtained from wildlife studies (see Fox, 1992 for review; also Flint and Vena,
Human Health Effects - SOLEC Background Paper 33
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1991), animal laboratory experiments, and from epidemiological studies describing occupational
exposure to high concentrations of chemicals (Whorton et al, 1977; 1979; Hemminki et al,
1983,1985; Olshan et al, 1990; Rowland et al, 1992). Although serious effects on reproduction
in animals and a potential hazard to human reproduction have been shown in these studies, it is
difficult to estimate the adverse reproductive effects in humans of chronic and low-level exposure
to environmental contaminants in the Great Lakes Basin due to the factors listed in the preceding
section. Furthermore, among the additional confounding variables in reproductive toxicology are
lifestyle factors such as alcohol consumption and smoking, which have been linked to an
increased risk of stillbirth (Prager et al, 1984) and congenital anomalies (Savitz et al, 1991).
Failure to account for these and other confounding factors in epidemiological studies makes it
difficult to establish cause-effect relationships.
Developmental Effects of Environmental Contaminants
The developing fetus and neonate are considered to be at particular risk as there is great potential
for exposure to environmental contaminants in utero and through breast milk. The developing
fetus is captive within its mother's environment and is not completely protected by the placenta,
animal experiments having shown that the placenta is an ineffective barrier to heavy metals and
chlorinated hydrocarbons (Buchet et al, 1978; Ando et al, 1985). As well, the transport of
persistent environmental contaminants in breast milk has been well documented (cited hi Foster
and Rousseaux, 1994 and reviewed by Sim and McNeil, 1992). The developmental consequences
of exposure to high concentrations of chemical contaminants and certain drugs include
intrauterine growth retardation (IUGR), shortened or prolonged gestational lengths, low
birthweight, congenital malformations, and spontaneous abortion (Foster and Rousseaux, 1994;
Jordan-Simpson et al, 1994). Examples of reproductive toxicants present in the Great Lakes and
known to induce such developmental effects include lead, methyhnercury, DDT/DDE, PCDFs,
PCBs, and polybrominated biphenyls (PBBs) (Foster and Rousseaux, 1994 and Jordan-Simpson
et al, 1994). Developmental toxicity in humans following occupational exposure to high levels
of chemical contaminants such as heavy metals, pesticides, PCBs, dioxins and organic solvents
has also been well documented (cited in Foster and Rousseaux, 1994 and reviewed by Rosenberg
et al, 1987; TasMnen, 1990; and Thomas and Ballantyne, 1990). However, there is a dearth of
data on low-level exposure and exposure to mixtures.
It is important to emphasize that the increased risk to the developing fetus and neonate is also
due to the nature of those stages in the life cycle. For example, in the fetus there are
physiological systems that have not yet differentiated into their mature, final form and function.
Damage at an early stage can thus affect whole organ systems, whereas in the adult organism
the same insult from exposure to an environmental contaminant may result in only limited,
reversible damage (Tong and Gorsky, 1994). Parental exposure to lead, a priority Great Lakes
contaminant, underscores the significance of prior contaminant exposure on reproductive
outcomes. Roughly 90% of ingested lead is deposited and stored in bone, from which it is
mobilized during pregnancy (Shannon et al., 1988b; Silbergeld et al, 1988; Markowitz and
Weinberger, 1990; Silbergeld, 1990). Exposure of the fetus to lead ingested and/or mobilized
from bone at critical developmental periods has been shown to adversely affect neurodevelopment
34
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(Sierra and Tiffany-Castiglioni, 1992), delay sexual maturation (Der et al., 1974; Kimmel et al.,
1980), and has been associated with an increased incidence of spontaneous abortions (Fahim et
al.t 1976; Odenbro and KiMstrom, 1977; Nordstrom et al., 1978; McMichael et al., 1986). Lead
is also mobilized from bone during lactation, thereby posing a continuing risk to the developing
infant.
Effects of Environmental Contaminants on Fertility
Occupational exposures to high concentrations of environmental contaminants and animal
experiments involving chronic exposure have shown the potential for adverse reproductive effects
on human fecundity and fertility. Known toxicants affecting female reproductive processes
include the heavy metals lead, methylmercury, and cadmium; the organochlorines
hexachlorobenzene (HCB), DDT, DDE, and PCBs; as well as alcohol and tobacco smoke (Foster
and Rousseaux, 1994).
Animal studies on female reproductive endpoints have shown altered menstrual function in
laboratory animals exposed to lead (Vermande-Van Eck and Meigs, 1960; Hilderbrand et al.,
1973; Laughlin et al., 1987; Franks et al., 1989), and suppression of circulating luteinizing
hormone (LH), follicle stimulating hormone (FSH), and estrogen (£2) levels during the follicular
phase of the menstrual cycle in the monkey (Foster, 1992). These results raise concerns
regarding the health of the developing follicle and ovum. In addition, primordial follicle numbers
in the ovary have been shown to be significantly reduced following exposure to reproductive
toxicants such as 7,12-dimethylbenz(a)anthracene, benzo(a)pyrene and hexachlorobenzene
(latropoulos et al,t 1976; Siracusa et al., 1992; Miller et al., 1992b; Weitzman et al., 1992; Jarrell
et al., 1993). Overall, the effects of environmental pollutants on female reproductive endpoints
such as oocyte (egg) maturation and quality, ovarian follicle development, ovarian function and
uterine receptivity require further study in order to elucidate the potential link between
environmental chemicals and adverse reproductive effects.
While considerable research attention has been directed to both developmental and female
reproductive toxicity, there has been comparatively little research on the effects of chemical
contaminants on male reproductive endpoints (for review see Colie, 1993). The majority of data
regarding the effects of chemicals on male reproductive processes have been derived from rodent
studies (Sullivan and Barlow, 1985; Working, 1989; Hess, 1990; Linder et al., 1992; Vachhrajani
et al., 1992), in which moderate to severe sperm damage has been detected in rodents following
acute exposure to suspected reproductive toxicants. In a broader context, other biomarkers of
male reproductive toxicity include fecundity; circulating concentrations of the hormones LH,
FSH, prolactin (PEL), inhibin, testosterone and dihydrotestosterone; semen quality and testicular
histomorphology (for review see Ewing and Mattison, 1987 and Mattison, 1991).
Regarding human males, the importance of male-mediated effects has been demonstrated in the
case of increased prevalence of congenital malformations in the offspring born to wives of fire-
fighters (Olshan et al., 1990). In addition, reduced fertility has been observed in men working
in pesticide manufacturing plants (Whorton et al., 1977). In a recent report (Carlsen et al., 1992)
Human Health Effects • SOLEC Background Paper 35
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a decline in semen quality was described on the basis of published reports on semen quality
appearing hi the literature over the preceding 50 years. It was suggested that the decline was
more likely the consequence of environmental than genetic factors although no direct evidence
to support this claim was presented. A decline in sperm quality, however, may also be related
to increased incidence of sexually transmitted disease, metabolic disorders such as diabetes, and
sample selection, among other factors. Nevertheless, sperm density has previously been
negatively correlated with tissue levels of persistent environmental contaminants (Lantz et al,
1981; Szymczynski and Waliszewski, 1981; Takahashi et al, 1981; Abdel-Rahman et al, 1982;
Couri et al, 1982; Mann and Lutwak-Mann, 1982; Jockenhovel et al, 1990). As well, reduced
sperm quality and unpaired fertility have been associated with men occupationally exposed to
lead (Jockenh5vel et al, 1990), although many other reports fail to demonstrate a relationship
between lead exposure and alterations hi fertility, which may be due to study design and various
confounding factors.
Alterations in male reproductive endpoints other than sperm quality have also been demonstrated
with lead treatment in experimental animals. For example, lead exposure has been associated
with altered hypothalamic-pituitary function (Sandstead et al, 1970; Braunstein et al, 1978;
Petrusz et al, 1979; McGivern and Sokol, 1990; Foster et al, 1993a) and testicular function
(Braunstein et al, 1978; Foster et al, 1993b). In addition, histopathological (i.e., structural)
alterations have been shown in lead-exposed rodents (Timm and Schulz, 1966; Hilderbrand etal,
1973), primates (Foster et al, 1993b) and occupationally exposed men (Lancranjan et al, 1975).
Altered sperm count (Golubovich et al, 1968), decreased sperm motility (Hilderbrand et al,
1973) and increased abnormal sperm (Eyden et al, 1978) have all been reported in rodents
treated with varying concentrations of lead. However, weight loss hi treated rats makes it
difficult to interpret these results as altered sperm counts, morphology, and motility could all be
explained by indirect effects of lead on other metabolic systems.
Hormone Disruption
A number of xenobiotics have the potential to disrupt the activities of certain naturally occurring
hormones hi an organism. This disruption can be manifested in a number of ways, including the
mimicing of a hormone or the blocking of its activity. For example, TCDD (a dioxin) may block
the activity of estrogens, the female sex hormones which play an important role hi the
development of the sexual organs and sexual behaviour. Under certain conditions dioxins can
also lower the levels of androgens and can affect the thyroid hormone levels in the body
(Birnbaum, 1994).
The best-studied of the xenobiotics that have been shown to alter hormone systems are
environmental estrogens, i.e., compounds which effects similar to those of estrogens (hence the
term hormone mimicry). These substances may either be man-made or occur naturally in the
environment Of the former, certain persistent environmental contaminants such as PCBs
(Korach et al, 1988), 3,9-dihydrobenz[a]anthracene, kepone, DDE, and o,p-DDT (McLachlan et
al, 1987) have been found to have weak estrogenic abilities. Concern exists regarding the
potential of both the natural and man-made estrogenic compounds to interact with the estrogen
36
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receptor and possibly induce adverse reproductive effects. Potential adverse consequences of
exposure to compounds with estrogenic activity include feminization of the male and premature
female sexual maturation (Foster and Rousseaux, 1994). For example, precocious puberty in
young boys and girls eating meat contaminated with diethylstilbestrol (DES), a synthetic
hormone, has been reported (New, 1985), and exposure to DES has also been shown to
infrequently induce vaginal adenocarcinoma in women whose mothers were given DES during
pregnancy to prevent miscarriage (Herbst et al, 1971; Greenwald et al, 1971).
