Vaccari D.A., Strom P.F., Alleman J.E. Environmental Biology for Engineers and Scientists
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to be much higher, averaging 40 to 80 Bq/m
3
(1 to 2 pCi/L). This is because the decay of
each gram of radium naturally present in the ground produces about 0.10 mL of radon gas
per day. As an ideal gas, radon moves readily through the soil, entering buildings through
the foundation. About 1.18% of potassium consists of the radioactive isotope
40
K. The
40
K in our bodies contributes about 0.17 mSv/yr. Cosmic rays produc e an exposure of
35 mR/yr at sea level, and 100 mR/yr at an altitude of 10,000 ft. Exposure to granitic
bedrock produces about 90 mR/yr from natural isotopes, and sedimentary rock produces
23 mR/yr.
Nuclear power results in emissions at a number of points in the fuel cycle, such as
mining, fuel processing, and p ower generation. A wide variety of radionuclides are pro-
duced in the power reactor. Besides the direct reaction produc ts, neutrons striking other
materials, such as air and impurities in cooling water, produce new radionuclides by neu-
tron activation. This creates radioactive forms of carbon, nitrogen, argon, oxygen,
copper, sodium, and many others. Some of these products are released to the environment.
Atmospheric nuclear weapons testing up to 1973 released far larger quant ities of radio-
nuclides to the environment than nuclear power has.
The prima ry risk of concern with radiation exposure is cancer and hereditable genetic
disorders. The International Commission on Radiation Protection (ICRP, 1990) estimates
the probability of fatal cancer of all types for the general population to be 5% per sievert
dosage and the probability of severe hereditary disorders to be 1% per sievert. Table 21.16
details these risks for individual tissues. Also given is the aggregated detriment, which
TABLE 21.16 Estimated Radiation Risk Probabilities for Specific Tissues and Organs
Probability of Aggregated
Fatal Cancer Detriment
(% per Sv) (% per Sv)
Whole Whole
Tissue or Organ Population Workers Population Workers
Bladder 0.30 0.24 0.29 0.24
Bone marrow 0.50 0.40 1.04 0.83
Bone surface 0.05 0.04 0.07 0.06
Breast 0.20 0.16 0.36 0.29
Colon 0.85 0.68 1.03 0.82
Liver 0.15 0.12 0.16 0.13
Lung 0.85 0.68 0.80 0.64
Esophagus 0.30 0.24 0.24 0.19
Ovary 0.10 0.08 0.15 0.12
Skin 0.02 0.02 0.04 0.03
Stomach 1.10 0.88 1.00 0.80
Thyroid 0.08 0.06 0.15 0.12
Remainder 0.50 0.40 0.59 0.47
Total 5.00 4.00 5.92 4.74
Probability of Severe Hereditary Disorders
Gonads 1.00 0.60 1.33 0.80
Grand Total 7.3 5.6
Source: Harley (1996).
838 TOXICITY OF SPECIFIC SUBSTANCES
takes into account fatal and nonfatal cancers, severe hereditary effects, and loss of relative
length of life.
The ICRP occupational guideline for radiation protection (1990) limit the dosage
received to an average of 20 mSv (2 rem) per year over five years, with a maximum of
100 mSv in any one year. A dosage of 20 mSv with a fatal cancer occupational risk factor
of 4% per sievert corresponds to an 8 10
4
risk. The NCRP (1993) has defined a neg-
ligible individual dose (NID) below which efforts to reduce radiation exposure further
are unwarranted. The NID was selected to be 0.01 mSv (1 mrem) per year. This corre-
sponds to 5 10
7
added risk of fatal cancer per year.
Acute effects in humans are found at higher dosages. The 30-day LD
50
for whole-body
radiation depends on individual factors and the level of medical support provided, but is
considered to be about 4 to 7 Gy (400 to 700 rad). At such levels the first symptoms
include nausea and vomiting within about a week. After two weeks sore throat and loss
of appetite occurs, followed by diarrhea, emaciation, and death. Suppression of the
immune system can result in infections that contribute to death rates. Exposure can
cause skin lesions, damage to leukocytes and lymphatic tissue, and ultimately the com-
plete elimination of antibody production. Bone marrow depression is obser ved at about 2
Gy, and changes in blood counts result at exposures from 0.14 to 0.50 Gy.
