Vaccari D.A., Strom P.F., Alleman J.E. Environmental Biology for Engineers and Scientists

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At high concentrations, ammonia seems to affect the central nervous system of ﬁsh,

resulting in hyperventilation, convulsions, and death. At chronic levels of exposure, the

toxicity seems to involve histological and reproductive effects. The LC

falls in the range

0.49 to 4.6 mg of nonionized ammonia per lite r for a variety of aquatic animals. These

include Daphnia, cray ﬁsh, and the ﬁsh bluegills, red shiners, channel catﬁsh, and large-

mouth bass. One group that seems more sensitive is the salmonids, which include pink

salmon (0.08 to 0.1 mg/L) and rainbow trout (0.2 to 1.1 mg/L). Chronic effects include

reduced uptake of food and reduced growth at levels as low as 0.002 to 0.15 mg/L NH

Ammonia is oxidized by bacteria such as Nitrosomonas to nitrite (NO



), which is

then converted to nitrate (NO



) by, among others, Nitrobacter. The ﬁrst step is usually

rate limiting. Thus, nitrite does not normally accumulate to appreciable levels in aquatic

systems. Nonionized ammonia inhibits Nitrobacter at 0.1 to 1.0 mg NH

/L and inhibits

Nitrosomonas at 10 to 150 mg/L. Thus, in between these two levels, the second step is

inhibited and not the ﬁrst, and nitrite can accumulate. Thus, lowering the pH can cause

nitrite accumulation by its effect on ammonia. Furthermore, nitrite is in equilibrium with

nitrous acid (HNO

), with a K

of about 3.39 at 10



C. Nitrous acid inhibits Nitrobacter

and Nitrosomonas at concentrations starting at about 0.22 to 2.8 mg/L. This inhibition also

favors nitrite formation. Some organic chemicals have similar effects. Concentrations of

nitrite up to 73 mg NO



-N /L have been found in lakes and streams.

Nitrite is toxic to ﬁsh and mammals by forming methemoglobin, limiting the oxygen-

carrying capacity of the blood (see Section ) LC

for ﬁsh has been measur ed at 0.1 to

0.4 mg NO



-N=L for rainbow trout, 1.6 mg NO



-N/L for mosquitoﬁsh, 7.5 to 13

mg NO



-N /L for catﬁsh, and greater than 67 mg NO



-N/L for the mottled sculpin.

Toxicity to ﬁsh decreases above pH 6.4, apparently due to decreasing HNO

levels.

Nitrate toxicity is very low. One of the most sensit ive aquatic species is the guppy

(Poecilia reticulata), with a 96-hour LC

of 180 to 200 mg NO



-N/L. Other species

range from 420 to 2000 mg NO



-N/L. Some of this toxicity may be related to a salinity

effect rather than a speciﬁc toxicity of nitrate.

In mammals, high concentrations of nitrites can react with some amines under the acid

conditions of the stomach to form N-nitroso compounds (nitrosamines and nitrosa-

mides). Many of these are highly carcinogenic. Nitrate is used to cure meats and to pre-

serve other foods and is found in water contaminated by agricultural fertilizers or

domestic wastewater. It is also found naturally in some vegetables such as turnip greens,

beets, and celery. Nitrate in food or water can be converted to nitrite by microorganisms in

the mouth and stomach. Nitrites and nitrates also cause ‘‘aging’’ of coronary arteries. N-

nitroso compounds can also be formed by cooking or drying foods over open ﬂames when

the NO

compounds formed in combustion react with amines in the food.

nitrosamine

Suspended solids may come from inert materials such as soil particles or from pollution

sources such as sewage. In the case of sewage, other harmful effects, such as oxygen limi-

tation, predominate over the physical effect of the solids. Forest streams typically have very

low suspended solids: less than 20 to 50 mg/L. Some rivers, such as the Mississippi River in

Louisiana, can reach almost 300 mg/L. The higher levels can be abrasive for aquatic

plants, and can coat the bottom, reducing survival of benthic organisms and ﬁsh eggs.

