Special Pesticide Re-vie-w G-ro\zp>
 Office of Pesticides Programs
        TJNITEJ3D STATES
                 PROTECTION
                   , OD.C. 2O4QO

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 MERCURIAL PESTICIDES,

            MAN, AND THE

           ENVIRONMENT
ENVIRONMENTAL PROTECTION AGENCY
        1971

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Prepared by the Special Pesticide Review Group of the Office of Pesticides
Programs, Environmental Protection Agency.

SPECIAL PESTICIDE REVIEW GROUP

O. Garth Fitzhugh, Ph.D., Chairman
LamarB. Dale, Jr., Ph.D.
William Barthel
G. A.Reich,M.D.,M.P.H.
William F. Durham, Ph.D.
Thomas E. DeVaney
Joseph G.  Cummings
Cipriano Cueto, Ph.D.
SPECIAL WORKING GROUP ON MERCURY

Aram Beloian
Edward P. Carter
Lee M. Loeser
With Library Assistance of:

Mrs. Claudia Lewis
                              ABOUT THIS REPORT

This staff report represents a scientific and technical assessment of mercurial products regis-
tered with the U.S. Environmental Protection Agency for pest control purposes. This informa-
tion was developed to assist the Agency in evaluating the past, present, and future impact of
these pesticides on man and his environment prior to determining whether their continued use
is in the public interest.

In making this determination, the Agency also will consider data supplied by  other scientific
sources, both governmental and private,  as well as pertinent economic and  social factors.
Therefore, any conclusions and recommendations for action contained in this preliminary
report should not be construed as  the position of the EPA or necessarily  indicative of the
course of action it might finally take with regard to mercurial pesticides.

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               MERCURIAL PESTICIDES, MAN,
                   AND THE ENVIRONMENT
                                CONTENTS
                                                                        Page

Introduction 	   i"
Foreword 	   Vl
Recommendations concerning the registrations of mercurial pesticides 	  viii
Chapter 1.    The Pesticide Uses of Mercury	    1
            Introduction 	    1
            Summary and Conclusions  	    1
            I.     Coatings 	    2
            II.    Fabrics and Textiles 	   10
            III.   Fibers and Cordage  	   13
            IV.   Food, Feed and Tobacco Crops 	   14
            V.    Food and Feed Containers 	   16
            VI.   Humans 	   16
            VII.   Ornamental Plants  	   17
            VIII.  Paper (mold resistant) 	   25
            IX.   Plastics 	   26
            X.    Rubber 	   28
            XI.   Sanitizers  	   29
            XII.   Seed Treatments-Field Crops 	   31
            XIII.  Surfaces (fungistats)  	   37
            XIV.  Tanneries (bacteriostats and fungistats)  	   38
            XV.   Wood  	   39
            XVI.  Dental and Surgical Instruments (disinfection) 	   40
            XVII. Miscellaneous 	   41
Chapter 2.    Analytical Methods for Mercury 	   43
Chapter3.    Prevalence of Mercury in the Environment  	   47
Chapter 4.    Pharmacology of Mercury  	   51
Chapter 5.    Toxicology of Mercury  	   71
Chapter 6.    Ecologic Effects of Mercury Contamination  	   79
Chapter7.    The Hazard of Mecurial Pesticide Use  	   85
Selected Bibliography	  94

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                                  INTRODUCTION
The  realization of the  toxicity  of  mercury
dates back as far as recorded history. Hip-
pocrates (460-377  B.C.), Pliney the Elder
(23-79 A.D.), Galen (131-200 A.D.), Avicen-
na (980-1037 A.D.),  and Paracelsus (1493-
1541 A.D.) have all written on the toxic ef-
fects of mercury (Battigelli, 1960; Goldwa-
ter,  1957). The first mention of mercury as
an industrial hazard appeared in the middle
of the 19th century in connection with hat-
ters employing mercury nitrate in the felting
process. In spite of the early realization of
the hazard involved with this use of mercu-
ry, it continued until recent times. In  1941,
the U.S. Public Health Service published the
results of a field study showing that  more
than  10% of the  workers  examined  were
suffering from  chronic mercury poisoning
(Neal, 1941). The expression "mad as a hat-
ter" is believed to have originated as a result
of one of the toxic manifestations of mercu-
ry poisoning. The hazard in this industry as
well as in many others, e.g., mining, manu-
facture of thermometers  and barometers,
testing  departments, and laboratories has
been either eliminated or greatly reduced.

Although  progress has been  made in  in-
dustrial safety,  "epidemic" outbreaks of
chronic mercury poisonings still occur. This
is due, in  part, to  the extensive increase in
the industrial and agricultural uses of mercu-
ry in recent decades. In  1958, Benning de-
scribed mercury intoxication in more than 60
workers in an Ohio plant employed in the
manufacture of carbon brushes. In another
episode, inhalation of mercury vapors from
a mercury-containing paint was  implicated
in an outbreak of neuromyasthenia in a Ken-
tucky electronics plant (Miller et al., 1967).

Reports of poisonings resulting from the use
of alkylmercury seed disinfectants soon fol-
lowed their introduction. In 1940 Hunter, et
al described in detail four cases of alkylmer-
cury  poisonings  resulting  from  industrial
exposure.  Ahlmark  (1948)  described  five
cases of  poisoning (two fatal) of workmen
involved  in manufacture and handling of
methylmercury compounds.  In 1949, Lund-
gren and Swensson reported eight cases of
occupational   poisoning  by  alkylmercury
compounds. Between 1956 and I960, there
were over three hundred patients suffering
from mercuric poisoning admitted to hospi-
tals in Mosul and Baghdad,  Iraq. They had
consumed wheat treated with ethylmercury
toluene   sulfonanilide  (Jalili  and Abbasi,
1961). Similar episodes occurred in Pakistan
(Haq, 1963) and Guatemala, (Ordones, et a],
1966). Numerous other cases  of poisoning
with alkylmercury compounds have been
reported  in the literature and by the press.
The most recent and the most publicized in
this country  occurred in Alamogordo,  N.
M., in 1969,  when three members of one
family were poisoned from eating pork from
hogs which had been fed grain treated with
an alkylmercury pesticide.

During the past 20 years, there  have been
two occurrences of human mercury poison-
ing in Japan resulting from the eating of con-
taminated fish. The first incident occurred in
Minamata in  1953. The outbreak reached
almost epidemic proportions. The source of
contamination was traced to a vinylchloride
and  acetaldehyde  plant which  discharged
large quantities of methylmercury into Mini-
mata Bay.  From 1953 to  1970, 121 persons
were reported poisoned after  having eaten
fish and shellfish caught in Minimata Bay.

There were 46 deaths recorded. It was some
time before  Japanese medical  authorities
recognized and documented the similar clini-
cal disorder of a large number of people in
the Minamata area.  A second incident oc-
curred in the riverside villages of the Agano
River in  Niigata prefecture  where 47 cases
and six deaths were observed through 1970.
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This syndrome, which has  become  to  be
known as the "Minamata disease" is char-
acterized by widespread involvement of the
central nervous system with granular cell
degeneration of the cerebellum, and  lesser
involvement of  the basal ganglia, hypothala-
mus,  midbrain, and cerebral  cortex. The
relative ease  with which  methylmercury
passes the "blood-brain barrier" in humans
accounts for the severe neurologic manifes-
tations.

The staff of the Kumamoto University, in a
series  of  carefully planned  investigations,
first identified the causative factor of  Mina-
mata disease as heavy consumption of fish
contaminated with an  organic form of mer-
cury,  later  identified  as  methylmercury.
Similar findings were  made by the staff of
the University of Niigata in the Niigata City
and Agano River outbreaks (Nelson, ef  al,
1971).

The first warning of the mercury problem in
Sweden came  in the early 1950's when the
populations  of  the yellow  bunting dropped
catastrophically. Deaths,  reproductive fail-
ures and population declines of both seed-
eating  and raptorial birds were soon  noted
(Otterlind, etal, 1964). Toxicity from mercu-
ry used in seed dressings to prevent  cereal
diseases   was  suspected.  Investigations
proved this assumption to be correct.  It was
soon discovered that mercury pollution was
serious in Swedish lakes, and  that leakage
from pulp  mills and  chlor-alkali  factories
was responsible.

Late in 1965, Westoo determined that  the
mercury she found in  eggs, fish,  and some
other  meats was  methylmercury.  Westoo
observed that both fish and mammals could
convert small amounts of inorganic mercury
to methylmercury in  their  livers. It was
shown  that Swedish eggs had four times the
mercury content of eggs from the rest  of
continental Europe. Johnels  published  an
opinion that  inorganic mercury could  be
converted to methylmercury by microorgan-
isms in anaerobic ecosystems such as mud
on lake bottoms. In 1965, it was shown that
the mercury in samples of eggs,  meat and
fish from Sweden was 80 to 100% methyl-
mercury. Subsequently, mercury  has been
shown to be methylated by aquarium and
natural  sediments  (Jensen  and  Jernelov,
1969).

Because  of  mercury  contamination, the
marketing of fish from certain lakes and riv-
ers has been banned in Sweden. This deci-
sion  is based on a temporary limit of 1 mg
Hg/kg of body weight with a recommenda-
tion not to eat fish from fresh waters  more
than once a  week. Recent investigations in
Denmark, Finland and Norway have  dem-
onstrated similar elevated  mercury concen-
trations in fish from coastal waters.

The National Poisons and  Pesticides  Board
of Sweden  revoked the licenses for  alkyl-
mercury compounds in Agriculture on Feb-
ruary 1, 1966. In the year following this ban,
the mercury content  of Swedish  eggs fell
almost to the level of the rest of continental
Europe or one-third of the level reported in
1966.

In 1969,  following  warnings of significant
mercury pollution in the central provinces,
studies were initiated by the Canadian Wild-
life Services to define the situation. Follow-
ing these studies, several commercial  catch-
es of fish (walleye,  northern pike, bass and
jackfish) taken from Lake  Winnipeg,  Cedar
Lake, Saskatchewan River, and Red River
in Manitoba Province were seized by the
Canadian Federal Department  of  Fisheries
and Forestries, because they contained mer-
cury residues ranging from 5 to 10 ppm (Sea-
gran, 1970). The Canadian Government then
publicly embargoed  all commercial fish tak-
en from Lake Saint Clair effective March 23,
1970.

In the United States,  results of analytical
studies on fish and wildlife showed mercury
IV

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levels up to 117 ppm in eagles from Minne-
sota and up to 4.4 ppm in fish collected from
the North Fork of  the Holston River. As a
result of this  information, restrictions  on
sport  and  commercial fishing  have been
placed on waters within at least  18 states as
of  September  1970 (Celeste  and Shane,
1970).


In the fall of 1970, the Food and Drug Ad-
ministration found  that canned tuna sold in
the United States contained up to 1.2 ppm
mercury (average 0.37 ppm) and that frozen
swordfish ranged from 0.18 to 2.4 ppm (aver-
age 0.93 ppm). The Food and Drug Adminis-
tration set an interim guideline  of 0.5  ppm
mercury in fish.


A 21 member  ad hoc committee of experts
reviewed the  Food and  Drug Administra-
tion's data on mercury  contamination  of
swordfish and were  unable to suggest any
basis on which swordfish consumption might
be continued without possible health hazard.
Accordingly, the FDA issued the statement
in May 1971 that the "public stop eating this
fish until and  unless the situation can  be
remedied."

On May 20, 1971, at a Senate subcommittee
hearing on chemical pollution, the first case
of mercury poisoning in the United States
from eating fish was reported. Dr. Roger C.
Herdman, New York State Deputy Health
Commissioner, reported the case of a house-
wife,  age 44.  He  stated  that  she became
"rigidly committed" to a weight loss pro-
gram. She started eating 10 oz of swordfish a
day, plus some shrimp, for 10 months "with-
out interruption." She lost  45 Ib but began
suffering lethargy,  visual   complaints and
tremor. Still, two or three times a year until
last November, she again ate swordfish for 3
to 6 weeks. In May 1966, she  began having
serious trouble speaking, walking, and un-
derstanding along with loss  of memory and
dizziness. Doctors  told her  it was probably
psychosomatic, and she  saw a psychiatrist
once a week for 2  1/2 years. Only recently
did a hair sample reveal a high mercury con-
centration (Washington Post, May 21, 1971).

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                                    FOREWORD
Charge — In a statement issued on March
18, 1971, the Administrator of the  Environ-
mental Protection Agency said that "Active
internal review is being initiated as to the
registrations of products containing benzene
hexachloride,  lindane,  chlordane,  endrin,
heptachlor and toxaphene, all products con-
taining  mercury,  arsenic, or lead, and all
others deemed necessary for review. The
function of review is not to make another
study of pesticides, but to identify which, if
any,  of the  presently  registered  products
present  substantial  questions  of  safety
which  should  trigger  the  administrative
process  of  cancellation."  (Ruckelshaus,
1971)
In order to activate this review process,  a
Special  Review Group  was established by
the Commissioner of the Office of Pesticides
to set priorities and appoint working groups
to study the  individual pesticides in ques-
tion. Accordingly, the first Working Group
was established and assigned the task of:

     (1) reviewing  the  currently registered
        uses of mercurial pesticides,

     (2) evaluating  these  uses in terms of
        human safety and  contamination of
        the environment, and

     (3) based on this  evaluation,  making
        recommendations  for  cancellation
        of registrations which  present  a
        substantial  question of safety  or of
        environmental contamination.

Basis for  Approach — In "Reasons Under-
lying the Registration Decisions Concerning
Products Containing DDT, 2,4,5,-T, Aldrin
and  Dieldrin," (Ruckelshaus, 1971) the En-
vironmental Protection  Agency  interpreted
its responsibilities under the Federal Insecti-
cide, Fungicide  and  Rodenticide  Act and
under the Food, Drug and Cosmetic Act as
being required to:

    (1) register  new economic  poisons if
       they meet certain standards of effi-
       cacy and safety, and

    (2) undertake a  continuous review  of
       previously registered pesticides  in
       order to insure continued  compli-
       ance with these requirements in  the
       light  of the developing scientific
       data and concern for public health.
       If this continuing review raises any
       substantial questions of safety,  no-
       tices of cancellation must be issued
       which  initiate   the  administrative
       process of review.

In continuing to define the Agency's respon-
sibilities, the  document interprets the thrust
of the Federal  Insecticide,  Fungicide  and
Rodenticide Act as prohibiting:

     (1) those economic poisons which do
        not contain directions for use which
        are necessary  and adequate for the
        protection of the public, and

     (2) those economic poisons which do
        not contain a  warning or caution
        statement which is adequate to pre-
        vent injury to man, vertebrate  ani-
        mals, or vegetation (except weeds).

The final decision with respect  to whether a
particular product should be registered ini-
tially or  should continue  to be registered
depends  upon  the intricate balance struck
between  the  benefits and dangers to public
health  and welfare resulting from its use.
"The fact that the danger results solely from
misuse does not determine that such danger
is to be ignored but  that this consideration
has a possible bearing on the magnitude and
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possibility  of  occurrence  of  the  risk."
(Ruckelshaus, 1971,6,10).

A product which has previously been regis-
tered  may either be cancelled  or suspended
if  the Administrator determines  that  the
product does not comply with the provisions
under which it  was registered. The  initial
step in the administrative process, cancella-
tion of  registration, is  triggered whenever
the Administrator determines from  all  the
data before  him that there  is a substantial
question as  to the safety of a product. The
cancellation decision does not turn on a sci-
entific decision  alone.  The  statute  leaves
room  to  balance the benefits of a pesticide
against its risks.  In other words, the type,
extent, probability, and duration of potential
or actual injury to man, plants, and animals
will be measured in the light of the positive
benefits accruing from the responsible use of
the pesticide. In its consideration  of a spe-
cific pesticide usage, the Agency is mindful
of its statutory directive and duty to the pub-
lic to  place the dictates  of health and safety
over economic considerations in its scale of
values.

In the consideration of the term  "safety"
one must realize that this is never absolute
(Mrak,  1969).  Health risks assumed by an
individual in his home  or in the street are
accepted as inevitable and may be limited to
some  extent by  the individual. Health haz-
ards stemming from  environmental  expo-
sure to chemical agents are beyond the ca-
pacity of the individual to control.  (Mrak,
1969).

In the consideration of "health" one must
realize that this  encompasses  more than an
absence of disease. Included is the feeling of
well-being  and capacity of happiness that
derives from a suitable environment - suita-
ble in the sense that makes possible the en-
joyment  of nature and her bountiful provi-
sions of flora and fauna (Mrak, 1969).

Based  on the above considerations, and as
directed by the Agency, the Working Group
will weigh the following criteria in determin-
ing the need for the continued registrations
of specific uses of mercurial pesticides:

    (1) the nature  and  magnitude of  the
       foreseeable hazards associated with
       each specific use will be evaluated.
       These hazards may apply directly to
       human health, or to domestic plants
       and animals, or to wildlife, or to the
       environment generally;

    (2) the nature of the benefit conferred
       by  each use will  be weighed. Some
       uses are obviously more important
       to public health and well-being than
       others. The nature of the benefit, if
       any, will be detailed;

    (3) an  attempt  will be made to assess
       the magnitude  of the social cost of
       foregoing any use recommended for
       cancellation; and
    (4) alternatives  for  each  use  will
        considered.
be
As the result of this review and the applica-
tion  of  the  above  criteria,  the  Working
Group will recommend the cancellation of
the registration for those uses which, in its
opinion, there is a substantial question of
safety.
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          RECOMMENDATIONS CONCERNING THE REGISTRATIONS
                           OF MERCURIAL PESTICIDES
 The Special  Pesticide  Review  Group  has
 reviewed  and evaluated the registered uses
 of  mercurial pesticides  on  a  use-by-use,
 benefit-versus-risk basis. Based on this eval-
 uation, the Special Pesticide  Review Group
 makes the following recommendations con-
 cerning the  continued registration of these
 pesticides.

 RECOMMENDATION 1:

 Suspend immediately the registrants for all
 pesticide  products containing alkylmercury
 compounds.

 The recommendation  of suspension  of all
 alkylmercury-containing pesticides- is  based
 on the high toxicity of these compounds to
 humans. The volatility and toxicity of the
 alkylmercuries present not only  a hazard in
 the use of the  pesticides  containing these
 compounds but also an unnecessary hazard
 in their manufacture, formulation, and stor-
 age. The alkylmercuries have a propensity
 for accumulating in the brain and producing
 an insidious onset of symptoms associated
 with damage to  the central nervous system.
 The registrations for-seed dressings contain-
 ing these compounds have been previously
 suspended. It is now considered that all oth-
 er pesticides containing  alkylmercury com-
 pounds present  an "imminent hazard  to the
 public" and  their registrations should be
 suspended.


 RECOMMENDATION 2:


 In addition to the  suspension recommended
 above, the Committee further recommends
 that in the absence of an imminent hazard
 finding, all other products containing mercu-
 ry be cancelled except  those intended for
 use as seed dressings for the prevention of
 stinking smut in wheat and leaf stripe  smut
 in growing barley. The  Group also  recom-
 mends that the Administrator request the
 Secretary of Agriculture to develop alterna-
 tive methods for the  prevention of these di-
 seases in  wheat and  barley. When this has
 been accomplished, the Environmental Pro-
 tection Agency  will cancel these two remain-
 ing uses of mercurial pesticides.


 RECOMMENDATION 3:

 Initiate monitoring activities to determine (1)
 the effect of the decreased use of mercury
 stemming from  the cancellation of mercury-
 containing pesticides  on  the general level of
 mercury  in  the environment,  and (2) the
 effect of  the continued use  of  mercury-
 treated wheat  and barley  on the mercury
 levels in man and his  environment in the re-
 gions in which these seeds are used.
   *
RECOMMENDATION 4:

Continue research on  the effects of mercury
in the environment, especially in the areas of
(1) development of more sensitive methods
of determining the effects in humans of low
level exposure to  mercury; and (2) the bio-
transformation of mercury compounds.
RECOMMENDATION 5:

The  nonpesticidal uses of mercury  should
be reviewed by the other components of the
Agency with the  goal of eliminating other
sources of  mercury  contamination  of  the
environment.
Vlll

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                                     SUMMARY
Although the toxic properties of  mercury
and its compounds have long been recog-
nized, it is only recently that the impact on
man and  the  environment of  the extensive
increase in industrial  and agricultural uses
has come to light. The first warnings of the
hazard to the environment resulting from the
agricultural use of mercury came from  Swe-
den in the 1950's where the drastic decline in
the populations of both seed-eating and rap-
torial birds was linked  to  mercury-treated
seeds. At about the same time the effects of
industrial pollution  on humans became ap-
parent in Japan where the first poisonings
from mercury-contaminated fish occurred in
Minamata in 1953. This was followed in 1965
by a similar occurrence in  Niigata. Soon it
was realized that mercury pollution of lakes
and rivers from industrial pollution was also
a serious problem  in  Sweden. In 1970 sys-
tematic surveys of fish and wildlife in both
Canada and the United States led to the real-
ization that North America was also  faced
with the mercury problem.

Human poisonings resulting from exposure
during the  manufacture, formulation, and
use of mercurial pesticides or from the acci-
dental  ingestion of mercury-treated  grain
date as far back as the use of  these  pesti-
cides,  especially  the  alkylmercury  pesti-
cides. While the accidental ingestion of mer-
cury-treated grain has resulted in many poi-
sonings and deaths in foreign countries, it
was  not  until the  recent highly publicized
incident in Alamogordo, New  Mexico, in
1969 that the American public became aware
of this potential hazard.

Inorganic and organic mercury  are used in
pesticides.  The organic compounds that
have gained importance all have the general
structure R-Hg-X, where R  is an  organic
radical,  alkyl,  alkoxyalkyl,  or  aryl. The
group X is  bound  to mercury with a  bond
more or less  having the character  of  a salt
and originating from  organic  or  inorganic-
substances with dissociable hydrogen ions,
e.g. acids, amides, phenols,  or thiols.  At
present, some one hundred combinations of
different organic  radicals and anions are
used in commercial preparations of mercury
fungicides.


All alkylmercury compounds used for seed
treatments and all mercury compounds used
as slimicides,  algicides,  and  in  laundries
have previously been cancelled. The regis-
trations of products containing hydroxymer-
curichlorophenol bearing directions for use
on vegetable and field crop fields, the regis-
trations of products containing hydroxymer-
curinitrophenol bearing directions for use on
potatoes and sweet potatoes, and the regis-
trations of products  containing phenylmer-
curic acetate or phenylmercuric ammonium
acetate bearing directions for use  on apples,
cherries, peaches,  strawberries, and sugar-
cane have previously been cancelled as the
result of implementing the NAS, NRC Advi-
sory Committee recommendations to abol-
ish "no residue" and "zero tolerance" reg-
istrations.
Inorganic and arylmercury compounds are
more acutely toxic than  the  alkyl  com-
pounds.  The  arylmercuries  are  relatively
rapidly degraded in the  body to inorganic
mercury, and their tissue  distribution resem-
bles inorganic  mercury.  Accumulation  of
mercury from these compounds is mainly in
the liver and  kidneys. The placenta  is  an
effective barrier to the entry of these com-
pounds. In addition, they are rapidly excret-
ed in the  urine and feces. In contrast, the
alkylmercuries are better absorbed, show a
more even tissue distribution and are more
slowly metabolized. They readily cross the
"blood-brain barrier" in man. They are able
to cross  the placenta!  barrier, where  accu-
mulation in the fetus  may exceed that in
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maternal tissues and may cause fetal neurol-
ogical  damage. All of  the  compounds of
mercury are capable of causing chromoso-
mal aberrations. This effect is more  marked
with the alkyl and aryl compounds than with
inorganic mercury.
A complicating feature of the mercury prob-
lem was the discovery that mercury in river
and  lake  bottoms can  be  converted  into
methylmercury.  This biotransformation  is
responsible   for   the  contamination   of
aqueous systems and their associated biota.
Indirectly, this  process may  also play,
through the evaporation of dimethylmercu-
ry,  a role in the  atmospheric transport of
mercury. In addition, microbial systems in
the interstinal flora of birds and mammals
may be involved in the methylation of mer-
cury.

Because of its volatility, mercury normally
circulates  in the environment between the
soil and water and the atmosphere.  Man's
use of mercury has added to this natural cir-
culation by increasing the concentration in
the atmosphere over the years through the
burning of fossil fuels and the smelting of
ores. Man has also produced areas of abnor-
mally  high   concentrations   of  mercury
through industrial  wastes and  the  use of
mercurial pesticides.  The pollution of rivers
and lakes with mercury from the effluents of
industrial plants has been abated. However,
the pesticidal use of mercury remains as the
largest intentional dissipative or nonrecycla-
ble use of mercury in  the United States.

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                                   CHAPTER I
                    THE PESTICIDE USES OF MERCURY
                                    Introduction
Because of incomplete records and the fact
that  specific  uses  for products registered
"For manufacturing use" can not always be
identified, we are not certain that we have
identified all pesticide  uses of mercury or all
available substitutes. It is estimated that the
following outline covers approximately 98%
of all such uses.

The  classification of uses is arbitrary and is
usually based on label claims which are  of-
ten so general in nature as to prohibit specif-
ic identification.

According to figures produced  by the  Bu-
reau of Mines, about 986,252  Ib of metallic
mercury were used in the production of pes-
ticides in 1969. This included  production of
products  from imported mercury and other
sources.
                              Summary and Conclusions
There  is a serious  lack of information on
nonagricultural uses of mercury-containing
pesticides, and data are not available for a
proper evaluation of the economic impact of
the withdrawal of such uses.

Mercury  compounds presently  registered
include alkyl, aryl and  inorganic types. All
alkylmercury  compounds  used  for  seed
treatments and all mercury compounds used
as slimicides, algicides and in laundries have
previously been cancelled and are  not  in-
cluded in this report. The remaining uses
involve many different commercial, house-
hold,  industrial  and institutional  applica-
tions. Uses requiring the largest amounts of
mercury include paints, seed treatments and
turf disease control.

A careful review of registrations of nonmer-
curial products indicates that no substitutes
are currently registered for the following
uses:

    (1)   barley - seed treatment for stripe
         disease
    (2)  broomcorn - for mildew control

    (3)  cellulose sponges - preservatipn

    (4)  sacks,  bins  and  containers  for
        treated seed - fungus and bacterial
        plant disease organisms

    (5)  seam and bedding compounds used
        in boat construction

    (6)  textures and other dry  products
        ultimately applied by dispersion in
        water

    (7)  elm  trees  (by injection) - Dutch
        Elm Disease

    (8)  wheat - seed  treatment  - seed-
        borne phase of smut control.

It is also recognized that, although substitute
materials appear to be available for all other
uses,  the general  patterns described  on
many product labels preclude an accurate
assessment of individual applications in spe-
                                                                                    1

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cific formulations or processes. Thus,  sub-
stitute materials may not be available for all
paint formulations, certain tanning process-
es or other uses. Conversely, the fact that no
substitute is presently registered for a spe-
cific formulation or process does not mean
that one  is not known which can be regis-
tered for  such use.
                                     I.  Coatings
1.  Adhesives

  A.  Mercury compounds

Phenylmercuric acetate: [Ref. I-P-08-00.091
For preservation of product: 45 to 250 ppm
For mildew control after application: 3500 to
15,000 ppm based on total wet weight.

  B.  Substitute compounds

    (1) Alkyl dimethyl benzyl  ammonium
chloride: [Ref. I-A-08-45.051  fungistat: 800
ppm by weight. [Ref.  I-A-08-50.01] preser-
vative: 50,000 ppm plus other fungistats.
    (2) Bis  (tributyltin) oxide: [Ref. I-D-09-
00.021 fungistat: use in amount required.
    (3) 4-Chloro-3, 5-xylenol: [Ref. I-C-21-
00.02] fungistat: use as  required.
    (4) Dehydroabietylamine  pentachloro-
phenate: [Ref. I-D-02-00.01] fungistat: 1700
to 8000 ppm by weight of adhesive.
    (5) Hexahydro-1,   3,  5-triethyl-s-tria-
zine:  [Ref.  I-H-04-00.01] fungistat: 100 ppm
by weight.
    (6) Monoethanolammonium 2-mercap-
tobenzothiazole: [Ref. I-M-21-00.01]
       (a) 2000 to  4000 ppm for low protein
adhesives by weight.
       (b) 800 to 12,000 ppm for high protein
adhesives by weight.
    (7) Parachlorometacresol: [Ref. I-P-01-
00.01] fungistat: 500 to 1500 ppm by weight
of product.
    (8) Sodium o-phenylphenate: [Ref. I-S-
 16-00.08] preservation: 500 to 1000 ppm by
weight.
    (9) Vinylene bisthiocyanate: [Ref. I-V-
01-00.01]
    (10) Tetrahydro-3, 5-Dimethyl-2H-l, 3,
5-thiadiazine-2-thione (Mylone): [Ref. I-T-
07-00.01] 0.01 to 0.5%  by weight of suspen-
sion.
    (11)  Ziram:  [Ref. I-Z-11-00.07] (1) plus
zinc-2-mercaptobenzothiazole  (2)  180  ppm
(1) plus 20 ppm (2) to 2300 ppm (1) plus 50
ppm (2) by weight.
  C. Comparative effectiveness and impact
    (1) In general, mercury compounds are
effective  at  lower dosages and  against  a
broader spectrum of  fungi than are the sub-
stitute materials.
    (2) Impact of withdrawal  of mercury
uses as pesticides in adhesives should  be
minimal.
2.  Coatings for outdoor fabrics

  A. Fungistatic:

    (1) Mercury compounds
Phenylmercuric oleate [Ref. I-P-14-00.0] 500
to 5000 ppm by weight of coating.
    (2) Substitute compounds
      (a)  None  specifically  identified  by
label claims but might include products used
in sealers and sizings, and certain plastics.
      (b) Bis (tributyltin) oxide:  [Ref.  I-S-
09-00.02] For furniture and similar items (vi-
nyl) 4,000 to 10,000 ppm by weight of nonvo-
latile components of formulation.
    (3) Comparative effectiveness  and im-
pact
      (a)  Comparative   effectiveness  un-
known.
      (b) Impact of  withdrawal of mercury
for this use on industry and consumer is also
unknown.

  B. Bacterial preservatives:

    (1)  Mercury compounds
Phenylmercuric hydroxide  17% (powdered):
[Ref. 6516-3]
Paint (unspecified) coatings for fabrics: 0.5
Ib product per 99.5 Ib media.

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    (2)  Substitute compounds
      (a)  Alkyl(50%C12,30%C14,  17%C,6,
3%C,S)  dimethyl  ethylbenzyl  ammonium
cyclohexylsulfamate  (80%):  [Ref.  1839-36]
0. 1% to 0.2% product by weight.
      (b)  l-(30chloroallyl)-3, 5,  7-triaza-l-
azoniadamantave chloride (90%): [Ref. 464-
3271
        (a)  latex paints: 2000 ppm product.
        (b)  polyvinyl  acetate  latex:  250
ppm product.
      (c)  Sodium 2-pyridinethio!   1-oxide
(40%): [Ref.  1258-843] 1.15  Ib product/10,-
000 Ib emulson, 115 ppm product.
      (d)  Captan (N-trichloromethylthio-4-
cyclohexene-1,   2-dicarboximide)   (90%):
[Ref.  1965-11]
0.2%  to 0.5% product by  weight  of total
formula.
      (e)  Alkyl  (5%  caprylyl,  7% capryl,
56% lauryl,  18%  myristyl, 7% palmityl, 5%
stearyl, 2%  linoleyl)  hydrochlorides (25%):
[Ref.  8489-13]
0.15% to 0.3% product based on total weight
of composition.
    (3)  Comparative  effectiveness  and im-
pact
      A.  Mercury compounds  are  color-
less. Some substitute chemicals  impart un-
desirable colors.
      B.  Substantivity of  some substitute
chemicals to  fabric  greater than  mercury
compounds.
      C.  Substitute chemicals appear to be
adequate.
      D.  Impact on industry expected to be
minimal. Increase in  costs to consumer ex-
pected.
3.  Cements and plasters (see also 7)
  A.  Fungistatic

    (1)  Mercury compounds
Phenylmercuric acetate: [Ref. I-P-08-00.09]
For preservation: 45 to  250 ppm   by  dry
weight.  For fungistat after application: 3500
to  15,000 ppm.
    (2)  Substitute compounds
Bis (tributyltin)  oxide: [Ref. I-B-09-00.02]
Tape-joint compounds: 150 ppm by weight.
    (3)  Comparative effectiveness  and im-
pact
      (a)  Bis (tributyltin) oxide is generally
comparable in effectiveness to PMA. Other
substitute  materials are probably  available
but cannot be identified specifically  from
label claims.
      (b)  Impact of withdrawal of mercury
for this use should be insignificant.
  B. Cement (bacterial preservative)
    (1)  Mercury compounds
Phenylmercuric acetate (95%) powder: [Ref.
6515-7] 2 ounces product per bag of  cement
(size not specified).
    (2)  Substitute compounds
      (a)  2, 3, 5, 5-Tetrachloro-4-(methyl-
sulfonyl)  pyridine  (82%):  [Ref.  464-353]
1.0% to 2.0% product by weight of formula-
tion.
      (b)  Sodium     pentachlorophenate
(79%):  [Ref.  464-125]  1.0% product  by
weight in water; 0.5% to 3.0% of solution by
weight of product in which incorporated.
      (c)  Dehydroabietylamine pentachlo-
rophenate (40%):  [Ref. 2829-56] 0.5% to 2%
product by weight of media.
    (3)  Comparative effectiveness  and im-
pact
      (a)  Other chemical compounds,  al-
though  not  specifically recommended for
this application, may also be used.
      (b)  Substitute compounds appear to
be adequate.
      (c)  Impact on industry may be signif-
icant in  that sufficient  substitute compounds
for a variety  of building applications may
not be available.  Impact on consumer may
also  be  significant  where  preservation
against  bacteria in humid climates is  a ne-
cessity. Mercurials have  had a long history
of  use  in building applications  and are
known to be highly effective.
4. Paints
   A.  Antifouling marine coatings
    (1)  Mercury compounds
      (a)  Mercuric oxide:  [Ref. Reg. No.

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2693-57, 2693-201
        (aa.) 0.5 to 6.0%, in combination
with 3.759? cuprous oxide and  1.4 to 6.5%
"mercury phenate."
        (hb.) 0.5 to 6.09?, in combination
with 17.59? cuprous oxide.
      (c)  Mercury phenate:
1.4 to 6.59?, in combination with mercuric
oxide (see 4 A (a) above)
      (d)  Phenylmercuric  acetate:   [Ref.
Reg. Nos.  3073-17, 25, and 26] 4.5%, used
alone.
      (e)  Phenylmercuric   oleate:    [Ref.
Reg. Nos. 539-214, 215, 216 and 218]
        (aa.) 0.95 to 1.11%, used alone, or
        (bb.) 0.89% in  combination with
23,88% metallic copper.
    (2)  Substitute compounds
      (a)  Copper  (metallic):   [Ref.  Reg.
Nos. 8120-3 and 9792-1] 15.0 to 48.2%  by
weight.
      (b)  Copper acetoarsenite: [Ref. Reg.
Nos. 390-11 and 390-38] 16 to 26.5% in com-
bination with 13.5% copper powders or 2.0%
Bis (tributyltin) oxide.
      (c) Copper  hydroxide:   [Ref.  Reg.
Nos. 3073-2 and 3073-34] 8 to 9% in combi-
nation with 48% copper oxide or 24% copper
oxide.
      (d)  Copper linoleate: [Ref. Reg. No.
2693-47] 9.4% in  combination  with  31.5%
cuprous oxide.
      (e) Copper oleate: [Ref. Reg.  Nos.
9461-50 and 9461-48] 3.4 to 8.0% in combina-
tion with 38.9 percent cuprous oxide or 10%
cuprous oxide.
      (f) Copper  resinate:  [Ref. Reg. No.
2568-7] 3% in combination with 16.8% cu-
prous oxide plus 12.6% capric acetoarsenite
plus 1.4% pine oil.
      (g) Cuprous oxide: [ref. Reg.  Nos.
10250-1 and 3658-2] 7.5 to 74.5% alone
      (h)  Bis (tributyltin) oxide: [Ref. Reg.
Nos. 390-30 and 568-20] 4.6 to 10% alone.
      (i) Dichlone: [Ref. Reg.  No.  3658-3]
5.5 percent in combination with 51.2% cu-
prous oxide.
      (j) Pentachlorophenol:   [Ref.   Reg.
No.  9461-52]  2.23%  in  combination  with
24.59% cuprous oxide plus 1.86% Bis (tribu-
tyltin) oxide.
       (k) Phenarsaxine chloride: [Ref. Reg.
Nos.  2693-35  and 2693-361 4.5 to 6.4%  in
combination with 19.4% cuprous oxide or
31.5% cuprous oxide.
       (I) Tributyltin  fluoride:  [Ref.  Reg.
Nos.  3658-14  and 8019-13]  5.55  to 14.3%
alone.
    (3) Comparative  effectiveness  and im-
pact
      (a)  Substitute compounds are effec-
tive  replacements for mercury in marine
finishes.
      (b)  Impact of withdrawal of mercury
from these uses will be insignificant.
  B.  Paints (bacterial preservative)
    (1)  Mercury compounds
Phenylmercuric  oleate (30%):  [Ref.  Reg.
Nos. 6516-10 and 8489-1]
      (a) 2 ounce by weight packet to 1 gal
of oil   based  paint, application to marine
surfaces on pleasure craft.
      (b) 0.5  Ib  product/100  gal  finished
formula.
         (2) Substitute compounds
       (a)  2,  3,   4,   6-Tetrachlorophenol
(74%): [Ref. Reg. No. 464-71] 1.0% to 3.0%
product by weight of formulation.
       (b) 2, 3, 5, 6-Tetrachloro-4-(methyl-
sulfonyl) pyridine  (82%): [Ref. Reg.  No.
464-333]
        (aa.)  Oil-based high zinc content:
0.25% to 0.5% by weight of formulation.
        (bb.)  Zinc-oxide free systems: 1  to
3% to weight of formulation.
        (cc.)  Interior paints: flat finishes -
0.3%; gloss  paints 0.7% by weight of formu-
lation.
       (c) 2-(Thiocyanomethylthio)  benzo-
thiazole (32%) and 2-Hydroxypropyl metha-
nethiosulfonate (28%): [Ref. Reg.  No  1448-
27]
        (aa.)  Oil paint,  zinc oxide: 0.1  to
0.5% by weight of formulation.
        (bb.)  Oil paint, zinc-free  alkyd: 0.3
to 1.0% by weight of formulation.

