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How a chemical enters a person's blood after the chemical has been swallowed, has come into contact with the skin, or has been breathed in.

Acute Exposure:
Contact with a chemical that happens once or only for a limited period of time. ATSDR defines acute exposures as those that might last up to 14 days.

Adverse Health Effect:
A change in body function or the structures of cells that can lead to disease or health problems.

The Agency for Toxic Substances and Disease Registry. ATSDR is a federal health agency in Atlanta, Georgia, that deals with hazardous substances and waste site issues. ATSDR gives people information about harmful chemicals in their environment and tells people how to protect themselves from coming into contact with chemicals.

Background Level:
An average or expected amount of a chemical in a specific environment. Or, amounts of chemicals that occur naturally in a specific environment.

Used in public health, things that humans would eat, including animals, fish and plants.

A group of diseases which occur when cells in the body become abnormal and grow, or multiply, out of control.

Cancer Slope Factor (CSF):
Used to define the relationship between exposure doses and the likelihood of an increased risk of developing cancer over a lifetime. CSFs are developed using data from animal or human studies and represent the upper-bound estimate of the probability of developing cancer at a defined level of exposure and tend to be very conservative (i.e., overestimate the actual risk) in order to account for a number of uncertainties in the data.

Cancer Risk Evaluation Guide (CREG):
An estimated contaminant concentration in water, soil, or air that would be expected to cause no more than one excess cancer in a million persons exposed over a 70-year lifetime, according to U.S. Environmental Protection Agency (EPA) estimates. As ATSDR's most conservative comparison value, the CREG merits special attention. Note that this does not mean that exposures equivalent to the CREG are actually expected to cause one excess cancer in a million persons exposed over a lifetime. Nor does it mean that every person in an exposed population of one million has a 1-in-a-million chance of developing cancer from the specified exposure. Although ATSDR CREGs continue to be useful devices for screening cancer-causing substances at a site, they cannot be used to predict cancer incidence rates at a site. Furthermore, the exposure assumptions on which EPA's cancer risk estimates and ATSDR's CREGs are based (i.e., essentially lifetime exposure) seldom apply at contaminated sites.

Chronic Exposure:
A contact with a substance or chemical that happens over a long period of time. ATSDR considers exposures of more than one year to be chronic.

Completed Exposure Pathway:
See Exposure Pathway.

Comparison Value (CV):
Concentrations or the amount of substances in air, water, food, and soil that are unlikely, upon exposure, to cause adverse health effects. Comparison values are used by health assessors to select which substances and environmental media (air, water, food and soil) need additional evaluation while health concerns or effects are investigated.

Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA):
CERCLA was put into place in 1980. It is also known as Superfund. This act concerns releases of hazardous substances into the environment, and the cleanup of these substances and hazardous waste sites. ATSDR was created by this act and is responsible for looking into the public health issues related to hazardous waste sites.

A belief or worry that chemicals in the environment might cause harm to people.

How much or the amount of a substance present in a certain amount of soil, water, air, or food.

See Environmental Contaminant.

Dermal Contact:
A chemical getting onto your skin. (see Route of Exposure).

The amount of a substance to which a person might be exposed, usually on a daily basis. Dose is often explained as "amount of substance(s) per body weight per day."

The amount of time (days, months, years) that a person is exposed to a chemical.

Environmental Contaminant:
A substance (chemical) that gets into a system (person, animal, or the environment) in amounts higher than that found in Background Level, or what would be expected.

Environmental Media:
Usually refers to the air, water, and soil in which chemicals of interest are found. Sometimes refers to the plants and animals that are eaten by humans. Environmental Media is the second part of an Exposure Pathway.

Environmental Media Evaluation Guide (EMEG):
A concentration of a contaminant in water, soil, or air that is unlikely to be associated with any appreciable risk of deleterious noncancer effects over a specified duration of exposure. EMEGs are derived from ATSDR Minimal Risk Levels by factoring in default body weights and ingestion rates. Separate EMEGs are computed for acute ( 14 days), intermediate (15-364 days), and chronic (365 days) exposures.

U.S. Environmental Protection Agency (EPA):
The federal agency that develops and enforces environmental laws to protect the environment and the public's health.

The study of the different factors that determine how often, in how many people, and in which people disease will occur.

Coming into contact with a chemical substance. (For the three ways people can come in contact with substances, see Route of Exposure.)

Exposure Assessment:
The process of finding the ways people come in contact with chemicals, how often and how long they come in contact with chemicals, and the amounts of chemicals with which they come in contact.

Exposure Pathway:
A description of the way that a chemical moves from its source (where it began) to where and how people can come into contact with (or get exposed to) the chemical.
ATSDR defines an exposure pathway as having five parts:
  1. Source of Contamination,
  2. Environmental Media and Transport Mechanism,
  3. Point of Exposure,
  4. Route of Exposure, and
  5. Receptor Population.

When all five parts of an exposure pathway are present, it is called a Completed Exposure Pathway. Each of these five terms is defined in this glossary.

How often a person is exposed to a chemical over time; for example, every day, once a week, twice a month.

Hazardous Waste:
Substances that have been released or thrown away into the environment and, under certain conditions, could be harmful to people who come into contact with them.

Health Effect:
ATSDR deals only with Adverse Health Effects (see definition in this glossary).

Indeterminate Public Health Hazard:
The category is used in public health assessments for sites where important information is lacking (missing or has not yet been gathered) about site-related chemical exposures.

