A

f

Toxicological Profile for

Glyphosate

August 2020
GLYPHOSATE II

DISCLAIMER

Use of trade names is for identification only and does not imply endorsement by the Agency for Toxic 

Substances and Disease Registry, the Public Health Service, or the U.S. Department of Health and Human 

Services.
GLYPHOSATE III

FOREWORD 

This toxicological profile is prepared in accordance with guidelines developed by the Agency for Toxic 

Substances and Disease Registry (ATSDR) and the Environmental Protection Agency (EPA). The 

original guidelines were published in the Federal Register on April 17, 1987. Each profile will be 

revised and republished as necessary.

The ATSDR toxicological profile succinctly characterizes the toxicologic and adverse health effects

information for these toxic substances described therein. Each peer-reviewed profile identifies and

reviews the key literature that describes a substance's toxicologic properties. Other pertinent literature is

also presented, but is described in less detail than the key studies. The profile is not intended to be an

exhaustive document; however, more comprehensive sources of specialty information are referenced.

The focus of the profiles is on health and toxicologic information; therefore, each toxicological profile 

begins with a relevance to public health discussion which would allow a public health professional to 

make a real-time determination of whether the presence of a particular substance in the environment 

poses a potential threat to human health. The adequacy of information to determine a substance's health 

effects is described in a health effects summary. Data needs that are of significance to the protection of 

public health are identified by ATSDR and EPA.

Each profile includes the following: 

(A) The examination, summary, and interpretation of available toxicologic information and

epidemiologic evaluations on a toxic substance to ascertain the levels of significant human

exposure for the substance and the associated acute, intermediate, and chronic health effects;

(B) A determination of whether adequate information on the health effects of each substance is

available or in the process of development to determine the levels of exposure that present a

significant risk to human health due to acute, intermediate, and chronic duration exposures;

and

(C) Where appropriate, identification of toxicologic testing needed to identify the types or levels

of exposure that may present significant risk of adverse health effects in humans.

The principal audiences for the toxicological profiles are health professionals at the Federal, State, and 

local levels; interested private sector organizations and groups; and members of the public. 

This profile reflects ATSDR’s assessment of all relevant toxicologic testing and information that has 

been peer-reviewed. Staffs of the Centers for Disease Control and Prevention and other Federal 

scientists have also reviewed the profile. In addition, this profile has been peer-reviewed by a 

nongovernmental panel and was made available for public review. Final responsibility for the 

contents and views expressed in this toxicological profile resides with ATSDR.

Patrick N. Breysse, Ph.D., CIH 

Director, National Center for Environmental Health and 

Agency for Toxic Substances and Disease Registry

Centers for Disease Control and Prevention 
VI

*Legislative Background

The toxicological profiles are developed under the Comprehensive Environmental Response,

Compensation, and Liability Act of 1980, as amended (CERCLA or Superfund). CERCLA section

104(i)(1) directs the Administrator of ATSDR to “...effectuate and implement the health related

authorities” of the statute. This includes the preparation of toxicological profiles for hazardous

substances most commonly found at facilities on the CERCLA National Priorities List (NPL) and

that pose the most significant potential threat to human health, as determined by ATSDR and the

EPA. Section 104(i)(3) of CERCLA, as amended, directs the Administrator of ATSDR to prepare a

toxicological profile for each substance on the list. In addition, ATSDR has the authority to prepare

toxicological profiles for substances not found at sites on the NPL, in an effort to “...establish and

maintain inventory of literature, research, and studies on the health effects of toxic substances” under

CERCLA Section 104(i)(1)(B), to respond to requests for consultation under section 104(i)(4), and

as otherwise necessary to support the site-specific response actions conducted by ATSDR.
GLYPHOSATE V

VERSION HISTORY

Date Description

August 2020 Final toxicological profile released

April 2019 Draft for public comment toxicological profile released
GLYPHOSATE VI

CONTRIBUTORS & REVIEWERS

Hana R. Pohl, M.D., Ph.D. (Lead)

Melanie Buser, M.P.H.

Breanna Alman, M.P.H.

Selene Chou, Ph.D. 

Mike Fay, Ph.D.

Carolyn Harper, Ph.D.

Susan Zells Ingber, A.B., M.S.P.P.

Jennifer Przybyla, Ph.D.

Jane Li, Ph.D.

Angela Ragin-Wilson, Ph.D.

Henry Abadin, M.S.P.H.

ATSDR, Division of Toxicology and Human Health 

Sciences, Atlanta, GA

David W. Wohlers, Ph.D.

Mario Citra, Ph.D.

Christina Coley, B.S.

Lisa Ingerman, Ph.D., D.A.B.T.

SRC, Inc., North Syracuse, NY

Kaley Beins, M.P.H.

Lauren Brown, M.S., D.A.B.T.

Paulina Do, M.P.H.

Adriana Antezana, M.P.H.

Hannah Derrick, B.S.

Kerry Diskin, Ph.D.

Andrea Chiger, M.P.H.

Abt Associates, Rockville, MD

Chimeddulam Dalaijamts, PhD

Texas A&M University (under 

subcontract to Abt Associates)

REVIEWERS

Interagency Minimal Risk Level Workgroup: 

Includes ATSDR; National Center for Environmental Health (NCEH); National Institute for

Occupational Health and Safety (NIOSH); U.S. Environmental Protection Agency (EPA); National 

Toxicology Program (NTP).

Additional reviews for science and/or policy: 

ATSDR, Division of Community Health Investigations; ATSDR, Office of Science; NCEH, Division of 

Laboratory Science; NCEH, Division of Environmental Health Science and Practice. EPA.

PEER REVIEWERS 

1. Annaclaire De Roos Ph.D., M.P.H., Associate Professor, Environmental and Occupational

Health, Dornsrife School of Public Health, Drexel University, Philadelphia, Pennsylvania

2. David A. Eastmond, Ph.D., Professor and Toxicologist, Department of Molecular Cell and

Systems Biology, University of California, Riverside, Riverside, California

3. Renata Marino Romano, Ph.D., Professora Adjunta, Departamento de Farmácia, Universidade

Estadual do Centro-Oeste – UNICENTRO, Guarapuava, Brazil

These experts collectively have knowledge of toxicology, chemistry, and/or health effects. All reviewers 

were selected in conformity with Section 104(I)(13) of the Comprehensive Environmental Response, 

Compensation, and Liability Act, as amended.
GLYPHOSATE VII

Peer reviewers for subsequent revision to Section 2.19 (Cancer) and Appendix A (MRL Worksheets) in

the Toxicological Profile for Glyphosate were:

1. James V. Bruckner, Ph.D., Professor of Pharmacology & Toxicology, Department of

Pharmaceutical & Biomedical Sciences, College of Pharmacy, University of Georgia

2. David A. Eastmond, Ph.D., Professor and Toxicologist, Department of Molecular Cell and

Systems Biology, University of California, Riverside, Riverside, California

3. Paul J. Mills, Ph.D., Professor of Family Medicine and Public Health, University of California,

San Diego

4. Renata Marino Romano, Ph.D., Professora Adjunta, Departamento de Farmácia, Universidade

Estadual do Centro-Oeste – UNICENTRO, Guarapuava, Brazil

ATSDR scientists review peer reviewers’ comments and determine whether changes will be made to the 

profile based on comments. The peer reviewers’ comments and responses to these comments are part of 

the administrative record for this compound.

The listing of peer reviewers should not be understood to imply their approval of the profile's final 

content. The responsibility for the content of this profile lies with ATSDR.
GLYPHOSATE X

CONTENTS

DISCLAIMER........................................................................................................................................................ II

FOREWORD..............................................................................................................................................................III

VERSION HISTORY ..................................................................................................................................................VI

CONTRIBUTORS & REVIEWERS ......................................................................................................................... VII

CONTENTS...... ......................................................................................................................................................VIII

LIST OF FIGURES .....................................................................................................................................................XI

LIST OF TABLES......................................................................................................................................................XII

CHAPTER 1. RELEVANCE TO PUBLIC HEALTH................................................................................................. 1

1.1 OVERVIEW AND U.S. EXPOSURES.....................................................................................................1

1.2 SUMMARY OF HEALTH EFFECTS ......................................................................................................3

1.3 MINIMAL RISK LEVELS (MRLs)..........................................................................................................7

CHAPTER 2. HEALTH EFFECTS ...........................................................................................................................10

2.1 INTRODUCTION ...................................................................................................................................10

2.2 DEATH....................................................................................................................................................47

2.3 BODY WEIGHT .....................................................................................................................................47

2.4 RESPIRATORY ......................................................................................................................................49

2.5 CARDIOVASCULAR.............................................................................................................................61

2.6 GASTROINTESTINAL ..........................................................................................................................62

2.7 HEMATOLOGICAL...............................................................................................................................64

2.8 MUSCULOSKELETAL..........................................................................................................................64

2.9 HEPATIC.................................................................................................................................................64

2.10 RENAL....................................................................................................................................................67

2.11 DERMAL.................................................................................................................................................69

2.12 OCULAR.................................................................................................................................................69

2.13 ENDOCRINE ..........................................................................................................................................70

2.14 IMMUNOLOGICAL...............................................................................................................................72

2.15 NEUROLOGICAL ..................................................................................................................................72

2.16 REPRODUCTIVE ...................................................................................................................................74

2.17 DEVELOPMENTAL...............................................................................................................................77

2.18 OTHER NONCANCER ..........................................................................................................................80

2.19 CANCER .................................................................................................................................................80

2.20 GENOTOXICITY..................................................................................................................................128

2.21 MECHANISMS OF ACTION...............................................................................................................139

CHAPTER 3. TOXICOKINETICS, SUSCEPTIBLE POPULATIONS, BIOMARKERS, CHEMICAL 

INTERACTIONS ...........................................................................................................................144

3.1 TOXICOKINETICS ..............................................................................................................................144

3.1.1 Absorption ......................................................................................................................................144

3.1.1.1 Inhalation Exposure ...................................................................................................................144

3.1.1.2 Oral Exposure ............................................................................................................................144

3.1.1.3 Dermal Exposure .......................................................................................................................145

3.1.2 Distribution.....................................................................................................................................146

3.1.2.1 Inhalation Exposure ...................................................................................................................146

3.1.2.2 Oral Exposure ............................................................................................................................146

3.1.2.3 Dermal Exposure .......................................................................................................................147

3.1.2.4 Other Routes of Exposure..........................................................................................................148

3.1.3 Metabolism .....................................................................................................................................148

3.1.4 Excretion.........................................................................................................................................150

3.1.4.1 Inhalation Exposure ...................................................................................................................150

3.1.4.2 Oral Exposure ............................................................................................................................150

3.1.4.3 Dermal Exposure .......................................................................................................................151

3.1.4.4 Other Routes of Exposure..........................................................................................................151

3.1.5 Physiologically Based Pharmacokinetic (PBPK)/Pharmacodynamic (PD) Models .......................152

3.1.6 Animal-to-Human Extrapolations...................................................................................................152
GLYPHOSATE X

3.2 CHILDREN AND OTHER POPULATIONS THAT ARE UNUSUALLY SUSCEPTIBLE...............152

3.3 BIOMARKERS OF EXPOSURE AND EFFECT.................................................................................153

3.3.1 Biomarkers of Exposure .................................................................................................................154

3.3.2 Biomarkers of Effect.......................................................................................................................154

3.4 INTERACTIONS WITH OTHER CHEMICALS.................................................................................154

CHAPTER 4. CHEMICAL AND PHYSICAL INFORMATION ...........................................................................156

4.1 CHEMICAL IDENTITY .......................................................................................................................156

4.2 PHYSICAL AND CHEMICAL PROPERTIES ....................................................................................156

CHAPTER 5. POTENTIAL FOR HUMAN EXPOSURE ......................................................................................159

5.1 OVERVIEW ..........................................................................................................................................159

5.2 PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL ............................................................159

5.2.1 Production.......................................................................................................................................159

5.2.2 Import/Export .................................................................................................................................163

5.2.3 Use ..................................................................................................................................................163

5.2.4 Disposal ..........................................................................................................................................166

5.3 RELEASES TO THE ENVIRONMENT...............................................................................................167

5.3.1 Air...................................................................................................................................................167

5.3.2 Water ..............................................................................................................................................168

5.3.3 Soil..................................................................................................................................................169

5.4 ENVIRONMENTAL FATE..................................................................................................................170

5.4.1 Transport and Partitioning ..............................................................................................................171

5.4.2 Transformation and Degradation ....................................................................................................174

5.5 LEVELS IN THE ENVIRONMENT.....................................................................................................181

5.5.1 Air...................................................................................................................................................183

5.5.2 Water ..............................................................................................................................................184

5.5.3 Sediment and Soil...........................................................................................................................184

5.5.4 Other Media ....................................................................................................................................184

5.6 GENERAL POPULATION EXPOSURE .............................................................................................194

5.7 POPULATIONS WITH POTENTIALLY HIGH EXPOSURES ..........................................................200

CHAPTER 6. ADEQUACY OF THE DATABASE ...............................................................................................201

6.1 Information on Health Effects................................................................................................................201

6.2 Identification of Data Needs..................................................................................................................204

6.3 Ongoing Studies.....................................................................................................................................208

CHAPTER 7. REGULATIONS AND GUIDELINES ............................................................................................210

CHAPTER 8. REFERENCES ................................................................................................................................. 212

APPENDICES

APPENDIX A. ATSDR MINIMAL RISK LEVELS AND WORKSHEETS.........................................A-1

APPENDIX B. LITERATURE SEARCH FRAMEWORK FOR GLYPHOSATE................................B-1

APPENDIX C. USER’S GUIDE.............................................................................................................C-1

APPENDIX D. QUICK REFERENCE FOR HEALTH CARE PROVIDERS.......................................D-1

APPENDIX E. GLOSSARY ................................................................................................................... E-1

APPENDIX F. ACRONYMS, ABBREVIATIONS, AND SYMBOLS ..................................................F-1
GLYPHOSATE XI

LIST OF FIGURES

1-1. Noncancer Health Effects Found in Animals Following Oral Exposure to Glyphosate Technical................. 4 

1-2. Summary of Sensitive Targets of Glyphosate Technical – Oral ..................................................................... 8

1-3. Overview of the Number of Animal Studies Examining Glyphosate Technical Health................................ 16

2-2. Overview of the Number of Studies Examining Glyphosate Formulations Health Effects* .. ......................17

2-3. Levels of Significant Exposure to Glyphosate Technical – Oral .................................................................. 29

2-4. Risk of non-Hodgkin’s Lymphoma Relative to Self-Reported Glyphosate Use or Exposure.................... 116

2-5. Risk of Multiple Myeloma Relative to Self-Reported Glyphosate Use or Exposure .................................. 117

3-1. Chemical Structures of Glyphosate and Aminomethylphosphonic Acid (AMPA) ..................................... 148

5-1. Agricultural Application Trends of Glyphosate in the United States According to U.S.

Geological Survey (USGS) Data ......................................................................................................................... 165

5-2. Degradation of Glyphosate Under Aerobic Conditions .............................................................................. 174

6-1. Summary of Existing Health Effects Studies of Animals Orally Exposed to Glyphosate by Endpoint)*...202

6-2. Summary of Existing Health Effects Studies on Glyphosate Formulations (Listed by Endpoint)*........... 203 
GLYPHOSATE XII

LIST OF TABLES 

1-1. Minimal Risk Levels (MRLs) for Technical Glyphosate ...................................................................... 9

2-1. Description of Selected Glyphosate Formulations ............................................................................. 11

2-2. Levels of Significant Exposure to Glyphosate Technical – Oral ........................................................ 18

2-3. Levels of Significant Exposure to Glyphosate Formulations – Oral .................................................. 34

2-4. Levels of Significant Exposure to Glyphosate Technical – Dermal ................................................... 46

2-5. Noncancer Outcomes in Humans Exposed to Glyphosate-Containing Products ............................... 51

2-6. Summary of Meta-Analyses of Results from Studies Examining Possible Association Between

Self-Reported Use of Glyphosate and Lymphohematopoietic Cancers ...................................................... 82

2-7. Cancer Outcomes for Solid Tumor-Types in Humans Exposed to Glyphosate-Containing

Products ...................................................................................................................................................... 87

2-8. Lymphohematopoietic Cancer Outcomes in Humans Exposed to Glyphosate-Containing

Products .................................................................................................................................................... 101

2-9. Incidences of Selected Tumors in Sprague-Dawley Rats Administered Technical Glyphosate

(98.7% purity) in the Diet for up to 26 Months ........................................................................................ 119

2-10. Incidences of Selected Tumors in Albino Sprague-Dawley Rats Administered Technical

Glyphosate (96.5% Purity) in the Diet for 2 Years ................................................................................... 120

2-11. Incidences of Renal Tubular Cell Tumors in Male CD-1 Mice Administered Technical

Glyphosate (99.78% Purity) in the Diet for up to 24 Months ................................................................... 123

2-12. Incidences of Tumors in Male and Female CD-1 Mice Administered Glyphosate (≥97.5%

Purity) in the Diet for up to 104 Weeks .................................................................................................... 123

2-13. Carcinogenicity Classification ........................................................................................................ 126

2-14. Genotoxicity of Glyphosate Technical In Vitro.............................................................................. 128

2-15. Genotoxicity of Glyphosate Technical In Vivo .............................................................................. 130

2-16. Genotoxicity of Glyphosate Formulations In Vitro........................................................................ 130

2-17. Genotoxicity of Glyphosate Formulations In Vivo......................................................................... 132

4-1. Chemical Identity of Glyphosate and Glyphosate Isopropylaminea................................................. 157

4-2. Physical and Chemical Properties of Glyphosate and its Isopropylamine Salta............................... 158

5-1. Glyphosate Salts ............................................................................................................................... 160

5-2. Companies Manufacturing Products Under Pesticide Code 417300 (Glyphosate) .......................... 161

5-3. Glyphosate AI (Pounds) Usage Trends from 1990 to 2014.............................................................. 166

5-4. Lowest Limit of Detection Based on Standards ............................................................................... 182

5-5. Summary of Environmental Levels of Glyphosate .......................................................................... 182

5-6. Outdoor Air Monitoring Data for Glyphosate .................................................................................. 183
GLYPHOSATE XIII

5-7. Glyphosate and its Degradation Products in Water Samples in Major U.S. River Basins ............... 184

5-8. Surface Water Monitoring Data for Glyphosate ............................................................................... 186

5-9. Groundwater Monitoring Data for Glyphosate................................................................................. 189

5-10. Sediment and Soil Monitoring Data for Glyphosate ...................................................................... 191

5-11. Available Glyphosate Human Monitoring Data ............................................................................. 196

6-1. Ongoing Studies on Glyphosate ....................................................................................................... 209

7-1. Regulations and Guidelines Applicable to Glyphosate .................................................................... 210
GLYPHOSATE 1

CHAPTER 1. RELEVANCE TO PUBLIC HEALTH

1.1 OVERVIEW AND U.S. EXPOSURES 

Glyphosate is a phosphonoglycine non-selective herbicide, first registered for use by the EPA in 1974. 

Glyphosate is typically manufactured for commercial use as a salt available in soluble liquid and granule 

formulations. Herbicide formulations employing glyphosate salts are commonly produced in 

combination with additives, inert ingredients, and surfactants. The salt derivatives enhance absorption of 

glyphosate from the surface of the plant or leaf structure, but are not the herbicidally active portion of the 

compound. Specific formulations vary in composition and are marketed under numerous trade names 

(NPIRS 2017; PAN 2009). Commercial products containing glyphosate may have concentrations ranging 

from 0.96 to 94 w/w%. For example, the common herbicide, Roundup®, has product formulations 

containing glyphosate in concentrations ranging from 0.96% to as much as 71% (w/w) (NPIRS 2017; 

PAN 2016b).

Glyphosate is the active ingredient in a variety of broad spectrum herbicidal products for residential, 

commercial, and agricultural purposes. Selected agricultural commodities such as roundup-ready corn 

and soybeans have been genetically modified to be resistant to damage when glyphosate is applied to 

control undesirable weeds. Glyphosate is produced commercially in the United States as a technicalgrade substance (glyphosate technical) with a purity of ≥80%, though the purity is usually >90% (IPCS 

1994, McBean 2011). In 2007, U.S. agricultural use of glyphosate was approximately 82,800 tons and 

non-agricultural use of glyphosate was approximately 9,300 tons (Battaglin et al. 2014). For the purposes 

of this Profile, the phrase “non-agricultural use” refers to the use of glyphosate outside of agriculture or 

farmland, such as to control weeds on a roadside, in a garden, or other use by homeowners.. In 2014, U.S. 

agricultural use of glyphosate was approximately 124,953 tons and non-agricultural use of glyphosate was 

approximately 13,260 tons (Benbrook 2016). The manufacture and use of glyphosate has led to its direct 

release into the environment (EPA 1993). Once glyphosate enters the environment, it has low potential 

for environmental bioavailability and is unlikely to bioaccumulate; the chemical is either degraded by 

microbial processes or inactivated by adsorption to soil (Shushkova et al. 2010; Smith and Oehme 1992). 

Glyphosate is expected to adsorb to soils under most environmental conditions; therefore, leaching into 

groundwater is minimal (Smith and Oehme 1992). Glyphosate may enter surface waters due to its use in 

some aquatic environments. Volatilization of glyphosate is not an important fate process based on its low 

vapor pressure and ionic nature (Smith and Oehme 1992). Transport in the air after spray applications is 
GLYPHOSATE 2

1. RELEVANCE TO PUBLIC HEALTH

dependent on meteorological conditions; ground and aerial applications can result in spray drift, which 

may affect non-target plants (PAN 2009; Yates et al.1978). 

The general population may be exposed to glyphosate by dermal contact with consumer products, crops, 

foliage, or soils containing residues of this chemical; ingestion of plants, crops, foods, or waters 

containing residues of this chemical; and inhalation of mist or spray during the use of products containing 

this chemical. As a result of its widespread usage, glyphosate is present at low levels in a wide range of 

foods (FAO and WHO 2016). The greatest potential for exposure can be expected for people who use 

glyphosate products at home and for populations residing near agricultural areas and crop farms, 

manufacturing and processing plants where glyphosate is produced or used, and hazardous waste disposal 

sites containing glyphosate.

Occupational exposure of glyphosate may occur via inhalation, dermal contact, and/or ocular contact 

during manufacture, transport, use, and disposal. Farmers and home gardeners using herbicides 

containing glyphosate may be exposed to glyphosate via inhalation, dermal contact, and/or ocular contact 

as well. People may be exposed to glyphosate upon entering areas where it has been recently applied. 

Dermal contact appears to be the major route of exposure to glyphosate for people involved in its 

application.

Children are expected to be exposed to glyphosate by the same routes as adults in the general population. 

Products containing glyphosate should be kept out of the reach of children. Due to increased hand-tomouth activity and playing habits, children are more likely to come into contact with glyphosate residues 

that may be present in soil. Glyphosate is not likely to bioaccumulate in breast milk (Bus 2015) and was 

not detected in breast milk from lactating mothers with detectable glyphosate in their urine (McGuire et 

al. 2016). In one small study, neither glyphosate nor its major degradation product, 

aminomethylphosphonic acid (AMPA), were detected in the maternal or fetal cord serum of pregnant 

subjects (Aris and LeBlanc 2011).

See Chapter 5 for more detailed information regarding concentrations of glyphosate in environmental 

media.
GLYPHOSATE 3

1. RELEVANCE TO PUBLIC HEALTH

1.2 SUMMARY OF HEALTH EFFECTS 

Information regarding the toxicity of glyphosate comes primarily from oral studies in laboratory animals 

exposed to glyphosate technical. No information was located regarding health effects in humans exposed 

to glyphosate technical; human exposures are to herbicides that contain glyphosate and other ingredients or 

to glyphosate residues in selected food sources. Human studies have reported possible associations

between glyphosate herbicide use and various health outcomes. A few animal studies evaluated the effects 

of inhalation or oral exposure to glyphosate formulations containing surfactant and additional unspecified 

substances. Reported effects may be due, at least in part, to the surfactant. Furthermore, glyphosate 

formulations vary in specific components and their relative proportions, thus precluding meaningful 

comparisons of toxic effect levels. Therefore, Figure 1-1 contains summary information related only to 

glyphosate technical. 
GLYPHOSATE 4

1. RELEVANCE TO PUBLIC HEALTH

Figure 1-1. Noncancer Health Effects Found in Animals Following Oral Exposure 

to Glyphosate Technical

* Classification of glyphosate used in each study is based on author-report. Technical-grade glyphosate has a purity 

of ≥80%, though the purity is usually >90% (IPCS 1994, McBean 2011). 
GLYPHOSATE 5

1. RELEVANCE TO PUBLIC HEALTH

As illustrated in Figure 1-1, gastrointestinal disturbance and effects on the salivary gland appear to be the 

most sensitive noncancer effects in animal studies that employed oral exposure to glyphosate technical. 

Ocular, hepatic, renal, and body weight effects have been reported as well. Developmental effects were 

observed at dose levels resulting in maternal toxicity. Effects observed in animals are considered relevant 

to human health in the absence of experimental data to indicate otherwise.

Gastrointestinal Effects. Gastrointestinal symptoms (e.g., nausea, vomiting, abdominal pain, sore throat, 

mucosal damage in mouth and esophagus) are commonly reported in patients ingesting glyphosate 

products (Chang et al. 1999; Lee et al. 2000, 2008; Moon and Chun 2010; Roberts et al. 2010; Sawada et 

al. 1988; Talbot et al. 1991; Tominack et al. 1991). Gastrointestinal effects have frequently been seen in 

animal studies. For example, soft stool/diarrhea were reported in pregnant rabbits gavaged with 

glyphosate technical during gestation (EPA 1992f, 2017b) and rats administered glyphosate technical in 

the diet for 2 generations (EPA 1992a). Inflammation of gastric mucosa was observed in female rats 

orally exposed to glyphosate technical for 2 years (EPA 1991a, 1991b). Cytoplasmic alterations were 

reported in salivary glands of glyphosate-treated rats and mice; the toxicological significance of these 

salivary gland changes is uncertain (NTP 1992).

Body Weight Effects. Depressed body weight was observed during intermediate- and chronic-duration 

oral exposure of laboratory animals to glyphosate technical at doses ≥1,183 mg/kg/day (EPA 1985a, 

1991a, 1991b, 1992a).

Hepatic Effects. Increased liver weight and increased serum markers of liver effects (alkaline 

phosphatase [AP], alanine aminotransferase [ALT], and/or bile acids) were observed in rats administered 

glyphosate technical for 13 weeks at ≥1,678 mg/kg/day (NTP 1992). Centrilobular hepatocellular 

necrosis was observed in livers from male mice administered glyphosate technical for 2 years at an 

estimated dose of 4,945 mg/kg/day (EPA 1985a). Other studies found less conclusive signs of hepatic 

effects such as changes in thiobarbituric acid reactive substances (Almeida et al. 2017; Milic et al. 2018) 

and significantly increased ROS levels in the liver (Milic et al. 2018). 

Renal Effects. Increased specific gravity of urine and decreased urinary pH were noted among male rats 

administered glyphosate technical for 2 years at 940 mg/kg/day (EPA 1991a, 1991b). Female mice 

administered glyphosate technical for 2 years at 6,069 mg/kg/day exhibited significantly increased 

incidence of renal proximal tubule epithelial basophilia and hypertrophy (EPA 2015a).
GLYPHOSATE 6

1. RELEVANCE TO PUBLIC HEALTH

Ocular Effects. In a report of human case series of 1,513 ocular exposures to glyphosate products, minor 

symptoms (primarily transient irritation) were observed in 70% of the cases; most (99%) complained of 

eye pain (Acquavella et al. 1999). Lens abnormalities were observed in male rats orally administered 

glyphosate technical for 2 years at 940 mg/kg/day (EPA 1991a, 1991b). According to EPA (1993),

glyphosate is considered mildly irritating to the eye following ocular instillation.

Developmental Effects. Limited epidemiology studies provided suggestive evidence of associations 

between maternal preconception exposure to glyphosate and increased risk of spontaneous abortion 

(Arbuckle et al. 2001) and parent-reported attention deficit disorder/attention deficit hyperactivity 

disorder (Garry et al. 2002). Depressed weight and increased incidence of unossified sternebrae were 

observed in gestation day (GD) 20 fetuses from rat dams treated with glyphosate technical by gavage at 

3,500 mg/kg/day during GDs 6–19 (EPA 1992e). In a study of rats exposed via the diet for 2 generations, 

up to 14–20% depressed pup body weight and/or body weight gain were noted at an estimated glyphosate 

technical dose of 3,134 mg/kg/day (EPA 1992a). In another 2-generation oral rat study, an estimated 

glyphosate technical dose of 1,234 mg/kg/day resulted in delayed preputial separation (EPA 2013a). A 3-

generation study in Sprague-Dawley rats using only 25 mg/kg/day glyphosate technical found delays in 

puberty in F1 males and significant increases in organ system diseases in F2 and F3 rats of both sexes

(Kubsad et al. 2019). 

Cancer Effects. The carcinogenic potential of glyphosate has been evaluated in six meta-analyses 

(Chang and Delzell 2016; IARC 2017; Schinasi and Leon 2014; Leon et al. 2019; Pahwa et al. 2019; 

Zhang et al. 2019a) and a number of case-control and cohort epidemiology studies (see Section 2.19 for 

detailed information and specific citations). The meta-analyses reported positive associations between 

glyphosate use and selected lymphohematopoietic cancers. Most of the case-control and cohort studies 

used self-reported ever/never glyphosate use as the biomarker of exposure, and subjects were likely 

exposed to other pesticides as well. Numerous studies reported risk ratios greater than 1 for associations 

between glyphosate exposure and risk of non-Hodgkin’s lymphoma or multiple myeloma; however, the 

reported associations were statistically significant only in a few studies.

Glyphosate-Containing Herbicide Formulations. Collectively, animal studies in which glyphosatecontaining herbicide formulations were tested by the oral exposure route have identified the following 

targets of toxicity:

• Body weight effects (depressed body weight gain in mice),
GLYPHOSATE 7

1. RELEVANCE TO PUBLIC HEALTH

• Hematological effects (decreases in red blood cells, hematocrit, and hemoglobin, and increases in

mean corpuscular volume and neutrophils in mice),

• Hepatic effects (increased serum liver enzyme activity and histopathologic liver lesions in male

rats),

• Renal effects (histopathologic kidney lesions in male rats), and

• Reproductive effects (increased percentage of morphologically abnormal sperm in rats).

A summary figure of sensitive targets of glyphosate-containing herbicide formulations is not included in 

this toxicological profile for glyphosate because formulations were not equivalent across studies and other 

ingredients (in addition to glyphosate as active ingredient) may have influenced the observed effects.

1.3 MINIMAL RISK LEVELS (MRLs) 

Animal studies submitted to EPA’s Office of Pesticides Programs to fulfill requirements for the 

registration of a particular glyphosate formulation for use in the United States involve exposure to 

glyphosate technical (typically >90% purity). Some animal studies in the open literature used glyphosate 

formulations that typically included 1–41% glyphosate technical (or glyphosate salts) and up to 18% 

surfactant (along with other “inert” ingredients). Surfactants in glyphosate formulations may be at least 

partly responsible for the toxic effects from overexposure to glyphosate formulations (Adam et al. 1997; 

Sawada et al. 1988; Williams et al. 2000). Human exposure to glyphosate formulations via its use in 

weed control includes exposure to all substances in a particular glyphosate formulation. No MRLs were 

derived for glyphosate formulations due to the wide variation in glyphosate content and surfactants used 

in various glyphosate formulations and the fact that surfactants can contribute to the toxicity of 

glyphosate formulations. However, because exposures of the general population via food or water 

sources with measurable glyphosate residues most likely involve glyphosate and/or its breakdown 

products rather than the intact glyphosate-based formulation, health effects data associated with oral 

exposure to glyphosate technical are considered relevant to potential derivation of oral MRLs for 

glyphosate. Oral MRLs based on glyphosate technical would not be applicable to intentional or 

accidental ingestion of a glyphosate formulation.

Available data for inhalation exposure to glyphosate technical are limited to a summary from a single 

4-week repeated-exposure rat study in which no effects were observed at the highest exposure level (EPA

1985c). The inhalation database was, therefore, not considered adequate for derivation of inhalation 

MRLs for glyphosate. As presented in Figure 1-1, available data have identified the gastrointestinal tract 
GLYPHOSATE 8

1. RELEVANCE TO PUBLIC HEALTH

as the most sensitive target of glyphosate toxicity following oral exposure. The oral database was 

considered adequate for derivation of acute- and chronic-duration oral MRLs for glyphosate. These 

MRLs are summarized in Table 1-1 and discussed in detail in Appendix A. The chronic-duration 

MRL value is adopted as the intermediate-duration oral MRL for glyphosate (see Appendix A). 

As illustrated in Figure 1-2, gastrointestinal disturbances (e.g., loose stools/diarrhea, decreased fecal 

production, inflammation of gastric mucosa, cytoplasmic alterations in salivary glands) appear to be 

the most sensitive effects of glyphosate technical toxicity in animals. The lowest-observed-adverseeffect levels (LOAELs) in Figure 1-2 reflect actual doses (levels of exposure) employed in animal 

studies. 

Figure 1-2. Summary of Sensitive Targets of Glyphosate Technical – Oral

The gastrointestinal tract is the most sensitive target of ingested glyphosate technical. 

Numbers in circles are the lowest LOAELs for all health effects in animals; no reliable doseresponse data were available for humans.
GLYPHOSATE 9

1. RELEVANCE TO PUBLIC HEALTH

Table 1-1. Minimal Risk Levels (MRLs) for Technical Glyphosatea

Exposure 

duration MRL Critical effect

Point of 

departure

Uncertainty 

factor Reference

Inhalation exposure (ppm)

Acute Insufficient data for MRL derivation

Intermediate Insufficient data for MRL derivation

Chronic Insufficient data for MRL derivation

Oral exposure (mg/kg/day)

Acute 1 Gastrointestinal effects 100 (NOAEL) 100 EPA 2017b

Intermediate The chronic-duration oral MRL of 1 mg/kg/day is adopted as the intermediate-duration 

oral MRL.

Chronic 1 Gastrointestinal effects 113 (NOAEL) 100 EPA 1991a, 

1991b

aSee Appendix A for additional information. 

LOAEL = lowest-observed-adverse-effect level; NOAEL = no-observed-adverse-effect level
GLYPHOSATE 10

CHAPTER 2. HEALTH EFFECTS

2.1 INTRODUCTION 

The primary purpose of this chapter is to provide public health officials, physicians, toxicologists, and 

other interested individuals and groups with an overall perspective on the toxicology of glyphosate. It 

contains descriptions and evaluations of toxicological studies and epidemiological investigations and 

provides conclusions, where possible, on the relevance of toxicity and toxicokinetic data to public health. 

When available, mechanisms of action are discussed along with the health effects data; toxicokinetic 

mechanistic data are discussed in Section 3.1. 

A glossary and list of acronyms, abbreviations, and symbols can be found at the end of this profile.

To help public health professionals and others address the needs of persons living or working near hazardous 

waste sites, as well as people exposed during production and/or use of glyphosate-containing products, the 

information in this section is organized by health effect. These data are discussed in terms of route of 

exposure (inhalation, oral, and dermal) and three exposure periods: acute (≤14 days), intermediate (15–

364 days), and chronic (≥365 days).

As discussed in Appendix B, a literature search was conducted to identify relevant studies examining health 

effect endpoints. Figure 2-1 for glyphosate technical and Figure 2-2 for glyphosate formulations provide an 

overview of the database of studies in humans or experimental animals included in this chapter of the profile. 

These studies evaluate the potential health effects associated with inhalation, oral, or dermal exposure to 

glyphosate, but may not be inclusive of the entire body of literature.

This ATSDR Toxicological Profile for Glyphosate includes data for glyphosate technical (purity typically 

>90%) and glyphosate formulations (typically 1–41% v/v glyphosate technical or glyphosate salts and 

≤18% polyoxyethyleneamine [POEA] surfactant). Surfactants in glyphosate formulations may be at least 

partly responsible for the toxic effects from exposure to glyphosate formulations (Adam et al. 1997; 

Sawada et al. 1988; Williams et al. 2000; Mesnage et al. 2013). As such, health effects observed in 

studies of animals exposed to relatively high levels of glyphosate technical may not accurately reflect 

health effects from human exposure to glyphosate formulations during application as an herbicide. 

However, because the general population may be exposed to glyphosate and/or its breakdown products 

(rather than to a particular glyphosate formulation) in selected food sources or contaminated drinking 
GLYPHOSATE 11

2. HEALTH EFFECTS

water, health effects from animal studies in which glyphosate technical was used as a test substance are 

considered relevant to human health.

Product names and reported descriptions for glyphosate-containing products included in this toxicological 

profile are summarized in Table 2-1 by reference (alphabetical order). Hereafter, each glyphosatecontaining formulation will generally be identified only by the reported product name.

Table 2-1. Description of Selected Glyphosate Formulations

Reference Product name Product descriptiona

Adam et al. 1997 Roundup® 41% w/v glyphosate isopropylamine salt and 

18% w/v POEA

Benedetti et al. 2004 Glyphosate-Biocarb® 360 g/L glyphosate and 18% w/v POEA

Bolognesi et al. 1997 Roundup® 30.4% glyphosate

Caglar and Kolankaya 

2008

Roundup® Monsanto of Brazil; 360 g/L glyphosate, 18% 

w/v POEA

Cassault-Meyer et al. 

2014

Roundup® Grand Travaux Plus 607 g/L glyphosate isopropylamine salt and 

adjuvants such as POEA

Contardo-Jara et al. 

2009

Roundup Ultra® 360 g/L glyphosate isopropylamine salt and 

surfactants of unspecified composition

Dallegrave et al. 2003, 

2007

Roundup® Monsanto of Brazil; 360 g/L glyphosate, 18% 

w/v POEA

Dimitrov et al. 2006 Roundup® Ingredients and proportions not specified

EPA 1985c Roundup® 33.3% use dilution (41.56% isopropylamine 

salt of glyphosate in concentrate)

Feng et al. 1990a Roundup® Unspecified proportion of glyphosate 

isopropylamine salt

Gasnier et al. 2009 Roundup Grands Travaux® 40% glyphosate

George et al. 2010 Roundup Original® 41% glyphosate and 15% POEA

Grisolia 2002 Roundup® 48% glyphosate isopropylammonium salt; 12% 

inerts, including POEA

Holečková 2006 Unspecified technical herbicide 62% w/w isopropylamine salt of glyphosate

and 38% unspecified inerts

Jasper et al. 2012 Roundup Original® 41% glyphosate and 16% POEA

Kale et al. 1995 Roundup® Glyphosate isopropylamine salt of unspecified 

concentration

Koller et al. 2012 Roundup Ultra Max® 450 g/L glyphosate acid

Maibach 1986 Roundup® 41% glyphosate as isopropylamine salt, water, 

surfactant

Mao et al. 2018 Roundup® Composition not specified

Moriya et al. 1983 Roundup® Composition not specified
GLYPHOSATE 12

2. HEALTH EFFECTS

Table 2-1. Description of Selected Glyphosate Formulations

Reference Product name Product descriptiona

Panzacchi et al. 2018 Roundup Bioflow® 41.5% glyphosate isopropylamine salt, 42.5% 

water, and 15% proprietary surfactant

Paz-y-Miño et al. 2007 Roundup-Ultra® Unspecified proportions of glyphosate, POEA, 

and the adjuvant Cosmoflux 411F

Peluso et al. 1998 Roundup® 30.4% glyphosate isopropylammonium salt

Piešová 2004, 2005 Unspecified product from 

Monsanto, Antwerp, Belgium

62% w/w isopropylamine salt of glyphosate 

and 38% unspecified inerts

Prasad et al. 2009 Roundup® >41% glyphosate isopropylamine salt

Raipulis et al. 2009 Roundup BIO® Ingredients not specified

Rank et al. 1993 Roundup® 480 g/L glyphosate isopropylamine salt

Romano et al. 2010 Roundup Transorb® 648 g/L isopropylamine salt of glyphosate and 

594 g/L inerts

Šiviková and 

Dianovskỳ 2006

Unspecified product from 

Monsanto Europe S.A., Belgium

62% glyphosate; 38% unspecified inerts

Vigfusson and Vyse 

1980

Roundup® Ingredients not specified

Wester et al. 1991 Roundup® Ingredients not specified

Wildeman and Nazar 

1982

Unspecified commercial 

formulation

Glyphosate-containing product (no additional 

details on composition)

Wunnapuk et al. 2014 Concentrate Roundup® 

Weedkiller

Monsanto Australia, containing 360 g/L of 

glyphosate (only ingredient specified)

aLimited to the glyphosate-containing substance description in the corresponding study report.

POEA = polyoxyethyleneamine (surfactant)

Animal oral study information for glyphosate technical is presented in Table 2-2 and Figure 2-3. Animal 

oral study information for glyphosate formulations is presented in Table 2-3. Animal dermal study 

information for glyphosate technical is presented in Table 2-4.

Levels of significant exposure (LSEs) for each route and duration are presented in tables and illustrated in 

figures. LSE tables and figures for animal inhalation studies of glyphosate technical and glyphosate 

formulations are precluded by lack of data. The points in the figures showing no-observed-adverse-effect 

levels (NOAELs) or lowest-observed-adverse-effect levels (LOAELs) reflect the actual doses (levels of 

exposure) used in the studies. LOAELs have been classified into "less serious" or "serious" effects. 

"Serious" effects are those that evoke failure in a biological system and can lead to morbidity or mortality 

(e.g., acute respiratory distress or death). "Less serious" effects are those that are not expected to cause 

significant dysfunction or death, or those whose significance to the organism is not entirely clear. 
GLYPHOSATE 13

2. HEALTH EFFECTS

ATSDR acknowledges that a considerable amount of judgment may be required in establishing whether 

an endpoint should be classified as a NOAEL, "less serious" LOAEL, or "serious" LOAEL, and that in 

some cases, there will be insufficient data to decide whether the effect is indicative of significant 

dysfunction. However, the Agency has established guidelines and policies that are used to classify these 

endpoints. ATSDR believes that there is sufficient merit in this approach to warrant an attempt at 

distinguishing between "less serious" and "serious" effects. The distinction between "less serious" effects 

and "serious" effects is considered to be important because it helps the users of the profiles to identify 

levels of exposure at which major health effects start to appear. LOAELs or NOAELs should also help in 

determining whether or not the effects vary with dose and/or duration, and place into perspective the 

possible significance of these effects to human health.

A User's Guide has been provided at the end of this profile (see Appendix C). This guide should aid in 

the interpretation of the tables and figures for LSEs and MRLs.

Glyphosate-containing products are among the most widely-used herbicides in commercial, agricultural,

and residential settings (NPIC 2015). Selected field crops have been genetically modified to resist 

damage from glyphosate; such crops can be sprayed with glyphosate formulations to control weed growth 

without harming the genetically-modified plants. Selected glyphosate-containing products are labeled for 

use as desiccants on some grain crops a few weeks prior to harvest.

Glyphosate technical (purity typically >90%) has been evaluated in numerous animal studies, most of 

which employed the oral exposure route and were submitted to EPA’s Office of Pesticide Programs

through the pesticide registration program as directed by the Federal Insecticide, Fungicide, and 

Rodenticide Act (FIFRA), Federal Food, Drug and Cosmetic Act (FFDCA), and Food Quality Protection 

Act (FQPA). The submitted studies are generally unpublished proprietary studies. EPA evaluated 

submitted study reports and produced summaries termed Data Evaluation Records or Data Evaluation 

Reports (DERs) that include study details and EPA’s own conclusions regarding study design, results, 

and conclusions of the study authors. Information from DERs received from EPA is summarized in this 

ATSDR Toxicological Profile for Glyphosate (note: selected DERs can be requested at: 

https://www.epa.gov/foia or viewed from a list of cleared reviews for glyphosate or glyphosate salts at 

https://archive.epa.gov/pesticides/chemicalsearch/chemical/foia/web/html/a.html). EPA evaluated and 

produced DERs for selected proprietary animal studies submitted by various chemical companies to 

agencies or organizations outside the United States for product registration purposes. Results from the 

DERs available to ATSDR were included in the Toxicological Profile for Glyphosate.
GLYPHOSATE 14

2. HEALTH EFFECTS

Epidemiological studies of glyphosate are predominantly case-control and cohort studies that examined 

possible associations between exposure to glyphosate (in glyphosate-containing herbicides) and selected 

health outcomes (noncancer and cancer endpoints), or case reports following accidental or intentional 

ingestion of glyphosate-containing products. These epidemiology studies are summarized in Table 2-5

(noncancer) and Table 2-7 (cancer). The majority of the studies used self-reported (or proxy reported) 

ever/never glyphosate use as the measure of exposure and some studies included a metric for frequency of 

exposure. There is no information regarding health effects in humans exposed to glyphosate technical.

Most reliable dose-response health effects data come from oral studies of animals administered 

glyphosate technical (seeFigure 2-1 for an overview of the number of animal studies examining potential 

endpoints of concern from oral exposure to glyphosate technical). No information was located regarding 

the effects of inhaled glyphosate technical. In a 4-week study that employed repeated inhalation exposure 

of rats to Roundup®, no adverse effects were observed at the highest exposure concentration tested 

(360 mg Roundup®/m3) (EPA 1985c). Limited animal data for dermal exposure to glyphosate technical 

indicate that glyphosate is not a dermal irritant. Results from the oral animal studies identify the 

following targets of glyphosate toxicity, albeit at relatively high dose levels:

• Gastrointestinal effects: Clinical signs and/or pathological evidence of glyphosate-induced 

irritation were observed in several animal studies; the lowest dose level resulting in 

gastrointestinal effects was 175 mg/kg/day for diarrhea and few feces in pregnant rabbits 

administered glyphosate acid by gavage. Gastrointestinal disturbances are signs and/or symptoms 

following ingestion of large amounts of glyphosate-containing products.

• Developmental effects: Glyphosate treatment-related developmental effects were noted in a few 

studies at dose levels (≥1,234 mg/kg/day) resulting in maternal toxicity as well.

• Body weight effects: Depressed body weight and/or depressed body weight gain resulted from 

repeated dosing of glyphosate technical at dose levels ≥1,183 mg/kg/day.

• Hepatic effects: Increases in liver weight and serum ALT activity were observed in one 

repeated-dose study at a dose level of 1,678 mg/kg/day.

• Ocular effects: Lens abnormalities were observed in one repeated-dose study at a dose level of 

940 mg/kg/day.

• Renal effects: Indicators of renal toxicity were noted in rats and mice administered glyphosate 

technical in the diet for 2 years at high doses (940 and 6,069 mg/kg/day, respectively).

• Other effects: Neurological, hematological, immunological, and reproductive endpoints have 

been evaluated, but do not appear to be particular targets of glyphosate toxicity.
GLYPHOSATE 15

2. HEALTH EFFECTS

• Cancer: Upon evaluation of available carcinogenicity studies in laboratory rodents, multiple

agencies or organizations have concluded that glyphosate technical does not appear to be an 

animal carcinogen. In contrast, IARC considered the animal data to provide “sufficient evidence” 

of glyphosate carcinogenicity.

An overview of the number of human and animal studies examining potential endpoints of concern from 

exposure to glyphosate formulations is presented inFigure 2-2. Results from available animal studies 

identify the following targets of toxicity: 

• Developmental effects: Histopathologic testicular lesions, decreased sperm production, and 

increased incidence of fetal skeletal malformations were reported in response to oral dosing of rat 

weanlings or pregnant rats with selected glyphosate formulations in the range of 5–

500 mg/kg/day.

• Endocrine effects: Decreased serum testosterone was noted in male rat weanlings administered 

a glyphosate formulation orally at 5 mg/kg/day.

• Body weight effects: Seriously depressed body weight gain was observed in mice administered a 

glyphosate formulation orally at 50 mg/kg/day.

• Renal effects: Histopathologic kidney lesions were noted in male rats gavaged once with a 

glyphosate formulation at 250 mg/kg.

• Hepatic effects: Increased serum liver enzyme activity and histopathologic liver lesions were 

reported in male rats repeatedly gavaged with a glyphosate formulation at 487 mg/kg/day.

• Hematological effects: Decreases in red blood cells, hematocrit, and hemoglobin, and increases 

in mean corpuscular volume and neutrophils were reported in mice administered a glyphosate 

formulation orally at 500 mg/kg/day.

• Reproductive effects: Increased percentage of morphologically abnormal sperm was reported 

among rats receiving a glyphosate formulation from the drinking water for 8 days at 

640 mg/kg/day.
GLYPHOSATE 16

2. HEALTH EFFECTS

7 

-

10 

5 

5 

1 

1 

4 

1 

8 

9 

-

8 

11 

-

-

20 

3 

-

-

-

-

Cancer

Other Noncancer

Developmental

Reproductive

Neurological

Immunological

Endocrine

Ocular

Dermal

Renal

Hepatic

Musculoskeletal

Hematological

Gastrointestinal

Cardiovascular

Respiratory

Body weight

Death

Figure 2-1. Overview of the Number of Animal Studies Examining Glyphosate Technical Health Effects*

Most studies examined the potential body weight, gastrointestinal, hematological, hepatic, and developmental effects of 

glyphosate technical (counts represent studies examining endpoint)

 

*Includes only animal studies that employed oral exposure to glyphosate technical as discussed in Chapter 2. A total of 30 studies include those finding no effect. 

Most studies examined multiple endpoints.

Oral

97%

Dermal

3%

Acute

27%

Intermediate

53%

Chronic

20%

Exposure Route Studies

Exposure Duration Studied
GLYPHOSATE 17

2. HEALTH EFFECTS

-

-

9 

13 

8 

1 

7 

1 

-

5 

8 

1 

3 

4 

-

2 

21 

3 

22 

6 

7 

3 

3 

-

3 

2 

6 

4 

1 

2 

1 

10 

13 

15 

-

8 

Cancer

Other Noncancer

Developmental

Reproductive

Neurological

Immunological

Endocrine

Ocular

Dermal

Renal

Hepatic

Musculoskeletal

Hematological

Gastrointestinal

Cardiovascular

Respiratory

Body weight

Death

Oral

91%

Inhalation 

2%

Figure 2-2. Overview of the Number of Studies Examining Glyphosate Formulations Health Effects*

Most epidemiological studies examined potential cancer, respiratory, and developmental effects associated with 

glyphosate-containing products; most animal studies examined potential body weight and developmental effects 

associated with glyphosate-containing products

More studies evaluated health effects in humans than animals (counts represent studies examining endpoint)

 

 

*A total of 85 studies, including those finding no effect. Many studies examined multiple endpoints. Reliable exposure route and duration information was not 

typically available for humans. Therefore, relative exposure route and duration proportions are plotted only for animal studies. 

Acute

29%

Intermediate

58%

Chronic

13%

Exposure Route Studies

(Animal studies only, 41 oral studies, 1 

inhalation study, 3 studies with other 

routes of exposure not included)

Exposure Duration Studied
GLYPHOSATE 18

2. HEALTH EFFECTS

Table 2-2. Levels of Significant Exposure to Glyphosate Technicala – Oral

Figure 

keyb

Species 

(strain)

No./group

Exposure 

parameters

Doses 

(mg/kg/day)

Parameters 

monitored Endpoint

NOAEL 

(mg/kg/day)

Less serious 

LOAEL 

(mg/kg/day)

Serious 

LOAEL 

(mg/kg/day) Effects

ACUTE EXPOSURE

1 RAT (Wistar) 

8M

Once

(G)

0, 2,000 

mg/kg

CS, GN, HP, 

LE, OW

Gastro 2000 M Diarrhea in 2/8 rats 

for 6 hours 

postdosing, prior to 

sacrifice at 24 hours

Adam et al. 1997 – Glyphosate technical, purity not specified

2 RAT 

(SpragueDawley) 5 

mixed

Once

(GW)

3,160, 3,980, 

5,010, 6,310

CS, GN, LE Death 4320 LD50

EPA 1992b – Glyphosate technical, purity not specified

3 RAT 

(SpragueDawley) 25 F

GDs 6–19

1 time/day

(GW)

0, 300, 1,000, 

3,500

BW, CS, DX, 

FX, GN, LE, 

MX, TG

Death 3500 F 6/25 Dams died

Bd wt 1000 F 3500 F 28.5% depressed 

mean maternal body 

weight gain

Gastro 1000 F 3500 F Diarrhea, soft stools

Develop 1000 F 3500 F 9% depressed mean 

fetal body weight, 

increased incidence 

of unossified 

sternebrae at serious 

maternally-toxic 

dose level

EPA 1992e – Glyphosate technical, purity 98.7%

4 RAT (Alpk: 

APfSD) 10 M, 

10 F

Once

(GW)

0, 500, 1,000, 

2,000 mg/kg

BW, CS, FI, 

GN, HP, LE, 

OF, OW

Bd wt 2000

Gastro 1000 2000 Diarrhea
GLYPHOSATE 19

2. HEALTH EFFECTS

Table 2-2. Levels of Significant Exposure to Glyphosate Technicala – Oral

Figure 

keyb

Species 

(strain)

No./group

Exposure 

parameters

Doses 

(mg/kg/day)

Parameters 

monitored Endpoint

NOAEL 

(mg/kg/day)

Less serious 

LOAEL 

(mg/kg/day)

Serious 

LOAEL 

(mg/kg/day) Effects

Neuro 1000 2000 Decreased activity, 

subdued behavior, 

hunched posture

Other 

noncancer

1000 2000 Hypothermia

EPA 2013c – Glyphosate technical, purity 95.6%

5 RAT (Alpk: 

APfSD) 24 F

GDs 7–16

1 time/day

(GW)

0, 250, 500, 

1,000

BW, CS, DX, 

FI, FX, GN, 

LE, MX, OW

Bd wt 1000 F

Develop 1000 F

EPA 2017b – Glyphosate acid, purity 95.6%

6 RAT SpragueDawley 10M2 wk-once/d

(W)

0, 2.5, 25 HP BI Endocr 25 M

Repro 25 M

Johansson et al. 2018 – glyphosate technical, purity 96%

7 RABBIT (New 

Zealand 

white) 20 F

GDs 8-20 1 

time/day

(GW)

0, 100, 175, 

300

BW, CS, DX, 

FI, FX, GN, 

LE, MX, OW

Bd wt 300 F NOAEL for maternal 

body weight

Gastro 100 Fc 175 F Diarrhea, few feces

Develop 300 F

EPA 2017b – glyphosate acid, purity 95.6%

INTERMEDIATE EXPOSURE

8 RAT 

(SpragueDawley) 30 M, 

30 F

2 Generation, up 

to 19 

weeks/generation

(F)

F0 M: 0, 137, 

754, 2,219 

F0 F: 0, 160, 

802, 3,134 

F1 M: 0, 165, 

818, 2,633 

F1 F: 0, 194, 

947, 3,035

NS Bd wt 802 F 3134 F Up to 18% 

depressed mean 

maternal body 

weight gain
GLYPHOSATE 20

2. HEALTH EFFECTS

Table 2-2. Levels of Significant Exposure to Glyphosate Technicala – Oral

Figure 

keyb

Species 

(strain)

No./group

Exposure 

parameters

Doses 

(mg/kg/day)

Parameters 

monitored Endpoint

NOAEL 

(mg/kg/day)

Less serious 

LOAEL 

(mg/kg/day)

Serious 

LOAEL 

(mg/kg/day) Effects

Bd wt 754 M 2219 M Up to 12% 

depressed mean 

paternal body weight 

gain

Gastro 802 F 3134 F Soft stool

Gastro 754 M 2219 M Soft stool

Repro 3134 F

Repro 2219 M

Develop 802 3134 Up to 14–20% 

depressed mean pup 

body weight or body 

weight gain during 

lactation at 

maternally-toxic 

dose level

EPA 1992a – Glyphosate technical, purity 97.67%

9 RAT 

(SpragueDawley) 12 M, 

12 F

3-Generation

(F)

0, 3, 10, 30 BW, CS, DX, 

FI, FX, GN, 

HP, LE, MX, 

OW

Bd wt 30

Repro 30

EPA 1992g – Glyphosate technical, purity 98.7%

10 RAT 

(SpragueDawley) 28 M, 

28 F

2 Generation, up 

to 19 

weeks/generation

(F)

M: 0, 121, 

408, 1,234; 

F: 0, 126, 

423, 1,273

BW, CS, DX, 

FI, FX, GN, 

HP, LE, MX, 

OF, OW, TG

Bd wt 1273 F

Bd wt 1234 M

Hepatic 1273 F

Hepatic 1234 M

Renal 1273 F
GLYPHOSATE 21

2. HEALTH EFFECTS

Table 2-2. Levels of Significant Exposure to Glyphosate Technicala – Oral

Figure 

keyb

Species 

(strain)

No./group

Exposure 

parameters

Doses 

(mg/kg/day)

Parameters 

monitored Endpoint

NOAEL 

(mg/kg/day)

Less serious 

LOAEL 

(mg/kg/day)

Serious 

LOAEL 

(mg/kg/day) Effects

Renal 1234 M

Repro 1273 F

Repro 1234 M

Develop 408 M 1234 M Delayed preputial 

separation

EPA 2013a – Glyphosate technical, purity 95.7%

11 RAT (Alpk: 

APfSD) 12 M, 

12 F

13 weeks

(F)

M: 0, 155.5, 

617.1, 

1,546.5

F: 0, 166.3, 

672.1, 

1,630.6

BW, CS, FI, 

GN, HP, LE, 

OF, OW

Neuro 1630.6 F

Neuro 1546.5 M

EPA 2013c – Glyphosate technical, purity 95.6%

12 RAT (F344/N) 

10 M, 10 F

13 weeks

(F)

M: 0, 205, 

410, 811, 

1,678, 3,393 

F: 0, 213, 

421, 844, 

1,690, 3,393

BC, BW, CS, 

EA, FI, GN, 

HE, HP, LE, 

OF, OW

Bd wt 3393 F

Bd wt 1678 M 3393 M 18% lower mean 

body weight and 

body weight gain

Gastro 213 F 421 F Increased severity of 

basophilia and 

hypertrophy of acinar 

cells in parotid and 

submandibular 

salivary glands
GLYPHOSATE 22

2. HEALTH EFFECTS

Table 2-2. Levels of Significant Exposure to Glyphosate Technicala – Oral

Figure 

keyb

Species 

(strain)

No./group

Exposure 

parameters

Doses 

(mg/kg/day)

Parameters 

monitored Endpoint

NOAEL 

(mg/kg/day)

Less serious 

LOAEL 

(mg/kg/day)

Serious 

LOAEL 

(mg/kg/day) Effects

Gastro 205 M 410 M Increased severity of 

basophilia and 

hypertrophy of acinar 

cells in parotid and 

submandibular 

salivary glands

Hemato 3393

Hepatic 1690 F 3393 F Increases in liver 

weight and serum 

AP, ALT, and bile 

acids

Hepatic 811 M 1678 M Increases in liver 

weight and serum 

ALT

NTP 1992 – Glyphosate technical, purity 99%

13 RAT SpragueDawley F0 8FGD 6 to PND 120-

once/d

(W)

0, 1.75 RX GN BC 

HP BI BW

Bd wt 1.75 F

Repro 1.75 F

Manservisi et al. 2019 – glyphosate technical, 99.5%

14 RAT SpragueDawley F1 8GD 6 to PND 120-

once/d, 6 wkonce/d

(W)

0, 1.75 RX GN BC 

HP BI FI WI 

BW

Bd wt 1.75

Endocr 1.75

Repro 1.75 M

Develop 1.75 M increased anogenital 

distance at PND 4

Manservisi et al. 2019 – glyphosate technical, 99.5%
GLYPHOSATE 23

2. HEALTH EFFECTS

Table 2-2. Levels of Significant Exposure to Glyphosate Technicala – Oral

Figure 

keyb

Species 

(strain)

No./group

Exposure 

parameters

Doses 

(mg/kg/day)

Parameters 

monitored Endpoint

NOAEL 

(mg/kg/day)

Less serious 

LOAEL 

(mg/kg/day)

Serious 

LOAEL 

(mg/kg/day) Effects

15 RAT SpragueDawley F1 10GD 6 to PND 120-

once/d, 13 wkonce/d

(W)

0, 1.75 RX GN BC 

HP BI FI WI 

BW

Bd wt 1.75

Endocr 1.75

Repro 1.75 M

Develop 1.75 M increased anogenital 

distance at PND 4

Manservisi et al. 2019 – glyphosate technical, 99.5%

16 MOUSE 

(B6C3F1/Crl) 

10 F

28 Days

(F)

0, 150.1, 

449.1, 

1,447.5

BW, CS, FI, 

GN, OF, OW, 

WI

Bd wt 1447.5 F

Immuno 1447.5 F

EPA 2013b – Glyphosate technical, purity 85.2%

17 MOUSE 

(B6C3F1) 10 

M, 10 F

13 weeks

(F)

M: 0, 507, 

1,065, 2,273, 

4,776, 10,780 

F: 0, 753, 

1,411, 2,707, 

5,846, 11,977

BW, CS, FI, 

GN, HP, LE, 

OF, OW

Bd wt 5846 F 11977 F 10% lower mean 

final body weight

Bd wt 2273 M 4776 M 11% lower mean 

final body weight

Gastro 1411 F 2707 F

Gastro 1065 M 2273 M Increased severity of 

basophilia of acinar 

cells in parotid 

salivary gland

Hepatic 11977 F

Hepatic 10780 M

NTP 1992 – Glyphosate technical, purity 99%
GLYPHOSATE 24

2. HEALTH EFFECTS

Table 2-2. Levels of Significant Exposure to Glyphosate Technicala – Oral

Figure 

keyb

Species 

(strain)

No./group

Exposure 

parameters

Doses 

(mg/kg/day)

Parameters 

monitored Endpoint

NOAEL 

(mg/kg/day)

Less serious 

LOAEL 

(mg/kg/day)

Serious 

LOAEL 

(mg/kg/day) Effects

18 RABBIT 

(Dutch belted) 

16 F

GDs 6-27 1 

time/day

(GW)

0, 75, 175, 

350

BW, CS, DX, 

FX, GN, LE, 

MX, TG

Death 350 F 10/16 maternal 

rabbits died

Bd wt 350 F

Gastro 175 F 350 F

Develop 350 F Increased incidence 

of soft stool and/or 

diarrhea

EPA 1992f – Glyphosate technical, purity 98.7%

CHRONIC EXPOSURE

19 RAT 

(SpragueDawley) 60 M, 

60 F

Up to 24 months

(F)

M: 0, 89, 362, 

940 

F: 0, 113, 

457, 1,183

BC, BW, CS, 

Fl, GN, HE, 

HP, LE, OW

Bd wt 457 F 1183 F 13% lower mean 

body weight at 

treatment week 81

Bd wt 940 M

Gastro 113 Fd 457 F Inflammation of 

gastric squamous 

mucosa

Gastro 940 M

Hemato 1183 F

Hemato 940 M

Hepatic 1183 F

Hepatic 940 M

Renal 1183 F

Renal 362 M 940 M Increased specific 

gravity and 

decreased pH of 

urine

Ocular 1183 F

Ocular 362 M 940 M Increased incidence 

of lens abnormalities
GLYPHOSATE 25

2. HEALTH EFFECTS

Table 2-2. Levels of Significant Exposure to Glyphosate Technicala – Oral

Figure 

keyb

Species 

(strain)

No./group

Exposure 

parameters

Doses 

(mg/kg/day)

Parameters 

monitored Endpoint

NOAEL 

(mg/kg/day)

Less serious 

LOAEL 

(mg/kg/day)

Serious 

LOAEL 

(mg/kg/day) Effects

EPA 1991a, 1991b – Glyphosate technical, purity 96.5%

20 RAT 

(SpragueDawley) 50 M, 

50 F

26 months

(F)

M: 0, 3.05, 

10.30, 31.45 

F: 0, 3.37, 

11.22, 34.02

BC, BW, CS, 

Fl, GN, HE, 

HP, LE, OF, 

OW, UR

Bd wt 34.02 F

Bd wt 31.45 M

Gastro 34.02 F

Gastro 31.45 M

Hemato 34.02 F

Hemato 31.45 M

Hepatic 34.02 F

Hepatic 31.45 M

Renal 34.02 F

Renal 31.45 M

EPA 1992d – Glyphosate technical, purity 98.7%

21 RAT Alpk: 

APfSD Wistar) 

64 M, 64 F

Up to 2 years

(F)

M: 0, 121, 

361, 1,214 

F: 0, 145, 

437, 1,498

BC, BH, BW, 

CS, EA, Fl, 

GN, HE, HP, 

LE, OF, OP, 

OW, UR

Bd wt 1498 F

Bd wt 1214 M

Gastro 1498 F

Gastro 361 M 1214 M Exocrine hyperplasia 

in pancreas in males

Hemato 1498 F

Hemato 1214 M

Hepatic 437 F 1498 F Increased serum AP 

and ALT

Hepatic 361 M 1214 M Increased serum AP, 

ALT, bilirubin
GLYPHOSATE 26

2. HEALTH EFFECTS

Table 2-2. Levels of Significant Exposure to Glyphosate Technicala – Oral

Figure 

keyb

Species 

(strain)

No./group

Exposure 

parameters

Doses 

(mg/kg/day)

Parameters 

monitored Endpoint

NOAEL 

(mg/kg/day)

Less serious 

LOAEL 

(mg/kg/day)

Serious 

LOAEL 

(mg/kg/day) Effects

Renal 437 F 1498 F Papillary necrosis in 

kidney

Renal 361 M 1214 M Papillary necrosis in 

kidney; decreased 

pH of urine

Ocular 1498 F

Ocular 1214 M

Neuro 1498 F

Neuro 1214 M

EPA 2015c – Glyphosate technical, purity 97.6%

22 RAT 

(SpragueDawley) 85 M, 

85 F

Up to 2 years

(F)

0, 10, 100, 

300, 1,000

BC, BW, CS, 

EA, Fl, GN, 

HE, HP, LE, 

OF, OP, OW, 

UR

Bd wt 300 1000 11–14% lower mean 

body weight and 

body weight gain

Gastro 100 300 Increased severity of 

basophilia and 

hypertrophy of acinar 

cells in parotid and 

mandibular salivary 

glands

Hemato 1000

Hepatic 1000

Renal 1000 F

Renal 300 M 1000 M Decreased pH of 

urine

Ocular 1000

EPA 2015c – Glyphosate technical, purity 98.7 and 98.9%
GLYPHOSATE 27

2. HEALTH EFFECTS

Table 2-2. Levels of Significant Exposure to Glyphosate Technicala – Oral

Figure 

keyb

Species 

(strain)

No./group

Exposure 

parameters

Doses 

(mg/kg/day)

Parameters 

monitored Endpoint

NOAEL 

(mg/kg/day)

Less serious 

LOAEL 

(mg/kg/day)

Serious 

LOAEL 

(mg/kg/day) Effects

23 MOUSE (CD1) 50 M, 50 F24 months

(F)

M: 0, 161, 

835, 4,945

F: 0, 195, 

968, 6,069

BW, CS, Fl, 

GN, HE, HP, 

LE

Bd wt 6069 F

Bd wt 4945 M

Gastro 6069 F

Gastro 4945 M

Hemato 6069 F

Hemato 4945 M

Hepatic 6069 F

Hepatic 835 M 4945 M Centrilobular 

hepatocellular 

necrosis

Renal 968 F 6069 F Renal tubular 

epithelial basophilia

Renal 4945 M

EPA 2015a – Glyphosate technical, purity 99.7%

24 MOUSE (CD1) 50 M, 50 F104 weeks

(F)

0, 100, 300, 

1,000

BW, CS, Fl, 

GN, HE, HP, 

LE, WI

Bd wt 1000

Hepatic 1000

Renal 1000

EPA 2015c – Glyphosate technical, purity ≥97.5%

25 DOG (Beagle) 

6 M, 6 F

1 year

(C)

0, 20, 100, 

500

BC, BW, CS, 

Fl, GN, HE, 

HP, LE, OP, 

OW, UR, WI

Bd wt 500

Hemato 500

Ocular 500

EPA 1986a, 1987 – Glyphosate technical, purity 96.13%
GLYPHOSATE 28

2. HEALTH EFFECTS

a Purities reported in this table are the information provided by the study authors in the study methodologies regarding the chemical used in the experiments.

bThe number corresponds to entries in Figure 2-3; differences in levels of health effects and cancer effects between male and females are not indicated in 

Figure 2-3. Where such differences exist, only the levels of effect for the most sensitive gender are presented.

cUsed to derive an acute-duration oral MRL for glyphosate; NOAEL divided by an uncertainty factor of 100 (10 for animal to human extrapolation and 10 for human 

variability); see Appendix A for more detailed information regarding the MRL.

dUsed to derive a chronic-duration oral MRL for glyphosate; NOAEL divided by an uncertainty factor of 100 (10 for animal to human extrapolation and 10 for 

human variability); see Appendix A for more detailed information regarding the MRL.

