EPA-570/9-79-012
A PRELIMINARY ASSESSMENT OF
SELENIUM IN DRINKING WATER
July 1979
FINAL REPORT
THE MITRE CORPORATION
Metrek Division
McLean, Virginia 22102
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DISCLAIMER
This report has been reviewed by the Office of Drinking Water,
U.S. Environmental Protection Agency, and approved f or publication.
Approval does not signify that the contents necessarily reflect the
views and policies of the U.S. Environmental Protection Agency, nor
does mention of trade names or commercial products constitute en—
dorseinent or recommendation for use.
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EPA-570/9-79-012
July 1979
A PRELIMINARY ASSESSMENT OF
SELENIUM IN
DRINKING WATER
by
J. Konz
The MITRE Corporation
Metrek Division
1820 Dolley Madison Boulevard
McLean, Virginia 22102
Contract No. 68-01-4635
Project Officer
Charles L. Trichilo, Ph.D.
Criteria and Standards Division
Office of Drinking Water
U.S. Environmental Protection Agency
Washington, D.C. 20460
Criteria and Standards Division
Office of Drinking Water
U.S. Environmental Protection Agency
Washington, D.C. 20460
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ABSTRACT
The current interim primary drinking water standard for selen —
ium is undergoing review. As part of that effort, this study defines
the major environmental sources of selenium exposure, identifies that
portion of an individual ’s total daily selenium uptake arising from
the consumption of drinking water, evaluates the toxicological sig—
nificance of such uptake, and assesses the adequacy of the current
standard in protecting the public health.
This preliminary review is intended to assist the Office of
Drinking Water/EPA in defining a priority sequence for the inorganic
contaminant standards review process. The data compiled in this
document were obtained prior to June 1978.
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ACKNOWLEDGEMENT
The author wishes to thank Dr. Charles L. Trichilo for his
continuous support and encouragement during the preparation of this
document.
This document was reviewed in final draft form by Dr. Paul
M. Newberne, Massachusetts Institute of Technology.
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TABLE OF CONTENTS
Page
List of Figures vi
List of Tables vi
EXECUTIVE SUMMARY ‘vii
1.0 INTRODUCTION 1
1.1 Background 2
1.2 Approach 3
2.0 ENVIRONMENTAL SOURCES OF SELENIUM EXPOSURE 5
2.1 Selenium Concentrations in Ambient Air 7
2.2 Selenium Concentrations in the Diet 9
2,3 Selenium Content in Drinking Water 9
2.4 Other Sources of Exposure 13
3.0 ABSORPTION, RETENTION AND ELIMINATION OF SELENIUM
IN HUMANS 14
3.1 Absorption Characteristics 14
3.1.1 Pulmonary Absorption 15
3.1.2 Gastrointestinal Absorption 15
3.1.3 Dermal Absorption 16
3.2 Retention Characteristics 16
3.3 Elimination Characterstics 18
4.0 TOXICITY 21
5.0 SOURCE CONTRIBUTIONS TO DAILY SELENIUM UPTAKE IN
HUMANS 26
5.1 Approach 26
5.2 Basic Assumptions 27
5.3 Estimated Daily Selenium Uptake from All Sources 29
5.4 Significance of Current Standard 33
5.5 Information Needs 34
6.0 REFERENCES 35
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LIST OF FIGURES
Figure
Number Page
2—1 DISTRIBUTION OF SELENIFEROUS VEGETATION 6
LIST OF TABLES
Table
Number Page
2—1 SELENIUM CONTENT OF AMBIENT AIR 8
2—2 SELENIUM CONTENT OF FOODSTUFFS 10
2—3 MAXIMUM SELENIUM CONCENTRATIONS REPORTED IN
DRINKING WATER SUPPLIES 12
3—1 SELENIUM IN HUMAN TISSUES, ppm WET WEIGHT 17
5—1 BASIC ASSUMPTIONS EMPLOYED IN THE CALCULATION
OF INDIVIDUAL SOURCE CONTRIBUTION FACTORS 28
5—2 REPRESENTATIVE ENVIRONMENTAL SELENIUM EXPOSURE
LEVELS 30
5—3 CALCULATION SEQUENCE IN DETERMINING SOURCE
CONTRIBUTION FACTORS 31
5—4 ESTIMATED DAILY SELENIUM UPTAKE 32
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EXECUTIVE SUMMARY
The Mitre Corporation/Metrek Division has been assisting the
Criteria and Standards Division, Office of Drinking Water, U.S.
Environmental Protection Agency in an assessment of the adequacy of
the current standard for selenium in drinking water. This report is
a preliminary review of the current selenium standard, and is intend-
ed to assist the Office of Drinking Water in defining a priority se-
quence for the inorganic contaminant standards review process.
Selenium is ubiquitous in the environment; it is present in
all rocks, soils, plants and animals. The major source of selenium
in the environment is the weathering of rocks. Large areas of the
Midwest and West contain high natural concentrations of selenium in
the soil. Anthropogenic inputs appear to be minor and confined to
the Immediate vicinity of the source. Most (62 percent) of the
selenium entering the environment from man’s activities can be traced
to coal combustion.
A major use of selenium is in the electronics industry. Xero-
graphy is becoming a major use due to the photoconducting properties
of selenium. Selenium also finds applications in the glass and
chemicals industries and as a nutritional additive in animal feeds.
The average concentration of selenium in the atmosphere appears
to be well below 0.01 g/m 3 . The maximum daily intake from air has
been reported as 0.07 big/day. The literature provides no indication
that pollution of the air by selenium is a problem at this time.
Food represents the major source of selenium intake for man.
The usual dietary intake averages 170 J.g/day, but can vary widely due
to dietary preferences. Sea foods (especially shrimp), meat, milk
products and grains provide the largest amounts of selenium in the
diet; fruits and vegetables contain relatively small amounts.