In organisms other than humans, the genotoxicity has been shown to be strongly related
to the amount of haploid DNA in the organism (Figure 21.5). This relationship seems to
be reflected in the lethal toxicity of radiation to various groups shown in Table 21.17.
The fate and transport of radionuclides is as varied as their chemical composition.
Radon, an ideal gas, is fairly soluble in water. Some of its daughters, however, are solids
that attach to particles in the air that in turn may be deposited in the lungs (see
Figure 21.4). Many of the metal radionuclides released by nuclear power plants have
been found to be strongly adsorbed by sediments. The concentration of plutonium in
aquatic organisms has been found not to exceed the concentration found in associated
sediments. It has also been found to decrease with trophic level.
−9.5
−9.0
−8.5
−8.0
−7.5
−7.0
−6.5
−6.0
0.01 0.1 1 10 100
Barley
Man
Tomato
Mouse
Fruit fly
Fungus
Yeast
E. Coli
DNA per haploid
g
enome
Log of specific locus mutations
per locus per rad
Figure 21.5 Relation between forward mutation rate per locus per rad and the DNA content per
haploid genome. The line is a regression line. The point for humans is estimated from the DNA
content.
IONIZING RADIATION 839
PROBLEMS
Write a research paper on one of the following topics:
21.1. Update Rachel Carson’s Silent Spring: Which of her fears were proved right; which
wrong? How did the pesticide industry respond to her book? What is the stance of
the pesticide industry today?
21.2. Look into the medical literature to find and summarize case histories of toxic effects
on humans of a chosen environmental toxin or class of toxins, such as a type of
pesticide or solvent.
21.3. Select several chemicals in each of two or three different categories, such as metals,
pesticides, and solvents, for which you can find information on the slope of the
toxicity curve. See if you can generalize about what you find. Do particular groups
have similar slopes? Does a particular chemical tend to have similar slopes in
different organisms? What does the slope indicate about the toxic mechanisms
involved?
21.4. Find journal articles discussing the extrapolation of animal toxicity test data to
humans, and summarize the information given and arguments made.
21.5. Research the stimulation of chemical sensitivity by formaldehyde.
21.6. Suppose that a woman has absorbed 1 mCi of
90
Sr into her bones. Compute the dose
rate, the initial dose rate, the dose delivered over 50 years, and the resulting added
risk of cancer. Assume that the total mass of bones is 5 kg.
REFERENCES
Anon., 1998. Arsenic crisis in Bangladesh, Chemic al and Engineering News, November 16,
pp. 27–29.
Brown, A. W. A., 1978. Ecology of Pesticides, Wiley, New York.
TABLE 21.17 Lethal Dosage of Radiation for Adult
Organisms of Several Groups
Group Lethal Dose (krad) Toxic Measurement
a
Bacteria 4.5–735 LD
90
Cyanobacter <400–>1200 LD
90
Other algae 3–120 LD
50
Protozoans ?–600 LD
50
Mollusks 20–109 LD
50/30
Crustaceans 1.5–56.6 LD
50/30
Fish 1.1–5.6 LD
50/30
a
LD
50/30
is the 30-day LD
50
.
Source: Connell and Miller (1984); original source I.L. Ophel, 1976, Tech.
Rep. Ser. 172, International Atomic Energy Agency, Vienna.
840 TOXICITY OF SPECIFIC SUBSTANCES
Connell, D. W., and G. J. Miller, 1984. Chemistry and Ecotoxicology of Pollution, Wiley, New York.
Esposito, M. P., T. O. Tiernan, and F. E. Dryden, 1980. Dioxin, EPA/600/2/80/197, U.S. Environ-
mental Protection Agency, Washington, DC.
Ferruzzi, G., and J. Gan, 2004. Pesticide Selection to Reduce Impacts on Water Quality, Publication
8119, University of California Division of Agriculture and Natural Resources, Berkeley, CA.
Gofman, J. W., 1981. Radiation and Human Health, Sierra Club Books, San Francisco, New York.