Swallowing something, as in eating or drinking. It is a way a chemical can enter your body (See Route of Exposure).

Breathing. It is a way a chemical can enter your body (See Route of Exposure).

Lifetime Health Advisory (LTHA):
A contaminant concentration that EPA deems protective of public health (considering the availability and economics of water treatment technology) over a lifetime (70 years) at an exposure rate of 2 liters of water per day.

Lowest Observed Adverse Effect Level. The lowest dose of a chemical in a study, or group of studies, that has caused harmful health effects in people or animals.

Maximum Contaminant Level (MCL):
A contaminant concentration in drinking water that EPA deems protective of public health (considering the availability and economics of water treatment technology) over a lifetime (70 years) at an exposure rate of 2 liters of water per day.

Minimal Risk Level (MRL):
An estimate of daily human exposure--by a specified route and length of time--to a dose of chemical that is likely to be without a measurable risk of adverse, noncancerous effects. An MRL should not be used as a predictor of adverse health effects.

National Priorities List:
Part of Superfund, a list kept by EPA of the most serious, uncontrolled, or abandoned hazardous waste sites in the country. An NPL site needs to be cleaned up or is being looked at to see if people can be exposed to chemicals from the site.

No Observed Adverse Effect Level. The highest dose of a chemical in a study, or group of studies, that did not cause harmful health effects in people or animals.

No Apparent Public Health Hazard:
The category is used in ATSDR's public health assessments for sites where exposure to site-related chemicals might have occurred in the past or is still occurring but the exposures are not at levels expected to cause adverse health effects.

No Public Health Hazard:
The category is used in ATSDR's public health assessments for sites where there is evidence of an absence of exposure to site-related chemicals.

A line or column of air or water containing chemicals moving from the source to areas further away. A plume can be a column or clouds of smoke from a chimney or contaminated underground water sources or contaminated surface water (such as lakes, ponds, and streams).

Point of Exposure:
The place where someone can come into contact with a contaminated environmental medium (air, water, food, or soil). For example:
the area of a playground that has contaminated dirt, a contaminated spring used for drinking water, the location where fruits or vegetables are grown in contaminated soil, or the backyard area where someone might breathe contaminated air.

A group of people living in a certain area; or the number of people in a certain area.

Public Health Assessment (PHA):
A report or document that looks at chemicals at a hazardous waste site and tells if people could be harmed from coming into contact with those chemicals. The PHA also tells if possible further public health actions are needed.

Public Health Hazard:
The category is used in PHAs for sites that have certain physical features or evidence of chronic, site-related chemical exposure that could result in adverse health effects.

Public Health Hazard Category:
PHA categories given to a site which tell whether people could be harmed by conditions present at the site. Each are defined in the glossary. The categories are:
  1. Urgent Public Health Hazard
  2. Public Health Hazard
  3. Indeterminate Public Health Hazard
  4. No Apparent Public Health Hazard
  5. No Public Health Hazard

Receptor Population:
People who live or work in the path of one or more chemicals, and who could come into contact with them (See Exposure Pathway).

Reference Dose (RfD):
An estimate, with safety factors (see safety factor) built in, of the daily, life-time exposure of human populations to a possible hazard that is not likely to cause harm to the person.

Reference Dose Media Evaluation Guide (RMEG):
The concentration of a contaminant in air, water, or soil that corresponds to EPA's RfD for that contaminant when default values for body weight and intake rates are taken into account.

Risk-Based Concentration (RBC):
EPA Region III combines reference doses and cancer slope factors with "standard" exposure scenarios to calculate risk-based concentrations, which are chemical concentrations corresponding to fixed levels of risk (i.e., a hazard quotient of 1, or lifetime cancer risk of 10-6, whichever occurs at a lower concentration) in water, air, fish tissue, and soil.

Route of Exposure:
The way a chemical can get into a person's body. There are three exposure routes:
- breathing (also called inhalation),
- eating or drinking (also called ingestion), and
- getting something on the skin (also called dermal contact).

Safety Factor:
Also called Uncertainty Factor. When scientists don't have enough information to decide if an exposure will cause harm to people, they use "safety factors" and formulas in place of the information that is not known. These factors and formulas can help determine the amount of a chemical that is not likely to cause harm to people.

The Superfund Amendments and Reauthorization Act in 1986 amended the Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA) and expanded the health-related responsibilities of ATSDR. CERCLA and SARA direct ATSDR to look into the health effects from chemical exposures at hazardous waste sites.

Source (of Contamination):
The place where a chemical comes from, such as a landfill, pond, creek, incinerator, tank, or drum. Contaminant source is the first part of an Exposure Pathway.

Another name for the Comprehensive Environmental Response, Compensation, and Liability Act, which created ATSDR.

A way to collect information or data from a group of people (population). Surveys can be done by phone, mail, or in person. ATSDR cannot do surveys of more than nine people without approval from the U.S. Department of Health and Human Services.

Synergistic effect:
A health effect from an exposure to more than one chemical, where one of the chemicals worsens the effect of another chemical. The combined effect of the chemicals acting together are greater than the effects of the chemicals acting by themselves.

Harmful. Any substance or chemical can be toxic at a certain dose (amount). The dose is what determines the potential harm of a chemical and whether it would cause someone to get sick.

The study of the harmful effects of chemicals on humans or animals.

Abnormal growth of tissue or cells that have formed a lump or mass.

Uncertainty Factor:
See Safety Factor.