828 TOXICITY OF SPECIFIC SUBSTANCES

Fish production is thought to be reduced at levels from 25 to 80 mg/L. From 80 to

400 mg/L, ﬁsh production is likely to be affected severely. Lethal effects in ﬁsh have been

measured at suspend ed solids levels ranging from 40,000 to 160,000 mg/L. However, a

single value cannot be determined because it will depend on shape and size distribution of

the particles. Presumably the lethality is due to clogging or abrasion of the gil ls.

21.7 TOXICITY TO MICROBES

Bacteria tend to be less sensitive than eukaryotic organisms to toxic substances. This may

be due to the relative simplicity of their metabolic processes and the lower degree of spe-

cialization. For example, organophosphate pesticides act on acetylcholinesterase in the

nervous system, which has no counterpart among bacteria. Thus, bacteria are fairly insen-

sitive to these substances. General metabolic inhibitors, however, can affect bacteria in a

manner similar to that of higher organisms. Bacterial membranes, cell walls, and slime layers

offer greater resistance to many toxins than animal structures such as gills, lungs, and intest-

inal surfaces. Furthermore, bacteria can become dormant when conditions are not favorable

for growth or survival. Cyst formation can be another barrier to a toxicant entering the cell.

Besides reduced sensitivity, three factors relating to microbial ecology serve to miti-

gate the impact of toxins on microbial communities:

1. Bacteria grow rapidly and can quickly regain their numbers if only part of the

population is eliminated.

2. Bacterial groups have redundant capabilities. That is, although bacteria may be

metabolically specialized individually, many different types share similar speciali-

zation. Consequently, when one type is poisoned, there will often be others ready to

take their place. There are some exceptions, such as the nitrifying bacteria. These

grow slowly, and are replaced slowly, yet are important to the ecosystem. Thus,

toxicity assessments should consider possible effects on this group.

3. Bacteria are ubiquitous in natural systems. Even in laboratory or industrial systems

it is very difﬁcult to sterilize an open system chemically and at the same time to

isolate it from external resupply. In the natural environment, it is all but impossible.

Nevertheless, inhibition of bacteria has been measured by various means, including plate

counts, biochemical measurements, respirometry, and biomass growth rates. Table 21.12

TABLE 21.12 Effect of Herbicides on Microbial Respiration

Erwinia carotovora Pseudomonas ﬂuorescens Bacillus sp.

Conc. % Conc. % Conc. %

Herbicide (mg/L) Inhibition (mg/L) Inhibition (mg/L) Inhibition

Diquat 25 40.8 50 0 25 100

Loxynil 25 71.0 50 0 10 29.0

Paraquat 50 25.5 25 43.7 5 100

PCP 10 29.6 25 65.8 5 100

Picloram 50 0 50 28.8 50 0

Nitralin 50 0 25 22.0 50 0

Source: Rand and Petrucelli (1985).

TOX ICITY TO MICROBES

829

shows the reduction in respiration measured with several herbicides. It is interesting

that Bacillus spp. were completely inhibited by diquat at levels that had no effect on

P. ﬂuorescens respiration. Note that inhibition of respiration does not necessarily mean

that the organisms were killed.

Toxic effects on bacteria can be studied by determination of effects on speciﬁc func-

tions, such as saprophytic activity, methanogenesis, nitriﬁcation, or other biogeochemi cal

cycle activities. Figure 21.3 shows an example of this. The amount of inhibi tion was

observed to vary with incubation time. For example, methylparathion’s inhibition

decreases up to 9 days, then increases again. This may be due to the degradation of the

pesticide, followed by an accumulation of an even more toxic by-product, aminophenol.

Nitrogen ﬁxation can be studied by measuring the conversion of acetylene to ethylene

in the absence of nitrogen. This is because the enzyme nitrogenase catalyzes both reac-

tions. Stimulation is often found with pesticides, as well as inhibition. For example,

malathion causes an initial period of inhibition, followed by more than double the activity

after 8 days. Other combinations of pesticides and species produced up to ﬁve times the

activity.

