Glyphosate Fact Sheets: Part 1 and Part 2

Glyphosate, Part 1: Toxicology

by Caroline Cox
Journal of Pesticide Reform, Volume 15, Number
3, Fall 1995. Northwest Coalition for
Alternatives to Pesticides, Eugene, OR.

Introduction

Glyphosate is a broad-spectrum herbicide widely used to kill unwanted plants both in

agriculture and in nonagricultural landscapes. Estimated use in the U.S. is between 19 and 26
million pounds per year.

Most glyphosate-containing products are either made or used with a surfactant, chemicals
that help glyphosate to penetrate plant cells.

Glyphosate-containing products are acutely toxic to animals, including humans. Symptoms

include eye and skin irritation, cardiac depression, gastrointestinal pain, vomiting, and
accumulation of excess fluid in the lungs. The surfactant used in a common glyphosate
product (Roundup) is more acutely toxic than glyphosate itself; the combination of the two is
yet more toxic.

In animal studies, feeding of glyphosate for three months caused reduced weight gain,
diarrhea, and salivary gland lesions. Lifetime feeding of glyphosate caused excess growth and
death of liver cells, cataracts and lens degeneration, and increases in the frequency of thyroid,
pancreas, and
liver tumors.

Glyphosate-containing products have caused genetic damage in human blood cells, fruit flies,
and onion cells.

Glyphosate causes reduced sperm counts in male rats, a lengthened estrous cycle in female
rats, and an increase in fetal loss together with a decrease in birth weights in their offspring.

It is striking that laboratory studies have identified adverse effects of glyphosate or

glyphosate-containing products in all standard categories of toxicological testing.

Two serious cases of fraud have occurred in laboratories conducting toxicology and residue
testing for glyphosate and glyphosate-containing products.

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Advertised as herbicides that can "eradicate weeds and unwanted grasses effectively with a
high level of environmental safety,"1 glyphosate-based herbicides can seem like a silver
bullet to those dealing with unwanted vegetation. However, an independent, accurate
evaluation of their health and environmental hazards can draw conclusions very different than
those presented by these advertisements. The following summary of glyphosate's hazards is
intended to serve that purpose. It will appear in two parts: Part 1 discusses the toxicology of
glyphosate, its metabolites, and the other ingredients of glyphosate products and Part 2 will
discuss human exposure to glyphosate and its ecological effects.

Glyphosate, N-(phosphonomethyl) glycine (Figure 1), is a post-emergent, systemic, and

non-selective herbicide used to kill broad-leaved, grass, and sedge species.2 It has been
registered as a broad spectrum herbicide in the U.S. since 1974 and is used to control weeds
in a wide variety of agricultural, lawn and garden, aquatic, and forestry situations.3

Most glyphosate herbicides contain the isopropylamine salt of glyphosate. A related

chemical, the sodium salt of glyphosate, acts as a growth regulator in sugar cane and peanuts
and is marketed for that purpose. The monoammonium salt of glyphosate is also marketed as
an herbicide and growth regulator.4

Glyphosate products are manufactured by Monsanto Company worldwide. The herbicide is

marketed under a variety of trade names: Roundup (including Roundup D-Pak, Roundup
Lawn and Garden Concentrate, and Roundup Ready-to-Use) and Rodeo are the most
common U.S. trade names.2 The sodium salt is sold as Quotamaster. The monoammonium
salt is sold as Deploy Dry.2 Other brand names used for the isopropylamine salt are Accord,5
Vision, Ranger, and Sting.2

As an herbicidal compound, glyphosate is unusual in that essentially no structurally related

compounds show any herbicidal activity.6

Use

Glyphosate is the eighth most commonly used herbicide in U.S. agriculture and the second
most commonly used herbicide in nonagricultural situations. Estimated annual use according
to
the U.S. Environmental Protection Agency (EPA) is between 15 and 20 million pounds in
agriculture and between 4 and 6 million pounds elsewhere.7 The largest agricultural uses are
in the production of soybeans, hay and pasture, corn, and oranges.4

About 25 million applications per year are made in U.S. households; most of these are made
on lawns or outdoor areas where a total vegetation kill is wanted.8

In California, where pesticide use reporting is more comprehensive than in other states, about
3.4 million pounds were used in 1992; about 25 percent of this was used along rights-of-way,
while 15 percent was used on almonds and 10 percent was used on grapes.9

Mode of Action

The mode of action of glyphosate is "not known at this time,"4 according to EPA. However,
"herbicidal action probably arises from the inhibition of the biosynthesis of aromatic amino
acids."10 These amino acids (phenylalanine, tyrosine, and tryptophan) are used in the
synthesis of proteins and are the essential for growth and survival of most plants. One
particular enzyme important in aromatic amino acid synthesis, called
5-enolpyruvylshikimate-3-phosphate synthase, is inhibited by glyphosate.10 Glyphosate also
"may inhibit or repress"4 two other enzymes, chlorismate mutase and prephrenate hydratase,
involved in other steps of the synthesis of the same amino acids. These enzymes are all part
of what is called the shikimic acid pathway, present in
higher plants and microorganisms but not in animals.11

Two of the three aromatic amino acids (tryptophan and phenylalanine) are essential amino
acids in the human diet because humans, like all higher animals, lack the shikimic acid
pathway, cannot synthesize these amino acids, and rely on their foods to provide these
compounds. Tyrosine is synthesized in animals through another pathway.12

Glyphosate can affect enzymes not connected with the shikimic acid pathway. In sugar cane,
it reduces the activity of one of the enzymes involved in sugar metabolism, acid invertase.
This reduction appears to be mediated by auxins, plant hormones.13

Glyphosate also affects enzyme systems found in animals and humans. In rats, injection into
the abdomen decreases the activity of two detoxification enzymes, cytochrome P-450 and a
monooxygenase, and decreases the intestinal activity of the enzyme aryl hydrocarbon
hydroxylase (another detoxification enzyme).14

"Inert" Ingredients in Glyphosate-containing Products

Virtually every pesticide product contains ingredients other than what is called the "active"
ingredient(s), those designed to provide killing action. Their purpose is to make the product
easier to use or more efficient. These ingredients are called "inert," although they are often
not biologically, chemically, or toxicologically inert. In general, they are not identified on the
label of the pesticide product.

In the case of glyphosate products, many "inerts" have been identified. Roundup contains a
polyethoxylated tallowamine surfactant (usually abbreviated POEA), related organic acids of
glyphosate, isopropylamine, and water. Both Rodeo and Accord contain glyphosate and
water.15 (However, label instructions usually require adding a surfactant during use.15) See
"Toxicology of 'Inert' Ingredients of Glyphosate-containing Products," p. 17, for basic
information about these "inert" ingredients.

