DRAFT
January 27, 1975
THE ENVIRONMENTAL IMPACT OF MERCURY
Work Performed
by
Biomedical Sciences Section
Information Center Complex
Information Division
Oak Ridge National Laboratory*
Oak Ridge, Tennessee 37830
for
Solid and Hazardous Waste Research Laboratory
National Environmental Research Center
U.S. Environmental Protection Agency
Cincinnati, Ohio ^5268
Interagency Agreement
EPA-IAG-D^-CA-03
*0perated by Union Carbide Corporation Nuclear Division for the
U.S. Energy Research and Development Administration. _. ,. , „ .
^ Biomedical Sciences
Section (EIGSCI)
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THE ENVIRONMENTAL IMPACT OF MERCURY
A. S. Hammons, B. L. Whitfield, H. M. Braunstein,
J. E. Huff, H. T. Kemp, E. B. Lewis,
H. B. Gerstner, and J. M. Chilton
with editorial and technical assistance
of
A. B. Gill and P. B. Hartman
-------
TABLE OF CONTENTS
Page
Section 1.0
Subsection 1.1
Section 2.0
Subsection 2.1
Subsection 2.2
Subsection 2.3
2.3.1
2.3.1.1
2.3.1.2
2.3.1.3
2.3.2
2.3.2.1
2.3.2.1.1
2.3.2.1.2
2.3.2.1.3
2.3.2.1.4
2.3.2.2
2.3.2.3
2.3.2.3.1
2.3.2.3.2
2.3.2.3.3
Subsection-2.4
2.4.1
2.4.1.1
2.4.1.2
1
,2.2
2.4.2
2.4.2.
2.4.
2.4.2.2.1
2.4.2.2.2
,4.2.2.3
,2.2.4
2.
2.4.
2.4.2.2.5
GENERAL SUMMARY
SUMMARY OF FINDINGS
CHEMICAL AND PHYSICAL PROPERTIES
AND ANALYSIS
SUMMARY
PHYSICAL CHARACTERISTICS
CHEMICAL CHARACTERISTICS
INORGANIC COMPOUNDS OF MERCURY
OXIDATION-REDUCTION EQUILIBRIA
ACID-BASE EQUILIBRIA
COMPLEX FORMATION
ORGANIC COMPOUNDS OF MERCURY
MERCURY-CARBON COMPOUNDS
REACTIVITY
REACTIONS
HYDROLYSIS
ACID CLEAVAGE
MERCURY-NITROGEN COMPOUNDS
MERCURY-SULFUR COMPOUNDS
SUBSTITUTION REACTIONS
EXCHANGE REACTIONS
COMPLEXES WITH NUCLEIC ACIDS
ANALYSIS FOR MERCURY
CONSIDERATIONS IN ANALYSIS
•SOURCES OF DISCREPANCY OF
ANALYTICAL RESULTS
EVALUATION OF EARLY ANALYTICAL
RESULTS
ANALYTICAL PROCEDURE
STORAGE AND PRESERVATION
CONCENTRATION AND SEPARATION
EVAPORATION
SOLVENT EXTRACTION
AMALGAMATION
CARBON ADSORPTION
ION EXCHANGE
1
2
5
5
5
6
8
11
11
13
13
16
16
17
18
18
19
19
20
20
21
23
26
26
28
29
29
29
30
30
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Subsection
Subsection
Section 4.0
Subsection
3.3.3
3.3.3.1
3.3.3.2
3.3.4
3.3.5
3.4
Subsection
4.1
4.1.1
4.1.2
4.2
4.2.1
4.2.1.1
4.2.1.2
4.2.2
4.2.2.1
4.2.2.2
4.2.2.3
4.3
Subsection
Section 5.0
Subsection 5.1
Subsection 5.2
Subsection 5.3
Subsection 5.4
Subsection 5.5
FUNGI 82
FUNGICIDES 82
PRESERVATIVES 85
ALGAE 86
PROTOZOA . 98
REFERENCES 101
BIOLOGICAL ASPECTS IN PLANTS 109
NONVASCULAR PLANTS 109
METABOLISM: UPTAKE, ABSORPTION, 109
AND RESIDUES
EFFECTS • 112
VASCULAR PLANTS 112
NONCROP PLANTS 112
METABOLISM: UPTAKE, ABSORPTION, 112
AND RESIDUE
EFFECTS 115
CROP PLANTS 116
METABOLISM: UPTAKE, ABSORPTION, 116
AND RESIDUES
TRANSLOCATION 120
EFFECTS 125
REFERENCES 130
ANIMAL STUDIES i% 135
SUMMARY 135
FISH 135
BIRDS . 139
MAMMALS 140
REFERENCES 143
Section 6.0
Subsection 6.1
Subsection 6.2
BIOLOGICAL ASPECTS IN HUMANS
SUMMARY
ANIMAL MODELS
144
144
147
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Subsection 6.3
METABOLISM
148
6.3.1
6.3.1.1
6.3.1.1.1
6.3.1.1.2
6.3.1.1.3
6.3.1.1.4
6.3.1.2
6.3.1.2.1
6.3.1.2.2
6.3.1.2.3
6.3.1.2.4
6.3.2
6.3.2.1
6.3.2.1.1
6.3.2.1.2
6.3.2.2
6.3.2.2.1
6.3.2.2.2
6.3.3
6.3.3.1
6.3.3.2
Subsection 6.4
6.4,
6.4,
6.4.
6.4,
,1
,2
,2.1
,2.1.1
6.4.2.1.2
6.4.2.1.3
6.4.2.1.4
6.4.3
6.4.3.1
6.4.3.2
6.4.3.3
Subsection 6.5
6.5.1
6.5.1.1
UPTAKE AND ABSORPTION
ORGANIC MERCURY
INHALATION
INGESTION
SKIN ABSORPTION
PLACENTAL TRANSFER
INORGANIC MERCURY
INHALATION
INGESTION
SKIN ABSORPTION
PLACENTAL TRANSFER
TRANSPORT AND DISTRIBUTION
ORGANIC MERCURY
DISTRIBUTION AND METABOLISM
IN BLOOD
TISSUE DISTRIBUTION
INORGANIC MERCURY.
DISTRIBUTION AND METABOLISM
IN BLOOD
TISSUE DISTRIBUTION
ELIMINATION AND BIOLOGICAL
HALF-LIFE
ORGANIC MERCURY
INORGANIC MERCURY
EFFECTS
NUTRITIONAL ROLE
CLINICAL STUDIES
TOXICOLOGY
SYMPTOMS
'ACUTE TOXICITY
GENETIC, TERATOGENIC, AND
CARCINOGENIC EFFECTS
ALTERATION OF MERCURY TOXICITY
NORMAL MERCURY LEVELS IN THE
HUMAN BODY
BLOOD LEVELS
URINE LEVELS
HAIR LEVELS
EFFECTS
CLINICAL AND EPIDEMIOLOGICAL
ASPECTS
CLINICAL STUDIES
148
148
148
150
151
151
152
152
153
154
155
155
156
156
158
162
162
164
165
165
171
171
171
172
172
172
175
175
182
183
183
187
191
192
192:
192
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Subsection 6.5.1.1.2
6.5.1.1.3
6.5.1.1.4
6.5.1.1.5
6.5.2
6.5.2.1
6.5.2.2
6.5.2.3
6.5.2.4
6.5.2.5
Subsection 6.6
Section 7.0
Subsection 7.1
Subsection 7.2
7.2.1
7.2.2
7.2.3
Subsection 7.3
7.3.1
7.3.2
7.3.3
Subsection- 7.4
Section 8.0
Subsection 8.1
Subsection 8.2
8.2.1
Subsection 8.3
8.3.1
8.3.2
8.3.3
ELEMENTAL MERCURY
INORGANIC MERCURY COMPOUNDS
ORGANIC MERCURY COMPOUNDS
THERAPY
EPIDEMIOLOGICAL EXAMPLES
ACUTE PULMONARY INJURY
CHRONIC BRAIN INJURY
ACUTE RENAL INJURY
METHYLMERCURY SYNDROME
TRANSPLACENTAL TRANSPORT
REFERENCES
ENVIRONMENTAL DISTRIBUTION
AND TRANSFORMATION
SUMMARY
DISTRIBUTION OF MERCURY
THE ENVIRONMENT
IN
DISTRIBUTION IN AIR
DISTRIBUTION IN WATER
DISTRIBUTION IN SOIL AND ROCK
ENVIRONMENTAL FATE
MOBILITY AND PERSISTENCE IN AIR
MOBILITY AND PERSISTENCE IN HATER
MOBILITY AND PERSISTENCE IN SOILS
REFERENCES
..ENVIRONMENTAL INTERACTIONS AND
THEIR CONSEQUENCES
SUMMARY
PRODUCTION AND USES
PRIMARY INDUSTRIAL SOURCES
ENVIRONMENTAL CYCLING OF
MERCURY
AIR
SOIL
WATER
192
193
194
194
196
196
196
196
197
198
198
207
207
208
208
211
212
230
230
231
232
234
240
240
240
240
245
247
247
247
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Subsection 8.3.3.1 EFFECTS OF INDUSTRIAL WASTE 248
CONTAMINATION
Subsection 8.4 FOOD CHAINS 248
Subsection 8.5 REFERENCES 253
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1.0 GENERAL SUMMARY
1.1 SUMMARY OF FINDINGS
Mercury—an extremely toxic heavy metal with a silvery appearance
and a liquid character—occurs naturally in the environment, but at low
levels: background concentrations in air approximate 1 nanogram/cubic
meter, in soils 50 parts per billion (ppb), and in water less than 5 ppb
(Section 7.1). However, because mercury is used extensively throughout
industry as well as in the -home, many additional sources and forms of
mercury impinge on the environment (Table 8.1 and Figure 8.2). For
instance, more than 70 percent of the mercury consumed in the United States
is lost to the environment (Section 8.1). Increased awareness of mercury
pollution on the other hand portends a decreased demand and use profile
for mercury (Table 8.2).
Probably the largest single source of particulate mercury emission
into the air is coal combustion, while one of the primary industrial
contributors of mercury contamination to waters is the chloral kali industry
through brine sludge containing mercury (Section 8.2.1). Mercury concen-
trations in environmental media reflect the proximity of pollution out-
falls or natural deposits of mercury. The natural circulation cycle of
mercury disperses it widely through rocks and soils, water, air, and the
biosphere (Figure 3.1 and Figure 8.1). Mercury compounds cycle in-
definitely among air, water, and land by the processes of evaporation,
vaporization, methylation, precipitation, and solution (Section 8.1).
Mercury accumulates in soils and sediments (Sections 8.3.2 and 8.3.3)
as well as in the tissues of most organisms.
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Because mercury is ubiquitous in the environment, essentially all
living organisms and foodstuffs contain existing background levels of
mercury (Section 8.4); even so, mercury has no known nutritional value.
Generally, the long-term intake of environmental levels of mercury by
humans does not appear to be hazardous; however, as evidenced by the
methylmercury poisoning incident in Minamata, Japan (Section 6.1) un-
restricted use and disposal of mercury and waste containing mercury can
create a serious hazard for the general population. Although remarkably
stable in air and water, organomercurials undergo a number of environ-
mentally and toxicologically important reactions. The relatively recent
discovery that methylation of mercury occurs under certain environmental
conditions has focused attention on the problem of environmental mercury
pollution.
Before the late 1960's many analyses determined total mercury in
biologic tissues and environmental samples without distinguishing between
the inorganic and organic forms; and further, the methods for mercury
detection gave inconsistent results. Trace metal analysis is presently
an active area of research primarily directed at establishing procedures
leading to increased sensitivity, precision, and accuracy. Trace mercury
analysis can now be successfully determined in the ppb range (Section 2.4.1.1)
Several analytical methods for mercury analysis are described in
Table 2.7. Cold vapor atomic absorption spectrometry is presently the
most acceptable method for trace mercury analysis (Section 2.4.2.4.5).
Because methylmercury is the most toxic form of mercury, the most
serious consequence of mercury contamination of the environment is the
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transformation of the mercury methylmercury and its subsequent
incorporation into the food chain (Figure 8.3). Methylation of mercury
occurs in sediments and probably in soils. Methyl mercury is water soluble
and readily absorbed and distributed to tissues of aquatic organisms
(Section 8.3.3). Research evidence indicates that mercury methylation
also occurs by microorganisms normally found in fish intestines and in
slime on fish; however, whether methylation occurs in fish or mammalian
tissues remains unclear (Section 3.2.2.1.1).
Mercury levels in animals reflect dietary intake; for example,
organisms inhabiting areas of high mercury concentrations resultantly
have increased bodily mercury levels (Sections 5.2, 5.3 and 5.4).
Because aquatic organisms accumulate methylmercury, food fish in mercury-
contaminated waters become important sources of mercury poisoning in
humans. Methylmercury has been shown to concentrate in fish muscle up to
3000 times the amount in the surrounding water (Section 8.4). Even in
heavily polluted waters, however, the concentration of mercury is usually
not high enough to kill fish (Section 5.1). Mercury also accumulates in
plants growing in contaminated soils; accumulation in foliage, seed, and
fruit of crop plants contributes to the growing mercury burden of humans
as well as domestic and wild animals (Section 4.2.2). Whether or not
mercury content of plant tissues originates from contaminated soils or
from surface residues is not determinate by chemical analysis alone.
Agricultural use of mercury compounds—as fungicidal treatment for seeds,
as soil applications or as sprays to crop plants—can lead to excessive
mercury accumulation in foods (Section 8.4).
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The biological activity of mercurials results primarily from their
tenacious affinity for sulfhydryl groups in proteins (Section 6.4.2.1).
Organic mercurials are the most toxic forms of mercury, the short-chain
alkyl derivatives being the most important toxicologically. The covalent
bond between the mercury and carbon atoms is particularly stable and
withstands virtually all in vivo detoxification pathways.
Methylmercury is readily and almost completely absorbed from the
digestive tract, whereas almost no elemental mercury enters the systemic
circulation through this route. Inhaled mercury vapor is quickly absorbed
via the respiratory system—nearly 80 percent enters the bloodstream;
dust or aerosols of inorganic mercury salts are also absorbed from the
respiratory tract, dependent mainly on particle size and solubility
(Section 6.3.1.2.1).
Metallic mercury and soluble mercury compounds have had a long history
of medicinal uses—treatment for syphilis, for example. The importance of
mercury in medicine has steadily diminished with the introduction of potent
nonmercurial diuretics, superior antiseptics, as well as antibiotics.
Nevertheless, both prescription and nonprescription preparations containing
mercury are available and are being used. Long-term use of these agents
has. resulted periodically in overt signs and symptoms of mercury poisoning
(Section 6.3.1.2.3). Alkyl and aryl mercury compounds can be absorbed
through the skin (Section 6.3.1.1.3).
Chronic poisoning causes disturbances of the central nervous system
(CNS), gastrointestinal tract, genitourinary system, respiratory tract,
skin and eyes (Table 6.4). Symptoms of acute mercury poisoning following
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inhalation and ingestion are listed in Table 6.3. With the exception of
respiratory tract involvement, the acute symptoms of mercury toxicity
are similar for both ingested and inhaled mercury. Although the complete
range of symptoms can be produced by either organic or inorganic mercury,
methylmercury is usually associated with CNS damage with substantial
time passage before symptoms appear, even after an acute exposure (Section
6.4.2.1.1); and inorganic mercury is more frequently associated with
damage to the alimentary canal and the kidneys (Section 6.5.1.1.3).
Symptoms occurring as a result of chronic exposure to mercury vapor, or
dusts of mercury salts, appear slowly and may be attributed falsely to
other causes. To identify mercury unequivocally as an etiological factor
in mild disturbances of the CNS remains a diagnostic barrier because the
signs and symptoms—for example, insomnia, shyness, loss of memory and
appetite—may be induced by many causes. Figure 6.6 shows dose-response
curves for several symptoms of methylmercury poisoning.
Methylmercury penetrates both the blood-brain and placental barriers,
reaches higher levels in the brain than other mercury compounds, and,
further complicating the toxicological profile, is eliminated from the body
more slowly than other forms. This slow elimination rate allows methyl-
mercury to accumulate in tissues, thereby contributing to the toxic potential
of methylmercury. The biological half-life of methylmercury in the body
approximates 65 to 70 days (Section 6.1); methylmercury preferentially
accumulates in red cells (Section 6.3.2.1.1). Tissue distribution of
monomethyl and ethylmercury is relatively unaffected by dose level, time
after a single exposure, or exposure time (Section 6.3.2.1.2); high levels
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are found in the liver, spleen, pancreas, and blood cells. Little
difference in toxicity or metabolism is evident among the various chemical
salts of methylmercury (Section 6.3.2.1.1). The main excretion routes for
monomethylmercury are feces, urine, and hair (Section 6.3.3.1). Radioactive
tracer studies in humans reveal that approximately ten percent of incor-
porated methyl mercury locates in the human head—the major portion pre-
sumably residing in the brain (Section 6.3.2.1.2).
Inorganic mercury compounds, due to their low solubility, rarely
reach the bloodstream in amounts large enough to be toxic. Therefore, the
primary concern with inorganic mercurials is the accidental or suicidal
ingestion of large amounts, or excessive occupational exposure. Because
almost any form of mercury entering the aquatic environment can be
biologically converted to methylmercury, mercury pollution is undesirable
and should be avoided.
Mercurials can alter enzyme activity, disrupt cell membrane integrity,
and combine with nucleic acids resultantly interfering with cell metabolism
and potentially causing death to the organism. Based on the known bio-
chemical activity of mercury compounds, a dose below which no effects occur
probably does not exist, although a dose below which no effects can be
measured or observed does exist. Persons poisoned in the Minamata incident
exhibited clinical signs of methylmercury poisoning when the concentration
in the brain reached one microgram/gram (ug/g) and death ensued beyond
5 ug/g (Section 6.1). Many exposed individuals, however, exhibited no
symptoms or signs—that is, remained subclinical.
Damage to the CNS and to the developing fetus is the most serious
consequence of mercury poisoning. Pathological changes in the brain are
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associated with CNS symptoms and signs (Section 6.4.2.1.1). Injuries to
the CNS are virtually irreparable, leading to permanent motor, sensory,
and mental deficiencies. Data at present are insufficient to correlate
or forecast the risks of mercury exposure to fetal injuries; it is known,
however, that the mother does not have to be affected before damage to
the fetus occurs.
In addition to general toxic effects, most mercurials also have
genetic activity, affecting mitosis, meiosis, and nucleic acids directly.
Genetic aberrations in some species have been demonstrated in laboratory
experiments. Some evidence indicates an increase in chromosome breaks in
populations consuming large amounts of fish containing methylmercury.
When populations having high fish consumption were compared with pop-
ulations having low fish consumption, the former displayed a higher number
of chromosome breaks in leukocyte cultures (Section 6.4.2.1.3). The full
implication of this phenomenon is poorly understood. Increased chromosome
breakage seemed to correlate with mercury levels in the blood.
Mutagenic, teratogenic, and carcinogenic effects of mercury have been
demonstrated in experimental studies; however, findings are still suggestive
rather than definitive (Section 6.4.2.1.3). Nevertheless, because effects
on genetic materials of cells occur at mercury levels below those which
produce any observable toxic effects, a long-term genetic effect may be
occurring in animal populations and in man (Section 6.4.2.1.3).
Dietary amounts of selenium obtained from tuna fish produced a
protective effect upon the toxicity of dimethylmercury in Japanese quail.
However, depending on dose and exposure levels, selenium itself is a toxic
material (Section 6.4.2.1.4).
-------
The present problem of mercury in the environment seems to center
mainly on mercury vapor in ambient air and the methyl mercury content in
food. A recent selected bibliography (1) containing 460 references on
mercury in the environment has been prepared by the Royal Ontario Museum.
Due to the bioaccumulation of mercury and the methylation of all forms
of mercury in aquatic environments, discharge of this material should be'
severely restricted. An October 1974 publication by the Environmental
Protection Agency (2) outlines background information on national emission
standards for mercury in the air.
1. Robinson S., and W. B. Scott, 1974. "A Selected Bibliography on
Mercury in the Environment, with Subject Listing," Life Sci. Misc. Publ.,
R. Ont. Mus. ISBN 0-88854-166-X, 54 pp.
2. United States Environmental Protection Agency, 1974. Background
Information on National Emission Standards for Hazardous Air Pollutants--
Proposed Amendments to Standards for Asbestos and Mercury, Office of Air
and Waste Management, Office of Air Quality Planning and Standards,
Research Triangle Park, North Carolina, 141 pp.
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1.2 CONCLUSIONS
1. Mercury is extremely toxic to all living organisms! methyl
and dimethylmercury are the most toxic forms of mercury;
and mercury can cause permanent damage to the central nervous
system and to the kidneys.
2. The significance of morphological chromosomal aberrations
has yet to be determined in persons showing high blood levels
of mercury.
3. The developing fetus is particularly susceptible to injury
from mercury exposure. Data are insufficient, however,
to adequately determine the statistical risks of maternal
exposure versus fetal damage.
4. Dose-response curves as well as minimal effect levels in all
organisms are lacking. Exposure group population studies
shed substantial light on the problem, but more definitive
guidelines can be established.
5. More data are required to fully understand mercury methylation
mechanisms for better evaluation of human health risks and
ecologiqal hazards.
6. Mercury in the food chain, particularly methylmercury in fish,
apparently remains the most serious hazard to the general
population.
7. Environmental cycling from every source—from mines, from
industry, from agriculture, from homes, as minimal examples--
eventual ly to the human organism has not been adequately
characterized and detailed with certainty.
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8. Deep soils and sediments function as environmental sinks
for mercury.
9. Extensive use of alkyl mercurial seed dressing presents
hazards to life, particularly wildlife.
10. Analytical analyses for mercury have been improved in recent
years—a gain in precision and increased sensitivity to the
ppb range.
11. Natural background concentrations of mercury in soils and
standing water as opposed to ambient levels are difficult
to determine due to widespread contamination of the
environment.
12. Mercury concentrations in water can be difficult to interpret
because of particulate adsorption and the influence of other
ions on the forms of mercury present.
13. Mercury in the environment—particularly from industrial
wastes—necessitates rapid regulatory and preventive action.
14. Literature on mercury as well as on most metals and
environmental contaminants continues to increase. To
qualitatively and quantitatively assess the potential and
real hazards, all published and unpublished reports
should be collected, analyzed, and categorized.
10
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2.0 CHEMICAL AND PHYSICAL PROPERTIES AND ANALYSIS
2.1 SUMMARY
Mercury and its compounds are best characterized by their uniqueness.
At ordinary temperatures, the metal exists as a liquid of high surface
tension and perceptible vapor pressure. Mercury tends to form covalent
rather than ionic bonds even in inorganic compounds, many of which are
more soluble in organic than inorganic solvents. It coordinates primarily
to two ligands and shows little tendency to increase this coordination.
Although remarkable for their stability to air and water, organomercurials
undergo a number of environmentally and toxicologically important reactions.
The chemistry of mercury as outlined in this section contains many
reactions and products observed in laboratory experiments. As cautioned
by Hem (1970),it is important to keep in mind the frequent departure
of natural systems from equilibrium conditions as established in laboratory
studies. Laboratory chemistry attempts to provide an understanding of
observed natural phenomena. In addition, even though equilibrium studies
often only demonstrate the inaccessibility and true complexity of naturally
occurring-events, they do indicate, if not actually predict, the extent to
T
which a given process may be expected, to. occur naturally.
A discussion of analysis for trace contaminants almost necessitates
a discussion of minute details. An attempt has been made here, however,
to present an overview of mercury determination, including only enough
detail to maintain an appreciation of the scope of the subject. The
problems to be considered in estimating the reliability of reported
analytical data will be covered along with a synoptic explanation and
-------
comparison of important and analytical methods both current and exploratory.
2.2 PHYSICAL CHARACTERISTICS
Mercury, a heavy, silvery liquid (density 13.5 g/ml), is practically
insoluble in water or organic solvents, and vaporizes slightly to a
colorless, odorless, tasteless gas. Like other metals, it is an excellent
electrical conductor. Unlike other liquids, however, 1 ml dropped on a
floor will disperse over a very large area in a multitude of tiny droplets
that defy collection due to its inherent high surface tension. The vapor
pressure of these finely dispersed droplets with a high surface-to-volume
ratio exceeds the saturation vapor pressure of a pool of the same liquid
with a plane surface (Lewis et al., 1961). Thus, since the vapor of mercury
rather than the liquid presents the health hazard, this hazard is increased
by the intrinsic physical properties of liquid metal mercury.
Many of the uses of elemental mercury depend upon its unique character-
istic of being a liquid metal at ordinary temperatures. As noted in
Table 2.1, the liquid state persists between -39 degrees C and 356 degrees
C. Its exceptionally low boiling point results in a small but not
insignificant vapor pressure at ordinary temperatures, which can result in
concentrations'.in the air in confined areas in excess of recommended
*.»
maximum allowances. At 20 degrees C, the"weight of mercury in one cubic
meter of air saturated with mercury vapor is about 10 mg/cubic meter
(see Fig. 2.1). This is 100 times 0.1 mg/cubic meter, an amount generally
agreed upon as causing mercurialism in man following prolonged exposure
(Hamilton and Hardy, 1974). Fortunately, mercury is rarely found in the
environment as the pure, confined liquid metal because it has a tendency
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Table 2.1. Sow Physical and Chemical Properties of Mercury Confounds3
OJ
Compound
Mercury
Qul cksl 1 vcr
Hcrcurous
Chloride
Co 1 omc 1
Mercuric
Chloride
Corros I va
Sub) imate
Prlrrary_ Use ^y/rbol
Occurrence Active Spec. cs
Chlor-alkol I Hg
Industry, mercury
dry cells (. lamps, Hg
dcnta 1 amo IgciO •
Fung I c t dc Hg.C 1 _
Insect i cl dc "*
Hg or Hg *
Fungici dc
Insecticide HgCl t, \
— '#
Chlor-jlkali Hg2*:
plant waste
Molecular Physical Melting Boiling
Weight Density St.Tte Point Point
(G/rolc) (g/cc) 20°C °C °C
200.6 13.55 silver - 38-9 35».6
, I iqut d
1.72.1 7.15 white sublimes
powder tOO
271.5 5.*4<* white 276 302
powder
Vopor Sol ubl 1 i ty
Pressure In water
20 C otncr
(fr.r.Hg) Solvents
0.0012 Insoluble
(3 x 10~13)b slightly
soluble
2 nig /I
(1 x 10 )b higher In
chlor i dc
conta i n-
ing waters
React I vi ty_
Toxic i ty
oxidi res under
proper condi-
t Ions to form
Inorgan I c nier-
(sec Soct. 2.3-1
dl sproport Io-
n.iics In sun-
light or h um i d
COnJi t ions .
Acute oral LO,.
(rot). 210 5°
Acute oral L0,_
(rat). 1 - 5 5°
mg/kg
760 g/l
cthono!
1*5 g/l ether
Dirr.cthy]
Mercury
Metnyl
Mercury
Diphcny 1
Mercury
Phcnyl
Ht_rcury
mercury
Acrt.itc or
ChlorU't,
Seed disinfectant /-u <\ u
/ . , . \^"t i o "9
(sold as organic 32
or Inorganic salts +
of me thy Inxircury ) CH. Hg
Paint Industry 652
CM OiCil ) M.jCl
S<-«-d trc.itfit.nc * or
— bulb-,, cuitini-,-;. CH G(Cll ) MijO II
potato. c,rc..l • Cll\(c^^ 2 '
Source,, of data. H.inJI/ook of Chi iiry .,nj Physic-,
Melsiur Pub. Co.. Vlllougt.by. Ohio, L.in.|.i'i HonuX&ok
colorless
230.7 3.0? liquid . 95
odor
35^-8 2.32 wh.tc 122
g l.tssy subl Imes
need 1 cs
295 2 - white
-Cj 318.7 crystal 1 Ino
42n*l Ed . Chemical Rutbwr Publishing Co., Clcv^ldnd, Ohio.
of Cht-oiistry, Jth £d., Handuook Pub, Inc. ,,1556.
2.5 1/1G__
«20) soluble/
alcohol ,
ether
3.5 r.G/ld
VOl ./Cnlo-
roform
si Ignt ly
sol ./ether
very
soluble
F lamnablc
Acute oral 1-0,.*
(rat) 'lO mg/k5
(pheny I mercury
acetate)
Acute oral
fjrm Chemicals Handbook, 1^72.
Personal cor/r.^nlcat ion H. Leo Vo1f>;. SC tnvi ron, ,c..ta I desearch Loboratory, EPA. Athens. Georgia.
-------
32 50 '58
3000
ce.
< 1000
Q
Ul
cc
cc
Ul
UJ
o
CO
IT
UJ
a.
en
X
300
100
30
10
3
1
ORNL-OWG 74-11871
TEMPERATURE (°F)
86 104 122 140 158 176 194 212
WEIGHT
VAPOR
PRESSURE
1.0
0.3
0.1
0.03
0.01
0.003
0.001
0.0003
E
~
UJ
cr
LU
cr
o_
0.0001
0 10 20 30 40 50 60 70 80 90 100
TEMPERATURE (°C)
Figure 2.1 WEIGHT PER CUBIC METER OF SATURATED AIR
AftD VAPOR'aBRESSURE OF MERCURY AS A
FUNCTION OF'TEMPERATURE.
-------
to form alloys (amalgams) and inorganic salts. Inorganic compounds of
mercury possess a lower vapor pressure than elemental mercury but some
f
organic mercury compounds like methylmercury, formed under proper
environmental and microbial conditions, have a vapor pressure orders of
magnitude higher than the metal. This property provides the mechanism
for distribution of mercury through the atmosphere and places mercury in
a form (vapor) that is a particular health hazard.
2.3 CHEMICAL CHARACTERISTICS
2.3.1 Inorganic Compounds of Mercury
Mercury metal is somewhat reactive; it can be dissolved with con-
centrated sulfuric acid or hot nitric acid. It does not react with air,
ammonia, carbon dioxide, nitrous oxide, or oxygen, but does react readily
with the halogens, sulfur, and hydrogen sulfide. Mercury forms two series
of inorganic compounds: mercurous with a valence of +1, and mercuric with
a valence of +2. All common mercury compounds are volatile and all of
these (except the halides) decompose to elemental mercury on heating.
Unlike most other metals, mercury exhibits a pronounced tendency to form
covalent rather than ionic bonds. The unique mercurous ion, for example,
consists of two .covalen^ly bonded mercury atoms, (+Hg:Hg+) possessing
*»
less than a total of two plus charges. 'With the exception of the nitrate
and perchlorate, most mercurous salts are relatively insoluble in water
(solubility <5 mg/1). Some of these, when moist, will decompose into the
corresponding salt and colloidal mercury.
2.3.1.1 Oxidation-Reduction Equilibria—The equilibrium thermodynamics
of mercury-sulfur interactions and the mercurous-mercuric disproportiona-
tion are important in understanding transformations of the mercury cycle
-------
in the environment. The oxidation-reduction potentials for some mercury
half-reactions are given in Table 2.2. It is clear from the positive
potentials for reaction (1) and reaction (7) reversed, that mercury, both
as the metal Hg , and as mercuric ion Hg , will easily be removed from
aquatic systems as insoluble HgS in the presence of sulfide ion or sulfur.
Mercuric sulfide is one of the most insoluble substances known (solubility
product = 4 x 10"53) (Wallace et al., 1971).
Mercurous chloride, too, is sparingly soluble in aqueous solution
and would provide another route for removal of mercury were it not so
readily decomposed into mercury and mercuric ion. Equations (4), (5),
and (6) of Table 2.2 indicate the very small differences between potentials
associated with the oxidation of Hg and Hg (1) to Hg (11). Consequently,
2+ 0 2+
the potential of the disproportionate equilibrium Hg2 = Hg + Hg is
only -0.131 volts. D'ltri (1972) indicates that 0.520 volts is the
potential commonly observed in oxygenated natural waters. This is far
in excess of the 0.131 volts necessary to drive the decomposition, a
process also observed to take place in the presence of heat and light.
(Mellor, 1952). For this reason, mercurous mercury is rarely found free
in the environment, but functions as an intermediary between the various
inorganic and organic species of mercury.
2.3.1.2 Acid-Base Equilibria--Mercuric mercury, the most prevalent form
of oxidized mercury, is important both environmentally and biologically.
2+
The ion Hg is fairly acidic (Hietanen and Sillen, 1952) resulting in
rapid hydrolysis in water:
,2+ + +
Hg^ + H20 = HgOH + H
HgOH+ + H,0 = Hg(OH)9 + H+.
-------
Table 2.2. OXIDATION - REDUCTION POTENTIALS OF MERCURY
(1)
(2)
(3)
(4)
(5)
(6)
(7)
Hg +
Hg +
2Hg +
2Hg =
Hg =
Hgp+=
HgS =
S"2 = HgS + 2e~
20H" = HgO + H20 + 2e
2C1" = Hg2Cl2 + 2e
Hg2+ + 2e
Hg2+ + 2e
2Hg2+ + 2e
S + Hg2+ + 2e
Volts
+0.
-0.
-0.
-0.
-0.
-0.
-1.
(25°C)
70
098
2675
789
854
920
05
Source:
Latimer and Hildebrand (1951).
-------
?_L I
Surprisingly, Hg differs from most acids in that it is less acidic than
the first hydrolysis product, HgOH . As a result, the relative amount of
HgOH* in equilibrium with Hg and Hg(OH)2 in aqueous systems will be quite
low, existing only over a very narrow range of pH (Fig. 2.2). In fact,
the presence of HgOH in high concentration would be exceptional
2+
considering the complexing behavior of Hg to be discussed in the next
section.
2+
Mercuric ion, Hg , again exhibits its acidic character in inter-
actions with Cl". Doubly coordinated mercury, HgCU, predominates in
aqueous solutions except at high chloride ion concentrations. In sea-
water (5 x 102 nM Cl") HgCl42~ is most important (see Fig. 2.3.).
2.3.1.3 Complex Formation—An examination of the complexing behavior of
mercury provides insight into some of the environmentally and biologically
important forms of mercury and their pathways. Mercury (11) forms com-
plexes with both inorganic and organic ligands. These are mainly
characterized by a two-coordinate linear arrangement (LHgL), although the
four-coordinate tetrahedral structure is not uncommon. In aqueous solution
2+ -2
Hg exists as HgCl^ in the presence of excess chloride ion, but its
structure has not been unequivo&ally determined (Webb, 1966). The
•*.»
octahedral configuration is rare.
Mercury forms stable complexes with halogens, sulfur, carbon, nitrogen,
phosphorus, and alkyl and aryl groups. Mercuric chloride (HgCl2) exemplifies
the two-coordinate linear complex. It is distinctly molecular; it
crystallizes in an essentially molecular lattice; it has a very low
melting and boiling point compared to ionic chlorides; it exists in aqueous
-------
PERCENT MERCURIC ION
CT5
CD
oo
CD
VJl >
IV)
O
Figure 2.2 DISTRIBUTION OF Hg(II) AS A FUNCTION
OF pH.
Source:
Baughman, Gordon, Wolfe and Zepp (1973).
-------
1.0
o.s
0.6
0.4
FRACTION
OF
TOTAL
0.2
10
-8
H«CI
10
- 6
10
10'
10
10
(CD
Figure 2.3 DISTRIBUTION OF Hg(II) AS A FUNCTION OF
CHLORIDE CONCENTRATION.
Source:
Webb (1966, p. 734 as cited from
Si 11 en, H49).
-------
solution and vaporizes as HgClg molecules; it is surprisingly soluble in
organic solvents (see Table 2.1). The exceptional stability of the doubly
coordinated complex compared to singly associated mercury is illustrated
in Table 2.3. D^ is the energy supplied in the process LHgL = LHg + L"
while D~ is the heat required to remove the second ligand, LHg = Hg +
L". The large difference between the first and second dissociation energy
is strik'ing. It requires three to seven times as much energy to sever
the first mercury-1igand bond as the second, while for dimethyl zinc, a
more normal organometallic compound, D, and D^ are almost the same
magnitude. Mercury has a powerful tendency to form two bonds, a character-
istic of considerable importance in its toxicological behavior.
2.3.2 Organic Compounds of Mercury
As noted by Coates (1956), organomercury compounds are not signifi-
cantly different from other organometallic compounds, except for a lower
than usual reactivity, especially toward air and water. Three major
types of organomercury compounds of interest are those in which mercury
is bonded to the organic group: (1) directly through a carbon atom, ••
(2) indirectly through a nitrogen atom, and (3) indirectly through a
sulfur atom. Because it is so Important for understanding the behavior
of mercury in the environment and its toxicity in organisms, the chemistry
of methylmercury and its compounds are emphasized.
2.3.2.1 Mercury-Carbon Compounds—Of all organomercurials, dimethyl-
mercury and methyl mercuric ion are critically important in the environ-
ment. Produced anaerobically in aquatic systems from other forms of
mercury (Wood et al., 1968), dimethylmercury undergoes a number of
11
-------
Table 2.3 BOND DISSOCIATION ENERGIES
(kcal/mole}
Compound D1 D
(CH3)2Hg
(C2H5)2Hg
HgCl2
CH3HgCl
C2H5HgCl
C6H5HgCl
(CN)2Hg
(GH3)2Zn
51.5
42.5 '•
81
64.3
60.3
66.4
123
47
6.9
5.9
24
24
24
24 '
23
35
Source:
Roberts (1968).
12
-------
conversion reactions producing end products, the particular species of
which depends upon.the pH and concentration of prevailing ions (Baughman,
Gordon, Wolfe* an<£ Zepp, 1973). Reactions producing dimethylmercury and
converting it to an organic salt are best classified by examining the
characteristics of the mercury-carbon bond.
2.3.2.1.1 Reactivity—The reactivity of an organometallic bond is
determined by the percent ionic character of the bond—the more ionic,
the greater the reactivity. The mercury-carbon bond is only 9 percent
ionic (Roberts, et al., 1968) making it 91 percent covalent. This pre-
dominantly covalent character of the Hg-C bond helps account for the unusual
inertness of organic derivatives of mercury toward oxygen, oxidizing agents,
water, oxygen containing organic compounds, and weak acids.
2.3.2.1.2 Reactions—Organomercurials are prepared fairly easily.
Although active metals will replace mercury from its organic compounds,
for example.
(C6H5)2 Hg + 2Na = 2CgH5Na + Hg,
mercuric halides will replace active hydrogen or active metals such as
magnesium and lithium from their organometallic salts to form organo-
mercurials (Markarova and Nesme^anov, 1967).
2RMgX + HgX2 = R2Hg = 2MgX2
2RLi + HgX2 = RgHg + 2LiX
RH + HgX2 = RHgX + HX.
These organomercury compounds, in turn, readily undergo important
reactions to form organomercury salts.
R2Hg + HgX2'= 2RHgX
For R = methyl or phenyl, the equilibrium for the gaseous reactions
13
-------
100
80
31
O
60
o
C£
LU
D-
40
20
0
CH3Hg'
CH-jHgOH
0 1 2 3 4 5 6 7_ 8 9 10
EH . '
Figure 2.4 ' DISTRIBUTION OF METHYLMERCURY AS A
FUN'CTION'OF pH- -
Source:
Baughman, Gordon, Wolfe, and Zepp (1973).
14
-------
100
re
o
cr>
SO
O
60
40
20
0
C6H5HgOH
2 ..4 6. .. 8
Figure 2.5 DISTRIBUTION OF PHENYLMERCURY AS A
FUNCTION OF pH.
Source:
10
Baughman, Gordon, Wolfe, and Zepp (1973).
15
-------
favors organomercurial salt formation by 6 kcal/mole (Skinner, 1964).
In aqueous solution the salt formation shows a strong pH dependence, the
reaction rate increasing dramatically as the pH is decreased. This may
be a significant degradative pathway for dimethylmercury in an acidic
natural environment (Baughman, Gordon, Wolfe, and Zepp, 1973).
2.3.2.1.3 Hydrolysis—Once formed, methyl and phenylmercury salts
dissociate in aqueous solution, the extent of dissociation depending upon
the particular salt (nitrates and sulfates completely dissociate; other
salts dissociate only partially) and its concentration. The methyl and
phenyl mercuric ions thus formed hydrolyze rapidly to form the respective
hydroxide, a process that is pH dependent as shown" in Figs. 2.4 and 2.5
It is clear that at pH factors encountered naturally, the hydroxides are
the principal species.
2.3.2.1.4 Acid cleavage--Baughman, Gordon, Wolfe, and Zepp (1973) also
studied the acid cleavage of dimethylmercury using mineral acids. The
results definitely show the reaction to be first order with respect to
concentration of both reactants and with a rate constant, extrapolated to
_c
25 degrees C, of 7 x 10 I/mole sec. The mechanism is thought to take
place directly.as showri below:.-
*.*
" *
-CH3 +
H3CHgCH3 ^ H3CHg^ «__>% + HgCH3
+
H+ H+
In summary, dimethylmercury can suffer any of a number of chemical
degradation pathways. All lead to methylmercury salt or methylmercuric
ion or the hydrolysis product of methylmercuric ion, methylmercuric
16
-------
hydroxide. The particular form depends upon pH and the anions present
in solution.