Although there have not been any reports of adverse effects following exposure to environmental
levels of estrogenic compounds in the human population, estrogenic effects of environmental
pollutants have been implicated in developmental abnormalities in wildlife species (Fox, 1992).
The presence of estrogenic contaminants in human tissues, and demonstration of effects in animal
species, have promoted speculation that effects in humans such as increased incidence of breast
cancer may occur among women exposed to organochlorines (Manz et al, 1991; Falck et al.,
1992; Wolff et al., 1993). However, the majority of these compounds have been shown to be
very weak estrogens (Soto et al., 1992) with few apparent biological effects. At present the link
between exposure to estrogenic compounds, such as PCBs, DDE and DDT, and breast cancer
cannot be established with confidence, and comprises a priority area for future research.
With respect to males, recent work suggests that chemicals with an estrogenic effect pose an
increased reproductive risk by decreasing semen quality (Carlsen et al, 1992). Further research
will be needed to confirm whether trace amounts of chemicals with an estrogenic effect do have
an effect on male reproduction.
5.2 Epidemiological Studies of the Effects of
Environmental Contaminants on Reproductive
Outcomes in Great Lakes Populations
Because fish consumption is considered one of the major routes by which humans are exposed
to environmental contaminants present in the Great Lakes, a number of studies have looked at
the association between maternal consumption of Great Lakes fish and the health of offspring.
Results from some of these studies indicate a relationship between PGB exposure in utero and
alterations in both neonatal health and health in early infancy (Swain, 1991). During the 1980s,
the Michigan Maternal/Infant Cohort study evaluated the impacts of consumption of contaminated
fish on the offspring of mothers who had consumed at least 11.8 kg of contaminated Lake
Michigan fish over a 6-year period. The study consisted of 313 infants of mothers who
consumed moderate to high amounts of Lake Michigan fish, and 71 infants whose mothers ate
no Lake Michigan fish. Effects were seen in the offspring of mothers in the former group, and
were attributed to intrauterine exposure to PCBs, These effects included lower birthweight,
reduced gestational age, and smaller head circumference compared to controls (Fein et al,
1984b). In later studies on the children at 4 years of age, researchers found that weight gain was
still lower compared to controls, indicating that the adverse effects may extend beyond infancy
Human Health Effects - SOLEC Background Paper 37
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(Jacobson et al, 1990a).
A second study, the Wisconsin Maternal/Infant Cohort study, consisted of mothers who ate fish
from Lake Michigan or the Sheboygan River for at least three years prior to the date of birth
(1980-81) of their offspring. The research showed that maternal PCB levels were associated with
increased incidence of infectious diseases suffered by the infants. The author concluded that PCB
exposure in utero resulted in the increased susceptibility to infectious illness in the first four
months of life (Smith, 1984).
Other research results are less alarming. In another study of mothers who consumed fish from
the Great Lakes, researchers examined prenatal exposure to PCBs and reproductive outcomes in
a population of 1112 women during 1987-1989 hi the Green Bay area. Following the pregnancy
period, reproductive outcomes were measured, including fetal wastage, stillbirths, birthweight,
birth length, and head circumference. The researchers expected to find that, as in the Michigan
cohort study, there would be a decrease in birthweight associated with an increase in PCB
exposure. However, the opposite was true: birthweights were often higher for infants of those
mothers who claimed to eat more Lake Michigan fish prior to pregnancy. The researchers noted,
however, that the amounts of fish these women consumed were much lower than in the Michigan
maternal cohort study, and speculated that the relatively low estimated exposure to PCBs
experienced by the Green Bay cohort did not appear to have an effect on birth outcomes.
Perhaps, the researchers concluded, there is a threshold exposure level below which there are no
observable negative effects (Dar et al,, 1992).
Likewise, in a recent study of a cohort of New York anglers, researchers examined the
relationship between consumption of PCB-contaminated fish from Lake Ontario and birthweight
of newborns. The New York cohort consisted of 11,717 people. Using a sample of recent births
(1986-91) from parents in this study, birthweight, gestational age, and other birth parameters were
abstracted from birth certificates. Preliminary results have shown no differences in mean
birthweights across estimated cumulative lifetime exposure to PCBs from contaminated fish
(Buck et al., 1993). An additional study was carried out on 1,820 women from the same cohort
to assess the relationship between PCB exposure due to consumption of contaminated Lake
Ontario sport fish and spontaneous fetal death (SFD), An analysis of fish consumption and
reproductive history data indicates that exposure to PCBs in contaminated sport fish does not
increase the risk of SFD (Mendola et al., 1994).
In conclusion, there is no doubt that accidental or occupational exposure to high concentrations
of certain chemicals presents an increased risk to human reproductive health. Although it is not
possible to state conclusively that exposure to environmental contaminants in the trace
concentrations currently reported in human tissues is or is not associated with adverse
reproductive effects, evidence from wildlife studies (Fox, 1992; Flint and Vena, 1991) and
epidemiological investigations of occupational exposures to various chemicals indicates that
environmental pollutants might be able to alter human reproduction. Epidemiological studies that
have addressed adverse pregnancy outcomes in populations in the Great Lakes have shown some
potential effects of concern, while other studies have shown little or no effects. Due to the
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current difficulties in estimating reproductive risk to the human population, and incompleteness
of the data base concerning reproductive effects of environmental contaminants, the real risk to
people residing within the Great Lakes region or elsewhere cannot be determined at present.
5.3 Neurotoxicity of Lead, Methylmercury, and
Polychlorinated Biphenyls (PCBs)
There are a number of contaminants in the Great Lakes that are neurotoxic or potentially so.
There is a large data base from animal and human epidemiological studies on two of these: lead
and methylmercury. The data base is less complete for a third class of contaminants, PCBs.
While it is reasonably certain that some PCBs are neurotoxic, particularly in developing
organisms, there are fewer human studies upon which to determine a "no observed adverse effect
level (NOAEL)" or "lowest observed adverse effect level (LOAEL)" than for lead or
methylmercury. For most other Great Lakes contaminants, there are no or scant data regarding
neurotoxicity, or the levels to which the general population is exposed via the Great Lakes Basin
are not cause for concern. For example, there is reason to be concerned about such substances
as toxaphene, HCB and HCHs based on their chemical structure, but neurotoxicity data based on
observations of humans are almost nonexistent. Other agents known to be neurotoxic, such as
organotin compounds and various pesticides, are found in the Great Lakes Basin at levels which
are orders of magnitude lower than those that have been tested in animals or at which
neurotoxicity has occurred in humans. Therefore, this discussion of neurotoxicity is restricted
to PCBs, methylmercury and lead.
PCBs
High doses of PCBs result in reproductive toxieity in humans (Rogan et al, 1988; Lione, 1988;
Safe, 1987). Less is known about the effects of PCBs on human neurobehaviour. However, in
laboratory monkeys behavioral deficits have been observed as a result of developmental exposure
to PCBs (Schantz et al, 1989, 1991). Research on other laboratory animals also links PCBs and
other toxic contaminants in the Great Lakes to adverse neurobehavioral effects. For example,
rats fed Lake Ontario salmon contaminated with PCBs, mercury and lead showed an increased
reactivity to aversive events (Daly, 1991).
It is clear from both the animal literature and epidemiological studies on humans that the
developing organism is more sensitive to behavioral deficits resulting from PCB exposure than
is the adult. Two well-designed prospective epidemiological studies in humans provide evidence
of behavioral deficits associated with low-level in utero exposure to PCBs. In one study,
exposure was via contaminated Great Lakes fish (Fein et al, 1984a, 1984b; Jacobson et al, 1984,
1985, 1989, 1990a, 1990b; Schwartz et al, 1983), while in the other, a North Carolina study,
there was no identified source of exposure (Gladen et al, 1988; Gladen and Rogan, 1991; Rogan
et al, 1986). Regarding the former, in a series of follow-up studies conducted over ten years,
the Jacobsons have tracked and evaluated the development of children born to mothers who had
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consumed at least 11.8 kg of contaminated Lake Michigan fish over a 6-year period. Data were
collected on the mothers' fish consumption habits, the PCB levels in their breast milk and in the
blood serum of both the mothers and their infants. Their research has shown that the cognitive,
motor and behavioral development of the infants were adversely affected by the mothers*
consumption of contaminated fish from Lake Michigan. The authors concluded that prenatal
exposure to PCBs was associated with deficiencies in the infants* cognitive ability to visually
discriminate between objects, and in their short-term memory scanning capabilities. In a follow-
up study of these children at age 4, the Jacobsons evaluated their processing efficiency (short-
term memory and visual discrimination) and sustained attention span. Processing efficiency was
measured because of its link to reading ability and the ability to master quantitative operations,
two dimensions of cognitive functioning fundamental to learning. The authors concluded that
prenatal exposure to PCBs was associated with less efficient visual discrimination processing and
more errors in short-term memory, but not with changes in sustained attention (Jacobson et al,
1992).
A possible limitation of these studies is the failure to assess and control for other potential
neurotoxicants possibly correlated with PCB levels, such as methylmereury. However, the
congruence between the laboratory monkey and human data suggests that the behavioral deficits
observed in the human studies are associated with developmental exposure to PCBs (Rice, 1994).
The most significant route of exposure to PCBs from the Great Lakes is the consumption of
contaminated fish. Estimates of PCB levels in Great Lakes fish tissue can vary by several orders
of magnitude among species and Lakes. One estimate of the present average PCB level in
recreational fish, taken from the Great Lakes is 0.037 ug/g (.04 ppm) (Rice, 1994), while the
Great Lakes Water Quality Board estimates the approximate PCB concentration to be 1.32 ppm,
which represents an average for all the Great Lakes (USEPA 1992, 1993). These figures suggest
that PCB levels in Great Lakes fish may present a potential hazard to offspring of women
consuming large quantities of fish, based on the behavioral data from human epidemiological
studies. Further studies, including prospective studies, should serve to define levels at which
toxicity is known to occur.