Many of the toxicology studies that will be summarized in this factsheet have been conducted
using glyphosate, the active ingredient, alone. Some have been conducted with commercial
products containing glyphosate and "inert" ingredients. When toxicology testing is not done
with the product as it is actually used, it is impossible to accurately assess its hazards.

We will discuss both types of studies, and will identify insofar as is possible exactly what
material was used to conduct each study.

Acute Toxicity to Laboratory Animals

Glyphosate's acute oral median lethal dose (the dose that causes death in 50 percent of a
population of test animals; LD50) in rats is greater than 4,320 milligrams per kilogram
(mg/kg) of body weight. This places the herbicide in Toxicity Category III (Caution).4 Its
acute dermal toxicity (dermal LD50) in rabbits is greater than 2,000 mg/kg of body weight,
also Toxicity Category III.4

If animals are given glyphosate in other ways, it is much more acutely toxic. When given
intraperitoneally (the dose applied by injection into the abdomen), glyphosate is between 10
and 20 times more toxic to rats (with an LD50 between 192-467 mg/kg)2,16 than it is when
given orally. Intraperitoneal injection also caused fever, cessation of breathing, and
convulsions.17 While this kind of exposure is not one that would be encountered under
conditions of normal use, these studies indicate the kinds of effects glyphosate can potentially
cause in mammals.

Commercial glyphosate-containing products are more acutely toxic than glyphosate alone.
Two recent (1990 and 1991) studies compared the amount of Roundup required to cause
death in rats with the amount of either glyphosate alone or POEA alone that would cause
death. The studies found that in combination, the amount of glyphosate and POEA required
to kill was about 1/3 of a lethal dose of either compound separately. The Roundup
formulation tested was also more toxic than POEA alone.18,19

As with glyphosate alone, glyphosate-containing products are more toxic when administered
other ways than orally. Inhalation of Roundup by rats caused "signs of toxicity in all test
groups,"20 even at the lowest concentration tested. These signs included a dark nasal
discharge, gasping, congested eyes, reduced activity, hair standing erect,21 and body weight
loss following exposure.20 Lungs were red or blood-congested.21 The dose required to cause
lung damage and mortality following pulmonary administration of Roundup Lawn and
Garden Concentrate or Roundup-Ready-to-Use (the glyphosate product is directly forced into
the trachea, the tube carrying air into the lungs) was only 1/10 the dose causing damage
through oral administration.18

Effects on the Circulatory System: When dogs were given intravenous injections of
glyphosate, POEA, or Roundup so that blood concentrations were approximately those found
in humans who ingested glyphosate, a variety of circulatory effects were found. Glyphosate
increased the ability of the heart muscle to contract. POEA reduced the output of the heart
and the pressure in the arteries. Together (Roundup), the result was cardiac depression.22

Eye Irritation: Glyphosate is classified as a mild eye irritant by EPA, with effects lasting up
to seven days4 although more serious effects were found by the World Health Organization.
In two of the four studies they reviewed, glyphosate was "strongly irritating"2 to rabbits' eyes
and a third test found it "irritating."2 In tests of glyphosate-containing products, all eight
products tested were irritating to rabbit eyes, and four of the products were "strongly" or
"extremely" irritating.2

Skin Irritation: Glyphosate is classified as a slightly irritating to skin. Roundup is a

"moderate skin irritant" and causes redness and swelling on both intact and abraded rabbit
skin. Recovery can take more than two weeks.20
 Acute Toxicity to Humans

The acute toxicity of glyphosate products to humans was first widely publicized by
physicians in Japan who studied 56 cases of Roundup poisoning. Most of the cases were
suicides or attempted suicides; nine cases were fatal. Symptoms of acute poisoning in
humans included gastrointestinal pain, vomiting, excess fluid in the lungs, pneumonia,
clouding of consciousness, and destruction of red blood cells.23 They calculated that the
mean amount ingested in the fatal cases was slightly more than 200 milliliters (about 3/4 of a
cup). They believed that POEA was the cause of Roundup's toxicity.23 More recent reviews
of glyphosate poisoning incidents have found similar symptoms, as well as lung congestion
or dysfunction,24-26, erosion of the gastrointestinal tract,24,26 abnormal
electrocardiograms,26 massive gastrointestinal fluid loss,27 low blood pressure,23,26 and
kidney damage or failure.24,25,27

Smaller amounts of Roundup also cause adverse effects. In general these include the skin or
eye irritation documented in animal studies, as well as some of the symptoms seen in humans
following ingestion. For example, rubbing of Roundup in an eye caused swelling of the eye
and lid, rapid heartbeat, palpitations, and elevated blood pressure. Wiping the face with a
hand that had contacted leaky Roundup spray equipment caused a swollen face and tingling
of the skin. Accidental drenching with Roundup (horticultural strength) caused recurrent
eczema of the hands and feet lasting two months.25

Different symptoms have been observed when a different type of exposure has occurred. In
Great Britain, a study compared the effects of breathing dust from a flax milling operation
that used flax treated with Roundup with the effects of dust from untreated flax. Treated flax
dust caused a decrease in lung function and an increase in throat irritation, coughing, and
breathlessness.28

Subchronic Toxicity

Experiments in which glyphosate was fed to laboratory animals for 13 weeks showed a
variety of effects. In experiments conducted by the National Toxicology Program (NTP),
microscopic salivary gland lesions were found in all doses tested in rats (200 - 3400 mg/kg
per day) and in all but the lowest dose tested in mice (1,000-12,000 mg/kg per day). Both the
parotid and submandibular salivary glands were affected in rats; in mice the lesions were
confined to the parotid gland. Based on further experiments, NTP concluded the lesions were
mediated by the adrenal hormone adrenalin.29

The NTP study also found evidence of effects on the liver: increases in bile acids as well as
two liver enzymes were found in both males and females. Other effects found in this study
were reduced weight gain in male and female rats and mice; diarrhea in male and female rats;
and changes in the relative weights of kidney, liver and thymus in male rats and mice.29

Other subchronic laboratory tests found decreased weight gains (using doses of 2500 mg/kg
per day)30 along with an increase in the weights of brain, hearts, kidney, and livers in mice.2
In rats, blood levels of potassium and phosphorus increased at all doses tested (60-1600
mg/kg/day) in both sexes. There was also an increase in pancreatic lesions in males.4
As in acute toxicity tests, glyphosate-containing products are more toxic than glyphosate
alone in subchronic tests. In a 7 day study with calves, 790 mg/kg of Roundup caused labored
breathing, pneumonia, and death of 1/3 of the animals tested. At lower doses decreased food
intake and diarrhea were observed.2