Soil fungi and actinomycetes were found to bioaccumulate organochlorine pesticides.

Bioconcentration factors ranged from 10 for lindane to 59,000 for chlordane. Bacteria are

also involved in biotransformation reactions that can enhance or reduce toxicity of sub-

stances to other organisms. One of the most important is the conversion of inorganic mer-

cury to methylmercury. Other examples include the conversion of crude oil components to

genotoxic agents, the conversion of P



S groups in organophosphate pesticides to the

more active P



O groups, and the formation of nitrosamines from secondary amines

and nitrites.

579111315

t (da

Percent activity

Fonofos

Guthion

Parathion

Methyl Parathion

Control

Figure 21.3 Effect of thiophosphorus pesticides on ammonia oxidation by estuarine nitriﬁers.

(From Rand and Petrucelli, 1985; original source: Jones and Hood, 1980, Can. J. Microbiol., Vol.

26, pp. 1296–1299.)

830

TOX ICITY OF SPECIFIC SUBSTANCES

21.8 IONIZING RADIATION

An important physical cause of toxic effects is a variety of forms of radiation. Ionizing

radiation possesses enough energy to strip an electron from an atom. This can result in

the formation of damaging free radicals or directly damage bonds in biochemical sub-

stances. The most sensitive system in living things is the DNA, since damage to a single

molecule can transform a cell to malignancy. It is not necessary for a radioactive emission

to damage a DNA molecule directly. The most abundant molecule in living things is

water. Water can form free radicals when irradiated, and these in turn can produce

toxic effects, including genotoxicity.

Ionizing radiation may be electromagnetic (g-rays, x-rays, ultraviolet rays) o r particu-

late. The major particulate forms of radiation are a and b, but they may include neutrons,

other subatomic particles, or larger particles; such as various atomic nuclei found in cos-

mic rays. Of primary interest here the a, b, and g emissions from the decay of radioactive

atoms, or radionuclides. Each particle of radiation possesses energy, commonly mea-

sured in millions of electron volts (MeV). A change to SI units is under way that will

replace the MeV with the joule: 1MeV ¼ 1:6  10

13

The energy of a particle relates to the amount of damage a particle can do to a tissue.

As radiation passes through material such as tissue, it is absorbed, depositing its energy in

the material. Much of this energy goes into stripping electrons from atoms. This requires

an average of 33.85 eV per electron. This ability to eject electrons confers a capacity to

disrupt chemical bonds with potentially damaging results.

Gamma (g) radiation is electromagnetic radiation (photons) of very high energy,

usually less than 1 MeV. They are produced by radioactive decay of unstable atomic

nuclei. X-rays are somewhat less energetic, up to 0.25 MeV for radiation from medical

x-ray machines. Ultraviolet (UV) are even less energetic, ranging from about 4.13 to 155

eV. X-ray and UV photons are produced by excitation of an atom’s electrons. Alpha (a)

particles consist of two protons and two neutrons (helium nuclei). They have energies that

range from 3 to 9 MeV. Beta (b) particles are high-energy electrons, with energies ranging

up to 3.5 MeV. Alpha, beta, and gamma particles are all emitted by spontaneous reactions

in the nuclei of unstable (radioactive) isotopes.

Although alpha particles are high in energy, they have the least penetrating power, due

to their mass and charge. They are strongly absorbed and deposit their energy rapidly,

producing a large amount of damage. For example , alpha particles with 5 MeV pene-

trate about 40 mm of soft tissue or about 5 cm in air. Thus, they do not penetrate the

skin. However, if they are inhaled or inge sted, they do not need to pe netrate very far

to reach cell nuclei, potentially causing gen etic damage. Beta particles are charged,

but have little mass. They penetrate about 3 m in a ir, but they are stopped by thin sheets

of many solids. Thus, alpha and be ta radiation is a problem mostly if their emitters

are ingested . Gamma rays are the most penetrating. Their range in air is about 4 m,

and th ey will penetrate several centimeters of lead. Co nsequently, g rays can cause

their effects o n living things eit her when emitters are ingested or by external radiation

sources.