Grosch, D. S., and L. E. Hopwood, 1979. Biological Effects of Radiations, Academic Press, New
York.
Harley, N., 1996. Toxic effects of radiation and radioactive materials, Chapter 25 in Casarett and
Doull’s Toxicology, 5th ed., C. D. Klaassen (Ed.), McGraw-Hill, New York.
ICRP, 1990. 1990 Recommendations of the International Commission on Radiological Protection.
ICRP Publication 60. International Commission on Radiation Protection, Pergamon Press,
Oxford, England.
IRIS database, other databases.
LaGrega, M. D., P. L. Buckingham, and J. C. Evans, 2001. Hazardous Waste Management, McGraw-
Hill, New York.
Lu, F. C., 1991. Basic Toxicology: Fundamentals, Target Organs, and Risk Assessment, 2nd ed.,
Hemisphere Publishing, Bristol, PA.
Manahan, S. E., 1989. Toxicological Chemistry, Lewis Publishers, Boca Raton, FL.
Newman, M. C., 1998. Fundamentals of Ecotoxicology, Ann Arbor Press, Ann Arbor, MI.
Rand, G. M., and S. R. Petrocelli, 1985. Fundamentals of Aquatic Toxicology: Methods and
Applications, Hemisphere Publishing, New York.
Rao, P. S. C., R. S. Mansell, L. B. Baldwin, and M. F. Laurent, 2004. Pesticides and Their Behavior in
Soil and Water, University of Florida, http://pmep.cce.cornell.edu/facts-slides-self/facts/gen-pubre-
soil-water.html.
Seinfeld, J., 1975. Air Pollution: Physical and Chemical Fundamentals, McGraw-Hill, New York.
U.S. EPA, 1985. Draft Superfund Public Health Evaluation Manual, U.S. Environmental Protection
Agency, Washington, DC.
Weast, R. C. (Ed.) 1979. CRC Handbook of Chemistry and Physics, 60th ed., CRC Press, Boca
Raton, FL.
Williams, P. L., and J. L. Burson (Eds.), 1985. Industrial Toxicology: Safety and Health Applications
in the Workplace , Van Nostrand Reinhold, New York.
REFERENCES 841
22
APPLICATIONS OF TOXICOLOGY
The results of toxicological studies are used by a number of government agencies to pro-
tect the health of individuals or of ecosystems. Risk assessment is used to provide a
rational basis for regulatory decision making. It may even be used in cost–benefit analyses
for regulations. In what is called a toxicity reduction evaluation, bioassays may be used to
find and eliminate the source of toxicity in wastewaters.
22.1 RISK ASSESSMENT
Risk is defined as the probability and magnitude of an adverse effect. Quantitative risk
assessment is the process of determining that probability and magnitude. Examples of
risk assessment include financial risk analysis, the determination of exposure to property
or other economic loss, and safety hazard analysis, the determination of the risk of low-
probability high-consequence effects. Here we are concerned with the following kinds of
risk assessment: Health risk assessment is the determination of the likelihood of adverse
effects in humans, generally from chronic low-level exposure to toxic agents. Ecological
risk assessment (also called hazard assessment) examines the risk of harm to species
other than humans. Risk assessment is usually considered to include the following four
steps:
1. Hazard identification is the selection of environmental agents that may be
responsible for a cause–effect relationship between an environmental agent and
some harmful effect. The identification may be made by the use of epidemiological
studies or laboratory animal studies compared with levels of the environmental
agent present.
Environmental Biology for Engineers and Scientists, by David A. Vaccari, Peter F. Strom, and James E. Alleman
Copyright # 2006 John Wiley & Sons, Inc.
842
2. Toxicity assessment is the determination of a quantitative relationship between
observed effects and environmental causes. These relationships can include the
determination of dose–r esponse relationships, LC
50
or other measurements, from
laboratory toxicity tests.
3. Exposure assessment is the measurement or prediction of the dosage to which
particular organisms may be subjected. This often involves tools such as mathe-
matical modeling of the fate and transport of pollutants in the environment.
4. Risk characterization (or risk estimation) is the determination of the risk, based
on integration of the toxicity and exposure information found in the preceding steps.