Chronic Toxicity

Glyphosate is also toxic in long-term studies. The following effects were found in lifetime
glyphosate feeding studies using mice: decreased body weight, excessive growth of particular
liver cells, death of the same liver cells, and chronic inflammation of the kidney. Effects were
significant only in males and at the highest dose tested (about 4800 mg/kg of body weight per
day). In females, excessive growth of some kidney cells occurred.31 At a lower dose (814
mg/kg of body weight per day) excessive cell division in the urinary bladder occurred.2

Lifetime feeding studies with rats found the following effects: decreased body weight in
females; an increased incidence of cataracts and lens degeneration in males; and increased
liver weight in males. These effects were significant at the highest dose tested (900-1200
mg/kg of body weight per day).4 At a lower dose (400 mg/kg of body weight per day)
inflammation of the stomach's mucous membrane occurred in both sexes.2

Carcinogenicity

The potential of glyphosate to cause cancer has been a controversial subject since the first
lifetime feeding studies were analyzed in the early 1980s. The first study (1979-1981) found
an increase in testicular interstitial tumors in male rats at the highest dose tested (30 mg/kg of
body weight per day).32 as well as an increase in the frequency of a thyroid cancer in
females.33 The second study (completed in 1983) found dose-related increases in the
frequency of a rare kidney tumor in male mice.34 The most recent study (1988-1990) found
an increase in the number of pancreas and liver tumors in male rats together with an increase
of the same thyroid cancer found in the 1983 study in females.35

All of these increases in tumor incidence are "not considered compound-related"35 according
to EPA. In each case, different reasons are given for this conclusion. For the testicular
tumors, EPA accepted the interpretation of an industry pathologist who said that the
incidence in treated groups (12 percent) was similar to those observed in other control (not
glyphosate-fed) rat feeding studies (4.5 percent).36 For the thyroid cancer, EPA stated that it
was not possible to consistently distinguish between cancers and tumors of this type, so that
the incidences of the two should be considered together. The combined data are not
statistically significant.33 For the kidney tumors, the registrants reexamined slides of kidney
tissue, finding an additional tumor in untreated mice so that statistical significance was lost.
This was despite a memo from EPA's pathologist stating that the lesion in question was not
really a tumor.34 For the pancreatic tumors, EPA stated that there was no dose-related trend
and no progression to malignancy. For the liver tumors and the thyroid tumors, EPA stated
that pairwise comparisons between treated and untreated animals were not statistically
significant and there was no progression to malignancy.35
EPA concluded that glyphosate should be classified as Group E, "evidence of
non-carcinogenicity for humans."35 They added that this classification "is based on the
available evidence at the time of evaluation and should not be interpreted as a definitive
conclusion that the agent will not be a carcinogen under any circumstances." 35 From a
public health perspective, the results of the laboratory tests leave many questions
unanswered. An EPA statistician wrote in a memo concerning one of the carcinogenicity
studies, "Viewpoint is a key issue. Our viewpoint is one of protecting the public health when
we see suspicious data."36 Unfortunately, EPA has not taken that conservative viewpoint in
its assessment of glyphosate's cancer-causing potential.

There are no studies available to NCAP evaluating the carcinogenicity of Roundup or other
glyphosate-containing products. Without such tests, the carcinogenicity of
glyphosate-containing products is unknown.

Mutagenicity

Laboratory studies of a variety of organisms have shown that glyphosate-containing products

cause genetic damage:

* In fruit flies, Roundup and Pondmaster (an aquatic herbicide consisting of glyphosate and a
trade secret surfactant)37 both increased the frequency of sex-linked, recessive lethal
mutations. (These are mutations that are usually visible only in males because two damaged
genes are required in order to be expressed in females.) In this study, the frequency of lethal
mutations was between 3 and 6 times higher in fruit flies that had been exposed to glyphosate
products during their larval development than in unexposed flies.38

* A laboratory study of human lymphocytes (one type of white blood cell) showed an
increase in the frequency of sister chromatid exchanges following exposure to high doses of
Roundup.39 (Sister chromatid exchanges are exchanges of genetic material during cell
division between members of a chromosome pair. They result from point mutations.)

* In Salmonella bacteria, Roundup was weakly mutagenic at high concentrations. In onion

root cells, Roundup caused an increase in chromosome aberrations.40

Glyphosate alone has rarely caused genetic damage in laboratory tests. None of the
mutagenicity studies required for registration of glyphosate have shown it to be mutagenic.
Tests included studies of mutations in hamster ovary cells, bacteria, and mouse bone marrow
cells.4 Glyphosate was also not mutagenic in other studies of rats, mice,2 and onion cells40
but caused chromosome stickiness and fragmentation in water hyacinth root cells.41

Reproductive Effects

Laboratory studies have demonstrated a number of effects of glyphosate on

reproduction,including effects on mothers, fathers, and offspring.

In rat feeding studiess, glyphosate reduced sperm counts (at the two highest doses tested)
andlengthened the estrous cycle, how often a female comes into heat (at the highest dose
tested).29 Other effects on mother rats in laboratory tests include soft stools, diarrhea,
breathing rattles, red nasal discharge, reduced activity, growth retardation, decreased body
weights, and increased mortality.2 Effects on offspring included an increase in fetal loss, a
decrease in the number of embryos successfully implanted into the uterus, a decrease in the
number of viable fetuses, a slight decrease in litter size, a decrease in fetal and pup weights,
and an increase in problems with breast bone formation.2 Effects were observed at the
highest doses tested (1500 and 3500 mg/kg of body weight per day).2

In a study of rabbits using doses that were lower than those used in the rat studies above,
glyphosate caused diarrhea, nasal discharge, and death in mothers.2 The only effect on
offspring was a decrease in fetal weight in all treated groups.42

A study in which glyphosate was fed to rats for three generations after which the offspring
were examined for birth defects found kidney damage at a relatively low dose (30 mg/kg of
body weight). However, a second study (only two generations long) did not find similar
effects, and EPA called the damage in the first study "spurious."4 From a public health
perspective, however, a new three generation study is crucial.

Toxicology of Glyphosate's Major Metabolite

In general, studies of the breakdown of glyphosate find only one

metabolite,aminomethylphosphonic acid (AMPA).2 (See Figure 5.) Although AMPA has
low acute toxicity (its LD50 is 8,300 mg/kg of body weight in rats)20 and is only slightly
irritating to eyes,43 it causes a variety of toxicological problems. In subchronic tests on rats,
AMPA caused decreased weight gain in males; an increase in the acidity of urine in both
males and females; an increase in the activity of an enzyme, lactic dehydrogenase, in both
sexes; a decrease in liver weights in males at all doses tested; and excessive cell division in
the lining of the urinary bladder and in part of the kidney in both sexes.20 AMPA is much
more persistent than glyphosate; studies in eight states found that the half-life in soil (the time
required for half of the original concentration of a compound to break down or dissipate)
were between 119 and 958 days.2

Quality of Toxicology Testing

Tests done on glyphosate to meet registration requirements have been associated with
fraudulent practices.