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    (3) Comparative effectiveness and im-
pact
       (a) Some substitute compounds  im-
part odors to finished paint film that may be
undesirable in food processing areas.
       (b) Listed   substitute   compounds
cannot be considered inclusive. Paint pre-
servative compounds used for  water-based
paints or synthetic emulsion-type paints may
also be substituted.
       (c) Substitute compounds appear to
be adequate.
       (d) Impact on industry  expected to
be small, impact  on consumer expected to
be negligible.
5. Paints, varnishes, stains
  A. Fungistatic (mildew control)
    (1) Mercury compounds
       (a) Chloromethoxy-acetoxymercu-
ripropane: [Ref. I-C-14-00.01]  Mfg. use la-
bel, no directions for use.
       (b) Di (phenylmercury)  dodecylsuc-
cinate: [Ref. I-D-21-00.01]
         (aa.) Household  use:  3750  ppm
added to paint.
         (bb.) Industrial use: add in amount
required.
       (c) Phenylmercuric acetate: [Ref. I-
P-08-00.09]
         (aa.) Preservation: 0.1  to 0.25 lb/
100 gal.
         (bb.) Mildew control:  1.0 to 3.0 lb/
100 gal.
         (cc.) Preservation of  protein  col-
loid components: 0.23 to 0.3 lb/100 gal.
         (dd.) Preservation of  carbohydrate
components: 0.1 to 0.15  lb/100 gal.
       (d) Phenylmercuric borate: [Ref.  I-P-
08-10.01] Mold control: 0.2 to 3.0 lb/100 gal.
       (e) Phenylmercuric hydroxide: [Ref.
I-P-09-50.01]  Aqueous systems: 4500 to 9000
ppm residual  in coating.
      (f)  Phenylmercuric oleate: [Ref. I-P-
14-00.01 and .02]
        (aa.) Mildew on  paint film, decay
on stained surfaces as  household  or com-
mercial  use:  1200 ppm plus 14,250  ppm of
pentachlorophenol added to coating.
        (bb.) Industrial use:
333 to 1666 ppm by weight of coating: 1.0 to
6.66 lb actual/100 gal.
      (g)  Phenylmercury  propionate: [Ref.
I-P-1500.01] Mildew  control:  1.5 to 4.0 lb
actual/100 gal.
      (2)  Substitute compounds
      (a)  Alkyl dimethyl benzyl ammonium
chloride: [Ref. I-A-08-25.06] Mildew con-
trol: aqueous systems—366 ppm plus  610
ppm TBTO.
      (b) Alkyl dimethyl  ethybenzyl  am-
monium cyclohexyl sulfamate: [Ref. I-A-17-
00.01] Aqueous exterior systems (latex): 600
to 800 ppm by weight.
      (c) Barium metaborate: [Ref. I-B-01-
00.91]
         (aa.) 8.35% by weight of paint.
         (bb.) 0.09 to 0.36% by weight for
preservation of finished  colors  containing
protein.
         (cc.) 0.09 to 0.27% by weight for
preservation of finished  colors  containing
carbohydrates.
      (d) trans-1,   2-Bis   (propylsulfonyl)
ethene: [Ref. I-B-07-80.01] 3000 to 5000 ppm
by weight—for oil-based paints.
      (e) Bis (tributyltin) oxide: [Ref. I-B-
09-00.01 and .02]
        (aa.) Household  use  in aqueous
systems: 610 ppm by volume.
        (bb.) Industrial use:  500  to  1000
ppm by weight of polyvinyl acetate formula-
tions;
1500 to 3000 ppm by weight of  acrylic  for-
mulations;
2500 to  3500 ppm by weight of styrenebuta-
diene formulations;
0.92 lb/100 gal of interior paint;
6 to 9 lb/100 gal of exterior paint;
8 to 12 lb/100 gal of roof paint.
      (f)  Captan:  [Ref.  I-C-10-00.15   and
.16]
        (aa.) Household uses:  l.Ooz/galof
oil-based paint.

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        (bb.)  Industrial  use: 3600  to 9000
ppm by weight of paint.
       (g)  4-Chloro-3, 5-xylenol:  [ref.  I-C-
21-00.01 and .02]
        (aa.)  Household use: 1.0 fluid oz of
45% solution/gal of interior, oil or emulsion
formulations.
        (bb.)  Industrial  use:   in  amounts
required.
       (h) Copper 8-quinolinolate:  [Ref. I-
C-34-00.01 and .02]
        (aa.)  Commercial use: 0.75 pint of
10.0% solution/gal.
        (bb.)  10,000 ppm by weight of  sol-
ids or by total  weight of paints, varnishes or
sealers.
       (i)  Parachlorometacresol: [Ref.  I-P-
01-00.01]  500  to  1500  ppm by weight of
aqueous system paints.
       (j)  Potassium o-phenylphenate: [Ref.
I-P-26-00.01]
        (aa.)  Preservation: 0.15 to 2.0 per-
cent by weight.
        (bb.)  Mildew  control: 10,000  to
20,000 ppm by weight of polyvinyl  acetate
formulation.
       (k) Potassium 2, 4, 6-trichlorophen-
ate: [Ref. I-P-28-80.01] Mildew control: 3750
to 22,500 ppm  by weight.
       (I)  Sodium  o-phenylphenate: [Ref. I-
S-16—00.09]
Preservation: 2000 to 5000 ppm by weight of
oil- or water-based formulations.
       (m) 2,  3, 5, 6-Tetrachloro-4-methyl-
sulfonyl pyridine:  [Ref. I-T-02-00.01] 500 to
30,000 ppm by weight of alkyl, latex or oil
formulations.
       (n) Tetrahydro-3,  5-dimethyl-2H-l,
3-.  5-thiadiazine-2-thione:  [Ref.   I-T-07-
00.03]
         (aa.)  Interior  paint   mildew: 1000
to 20,000 ppm  by weight of paint.
        (bb.)  Aqueous    components
molds: 100 to 5000 ppm. by weight of sus-
pension.
       (o) 2-(4-Thiazolyl)    benzimidazole:
[Ref.  I-T-09-00.02 and .03]
         (aa.) Exterior paints:
0.25to2.01b/100gal.
         (bb.) Interior paints:
0.1 tol.Olb/lOOgal.
      (p) 3,  4',  5-Tribromosalicylanilide:
[Ref. I-T-11-00.02] 1000 ppm  by weight of
butadiene - styrene latex formulation.
      (q) Tributyltin salicylate:  [Ref.  I-T-
12-80.01] Amount as required.
      (r) Zineb: [Ref. I-Z-10-00.14]
Household use:  1.0 to 1.5 ounces/gal.
    (3)  Comparative  effectiveness and im-
pact
      (a) Very  little  is known  about the
comparative  effectiveness of  mercury  and
substitute compounds in paints. Mercury is
compatible with most  types and formula-
tions  of  both oil- and  water-based types.
Most substitute compounds are limited as to
type of  paint and specific  formulation in
which they can be used or that has been test-
ed.
      (b) The industry  recognizes the need
to develop substitute materials but has indi-
cated that time is needed to test compounds
now available.
      (c) The impact of withdrawal of mer-
cury from the pesticide uses in paints, var-
nishes and lacquers would be very severe on
the manufacturers  and could leave the pub-
lic in a "distress situation" in regard to mil-
dew control  on  paint films, particularly in
areas with severe mildewing conditions.
  B.Paint and premanufactured paint com-
ponents preservation (bacteriostatic):
    (1)  Mercury compounds
Phenylmercuric  acetate  (100%  powder):
[Ref. Reg. No. 8489-5]
      (a) Preservative  for  polyvinyl ace-
tate,  acrylic and  butadiene-s styrene sys-
tems. Package stability for aqueous systems
such  as  paint and carbohydrate thickener
solutions: 2 to 4 ounces product/100 gal me-
dia by weight.
      (b) Preservation  of  protein  colloids
and systems containing  same: 4 to 8 ounces
product/100 gal media by weight.

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    (2)  Substitute compounds
      (a)  Sodium      pentachlorophenate
(79%): [Ref. Reg. No. 464-299] 0.1% to 0.2%
product by weight of particular substrate.
      (b)  l-(3-chloroallyl)-3,  5, 7-triaza-l-
azoniaadamatane chloride (90%): [Ref. Reg.
No. 464-327]
        (aa.) Aqueous paint systems: 0.1%
to 0.2%  product by weight of formulation.
        (bb.) Paint components: 0.05% to
0.15% product by weight of media.
      (c)  Sodium 2, 4, 5-trichloropihenate
(85%): [Ref. Reg. No. 464-131] For preser-
vation of polyvinyl acetate emulsions:0.4%
product by weight of media.
      (d)  Sodium  o-phenylphenate:  [Ref.
Reg. No.  464-78]  Preservation  of carbohy-
drate  thickener solutions:  0.05%  to  0.2%
product by weight of media.
      (e.) 50:50  mixture  o-phenylphenol
and Pentachlorophenol: [Ref. Reg.  No. 464-
70 and 464-72]
0.5%  of mixture  based on weight of wet
formulation for preservation of protein col-
loids.
      (f)  Sodium  2-pyridinethiol   1-oxide
(2%): Ref. Reg. No.  1258-846] Preservation
of acrylic  latex paint,  0.25%  product  by
weight of formulation.
      (g)  2-(Thiocyanomethylthio)  benzo-
thiazole (32%) and 2-Hydroxypropyl metha-
nethiosulfonate (28%): [Ref. Reg. No. 1448-
27]
Alkyl-modified emulsion paint preservative:
0.3% to 1.0% product by weight of formula-
tion.
      (h)  AlkyI (50%C,2, 30%C,4, 17%C,6,
3%C,8)  dimethyl  ethylbenzyl  ammonium
cyclohexylsulfamate (80%): [Ref. Reg. No.
1839-36]
        (aa.) Latex   paint  preservative:
0.1% to  0.2% product by weight of paint.
        (bb.) Carbohydrate  and   protein
colloid preservative: up to 0.1% product by
weight of formulation.
      (i) Dehydroabjetylamine  pentachlor-
phenate (50%):  [Ref.  Reg. No.  2829-59]
Water-based  paint  preservative:   0.35%
product based on finished weight of formula-
tion.
      (j) Alkyl (5% caprylyl, 56% lauryl,
18% myristyl, 7% palmityl, 5% stearyl, 2%
linoleyl) hydrochlorides (25%): [Ref.  Reg.
No. 8489-13] Preservation of water-contain-
ing and emulsion-type adhesives, Paints and
their components:  0.15% to  0.3% product
based on total weight of composition.
      (k)  1,       2-benzisothiazolin-3-one
(23%): [Ref. Reg. No. 10182-1] Preservation
of water-based  paints, emulsion  paints and
components: [0.15% product based on total
weight of paint.
    (3)  Comparative effectiveness and im-
pact
      (a)  Mercury  compounds  can  cause
"browning" of certain paint formulations,
substitute compounds much less so.
      (b)  Some substitute  compounds im-
part  objectionable  odor  to finished  paint
film.
      (c)  Substitute compounds appear to
be adequate.
      (d)  Impact on  industry expected to
be negligible, price  of end-product to con-
sumer expected to rise.
  C. Latex vinyl paint finish on asbestos ceil-
ing  tile  (bacteriostatic  and  self-sanitizing
against bacteria)
    (1)  Mercury compounds
      (a)  Phenylmercuric acetate (0.0034%
to 0.004%  by weight of total product):  [Ref.
Reg. Nos.  7816-3, 8700-2] Product is compo-
nent of tile vinyl latex paint applied at rate of
3.13 gal  paint per 100 sq ft. of ceiling tiles or
panels, equal to 0.02 Ib phenylmercuric ace-
tate per  1000 sq  ft.
      (b)  Phenylmercuric        propionate
(0.0013% to 0.005% by weight of total tile):
[Ref. Reg. Nos. 7850-11, eta/]
Product is  component of vinyl latex  paint
applied to asbestos ceiling tile. Bears bacter-
iostatic (bacterial growth inhibiting) and self
-sanitizing (reduction of bacterial numbers)
claims; used primarily in hospitals and  nurs-
ing homes.
                                                                                    7

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      (c) Chloromethoxypropylmercuric
acetate (0.002% based on total weight of tile)
and  copper  pentachlorophenate  (0.02%):
[Ref. Reg. No. 10591-1]
Product component of white latex paint and
clay primer applied to ceiling tile and wall-
board applied at rate of 0.013 pounds prod-
uct (in latex paint) per 1000 square feet  of
surface.
    (2)  Substitute compounds
      (a) l-(3-chloroally1)-3,  5, 7-triza-l-
azoniaadamantane  chloride  (90%):  [Ref.
Reg. Nos. 464-3271
0.1% to 0.2% product by weight of formula-
tion.
      (b) 2, 3, 5, 6-Tetrachloro-4-(methyl-
sulfonyl) pyridine  (82%):  [Ref.  Reg. No.
464-353]
0.5 to 1.0%  by weight of formulation.
      (c) Captan (N-trichloromethylthio-4
cyclohexene-1,  2-dicarboximide)   (90%):
[Ref. Reg. No. 1965-111
0.25% to 1.0% product by weight of formu-
lation.
      (d) Alkyl  (5%  caprylyl,  7% capryl,
56% lauryl,  18% myristyl, 7%. palmityl, 5%
stearyl, 2%  linoleyl) hydrochlorides (25%):
[Ref. Reg. No. 8489-13]
0.15 to 0.3%- product on total weight of me-
dia.
      (e) Phenol  (1.41%),  Sodium  borate
(0.47%) and Sodium phenate (0.24%): [Ref.
Reg. No. 8383-1] 2% to 5% by weight of ac-
tive ingredients.
      (f) 2-(Thiocyanomethylthio)   benzo-
thiazole (32%) and 2-Hydroxypropyl metha-
nethiosulfonate (28%): [Ref. Reg. No. 1448-
27]
0.03 to 0.05% product based on  formula
weight.
      (g) Alkyl (50%C,2,30%C14,  17%C,6,
3%C]8) dimethyl  ethylbenzyl  ammonium
cyclohexylsulfamate (80%): [Ref. Reg. No.
1839-36]
0.1 to 0.2% product by weight of formula-
tion.
    (3)  Comparative  effectiveness and im-
pact
      (a)  Comparative costs of substitutes
and mercury compounds not known.
      (b)  Substitute  compounds appear to
be adequate.
      (c)  Impact on industry expected to be
minimal, consumer impact somewhat varia-
ble.
      (d)  Impact on uses of product in criti-
cal hospital areas requiring  low bacterial
counts cannot be assessed.
  D. Vinyl latex interior paint (bacteriostatic
finish)
    (1)  Mercury compounds
Phenylmercuric  acetate: [Ref.  Reg. No.
10751-1]
Component of paint, 0.27% by weight.
    (2)  Substitute compounds
      (a)  Phenol (1.4%) and Sodium borate
(0.47%), and Sodium phenate (0.24%): [Ref.
Reg. No. 8383-1]
2 to 5% by weight of active ingredients.
      (b)  1-(3-chloroallyl)-3,  5,  7-triaza-l-
azoniaadamantane  chloride  (90%):  [Ref.
Reg. No. 464-327]
0.1 to 0.2% product by weight of formula-
tion.
      (c)  Sodium   2-pyridinethioI-l-oxide
(90%,): [Ref. Reg. No. 1258-842]
        (aa.) 0.5 lb/10,0001b formulation.
      (d)  Captan  (N-trichloromethylthio-4
cyclohexene-1,   2-dicarboximide)   (90%):
[Ref. Reg. No. 1965-11]
0.25 to 1.0% product by weight of paint.
      (e)  Alkyl  (5% caprylyl,  7%  capryl,
56% lauryl, 18% myristyl, 7% palmityl, 5%
stearyl, 2% linoleyl)  hydrochlorides (25%):
[Ref.  Reg. No. 8489-13] 0.15 to 0.3% prod-
uct based on total weight of media.
      (f)  2-(Thiocyanomethylthio)   benzo-
thiazole (32%) and 2-Hydroxypropyl metha-
nethiolsulfonate (29%): [Ref. Reg. No. 1448-
27] 0.03 to 0.05% product based on formula
weight.
      (g)  Alkyl (50%C,2, 30%C,4, 17%C,6,
3%C18)  dimethyl  ethylbenzyl  ammonium
cyclohexylsulfamate (80%): [Ref. Reg No
1839-36]
8

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0.1 to 0.2% product by weight of formula-
tion.
      (h)  2, 3, 5, 6-Tetrachloro-4-(methyl-
sulfonyl) pyridine (82%): latex media: [Ref.
Reg..No. 464-3531
0.5,to 1.0% product by weight latex media.
    (3) Comparative effectiveness and im-
pact
      (a)  Substitute compounds  appear to
be adequate.
    (b) Impact on  industry  and  consumer
appear to be minimal.
6. Sealers and Sizings

  A.  Mercury compounds

    (1)  Phenylmercuric acetate: [Ref. I-P-
08-00.09]
      (a)  Preservation: 0.1  to  0.25  lb/100
gal.
      (b)  Mildew control: 1 t,o 3 lb/100 gal.
      (c)  Preservation of carbohydrate so-
lutions: 0.1 lb/100 gal.
      (d)  Preservation of protein solutions:
0.23 to 0.3 lb/100 gal.
    (2)  Phenylmercuric oleate: [Ref. I-P-14-
00.01] mildew  control:  1200  ppm by weight
of formulation.

   B.  Substitute com pounds

    (1) Alkyl  dimethyl benzyl ammonium
chlorides: [Ref. I-A-08-45.051
Preservation: 50,000 ppm  plus other fungis-
tats.
    (2)  4-Chloro-3, 5-xylenol: [Ref, I-C-21-
00.021 As required.
    (3)  Copper  8-quinolinolate:  [Ref. I-C-
3400.02] 1.0% by weight.
    (4)  Monoethanolamine    2-mercapto-
benzothiazole:  [Ref. I-M-21-00.01] 0.15 to
0.4% by weight.
    (5)  Sodim _o-phenylphenate: [Ref. I-S-
16-00.101 2.0% by weight.
    (6)  Tetrahydro-3, 5-dimethyl-2H,  -1, 3,
5-thiadiazine-2-thione (Mylone):  [Ref. I-T-
07-00.03]
100 to 5000 ppm by weight.
  C. Comparative effectiveness and impact
    (1)  Substitute compounds are generally
less effective than mercury at  comparable
dosage rates.
    (2)  Mercury compounds are less expen-
sive and adapted to use in a wider range of
products than are substitutes.
    (3)  Impact of withdrawal  of mercury
for these uses should have slight to moder-
ate effect on manufacturers and consumers.
                              *
7. Textures and other dry products ultimate-
ly applied by dispersion in water (see also 1,3
cements and plasters).
  A. Mercury compounds
Phenylmercuric acetate: [Ref. I-P-08-00.09]
      (a)  Preservation: 45 to 250 ppm by
weight.
      (b)  Mildew  control: 3500 to  15,000
ppm by weight.
  B. Substitute com pounds
None identified.
8.  Wallpaper coatings
  A. Mercury compounds
Di(phenylmercury)     dodecenylsuccinate:
[Ref. I-D-21-00.01]
Add to deposit 0.01 ounce of a 10.5 or 12.0%
product/square yard of finished paper.
  B. Substitute compounds
    (1)  3, 4, 5-Tribromosalicylanilide( [Ref.
I-T-11-00.02]
Incorporate  0.1% into  plastic laminate be-
fore calendering.
    (2)  See  additional  probable substitutes
under IX - Plastics.
  C. Comparative effectiveness and impact
    (1)  Substitute compounds must be em-
ployed at higher concentrations than mercu-
ry to achieve comparable fungistasis.
    (2)  Mercury has a  broader  spectrum of
fungal control  than most substitute com-
pounds.
    (3)  Impact of withdrawal  of mercury
for this use would appear to be slight.

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                                II.  Fabrics and Textiles
 1. Fungistats
   A. Mercury compounds
     (1) Phenylmercuric  acetate:  fungistat
 for mildew control; industrial use in finishing
 processes. [Ref. I-P-08-00]
       (a) 25 to 180 ppm in final rinse.
       (b) 30 to 90 ppm by padding.
       (c) 150 to 225 ppm by spraying.
     (2) Phenylmercuric  borate  and chlor-
 ide:  fungistat,  industrial use  in  finishing
 process. [Ref. I-P-08-10.01] 2.0 Ib of a 1.1%
 PMB plus 0.10% PMC soln./lOO gal in finish-
 ing bath  = 26.5 ppm PMB plus  2.4 ppm
 PMC.
     (3) Phenylmercuric  oleate:  fungistat;
 consumer use on awnings, boat covers, navy
 tops, curtains, sail covers. [Ref. I-P-14-00]
       (a) 2000  to 2800 ppm alone or with
 TBTO and zinc naphthenate, by brush.
       (b) coatings for outdoor fabrics: 0.05
 to 0.5% of a 30% product, based on weight
 of coating. [Ref. l-P-14-00.02]
     (4) Phenylmercuric propionate: fungis-
 tat; industrial use in finishing process. [Ref.
 I-P-15-00] 250 to 500 ppm by impregnation.
     (5) Phenylmercuric triethanol ammon-
 ium  lactate: fungistat  for mildew,  rot and
 decay; industrial use in finishing process.
 [Ref. I-P-17-00] 560 to  1130 ppm by impreg-
 nation  or in size.
     (6) Pyridyl  mercuric chloride: (0.06%
 plus 7.5%) alkyl dimethyl benzyl ammonium
 chloride; industrial use in finishing process.
 [Ref. I-A-08-10.02] 1.2  to 1.3% of mixture
 retained on fabric by padding.
   B. Substitute compounds

    (1) Alkyl  amine  salts  of  tetrachloro-
 phenol (alone or with TBTO); fungistat; in-
dustrial use in finishing process. [Ref. I-A-
06-00.01]
       (a) cotton, sisal, jute, hemp and simi-
 lar materials: 10,000 to 20,000 ppm alone or
 1090 ppm plus 210 ppm TBTO.
       (b) carpet underlay:  1500 ppm plus
 250 ppm TBTO.
    (2) Alkyl dimethyl benzyl  ammonium
 chlorides: fungistat; industrial processes.
       (a) padding to retain  1.2  to 1.3%  by
 weight of a mixture  of quaternary plus o-
 phenylphenol  and  2, 3-thiobis  (4-chloro-
 phenol).  [Ref. I-A-08-10.02]
       (b) 1500 to  6000 ppm quaternary  by
 finishing equipment. [Ref. I-A-08-15.02]
       (c) 5000 ppm  quaternary plus 250
 ppm TBTO by spraying. [Ref. I-A-08-15.02]
       (d) 500 to 2500 ppm quaternary plus
 150 to 500 ppm TBTO by padding or other
 suitable equipment. [Ref. I-A-08-15.02]
    (3) Ammonium   hydroxide   C8  fatty
acid-silver complex:  fungistat;  consumer
use. [Ref. I-A-25-00.01] 800 ppm spray.
    (4) Bis  (tributyltin) oxide:  fungistat;
industrial use in finishing process. [Ref. I-B-
09-00.03]
      (a) 250 to 500 ppm on clothing, etc.
      (b) 500 to 1000 ppm on awnings, etc.
    (5) Captan: fungistat; industrial use  in
finishing process. [Ref. I-C-10-00.16] Depos-
it 0.90 to 1.7% by weight of fabric.
    (6) 4-or  6-chloro-2-phenylphenol: fun-
gistat; consumer  use.  2000  ppm  spray,
 sponge or dip. [Ref. I-C-18-00.01]
    (7) 4-chloro-3,   5-xylenol:   fungistat;
 consumer use. [Ref. I- -21-00]  1200 ppm
 alone or 600 to 2000 ppm  in combination
 with other fungistats.
    (8) Copper  8-quinolinolate:  fungistat;
 industrial use in finishing process. [Ref. I-C-
 34-00.03] 0.02 to 1.0% metallic copper equiv-
 alent  deposited. Note:  objectionable color
 for many types of fabric.
    (9) Dehydroabiethylamine  salt of pen-
 tachlorophenate: Industrial use  in finishing
 process. [Ref. I-D-02-00.01]
       (a) indoor fabrics: 0.25 to 1.25%  by
 weight of fabric.
       (b) outdoor fabrics: 0.8 to 1.5%  by
 weight of fabric.
10

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    (10) Dialkyl dimethyl ammonium chlor-
ide:  fungistat;  industrial use  in  finishing
process. [Ref. I-D-04-20.02]  Deposit 28.1 to
3750 ppm quaternary plus 142.5 to 1250 ppm
TBTO by weight.
    (11) Diisobutylphenoxyethoxyethyl
dimethyl benzyl ammonium  chloride:  fun-
gistat; industrial  use in finishing  process.
[Ref.  I-D-13-00.04] 1635 to 2045 ppm quater-
nary  plus 468 to 585 ppm tributyltin  ben-
zoate by weight of fabric.
    (12) Dodecyl-di    (beta-hydroxyethyl)
benzyl  ammonium  chloride: fungistat;  in-
dustrial use in finishing process. [Ref. I-D-
26-10.01] For  suitings, linings,  blankets,
upholstery fabrics, carpets and other articles
seldom, if  ever, laundered. 0.2 to 1.0 gram/
liter of water by exhaustion or padding.
    (13) N-Dodecylquanidine   terephthal-
ate:  fungistat; industrial use  in   finishing
process. [Ref. I-D-27-90.01] For  awnings,
tents, tarpaulins, sails and  similar  textiles:
2500 to 5900 ppm by padding.
    (14) Lauryl pyridinium salt of 5-chloro-
2-mercaptobenzothiazole:   fungistat;    in-
dustrial  use in finishing process.  [Ref.  I-L-
01-00.01]
       (a)  For burlap: 3375 to 10,000 ppm.
       (b)  Duck, mattress  ticking, similar
fabrics:  1250 plus 2500 ppm.
       (c)  Industrial fabrics  and yarns: 5000
plus 10,000 ppm.
     (15) 2, 2 -Methylenebis - (3,  4,  6-tri-
chlorophenol):  fungistat;  industrial  uses,
finishing process. [Ref. I-M-13-00.03]
       (a)  -200 to 2500 ppm.
       (b)  2500  to  6000 ppm plus  2500 to
6000 ppm o-phenylphenol.
    (16) 10, 10   Oxybisphenoxarsine: fun-
gistat; industrial  uses in finishing  process.
[Ref. I-O-03-00.011  For cotton  fabrics to be
coated  with  thermoplastic systems: 400 to
1000 ppm by padding.
    (17) Pentachlorophenol: consumer use.
30,000 to 50,000 ppm as a soak. [Ref. I-P-05-
00.01]
    (18) Sodium dimethyldithiocarbamate:
fungistat; industrial uses in  finishing proc-
ess.  [Ref.  I-S-09-00.05]  1.38% plus 0.12^
sodium  2-mercaptobenzothiazole  by  pad-
ding to 100% wet pick up. Set with zinc ace-
tate.
    (19)  Sodium  pentachlorophenate:  fun-
gistat;  industrial  use in finishing process.
[Ref.  I-S-15-00.04]  For suit linings, uphol-
stery fabrics: 1000 to 5000 ppm by dipping,
padding or spraying.
    (20) Sodium  orthophenylphenate:  fun-
gistat for preservation of  unfinished cloth
and yarns. [Ref. I-S-16-00.10]0.2 to 1.0%.
    (21) Sodium   salt  of  2-mercaptoben-
zothiazole: fungistat; industrial use in finish-
ing process.  [Ref.  I-S-20-00.01]  0.2% by
weight deposited on fabric.
    (22) Thiram: fungistat; industrial uses.
[Ref. l-T-10-00.08]  For belting, ducks, other
heavy industrial fabrics: 1875 to 3750 ppm
by weight of fabric.
    (23) 3,   4',   5-Tribromosalicylanilide:
fungistat; industrial use in finishing process.
[Ref. I-T-11-00.01 and 0.2]
       (a) For fabrics to be coated with vi-
nyl thermoplastics: 20,000 ppm prior to coat-
ing.
       (b) Other textiles: 500 to 7500 ppm by
weight.
    (24) Tributyltin  acetate:  fungistat;  in-
dustrial use in  finishing process. [Ref.  I-T-
12-00.01] Deposit 1.8% of product by weight
of fabric by padding.
    (25) Zinc dehydroabietylammonium  2-
ethylhexoate:  fungistat; industrial  use  in
finishing process.  [Ref.  1-2-03-00.01] 2.0  to
2.5% or more by weight of fabric of a formu-
lation  containing  42.8% plus 29.2% zinc
ethylhexoate and 19.2% 2-ethylhexoate salt
of magnesium quinolinolate.

  C.  Comparative effectiveness and impact.
    (1) Various  mercury  compounds are
used as fungistats in textile finishing at levels
of 25 to 1130 ppm by impregnation. Substi-
tute materials are used  at levels  from 200 to
20,000 ppm.
    (2)  Mercury  compounds are "broad
spectrum" fungistats controlling most, if not
                                                                                     11

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all, of the problem  organisms.  Substitute
materials are less broad and frequently re-
quire combinations of materials to aid effec-
tiveness.
    (3)  Mercury compounds are useful on a
broad range of fabric and textile  substrates
(cotton, jute, wool, etc.). Substitute  materi-
als are adapted to more specific uses.
    (4)  Mercury compounds are less expen-
sive than substitute materials, frequently by
a factor of 10.
    (5)  Mercury compounds do not impart
objectionable coloration nor do they affect
the "hand" of textiles as do many substitute
compounds.
    (6)  Impact of withdrawal of mercury
for use  on fabrics and textiles may affect
financial situation of certain economic poi-
son formulators and may require revision of
certain  Federal  specifications.  Impact on
consumer of treated  goods  should be slight
to moderate.

2.  Bacteriostats

   A.  Mercury compound!)

    (1)  Phenylmercuric borate: (1.1%)  and
alkyl (40% C,2, 50% C,4, 10% C16) dimethyl
benzyl  ammonium   chloride (0.12%)  and
Phenylmercuric   chloride   (0.10%):  [Ref.
3673-10] Add 2 Ib product to 100 gal of fin-
ishing bath; for cotton,  wool, nylon and ray-
on fibers.
    (2)  Pyridyl mercuric acetate  (2%)  and
alkyl  (67% C,2, 25% C14,  7% C,6,  1% C8-
C|8)  dimethylbenzyl ammonium chorides
(7.5%):  [Ref. 5817-2]
2% solution of product at 100°F, 60-65% wet
pickup by fabric resulting in 1.2 to 1.3% of
product on fabric (types not specified)
    (3)  Phenylmercuric    triethanolamm-
onium lactate (22.5%): [Ref. 6516-4] Typical
formula: 3.75 Ib product to makeup  100 gal
of water. Padding application from aqueous
solution sufficient to  deposit 0.25% of prod-
uct manufactured dry weight of fabric (un-
specified).
  B. Substitute compounds
    (1)  Bis (tributyltin) oxide (0.84%) and
dialkyl (alkyl from coconut oil fatty acids)
dimethyl ammonium chloride (1.25%): [Ref.
10466-2]  1.25% product on weight of goods.
    (2)  Alkyl (average = Cp) amine salts of
tetrachlorophenol  (100%):  "[Ref.  3090-461
0.25% to 2% product based  on weight of dry
fabric.
    (3)  Bis  (tri-n-butyltin)  oxide  (25%):
[Ref. 6390-2] 0.1 to 0.2% product based on
dry weight of fabric.
    (4)  n-alkyl (60% C]4, 30% C,6, 5% C,2,
5% C)8) dimethyl benzyl ammonium choride
(50%):  [Ref. 6390-9] Apply to leave  0.25%
product on dry weight of fabric.
    (5)  n-alkyl (60% C,4, 30% C,6, 5% C,2,
5% C,8) dimethyl benzyl ammonium 2 ethyl
hexoate (25%):  [Ref. 6390-13] 0.1% pickup
or 0.025% active ingredient  on dry weight of
fabric.
    (6)  Tributyltin  neodecanoate  (98%).
[Ref. 8314-5] 0.025% to 0.05% product based
on weight of fabric.
    (7)  Zinc      dimethyldithiocarbamate
(46%) and zinc mercaptobenzothiazole (4%):
[Ref.  1965-26] 2.5% product by weight of
cloth.
    (8)  Sodium pentachlorophenate  (79%)
[Ref. 464-125] 0.1% to 0.75% by weight of
treated material.
    (9) 2, 2 -methylenebis (4-chlorophenol):
[Ref. 824-6] 40%  solution  used  to deposit
0.5% to  1.0%  on fabric, concentration of
product in  pad liquor  varies with percent
pickup.

  C. Comparative effectiveness and impact

    (1) Substitute compounds exhibit great-
er substantivity to fabrics than mercurials.
    (2) Substitute compounds appear to be
satisfactory.
    (3)  Impact  on  certaiin  individual  firms
selling mercurials may  be  substantial, im-
pact on  industry and consumer expected to
be minimal.
12

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                               III.   Fibers and Cordage
1.  Fungistats
  A. Mercury compounds
    (1)  Phenylmercuric acetate: [Ref. I-P-
08-00.10] For interior components of furni-
ture and mattresses (alpha cellulose, cotton,
latex impregnated  curled hair, sisal, etc.)
fungistat: 150 to 300 ppm by spraying.
    (2)  Phenylmercuric borate and  phenyl-
mercuric chloride plus alkyl dimethyl benzyl
ammonium chloride:  [Ref. I-A-08-45.05] For
cotton, wool,  and  synthetic fibers   fungis-
tat: 0.22 Ib  of PMB  plus  0.020 Ib of PMC
plus  quaternary/100  gal by dip,  spray,  or
brush (264 ppm PMB  plus 24 ppm PMC).
    (3)  Phenylmercuric  oleate  plus zinc
naphthenate: [Reg. No. 2553-6 and I-P-14-
00.01] For rope, twine.
      (a)  Household use: dip  cordage  to
saturate fibers in 2.5% PMO plus 12.5% zinc
naphthenate.
      (b)  Household use: dip  cordage  to
saturate all fibers in 0.6% PMO plus 7.125%
pentachlorophenol.
      (c)  Industrial  use: animal, vegetable
and synthetic filling  material for furniture,
mattresses,  pillows:  spray with  10 parts  of
30% PMO in 90 parts of spray oil and water
(30,000 ppm PMO).
   B. Substitute compounds
    (1)  Alkyl dimethyl benzyl ammonium
chlorides:  [Ref.   I-A-08-45.02,  Reg.  No.
3533-29] Air conditioning filters:  1000 ppm
or 2.8% mixture of quaternary,  sodium di-
methyl-dithiocarbonate and sodium 2-mer-
captobenzothiazole.
    (2)  Copper  naphthenate    cordage:
[Ref. I-C-30-00.01] 1.0 to 2.0% metallic cop-
per equivalent.
    (3)  Copper  8-quinolinolate   cordage:
[Ref.  I-C-34-00.01] To, retain 1.0% or more
actual.
    (4)  Creosote - cordage: [Ref.  I-C-41-
00.01] 40 to 100% dip.
    (5)  Dialkyl dimethyl ammonium chlor-
ide: [Ref. I-D-04-20.01]
       (a) Air conditioning  filters:  Deposit
 1432 ppm quaternary plus 285 ppm benzoic
 acid and 263 ppm  salicylic  acid  by dip,
 spray, or sponge.
       (b) For interior components of furni-
 ture and mattresses:  1.3 Ib quaternary plus
 0.26% TBTO by spraying; or 0.0375 Ib qua-
 ternary plus 0.05% TBTO in dye   beck or
 padder; or 0.025% quaternary plus 0.008%
 TBTO for cotton batting only.
    (6) Lauryl pyridinium salt of 5-chloro-
 2-mercaptobenzothiazole:   [Ref.   I-L-01-
 00.01]  Industrial use in finishing process:
       (a) Burlap: 3,375 to 10,000 ppm.
       (b) Duck,  mattress  ticking, similar
 fabrics: 1200 to 2500 ppm.
       (c) Industrial  fabrics  to yarns:  5,000
 to 10,000 ppm.
    (7) Pentachlorophenol   cordage:  [Ref.
 I-P-05-00.01 ]3.0 to 5.0% by dipping.
    (8) Sodium   o-phenylphenate:  [Ref. I-
 S-16-00.08]  Air  filters:  spray using  0.   o
 SOPP  plus 0.2%  sodium  propionate and
 0.2% 2,  2-methylenebis  ( 3, 4, 6-trichloro-
 phenol)
    (9) Zinc dehydroabietylammonium  2-
 ethylhexoate  cordage:  [Ref.  I-Z-03-00.01]
 Use 2.5 to 5.0% or more by weight.
    (10) Zinc naphthenate   cordage:  [Ref.
 I-Z-05-00.01] Use  1.8 to  5.0% product as a
 dip.
  C. Comparative effectiveness and impact
    (1) Several  substitute  materials are
available for use on  air  conditioning filter
fibers and interior  components of furniture
and mattresses.
    (2) The impact of withdrawal of mer-
 cury on fibers and  cordage would appear to
be slight on industry and insignificant on the
consumer.

2.  Bacteriostats

  A. Mercury compounds
    (1) Phenylmercuric   acetate   (30%):
 [Ref. 3090-127] 1 Ib product per 3333 Ib ma-
                                                                                    13

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terial,  or 0.03% product based on  finished
weight of material; apply as spray.
    (2) Phenylmercuric acetate (15%): [Ref.
3090-28] 10 parts product to 90 parts water;
spray on material  depositing 0.3%  of total
mixture in the filling material.

  B. Substitute compounds

    (1)  Bis   (tri-n-butyltin)  oxide  (25%):
[Ref. 6390-7]  0.1 to 0.2% by weight of mate-
rial.
    (2)  n-Alkyl (60%. C,4, 30% C,6, 5% C,2,
5% C,8) dimethylbenzyl  ammonium chloride
(50%):  [Ref. 6390-9] Apply to leave 0.25 to
1% product by weight.
    (3)  n-Alkyl (60% C,4, 30% C]6, 5% C12,
5%  C)8)  dimethyl benzyl  ammonium 2
ethylhexoate  (25%): [Ref. 6390-13] Apply to
yield 0.025% active ingredient by weight.
    (4) Tributyltin  neodecanoate  (98%):
[Ref. 8314-5]  0.1 to 2% product by weight of
material.
    (5) AlkyI (average CJ2) amine salts of
tetrachlorophenol  (100%):  [Ref. 3090-146]
0.25 to 2% product based on dry weight of
material.
    (6) Sodium pentachlorophenate  (79%)
and sodium  salts  of  other  cholorophenols
(11%): [Ref.  464-125] 0.1 to 0.75% product
by weight of material treated.
    (7) Zinc      dimethyldithiocarbamate
(46%)  and  zinc  2-mercaptobenzothiazole
(4%):  [Ref.  1965-26]  1 to 1.5%  product by
weight of material.
    (8) Sodium pentachlorophenate (79%):
[Ref.   464-1251  0.1 to  0.75%  product  by
weight of treated material.

  C. Comparative effectiveness and impact

    (1) Substitute compounds appear to be
adequate.
    (2) Impact  on industry and consumer
expected to be minimal.
                           IV.  Food, Feed and Tobacco Crops
                              (see also XI, Seed Treatments)
 1. Cotton

  A.  Mercury compounds

 Cyano (methylmercuric)  guanidine:  [Ref. I-'
 C-46-00.01] 0.016 Ib plus 0.68 to 0.72 Ib of
 pentachloronitrobenzene/acre (12,400 linear
 ft of row) in furrow and covering soil at time
 of planting. For soil-borne seedling diseases.