ALT = alanine aminotransferase; AP = alkaline phosphatase; BC = biochemistry; BW or Bd Wt = body weight; C = capsule; CS = clinical signs; 

Develop = developmental; DX = developmental toxicity; EA = enzyme activity; (F) = exposure in feed; F = female(s); FI = food intake; FX = fetal toxicity; 

G = gavage, neat; Gastro = gastrointestinal; GD = gestation day; GN = gross necropsy; GW = gavage in water vehicle; HE = hematology; 

Hemato = hematological; HP = histopathology; Immuno = immunological; LD50 = lethal dose, 50% kill; LE = lethality; LOAEL = lowest-observed-adverse-effect 

level; M = male(s); MRL = Minimal Risk Level; MX = maternal toxicity; NOAEL = no observed-adverse-effect level; NS = not specified; OF = organ function; 

OP = ophthalmology; OW = organ weight; Repro = reproductive; TG = teratogenicity; UR = urinalysis; WI = water intake
GLYPHOSATE 29

2. HEALTH EFFECTS

Figure 2-3. Levels of Significant Exposure to Glyphosate Technical – Oral

Acute (≤14 days)
GLYPHOSATE 30

2. HEALTH EFFECTS

Figure 2-3. Levels of Significant Exposure to Glyphosate Technical – Oral

Intermediate (15-364 days)
GLYPHOSATE 31

2. HEALTH EFFECTS

Figure 2-3. Levels of Significant Exposure to Glyphosate Technical – Oral

Intermediate (15-364 days)
GLYPHOSATE 32

2. HEALTH EFFECTS

Figure 2-3. Levels of Significant Exposure to Glyphosate Technical – Oral

Chronic (≥365 days)
GLYPHOSATE 33

2. HEALTH EFFECTS

Figure 2-3. Levels of Significant Exposure to Glyphosate Technical – Oral

Chronic (≥365 days)
GLYPHOSATE 34

2. HEALTH EFFECTS

Table 2-3. Levels of Significant Exposure to Glyphosate Formulationsa – Oral

Species 

(strain)

No./group

Exposure 

parameters

Doses 

(mg/kg/day)

Parameters 

monitored Endpoint

NOAEL 

(mg/kg/day)

Less serious 

LOAEL 

(mg/kg/day)

Serious 

LOAEL 

(mg/kg/day) Effects

ACUTE EXPOSURE

RAT 

(Wistar) 15 

F

GDs 6–15, 

1 time/day

(GW)

0, 500, 750, 

1,000

BW, DX, FI, 

FX, GN, HP, 

LE, MX, OW, 

TG, WI

Death 1000 F 8/15 died

Bd wt 1000 F

Develop 500 Increased incidence of fetal skeletal 

malformations

Dallegrave et al. 2003 – Glyphosate Formulation – Roundup® (Monsanto of Brazil; 360 g/L glyphosate, 18% w/v POEA)

RAT 

(Wistar) 4 

M

Once

(GW)

0, 250, 500, 

1,200, 2,500 

mg/kg

HP, OF Renal 48.7 M 487 M Histopathologic kidney lesions.

Wunnapuk et al. 2014 – Glyphosate Formulation – Concentrate Roundup® Weedkiller (Monsanto Australia, containing 360 g/L of glyphosate)

RAT 

(Wistar) 

8M

Once

(G)

0, 2,000 

mg/kg

CS, GN, HP, 

LE, OW

Gastro 2000 M Diarrhea in rats administered 

Roundup® (41% w/v glyphosate 

isopropylamine salt and 18% w/v 

polyoxyethyleneamine [POEA]) or 

glyphosate isopropylamine salt + 

POEA at the same concentrations as 

contained in the Roundup® 

formulation

Adam et al. 1997 – Glyphosate Formulation – Roundup® (41% w/v glyphosate isopropylamine salt and 18% POEA)

RAT 

(SpragueDawley) 15 

M

8 days

(W)

0, 640 BW, OF, 

OW, WI

Repro 640 M Up to 18% increased percent 

abnormal sperm morphology

Cassault-Meyer et al. 2014 – Glyphosate formulation – Roundup® Grand Travaux Plus (607 g/L glyphosate isopropylamine salt and adjuvants 

such as POEA)
GLYPHOSATE 35

2. HEALTH EFFECTS

Table 2-3. Levels of Significant Exposure to Glyphosate Formulationsa – Oral

Species 

(strain)

No./group

Exposure 

parameters

Doses 

(mg/kg/day)

Parameters 

monitored Endpoint

NOAEL 

(mg/kg/day)

Less serious 

LOAEL 

(mg/kg/day)

Serious 

LOAEL 

(mg/kg/day) Effects

RAT 

(Wistar) 5F

Day 1 to 7 of 

pregnancy

(G)

0, 500 BI BW HP 

RX

Hepatic 500 F significantly higher (19-23%) 

thiobarbituric acid reactive 

substances (TBARS) levels in liver 

tissue compared to control

Neuro 500 F 16-26% decrease of glutathione

Repro 500 F lighter ovaries, decreased number of 

implanted sites (42% less than 

controls), reduced total number of 

corpus luteum (seen after Roundup 

exposure alone and co-exposures to 

multiple pesticides), increased 

percentage of pre-implantation loss

Almeida et al. 2017 – Glyphosate formulation – Roundup® (360 g/L of glyphosate (N-phosphonomethyl glycine))

RAT 

SpragueDawley 

10M

2 wk-once/d

(W)

0, 25 HP BI Endocr 25 M

Repro 25 M

Johansson et al. 2018 – Glyphosate formulation – Glyfonova 450 Plus® (FMC Corporation, 450 g/L glyphosate acid equivalent)

RAT 5M 14 d-once/d

(NS)

0, 5, 10, 25, 

50, 100, 250

HP BI BW Bd wt 100 M estimated decrease of 37%

Hepatic 100 M increased liver index and liver weight 

(approximately 17%), increased 

cytokine expression

Pandey et al. 2019 – Glyphosate formulation – Roundup® (Monsanto India, 41% w/w glyphosate)

MOUSE 

(Swiss) 6M

Once

(G)

0, 250, 500 BW NX Bd wt 500 M

Neuro 500 M

Ait Bali et al. 2017 – Glyphosate formulation – Roundup® (glyphosate concentration 360 g/L in the form of glyphosate isopropylamine salt 486 

g/L)
GLYPHOSATE 36

2. HEALTH EFFECTS

Table 2-3. Levels of Significant Exposure to Glyphosate Formulationsa – Oral

Species 

(strain)

No./group

Exposure 

parameters

Doses 

(mg/kg/day)

Parameters 

monitored Endpoint

NOAEL 

(mg/kg/day)

Less serious 

LOAEL 

(mg/kg/day)

Serious 

LOAEL 

(mg/kg/day) Effects

MOUSE 

(Swiss) 6M

Once

(G)

0, 250, 500 GN NX Gastro 500 M

Neuro 500 M

Aitbali et al. 2018 – Glyphosate formulation – Roundup® (glyphosate concentration 360 g/L in the form of glyphosate isopropylamine salt 486 

g/L)

MOUSE 

(Swiss) 6M

Once

(G)

0, 250, 500 NX Neuro 250 M decrease in aversive memory 

performance

Ait Bali et al. 2019 – Glyphosate formulation – Roundup® (glyphosate concentration 360 g/L in the form of glyphosate isopropylamine salt 486 

g/L)

INTERMEDIATE EXPOSURE

RAT 

(Wistar) 14 

or 16 M

75 days, 

1 time/2 days

(GW)

0, 4.87, 

48.7, 487

EA, OF Hepatic 48.7 M 487 M Increased serum liver enzyme 

activity, histopathologic liver lesions

Benedetti et al. 2004 – Glyphosate Formulation – Glyphosate-Biocarb® (360 g/L glyphosate and 18% w/v POEA)

RAT 

(Wistar) 

NS

5 weeks, 

1 time/day

(GW)

0, 56, 560 BW, EA, FI, 

HE, HP, OF, 

OW, WI

Bd wt 560

Hepatic 560

Caglar and Kolankaya 2008 – Glyphosate formulation – Roundup® (Monsanto of Brazil; 360 g/L glyphosate and 18% w/v POEA)

RAT 

(Wistar) 

NS

13 weeks,

1 time/day

(GW)

0, 56, 560 BW, EA, FI, 

HE, HP, OF, 

OW, WI

Bd wt 560

Hepatic 560

Caglar and Kolankaya 2008 – Glyphosate Formulation – Roundup® (Monsanto of Brazil; 360 g/L glyphosate and 18% w/v POEA)

RAT 

(Wistar) 15 

F

42–44 days 

(gestation, 

lactation)

(GW)

0, 50, 150, 

450

BW, CS, DX, 

FX, HP, LE, 

MX, OW, TG

Bd wt 450 F
GLYPHOSATE 37

2. HEALTH EFFECTS

Table 2-3. Levels of Significant Exposure to Glyphosate Formulationsa – Oral

Species 

(strain)

No./group

Exposure 

parameters

Doses 

(mg/kg/day)

Parameters 

monitored Endpoint

NOAEL 

(mg/kg/day)

Less serious 

LOAEL 

(mg/kg/day)

Serious 

LOAEL 

(mg/kg/day) Effects

Develop 50 M Decreased sperm production, 

histopathologic testicular lesions

Dallegrave et al. 2007 – Glyphosate Formulation – Roundup® (Monsanto of Brazil; 360 g/L glyphosate and 18% w/v POEA)

RAT 

(Wistar) 

16-18 M

30 days, 

(PPDs 23–53)

(GW)

0, 5, 50, 250 BW, DX, HP, 

OF, OW

Bd wt 250 M

Endocr 5 M Decreased serum testosterone

Develop 5 M Decreased epithelial thickness and 

increased luminal diameter in 

seminiferous tubules

Romano et al. 2010 – Glyphosate Formulation – Roundup Transorb® (648 g/L isopropylamine salt of glyphosate and 594 g/L inerts)

RAT 

(Wistar) 

7M

daily

8 weeks

(F)

0, 375 HP RX Repro 375 M significant decrease in abnormal 

sperm rate in both GLF exposed 

groups; increased testes MDA levels, 

decreased GSH levels; DNA damage 

in sperm cells; decreased sperm 

concentration and degeneration of 

Sertoli cells in testes

Avdatek et al. 2018 – Glyphosate formulation – Knockdown 48 SL (Hektaş company; glyphosate formulation not otherwise described)

RAT 

(Wistar) 6 

M,F

Continuously

120 days

(NS)

0, 500 BC BI BW 

HP

Resp 500

Hepatic 500 increase in mean liver MDA levels, 

decrease SOD concentration, 

decrease CAT activity, and 

decreased enzymatic activity of GSHPx compared to control; moderate 

hepatocytic degeneration and 

necrosis; increase in ALT, AST, and 

LDH in all exposed groups compared 

to control
GLYPHOSATE 38

2. HEALTH EFFECTS

Table 2-3. Levels of Significant Exposure to Glyphosate Formulationsa – Oral

Species 

(strain)

No./group

Exposure 

parameters

Doses 

(mg/kg/day)

Parameters 

monitored Endpoint

NOAEL 

(mg/kg/day)

Less serious 

LOAEL 

(mg/kg/day)

Serious 

LOAEL 

(mg/kg/day) Effects

Dar et al. 2019 – Glyphosate formulation – Roundup® (glyphosate 41% EC, not otherwise described)

RAT 

(Wistar) 4F 

(F0), 16M 

(F1)

maternal 

exposure GD 5 

to PND 21 then 

offspring 

exposed from 

PND 21 to 60

(W)

0, 70 BI BW CS 

GN HP NX

Neuro 70 M 23% inhibition of hippocampus 

cholinesterase after post-natal day 

60; glutamate excitotoxicity, 

misregulation of cholinergic 

transmission, oxidative damage and 

astrocyte dysfunction in offspring 

hippocampus

Develop 70 M 14% decreased body weight gain in 

offspring at day 60 compared to 

controls

Cattani et al. 2017 – Glyphosate formulation – Roundup Original® (360 g/L glyphosate, not otherwise described)

RAT 

(Wistar) 6-

12F

Daily

60 days

(GW)

0, 126, 315 BI HP LX 

RX OW

Death

Bd wt 315 F

126 F 6/12 rats died

Repro 126 F 315 F 38% decrease in relative ovary 

weight compared to control (58% 

decrease in the high-dose group); 

109% increase in percent atretic 

follicles; 14% increased MDA levels 

in ovary homogenates; decreased 

enzymatic antioxidant activity in 

ovaries; necrosis, vacuolization of 

follicles and oocytes in ovaries

Hamdaoui et al. 2018 – Glyphosate formulation – Kalach 360 SL (KL) commercial formulation (Monsanto Europe, 360 g/L glyphosate, 41.5% 

isopropylamine salt of n-phosphonomethylglycine, 15.5% surfactant and 43% water)
GLYPHOSATE 39

2. HEALTH EFFECTS

Table 2-3. Levels of Significant Exposure to Glyphosate Formulationsa – Oral

Species 

(strain)

No./group

Exposure 

parameters

Doses 

(mg/kg/day)

Parameters 

monitored Endpoint

NOAEL 

(mg/kg/day)

Less serious 

LOAEL 

(mg/kg/day)

Serious 

LOAEL 

(mg/kg/day) Effects

RAT 

(Wistar) 5-

10M, 5-

10F

GD 0 to 

weaning on 

PND 21 

(maternal 

exposure)

(W)

0, 100, 200 BI HP NX Develop 100 F impaired recognition memory, 

oxidative stress in whole brain, 

decrease in lipid peroxidation and 

enzyme activity alterations in female 

F1 offspring

Develop 100 M 200 M SLOAEL: impaired recognition 

memory

LOAEL: 23% inhibition of striatum 

acetylcholinesterase activity; 

oxidative stress in whole brain; 

enzyme activity alterations

Gallegos et al. 2018 – Glyphosate formulation – Glifloglex® (480 g/L glyphosate isopropylamine salt equivalent to 35.6% w/v of Gly acid with 

unspecified mix of inerts and adjuvants)

RAT 

Wistar 

10M

36 wk-once/d

(GW)

0, 14.4, 375, 

750

HP BC Endocr 14.4 M degeneration of pancreatic acinar 

cells and islets of Langerhans

Tizhe et al. 2018 – Glyphosate formulation – Bushfire® (360 g glyphosate/L)

RAT 

Wistar F0 

7F

GD 9 to LD 21-

once/d

(F)

0, 3.69, 

352.20

RX DX BW Bd wt 352.2 F

Repro 352.2 F

Milesi et al. 2018 – Glyphosate formulation – MAGNUM SUPER II (Grupo Agros S.R.L., Argentina, 66.2% glyphosate potassium salt)

RAT 

Wistar F1 

20-25F

GD 9 to LD 21-

once/d

(F)

0, 3.69, 

352.20

RX DX BW Bd wt 352.2 F

Repro 3.69 F increased rate of preimplantation loss 

(estimated 71% increase), fewer 

implantation sites in the uterus (not 

otherwise described)
GLYPHOSATE 40

2. HEALTH EFFECTS

Table 2-3. Levels of Significant Exposure to Glyphosate Formulationsa – Oral

Species 

(strain)

No./group

Exposure 

parameters

Doses 

(mg/kg/day)

Parameters 

monitored Endpoint

NOAEL 

(mg/kg/day)

Less serious 

LOAEL 

(mg/kg/day)

Serious 

LOAEL 

(mg/kg/day) Effects

Develop 3.69 F 352.2 F LOAEL: 2% decrease in fetal length, 

6% decrease in body weight, and an 

increased relative risk of small for 

gestational age F2 fetuses

SLOAEL: increased fetal anomalies 

(conjoined fetuses and abnormal 

limbs)

Milesi et al. 2018 – Glyphosate formulation – MAGNUM SUPER II (Grupo Agros S.R.L., Argentina, 66.2% glyphosate potassium salt, equivalent 

to 54% w/v of glyphosate acid)

RAT 

Albino 8M

12 wk-once/d

(G)

0, 3.6, 50.4, 

248.4

BC HP RX Endocr 3.6 M decrease in testosterone (about 

13%), FSH (about 17%), and LH 

(about 14%), increase in prolactin 

(about 31%)

Repro 3.6 M testicular degeneration and increased 

sperm abnormalities

Owagboriaye et al. 2017 – Glyphosate formulation – Roundup® (Monsanto, Belgium, 360 g/L glyphosate)

RAT 

SpragueDawley F0 

8F

GD 6 to PND 

120-once/d

(W)

0, 1.75 RX GN BC 

HP BI BW

Bd wt 1.75 F

Repro 1.75 F

Manservisi et al. 2019 – Glyphosate formulation – Roundup® Bioflow (360 g/L of glyphosate acid, 42.5% water, 16% surfactant)

RAT 

SpragueDawley F1 

8

GD 6 to PND 

120-once/d, 6 

wk-once/d

(W)

0, 1.75 RX GN BC 

HP BI FI WI 

BW

Bd wt 1.75

Endocr 1.75

Repro 1.75 M
GLYPHOSATE 41

2. HEALTH EFFECTS

Table 2-3. Levels of Significant Exposure to Glyphosate Formulationsa – Oral

Species 

(strain)

No./group

Exposure 

parameters

Doses 

(mg/kg/day)

Parameters 

monitored Endpoint

NOAEL 

(mg/kg/day)

Less serious 

LOAEL 

(mg/kg/day)

Serious 

LOAEL 

(mg/kg/day) Effects

Develop 1.75 increased anogenital distance at 

PND 4 in males; delayed first estrous 

in females

Manservisi et al. 2019 – Glyphosate formulation – Roundup® Bioflow (360 g/L of glyphosate acid, 42.5% water, 16% surfactant)

RAT 

SpragueDawley F1 

10

GD 6 to PND 

120-once/d, 13 

wk-once/d

(W)

0, 1.75 RX GN BC 

HP BI FI WI

Bd wt 1.75

Endocr 1.75 F increased serum TT hormone, 

decreased DHT/TT ratio, increased 

E2/TT ratio

Endocr 1.75 M decreased serum DHT hormones, 

increased plasma TSH hormones, 

decreased DHT/TT and fT/TT ratios

Repro 1.75 F

Repro 1.75 M

Develop 1.75 M increased anogenital distance at 

PND 4

Manservisi et al. 2019 – Glyphosate formulation – Roundup® Bioflow (360 g/L of glyphosate acid, 42.5% water, 16% surfactant)

MOUSE 

(albino 

Swiss) 10 

M, 10 F

15 days

1 time/day

(GW)

0, 50, 500 BW, EA, HE, 

HP, OF

Bd wt 50 60–66% depressed mean body 

weight gain

Hemato 50 500 Decreased red blood cells, 

hematocrit, hemoglobin; increased 

mean corpuscular volume, 

neutrophils

Hepatic 500

Jasper et al. 2012 – Glyphosate Formulation – Roundup® Original (41% glyphosate and 16% POEA
GLYPHOSATE 42

2. HEALTH EFFECTS

Table 2-3. Levels of Significant Exposure to Glyphosate Formulationsa – Oral

Species 

(strain)

No./group

Exposure 

parameters

Doses 

(mg/kg/day)

Parameters 

monitored Endpoint

NOAEL 

(mg/kg/day)

Less serious 

LOAEL 

(mg/kg/day)

Serious 

LOAEL 

(mg/kg/day) Effects

MOUSE 

(Swiss) 6M

Daily

6 weeks

(G)

0, 250, 500 BW BC NX 

OW

Bd wt 250 M significant reduced body weight gain 

(46%) after 40 days

Resp 500 M

Hepatic 500 M 43% decrease in relative liver weight

Renal 500 M

Neuro 250 M decreased locomotor activity, 

increased anxiety-like behavior and 

anxiety index (p<0.001) compared to 

control, decreased grooming time

Ait Bali et al. 2017 – Glyphosate formulation – Roundup® (glyphosate concentration 360 g/L in the form of glyphosate isopropylamine salt 486 

g/L)

MOUSE 

(Swiss) 6M

Daily 

6 weeks

(G)

0, 250, 500 GN NX Gastro 250 M decrease in total bacterial count in 

gut (p<0.001) compared to control

Neuro 250 M increase in anxiety index (p<0.001)

Aitbali et al. 2018 – Glyphosate formulation – Roundup® (glyphosate concentration 360 g/L in the form of glyphosate isopropylamine salt 486 

g/L)

MOUSE 

(Swiss) 6M

Daily

6 weeks

(G)

0, 250, 500 NX Neuro 250 M decreased recognition and aversive 

memory performance

Ait Bali et al. 2019 – Glyphosate formulation – Roundup® (glyphosate concentration 360 g/L in the form of glyphosate isopropylamine salt 486 

g/L)

MOUSE 

Kumming 

8M

35 d-once/d

(W)

0, 60, 180, 

540

BW OW RX Bd wt 540 M
GLYPHOSATE 43

2. HEALTH EFFECTS

Table 2-3. Levels of Significant Exposure to Glyphosate Formulationsa – Oral

Species 

(strain)

No./group

Exposure 

parameters

Doses 

(mg/kg/day)

Parameters 

monitored Endpoint

NOAEL 

(mg/kg/day)

Less serious 

LOAEL 

(mg/kg/day)

Serious 

LOAEL 

(mg/kg/day) Effects

Repro 60 M 180 M decreased sperm motility (estimated 

10% decrease in rapid progressive 

sperm, estimated 13% increase in 

immotile sperm), increased sperm 

abnormality (estimated 8% increase 

in total sperm abnormality)

Jiang et al. 2018 – Glyphosate formulation – Roundup® (360 g/L glyphosate, 18% w/v POEA)

MOUSE 

F0 

C57B1/6 

9-11F

GD 4 to PND 

30-once/d

(W)

0, 420 BW OW RX Bd wt 420 F 17% decreased body weight and 

approximately 25% decreased body 

weight gain

Renal 420 F

Endocr 420 F

Repro 420 F

Teleken et al. 2019 – Glyphosate formulation – Roundup® Original (Monsanto, Brazil, not otherwise described)

MOUSE 

F1 8-12M

GD 4 to PND 

30-once/d

(W)

0, 420 RX HP BI 

BW

Bd wt 420 M

Endocr 420 M intratesticular testosterone content 

195% higher than control mice, 

approximately 60% increase in 

plasma LH concentration, 111% 

increase in β-LH pituitary protein 

content
GLYPHOSATE 44

2. HEALTH EFFECTS

Table 2-3. Levels of Significant Exposure to Glyphosate Formulationsa – Oral

Species 

(strain)

No./group

Exposure 

parameters

Doses 

(mg/kg/day)

Parameters 

monitored Endpoint

NOAEL 

(mg/kg/day)

Less serious 

LOAEL 

(mg/kg/day)

Serious 

LOAEL 

(mg/kg/day) Effects

Repro

Develop

420 M

420 M

70% reduction of sperm in cauda 

epididymis, estimated 5% decreased 

epithelial height

delayed testes descent

Teleken et al. 2019 – Glyphosate formulation – Roundup® Original (Monsanto, Brazil, not otherwise described)

MOUSE 

(Swiss) 6M

Daily

12 weeks

(G)

0, 250, 500 BW IX NX 

OW

Bd wt 250 M significant reduced body weight gain 

(33%) after 90 days, decreased 

grooming time

Resp 250 M 50% decrease in relative lung weight

Hepatic 250 M 44% decrease in relative liver weight

Renal 250 M 50% decrease in relative kidney 

weight

Neuro 250 M decreased locomotor activity, 

increased anxiety-like behavior and 

anxiety index (p<0.001) compared to 

control

Ait Bali et al. 2017 – Glyphosate formulation – Roundup® (glyphosate concentration 360 g/L in the form of glyphosate isopropylamine salt 486 

g/L)

MOUSE 

(Swiss) 6M

Daily

12 weeks

(G)

0, 250, 500 GN NX Gastro 250 M decrease in total bacterial count in 

gut (p<0.001) compared to control

Neuro 250 M increase in anxiety index (p<0.01) 

and decreased grooming time 

(p<0.001) compared to controls

Aitbali et al. 2018 – Glyphosate formulation – Roundup® (glyphosate concentration 360 g/L in the form of glyphosate isopropylamine salt 486 

g/L)
GLYPHOSATE 45

2. HEALTH EFFECTS

Table 2-3. Levels of Significant Exposure to Glyphosate Formulationsa – Oral

Species 

(strain)

No./group

Exposure 

parameters

Doses 

(mg/kg/day)

Parameters 

monitored Endpoint

NOAEL 

(mg/kg/day)

Less serious 

LOAEL 

(mg/kg/day)

Serious 

LOAEL 

(mg/kg/day) Effects

MOUSE 

(Swiss) 6M

Daily

12 weeks

(G)

0, 250, 500 NX Neuro 250 M decreased recognition, working, and 

aversive memory performance; 

>60% decrease of whole brain 

acetylcholinesterase activity after 12 

weeks

Ait Bali et al. 2019 – Glyphosate formulation – Roundup® (glyphosate concentration 360 g/L in the form of glyphosate isopropylamine salt 486 

g/L)

a Purities reported in this table are the information provided by the study authors in the study methodologies regarding the chemical used in the experiments.

Bd Wt or BW = body weight; CS = clinical signs; Develop = developmental; DX = developmental toxicity; EA = enzyme activity; Endocr = endocrine; F = female(s); 

FI = food intake; FX = fetal toxicity; Gastro = gastrointestinal; GD = gestation day; GN = gross necropsy; GW = gavage in water vehicle; HE = hematology; Hemato 

= hematological; HP = histopathology; IT = intratracheal; LE = lethality; LOAEL = lowest-observed-adverse-effect level; M = male(s); MX = maternal toxicity; 

NOAEL = no observed-adverse-effect level; NS = not specified; OF = organ function; OW = organ weight; POEA = polyoxyethyleneamine; PPD = post-parturition 

day; Repro = reproductive; TG = teratogenicity; W = water vehicle; WI = water intake
GLYPHOSATE 46

2. HEALTH EFFECTS

Table 2-4. Levels of Significant Exposure to Glyphosate Technicala – Dermal

Species (strain)

No./group

Exposure 

parameters

Doses 

(mg/kg/day)

Parameters 

monitored Endpoint NOAEL 

Less 

serious 

LOAEL 

Serious 

LOAEL Effect

INTERMEDIATE EXPOSURE

Rabbit (New 

Zealand)

10 M, 10 F

21 days, 

5 days/week, 

6 hours/day

0, 100, 

1,000, 

5,000 

BC, BW, 

CS, EA, FI, 

GN, HE, 

HP, LE, OW

Bd Wt 5,000

Hemato 5,000

Hepatic 5,000

Dermal 1,000 5,000 Very slight erythema and edema at 

application site

EPA 1992c – glyphosate technical, purity not specified

a Purities reported in this table are the information provided by the study authors in the study methodologies regarding the chemical used in the experiments.

BC = biochemistry; BW or Bd wt = body weight; CS = clinical signs; EA = enzyme activity; F = female(s); FI = food intake; GN = gross necropsy; 

HE = hematology; Hemato = hematological; HP = histopathology; LE = lethality; LOAEL = lowest-observed-adverse-effect level; M = male(s); NOAEL = no 

observed-adverse-effect level; OW = organ weight
GLYPHOSATE 47

2. HEALTH EFFECTS

2.2 DEATH 

Several case report series have reported deaths in individuals intentionally ingesting glyphosate products 

(Chen et al. 2009; Kim et al. 2014; Moon et al. 2018; Roberts et al. 2010; Sawada et al. 1988; Talbot et al. 

1991; Tominack et al. 1991). The predominant cause of death was often shock (hypovolemic or 

cardiogenic), hypotension, and respiratory failure, often due to aspiration (Chen et al. 2009; Kim et al. 

2014; Moon et al. 2018; Talbot et al. 1991). Among 107 patients who ingested glyphosate isopropylamine 

salt, eleven fatalities were reported (10.3% rate) while none were observed in the glyphosate ammonium 

salt group, for which there were 40 patients (Moon et al. 2018). A retrospective cohort study reported that 

14 of 150 patients with glyphosate surfactant herbicide poisoning died and that nonsurviving patients 

were statistically older compared to surviving patients (Cho et al. 2019). 

An acute oral LD50 value of 4,320 mg/kg/day was reported following single oral dosing of rats with 

glyphosate technical (EPA 1992b). In a developmental toxicity study, 6/25 pregnant rats died during oral 

dosing of glyphosate technical at 3,500 mg/kg/day; there were no deaths during treatment at 

1,000 mg/kg/day (EPA 1992e). No adequate sources were located regarding death in laboratory animals 

exposed to glyphosate technical by inhalation or dermal routes.

In a study of female Wistar rats exposed to 126 or 315 mg/kg/day of a glyphosate formulation for 60 

days, 6/12 rats died (Hamdaoui et al. 2018). In a study that employed oral dosing of pregnant rats with 

Roundup®, 8/15 dams died during the first 8 days of treatment at 1,000 mg/kg/day glyphosate 

(Dallegrave et al. 2003). No deaths occurred in a 4-week study of rats intermittently exposed to 

Roundup® at exposure levels as high as 360 mg/m3(approximately 36 mg Roundup®/m3) (EPA 1985c). 

No adequate sources were located regarding death in laboratory animals exposed to glyphosate 

formulations by the dermal route.

2.3 BODY WEIGHT 

Oral exposure of rats to glyphosate technical at relatively high doses resulted in significant effects on

body weight and/or body weight gain. Pregnant rats gavaged at 3,500 mg/kg/day during GDs 6–19 

exhibited as much as 28.5% lower mean body weight gain than controls (EPA 1992e). Body weight gain 

was 12–18% less than that of controls in two generations of parental male and female rats exposed via the

diet for 14–19 weeks at 2,219 or 3,134 mg/kg/day, respectively (EPA 1992a). No treatment-related effects 

on body weight were seen among young female mice treated for 28 days at estimated doses up to 

1,447.5 mg/kg/day (EPA 2013b). In 13-week oral studies, body weight and/or body weight gain among 
GLYPHOSATE 48

2. HEALTH EFFECTS

rats and mice at oral doses in the range of 2,273–11,977 mg/kg/day were 10–18% less than controls (NTP 

1992). In a 2-year study, female rats dosed at 1,183 mg/kg/day exhibited 13% lower mean body weight 

than controls at treatment week 81 (EPA 1991a).

Evidence of treatment-related effects on body weight among laboratory animals receiving lower oral 

doses of glyphosate or glyphosate-based herbicides varied by study. Studies using doses of glyphosate

technical at ≤1,000 mg/kg/day during acute-, intermediate-, or chronic-duration exposure found no effects 

on body weight (Baier et al. 2017; El-Shenawy 2009; EPA 1986a, 1987, 1991a, 1991b, 1992a, 1992d, 

1992e, 1992f, 1992g, 2013a, 2013b, 2017b; Manservisi et al. 2019). In contrast, body weight changes 

were sometimes observed in lower dose oral studies using glyphosate formulations (Ait Bali et al. 2017; 

Almeida et al. 2017; Cattani et al. 2017; Hamdaoui 2018; Pandey et al. 2019; Teleken et al. 2019). 

Several studies evaluated effects of oral exposure to glyphosate formulations on body weight. Limited 

results indicate that mice may be more sensitive than rats to body weight effects from repeated oral 

exposure to glyphosate formulations. In intermediate studies on male mice, significantly reduced body 

weight gain (>70%) occurred at 250 mg/kg/day after 6-12 week exposure (Ait Bali et al. 2017), and in 

offspring exposed in utero, during lactation and then orally from post-natal day 21 to 60 (14% less than 

controls) (Cattani et al. 2017). However, in another intermediate oral study, pregnant C57B1/6 mice 

showed a 17% decrease in body weight and an approximate 25% decrease in body weight gain, while 

their male offspring exposed in utero and during lactation did not have significantly different body weight 

or body weight gain when compared with controls (Teleken et al. 2019). Seriously-depressed mean body 

weight gain (60–66% less than controls) was reported for albino Swiss mice gavaged with Roundup 

Original® at 50 mg/kg/day for 15 days and approximately 10% body weight loss for mice dosed at 500 

mg/kg/day (Jasper et al. 2012). When compared to controls, male rats orally exposed to a range of 

concentrations of Roundup® for two weeks showed an estimated 37% decrease in body weight when 

exposed to 100 mg/kg/day and an estimated 33% decrease in body weight when exposed to 250 

mg/kg/day. Pregnant rats fed 500 mg/kg/day Roundup® via gavage for 7 days had 10% less body weight 

gain compared to controls, when exposed simultaneously with paraquat (Almeida et al. 2017). In rats, 8-

10% less body weight gain was seen after exposure to 126 mg/kg/day in feed for 60 days (Hamdaoui 

2018).

However, other studies found no effects of oral glyphosate exposure on body weight. No significant 

effects on body weight were observed among Wistar rats gavaged with Roundup® at 56 or 560 

mg/kg/day for up to 13 weeks (Caglar and Kolankaya 2008), male mice orally exposed to Roundup® for 
GLYPHOSATE 49

2. HEALTH EFFECTS

35 days (Jiang et al. 2018). pregnant Wistar rats gavaged with Roundup® at 1,000 mg/kg/day during 

GDs 6–15 (Dallegrave et al. 2003), or maternal Wistar rats gavaged with Roundup® at 50–

450 mg/kg/day during gestation and lactation (Dallegrave et al. 2007). No effects on body weight were 

observed among male Wistar rats gavaged with Roundup Transorb® at 250 mg/kg/day during postnatal 

days (PNDs) 23–53 (Romano et al. 2010). After exposure to 1.75 mg/kg/day of glyphosate technical or 

Roundup® Bioflow during pregnancy and lactation, no weight changes were observed in SpragueDawley F0 females or their male offspring (Manservisi et al. 2019). At higher exposure levels to 

glyphosate formulations (3.69 mg/kg/d and 352.2 mg/kg/d) during pregnancy, F0 and F1 female Wistar 

rats showed no signs of glyphosate-associated weight changes (Milesi et al. 2018).

Non-oral exposure to glyphosate and glyphosate formulations was not associated with changes in body 

weight. No significant body weight effects occurred in a 4-week inhalation study of rats intermittently 

exposed to Roundup® at exposure levels as high as 360 mg/m3(approximately 36 mg Roundup®/m3) 

(EPA 1985c). A study on male albino rats intraperitoneally exposed to 269.9 mg/kg/day of Roundup® for 

up to two weeks (El-Shenawy 2009) also found no changes in body weight, No significant treatmentrelated effects on body weight were observed among rabbits administered repeated dermal applications of 

glyphosate technical at doses in the range of 100–5,000 mg/kg/application for 21 days (EPA 1992c).

When mice were acutely exposed subcutaneously to 2 mg/kg/bw, no effects on body weight were seen 

(Altamirano et al. 2018; Guerrero Schimpf et al. 2017; Guerrero Schimpf et al. 2018). No effects on body 

weight were seen in male mice after intranasal exposure to 50 mg/kg/day for 3 times a week for 4 weeks 

(Baier et al. 2017). 

2.4 RESPIRATORY 

As summarized in Table 2-5, several investigations of the Agricultural Health Study participants have 

examined the possible associations between use of glyphosate-containing products and increased risk of 

rhinitis, wheezing, atopic asthma, allergic asthma, or chronic bronchitis (Hoppin et al. 2002, 2006a, 

2006b, 2007, 2008, 2009; Slager et al. 2009, 2010). No associations were found for diagnosed chronic 

bronchitis (Hoppin et al. 2007) or for wheezing after adjusting for confounding exposure to other 

pesticides (Hoppin et al. 2002, 2006a, 2006b). Current rhinitis was associated with glyphosate use among 

commercial applicators (Slager et al. 2009) and farmers (Slager et al. 2010), but no relationship between 

risk and the number of days of use per year was found among the commercial applicators (Slager et al. 

2009). The relationship seen in commercial applicators was limited to applicators that also reported using 

2,4-D. Applicators using 2,4-D or glyphosate alone did not show an increased risk of rhinitis (Slager et al. 
GLYPHOSATE 50

2. HEALTH EFFECTS

2009). An association between glyphosate use and the risk of atopic asthma was found among farm 

women, but there was no association with nonatopic asthma (Hoppin et al. 2008). No associations were

found between glyphosate use by male farmers and risk of allergic or nonallergic asthma (Hoppin et al. 

2009). An association between glyphosate use and the risk of both allergic and nonallergic wheeze was 

found among male farmers, with an increase in risk for allergic wheeze with increasing days of use per 

year (Hoppin et al. 2017). It is noted that many of these studies did not account for use of other 

pesticides. 

A study by Camacho and Mejia (2017) investigated the association between aerial applications of 

glyphosate in Colombia and health effects of individuals living in the sprayed areas. The association was

assessed using individual medical record data and information about Colombia’s aerial spraying program.

Several health outcomes including respiratory illnesses was examined and a positive association was 

observed. For each additional square kilometer increase in area sprayed with glyphosate there was an 

increase in the proportion of respiratory diagnoses 7 to 15 days following exposure.

Respiratory failure or distress was reported in about 10–25% of the cases of intentional ingestion of 

glyphosate products (Lee et al. 2000; Moon and Chun 2010; Picetti et al. 2018; Tominack et al. 1991).

Cho et al. (2019) found that the most common complication occurring in patients who had ingested 

glyphosate surfactant herbicide was acute respiratory distress syndrome.
GLYPHOSATE 51

2. HEALTH EFFECTS

Table 2-5. Noncancer Outcomes in Humans Exposed to Glyphosate-Containing Products

Reference and study population Exposure Outcomes

Death

Cho et al. 2019

Retrospective cohort study of 150 adults who 

presented with glyphosate poisoning at a Korean 

hospital between January 2006 and April 2017.

Exposure: ingestion of glyphosate-based 

herbicides

Multivariate logistic regression: age, 

amount of glyphosate-based herbicide 

ingested, elapsed time since ingestion, 

qSOFA score

14/150 patients died (9.3% mortality), and age 

was determined to be a statistically significant 

factor (p<0.001). Higher qSOFA scores were 

associated with greater odds of death 

(OR:2.73, 95% CI: 1.41–5.76) and lifethreatening complications (OR: 17.19, 95% CI:

6.25–72.65). 

Respiratory

Camacho and Mejia 2017

Cross-sectional study examining individual health 

records from the general public over a five-year 

period (2003 to 2007) merged with data of aerial 

spraying events. The study examined the data 

under several specifications:

• Complete sample set: 39,766,259

observations

• Municipalities with positive aerial

spraying: 7,264,691 observations

• Municipalities with non-immigrant

population: 37,736,485 observations

• High and low income municipalities:

20,131,375and 19,634,884 observations,

respectively

Exposure: aerial spraying of glyphosate 

on coca crops and the general population 

living in the spray areas within study period 

2003 to 2007

Regression Adjustments: age, age 

square, health regime, municipal tax 

income, population, area in square km, 

rurality index, average monthly rainfall, 

municipal spending on education and 

health, subsidized regime coverage, year 

and month dummy

Increased number of respiratory illnesses 

consistent across all specifications analyzed

(only statistically significant p values were 

presented). 

Hoppin et al. 2002

Cohort study of 20,468 participants in the 

Agricultural Health Study in Iowa and North 

Carolina

Exposure: glyphosate ever use and 

application frequency categories

Logistic regression adjustments: age, 

state, smoking history, asthma-atopy 

status 

Wheeze, self-reported

OR 1.05 (0.95–1.17), p=0.04 for trend of 

increasing exposure days

Hoppin et al. 2006a Exposure: glyphosate ever use in the 

year prior to enrollment

Wheeze, self-reported

OR 1.05 (0.94–1.17), farmers
GLYPHOSATE 52

2. HEALTH EFFECTS

Table 2-5. Noncancer Outcomes in Humans Exposed to Glyphosate-Containing Products

Reference and study population Exposure Outcomes

Prospective cohort study of 20,175 participants in 

the Agricultural Health Study in Iowa and North 

Carolina (17,920 farmers and 2,255 commercial 

pesticide applicators)

Logistic regression adjustments: age, 

state, smoking history, BMI 

OR 1.14 (0.83–1.57), applicators

Hoppin et al. 2006b

Cohort study of 2,255 commercial pesticide 

applicators participating in the Agricultural Health 

Study in Iowa and North Carolina 

Exposure: glyphosate ever use in the 

year prior to enrollment

Logistic regression adjustments: age, 

smoking status, asthma and atopy history, 

BMI 

Wheeze, self-reported

OR 1.38 (1.03–1.86)

OR 1.14 (0.83–1.57), with adjustment for 

use of chlorimuron-ethyl pesticide

Hoppin et al. 2007

Prospective cohort study of 20,908 participants in 

the Agricultural Health Study in Iowa and North 

Carolina 

Exposure: glyphosate ever use

Logistic regression adjustments: age, 

state, sex, smoking (pack-years)

Chronic bronchitis 

OR 0.99 (0.82–1.19)

Hoppin et al. 2008

Prospective cohort study of 25,814 farm women 

participating in the Agricultural Health Study in 

Iowa and North Carolina 

Exposure: glyphosate ever use

Logistic regression adjustments: age, 

state, smoking status, “grew up on farm” 

Atopic asthma

OR 1.31 (1.02–1.67)

Nonatopic asthma

OR 1.13 (0.92–1.39)

Hoppin et al. 2009

Prospective cohort study of 19,704 male farmers 

participating in the Agricultural Health Study in 

Iowa and North Carolina 

Exposure: glyphosate ever use

Logistic regression adjustments: age, 

state, smoking status, BMI 

Allergic asthma

OR 1.37 (0.86–2.17)

Nonallergic asthma

OR 1.15 (0.87–1.51)

Hoppin et al. 2017

Prospective cohort study of 22,134 male farmers 

participating in the Agricultural Health Study in 

Iowa and North Carolina

Exposure: glyphosate ever use

Logistic regression adjustments: age, 

BMI, state, smoking status, current 

Allergic wheeze

OR 1.56 (1.19–2.03), higher prevalence 

with increasing use days per year

Nonallergic wheeze

OR 1.24 (1.07–1.44)
GLYPHOSATE 53

2. HEALTH EFFECTS

Table 2-5. Noncancer Outcomes in Humans Exposed to Glyphosate-Containing Products

Reference and study population Exposure Outcomes

asthma, days applying pesticides, days 

driving diesel tractors

Slager et al. 2009

Prospective cohort study of 2,245 commercial 

applicators participating in the Agricultural Health 

Study in Iowa 

Exposure: any glyphosate use and 

application frequency categories during the 

past year

Logistic regression adjustments: age, 

education, “growing up on farm” 

Current rhinitis 

OR 1.32 (1.08–1.61), p=0.735 for trend for 

increasing use days per year

Slager et al. 2010

Prospective cohort study of 19,565 farmers 

participating in the Agricultural Health Study in 

Iowa and North Carolina

Exposure: any glyphosate use and 

application frequency categories during the 

past year

Logistic regression adjustments: age; 

race; education; state; BMI; currently 

working on farm; years mixing pesticides, 

repairing engines or pesticide equipment, 

welding, painting, handling stored grain or 

hay, working in swine areas, working with 

hogs or other farm animals, butchering 

animals, and growing cabbage, Christmas 

trees, field corn, sweet corn, and hay

Current rhinitis 

OR 1.09 (1.05–1.13)

Cardiovascular Effects

Dayton et al. 2010

Case control study of 168 cases of nonfatal 

myocardial infarction and 22,257 controls in 

women in Iowa and North Carolina participating in 

the Agricultural Health Study 

Exposure: glyphosate ever use

Logistic regression adjustments: age, 

BMI, smoking, state

Nonfatal myocardial infarction

OR 0.8 (0.6–1.2)

Mills et al. 2009

Prospective study of male participants in the 

Agricultural Health Study in Iowa and North 

Carolina (n=54,069 for fatal myocardial infarction 

and 32,024 for nonfatal incidence)

Exposure: glyphosate ever use

Cox proportional regression 

adjustments: age, state, smoking, BMI 

(nonfatal analysis only)

Fatal myocardial infarction

HR 0.99 (0.80–1.23)

Nonfatal myocardial infarction 

HR 1.10 (0.93–1.31)
GLYPHOSATE 54

2. HEALTH EFFECTS

Table 2-5. Noncancer Outcomes in Humans Exposed to Glyphosate-Containing Products

Reference and study population Exposure Outcomes

Musculoskeletal Effects

De Roos et al. 2005b

Nested case control study of 135 cases of 

physician-confirmed rheumatoid arthritis and 

675 controls participating in the Agricultural 

Health Study in Iowa and North Carolina (female 

participants only)

Exposure: glyphosate ever use

Logistic regression adjustments: birth 

date, state

Rheumatoid arthritis 

OR 1.2 (0.8–1.8)

Parks et al. 2016

Nested case-control study of cases of physicianconfirmed rheumatoid arthritis or self-reported 

use of disease modifying antirheumatic drugs and 

noncases participating in the Agricultural Health 

Study in Iowa and North Carolina (female 

spouses of licensed pesticide applicators only); 

enrolled between 1993 and 1997 and followed 

through 2010

Exposure: glyphosate ever use

Logistic regression adjustments: age, 

state, pack-years smoking

Rheumatoid arthritis 

OR 1.2 (0.95–1.6); based on 100 prevalent 

cases

OR 1.4 (1.0–2.0); based on 54 incident 

cases

Hepatic Effects

Mills et al. 2019

Case-control study of 97 participants, 63 with 

nonalcoholic steatohepatitis (NASH) and 34 

without NASH

Exposure: glyphosate and glyphosate 

residue measured from fasting urine; 

glyphosate residue (calculated) which 

estimates dietary intake and exposure to 

residues

Multivariable linear adjustments: age, 

sex, body mass index

Glyphosate residue significantly higher in 

patients with NASH compared with patents 

without NASH (p=0.008)

Significant dose-dependent increase of 

glyphosate exposure with increase in fibrosis 

stage when comparing patients without 

advanced fibrosis to those with Stage 2,3 or 4 

fibrosis (glyphosate: 0.230 mg/L, SD: 0.19 vs. 

0.351 mg/L, SD: 0.45; glyphosate residue: 

0.525 mg/L, SD 0.38 vs. 0.938 mg/L, SD: 

0.372,p <0.001).

NASH cases confirmed through liver biopsy.

Dermal Effects
GLYPHOSATE 55

2. HEALTH EFFECTS

Table 2-5. Noncancer Outcomes in Humans Exposed to Glyphosate-Containing Products

Reference and study population Exposure Outcomes

Camacho and Mejia 2017

Cross-sectional study examining individual health 

records from the general public over a five-year 

period (2003 to 2007) merged with data of aerial 

spraying events. The study examined the data 

under several specifications:

• Complete sample set: 39,766,259 

observations

• Municipalities with positive aerial 

spraying: 7,264,691 observations

• Municipalities with non-immigrant 

population: 37,736,485 observations

• High and low income municipalities: 

20,131,275 and 19,634,884 observations, 

respectively

Exposure: aerial spraying of glyphosate 

on coca crops and the general population 

living in the spray areas within study period 

2003 to 2007

Regression Adjustments: age, age 

square, health regime, municipal tax 

income, population, area in square km, 

rurality index, average monthly rainfall, 

municipal spending on education and 

health, subsidized regime coverage, year 

and month dummy

Increased number of dermatological illnesses 

consistent across all specifications analyzed 

(only statistically significant p values were 

presented).

Maibach 1986

Experimental study of 24 males and females

Exposure: 0.1 mL applied to intact and 

Draize-type abraded skin; patch removed 

after 24 hours

No skin irritation 24 or 48 hours after 

application to intact skin

Irritancy scores 24 hours after application to 

abraded skin were negative in 10 subjects, 

equivocal in 4 subjects and erythema was 

noted in 10 subjects; at 48 hours, the scores 

were negative in 10 subjects, equivocal in 

6 subjects, and erythema was noted in 

8 subjects

Maibach 1986

Experimental study of 23 males and females

Exposure: 0.1 mL applied 5 days/week 

for 21 days 

The average score was 1.4 where a score of 

1 indicates erythema and 2 indicates erythema 

and induration; none of the subjects reported 

burning, stinging, or itching from the test 

compound

Maibach 1986

Experimental study of 204 males and females

Exposure: 0.2 mL applied 3 days/week 

for 3 weeks with patches remaining in 

No skin irritation was observed
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Table 2-5. Noncancer Outcomes in Humans Exposed to Glyphosate-Containing Products

Reference and study population Exposure Outcomes

place for 48–72 hours; a challenge patch 

was applied after a 2-week rest period

Maibach 1986

Experimental study of 15 males and females

Exposure: Full-strength glyphosate was 

applied to skin stripped of the stratum 

corneum; the test site received irradiation 

with ultraviolet A and ultraviolet B light

No positive results for photoirritation or 

photosensitization were found

Ocular Effects

Kirrane et al. 2005

Prospective study of 31,173 female spouses of 

commercial pesticide applicators participating in 

the Agricultural Health Study in Iowa and North 

Carolina

Exposure: glyphosate ever use

Hierarchical regression adjustments: 

age, state

Retinal degeneration

OR 1.1 (0.8–1.5)

Endocrine Effects

Goldner et al. 2010

Prospective study of 16,529 participants (female 

spouses only) in the Agricultural Health Study in 

Iowa and North Carolina

Thyroid disease was self-reported as clinically 

diagnosed

Exposure: glyphosate ever use

Polytomous logistic regression 

adjustments: age, education, smoking 

status, hormone replacement therapy, BMI

Hyperthyroid disease

OR 0.98 (0.78–1.2)

Hypothyroid disease

OR 1.0 (0.91–1.2)

Other thyroid disease

OR 0.97 (0.81–1.2)

Kongtip et al. 2019

Cross sectional study of 195 conventional 

farmers and 222 organic farmers in Thailand. 

Sera were collected and analyzed for the 

following thyroid levels: TSH, T3, T4, FT3 and 

FT4

Exposure: glyphosate use, amount 

recorded in a diary 

Generalized linear regression 

adjustments: sex, current smoking, 

current alcohol use, insecticide use at 

home in the past year, triglyceride levels, 

and any stress symptoms in the past 2–4 

weeks

Log(e) estimates of thyroid hormone levels 

predicted by models of glyphosate sprayed in 

past year

Expβ(95%CI):

TSH: 0.992 (0.957–1.027)

FT3: 1.002 (0.998–1.007)

FT4: 0.999 (0.993–1.005)

T3: 1.006 (0.999–1.012)

T4: 1.007 (1.001–1.014)
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Table 2-5. Noncancer Outcomes in Humans Exposed to Glyphosate-Containing Products

Reference and study population Exposure Outcomes

Increased use of glyphosate sprayed

(measured in moles) was found to increase T4

levels.

Shrestha et al. 2018

Prospective study of 35,150 male and female 

pesticide applicators in the Agricultural Health 

Study in Iowa and North Carolina followed over 

20 years

Thyroid disease was self-reported as clinically 

diagnosed

Exposure: glyphosate ever use

Logistic regression adjustments: sex, 

education, state of residence, smoking

Hypothyroid disease

HR 1.28 (1.07–1.52), ever use

HR 1.27 (1.03–1.56), >0–≤686 intensityweighted days

HR 1.38 (1.12–1.69), >686–≤2,604 

intensity-weighted days

HR 1.17 (0.94≤1.45), >2,604 intensityweighted days

Neurological Effects

Kamel et al. 2007

Case control study of cases of self-reported 

Parkinson’s disease (n=83 prevalent cases 

and 78 incident cases) and controls 

(n=79,557 prevalent controls and 55,931 incident 

controls) participating in the Agricultural Health 

Study in Iowa and North Carolina

Exposure: glyphosate ever use

Logistic regression adjustments: age, 

state, type of participant 

Parkinson’s disease

OR 1.0 (0.6–1.7), prevalent disease

OR 1.1 (0.6–2.0), incident disease

Prevalent disease defined as reporting 

Parkinson’s disease at enrollment and incident 

disease defined as Parkinson’s disease 

reported at the study follow-up

Zhang et al. 2018

A cross-sectional study of 218 farmers in China. 

Abnormalities of peripheral nerve conduction 

including nerve conduction velocity, distal motor 

latency, and amplitude were measured with a 

conventional nerve conduction assessment.

Exposure: glyphosate agriculture use

Logistic regression adjustments: 

age, gender, smoking habit, alcohol 

consumption, whether adopting personal

protective equipment, and whether 

suffering from diabetes mellitus 

Abnormalities in nerve conduction velocity

OR 0.70 (0.38-1.30), overall

OR 1.34 (0.30-6.03), motor

OR 0.64 (0.35-1.18), sensory

Abnormalities in nerve conduction distal motor 

latency

OR 1.05 (0.81-1.37)

Abnormalities in nerve conduction amplitude

OR 1.21 (0.75-1.97)

Reproductive Effects

Camacho and Mejia 2017 Exposure: aerial spraying of glyphosate 

on coca crops and the general population 

Increased number of miscarriages consistent 

across all specifications analyzed (only 
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Table 2-5. Noncancer Outcomes in Humans Exposed to Glyphosate-Containing Products

Reference and study population Exposure Outcomes

Cross-sectional study examining individual health 

records from the general public over a five-year 

period (2003 to 2007) merged with data of aerial 

spraying events. The study examined the data 

under several specifications:

• Complete sample set: 39,766,259 

observations

• Municipalities with positive aerial 

spraying: 7,264,691 observations

• Municipalities with non-immigrant 

population: 37,736,485 observations

• High- and low-income municipalities: 

20,131,275 and 19,634,884 observations, 

respectively

living in the spray areas within study period 

2003 to 2007

Regression Adjustments: age, age 

square, health regime, municipal tax 

income, population, area in square km, 

rurality index, average monthly rainfall, 

municipal spending on education and 

health, subsidized regime coverage, year 

and month dummy

statistically significant p values were 

presented).

Curtis et al. 1999

Retrospective cohort study of 2,012 planned 

pregnancies among participants in the Canadian 

Ontario Farm Family Health Study 

Exposure: glyphosate use on the farm

Cox proportional hazard adjustments: 

age when beginning to try to conceive, 

recent oral contraceptive use, men’s and 

women’s smoking, and use of other 

pesticides 

Fecundability 

CFR 0.61 (0.30–1.26), pesticide use on the 

farm and women reported pesticide 

activities

CFR 1.30 (1.07–1.56), pesticide use on the 

farm, but no pesticide activities reported 

by women

Developmental Effects

Arbuckle et al. 2001

Retrospective cohort study of 2,110 female 

participants in the Canadian Ontario Farm Family 

Health Study

Exposure: glyphosate use during 

gestation

Logistic regression adjustments: none

Spontaneous abortion, preconception 

exposure

OR 1.4 (1.0–2.1), all gestational ages

OR 1.1 (0.7–1.9), <12 weeks gestation

OR 1.7 (1.0–2.9), >12 weeks gestation

Spontaneous abortion, postconception 

exposure

OR 1.1 (0.7–1.7), all gestational ages

OR 0.8 (0.4–1.6), <12 weeks gestation

OR 1.4 (0.8–2.5), >12 weeks gestation

Garcia et al. 1998 Exposure: paternal glyphosate use Congenital malformations
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Table 2-5. Noncancer Outcomes in Humans Exposed to Glyphosate-Containing Products

Reference and study population Exposure Outcomes

Case control study of 261 cases of congenital 

malformations and 261 matched controls in Spain

Conditional logistic regression 

adjustments: paternal age and paternal 

job and maternal history of spontaneous 

abortion, twins, drug consumption, heavy 

smoking, education, occupation

OR 0.94 (0.37–2.34) for the acute risk 

period (during 3 months preceding 

conception or during the first trimester of 

pregnancy or both for the father and during 

1 month preceding conception or during the 

first trimester of pregnancy or both for the 

mother)

Garry et al. 2002

Cross sectional study of 695 families and 

1,532 children in Minnesota

Exposure: glyphosate ever use

Regression adjustments: maternal age, 

smoking status, alcohol use, season of 

conception

ADD/ADHD, parent reported

OR 3.6 (1.35–9.65)

Parvez et al. 2018

Birth-cohort study of 71 women with singleton 

pregnancies in Central Indiana

Exposure: maternal glyphosate levels in 

urine specimens

Nonparametric Spearman correlation 

adjustments: maternal age, prepregnancy BMI, tobacco use, alcohol use, 

trimester of pregnancy

Shortened gestational length

(r = -0.30, p = 0.01)

Reduced birth weight

(r = -0.14, p = 0.27)

Head circumference

(r = -0.06, p = 0.64)

Rull et al. 2006

Case control study of 731 cases of neural tube 

defects and 940 controls in California 

Exposure: maternal residential proximity 

to glyphosate application (within 1,000 m)

Logistic regression adjustments: 

maternal ethnicity, education, 

periconceptional smoking, vitamin use 

Neural tube defects

OR 1.5 (1.0–2.4)

OR 1.5 (0.8–2.9) with adjustment for other 

pesticide exposure 
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Table 2-5. Noncancer Outcomes in Humans Exposed to Glyphosate-Containing Products

Reference and study population Exposure Outcomes

Sathyanarayana et al. 2010

Prospective study of 2,246 women whose most 

recent singleton birth occurred within 5 years of 

enrollment in the Agricultural Health Study in 

Iowa and North Carolina

Exposure: maternal glyphosate ever use 

(n=700)

Linear regression adjustments: 

maternal BMI and height, parity, preterm 

status, state, maternal smoking during 

pregnancy

Multiple regression estimates of change in 

birth weight (g) in relation to maternal selfreported glyphosate use (coefficient = 4 g; 

95% CI -40 to +48 g) indicate no significant 

association between birth weight and maternal 

use of glyphosate

Savitz et al. 1997

Retrospective cohort study of 1,898 couples 

participating in the Canadian Ontario Farm Family 

Health Study 

Exposure: any paternal glyphosate use 

from 3 months prior to conception through 

the month of conception

Logistic regression adjustments: 

maternal age, parity, maternal and paternal 

education, income, maternal and paternal 

off farm job, maternal smoking and alcohol 

use during pregnancy, conception to 

interview interval

Miscarriage

OR 1.5 (0.8–2.7)

Preterm delivery

OR 2.4 (0.8–7.9)

Small for gestational age

OR 0.8 (0.2–2.3)

Other Noncancer Effects

Montgomery et al. 2008

Prospective study of 33,457 participants (white 

males only) in the Agricultural Health Study in 

Iowa and North Carolina

Exposure: glyphosate ever use

Logistic regression adjustments: age, 

state, BMI

Diabetes incidence

OR 0.85 (0.74–0.98)

Saldana et al. 2007

Prospective study of 11,273 participants in the 

Agricultural Health Study in Iowa and North 

Carolina

Exposure: any agricultural glyphosate 

exposure during the first trimester

Logistic regression adjustments: BMI at 

enrollment, mother’s age at pregnancy, 

parity, race, state, commonly used 

pesticides by women

Gestational diabetes mellitus 

OR 0.7 (0.2–1.75)

ADD/ADHD = attention deficit disorder/attention deficit hyperactivity disorder; BMI = body mass index; CFR = conditional fecundability ratio; CI = confidence 

interval; HR = hazard ratio; OR = odds ratio
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Available data regarding respiratory effects in laboratory animals exposed to glyphosate are limited. In 

mice, a 50% decrease in relative lung weight was observed following exposure to 250 mg/kg/day for 12 

weeks (Ait Bali et al. 2017). No other observations were made in the lungs. Kumar et al. (2014) reported 

an inflammatory respiratory response (evidenced by increased eosinophil and neutrophil counts, mast cell 

degranulation, and production of IL-33, TSLP, IL-13, and IL-5) in anesthetized mice exposed intranasally 

to glyphosate. Adam et al. (1997) designed a study to evaluate the effects of glyphosate technical (200 

mg/kg), glyphosate + POEA (200 and 100 mg/kg, respectively), POEA alone (100 mg/kg), and 

Roundup® in rats evaluated for 24 hours following intratracheal instillation (Adam et al. 1997). Control 

rats received normal saline. Obvious clinical signs of adverse pulmonary effects and mortalities occurred 

in each group except the saline controls. The study authors stated that the pulmonary effects were more 

severe and lasted longer in rats treated with POEA alone or in combination with glyphosate compared to 

responses in glyphosate only-treated rats. These results suggest POEA was more acutely toxic than 

glyphosate to the lungs. No respiratory effects occurred in a 120-day study where rats were exposed to 

250 mg/kg/day (Dar et al. 2019). No respiratory effects occurred in a 4-week study of rats intermittently 

exposed to Roundup® at exposure levels as high as 360 mg/m3(approximately 36 mg Roundup®/m3)

(EPA 1985c).

2.5 CARDIOVASCULAR 

Two studies of Agricultural Health Study participants did not find associations between the use of 

glyphosate-containing products and the risk of myocardial infarctions (Dayton et al. 2010; Mills et al. 

2009); see Table 2-5 for details. An association was found between using a glyphosate-based herbicide 

and vasculitic neuropathy in a 70 year old man who sprayed approximately 2,000 mL of the herbicide for 

several hours without using protective gear 4 months before presenting with symptoms (Kawagashira et 

al. 2017). In case series reports, abnormal electrocardiogram (EKG) readings have been found in patients 

ingesting large doses of glyphosate-containing products (Kim et al. 2014; Lee et al. 2000, 2008; Moon 

and Chun 2010; Moon et al. 2018; Talbot et al. 1991). The most commonly reported alterations included 

prolonged QTc interval and sinus tachycardia. In the most severe poisoning cases, hypotension and shock 

have been reported (Picetti et al. 2018; Roberts et al. 2010; Sawada et al. 1988; Tominack et al. 1991).

Additionally, adverse cardiovascular events (myocardial injury, shock, ventricular dysrhythmia, or 

cardiac arrest) have been reported among patients who ingested glyphosate (Moon et al. 2018).

No data were available regarding evaluation of cardiovascular endpoints in laboratory animals exposed to 

glyphosate technical or glyphosate formulations by any exposure route.
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2.6 GASTROINTESTINAL 

Gastrointestinal symptoms are commonly reported in case series reports of patients who ingested

glyphosate products. In numerous reports, over 40% of the patients reported nausea/vomiting (Eriguchi et 

al. 2019; Lee et al. 2000, 2008; Luo et al. 2019; Picetti et al. 2018; Roberts et al. 2010; Sawada et al. 

1988; Tominack et al. 1991). Other effects reported included abdominal pain (Lee et al. 2000, 2008; 

Moon and Chun 2010; Roberts et al. 2010; Sawada et al. 1988; Talbot et al. 1991), sore throat (Lee et al. 

2000; Tominack et al. 1991), poor appetite (Luo et al. 2019), and damage to mucosal tissue in the mouth 

and esophagus (Chang et al. 1999; Picetti et al. 2018; Sawada et al. 1988; Talbot et al. 1991; Tominack et 

al. 1991). One case study reported gastric ulcer and a large pyloric antrum ulcer (Luo et al. 2019). In a 

woman who accidentally ingested glyphosate-surfactant herbicide, a CT scan showed aspiration 

pneumonitis and ileus of the intestine (Ozaki et al. 2017).

Several studies evaluated effects of glyphosate technical oral exposure in laboratory animals. The most 

common effect was clinical signs of gastrointestinal disturbances. Such clinical signs are commonly

observed in studies of laboratory animals receiving bolus gavage doses of test substances, in which cases 

the clinical signs may be at least partially the result of the method of gavage dosing. Diarrhea was 

observed among rats gavaged once with glyphosate technical at 2,000 mg/kg (EPA 2013c). 