Drinking water rarely contains selenium at levels above a few
micrograms per liter. Most of the analyses reported are well below
the current standard of 10 ig/l. However, selenium is easily leached
from soils resulting in high selenium content of some ground water
supplies. Levels as high as 12,000 g/l have been reported in well
water in isolated cases. Toxic symptoms (e.g., depression, pallor,
nervousness, gastrointestinal disturbances, dermatitis and garlic
odor of breath and perspiration) have been noted in individuals
drinking water containing these high concentrations.
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Selenium can be absorbed into the body via ingestion, inhalation
and through dermal contact. The only significant exposure route
under ambient conditions is ingestion. Selenium is rapidly and
efficiently absorbed from the gastrointestinal tract and is widely
distributed to all body tissues. There does not appear to be any
extensive accumulation in the tissues under normal circumstances.
The major excretory route for selenium in man is the urine.
Other routes include feces, breath and perspiration.
The absorption, retention and distribution of selenium within
the body and the amounts, forms and routes of excretion are functions
of the chemical forms and amounts ingested as well as of the dietary
levels of other elements such as arsenic, cadmium, sulfur and mer-
cury. Within certain physiologic limits, the body appears to have a
hLraeostatic mechanism for retaining trace amounts of selenium and ex—
.reting the excess.
Selenium is an essential trace element but can be toxic at high
concentrations. Chronic selenosis has been reported in humans
drinking water containing 9 ppm selenium. This is characterized by
bad teeth, jaundice, chloasma, vertigo, chronic gastrointestinal
disease, dermatitis, nail and hair changes, arthritis, edema, lassi-
tude and fatigue. Epidemiological evidence indicates that selenium
may increase the incidence of dental caries in children. It has
been suggested that selenium may be a teratogen in man.
Selenium is also recognized as an essential element at trace
levels. Its metabolic role concerns membrane elasticity, hence it is
involved in the production and maintenance of membranes. Other
studies indicate that selenium may influence the synthesis of gluta—
thione and protein. Additional evidence suggests that selenium may
have therapeutic value against cancer in man. Selenium is also pro-
tective against cadmium toxicity.
To determine whether the current drinking water standard is
adequate, an evaluation of selenium content from the different
sources is necessary. Ambient exposure levels and absorption rates
for each exposure route are used to estimate total daily uptake.
Food is the major source of selenium. Somewhat more than 90
percent of the daily uptake can be attributed to this source, de-
pending on the level assumed to be contributed by water. At the
current interim drinking water standard of 10 pg/i, water would
contribute approximately 10 percent of the daily selenium uptake. No
good national estimates of selenium concentrations in drinking water
viii
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are available. However, most reported values are below the current
standard. Since most of the waters analyzed contained a much lower
concentration, water actually contributes less than 10 percent of the
total daily uptake. In certain instances, drinking water can be the
major source of selenium, however. In those cases where well water
samples contained from 9,000—12,000 p.g/l selenium, it would be
expected that approximately 99 percent of an individual’s daily
selenium uptake could be attributed to drinking water.
The current uptake of selenium under normal conditions appears
to be approximately 200 ig/day. Since toxic symptoms have been
observed at levels as low as 600 kg/day, the current uptake represents
a safety factor of only three. However, since neither deficiency nor
toxicity have been reported at the 200 1 j.g/day level, it is believed
that the current uptake is in the required range.
A characteristic of selenium is the rather narrow range between
toxicity and nutritional requirement. However, no symptoms of toxic-
ity have been reported at levels generally encountered in the ambient
environment. It appears that selenium deficiency may be a more
serious health problem than selenium toxicity.
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1.0 INTRODUCTION
The Office of Drinking Water (ODW) within the United States
Environmental Protection Agency (EPA) in accordance with the Safe
Drinking Water Act as amended has promulgated National Interim
Primary Drinking Water Regulations for a number of physical, chemi-
cal, biological and radiological contaminants in potable water
systems. Those interim regulations specify maximum contaminant level
(MCLs) for substances in drinking water, and will be replaced by
final Primary Drinking Water Regulations, as more definitive informa-
tion describing the health risks associated with each contaminant is
accumulated and analyzed.
The MITRE Corporation/Metrek Division has been assisting the
Criteria and Standards Division, Office of Drinking Water, in their
assessment of the adequacy of the current standard for selenium in
drinking water*. In this preliminary assessment, the biological
effects of selenium exposure are reviewed, the major environmental
sources of selenium exposure (i.e., air, food, drinking water) are
defined, and a discussion of the adequacy of the current interim
standard is presented.
This initial review of the current selenium standard is being
conducted concurrently with several other contaminants. This docu-
ment is not intended to be a comprehensive assessment of the selenium
standard, but rather a preliminary critique in order to assist
*Current interim selenium standard — 10.0 ig/1.
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the Office of Drinking Water in defining a priority sequence to
be instituted for its inorganic contaminant standards review
process.
1.1 Background
Selenium occurs in several chemical forms in the environment;
i.e., elemental selenium, inorganic complexes (soluble and insoluble
forms) and organic forms. Both availability to biological systems
and toxicity vary depending on the chemical form present. Unfor-
tunately, the literature does not consistently differentiate between
the forms but presents the data based on quantitative analyses of
the total selenium present. Where possible data will be presented
according to chemical form.
Selenium is widely distributed in the environment, occurring
primarily in foods. Some drinking water sources contain selenium at
very high concentrations but the overwhelming majority of drinking
waters sampled have levels well below the current standard. The
amount of selenium in air appears to be insignificant.
Selenium is a paradoxical element; either a deficiency or an
excess produces adverse biological effects. There is a relatively
narrow margin of safety; a few parts per million can be toxic but
trace amounts are required.