Methylmercury
Methylmereury was recognized as a neurotoxic agent following outbreaks of human poisoning
in Japan in the 1950s and 1960s through consumption of contaminated fish (Japan Environment
Agency, 1975). A later episode of human poisoning in Iraq following consumption of grain
treated with methylmereury fungicide resulted in neurotoxic effects, and provided detailed
estimates of thresholds for various health endpoints (WHO, 1976,1989,1990). It became evident
that the developing fetus is much more sensitive than is the adult. There also exists a reasonably
good animal data base replicating effects observed in humans.
Consumption of contaminated fish represents the main exposure route for methylmercury hi the
Great Lakes Basin. The most sensitive endpoints affected by MeHg are developmental delays
in children exposed in utero (Amin-Zaki etal., 1980; Marsh, 1987; Chang, 1977; Harada, 1968).
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There have been few epidemiological studies of Great Lakes populations in this regard. In one
recent study of mercury levels in the Chippewa Tribe at the Red Cliff Reservation on Lake
Superior (the least polluted of the Great Lakes), researchers at the University of Wisconsin found
no obvious adverse behavioral effects that could be related to consumption of Lake Superior fish,
as there were no significant methylmercury body burdens found in the study (Dellinger et al,
1993). It is unclear whether the body burdens of MeHg in subpopulations who consume fish
from the other Great Lakes are associated with adverse behavioral effects.
Lead
Lead has been known to be neurotoxic since ancient times (Cantarow and Trumpet, 1944; Oliver,
1914). The present body burden of lead in the general population is 2-3 orders of magnitude
above historical background levels, as a result of human activity (NAS, 1980). In the last decade
and a half, it has become clear that exposure to lead in utero and/or during childhood at body
burdens that are presently typical of humans in industrialized countries results in deficits in IQ,
and in distractibility, inattention and other behavioral problems (Needleman et al, 1979).
Approximately 20 epidemiological studies, both prospective and retrospective, provide extremely
strong and consistent evidence (Rice, 1994). The retrospective studies have been extensively
reviewed (see Rutter and Russell Jones, 1983; Mahaffey, 1985; Mushak et al, 1989), and the
most recent ones have utilized populations with lower body burdens of lead than the children
assessed by Needleman. Effects of lead on intellectual and behavioral functions in children in
these studies include intellectual deficit, hyperactivity, inattention, and increased reaction time.
Prospective studies also provide convincing data regarding developmental deficits produced by
low-level lead exposure (for review see Mushak et al., 1989; Hammond and Dietrich, 1990),
including deficits in cognitive performance, abstract thinking, sustained attention, and
psychomotor development. There is also a large body of animal data that indicates that lead
produces behavioral impairment consistent with the types of impairment observed in lead-exposed
children and the blood levels at which they occur (for review see Cory-Slechta, 1984; Rice, 1992,
1993). Among other findings is the association between an elevated maternal blood lead level
and abnormal reflexes, poor muscle tone, and neurological soft signs such as jitteriness,
hypersensitivity, and abnormal cry in the infant following exposure in utero (Ernhart et al., 1985,
1986).
It is also becoming increasingly clear that there is no apparent threshold for these effects at
present day body burdens. An important unanswered question is the contribution of total maternal
body burden, rather than blood level, to the risk to the infant. Bone contains over 90% of body
lead stores, and it is established that lead increases in bone throughout the life-span of humans
(Barry, 1975). Women currently at reproductive age have been exposed to the most lead since
ancient times, and thus will generally have a significantly higher total body burden of lead than
previous generations and will provide a significant source of both in utero and neonatal exposure
via mobilization of lead from bone stores during pregnancy and lactation, long after exposure has
ceased (Thompson et al., 1985).
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The most significant sources of lead exposure are food (indirectly from environmental fallout)
and drinking water via lead or lead-soldered plumbing, or environmental contamination. The
Great Lakes Basin does not present a particular hazard with regard to lead exposure. However,
as there is no apparent threshold for intellectual impairment produced by lead in the developing
organism, every reasonable effort should be made to minimize point sources of lead
contamination in the Great Lakes Basin (Rice, 1994).
5.4 Immunotoxicology of Heavy Metals, PCBs, Dioxins
and Organochlorine Pesticides
The immune system plays a crucial role in maintaining health. However, accumulating evidence
indicates that this system can be the target for immunotoxic effects caused by a variety of
chemicals, including environmental pollutants such as PCBs and chlorinated dibenzo-p-dioxins;
the pesticides HCB, mirex, dieldrin and DDT; and the heavy metals cadmium, mercury and lead.
Their immunotoxic potential raises concerns regarding subsequent effects on human health.
Limited human epidemiological data and data derived from studies using experimental animal
models and in vitro cell culture systems indicate that certain human populations might be vulner-
able to the immunomodulating effects of these pollutants (Tryphonas, 1994; Bernier et al., 1994;
Thomas, 1994; Kerkvliet, 1994). Adverse immunomodulation may be expressed either as
immunosuppression or irnmunoenhancement. The former may be manifested either as decreased
resistance to opportunistic viral, bacterial, fungal and other agents or increased susceptibility to
cancer. Immunoenhancement, on the other hand, may either increase the risk of autoimmune
reactions or result in allergic reactions (Bradley and Morahan, 1982; Koller and Exon, 1983;
Roller et al., 1983; Munson et al., 1982; Vos, 1977), Following is a description of the current
status of knowledge on the immunomodulatory effects of selected groups of contaminants present
in the Great Lakes.
Heavy Metals
The existing limited data on humans exposed to heavy metals accidentally or occupationally and
data derived from experimental animal models and in vitro studies reveal that such metals are
among the most potent immunotoxic inorganic chemicals. Frequently, these chemicals exert their
adverse effects on the immune system at doses much lower than those required for overt
toxicologic effects (Exon, 1984). The adverse immunomodulating effects of mercury, lead and
cadmium on the immune system have been the subject of numerous studies, and have been
reviewed by Bernier et al, (1994) in a background paper prepared for Health Canada, highlights
from which are presented below.
Cadmium-induced immunosuppression is suspected to cause decreased resistance to infections
by adversely affecting the activity of various important components of the immune system,
including reduced macrophage phagocytosis and natural killer cell activity. However, the role
of cadmium in reducing host resistance to experimental infections is not conclusive. With respect
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to cancer, the carcinogenic potential of cadmium in man is questionable. Yet, animal studies
show a strong association between cadmium exposure and tumorigenesis. Overall, the
mechanism of cadmium-induced immunotoxicity remains elusive and further mechanistic studies
are required.
Inorganic and organic forms of mercury have definitive toxic effects on the immune system (e.g.
altered levels of lymphocyte subsets in rodents). In vitro studies have shown increased DNA
synthesis in lymphocytes at low mercury concentrations, whereas in vivo mercury exposure has
resulted in decreased antibody response to certain antigens. Among other effects, mercury
exposure can alter non-specific host defenses such as suppression of natural killer cell activity.
In addition, it has been well documented that mercury has the potential to induce allergy and
autoimmunity, phenomena possibly dependent upon genetic susceptibility.
Lead is immunotoxic, as it has been shown to depress the antibody response in mammals and
to diminish host resistance to pathogens in experimental infections in laboratory animals. Lead
can also moderately enhance certain immune responses such as B cell differentiation and mixed
lymphocyte culture responses. These phenomena are probably mediated through an increase in
activity of the T-helper cell. Regarding possible carcinogenic effects, there is no epidemiological
evidence that implicates lead as a human carcinogen, although it has been shown to cause tumors
in experimental animals.
Generally, the immunosuppressive effects of cadmium, mercury and lead have been shown to
increase the susceptibility of laboratory animals to infectious agents (Bernier et al, 1994). In
addition, these three contaminants should be regarded as potential epigenetic carcinogens, acting
possibly through interference with the immunosurveillance mechanisms (Exon, 1984).
PCBs
The results of in vivo and in vitro experimental animal studies indicate that commercially
available PCB mixtures, known as Aroclors, alter several morphologic and functional aspects of
the immune system (reviewed by Vos and Luster, 1989; see also Tryphonas, 1994). High but
sublethal dermal and oral PCB exposure have resulted in (a) structural alterations of immune
system organs (loss of thymic cortical lymphocytes, reduction of germinal center size, and
reduction of leukocyte and T lymphocyte counts in peripheral blood) and (b) altered functional
reactivity of the immune system, characterized by reduced antibody production against foreign
antigens and reduced skin reactivity to specific antigens (delayed type hypersensitivity);
functional defects in the mononuclear phagocytic cells and natural killer cell activity, both of
which play primary roles in combating infection; and increased susceptibility to normally
tolerated doses of bacterial and viral infections and parasitic infestations. Although the degree
of immunotoxicity has been shown to vary across species with dose, duration of exposure and
PCB mixture, the more highly chlorinated PCB mixtures (Aroclors 1260, 1254, and 1248) have
been found to be more immunotoxic than the less chlorinated Aroclors 1232, 1016 and 1242.
Despite the evidence that PCB-induced immunosuppression impairs the immune surveillance,
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Aroclor 1254 has been shown to protect mice and rats against certain kinds of experimentally
induced tumours (reduced tumour growth and metastasis) (Keck, 1981; Koller, 1977; Kerkvliet
and Kimedorf, 1977). This paradox points to the need for additional studies on PCBs and their
relationship to tumour formation and growth.
While the degree of human sensitivity to PCBs relative to that observed in laboratory monkeys
is not well characterized, the results of chronic immunotoxicity studies have revealed that
monkeys with blood and fat PCB levels comparable to background levels of PCBs found in
humans had significant immunotoxic manifestations. In one such study, reduced antibody levels
to the T-dependent antigen sheep red blood cells were observed at levels as low as 0.005 mg/kg
body weight/day (Tryphonas et al., 1989, 1991a, 1991b). Furthermore, a no-effect dose was not
identified in this study. The impact of these findings on the evaluation of the potential risk PCBs
pose to humans is presently unclear.
Epidemiological studies (Smith, 1984 and Humphrey, 1988) suggest that PCBs in the Great Lakes
may have an immunosuppressive effect in humans. Significant positive correlations were revealed
(a) between the maternal serum PCB level during pregnancy and the number and type of
bacterial infections suffered by the breast-fed infant during the first four months of life and (b)
between the incidence of infections in the breast-fed infant and cumulative fish consumption by
the mother (Swain, 1991). Limited data from recent studies on rodents fed fish diets from
selected areas of Great Lakes suggest that the immune system may be affected. Further studies
are needed to determine the risk that Great Lakes contaminants pose to the human immune
system and consequently to human health.