   B.  Substitute compounds
    (1) Captan: [Ref. I-C-10-00.11] 4 to 6 Ib/
 acre (12,400 linear ft of row) or 1.0  Ib plus
 1.0 Ib pentachloronitrobenzene/12,400 linear
 ft of row in furrow and covering soil  at time
 of planting.
    (2) Chloroneb: [Ref. I-C-16-00.11]  1.0
 to 2.0 lb/12,400 linear ft of row
    (3) Dichlone: [Ref. I-D-06-00.04] 0.5 Ib/
 12,400 linear ft of row.
    (4)  5-Ethoxy-3-trichloromethyl-l, 2, 4-
thiadiazole: [Ref. I-E-01-00.01]  0.25 to 0.37
Ib  plus  1.0  to  1.5 Ib  of  pentachloroni-
trobenzene/12,400 linear ft or row.
    (5)  Monosodium salt of 2,  2-Methyle-
nebis- (3, 4,  6-trichlorophenol): [Ref.  I-M-
22-00.01] 0.560 to 1.125 oz/12,400 linear ft of
row.
    (6)  Pentachloronitrobenzene: [Ref. I-P-
04-00.06] 1.0 to 5.0 lb/12,400  linear ft of row.
    (7)  Zinc  ion- maneb coordination prod-
uct: [Ref. I-Z-04-00.06]
      (a) 0.45 to 1.2 lb/12,400  linear ft of
row.
      (b) 0.3 Ib plus  0.3 Ib PCNB/12,400
linear ft of row.
    (8)  Zineb: [Ref. I-Z-10-00.08]
      (a) 2.25 to 3.75  lb/12,400 linear ft of
row.
      (b) 1.3 Ib  plus 0.75 Ib  captan and 1 15
Ib PCNB/12,400  linear ft of row.
 14

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  C. Comparative effectiveness and impact
  C. Comparative effectiveness and impact
    (1)  Mercury is a highly effective fungi-
cide at very low dosage rates, and the spec-
trum of organisms it controls is broadened
by formulating with PCNB.
    (2)  Substitute compounds must be used
at dosages from 30 to almost 400 times more
than mercury.
    (3)  The cost of using substitute materi-
als is 50 to 1000 times the cost of mercury.
    (4)  Substitute compounds  are  some-
times  as effective as  mercury when used as
directed for this purpose.
    (5)  The impact of withdrawal of mercu-
ry for this use will be very slight on industry
but will add to the farm cost of growing cot-
ton.

2. Tobacco

  A.  Mercury compounds

Hydroxymercurichlorophenol: [Ref. I-H-06-
00.01] For seed beds only, where plants are
withdrawn and  transplanted:  0.0143  to
0.0214 lb/10 sq ft (9.15 Ib/acre). For damp-
ing-off control.

  B.  Substitute compounds

    (1) Chloranil  (shade   tobacco  only):
[Ref.  I-C-12-00.03] 0.5 lb/25 gal as a drench.
    (2)  Formaldehyde: [Ref. I-F-03-00.02] 1
gal of 8000 ppm solution.
    (3) Methyl  bromide:   [Ref.   I-M-06-
00.02] 1 to 2 lb/100 sq ft with tarpaulin, or 20
to 50 gal of 69.0% formulation/acre by chisel
method.
    (4) Tetrahydro-3, 5-dimethyl-2H, 1, 3,
5-thiadiazine- 2-thione (Mylone):  [Ref. I-T-
07-00.01] 4.1 lb/80 to 100 sq yd.
    (1)  Substitute materials  are  about as
effective as mercury.
    (2)  Mercury is much less expensive to
purchase and  apply, but substitute chemi-
cals also control other diseases at the same
time.
    (3)  Mercury has not been used exten-
sively for this  purpose in recent years, and
the impact  on  manufacturer and consumer
of withdrawal of mercury for this use will be
negligible. Note: The manufacturer of this
mercury product has stated that it is being
withdrawn  from  production.  Registration
has continued to cover stocks still in dealers
hands.

3. Farm and Greenhouse Equipment

  A. Mercury compounds

Cyano (methylmercuric) guanidine: [Ref. I-
C-46-00.03]  For  farm   machinery, green-
house benches, empty flats, pots,  tools and
walks. Plant pathogen disinfection. 1.7 ppm
spray or dip. No food contamination.

  B. Substitute com pounds

Alkyl dimethyl benzyl ammonium chlorides.
[Ref. I-A-08-05.01 and I-A-08-50.01] 1800 to
5900 ppm.

  C. Comparative effectiveness and impact

    (1)  Mercury compounds are  far  more
effective than  substitute materials for this
use and  at very low dosage rates.
    (2)  Impact of withdrawal of mercury
for this  use will be severe  on nurserymen
and potato  growers; slight  on manufactur-
ers.
                                                                                   15

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                             V.  Food and Feed Containers
                      (Sacks, Seed Bins, and Containers for Treat-
                      ed Seed Subject to Diversion to Food and Feed
                                        Uses)
 1.  Mercury compounds

 Hydroxymercurichlorophenol: [Ref. I-H-06-
 00.05]  690 ppm  suspension. Spray  or dip
 before refilling. Fungistat.

 2.  Substitute compounds

 None registered.

 3.  Comparative effectiveness and impact

   a.  Several substitute materials  could  be
 accepted for this use, particularly the non-
 residual disinfectants such as the hypochlor-
 ites.  Quaternary compounds,  TBTO, etc.
 would require  tolerances for use on  seed
 which could be  diverted to food  or  feed
 uses. Copper naphthenate and zinc petrole-
 um sulfonate can also be used.
   B.  Impact of withdrawal of this use for
 mercury would  be  negligible.  Note:  The
 manufacturer has indicated that the product
 is being discontinued.  Registration  remains
 in effect to cover stocks still on distributors
 shelves.                               [
                                    VI.  Humans
I.  Mercury compounds
  A. Metallic  mercury: [Ref. Reg.  Nos.:
140-20; 223-12; 372-19; 1091-5; 1471-3; 5231-
3;  6253-3; 9850-1] 9.0 or 10% mercury for
louse control applied as an ointment.
  B. Ammoniated  mercury:  5.0%  [Ref.
Reg. Nos.  994-5] (3.9% metallic mercury)
for louse control applied as an ointment.
  C. Metallic mercury: (10%) plus Mercury
oleate (0.8%) [Ref. Reg. No. 4476-30; 6253-
3] For louse control applied as an ointment.

2.  Substitute compounds

   A.  Premium grade Malathion:  1% dust for
head and  body lice [Ref.  Reg. No.  241-68]
(Basic manufacturer of  malathion does not
market for this purpose).
  B. Carbaryl  (Sevin):  5% dust for crab,
head and body lice [Ref. Reg. No. 9734-3]
  C.  Lindane:  1% dust is registered for use
by the military or under prescription from  a
physician.
  D. Thanite: 5%  water  emulsion  [Ref.
Reg. No. 718-1]
  E. Products containing  pyrethrins,  saba-
dilla, and larkspur have also been registered
for control of lice on humans; however, we
can not identify any products which are cur-
rently being marketed for this purpose.
  F. DDT has been registered for control of
lice on humans;  however, all uses of DDT
have  been  cancelled,  and administrative
hearings are  to take place in the near future.

3.  Comparative effectiveness and impact

The  primary problems with products used
against lice are in two areas:
    (1) resistance  in  certain parts of  the
world has developed to one or more of the
chemicals registered for control of lice;
    (2)  Malathion  and certain of the other
compounds  are not readily available to the
general public.
16

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                               VII.   Ornamental Plants
1.  Bulbs and Corms

  A. Mercury compounds

    (1)  Cyano (methylmercuric) guanidine:
[Ref.  I-C-46-00] For  root, stem  and bulb
rots: 5.0 ppm solution. Soak.
    (2)  Mercurous chloride: (alone or with
mercuric chloride) [Ref. I-M-0500.01] Gladi-
olus corms only. 0.9 lb/5 gal. Dip.
    (3)  N-Methylmercuri-1, 2, 3, 6-tetrahy-
dro-3,  6-endomethano-3, 4, 5, 6, 7, 7-te-
trachlorophthalimide:   [Ref.  I-M-15-00.01]
Gladiolus  corms only: 1 pt of 10.0% formu-
lation/50 gal. Soak.
    (4)  Phenylmercuric acetate:  [Ref. I-P-
08-00.03]  Bulbs: 2.0 fl. oz of 10% formula-
tion/2 gal. Soil soak.
    (5)  Phenylmercuric triethanol ammon-
ium lactate: [Ref.  I-P-17-00.02]  117  to 750
ppm dip.
    (6)  Sodium ethylmercuri thiosalicylate:
[Ref. I-S-11-00.01]  For bulbs and corms: 2 to
3ptof 12% solution/100gal. Soak.

  B. Substitute compounds

    (1)  Copper chloride: [Ref. I-C-26-50.01]
Household use: For  Fusarium rot only    1
tbs/gal/12  sq  ft of soil. Minimal  effective-
ness.
    (2)  p-(Dimethylamino)   benzenediazo
sodium  sulfonate: [Ref. I-D-14-00.02] 1.25 to
2.8 oz/50  gal/400 sq ft, or use 0.5 pt above
solution/each 6-inch pot.
    (3)  Methyl isothiocyanate:  [Ref. I-M-
07-00.01] 25 to 50 gal/acre.
    (4)  Sodium o-phenylphenate: [Ref. I-S-
16-00.07] Bulbs, Corms - rots: 514 ppm. sol-
ution as tetrahydrate. Soak.
    (5)  2-(4-thiazolyl) benzimidazole (Thia-
bendazole):   [Ref.   I-T-09-00.01]:   Bulbs,
Corms-Fusarium rot: 1080 ppm. Soak.
    (6)  Thiram: [Ref. I-T-10-00.08]  Bulbs,
Corms- decays. Dust with 4.0 to 12.0% for-
mulation.
  C. Comparative effectiveness and impact

    (1)  Effectiveness  of  substitute  com-
pounds  ranges from low to  comparable to
mercury compounds.
    (2)  Impact of withdrawal of mercury
for these uses will be slight on manufacturer
but much more costly to florist and nursery-
man.

2. Cuttings

   A. Mercury compounds

    (1)  Cyano (methylmercuric) guanidine:
[Ref.  I-C-46-00.02]  2.5  ppm  solution. Dip.
Soil-borne diseases.
    (2)  Methylmercury hydroxide: [Ref. I-
M-18-00.01] Carnation  cuttings  only:  2.2
ppm. Dip.

   B.  Substitute compounds

    (1)  8-Quinolinol benzoate: [Ref. I-Q-01-
00.01] 250 to  500 ppm  solution. Soak soil.
Damping-off.
    (2)  8-Quinolinol sulfate: [Ref. I-Q-03-
00.01] 180 to 260 ppm solution.  Dip cuttings
or soak  soil. Soil-borne diseases.
    (3)  Thiram: [Ref.  I-T-10-00.04]  15,000
ppm dust as dip for hardwoods, or 3 oz of
 15% formulation/pt as softwood dip.

   C.  Comparative effectiveness and impact

    (1)  Mercury is more effective than the
substitute* compounds  against  a broader
range of pathogens and at lower dosages and
lower costs.
    (2)  Other, now unregistered products,
are available or will soon be available with
good  effectiveness for  these  uses  but at
much higher cost.
    (3)  The impact of withdrawal of  mercu-
ry for treating cuttings  will be negligible on
the manufacturer but severe on the nursery-
                                                                                    17

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man or florist until suitable inexpensive re-
placements are available.

3.  Flowering and Foliage Plants (Soil treat-
ments)

  A. Mercury compounds

    (1)  Cyano  (methylmercuric) guanidine
[Ref. I-C-46-00.02]  2.5  to 5.3  ppm  as soil
drench for soil-borne diseases.
    (2)  Hydroxymercurichlorophenol:
[Ref. I-H-06-00.01] 0.0143 to 0.0214 lb/10 sq
ft.
    (3)  Phenylmercuric acetate:  [Ref. I-P-
08-00.04] 26 ppm solution as soil spray.


  B.  Substitute compounds

     (1)  Captan: [Ref. I-C-10-00.12] 15 gal of
1200 ppm solution/1000 sq ft.
     (2)  Chloropicrin: [Ref. I-C-19-00.01]
      (a) 485 to 1976 Ib/acre with cultipack
or water seal.
      (b) 150 to 200 Ib/acre  with plastic
seal.
      (c) 82 to 115 Ib plus  168 to 235 Ib
methyl bromide/acre with plastic seal.
      (d) 319 Ib plus 240 Ib Dichloropro-
penes/acre with plastic seal.
     (3)  p-(Dimethylamino)   benzenediazo
sodium sulfonate: [Ref. I-D-14-00.02]: 1.25
to 2.8 oz/50 gal/400 sq ft or 1 pt above solu-
tion/each 6-inch pot.
     (4)  Methyl   bromide:   [Ref.  I-M-06-
00.02] 1 to 2 lb/100 sq ft with tarpaulin, 20 to
50  gal of 65%  formulation/acre by chisel
application.
     (5)  Methyl  isothiocyanate: [Ref. I-M-
07-00.01] 25 to 50 gal/acre
     (6)  Pentachloronitrobenzene: [Ref. I-P-
04-00.07] 27 to 232 lb/100 gal or 65 to 232 Ib
as a dust/acre.
     (7)  Tetrahydro-3,  5-dimethyl-2H-l,  3,
5: thiadiazine-2-thione (Mylone): [Ref. I-T-
07-00.02]: 4. lib/10 to 80 sq yd.
  C. Comparative effectiveness and impact

    (1)  Highly  effective   substitute  com-
pounds  are  already  registered  for  this use
and are widely employed.
    (2)  Impact of withdrawal will be slight
on manufacturers and consumers alike.

4.  Flowering and Foliage Plants (Foliar treat-
ments)

  A. Mercury compounds

    (1)  Cyano (methylmercuric) guanidine:
[Ref. I-C-46-00.02] 25 ppm. Apply as neces-
sary.
    (2)  Phenylmercuric triethanol  ammon-
ium  lactate:  [Ref.  I-P-17-00.01]  Gladiolus
only.  146 ppm. Dip flower  spikes before
shipment or storage. Laurel and Rhododen-
dron: 94 ppm in 2 or 3 applications.

  B. Substitute compounds

    (1)  Benomyl: [Ref. I-B-02-00.02] 4 oz/
100gal, as required.
    (2)  Captan: [Ref.  I-C-10-00.11  through
.13] 1.0 lb/100 gal or 2.1 Ib as  a dust/acre, as
required.
    (3)  Copper-Bordeaux:   [Ref.   I-C-25-
00.08] Use 2-2-50 to 4-4-50 mixtures as re-
quired.
    (4)  Copper  oleate: [Ref. I-C-30-50.03]
Up to 4 Ib of 25%  formulation/gal. Home-
owner use, as required.
    (5)  Copper oxychloride: [Ref. I-C-32-
00.06 and .07] 2.1 Ib metallic  copper equiva-
lent/100 gal; 0.125 to 0.25 oz of  metallic cop-
per plus 0.1 to 0.2 oz of sulfur and 0.025 to
0.050 oz  of  zineb/gal. Household use, as
required.
    (6)  Copper oxychloride sulfate: [Ref. I-
C-33-00.08]  1.25 to  2.2 Ib metallic copper
equivalent/100 gal, or 1.4 to 3.5 Ib as a dust/
acre. As required.
    (7)  Copper 8-quinolinolate: [Ref.  I-C-
34-00.01]  1.0  oz of 2.0%  formulation  plus
Karathane (dinocap) and  petroleum  distil-
18

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late/3000 cu ft of greenhouse space, as re-
quired.
    (8) Copper sulfate, basic: [Ref. I-C-36-
00.09]  2.0 Ib metallic copper equivalent/100
gal. As required.
    (9) Copper dihydrazinium sulfate: [Ref.
I-C-28-00.01] 3000 to 4000 ppm solution, as
necessary. Roses only.
    (10) Copper  oleate:  [Ref. I-C-30-50.03]
Up to  4 tbs./gal  as necessary. Homeowner
use.
    (11) Copper  oxychloride: [Ref. I-C-32-
00.06]  2.12 Ib as metallic copper equivalent/
100 gal (2545 ppm) as necessary.
    (12) Copper  oxychloride sulfate, basic:
[Ref. I-C-33-00.07 and .08] 1.2 to 2.2 Ib as
metallic copper equivalent/100 gal (2640 to
6940 ppm) as necessary.
    (13) Copper  sulfate, basic:  [Ref.  I-C-
36-00.09 and . 10]  3.0 to 3.18 Ib metallic cop-
per equivalent/100 gal (approx. 3600 ppm) as
necessary.
    (14) Copper-Zinc-Chromate  Complex:
[Ref. I-C-40-00.03 and .04] 1.8 Ib actual/100
gal or  1.7 to 2.3 Ib/acre dust.
    (15) 2, 6-Dichloro-4-nitroaniline:  [Ref.
I-D-09-00.06] 0.28 to 0.56 lb/100 gal or-0.64
to 1.8  Ib as a dust/acre at 5- to 14-day inter-
vals.
    (16) Cycloheximide:   [Ref.    I-D-16-
00.01]  2.0 ppm solution at 3- to 7-day inter-
vals.
    (17) Ferbam:  [Ref.  I-F-01-00.08  and
.09] 0.76 to 1.14 lb/100 gal or dust to cover at
7- to 10-day intervals
    (18) Folpet:  [Ref. I-F-02-00.05 and .06]
0.5 to 1.0 lb/100 gal (600 to 1200 ppm)
    (19) Glyodin: [Ref. I-G-02-00.02] 200 to
480 ppm solution  as required.
    (20) Maneb:   [Ref.  I-M-02-00.09  and
.10] 0.8 to 1.2 lb/100 gal  (1000 to  1500 ppm)
or 1.2 to 2.4 Ib dust/acre.
    (21) Karathane (dinocap): [Ref. I-M-14-
00.04]  1.5 to 3.84 lb/100 gal as necessary.
    (22) 3  (2-methylpiperidino) propyl 3, 4-
dichlorobenzoate: [Ref.  I-M-26-00.01]  0.25
to 0.5 lb/100 gal (300 to 600 ppm) at 7-day
intervals.
    (23) Nabam: [Ref. I-N-01-00.08] o.43 to
0.86 lb/100 gal at 7-day intervals.
    (24) Potassium  polysulfide:  [Ref.  I-P-
27-00.01] 3 ft oz of 2.9% solution/100 gal at 7-
to 10-day intervals.
    (25) 8-Quinolinol sulfate: [Ref. I-Q-03-
00.01] 180 to 390 ppm solution at 7-day inter-
vals.
    (26) Sodium o-phenylphenate: [Ref. I-
S-16-00.07] 514  to 1030 ppm at 7- to  14-day
intervals.
    (27) Streptomycin:  [Ref.  I-S-23-00.03]
50 to  200 ppm at 3- to 7-day intervals.
    (28) Sulfur: [Ref. I-S-24-00.09 through
.11] 4.75 to 5.6 lb/100 gal or dust  to cover at
5- to  10-day intervals.
    (29) 1, 2, 4, 5-Tetrachloro-3-nitroben-
zene: [Ref. I-T-03-00.01] 1 oz/10,000 cu ft of
greenhouse space by vaporization.
    (30) Tetrachloroisophthalonitrile: [Ref.
I-T-05-00.01] 0.75 to 1.126 lb/100 gal or 8.0
gm/4000 cu ft of greenhouse space by vapor-
ization.
    (31) Thiram: [Ref. I-T-10-00.03 through
.05] 0.65 lb/100 gal or 5.0 to 12.0% dusts.
    (32) Zinc ion-maneb complex: [Ref. I-
Z-04-00.07 through .09] 1.2 lb/100 gal at 7- to
10-day intervals.
    (33) Zineb:  [Ref. I-Z-10-00.09] 1.125 to
1.5 lb/100 gal as required
    (34) Ziram: [Ref. I-Z-11-00.05 and .06]
1.14 to 6.3  lb/100 gal at 7-  to 10-day inter-
vals.


  C.  Comparative effectiveness and impact

    (1)  Most  substitute  compounds  are
more  effective  than mercury compounds
against the foliar diseases of flowering and
foliage plants.
    (2)  Impact of withdrawal  of mercury
compounds for such uses will  be insignifi-
cant on manufacturer and consumer.
                                                                                     19

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5.  Trees  and Shrubs (Foliar application for
disease control)


  A. Mercury compounds


    (!) Methylmercury    8-hydroxyquino-
linolate:  [Ref.  I-M-19-00.01  and .02]  For
anthracnose, leaf blights, leaf  spots,  twig
blights.  1  oz/100  gal  (75  ppm  solution).
Spray.
    (2) Phenylmercuric acetate: [Ref.  I-P-
08-00]  For  anthracnose,  leaf  blight,  leaf
spots, twig blights. 125 ppm solution, spray.
    (3) Phenylmercuric       dimethyldit-
hiocarbamate: [Ref. I-P-] For twig blight on
eastern red cedar only, in nurseries. 180 ppm
solution, spray at 10- to 14-day intervals.
    (4) Phenylmercuric triethanol ammon-
ium lactate: [Ref. I-P-]
       (a) For elm leaf  spot only: 9.4  ppm
spray at 1- to 3-week intervals.
       (b) For  hickory,  maple,  oak,  etc.
anthracnose, leaf spots.  Use 9.4 to 19.0 ppm
spray as required.

   B. Substitute compounds
None directing use on  trees specified for
mercury  compounds. Maneb is used for an-
thracnose on dogwood  and might be some-
what effective on other trees.


  C. Comparative effectiveness and impact


    (1) Adequate  substitutes for  mercury
are not registered.

    (2) Impact of withdrawal  of mercury
compounds for these uses would be slight on
the manufacturer but severe on the consum-
er and would result in loss of many trees,
particularly Sycamore  severely  injured by
anthracnose. Cost of  tree removal  on city
streets and in parks is very high.
6.  Trees and Shrubs (Injection application)

  A. Mercury compounds

Mercuric chloride: [Ref. I-M-04-00.02] For
Dutch Elm disease. Inject 0.12% solution in
methyl alcohol.

  B. Substitute compounds

None

  C. Comparative effectiveness and impact

Impact of  withdrawal  of mercury for this
will be highly important to the manufactur-
er, but product is of doubtful or marginal
value, and impact on disease control will be
very slight to negligible.

7.  Trees and Shrubs (wound dressings)

  A. Mercury compounds

    (1) Mercuric   chloride:  [Ref. I-M-04-
00.02] 1930 ppm.
    (2) Phenylmercuric nitrate:  [Ref.  I-P-
13-00.01] 3000 ppm.

  B. Substitute compounds

    (1) Copper naphthenate: [Ref.  I-C-30-
00.01] 3.3 to 10.0% in asphalt.
    (2) Copper sulfate, basic:  [Ref. I-C-36-
00.10]  1.9% as metallic  copper  equivalent
plus  1.2% phenol.
    (3) Sodium o-phenylphenate: [Ref. I-S-
16-00.07] 2.0% tetrahydrate paste.
    (4) Thiram: [Ref.  I-T-10-00.05]  1.0%
paste or in asphalt.

  C. Comparative effectiveness and impact

    (1) Effectiveness  of  substitute  com-
pounds is probably about equal to  that of
mercury.
    (2) Impact on withdrawal of mercury
for this use would  be neglibible.
20

-------
VII. 8. Turf Disease Control
Compounds
A. Mercury compounds:
(1) Cyano (methyl-
mercuric) guanidine
[Ref. I-C-4 6-00.02]
(2) Hydroxymercuric -
chloro phenol:
[Ref.I-M-06-00.011
(3) Mercuric chloride
[Ref. I-M-04-00.01}
(4) Mercuric chloride
plus
1 Mercurpus chloride
[Ref. I-M-04-00.01]
(5) Mercuric dimethyl -
dithiocarbarnate
[Ref. I-M-04-05.01]
(6) Methylmercuri
tetrahydroendo -
methano hexachloro
phthalimide
[Ref.I-M-15-00.01]
(7) Mercuious chloride
[Ref. I-M-05-00.01]
(8) Phenylmercuric
acetate
[Ref. I-P-08-00.04]
(9) Phenylmercuric
dimethyldithio-
carbamate
[Ref. I-P-09-00,01]

.033
.823
1 -3
.3 - .9
+
.6 -2.4
.444
.1
.9 - 1.5
.1
.1 - .2
.033
.300


.444
.1

.1
.1 - .2
.066






.1

ounces actual per 1000 square feet
.033
.823

.3 - .9
+
.6 -2.4
.444
.1
.9 - 1-8
.1
.1 - .2
.066
.300


.444
.1

.1


.300


.444


.1






.2

.1

.066
.800
4




.1 - .2


-------
VII.  8. Turf Disease Control-Continued
Compounds
(10) Phenylmercuric
monoethanol
ammonium lactate
[Ref.I-P-12-00.01]
(11) Phenylmercuric
triethanol
ammonium lactate
[Ref. I-P-17-00.01]
B. Substitute compounds:
(1) Benomyl
[Ref. I-B-02-00.02]
(2) Cadmium-calcium-
copper-zinc-chromate
complex
[Ref. I-C-01-00.01]
(3) Cadmium carbonate
[Ref. I-C-02-00;01
(4) Cadmium chloride
[Ref. I-C-0 3-00.01]
(5) Cadmium sebacate
[Ref. I-C-04-00.01]
(6) Cadmium succinate
[Ref.I-C-05-00.01]
(7) Captan
[Ref. I-C-10-QQ.12]
(8) Chloranil
[Ref. I-C-12-00.03]
ounces actual per 1000 square feet


.13



.15


.5 - 1



3 -4



.2

.1 - .4



16 -32

3.2



.13



.15






3 -4

.23

.2

.1 - .4

.3

16 -32
















3



.2





16 -32





.13



.15


.5 - 1



3 -4

.23

.2



.3







.13



.15










.2

.1 - .4



16 -32





.13



.15






3-4*

.23*

.2*

.1 - .4*

.3*


































.13 to .26



.15 to .20


.5 -1



8-12



.2 - .4



1.2 to 2.4






-------
VII.  8.  Turf Disease Control-Continued
Compounds
(9) Chloroneb
[Ref. I-C-12-00.02]
?10) Copper-zinc-chromate
complex
[Ref. I-C-40-00.04]
(11) Crystal violet-
auramine-malachite
green
[Ref.I-C-45-00.01]
(12) 2, 4-Dichloro-6-
(o-chloroanilino)-
s-triazine (Dyrene)
[Ref. I-D-07-00.03]
(13) p-(Dimethylamino)
benezenediazo sodium
sulfonate
[Ref. I-D-14-00.02]
(14) Cycloheximide
[Ref. I-D-1 6-00.01]
(15) Folpet
[Ref. I-P-02-00.06]
(16) Maneb
[Ref. I-M-02-00.10]
(17) Pentachloronitro-
benzene
[Ref. I-P-04-00.08]
(18) Chlorophthalonil
[Ref. I-T-05-00.02]
ounces actual per 1000 square feet

1 gal. of
.1 - .33
%soln.
.5
2 to 4

.318

2.4 to 6.4
2.15 to
78.4
1.5 to
6.0



2 to 4



















2 to 4



4.8 to 6.4
78.4 to
158.4
1.5 to
3.0



2 to 4

.318
3
2.4 to 6.4

1.5 to
6.0










2.6



1.4 to 1.8





3.9 to 5. 9
1 gal. of
.1 - .3
% soln.

2




16.0 to
78.4
4.5 to
6.0

-------
Ni
                                                          VII. 8. Turf Disease Control-Continued
Compounds
(19) 2-(4-Thiazolyl)
benzimidazole
[Ref. I-T-09-00.02]
(20) Thiram
[Ref. I-T-10-00.04]
(21) Zinc ion-maneb
complex
[Ref. I-Z-04-00.08]
(22) Zineb
[Ref.I-Z-10-00.12]
ounces actual per 1000 square feet
.6 - 1.2
1.9 to
4.5
3.2 to
6.4


2.0 to
3.25
3.2 to
6.4





.6 - 1.2
1.9 to
4.5
3.2 to
6.4


2.25 to
3.38
3.2 to
6.4
1.5






6.4
1.0 to
1.5
.6 - 1.2
4.5 to
6.0
4.8 to
6.4

    •Cadmium resistant stains of this pathogen are common.

-------
  C.  Comparative effectiveness and impact

    (1) Mercury  compounds have a broad
spectrum  of  turf pathogen control  at high
efficiency for low dosage rates. Substitute
compounds are usually used in combination
to achieve broad spectrum control at higher
dosage rates, higher cost and more  difficult
application procedures.
    (2) The impact of withdrawal of mercu-
ry for turf disease  control  will be very  se-
vere on some manufacturers, on golf greens
management budgets and on turf quality.
9. Turf Weed Control (Crabgrass)

  A.  Mercury compounds

Phenylmercuric  acetate:  [Ref.  Reg.  Nos.
702-14, 1001-14,  1001-24, 1439-173, etc.]
       (a) 0.25 to 0.4 oz actual/1000 sq ft.
       (b) 0.0003 oz actual  plus 0.1391 oz
dimethylamine salt of 2, 4-D and  0.005 oz
isopropyl  N-(3-chlorophenyl)  carbamate/
lOOOsqft.
       (c) 0.009 oz actual plus 2.25 oz Thir-
am/lOOOsqft.

  B.  Substitute compounds

    (1) Octyl  ammonium  methanersenate
plus  dodecylammonium  methanearsenate
[Ref.   Reg. No.  2853-6]  0.64 oz  actual
each of/lOOOsqft.
    (2) Calcium   methanearsenate   [Ref.
Reg.  Nos.  264-147 and  2853-4] 0.83 oz ac-
tual /1000 sq ft.
    (3) Disodium  methanearsenate:  [Ref.
Reg. No. 572-199] 0.76 oz actual/1000 sq ft.
    (4) Monosodium acid methanearsenate:
[Ref. Reg. No. 728-79]  0.52 oz actual/1000
sqft.

  C.  Comparative Effectiveness and Impact

     (1) Substitute materials are about equal
to mercury for  crabgrass  control in post-
emergence application and are safer from
point of view of injury to desirable grasses.
     (2) Other substitute materials are avail-
able for use before crabgrass emerges.
     (3) Impact of withdrawal  of mercury
for this use will be minimal.

10. Turf Weed Control (moss)

  A. Mercury compounds

     (1) Phenylmercuric acetate: [Ref. Reg.
Nos. 538-5, 24,  36] 0.02 to 0.51 oz  actual/
lOOOsqft.
     (2)  Phenylmercuric  triethanol ammon-
ium lactate: [Ref. Reg. No. 802-233]  0.17 to
0.5 oz actual/1000 sqft.

   B. Substitute com pounds

     (1)  Ferrous  ammonium  sulfate: [Ref.
Reg. No. 7923-3] 9.8 Ib actual/100 sq ft.
     (2)  Ferrous  sulfate:  [Ref.  Reg. No.
7404-3] 2.0 Ib actual/1000 sq ft.
     (3)  Ferrous sulfate heptahydrate: [Ref.
Reg. No. 5584-17] 1.5 Ib actual/1000 sq ft.

   C. Comparative effectiveness and impact

     (1)  Substitute  materials   are  equally
effective for moss control but require much
higher dosage.
     (2)  Impact  of withdrawal  of mercury
for moss control will be minimal.
                              VIII.  Paper (mold resistant)
1.  Mercury compounds
Phenylmercuric acetate: [Ref. I-P-08-00.10]
  A. Beater application: 0.8 Ib/ton of fiber,
dry weight.
  B. Coating application: 0.1 to 0.3 lb/side/
ton or 150 to 225 ppm as a spray.
  C. Calender application:  0.1  to 0.3  Ib/
side/ton or 0.5% solution.
                                                                                   25

-------
2.  Substitute compounds

  A.  Alkyl  dimethyl  benzyl  ammonium
chlorides and Bis (tributyltin) oxide: [Ref.  I-
A-08-15.02]
    (1)  3750 ppm quaternary alone.
    (2)  5000 ppm quaternary plus 250 ppm
TBTO.
    (3)  625 to 2500 ppm quaternary plus 125
to 500 ppm TBTO.

   B.  Captan:
0.15 to 0.90% by weight.

   C.  4-Chloro-3,  5-Xylenol:  [Ref.  I-C-21-
00.02] Use as required.

   D.  Copper 8-quinolinolate: [Ref.  I-C-34-
00.02] Use as  required or 0.04% metallic
copper equivalent in wax sizing.

   E.  Diisobutylphenoxyethoxyethyl  dime-
thyl benzyl ammonium chloride: [Ref. I-D-
 13-00.011  Use 0.4% of a mixture of 40.9%
quaternary plus 11.7% tributyltin salicylate
based on dry weight of solids; or use 0.5  of
above in the tub size.

   F  N-Dodecylguanidine   hydrochloride:
[Ref. I-D-27-80.01] 0.4 to 0.8% on weight  of
paper.

   G.  Dodine: [Ref.  I-D-28-00.04] 0.8% on
weight of paper.

   H. 2, 2'-Methylenebis-(3, 4, 6-trichloro-
phenol): [Ref.  I-M-13-00.03] 0.02 to 0.25%
on weight of paper.
  I.  Sodium      dimethyldithiocarbamate:
[Ref. I-S-09-00.05] 0.455 to 0.911% plus 0.04
to 0.08%  sodium 2-mercaptobenzothiazole
based on weight of sheet.

  J.  Sodium pentachlorophenate: [Ref. I-S-
15-00.03] 0.1  to  0.5%  based  on weight of
sheet.

  K. Sodium ^-phenylphenate:  [Ref.  I-S-
16-00.09] 0.1 to 0.3% on weight of stock.

  L.Thiram: [Ref. I-T-10-00.08] 0.3 to 1.2%
plus  0.3 to 1.2% of zinc pentachlorophenate
based on weight of finished paper.

  M. 3,4' 5-Tribromosalicylanilide: [Ref. I-
T-l 1-00.01] 0.025 to 0.25% or 200 or more
ppm  based on weight of paper.

  N. Ziram: [Ref. I-Z-11-00]  0.46 to 0.86%
plus  0.02  to  0.037%  zinc-2-mercaptoben-
zothiazole on weight of  sheet.

3. Comparative effectiveness and impact

  A. Mercury compounds are highly effec-
tive at  low concentrations. Substitute mate-
rials  require higher dosages.

  B. Mercury compounds  are colorless.
Some substitute compounds impart undesir-
able  colors, others do not.

  C. Substitute  compounds  appear  to be
adequate.

  D. Impact on industry will be very small,
none on consumer.
                                     IX.  Plastics
 1. Plastics (unspecified)

   A.  Mercury compounds
     (1) Phenylmercuric  acetate:  [Ref. I-P-
 08-00.01]  Fungistatic surface treatment: 150
 to 225 ppm spray.
    (2)  Phenylmercuric borate:  [Ref.  I-D-
13-00.04] Fungistatic film: 50 ppm phenyl-
mercuric borate  plus 31.25 ppm  diisobutyl-
phenoxy    ethoxyethyl  dimethyl  benzyl
ammonium chloride by weight  of pellets
before molding.

-------
    (3)  Phenylmercuric propionate: [Ref.  I-
P-15-00.01] Fungistatic disposable bags for
garbage and other wastes: 0.02% by weight.


  6. Substitute com pounds

    (1)  Alkyl  dimethyl  benzyl  ammonium
chloride:  [Ref.  I-A-08-15.02]  Fungistatic
surface  treatment:  5000 ppm  plus 250 ppm
TBTO.
    (2)  Bis   (tributyltin)  sulfosalicylate:
[Ref.  I-B-12-00.01] 0.05% by weight or as
required.
    (3)  4-Chloro-3, 5-xylenol: [Ref. I-C-21-
00.02] Use as required.
    (4)  3,4', 5-Tribromosalicylanilide: [Ref.
I-T-11-00.02]
    (5)  Tributyltin linoleate:  [Ref.  I-T-12-
50.01] 0.43%,  more or less as required, by
weight of resin.
    (6)  Tributyltin  monopropylene  glycol
maleate: [Ref. I-T-12-60.01]
      (a)  For floor tile use 0.8% by weight
of plasticizer.
    (b) For calendered film use 0.2 to 1.0%
by weight of plasticizer.
  C. Comparative effectiveness and impact

    (1)  Higher concentrations of substitute
compounds at higher costs are needed to
secure adequate  protection in place of mer-
cury.
    (2)  Relative spectrums of microorgan-
ism control not known.
    (3)  Impact on manufacturer  and con-
sumer not known but probably insignificant,
since  no replies were received  to our  De-
cember 3, 1970, Federal Register request for
comments and views.

2. Plastics (polyethylene)

  A. Mercury compounds

Phenylmercuric  borate: [Ref. I-P-08-10.01]
50 ppm PMB plus 31.25 ppm diisobutyl-
phenoxyethoxyethyl  dimethyl  benzyl  am-
monium chloride by weight of pellets before
molding. Fungistat.

  B. Substitute compounds

    (1)  Captan:  [Ref. I-C-10-00.16] 0.44 to
1.74% by weight of stabilizer.
    (2)  Ziram:  [Ref.  I-Z-11-00.07] 0.225%
plus  0.0195%   of   zinc   2-mercaptoben-
zothiazole by weight of resins.

  C. Comparative effectiveness and impact

    (1)  Substitute compounds require dos-
age rates of 85 to 248 times  that of mercury
for effective fungal control.
    (2)  Relative spectrums  of microorgan-
ism control are unknown.
    (3)  Impact on  withdrawal of mercury
for this  use is  unknown but assumed to be
minimal.

3.  Plastics (polystyrene)

  A. Mercury compounds

Phenylmercuric borate:  [Ref. I-P-08-10.01]
50 ppm PMB plus 31.25 ppm diisobutyl-
phenoxyethoxyethyl dimethyl benzyl  am-
monium chloride by weight of pellets before
molding. Fungistat.

  B. Substitute compounds

Ziram:  [Ref.  I-Z-11-00.07]  0.255%  plus
0.0195% of  zinc 2-mercaptobenzothiazole
by weight of resin.

  C. Comparative effectiveness and impact

    (1)  Substitute compound requires dos-
age rate 85 times that of mercury for compa-
rable effectiveness.
    (2)  Relative spectrums of microorgan-
ism control are unknown.
    (3)  Impact of withdraw! of mercury use
is unknown but assumed to be minimal.
                                                                                   27

-------
4.  Polyvinyl Chloride Film (bacteriostatic at
surface)

  A. Mercury compounds

Phenylmercuric  propionate  (0.62%): [Ref.
Reg. No. 7101-2] Product is disposable plas-
tic bag impregnated with mercurial and bear-
ing bacteriostatic (bacterial  growth  inhibit-
ing) claim.

  B. Substitute compounds

    (1) Captan    (N-trichloromethylthio-4-
cyclohexene-1,   2-dicarboximide)   (90%):
[Ref. Reg. No. 1965-11] 0.2 to 0.5% product
by weight of total formula.
    (2) 4-chloro-3, 5-xylenol (100%): [Ref.
Reg. No. 4026-4] Recommended for "plas-
tics" but no dosages available.
    (3) Tri-n-butyltin linoleate (75%): [Ref.
Reg. No. 5204-15] 0.15 to 0.2% product by
weight based on plastic mix weight.
    (4) Diphenylstibine      2-ethylhexoate
(10%): [Ref. Reg. No.  5204-42] 1.3 to 5%
product based on weight of film.
    (5) Tributyltin  linoleate (98%): [Ref.
Reg. No. 8314-4] 0.43% product by weight
of plastic mix.
    (6) 3,    4,    5-Tribromosalicylanilide
(97%)  and  3, 5  Dibromosalicylanilide (2%):
[Ref. Reg.  No. 6390-29] 2.0% product based
on total weight of media.