Gastrointestinal disturbances (e.g., soft stool, diarrhea, few feces) were reported among pregnant rats 

gavaged at 3,500 mg/kg/day during GDs 6–19 (EPA 1992e) and pregnant rabbits gavaged at 

350 mg/kg/day during GDs 6–27 (EPA 1992f) or 175 mg/kg/day during GDs 8–20 (EPA 2017b). A slight 

increase in observations of soft stool and/or diarrhea was noted in the rabbits dosed at 175 mg/kg/day

during GDs 6–27 as well (EPA 1992f). Soft stools were observed in rats exposed via the diet for 

2 generations at concentrations resulting in estimated doses in the range of 2,219–2,633 and 3,035–

3,134 mg/kg/day for parental males and females, respectively (EPA 1992a). Mao et al. (2018) reported 

that glyphosate added to the drinking water of rat dams from GD 6 through lactation and to F1 offspring 

up to PND 125 at a concentration resulting in a daily dose of 1.75 mg/kg/day (the U.S. acceptable daily 

intake [ADI]) resulted in modifications to the gut microbiota in early development, particularly among 

prepubertal rats. 

In a 2-year study of rats exposed via the diet (EPA 1991a, 1991b), inflammation of gastric squamous 

mucosa was observed in females at an estimated dose level of 457 mg/kg/day; there were no signs of 

gastrointestinal effects in males at estimated doses as high as 940 mg/kg/day. In another chronic-duration 

oral rat study (EPA 1992d), there were no signs of treatment-related gastrointestinal effects at the highest 
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estimated dose level (31.45–34.02 mg/kg/day). No clinical signs or histopathological evidence of 

treatment-related gastrointestinal effects were seen among male or female mice exposed via the diet for 

24 months at estimated doses as high as 4,945 and 6,069 mg/kg/day, respectively (EPA 1985a, 2015a).

Increased incidence of exocrine hyperplasia in the pancreas was reported for male rats receiving 

glyphosate technical from the diet for up to 2 years at an estimated dose of 1,214 mg/kg/day (EPA 

2015c). Increased severity of cytoplasmic changes in salivary gland cells (basophilia and hypertrophy of 

acinar cells in parotid and submandibular salivary glands) was reported for male and female rats receiving 

glyphosate from the diet for 13 weeks at 410 and 421 mg/kg/day, respectively (NTP 1992) and other rats 

similarly treated at 300 mg/kg/day for up to 2 years (EPA 2015c). Similar effects on salivary glands were 

observed in male and female mice treated for 13 weeks at much higher doses (1,065 and 2,707 

mg/kg/day, respectively; not observed at 507 and 753 mg/kg/day, respectively) (NTP 1992). Although 

salivary gland cytoplasmic changes were noted in rats at doses <300 mg/kg/day as well, the changes were 

reported to be only of minimal or mild severity; therefore, they are not considered adverse effects. The 

toxicological significance of the glyphosate treatment-related effects on salivary glands is uncertain.

Limited information was located regarding gastrointestinal effects in laboratory animals following oral 

exposure to glyphosate formulations. Rats exposed daily for 6-12 weeks to 250 mg/kg/day exhibited a 

decreased in total bacterial count in the gut (Aitbali et al. 2018). Lozano et al. (2018) reported significant 

differences in microbiome genomic diversity, characterized by an increase in the Bacteroidetes family 

S24-7 and a decrease in Lactobacillaceae, between treated female rats exposed to 5,000 ppm of Roundup 

for 673 days when compared to control males, control females, and treated males. The study found that 

Roundup had a direct selective bactericidal action on isolated gastrointestinal strains. In a study designed 

to evaluate the effects of glyphosate technical (2,000 mg/kg), rats were administered glyphosate + POEA 

(2,000 and 1,000 mg/kg, respectively), POEA alone (1,000 mg/kg), or Roundup® by gavage, followed by 

24 hours of posttreatment observation (Adam et al. 1997). Control rats received normal saline. Two rats 

in the POEA-only treatment group died. Diarrhea was noted in all groups except the control group. The 

study authors stated that the groups given POEA or mixtures that included POEA experienced more rapid 

and severe diarrhea than those given glyphosate alone. These results suggest that POEA was more acutely 

toxic than glyphosate to the gastrointestinal system. Mao et al. (2018) reported that Roundup® added to 

the drinking water of rat dams from GD 6 through lactation and to F1 offspring up to PND 125 at a 

concentration designed to deliver a daily dose of 1.75 mg glyphosate/kg/day (the U.S. glyphosate ADI)

resulted in modifications to the gut microbiota in early development, particularly among prepubertal rats.
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2.7 HEMATOLOGICAL 

After the accidental ingestion of 100 mL of glyphosate-surfactant herbicide a woman exhibited 

hypoxemia, hyperkalemia, hypotension, and hemoconcentration (Ozaki et al. 2017). Results from 

available animal studies do not implicate the hematological system as a sensitive target of glyphosate 

toxicity. There were no apparent treatment-related hematological effects in chronic-duration oral studies 

of rats, mice, or dogs administered glyphosate technical at oral doses as high as 940–1,183 mg/kg/day for 

rats (EPA 1991a, 1991b, 1992d), 4,945–6,069 mg/kg/day for mice (EPA 2015a), and 500 mg/kg/day for 

dogs (EPA 1986a, 1987). Rabbits administered repeated dermal applications of glyphosate technical at 

doses in the range of 100–5,000 mg/kg/application for 21 days exhibited no evidence of treatment-related 

hematological effects (EPA 1992c). Small changes in hematological parameters were seen in both male 

and female rats following dietary exposure to glyphosate technical in the 13-week NTP (1992) study. 

These were considered to be unremarkable and most likely due to mild dehydration.

Available information regarding hematological effects related to glyphosate formulations is limited. No 

hematological effects occurred in a 4-week study of rats intermittently exposed to Roundup® at exposure 

levels as high as 360 mg/m3(approximately 36 mg Roundup®/m3) (EPA 1985c). Decreases in red blood 

cell count, hematocrit, and hemoglobin, and increases in corpuscular volume and neutrophil count were 

reported in mice gavaged with Monsanto Roundup® Original for 15 days at 500 mg/kg/day (Jasper et al. 

2012).

2.8 MUSCULOSKELETAL 

De Roos et al. (2005b) did not find an association between glyphosate use and the risk of rheumatoid 

arthritis among participants of the Agricultural Health Study. In a subsequent study of female spouses of 

licensed pesticide applicators, Parks et al. (2016) reported a weakly positive association between spousal 

use of glyphosate and risk of rheumatoid arthritis (based on incident cases). See Table 2-5 for additional 

study details.

No data were available regarding evaluation of musculoskeletal endpoints in laboratory animals exposed 

to glyphosate technical or glyphosate formulations by any exposure route.

2.9 HEPATIC 
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Human studies evaluating the relationship between glyphosate and hepatic endpoints is limited. One 

retrospective cohort study reported acute liver failure as a complication associated with organ injury (Cho 

et al. 2019). In a case-control study evaluating the association between glyphosate and patients with 

nonalcoholic steatohepatitis (NASH), Mills et al. (2019) reported significantly higher levels of glyphosate

residue in NASH patients compared to non-NASH (p=0.008) patients. Furthermore, a dose-dependent 

increase of glyphosate exposure was observed with advanced stages of fibrosis (stage 2, 3 or 4). No other

information was located regarding hepatic effects in humans exposed to glyphosate-containing products. 

The potential for glyphosate technical to cause liver toxicity was evaluated in studies of rats and mice. In 

a 7-day study of pregnant rats, the liver had a 19-23% increase in thiobarbituric acid reactive substances 

(TBARS) levels in liver tissue compared to controls, following exposure to 500 mg/kg/day by oral gavage 

(Almeida et al. 2017). In rats orally administered glyphosate for 28-days up to 10 mg/kg bw/day, no 

treatment related findings were reported after gross necropsy. Further, no significant differences in liver 

weights were reported between glyphosate treated groups and the control (Milic et al. 2018). However, 

ROS levels in the liver were significantly increased at 10 mg/kg bw/day, while TBARS concentrations

decreased at 0.5, 1.75 and 10 mg/kg bw/day compared to controls. GHS levels in liver decreased by 

22.7% and 27% at 1.75 and 10 mg/kg bw/day concentrations, respectively (Milic et al. 2018). Similarly, 

GHS peroxidase (GSH-Px) activity in the liver was noticeably higher among rats exposed to 0.5, 1.75 and 

10 mg/kg bw/day glyphosate compared to controls. Elevated levels of GSH-Px is reflective of glyphosate 

inducing the antioxidant defense system in the liver (Milic et al. 2018).

In a 13-week rat dietary study of glyphosate technical, increases in liver weight and serum ALT were 

observed in males at 1,678 mg/kg/day; increased liver weight and increased serum AP, ALT, and bile 

acids were noted in females at 3,393 mg/kg/day. There were no indications of treatment-related liver 

effects among male and female rats treated via the diet for 2 generations at estimated doses as high as 

1,234–1,273 mg/kg/day (EPA 2013a) or other rats treated for 2 years to doses as high as 940–

1,183 mg/kg/day (EPA 1991a, 1991b). Male mice exposed via the diet for 13 weeks at doses ≥2,273 

mg/kg/day exhibited increased mean relative liver weight (4–9% greater than controls) in the absence of 

histopathologic liver lesions; there were no effects on liver weight in similarly-treated female mice at 

doses up to and including 11,977 mg/kg/day (NTP 1992). Male mice exposed via the diet for 2 years at an 

estimated dose of 4,945 mg/kg/day exhibited increased incidence of histopathologic central lobular 

hepatocyte necrosis; there was no evidence of treatment-related liver effects in similarly-treated female 

mice at an estimated dose of 6,069 mg/kg/day (EPA 2015a).
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Following oral exposure to glyphosate (1.0 g/L in drinking water) for 72 weeks, wild type and multiple 

myeloma model mice (Vk*MYC strain) showed hepatic fibrosis and hematological abnormalities 

including decreases in hemoglobin levels (i.e. anemia); lower levels of platelet counts and hematocrit 

were observed in model multiple myeloma mice (Wang et al. 2019). This study was part of a larger effort 

to understand the effect of glyphosate on multiple myeloma development, which is discussed in Section 

2.19.

Available information regarding hepatic endpoints in animals exposed to glyphosate formulations is 

limited. No hepatic effects occurred in a 4-week study of rats intermittently exposed to Roundup® at 

exposure levels as high as 360 mg/m3(approximately 36 mg Roundup®/m3) (EPA 1985c). Increased 

serum ALT and aspartate aminotransferase (AST) activity and histopathologic liver lesions (increased 

Kupffer cells in hepatic sinusoids and deposition of reticulin fibers) were seen in male rats treated with 

Glyphosate-Biocarb® by gavage for 75 days (one dose every 2 days) at 487 mg/kg/dosing (Benedetti et 

al. 2004). In an acute oral exposure study, a significant increase in liver index, liver weight, and cytokine 

expression (IL-1β and TNF-α) was observed in male rats exposed to 100 or 250 mg/kg/day Roundup®. 

Lower doses of Roundup®, including exposure to 25 or 50 mg/kg/day, resulted in increased liver weight, 

higher numbers of liver macrophages, and changes in glycogen storage. However, these results were less 

consistent and did not adhere to a dose-response relationship (Pandey et al. 2019). Following a 120-day 

exposure to 500 mg/kg/day Roundup®, rats exhibited increased mean liver malondialdehyde levels, 

decreased superoxide dismutase concentration, catalase activity, increased alanine aminotransferase, 

aspartate amino transferase, lactate dehydrogenase and enzymatic activity of GSH-Px, moderate 

hepatocytic degeneration and necrosis (Dar et al. 2019). Following 6-12 weeks of daily exposure to ≥250 

mg/kg/day of Roundup ®, mice showed a 44% decrease in relative liver weight, no other liver 

observations were made (Ait Bali et al. 2017).

Rabbits administered repeated dermal applications of glyphosate technical at doses in the range of 100–

5,000 mg/kg/application for 21 days exhibited no evidence of treatment-related hepatic effects (EPA 

1992c). However, male albino rats intraperitoneally exposed to 134.95 mg/kg/day glyphosate technical 

for up to two weeks showed significantly increased serum AST, ALT, and ALP, decreased serum GSH, 

increased hepatic nitric oxide, and increased hepatic lipid peroxidation, which the author attributed to 

impairment of liver enzymes and hepatic metabolism (El-Shenawy 2009).

Two-week intraperitoneal exposure of albino rats to 269.9 mg/kg/day Roundup® demonstrated the same 

liver effects as intraperitoneal exposure to 134.95 mg/kg/day glyphosate technical, including increased 
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serum AST, ALT, and ALP, decreased serum GSH, increased hepatic nitric oxide, and increased hepatic 

lipid peroxidation. Most of these observed effects were similar in both Roundup®-exposed and 

glyphosate-exposed rats. However, compared to controls, rats exposed to glyphosate technical showed a 

larger increase in hepatic nitric oxide than rats exposed to Roundup® (72% increase and 21% increase 

respectively). Conversely, the increase in hepatic lipid peroxidation compared to controls was much more 

pronounced in Roundup ®-exposed rats than in glyphosate-exposed rats (630% increase and 432% 

increase respectively) (El-Shenawy 2009). 

In vivo metabolome and proteome profiling of liver obtained from rats chronically exposed to long-term 

exposure at low levels of Roundup® (4 ng/kg bw/day) for two years indicate effects to the liver including

metabolite alterations associated with non-alcoholic fatty liver disease and steatohepatosis (Mesnage et al. 

2017). Metabolome profiling, or the analysis of metabolites characterizing the range of chemical 

processes, analogous to chemical fingerprinting, revealed a lipotoxic condition, oxidative stress, and 

markers of hepatotoxicity in the liver (Mesnage et al. 2017). Results from the proteome analysis, which 

characterizes the expression of protein products and their interaction, reported rats exposed to Roundup ® 

had alterations reflective of peroxisomal proliferation, steatosis, and necrosis (Mesnage et al. 2017).

2.10 RENAL 

Available human data regarding the possible association between exposure to glyphosate and risk of renal 

effects is limited to a few case-control studies, two case reports and one retrospective cohort study. One

case-control study of patients with chronic kidney disease found an increased risk of chronic kidney 

disease among glyphosate applicators (Jayasumana et al. 2015). However, uncertainty regarding an 

association between exposure to glyphosate-containing products and risk of chronic kidney disease 

includes the finding that the applicators were also exposed to high levels of calcium, magnesium, barium, 

strontium, iron, titanium, and vanadium by drinking water from abandoned wells. In the case of a 55 year 

old man who ingested 200 mL of a glyphosate formulation, acute renal failure occurred (Picetti et al. 

2018). Acute kidney injury and metabolic acidosis occurred in a woman who accidentally ingested 

glyphosate-surfactant herbicide (Ozaki et al. 2017). Acute kidney injury associated with glyphosate-based 

herbicide ingestion was also reported in a retrospective cohort study as a complication associated with

organ injury (Cho et al. 2019).

Several studies evaluated possible renal toxicity in laboratory animals treated with glyphosate technical. 

In a 2-generation reproductive toxicity study (EPA 2013a), slightly increased absolute and relative kidney 

weights (7–11% greater than controls) were reported among F0 parental female rats dosed at 
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1,273 mg/kg/day; there was no evidence of histopathologic kidney lesions. Therefore, the slightly 

increased kidney weight was not considered to represent an adverse effect. During 2 years of dietary 

treatment of rats, urinalysis revealed increased specific gravity of urine and decreased urinary pH among 

males treated at an estimated dose of 940 mg/kg/day (NOAEL=362 mg/kg/day); there were no signs of 

treatment-related renal effects in urinalysis results from females treated at an estimated dose as high as 

1,183 mg/kg/day (EPA 1991a, 1991b). Papillary necrosis (males and females) and decreased pH of urine 

(males only) were observed in a study of rats administered glyphosate in the diet for up to 2 years at 

estimated doses of 1,214 mg/kg/day (males) and 1,498 mg/kg/day (females); respective NOAELs were 

361 and 437 mg/kg/day (EPA 2015c). Another 2-year rat study reported decreased pH of urine among 

males treated at 1,000 mg/kg/day (NOAEL=300 mg/kg/day); no renal effects were observed in females at 

doses as high as 1,000 mg/kg/day (EPA 2015c). Female mice treated for 2 years at an estimated dose of 

6,069 mg/kg/day exhibited significantly increased incidence of renal proximal tubule epithelial basophilia 

and hypertrophy (NOAEL=968 mg/kg/day); there was no evidence of renal effects in similarly-treated 

male mice at doses as high as 4,945 mg/kg/day (EPA 2015a).

Shorter-term studies on rodents exposed to glyphosate technical found signs of potential renal damage. 

Myeloma model mice orally exposed to glyphosate (1.0 g/L in drinking water) for 72 weeks showed renal 

damage, including tubular obstruction by casts (Wang et al. 2019). This study was part of a larger effort 

to understand the effect of glyphosate on myeloma development, which is discussed in Section 2.19. In a 

two-week study albino rats exposed intraperitoneally to 134.95 mg/kg/day glyphosate showed serum 

changes indicative of potential kidney effects. Compared to control rats, glyphosate-exposed rats had 

33.8% decreased serum creatinine, 110% increased serum urea, and 146% increased uric acid. Similar 

results were seen in the male rats exposed to 269.9 mg/kg/day Roundup® (El-Shenawy 2009).

Information regarding renal effects in animals exposed to glyphosate formulations is limited. A 

multigenerational study on reproductive effects measured F0 dam kidney weight and found no difference 

between controls and dams exposed to 420 mg/kg/day of Roundup® (Teleken et al. 2019). In mice, 

decreased relative kidney weight (50% less than controls) was reported after daily exposure to ≥250 

mg/kg/day for 12 weeks (Ait Bali et al. 2017). No other kidney observations were made. No renal effects 

occurred in a 4-week study of rats intermittently exposed to Roundup® at exposure levels as high as 360 

mg/m3(approximately 36 mg Roundup®/m3) (EPA 1985c). Histopathologic kidney lesions (necrotic and 

apoptotic cells, localized primarily in tubular epithelium of the proximal straight tubule and thick 

ascending limb of the loop of Henle) were reported in male rats gavaged once with Concentrate 
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Roundup® Weedkiller at dose levels ranging from 250 to 2,500 mg/kg (Wunnapuk et al. 2014). There is 

some uncertainty regarding the role of glyphosate in the reported effects.

2.11 DERMAL 

One woman developed skin lesions after accidental dermal exposure to glyphosate in an herbicide and 

was diagnosed with toxic hand dermatitis (Elsner et al. 2018). After treatment did not fully resolve the 

lesions, she was diagnosed with koebnerization of psoriasis caused by acute irritant contact dermatitis.

In another study, Camacho and Mejia (2017) evaluated the association between aerial applications of 

glyphosate in Colombia and health effects of individuals living in the sprayed areas. The association was 

assessed using individual medical record data and information about Colombia’s aerial spraying program.

Several health outcomes including dermatological effects. Their results observed that for each additional 

square kilometer increase in area sprayed with glyphosate there was an increase in the proportion of 

dermatological diagnoses 7 to 15 days following exposure. 

One study evaluated the potential dermal toxicity of glyphosate in humans. In an experimental study (see 

Table 2-5), a single application of Roundup® to intact skin for 24 hours did not result in irritation 

(Maibach 1986). When applied to abraded skin, erythema was noted in 42% of the subjects after 

24 hours. Mild skin irritation was observed in a repeated exposure test study (Maibach 1986). No skin 

irritation was observed in a Draize skin sensitization test or in a photosensitivity/photoirritation test 

(Maibach 1986).

Available information regarding dermal effects in animals is limited. Minor dermal irritation was 

reported in response to dermally-applied glyphosate technical. At the application site, very slight 

erythema and edema were observed in rabbits during 21 days of repeated dermal application of 

glyphosate technical at 5,000 mg/kg/application; no dermal effects were seen at doses ≤1,000 mg/kg/

application (EPA 1992c). According to EPA (1993), glyphosate is considered a slight dermal irritant 

following acute dermal application.

2.12 OCULAR 

In a study of wives of commercial pesticide applicators, no association was found between glyphosate use 

among the wives and retinal degeneration (Kirrane et al. 2005); see Table 2-5 for details. In a case series 

report of 1,513 ocular exposures to glyphosate, minor symptoms (primarily transient irritation) were 
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observed in 70% of the cases; most (99%) complained of eye pain (Acquavella et al. 1999). Moderate 

effects, such as persistent irritation or low-grade corneal burns or abrasions, were observed in about 2% of 

the cases. Among the cases with moderate effects, 93% reported eye pain, 20% reported lacrimation, and 

27% reported blurred vision.

Two chronic-duration oral studies included ophthalmoscopic examinations of laboratory animals exposed 

to glyphosate technical. EPA (1991a, 1991b) reported significantly increased incidence of lens 

abnormalities in male rats treated via the diet for 2 years at an estimated dose of 940 mg/kg/day; there 

were no indications of a treatment-related ocular effect in female rats at the highest estimated dose level 

(1,183 mg/kg/day). No signs of treatment-related ocular effects were seen among dogs treated via 

capsule for 1 year at estimated doses as high as 500 mg/kg/day (EPA 1986a). 

According to EPA (1993), glyphosate is considered mildly irritating to the eye following ocular 

instillation. According to FAO and WHO (2016), glyphosate was moderate to severely irritating to the 

rabbit eye. EFSA (2015) stated that glyphosate acid was a severe ocular irritant, but that salts of 

glyphosate do not require classification as ocular irritants. There were no signs of exposure-related 

effects in ophthalmologic examinations of rats intermittently exposed to Roundup® for 4 weeks at 

exposure levels as high as 360 mg/m3(approximately 36 mg Roundup®/m3) (EPA 1985c).

2.13 ENDOCRINE 

Available human information regarding possible associations between exposure to glyphosate or 

glyphosate-containing products and risk of endocrinological effects is limited to three studies with 

conflicting results. Goldner et al. (2010) reported no associations between any glyphosate exposure and 

the risks of thyroid diseases. Shrestha et al. (2018) found a significant association between ever-use of 

glyphosate and hypothyroidism (HR 1.28; 95CI 1.07–1.52). Kongtip et al. (2019) reported a positive 

association between increasing use of glyphosate and increased T4 thyroid hormone levels (1.007; 95%CI 

1.001–1.014). These studies are summarized in Table 2-5.

In a weight-of-evidence approach to evaluate the potential for glyphosate to affect the endocrine system, 

EPA (2015b) subjected glyphosate to the Endocrine Disruptor Screening Program Tier 1 (a battery of in 

vitro assays designed assist in evaluation of the potential for a substance to interact with estrogen, 

androgen, or thyroid signaling pathways). EPA evaluated results from the battery of in vitro assays and 

relevant laboratory mammalian and wildlife studies. Using this approach, EPA determined that there is 
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no convincing evidence of potential interaction between glyphosate and estrogen, androgen, or thyroid 

pathways in mammals or wildlife. Included in the evaluation of the estrogen pathway were estrogen 

receptor (ER) binding assays, an ER transactivation assay, aromatase and steroidogenesis assays, a fish 

short-term reproduction assay, and mammalian and wildlife studies that assessed female reproductive 

parameters. Included in the evaluation of the androgen pathway were androgen receptor (AR) binding 

and steroidogenesis assays, a fish short-term reproduction assay, Hershberger and male pubertal assays, 

an AR transactivation assay, and mammalian and wildlife studies that assessed male reproductive 

parameters. Included in the evaluation of the thyroid pathway were male and female pubertal assays, an 

amphibian metamorphosis assay, and mammalian and wildlife studies that assessed thyroid parameters 

Refer to EPA (2015b) for study summaries and EPA (2015d) for DERs from most studies that contributed 

to EPA’s conclusions regarding the potential for glyphosate to affect the endocrine system.

Limited information was located regarding the potential for glyphosate formulations to affect the 

endocrine system. While one study reported degeneration of pancreatic acinar cells and islets of 

Langerhans after male Wistar rats were exposed to 14.4, 375, or 750 mg/kg/day of the herbicide Bushfire 

via drinking water (Tizhe et al. 2018), most of the observed endocrine effects in glyphosate formulation 

animal studies involved changes in hormone levels. Romano et al. (2010) reported dose-related 30–50% 

decreased serum testosterone in young male rats gavaged with Roundup Transorb® at 5–250 mg/kg/day 

during postpartum days 23–53. Romano et al. (2012) implicated disruption of gonadotropin expression as 

a mechanism of action for glyphosate-induced effects on male rat sexual development. Pregnant C57B1/6 

mice exposed to 420 mg/kg/day Roundup® in their drinking water showed no difference in pancreas 

weight compared to controls, but their male F1 offspring had 195% higher intratesticular testosterone, an 

estimated 60% increase in plasma LH, and a 11% increase in β-LH pituitary protein compared with male 

F1 controls (Teleken et al. 2019).

A multi-generational study of F0 Sprague-Dawley rats exposed to either 1.75 mg/kg/day glyphosate 

technical or Roundup Bioflow® found no evidence of endocrine organ lesions in F1 offspring for either 

exposure. However, exposure to Roundup Bioflow® was associated with changes in hormone ratios in F1 

offspring when compared to controls. Specifically, after 13 weeks of exposure to Roundup Bioflow® in 

addition to exposure during gestation and lactation, female F1 rats had increased serum total testosterone 

(TT), decreased 5α-dihydrotestosterone (DHT)/TT ratios, and increased 17β-estradiol (E2)/TT ratios, 

while male F1 rats had decreased serum DHT and increased plasma thyroid stimulating hormone (TSH)

(Manservisi et al. 2019). A 12-week study on male albino rats orally exposed to Roundup® also found 

changes in hormone levels (13% decrease in testosterone, 17% decrease in follicle stimulating hormone, 
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approximately 14% decrease in luteinizing hormone, and approximately 31% increase in prolactin) at 

doses as low as 3.6 mg/kg/day (Owagboriaye et al. 2017). 

However, in an exposure study that exposed male Sprague-Dawley rats to either glyphosate technical (2.5 

mg/kg/day or 25 mg/kg/day) or the glyphosate formulation Glyfonova (25 mg/kg/day) via their drinking 

water, no changes in intratesticular testosterone levels were observed. While the rats exposed to 

Glyfonova showed a statistically significant upregulation in P450 encoding genes in the testes, the authors 

concluded this was not indicative of endocrine effects (Johansson et al. 2018). Nevertheless, other studies 

reported changes in gene and protein expression attributed to glyphosate formulation exposures (Romano 

et al. 2012; Teleken et al. 2019; Varayoud et al. 2017).

2.14 IMMUNOLOGICAL 

Studies examining possible associations between glyphosate exposure and asthma risk or rheumatoid 

arthritis risk are discussed in Sections 2.4 and 2.8, respectively.

Limited information is available regarding immunological effects. There was no evidence of treatmentrelated effects on spleen or thymus of mice administered glyphosate technical in the diet for 28 days at 

estimated doses as high as 1,447.5 mg/kg/day and no evidence of treatment-related effects on splenic antisheep red blood cell (SRBC) anti-body forming cell (AFC) responses to SRBC (EPA 2013b). EPA 

(1992d) reported significantly increased incidences of lymphocytic hyperplasia in the thymus from female 

rats administered glyphosate technical in the diet for up to 26 months at doses of 3.37, 11.22, and 

34.02 mg/kg/day (13/32, 18/37, and 17/34, respectively, versus 5/25 controls). However, EPA (1992d) 

did not consider the lesion to be compound-related because the lesion occurs spontaneously in older rats 

and is quite variable in the thymus, there was no apparent effect on lymphocytes in the spleen (a much 

less variable indicator for lymphocytic hyperplasia), and the severity of the lesion was similar among 

controls and glyphosate-treated groups. Kumar et al. (2014) reported an inflammatory respiratory 

response (evidenced by increased eosinophil and neutrophil counts, mast cell degranulation, and 

production of interleukin-33, thymic stromal lymphopoietin, interleukin-13, and interleukin-5) in

anesthetized mice exposed intranasally to glyphosate.

2.15 NEUROLOGICAL 

Available information regarding possible associations between exposure to glyphosate-containing 

products and risk of neurological effects in humans is limited. One case-control study did not find an 
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association between glyphosate exposure and Parkinson’s disease (see Table 2-5 for details) (Kamel et al. 

2007). In a cross-sectional study conducted on farmers in China, Zhang et al. (2018) reported glyphosate

use was not associated with increased odds or incidence rates of abnormalities of peripheral nerve 

conduction.

One case study found that a man who ingested 200 ml of glyphosate developed Parkinson’s symptoms 4 

years after exposure (Eriguchi et al. 2019). A spatial analysis of exposure to pesticides in Washington 

State found an association between glyphosate exposure and increased odds of premature mortality 

attributable to Parkinson’s disease (OR = 1.33; 95% CI = 1.06-1.67) (Caballero et al. 2018). 

Several animal studies in rats and mice have evaluated the neurological effects of glyphosate. Mice 

exposed once to 250 mg/kg/day RoundUp® via gavage showed a decrease in aversive memory 

performance (Ait Bali et al. 2019). However, no neurological effects were seen in mice given ≤500 

mg/kg/day once by oral gavage (Ait Bali et al. 2017; Aitbali et al. 2018). At 6-12 weeks of daily 

exposure, mice showed behavioral changes in locomotor activity, increase of anxiety and depression-like 

behavior levels, decreased memory performance and decreased grooming time with 250 mg/kg/day

RoundUp® exposure (Ait Bali et al. 2017; Ait Bali et al. 2019; Aitbali et al. 2018). The observed 

neurobehavioral changes were attributed to neurodevelopmental impairment as evidenced by a reduction 

in serotonin (5-HT) immunoreactivity following 6 or 12 weeks of oral exposure to 250 or 500 mg/kg/day 

RoundUp® and a reduction in tyrosine hydroxylase (TH) immunoreactivity following 12 weeks of 

exposure to 250 or 500 mg/kg/day RoundUp® (Ait Bali et al. 2017).

Ait Bali et al. (2019), measured acetylcholinesterase activity in rat whole brain, prefrontal cortex and 

hippocampus, which was inhibited at ≥250 mg/kg/day by >25%, >35%, >25%, respectively. Inhibition in 

all measured parts was dose-dependent (Ait Bali et al. 2019). In pregnant rats, glutathione was decreased 

by 16-26% following exposure to 500 mg/kg/day RoundUp® on days 1 to 7 of pregnancy (Almeida et al. 

2017). In male offspring exposed in utero, during lactation then from post-natal day 21 to 60 to 70 

mg/kg/day RoundUp®, there was a 23% inhibition of hippocampus cholinesterase after post-natal day 60

(Cattani et al. 2017). Oxidative damage, astrocyte dysfunction, glutamate excitotoxicity, and 

misregulation of cholinergic transmission were also seen (Cattani et al. 2017). 

In rats treated via the diet for 13 weeks at doses as high as 1,547–1,631 mg/kg/day and in rats 

administered glyphosate technical once by gavage at up to 2,000 mg/kg, there was no evidence of 

treatment-related neurotoxicity seen by functional observational battery, motor activity testing, and gross 
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and histopathologic examination of brain and peripheral nervous tissue (EPA 2013c). However, clinical 

signs included decreased activity, subdued behavior, and hunched posture.

Glyphosate technical was observed to affect monoaminergic neurotransmitters in the central nervous 

system. In rats administered glyphosate orally up to 800 mg/kg bw/day for 6 days, serotonin 

neurotransmitter levels were significantly decreased in a dose dependent manner at 75, 150 and 800 

mg/kg bw in various regions of the brain including the striatum, hippocampus, prefrontal cortex, 

hypothalamus and midbrain region (Martinez et al. 2018). Similarly, dopamine and norepinephrine levels 

were reported to decrease with increasing concentrations of glyphosate starting at 75 mg/kg bw/day. 

Turnover rates of the neurotransmitters were measured, and their metabolites were altered; there was a 

significant increase in turnover between serotonin and dopamine, and a decrease in turnover with 

norepinephrine (Martinez et al. 2018). 

Rats orally exposed to 5 mg/kg/day of glyphosate or glyphosate-based formulation perinatally from day 9 

gestation to day 22 post-natal were found to have increased expression of synaptophysin a marker of 

synaptic terminals in the hippocampus of both groups (Dechartres et al. 2017). Maternal behavior was 

also observed; at day 1 post-natal, dams were observed to spend less time licking and grooming offspring 

whereas between day 2 and 6 post-natal, more time was spent with offspring. 

In vitro studies have also examined glyphosate and glyphosate-based herbicides for neurotoxicity. 

Glyphosate and an herbicide containing glyphosate isopropylamine as its active ingredient were tested in 

vitro at concentrations of 0.005% to 0.0005%. Although no effect was observed for pure glyphosate, 

glyphosate-based herbicides were reported to interfere with myelination and also as a demyelinating agent 

in a dose-dependent manner (Szepanowski et al. 2018). However, after testing for demyelination using 

glyphosate and isopropylamine additively (rather than as formulated), the authors note that this effect may 

be due to undisclosed additives. Neither glyphosate (pure) nor glyphosate-based herbicide were found to 

impair neurite development (Szepanowski et al. 2018).

2.16 REPRODUCTIVE 

No association between glyphosate use and fecundability was found among women living at farms in 

which pesticides were used and were involved in pesticide activities (Curtis et al. 1999). This study also 

reported an association with improved fecundability when the women were not involved in pesticide 

activities; see Table 2-5 for additional information. Sanin et al. (2009) examined the fertility of women 
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living in regions of Columbia with varying agricultural usage of glyphosate. Although time to pregnancy 

varied widely by region, no significant associations were found with level of glyphosate usage.

In another study, Camacho and Mejia (2017) evaluated the association between aerial applications of 

glyphosate in Colombia and miscarriages by women living in the sprayed areas. Their results observed a 

positive association. For each additional square kilometer increase in area sprayed with glyphosate there 

was an increase in the number of miscarriage diagnoses. However, the authors note the way miscarriage 

was defined in the study may overestimate the number of actual miscarriages. In the study, miscarriage 

was defined when a mother was observed to have attended a prenatal care visit, but a corresponding birth 

registry was not located after 10 months. 

Rodent studies frequently reported reproductive effects in males. Increased incidence of prostatitis was 

reported among male rats receiving glyphosate technical from the diet for up to 2 years at estimated doses 

of ≥361 or 1,214 mg/kg/day (EPA 2015c). In male rats exposed to 375 mg/kg/day of glyphosate for 8 

weeks, a significant decrease in abnormal sperm rate, increased testes malondialdehyde levels, decreased 

glutathione levels, DNA damage in sperm cells, decreased sperm concentration, and degeneration of 

Sertoli cells in testes were observed (Avdatek et al. 2018). Cassault-Meyer et al. (2014) reported 

increased abnormal sperm morphology in rats receiving Roundup® Grand Travaux Plus from the 

drinking water for 8 days at 640 mg/kg/day (the only dose level tested). Male F1 offspring of C57B1/6 

mice exposed to 420 mg/kg/day Roundup® in utero through the end of lactation showed an estimated 5% 

decrease in epithelial height and a 70% reduction of sperm in the cauda epididymis (Teleken et al. 2019). 

Male Kumming mice exposed to 60, 180, or 540 mg/kg/day Roundup® showed no reproductive effects at 

the lowest dose, but had significantly decreased sperm motility and increased sperm abnormality at the 

higher two doses (Jiang et al. 2018). Two low dose studies using glyphosate and glyphosate-based 

herbicides with exposures ranging from 1.75 mg/kg/day to 25 mg/kg/day showed no effects on sperm 

parameters or evidence of lesions or degeneration (Johansson et al. 2018; Manservisi et al. 2019). 

However, male albino rats orally exposed to Roundup® for 12 weeks showed testicular degeneration and 

increased sperm abnormalities in doses as low as 3.6 mg/kg/day (Owagboriaye et al. 2017).

While most studies on male rodents showed reproductive effects, reproductive effects in female rodents 

exposed to glyphosate or glyphosate formations were not observed consistently. In female rats exposed to 

126 mg/kg/day of a glyphosate-based herbicide for 60 days, relative ovary weight decreased by 38% 

compared to controls (Hamdaoui 2018). Additionally, there was a 109% increase in atretic follicles, 14% 

increase in malondialdehyde levels in ovary homogenates, decreased enzymatic antioxidant activity in 
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ovaries, necrosis, and vacuolization of follicles and oocytes in ovaries (Hamdaoui 2018). In pregnant rats 

acutely exposed, ovaries were lighter, implanted sites decreased by 42%, total number of corpus luteum 

were reduced, and pre-implantation loss increased following exposure to 500 mg/kg/day (Almeida et al. 

2017). However, no reproductive effects were reported in pregnant female C57B1/6 mice orally exposed 

to 420 mg/kg/day (Teleken et al. 2019) or in female Wistar rats subcutaneously exposed to 0.5, 5, or 50 

mg/kg/day of a glyphosate formulation (Varayoud et al. 2016).

In multi-generational studies on female rodents, reproductive effects varied by generation. While F0 

female Wistar rats exposed to 1.75 mg/kg/day of Roundup® showed no signs of reproductive effects (no 

changes in gestational length, litter size, sex ratio, or mean live birth index), their female F1 offspring 

who were exposed postnatally for an additional 6 to 13 weeks had a significantly delayed first estrous 

(Manservisi et al. 2019). Similarly, F0 Wistar rats exposed via feed to 3.69 or 352.52 mg/kg/day of the 

glyphosate-based herbicide MAGNUM SUPER II did not show changes in litter size or length of 

gestation at either dose, but their female F1 offspring had an increased rate of preimplantation loss and 

fewer implantation sites at both doses of exposure (Milesi et al. 2018). There was no evidence of 

treatment-related reproductive effects among parental male or female rats administered glyphosate 

technical in the diet for 2 generations at estimated doses as high as 1,234–3,134 mg/kg/day (EPA 1992a, 

2013a). See Section 2.17 for information regarding treatment-related effects on the reproductive system 

of male rats exposed to glyphosate formulations during in utero and/or postnatal development.

Anifandis et al. (2017) investigated the effects of direct exposure of human sperm samples to 1 mg/L 

Roundup® (corresponding to 0.36 mg/L of glyphosate) on mitochondrial integrity and motility. Results 

found that the percentage of sperm motility in Roundup-treated samples upon one hour of incubation was 

significantly lower than in controls; after three hours of incubation, the percentage of sperm motility in 

Roundup-treated samples was also significantly lower than in controls. Mitochondrial incorporation of 

CMX dye was reduced in sperm samples exposed to Roundup at the first hour of incubation, indicating 

mitochondrial dysfunction. Anifandis et al. (2018) also found that human sperm motility decreased more 

significantly in samples exposed to 0.36 mg/L of glyphosate than in control samples at the first hour of 

incubation. This study also found that sperm DNA fragmentation of glyphosate-treated samples was not 

significantly different than sperm DNA fragmentation in controls.

Zhang et al. 2019b evaluated in vitro the effect of glyphosate on the maturation of oocytes. Mouse 

oocytes were exposed up to 500 μM glyphosate for either 2 or 14 hours. Glyphosate was reported to 

reduce the rates of germinal vesicle breakdown (GVBD) and first polar body extrusion (PBE), which are 
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key events in oocyte maturation. Glyphosate was also observed to increase ROS levels, damage DNA, 

induce abnormal spindle morphology, and impair mitochondrial aggregation. Consequently, findings 

suggest glyphosate disrupts the development and maturation of oocytes by generating oxidative stress and 

inducing early apoptosis (Zhang et al. 2019b).

Vanlaeys et al. (2018) investigated the effects of various concentrations of glyphosate and glyphosatebased herbicide formulations on the immature mouse Sertoli cell line (TM4). During the first 24 hours of 

treatment, glyphosate at concentrations ranging from 10 ppm to an agricultural dilution 1000 times 

greater did not impact cell viability, while glyphosate-based formulations resulted in dose-dependent cell 

death. Glyphosate–based formulations also inhibited glutathione-S-transferase activity, but glyphosate 

alone did not. Additionally, glyphosate-based formulations induced accumulation of intracellular lipids. 

Both glyphosate and glyphosate-based formulations resulted in mitochondrial dysfunction signified by 

reduced Succinate dehydrogenase activity. The authors concluded that herbicide-induced mitochondrial 

function alterations are formulation-dependent. The study also assessed TM4 cell viability after acute or 

24-hour exposure to Glyphogan formulants or Glyphogan, and results indicate that this mixture of

compounds leads to rapid induction of cell mortality. Glyphogan formulants at sub-agricultural doses 

were able to rapidly penetrate and accumulate in cells.

2.17 DEVELOPMENTAL 

Several epidemiology studies have examined possible associations between glyphosate use and 

developmental toxicity; these studies are summarized in Table 2-5. Given that only one study examined 

each endpoint and the lack of quantification of glyphosate exposure across studies, these results were not 

considered sufficient for drawing conclusions on the risk of developmental toxicity associated with 

glyphosate exposure in humans. Arbuckle et al. (2001) reported a positive association between maternal 

preconception exposure to glyphosate and increased risk of spontaneous abortion (miscarriage). Garry et 

al. (2002) reported a positive association between phosphonamino- herbicides (glyphosate, Roundup®) 

exposure and parent-reported attention deficit disorder/attention deficit hyperactivity disorder 

(ADD/ADHD). No associations were found between paternal exposure and risk of miscarriages (Savitz et 

al. 1997), preterm delivery (Savitz et al. 1997), small for gestational age risk (Savitz et al. 1997), or 

congenital malformations (Garcia et al. 1998). Similarly, no associations were found between maternal 

glyphosate exposure and birth weight (Sathyanarayana et al. 2010; Parvez et al. 2018), neural tube defects

(Rull et al. 2006), or head circumference (Parvez et al. 2018). 
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Developmental endpoints were evaluated in animals orally exposed to glyphosate technical. Depressed 

weight and increased incidence of unossified sternebrae were observed in fetuses from rat dams treated by 

gavage at 3,500 mg/kg/day during GDs 6–19 (EPA 1992e). This dose level resulted in maternal toxicity, 

thus the developmental effects noted may be secondary to the maternal effects. Increased incidence of 

kidney tubular dilation was reported for F3b male weanlings in a 3-generation study of glyphosate 

technical (98.7% purity) administered to male and female Sprague-Dawley rats in the diet at an estimated 

dose level of 30 mg/kg/day; the reported NOAEL was 10 mg/kg/day (EPA 1992g). However, there were 

no signs of treatment-related effects on kidneys of rat offspring in two subsequent 2-generation rat studies

at dose levels up to 1,234 mg/kg/day (EPA 2013a) or 3,134 mg/kg/day (EPA 1992a). Therefore, the 

finding of increased incidence of kidney tubular dilation in the 3-generation rat study (EPA 1992g) was 

considered a spurious result rather than a glyphosate-induced adverse developmental effect. In one 2-

generation oral rat study, exposure via the diet at an estimated dose level of 1,234 mg/kg/day resulted in 

delayed preputial separation in male pups (EPA 2013a). In the other 2-generation study, the highest dose 

level (3,134 mg/kg/day) resulted in up to 14–20% depressed pup body weight and/or body weight gain 

during the lactation period (EPA 1992a), though the authors state it is unclear if this effect is compound 

related or due to the ingestion of the treated diet. There were no apparent treatment-related developmental 

effects in a study of rabbits treated by gavage at up to 350 mg/kg/day glyphosate technical during GDs 6–

27 (EPA 1992f). No developmental effects were seen in rat pups exposed to 2 mg/kg/day every 48 hours 

on post-natal day 1 to 7 (Guerrero Schimpf et al. 2017). Depressed mean fetal weight (8% less than 

controls) was noted in a study of pregnant rabbits administered glyphosate acid at 300 mg/kg/day during 

GDs 8–20 (EPA 2017b). However, on a per litter basis, there was no statistically significant difference 

between controls and glyphosate-treated groups. Therefore, the 300 mg/kg/day dose level is considered a 

NOAEL for fetal body weight. In a 3-generation study, female Sprague-Dawley rats were acutely exposed 

to 25 mg/kg/day of glyphosate technical during GDs 8-14 (Kubsad et al. 2019). Offspring in the F1 

generation showed delays in puberty in males and decreases in weaning weights of both sexes. More 

serious effects were observed in the F2 and/or F3 generations: significant increases in testis disease, 

prostate disease, kidney disease, ovary disease, obesity, tumors and parturition abnormalities. Almost a 

third of F2 generation females (7/20) died during late gestation or experienced litter mortality, whereas 

neither of these abnormalities were observed in the 16 controls.

Pham et al. (2019) administered glyphosate or Roundup® 3 Plus at doses of 0.5, 5 or 50 mg/kg/day to 

pregnant rats from embryonic day 10.5 to 20 days postpartum. Male offspring were assessed for 

reproductive effects after sacrifice at 5 days, 20 days, 35 days, or 8 months old. Significant decreases in 

sperm counts were observed in males prenatally exposed to both formulations of glyphosate: 0.5 
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mg/kg/day of Roundup® and 5 mg/kg/day of glyphosate were associated with 89% and 84% reductions, 

respectively. Exposure to glyphosate technical was associated with decreased serum testosterone and 

altered testes morphology in rats sacrificed at 20 days old. Testosterone was also reduced in 8-month old 

rats exposed to Roundup®. 

Developmental endpoints were evaluated in three open-literature studies that employed oral exposure to 

glyphosate formulations. The specific role of glyphosate in the reported results is uncertain. Dallegrave 

et al. (2003) observed an increased incidence of skeletal malformations in fetuses from rat dams gavaged 

with Roundup® at 500 mg/kg/day during GDs 6–15. Dallegrave et al. (2007) reported decreased sperm 

production and histopathologic testicular lesions in offspring of rat dams gavaged with Roundup® at 

50 mg/kg/day during gestation and lactation. Romano et al. (2010) reported decreased epithelial 

thickness and increased luminal diameter in seminiferous tubules of male rat pups treated with Roundup 

Transorb® by gavage at 5 mg/kg/day on postpartum days 23–53 and delayed preputial separation at a 

dose level of 50 mg/kg/day. An additional study on C57B1/6 mice also documented developmental 

effects on the reproductive system when male F1 offspring exposed to 420 mg/kg/day Roundup® in utero 

through the end of lactation showed increased age at testes descent (Teleken et al. 2019).

Multi-generational rat studies using intermediate oral exposure to glyphosate-based herbicides found 

developmental effects of varying severity. When pregnant F0 Sprague-Dawley dams were exposed to 

1.75 mg/kg/day Roundup® Bioflow in their drinking water from gestation day 6 to postnatal day 120, 

male and female offspring showed increased anogenital distance at postnatal day 4. Increased anogenital 

distance was also observed in offspring of F0 dams exposed to glyphosate technical, but, unlike 

Roundup® Bioflow exposure, glyphosate exposure was only associated with this effect in male offspring 

(Manservisi et al. 2019). When pregnant F0 Wistar dams fed paste with 3.69 or 352.2 mg/kg/day of the 

glyphosate-based herbicide MAGNUM SUPER II from gestation day 9 to lactation day 21, 

developmental effects were observed in F2 offspring. F1 females from the lower exposure group gave 

birth to offspring with a 2% decrease in fetal length, 6% decrease in body weight, and an increased risk of 

being small for gestational age (RR= 2.43, 91% CI: 1.66, 3.55) compared to controls. F1 females from the 

higher exposure group gave birth to offspring that showed increased fetal anomalies (conjoined fetuses 

and abnormal limbs) compared to controls, as well as the fetal growth effects found in the lower exposure 

group (Milesi et al. 2018).

In a study on rats exposed from gestation day 0 to post-natal day 21, exposure to a glyphosate formulation 

was associated with impaired neurological development. Impaired recognition memory, whole brain 

oxidative stress, decreased lipid peroxidation, and enzyme activity alterations were seen in female 
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offspring rats exposed to 100 mg/kg/day Glifloglex® (Gallegos et al. 2018). In male offspring, impaired 

memory was only seen at higher doses of 200 mg/kg/day. At 100 mg/kg/day, striatum 

acetylcholinesterase activity was inhibited by 23%, in addition to other effects seen in females at the same 

dose (Gallegos et al. 2018).

Chronic glyphosate exposure to pregnant mice at 0.5% glyphosate solution altered several biochemical 

indices related to liver status and metabolism in the offspring. Serum triglyceride levels increased in 

gestational day 19 fetuses and postnatal day 21 female offspring and total cholesterol was elevated in 

postnatal day 7 (males) and 21 (female) offspring. LDL levels were noticeably elevated in postnatal day 7 

mice and in females, AST levels were significantly increased suggesting damage to the liver. Histological 

examination revealed clustering of monocytes, indicative of inflammation, in postnatal day 7 females and 

hepatic lipid droplets in hepatocytes of the offspring mice, with effects more pronounced in males (Ren et 

al. 2019). Overall, offspring mice exhibited hepatic steatosis and excessive lipid droplets formation within 

hepatocytes suggesting glyphosate alters lipid metabolism (Ren et al. 2019). 

Other developmental endpoints evaluated include developmental neurotoxicity. Frank et al. (2017) 

conducted in vitro assays at concentrations ranging between 0.03 to 30 μM of glyphosate to examine 

whether it disrupts normal cortical development. Glyphosate was not found to exert neurodevelopmental 

toxicity in vitro.

2.18 OTHER NONCANCER 

No associations were found between glyphosate exposure and increased risks of diabetes (Montgomery et 

al. 2008) or gestational diabetes (Saldana et al. 2007) in epidemiology studies (see Table 2-5). Metabolic 

acidosis (Kim et al. 2014; Lee et al. 2008; Moon and Chun 2010; Tominack et al. 1991), hyperkalemia 

(Kim et al. 2014; Lee et al. 2008; Moon and Chun 2010), and acute pancreatitis (Hsiao et al. 2008; Kim et 

al. 2014; Moon and Chun 2010) have been reported in case series of individuals ingesting glyphosate; 

metabolic acidosis was typically reported in >35% of the cases.

Hypothermia was reported among rats following single gavage dosing of glyphosate technical at 

2,000 mg/kg (EPA 2013c).

2.19 CANCER 

Meta-Analyses of Epidemiological Studies
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Lymphohematopoietic Cancers. From 2014 to 2016, several meta-analyses were conducted for 

lymphohematopoietic cancers. The results of these analyses are presented in Table 2-6. The primary 

literature used in these meta-analyses is discussed later in this section.

Schinasi and Leon (2014) conducted a systematic review and meta-analysis of 21 pesticide active 

ingredients and chemical groups including glyphosate. The authors reported a positive association 

between glyphosate use and B-cell lymphoma based on two studies (meta-relative risk [RR] 2.0; 95% 

confidence interval [CI] 1.1–3.6) and a positive association between glyphosate use and non-Hodgkin’s 

lymphoma (NHL) based on six studies (meta RR 1.5; 95% CI 1.1–2.0).

Chang and Delzell (2016) performed meta-analyses for NHL subtypes (diffuse large B-cell lymphoma, 

B-cell lymphoma, chronic lymphocytic leukemia/small lymphocytic leukemia [CLL/SLL], and hairy-cell 

leukemia), as well as other types of lymphohematopoietic cancers (leukemia, multiple myeloma, and 

Hodgkin’s lymphoma). The authors reported a positive association between glyphosate use and the risk

of NHL (meta RR 1.3; 95% CI 1.0–1.6; six studies), multiple myeloma (meta RR 1.4; 95% CI 1.0–1.9; 

four studies), and the NHL subtype B-cell lymphoma (meta RR 2.0; 95% CI 1.1–3.6; two studies). The

authors concluded that associations were statistically null for Hodgkin’s lymphoma (meta RR 1.1; 95% 

CI 0.7–1.6; two studies), leukemia (meta RR 1.0; 95% CI 0.6–1.5; three studies); and the NHL subtypes 

diffuse large B-cell lymphoma (meta RR 1.1; 95% CI 0.5–2.3; two studies), CLL/SLL (meta RR 1.3; 95% 

CI 0.2–10; two studies), follicular lymphoma (meta RR 1.7; 95% CI 0.7–3.9; two studies), and hairy cell 

leukemia (meta RR 2.5; 95% CI 0.9–7.3; two studies). Some of the RR CIs were wide, indicating 

uncertainty in the point estimate.

The IARC Working Group conducted a meta-analysis for NHL using the same six studies as Schinasi and 

Leon (2014) and Chang and Delzell (2016). The Working Group reanalyzed the data, but used the most 

fully adjusted risk estimates for the studies by Hardell et al. (2002) and Eriksson et al. (2008) and 

estimated a slightly lower meta-analysis relative risk (meta RR 1.3; 95% CI 1.03–1.65) (IARC 2017).

Zhang et al. (2019a) conducted a meta-analysis of the association between glyphosate exposure and NHL 

based on five case-control studies and the 2018 update of the Agricultural Health Study. The most highly 

exposed individuals had a 41% higher risk of NHL as compared to unexposed controls (meta RR 1.41; 

95% CI 1.13–1.75).
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Table 2-6. Summary of Meta-Analyses of Results from Studies Examining Possible Association Between SelfReported Use of Glyphosate and Lymphohematopoietic Cancers

Outcome

Studies included in 

analysis Number of participants

Number reporting

glyphosate use

Meta-analysisa

relative risk or hazard ratio

(95% CI) Reference

NonHodgkin’s 

lymphoma

De Roos et al. 2003

De Roos 2005a

Eriksson et al. 2008

Hardell et al. 2002

McDuffie et al. 2001

Orsi et al. 2009

650 cases/1,933 controls

54,315

1,163 cases/1,016 controls

515 cases/1,141 controls

517 cases/1,506 controls

244 cases/436 controls

36 cases/61 controls

71 cases

29 cases/18 controls

8 cases/8 controls

51 cases/133 controls

12 cases/24 controls

1.5 (1.1–2.0)

I

2=32.7%

Schinasi and 

Leon 2014

NonHodgkin’s 

lymphoma

De Roos et al. 2003

De Roos 2005a

Eriksson et al. 2008

Hardell et al. 2002

McDuffie et al. 2001

Orsi et al. 2009

Not stated

54,315

910 cases/1,016 controls

404 cases/741 controls

517 cases/1,506 controls

244 cases/436 controls

Not stated

Not stated

29 cases

8 cases

51 cases

12 cases

1.3 (1.03–1.65)

I

2=0.0%, p=0.589 for 

heterogeneity

IARC 2017

NonHodgkin’s 

lymphoma

De Roos et al. 2003

De Roos 2005a

Eriksson et al. 2008

Hardell et al. 2002

McDuffie et al. 2001

Orsi et al. 2009

650 cases/1,933 controls

49,211 

995 cases/1,016 controls

515 cases/1,141 controls

517 cases/1,506 controls

244 cases/436 controls

36 cases/61 controls

71 cases

29 cases/18 controls

8 cases/8 controls

51 cases/133 controls

12 cases/24 controls

1.3 (1.0–1.6)

I

2=0.0%, p=0.84 for heterogeneity

Chang and 

Delzell 2016

NonHodgkin’s 

lymphoma

Leveque-Morlais et al. 

2015

Kristensen et al. 1996

Alavanja et al. 1996

127,282

137,821

51,167

Estimated 36%

Estimated 38%

Estimated 83%

mHR 0.95 (0.77–1.18)

I

2=57.0%, p=0.10 for 

heterogeneity

Leon et al. 

2019

NonHodgkin’s 

lymphoma

McDuffie et al. 2001

Cantor et al. 1992

Hoar et al. 1986

Zahm et al. 1990

517 cases/1,506 controls

622 cases/1,245 controls

200 cases/1,005 controls

201 cases/725 controls

mOR 1.43 (1.11–1.83)

I

2= not reported

Pahwa et al. 

2019

NonHodgkin’s 

lymphoma

Andreotti et al.2018

De Roos 2003

De Roos 2005a

Eriksson et al. 2008

Hardell et al. 2002

54,251

650 cases/1,933 controls

54,315

910 cases/1,016 controls

515 cases/1,141 controls

Estimated 83%

36 cases

Estimated 76%

Estimated 2%

8 cases

1.41 (1.13–1.75)

p=0.14 for heterogeneity

Zhang et al. 

2019a
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Table 2-6. Summary of Meta-Analyses of Results from Studies Examining Possible Association Between SelfReported Use of Glyphosate and Lymphohematopoietic Cancers

Outcome

Studies included in 

analysis Number of participants

Number reporting

glyphosate use

Meta-analysisa

relative risk or hazard ratio

(95% CI) Reference

McDuffie et al. 2001

Orsi et al. 2009

517 cases/1,506 controls

244 cases/435 controls

51 cases

12 cases

B-cell 

lymphoma

Cocco et al. 2013

Eriksson et al. 2008

2,348 cases/2,462 controls

1,163 cases/1,016 controls 

4 cases/2 controls

Not stated

2.0 (1.1–3.6)

I

2=0.0%, p=0.58 for heterogeneity

Chang and 

Delzell 2016;

Schinasi and 

Leon 2014

Leukemia Brown et al. 1990 

De Roos et al. 2005a

Kaufman et al. 2009

578 cases/1,245 controls

49,211

180 cases/756 controls

15 cases/49 controls

43 cases

1 case/3 controls

1.0 (0.6–1.5)

I

2=0.0%a

, p=0.92 for 

heterogeneity

Chang and 

Delzell 2016

Multiple 

myeloma

Brown et al. 1993

De Roos et al. 2005a

Kachuri et al. 2013

Orsi et al. 2009

Pahwa et al. 2012

Sorahan 2015

173 cases/650 controls

19 cases

342 cases/1,357 controls

56 cases/456 controls

32 cases/133 controls

40,719

11 cases/40 controls

Not stated

32 cases/131 controls

5 cases/24 controls

Not stated

24 cases

1.4 (1.0–1.9)

I

2=0.0%, p=0.63 for heterogeneity

Chang and 

Delzell 2016

Multiple 

myeloma

Leveque-Morlais et al. 

2015

Kristensen et al. 1996

Alavanja et al. 1996

127,282

137,821

51,167

Estimated 36%

Estimated 38%

Estimated 83%

mHR 0.87 (0.66–1.15)

I

2=0.0%, p=0.95 for heterogeneity

Leon et al. 

2019

Hodgkin’s 

lymphoma

Karunanayake et al. 2012

Orsi et al. 2009

316 cases/1,506 controls

87 cases/496 controls

38 cases/133 controls

6 cases/24 controls

1.1 (0.7–1.6)

I

2=0.0%, p=0.36 for heterogeneity

Chang and 

Delzell 2016

Diffuse large 

B-cell 

lymphoma

Eriksson et al. 2008

Orsi et al. 2009

955 cases/1,016 controls

456 controls

Not stated

5 cases/24 controls

1.1 (0.5–2.3)

I

2=0.0%, p=0.79 for heterogeneity

Chang and 

Delzell 2016

Diffuse large 

B-cell 

lymphoma

Leveque-Morlais et al. 

2015

Kristensen et al. 1996

Alavanja et al. 1996

127,282

137,821

51,167

Estimated 36%

Estimated 38%

Estimated 83%

mHR 1.36 (1.00–1.82) 

I

2=0.0%, p=0.48 for heterogeneity

Leon et al. 

2019
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Table 2-6. Summary of Meta-Analyses of Results from Studies Examining Possible Association Between SelfReported Use of Glyphosate and Lymphohematopoietic Cancers

Outcome

Studies included in 

analysis Number of participants

Number reporting

glyphosate use

Meta-analysisa

relative risk or hazard ratio

(95% CI) Reference

Diffuse large 

B-cell 

lymphoma

McDuffie et al. 2001

Cantor et al. 1992

Hoar et al. 1986

Zahm et al. 1990

517 cases/1,506 controls

622 cases/1,245 controls

200 cases/1,005 controls

201 cases/725 controls

51 cases/133 controls

26 cases/49 controls

Not stated

Undetermined

mOR 1.60 (1.12–2.29)

I

2 not reported; p=0.08 for 

heterogeneity

Pahwa et al. 

2019

CLL/SLL Eriksson et al. 2008

Orsi et al. 2009

955 cases/1,016 controls

456 controls

Not stated

2 cases/18 controls

1.3 (0.2–10)

I

2=83.7%, p=0.01 for 

heterogeneity

Chang and 

Delzell 2016

CLL/SLL Leveque-Morlais et al. 

2015

Kristensen et al. 1996

Alavanja et al. 1996

127,282

137,821

51,167

Estimated 36%

Estimated 38%

Estimated 83%

mHR 0.92 (0.69–1.24)

I

2=0.0%, p=0.38 for heterogeneity

Leon et al. 

2019

CLL/SLL McDuffie et al. 2001

Cantor et al. 1992

Hoar et al. 1986

Zahm et al. 1990

517 cases/1,506 controls

622 cases/1,245 controls

200 cases/1,005 controls

201 cases/725 controls

51 cases/133 controls

26 cases/49 controls

Not stated

Undetermined

mOR 1.77 (0.98–3.22)

I

2 not reported; p=0.04 for 

heterogeneity

Pahwa et al. 

2019

Follicular 

lymphoma

Eriksson et al. 2008

Orsi et al. 2009

955 cases/1,016 controls

456 controls

Not stated

3 cases/24 controls

1.7 (0.7–3.9)

I

2=0.0%, p=0.73 for heterogeneity

Chang and 

Delzell 2016

Follicular 

lymphoma

Leveque-Morlais et al. 

2015

Kristensen et al. 1996

Alavanja et al. 1996

127,282

137,821

51,167

Estimated 36%

Estimated 38%

Estimated 83%

mHR 0.79 (0.52–1.21)

I

2=0.0%, p=0.56 for heterogeneity

Leon et al. 

2019

Follicular 

lymphoma

McDuffie et al. 2001

Cantor et al. 1992

Hoar et al. 1986

Zahm et al. 1990

517 cases/1,506 controls

622 cases/1,245 controls

200 cases/1,005 controls

201 cases/725 controls

51 cases/133 controls

26 cases/49 controls

Not stated

Undetermined

mOR 1.00 (0.65–1.54)

I

2 not reported; p=0.04 for 

heterogeneity

Pahwa et al. 

2019

Hairy cell 

leukemia

Orsi et al. 2009

Nordstrom et al. 1998

456 controls

111 cases/400 controls

2 cases/18 controls

4 cases/5 controls

2.5 (0.9–7.3)

I

2=0.0%, p=0.63 for heterogeneity

Chang and 

Delzell 2016
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Table 2-6. Summary of Meta-Analyses of Results from Studies Examining Possible Association Between SelfReported Use of Glyphosate and Lymphohematopoietic Cancers

Outcome

Studies included in 

analysis Number of participants

Number reporting

glyphosate use

Meta-analysisa

relative risk or hazard ratio

(95% CI) Reference

a

I

2

is a measure of total variance explained by study heterogeneity and measure of inconsistency in results; higher values indicate greater inconsistency.

CI = confidence interval; CLL/SLL = chronic lymphocytic leukemia/small lymphocytic lymphoma
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Leon et al. (2019) performed meta-analyses for exposure to glyphosate with NHL, diffuse large B-cell 

lymphoma, chronic lymphocytic leukemia/small lymphocytic leukemia (CLL/SLL), multiple myeloma, 

Hodgkin’s lymphoma, and follicular lymphoma based on three cohort studies included in the AGRICOH 

consortium; this includes agricultural workers in France, Norway, and the US. Of these, a significant

association was observed between diffuse B-cell lymphoma and glyphosate (meta hazard ratio [HR] 1.36; 

95% CI 1.00–1.85; I2 = 0%). The authors concluded that associations were statistically null for NHL 

(meta HR 0.95’ 95% CI: 0.77-1.18), multiple myeloma (meta HR 0.87; 95% CI: 0.66-1.15), CLL/SLL 

(meta HR 0.92; 95% CI: 0.69-1.24), and follicular lymphoma (meta HR 0.79;95% CI: 0.52-1.21).

Findings for other cancer types are listed in Table 2-6.

Pahwa et al. (2019) conducted meta-analyses for exposure to glyphosate with NHL, diffuse large B-cell 

lymphoma, CLL/SLL, and follicular lymphoma based on four case-control studies in the US and Canada. 

The authors reported a positive association between glyphosate use and NHL (meta odds ratio [OR] 1.43; 

95% CI: 1.11, 1.83) and diffuse large B-cell lymphoma (meta OR 1.60; 95% CI: 1.12-2.29). The authors 

concluded that associations were statistically null for CLL/SLL (meta OR 1.77; 95% CI: 0.98-3.22) and 

follicular lymphoma (meta OR 1.00; 95% CI: 0.65, 1.54).

Epidemiological Studies

A number of case-control and prospective cohort epidemiology studies have examined possible 

associations between use of glyphosate-containing compounds and increased cancer risks. Detailed 

overviews—including a description of the exposure metric used, the results, and the conclusions and 

limitations as reported by the study authors—are presented in Table 2-7 for solid tumor types and Table 

2-8 for lymphohematopoietic cancers. 

The majority of the studies examined individuals who were occupationally exposed to pesticides and used 

self-reported or proxy-reported (ever/never use of glyphosate-containing compounds) use as the marker of 

exposure. A few studies examined potential cancer risk among family members (i.e., wife and children) 

of pesticide applicators. The cohort studies utilized data on participants from the Agricultural Health 

Study, a prospective study of cancer and other health outcomes. The cohort consisted of >89,000 licensed 

pesticide applicators and their spouses (52,394 applicators and 32,345 spouses) who were recruited 

between 1993 and 1997 from Iowa and North Carolina. Study limitations included self-reported exposure 

information, few cases for many of the cancer subtypes, limited information regarding the timing and 

duration of exposure, and recall bias.
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Table 2-7. Cancer Outcomes for Solid Tumor-Types in Humans Exposed to Glyphosate-Containing Products

Reference and study overview Methods and outcomes Results (with 95% CI)

Study author conclusions and 

limitations

Andreotti et al. 2018

Prospective cohort study of 

54,251 licensed pesticide applicators 

(97% white, 97% male) recruited between 

1993 and 1997 in Iowa and North 

Carolina from the Agricultural Health 

Study to evaluate agricultural exposure to 

50 pesticides (including glyphosate) and 

cancer incidence cases.

44,932 participants reported ever use of 

glyphosate, including 5,779 participants 

with incident cancer cases.

Exposure: Self-reported 

ever/never use of any glyphosate 

pesticides, lifetime days of 

glyphosate use (days per year x 

number of years), and intensityweighted lifetime days (lifetime 

days x intensity score) at

enrollment (1993–1997) or followup (1999–2005). 