There are very few data in the literature which report ad-
verse health effects in man from either a deficiency or an excess
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of selenium. Selenium in water has been the cause of severe sele—
nosis in a few isolated instances where geologic factors produced
high concentrations of selenium in the well water of the area.
Because of the multiple exposure pathways, the interim primary
drinking water standard for selenium is being reviewed and the rela-
tive contributions to an individual’s daily selenium uptake arising
from specific environmental media are being defined. In this way,
if selenium appears to pose a significant health risk as a result of
exposure via daily drinking water intake alone, or if drinking
water intake contributes significantly to the total daily selenium
intake, then an intensive review and analysis of the problem will be
initiated.
1.2 Approach
In order to properly assess the health significance of exposure
resulting from the ingestion of selenium—contaminated drinking water,
it becomes necessary to define an individual’s total daily selenium
uptake from all pertinent sources, to assess the health impacts
associated with that total daily uptake, and to identify that propor-
tion of the total daily uptake arising from the ingestion of drinking
water. In this preliminary assessment, the following sequence of
steps is followed:
• quantify the major environmental sources of selenium exposure;
• determine the absorption/retention/elimination characteris—
tics of those selenium compounds commonly found in the
environment;
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• define the toxicological impacts associated with selenium
exposure, especially the low—level chronic effects;
• develop estimates of total daily selenium uptake in man based
on ambient exposure levels and absorption/retention charac-
teristics;
• assess the public health significance of various levels of
selenium in drinking water, given ambient selenium contamina-
tion in other environmental media.
In developing this report, time constraints would not permit an
exhaustive review of the scientific literature. Review articles were
utilized as information sources when the primary citations were
unavailable. Those instances when critical data were insufficient or
lacking are pointed Out in the text.
This review is intended to be a preliminary assessment of the
current interim primary drinking water standard for selenium. Should
the Office of Drinking Water decide that the selenium standard is
high on its priority standards review list, then a comprehensive
evaluation will be initiated to define the adequacy of the current
interim standard.
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2.0 ENVIRONMENTAL SOURCES OF SELENIUM EXPOSURE
Selenium can be found in all rocks, soils, plants and animals.
It is present in the earth’s crust at an average range of 0.03—0.8
ppm (NAS, 1976). The most commonly accepted average appears to
be 0.09 ppm. Many areas of the United States contain high natural
concentrations of selenium in the soil and in the plants. Figure 2—1
identifies these seleniferous areas.
Natural sources of selenium include weathering of rocks, volcan-
ism, microbial action, volitilization by plants and animals and spray
from large bodies of water (Johnson, 1976). Volcanic activity may be
a significant source of the pollutant in air and soil (NAS, 1976).
Probably the major source of selenium in the environment is the
weathering of natural rock. Natural inputs of selenium appear to be
much more important than those contributed by man’s activities. It
is believed that the impact of any industrial pollution on ambient
selenium levels would be restricted to the immediate vicinity of the
source (NAS, 1976).
Sources of industrial pollution by selenium include mining and
milling; smelting and refining; and the manufacture of glass, steel,
electronic components, and various chemicals. Most of the selenium
entering the environment from anthropogenic sources can be traced to
coal combustion (WHO, 1975; EPA, 1975a). For example, of the
1,215 tons of selenium released to the environment from industrial
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N
FIGURE 2-1
DISTRIBUTION OF SELENIFEROUS VEGETATION
Source: Lansche, 1967, as cited in Stahl, 1969
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sources in 1970, 62% was from coal combustion (NAS, 1976). The
burning of fossil fuels, in general, constitutes a major source of
selenium input to the atmosphere, emitting an estimated 4,000 tons
per year (Lakin, 1973). The burning of other organic matter also
adds selenium to the atmosphere.
2.1 Selenium Concentrations in Ambient Air
A significant amount of the selenium in air probably has a
natural source. At this time the portion attributable to natural
sources cannot be quantified. Pollution from industrial sources
seems to be confined to a small area in the immediate vicinity of
the source. At a distance of 2 km from an electrolytic copper plant,
the selenium concentration dropped from 0.50 ig/m 3 to 0.07 jIg/rn 3 .
At another plant, the concentration fell from 0.39 jig/rn 3 to an un-
detectable level 2 km from the plant (NAS, 1976).
The average concentration of selenium in ambient air is probably
well below 0.01 jig/ni 3 . It seems unlikely that pollution of the air
by selenium is a problem at this time (NAS, 1976). Table 2—1 summa-
rizes the data available concerning the levels of selenium in ambient
air.
Daily selenium intake from air has been estimated at 0.07 jig/day
(Woolrich, 1973), 0.02 ig/day (Casarett and Doull, 1975) and <1
jig/day (Schroeder et al., 1970).
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TABLE 2-1
SELENIUM CONTENT OF AMBIENT AIR
Selenium Concentration
( gJm 3 )
0.006 (avg)
0.001
0.0025
0.0038
0.0014
0.0044 (max)
Location
Buffalo, NY
Cambridge, MA
Niles, MI
East Chicago, IN
Boston area
Northwest Indiana
Reference
Pillay et al., 1971
Hashimoto et al., 1967
Dams et al., 1970
Dams et al., 1970
Cordon et al., 1973
Harrison et al., 1971
Remarks
14 samples with range of 0.0036—0.0095 1 gfm 3
Based on concentration in rain and snow
Concentration in suspended particulates
Concentration in suspended particulates
Data from 24 hour samples at 25 sites
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2.2 Selenium Concentrations in the Diet
Food represents the major source of selenium intake for man
(Sterrett, 1977; WHO, 1973). There is a wide range in the selenium
content of foods. Several factors influence these differences:
• The class of food — seafood, meat and grains tend to have
high concentrations of selenium while fruits and vegetables
have rather low concentrations.
• The origin of the food — foods from areas with high concentra-
tions of selenium in the soil tend to contain more selenium.