  C. Comparative effectiveness and impact

    (1) Substitute compounds appear to be
more than adequate.
     (2) Impact on  industry and  consumer
appears to be nil.

5. Vinyl (bacterial preservatives)

  A.  Mercury compounds

Phenylmercuric hydroxide (17%): [Ref. Reg.
No.  6516-3] Vinyl  (otherwise unidentified)
coating for  fabrics, ground  together with
chlorinated paraffin: 0.5  Ib product/99.5 Ib
media.

  B.  Substitute compounds

    (1) Diphenylstibine     2-ethylhexoate
(10%): [Ref.  Reg.  No. 5204-42]  Polyvinyl
chloride: 1.3 to 5% product by weight.
    (2) Captan   (N-trichloromethylthio-4-
cyclohexene-1,  2-dicarboximide)  (90%):
[Ref. Reg. No. 1965-11] Polyvinyl chloride:
0.2 to 0.5% product by weight.
    (3) Bis  (tri-n-butyltin)  oxide (.075%)
and alkyl (61%C,2, 23%C,4, 11%C,6, 5%Cg-
C,8) dimethyl benzyl ammonium chlorides
(1.5%): [Ref.  Reg.  No.  3090-137] 1 part
product to 2 parts water, "spray surface uni-
formly."

  C.  Comparative effectiveness and impact

    (1) Substitute compounds appear  to be
adequate.
    (2) Impact on industry expected  to be
minimal. Cost to consumer expected  to in-
crease.
                                     X.  Rubber
I.  Fungistats

  A. Mercury compounds

    (1)  Phenylmercuric acetate: [Ref.  I-P-
08-00.10] Fungistat: 125-225 ppm, spray sur-
faces.
    (2)  Phenylmercuric borate: [Ref.  I-D-
13-00.02 and I-P-08-10.01] Fungistat: 50 ppm
plus    31.25    ppm.    diisobutylphenox-
yethoxyethyl dimethyl  benzyl ammonium
chloride, before molding.

  B. Substitute compounds: [Ref. I-Z-08-15.
.01]

    (1) Alkyl dimethyl benzyl ammonium
chloride and Bis (tributyltin) oxide: [Ref. I-
28

-------
A-08-15.01] 5000 ppm quaternary  and 250
ppm TBTO, spray surfaces.
     (2) Bis  (tributyltin)   sulfosalicylate:
[Ref. I-B-12-00.01] 0.5% by weight of rub-
ber.
     (3) 4-Chloro-3, 5-xylenol:  [Ref. I-C-21-
00.02] As required.
     (4) Dehydroabietylamine  pentachloro-
phenate: [Ref. I-D-02-00.01] 0.5 to 1.0% by
weight.
     (5) Salicylanilide:  [Ref.  I-S-01-00.01]
0.5% by weight.
     (6) Ziram:  [Ref. I-Z-11-00.07]  0.5% by
weight of formulation containing 46% ziram
plus 4% zinc-2-mercaptobenzothiazole.

2. Bacteriostats

   A. Mercury compounds

Phenylmercuric hydroxide (17%); [Ref. Reg.
No. 6516-3] Chlorinated rubber coatings for
fabrics: 0.5 Ib product/99.5 Ib media.

   B. Substitute compounds

     (1) Ziram      (Zinc     dimethyldit-
hiocarbamate)  and   Zinc   2-mercaptoben-
zothiazole  (total Zn metallic 19.8%);  [Ref.
Reg. No. 1965-19] 0.2 to 1.5% product by
weight of finished media.
     (2) l-(3-chloroallyl)-3,   5,   7-triaza-l-
azoniaadamantane  chloride  (90%):  [Ref.
Reg. No. 464-32710.5 to 0.15% product by
weight.
     (3) Sodium pentachlorophenate (90%):
[Ref. Reg. No. 464-125] 0.3% product by
weight.
     (4) Sodium o-phenylphenol: [Ref. Reg.
No. 464-78] 0.3% product by weight.
     (5) Captan   (N-trichloromethylthio-4-
cyclohexene-1,   2-dicarboximide    (90%):
[Ref. Reg. No. 1965-11] 0.4% product by
weight of latex.
     (6) Dehydroabietylamine  pentachloro-
phenate (45%): [Ref. Reg. No. 2829-55] 0.5
to 1%  active ingredient based on weight of
finished product.
     (7) 4-chloro-3,  5-xylenol (100%): [Ref.
Reg. No. 4026-4] Product recommended for
neoprene and rubber preservation,  no dos-
ages stipulated.

  C. Comparative effectiveness and impact

     (1) Substitutes  appear to be adequate.
     (2) Impact on industry expected to be
minimal.
     (3) Cost to consumer  expected to in-
crease.
                                   XI.  Sanitizers
1.  Dust and cleaning cloth (bacteriostatic)
  A.  Mercury compounds
Phenylmercuric  oleate (0.01%):  [Ref. Reg.
No. 8618-1] Product inpregnated into fabric
using mineral oil.

  B.  Substitute compounds

    (1) Dilauryl dimethyl ammonium brom-
ide (0.25%): [Ref. Reg. No. 303-56]  1 fluid
ounce/6 inches mop or cloth.
    (2) n-Alkyl (50%C12, 30%C]4, 17%C,6,
3%C,8) dimethyl  ethylbenzyl  ammonium
chloride,  and n-alkyl (60%C]4,  30%C16,
5%C)2, 5%C18) dimethylbenzyl ammonium
chlorides. (0.2% total): [Ref. Reg. No. 1270-
92] 1 fluid ounce/6 inches of mop or cloth.
    (3) Lauryl pyridinium  salt of 5-chloro-
2-mercaptobenzothiazole:   [Ref.  Reg.  No.
1750-42] Spray on cloth undiluted.
(4) Dialkyl
                         8%C,  7%C
                                      10.
48%C,2, 17%C14, 9%C16, 10%Clg) dimethyl
ammonium chloride: [Ref. Reg. No. 1878-9]
Mix 1 1/2 gal product with 55 gal mineral oil
and add 2.5 to 3 gal/100 Ib dry weight cloth.
    (5) 2,  2'-methylenebis (3, 4,  6-trichlo-
rophenol)  (0.5%): [Ref. Reg. No. 2915-29] 6
to 16 ounces per mop depending on size.
                                                                                   29

-------
    (6) o-benzyl-p-chlorophenol    (1.0%):
[Ref. Reg. No. 4878-17] Used undiluted as a
dip.
    (7) 4-and      6-chloro-2-phenylphenol
(1.0%):  [Ref.  Reg.  No.  6831-5] 25  fluid
ounces/100 Ib dry cloth.

  C. Comparative effectiveness and impact

    (1) Substitute  compounds  are  ade-
quate.
    (2) Impact on industry and consumer
expected to be negligible.

2.  Floor Covering Finishes (bacteriostatic)

  A. Mercury compounds

Phenyl  mercuric  acetate  (0.025%): [Ref.
Reg. No. 52-145] Used undiluted for institu-
tional floor care.

  B. Substitute compounds

    (1) 2, 2' methylenebis (3, 4, 6-trichloro-
phenol):  [Ref. Reg.  No.  824-1]  1% to 4%
product by weight of media.
    (2) Alkyl  (derived  from fatty acids of
coconut  oil)  amine  hydrochlorides: [Ref.
Reg. No. 4313-37] 0.063% product by weight
of media.
    (3) Sodium pentachlorophenate (79%):
[Ref. Reg. No. 464-299] 0.025 to 0.15% prod-
uct by weight of formulation.
    (4)  l-(3-chloroallyl)-3,  5,   7-triaza-l-
azoniaadamantane chloride  (90%):  [Ref.
Reg. No. 464-327] 0.025% product by weight
of formulation.
    (5) 4-chIoro-3, 5, -xylenol (100%): [Ref.
Reg. No. 4026-4] Dosage not stated.

  C. Comparative effectiveness  and impact

    (1) Substitute  compounds  are  ade-
quate.
    (2) Impact on industry and consumer
expected to be negligible.

3. Floor Wax (bacteriostatic)

  A.  Mercury compounds

Phenyl mercuric acetate: [Ref. Reg. No. 52-
145] Applied to floor undiluted.

  B.  Substitute compounds


    (1) 2-Bromo-2-nitropropane-l,  3-diol:
[Ref.  Reg. No. 1839-60]  .05 to 0.1% product
by weight of formula.
    (2)  Dialkyl  (1%C6,   8%C8,   7%C,0,
48%C12, 17%C]4, 9%C]6, 10%C,8)  dimethyl
ammonium chloride:  [Ref. Reg. No. 1839-8]
1.5 to 2% product by weight of formula.
    (3)  l-(3-chloroallyl)-3,   5,   7-triaza-l-
azoniaadamantane chloride: [Ref. Reg. No.
464-327] 0.025% product by weight of for-
mula.
    (4)  4-chloro-3,  5-xylenol:  [Ref.  Reg.
No. 4026-4] Dosage not specified.

    (5) 2, 2'   methylenebis (3, 4, 6-trichlo-
rophenol):  [Ref. Reg. No. 824-1]  1 to  4%
product by weight of formulation.
    (6) 2, 2'-methylenebis  (4-chlorophen-
ol): [Ref. Reg. No. 824-6] 1 to 7% product by
weight of formulation.

  C.  Comparative effectiveness and  impact

    (1) Substitute   compounds  are  ade-
quate.
    (2) Impact on industry and consumer
expected to be nil.
30

-------
                                    XII.  Seed Treatments -
                                           Field Crops
   A.  Mercury compounds:
Phenylmercuric acetate-see tables 1 through
7, attached.
B.  Substitute compounds:

see tables 1 through 7, attached
                                          XII. Seed Treatments

                                                1. Bailey

Black loose smut,
covered smut
Damping-off, seed decay,
seedling blights

Stripe


0.019
to
0.038
0.019
to
0.038
0.019
to
0.038

1.2-1.9



ounces actual per bushel
0.75-2.10
0.75-2.10



0.18




2.04
2.04



1.5




1.6
1.6




0.42-0.53








p.p.m.
1200 to
1600




                                          XII. Seed Treatments

                                              2. Cotton


Sore shin


Surface seed-borne

anthracnose
Damping-off, Seed rot
and decay, seedling
blights
ounces actual per 100 pounds
0.075
to
0.338
0 075


0.338
0.075
to
0.338


3.0-3.5






3.0-3.5









2.7-4.0









2.9-5.7


6.5






6.5






1.4-2.1


1.4-2.1









9.6







0.9
to
1.3
4.0
to
6.0




4.0
to
6.0
1.0
to
2.5




1.0
to
2.5







1.89
to
3.00







0.84
to
2.94
12-(Thiocyanomethylthio) benzothiazole
2Used as a supplement to suitable standard seed treatments.
3p-(Dimethylamino) benzenediazo sodium sulfonate.
         H5-ethoxy-3-trichloromethyl-l,2,4-thiadiazole.
          with PCNB.
         5Used in combination with Captan.
                                                                                                  31

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                                                 XII. Seed Treatments
                                                        3. Flax

Damping-off,
Root Rots,
Seed decay
ounces actual per bushel
0.057
to
0.114
1.02
to
1.46
2.05
to
2.21
0.75
to
3.20

1.45

2.4
to
3.2
0.95
to
1.26
  *Used only as supplemental treatment to suitable standard seed protectants.
  ^Used only in combination with Captan.

                                                  XII. Seed Treatments
                                                         4. Oats


Leaf stri

Seed decay
Seedling blights
Covered smut,
Loose smut

ounces actual pet bushel
0.019
to
0.038







0.48
to
0.90






1.92






0.75
to
2.10
0.75
to
2.10





0.18





0.47
to
0.53





1200
to
1600
   1 Used as supplemental treatment to suitable standard treatments.
   2 In combination with Captan.
                                                 XII.  Seed Treatments
                                                        5. Rice

Damping-off,
Seed rots


0.042
to
0.084


1.7-3.75

ounces actual per 100 pounds

1.9-2.4


7.2


1.0


1.55-3.3


1.6-3.2

1 Used only as a supplemental treatment to suitable standard seed protectants.

32

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                                                                            XI i. Seed Treatments
                                                                                  6. Sorghum

Covered kernel smut,
Loose smut
Damping-off,
Seed decay
ounces actual per 100 pounds
0.019
to
0.038
0.019
to
0.038
1.9-3.0
1.9-3.0

1.9-2.9
0.7-1.4
0.7-1.4

1.0

1.8-2.3
0.57-1.34
0.57-1.34
2.4'
0.52
2.57


0.125
1.34-1.79
1.34-1.79

1.32-1.41
oz.
Cu/100""
1.07-1.43


1200
to
1600

1 In combination will, Dexon.
2 In combination with Terrazole.
3 Used only as a supplement to suitable standard seed treatments.
4p-(Dimethylamino) benzenediazo sodium sulfonatc.
511.6% Sodium dimethyl dithiocarbamate + 2.4% Sodium 2-mercaptobenzothiazole.
'In combination with PCNB.
7 In combination with Captan.

-------
                                                               XII. Seed Treatments
                                                                     7. Wheat

Dwarf bunt, Bunt
(stinking smut)
Flag smut, covered smut

Kernel smudge

Seed decay,
Seedling blights

ounces actual per bushel
0.019
to
0.038
0.019
to
0.038
0.019
to
0.038
|
0.66
to
1.20



0.66
to
1.20
0.20
to
0.53






0.75
to
2.10



0.75
to
2.10
0.50
to
0.75



0.50
to
0.75

1.44








0.125





0.125


1.0





1.0


1.8








1.6





1.6

0.47
to
0.52



0.47
to
0.52
oz. copper/bushel

0.4-0.8








1.0-2.0







p.p.m.
1200
to
1600






'27.6% Sodium dimethyl dithiocarbamate + 2.4% Sodium 2-mercaptobenzothiazoIe.
2 In combination with PCNB.
3 Limited to foundation and registered seed.
4 In combination with Captan.

-------
  C.  Comparative effectiveness and impact;

    (1) Mercury as PMA is the only availa-
ble control for stripe (Helminthosporium) of
barley.
    (2) Mercury  compounds  are  broad
spectrum fungistats for a wide range of path-
ogens on  field crop seeds. They control sev-
eral diseases for which  label claims have
never been noted, such as  certain bacterial
pathogens on cotton seed and fusarium scab
of cereals.
    (3) Mercury as PMA  is effective  at 0.1
to 0.01 of  the concentration of substitute
materials.
    (4) The impact on withdrawal  of these
uses for PMA would be severe and result in
greatly increased  costs to the commercial
seed  treater, the farmer  and consumer  of
crops grown from the treated seed.

  D.  An  estimation of the potential use of
PMA for the preceeding seven field  crops is
given in table 8.
                          Table 8. Estimated Potential Use of Phenylmercuric Acetate
                                   Field Crop Seed Treatments - Based
                                      On 1969 Seed Requirements
Crop Seed
Barley
Cotton
acid delinted
reginned
fuzzy
Flax
Oats
Rice
Sorghum
Wheat
Totals
Seed Used- 1969
XI, 000
1 6,000 bu.

95,1841b.
179,897 Ib.
ll,4221b.
72 bu.
59,563 bu.
2,119bu.
129,041 Ib.
l,552bu.

PMA
Ib. act. X 1,000
2.46

671.05
1,902.42
181.18
0.64
106.10
0.08
4.10
3.40
2,871.43
Hg
Ib. X 1,000
1.47

399.74
1,133.27
107.93
0.38
63.20
0.05
2.45
2.03
1,710.52*
     *Note that the Pesticide Review — 1970 shows that only 204,364 pounds of mercury was used in 1969 for all
      agricultural purposes. Assuming that all of the 204,364 pounds was used for treating seed, only about 8 per-
      cent of the seed was treated with mercury.


                                      XII. Seed Treatments
                                         8. Flower Seeds
 A. Mercury compounds:
                            [Ref. I-N-06-00.02]
                     Hydroxymercurichlorophenol Ornamental Seed and Bulb Treatments


Name of Seed

Acroclinium
Ageratum
Agrosteman
Amaranthus
Antirrhinum
(snapdragon)
Treatment
Avdp. oz.
28.6%
per 15 pounds
seed
1 oz.
1 oz.
1 oz.
Vi oz.
Vioz.


Soak time
in normal
solution
	
60 min.
60.min.
30 min.
60 min.













Name of Seed

Aquilegia
Arabis alpina
Arctotis
Aster
Balsam
Browallia
Treatment
Avdp. oz.
28.6%
per 15 pounds
seed
V4 OZ.
1 oz.
1 oz.
loz.
V4 oz.
1 oz.

Soak time
in normal
solution
60 min.
60 min.
90 min.
60 min.
30 min.
30 min.
                                                                                           35

-------

Name of Seed

Calendula
Calla Lily
Campanula
Carnary Bird Flower
Canterbury
Cardiospermum
Carnation
Celosia plumosa
Centaurea
Chrysanthemum
Clarkia
Clematis
Convolvulus
Coreopsis
Cosmos
Crimson Flax
Crocus
Daffodil (bulb)
Dahlia (Tuber)
Dahlia (Seed)
Delphinium
Digitalis
Dimorphoteca
Eschscholtzia
Four O'Clock
Freesia (Germs)
Gaillardia
Geum
Gladiolus (Corms)
Globeamaranth
Godetia
Gypsophila
Helianthus
Helichrysum
Heliotrope
Hibiscus
Hollyhock
Treatment
Avdp. oz. 28.6%
per 15 pounds
seed
loz.
	
loz.
1 oz.
	
Vioz.
loz.
1 oz.
loz.
1 oz.
V4oz.
loz.
1 oz.
1 oz.
Vi OZ.
1 oz.
	
	
	
Vi oz.
loz.
loz.
Vi oz.
loz.
loz.
	
1 oz.
loz.
	
	
1 oz.
loz.
loz.
loz.
loz.
loz.
1 oz.
Soak time
in normal
solution
60 min.
60 min.
30 min.
60 min.
15 min.
60 min.
30 min.
30 min.
30 min.
30 min.
60 min.
60 min.
60 min.
30 min.
	
	
2hrs.
2hrs.
30 min.
	
30 min.
30 min.
	
90 min.
60 min.
60 min.
15 min.
	
7 hrs.2
30 min.
60 min.
60 min.
30 min.
30 min.
60 min.
90 min.
30 min.









































Name of Seed

Humulus
Hyacinth (bulb)
Ipomeoa
Jonquil (bulb)
Kochia
Kudzu Vine
Larkspur
Lavatera
Lupinus
Marigold
Mignonette
Myosotis
Narcissus (bulb)
Nasturtium
Pansy
Peony (Roots)
Petunia
Phlox
Poppy
Portulaca
Pyrethrum
Salpiglossis
Salvia
Scabiosa
Stevia
Stock
Sweet Alyssum
Sweet Pea
Sweet William
Tuberose
(bulb)
Tulip (bulb)
Valerian
Verbena
Violet
Wallflower
Zinnia
Treatment
Avdp. oz. 28.6%
per 15 pounds
seed
1 oz.
	
1 oz.
	
Vi OZ.
1 oz.
1 oz.
1 oz.
Vi OZ.
'/2 OZ.
Vi oz.
'/20Z.
	
1 oz.
1 oz.
	
Vi oz.
1 oz.
Vi oz.
Vi oz.
]/2 OZ.
1 oz.
Vi oz.
1 oz.
1 oz.
Vioz.
Vi OZ.
1 oz.
loz.
	

	
1 oz.
loz.
1 oz.
1 oz.
1 oz.
Soak time
in normal
solution
60 min.
2 hrs.
60 min.
2 hrs.
30 min.
60 min.
60 min.
60 min.
60 min.
60 min.
60 min.
60 min.
2 hrs.3
30 min.
30 min.
30 min.1
30 min.
30 min.
30 min.
30 min.
30 min.
60 min.
30 min.
60 min.
60 min.
30 min.
60 min.
30 min.
30 min.
30 min.

2 hrs.
30 min.
30 min.
30 min.
30 min.
60 min.
1 Preplanting treatment only.
J Use extra strength solution.
3Use double strength solution.
  B.  Substitute compounds:

Thiram:  [Ref. I-T-10-00.08] dust thoroughly
with 4 to 12% dusts
  C. Comparative effectiveness and impact:

    (1) Mercury   compounds  are   more
effective than the available  substitute com-
36

-------
pounds  for controlling  most  seed-borne
pathogens and some soil-borne organisms.
    (2) The impact of withdrawal of mercu-
ry for these uses will be minimal.
    (3)  Note: The manufacturer has already
ceased production of  this chemical. Regis-
trations are now continued in effect only to
cover merchandise in channels of trade.
                           PESTICIDE USES OF MERCURY

                              XIII.   Surfaces (fungistats)
                                (see also XI. Sanitizers)
1.  Fungistats on Commercial, Institutional
and  Household  Surfaces  e.g.  [cabinets,
floors, walls, ceilings, garbage cans, lockers,
masonry,  tile, refrigerator  and other  hard
surfaces; blankets, canvas goods, carpeting,
clothing, cubicle curtains, hampers, laundry
bags, leather goods, linens,  mattresses, uni-
forms, upholstery and similar porous sur-
faces.]

  A.  Mercury compounds

20    ppm   of   Sodium   ethylmercurit-
hiosalicylate plus 4860 ppm alkyl dimethyl
benzyl ammonium chloride, 360 ppm tribu-
tyltin benzoate, 240 ppm tributyltin isopro-
pyl succinate, 120 ppm  tributyltin  linoleate
and 250 ppm isopropyl alcohol, applied as a
low-pressure  bomb  spray.  [Ref.  I-A-08-
25.04]

  B.  Substitute compounds

    (1)  Alkyl dimethyl  benzyl ammonium
chlorides: [Ref. I-A-08-00.01, I-A-08-15.01,
I-A-08-20.01,  I-A-08-25.04,  I-A-08-35.01, I-
A-08-45.04, I-A-08-50.01] 200 to 30,000 ppm
alone or in combination with a large number
of other active ingredients  as low  pressure
bomb  sprays or  by  mopping,  wiping  or
washing.
    (2)  Alkyl dimethyl  benzyl ammonium
saccharinate:  [Ref. I-A-11-00.01]
      (a)  400 ppm plus  100 ppm sodium o-
phenylphenate by mop or spray.
      (b)  10,000 ppm plus 2500 ppm sodium
o-phenylphenate and  237,000 ppm isopro-
panol by low pressure bomb.
    (3)  Aklyl dimethyl 3,  4-dichlorobenzyl
ammonium chloride: [Ref.  I-A-14-20.01] 700
ppm plus  138 ppm tributyltin benzoate and
isopropanol by mop, sponge, brush or spray.
    (4)  Alkyl dimethyl ethylbenzyl ammon-
ium  cyclohexyl  sulfamate:  [Ref. I-A-17-
00.01] 3,000 to 3,200 ppm  plus 645, 000 to
675,500  ppm ethyl alcohol and 50,000 ppm
propylene  glycol  by  low-pressure  bomb
spray.
    (5)  Ammonium  hydroxide-C8   Fatty
acid-Silver Complex: [Ref.  I-A-32-00.01] 860
ppm metallic silver equivalent as a  low-
pressure bomb spray.
    (6)  Bis (tributyltin) oxide: [Ref. I-B-09-
00.01] 420 ppm in low-pressure bomb spray.
    (7)  Calcium hypochlorite: [Ref. I-C-07-
00.01] 7300 ppm by brush or sponge.  Note:
Not a substitute for residual  properties of
mercury compounds.
    (8)  Captan: [Ref. I-C-10-00.15] 375 ppm
plus 240,600 ppm isopropanol as low pres-
sure bomb spray.
    (9)  Chlorine  dioxide:   [Ref.  I-C-13-
60.01] 1000 ppm plus  292,000 ppm ethanol
and 3000 ppm sodium carbonate as low pres-
sure bomb spray. Note: Not a substitute for
residual properties of mercury compounds.
    (10) 4-Chloro-3,  5-xylenol: [Ref. I-C-
21-00.01] 3300 ppm as a spray.
    (11) Diisobutylphenoxyethoxyethyl
dimethyl benzyl ammonium chloride: [Ref.
I-D-13-00.01] 700 to 2000 ppm plus isopropyl
alcohol or other agents.
    (12) 80 percent  methyldodecylbenzyl
trimethyl  ammonium  chloride  plus  20%
methyldodecylxylene bis (trimethyl ammon-
ium chloride): [Ref. I-M-09-00.02]
                                                                                  37

-------
      (a)  2000 to 5000 combined quaternar-
ies plus 600,000 ppm ethanol as low pressure
bomb spray, or
      (b)  2500  to 5000 ppm  combined qua-
ternaries plus 750 to 2000 ppm brominated
salicylanilides and 630,000 ppm  ethanol or
isopropanol as low-pressure bomb spray.
    (13) 2, 2'-methylenebis-(3, 4, 5-trichlo-
rophenol): [Ref. I-M-13-00.03] 200 ppm plus
400 ppm 2, T methylenebis (4-chlorophenol)
as low pressure  bomb spray.
    (14) o-Phenylphenol:[Ref. I-P-19-00.03]
1000 to  2000 ppm plus various amounts of
other fungistats, mostly  as  low-pressure
bomb sprays.
    (15) Sodium dimethyldithiocarbamate
      (a)  plus    sodium   2-mercaptoben-
zothiazole [Ref. I-S-09-00.06]
      (b)  1400  to 5800 ppm
      (c)  plus 120 to 500 ppm
      (d)  as wash, mop, sponge or spray.
    (16) Sodium  g-phenylphenate: [Ref. I-
S-16-00.08]  1500 ppm  plus 930 ppm methyl
salicylate  and  9300 ppm  isopropanol as a
spray.
    (17) Zineb:  [Ref.  I-Z-10-00.15]  10,000
ppm as low-pressure bomb spray.

  C.  Comparative effectiveness and impact

    (1)  Substitutes are available which  are
as effective as mercury compounds for fun-
gistasis on surfaces.
    (2)  Impact of withdrawal of these uses
will be slight to the consumer but may be
more severe on  the manufacturer.
 XIV. Tanneries (bacteriostats and fungistats)

  A.  Mercury compounds

Phenylmercuric acetate

For hides and skins (in cellars of meat pack-
ing plants and tanneries): [Ref. I-P-08-00.09]
305 ppm solution of a combination of PMA,
sodium  pentachlorophenate  and  sodium
trichlorophenate. For processing: [Ref. I-P-
08-00.10 and  I-P-08-00.11] soaking - 0.05 to
0.10 Ib  PMA (I) plus 0.25 to 0.50 Ib potas-
sium trichlorophenate (ID/1000 Ib. Add  to
soak water, pickling - 0.03 Ib (I) plus 0.15 to
0.25 Ib 11/1000 Ib wet  stock. Add to pickling
solution.
Chrome tanning: 0.03 to 0.06 Ib (I) plus 0.15
to 0.30 Ib  (II)/1000 Ib  wet stock. Add  to
chrome liquor.
Vegetable tanning:  0.03 to 0.06 Ib (I) plus
0.15 to  0.30 Ib (II)/1000 Ib of tanned stock.
Add to  wash  water  or to final bleaching liq-
uor.
Samming: Treat sawdust with 0.05 Ib (I) plus
0.25 Ib (II)/50 gal of water [120 ppm (I) plus
600 ppm (II)].
Fatliquoring:  500 to 1500 ppm (I) plus 2500
to 7500 ppm (II) on weight of fatliquor.

  B. Substitute compounds

    (1)  Pentachlorophenol:  [Ref.  I-P-05-
00.03] 0.1 to 3.5% in processing solution or
dressing formulations,
    (2)  22.5%  of  potassium  pentachloro-
phenate plus 22.5% of potassium  4 (or 6;-
chloro-2-phenylphenate: [Ref.  I-P-25-00.01]
Pickling: 0.1% by weight of stock. Chrome
tanning: 0.1% by weight of stock. Vegetable
tanning: 0.3% by weight of stock.  Brusting,
pearling or staining:  0.1% solution. Dying
and fatliquoring: 0.1 to 0.2% solution.
    (3)  Sodium o-phenylphenate: [Ref' I-S-
16-00.09] 0.1  to 3.5% by weight of'process-
ing solutions.
    (4)  17.5% of sodium tejrachlorophenate
plus 7.7% of sodium o-phenylphenate: [Ref.
I-S-21-00.01]
Soaking: 1 to  2 Ib/lOOgal.
Pickling: 3 to  5 Ib/1000 Ib stock. Chrome and
vegetable tanning: 3 to 5 lb/1000 Ib stock.
    (5)  Tetrahydro-3, 5-dimethyl-2H,  1, 3,
5-thiadiazine-2-thione: [Ref. I-T-07-00.03]
Soaking: 2 to 4 oz/100 gal.
Padding, tanning, fatliquoring and coloring:
0.5 to 1.5oz/100gal.
38

-------
Final rinse (leather to be used in clothing):
l.Ooz/lOOgal.
    (6) Tributyltin  salicylate  plus 40.9%
Diisobutylphenoxyethoxyethyl    dimethyl
benzyl ammonium chloride and 6.5% isopro-
phanol:  [Ref. I-D-13-00.03] Fatliquor  and
long bath: 0.5% of formulation by weight of
leather.

  C. Comparative effectiveness and impact

    (1) Substitute  chemical  products  are
more expensive than the mercury materials.
1.  Logs, lumber (sap stain and mqld during
seasoning, storage and shipment):

  A. Mercury compounds

    (1)  Ethylmercury phosphate: [Ref. I-E-
07-00.01] 150 to 300 ppm solution, or  72 to
1200 ppm plus sodium pentachlorophenate,
or 225 to 450 ppm for heavy timbers.
    (2)  Phenylmercuric    acetate:    [Ref.
I-P-08-00.08]  2 pints of 5% PMA  plus 25%
sodium  trichlorophenate/75  gal  (approxi-
mately 1600 ppm PMA).
    (3)  Phenylmercuric hydroxide: [Ref. I-
P-09-50.01] 1 to 2 gal of 0.2% PMH plus
14.54%   sodium  pentachlorophenate   and
3.16% sodium metaborate/40 to 50 gal.
    (4)  Phenylmercuric  lactate:  [Ref.  I-P-
10-00.01; I-S-15-00.02; I-S-21-00-01] Use 1 to
2 gal of 0.4% PML plus 1.0% sodium  octa-
borate  and 22.82% technical sodium  pen-
tachlorophenate/100 gal,  1  to 2  gal  0.4%
PML plus  13.3%  sodium  metaborate and
22.82%   technical  sodium   pentachlorop-
henate/100  gal, or 2 to 3 gal of 3.19%  PML
plus 49.23% sodium trichlorphenate/100 gal
for  western species including Douglas Fir,
Hemlock and pine.
             ''-1
  B. Substitute compounds

    (1)  2.0% Bis  (tributyltin)  oxide  plus
4.5% l-(Alkyl amino)-!,  3-amino  propane
     (2) We are not familiar with the various
problems of color,  hand and other quality
factors which may influence the usability of
substitute materials.
     (3) Based on the fact that the industry
failed  to  respond  to the  Federal Register
request for views and comments, we believe
that the  impact of  withdrawal  of mercury
registrations will have little impact on  the
tanning industry.
                                     XV.  Wood
monoacetate,  21.0%  sodium  tetrachloro-
phenate and  5.7%  sodium  salts  of other
chlorphenols:  [Ref.  I-A-07-00.01]  0.5  to
0.75% solution
    (2) 2.5%  Q-Phenylphenol   plus  2.5%
pentachlorophenol:  [Ref. I-P-19-00.02] dip
in above formulation
    (3) 14.4%   Potassium   pentachloro-
phenate plus  1.5% alkyl amino-3-aminopro-
pane, 8.3% potassium trichlorophenate and
1.7% of other potassiums salts of chlorophe-
nols: [Ref. I-P-25-00.02] Use 0.5 to 0.75% of
above formulation in water. Dip or spray.
    (4) 13 to 65% Sodium borate plus 27.7
to 36.0%  sodium pentachlorophenate  and
4.0 to 12.3% sodium carbonate:  [Ref. I-S-04-
00.01] 10 o 20 Ib formulation/100 gal.
    (5) Sodium pentachlorophenate: [Ref.
I-S-15-00.02] 3 to 12 lb/100 gal.
    (6) Sodium tetrachlorophenate: [Ref. I-
S-21-00.01] 4.8 lb/100 gal.

  C. Comparative effectiveness and impact

    (1) Mercury compounds are the  most
effective, require much smaller dosage rates
and control more fungus species than the
substitute   materials.  The  mercury  com-
pounds are also much less expensive.
    (2) The impact of withdrawal of mercu-
ry for this use will be great on the manufac-
turers of such formulations and will be very
                                                                                   39

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great  on the  consuming  lumber industry
where  federal  specifications now  require
such treatment or where it  is required  by
foreign purchasers of lumber.

2.  Fence posts (rot and decay application)

  A. Mercury compounds

    (1)  Mercuric chloride:  [Ref.  I-M-04-
00.01] 1 tbs of 33.2% mercuric chloride plus
33.2% arsenious oxide/0.75 inch x 2.0 hole
bored 6 inches  above ground line, in green
posts. Posts over 4 inches in diameter  re-
quire 2 to 3 holes. Plug holes after filling. No
access to livestock.
    (2)  Phenylmercuricoleate: [Ref. I-P-14-
00.01] 1.0 to 1.25% solutions - soak

  B. Substitute compounds

    (1)  Anthracene oil:  [Ref. I-A-35-00.01]
soak
    (2)  Coal for neutral oils: [Ref.  I-C-22-
00.01] soak.
    (3)  Copper naphthenate: [Ref.  I-C-30-
00.01] soak.
    (4)  Copper sulfate plus sodium fluoride
or  sodium  chromate:  [Ref.  I-C-38-00.01]
soak.
    (5)  Creosote (coal  tar):  [Ref.  I-C-41-
00.01] soak.
    (6)  Creosote  (wood):   [Ref.   I-C-42-
00.01]soak.
    (7)  Pentachlorophenol:  [Ref.  I-P-05-
00.01] 5% solution, soak.
    (8)  5.09%  sodium   dichromate  plus
5.36% copper sulfate and 0.2% chromic acid
solution: [Ref. I-S-07-50.01] soak.
    (9)  Tetrachlorophenol:  [Ref.   I-T-06-
00.01] 5% solution, soak.
    (10)  Zinc  naphthenate:  [Ref,  I-Z-05-
00.01] 20% solution, soak.

  C. Comparative effectiveness and impact

    (1) Substitute compounds are at least as
effective  as mercury compounds for the con-
trol of rot and decay of fence posts.
    (2) Substitute  compounds  frequently
provide objectionable coloration  to treated
wood, mercury does not.
    (3) Substitute  compounds  frequently
impair the paintability of treated wood, men-
cury does not.                           '>
    (4) Impact of  withdrawal  of mercury
for treating fence posts will be negligible.
3. Lumber and timbers (rot and decay - con-
sumer application)

   A. Mercury compounds               ;

    (1)  Phenylmercuricoleate: [Ref. I-P-14-
00.01] 1.0 to 1.25% solution by brush, spray
or dip.
    (2)  0.6%  Phenylmercuric  oleate  plus
7.125% technical pentachlorophenol: [Ref.
I-P-14-00.01] brush, spray or dip.

   B. Substitute compounds

See 2, B  above. Apply by dip, spray or soak.
   C. See 2, Cabove.

   D. Addendum

    (1)  Mercury compounds

0.28% Phenylmercuric  oleate plus 0.28%
TBTO and 12.5% zinc naphthenate - house-
hold use by brush spray OF dip.  [Ref. Reg.
No. 390-3]
                         XVI. Dental and Surgical Instruments
                                    (disinfection)
 1. Mercury compounds
   A.  Phenylmercuric borate (0.1%):  [Ref.
Reg.  No.  1293-1] Instrument  disinfectant
used undiluted.
   B.  3-(Hydroxymercuri)^4-nitro-o-cresol
 (0.48%): [Ref. Reg. No. 275-3] Disinfectant,
 used undiluted.
40

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2. Substitute compounds
  A. n-Alkyl  (60%C,4,  30%C]6,  5%C,2,
5%C,8) dimethylbenzym  ammonium chlo-
ride (total 10%): [Ref. Reg. No. 859-7] Use-
dilution: 1 fluid oz/2 gal water.
  B. Potassium o-phenylphenate, and  po-
tassium o-benzyl-p-chlorophenate (and solu-
bilizing and  sequestering  agents)  (total
19.2%): [Ref.  Reg. No. 1750-32] Use-dilu-
tion: 1-100.
  C. Tetradecyl  dimethyl  benzyl  ammo-
nium chloride (1.25%), dodecyl  dimethyl-
benzyl  ammonium chloride (0.25%),  and
isopropyl  alcohol  (17.5%):  [Ref.  Reg. No.
3625-1] Use-dilution:  4 fluid oz product/gal
water.
  D. Isopropanol, and  n-alkyl  (50%C14,
40%C,2,  10%C16)  dimethylbenzyl ammon-
ium chloride (total 29% actives):  [Ref. Reg.
No. 4330-1] Use-dilution:  1-32
  E. Cresol, benzaldehyde,  safrole,  and
formaldehyde (total 30% actives): [Ref. Reg.
No. 5493-2] Use-dilution: 1-32.
  F. Cresols,  formaldehyde, phenylethyl,
alcohol,  and benzyl alcohol (total 95%):
[Ref. Reg. No. 5493-4]  Use-dilution: 2 fluid
oz/gal of water.
  G. Diisobutylcresoxyethoxyethyl-dime-
thylbenzyl ammonium chloride and o-phen-
ylphenol   ethoxynonyl-phenol    complex
(1.1%),   and   methyl-p-hydroxybenzoate
(0.3%): [Ref. Reg. No. 7150-4] Use-dilution:
1 part product to 3 parts water.

3. Comparative effectiveness and impact

  A. Substitute compounds are better disin-
fectants than mercury compounds.
  B. No impact on industry or the consum-
er expected.
                                XVII.  Miscellaneous
 1. Broomcorn

   A.  Mercury compounds

 Phenylmercuric acetate: [Ref.  I-P-08-00.09]
 200 ppm in dye bath by weight of solution.

   B.  Substitute compounds

 None.

   C.  Impact

    (1) Broomcorn brooms  and  brushes
 must  have a bright color and clean appear-
 ance to be saleable. A  fungistatic agent with
 residual qualities  is  necessary  in  broom
 manufacture.
    (2) Although no substitutes for mercury
 are registered for this use, it would appear
 that a suitable replacement compound could
 be found  with little effort. Therefore, the
 impact of withdrawal of mercury for this use
 should be slight to moderate on the manu-
 facturer and consumer.
2. Cellulose sponges

  A.  Mercury compounds

Phenylmercuric acetate: [Ref. I-P-08-00.09]
750 ppm solution.

  B. Substitute compounds

None.

  C. Impact

Unknown. Substitute compounds should not
be difficult to find  once the consumers are
aware of the withdrawal of mercury for this
use.