2.3.2.2 Mercury-Nitrogen Compounds—The nature of the mercury-nitrogen
bond, important for understanding possible interactions of mercury with
living systems, follows that of general mercury complexing behavior:
the formation of a linear, two-ligand grouping. Amines, amides, and
imides are formed by direct reaction of the halide with ammonia:
HgCl2 + 2NH3 = (NH3)2HgCl2
HgCl2 + NH3 + NH4OH = HgNH2Cl
HgCl2 + (excess) NH4OH = (Hg2N)OH-2H20
The product in the first reaction contains the linear amine group
2+
(H^N-Hg-NH-) . If nitrogen is bonded to electronegative groups rather
w *5
than hydrogen, a pseudohalogen of mercury is formed:
HgF2 + 2(CF3-N=CF2) = (CF3)N:Hg:N(CF3)
where N(CF,)2 behaves like a halogen (Roberts, 1968).
The affinity of mercury for amine constituents is assumed responsible
for the complexing of mercury by amino acids shown to reduce the
?«
bactericidal activity of HgCl2 (Webb, 1966). The mercury atom, thought
to form a bridge between the alpha amine and the carboxyl group, has the
capacity of complexing either one or two amino acids, the two amino acid
grouping satisfying the double coordination tendency of mercury.
17
-------
-
IT 0-CO
\
-
/ oc-o
OC-0. H2
single double
bridge bridge
2.3.2.3 Mercury-Sulfur Compounds—A large measure of the well-known toxic
effects of mercury can be attributed to the strong covalent mercury-sulfur
interaction. Because of this interaction, the active enzyme sulfhydryl
groups and the sulfur-sulfur linkages in proteins are logical sites for
attack by mercurials.
2.'3.2.3.1 Substitution reactions—Mercuric oxide reacts with alkyl thiols
(mercaptans), often violently, to form alkyl mercaptides,
2CH3SH + HgO =
while the phenyl derivative is obtained by direct reaction with the metal
C6H5SSC6H5 + Hg = (CgH^Hg.
In the above 'reversible reaction one S-S link is replaced by two Hg-S
links. The observed lack of an appreciable heat effect thus provides an
estimate of the average Hg-S bond energy as 32 kcal/mole since the S-S
bond energy is 64 kcal/mole (Sidgwick, 1950). The destruction of S-S
linkages between peptide chains in proteins to form Hg-S linkages
undoubtedly is the mechanism for denaturation of proteins by mercury
compounds. Although denaturation may not be energetically advantageous
18
-------
under physiological conditions, so that the process is not generally
considered of major importance for disruption of protein activity, a
reversible equilibrium exists such that a progressive loosening of the
protein structure may take place exposing heretofore protected SH groups to
irreversible attack by mercury (Webb, 1966).
2.3.2.3.2 Exchange reactions—Like so many compounds of the R2Hg type,
(RS)pHg exchanges with mercuric halides to form the half halide
(RS)2Hg + HgCl2 = 2RSHgCl
which upon dissociation yields the active ion, RSHg . A reaction
possibly indicative of biological effects involves the interaction of
mercuric chloride with monothiols such as amino acids or small peptides
cystein
HgCl2 + glutathione = RSHgSR
thioglycolate
to form dimercaptides (Webb, 1966). Dimercaptides, unexpectedly, are
also found to be toxic. This is thought to be due to an exchange reaction
in which mercury attaches itself to critical enzymatic sulfhydryl groups,
R'fHgSR" . -F^RSH = R'HgSR + R" SH
1' "*
an exchange that proceeds at room temperature and blood pH (Webb, 1966).
2.3.2.3.3 Complexes with nucleic acids—The general effects of mercury
complexation with nucleic acids has been summarized by Webb (1966).
Mercury forms complexes with nucleic acids obtained from animal and
plant tissue, bacteria, and viruses. The site of binding is believed
to be the bases with a Hg:base combining ratio of 1:2 in most cases, Hg
apparently bridging the double strands of the DNA helix.
19
-------
As noted by Webb (1966), one must assume that in most physiological
media organic mercurials will exist in a variety of complexes—organic,
inorganic, and mixed—and that the nature of the competition between
these ligands will determine the extent of reaction with protein and
enzyme sulfhydryl groups.
2.4 ANALYSIS FOR MERCURY
2.4.1 Considerations In Analysis
Analysis is implicit in every document or article citing a mercury
concentration, regardless of whether the source of mercury is experi-
mental, environmental, animal or human. It is important to know the
reliability of trace level and analysis. Hume (1973) has examined the
present state-of-the-art trace metal analysis and its implications;
this discussion follows his general comments.
He points out first the general lack of interlaboratory agreement in
analyses of blind samples. An example is given from an unpublished
report dated 1970 of 13 laboratories that participated in analyzing the
trace metal content (not mercury) of three subsamples, each taken frpm
two large, primary samples of seawater. Conventional atomic absorption
spectroscopy, -neutron'activatfpji analysis or colorimetric procedures
1' »
were used. Values reported ranged from 3.7 to 47 yg/kg (ppb), with a
range of standard deviations per set of analyses between 3 and 70 percent.
Before it is assumed that water chemists are particularly inept, Hume
hastens to point out the same lack of consistency is in some degree
characteristic of all experimental measurements. Discrepancies, however,
are not obvious except in demanding procedures such as trace metal
20
-------
analyses where the "signal to noise" ratio is unfavorable and the pitfalls
are numerous. Nonetheless, some sources of discrepancy can be isolated,
examined, and possibly eliminated.
2.4.1.1 Sources of Discrepancy of Analytical Results—Operator and
instrument variability, understandable sources of disagreement, can be
controlled somewhat by automated procedures and instrumental techniques
now largely implemented at government agencies such as the U.S. Environmental
Protection Agency (Manual of Methods for Chemical Analysis of Water and
Wastes, 1974). Other sources require an appreciation of the minute
quantities of metal measured (Table 2.4). A natural mercury concentration
of 0.001 yg/g or 1 ppb corresponds to less than one atom of mercury, for
every 10 (billion) atoms of other substances. Detection of this
concentration is a result of a multistage process, each step of which
provides a means for introduction of errors. Preceding the actual
instrumental measurement, the sample is usually collected, stored, pre-
treated for quantitative subsampling, then chemically treated for separation
or concentration. A typical chemical treatment for a biologic samplers
shown in Table 2.5 (Smith and Windom, 1972). At each step, metal can be
lost or gained. ' Reagents are notorious for background metal ion con-
'' *
centration, often far in excess of the sample (Handbook for Analytical
Quality Control in Water and Wastewater Laboratories, 1972). Possible
loss of mercury compounds by volatilization during chemical processing
has long been recognized as another potential source of error. Likewise,
during storage, mercury can be leached into solution from laboratory or
container materials or lost to container walls by sorption (Campbell et
al., 1972). This is one of the reasons for promotion of neutron activation
21
-------
Table 2.4. UNITS OF HEIGHT AND CONCENTRATION
Units of weight
1 kilogram (kg) = 1000 grams (g)
1 milligram (mg) = 10'3 g
1 microgram (yg) = 10~6 g
1 nanpgram (ng) = 10"9 g
1 picogram (pg) = 10"12g
Units of concentration
For foods, body organs, and other solids—weight: weight basis:
1 part per million (ppm) = 1 mg/kg or 1 vg/g
1 part per billion (ppb) = 1 yg/kg or 1 ng/g
1 part per trillion
-------
analysis, namely, the accessibility of a blank container count before
sample collection (Thatcher and Johnson, 1971). A recent publication,
however (Weiss and Chew, 1973), presents data indicating a 30 percent
loss of expected induced activity (12 percent to the walls of the vial)
in irradiation of unacidified aqueous mercury solutions. The loss is
thought to occur by two routes: adsorption and volatilization during
irradiation.
Environmental samples contain an unpredictable assortment of in-
organic and organic substances, in addition to the trace metal, that can
contribute to analytical interference. Natural chelating agents derived
from decomposition of plant and animal matter can prevent water-organic
liquid extraction of the metal. Algal or bacterial action on mercury may
continue in stored natural fluids while mercury in tissue samples continues
to change during decomposition. Both processes can be controlled by
proper treatment at the time of collection.
In conclusion, trace mercury analysis, in the ppb range can be
successfully accomplished by considering and avoiding or compensating .for
all the known pitfalls. Only those analyses utilizing proven or standard-
ized procedures -and reporting standard deviations as well as calibrations
using a known standard or spiked sample should be accepted. Trace metal
analysis is presently an extremely active area of research directed at
establishing procedures leading to increased sensitivity, precision, and
accuracy.
2.4.1.2 Evaluation of Early Analytical Results—It is generally accepted
that techniques in trace metal analysis have undergone considerable
23
-------
improvement in the past ten years leading to a need for assessment of
earlier analyses. To do this, it is important to recognize not so much
the change itself as the direction of change. Prior to the mid-1960's,
for instance, many analyses of biologic tissue determined total mercury
without distinguishing between inorganic and organic forms. Westoo (1966),
in identifying methylmercury as the prevalent form in fish, focused
attention on the importance of analysis for organomercury compounds.
Today, analyses of environmental or biological samples for mercury are
more likely to involve detection of the form as well as the quantity.
Likewise, as improvements in analytical techniques were instituted, greater
sensitivity, selectivity, and reliability were attained. These lead to
improved detection of the mercury in a sample, even as the concentrations
diminish.
Since there are more pathways for error leading to apparent low
rather than apparent high determinations, it is probably safe to assume
that, if in error, earlier analyses were more likely to have reported
concentrations lower than the true value rather than higher. Mercury was
reported absent because of poor detectability; for example, volatile
mercury compounds were lost in.hjrt digestion of samples or mercury was
1' *
not totally recovered because of inefficient oxidizing reagents.
Processing for total mercury analyses often neglected organic mercury
compounds entirely.
On the other hand, the commonly cited mechanism for higher than
true mercury determination, contamination of reagents and laboratory ware,
can contribute parts per billion and possibly parts per million in
24
-------
Table 2.'5. PROCEDURE FOR CHEMICAL TREATMENT OF
SAMPLE TO DETERMINE TOTAL MERCURY CONTENT
1. Weigh 0.5 gm of frozen tissue into 100 ml beaker.
2. Add 4.0 ml of cone. H SO and 2.5 ml of cone. HNO .
£. * O
3. Cover beaker with a watch glass and place in a water bath at 58 degrees
centigrade overnight.
4. Carefully transfer the sample solution to a BOD bottle, washing the -
original sample beaker with redistilled water.
5. Dilute sample solution to 100 ml and add 1 ml of KMnOu solution.
6. Shake and add additional portions of KMnOu until the purple color persists
at least 15 minutes.
7. Add 2 ml of K0S000 solution and allow to stand 30 minutes.
Z Z o
8. Add NaCl-hydroxysulfate in 2 ml increments until a clear solution is observed.
9. Add 5 ml of stannous sulfate and immediately attach to aeration assembly.
10. From recorder peak height, find the micrograms Hg from a c libration curve.
Source:
Smith and Winddrn (1972).
25
-------
particularly aggravated cases. Blank determinations along with
purification of reagents and labware help eliminate this source of
error, Another i-rapgrta-nt route that leads to apparent high values
involves loss of mercury from synthetic standard solutions. Standard
solutions are almost invariably prepared with distilled or deionized
water. As noted in Table 2.6, unless carefully treated, the half-life
of mercury in distilled water is as little as one-half that of mercury
in natural water. Natural water contains an abundance of soluble ions*
thought to prolong the half-life of mercury (Rosain and Wai, 1973).
Feldman (1974) noted an apparent increase with time in the mercury con-
centration in natural water samples, attributable to a decrease with time
in the strength of his synthetic standard solution. His recommendations
for preservation of standard solutions are discussed in Section 2.4.2.3.
It is likely that a fair portion of the systematic errors in
mercury analysis have now been detected and documented. Although there
is always a lag between documentation and implementation, the improvement
in agreement in interlaboratory analyses (Section 2.4.3.2) may be indicative
of improved analyses in general. Likewise, the utilization of standard
methods and standard environmental samples lends added confidence to
3»
recent analyses. "
2.4.2 ANALYTICAL PROCEDURE
2.4.2.1 Storage and Preservation—A sample that cannot be analyzed
immediately must be stored. Contrary to expectation, this is not a static
phase of the analytical procedure and, in fact, it presents another route
for loss of mercury. In this case "loss" indicates mercury originally
26
-------
Table 2.6. HALF-LIFE IN DAYS OF 26 ppb MERCURY IN
AQUEOUS SOLUTION
Container
Polyethylene
Polyvinyl chloride
Soft glass
Distilled
1.58
1.98
2.98
pH7
water Creek water
3.95
4.38
4.44
pH2
Creek water
4.0
1.7
3.5
Source:
Rosain and Wai (1973).
27
-------
present; this is undetectable. Rosain and Wai (1973) studied the rate
of mercury loss from solutions of natural and distilled water, spiked
with 25 ppb mercuric ion, when stored in stoppered polyethylene, poly-
vinyl chloride, and soft glass containers. Severe losses, observed at
pH 2 and 7, were considerably curtailed by acidification with, nitric
acid to pH 0.5. The half-lives of stored mercury is given in Table 2.6.
The loss is exponential, only half the original quantity remaining after
as little as 1 1/2 days. At pH 0.5, loss was not detected after 4 1/2
days and was barely detected (2 percent loss) after 15 days. Feldman
(1974), working at the 0.1 to 10.0 ppb range, found losses of mercury
from both glass and polyethylene containers in spite of acidification
and preservation with potassium permanganate. Addition of 0.01 percent
dichromate ion in place of permanganate stabilized the acidified solutions
for as long as 5 months.
Solid biological samples are adequately stored without loss of
mercury by freezing immediately after collection. Preservation and
storage of urine samples have been discussed by Trujillo et al. (1974.1.
Potassium persulfate, added to the sample at the time of collection,
preserves the sample for several,days.
2.4.2.2 Concentration and Separation—In principle, any mercury con-
centration, no matter how small, can be determined if a sufficiently
•large sample is collected and the total mercury separated into a small
volume. However, any process, no matter how judiciously applied,
represents a route for loss of mercury.
28
-------
2.4.2.2.1 Evaporation—Concentration and separation are essentially the
same process. The 'first removes the matrix from the metal; the second
removes metal from ihe matrix. The simplest concentration technique is
evaporation, a valuable but frequently undesirable method considering
the volatility of many mercury compounds, particularly organomercurials.
Nonetheless, it has been used advantageously to concentrate mercurials
in benzene solution by evaporation of a portion of the benzene after
liquid-liquid extraction of organomercury salts preparatory to gas chroma-
tographic injection (Longbottom, 1973).
2.4.2.2.2 Solvent extraction—Solvent extraction, widely used in aqueous
analysis for separating and concentrating organic mercury compounds,
depends upon the differential solubility of mercury compounds in mutually
immiscible liquids, e.g., benzene and water. Specifically, benzene or
toluene is added to a mercury containing aqueous solution;' the mixture
is agitated sufficiently to allow optimum transfer of the solute between
the two phases, and then the mixture is allowed to separate and the organic
phase containing mercury is drawn off. This procedure may be repeated'
with fresh solvent as often as necessary to effect as complete a recovery
, -r
\as possible. Inorganic mercury frtay be extracted into an organic solvent
by addition of an organic chelating agent to form an organic mercury
complex. Dithizone, widely used for extraction of inorganic mercury, not
only complexes quantitatively, but forms a colored complex that is detected
spec-trophotometrically (Sandell, 1959). The principles and applications
of solvent extraction to water analysis are discussed by Andelman (1971).
2.4.2.2.3 Amalgamation—Like solvent extraction, amalgamation depends
upon the differential solubility of a solute, in this case elemental
29
-------
mercury, in each of two different phases. Traces of metallic mercury are
immediately soluble in gold and silver. Grids of gold or silver are placed
in an airstream to collect airborne elemental mercury and a gold-coated
fritted glass disk has been used to capture mercury by passing air
through it at one liter per minute (Instrumentation for Environmental
Monitoring—Air, 1974). Similarly, mercury has been collected from
acidified water samples by amalgamation on a silver wire (Fishman, 1970)
or by electrodeposition onto a copper cathode (Doherty and Dorsett, 1971),
although the presence of sulfide ion in the water causes low results
(Fishman, 1970). Amalgamated mercury is released (usually into an atomic
absorption cell) by simple heating to drive off the volatile metal.
2.4.2.2.4 Carbon adsorption—Atmospheric mercury can be concentrated on
activated carbon. Moffitt and Kupel (1970) used a commercially available
impregnated charcoal to trap mercury in industrial atmospheres. Air is
pumped through a sampling tube containing two tandem charcoal sections
separated from each other and from the atmosphere by glass wool plugs.
The glass wool plug at the inlet end of the tube is analyzed for particulate
bound mercury while adsorbed volatile mercury is determined by atomic
absorption spectroscopyf. The ef-fectiveness of the charcoal filter is
.3*
determined by the absence of mercury on the second section.
2.4.2.2.5 Ion exchange—Ion exchange separation is a well-established
analytical technique, although applications to mercury analysis have been
few. Selectivity occurs as a result of the relative affinity of a given
ion exchange resin for particular ions (Andelman, 1971). An anion ex-
change resin-loaded filter paper has been used to remove mercury from
30
-------
natural water containing from 0.03 to 6.5 ppb mercury (Becknell et al.,
1971). Both the inorganic and organic forms of mercury are converted
to HgCK before filtering. The mercury loaded papers are air dried
and then sealed in mylar film for irradiation prior to neutron activation
analysis. In another study, mercury collected directly on a chea.lting
resin from seawater was so strongly retained no reagent was found to
elute it completely for analysis by atomic absorption spectroscopy
(Riley and Taylor, 1968).
2.4.2.3 Chemical Treatment of Samples
2.4.2.3.1 Aqueous mercury—Mercury in aquatic samples appears as in-
organic or organic species either dissolved, sorbed onto particulate
matter, or entrained within a particulate matrix. Total mercury deter-
mination measures all of these. Thus, samples require pretreatment to
release mercury from all the forms in which it is collected and transform
it into a state compatible with the measuring technique. Kopp et al.
(1972) have described some of the obstacles inherent in the pretreatment
procedure for lake and river waters and also proposed methods for over.r
coming them. Addition of acids to aqueous samples, for example, generates
heat which can lead to losses oCjiiercury compounds by volatilization.
' *
Aquatic materials also require an oxidizing agent strong enough to effect
the complete decomposition of organomercury compounds. The authors
demonstrated the ineffectiveness of commonly used KMnO, (only) for
release of all organically bound mercury, and the success of added
K2S2Og in conjunction with KMn04 in total recovery of mercury from dissolved
phenyl and methyl mercuric salts. The procedures, now incorporated into
31
-------
the standard methodology for water and wastes (Manual of Methods for
Chemical Analysis of Water and Wastes, 1974), are outlined briefly:
1. An aliquot is acidified with H2$04 and HN03;
2. KMnCL solution is added until purple color persists for
at least 15 minutes;
3. K0S000 is added and heat is applied for 2 hours at
c. c o
95 degrees centigrade;
4. Sodium chloride- hyroxylamine sulfate is added to
reduce excess permanganate;
5. Stannous sulfate is added just prior to aeration
into the atomic absorption cell.
2.4.2.3.2 Biologic mercury—It is important in analyzing for mercury in
biologic tissue to determine the total mercury content and also the
fraction of organomercury compounds, in particular, methylmercury.
Uthe (1971) describes a thoroughly tested total mercury procedure
essentially like that shown in Table 2.5 except for semiautomation of
the method. It consists of cold wet acid oxidation to decompose the .organic
matter releasing mercuric mercury which is then reduced to elemental
mercury, the form aerated from'solution for atomic absorption measurement.
Alkylmercury determinations require a completely different approach
to preserve the organic-bound form during extraction from the matrix.
Most techniques reported are variations of the original Westoo method
(Westoo, 1966, 1967, 1968). These consist basically of organic solvent
extraction and reextraction. Chemical treatment precedes extraction to
remove interfering substances such as sulfides and to convert the organo-
mercury compound to the halide salt (e.g., chloride or bromide), the
32
-------
form most accessible to electron capture detection after chromatographic
separation. Dialkylmercury compounds such as dimethyl mercury are not
as strongly bound to the matrix and are easily extracted into an organic
medium (benzene or toluene) as a first step prior to chemical treatment
of the remaining sample. Care is required, however, to prevent loss of.
the highly volatile dimethylmercury. This extracted mercury is then
subjected to halide treatment producing monomethylmercury halide which
is analyzed by gas chromatography (Mushak, 1973).
A procedure, proposed for adoption by the Environmental Protection
Agency for methylmercury determination in biologic media, has been
described by Longbottom et al. (1973). It includes preservation, storage,
chemical treatment, extraction, and cleanup. Copper sulfate is introduced
at the time of collection to preserve the integrity of mercury compounds
until analysis. Fish and sediment samples are frozen upon collection,
thawed before use, then treated with CuSCL to displace methylmercury from
its strong, natural inorganic and organic sulfur bonds. The free methyl-
mercury is converted to the bromide salt by addition of excess KBr to-a
solution strongly acidified with H2SCL (pH below 0.5); then it is
.-•—
extracted into'a toluene layer.** The extract cannot be injected into the
' . *
gas chromatograph until sulfur compounds are completely removed. This is
the purpose of the cleanup step, accomplished by a high efficiency
extraction of methylmercury into an aqueous thiosulfate phase, addition
of KI, then reextraction into benzene or toluene for injection into the
gas chromatograph. Any of the extraction or cleanup steps may be repeated
for improved recovery.
33
-------
2.4.2.3.3 Airborne mercury—Mercury appears in air in several forms: '•
as elemental free mercury atoms, as inorganic or organic mercury molecules,
and as any of these sorbed on particulate matter in the air. All forms
present a hazard necessitating their detection and monitoring.
Elemental mercury vapor, the form usually monitored, requires no
pretreatment and is detected directly in the field by drawing air through
a high sensitivity atomic absorption spectrometer (Jepsen, 1973).
Alternatively, mercury vapor can be collected before analysis by metering
air flow through flasks containing potassium permanganate--sulfuric acid
or iodine—potassium iodide solution, by adsorption onto impregnated
charcoal, or by deposition on filter materials (Lindstedt and Skerfving,
1972; Bogen, 1973). Airborne mercury trapped in solution is recovered
for analyses by any of the standard pretreatment methods while that de-
posited on filters, including particulate matter, may be determined
directly by neutron activation analysis (Bogen, 1973).
The collection systems discussed are inadequate for detection of
organic mercurials. Linch et al. (1968) found less than 20 percent of
dimethylmercury and less than 50 percent of diethylmercury in air re-
tained by an aqueous iodine—potassium iodine reagent and less than
.T»
5 percent of dimethylmercury is "retained by potassium permanganate—sulfuric
acid solution. Recoveries averaging 98 percent for dimethylmercury in
the 2 to 60 jjg range, however, were attained using an iodine monochloride
reagent. Near quantitative collection of diethylmercury, methylmercury
chloride, and ethylmercury chloride also was established. Iodine mono-
chloride is considered the only known absorbent efficient for collecting
34
-------
both inorganic and organic mercury (Instrumentation for Environmental
Monitoring-Biomedical, 1973, p. 3). The final mercury determination,
however, requires a method free of interference from iodine (i.e.,
atomic absorption spectroscopy cannot be used).
2.4.2.4 Methods of Analysis—The reliability of any analytical procedure
can be no more dependable than the least reliable step in the procedure.
Even assuming no systematic errors, the uncertainty of an analysis is the
sum of the uncertainty contribution of the individual analytical processes,
This arises from random error associated with any experimental procedure.
For this reason, an analysis is a continual checking process, first to
eliminate any systematic error and second to minimize random error.
The crucial instrumental operation often proves to be the limiting
factor in an analysis and most of the preliminaries are preparatory to
the instrumental step. In fact, an analytical method is named for the
instrumental step even though it often requires the least time and effort.
Table 2.7 shows the commonly used instrumental methods including a very
brief description of sample preparations and measurement techniques...
The sensitivity (column 6) is largely instrument dependent, experi-
mentally determined, a'nd defined differently by different authors. It
" *
is essentially the smallest quantity of substance that can be determined
reliably by the instrumental technique. In atomic absorption, for
instance, sensitivity has been defined as that concentration of analyte
that yields a 1 percent of full-scale reading or that will produce an
absorption of 1 percent (Minear and Murray, 1974) or that is three times
the standard deviation of blank readings (Standardization of Methods for
35
-------
Determination of Traces of Mercury, 1974).
The precision of the method is given in column 7 as the relative
standard deviation (i.e., the standard deviation of a set of sample
measurements divided by the concentration of the sample). The sample
concentration is also shown here since the precision is strongly
dependent upon it. (
Column 8, accuracy, is really a procedural calibration technique
that measures accuracy. Kaiser (1973) has discussed the three main
calibration methods for trace determination: with synthetic standard
samples, with analyzed standard samples, or by differential additions.
Ideally, synthetic standards are prepared and processed with the sample.
With mercury, however, it is exceedingly difficult, if not impossible,
to prepare synthetic trace samples from truly pure substances and to
transfer them into a state that duplicates the natural analysis sample.
Use of preanalyzed natural samples solves this problem but presupposes
that the problem of analyzing a natural trace sample with adequate
calibration procedures has already been solved (Alvarez, 1974). None-
theless, NBS biological preanalyzed samples are available and their use
is increasing (Catalog, of Standard Reference Materials, 1973). The most
*•»
prevalent calibration method, by differential additions, is the one
listed here. Small but known quantities of mercury compound are added
to the unknown samples before processing. Recovery of this quantity
measures the accuracy of the procedure. The main problem is to insure
that the spike is in the same physical and chemical condition as the
natural mercury component.
36
-------
PAGE NOT
AVAILABLE
DIGITALLY
-------
Other than the^ columns discussed, Table 2.6 is intended to be
•self-explanatory. • However, it is not intended to be a complete des-
cription of analytical methods. For instance, although total mercury
is determined in atomic absorption spectroscopy, this does not preclude
determination of organomercury concentrations. First, an intact sample
is processed; then a sample in which the organomercurials have been
separated by organic liquid extraction is processed. The difference
between the two determinations gives the concentration of organomercury
compounds. The species of organomercurial, however, cannot be determined
by atomic absorption. A brief description is given in the following
sections of the listed instrumental methods preceded by a few well-known
chemical methods. Some newer exploratory techniques are discussed in
Section 2.4.2.5.
2.4.2.4.1 Gravimetric analysis—All gravimetric procedures are
essentially alike. The sample is digested with a reducing solution to
convert all mercury to the elemental form. The mercury is driven off as
a vapor for heating and collected on a metal foil or screen with which
it amalgamates. Gold or silver is usually used, and the mercury is
determined by'the difference fn, weight before and after the amalgamation.
'' »
With routine analytical balances, a few milligrams of mercury can be
determined with reasonable accuracy; with the newer micro balances,
this level can be extended to a few micrograms. A variation of this
method involves the deposition of the mercury on a platinum cathode.
This is the method recommended by the American Society for Testing and
Materials for Mercury in Paint (Annual "Book of ASTM Standards, 1972).
38
-------
ABSORPTION
CELL
SAMPLE SOLUTION'
IN BOD BOTTLE
SCRUBBER
3f* CONTAINING
J A MERCURY
ABSORBING
MEDIA
Figure 2.6 APPARATUS FOR FLAMELESS
MERCURY DETERMINATION
Source:
Manual of Methods for Chemical Analysis
of Water and Wastes, 1974.
39
-------
2.4.2.4.2 Volumetric analysis—Aqueous volumetric procedures depend upon
2+
conversion of mercury to Hg ion, complexation of the ion, then
titration to a readable end point. In one widely used method, the
Volhard titration, potassium thiocyanate is added in excess to form
the sparingly soluble compound Hg(SCN)2. The excess thiocyanate is
titrated with ferric ion to produce a brilliant red color. The
advantage of the Volhard titration is that very few metals interfere;
the disadvantage is that the reaction is not entirely stiochiometric,
necessitating corrections that may introduce uncertainties beyond the
accepted tolerances for some trace analyses (Coetzee, 1961).
2.4.2.4.3 Micrometric determination—In this method mercury is .
electrodeposited from solution on copper wire; the mercury is then
distilled from the copper wire in a capillary tube. The volatilized
mercury condenses in a cooled section of the tube, the condensate is
united into a globule, and the diameter of the globule is measured with
a microscope. Under favorable conditions, amounts exceeding 0.5 yg
can be determined with an accuracy of +_ 2 percent and as little as 0.01 yg
with an accuracy of +_ 10 percent (Coetzee, 1961).
2.4.2.4.4 Colbrimetrfc spectrophotometry—Until the development of more
1 \
sensitive instrumental methods, dithizone extraction followed by
photometric analysis was the method of choice for trace environmental
mercury samples. Dithizone (diphenylthiocarbazone) complexes quantitatively
with mercuric ion in acidic aqueous solution. The complex is extracted
with chloroform as orange mercury dithizonate which exhibits an absorption
maximum at 490 nm. Various techniques are required to eliminate inter-
fering metals (Sandell, 1959). The sensitivity and procedures of the
40
-------
method are outlined in Table 2.7.
2.4.2.4.5 Cold vapor atomic absorption spectrometry--The use of a cold
vapor atomic absorption method for trace mercury analysis is so direct
and accessible under ordinary laboratory conditions that it has been
detailed as an experiment for (instruction in an undergraduate course in
analytical chemistry (Lieu et al., 1974). The equipment is shown in
Fig. 2.6. A hollow cathode mercury discharge lamp supplies radiation
at 253.7 nm for absorption by atomic mercury vapor aerated from solution
into the absorption cell. Mercury ions in solution are reduced to
elemental mercury by stannous chloride, then swept with helium into the
cell where radiation is absorbed by the mercury atoms. The concentration
of atoms is determined from the absorbance compared to a standard curve.
Atomic absorption is highly specific for the particular metal under
investigation; most interfering agents are readily removed, and it is
suitable for measurement of most environmental materials after pre-
treatment. Elemental mercury in air, for instance, is monitored directly
by passage of air through an atomic absorption cell (Jepsen, 1973). ••
. Unfortunately, atomic absorption determines only total mercury content
giving no information 'about tha,species or form of the mercury.
'' \ -
The cold vapor method has been readily adopted and likely will
eventually become the method. It is specific for mercury, all sorts of
pretreatment variations exist, it is applicable to extremely low
concentrations, it is fast, and above all, the equipment is readily
available and reasonable in cost. The Bureau International Technique
Du Chlor has selected cold vapor atomic absorption spectrometry as
-------
their standard (Standardization of Methods for the Determination of Traces
of Mercury, 1974),.and the sensitivity and accuracy are well within the
0.1 yg/g +. 10 percent cited as desirable for regulatory purposes (Alvarez,
1974).
2.4.2.4.6 Gas chromatography using an electron capture detector—Gas
chromatography actually refers to a separation technique. Coupling this
with a detector for sensing the separated components constitutes an
instrumental method, the only one in wide use which will determine organic
mercury compounds directly. These are converted to organomercury halides
to make the mercury volatile and chromatographable. After extraction into
an organic solvent, the organic mercury compounds are injected into a
GC inlet where they are vaporized and the gases passed through a chromato-
graphic column. The absorbent in the column is often a high-boiling
liquid adsorbed on a solid substrate; hence, the term gas-liquid chromato-
graphy. The volatile organics, partitioned between the stationary phase
and the mobile carrier gas, emerge from the column at different times and
are determined by one of several detection devices.
The electron capture detector, used almost exclusively in organo-
mercury determination by gas chfpmatography, employs a tritium or nickel-63.
- • • i ^
These are captured by sample molecules, reducing the current of electrons
to an anode under fixed voltage. The decrease in current is a measure of
the amount and electron affinity of the component, (Andelman, 1971).
Dressman (1972) found that phenylmercuric salts, except phenylmercuric
chloride, are converted in the gas chromatographic injection block to
diphenylmercury, as the major product, which is overlooked by electron
41
-------
capture detection. Baughman, Carter, Wolf, and Zepp (1973) found a similar
conversion of methylmercury salts to dimethylmercury and he suggests the
use of specially treated columns for reliable analyses.
2.4.2.4.7 Neutron activation analysis—The use of neutron activation
analysis of mercury in bio-environmental materials is now well established.
Usually, the sample is sealed in quartz vials and irradiated with neutrons
to convert Hg to Hg, a radioactive isotope with a 65-hour half-life.
The Hg is identified using a multichannel analyzer and Ge(Li) detector
(Westermark, 1972). The most important and useful aspect of activation
analysis is that no treatment of the sample is needed prior to neutron
irradiation, although post-irradiation separation can be performed to
increase sensitivity by removal of interfering substances.
The major limitation in activation analysis is the inability to
distinguish the chemical state of mercury in the sample. Additionally,
the excessive equipment cost relative to other methods, as well as the
need for a nearby neutron source (reactor), has to some extent reserved this
method primarily for referee analyses.
2.4.2.5 Newer Methods of Analysis
2.4.2.5.1 Atomic fluorescence gfiectrometry—-Atomic fluorescence depends
upon excitation of mercury atoms with a mercury lamp followed by detection
of the emitted radiation when the atoms return to the ground state. It
is reported to have a sensitivity advantage of at least a factor of 10 over
atomic absorption (Subber, 1974). It is useful in detecting mercury in
amounts between 0.1 ng and 1 pg. Above 1 yg, the calibration curve becomes
nonlinear (Subber, 1974).
42
-------
The techniques for pretreatment and for reduction and release of
mercury from solution are exactly the same as for atomic absorption. Here,
however, the 253.7 nm radiation from a mercury line source is focused onto
the vapor, and the resulting 253.7 nm fluorescence emission is monitored.
The added sensitivity is derived in part from the fact that the absorption
is a very small quantity determined as the difference between two large
quantities, whereas emission is this same quantity, determined directly
(Minear and Murray, 1974). Additionally, the emission is a function of
the intensity of the impinging radiation which can be varied to some ex-
tent to increase the signal. Muscat et al. (1972) used atomic fluorescence
to determine mercury in a number of environmental reference materials and
sediments. For a water sample from the Analytical Quality Control
Laboratory, Cincinnati, containing 4.2 ng/ml, a value of 4.2 j^ 0.4 ng/ml
was obtained. Wheat flour samples (International Atomic Energy Agency,
Code 66/10) yielded 5.1 +_ 0.5 ppm compared to a pooled analysis of
4.59 +_ 1.32 ppm by neutron activation or 4.92 +_ 0.45 ppm by atomic ab-
sorption. Atomic fluorescence appears to be a promising technique in-'terms
of sensitivity, availability, and ease of operation.
2.4.2.5.2 Spark source mass spestrometry—In an analytical program under-
»
taken by the NBS to provide a reliable value for the mercury content of
the ground Orchard Leaves, SRM 1571, a standard environmental reference
material, three analytical methods were used: atomic absorption spectro-
metry; neutron activation; and stable-isotope dilution with spark source
mass spectrometry (Alvarez, 1974). The first two are well-tested,
reliable methods. Spark source mass spectrometry has not been previously
43
-------
Table 2.8.
COMPARISON OF MERCURY RESULTS BY ISOTOPE DILUTION WITH
OTHER ANALYTICAL METHODS FOR ORCHARD LEAVES, SRM 1571
Average concentration and 95%
confidence limits in ug g"
Number of
determinations
Method
Lab
0.141 + 0.009
0.160 + 0.012
0.155 + 0.006
0.145 + 0.014
0.148 + 0.010
6
15
n
5
4
Isotopic dilution
Atomic absorption
Neutron activation
Neutron activation
Neutron activation
NBS
NBS
NBS
A
B
Source:
Alvarez (1974).
44
-------
Table 2.9. COMPARISON BETWEEN ELECTRON CAPTURE AND PLASMA
EMISSION SPECTROSCOPY SYSTEMS
n capture
1'l.iMiu emission
Selectivity Response to olcctron-alvsorbtng
compounds, cspci uily halogens,
nitrates, and conjugated earbonyls
Sensitivity IVo^ram level
Linear range" 50 lo 1UO
Stability I'air
lempcralurc limit 250°C(3II). 35trC(6JNi)
Carrier gas Nj or Ar-10'/ Cll^
Repairs I)y producer only
Life expectancy Limned by "poisoning" compounds
Renuik.s hasilv contaminated, easily i leaned,
sejisitivc lo u.ilcr, carrier gas
must bo dried
SpCLlroMnpii.il si'k'clivil) SensiiiNO (o
pr.KliL.ill) .ill ok'im'iils ( .in lie used
luilli as selOLtivo and geik'ial-purpose
dc'leclor
level
103 to
(iood to e\i.clli'iit
I'raclically tinlimiled
Ar ami lie
Very simple pioccdine, usually involves
a replacement of I lie quart/ i.ipill.ny
1'iaclie.ill) unlimited, un.illei.U-d by an>
compoiinds
No I emit > nun a led, voiy i'.is\ to ilean, insensitive
lo water, sensitive to tiiliogon liacei'.s
Note:
aLinear range is defined as the ratio of the highest to the lowest
concentration values which lie on a linear calibration curve.
^~
Source: ' ' ^
fc—BW^i^^l^^"^"^^^" t , ^ "
Talmi (1974).
45
-------
applied to environmental mercury problems, although it has been used at
NBS for standardization needs. The apparatus consists of a spark source
mass spectrometer with Mattauch-Herzog geometry (double-focusing). The
environmental standards were processed routinely to oxidize the organic
matter; then the mercury containing solution was spiked with 0.370 yg
?m 198
Hg and 50 yg Hg as a carrier. The mercury was electrodeposited onto
high-purity gold wires for sparking in the mass spectrograph. The con-
201 202
centration was calculated from the altered isotope ratio, Hg/ Hg.
The results are given in Table 2.8. The average concentration, 0.141 +_
0.009 yg/g, is seen to be in good agreement with averages determined not
only by other methods but by other laboratories.
2.4.2.5.3 Gas chromatography using a microwave emission spectrometric
detector—A gas chromatograph-microwave excited spectrometric detector
(GC-MES) has been built and applied to the detection of (CH,)9Hg,
*J L.
CH3HgCl and (CpH^HgCl at the 6, 7 and 4 picogram level, respectively
(Talmi, 1974). The relative sensitivity is at the 5 ppb level. The
technique is reported to be substantially faster and simpler than most
presently available ones. In this detector, the intensity of the 253.7
nm line emitted.from the microwave-generated plasma used as a GC detector,
3-%
is monitored to characterize the molecu'le and to determine its con-
centration. A comparison with a conventional electron capture detector
is given in Table 2.9. The GC-MES appears to be equal in sensitivity, yet
superior in all other respects to the GC-ECD.
2.4.2.5.4 Gas chromatograph using a mass-spectrometric detector—Although
gas chromatography mass-spectrometry has been applied for at least five
46
-------
years to the study of various organic pollutants (Webb et al., 1973), it
has only been used'sparingly for the detection of organomercury compounds
(Johansson, 1970). Baughman, Carter, Wolf, and Zepp (1973) utilized a
GLC-MS apparatus to demonstrate that ionic methylmercury compounds undergo
decomposition during gas-liquid chromatography (Section 2.4.2.4.6').
Johansson et al. (1970) analyzed eight samples of fish flesh containing
from 0.14 to 3.2 ppm mercury as methylmercury. Excellent agreement was
obtained in a comparison to the results using gas chromatography-mass
spectrometry, gas-chromatography-electron capture detection, and neutron
activation analysis. The three methods coincided with a deviation of
less than +_ 10 percent from the average value. The mass-spectrometer
provides a positive identification of organomercury compounds including
organomercuric iodide.
2.4.2.5.5 Stripping vo1tanimetry--Anodic stripping voltammetry is a
convenient, sensitive method for metals analysis in aqueous media,
particularly seawater (Smith and Windom, 1972). The customary electrode,
a mercury drop or mercury film, however, is obviously unsuitable for *•
mercury^determination; and since mercury amalgamates with platinum or
c
gold electrodes, another electrdde. material was required. Allen and
Johnson (1973) utilized a rotating ring-disk electrode having a glossy
carbon disk plated with a thin film of gold. Mercurous ion in 1.0 M
sulfuric acid solution was determined in the 0.10 to 4.00 ppb range with
a relative standard deviation of 7.5 percent. The limit of detection for
the technique is approximately 0.01 ppb. This particular method is academic
and will probably never be used in real-life analysis for mercury.
47
-------
2.4.3 Comparison of Analytical Methods
Gas chromatography is generally accepted as the most sensitive,
accurate method for organomercury determination. Controversy still
exists, however, between atomic absorption spectroscopy and neutron
activation analysis for total mercury determination. Wood (1972) claims
the latter technique is superior, asserting consistently lower results
are obtained using atomic absorption analysis. Hume (1973), however,
cites a comparison of analytical results for cobalt on two samples of
seawater from eight laboratories, four using atomic absorption with
chelation-extraction and four using neutron activation. Averages were
five- to sixfold larger by absorption than activation.
Interlaboratory comparisons using different instrumental methods
are necessary for elucidating the advantages and pitfalls of various
techniques while displaying to some extent the uncertainty inherent in
some trace analyses. However, trace analysis has been the subject of
rapidly advancing research directed toward improvement of precision and
accuracy through technique and instrumentation.
.2.4.3.1 Standard!zation—Analyses for trace levels of mercury are per-
formed in laboratories''throughout the world. Comparison of these results,
'' "*
however, is difficult due to lack of uniformity. Kaiser (1973) has
addressed this problem in terms of trace analyses in general, presenting
an excellent treatment of expressions of accuracy as discussed in
Section 2.4.2
All measured values are subject to errors—systematic and random.