Urgent Public Health Hazard:
This category is used in ATSDR's public health assessments for sites that have certain physical features or evidence of short-term (less than 1 year), site-related chemical exposure that could result in adverse health effects and require quick intervention to stop people from being exposed.

Volatile Organic Compound (VOC):
A substance containing carbon and different proportions of other elements, such as hydrogen, oxygen, fluorine, chlorine, bromine, sulfur, or nitrogen. VOCs easily become vapors or gases, and a significant number of them are commonly used as solvents (paint thinners, lacquer thinner, degreasers, and dry cleaning fluids).


Estimates of Human Exposure Doses and Determination of Health Effects

Deriving Exposure Doses

The Agency for Toxic Substances and Disease Registry (ATSDR) estimated human exposure dosesfrom ingestion of shellfish and fish harvested from Willoughby Bay. Deriving exposure dosesrequires evaluating the concentrations of the contaminants to which people might have been ormight be exposed and how often and for how long exposures to those contaminants occur. Together,these factors help influence individual physiological responses to contaminant exposure andpotential for noncancer or cancer outcomes. In the absence of exposure-specific information,ATSDR applied several conservative assumptions to define site-specific exposures as accurately aspossible for people consuming contaminated fish and shellfish.

Evaluating Potential Health Hazards

Estimated exposure doses are used to evaluate potential noncancer and cancer effects associated withcontaminants detected in site media. When evaluating noncancer effects, ATSDR first comparesthe estimated exposure dose to standard toxicity values, including ATSDR's minimal risk levels(MRLs) and the U.S. Environmental Protection Agency's (EPA's) reference doses (RfDs), toevaluate whether adverse effects might occur. The MRLs and RfDs are estimates of daily humanexposure to a substance that is likely to be without appreciable risk of adverse noncancer effectsover a specified duration. The MRLs and RfDs are conservative values, based on the levels ofexposure reported in the literature that represent no observed adverse effects levels (NOAELs) orlowest observed adverse effects levels (LOAELs) for the most sensitive outcome for a given route ofexposure (e.g., dermal contact, ingestion). In addition, uncertainty (safety) factors are applied toNOAELs or LOAELs to account for variation in the human population and uncertainty involved inextrapolating human health effects from animal studies. If estimated exposure doses are greater thanthe appropriate MRL or RfD, ATSDR reviews the toxicological literature to determine thelikelihood of adverse effects.

When evaluating the potential for cancer to occur, ATSDR uses cancer slope factors (CSFs) thatdefine the relationship between exposure doses and the likelihood of an increased risk of developingcancer over a lifetime. The CSFs are developed using data from animal or human studies and oftenrequire extrapolation from high exposure doses administered in animal studies to lower exposurelevels typical of human exposure to environmental contaminants. CSFs represent the upper-boundestimate of the probability of developing cancer at a defined level of exposure; therefore, they tend tobe very conservative (i.e., overestimate the actual risk) in order to account for a number ofuncertainties in the data used in the extrapolation.

ATSDR estimated the potential for cancer to occur using the following equation. The estimatedexposure doses and CSF values for the contaminants of concern are incorporated into the equation:

Lifetime cancer risk =Estimated exposure dose (milligrams of contaminants per kilogram bodyweight per day [mg/kg/day]) x CSF (mg/kg/day)-1

Although no risk of cancer is considered acceptable, because a zero cancer risk is not possible toachieve, ATSDR often uses a range of 10-4 to 10-6 estimated lifetime cancer risk (or 1 new case in10,000 to 1,000,000 exposed persons), based on conservative assumptions about exposure, todetermine whether there is a concern for cancer effects.

Estimated Exposure Dose for Consumption of Shellfish or Fish from Willoughby Bay

Shellfish and fish samples collected from Willoughby Bay over the last 30 years have containedelevated levels of PAHs, pesticides, PCBs, and metals. People consuming fish and shellfish might beexposed to these contaminants. Levels would be expected to have been at their highest prior to themid-1970s, before Naval Station Norfolk's industrial wastewater was rerouted to an industrialwastewater treatment plant. In addition, increasing wastewater and stormwater managementrequirements would be expected to result in a decline in levels of contaminants reaching the bay insubsequent years.

To determine whether exposures to contaminants in shellfish or fish might be related to adversehealth effects, ATSDR estimated exposure doses for people consuming these aquatic biota. We didnot identify any information suggesting that subsistence fishing occurs in Willoughby Bay. Inestimating to what extent people might be exposed to contaminants, we used conservativeassumptions about how much fish and shellfish people eat, how often exposures occur, and for howlong exposures last, as well as conservative assumptions about contaminant concentrations (i.e., thatall exposures were to the highest levels of contaminants detected). These assumptions allow ATSDRto estimate the highest likely exposure dose, on the basis of our understanding of site-specificconditions, and evaluate the corresponding health effects. Although we expect that few people areregularly exposed at these levels, the conservative estimates are used to protect public health.ATSDR used the following equation and exposure assumptions to estimate exposure doses:

Estimated exposure dose equals C times IR times EF times ED divided by BW times AT