With respect to the interactive effects of PCBs, the existing limited data suggest that under
certain experimental conditions PCB congeners in mixtures may either have additive effects or
antagonize the immunotoxic effects of other chemicals, including those of dioxin (Davis and
Safe, 1989).
The mechanism of PCB-induced immunomodulation has not been adequately elucidated. Many
of the immunotoxic effects of PCB congener mixtures depend on the presence of the aromatic
hydrocarbon (Ah) receptor and on the ability of the PCBs to bind to this receptor. The molecular
events following binding of certain PCBs to the receptor are believed to be similar to those of
dioxin. It should be noted, however, that other PCB congeners do not share a common
mechanism with dioxins, suggesting a different mechanism of action (Tryphonas, 1994).
Poly chlorinated Dibenzo-p-dioxins (Kerkvliet, 1994)
Immunosuppression is a widely recognized toxic effect following exposure of animals of various
species to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), expressed as lymphoid tissue depletion,
especially in thymus and bone marrow, functional alteration in immune responsiveness, and
increased susceptibility to infectious disease. Some studies suggest that prenatal exposure to
TCDD is more immunosuppressive than comparable exposure in adults, which may be related
to effects on the thymus. Since the thymus is critical for the development of T-cells that can
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appropriately discriminate between self and non-self, prenatal exposure to TCDD has the potential
to produce serious, long-term effects on immune function.
The immunotoxicity of TCDD depends on the aromatic hydrocarbon (Ah) receptor, and the
expression of this receptor in different species or tissues is thus a very important factor
determining the toxicity of dioxins and related compounds. Although the effects of TCDD
exposure on immunity have been widely studied over the last 15 years, there is still no consensus
regarding the target cells and functions that mediate TCDD immunotoxicity. There is a fair
amount of conflicting data. In mice, the generation of a primary antibody response appears to
be particularly sensitive to suppression when mature animals are exposed to TCDD. The effect
on antibody production may result from effects on both T and B lymphocytes. Although most
macrophage functions appear to be resistant to TCDD-induced alterations, recent studies indicate
that macrophage production of inflammatory cytokines is enhanced following TCDD exposure.
Natural killer cell cytotoxicity is not altered in mice exposed to relatively high doses of TCDD.
Mitogen-induced blastogenesis of lymphocytes from adult mice is not altered by doses of TCDD
that significantly suppress antibody production. Delayed type hypersensitivity (DTK) responses
and T-eell mediated cytotoxic responses are suppressed by TCDD, but require higher doses than
those capable of affecting antibody production.
The immunotoxicity of TCDD in humans has been the subject of a limited number of studies,
primarily based on accidentally or occupationally exposed humans (e.g., in Italy and in Missouri).
A decrease in the level of the thymus peptide, thymosin alpha-1, has been reported; however this
change was not associated with changes in other immune system parameters nor with any
increased incidence of clinically diagnosed immune suppression. The decrease in thymosin
alpha-1 levels in humans contrasts with an increase of this peptide seen in PCB-exposed
monkeys. The lack of clearly documented immunotoxic effects of TCDD in humans may relate
to both the exposure status of the cohorts studied which may have been lower than the
immunotoxic dose, as well as the assays chosen to assess immune function, which may have been
insensitive to the effects of TCDD.
Organochlorine Pesticides (Thomas, 1994)
There are several pesticides in the Great Lakes Basin which are known to have
immunomodulatory effects. These include hexachlorobenzene (HCB), mirex, dieldrin and DDT
and its metabolites. At present there is no clear evidence that environmental exposure to these
pesticides through consumption of contaminated fish or wildlife poses a threat of immune-
mediated health effects in humans. However, laboratory animal studies have shown that these
compounds are immunomodulatory (albeit at exposure levels that are orders of magnitude higher
than those reported for human exposure), with immunotoxic effects ranging from an increased
severity of experimental infection, to specific effects on immune system structure
(histopathology) and function.
In rodent studies, hexachlorobenzene (HCB) has been shown to be immunomodulatory based
upon increased susceptibility to infection, increased sensitivity to endotoxin challenge and
Human Health Effects - SOLEC Background Paper 45
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histopathologic alterations, while altered immune responses suggestive of impaired host defense
mechanisms have been observed in mice exposed to dieldrin. With respect to mirex, little is
known about the potential immunotoxicity of this compound.
In contrast to the other priority pesticides found in the Great Lakes Basin, there have been
numerous studies of the effect of DDT on the immune system of laboratory animals. The results
included suggestions of immunosuppression. However, there is no evidence of any adverse long-
term effects resulting from small daily doses of DDT, and no conclusive evidence that DDT is
immunosuppressive in humans exposed through the food chain. There have been recent reports
of an association between DDT exposure and appearance of breast cancer. However, the
relationship of this observation to changes in tumour surveillance mechanisms remains unclear.
In summary, there is limited direct evidence that exposure to heavy metals, PCBs, dioxins, and
pesticides induces significant immune dysfunction in humans. However, data derived from
wildlife (Fox, 1993) and laboratory animal models including monkeys provide evidence of
structural changes in tissues of the immune system and of functional deficits in both humoral and
cell-mediated immunity. While more information is needed on the mechanism(s) underlining the
immunomodulatory effects of these chemicals, the existing limited data suggest that these
chemicals may have potential adverse immune-mediated effects in humans who consume large
quantities of fish from the Great Lakes.
An important consideration regarding the potential immunotoxic effects of Great Lakes
contaminants is that, unlike certain other health effects areas, adverse health effects related to
immune dysfunction can be quite subtle yet significant following prolonged exposure. Research
in this area is problematic due to a number of confounding factors, including the difficulty in
assessing subclinical immunomodulation in a heterogeneous human population, and in quantifying
associated health effects. Therefore, there is a strong need to establish a broad database of
normal values for the clinical immunology endpoints that may be of use as biomarkers of
immune function in immunotoxicity assessment in humans. To validate these biomarkers, there
is a parallel need for animal research to identify sensitive immune endpoints that can also be
measured in humans in order to establish correlative changes in the biomarker and immune
function.
5.5 Carcinogenicity and Genotoxicity
While laboratory animal studies (Parfett et al., 1994) and wildlife studies on Great Lakes fish
populations and Beluga whales in the St. Lawrence River (Flint and Vena, 1991) provide
evidence that a number of critical pollutants are potentially carcinogenic, there are few
epidemiological data on human cancer incidence and mortality and their association with Great
Lakes pollutants. In their review conducted for Health Canada, Parfett et al. (1994) examined
selected persistent chlorinated organic chemicals, volatile organic chemicals, polyaromatic
hydrocarbons (PAHs), metals, minerals, and nitrates known to contaminate Great Lakes drinking
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water, and concluded that there is limited epidemiological evidence to indicate that some drinking
water sources with Great Lakes origin may be associated with increases in the incidence of
several types of cancer in humans. Some of these drinking water sources currently have elevated
levels of certain contaminants represented by alpha-hexachlorocyclohexane (a-HCH), nickel, and
trihalomethanes. However, the epidemiological evidence is not of sufficient strength to link the
presence of these compounds with the elevated cancer incidences.
Case-control studies have also examined the association between Great Lakes pollutants and
human cancer incidence and mortality. Vena et al. (1993) investigated the occurrence of bladder
cancer in white males, and a possible association with overall fluid intake and the consumption
of specific beverages. Their study involved 351 cases of confirmed transitional cell carcinoma
and 855 controls selected from the Erie, Niagara, and Monroe counties of western New York
state, all counties bordering the Great Lakes. For more than 95% of the cancer cases and
controls in this study, the source of tap water was the public supply obtained from the surface
waters of Lake Erie, the Niagara River, and Lake Ontario. After controlling for numerous
potential confounding factors, total fluid consumption was found to be a strong risk factor for
bladder cancer. More importantly, tap water was associated with an increased risk of bladder
cancer, with a clear dose-response relationship (Vena et al., 1993).
While this study links the ingestion of tap water and bladder cancer risk, it does not link
exposure to specific contaminants in Great Lakes drinking water with elevated cancer incidences.
However, the authors do note that surface waters from which drinking water is drawn have much
higher levels of naturally occurring organic substances than does groundwater. The chlorine
added to drinking water as a disinfectant reacts with these organic compounds during the
chlorination process to form a variety of volatile organic compounds such as trihalomethanes, and
a host of other chlorinated non-volatile compounds that have been found to be carcinogenic in
laboratory rodents. Among recent research efforts in this area is a case-control study currently
being conducted by the Ontario Cancer Treatment and Research Foundation (OCTRF). The
OCTRF is examining the possible association between consumption of Great Lakes drinking
water and the risk of cancers of the bladder, colon and rectum in residents of Ontario; however,
no results are yet available. As well, a national study being initiated by Health Canada will
investigate potential risks from Great Lakes water consumption and trihalomethanes based on
historical residence. Cancer sites and types under study include liver, testes, brain, pancreas,
prostate, stomach, leukaemia, kidney, non-Hodgkin's lymphoma and lung (Johnson, 1993).
It is important to consider that the potential risks associated with the ingestion of drinking water
is much lower than the risks associated with other types of exposures. For example, the U.S.
Environmental Protection Agency considers the risk of cancer posed by drinking water from the
Great Lakes much lower than that for other exposure routes. According to USEPA estimates,
the potential number of excess cancer cases related to the ingestion of drinking water across the
Basin may total approximately 66 over a 70-year span. On the other hand, the estimated total
number of potential excess cancer cases related to consumption of Great Lakes fish is 30,000
over a 70-year span — several orders of magnitude higher (USEPA Great Lakes National Program
Office, 1992). The USEPA based its estimate on the following assumptions: that the residents
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of the Great Lakes Basin who derive their drinking water from surface water sources ingest 2.0
litres of contaminated water per person per day; an estimated duration of exposure of 70 years
(lifetime) and an estimated average body weight of 70 kg; a Great Lakes population of
12,700,000 relying on drinking water from surface water supplied systems within the Great Lakes
counties in the U.S.; and concentrations of lindane, a-BHC (a by-product of lindane), dieldrin,
p'p-DDE, PCBs, and HCB for all of the Great Lakes as estimated by the International Joint
Commission's (DC) Water Quality Board (1989).