Laboratory fraud first made headlines in 1983 when EPA publicly announced that a 1976
audit had discovered "serious deficiencies and improprieties" in toxicology studies conducted
by Industrial Biotest Laboratories (IBT).44 Problems included "countless deaths of rats and
mice that were not reported," "fabricated data tables," and "routine falsification of data."44

IBT was one of the largest laboratories performing tests in support of pesticide
registrations.44 About 30 tests on glyphosate and glyphosate-containing products were
performed by IBT, including 11 of the 19 chronic toxicology studies.45 A compelling
example of the poor quality of IBT data comes from an EPA toxicologist who wrote, "It is
also somewhat difficult not to doubt the scientific integrity of a study when the IBT stated
that it took specimens from the uteri (of male rabbits) for histopathological examination."46
(Emphasis added.)
In 1991, laboratory fraud returned to the headlines when EPA alleged that Craven
Laboratories, a company that performed contract studies for 262 pesticide companies
including Monsanto, had falsified test results.47 "Tricks" employed by Craven Labs included
"falsifying laboratory notebook entries" and "manually manipulating scientific equipment to
produce false reports."48 Roundup residue studies on plums, potatoes, grapes, and sugarbeets
were among the tests in question.49

The following year, the owner/president of Craven Laboratories and three employees were
indicted on 20 felony counts. A number of other employees agreed to plead guilty on a
number of related charges.50 The owner was sentenced to five years in prison and fined
$50,000; Craven Labs was fined 15.5 million dollars, and ordered to pay 3.7 million dollars
in restitution.48

Although the tests of glyphosate identified as fraudulent have been replaced, these practices
cast shadows on the entire pesticide registration process.

References

1. Monsanto, the Agricultural Group. Undated. Roundup into the twenty-first century. St.
Louis, MO.

2. World Health Organization, United Nations Environment Programme, the International

Labour Organization. 1994. Glyphosate. Environmental Health Criteria #159. Geneva,
Switzerland.

3. U.S. Environmental Protection Agency. 1986. Pesticide fact sheet: Glyphosate. No. 173.
Washington, D.C.: Office of Pesticide Programs. (June.)

4. U.S. EPA. Office of Pesticide Programs. Special Review and Reregistration Division.
1993. Reregistration eligibility decision (RED): Glyphosate. Washington, D.C. (September.)

5. Monsanto Company Agricultural Products. 1992. Accord label. St. Louis, MO.
(December 1.)

6. Carlisle, S.M. and J.T. Trevors. 1988. Glyphosate in the environment. Water, Air, and Soil
Pollution 39:409-420.

7. Aspelin, A.L. 1994. Pesticide industry sales and usage: 1992 and 1993 market estimates.
U.S. EPA. Office of Prevention, Pesticides and Toxic Substances. Office of Pesticide
Programs. Biological and Economic Analysis Division. Washington, D.C. (June.)

8. Whitmore, R.W., J.E. Kelly, and P.L. Reading. 1992. National home and garden pesticide
use survey. Final report, Vol. 1: Executive summary, results, and recommendations. Research
Triangle Park, NC: Research Triangle Institute.

9 California Environmental Protection Agency. Dept. of Pesticide Regulation. Information

Services Branch. 1994. Pesticide use report: Annual 1992. Indexed by chemical.
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10. Cremlyn, R.J. 1991. Agrochemicals: Preparation and mode of action. Chichester, U.K:
John Wiley & Sons. Pp.257-258.

11. Gilchrist, D.G. and T. Kosuge. 1980. Aromatic amino acid biosynthesis and its
regulation. In Miflin, B.J. (ed.) The biochemistry of plants. New York: Academic Press. Pp.
507-513

12. Metzler, D.E. 1977. Biochemistry: The chemical reactions of living cells. Pp. 849-850.
New York, NY: Academic Press.

13. Su, L.Y. et al. 1992. The relationship of glyphosate treatment to sugar metabolism in
sugarcane: New physiological insights. J. Plant Physiol. 140:168-173.

14. Hietanen, E., K. Linnainmaa, and H. Vainio. 1983. Effects of phenoxy herbicides and
glyphosate on the hepatic and intestinal biotransformation activities in the rat. Acta Pharma.
et Toxicol. 53:103-112.

15. U.S. Dept. of Agriculture. Forest Service. Pacific Northwest Region. 1994. Glyphosate
herbicide information profile. (October.)

16. Olorunsogo, O.O., E.A. Bababunmi, and O. Bassir. 1977 Proc. 1st Intern. Cong. of
Toxicol. (Toronto, Canada). Cited in Olorunsogo, O.O., E.A. Bababunmi, and O. Bassir.
1979. Effect of glyphosate on rat liver mitochondria in vivo. Bull. Environ. Contam. Toxicol.
22:357-364.

17. Olorunsogo, O.O. 1976. Ph.D. thesis, University of Ibadan, Ibadan, Nigeria. Cited in
Olorunsogo, O.O., E.A. Bababunmi, and O. Bassir. 1979. Effect of glyphosate on rat
liver mitochondria in vivo. Bull. Environ. Contam. Toxicol. 22:357-364.

18. Martinez, T.T., W.C. Long, and R. Hiller. 1990. Comparison of the toxicology of the
herbicide Roundup by oral and pulmonary routes of exposure. Proc. West. Pharmacol. Soc.
33:193-197.

19. Martinez, T.T. and K. Brown. 1991. Oral and pulmonary toxicology of the surfactant
used in Roundup herbicide. Proc. West. Pharmacol. Soc. 34:43-46.

20. Agriculture Canada. Food Production and Inspection Branch. Pesticides Directorate.
1991. Discussion document: Pre-harvest use of glyphosate. Ottawa, Ontario, Canada.
(November 27.)

21. U.S. EPA. Office of Pesticides and Toxic Substances. 1982. Memo from William
Dykstra, Toxicology Branch, to Robert Taylor, Registration Division. (April 29.)

22. Tai, T. 1990. Hemodynamic effects of Roundup, glyphosate and surfactant in dogs. Jpn.
J. Toxicol. 3(1): 63-68. Cited in World Health Organization, United Nations Environment
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Criteria #159. Geneva, Switzerland.

23. Sawada, Y., Y. Nagai, M. Ueyama, and I. Yamamoto. 1988. Probable toxicity of
surface-active agent in commercial herbicide containing glyphosate. Lancet 1(8580):299.