Furthermore, risk characterization should include a discussi on of the uncertainty in
the computed risk and qualitative factors. This discussion could include compar-
isons between different toxicity and exposure assessment approaches, and compar-
isons between different target populations.
These steps may be taken in different orders. For example, exposure assessment pre-
cedes toxicity assessment in the Superfund risk assessment process. If the exposure is
found to exceed established standards, such as drinking water MCLs or air NAAQSs
(see Appendixes D and E, respectively), remediation is considered. In environmental
risk assessment, toxicity assessment and exposure assessment are considered to be paral-
lel steps rather than in sequence.
Whereas the first two steps above are the province of biologists, the last two steps con-
tain roles for the environmental engineer. Furthermore, risk assessment is typically fol-
lowed by risk management, which may also involve engineers. Risk management is
the selection and implementation of actions to control the risk. This may require design,
construction, and operation of facilities to remediate or treat sources of environmental
pollution.
Virtually this entire textbook might be thought of as providing an understanding of nor-
mal and perturbed functioning of living things so as to b e able to attribute effects observed
to particular environmental causes. These topics covers the hazard identi fication portion
of risk assessment. In Chapter 19 and Section 20.1 we described the techniques of toxicity
assessment. In the following sections we describe the remainin g steps: exposure asse ss-
ment and risk characterization.
22.1.1 Human Health Risk Assessment
Human health risk assessments are used for many regulatory purposes. These include the
setting of standards and guidelines for drinking water and air quality and the determina-
tion of cleanup go als under the Resour ce Conservation and Recovery Act (RCRA) or the
Comprehensive Environmental Responsibility and Liability Act (CERCLA, the Super-
fund Act).
Exposure Assessment Exposure assessment has three parts. First is the determination of
exposure pathways, such as breathing of air or ingestion of food, soil, or water. Second,
mathematical models of pollutant fate and transport are often used to predict exposure
based on release rates from the sources coupled with the physicochemical properties of
the pollutant. Exposure is defined as the amount of pollutant contacting bod y boundar ies
(skin, lungs, gastrointestinal tract, etc.). Exposure may also be measured directly by per-
RISK ASSESSMENT 843
sonal monitoring devices, such as air samplers that are carried by people for a period of
time. Prediction of fat e and transport is a part of the risk assessment process that has the
major role for engineers.
Once the concentration of a pollutant at the point of exposure is determined, the third
and final step of the exposure assessment in human risk assessment is the calculation of
receptor dosage or chemical intake rate. Th is is usually expressed in units of milligrams
of intake per kilogram of body weight per day. The calculation depends on the route of
exposure and other factors. A typical form of the relationship could be
I ¼ C
CR EF ED ABS
BW
1
AT
ð22:1Þ
where
I ¼ intake rate ðmg=kg day
1
Þ
C ¼ exposure concentration ðmg=L for water; mg=m
3
for air; mg=g for soilÞ
CR ¼ contact rate ð L = day; m
3
=day; or g=dayÞ
EF ¼ exposure frequency ðdays=yrÞ
ED ¼ exposure duration ð yrÞ
ABS ¼ absorption efficiency ðfractionÞ
BW ¼ body weight ðkgÞ
AT ¼ averaging time ðyrÞ
Formulations that are more complex may be used. For example, if the exposure con-
centration is time varying, an expression that integrates the exposure could be used. The
absorption efficiency reflects the fact that not all contaminants inhaled or ingested are
actually taken into the bloodstream. Inhaled gases may not be absorbed completely
because of the limited time for mass transfer. Contaminants associated with particulates,
such as dust and soil, may be sequestered in the interior of particles or in highly insoluble
forms. The fraction that is not sequestered is called the bioavailability.
The exposure concentration may be based on measurements or best estimates based on
modeling results. If the risk assessment is retrospective (i.e, it is for the purpose of com-
puting risk based on historical exposure), the best estimate of concentration is used. How-
ever, if the risk assessment is prospective (i.e., it is a prediction of risks for the future), it is
common practice to use an upper 95% confidence limit for the exposure concentration.
This could be done by adding 1.96 times the standard deviation to the average value.