In addition, the USEPA's Great Lakes Basin Risk Characterization study has estimated cancer
risks from multiple exposure to contaminants Basin-wide. The study results indicate that health
risks related to Basin-wide exposure to contaminants in Great Lakes fisheries and ambient water
are driven primarily by PCB exposure. With regard to Great Lakes fish consumption, chemical
risk analyses suggest that PCB exposure accounts for 85% of human cancer risks. Indeed, there
have been studies linking PCB levels in certain populations with breast cancer incidence. For
example, recent studies conducted on cohorts from Connecticut and New York state provide some
evidence linking organocMorine pollutants such as DDT and PCBs to breast cancer incidence
(Falck et al, 1992, Wolff et aL, 1993). These studies point to potential adverse effects that
should be considered in health studies for the Great Lakes region. This is based on predictive
modeling and assuming that 3.4 million people consume 19 grams of Great Lakes fish per day
over a 70 year life time exposure, which is a conservative estimate. In addition, concentrations
for fish contaminants were averaged for all the Great Lakes and based on figures from the DC
Great Lakes ,Water quality Board's Report on Water Quality for PCB, DDT, Dieldrin and
mercury and assumes that contminant level would not decline.
Regarding mixtures of chemicals from the major groups discussed in this review, these have been
linked to excess cancer mortality associated with occupational exposures. Consistent with
exposure to qualitatively similar hazards, cancer sites implicated in these studies overlap with the
cancer sites.identified in Ontario drinking water studies. Occupational exposures to PAHs,
TCDD, cadmium and nickel have been associated with increased lung cancers; pesticide
exposures have been associated with lung cancer and non-Hodgkin's lymphoma; and various
exposures to some volatile organic chemicals have been associated with oesophageal, cervical,
and non-Hodgkin's lymphatic cancers (Parfett et a/., 1994).
With respect to relevant data from animal studies, most Great Lakes contaminants for which
animal carcinogenicity data are available are classifiable as animal carcinogens at high doses.
Consistent with exposure to qualitatively similar hazards, the listing of tumour sites obtained
from positive animal studies overlap with human tumour sites associated with "contaminated"
Great Lakes drinking water sources. However, no cause-effect relationships have been
established regarding the very low concentrations of environmental contaminants. In laboratory
animals, lung and kidney cancers have resulted from treatments with members of all groups of
contaminants (PAHs; certain volatile, chlorinated organics; metals; pesticides; dibenzodioxins,
dibenzofurans and PCBs). As well, thyroid tumours have resulted from treatments with
individual volatile, halogenated alkanes and alkenes, pesticides, chlorinated dioxins and PCBs,
while leukaemias were found in animals treated with some pesticides, and cadmium treatment
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gave rise to lymphomas (Parfett et al, 1994).
Evidence also indicates that TCDD is active in rodent and human systems at lower concentrations
than any of the other contaminants discussed and identified as carcinogenic risks by Parfett et
al, in their review. TCDD induces gene expression and transformation of human cells in vitro
at concentrations similar to the background levels in the sera of the majority of North Americans.
Levels and effects (e.g., likely cancer sites, gene inductions, etc.) of this persistent compound
should receive special attention in populations receiving greatest exposure to Great Lakes
contaminants (Parfett et al, 1994).
In addition, available data further indicate that in human cells certain volatile, chlorinated alkanes
and alkenes (trichloroethylene, tetrachloroethylene, chloroform) cause sister chromatid exchanges
in vivo, and induced cell proliferation in vitro at concentrations only ten-fold higher than those
in the guidelines established for drinking water contamination (Parfett et al, 1994). (Note: levels
in drinking water can be compared to levels in culture fluid used to incubate cells. They cannot
be compared with levels in vivo (i.e., tissue fluids) because only 2 litres of water per day are
consumed and most of the water is excreted. The tissue or blood levels are the result of a
composite exposure through food consumption, inhalation, and dermal contact with water).
Lastly, combinations of Great Lakes contaminants known to have carcinogenesis-related effects
at low doses in human cells have received little or no attention with regard to effectiveness hi
chemical mixtures. This represents an important area for future research.
5.6 Respiratory Health Effects
The effects of air pollution on respiratory health can range from severe (aggravation of
respiratory disease, death) to moderate (reduced lung function with or without symptoms) to
minor (eye, nose and throat symptoms). Certain effects, such as mild inflammation in the lungs
without symptoms, may or may not have any significance (American Thoracic Society, 1985).
Some researchers have suggested that there is a logical "cascade" of these effects (Bates, 1992);
in other words, if a few people die as a result of air pollution, men more should experience
worsening of respiratory disease, even more should experience reduced lung function, and a very
large number should experience eye, nose and throat symptoms, so that the total burden of illness
could be very large. This means that research which demonstrates increased death rates and rates
of hospital admission due to air pollution could reflect a very large overall burden of illness hi
the population.
Effects on Death Rates
Several studies have examined the relationship between air pollution and death rates, two of
which were carried out in the Great Lakes Basin. A study in Hamilton, Ontario looked at the
geographic distribution of lung cancer deaths between 1972 and 1976, comparing industrial and
non-industrial areas of the city (Shannon et al, 1988a). A 15% excess of lung cancer deaths was
Human Health Effects - SOLEC Background Paper 49
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observed in industrial areas, after taking into account different age and smoking patterns. Air
pollution levels were not reported.
A second study in Detroit, Michigan examined parallels between daily death rates and air
pollution levels (Schwarz, 1991). This study used statistics on all causes of death other than
accidents between 1973 and 1982 and measured weather variables and levels of airborne
particles, ozone, and sulphur dioxide. There was a clear relationship noted between increased
death rates and increased levels of airborne particles and, to a lesser extent, sulphur dioxide, even
when the effects of weather and other variables were taken into account. It was estimated that
when daily levels of airborne particles increased from the low end to the high end of levels
observed in the study (100 ug/m3), the death rate increased by 6%. As described in the section
on airborne particles, levels such as this are commonly observed in Great Lakes cities in Ontario.
Other studies have linked increased death rates with elevated levels of sulphur dioxide, sulphate
and particles (Plagiannakos and Parker, 1988), as well as ozone (Kinney and Ozkaynak, 1991).
In addition, increased death rates from asthma have been observed worldwide in recent years
(Mao et al., 1987), which may be partially attributable to exposure to air pollution.
Effects on Hospital Admission Rates
Three studies have examined the relationship between daily air pollutant levels and rates of
hospital admission in Great Lakes cities. The first study, based on data for southern Ontario
between 1974 and 1983, looked at the effect on hospital admissions of levels of ozone, nitrate,
sulphur dioxide, airborne particles, and sulphate (Bates and Sizto, 1987). Increased temperature,
ozone, sulphate and sulphur dioxide accounted for an increase in respiratory admissions of about
5%. These effects were observed within the range of pollutant levels described in the sections
on ground-level ozone and acid aerosols.
The second study took a similar approach, using data for the years 1983-1988 for a larger number
of Ontario communities, some of which were in the Great Lakes Basin (Burnett et aL, 1993).
This study attributed 5% of respiratory admissions to ozone, and an additional 1% to sulphates.
The largest impact appeared to be on children under 2 years of age, in whom 15% of hospital
admissions were attributed to ozone and sulphate together. Again, these effects were observed
within the range of pollutant levels described in the sections on ground-level ozone and acid
aerosols.
The third study looked at hospital admissions in Toronto during July and August 1986-1988
(Thurston, 1993). This study found significant associations between hospital admission rates and
elevated temperature and pollutant levels, including ozone and acid aerosols.
With regard to the health impact of exposure to air pollutants on the U.S. side of the Great Lakes
Basin, the U.S. Environmental Protection Agency has conducted a risk assessment of populations
in the Basin and estimated that exposure to toxic air pollutants results in 148 premature deaths
and approximately 470 hospital admissions annually. In addition, the USEPA estimates that over
50
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33,000 children and nearly 110,000 adults in the Basin experience respiratory symptoms as a
result of exposure to sulphates. Consequently, the costs arising from the 148 predicted premature
deaths and the 470 hospital admissions are $11 million and $2.1 million, respectively (USEPA
Risk Characterization Study, 1992).
Effects on Lung Function
A number of studies have examined the relationship between levels of various pollutants and
decreases in lung function, particularly in children. A study conducted in Hamilton between
1978 and 1982 measured exposure to suspended particles and sulphur dioxide, and correlated
these with symptoms and lung function measurements in children aged 6 to 11 years (Pengelly
et a/., 1986). Children living in the most industrial areas of the city, who had the greatest
exposure to small particles, had poorer lung function, although the effect was smaller than that
of maternal smoking.
A second study was conducted in a girls' camp on the north shore of Lake Erie in the summer
of 1986 (Raizenne et al., 1989). This study examined the relationship between ozone, acid and
sulphate levels (measured on site) and lung function hi girls aged 8-14. Small (up to 5-10 %)
decreases in lung function were observed on days when pollutant levels were high. The highest
ozone, acid and sulphate levels were 143 ppb, 550 nmol/m3 and 83 ug/m3, respectively, which
are much higher than average levels observed in southern Ontario, but are typical of air pollution
episodes in this area.
A more recent study in 24 North American communities related measurements of acid aerosols,
small particles (PM2il ;<2,1 urn), larger particles (PM,0;<10 urn), and sulphate, to lung function
measurement in children. Two of these communities (Dunnville - near Hamilton, and
Leamington - near Windsor) were in the Great Lakes Basin area and experienced pollutant levels
which were intermediate compared to other communities. Children exposed to the highest acid
aerosol levels were 2.5 times as likely to have lung function below 85% of that predicted for
healthy children based on sex, height, weight and other factors.
In conclusion, there is strongly suggestive evidence from the Great Lakes Basin linking ozone,
airborne particles and acid aerosols to significant respiratory health effects including death and
illness requiring hospital admission. There is also evidence from the Great Lakes Basin that
these pollutants cause reduced lung function hi children. This evidence is consistent with data
from elsewhere in North America and Europe.