Many of the environmentally important radionuclides are products of the sequence of

nuclear decay reactions that start with

238

U. Each beta emission increases the atomic num-

ber without signiﬁcantly changing the atomic mass by converting a neutron to a proton.

An alpha emission reduces the atomic number by two and the atomic mass by four.

Figure 21.4 shows the members of the series, with their half-lives and the energy carr ied

IONIZING RADIATION 831

238

234

230

226

222

218

214

210

206

92 - (U)

Uranium

U-238

4.5e9 yr

4.2 MeV

U-234

2.5e5 yr

4.7-4.8 MeV

91 - (Pa)

Protactinium

Pa-234m

1.2 months

2.3 MeV

Alpha Decay

(helium nucleus

ejected)

90 - (Th)

Thorium

Th-234

24 days

0.2

0.1 MeV

Th-230

8.0e4 yr

4.6-4.7 MeV

89 - (Ac)

Actinium

Beta Decay

(electron

ected)

88 - (Ra)

Radium

Ra-226

1600 yr

4.8 MeV

87 - (Fr)

Francium

86 - (Rn)

Radon

Rn-222

3.82 days

5.5 MeV

85 - (At)

Astatine

84 - (Po)

Polonium

Po-218

3.05 min

6.0 MeV

Po-214

1.6e-4 sec

7.7 MeV

Po-210

138 days

5.3 MeV

83 - (Bi)

Bismuth

Bi-214

19.7 min

0.4-3.3 MeV

Bi-210

5.0 days

1.2 MeV

82 - (Pb)

Lead

Pb-214

26.8 min

0.7, 1.0 MeV

Pb-210

22 yr

<0.1 MeV

Pb-206

Stable

MASS NUMBER

ATOMIC NUMBER

Figure 21.4

Uranium-238 decay series.

832

by their alpha and beta particles. Some of these reactions may also produce g radiation,

usually at lower energies.

Table 21.13 summarizes the emissions from some other important radionuclides. Note

that the smaller radionuclides tend not to emit alpha radi ation.

Each type of decay is characterized by its half-life, the type of particle(s) emitted, and

the energy carried by the particles. The half-life deﬁnes the rate of disintegrations. The

half-life is related to the decay rate coefﬁcient, k, by equation (18.25). The rate coefﬁcient

can then be used in equation (18.23) to compute the rate of decay.

Example 21.1 One gram of

226

Ra has a half-life of 1600 years. Thus, k ¼ 0:693=

1600 years ¼ 4:33  10

4

1

or 1:374  10

11

1

. The number of atoms in 1 g of

radium is

226 g=mol

ð6:022  10

Þ¼2:665  10

atoms

TABLE 21.13 Some Important Radionuclides and Energies of Dominant Radiation Particle

Avg. Particle Nutrient Relative Food

Dominant Energy Analogs and Chain

Particle (MeV) Critical Transport

Isotope Half-Life Emission (% intensity) Tissue (BAF) Source

H 12.26 yr b 0.01861 H, whole body High (1) Nuclear weapons,

nuclear power

C 5730 yr b 0.156 C NA Natural, nuclear

power

K1:28  10

yr b 1.35 (1.35%) K, whole body High (1) Natural

P 14.3 days b 1.71 P NA Natural

Kr 10.76 yr b 0.67 NA NA Nuclear weapons,

nuclear power

Rb 4:8 10

yr b 0.274 NA NA Natural

Sr 28.1 yr b 0.546 Ca, bones High (1) Nuclear weapons

106

Ru 367 days b 0.0392 NA NA Nuclear weapons

129

I1: 6  10

yr b 0.189 NA NA Nuclear power

131

I 8.07 days b 0.582 I, thyroid High (10) Nuclear weapons,

power, medical

134

Cs 2.05 yr b 0.499 NA NA Nuclear power

135

Cs 3  10

yr b 0.210 NA NA Nuclear weapon

tests

137

Cs 30.23 yr b 0.551 K, whole body High (3.0) Nuclear power

222

Rn 3.82 days a NA None, lungs, Negligible Natural

S, Se?