24. Tominack, R.L. et al. 1991. Taiwan National Poison Center: Survey of
glyphosate-surfactant herbicide ingestions. Clin. Toxicol. 29(1):91-109.

25. Temple, W.A. and N.A. Smith. 1992. Glyphosate herbicide poisoning experience in New
Zealand. N.Z. Med. J. 105:173-174.

26. Talbot, A.R. et al. 1991. Acute poisoning with a glyphosate-surfactant herbicide
('Roundup'): A review of 93 cases. Human Exp. Toxicol. 10:1-8.

27. Menkes, D.B., W.A. Temple, and I.R. Edwards. 1991. Intentional self-poisoning with
glyphosate-containing herbicides. Human Exp. Toxicol. 10:103-107.

28. Jamison, J.P., J.H.M. Langlands, R.C. Lowry. 1986. Ventilatory impairment from
pre-harvest retted flax. Brit. J. Ind. Med. 43:809-813.

29. U.S. Dept. of Health and Human Services. Public Health Service. National Institutes of
Health. NTP technical report on toxicity studies of glyphosate (CAS No. 1071-83-6)
administered in dosed feed to F344/N rats and B6C3F1 mice. (NIH Publication 92-3135).
Toxicity Reports Series No. 16. Research Triangle Park, NC: National Toxicology Program.

30. U.S. EPA. Office of Toxic Substances. 1980. EPA Reg. #524-308; glyphosate; 3-month
mouse feeding study. Memo from William Dykstra, Health Effects Division, to Robert
Taylor,
Registration Division. Washington, D.C. (September 29.)

31. U.S. EPA. Office of Pesticides and Toxic Substances. 1985. Glyphosate; EPA
Reg.#524-308; Mouse oncogenicity study. Washington, D.C. (April 3.)

32. U.S. EPA. Office of Pesticides and Toxic Substances. 1982. EPA Reg. #524-308;
Lifetime feeding study in rats with glyphosate. Memo from William Dykstra, Health Effects
Division to Robert Taylor, Registration Division. Washington, D.C. (February 18.)

33. U.S. EPA. Office of Pesticides and Toxic Substances. 1983. Glyphosate; EPA Reg.
#524-308; A lifetime feeding study of glyphosate in Sprague-Dawley rats; a preliminary
addendum to review dated 2/18/83. Memo to Robert Taylor, Registration Division.
Washington, D.C. (February 15.)

34. U.S. EPA. Office of Pesticides and Toxic Substances. 1985. Glyphosate Q Evaluation of
kidney tumors in male mice. Chronic feeding study. Memo from L. Kasza, Toxicology
Branch, to W. Dykstra, Toxicology Branch. Washington, D.C. (December 4.)
35. U.S. EPA. Office of Pesticides and Toxic Substances. 1991. Second peer review of
glyphosate. Memo from W. Dykstra and G.Z. Ghali, Health Effects Division to R. Taylor,
Registration Division, and Lois Rossi, Special Review and Reregistration Division.
Washington, D.C. (October 30.)

36. U.S. EPA Office of Pesticides and Toxic Substances. 1985. Use of historical data in
determining the weight of evidence from kidney tumor incidence in the glyphosate two-year
feeding study; and some remarks on false positives. Memo from Herbert Lacayo to Reto
Engler (both Office of Pesticide Programs, Health Effects Division). Washington, D.C.
(February 26.)

37. Monsanto Co. 1988. Material safety data sheet: Pondmaster aquatic herbicide. St. Louis,
MO. (April.)

38. Kale, P.G. et al. 1995. Mutagenicity testing of nine herbicides and pesticides currently
used in agriculture. Environ. Mol. Mutagen. 25:148-153.

39. Vigfusson, N.V. and E.R. Vyse. 1980. The effect of the pesticides, Dexon, Capton and
Roundup on sister-chromatid exchanges in human lymphocytes in vitro. Mutation Research
79:53-57.

40. Rank, J. et al. 1993. Genotoxicity testing of the herbicide Roundup and its active
ingredient glyphosate isopropylamine using the mouse bone marrow micronucleus test,
Salmonella mutagenicity test, and Allium anaphase-telophase test. Mut. Res. 300:29-36.

41. Goltenboth, F. 1977. The effect of glyphosate and ametryn on the root tip mitosis of water
hyacinth. Proc. Asian Pac. Weed Sci. 6th Conf. 2:255. Cited in Hess, F.D. 1989. Herbicide
interference with cell division in plants. Chapter 5 of Bgez, P and Sandmann, G. (eds.) Target
sites of herbicide action. Boca Raton, FL: CRC Press, Inc.

42. U.S. EPA. Office of Toxic Substances. 1980. EPA Reg. #524-308; glyphosate;
submission of rat teratology, rabbit teratology, dominant lethal mutagenicity assay in mice.
Memo from W. Dykstra, Health Effects Division, to Robert Taylor, Registration Division.
Washington, D.C. (Undated.)

43. U.S. EPA. Office of Pesticides and Toxic Substances. 1986. Guidance for the
reregistration of pesticide products containing glyphosate as the active ingredient.
Washington, D.C. (June.)

44. U.S. Congress. House of Representatives. Committee on Government Operations. 1984.

Problems plague the Environmental Protection Agency's pesticide registration activities.
House Report 98-1147. Washington, D.C.: U.S. Government Printing Office.

45. U.S. EPA. Office of Pesticides and Toxic Substances. 1983. Summary of the IBT review
program. Washington, D.C. (July.)

46. U.S. EPA. 1978. Data validation. Memo from K. Locke, Toxicology Branch, to R.
Taylor, Registration Branch. Washington, D.C. (August 9.)
47. U.S. EPA. Communications and Public Affairs. 1991. Note to correspondents.
Washington, D.C. (March 1.)

48. U.S. EPA. Communications, Education, And Public Affairs. 1994. Press advisory.
Craven Laboratories, owner, and 14 employees sentenced for falsifying pesticide tests.
Washington, D.C. (March 4.)

49. U.S. EPA. Communications and Public Affairs. 1991. Press advisory. EPA lists crops
associated with pesticides for which residue and environmental fate studies were allegedly
manipulated. Washington, D.C. (March 29.)

50. U.S. Dept. of Justice. United States Attorney. Western District of Texas. 1992. Texas
laboratory, its president, 3 employees indicted on 20 felony counts in connection with
pesticide testing. Austin, TX. (September 29.)

========================================================
| Northwest Coalition for Alternatives to Pesticides |
| P.O. Box 1393 Eugene, OR 97440 |
| Phone: (541) 344-5044 |
| email: [email protected] |
========================================================
 Glyphosate, Part 2:
Human Exposure and Ecological Effects
by Caroline Cox
Journal of Pesticide Reform, Volume 15, Number 4, Winter 1995
Northwest Coalition for Alternatives to Pesticides, Eugene, OR.