The random error is usually evaluated by the individual investigator or
laboratory from a statistical evaluation of the data. Systematic errors,
48
-------
on the other hand, are not readily accessible to evaluation individually,
although blank readings are intended to eliminate them. Moreover, this
type of error acquires additional importance in trace element determinations
since it may contribute disproportionately to the "analytical signal."
Wilson (1974) has reviewed the role of systematic and random error in
standardization procedures. An acceptable test for systematic error
includes the use of biologic and environmental standard reference materials.
These enable the analyst to verify the accuracy (absence of systematic
error) in his analytical procedure. The NBS supplies certified biological
and environmental samples tested by a multiplicity of techniques, the
results of which are shown in Table 2.8 for Orchard Leaves SRM 1571
(Alvarez, 1974).
2.4.3.2 Interlaboratory Comparison--Inter1aboratory comparison studies
have been conducted since the mid 1960's. These have involved not only
different establishments, but also different instrumental methods. An
examination of the results of a few of these studies indicates a trend
toward increased accuracy, although this is not always immediately
apparent since comparisons have migrated from the ppm to the ppb range.
A comparative analysis of a-standard plant material submitted before
?%
1967 to laboratories around the world resulted in the inconsistent
average mercury content of 0.150 +_ 0.008 ppm by activation analysis and
0.0122 +_ 0.0024 ppm by colorimetric analysis (Bowen, 1967). Rottschafer
et al. (1971) reported results of replicate fish tissue samples analyzed
for mercury in 1970 or earlier by different laboratories and different
techniques:
49
-------
Method Results, ppm
Atomic absorption, laboratory 1 0.60
2 1.0
3 0.85
X-Ray fluoresence 0.40
Destructive neutron activation 0.87
A similar study with contrasting results was reported in 1974 and
is shov/n in Table 2.8. Not only was excellent agreement obtained between
different laboratories using the same technique, but also by one laboratory
using three different methods. It is worth noting that the 100 ppb
concentration range was chosen as desirable for regulatory purposes
(Alvarez, 1974). Another recent study (Standardization of Methods for
the Determination of Traces of Mercury, 1974) involved one method, atomic
absorption spectroscopy, 37 laboratories and samples containing mercury
that varied over three orders of magnitude of concentration from 20 ppm
to 20 ppb. The results are shown in Table 2.10. The relative standard
deviation from the mean is plotted against the concentration in
Figure 2.7 to show the' strong functional dependence of the reproducibility
'' *
on concentration. Although the authors were apologetic about the high
relative standard deviations at low concentrations, this is not un-
expected insofar as "analytical noise" is concerned (Kaiser, 1973).
The studies cited here are definitely not intended to be a com-
prehensive treatment of interlaboratory comparisons of analytical ability.
Rather, they are meant to demonstrate a definite trend toward improved
precision and accuracy in procedures for analyzing mercury in the
50
-------
Table 2.10. RESULTS OF STATISTICAL EVALUATION OF INTERLABORATORY
ANALYSIS FOR MERCURY
Results •% *
Arithmetic rrcan
Repeatability"
Standard dev.ation
Relati\e stirdard deviation
Reproduc'b.lr.y"
Standard dcsiation •
Re!ati\e standard dc\iai;on
Standard samples
Ctg. 5 0 my H(j kg
5.03 mgkg"1
OlSmgkg"1
3.5%
0.30 mg kg"1
5 9°'
->•' /o
Watte Caustic "ioiin
' ' Ctg. 20 0 imj Ilg l.g ' ' Sample 1 Sample ?
•203mgkg-' 3 IS rrg ks"1 214/igkg"1 201/igkg"1
08ms kg"1 0.10 rrg kg"1 1.7 pa kg"1 llpc'-.g"'
40?; 3.1% 8% 54%
llmgkg"1 034mgkg"1 48/igkg"1 38 ;ig kg
54% 11% 22% 19%
Notes:
Repeatability means single laboratory, single operator and single apparatus
precision; reproducibility means multi-laboratory, multi-operator and
multi-apparatus precision.
Source:
Standardization of Methods for the Determination of Traces of Mercury, 1974.
-------
10.
9_
8.
7_
6_
-H-
±t±t
_j_L I
I -.
> U
O «
I - --•-•
.- -.1
I 1
J < / 9_
_i_L_
±tt
~r-|— i--
~i~'"r
_ I
\ I
-1—
-t-'-
-| -;••
":^>. /"/
-l-t-:—
-------
environment. Currently, mercury and organomercurials can be determined
about as well as any trace element or trace organometallic of environmental
significance (Shults, 1975).
2.5 REFERENCES
1. Allen, R. E., and D. C. Johnson, 1973. "Determination of Hg(II)
in Acidic Media by Stripping Voltammetry with Collection,"
Talanta (Great Britain), 2£: 799-809. . .
2. Alvarez, R. , 1974. "Sub-microgram Per Gram Concentrations of
Mercury in Orchard Leaves Determined by Isotope Dilution and ,
Spark - Source Mass Spectrometry," Anal. Chem. Acta (Amsterdam),
73;33-38.
3. Andelman, J. B., 1971. "Concentration and Separation Techniques,"
i_n_: Instrumental Analysis for Water Pollution Control. K. H. Mancy
(ed.), Ann Arbor Science Pubs. Inc., Ann Arbor, Mich. 48106,
pp. 33-62.
4. Annual Book of ASTM Standards, Part 21, 1972. American Society
for Testing and Materials, Philadelphia, Pa.
5. Baughman, G. L., M. H. Carter, N. L. Wolf, and R. G. Zepp, 1973.
-—
"Gas-Liquid Chromatograptiy - Mass Spectrometry of Organomercury
Compounds," Journal of Chromatography, 76:471-476.
6. Baughman, G. L., J. A. Gordon, N. L. Wolfe, and R. G. Zepp, 1973.
Chemistry of Organomercurials in Aquatic Systems. National
Environmental Research Center, Office of Research and Development,
U.S. Environmental Protection Agency, Corvallis, Oregon 97730,
EPA-660/3-73-012, 98 p.
53
-------
7. Becknell, D. E., R. H. Marsh, and W. Allie, Jr., 1971. "Use of
Anion Exchange Resin-Loaded Paper in the Determination of Trace
Mercury in Water by Neutron Activation Analysis," Anal. Chem.,
43_( 10): 1230-1233.
8. Bogen, J., 1973. "Trace Elements in Atmospheric Aerosol in the
Heidelberg Area Measured by Instrumental Neutron Activation
Analysis," Atmospheric Environment (Great Britain), 7_:1117-1125, 1973.
9. Bowen, H.J.M., 1967. "Comparative Elemental Analyses of a
Standard Plant Material," Analyst. 92^:124-131.
10. Campbell, E. E., G. 0. Wood, P. E. Trujillo, and P. Stein, 1972.
Evaluation of Methods for Determining Mercury. LASL Project R-060,
Los Alamos Scientific Laboratory of the University of California,
Los Alamos, N.M. 87544, LA-5188-PR. 7 pp.
11. Catalog of Standard Reference Materials, NBS Special Publication
260. 1973. U.S. Govt. Printing Office, Washington, D.C.
12. Coates, G. E., 1956. Orango-Metallic Compounds, Methuen & Co.
Ltd. London , 197 pp.
13. Coetzee, J. F., 1961. "Mercury," in: Treative and Analytical
Chemistry, Part JI, Vol.--3, Kolthoff, I. M., P. J. Elving, and
j»
E. B. Sandell (eds.), Inters'cience Publishers, New York, N.Y.,
pp. 231-326.
14. Cotton, F. A., and G. Wilkinson, 1962. Advanced Inorganic Chemistry,
Interscience Publishers, New York, 959 pp.
15. D'ltri, F. M., 1972. The Environmental Mercury Problem, CRC Press,
Cleveland.
54
-------
16. Doherty, P. E., and R. S. Dorsett, 1971. "Determination of Trace
Concentrations of Mercury in Environmental Water Samples,"
Anal. Chem., 43_( 13): 1887-1888.
17. Dressman, R. C., 1972. "The Conversion of Phenylmercuric Salts
to Diphenylmercury and Phenylmercuric Chloride Upon Gas
Chromatographic Injection," Journal of Chromatographic Science,
10:468-472.
18. Farm Chemicals Handbook, 1972. Meister Pub. Co., Willoughby, Ohio.
19. Feldman, C., 1974. "Preservation of Dilute Mercury Solutions,"
Anal. Chem., 46(1):99-102.
20. Fishman, M. J., 1970. "Determination of Mercury in Water,"
Anal. Chem., 42(12):1462-1463.
21. Friberg, L., and J. Vostal (eds.), 1972. Mercury in the Environment
A Toxicolpgical and Epidemiological Appraisal, CRC Press,
Cleveland, 215 pp.
22. Hamilton, A., and H. L. Hardy, 1974. Industrial Toxicology, 3rd
Ed., Publishing Sciences Group, Inc., Acton, Mass., 575 p.
23. Handbook of Analytical Quality Control in Water and Wastev/ater
Laboratories, 1972. Analytical Quality Control Laboratory,
" *
U.S. Environmental Protection Agency, Cincinnati, Ohio, 45268.
24. Handbook of Chemistry and Physics. 1962. 42nd ed., CRC Press,
Cleveland, Ohio.
25. Hatch, W. R., and W. L. Ott, 1968. "Determination of Sub-Microgram
Quantities of Mercury by Atomic Absorption Spectrophotometry,"
Analytical Chemistry. 40:2085-2087.
55
-------
26. Hem, J. D., 1970. "Chemical Behavior of Mercury in Aqueous
Media," UK Mercury in the Environment, Geological Survey
Professional Paper 713, U.S. Govt. Printing Office, Washington,
D.C., pp. 19-24.
27. Hietanen, S., and L. G. Sillen, 1952. "Studies of the Hydrolysis
of Metal Ions II. The Hydrolysis of the Mercury (II) Ion Hg2+,"
Acta Chem. Scand. (Copenhagen), £:747-758.
28. Hume, D. N., 1973. "Pitfalls in the Determination of Environmental
Trace Metals," jjv. Chemical Analysis of the Environment. Ahuja, S.,
E. M. Cohen, T. J. Knelp, J. L. Lambert, and G. Zeveig (eds.),
Plenum Press, New York, pp. 3-16.
29. Instrumentation for Environmental Monitoring - Biomedical," 1973.
Lawrence Berkeley Laboratory, University of California,
Berkeley, (Mercury, 23 pp.).
Instrumentation for Environmental Monitoring - Air, 1974.
Lawrence Berkeley Laboratory, University of California, Berkeley,
(Mercury).
30. Jepsen, A. F., 1973. "Measurements of Mercury Vapor in the
Atmosphere," in> Trace Clements in the Environment, Kothny, E. L.
' »
(ed.), Advances in Chemistry Series 123, American Chemical Society,
Washington, D.C., pp. 81-95.
31. Johansson, B., R. Ryhage, and G. Westoo, 1970. "Identification
and Determination of Methylmercury Compounds in Fish Using
Combination Gas Chromatograph - Mass Spectrometer," Acta Chem. Scand.
(Copenhagen), 14(7):2349-2354.
56
-------
32. Kaiser, H., 1973. "Guiding Concepts Relating to Trace Analysis," '
j_nj Analytical Chemistry - 4, International Union of Pure and
Applied Chemistry, Crane, Russak and Co. Inc., New York, pp. 35-61,
33. Kopp, J. F., M. C. Longbottom, and L. B. Lobring, 1972. "vCold
Vapor' Method for Determining Mercury," Journal AHWA., pp. 20-25.
34. Lange's Handbook of Chemistry, 1956. 9th Ed., Handbook Pub. Inc.,
New York.
35. Latimer, W. M., 1952. "Oxidation Potentials," 2nd Ed.,
Prentice-Hall, Inc., New York, 392 p.
36. Latimer, W. M., and 0. H. Hildebrand, 1951. Reference Book of
Organic Chemistry, 3rd Ed., The MacMillan Co., New York, p. 141.
37. Lewis, G. N., M. Randall, K. S. Pitzer, and L. Brewer, 1961.
Thermodynamics, 2nd Ed., McGraw-Hill Pub. Co., New York, 732 pp.
38. Lieu, V. T., A. Cannon, and W. E. Huddleston, 1974. "A Non-Flame
Atomic Absorption Attachment for Trace Mercury Determination,"
J. Chem. Ed.. 51_(1):752-753.
39. Linch, A. L., R. F. Stalzer, and D. T. Leffers, 1968. "Methyl and
Ethyl Mercury Compounds - Recovery from Air and Analysis,"
Amer. Indust. Myg. Assoct-J.. 29_(l):79-86.
3 %
40. Lindstedt, G., and S. Skerfving,'1972. "Methods of Analysis," UK
Mercury in the Environment, Friberg, L., and J. Vostal (eds.),
CRC Press, Cleveland, Ohio, pp. 3-13.
41. Longbottom, J. E., R. C. Dressman, and J. J. Lichtenberg, 1973.
"Gas Chromatographic Determination of Methyl Mercury in Fish,
Sediment and Water," J. Ass. Offie. Anal. Chem.. 56(6):1297-1303.
57
-------
42. Makarova, L. G., and A. N. Nesmeyanov, 1967. "The Organic Compounds
of Mercury," UK Methods of Elements-Organic Chemistry, Vol. IV,
Nesmeyanov, A. N., and K. A. Kocheskhov (eds.), North-Holland
Publishing Company (Amsterdam), 532 pp.
43. Manual of Methods for Chemical Analysis of Hater and Hastes, 1974.
National Environmental Research Center, U.S. Environmental
Protection Agency, Cincinnati, Ohio, 45268, EPA-625-/6-74-003,
289 pp.
44. Mellor, J. W., 1952. A Comprehensive Treatise on Inorganic and
Theoretical Chemistry, Vol. IV, Longmans, Green and Co., London ,
p. 761.
45. Minear, R. A., and B. B. Murray, 1974. "Methods of Trace Metals
Analysis in Aquatic Systems," in: Trace Metals and Metal Organic
Interaction in Natural Haters, Singer, P. C. (ed.), Ann Arbor
Science Publishers Inc., Ann Arbor, Mich., p. 1-42.
46. Moffitt, A. E., Jr., and R. E. Kupel, 1970. "A Rapid Method
Employing Impregnated Charcoal and Atomic Absorption Spectro-
photometry for the Determination of Mercury in Atmospheric,
Biological and Aquatic SaTnples," Atomic Absorption Newsletter,
5"» ' " ' ' • '• •" ' ' '• • •' •-• —••" " -• —
i(6):113-118.
47. Muscat, V. I., T. J. Vickers, and A. Andren, 1972. "Simple and
Versatile Atomic Fluorescence System for Determination of Nanagram
Quantities of Mercury," Anal. Chem., 44_(2): 218-221.
48. Mushak, P., 1973. "Gas-Liquid Chromatography in the Analysis of
Mercury (II) Compounds," Environmental Health Perspectives.
pp. 55-60.
58
-------
49. Proposed Hater Quality Information, Volume II, 1973. U.S.
Environmental Protection Agency, Washington, D.C. 20460, 164 pp.
50. Riley, 0. P., and D. Taylor, 1968. "Chelating Resins for the
Concentration of Trace Elements from Sea Water and Their Analytical
Use in Conjunction with Atomic Absorption Spectrophatometry,"
Anal. Chem. Acta (Amsterdam), 40_:479-435.
51. Roberts, H. L., 1968. "Some General Aspects of Mercury Chemistry,"
j_n_; Advances in Inorganic Chemistry and Radiochemistry,
Emeleus, H. J., and A. G. Sharpe (eds.), Academic Press, New York,
P. 309-339.
52. Rosain, R. M., and C. M. Wai, 1973. "The Rate of Loss of Mercury
from Aqueous Solution when Stored in Various Containers,"
Analytical Chimica Acta (Amsterdam), £5:279-284.
53. Rottschafer, J. M., 0. D. Jones, and H. B. Mark, Jr., 1971.
"A Simple, Rapid Method for Determining Trace Mercury in Fish
via Neutron Activation Analysis," Environ. Sci. Techno!.,
5^(4) :336-338.
54. Sandell, E. B., 1959. Colorimetric Determination of Traces of
Metal's j. 3rd Ed. ,f Intersci-ence Publishers Inc., New York, 1032 pp.
3%
55. Shults, W. D., 1975. Analytical' Chemistry Division, Oak Ridge
National Laboratory, Oak Ridge, Tenn. 37830, Personal
Communication, Jan. 1975.
56. Sidgwick, N. V., 1950. The Chemical Elements and Their Compounds,
Vol. I, Oxford University Press (London), 853 pp.
57. Sillen, L. G., 1949. "Electromagnetic Investigation of Equilibria
V
Between Mercury and Halogen Ions. VIII. Survey and Conclusions,"
Acta. Chem. Scand.. 3_: 439-553.
59
-------
58. Skinner, H. A., 1964. "The Strength of Metal-to-Carbon Bonds,"
jn_: Advances in Organometallic Chemistry, Vol. II, Stone, F. G.,
and R. Hest (eds.), Academic Press, New York, pp. 49-114.
59. Smith, R. G., Jr., and H. I. Windom, 1972. Analytical Handbook
for the Determination of Arsenic, Cadmium, Cobalt, Copper, Iron.
Lead, Manganese, Mercury, Nickel, Silver and Zinc in the Marine
and Estuarine Environments, Scidaway Institute of Oceanography,
55 West Bluff Road, Savannah, Ga. 31406, p. 42. University System
of Georgia (to be cited as unpublished manuscript).
60. "Standardization of Methods for the Determination of Traces of
Mercury, Part I," 1974. Anal. Chim. Acta (Amsterdam), 72_:37-48.
61. Subber, S. W., S. D. Fihn, and C. D. West, 1974. "Simplified
Apparatus for the Flameless Atomic Fluorescence Determination
of Hg," Amer. Lab., 6/11):38-40.
62. Talmi, Y., 1974. "Separation, Detection and Other Identification
of Organically Bound Toxic Metals and other Hazardous Materials,"
in: Ecology and Analysis of Trace Contaminant, Fulkerson, W.,t
W. D. Shults, and R. I. Van Hook (eds.), Oak Ridge National
Laboratory, Oak Ridge, I$nn., 37830, ORNL-NSF-EATC-6.
63. Thatcher, L. L., and J. 0. Johnson, 1971. "A Comprehensive
Program in Neutron Activation Analysis in Water Quality," j_n_:
Nuclear Techniques in Environmental Pollution, International
Atomic Energy Agency, Vienna, pp. 323-328.
64. Trujillo, C., P. Stein, and E. Campbell, 1974. "Preservation of
Dilute Mercury Solutions," Anal.-Chem., 46(1):99-102.
60
-------
65. Uthe, J. F., 1971. "Determination of Total and Organic Mercury
Levels in Fish Tissue," in: Identification and Measurement of
Environmental Pollutants, National Research Council of Canada,
Campbell Printing, Ottawa, Canada, pp. 207-212.
66. Wallace, R. A., W. Fulkerson, W. D. Shultz, and W. S. Lyon, 1971.
Mercury in the Environment, Oak Ridge National Laboratory,
Oak Ridge, Tenn. 37830, ORNL NSF-EP-1, 61 p.
67. Webb, J. L., 1966. Enzyme and Metabolic Inhibitions, Vol. II,
Academic Press, New York, 1237 p.
68. Webb, R. G., A. W. Garrison, L. H. Keith, and J. M. McGuire, 1973.
Current Practice in GC-MS Analysis of Organics in Hater, National
Environmental Research Center, U.S. Environmental Protection
Agency, Corvallis, Oregon, 97330, 91 pp.
69. Weiss, H. V., and K. Chew, 1973. "Neutron Irradiation of Mercury
in Polyethylene Containers," Analytica Chemica Acta (Amsterdam),
67_: 444-447.
70. Westermark, T., 1972. "Activation Analysis of Mercury in
Environmental Studies," in: Advances in Activation Analysis,
Vol. 2, Academic" Press,'New York, pp. 57-88.
71. Westoo, G., 1966. "Determination of Methylmercury Compounds in
Foodstuffs," I. Methylmercury Compounds in Fish, Identification
and Determination," Acta Chem. Scand. (Copenhagen), 20:2131.
72. Westoo, G., 1967. "Determination of Methylmercury Compounds in
Foodstuffs. II. Determination of Methylmercury in Fish,Egg,
Meat and Liver," Acta Chem. Scand. (Copenhagen), 21:1790-1800.
61
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73. Westoo, G., 1968. "Determination of Methyl mercury Salts in
Various Kinds of Biological Media," Acta Chem. Scand. (Copenhagen),
22:2277.
74. Wilson, A. L., 1974. "Performance Characteristics of Analytical
Methods - IV," Talanta (Great Britain), 2^:1109-1121.
75. Wood, J. M., 1972. "A Progress Report on Mercury," Environment,
14_(l):33-39.
76. Wood, J. M., F. S. Kennedy, and C. G. Rosen, 1968. "Synthesis
of Methyl-Mercury Compounds by Extracts of a Methanogenic
Bacterium," Nature (London), 220:173-174.
62
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3.0 BIOLOGICAL ASPECTS IN MICROORGANISMS
3.1 INTRODUCTION -
In aquatic environments mercury undergoes repeated transformations
as a result of multiple natural processes, including microbial activity.
The status of research at present is such that no finalized mercury
cycle(s) in these environments can be easily elucidated. Most micro-
biological studies investigating some aspect of mercury transformations
are conducted in the laboratory using a single species. Naturally
occurring mixed microbial populations contain a much greater range of
biochemical potential, that is, transformation capability, than single
species cultured under optimal laboratory conditions. The species
composition and concentration of microorganisms in natural mixed
populations change as the environment changes. Thus microbial trans-
formation capability is continuously enlarged or diminished by the
environment. Only a few laboratory studies report interrelationships
between microorganisms that may result in a stepwise biochemical process
that might otherwise not have occurred. Furthermore, environmental •.
conditions in natural aquatic situations seldom are well described.
Elemental facts such ars pH, nutrient status, other toxicants present,
and oxygen content of the aquatic milieu under investigation are usually
lacking. Attempts to protray mercury cycling to date therefore appear
to be somewhat oversimplified.
3.2 METABOLISM AND TRANSFORMATIONS
3.2.1 Chemical Transformations
First consideration of these transformations must be given to the
chemical and physical properties of mercury (see Section 2).
63
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The geochemistry of metallic and inorganic mercury involves numerous
interconversions and transformations. Mercury in the natural state is
f
generally present in the aquatic environment as the metallic form; as a
variety of inorganic compounds and organic complexes, for example, humates,
which can interchange with one another; and as the relatively nonionized
and chemically stable mercuric sulfide. Oxidizing conditions result in
slow conversion of mercuric sulfide to mercuric sulfate which dissociates
and releases inorganic mercury. Conversion of metallic mercury to mercuric
ion in soils or sediments also occurs under oxidizing conditions. In
this case the inorganic mercury is usually firmly bound to soil and
sediment constituents. Under the action of sunlight, mercuric compounds
will generally degrade to metallic mercury and volatile. Mercuric
compounds washed or settled into anaerobic aquatic environs combine with
the hydrogen sulfide present to form the insoluble mercuric sulfide.
Superimposed on naturally occurring mercury are the hundreds of
commercially prepared mercurials released into waterways from point
sources such as industrial plants and accidental spills or from nonpqint
sources such as agricultural usage and materials applications.
3.2.2 Biotrarisformatiens
•- • - • —— • • • -J%
''. \
Microorganisms can be considered as agents that accelerate environ-
mental change, for example, degradation of dead plant and animal matter,
utilization of organic matter to form carbon dioxide and water, and
conversion of relatively simple compounds to more complex ones. Following
this concept, microorganisms can be considered accelerators of mercury
transformations that occur more slowly in natural geochemical or chemical
processes.
64
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3.2.2.1 Mercury Cycling—In an attempt to outline the aquatic inter-
conversions of mercury, Jonasson and Boyle (1971) have presented a mercury
cycle as shown in Fig. 3.1. Despite the attempt to present the cycle in
relative simplicity, the complexity of mercurial transformations in
nature is abundantly illustrated. The precise roles of microorganisms,
bacteria in particular, in this scheme are not known to be fully doc-
umented, but data suggesting many of the varied pathways have been
published. D'ltri (1972), for example, has discussed this mercury cycle
and others.
As mentioned previously, Hg° is readily converted to Hg in aquatic
situations whether microorganisms are present or not. Microorganisms
and other living organisms appear to mediate this reaction, but the extent
of involvement is not known.
The reduction of Hg to Hg° is well documented (Ben-Bassett et al., 1972-;
Komura et al., 1971; Komura and Izaki, 1971; Summers and Lewis, 1973; and
Tonomura et al., 1968). In a few studies, elemental mercury has been
found in culture media when HgCl? was the initial mercurial. In some% cases
volatile mercury was collected and analyzed, but there was a question of
whether the"mercury was truly 1* elemental form. Bacteria resistant to
3*
the toxic effect of mercury appear to play an important role in this
reaction. The reaction also occurs in the presence of cell-free extracts
(enzymes) of a pseudomonad strain and methanogenic bacteria.
3.2.2.1.1 Methylmercury—The most serious consequence of mercury cycling
is transformation of the mercuric ion to methylmercury (generally represented
in Fig. 3.1) as reaction (Rx) 3. Methylmercury is much more toxic than
65
-------
I
inorganic mercurials and, further, is the form of mercury that accumulates
in animals, particularly fish--and is passed on to man. Initial studies
indicated that methylmercury was formed from the mercuric ion by the
activity of anaerobic microorganisms. Although true, more recent studies
indicate that mercury methylation occurs principally as aerobic micro-
biological processes (Ghosh and Zugger, 1973; Summers and Lewis, 1973;
and Vonk and Sijpesteijn, 1973).
Studies have been conducted to determine if methylation of mercury
and mercury compounds occurs in fish. Jernelov (1972) injected inorganic
mercury into liver and muscles of pike or added it to slime on the sur-
face of the fish or to the intestines. He concluded that microorganisms
which are predominant in fish slime and fish intestines have the ability
to methylate mercury, but found no evidence of mercury methylation
occurring in the fish itself. The name of the compound used was not
reported. The capacity of these microorganisms to methylate inorganic
mercury was greater in late winter and early spring. Also, methylation
occurred only when the fish were kept on a fish extract substrate as.
opposed to a meat extract substrate.
The possibility of methylation of inorganic mercury by various
~f , 3«
•3>
fish-liver homogenates was investigated by Ukita and Imura as cited by
Kojima and Fujita (1973). Yellow fin tuna liver homogenates were found
to methylate inorganic mercury after 5 hours in the dark at 37 degrees
or after sterilization at 120 degrees for 15 minutes. Methylation
reactions were not observed with other fish or mammalian liver homogenates.
In the anaerobic process, an acetate synthetase mechanism has been
postulated as the biochemical pathway for the methylation reaction.
66
-------
I
Chemical transfer and enzyme regeneration cycles have been outlined and -
discussed by D'ltri (1972). For methylation to occur, a methyl carbon ion
donor is required. The only naturally occurring compound known to
accomplish this transformation is the vitamin B12 derivative, methyl-
cobalamin. Complicating this sequence, inorganic mercurials—in
particular HgClp—react nonenzymatically with methylcobalamin in mildly
reducing conditions to form methylmercury and other methylated mercurials
having toxicological significance. Another study reported that the
methylation reaction proceeded at an unexpectedly high rate after methyl -
cobalamin was mixed with inorganic mercury in neutral aqueous solutions
in the absence of reducing conditions. When small amounts of HgCl^ were
used, the initial product of the reaction was dimethylmercury. Addition
of more HgClp resulted in conversion of the dimethylmercury to monomethyl-
mercury chloride. Another complication is the formation of trace amounts
of methylmercury from the reaction of inorganic mercury with amorphous
(electrode) carbon. These nonenzymatic methylations of mercuric ion are
of potentially great significance. As shown in Fig. 3.1, organomercurials
can provide Hg° and Hg for the methylation process via Rx 4 and Rx 10
or can be converted directly to jnethylmercury (Rx 13). These trans-
r
-x%
formations also are significant to1 the mercury methylation process.
Clearly, however, more data are required to fully elucidate mercury
methylation mechanisms for better evaluation of ecological and human
health impact.
Methylmercury bromide and chloride (Tonomura et al., 1968; Spangler,
Spigarelli, Rose, Flippin, and Miller, 1973), ethylmercuric acetate
(Nelson, Blair, Brinckman, Colwell, and Iverson, 1973) and phosphate
67
-------
(Tonomura and Kanazki, 1969; Selikoff, 1971), and phenylmercuric
acetate (Nelson, Blair, Brinckman, Colwell, and Iverson, 1973; Tonomura
et al., 1968) have been acted upon by various microorganisms to form Hg°
and the corresponding carbonaceous gasses-methane and ethane--as well as
benzene (Rx 10). Demethylation of methyl mercury has occurred in aerobic
and anerobic conditions (Spangler, Spigarelli, Rose, Flippin, and Miller,
1973). Cleavage of the C-Hg bond of phenylmercuric acetate has also been
demonstrated with cell-free extracts of a mercury-resistant pseudomonad
(Tonomura and Kanzaki, 1969). Resistant microbial strains also appear
to be important in this type of mercury transformation (Tonomura et al.,
1968; Nelson, Wan, Vaituzis, and Colwell, 1973; Walker and Colwell, 1974).
Apparently, dialkyl mercurials can be converted to methyl mercury
(Rx 13) by purely chemical processes (Greeson, 1970). Similarly,
dimethylmercury (at low pH) and phenylmercuric acetate can be converted
chemically to methylmercury (D'ltri, 1972; Greeson, 1970). Bacteria
also appear to be involved in demethylation.
The remaining parts of the cycle of mercury interconversions,
notable Rx 5, 6, 7, 8, 11, and 12, occur in the laboratory and undoubtedly
in nature with relative-ease. - Although important for complete under-
standing, these particular interconversions are probably significant only
as intermediate reactions in two- or three-step conversion processes to
mercury states already discussed. Microbial involvement is indicated
for some of these reactions (Rx 5, 7, and 8), but no recent reports confirm
this (Jonasson and Boyle, 1971).
68
-------
3.2.3 Uptake and Absorption
Uptake and absorption of mercurials by microorganisms occur rapidly,
often within minutes and hours. As discussed in the Effects Section 3.3,
resistant microbial strains, reversal of mercury uptake by medium
constitutents, inactivation of mercury by SH-containing compounds, and
other allied factors are all important considerations in studies of
mercury toxicity. In the context of these factors—with awareness of the
limited knowledge about them—discussion of absorption and uptake of
mercury by microorganisms would be meaningless at this time.
Few studies report residues of mercury in microorganisms. However,
planktonic algae accumulated mercury at higher concentration levels
(2.8 to 81.0 ppm) than were found in associated bottom sediments (Pillay
et al., 1972). Concentration factors up to 24X were reported for a variety
of sampling locations in and around Lake Erie. In another study,
phytoplankton was reported to concentrate mercury to a greater extent than
zooplankton (0.19 ppm vs. 0.11 ppm) (Cocoros et al., 1973). Marine
phytoplankton, primarily diatoms, contained significantly more mercury
than zooplankton (207 ppm av vs. 119 ppm av); seasonal variations were also
found (Knauer. and Martin, 1972}.. These data are summarized in Table 3.1.
t
•7%
In a laboratory study, living or *dead cells of Selenastrum capricornutum
examined either'in a light or dark environment absorbed essentially the
same amounts (about 40%) of mercury in solution (Filip and Lynn, 1972).
The mechanism of mercury uptake in this situation was entirely passive
absorption.
69
-------
Table 3.1. MERCURY RESIDUES IN PHYTOPLANKTON
Phytoplankton
a
type Concentration Reference
Freshwater
Estuarine
Marine
2.8-81.0
.11-. 19
104-590
ng/g
Pillay et al .
Cocoros et al .
(1972)
(1973)
Knauer and Martin (1972)
Note:
appm unless otherwise noted.
70
-------
3.3 EFFECTS
3.3.1 ' Viruses
Mercurials are seldom used as antiviral agents, although research
reviewed by Dunham (1968) indicates some in vitro efficacy. At a
concentration of 1:1000, mercuric chloride rapidly (within 3 min.)
inactivated influenza and vaccinia viruses. Using a 1:10,000 concentration,
however, merthiolate (sodium ethylmercurithiosalicylate) had little effect
on neurotropic viruses. These viruses remained infective for months
despite exposure in suspension to this compound. Phenylmercuric salts
(concentration not stated) reduced the number of infective encephalomyo-
carditis and herpes viruses in vitro. Inactivating effects of 0.1%
concentrations of phenylmercuric borate were reported in a study of polio
(types I, II, and III) and adeno (types 7, 8) viruses in suspension
(Dunham, 1968).
As with bacteria (Section 3.2.2), inactivation and reactivation of
viruses by mercurials have been reported by Brewer (1968). The bacteriophage
of Staphylococcus aureus was completely inactivated by mercuric chloride
and reactivated by hydrogen sulfide. Briefly, phage titer (8.7 x 10
particles/ml) w.as reduqed 99(%)^y a 1:10,000 concentration of mercuric
\y 3t
chloride but reactivated by a 1:50 dilution of sodium thioglycolate.
A combination of sodium thioglycolate and BAL (2,3-dimercaptopropanol)
was also effective in reactivating influenza A virus.
Studies of mercury effects on plant disease viruses are limited to
in vitro laboratory experimentation in which the biophysics of viral
inactivation or protein binding are the usual subjects. Far from being
71
-------
merely tools for biophysical studies or simply laboratory curiosities,
studies of this type provide insight into why some living organisms are
more resistant to mercury compounds than others and why the effect of
mercury on some is temporary. Some recent findings are summarized in
Table 3.2.
3.3.2 Bacteria
A summary of recent studies of toxic levels and other effects of
mercurials on bacteria is shown in Table 3.4. Mercury toxicity obviously
varies both with the chemical form of the compound used and bacterial
species tested. Less obvious is the fact that mercury toxicity varies
with pH, type of culture medium (whether nutrient or simple aqueous media),
temperature, and other aspects of test systems. Not all systems are fully
and carefully described by research authors. Inactivation and reactivation
(dissociation and reassociation) are not limited to viruses (see Section
3.3.1). Hydrogen sulfide, glutathione, and 2,3-dimercaptopropanol, for
instance, have been shown to reactivate hemolytic streptococci, Pseudomonas
aeruginosa, and varied microbial enzyme systems inactivated by mercur-ic
chloride.
3.3.2.1 Antisepti os—lted ical •u'Ca.ge of mercurials in skin disinfection and
in preserving varied fluids was reviewed by Brewer (1968), Grundy (1968),
Hart (1973), and Lawrence and Block (1968). Brewer (1968) has summarized
data on examples of mercurial antiseptics as shown in Table 3.4. Mercury
usage medically has had only limited success. Gepper showed in 1889
(Brewer, 1968) that inorganic mercurial compounds are inactivated or
neutralized by ammonium sulfide. Subsequently, other chemicals, organic
72
-------
Table 3.2. STUDIES OF MERCURY EFFECTS ON PLANT VIRUSES
Virus studied
Type of study
Compound
Comments
Turnip yellow
mosaic virus
Turnip yellow
mosaic virus
Binding of mercury to
sulfhydryl and non-
sulfhydryl sites
viral vprotein,
Methylmercury
of
Virus particle dis-
sociation and re-
association.
Mercuric
chloride
At pH range of 3 to 6, the fast
reaction phase (non-sulfhydryl )
was at a constant rate but increased
substantially at pH 6 to 8. The
slower reaction phase (sulfhydryl)
had a pH minimum of 4. The latter
resulted in disintegration of the
virus particle (Godshalk, 1970).
Initial addition of HgCl^ to
isolated virus particles re-
sulted in dissociation into
RNA-free protein and a nucleo-
protein. Addition of further
HgClp caused reassociation of the
protein and nucleoprotein into
particles less regular in size and
shape than the original viral
particles (Dome et al . , 1971).
-------
Table;3.2. STUDIES OF MERCURY EFFECTS ON PLANT VIRUSES (cont'd)
Virus studied
Type of study
Compound
Comments
Prunus necrotic
ringspot virus
Tulare apple
mosaic virus
Brome grass
mosaic virus
Response of isolated
virus to stabilizing
agents.
Response of isolated
virus to stabilizing
and inactivating agents,
Reversible reaction
of isolated virus
and mercuric ions.
p-chloromercuri-
benzoate (PCMB)
p-chlcromercuri-
benzoate (PCMB)
Mercuric chloride
Of varied agents studied, PCMB slowly
inactivated this virus as determined
by fewer local leaf lesions in the
Mormordica balsamina test species
(Barnett and Fulton, 1971).
PCMB rapidly inactivated this virus
as determined by few local leaf
lesions in the test species,
Phaseolus vulgaris cv. Bountiful
(Barnett and Fulton, 1971).
Mercuric ions reacted with RNA from
the virus itself without degradation
of the virus particle. Infectivity
of both RNA and the virus decreased
with increased mercury binding. All
virus modifications by mercury could
be easily reversed by strong complex-
ing agents such as EDTA, mercapto-
ethanol , and CN (Pfeiffer and Dome,
1971).
-------
Table 3.3. 'TOXICITY AND OTHER EFFECTS OF MERCURIALS ON BACTERIA
en
Chemical3
Ethylmercuric
bromide
Ethylmercuric
oxalate
Ethylmercuric
phosphate
Mercuric
chloride
-Bacteria
Escherichia coli,
* \
. t
E. coli
Pseudomonas spp.
(resistant strain)
Sewage
organisms
£". coli.
Pseudomonas spp.
(resistant strain)
Pseudomonas spp.
(onion seed isolate)
Heterotrophic-
Toxicity
ppmb
0.2 (L)
0.3 (K)
20 (I)
1.0 (SB)
2.0 (K)
0.2 (K)
450 (I)
100 (I)
0.1-1.0 (I)
Reference
Wallace et al. (
Selikoff (1971)
Kemp et al . (197
Wallace et al . (
Selikoff (1971)
1971)
1)
1971)
Mallery and Mel era (1973)
Albright et al.
(1972)
water bacteria
-------
Table 3.3. TOXICITY AND OTHER EFFECTS OF MERCURIALS ON BACTERIA (cont'd)
CTl
Chemical
"Mercury
metal"
Mercuric
cyanide
Methylmercury
dicyandi amide
-£acteriaa
Pseudomonas spp.
(resistant strain)
" i
. *
Pseudomonas spp.
(nonresistant)
Bacillus spp.
Sewage organisms
Soil bacteria
(aerobic and anaerobic)
E. coli
E. coli
Sarcina lutea
B. subtilis .
Strep tony ces- scabies
S. griseus
Toxicity
ppm Reference
25 (NTE) Nelson, Wan, Vaituzis, and
Colwell, 1973.
15 (AB)
5 (AB) Ghosh and Zugger (1973)
2.5-5.0 (I)
1.0 (I) Fujihara et al. (1973)
0.2 (K) Wallace et al . (1971)
100 (I) Chinn (1973)
10 (I)
100 (I)
10 (I)
10 (I)
-------
Table 3.3. TOXICITY AND OTHER EFFECTS OF MERCURIALS ON BACTERIA (cont'd)
Chemical3
Phenylmercuric
acetate
Phenylmercuric
chloride
Phenylmercuric
nitrate
^Bacteria5
Pseudomonas spp.
(resistant strain)
w \
t
E. ooli
B. subt-ilis
NCTC 8236 (spores)
Toxicity
ppm Reference
120 (I) Selikoff (1971)
0.3 (K) Wallace et al . (1971)
40 (I) Deasy et al . (1971)
+ irradiation
Notes:
aAs named by authors.
Abbreviations are:
K = kill or lethality
I = significant inhibition
SB = sublethal
AB = abnormal morphology
MTE = no toxic effect.
-------
Table,3.4. MERCURIALS COMMONLY USED AS ANTISEPTICS
oo
Name
Merthiolate
Metaphen
Merphenyl
nitrate
Chemical
-name
Sodium salt of
ethyj >,mercuri
thitfsalicylic
acid
Anhydride of
4, ,nitro-5-
hydroxy mer-
curi ortho
cresol
Phenylmer-
curic nitrate
(basic)
Mercury
content
(per cent)
49
56-57
63
Empirical
formula
C9H902S Hg Na
C7H5OkHg N
C6H5HgOH,
C6H5HgM03
Concentration
of
pH type used
9.8 1:1,000
isotonic solution
10.5 1:2,500
aqueous germicidal
solution
4.2 1:1,500
boric acid
solution
Mercarbolide
Ortho
hydroxy phenyl
mercury
chloride
60.95
C6H50 HgCl
6.5 1:1,000
aqueous solution
-------
Table 3.4-. MERCURIALS COMMONLY USED AS ANTISEPTICS (cont'd)
Name
Mertoxol
Mercurochrome
Meroxyl
flercury
oxycyanide
Chemical
" name
Acetoxy mer-
curvh2-ethyl-
hex'yl -phenol
sulfonic acid
Sodium salt of
di-brom hydroxy
mercuri fluo-
rescein
Sodium salt of
2-4 di hydroxy-
3-5 di hydroxy-
mercury benzo-
phenone 2' sul-
fonic acid
Mercury Concentration
content Empirical of
(per cent) formula pH type used
40 C16H21t05S Hg 3.5 1:1,000
isotonic
24-26 C10H305Br2Hg Ma 9.1 1:50
aqueous
solution
solution
26-29 C13H906Hg2SNa 7.1 1:200
stabilized aqueous
85.5 Hg(CN)2 HgO 9.1 1:6,000
aqueous
-------
Table 3.4". MERCURIALS COMMONLY USED AS ANTISEPTICS (cont'd)
CO
o
Name
Mercuric
cyanide
Potassium
mercuric
iodide
Mercury
chloride
Mercury
Chemical content Empirical
name (per cent) formula
83.3 Hg(CN)2
? ''
25.5 K2Hg I4
Mercuric 83.3 HgCl2
chloride,
"corrosive
sub! imate"
Concentration
of
pH type used
6.2 1:1,000
aqueous
9.2 1:1,000
aqueous
5.9 1:1,000
aqueous
Source:
Brewer (1968).