238

U3:5  10

yr a 4.2 GI tract, Low–moderate Natural,

kidney, lung (<1.0) contaminant in

depleted

uranium

projectiles

239

Pu 24,400 yr a 5.149 None, bone, Very low Nuclear weapons

lung (<0.01)

Energy of dominant radiation particle given, or weighted average for type of particles. NA, not available.

Source: Based on Connell and Miller (1984); Weast (1979); Newman (1998).

IONIZING RADIATION

833

Then the rate of decay can be computed as

r ¼ kc ¼ð1:374  10

11

1

Þð2:665  10

atomsÞ¼3:66 10

atoms=s

That is, 1 g of radium disintegrates at the rate of 3:66  10

atoms per second.

21.8.1 Dosimetry

In measuring radiation, it is necessary to discriminate among emission, exposure, and

dose. Emission is the rate at which particles are produced or energy is released. One dis-

integration per second is termed a becquerel (Bq). The curie (Ci) is deﬁned as

1Ci¼ 3:70  10

Bq. Note that this is approximately the number of becquerels emitted

by 1 g of radium. Historically, the Curie was deﬁned in terms of radium decay, although

now it is given the ﬁxed value. Also, note that 1 curie emitted by different radionuclides

can have different amounts of energy. Thus, the number of curies by itself does not indi-

cate the amount of potential harm that might be cause d by a radionuclide. Environmental

concentrations of radionuclides are often expressed in picocuries: 1 pCi ¼ 10

12

Ci ¼

0:037 Bq. For example, radon in drinking water is regulated in terms of pCi/L. The

U.S. EPA has proposed a maximum contaminant level for radon in drinking water of

300 pCi/L and has an action level in ambient air of 4 pCi/L.

Exposure is deﬁned only for electromagnetic radiation such as g -rays. The SI unit is

based on the number of charges of one sign produced by complete absorption in air. The

unit is coulombs per kilogram of air. The older unit of exposure is the roentgen (R):

1 roentgen ¼ 2:58  10

4

C=kg

Exposure can occur due to external sources, such as g-, b-, or x-ray emissions from

outside the body. Alternatively, they may be from internal sources, such as any radionu-

clide that is ingested or absorbed and decays within the body.

The dose refers to the amount of energy actually absorbed. The SI unit is the gray

(Gy), which is 1 J/kg. The older unit is the rad. The conversion is 100 rad ¼ 1 Gy.

Because of the previously mentioned average ionization energy, exposure can be con-

verted into dosage in either system of units assuming 100% absorption of the energy:

1C=kg ¼ 33:85 Gy

1 roentgen ¼ 0:87 radðin airÞ

For tissues this conversion is approximate and may vary with type of tissue and g

energy. Exposure and dose have frequently been confused with each other, partly because

in the units of roentgens and rads they are numerically similar. Exposure refers only to

ionization that would occur in air due to electromagnetic radiation such as g- or x-rays.

It is the radiation that would be measured by an external dosimeter, such as a ﬁlm badge

clipped to the shirt of a worker. However, it only indirectly indicates how much radiation

has been absorbed by the worker. Dose applies to energy absorbed by any material and

due to any type of radiation.

The differing ability of various emissions to damage living tissue is accounted for by

what is called the relative biological effectiveness (RBE) in biology. It is deﬁned as the

ratio of the toxicological effect of the radiation in question to the effect produced by g

834 TOXICITY OF SPECIFIC SUBSTANCES

radiation of the same dose. The value depends not only on the radiation but on the type of

endpoint (e.g., cancer, cell necrosis). Because the RBE is difﬁcult to determine for human

health effects, the relative rate at which energy is deposited in water by the emission, com-

pared to g radiation, is used in place of RBE. This ratio is called the radiation weighting

factor (W

; formerly the quality factor). Thus; g radiation has a W

value of 1. The W

a radiation is about 20. The W

for b is also about 1. Th e product of dose and W

gives the

dose equivalent (H), which is measured in sieverts (Sv); Gy W

¼ Sv. (In the older

measurement units, rad  W

¼rem. Then 100 rem ¼ 1 Sv.) An interpretation of dose

equivalent is that it is the dose of g radiation that would produce the same amount of tis-

sue damage as the radiation under consideration.