Overview

Residues of the commonly-used herbicide glyphosate have been found in a variety of fruits
and vegetables. Residues can be detected long after glyphosate treatments have been made.
Lettuce, carrots, and barley planted a year after glyphosate treatment contained residues at
harvest.

In California, where reporting of pesticide-caused illnesses is more comprehensive than in

other states, glyphosate exposure was the third most commonly-reported cause of pesticide
illness among agricultural workers. For landscape maintenance workers, glyphosate ranked
highest.

Glyphosate can drift away from the site of its application. Maximum drift distance of 400 to
800 meters (1300-2600 feet) have been measured.

Glyphosate residues in soil have persisted over a year.

Although not expected for an herbicide, glyphosate exposure damages or reduces the
population of many animals, including beneficial insects, fish, birds, and earthworms. In
some cases glyphosate is directly toxic; for example, concentrations as low as 10 parts per
million can kill fish and 1/20 of typical application rates caused delayed development in
earthworms. In other cases, (small mammals and birds, for example) glyphosate reduces
populations by damaging the vegetation that provides food and shelter for the animals.

Glyphosate reduces the activity of nitrogen-fixing bacteria. These bacteria transform

nitrogen, an essential plant nutrient, into a form that plants can use. Glyphosate reduces the
growth of mycorrhizal fungi, beneficial fungi that help plants absorb water and nutrients.
Glyphosate also increases the susceptibility of plants to diseases, including Rhizoctonia root
rot, take-all disease, and anthracnose.
-------------------------------------------------------
Glyphosate is a widely-used, broad-spectrum herbicide that is used to kill unwanted plants in
a wide variety of agricultural, lawn and garden, aquatic, and forestry situations. It ranks
among the top ten herbicides used in the U.S., both in agricultural and nonagricultural
situations. Common brand names are Roundup, Rodeo, Accord, and Vision. This is the
second part of a summary of glyphosate's hazards. Part 1 (JPR 15(3):14-20) discussed the
toxicology of glyphosate, its breakdown products, and the other ingredients in
glyphosate-containing products. This part discusses human exposure to glyphosate and its
ecological effects.
 Human Exposure

The most important ways that people are exposed to glyphosate are through workplace
exposure (for people who use glyphosate products on the job), eating of contaminated food,
exposure caused by off-target movement following application (drift), contact with
contaminated soil, and drinking or bathing in contaminated water. The next five sections of
this factsheet summarize information about these five routes of exposure. The third section,
discussing drift, also covers impacts on plants.

Contamination of Food

Analysis of glyphosate residues is "in general laborious, complex, and costly."1 For this
reason, it is not included in government monitoring of pesticide residues in food.1 The only
information available about contamination of food comes from research situations. Such
studies demonstrate several important points:

* First, glyphosate can be taken up by plants and moved to parts of the plant that are used for
food. For example, glyphosate has been found in strawberries,2 wild blueberries and
raspberries,3 lettuce, carrots, barley,4 and fish5,6 following treatment.

* Second, pre-harvest use of glyphosate on wheat (to dry out the grain prior to harvest)
results in "significant residues in the grain,"1 according to the World Health Organization.
Bran contains between 2 and 4 times the amount on whole grains. Residues are not lost
during baking.1

* Third, glyphosate residues can be found in food long after treatments have been made. For
example, lettuce, carrots, and barley contained glyphosate residues at harvest when planted
a year after treatment.4

Occupational Exposure

Workers in a variety of occupations are exposed to glyphosate. Researchers have documented

exposure for forestry workers in Finland7 and the southeastern U.S., palm plantation workers
in Malaysia1 and conifer nursery workers in Mississippi and Oregon.8 All of these studies
generally found low, but consistent, exposure rates.

Physicians, however, paint a different picture. In California, the state with the most
comprehensive program for reporting of pesticide-caused illness, glyphosate was the third
most commonly-reported cause of pesticide illness among agricultural workers.9 Among
landscape maintenance workers, glyphosate was the most commonly reported cause.10 (Both
these statistics come from reviews of illness reports collected between 1984 and 1990.) Even
when glyphosate's extensive use in California is considered, and the illness statistics
presented as "number of acute illnesses reported per million pounds used in California,"
glyphosate ranked twelfth.9
 Drift

In general, movement of a pesticide through unwanted drift is "unavoidable."11 Drift of

glyphosate is no exception. Glyphosate drift, however, is a particularly significant problem.
Its wide use means that there is a correspondingly large potential for drift.12 When drift does
occur, "damage is likely to be much more extensive and more persistent than with many other
herbicides. "13 This is because glyphosate translocates (moves) within plants readily so that
even unexposed parts of a plant can be damaged. Damage to perennial plants (when not
exposed to enough glyphosate to kill them) is persistent, with some symptoms lasting several
years.13 In addition, plant susceptibility varies widely. Some wildflowers are almost a
hundred times more sensitive than others; small amounts of drift will damage these
species.14

A fundamental question about drift is "How far can I expect glyphosate to travel off-site?"
Unfortunately, the question is difficult to answer, since drift is "notoriously variable."15
Factors that increase drift are aerial application techniques, high wind speeds (over 10
kilometers, or 6 miles, per hour), spray nozzles that produce a high proportion of fine
droplets, and calm conditions (without enough turbulence to drive the glyphosate droplets
onto plant foliage).15 Drift distances that have been measured for the major application
techniques include the following:

* Ground Applications: Between 14 and 78 percent of glyphosate applied as ground sprays

moves off-site.15 Seedling mortality has been demonstrated 20 meters (66 feet) downwind
when using a tractor-mounted sprayer. Sensitive species were killed at 40 meters (131
feet).16 Models indicate that even more sensitive species would be killed at distances
approaching 100 meters (328 feet).14 Glyphosate residues have been measured 400 meters
(1312 feet) downwind from ground applications.17

* Helicopter applications: Between 41 and 82 percent of glyphosate applied from helicopters

moves off the target site.15 Two studies done in Canada18,19 measured glyphosate residues
200 meters (656 feet) from target areas following helicopter applications to forest sites. In
both studies, 200 meters was the farthest distance at which samples were taken, so the longest
distance glyphosate travelled is not known.18,19 A third study (from California) found
glyphosate 800 meters (2624 feet) downwind following a helicopter application. Again, this
was the farthest distance at which measurements were made. Plant injury was recorded 400
meters (1312 feet) downwind.17