-------
matter, and particularly proteins with -SH groupings were shown to
inactivate mercurials. Such compounds include arginine, aspartic acid,
cysteine, glutamic acid, glycine, glutathione, lysine, thiolacetate,
sodium metabisulfite, and hydrogen sulfide.
3.3.2.2 Fungicides—In a study of the effect of mercurial fungicides
(phenylmercuric acetate, phenylmercuric chloride, phenylmercuric hydroxide,
and phenylmercuric pyrochatechine), Hansen (1972) reported that these
compounds at a concentration of 0.025% were more inhibitory to Gram
positive bacteria (97% sensitivity) than to Gram negative bacteria (53%
sensitivity). The number of bacterial strains investigated was 211, but
the author presented no further breakdown of the data on toxicity of the
individual fungicides.
3.3.2.3 Preservatives—Phenylmercuric nitrate (PMN) alone.or in
combination with other antibacterial agents is an effective preservative
against bacteria at concentrations as low as 20 ppm in ophthalmic and
injectable medicaments such as atropine, physostigmine, and pilocarpine
(Buckles et al., 1971; Hart, 1973; Richards, 1971; Richards and McBride,
1971, 1972). Test organisms were P. aeruginosa and Staphylococcus aureus.
PMN in combination with, other preservatives was effective against resistant
j»
pseudomonas strains. The concentration of PMN in solutions containing
sodium metabisulphite was reduced during relatively short storage periods.
At acid pH after autoclaving, a PMN-metabisulfite complex formed that was
most effective. Usually, however, autoclaving and heating were found to
reduce PMN concentrations, while solution filtration was found to be the
best method of sterilization. P. aeruginosa survived PMN better at pH
6.3 than at 3.9 or 8.4, a fact no reported previously (Richards and McBride,
81
-------
1972). In view of PMN loss during storage and its known mammalian
toxicity, other preservative agents (benzalkonium, chlorbutal, EDTA, and
phenylethanol) alone or in combination are safer and more effective
storage preservatives (Richards and McBride, 1972; Richards, 1971).
3.3.2.4 Sludge—At loadings of biological sludge solids of 2000 pm as
determined by chemical oxygen demand (COD), slug doses of 2.5 to 5.0 ppm
mercuric chloride definitely inhibited aerobic biological processes
(Ghosh and Zugger, 1973). This inhibitory effect was temporary, that is,
microorganisms apparently acclimated to moderately high doses of mercury.
Nevertheless, at 5 ppm Hg , COD removal was 55% of the control after 1 hr.
Maximal removal (86%) at this mercury concentration occurred after 5 hr.
Van Loon (1973) compared mercury content (1 to 26 ppm) of dried sludges
and sludge fertilizers from varied sources in Canada to mercury levels in
dried soils (0.1 to 3ppm) with no sludge amendments. Sludges can therefore
add significantly to mercury content of soils, some of which may be used
for growing crops. This work is continuing.
3.3.3 Fungi
3.3.3.1 Fungicides--Agricultural usage of mercury compounds as fungicidal
treatments for.seed, as. s,oil applications, or as sprays to crop plants
*.»
has been broadly documented. D'ltri (1972) listed 162 mercurial formu-
lations marketed at that time. Because mercurials used for these purposes
resulted in poisoning of animals and humans, these uses were subsequently
banned in Japan and Sweden. Excessive accumulation of mercury in foods
for humans has caused considerable concern throughout the world; wildlife
becomes involved directly by ingestion of treated seed. Although
82
-------
agricultural application of mercurials as fungicides has diminished great'ly,
investigations of various mercury compounds continue as documented in
recent reports (Chinn, 1971, 1973; Greenaway, 1972; Meyer et al., 1973;
Pero and Owens, 1971; Rawlinson and Col noun, 1970; and Fujihara et al.,
1973). Mercurials are often used in tests as standards for the development
of nonmercurial fungicides.
Panogen PX (methylmercury dicyandiamide or MMD) applied to soil at a
rate of 5 ppm had little direct effect on Cochliobolus sativus (causal
agent of wheat root rot), but increased seedling growth and reduced
incidence of root rot were observed (Chinn, 1971). At 25 ppm, disease
incidence was reduced by MMD but phytotoxic effects occurred. Chinn (1973)
also reported that C_. sativus, Fusarium culmorum, and Urocladium atrum
were controlled by 10 ppm MMD mixed with soil and then applied to nutrient
agar contained in petri plates. The compound was ineffective at 1.0 ppm.
In Ritzville slit loam, according to Fujihara et al. (1973), mercury
controlled fungi and other soil microflora at concentration levels as low
as 1 ppm (1 ug/g soil).
Ceresan Wet (methoxyethylmercury chloride) and mercuric chloride in
combination with other.fantimicr-ebials were used in two selective media for
•*.»
the isolation and enumeration of Macrophomina phased i, causal agent of
root and stem rot of corn, sorghum, soybean, and sugar pine. Mercury
concentrations employed were 0.25 mg/1 (as mercury) for Ceresan Wet and 7.0
mg/1 for mercuric chloride. Recovery of M_. phaseoli was close to 100% with
either medium (Meyer et al., 1973).
Ceresan dryseed dressing (1.5% mercury), applied at a rate of 74 g per
250 g of seed, protected oat seedlings (var. Powysand Pennant) and mesocotyls
83
-------
from Cylindrocarpon radicola and Fusarium sambucinum (Rawlinson and Colhoun,
1970). These fungi are normally regarded as saprophytes but have been
associated with lesions and discoloration of mesocotyls and reduced oat
plant vigor. Ceresan reduced the occurrence of some fungal series present
on the oat seed and at the same time broadened the numbers of species
present. Increased vigor of wheat and barley was also found. Response was
greatest when seedlings were grown at low temperatures under low light
intensities.
Resistant and susceptible (to phenylmercuric acetate or PMA) isolates
of Pyrenophora avenae were found to absorb similar amounts of phenyl-
mercury(+)ions from water solutions (Greenaway, 1972). Water rinses of
mercury-treated mycelia resulted in greater removal of mercury from
susceptible strains, while cysteine removed similar amounts from suceptible
and resistant strains. Greenaway concluded that:
1. cell permeability is not a factor in mercury
resistance of this fungus,
2. resistance is based on an intracellular process,
3. resistance may result from binding and
inactivation of the tq&ic ion by metabolically
inessential compounds,
4. detoxification is initially based on ligand
saturation of the mercuric ion, and
5. anthraqu.inone molecules may be involved in
the mercury binding process.
Further research is in progress.
84
-------
As noted by Manowitz (1968), phenylmercury salts (acetate, borate, and
benzoate) are very effective antimicrobial agents in cosmetics. However,
these organic mercurials are used with reluctance because of their potential
toxicity. In a new technique for rapidly evaluating preservatives,
phenylmercuric nitrate was shown to inhibit spore swelling of Bacillus
subtilis^. Spore swelling preceded spore germination and subsequent cell
division and growth. The swelling could be measured by direct microscopic
examination, spectrophotometric measurement of optical density, total
packed cell volume with hematocrit tubes, and sizing by means of a Coulter
counter. This technique was useful for evaluating comparative inhibitory
effects of chemicals on spores and cells from a number of bacterial and
fungal species, including yeasts (Parker, 1971).
3.3.3.2 Preservatives--Mercurials are used broadly in industry to preserve,
for example, wood, paper, cotton fibers, wool, leather, petroleum products,
concrete, adhesives, electronic and optical equipment, and bedding. Careful
consideration of mercurial preservatives is exercised in situations where
these materials come into contact with humans. In a recent review (Brand
and Kemp, 1973) Of Aureobasidum pullulans (the principal fungus causing
paint film disfigurement and deterioration), mercury fungicides were found
-»»
to control this fungus in a variety of situations:
1. Ceresan U-564 - flax seed treatment,
2. ethylmercury chloride - wood protectant,
3. mercury acetate - wood pulp disinfectant,
4. p-chloromercuribenzoate - in vitro inhibition of A_. pullulans,
5. phenylmercuric acetate - wood protectant and blue stain
preservative, and
6. phenylmercuric oleate - wood and paper preservative.
85
-------
Among mercurials used in preserving paint films are phenylmercury
acetate, phenylmercury propionate, phenylmercury oleate, phenylmercury
dimethyldithiocarbamate, and to a lessor extent phenylmercury succinate,
phenylmercury sterate, phenylmercury hydroxide, and chloromethoxyacetoxy
mercuripropane. Other mercurials, for example, phenylmercury chloride
and phenylmercury nitrate, are too volatile and water soluble for utility
as paint fungicides. Although mercurials have been the best paint fungicides
available in the past, their performance in this application has not been
uniformly successful. Reasons for this include mercury inactivation by
sulfhydryl groups, mercury-resistant microorganisms, and complexing by
components of the paint formulation. These facts, along with regulations
limiting use of mercurials in paints, have resulted in intensive searches
by paint formulators and manufacturers for effective, nonmercurial paint
fungicides.
3.3.4 Algae
Toxicity and other effects of mercurials on algae have been reported
or summarized in a variety of documents. Brief summaries of this information
are presented in Table 3.5. Comparison of these data with similar data for
bacteria seems to indicate that'Tnercurials are more toxic to algae by at
" v
least one order of magnitude. As noted by a number of researchers, media
nutrients (especially proteins) directly affect the toxicity of mercurials.
Bacterial test media usually contain proteinaceous nutrients while algae
media usually do not. This in part may explain the wide difference in
mercury toxicity to these organisms. This fact notwithstanding, algae
appear to be more sensitive to mercury compounds than bacteria. The
86
-------
Table 3.5. ' LETHALITY AND OTHER EFFECTS OF MERCURIALS ON ALGAE
oo
Chemical3
Alkyl mercury
Dimethylmercury
-
Diphenylmercury
Ethylmercury
Algal
^ species3
• Phytoplankton
1 'chlorella
. pyrenoidosa
' Phaeodac ty li-jn
• tr-Lcornitwn
Cyclotella nana
Chaetoceros
galvestonens-is
Nitzsch-i.a
de l-icatisszma
Phytoplankton
Phytoplankton
Type
M
FW
M
M
M
FW
M
Toxicity
ppmc
001-006 (SB)
0.1 (I)
1-10 ppb (SB)
0 - 1 (SB)
0.06 (K)
Reference
Wallace (1971)
Hannan and Patouillet
(1972)
Harriss et al . (1970)
Wallace et al . (1971)
phosphate
-------
Table 3.5. LETHALITY AND OTHER EFFECTS OF MERCURIALS ON ALGAE (cont'd)
CD
oo
Chemical
Lignasan
Mercuric acetate
Algal
species
Type
Toxicity
ppmc
Protococaus sp.
Duna.li.ella euchlora
Phaeodactylum
tricornuturn
Monochrysis lutheri
Cy lindrospervniMn
Microct/stis
aeruginosa
Scenedesmus
obliquus
FW
FW
0.006 (K)
0.006 (K)
0.06 (K)
0.006 (K)
0.06 (K)
2.0 (SB)
Reference
Kemp et al . (1971)
Kemp et al . (1971)
-------
Table 3.5. LETHALITY AND OTHER EFFECTS OF MERCURIALS ON ALGAE (cont'd)
CO
Chemical3
Mercuric acetate
Mercuric chloride
Mercuric chloride
(203Hg)
Mercuric chloride
Algal
species3
, Chlorella variegata
_ • Gomphonema
parvulwr.
' Nitzschia palea
Scenedesnrus sp.
Clnlorella.
pyrenoidosc.
Ankis trade suras
braun-ii
Euglena gracilis
Scsnedesmus sp.
Antithamnion
Toxicity
-r b C
Type ppm
FW 0.03 (K)
FW 5-30 uM (SB)
FW 1-4 (SB)
FW 0.03 (K)
M • 5.0 (L)
Reference
Wallace et al . (1971)
Shieh and Barber (1973)
Matson et al . (1972)
Wallace et al . (1971)
Boney (1971)
plwnula
Ceramiicn
flc.be 1 l-igenun
3.2 (L)
-------
Table 3.5. LETHALITY AMD OTHER EFFECTS OF MERCURIALS ON ALGAE (cont'd)
<£>
O
Algal
Chemical3 -« species3
Mercuric chloride C, pedicellatum
. Poly siphonia
brodiaei.
' P. fruticulosa.
P. lanosa
PZ'amaria. elegans
Spermafkann-Lon
rep ens
Chlorella
pyrenoidosa
Phaeodacty turn
tricomutwn
Cycloteljla ncna
Chaetocer-os
Typeb
4
3
1
8
6
3
FW 0
M
M
M
Toxicity
ppmc Reference
.2 (L)
.2 (L)
.8 (L)
.0 (L)
.7 (L)
.0 (L)
.1 (I) Hannan and Patouillet (1972)
-
galvestoner.sis
-------
Table 3.5. LETHALITY AND OTHER EFFECTS OF MERCURIALS ON ALGAE (cont'd)
Chemical'
Algal
species'
Type
Toxicity
ppmc
Reference
Mercuric chloride
Methyl mercury
Mercuric
cyanide
Methyl mercury
acetate
Methyl mercuric
chloride
Chlorella sp.
•j Phaeodactylim
tricornatum
Chlamydomonas sp.
phytoplankton
Scenedesmus spp.
Chlovella
vulgar is
Rhodospirillum
rubnvn
Rhodopseudomonas
aeruginosa
AnkistPodesrrrus
braunii
E 0.015 (K)
FW (?) 0.025 (K)
M
FW
FW
FW
0.
0.
0.
1
025 (K)
001 (SB)
15 (K)
11
x 10 M
(I)
FW
1 - 2 (B)
Nuzzi (1972)
Wallace et al. (1971)
Wallace et al. (1971)
Jeffries and Butler (1972)
Matson et al. (1972)
-------
Table 3.5. LETHALITY AND OTHER EFFECTS OF MERCURIALS OH ALGAE (cont'd)
IVJ
Chemical a
Methylmercuric
chloride
n-methylmercuric-1 ,2
3,6-tetrahydro-3,6
methano-3,4,5,6,7,7-
hexachlorophthal imide
Methyl mercury
Algal
species3
Eug lena
gxacilis
. Nitzschia
delicatissima
phytoplankton
Nitzschia
Type
•8
FW
M
Toxicity
ppmc
-O.lppb (SB)
-O.lppb (SB)
-O.lppb (SB)
Reference
Harriss et al . (1970)
Harriss et al . (1970)
dicyandiamide
Phenylmercuric
acetate
de licatissisxa
phytoplankton
Chlorella sp.
Phaeodactylum
tricornatum
0.003 (K)
FW (?) 0.003 (I)
Nuzzi (1972)
Chlcanydomonas sp.
0.009 (I)
-------
Table 3.5. LETHALITY AND OTHER EFFECTS OF MERCURIALS ON ALGAE (cont'd)
Chemical
Algal
species
Type
Toxicity
ppmc
Reference
CO
Phenylmercuric
acetate
Phenylmercuric
hydroxide
Nitzschia
deUcat'Css'una
i
phytoplankton
Cy lindrosperrrum
licheni forme
Miarocystis
aeruginosa
Scenedesmus
obliquus
Chlorella
variegata
Gomphonena
parvulwr.
N-itzsch-ia
palca
M
FW
P
0.1 - 0.5 ppb (SB) Harriss et al. (1970)
2.0 (K)
Kemp et al. (1971)
-------
Table 3.5. LETHALITY AND OTHER EFFECTS OF MERCURIALS ON ALGAE (cont'd)
IO
Chemical3
Phenylmercuric
nitrate
Algal Toxicity
species3 Type ppmc Reference
• Cylindrospermum P 2.0 (K) Kemp et al . (1971)
^cheni forme
. Microcystis
aerug-inosc.
, Scenedesmus
obliquus
Chlorella
variegata
Gcmphoner.a
parvulum
Nitzschia
palea
Phenylmercury
phytoplankton
0.001 (SB)
Wallace et al. (1971)
-------
Table 3.5. LETHALITY AND OTHER EFFECTS OF MERCURIALS ON ALGAE (cont'd)
10
en
Chemical3
n-propylmercuric
chloride
Algal
species3
Antithccnnion
plumula
»
- Ceramium
' flabelligervsn
Ceramium
• pedicellatum
Po ly siphonia
brodiasi
Po ly siphonia
fruticulosa
Po ly siphonia
Toxicity
b c
Type ppm Reference
M 0.05 (L) Boney (1971)
0.08 (L)
0.15 (L)
0.09 (L)
0.09 (L)
0.03 (L)
lanosa
-------
Table 3.5. LETHALITY AND OTHER EFFECTS OF MERCURIALS ON ALGAE (cont'd)
cr>
Chemical3
Algal
- species3
Plumaria elegans
• V
. ' Spermothcmn-Lon
repens
Toxicity
Type ppmc Reference
0.02 (L)
0.01 (L)
Notes:
As named by author.
FW = freshwater
M = marine
E = estuarine
K = kill or lethality
SB = sublethal
I = inhibitory
L = LD50
cppm unless otherwise designated.
-------
disparity is probably less than that indicated by comparison of toxicity
values. Nuzzi (1972) found that sublethal effects of mercurials (0.003 to
0.006 ppm) on algae occur at concentrations of mercury equivalent to those
ordinarily found in seawater and, further, that algal productivity may be
affected be even lower concentrations. ;
Hannan and Patouillet (1972) reported that mercury was more toxic to
four species of algae than other metals tested (silver, cadmium, lead, and
copper) in a system containing minimal nutrients. Mercuric chloride was
more toxic than dimethylmercury. Toxicity of mercury varied inversely with
the concentrations of nutrients present. The authors stressed that toxicity
must be defined in the context of a given nutrient level. Mercury toxicity
was "comparatively irreversible under the conditions of the experimentation".
Few algal studies reporting reversal of mercury toxicity have been
documented. However, glutathione completely reversed the effect of phenyl-
mercuric acetate on Phaeodactylum tricornutum (Nuzzi, 1972). Cysteine
apparently reversed one effect of mercury chloride on Clilorella pyrenoidosa
(Shieh and Barber, 1973). No studies of resistant strains of algae were
found.
Mercuric chloride ('3.5 ppm)-*and methylmercuric chloride (2.0 ppm)
significantly inhibited galactolipid and chlorophyll biosynthesis in
Ankistrodesmus braunii and Euglena gracilis (Matson et al., 1972). The
methylmercuric ion was more inhibitory than the inorganic mercury ion.
Inhibition of the galactolipid synthesis was confirmed in vitro with
isolated chloroplasts of E. gracilis.
97
-------
Mercuric chloride affected the cell membrane permeability of •
£. pyrenoidosa and enhanced the potassium ion turnover rate (release or
efflux) (Matson et al., 1972). This effect was inhibited by low temperature.
Methylmercuric chloride had no effect on cell permeability or potassium
exchange at similar concentrations.
The mercurial, p-mercuriphenylsulfonic acid, is used to modify
chromophore-protein reactions in studies of the structure of phycoerythrins
(Fujimori and Pecci, 1970, 1971). Fresh and aged cells of the blue-green
algae, Hydrocoleum sp, have single and double absorption maxima, respectively,
as determined by spectropolarimetry. Changes in circular dichroic (CD)
properties of varied phycoerythrins due to treatment with the mercury
compound were fully or partly reversed by mercaptoethanol removal of the
mercury. While this is pure laboratory experimentation for other purposes,
these studies point out an effect of mercury that may occur in nature.
3.3.5 Protozoa
Although important in aquatic food chains, protozoa have been
investigated less than bacteria and fungi. Recent published data are..
briefly summarized in Table 3.6. Many factors affecting mercury toxicity
to other microorganisms' are als'a,applicable to protozoa. On the basis of
relatively scanty data, protozoa appear to be in an intermediate position
between bacteria and algae in regard to toxic effects of mercurials, that
is, less sensitive than algae, but more sensitive than bacteria.
98
-------
Table 3.6. EFFECT OF MERCURIAL COMPOUNDS ON PROTOZOA
1C
Chemical
Ethyl mercuric
chloride
Mercuric
chloride
Mercuric
chloride
Mercuric
chloride
Mercuric
chloride
Organism3
Tetrakumena
pyri-fpymis
Amoeba
pro tens
Englena
grac-Llis
Parcmecium
aaudatium
T. pyr"ifoYmi.s
M-iororegma sp.
Crist'ige'ca. sp.
Toxicity
Type ppmc
FW 0.3 (K)
0.08 (SB)
FW 0.025 (SB)
FW 3.1 (K)
(soft water)
1.9 (K)
(hard water)
FW 0.15 (K)
M 0.0025 (SB)
Reference
Thrasher (1973)
Mills (1973)
Carter and Cameron (1973)
Wallace, et al . (1971)
Gray and Ventilla (1973)
-------
Table 3,-6. EFFECT OF MERCURIAL COMPOUNDS ON PROTOZOA (cont'd)
o
o
Chemical ^Organism3
Mercuric T. pyriformis
chloride
* \
Methylmercuric :T. pyr-iformis
chloride
Mercuric Micrcregma sp.
cyanide
Phenyl mercuric y. pyrifomis
acetate
Toxicity
Type ppmc Reference
FW 5.8 (K) Thrasher (1973)
3.4 (SB)
FW 0.2 (K) Thrasher (1973)
FW 0.16 (K) Wallace et al . (1971)
FW 0.5 (K) Thrasher (1973)
0.3 (SB)
Notes:
As named by author.
DFW = freshwater
M = marine
: K = kill
SB = sublethal
-------
3.4 REFERENCES
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t
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8. Chinn, S. H., 1971. "Biological Effect of Panogen PX (0.9%
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101
-------
9. Chinn, S. H., 1973. "Effect of Eight Fungicides on Microbial
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10. Cocoros, 6., P. H. Cahn, and W. Siler, 1973. "Mercury Concentrations
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11. Deasy, P. B., E. Keuster, and R. F. Timoney, 1971. "Resistance
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12. D'ltri, F. M., 1972. The Environmental Mercury Problem, CRC Press,
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13. Dome, B., G. Jonard, J. Witz, and L. Hirth, 1971. "Interactions
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Virology, 43_(1): 279-290.
14. Dunham, W. B., 1968. "Virucidal Agents," j_n_: Disinfection,
Sterilization, and Preservation, Lawrence, C. A., and S. S. Block
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15. Filip, D. A., and R. I. Lynn, 1972. "Mercury Accumulation by
the Fresh Water Alga Selenastrum capricornutum," Chemosphere.,
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16. Fujihara, M. P., T. R. Garland, R. E. Wildung, and H. Drucker,
1973. "Response of Microbiota to the Presence of Heavy Metals
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102
-------
17. Fujimori, E., and J. Pecci, 1970. "Circular Dichroism of Single"
and Double-Peacked Pyco Erythrin Mercurial Induced Changes,"
Biochim. Biophys. Acta.. 221(1);132-134.
18. Fujimori, E., and J. Pecci, 1971. "Changes in Circular Dichroism
and Absorption Spectrum of Phycoerythrin Chromophores by Organic
Mercurial," Phytochemistry., 10_( 10): 2519-2523.
19. Ghosh, M. M., and P. D. Zugger, 1973. "Toxic Effects of Mercury
on the Activated Sludge Process," J. Hater Pollut. Contr. Fed.,
4^(3):424-433.
20. Godschalk, W., 1970. "pH Dependence of the Interaction of Turnip
Yellow Mosiac Virus with Alifatic Mercurials," Biophys. Soc. An.
Meet. Abstr.. 14_:157A.
21. Gray, J. S., and R. J. Ventilla, 1973. "Growth Rates of Sediment
Living Marine Protozoan as a Toxicity Indicator for Heavy Metals,"
Ambio., 2_(4): 118-121.
22. Greenaway, W., 1972. "Permeability of Phenyl-Hg+-Resistant and
Phenyl-Hg -Susceptible Isolates of Phyrenophora avenae to the
Phenyl-Hg+-Ion," J. Gen. Microbiol.. 73_(Pt. 2):251-255.
23. Greesoh, P. E.,- 1970. . -^Biological Factors in the Chemistry of
'' \
Mercury," in: Mercury in the Environment, Geological Survey
Professional Paper 713, U.S. Govt. Printing Office, Washington,
D.C., pp. 32-34.
24. Grundy, W. E., 1968. "Antimicrobial Preservatives in Pharmaceuticals,"
j_n_: Disinfection, Sterilization, and Preservation, Lawrence, C. A.,
and S. S. Block (eds)., Lea and Febiger, Philadelphia, pp. 566-574.
103
-------
25. Hannah, P. J., and C. Patouillet, 1972. "Effect of Mercury on
Algal Growth Rates," Biotechnol. Bioen., 14_(1): 93-101.
26. Hanse, J. C., 1972. "Effect of Some Sulfur- and Mercury-Containing
Fungicides on Bacteria," Chemosphere, 1_(4): 159-162.
27. Harriss, R. C., D. B. White, and R. B. MacFarlane, 1970. "Mercury
Compounds, Reduced Photosynthesis by Plankton," Science,
170(3959)-.736-737.
23. Hart, A., 1973. "Antibacterial Activity of Phenylmercuric
Nitrate in Zinc Sulfate and Adrenaline Eye Drops B.P.C. 1968,"
Pharm. Pharmacol., 25_(6): 507-508.
29. Jeffries, T. W., and R. G. Butler, 1972. "Inhibitory and .
Stimulatory Effects of Methyl Mercury on Photosynthetic
Microorganisms," Abstr. An. Meet. Am. Soc. nicrobiol., 72_:71.
30. Jernelov, A., 1972. "Factors in the Transformation of Mercury to
Methylmercury," in: Environmental Mercury Contamination,
Hartung, R., and B. D. Dinman (eds.), Ann Arbor Science Publishers,
Ann Arbor, Mich., pp. 167-201.
31. Jonasson, I. R., and R. W. Boyle, 1971. "Geochemistry of Mercury,"
in: Mercury in Man's.'Environment, Proc. Symp., Ottawa, 201 pp.
32. Kemp, H. T., J. P. Abrams, and R. C. Overback, 1971. "Effects
of Chemicals on Aquatic Life," UK Hater Quality Criteria Data
Book, 3, U.S. Environmental Protection Agency, Washington, D.C.,
528 pp.
33. Knauer, G. A., and J. H. Martin, 1972. "Mercury in a Marine
Pelagic Food Chain," Limnol. Qceanogr., 17(6):868-876.
104
-------
34. Kojima, K., and M. Fujita, 1973. "Summary of Recent Studies in
Japan on Methyl Mercury Poisoning," Toxicology., l_:43-62.
35. Komura, I., T. Funaba, and K. Izaki, 1971. "Mechanism of Mercuric
Chloride Resistance in Microorganisms. Part 2. NADPH Dependent
Reduction of Mercuric Chloride and Vaporization of Mercury from
Mercuric Chloride by a Multiple Drug Resistant Strain of
Escherichia-coli, J. Biochem. . (Tokyo), 70_(6) :895-901.
36. Kamura, I., and K. Izaki, 1971. "Mechanisms of Mercuric Chloride
Resistance in Microorganisms. Part I. Vaporization of a Mercury
Compound From Mercuric Chloride by Multiple Drug Resistant Strains
of Escherichia-coli." J. Biochem. (Tokyo), 70_(6): 885-893.
37. Lawrence, C. A., and S. S. Block (eds.), 1968. Disinfection,
Sterilization, and Preservation, Lea and Febiger, Philadelphia,
808 pp.
38. Mallery, C. H., and P. W. Melera, 1973. "Elimination of Bacterial
Contamination from Onion Seed." Plant Physio!., Sl[6):ll50-llS3.
39. Manowitz, M., 1968. "Cosmetic Preservatives," jm: Disinfection,
Sterilization, and Preservation, Lawrence C. A., and S. S. Block,
3-»
(eds.), Lea & Febiger, Phi'ladeTphia, pp. 555-565.
40. Matson, R. S., G. E. Mustoe, and S. B. Chang, 1972. "Mercury
Inhibition on Lipid Biosynthesis in Freshwater Algae,"
Environ. Sci. Techno., 6_(2):158-160.
41. Meyer, W. A., J. B. Sinclair, and M. N. Khare, 1973. "Biology of
Macrophomina phaseoli in Soil Studied with Selective Media,"
Phytopathology. 63_(5):613-620.
105
-------
42. Mills, W. L., 1973. "Mercury Toxicity to Selected Protozoa,"
J. Protozool.. 2£(4):497.
43. Nelson, J. D., W. Blair, F. E. Brinckman, R. R. Colwell, and
W. P. Iverson, 1973. "Biodegradation of Phenylmercuric Acetate
by Mercury-Resistant Bacteria," Appl. Microbiol., 26_(3): 321-326.
44. Nelson, J. D., L. W. Wan, Z. Vaituzis, and R. R. Colwell, 1973.
"Effects of Mercuric Chloride on the Morphology of Selected
Bacterial Strains," Abstr. An. Meet. Am. Soc. Microbiol., ^3_:31.
45. Nuzzi, R., 1972. "Toxicity of Mercury of Phytoplankton,"
Nature (London), 237(5349):38-40.
46. Parker, M. S., 1971. "The Rapid Screening of Preservatives
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7.(2): 47-53.
47. Pero, R. W., and R. G. Owens, 1971. "A Micro-Technique for
Evaluation of Anti-Fungal Activity," Phytopathology, 61_(2):132.
48. Pfeiffer, P., and B. Dome, 1971. "The Reversible Reaction of
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'' *
1972. "Mercury Pollution of Lake Eric Ecosphere," Environ. Res.,
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50. Rawlinson, C. J., and J. Colhoun, 1970. "Chemical Treatment of
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51. Richards, R.M.E., 1971. "Inactivation of Resistant Pseudomonas
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106
-------
52. Richards, R.M.E., and R. J. McBride, 1971. "The Preservation of
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53. Richards, R.M.E., and R. J. McBride, 1972. "The Preservation of
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54. Selikoff, I. J. (ed.), 1971. "Hazards of Mercury," Environ.
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57. Spangler, W. J., J. L. Spigarelli, J. M. Rose, and H. M. Miller,
1973. "Methyl Mercury Bacterial Degradation in Lake Sediments,"
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.-—
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107
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60. Tonomura, K., and F. Kanzaki, 1969. "The Reductive Decomposition
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62. Van Loon, J. C., 1973. "Agricultural Use of Sewage Treatment
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64. Walker, J. D., and R. R. Colwell, 1974. "Mercury Resistant
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108
-------
4.0 BIOLOGICAL ASPECTS IN PLANTS
4.1 NONVASCULAR PLANTS
4.1.1 Metabolism: Uptake, Absorption, and Residues
"Normal" soils supporting vegetative growth contain very small
amounts of mercury (10-300 ppb) (Shaklette, 1970). Until recently,
mercury was thought not to accumulate excessively in tissues of plants
that grow in these soils. We now know this is not true. Macro-algae
accumulate mercury rapidly from water and subsequently pass the mercury
burden to organisms feeding on them. Data from recent reviews and
research papers on mercury content of noncrop plant species are
summarized in Table 4.1.
Mushrooms (higher fungi) were unexpectedly found to concentrate
mercury with contents up to 80.5 ppm (dry wt.) for Lactarius sp. and
74.0 ppm for Lycoperdon perlatum (Stegnar et al., 1973). These values
were significantly greater than the mercury content of soil in which
the mushrooms grew. Of the mushrooms studied (see Table 4.1), most are
edible. The authors noted that this was one of the first times methyj-
mercury was detected in plants.
tf-
Mosses were founci to contain significantly greater mercury concen-
'' • *
trations than other plants collected at the same locations. Experiments
203
with Hg-labeled fly ash showed mosses take up and retain mercury to a
greater extent than grasses (Huckabee, 1973; Huckabee and Blaylock, 1973).
These results were confirmed in microcosm studies. Although litter and
soil contained more mercury than did mosses after 27 days, the suggestion
was made that mosses could be utilized as reliable monitors of airborne
109
-------
Table 4.1. MERCURY CONTENT OF NON-VASCULAR PLANT SPECIES
Organism3
ALGAE
Ascophyllum nodosum
Ceramium rubrurn
Caldophora rupestris
Enteromorpha compressa
Fucus serratus
F. vesiculosus
Laminaria digitata
Polysiphonia lanosa
Porphyra umbilicalis
FUNGI
Agaricus arvensis '
Boletus edulis
Clavaria sp.
Hypholoma sp.
Kuehneromyces mutabilis
Lacterius sp.
Mercury
content
b
Ppm
.319
3.031
.826
1.007
1.153
.083-. 206
.794
.612
2.353
• :& 4-1.1
2.2-2.4fc
6.6-16.4
15.5-20.2
.35-. 92
80. 5C
Reference
Jones et al. (1972)
s
Stegnar et al. (1973)
110
-------
Table 4.1. MERCURY CONTENT OF NON-VASCULAR PLANT SPECIES (cont'd)
Organism0
Mercury
content
ppnib
Reference
Lycoperdon perlatum
Polypovus sp.
Russula sp.
Scleroderma vulgare
MOSSES
Fontinalis sp.
Eurhynchiwn hians
Brachythecitm rivulare
Sharpiella striatella
Dicramm sp.
Polytrichum
32.2-74.01-
0.4
23.9-36.0
.01-.02
3.70
.012-.080
.012-.080
.012-.080
.118
.092
Wallace et al. (1971)
Huckabee (1973)
Huckabee and Blaylock
(1973)
Notes:
As named by author.
ppm, dry weight unless otherwise noted, of plants growing naturally or
experimentally treated with mercury compounds. Abbreviations are
MM=methylmercury, EM=ethylmercury, PMA=phenylmercury acetate, Hg=mercury (Hg )
cMethylmercury also found.
Ill
-------
mercury pollution. Fontinalis (water moss) contained considerably more
mercury below a pollution outfall (3.70 ppm) than above it (0.08 ppm)
(Wallace et al., 1971).
4.1.2 Effects
No information was found on effects of mercury on nonvascu.lar
plants. Mercury, however, is known to be toxic to micro-algae (see
Section 3.0).
4.2 VASCULAR PLANTS
4.2.1 Noncrop Plants
4.2.1.1 Metabolism: Uptake, Absorption, and Residue—Few studies
report transformation of mercury and mercurials within higher plants.
Fang (1973) using laboratory aquaria showed that the aquatic plants
203
Ceratophyllum demersum and Elodea canadensis converted Hg-phenyl
mercuric acetate to methylmercury, ethylmercury, and Hg (see Table
4.2). Uptake was related to the length of exposure time and phenyl-
mercuric acetate concentration.
Metabolic data for aquatic plants indicate that organomercury
metabolism in higher plants constitutes a detoxification mechanism, i.e.,
trans formation of the more to'^jc organic mercurials to the less toxic
" "i
mercuric ion. Whether or not this mechanism could be a significant
operating factor environmentally needs further clarification.
Woody plants and grasses contain minor amounts of mercury, with
the exception of greenhouse-grown species, which contained up to
808 ppm (see Table 4.2). Wide varietal differences were seen between
leaves from the Briarcliff and Coolidge roses, which accumulated
112
-------
Table 4.2. MERCURY CONTENT OF VASCULAR PLANT SPECIES
Organism
Mercury
content
b
ppm
Reference
AQUATIC PLANTS
Ceratophyllum demersum
Elodea canadenesis
Water lily
GRASSES
Andropogon sp.
Festuoa eliator
WOODY PLANTS
Rhododendron maximum
Tsuga canadensis
Acer saccharinum
Ailanthus dltissima
Picea abies
Pinus nigra
Platanus aaerifolia
Onerous palustr-is
0-.003(MM)
.003-.039(EM)
.21-6.22(PMA)
1.28-6.95(Hg)
0-.009(MM)C
.030-.170(EM)
2.68-9.35(PMA)
1.80-6.65(Hg)
0.52
0.68
.002-.005
--.024 (
.004-.023
.81
.61
.22
.08-.17
.13-.71
.76
Fang (1973)
Huckabee and Blaylock
(1973)
Huckabee (1973),
Huckabee (1973)
Smith (1972)
113
-------
Table 4.2. MERCURY CONTENT OF VASCULAR PLANT SPECIES (cont'd)
Organism3
Taxus sp.
Tilia cordata
Alnus crispa
Be tula nana
B. papyri f era
Juniperus virginiana
Ledum palustre
Quercus alba, Q. lyrata,
Q. stellata
Rhus glabra}
R. copallina
Spirea beauverdiana
Rosa sp. r
Mercury
, content
ppm Reference
.85
1.10
1.0 Shaklette (1970)
.5-1.0
.5-2.0
.5
1.0-3.5
.5
.5
M
.3
. -1.3-808.0 Stahl (1969)
, -
Notes:
aAs named by author.
ppm, dry weight unless otherwise noted, of plants growing naturally or
experimentally treated with mercury compounds. Abbreviations are
MM=methylmercury, EM=ethylmercury, PMA=phenylmercury acetate, Hg=mercury (Hg++)
cPUnts treated initially with PMA.
114
-------
317 and 808 ppm, and other rose varieties nearby accumulating only
1.3 ppm (Stahl, 1969). Eight weeks after a single injection of mercuric
OQO
nitrate ( Hg(N(L)2) into the trunk of an Eastern red cedar, the
labelled radioactive mercury distribution pattern was: 1.7% to branches,
1.5% to foliage, with 96.5% remaining in the trunk. Only 0.3% of the
radioactivity was leached by rain into the underlying litter (Huckabee
and Blaylock, 1973).
4.2.1.2 Effects—In a brief review of mercury phytotoxicity, D'ltri
(1972) noted that older plant parts are generally more susceptible to
injury than younger plant parts.
No reports were found describing mercury-induced toxic effects to
plants from naturally occurring sources. The extent of damage to a
plant, however, is dependent on such factors as chemical species of
mercury, initial concentration, temperature, sunlight, and air flow
rate. Additionally, varietal and strain differences are important
functional factors in determining the toxic response of plants belonging
to the same species.
According to Stahl, in 1969 few papers existed that described the
phytotoxic effect on plants. --When measurable, mercury content of the
3»
air was 10 micrograms/cubic meter in'some cases, but below the limit of
detection (10 micrograms/cubic meter) in others. Decomposing organic
matter in tankage fertilizer apparently enhanced mercury release.
Tobacco leaves accumulated large amounts of mercury—up to 4000 ppm
dry weight—whereas rose leaves accumulated only 3.3 ppm dry weight.
115
-------
A generalized concept holds that-phytotoxicity arises primarily
from metallic vapors formed by thermal decomposition or catalytic
reduction of mercury compounds (Stahl, 1969). In this review, analytical
procedures are not described sufficiently to determine whether metallic
mercury was distinguishable from volatile organic mercury compounds.
Most of the research was conducted in confined spaces such as green-
houses.
4.2.2 Crop Plants
Mercury can accumulate in the foliage, seed, and fruit of crop'
plants, thereby contributing to the mercury burden of humans and of
domestic and wild animals. The amounts of mercury found in plants and
plant parts may be large, but chemical analysis alone does not indicate
whether a mercury compound was absorbed into and translocated through-
out plant tissues or whether the content was a surface residue
(Shaklette, 1970). All studies reviewed did not take this factor into
consideration. The most important aspect of crop plant accumulation of
mercury is how much residue remains in food products consumed by humans.
Although mercury residue concentrations have been widely reported
3»
(Table 4.3), an obvious need exists for "more comprehensive and precise
mercury analyses of foods.
4.2.2.1 Metabolism: Uptake, Absorption, and Residues—Harvested sweet
potato tubers contained 0.02 to 0.03 ppm mercury, values similar to
control levels; evidence thus implies no detectable translocation of
mercury from Semesan (mixture of hydroxymercurichlorophenols and
hydroxymercurinitrophenols) and other mercurial fungicide treatments of
116
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PAGE NOT
AVAILABLE
DIGITALLY
-------
i
propagative roots (Huisingh and Kline, 1972). However, foliage of
plants grown from Semesan-treated roots had increased mercury content.
Harvested grain (wheat and barley) similarly had no increased
mercury content due to Panogen PX (methylmercury dicyandiamide)
treatment of seed (Saha et al., 1970). When Panogen PX was app.lied to
soil, however, mercury was translocated to the ears of grain.
203
When directly contaminated with Hg at various stages of growth,
barley had mercury residues primarily in stems (55-60%), to some extent
in husks (30-35%), and to a minor degree in grain (10%) (Aarkrog and
Lippert, 1971). Translocation of mercury within the plant was apparently
quite small. The order of uptake in barley for the radionuclides studied
was Zn less than Co less than Fe less than Cr less than Pb less than Hg.