Dose equivalent, however, still does not provide enough information to estimate the

risk of cancer. The reason is that all parts of the body rarely receive the same exposure,

and in the case of ingested radionuclides, they often concentrate in various organs or tis-

sues with varying sensitivities. For example, dent al x-rays are concentrated on the head

and neck area, and ingested radioactive iodine tends to concentrate in the thyroid gland.

To account for factors such as these, dose equivalent is multiplied by a tissue weighting

factor, w

, which is the ratio of the cancer risk to the organ per sievert divided by the

cancer risk per sievert to the whole body. The product of dose equivalent and w

is called

the effective dose equivalent (H

). The w

for the gonads is 0.20; for bone marrow, colon,

lung, and stomach it is 0.12; for the bladder, breast, liver, esophagus, and thyroid it is

0.05; for the skin and bone surface it is 0.01; for the rest of the body it is 0.05. The effec-

tive dose for parts of the body are computed separately because the dose received by the

different parts are rarely the same. The sum of the effective dose equivalents for all the

parts of the body is used to compute overall effective dose equivalent. This value is then

used to compute a person’s risk of cancer. Table 21.14 summarizes the units used in radia-

tion dosimetry.

The dosage values described so far are in units of energy deposited per unit mass of

tissue. However, the dosage may decrease with time because of the elimination of the

radionuclide by radioactive decay, by biological elimination, or by both. The decrease

TABLE 21.14 Units and Conversion Factors Used in Radiation Health Measurements

Fundamental Units Traditional Units SI Units

Disintegration Rate

1 disintegration/s 1 becquerel (Bq) 27.0 picocuries (pCi)

3:70 10

Bq 1 curie (Ci)

Exposure (g- or X-Rays): Number of Charges of One Sign Produced by Complete Absorption in Air

2:58 10

4

C/kg 1 roentgen (R) 2:58 10

4

C/kg

3876 R 1 C/kg

Dose: Amount of Energy Actually Absorbed

1 J/kg 100 rad 1 gray (Gy)

Dose Equivalent: Dose  RBE or Dose  W

: Capability to Damage Living Tissue

100 rem 1 sievert (Sv)

Effective Dose Equivalent: Dose Equivalent  Tissue Weighting Factor

100 rem 1 sievert (Sv)

Units on the same row are equal to each other.

IONIZING RADIATION

835

is a ﬁrst-order process, with an effective rate constant, k

, equal to the sum of the rate

constants for radioactive decay, k

, and for biological elimination, k

. The initial rate at

which energy is being deposited in a tissue is D

. Then the amount that will be deposited

in the ﬁrst t time units will be

D ¼

½1  expð k

tÞ ð21:3Þ

The dose that is deposited over a lifetime (assumed to be 50 years for adults and

70 years for exposure to children) is called the committed effective dose (CED).

For an inﬁnite time period, or for practical purposes when the lifetime is four or

more times the effective half-life (1=k

), the committed effective dose is equal to the

total dose:

D ¼

ð21:4Þ

Internal nuclides with long effective half-lives do not change appreciably in concentra-

tion in the body over a person’s lifetime . In such cases it is appropriate to expressed the

dosage as a rate of energy delivered per mass of tissue per unit time, D

Example 21.2

131

Iisab emitter with a half-life of 8 days and a 180-day biological half-

life in the thyroid. Thus, k

¼ 0:693=8:07 days ¼ 0:0859day

1

and k

¼ 0:693=

180 days ¼ 0 :00385 day

1

. Then k

¼ 0:0897 and the effective half-life is 7.72 days.