Fixed-wing aircraft: Long drift distances occur following applications of glyphosate made
from fixed-wing airplanes. Three studies on forested sites conducted by Agriculture Canada
(the Canadian agricultural ministry) showed that glyphosate was consistently found at the
farthest distance from the target areas that measurements were made (200, 300, and 400
meters, or 656, 984, and 1312 feet).20-22 A California study found glyphosate 800 meters
downwind of an airplane application. Again, this was the farthest distance at which
measurements were made. Plant injury was observed at 100 meters (328 feet). Unlike the first
three studies, this study used a grass field as the test site.17

One of the Canadian studies22 calculated that buffer zones of between 75 and 1200 meters
(246 feet - 0.75 miles) would be required to protect nontarget vegetation.
 Soil Contamination

Persistence: Glyphosate's persistence in soil varies widely, so giving a simple answer to the
question "How long does glyphosate persist in soil?" is not possible. Half-lives (the time
required for half of the amount of glyphosate applied to break down or move away) as low as
3 days and as long as 141 days have been measured by glyphosate's manufacturer.4 Initial
degradation (breakdown) is faster than the subsequent degradation of what remains, resulting
in long persistence.23 Long persistence has been measured in the following studies: 55 days
on an Oregon Coast Range forestry site24; 249 days on Finnish agricultural soils25; between
259 and 296 days on eight Finnish forestry sites23; 335 days on an Ontario (Canada) forestry
site26; 360 days on 3 British Columbia forestry sites27; and, from 1 to 3 years on eleven
Swedish forestry sites.28 These are minimum estimates because, in all but two of these
studies, glyphosate was detected on the last date samples were analyzed.

Glyphosate is thought to be "readily bound to many soils and clay minerals"1 and therefore
"immobile or slightly immobile in many soils."1 This means that the glyphosate will be
unlikely to move away from the application site and contaminate water or soil elsewhere.
However, a new study29 paints a different picture. The researchers found that glyphosate
bound readily to the four soils studied. However, desorption, when glyphosate unbinds from
soil particles, also occurred readily. In one soil, 80 percent of the added glyphosate desorbed
in a two hour period. The study concludes that "this herbicide can be extensively mobile in
the soil environment.."29

Water Contamination

Based on the prevailing view that glyphosate binds readily to soil particles, it does not have
the chemical characteristics of a pesticide that is likely to leach into either ground or surface
water.1 (If it readily desorbs, as described above, this picture would change.) In either case,
glyphosate can move into surface water when the soil particles to which it is bound are
washed into streams or rivers.4 How often this happens is not known, because routine
monitoring for glyphosate in water is infrequent.1

However, glyphosate has been found in both ground and surface water. Examples include
two farm ponds in Ontario, Canada, contaminated by run-off from an agricultural treatment
(one pond) and a spill (the other pond)30; the run-off from a watersheds treated with
Roundup during production of no-till corn and fescue31; contaminated surface water in the
Netherlands1; and seven U.S. wells (one in Texas, six in Virginia) contaminated with
glyphosate.32

Glyphosate's persistence in water is shorter than its persistence in soils. Two Canadian studies
found glyphosate persisted 12 to 60 days in pond water following direct application.33,34
Glyphosate persists longer in sediments. For example, a study of Accord applied to forest
ponds found glyphosate residues in sediment 400 days after application.1 The half-life in
pond sediments in a Missouri study was 120 days; persistence was over a year in pond
sediments in Michigan and Oregon.4
 Ecological Effects

Glyphosate can impact many organisms not intended as targets of the herbicide. The next
two sections describe both direct mortality and indirect effects, through destruction of food or
shelter.

Effects on Nontarget Animals

Beneficial insects: Glyphosate-containing products pose hazards to insects that are

economically beneficial because they kill pest insects. The International Organization for
Biological Control found that exposure to freshly dried Roundup killed over 50 percent of
three species of beneficial insects: a parasitoid wasp, a lacewing, and a ladybug.35 Over 80
percent of a fourth species, a predatory beetle, was killed.

Similar impacts on beneficial insects have been shown in field studies. In North Carolina
winter wheat fields, populations of large carabid beetles declined after treatment with a
commercial glyphosate product and did not recover for 28 days.36 A study of Roundup
treatment of pasture hedgerows in the United Kingdom showed a similar decline in carabid
beetles.37

Roundup treatment of a Maine clear-cut caused an 89 percent decline in the number of

herbivorous (plant-eating) insects. While these are not usually considered beneficial insects,
they serve as an important food resource for birds and insect-eating small mammals.38

Aquatic insects can also be affected by glyphosate. Midge larvae (important food for
breeding waterfowl39) are killed by glyphosate in amounts that vary widely. For example,
one study found that 55 parts per million (ppm) of glyphosate killed midge larvae6 while
other studies found that 65040 -560039 ppm of Rodeo (containing glyphosate and water)
were required to kill the larvae. Part of the variability is related to water hardness.39

The U.S. Fish and Wildlife Service has identified one endangered species of insect, a
longhorn beetle, that would be jeopardized by use of glyphosate.41

Other arthropods: Glyphosate and glyphosate-containing products kill a variety of other

arthropods. For example, over 50 percent of test populations of a predatory mite that is an
important predator of pest mites was killed by exposure to Roundup.35 In another laboratory
study, Roundup exposure caused a decrease in survival and a decrease in body weight of
woodlice. These arthropods are important in humus production and soil aeration.42 Roundup
treatment of pasture hedgerows reduced the number of spiders, probably by killing the plants
they preferred for web-spinning.37 The water flea Daphnia pulex is killed by concentrations
of Roundup between 3 and 25 ppm.6,43,44 Young Daphnia are more susceptible than mature
individuals, and suspended sediments in the water increased the toxicity.43 The red swamp
crawfish, a commercial species, was killed by 47 ppm of Roundup.45
Fish: Both glyphosate and the commercial products that contain glyphosate are acutely
toxic to fish. In general, glyphosate alone is less toxic than the common glyphosate product,
Roundup, and other glyphosate products have intermediate toxicity. Part of these differences
in toxicity to fish can be explained by the toxicity of the surfactant (detergent-like ingredient)
in Roundup. It is about 30 times more toxic to fish than glyphosate itself.44

Acute toxicities of glyphosate vary widely: median lethal concentrations (LC50s; the
concentrations killing 50 percent of a population of test animals) from 10 ppm to over 1000
ppm have been reported depending on the species of fish and test conditions.1 In soft water
there is little difference between the toxicities of glyphosate and Roundup.