Velvet bentgrass, Agrostis canina, exhibited no detrimental effects
when growning in soils containing 455 ppm mercury from annual organo-
mercurial treatment (Estes et al., 1973). The grass contained 1.68 ppm
Hg with normal levels of Mn, Fe, Cu, and Zn. This organomercurial
accumulated in surface soils, but exhibited negligible lateral migration
through the soil. The treatments were made over a period of 15 years in
conjunction with golf green maintenance.
Regarding mercury contamination of foods, Somers (1971a) listed 12
food types and found that noncontained more than 0.02 ppm, the limit
of detection for the atomic spectrophotometric technique employed
(Table 4.4). Somers (1971b) estimated that the normal daily intake of
mercury is 20 micrograms/person maximum, based on the detection limit
of 0.02 ppm.
118
-------
Table 4.4. MERCURY IN TOTAL CANADIAN DIET, 1969
Food group
1. Milk and dairy products
2. Meats
3. Cereals
4. Potatoes
5. Leafy vegetables
6. Legumes
7. Root vegetables
8. Garden fruits
9. Fruits
10. Oils and fats
11. Sugar, jams, pickles
12. Coffee, tea, soft drinks
No mercury residues above detection limit, 0.02 ppm
c
J»
" *
Source:
Somers (1971b).
119
-------
Analytical techniques, absorption of mercury on laboratory glass-
ware, proper sampling techniques, and ease of mercury reactivity are all
problems contributing to difficulties in accurately detecting the very
low mercury concentrations present in food residues. Analytical chemistry
of mercury is discussed previously in Section 2.0. Comparison of three
analytical techniques is shown in Table 4.5. The wide discrepancies are
obvious and difficult to explain.
4.2.2.2 Trans1ocation--A review by D'ltri (1972) summarizes data on
translocation in crop plants. Care is exerted to distinguish between
true translocation of mercury within the plant and mercury content
resulting from spray residues:
For apples, mercury translocation was documented in a series of
well-designed experiments. Mercury accumulated excessively in fruit,
with translocation being the only reasonable explanation. Mercury
residues in fruit ranged from 0.005 ppm (single treatment) to 0.07 ppm
(multiple treatments) when mercurial fungicides were applied. In one
case, most of the residue was found in the pulp (73%), with less in peel
(18%), and..core(9%). One study reported translocation of mercury from
apple tree bark to roots, buds.^and leaves. Application of mercury early
in the growing season resulted in higher mercury content in harvested
fruit than applications at later dates. Furthermore, low levels of
mercury persisted in apple trees that had not been sprayed for 10 or
more years (D'ltri, 1972).
For potatoes, experiments reviewed indicated that mercury can be
absorbed and translocated by root systems, potato skin, or leaves.
120
-------
Table 4.5. COMPARATIVE MERCURY ANALYSIS OF WHEAT AND FLOUR
(ppm)
F.D.D
No.
18464
20445
18465
20389
32573
32574
32575
Notes:
Sample Neutron Atomic Neutron
Activation Absorption Activation
Wheat 0.079 0.005 0.007b
Wheat y '» 0.30 0.007 0.014,b 0.004a
Wheat 0.40 0.007 0.012b
Wheat * 0.34 0.009 0.016,b 0.010a
Flour 0.38, 0.29 0.007 0.010,b 0.015,3
0.02,C 0.011d
Flour 0.26, 0.14 0.007 . 0.005,b 0.013a
Flour 0.22 0.005 0.008,b 0.0363
?Atomic Energy of Canada Limited.
Oak Ridge National Laboratory.
"jF.D.A. (Nine replicates).
Gulf General Atomic.
Source:
•
Somers (1971b).
-------
Normal spraying resulted in tuber residues of 0.040 ppm, while un-
sprayed controls contained greater than 0.005 ppm. Soil applications
of phenylmercuric chloride in the year prior to planting did not result in
significant residues; mercury was believed to be converted into
insoluble mercuric sulfide which is not available to plants (D'ltri,
1972).
For tomatoes, review data indicated total residual mercury was as
high as 0.5 ppm in fruit cultured in greenhouse. Mercury was rapidly
absorbed and the residue persisted. In other studies, residues usually
did not exceed 0.01 or 0.05 ppm, but in one circumstance total whole
fruit mercury residue was 0.110 ppm after multiple applications (D'ltri,
1972).
Translocation of mercury within tomato plants was demonstrated best
in hydroponic culture (Haney and Lipsey, 1973). In only two days seedling
tomato plants grown in nutrient solution containing, for example, 0.0006
ppm of methylmercury hydroxide (MMH), responded by accumulating mercury
in roots (8.2 ppm, concentration factor = 1367) and shoot terminals
(1.5 ppm, concentration factor = 250). As determined by inhibition of
shoot length and terminal wet'Iweight, growth of the plants was moderately
' • *
inhibited, averaging 30%. Interestingly, aphids and lacewing larvae
placed on these plants accumulated mercury at a high rate (concentration
factors in relation to mercury content of nutrient solution - 1670 and
4187 ppm, respectively, after 4 to 8 days). Similar sensitivity to MMH
was found for corn and bean in 13 to 15 days, but these plants were not
studied in detail.
122
-------
Bache et al. (1972) have reported increased accumulation of mercury
from treatment of soil (Howard gravelly loam) with methylmercury
dicyandiamide (10 ppm) in tomato fruit (0.013 ppm increase over controls)
and foliage (0.341 ppm increase). A similar amount (0.231 ppm increase)
was found in foliage of tomato plants grown in eel slit loam containing
10 ppm mercuric chloride. Less pronounced residue amounts were found
at a 1 ppm application rate for these soils and another, Oswego muck, and
for phenylmercuric nitrate. Thus, soil type, type and concentration of
mercury compound, and plant part to which mercury is translocated all had
a bearing on experimental results.
For grains, articles reviewed by D'ltri (1972) indicated appreciable
uptake and translocation of mercury from cereal seed to seedlings:
203
One study involving HgCl^ demonstrated translocation and
accumulation of mercury from treated seed into growing seedlings and
from foliage to storage organs (seed). The plants studied were wheat,
barley, oats, and corn. Another cites residues in barley and oats that
203
were twice the amount in untreated seed. When Hg-phenylmercuric •
203
acetate -was applied to rice leaves, Hg was rapidly translocated to
t
other parts of the plant, particularly newly developing plant parts.
In Japan, rice grains treated with mercurials had up to 1.0 ppm mercury
while nontreated rice contained 0.227 to 0.238 ppm. Other studies reported
residues up to 0.61 ppm. Polishing rice tended to reduce mercury content.
Nearly 5% of mercury sprayed on rice plant foliage was translocated to
ripe grain. Greatest mercury concentrations occurred in rice grain when
the plants were treated at later stages of growth. 'From studies on rice,'
123
-------
the United Kingdom reported negligible amounts of mercury in rice
(0.010 to 0.015 ppm). Millet accumulated mercury residues of 0.058
ppm (increase over control) in harvested grain and 0.123 ppm increase
in stems and leaves when grown in Howard gravelly loam containing 10 ppm
methylmercury dicyandiamide. In studies of other soils, significant
increases in mercury content were also observed for grain, but less
significant increases for stems and leaves (D'ltri, 1972).
Although the data were contested, James (1971) reported that seed
treatment with Ceresan M (N-ethylmercuric p-toluene sulfonamide) resulted
in mercury accumulation in seed of the succeeding generation of peas
and wheat. Accumulation was greater at pH 5.6 for peas (0.065 to 0.248
ppm) than for wheat (0.003 to 0.061 ppm). In a similar study of barley,
seed treatment with various organomercurial fungicides at 0.5, 1, 2, and
5 times recommended rates resulted in absorption and translocation of
mercury from treated seed to seedling leaves and roots (Huisingh and
Kline, 1972). The results showed definite dose-response relation.
Using radiotracers, Aarkrog and Lippert (1971) reported translation
of mercury (as well as chromium and lead) was minimal in barley grown
in experimental plots/ Barle/jplants were sprayed at six different stages
of development. Of various metals studied, mercury, lead, chromium,
and iron followed the same approximate pattern of retention, i.e., grain
(10%), husks (30 to 35%), and straw (55 to 60%). Distribution for cobalt
and zinc was somewhat different. Mercury was translocated to barley
grain to a lesser extent than any of the other metals studied.
124
-------
A variety of crop plants grown in three different soils each
treated with one of three mercurial fungicides absorbed and translocated
mercury to different plant parts (Bache et al., 1972). The most consistent
study involved Panogen (cyano(methylmercuri)guanidine) and a gravelly
loam soil. Results from this report are summarized in Table 4.6; In
general, mercury content could be correlated directly with application
rate of Panogen. Mercury tended to accumulate more in edible parts of
millet and onion, but accumulation was greatest in stems and leaves of
bean, carrot, and tomato. However, analysis for methylmercury indicated
this compound tended to accumulate more in fruit than in stems and leaves.
The highest total mercury content occurred in onions (1.065 ppm).
Although the mercury application rates (1.0 and 10.0 ppm) were admittedly
greater than normal, the experiment definitely demonstrated uptake and
translocation of mercury. Results with other soils and other mercurials
were somewhat similar, but less definitive. The highest residues for
methylmercury were found in beans (0.127 ppm) and potatoes (0.183 ppm).
Of the three chemicals studied, Panogen was more persistent in all thr.ee
soils than mercuric chloride or phenylmercuric acetate.
There is no doubfthat tra'aslocation, redistribution, and residue
'' *
accumulation of mercury occur in crop plants. Except for unusual cultural
situations, plant products produced by normal agricultural practice can
be considered safe for human consumption in regard to mercury content.
4.2.2.3 Effects--App1ication of mercury-containing fungicides directly
onto crop plants and to soils from which transformed (usually as metallic
vapor) mercury is released results in widely varied phytotoxic effects on
plants.
125
-------
Table 4.6. 'TOTAL MERCURY AND METHYLMERCURY CONTENT OF PARTS OF
CROP PLANTS CULTIVATED IN HOWARD GRAVELLY LOAM
CONTAINING VARYING AMOUNTS OF PANOGEN
(METHYLMERCURY DICYANDIAMIDE)
Residue, ppm
Edible fruit, seed,Stems and
Application or vegetable leaves
rate, ppnv \ . .
Crop plant (as mercury) Total Hg Methyl Hg Total Hg Methyl Hg
0 .024 .002 .083 " .002
Bean 1 • .061 .050 .135 .048 '
10 .205 .127 .173 .030
0 .029 .001
Cabbage 1 .029
10 .162 .004
0 .006 nd .026 nd
Carrot 1 .037 .130
10 .285 .003 .240 .001
-------
TABLE 4.6. TOTAL MERCURY AND METHYLMERCURY CONTENT OF PARTS OF
CROP PLANTS CULTIVATED IN HOWARD GRAVELLY LOAM
CONTAINING VARYING AMOUNTS OF PANOGEN
(METHYLMERCURY DICYANDIAMIDE) (cont'd)
Residue, ppmc
Crop plant
Application
rate, ppm -1
(as mercury^ '>
Edible fruit, seed,
or vegetable
Stems and
leaves
Total Hg
Methyl Hg1
Total Hg
Methyl Hg[
ro
Millet
0
1
10
.048
.142
.106
nd
.081
.020
.044
.123
Onion
0
1
10
.021
.021
1.065
.001
.007
.022
.022
.035
Potato
0
1
10
.003
.052
.335
.001
.057
.081
,067
,067
,570
nd
.006
.009
-------
Table 4.6. ; TOTAL MERCURY AND METHYLMERCURY CONTENT OF PARTS OF
CROP PLANTS CULTIVATED IN HOWARD GRAVELLY LOAM
.' CONTAINING VARYING AMOUNTS OF PANOGEN
(METHYLMERCURY DICYANDIAMIDE) (cont'd)
rv>
oo
Residue, ppma
Crop plant
Tomato
Application
rate, ppm ,
(as mercury)
0 -
1
10
Edible fruit, seed
or vegetable
Total Hg Methyl Hgb
nd
nd
.013
Stems and
Total Hg
.091
.091
.432
leaves
Methyl Hgb
nd
.002
.003
Notes:
nd=not detected (below level of detectability), blanks indicate no analysis made.
Analyses made only when high total mercury was found.
Source:
Adapted from Bache et al. (1972).
-------
Byford (1971) reported that a 1.2% solution of ethylmercuric
phosphate applied as a mist to sugar beet seed at a 1.0% (V/VI) rate
caused reduced germination rate and a significant number of abnormal
seedlings. Because of these findings, further testing of the mist
treatment was abandoned.
Kojima and Fujita (1973) briefly summarized experimental data of
other Japanese workers who investigated the decomposition of organic
mercurials by roots and other organs of soybeans. Decomposition rates
decreased in the following order: ethylmercuric chloride greater than
butylmercuric chloride greater than phenylmercuric chloride greater
than methyl mercuric chloride. Cysteine and dihydrothioctic acid
accelerated the in vitro decomposition of methylmercury compounds.
According to Kojima and Fujita (1973), this may explain why phenyl-
mercuric acetate rapidly decomposes in plant tissue.
Phenylmercuric acetate (PMA) has been studied as an antitranspirant
for tomato and grain sorghum (Cotter, 1970; Fuehring, 1973). Results
with tomato showed that 100 ppm PMA- reduced transpiration significantly
when available water was adequate. At night or under a water deficit,
however, transpiration, increased (Cotter, 1970). In some cases of the
.T»
grain sorghum study, single applications of PMA at rates up to 80 g/ha
resulted in yield increases of 16.9%. Spraying young (boot stage)
sorghum at the beginning of maximum mositure uptake gave the best results,
Atrazine and Folicote were as effective as PMA. Cotter (1970) noted the
lack of data concerning rates and volume of spray, but also that use of
antitranspirants offers possibilities of conserving water over wide areas
129
-------
and on an important economic scale. Although not yet reduced to practice,
PMA application as an antitranspirant to crop plants presents an additional
source of mercury contamination of the environment. Earlier studies
reviewed by these authors involved PMA transpiration reduction in apple,
citrus, corn, cotton, red pine, tobacco, and wheat.
Relatively few studies relating mercury effects on plant genetics
have been reported. Saha (1972) summarized earlier research in which
organomercurials affected the mitotic spindle of onion roots (Aliiurn
cepa): Chromosome numbers doubled or individual chromosomes were
defectively distributed during mitosis.
Methylmercury dicyandiamide (Panogen 15) was found to cause C-mitoses,
multinucleated cells, and polyploidy in Tradescantia and Vicia faba root
tips (Ahmed et al., 1972). These effects are similar to those caused by
colchicine, a known inhibitor of spindle formation. Treatment concen-
trations were 1, 2, and 5 ppm for 1, 2, and 3 hours. The authors warn
that considerable precaution should be taken in using this fungicide.
Panogen 15 is used for treating seeds of cereal grains, flax, soybeans,
peas, rape, safflower, and seeds of numerous other crop plants.
4.3 REFERENCES- < •''
•t *
'' "*
1. Aarkrog, A., and J. Lippert, 1971. "Direct Contamination of
Barley with Chromium-51, Iron-59, Zinc-65, Mercury-203, and
Lead-210," Radiat. Bot., U_(6):463-472.
2. Ahmed, M., and W. F. Grant, 1972. "Cytological Effects of the
Mercurial Fungicide Panogen 15 on Tradescantia and Vacia faba
Root Tips," Mutat. Res., 14(4):391-396. '
130
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3. Bache, C. A., W. H. Gutenmann, L. E. St. John, R. D. Sweet, and
M. Barelli, 1972. "The Use of a Pelagic Trophodynamic Chain for
Studying the Transfer of Metallic Pollutants," R'ev. Int. Oceanogr.
Med., 28:27-52.
4. Byford, W. J., 1971. "Organo Mercury Fungicide Treatment of
Sugar Beet-D Seed," Ann. Appl . Biol., 6£(3): 245-252.
5. Cotter, D. J., 1970. "Phenylmercuric Acetate Effect on Water Loss
of the Tomato," J. Amer. Soc. Hort. Sci., 95_(6): 774-776.
6. Cunningham, H. M., and J. C. Merangner, 1972. "Mercury Content
of Canadian Foods and Cereals Determined by Different Methods,"
Environ. Mercury Contam., Int. Conf. (25UOA5), 4_:41-145.
7. D'ltri, F. N., 1972. The Environmental Mercury Problem, CRC Press,
Cleveland, pp. 20-85.
8. Estes, G. 0., W. E. Knoop, and F. D. Houghton, 1972. "Soil-Plant
Response to Surface-Applied Mercury," J. Environ. Qua! . ,
2!(4):451-452.
9. Fang, S. C., 1973. "Uptake and Biotransformation of Phenylmercuric
Acetate by Aquatic Organisms," Arch. Environ. Contam. Toxicol.,
10. Fuehring, H. D., 1973. "Effect of Anti Transpirants on Yield of
Grain Sorghum Under Limited Irrigation," Agron, J., 55/3) : 348-351.
11. Goldwater, L. J., 1971. "Mercury in the Environment," Scientific
American, 224(5) :15-21.
12. Haney, A., and R. L. Lipsey, 1973. "Accumulation and Effects of
Methyl Mercury Hydroxide in a Terrestrial Food Chain Under
Laboratory Conditions," Environ. Pollut.. 5_(4):305-316.
131
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13. Huckabee, J. W., 1973. "Mosses: Sensitive Indicators of
Airborne Mercury Pollution," in: Atmospheric Environment,
Pergamon Press, London, pp. 749-754.
14. Huckabee, J. W., and B. G. Blaylock, 1973. "Transfer of Mercury
and Cadmium from Terrestrial to Aquatic Ecosystems," in: Metal
Ions in Biological System Studies of Some Biochemical and
Environmental Problems, Plenum Press, New York, London, pp. 115-160.
15. Huisingh, D., and D. M. Kline, 1972. "The Fate of Mercury in
Vegetative Parts of Barley Grown from Seed Treated with Mercury
Fungicides," Phytopathology. 62_(7):766.
16. James P. E., 1971. "Translocation of Mercury from Seed Treatment,"
in: Identification and Measurement of Environmental Pollutants,
Symposium, Ottawa, Canada, June 14-17, 1971, B. Westley (ed.),
National Research Council, Canada, pp. 213-215.
17. Jervis, R. E., and B. Tiefenbach, 1971. "Trace Mercury Deter-
minations in a Variety of Foods," in: Nuclear Methods in
Environmental Research, J. R. Vogt (ed.), Univ. of Missouri, •.
Columbia, pp. 188-198.
18. Jones, A. M., V. Jones and W. D. Stewart, 1972. "Mercury in
" »
Marine Organisms of the Tay Region," Nature (London), 238(5360):
164-165.
19. Kojima, K., and M. Fujita, 1973. "Summary of Recent Studies in
Japan on Methylmercury Poisoning," Toxicology,1:43-62.
20. Sana, J. G., 1972. "Significance of Mercury in the Environment,"
Residue Reviews, 42:111-132.
132
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21. Saha, J. G., Y. W. Lee, R. D. Tinline, S.H.F. Chirm, and
H, M. Austenson, 1970. "Mercury Residues in Cereal Grains from
Seeds or Soil Treated with Organo Mercury Compounds," Can. J.
Plant Sci.. 50_(5): 597-599.
22. Shaklette, H. T., 1970. "Mercury Content of Plants," in: •
Mercury in The Environment, Geological Survey Professional
Paper 713, U.S. Govt. Printing Office, Washington, D.C.,
pp. 35-36.
23. Smith, W. H., 1972. "Lead and Mercury Burden of Urban Woody
Plants," Science. 176.(4040): 1237-1239.
24. Somers, E., 1971a. "Heavy Metals in Foods," in: Int. Symp.
Identification Meas. Environ. Pollut., pp. 199-201.
25. Somers, E., 1971b. "Mercury Contamination of Foods," in:
Mercury in Man's Environment, Proc. Symp., Ottawa, pp. 99-106.
26. Stahl, Q. R., 1969. Preliminary Air Pollution Survey of Mercury
and Its Compounds, National Air Pollution Control Administration,
Raleigh, N.C., Pub. No. APTD 69-40, pp. 15-29.
27. Stegnar, R., L. Kosta, A. R. Byrne, and V. Ravnik, 1973.
"Accumulation of Mercury "Jjy, and the Occurrence of Methyl mercury
11 ^
in, Some Fungi," Chemosphere, 2_(2): 57-63.
28. Tanner, J. T., M. H. Friedman, D. N. Lincoln, L. A. Ford, and
M. Jaffee, 1972. "Mercury Content of Common Foods Determined by
Neutron Activation Analysis," Science, 177(4054):.1102-1103.
133
-------
29. Tolan, A., and G.A.H. Elton, 1972. "Mercury in Food,"
Biochem, J., 130(2):69-70.
30. Wallace, R. A., W. Fulkerson, W. D. Shultz, and W. S. Lyons,
1971. Mercury in The Environment, Oak Ridge National Laboratory
ORNL-NSF-EP-1.
134
-------
5.0 ANIMAL STUDIES
5.1 SUMMARY
Due to the natural and ambient background levels of mercury in the
environment, essentially all living organisms contain low levels of mercury.
Organisms higher up the food chain generally have higher mercury levels
than those lower in the chain. In areas where man's activities increase
the mercury content in the environment, the mercury levels in animals
inhabiting that area are also raised. The large number of epidemiological
.studies and the vast amount of data on mercury content of various
organisms in the environment make a complete overview impractical. This
section will present representative data from three levels of the food
chain: fish, birds, and mammals.
5.2 FISH
About 10,000 tons of mercury per year enter the oceans via rivers
and rainfall, half from natural weathering processes and half from man's
activities (Hartung and Dinman, 1972). The concentration of mercury in
fresh waters varies, being high in mineralized or industrial areas an,d
lower elsewhere. As an example of natural levels of mercury in fresh
water, the mercury concentration in waters of the Northeastern United
States was determined to be 0.055 plus or minus 0.035 ppb from analysis
of samples taken from lakes, rivers, and ponds (Hartung and Dinman,
1972). This value probably represents the current natural background
level. Higher values ranging to 2.8 ppb were found and possibly
represent contamination by man.
135
-------
Mercury levels in fish vary depending on the water concentration of
mercury. Also, predatory fish, such as tuna and swordfish, have higher
levels than other varieties of fish. Mercury in fish muscle accumulates
mostly as methylmercury, presenting a serious hazard to man. Some
examples of mercury concentrations in freshwater fish are shown in
Table 5.1.
Mercury in marine fish are listed in Table 5.2 by species rather
than country since the oceans are multinational. The countries listed
either caught, processed, or consumed the fish.
The lethal concentration of mercuric chloride for stickleback (fish)
is 4 to 20 ppb, 20 ppb for guppy, 27 ppb for eel, and 9,200 ppb for
rainbow trout. The lethal concentration of mercuric nitrate is 20 ppb
for stickleback and 20 ppb for guppy (U.S. Environmental Protection Agency,
1973). Because mercuric sulfate decomposes in cold water into a yellow
insoluble basic sulfate and free sulfuric acid and because mercury and
mercury diammonium chloride are insoluble in cold water, no data are
available on the toxicity of these compounds in aquatic organisms.
Even in heavily polluted areas the concentration of mercury is
usually not high enough to kill fish. Fish and shellfish killed in the
Minamata area of Japan, for example, contained a high level of mercury
(9-24 mg/kg) in their tissues (Holden, 1973). Fifteen mg Hg/kg was found
in body muscle of pike and rainbow trout after an oral LD5Q of methyl-
mercury (Holden, 1973).
As indicated in many studies, a mercury concentration of 0.1 mg/kg
is probably normal for most marine fish with the exception of large
predatory fish where the concentration may be higher. In freshwater fish,
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Table 5.1. MERCURY CONCENTRATIONS IN FRESHWATER FISH
Country
Source:
Holden (1973).
Species
Concentration
(parts per million)
Range Mean
Canada
Lake Winnipeg
Lake St. Clair
Finland
Netherlands
Norway
United Kingdom
United States
Pike
Yellow perch
Sucker
Pike
Yellow perch
Sucker
Pike
Common perch
Bream
Pike .
Common perch
Pike
Perch
Brown trout
Pike
Perch
Bream
Sea trout
Yellow perch
Walleye
Channel catfish
0.14-1.27
0.07-1.14
0.02-0.55
0.85-2.97
0.31-2.25
0.22-5.13
0.02-5.80
0.11-4.70
0.06-1.78
0.19-0.59
0.57-1.90
0.12-1.27
0.08-2.39
0.04-1.56
0.08-1.60
0.07-0.60
0.06-0.18
0.10-1.00
0.32-1.70
1.40-3.57
0.32-1.80
0.41
0.48
0.11
1.76
1.14
1.97
_
-
-
0.44
0.85
0.44
0.56
0.19
' 0.47
0.30%%
0.13
0.33
•.
-
137
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Table 5.2.. MERCURY CONCENTRATIONS IN MARINE FISH
Species
Plaice
Flounder
Cod
Tuna
Swordfish
Lobster
Oyster
Country
Denmark
Sweden (Baltic)
U. K. (Thames)
Denmark
Sweden (Baltic)
U. K. (Thames)
Canada (Atlantic)
Denmark (Baltic)
Sweden (Baltic)
U. K. (Thames)
Canada (Atlantic)
Canada (Atlantic)
Sweden (Japan, canned)
(USA, canned)
(USSR, canned)
Canada (Atlantic)
Canada (Atlantic)
U. K. (Scotland)
Canada (Atlantic
U. K.
Concentration Range
(parts per million)
0.038 -
0.031 -
0.09 -
0.07 -
0.06 -
0.08 -
0.07 -
0.14 -
0.02 -
0.11 -
0.02 -
0.33 -
0.14 -
0.08 -
0.53 -
0.82 -
0.08 -
0.12 -
0.02 -
0.03 -
0.496
0.076
0.60
0.89
0.26
2.5
0.17
1.29
0.36
1.2
0.23
0.86
0.30
0.33
0.77
1.00
0.20
0.75
0.14
0.20
Source:
Holden (1973).
138
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concentrations as high as 0.5 nig/kg may be normal for some predatory species.
5.3 BIRDS
The amount of mercury found in various bird species and in birds
from various areas should reflect their dietary habits. Birds that eat
fish or grain and seeds from agricultural areas where mercurial pesticides
or seed dressings are used can be expected to have higher mercury levels
than birds from areas of low mercury concentration. For example, a sharp
rise in the mercury concentration in feathers of goshawks shot between
the early 1900's and 1965 occurred about the time methylmercury seed
dressings became widely used in Sweden (Friberg and Vostal, 1972).
Following restriction and regulation of the use of mercurial seed dressings,
the mercury levels in seed-eating birds and their predators decreased
substantially.
In 1971 starlings were collected in the United States from 50 sites
selected to give a cross section of environmental conditions (Martin and
Nickerson, 1973). Mercury levels were generally well below 0.50 ppm
(whole body wet weight), with 76 percent at or below 0.05 ppm.
Mercury residues in the wings of mallards and black ducks were
determined from samples supplied by hunters across the United States
during the 1969-1970 hunting season (Heath and Hill, 1974). Pools of
wings from all areas had at least 0.05 ppm mercury, but levels in only
three pools (one each from New York, Wisconsin, and Nevada) exceeded
0.50 ppm. The mercury content was less than 0.05 ppm (wet weight) in
breast muscle of 93 percent of mourning doves sampled from the Eastern
United States during 1970-1971 (Kreitzer, 1974).
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The effects of feeding habits on the mercury levels in birds can be
seen from a report by Spronk and Hartog (1970) on mercury levels in flight
feathers of the goshawk and the buzzard in the Netherlands. Mercury levels
in the goshawk, one-third of whose diet consists of seed-eating pigeons,
varied from 26 to 72 ppm, while levels in the buzzard, which mainly preys
on sprout-and root-eating mice, varied from 2 to 23 ppm.
5.4 MAMMALS
As in fish and birds, mercury levels in various mammals reflect
their diet. In an area of mercury contamination the mercury progresses
up the food chain, becoming more concentrated with each step. Since wild
mammals are not a major food supply for humans, mercury should not be a
problem through this route. The feed provided to domestic animals can be
controlled; therefore, except for accidents or ignorance, mercury levels
in these animals should normally not be above background levels.
Table 5.3 lists mercury levels found in tissues of black bear
collected during the October and November 1972 hunting season in Idaho.
Table 5.4 lists mercury levels in tissue samples from northern fur seals
and their lice collected on St. Paul Island, Alaska in July 1972.
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Table 5.3. MERCURY IN BEAR TISSUE
(parts per billion)
Sex
Tissues
Mercury
M
M
M
M
M
Hair
Muscle
Fat
Hair
Muscle
Fat
Hair
Muscle
Fat
Hair
Muscle
Fat
Muscle
Muscle
110.0
40.0
51.0
183.0
42.0
60.0
275.0
48.0
48.0
160.0
53.0
48.0
42.0
160.0
F
F
Range:
Muscle
Fat
Muscle
Fat
Hair
Muscle
Fat
48.0
114.0
171.0
120.0
100-275
40-171
48-120
Source:
Benson et al.(1974).
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Table 5.4. MEAN MERCURY CONTENTS IN TISSUES AND THE
SUCKLING LICE SAMPLES OF THE NORTHERN
FUR SEALS, Callorhinus ursinus (ppm)
Seals
Nursing cows
Newborn pups
Pups (2 months)
No. of
samples
2
2
3
Hair3
4.87
3.68
5.36
Bloodb Milkc
0.0995 0.0145
0.0195
0.0686
Suckling
Acd
0.221
0.630
lice
Pfe
--
—
0.513
Notes:
aAir dried
bWhole blood
cWhole milk
Ac = Antarctophth-irus callorhini
P
Pf = Proechinophthirus fliictus
Source:
Kim et al. (1974).
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5.5 REFERENCES
1. Benson, W. W., J. Gabica, and 0. Beecham, 1974. "Pesticide and
Mercury Levels in Bear," Bull. Environ. Contam. Toxicol., ll(l):l-4.
2. Friberg, L., and J. Vostal (eds.), 1972. Mercury in the Environment -
a Toxicological and Epidemiological Appraisal, CRC Press,
Cleveland, 215 pp.
3. Hartung, R., and B. D. Dinman (eds.), 1972. Environmental Mercury
Contamination, Ann Arbor Science Publishers, Ann Arbor, Mich., 349 pp.
4. Heath, R. G., and S. A. Hill, 1974. "Nationwide Organochlorine and
Mercury Residues in Wings of Adult Mallards and Black Ducks During
the 1960-1970 Hunting Season," Pestic. Monit. J., 7(3-4):127-138.
5. Holden, A. V., 1973. "Mercury in Fish and Shellfish, a Review,"
J. Food Techno!.. 8(l):l-25.
6. Kim, K. C., R. C. Chu, and G. P. Barren, 1974. "Mercury in Tissues
and Lice of Northern Fur Seals," Bull. Environ. Contain. Toxicol.,
11(3):281-284.
7. Kreitzer, J. F., 1974. "Residues of Organochlorine Pesticides,
Mercury, and PCB's in Mourning Doves from Eastern United States -
1970-1971," Pestic. Monit. J.. 7(3-4):195-199.
8. Martin, W. E., and P. R. Nickerson, 1973. "Mercury, Lead, Cadmium,
and Arsenic Residues in Starlings - 1971," Pestic. Monit. J..
7jl):67-72.
9. Spronk, N., and G. C. Hartog, 1970. "Mercury in Birds of Prey,"
Ardea_, 59 (1-2): 34-37.
10. U.S. Environmental Protection Agency, 1973. National Disposal Site
Candidate Profile Reports - Mercury, Arsenic, Chromium, and Cadmium
Compounds. Vol. VI (Draft), TRW Systems Group Report No. 21485-6013-
RU-00, 212 p.
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6.0 BIOLOGICAL ASPECTS IN HUMANS
6.1 SUMMARY
Within recent years, particularly within the last decade, laboratory
methods for the determination of trace amounts of mercury have been
developed sufficiently to allow accurate measurements of this element
in the environment and in biological materials (see Section 2.0). More
accurate data from both clinical and epidemiological studies are presently
being added to the literature. Despite the possible deficiencies of
earlier mercury determinations and the state of flux caused by the input
of new data, the biological effects of mercury in the environment are
quite clear.
The biological activity of mercurials is primarily a result of their
affinity for sulfhydryl groups. It might be expected that the combination
of a mercury ion with a sulfhydryl group in an enzyme molecule could
change enzyme activity. In fact, various mercury compounds such as
p-chloromercuribenzoate are routinely used by enzyme chemists as sulf-
hydryl specific reagents when studying enzyme structure and activity.-.
In addition to the effect on enzymes, mercurials can also react with
phosphoryl groups of membranes (Passow, et al., 1961) and directly with
i
nucleic acids (Friberg and Vostal, 1972). Obviously, any agent that can
alter enzyme activity, that can disrupt cell membrane integrity, and that
can combine with nucleic acids could have a deleterious effect on cellular
metabolism, resulting in cell death and ultimately in death of the entire
organism.
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Mercury in its various forms is a natural constituent of the
environment. Elemental mercury vapor when inhaled is absorbed through
the lungs, penetrating both the blood-brain and the placental barriers.
Thus, when inhaled, mercury vapor has a toxic effect, particularly on
the central nervous system (CNS) and on the developing fetus (Friberg
and Vostal, 1972). After absorption by tissues, the mercury is oxidized
to the mercuric form which is retained in the tissue with a half-life of
several months (Friberg and Vostal, 1972). Continuous low-level exposure,
for example, would therefore lead to an accumulation of mercury in the
body. Although generally lying well below clinical thresholds, the
mercury content of ambient air occasionally approaches critical levels
in highly industrialized metropolitan areas and in areas with rich ore
deposits. From a diagnostic standpoint, it is difficult to identify
mercury as an unequivocal etiological factor in mild disturbances of the
CNS since the signs and symptoms—such as insomnia, shyness, loss of
memory and appetite, and others—may be elicited by many causes.
Inorganic mercury compounds are also ubiquitous in the human
environment, entering the body through food and beverages as well as
through dust in the inhaled air; however, because of their low solubility,
only small amounts reach the bloodstream, penetrating neither the blood-
brain nor the placental barriers (Friberg and Vostal, 1972). Even in the
kidney - the critical organ - concentrations remain so low that clinical
disturbances are not encountered under normal circumstances. Toxic levels,
however, are reached occasionally in those situations where mistakes or
poor industrial hygiene lead to occupational overexposure and where large
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quantities are ingested either by accident or intent. For all practical
purposes, inorganic mercury compounds thus pose a potential hazard to
workers in certain industries but not to the general public directly. This
judgment, of course, does not take into account possible conversion of
inorganic into organic mercurials which may proceed outside the human
body, in the environment, for instance.
Organic mercury compounds vary widely in molecular structure and
their fate in the human body varies accordingly (Friberg and Vostal, 1972).
The short-chain alkyl derivatives - especially methylmercury - are most
important. Their elimination from the body is slow, and the bond between
the mercury and carbon atoms is stable and withstands virtually all attacks
by tissue metabolism. From an environmental point of view, the problem
of organic mercurials thus reduces itself essentially to that of methyl-
mercury especially with its widespread presence in human food. Being
readily absorbed in the digestive tract, methylmercury enters the blood-
stream and penetrates both the blood-brain and placental barriers,
endangering the CNS as well as the developing fetus. The toxic potent.ial
receives further enhancement through a long retention time allowing the
accumulation of high tissue concentrations. Generally, the biological
half-life of methylmercury in the human body is 65 to 70 days; however,
evidence indicates the retention times of brain and cerebellum considerably
exceed the mean values of other tissues and organs (Friberg and Vostal,
1972). Moreover, injuries to the CNS are virtually irreparable, leading
to permanent motor, sensory, and mental deficiencies.
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The outbreak of mercury poisoning in Minamata, Japan is the classic
example of environmental contamination with mercury and, in fact, mercury
poisoning is often called "Minamata Disease." Several hundred persons
were poisoned by eating fish and shellfish which contained large amounts
of methylmercury as a result of chemical discharge from an industrial
operation along Minamata Bay. Clinical signs became evident when the
mercury concentration in the brains of those persons reached 1 ug/g and
death ensued beyong 5 ug/g (McAlpine and Shukuro, 1958; Friberg and
Vostal, 1972).
Briefly summarized, the problem of mercury in the environment is
mainly a question of mercury vapor in ambient air and the content of
methylmercury in food; exposure to either can result in CNS damage.
Reliable dose-response curves are essential if "safe" exposure
levels for mercurials are to be established. Unfortunately, the number
of variables involved, including differences in individual susceptibility,
and technical problems in determining actual mercury levels prior to 1970
make this very difficult.
6.2 ANIMAL MODELS
Most controlled studies on the biological effects of mercury or any
other biologically active agent must use animal models in place of humans.
Although the applicability to humans of information gained from animal
studies can be questioned due to species differences, dose response, and
a number of other factors, the information is probably as useful as the
uncontrolled, unquantitated data derived from epidemiological studies of
human exposures. In fact, the uptake and absorption of mercury and its
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various compounds in humans follow essentially the same patterns as those
determined experimentally in animals. Proper selection of animal models
to most closely parallel the particular human system or function being
studied can minimize the objections. Obviously, some of the more subtle
behavioral changes found in humans following chronic mercury exposure
cannot be examined directly in animals.
In the following section, 'the preponderance of data reported relates
effects of mercury exposure in experimental animals; where available, the
human data have been emphasized.
6.3 METABOLISM
6.3.1 Uptake and Absorption
6.3.1.1 Organic Mercury—Organic mercury compounds are divided into two
general classes: the arylmercurials such as the phenyl and methoxymethyl
compounds and the alkylmercurials such as methyl and ethylmercury.
Arylmercury compounds are metabolized to inorganic mercuric ion-forms in
the animal body and are then distributed and excreted as discussed in
section 6.3.1.2 on inorganic mercurials (Friberg and Vostal, 1972). T.he
alkylmercurials are quite stable because of the strong carbon-to-mercury
bonding characteristic, exerting their toxic effects as intact molecules.
The short carbon chains of methyl or ethyl mercurials permits passage
across biological membranes, a property that explains their ability to
affect the central nervous system (CNS) and to cross the placental barrier
in mammals.
6.3.1.1.1 Inhalation—Inhalation is not a major-route of uptake of
alkylmercury compounds although several (for example, methyl mercury
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iodide, chloride, and dicyandiamide) are relatively volatile at room
temperature. Poisoning via inhalation has been reported in mice, rats,
and monkeys (Friberg and Vostal, 1972). Mice under light anesthesia
were exposed to single inhalation of dimethylmercury (Ostlund, 1969a,
1969b); about 50 to 80 percent of the inhaled compound was transferred
to the mouse within 45 second after exposure. The concentration of
inhaled dimethylmercury was not given but the amount retained in the
mouse was 5 to 9 mg Hg/kg body weight. Most of the dimethylmercury was
subsequently exhaled as dimethylmercury but a small amount was metabolized
to methylmercury and distributed as such. No experimental data are
available on the respiratory uptake of ethyl or longer carbon chain mercury
compounds although vapors of ethylmercury salts have caused poisoning
(Friberg and Vostal, 1972).
Poisoning has been reported following inhalation of the arylmercury
compound phenylmercury acetate (Friberg and Vostal, 1972). Mice exposed
to phenylmercury acetate dust particles of 0.6 to 1.2 microns in size
died after about one hour while those inhaling particles with a size ,.
range of 2 to 40 microns were apparently still healthy 30 hours after
exposure. Almost no information is available on respiratory uptake of
alkoxyalkylmercury compounds, although mice have died following inhalation
of methoxyethyl mercury silicate dust (Friberg and Vostal, 1972). There
are no experimental data available on uptake and absorption of inhaled
organic mercury compounds in humans; however, poisonings have occurred
following accidental inhalation of several alkylmercury compounds (Friberg
and Vostal, 1972).
Respiratory uptake of organic mercurials has not been a major
concern and little experimental work has been done.
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6.3.1.1.2 Ingestion--Ingestion is a much more probable route of uptake '<
and absorption of organic mercurials than inhalation and was the route
responsible for the classic outbreak of mercury poisoning in Minamata,
Japan. Experimental studies in both animals and humans have shown that
methylmercury is almost completely absorbed from the gastrointestinal
tract (Friberg and Vostal, 1972). Clarkson (1971) found that mice
absorbed almost all of the methylmercury chloride ingested in food.
Similar results were found in cats and monkeys (Friberg and Vostal, 1972),
where more than 90 percent of ingested methylmercury was absorbed.
Gastrointestinal absorption of ethylmercury compounds was comparable to
that of methylmercury as determined in rats (Ulfvarson, 1962) and cats
(Friberg and Vostal, 1972). Although no experimental data are available,
absorption of ethylmercury in humans is probably also similar to that of
methylmercury.
Gastrointestinal absorption of aryl and alkoxyalkylmercury compounds
has not been examined in humans, but rats absorbed 50 to 80 percent of
ingested phehylmercuric acetate (PMA). Mercury was found in the urine of
a person who had ingested PMA as well as in the kidneys of persons treated
orally with substituted alkoxyalkylmercury diuretics (Friberg and Vostal,
1972). In general, PMA is absorbed better than inorganic mercury salts but
not as well as methylmercury compounds.