C = Maximum concentration (milligrams per kilogram [mg/kg])
IR = Intake rate:
Chronic intake for adults = 0.035 kg/day (approximately five 8-ounce fish or shellfish servings/month); for children = 0.0175 kg/day (approximately five 4-ounce fish or shellfish servings/month)(3)
Acute intake for adults = 0.326 kilograms/serving (11.4 ounces);
for children = 0.170 kilograms/serving (about 6 ounces)(4)
EF = Exposure frequency: 365 days/year
ED = Exposure duration or the duration over which exposure occurs:
adult = 30 years; child = 5 years
BW = Body weight: adult = 70 kg (154 pounds); child = 10 kg (22 pounds)
AT = Averaging time or the period over which cumulative exposures are averaged:
5 years or 30 years x 365 days/year for noncancer effects and 70 years
(considered a lifetime) x 365 days/year for cancer effects

On the basis of estimated exposure doses and review of the relevant toxicologic literature, ATSDR concluded that exposures to contaminants in fish and shellfish harvested from Willoughby Bay would not be expected to result in any long-term health effects. However, acute exposure to some of the elevated levels of zinc in fish or shellfish might cause temporary decreases in serum cortisol levels or short-term gastrointestinal distress. For the most part, these concentrations were detected in oysters, but there has been no documented oyster harvest from Willoughby Bay since 1972. In 2001 samples from a range of seafood species, the detected concentrations of zinc in species other than oysters would not be expected to cause any adverse health effects. ATSDR's evaluation of chemical-specific exposures is detailed as follows.


Not all of the contaminants detected in fish and shellfish from Willoughby Bay have the potential tocause cancer. ATSDR evaluated contaminants that could potentially cause cancer, includingarsenic, benzo(a)pyrene, benzo(b)fluoranthene, 4,4'-DDD, 4,4'-DDE, 4,4'-DDT, heptachlor epoxide,and PCBs/Aroclor-1254. For all contaminants, the derived lifetime cancer risk for exposure tocontaminants is below levels that are likely to result in increased instances of cancer.


ATSDR's calculated noncancer doses assume that people were exposed to the maximum detectedconcentration over the entire exposure period. ATSDR used conservative assumptions aboutconsumption rates and levels and the length of exposures. The calculated doses were then comparedto ATSDR's MRLs or EPA's RfDs. Calculated noncancer doses were below the associated MRLsor RfDs for most contaminants. The exceptions are discussed below. The contaminants for whichnoncancer doses calculated using ATSDR's conservative assumptions exceeded MRLs or RfDswere arsenic, cadmium, mercury, thallium, and zinc. ATSDR concluded that ingestion of arsenic,cadmium, mercury, and thallium in aquatic biota from Willoughby Bay would not be expected toresult in any adverse health effects and that ingestion of zinc would not be expected to result in anylasting health consequences, but might cause serum cortisol levels to decline temporarily or mightcause short-term gastrointestinal distress. The calculated doses for chromium are below the RfD forchromium III, the type of chromium expected to be present in aquatic biota.

There are no MRLs or RfDs for lead. ATSDR's evaluation of the potential for adverse health effectsfrom lead, provided below, is based on expected increases in blood lead levels, which have beenshown to be correlated to adverse health effects. This evaluation concluded that adverse healtheffects due to consumption of lead in fish or shellfish from Willoughby Bay would not be expected.


Arsenic exists in nature in both organic and inorganic forms. Organic forms are essentially non-toxic, while inorganic forms can produce a variety of health effects. Available samples fromWilloughby Bay measured total arsenic. The detected concentrations in fish and shellfish fromWilloughby Bay ranged from <0.5 mg/kg in (a 1998 spot sample and 2001 samples of blue crabs,croaker, spot, oysters, and hard clams), to 1.1 mg/kg in a 1998 crab sample, to 2.5 mg/kg in a 1986clam sample, to 3.0 mg/kg in a 1994 oyster sample. Scientific research indicates that most arsenicpresent in fish and shellfish is in a non-toxic organic form. According to studies, the inorganiccomponent of arsenic accounts for 10%-20% of the total arsenic in fish and shellfish (FDA 1993a,ATSDR 2000). ATSDR's dose calculations for inorganic arsenic are based, therefore, on exposureto a conservatively estimated 20% of the maximum concentration of total arsenic detected in asample, or 0.6 mg/kg.

ATSDR's estimated chronic dose for adults (0.0003 mg/kg/day) does not exceed the chronic MRLof 0.0003 mg/kg/day, and ATSDR's estimated chronic dose for children (0.001 mg/kg/day) onlyslightly exceeds the chronic MRL. Furthermore, the doses estimated based on chronic exposure tothe maximum level of arsenic detected are lower than the lowest level at which health effects werereported in the scientific literature (the lowest LOAEL), 0.005 mg/kg/day. Because continuousexposures to the highest detected concentration of inorganic arsenic in fish or shellfish fromWilloughby Bay is unlikely to occur, chronic exposure to arsenic is not expected to cause anyadverse health effects.

The estimated acute dose of arsenic to children was estimated at 0.01 mg/kg/day, which exceedsATSDR's provisional acute MRL (0.005 mg/kg/day). However, ATSDR's assumption that a smallchild is consuming an approximately 6-ounce serving of fish or shellfish in one meal (acuteexposure) is very conservative. Also, the lowest LOAEL reported in the literature for acute exposureis 0.05 mg/kg/day, 10 times higher than the MRL and higher than the worst-case dose that ATSDRestimated (ATSDR 2000). Thus, adverse effects from acute exposures to arsenic are not expected.