• Food processing — more refined and/or processed foods usually
contain less selenium; cooking and heating may reduce the
selenium level due to volitilization (WHO, 1973).
Due to the nature of food distribution throughout the United
States, there is no reason to expect either an inadequate or an
excess amount of selenium in our diets (NAS, 1976).
Selenium content of foods has been monitoried by the FDA in its
Total Diet Studies. Data from this study and other sources are pre-
sented in Table 2—2. The usual dietary intake has been reported as
150 p.g/day (Mahaf fey et al., 1975; ICRP, 1975), 60—150 } i.g/day
(Schroeder et al., 1970), 170 pg/day (FDA, 1977), and 200 kg/day
(EPA, 1976).
2.3 Selenium Content In Drinking Water
Data reporting the selenium content of waters are limited. The
forms of selenium in drinking water have not been investigated;
moreover, the current standard for selenium In drinking water is
based on the total selenium content (EPA, 1976).
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TABLE 2—2
SELENIUM CONTENT OP FOODSTUFFS
FOOD CLASS* CONCENTRATION (ppm) REFERENCE
I. Dairy Products 0.063 FDA, 1977
Trace Johnson and I4anake, 1977
0.069 Morris and Levander, 1970
0.37 Schroeder et al., 1970
Whole milk 013 Morris and Levander, 1970
Human milk 0.018 Shearer et al., 1975
II. Meat, Fish and Poultry 0.221 FDA, 1977
0.25 Johnson and Manske, 1977
Meat 0.224 Morris and Levander, 1970
0.92 Schroeder et al., 1970
0.48 HAS, 1976
Processed meat 0.33 HAS, 1976
Seafood 0.532 Morris and Levander, 1970
0.99 Schroeder et al., 1970
III. Grains and Cereals 0.244 FDA, 1977; Johnson and Manske, 1977
0.387 Norris and Levander, 1970
0.15 Schroeder et al., 1970
IV. Potatoes 0.005 FDA, 1977
0.005 Morris and Levander, 1970
Not detected Schroeder et al., 1970
Irate Johnson ant Manske, 1977
V. Leaf vegetables 0.002 FDA, 1977
0.012 Morris and Levander, 1970
0.17 Schroeder et al., 1970
VI. Legume Vegetables 0.004 FDA, 1977
0.006 Morris and Levander, 1970
0.01 Schroeder et al., 1970
Trace Johnson and Manske, 1977
VII. Root Vegetables 0.001 FDA, 1977
0.021 Morris and Levander, 1970
0.06 Schroeder et al., 1970
Trace Johnson and Manske, 1977
Garlic 0.276 Morris and Levander, 1970
VIII. Garden Fruits 0.001 FDA, 1977
0.005 Morris and Levander, 1970
Not detected Schroeder et al., 1970
Trace Johnson and Manske, 1977
IX. Fruits 0.001 FDA, 1977
(Canned and Fresh) 0.006 Morris and Levander, 1970
Not detected Schroeder et al., 1970
X. 011 and Fats 0.002 FDA, 1977
Trace Johnson and Manske, 1977
XI. Sugar and Adjuncts 0.002 FDA, 1977
Trace Johnson and Manske, 1977
0.15 Schroeder et al., 1970
Brown sugar 0.012 Morris and Levander, 1970
White sugar 0.003 Morris and Levander, 1970
XII. Beverages 0.001 FDA, 1977
0.057 Schroeder et al., 1970
Coffee (ground) 0.124 FDA, 1977
Coffee (instant) 0.069 FDA, 1977
Coffee (ground and instant) 0.101 Shah et al., 1971
Tea 0.116 FDA, 1977; Shah et al., 1971
*Accordang to FDA
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The selenium content of water is a function of the pH of the
water. Acid waters (pH 6.3—6.7) tend to precipitate selenium as a
basic ferric selenite, while in alkaline waters (pH 8) selenium may
be oxidized to soluble, toxic selenate (Lakin, 1973). Thus, areas
with alkaline waters may be of special concern.
Natural waters are usually low in selenium content with an
average concentration of 0.25 ig/l (Johnson, 1976). Available data
suggest that surface waters rarely contain toxic levels of selenium
or even amounts which would be significant in terms of nutritive
requirements (NAS, 1976).
Drinking water rarely contains selenium at levels above a few
micrograms per liter. However, the concentration of selenium in
wells in seleniferous areas can be quite high. Levels as high as
210 g/l have been reported tn South Dakota (NAS, 1977). Under aver-
age conditions, drinking water cannot be considered a significant
source of selenium (NAS, 1976). Table 2—3 provides a summary of the
maximum values reported in drinking water samples analyzed for selen-
ium. No explanation was given for the extremely high values reported
in the table for Alabama and Utah. Though no fatalities occurred due
to ingestion of these waters, symptoms of selenosis were reported.
The estimated daily intake from drinking water ranges from negligible
amounts (Sakurai and Tsuchiya, 1975) to <1 big/day (Schroeder et al.,
1970).
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TABLE 2—3
AXIM1N SELENIUM CONCENTRATIONS REPORTED IN DRINEING WATER SUPPLIES
Maximum
Selenium Concentration
( jig/i) Location Reference Remarks
70 9 areas of U.S. McCabe ec al., 1970 Based on 2595 distribution samples; 10 samples (0.4%) exceeded
10 &g/l limit.
15 Interstate carriers EPA, 1975 Based on analyses of 418 samples, only 1 (0.2%) failed the
mandatory limit of 10 gI1.
10 194 finished water Taylor, 1963 Results of a two year study; mean concentration was 8 ig/1.
supplies
0.11 Cambridge, MA Hashiinoto et al., 1967 Tap water samples
0.090 Cambridge, MA Hashjjnoto et al., 1967 Well water samples
11 New York State Public Water Supply Found in 64% of the 312 distribution samples analysed; average
Report, 1974 concentration was 3.16 j ig/i
12,000 Alabama EPA, 1975a Two well water supplies with concentration of 8,000 and 12,000
j gI 1.