5.7 Health Effects Associated with Radlonuclides
The Great Lakes Basin is an area of radiological concern as a result of the large population that
may be exposed to actual or potential sources of ionizing radiation arising from both natural and
artificial sources. Exposure to ionizing radiation can affect the various organs and tissues of the
body, and may result from rediation originating in deep space, or emitted by the decay of
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radioactive elements found in the environment. These radioactive elements, or radionucUdes, are
unstable nuclides of a particular atomic species that return to stability by emitting ioning
radiation. Specific radionucUdes of interest in the Basin arising from natural and artificial
sources include tritium (3H), carbon-14 (14C), strontium-90 (*°Sr), radioiodine (I291,13II), cesium-
137 (I37Cs), radon-222 (mRn), radium-226 (^Ra), uranium isotopes p'U, 238U),and plutonium
isotopes (e.g., 239Pu, MOPu, M1Pu).
By far, the greatest contribution to the average public radiation exposure is the natural
background radiation that comes from radioactive elements in the earth's crust and from cosmic
radiation originating in deep space. Natural sources contribut on average more than 98% of the
human radiation dose, excluding medical exposures. The global average dose from natural
sources as estimated by the United Nations Scientic Committee on the Effects of Atomic
Radiation (UNSCEAR, 1993) is about 2.4 milliSieverts (mSv — a unit of effective dose) per year,
which can be compared with the national Council on Radiation Protection and Measurments
estimate of 2.6 mSv a"1 for Canada (NCRP, 1987a). this dose results mainly from internal and
external exposure to radioactive potassium t40!^), and from the inhalation and accumulation in the
respiratory system of the short-lived radon decay products (the rapidly decaying radionucUdes
formed as a result of successive decays of 222Rn). The natural radiation dose provides a measure
by which contributions from human activities can be evaluated.
Global fallout of radionucUdes produced during atmospheric nuclear weapons tests has resulted
in the largest total input of anthropogenic radioactivity into the Lakes (Table 8), although the
1963 moratorium on atmospheric detonations of nuclear weapons has resulted in declining
radiation levels since the mid-1960s. The total committed dose (the average total dose resulting
from radionuclides accumulated in the body) to the year 2050 to each individual in the Basin
from weapons tests conducted between 1945-1980 has been estimated to be about 1.9 mSv
(UNSCEAR, 1993), Most of which has already been received. This truncated dose provides a
measure of the radiation hazard presented to those living during the period of intensive testing
prior to 1963, and is equvalent to sUghtly less than one extra year of exposure to natural
background radiation.
Increases in local exposure above background levels may result from radionucUdes released
during the various stages of the nuclear fuel cycle. Nearly all components of the nuclear fuel
cycle are found within the Basin, the main elements of which are uranium mining, fuel
preparation, power generation, and waste management (see Figure 6). Normal fuel cycle
operations result in controlled and regulated release of radionucUdes into the atmosphere and
aquatic environments (Table 8), adding to the radiation exposure from both natural sources and
radioactive fallout from atmospheric nuclear weapons tests (see Table 9).
The doses from these three sources can be compared in terms of the total collective doses to the
Basin population from 50 years of exposure at current levels, or to the year 2050 in the case of
nuclear weapons fallout. These doses >are obtained by multiplying the average annual individual
exposure by the number of people exposed and the number of years considered (Table 9). The
collective dose to the Basin population from 50 years of expsoure to natural background radiation
52
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is therefore of the order of 4.7 x 106 man-sievert (man-Sv). The collective dose from 50 years
of fuel cycle operation in the Basin based on actual radionuclide emmissions from 1985-1989
(UNSCEAR, 1993) has been estimated to be about 2.8 x 103 man-Sv, or about 3 orders of
magnitude less than the exposure due to natural background radiation. Although currently very
low, the dose from fuel cycle activities can be expected to increase if there is continued growth
of the nuclear industry.
TABLES
INVENTORY OF RADIONUCLIDES IN THE GREAT LAKES FROM FALLOUT
TO 1983 AND NUCLEAR FACILITY RELEASES, AND 1989 INVENTORIES
STORED AT THE FACILITIES
ESTIMATED RADIONUCLIDE INPUTS AND INVENTORIES BY LAKE (TBq)
SOURCE Superior
Tritium (*H):
Fallout* 7 x 104
Nuclear Facilities
Strontium-90:
Fallout* 123
Nuclear Facilities
Stored at Facilities
Cesium-137:
Fallout* 200
Nuclear Facilities
Stored at Facilities
Michigan
6x 104
2x 103
98
0.015
5x 10*
159
9
8x 10*
Huron
7x 10*
1.5 x 104
98
0.11
3.5 x 10*
159
0.12
5x 106
Erie
4x 104
2x 102
45
1.5
6x 10s
74
0.2
7x 105
Ontario
3x 104
5x 102
33
0.15
4x 10*
54
25
7x 10*
* Input from fallout calculated using deposition flux at mid-basin location for each Lake using New York City
data, adjusted for latitude.
Source: Joshi, 1991 (cited in Ahier and Tracy, 1994)
Human Health Effects - SOLEC Background Paper
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Radiological Effects and Health Implications of Human Exposure to Radionuclides
In their review of radionuclides in the Great Lakes Basin, Ahier and Tracy (1994) present an
informative discussion of the radiological and health effects of exposure to radionuclides, on
which the following summary is based. In essence, the decay of a radionuclide results in the
emission of ionising alpha, beta, and gamma radiation, which can disrupt cells in the human body
as energy is transferred from the radiation to the tissue. A measure of this disruption is the
absorbed dose, defined as the amount of energy imparted by ionising radiation to a unit mass of
tissue. The term effective dose is introduced to account for the difference in effectiveness of the
type of radiation and the different susceptibilities of bodily organs. Generally, the effective dose
can be considered a broad indicator of the risk to health from any exposure irrespective of the
type and energy of the radiation, or of the organ or organs exposed.
Exposure to ionising radiation, whether natural or man-made, can cause two kinds of health
effects. Effects for which the severity of the damage caused is proportional to the dose, and for
which a threshold exists below which the effect does not occur, are called deterministic effects.
These are generally manifested in the individual within a few days or weeks following exposure.
Deterministic effects have not been observed at exposures below 0.5 Sv. Under normal
conditions, doses received from natural radioactivity and routine exposures from regulated
practices are well below the threshold levels. Effects for which the probability of occurrence,
rather than the severity, is proportional to dose are known as stochastic effects, and it is assumed
that there is no threshold below which they do not occur. Stochastic effects are the most
important consequence of environmental levels of radiation.
Stochastic effects can be either hereditary or somatic in nature. Hereditary effects appear in
future generations as a result of radiation-induced changes in the reproductive cells of an exposed
individual. Although studies have been conducted on the hereditary damage induced in
experimental animals, no conclusive evidence for hereditary effects attributable to exposure from
either natural or artificial radiation has been found in human offspring.
The stochastic effects of concern are late somatic effects, mainly cancer, which follow a variable
latent period of up to several decades. These effects result primarily from relatively low
exposures received over an extended period of time, although they can result from massive doses
that have caused immediate effects (e.g., atomic bomb survivors). The main somatic hazards
from environmental radiation are the development of leukaemia and other cancers, particularly
in the bone, thyroid, lung, or breast.
The primary sources of epidemiological information on radiation effects have come from studies
of individuals or groups who have received high or intermediate levels of exposure. As it is
impossible to obtain dose-effect relationships in humans at low levels of exposure, a linear, no-
threshold model is assumed, extrapolated from the epidemiological studies of the effects of high
dose and dose-rate exposures. Thus, health effects are generally assumed to be proportional to
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the dose received, without a dose threshold (i.e., there is no dose, however small, that may in
principle be considered without risk). The no-threshold hypothesis is believed to be conservative,
and estimates of risk based on this model are upper limits. One consequence of the no-threshold
approach is that even when the risk to an individual is small, a finite number of theoretically
attributable radiation-induced cancers is predicted if a sufficiently large population is exposed.
Based on the epidemiological data, the International Commission on Radiological Protection
(ICRP, 1991) has established a risk of 5 x 10 "5 per mSv for the induction of fatal cancer after
low dose, low dose-rate whole body irradiation of a member of the general population. The
ICRP has alsorecognized that not all cancers are fatal, and that this, in addition to the possibilty
of hereditary effects, should be considered. Therefore, the ICRP has estimated the risk of
incidence of non-fatal cancers, weighted for severity, and of hereditary effects. The total risk
coefficient for fatal and weighted non-fatal cancers, and hereditary effects, based on all
epidemiologic data, has been estimated to be 7.3 x 10*5 per mSv (ICRP, 1991).
Radiological Risk Assessment in the Great Lakes Basin
Risk assessments of exposures in the Great Lakes Basin require estimates of total effective dose
for both local and regional populations, as well as for the maximally exposed individual or group
living in the vicinity of a nuclear facility (see Table 9). Assuming a no-threshold model for
radiation effects, the ICRP risk estimate for fatal cancer can be applied to the total effective dose
for the relevant population. Estimates of collective dose and risk committed by 50 years of
exposure have been derived by Abler and Tracy (1994) for the current Basin population of 36
million. The total number of predicted fatalities over the lifetime of the current Basin population
that could be theoretically attributed to a 50-year exposure to natural background radiation is of
the order of 2.4 x 105. By comparison, the total number of predicted fatalities theoretically
attributable to radioactive fallout from all weapons tests to date would be of the order of 3,400.
Estimates of theoretically attributable fatalities due to 50 years of exposure to current nuclear fuel
cycle effluent (from exposures mainly to 3H and 14C releases) based on environmental models and
actual radionuclide emission rates (UNSCEAR, 1993) are on the order of 140. These numbers
are hypothetical values based on conservative exposure models, rather than predictions of actual
effects from either natural or artificial sources. These numbers should be taken as upper limits,
and show that the inpact from man-made sources is small compared to the effects of normal
background radiation.