Cadmium occurs naturally in the earth's crust, but it is also used to plate certain aircraft parts and inother products used at Naval Station Norfolk. The highest detected concentrations of cadmium inaquatic biota from Willoughby Bay, 6.06 mg/kg (1971) and 3.7 mg/kg (1976), have been found inoyster samples. Since 1985, all detected concentrations have been below 1 mg/kg, except in one1987 sample, which contained 3.1 mg/kg of cadmium. A 2001 VDEQ oyster sample contained 0.1mg/kg of cadmium. Only a few samples from aquatic biota other than oysters have been analyzedand the maximum detected concentration was 0.02 mg/kg (in spot, collected in 1998). In 2001,samples of blue crab, croaker, spot, and hard clams were found to contain cadmium levels lowerthan the detection limit (0.01 mg/kg).

Using conservative assumptions for estimating seafood exposure doses based on the maximumdetected concentration of cadmium in oysters, ATSDR estimated a chronic adult dose (0.003mg/kg/day) and a chronic child dose (0.011 mg/kg/day) that exceeds the chronic oral RfD, 0.001mg/kg/day for food intake. Because the absorption and distribution of cadmium in the body has beenwell studied, scientists have been able to predict (using a model) the NOAEL or level of cadmiumintake at which adverse health effects would not be expected to result after chronic exposure. TheRfD is based on this NOAEL, which is 0.01 mg/kg/day, multiplied by an uncertainty factor of 10 toaccount for variability between people. A review of most chronic toxicity studies showed LOAELsat doses above 1 mg/kg/day (ATSDR 1999b).

The oyster population in Willoughby Bay is not sufficiently large for any commercial oyster harvestto have reported since 1972, when Virginia first implemented a voluntary commercial catchreporting system (which became mandatory in 1992) (VMRC 2001). For about the last 20 years,any recreational harvesting of oysters has been limited because disease caused a steep decline in thepopulation. Hard clams, blue crabs, and fish are sufficiently abundant that they are commerciallyharvested. Since 1985, levels of cadmium measured in oyster samples have generally been below 1mg/kg. Doses associated with these concentrations are well below levels shown to result in adversehealth effects. Oysters are reported to bioaccumulate cadmium at substantially higher rates thanother marine species, including other bivalves (Dixon et. al 1993). Results from VDEQ's 2001samples of hard clams, blue crabs, fish, and oysters were consistent with this finding.

Because ATSDR's conservative dose estimates resulted in doses lower than the LOAELs and theNOAEL, oyster consumption is infrequent, and other aquatic biota are expected to contain lowerlevels of cadmium than those found in oysters, exposures to cadmium are not expected to causeadverse health effects.


Chromium is present in the environment in several different forms, including chromium VI andchromium III. Chromium III is an essential nutrient (i.e., required by the human body). TheNational Academy of Sciences recommends that the adult diet include 0.05 to 0.2 mg/kg ofchromium III/day and that the diet of a child (aged 4 to 6) include 0.03 to 0.12 mg/kg/day(recommendations for younger children are lower). Chromium III occurs naturally in theenvironment and is used in certain industrial processes, while chromium VI is generally produced byindustrial processes. Chromium VI is reduced to chromium III in water.

The forms of chromium present in fish and shellfish samples from Willoughby Bay were notspecified, but chromium in fish and shellfish is normally present entirely as chromium III.Chromium was only detected in 12 of 41 samples, and the highest concentration was 74 mg/kg. Nochromium was detected in any of the fish or shellfish samples collected in 2001 (at concentrationsabove the detection limit of 0.05 mg/kg). Using the highest reported concentration, ATSDRestimated an adult dose of 0.04 mg/kg/day and a child dose of 0.13 mg/kg/day. While these dosesexceed ATSDR's provisional guidance for oral exposure to chromium VI (0.003 mg/kg/day, basedon the upper range of the estimated safe and adequate daily dietary intake), they are well below theRfD for chromium III (1.5 mg/kg/day), the type of chromium expected to be present in aquatic biota(ATSDR 2001b; FDA 1993b). Thus, exposure to chromium is not expected to result in adversehealth effects.


The highest detected concentrations of lead in biota samples from Willoughby Bay were 6.19 mg/kg(blue crab) and 2.52 mg/kg (spot), both measured in 1971. A second spot analyzed in 1971contained 1.35 mg/kg of lead. No samples were analyzed for lead between 1971 and 1985. Duringmuch of this period, a fishing ban was in effect in Willoughby Bay due to the upstream release ofkepone. In 18 oyster samples collected between 1985 and 1993, lead levels reached only 2 mg/kg,and in 13 oyster samples collected since 1994, lead levels have been below 1 mg/kg. In 2001samples from oysters and hard clams, the detected concetrations of lead were 0.10 mg/kg and 0.13mg/kg, respectively. In 1998 and 2001, two spot samples, a croaker sample, and two blue crabsamples did not contain levels of lead exceeding 0.1 mg/kg. Based on our understanding of likelyfish and shellfish consumption patterns, data from available samples, and our review of thetoxicology literature addressing lead, ATSDR concluded that lead levels in fish and shellfish fromWilloughby Bay are not expected to cause adverse health effects.

Scientific literature does not reveal a clear threshold level (i.e., a level at which no adverse health effects will occur) for many health effects from lead exposure and there are no MRLs or RfDs for exposure to lead. Correlations between blood lead levels and adverse effects are fairly well understood, however, and are studied to evaluate the potential for adverse health effects (e.g., nervous system effects, impaired neurobehavioral development of children, and hematological effects). The Centers for Disease Control and Prevention (CDC) considers children to have an elevated level of lead if the amount of lead in the blood is at least 10 micrograms per deciliter (µg/dL). Medical evaluations and environmental investigations and remediation are recommended when blood lead levels in children reach 20 µg/dL. Medical treatment might be necessary in children if the lead concentration in blood is higher than 45 µg/dL. CDC considers blood lead levels of adults to be elevated if they exceed 25 µg/dL (ATSDR 1999c).