High concentrations of mercury have been found in the kidneys of
persons treated orally with alkoxyalkylmercury compounds; however, no
experimental data are available on gastrointestinal absorption of these
compounds (Friberg and Vostal, 1972).
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6.3.1.1.3 Skin absorption—Alkylmercury compounds are absorbed through ''
the skin. About 6 percent of the methylmercury dicyandiamide applied in
a water solution to intact skin of guinea pigs was absorbed in 5 hours
(Friberg, 1961; Wahlberg, 1965). Humans treated topically with prep-
arations containing methylmercury thioacetamide developed mercury
poisoning, although inhalation of vapors could not be excluded and
quantitative data were not obtained (Friberg and Vostal, 1972). Aryl-
mercury compounds can also be absorbed through the skin. Following
application of a phenylmercury dinaphthylmethane disulphonate solution
in buffered water to the skin of rabbits, mercury was found in the skin,
subdermal connective tissue, and muscles (Friberg and Vostal, 1972).
Twenty-five percent of the PMA applied intravaginally to rats was present
in the liver and kidneys 24 hours after application (Friberg and Vostal,
1972).
6.3.1.1.4 Placenta! transfer—Methylmercury salts readily cross the
placental barrier as shown experimentally in mice, rats, cats, and guinea
pigs (Friberg and Vostal, 1972) and as demonstrated following accidental
ingestion in humans (McAlpine and Shukuro, 1953). Following injection
of ethylmercury phosphate into pregnant mice, higher levels of mercury
were found in the fetuses' brains than in the mothers' brains (Ukita et
al., 1967). Only low levels of mercury were found in fetuses after
inhalation or intravenous exposure of pregnant mice to dimethylmercury.
Severe or fatal poisoning of the fetus can occur even when the mother is
affected little or not at all by the amount of mercury (Friberg and Vostal,
1972).
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6.3.1.2 Inorganic Mercury—The inorganic mercurials include elemental
mercury of any of the variety of ionic compounds such as mercuric or
mercurous chloride.
6.3.1.2.1 Inhalation—Because mercury is volatile at room temperature,
the main route of absorption of elemental mercury is via the respiratory
system. The vapor diffuses rapidly across the alveolar membranes and,
according to several reports, almost all the inhaled mercury vapor is
absorbed (Friberg and Vostal, 1972). In fact, about 80 percent of
inhaled mercury vapor enters the bloodstream (Teisinger and Fiserova-
Bergerova, 1965; Nielson Kudsk, 1965). The rapid diffusion of elemental
mercury vapor across membranes is due to the lipid solubility of the
uncharged mercury molecule (Friberg and Vostal, 1972). The ease with
which mercury vapor crosses the alveolar membrane was demonstrated by
Magos (1967) when 20 percent of the mercury vapor he injected intra-
venously into rats was exhaled in 30 seconds.
Dusts or aerosols of inorganic mercury salts are absorbed from
the respiratory tract depending on particle size and solubility (Friberg
and Vostal, 1972). Relatively large mercury-containing particles
deposited in the upper respiratory tract should be cleared by sneezing,
coughing, and ciliary movement in the trachea and large bronchi. With
decreasing particle size, however, the material penetrates deeper into
the lungs where soluble salts may enter the bloodstream in significant
amounts. The water solubility of a mercury compound is also important.
For example, 45 percent of a highly insoluble mercuric oxide aerosol with
a mean particle diameter of 0.16 urn was cleared from the lungs of dogs
in 24 hours, while the remainder cleared slowly with a half-life of
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33 ^ 5 days (Friberg and Vostal, 1972). In general, inorganic mercury
compounds are absorbed via the respiratory tract to a lesser extent than
mercury vapor. When rats and mice were exposed to equivalent mercury
concentrations as mercury vapor or aerosol mercurous chloride, less mercury
was retained in all tissues of the aerosol-exposed group (Viola and
Cassano, 1968), with the greatest difference being found in the brain and
heart.
6.3.1.2.2 Ingestion--Almost no elemental mercury is absorbed from the
gastrointestinal tract. Bornmann et al. (1970) measured the mercury content
in the blood and organs of rats following ingestion of elemental mercury
and found that less than 0.01 percent had been absorbed. This result would
have been expected based on earlier experience: metallic mercury had been
used for centuries to treat bowel obstructions in humans with no reported
poisonings. Also, more recently, mercury has been released accidentally
into the gastrointestinal tract during medical procedures with no result-
ing mercury poisoning (Friberg and Vostal, 1972).
Absorption of various inorganic mercury compounds from the gastro-
intestinal tract depends on their solubility in water or gastrointestinal
fluids at various pH values. About 20 percent of the relatively soluble
mercuric acetate was absorbed following oral administration to rats at
doses varying from 0.5 mg Hg/kg to 4 mg Hg/kg (Friberg and Vostal, 1972).
Clarkson (1971) reported that less than 2 percent of ingested mercuric
chloride was absorbed from the gastrointestinal tract of mice following
doses of 0.5 to 5 ppm of the dry food. Mercurous chloride is much less
soluble in water than mercuric chloride and has been used (as calomel)
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in the treatment of syphilis and as a diuretic in man without serious
mercury poisoning; however, excessive long-term use has resulted in
symptoms of mercury poisoning in man (Friberg and Vostal, 1972). At
equivalent doses of mercury, mercuric chloride can be fatal, while
mercurous chloride is not. Also, autoradiographic studies in mice have
shown that mercurous mercury was poorly absorbed (Viola and Cassano, 1968).
6.3.1.2.3 Skin absorption—Without doubt, elemental mercury can be
absorbed through the skin, although no quantitative data on rates of
penetration are available. Absorption through the skin has been shown
experimentally in rats, rabbits, and dogs (Friberg and Vostal, 1972) when
precautions were taken to prevent inhalation of mercury vapors. Metallic
mercury has been used in the past in ointments for treatment of syphilis
and skin diseases in humans. Mercury poisoning resulted from this use,
although inhalation of vapor was certainly a contributing factor.
Soluble mercury compounds have also been used topically for treatment
of skin disorders, such as psoriasis and seborrheic dermatitis, as well
as for treatment of venereal diseases. Mercury poisoning has been reported
following such treatment.
The ointment base has an effect on mercury absorption. With an
ointment base of 50 percent lard and 50 percent lanolin, the average
kidney concentration in rats was 8.8 yg/g for mercurous chloride, 19 yg/g
for ammoniated mercury, 14 yg/g for metallic mercury, and 23 yg/g for
yellow oxide mercury. Absorption was lower with an ointment base of 50
percent petrolatum and 50 percent lanolin (Friberg and Vostal, 1972).
Friberg et al. (1961) showed that mercuric chloride was absorbed to a
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maximum of 6 percent in guinea pigs in 5 hours at a mercury concentration
of 16 mg/ml. Electron dense granules were found with the electron
microscope, both intracellularly and extracellularly following application
of mercuric mercury to human skin (Frithz and Lagerholm, 1968; Silberberg
et al., 1969). Autoradiographic study showed that penetration of human
skin took about 8 hours (Friberg and Vostal, 1972).
6.3.1.2.4 Placenta! transfer—Transfer of elemental mercury across the
placenta has not been shown experimentally, but mercury was detected in
stillborn babies of mothers treated with mercury inunctions against
spyhilis. Since elemental mercury vapor is lipid soluble and crosses
membranes easily, placental transfer should be possible.
The placental membrane is an effective barrier against the penetra-
tion of mercuric ions into the fetus. Following intravenous injection of
0.5 mg/kg mercuric chloride into mice, a significant accumulation of
mercury was found in the placenta but a much lower accumulation was found
in the fetus (Friberg and Vostal, 1972). Suzuki et al. (1967) found the
ratio of mercury in maternal blood: placenta: fetus to be 1:19:0.4
after administration of mercuric chloride to mice. No data are available
in humans.
6.3.2 Transport and Distribution
Regardless of the route of uptake and absorption of mercury, it is
ultimately transported and distributed to various organs via the circulatory
system. This distribution depends to a large degree on the physical -
chemical properties of the mercury absorbed (see Section 2.0). In this
process, two factors are particularly important: firstly, for the
majority of substances, tissue infiltration is not homogeneous because
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certain organs have a strong affinity for particular chemicals, allowing
highly preferential accumulations leading to specific toxic reactions;
often these critical organs determine not only the clinical picture but
also the permissible body burden. Secondly, between blood capillaries
and tissue cells significant barriers exist in the brain as well as in
the placenta. Only those substances which are able to overcome these
barriers may provoke disturbances of the CNS or the developing fetus.
Ionic forms of mercury are responsible for the biological effects because
elemental mercury (Hg°) cannot form chemical bonds. The partition between
plasma proteins and red blood cells (RBC) in the blood is a function of
the ionic form of the mercury and interconversions can take place in the
blood.
6.3.2.1 Organic Mercury
6.3.2.1.1 Distribution and metabolism in blood—Organic mercury compounds
differ widely in behavior during blood transport. Short-chain alkyl
derivatives - particularly methyl mercury - are quite stable in the body
and preferentially accumulate within red cells (Friberg and Vostal, 1972).
In humans the ratio of mercury in cells to that in plasma is ten to one.
In mice 75 to 90 percent, depending on dose, binds to blood cells; rats
95 percent; rabbits and monkeys 90 percent; cats more than 95 percent; and
pigs 80 percent (Friberg and Vostal, 1972). There is apparently little
difference in toxicity or metabolism among the various chemical salts of
methylmercury.
Following exposure of mice to dimethylmercury via inhalation or
intravenous injection, the mercury was transported to fat deposits and
156
-------
blood levels were low (Friberg and Vostal, 1972).
The carbon-mercury bond of monomethylmercury is quite stable as
indicated by the slow, even elimination of mercury following administra-
tion to mice (Ostlund, 1969) and monkeys (Nordberg et al., 1969, 1971)
as well as the rather constant mercury distribution in organs with time
after a single administration to mice and rats (Friberg and Vostal, 1972).
Other studies using rats showed that 90 percent or more of the mercury
found in hair, spleen, and blood cells 6 weeks after injection with
methylmercury dicyandiamide was in an organic form (Friberg and Vostal,
1972). Some breakdown of methylmercury to inorganic mercury does occur
and was demonstrated by Norseth and Clarkson (1970) in rat liver. Some
breakdown also occurs in intestinal lumen and in the kidney. Most mercury
in the brain is methylmercury (Friberg and Vostal, 1972).
Mice intravenously injected with dimethylmercury rapidly exhaled
80 to 90 percent as dimethylmercury, but some was retained and within
20 minutes was found in the liver, the bronchi, and nasal mucosa. The
la.ter distribution pattern resembles that of monomethylmercury (Friberg
and Vostal, 1972).
Ethylmercury is similar to methylmercury because both bind to blood
cells and distribute in a like manner; however, ethylmercury is less
stable in the body than methylmercury and is more easily altered to an
inorganic form (Friberg and Vostal, 1972).
Most data on the metabolism of arylmercurials were obtained using
phenylmercury compounds. Shortly after administration of phenylmercury
compounds to various animals blood distribution resembles that of the
157
-------
alkylmercury compounds; with time, however, distribution becomes similar
to that found after administration of inorganic mercury salts (Ulfvarson,
1962). The carbon-mercury bond in phenylmercurials is less stable than
that in methylmercury and there is a relatively rapid breakdown to
inorganic mercury.
Methoxyethylmercury, the only alkoxyalkylmercury compound for which
there is any experimental data, is distributed in the blood like
phenylmercury, although the initial level in the blood cells is lower
than after phenylmercury administration. One day after the administration
of methoxyethylmercury chloride to rats, all the mercury in the kidney
was in an inorganic form (Friberg and Vostal, 1972). At present,
observations on blood effects in humans are too scanty to permit a more
detailed analysis.
6.3.2.1.2 Tissue distribution--The distribution pattern of monomethyl
and ethylmercury is relatively unaffected by dose level, time after a
single exposure, or exposure time. High mercury levels are found in the
liver, kidney, spleen, pancreas, and blood cells (Friberg and Vostal,
1972). The short carbon chain of these molecules permits them to cross
.biological membranes and thus reach the brain and fetus. Figure 6.1
summarizes data drawn from many sources on the total mercury body burden
in equilibrium from continuous daily ingestion of methylmercury.
Although the mercury level in the brain from methylmercury is low
compared to the level in liver or kidney, it is high compared to mercury
brain levels found after administration of inorganic mercury salts
(Friberg and Vostal, 1972). Radioactive tracer studies in humans
revealed that approximately 10 percent of incorporated methylmercury was
158
-------
ORNL-DWG 74-10376
Ul
ID
. en
E
cr
O
UJ
LU
O
cr
ID
CD
Q
O
CD
O
50
30
20
0
CLINICAL THRESHOLD
OIL
0 0.1 0.2 0.3 . 0.4 0.5 0.6 0.7 0.8
CONTINUOUS DAILY INGESTION OF METHYLMERCURY (mg)
Figure 6.1 CORRELATION OF BODV BURDEfl OF MERCURY '/'ITH '-'ETHYLMERCURY INTAKE
-------
located fn the human head, the major portion presumably residing in the
brain (Friberg and Vostal, 1972). In mice and rats the mercury level
in the brain reached a maximum several days later than in the other
organs. The blood-brain barrier evidently slows penetration but does
not prevent it. Figure 6.2 plots from many sources data on the mean
brain mercury concentration against continuous daily ingestion of
methylmercury.
Almost all the mercury in the rat brain was found in the protein
fraction, while in rat liver cells most was found in the microsomes'
(Friberg and Vostal, 1972).
The ratio of mercury levels in whole blood to brain differs widely
between species varying from 10-20 to 1 in rats to 0.1-0.2 to 1 in
monkeys and man. The ratios between mercury levels in plasma to brain
are more consistent reflecting species differences in ratios of blood
cells to plasma. As mentioned previously, methylmercury crosses the
placental barrier and in the mouse fetus the distribution is relatively
even and similar to that in the mother (Berlin and Ullberg, 1963b). ..
Initially dimethylmercury is distributed differently in mice than
monomethylmercury (Ostlund, 1969a, 1969b). Most goes to fat deposits
and only low concentrations are found in the CNS and blood. Somewhat
higher concentrations are found in the liver and kidneys. Dimethyl-
mercury is rapidly exhaled and the small amount retained in the body
is converted to monomethylmercury and is distributed as such. Overall,
however, distribution of ethylmercury is comparable to that of methyl-
mercury.
160
-------
cr>
3.0
en
2 2.0
H
cc
1-
I 1.5
o
o:
CD
UJ
0.5
0
ORNL DWG 74-10378
CLINICAL THRESHOLD
o
_i
o
X
UJ
o:
x
h-
U
0 0.1 0.2 0.3 0.4 • 0.5 O.6 0.7
CONTINUOUSi DAILY INGESTION OF METHYLMERCURY (mg)
Figure 6.2 CORRELATION OF BRAIN MERCURY CONTENT WITH METHYLMERCURY INTAKE
-------
The distribution pattern following administration of phenylmercury
compounds is complex because disposition is dose-dependent and changes
as the phenylmercury is transformed into organic mercury. Initially
the distribution in mice and rats is similar to the pattern seen after
administration of short-chain alkylmercury compounds but with time
resembles that of inorganic mercury salts (Friberg and Vostal, 1972).
The highest mercury level is in the kidneys, followed by liver; brain
levels are low. No information is available on distribution in humans.
Following administration of methoxyethylmercury compounds the
distribution pattern is similar to that for phenylmercury except there
is less change with time and the initial level in the liver is lower
(Friberg and Vostal, 1972). Table 6.1 shows organ mercury levels
following administration of methylmercury to various mammals.
6.3.2.2 Inorganic Mercury
6.3.2.2.1 Distribution and metabolism in blood — Inorganic mercury
exists in three forms: elemental (Hg°), mercurous (Hg2 ), and mercuric
(Hg ). In the body elemental mercury is rapidly oxidized through the
mercurous stage to the mercuric ion form (2Hg ->Hgp ->-2Hg ). Clarkson
et al. (1961) concluded that since elemental mercury was converted to
mercuric ions, no difference should exist in distribution or toxicity
between inhaled mercury vapor and absorbed mercuric salts. However,
experiments in mice, rats, rabbits, monkeys, and guinea pigs (Friberg
and Vostal, 1972) showed a greater uptake of mercury by the brain, blood
cells, and myocardium after exposure to mercury vapor than after ex-
posure to mercuric salts. Magos (1967) extrapolated from his data
162
-------
PAGE NOT
AVAILABLE
DIGITALLY
-------
that most of the mercury in the blood is in the elemental form during
the first 30 seconds following exposure to mercury vapor, thus giving
time for this diffusible form to be carried to the brain and other
tissues. Elemental mercury is eventually converted to mercuric ions,
probably by enzymatic processes; and once in the ionic form the mercury
is about equally distributed in blood cells and plasma (Friberg and
Vostal, 1972).
Mercury from various inorganic mercury compounds is also distributed
about equally in blood cells and plasma (Ulfvarson, 1962), although
penetration of mercuric mercury into RBC required 2 hours in rabbits and
4 days after subcutaneous injection in rats (Friberg and Vostal, 1972).
The route of administration in rabbits was not given. Almost all the
mercuric mercury in the plasma is bound to proteins.
6.3.2.2.2 Tissue distribution—Except for the brain, blood, and myocardium,
the distribution pattern of mercury following exposure to mercury vapor
is the same as that following exposure to mercuric mercury. In comparison
with inorganic compounds, exposure to corresponding amounts of the
elemental metal causes a ten-times higher mercury concentration in the
brain (Friberg and Vostal, 1972). Unfortunately, the distribution pattern
of mercury following administration of inorganic mercury compounds is
complicated because the pattern changes with time, mode of administration,
dose, and species. One constant factor, however, is that the highest
mercury levels are found in the kidney with lesser concentrations in the
liver, spleen, and thyroid (Berlin and Ullberg, 1963a).
164
-------
PAGE NOT
AVAILABLE
DIGITALLY
-------
Little data are available on the distribution of mercuric mercury
1n humans; the principal distribution pattern is probably similar to
that determined in animal studies. High mercury levels are found in the
blood immediately after administration to mice or rats but the level drops
faster than in other tissues. .Although little mercury enters the brain, it is
very slowly eliminated. Cassano et al. (1966) studied the distribution
of mercury in the CNS following exposure to elemental mercury and found
a higher concentration in grey matter than in white. The highest levels
were found in certain neurons of the cerebellum, spinal cord, medulla,
pons, and midbrain. Mercury distribution in the kidney also varies.
Rabbits injected subcutaneously with mercuric chloride at 2 mg Hg/kg
accumulated most mercury in the distal parts of the proximal tubules and
some in the wide part of Henle's loop and in the collecting ducts (Friberg
and Vostal, 1972). Metallothionine binds the largest part of the mercury
in the kidney. Chronic dosing of rats with mercuric chloride induces
the synthesis of metallothionine, indicating that this response may be a
protective reaction (Clarkson, 1972).
No experimental data are available on the distribution of mercurous
mercury, but it probably is oxidized to mercuric mercury and distributed
as such. Table 6.2 shows distribution of mercury in organs following
exposure of mammals to mercury vapor.
6.3.3 Elimination and Biological Half-Life
6.3.3.1 Organic Mercury—Elimination of organic mercury compounds depends
to a large extent on the rate of degradation into inorganic mercury.
Methylmercury, being quite stable, has a long half-life. As indicated
165
-------
Table 6.2. DISTRIBUTION OF MERCURY IN ORGANS AFTER EXPOSURE TO ELEMENTAL MERCURY VAPOR IN MAMMALS
en
en
Species
Mouse
Guinea
pig
No. of
animals
6
2
2
4
2
3
3
Exposure
air con-
centration
mg/Hg/m3
and time
(single
exposure
1.v. Hg°
vaporjj
4 hrs°
r>
4 hrsc
h
4 hrsD
4 hrs
7;5 hrs
7;5 hrs
Time to
sacrifice
(single
exp.) Ex-
posure
time
5 min
1 day
1 day
16 days
16 days
1 day
16 days
Ratios betv/een concentrations in organs
Blood/ Blood/ Liver/
brain kidney brain
1.24 0.28
1.31
0.96
0.28
0.14
• 1.33 0.026 1.28
0.10 0.002 1.37
Kidney/
brain
4.5
12.2
10.2
5.4
1.1
38.5
40.9
Kidney/
1 iver
9 '
11
19
8
30
30
Reference
Magos (1968)
Berlin, Jerksell ,
and von Ubisch (1966)
Berl in, Jerksell ,
and von Ubisch (1966)
Berlin, Jerksell ,
and von Ubisch (1966)
Berl in, Jerksell ,
and von Ubisch (1966)
Nordberg and Serenius
(1969)
Nordberg and Serenius
(1969)
-------
Table 6.2. DISTRIBUTION OF MERCURY IN ORGANS AFTER EXPOSURE TO ELEMENTAL MERCURY VAPOR IN MAMMALS (cont'd)
cr>
No. of
Species animals
Rat 3
2
3
2
2
2
2
3
3
4
2
7
2
Exposure
air con-
cencentration
mg Hg/m3
and time
(single
exposure
1.4;5 hrs
1.0 ;4 hrs
1.4;5 hrs
1.0;4 hrs
1
1
0.02-0.03
0.008-0.01
0.002-0.005
0.1
0.1
0.1
0.1
Time to
sacrifice Ratio between concentrations in organs
(single
exp.) Ex-
posure Blood/
time brain
1 day
1 day 0.38
15 days
16 days 0.02
6 v/eeks
4 months
6. 5 months
6.5 months
6.5 months
7-9 v/eeks
3.5 months ,
13-15 months
17 months
Blood/ Liver/
kidney brain
0.0006
0.011 1.03
0.002 0.16
0.09
0.02
2.5
2.8
4.7
;
Kidney/
brain
31.4
13.0
15.5
23.8
5.6
9.8
8.6
Kidney/
liver
33
31
320
78
179
1167
2
3
2
29
75
23
22
Reference
Hayes and Rothstein
(1962)
Berlin, Fazackerly,
and Nordberg (1969)
Hayes and Rothstein
(1962)
Berlin, Fazackerly,
and Nordberg (1969)
Gage (I961a)
Gage (1961a)
Kournossov (1962)
Kournossov (1962)
Kournossov (1962)
Ashe et al . (1953)
Ashe et al. (1953)
Ashe et al . (1953)
Ashe et al . (1953),-
-------
Table 6.2. DISTRIBUTION OF MERCURY IN ORGANS AFTER EXPOSURE TO ELEMENTAL MERCURY.VAPOR IN MAMMALS (cont'd)
CT)
CO
Species
Rabbit
No. of
animals
2
1
4
2
11
4
1
2
4
2
Exposure
air con-
centration
mg Hg/m3
and time
(single
exposure
1;4 hrs
1;4 hrs
6
6
0.9
0.9
0.1
0.1
0.1
0.1
Time to
sacrifice
(single
exp.) Ex-
posure
time
4 days
16 days
6-8 weeks
10-11 weeks
6-8 weeks
10-12 weeks
8 weeks
3.5 months
10.5 months
19 months
Ratios between concentrations in organs
Blood/
brain
0.25
0.15
0.06
0.30
0.12
0.23
0.25
0.27
Blood/
kidney
0.003
0.015
0.006
0.012
0.004
0.015
0.007
0.003
0.04
Liver/
brain
1.8
3.5
0.36
0.50
2.24
3.53
2.23
5.4
2.8
Kidney/
bra i n
83
74
9.7
9.4
25.9
27.6
31.6
30.0
7.1
Kidney/
1 iver
45
21
27
19
12
8
16
14
6
3
Reference
Berlin, Fazackerly,
and Nordberg (1969)
Berlin, Fazackerly,
and Nordberg (1969)
Ashe et al. (1953)
Ashe et al . (1953)
Ashe et al . (1953)
Ashe et al . (1953)
Ashe et al . (1953)
Ashe et al . (1953)
Ashe et al . (1953)
Ashe et al . (1953)
-------
Table 6.2. DISTRIBUTION OF MERCURY IN ORGANS AFTER EXPOSURE TO ELEMENTAL MERCURY VAPOR IN MAMMALS (cont'd)
en
Exposure
air con-
Time to
s
centration sacrifice Ratio between concentrations in organs
mg Hg/m3 (single
Species
Dog
Monkey
Notes:
gSingle
Single
.Single
Brain
Source:
No. of
animal
1
1
2
1
and time
(single
s exposure
0.1
0.1
1;4 hrs
1;4 hrs
exposure corresponding to
exposure corresponding to
exposure corresponding to
weight assumed to be 1.8 g
exp.) Ex-
posure Blood/ Blood/ Liver
time brain kidney brain
14 months 0.026 0.0013 1.86
19 months 0.012 0.0005 7.37
4 days 0.19 0.011 2.0
16 days 0.57 0.010 15.9
0.005 pg Hg/kg.
0.01 mg Hg/kg.
0.5 mg Hg/kg.
, liver weight 12 g, and kidney weight 2.0 g.
Kidney/ Kidney/
brain liver Reference
20.0 11 Ashe et al . (1953)
25.1 3 Ashe et al . (1953)
17 17 Berlin, Fazackerly,
and Mordberg (1969)
58 4 Berlin, Fazackerly,
and Nordberg (1969)
_
Friberg and Vostal (1972).
-------
by human tracer studies, the total body burden of incorporated methyl-
mercury decreases to one-half within 70 to 90 days (Friberg and Vostal,
1972). Half of a single dose given to rats was eliminated in the feces
and urine in 20 days (Friberg and Vostal, 1972). Elimination from the
brain was slower than from other organs. In monkeys, the biological
half-life in blood was 50 to 60 days but whole body measurements indicated
a half-life of. 150 days.
The main routes of excretion of monomethylmercury are feces, urine,
and hair. Fecal elimination is about 10 times greater than urinary
elimination. For individual tissues and organs, the clearance rates of
methylmercury generally parallel that of the total body burden; however,
the CNS apparently is an exception, showing a somewhat slower rate of
release. Since methylmercury is attached largely and firmly to RBC
constituents, urinary excretion accounts for not more than 10 percent of
the elimination; urine contains mercury mostly in an inorganic form.
The major pathway for methylmercury removal is through the gastrointestinal
tract, with excretion by bile probably the most important factor (Friberg
and Vostal, 1972). In mice and rats most of the mercury in the feces
was inorganic while in the urine a large fraction was organic (Friberg
and Vostal, 1972).
Kinetics of retention and excretion of ethyTmercury are similar to
those of methyl mercury, although fecal elimination may be somewhat less.
Elimination of mercury following administration of phenylmercury is
similar to that after inorganic mercury exposure. In rats the rate of
elimination is dose dependent, increasing with increasing dose (Friberg
and Vostal, 1972). In the rat the half-life is 4 to 10 days at repeated
170
-------
administrations of 0.1 nig Hg/kg body weight. The elimination pattern
changes with time, probably because of the conversion of phenylmercury
into inorganic mercury and redistribution of mercury within the body.
Elimination from the kidney is slower than from the rest of the body.
Most of the mercury excreted following administration of phenylmercury
is in the feces. Although the fraction excreted in feces varied in
different experiments, it was at least two-thirds in most cases (Friberg
and Vostal, 1972). Excretion of methoxyethylmercury is similar to phenyl--
mercury.
6.3.3.2 Inorganic Mercury—The half-life of inorganic mercury in humans
is 30 to 60 days. Humans given 6 yg of radioactive inorganic mercury
excreted 85 percent in the feces within the first four or five days.
The half-life of the remaining 15 percent was 42 +_ 3 days for all persons,
37 +_ 3 days for women, and 48 +_ 5 days for men (Friberg and Vostal, 1972).
Excretion occurs mainly through the urine and feces in approximately
equal amounts. Inorganic mercury is removed from the blood by the kidneys;
urinary excretion probably involves passive glomerular filtration as
well as active tubular transport (Friberg and Vostal, 1972). Fecal
excretion probably involves an active transport .across membranes of the
gastrointestinal mucosa. A small amount of the mercury can leave the
body through the lungs and body surface. Since there is a large uptake
of mercury in the kidney with slow excretion, chronic exposure can lead
to accumulation in this organ. A similar situation exists for the brain.
6.4 EFFECTS
6.4.1 Nutritional Role
There is no known nutritional role for mercury in humans or animals.
171
-------
6.4.2 Clinical Studies
6.4.2.1 Toxicology—The biological activity of mercurials rests
primarily on the ability to combine with sulfhydryl groups in proteins,
although they do possess some other reactivities. Potentially, almost
all proteins in the body could form complexes with mercury. How damaging
this is depends on what effect the mercury has on the protein's function,
how essential this function is, and what proportion of this protein is
affected.
Basically, the toxicity of a given mercury compound depends on its
ability to reach a critical target in sufficient concentrations and remain
long enough to react. For example, methylmercury--one of the most toxic
mercurials—is almost completely absorbed from the gastrointestinal
tract, reaches a higher level in the brain than other mercury compounds,
and is eliminated from the body more slowly than other forms of mercury.
On an individual level, an organism's general health and reserve
capacity will help determine the dose level required to produce overt
symptoms of mercury poisoning. Based on the known biochemical activity
of mercury compounds, a dose below which no effects occur probably does
not exist, although a dose below which no effects can be measured or
observed does exist.
6.4.2.1.1 Symptoms--Symptoms of acute mercury poisoning following
ingestion of any of various mercury compounds and acute symptoms following
inhalation are listed in Table 6.3 (D'ltri, 1972). In addition,
corrosion of the alimentary tract, renal tubular necrosis and sometimes
central necrosis of the liver may be found at autopsy. With the primary
exception of respiratory tract involvement, the acute symptoms of mercury
172
-------
MERCURY POISONING
ion
ed mucus
lectrolytes
Eschar of mouth and lips
Gastrointestinal irritation
Severe abdominal pain
Shock
Slow breathing
tion
ns
Abdominal cramps
Cough
Restlessness
Central cervous system signs
Kidney damage
f.-
j -•
4 c
B. -.•--,
-------
Table 6.3. ACUTE SYMPTOMS OF MERCURY POISONING (cont'd)
Salivary gland swelling
Ulcerative colitis
Bad breath
Anuria
Hematuria
Delayed reactions up to two v/eeks
Excessive salivation
Loose teeth
Blue-black line on the gums
Possible symptoms
Uremia
Proteinuria
Metallic taste
Soft spongy gums
Albriminuria
Acidosia
Source:
Based on information from D'ltri (1972)
-------
toxicity are very similar for both routes of exposure.
Symptoms occurring as a result of chronic exposure to mercury
vapor or dusts of mercury salts (see Table 6.4) appear slowly and may
be attributed falsely to other causes.
Pathological changes in the brain are associated with the CNS
symptoms which include cerebral edema, atrophy of the calcarine and
pre- and postcentral cerebral cortex, cerebellar atrophy, and punctate
hemorrhages. A diffuse cellular degeneration with gliosis occurs.
Similar histological changes have been observed in swine, cats, crows,
sea birds, and fish that died of mercury poisoning and also in experi-
mental animals.
The areas of mercury concentration in the brain of mice exposed
to mercuric chloride correlated well with the areas of pathological
lesion development.
Although the complete range of symptoms can be produced by either
organic or inorganic mercury, organic mercury—especially methylmercury--
is usually associated with CNS damage with some time passing before
symptoms appear, even after an acute exposure.
6.4.2.1.2 Acute toxicity--LD5Q values for various arylalkyl and in-
organic mercury compounds as compiled by Lu et al. (1972, Chapter 6)
are listed in Tables 6.5, 6.6, and 6.7.
6.4.2.1.3 Genetic, teratogenic, and carcinogenic effects — In addition
to the toxic effects, most mercurials also have genetic activity,
affecting mitosis, meiosis, and nucleic acids directly.
Mercury compounds are very efficient c-mitotic agents. C-mitosis
(from colchicine-mitosis) is a disruption of the spindle fiber mechanism
175
-------
Table 6.4. CHRONIC SYMPTOMS OF MERCURY POISONING
Central Nervous
System
Headache
Vertigo
Ataxia
Vasomotor
disturbance
Peripheral neuritis
Muscular tremor
Pain
Numbness in the
extremities
Gastrointestinal
Increased salivation
Stomatitis
Gingivitis
Loss of appetite
and weight
Nausea
Diarrhea
Vomiting
Swollen salivary
glands
Soft spongy gums
Bad breath
Metallic taste
Liver damage
(sometimes)
Genitourinary
Proteinuria
Hematuria
Anuria, and nephritis
with renal damage and
finally renal failure
with anuria
Respiratory
Inflammation of
nose
Loss of smell
Cough
Fever
Skin
Erythemateous
papulor
Vesicular
lesions
Urticaria progressing
to weeping
dermatitus
Eye
Constriction of visual
field and
mercurialentis
Muscular
General muscular
weakness and
fatigue
Erethism
Irritability
Restlessness
Resentment of
criticism
Insomnia
Others
Loss of self confidence,
concentration, memory,
drive, energy, and
interest.
Melancholia
Hallucinations
Mental depression
Excessive perspiration
Source:
Based on information from D'ltri (1972).
176
-------
Table 6.5. ACUTE TOXICITY OF ARYLMERCURY COMPOUNDS
Compound
Phenylmercuric
acetate
Phenylmercuric
acetate
Phenylmercuric
acetate
Phenylmercuric
acetate
Phenylmercuric
acetate
Phenylmercuric
acetate
Phenylmercuric
acetate
Species
Mouse
Rat
Mouse
Rat
Chicken
Rat
Mouse
Route
oral
oral
oral
oral
oral
i.p.
1 .V.
LD50
(mg/kg body-weight)
13
60
70
46
ca 60
ca 10
27
Reference
Piechocka and Krauze (
Piechocka and Krauze (
Goldberg et al . (1950)
Ikeda (1968a)
Miller et al . (1960)
Swensson (1952)
Wein (1939)
1967)
, t
1967J
'j
'|
f
Source: -
Lu (1972, Chapter 6).
-------
Table 6.6. ACUTE TOXICITY OF ALKYLMERCURY COMPOUNDS
CD
Compound
Methylmercuric
chloride
Methylmercuric
chloride
Methylmercuric
dicyandi amide
Ethylmercuric
chloride
Ethylmercuric
chloride
n-Propylmercuric
chloride
n-Bu thy! mercuric
chloride
Species
Mouse
Rat
Rat
Mouse
Rat
Mouse
Mouse
Route
i.p.
oral
oral
i.p.
oral
i.p.
i.p.
LD50
(mg/kg body-weight)
47
58
26
28
50
18
15
Reference
Nose (1969)
Ikeda (1968a)
Swensson and Ulfvarson (1963)
Nose (1969)
Ikeda (1968a)
Nose (1969)
Nose (1969)
Source:
Lu (1972, Chapter 6).
-------
Table 6.7. ACUTE TOXICITY OF INORGANIC MERCURY SALTS
Compound
Mercurous iodide
Mercurous iodide
Mercuric acetate
Mercuric iodide
Mercuric iodide
Mercuric chloride
Mercuric chloride
Species
Mouse
Rat
Rat
Mouse
Rat
Rat
Mouse
Route
oral
oral
oral
oral
oral
s.c.
s.c.
LD50
(mg/kg body-weight)
110
>310
104
80
40
3
6
Reference
Gothe and Sundell
Gothe and Sundell
Ikeda (1968a)
Gothe and Sundell
Gothe and Sundell
Clarkson (1968)
Clarkson (1968)
(1964)
(1964)
(1964)
(1964)
Source:
Lu (1972, Chapter 6).
-------
during cell division that results in polyploidy or other abnormal
chromosome numbers-in cells. Colchicine is the classic inducer of this
process and with increasing dose the spindle fiber mechanism is completely
blocked. Organic mercury compounds produce a gradual transition between
normal and c-mitosis (Ramel, 1969). Total blockage, which affects the
entire set of chromosomes, is almost always lethal at an early stage;
the incomplete c-mitosis produced by mercurials is more dangerous
genetically because chances for survival are greater. Phenylmercury and
methylmercury have induced c-mitosis in (onion) Alii urn cepa roots at a
dose equivalent to 0.05 ppm mercury (Ramel, 1967). Methoxyethylmercury
was less active, with 0.6 ppm mercury required for the same effect.
Phenyl- and methylmercury are 200 times more effective as c-mitotic
agents than inorganic mercurials and 1000 times more effective than
colchicine (D'ltri, 1972). The differences are not a result of different
cellular uptake. C-mitosis was demonstrated in human leucocytes in
culture after treatment with methylmercury chloride at a concentration
of 1 to 2.0 x 10" M. Mercurials probably produce c-mitosis by reacting
with sulfhydryl groups in the proteins involved in spindle fiber formation
(D'ltri, 1972).
Organic mercury compounds can directly affect the genetic material
and cause chromosome breakage independent of c-mitosis (Ramel, 1969). When
populations having high and low fis'h consumptions were compared, the former
displayed a higher number of chromosome breaks in leukocyte cultures
(Skerving et al., 1970). The increase in breakage seemed to correlate
with the mercury level in blood and thus with body burden; hov/ever, the
180
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findings are still suggestive rather than definitive. Meiosis is also
affected by mercurials as shown by the increased number of exceptional
daughter offspring (xxy) in Drosophila melanogaster after treating larvae
with 0.25 rng methyl mercury/1 and adults with 5 nig methylmercury/1 (Ramel,
1967; Ramel and Magnusson, 1969). Evidently the x chromosomes were
preferentially distributed to the pole from which the egg cell arose, a
process called-"meiotic drive."
Methylmercury has a minor mutagenic effect (Ramel, 1969). Possibly
the effect is so small because little mercury reaches the DNA, most
reacting with the various proteins in the cell. Mutations have been studied
in mammals using dominant lethals. Pregnant CBA mice given a single dose
of an organic mercurial on day 10 of gestation had a high frequency of
resorbed litters and an increased percentage of dead fetuses (Ramel,
1967).
Teratogenic effects have occurred in mice treated with phenylmercury
acetate (WHO, 1972); a 31.6 percent incidence of cleft palate was found
in rats born after their mothers were given single high-level dose of
methylmercury phosphate on day 10 of gestation (Oharazawa, 1968).
In rats, sarcomas have developed in areas in direct contact with
metallic mercury injected intraperitoneally (Druckery et al., 1957).
Mercury could be seen in all tumors. No metastases occurred.
Since effects on the genetic material of cells occur at mercury
levels below those which produce any observable toxic effects, a long-term
genetic effect may be occurring in animal populations and in man.
181
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6.4.2.1.4 Alteration of mercury toxicity--Ganther et al. (1972) reported
dietary amounts of selenium obtained from tuna fish had a protective
effect against the toxicity of dimethylmercury in Japanese quail.
Experiments carried out subsequently (Ganther et al., 1973) show selenium
is definitely associated with a reduction in toxicity of methylmercury.
Ten ppm methylmercury hydroxide was added to the drinking water of two
groups of weanling rats; one group also received 0.5 ppm selenium as
sodium selenite in the diet. At six weeks only those animals receiving
selenite were still alive. Administration of 25 ppm mercury in the
drinking water, however, caused 100 percent mortality by six weeks, but
those animals receiving selenium showed markedly improved growth and
prolonged survival at four weeks.
Parizek et al. (1974) notes an especially complex character to the
selenium-mercury interaction. Although an essential element, selenium
at high concentrations is by itself a toxic material. In contrast to
the observed improved survival of rats receiving selenite a few hours
after administration of mercuric salts, administration of these two .•
compounds in reverse order results in a high mortality, especially of
adult male rats. Mercuric salts appear to intensify the toxic effects
of dimethylselenide by several orders of magnitude, with greatest
sensitivity in adult male and lactating female rats (Parizek et al.,
1971). Dimethylselenide is normally excreted in respiration. Additionally,
small amounts of mercury can decrease the biological availability of
selenium without actually removing this essential nutrient from the
organism.
182
-------
Although the preventive mechanism for selenium protection against
mercury toxicity is not at all clear, it does not involve an effect on
mercury absorption or excretion. In fact, mercury retention in the
organism is increased but organ distribution and reactivity is changed
(Parizek et al., 1971).
Ethyl alcohol has been shown to affect absorption of mercury in
inspired air in humans. Retention of mercury fell from 75 to 85 percent
to 50 to 60 percent in persons who had consumed moderate amounts of
ethyl alcohol (Friberg and Vostal, 1972).
6.4.3 Normal Mercury Levels in the Human Body
Because of long retention times - or slow clearance rates from the
human body - and because of the ubiquity, both inorganic mercury and
methyl mercury present a potential environmental hazard not only to
professionally exposed persons but also to the public in general. Through
air, food, and beverages, every individual each day takes up certain
amounts of mercury which maintain more or less an equilibrium with body
burden and excretion. Ideally, the accumulated concentrations in critical
organs - CNS, kidneys, and liver - are the best indicators of the serious-
ness of the problem. From a practical standpoint, however, these
critical organs remain inaccessible to routine analysis. Biopsy, for
example, entails sufficiently high risk to justify the procedure only in
exceptional clinical situations. Therefore, the body burden must be
assessed indirectly by determining the mercury content of easily obtainable
biological specimens - particularly blood, urine, and hair.
6.4.3.1 Blood Levels—Thus far, human populations have not been sub-
jected to large-scale epidemiological studies employing modern analytical
183
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and statistical methods. As a result, the "normal" blood level of
mercury remains somewhat elusive. Furthermore - even within a given
population - the level varies throughout a broad range, showing no
clear-cut relationship to either age, sex, or body weight. The mercury
content obviously is not regulated by a biological control mechanism as
are the levels of iron and copper, for example. Table 6.8 lists "normal"
mercury levels in whole blood in samples from.various countries.