Intensity-weighted lifetime days of 

glyphosate use was categorized 

into quartiles, tertiles, or the 

median, such that there were at 

least five exposed cases in each 

category.

Outcome: Incident cancer 

diagnoses ascertained via linkage 

to cancer registries in Iowa 

(enrollment through 2013) and 

North Carolina (enrollment through 

2012).

Data analysis: Poisson regression 

Adjustments: Age, cigarette 

smoking status, alcohol drinks per 

month, family history of any 

cancer, state of recruitment, and 

the five pesticides (atrazine, 

alachlor, metolachlor, trifluralin, 

and 2,4-D).

Confounders considered included 

BMI and pack-years of cigarettes 

smoked.

Oral cavity:

Q4: RR 0.84 (0.48–1.46)

p-trend: 0.54

Colon: 

Q4: RR 1.01 (0.74–1.38)

p-trend: 1.00

Rectum:

Q4: RR 0.84 (0.52–1.34)

p-trend: 0.43

Pancreas:

Q4: RR 1.06 (0.57–1.97)

p-trend: 0.14

Lung:

Q4: RR 1.00 (0.76–1.33)

p-trend: 0.78

Melanoma:

Q4: RR 1.17 (0.78–1.74)

p-trend: 0.53

Prostate: 

Q4: RR 0.99 (0.86–1.13)

p-trend: 0.89

Testicular: 

T3: RR 0.57 (0.20–1.67)

p-trend: 0.07

Bladder: 

Q4: RR 1.26 (0.87–1.82)

p-trend: 0.42

Conclusions: The authors 

observed no associations 

between glyphosate use and 

overall cancer risk or risk of 

cancer of the oral cavity, colon, 

rectum, pancreas, lung, skin, 

prostate, testes, bladder or 

kidney. Risk estimates were 

similar in magnitude between the 

unlagged and lagged (5 or 

20 years) exposure analyses for 

all sites evaluated.

Limitations: Some 

misclassification of exposure 

undoubtedly occurred; because 

many cancer sites were 

evaluated, there is the possibility 

that results were observed by 

chance, and should be 

interpreted with caution.

However, 37% of the participants 

did not respond to follow-up, 

which may have resulted in an 

underestimation of glyphosate 

exposure though imputation 

procedures were used in an 

attempt to mitigate this issue.
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Table 2-7. Cancer Outcomes for Solid Tumor-Types in Humans Exposed to Glyphosate-Containing Products

Reference and study overview Methods and outcomes Results (with 95% CI)

Study author conclusions and 

limitations

Kidney:

Q4: RR 1.03 (0.66–1.61)

p-trend: 0.95

De Roos et al. 2005a

Prospective cohort study of 

54,315 certified pesticide applicators 

(97% male, 97% Caucasian) in Iowa and

North Carolina (Agricultural Health Study) 

to evaluate agricultural exposure to 

glyphosate and cancer incidence. 

Among 54,315 subjects included in ageadjusted analyses, 41,035 subjects 

reported exposure to glyphosate and 

13,280 reported no exposure.

Number cases (exposed percent) for 

different cancer sites: 

All cancers: 2,088 (73.0%)

Lung: 204 (72.1%)

Oral cavity: 59 (76.3%)

Colon: 174 (75.3%)

Rectum: 76 (77.6%)

Pancreas: 38 (76.3%)

Kidney: 63 (73.0%)

Bladder: 79 (76.0%)

Prostate: 825 (72.5%)

Melanoma: 75 (84.0%)

Exposure: Self-reported 

never/ever use of glyphosate. 

Cumulative exposure days 

(CEDs): 1–20 (reference), 21–56, 

and 57–2,678 days. 

Intensity weighted exposure days 

(IWEDs) of 0.1–79.5 (reference), 

79.6–337.1, and 337.2–

18,241 units. 

Outcomes/endpoints: Cancer 

registry files in Iowa and North 

Carolina for case identification. 

Incident cases were identified from 

enrollment to 2001 (median followup time: 6.7 years). 

Data analysis: Poisson regression 

analyses for all cancers combined 

and 12 specific cancer sites (with 

at least 30 cases).

Adjustments: Age at enrollment, 

education, pack-years of cigarette 

smoking, alcohol consumption, 

family history of cancer, state of 

residency, and co-exposure to 

10 other pesticides (2,4-D, 

alachlor, atrazine, metolachlor, 

trifluralin, benomyl, maneb, 

paraquat, carbaryl, and diazinon).

All cancers:

Ever used: RR 1.0 (0.9–1.2)

CED T3: RR 1.0 (0.9–1.1)

p-trend: 0.57

IWED T3: RR 0.9 (0.8–1.1)

p-trend: 0.35

Lung:

Ever used: RR 0.9 (0.6–1.3)

CED T3: RR 0.7 (0.4–1.2)

p-trend: 0.21

IWED T3: RR 0.6 (0.3–1.0)

p-trend: 0.02

Oral cavity:

Ever used: RR 1.0 (0.5–1.8)

CED T3: RR 0.8 (0.4–1.7)

p-trend: 0.66

IWED T3: RR 1.0 (0.5–2.3)

p-trend: 0.95

Colon:

Ever used: RR 1.4 (0.8–2.2)

CED T3: RR 0.9 (0.4–1.7)

p-trend: 0.54

IWED T3: RR 1.4 (0.8–2.5)

p-trend: 0.10

Rectum:

Ever used: RR 1.3 (0.7–2.3)

Conclusions: No association 

between glyphosate exposure 

and all cancer incidence or most 

of the specific cancer subtypes, 

including NHL. A small number 

of cases suggested a positive 

association between multiple 

myeloma and glyphosate 

exposure.

Limitations: Self-reported 

exposure information, few cases 

for many of the cancer subtypes, 

most applicators were male, there 

is no information on timing of 

pesticide use in relation to 

disease. 
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Table 2-7. Cancer Outcomes for Solid Tumor-Types in Humans Exposed to Glyphosate-Containing Products

Reference and study overview Methods and outcomes Results (with 95% CI)

Study author conclusions and 

limitations

CED T3: RR 1.1 (0.6–2.3)

p-trend: 0.70

IWED T3: RR 0.9 (0.5–1.9)

p-trend: 0.82

Pancreas:

Ever used: RR 0.7 (0.3–2.0)

CED T3: RR 1.3 (0.5–3.6)

p-trend: 0.83

IWED T3: RR 0.5 (0.1–1.9)

p-trend: 0.06

Kidney:

Ever used: RR 1.6 (0.7–3.8)

CED T3: RR 0.7 (0.3–1.6)

p-trend: 0.34

IWED T3: RR 0.5 (0.2–1.0)

p-trend: 0.15

Bladder:

Ever used: RR 1.5 (0.7–3.2)

CED T3: RR 1.2 (0.6–2.2)

p-trend: 0.53

IWED T3: RR 0.8 (0.3–1.8)

p-trend: 0.88

Prostate:

Ever used: RR 1.1 (0.9–1.3)

CED T3: RR 1.1 (0.9–1.3)

p-trend: 0.69

IWED T3: RR 1.1 (0.9–1.3)

p-trend: 0.60

Melanoma:

Ever used: RR 1.6 (0.8–3.0)
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Table 2-7. Cancer Outcomes for Solid Tumor-Types in Humans Exposed to Glyphosate-Containing Products

Reference and study overview Methods and outcomes Results (with 95% CI)

Study author conclusions and 

limitations

CED T3: RR 0.9 (0.5–1.8)

p-trend: 0.77

IWED T3: RR 0.7 (0.3–1.2)

p-trend: 0.44

Engel et al. 2005

Prospective cohort study of 30,454 wives 

(98% Caucasian) of private pesticide 

applicators (largely farmers) in Iowa and 

North Carolina (Agricultural Health Study) 

to evaluate breast cancer risk in relation 

to use of individual pesticides by the 

women themselves or by their husbands. 

Glyphosate analysis for wife’s pesticide 

use among all wives in the cohort 

included 82 exposed and 227 unexposed 

cases (n= 309) and 10,016 exposed and 

20,129 (n= 30,145) unexposed controls. 

Further analysis of husband’s pesticide 

use among wives who reported never 

having used pesticides themselves 

included 109 “exposed” (husband used 

pesticide) and 43 “unexposed” cases and 

9,304 “exposed” and 3,993 “unexposed” 

controls.

Exposure: Self-reported 

ever/never use of any glyphosate 

products at enrollment (1993–

1997). Husband’s information was 

used as a measure of possible 

indirect pesticide exposure for 

their wives.

Outcomes/endpoints: Breast 

cancer incident cases identified 

through state cancer registries 

from enrollment to 2000 (mean 

follow-up period: 4.8 years).

Data analysis: Poisson regression

Adjustments: Age, race, and state 

of residence.

Confounders considered included 

BMI, age at menarche, parity, age 

at first birth, menopausal status, 

age at menopause, family history 

of breast cancer, physical activity, 

smoking, alcohol consumption, 

fruit and vegetable consumption, 

and education.

Breast cancer:

Wife’s pesticide use among all 

wives in cohort: RR 0.9 (0.7–

1.1)

Husband’s pesticide use among 

wives who never used 

pesticides: RR 1.3 (0.8–1.9)

Conclusions: No specific 

conclusion was given on 

glyphosate exposure and breast 

cancer.

Limitations: Some associations 

may have occurred by chance, 

data on pesticide-specific 

exposure-response relations 

were only available for the 

husband, lack of information on 

how long each woman had been 

married to her current partner, 

limited power to assess 

associations for less commonly 

used pesticides, pesticide use 

was based on self-reporting.
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Table 2-7. Cancer Outcomes for Solid Tumor-Types in Humans Exposed to Glyphosate-Containing Products

Reference and study overview Methods and outcomes Results (with 95% CI)

Study author conclusions and 

limitations

Flower et al. 2004

Prospective and retrospective cohort 

study of 17,280 children (52% male, 96% 

Caucasian) of pesticide applicators in 

Iowa (Agricultural Health Study) to 

evaluate parental exposure to 

50 pesticides (including glyphosate) and 

childhood cancer risk.

Glyphosate analysis included 

6,075 children (13 cases) with maternal 

use and 3,231 children (6 cases) with 

paternal use of glyphosate. 

Exposure: Self-reported parental 

ever/never use of any glyphosate 

product by both applicators and 

spouses at enrollment (1993–

1997).

Outcomes/endpoints: Childhood 

cancer cases were both 

retrospectively and prospectively 

identified after parental enrollment 

through Iowa Cancer registries 

from 1975 to 1998.

Data analysis: Multiple logistic 

regression.

Adjustments: Child’s age at 

parent’s enrollment.

Confounders considered included 

parental age at child’s birth, child’s 

sex, child’s birth weight, history of 

parental smoking, paternal history 

of cancer, and maternal history of 

miscarriage.

Childhood cancers:

Maternal use (ever): OR 0.61 

(0.32–1.16)

Paternal use (prenatal): OR 

0.84 (0.35–2.34)

Conclusions: No significant 

associations were observed 

between maternal (or paternal) 

pesticide (including glyphosate) 

application, including increased

frequency of application, and risk 

of childhood cancer risk.

Limitations: Small number of 

cases limits statistical power, 

maternal use is limited by lack of 

data on timing of exposure in 

relation to child’s birth, paternal 

prenatal use constitutes a broad 

window of exposure and not 

necessarily just prenatal.
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Table 2-7. Cancer Outcomes for Solid Tumor-Types in Humans Exposed to Glyphosate-Containing Products

Reference and study overview Methods and outcomes Results (with 95% CI)

Study author conclusions and 

limitations

Koutros et al. 2013a, 2013b

Prospective cohort study of 

54,412 certified pesticide applicators in 

Iowa and North Carolina (Agricultural 

Health Study) to evaluate agricultural 

exposure to 50 pesticides (including 

glyphosate) and prostate cancer risk. 

There were 1,962 incident prostate 

cancer cases, 919 of whom had 

aggressive prostate cancer. 

Glyphosate analysis included 

1,464 exposed and 498 unexposed cases 

(n=1,962) and 42,420 exposed and 

10,015 unexposed controls (n=52,435).

Exposure: Self-reported 

ever/never glyphosate use, lifetime 

days of glyphosate use (years of 

use x days/year used), intensityweighted lifetime days of 

glyphosate use (lifetime days x 

exposure intensity) at enrollment 

(1993–1997). Exposure was 

categorized into non-exposed and 

quartiles exposure on the basis of 

the distribution of exposed cases.

Outcomes/endpoints: Prostate 

cancer incidences determined 

through state cancer registries 

from enrollment to 2007.

Data analysis: Poisson 

regression.

Adjustments: Age at enrollment,

race, state, family history of 

prostate cancer, smoking, fruit 

servings, and leisure-time physical 

activity in the winter.

Separate glyphosate analyses 

were conducted by disease 

aggressiveness and family history 

of prostate cancer (yes, no).

Cumulative lifetime exposure 

based on intensity-weighted 

days: 

Total prostate cancer:

Q4: RR 0.99 (0.86–1.15)

Aggressive prostate cancer:

Q4: RR 0.94 (0.75–1.18)

Total prostate cancer, no family 

history:

Q4: RR 1.02 (0.86–1.21)

p-trend: 0.27

Total prostate cancer, with 

family history:

Q4: RR 0.95 (0.64–1.40)

p-trend: 0.71

Conclusions: No significant 

association was found between 

any specific pesticide (including 

glyphosate) and risk of total 

prostate cancer.

Limitations: Information on 

Gleason score of severity was 

missing for some and not 

standardized, which most likely 

led to an underestimation of 

advanced cases; use of takehome questionnaire could 

introduce selection bias and 

exposure misclassification; large 

number of pesticides investigated

so cannot rule out the possibility 

that some findings may be due to 

chance.
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Table 2-7. Cancer Outcomes for Solid Tumor-Types in Humans Exposed to Glyphosate-Containing Products

Reference and study overview Methods and outcomes Results (with 95% CI)

Study author conclusions and 

limitations

Koutros et al. 2016

Prospective cohort study of 54,344 male 

pesticide applicators in Iowa and North 

Carolina (Agricultural Health Study) to 

evaluate agricultural exposure to 

65 pesticides (including glyphosate) and 

bladder cancer risk (n=321 incident cases 

identified).

Glyphosate analysis included 

248 exposed and 73 unexposed cases 

(n=321) and 54,023 controls.

Exposure: Self-reported 

ever/never glyphosate use, lifetime 

days of glyphosate use (years of 

use x days/year used), intensityweighted lifetime days of 

glyphosate use (lifetime days x 

exposure intensity) at enrollment 

(1993–1997).

Outcomes/endpoints: Bladder 

cancer incidences determined 

through state-based cancer 

registries from enrollment through 

2010 in North Carolina and 2011 

in Iowa.

Data analysis: Poisson 

regression.

Adjustments: Age, race, state, 

cigarette smoking, and pipe 

smoking.

Bladder cancer:

Ever use: RR 1.17 (0.78–1.77)

Cumulative lifetime exposure 

based on intensity-weighted 

days: 

Overall

Q4: RR 1.07 (0.73–1.56)

p-trend: 0.99

Stratification by smoking status

Never smoker: 

Q4: RR 1.93 (0.95–3.91) 

p-trend: 0.03

Former smoker: 

Q4: RR 1.00 (0.58–1.72)

p-trend: 0.67

Current smoker: 

Q4: RR 0.58 (0.25–1.34)

p-trend: 0.17

Conclusions: No specific 

conclusion given on glyphosate 

exposure and bladder cancer. 

Never smokers who were heavy 

users of the glyphosate had 

increased risk of bladder cancer. 

Limitations: Potential for 

exposure misclassification, 

findings may be due to chance, 

due to small number of cases.
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Table 2-7. Cancer Outcomes for Solid Tumor-Types in Humans Exposed to Glyphosate-Containing Products

Reference and study overview Methods and outcomes Results (with 95% CI)

Study author conclusions and 

limitations

Lee et al. 2007 

Prospective cohort study of 

56,813 certified pesticide applicators 

(97% male, 97% Caucasian) in Iowa and 

North Carolina (Agricultural Health Study) 

to evaluate agricultural exposure to 

50 pesticides (including glyphosate) and 

colorectal cancer risk. 

Glyphosate analysis included 

225 exposed and 67 unexposed for 

colorectal cancer cases (n=305), 

151 exposed and 49 unexposed for colon 

cancer cases (n=212), and 74 exposed 

and 18 unexposed for rectal cancers 

(n=93). 

Exposure: Self-reported ever use 

of any glyphosate pesticides at 

enrollment (1993–1997).

Outcomes/endpoints: Colorectal 

cancer incidences determined 

through cancer registries from 

enrollment to 2002 (mean followup period: 7.3 years).

Data analysis: Unconditional 

multivariate logistic regressions. 

Adjustments: Age, state of 

residence, smoking history, total 

pesticide application days to any 

pesticide. 

Confounders considered included 

BMI, race, license type, education 

level, aspirin intake, family history 

of colorectal cancer, physical 

activity, smoking, and intakes of 

meat, fruits, vegetables, and 

alcohol.

Colorectal cancer:

OR 1.2 (0.9–1.6)

Colon cancer:

OR 1.0 (0.7–1.5)

Rectal cancer:

OR 1.6 (0.9–2.9)

Conclusions: No specific 

conclusion was given on 

glyphosate exposure and 

colorectal cancers. 

Limitations: Since the study 

examined risks for 50 pesticides, 

it is possible that some significant 

findings might occur by chance 

alone due to the multiple 

comparisons. Potential recall 

bias and thus exposure 

misclassification associated with 

subjects recalling pesticide use 

from many years ago.
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Table 2-7. Cancer Outcomes for Solid Tumor-Types in Humans Exposed to Glyphosate-Containing Products

Reference and study overview Methods and outcomes Results (with 95% CI)

Study author conclusions and 

limitations

Andreotti et al. 2009

Nested case-control study of 93 cases of 

pancreatic cancer (64 applicators and

29 spouses) and 82,503 controls 

(52,721 applicators and 29,782 spouses) 

from the Agricultural Health Study, 

conducted in Iowa and North Carolina, to 

evaluate the association of pancreatic 

cancer and use of 24 pesticides 

(including glyphosate).

Glyphosate analysis included 55 exposed 

and 35 unexposed cases (n= 90) and 

48,461 exposed and 31,282 unexposed 

controls (n= 79,743).

Exposure: Self-reported

ever/never use of any glyphosate 

product for applicators and 

spouses and intensity-weighted 

lifetime exposure days for 

applicators at enrollment (1993–

1997). 

Outcomes/endpoints: Pancreatic 

cancer incidences identified 

through state cancer registries 

from enrollment to 2004 (over 

9 years of follow-up time).

Data analysis: Unconditional 

logistic regression.

Adjustments: Age, cigarette 

smoking, diabetes, and subject 

type for ever/never pesticide 

exposure (applicator versus 

spouse).

Pancreatic cancer:

Ever/never among applicators 

and spouses: OR 1.1 (0.6–1.7)

Intensity weighted pesticide 

exposure among applicators:

Never: 1.0 (reference)

≤184: 1.9 (0.9–3.8)

≥185: 1.2 (0.6–2.6)

p-trend: 0.85

Conclusions: No specific 

conclusion given on glyphosate 

exposure and pancreatic cancer.

Limitations: There was a limited 

number of exposed cases and 

limited in generalizability due to 

predominantly white male study 

population.
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Table 2-7. Cancer Outcomes for Solid Tumor-Types in Humans Exposed to Glyphosate-Containing Products

Reference and study overview Methods and outcomes Results (with 95% CI)

Study author conclusions and 

limitations

Band et al. 2011

Case-control study on male cancer 

patients (96.8% Caucasian) in British 

Columbia, Canada, to evaluate exposure 

to 139 specific active compounds in 

pesticides (including glyphosate) and 

prostate cancer risk. 

Glyphosate analysis included 25 exposed 

and 1,128 unexposed cases (n=1,153) 

and 60 exposed and 3,939 age-matched 

internal controls (patients with cancer of 

other primary site) controls (n=3,999).

Exposure: Self-reported

ever/never use of glyphosate 

pesticides from questionnaire. 

Agricultural job exposure matrix 

(JEM) was developed for farm 

workers in British Columbia for the 

period of 1950–1998. 

Outcomes/endpoints: Prostate 

cancer cases identified through 

British Columbia Cancer Registry 

for 1983–1990 and histologically 

confirmed.

Data analysis: Conditional logistic 

regression on age-matched sets of 

cases and controls.

Adjustments: Alcohol 

consumption, cigarette years, 

education level, p-years, and 

respondent.

Confounders considered included 

marital status, smoking (age 

started smoking, average number 

of cigarettes, pipe or cigars 

smoked per day, total years 

smoked), and ethnicity.

Prostate cancer:

OR 1.36 (0.83–2.25)

Conclusions: No specific 

conclusion given on glyphosate 

exposure and prostate cancer. 

JEM likely to result in nondifferential misclassification and 

may underestimate the true 

association; thus, negative 

findings should be regarded as 

inconclusive.

Limitations: Lack of information 

on familial history, potential for 

misclassification of exposure due 

to use of JEM, use of cancer 

controls may result in selection 

bias, statistically significant 

associations could have occurred 

by chance as a result of multiple 

comparisons since 142 active 

chemicals were examined. 
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Table 2-7. Cancer Outcomes for Solid Tumor-Types in Humans Exposed to Glyphosate-Containing Products

Reference and study overview Methods and outcomes Results (with 95% CI)

Study author conclusions and 

limitations

Lee et al. 2004b

Case control study of white men and 

women (ages ≥21 years) diagnosed with 

stomach adenocarcinoma (n=170) or 

esophagus adenocarcinoma (n=137) and 

502 controls in eastern Nebraska to 

evaluate the risk of the stomach and 

esophageal adenocarcinomas associated 

with farming and agricultural use of 16 

insecticides and 14 herbicides (including 

glyphosate). 

Glyphosate analysis included

12 cases of stomach cancer and 

12 cases of esophageal cancer among 

farmers, and 46 controls compared to 

non-farmers (59 stomach cancer, 

62 esophageal cancer cases and 

184 controls). 

Controls were randomly selected from a 

group of controls interviewed in 1986–

1987 for a previous population-based 

case-control study. Controls were 

frequency-matched by sex and age to the 

combined distribution of the stomach and 

esophagus cases.

Exposure: Self- or proxy-reported 

ever use of glyphosate pesticide at 

enrollment (1992–1994).

Outcomes: Stomach and 

esophageal cancer cases were 

identified from the Nebraska 

Cancer Registry (1988–1990) or 

by review of discharge diagnosis 

and pathology records at 

14 hospitals (1991–1993).

Data analysis: Unconditional 

logistic regression.

Adjustments: Age, sex. 

Confounders considered included 

BMI, smoking, alcohol 

consumption, educational level, 

family history of stomach or 

esophageal cancer, respondent 

type, dietary intake of vitamin A 

and C, b-cryptoxanthin, riboflavin, 

folate, zinc, dietary fiber, protein, 

and carbohydrate. 

Stomach cancer:

OR 0.8 (0.4–1.5)

Esophageal cancer:

OR 0.7 (0.3–1.4)

Conclusions: “No significant 

associations were found between 

specific agricultural pesticide 

exposures (including glyphosate) 

and the risk of stomach or 

esophageal adenocarcinomas 

among Nebraska farmers.”

Limitations: Possible 

misclassification of pesticide 

exposure and generally small 

number of farmers exposed to 

some of the individual pesticides.
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Table 2-7. Cancer Outcomes for Solid Tumor-Types in Humans Exposed to Glyphosate-Containing Products

Reference and study overview Methods and outcomes Results (with 95% CI)

Study author conclusions and 

limitations

Lee et al. 2005

Case control study of 251 white men and 

women (ages ≥21 years) diagnosed with 

gliomas and 498 controls in eastern 

Nebraska (Nebraska Health Study II) to 

evaluate adult glioma associated with 

farming and agricultural use of 

20 insecticides and 17 herbicides 

(including glyphosate). 

Glyphosate analysis (only conducted 

among male farmers) included 17 cases 

and 32 controls among farmers compared

to non-farmers (49 cases and 

112 controls). Among these, selfreported respondents included 

4 cases/17 controls for glyphosate users 

and 20 cases/40 controls for reference 

non-farmers; proxy-reported respondents 

included 13 cases/15 controls for 

glyphosate users and 29 cases/

72 controls for reference non-farmers.

Controls were randomly selected from a 

group of controls interviewed in 1986–

1987 for a previous population-based 

case-control study. Controls were 

frequency-matched by sex, age, and vital 

status to the combined distribution of the 

cases.

Exposure: Self- or proxy-reported 

ever use of glyphosate pesticide at 

enrollment (1992–1994).

Outcomes: Incident primary adult 

glioma cases diagnosed between 

1988 and 1993 were identified 

from the Nebraska Cancer 

Registry or from 11 hospitals.

Data analysis: Unconditional 

logistic regression. Separate 

analyses by sex and respondent 

type (self- versus proxy-reported) 

were also conducted. 

Adjustments: Age, sex, and 

respondent type. 

Confounders considered included 

history of head injury, marital 

status, education level, alcohol 

consumption, medical history of 

diabetes mellitus, dietary intake of 

a- and b-carotene, and dietary 

fiber.

Glioma among male farmers:

OR 1.5 (0.7–3.1), all reported 

glyphosate use

OR 0.4 (0.1–1.6), self-reported 

glyphosate use

OR 3.1 (1.2–8.2), proxy-reported 

glyphosate use

Conclusions: “Glioma risk was 

also significantly increased 

among men who used specific 

pesticides (including glyphosate) 

and pesticide chemical classes; 

however, the positive results 

were mostly limited to proxy 

respondents.”

Limitations: The major limitation 

was the large proportion of proxy 

respondents. Most of the 

associations observed were 

limited to proxy respondents.
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Table 2-7. Cancer Outcomes for Solid Tumor-Types in Humans Exposed to Glyphosate-Containing Products

Reference and study overview Methods and outcomes Results (with 95% CI)

Study author conclusions and 

limitations

Pahwa et al. 2011

Case control study of 357 soft tissue 

sarcoma cases and 1,506 controls in 

Canada (all males, ≥19 years of age) to 

investigate the putative associations of 

pesticides (including glyphosate) with 

soft-tissue sarcoma (STS).

Glyphosate analysis included 36 exposed 

and 321 unexposed cases and 

147 exposed and 1,359 unexposed 

controls.

Potential controls were selected randomly 

within age constrains (±2 years) from 

provincial health records, comprehensive 

telephone lists, or voters’ lists. 

Exposure: Self-reported ever use 

of glyphosate herbicides collected 

through self-administered postal 

questionnaire and telephone 

interviews. 

Outcomes: STS cases (first 

diagnosed in 1991–1994) 

ascertained from provincial cancer 

registries, except in Quebec, 

where hospital ascertainment was 

used. 

Data analysis: Conditional logistic 

regression. 

Adjustments: Age, province of

residence, medical history.

Soft tissue sarcoma:

OR 0.93 (0.60–1.42), stratified 

by age group and province of 

residence

OR 0.90 (0.58–1.40), adjusted 

for medical history and with 

strata for age group and 

province of residence

Conclusions: “No association 

between herbicides (individual 

compound or major chemical 

class) (including glyphosate) and 

STS.”

Limitations: Limitations common 

to epidemiological case-control 

studies. 
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Table 2-7. Cancer Outcomes for Solid Tumor-Types in Humans Exposed to Glyphosate-Containing Products

Reference and study overview Methods and outcomes Results (with 95% CI)

Study author conclusions and 

limitations

Yiin et al. 2012

Case control study of 798 cases of glioma 

and 1,175 controls (98% white, aged 18–

80 years) in Iowa, Michigan, Minnesota, 

and Wisconsin (Upper Midwest Health 

Study) to investigate association between 

exposure to pesticides (including 

glyphosate) and risk of glioma in male 

and female participants. 

Pesticide use in non-farm jobs: 

Glyphosate analysis included 12 exposed 

and 786 unexposed cases and 

147 exposed and 1,359 unexposed 

controls. Analysis included 8 exposed 

and 430 unexposed cases and 

19 exposed and 1,122 unexposed 

controls excluding proxy respondents.

House and garden pesticide use:

Glyphosate analysis included 51 exposed 

and 747 unexposed cases and 

76 exposed and 1,099 unexposed 

controls. Analysis included 28 exposed 

and 410 unexposed cases and 

75 exposed and 1,066 unexposed 

controls excluding proxy respondents.

Randomly-selected, population-based 

controls were frequency-matched within a 

state.

Exposure: Self- or proxy-reported 

ever/never use of glyphosate 

pesticide through 1992.

Outcomes: Cases with a 

histologically confirmed primary 

intracranial glioma were identified 

through medical facilities, 

oncologists, neurosurgeons, and 

cancer registries (1995–1997). 

Data analysis: Unconditional 

logistic regression. Analyses were 

separately conducted with or 

without proxy respondents.

Adjustments: Age, sex, education.

Glioma 

Non-farm job use: OR 0.83 

(0.39–1.73) including proxy 

respondents; OR 0.79 (0.33–

1.86) excluding proxy 

respondents.

House and garden use: OR 

0.98 (0.67–1.43) including proxy 

respondents; OR 0.84 (0.52–

1.33) excluding proxy 

respondents

Conclusions: “No individual 

pesticides (including glyphosate) 

or broader category of pesticides, 

with or without proxy respondent, 

was associated with a statistically 

significant decrease or elevation 

in glioma risk.”

Limitations: A limitation of this 

study is the high proportion (45%) 

of proxy interviews for case 

participants compared to 2.9% 

control interviews that were with 

proxies. The accuracy and 

completeness of information 

given by proxy respondents 

varies by many factors. 

Another concern is the validity 

and reliability of the pesticide 

exposure assessment. 

BMI = body mass index; CED = cumulative exposure day; CI = confidence interval; IWED = intensity weighted exposure day; JEM = job exposure matrix; 

NHL = non-Hodgkin’s lymphoma; OR = odds ratio; RR = relative risk; Q = quartile; STS = soft tissue sarcoma; T = tertile
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Table 2-8. Lymphohematopoietic Cancer Outcomes in Humans Exposed to Glyphosate-Containing Products

Reference and study overview Methods and outcomes Results (with 95% CI)

Study author conclusions and 

limitations

Andreotti et al. 2018

Prospective cohort study of 

54,251 licensed pesticide applicators 

(97% white, 97% male) recruited 

between 1993 and 1997 in Iowa and 

North Carolina from the Agricultural 

Health Study to evaluate agricultural 

exposure to 50 pesticides (including 

glyphosate) and cancer incidence 

cases.

44,932 participants reported ever use of 

glyphosate, including 5,779 participants 

with incident cancer cases. 

Exposure: Self-reported 

ever/never use of any glyphosate 

pesticides, lifetime days of 

glyphosate use (days per year x 

number of years), and intensityweighted lifetime days (lifetime 

days x intensity score) at

enrollment (1993–1997) or followup (1999–2005). 

Intensity-weighted lifetime days of 

glyphosate use was categorized 

into quartiles, tertiles, or the 

median, such that there were at 

least five exposed cases in each 

category.

Outcome: Incident cancer 

diagnoses ascertained via linkage 

to cancer registries in Iowa 

(enrollment through 2013) and 

North Carolina (enrollment through 

2012).

Data analysis: Poisson regression 

Adjustments: Age, cigarette 

smoking status, alcohol drinks per 

month, family history of any 

cancer, state of recruitment, and 

the five pesticides (atrazine, 

alachlor, metolachlor, trifluralin, 

and 2,4-D).

Confounders considered included 

BMI and pack-years of cigarettes 

smoked. 

Lymphohematopoietic:

Q4: RR 1.00 (0.74–1.34)

p-trend: 0.43

Hodgkin’s lymphoma:

M2: RR 0.90 (0.25–3.24)

p-trend: 0.94

NHL:

Q4: RR 0.87 (0.64–1.20)

p-trend: 0.95

B-cell:

Q4: RR 0.86 (0.62–1.19)

p-trend: 0.86

CLL/SLL: 

Q4: RR 0.87 (0.48–1.58)

p-trend: 0.71

Diffuse large B-cell lymphoma:

Q4: RR 0.97 (0.51–1.85)

p-trend: 0.83

Marginal-zone lymphoma:

M2: RR 0.44 (0.09–2.17)

p-trend: 0.67

Follicular lymphoma:

T3: RR 0.85 (0.36–2.03)

p-trend: 0.95

Multiple myeloma:

Q4: RR 0.87 (0.45–1.69)

p-trend: 0.84

Conclusions: The authors 

observed no associations 

between glyphosate use and 

overall cancer risk or with total 

lymphohematopoietic cancers, 

including NHL, multiple myeloma, 

and any other NHL subtypes. 

There was some evidence of an 

increased risk of acute myeloid 

leukemia for applicators, 

particularly in the highest 

category of glyphosate exposure 

compared with never users of 

glyphosate. Risk estimates were 

similar in magnitude between the 

unlagged and lagged (5 or 

20 years) exposure analyses for 

all sites evaluated.

Limitations: Some 

misclassification of exposure 

undoubtedly occurred; because 

the authors evaluated many 

cancer sites, there is the 

possibility that results were 

observed by chance and should 

therefore be interpreted with 

caution; the fact that no other 

studies have reported an 

association with acute myeloid 

leukemia also calls for cautious 

interpretation. However, 37% of 

the participants did not respond 

to follow-up, which may have 

resulted in an underestimation of 
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Table 2-8. Lymphohematopoietic Cancer Outcomes in Humans Exposed to Glyphosate-Containing Products

Reference and study overview Methods and outcomes Results (with 95% CI)

Study author conclusions and 

limitations

NHL T-cell: 

M2: RR 1.53 (0.23–10.38)

p-trend: 0.31

Acute myeloid leukemia:

Q4: RR 2.44 (0.94–6.32)

p-trend: 0.11

Chronic myeloid leukemia:

M2: RR 0.82 (0.23–2.98)

p-trend: 0.36

glyphosate exposure though 

imputation procedures were used 

in an attempt to mitigate this 

issue.

De Roos et al. 2005a

A prospective cohort study in 

57,311 licensed pesticide applicators 

(>97% males) recruited between 1993 

and 1997 in Iowa and North Carolina 

from the Agricultural Health Study to 

study cancer incidence associated with 

glyphosate use.

All lymphohematopoietic: 190 (75.3%)

NHL: 92 (77.2%)

Leukemia: 57 (75.4)

Multiple myeloma: 32 (75.0%)

Exposure: Self-reported 

never/ever use of glyphosate. 

Cumulative exposure days (CEDs): 

1–20 (reference), 21–56, and 57–

2,678 days. 

Intensity weighted exposure days 

(IWEDs) of 0.1–79.5 (reference), 

79.6–337.1, and 337.2–18,241 

units. 

Outcomes: Incident cases 

identified between enrollment and 

Dec 31st of 2001 from cancer 

registry files.

Data analysis: Poisson regression 

adjusted for age, education, 

smoking status, alcohol 

consumption, family history of 

cancer in 1st degree relative, state 

of residence. 

All lymphohematopoietic cancers:

Ever use: RR 1.1 (0.8–1.6)

CED T3: RR 1.2 (0.8–1.8) 

p-trend: 0.69

IWED T3: RR 1.0 (0.7–1.6)

p-trend: 0.90

NHL cancers:

Ever use: RR 1.1 (0.7–1.9)

CED T3: RR 0.9 (0.5–1.8)

p-trend: 0.73

IWED T3: RR 0.8 (0.5–1.4)

p-trend: 0.99 

Leukemia:

Ever use: RR 1.0 (0.5–1.9)

CED T3: RR 1.0 (0.4–2.9)

p-trend: 0.61

IWED T3: RR 0.7 (0.2–2.1)

p-trend: 0.11

Conclusions: Glyphosate 

exposure was not associated with 

overall cancer incidence or with 

most cancer subtypes, but there 

was a suggested association of 

glyphosate exposure with multiple 

myeloma incidence.

Limitations: Small number of 

specific cancers cases, only 

males included in the analysis, no 

information on timing of pesticide 

use.
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Table 2-8. Lymphohematopoietic Cancer Outcomes in Humans Exposed to Glyphosate-Containing Products

Reference and study overview Methods and outcomes Results (with 95% CI)

Study author conclusions and 

limitations

Multiple myeloma:

Ever use: RR 2.6 (0.7–9.4)

CED T3: RR 1.9 (0.6–6.3)

p-trend: 0.27

IWED T3: RR 2.1 (0.6–7.0)

p-trend: 0.17

Sorahan 2015

Cohort study of 55,934 licensed 

pesticide applicators in Iowa and North 

Carolina (Agricultural Health Study).

Set 1: 54,315 applicators, excluded 

those with cancer diagnosis before 

enrollment, those lost to follow-up, those 

who had missing data for age at 

enrollment, those who did not provide 

information on glyphosate use. (“Not 

known/missing” data included as a 

separate category for each variable.) 

n=32 cases.

Set 2: 49,211 applicators, additionally 

excluded those with missing data on 

education, smoking history, or alcohol 

used. n=26 cases.

Set 3: 40,719 applicators, additionally 

excluded those missing data on 

additional pesticide use. n=22 cases.

Set 4: 55,934 applicators, excluding 

those with any cancer diagnosis prior to 

enrollment, those lost to follow up, and 

Exposure: Self-reported 

never/ever use of glyphosate. 

CEDs: 1–20 (reference), 21–56, 

and 57–2,678 days. IWEDs of 

0.1–79.5, 79.6–337.1, and 337.2–

18,241 units. 

Outcomes: Incident cases 

identified between enrollment and 

December 31st from 2001 cancer 

registry files. 

Data analysis: Poisson regression 

adjusted for the following:

Set 2: Age at enrollment, cigarette 

use, alcohol use, education.

Set 4: Age at enrollment, cigarette 

use, alcohol use, education, family 

history of cancer.

Sets 1 and 3: Age at enrollment, 

cigarette use, alcohol use, 

education, family history of cancer, 

use of some pesticides (2,4-D, 

alachlor, atrazine, metolachlor, 

trifluralin), ever use of other 

Multiple myeloma:

Set 1:

Ever use: RR 1.24 (0.52–2.94)

CED Q4: RR 1.38 (0.42–4.45) 

p-trend: 0.48

IWED Q4: RR 1.87 (0.67–5.27)

p-trend: 0.22

Set 2:

Ever use: RR 2.07 (0.71–6.04)

Set 3:

Ever use: RR 2.79 (0.78, 9.96)

Set 4:

Ever use: RR 1.18 (0.53–2.65)

CED Q4: RR 1.17 (0.40–3.41)

p-trend: >0.50

IWED Q4: RR 1.58 (0.62–4.05)

p-trend: 0.30

Conclusions: Glyphosate is not a 

risk factor for multiple myeloma.

Limitations: The small number of 

cases, absence of information on 

timing of pesticide exposure,

unable to adjust for state of 

residence. 
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Table 2-8. Lymphohematopoietic Cancer Outcomes in Humans Exposed to Glyphosate-Containing Products

Reference and study overview Methods and outcomes Results (with 95% CI)

Study author conclusions and 

limitations

those missing data for age at 

enrollment. n=34 cases.

Re-analysis of data reported by De 

Roos et al. (2005a).

pesticides (maneb, paraquat, 

carbaryl, diazinon, benomyl).

Brown et al. 1990

Case-control study of 578 cases of 

leukemia and 1,245 controls (all white

males, ages ≥30 years) in Iowa and 

Minnesota to investigate agricultural 

exposure to 24 animal insecticides, 

34 crop insecticides, 38 herbicides, and 

16 fungicides (including glyphosate) and 

risk of leukemia. 

Glyphosate analysis included 15 cases 

and 49 controls who used glyphosate 

herbicide compared to never-farmers 

(243 cases and 547 controls).

Controls were a population-based, 

stratified sample of white men 

frequency-matched to the cases by 

5-year age group, vital status at 

interview, and state of residence.

Exposure: Self-reported ever 

mixing/handling/applying 

glyphosate herbicides at 

enrollment (1981–1984).

Outcomes: Leukemia cases

ascertained from Iowa Tumor 

Registry or hospital records in 

Minnesota from 1 year before 

(retrospectively) to 2 years after 

the start of the study 

(prospectively).

Data analysis: Unconditional 

logistic regression.

Adjustments: Vital status, age, 

state, tobacco use, family history of 

lymphopoietic cancer, high-risk 

non-farming occupations, high risk 

exposures (benzene, naphtha, hair 

dyes).

Leukemia

OR 0.9 (0.5–1.6)

Conclusions: “Risks for all 

leukemia were not significantly 

increased among subjects who 

personally mixed, handled, or 

applied specific herbicides 

(including glyphosate).”

Limitations: With the case-control 

study design, the associations 

found or failure to find an 

association could be due to bias. 

Potential inaccuracies in the 

evaluation of pesticide exposure 

could lead to exposure 

misclassification. Multiple 

statistical comparisons make it 

difficult to separate real 

association from chance findings.
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Table 2-8. Lymphohematopoietic Cancer Outcomes in Humans Exposed to Glyphosate-Containing Products

Reference and study overview Methods and outcomes Results (with 95% CI)

Study author conclusions and 

limitations

Brown et al. 1993

Case control study to evaluate the 

association between multiple myeloma, 

agricultural risk factors, and exposure to 

individual pesticides in 823 white males 

aged ≥30 years in Iowa. 

173 cases and 650 frequency-matched 

controls from random digit dialing, 

Medicare records, and death certificate 

files.

Glyphosate analysis included 

11 exposed and 162 unexposed cases 

(n=173) for multiple myeloma and 

40 exposed and 610 unexposed 

controls (n=650).

Exposure: Self-reporting 

never/ever mixing, handling, or 

applying glyphosate.

Outcomes: Multiple myeloma 

cases from the Iowa Health 

Registry from 1981 to 1984.

Data analysis: Logistic models 

adjusted for vital status and age. 

Other confounders considered 

included smoking and education.

Multiple myeloma:

OR 1.7 (0.8–3.6)

Conclusions: Little evidence of 

an association between risk of 

multiple myeloma and exposure 

to pesticides (including 

glyphosate).

Limitations: Small number of 

cases and controls, multiple 

statistical comparisons, and 

possibility of recall bias or 

chance.

Cocco et al. 2013

Case control study of 4,810 in the 

EPILYMPH study from six European 

countries to investigate the role of 

occupational exposure to agrochemicals 

(including glyphosate) in etiology of 

lymphoma, B cell lymphoma and 

subtypes. 

2,348 incident lymphoma cases and 

2,462 controls (n=4,810).

Glyphosate analysis included 

four exposed B cell lymphoma cases

and two exposed controls.

Exposure: Self-reported 

questionnaires: never/ever 

glyphosate exposure.

Outcomes: First diagnosis 

according to 2001 WHO 

classification of lymphoma 

between 1998 and 2004; patients 

referred from centers within referral 

area. 

Data analysis: Unconditional 

logistic regressions. 

Adjustments for age, gender, 

education, center. 

B cell lymphoma:

OR 3.1 (0.6–17.1)

Conclusions: No support to the 

role of occupation exposure to 

agrochemicals (including 

glyphosate) in etiology of B cell 

lymphoma.

Limitations: Low response rate 

may have resulted in selection 

bias.
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Table 2-8. Lymphohematopoietic Cancer Outcomes in Humans Exposed to Glyphosate-Containing Products

Reference and study overview Methods and outcomes Results (with 95% CI)

Study author conclusions and 

limitations

De Roos et al. 2003

Pooled data from three case-control 

studies conducted by the National 

Cancer Institute to investigate exposure 

to multiple pesticides in farming as risk 

factors for NHL among 3,417 white 

males from Nebraska, Iowa, Minnesota, 

and Kansas.

Glyphosate analysis included 

36 exposed and 614 unexposed cases 

(n=650) and 61 exposed and 

1,872 unexposed population based 

matched controls (n=1,933).

Exposure: Interview self-reported 

never/ever glyphosate exposure.

Outcomes: In Nebraska, cases 

were identified through Nebraska 

Lymphoma Study Group and area 

hospitals among males aged 

≥21 years from July 1983 to June 

1986. In Iowa, cases were 

ascertained from Iowa State Health 

Registry from 1981 to 1983 from 

males ≥30 years of age. In 

Minnesota, cases were ascertained 

from a surveillance system of 

Minnesota hospitals and pathology 

laboratories from 1980 to 1982 in 

males ≥30 years of age. In 

Kansas, cases were randomly 

selected from statewide cancer 

registry from males ≥21 years of 

age.

Data analysis: Two models were 

used: (1) standard logistic 

regression and (2) hierarchical 

regression adjusted for age and 

study site.

Logistic regression:

NHL:

OR 2.1 (1.1–4.0)

Hierarchical regression:

NHL:

OR 1.6 (0.9–2.8)

Conclusions: No specific 

conclusions for glyphosate and 

NHL.

Limitations: Crude exposure 

metric, no information on timing 

of exposure versus NHL onset or 

timing of use of pesticides to 

each other. Potential bias for 

missing data exclusion.
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Table 2-8. Lymphohematopoietic Cancer Outcomes in Humans Exposed to Glyphosate-Containing Products

Reference and study overview Methods and outcomes Results (with 95% CI)

Study author conclusions and 

limitations

Eriksson et al. 2008

Case control study of 1,926 male and 

female subjects aged 18–74 years were 

recruited between December 1, 1999 

and April 30, 2002 in Sweden to 

evaluate pesticides (including 

glyphosate) as a risk factor for NHL.

Glyphosate analysis included 

29 exposed and 881 unexposed cases 

(n=910) and 18 exposed and 

998 unexposed frequency-match 

controls (n=1,016).

Exposure: Self-reporting 

questionnaires; never/ever 

exposed and days of exposure.

Outcomes: Newly diagnosed NHL, 

identified through physicians and 

pathologists recruited between 

December 1, 1999 and April 30, 

2002. Subtypes divided according 

to WHO classification.

Data analysis: Unconditional 

logistic regression analysis 

adjusted for age, sex, year of 

diagnosis/enrollment.

NHL:

Ever: OR 2.02 (1.10–3.71)

Ever (adjusted for other 

pesticides):

OR 1.51 (0.77–2.94)

Ever (1–10-year latency):

OR 1.11 (0.24–5.08)

Ever (>10-year latency):

OR 2.26 (1.16–4.40) 

≤10 days: OR 1.69 (0.70–4.07)

≥10 days: OR 2.36 (1.04–5.37)

B-cell lymphomas:

Ever: OR 1.87 (0.998–3.51)

Lymphocytic lymphoma:

Ever: OR 3.35 (1.42–7.89)

Follicular, grade I-III:

Ever: OR 1.89 (0.62–5.79)

Diffuse large B-cell lymphoma:

Ever: OR 1.22 (0.44–3.35)

Other specified B-cell lymphoma:

Ever: OR 1.63 (0.53–4.96)

Unspecified B-cell lymphoma:

Ever: OR 1.47 (0.33–6.61)

T-cell lymphoma:

Ever: OR 2.29 (0.51–10.4)

Unspecified NHL:

Ever: OR 5.63 (1.44–22.0)

Conclusions: The association of 

NHL with glyphosate was 

strengthened by the study.

Limitations: No registries of 

pesticide use kept in Sweden, 

possible misclassification of 

pesticide exposure, no 

information gathered on 

protective equipment use.
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Table 2-8. Lymphohematopoietic Cancer Outcomes in Humans Exposed to Glyphosate-Containing Products

Reference and study overview Methods and outcomes Results (with 95% CI)

Study author conclusions and 

limitations

Hardell et al. 2002

Pooled analysis of two case-control 

studies of 1,656 male and female 

subjects from Sweden to investigate 

pesticides in etiology of NHL and HCL.

Glyphosate analysis included 8 exposed 

and 507 unexposed cases (n=515) and 

8 exposed and 1,133 unexposed 

county-matched controls (n=1,141).

Exposure: Self-reporting 

questionnaires; never/ever 

glyphosate exposure.

Outcomes: Histopathologically 

verified NHL cases from regional 

cancer registries in males age 

≥25 years from 1987 to 1990. HCL 

diagnosed cases from the national 

Swedish Cancer Registry in males 

from 1987 to 1992.

Data analysis: Conditional logistic 

regression analysis adjusted for 

both univariate and multivariate.

NHL and HCL (pooled):

Ever (univariate analysis):

OR 3.04 (1.08–8.52)

Ever (multivariate analysis):

OR 1.85 (0.55–6.20)

Conclusions: Glyphosate is a risk 

factor for developing NHL.

Limitations: Possible recall bias. 

Correlation of pesticides.

Kachuri et al. 2013

A population-based, case-control study 

in 1,506 males from six Canadian 

provinces to investigate the association 

between lifetime use of multiple 

pesticides and multiple myeloma.

Glyphosate analysis included 

32 exposed cases and 310 unexposed 

cases (n=342) and 121 exposed and 

1,236 unexposed frequency-matched 

controls (n=1,357). Excluding proxy 

respondents, analysis included 

23 exposed cases and 108 exposed 

frequency-matched controls.

Exposure: Self-reporting 

questionnaires; ever/never, 

days/year glyphosate use.

Outcomes: Incident multiple 

myeloma cases among men aged 

≥19 years who were diagnosed 

between September 1, 1991 and 

December 31, 1994 ascertained 

from provincial cancer registries.

Cases in Quebec were ascertained 

from hospitals. 

Data analysis: Logistic regression.

Adjusted for age, province of 

residence, use of proxy 

responders, smoking, and selected 

medical history.

Multiple myeloma:

Ever: 

OR 1.19 (0.76–1.87)

Ever (exclude proxies):

OR 1.11 (0.66–1.86)

>0 and ≤2 days/year:

OR 0.72 (0.39–1.32)

>0 and ≤2 days/year

(exclude proxies):

OR 0.70 (0.35–1.40)

>2 days/year:

OR 2.04 (0.98–4.23)

>2 days/year (exclude proxies):

OR 2.11 (0.95–4.70)

Conclusions: No specific 

conclusions for glyphosate and 

multiple myeloma.

Limitations: Low response rates 

observed for cases and controls, 

possibility of recall bias. 
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Table 2-8. Lymphohematopoietic Cancer Outcomes in Humans Exposed to Glyphosate-Containing Products

Reference and study overview Methods and outcomes Results (with 95% CI)

Study author conclusions and 

limitations

Karunanayake et al. 2012

Case-control study of 1,822 men to 

evaluate exposure to pesticides and 

incidence of Hodgkin lymphoma in six

Canadian provinces.

Glyphosate analysis included 

38 exposed and 278 unexposed 

Hodgkin lymphoma cases (n=316) and 

133 exposed and 1,373 unexposed agematched controls (n=1,506).

Exposure: Any self-reported 

glyphosate use. 

Outcomes: Hodgkin lymphoma 

incidences determined using 

Internal Classification of Diseases 

for Oncology, 2nd Edition (ICD-O-2) 

from September 1, 1991 to 

December 31, 1994.

Data analysis: Conditional logistic 

regression. Adjustments for age, 

province of residence, personal 

and family medical history.

Hodgkin lymphoma:

OR 0.99 (0.62–1.56)

Conclusions: This study shows a 

lack of association between 

Hodgkin lymphoma and 

glyphosate.

Limitations: Inability to ascertain 

Epstein-Barr virus exposure.

Potential for recall bias and for 

misclassification of exposure to 

pesticides, as well as 

misclassification of exposure 

duration. Low response rates 

resulted in inability to evaluate 

dose-response relationship and 

women were not included in the 

study. 

Lee et al. 2004a 

Case control study of 3,253 in Iowa, 

Minnesota, and Nebraska to evaluate if 

asthma modifies risk associated with 

pesticide exposure.

872 cases of NHL and 2,381 frequencymatched controls.

Glyphosate analyses, 259 cases and 

684 controls for non-asthmatic nonfarmers (reference), 53 cases and 

91 controls for non-asthmatic farmers, 

and 6 cases and 12 controls for 

asthmatic farmers.

These data were used in the pooled 

analysis by De Roos et al. (2003). 

Exposure: Self-reported 

ever/never glyphosate use. Selfreported asthma from physician 

diagnosis. 

Outcomes: Cases identified 

through Iowa State Health Registry 

and Minnesota’s surveillance 

system of hospital and pathology 

laboratories from 1980 to 1983 

(n=530). Cases identified through 

Nebraska Lymphoma Study group 

and area hospitals between July 

1983 and June 1986 (n=346).

Data analysis: Unconditional 

logistic regression adjusted for 

age, state, vital status.

NHL(non-asthmatic farmers):

OR 1.4 (0.98–2.1)

NHL (asthmatic farmers):

OR 1.2 (0.4–3.3)

Conclusions: No specific 

conclusion concerning exposure 

to glyphosate, asthma, and NHL. 

Limitations: Self-reported 

exposure and asthma diagnosis 

may be subject to 

misclassification bias. 
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Table 2-8. Lymphohematopoietic Cancer Outcomes in Humans Exposed to Glyphosate-Containing Products

Reference and study overview Methods and outcomes Results (with 95% CI)

Study author conclusions and 

limitations

McDuffie et al. 2001

Case-control study to investigate the 

association between non-occupational 

exposure to pesticides (including 

glyphosate) and NHL among 2,023 men 

in six Canadian provinces.

Glyphosate analysis included 

51 exposed and 466 unexposed NHL

cases (n=517) and 133 exposed and 

1,373 unexposed age-matched controls 

(n=1,506).

Exposure: Self-reported 

ever/never use of any glyphosate 

use and number days/year use.

Outcomes: First diagnosis of NHL 

between September 1, 1991 and 

December 31, 1991 from cancer 

registries for five providences, in 

Quebec where hospital records 

were used.

Data analysis: Conditional logistic 

regression adjusted for age, 

province of residence, medical 

history (measles, mumps, cancer, 

allergy desensitization shots, 

positive family history of cancer in 

1

st-degree relative).

NHL:

Ever use:

OR 1.20 (0.83–1.74)

Exposure >0 and ≤2 days/year:

OR 1.00 (0.63–1.57)

Exposure >2 days/year:

OR 2.12 (1.20–3.73)

Conclusions: No conclusions 

stated for glyphosate ever use. 

When stratified by average 

number of days per year of 

exposure, glyphosate was not 

significantly associated with NHL

for exposure, but demonstrated a 

dose-response relationship. 

Limitations: Potential for recall 

bias and misclassification of 

pesticide exposure. Inclusion of 

occupational groups without 

extensive validations studies 

could bias findings towards null. 

Less-than-optimal response 

rates. Due to multiple 

comparison, a small number of 

statistically significant results may 

be attributable to chance.

Because of limited statistical 

power, analysis was restricted to 

exposure that at least 1% of 

respondents ever used. 
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Table 2-8. Lymphohematopoietic Cancer Outcomes in Humans Exposed to Glyphosate-Containing Products

Reference and study overview Methods and outcomes Results (with 95% CI)

Study author conclusions and 

limitations

Nordstrӧm et al. 1998

Case-control study of 511 Swedish adult 

males to evaluate occupational 

exposures (including glyphosate) as risk 

factors for HCL.

Glyphosate analysis included 4 exposed 

and 107 unexposed cases (n=111) of 

HCL and 5 exposed and 395 controls 

(n=400) in Sweden.

These data were used in pooled 

analysis by De Roos et al. (2003).

Exposure: Self-reported 

never/ever glyphosate exposure 

determined by at least 1 working 

day (8 hours) and induction of at 

least 1 year.

Outcomes: HCL reported to 

Swedish Cancer Registry from 

1987 to 1992. One case 

diagnosed in 1993 included in 

analysis.

Data analysis: Logistic regression 

adjusted for age. 

HCL:

OR 3.1 (0.8–12)

Conclusions: No specific 

conclusions were given for 

glyphosate and HCL.

Limitations: Possible correlation 

of occupational exposures 

resulting in confounding. Multiple 

comparisons may result in some 

correlations to occur by chance. 

Possibility of elevated OR due to 

recall bias. 
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Table 2-8. Lymphohematopoietic Cancer Outcomes in Humans Exposed to Glyphosate-Containing Products

Reference and study overview Methods and outcomes Results (with 95% CI)

Study author conclusions and 

limitations

Orsi et al. 2009

Case-control study to investigate the 

relationship between occupational 

exposure to pesticides and lymphoid 

neoplasms in 947 18–75-year-old males 

from six hospitals in France from 2000 

to 2004.

Glyphosate analysis included:

12 exposed and 232 unexposed NHL 

cases (n=244) and 24 exposed and 

412 unexposed center, age, sexmatched controls (n=436).

6 exposed and 81 unexposed cases of 

Hodgkin’s lymphoma (n=87) and 

15 exposed and 250 unexposed center, 

age, sex-matched controls (n=265).

5 exposed and 51 unexposed cases of 

multiple myeloma (n=56) and 

18 exposed and 295 unexposed center, 

age, sex-matched controls (n=313). 

27 exposed and 464 unexposed cases 

of lymphoid neoplasms (n=491) and 

24 exposed and 432 unexposed center, 

age, sex-matched controls (n=456).

Exposure: Self-reported none and 

probable/definite glyphosate 

exposure, after expert review of 

pesticide use questionnaire.

Outcomes: Cases determined 

using ICD-O-3 code diagnosis from 

September 2000 to December 

2004.

Data analysis: Unconditional 

logistic regression, adjusted for 

age, center, socioeconomic 

category (white collar/blue collar).

Lymphoid neoplasms:

OR 1.2 (0.6–2.1)

NHL:

OR 1.0 (0.5–2.2), all subtypes

OR 1.0 (0.3–2.7) for diffuse large 

cell lymphoma

OR 1.4 (0.4–5.2) for follicular 

lymphoma

Hodgkin’s lymphoma:

OR 1.7 (0.6–5.0)

Lymphoproliferative syndrome:

OR 0.6 (0.2–2.1), all subtypes

OR 0.4 (0.1–1.8) for chronic 

lymphocytic leukemia

OR 1.8 (0.3–9.3) for HCL

Multiple myeloma:

OR 2.4 (0.8–7.3)

Conclusions: No specific 

conclusions for glyphosate and 

development of lymphoid 

neoplasms.

Limitations: Potential nondifferential misclassification 

resulting in reduced power.
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Table 2-8. Lymphohematopoietic Cancer Outcomes in Humans Exposed to Glyphosate-Containing Products

Reference and study overview Methods and outcomes Results (with 95% CI)

Study author conclusions and 

limitations

Pahwa et al. 2012

Case-control study to investigate the 

association between non-occupational 

exposure to pesticides (including 

glyphosate) and multiple myeloma 

among 1,848 men in six Canadian 

provinces.

Glyphosate analysis included 

32 exposed and 310 unexposed cases 

(n=342) and 133 exposed and 

1,373 unexposed controls (n=1,506).

Exposure: Self-reported 

glyphosate never/ever use.

Outcomes: First diagnosis of 

multiple myeloma between 

September 1, 1991 and December 

31, 1994 from cancer registries for 

five providences, in Quebec where 

hospital records were used.

Data analysis: Conditional logistic 

regression adjusted for age, 

province of residence, medical 

history (measles, mumps, cancer, 

allergy desensitization shots, 

positive family history of cancer in 

1

st degree relative). 

Multiple myeloma:

OR 1.22 (0.77–1.93)

Conclusions: No specific 

conclusion for glyphosate and 

multiple myeloma.

Limitations: Low response rates, 

potential for selection bias, recall 

bias, and misclassification of 

pesticide exposure.

BMI = body mass index; CED = cumulative exposure day; CI = confidence interval; CLL/SLL = chronic lymphocytic leukemia/small lymphocytic lymphoma;

DLBCL = diffuse large B-cell lymphoma; HCL = hairy cell leukemia; IWED = intensity weighted exposure day; M = median; NHL = non-Hodgkin’s lymphoma; OR = 

odds ratio; Q = quartile; RR = relative risk; T = tertile; WHO = World Health Organization
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Solid Tumors. The epidemiological studies on the association between glyphosate use and solid-type 

tumors are presented in Table 2-7. Overall, these studies did not detect a statistically significant 

association between glyphosate use and all cancer types studied, including melanoma, childhood cancers,

soft tissue sarcoma, colorectal cancer, and cancers of the lung, oral cavity, colon, rectum, pancreas, 

kidney, prostate (including total prostate and aggressive prostate cancers), testes, breast, bladder, stomach, 

and esophagus. A statistically significant association with glyphosate use and solid tumors was reported 

in one study. Lee et al. (2005) reported an association between proxy-reported glyphosate use and glioma 

cancer (odds ratio [OR] 3.1; 95% CI 1.2–8.2). However, when using self-reported glyphosate use or 

combined self- and proxy-reported glyphosate use, no association with glioma was observed (OR 0.4; 

95% CI 0.1–1.6 and OR 1.5; 95% CI 0.7–3.1, respectively).

Lymphohematopoietic Cancers. Overviews of epidemiological studies that focused on the association 

between glyphosate use and lymphohematopoietic cancers are presented in Table 2-8. A majority of the 

studies did not report statistically significant associations between glyphosate use and many of the 

lymphohematopoietic cancer subtypes. These statistically null associations were reported for the 

following subtypes: all lymphohematopoietic cancers (Andreotti et al. 2018; De Roos et al. 2005a); NHL 

(Andreotti et al. 2018; De Roos et al. 2005a; Lee et al. 2004a; Orsi et al. 2009); leukemia (Brown et al. 

1990; De Roos et al. 2005a); multiple myeloma (Andreotti et al. 2018; Brown et al. 1993; De Roos et al. 

2005a; Kachuri et al. 2013; Orsi et al. 2009; Pahwa et al. 2012; Sorahan 2015); B-cell lymphoma 

(Andreotti et al. 2018; Cocco et al. 2013; Eriksson et al. 2008); follicular lymphoma (Andreotti et al. 

2018; Eriksson et al. 2008; Orsi et al. 2009); diffuse large B-cell lymphoma (Andreotti et al. 2018; 

Eriksson et al. 2008; Orsi et al. 2009); other specified B-cell lymphoma (Eriksson et al. 2008); 

unspecified B-cell lymphoma (Eriksson et al. 2008); T-cell lymphoma (Andreotti et al. 2018; Eriksson et 

al. 2008); Hodgkin’s lymphoma (Andreotti et al. 2018; Karunanayake et al. 2012; Orsi et al. 2009); hairy 

cell leukemia (Nordström et al. 1998; Orsi et al. 2009); lymphoid neoplasms (Orsi et al. 2009); marginalzone lymphoma (Andreotti et al. 2018); chronic myeloid leukemia (Andreotti et al. 2018); and 

lymphoproliferative syndrome, all subtypes and chronic lymphocytic leukemia (Andreotti et al. 2018; 

Orsi et al. 2009). Andreotti et al. (2018) reported an increased risk of acute myeloid leukemia among 

applicators in the highest exposure quartile, compared with never users (RR 2.44; 95% CI 0.94–6.32), 

although the authors noted that this association was not statistically significant. However, in a letter to the 

editor, Sheppard and Shaffer (2018) argued that the statistical procedure used by Andreotti et al. (2019) to 

account for the 37% loss to follow-up was not sufficient given health outcomes were not included in their 

imputations. Therefore, the results of the analysis may have been biased towards the null (Sheppard and 

Shafer 2019). Andreotti et al (2019) responded to this comment stating that although the argument in 
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Sheppard and Shafer (2019) is theoretically possible, however based on a sensitivity analysis, Andreotti 

et al. argue their imputation likely did not impact risk estimates. 

In contrast, Eriksson et al. (2008) reported positive associations between glyphosate use and lymphocytic 

lymphoma (OR 2.56; 95% CI 1.17–5.60) and unspecified NHL (OR 5.29; 95% CI 1.60–17.50). Several 

other studies reported significant associations between glyphosate use and NHL, but these studies reported 

conflicting results depending on the statistical methods used, adjustment for confounders, or inclusion 

criteria. De Roos et al. (2003) reported a positive association between glyphosate use and NHL using 

logistic regression (OR 2.1; 95% CI 1.1–4.0); however, analysis using hierarchical regression did not find 

an association (OR 1.6; 95% CI 0.9–2.8). Similarly, Eriksson et al. (2008) reported a positive association 

with NHL (OR 2.02; 95% CI 1.10–3.71); when this analysis further adjusted for other pesticide use, the 

reported OR was 1.51 (95% CI 0.7–2.94). Hardell et al. (2002) investigated the association between 

glyphosate use and combined cases of NHL and hairy cell leukemia. The authors reported an OR of 

3.04 (95% CI 1.08–8.52) in unadjusted models, but after adjusting for potential confounders, the reported 

OR was 1.85 (95% CI 0.55–6.20). McDuffie et al. (2001) reported that glyphosate use was not associated 

with NHL (OR 1.20; 95% CI 0.83–1.74); however, after restricting analyses to individuals who reported 

using glyphosate >2 days a year, there was a positive association with NHL (OR 2.12; 95% CI 1.20–3.73).

Results for risk of non-Hodgkin’s lymphoma and self-reported glyphosate use or exposure from 

individual studies summarized in Table 2-8 and meta-analyses summarized in Table 2-6 are plotted in

Figure 2-4. Results for risk of multiple myeloma and self-reported glyphosate use or exposure from 

individual studies summarized in Table 2-8 and the meta-analysis summarized in Table 2-6 are plotted in

Figure 2-5.
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Figure 2-4. Risk of non-Hodgkin’s Lymphoma Relative to Self-Reported 

Glyphosate Use or Exposure

*Logistic Regression; **Hierarchical regression; ***Non-Asthmatic farmers; ****Asthmatic farmers

a = adjusted; CED = cumulative exposure; IWED = intensity-weighted exposure days; IWLD = intensity-weighted 

lifetime days; OR = odds ratio; Q4 = 4

th quartile; RR = rate ratio; T3 = 3rd tertile
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Figure 2-5. Risk of Multiple Myeloma Relative to Self-Reported Glyphosate Use or 

Exposure

*Set 1 included 54,315 applicators; **Set 2 included 49,211 applicators; ***Set 3 included 40,719 applicators; ****Set 

4 included 55,934 applicators

a = adjusted; CED = cumulative exposure; IWED = intensity-weighted exposure days; IWLD = intensity-weighted 

lifetime days; IRED = intensity-rated exposure days; OR = odds ratio; Q4 = 4th quartile; RR = rate ratio; T3 = 3rd tertile
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Laboratory Animal Studies

EPA evaluated results from four unpublished rat studies in which the carcinogenicity of glyphosate 

technical was assessed; EPA summarized the findings in publicly available DERs (EPA 1991a, 1991b, 

1992d, 2015c).