3. Seam and bedding compounds (boat con-
struction)

  A. Mercury compounds

Phenylmercuric oleate: [Ref. I-P-14-00.01]
400 ppm PMO plus 1425 ppm. Pentachloro-
phenol by volume of compound.
                                                                                  41

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   6.  Substitute compounds

None.

   C.  Impact

Unknown. Mercury is  thought to be  of
doubtful necessity or value in this use. Sub-
stitute materials should  not be difficult to
find.

4. Milk sample preservation  (for dairy herd
improvement)

   A.  Mercury compounds

Mercuric chloride (32.2%):  [Ref. Reg. No.
2955-9] One tablet weighing 0.28 grams to
140 ml  of milk sample; preservation for
Babcock laboratory test.

  B. Substitute compounds

Potassium dichromate (65.9%): [Ref.  Reg.
No. 2955-21]  1  tablet weighing 0.23 grams
added to 180 ml milk provides  preservation
for 3 weeks.

  C. Comparative effectiveness and impact

    (1)  Substitute compounds  cannot pre-
serve milk samples as long as mercurial.
    (2)  Substitute chemical  is satisfactory.
    (3)  Impact on industry  expected to  be
minimal; consumer impact may call for in-
creased  cost.
42

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                                   CHAPTER 2
                ANALYTICAL METHODS FOR MERCURY
Probably the single most important cause of
the sudden increase  in  apprehension  over
mercury  in the environment has been the
rapid  strides  made in analytical  methods
used to detect trace amounts of mercury and
its compounds. It can now be found in hith-
erto unsuspected substrates.

II.A. Colorimetric— For years the classical
method for determination of mercury was
the AOAC  dithizone  spectrophotometric
procedure (Horwitz,  1970). In  this  proce-
dure the  sample, for  instance, grain or tis-
sue, is digested with nitric and sulfuric acids
under reflux. Even after  the solution be-
comes clear, indicating complete destruction
of most of the organic matter, some of the
organic mercury may still be so bound that it
will not complex with dithizone  reagent. In
such a case, the results would be low. Fur-
ther, some mercury can be lost by volatiliza-
tion or absorption on the glass container.

Then, too, copper, gold,  silver, palladium
and platinum in trace amounts interfere giv-
ing high results.  In the same manner,  lead,
zinc, nickel, and cobalt in larger amounts
cause high results. The mercury dithizone
complex  is not stable to  light  and  breaks
down readily giving low results.

However, within the limits of its sensitivity
and problems of interference, the dithizone
method is satisfactory. A description of the
method follows:

A sample equivalent to not more than 10 g
dry weight  is  digested  with   HNO3 and
FLjSC^ under reflux in a special apparatus
designed  to prevent loss of Hg by volatiliza-
tion. The mercury is extracted from  the di-
gest with  a chloroform solution of dithizone
and is then separated  from copper as a mer-
cury thiosulfate  complex. The complex is
decomposed and  the mercury again taken up
in a chloroform  solution  of dithizone. The
absorbance of the dithizone solution is mea-
sured at 490 nm and the mercury determined
by  comparison  with  the  absorbance  of
standards.  As  little as  3/ig of Hg may be
determined. For a dry produce such as grain
using a 10-g sample, 3 g would be equivalent
to a  sensitivity of 0.3  ppm.  With fish  and
other high moisture products a larger sample
could be used. Assuming the use of a 20-g
sample, the sensitivity of  the method would
be better than 0.2 ppm.

The method has little value in studying cases
of mercury poisoning because of the  larger
amount of sample needed, the low limit of
sensitivity and  the many interferences.


Reviews of the  methods for  colorimetric
analysis are given by Sandell (1959) and by
Snell & Snell (1949).

II.B. Atomic Absorption — Even the advent
of atomic absorption spectrophotometry did
not immediately result in improvement in
mercury analysis as  mercury is one of the
least sensitive  of the metals to this method.
However,  a number of  modifications of
classical atomic  absorption analysis permit
greater sensitivity, reproducibility and ease
of analysis. Some of these developments are
as follows:

Jacobs and Goldwater  (1960) digested sam-
ples of apples with permanganate, extracted
the mercury with a chloroform solution of
dithizone, evaporated, off the CHC13, vola-
tized the mercury by heating the dry dithi-
zone  residue, swept  the  mercury  vapor
through a quartz  windowed cell in a modified
                                                                                  43

-------
Kruger  mercury  vapor meter  and deter-
mined the mercury content  by its absorb-
ance.  Values as low as 0.01 ppm Hg were
reported.


Pappas and Rosenberg (1966) used a Schoni-
ger combustion flask to burn samples. The
released  mercury  was absorbed  in  dilute
HC1 and  collected on a CdS-impregnated
asbestos pad. The pad was pyrolyzed at
650°C and the released Hg vapor swept into
a quartz-windowed cell where its absorb-
ance was measured by a photometer using a
mercury lamp as the light source. Sensitivity
of 0.01  ppm Hg  was  reported  for wheat
samples.

Lidums and  Ulfvarson (1968) burnt small
samples (20-200 mg) of biological material in
a stream of oxygen, and collected the Hg on
gold foil. The gold foil was then heated, re-
leasing mercury vapor which was swept into
a cell and its absorbance measured by a pho-
tocell using  a  mercury lamp  as  the  light
source.  As little as 0.001 p  g  Hg/g sample
could be  determined. The  procedure was
said to work well  for blood, plasma, urine
and sea bottom sediments, but the authors
were not quite satisfied with it for more diffi-
cult organic samples.

A.O.  Rathje (1969) determined mercury in
urine without digestion. The urine (2 ml) was
treated with 5 ml cone. HNO3, diluted to 50
ml and the mercury reduced  by the addition
of stannous  chloride. Air or nitrogen was
then bubbled through the solution and the
mercury vapor  swept through a drying tube
into the cell of the detector.  The instrument
used was  a Perkin Elmer  Model 303 atomic
absorption spectrophotometer  with  a  GE
64811 mercury discharge lamp to provide the
253.7-mm line and with the burner assembly
removed and replaced by an  8-inch cell with
quartz windows. As little as 6 ng Hg could
be detected,  thus for a 2-ml  sample indicat-
ing a sensitivity of 0.003 ppm.
44
Uthe, Armstrong and Stainton (1970) of the
Fisheries Research Board of Canada deter-
mined mercury in fish using very small sam-
ples (0.1-0.5 g). The sample was first digested
with  H2SO4 at 50°-60°C  and  then with
KMnO4 at room temperature. The mercury
was reduced with stannous sulfate and the
mercury  vapor swept  by  an  air stream
through a drying tube and a gas cell in a Per-
kin-Elmer atomic  absorption  spectrophoto-
meter.

More  recently  the Association of Official
Analytical Chemists has accepted the pre-
scribed atomic absorption method as official.
A brief description of the method is  as fol-
lows:

Five gram samples of fish are digested under
a water condenser  first with H2SO4,  HNO3
and NaMoO4 and  then with  HNO3 and
HC104. The  digest is made up  to 100 ml, and
a 25-ml aliquot taken for atomic absorption
analysis.  Using a  closed system consisting
of a reaction flask, a drying flask,  a gas cell
in an  atomic absorption spectrophotometer
and a  recirculating  air  pump, the mercury is
reduced with stannous chloride  and the  re-
sulting mercury vapors swept through the
gas cell where the absorbance is measured.

II.C. Neutron Activation — The use of neu-
tron activation analysis has excited the at-
tention of many analysts, because  of certain
apparent advantages.   It purports to be a
nondestructive  method. Also, it  can yield
definitive results with very small samples of
even such materials as skin or hair. Further,
in a reactor designed for automatic analysis,
practically  the entire operation   becomes
automatic  including  irradiation,   counting
and calculations.

However, the accuracy  of  the method  is
affected by the fact that sodium is  present in
practically all biological samples. If the level
of sodium  activity following irradiation is
permitted to decay to tolerable limits, often
the  mercury has decayed to the  point that it

-------
cannot be measured against the interference
background.
ucts  and phenylmercury in rice to  levels
lower than 0.01 ppm.
The method of getting around this problem
is to irradiate the sample and then add a few
milligrams  of carrier  mercury,  generally
mercuric chloride. The  sample is then di-
gested, the mercury precipitated or extract-
ed and the analysis completed by counting
the isolated portion and calculating the mer-
cury content from the radioactivity remain-
ing.

However, that is unsatisfactory with many
biological samples such as fish in which most
of the mercury is present as methylmercury
compounds. The mercury becomes radioac-
tive on irradiation, but in the isolation step,
much of  the radioactive  mercury is lost be-
cause of the difficulty in  digestion. It simply
is not precipitated or extracted with the car-
rier.  Results  may  reflect only 10% of the
actual level in such cases.

Sjostrand (1964)  described  the  procedure
used in  Sweden.  The sample, sealed  in a
quartz tube, was exposed to neutron radia-
tion  in a nuclear reactor. The sample was
then transferred to a flask and 20  mg of Hg
(HgCl-,)  added as carrier and digested. The
mercury  was  distilled from a perchloric acid
solution  and electrolytically plated out on a
weighed  gold foil. The foil was weighed to
determine percent recovery of Hg and the
197Hg measured by y -spectrometry. Sensi-
tivity of the procedure is said to be about 10"
5 ppm Hg.

II.D. Gas-Liquid Chromatography  — Since
alkylmercury compounds tend to be difficult
to analyze and yet are  prevalent  in many
substrates, a number  of scientists have at-
tempted to devise methods suitable for sam-
ples containing such mercury derivatives.

K. Sumino (1968) used gas chromatography
to determine methylmercury in marine prod-
Westo'6 (1967, 1968) used electron capture
GLC  to  determine  methylmercury  in  fish
and other foods of animal origin. She report-
ed that most of the mercury present in fish,
eggs and meat was  in the form of methyl-
mercury, 82% for ocean  fish  and 92% in
fresh water fish.
In contrast to the two above methods in
which the organic mercurials were chroma-
tographed  as  the chlorides,  Tatton  and
Wagstaffe (1969)  extracted and  chromato-
graphed these compounds as their dithizon-
ates.  Apparently  the  intact  dithizonajes
chromatographed  and  the specific organic
mercurials could be identified by their reten-
tion time. Both these authors  and West66
also used TLC as an  additional means of
identification.

II.E. Miscellaneous Methods —  Tong, Gu-
tenman and Lisk (1969) applied  the use of
spark source mass spectrometry  to analysis
of apples for mercury. In this, a pair of in-
dium electrodes was used to make a graded
series of exposures on the same photograph-
ic plate  for  emulsion calibration relating
microdensitometric measurements of mass
line optical transmittance (%T) to exposure
level (E). The  %T values for silver (m/e
107), mercury (m/e 198, 199, 201, and 202),
and their corresponding backgrounds were
measured. These values were converted into
E values according to the emulsion calibra-
tion curve. The  ratio of mercury to silver
was then determined by the exposure  (E)
ratio of mercury to silver (each element hav-
ing been corrected for the isotopic abund-
ance and background) according to Equation
 mercury/silver (mole ratio) =
 (^mercury - ^-mercury background) ^silver
 C       f                  .         /1 \
 (^silver - ^silver background) Amercury

                                      45

-------
where A mercury and A silver are the iso-
topic abundances of the respective lines of
interest.
Mtusiak and coworkers (1964) described a
method for analysis of mercury in biological
substances wherein they passed wet digests
or urine over copper powder over a period
of 1  hour  using suction to control the flow
rate. The copper powder was then placed in
the crater of the electrode of a spectrograph
and the 2537  A mercury line used for analy-
sis.

Pakter (1968) describes a method he  devel-
oped for  determination of mercury in or by
absorption on manganese dioxide. The mer-
cury can then be driven from the manganese
dioxide by heat and measured by conven-
tional  methods  such as dithizone or atomic
absorption methods.
46

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                                   CHAPTER 3
         PREVALENCE OF MERCURY IN THE ENVIRONMENT
Mercury is one of the elements which make
up the earth.  In its  elemental state at the
earth's surface, it is  a silvery liquid metal,
approximately 13 1/2 times as heavy as wa-
ter. Mercury is the only metal which occurs
in the liquid state at ordinary earth tempera-
tures. Like other liquids,  it vaporizes  and
condenses  in  a pattern  determined by its
own vapor pressure and the barometric pres-
sure of the environment in which it exists.
Mercury is absorbed  and is bound tightly by
a variety of materials such  as plant fibers
and soils. It reacts with a variety of inorgan-
ic and organic compounds to form simple
and complex molecules ranging from cinna-
bar, a mercury sulfide and the most common
ore mineral, to the metallo-organic complex-
es which are  used in pesticides and which
are now found  as a contaminant  in  fish
(Fleischer, et al., 1970). At this point in time,
it is difficult to separate the "natural" back-
ground levels of mercury from those which
are man-made. Certainly,  a portion of the
mercury found in  water,  soil, plants,  and
animals arises from  "natural" sources. In
areas where mercury pollution is known to
occur from sources such as agricultural run-
off,  industrial wastes, and  mining opera-
tions, increases above the "natural" levels
can be expected.  There  remains,  however,
the question of just how much of the remain-
ing background is due to the combustion of
paper products and fossil fuels, the smelting
of ores, weathering of paints, and other ac-
tivities of man.


III.A. Minerals and Rocks — Cinnabar is the
most  commonly   found  mercury-bearing
mineral. It contains 86% mercury by weight.
Cinnabar is generally found in mineral veins
or fractures,  as impregnations,  or  having
replaced quartz, in rocks near recent volcan-
ic or hot-spring areas. The mercury content
of broad categories of rocks in the earth's
crust range from 10 to 20,000 ppb. Less than
20% of  recorded  rock samples have more
than 1,000 ppb. Igneous rocks are the basic
sources  of mercury. These contain less than
200 ppb of mercury and average about 100
ppb. The mercury content of soils averages
about 100 ppb and  varies within relatively
narrow  limits. The  background concentra-
tion of soils  in California are 20 to  40 ppb.
The Franciscan Formation of California, in
which most of the State's mercury mines are
located, has background levels of 100 to 200
ppb; anomalies in  soils around these mercu-
ry deposits are in the  range  of 10,000 to
100,000  ppb (Fleischer, etal., 1970).


III.B. Atmosphere — Because of the tenden-
cy of mercury to vaporize, it is distributed in
the environment through  aerial  circulation.
The atmosphere  measured at ground  level
near mercury ore deposits may contain as
much as 20,000 ng/m3 of mercury. The con-
centrations over the ocean usually measure
less than 1 ng/m3.  Land sources of airborne
mercury apparently are subject to meteoro-
logical controls, i.e., mercury released into
the air as a function of barometric pressure,
time of day, and season. Rain serves to wash
the mercury  from  the atmosphere. Immedi-
ately after a rainfall, mercury concentration
in the air are negligible even near ore depos-
its (Wallace,  et al.,  1971). The  same author
lists  the air  concentrations of  mercury at
various  mineralized and  nonmineralized
areas  of the United States in Table 1. Air
over urban industrial areas contains mercury
levels higher  than background,  and several
measurements have indicated average val-
ues of 0.01 (Chicago, 111.), 0.10 (Cincinnati,
Ohio), and 0.17 (Charleston, W. Va.) Mg/
m3. Concentrations of 1  to 14  ,ug/m3  have
been cited for New York City. Air  concen-
                                                                                  47

-------
                      Table 1. Maximum mercury concentration in air measured at scattered
                                  mineralized and nonmineralized areas
                                     of the western United States*
                 Sample location
      Maximum Hg concentration Gug/m3)1
    Ground surface   400 feet above ground2
            Ord mine, Mazatzal Mtns., Ariz.
            Silver Cloud Mine, Battle Mtn., Nev.
            Dome Rock Mtns., Ariz.
Mercury mines
     20.000 (50)
      2.000 (50)
      0.128(6)
                                    Base and precious metal mines
            Cerro Colorado Mtns., Ariz.
            Cortez gold mine, Crescent Valley, Nev.
            Coeur d'Alene mining district, Wallace, Idaho
            San Xavier, Ariz.
      1.500 (5)
      0.180 (60)
      0.068 (40)
                                       Porphyry copper mines
             Number of measurements shown in parentheses.
            2 Samples taken from single-engine aircraft.
            * From Wallace, etal., 1971.
0.108(4)
0.024 (8)
0.057 (20)
0.024 (2)
0.055 (4)

0.025 (3)
Silver Bell mine, Ariz.
Esperanza mine, Ariz.
Vekol Mtns., Ariz.
Ajo mine, Ariz.
Mission mine, Ariz.
Twin Buttes mine, Ariz. 0.020
Pima mine, Ariz.
Safford, Ariz.
Unmineralized areas
Blythe, Calif.
Gila Bend, Calif.
Salton Sea, Calif.
Arivaca, Ariz.
0.053 (3)
0.032.(3)
0.032 (4)
0.030 (3)
0.024 (3)
0.022 (3)
0.013(3)
0.007 (2)

0.009 (20)
0.004 (2)
0.004 (2)
0.003 (2)
trations of 100 Mg/m3 or larger  have been
reported  within  industrial buildings (Wal-
lace, etal., 1971).

III.C. Water — Contact of water with  soil
and rock  during storm  runoff,  percolation
into  the  ground, and  movements under-
ground where different geochemical stresses
prevail, results in a natural distribution of
mercury in  water.  Surface waters, except
where they are influenced by special geolog-
ic conditions, or more recently by man-made
pollution, generally contain less than 0.1  ppb
mercury.  This  reflects  the relatively   low
concentration of  mercury in rain water  and
the relatively tight binding of mercury in
  organic and inorganic materials over which
  the  water  passes in its  travel  through  the
  environment. A recent  reconnaissance  of
  river waters in 31 states showed that 65% of
  the samples tested were below 0.1 ppb, 15%
  exceeded 1.0 ppb, and only 3% were more
  than 5.0 ppb - the maximum considered safe
  for drinking water (Fleischer, era/., 1970).

  Because of  mercury's  tendency  to sorb
  readily on a variety of earth materials, parti-
  culate  matter suspended  in water and bot-
  tom sediments of streams are more likely to
  contain high concentrations of mercury than
  the  water  itself. The best  estimate  is that
  suspended matter may contain from 5 to 25
48

-------
times as much mercury as the water around
it in areas of industrial pollution (Fleischer,
efa/., 1970).

Sea  water  contains  from 0.03 to 2.0 ppb
mercury, depending on area, depth, and ana-
lytical procedures. Mercury concentrations
increase from surface values of 0.10 ppb to
0.15 - 0.27 ppb at greater depths. The deple-
tion of mercury in surface waters is attribut-
ed to its uptake by plankton arid subsequent
conveyance to depths by the biological  ac-
tivities of the marine food web (Wallace, et
a/., 1971).

In  the United States, the range of mercury
levels in rivers is from less than 0.1 ppb to
6.0 ppb. Wallace, et a/., 1971 give a table of
mercury  content of  selected rivers  in  the
United States in 1970. In  Minamata Bay,
Japan, the values of  mercury in water aver-
aged from 1.6 to 3.6 ppb. Oceanic mercury is
generally  present  as an anionic  complex
(HgCl42\ which does not have a pronounced
tendency to bind to particulate  substances
and subsequently settle out as  do mercury
compounds  in freshwater  situations  (Wal-
lace, et a/., 1971).


III.D.  Plants —  Terrestrial  plants,  like
aquatic organisms, absorb  minor elements,
including mercury, from  the soils in  which
they grow at rates depending on the quality
of the environment and the genetic charac-
teristics of the plants. Unlike aquatic organ-
isms, there  seems to be  little tendency for
terrestrial plants to  concentrate mercury
above environmental levels. Typical soils
contain from 30 to  500  ppb mercury,  and
most of the plants which grow in them are
likely to contain less than 500  ppb.  When
soil concentrations of mercury are extreme-
ly high (40,000 ppb) in the vicinity of cinna-
bar deposits, plants growing in them actually
are likely to have mercury contents far be-
low*  the level of their environment, for ex-
ample, 1000 to  3000 ppb. Even in these in-
stances, it is primarily the  plants which are
rooted through the surface soil into the mer-
cury ore which have high mercury contents
(Fleischer, et a/., 1970).

Smart (1968) reported results of studies car-
ried  out  by various  workers in  the field
which indicated translocation of mercury to
fruit, tuber or seed following the foliar appli-
cation of mercury fungicides. For example,
tomatoes from untreated plants contain 0.01
ppm mercury, while tomatoes from plants
which have been treated with mercurial fun-
gicides contain 0.10 ppm.

Lindberg  (1961) has  also reported on  the
translocation of mercury from the  leaves to
the grain  in plants  which  have had foliar
treatment with phenylmercuric acetate. The
translocation of mercury from treated seed
to harvested grain is  small. Westermark et
a/., (1966), found 0.01 ppb mercury in grain
grown from treated  wheat seed containing
15 ppm mercury. Lagerwerff of the United
States Department of Agriculture, in coop-
eration with Emry of the Oak Ridge Nation-
al Laboratory  and with analytical  chemists
of the National Bureau of Standards, dem-
onstrated  that leaves of corn  plants grown
from seed treated with ethylmercury-o-sul-
fonanilide, contained  0.14 ppm  mercury
(Mercurial Pesticide Review Panel Report).

It is known that plants take up and concen-
trate mercury from the soil or water to a var-
iable  extent. Marine algae,  for  example,
have  been found to contain from  0.023 to
0.037 ppm mercury. This is several hundred
times the accepted concentration of mercury
in sea water. Trees and shrubs growing near
known cinnabar veins contain up to 3.5 ppm
mercury.  Rice  from  paddies  treated with
mercurial  pesticides have  higher  mercury
content, e.g., Japanese rice versus rice from
other countries. However, Yamada (1970)
treated rice  with  203Hg-treated phenylmer-
curic acetate and failed to grow rice with  a
higher mercury content than  the "normal"
background. Again, on the other side of the
                                                                                   49

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coin. Wallace, et a/., report on the work of
Furutani and Osajima  which gave positive
results.  They  demonstrated  that a well-
drained  soil  containing  0.3  ppm  mercury
grew rice containing0.3 ppm, while a poorly
drained soil containing 1.4 ppm yielded rice
containing 0.8 ppm mercury.

Evidence is in favor of the translocation of
mercury from soil  to  plants,  including the
edible portions. In addition, evidence is also
in favor  of  the  conclusion  that mercury-
treated plants will  bear fruit with a higher
mercury  content  than the  normal  back-
ground.

I1I.E. Animals  — "Background" levels  of
mercury for animals are difficult to assess,
since the agricultural use of mercury prodr
nets is so widespread, and  completely un-
contaminated food  sources  are rare. Wal-
lace, ef a/., (1971), give the normal value for
eggs and the flesh  of birds  and animals  as
generally less than 0.02 ppm.  Marine fish
have mercury concentrations usually below
0.10 ppm and nearly always below 0.15 ppm,
whereas  the mercury levels  of 0.20 ppm  or
less  are assumed to be  normal for fresh wa-
ter fish. The higher background levels found
for fish when compared to other animals  or
fruits and vegetables is due to the marked
ability of fish to accumulate mercury.
III.F. Fossil Fuels — From the beginning of
time, the products and residues of geochem-
ical processes and the life cycles of terrestri-
al and  aquatic organisms have combined to
yield very appreciable mercury contents and
distinct regional patterns  in fossil fuel de-
posits. Joensuu (1971) analyzed 36 American
coals and found an average mercury content
of 3.3 ppm.
Applying a conservative estimate of 1  ppm
mercury in coal to the yearly world produc-
tion of coal of 3 x 109 tons per year. Joensuu
concluded  that 3000  tons of mercury per
year are released into the environment. He
compares  this to  the calculated  upper  limit
of natural  release of mercury due to chemi-
cal weathering of 230 tons per year.
III.G. Other  Sources — Other sources  of
mercury  in the environment have included
mine tailings, discharges  from chlor-alkali
plants, and dissipative uses such  as paints,
agricultural pesticides, pulp and paper, and
Pharmaceuticals.  Of  the  dissipative  uses,
paint and agricultural pesticides are the larg-
est. Mercury  losses from chlor-alkali plants
have been greatly reduced  in the  past year,
and the pulp and paper uses have been cur-
tailed.
50

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                                    CHAPTER4
                         PHARMACOLOGY OFMERCURY
The basic pharmacological  activity of mer-
cury is centered about the strong attraction
of this metal for certain  sensitive ligands of
proteins  located  in  enzymes, cell  mem-
branes, and  cell stroma. The total body re-
sponse to this binding is dependent upon the
cells, tissues, and enzyme systems affected
and the concentration of mercury present in
these sites. Therefore, the degree of absorp-
tion and excretion and the tissue distribution
play a major role in the final effect of mercu-
ry on the  organism.  The different forms of
mercury  vary  in their absorption,  distribu-
tion,  and  excretion characteristics   and,
therefore, vary in their effects upon man or
animal.

IV.A. Absorption

The  absorption of  mercury and its  com-
pounds varies  considerably with the chemi-
cal form of the metal and with the route of
exposure.

IV. A. 1.  Oral Absorption — It is generally
considered that elemental  mercury  is not
absorbed from  the intestinal tract. The mild
catharsis, diuresis, or intoxication  resulting
from  the ingestion of mercury results from
small particles of oxides or sulfides found
on the surface  of mercury. These oxides and
sulfides are the result of atmospheric expo-
sure and oxidation.  In water, especially in
the presence of the  chloride ion,  mercury
can be slowly  oxidized to the mercuric ion.
So long as the state of subdivision  of the
mercury is quite coarse, the rate of solution
in body fluids  is too  slow to give rise to cu-
mulative  effects  (Goodman and  Oilman,
1965).

Soluble inorganic mercurials,  such as  mer-
curic chloride, are absorbed from the gas-
trointestinal tract but only to the extent of
about 2% (Clarkson,  1971). This is probably
because these compounds  show a  strong
avidity for a large number of groupings on
proteins, and after binding to SH groups, the
mercuric ion still  contains a frde valence
capable of  combining :with  some  other
properly placed group. This fixes the mer-
curic  ion  to the  protein of  the intestinal
mucosa preventing or delaying absorption,
and  producing  local  irritation  (Hughes,
1957).

Swensson, Lundgfen and Lindstrom  (1959)
studied the absorption of mercuric chloride
and mercuric  nitrate from  subacute  oral
administration in rats.  The animals were
administered the compounds  in  water, fed
ad libitum, at a concentration of 2 mg Hg/li-
ter of  water. The animals were sacrificed at
1, 2, and 3 weeks. Absorption of both mer-
curial  salts occurred as indicated  by very
low levels of mercury in the blood,  brain,
and liver as compared to organic mercurials.

Fitzhugh,  Nelson, Laug, and Kunze  (1950)
studied  the absorption of mercuric acetate
and phenylmercuric  acetate from chronic
oral administration in rats. The animals were
administered the compounds in their diets at
levels ranging from 0.1 to 160 ppm, ad libi-
tum, for up to 2 years. Feces and urine sam-
ples were analyzed for mercury at 6 months
and 1 year. The livers and kidneys were  ana-
lyzed  for mercury in animals sacrificed at  1
year and at termination. Diets containing the
same  quantity of mercury  but in  different
forms,  viz., phenylmercuric  acetate  and
mercuric acetate,  produced  a large  differ-
ence in tissue concentration of mercury. For
example, at a dosage level of 0.5 ppm mer-
cury,  the liver contained, on the average,  2
1/2 times and the kidneys 28 times as much
                                                                                   51

-------
mercury after administration of phenylmer-
curic acetate as after  mercuric  acetate. On
the whole, there was  a significant positive
regression for both compounds relating dos-
age level with storage. Forty-three percent
of the mercury ingested as mercuric acetate
appeared in the feces, whereas only 20 per-
cent of mercury ingested as phenylmercuric
acetate appeared in the feces. This figure  is
not in agreement with Clarkson who  found
only 2% absorption of mercuric chloride by
the oral route. One possible explanation for
the low  fecal excretion  of mercury  after
mercuric acetate ingestion is that of Hughes
cited above. The bivalency of the mercuric
ion causes it to link protein of the intestinal
mucosa, becoming fixed and thus limiting its
absorption and also excretion in the  feces.
However -no firm conclusions may be drawn
from fecal excretion, since Ulfvarson  (1962)
has shown that a  significant proportion of
absorbed mercury  is excreted  by the  fecal
route.

In the  study of Swensson, Lundgren, and
Lindstrom,  cited  above,  phenylmercuric
acetate,  an arylmercury  compound, was
absorbed to a much greater extent than ei-
ther mercuric chloride or mercuric nitrate as
indicated by blood  levels of mercury. Much
higher levels were also reached in the brain,
kidney, and  liver. These  findings are  in
agreement with Fitzhugh, etal. (1950). Ulfv-
arson (1962) also found much higher levels
of mercury in blood plasma, brain, liver, and
kidneys in rats dosed with phenylmercuric
acetate than those dosed with mercuric ni-
trate.

The absorption  after oral  administration
appears to be much greater for the alkylmer-
cury compounds  than for  either inorganic
mercury   or   arylmercury   compounds.
Swensson, ef al. (1959) found much higher
levels of mercury  in the  tissues of animals
fed methylmercuric   hydroxide or  cyano
(methylmercuric) guanidine than in the tis-
sues of animals fed mercuric chloride.  Ulfv-
arson  (1962)  found  that  methylmercuric
cyanide,  methylmercuric  hydroxide,  and
methylmercuric propandiolmercaptide were
absorbed to about the same extent via the
oral route. In reviewing the available data on
both man and  the rat, Berglund and Berlin
(1969) concluded that the intestinal absorp-
tion of methylmercury is more than 90%.

Clarkson (1971) studied the rate of absorp-
tion  of  inorganic  and methylmercury com-
pounds,  labelled  with 203  Hg  in  food by
whole-body counting techniques. The exper-
imental results indicated that when  mercuric
chloride was  added  to food,  absorption
across  the  gastrointestinal tract was small,
averaging less  than  2% of the daily intake.
When the total body burden of mercury was
plotted against the time on diet, in days, the
curve showed  a sharp rise within the first
day  of  administration of radioactive food
and a sharp fall after the animals  were re-
turned  to normal  food.  The sharp rise and
fall  were equal  in  magnitude and  corre-
sponded to approximately 25% of the daily
intake. Such curves are typical of isotopes
that are poorly absorbed  by the gastrointes-
tinal tract. The rapid rise and fall correspond
to the effect on whole-body count of the iso-
tope's entry into and removal from the gas-
trointestinal tract, respectively. The curve
also exhibits a slowly rising phase during the
remainder of the times the animals are fed
radioactive food. The slope of the curve cor-
responds to the daily net absorption of the
isotope  into the blood stream and body tis-
sues.  When  radioactive  methylmercury
chloride was fed in  the diets of  the animals,
the curve describing the whole-body counts
was entirely different from those above. The
whole-body  count   rose    continuously
throughout the period  of  exposure.  The
curves suggest that  the absorption  of meth-
ylmercury  from food is practically  com-
plete.

Clarkson's data are difficult to reconcile with
the data of Fitzhugh, et al. and with the high
52

-------
acute oral toxicity of the inorganic mercuri-
als as compared with the organic mercurials.

IV.A.2. Absorption through the Lungs —
Metallic mercury and all of its compounds
are absorbed in the lungs.  The organomer-
     curials vary in their volatility and, therefore,
     differ in their hazards  via  the  inhalation
     route. The following table of the saturated
     vapor concentrations of organic mercurial
     compounds and of metallic mercury comes
     from Swensson and Ulfvarson (1963).
                            Saturated Vapor Concentration of Some Mercurial
                                      Fungicides at 20° C
Organomercury
Cation
methylmercury
»t






ethyl mercury
i»
»»
»>
"
methoxyethylmeicury
»»
Anion
chloride
bromide
iodide
acetate
hydroxide
toluenesulfonate
benzoate
dicyandiamide
chloride
bromide
iodide
dicyandiamide
monohydrophosphate
chloride
acetate
Saturated^
Vapor Cone.
Mg/M3
94,000
94,000
90,000
75,000
10,000
15,000
2,000
300
8,000
7,000
9,000
400
50
2,600
2
               phenylmercury
               metallic mercury
atietate
chloride
nitrate
methanedinaphthyldisulfonate
   17
    5
    1
    2

14,000
In a study in which mice were exposed to a
vapor stream  of  air containing various or-
ganomercurials, Swensson (1952) found the
chlorides  were more toxic than the dicy-
anamides of alkylmercury compounds. This
is  in agreement with the lower vapor pres-
sure of the latter. Gage  (1961) has shown in
his experiments in which rats were exposed
to an atmosphere  containing 1 mg of mercu-
ry per cubic meter of air for varying periods,
that absorption is rapid and complete and
the turnover in all tissues, except the brain,
is  rapid; most of the mercury is removed
within a week after exposure has ceased.
     In a study designed to measure the absorp-
     tion, distribution, and excretion of inhaled
     mercury vapor, female rats were exposed 24
     hours per day for 28 days to a concentration
     of 1 mg Hg/M3 of air.  The rats survived but
     lost weight,  became lethargic, and showed
     slight tremors, especially  when  lifted by
     their tails.

     A second series of rats were given repeated
     continuous exposures to the  same concen-
     tration  of mercury vapor for 100 hours from
     Monday through Friday in each week for six
     weeks. As a  result, growth was retarded, the
                                                                                    53

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rats appeared lethargic and  squeaked when
touched, and after 5 weeks these rats also
showed fine tremors when lifted by their
tails.

In a third series  of  experiments, rats were
exposed to the same mercury vapor concen-
tration for 7 hours per day for 5 days  per
week for 18 successive weeks. The resulting
symptoms were similar to those in the first
and second experiments but appeared more
slowly, the only  difference being that  the
rats showed a  slight increase in weight dur-
ing the experiment.

The author calculates that if the results ob-
tained in rats in these experiments with mer-
cury vapor at 1 mg Hg/M3 can be applied to
a man  breathing 10  M3/day  for 5 days with
the maximum allowable concentration  of
mercury vapor of 0.1 mg/m3, then the daily
absorption might be expected  to be about
500 fjL g, with a total excretion over 7 days of
approximately 2.5 mg. If the total exposure
were short, the bulk of the mercury would
be eliminated in a few days, but if the expo-
sure continued for several weeks, the result-
ing accumulation of mercury would be ex-
creted  for a considerable  time  and could
amount to several hundred  micrograms per
day (Gage, 1961).

Kosmider (1965) studied the pathogenetic
mechanisms of poisoning in  rabbits resulting
from the  inhalation of mercury vapors. In
these experiments, rabbits were exposed to
mercury vapor concentrations of 10.6 mg/m3
for 1 to 5 hours daily for 30 days. This expo-
sure resulted in the alteration of function of
a number of enzymes and damage to  several
organs.

IV.A.3.  Absorption through the Skin — All
forms of mercury may be absorbed through
the intact skin. Laug, et al. (1947 a,b,c) stud-
ied the dermal absorption in rats and rabbits
of several of the  official  mercurial oint-
ments. The preparations studied were Mild
Mercurous Chloride Ointment,  NF (Calomel
Ointment)  which  contains  30%  HgCl;
Strong Mercurial Ointment, NF (Mercurial
Ointment) which  contains  50%  Hg;  Mild
Mercurial Ointment, NF (Blue  Ointment)
which contains 10%  Hg; and Ointment of
Oleated Mercury, USP which contains 23%
Hg.  Both Strong  Mercurial  Ointment, NF
and Mild  Mercurial Ointment, NF contain
finely divided metallic Hg. A small amount
(5%) of mercuric oleate is added to the mer-
cury in  the preparation of the ointment to
form a film over the globules of mercury to
facilitate the dispersion in the ointment.

It was determined that dermal absorption of
mercury was proportional to (1) the duration
of contact, and (2) the area of skin exposed.
The mercury content of the kidneys of rats
after 24 hours continuous skin contact to 8%
of the body surface with 0.4 g of Mild Mer-
curous Chloride Ointment, NF was about
90-fold that found  in the controls (27.2 M g
Hg versus 0.3^8 Hg/g wet kidney) and about
130-fold after 48 hours contact. In this exper-
iment, mercury levels in rat liver  increased
by 10- to 20-fold (0.8 /u. g at 48 hours versus
0.06 \JL gig wet liver of controls). The great-
est  absorption occurred with Ointment of
Oleated Mercury, which gave 30.1  ft gig wet
tissue.

The vehicle in which mercury is suspended
and the particle size of mercury have an in-
fluence on the  dermal absorption. However,
the concentration of mercury in the test oint-
ments appeared to have little influence on
total mercury absorbed. The kidney concen-
trations of mercury after application of Mild
Mercurial Ointment  and Strong  Mercurial
Ointment were almost identical.

Recent studies in humans conducted by the
Food and Drug Administration with  a 1%
ammoniated mercury bleach cream to which
3% 203Hg had been added, showed that an
average of 2.4 JJL g/cm2 mercury  penetrated
intact skin in a 24-hour period (unpublished
data). The author extrapolates these results
54

-------
to application of this type of product to a 10-
by 15-cm area on each hand or arm (300 cm2
total skin area) from which a theoretical 720
V  g mercury could penetrate skin in a  24-
hour day. According to  these studies,  the
urinary excretion rate may be as little as  4%
in 5 days, indicating a possible problem of
heavy metal poisoning from skin absorption.
Cases  of  nephrotic syndrome in humans
from topical use of ammoniated  mercury
have been reported (Becker,  1962;  Silver-
bert,efa/., 1967).

Mercury is absorbed slowly through intact
skin and much more rapidly through broken
skin. The  mucosa  offers  little resistance to
penetration of mercury. Instillation of 0.1 ml
of a 0.05% solution of phenylmercuric ace-
tate into the vaginal tracts of rats (9 M g/kg)
resulted in about 28% residue of mercury in
the kidney and  liver combined immediately
following a 24-hour exposure.

IV.B. Distribution

The distribution of mercury  in the organs
and tissues of animals after absorption var-
ies with the form  in which the mercury is
administered and  with the species of the
animal studied. Mercury derived from inor-
ganic and  aryl compounds appears to accu-
mulate in the liver and  kidneys,  whereas
mercury derived from alkyl compounds is
more   evenly  distributed  throughout  the
body. There are  considerable species differ-
ences in the distribution patterns of mercury
among different  mammalian species — most
pronounced  is the low brain content of mer-
cury in the  rat as compared  with other
species after the administration of alkylmer-
cury compounds.

IV.B.I. Bloo<}— The distribution of mercu-
ry in the blood  between the red blood cells
and the plasma is dependent upon the type
of mercury administered. There appear to be
significant differences between the red blood
cell/plasma  distribution  characteristics  of
metallic mercury,  inorganic mercury, aryl-
mercury,  and alkylmercury.  Some  species
variations have been,noted.

Metallic mercury, inhaled as mercury vapor,
results in a higher concentration of mercury
in the red blood cells than in the plasma.
After inhalation  of mercury vapors, 67% of
the mercury in monkeys' blood and 84% of
the mercury in rabbits' blood was bound to
the red blood cells (Berlin, 1969).

Inorganic  mercury accumulates in the plas-
ma of the  blood. This has been demonstrat-
ed after oral administration to rats and intra-
venous administration to rats, rabbits, and
dogs by Swensson, et al. (1959a; 1959b). In
rabbits and monkeys injected with inorganic
mercury,  the red blood cell  level  was ap-
proximately 25% of the blood mercury level
(Berlin, 1969). Inorganic mercury  reacting
with the red blood cells binds to hemoglobin,
not only with the sulfhydryl groups but also
with the imidazole residues (Resnik, 1964).