About 60% of the iodine in the body concentrates in the thyroid gland. If a person receives

3 mCi of

131

I, what will be the effective dose rate to the thyroid? What will be the effec-

tive dose delivered over the ﬁrst 15 days, and what will be the total dose?

Answer From Table 21.13,

131

I produces 0.582 MeV per disintegration; 60% of the

total dose results in ð0:6Þð3ÞmCi ¼ 1:8 mCi dose to the thyroid. Thus, the dose rate will

ð1:8 mCiÞ

3:7 10

mCi



0:582 MeV

Bq  s



1:6  10

13

MeV



86; 400 s

day



¼ 5:3610

4

J=day

This is also the dose equivalent, H, since the radiation weighting factor can be taken as 1.0

for b emiss ions. Also, since we are dealing with a known dose to an organ rather than a

whole-body dose, a tissue weighting factor is not needed and the dosage we are computing

is the effective dose equivalent, H

. Assume that the mass of the thyroid is 25 g. Since the

penetration depth of b emissions is much smaller than the thyroid, one can assume that all

the energy is deposited in that organ. Thus, the initial dose rate, D

, will be

5:36  10

4

J=day

0:025 kg

¼ 0:0214 Gy=day ¼ 0:0214 Sv=day

The dose delivered over the ﬁrst 15 days will be

D ¼

0:0214 Sv=day

0:0897 day

1

½1  expð 0 :0897 day

1

Þð15 dayÞ ¼ 0:177 Sv

836 TOXICITY OF SPECIFIC SUBSTANCES

Over the long term, the total dose will be

D ¼

0:0214 Sv=day

0:0897 day

1

¼ 0:239 Sv

Dosimetry calculations can easily become complicated by additional factors not con-

sidered here. The distribution of radionuclides can be described by pharmacokinetic mod-

els to more accurately describe their spatial and temporal distributions in the b ody.

Conversion of exposure to absorbed dose can be complicated by external and internal

shielding, which can be difﬁcult to quantify. Often, it is necessary to take into account

not only a particular radionuclide, but its daughters as well. Radon is one example

where this is critical (see below). In such cases the daughters can have greatly different

emission characteristics and pharmacokine tics. Once the radionuclide loading to a parti-

cular tissue is determined, it may be necessary to consider secondary forms of radiation as

the energy interacts with the matter (e.g., neutrons or positrons). It may be necessary to

examine radiation to tissues adjacent to the organ containing the radionuclide. An exam-

ple of the latter is that some of the radioactive isotopes of strontium may deposit at the

inner surface of hard bone tissue, where their emissions can irradiate the sensitive bone

marrow tissue. Many radioisotopes produce more than one type of emission. For example,

some 8% of the emission from

131

Iisg radiation. In the case of g-ray dosimetry from

internal emitters, the spatial distribution of the nuclides affects the absorbed dose. This

can be taken into account either by detailed integration or by use of predetermined

geometry factors.

21.8.2 Radiation Exposure and Risks

The major sources of radionuclides in the environment are natural sources, fallout from

nuclear detonations in the atmosphere, and sources associated with nuclear power. Natural

sources include a number of minerals, such as

238

U and its derivatives (Figure 21.4),

and the gas tritium (

H), and

C, which is continually produced by cosmic ray bombard-

ment of the atmosphere. One of the more important by-products of

238

U is radon ,

222

Rn.

The natural backgr ound radiation to which the public is exposed is about 3 mSv per year,

as shown in Table 21.15.

Inhalation of radon is the largest source of natural exposure. Outdoor radiation in the

United States has been measured at an average of 7 Bq/m

(0.19 pCi/L); indoor levels tend

TABLE 21.15 Estimated Total Effective Dose

from Several Forms of Natural Radiation for the U.S.

and Canadian Populations

Source Dose Rate (mSv/yr)

Cosmic 0.27

Cosmogenic 0.01

Terrestrial 0.28

Inhaled 2.0

In body 0.40

Total 3.0

Source: Harley (1996).

IONIZING RADIATION

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