Groups of weanling Sprague-Dawley rats (50/sex/group) were administered glyphosate technical (98.7% 

purity) in the diet for up to 26 months at initial concentrations of 0, 30, 100, or 300 ppm (EPA 1992d). 

Based on body weight and food consumption data, concentrations of glyphosate technical were adjusted 

to achieve oral doses of 0, 3.05, 10.30, and 31.49 mg/kg/day, respectively, for males and 0, 3.37, 11.22, 

and 34.02 mg/kg/day, respectively, for females. Incidences of testicular interstitial cell tumors in the

control, low-, mid-, and high-dose male rats were 0/50 (0%), 3/50 (6%), 1/50 (2%), and 6/50 (12%), 

respectively (Table 2-9). The incidence in the high-dose males was statistically significant (p=0.013) in 

pairwise comparison to the control incidence. Although the incidence in the mid-dose group was less 

than that in the low-dose group, trend analysis revealed a significant trend (p=0.009) for increasing 

incidence of testicular interstitial cell tumors with increasing dose. Evaluation of historical control 

incidences resulted in testicular interstitial cell tumor incidences in the range of 0–12%, with a mean 

incidence of 4.5% (range: 3.4–6.7%) among lifetime studies that employed the same rat strain and were 

conducted concurrently with the 26-month study.

Incidences of thyroid c-cell tumors (adenoma, carcinoma, combined adenoma or carcinoma) in the female 

rats are presented in Table 2-9. An increased incidence of thyroid c-cell carcinomas in female rats 

approached statistical significance (p=0.055) at the highest dose (6/47 versus 1/47 for controls) (EPA 

1992d). The combined incidence of combined c-cell carcinomas or adenomas was not significantly 

increased (9/47 high-dose females versus 6/47 controls), and time-to-tumor analysis revealed no sign of a 

treatment-related effect. Historical control incidences of spontaneous thyroid c-cell tumors in female 

Sprague-Dawley rats were as high as 17%.
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Table 2-9. Incidences of Selected Tumors in Sprague-Dawley Rats Administered 

Technical Glyphosate (98.7% purity) in the Diet for up to 26 Months

Glyphosate dose (mg/kg/day) Historical control 

0 3.05 10.3 31.49 incidence

Male rats

Testes interstitial cell tumors

Interstitial cell tumors 0/50 (0%) 3/50 (6%) 1/50 (2%) 6/50a(12%) 0–12%

Female rats

Thyroid c-cell tumors

Adenoma 5/47 (11%) 3/49 (6%) 6/50 (14%) 3/47 (6%) 0–17%

Carcinoma 1/47 (2%) 0/49 (0%) 2/50 (4%) 6/47 (13%) 0–5%

Adenoma or carcinoma 

(combined)

6/47 (13%) 3/49 (6%) 8/50 (16%) 9/47 (19%) 0–17%

aSignificantly different from concurrent control according to Fisher’s Exact Test (p<0.05).

NA = not applicable; NS = not specified

Sources: EPA 1992d

Groups of albino Sprague-Dawley rats (60/sex/group) were administered technical glyphosate (96.5% 

purity) in the diet at target concentrations of 0, 2,000, 8,000, or 20,000 ppm (mean measured 

concentrations of 0, 1,900, 7,600, and 19,000 ppm, respectively) for up to 24 months (EPA 1991a, 

1991b). Based on mean body weight and food consumption data, estimated glyphosate doses to controls 

and low-, mid-, and high-dose groups were 0, 89, 362, and 940 mg/kg/day, respectively, for the males and 

0, 113, 457, and 1,183 mg/kg/day, respectively, for the females.

As shown in Table 2-10, low-dose (but not mid- or high-dose) males exhibited significantly increased 

incidences of pancreatic islet cell adenoma (p=0.015) in pairwise comparison to control incidence (EPA 

1991a, 1991b). Incidences of pancreatic islet cell carcinoma in low-, mid-, and high-dose males were not 

significantly different from control incidences. Incidences of combined adenoma or carcinoma among 

mid-, and high-dose males were not significantly different from control incidences. After excluding those 

male rats that died or were sacrificed prior to treatment week 55 (before the first adenoma or carcinoma 

were observed), incidences of pancreatic islet cell adenoma in the low-dose group remained significantly 

(p=0.018) higher than controls. However, exclusion of the early deaths resulted in only borderline 

significantly increased incidence of combined adenoma or carcinoma (p=0.052) in the low-dose group. 

Historical control incidences for pancreatic islet cell adenoma in male rats from 2-year studies conducted 

at the same testing facility ranged from 1.8 to 8.5%. In the female rats, no significant differences were 
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observed between controls and treated rats regarding pancreatic islet cell tumor incidences in pairwise 

comparisons with controls.

Table 2-10. Incidences of Selected Tumors in Albino Sprague-Dawley Rats 

Administered Technical Glyphosate (96.5% Purity) in the Diet for 2 Years

Glyphosate dose (mg/kg/day) Historical control 

0 89 362 940 incidence

Male rats

Pancreatic islet cell tumors

All deaths considered

Adenoma 1/58 (2%) 8/57a(14%) 5/60 (8%) 7/59 (12%) 1.8–8.5%

Carcinoma 1/58 (2%) 0/57 (0%) 0/60 (0%) 0/59 (0%) NS

Adenoma or carcinoma 

(combined)

2/58 (3%) 8/57 (14%) 5/60 (8%) 7/59 (12%) NA

Excluding deaths prior to treatment week 55 (first adenoma at week 81; first carcinoma at week 105)

Adenoma 1/43 (2%) 8/45a(18%) 5/49 (8%) 7/48a(15%) NA

Carcinoma 1/43 (2%) 0/45 (0%) 0/49 (0%) 0/48 (0%) NA

Adenoma or carcinoma 

(combined)

2/43 (2%) 8/45 (18%) 5/49 (10%) 7/48 (15%) NA

Thyroid c-cell tumors

All deaths considered

Adenoma 2/60 (3%) 4/58 (7%) 8/58b(14%) 7/60 (12%) 1.8–10.6%

Carcinoma 0/60 (0%) 2/58 (3%) 0/58 (0%) 1/60 (2%) NS

Excluding deaths prior to treatment week 55 (first adenoma at week 54; first carcinoma at week 93)

Adenoma 2/54 (4%) 4/55 (7%) 8/58 (14%) 7/58 (12%) NA

Carcinoma 0/54 (0%) 2/55 (4%) 0/58 (0%) 1/58 (1%) NA

Adenoma or carcinoma 

(combined)

2/54 (4%) 6/55 (11%) 8/58 (14%) 8/58 (14%) NA

Liver tumors

All deaths considered

Adenoma 2/60 (3%) 2/60 (3%) 3/60 (5%) 7/60 (12%) 1.4–18.3%

Carcinoma 3/60 (5%) 2/60 (3%) 1/60 (2%) 2/60 (3%) 0–6.7%

Excluding deaths prior to treatment week 55 (first adenoma at week 88; first carcinoma at week 85)

Adenoma 2/44 (5%) 2/45 (4%) 3/49 (6%) 7/48 (15%) NA

Carcinoma 3/44 (7%) 2/45 (4%) 1/49 (2%) 2/48 (4%) NA

Adenoma or carcinoma 

(combined)

5/44 (11%) 4/45 (9%) 4/49 (8%) 9/48 (19%) NA
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Table 2-10. Incidences of Selected Tumors in Albino Sprague-Dawley Rats 

Administered Technical Glyphosate (96.5% Purity) in the Diet for 2 Years

Glyphosate dose (mg/kg/day) Historical control 

0 89 362 940 incidence

Female rats

Pancreatic islet cell tumors

All deaths considered

Adenoma 5/60 (8%) 1/60 (2%) 4/60 (7%) 0/59 (0%) NS

Carcinoma 0/60 (0%) 0/60 (0%) 0/60 (0%) 0/59 (0%) NS

Adenoma or carcinoma 

(combined)

5/60 (8%) 1/60 (2%) 4/60 (7%) 0/59 (0%) NA

Thyroid c-cell tumors

All deaths considered

Adenoma 2/60 (3%) 2/60 (3%) 6/60 (10%) 7/60 (10%) 3.3–10%

Carcinoma 0/60 (0%) 0/60 (0%) 1/60 (2%) 0/60 (0%) 0–2.9%

Adenoma or carcinoma 

(combined)

Excluding deaths prior to treatment week 55 (first adenoma at week 72; first carcinoma at week 93)

Adenoma 2/57c(4%) 2/60 (3%) 6/59 (10%) 6/55 (11%) NS

Carcinoma 0/57 (0%) 0/60 (0%) 1/59 (2%) 0/55 (0%) NS

Adenoma or carcinoma 

(combined)

2/57c(4%) 2/60 (3%) 7/59 (12%) 6/55 (11%) NA

aSignificantly different from concurrent control according to Fisher’s Exact Test (p<0.05).

bMarginally significantly different from concurrent control according to Fisher’s Exact Test (p=0.051).

cSignificant trend (p<0.05) for increasing incidence of adenoma and adenoma/carcinoma combined, excluding 

deaths prior to treatment week 55.

NA = not applicable; NS = not specified

Sources: EPA 1991a, 1991b

As shown in Table 2-10, the incidence of thyroid c-cell adenoma in mid-dose (but not low- or high-dose) 

male rats was marginally significantly (p=0.051) greater than that of controls. Historical control 

incidences for thyroid c-cell adenoma in male rats ranged from 1.8 to 10.6%. Pairwise comparison with 

concurrent controls revealed no significant difference between controls and low-, mid-, or high-dose

groups regarding incidences of thyroid c-cell adenoma or carcinoma. There were no significant 

differences between controls and low-, mid-, or high-dose groups regarding incidences of thyroid c-cell 

adenoma after excluding those male rats that died prior to week 54 (EPA 1991a, 1991b). In the female 

rats, no significant differences were observed between controls and treated rats regarding thyroid c-cell 

tumor incidences in pairwise comparisons with controls. Significant trends (p<0.05) for increasing 
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incidence of adenoma and adenoma/carcinoma combined were noted after excluding those female rats 

that died prior to week 55 (EPA 1991a, 1991b).

As shown in Table 2-10, incidences of liver tumors in the glyphosate-treated male rats were not 

significantly different from incidences among controls. Lack of statistical significance remained after 

excluding those rats that died or were sacrificed prior to study week 55 and upon combining incidences of 

adenoma or carcinoma combined.

EPA summarized results from two unpublished rat studies in which the carcinogenicity of glyphosate 

technical was assessed. In one study, groups of Alpk:APfSD Wistar rats (64/sex/group) received 

glyphosate (97.6% purity) from the diet for up to 2 years at 0, 121, 361, or 1,214 mg/kg/day (males) and 

0, 145, 437, or 1,498 mg/kg/day (females) (EPA 2015c). An interim sacrifice was performed on 

12 rats/sex/group after 1 year. Incidences of hepatocellular adenoma among controls, low-, mid-, and 

high-dose male rats were reported as 0/52 (0%), 2/52 (4%), 0/52 (0%), and 5/52 (10%), respectively. The 

incidence in the high-dose group was significantly greater than that of controls (p=0.028 by Fisher’s exact 

test). EPA (2015c) noted a range of 0–11.5% for this tumor type among historical controls reported by 

Greim et al. (2015). In the other study, there were no treatment-related increased incidences of any tumor 

type among Sprague-Dawley rats (50/sex/group) that received glyphosate (98.9 purity) from the diet for 

up to 104 weeks at 0, 100, 300, or 1,000 mg/kg/day (EPA 2015c).

In a combined chronic toxicity/carcinogenicity study, groups of Sprague-Dawley rats (50/sex/group for 

the carcinogenicity portion) received glyphosate (98.9 purity) from the diet for up to 104 weeks at 0, 100, 

300, or 1,000 mg/kg/day (EPA 2015c). There were no treatment-related increased incidences of any 

tumor type.

EPA also evaluated results from two unpublished mouse studies in which the carcinogenicity of 

glyphosate technical was assessed; EPA summarized the findings in publicly-available DERs.

In one study, groups of CD-1 mice (50/sex/group) were administered technical glyphosate (99.78% 

purity) for 24 months at doses of 0, 161, 835, or 4,945 mg/kg/day to the males and 0, 195, 968, or 

6,069 mg/kg/day to the females (EPA 2015a; selected results also available in EPA 1985a, 1985b, 1986b, 

1989, and 1993). Guidelines for testing of chemicals for carcinogenicity generally consider 

1,000 mg/kg/day as an upper limit for oral dosing (e.g., OECD Test Guideline 451, available at: 

http://www.oecd.org/chemicalsafety/testing/41753121.pdf). The highest dose tested in the mouse study 
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far exceeds the upper limit and the mid-dose level approached the upper limit. There were no treatmentrelated effects on tumor incidences in the female mice. Table 2-11 shows incidence data for renal tubular

cell tumors in the male mice summarized by EPA (2015a). There were no statistically significant trends 

for increased incidence of renal tubule adenoma, carcinoma, or combined carcinoma or adenoma and no 

statistically significant differences between groups upon pairwise analyses.

Table 2-11. Incidences of Renal Tubular Cell Tumors in Male CD-1 Mice 

Administered Technical Glyphosate (99.78% Purity) in the Diet for 

up to 24 Months 

Dose (mg/kg/day)

0 161 835 4,945

Adenoma 1/49 (2%) 0/49 (0%) 0/50 (0%) 1/50 (2%)

Carcinoma 0/49 (0%) 0/49 (0%) 1/50 (2%) 2/50 (4%)

Adenoma or carcinoma (combined) 1/49 (2%) 0/49 (0%) 1/50 (2%) 3/50 (6%)

Source: EPA 2015a

In the other study, groups of CD-1 mice (50/sex/group) received glyphosate (≥97.5% purity) from the diet 

at 0, 100, 300, or 1,000 mg/kg/day for 104 weeks (EPA 2015c). Incidence data for tumors reported by 

EPA are summarized in Table 2-12. Compared to controls, the incidence of hemangiosarcoma in the 

high-dose males approached the level of statistical significance (p=0.056 according to Fishers exact test). 

A significant trend (p=0.00296) was noted for increased incidence of hemangiosarcoma with increasing 

dose. All tumors were malignant and were located in the liver and spleen of one mouse; liver of another 

mouse; spleen of a third mouse; and liver, spleen, and prostate of the fourth mouse. Hemangiosarcoma 

incidences among glyphosate-treated female mice were not significantly increased relative to controls. 

All tumors were malignant and were located in the uterus of one low-dose female, spleen of another lowdose female, and liver of the high-dose female.

Table 2-12. Incidences of Tumors in Male and Female CD-1 Mice Administered 

Glyphosate (≥97.5% Purity) in the Diet for up to 104 Weeks

Dose (mg/kg/day)

0 100 300 1,000

Males

Hemangiosarcoma 0/50a(0%) 0/50 (0%) 0/50 (0%) 4/50 (8%)

Histiocytic sarcoma 0/50 (0%) 2/50 (4%) 0/50 (0%) 2/50 (4%)

Females
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Table 2-12. Incidences of Tumors in Male and Female CD-1 Mice Administered 

Glyphosate (≥97.5% Purity) in the Diet for up to 104 Weeks

Dose (mg/kg/day)

0 100 300 1,000

Hemangiosarcoma 0/50 (0%) 2/50 (4%) 0/50 (0%) 1/50 (2%)

Histiocytic sarcoma 0/50 (0%) 3/50 (6%) 3/50 (6%) 1/50 (2%)

aSignificant trend (p=0.00296) for increasing incidence of hemangiosarcoma

Source: EPA 2015c

Additional studies were conducted evaluating the potential carcinogenicity and pathogenic role of 

glyphosate or glyphosate formulation in cancer, specifically multiple myeloma. George et al. (2010) 

evaluated the potential carcinogenicity of Roundup Original® using the 2-stage mouse skin 

carcinogenesis model. The study included groups of male Swiss albino mice (20/group) receiving the 

glyphosate formulation topically 3 days/week for 32 weeks, single topical application of 

dimethylbenz[a]anthracene (DMBA; a tumor initiator) followed by repeated dermal applications of 

12-O-tetradecanoyl-phorbol-13-acetate (TPA; a tumor promoter), single or multiple topical application of 

the glyphosate formulation followed by dermal applications of TPA (test for initiation potential of the 

glyphosate formulation), single application of DMBA followed by repeated dermal application of the 

glyphosate formulation (test for promotion potential of the glyphosate formulation), single DMBA 

application, repeated TPA application, and untreated controls. Skin tumors were observed in 100% of the 

DMBA + TPA treatment group; the first tumor appeared at 52 days. Tumors were noted in 40% of the 

DMBA + glyphosate formulation treatment group; the first tumor appeared at 130 days. No tumors were 

observed in other groups. The results indicate that the glyphosate formulation functioned as a tumor 

promoter, but not a tumor initiator or complete carcinogen.

In an effort to understand whether glyphosate is involved in the pathogenesis of multiple myeloma, Wang 

et al. (2019) treated wild type and multiple myeloma model mice (C57b1/b strain) with drinking water 

containing up to 30 g/L glyphosate for 7 days or 1.0 g/L of glyphosate for 72 weeks. Vk*MYC mice with 

sporadic MYC activation in germinal B cells have been found to be the best available animal model for 

multiple myeloma (MM); this model follows the biological and clinical progression of human multiple 

myeloma. In the acute study, neither spleen, body weight nor serum creatinine levels were altered, 

however, plasma cells in bone marrow, spleen and lymph nodes were elevated (Wang et al. 2019). In the 

chronic study of 72 weeks, Wang et al. (2019) observed glyphosate to damage the liver and kidney and 

induce splenomegaly and benign monoclonal gammopathy in wildtype (WT) mice, an early indicator of 
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MM in humans; in MM model mice, glyphosate was seen to cause splenomegaly and organ dysfunction 

including lytic bone lesions, renal, liver, lung and kidney damage. Glyphosate also promoted the 

progression of multiple myeloma in Vk*MYC mice as shown by the development of plasma cell 

neoplasms. Upregulation of activation-induced cytidine deaminase (AID), a B-cell genome mutator, in 

bone marrow and spleen was exhibited in wild type and MM model mice in both acute and chronic study 

duration (Wang et al. 2019). 

Assessment of Carcinogenicity. Several national and international agencies and organizations have 

assessed the carcinogenicity of glyphosate (Table 2-13). These evaluations provide different types of 

determinations—some focused on hazard identification, or whether there is evidence that a chemical can 

cause an effect, and others focused on carcinogenic risk, or the likelihood of cancer effects at levels of 

exposure typically experienced by humans. In addition, there are large numbers of unpublished guideline 

studies on glyphosate and the inclusion or exclusion of these may account for the differences in the 

conclusions reached by these various agencies. For additional discussion regarding the carcinogenicity of 

glyphosate, refer to the following sources: Acquavella et al. 2016; Greim et al. 2015; McClellan 2016; 

Portier et al. 2016; Samsel and Seneff 2015; Tarazona et al. 2017; Williams et al. 2016.
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Table 2-13. Carcinogenicity Classification

Organization Reference Classification Justification

Domestic organizations 

U.S. Environmental 

Protection Agency

EPA 2017c, 

EPA 2017d, 

EPA 2020

Not likely to be 

carcinogenic to humans

EPA’s January 2020 Glyphosate Interim Registration Review Decision finalized 

the Glyphosate Draft Human Health Risk Assessment in Support of Registration 

Review. Based on a weight of evidence analysis of animal, human, and 

genotoxicity studies, EPA concluded glyphosate is “not likely to be carcinogenic 

to humans.” EPA (2017c) concluded “there is not strong support for the 

‘suggestive evidence of carcinogenic potential’ cancer classification descriptor 

based on the weight-of-evidence, which includes the fact that even small, nonstatistically significant changes observed in animal carcinogenicity and 

epidemiological studies were contradicted by studies of equal or higher quality.”

International organizations

Australian Pesticides 

and Veterinary 

Medicines Authority

APVMA 

2017

Exposure does not pose 

a carcinogenic risk to 

humans

Concluded “that the scientific weight-of-evidence indicates that exposure to 

glyphosate does not pose a carcinogenic risk to humans”.

European Chemical 

Agency

ECHA 2016 No hazard classification 

for carcinogenicity is 

warranted

Conclusion is “based on epidemiological data as well as on data from long-term 

studies in rats and mice, taking a weight of evidence approach, no hazard 

classification for carcinogenicity is warranted for glyphosate according to the CLP 

criteria” 

European Food Safety

Authority 

EFSA 2015 Unlikely to pose a 

carcinogenic hazard to 

humans

Conclusion is based on very limited evidence for an association between 

glyphosate-based formulations and non-Hodgkin lymphoma, overall inconclusive 

for a causal or clear associative relationship between glyphosate and cancer in 

human studies, “no evidence of carcinogenicity” in rats or mice, and “unlikely to 

be genotoxic”.

Food and Agricultural 

Organization/World 

Health Organization 

Joint Meeting on 

Pesticide Residues

FAO and 

WHO 2016

Unlikely to pose a 

carcinogenic risk to 

humans from dietary 

exposure

Conclusions were “in view of the absence of carcinogenic potential in rodents at 

human-relevant doses and the absence of genotoxicity by the oral route in 

mammals, and considering the epidemiological evidence from occupational 

exposures.” 

Health Canada Health 

Canada 

2015, 2017

Unlikely to pose a 

human cancer risk

In consideration of the strength and limitations of the large body of information on 

glyphosate, which included multiple short- and long-term (lifetime) animal toxicity 

studies and numerous in vivo and in vitro genotoxicity assays, as well as the 

large body of epidemiological information.
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Table 2-13. Carcinogenicity Classification

Organization Reference Classification Justification

International Agency 

for Research on 

Cancer 

IARC 2017 Group 2A (probably 

carcinogenic to humans)

This classification is based on IARC’s conclusions that there is “limited evidence” 

in humans, “sufficient evidence” in animals, and evidence that glyphosate and 

glyphosate-based formulations are genotoxic and capable of inducing oxidative 

stress.

New Zealand 

Environmental 

Protection Agency

NZ EPA

2016

Unlikely to be genotoxic 

or carcinogenic to 

humans

This conclusion is “based on a weight of evidence approach, and taking into 

account the quality and reliability of the available data – glyphosate is unlikely to 

be genotoxic or carcinogenic to humans.”
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2. HEALTH EFFECTS

2.20 GENOTOXICITY 

The potential genotoxicity of glyphosate technical and glyphosate formulations has been extensively 

evaluated. The intent of this section of the Toxicological Profile for Glyphosate is to present 

representative results from available sources of information on glyphosate technical and glyphosate 

formulations. Results from selected in vitro and in vivo genotoxicity tests for glyphosate technical are 

presented in Table 2-14 and Table 2-15, respectively. Results from selected in vitro and in vivo

genotoxicity tests for glyphosate formulations are presented in Table 2-16 and Table 2-17, respectively. 

Table 2-14. Genotoxicity of Glyphosate Technical In Vitro

Species (test system)

Test 

substance 

purity Endpoint

Result

Reference

Activation

With Without

Salmonella typhimurium

TA98, TA100, TA1535, 

TA1537

NS Gene mutation – – EPA 1992i

S. typhimurium TA98, 

TA100

NS Gene mutation – – Kubo et al. 2002

S. typhimurium TA97a, 

TA98, TA100, TA102

NS Gene mutation – – Chruscielska et al. 

2000

S. typhimurium TA98, 

TA100, TA1535, 

TA1537, TA1538

98% Gene mutation – – Li and Long 1988

S. typhimurium TA97, 

TA98, TA100, TA1535

98.6% Gene mutation – – NTP 1992

Escherichia coli WP2 

hcr

98% Gene mutation – – Li and Long 1988

Chinese hamster ovary 

cells

98% Gene mutation – – Li and Long 1988

Bacillus subtilis rec+, 

rec98% rec assay NT – Li and Long 1988

Human peripheral blood 

lymphocytes

>98% Chromosomal aberrations NT + Lioi et al. 1998a

Bovine peripheral blood 

lymphocytes

≥98% Chromosomal aberrations NT + Lioi et al. 1998b

Human peripheral blood 

lymphocytes

>96% Chromosomal aberrations NT – Mañas et al. 2009

Human peripheral blood 

lymphocytes

>98% Sister chromatid exchange NT (+) Lioi et al. 1998a

Human peripheral blood 

lymphocytes

99.9% Sister chromatid exchange NT + Bolognesi et al. 

1997

Bovine peripheral blood 

lymphocytes

≥98% Sister chromatid exchange NT (+) Lioi et al. 1998b
GLYPHOSATE 129

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Table 2-14. Genotoxicity of Glyphosate Technical In Vitro

Species (test system)

Test 

substance 

purity Endpoint

Result

Reference

Activation

With Without

Human-derived buccal 

epithelial cells

95% Micronuclei NT + Koller et al. 2012

Chinese hamster CHOK1 cellsNS Micronuclei – + Roustan et al. 2014

Rat hepatocytes 98% Unscheduled DNA 

synthesis

NT – Li and Long 1988

Human fibroblast 

CM5757 cells

96% DNA damage NT + Alvarez-Moya et al. 

2014

Human fibroblasts 98.4% DNA damage NT + Lueken et al. 2004

Human peripheral blood 

lymphocytes

96% DNA damage NT + Mañas et al. 2009

Human GM38 cells Technical 

grade

DNA damage NT + Monroy et al. 2005

Human HT1080 

(fibrosarcoma) cells

Technical 

grade

DNA damage NT + Monroy et al. 2004, 

2005

Chinese hamster ovary 

cells

Technical 

grade

DNA damage NT + Monroy et al. 2004

Raji cells 95% DNA damage NT + Townsend et al. 

2017

Human lymphocytes NS DNA damage NT + Suarez-Larios et al. 

2017

Human lymphocytes NS Chromosomal aberrations NT + Santovito et al. 2018

Human lymphocytes NS Micronuclei NT + Santovito et al. 2018

Peripheral blood 

mononuclear cells

NS DNA damage NT + Kwiatkowska et al. 

2017

HEPG2 Standard 

purity 

<100%

DNA damage NT + Kasuba et al. 2017

HEPG2 Standard 

purity 

<100%

Micronuclei NT + Kasuba et al. 2017

HEC1A 99.5% DNA damage NT + De Almeida et al. 

2018

MDA MB 231 99.5% DNA damage NT + De Almeida et al. 

2018

MCF7 99.5% DNA damage NT - De Almeida et al. 

2018

Mouse (oocytes) NS DNA Damage NT + Zhang et al. 2019b

Mouse (oocytes) NS Abnormal chromosome 

spindle

+ Zhang et al. 2019b

– = negative result; + = positive result; (+) = weakly positive result; +/– = equivocal result; DNA = deoxyribonucleic 

acid; NS = not specified; NT = not tested
GLYPHOSATE 130

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Table 2-15. Genotoxicity of Glyphosate Technical In Vivo

Species (test system)

Test 

substance 

purity Endpoint Result Reference

Oral exposure

Mouse (bone marrow) 98.6% Micronuclei – NTP 1992

Mouse (male germ cells) 98.7% Dominant lethal mutation – EPA 1992j

Intraperitoneal injection

Rat (bone marrow) 98% Chromosomal aberrations – Li and Long 1988

Mouse (bone marrow) 99.9% Micronuclei + Bolognesi et al. 1997

Mouse (bone marrow) 96% Micronuclei + Mañas et al. 2009

Mouse (bone marrow) NSa Micronuclei – Rank et al. 1993

Mouse (liver DNA) 99.9% DNA damage + Bolognesi et al. 1997

Mouse (kidney DNA) 99.9% DNA damage + Bolognesi et al. 1997

Mouse (liver DNA) 99.9% Oxidative DNA damage + Bolognesi et al. 1997

Mouse (kidney DNA) 99.9% Oxidative DNA damage – Bolognesi et al. 1997

Mouse (liver, kidney DNA) NSa DNA adducts – Peluso et al. 1998

Rats (leukocytes, liver 

DNA)

≤100 % DNA damage + Milic et al. 2018

aTest substance: glyphosate isopropylamine salt.

– = negative result; + = positive result; DNA = deoxyribonucleic acid; NS = not specified

Table 2-16. Genotoxicity of Glyphosate Formulations In Vitro

Test system

Glyphosate 

formulation End point

Result

Reference

Activation

With Without

Salmonella typhimurium

TA98, TA100, TA1535, 

TA1537, TA1538

Roundup®

(composition NS)

Gene mutation – – Moriya et al. 1983

S. typhimurium TA98 Roundup® (48% 

glyphosate 

isopropylamine salt)

Gene mutation – (+)a Rank et al. 1993

S. typhimurium TA100 Roundup® (48% 

glyphosate 

isopropylamine salt)

Gene mutation (+)b – Rank et al. 1993

S. typhimurium TA98, 

TA100

Glyphosate 

(Unspecified 

commercial 

formulation)

Gene mutation – – Wildeman and 

Nazar 1982

Escherichia coli WP2 hcr Roundup®

(composition NS)

Gene mutation – – Moriya et al. 1983
GLYPHOSATE 131

2. HEALTH EFFECTS

Table 2-16. Genotoxicity of Glyphosate Formulations In Vitro

Test system

Glyphosate 

formulation End point

Result

Reference

Activation

With Without

Bovine peripheral blood 

lymphocytes

Glyphosate (62% 

w/w isopropylamine 

salt; 38% unspecified 

inerts)

Chromosomal 

aberrations

NT – Holečková 2006

Bovine peripheral blood 

lymphocytes

Glyphosate (62% 

isopropylamine salt; 

38% unspecified 

inerts)

Chromosomal 

aberrations

NT – Šiviková and 

Dianovskỳ 2006

Human peripheral blood 

lymphocytes

Roundup® (not 

otherwise described)

Sister chromatid 

exchange

NT (+) Vigfusson and 

Vyse 1980

Human peripheral blood 

lymphocytes

Roundup® (30.4% 

glyphosate)

Sister chromatid 

exchange

NT + Bolognesi et al. 

1997

Bovine peripheral blood 

lymphocytes

Glyphosate (62% 

isopropylamine salt; 

38% unspecified

inerts)

Sister chromatid 

exchange

+ + Šiviková and 

Dianovskỳ 2006

Human-derived buccal 

epithelial cells

Roundup Ultra Max®

(45% glyphosate)

Micronuclei NT + Koller et al. 2012

Bovine peripheral blood 

lymphocytes

Glyphosate (62% 

isopropylamine salt; 

38% unspecified 

inerts)

Micronuclei NT (+) Piešová 2004

Bovine peripheral blood 

lymphocytes

Glyphosate (62% 

isopropylamine salt; 

38% unspecified 

inerts)

Micronuclei NT (+) Piešová 2005

Human liver HepG2 cells Grands Travaux®

(40% glyphosate)

DNA damage NT (+) Gasnier et al. 2009

E. coli PQ37 Roundup BIO® (NS) DNA damage NT + Raipulis et al. 2009

HEC1A Roundup DNA damage NT + De Almeida et al. 

2018

MDA MB 231 Roundup DNA damage NT + De Almeida et al. 

2018

MCF7 Roundup DNA damage NT - De Almeida et al. 

2018

HEC1A Wipeout DNA damage NT + De Almeida et al. 

2018

MDA MB 231 Wipeout DNA damage NT + De Almeida et al. 

2018

MCF7 Wipeout DNA damage NT - De Almeida et al. 

2018

peripheral blood 

mononuclear cells

Roundup DNA damage NT + Wozniak et al. 

2018
GLYPHOSATE 132

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Table 2-16. Genotoxicity of Glyphosate Formulations In Vitro

Test system

Glyphosate 

formulation End point

Result

Reference

Activation

With Without

aWeakly positive at 360 μg/plate in one test (4-fold increase in revertants/plate) but not in another test; cytotoxicity at 

concentrations ≥360 μg/plate.

bWeakly positive at 720 μg/plate (3.3-fold increase in revertants/plate); cytotoxicity at concentrations ≥360 μg/plate.

– = negative result; + = positive result; (+) = weakly positive result; NS = not specified; NT = not tested

Table 2-17. Genotoxicity of Glyphosate Formulations In Vivo

Species (test system)

Test substance 

(purity) End point Result Reference

Drosophila (sex-linked 

recessive lethal 

mutation assay)a

Roundup® (glyphosate 

isopropylamine salt; 

purity NS)

Gene mutation + Kale et al. 1995

Oral

Mouse (bone marrow) Roundup® (9.8% active 

ingredient)

Chromosomal 

aberrations

– Dimitrov et al. 2006

Intraperitoneal injection

Mouse (bone marrow) Roundup® (>41% 

glyphosate 

isopropylamine salt)

Chromosomal 

aberrations

+ Prasad et al. 2009

Mouse (bone marrow) Roundup® (48% 

glyphosate 

isopropylamine salt)

Micronuclei – Rank et al. 1993

Mouse (bone marrow) Roundup® (30.4% 

glyphosate)

Micronuclei + Bolognesi et al. 1997

Mouse (bone marrow) Roundup® (9.8% 

glyphosate)

Micronuclei – Dimitrov et al. 2006

Mouse (bone marrow) Roundup® (>41% 

glyphosate 

isopropylamine salt)

Micronuclei + Prasad et al. 2009

Mouse (bone marrow) Roundup® (48% 

glyphosate 

isopropylammonium 

salt; 12% inerts 

including POEA)

Micronuclei – Grisolia 2002

Mouse (liver DNA) Roundup® (30.4% 

glyphosate)

DNA damage + Bolognesi et al. 1997

Mouse (kidney DNA) Roundup® (30.4% 

glyphosate)

DNA damage + Bolognesi et al. 1997

Mouse (liver DNA Roundup® (30.4% 

glyphosate)

Oxidative DNA 

damage

– Bolognesi et al. 1997

Mouse (kidney DNA) Roundup® (30.4% 

glyphosate)

Oxidative DNA 

damage

+ Bolognesi et al. 1997
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2. HEALTH EFFECTS

Table 2-17. Genotoxicity of Glyphosate Formulations In Vivo

Species (test system)

Test substance 

(purity) End point Result Reference

Mouse (liver, kidney 

DNA)

Roundup® (30.4% 

glyphosate 

isopropylammonium 

salt)

DNA adducts + Peluso et al. 1998

aDrosophila larvae were exposed to test substance in growing medium.

+ = positive result; – = negative result; DNA = deoxyribonucleic acid; NS = not specified

Glyphosate Technical. Glyphosate did not induce gene mutations either with or without exogenous 

metabolic activation in numerous bacterial assays, or in assays using mammalian cells (Chruscielska et al. 

2000; EPA 1992i, Kubo et al. 2002; Li and Long 1988; NTP 1992). Lioi et al. (1998a, 1998b) reported 

concentration-related significant increases in chromosomal aberrations in human and bovine peripheral 

blood lymphocytes exposed to glyphosate, although concomitant decreases in mitotic index were 

indicative of some degree of cytotoxicity at least at the highest glyphosate concentrations. Mañas et al. 

(2009) found no evidence of glyphosate-induced chromosomal aberrations in human peripheral blood 

lymphocytes. Glyphosate was positive for induction of sister chromatid exchange in one assay using 

human peripheral blood lymphocytes (Bolognesi et al. 1997); weakly positive responses were obtained in 

other assays using human lymphocytes (Lioi et al. 1998a) and bovine lymphocytes (Lioi et al. 1998b). 

There was some evidence of cytotoxicity in the assays of Lioi et al. (1998a, 1998b). The result was 

considered equivocal due to significant apoptosis at concentrations resulting in significantly increased 

micronuclei frequency. Koller et al. (2012) reported significantly increased frequency of micronuclei in 

an assay using human-derived buccal epithelial cells exposed to glyphosate. Roustan et al. (2014) 

reported significantly increased micronuclei frequency in Chinese hamster ovary K1 cells exposed to 

glyphosate without (but not with) exogenous metabolic activation. Negative results were obtained in an 

assay that evaluated the potential for glyphosate to induce unscheduled DNA synthesis in rat hepatocytes 

(Li and Long 1988). Mañas et al. (2009) and Lueken et al. (2004) reported positive results for DNA 

damage in glyphosate-exposed human fibroblasts. Alvarez-Moya et al. (2014) reported DNA damage in 

human fibroblast CM5757 cells exposed to glyphosate technical. Exposure-related DNA damage was 

observed in assays of human GM38 cells (Monroy et al. 2005), human HT1080 (fibrosarcoma) cells 

(Monroy et al. 2004, 2005), and Chinese hamster ovary cells (Monroy et al. 2004) exposed to glyphosate 

technical. 
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2. HEALTH EFFECTS

Townsend et al (2017) evaluated DNA damage in human Raji cells exposed to various concentrations of 

glyphosate. Significant DNA damage occurred after exposure to concentrations of 1 or 5 mM for 30 to 

60 minutes. However, after two hours, DNA damage was no longer apparent. One hour after the initial 

exposure, cells were again exposed to the same concentrations for the same length of time. DNA repair 

was not observed in any cells after two exposures (Townsend et al. 2017). Suarez-Larios et al (2017) also 

reported DNA damage in the form of double strand breaks in human lymphocytes after exposure to 

glyphosate. Santovito et al (2018) reported increases in chromosomal aberrations, micronuclei, and 

nuclear microplasmic bridges with increasing doses of glyphosate in human lymphocytes. Kwiatkowska 

et al (2017) also reported DNA damage in the form of single and double stand breaks in human 

lymphocytes after exposure to glyphosate. However, after two hours, significant repair of the DNA had 

occurred. The authors also reported a significant decrease in DNA methylation levels. 

DNA damage was also reported in HEPG2 cells after 4 hours of exposure but not after 24 hours of 

exposure (Kasuba et al. 2017). Kasuba et al (2017) also report statistically significant increases in 

micronuclei and nuclear buds after four hours of exposure. Increases were also reported for 

nucleoplasmic bridges, but not at statistically significant levels after four hours of exposure. After 24 

hours of exposure, decreases in micronuclei and nucleoplasmic bridges were noted (Kasuba et al. 2017). 

De Almeida et al (2018) also reported DNA damage in two of three cell lines assessed: HEC1A and MDA 

MB 231. No significant damage was reported for the MCF7 cell line. Wozniak et al (2018) reported 

DNA damage for human peripheral blood mononuclear cells after exposure to glyphosate for 24 hours.

Elie-Caille et al. (2010) examined the effects of glyphosate on human keratinocyte cell lines and found 

alterations in cell morphology and size that were indicative of apoptosis.

Koureas et al. (2014) investigated the effects of occupational exposures to pesticides on oxidative DNA 

damage. Use of herbicides (defined as glyphosate, ammonium or glufosinate) was significantly associated 

with increased risk of oxidative damage, as measured by levels of 8-hydroxy-2-deoxyguanosine in whole 

blood (RR = 2.60; 95% CI: 1.35-5.04). However, no significant associations were found between levels 

of this marker and glyphosate exposure specifically (RR = 1.47; 95% CI: 0.78-2.77).

Zhang et al. (2019b) reported DNA damage in the form of double strand breaks as well as abnormal 

spindly morphology in mouse oocytes after exposure to up to 500 μM glyphosate for 14h. See section 

2.16 for a discussion of non-genotoxic reproductive effects associated with glyphosate exposure.
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2. HEALTH EFFECTS

The genotoxicity of glyphosate technical has been evaluated in a number of in vivo tests; results are 

mixed across a variety of cell types. Glyphosate did not induce dominant lethal mutations following oral 

dosing of male CD-1 mice once by gavage at up to 2,000 mg/kg (EPA 1992j). Glyphosate did not 

increase the frequency of micronuclei in bone marrow cells from B6C3F1 mice administered glyphosate 

in the diet for 13 weeks at concentrations resulting in estimated doses as high as 10,780–

11,977 mg/kg/day (NTP 1992). Glyphosate did not increase the frequency of micronuclei in bone 

marrow cells from C3H mice administered glyphosate technical via single intraperitoneal injection 

(Chruscielska et al. 2000) or NMRI-bom mice administered glyphosate (as isopropylammonium salt) via 

two intraperitoneal injections 24 hours apart (Rank et al. 1993). Glyphosate did not induce chromosomal 

aberrations in bone marrow cells from rats administered glyphosate via intraperitoneal injection at 

1,000 mg/kg (Li and Long 1988). Kier and Kirkland (2013) summarized results from 10 industry studies 

that evaluated frequency of micronuclei in bone marrow cells from mice or rats administered glyphosate 

orally or via intraperitoneal injection; results were consistently negative for glyphosate-induced 

micronuclei, although an inconclusive result was determined for one study. 

However, other investigators reported positive results for micronuclei induction in bone marrow cells 

from mice administered glyphosate via intraperitoneal injection by single 300 mg/kg dose (Bolognesi et 

al. 1997) or two 200 mg/kg doses 24 hours apart (Mañas et al. 2009). Bolognesi et al. (1997) reported 

significantly increased frequency of DNA damage (single strand breaks) in liver and kidney and 

significantly increased frequency of oxidative DNA damage in liver (but not kidney) from mice 

administered glyphosate via single intraperitoneal injection at 300 mg/kg. Peluso et al. (1998) found no 

evidence of the formation of DNA adducts in liver or kidney from mice following intraperitoneal 

injection of glyphosate (as isopropylammonium salt) at up to 270 mg/kg. It should be noted that 

intraperitoneal injection studies typically employed lethal dose levels; a positive result at such high dose 

levels does not necessarily indicate potential for genotoxicity at doses relevant to human exposure. Rats 

exposed up to 10 mg/kg bw/day glyphosate orally for 28 days were reported to have DNA damage in 

leukocytes and liver cells compared to controls (Milic et al. 2018). Furthermore, liver cell DNA damage 

was greatest in the lowest (0.1 mg/kg bw/day) and highest (10 mg/kg bw/day) exposure groups (Milic et 

al. 2018). 

DNA damage in human fibroblast cells and peripheral blood lymphocytes were the most frequently 

reported clearly positive results from available in vitro assays that employed glyphosate technical. From 

available in vivo assays that employed glyphosate technical, DNA damage in mouse kidney and liver was 
GLYPHOSATE 136

2. HEALTH EFFECTS

the most frequent positive result. Summaries should be interpreted with caution because the genotoxicity 

of glyphosate technical was assessed based on a limited number of primary results available to ATSDR.

Glyphosate Formulations. Glyphosate formulations (active ingredient typically ranging from 

approximately 30 to 62% of the formulation) were not mutagenic to bacterial test systems in available 

published studies (Chruscielska et al. 2000; Moriya et al. 1983; Wildeman and Nazar 1982), numerous 

unpublished industry studies summarized by Kier and Kirkland (2013), or several other studies 

summarized by Williams et al. (2000). Weakly positive results were obtained for Salmonella

typhimurium strain TA98 in the absence (but not presence) of exogenous metabolic activation and strain 

TA100 in the presence (but not absence) of exogenous metabolic activation (Rank et al. 1993); however, 

the positive responses were observed at concentrations exhibiting cytotoxicity and in only one of two tests 

in strain TA98. Glyphosate formulations did not induce chromosomal aberrations in bovine peripheral 

blood lymphocytes in two assays that employed 24-hour exposures (Holečková 2006; Šiviková and 

Dianovskỳ 2006); however, a significant increase in sister chromatid exchange was noted both with and 

without exogenous metabolic activation (Šiviková and Dianovskỳ 2006). A slight, (statistically 

significant) 1.1–1.3-fold increase in frequency of sister chromatid exchange was observed in human 

peripheral blood lymphocytes exposed to Roundup® (Vigfusson and Vyse 1980). Bolognesi et al. (1997) 

reported significantly increased sister chromatid exchange (1.3–1.5-fold greater than that of controls) in 

human peripheral blood lymphocytes exposed to Roundup® for 72 hours at concentrations of 0.1 and 

0.33 mg/mL. The magnitude of this effect was comparable to that obtained using analytical-grade 

glyphosate at 10 times the concentration of the Roundup® formulation, indicating that other substances in 

the Roundup® formulation may have been at least partly responsible for the effect. In two assays, 

unspecified glyphosate formulations induced micronuclei in cultured bovine peripheral blood 

lymphocytes at noncytotoxic concentrations (Piešová 2004, 2005). Koller et al. (2012) reported 

significantly increased numbers of micronuclei in human-derived buccal epithelial cells exposed to 

Roundup Ultra Max® for 20 minutes, including concentrations that were noncytotoxic; this effect was 

more pronounced than that resulting from similar treatment using analytical grade glyphosate. A weakly 

positive result for DNA damage was reported for human liver HepG2 cells exposed to Roundup Grands 

Travaux® (Gasnier et al. 2009). Roundup® induced dose-dependent increases in DNA damage and the 

proportion of apoptotic cells in human alveolar carcinoma cells (Hao et al. 2019). In the same study, DNA 

single-strand and double-strand breaks, and the collapse of mitochondrial membrane were induced by 

RoundUp® concentrations ranging from 50 to 125 μg/mL (Hao et al. 2019). Exposure to non-specified 

concentrations of glyphosate resulted in treatment-related DNA damage in Escherichia coli PQ37 cells

(Raipulis et al. 2009). Wozniak et al (2018) reported DNA damage for human peripheral blood 
GLYPHOSATE 137

2. HEALTH EFFECTS

mononuclear cells after exposure to Roundup 360 plus for 24 hours at a dose two orders of magnitude 

lower than glyphosate. De Almeida et al (2018) also reported DNA damage in two of three cell lines 

exposed to Roundup and Wipeout: HEC1A and MDA MB 231. No significant damage was reported for 

the MCF7 cell line.

Several studies were designed to evaluate the genotoxicity of selected glyphosate formulations in vivo; 

similar to findings from in vivo studies using glyphosate technical, mixed results were obtained from in 

vivo exposure to glyphosate-containing products. Roundup® induced mutations in Drosophila in a sexlinked recessive lethal mutation assay (Kale et al. 1995). Roundup® did not induce chromosomal 

aberrations or micronuclei in mice administered the test chemical orally at a 1,080 mg/kg dose, reported 

by the study authors as one-half the LD50 (Dimitrov et al. 2006). The potential for Roundup® to induce 

chromosomal aberrations and/or micronuclei in bone marrow cells has been assessed in several studies in 

which the test chemical was administered to mice via intraperitoneal injection. Although intraperitoneal 

administration of Roundup® at 25 and 50 mg/kg resulted in significantly increased frequencies of 

chromosomal aberrations and micronuclei, both doses appeared to be cytotoxic, as indicated by time- and 

dose-related significant decreases in mitotic indices (Prasad et al. 2009). Roundup® induced micronuclei 

in bone marrow from mice administered the chemical via intraperitoneal injection at 300 mg/kg 

(expressed as glyphosate) (Bolognesi et al. 1997). Negative results were reported in two other studies that 

evaluated micronucleus induction in bone marrow cells from mice treated by intraperitoneal injection of 

Roundup® (Grisolia 2002; Rank et al. 1993). In the study of Grisolia (2002), polyoxyethylene amine 

surfactant accounted for 12% of the formulation. Negative results were also reported for micronucleus 

induction in bone marrow cells from mice treated by intraperitoneal injection of a commercial 

formulation identified only as Perzocyd 10 SL (Chruscielska et al. 2000). Roundup® induced singlestrand breaks in DNA from liver and kidney of mice administered the chemical via intraperitoneal 

injection at 300 mg/kg (expressed as glyphosate) and oxidative DNA damage in kidney (but not liver) 

cells (Bolognesi et al. 1997). However, Heydens et al. (2008) repeated the study design of Bolognesi et 

al. (1997) and found a 300 mg/kg intraperitoneally-injected dose to be highly toxic to liver and kidney. It 

was suggested that the genotoxic effects observed by Bolognesi et al. (1997) might have been secondary 

effects mediated by local toxicity. Peluso et al. (1998) reported the formation of DNA adducts in liver 

and kidney from mice following intraperitoneal injection of Roundup® at doses in the range of 122–

182 mg active ingredient/kg. The DNA adduct formation was considered likely related to other 

components of the Roundup® formulation because DNA adduct formation was not observed in mice 

similarly treated with analytical-grade glyphosate at 270 mg/kg.
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Exposure to glyphosate-containing products and evidence of genetic damage was reported in limited 

human studies that did not measure specific exposure levels. Paz-y-Miño et al. (2007) evaluated 

prevalence of DNA strand breaks in blood samples from 24 residents of an area in northern Ecuador at 2 

weeks to 2 months following aerial applications of Roundup-Ultra®; the study included 21 unexposed 

control individuals. The exposed individuals exhibited a higher degree of DNA damage (comet length 

35.5±6.4 μm) than the unexposed controls (comet length 25.94±0.6 μm). There was no evidence of 

exposure-related chromosomal damage among 92 individuals from 10 communities near the northern 

Ecuador border evaluated at 2 years following the last aerial applications of glyphosate-containing 

herbicides (Paz-y-Miño et al. 2011). Bolognesi et al. (2009) reported increases in micronuclei in 

peripheral blood lymphocytes from nearby residents following aerial spraying of glyphosate-based 

formulation with adjuvant to coca and poppy crops, or without adjuvant on sugar-cane plantations. These 

residents were evaluated both prior to and following aerial spraying.

DNA damage in human cells was the most frequently reported clearly positive results from available in 

vitro assays that employed glyphosate formulations. However, comparison of results across available 

studies was precluded due to lack of information regarding the composition of the various formulations 

tested. From available in vivo assays that employed glyphosate formulations, DNA damage in mouse 

kidney and liver was the most frequent positive result. Summaries should be interpreted with caution 

because the genotoxicity of glyphosate technical was assessed based on a limited number of primary 

results available to ATSDR.

Additional unpublished genotoxicity assays were submitted to EPA and/or the European Commission 

(EC) during re-registration of products containing glyphosate. Many agencies, organizations, and/or 

expert panels have reviewed available genotoxicity data and concluded that the data do not support a 

genotoxicity role for glyphosate, at least at concentrations relevant to human exposure (e.g., APVMA 

2017; Brusick et al. 2016; EFSA 2015; EPA 2017c; FAO and WHO 2016; Health Canada 2017; Kier and 

Kirkland 2013; NZ EPA 2016; Williams et al. 2016). In contrast, IARC (2017) concluded that there is 

strong evidence for the genotoxicity of glyphosate. For more detailed information regarding genotoxicity 

evaluations and conclusions of these agencies, organizations, and/or expert panels, consult corresponding 

references.
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2.21 MECHANISMS OF ACTION 

Mechanism of Action in Plants. Glyphosate-based herbicides act on the shikimate pathway in plants by

blocking the activity of the enzyme, 5-enolpyruvylshikimate-3-phosphate synthetase (EPSPS), thereby 

inhibiting the biosynthesis of essential aromatic amino acids in plants (see Funke et al. 2006; Martinez et 

al. 2018; Pollegioni et al. 2011 for more specific information regarding mechanisms of action). The 

action of glyphosate on the shikimate pathway is not of direct human concern because this pathway does 

not exist in mammals. However, animal exposures to glyphosate could impact the shikimate pathway of 

gut bacteria, thereby affecting the gut microbiome (Aitbali et al. 2018; Deschartres et al. 2019; Lozano et 

al. 2018). The implications of microbiome effects are further discussed in Section 3.1.3.

Some crop plants have been genetically modified to resist the action of glyphosate by the addition of a 

glyphosate-insensitive form of EPSPS (CP4 EPSPS) obtained from Agrobacterium sp. strain CP4 (Funke 

et al. 2006). Some transgenic plants have been genetically altered to express N-acetyltransferase proteins 

(e.g., glyphosate acetyltransferase [GAT4601] from Bacillus licheniformis), which acetylate glyphosate to 

a non-phytotoxic metabolite (N-acetylglyphosate) (Pioneer 2006).

Proposed Mechanisms of Action with Human Relevance. Although glyphosate is generally considered 

to be of relatively low toxicity to mammals, the following mechanisms of action have been proposed:

Hepatotoxicity. Ford et al. (2017) administered glyphosate to male C57BL/6 mice by intraperitoneal 

injection at 200 mg/kg/day for 7 days, after which livers were evaluated for levels of glyphosate, 

aminomethylphosphonic acid (AMPA), and glyoxylate (a reactive substance produced endogenously). 

Glyphosate treatment at this high dose level resulted in measurable levels of AMPA, indicating some 

degree of glyphosate metabolism. Glyphosate treatment also resulted in an approximately 2-fold increase 

in glyoxylate. Because glyoxylate is formed endogenously, the increase in glyoxylate level in the liver 

may be a result of glyphosate acting on mechanisms responsible for endogenous production of glyoxylate. 

The study authors demonstrated that glyoxylate inhibited liver fatty acid oxidation enzymes in mice and 

that glyphosate treatment increased triglycerides and cholesteryl esters, which was considered a likely 

result of the diversion of fatty acids toward lipid pathways other than oxidation. In another study, Astiz et 

al. 2009 exposed rats to 10 mg/kg/bw of glyphosate three times a week for five weeks via injection and 

measured oxidative stress and cell damage. In the liver, lipid peroxidation as measured by thiobarbituric 

acid-reactive substances (TBARS) was two times greater than control; antioxidant (alpha-Tocopherol) 

and SOD levels were significantly decreased suggestive of oxidative damage induced by glyphosate. 
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Enzyme levels of γ-glutamyl transpeptidase, a sensitive biomarker for hepato-cellular damage, increased 

by 125% compared to controls indicating glyphosate induces cell damage. No clinical signs of animal 

toxicity were observed during the experiment. An in vitro assessment of Roundup® cytotoxicity on 

human L-02 hepatocytes determined that exposure induced structural and morphological changes in cell 

membranes, mitochondria and nuclei, in addition to cell shrinkage, nuclear fragmentation, and 

mitochondrial vacuolar degenerations (Luo et al. 2017). Study authors determined that the Roundupinduced overproduction of reactive oxygen species led to oxidative stress responses affecting normal cell 

function.

Renal toxicity. Mohamed et al. (2016) observed increases in serum and urinary cystatin C and urinary 

interleukin-18, cytochrome C, and neutrophil gelatinase-associated protein (NGAL) in patients presenting 

with poisoning from glyphosate-based formulations. The study authors noted that the increases in 

cystatin C and interleukin-18 suggest that glyphosate-based formulations might induce apoptosis and 

mitochondrial toxicity.

Astiz et al. 2009 reported increases in oxidative stress in the kidney tissues of rats exposed to 10 

mg/kg/bw day glyphosate as measured by TBARS and a decrease in superoxide dismutase activity (SOD) 

level. Dedeke et al. (2018) administered glyphosate alone or a glyphosate-based formulation to rats by 

daily gavage for 12 weeks at dose levels of 3.6, 50.4, or 248.8 mg glyphosate/kg/day. The rats 

administered the glyphosate-based formulation exhibited significantly altered markers of kidney changes 

(serum urea and creatinine, plasma cystatin-C, NGAL), oxidative stress, and activities of selected 

membrane-bound enzymes compared to the rats treated with glyphosate alone. Those rats administered 

glyphosate-based formulation were the only ones to exhibit severe histopathologic kidney lesions. The 

study authors suggested that these results did not support a nephrotoxic role for glyphosate alone.

Dermal Toxicity. George and Shukla (2013) examined whether the mechanism of action for glyphosate 

and its potentially tumor-promoting properties could be elucidated; previously the research group found 

glyphosate to cause tumor promotion in mouse skin carcinogenesis (George et al. 2010). In an in-vitro 

model, human skin keratinocyte, or HaCaT cells, were exposed to up to 1 mM of glyphosate for 72 hours. 

Glyphosate was observed to induce proliferation, decrease Ca+2 and increase reactive oxygen species 

(ROS) generation in HaCaT cells. Taken together, these suggest glyphosate may possibly have a 

proliferative effect on HaCaT cells by disturbing the homeostasis levels of Ca+2 and decrease SOD1 to 

increase ROS generation potentially leading to neoplastic growth in the mammalian skin system.
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Gehin et al. (2005) evaluated the cytotoxic effect of glyphosate or glyphosate formulation (Roundup 3® 

plus) in relation to antioxidants such as Vitamin C and E, glyphosate formulation was found to be more 

toxic than glyphosate after epidermal HaCaT cells were exposed to the herbicide for 24 hours. Taken 

together, glyphosate-based formulations, and comparatively to a lesser degree, glyphosate, are implicated 

in generating oxidative damage, which in turn may lead to dermal toxicity. The interaction between 

glyphosate and other chemicals (e.g. surfactants) may explain this observation; Section 3.4 discusses this 

further.

Neurotoxicity. Astiz et al. 2009 reported increases in oxidative stress in the brain of rats exposed to 10 

mg/kg/bw day glyphosate as measured by increased concentrations of TBARS, altered levels of 

antioxidant enzymes (decrease in superoxide dismutase and increase in catalase activity), and nitric oxide 

metabolites.

Cattani et al. (2014) added 1% Roundup® (0.38% glyphosate) to the drinking water of rat dams from 

gestation day 5 through lactation day 15. Hippocampal slices from 15-day-old pups were exposed to 

Roundup® (0.00005–0.1%) for 30 minutes. The study authors reported that Roundup® treatment 

resulted in increased Ca2+ influx via activation of NMDA receptors and voltage-dependent Ca2+ channels,

activation of Ca2+/calmodulin-dependent protein kinase II (CaMKII) and extracellular signal-regulated 

kinase (ERK), increased glutamate release into the synaptic cleft, decreased glutathione content, increased 

lipoperoxidation, decreased glutamate uptake and metabolism, and induced Ca2+ uptake and methylamino-isobutyric acid accumulation. The study authors suggested that exposure to Roundup® might lead 

to excessive extracellular glutamate levels and resulting glutamate excitotoxicity and oxidative stress in 

rat hippocampus.

Martinez and Al-Ahmad (2019) examined the effects of glyphosate on the blood brain barrier in vitro on 

induced pluripotent stem cells (iPSCs) after a single exposure. The study used a range of concentrations 

similar to levels found in patients and occupational exposures. Following treatment of 1 to 10 μM 

glyphosate for 24 hours, there was increased blood brain barrier permeability to fluorescein (dye)

indicating disruption of the barrier function. Glyphosate permeated across the blood brain barrier via a 

transcellular mechanism. Subsequently, neuronal cell metabolic activity and glucose uptake in brain 

microvascular endothelial cells was observed. Study authors suggest that exposure to glyphosate may lead 

to increased blood brain barrier permeability and alteration of glucose metabolism resulting in 

neurological damage.
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Reproductive/endocrine effects. Perego et al. (2017) reported results from an in vitro study designed to 

evaluate the effects of glyphosate treatment (up to 5 μg/mL) on bovine granulosa cells and theca cells. 

Granulosa cell proliferation and estradiol production were impaired, but no effects were observed on 

theca cell proliferation or steroidogenesis. The results suggest that glyphosate may affect the 

reproductive system in cattle via direct action on ovarian function. EPA evaluated results from the battery 

of in vitro assays and relevant laboratory mammalian and wildlife studies. Using this approach, EPA 

determined that there is no convincing evidence of potential interaction between glyphosate and estrogen 

or androgen.

Zhang et al. (2019b) evaluated the effects of glyphosate on mice oocytes, and found reduced rates of 

germinal vesicle breakdown (GVBD) and first polar body extrusion (PBE), indicating disruption of 

nuclear oocyte maturation after treatment with 500 μm glyphosate. In response to glyphosate exposure, 

cells produced excess reactive oxygen species, displayed abnormal spindle morphology, DNA double 

strand breaks, aggregated distribution of mitochondria and decrease in membrane potential of oocytes. 

Genes related to oxidative-stress (cat, sod2, gpx) were found expressed at greater levels than the control 

group; on the other hand, expression of apoptosis related genes including Bcl-2 (inhibits apoptosis) 

decreased, while Bax (pro-apoptosis gene), increased. Zhang et al. (2019b) suggests these changes led to 

the generation of oxidative stress and early apoptosis that result in the interference of mouse oocyte 

maturation and development.

Romano et al. (2010) reported decreased serum testosterone in young male rats gavaged with Roundup 

Transorb®. Romano et al. (2012) implicated disruption of gonadotropin expression as a mechanism of 

action.

Vanlaeys et al. (2018) evaluated the effects of Roundup Bioforce® and Glyphogan on cultured mice TM4 

Sertoli cell lines. These formulations induced dose-dependent cell death, and induced cell mitochondrial 

dysfunction, lipid droplet accumulation, and disruption of cell detoxification systems. Additionally, the 

penetration and accumulation of glyphosate formulants in cells led to cell death. Vanlaeys et al. (2018)

suggests these mechanisms can lead to disruption of reproductive function in pre-pubertal mammals. 

Carcinogenicity. As stated in Section 2.20 (Genotoxicity), IARC (2017) concluded that there is strong 

evidence for the genotoxicity of glyphosate, although other agencies, organizations, and/or expert panels 

have concluded that the data do not support a genotoxicity role for glyphosate (e.g., APVMA 2017; 

Brusick et al. 2016; EFSA 2015; EPA 2017c; FAO and WHO 2016; Health Canada 2017; Kier and 
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Kirkland 2013; NZ EPA 2016; Williams et al. 2016). IARC (2017) also concluded that there is strong 

evidence for glyphosate-induced oxidative stress based on results from studies of animal models in vivo

and human cells in vitro.
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POPULATIONS, BIOMARKERS, CHEMICAL 

INTERACTIONS

3.1 TOXICOKINETICS 

Toxicokinetic data for glyphosate are summarized below. 

• Glyphosate is readily absorbed from the gastrointestinal tract; very little glyphosate is absorbed 

through the skin; it is assumed that glyphosate is readily absorbed from the respiratory tract.

• Absorbed glyphosate is readily distributed via the blood, but does not accumulate in any 

particular organ or tissue.

• Glyphosate does not undergo significant metabolism in mammals; <1% is metabolized to 

aminomethylphosphonic acid (AMPA).

• Approximately two-thirds of an oral dose of glyphosate is excreted in the feces as unabsorbed 

parent compound. Most absorbed glyphosate is rapidly excreted in the urine as parent compound.

3.1.1 Absorption 

3.1.1.1 Inhalation Exposure 

Limited information is available regarding the toxicokinetics of inhaled glyphosate. Observations of 

increased urinary glyphosate levels among 48 farmer-applicators following application of glyphosatecontaining products is evidence that inhaled glyphosate can be absorbed (Acquavella et al. 2004). 

However, dermal absorption was likely involved in some cases because mean urinary glyphosate was 

higher among those farmers (14/48) who did not use rubber gloves. Detectable levels of urinary 

glyphosate were also measured in children of the farmers who were present during mixing, loading, or 

application of the herbicide; exposures among the children may have involved inhalation and/or dermal 

routes. No information was located regarding the toxicokinetics of inhaled glyphosate in laboratory 

animals.

3.1.1.2 Oral Exposure

Information regarding the toxicokinetics of ingested glyphosate in humans is limited. The detection of 

glyphosate in serum and/or urine samples from individuals who had intentionally or unintentionally 
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ingested glyphosate-containing products is confirmation of absorption from the gastrointestinal tract 

(e.g., Hiraiwa et al. 1990; Hori et al. 2003; Sribanditmongikol et al. 2012; Zouaoui et al. 2013). 

Numerous reports of systemic effects following intentional or unintentional ingestion of glyphosatecontaining products serve as additional evidence that ingested glyphosate is absorbed (e.g., Chang and

Chang 2009; Chen et al. 2009; Hsiao et al. 2008; Kim et al. 2014; Lee et al. 2000; Menkes et al. 1991; 

Moon and Chun 2010; Roberts et al. 2010; Sato et al. 2011; Sawada et al. 1988; Sørenson and Gregersen 

1999; Stella and Ryan 2004; Talbot et al. 1991; Tominack et al. 1991).

Several groups of investigators have evaluated the absorption of glyphosate following oral exposure in 

laboratory animals, particularly rats. In one study (NTP 1992), male F344/N rats were administered a 

single gavage dose of 14C-glyphosate (purity 99%) in distilled water at 5.6 or 56 mg/kg. Other rats were 

administered a single dose of glyphosate at 5.6 mg/kg via intravenous injection, intraperitoneal injection, 

or oral (gavage) to compare 24-hour urinary and fecal elimination by these administration routes. Results 

from comparative studies of oral, intravenous, and intraperitoneal administration of glyphosate indicated 

that urinary radioactivity represented the amount of glyphosate absorbed and fecal radioactivity 

represented the amount of unabsorbed glyphosate following oral exposure. Although quantitative data 

were not included in the study report, the study authors estimated that 30% of the 5.6 mg/kg dose of 

14C-glyphosate was absorbed and that a slightly higher percentage (34%) of the 56 mg/kg dose was 

absorbed. In another study, male Sprague-Dawley rats received a single gavage dose of 12C- and 

14C-glyphosate at 10 mg/kg (Brewster et al. 1991). Based on urinary radioactivity, it was estimated that 

35–40% of the oral dose had been absorbed from the gastrointestinal tract. Anadón et al. (2009) reported 

an absorption half-life of 2.29 hours following administration of an oral dose of 400 mg glyphosate/kg to 

rats; an estimated peak plasma glyphosate of 4.62 μg/mL was reached at 5.16 hours postdosing. Results 

from a number of unpublished industry studies cited in EPA (1993), FAO and WHO (2016), IPCS (1994), 

and/or Williams et al. (2000), but not available to ATSDR, demonstrate that single or repeated oral dosing 

of glyphosate to rats at doses in the range of 10–1,000 mg/kg/day result in urinary excretion of 7–36% of 

the administered dose during ≤7 days of posttreatment, which presumably represents the proportion of 

absorbed glyphosate.

3.1.1.3 Dermal Exposure 

Limited human data are available regarding the toxicokinetics of glyphosate following dermal exposure. 

Increased urinary glyphosate levels among 48 farmer-applicators following application of glyphosatecontaining products is evidence that glyphosate can be absorbed (Acquavella et al. 2004). Dermal 
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absorption was likely involved in some cases because mean urinary glyphosate was higher among those 

farmers (14/48) who did not use rubber gloves.

In vitro studies using human skin samples indicate that dermal penetration of glyphosate is very low. 