For example, if historical data indicate that a population has been exposed to an average
concentration of 8.0 mg/m
3
of a toxin, with a standard deviation of 0.5 mg/m
3
, the expo-
sure concentration should be taken to be 8.0 + (1.96) (0.5) = 8.98 mg/m
3
.
The averaging time, AT, is 70 years for carcinogens and is equal to the exposure dura-
tion (ED) for noncarcinogens. The contact rate, exposure frequency, and duration are
usually based on average or reasonable maximum (e.g., 90th percentile) values, as
shown in Table 22.1.
The intake rate may be based on long-term exposures as shown in Table 22.1, or up to a
lifetime of 70 years. This produces a chronic daily intake (CDI). Risk assessment may
also be based on short-term concentrations averaged over a 10- to 90-day period. The
844 APPLICATIONS OF TOXICOLOGY
resulting intake is called the subchronic daily intake (SDI). In some cases, instead of
estimating intake of a contaminant, the body burden will be measured directly, such as
by blood or tissue sampling.
Risk Characterization Toxic effects in humans are broadly classified for risk assessment
purposes as either carcinogenic or noncarcinogenic. Carcinogenic effects are the forma-
tion of tumors. Noncarcinogenic effects include all toxic responses other than tumor for-
mation, which may include, for example, respiratory, neurological, or reproductive
effects. The U.S. EPA makes the following important distinction between these two cate-
gories: Carcinogenic effects are always assumed to have no threshold; any finite dosage is
capable of producing cancer. Noncarcinogenic effects, on the other hand, are always
assumed to have a threshold below which no effect will occur. The characterization of
risk is different for the two types. Some chemic als may exhibit both types of effect, so
both need to be checked whe n doing a risk assessment for any chemical.
Noncarcinogenic Risk Characterization Toxicologica l effects other than carcinogen-
esis are assumed to produce their effect only above a threshold. The threshold is
determined experimentally from bioassay and epidemiological data. The highest level
at which no toxic effect is found is termed the no observed adverse effect level
(NOAEL). The NOAEL is often divided by a safety factor of 10 to take into account
differences between the typical members of a population and its more sensitive members.
Table 22.1 Exposure Factors Used by the EPA for Risk Assessment
Exposure
Exposure Frequency Exposure Body
Land Use Pathway Daily Intake (days/yr) Duration (yr) Weight (kg)
Residential Ingestion of 2 L (adult) 350 30 70 (adult)
potable water 1 L (child) 15 (child)
Ingestion of 100 mg (adult) 350 24 as adult 70 (adult)
soil and dust 200 mg (child) +6 as child 15 (child)
Food intake 1500 g
(wet weight)
Inhalation of 20 m
3
(adult) 350 30 70
contaminants 10 m
3
(child)
Industrial and Ingestion of 1 L 250 25 70
commercial potable water
Ingestion of 50 mg 250 25 70
soil and dust
Inhalation of 20 m
3
250 25 70
contaminants (workday)
Agricultural Consumption 42 g (fruit) 350 30 70
of homegrown 80 g (veg.)
produce
Recreational Consumption 54 g 350 30 70
of locally
caught fish
Source: Kolluru et al. (1996); Doull et al. (1980).
RISK ASSESSMENT
845
The resulting safe threshold is called the reference dose (RfD) [formerly called the
acceptable daily intake (ADI)]. Appendix C gives RfDs for several important environ-
mental toxins. Unless information to the contrary is available, noncarcinogenic risks are
assumed to be additive.
The RfD is used to compute a hazard index (HI), which represents a summary of all
exposures over all pathways:
HI ¼
X
i
E
i
RfD
i
ð22:2Þ
where E
i
is the exposure or intake in mg/kgday. If the hazard index exceeds 1.0, a more
detailed study on the risk and control measures would be required. If several chemicals
are known to produce their noncarcinogenic effect on different organs, the summation
may be carried out separately for each organ.