9,000 Utah EPA, 19758 Well water samples
20 National data Lassovszky, 1978 Based on 1332 distribution samples from surface water sources;
2 samples (0.1%) exceeded the 10 ig/l limit.
30 National data Lassovszky, 1978 Based on 2898 distribution samples from groundwater source;
11 samples (0.3%) exceeded the 10 ig/l limit.
Interim Primary Standard — 10 j.ig/l
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2.4 Other Sources of Exposure
Smoking is an additional source which could add significant
amounts of selenium to the body via the respiratory tract. The
selenium content of cigarette tobacco has been reported at average
concentrations of 0.08 ppm (Olson and Frost, 1970) and 0.35 ppm
(Schroeder et al., 1970). The paper from these cigarettes adds an
additional 0.05 ppm selenium (Olson and Frost, 1970; Schroeder et
al., 1970). Pipe and cigar tobacco reportedly contain 0.08 and
0.33—1.01 ppm selenium, respectively (Olson and Frost, 1970).
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3.0 ABSORPTION, RETENTION AND ELIMINATION OF SELENIUM IN HUMANS
Selenium is absorbed into the body via ingestion, inhalation
and, to a lesser extent, through derinal contact. The concentration
of selenium in the body is a function of intake levels, absorption
rates, metabolic requirements and excretion rates.
Selenium is widely distributed in the internal organs. The
liver and kidneys contain the largest amounts.
The amount of selenium in the diet has a major influence on the
amount excreted via the different pathways. The main excretion route
in humans is generally the urine but other routes include the feces,
breath and perspiration.
The absorption, retention and distribution of selenium within
the body and the amounts, forms and routes of excretion vary with the
chemical forms and amounts ingested and with the dietary levels of
other elements such as arsenic and sulfur (Underwood, 1977). Within
certain physiologic limits, the body appears to have a homeostatic
mechanism for retaining trace amounts of selenium and excreting the
excess material (Casarett and Doull, 1975).
3.1 Absorption Characteristics
Absorption characteristics vary greatly with the chemical forms
and amounts of selenium taken into the body and with the dietary
levels of other elements such as arsenic, cadmium and mercury.
Following absorption, selenium is transported by albumin to more
stable binding sites in blood and tissues (Underwood, 1977).
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3.1.1 Pulmonary Absorption
Due to the low concentrations in ambient air, the intake of
selenium via the respiratory route is considered negligible (Sakurai
and Tsuchiya, 1975). However, selenium may pose a possible hazard
since it exists in air in a readily respirable physical state. In
addition, selenium is localized on the surface of particulate matter
and thus is readily available to dissolve and interact in vivo
(Hausknecht and Ziskind, 1976).
Practically no quantitative data concerning pulmonary absorp-
tion of gaseous or particulate selenium compounds were found in the
literature. The International Commission on Radiation Protection
suggests an absorption rate of 70 percent for inhaled selenium
compounds (ICRP, 1959). In subsequent calculations in this document,
a pulmonary absorption rate of 70 percent has been assumed.
3.1.2 Gastrointestinal Absorption
Selenium is rapidly and efficiently absorbed from the gastro-
intestinal tract (McKee and Wolf, 1963; Diplock and Hoekstra, 1976).
Rat studies indicate higher gastrointestinal absorption of selenium
from grains grown in seleniferous areas than from selenites and
selenates and very low absorption from selenides and elemental selen-
ium (Underwood, 1977). Blood levels respond readily to the concen-
tration of selenium in the diet (Lee, 1977). It is believed that the
small intestine is the primary site of absorption (Lee, 1977). An
absorption rate of 90% has been reported for humans (ICRP, 1959).
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In addition, 50—80% of the ingested selenium is excreted via the
kidneys in humans (Waldbott, 1973) so it can be assumed that at least
these amounts are absorbed. In another study of three young women,
intestinal absorption rates were reported as 70%, 64% and 44% (Under-
wood, 1977). Estimated absorption rates ranging from 95—100% have
been reported for other mammals (NAS, 1976) s. hich tends to support
human rates reported. In subsequent calculations in this document,
a CI absorption rate of 90 percent has been assumed.
3.1.3 Dermal Absorption
The absorption of selenium through the skin has been known
to occur. This is usually in an industrial setting and does not
appear to present a problem in the ambient environment.
3.2 Retention Characteristics
The selenium that is retained in the body is widely distributed.
Although tissues do not appear to accumulate selenium to any great
extent, some accumulation does occur in hair, liver and the kidneys
and to a lesser extent in muscles. The kidneys retain the highest
concentrations. Table 3—1 shows the distribution of selenium in the
tissues of six humans at autopsy. Selenium is not stored but rather
Is rapidly eliminated from the body after the dietary source is
removed. However, the liver may store selenium for a few weeks (Lee,
1977). At high doses, a balance between intake and excretion Is
found which prevents further accumulation (Schroeder et al., 1970).
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TABLE 3--i
SELENIUM IN HUMAN TISSUES, ppm WET WEIGHT
9 Months 41 yr 68 yr 69 yr 52 yr 68 yr
Tissue Male Male Male Male Female Female Mean
Liver 0.33 0.42 0.81 0.65 0.72 0.28 0.54
Lung 0.24 0.26 0.20 0.14 0.05 0.10 0.15
Heart 0.25 0.25 0.26 0.25 0.37 — 0.28
Kidney 0.70 0.75 1.84 1.52 1.12 0.61 1.09
Spleen 0.47 0.29 0.32 0.28 — 0.34
Bone (rib) 0.42 — (0.42)
Muscle 0.18 0.17 0.36 0.38 0.11 0.24
Pancreas 0.34 0.29 0.27 — 0.30
Testes 0.15 0.36 0.38 — 0.30
Brain 0.04 0.21 — 0.13
Small intestine 0.18 0.32 0.12 — 0.21
(Fat) intestine — N.D.