Mercury  derived from  arylmercury  com-
pounds is  bound to the red blood cells to a
greater extent than is mercury derived from
inorganic compounds. Berlin (1969) states it
is evenly distributed between the plasma and
the red cells, while Swensson (1959a, 1959b)
states that phenylmercury  compounds are
bound mainly to the red blood cells. In either
case,  it appears to be intermediate  between
inorganic mercury and alkylmercury.

Mercury derived  from alkylmercury  com-
pounds is  bound mainly to the  red  blood
cells (Swensson,  era/., 1959a, 1959b). Burg-
land and Berlin (1969) reported that, in all
species studied, 90% of the methyl mercury
in the blood is bound to the red blood cells.
The fraction in the plasma varies with the
species; in man 10%, in the rat 4.5%, in the
rabbit 10%, and in the squirrel monkey 9%.
Takeda (1968a) found  that,  of the alkylmer-
cury compounds studied  (methylmercuric
                                                                                   55

-------
chloride, ethylmercuric chloride, and n-bu-
tylmercuric chloride), there  was a marked
accumulation of alkylmercury in the blood,
especially in the nonstromal fractions of the
erythocytes.  Ethylmercuric  chloride  gave
lower concentrations in the blood than did n-
butylchloride.  In  a  later  study,  Takeda
(1968b)  found that  more than 97%- of the
mercury in the blood after the administra-
tion of -^ Hg-labeled ethylmercuric chloride
was in the form of ethylmercury. The ethyl-
mercury residues accumulated in the hemo-
globin,  forming a mercaptide  linkage with
SH group:, of cysteine residues in the hemo-
globin molecules.  He attributes the high,
long-lasting accumulation of aklylmercury in
the blood to the high affinity of alkylmercury
for hemoglobin.

Phenylmercuric acetate  appears to be ab-
sorbed unchanged, regardless of the route of
administration. The transportation via the
blood appears to be as phenylmercury. The
phenylmercury present in the blood after 48
hours appears to account for the total mer-
cury in the blood (Miller, et a/., 1960).

IV.B.2.  Brain —The concentrations of mer-
cury found in the brain after administration
of inorganic, aryl, and alkylmercury com-
pounds  are  lower than  the  concentrations
found in other organs and tissues. While the
blood-brain barrier is a relative hindrance to
their passage, the alkylmercury compounds
reach a higher concentration  in the brain
than do the arylmercury compounds. How-
ever, there is some disagreement in the liter-
ature  as to these differences, especially in
the rat.  In addition, there are  considerable
species  differences in  mercury levels  in the
brain. In the rat, short-chain alkylmercury
compounds reach a higher level in the brain
than do  the longer chain compounds.

Swensson, ef a/., (1959a) administered 203
Hg-iabeled mercuric chloride, mercuric  ni-
trate, phenylmercuric acetate, cyano (meth-
ylmercuri) guanidine, and methylmercuric
hydroxide to rats in their drinking water at 2
mg Hg per liter for 3 weeks and determined
the distribution of mercury in  the  various
organs. He found  that the inorganic com-
pounds gave a very low mercury content in
the brain:  In fact, no  mercury could be dem-
onstrated after 1 week exposure  and very lit-
tle after 2 or 3 weeks. The animals which
received phenylmercuric  acetate had some-
what higher mercury contents in the brain,
and the animals exposed to cyano (methyl-
mercuri) guanidine had much higher levels.
The ratio between  blood and  brain mercury
contents  seemed  to  be constant for each
substance and indicated a distribution equi-
librium.  However,  in   an   earlier  study
(1959b) Swensson  failed to demonstrate
these differences after a  single  intravenous
administration of 100 /u. g 203Hg as mercuric
nitrates, phenylmercuric acetate, or  methyl-
mercuric hydroxide.

Friberg (1957) compared the tissue distribu-
tion of mercury in rabbits after the single
                                   om
subcutaneous administration  of 2 mg 2U-Hg
per kg. of body weight as  mercuric chloride
or phenylmercuric acetate.  Readings were
made after 1, 6, and 40 days. The readings in
the cerebrum,  cerebellum and brain stem
were less than 1% of the corresponding renal
levels.  He found no significant difference in
the mercury  concentration in the brain re-
sulting from the administration  of mercuric
chloride or phenylmercuric acetate.

Gage (1964) studied the distribution, metab-
olism and excretion of phenylmercuric ace-
tate and  methylmercuric dicyandiamide af-
ter repeated subcutaneous administration of
0.15 mg Hg per rat and after a single 0.5 mg
dose.

More mercury accumulated in the brain with
methylmercuric dicyandiamide  than  with
phenylmercuric acetate.  Gage  postulated
that the higher  concentration of methylmer-
cury in the brain was due to the sustained
higher  concentration in the plasma  and not

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that methylmercury  had a greater ease of
penetration into the central nervous system.

Ulfvarson (1962) administered 203Hg-labe!ed
mercuric  nitrate,  methylmercuric hydrox-
ide, methylmercuric dicyandiamide, phenyl-
mercuric  hydroxide,  and  methoxyethyl-
mercuric hydroxide subcutaneously to rats
at a dosage level of 0.1 /* gm Hg per gram of
body  weight every other day. He analyzed
the radioactivity in the tissues at 6, 16, and
18  days.  He  concluded that  radioactivity
found in the brain  could be attributed to the
blood content  of this organ and that there is
no  reason to believe that  alkyl compounds
have a greater  affinity for the brain.

In a series of  experiments  on the rabbit by
Swensson et al. (1959b), intravenous injec-
tions  of  methylmercuric   hydroxide  were
given at approximately  10  mg mercury  per
kilogram of body  weight,  corresponding to
approximately the LD5Q. He compared  the
brain  concentrations of mercury  resulting
from this dose to the concentration in an ear-
lier study in which only 1  mg mercury  per
kilogram of body weight was administered.
The mercury  contents  of  the  organs agree
closely with the amount injected, except the
brain  where the increase in the mercury con-
tent was much less than would be expected
from the increase in dose.

Berlin,  et al.  (1965)  demonstrated that, al-
though the blood-brain barrier is  a relative
hindrance  to  methylmercury  penetration,
the diffusion of mercury into the  brain can
be accelerated by the simultaneous adminis-
tration of dimercaprol (BAL).

Short-chain alkylmercury  compounds may
accumulate more in  the brain than do  the
long-chain compounds.  Takeda, et al. (1968)
found that the brain/blood  ratios for ethyl-
mercury were  higher  than those for n-butyl-
mercury. When ethylmercuric chloride was
administered,  the concentration of mercury
in the brain was 2  to 3  times higher than in
plasma, while the concentration in the brain
was approximately equal to that in plasma
when n-butylmercuric chloride was adminis-
tered. Sebe, et al. (1962) studied the toxicity
of a number of alkylmercury compounds.
The alkyl compounds containing a R-Hg, or
R-Hg-S radical,  with a methyl,  ethyl, or n-
propyl chain administered orally to rats were
toxic  to the central nervous system and in-
duced paralysis  of the legs. Isopropylmer-
cury  compounds and other alkylmercury
compounds with 4 to 5 carbon  atoms were
shown not  to cause injuries to the nervous
system. Suzuki, et al. (1963) studied the dis-
tribution of mercury  in mice administered
methyl, ethyl, or  propylmercuric acetate.
The highest concentration of mercury in the
brain  was obtained with ethylmercuric  ace-
tate. In addition, the mercury in  the brain
resulting from  the  administration  of  the
ethylalkyl compound  was more rapidly dissi-
pated than  that from  the methyl or propyl
derivatives. In a later study, Suzuki, et al.
(1964) compared the distribution of mercury
resulting from the administration of n-butyl,
isobutyl, propyl, and amylmercuric  ace-
tates.  The  mercury   concentration in  the
brain  was  lowest for the amyl  compound.
There was  no marked difference in the up-
take of mercury  in the brain from  the other
acetates. However, when graded  doses of
the compounds were given,  there was a very
marked increase in mercury concentration in
the brain in relation  to dose for the  n-pro-
pylmercuric acetate.

In three separate studies, Berlin,  et al.
(1963a, 1963b,  1963c)  used an autoradiogra-
phic technique to differentiate the distribu-
tion of  mercuric chloride,  phenylmercuric
acetate, and methylmercuric dicyandiamide.

With mercuric chloride, Berlin,  et al. found
that the brain takes up mercury slowly and
retains it for a long time in comparison  with
other organs, but appreciable levels are ac-
cumulated  only in parts which  constitute  a
small  fraction of the total brain tissue. They
                                                                                   57

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speculate  that this  may  explain why pre-
vious investigators have been unable to find
deposits of mercury  in the brain adequate to
explain the clinical  picture; measurements
were made on the whole organ or large parts
of it and generally at  relatively short times
after  administration.  The  localization  of
mercury in tissues adjacent to the cerebro-
spinal canal causes Berlin to  suggest that
mercury reaches the brain through the cere-
brospinal fluid rather than the  blood. There
is a relatively high concentration of mercury
in the gray matter of the cerebellum, area
postrema, the  subfornical body, and the
tuber cinereu-m.

After phenylmercuric  acetate, the picture  is
quite similar to that of  mercuric chloride; the
autoradiograms  of  the brain, brain stem,
and  spinal cord in  the first 24 hours after
exposure show a uniform density which  is
slight in comparison with the other organs.
After 4 days, there is a more differential
accumulation  of mercury  which  is  even
greater at  16 days. As  with inorganic mercu-
ry, there is an accumulation in  the  dorsal
part of the brain stem, especially in the area
corresponding to the area  postrema, in areas
adjacent to the lateral ventricle, and in the
area corresponding to  the hypothalamus and
tuber cinereum. It also accumulated in the
gray substance of the cerebellum.

After an  injection  of methylmercuric di-
cyandiamide, as with inorganic mercury and
phenylmercury, very little mercury is taken
up by the central nervous system in the first
few  hours. Accumulation occurs gradually
over a period of several days and is not cor-
related with  the  level of  mercury in the
blood. The distribution in the brain is quite
different from that seen after the injection of
inorganic mercury or  phenylmercury. With
these compounds, the distribution was het-
erogeneous, but after methylmercury it  is
more uniform. Although the gray substances
takes up more mercury than the white, as  in
the case of inorganic  mercury, the regions
which show the maximum concentration of
mercury  are  not  the  same.  These are the
hippocampus and  the gray matter of the cer-
ebellum.

IV.B.3.  Liver,  Kidney, and Other Organs
and Tissues— After absorption, the aryl and
alkylmercury  compounds   accumulate at
higher concentrations in  the liver and kid-
neys than do the inorganic  compounds of
mercury. The alkylmercurys are more even-
ly distributed throughout the body than the
other two groups  of compounds. Inorganic
and phenylmercury compounds translocate
from the  liver to the kidneys with time. The
spleen and muscle concentrations of mercu-
ry are lower than those found in the liver and
kidneys.  Both aryl  and alkylmercury  com-
pounds give a high content of mercury in the
hair. With methylmercury,  the  concentra-
tion of mercury in the hair is greater than in
the other tissues.

Swensson, et a/. (1959a,  1959b) studied the
distribution of mercury in the body of rats,
rabbits, and dogs  after the administration of
inorganic,  aryl,  and  alkylmercury  com-
pounds,  both by  the oral and intravenous
routes. He found  that administration of the
organic compounds by the oral route in rats
resulted in much higher mercury  concentra-
tions in the liver and kidneys than the inor-
ganic compound.

On the other hand, after intravenous admin-
istration  to rabbits,  mercuric nitrate and
phenylmercuric   acetate  were  deposited
chiefly in the kidneys, whereas methylmer-
curic hydroxide appeared to be more uni-
formly distributed throughout the body. El-
lis,  ef a/.  (1967) studied the tissue  distribu-
tion of mercury  after single oral doses of
-°-Hg-labeled  mercuric acetate  or  phenyl-
mercuric acetate.  With both compounds, the
highest  concentrations of  mercury  were
found in the kidneys and then the liver, lung,
and heart; accumulations in  other organs
were comparatively small. In the kidney and
58

-------
 liver,  subcellular  distribution of the com-
 pounds was quite similar.  Takeda, et al.,
 (1968), administered  single  subcutaneous
 doses of inorganic mercury, phenylmercury,
 ethylmercury,  and  n-butylmercury  com-
 pounds. With the alkylmercury compounds,
 there was a gradual increase in the accumu-
 lation of mercury in the kidneys. There  was
 a difference in the distribution of ethylmercu-
 ry and h-butylmercury. With butylmercury,
 there was a larger amount of mercury in the
 blood than in the muscles. The opposite  was
 true with ethylmercury.

 Friberg, et a\. (1957) studied the distribution
 of  203Hg-labeled  mercuric  chloride   and
 phenylmercuric acetate  in  rabbits after  a
 single  subcutaneous injection.  In the  kid-
 neys, almost all of the mercury was in the
 cortex. The mercury  concentrated  in  the
 tubules and not in the glomeruli.  Bergstrand,
 et  al.   (1958),  administered  203Hg-labeled
 mercuric chloride  and phenylmercuric ace-
 tate subcutaneously to rabbits at a dose  of 2
 mg per kilogram of  body weight. The  kid-
 neys were  studied 1  and 6 days after injec-
 tion. Mercury invariably accumulated in the
 cortex and  subcortical stratum  of the  kid-
 neys. Much of  the activity in  the renal cor-
 tex was derived from the regions around the
 intralobular  vein   and  the   neighboring
 straight tubules. In the subcortical stratum,
 the activity could be traced to  the tubular
 epithelium  between the arciform veins. No
 activity was demonstrated in the glomeruli.
 In sections taken  6  days after injection of
 organic mercury, the activity in the subcorti-
 cal stratum was even higher. Whether or not
 this is specific for organic mercury could not
 be definitely decided.

 Organic mercurials reach a higher concen-
 tration in the kidneys than do  the inorganic
 mercurial   compounds  (Swensson,  et  al.,
 1959a,  1959b).  In the kidneys, almost all of
the mercury is found in the cortex. The mer-
cury is concentrated in the tubules and not in
the glomeruli (Friberg, et al., 1957;  Berg-
strand, et al., 1958). This localization of mer-
cury in  the  renal cortex  is to be expected,
since this is the basis for the pharmacologi-
cal action of the  mercurial diuretics.  Two
mechanisms may contribute.  In  the  first
place,  organic  mercurials  are weak acids
which are secreted in the proximal region of
the renal tubule. In the  second place, the
hemodynamics of the kidney  are favorable
to cortical deposition. The cortex is the first
area of  the  kidneys with which mercury in
the arterial blood will equilibrate. Moreover,
since mercury is present in the blood  as a
nonultrafilterable protein-complex, it will be
retained in the bloodstream during the glom-
erular filtration process.  Consequently, the
concentration of the mercurial in the blood-
stream just  distal to the glomerulus  will  be
increased by 20%, depending upon the  frac-
tion of plasma filtered. In addition, the dis-
tribution of blood vessels in the medulla is
such as to produce a low effective blood flow
in the region of the  loop of Henle and the
distal tubule (Passow, eta/., 1961).

With inorganic mercury  there is a marked
concentration of mercury in the liver, in the
periportal connective tissue, lymph space,
or in the bile ducts. Organic  mercury  pro-
duces a more even distribution pattern, ex-
cept for areas of slightly increased density
around  the  portal vein.  There is a higher
concentration of mercury in the red pulp of
the spleen than in the white pulp (Friberg, et
al., 1957).

The placenta apparently constitutes a barrier
to mercury after the administration of  mer-
curic chloride.  In the  24-hour autoradi-
ograms, it  appears strongly  darkened; the
visceral yolk sac epithelium  adjacent to the
fetus shows only traces of mercury. Locali-
zation apparently corresponds to that of the
maternal organs,  as  judged from  the  faint
pictures (Bolin 1963a).

The placenta affords  a barrier to mercury
after the administration of phenylmercuric
                                                                                    59

-------
acetate as it does with mercuric chloride.
While the placenta takes up a large amount
of mercury,  only traces are demonstrable in
the fetus. After 8 to 16 days, however,  the
yolk sac epithelium and the fetal membranes
show a greater amount than the placenta.

The placenta does not constitute a barrier to
mercury  after the administration of methyl-
mercuric dicyandiamide.  In the fetus,  the
concentration equals that in the mother, and
the distribution  differs  only  in  that there
appears to be more mercury in the fetal skin.

IV.C. Metabolism and Excretion

Inorganic mercury and phenylmercury com-
pounds may be  slowly  metabolized  in  the
liven and kidneys, while alkyl and alkoxy-
alkyjmercury compounds  are  relatively sta-
ble iftthe body. Ulfvarson (1962) studied  the
distribution  and excretion of mercuric  ni-
trate, phenylmercuric hydroxide, methoxy-
ethylmercuric hydroxide,  methylmercuric
hydroxide, and  methylmercuric dicyandia-
mide after subacute, subcutaneous adminis-
tration to rats. He found that a simple distri-
bution equilibrium between different organs
existed  for  the  alkyl  and  alkoxyalkyl-
mercury  compounds. This was not the case
for mercuric nitrate or phenylmercuric  hy-
droxide which were continuously translocat-
ed toward the kidneys. There is no reason to
believe such a gradual accumulation should
occur with stable substances which are able
to  pass  permeable membranes. It is very
likely  that this  translocation is connected
with a chemical change of the compounds,
which results in a gradual change of the par-
tition coefficients. The chemical reactions to
the final  product must also be rather slow,
since otherwise  the  new derivatives  would
immediately distribute  in the  final  way.
Ulfvarson  estimated the half-life  of  the
methylmercury salts as between  15 and 20
days and the methoxyethylmercury hydrox-
ide as between 4 and 10 days. Since mercu-
ric nitrate  and  phenylmercuric hydroxide
were unstable in the body, the estimation of
their half-life was more difficult. The excre-
tion data indicate  a  half-life of between 4
and 10 days in  the beginning of the experi-
ment.

Berlin  (1963) studied the renal  uptake,  ex-
cretion, and retention of mercury  in rabbits
during an infusion of phenylmercury acetate
or methylmercuric dicyandiamide. The renal
excretion did not exceed 10% of the amount
of mercury in the blood passing through the
kidneys in the case of either  compound.
There  was  no correlation  between  the
amount of mercury accumulated in the kid-
neys and the urinary excretion  of mercury,
although there was  a correlation  between the
urinary excretion of mercury and  the blood
concentration. In the case of phenylmercu-
ric acetate, a small  percentage of the infused
mercury was excreted in the  urine  while
about 30% was  accumulated in the kidneys.
After infusion with methylmercuric dicyan-
diamide, the urinary excretion  of mercury
did not exceed  a few parts per  thousand of
the infused dose and less than 10% accumu-
lated in the kidneys.

Miller, era/. (1960, 1961) administered phen-
ylmercuric  acetate  and  ethylmercuric  chlo-
ride intravenously, intramuscularly, and oral-
ly to chicks, rats, and dogs. Phenylmercuric
acetate appeared to be absorbed unchanged,
regardless of the route of administration. In
rats, slightly over half of the urinary mercu-
ry was in a form other than phenylmercuric
acetate. Metabolism was  fairly  rapid  and
occurred mainly in the liver and  kidney, with
accumulation of mercury  in these organs.
With dogs, a greater proportion of the  uri-
nary mercury was not present as phenylmer-
cury. Phenylmercuric acetate was detecta-
ble only for 96  hours. Less than 10% of the
initial dose was excreted unchanged in the
urine.   In  contrast,  when  ethylmercuric
chloride was given to chicks and rats orally,
the intact ethylmercury was detectable in
the liver and kidneys for 21 days. The excre-
,60

-------
tion of mercury in the urine of rats was not
as rapid as that observed with phenylmercu-
ry, nor was there any appreciable excretion
of the unchanged compound. However,  to-
tal mercury levels in the  kidneys showed a
marked  increase. In  addition, the fecal ex-
cretion of mercury over a 7-day period fol-
lowing administration of  ethylmercury was
only one-twentieth of that observed in the
phenylmercury study,  suggesting the liver
was not involved  in the metabolism  and ex-
cretion  of  ethylmercury. Chicks did not
show  accumulation of  mercury  in the kid-
neys following the administration of ethyl-
mercury, and it appeared  the liver was the
major organ  involved  in detoxication.  A
comparison of the excretion of mercury  in
rats fed 203Hg-labeled phenylmercuric ace-
tate or mercuric acetate showed that 68% of
the activity from a single dose of phenylmer-
curic acetate accumulated in the feces, and
12.6% of the inorganic  mercury was excret-
ed in the feces and only 1 to 4% in the urine
(Ellis and Fang, 1967).

Swensson, et al. (1959) studied the distribu-
tion and excretion of 203Hg-labeled mercuric
nitrate, phenylmercuric acetate and  methyl-
mercuric hydroxide in rats and dogs. There
was a continuous outflow of mercury from
the various organs until 32 to 64 days after
the initial injection when the  organs were
practically free from mercury.  The kidney
level of mercury fell very slowly after meth-
ylmercury. This was probably due to a con-
tinuous supply from other parts of the body
that were being depleted of mercury. There
were considerable differences  between the
rate of excretion of the  three compounds.
The mercury concentration was appreciably
lower in the case of methylmercury than af-
ter mercuric nitrate or  phenylmercury. The
total excretion within 4 hours of injection
was essentially lower for the methylmercury
compound than for the other two. The meth-
yl and phenyl compounds  were excreted
most rapidly at the beginning of the experi-
ment when the concentration of  mercury in
the blood was highest, the rate decreasing
with the fall in concentration  of mercury in
the blood was highest, the rate decreasing
with the fall in concentration in the blood.
After the injection of inorganic mercury, a
high initial excretion was followed  by a peri-
od of anuria, after which only traces of urine
with a very high mercury  content were ex-
creted. The rate  of  urinary excretion  was
greater after phenylmercury than with meth-
ylmercury. Although, in both cases, there
was  a steady excretion of mercury which
was  related to  the  concentration  in  the
blood. The anuria following mercuric nitrate
administration  suggests that this compound
is more toxic to the kidneys than the organic
compounds.

Gage (1964) studied the distribution and ex-
cretion of mercury after the  subcutaneous
injection  of phenylmercuric acetate and of
methylmercuric dicyanidamide  in the  rat.
He found that  phenylmercury is readily ab-
sorbed from the injection site  and  is rapidly
removed  from  the blood   by the tissues.
Some concentration  and   probably  some
metabolism of  phenylmercury occurs in the
skeletal  muscles,  but the  bulk is  removed
from  plasma by the  liver  and the kidneys
where it is rapidly metabolized and excreted
with only a small proportion  appearing un-
changed in the feces  and urine. Absorption
of methylmercury was rapid from  the injec-
tion  site  and was  taken up by all tissues,
especially in the skeletal muscle and intes-
tine. The major route of excretion is through
the gut, but the ratio of organic mercury in
the liver and feces indicates methylmercury
is  also excreted by this route more slowly
than  phenylmercury  acetate.  With  both
methylmercury and phenylmercury, there is
a high content of mercury in  the hair; with
methylmercury the concentration  is greater
than in any other tissue, and there may be an
appreciable excretion of  mercury by  this
route. There  is  no  evidence  whether the
mercury is excreted in sebum  or incorporat-
ed into the hair proteins.
                                                                                   61

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The  mouse excretes methylmercury  in the
bile and also via the intestinal mucosa  (Berg-
lund and  Berlin,  1969).  Clarkson  (1970)
demonstrated that the rat excretes methyl-
mercury in the form of methylmercury cys-
teine  in  the  bile.  This  is completely  re-
sorbed in the upper gastrointestinal tract,
since none is detectable  in the large intes-
tine. The rate of turnover of epithelial cells
may be a determining factor  in the rate of
excretion  of  methylmercury, since studies
have shown some accumulation of mercury
in the mucosal  epithelium. The turnover of
epithelial cells in rats is five times faster than
the turnover in man. This correlates with the
difference observed in rate of elimination of
methylmercury in the two species (Berglund
and Berlin, 1969).

Biotransformation of  methylmercury to in-
organic mercury occurs  before excretion.
About 40% of  the total  mercury  excretion
was found to be inorganic mercury.  About
50% of the fecal excretion and from 5 to 20%
of the urinary excretion is inorganic mercu-
ry. Enterohepatic circulation of  mercury
from  methylmercuric chloride is important
in the distribution and excretion of mercury.
About 10% of  an administered dose is ex-
creted in the first day. This falls to about 3%
by the  10th day. During this period only
about 3% is excreted in the feces. Almost all
of the mercury  present in the bile was in the
form  of  methylmercury  cysteine  and inor-
ganic mercury  bound to protein. The  cys-
teine complex  is  rapidly and completely
reabsorbed in contrast to the inorganic mer-
cury. Other sources of mercury in the feces
are the sheddings of intestinal epithelium,
pancreatic secretion, and some  secretion
from the pylorous. Biotransformation within
the intestinal lumen in the cecum is the ma-
jor source of inorganic mercury in the feces.

Enzyme systems may participate in the me-
tabolism of organomercurials. Studies by
Clarkson (1969) indicate that different com-
pounds release  inorganic mercury at  differ-
ent rates. Paramercurbenzoate was metabol-
ized  the  fastest  and  methylmercury the
slowest of seven compounds studied. These
studies  indicate the  nephrotoxic action of
mercurials may be related to the rate of their
biotransformation.

The metabolism of methylmercury has been
studied in man by Aberg, et al. (1969). After
the oral  administration of  203Hg-labeled
methylmercury, 203Hg was detected in the
whole blood within 15 minutes and reached a
maximum  blood   concentration  within  6
hours. The blood/plasma quotient remained
constant for 24 days.  The orally adminis-
tered methylmercury was almost completely
absorbed. The principal route of excretion
was by the  feces with  13 to 14.2% of the
dose excreted during the first 10 days and
33.4  to  34.7% of the dose excreted  in 49
days.  The  urinary excretion  was low and
accounted for only 0.18  to 0.27% in  10 days
and 3.29 to 3.33% in 49 days. Urinary excre-
tion was still taking place at 71 days. The
biological half-life of methylmercury in man
was estimated at 70.4 to 74.2 days. During
the 240-day test period, there was never any
measurable  amount  of  mercury  in the
sperm. Only traces  of mercury were found
in the hair. Step scanning revealed the main
uptake of 203Hg was in the abdominal cavity
with possible localization in the cerebellum.
Whole-body measurements over a  240-day
period did not reveal any marked difference
in the biological half-life in any region. Miet-
tinen,  et  al. (1969)  fed burbot containing
bound 203Hg methylmercury to humans. His
results  were similar to those reported by
Aberg.

Mercury may be  excreted by rats  through
volatilization. In an experiment designed to
determine if mercury is lost from  animals
through  volatilization,  Clarkson (1965) in-
jected  203Hg  complexed  with glutathione
into  the hearts of rats. The animals were
placed  in a chamber  so constructed that
urine, feces, and  air circulating through the
62

-------
cage could be  collected and analyzed  for
203Hg content. As soon as the animals were
placed in the  chamber,  volatile  mercury
began to build up in the air sampler. It was
determined that  the radioactivity in the air
sampler was not  due to volatile release from
the urine and feces. In a series of experi-
ments in which animals were given varying
amounts of -03Hg, volatile excretion varied
from 0 to 7% of the administered dose and
averaged approximately 4%.

There seems to  be a  steady state between
intake, distribution and excretion of mercu-
ry. Gage (1964)  demonstrated that rats re-
ceiving  repeated  subcutaneous  doses  of
phenylmercuric  acetate  reached a  steady
state by the end of the second week when
excretion balanced intake.  No significant
amount of mercury was found in the brain.
In contrast, rats receiving similar doses of
methylmercury dicyanidiamide showed no
indication of reaching a steady  state after 6
weeks. Further,  there was an accumulation
of organic mercury in all tissues, particularly
in the erythrocytes  and  the brain. Although
these short-term studies with methylmercu-
ry failed to demonstrate a steady state, Ber-
glund and  Berlin (1969b) showed that the
continuous administration of dietary methyl-
mercury (1-5 ppm) to  rats  resulted  in a
steady state between  body burden and ex-
cretion in about 6 months. At  equilibrium,
the daily excretion corresponded  to  about
1% of the body  burden. There was a linear
correlation between dose and body burden.

The highest concentration of methylmercury
in the brain  was  8 /u, g/g of  brain  tissue.
There were no  effects  on body  weight or
conditioned  behavior  and no pathologic or
anatomic changes were observed.

IV.D. Chemical  Interactions and Biological
Activity

Mercury is capable of combining with a wide
variety of organic molecules. Because of its
interactions with ligands present in proteins,
it is a particularly potent enzyme inhibitor.
The enzyme  systems or other biologically
important molecules known to be inactivat-
ed by mercury would include  all  of the es-
sential chemical components of the cell.

The action of mercury depends upon biolog-
ical factors, the chemical composition, and
the structural as well as the functional or-
ganization of cells. In living systems,  large
numbers of reactive substances compete for
traces of  mercury.  Each chemical constitu-
ent has a certain significance  in  relation to
cellular function, but the relative importance
of the individual substances in maintaining a
specific function varies greatly. Consequent-
ly, mercury binding will occur simultaneous-
ly at  "sensitive"  and  "insensitive"  sites,
and the toxic action may be  produced by
only a small proportion  of the  total mercury
fixed. This tends  to obscure  the  relation
between mercury binding and pharmacologi-
cal response (Passow,  H.,  Rothstein, A.,
andClarkson,T. W., 1961).

IV.D.I. Cellular Level— Cell structure gov-
erns the accessibility of sensitive ligands and
decisively influences the time   course  of
mercury action. The cell membrane  as  a
diffusion  barrier protects the cell  interior
from  poisonous action of the metal. On the
other hand, sensitive ligands located within
the membrane structure or on  the outer cell
surface are separated from the large reser-
voir  of  protective  complex-forming  sub-
stances inside the cell. Therefore, functions
associated with the cell membrane are  par-
ticularly susceptible to the action of mercu-
ry.

The first reactions  of mercury are with the
ligands of the cell  surface, with associated
disturbances of membrane function. Next, a
redistribution of the metal may take place.
As mercury penetrates  into the cell,  addi-
tional effects develop; and the initially inhib-
ited functions may begin to recover.  The
inactivation of  one sensitive site  usually
                                                                                    63

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induces a  whole  sequence  of  secondary
changes which may ultimately  affect the
physiological state of the whole cell  (Pas-
sow, etal., 1961).

IV.D.2. Organ Level— All of the generaliza-
tions  concerning  the cells  are valid when
considering the actions of mercury on organ
systems and on the intact animal. The matter
is  complicated by the fact that, in  the or-
gans, several  cell populations of different
susceptibilities may exist in a complex ana-
tomical arrangement. In animals, the effec-
tive concentration of mercury at the  cellular
sites of damage and the time of exposure are
determined  by the  patterns of  absorption,
distribution, deposition,  and excretion (Pas-
sow, etal., 1961).

IV.D.3. Chemical  Interactions  —  Most
heavy metals, including  mercury, are capa-
ble of forming complexes with ligands con-
taining sulfur, nitrogen,  or oxygen as elec-
tron donors. Nitrogen is  the preferred donor
in the  formation  of   coordination  com-
pounds. Oxygen  rarely  forms coordination
complexes, but when present in such disso-
ciable groups as  carboxyl and phosphoryl,
forms strong ionic bonds with heavy metals.
In any living cell, the following ligands are
present:

—OH, —COOH, —PO3H2, —SH,  —NH2,
—imidazole

These ligands, which form the integral parts
of almost  any molecule of biological signifi-
cance, are frequently essential to the normal
functioning of the cells. Mercury does not
have  the  same affinity for the  different  li-
gands. While it apparently has little affinity
for —COO-groups, it has high affinity for  —
NH-,  and  —SH groups  (Gurd and Wilcox,
1956: Klotz and Klotz, 1959).

Hydroxyl groups  of water can participate in
complex formation and  in the formation  of
insoluble hydroxides. These complexes may
have a very complicated structure, and their
electrochemical behavior may be quite dif-
ferent from the behavior of simply hydrated
ions.  Chloride ions also  form strong com-
plexes with mercury (Sillen,  1949).  Com-
plications in pharmacological studies  arises
immediately  after  dissolving mercury  in
water. In addition, all the  listed biological
ligands contain dissociable  protons. Mercu-
ry ions will replace these protons in complex
formation (Passow, etal., 1961).

Mercury binding  by biological  materials is
strong but not specific with regards to  the
ligands. The  only rules that  can be estab-
lished are concerned with affinities.  Chelate
formation may introduce specificity patterns
that invalidate the lists of relative affinities
(Martell and Calvin, 1952). Many metabol-
ites like  amino acids  or  dicarboxylic acids
are  capable of forming  chelates.  Chelate
formation generally leads to an  increase of
association   constants.  Since   chelating
agents may  exhibit high  specificity toward
mercury cations,  the rules regarding orders
of affinities of mercury for ligands can  be
applied to biological systems only with cau-
tion. For example,  if mercury, which has a
high affinity toward sulfhydryl groups, pro-
duces  a pharmacological effect, it is  not
permissible to ascribe the effect  to the inac-
tion of sulfhydryl groups. The observations
must  be supplemented by  studying the ef-
fects of additional sulfhydryl reagents (Cal-
vin, 1954). The arrangement of ligands with-
in a single macromolecule may also  favor
chelate formation. Chelates of high specific-
ity play an important role in the inactivation
of enzymes by metals (Malmstrom  and  Ro-
senberg, 1959).

IV.D.4. Action on Enzyme  Systems  — Mer-
cury is potentially able to combine  with all
of the components of an  enzyme  system.
The possibilities of metal interactions with
the enzyme or with the enzyme-coenzyme-
substrate complex are manifold, because of
the presence  of many reactive ligands. The
64

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reduction of enzyme activity  is dependent
upon the accessibility and on the functional
significance of  the  various  metal-binding
groups. Of primary importance are the inter-
actions with the ligands which are functional
in bond formation with the components  of
the enzyme-substrate complex at the active
center of^ the enzyme.  Other changes are
brought about by metal combination with
groups linked to the active center. The metal
bindings with no functional significance play
an indirect role.  By combining with mercu-
ry, they  reduce  the  amount  available for
reaction  with functional  ligands, thereby
affording protective  action (Passow, et a/.,
1961).

Summer  and  Myrback (1930) found that
90% inhibition of urease activity resulted
when 50 atoms of mercury were attached to
one  molecule  of  urease: Only 15 atoms  of
silver were required to yield 95% inhibition.
It was concluded that a large fraction of the
mercury atoms bound to the enzyme is asso-
ciated with ligands which play  no role in ca-
talysis. Thus  in  urease  inhibition by SH-
seeking metals chemical affinities, functional
importance of ligands, diversion to "insensi-
tive" sites, and accessibility of "sensitive"
ligands all play a role (Passow,  et a/., 1961).

Inhibitory effects of  heavy metals may also
result from interactions with ligands which
are not directly involved in the active center
of the enzyme. The binding of the mercury
cation to the side-chain residues of the pro-
tein  may  result in electrostatic charge and a
shift in the ionization constant of the active
center, leading to changes in  the  catalytic
activity (Klotz, 1959). The inhibitory  effect
of relatively high concentrations of Hg+ +
on  chymotrypsin have  been  attributed  to
changes in the polymeric forms of the en-
zyme (Green, Glander, Cunningham, 1952).

A second type of indirect action may be a
consequence of  structural changes  in the
protein. In the presence of mercury, oxygen
uptake by hemoglobin increases, particular-
ly at low O2 pressures (Riggs,  1952). The
author stated that the metal  is not attached
to the heme-ring but probably exerts its in-
fluence  by changing  the  structure of the
globin moiety of the hemoglobin molecule.
More recently Resnik demonstrated that the
addition of more than 10 equivalents of mer-
cury  per hemoglobin  molecule  produced
marked changes in the absorption spectra
and  the  rotary dispersion curves of both
HbO2 and metHb. The final product in both
instances was similar to acid-denatured pro-
tein. He postulated that mercuric chloride is
capable of reaction not only with the sulfhy-
dryl  groups but also the imidazole residues
of hemoglobin (Resnik, 1964).

Cell  membranes contain large quantities of
lipids,  mainly  phospholipids.   It is  well
known that  very small amounts of  heavy
metals produce appreciable changes of sur-
face tension and  surface charge of lipid
films. Alterations of these variables may be
expected  to  lead  to  marked  changes of
permeability and metabolic activities of sur-
face enzymes (Passow, 1961).

IV.D.5.  Action on  Cells — The cell  mem-
brane is the  first and most important  site of
action  of metals. Frequently, almost  all of
the metal applied is rapidly absorbed  by the
easily accessible ligands of the outer surface
of the membrane. The interior of the cell, on
the other hand, is  protected by the  mem-
brane as a diffusion barrier and also  by the
many inert substances in the cytoplasm that
can react with and divert the metal. Many of
the metal-binding ligands are essential  to the
maintenance of the membrane as a diffusion
barrier or are necessary for  the functioning
of the enzyme of the membrane. The general
pharmacology  of  mercury,  therefore,  is
largely concerned with pathological changes
of functions  associated with the cell  mem-
brane (Rothstein, 1959).

Studies with yeast cells have  revealed much
about the interaction of heavy metals with
                                                                                   65

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the ionized ligands on the cell's outer sur-
face. There is strong evidence for the exist-
ence of three types of metal-binding ligands
on the surface  of the cell, namely sulfhy-
dryl, phosphoryl, and carboxyl groups. Ev-
idence indicates that ribonucleic acid is the
source of the phosphoryl groups on the cell
membrane. The sulfhydryl group is the prin-
cipal binding site for mercury. Metal interac-
tions with SH-groups lead to a generalized
breakdown of the permeability of the barrier
of the cell (Passow, eta/., 1961).

Several types of enzymes are located on the
cell's outer surface. These include: enzymes
that digest external  substrates (such as in-
vertase and phosphatases), enzymes  con-
cerned in active transport phenomena, and
enzymes involved in membrane  synthesis.
These  enzymes are  probably found  in all
cells and have been verified in  red blood
cells. Because of their location, the enzymes
of the  cell surface are particularly suscepti-
ble to heavy metals.

Some  sugars enter cells slowly  by simple
diffusion. Certain other sugars enter quite
rapidly by a special  mechanism. Evidence
indicates that the entry mechanism involves
a definite chemical specificity, that pairs of
sugars compete with  each other, that the
kinetics of entry follow mass-law behavior,
and that the entry is  susceptible to traces of
heavy metals.

Mercury often  produces an all-or-none re-
sponse in which no effect is observed until  a
certain threshold concentration is attained.
The response once elicited is maximal for  a
given  cell.  The  curves  relating  dose and
effect do not represent the parameters of the
chemical reaction of  the metal  and cellular
receptors,  but  rather the  distribution of
thresholds in the population. A distribution
equation, usually the normal curve, can fit
the data, whereas a  mass-law equation will
not. If mercury is added to a suspension of
yeast cells,  rapid loss of potassium occurs.
The defect in the membrane is not specific
for potassium. It represents a general break-
down of the permeability barrier. The indi-
vidual  cells respond in an  "all-or-none"
fashion. The reason for this is that mercury
is  acting on sites maintaining structural in-
tegrity, possibly  SH groups  in the mem-
brane. No single one of these ligands plays
any measurable  functional role. However,
when many of these groups are cross-linked
by reaction with mercury, the stress on the
membrane  is sufficient to  destroy it as  a
permeability  barrier.  In other  words, if
groups of ligands acting in unison are essen-
tial for a particular function, all-or-none re-
sponses may occur (Passow, et a/.,  1961).