Collectively, elevated blood values among a population tend to indicate
overexposure and increased body burden; blood levels hence possess a
certain epidemiological significance. In individual cases, however, the
blood concentration allows no reliable conclusions about the amount of
incorporated inorganic compounds. Because there is an equilibrium be-
tween tissue concentrations and blood levels of mercury following
exposure to methyl mercury, blood levels can mirror the total body burden.
When repeated blood measurements show a rising or highly elevated mercury
level, with a plasma to cell ratio approximating one to ten, the person
is likely to be continuously overexposed to methyl mercury. Figure 6.3.-
illustrates the mercury blood concentration resulting from continuous
daily ingestion of methylmercury.
Certain amounts of methylmercury are contained in normal human food
sources, particularly in fish; populations with large fish consumption
have mercury concentrations in the blood which are significantly higher
than those of populations rarely eating fish (Friberg and Vostal, 1972).
In the former case, the plasma-to-cell ratios lie around one-to-three or
one-to-four, presumably indicating a mixed uptake of inorganic and organic
184
-------
Table 6.8. "NORMAL" MERCURY LEVELS (ATOMIC ABSORPTION SPECTROMETRY)
IN WHOLE BLOOD IN SAMPLES FROM DIFFERENT COUNTRIES
Country
Argentina
Chile
Czechoslovakia
Finland
Israel
Italy
Japan
Netherlands
Peru
Poland
Sweden
Yugoslavia
U.A.R. (Egypt)
U.K.
U.S.
California
New York
Ohio
Total
Total
number
of
samples
49
35
20
46
67
27
40
60
58
95
30
67
28
30
160
33
87
40
812
Percent
of samples
< 5 ng Kg/ml
80
69
60
70
90
78
80
93
29
72
90
72
93
93
82
79
83
85
77
Highest
level
ng Hg/ml
30
30
21
75
39
30
30
21
200
370
90
270 •'
10
75
240
51
45
240
370
Source:
Friberg and Vostal (1972).
185
-------
oo
en
^ 50
o
o
40
o
cr
h-
30
o 20
-z.
o
o
o
3
CD
0
ORNL-DWG 74-10375
CLINICAL THRESHOLD
_
< o
O X
^ 00
^ LU
—I QC
O X
I-
0
0.1 0.2 0.3 0.4 0.5 0.6 0.7 ' 0.8
CONTINUOUS DAILY INGESTICN OF METHYLMERCURY (mg)
Figure 6.3 BLOOD MERCURY COMCENTRATIO:; VS METHYLMERCURY INTAKE
-------
mercury compounds. Metabolic degradation of long-chain alkyl as well as
aryl derivatives complicate the blood level pattern making conclusions
from blood levels misleading at best.
6.4.3.2 Urine Levels--Depending on fluid intake, type of food, and many
other factors, the mercury content of urine displays such wide individual
variation that any meaningful definition of normal values and any definite
conclusions about the body burden are impossible. According to an
international survey encompassing 1,107 samples from 15 countries, 79
I
percent of the world population excrete less than 0.5 yg Hg/1 of urine,
the remaining 21 percent are scattered broadly throughout levels ranging
up to 221 yg Hg/1 (WHO, 1966). Table 6.9 lists "normal" mercury levels
in urine in samples from various countries.
Smith (1972) describes a thorough study of about one thousand
workers exposed to various levels of elemental mercury. His most
important finding is the existence of a close statistical correlation
between mercury concentrations in air, blood, and urine -- see Figures
6.4 and 6.5. These observations indicate that urinary excretion quite
accurately reflects the level of chronic exposure to elemental mercury;
hence, urinary excretion also permits cautious inferences about the body
burden under these specific circumstances. Another important finding
of the same study is the existence of an air threshold value lying
around 100 yg Hg/cubic meter.
Generally, the mercury content of urine yields little information
about the body burden resulting from chronic exposure to inorganic
mercury compounds. Occasionally, however, the determination of urine
mercury becomes an important diagnostic tool. For example, after a sudden
187
-------
Table 6.9. "NORMAL" MERCURY LEVELS (ATOMIC ABSORPTION SPECTROMETRY)
IN URINE IN SAMPLES FROM DIFFERENT COUNTRIES
Country
Argentina
Chile
Czechoslovakia
Finland
Israel
Italy
Japan
Netherlands
Peru
Poland
Sweden
Yugoslavia
U.A.R. (Egypt)
U.K.
U.S.
California
New York
Ohio
Total
Total
number
of
samples
49
35
20
46
83
25
40
60
64
98
30
65
14
30
434
31
363
40
1,107
Percent
of samples
< 5 pg Hg/1
84
69
85
67
87
76
85
87
50
71
80
83
64
87
82
87
80
93
79
Highest
level
yg Hg/1
21
21
11
30
95
37
45
15
107
158
74
69
12 •'
38
221
15
97
221
221
Source:
Friberg and Vostal (1972).
188
-------
ORNL-DWG 74-10380
OD
VO
\ CM
CP O
500
LU H
1 § 375
o
2 ^
o [3
U LU
>- o:
cc o:
3 °
o:
LU
250
125
0
CLINICAL
THRESHOLD
D
_J -I
< O
X
^ <"
? UJ
_J 01
O X
0 ' 100 200 •
INORGANIC MERCURY CONCENTRATION IN AIR
Figure 6.4 MERCURY CONTENT OR URINE VS MERCURY CONTENT IN AIR
Source:
300
Smith (1972).
-------
ORNL-DWG 74-10379
20
o cr
rr
i-
:z
UJ
o
o
or
o
cr
UJ
o
a
o
3
QQ
15
10
0
CLINICAL
THRESHOLD
CLINICAL
iTHRESHOLD
I
j
0 .100 200 300
- INORGANIC MERCURY CONCENTRATION IN AIR
Figure 6.5 MERCURY CONTENT OF BLOOD VS MERCURY CONTENT IN AIR
Source:
Smith (1972).
400
-------
and known ingestion of mercury salts, the urinary content serves as an
indicator of uptake. Also when a patient receives treatment aiming at
removal of a high body burden, the urinary content rises with tissue
release of incorporated mercury and thus indicates effectiveness of the
therapeutic procedure.
Urinary assays are virtually useless in assessing body burden after
exposure to short-chain alkyl derivatives since fecal excretion is the
predominant elimination route.
6.4.3.3 Hair Levels—Hair has an important role in the assessment of
both mercury exposure and body burden. First of all, its major protein -
keratin - contains large numbers of sulfhydryl groups which act as binding
sites for mercury ions and radicals. As a general rule, the mercury
concentration in hair is between 250 and 300 times higher than that in
blood. Furthermore, each individual hairshaft carries a coating of
natural oils which largely prevents external contaminations from reaching
the binding sites; hence samples of washed hair quite reliably reflect
the existing mercury blood level. Secondly, since the formation of new
hair takes place only at the base, a record of mercury content throughout
a considerable length of time is available. "Normal" mercury levels in
hair expectedly cover a broad range. Among persons who are exposed
neither professionally nor accidentally, the mean concentrations of total
mercury in hair generally lie between 1 and 5 yg Hg/g. Several examples
follow: Canada - 1.8 yg Hg/g (Perkins and Jervis, 1966), Japan - 5.0 yg
Hg/g (Yamaguchi et al., 1971), England - 5.1 yg Hg/g (Al-Shahristani and
Shihab, 1974).
191
-------
Nord et al. (1973) compared the population from an industrialized
urban area - Pasadena, California - with that from a nonindustrialized
region - Los Alamos, New Mexico. Geometric mean concentrations of mercury
in hair were as follows: Pasadena - 25.0 yg Hg/g; Los Alamos - 18.9 yg
Hg/g; individual values ranged from 5 yg Hg/g to over 100 yg Hg/g.
By sectioning long bundles of hair, it is possible not only to
retrace the dates and the durations of ingestion but also to determine
the approximate amount of methylmercury incorporation. After exposure
stops, the exponential decline of hair concentration yields valuable
information about the half-life of methylmercury in blood and tissues.
6.5 EFFECTS
6.5.1 Clinical and Epidemiological Aspects
6.5.1.1 Clinical studies—The symptoms and toxicological aspects of
mercury poisoning have been covered in Section 6.4.2 for animals; since
animal response is quite similar to human response and because most
experimental data were obtained from animal studies, only a few specific
points will be covered in this section.
6.5.1.12 Elemental mercury—Exposure to very high concentrations of
mercury vapor triggers a clinical picture that centers primarily around
the lungs. Usually a one-to-four hour delay elapses from time of exposure
until onset of symptoms. Fever, chills, nausea, and general malaise
develop rapidly and are accompanied frequently by shortness of breath,
pain and tightness in the chest, and by episodes of paroxysmal coughing.
In the most severe cases patients die from lung edema within three days.
Both gross and microscopic examination reveal diffuse interstitial
192
-------
pneumonitis with profuse fibrinous exudation into the alveoli and with
erosion of the bronchial and bronchiolar linings (Milne et al., 1970).
In mild cases patients recover completely within a few days or weeks.
Chronic exposure to levels which do not trigger the acute pulmonary
syndrome can lead to classical mercurial ism.
6.5.1.1.3 Inorganic mercury compounds—The clinical picture of inorganic
mercury poisoning can be demonstrated by cases where mercuric chloride
has been ingested. Signs and symptoms of the poisoning essentially
spring from the mercuric cation; clinical experience on a limited number
of patients indicates that the type of anion exerts only a minor
influence, if any at all. Therefore, the classical picture applies
equally well to every inorganic mercuric compound.
Clinical problems involve the alimentary canal and the kidneys.
When ingested, the corrosive action of mercuric chloride causes an
immediate necrosis in the superficial cell layers of the mucosa. In
severe cases shock and peripheral vascular collapse can lead to death.
Usually, however, the primary lesions begin to heal within a few days-.
and the patient shows marked improvement. A secondary phase of
deterioration then results from excretion of mercury through the salivary
glands and through the gastrointestinal mucosa, particularly that of
the colon. The excretion leads to stomatitis, gingivitis, and a metallic
taste in the mouth; also, the gastrointestinal tract develops inflammation,
bowel motility declines occasionally to complete ileus, while the
abdomen becomes distended and tender to the touch. The colon often reacts
with severe ulcerative colitis entailing tenesmus and heavy blood loss.
193
-------
The secondary phase lasts about one week and complete recovery ensues
within a few weeks,
Since inorganic mercury ions are excreted through the kidneys as
well as through the alimentary canal, kidney damage may be more important
than damage to the alimentary canal. The epithelium of the proximal
convoluted tubules may be destroyed leading to oliguria or anuria
(Clarkson, 1972). Renal insufficiency or failure can thus lead to
death. If the patient can be maintained through the critical period,
the tubular epithelium can begin to regenerate and prognosis is good.
6.5.1.1.4 Organic mercury compounds—The clinica.l picture of methyl -
mercury poisoning resembles that of chronic exposure to elemental
mercury; that is, the primary effect is on the CNS. Motor and sensory
systems are affected as well as the mental facilities. Dose-response
curves for several symptoms of methylmercury poisoning are shown in
Figure 6.6.
Long-chain alkyl and aryl derivatives are readily eliminated from
the human body either in an unchanged form or after undergoing metabal.ic
alteration. Toxicity of these is thus quite low. Both histological
damage and functional impairment closely resemble that which is caused
by inorganic mercuric compounds (Friberg and Vostal, 1972). Ethylmercury
occupies a middle position; its toxicity is lower than that of methyl-
mercury but not as low as that of the other organomercurials; its
injurious action affects both the CNS and the kidneys.
6.5.1.1.5 Therapy—Treatment of mercury poisoning aims primarily at
removing mercury from the body. Unabsorbed and unbound mercury can
194
-------
obviously be removed from the stomach by vomiting and gastric lavage.
A resin containing-a high concentration of thiol groups has been used to
sequester unbound methylmercury from the intestines (Clarkson, 1973).
The resin is not digested and hastens the fecal elimination of mercury.
Several other agents are used once mercury has entered the bloodstream
and organs. BAL or British Anti-Lewisite (2,3-dimercapto-l-propanol),
NAP (N-acetyl-D,L-penicillamine, and CaEDTA (calcium ethylene-diaminote-
traacetate) are sometimes used. Good results after administration of
BAL were reported by several investigators (Roskam et a!., 1948; Longcope,
1952; Bell et al., 1955; Hadengue et al., 1957). Hadengue et al, (1957)
tried EDTA in a case of severe tremor after mercury fulminate poisoning
and found no benefit in either urinary excretion of mercury or relief
of symptoms. Bell et al. (1955) found that EDTA actually decreased
excretion of mercury in a case of metallic mercury poisoning; however,
in another case of mild metallic mercury'poisoning, Woodcock (1958)
-found BAL to be ineffective and EDTA to be beneficial. BAL was effective
in acute mercuric chloride poisoning when given promptly after exposure.
(Longcope, 1952); however, another report indicated that treatment
with BAL, while increasing urinaryexcretion of mercury, also increased
the mercury concentration in the brain (Berlin et al., 1965). NAP was
not effective in treating chronic poisoning in man, even though it did
increase urinary mercury excretion (Elkins, 1960). Based on a limited
number of cases, effectiveness of BAL, EDTA, and NAP is as follows
(Kark et al., 1971):
BAL improvement in 32 percent of patients;
CaEDTA improvement in 50 percent of patients;
NAP improvement in 88 percent of patients.
195
-------
6.5.2 Epidemiological Examples
Study of case histories of accidental or self-inflicted mercury
poisoning is the only acceptable method of obtaining dose-response and
other types of human data. Although exact doses are not always known
in these cases, the data may be more useful than that extrapolated from
animal experiments. Several examples follow to show the specific types
of information that can be obtained from case histories.
6.5.2.1 Acute Pulmonary Injury—A 2.5-hour exposure to a concentration
of mercury vapor estimated to be 1000 yg/cubic meter was sufficient to
cause pulmonary symptoms (shortness of breath, coughing, pain) in a
46-year-old man (Milne et al., 1970). Mercury levels in the urine
10 to 14 days after exposure were 100 yg/1 and 170 yg/24 hours. One
i
month later the level declined to 70 yg/1 and 100 yg/24 hours.
6.5.2.2 Chronic Brain Injury—A 25-year-old man was exposed to mercury
i
vapor concentrations varying from 100 to 2200 yg/cubic meter or higher
for two years (Kark et al., 1971). Classical signs of mercury poisoning
were apparent after one year and grew in severity during the second -year
until the man was totally disabled from CNS involvement. Four courses
of treatment with NAP over a ten-week period led to a gradual improvement
in condition. During treatment, mercury levels declined in: cerebrospinal
fluid - from 7.5 yg/100 ml to undetectable; blood plasma - 5 to 7 yg/100
ml to 0 to 2 yg/100 ml; feces - 100 yg/day to 50 yg/day; and urine -
2000 to 8600 yg/24 hours to 600 yg/24 hours. Some permanent damage to the
CNS resulted.
6.5.2.3 Acute Renal Injury—Acute renal injury was produced in a
20-year-old woman following ingestion of 1.5 grams of mercuric chloride
196
-------
(Davis et a!., 1974). The actual dose insult was probably much smaller
because of almost'immediate vomiting and gastric lavage within one
hour; however, the caustic effect to the gastrointestinal tract was
severe. Treatment with 125 mg BAL every four hours did not prevent
kidney damage and urinary output fell to below the necessary limit of
500 ml/24 hours. The kidneys were able to repair themselves in time,
but hemodialysis was required until urinary output rose to acceptable
levels.
An ingested dose of 10 grams of mercuric chloride was fatal to a
35-year-old man (Davis et al., 1974). Acute tubular necrosis and signs
of regeneration and focal interstitial nephritis were found in the
kidneys. The mercury level in renal tissue was 19 yg/g and in hepatic
tissue was 63 yg/g.
6.5.2.4 Methylmercury Syndrome—An indication of morphological changes
j
associated with methylmercury poisoning in humans was obtained upon
autopsy of a 38-year-old man who had been totally disabled for 15 years
as a result of exposure to methylmercury phosphate and nitrate (Hunter.
et al., 1940; Hunter and Russell, 1954). Pathological changes were
confined almost exclusively to the CHS. Methylmercury was quite selective
in its toxic action, preferentially destroying the optical cortex and
certain parts of the cerebellum. Other cortical areas are affected to
a lesser degree and only in sharply localized spots. The spinal cord
and peripheral nerves showed no pathological changes.
197
-------
6.5.2.5 Transplacental Transport--Transp1acenta1 transport of methyl -
mercury in humans has been demonstrated following accidental ingestion.
During the second trimester of pregnancy, a woman ate pork from a pig
that had eaten grain treated with methylmercury fungicides (Snyder, 1971;
Curley et al., 1971; Snyder, 1972). Prenatal examinations during the
seventh and eighth month of pregnancy revealed no abnormal findings
except above-normal levels of mercury in the mother's urine. Mercury
concentrations in the baby's urine were: first day - 2.7 ug/1;
fourth day - 2.0 yg/1; and sixth week - 0.01 yg/1. About three months
after birth abnormalities appeared in the baby's electroencephalogram
(in the absence of breast feeding) and became more severe with time.
Neurological examination at 16 months revealed that development had
been arrested at three months. The child was blind and mentally
retarded and had severe motor disorders.
A similar case was reported by Mat'sumoto et al. (1965). Autopsy
of this baby at two years and six months of age showed extensive
destruction of nerve cells in the cerebral cortex and cerebellar folia.
6.6 REFERENCES
1. Al-Shahristani, H., and K. M. Shihab, 1974. "Variation of
Biological Half-Life of Methylmercury-in Man," Arch. Environ.
Health.. 28:342-344.
2. Bell, R. F., J. C. Gilliland, and W. S. Dunn, 1955. "Urinary
Mercury and Lead Excretion in a Case of Mercurial ism:
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Calcium and Dimercaprol," Arch. TnHnqtr, Health. ,11:231-233.
198
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3. Berlin, M., and S. Ullberg, 1963a. "Accumulation and Retention'
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A.W.R.E. Aldermaston, 1967. "The Trace Element Content of
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W. F. Barthel, P. E. Pierce, and W. H. Likosky, 1971. "Organic
Mercury Identified as the Caus'e of Poisoning in Humans and
and Hogs," Science, 172:65-67.
14. Davis, L. E., et al., 1974. "Central Nervous System Intoxication
from Mercurous Chloride Laxatives," Arch. Neurol., 30_: 428-341.
15. D'ltri, F. M., 1972. The Environmental Mercury Problem, CRC
Press, Cleveland, pp. 20-85.
16. Druckery, H., H. Hamperl, and D. Schmahl, 1957. "Carcinogenic
Action of Metallic Mercury After i.p. Administration in Rats,"
1. Krebsforsch.. 61^:511-519.
17. Elkins, H. G., 1960. An. Meet. Am. Ind. Hyg. Assoc.,
Rochester, N.Y.
200
-------
18. Friberg, L., 1961. "On the Value of Measuring Mercury and
Cadmium Concentrations in Urine," Pure Appl. Chem., 3_:289.
19. Friberg, L., E. Skog, and J. E. Wahlberg, 1961. "Resorption
of Mercuric Chloride and Methyl Mercury Dicyandiamide in
Guinea-Pigs Through Normal Skin and Through Skin Pre-Treated
with Acetone, Alkylaryl-Sulphonate and Soap," Acta Dermatovener,
41.: 40-52.
20. Friberg, L., and J. Vostal (eds.), 1972. Mercury in the
Environment - A Toxicological and Epidemiological Appraisal,
CRC Press, Cleveland, 215 pp.
21. Frithz, A., and B. Lagerholm, 1968. "Cellular Changes in the
Psoriatic Epidermis. VI. The Submicroscopic Intracellular
Distribution of Mercury Compound in the Normal Epidermis in
Comparison with That in the Psoriatic Epidermis," Acta Derm.
Venereal, 48_:403.
22. Ganther, H. E., C. Gondie, M. L. Sunde, M. J. Kopecky, P. Wagner,
Sang-Hwan Oh, and W. G. Hoekstra, 1972. "Selenium: Relation to
Decreased Toxicity of Methylmercury Added to Diets Containing
Tuna," Science, 175:1122-1124.
23. Ganther, H. E., P. A. Wagner, M. L. Sunde, and W. G. Hoekstra,
1973. "Protective Effects of Selenium Against Heavy Metal
Toxicities," iji_: Trace Substances in Environmental Health VI.
Hemphill, D. 'D. (ed.), Curators of University of Missouri,
Columbia, pp. 247-252.
201
-------
24. Hadengue, A., Y. Barre, J. Manson, R. LeBreton, and J. Charlier,
1957. "Tremblement Mercurial Effects des Traitments par EDTA
et BAL." Arch. Mai. Prof.. 18:561.
25. Hunter, D., R. R. Bomford, and D. S. Russell, 1940. "Poisoning
by Methyl Mercury Compounds," Quart. J. Med., Sk 193-213.
26. Hunter, D., and D. S. Russell, 1954. "Focal Cerebral and Cerebellar
Atrophy in a Human Subject Due to Organic Mercury Compounds,"
J. Neurosurg. Psychiat., V7_:235-241.
27. Kark, R.A.P., D. C. Poskanzer, J. D. Bullock, and G. Boylen, 1971.
"Mercury Poisoning and Its Treatment with N-Acetyl-D,
L-Penicillamine," New Engl. J. Med.. 285:10-16.
28. Longcope, W. T. , 1952. Bull. Ayer Clin. Lab. Penn. Hosp., 4_:61.
29. Lu, F. C., P. E. Berteau, and D. J. Clegg, 1972. Mercury
Contamination in Man and His Environment, Int. Atomic Energy
Agency, Vienna, Chap. 6., pp. 67-85.
30. Magos, L., 1967. "Mercury-Blood Interaction and Mercury Uptake
by the Brain After Vapor Exposure," Environ. Res., j_(4):323-337.
31. Matsumoto, H., G. Koya, and T. Takeuchi, 1965. "Fetal Minamata
Disease: A Neuropathological Study of Two Cases of Intrauterine
Intoxication by a Methyl Mercury Compound," J. Neuropath. Exp.
Neurol., 24_: 563-574.
32. McAlpine, D., and A. Shukuro, 1958. "Minamata Disease. An
Unusual Neurological Disorder Caused by Contaminated Fish,"
Lancet, 2:629-631.
202
-------
33. Milne, J., A. Christophers, and P. DeSilva, 1970. "Acute .
Mercurial Pneumonitis," Brit. J. of Ind. Med., 27_:334-338.
34. Nielson Kudsk, F., 1965. "Absorption of Mercury Vapor from the
Respiratory Tract in Man," Acta. Pharmacol., 23_:250.
35. Nord, P. J., M. P. Kadaba, and J.R.J. Sorensen, 1973. "Mercury
in Human Hair. A Study of the Residents of Los Alamos, NM, and
Pasadena, CA, by Cold Vapor Atomic Absorption Spectrophotometry,"
Arch. Environ. Health., Z7_:40-44.
36. Nordberg, G. G., M. H. Berlin, and C. A. Grant, 1971. "Methyl-
Mercury in the Monkey - Autoradiographical Distribution and
Neurotoxicity," Proc. 16th Int. Congr. Occup. Health, Tokyo,
Sept. 22-27. 1969. pp. 234-237.
37. Norseth, T., and T. W. Clarkson, 1970. "Studies on the
203
Biotransformation of Hg-Leveled Methyl Mercury Chloride in
Rats," Arch. Environ. Health.. 21_:/17-727.
38. Oharazawa, H., 1968. "Effect of Ethyl Mercuric Phosphate in the
Pregnant Mouse on Chromosome Abnormalities and Fetal Malformation,"
J. Jap. Qbstet. Gynecol. Soc.. 29;14-79.
39. Ostlund, K., 1969a. "Separation of Organic Mercury Compounds by
Thin-Layer Chromatography," Nord. Hyg. T., 50_:82-84.
40. Ostlund, K., 1969b. "Studies on the Metabolism of Methyl Mercury
and Dimethyl Mercury in Mice," Acta. Pharmacol.. 2_7_, Suppl. 1:1-132.
203
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41. Parizek, J., I. Ostadalova, J. Kalouskova, A. Babkky, and
J. Beres, 1971. "The Detoxifying Effects of Selenium.
Interrelation Between Selenium and Certain Metals" in:
Newer Trace Elements in Nutrition, Mertz, W. and W. E. Cornatzer
(eds.), Morcel Dekker, New York, pp. 85-122.
42. Parizek, J., J. Kalouskova, A. Babicky, J. Beres, and L. Pavlik,
1974. "Interaction of Selenium with Mercury, Cadmium and other
Toxic Metals" in: Trace Element Metabolism in Animals - 2,
Hoekstra, W. 6., J. W. Suthe, H.- E. Ganther, and W. Mertz (eds.),
University Park Press, Baltimore, pp. 119-131.
43. Passow, H., A. Rothstein, and T. W. Clarkson, 1961. "The General
Pharamacology of Heavy Metals," Pharmacol. Rev., ^3_:185-224.
44. Perkins, A. K., and R. E. Jervis, 1966. "Trace Elements in Human
Head Hair," J. Forensic Sci.. 11;50-63.
i
45. Ramel, C., 1967. "Effects of Organic Mercury Compounds,"
Hereditas, 57;445-447.
46. Ramel, C. 1969. "Genetic Effects of Organic Mercury Compounds. •.
I. Cytological Investigations on Allium Roots," Hereditas,
6J_: 208-230.
47. .Ramel* C., and J. Magnusson, 1969. "Genetic Effects of Organic
Mercury Compounds. II. Chromosome Segregation in Drosophila
melanogaster," Hereditas, 61;231-254.
48. Roskam, J., J. Heusghem, C. Renard, and L. Swalue, 1948.
"Intoxication Mercurielle Aigue et BAL," Schweiz. Med. Hschr..
78:932.
204
-------
49. Silberberg, I., L. Prutkin, and M. Leider, 1969. "Electron
Microscopic Studies of Transepidermal Absorption of Mercury,"
Arch. Environ. Health., _19_: 7.
50. Skerving, S., A. Hansson, and J. Lindsten, 1970. "Chromosome
Breakage in Human Subjects Exposed to Methyl Mercury Through
Fish Consumption," Arch. Environ. Health., 21_:133-139.
51. Smith, R.' G., 1972. "Dose-Response Relationship Associated with
Known Mercury Absorption at Low Dose Levels of Inorganic Mercury,"
in: Environmental Mercury Contamination, Hartung, R. and B. Dinman,
(eds.), Ann Arbor Science Publishers Inc., Ann Arbor, Mich.,
pp. 207-222.
52. Snyder, R. D., 1971. "Congenital Mercury Poisoning,". New Engl.
J. Med., 284:1014-1016.
53. Snyder, R. D., 1972. "The Involuntary Movements of Chronic
Mercury Poisoning," Arch. Neurol. ,'• 26:379-381.
54. Suzuki, T., N. Matsumoto, T. Miyama, and H. Katsunuma, 1967.
"Placenta! Transfer of Mercuric Chloride, Phenyl Mercury
Acetate and Methyl Merucury Acetate in Mice," Industr. Health.,
5_: 149-155.
55. Teisinger, J., and V. Fiserova-Bergerova, 1965. "Pulmonary
Retention and Excretion of Mercury Vapors in Man," Ind. Med. Surg.,
34:580-584.
56. Ukita, T., Y. Takeda, Y. Sato, and T. Takahashi, 1967.
203
"Distribution of Hg Labelled Mercury Compounds in Adult and
Pregnant Mice Determined by Whole-Body Autoradiography,"
Radioisotopes, 16:439-448.
205
-------
57. Ulfvarson, U., 1962. "Distribution and Excretion of Some Mercury
Compounds After Long Term Exposure," Int. Arch. Gevjerbepath..
191:412-422.
58. Viola, P. A., and G. B. Cassano, 1968. "The Effect of Chlorine on
Mercury Vapor Intoxication. Autoradiographic Study," Ned. Lavoro.,
59_(6-7):437-444.
59. Wahlberg, J. E., 1965. "Disappearance Measurements - a Method
for Studying Percutaneous Absorption of Isotope-Labelled Compounds
Emitting Gamma-Rays," Acta. Dermatovener, 45_: 397-414.
60. WHO (World Health Organization), 1966. "Meeting of Investigators
for the International Study of Normal Values for Toxic Substances
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61. Woodcock, S. M., 1958. "A Case Illustrating the Effect of
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1971. "Relationship Between Mercury Content of Hair and Amount
of Fish Consumed," Health Services and Mental Health Administration
Health Rep., 86(10):904-909.
206
-------
7.0 ENVIRONMENTAL DISTRIBUTION AND TRANSFORMATION
7.1 SUMMARY
Mercury is distributed widely in the natural state, usually in low
concentrations. It reacts with a variety of compounds, forming complexes
ranging from simple ores to metallo-organic pesticides. Due to the
ubiquity of mercury and the many sources of mercury contamination, it is
often difficult to separate natural background concentrations from those
which are man-made.
Because of its natural tendency to vaporize, mercury can be distributed
throughout the environment by aerial circulation. Atmospheric concen-
trations of mercury are highest over natural deposits or sources of
industrial contamination, and background concentrations in the atmosphere
are about 1 ng/cubic meter. Mercury leaves the atmosphere by way of dust
and rain.
Mercury is usually found in water a't concentrations less than 5 parts
per billion and is probably transported primarily by particles suspended
in the water. Biological methylation of mercury converts the element-to
more soluble forms. Mercury leaves water by sedimentation, adsorption,
and volatilization.
The mercury content of the world's soils is generally about 50 parts
per billion. However, concentrations may be greater in soils with high
organic matter content. In some areas the use of mercuric pesticides
has contributed to a high level of contamination. Mercury leaves soils
by the processess of evaporation, plant uptake, runoff, or percolation.
207
-------
7.2 DISTRIBUTION OF MERCURY IN THE ENVIRONMENT
7.2.1 Distribution in Air
al degassing of the earth's crust and upper mantle has been
suggested as the primary source of atmospheric mercury (Krenkel, 1973;
Weiss et al., 1971). Hence, land surface is the main natural source of
airborne mercury, and concentrations above land masses are higher than
those above oceans (McCarthy et al., 1970). Volatile forms of mercury
in aquatic areas are also released into the atmosphere. The atmospheric
background concentrations of mercury appear to be about 1 ng/cubic meter
(Krenkel, 1973).
Krenkel (1973) has calculated that the world's atmosphere contains
50 million pounds of mercury. Atmospheric concentrations of mercury are
highest over areas with ore deposits or industries with mercury release
into the environment (Table 7.1). Ground -surface air concentrations are
usually higher than concentrations abov^ the ground. Over an Arizona
ore mine ground surface air concentration was 20,000 ng/cubic meter,
while measurements above the ground indicated a concentration of 108
ng/cubic meter (Friberg and Vostal , 1972).
Mercury enters the atmosphere in both particulate and gaseous forms.
In 1970 atmospheric concentration of particulate mercury in the industrial
area of Chicago was 4.8 ng/cubic meter compared with a rural area
concentration of 1.9 ng/cubic meter (Jenne, 1970). Ionized forms of
mercury can enter the atmosphere by volatilization, theoretically occurring
by three processes: 1) chemical reduction into the elemental form,
2) reduction through the activity of microbes, plants, or other living
208
-------
Table 7.1. MERCURY IN AIR
(nanograms per cubic meter)3
ro
o
UD
Sample
"Unpolluted air"
Over Pacific Ocean, 20 miles offshore
California, winter
California, summer
Background, Arizona and California
Chicago area
Kamrht' ka
Mn<;rnw and Tula rpainn<; fnn nrp Hpnnsit
Number of
samples
analyzed
2
--
--
--
22
i n
Range
Min
Air
0.6
1
1.5
1.6
3
nn
Max
0.7
25
50
7.2
39
inn
Average
Reference
R Sfnrk and fiirupl (1934)
Williston (1968).
Do.
Do.
4.5 McCarthy and others (1969).
9.7 Brar and others (1969).
1QO fliHi'n' va n ^nrf f)7Prova i 1 ^Ffi
nn
-------
Table 7.1. MERCURY IN AIR
(nanograms per cubic meter) (cont'd)
Sample
Number of
samples_
analyzed
Range
Average
Min
Max
Reference
IV)
I—-
o
Air
Over porphyry copper deposit
Do.
Over mercury deposit
Do.
Do.
12
18.5
12
58
200
30
53
57.5
66
1,200
18.8 McCarthy and others (1969)
28 Do.
31.4 Do.
62 Do.
Karasik and Bol'shakov,
quoted by Aidin'yan and
Ozerova (1966).
Note:
a _9
1 nanogram = 10 grams.
Source:
Fleischer (1970).
-------
organisms, and 3) biotransformation into volatile organomercury
compounds, mainly short chain alkyl mercurials (Friberg and Vostal,
1972).
Certain industries such as chloral kali or ore processing facilities
contribute directly to the atmospheric concentration of mercury when small
amounts of gaseous and particulate mercury are vented into the surrounding
air. The U.S..Environmental Protection Agency has recently limited
discharges from the two above mentioned industries to 2300 g of Hg/day
(Fed. Reg., 1974). Probably the largest single source of mercury emission
into the air is from coal combustion - estimated to be from 275 to 1800
tons per year (U.S. Environmental Protection Agency, 1972). Another
estimate resulting from an anlysis of 36 United States coals for mercury
was 3000 tons per year (Joensuu, 1?71). Incinerators, power plant boilers,
and paints are thought to contribute 66 percent of the total United States
mercury emissions (Flinn and Remiers, 1974).
7.2.2 Distribution in Hater
Mercury concentration measurements in water can be difficult to
interpret due to particulate adsorption of mercury and the influence of
other ions on the forms of mercury present. Particulate matter in water
is more likely to contain high concentrations of mercury than the water
itself (Klein, 1973). Higher concentrations of mercury are likely to
occur in underground'water due to the length of exposure and close contact
with mineral grains and other environmental factors (U.S. Geological
Survey, 1970).
211
-------
Water from drainage areas near industrial sources or high natural
deposits of mercury usually contains higher levels of mercury. In 1970,
more than 500 samples of industrial effluents in the United States were
analyzed for mercury (Friberg and Vostal, 1972). Eighty-three percent
of all samples were below 5 ng/g, 12 percent ranged between 5 and 100
ng/g, and less than 5 percent had concentrations higher than 100 ng/g.
Two samples contained over 10,000 ng/g.
Surface waters representing 31 states as shown in Table 7.2, ranged
in concentration of mercury from less than 0.1 to 17 parts per billion
(ppb); only two areas had levels higher than 5 ppb, the Public Health
Service limit for potable water supplies (Wershaw, 1970). Many of ,the
samples were collected in areas of suspected mercury contamination. The
i
mercury content of v/ater samples from all 50 states ranged from 0.5 ug/1
to 6.9 ug/1 in 1970 (U.S. Environmental Protection Agency, 1973). The
mercury content of some natural waters is presented in Table 7.3.
7.2.3 Distribution in Soil and Rock
Due to widespread contamination of the environment, background
concentrations of soil mercury are often difficult to determine. The
natural geological occurrence of mercury and mercury contamination of
air adds to soil concentrations of mercury (Rissanen and Miettinen, 1972)
Agricultural use of mercury also contributes to soil concentrations,
usually in small amounts, either directly or by the decomposition of
plant material.
Global deposits of mercury with the highest concentrations are
contained in mercuriferous belts which correspond to the mobile dis-
location zones of the earth (Jonasson and Boyle, 1971). In the
212
-------
Table 7.2. MERCURY IN SELECTED RIVERS OF THE UNITED STATES, 1970
PO
1—"
CO
Source and location
Gold Creek at Juneau, Alaska
Colorado River near Yuma, Ariz.
Wei ton Mohawk Drain near Yuma, Ariz.
Ouachita River downstream from Camden, Ark.
St. Francis River at Marked Tree, Ark.
Santa Ana River below Prada Dam near Riverside, Calif.
South Platte River at Henderson, Colo.
Blue River upstream of Dillon Reservoir, Colo.
French Creek near Breckenridge, Colo.
Time sample collected
Month-day Hour
6-10 1350
6-18
6-19
6-18 0900
6-19 1000
6-29
5-19 1410
6-22
6-22
Mercury
(in ppb)
< 0.1
< 0.1
< 0.1
< 0.1
0.1
< 0.1
0.3
< 0.1
< 0.1
-------
Table 7.2. MERCURY IN SELECTED RIVERS OF THE UNITED STATES, 1970 (cont'd)
Source and location
Animas River at Silverton, Colo.
Cement Creek at Silverton, Colo.
Red Mountain Creek near Ouray, Colo.
Red Mountain Creek at Ironton, Colo.
Nuuanu Stream near Honolulu, Hawaii
Honolii Stream near Papaikou, Hawaii
North Fork Kaukonahua near Wahiawa, Hawaii
Time sample
Month-day
6-22
6-22
6-22
6-22
6-8
6-8
6-11
collected
Hour
0930
1405
1800
Mercury
(in ppb)
0.1
< 0.1
17.0
< 0.1
0.6
< 0.1
0.4
Ohio River near Grand Chain, 111.
6-26
1040
0.1
Floyd River at Sioux City, Iowa
6-9
1645
0.2
Kansas River downstream from Topeka, Kans.
5-19
1130
3.5
-------
Table 7.2. MERCURY IN SELECTED RIVERS OF THE UNITED STATES, 1970 (cont'd)
ro
t—'
tn
Source and location
Mississippi River near Hickman, Ky.
Merrimack River above Lowell, Mass.
Wolf Creek near Cedar Lake, Mich.
Unnamed tributary to Wolf Creek near Edmore, Mich.
Rainy River at International Falls, Minn.
St. Louis River at Scanlon, Minn.
Pearl River at Byram, Miss.
Pascagoula River at Merrill, Miss.
Yellowstone River near Bill ings,' Mont.
Missouri River near Great Falls, Mont.
Time sample
Month-day
6-25
6-8
6-7
6-7
5-14
6-8
6-17
6-9
5-14
5-18
collected
Hour
1030
1100
1100
1000
1245
1015
1445
1500
1500
1730
Mercury
(in ppb)
< 0.1
1.2
< 0.1
0.1
< 0.1
< 0.1
0.1
3.0
< 0.1_-
< 0.1
-------
Table 7.2. MERCURY IN SELECTED RIVERS OF THE UNITED STATES, 1970 (cont'd)
ro
i—"
en
Source and location
Missouri River near St. Louis, Mo.
Missouri River at Hermann, Mo.
Salt Creek near Lincoln, Neb.
Las Vegas Wash at Henderson, Nev.
Pern igewas set River at Woodstock, N.H.
Canadian River near Glenrio, N. Mex.
Hudson River downstream from Poughkeepsie, N.Y.
Roosic River near North Pownal , Vt. , in Rennsselaer County, N.Y.
Wappinger Creek near Wappingers 'Falls, N.Y.
Time sample
Month-day
6-23
6-24
6-24
5-14
6-8
6-10
4-7
4-7
4-23
col lected
Hour
1430
1030
0915
1700
1100
1045
Mercury
(in ppb)
2.8
0.2
0.5
< 0.1
3.1
< 0.1
0.1
0.1
< 0.1
-------
Table 7.2. MERCURY IN SELECTED RIVERS OF THE UNITED STATES, 1970 (cont'd)
ro
Source and location
Delaware River at Port Jervis, N.Y.
Beaver Kill at Cooks Falls, N.Y.
Dear River near Helena, N.Y.
Raquette River at Raymondville, N.Y.
Oswegatchie River at Gouverneur, N.Y.
Oswegatchie River at Gouverneur, N.Y.
Black River at Watertown, N.Y.
Black River near Watertown, N.Y.
Lake Champlain near Whitehall, N.Y.
Lake Champlain near Ticonderoga, N.Y.
Lake Champlain near Crown Point, ;N.Y.
Raquette River at Massena, N.Y.
Time sample
Month -day
4-23
4-24
5-5
5-5
5-6
6-16
5-6
5-6
6-16
col lected
Hour
1420
1320
0735
0945
0800
1200
1015
1155
0840
Mercury
(in ppb)
< 0.1
0.1
< 0.1
0.2
0.7
1.2
< 0.1
< 0.1
< 0.1
< 0.1
0.1
< 0.1 "
-------
Table 7.2. MERCURY IN SELECTED RIVERS OF THE UNITED STATES, 1970 (cont'd)
Source and location
Raquette River at Raymondville, N.Y.
£2 Raquette River at Potsdam, N.Y.
oo
Oswegatchie River below Natural Dam, St. Lav/rence County, N.Y.
Oswegatchie River at Hailsboro, N.Y.
Chemung River near Wellsburg, N.Y.
Susquehanna River at Johnson City, N.Y.
Maumee River at Antwerp, Ohio
Scioto River near Chill icothe, Ohio
Great Miami River near Miamisburg, Ohio
North Canadian River near Harrahj Okla.
North Canadian River near Oklahoma City, Okla.