Fat — 0.04
Human milk 0.24
Breast — 0.11
Mean 0.36
Source: Schroeder et al., 1970
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The long—terni fate of an oral dose of 75 Se—labeled seleno—
methionine was reported by Griffiths et al. (1976). In this study
involving four women, whole body radioactivity decreased exponential-
ly with a half—time of 90 to 207 days.
3.3 Elimination Characteristics
Selenium is excreted from the human body via urine, feces,
respiration, milk and perspiration. The urine is the predominant
route of elimination under chronic conditions and may be an indicator
of exposure (EPA, 1975). The feces is considered a minor route. In
humans 50—80% of ingested selenium is excreted through the kidneys
(Waldbott, 1973). The urine is believed to contain at least twice as
much selenium as the feces (Casarett and Doull, 1975). Urinary
output has been estimated at 50% or more of the ingested dose in
humans where input and output are considered to be in an approximate
balanced state (Sakurai and Tsuchiya, 1975). Animal studies tend to
show agreement with these figures. Eats given a diet containing
selenium as Na 2 SeO 4 over a two—week period excreted about 50% of
the ingested selenium In the urine and 12% in the feces within two
weeks (Diplock and Roekstra, 1976). In contrast to this, the Task
Group on Reference Man reports only 33% excretion via the urine, 13%
via the feces and 53% via sweat (ICRP, 1975).
Elimination characteristics are highly dependent upon chemical
form, amount Ingested and the presence of modifying factors
18
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(Underwood, 1977). Animal experiments suggest that at low concen-
trations the urinary and fecal excretion routes attain a steady
state. It appears that the body has effective removal mechanisms so
that toxic levels do not occur (Stahl, 1969). As the dosage becomes
larger, respiration and perspiration become important routes of
excretion. The formation of volatile selenium is significantly
greater and elimination via the lungs and perspiration increases
(Diplock and Hoekstra, 1976). Selenium also appears to accumulate in
hair which serves as an elimination mechanism (Casarett and Doull,
1975).
In the human body, natural detoxification occurs through reduc-
tion of selenium compounds to elemental selenium which is excreted
through the kidneys and liver. Elemental selenium is also converted
to diiuethyl selenide which is excreted through the breath and per-
spiration (Stahl, 1969).
There are few data available which quantify the rates of excre-
tion from the different routes. The selenium balance for reference
man has been reported. Of the average 150 i.g/day intake from foods
and fluids (unknown inputs via atmosphere), 50 pg/day are reportedly
excreted via the urine, 20 1 j.g/day via the feces, 80 pig/day via
perspiration, 0.3 p.g/day are deposited in hair and trace amounts
are lost through other fluids (ICRP, 1975).
19
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Human body burden has been reported by two sources. The figures
reported are 14.6 mg, with a range from 13.0—20.3 mg (Schroeder
et al., 1970) and 15 mg (Casarett and Doull, 1975).
20
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4.0 TOXICITY
Selenium is considered an essential trace element in animals.
It is a micronutrient at levels up to 1 ppm (Waldbott, 1973) but
toxic at levels above 4 ppm (Lakin, 1973). Toxic levels for man are
estimated to be in the range of 600—6300 g/day (EPA, 1976). Selen-
ium is believed to be an essential trace element in man. Though no
recommended daily intake has been established for humans, it has been
determined that selenium performs certain nutritional functions.
The metabolic role of selenium deals with the production and
maintenance of membranes (WHO, 1973). Selenium inhibits the oxida-
tion of polyunsaturated fatty acids. This function curtails the
production of “free radicals” which polymerize body proteins and
diminish the elasticity of membrane tissues (Woolrich, 1973). Selen-
ium may have a function in maintaining transmembrane cation gradi-
ents. Other studies indicate that selenium may influence the
synthesis of glutathione and protein (WHO, 1973).
The toxicity of selenium depends on many factors, including the
chemical form of the selenium compound and its solubility. The route
of exposure is also important. Other factors include quantity
consumed and the presence of modifying factors (e.g., other chemi-
cals) in the diet.
Elemental selenium is relatively nontoxic. It is converted by
the body into dimethyl selenide which is eliminated through the
21
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breath and perspiration. The most toxic compounds are hydrogen
selenide, methyl selenide and ethyl selenide. These compounds are
retained in the tissues longer and In greater quantities (Waldbott,
1973).
Selenate and selenite are the forms which occur most often In
water. Selenate compounds are of major concern due to their stabil-’
ity, solubility and ready availability to plants. Selenate is
the form found in plants which accumulate selenium. Selenite, on the
other hand, is less hazardous since it Is likely to form insoluble
compounds or be reduced to elemental selenium. Elemental selenium
appears to be a major Inert sink for selenium Introduced into the
environment. Though selenide forms are highly toxic, they represent
an industrial hazard only due to rapid decomposition to elemental
selenium in air (NAS, 1976).
Most toxicological data deal with acute exposure to selenium
in animals. Acute exposures in man result in such symptoms as irri-
tation of eyes and mucous membranes, sneezing, coughing, dizziness,
dyspnea,* dermatitis, headaches, pulmonary edema,** nausea and garlic
breath odor (NAS, 1977). Selenium is easily detected in fumes due to
its unpleasant odor. Because of this, acute selenium poisoning
Is rare (Waldbott, 1973).
*Djffjcult or labored breathing.
**Abnorinal accumulation of fluids in the pulmonary tissues.
22
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Chronic intoxication is reported to produce the following symp-
toms: depression, marked pallor, coated tongue, languor, nervous-
ness, occasional dermatitis, gastrointestinal disturbances, giddiness
and garlic odor of breath and perspiration. Garlic odor is believed
to be one of the earliest and most characteristic symptoms of expo-
sure (Stahl, 1969).