Erythrocytes of man and rodents are readily
permeable to glycerol. Entry of glycerol into
the cells is prevented by traces of  mercury.
Mercury is probably temporarily fixed to li-
gands in the membrane that control glycerol
permeability. Subsequently,  it moves into
the interior of the cell and combines with the
many complexing substances. As  long as
some mercury is bound to  the membrane,
inhibition of glycerol takes place. The inhibi-
tion disappears as soon as all of the mercury
has passed through the  membrane. At very
high mercury concentrations, the complex-
ing ligands of the cell interior become satu-
rated. The excess mercury remains attached
to the  cell membrane and a permanent re-
duction of glycerol permeability is produced
(Passow, eta/., 1961).

Mercury inhibits the uptake of  glucose  by
the rat diaphragm. The inhibition reaches a
concentration-dependent maximal  value in
less than 20 minutes. After a lag of over 30
minutes, a second effect gradually develops:
respiration becomes progressively inhibited,
provided relatively high concentrations of
mercury are applied. Upon addition of slow-
ly penetrating complexing agents like BAL
or cysteine, the  inhibition of glucose trans-
port can be reversed whereas that of respira-
tion  cannot. The respiration of  muscle ho-
66

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mogenates is reduced almost immediately on
addition of mercury, and the inhibition  can
be rapidly reversed by the  addition of cy-
steine.Jt  appears that the metal first inter-
acts  with  functional groups  at the cell sur-
face, therefore inhibiting the transport of
sugar. Subsequently  it slowly  enters  the
cells, and the  respiration is progressively
inhibited (Demis and Rothstein, 1955). Stud-
ies of binding of mercury by rat diaphragm
confirm this  interpetation.  Uptake of mercu-
ry by the excised diaphragm proceeds fairly
rapidly for about 20 minutes. Thereafter, the
rate  of mercury uptake proceeds at a much
lower rate constant. The time-sequence in-
volves a rapid diffusion through the intersti-
tial spaces and immediate binding on the cell
surface,  followed by  a  slow penetration
through the  membrane to  the  respiratory
sites within the interior of the cell.

In epithelial tissues such as  the small intes-
tine  and the kidney, several  populations of
cells are found in  a definite geometrical ar-
rangement. The actions of mercury here are
more complicated than in a homogeneous
population of cells. Similarities are found,
however,  because  the absorptive and secre-
tory functions of the epithelia represent spe-
cialized use of mechanisms present in nearly
all cells. It can be stated that any  observed
inhibition  of mercury of the  net transport of
salt solutions or of glucose across epithelia
can  be explained  in terms  of  mechanisms
similar to  those active in the cells  (Passow,
eta/!, 1961).

The  action of mercury on the membrane of
the columnar epithelial cells of the jejunum
is similar  to its action on the membranes of
muscle and red blood cells. Immediately fol-
lowing the addition of mercury (as mercuric
chloride)  to  the mucosal side,  rapid re-
sponses are observed in the electrical poten-
tial across the intestine, the loss of cellular
K+,  and  the cessation of glucose uptake.
Each of these responses is associated with
the action of mercury  on the membrane fac-
ing the  lumen.  After  a delay period, other
functions  are inhibited. These include Na+
and glucose transfer into the serosal solution
and the production of lactic acid. Similar
disturbances in electrolyte equilibrium have
been reported for the action of mercury on
kidney slices (Kleinzeller, etal., 1957).
Mercury can produce one kind of response
when added to the mucosal side of an epi-
thelial tissue and a different response when
introduced on the serosal side. When mercu-
ry at  10-4 M is in contact with  the mucosal
surface  of frog skin, transport  of salts and
water is reduced, because of the specific in-
hibition   of  the sodium  transfer system.
Since the effects are noted at mercury levels
which do  not produce  inhibition of cellular
metabolism, it  seems likely  that the toxic
action of mercury is mediated through a di-
rect effect on the outward-facing membrane
of the  epithelial  cells.  When  mercury  is
present  on the serosal side in the same con-
centration, sodium transport is  accelerated.
This response  has been attributed to an in-
teraction of  mercury with the inward-facing
membrane of the epithelial cells (Passow, et
a/., 1961).
IV.D.6. Differences  in Biological Behavior
of Various Mercury  Compounds — Hughes
(1957) offered a physio-chemical explanation
for the differences in biological behavior of
metallic mercury, inorganic  mercury, and
alkyl and  arylmercury compounds.  Hughes
states  that alkylmercury  halide possesses
both a stable carbon-mercury bond and the
essentially ionic mercury-halide bond. Car-
bon-mercury bonds possess a wide range of
stabilities. In general, aliphatic carbon com-
bines more stably with mercury than aro-
matic carbon;  however, both would appear
to be sufficiently  stable to resist usual phy-
siological  processes. The  pharmacology, of
methylmercury halides may be discussed in
terms of the  affinity of methylmercury ion
                                                                                    67

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for biological substances. This affinity  may
be described by the equation:

        CH3Hg+ + X-=CH3HgX

Relative  affinities for  various   biological
substances may then  be  obtained by corn-
paring the equilibrium constants for this re-
action.
         K =
             CH3HgX
             CH3Hg-
Hughes  has  measured  some  equilibrium
constants and the values are given below:

 Association Constants of Methylmercury for Certain Ligands
Ligand
Log,0 K
RS~
17
OH"
9.7
I"
9.0
Br Cl~
7.0 5.7
   Equilibrium Constants of CH3HgI for several Proteins
       Protein
Kx 10°
Human serum albumin
Bovine serum albumin
Bovine oxyhemoglobin
Bovine carbonylhemoglobin
 25
  7
 20
  6
Hughes argues that from the magnitude of
these association constants,  methylmercury
ion can exist only in infinitesimal concentra-
tions in biological  solutions. Thus at pH 7,
there must be 500 times as much methylmer-
cury  hydroxide as methylmercury ion.  If
chloride is also present at physiological con-
centrations (0.1M), Hughes  calculates  that
there must be 100 times as much methylmer-
cury chloride as methylmercury  hydroxide.
However, since all biological systems con-
tain thiols, the extremely large association
constant for this reaction must mean that all
but traces of the mercurial will be bound to
thiols, provided that they exceed the amount
of mercury present. This is usually the case,
since human blood plasma is 0.5  millimolar
thiol, and the red cells contain 60 times as
much sulfhydryl in their hemoglobin. Man's
plasma alone should be able to combine with
1  1/2 M of mercurial  containing 300 mg of
mercury. Methyl mercury also has a strong
affinity for many other groupings present in
biological substances as  discussed  in  the
previous section (Hughes, 1957).

One can modify the relative affinity of the
mercurials   for  various  sulfhydryl  com-
pounds  by  replacing  the CH-, group  with
larger organic radicals and with organic radi-
cals containing other functional groups. One
may expect interference from a large group-
ing if the SH group were located in a "tight"
part of the protein molecule, or if there were
charges on groups adjoining the SH group;
and  if the  mercurial carried  an  identical
charge.  If the mercurial  carried the  charge
opposite to  that of the  region  surrounding
the SH group,  the  affinity should  be in-
creased. Similarly, after binding to  SH, the
mercuric ion still  contains  a  free  valence
capable  of  combining   with  some  other
properly placed group. Therefore, in gener-
al,  mercuric ions should bind more tightly
than  simple  mercurials, and  considerable
variation in affinity should exist from protein
to protein (Hughes, 1957).

Most of the thiols of human plasma can be
accounted for by serum mercapto-albumin
containing  1  thiol group per protein  mole-
cule.  However,  5 to 10% of the total  thiol
content of human plasma is present in the
form of small molecules. Thus a mechanism
is provided for the egress of mercury from
the blood stream in combination with one of
the small diffusible thiols.  Simple mercuri-
als, such as  methylmercury  halides, are 100
times as  soluble in  lipids  as  water.  The
amount of mercury present at any one site
must be small  in the presence of  thiol, a
definite  infinitesimal amount is  always pres-
ent, and if  any leaves  the  system by  dis-
solving in a lipoid membrane, more  will dis-
sociate from the protein-mercurial complex
68

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to maintain the equilibrium. It is thus possi-
ble for all the mercury to diffuse through the
membrane;  Hughes postulates  that  these
mechanisms would  explain the rapid distri-
bution of methylmercuric halide to all  tis-
sues of the body. Other compounds of mer-
cury show a different distribution pattern.

Larger compounds  of  mercury  do not  ap-
pear to be selectively  soluble in lipid sol-
vents; they seem to be of such large size as
not to diffuse through  pores  in cell mem-
branes. The upper  limit of size for ready
diffusion is not known; however, even glu-
cose, an uncharged molecule, appears  to
enter cells  only by active transport. In the
case  of charged  molecules, even  smaller
molecules may be excluded.

The bivalency of inorganic mercury, despite
its small size, may act to restrict further its
diffusibility since,  with both bonds clinging
to protein, the amount of time when it is free
for diffusion  must be reduced still further.
This bivalency may also explain its ability to
coagulate proteins since, by bonding to adja-
cent protein molecules, it can link them to-
gether causing aggregation (Hughes, 1957).
                                                                                     69

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                                    CHAPTER 5
                          TOXICOLOGY OF MERCURY
V.A.  Toxicity to Laboratory Animals

The  absorption,  distribution,  metabolism,
excretion, and the action of mercury at cel-
lular and subcellular levels has  previously
been discussed.  This section will deal with
the toxic effects of mercury on the intact
animal.

V.A.I. Acute and Subacute Toxicity— The
acute toxicity of inorganic mercury is great-
er than that of the organic mercurials, re-
gardless of the route of administration. The
arylmercury, alkylmercury, and the alkoxy-
mercury compounds seem to be equally tox-
ic. The symptoms of  poisoning with alkyl-
mercury compounds  may appear several
weeks after administration, but the toxicity
is still less than that of  inorganic mercury
when the observation period is prolonged to
1 month (Swensson and Ulfvarson, 1963).

Swensson (1952) studied the relative acute
toxicities of mercuric  chloride, methylmer-
curic  chloride, and methylmercuric dicyan-
diamide, intraperitoneally,  in mice.  In this
study, mercuric chloride was found to be the
most toxic. Thereafter, with decreasing tox-
icity,  were phenylmercuric acetate, the al-
kylmercuric chlorides, and the alkylmercu-
ric dicyandiamides. No difference in toxicity
was noted between ethyl and methylmercur-
ic chlorides.  Methylmercuric chloride  and
methylmercuric dicandiamide were of equal
toxicity by the intravenous route in rabbits.
With  repeated intraperitoneal injections of
one-tenth to one-fourth of the Probable Le-
thal Dose (PLD),  there  was  a gradual in-
crease in the appearance of central nervous
system effects. Histological studies revealed
diffuse injuries in the  CNS with all com-
pounds tested (inorganic mercury was not
included  in  this  study). Gage and  Swan
(1961) demonstrated that only alkylmercury
compounds  gave evidence  of neurotoxic
effects which developed in survivors of the
median lethal dose in animals receiving sub-
lethal doses.  Short term tests  with methyl-
mercury (10  to 90 days) showed that a daily
intake of 0.4 to 1.0 mg Hg/kg of body weight
caused neurological  symptoms in rabbits,
dogs, and cats (Lefroth, 1969). The acute
toxicities of  the mercurials are summarized
in Table 1.
Methylmercuric chloride, suspended in olive
oil, was administered  to mice, orally via
stomach tube, at levels of 4.6 to 100 mg Hg/
kg of body weight. The animals  at the lower
levels (4.6 to 14.7 mg Hg/kg) received seven
daily  injections,  while the  animals at the
higher dosage levels received only a single
injection. Neurological symptoms appeared
in two groups given one  dose of 32 and 46
mg Hg/kg,  respectively. In groups which
received a  dose larger than 46 mg Hg/kg,
death  occurred  before  any  neurological
symptoms could be detected. Mice receiving
a dose  less than  32 mg  Hg/kg showed no
neurological symptoms up to the 30th day
after the dose was administered. Seven daily
doses of 10 and 14.7 mg Hg/kg administered
to two  different groups of mice induced neu-
rological symptoms; all mice from the latter
group died  within 5 days  after the last dose
was administered. Only one of ten mice died
as the  result of the lower dose. The domi-
nant neurological  symptoms  related to cere-
bellar,  or  vestibulocerebellar regulation of
movement of posture. A brain concentration
of mercury of 20 Mg/g  of  wet tissue  was
found only  in those groups which had shown
some neurological symptoms (Suzuki, 1969).
                                                                                   71

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                          Table 1. Toxicity of Various Compounds of Mercury*
      Compound
                                                Animal
                 Route of
               Administration
                 Toxicity
                  mg/kg
 Inorganic
 Mercuric chloride
Alkylmercury
Ethylmercuric chloride
Ethylmercuric dicyandiamide
Ethylmercuric phosphate
Ethylmercuric thioglycolate
Ethylmercuric thioglycolate
Ethylmercuric toluenesulfonate
Isopropylmercuric hydroxide
Methylmercuric chloride
Methylmercuric chloride
Methylmercuric dicyandiamide
Methylmercuric dicyandiamide
Methylmercuric dimercaptopropanol
Methylmercuric hydroxide
Methylmercuric propanediolmercaptide

Arylmercury
Phenylmercuric acetate
Phenylmercuric catecholate
Phenylmercuric dinaphthylmethane-disulfonate
Phenylmercuric dinaphthylmethane-disulfonate
Phenylmercuric nitrate

Alkoxyalkyl
Methoxyethylmercuric acetate
Methoxyethylmercuric silicate
                                                Rat
                                                Mouse
                                                Mouse
                                                Rabbit
                                                 Mouse
                                                 Mouse
                                                 Rat
                                                 Rat
                                                 Rabbit
                                                 Mouse
                                                 Mouse
                                                 Rabbit
                                                 Mouse
                                                 Rat
                                                 Mouse
                                                 Mouse
                                                 Mouse
                                                 Mouse
                                                 Mouse
                                                 Mouse
                                                 Mouse
                                                 Mouse
                                                 Mouse
Rat
Mouse
                    oral
                    sc
                    iv
                    sc
                    oral
                    oral

                    iv
                    iv

                    oral
                    ip
                    iP
                    ip
                    iP
                    IP

                    iP
                    oral
                    iv
oral
iP
               37 (LD50)
               23
                7.6  "
               10 (LD)
               16(LDSO)
               19
               30   "
               20
               20 (MLD)
               28(LD50)
               12   "
               15 (LD)
               20(LD50)
               32   "
               20   "
               22 (PLD)
               17 (LD50)
               29
               13(LD50)
               50-100 (LDSO)
               25 (LDSO)
               ,70   "
               27
                                                                                      > (LDSO)
                                                                                    50
 'Adapted from Swensson and Ulfvarson (1963) and Spector (1955)
 Suzuki (1969) administered  methylmercuric
 acetate labeled  with 203Hg dissolved in dis-
 tilled water subcutaneously to mice daily for
 10 successive days. The daily dose was ei-
 ther 50 or 100 /A g/203Hg/mouse.  During the
 course of the experiment, the mercury con-
 centrations of the various organs  and tissues
 did not reach saturation. The concentrations
 of mercury in the blood was  constantly high-
 er than that in the  brain in the course of ad-
 ministration and for a short period  after it,
 but the  decrease of mercury concentration
 in the blood was faster than that in the brain.
 The biological  half-life of  mercury in  the
 brain  was calculated to be 7.2 and 6.2 days
                                                  respectively and that in the blood 4.2 and 4.1
                                                  days respectively for the 50 and 100 ^u g Hg/
                                                  mouse.
                                                  Sebe, et a/., (1962) studied the toxicity of a
                                                  series  of alkylmercury compounds.  Com-
                                                  pounds of alkylmercury Containing R-Hg or
                                                  R-Hg-S with  the methyl,  ethyl, or  n-propyl
                                                  chain administered orally to rats were toxic
                                                  to the central nervous system and induced
                                                  paralysis of the  legs. Iso-propyl compounds
                                                  and  other alkylmercury  Compounds  with 4
                                                  or 5  carbon atoms were shown not to cause
                                                  these injuries.
72

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Meshkov, Glezer, and Panov (1963) studied
the effects of lethal and toxic doses of die-
thylmercury on the kidneys of rats. In these
experiments, albino rats were administered
doses of 25 to 100 mg/kg of body weight of
diethylmercury. The animals at the 100 mg/
kg dosage level died  within 24  hours and
were found  to have pronounced degenera-
tive changes in the kidneys, involving prima-
rily the  proximal tubules.  The  loops of
Henle and the straight tubules in the medulla
were almost unchanged. The lower doses of
25  to  50 mg/kg  produced  similar  renal
changes in 10 to 20 days. The exact nature of
the histochemical change produced depend-
ed upon the extent of the degenerative  proc-
esses. In the early stages (sublethal doses),
there is  a decrease in the nuclear DNA con-
centration of the epithelial cells of the proxi-
mal and thin segments, while the cytoplas-
mic RNA content increases. Further changes
in the tubules are accompanied by a marked
reduction in  the  DNA and  RNA  content.
Sublethal    doses  produced   significant
changes in the ultrastructure of the proximal
tubular  epithelium:  appearance  of  large
numbers of  vacuoles in the  cytoplasm, de-
struction  of the  membranes of the endo-
plasmic reticulum, swelling and splitting the
cell membrane, and,  most  important, de-
struction  of  the  mitochondria!  apparatus,
swelling of  the  mitochondria and  granular
disintegration of their cristae.

In the experiments  cited earlier, Swensson
(1952) limited his histological examinations
to the central nervous system, particularly
the spinal cord,  although, the cerebellum
was also examined. Cell injuries  were  dem-
onstrated  in the,granular  cell  layer of the
cerebellum,  in  the  Purkinje's cells in the
cerebellum and  in  the cells  of  the  spinal
cord. The same changes were observed with
all  compounds  studied;  methylmercuric
chloride,  ethylmercuric  chloride,  methyl-
mercuric  dicyandiamide, ethylmercuric di-
cyandiamide, and phenylmercuric acetate.
No essential differences were noted between
the  compounds.  Injury  to  the  myelin
sheaths in the spinal cord were noted as well
as selective Marchi degeneration in the pos-
terior columns of the cord. Swensson found
that injury to nerve cells occurred even after
very small doses. When  the injuries  were
sufficiently  extensive,  nerve   symptoms
arose.  The degree of severity was clearly
connected with the degree of severity of the
poisoning and, to some extent with the peri-
od of time elapsing after the administration
of the compound.

V.A.2. Chronic  Toxicity— Fitzhugh, et a!.,
(1950) showed, that although inorganic mer-
cury compounds are more acutely toxic than
organic mercury compounds, phenylmercu-
ric acetate was more toxic, chronically, than
was mercuric acetate. Significant toxicity in
the form  of kidney damage was observed
from 0.5  ppm dietary mercury in the form of
phenylmercuric acetate. Ten to twenty times
this amount of mercury in the form of mer-
curic acetate  was required to cause similar
damage.  Mercury was accumulated  in the
liver and kidneys of animals fed phenylmer-
curic acetate, although no damage of a func-
tional nature was observed. There was con-
siderably more mercury stored in these or-
gans after feeding phenylmercuric acetate
than after feeding  mercuric acetate. The
results indicated  that as the mercury concen-
tration increased 100 times,  the organ con-
centration was increased only about 10 times
for both compounds. This  suggests that
there is  a saturation phenomenon present,
with excretion increasing with the dose.

V.A.3. Genetic  and Teratogenic Effects —
Experimentally,  in certain systems of plants
and in drosophilia, organic mercurials may
produce  genetic mutations and  chromoso-
mal aberrations.

Organic  mercurials  cause c-mitosis in the
cells of Allium cepa roots. The aryl and alkyl
compounds are most active and produce this
effect at  levels as low as  15 x  10"7M. The
                                                                                   73

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alkoxyalkyl compounds are less active and
produce a comparable effect at levels as high
as 30 x 10~7M. All of the mercurials studied
produced c-mitosis, however, there was  a
difference in their effects. The aryl com-
pounds gave rise to distinctly more bridges
and fragments  than the  other mercurials.
The phenyl  compounds  produced a higher
frequency of multipolar  spindles  and other
spindle irregularities than the alkyl of alkox-
yalkyl  compounds  (Ramel,  1967). These
compounds  are  200 to  1,000 times more
effective than colchicine in producing c-mi-
tosis.  Rats which have been maintained on
methylmercury for up to  8 months and in
which mercury has reached a steady  state
showed no chromosomal aberrations in the
blood cells (Ahlberg, et a/., loc cit, Berglund
and Berlin, 1969).

As a result of the c-mitotic action, polyploid
as well  as aneuploid cells occur. The  mer-
curial compounds  cause c-mitotic  tumors,
and hook-like growths of the roots  are also
observed, which  represent incomplete tu-
morous action. Fahmy reported studies on
the cytologic  effects  of  organic mercury
compounds,  the  results of which  are  in
agreement with the results given by Ramel.
In addition,  inorganic  mercury is about 200
times less effective than  organic mercury in
the production  of c-mitosis (Nelson, et a/.,
1971).

In a study with Drosophila melanogaster,
selected so that dysfunction of the sex chro-
mosomes in either the female or the male
would result in non-yellow (XXY) daughters
or yellow (Xo) sons, treatment of the female
larvae with aryl or alkylmercury resulted in
a significant increase  in  the number of ex-
ceptional daughters (XXY) showing irregu-
larities of meiotic chromosomal disjunction
(Ramel, 1967). It has been  shown that meth-
ylmercuric hydroxide binds  to DNA and
causes irreversible denaturation of  DNA in
vitro. Therefore,  it may  be suspected that
methylmercury could induce mutations. Fol-
lowing the results of the Drosophila study,
Ramel  (1969)  concluded  methylmercury
induces mutations, but the mutagenic effect
should be considered minimal. He considers
the genetic risks may be recognized at two
levels. First, if a sufficiently high concentra-
tion should reach the gonads, a segregation
disturbance  like the one with Drosophila
may occur. In these cases, one may expect
the human defects will  increase  which are
caused by the additional chromosome, e.g.,
Down's  Syndrome  or   Klinefelters  Syn-
drome. Secondly are the teretogenic effects
of methylmercury; the accumulation in the
fetus  may  cause disturbances in  chromo-
some  segregation during development (Ra-
mel, 1969).

As  reported earlier,  rats which have  been
maintained on  methylmercury for  7  to  8
months, until a steady state for mercury  is
reached, showed no chromosomal  aberra-
tions in any blood cells.

Oharazawa (1968) carried out investigations
on the effects of ethylmercuric phosphate on
mouse embryos with particular emphasis on
embryopathy, teratology* and cytogenetics.
Prior to the experiments, the LD50 of ethyl-
mercuric phosphate was determined as 76
mg/kg for the normal, nonpregnant female
mouse of the ICR-JCL strain. To  study pos-
sible fetal malformations induced by ethyl-
mercuric phosphate,  40  mg/kg of the com-
pound was injected subcutaneously on the
10th day of pregnancy.  Controls received
only distilled water and no other  treatment.
On the 19th day, the mice were sacrificed
and the  fetuses removed for comparison
between the two groups. There were no dif-
ferences between food and water intake of
the two  groups.  The incidence of young
from  one litter was not significant.  The
weights of the young in the  treated group
were  decreased.  There  was  a 31.6% inci-
dence of cleft palate among the treated mice,
but no malformations of the bones or skin
were found. The mice weje similarly treated
with ethylmercuric phosphate  for the  chro-
mosome studies. Sacrifice was at  5,9, and  19
74

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days. Using  the  plasma clot  method, the
number of cells from the two groups was
compared with normal for abnormal chromo-
somal patterns. The incidence of unstable
chromosomes characterized  as  polyploid,
chromatid gap, or fragmented was 19.3% on
day 5; on day 9,  this incidence was 16.6%
compared to 3.2% for the control group.

Murakami, et a/., (1955) investigated the ter-
atogenic properties of phenylmercuric ace-
tate, an ingredient of a vaginal contraceptive
product, in mice. One-fourth of  a  vaginal
contraceptive tablet containing phenylmer-
curic acetate was placed in the vaginas of
mice on the 7th day of pregnancy. In  another
group of mice, an aqueous  solution of the
tablet  with the corresponding amount of
phenylmercuric acetate was  injected subcu-
taneously on the 8th  day of pregnancy.  A
control group of mice was also utilized. The
rate of  occurrence of abnormalities was
highest in the mice which received  phenyl-
mercury vaginally (15.1%) and lowest in the
controls (2.7%). The group receiving phenyl-
mercury subcutaneously was intermediate
between the two (9.1%). Clegg (1970) report-
ed that the administration of a single dose of
14 mg/kg of body weight of methylmercuric
phosphate to pregnant rats on the 10th day
of  pregnancy  resulted  in  reduced  body
weight of the offspring and an incidence of
31.6% cleft palates.

V.B. Toxicity to Humans

The symptoms resulting from poisoning with
the inorganic" mercurials differ in essential
points from those resulting  from  poisoning
with the organic  mercury compounds. The
symptomology  df  human  poisoning with
both  types of  compounds  resembles  that
seen in laboratory animals.

V.B.I.  Inorganic  Mercury  Compounds —
Soluble  inorganic- compounds of  mercury
are irritating to the skin and mucous mem-
branes. This effect is  marked with mercuric
chloride. Concentrations of  1 to 5% cause
irritation, vesiculation, and corrosion of the
skin and mucous membranes. More dilute
solutions produce irritation to sensitive skin.
Mercuric chloride may be absorbed from the
intact skin and mucous membranes  to the
extent of producing symptoms of poisoning
(Bidstrup, 1964).

V.B. 1.1.  Acute Poisoning — The oral inges-
tion  of doses as low as 0.5 g of  mercuric
chloride has produced death. The  mean le-
thal dose in adults is probably between 1 and
4 g (Gleason, Gosselin, and Hodge, 1963.)

When ionizable mercuric salts are  ingested,
necrosis begins immediately in  the mouth,
throat, esophagus, and  stomach.  Within  a
few minutes, violent pain, profuse vomiting,
and severe purging is experienced. The pa-
tient may die within a few hours from peri-
pheral vascular collapse secondary to fluid
and electrolyte losses. If the patient survives
this phase, the primary  gastroenteritis sub-
sides spontaneously within a few days. A
second phase, developing within 1  to 3 days
after exposure, is characterized by stomati-
tis, membranous colitis, and  tubular nephri-
tis. This second phase which is seen even in
noncorrosive preparations of  mercury is
independent of the portal of entry,  and is
associated with a slow and prolonged  excre-
tion of mercury  by the salivary glands, the
gastrointestinal mucosa, and the kidneys.
Death in this phase is usually the result of
complete  renal failure (Gleason,  Gosselin,
and Hodge, 1963). Postmortem examination
shows inflammation and corrosion along the
alimentary canal and severe damage to the
kidneys. The glomeruli as well as the tubules
are involved (Goldwater, 1957).


V.B.1.2.Chron/c Poisoning— The most fre-
quent manifestations  of chronic  inorganic
mercurial poisoning  are (1) gingivitis  and
stomatitis, often associated with loss of
teeth; (2) tremor,  involving  the hands and
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later other parts of the body; and (3) person-
ality change known as erethism. This condi-
tion is characterized by irritability, bursts of
temper, and excitability, sometimes  alter-
nating with depression. There are numerous
other signs and symptoms including saliva-
tion, loss of appetite,  weight loss, weakness,
and disturbances of urinary and gastrointes-
tional function (Goldwater, 1957).

There is little or no correlation between uri-
nary mercury  levels  and severity of symp-
toms.  While  urinary mercury levels  may
give some indication  of the degree of expo-
sure, they are of limited value in diagnosis of
poisoning, since high levels can be found in
human subjects who  are  symptom free, and
low levels in those exhibiting marked evid-
ence of mercurialism. Albuminuria severe
enough to result in nephrotic syndrome can
occur (Goldwater, 1957).

V.B.2. Organic Mercury Compounds— The
organic compounds of importance in pesti-
cides  are  the  aryl and alkylmercury com-
pounds.

V.B.2.1. Arylmercury Compounds— Cases
of clinical poisoning with  phenylmercury
salts are rare in the literature in comparison
with  inorganic  and alkylmercury  com-
pounds. However, the toxicity of the phen-
ylmercuries can not be discounted. One may
conclude from the animal data that these
compounds are  highly toxic. In addition,
since phenylmercury  is metabolized to  inor-
ganic mercury in the  liver, one may expect
kidney  involvement  resulting from  toxic
doses  of  the  compound. Phenylmercuric
acetate is irritating to the skin and may also
produce  a delayed sensitivity (Sunderman,
et a/.,  1956).  Hypersensitivity has been re-
ported to occur with  several phenylmercury
salts (Matthews, 1968). Acrodynia  (Hirsch-
man,  et a/.,   1963; Matthes, et a/.,  1958;
Schrager, 1964) and neuromyasthenia (Mill-
er, et  a/.,  1967) have been  reported  from
inhalation of  phenylmercury vapors  from
paints. Dunn reported four cases of mercury
poisoning resulting  from the use of  fiber
glass  air filters containing phenylmercury
acetate from forced draft heaters. Becker, et
a/., (1962), reported  on 5 cases of nephrotic
syndrome associated with contact with mer-
cury. Three of these cases involved the use
of ammoniated mercury ointment, one asso-
ciated with the use of phenylmercury paint
additive, and one with a mercurial diuretic.

V.B.2.2. Alkylmercury  Compounds  — If
alkylmercury compounds come  in contact
with the skin, dermatitis may develop. The
first symptoms are warmth,  swelling  and  a
burning sensation. Later, blisters may form
which may break, producing a sodden, gray-
ish-white appearance. These symptoms may
occur at any time, from a few days to sever-
al weeks, after the first contact. Irritation of
the mucous membranes of the nose, mouth
and throat are often  described in connection
with alkylmercury compounds. These sensa-
tions may come after  a short exposure and
usually disappear quickly when the  expo-
sure is terminated (Lundgren  and Swensson,
1949).

V.B.2.2.1. Acute Poisoning— In acute al-
kylmercury  poisoning,  symptoms of in-
volvement of the  respiratory tract and the
alimentary  tract are described.  Headache,
fatigue, and other nervous symptoms have
been reported. Myalgia has been noted and
albuminuria is a transient symptom (Lund-
gren and Swensson, 1949).

V.B.2.2.2. Chronic  Poisoning— In chronic
poisoning, symptons are fatigue, headache,
impairment of memory  and  of  concentra-
tion,  numbness and  tingling of lips  and
tongue  and  later   of the   limbs, slurred
speech, increasing ataxia and impaired gait.
There may be concentric narrowing of the
visual fields and impairment of hearing. The
symptoms may first appear  as  long  as  2
months after the exposure has ceased.  The
sympsoms may increase, remain static, or
decrease. In cases of  severe poisoning, the
76

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physical defects and the mental deteriora-    The clinical details of the Minamata, Japan,
tion often remain.  This clinical  picture has    and the Alamogordo,  N. Mex., poisonings
been  reproduced  in  animal experiments    have been reported by Takeuchi (1970) and
(Lundgren and Swensson, 1949).               Gregg, etal., (1971), respectively.
                                                                                  77

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                                   CHAPTER 6
             ECOLOGIC EFFECTS OF MERCURY CONTAMINATION
Sources  of  mercury  in  the  environment,
both natural and man-made have been con-
sidered. While all forms of mercury are tox-
ic to life, it has been pointed out that aryl-
mercury, or methylmercury specifically, has
the most profound effect on animal life. It
has been demonstrated that all forms  of
mercury  may  be transformed into methyl-
mercury in an aquatic environment.


VI.A. Biotransformation of Mercury — The
methylation of mercury in sediments in river
and lake  bottoms is the process which, to a
substantial degree, is responsible for current
and  potentially  future  contamination  of
aqueous systems and their associated  biota.
Indirectly this methylation process may also
play, through the evaporation of dimethyl-
mercury, a large role in atmospheric  trans-
port of mercury.

Natural methylation  of  mercury was sus-
pected in the Minamata episode (Fujiki 1963
cited in Wood, et a/., 1968), but the  suspi-
cion was put aside as being of no signifi-
cance when methylmercury was identified in
the  discharge from the acetaldehyde plant
(Irukayama, et a/., 1962). Mercury has been
shown to be  methylated  by aquarium and
natural sediments  (Jensen  and  Jernelov,
1969) and enzymatically by extracts of meth-
anogenic  bacteria (Wood et a/., 1968). These
workers also  found that  small amounts  of
methylmercury were produced nonenzyma-
tically. Both groups found both monomethyl
and dimethyl mercury as initial products,
with high mercurial  concentration favoring
the  monomethyl  form (Wood et a/.,  1968),
and alkaline pH favoring the dimethyl form
(Larsson  1970).  The latter compound  de-
composes to  monomethyl form at an acid
pH. Jensen and Jernelov (1968) suggest that
the methylation might proceed as follows:
    ,2+
Wood et a/., (1968)  suggest the following
scheme  of  methylation by Methanobacter-
ium omelianskii or by solutions of  methyl-
cobalamin:
                              neutral pH
      enzymatic
    regeneration
The tendency of alkaline pH to favor a high-
er production of the more volatile dimethyl
form also would produce a larger discharge
of methylated mercury by evaporation into
the atmosphere; contrarily, a more acid pH
should then favor  (1) a higher proportion of
the less volatile monomethyl form, (2) ready
decomposition of  the smaller proportion of
the dimethyl  compound, and  (3) a greater
total retention, with less loss to the atmos-
phere (Larsson  1970). These  mechanisms
have been cited as possible factors (Hohnels
1970) leading to the contamination of remote
acid  lakes with high levels of mercury in
fish,  in the absence  of known sources of
contamination. All forms of mercury appear
to be directly or indirectly capable of  con-
version to methylmercury (Jernelov 1969).
                                                                                 79

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Jernelov  suggests that phenylmercuric ace-
tate slimicides are more  efficient sources of
mercury for subsequent  methylation than is
inorganic mercury.

Although methylation of mercury will occur
anaerobically, it appears to be more efficient
in aerobic systems.

VII.B. Sweden — Wildlife served its  tradi-
tional role  as an early warning system for
man when  problems with mercury arose in
Sweden.  About 1955, several ornithologists
in various  parts of  Sweden  observed  a de-
cline in the populations  of some seed-eating
birds. The increase in the number of birds of
prey found ill or dead also attracted atten-
tion. In 1958, Borg drew  attention to the fact
that birds found dead and sent to the  State
Veterinary Medical Institute had remarkably
high residues of mercury in their livers and
kidneys.  Studies of shot and trapped  birds
also revealed high  levels.  The conclusion
was that the large numbers of dead speci-
mens of  seed-eating birds (pheasants, par-
tridges, pigeons, finches) and birds of prey
(eagles, buzzards, hawks, falcons, owls) in
particular,  and of corvine birds indicated a
very general poisoning in birds. The source
of the mercury was attributed to the use of
mercury  compounds in agriculture. The de-
cline in the  population of several bird species
in Sweden  was attributed to the use of  pesti-
cides  (Johnels  and  Westermark,   1969).
News of  the Minamata problem in Japan led
to broader and deeper  studies (Nelson,  et
ai, 1971).

Analyses soon revealed  that mercury  pollu-
tion was  serious in Swedish lakes and  rivers
and that seed dressings were not the  sources
of  this contamination.  Waste and  leakage
from  pulp mills and chlor-alkali factories
were  chiefly responsible. The result was lo-
cal and spotty contamination, often heavy.
Many  lakes and streams remained  free or
nearly free of mercury. Even today,  most
waters of Sweden are not and need not be
monitored. This localization of contamina-
tion means that one must look at the right
spots  to find it. Early efforts to repeat the
Swedish findings in the United States, failed
because the animal samples that were taken
did not come from near sources of mercury,
despite the fact that they were taken from
some  of the most polluted estuaries of the
eastern United States (Nelson, etal., 1971).

It was evident in Sweden that mercury from
seed dressings was  responsible for the de-
cline of seed-eating  birds. The  birds of prey
obtained their high  levels of mercury from
fish. As stated above, the levels of mercury
in the rivers and streams arose chiefly from
industrial waste and to a smaller extent from
agricultural runoff. Mercury levels up to 9.8
ppm were recorded in Swedish fish.

It became apparent that mercury contamina-
tion of the Swedish environment was even
more  widespread than had been previously
believed. In order  to assess the historical
development of this contamination,  neutron
activation analyses  of the mercury content
of bird  feathers  from museum specimens
collected over the  previous  century were
performed  (Johnels  and Westermark,  1969).
These studies revealed that in birds with a
terrestrial food chain, a nearly constant level
of mercury was maintained from the middle
of the previous  century  until  1940. Subse-
quently, an increase in the mercury concen-
tration of feathers occurred amounting to at
least  10 to 20 times the previous level. Short-
ly after 1940, liquid treatments for seed grain
using  alkylmercury  ingredients  replaced
dusting with other types of organic mercury
compounds in many of the developing na-
tions, because of the reduced  hazards and
inconvenience to operators dressing grain
with  specially designed  machines. The  si-
multaneous appearance of increased mercu-
ry accumulations in birds with a terrestrial
food  chain thus suggests that  the alkylmer-
cury  seed-dressings are the main source of
contamination  of  the  terrestrial  environ-
ment. In contrast, fish-eating birds showed a
gradual increase in mercury content since
80

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the previous century, suggesting  that the
mercury contamination of water follows the
general  increased  industrial activity (Wal-
lace, etal., 1971).

In 1966, Westermark,  et a/., demonstrated
that  part of the mercury content in bird's
feathers is metallo-organic. In 1967, Noren
and  Westoo  demonstrated  that  almost all
mercury present in fish muscle appears in
the form  of methylmercury (Johnels  and
Westermark, 1969).  Methoxyethylmercury
compounds were substituted for alkylmer-
cury compounds in seed-dressing  formula-
tions after February 1966,  and the relative
amount of dressed seed used for sowing
was also reduced from 80% (prior to 1966) to
12% (1967). These changes  apparently had
no deleterious effect on crop yield. In  1966
and  1967,  the mercury  levels in the feathers
of predatory birds with a terrestrial food
chain abruptly dropped to levels about  50%
above those typical for the previous century
(Wallace,  et a/., 1971).

VI.C. Canada and the United States — In
1967, a limited study of mercury residues in
U.S. foods was conducted by the Food and
Drug Administration as part of the Pesticide
Total Diet Study. Six food classes were  ana-
lyzed by neutron activation analysis, and the
results indicated background level of mercu-
ry in the order of 0.002 to 0.050 ppm. No fur-
ther  testing was performed in this country
until 1970. In 1969, following warnings of
significant mercury pollution in the central
provinces, studies  were initiated by the
Canadian Wildlife Services to define the sit-
uation. Shortly thereafter, several commer-
cial catches of fish (walleye, northern pike,
bass, and  jackfish) taken from Lake Winni-
peg, Cedar Lake, Saskatchewan River, and
Red River in the Province of Manitoba were
detained by the Canadian Federal Depart-
ment of Fisheries  and Forestries, because
they contained < mercury residues ranging
from 5 to  10 ppm.  As a result of concurrent
testing  by Ontario officials,  the  Canadian
Government  publicly embargoed all  com-
mercial fish taken from Lake  Saint  Clair
effective March 23, 1970.