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TABLE 9
MAXIMUM INDIVIDUAL AND COLLECTIVE EFFECTIVE DOSES AND RISKS
FROM RADIATION SOURCES IN THE GREAT LAKES BASIN
SOURCES ANNUAL DOSES
Individual Collective
(mSv a"1) (man-Sv a'1)
50 YEAR DOSE AND RISK
Collective Risk
(man-Sv) (fatalities)
Natural 2.6
Fallout 1.9 (mSv
Nuclear Fuel Cycle
Mining, milling1
Conversion2
Reactor operation3
Low-level waste
94,00
to 2050)
0,65
0.044
0.01 - 0.04
4.7 x 106
6.8 x 104
15
0.1
40
<0.1
2,4 x 10s
3.4 x 103
Total Fuel Cycle
55
2.8 x 103
140
50-Year Collective Risk to Basin Population
Natural 2.4 x 10s
Weapons Fallout 3.4 x 103 (to year 2050)
Nuclear Fuel Cycle 140
Collective doses and risk for natural and fuel cycle exposures integrated over 50 years based on current dose rates;
integrated to the year 2050 for weapons fallout exposure.
Collective doses for nuclear fuel cycle based on doses per unit release, and measured emissions for Basin facilities,
1985 -1989 (UNSCEAR, 1993).
' maximum individual dose from mining activities from (NCRP 1987)
2 maximum dose from Health Canada Port Hope study (Ahier and Tracy, 1993)
3 maximum dose for reactors based on Ontario Hydro estimates (Ontario Hydro, 1994)
Source:
(Ahier and Tracy, 1994)
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Concentrations of important radionuclides in Great Lakes water that would result in a 50-year
committed effective dose equal to the ICRP (1991, 1991a) public exposure limit of 1 mSv from
a single year of consumption of drinking water (550 1 per year) are shown in Table 10, These
are compared with actual measured concentrations, which are well below the maximum derived
concentrations. The effective doses for drinking water for each lake are shown in Table 11. The
total average dose for Great Lakes water is estimated to be about 1.0 uSv for Lakes Ontario, Erie,
and Huron, and 0.7 uSv for Lake Michigan (Ahier and Tracy, 1994). These are well below the
ICRP exposure limit, and would result in two additional fatalities per year based on the maximum
effective dose to the entire Basin population. As with other estimates of risk, this estimate is an
upper limit based on the conservative assumption of a no-threshold dose model.
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TABLE 10
COMPARISON OF PROPOSED CANADIAN FEDERAL GUIDELINE CONCENTRATIONS FOR RADIONUCLIDES
IN WATER, AND ACTUAL CONCENTRATIONS IN THE GREAT LAKES
RADIONUCLJGDE
GUIDELINE CONCENTRATION
Superior
OBSERVED CONCENTRATION (Bq L'1)
Michigan Huron Erie Ontario
3H
*>Sr
137Cs
2MRa
B9JM0P,,
7,000
4
7
0.6
0.3
5.4 6.6
1.5 x 10'2 1.9 x 10 2
1.7 x IO3 1.4 x Iff3
_ —
4.4 x ID'7
9.1
2.7 x
io-2
1.1 x Iff3
0.7
4.8 x
x 10'3
Iff7
12
2.3 x
0.6 x
—
1.8 x
10'2
Iff3
io-7
8.7
2.9
1.0
1.2
1.7
x
x
X.
X
Iff2
IO3
Iff3
Iff7
U (Mg L'1)*
200
0.08
0.38
0.39
0.59
0.42
Maximum allowable concentrations in water based on an annual exposure limit of 0.1 mSv and an annual water consumption of 730 L. Water contrations from
IJC (1983) and Joshi (1991.
•"Uranium concentration given in units of ng L"1; guideline concentration corresponds to approximately 6 Bq/L.
The limit based on chemical toxicity 100 ng L"1.
Source: Ahier and Tracy, 1994.
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TABLE 11
50 YEAR COMMITTED EFFECTIVE DOSE FROM THE INGESTION OF GREAT LAKES WATER
FOR ONE YEAR
RADIONUCLIDE
50 YEAR COMMITTED EFFECTIVE DOSE (uSv)
Superior Michigan Huron Erie Ontario
3H
""Sr
137Cs
226Ra
U (natural)
0.08
0,4
0.02
0.2
0.04
0.09
0.5
0.02
0.2
0.2
0.1
0.7
0.02
0.2
0.2
0.2
0.6
0.01
0.2
0.3
0.1
0.7
0.01
0.2
0.2
TOTAL (|iSv) 0.7 1.0 1.2 1.3 1.2
Average Risk: 2 theorectically attributable fatalities per year from consumption of Great Lakes waters
Does based on concentrations from Table 10, except for226 Ra, for which a concentration of 1 mBq L"1 is assumed. Average basin
risk based on a committed effective dose of 1.2 uSv for a population of 36 million.
Source: Ahier and Tracy, 1994
Human Health Effects - SOLEC Background Paper
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In spite of strict regulations concerning the design and operation of nuclear power facilities, the
potential exists for a serious nuclear accident as a result of the large inventories of radionuclides
contained in the reactor core and spent fuel bays. Although the probability of occurrence is
small, the release into the environment of a significant fraction of this inventory could lead to
many deaths and other health effects, and would have severe social and economic consequences.
Long-range atmospheric transport and dispersion of radioactive plumes could result in the
exposure of many people to marginally or significantly elevated levels of radiation. In a similar
fashion, serious accidents outside of the Basin could also affect local ecosystems. Additional
future deaths due to cancer could occur as a result of increased collective doses. With the
engineered safeguards of North American reactors, the risks associated with a severe accident are
orders of magnitude less than risks from other natural and man-made hazards.
An area of priority over the next few decades will be the management of the substantial amounts
of high-level and low-level wastes generated by the nuclear facilities in the Basin. Current and
historic low-level waste sites are situated in the Basin. Proposed methods for permanent disposal
of high-level wastes include the deep-geological disposal concept, which is currently under
environmental review in both Canada and the United States. It is conceivable that a Canadian
facility could be located within the Baste. Due to the presence of long-lived radionuclides in the
spent fuel, the technical requirements of any disposal method are momentous. Considerable effort
is being expended to ensure that the impact on any environment in which a repository is sited
will be negligible to the far future.
5.8 Health Effects Associated with Microbial
Contaminants
Water in the Great Lakes Basin is used for drinking and recreational purposes by an estimated
40 million people. Microbial contamination of the water by human and animal sewage has been
documented at numerous sites in the region. Those drinking the water at these locations run the
risk of developing giardiasis, cryptosporidiosis, or gastrointestinal illness (Xu et al, 1994). The
largest documented waterborne outbreak in the United States history occurred hi Milwaukee,
Wisconsin during March and April of 1993. Cryptosporidium was the etiologic agent. As a result,
880,000 customers served by the Milwaukee Water Works were advised to boil their water
(Gradus, 1994). During March and April, before and after the advisory, an estimated 370,000 city
residents (roughly one quarter of those living in the metropolitan area) experienced severe
diarrhea, nausea, and stomach cramps (Edwards, 1993). There are a number of possible causes
of the outbreak of the parasite cryptosporidia in Milwaukee: 1) a combination of spring water
runoff, which overstressed the treatment system and most likely brought the parasite into the city,
2) a substitute coagulant used to settle particulates prior to sand filtration which did not filter out
the parasite, and 3) chlorination, a standard procedure in water treatment, is not effective in
killing the parasite hence making the other physical treatment procedures all the more important.
Among bathers, higher rates of gastrointestinal, respiratory, eye, ear, and skin infections have
been noted. A Canadian prospective study of swimming-related illness showed that swimmers
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experienced respiratory ailments most frequently followed by gastrointestinal, eye, ear, and skin
symptoms (Seyfried et al, 1985a, 1985b). A second Canadian prospective study in 1989 reported
similar results (Lightfoot, 1989). A similar survey in New Jersey showed that the beachgoers had
red itchy eyes and sore throat most commonly, followed by skin rash, gastrointestinal illness and
ear infections (New Jersey Department of Health, 1990), The New Jersey researchers suggested
that the illnesses may have resulted from person to person transmission of viruses rather than
sewage contamination. The difference between gastrointestinal illness rates among swimmers
and nonswimmers in the 1985 Canadian epidemiological study was similar to those observed by
Cabelli (1982, 1983) and the New Jersey survey, i.e. an excess of 13.3 cases per 1000 in Canada
compared with excesses of 4.0 to 16.0 cases per 1000 in Cabelli's studies and an excess of 12.2
cases per 1000 in the New Jersey survey.
The bacteria used as water quality indicators in the epidemiological surveys are not the
etiologieal agents of the illnesses which they index. For this reason it has been difficult to
demonstrate a relationship between the bacteriological quality of the water and adverse health
effects. A number of new water quality indicators, such as the F2 bacteriophage to assess viral
survival in receiving waters, have been proposed but are still under investigation (Xu et al.,
1994).
Future studies on the relationship between health effects and water quality in the Great Lakes
Basin should include other bacteria and viruses, in addition to the usual fecal indicator bacteria.
Furthermore, water sampling and microbial monitoring should be carried out as frequently as
possible during the survey. Finally, clinical investigations could be included in the determination
of illness rates in order to rninirnize the effects caused by respondents and interviewers.
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6.0 Knowledge Gaps and Directions
for Future Research
Recent research into the human health effects of exposure to Great Lakes contaminants, including
risk assessment methodologies, has focused on the potential for pollutants to cause cancer, birth
defects and related readily observable health outcomes. This traditional evaluation of the
significance of environmental pollution in terms of adverse health effects pervades both health
policy and regulatory policy. The focus on cancer as a health effect endpoint of environmental
contamination reflects a valid scientific and public concern. However, an important point arising
from the Great Lakes research community is that the public health implications of toxic pollution
go well beyond cancer to other health effects priorities. Great Lakes researchers have revealed
evidence that some health effects of toxic pollutants may be more subtle and far-reaching than
previously thought. Accordingly, a more holistic approach to evaluating human health effects
requires identifying, assessing and monitoring potential noncancer endpoints in order to develop
and implement effective remedial action strategies. The Great Lakes research community is
currently breaking new ground in its research into potential human health impacts in a number
of areas, such as immunotoxicity, reproductive outcomes additional to birth defects, neurotoxicity
and developmental effects, respiratory health effects, and newer concerns such as multiple
chemical sensitivity (MCS) (Bell, 1994; Miller, 1994). As a result, the Great Lakes research
agenda provides a fitting model for such environmental health effects research worldwide.