The relationship between exposure to high levels of selenium in
drinking water and human health effects was recently reported. Indi-
viduals drinking water containing selenium at concentrations between
50 and 125 1 j.g/l were compared with controls consuming water contain-
ing 16 g/l selenium or less. Even though urinary selenium levels
were higher in the exposed group, there were no significant differ-
ences in the incidence or prevalence of any disease studied (Tsongas
and Ferguson, 1977). Chronic selenosis has been reported in humans
drinking water containing 9 ppm selenium. Lassitude, loss of hair
and discoloration or loss of nails were symptoms noted (Cooper,
1967).
Epidemiological evidence indicates that selenium may increase
the incidence of dental caries in children (Hadjimarkos, 1970).
Little informaton exists concerning the effects of long—term
exposure to low levels of selenium. It does not appear that long—
term systemic effects occur as a result of low—level, long—term
exposure (Stahl, 1969).
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Selenium toxicity is generally attributed to its interference
with sulfur metabolism (Luckey and Venugopal, 1977). The harmful
effects are believed to be caused by the organism’s inability to
distinguish between selenium and sulfur (Hausknecht and Ziskind,
1976).
Selenium interacts with many other compounds. Adequate dietary
protein, organic sulfur, sulfate or arsenic decrease the toxicity of
selenium by increasing its excretion rate (Luckey and Venugopal,
1977). Selenium has also been shown to stimulate gastrointestinal
excretion of arsenic (Lee, 1977).
Selenium shows antagonistic properties with certain other ele-
ments. It has been shown to be highly effective in reducing the
toxic effects of cadmium, mercury and arsenic (Diplock and Hoekstra,
1976).
Teratogenic effects have been reported in animals. Selenium has
been shown to cross the placental barrier in several animal species.
From the very limited data available, it has been suggested that
selenium may be a teratogen in man (NAS, 1976).
Selenium has produced an increase in the incidence of liver
tumors in rats but data are insufficient to evaluate the carcino—
genicity of selenium compounds (IARC, 1975). Selenium has been sus-
pected of being carcinogenic in man; however, there have been no
direct reports of selenium carcinogenicity in humans. Moreover,
24
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epidemiologic evidence suggests that selenium compounds may have
therapeutic value against cancer in humans. These studies reveal an
inverse relationship between human cancer mortality and environmental
and blood selenium levels (Luckey and Venugopal, 1977). It is now
believed that selenium can have an inhibitory effect on human cancer
(Underwood, 1977). It is also possible that human breast cancer
incidence and mortality could be lowered by appropriate dietary
supplementation (Schrauzer and Ishmael, 1974).
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5.0 SOURCE CONTRIBUTIONS TO DAILY SELENIUM UPTAKE IN HUMANS
To determine whether the current drinking water standard is
adequate, an evaluation of selenium content from the different
sources is necessary. An appreciation of the percent contributed via
drinking water is needed to determine whether the dose contributed by
drinking water is significant. An evaluation of the exposure from
the other routes is also important in determining the overall hazards
of exposure.
5.1 Approach
The method employed in this study to estimate the degree to
which each major environmental source of selenium exposure contri-
butes to an individual’s total daily uptake is based on probable
exposure conditions (i.e., ambient selenium levels) as well as ab-
sorption rates for each exposure route. The method consists of a
five—step process:
• definition of ambient concentrations of selenium in the major
exposure sources (i.e., air, food, and drinking water);
• determination of daily selenium intake from each exposure
source according to the relationship:
Ij = Cj [ Seli
where I is the daily selenium intake from each source i,
Cj is the consumption per day of each source (i.e., air,
food, drinking water), and [ Se ] 1 is the concentration of
selenium in each source i;
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• calculation of the amount of selenium absorbed from each
exposure source:
Uj I Aj
where Uj is seleni&tm uptake for each exposure source
Ij is daily selenium intake from each source i, and A
is the fraction of selenium absorbed for each particular
exposure route j (i.e., inhalation or ingestion);
• calculation of the total daily selenium uptake (Ut):
U (I Aj) =
for all appropriate pairs of i and j;
• determination of percent (P 1 ) of total daily uptake pro-
vided by each of the three exposure sources (i.e., source
contribution factors):
P = — - • 100
i Ut
5.2 Basic Assumptions
Several assumptions were made in defining the amount of each
source material consumed each day. When possible, Reference Man*
Values were utilized for daily air and food consumption rates (see
Table 5—1). Daily consumption of drinking water is that value
suggested by NAS and EPA (NAS, 1977).
Pulmonary and gastrointestinal absorption rates utilized in the
calculations are also specified in Table 5—1. These figures repre—
sent reasonable absorption values for inhaled or ingested selenium,
as reported in the scientific literature.
*Fr the ICRP Reference Man Tables (IcRP, 1975).
27
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TABLE 5—1
BASIC ASSU1’iPTIOi S EMPLOYED IN THE
CALCULATION OF INDIVIDUAL SOURCE CONTRIBUTION FACTORS
Basic Assumptions Remarks
• Reference Man:
Adult consumes: 2.O H 2 O/day — Daily intake as suggested by NAS (1977);
conservative estimate, since all beverages
assumed to be water, which has higher [ Se ]
than generic beverages
‘u2200g food/clay — Approximate daily intake for 18—yr. old in
FDA total diet studies; comparable to
Reference Nan (ICRP report 23); however,
since daily Se intake from the total diet
will be assumed, this figure is not used in
3 the calculations
22.8 m air/day — Assumes 8 hrs. light work, 8 hrs. non—
occupational, and 8 hrs. resting
• Absorption Characteristics:
Gastrointestinal
Adult 90% — Approximation based on limited data
Pulmonary
Adult 70% — From ICRP (1959) data
Dermal Insignificant — Relatively unimportant, except in rare
circumstances
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5.3 Estimated Daily Selenium Uptake From All Sources
The relative contribution to an individual’s daily selenium up-
take from each of the three exposure routes was determined by using
average environmental selenium occurrence data in the calculation
sequence previously described. Several concentrations of selenium
in drinking water and several values of daily intake from food are
utilized to represent the range of values reported. The maximum
reported value from Table 2—1 was used for ambient air concentration.