Wester et al. (1996) applied 300 μL of a 1% aqueous dilution of analytical-grade 14C-labeled glyphosate 

to human cadaver skin (0.8 cm2 of available skin area). The study authors reported a permeability 

constant of 4.59x10-4cm/hour, with a lag time of 10.48 hours, which resulted in a calculated flux of 

4.12 μg glyphosate/hour. Wester et al. (1991) used a 14C-labeled Roundup® formulation to evaluate 

dermal absorption of glyphosate through human skin (in vitro) and abdominal skin of Rhesus monkeys (in 

vivo). Undiluted application to human skin samples at doses ranging from 15.4 to 154 μg/cm2resulted in 

0–0.4% dermal absorption over 8 hours postapplication; dermal absorption of glyphosate from aqueous 

dilutions of test substance (1:20 or 1:32 test substance:water, v/v) during 16 hours postapplication was 

≤2.2%. Twelve-hour in vivo application of the test substance diluted 1:29 with water at concentrations of 

25 or 270 μg/cm2resulted in 7-day recovery of 0.8 and 2.2% of the applied dose, respectively, in the urine 

and 3.6 and 0.7%, respectively, in the feces. These results indicate that approximately 3–4% of the 

applied dose had been absorbed. An in vitro study using rat skin membranes, applied glyphosate 

formulations, concentration and field diluted, for 8 hours at concentrations of 6.249 and 0.08 mg/cm2for 

MON 35012 and 6.343 and 0.08 mg/cm2 for MON 0139 (van Burgsteden 2002). Over a period of 48 

hours, penetration of concentrates was higher, with 10% penetration of MON 35012 concentrate through 

rat skin membrane and 1.3% penetration of MON 0139 concentrate. 

3.1.2 Distribution 

3.1.2.1 Inhalation Exposure 

No human or animal data were located regarding distribution of glyphosate following absorption via the 

inhalation exposure route.

3.1.2.2 Oral Exposure 

Limited human data were located regarding distribution of glyphosate following absorption via the oral 

exposure route. Menkes et al. (1991) reported measurable glyphosate in kidney, liver, blood, and brain in 

postmortem examination of an individual who had ingested 200–250 mL of Roundup®.
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Following oral administration, absorbed glyphosate is readily distributed and rapidly eliminated without 

significant accumulation in any particular tissue. In male F344/N rats administered a single gavage dose 

of 14C-glyphosate (purity 99%) in distilled water at 5.6 or 56 mg/kg, peak blood radioactivity occurred at 

1 and 2 hours postdosing, respectively, mean peak blood concentration was 30-fold higher in the highdose group (NTP 1992). Among rats gavaged at 5.6 mg radiolabeled glyphosate/kg and evaluated for 

tissue distribution, total tissue radioactivity amounted to approximately 12, 11.7, 5.5, 0.9, and 0.1% of the 

administered dose at 3, 6, 12, 24, and 96 hours postdosing, respectively. The highest radioactivity level 

was found in the small intestine, reaching a peak level of approximately 10% of the administered dose at 

6 hours postdosing; radioactivity in the large intestine peaked at approximately 1.2% at 3 hours 

postdosing. Liver, kidney, skin, and blood each accounted for <1% of the administered dose at each time 

point. By 24 hours postdosing, <1% of the administered dose remained in all tissues combined. Brewster 

et al. (1991) administered 12C- and 14C-glyphosate by a single gavage dose at 10 mg/kg to male SpragueDawley rats and found approximately 34% of the administered dose in the small intestine (not associated 

with intestinal content) at 2 hours postdosing, decreasing to 0.05% of the administered dose by 96 hours 

postdosing. Radioactivity levels in most other tissues (blood, colon, kidney, liver, stomach, abdominal 

fat, testicular fat) peaked at 2–6 hours postdosing; each of these tissues accounted for ≤1.3% of the 

administered dose at peak and ≤0.06% by 96 hours postdosing. Radioactivity in bone peaked at 6 hours 

postdosing (4.7% of the administered dose) and remained at 1.7% at 96 hours postdosing. The tissue to 

blood ratio for bone increased with time suggesting a slower elimination from bone compared to blood. 

Anadón et al. (2009) reported an absorption half-life of 2.29 hours following administration of an oral 

dose of 400 mg glyphosate/kg to rats; an estimated peak plasma glyphosate level of 4.62 μg/mL was 

reached at 5.16 hours postdosing.

3.1.2.3 Dermal Exposure 

No human data were located regarding distribution following dermal exposure to glyphosate.

Limited animal data are available. The observation of radioactivity in urine and feces collected from 

rhesus monkeys following dermal application of a 14C-labeled Roundup® formulation is demonstration of 

systemic distribution following dermal absorption (Wester et al. 1991). However, at sacrifice 7 days 

posttreatment, no radioactivity was detected in spleen, ovaries, kidney, brain, abdominal fat, bone 

marrow, upper spinal column, or central nervous system fluid.
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3.1.2.4 Other Routes of Exposure

Limited data are available regarding the distribution of parenterally administered glyphosate. Male and 

female Sprague-Dawley rats were administered 14C-glyphosate via intraperitoneal injection at 

1,150 mg/kg (EPA 1992h). Radioactivity measured in bone marrow samples taken 30 minutes 

postinjection amounted to approximately 0.0044 and 0.0075% of the administered activity for the males 

and females, respectively. Anadón et al. (2009) administered glyphosate (95% purity) to male Wistar rats 

via intravenous injection at 100 mg/kg. Plasma levels of glyphosate and its metabolite, AMPA, were 

measured using high-performance liquid chromatography (HPLC). Reported fast plasma distribution 

(half-life of 0.345 hours) and high volume of distribution at steady state (2.99 L/kg) were interpreted to 

indicate that glyphosate was extensively distributed to extravascular tissues.

3.1.3 Metabolism 

Glyphosate does not undergo significant metabolism in mammals. Available data are limited to the oral 

exposure route and indicate that ingested glyphosate is eliminated mostly as parent compound; only a 

small amount may be metabolized to AMPA. Figure 3-1 depicts the chemical structures of glyphosate 

and AMPA. In one human case of intentional ingestion of an herbicide in a suicide attempt, glyphosate 

and its metabolite, AMPA, were detected in serum and urine (Hori et al. 2003). At 16 hours 

postingestion, serum levels of glyphosate and AMPA were 4.4 and 0.03 μg/mL, respectively (147:1, 

glyphosate:AMPA). Total urinary excretion of glyphosate and its metabolite during 4 days postingestion 

was 3.7 g and 25 mg, respectively (148:1, glyphosate:AMPA).

Figure 3-1. Chemical Structures of Glyphosate and Aminomethylphosphonic 

Acid (AMPA)

Results from available animal studies also indicate that very little ingested glyphosate is metabolized. 

Anadón et al. (2009) administered glyphosate (95% purity) to male Wistar rats by gavage at 400 mg 

glyphosate/kg. Plasma glyphosate peaked at 5.16 hours postdosing and measured 4.62 μg/mL; plasma 

AMPA peaked at 2.42 hours postdosing and measured 0.416 μg/mL. Based on the ratios between the 

OH

O

N

H

P

OH

O

OH

NH2 P

OH

O

OH

Glyphosate Aminomethylphosphonic acid (AMPA)
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area under the curve (AUC) for AMPA and the AUC for glyphosate, it was estimated that the metabolite 

represented 6.49% of the parent compound plasma concentration. In an unpublished study summarized 

by EPA (1993) and Williams et al. (2000), following oral administration of radiolabeled glyphosate 

(>99% purity) to Sprague-Dawley rats at 10 mg/kg, the glyphosate metabolite (AMPA) was detected in 

the urine (0.2–0.3% of the administered dose) and feces (0.2–0.4% of the administered dose). The 

formation of AMPA was thought to have occurred in the gastrointestinal tract (possibly by microflora) 

because AMPA was not detected in other rats administered glyphosate via intravenous injection. 

Following a single gavage dose of administered radiolabeled glyphosate (>99% purity) to SpragueDawley rats, expired air accounted for <0.27% of the administered radioactivity at 24 hours postdosing, 

indicating that glyphosate metabolism had occurred to a slight extent (EPA 1993).

In addition to its potential role in glyphosate metabolism, gut microflora can also be impacted by 

exposure to glyphosate and glyphosate-based herbicides. Though the shikimate pathway is absent in 

mammals, the shikimate pathway in animal gut microbes synthesizes amino acids (Aitbali et al. 2018; 

Nielsen et al. 2018). Rodents orally exposed to doses of glyphosate-based herbicides ranging from 5 to 

500 mg/kg/d showed a significant decrease in bacteria count and changes in community composition 

(Aitbali et al. 2018; Dechartres et al. 2019). A study using fecal samples from Roundup®-exposed

Sprague-Dawley rats also found changes in bacterial community composition (Lozano et al. 2018). 

Decreases in bacteria count were also observed in rodents orally exposed to 5 mg/kg/d of glyphosate 

technical (Aitbali et al. 2018). However, fecal samples from Sprague-Dawley rats orally exposed to doses 

of glyphosate or Glyfonova® found that while minimal changes in bacteria composition were observed, 

exposure to the glyphosate formulation appeared to have a more pronounced effect than exposure to 

glyphosate technical (Nielsen et al. 2018). While the implications of alterations in the gut microbiome are 

unclear, some animal studies suggest neurologic and behavioral changes (Aitbali et al. 2018; Dechartres 

et al. 2019; Lozano et al. 2018) and greater susceptibility to infection may be associated with loss of 

microbiome diversity, especially in cases of malnutrition (Nielsen et al. 2018; Shehata et al. 2013).

Ford et al. (2017) administered glyphosate to male C57BL/6 mice by intraperitoneal injection at 

200 mg/kg/day for 7 days. Glyphosate treatment at this high dose level resulted in measurable levels of 

AMPA (approximately 4% of the dose of glyphosate) and an approximately 2-fold increase in hepatic 

glyoxylate (a reactive substance produced endogenously). Because glyoxylate is formed endogenously, 

the increase in glyoxylate level in the liver may be a result of glyphosate acting on mechanisms 

responsible for endogenous production of glyoxylate.
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3.1.4 Excretion 

3.1.4.1 Inhalation Exposure 

Limited information is available regarding elimination and excretion of glyphosate in humans following 

inhalation exposure. In one study, urinary glyphosate levels were evaluated in 48 farmer-applicators prior 

to application of glyphosate-containing products, immediately following application, and for 3 days 

thereafter (Acquavella et al. 2004). Urinary glyphosate was detectable in 15% (7/47) of the farmers prior 

to application, in 60% (29/48) of the farmers immediately following application, and in only 27% (13/48) 

of the farmers on postapplication day 3. No information was located regarding elimination or excretion 

following inhalation exposure of laboratory animals to glyphosate.

3.1.4.2 Oral Exposure 

Roberts et al. (2010) estimated a half-life of 3–4 hours for elimination of glyphosate from the blood of 

patients who had intentionally ingested large amounts of glyphosate-containing herbicide products. In 

other cases of poisoning victims, plasma glyphosate levels dropped rapidly (within 2–3 days) following 

the onset of observation (e.g., Talbot et al. 1991). Glyphosate has been detected in feces and urine of 

individuals who intentionally or accidentally ingested relatively large amounts of glyphosate. 

Results from animal studies identify the feces and urine as major routes of elimination following oral 

exposure to glyphosate. For example, among male and female Sprague-Dawley rats administered 

14C-glyphosate (99% purity) via a single gavage dose at 10 mg/kg, during 7 days posttreatment, 

radioactivity recovered in the feces averaged 62.4 and 69.4% of the administered dose (males and 

females, respectively); another 28.6 and 22.5% of the administered dose (males and females, respectively) 

was recovered in the urine (IPCS 1994). Thus, feces and urine accounted for approximately 88–91% of 

the administered dose. HPLC analysis revealed that parent compound accounted for 98.5–99.3% of the 

radioactivity in feces and urine. There were no significant differences in fecal and urinary excretion 

among rats dosed with unlabeled glyphosate for 14 days followed by a single oral dose of radiolabeled 

glyphosate. Following a single gavage dosing of 14C-glyphosate (>96% purity) to male and female 

Sprague-Dawley rats at 30 mg/kg, the feces accounted for 57–59% of the administered radioactivity and 

the urine accounted for 27–29% during the first 36 hours posttreatment; indicating that fecal and urinary 

excretion occur relatively rapidly following oral exposure to glyphosate (IPCS 1994). In male F344/N 

rats administered a single gavage dose of 14C-glyphosate (purity 99%) in distilled water at 5.6 or 56 

mg/kg, 72-hour collection of feces and urine resulted in the recovery of 91–92% of the administered 
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radioactivity; 74 and 19%, respectively, at the low dose and 58 and 34%, respectively, at the high dose 

(NTP 1992). In one study (NTP 1992), male F344/N rats were administered a single dose of glyphosate 

at 5.6 mg/kg via intravenous injection, intraperitoneal injection, or oral (gavage) to compare 24-hour 

urinary and fecal elimination by these administration routes. Results from comparative studies of oral, 

intravenous, and intraperitoneal administration of glyphosate indicated that urinary radioactivity 

represented the amount of glyphosate absorbed and fecal radioactivity represented the amount of 

unabsorbed glyphosate following oral exposure. Although quantitative data were not included in the 

study report, the study authors estimated that 30–34% of the oral doses of 14C-glyphosate was absorbed

and excreted in the urine. Therefore, approximately 66–70% was unabsorbed and eliminated in the feces.

Very little ingested glyphosate is eliminated via routes other than feces and urine. Among SpragueDawley rats administered radiolabeled glyphosate (>99% purity) by a single gavage dose, <0.27% of the 

administered radioactivity was recovered in expired air at 24 hours postdosing (EPA 1993).

3.1.4.3 Dermal Exposure 

No information was located regarding elimination or excretion following known dermal exposure to 

glyphosate in humans. However, in a study that evaluated urinary glyphosate levels in 48 farmerapplicators involved in application of glyphosate-containing products, mean urinary glyphosate was 

higher among those farmers (14/48) who did not use rubber gloves, indicating that some glyphosate had 

been absorbed through the skin (Acquavella et al. 2004). Limited information is available for laboratory 

animals. Wester et al. (1991) applied a 14C-labeled Roundup® formulation to the abdominal skin of 

Rhesus monkeys (in vivo) to evaluate dermal absorption of glyphosate. Twelve-hour application of the 

test substance at concentrations of 25 or 270 μg/cm2resulted in 7-day recovery of 0.8 and 2.2% of the 

applied dose, respectively, in the urine and 3.6 and 0.7%, respectively, in the feces.

3.1.4.4 Other Routes of Exposure

Male and female Sprague-Dawley rats were administered 14C-glyphosate via intraperitoneal injection at 

1,150 mg/kg (EPA 1993). Assuming first-order kinetics, the half-life of elimination from the bone 

marrow was estimated at 7.6 and 4.2 hours for males and females, respectively. A half-life for 

elimination of radioactivity from plasma was approximately 1 hour for both sexes. These results indicate 

that glyphosate reaching the blood was rapidly eliminated and that the small fraction reaching bone 

marrow was rapidly eliminated. Anadón et al. (2009) reported a half-time of 9.99 hours for elimination of 
GLYPHOSATE 152

3. TOXICOKINETICS, SUSCEPTIBLE POPULATIONS, BIOMARKERS, CHEMICAL INTERACTIONS

glyphosate from the blood of male Wistar rats administered glyphosate (95% purity) via intravenous 

injection at 100 mg/kg. 

3.1.5 Physiologically Based Pharmacokinetic (PBPK)/Pharmacodynamic (PD) Models 

PBPK models use mathematical descriptions of the uptake and disposition of chemical substances to 

quantitatively describe the relationships among critical biological processes (Krishnan et al. 1994). PBPK 

models are also called biologically based tissue dosimetry models. PBPK models are increasingly used in 

risk assessments, primarily to predict the concentration of potentially toxic moieties of a chemical that 

will be delivered to any given target tissue following various combinations of route, dose level, and test 

species (Clewell and Andersen 1985). Physiologically based pharmacodynamic (PBPD) models use 

mathematical descriptions of the dose-response function to quantitatively describe the relationship 

between target tissue dose and toxic endpoints. 

PBPK models for glyphosate were not located.

3.1.6 Animal-to-Human Extrapolations 

No information was located to suggest significant differences between animals and humans regarding the 

toxicokinetics of glyphosate.

3.2 CHILDREN AND OTHER POPULATIONS THAT ARE UNUSUALLY SUSCEPTIBLE

This section discusses potential health effects from exposures during the period from conception to 

maturity at 18 years of age in humans. Potential effects on offspring resulting from exposures of parental 

germ cells are considered, as well as any indirect effects on the fetus and neonate resulting from maternal 

exposure during gestation and lactation. Children may be more or less susceptible than adults to health 

effects from exposure to hazardous substances and the relationship may change with developmental age. 

This section also discusses unusually susceptible populations. A susceptible population may exhibit 

different or enhanced responses to certain chemicals than most persons exposed to the same level of these 

chemicals in the environment. Factors involved with increased susceptibility may include genetic 

makeup, age, health and nutritional status, and exposure to other toxic substances (e.g., cigarette smoke). 

These parameters can reduce detoxification or excretion or compromise organ function. 
GLYPHOSATE 153

3. TOXICOKINETICS, SUSCEPTIBLE POPULATIONS, BIOMARKERS, CHEMICAL INTERACTIONS

Populations at risk of exposure to glyphosate at unusually high levels are discussed in Section 5.7, 

Populations with Potentially High Exposures.

Limited information was located regarding possible age- or gender-related differences in susceptibility to 

toxic effects from glyphosate technical or glyphosate formulations. Mao et al. (2018) added glyphosate 

or Roundup Bioflow® to the drinking water of rat dams from GD 6 through lactation and to their 

offspring up to postpartum day 125 at a concentration resulting in a dose of 1.25 mg glyphosate/kg/day. 

Microbiome profiling of the gut resulted in significant changes in overall bacterial composition in the 

pups only (particularly apparent prior to puberty); this effect was noted for glyphosate and for Roundup 

Bioflow®. Romano et al. (2010) employed Roundup Transorb® as a test substance and found decreased 

serum testosterone in young male rats gavaged at a dose as low as 5 mg/kg/day; however, the effect may 

have been caused, at least in part, by other ingredients in the glyphosate formulation.

3.3 BIOMARKERS OF EXPOSURE AND EFFECT 

Biomarkers are broadly defined as indicators signaling events in biologic systems or samples. They have 

been classified as biomarkers of exposure, biomarkers of effect, and biomarkers of susceptibility 

(NAS/NRC 1989).

A biomarker of exposure is a xenobiotic substance or its metabolite(s) or the product of an interaction 

between a xenobiotic agent and some target molecule(s) or cell(s) that is measured within a compartment 

of an organism (NAS/NRC 1989). The preferred biomarkers of exposure are generally the substance 

itself, substance-specific metabolites in readily obtainable body fluid(s), or excreta. Biomarkers of 

exposure to glyphosate are discussed in Section 3.3.1. The National Report on Human Exposure to 

Environmental Chemicals provides an ongoing assessment of the exposure of a generalizable sample of 

the U.S. population to environmental chemicals using biomonitoring (see http://www.cdc.gov/

exposurereport/). If available, biomonitoring data for glyphosate from this report are discussed in 

Section 5.6, General Population Exposure. 

Biomarkers of effect are defined as any measurable biochemical, physiologic, or other alteration within an 

organism that (depending on magnitude) can be recognized as an established or potential health 

impairment or disease (NAS/NRC 1989). This definition encompasses biochemical or cellular signals of 

tissue dysfunction (e.g., increased liver enzyme activity or pathologic changes in female genital epithelial 

cells), as well as physiologic signs of dysfunction such as increased blood pressure or decreased lung 
GLYPHOSATE 154

3. TOXICOKINETICS, SUSCEPTIBLE POPULATIONS, BIOMARKERS, CHEMICAL INTERACTIONS

capacity. Note that these markers are not often substance specific. They also may not be directly 

adverse, but can indicate potential health impairment (e.g., DNA adducts formed by covalent bonding of a 

chemical to DNA, the formation of which can induce abnormal replication, mutation, and/or prevent 

proper DNA repair). Biomarkers of effect caused by glyphosate are discussed in Section 3.3.2.

A biomarker of susceptibility is an indicator of an inherent or acquired limitation of an organism's ability 

to respond to the challenge of exposure to a specific xenobiotic substance. It can be an intrinsic genetic or 

other characteristic or a preexisting disease that results in an increase in absorbed dose, a decrease in the 

biologically effective dose, or a target tissue response. If biomarkers of susceptibility exist, they are 

discussed in Section 3.2, Children and Other Populations that are Unusually Susceptible.

3.3.1 Biomarkers of Exposure

Glyphosate and the metabolite, AMPA, have been measured in blood and urine (e.g., Connolly et al. 

2018; Conrad et al. 2017; Mills et al. 2017; Soukup et al. 2020; Zhang et al. 2020; Zoller et al. 2020;

Zouaoui et al. 2013). However, most absorbed glyphosate is rapidly excreted as parent compound, and 

urine is generally considered to be a stronger biomarker of exposure given that the level of detection

(LOD) for glyphosate in urine is much lower than the LOD for glyphosate in blood (see Table 5-4). 

Meaningful quantification of exposure would require analysis of blood and/or urine within hours 

following exposure, though a case study on glyphosate poisoning reported plasma glyphosate levels over 

the course of 2 to 3 days, rather than hours (Talbot et al. 1991).

3.3.2 Biomarkers of Effect

No information was located regarding biomarkers of effect specific to glyphosate toxicity.

3.4 INTERACTIONS WITH OTHER CHEMICALS 

Information on the toxicological effects of glyphosate interacting with other chemicals such as inert 

ingredients is limited. Inert ingredients include other substances that alter the physico-chemical properties 

to improve plant absorption or stability of the active ingredient(s) (Defarge et al. 2016). Inert ingredients 

include surfactants. Surfactants such as polyethoxylated tallow amine (POEA) in glyphosate-containing 

products might enhance the toxicity of glyphosate; results from one study indicate that the surfactant may 

be more acutely toxic than glyphosate or the combination of glyphosate and POEA (e.g., Adam et al. 

1997). In an in vitro study using three human embryotic cell lines (kidney, liver, and placenta), glyphosate 
GLYPHOSATE 155

3. TOXICOKINETICS, SUSCEPTIBLE POPULATIONS, BIOMARKERS, CHEMICAL INTERACTIONS

formulations and formulation additives were found to be more toxic than glyphosate technical alone. 

Based on measured cytotoxicity evaluated via mitochondrial respiration, membrane disruption, and 

caspases 3/7 activity, the glyphosate formulations were more toxic than glyphosate alone, and the 

adjuvants POE-15 and Genamin were more toxic than either the glyphosate formulations or glyphosate 

alone (Mesnage et al. 2013).

Increased toxicity of glyphosate formulations compared to glyphosate technical was also observed in 

another in vitro study. Defarge et al. (2016) observed in vitro that co-formulants including 

polyethoxylated tallow amine (POEA), alkyl polyglucoside (APG), polyoxyethylenealkyl ether phosphate 

(POE-APE), quaternary ammonium compound (QAC) and glyphosate formulations (inert and glyphosate 

combined) to exert toxic effects far greater than glyphosate alone. Cytotoxicity was determined by 

measuring mitochondrial respiration and endocrine disrupting activity was measured by aromatase 

activity inhibition. Although, Defarge et al. did not find that glyphosate inhibited mitochondrial 

respiration, disturbed cell membranes, or disrupted endocrine activity, co-formulants APG and POAE 

were up to 18 times and 200 times more cytotoxic than glyphosate, respectively, and co-formulants and 

glyphosate-based herbicide formulations were cytotoxic at concentration 18-2000 times and 8-141 times 

lower, than the recommended agricultural dilution of 1%, respectively. In short, co-formulants POEA, 

APG, POE-APE, QAC and glyphosate formulation including R classic were found to be more toxic than 

the active ingredient glyphosate.
GLYPHOSATE 156

CHAPTER 4. CHEMICAL AND PHYSICAL INFORMATION

4.1 CHEMICAL IDENTITY 

Glyphosate is an organic acid composed of a phosphonomethyl and glycine component. The chemical 

name for glyphosate is N-(phosphonomethyl) glycine. Glyphosate is a zwitterion with four distinct 

dissociation constants (pKa values are depicted below) and exists as different ionic species depending on 

the pH of its surroundings. Glyphosate is an amphoteric chemical and may react as an acid or a base 

under certain conditions.

OH

P

OH

O

N

H2

+

O

OH O

P

OH

O

N

H2

+

O

OH

O

P

OH

O

N

H2

+

O

O

O

P

O

O

N

H2

+

O

O

O

P

O

O

NH

O

O

pKa < 2 pKa = 2.6 pKa = 5.6 pKa =10.6

Glyphosate isopropylamine (Chemical Abstracts Registry Number [CASRN] 38641-94-0) is one of the 

salt forms of glyphosate used in commercial herbicides employing glyphosate as an active ingredient. 

This substance is registered as a pesticide by the EPA (1993) and is used to control broadleaf weeds and 

grasses; in food and nonfood settings, flower gardens, lawns, turf, residential areas, and forests; and along 

roadsides. Use of glyphosate as a pesticide outside of an agricultural context would be considered nonagricultural. Some labels may list the active ingredient in a formulation of glyphosate and the acid 

equivalents (AE), which is the theoretical yield of the parent acid from the formulated ester or salt. For 

example, the AE of glyphosate isopropylamine salts is 74%. 

Detailed information on the chemical identity of glyphosate and glyphosate isopropylamine is provided in

Table 4-1.

4.2 PHYSICAL AND CHEMICAL PROPERTIES 

Detailed information on the physical and chemical properties of glyphosate and glyphosate 

isopropylammonium is provided in Table 4-2.
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4. CHEMICAL AND PHYSICAL INFORMATION

Table 4-1. Chemical Identity of Glyphosate and Glyphosate Isopropylaminea

Characteristic Information

Chemical name Glyphosate Glyphosate isopropylamine

Synonym(s) Glyphosphate; N-(phosphonomethyl) Glycine, N-(phosphonomethyl)-, compound 

glycine; phosphonomethyliminoacetic with 2-propanamine (1:1); glyphosateacid; glyphosate acid isopropylammonium; glyphosate 

mono(isopropylamine) salt; glyphosatemono(isopropylammonium); 

N-(phosphonomethyl)glycine, 

isopropylamine salt

Partial list of Pondmaster; Roundup® Max; Roundup®; Rondo; Rodeo; Glifonox; Glycel; 

b registered trade Glifoglex; Glycel; Muster; Rondo; MON-0139; CP 70139; Shackle

name(s) Sonic; Spasor; Sting; Tumbleweed; 

MON-0573; CP 67573

Chemical formula C3H8NO5P C3H8NO5P.C3H9N

Chemical structure

CAS Registry 1071-83-6 38641-94-0

Number

aAll information obtained from McBean (2011), O’Neil et al. (2013), and/or ChemIDplus (2017) unless noted 

otherwise.

bEPA 1993.

CAS = Chemical Abstracts Service
GLYPHOSATE 158

4. CHEMICAL AND PHYSICAL INFORMATION

Table 4-2. Physical and Chemical Properties of Glyphosate and its 

Isopropylamine Salta

Property Glyphosate Glyphosate isopropylamine salt

Molecular weight 169.1 228.2

Color White White

Physical state Solid; crystals Powder

Melting point 230°C (decomposes) Two stages: 143–164 and 189–223°C

Boiling point No data Decomposes without boiling

Density at 20°C 1.705 1.482

Odor Odorless Odorless

Odor threshold:

Water No data No data

Air No data No data

Solubility:

Water at 25°C 12,000 mg/L

10,500 mg/L (pH 1.9, 20°C)

1,050,000 mg/L (pH 4.3, 25°C)

Organic solvent(s) Insoluble in most organic solvents: 

acetone, ethanol, and xylene

Dichloromethane 184 mg/L at 20°C; methanol 

15,880 mg/L at 20°C

Dissociation 

constants:

pKa1 0.8; pKa2 3; pKa3 6; pKa4 11;

pKa1

b <2; pKa2b 2.6; pKa3b 5.6;

pKa4

b 10.6

pKa1 2.18 at 20°C (monophosphate); 

pKa2 5.77 at 20°C (carboxylic acid) 

Partition coefficients:

Log Kow <-3.4 -5.4

Log Koc 3.4–3.7 (Koc=2,600–4,900)c

-2.8–3.1 (Koc=0.00169–2,080 L/kg)

d

3.3 (Koc = 2,080 L/kg)d

Vapor pressure at 

25°C

9.8x10-8 mmHg 1.58x10-8 mmHg

Henry's law constant 2.1x10-12 atm-m3

/mol at 25°Cd 3.3x10-15 atm-m3

/mol at 25°Ce

Autoignition 

temperature

No data No data

Flashpoint Not flammable No data

Flammability limits No data No data

Explosive limits No data No data

aAll information obtained from either McBean (2011) or O’Neil et al. (2013).

bSprankle et al. 1975.

cGlass 1987.

dPredicted values from EPA CompTox Chemicals Dashboard

dEPI Suite 2012.
GLYPHOSATE 159

CHAPTER 5. POTENTIAL FOR HUMAN EXPOSURE

5.1 OVERVIEW 

Glyphosate has not been identified in any of the 1,832 hazardous waste sites that have been proposed for 

inclusion on the EPA National Priorities List (NPL) (ATSDR 2015). However, the number of sites 

evaluated for glyphosate is not known. 

• Occupational and residential exposure is a result of glyphosate’s use in agricultural, industrial, 

and residential settings. The highest potential for dermal, inhalation, and ocular exposure is 

expected for pesticide applicators, farm workers, and home gardeners who use herbicides 

containing glyphosate. 

• The general population is exposed to glyphosate via ingestion of crops, plants, and foods with 

residues of this chemical. Residential exposure may occur via inhalation, dermal contact, and/or 

ocular contact during mixing or application of consumer products containing glyphosate or by 

coming into contact with crops, soils, or water to which glyphosate-containing products have 

been applied. 

• Occupational exposure to glyphosate may occur via inhalation, dermal contact, and/or ocular 

contact during manufacture, transport, mixing, loading, application, and disposal processes. 

Accidental oral exposure may occur via unintentional ingestion. Dermal contact appears to be 

the major route of exposure to glyphosate for individuals involved in its application.

• Glyphosate mainly enters the environment as a direct result of its herbicidal use. Fate of this 

chemical in the environment includes degradation, transport, and partitioning processes, which 

are governed by its physicochemical properties and by abiotic or biotic degradation under certain 

environmental conditions. Glyphosate is a nonvolatile, highly polar, non-residual herbicide that 

has low potential for environmental persistence and is unlikely to bioaccumulate.

5.2 PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL 

5.2.1 Production

No information is available in the Toxics Release Inventory (TRI) database on facilities that manufacture 

or process glyphosate because this chemical is not required to be reported under Section 313 of the 

Emergency Planning and Community Right-to-Know Act (Title III of the Superfund Amendments and 

Reauthorization Act of 1986) (EPA 2005b).

Production of glyphosate is achieved through heating phosphorous acid and a-amino acetic acid followed 

by the addition of formaldehyde (Muller and Applebyki 2010). Glyphosate may also be produced by 

heating glycine and chloromethylphosphonic acid in aqueous sodium hydroxide (IPCS 1994). 
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5. POTENTIAL FOR HUMAN EXPOSURE

Glyphosate is produced commercially in the United States as a technical-grade substance with a purity 

≥80%, but usually over 90% (IPCS 1994, McBean 2011). 

Glyphosate is typically manufactured for commercial use as a salt available in soluble liquid and soluble 

granule formulations. Salt forms of glyphosate include the isopropylamine salt, sodium salt, and 

monoammonium salt. Table 5-1 summarizes some of the common glyphosate salts that may be used as 

active ingredients in herbicides. Due to the various salt forms, the active ingredient listed on products is 

sometimes expressed in terms of acid equivalent. 

Table 5-1. Glyphosate Salts

Name

CAS Registry 

Number

EPA 

PC Code Cation U.S. registrationa

Glyphosate isopropylamine salt 38641-94-0 103601 Yes

Glyphosate mono ammonium 40465-66-5 103604 NH4

+ Yes

Glyphosate ethanolamine salt 40465-76-7 103605 Yes

Glyphosate triammonium salt 114370-14-8 103607 NH4

+ Yes

Glyphosate diammonium salt 69254-40-6 103607 NH4

+ Yes

Glyphosate dimethylammonium salt 34494-04-7 103608 Yes

Glyphosate potassium salts 70901-12-1; 

70901-20-1; 

39600-42-5

103613 Yes

Glyphosate monosodium salt 34494-03-6 103603 No

Glyphosate sesquisodium salt 70393-85-0 103603 No

Glyphosate trimesium 81591-81-3 128501 No

aPan 2014

CAS = Chemical Abstracts Service; EPA = U.S. Environmental Protection Agency; PC = pesticide chemical

Herbicide formulations employing glyphosate salts are commonly produced in combination with 

additives, inert ingredients, and surfactants. The salt derivatives enhance absorption of glyphosate from 

the surface of the plant or leaf structure, but are not the herbicidally active portion of the compound. 

Specific formulations vary in composition and are marketed under numerous trade names (NPIRS 2017; 

PAN 2009). Polyoxyethylene amine (POEA) (CASRN 24911-53-5) is a surfactant used in the 

NH3+

3CH CH3

OH

NH3+

H

N

+

H

3CH CH3

K

+

Na

+

Na

+

S

+

3CH

CH3

CH3
GLYPHOSATE 161

5. POTENTIAL FOR HUMAN EXPOSURE

commercial product Roundup® (PAN 2009). Surfactants are used in herbicide formulations to increase 

penetration of glyphosate into plants. Sulfuric acid (CASRN 7664-93-9), phosphoric acid (CASRN 7664-

38-2), propylene glycol (CASRN 57-55-6), and sodium benzoate (CASRN 532-32-1) are examples of 

additives used in some formulations (IPCS 1994; PAN 2009). Products may contain other active 

ingredients such as simazine (CASRN 122-34-9) and 2-methyl-4-chlorophenoxyacetic acid (CASRN 94-

74-6). The herbicide 2,4-dichlorophenoxyacetic acid (CAS 94-75-7) may also be present at 

concentrations ranging from 11.1 to 20.6% (IPCS 1994). Commercial products containing glyphosate 

have been reported with concentrations ranging from 0.96 to 94 w/w%. The common herbicide,

Roundup®, has product formulations containing glyphosate concentrations ranging from 0.96% to 71% 

(w/w) (NPIRS 2017; PAN 2016b). These products may be diluted depending upon the labeled use as per 

manufacturers specifications. 

The introduction of glyphosate-resistant crops such as soybeans in 1996, canola and cotton in 1997, and 

maize in 1998, along with the distribution of their genetically engineered seeds, had major impacts on the 

production and demand for glyphosate. 

According to the National Pesticide Information Retrieval System (NPIRS), as of May 2017, there were 

43 companies manufacturing EPA federally registered products under the active pesticide code 417300 

(glyphosate) (since many chemical names are too long to be handled easily, EPA assigns a 6-digit 

chemical code number for every active chemical ingredient), which are available for use in the United 

States; see Table 5-2 (NPIRS 2017). In addition, there were 72 companies in the United States that were 

manufacturing chemicals under the active pesticide code 103601 (glyphosate isopropylamine salt) 

(NPIRS 2017). 

Table 5-2. Companies Manufacturing Products Under 

Pesticide Code 417300 (Glyphosate)

Company Address City, State, Zip Code

Syngenta Crop Protection, LLC 410 Swing Road Greensboro, North Carolina 27419

The Scotts Company D/B/A The Ortho Group, 

14111 Scottslawn Road

Marysville, Ohio 43041

FMC Corporation, Agricultural 

Products Group

1735 Market Street Philadelphia, Pennsylvania 19103

Monsanto Company Chesterfield Village Research 

Center, 700 Chesterfield 

Parkway North

Chesterfield, Missouri 63017

Winfield Solutions, LLC P.O. Box 64589 St. Paul, Minnesota 55164
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5. POTENTIAL FOR HUMAN EXPOSURE

Table 5-2. Companies Manufacturing Products Under 

Pesticide Code 417300 (Glyphosate)

Company Address City, State, Zip Code

ABC Compounding Co., Inc. P.O. Box 16247 Atlanta, Georgia 30321

Cheminova A/S P.O. Box 9 DK-7620 Lemvig

Helena Chemical, Co. 225 Schilling Boulevard, 

Suite 300

Collierville, Tennessee 38017

Chemsico, A Division of United 

Industries Corporation

P.O. Box 142642 St. Louis, Missouri 63114

Adama Agan Ltd P.O. Box 262 Ashdod, 77102, Israel

Drexel Chemical Company P.O. Box 13327 Memphis, Tennessee 38113

Loveland Products, Inc. P.O. Box 1286 Greeley, Colorado 80632

Nufarm Limited 103–105 Pipe Road Laverton North, Victoria 3026 Australia

Albaugh, LLC P.O. Box 2127 Valdosta, Georgia 31604

Atanor S.A. Foreign Trade Department, 

Albarellos 4914

B1605 AFR, Munro, Providence de 

Buenos Aires

BASF Sparks, LLC P.O. Box 13528 Research Triangle Park, North Carolina 

27709

Control Solutions, Inc. 5903 Genoa-Red Bluff Road Pasadena, Texas 77507

Tenkoz, Inc. 1725 Windward Concourse Alpharetta, Georgia 30005

Dow AgroSciences, LLC 9330 Zionsville Rd 308/2e Indianapolis, Indiana 46268

Makhteshim Agan of North 

America, Inc.

d/b/a Adama, 3120 Highwoods 

Boulevard, Suite 100

Raleigh, North Carolina 27604

United Phosphorus, Inc. 630 Freedom Business Center, 

Suite 402

King of Prussia, Pennsylvania 19406

Monsanto Company Lawn & Garden Products, 

600 13th Street, NW, Suite 660

Washington, DC 20005

Helm Agro US, Inc. 401 E. Jackson Street, 

Suite 1400

Tampa, Florida 33602

Mey Corporation 121 South Estes Drive, 

Suite 101

Chapel Hill, North Carolina 27514

Sharda Cropchem, Limited Domnic Holm, 29th Road Bandra (West), Mumbai 400050

Rotam Agrochemical Company, 

Ltd.

26/F, E-Trade Plaza, 24 Lee 

Chung Street

Chaiwan, Hong Kong

Sharda USA LLC P.O. Box 640 Hockessin, Delaware 19707

Ragan and Massey, Inc. 101 Ponchatoula Parkway Ponchatoula Louisiana 70454

Tide International, USA, Inc. 21 Hubble Irvine, California 92618

Agsaver II, LLC P.O. Box 111 McGehee, Arkansas 71654

Repar-Glypho, LLC 8070 Georgia Avenue, 

Suite 209

Silver Spring, Maryland 20910

Farmway, Inc. P.O. Box 640 Hockessin, Delaware 19707

Consus Chemicals, LLC 22 Pine Tree Drive Wayne, New Jersey 07470

Axss Technical Holdings, LLC 111 Martin Road Fulton, Mississippi 38843

Cinmax International, LLC 3050 Suite 113 Bloomington, Minnesota 55425
GLYPHOSATE 163

5. POTENTIAL FOR HUMAN EXPOSURE

Table 5-2. Companies Manufacturing Products Under 

Pesticide Code 417300 (Glyphosate)

Company Address City, State, Zip Code

Agromarketing Co., Inc. 133 Mavety Street Toronto, Ontario, Canada M6P

Glysorttech, LLC 281 Hampshire Drive Plansboro, New Jersey 08536

Liberty Crop Protection, LLC 4850 Hahns Peak Drive, 

Suite 200

Loveland, Colorado 80538

Gly-Peak, LLC 224 South Bell Avenue Ames, Iowa 60010

Tundra Agroindustrial, Ltd. P.O. Box 10 Lemars, Iowa 51031

Argustoli H.C., LLC 10191 Park Run Drive, 

Suite 110

Las Vegas, Nevada 89145

Genmerica NA LLC P.O. Box 1603 Cheyenne, Wyoming 

Gruhn Mill Crop Solutions, LLC 701 Fifth Avenue, Suite 6100 Seattle, Washington 98104

Source: NPIRS 2017 

5.2.2 Import/Export

No information was found concerning U.S. imports and exports of glyphosate.

5.2.3 Use

Glyphosate is a phosphonoglycine herbicide, first registered for use by the EPA in 1974. In June 1986, 

glyphosate was issued a Registration Standard (EPA 1986c) requiring additional data, which included 

phytotoxicity, environmental fate, toxicology, product chemistry, and residue chemistry studies; 

reregistration of single active ingredient formulations, plus one additional active ingredient formulation,

were finalized in 1993 (EPA 1993). Glyphosate is registered for pre- and post-emergent applications for 

weed control in the production of various fruit, vegetable, and field crops. Glyphosate may be applied to 

fields prior to planting in order to remove unwanted weeds and vegetation or in preparation for harvesting 

in glyphosate resistant crops. Recommended application rates, methods of application and timing, 

temperature considerations, etc. may be found on individual product labels. Glyphosate is in the process 

of registration review by EPA; docket ID: EPA-HQ-OPP-2009-0361-0066 (EPA 2017c).EPA published 

an interim registration review decision in January 2020; docket ID: EPA-HQ-OPP-2009-0361 (EPA 

2020), which will be finalized after an EPA Endocrine Disruptor Screening Program FFDCA 
GLYPHOSATE 164

5. POTENTIAL FOR HUMAN EXPOSURE

determination, evaluation of glyphosate under the Endangered Species Act, and the resolution of a 

petition by the Environmental Working Group.

Glyphosate is used as a non-selective contact herbicide. Formulations are applied directly to control 

native and invasive weeds and vegetation around food crops and non-food field crops, and in non-crop 

areas such as roadsides, golf courses, right-of-way locations, and aquatic areas. Glyphosate is used in 

agriculture, forestry, industrial, lawn and garden, and aquatic (e.g., Rodeo®, Clearcast®) environments 

for weed control. In aquatic usage, the formulation typically contains no surfactant or a surfactant that is 

nontoxic to aquatic organisms and applications must be made as per the product instructions to avoid 

rapid vegetative decay, which can lead to anaerobic environments and potential fish kills (Dow 2017). 

Glyphosate is applied to control broad-leaved weeds and woody brush, as well as annual and perennial 

grasses (Muller and Applebyke 2010; Plimmer et al. 2004). The sodium salt (CASRN 34494-03-6) can 

be used as a plant growth regulator for peanuts and sugarcane (EPA 1993). Glyphosate is a foliar-applied 

herbicide. Before the introduction of genetically modified glyphosate-resistant crops, application 

generally occurred before crops were planted (Duke and Powles 2008). After successful production and 

approval of glyphosate-resistant crops, such as soybean, cotton, maize, and canola, application generally 

occurs after planting and before harvest; the timing depends on the specific application (Duke and Powles 

2008; Muller and Applebyke 2010). The introduction of these glyphosate-resistant crops increased the 

use of herbicidal products containing this chemical because it is possible to use it post-emergence without 

actually harming the crop. Greater than 90% of the soybeans produced in the United States are 

glyphosate tolerant, and most cotton (72%) and about half of the corn (52%) planted in 2007 were

glyphosate tolerant (Coupe et al. 2012). It has been estimated that genetically engineered glyphosatetolerant crops now account for about 56 % of its global usage (Benbrook 2016). Application techniques 

include aerial treatments, typically used for large-scale purposes, and wiping equipment or spraying 

equipment attached to vehicles, generally used for small-scale applications (FAO 1997; IPCS 1994).

Newer application practices, such as the addition of glyphosate to crops to simplify the harvesting process

(referred to as “green burndown”), may have implications for usage rates of the herbicide (Zhang et al. 

2019a). 

According to data from the Pesticide Action Network (PAN) Pesticide Database, there are 102 products 

containing glyphosate (CASRN 1071-83-6) as the active ingredient, 94 of which have active registrations 

in the United States. There are 848 products containing glyphosate isopropylamine salt (CASRN 38641-
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94-0) as the active ingredient, of which 739 have active registrations in the United States (PAN 2016a, 

2016b).

Increasing trends in annual agricultural use data for the United States are reflected from the use statistics 

available from the U.S. Geological Survey (USGS) National Water-Quality Assessment (NAWQA) 

Program. Estimated yearly usage increased from approximately 20 to 60 million pounds from 1992 to 

1998, from approximately 70 to 130 million pounds from 1999 to 2003, from approximately 140 to 

250 million pounds from 2004 to 2011, and steady use of approximately 285–290 million pounds from 

2012 through 2014 (USGS 2017). Figure 5-1 illustrates the agricultural use of glyphosate from 1992 to 

2009 in the United States (USGS 2013). 

Figure 5-1. Agricultural Application Trends of Glyphosate in the United States 

According to U.S. Geological Survey (USGS) Data

Source: USGS 2017

Benbrook (2016) compiled data from the National Agricultural Statistical Service (NASS) to estimate the 

amount of glyphosate applied for weed control in the production of major agricultural crops and nonagricultural (residential uses) in the United States from 1990–2014. The trends are summarized in Table 

5-3.
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Table 5-3. Glyphosate AI (Pounds) Usage Trends from 1990 to 2014

Crop 1990 Active ingredient (pounds) 2014 Active ingredient (pounds) % Increase

Soybean 2,663,000 122,473,987 4,499.10%

Corn 880,066 68,949,452 7,734.58%

Cotton 192,429 17,421,787 8,953.62%

Wheat (winter) 331,758 12,353,488 3,623.64%

Alfalfa 381,525 8,853,600 2,220.58%

Sorghum 236,305 4,178,573 1,668.30%

Sugar beets 36,130 2,763,075 7,547.59%

Canola 0 219,392 NA

Wheat (spring) 75,308 1,201,807 1,495.86%

Barley 13,1568 1,064,160 708.83%

Other cops 1,897,522 4,526,043 138.52%

Total 7,683,070 249,906,307 3,152.69%

Non-Agricultural Use

5,300,000 26,519,000 400.36%

Source: Benbrook 2016

The EPA recently granted the registration of a new herbicide named Enlist DuoTM containing 2,4-D 

choline salt and glyphosate for use on genetically modified corn and soybean crops designed to be 

resistant to 2,4-D and glyphosate (EPA 2014). 

5.2.4 Disposal

Wastes resulting from products containing glyphosate should be disposed of at an approved waste 

disposal facility or in landfills approved for pesticide disposal. Disposal practices should be in 

accordance with federal, state, and local procedures. Non-refillable containers should never be reused. 

Empty containers should be rinsed thoroughly and offered for recycling, if available, or disposed of in 

accordance with container labels. Rinse-water can be emptied into formulation equipment and applied as 

residual pesticide in the appropriate manner. Do not contaminate fresh waters when disposing of 

equipment wash waters or container rinse waters. Containers that have not been completely rinsed may 

be considered hazardous and should be disposed of with regard to federal, state, and local regulations.

Any unused product may be recycled by applying the product in an approved use setting or returning it to 

the manufacturer or supplier for safe disposal (Agrisolutions 2010; EPA 1993, 2011). 
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5.3 RELEASES TO THE ENVIRONMENT 

TRI data should be used with caution because only certain types of facilities are required to report (EPA 

2005b). This is not an exhaustive list. Manufacturing and processing facilities are required to report 

information to the TRI only if they employ ≥10 full-time employees; if their facility is included in 

Standard Industrial Classification (SIC) Codes 10 (except 1011, 1081, and 1094), 12 (except 1241), 20–

39, 4911 (limited to facilities that combust coal and/or oil for the purpose of generating electricity for 

distribution in commerce), 4931 (limited to facilities that combust coal and/or oil for the purpose of 

generating electricity for distribution in commerce), 4939 (limited to facilities that combust coal and/or 

oil for the purpose of generating electricity for distribution in commerce), 4953 (limited to facilities 

regulated under RCRA Subtitle C, 42 U.S.C. section 6921 et seq.), 5169, 5171, and 7389 (limited S.C. 

section 6921 et seq.), 5169, 5171, and 7389 (limited to facilities primarily engaged in solvents recovery 

services on a contract or fee basis); and if their facility produces, imports, or processes ≥25,000 pounds of 

any TRI chemical or otherwise uses >10,000 pounds of a TRI chemical in a calendar year (EPA 2005b).

No information is available in the TRI database on facilities that manufacture or process glyphosate 

because this chemical is not required to be reported under Section 313 of the Emergency Planning and 

Community Right-to-Know Act (Title III of the Superfund Amendments and Reauthorization Act of 

1986) (EPA 2005b).

The use of glyphosate as an herbicide for crops and non-crop applications is the major source of 

glyphosate that intentionally enters the environment. Some glyphosate may be released from the 

manufacture, transport, and disposal of glyphosate or glyphosate-containing products. The majority of 

herbicidal formulations with glyphosate are directly applied to weeds to remove unwanted vegetation in 

residential and agricultural settings. Depending on its application, glyphosate may enter aquatic 

environments through direct application to control aquatic weeds (Dow 2017) or as a result of overspray 

in areas near aquatic environments. Aerial applications of glyphosate may result in unintended transport,

depending on application technique and meteorological conditions, such as wind drift (EPA 1993; IPCS 

1994; PAN 2009; Yates et al. 1978).

5.3.1 Air 

There is no information on releases of glyphosate to the atmosphere from manufacturing and processing 

facilities because these releases are not required to be reported (EPA 2005b).
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Glyphosate released to the air from aerial and ground equipment has the potential for downwind transport. 

Yates et al. (1978) assessed the loss due to drift after application. The lowest drift losses resulted when 

ground sprayers operating at low pressure were employed. The highest drift losses occurred when jet 

nozzles were employed during aerial application performed by helicopter.

The Air Quality System (AQS) database is EPA’s repository of criteria air pollutants and hazardous air 

pollutants (HAPs), containing monitoring data from >2,600 monitoring sites across the United States. 

Glyphosate has not been included in the AQS ambient air monitoring data as of 2016 (EPA 2017a).

5.3.2 Water 

There is no information on releases of glyphosate to water from manufacturing and processing facilities 

because these releases are not required to be reported (EPA 2005b). 

Glyphosate may enter surface water systems either directly as a result of its aquatic use or indirectly due 

to overspray near surface water. Aquatic applications of glyphosate are used to control invasive aquatic 

species such as water chestnut (Trapa natans) or other labeled weeds (EPA 2010); however, no 

quantitative data are available regarding how much glyphosate is applied to aquatic waterways in the 

United States. Glyphosate may also enter surface waters indirectly due to transport of residues in run-off 

or erosion events. The amount of glyphosate transported to nearby water bodies from runoff and erosion 

is dependent upon several factors, including the frequency, timing, and application rate of glyphosate to 

nearby areas, meteorological conditions (e.g., rainfall events and duration), and the characteristics of the 

soils in the treated areas. Hydrological factors such as input to the waterbody from overland flow as 

compared to subsurface infiltration also effect potential pesticide loadings. Coupe et al. (2012) studied 

the glyphosate levels at three locations located in the United States (South Fork River Basin, Iowa; Sugar 

Creek River Basin, Indiana; and Bogue Phalia Basin, Mississippi). The basins are located in agricultural 

areas dominated by soybean, corn, rice, and cotton (Mississippi only) production, but have differing 

climates and soil characteristics. Water samples collected from 2007 to 2008 at three sites located in the 

Bogue Phalia basin all had detectable levels of glyphosate and its degradation product,

aminomethylphosphonic acid (AMPA). Glyphosate concentrations at the sites ranged from 0.03 to 73 

μg/L. Levels showed a distinctive seasonal pattern with lowest levels occurring in winter, followed by a 

steady increase into late fall, which coincided with seasonal application timings of glyphosate. Moreover, 

both glyphosate and AMPA loads into the basin were greater in 2008 as compared to 2007, which 

corresponded to a higher rainfall rate for that year. Approximately 59–72% of the water samples 
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collected from the South Fork River basin had detectable levels of glyphosate ranging from <0.02 to 5.7 

μg/L. Higher glyphosate loadings as a percentage of usage into the Bogue Phalia Basin as compared to 

the South Fork River Basin is a result of a higher overland flow in the basin (as compared to subsurface 

water infiltration) and the fact that the majority of soils in the Bogue Phalia Basin are characterized as 

heavy clay soils classified as hydrologic soil groups C and D, which have higher runoff potential than the 

predominant soil types in the South Fork River Basin. 

Glyphosate levels in the Sugar Creek River Basin, Indiana were limited to measurements taken during 

two heavy rainfall storm events in which 2.6 and 5.7 cm of rain were recorded. Glyphosate levels ranged 

from 0.16 to 430 μg/L, with the highest level recorded during the heavier rainfall event. 

Battaglin et al. (2005) discussed the occurrence of glyphosate in 51 streams in the Midwestern United 

States from pre-emergence, post-emergence, and harvest runoff samples. Maximum levels in runoff 

water ranged from 1.00 μg/L (pre-emergence runoff) to 8.7 μg/L in harvest season runoff samples. 

Glyphosate levels in surface water are summarized in Section 5.5.2. 

Aparicio et al. (2013) measured the environmental fate of glyphosate and AMPA in surface water of 

agriculture basins in Argentina. Forty-two streams were sampled in April, August and September of 2012. 

Between the collection months, glyphosate was measured in 4% to 35% of samples with levels ranging 

between trace to 7.6 μg l-1. AMPA was detected in up to 33% of samples collected and concentration 

levels were measured between non-detect to 2.3 μg l-1. There was a decrease in the number of samples 

detecting glyphosate or AMPA overtime, and this may be due to the dilution effect caused by rainfall, 

which was measured as 65.7 mm (April) and 253.5 mm (August) (Aparcio et al. 2013).

5.3.3 Soil 

There is no information on releases of glyphosate to soil from manufacturing and processing facilities 

because these releases are not required to be reported (EPA 2005b).

Glyphosate applied directly to vegetation may migrate to the soil from foliar washoff or translocation 

from the plants to the root zone. As discussed in Section 5.2.3, glyphosate agricultural uses in the United 

States increased from about 20 million pounds in 1992 to about 300 million pounds by 2014 (USGS 

2017). Battaglin et al. (2014) estimated that nonagricultural uses of glyphosate were about 9,300 metric 
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tons (20.5 million pounds) in the United States in 2007 and Benbrook (2016) estimated that about 

26.5 million pounds were used for nonagricultural purposes in 2014. 

A 2008 survey of pesticide application in Ontario, Canada, conducted by the Ministry of Agriculture, 

Food, and Rural Affairs reported that glyphosate use increased from an estimated 1,170,762 kg active 

ingredient in 2003 up to an estimated 2,062,648 kg active ingredient in 2008 (OMAFRA 2008). A total 

of 527,952 kg of glyphosate were used on field crops, 6,700 kg were used on fruit, 6,110 kg were used on 

vegetables, and 6,635 kg of glyphosate were used on nursery crops, sod, and ginseng; greenhouse crops 

were not included. Specific 2008 glyphosate applications for weed control by crop use amounted to 

527,952 kg in production of field corn, 1,253,773 kg for soybean production, 11,087 kg for canola, 

155,428 kg for wheat, 9,206 kg for oats, 6,588 kg for barley, 6,167 kg for mixed grains, 3,185 kg for rye, 

18,054 kg for white beans, 18,661 kg for dry beans, 27,011 kg for hay, 2,717 kg for pasture, 1,386 kg for

sugar beets, and 1,991 kg for other field crops (OMAFRA 2008).

A 2013/2014 survey of pesticide application in Ontario, Canada, conducted by the Ministry of 

Agriculture, Food, and Rural Affairs reported pesticide use for glyphosate (OMAFRA 2015). An 

estimated total of 2,909,184 kg of glyphosate were used on all surveyed field crops in 2013/2014; 13,194 

kg were used for fruit and 9,869 kg were used for vegetables. Specific crop use in 2013 for the amount of 

the active ingredient glyphosate applied as an herbicide equaled 1,151,051 kg for field corn, 1,544,954 kg 

for soybeans, 65,230 kg for wheat, 34,573 kg for oats and mixed grains, 11,542 kg for white beans, 

27,980 kg for hay and pasture, and 24,144 kg for other field crops (OMAFRA 2015).

5.4 ENVIRONMENTAL FATE 

The environmental fate of glyphosate, which includes the transport, partitioning, and transformation of 

this substance, is controlled by various physicochemical properties, degradation, and other loss processes. 

Glyphosate is a non-volatile, highly polar, non-residual herbicide that has low potential for environmental 

persistence and is unlikely to bioaccumulate; the chemical is either degraded or inactivated by adsorption 

to soil (Smith and Oehme 1992). Microbial degradation in soils and water is an important fate process; 

reported half-lives range from 2 to 215 days in soils and from 1.5 to 130 days in waters (Battaglin et al. 

2014; IPCS 1994; PAN 2009; Rueppel et al. 1977). The wide range of half-lives is a result of 

environmental conditions such as soil characteristics, pH, and endogenous microbial populations, which 

are factors that influence the rate of degradation. Glyphosate is not expected to be susceptible to 
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hydrolysis; photodegradation has not been confirmed as an important fate process in any environmental 

media (Smith and Oehme 1992).

5.4.1 Transport and Partitioning 

Glyphosate is not expected to change ionic form at pH levels of 5–8 and is expected to exist in its anionic 

form under most environmental conditions. 

Air. Glyphosate has a low vapor pressure and is expected to exist in the particulate phase in the ambient 

atmosphere. There is potential for spray drift after application of herbicides, the extent of which is 

dependent on the mode of application. Aerial applications may result in considerable transport depending 

on climate conditions (Silva et al. 2018; IPCS 1994; Yates et al. 1978). Drift analysis has shown that 10–

37% of applied herbicide can drift to non-target plants. Seedling and plant fatalities were found 20–100 

m downwind after application, and residues have been detected at 400 and 800 m downwind following 

ground and aerial applications, respectively (PAN 2009). Wind erosion is one pathway in which 

glyphosate and its primary metabolite, AMPA, are transported into the atmosphere; Silva et al. (2018) 

estimated wind only can contribute between 1941 to 30,000 mg/ ha-1 year-1in offsite transport in soils 

with low to medium and high glyphosate content, respectively (Silva et al. 2018). Furthermore, Bento et 

al. (2017), reported that glyphosate and AMPA content were highest in the smallest particle sample size 

(8 μm) tested across three soil types (clay, organic matter, and silt). Glyphosate concentration ranged 

between 5.5 to 15 μg/g and AMPA content ranged between 0.07 to 0.7 μg/g when particle sizes (8 μm to

715 μm) were analyzed. Because particles <20 μm can be transported in long-term suspension, it’s 

possible that combined with wind speeds, glyphosate particles have the potential to travel long distances 

and be transported into non-agricultural areas, particularly in conditions where topsoil is sufficiently dry

(Bento et al. 2017). 

Particulate-phase glyphosate can be removed from the atmosphere by wet or dry deposition. Wet 

deposition of glyphosate and its major degradation product, AMPA, from the atmosphere ranged from 3.9 

to 16 μg/m2and from 1.7 to 5.2 μg/m2, respectively, as reported in a study conducted in Pace, 

Mississippi, and Blairsburg, Iowa in 2007 and 2008 (Chang et al. 2011). In a study conducted in 2001, 

the total annual deposition for glyphosate was reported as 49,000 ng/m2and the maximum concentration 

detected was 6,200 ng/L. Glyphosate was detected in about 10% of the collected samples. The total 

annual deposition for AMPA was reported as 12,757 ng/m2and the maximum concentration detected was 

1,200 ng/L. The majority of glyphosate detections occurred during the spraying season. Deposition rates 
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and concentrations of glyphosate were higher at the urban sites; this was attributed to its non-agricultural 

uses. The concentration of glyphosate and several other herbicides/pesticides were monitored in 

rainwater in Belgium from 1997 to 2001, and glyphosate was found to have an average annual 

concentration of 78 ng/L. The concentration increased dramatically during spraying season, reaching a 

maximum of 6,200 ng/L (Quaghebeur et al. 2004).

Water. Depending on its application, glyphosate may enter aquatic environments through direct 

application, or as a result of overspray in areas near aquatic environments .Water erosion is another route 

in which glyphosate and AMPA are transported into surface water bodies; Silva et al. (2018) estimated

water erosion can contribute between 9753 to 47,557 mg/ ha-1 year-1in soils with low to medium and high 

glyphosate content, respectively (Silva et al. 2018). There is evidence of limited run-off and leaching 

with sandy soils and heavy rainfall (Borggaard and Gimsing 2008). Partitioning into aqueous 

environments is attenuated by adsorption to soils and sediments.

Sediment and Soil. Glyphosate will have strong adsorption to most soils due to its ionic nature and is 

expected to bind to positively charged metal surfaces present in clay and soils. Adsorption occurs 

through hydrogen bonding ion exchange or complexes of the phosphonate anion as well as the 

ammonium cation with minerals present in soils (Miles and Moye 1988). In an unpublished report by 

Monsanto in 1978, <0.1–6.6% of applied activity was recovered in the solution that washed off of the soil 

columns under leaching conditions simulating a heavy rainfall (IPCS 1994). The potential for run-off and 

leaching ability of glyphosate was examined by Rueppel et al. (1977) in three soils. Using inclined soil 

beds and artificial rainfall scenarios, a maximum runoff off <2x10-4 kg/ha was reported. Using thin layer 

chromatography and beta camera analysis, 97–100% adsorption to all three soils indicated that there is 

minimal possibility for leaching into groundwater. Although glyphosate is expected to adsorb strongly to 

soil particles and clay minerals, desorption may occur under certain conditions. It has been demonstrated 

that sorption decreases with increasing soil pH, increasing concentrations of inorganic soil phosphate, and 

decreasing mineral concentrations (Glass 1987; Gerritse et al. 1996; Piccolo et al. 1994; Plimmer et al. 

2004; Smith and Oehme 1992; Sprankle 1975). However, because of the strong sorption to most soils, 

mobility and the potential for migration into groundwater are low. It is known that glyphosate and 

AMPA strongly adsorb and accumulate in the top of soils (Silva et al. 2018). The major degradation 

product, AMPA (CASRN 1066-51-9), also binds to soils and may be more mobile than glyphosate (Duke 

and Powles 2008; IPCS 1994). Leaching of glyphosate may be possible under certain environmental 

conditions. In a study examining the environmental fate and leaching risk of aged glyphosate and its 

metabolite, AMPA, large amounts of glyphosate and AMPA were extracted from soil after treating it with 
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phosphate solution (to simulate rainwater in the presence of fertilizer) compared to pure water (to 

stimulate rainwater in non-fertilized soil). The presence of phosphate based fertilizer in soil appears to 

enhance the probability that glyphosate and its metabolite residue will leach from the soil matrix 

(Simonsen et al. 2008). While glyphosate and AMPA have been reported to reach shallow groundwater 

and then transfer to surface water (Grandcoin et al. 2017), the chemical is not expected to leach into 

groundwater as it is mostly concentrated in the topsoil layers; Glyphosate and AMPA are infrequently 

detected in deep groundwater systems, and when found, concentrations are generally at low levels (Silva 

et al. 2018). 

Other Media. Glyphosate is not generally taken up from the soil by a plant’s root system since it 

typically forms bound residues with organic matter in most soils. Absorption of glyphosate via the roots 

has been discussed in a review by Saunders and Pezeshki (2015); however, many of the studies cited were 

conducted under hydroponic conditions, which are not likely to be typical of field environments. 

However, some uptake has been demonstrated to occur under field conditions with low organiccontaining soils and in laboratory growing conditions. The EPA Registration Eligibility Decision (RED) 

document for glyphosate showed that lettuce, carrots, and barley contained glyphosate and AMPA 

residues after a sandy loam containing 0.3–0.5% organic matter was treated with 3.71 pounds of 

glyphosate per acre, but accumulation decreased as the length of rotation increased. For example, 

glyphosate residues were 0.097 ppm in lettuce planted 30 days post-treatment, but only 0.037 ppm in 

lettuce planted 119 days post-treatment (EPA 1993). After surface application of glyphosate, it may 

move from the point of application, typically the leaves, to other parts of the plant. In a plant uptake 

study where glyphosate was aged for 6.5 months in soil before either rape or barley seeds were planted, 

radioactivity demonstrated translocation of glyphosate into the parts of the plant above the soil after a 

growth period of 41 days. The measured uptake for rape and barely were equivalent to 14.0 and 11.5 

ng/glyphosate/g plant fresh weight, respectively (Simonsen et al. 2008). Glyphosate can be absorbed into 

the plant or vegetable through its outer wall or skin and can move throughout the stem and leaves of the 

entire plant. Metabolism of glyphosate within the plant occurs slowly (Doublet et al. 2009; Smith and 

Oehme 1992; WHO 2005). Glyphosate is mobile inside the plant and may be transported within the 

phloem system into other tissues before the plant is killed (Duke and Powles 2008; Pankey 2000; 

Plimmer et al. 2004). Boerboom and Wyse (1988) investigated absorption and translocation of 

glyphosate using Canada thistle seeds with various concentrations of a formulation of glyphosate (356 

g/L) and the surfactant POEA (178 g/L). Translocation from the treated leaf to the root was clearly 

observed. Translocation generally decreased as the concentration of glyphosate increased. Application of 
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the smaller droplets resulted in greater translocation to the roots compared to application of larger 

droplets. 

5.4.2 Transformation and Degradation 

Glyphosate is readily and completely degraded in the environment mainly by microbial processes. 

Microorganisms that degrade glyphosate into its metabolite include Pseudomonas sp., Arthrobacter 

atrocyaneus and Flavobacterium sp. (Singh and Singh 2016). Modes of degradation involving glyphosate 

oxidoreductase (GOX) and C-Plyase enzymatic pathways have been suggested. AMPA has been 

identified as the major metabolite in both soils and water. Sarcosine is an additional degradation product 

produced by the C-Plyase enzymatic pathway (Singh and Singh 2016). However, sarcosine has mostly 

been found in pure culture experiments, likely due to its fast degradation compared to AMPA (Borggaard 

and Gimsing 2008). Glyoxylic acid (CASRN 298-12-4) is an additional degradation product by the GOX 

enzymatic pathway. Both pathways result in complete mineralization to inorganic phosphate, carbon 

dioxide, ammonium, and water (Balthazor and Hallas 1986; Kishore and Jacob 1987; Shinabarger and 

Braymer 1986). AMPA is more persistent than glyphosate and has reported soil half-lives ranging from 

32 to 240 days depending on edaphic and environmental conditions such as temperature and soil moisture

(Simonsen et al. 2008; Battaglin 2014; Silva et al. 2018). At colder and drier conditions, degradation of 

AMPA is slower (Silva et al. 2018). Aquatic half-lives are similar to glyphosate (Battaglin 2014). Figure 

5-2 illustrates the degradation of glyphosate under aerobic conditions.