However, researchers have identified a number of gaps in our knowledge of the actual and
potential human health effects of chronic, low-level exposure to Great Lakes contaminants.
Consequently, there are several potential research areas that decision-makers might consider in
efforts to expand our knowledge in this field:
* Exposure: Further research is required to improve exposure data (including expanded routine
monitoring of priority air pollutants) so that quantitative exposure-response relationships can be
determined -- i.e., linking tissue contaminant levels with health effects endpoints, including
noncancer endpoints (e.g., immunological, neurological, reproductive).
* There is also a need to monitor Great Lakes populations exposed to persistent toxic substances
to evaluate whether or not they are accumulating body burdens at higher rates than the national
average, and to identify highly exposed groups. Monitoring could include long-term surveillance
to determine trends in contamination.
4 As well, further study of pathways of exposure other than fish consumption is required, and
related risks assessed ~ e.g., for ingestion of drinking water, inhalation of polluted air, and
consumption of contaminated locally grown meat and dairy products. Research is also needed
to examine the potential for dermal absorption of Basin water contaminants during bathing at
home or in Great Lakes waters. PAHs from Basin sludge located near the lakeshores in
contaminated areas needs special attention.
Human Health Effects • SOLEC Background Paper 63
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* Chemical Mixtures: Additional research is required to better define the potential interactions
among the many Great Lakes contaminants to determine the net effect of exposure to mixtures
of environmental pollutants, i.e., a more holistic evaluation of the risk these chemicals pose to
human health. Research is also required to develop better technologies for measuring exposure
to multiple chemicals and subtle related effects on health.
* Range of Endpoints: There is a need to identify the most sensitive and reliable health effect
endpoints and to broaden the range beyond cancer and birth defects in order to better assess the
risks to human health associated with chronic low-level exposure to Great Lakes contaminants.
The endpoints monitored should include neurological, endocrinological, immunological,
respiratory, cancer and reproductive effects ~ including those of growing public concern, such
as breast cancer and multiple chemical sensitivity.
* In addition, the majority of biomarkers of effect and susceptibility are currently limited in their
use because they are non-specific and can apply to a variety of environmental contaminants.
There is a need to develop biomarkers that are more sensitive and specific to particular chemical
exposures.
• Epidemiological studies: Baseline data from epidemiological studies are required to quantify
the health effects of exposure to low environmental concentrations of specific contaminants,
including air pollutants, in a way that accounts for them apart from the many other known risk
factors (e.g., socio-economic and lifestyle factors, biological and occupational exposures); and
to determine whether the incidence of adverse health effects for individuals living within the
Great Lakes Basin differs from that observed in other areas of Canada and the United States.
• In the design of epidemiological studies, identification and verification of high-risk, high-
exposure cohorts, consideration of past exposure histories and other risk factors for adverse health
effects are critical.
4 There is a further need for information on the long-term health effects on children exposed in
utero and in early childhood to low levels of persistent environmental Great Lakes toxicants.
Indications are that such health effects as might exist are not necessarily expressed as classical
physical disease. Rather, the endpoints may be psychosocial in nature and require long-term
neurobehavioral and biochemical assessments to detect what might be subtle effects. For
example, there have been calls for more studies of behavioral, developmental, and immune
system characteristics as well as of stages of sexual development in growing children (Colborn
el al, 1990, cited in Jordan-Simpson et al, 1994). There is also a need to study delayed effects
that may occur after puberty, such as endometriosis and premature reproductive senescence.
4 Subpopulations at special risk: With regard to relative risks, future public research efforts
should be focused on those subpopulations which have the highest potential for exposure, such
as people who eat large amounts of contaminated fish or wildlife from the Great Lakes, and those
who live near hazardous waste sites. Of particular concern are people whose immune systems
are already suppressed either through medication or certain disease states; developing fetuses and
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infants; the oldest population groups, and others who are especially vulnerable to adverse health
effects.
Human Health Effects - SOLEC Background Paper 65
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7.0 Conclusions
It is clear that occupational or accidental exposure to high levels of certain contaminants
discussed in this paper — PCBs, dioxins, organochlorine pesticides, lead, and
metkylmercury — pose a risk to human health. While the exact nature and extent of the
health risk from exposure to environmental levels of these chemicals in the Great Lakes
ecosystem are unclear and require further study.
Because of the limitations inherent in human health effects research, the study of potential
effects and their use as a gauge for "State of the Lakes" water quality are problematic,
and thus the "weight of evidence" approach includes a substantial amount of data from
laboratory animal and wildlife studies. In addition to data from (limited) epidemiologic
studies, adverse reproductive, developmental, behavioural, endocrine, and immunologic
effects have been observed in laboratory animal studies and across a range of wildlife
species exposed to mixtures of these persistent toxic chemicals present in the Great Lakes
Basin. While differences exist between humans and animal life, these findings are
indicators of a potential risk to human health at certain levels of exposure, and warrant
further study.
Furthermore, traditional health outcomes such as cancer and birth defects, which are
relatively severe and well recorded, may be comparatively insensitive indicators of the
effects of low-level exposure to environmental contaminants. There is a need for further
study of the less severe, more subtle adverse health effects of long-term, low-level
exposures to mixtures of chemicals, including effects on human reproduction (additional
to birth defects), the immune, endocrine, respiratory and circulatory systems; and on
neurobehaviour, development in children, and psycho-social health status.
The uncertainty as to whether these chemicals (PCBs, dioxins, organochlorine pesticides,
lead, and methylmercury) have long-term adverse health effects on humans is
predominantly in the quantification of the dose-response relationship; i.e., what level of
exposure is required to observe an adverse effect.
Comprehensive data on contaminant exposure levels in Great Lakes populations compared
to those in other populations worldwide are lacking. With regard to fish consumption as
a major route of exposure, there is some evidence that the contaminant levels seen in
people who live in the Basin and consume fish are no greater than levels in populations
elsewhere. Whether or not this is attributable to lower levels of toxic chemicals in fish
is uncertain. However, recent evidence suggests that certain subpopulations that are
traditionally large fish-eaters (i.e., sports anglers and Native people) have changed their
fish consumption habits, either by consuming less fish or by modifying their fish-cleaning
and preparation methods in response to health advisories.
Human Health Effects - SOLEC Backgmund Paper 67
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4) While it is clear that fish consumption is a major route of human exposure to persistent
chemicals in the Great Lakes, those other than Native people who consume large amounts
of fish make up a minority of the Great Lakes population. When measuring total
exposure to Great Lakes contaminants as part of an integrated exposure assessment, other
exposure routes — i.e., ingestion of drinking water, inhalation of polluted air,
consumption of contaminated meat or dairy products and, to a much lesser degree, dermal
exposure to water contaminants — must also be considered.
5) With respect to the other groups of environmental contaminants discussed in this paper,
there is strongly suggestive evidence from the Great Lakes Basin linking ground-level
ozone, airborne particles and acid aerosols to significant respiratory health effects,
including illness requiring hospital admission, and death. There is also evidence from the
Basin that these pollutants cause reduced lung function in children. This evidence is
consistent with data from elsewhere in North America and Europe.
Available data show that the health impact of exposure to radionuclides from man-made
sources appears to be small compared to the effects of normal background radiation.
Health effects of microbial contaminants have not been adequately studied, but there are
indications of increased incidences of short-term infections in users of recreational waters
and in consumers of treated drinking water.
7) Based on our knowledge thus far, it would appear that some subpopulations in the Great
Lakes Basin may have greater sensitivity to low levels of environmental contaminants,
and could be at higher risk than is the general population. These would include the fetus
and newborn infant, children, the elderly, and those in ill health. Sportsmen and Native
people who consume large amounts of contaminated fish and wildlife may also be at
higher risk because of their increased exposure to persistent toxic chemicals.
8) Finally, identifying research data gaps (as outlined in the preceding section) and
exploring directions for future essential research ~ ranging from integrated exposure
assessments, to body burden estimates, to a broader spectrum of health effect endpoints -
- should be a priority to help reduce the uncertainties in our knowledge of the potential
short- and long-term adverse human health effects of exposure to environmental
contaminants in the Great Lakes Basin.
68
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Legend
15
Figure 1. Number of days per year with ozone levels in excess of the one-hour air quality objective of 82 ppb.
Data Source: Hilborn, J, and Still, M,, 1990. A State erf the Environment Report: Canadian Perspectives on Air Pollution. Ministry of the Environment
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120ug/m3
160
Oug/m3
I Average PMio Concentration
•Maximum PMio Concentration
SaultSte. Marie
Source: Ontario Ministry of the Environment and Energy, 1992.
Flaure 2. PMm Concentrations at 9 Urban Sites in Ontario, 1991.
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Sulphate Levels
10 ug/n?
Dug/in
Source: Burnett etal 1993
Figure 3. Sulphate Concentrations at Selected Sites in Ontario, 1983 -1988.
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B1OMARKERS OF EXPOSURE
HAIR
BLOOD
MILK
URINE
FECES
FOOD
WATER
AIR
SOIL
Absorption
Distribution
Excretion
Residue Analysis
Residue Analysis
SOUHOB: Feetey, 1993.
Rgure 4.
-------
Gastrointestinal!
Tract
Dermal or
Eye Contact 1
Other Body
Organs
Blood & Lymph
(Heart, Blood V<
Lymphatic System)
Bladder
Exposure
Absorption
Storage
Extracellular
Fluid
L
Secretory
Glands
t
[
L
r
^
^
-+
Fat I
Bones |
- « •
""""T"""
I
:
T , +
Expired f
Urine
t
Secretion
5
Excretion
Source: RodrickB, J.V., 1992
Rgure 5.
-------
Zion
Legend
a Uranium Mining Area (Closed)
t Uranium Mining Area
ift Nuclear Generating Stations
m Uranium Refinery/Fuel Fabrication Plant
e Waste Management Sites
I Fuel Reprocessing Plant (Closed)
^Bancroft
iPeterborough /
Nine Mile Point
Fitepatrick
Source: Abler, Tracy, 1993.
Figure 6. Nuclear facilities in the Great Lakes Basin.
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