Acute toxicities of Roundup to fish range from an LC50 of 3.2 ppm to an LC50 of 52 ppm.1
Acute toxicities of Rodeo (used with the surfactant X-77 per label recommendations) vary
from 120 to 290 ppm.46

Factors important in determining the toxicity of glyphosate or glyphosate-containing products

to fish include the following:

* First, different species of fish have different susceptibilities. For example, coho and
chinook salmon are more tolerant of glyphosate than pink or chum salmon.47

* Water quality is important: glyphosate in soft water was 20 times more toxic to rainbow
trout than was glyphosate in hard water. For Roundup, the reverse is true: it is more toxic in
hard water than in soft.47,48

* Age affects the susceptibility of fish because juveniles are often more susceptible than
adults. For example, Roundup was four times more toxic to rainbow trout fry and fingerlings
than it was to larger fish.6

* Nutrition also can determine toxicity. Hungry fish are more susceptible to glyphosate than
fed fish. For example, fed flagfish were 10 times more tolerant of glyphosate than unfed
fish.49

* Finally, glyphosate toxicity increases with increased water temperature. In both rainbow
trout and bluegills, toxicity about doubled between 7 and 17!C (45 and 63!F).6 Treatment of
riparian areas with glyphosate causes water temperatures to increase for several years
following treatment 50 because the herbicide kills shading vegetation. This means that
repeated use of glyphosate in a watershed could favor its increased toxicity to fish. In
addition, the temperature increase itself could be critical for fish, like juvenile salmon, that
are sensitive to water temperature.

Sublethal effects of glyphosate on fish are also significant and occur at low concentrations.
Studies of rainbow trout and Tilapia found that concentrations of about 1/2 and 1/3 of the
LC50 (respectively) caused erratic swimming.51,52 The trout also exhibited labored
breathing.51 Behavioral effects can increase the risk that the fish will be eaten, as well as
affecting feeding, migration, and reproduction.52
Birds: Glyphosate is acutely toxic to birds, but only in large amounts. The LC50, the
amount in food that kills 50 percent of a population of test animals, is often above 4000
milligrams per kilogram of food.1

Glyphosate also has indirect impacts on birds. Because glyphosate kills plants, its use creates
a dramatic change in the structure of the plant community. This affects bird populations,
since the birds depend on the plants for food, shelter, and nest support.

For example, a study of four glyphosate-treated clear-cuts (and an unsprayed control plot) in
Nova Scotia found that the densities of the two most common species of birds
(white-throated sparrow and common yellowthroat) decreased for two years after glyphosate
treatment. By the fourth year post-spray, densities had returned to normal for these two
species. However, the unsprayed plot had by then been colonized by new species of birds
(warblers, vireos, and a hummingbird). These species did not appear on the sprayed plots.53

An earlier three year study of songbird abundance following glyphosate treatment of

clear-cuts in Maine forests showed similar results. Abundances of the total number of birds
(Figure 2) and three common species decreased. The decrease in bird abundance was
correlated with decrease in the diversity of the habitat.54

Black grouse avoided glyphosate-treated clear-cuts in Norway for several years after
treatment.55 Researchers recommended that the herbicide not be used near grouse courtship
areas.

Small mammals: In field studies, small mammals have also been indirectly affected when
glyphosate kills the vegetation they (or their prey) use for food or shelter. This was first
shown in studies of clear-cuts in Maine.38 Insect-eating shrews declined for three years
post-treatment; plant-eating voles declined for two. A second study in Maine56 found similar
results for voles, but not shrews. A British Columbia study found that deer mice populations
were dramatically (83 percent) lower following glyphosate treatment.57 While some other
studies have found no affect on mice, this may have occurred because treated areas were
small.1 This suggests that effects are more severe when large areas are treated.

In Norway, there was a "strong reduction" in use of sprayed clear-cuts by mountain hare.58

Earthworms: A study of the most common earthworm found in agricultural soils in New
Zealand showed that glyphosate significantly affects growth and survival of earthworms.
Repeated biweekly applications of low rates of glyphosate (1/20 of typical rates) caused a
reduction in growth, an increase in the time to maturity, and an increase in mortality.59

Effects on Nontarget Plants

As a broad-spectrum herbicide, glyphosate has potent acutely toxic effects on most plant
species. However, there are other kinds of serious effects. These include effects on
endangered species, reduction in the ability to fix nitrogen, increased susceptibility to plant
diseases, and reduction in the activity of mycorrhizal fungi.
Endangered species: Because essentially all plants are susceptible to glyphosate-caused
damage or mortality, glyphosate can seriously impact endangered plant species. The U.S.
Fish and Wildlife Service has identified 74 endangered plant species that it believes could be
jeopardized by use of glyphosate. This list is based on the use of glyphosate on 9 crops, and
does not include over 50 other uses.41

Nitrogen fixation: Nitrogen is important because of its "near omnipresence" in membranes,

proteins, and genetic material of living things. Most living things cannot use nitrogen in its
common form and instead use ammonia and nitrates, much rarer compounds. The processes
by which ammonia and nitrates are created are called nitrogen fixation and nitrification. They
are carried out by certain bacteria.60

A number of studies (from Iowa,61 Australia,62 eastern Canada,63 and Ontario

(Canada)64,65) have shown that commercial glyphosate products can reduce nitrogen-fixing
or nitrification activity of soils. The amount of glyphosate that produces inhibitory effects
varies from 262 to 200063 ppm. Effects can be persistent; the formation of nitrogen-fixing
nodules on clover roots was inhibited 120 days after treatment. 62

In addition, tests of cultured nitrogen-fixing bacteria have also shown that glyphosate inhibits
nitrogen-fixation. These studies included the nitrogen-fixing species in roots of soybeans66
and clover.67-68

Given the importance of nitrogen-fixation to agriculture, more research is crucial.

Mycorrhizal fungi: Mycorrhizal fungi are beneficial fungi that live in and around plant
roots. They help plants absorb nutrients and water and can protect them from cold and
drought.69 Glyphosate is toxic to many species of mycorrhizal fungi. Effects, mostly growth
inhibition, have been observed at concentrations between 1 and 100 ppm.70-73

Plant diseases: Glyphosate treatment increases the susceptibility of crop plants to a number
of diseases. For example, glyphosate reduced the ability of bean plants to defend themselves
against the disease anthracnose.74 Glyphosate increased the growth of take-all disease in soil
from a wheat field. In addition, the proportion of soil fungi which was antagonistic to the
take-all fungus decreased.75 Bean seedlings also survived glyphosate treatment when grown
on sterile soil, but not when grown on normal (not sterilized) soil.76 Spraying of Roundup
prior to planting barley increased the severity of Rhizoctonia root rot and decreased barley
yield.77 In addition, Roundup injection of lodgepole pine inhibited the defensive response of
the tree to blue stain fungus.78
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| Northwest Coalition for Alternatives to Pesticides |
| P.O. Box 1393 Eugene, OR 97440 |
| Phone: (541) 344-5044 |
| email: [email protected] |
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