Carcinogenic Risk Characterization The different models for extrapolating carcino-
genic risk, including the linearized multistage model, result in a linear relationship
between risk and dose at low dose. The slope of that relationship is the carcinogenic
potency factor (CPF) or slope factor (SF) and relates the probability of contracting cancer,
p, to the exposure or intake:
p ¼ CDI CPF ð22:3Þ
where CDI is the chronic daily intake in mg/kg day (equivalent to exposure E). CPFs for
some p ollutants are given in Appendix C. The potency factor includes a safety factor to
take into accoun t the uncertainty in ‘‘mouse-to-human’’ extrapolation. The value of the
safety factor varies from 10 to 1000, and depends on the quality and quantity of the evi-
dence of toxicity. If toxicity has been tested in only a single species, a larger safety factor
is called for. If multiple species have been tested, a smaller safety factor, together with
using the most sensitive species, would give reasonable protection. Other considerations
affecting the safety factor include whether there is specific knowledge of toxic mechan-
isms such as specific biotransformations that occur, or of pharmacokinetic behavior. There
may be different potency factors for different routes of absorption.
Both the RfD and the potency factor include safety factors and conservative assump-
tions. To summarize, the risk assessment is conservative because of the emphasis on data
from the most sensitive species, strain, and sex; extrapolation by body surface area instead
of body weight, the use of safety factors for extrapolation from animals to humans; use of
the upper confidence limit of the dose–response model; and the assumption of no thresh-
old for carcinogens.
In performing human health risk assessments for exposures involving the public, an
excess lifetime risk less than 10
6
is generally considered acceptable for regulatory pur-
poses. In some cases, such as occupational exposures or other populations that have a
stake in the costs, higher risks may be acceptable. It must be noted that the public percep-
tion of risk is quite different from the probabilistic definition given here. Although engi-
neers and scientists recognize that ‘‘zero risk’’ is an impossibility, the public rightfully
demands that the goal should be zero risk. That is, although the goal may not be achiev-
able, all reasonable exertions should be made to attempt it.
846 APPLICATIONS OF TOXICOLOGY
Example Risk Characterization CPF and RfD values for some pollutants are given in
Appendix C. More complete and up-to-date information can obtained online from U.S.
EPA’s Integrated Risk Information Systems (IRIS) database at http://www.epa.gov/iris.
Example 22.1 Estimate and characteri ze the risk to an adult from a lifetime of drinking
water containing 1 mg/L of perchloroethylene (PCE) and 10 mg/L of carbon tetrachloride
(CT).
RfD (mg/kg day) Oral CPF (mg/kg day)
PCE 0.010 0.13
CT 7.0e10
4
0.051
Solution Calculation of intake:
CDI
PCE
¼
ð0:001 mg=LÞð2:0L=dayÞ
70 kg
¼ 2:86 10
5
mg=kg day
CDI
CT
¼
ð0:01 mg=LÞð2:0L=dayÞ
70 kg
¼ 2:86 10
4
mg=kg day
Calculation of hazard index:
HI ¼
2:86 10
5
0:010
þ
2:86 10
4
0:0007
¼ 0:00286 þ 0:408 ¼ 0:411
Although most of the risk comes from carbon tetrachloride, the hazard index is well below
1.0, indicating that the person is below the threshold for noncarcinogenic effects. The car-
cinogenic risk is calculated as follows:
p
PCE
¼ð0:13Þð2:86 10
5
Þ¼3:72 10
6
p
CF
¼ð0:051Þð2:86 10
4
Þ¼1:46 10
5
Both of these risks exceed the acceptable level of 10
6
. The water supply may need treat-
ment or remediation, or a substitute water supply may have to be provided. Keep in mind
all the sources of uncertainty in these calculations, notably measurement error in the
bioassay and error associated with low-dose extrapolation and extrapolation between species.
Having computed a numeric risk, it is tempting to believe in it too much. Remember all
of the sources of uncertainty: error in laboratory experiments, low-dose extrapolation,
animal-to-human extrapolation, variation in human populations, and so on. Nevertheless,
the computed risk is conservative, is based on what is known, and may often be the best
information available for planning purposes.
22.1.2 Ecological Risk Assessment
Like human health risk assessments, ecological risk assessments (ERAs) are called for
under provisions of numerous laws and regulations, including RCRA, CERCLA, and
RISK ASSESSMENT 847