ATSDR applied an approach that has been devised to estimate blood lead levels from known,media-specific contaminant concentrations. The approach has been developed based on the results ofnumerous studies that have attempted to correlate environmental lead levels with blood lead levels(ATSDR 1999c, FDA 1993c). The model that has been developed to estimate blood lead levelsconsiders the extent to which lead exposures might cause blood lead levels to rise. ATSDR regardsthe model as a useful screening tool and used it to evaluate exposures to lead in fish and shellfishfrom Willoughby Bay.

ATSDR estimated the possible contribution of chronic exposure to lead in fish or shellfish to blood lead levels. Studies indicate that the blood lead levels of adults and children are estimated to increase up to 0.034 µg/dL and 0.24 µg/dL, respectively, for every microgram of lead in food ingested (ATSDR 1999c). Based on this screening approach, chronic exposures to the highest detected concentration of lead (6.19 mg/kg, measured in an oyster sample in 1971) would result in an estimated increase of 26.0 µg/dL in blood lead levels of children and an estimated increase of 7.4 µg/dL in blood lead levels of adults. These estimates, however, are extremely conservative and are expected to overestimate increases in blood lead levels due to consumption of fish and shellfish from Willoughby Bay. They assume that people consumed almost 5 meals per month containing the maximum detected lead level of 6.19 mg/kg, measured in 1971. However, the second highest detected concentration of lead was 2.52 mg/kg, also measured in 1971. All other fish and shellfish samples analyzed for lead have contained concentrations of lead below 2 mg/kg. The fish and shellfish samples collected in 2001 had even lower levels (below 0.2 mg/kg). Chronic exposure to lead levels below 2 mg/kg would be estimated to cause the blood lead levels of children to increase less than 10 µg/dL and of adults to increase less than 2.5 µg/dL. Therefore, adverse health effects due to consumption of lead in fish or shellfish from Willoughby Bay would not be expected.


Mercury exists in several forms, including metallic mercury, inorganic mercury, and organicmercury, each of which occur naturally in the environment. Certain microorganisms and naturalprocesses can convert mercury from one form to another, most commonly to methylmercury, a typeof organic mercury that can accumulate in the food chain (ATSDR 1999a). Nine samples fromWilloughby Bay have been analyzed for mercury. One 1971 sample contained 0.49 mg/kg mercury,but the other three samples from 1971 contained less than 0.04 mg/kg mercury. All five samplescollected in 2001 (from blue crabs, croaker, spot, oysters, and hard clams) contained mercury levelsbelow the detection limit of 0.01 mg/kg.

ATSDR's estimated chronic dose for a child (0.0009 mg/kg/day) would exceed the chronic MRLfor methylmercury (0.0003 mg/kg/day). The MRL was derived from a study indicating a NOAELfor humans of 0.0013 mg/kg/day, which is higher than the estimated child dose (ATSDR 1999a).Furthermore, no one is expected to be regularly exposed to mercury at the highest detectedconcentration. This conclusion is supported by the 2001 VDEQ data, in which all reported mercuryconcentrations were lower than the detection limit of 0.01 mg/kg. Although data on mercuryconcentrations in shellfish and fish in Willoughby Bay are limited, available data do not indicatethat exposure to mercury would result in adverse health effects.


Six samples from Willoughby Bay were analyzed for thallium. In 1986, a hard clam sample wasanalyzed and found to contain 2 mg/kg of thallium. In 2001, a single sample of each of thefollowing species was analyzed for thallium: blue crab, croaker, spot, oyster, and hard clam. In allfive of these samples, thallium levels were below the detection limit of 0.3 mg/kg. Chronic exposureto the level of thallium reported in 1986 (2 mg/kg) would result in an adult dose (0.001 mg/kg/day)and a child dose (0.004 mg/kg/day) that both exceed the RfD (0.00008 mg/kg/day). However, therelatively limited available scientific literature reports that the NOAEL for thallous compounds (theforms of thallium most common in the environment) in animals is generally in the range of 0.2mg/kg/day, 50 times higher than the estimated dose to children and 200 times higher than theestimated dose to adults. Furthermore, the 2001 thallium sampling data suggest that the 1986measurement is not representative of the concentrations of thallium generally currently present inshellfish and fish from Willoughby Bay. Even at concentrations 10 times higher than the highestvalue observed (2 mg/kg in clams) no adverse health effects from exposure to thallium would beexpected (ATSDR 1992). Further, ATSDR's assumptions likely overestimate the extent to whichoysters from Willoughby Bay are consumed, particularly by children.


Sixty-two oyster samples from Willoughby Bay have been analyzed for zinc since the 1970s, but atotal of only eight samples have been analyzed from blue crab, spot (a popular species of ediblefish), croaker (another species of edible fish), and hard clam. The maximum detected concentrationof zinc in an oyster sample was 1,440 mg/kg, measured in 1994. The average detected concentrationin all oyster samples, however, was 647 mg/kg. The three spot samples available (the first twocollected in 1971 and the third in 2001) contained 91 mg/kg, 124 mg/kg, and 5.1 mg/kg zinc(respectively). The 2001 croaker sample contained 4.7 mg/kg zinc. The zinc concentration in a1971 blue crab sample was 65 mg/kg and 22 mg/kg in a 2001 blue crab sample. The zincconcentration in a 1986 hard clam sample was 38 mg/kg, while a 2001 hard clam sample wasreported to contain 8.4 mg/kg.