Figure 5-2. Degradation of Glyphosate Under Aerobic Conditions

Source: Adapted from Schuette 1998
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The high water solubility, low log Kow, and ionic nature of glyphosate suggest that this compound would 

not be expected to bioaccumulate in aquatic organisms (IPCS 1994; WHO 2005). Jackson et al. (2009) 

measured whole-body bioconcentration factor (BCF) values for glyphosate in bluegill fish (Lepomis 

macrochirus) using EPA guideline method OPPTS 850.1730 for an exposure period of 28 days. A BCF 

value of 0.52 (log BCF -0.284) was reported, suggesting that bioconcentration was low. Accumulated 

residues of glyphosate in fish, crustaceans, and mollusks exposed to water containing glyphosate declined 

approximately 50–90% over 14–28 days after removal from the glyphosate water into glyphosate-free 

water (WHO 2005). Bioaccumulation of glyphosate in blackworms (Lumbriculus variegatus), following 

soil application of glyphosate and a commercial formulation, was investigated (Contardo-Jara et al. 2009). 

BCF values after 4 days of exposure to concentrations of 0.05–5 mg/L of both 98% pure glyphosate and 

the formulation Roundup Ultra® were measured at 20°C (Contardo-Jara et al. 2009). BCF values based 

on the fresh weight of the worms ranged from 1.2 to 5.9; the BCF values for pure glyphosate at 0.05, 0.5, 

and 5.0 mg/L were approximately 2.9, 1.1, and 2.8, respectively and BCF values for Roundup Ultra® at 

0.05, 0.5, and 5.0 mg/L were approximately 5.9, 3.8, and 2.7, respectively. The greater uptake of 

glyphosate from the Roundup Ultra® sample was attributed to the surfactant in the formulation, POEA. 

The mechanism of action for glyphosate’s herbicidal properties involves the inhibition of enzymes in the 

shikimate pathway. Specifically, the enzyme enolpyruvylshikimate-3-phosphate synthase is inhibited, 

creating a deficiency of enolpyruvylshikimate-3-phosphate and an abundance of shikimate. It has been 

suggested that the actual death of the plant is due to the disruption of plant processes regulated by the 

shikimate pathway essential to plant health and growth such as the primary biosynthesis of aromatic 

amino acids like phenylalanine, tryptophan, and tyrosine, as well as lignin and chlorophyll, and secondary 

processes such as flavonoid synthesis. These primary processes are exclusive to plants and some 

microorganisms and do not occur in any animals; therefore, the inhibition of enzyme production induced 

by glyphosate only affects species in the plant kingdom. It has also been suggested that the increased 

carbon flow to the shikimate pathway decreases carbon available for other essential photosynthetic 

processes (Muller and Applebyke 2010; Pankey 2000; Plimmer et al. 2004; Servaites et al. 1987).

In one version of transgenic plants modified to be glyphosate tolerant, glyphosate is converted to Nacetylglyphosate (CASRN 129660-96-4), a chemical that lacks herbicidal properties (Pioneer 2006). This 

chemical may be further metabolized to N-acetyl (aminomethyl)phosphonic acid (N-acetyl-AMPA) (PAN 

2009). However, the more common method of conferring glyphosate-resistance to plants is promoting the 
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expression of enolpyruvulshikimate-3-phosphate synthase variants that are resistant to glyphosateinhibition (Pioneer 2006). 

Air. Glyphosate has low vapor pressure and is considered stable in ambient air. Experimental and 

monitoring studies have confirmed wind-driven transportation of both glyphosate and AMPA including in 

areas that never had glyphosate application (Silva et al. 2018; Aparicio et al. 2018).

Water. Glyphosate is polar, has high water solubility and is expected to exist as an anion at neutral pH 

(IPCS 1994; O’Neil et al. 2013; Singh and Singh 2016). Based on experimental adsorption coefficients 

ranging from 8 to 377 dm3/kg for various soil and clay substrates, glyphosate is expected to adsorb to 

suspended solids and sediments in water. Precipitation from water has been suggested due to waterinsoluble metal complexes with iron(III), copper(II), calcium, and magnesium that have been found; 

coordination occurs through the amine nitrogen, the carboxylic oxygen, and the phosphate oxygen 

(Subramaniam and Hoggard 1988). Photodegradation in water is not expected to be an important fate 

process for glyphosate under environmentally relevant conditions. Experimental half-lives of <28 days 

upon exposure to natural light have been reported (IPCS 1994; Rueppel et al. 1977). No detectable 

photodegradation was observed in a study using sterile water and exposure to ultraviolet (UV) light or 

natural sunlight (Smith and Oehme 1992). Lund-Hoie and Friestad (1986) exposed RoundUp® to UV 

light at 254 nm at 20°C in the laboratory and exposed 1% RoundUp® solutions in deionized water, 

polluted water, and water with suspended sediments to natural sunlight (measured λ=295–385 nm) 

outside at temperatures ranging from 20 to -5°C. Results indicated that photodegradation occurred faster 

in pure water as opposed to polluted water or water with sediments in which adsorption accounted for the 

majority of dissipated glyphosate. A photolytic half-life of 3–4 weeks was observed for glyphosate, at an 

initial concentration of 2,000 ppm in the deionized water exposed to UV light. A photolytic half-life of 5 

weeks at 100 ppm was observed for glyphosate in deionized water, exposed to natural sunlight. The rate 

of hydrolysis is considered very slow. In a study at 35°C, glyphosate did not undergo hydrolysis in 

buffered solutions with a pH of 5, 7, or 9. Laboratory studies have reported 50% degradation in ≤14 days 

in water and sediment under aerobic conditions and 14–22 days under anaerobic conditions for glyphosate 

(IPCS 1994). In an aqueous hydrolysis study at 25°C in buffered solutions of pH 5, 7, and 9, glyphosate 

was considered hydrolytically stable, with extrapolated half-lives beyond 3 years (EPA Undated).

Rapid dissipation of glyphosate in small forest ponds was observed as a result of sediment sorption and 

microbial degradation (Goldsborough and Beck 1989). Dissipation in three ponds, pH 5.0–7.7, resulted 
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5. POTENTIAL FOR HUMAN EXPOSURE

in half-lives of 1.5–3.5 days. After 38 days, glyphosate was not detected in any of the samples. AMPA 

concentrations were consistently low throughout the study.

Microbial degradation of glyphosate in water sediments has been investigated. AMPA has been 

identified as the major metabolite in water. Rueppel at al. (1977) performed non-sterile and sterile 

soil/water shake flask experiments to examine the degradation of glyphosate under aerobic and anaerobic 

conditions. The 14C-labeled glyphosate samples used were between 94.8 and 98.1% pure. Ray silt loam, 

Norfolk sandy loam, and Drummer silty clay loam soil samples were used. In the sterile soil test, 1.0% 

degradation was achieved after 7 days; the report suggests that abiotic chemical degradation is not a likely

fate process for glyphosate. In non-sterile aerobic and anaerobic tests using Ray silt loam and 14C-labeled 

glyphosate, 46.8–55.3 and 33.5–51.4% TCO2 (theoretical CO2 evolution), respectively, was achieved after 

28 days. In the non-sterile aerobic tests using fresh and bin-stored Drummer loams, just over 40% and just 

under 20% TCO2, respectively, was achieved after 28 days. In the fresh Drummer loam and Ray loam 

samples, no lag phases were observed, and the bulk of the degradation occurred by day 7, after which 

time, the rate of degradation declined. The slowing of degradation was attributed to adsorption to soil. In 

Ray silt loam and Drummer silty clay loam, degradation of glyphosate reached 90% after 14 and 80 days, 

respectively, and half-lives were reported as 3 and 25–27 days, respectively. The results were similar at 

different concentrations of glyphosate. In the non-sterile aerobic test in Norfolk sandy loam, carbonlabeled glyphosate achieved <10% mineralization after 28 days, measured by applied 14C as CO2 

evolution, and 43% dissipation occurred after 112 days. A half-life of 130 days was reported for Norfolk 

soil. The principle degradation product identified, AMPA, was confirmed in soil samples by nuclear 

magnetic resonance (NMR) imaging, mass spectral analysis, ion-exchange chromatography, and thinlayer chromatography. Minor degradation products identified included N-methylaminomethylphosphonic 

acid, glycine, N,N-dimethylaminomethylphosphonic acid, and hydroxymethylphosphonic acid, all of 

which were typically present at <1% (Rueppel et al. 1977). The metabolite, AMPA, achieved 16.1 and 

34.8% degradation after 63 days in Drummer and Ray loams, respectively, measured by applied 14C as 

CO2 evolution.

Abiotic degradation was examined by Ascolani Yael et al. (2014) in aqueous solution in the presence of 

copper salts; results indicated that glyphosate interactions with metal ions in soils may catalyze 

degradation to AMPA. Further investigation was proposed.

Sediment and Soil. Glyphosate is readily degraded in the terrestrial environment by a variety of 

microorganisms. Bacteria, actinomycetes, fungi, and other soil microbes have the ability to degrade 
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5. POTENTIAL FOR HUMAN EXPOSURE

glyphosate. AMPA has been identified as the major metabolite in soil. Glyphosate may also be degraded 

in soil to sarcosine and inorganic phosphate. Photodegradation is not expected to be an important fate 

process in soil.

After application of Roundup® at about 2.0 kg/ha (acid equivalent of isopropylamine salt of glyphosate)

to Carnation Creek watershed (10 km2study area), 50% of the glyphosate residues in soil dissipated after 

45–60 days and 82–94% dissipated after 360 days (Feng et al. 1990a). 

It has been demonstrated that inorganic phosphate present in soils may inhibit some microbial degradation 

of glyphosate (Kishore and Jacob 1987). Strains capable of using glyphosate as a sole carbon, nitrogen, 

or phosphorus source, thereby degrading glyphosate, include Flavobacterium sp. (Balthazor and Hallas 

1986), which is known to degrade glyphosate in the presence of phosphate, Pseudomonas sp. PG2982 

(Kishore and Jacob 1987; Shinabarger and Braymer 1986), Arthrobacter atrocyaneus (Pipke and 

Amrhein 1988), and Rhizobium spp. (Liu et al. 1991). Biodegradation may involve co‐metabolism with 

other energy sources as well (Sprankle et al. 1975). Degradation products include AMPA and glyoxylic 

acid, which are subsequently degraded to inorganic phosphate, carbon dioxide, and ammonium. In 

addition, some bacterial degradation results in the production of sarcosine and inorganic phosphate 

(Borggaard and Gimsing 2008; Kishore and Jacob 1987; Liu et al 1991; Pipke and Amrhein 1988; 

Shinabarger and Braymer 1986).

Microbial degradation of bound and unbound glyphosate in several soils resulted in 17.4–45% ultimate 

degradation after 28 days; the highest degradation rate was observed in Conover sandy clay loam soil 

(Sprankle et al. 1975). The majority of the degradation was attributed to co-metabolic processes of soil 

microbes, with possible chemical degradation occurring.

In a biodegradation experiment with activated sludge, the bacterial strain, Flavobacterium sp., was 

identified as the microorganism metabolizing glyphosate to AMPA. This degradation was followed by 

complete mineralization of AMPA, using the enzyme phosphonatase, to carbon dioxide (CO2), phosphate 

(PO4

3-

), ammonium (NH4+), and water (H2O) (Balthazor and Hallas 1986). 

A variety of microorganisms are capable of degrading glyphosate. In one degradation pathway, the initial 

step involves cleavage of the carbon-phosphate bond to produce sarcosine and inorganic phosphate. This 

is followed by conversion of sarcosine to glycine and formaldehyde. Pseudomonas sp. PG2982 uses the 

enzyme, C-P lyase, to cleave the carbon-phosphate bond in glyphosate, producing sarcosine. This is 
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5. POTENTIAL FOR HUMAN EXPOSURE

followed by the cleavage of sarcosine into glycine and formaldehyde (Kishore and Jacob 1987; 

Shinabarger and Braymer 1986). Glycine and formaldehyde are metabolized in other biosynthesis 

processes, such as the oxidation of formaldehyde to carbon dioxide. Multiple strains in the bacterial 

family Rhizobiaceae have the ability to metabolize glyphosate. Liu et al. (1991) found that rhizobia 

bacterial cells took up close to 85% of available glyphosate within 30 minutes, after which time, the 

percentage began to decrease. Thin layer chromatography confirmed the presence of sarcosine and 

glycine as degradation products. 

Doublet et al. (2009) studied the degradation of plant absorbed glyphosate in soils. Plants containing 

residues of glyphosate can enter the soils during crop cycling or harvesting. Degradation of glyphosate 

was different depending on the plant tissue in which it was absorbed. Mineralization rate constants 

(k (day-1)) ranged from 0.031 to 0.097 in the apex of oilseed rape and in the lamina of maize, respectively. 

It was noted that absorption of glyphosate in plants delayed degradation in soil. 

Glyphosate is expected to adsorb strongly to soil particles and clay minerals; however, the amount of 

glyphosate sorbed decreases with increasing soil pH. Adsorption and desorption of glyphosate were 

examined using HPLC (Gerritse et al. 1996; Glass 1987; Piccolo et al. 1994; Sprankle et al. 1975). 

Adsorption to agricultural soils and clay minerals and the effects of pH and cation saturation were 

examined by Glass (1987). The Koc values were 4,900 for clay loam with pH 7.5 and organic content 

(OC) of 1.56%; 3,400 for silt loam with pH 5.8 and OC of 1.64%; and 2,600 for sandy loam with pH 5.6 

and OC of 1.24%. The adsorption and desorption of glyphosate and the effects of soil characteristics in 

four various soil types were assessed (Piccolo et al. 1994). Some characteristics for the four soils follow: 

Sample A, pH 8.0 and 0.00 OC % (64.1% silt); sample B, pH 5.8 and 3.73 OC% (46.3% sand); sample C, 

pH 4.6 and 9.23 OC % (81.5% sand); and sample D, pH 8.3 and 0.45 OC % (82.4% silt). The greatest 

adsorption occurred in the soil with the highest concentrations of iron (4.74%) and aluminum (1.57) 

oxides (sample B); the greatest desorption occurred in the soil with lowest concentration of iron (0.18%) 

and aluminum (0.16%) oxides (sample A). The percent desorptions of glyphosate from the four soils 

were 81% in sample A, 15% in sample B, 72% in sample C, and 35% in sample D. A ligand exchange 

mechanism is hypothesized for the adsorption of glyphosate involving either the phosphonic component 

or the carboxylic component of this substance and adsorption to iron and aluminum sites (Benetoli et al. 

2010; Piccolo et al. 1994). The adsorption and desorption of both glyphosate and its metabolite, AMPA, 

were examined by Gerritse et al. (1996) using five soil types. Koc values calculated for soil organic 

carbon ranged from 8.5 to 5x106after 1 day and from 45 to >5x106after 1 week. The strongest 

adsorption occurred in the soil with the highest iron and aluminum content. The weakest adsorption 
GLYPHOSATE 180

5. POTENTIAL FOR HUMAN EXPOSURE

occurred in the soil with the highest organic content. These results indicate that glyphosate has a notable 

affinity towards some soils, particularly with lower pH values and greater mineral content, and desorption 

occurs under certain environmental conditions especially as pH values increase and mineral 

concentrations decrease. The EPA CompTox Chemicals Dashboard provided a predicted Koc range of 

0.00169–2,080 L/kg, which again indicates a range of mobility in soil likely determined by affinity 

towards these soil properties.

During a monitoring study with mixtures of Roundup® plus an additional herbicide, soil adsorption and 

desorption studies were performed on soils from Baton Rouge, Bridge City, and Hammond Louisiana 

(LaDOTD 1995). The Hammond soil with a pH <8 adsorbed >90% of the applied glyphosate. 

Adsorption values (Kf) were 8.7, 0.1, and 0.34 for Baton Rouge, Bridge City, and Hammond soils, 

respectively. Desorption values (Kd) were 355, 0.04, and 0.005 μg/g for Baton Rouge, Bridge City, and 

Hammond soils, respectively. 

Greater than 90% of the glyphosate residues detected in forest soil samples (pH 4.20–5.28), where 

herbicides containing glyphosate had been sprayed, were found in the upper layers (depth of 0–15 cm) of 

the soils in both seasonally flooded and well-drained soils, indicating minimal leaching of glyphosate 

(Feng et al. 1990b). 

Glyphosate dissipates from soil under certain environmental conditions. Half-life values between 2 and 

215 days have been reported (Battaglin et al. 2014). In field experiments, dissipation from the soil due to 

run‐off has been demonstrated (IPCS 1994). Landry et al. (2005) examined the leaching potential and 

mineralization of glyphosate in vineyard soils by monitoring outdoor soil columns from May 2001 to 

May 2002. Bare and grass-covered soils with pH values ranging from 8.0 to 8.4 were studied. Sand, silt, 

and clay contents were 23.8–34.4, 36.5–39.6, and 29.1–36.9%, respectively, of the bare soils and 26.2–

35.6, 34.2–41.3, and 29.6–32.5%, respectively, of grass-covered soils. An aqueous solution of herbicide 

containing 340 mg/L glyphosate was applied to both soil column surfaces. Effluents from the bare and 

grass-covered soils were collected weekly and after heavy precipitation to evaluate leaching of glyphosate 

and AMPA. Glyphosate was detected in 37% of the bare soil leachates and 27% of the grass-covered soil 

leachates. The highest concentrations measured from the bare soil leachate and grass-covered leachate 

were 17 and 2.7 μg/L, respectively. AMPA was detected in 90% (maximum concentration 9.4 μg/L) of 

the bare soil leachates and 41% (maximum concentration 3.5 μg/L) of the grass-covered soil leachates. 

Mineralization analysis was performed at 20°C for 42 days in both soils. In the grass-covered soil and 

bare soil, 14C-labeled glyphosate achieved 46.5 and 43.5% CO2 evolution after 42 days, respectively. 
GLYPHOSATE 181

5. POTENTIAL FOR HUMAN EXPOSURE

Rapid degradation was observed with no lag phase; the highest rate of degradation occurred within the 

first 2 days. It was suggested that the initial rapid degradation was based on the degradation of free 

glyphosate and slowing rates of degradation were attributed to the degradation of adsorbed glyphosate. 

Other Media. After application of herbicides, 30–97% of the applied glyphosate may be taken up by 

the plant by absorption from the treated leaves. Glyphosate-based formulations containing surfactants 

(and adjuvants) have a higher rate of absorption compared to glyphosate water solutions (Doublet et al. 

2009). Surfactants in herbicide formulations aid in the adsorption and absorption of the active ingredient. 

Glyphosate is absorbed by plant foliage and transported or moved through the plant via phloem vessels; 

translocation patterns depend on the specific species of plant. Glyphosate enters these vessels slowly, but 

once inside, it becomes ‘trapped’ because of the pH within the vessels, which causes ionization (Gomes et 

al. 2014; IPCS 1994). Glyphosate may be degraded or metabolized in plants, AMPA is a notable 

degradation product (Duke 2011). An examination of the metabolism of glyphosate in soybean and 

canola suggest that some plants use a GOX enzyme for the conversion of glyphosate to AMPA. 

Degradation of glyphosate in glyphosate-resistant crops may give a better picture of the metabolic 

processes without interferences found in conventional crops. In transgenic plants modified to be 

glyphosate tolerant, glyphosate is converted to N-acetylglyphosate, which lacks herbicidal properties

(Pioneer 2006). This chemical may be further metabolized to N-acetyl-AMPA (PAN 2009). Glyphosate 

and AMPA accumulate less in glyphosate-resistant crops than in conventional crops. Lower glyphosate 

and AMPA levels in glyphosate-resistant canola compared to conventional crops suggested that 

metabolism is more rapid in glyphosate-resistant canola (Duke 2011). 

5.5 LEVELS IN THE ENVIRONMENT 

Reliable evaluation of the potential for human exposure to glyphosate depends, in part, on the reliability 

of supporting analytical data from environmental samples and biological specimens. Concentrations of 

glyphosate in unpolluted atmospheres and in pristine surface waters are often so low as to be near the 

limits of current analytical methods. In reviewing data on glyphosate levels monitored or estimated in the 

environment, it should also be noted that the amount of chemical identified analytically is not necessarily 

equivalent to the amount that is bioavailable.

Table 5-4 shows the lowest limits of detection (LODs) that are achieved by analytical analysis in 

environmental media. An overview summary of the range of concentrations detected in environmental 

media is presented in Table 5-5.
GLYPHOSATE 182

5. POTENTIAL FOR HUMAN EXPOSURE

Table 5-4. Lowest Limit of Detection Based on Standardsa

Media Detection limit Reference

Air 0.01 ng/m3 Chang et al. 2011

Drinking water 5.99 μg/L (ppb) EPA 1990

Surface water and groundwater Glyphosate and AMPA 0.02–0.10 μg/L

0.005 μg/L

Lee et al. 2002; USGS 2002

Ibanez et al. 2005

Soil and sediment Organic soil =0.05 μg/g

Mineral soil=0.02 μg/g

Foliage=0.10 μg/g

Sediment=0.03 μg/g

Soil=0.005 μg/g

Thompson et al. 1989

Ibanez et al. 2005

Whole blood 15 ng/mL Aris and LeBlanc 2011

Urine 0.09 ng/mL

0.1 ng/mL

Biagini et al. 2004

Jensen et al. 2016

Milk (human and bovine) 10 μg/L (ppb) Jensen et al. 2016

Crops and commodities 0.01 mg/kg Alferness 1993

aDetection limits based on using appropriate preparation and analytics. These limits may not be possible in all 

situations.

AMPA = aminomethylphosphonic acid

Table 5-5. Summary of Environmental Levels of Glyphosate

Media Low High For more information

Outdoor air (ng/m3) <0.01 (glyphosate)

<0.01 (AMPA)

9.1 (glyphosate)

0.97 (AMPA)

Table 5-6

Surface water (ppb) 0.02 427 Table 5-8

Ground water (ppb) 0.01 4.7 Table 5-9

Drinking water (ppb) Not detected Table 5-9

Food (ppb) 0.078 5.47 Section 5.5.4, Other Media

Sediment Not detected Table 5-10

AMPA = aminomethylphosphonic acid

A study by the USGS evaluated 3,732 environmental samples across 38 states and the District of 

Columbia from several studies examining glyphosate in the environment; the samples were collected 

between 2001 and 2010 from 1,341 different sites, including groundwater; lakes, ponds, and wetlands; 

soil water; streams; large rivers; precipitation; ditches and drains; soil and sediment; and waste water 

treatment plant outfall (Battaglin et al. 2014). Glyphosate was detected in 39.4% of all the samples, with 

a median value of <0.02 μg/L and a maximum value of 476 μg/L. Its degradation product, AMPA, was 

detected in 55% of all the samples, with a median value of 0.04 μg/L and a maximum value of 397 μg/L. 
GLYPHOSATE 183

5. POTENTIAL FOR HUMAN EXPOSURE

Groundwater (n=1,171) had the smallest percentage of detections, with 5.8% for glyphosate and 14.3% 

for AMPA. Glyphosate was detected in 53% of the 1,508 stream samples and AMPA was detected in 

72%. Glyphosate was detected in 34% and AMPA was detected in 30% of the 104 small body water 

samples such as lakes and ponds. Out of 11 wastewater treatment plant (WWTP) samples, glyphosate 

and AMPA were detected in 9.1 and 82%, respectively. Out of 85 precipitation samples, glyphosate was 

detected in 71% and AMPA was detected in 72%. Glyphosate was detected in 71% of the 374 ditch and 

drain samples, with a median value of 0.02 μg/L and a maximum value of 427 μg/L. Glyphosate was 

only detected without its degradation product, AMPA, in 2.3% of all of the samples; AMPA was detected 

without glyphosate in 17.9% of the samples. In 42.7% of all of the samples, neither analyte was detected. 

Several sites with multiple samples during the years 2001–2005 and 2006–2010 indicated that the 

detection frequency and median concentration of both glyphosate and AMPA had increased in the 

environment (Battaglin et al. 2014). The highest level of glyphosate was detected in soils and sediments. 

Out of 45 samples, glyphosate was detected in 91%, with a median value of 9.6 μg/kg and a maximum 

value of 476 μg/kg. AMPA was detected in 93.3% of 45 samples, with a median value of 18 μg/kg and a 

maximum value of 341 μg/kg. 

5.5.1 Air 

Ambient air monitoring data for glyphosate are compiled in Table 5-6.

Table 5-6. Outdoor Air Monitoring Data for Glyphosate

Location Date

Median concentration 

(range) in ng/m3 Notes Reference

Agricultural 

ambient air;

Mississippi

2007

2008

Glyphosate: 0.48 (<0.01–9.1)

AMPA: 0.06 (<0.01–0.49)

Glyphosate: 0.24 (<0.01–1.5)

AMPA: 0.02 (<0.01–0.09)

Glyphosate and AMPA detected in 

19/22 air samples

Glyphosate and AMPA detected in 

27/27 and 19/27 air samples, 

respectively

Chang et al. 

2011

Agricultural 

ambient air;

Iowa

2007

2008

Glyphosate: 0.08 (<0.01–5.4)

AMPA: 0.02 (<0.01–0.97)

Glyphosate: 0.22 (<0.01–7.7)

AMPA: 0.04 (<0.01–0.38)

Glyphosate and AMPA detected in 

11/18 and 10/18 air samples

Glyphosate and AMPA detected in 

13/18 and 11/18 air samples

Chang et al. 

2011

Agricultural 

breathing 

zones;

Baton 

Rouge, 

Bridge City, 

June 

19, 

1990–

October 

9, 1990

<0.1–138.6 μg/m Breathing zone air (110 samples); 

sampled in areas where mixtures of 

commercial herbicides were 

applied using spray equipment with 

operating capabilities of 

0.37 L/minute

LaDOTD 

1995
GLYPHOSATE 184

5. POTENTIAL FOR HUMAN EXPOSURE

Table 5-6. Outdoor Air Monitoring Data for Glyphosate

Location Date

Median concentration 

(range) in ng/m3 Notes Reference

Hammond, 

Louisiana; 

AMPA = aminomethylphosphonic acid

5.5.2 Water 

A comprehensive study conducted by the USGS from 2001 to 2006 examined glyphosate and its 

degradation product, AMPA, in 2,135 groundwater and surface water samples, 14 rainfall samples, and 

193 soil samples in major river basins in the United States (USGS 2007). Results indicated that AMPA 

was detected more frequently and at similar concentrations than parent glyphosate in many samples. The 

results are summarized in Table 5-7.

Table 5-7. Glyphosate and its Degradation Products in Water 

Samples in Major U.S. River Basins

N

Glyphosate AMPA

Detections

Maximum

(μg/L)

Minimum 

(μg/L) Detections

Maximum

(μg/L)

Minimum 

(μg/L)

Groundwater

873 68 4.7 0.02 133 2.6 0.02

Surface water

1,262 489 427 0.02 725 41 0.02

Rainfall

14 12 1.1 0.3 12 0.47 0.02

Source: USGS 2007

Additional water monitoring data for glyphosate are compiled in Tables Table 5-8 and Table 5-9.

5.5.3 Sediment and Soil 

Sediment and soil monitoring data for glyphosate are compiled in Table 5-10.

5.5.4 Other Media 
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5. POTENTIAL FOR HUMAN EXPOSURE

In 2006, 20 prepared food samples were examined for glyphosate residues using electrospray ionization–

liquid chromatography tandem mass spectrometry with limit of quantitation of 0.01 mg/kg and an LOD of 

0.005 mg/kg (McQueen et al. 2012). Composite food samples assessed had a mean concentration of 

0.08 mg/kg. 

Four weeks post application of glyphosate at 4.5 kg/ha to separate pots planted with conventional corn, 

cotton, soybeans, and wheat, concentrations of glyphosate were 0.21, 0.26, 0.20, and 0.20 mg/kg, 

respectively. Six weeks after application, concentrations in corn, cotton, soybeans, and wheat were 0.14, 

0.21, 0.29, and 0.18 mg/kg, respectively, and 8 weeks after application, concentrations in corn, cotton, 

soybeans, and wheat were 0.079, 0.42, 0.076, and 0.35 mg/kg, respectively (FAO 2005). Four-week 

concentrations of glyphosate in control crops of corn, cotton, soybeans, and wheat were 0.068, 0.04, 

0.029, and 0.008 mg/kg, respectively. Six-week concentrations in control crops of corn, cotton, soybeans, 

and wheat were 0.089, 0.020, 0.11, and 0.015 mg/kg, respectively, and 8-week concentrations in control 

crops of corn, cotton, soybeans, and wheat were 0.022, 0.27, 0.045, and 0.061 mg/kg, respectively (FAO 

2005).
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5. POTENTIAL FOR HUMAN EXPOSURE

Table 5-8. Surface Water Monitoring Data for Glyphosate

Location Date Concentration (range) in μg/L Notes Reference

Surface water

United States

2016 Mean: 0.30 ; Median 0.10; (0.02–5.1) EPA STORET data: Routine monitoring samples from

USGS Science Centers in Arkansas, California, Colorado, 

Connecticut, Georgia, Idaho, Illinois, Indiana, Iowa, 

Kansas, Kentucky, Louisiana, Michigan Center, Maryland, 

Massachusetts, Minnesota, Mississippi, Missouri, 

Montana, Nebraska, Nevada, New Jersey, New Mexico, 

New York, North Carolina, North Dakota, Oregon, South 

Carolina, Texas, Utah, Washington, and Wyoming

WQP 2017

Surface water

United States

2015 Mean: 0.27; Median 0.08; (0.02–24.20) EPA STORET data: Routine monitoring samples from

Minnesota Department of Agriculture–Pesticide and 

USGS Science Centers in Alabama, Arizona, Arkansas, 

California, Colorado, Connecticut, Georgia, Idaho, Illinois, 

Indiana, Iowa, Kansas, Kentucky, Louisiana, Maryland, 

Massachusetts, Michigan Center, Minnesota, Mississippi, 

Missouri, Montana, Nebraska, Nevada, New Jersey, New 

Mexico, New York, North Dakota, North Washington, 

Ohio, Oklahoma, Oregon, South Carolina, South Dakota, 

Texas, Utah, Washington, and Wyoming

WQP 2017

Surface water

United States

2014 Mean: 0.38; Median 0.10; (0.02–8.10) EPA STORET data: Routine monitoring samples from

Minnesota Department of Agriculture–Pesticide and 

USGS Science Centers in Alabama, Arizona, Arkansas, 

California, Colorado, Connecticut, Florida, Georgia, 

Hawaii, Idaho, Illinois, Indiana, Iowa, Kansas, Kentucky, 

Louisiana, Maryland, Massachusetts, Michigan, 

Minnesota, Mississippi, Missouri, Montana, Nebraska, 

Nevada, New Jersey, New Mexico, New York, North 

Carolina, North Dakota, Ohio, Oklahoma, Oregon, 

Pennsylvania, South Carolina, Texas, Utah, Virginia, 

Washington, and Wyoming

WQP 2017

Surface water

United States

March to 

October 

2013

Mean: 0.85; Median 0.34; (0.02–27.80) EPA STORET data: Routine monitoring samples from 

Minnesota Department of Agriculture and USGS Science 

Centers in Idaho, Illinois, Indiana, Iowa, Kansas, 

Kentucky, Minnesota, Missouri, Nebraska, New York, 

North Carolina, Ohio, South Dakota, Wisconsin, and 

Wyoming

WQP 2017
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5. POTENTIAL FOR HUMAN EXPOSURE

Table 5-8. Surface Water Monitoring Data for Glyphosate

Location Date Concentration (range) in μg/L Notes Reference

Rivers, small 

streams, 

agricultural 

ditches, and 

low-flow 

wetlands

Southern 

Ontario

May and 

midDecember 

2004; April 

and 

November 

2005

5–41 2004: 203 surface water samples collected from 26 sites

2005: 299 samples taken from 58 sites

~50% of sites detected glyphosate multiple times

AMPA detected at trace levels (20–66 μg/L in 5.4% of 

samples)

Struger et al. 

2008

Streams

Minnesota, 

Wisconsin, 

Nebraska, 

Iowa, Illinois, 

Indiana, Ohio, 

Kansas, and 

Missouri

2002 Minimum: 0.10–0.46 detected in Iowa, 

Missouri, and Wisconsin

Maximum: 0.54–8.7 detected in Illinois, 

Indiana, Kansas, Minnesota, Nebraska, 

and Wisconsin

51 locations (155 total samples); samples collected postapplication of pre-emergence herbicides, post-application 

of post-emergence herbicides, and during the harvest 

season. Glyphosate detected at levels above the method 

reporting limit of 0.10 μg/L in 35% of pre-emergence 

samples, 40% of post-emergence samples, and 31% of 

harvest season samples. AMPA detected at levels 

>0.10 μg/L in 53% of pre-emergence samples, 83% of 

post-emergence samples, and 73% of harvest season 

samples.

Battaglin et al. 

2005

Drainage 

basins for 

surface-water

or rainwater

sampling sites 

from multiple 

USGS studies 

in Florida, 

Georgia, 

Illinois, Iowa, 

Kansas, 

Mississippi, 

Nebraska, 

South Dakota, 

Vermont, and 

Washington

2001 

through 

2006

0.02–427 in surface water

0.3–1.1 in rainwater

Glyphosate and AMPA measured in 1,262 surface water 

samples and 14 rainwater samples. Glyphosate detected 

in 489 surface water samples and in 12 rainwater 

samples. AMPA detected in 725 surface water samples 

and 12 rainwater samples.

USGS 2007
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5. POTENTIAL FOR HUMAN EXPOSURE

Table 5-8. Surface Water Monitoring Data for Glyphosate

Location Date Concentration (range) in μg/L Notes Reference

Rainwater

Mississippi

2007

2008

Glyphosate: Median: 0.2 (<0.1–1.9)

AMPA: Median: 0.1 (<0. 1–0.3)

Glyphosate: Median: 0.15 (<0.1–1.6)

AMPA: Median: <0.1 (<0. 1–0.48)

Glyphosate and AMPA detected in 8/11 and 8/11 

samples, respectively

Glyphosate and AMPA detected in 13/11 and 

14/19 samples, respectively

Chang et al. 

2011

Rainwater

Iowa

2007

2008

Glyphosate: Median: 0.2 (<0.1–2.5)

AMPA: Median: <0.1 (<0. 1–0.2)

Glyphosate: Median: 0.1 (<0.1–1.8)

AMPA: Median: <0.1 (<0. 1–0.24)

Glyphosate and AMPA detected in 10/14 and 

5/14 samples, respectively

Glyphosate and AMPA detected in 15/24 and 

12/24 samples, respectively

Chang et al. 

2011

Rainwater

Indiana

2004 Glyphosate: Median: 0.14 (<0.1–1.1)

AMPA: Median: <0.1 (<0.1–47)

Glyphosate and AMPA detected in 11/12 and 

11/12 samples, respectively

Chang et al. 

2011

Rainwater

Flanders, 

Belgium

2001 Maximum during spraying season:

Glyphosate: 6,200 ng/L

AMPA: 1,200 ng/L

Average annual concentrations:

Glyphosate: 78 ng/L

AMPA: 20 ng/L

Glyphosate detected in 10% of samples; AMPA detected 

in 13% of samples

Quaghebeur et 

al. 2004

Streams of 

Southeast 

Buenos Aires, 

Argentina

2012 Glyphosate: 0.5 μg/L – 7.6 μg/L

AMPA: non-detect to 2.3 μg/L

Glyphosate detected in 35%, 10% and 4% samples 

collected in April, August and September, respectively. 

AMPA detected in 33% and 7%, of samples in April and 

August, respectively. AMPA was not detected in samples 

collected in September. 

Aparicio et al. 

2013

Gualeguay or 

Gualeguaychu 

River, 

Argentina

2012 Glyphosate: 0.73 μg/L

AMPA: 0.53 μg/L

Glyphosate detected in 3/11 samples; AMPA detected in 

6/11 samples.

Primost et al. 

2017

AMPA = aminomethylphosphonic acid; EPA = U.S. Environmental Protection Agency; MDL = method detection limit; STORET = STOrage and RETrieval; 

USGS = U.S. Geological Survey
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5. POTENTIAL FOR HUMAN EXPOSURE

Table 5-9. Groundwater Monitoring Data for Glyphosate

Location Date

Concentration 

(μg/L) Notes Reference

Drainage 

basins for 

surfacewater or 

rainwater 

sampling 

sites from 

multiple 

USGS 

studies in 

Florida, 

Georgia, 

Illinois, Iowa, 

Kansas, 

Mississippi, 

Nebraska, 

South 

Dakota, 

Vermont, and 

Washington

2001 through 

2006

0.02–4.7 Glyphosate and AMPA measured in 873 groundwater samples. Glyphosate 

detected in 68 groundwater samples, and AMPA detected in 133 groundwater 

samples.

USGS 2007

Groundwater

Wyoming 

September 9, 

2010

1.6 EPA STORET data: Routine monitoring sample from USGS Wyoming Water 

Science Center

WQP 2017

Groundwater

Florida 

March 2, 2010 0.14 EPA STORET data: Routine monitoring sample from USGS Florida Water 

Science Center

WQP 2017

Groundwater

Louisiana 

April, October, 

and November 

2011

0.03–2.2 EPA STORET data: Routine monitoring sample from USGS Louisiana Water 

Science Center; depths 43.5–82 feet

WQP 2017

Groundwater

Alabama

Texas

February and 

April, 2012

0.01–0.06 EPA STORET data: Routine monitoring sample from USGS Alabama Water 

Science Center; USGS Texas Water Science Center

WQP 2017

Groundwater

Kansas 

June and August 

2014, June 2015, 

July 2016

0.02–0.24 EPA STORET data: Routine monitoring sample from USGS Kansas Water 

Science Center

WQP 2017
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5. POTENTIAL FOR HUMAN EXPOSURE

Table 5-9. Groundwater Monitoring Data for Glyphosate

Location Date

Concentration 

(μg/L) Notes Reference

Groundwater

23 U.S. 

states

2001–2010 Median: <0.02 

Maximum: 2.03

Detected in 68 out of 1,171 samples Battaglin et al. 

2014

Groundwater 

Washington, 

DC

2008 0.02 Detected in 1 out of 13 well; not detected in 14 wells sampled in 2005 USGS 2010

Well water

Minnesota

October and 

November 2014, 

2015

Not detected EPA STORET data: Routine monitoring sample from Minnesota Department 

of Agriculture Pesticide Monitoring Program; activity depth reported at 0 m

WQP 2017

Aquifer, 

Mesopotamia 

Pampas, 

Argentina

January and 

March 2012

Not detected Ground water collected from pump 40 to 60 meter deep aquifer Primost et al. 

2017

EPA = U.S. Environmental Protection Agency; STORET = STOrage and RETrieval; USGS = U.S. Geological Survey
GLYPHOSATE 191

5. POTENTIAL FOR HUMAN EXPOSURE

Table 5-10. Sediment and Soil Monitoring Data for Glyphosate

Location Date Concentration (μg/g) Notes Reference

Sediment

Big Valley 

Rancheria, 

California

July 6, 2010 Not detected EPA STORET data: Routine monitoring samples 

from Big Valley Band of Pomo Indians of the Big 

Valley Rancheria, California: two samples; depth: 

0.152 m; MDL: 0.017 mg/kg

WQP 2017

Soil and 

sediment

Indiana, 

Mississippi

2001–2010 Median: 0.0096; maximum: 0.476 Detected in >90% of 45 samples Battaglin et 

al. 2014

Estuary

Willapa Bay, 

Washington

July 1997–

1999

1997 mudflat samples: 2.58–16.3

1998 mudflat samples: 3.11–9.94

1999 mudflat samples: 0.311–1.21

1997 meadow samples: 0.090–0.265

1998 meadow samples: 0.163–2.30

1999 meadow samples 0.472–1.32 (dry weight)

Aqueous herbicide formulated with Rodeo (5% 

solution v/v) and LI-700 (2% solution) applied in 

mudflat and cordgrass plots of land in 1997 and 

1998

Kilbride and 

Paveglio 

2001

Major river 

basins in the 

United States

2011–2006 193 samples collected; 119 glyphosate 

detections (0.001–0.476); 154 detections AMPA, 

(0.001–0.956)

Samples collected as part of USGS study USGS 2007

Streams 

Southeast 

Buenos Aires, 

Argentina

September 

2012

Glyphosate minimum: 5.7 μg/kg; maximum: 

221.2 μg/kg

AMPA minimum: 5.1 μg/kg; maximum: 235 

μg/kg

Glyphosate was detected in 66% of samples from 

44 streams in Southeast Buenos Aires

AMPA was found in 89% of samples from 44 

streams in Southeast Buenos Aires

Aparicio et 

al. 2013

Soils of 

Southeast 

Buenos Aires, 

Argentina

September 

2012

Glyphosate: 35 to 1502 μg/kg

AMPA: 299 to 2256 μg/kg

Sixteen farms were selected for soil sampling in 

the southeast of the Province of Buenos Aires

where glyphosate had been used

Aparicio et 

al. 2013

Los Frentones

(Chaco), 

Argentina

November 

2004 to 

November 

2010

Glyphosate: 2.4 μg/kg

AMPA: 6.3 μg/kg

Soil analysis conducted in semiarid regions of 

Argentina; no history of herbicide application, but 

in the surrounding area, there were patches with 

2 and 3 years of annual crops (mainly soybean)

Aparicio et 

al. 2018

Santa Rosa (La 

Pampa), 

Argentina

November 

2004 to 

Glyphosate: 9.5 μg/kg

AMPA: 66.2 μg/kg

Soil analysis conducted in semiarid regions of 

Argentina in soils with 4 years of annual crops 

Aparicio et 

al. 2018
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5. POTENTIAL FOR HUMAN EXPOSURE

November 

2010

(oats, rye, and sorghum) under conventional 

tillage with little use of pesticides.

Villa Mercedes 

(San Luis), 

Argentina

November 

2004 to 

November 

2010

Glyphosate: 131. 5 μg/kg

AMPA: 703.5 μg/kg

Soil analysis conducted in semiarid regions of 

Argentina in soil with 5 years of agricultural 

activity, mainly annual crops under no tillage and 

a high use of pesticides.

Aparicio et 

al. 2018

Mesopotamia 

Pampas, 

Argentina

January and 

March 2012

Glyphosate: 2,299 μg/kg (average)

AMPA: 4,204 μg/kg (average)

Samples were collected from 17 agricultural 

farms. Glyphosate detected in 5/6 samples

detected. AMPA detected in 6/6 samples.

Primost et al. 

2017

AMPA = aminomethylphosphonic acid; EPA = U.S. Environmental Protection Agency; MDL = method detection limit; STORET = STOrage and RETrieval; 

USGS = U.S Geological Survey
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5. POTENTIAL FOR HUMAN EXPOSURE

A Joint FAO/WHO Meeting on Pesticide Residues summarized glyphosate concentrations found in edible 

foods following applications of glyphosate formulations representative of several authorized use patterns. 

Glyphosate concentrations ranged from undetectable, ≤0.05 mg/kg, in several foods like bananas and 

selected meats to 3.7 mg/kg in a variety of grains and grain-based products (FAO 2005; FAO and WHO

2016). Genetically modified, and conventional food samples were studied. Herbicidal application 

techniques used on the food samples examined included pre-harvest application, directed ground spray, 

pre-emergence, and recirculating spray application methods. Application rates ranged from 0.36 to 7.7 

kg/ha. The highest concentration found in banana pulp was 0.16 mg/kg. All kiwifruit assessed in the 

study had undetectable residues. Olives had residues ranging from undetectable to 12 mg/kg. Dry beans 

had residues ranging from undetectable to 10 mg/kg. Dry peas had residues ranging from undetectable to 

8.9 mg/kg. Lentils had residues ranging from undetectable to 17 mg/kg. Glyphosate-tolerant sugar beet 

root had residues ranging from undetectable to 8.6 mg/kg. Conventional maize had residues ranging from 

undetectable to 3 mg/kg. Glyphosate-tolerant maize had residues ranging from undetectable to 0.83 

mg/kg. Oats had residues ranging from undetectable to 19 mg/kg. Rye grain had residues ranging from 

0.1 to 4.6 mg/kg. Wheat grain had residues ranging from 0.09 to 6.4 mg/kg. Sugarcane had residues 

ranging from undetectable to 15 mg/kg. Coffee and tea had levels ranging from undetectable to 9.6 

mg/kg. Glyphosate residues in Kona Hawaiian coffee beans prior to roasting were 0.58 mg/kg, and the 

roasted beans had residues of 0.06 mg/kg. 

Glyphosate was not included in compounds tested for by the Food and Drug Administration’s (FDA) 

Pesticide Residue Monitoring Program (PRMP), nor in the United States Department of Agriculture’s 

Pesticide Data Program (PDP) (FDA 2015; NPIC 2015).

A review by WHO reported that glyphosate was not detected in cereal grains at harvest when application 

of the herbicide occurred before planting (WHO 2005). Glyphosate was detected in cereals at mean 

residue levels of 0.2–4.8 mg/kg when application of the herbicide was prior to harvesting. In one 

assessment, levels of glyphosate were found to decrease upon industrial processing grains to flour from 

1.6 to 0.16 mg/kg (WHO 2005). In wheat treated with either Glyfos or Roundup® herbicides, levels of 

glyphosate were also found to decrease upon processing grains to flour from 0.28–1.0 mg/kg in the grains 

to <0.05 mg/kg in the flour (FAO 2005). Glyphosate residues in oats stored at room temperature 

compared to frozen storage were similar, 3.5 and 3.1 mg/kg, respectively (FAO 2005). After exposure to 

glyphosate at 10 mg/L for 14 days, fish concentrations ranged from 0.2 to 0.7 mg/kg and decreased upon 

exposure to glyphosate-free water (WHO 2005). 
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5. POTENTIAL FOR HUMAN EXPOSURE

A review by Williams et al. (2000) reported U.S. glyphosate residue data for wheat treated with 

maximum rates of Roundup®. Wheat crop residues consisted of a mean glyphosate concentration of 

0.69 μg/g (mg/kg), with a maximum concentration of 2.95 μg/g (mg/kg). Glyphosate-tolerant soybeans 

treated with maximum rates of Roundup® showed a mean glyphosate concentration of 2.36 μg/g (mg/kg) 

and a maximum concentration of 5.47 μg/g (mg/kg). 

Glyphosate was detected in carrot samples at average concentrations of 0.078±0.002 mg/kg and in 

spinach at 0.104±0.005 mg/kg (Zhao et al. 2011).

Glyphosate residues were examined on alder and salmonberry foliage and leaf litter sprayed with 

glyphosate at 2.0–2.1 kg/ha (Feng et al. 1990b). Foliar residues on alder and salmonberry were 261 and 

448 ppm (dry weight), respectively, after the initial application of the herbicide. Leaf litter of alder and 

salmonberry collected 15 days post-application had glyphosate residues of 12.5 and 19.2 ppm (mg/kg), 

respectively. After 8–9 days, 50% dissipation was reported for the glyphosate residue. AMPA residues 

in the leaf litter decreased, and at 29 days after application of the herbicide, concentrations of AMPA 

were not detected.

5.6 GENERAL POPULATION EXPOSURE 

The main routes of exposure to glyphosate for the general public result from the ingestion of foods with 

residues of glyphosate and foods made from these crops, as well as dermal, ocular, or inhalation exposure 

from application of herbicides containing glyphosate (EPA 2009c). Glyphosate has been detected in dust 

samples from homes near glyphosate application sites or from people who brought it indoors on their 

bodies and/or clothing from glyphosate-treated areas (Curwin et al. 2005). Additionally, pesticide 

application equipment, such as backpack sprayers, may leak, causing workers to be dermally exposed to

glyphosate formulations (NIOSH 2017). Upon dermal exposure, absorption through the skin is expected 

to be low based on dermal absorption studies, where an estimated 0.8–2.2% percutaneous absorption of 

glyphosate occurred in a study using 14C-radiolabeled glyphosate in Roundup® (Wester et al. 1991). 

Evidence has shown that proper hygiene removes glyphosate from skin and will deter absorption through 

the skin (Wester et al. 1991). Limited monitoring data indicate that oral exposure may occur from 

drinking contaminated well water supplied from groundwater contaminated with glyphosate; 

concentrations reported in groundwater are relatively low, and this chemical has low leaching potential

from soil to groundwater. Exposure may also occur via ingestion of food with herbicidal residues 

containing glyphosate as a result of its application. The FDA has not performed a total diet study on 
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5. POTENTIAL FOR HUMAN EXPOSURE

glyphosate. Glyphosate has not been included in the FDAs Pesticide Residue Monitoring Program 

Reports for the fiscal years 2009 through 2015 (FDA 2013a, 2013b, 2014, 2015, 2016, 2017); however, 

the FDA in 2016 and 2017 began preliminary testing of samples of soybeans, corn, milk, and eggs for 

glyphosate residues (FDA 2018). Preliminary results showed no pesticide residue violations for 

glyphosate in all four commodities tested (soybeans, corn, milk, and eggs). The Joint FAO/WHO 

Meeting on Pesticide Residues listed International Estimated Daily Intake (IEDI) of glyphosate from 17 

GEMS/Food (Global Environment Monitoring System-Food Contamination Monitoring and Assessment 

Programme) cluster diets to range from 140.5 to 443.0 μg/person (FAO and WHO 2016). Glyphosate is a 

non-volatile compound, and drift of herbicidal sprays may occur with aerial and ground equipment (Yates 

et al. 1978); therefore, some exposure via inhalation and direct contact with skin and eyes may occur after 

members of the general population apply glyphosate during residential use. Although the effects of 

glyphosate exposure of populations living in areas where glyphosate-containing products have been 

aerially-applied to eradicate coca crops have been evaluated (Paz-y-Miño et al. 2007, 2011; Solomon et 

al. 2009), such reports did not include monitoring of exposure levels.

Occupational exposure may occur in both forestry, landscaping, and agricultural settings from the direct 

use of herbicides containing glyphosate. The most probable routes for occupational exposure are via 

inhalation and dermal contact with this chemical at workplaces where glyphosate or products containing 

this chemical are produced or used. Oral exposure may occur from accidental ingestion. During the 

years 1990–1993, exposure to glyphosate of field workers applying mixtures of Roundup® plus an 

additional herbicide in areas of Louisiana was assessed (LaDOTD 1995). Mixtures of Roundup® (active 

ingredient glyphosate) plus Garlon-3A (active ingredient triclopyr) and Roundup® (active ingredient 

glyphosate) plus 2,4-D (active ingredient 2,4-dichlorophenoxyacetic acid) were applied by 13 workers 

using spray equipment with operating capabilities of 0.37 L/minute. Glyphosate was detected in the 

workers’ urine using HPLC with a detection limit of 100 ppb. Total excreted urinary amounts of 

glyphosate ranging from non-detectable to 175 μg/day were reported for both working and non-working 

days. Urine concentrations were higher than concentrations found in the collected air samples of the 

breathing zone. It was noted that inhalation exposure was very low compared with threshold limits; the 

maximum air concentration was 17.9 μg/m3. Dermal contact and improper hygiene leading to ingestion 

of the herbicides were noted as the probable routes of exposure. 

One-hundred adults older than 50 years who resided in Southern California, as part of the Rancho 

Bernardo study, were sampled for glyphosate and its metabolite AMPA in 1993-1996 and again in 2014-

2016 (Mills et al. 2017). The study did not indicate that any of these adults were involved in application 
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5. POTENTIAL FOR HUMAN EXPOSURE

of pesticides containing glyphosate. In 1993-1996, only 12 participants had glyphosate above the level of 

detection (LOD=0.03 μg/L) in urine and mean levels were 0.024 for all participants, and 5 participants 

had detected levels of AMPA (LOD=0.04 μg/L) with the mean levels of 0.008 μg/L for all participants. 

By 2014-2016 sampling, 70/100 participants had detectable levels of glyphosate and 71/100 of AMPA. 

Means levels in all 100 participants were 0.314 μg/L and 0.285 μg/L for glyphosate and AMPA, 

respectively (Mills et al. 2017).

Farmers, with an average age of 45 years licensed as pesticide applicators in South Carolina and 

Minnesota, who applied herbicides containing glyphosate had average urinary glyphosate levels of 3 μg/L

on the day of application (Acquavella et al. 2004). Lack of wearing rubber gloves was associated with 

higher concentrations in farmers’ urine. Spouses, with an average age of 42.2 years residing with the 

farmers but having minimal or no involvement in the preparation or application of the herbicide, had 

relatively low and consistent urine concentrations of glyphosate, while children (ages 4–18 years) had an 

increase followed by a decrease in urine concentrations correlated with application (see Table 5-11). For 

the entire assessment period, 88–95% of all samples of children’s urine were below the detection limit (1 

μg/L [ppb] for a 100-mL urine sample). Farmers applying the pesticide had the highest concentrations. 

The highest concentration of glyphosate found in a child was from a teenage male (29 μg/L [ppb]) who 

had assisted with mixing and application of the herbicide. An estimated dermal and inhalation exposure 

value of about 8,000 μg/hour was reported as the highest value from a study of workers employing spray 

applicators; when corrected for incomplete absorption, this corresponds to an approximate exposure of 

50 μg/kg body weight/day (8-hour working day for a 70-kg adult) (IPCS 1994).

Table 5-11. Available Glyphosate Human Monitoring Data

Medium

Concentrations/ 

minimum, maximum Average Notes Reference

Tissue

(brain, 

blood, 

liver, 

kidney)

Postmortem, 

approximately 12–

13 hours after 

ingestion

Glyphosate (ppm): 

kidney 3,650; liver 

600; blood; 550; brain; 

100

After one individual 

ingested 200–250 mL 

Roundup® with 72–

91 g/mL glyphosate

Menkes et 

al. 1991

Urine Pre-application <1–15 μg/L (ppb) Not reported Farmers applying 

pesticide; average age: 

45 years

Acquavella 

Day of pesticide et al. 2004

application

<1–233 μg/L (ppb) Geometric 

mean: 

3.2 μg/L (ppb)

1-Day postpesticide application<1–126 μg/L (ppb) Geometric 

Mean: 

1.7 μg/L (ppb)
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5. POTENTIAL FOR HUMAN EXPOSURE

Table 5-11. Available Glyphosate Human Monitoring Data

Medium

Concentrations/ 

minimum, maximum Average Notes Reference

2-Day postpesticide application<1–81 μg/L (ppb) Geometric 

mean: 

1.1 μg/L (ppb)

3-Day postpesticide application<1–68 μg/L (ppb) Geometric 

mean: 

1.0 μg/L (ppb)

Pre-application <1–3 μg/L (ppb) Not reported Spouses not involved 

with application; 

average age: 42 years

Day of pesticide 

application

<1–2 μg/L (ppb) Not reported

1–3-Day postpesticide application<1–1 μg/L (ppb) Not reported

Pre-application <1–17 μg/L (ppb) Not reported Children not involved 

with application; 

average age: 

11.5 years

Day of pesticide 

application

<1–29 μg/L (ppb) Not reported

1-Day postpesticide application<1–24 μg/L (ppb) Not reported

2-Day postpesticide application<1–12 μg/L (ppb) Not reported

3-Day postpesticide application<1–6 μg/L (ppb) Not reported

Daily during 1-week 

working period 

<0.1 ng/μL Forest workers using 

pressurized herbicide 

sprayers; 8% 

Roundup® (active 

ingredient 360 g/L 

isopropylamine salt)

Jauhiainen 

et al. 1991

3 Weeks after 

1-week working 

period

<0.1 ng/μL

General population 

exposure

Not reported 0.024 μg/L 

(ppb)

Adults >50 years of 

age not involved in 

application in 1993-

1996 Mills et al. 

General population 2017

exposure

Not reported 0.314 μg/L 

(ppb)

Adults involved in 

application in 2014-

2016; average age: 

77.7 years

Following mild to 

fatal ingestions of 

20–500 mL 

pesticide

Glyphosate: 228 mg/L 

mild/moderate case; 

22,300 mg/L fatal 

case; AMPA: 

0.54 mg/L 

mild/moderate case;

91.5 mg/L fatal case

13 individuals ages 25–

69 years

Zouaoui et 

al. 2013

Two occasions 

(1 month apart) 

during spring and 

0.13–5.4 μg/L 1.4 μg/L Farm fathers Curwin et al. 

2007b 0.20–18 μg/L 1.9 μg/L Non-farm fathers

0.062–5.0 μg/L 1.2 μg/L Farm mothers

0.10–11 μg/L 1.5 μg/L Nonfarm mothers
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5. POTENTIAL FOR HUMAN EXPOSURE

Table 5-11. Available Glyphosate Human Monitoring Data

Medium

Concentrations/ 

minimum, maximum Average Notes Reference

summer of 2001 

(LOD 0.9 μg/L)

0.10–9.4 μg/L 2.7 μg/L Farm children

0.022–18 μg/L 2 μg/L Non-farm children

Blood Following mild to 

fatal ingestions of 

20–500 mL 

pesticide

Glyphosate: 3.7 mg/L 

mild/moderate case; 

6,640 mg/L fatal case; 

AMPA: 0.13 mg/L 

mild/moderate case;

15.4 mg/L fatal case

Zouaoui et 

al. 2013

AMPA = aminomethylphosphonic acid; LOD = limit of detection

Acquavella et al. (1999) evaluated 1,513 reported cases to the American Association of Poison Control 

Centers during the years 1993–1997 of ocular or dermal/ocular exposure to Roundup® herbicides with 

glyphosate concentrations ranging from <2 to >20%. Of all exposure cases, 62% involved male subjects, 

>80% were in a residential setting, and about 15% were in occupational settings. During the time period, 

California and Texas had the greatest number of reported cases. Dilute Roundup® formulations 

accounted for about 82% of the exposures; 5% were with concentrated Roundup®.

Acquavella et al. (2005) analyzed biomonitoring data of farmers before, during and after pesticide 

application and para-occupational exposure to their spouses and children over a course of five days (1 day 

before, 1 day during and 3 days post-exposure). Glyphosate was measured in urine at a peak of 3 ppb 

(LOD 1 ppb) on the day of application and then decreased rapidly. Among the spouse and children of 

farmers, glyphosate urinary levels remained relatively stable with only appreciable changes in 

concentration after exposure to pesticide application.

Brouwer et al. (2016) pooled exposure data from three agriculture cohorts from USA, France and 

Norway, specifically, the Agricultural Health Study (AHS), Agriculture and Cancer Study (AGRICAN) 

and the Cancer in the Norwegian Agricultural Population (CNAP), respectively. Among 316,270 

participants who were pesticide applicators or farmers (active or retired), 99% reported ever using any 

pesticide of which 44% reported to have ever been exposed to glyphosate, ranging between 1 to 21 years

of exposure. Specifically, 129,327 men (54%) and 41,276 (14%) females were exposed to glyphosate 

across the three cohorts.

Aris and LeBlanc (2011) examined blood concentrations of glyphosate in a group of 30 pregnant and 

39 non-pregnant females residing in Sherbrooke, Canada. The study noted that none of the subjects 
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5. POTENTIAL FOR HUMAN EXPOSURE

worked or lived with an individual who worked with pesticides. Neither glyphosate nor AMPA were 

detected in the maternal or fetal cord serum of pregnant subjects. Additionally, AMPA was not detected 

in non-pregnant subjects. Glyphosate was detected in 5% of the non-pregnant subjects at a range of not 

detectable to 93.6 ng/mL, with a mean of 73.6 ng/mL (LOD=15 ng/mL). 

The Fourth National Report on Human Exposures to Environmental Chemicals, published and updated by 

the Centers for Disease Control and Prevention reporting biomonitoring data from the National Health 

and Nutrition Examination Survey (NHANES), does not include data for glyphosate or its metabolite, 

AMPA (CDC 2019). 

As with the adult general population, exposure of children to glyphosate may occur through ingestion of 

foods with residues of glyphosate and foods made from these crops, as well as inhalation, dermal contact, 

and/or ocular contact when in the proximity of areas where glyphosate containing herbicides have been 

recently applied. Glyphosate has been detected in dust samples from homes near glyphosate application 

sites or from people who brought it indoors on their bodies and/or clothing from glyphosate-treated areas 

(Curwin et al. 2005). Limited monitoring data indicate that oral exposure may occur from drinking 

contaminated well water supplied from groundwater contaminated with glyphosate; concentrations 

reported in groundwater are relatively low, and this chemical has low leaching potential from soil to 

groundwater. It is unclear if breastmilk is a route of exposure for glyphosate as there are only two studies 

which have evaluated this route (Bus 2015 and McGuire et al., 2016). According to Bus (2015) 

glyphosate is not likely to bioaccumulate in breast milk and McGuire et al., 2016 did not detect it in 

breast milk from lactating mothers with detectable glyphosate in their urine (McGuire et al. 2016).

During the spring and summer of 2001, urinary pesticide concentrations were investigated in families 

residing in non-farm and farm households located in Iowa (Curwin et al. 2007a, 2007b). Urinary

glyphosate levels were fairly similar between farm and non-farm households. In addition, glyphosate 

concentrations were fairly similar when comparing individuals living on farms where the pesticide was 

used with those living on farms where the pesticide was not used. Glyphosate was detected at urinary 

levels equal to or greater than the LOD (0.9 μg/L) in 66% of the 23 non-farm fathers, 75% of the 24 farm 

fathers, 65% of the 24 non-farm mothers, 67% of the farm mothers, 88% of the non-farm children, and 

81% of the farm children (Curwin et al. 2007b). Estimated glyphosate intakes among 40 children 

(17 homes) living on farms where glyphosate was applied ranged from 0.001 to 0.33 μg/kg/day, with 16% 

of the samples below the LOD (Curwin et al. 2007a). Estimated glyphosate intakes among 25 children 
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5. POTENTIAL FOR HUMAN EXPOSURE

(8 homes) living on farms where glyphosate was not applied ranged from 0.003 to 0.64 μg/kg/day, with 

20% of the samples below the LOD. 

McQueen et al. (2012) estimated the mean glyphosate dietary exposure of 43 pregnant women at 

0.001 mg/kg body weight/day and these exposures were well below applicable health guidelines. Since 

only a small percentage of glyphosate crosses the placenta, fetal exposure resulting from maternal 

exposure to glyphosate was minimal.

5.7 POPULATIONS WITH POTENTIALLY HIGH EXPOSURES 

Farm workers, farming families, landscaping workers, and people of all ages living and or working in 

agricultural sectors will incur higher exposure to glyphosate, as agriculture is the largest industry for 

herbicide use. Field workers who apply herbicides containing glyphosate will likely incur higher 

exposures to this chemical. Levels of glyphosate in field workers’ urine has been shown to increase 

during spraying season; however, glyphosate levels did not appear to carry over from previous seasons 

(LaDOTD 1995).
GLYPHOSATE 201

6. ADEQUACY OF THE DATABASE

CHAPTER 6. ADEQUACY OF THE DATABASE

Section 104(i)(5) of CERCLA, as amended, directs the Administrator of ATSDR (in consultation with the 

Administrator of EPA and agencies and programs of the Public Health Service) to assess whether 

adequate information on the health effects of glyphosate is available. Where adequate information is not 

available, ATSDR, in conjunction with NTP, is required to assure the initiation of a program of research 

designed to determine the adverse health effects (and techniques for developing methods to determine 

such health effects) of glyphosate.

Data needs are defined as substance-specific informational needs that, if met, would reduce the 

uncertainties of human health risk assessment. This definition should not be interpreted to mean that all 

data needs discussed in this section must be filled. In the future, the identified data needs will be 

evaluated and prioritized, and a substance-specific research agenda will be proposed. 

6.1 Information on Health Effects

Studies evaluating the health effects of inhalation, oral, and/or dermal exposure of humans and animals to 

glyphosate that are discussed in Chapter 2 are summarized in Figure 6-1 for glyphosate technical and 

Figure 6-2 for glyphosate formulations. As described in Chapter 2, data on inhalation and dermal 

exposure to glyphosate technical were limited. Therefore, Figure 6-1 only summarizes oral exposure 

studies. The purpose of these figures is to illustrate the information concerning the health effects of 

glyphosate. The number of human and animal studies examining each endpoint is indicated regardless of 

whether an effect was found and the quality of the study or studies.

The health effects of glyphosate have been evaluated in epidemiology and animal studies. 

Epidemiological studies are predominantly case-control and cohort epidemiology studies that examined 

possible associations between glyphosate exposure and selected health outcomes (noncancer and cancer 

endpoints), or case reports following accidental or intentional ingestion of glyphosate-containing 

products. These studies do not include data regarding the extent of the exposure or relative contribution 

of inhalation, oral and/or dermal exposure. Most health effects data come from animal studies that 

employed oral exposure and examined potential body weight, gastrointestinal, hematological, hepatic,

and/or developmental effects.
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5. POTENTIAL FOR HUMAN EXPOSURE

Figure 6-1. Summary of Existing Health Effects Studies of Animals Orally 

Exposed to Glyphosate Technical (Listed by Endpoint)*

 

Potential body weight and gastrointestinal effects of glyphosate technical were the most studied 

endpoints 

*Includes studies discussed in Chapter 2; the numbers of studies include those finding no effect.
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5. POTENTIAL FOR HUMAN EXPOSURE

Figure 6-2. Summary of Existing Health Effects Studies on Glyphosate 

Formulations (Listed by Endpoint)*

Potential cancer, respiratory, and developmental effects were the most studied in humans; 

potential body weight and developmental effects were the most studied in animals

*Includes studies discussed in Chapter 2; the numbers of 

studies include those finding no effect. Human 

exposures likely included multiple exposure routes.
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6. ADEQUACY OF THE DATABASE

6.2 Identification of Data Needs 

Missing information in Figure 6-1 and Figure 6-2 should not be interpreted as a “data need”. A data need, 

as defined in ATSDR’s Decision Guide for Identifying Substance-Specific Data Needs Related to 

Toxicological Profiles (ATSDR 1989), is substance-specific information necessary to conduct 

comprehensive public health assessments. Generally, ATSDR defines a data gap more broadly as any 

substance-specific information about glyphosate technical missing from the scientific literature.