Time sample
Month-day
6-16
6-16
6-16
6-16
7-6
7-6
6-10
6-25
6-11
6-30
6-30
collected
Hour
0910
0950
1130
1230
1015
1330
1215
1115
1815
1000
1345
Mercury
(in pbb)
< 0.1
0.1
< 0.1
0.2
0.2
0.1
6.0
< 0.1
C.9
1.1
0.1
-------
Table 7.2. MERCURY IN SELECTED RIVERS OF THE UNITED STATES, 1970 (cont'd)
U3
Source and location
Whitev/ood Creek near Vale, S. Dak.
Paper Mill Creek near Herty, Tex.
San Antonio River near Elmendorf, Tex.
Blackwater River at Franklin, Va.
Jackson River near Covington, Va.
Bailey Creek near Hopewell , Va.
Snohomish River near Monroe, Wash.
North Branch Potomac River near Barnum, W. Va.
Time sample
Month-day
5-22
6-9
6-11
6-15
6-16
6-18
7-1
6-3
collected
Hour
1100
1015
1100
0930
0820
0945
1050
1600
Mercury
(in ppb)
< 0.1
0.1
< 0.1
1.1
< 0.1
0.4
< 0.1
1.2
-------
Table 7.2. MERCURY IN SELECTED RIVERS OF THE UNITED STATES, 1970 (cont'd)
Wisconsin Ri
Wisconsin Ri
North Platte
Source and location
ver at Wisconsin Rapids, Wis.
ver near Nekoosa, Wis.
River near Casper, Wyo.
Bighorn River at Kane, Wyo.
Time sample
Month-day
6-10
6-10
6-23
6-30
collected
Hour
1300
1230
1215
1600
Mercury
(in ppb)
0.9
2.4
0.1
< 0.1
Source:
Wershaw (1970). (Analyses by M. J. Fishman (U.'S. Geological Survey, written commun., 1970)}.
-------
Table 7.3. MERCURY CONTENT OF NATURAL WATERS
(micrograms per liter)3
rv>
ro
Sample
Number of Range
samples
Min Max
Average
Reference
Rivers
Rhine River
Saale River, Germany
Elbe River, Germany
Danube River
Sweden
European SSSR
Armenian SSR
Armenian SSR
8 0.05 0.19b
i
in 7 n
4 0.02 0.2
24 0.4 2.8
7 1.0 20.0
6 1.0 2.0b
300 0.01 136. 0C
0.10
0.07
0.09
1.1
4.2
1.5b
< 0.1
Stock and Cucuel (1934).
Heide and Bohm (1957), and
Heide, Lerz, and Bohm (1957)
Do.
Aidin'yan and Balavskaya
(1963).
Wikander (1968).
Aidin'yan (1962).
Aidin'yan (1963).
Do.
-------
Table 7.3. MERCURY CONTENT OF NATURAL WATERS
(micrograms per liter)9 (cont'd)
IN3
IV)
Number of Range
Sample samples
analyzed Min Max
Average
Reference
Sea water
„-
Atlantic, Indian, Red Sea, Black Sea, etc. 14 0.7 2.0
Atlantic Ocean 9 0.4 1.6
Pflp'i'F'ipnrp^n RAmAnnDppn ..... OOR 0 1 ^
Do. 4 0.15 0.27
Minamata Rav. .lanan IK "} fi
0.03
0.03
1.1
1.2
0.1
0.2
Stock and Cucuel (1934).
Heide and Bohm (1957).
Aidin'yan (1962).
Aidin'yan, Ozerova, and •
Gipp (1963).
Hamaguchi and others (1961)
Hosohara (1961).
Hncnhara anrl nfhorc MQfil\
-------
Table 7.3. MERCURY CONTENT OF NATURAL WATERS
(micrograms per liter)9 (cont'd)
ro
rsi
oo
Sample
Number of
samples
analyzed
Range
Average
Reference
Min
Max
Ground water and miscellaneous samples
Rainwater 0.05 0.48 0.2
Spring water, Germany 0.01 0.05
Surface waters, Northwest Caucasus { 0.27 0.68
7,000{
Subsurface waters, Northwest Caucasus { 0.25 1.25
Springs, Elbrus region 37 < 0.05 80.0 ==1.0
(No data in abstract on nature of water.) 0.0 140,000.0
Ground water, Kerch, U.S.S.R. < 1.0 2.5
Ground water, near mud volcanoes, Kerch 1.0 2.5
Ground water, Abkhazia, U.S.S.R. < 0.5
Mine waters, Abkhazia, U.S.S.R. 0.5 3.0
Stock and Cucuel (1934).
Do.
Baev (1968).
Do.
Krainov, Volkov, and
Korol'kova (1966).
Ishikura and Shibuya (1968)
Morozov (1965).
Karasik and Morozov (1966).
Zautashvili (1966).-
Do.
-------
Table 7.3. MERCURY CONTENT OF NATURAL WATERS
(micrograms per liter)3 (cont'd)
Sample
Number of Range
samples Average Reference
analyzed Min Max
Ground water and miscellaneous samples
Mineralized waters, Abkhazia, U.S.S.R.
Waters of Permian salt beds, Donets Basi
Brines associated with petroleum, Cymric
oilfield, California.
Brine, geothermal well, Salton Sea,
Calif.
in 'in Do
n 7 A — — KaraciLr ftnnrhfl rnv ^ nH
Vasilevskaya (1965).
inn n Ann Ra il PV anH nfhpr<; MQP1}
i c n ^kinnpr ^nd nthpr<; H967)
Notes:
a
l microgram per liter ~1 part per billion mercury.
The value 0.19 (next highest 0.08) is ascribed to waste water from an industrial plant.
Excluding the highest value.
Values above 0.1 ppb were in the drainage area of mercury deposits.
-------
ro
tn
Table 7.3. MERCURY CONTENT OF NATURAL WATERS
(micrograms per liter)9 (cont'd)
'Notes:
eAnother sample, a concentrated brine, contained 220 ppb Hg.
Source:
Fleischer (1970).
-------
United States, mercury deposits are confined mainly to the west coast
area in a belt of late tertiary orogeny and volcanism (Stahl, 1969).
Rocks of all classes contain some mercury ore. However, it is
most commonly found in limestone, calcareous shales, sandstone, serpentine
chert, andesite basalt, and rhyolite. Elemental mercury can be found in
some ores but only in small quantities (Krenkel, 1973). Mercury
concentrations in sedimentary layers 'of the earth's crust are much
higher than in igneous rocks. Concentrations in the earth's deep crust
and upper mantle range from 0.78 to 1.48 ppm (Saha, 1972).
Klein (1971) has estimated mercury concentrations in world soils
to a one meter depth to be 50 ppb, with a total content of 2 x 107 tons.
Jonasson and Boyle (1971) have also arrived at a figure of 50 ppb.
Eriksson (1967) has estimated mercury storage in the earth's soils at
1.5 kg/ha. Background mercury values for selected soil sampling areas
in Great Britain were estimated to be Between 0.01 and 0.06 ppm (Warren
and Delavault, 1969). Pierce et al. (1970) have suggested a background
value of 500 ppb for soils of the western United States.
Variability of soil mercury content is shown in Table 7.4.
Andersson (1967) found that Swedish topsoils contained 0.1 to 1.2
kg/ha. Of these, organic soils contained 300-510 ng Hg/g; moraine soils,
125-250 ng/g; clay soils, 80-150 ng/g; and sandy and silty soils 50-350
ng/g. Other analyses by Andersson revealed a mercury content of 50 ng/g
for a French soil sample and values of 70, 20, and less than 15 ng/g
for three Sudan soils. Soils from selected areas in Great Britain
have been found to contain between 0.25 and 15 ppm mercury (Warren and
Delavault, 1969). Analyses of soil samples representing 30 soil series
226
-------
Table 7.4. ANALYSES OF SOILS FOR MERCURY
(parts per billion)
PO
IV)
Number of
Sample samples
analyzed
Most soils, California —
Soils, Franciscan Formation, California —
Soils, unmineralized areas, California - —
Unmineral ized areas, British Columbia —
Near mineralization, British Columbia —
Very near mineralization, British —
Columbia
Soils, Germany —
Tnncnil c QwpHpn ")T\
Range
Average
Min Max
on An
£U HU — -
inn ?nn
1UU £UU ~ ~
An fin
in Rn
en 7 snn
9t;n ? f^nn -
on ?Qn
fin
Reference
Williston (1968)
Do.
Friedrich and Ha
(1966).
Warren, Delavaul
Barakso (1966).
Do.
Do.
Stock and Cucuel
Anrlov-ccpn MQfi?^
v/kes
t, and
(1934
-------
Table 7.4. ANALYSES OF SOILS FOR MERCURY
(parts per billion) (cont'd)
Sampl e
Number of
samples
Range
Min
Max
Average
Reference
ro
ro
cc
ils, European U.S.S.R.
Soils, Donets Basin
Soils, Donets Basin
Soils, Kerch Peninsula
Soils, Kerch-Tama area
Soils, Viet Nam
14
130
248
264
20
1,000
< 50 10,000 300
100 2,400 1,300
< 100 3,000
240 1,900
300
Do.
Aidin'yan, Trotskii,
and Balavskaya (196£),
Dvornikov (1963).
Dvornikov and Petrov
(1961).
Morozov (1965).
Karasik and Morozov
(1966).
Aidin'yan, Trotskii,
and Balavskaya (1964)
Source:
Fleischer (1970.
-------
in California revealed mercury content of 0.0002 to 0.0109 ppm, with a
mean of 0.0024 ppm (Bradford et al., 1971). A mean mercury concentration
of greater than 7000 ppm has been found in surface sediment of the
Pallanza Basin in Italy (Damiani and Thomas, 1974). Wiersma and Tai
(1974) found that actual levels of mercury residue in soils of the
eastern United States ranged from 0.05 to 0;10 ppm. No significant
difference in mercury content was found between cropland and noncrop-
land soils.
Mercury content is higher in soils near natural mercury deposits
or pollution outfalls '(Krenkel, 1973; Jonasson and Boyle, 1971; Fleischer
et al., 1970). Klein (1972a) found that concentrations in soil distant
or windward from industrialized areas averaged approximately 0.02 ppm,
as opposed to concentrations in industrialized regions which were
elevated tenfold. Bothner and Piper (1973) revealed that mercury
concentration in surface sediment decreased as a function of radial
distance from a chloral kali plant. Mercury content in Michigan soils
has been correlated with land use patterns (Klein, 1972b). Residential
areas contained a mean mercury concentration of 0.10 ppm; agricultural
areas, 0.11 ppm; industrial areas, 0.14 ppm; and airport areas, 0.33 ppm.
Mercury levels in the surface soil may be 5 to 10 times greater than
those found in subsoils (Krenkel, 1973). In some instances the greater
topsoil concentration may result from the use of fungicides, which are
normally bound in the upper 10 cm of soil (Ross and Stewart, 1962;
Fukunaga et al., 1972).
229
-------
7.3 ENVIRONMENTAL FATE
7.3.1 Mobility and Persistence in Air
Due to its high vapor pressure, the easiest way for elemental
mercury to enter the atmosphere is through vaporization. The mobility
of mercury is greatly increased by the high vapor pressure of its
metallic form and some of its compounds, especially the methyl and
ethyl forms. Atmospheric mercury can be widely distributed by wind
currents (U.S. Environmental Protection Agency 1971). Airborne mercury
is continuously removed from the atmosphere and deposited on the earth
or water surface by precipitation (Friberg and Vostal, 1972).
Daily and seasonal variations in atmospheric mercury concentrations
which appear to be due to changes in barometric pressure or temperature
have been documented. The maximum daily mercury concentration over the
Ord mine in Arizona was recorded when the rate of decrease in the
t
barometric pressure was greatest (McCarthy et al., 1970). The maximum
daytime concentration was 600 ng/cubic meter of mercury at midday with
a minimum concentration of 20 ng/cubic meter at 2:00 a.m. Background.
air concentrations of mercury 400 feet above ground in the Southwestern
United States range from 3 to 9 ng/cubic meter.
Mercury residence time in the atmosphere is not known; however,
both particulate and gaseous mercury can be washed out by rain (Friberg
and Vostal, 1972; McCarthy et al., 1970). Some of the particulate
mercury returns to the earth's surface as dry fallout.
Wind velocity and direction, temperature, and solar insolation
appear to affect the atmospheric concentration of mercury. Smog may
230
-------
also have an effect and sometimes coincides with high mercury
concentrations (Krenkel, 1973). Therefore, atmospheric mercury
residence time is variable, depending on weather conditions.
7.3.2 Mobility and Persistence in Hater
Mercury is largely removed from water by adsorption on clay-rich
sediments, hydrous oxides of iron and manganese, and by algae and
plankton (Fleischer, 1970). Removal from water also depends on the
volatility and solubility of the forms present (see Section 2.0). The
levels of mercury tend to be kept near normal background concentrations
except at points of actual mercury discharge.
Mercury accumulates in sediments due to its high reactivity with
particulates and physical characteristics conducive to high sedimentation
rates (Lindberg and Harriss, 1974). The concentration of mercury in
sediments correlates strongly with the organic content and the amount
of fine particulates (Klein, 1973). Methylation by organic materials
accelerates its release into the water and its vaporization into the
atmosphere.
Usual conditions of temperature and pressure occurring in river
and lake water and water-saturated sediment allow the presence of
mercury in one or more of three oxidation states (Hem, 1970). The metal
in a chemical sense is the most reduced, whereas the other forms are
mercurous and mercuric ions. Predominant inorganic mercury forms depend
on chloride concentration and pH (Hahne and Kroontje, 1973). Above
pH 5 the predominant mercury form in solution is undissociated mercury.
The solubility of mercury in oxygenated water containing high chloride
concentrations may be greatly increased by the formation of the
231
-------
-2 '
unchanged HgCl2 complex or anionic complexes such as HgCl^" (Hem,
1970) (see Section 2.0).
Mercury is probably transported primarily in the suspended load
of rivers. According to reports on mobilization of metals in the
Rhine River (de Groot and de Goeij, 1971), mercury remains fixed to
the suspended matter as long as there is no interference from tidal
areas. Under the influences.of the sea, mercury is mobilized, going
into solution in the surrounding water as organometallic complexes.
Chloride concentrations of the water may influence the mobility of
mercury in the sediments, since more mercury is adsorbed on the
particles if chloride content is high (Krenkel, 1973; de Groot and
de Goeij, 1971). Biological methylation may be a significant factor
in the mobilization of mercury from deposits in bottom sediments and
its eventual release into the general environment (Kazantzis, 1971).
7.3.3 Mobility and Persistence in Soiils
Mercury binds strongly to humic substances, particularly those
with S and SH function groups. Due to this high affinity for organic
matter, leaching of mercury from many soils may be retarded (Page,
1974; Goldwater and Clarkson, 1972). Soils high in organic matter
carry appreciably more mercury than soils low in organic matter (Warren
and Delavault, 1969; Jonasson and Boyle, 1971). Andersson (1967) found
a direct relationship between soil organic matter content and mercury
content. The mercury content of the organic constituent of soil was
1,100 ng/g of humus, while the corresponding content of the mineral
component was 80 ng/g. Eriksson (1967) has estimated values of 1,000
ng/g for soils rich in organic matter. Klein (1973) determined a
232
-------
correlation of 0.86 between mercury content and organic content of soil.
Greater amounts of mercury are adsorbed on humus at low pH levels.
As pH increases, more mercury is adsorbed by the mineral fraction
(D'ltri, 1972; Krenkel, 1973; Rissanen and Mittinen, 1972). Increasing
salinity decreases the mercury complexing capacity of humic soils
(Krenkel, 1973; Lindberg and Harriss, 1974).
In surface soils mercury may be lost as volatile mercury (Page,
1974). An increase in soil moisture content decreases the rate of
vaporization (Kimura and Miller, 1964). Elemental mercury may also
form under reducing conditions.
Both metallic mercury and many mercury compounds are metabolized
by microorganisms (see Section 3.0). Aerobic bacteria can convert
metallic mercury to either methyl or dimethyl mercury by way of the
mercurous ion. Under acidic conditions dimethyl mercury is converted
\
to monomethylmercury. Demethylation by anaerobic bacteria occurs in
anoxic sediments (Mitchell, 1974). Bacterial conversion to methyl-
mercury is said to be prevented by maintaining a pH above 10 (Dean .,
et al., 1971).
Methylmercury compounds are slowly removed from soil by rainwater,
plants, and evaporation (Rissanen and Miettinen, 1972). Five months
after application of methylmercury dicyandiamide 51 to 53 percent has
been found in the soil (Sana et al., 1970). Kimura and Miller (1964)
investigated soil losses of ethyl and phenylmercury compounds. After
a 28-day period following application, 83 to 93 percent of the
phenylmercury acetate remained in the soil. Sixty-eight to 79 percent
of the ethylmercury acetate remained after a 53-day period.
233
-------
7.4 REFERENCES
1. Andersson, A., 1967. "Mercury in Swedish Soils," Qikos
(Copenhagen), Supplement 9;13-14.
2. Bothner, M. H., and D. Z. Piper, 1973. "The Distribution of
Mercury in Sediment Cores from Bellingham Bay, Washington," UK
Mercury in the Western Environment, Buhler, D. R. (ed.), Oregon
State University, Corvallis, pp. 34-44.
3. Bradford, G. R., F. L. Bair, and V. Hunsaker, 1971. "Trace and
Major Element Contents of Soil Saturation Extracts," Soil Sci.,
U2_(4): 225-230.
4. Damiani, V., and R. L. Thomas, 1974. "Mercury in the Sediments
of the Palanza Basin," Nature, 251:696-697.
5. Dean, R. B., R. T. Williams, and R. H. Wise, 1971. "Disposal
of Mercury Wastes from Water Laboratories," Environ, Sci. Tech.,
5.( 10): 1044-1045. \
6. De Groot, A. J., and J.J.M. de Goeij, 1971. "Contents and
Behavior of Mercury as Compared with Other Heavy Metals in
Sediments from the Rivers Rhine and Ems," Geologic en Minjnbower,
(Rotterdam), 50(3):393-398.
7. D'ltri, F. M., 1972. "Sources of Mercury in The Environment," in:
Environmental Mercury Contamination, Hartung, R., and B. Dinman
(eds.), Ann Arbor Science Publishers, Inc., Ann Arbor, Mich.,
pp. 5-25.
234
-------
8. D'ltri, F. M., 1972. The Environmental Mercury Problem, CRC Press,'
Cleveland, 124 pp.
9. Eriksson, E., 1967. "Mercury in Nature", Oikos (Copenhagen),
Supplement 9_» 13.
10. Federal Register, Oct. 25, 1974. 39_(208).
11. Fleischer, M., 1970. "Summary of the Literature on the
Geochemistry of Mercury, "Mercury in The Environment, U.S. Geological
Survey Professional Paper 713, U.S. Govt. Printing Office,
'Washington, D.C., pp. 6-13.
12. Flinn, J. E., and R. S. Reimers, 1974. Development of Predictions
of Future Pollution Problems, U.S. Environmental Protection Agency,
Washington, D.C., EPA-600/5-74-005, 207 pp.
13. Friberg, L., and J. Vostal, 1972. Mercury in the Environment: A
Toxicological and Epidemiological Appraisal, CRC Press, Cleveland,
215 pp. ',
14. Fukunaga, K., Y. Tsukano, and J. Kanazawa, 1972. "Residue Analysis
of Organomercury Fungicides Sprayed on Rice Plants," in: Environmental
Toxicology of Pesticides, Matsamura, F., G. M. Boush, and T. Misato
(eds.), Academic Press, New York, pp. 177-189.
15. Goldwater, L. J., and T. W. Clarkson, 1972. "Mercury," UK Metallic
Contaminants and Human Health, Lee, D.M.K. (ed.), Academic Press,
New York, pp. 17-56.
16. Hahne, H.C.N., and W. Kroontje, 1973. "The Simultaneous Effect of
pH and Chloride Concentrations upon Mercury (II) as a Pollutant,"
Proc. Soil Sci. Soc. Am.. 37:838-843.
235
-------
17. Hem, J. D., 1970. "Chemical Behavior of Mercury in Aqueous Media,"
JJT_: Mercury in The Environment, Geological Survey Professional
Paper 713, U.S. Govt. Printing Office, Washington, D.C., pp. 19-24.
18. Jenne, E. A., 1970. "Atmospheric and Fluvial Transport of Mercury,"
in: Mercury in The Environment, Geological Survey Professional
Paper 713, U.S. Govt. Printing Office, Washington, D.C., pp. 40-45.
19. Joensuu, 0. I., 1971. "Fossill Fuels as a Source of Mercury
Pollution," Science, 172:1027-1028.
20. Jonasson, I. R., and R. W. Boyle, 1971. "Geochemistry of Mercury,"
in: Mercury in Man's Environment, Roy. Soc. Can., Ottawa, pp. 5-21.
21. Kazantzis, G., 1971. "The Poison Chain for Mercury in the
Environment," Int. J. Environ. Studies, 1_:301-306.
22. Kimura, Y., and V. L. Miller, 1964. "The Degradation of
Organomercury Fungicides in Soil," Agr. and Food Cheiii., 12(3): 253-257.
23. Klein, D. H., 1971. "Sources and Present Status of the Mercury
Problem," in: Mercury in the Western Environment, Bubler, D. R.
(ed.), Oregon State University, Corvallis, pp. 3-15.
24. Klein, D. H., 1972a. "Some Estimates of Natural Levels of Mercury
in the Environment," inj Environmental Mercury Contamination,
Hartung, R., and B. Dinman (eds.), Ann Arbor Science Publishers, Inc.,
Ann Arbor, Mich., pp. 25-29.
25. Klein, D. H., 1972b. "Mercury and Other Metals in Urban Soil,"
Env. Sci. Tech., 6(6):560-562.
236
-------
26. Klein, D. H., 1973. Mercury in The Environment, U.S. Environmental
Protection Agency, Washington, D.C., Report No. EPA-660/2-73-008,
pp. 1-23.
27. Krenkel, P. A., 1973. Mercury Environmental Considerations, Part I,
CRC Press, Cincinnati, pp. 303-373.
28. Lindberg, S. E., and R. C. Harris, 1974. "Mercury-Organic Matter
Associations in Estuarine Sediments and Interstital Water,"
Env. Sci. Tech., 8(5):459-462.
29. McCarthy, J. H., Jr., J. L. Mueschke, W. H. Ficklin, and
R. E. Learned, 1970. "Mercury in the Atmosphere," in: Mercury in
The Environment, Geological Survey Professional Paper 713, U.S.
Govt. Printing Office, Washington, D.C., pp. 37-39.
30. Mitchell, R., 1974. Introduction to Environmental Microbiology,
Prentice-Hall, Inc., Englewood, 355 p.
31. Page, A. L., 1974. Fate and Effect's of Trace Elements in Sewage
When Applied to Agricultural Lands, U.S. Environmental Protection
Agency, Cincinnati, Report No. EPA-670/2-74-005, 96 p.
32. Pierce, A. P., J. M. Botkol, and R. E. Learned, 1970. "Mercury
Content of Rocks, Soils, and Stream Sediments," in: Mercury in The
Environment, U.S. Geological Survey Professional Paper 713, U.S.
Govt. Printing Office, Washington, D.C., pp. 14-16.
33. Rissanen, K., and J. K. Miettinen, 1972. "Use of Mercury Compounds
in Agriculture and its Implications," in: Mercury Contamination in
Man and His Environment. International Atomic Energy Agency, Vienna,
Technical Reports Series No. 137, pp. 5-34.
237
-------
34. Ross, R. G., and D.K.R. Stewart, 1962. "Movement and Accumulation '
of Mercury in Apple Trees and Soil," Can. J. Plant Sci., 42_:280-285.
35. Sana, J. G., Y. W. Lee, R. D. Tinline, S.H.F. Chinn, and
H. M. Austenson, 1970. "Mercury Residues in Cereal Grains from
•, Seeds or Soil Treated with Organomercury Compounds," Can. J. Plant
Sci., 50_:597-599.
36. Sana, J. G., 1972. "Significance of Mercury in The Environment,"
Residue Reviews, 42_: 103-163.
37. Stahl, Q. R., 1969. Preliminary Air Pollution Survey of Mercury
and its Compounds, National Air Pollution Control Administration,
Raleigh, N.C., Publication No. APTD 69-40, 96 p.
38. U.S. Environmental Protection Agency, 1971. Background Information -
Proposed National Emission Standards for Hazardous Air Pollutants :
Asbestos. Beryllium, Mercury, Office of Air Programs, Raleigh, N.C.,
Publication No. APTD-0753, 28 p.
39. U.S. Environmental Protection Agency, 1972. Control of Mercury
Pollutions in Sediments, Environmental Protection Technology Series,
Washington, D.C., EPA-R2-72-043, pp. 1-55.
40. U.S. -Environmental Protection Agency, 1973. Proposed Water Quality
Information, Vol. II., Washington, D.C., 164 pp.
41. U.S. Geological Survey, 1970. Mercury in The Environment,
Geological Survey Professional Paper 713, U.S. Govt. Printing
Office, Washington, D.C., pp. 1-5.
42. Warren, H. V., and R. E. Delavault, 1969. "Mercury Content of
Some British Soils," Oikos (Copenhagen), 20(2):537-539.
238
-------
43. Weiss, H. V., M. Koide, and E. D. Goldberg, 1971. "Mercury in a
Greenland Ice Sheet: Evidence of Recent Input by Man," Science,
174:692-694.
44. Wershaw, R. L, 1970. "Sources and Behavior of Mercury in Surface
Waters," in; Mercury in The Environment, Geological Survey
Professional Paper 713, U.S. Govt. Printing Office, Washington, D.C.,
pp. 29-31.
45. Wiersma, G. B., and H. Tai, 1974. "Mercury Levels in Soils of the
Eastern United States," Pest. Monit. J., 7(3-4):214-216.
239
-------
8.0 ENVIRONMENTAL INTERACTIONS AND THEIR CONSEQUENCES
8.1 SUMMARY
Mercury enters the environment from natural sources, industrial
effluents, and consumer use, misuse, and disposal of products containing
mercury (D'ltri, 1972). More than 70 percent of the mercury consumed in
the United States (about 33 percent of the world production) is lost to
the environment (Saha, 1972).
Environmental mercury is widely dispersed through air, soil, water,
and the biosphere (Figure 8.1). Mercury compounds cycle indefinitely
among air, water, and land by the processes of methylation, evaporation,
precipitation, and solution.
At present the most serious consequence of mercury contamination of
the environment is the transformation of the mercuric ion to methylmercury
and its incorporation into the food chain.
8.2 PRODUCTION AND USES
The consumption of mercury according to uses in the United States
from 1967 to 1971 is shown in Table 8.1. In 1968, 36 percent of the ..
United States supply of mercury came from United States mining, 24 percent
from Government stockpile releases, 22 percent from net imports, and
18 percent from recycled material. A decrease in demand for mercury has
been forecasted in agricultural uses, electrolytic preparation of chlorine
and soda, installation and expansion of chloralkali industries, paints,
and paper pulp manufacture (see Table 8.2).
8.2.1 Primary Industrial Sources
The largest source of commercial discharges of mercury during 1968
was from inventory losses suffered by chloralkali industries. However,
240
-------
ATMOSPH
COASTAL | e t
DEEP SEA
SEOIMtNT
M-icc'0 c
CONTINENTAL
SHELF
Figure 8.1 THE CYCLE OF MERCURY IN NATURE.
(Dots represent sources and
arrowpoints are the sink for
each route. Numbers on the
routes are tons per day.
Residence time in years (y)
and months (m) are above each
entity. Immobilized tonnage
(metric, t) is indicated below
each entity.)
Source:
Kothny (1973).
241
-------
Table 8.1. MERCURY CONSUMED IN THE UNITED STATES BY USES
1X3
-P>
rxi
Consumption
Use
Agriculture (includes fungicides and bactericides
for industrial purposes)
Amalgamation
Catalysts
Dental preparations
Electrical apparatus
Electrolytic preparation of chlorine & caustic soda
General laboratory uses
Industrial & control instruments
Paint:
Antifoul ing
Mildev/ proofing
Paper & pulp manufacture
1967
3,732
219
2,689
1,359
14,610
14,306
1,133
3,865
152
7,026
446
1968
3,430
267
1,914
2,089
17,484
17,458
1,246
3,935
392
10,174
417
, flasks (76 pounds)
- 1969
2,689
195
2,958
3,083
18,650
20,720
2,041
6,981
244
9,486
588
1970
1,812
216
2,041
1,799
15,789
14,977
1,513
4,035
193
8,771
316
1971
1,477
a
1,141
2,387
16,938
12,262
1,809
4,871
414
8,191
a
-------
Table 8.1. MERCURY CONSUMED IN THE UNITED STATES BY USES (cont'd)
ro
-p>
CO
Consumption,
Use
Pharmaceuticals
Redistilled13
Other0
Total known uses
Total uses unknown
Grand total
1967
283
7,129
12,568
69,517
--
69,517
1968
424
8,247
7,945
75,422
--
75,422
flasks (76 pounds)
1969
724
—
9,689
78,048
1,056
79,104
1970
571
6,521
58,554
2,936
61,490
1971
682
2,300
52,472
3
52,475
Notes:
aWithheld to avoid disclosing individual company confidential data; included with "Other".
"Redistilled" used in industrial instruments, dental preparations, and electrical apparatus.
Figures for the Redistilled category are not available after 1969, but have probably been
broken down and added to the figures of the individual use categories.
c"0ther" includes mercury used for installation and expansion of chloralkali plant.
Source:
U.S. Environmental Protection Agency (1973).
-------
Table 8.2. TRENDS IN USES OF MERCURY OVER
THE PERIOD 1967 to 1971
Use
Decreasing level of
Agriculture
Catalysts
Electrolytic preparation of chlorine
and soda
Other uses3
Subtotal
No significant changes
Dental preparations
Electrical apparatus
General laboratory uses
Industrial and control instruments
Paints
Pharmaceuticals
Subtotal
Grand total
1971
Flasks
consumption
1,477
1,141
12,262
2,300
17,180
in consumption
2,387
16,938
1,809
4,871
8,605
682
35,292
52,472
Consumption
Percent of total
2.8
2.2
23.4
4.4
32.8
4.5
32.3
3.4
9.3
16.4
1.3
67.2
100.0
Note:
aOther uses include mercury used for installation and expansion of
chloral kali plants, amalgamation, and in paper and pulp manufacture.
Source:
U.S. Environmental Protection Agency (1973).
244
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monitoring by the Department of Interior determined the overall level of
mercury emission to receiving waters had dropped 86 percent from 287
pounds/day in July to 40 pounds/day in September, 1970 (U.S. Environmental
Protection Agency, 1973).
Currently, the major problem associated with the chloral kali industry
is the safe disposal of the mercury containing brine sludges. These
losses are estimated to be 12,500 pounds annually via 58,000 tons of
brine sludges.
Other man-made sources of environmental mercury include:
1. mine tailings and vapor released by the mining and
smelting of mercury (estimated 31 tons annually),
2. smelting of tin, zinc, copper, and gold (estimated
10 Ib/day/smelter),
3. combustion of paper products and fossil fuel
(estimated 550 tons annually) (U.S. Environmental
Protection Agency, 1973).
8.3 ENVIRONMENTAL CYCLING OF MERCURY
The principal pathways of mercury contamination and environmental
movement are shown in Figure 8.2. Mercury enters the atmosphere in both
vapor and particulate forms. Sources of mercury vapor include degassing
of the earth's crust, methylation of inorganic mercury by microorganisms,
and improper use and disposal of mercury by man. Mercury in particulate
form originates from combustion, with coal serving as the primary source
(U.S. Environmental Protection Agency, 1972).
245
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Agriculturol Hg compounds
ogents in industry
Hg metal
in industry
Hg Other uses
metallurgy ot Hg metal
Medicaments
cosmetics
• Dusting —
- Spraying -
-Tilling —
5
--Wastes- 1 i- Vapor
r-Contact-J r- Wastes —
' rAmalgamsJ
I 1
j !_,
1 1 1_
q
L
ftir
\
Spillage
Vapor —
Wastes
I—Spillage
I -Vapor—J
Objects
=^-Crops
External use
Ingestion
Excreta —
Figure 8.2 PRINCIPAL PATHWAYS OF MERCURY
CONTAMINATION AND ENVIRONMENTAL
MOVEMENT.
Source:
Fishbein (1973).
246
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8.3.1 Air
Once in the air, mercury is widely distributed by wind currents. The
atmospheric concentration and residence time of mercury are variable and
j
depend on factors such as wind speed and duration, temperature, and
barometric pressure. Mercury eventually leaves the atmosphere and
recontaminates land or water surfaces by particulate fallout or pre-
cipitation.
8.3.2 Soil
The soil is an environmental sink for mercury from the natural
processes of dustfall, precipitation, plant and animal decay, and erosion
of bedrock. In recent years, man-made contamination has also increased,
primarily through waste dumping and the use of organomercuric chemicals
in agriculture.
Mercury added to normal soils usually stays in the upper horizons
and is slowly mobile. Some of the mercu'ry is converted by soil microbes
into more soluble or volatile forms and is removed by plant uptake,
leaching, runoff, and evaporation. The rate of removal depends on soil
moisture content, pH, and organic matter content, oxygen content, and
other factors.
8.3.3 water
Aqueous systems receive mercury from soil waters, industrial wastes,
and the atmosphere. Mercury in aqueous systems is primarily removed by
combination with suspended matter and accumulation in bottom sediments.
However, inorganic mercury in sediments or water can be converted by
bacteria to highly toxic methyl and dimethylmercury. Dimethylmercury
reenters the atmosphere by evaporation. Methylmercury is water soluble
247
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and is readily taken up by tissues of aquatic organisms where it may
accumulate (Wood, 1972).
8.3.3.1 Effects of Industrial Haste Contamination—Results from a series
of methylation studies on sediment samples from a 26-mile section of a
river in Canada receiving wastes from a chloral kali plant and on goldfish
maintained in this river'are shown in Table 8.3 (Langley, 1973).
Methylation rates varied from 0.12 to 4.83 ng Hg/wk/sq cm. The control
fish contained an average of 25 ng/g methylmercury with a standard
deviation of 5.1. Fish containing greater than 30 ng/g were assumed to
have taken in methylmercury. Cell fine which showed the highest rate of
methylation yielded a much greater number and variety of bacteria than
other cells.
The cells holding the fish were monitored regularly for dissolved
oxygen, temperature, and pH. Controls were used to determine background
<
I
levels.
Table 8.4 shows the results of similar experiments in areas where
the mercury-contaminated sediments were sealed off with fluorspar tail'tngs.
Langley concluded that environmental mercury methylation is too slow to
permit a natural rehabilitation through purging of contaminated sediments,
possibly requiring many decades to return to normal levels, and that
sealing off mercury-contaminated sediments shows promise as a rehabilitation
measure.
8.4 FOOD CHAINS
As mercury cycles through the environment, it may be incorporated
into food chains (Figure 8,3). This is particularly important in aquatic
systems, since fish constitutes a large portion of many people's diet.
248
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Table 8.3. METHYLMERCURY UPTAKE BY FISH
Amount MeHg
uptake by fish
Location
Control upstream
Outfall
0.4 mile
3 mile
8 mile
26 mile
Outfall ditch
Cell
no.
1
2
3
4
5
6
7
Total Hg
in surface
sediment
(mg/1 Hg)
0.1
15.6
68.1
6.4
3.8i
0.1
9.2
During
5 wk
(ng)
220a
252
300
372
744
104
24
Calculated
weekly
average
(ng/ Hg/sq/cm)
1.43
1.31
1.56
1.93
4.83
0.54
0.12
Notes:
Miles X 1.6 = km.
10 fish/cell.
aUptake value for 4 wk only.
Source:
Langley (1973).
249
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Table 8.4. EFFECT OF FLUORSPAR TAILINGS DEPOSITION
ON METHYLMERCURY UPTAKE
Note:
Miles x 1.& = km.
Source:
Langley (1973).
Methyl mercury uptake
by fish
Location
Outfall
0.4 mile
Cell
no.
2
2a
2b
2c
2d
3
3a
3b
3c
3d
Depth of
fluorspar
deposit
(cm)
0.0
0.5
2.0
5.0
10.0
0.0
0.5
2.0
5.0
10.0,
During
5 wk
(ng.
Hg)
252
90
32
16
56
300
84
56
60
54
Calculated
v/eekly
average
(ng Hg/sq cm)
1.31
0.47
0.17
0.08
0.29
1.56
0.44
0.29
0.31
0.28
250
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decay
en
Fish
Animal Feed
Capture
Farm Animals
Food Products
Fish for Eating
Other Food Products
Man
Microorganisms Methyl mercury Solution'
decay
Birds
Algae, Plankton, Insects,
Other Aquatic Life
Figure 8.3 A SIMPLE FOOD CHAIN
'Source:
Fishbein (1973).
-------
Plankton take up methyl mercury by passive absorption. Fish accumulate
methylmercury directly through their food, which is mainly plankton, or
through their gills. Predatory or carnivorous fish usually have the
highest mercury levels. Bottom-feeding fish concentrations are some-
what lower, and plankton-feeding fish are almost always below the 0.5 ppm
FDA limit (Krenkel, 1973). Species of fish that breathe faster and eat
more, such as tuna, accumulate more mercury in their lifetime than do
other fish (Waldbott, 1973). Mercury concentrations in fish muscle can
be 3,000 times- that of the surrounding water (Saha, 1972). The potential
for mercury concentration in aquatic life has been estimated to be on the
order of 1,000 times for freshwater macrophytes and phytoplankton, 1,000
times for fish, and 100,000 times for freshwater invertebrates (Krenkel,
1973).
Terrestrial food chains have also been contaminated with mercury,
i
primarily by agricultural chemicals. Since the 1940's the increased use of
organomercuric fungicides and pesticides has added to the mercury con-
tamination of soils and plants. The use of these chemicals has also ••
resulted in elevated residues in game birds (Rissanen and Miettinen,
1972; McEwen et al., 1973). The extensive use of alkyl mercurials for
seed dressing has been hazardous to wildlife and humans. Some of the
effects reported for wildlife are increased mortality and a high fre-
quency of fetal malformations. After the use of alkyl mercurials as seed
dressing was condemned in Sweden, tissue levels of mercury in seed-eating
birds and their predators immediately decreased substantially (Friberg
and Vostal, 1972). Human mercury poisonings have been reported in Iraq,
252
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Pakistan, and Guatemala as a result of the ingestion of mercury-treated
grain. An American family suffered mercury poisoning after eating
meat from a hog which had been fed mercury-treated grain.
Small amounts of mercury are found naturally in all foodstuffs;
therefore, man is exposed to mercury by virtually all the food he
ingests. In general, the average level of mercury of food is 20 ppb
(Friberg and Vostal, 1972), which is below the Federal Drug Administration
limit. The direct human health hazard regarding food appears to be
limited to those persons for whom fish composes the major portion of
their diet (Peakall and Lovett, 1972), or who ingest food that has been
treated with unusually high levels of mercuric chemicals.
8.5 REFERENCES
1. Fishbein, L., 1973. Chromatography of Environmental Hazards,
Vol. 2, Elsevier Scientific Publishing Company, New York,
i
p. 144.
2. Friberg, L., and J. Vostal, 1972. Mercury in the Environment: A
Toxicological and Epidemiological Appraisal, CRC Press,
Cleveland, 215 pp.
3. Kothny.'E. L., 1973. "The Three-Phase Equilibrium of Mercury
in Nature," j_n_: Trace Contaminants in the Environment. Kothny, E. L.
(ed.), American Chemical Society, Washington, D.C., p. 54.
4. Krenkel, P. A., 1973. Mercury Environmental Considerations,
Part 1, 'CRC Critical Reviews in Environmental Control, CRC Press,
Cleveland, Ohio, pp. 303-373.
253
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5. Langley, D. G., 1973. "Mercury Methylation in an Aquatic
Environment," J. Hater Pol. Control. Federation. 45jl):44-50.
6. McEwen, L. C., R. K. Tucker, J. 0. Ells, and M. A. Haegele,
1973. "Mercury-Nildlife Studies by the Denver Wildlife Research
Center," UK Mercury in the Western Environment, Buhler, D. R. (ed.),
Oregon State University, Portland, Oregon, pp. 146-156.
7. Peakall, D. B., and R. J. Lovett, 1972. "Mercury: Its
Occurrence and Effects in the Ecosystem," BioScience, 22(l):20-25.
8. Rissanen, K., and J. K. Miettinen, 1972. "Use of Mercury Compounds
in Agriculture and its Implications," in: Mercury Contamination in
Man and His Environment, Technical Reports Series No. 137,
International Atomic Energy Agency, Vienna, pp. 5-34.
9. Sana, J. G., 1972. "Significance of Mercury in the Environment,"
Residue Reviews, 42_: 103-163.
i
10. U.S. Environmental Protection Agency, 1972. Control of Mercury
Pollutions in Sediments, Environmental Protection Technology Series,
Washington, D.C., EPA-R2-72-043, pp. 1-55.
11. U.S. Environmental Protection Agency, 1973. National Disposal Site
Candidate Waste Stream Constituent Profile Reports - Mercury.
Arsenic, Chromium, and Cadmium Compounds, Vol. VI. (Draft), TRW
Systems Group, Report No. 21485-6013-RU-OO, 212 pp..
12. Waldbott, G. S., 1973. Health Effects of Environmental Pollutants,
The G.U. Mosby Company, St. Louis, Missouri, pp. 139-149.
13. Wood, J. M., 1972. "A Progress Report on Mercury," Environment,
14(l):33-39.
254
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