On April 10, 1970, a formal monitoring pro-
gram  was  initiated  by  the United States
Food and Drug Administration in all 17  of its
districts. All  of the  75  known, chlor-alkali
plants in the United States were visited. Ag-
ricultural   run-off  and  other   industrial
sources of pollution were  also  examined
during the investigation. When the industrial
process was  suspected  of  polluting water,
samples of fish were  collected and analyzed
to determine  the  impact of the contamina-
tion on the environment. Any fish  exceeding
the interim guideline level of 0.5 ppm mercu-
ry  in  commercial channels were  recom-
mended  for  seizure (Mercurial  Pesticide
Review Panel Report, 1971).

The majority of the fish analyzed have  been
collected from areas where investigations
have shown  contamination with mercury
wastes. Of 763 composite  samples  of fish
examined by the Food and Drug Administra-
tion, 683 samples  were below 0.5  ppm  mer-
cury,  while 124 were above.  The highest
mercury residue thus far encountered was a
Lake  Onondaga  catfish composite which
was found to contain  4.3 ppm. In areas such
as the Rocky Mountains  with no known pol-
lution  sources, "background"  can  run as
high as 0.2 ppm mercury but averages less
than 0.1 ppm, depending upon the species
(Mercurial  Pesticide  Review Panel Report,
1971).

The Review Panel reached the following ten-
tative conclusions on mercury contamina-
tion of the environment:

(1.) Where  there  are  chlor-alkali  plants,
there is a great possibility of mercury escap-
ing into the environment. Since fish have a
great  propensity  for bioconcentration  of
mercury, the fish level reflects the degree of
pollution of the water.
                                                                                   81

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(2.)The mercury content of fish is related to
the species, the size, locality, and length of
exposure to mercury.
(3.)  Agricultural  runoff from  areas  where
heavy use has been made of mercury-treated
seeds can  result  in residues in fish greater
than 0.5,ppm mercury.

 A systematic survey of wildlife and  animal
 food products  (including  freshwater  and
 marine fish)  has been underway in Canada,
 and the initial results were made available in
 the summer of 1970. At that time,  using neu-
 tron  activation  analysis, elevated levels of
 mercury were  found in several  pheasants
 from Alberta and  in  pike,  pickerel,  and
 whitefish from the Great 'Lakes area. Avian
 products generally contained less than  0.05
 ppm, and most fish (except those from heav-
 ily contaminated areas) averaged 0.2 ppm or
 less. The levels of  mercury found in these
 fishwere omewhat lower than those found by
 other laboratories, and the explanation given
 was that smaller fish were sampled for anal-
 ysis.

In the fall  of 1970,  the United States Food
and Drug Administration found that canned
tuna sold in the United States contained up
to 1.2 ppm mercury (average 0.37  ppm) and
that frozen swordfish ranged from 0.18 to
2.4 ppm (average 0.93). Surprisingly high
levels (25   170 ppm) were also found in liv-
ers of fur seals and sea lions off the western
coast of North America. A 21  member ad
hoc committee  of experts  reviewed  the
FDA's  data  on  mercury contamination in
swordfish and suggested that swordfish con-
sumption be  curtailed in the United States.
In May 1971, the Food and Drug Adminis-
tration issued the statement that the "public
stop eating this fish until and unless the situ-
ation can be remedied."

VI.D. Mercury in Fish — In  Sweden, the
pike contain two to three times more mercu-
ry than do the other fish in the same waters.
This fish is taken as the standard for  black-
listing waters. A body of water is blacklisted
in Sweden when a sample of five pike shows
residues  of  1  ppm or more of mercury  in
most of the five.  If one or two of the five
have a higher level, another sample  may be
requested. Statisticians have advised a sam-
ple of at least 11, but costs would be prohibi-
tive. At present, the judgment is made more
or less  subjectively from the sample  of five.
If residues  are  between 0.2  and  1  ppm,
Swedes are  advised to eat  fish from  these
waters no more often than once a week. The
Swedish action level of 1  ppm is considered
too high, but if 0.5 ppm were the criterion,
as in  the United States  and  Canada, five
times as  many waters would be blacklisted
and monitoring costs would be extravagant
(Nelson,  eta/., 1971).     ,

When  comparing residues  of  mercury for
blacklisting purposes, levels in pike  are ad-
justed to  fit a pike weighing 1  kg., or about
2.2 pounds. This is done, because pike keep
growing and keep increasing  in concentra-
tion of  mercury. The curve of the increase in
the level of mercury tends to flatten in large,'
old  pike, but it does not seem to reach  a
steady  state (Nelson, et a/., 1971).

Fish and  shellfish found dead at Minamata
contained 9  to 24 ppm mercury  on  a wet-
weight  basis. One Swedish  pike was taken
which  contained  17  ppm,  however, pike
have been killed experimentally at  muscle
levels of  mercury of 5 to 9.1 ppm.  Stickel
(Nelson,  et  al.,  1971)  states  that there  is
clearly an overlap between the curves of res-
idue distribution in living wild  pike and ex-
perimentally killed pike.  He  believes that
Swedish  pike have died from mercury poi-
soning  in the wild, and losses were gradual
and unobserved.

The lethal concentration  of mercury  com-
pounds found for various  aquatic organisms
is listed in the appendix.  While such infor-
mation indicates that  mercury  compounds
are remarkably toxic at low concentrations,
it does not define the maximal levels which
should  be avoided  to  maintain a  healthy
82

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aquatic ecosystem. While 60 ppb ethylmer-
cury is lethal to marine phytoplankton, as lit-
tle as 0.1 to 0.6 ppb alklymercury introduced
into seawater will produce a measurable in-
hibition of photosynthesis and  growth. It
appears  that  concentrations  of  mercurial
compounds well below the proposed water-
quality standards of 5 ppb can have a detri-
mental effect on  phytoplankton (Harriss and
White, 1970). The authors also conclude that
the use of organomercurial compounds in
any way that  permits  their discharge  into
natural waters should be stopped as soon as
possible. The  long-term effects of mercury
pollution  below concentrations of  1  ppb
must be determined to establish adequate
water-quality  standards.  In another study,
half of the goldfish continuously exposed to
a concentration of 820 ppb mercuric chloride
died within 7 days, yet  an exposure for only
2 days to 3 ppb mercuric chloride produced a
measurable impairment in learning behavior
(Weir and Mine,  1970).

VI.E. Mercury in Birds — Stickel, in "Haz-
ards of  Mercury"  (Nelson,  et al., 1971),
gives an excellent account of the effect of
mercury on birds in Sweden.

According to Stickel, birds have been seri-
ously affected  by mercury in Sweden. Treat-
ed seed had the  most dramatic effect, while
aquatic contamination  had less sudden and
dramatic effects. The world-wide  ramifica-
tions are just beginning to be known.

The acute toxicity  of methylmercury  to
birds results from levels  about the same as
those toxic for laboratory mammals, around
12 to 20 mg/kg of body  weight. Chronic tests
with birds have been carried out largely with
seed operationally dressed with about 15 to
20  ppm methylmercury.  These  seed killed
pheasants in 29  to 61 days and jackdaws in
26 to 38 days.

Mercury residues in liver-kidney composites
of birds killed experimentally with treated
seed ranged from 30 to 130 ppm for pheas-
ants, 70 to 115 ppm for jackdaws, and 50 to
200  ppm  for magpies.  Muscle  levels in
pheasants ranged from 20 to 45 ppm. Stickel
concludes  that kidney-liver  residues of 30
ppm or more in birds indicated critical expo-
sure and perhaps death; normal levels, by
contrast, are less than 1  ppm. Using these
criteria  in  judging  wild  birds, both those
found dead and those taken alive, more than
half the bird populations of Sweden  were
carrying increased  levels of mercury and
many birds had died outright. Population
declines occurred  in a  number of  species
(Nelson, et a/., 1971).

Stickel reported that Tehning demonstrated
that  pheasants could readily eat enough
dressed  seed to create the observed tissue
levels of mercury and to cause death. Seed
is often  available on the surface, especially
at the turn-around areas at the ends of fields.
The effects of mercury were complicated by
the presence of  aldrin and  dieldrin in the
seed dressing, and the amount of aldrin and
dieldrin in the birds was not determined. The
use of aldrin or dieldrin is no longer legal in
Sweden.

Stickel also reports that while seed-eating
birds were declining, predatory  birds that
fed on them—or on fish—were in a worse
situation.  He states that  all  studies  he has
seen support the view that free and protein-
bound methylmercury acts in the same way
and with equal force (Nelson, eta/., 1971).

Hawks  and  owls   were  hard-hit.   Wild
seed-eaters had liver residues ranging up to
140 ppm, but predatory birds had levels up
to  300 ppm. As  predatory birds are rarely
numerous  and have  relatively low reproduc-
tive rates, they might have been exterminat-
ed over large areas, if the release of mercury
had not been stopped.  However,  since the
ban on  seed dressing with  methylmercury
took force in 1966, goshawks have been re-
covering, and their residues of mercury have
dropped (Nelson, eta/., 1971).
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Stickel reports that the seed-eaters respond-
ed more promptly, and that levels of mercu-
ry in pheasants were back to normal the year
after the ban.  The methoxymethylmercury
dressings which are now used (only when
and  where  needed) are  less toxic and are
much more easily  excreted  than are the
methylmercury dressings.

The  half-life of mercury in birds does not
appear to be excessive by  comparison with
that in mammals. The half-life in chickens is
35 days. Male quail excrete mercury slowly,
while the female excretes it much more rap-
idly due to excretion in eggs. Pheasants have
a relatively rapid loss of mercury.

The  reproduction of birds  has been greatly
reduced by dietary exposure to  mercury.
Hatchability is reduced, but there appears to
be no drop  in egg production. The pheasant
eggs with  demonstrated poor hatchability
contained 1.3 to 2 ppm mercury.

VI.F. Mercury in Farm Animals — There are
a few reported injuries of livestock from the
feeding  of mercury-treated seed  grain.
Loosemore, et a/., (1967), reported experi-
mental results  with pigs fed grain  treated
with 6 ppm  mercury. Pigs which  survived 10
to 21 days on the mercury-treated grain suf-
fered  tubular necrosis of the kidneys, and
their livers contained 60 ppm mercury. Their
kidneys contained 65 ppm mercury.

Trabash (1970) reported condemnation of 7
cattle  carcasses in Oregon, because of mer-
cury content. The  kidneys  of  one of the
animals contained 67 ppm mercury; muscle
ranged from  0.1. to  1.63 ppm among the 7
carcasses.  Kahrs reported  on  a  herd of
swine fed for several weeks a diet one-half
of which consisted of seed grain treated with
methylmercuric dicyandiamide.  Almost all
of this herd of 44 adults and  5 litters of pigs
died within a 3 month feeding period (Mer-
curial Pesticide Review Panel Report).

Westoo (1967) reported that  hens fed grain
treated with  methylmercury lay eggs with
higher mercury content than  those fed grain
treated  with  alkoxyalkyl  mercury  com-
pounds. Tehning (1967) found that hens fed
grain containing 18.4 ppm methylmercury in
half their feed intake laid eggs  with  more
than 20 ppm methylmercury  in the albumin.
Other workers have  reported lower amounts
of methylmercury in eggs of chickens fed
treated grain.
84

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                                     CHAPTER 7
                 THE HAZARDS OF MERCURIAL PESTICIDE USE
Approximately one million pounds of metal-
lic mercury were used in the United States in
1969 in the production of pesticide chemi-
cals. About 85% of this one million pounds
was used in preserving and mildew-proofing
paints while the remainder was used in agri-
culture, the paper and pulp industry, and in
miscellaneous pesticides. The pesticide uses
of mercury  are the  largest  dissipative or
nonrecyclable uses in this country today.

Elemental, inorganic, and organic mercury
are used in pesticides. The organic com-
pounds that have gained importance all have
the general structure R-Hg-X, where R is an
organic radica], alkyl, alkoxyalkyl, or aryl.
The group X is bound to mercury with a bond
more or less  having the character of a salt
and originating from  organic or  inorganic
substances with dissociable hydrogen ions,
e.g., acids, amides, phenols, or thiols. At
present, some hundred combinations of dif-
ferent organic radicals and anions are used
in commercial preparations of mercury  fun-
gicides.

The different compounds of mercury differ
in their solubility, volatility, and their toxici-
ty to man and animals. Therefore, in consid-
eration  of the hazard  of  a particular  use,
both the nature of the compound and the
usage pattern must be considered.

VILA. Cancelled or Suspended Uses

Steps  have already been  taken that have
reduced or eliminated certain uses  of mercu-
ry.

VII.A.I. Paper and Pulp —The  paper and
pulp use fell  sharply in 1965 consequent to
Food  and Drug Administration  action re-
quiring that paper used to wrap food be free
of mercury. Although, the 1969 paper and
 pulp use was above the 1968 level, it was
 only 25% of the 1964 level. This use will be
 reduced to zero as the result of the August 7,
 1970, cancellation of the registered uses  of
 all mercury products bearing the claims  or
 directions for use as  slimicides, algicides,  or
 for use in laundering. These  cancellations
 were based on the potential of these uses to
 result in contamination of water.

VILA.2. Alky/mercury Seed Treatments—As
a result of the poisonings in Alamogordo, N.
Mex., which  resulted from the ingestion of
pork from hogs fed seed treated with cyano
(methylmercuri) guanidine, all registrations of
products containing  this  compound  were
suspended February  18, 1970. On March 4,
 1970, and ad hoc committee  appointed by
the National Academy of Sciences, National
Research  Council recommended  that all
compounds containing  a short chain  alkyl
group bonded chemically to a mercury atom
through a carbon-mercury bond should be
considered lexicologically alike regardless
of the associated anion until proven other-
wise by a  detailed  review of appropriate
data. Accordingly, a notice of suspension of
the registrations containing  alkylmercury
compounds  bearing  directions for use as
 seed treatments was issued March 9, 1970.

VII.A.3. "Zero Tolerance" and "No  Resi-
 due" Registrations —The registrations of
products    containing    hydroxymercuri-
chlorophenol bearing directions for use on
vegetable and field crop seeds,  the registra-
tions of products containing hydroxymercu-
rinitrophenol bearing directions for use on
potatoes and sweet potatoes, and the  regis-
trations of products  containing phenylmer-
curic acetate or phenylmercuric ammonium
acetate bearing directions for use on applies,
cherries, peaches, strawberries, and sugar-
cane were cancelled  by the March  12, 1971,
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PR  Notice.  These  cancellations  were the
result of implementing the recommendations
of a National Academy of Sciences, Nation-
al Research Council Advisory Committee to
abolish "no  residue" and "zero tolerance"
registrations. Registrations are being contin-
ued  on  certain other pesticides  based on
pending  petitions  for  finite  tolerances or
upon request of a Federal Agency.

VII. A.4.  Algicide Use in Swimming Pool —
Aglimycin 200 and Algimycin 300 are prod-
ucts containing phenylmercuric acetate for
the control  of algae  in swimming pools.
These products were first registered in  1962,
under protest,  as  provided in  the Federal
Insecticide, Fungicide, and Rodenticide Act
of 1947.  It was the decision  of the United
States Department of Agriculture that the
registrant had  not  clearly demonstrated the
safety of the products.  Termination of the
registrations was affected in 1964, pursuant
to Public Law 88-305  eliminating registra-
tions under  protest. The firm reapplied for
registration in 1964 with supplemental data.
Questions were raised by the United States
Department of Agriculture, Food and  Drug
Administration, and the Public Health  Serv-
ice regarding the data submitted by the firm
purporting to  show an  adequate  margin of
safety to humans when used  as directed.
The products  were registered in  1965  with
the provision  that specific additional  data
would be submitted. Since that date,  regis-
trant has failed to furnish all the data set
forth by the United States Department of
Agriculture. Notice of  cancellation of the
registrations for Algimycin 200 and Algimy-
cin 300 was made  on July 22, 1969. The re-
gistrant requested  an advisory committee to
review the cancellation action.

VII.E. Currently Registered Uses

In  May  1970,  the Department of  Health,
Education,  and Welfare,  acting  under the
provisions of the Interagency Agreement on
Pesticide Registrations, requested the for-
mation of a registration review panel for the
purpose of considering the current registra-
tions of  mercurial pesticides. As provided
by the Interagency Agreement, the  panel
was  composed  of  representatives of  the
Department of Agriculture, the Department
of Interior, and  the Department of Health,
Education, and Welfare.

The  panel was  dissolved  on  January  20,
1971, following the  transfer of all pesticide
responsibilities  to the Environmental Pro-
tection Agency.  However, the panel submit-
ted their report, although incomplete, so that
it would be available to those responsible for
pesticide regulatory activities.

This report, "A Report  on  the  Mercury
Hazards  in the  Environment," contain no
unified recommendations for  actions to be
taken with the currently registered uses of
pesticides. However,  it does contain recom-
mendations from the  individual panel mem-
bers. Without exception, the members rec-
ommended cancellation of the registrations
of all  alkylmercury  containing pesticides.
The members were also in agreement that
only the registrations for essential uses of
pesticides  containing inorganic  mercury or
arylmercury compounds should be retained.
However,  even these registrations  should
not be retained if the  use poses a water con-
tamination hazard.  Consideration  has been
given this report in the present study.

While it  would be ideal to follow the outline
of uses employed in Chapter 1 of this report,
this was  not done in consideration  of the
human hazards  associated with the  use of
mercurial  pesticides.  Therefore,  the uses
have been categorized under two headings:
VII.B.I. Pesticides Containing Alkylmercury
Compounds, and VII.B.2.  Pesticides Con-
taining Metallic Mercury, Arylmercury or
Inorganic Mercury  Compounds. The human
toxicity  of the  alkylmercuries is discussed
under VII.B.I.  without regard  to the envi-
ronmental  contamination   potentials.  The
 86

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environmental contamination potentials  of
mercurial pesticides are considered in detail
under VII.B.2. before the listing of the spe-
cific pesticide uses. Individual uses will  be
discussed at length where necessary; other-
wise reference will be made to the particular
hazard, if any, which the use involves.
that found in the blood. However, this con-
centration increases with time as the  result
of the conversion of phenylmercury to inor-
ganic mercury in the liver. The concentra-
tion of alkylmercury compounds in the kid-
ney is about  1.0 to  1.4  times that in  the
blood.
VII. B. 1.  Pesticides Con taining A Iky 1m ercu-
ry Compounds — The different members of
the  homologous  series  of  alkylmercury
compounds behave in the same manner and
can cause the same type of poisoning. The
anion of the compounds has no influence on
the biological reaction of mammals but may
influence some  of the physical characteris-
tics of the salt, such as volatility.

The acute toxicity of the alkylmercury com-
pounds is lower than the acute toxicity of
the soluble  inorganic mercury compounds
and of the arylmercury compounds.  How-
ever, the alkylmercury compounds are ab-
sorbed from the  gastrointestinal  tract to a
much greater extent  than are the  inorganic
or arylmercury compounds.

The  greatest physiological distinction  be-
tween the alkyl and aryl or inorganic mercu-
ry compounds is [the distribution of mercury
within the body after single or repeated ad-
ministrations.   Inorganic  mercury   com-
pounds disappear rapidly  from the  blood,
and the  blood  concentrations of mercury
remain low even after repeated administra-
tions. The  arylmercury compounds  disap-
pear  rapidly after a single administration,
but after repeated administrations, there is a
considerable increase in the blood content of
mercury. The  greatest increase  by  far is
caused by the alkylmercury compounds.

Inorganic compounds of mercury give con-
centrations of mercury in  the kidneys of
from 100 to 1,000 times that found  in the
blood.  The arylmercury compounds give
kidney concentrations of from 2 to  100 times
The concentration of  mercury in the  liver
after  inorganic mercury  administration is
from 5 to 20 times that found in the blood.
The arylmercury  compounds give  about 2
times  that  in  the blood.  The alkyl com-
pounds  give a liver concentration of  only
about 0.2 to 0.4 times that in the blood.

The mercury concentration in the  brain after
the administration  of inorganic  mercury
salts is  about equal to the blood concentra-
tion. After the administration of aryl com-
pounds, it  is only  1 to 3%  of that in the
blood.  Alkylmercury  compounds  give a
brain concentration of only about 4 to 6% of
that found in  the blood. However, as the
mercury in the blood is much higher  after
the administration of the alkylmercury com-
pounds, the mercury  retained in the brain
after the administration of this compound is
by far higher than after equivalent amounts
of the other comppunds of mercury.


The placenta is an effective barrier to mercu-
ry derived  from  inorganic or arylmercury
compounds. However, this is not true with
alkylmercury compounds. After the admin-
istration of these compounds, the  mercury
concentrations in  the fetus may reach higher
levels than those  found in the maternal tis-
sues.  The chromosome-damaging and  tera-
togenic  effects of the alkylmercury  com-
pounds  are greater than those of inorganic or
arylmercury compounds.
The alkylmercury compounds are excreted
much more slowly than are the aryl or inor-
ganic mercury compounds. This indicates a
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considerable risk for accumulation of alkyl-
mercury compounds on repeated exposure.

Serious poisonings  and fatalities resulting
from the manufacture  and  handling of the
alkylmercury  compounds  have been  de-
scribed in the literature. Hundreds of people
have been poisoned from the consumption
of wheat treated with  these compounds; an
entire family was poisoned  from the eating
of meat from hogs fed alkylmercury-treated
grain.  The fish which caused the epidemic
poisonings  in Minamata and Niigata con-
tained  this compound as did the seeds which
caused the drastic reduction in the bird pop-
ulations in Sweden. It is the opinion of this
Special Group that  pesticides  containing
alkylmercury compounds can not be labeled
adequately to protect the safety of the pub-
lic. The Group recommends that the regis-
trations for  pesticides  containing alkylmer-
cury compounds  be suspended, because  of
the immininent hazard to human health.

VII. B. 2.  Pesticides  Containing  Metallic
Mercury, Arylmercury or Inorganic Mercu-
ry— The pesticides comprising this catego-
ry are considered on the basis of their poten-
tial for environmental  contamination and on
the basis of the possible effect the particular
use may have on human health.

VII.B.2.1. Pesticidal Mercury and the envi-
ronment—  Mercury resulting from pestici-
da! use may contaminate the soil, water,  or
atmosphere.  Because  of the  volatility  of
mercury and  its  natural circulation in the
environment, mercury  contamination of the
soil or atmosphere will eventually  result  in
water and food residues.

Pesticidal mercury may reach the soil from a
number of sources: from treated seeds  or
grain;  from fall-out following sprayed appli-
cations  to   agricultural and  ornamental
plants; from the treatment of lawns and turf;
from the wash-off of painted structures; and
from the emptying  of  vats  in which bulbs.
corms, textiles, fabrics, fibers, logs, or lum-
ber were treated.

Mercury may reach water  either directly
from one of the  above applications, e.g.,
emptying of vats in which fabrics were treat-
ed. Mercury may also reach the aquatic envi-
ronment bound to soil particles or from the
washing of the atmosphere by rain.


Mercury may become  firmly bound  to the
soil. This phenomenon of mercury adsorp-
tion is intimately related to the type of soil
with which the mercury comes in  contact.
The nature of  the colloidal soil  particles,
whether they are high in organic content or
are of  clay  or sandy composition, affects
adsorption. The solubility  of  the  mercury
compound and the pH of the soil also affects
soil adsorption. The temperature  and the
condition of soil moisture also play an im-
portant role in adsorption (Mrak, 1969). The
affinity of certain soils  for mercury is indi-
cated by the  failure  of mercury applied as
orchard  sprays (phenylmercuric  acetate)
over a period of several years to migrate
below the surface 2 inches; the soil con-
tained 500 or 1,100 ppb mercury depending
on the  number of spray applications (Ross
and Stewart,  1962).

Even in those instances in which mercury is
firmly adsorbed to soil,  water contamination
may result. Mercury  held in the soil may be
carried  by water  with  possible subsequent
contamination of water courses, water sup-
plies, and groundwater. Runoff after either
rainfall  or irrigation  may physically trans-
port particles to which  mercury adheres, or
the water may  leach the pesticide from the
soil particles (Mrak, 1969).

Much has been said about the  natural back-
ground  of mercury in  the environment.
However, it is difficult, if not impossible, to
separate the naturally  occurring  mercury
levels from the levels created  by man. The
 88

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upper limit for the natural release of mercu-
ry due to chemical weathering can be esti-
mated  by comparison with the correspond-
ing figures for sodium. The sodium leached
by weathering is  almost completely carried
to the  sea by rivers, 8 x  107 tons per year
(runoff of rivers, 3.2  x 1013 tons per year;
noncyclic sodium in river waters, 2.5  ppm).
In the  weathered rock masses, the ratio of
mercury to  sodium can be estimated to be
the same as the  ratio  of their lithospheric
abundances (2.8  x 10~6), which yields  an
upper limit of 230 tons per year for leached
mercury. The amount of mercury released is
probably less than this  estimate, because
proportionally more mercury than sodium is
absorbed on clays, hydroxides,  organics,
and so forth (Joensuu, 1971).
Another source of mercury is the burning of
fossil fuels and ores. In order to estimate the
amount of mercury released into the atmos-
phere by the burning of coal, Joensuu ana-
lyzed  samples of  36 American coals by
means of a mercury vapor detector that had
been  modified to eliminate organic vapors
which interfere in the detection process. The
mercury content of the Illinois coal samples
that were  analyzed  contained an average of
180 x 10"9g/g mercury. The author applied a
more  conservative estimate of 1 ppm to the
yearly production of coal and concluded that
about 3,000 tons of  mercury per year are re-
leased to the environment by the burning of
coal.
The burning of fossil fuels by man contrib-
utes more than 13 times as much mercury to
the environment as does the natural weath-
ering process. The use of pesticides contrib-
utes over two times as much mercury to the
environment as does the natural weathering
process.  It is obvious that man  is contribut-
ing a  substantial  amount  to the "natural"
background of mercury, and we* must elimi-
nate all but the essential dissipative uses of
mercury.
VII.B.2.2. Coatings

VII.B.2.2.1. Paints,  Varnishes, and Stains
— This  is a highly significant use of mercu-
ry. In 1969, 720,000 pounds of metallic mer-
cury were used in paint as follows:

 Interior latex 	  45,000 Ib
 Exterior latex  	351,000 Ib
 Exterior oil  	324,000 Ib

Mercurials  are  added  to  interior water-
thinned  (latex)  paints to  prevent  spoilage
during manufacture and in the container dur-
ing storage. The concentration employed for
this use  ranges from 0.015 to 0.02% mercury
as the metal. Solvent-thinned interior paints
do not require the use of mercury for preser-
vation.

Mercurials  are  used  in   exterior water-
thinned  paints both for  preservation in the
container and as a fungicide to minimize dis-
coloration from mold  or mildew growth on
the dry  paint film. For this use, mercury, as
the metal, is used in  the  range of 0.05 to
0.09%. Solvent-thinned  exterior paints may
also   contain  mercury  to  prevent  mold
growth on the dry film.

The  mercury compounds generally used in
paints are:

Phenylmercuric acetate
Phenylmercuric oleate
Diphenyl mercuric dodecenyl succinate
Phenylmercuric propionate
Chlormethoxypropylmercuric acetate

(1) Interior Paints — In order to satisfy the
labeling  requirements  under  the   Federal
Hazardous Substances Labeling Act,  acute
oral and dermal toxicity  studies were carried
out by  Hazleton  Laboratories for the Na-
tional Paint, Varnish,  and Lacquer Associa-
tion.  These studies  indicated  paint  could
contain  up to 0.2% elemental mercury with-
out hazard of acute oral or dermal toxicity or
dermal irritation.
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A  study  was conducted by Goldwater and
Jacobs (1964) to determine the concentration
obtained  in a room painted with paint con-
taining mercury and the effects on the inhab-
itants of  the room. It was  found that a con-
centration of 0.17  mg/m3 of mercury  vapor
was  reached in  90 minutes after  painting.
The  total mercury concentration was of the
order of  0.20 mg/m3 for about 4 1/2 hours.
After 24  hours with no exceptional attempts
at ventilation, the concentration of mercury
decreased to insignificant levels. Some mer-
cury was absorbed by the inhabitants  of the
room, as measured by  comparative excre-
tion  concentrations of mercury in the  urine.
However, the mercury concentration  in the
urine of the test subjects was no greater than
found in  the urine of unexposed "normals."
No  evidence was  found of mercury  expo-
sure or  absorption in a degree that would
constitute a hazard to the painters or  to the
occupants of the room.

As  reported  earlier,  Hirschman,  et a/.
(1963), associated  acrodynia in a 5-year-old
child to the inhalation of mercury vapors in a
freshly painted room.  Miller,  et al. associat-
ed neuromyasthenia in 49 employees to the
exposure of  organic mercury from freshly
painted walls.

(2) Exterior Paints — In  their reply to the
Federal  Register Notice  on Mercury, the
National Paint, Varnish and Lacquer  Asso-
ciation  stated  that mercury  is lost  from
painted exterior surfaces.  The majority of
this  is washed from the painted surface and
goes into the ground. The statement is made
that  the  mercury (phenylmercury) is firmly
bound to the soil and is not removed by dilu-
tion  with water or saline solution. The  Asso-
ciation therefore contends that the mercury
thus  removed  from the  painted  surfaces
does not  enter the aquatic eco system.

The  thesis that mercury thus bound will not
eventually end  up in  water  is untenable.
Mrak (1969) stated that because of the tight
binding characteristics of pesticide residues
to soil particles, the general pollution  of
water  by  pesticides  occurs  through  the
transport of soil particles to which the resi-
due is attached. Soil residues  may, there-
fore, be a cause for concern; since they may
reach man by a number of routes; uptake
from soil by consumable crops; leaching into
water supplies;  and volatilization into the
air.

The  National Paint, Varnish, and Lacquer
Association states that there are no substi-
tutes now available for mercury for the pres-
ervation of paint; and without preservatives,
latex  paints will spoil during manufacture.
The Association states that it will  require 1
year  to  develop a suitable  substitute for
mercury  in interior  paint and 3 years to de-
velop a substitute for mercury for exterior
paint.

Paint manufacturers do recycle wash water
and use it in the preparation of other batches
of paint,  thus the manufacture of paint does
not contribute to mercury pollution.

This is a highly significant use of mercury. It
is the largest dissipative use of mercury in
the United States today.

There are latex paints on the market which
contain preservatives other  than  mercury.
Therefore, there seem to be suitable substi-
tutes  for mercury  in  the  preservation  of
paint.

(3) Ship  bottom antifouling  paints — This
use  constitutes  a direct contamination of
water with mercury. This  contamination
may result from the slow leaching of mercu-
ry from the painted ship bottom or from dust
and chips from  the ship bottom when it is
scraped  and  sanded  prior  to repainting.
Mercury may be released in acutely  toxic
amounts  during  this  sanding operation.
Schrager (1964)  reported on  the occurrence
of tubular  necrosis in a 2-year-old child  ex-
90

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posed to mercury during  the sanding of a
boat bottom. There  are safer and  equally
effective substitutes available for this use.

VII.B.2.2.2.  Other Coatings — Adhesives,
Starches, Glues,  Emulsions, etc. — These
uses include glues for labels of cans, wallpa-
per paste,  glues  for various fabrics,  spac-
kling compounds, joint cements. These  are
in liquid or dry form  which are ultimately to
be applied by dispersion in  water.  Phenyl-
mercuric acetate and  phenylmercuric am-
monium acetate are used for preservation of
the products  at levels of 45 to 250 ppm. For
mildew control in finished  products, phenyl-
mercuric acetate  or phenylmercuric ammo-
nium acetate  levels range from 3,500 to 15,-
000 ppm.

RECOMMENDATION:

(a) Interior paints — The Committee recom-
mends the cancellation of  this use, because
of the  environmental contamination poten-
tial. The Committee believes there is insuffi-
cient evidence to consider this use as  a  hu-
man health hazard.

(b)  Exterior paints — The Committee rec-
ommends cancellation of this use, because
of environmental  contamination.

(c)  Shipbottom antifouling  paints  —  The
Committee recommends cancellation of this
use, because  of direct contamination of wa-
ter with mercury, and because of acute tox-
icity to humans.

(d)  The  Committee  considers  the  use of
mercury in adhesives, starches, glues, emul-
sions, etc., to be equivalent to paint use and
recommends  that the registrations be can-
celled.

VII.B.2.3. Fabrics and Textiles — Mercurial
pesticides are used as mildew preventatives
in fabrics and textiles.
Indoor  Use — These  fabrics are used as
bedding, dust cloths, mops, rugs, shoe lin-
ings, etc. As such articles will come into* inti-
mate contact with humans.

Outdoor Use — These fabrics and  textiles
are used as awnings, sails, tarpaulins, etc.


RECOMMENDATION:

The Committee recommends that all regis-
trations be cancelled.

VII.B.2.4. Fibers and cordage — These uses
include the interior components of furniture,
mattresses,  pillows,  etc.,  air-conditioner
filters, and rope and twine.

The use in interior components of furniture,
mattresses, pillows, etc., and the use in air-
conditioner filters may act to increase the
body burden of mercury. These uses present
a potential human health hazard.

The uses in rope and  twine constitute  an
environmental hazard.
RECOMMENDATION:

The Committee recommends cancellation of
the uses on interior components of furni-
ture, mattresses, pillows, and the use in air-
conditioner filters.

The Committee recommends cancellation of
the registrations in rope and twine.

VII.B.2.5.  Food, Feed, and Tobacco Crops
— These uses of mercury result in a direct
contamination of the environment. Alterna-
tives are available. (See Chapter 1).
RECOMMENDATION:

Cancel the food,  feed, and tobacco crop
uses of mercury.
                                                                                   91

-------
VII.B.2.6.  Feed  Containers  —  These are
sacks, seed bins,  and containers for treated
seeds subject to diversion to food and feed
use. This use presents not only an environ-
mental contamination hazard  but also a po-
tential human health hazard.

RECOMMENDATION:

Cancel this use of mercury.

VII.B.2.7.  Humans — These registrations
are for Mild Mercurial Ointment (Blue Oint-
ment) as a treatment for pediculosis pubis.
This  product contains  elemental mercury
which is absorbed through the intact skin.
Fatal accidents  have been reported in which
the entire body surface  was  covered  with
Blue Ointment.

RECOMMENDATION:

Cancel  the registrations for Mild  Mercurial
Ointment as a treatment  for pediculosis pu-
bis.

VII.B.2.8. Ornamental Plants

1. Bulbs and Conns —The mercurial fungi-
cides are used  to control root,  stem,  and
bulb  rots.  The registrations  include alkyl,
aryl,  and inorganic mercury compounds. In
Washington and Oregon, bulb dipping vats
have capacities up to 10,000 gallons. The
drainage of the vats after treatment of the
bulbs and corms has been completed poses a
significant potential for contamination of the
soil and water.

2.  Cuttings  —  Only  alkylmercury com-
pounds are employed in this use.

3.  Flowering and Foliage Plants — These
uses are directly on the foliage of the plants
or on the soil in which they are planted. This
usage pattern provides  a direct contamina-
tion of the environment.
4.  Trees and Shrubs — This use provides a
direct  contamination  of the  environment
with mercury.

RECOMMENDATION:

Cancel the registrations  for the use of mer-
curials on ornamental plants.

VII.B.2.9.  Paper— Mercurials are used for
moldproofing paper, paperboard, and wall-
paper. This use provides a direct contamina-
tion of the environment with mercury.

RECOMMENDATION:

Cancel the registrations  for the use of mer-
curials in paper.

VII.B.2.10. Plastics — Mercurials are used
as fungistats in the plastic films. The use of
plastics thus  treated  range from garbage
bags, shower  curtains, to almost any non-
food use of plastics. Garbage bags treated
with mercury are often misused for the stor-
age of foods.
RECOMMENDATION:

Cancel the registrations  for the use of mer-
curials in plastics.

VII.B.2.11. Rubber — The use of mercurials
in rubber is similar to the use in plastics.

RECOMMENDATION:

Cancel the registrations  for the use of mer-
curials in rubber.

VII.B.2.12. Sanitizers— This  category in-
cludes impregnated dust cloths  and floor
wax. Mercury from this usage pattern will
eventually enter the sanitary sewers.

RECOMMENDATION:

Cancel the registrations  for the use of mer-
curial pesticides in sanitizers.
92

-------
VII.B.2.13. Seed  Treatments — Petitions
for tolerance are pending for some  uses of
mercurial  pesticides  as  seed  treatments.
Substitutes are available for all uses except
for stinking smut on wheat and striped smut
on barley.

RECOMMENDATION:

Cancel all registrations for use as seed treat-
ment except for stinking smut on wheat and
stripped smut on barley.

VII.B.2.14. Tanneries  — Mercurials are
employed in  the tanning  process as fungi-
stats. The liquor from this process  is  a po-
tential contaminant of the environment.

VII.B.2.15. Wood — Mercurial pesticides
are used to  prevent sap stain in  freshly
sawed logs  and lumber and as a preservative
of wood against fungi. These uses are a di-
rect contamination of the  environment with
mercury.

RECOMMENDATION:

Cancel  the use of mercurial pesticides as
preservatives for wood against sap stain and
fungi.

VII.B.2.16. Sterilization of Dental and Sur-
gical Instruments —  The  solution in which
instruments are sterilized is discarded into
the sanitary  sewage  system  and contami-
nates water with mercury.

RECOMMENDATION:

Cancel the  uses of mercurial pesticides for
the sterilization of dental and surgical instru-
ments.
VII.B.2.17.  Surfaces  — As  fungistats  on
commercial, institutional and household sur-
faces such as cabinets, floors,  walls, ceil-
ings, garbage cans, lockers, masonry, tile,
refrigerator and  other hard surfaces; blan-
kets, canvas goods, carpets, clothing, cubi-
cle curtains, hampers, laundry bags, leather
goods, linens, mattresses, uniforms, uphol-
stery and similar  porous  surfaces. These
uses bring mercury into intimate contact
with humans  and also provide a contamina-
tion of the environment.

RECOMMENDATION:

Cancel the uses  of  mercurial pesticides  on
environmental surfaces.

VII.B.2.18. Miscellaneous

1. Seam and Bedding Compounds — These
compounds are  used  in boat-building and
provide a direct contamination of water.

2.  Broomcorn — Mercurial pesticides are
used in the process of dying broomcorn as a
fungistatic agent to prevent discoloration.

3.  Cellulose Sponges — Cellulose sponges
are  dipped in solutions of  phenylmercuric
acetate for preservation. Disposal of these
solutions after use will provide a direct con-
tamination of the environment.

4.  Milk  and  Urine Samples —  Mercuric
chloride is added to milk and urine samples
as a preservative. Disposal of these samples
will provide a direct contamination of water.

RECOMMENDATION:

Cancel the registrations of  mercurial pesti-
cides for the above uses.
                                                                                   93

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