Scientific literature indicates that zinc bioaccumulates in oysters at substantially higher rates than inother molluscan bivalves. Specifically, research indicates that zinc bioconcentrates in oysters almost200 times more than it does in soft-shell clams and more than 30 times more than it does in mussels(NPS 1997). Bioconcentration factors have not been identified for hard clams, the type of clamsfound in Willoughby Bay, or blue crabs. However, a study of zinc levels in oysters and hard clamscollected from part of western Florida indicated that zinc levels were 20 or more times higher inoysters than in hard clams (Dixon et. al 1993). Thus, available data suggest that levels of zinc inaquatic biota other than oysters would be expected to be lower than the levels found in oysters.

Zinc is one of the most common elements in the earth's crust and is one of the most widely usedmetals in the world. Its most common use is as a protective coating for other metals, and it is alsopresent in a number of metal alloys and paints, as well as in domestic wastewater. It is an essentialnutrient. Too little zinc in a person's diet can lead to a lowered ability to resist disease and otherhealth problems. Too much zinc in a person's diet, however, can lead to health problems, such asgastrointestinal distress or effects on other human systems. Potential health effects from acute andchronic dietary exposures to zinc are discussed in more detail below.

Because exposure to oysters is expected to be infrequent based on the limited oyster population inWilloughby Bay, ATSDR evaluated occasional, one-time exposures. ATSDR calculated the acutedoses to adults and children that would result from a single meal of fish or shellfish containingvarying levels of zinc. The following table presents these dose calculations.

Zinc Concentration (mg/kg) Resulting Acute Dose (mg/kg/day) Acute MRL (mg/kg/day) Human LOAELs,
Acute Exposure6
Adult (11.4 oz) Child (6 oz.)
1,4401 6.7 24.5 None 0.5 - 7
6472 3.0 11.0
1243 0.6 2.1
454 0.2 0.8
225 0.1 0.4

1 - maximum level detected in oysters
2 - average level detected in oysters
3 - maximum level detected in a non-oyster sample, from spot
4 - average level detected in all eight available non-oyster samples
5 - maximum value detected in summer 2001 non-oyster samples, from blue crab
6 - few human studies of acute exposure to zinc are available

Ingestion of zinc or zinc-containing compounds has been shown to result in a variety ofgastrointestinal effects and other systemic effects on humans, but extensive data are not available.No oral acute MRL is available for zinc due to insufficient scientific data. The few available casereports of acute exposure in humans have reported short-term health effects at doses as low as 0.5mg/kg/day. One report of one-time ingestion of 0.5 mg/kg/day of zinc (as zinc sulfate) indicated atransitory decrease in serum cortisol levels. No effects on the adrenal gland itself from exposure tozinc have been reported in humans, and ATSDR did not locate any other studies showing the effectsof zinc on adrenal cortisol output (ATSDR 1994).(5) Another case report involved a one-time incidentin which military personnel in two army companies inadvertently ingested approximately 7mg/kg/day of zinc as zinc oxide and 80% of the personnel had gastrointestinal distress and diarrhea.Other case reports suggest gastrointestinal effects might occur after ingestion of zinc as zinc sulfateat doses above 2 mg/kg/day. However, a great deal of uncertainty exists regarding the exposurelevels for these acute studies (ATSDR 1994).

Based on the available scientific evidence, estimated acute exposure doses for adults and childreneating oysters at the maximum and average detected concentrations are within the range of dosesthat might result in decreased serum cortisol levels and short-term gastrointestinal effects. However,the oyster population in Willoughby Bay is sufficiently limited that there has been no reportedcommercial oyster harvest since 1972. The recreational harvest is expected to be very limited, if itexists at all.

ATSDR's conservative estimate of the adult dose resulting from acute exposures to concentrationsof zinc detected in eight available samples from other aquatic biota suggests that a temporarydecrease in serum cortisol levels might occur, on the basis of evidence from one study. ATSDR'sconservative estimate of the acute child dose resulting from exposures to seafood species other thanoysters exceeds zinc doses reported to cause a short-term decline in serum cortisol levels and some ofthe doses that have reportedly caused temporary gastrointestinal distress. However, 2001 samplesfrom non-oyster species contained levels of zinc lower than those reported to cause these temporaryeffects. The limited data that exist make it difficult for ATSDR to evaluate the representativeness ofthe available non-oyster samples. Therefore, ATSDR concludes that if there is consumption ofWilloughby Bay biota containing zinc levels similar to those previously reported in oysters or thosereported in other fish and shellfish species prior to 2001, temporary effects might result, but nolasting health effects would be expected.

ATSDR also considered longer-term exposures by calculating the chronic doses to adults andchildren that would result from chronic ingestion of fish or shellfish containing zinc. The followingtable presents the results of ATSDR's chronic dose calculations.