Even at this level the contribution to an individual’s daily uptake
is negligible. Table 5—2 provides the exposure values used in the
calculations.
It should be noted that selenium levels in the diet reflect
daily selenium intake excluding any contribution by beverages. The
selenium intake reported in beverages by FDA studies was much lower
than that calculated for drinking water using the basic assumptions
as previously outlined. Therefore, any error due to this manipula-
tion would be a conservative one. Water is assumed to be the only
beverage intake.
Table 5—3 provides an example of the actual calculation sequence
employed. The source contribution factors for air, food and drinking
water are summarized in Table 5—4.
Food is the major source of selenium under normal conditions,
accounting for more than 90% of the total daily selenium uptake. At
the level of the current interim drinking water standard (10 g/1),
29
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TABLE 5—2
REPRESENTATIVE ENVIRONMENTAL SELENIUM EXPOSURE LEVELS
Exposure Routes Exposure Levels Rema
Diet 150 kg/day Selenium concentration in food is highly
200 p g/day variable; dietary preferences are a
major factor
Ambient Air 0.006 .g/m 3 Highest reported concentration (see
I Table 2—1)
U)
C
Drinking Water 1 p.g/
10 p.g/2 National Interim Primary Drinking Water
Standard
30 p.g/ 2 Highest concentration reported in large
National Survey (See Table 2—3)
12,000 g/2 Highest concentration reported in
isolated case (see Table 2—3)
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TAELE 5—3
CALCULATIO SEQUENCE IN DETERMINING SOURCE CONTRIBUT ION FACTORS
Percent of
Source Ambient Concentration x Consumption Rate x Absorption Rate = Daily Uptake Total Uptake
Drinking Water 10 ig/2 2i 0.9 18 Mg/day 9.1%
Food 200 Mg/day 0.9 180 Mg/day 90.9%
Air 0.006 Mg/rn 3 22.8 rn 3 /day 0.7 0.096 Mg/day
TOTAL 198.1 Mg/day 100.0%
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TABLE 5—4
*
ESTIMATED DAILY SELENIUM UPTAICE
Total Daily Source Contribution Factors
Selenium Concentration Selenium Uptake ( Percent of Total Uptake)
Drinking Water Air Food Drinking Water Air Food
1 ug/L 0.006 g/m 3 150 ig/day 137 gIday 1.4% 98.6%
1 ig/t 0.006 ug/m 3 200 pg/day 182 gJday 1.1% ———— 98.97.
10 ig/L 0.006 pg/rn 3 150 pg/day 153 pg/day 11.8% 88.2%
10 pgf9. 0.006 pg/rn 3 200 pg/day 198 pglday 9.17. 90.9%
50 pg/ 9 . 0.006 gfm 3 150 pg/day 226 pg/day 40.0% 60.0%
50 pg/I 0.006 pg/rn 3 200 pg/day 270 pg/day 33.3% 66.7%
12,000 pg/I 0.006 pg/rn 150 pg/day 21,735 pg/day 99.4% .6%
12,000 pg/ I 0.006 pg/rn 200 pg/day 21,780 pg/day 99.2% .8%
* Selenium uptake — selenium absorbed
** Contribution < 0.1%
-------
water represents approximately 10% of the daily selenium uptake.
Since most of the values reported for water were less than 10
the contribution is actually less than this figure. A level of
12,000 p g/l was reported for one drinking water source. It can be
seen from the table that at this level water would be the source of
over 99Z of the selenium uptake. This represents an isolated case,
however, and is not a common occurrence. Toxic effects were reported
for people drinking this water which shows that water can be the
source of selenium toxicity.
5.4 Significance of Current Standard
The current uptake of selenium under normal conditions appears
to be approximately 200 pg/day. Since toxic symptoms have been
reported in man at daily uptake levels of 600—6300 pg/day, the cur-
rent levels represent a safety factor of only three. However, no
data have been found which indicate toxicity at the current levels.
There is not a very broad range between toxicity and nutritional
requirements. The current standard appears to be in the range where
neither deficiency diseases nor symptoms of toxicity occur.
There do not appear to be any groups within the general popula-
tion who are at great risk from selenium exposure. However, since
infants can be exposed in utero as well as through breast feeding,
they may represent a sensitive population. Human milk contains an
average of 0.021 ppm selenium. This means that a breast—fed infant
33
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at 6 months might consume about 17 .ig Se/day (ICR.P, 1975). Available
information does not permit an accurate assessment of the risk such
an exposed infant may be assuming.
As more information becomes available concerning these points,
the data will need to be taken into account when developing any new
standard for selenium in drinking water.
5.5 Information Needs
In this preliminary review, there are several areas where data
are limited or lacking:
• National ambient levels of selenium * more complete data are
needed on levels, chemical forms and solubility of selenium
in the environment.
• Human nutritional requirements — it is not definitively known
at what levels selenium is required by man, although values
averaging 150 pg/day have been suggested.
• Acute/chronic human toxicity levels — there is no clear dif-
ferentiation between selenium exposure resulting in acute or
chronic toxicity.
• Human absorption/retention/excretion rates and biological
half—life — no human studies are currently available that
provide definitive absorption/retention/excretion rates.
• Metabolic interactions with other elements — the interactions
of selenium with mercury, cadmium and arsenic, among others,
need to be more clearly defined.
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