Zinc Concentration (mg/kg) Resulting Chronic Dose (mg/kg/day) (about 5 meals/month) Intermediate and Chronic MRL
Human LOAELs, Intermediate Exposure6
Adult Child
1,4401 0.72 2.52 0.3 0.7 - 4.3
6472 0.32 1.13
1243 0.06 0.22
454 0.02 0.08
225 0.01 0.04

1 - maximum level detected in oysters
2 - average level detected in oysters
3 - maximum level detected in a non-oyster sample, from spot
4 - average level detected in all four available non-oyster samples
5 - maximum value detected in summer 2001 non-oyster samples, from blue crab
6 - intermediate LOAELs are reported because few human studies of chronic exposure to zinc are available

Few studies of chronic exposure to zinc have been performed. For this reason, the MRL forintermediate exposure to zinc, 0.3 mg/kg/day, has also been adopted as the chronic MRL. The MRLis based on a study of human exposure to zinc that reported hematological effects (decreasedhematocrit, serum ferritin, and erythrocyte superoxide dismutase activity) from exposure to 1mg/kg/day zinc (0.16 mg/kg/day from dietary sources and 0.83 mg/kg/day from dietarysupplements). Thus, the lowest observed adverse effect level (LOAEL) in humans of 1.0 mg/kg/daywas derived. Other human studies have shown decreased serum HDL-cholesterol ("goodcholesterol") as a result of intermediate exposure to doses ranging from 0.7 mg/kg/day to 4.3mg/kg/day zinc (ATSDR 1994).

Based on the assumption that people consume fish and shellfish from Willoughby Bay about fivetimes per month, adult and child doses resulting from chronic exposure to the highest detectedconcentration of zinc in oysters and the adult and child dose resulting from chronic exposure toaverage levels of zinc detected in oyster samples exceed the MRL. However, consumption of oystersis thought to be uncommon and to occur substantially less frequently than the conservativeassumptions ATSDR used in its dose calculations. Furthermore, people are unlikely to consistentlyconsume the maximum zinc concentration measured in oyster samples. Regular exposure to oystersfrom Willoughby Bay is no longer possible, as the oyster population is very limited. Childrenexposed to the average concentration of zinc detected in oyster samples in fewer than three 4-ouncemeals per month (or four and one-half 4-ounce meals per month during the 8 months of the yearwhen fishing and shellfish harvesting would be likely to occur) would receive zinc doses below thelowest LOAELs and would not be expected to experience adverse health effects.

The estimated adult and child doses resulting from chronic exposure to levels of zinc measured inavailable clam, crab, and fish samples are below the MRL. Samples from these biota are limited, buteven if zinc levels were twice as high as the maximum detected concentration, adverse health effectsfrom chronic exposure to these biota would not be expected to occur.


Agency for Toxic Substances and Disease Registry (ATSDR). 1992. Toxicological Profile forThallium. July 1992.

ATSDR. 1994. Toxicological Profile for Zinc (Update). May 1994.

ATSDR. 1999a. Toxicological Profile for Mercury (Update). March 1999.

ATSDR. 1999b. Toxicological Profile for Cadmium (Update). July 1999.

ATSDR. 1999c. Toxicological Profile for Lead (Update). July 1999.

ATSDR. 2000a. Toxicological Profile for Arsenic (Update). September 2000.

ATSDR. 2000b. Toxicological Profile for Chromium. September 2000.

Dixon, L.K. et al. 1993. Bivalved shellfish contamination assessment. Prepared for the Sarasota BayNational Estuary Program. Mote Marine Laboratories Technical Report No. 224. January 4, 1993.

U.S. Environmental Protection Agency (EPA). 1997. Exposure Factors Handbook, Volume II, FoodIngestion Factors. EPA/600/P-95/002Fb. August 1997.

U.S. Food and Drug Administration, Center for Food Safety and Applied Nutrition (FDA). 1993a.Guidance Document for Cadmium in Shellfish. January 1993.

FDA. 1993b. Guidance Document for Chromium in Shellfish. August 1993.

FDA. 1993c. Guidance Document for Lead in Shellfish. August 1993.

MEDLINEplus. 2001. MEDLINEplus Health Information: A Service of the National Library ofMedicine. Medical Encyclopedia: Cortisol Level. Last Updated 3 October 2001.

National Park Service (NPS). 1997. NPS Water Resources Divisions, Water Operations Branch.Environmental contaminants encyclopedia: zinc entry. Roy J. Irwin, ed. July 1, 1997.

Stöppler, M. C., M.D. n.d. Cortisol: The "Stress Hormone." Undated.

3. The estimate for adult chronic intake is based on the 90th percentile intake of recreationally-caught fish and shellfish by recreational fisherman who consumed their catch, according to data from a 1981 study of marine finfish and shellfish consumption survey in metropolitan Los Angeles (reanalyzed in 1994). ATSDR did not identify any studies reflecting intake rates of marine fish and shellfish for populations in the Mid-Atlantic area. The estimate for child chronic intake is 50% of the adult intake (EPA 1997).
4. The estimate for adult acute intake is based on the 95th percentile fish or shellfish serving size from 1989 to 1991 United States Department of Agriculture data. The estimate for child acute intake is based on the 95th percentile fish or shellfish serving size for children aged 3 to 6 from a 1977-1978 United States Department of Agriculture food consumption survey for which data were collected by age (EPA 1997).
5. Cortisol is a hormone secreted by the adrenal cortex that plays a role in regulating blood pressure, cardiovascular function, and the body's use of proteins, carbohydrates, and fats. It is normal for cortisol levels to rise and fall during the day; they are usually at their highest in the early morning and at their lowest around midnight. Cortisol is also secreted in response to stress, increasing the blood sugar level and reducing inflammation, among other effects (MEDLINEplus 2001; Stöppler n.d.).

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