Therefore, uncertainties with regard to glyphosate-based formulations (GBFs) would not be considered a 

data gap for the purposes of this Profile. However, exposure to GBFs is widespread, and studies 

investigating the toxicity and components of the individual GBFs are important. EPA’s 2016 Glyphosate 

Issue Paper states, “additional research could also be performed to determine whether formulation 

components, such as surfactants, influence the toxicity of glyphosate formulations,” and describes plans 

to investigate the potential toxicity of GBF components (EPA 2016c).

Oral studies in animals indicate that glyphosate technical toxicity is associated with oral doses levels 

many times higher than levels allowed as residues in food products. The general population is most likely 

to be exposed to glyphosate residues in food sources. Humans should continue to be monitored for 

possible associations between glyphosate intake from food sources and adverse health outcomes. 

Individuals can also be exposed to glyphosate via inhalation, dermal contact, and/or ocular contact during 

application of the herbicide or by being in the vicinity where it is applied. However, available dermal 

studies indicate that only 3–4% of dermally-applied glyphosate enters the blood, though local dermal 

toxicity is possible (see Section 2.11). Data regarding the extent of absorption and potential health effects 

following inhalation exposure are lacking. Therefore, human and animal studies should be designed to 

evaluate airborne exposure levels and possible health effects from inhalation exposure. Additional animal 

studies should be designed to assess the toxic effects of exposure to a variety of glyphosate formulations

and individual components suspected to be toxic. Such studies could also be designed to evaluate 

possible interactions among individual components that might enhance toxicity.

Acute-, Intermediate-, and Chronic-Duration MRLs. No inhalation MRLs were derived for 

glyphosate due to the lack of quantitative exposure-response data for humans or animals.

As stated previously, most information is available from animal studies submitted to EPA’s Office of 

Pesticides Programs using glyphosate technical (typically >90% purity) to fulfill requirements for the 

registration of a particular glyphosate formulation for use in the United States. Some animal studies in 
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6. ADEQUACY OF THE DATABASE

the open literature used glyphosate formulations that typically included 1–41% glyphosate technical (or 

glyphosate salts) and up to 18% surfactant (along with other “inert” ingredients). Surfactants in 

glyphosate formulations may be at least partly responsible for the toxic effects from overexposure to 

glyphosate formulations (Adam et al. 1997; Sawada et al. 1988; Williams et al. 2000). Human exposure 

to glyphosate formulations via its use in weed control includes exposure to all substances in a particular 

glyphosate formulation as well as to other substances that may be added by the end user. No MRLs were 

derived for glyphosate formulations due to the wide variation in glyphosate content and surfactants used 

in various glyphosate formulations and the fact that surfactants can contribute to the toxicity of 

glyphosate formulations. However, because exposures of the general population via food or water 

sources with measurable glyphosate residues most likely involve glyphosate and/or its breakdown 

products rather than the intact glyphosate-based formulation, health effects data associated with oral 

exposure to glyphosate technical are considered relevant to potential derivation of oral MRLs for 

glyphosate. Oral MRLs based on glyphosate technical would not be applicable to intentional or 

accidental ingestion of a glyphosate formulation. 

Acute- and chronic-duration oral MRLs were derived for glyphosate based on gastrointestinal effects in 

animal studies. The chronic-duration oral MRL was adopted as the intermediate-duration oral MRL. 

Health Effects

Respiratory. Limited information was located regarding the effects of inhalation exposure in 

laboratory animals. A single 4-week repeated-exposure rat study found no effects at the highest 

exposure concentration tested (36 mg Roundup®/m3). Studies should be designed to evaluate 

respiratory effects in animals exposed to glyphosate by inhalation.

Developmental. Developmental toxicity studies in animals that employed oral exposure to 

glyphosate technical found no evidence of treatment-related effects at levels below the threshold of 

maternal toxicity. One study reported testicular lesions in weanling rats administered a glyphosate 

formulation orally at doses as little as 5 mg/kg/day. Additional studies should be designed to 

substantiate or refute this finding and to determine whether glyphosate or other ingredients in 

glyphosate formulations are involved in developmental effects on male reproductive organs.

Epidemiology and Human Dosimetry Studies. Limited information was located regarding 

respiratory effects associated with human exposure to glyphosate-based formulations. Additional studies 
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6. ADEQUACY OF THE DATABASE

should be designed to monitor exposure levels and health effects associated with individuals involved in 

the application of glyphosate-based products. There is limited evidence for glyphosate-related 

developmental effects in humans. Additional studies should be designed to evaluate possible associations 

between exposure to glyphosate and developmental endpoints in humans. Numerous agencies have 

evaluated glyphosate for possible associations between exposure and risk of various cancers. The 

majority of the human studies used self-reported ever/never glyphosate use as the biomarker of exposure. 

The results of these studies should be interpreted cautiously given the lack of quantitative or semiquantitative glyphosate exposure information and the likely exposure to other pesticides. Most studies 

found no association between exposure to glyphosate-based products and risk of cancer. However, a 

possible association between exposure to glyphosate and risk of non-Hodgkin’s lymphoma could not be 

ruled out, based on conflicting results.

Biomarkers of Exposure and Effect. The most reliable biomarker of exposure to glyphosate is its 

detection in blood and urine. However, the limit of detection (LOD) for glyphosate in blood is higher than 

the LOD for glyphosate in urine (see Table 5-4), meaning using urine as a biomarker of exposure may be 

more informative, especially in cases where human glyphosate levels are expected to be low. Recent 

biomarker studies seem to show a preference for urine as a biomarker (Soukup et al. 2020, Zoller et al. 

2020, Zhang et al. 2020).

Absorption, Distribution, Metabolism, and Excretion. The toxicokinetics of glyphosate 

following oral and dermal exposure have been adequately described. Additional studies should be 

designed to evaluate the toxicokinetics of inhaled glyphosate.

Comparative Toxicokinetics. Significant species differences in the toxicokinetics of glyphosate are 

not likely.

Children’s Susceptibility. Age-related differences in susceptibility to glyphosate have not been 

elucidated. Due to relatively large oral doses required to elicit adverse effects in glyphosate-exposed 

animals, it may be difficult to evaluate age-related differences in susceptibility. As additional 

epidemiological data become available, age-related issues regarding susceptibility to glyphosate toxicity 

should be evaluated.

Physical and Chemical Properties. The physical chemical properties of glyphosate are 

summarized in Chapter 4. No data needs are identified.
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6. ADEQUACY OF THE DATABASE

Production, Import/Export, Use, Release, and Disposal. No information is available in the TRI 

database on facilities that manufacture or process glyphosate because this chemical is not required to be 

reported under Section 313 of the Emergency Planning and Community Right-to-Know Act (Title III of 

the Superfund Amendments and Reauthorization Act of 1986) (EPA 2005b). There is no information on 

releases of glyphosate from manufacturing and processing facilities because these releases are not 

required to be reported (EPA 2005b). Data on current manufacturing, processing, import/export values 

would be useful information. Data on current uses and disposal practices are outlined in Sections 5.2.3 

and 5.2.4. Further studies on these practices do not appear to be essential.

Environmental Fate. Transport, partitioning, and bioconcentration data are available for glyphosate 

summarized in Section 5.4. In glyphosate-tolerant plants, glyphosate is converted to N-acetylglyphosate; 

therefore, studies evaluating the possibility of additional crop and plant metabolites, along with the 

characteristic fates, may be beneficial (Pioneer 2006). Additional studies should be designed to further 

assess potential for glyphosate to persist in foods, water, and soil.

Bioavailability from Environmental Media. Glyphosate degrades quickly in the environment and 

adsorbs to soils and sediment and possesses low bioconcentration in aquatic organisms, suggesting that 

bioavailability from environmental media is low. A study regarding the bioavailability of glyphosate in 

soil indicated that degradation rates decreased in lower soil horizons as microbial populations of 

glyphosate degrading organisms decreased, but bioremediation practices that incorporate anthropic 

bacteria can be useful to remediate highly polluted glyphosate-containing soils and maintain low 

bioavailability (Shushkova et al. 2010). Additional studies on glyphosates bioavailability from different 

types of soil would be helpful to expand our understanding of potential human exposures to glyphosate 

bound residues. 

Food Chain Bioaccumulation. Studies are available that indicate that glyphosate has very low 

potential to bioconcentrate in aquatic organisms and is not expected to bioaccumulate in the food chain.

No data needs are identified.

Exposure Levels in Environmental Media. Reliable monitoring data for the levels of glyphosate 

in environmental media surrounding areas where it is applied are available (Chang et al. 2011; USGS 

2007; WQP 2017). The USGS NAWQA frequently reports on levels of glyphosate and other substances 
GLYPHOSATE 208

6. ADEQUACY OF THE DATABASE

in both surface water and groundwater. No data needs are identified; however, monitoring studies in air, 

water, soil, and other environmental media should continue as this is an herbicide used globally.

Exposure Levels in Humans. Studies are needed to investigate human intake of glyphosate via 

food and water, such as total diet studies. Up until 2016–2017, the FDA did not test for glyphosate 

residues in food sources because its multi-residue testing protocols did not include glyphosate. The FDA 

has now developed a method to specifically test for glyphosate residues in foods and results are expected 

to be provided through the FDA Pesticide Residue Monitoring Program (FDA 2018). Biomonitoring 

information of glyphosate for the general population would be useful in conducting future risk 

assessments. 

Exposures of Children. Monitoring of children’s exposure to glyphosate would be useful, in 

combination with children’s health and susceptibility information, to assess the potential risk for 

deleterious effects.

Analytical Methods. Standardized methods that yield low detection limits for glyphosate and 

aminomethylphosphonic acid (AMPA) in biological samples (e.g., urine analysis, blood analysis) may 

provide more sensitivity and a more complete exposure analysis.

6.3 Ongoing Studies 

Glyphosate is a potential candidate for addition to the California Environmental Contaminant 

Biomonitoring Program (CDPH 2013). Ongoing research identified in the National Institutes of Health 

(NIH) RePORTER (2017) database is summarized in Table 6-1. In addition, NTP (2017) is performing 

research to investigate potential genetic and mechanistic toxicity of glyphosate and glyphosate 

formulations. NTP will also evaluate published literature for information regarding glyphosate on noncancer outcomes. Researchers at the Cesare Maltoni Cancer Research Centre at the Ramazzini Institute in 

Italy are conducting research into potential genetic, reproductive, and developmental effects in rats 

administered glyphosate at levels equivalent to those allowed in humans.
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6. ADEQUACY OF THE DATABASE

Table 6-1. Ongoing Studies on Glyphosate

Investigator Affiliation Research description Sponsor

De Roos, AJ Drexel 

University

Occupational pesticide use and risk 

of lymphoid cancers

National Cancer Institute

Keating, AF Iowa State 

University

Investigating modes of action of 

glyphosate-induced ovotoxicity

National Institute of 

Environmental Health Sciences

Curl, CL Boise State 

University

Measurement of agricultural and 

dietary glyphosate exposure among 

pregnant women

National Institute of 

Environmental Health Sciences

Ford, B University of 

California 

Berkeley

Understanding complex toxicological 

mechanisms of glyphosate and 

mechanism-sharing environmental 

chemical mixtures

National Institute of 

Environmental Health Sciences

Newman, LS University of 

Colorado 

Denver

Etiologic and mechanistic factors 

underlying chronic kidney disease in 

Guatemalan sugarcane workers

National Institute of 

Environmental Health Sciences

Petropoulos, Z Boston 

University 

Medical 

Campus

Occupational heat exposure and 

gene-environment interactions in 

Mesoamerican nephropathy

National Institute of 

Environmental Health Sciences

Scammell, M Boston 

University

Medical 

Campus

Longitudinal study of risk factors for 

Mesoamerican nephropathy among 

agricultural workers in El Salvador, 

central America

National Institute of 

Environmental Health Sciences

Von Ehrenstein, 

O

University of 

California Los 

Angeles

Pesticide exposure and birth 

outcomes

National Institute of 

Environmental Health Sciences

Mitchell, KS VA Boston 

Health Care 

System

Eating disorders in veterans: risk, 

resilience, and service use

Not specified

Source: RePORTER 2020
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CHAPTER 7. REGULATIONS AND GUIDELINES

Pertinent international and national regulations, advisories, and guidelines regarding glyphosate in air, 

water, and other media are summarized in Table 7-1. This table is not an exhaustive list, and current 

regulations should be verified by the appropriate regulatory agency.

ATSDR develops MRLs, which are substance-specific guidelines intended to serve as screening levels by 

ATSDR health assessors and other responders to identify contaminants and potential health effects that 

may be of concern at hazardous waste sites. See Section 1.3 and Appendix A for detailed information on 

the MRLs for glyphosate.

Table 7-1. Regulations and Guidelines Applicable to Glyphosate

Agency Description Information Reference

Air

EPA RfC Not evaluated IRIS 1989

WHO Air quality guidelines No data WHO 2010

Water & Food

EPA Drinking water standards and health advisories EPA 2012d

1-Day (10-kg child) 20 mg/L

10-Day (10-kg child) 20 mg/L

DWEL 70 mg/L

National primary drinking water regulations EPA 2009b

Maximum Contaminant Level 0.7 mg/L

Maximum Contaminant Level Goal 0.7 mg/L

RfD 1.0 mg/kg/daya EPA 2017d

WHO Drinking water quality guidelines Not establishedb WHO 2017

FDA EAFUS No datac FDA 2013c

Cancer

HHS Carcinogenicity classification No data NTP 2016

EPA Carcinogenicity classification Not likely to be 

carcinogenic to 

humans

EPA 2017c, 2017d, 2020

IARC Carcinogenicity classification Group 2AdIARC 2017

Occupational

ACGIH TLV No data ACGIH 2016

OSHA PEL (8-hour TWA) for general industry No data OSHA 2016b

PEL (8-hour TWA) for shipyards and 

construction

No data OSHA 2016c

PEL (8-hour TWA) for construction No data OSHA 2016a
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7. REGULATIONS AND GUIDELINES

Table 7-1. Regulations and Guidelines Applicable to Glyphosate

Agency Description Information Reference

NIOSH REL (up to 10-hour TWA) No data NIOSH 2016

Emergency Criteria

EPA AEGLs-air No data EPA 2016b

DOE PACs-air No data DOE 2018

aEPA’s Office of Pesticides Program (OPP) published an interim registration review decision on glyphosate in 

January 2020, which finalized the Glyphosate Draft Human Health Risk Assessment in Support of Registration 

Review. The human health risk assessment derived an RfD of 1.0 mg/kg/day based on the same study that ATSDR 

used for derivation of the acute-duration MRL.

bGlyphosate and aminomethylphosphonic acid occur in drinking water at concentrations well below those of health 

concern, so a guideline value was not deemed necessary.

cThe EAFUS list of substances contains ingredients added directly to food that FDA has either approved as food 

additives or listed or affirmed as GRAS.

dGroup 2A: Probably carcinogenic to humans.

ACGIH = American Conference of Governmental Industrial Hygienists; AEGL = acute exposure guideline levels; 

CFR = Code of Federal Regulations; DOE = Department of Energy; DWEL = drinking water equivalent level; 

EAFUS = Everything Added to Food in the United States; EPA = Environmental Protection Agency; FDA = Food and 

Drug Administration; HHS = Department of Health and Human Services; IARC = International Agency for Research 

on Cancer; NIOSH = National Institute for Occupational Safety and Health; NTP = National Toxicology Program; 

OSHA = Occupational Safety and Health Administration; PAC = Protective Action Criteria; PEL = permissible 

exposure limit; REL = recommended exposure limit; RfC = inhalation reference concentration; RfD = reference dose

TLV = threshold limit values; TWA = time-weighted average; WHO = World Health Organization
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GLYPHOSATE A-1

APPENDIX A. ATSDR MINIMAL RISK LEVEL WORKSHEETS

MRLs are derived when reliable and sufficient data exist to identify the target organ(s) of effect or the 

most sensitive health effect(s) for a specific duration for a given route of exposure. An MRL is an 

estimate of the daily human exposure to a hazardous substance that is likely to be without appreciable risk 

of adverse noncancer health effects over a specified route and duration of exposure. MRLs are based on 

noncancer health effects only; cancer effects are not considered. These substance-specific estimates, 

which are intended to serve as screening levels, are used by ATSDR health assessors to identify 

contaminants and potential health effects that may be of concern at hazardous waste sites. It is important 

to note that MRLs are not intended to define clean-up or action levels.

MRLs are derived for hazardous substances using the NOAEL/uncertainty factor approach. They are 

below levels that might cause adverse health effects in the people most sensitive to such chemicalinduced effects. MRLs are derived for acute (1–14 days), intermediate (15–364 days), and chronic 

(≥365 days) durations and for the oral and inhalation routes of exposure. Currently, MRLs for the dermal 

route of exposure are not derived because ATSDR has not yet identified a method suitable for this route 

of exposure. MRLs are generally based on the most sensitive substance-induced endpoint considered to 

be of relevance to humans. Serious health effects (such as irreparable damage to the liver or kidneys, or 

birth defects) are not used as a basis for establishing MRLs. Exposure to a level above the MRL does not 

mean that adverse health effects will occur.

MRLs are intended only to serve as a screening tool to help public health professionals decide where to 

look more closely. They may also be viewed as a mechanism to identify those hazardous waste sites that 

are not expected to cause adverse health effects. Most MRLs contain a degree of uncertainty because of 

the lack of precise toxicological information on the people who might be most sensitive (e.g., infants, 

elderly, nutritionally or immunologically compromised) to the effects of hazardous substances. ATSDR 

uses a conservative (i.e., protective) approach to address this uncertainty consistent with the public health 

principle of prevention. Although human data are preferred, MRLs often must be based on animal studies 

because relevant human studies are lacking. In the absence of evidence to the contrary, ATSDR assumes 

that humans are more sensitive to the effects of hazardous substance than animals and that certain persons 

may be particularly sensitive. Thus, the resulting MRL may be as much as 100-fold below levels that 

have been shown to be nontoxic in laboratory animals.
GLYPHOSATE A-2

APPENDIX A

Proposed MRLs undergo a rigorous review process: Health Effects/MRL Workgroup reviews within the 

Division of Toxicology and Human Health Sciences, expert panel peer reviews, and agency-wide MRL 

Workgroup reviews, with participation from other federal agencies and comments from the public. They 

are subject to change as new information becomes available concomitant with updating the toxicological 

profiles. Thus, MRLs in the most recent toxicological profiles supersede previously published MRLs. 

For additional information regarding MRLs, please contact the Division of Toxicology and Human 

Health Sciences, Agency for Toxic Substances and Disease Registry, 1600 Clifton Road NE, Mailstop 

S102-1, Atlanta, Georgia 30329-4027.

Human exposure to glyphosate formulations via its use in weed control includes exposure to all 

substances in a particular glyphosate formulation. No MRLs were derived for glyphosate formulations 

due to the wide variation in glyphosate content and surfactants used in various glyphosate formulations 

and the fact that surfactants can contribute to the toxicity of glyphosate formulations. However, the 

general population may be exposed via food or water sources containing glyphosate residues from 

glyphosate-based formulations registered for use in agricultural and residential environments. Therefore, 

health effects data associated with oral exposure to glyphosate technical are considered relevant to 

potential derivation of oral MRLs for glyphosate.
GLYPHOSATE A-3

APPENDIX A

MINIMAL RISK LEVEL (MRL) WORKSHEET

Chemical Name: Glyphosate technical

CAS Numbers: 1071-83-6

Date: August 2020

Profile Status: Final 

Route: Inhalation

Duration: Acute

MRL Summary: There are insufficient data for derivation of an acute-duration inhalation MRL.

Rationale for Not Deriving an MRL: No acute-duration inhalation exposure-response studies were 

identified for glyphosate.

Agency Contact (Chemical Manager): Hana R. Pohl, M.D., Ph.D.
GLYPHOSATE A-4

APPENDIX A

MINIMAL RISK LEVEL (MRL) WORKSHEET

Chemical Name: Glyphosate technical

CAS Numbers: 1071-83-6

Date: August 2020

Profile Status: Final 

Route: Inhalation

Duration: Intermediate

MRL Summary: There are insufficient data for derivation of an intermediate-duration inhalation MRL.

Rationale for Not Deriving an MRL: No intermediate-duration inhalation exposure-response studies 

were identified for glyphosate.

Agency Contact (Chemical Manager): Hana R. Pohl, M.D., Ph.D.
GLYPHOSATE A-5

APPENDIX A

MINIMAL RISK LEVEL (MRL) WORKSHEET

Chemical Name: Glyphosate technical

CAS Numbers: 1071-83-6

Date: August 2020

Profile Status: Final 

Route: Inhalation

Duration: Chronic

MRL Summary: There are insufficient data for derivation of a chronic-duration inhalation MRL.

Rationale for Not Deriving an MRL: No chronic-duration inhalation exposure-response studies were 

identified for glyphosate.

Agency Contact (Chemical Manager): Hana R. Pohl, M.D., Ph.D.
GLYPHOSATE A-6

APPENDIX A

MINIMAL RISK LEVEL (MRL) WORKSHEET

Chemical Name: Glyphosate technical

CAS Numbers: 1071-83-6

Date: August 2020

Profile Status: Final 

Route: Oral

Duration: Acute

MRL: 1 mg/kg/day

Critical Effect: Gastrointestinal effects

Reference: EPA 2017b

Point of Departure: NOAEL of 100 mg/kg/day

Uncertainty Factor: 100

LSE Graph Key: 7

Species: Rabbit

MRL Summary: An acute-duration oral MRL of 1 mg/kg/day was derived for glyphosate based on 

gastrointestinal effects (diarrhea, few feces) observed in pregnant female New Zealand white rabbits 

administered glyphosate acid (96.5% purity) by daily gavage (in deionized water) during GDs 8–20 

(EPA 2017b). The MRL is based on a NOAEL of 100 mg/kg/day and a total uncertainty factor of 100 

(10 for animal to human extrapolation and 10 for human variability). 

Selection of the Critical Effect: Several acute-duration oral studies were available regarding the toxicity 

of glyphosate technical following acute-duration oral exposure (see Table A-1). The lowest LOAELs 

were 175 mg/kg/day for gastrointestinal effects (diarrhea, few feces) in maternal rabbits and 

300 mg/kg/day for developmental effects (depressed fetal weight) following gavage treatment with 

glyphosate technical during GDs 8–20 at 175 mg/kg/day. Based on available data, gastrointestinal 

disturbance is considered to represent the most sensitive effect of glyphosate toxicity following oral 

exposure in laboratory animals. 

Table A-1. NOAELs and LOAELs Identified in Acute-Duration Oral Studies of 

Glyphosate Technical

Endpoint Effect

NOAEL 

(mg/kg/day)

LOAEL 

(mg/kg/day) Reference

Body weight 28.5% depressed maternal body weight 

gain in rats

1,000 3,500 EPA 1992e

No effect in pregnant rats 1,000 EPA 2017b

No effect in pregnant rabbits 300 EPA 2017b

Gastrointestinal Diarrhea in 2/8 rats gavaged once 2,000 Adam et al. 1997

Diarrhea in rats gavaged once 1,000 2,000 EPA 2013c

Diarrhea, soft stools in pregnant rats 

gavaged on GDs 6–19

1,000 3,500 EPA 1992e

Diarrhea, few feces in pregnant rabbits 

gavaged on GDs 8–20

100 175 EPA 2017b
GLYPHOSATE A-7

APPENDIX A

Table A-1. NOAELs and LOAELs Identified in Acute-Duration Oral Studies of 

Glyphosate Technical

Endpoint Effect

NOAEL 

(mg/kg/day)

LOAEL 

(mg/kg/day) Reference

Developmental Decreased fetal weight; delayed 

ossification

1,000 3,500 EPA 1992e

No effect in fetuses from pregnant rats 

gavaged on GDs 7–16

1,000 EPA 2017b

Depressed weight in fetuses from 

pregnant rabbits gavaged on GDs 8–20

175 300 EPA 2017b

Other Hypothermia in rats gavaged once 1,000 2,000 EPA 2013c

GD = gestation day; LOAEL = lowest-observed-adverse-effect level; NOAEL = no-observed-adverse-effect level

Selection of the Principal Study: Among available acute-duration oral toxicity studies for glyphosate, 

the developmental toxicity study in rabbits (EPA 2017b) identified the lowest LOAEL (gastrointestinal 

effects in pregnant rabbits gavaged with glyphosate acid); the corresponding NOAEL was 100 mg/kg/day. 

Therefore, this study was selected as the principal study for deriving an acute-duration oral MRL for 

glyphosate.

Summary of the Principal Study:

EPA. 2017b. Memorandum. December 13, 2017. Glyphosate: Preparation of data evaluation records 

for developmental rat and rabbit toxicity studies. MRID No.: 43320615, 43320616. Washington, DC: 

U.S. Environmental Protection Agency, Office of Chemical Safety and Pollution Prevention.

Groups of sperm-positive female New Zealand white rabbits (20/group) were administered glyphosate 

acid (95.6% active ingredient) by daily gavage (in deionized water vehicle; dosing volume 2 mL/kg body 

weight) on GDs 8–20 at target concentrations of 0, 100, 175, or 300 mg/kg/day (adjusted for purity of 

active ingredient). Dams were monitored for survival, clinical signs, body weight, and food intake. On 

GD 30, dams were sacrificed and subjected to gross external and internal examination, pregnancy status, 

weight of gravid uteri, number of corpora lutea, number and position of implantations, live fetuses, and 

early and late intrauterine deaths. Fetuses were evaluated for weight and sex. External, visceral, and 

skeletal examinations were performed; brains were subjected to macroscopic examination.

The 100 mg/kg/day dose level represented a NOAEL for maternal toxicity. At 175 and 300 mg/kg/day,

maternal rabbits exhibited diarrhea and reduced production of feces. Mean body weight in the 

300 mg/kg/day group of maternal rabbits ranged from 5.2 to 7.4% less than that of controls during 

GDs 16–26. The depressed maternal body weight was <10% in magnitude, and was therefore not 

considered to represent an adverse effect. Furthermore, there were no statistically significant differences 

between controls and glyphosate-treated groups regarding GD 30 mean maternal body weight. Gross 

pathologic examination of maternal rabbits revealed no treatment-related effects. There were no 

treatment-related effects on pregnancy rate, numbers of corpora lutea, total number of implantation sites, 

litter size, sex ratio, or pre- or post-implantation loss. The 300 mg/kg/day dose group exhibited 8.3% 

lower mean fetal weight (p<0.05). Gross and visceral examination of fetuses revealed no treatmentrelated effects. Increased incidences of fetuses with selected minor skeletal defects (e.g., delayed 

sternebral and vertebral ossification) were observed at the 300 mg/kg/day maternal dose level. However, 

incidences of these skeletal defects did not appear to be increased in glyphosate-treated groups when 
GLYPHOSATE A-8

APPENDIX A

evaluated on a per litter basis; therefore, they were not considered treatment-related developmental 

effects.

Selection of the Point of Departure: Incidence data for the gastrointestinal effects were not presented in 

the available data evaluation record (DER) for the study, thus precluding a benchmark dose (BMD) 

approach to deriving an MRL. Therefore, the NOAEL of 100 mg/kg/day was selected as the point of 

departure for deriving an acute-duration oral MRL for glyphosate.

Uncertainty Factor: The NOAEL of 100 mg/kg/day was divided by a total uncertainty factor of 100:

• 10 for animal to human extrapolation

• 10 for human variability

Other Additional Studies or Pertinent Information: Glyphosate-induced gastrointestinal effects were 

observed in acute-duration oral studies of rats (Adam et al. 1997; EPA 1992e, 2013c), although rabbits 

appear to be much more sensitive than rats to glyphosate-induced gastrointestinal effects following oral 

dosing.

Agency Contacts (Chemical Managers): Hana R. Pohl, M.D., Ph.D.
GLYPHOSATE A-9

APPENDIX A

MINIMAL RISK LEVEL (MRL) WORKSHEET

Chemical Name: Glyphosate technical

CAS Numbers: 1071-83-6

Date: August 2020

Profile Status: Final 

Route: Oral

Duration: Intermediate

MRL Summary: The chronic-duration oral MRL of 1 mg/kg/day is adopted as the intermediate-duration 

oral MRL.

Rationale for Not Deriving an MRL: Several intermediate-duration oral animal studies were available 

for glyphosate technical (see Table A-2).

Table A-2. NOAELs and LOAELs Identified in Intermediate-Duration Oral Studies 

of Glyphosate Technical

Endpoint Effect

NOAEL 

(mg/kg/day)

LOAEL 

(mg/kg/day) Reference

Body weight 12–18% depressed paternal body 

weight gain in rats

M: 754

F: 802

M: 2,219

F: 3,134

EPA 1992a

No effect in rats (highest dose) M, F: 30 EPA 1992g

No effect in rats (highest dose) M: 1,234

F: 1,273

EPA 2013a

18% lower mean body weight and 

body weight gain in male rats

M: 1,678

F: 3,393

M: 3,393 NTP 1992

No effect in mice (highest dose) F: 1,447.5 EPA 2013b

10–11% lower mean final body 

weight in mice

M: 2,273

F: 5,846

M: 4,776

F: 11,977

NTP 1992

No effect in maternal rabbits 

(highest dose)

F: 350 EPA 1992f

Gastrointestinal Soft stool in rats M: 754

F: 802

M: 2,219

F: 3,134

EPA 1992a

Increased severity of basophilia 

and hypertrophy of acinar cells in 

parotid and submandibular salivary 

glands of rats

M: 205

F: 213

M: 410

F: 421

NTP 1992

Increased severity of basophilia of 

acinar cells in parotid salivary gland

of mice

M: 1,065

F: 1,411

M: 2,273

F: 2,707

NTP 1992

Increased incidence of soft stool 

and/or diarrhea in pregnant rabbits

175 350 EPA 1992f

Hematological No effect in rats (highest dose) M, F: 3,393 NTP 1992
GLYPHOSATE A-10

APPENDIX A

Table A-2. NOAELs and LOAELs Identified in Intermediate-Duration Oral Studies 

of Glyphosate Technical

Endpoint Effect

NOAEL 

(mg/kg/day)

LOAEL 

(mg/kg/day) Reference

Hepatic No effect in rats (highest dose) M: 1,234

F: 1,273

EPA 2013a

M: Increases in liver weight and 

serum ALT

F: Increases in liver weight and 

serum AP, ALT, and bile acids

M: 811

F: 1,690

M: 1,678

F: 3,393

NTP 1992

No effect in mice M: 10,780

F: 11,977

NTP 1992

Renal No effect in rats (highest dose) M: 1,234

F: 1,273

EPA 2013a

Immunological No effect in mice (highest dose) F: 1,447.5 EPA 2013b

Neurological No effect in rats (highest dose) M: 1,546.5

F: 1,630.6

EPA 2013c

Reproductive No effect in rats (highest dose) M: 2,219

F: 3,234

EPA 1992a

No effect in rats (highest dose) M, F: 30 EPA 1992g

No effect in rats (highest dose) M: 1,234

F: 1,273

EPA 2013a

Developmental 14–20% depressed pup body 

weight during lactation (maternally 

toxic dose level)

802 3,134 EPA 1992a

Delayed preputial separation 408 1,234 EPA 2013a

No effect in rabbits (highest dose) 350 EPA 1992f

ALT = alanine aminotransferase; AP = alkaline phosphatase; F = female; LOAEL = lowest-observed-adverse-effect 

level; M = male; NOAEL = no-observed-adverse-effect level

Increased incidence of kidney tubular dilation was reported for F3b male weanlings of a 3-generation 

study of glyphosate technical (98.7% purity) administered to male and female Sprague-Dawley rats in the 

diet at an estimated dose level of 30 mg/kg/day; the reported NOAEL was 10 mg/kg/day (EPA 1992g). 

However, there were no signs of treatment-related effects on kidneys of rat offspring in two subsequent 

2-generation rat studies at dietary doses up to 1,234 or 1,273 mg/kg/day for parental males and females, 

respectively (EPA 2013a), or 2,633 or 3,134 mg/kg/day for parental males and females, respectively 

(EPA 1992a). Therefore, the finding of increased incidence of kidney tubular dilation in the 3-generation 

rat study (EPA 1992g) was considered a spurious result rather than a glyphosate-induced adverse 

developmental effect. In one 2-generation oral rat study, exposure via the diet at estimated parental dose 

levels of 1,234 or 1,273 mg/kg/day (parental males and females, respectively) resulted in delayed 

preputial separation in male pups (EPA 2013a). In the other 2-generation study, the highest dietary dose 

level (up to 2,633 and 3,134 mg/kg/day for parental males and females, respectively) resulted in up to 14–

20% depressed pup body weight and/or body weight gain during the lactation period (EPA 1992a). There 

were no apparent treatment-related developmental effects in a study of rabbits treated by gavage at up to 

350 mg/kg/day during GDs 6–27 (EPA 1992f).
GLYPHOSATE A-11

APPENDIX A

Consideration was given to the increased anogenital distance (AGD) reported by Manservisi et al. (2019). 

This pilot study found that male F1 Sprague-Dawley rats exposed to 1.75 mg/kg/day glyphosate technical 

from gestation day 6 to post-natal day 120 showed increased anogenital distance at postnatal day 4. 

However, this result was determined to be insufficient for MRL derivation. The study used only one dose, 

which was substantially lower than the other lowest observed adverse effect levels (LOAELs) and the no 

observed adverse effect levels (NOAELs) identified in the body of literature. Furthermore, while 

decreases in AGD are sometimes considered an adverse effect related to endocrine disruption, increases 

in AGD are less commonly used because the toxicological significance of such increases is not well 

understood (Schwartz et al. 2019). Given that only one dose was tested, the observed effect was small 

(6%) and not observed in other studies, and because the relevance of such an effect to human health is not 

well-understood, it is not appropriate to use this study for MRL derivation. 

As shown in Table A-2, gastrointestinal endpoints are the most sensitive to intermediate-duration oral 

exposure of laboratory animals to glyphosate technical. Pregnant rabbits gavaged with glyphosate 

technical daily at 350 mg/kg/day (LOAEL) during GDs 6–27 exhibited increased incidence of soft stool 

and/or diarrhea; the NOAEL was 175 mg/kg/day (EPA 1992f). Similar results were observed among 

other pregnant rabbits gavaged daily with glyphosate technical at 175 mg/kg/day (LOAEL) during GDs 

8–20 (an acute-duration oral exposure scenario); the NOAEL was 100 mg/kg/day (EPA 2017b).

Increased severity of basophilia and hypertrophy of acinar cells in parotid and submandibular salivary 

glands were observed among male and female rats receiving glyphosate from the diet for 13 weeks at 

410 and 421 mg/kg/day, respectively; NOAELs were 205 and 213 mg/kg/day, respectively (NTP 1992). 

Increased severity of basophilia of acinar cells in parotid salivary glands were observed in male and 

female mice similarly treated at estimated doses of 2,273 and 2,707 mg/kg/day, respectively; NOAELs 

were 507 and 753 mg/kg/day, respectively (NTP 1992). Thus, rats appear to be much more sensitive than 

mice to glyphosate treatment-related effects on salivary glands.

Among reliable animal study results, the LOAEL of 350 mg/kg/day for gastrointestinal effects (increased 

incidence of soft stool and/or diarrhea) in maternal rabbits gavaged daily during GDs 6–27 represents the 

most sensitive adverse effect from intermediate-duration oral exposure to glyphosate technical (EPA 

1992f); the corresponding NOAEL is 175 mg/kg/day (see Table A-2). Incidence and severity data were 

not available for review. Application of a NOAEL/LOAEL approach using the NOAEL of 

175 mg/kg/day as the point of departure and a total uncertainty factor of 100 (10 for extrapolation from 

animals to humans and 10 for human variability) would result in an intermediate-duration oral MRL of 

2 mg/kg/day (rounded up from 1.75 mg/kg/day). An intermediate-duration oral MRL was not derived for 

glyphosate because an intermediate-duration oral MRL of 2 mg/kg/day is higher than the acute- and 

chronic-duration oral MRL of 1 mg/kg/day. Glyphosate-induced microscopic changes in salivary glands 

of the rats treated orally for 13 weeks are not considered an adequate basis for MRL derivation due to 

uncertainty regarding the adversity of the effect. However, application of a total uncertainty factor of 

100 (10 for extrapolation from animals to humans and 10 for human variability) to the NOAEL of 

205 mg/kg/day for salivary gland changes in male rats administered glyphosate in the diet for 13 weeks 

would result in an intermediate-duration oral MRL of 2 mg/kg/day. The chronic-duration oral MRL of 1 

mg/kg/day for glyphosate is adopted as the intermediate-duration oral MRL because 1 mg/kg/day is 

considered protective of intermediate-duration oral exposure to glyphosate as well.

Agency Contact (Chemical Manager): Hana R. Pohl, M.D., Ph.D.
GLYPHOSATE A-12

APPENDIX A

MINIMAL RISK LEVEL (MRL) WORKSHEET

Chemical Name: Glyphosate technical

CAS Numbers: 1071-83-6

Date: August 2020

Profile Status: Final 

Route: Oral

Duration: Chronic

MRL: 1 mg/kg/day

Critical Effect: Inflammation of gastric squamous mucosa

Reference: EPA 1991a, 1991b

Point of Departure: NOAEL of 113 mg/kg/day

Uncertainty Factor: 100

LSE Graph Key: 19

Species: Rat

MRL Summary: A chronic-duration oral MRL of 1 mg/kg/day was derived for glyphosate based on 

gastrointestinal effects (inflammation of gastric squamous mucosa) observed in female rats administered 

glyphosate technical in the diet for up to 24 months at an estimated dose of 457 mg/kg/day; the NOAEL 

was 113 mg/kg/day (EPA 1991a, 1991b). The MRL is based on a NOAEL of 113 mg/kg/day and a total 

uncertainty factor of 100 (10 for animal to human extrapolation and 10 for human variability). 

Selection of the Critical Effect: Several chronic-duration oral animal studies were available for 

glyphosate technical (see Table A-3).

Table A-3. NOAELs and LOAELs Identified in Chronic-Duration Oral Studies of 

Glyphosate Technical

Endpoint Effect

NOAEL 

(mg/kg/day)

LOAEL 

(mg/kg/day) Reference

Body weight 13% lower body weight in female 

rats at treatment week 81

M: 940

F: 457 F: 1,183

EPA 1991a, 1991b

No effect in rats (highest dose) M: 31.45

F: 34.02

EPA 1992d

No effect in rats (highest dose) M: 1,214

F: 1,498

EPA 2013a

11–14% lower body weight and 

body weight gain in rats

300 1,000 EPA 2015c

No effect in mice (highest dose) M: 4,945

F: 6,069

EPA 2015a

No effect in mice (highest dose) 1,000 EPA 2015c

No effect in dogs (highest dose) 500 EPA 1986a, 1987
GLYPHOSATE A-13

APPENDIX A

Table A-3. NOAELs and LOAELs Identified in Chronic-Duration Oral Studies of 

Glyphosate Technical

Endpoint Effect

NOAEL 

(mg/kg/day)

LOAEL 

(mg/kg/day) Reference

Gastrointestinal Inflammation of gastric squamous 

mucosa

M: 940

F: 113 F: 457

EPA 1991a, 1991b

No effect in rats (highest dose) M: 31.45

F: 34.02

EPA 1992d

Increased severity of basophilia 

and hypertrophy of acinar cells in 

parotid and mandibular salivary 

gland in rats

100 300 EPA 2015c

No effect in mice (highest dose) M: 4,945

F: 6,069

EPA 2015a

Hematological No effect in rats (highest dose) M: 940

F: 1,183

EPA 1991a, 1991b

No effect in rats (highest dose) M: 31.45

F: 34.02

EPA 1992d

No effect in rats (highest dose) M: 1,214

F: 1,498

EPA 2015c

No effect in rats (highest dose) 1,000 EPA 2015c

No effect in mice (highest dose) M: 4,945

F: 6,069

EPA 2015a

No effect in dogs (highest dose) 500 EPA 1986a, 1987

Hepatic No effect in rats (highest dose) M: 940

F: 1,183

EPA 1991a, 1991b

No effect in rats (highest dose) M: 31.45

F: 34.02

EPA 1992d

Increased serum AP, ALT, bilirubin 

in male rats; increased serum AP, 

ALT in female rats

M: 361

F: 437

M: 1,214

F: 1,498

EPA 2015c

No effect in rats 1,000 EPA 2015c

Centrilobular hepatocellular 

necrosis in male rats

M: 835

F: 6,069

M: 4,945 EPA 2015a

No effect in mice (highest dose) 1,000 EPA 2015c

Renal Increased specific gravity, 

decreased pH of urine in male rats

M: 362

F: 1,183

M: 940 EPA 1991a, 1991b

No effect in rats (highest dose) M: 31.45

F: 34.02

EPA 1992d

M: Decreased pH of urine in rats

M, F: Papillary necrosis in kidney in 

rats

M: 361

F:437

M: 1,214

F: 1,498

EPA 2015c

Decreased pH of urine in male rats M: 300

F: 1,000

M: 1,000 EPA 2015c

Renal tubular epithelial basophilia 

in female mice

M: 4,945

F: 968 F: 6,069

EPA 2015a

No effect in mice (highest dose) 1,000 EPA 2015c
GLYPHOSATE A-14

APPENDIX A

Table A-3. NOAELs and LOAELs Identified in Chronic-Duration Oral Studies of 

Glyphosate Technical

Endpoint Effect

NOAEL 

(mg/kg/day)

LOAEL 

(mg/kg/day) Reference

Ocular Lens abnormalities in male rats M: 362

F: 1,183

M: 940 EPA 1991a, 1991b

No effect in rats M: 1,214

F: 1,498

EPA 2015c

No effect in rats 1,000 EPA 2015c

No effect in dogs (highest dose) 500 EPA 1986a, 1987

Neurological No effect in rats (highest dose) M: 1,214

F: 1,498

EPA 2013c

ALT = alanine aminotransferase; AP = alkaline phosphatase; F = female; LOAEL = lowest-observed-adverse-effect 

level; M = male; NOAEL = no-observed-adverse-effect level

As shown in Table A-3, gastrointestinal endpoints are the most sensitive to chronic-duration oral 

exposure of laboratory animals to glyphosate technical. Inflammation of gastric squamous mucosa was 

observed in female (but not male) rats administered glyphosate technical in the diet for up to 24 months at 

an estimated dose of 457 mg/kg/day; the NOAEL was 113 mg/kg/day (EPA 1991a, 1991b). Increased 

severity of cytoplasmic changes in salivary gland cells (basophilia and hypertrophy of acinar cells in 

parotid and submandibular salivary glands) was reported for rats receiving glyphosate from the diet for 

2 years at doses ≥300 mg/kg/day (EPA 2015c). Although salivary gland cytoplasmic changes were noted 

in rats at doses <300 mg/kg/day as well, the changes were reported to be only of minimal or mild 

severity; therefore, they are not considered adverse effects. Furthermore, the toxicological significance of 

the glyphosate treatment-related effects on salivary glands is uncertain. One chronic-duration oral study 

of male and female mice found no evidence of glyphosate treatment-related gastrointestinal effects at 

doses as high as 4,945 and 6,069 mg/kg/day, respectively (EPA 1985a, 1985b, 1986b, 1989, 1991c, 1993, 

2015a).

Summary of the Principal Study:

EPA. 1991a. June 03, 1991. Memorandum. 40 Page(s). William Dykstra. Toxicology Branch. 

Glyphosate; 2-Year combined chronic toxicity/carcinogenicity study in Sprague-Dawley rats - List A 

Pesticide for Reregistration Pages 29-40 removed-registrant data. MRID 416438-01. Tox review 

008390. U.S. Environmental Protection Agency. 

https://archive.epa.gov/pesticides/chemicalsearch/chemical/foia/web/pdf/103601/103601-263.pdf. April 

10, 2016. 

EPA. 1991b. December 13, 1991. Memorandum. 38 Page(s). William Dykstra. Toxicology Branch I. 

Glyphosate - EPA Registration No. 524-308 - 2-Year chronic feeding/oncogenicity study in rats with 

technical glyphosate. MRID 416438-01. Tox review 008897. U.S. Environmental Protection Agency. 

https://archive.epa.gov/pesticides/chemicalsearch/chemical/foia/web/pdf/103601/103601-268.pdf. April 

10, 2016.

Groups of albino Sprague Dawley rats (60/sex/group) were administered technical glyphosate (96.5% 

purity) in the diet at target concentrations of 0, 2,000, 8,000, or 20,000 ppm (mean measured 

concentrations of 0, 1,900, 7,600, and 19,000 ppm, respectively) for up to 24 months. Rats were 

monitored for survival, clinical signs, food intake, and body weight. Ten rats/sex/dose were subjected to 
GLYPHOSATE A-15

APPENDIX A 

comprehensive evaluations at 12-month interim sacrifice. Rats were subjected to ophthalmologic 

examinations prior to the initiation of treatment and twice prior to scheduled terminal sacrifice. Blood 

and urine samples were collected at 6, 12, 18, and 24 months for hematology, clinical chemistry, and 

urinalysis. Evaluations of all rats that died or survived until scheduled sacrifice included organ weight 

determinations (brain, liver, kidneys, testes, epididymides, prostate) and comprehensive gross and 

histopathologic examinations. 

There were no indications of glyphosate-related clinical signs or effects on survival. Mean body weights 

of all glyphosate-treated male rats were not significantly different from that of controls. Mean body 

weights and of high-dose female rats were significantly lower than that of controls at weeks 7, 13, 81, and 

104 (approximately 3–4% less than that of controls); by week 81, the magnitude of the mean body weight 

difference between high-dose females and their controls reached 13% (470.6 g versus 543.2 g for 

controls). There were no significant differences between controls and glyphosate-treated groups 

regarding food consumption. Based on mean body weight and food consumption data, estimated 

glyphosate doses to controls and low-, mid-, and high-dose groups were 0, 89, 362, and 940 mg/kg/day, 

respectively, for the males and 0, 113, 457, and 1,183 mg/kg/day, respectively, for the females. 

Glyphosate treatment-related nonneoplastic effects included increased incidence of ocular effects (lens 

abnormalities), renal effects (increased specific gravity and decreased pH of urine) in high-dose 

(940 mg/kg/day) male rats, and significantly increased incidence of inflammation of gastric squamous 

mucosa in female rats at 457 and 1,183 mg/kg/day (incidences of 0/59, 3/60, 9/60 [p=0.0015], and 

6/59 [p=0.014] among controls, low-, mid-, and high-dose groups, respectively; statistical significance 

determined using Fisher's exact test). The high-dose (1,183 mg/kg/day) group of female rats exhibited as 

much as 13% lower mean body weight at treatment week 81. Relative liver weight was significantly 

increased in high-dose male rats evaluated at 12 months and terminal sacrifice (13–14% greater than 

controls); however, histopathologic examinations of liver sections revealed no evidence of significant 

treatment-related nonneoplastic effects. 

Selection of the Point of Departure: A chronic-duration oral MRL can be derived for glyphosate based 

on incidences of female rats exhibiting gastric lesions in the 2-year dietary study of rats (EPA 1991a, 

1991b). Incidences of female rats with gastric lesions were 0/59, 3/60, 9/60, and 6/59 for controls, low-, 

mid-, and high-dose groups, respectively. All dichotomous models in the Benchmark Dose Modeling 

Software (BMDS; Version 2.6) were fit to the incidence data for female rats exhibiting inflammation of 

gastric squamous mucosa. A benchmark response (BMR) of 10% extra risk was applied. None of the 

models produced adequate fit to the dataset, likely due to 33% lower incidence for the gastric lesion in the 

high-dose group compared to the mid-dose group. Therefore, a NOAEL/LOAEL approach was employed 

to derive a chronic-duration oral MRL for glyphosate. The point of departure is the NOAEL of 113 

mg/kg/day for gastrointestinal lesions in the female rats of the 2-year dietary study (EPA 1991a, 1991b). 

Uncertainty Factor: The NOAEL of 113 mg/kg/day was divided by a total uncertainty factor of 100: 

• 10 for animal to human extrapolation

• 10 for human variability

Per ATSDR guidance, MRLs are expressed to one significant figure, making the MRL 1 mg/kg/day.

The glyphosate-induced cytoplasmic changes in salivary glands of the chronically-treated rats were not 

considered for MRL derivation because the toxicological significance of the changes is uncertain. 

However, consideration of the NOAEL of 113 mg/kg/day (EPA 2015c) as a point of departure,

application of a total uncertainty factor of 100 (10 for extrapolation from animals to humans and 10 for 

human variability) would also result in a chronic-duration oral MRL of 1 mg/kg/day.
GLYPHOSATE A-16

APPENDIX A

Other Additional Studies or Pertinent Information: Glyphosate-induced gastrointestinal effects were 

observed in acute-duration oral studies of rats and rabbits (Adam et al. 1997; EPA 1992e, 2013c, 2017b), 

intermediate-duration oral studies of rats, mice, and rabbits (EPA 1992a, 1992f; NTP 1992), and chronicduration oral studies of rats (EPA 1991a, 1991b, 2015c).

Agency Contact (Chemical Manager): Hana R. Pohl, M.D., Ph.D.
GLYPHOSATE B-1

APPENDIX B. LITERATURE SEARCH FRAMEWORK FOR GLYPHOSATE 

The objective of the toxicological profile is to evaluate the potential for human exposure and the potential 

health hazards associated with inhalation, oral, or dermal/ocular exposure to glyphosate. 

B.1 LITERATURE SEARCH AND SCREEN 

A literature search and screen was conducted to identify studies examining health effects, toxicokinetics, 

mechanisms of action, susceptible populations, biomarkers, chemical interactions, physical and chemical 

properties, production, use, environmental fate, environmental releases, and environmental and biological 

monitoring data for glyphosate. ATSDR primarily focused on peer-reviewed articles without publication 

date or language restrictions. Non-peer-reviewed studies that were considered relevant to the assessment 

of the health effects of glyphosate have undergone peer review by at least three ATSDR-selected experts 

who have been screened for conflict of interest. The inclusion criteria used to identify relevant studies 

examining the health effects of glyphosate are presented in Table B-1.

Table B-1. Inclusion Criteria for the Literature Search and Screen

Health Effects

Species

Human

Laboratory mammals

Route of exposure

Inhalation

Oral

Dermal (or ocular)

Parenteral (these studies will be considered supporting data)

Health outcome

Death

Systemic effects

Body weight effects 

Respiratory effects

Cardiovascular effects

Gastrointestinal effects

Hematological effects

Musculoskeletal effects

Hepatic effects

Renal effects

Dermal effects

Ocular effects

Endocrine effects

Immunological effects

Neurological effects

Reproductive effects

Developmental effects
GLYPHOSATE B-2

APPENDIX C

Table B-1. Inclusion Criteria for the Literature Search and Screen

Other noncancer effects

Cancer

Toxicokinetics

Absorption

Distribution

Metabolism

Excretion

PBPK models

Biomarkers

Biomarkers of exposure

Biomarkers of effect

Interactions with other chemicals

Potential for human exposure

Releases to the environment

Air

Water

Soil

Environmental fate

Transport and partitioning

Transformation and degradation

Environmental monitoring

Air

Water

Sediment and soil

Other media

Biomonitoring

General populations

Occupation populations

B.1.1 Literature Search

The following main databases were searched in February 2015 and September 2017:

• PubMed 

• National Library of Medicine’s TOXLINE

• Scientific and Technical Information Network’s TOXCENTER

The search strategy used the chemical names, Chemical Abstracts Service (CAS) numbers, 

synonyms, and Medical Subject Headings (MeSH) terms for glyphosate. The query strings used for 

the literature search are presented in Table B-2. 

The search was augmented by searching the Toxic Substances Control Act Test Submissions (TSCATS), 

NTP website, and National Institute of Health Research Portfolio Online Reporting Tools Expenditures 

and Results (NIH RePORTER) databases using the queries presented in Table B-3. Additional databases 
GLYPHOSATE B-3

APPENDIX C

were searched in the creation of various tables and figures, such as the TRI Explorer, the Substance 

Priority List (SPL) resource page, and other items as needed. Regulations applicable to glyphosate were 

identified by searching international and U.S. agency websites and documents.

Review articles were identified and used for the purpose of providing background information and 

identifying additional references. ATSDR also identified reports from the grey literature, which included 

unpublished research reports, technical reports from government agencies, conference proceedings and 

abstracts, and theses and dissertations. The reference sections of the gray literature were used as quality 

assurance (QA) to ensure that no studies were missed during the literature review process. The 

ToxProfiles rely on peer reviewed data such as published studies and reports from government agencies 

or international organizations. In certain cases (e.g. ATSDR’s use of EPA’s DERs), ATSDR will rely on 

peer reviewed studies and reports evaluating unpublished data or original studies that are not available to 

ATSDR. 

Table B-2. Database Query Strings Pre-Public Comment Searches

Database

search date Query string

PubMed

9/2017

("glyphosate"[nm] OR "1071-83-6"[tw] OR "(Carboxymethylamino)methylphosphonic 

acid"[tw] OR "Carboxymethylaminomethanephosphinic acid"[tw] OR "C-K Yuyos FAV"[tw] 

OR "CP 67573"[tw] OR "Folusen"[tw] OR "Forsat"[tw] OR "Glialka"[tw] OR "Glifoglex"[tw] 

OR "Glifosan 747"[tw] OR "gliphosate"[tw] OR "Gliz"[tw] OR "Glyfos"[tw] OR "GlyGran"[tw] 

OR "Glyphodin A"[tw] OR "Glyphomax"[tw] OR "Glyphosate"[tw] OR "Glyphosphate"[tw] 

OR "Ground Bio"[tw] OR "Herbatop"[tw] OR "HM 2028"[tw] OR "Kickdown"[tw] OR "Lancer 

herbicide"[tw] OR "MON 2139"[tw] OR "MON 3539"[tw] OR "MON 6000"[tw] OR "N-

(Phosphonomethyl)glycine"[tw] OR "N-(phosphonomethyl)-Glycine"[tw] OR "NPhosphomethylglycine"[tw] OR "N-Phosphonomethylglycine"[tw] OR "Phorsat"[tw] OR 

"Phosphonomethylglycine"[tw] OR "Phosphonomethyliminoacetic acid"[tw] OR 

"Pondmaster"[tw] OR "Rebel Garden"[tw] OR "Roundup Max"[tw] OR "Safal"[tw] OR 

"Scout herbicide"[tw] OR "Silglif"[tw] OR "yerbimat"[tw] OR "Roundup"[tw] OR "34494-03-

6"[tw] OR "MON 0459"[tw] OR "40465-66-5"[tw] OR "MON 14420"[tw] OR "MON 8750"[tw] 

OR "Roundup Hi-Load"[tw] OR "Roundup PRODry"[tw] OR "70393-85-0"[tw] OR "MON 

8000"[tw] OR "Monsanto 8000"[tw] OR "Polado"[tw] OR "Trisodium hydrogen bis(N-

(phosphonatomethyl)aminoacetate"[tw] OR "39600-42-5"[tw] OR "Glyphosate 

potassium"[tw] OR "Glyphosate monopotassium salt"[tw] OR "Glyphosate potassium"[tw] 

OR "Glyphosate-potassium"[tw] OR "Monopotassium glyphosate"[tw] OR "Roundup 

Attack"[tw] OR "Roundup Energy"[tw] OR "Roundup Maxload"[tw] OR "Roundup Original 

Max"[tw] OR "Roundup Power Max"[tw] OR "Roundup Ultramax II"[tw] OR "Roundup 

Weathermax"[tw] OR "Touchdown Forte HiTech"[tw] OR "Transorb R"[tw] OR 

"Weathermax"[tw] OR "Zapp Qi"[tw] OR "70901-12-1"[tw] OR "Glyphosate-potassium"[tw] 

OR "Potassium glyphosate"[tw] OR "Potassium N-(phosphonomethyl)glycine"[tw] OR 

"Uragan Forte"[tw] OR "VisionMAX"[tw] OR "N-(phosphonomethyl)glycine potassium 

salt"[tw] OR "114370-14-8"[tw] OR "Glyphosate ammonium"[tw] OR "N-

(phosphonomethyl)glycine ammonium salt"[tw] OR "69254-40-6"[tw] OR "Glyphosatediammonium"[tw] OR "Diammonium N-(phosphonomethyl)glycine"[tw] OR "N-

(phosphonomethyl)glycine diammonium salt"[tw]) AND (cancer[sb] OR "neoplasms"[mh] 

OR "carcinogenicity tests"[mh] OR "carcinogens"[mh] OR "cell division/drug effects"[mh] 

OR "cell cycle/drug effects"[mh] OR "cell line, tumor/drug effects"[mh] OR "gene 

expression regulation, neoplastic"[mh] OR "neoplasm proteins/drug effects"[mh] OR 

"angiogenesis inducing agents"[mh] OR "myelodysplastic-myeloproliferative diseases"[mh] 

OR cancer*[tw] OR carcinog*[tw] OR carcinom*[tw] OR cocarcinog*[tw] OR lymphoma*[tw] 

OR neoplas*[tw] OR oncogen*[tw] OR precancer*[tw] OR tumor*[tw] OR tumour*[tw]) AND 
GLYPHOSATE B-4

APPENDIX C

Table B-2. Database Query Strings Pre-Public Comment Searches

Database

search date Query string

(2014/02/01 : 3000[dp] OR 2015/02/01 : 3000[mhda] OR 2015/02/01 : 3000[crdat] OR 

2015/02/01 : 3000[edat])

("glyphosate, isopropyl amine salt"[nm] OR "N-(phosphonomethyl)glycine 

trimethylsulfonium salt"[nm] OR "38641-94-0"[tw] OR "Glyphosateisopropylammonium"[tw] OR "Glyphosate isopropylamine salt"[tw] OR "Azural AT"[tw] OR 

"CP 70139"[tw] OR "Fosulen"[tw] OR "Glifosato estrella"[tw] OR "Glycel"[tw] OR "Glycine, 

N-(phosphonomethyl)-, cmpd with 2-propanamine (1:1)"[tw] OR "Glyfos AU"[tw] OR 

"Glyfos BIO"[tw] OR "Glyphosate isopropylamine salt"[tw] OR "Glyphosate 

mono(isopropylamine) salt"[tw] OR "Glyphosate-isopropylammonium"[tw] OR "Glyphosatemono(isopropylammonium)"[tw] OR "Landmaster"[tw] OR "MON 139"[tw] OR "MON 

39"[tw] OR "N-(Phosphonomethyl)glycine isopropylamine salt"[tw] OR "N-

(Phosphonomethyl)glycine isopropylammonium salt"[tw] OR "N-(Phosphonomethyl)glycine 

monoisopropylamine salt"[tw] OR "Nitosorg"[tw] OR "Ron-do"[tw] OR "Utal"[tw] OR "Utal 

(herbicide)"[tw] OR "Vision (herbicide)"[tw] OR "2-Propanamine, compd, with N-

(phosphonomethyl)glycine (1:1)"[tw] OR "Glycine, N-(phosphonomethyl)-, compd. with 2-

propanamine (1:1)"[tw] OR "N-(Phosphonomethyl)glycine, compound with 2-propylamine 

(1:1)"[tw] OR "Isopropylamine glyphosate"[tw] OR "81591-81-3"[tw] OR "Glyphosatetrimesium"[tw] OR "Glyphosphate-trimesium"[tw] OR "Avans 330"[tw] OR "Glyphosate 

mono(trimethylsulfonium) salt"[tw] OR "Glyphosate trimethylsulfonium salt"[tw] OR 

"Glyphosate-trimesium"[tw] OR "Medallon"[tw] OR "Ouragan"[tw] OR "R 50224"[tw] OR 

"SC 0224"[tw] OR "Sulfosate"[tw] OR "Sulphosate"[tw] OR "Touchdown herbicide"[tw] OR 

"Trimethylsulfonium carboxymethylamino-methylphosphonate"[tw] OR "Trimethylsulfonium 

glyphosate"[tw] OR "Glycine, N-(phosphonomethyl)-, ion(1-), trimethylsulfonium"[tw] OR 

"Sulfosate"[tw]) AND (cancer[sb] OR "neoplasms"[mh] OR "carcinogenicity tests"[mh] OR 

"carcinogens"[mh] OR "cell division/drug effects"[mh] OR "cell cycle/drug effects"[mh] OR 

"cell line, tumor/drug effects"[mh] OR "gene expression regulation, neoplastic"[mh] OR 

"neoplasm proteins/drug effects"[mh] OR "angiogenesis inducing agents"[mh] OR 

"myelodysplastic-myeloproliferative diseases"[mh] OR cancer*[tw] OR carcinog*[tw] OR 

carcinom*[tw] OR cocarcinog*[tw] OR lymphoma*[tw] OR neoplas*[tw] OR oncogen*[tw] 

OR precancer*[tw] OR tumor*[tw] OR tumour*[tw]) AND (2014/02/01 : 3000[dp] OR 

2015/02/01 : 3000[mhda] OR 2015/02/01 : 3000[crdat] OR 2015/02/01 : 3000[edat])

2/2015 ("glyphosate"[nm]) OR (("1071-83-6"[tw] OR "(Carboxymethylamino)methylphosphonic 

acid"[tw] OR "Carboxymethylaminomethanephosphinic acid"[tw] OR "C-K Yuyos FAV"[tw] 

OR "CP 67573"[tw] OR "Folusen"[tw] OR "Forsat"[tw] OR "Glialka"[tw] OR "Glifoglex"[tw] 

OR "Glifosan 747"[tw] OR "gliphosate"[tw] OR "Gliz"[tw] OR "Glyfos"[tw] OR "GlyGran"[tw] 

OR "Glyphodin A"[tw] OR "Glyphomax"[tw] OR "Glyphosate"[tw] OR "Glyphosphate"[tw] 

OR "Ground Bio"[tw] OR "Herbatop"[tw] OR "HM 2028"[tw] OR "Kickdown"[tw] OR "Lancer 

herbicide"[tw] OR "MON 2139"[tw] OR "MON 3539"[tw] OR "MON 6000"[tw] OR "N-

(Phosphonomethyl)glycine"[tw] OR "N-(phosphonomethyl)-Glycine"[tw] OR "NPhosphomethylglycine"[tw] OR "N-Phosphonomethylglycine"[tw] OR "Phorsat"[tw] OR 

"Phosphonomethylglycine"[tw] OR "Phosphonomethyliminoacetic acid"[tw] OR 

"Pondmaster"[tw] OR "Rebel Garden"[tw] OR "Roundup Max"[tw] OR "Safal"[tw] OR 

"Scout herbicide"[tw] OR "Silglif"[tw] OR "yerbimat"[tw]) AND (to[sh] OR po[sh] OR ae[sh] 

OR pk[sh] OR (me[sh] AND ("humans"[mh] OR "animals"[mh])) OR ci[sh] OR bl[sh] OR 

cf[sh] OR ur[sh] OR "environmental exposure"[mh] OR "endocrine system"[mh] OR 

"hormones, hormone substitutes, and hormone antagonists"[mh] OR "endocrine 

disruptors"[mh] OR (("Computational biology"[mh] OR "Medical Informatics"[mh] OR 

Genomics[mh] OR Genome[mh] OR Proteomics[mh] OR Proteome[mh] OR 

Metabolomics[mh] OR Metabolome[mh] OR Genes[mh] OR "Gene expression"[mh] OR 

Phenotype[mh] OR genetics[mh] OR genotype[mh] OR Transcriptome[mh] OR ("Systems 
GLYPHOSATE B-5

APPENDIX C

Table B-2. Database Query Strings Pre-Public Comment Searches

Database

search date Query string

Biology"[mh] AND ("Environmental Exposure"[mh] OR "Epidemiological Monitoring"[mh] 

OR analysis[sh])) OR "Transcription, Genetic "[mh] OR "Reverse transcription"[mh] OR 

"Transcriptional activation"[mh] OR "Transcription factors"[mh] OR ("biosynthesis"[sh] AND 

(RNA[mh] OR DNA[mh])) OR "RNA, Messenger"[mh] OR "RNA, Transfer"[mh] OR 

"peptide biosynthesis"[mh] OR "protein biosynthesis"[mh] OR "Reverse Transcriptase 

Polymerase Chain Reaction"[mh] OR "Base Sequence"[mh] OR "Trans-activators"[mh] OR 

"Gene Expression Profiling"[mh])) OR cancer[sb] OR "pharmacology"[Majr])) OR (("1071-

83-6"[tw] OR "(Carboxymethylamino)methylphosphonic acid"[tw] OR 

"Carboxymethylaminomethanephosphinic acid"[tw] OR "C-K Yuyos FAV"[tw] OR "CP 

67573"[tw] OR "Folusen"[tw] OR "Forsat"[tw] OR "Glialka"[tw] OR "Glifoglex"[tw] OR 

"Glifosan 747"[tw] OR "gliphosate"[tw] OR "Gliz"[tw] OR "Glyfos"[tw] OR "GlyGran"[tw] OR 

"Glyphodin A"[tw] OR "Glyphomax"[tw] OR "Glyphosate"[tw] OR "Glyphosphate"[tw] OR 

"Ground Bio"[tw] OR "Herbatop"[tw] OR "HM 2028"[tw] OR "Kickdown"[tw] OR "Lancer 

herbicide"[tw] OR "MON 2139"[tw] OR "MON 3539"[tw] OR "MON 6000"[tw] OR "N-

(Phosphonomethyl)glycine"[tw] OR "N-(phosphonomethyl)-Glycine"[tw] OR "NPhosphomethylglycine"[tw] OR "N-Phosphonomethylglycine"[tw] OR "Phorsat"[tw] OR 

"Phosphonomethylglycine"[tw] OR "Phosphonomethyliminoacetic acid"[tw] OR 

"Pondmaster"[tw] OR "Rebel Garden"[tw] OR "Roundup Max"[tw] OR "Safal"[tw] OR 

"Scout herbicide"[tw] OR "Silglif"[tw] OR "yerbimat"[tw]) NOT medline[sb])

("Roundup"[tw] AND (monsanto[tw] OR "antifungal agents"[Pharmacological Action] OR 

"antifungal agents"[MeSH Terms] OR "antifungal"[tw] OR "anti-fungal"[tw] OR "enzyme 

inhibitors"[Pharmacological Action] OR "enzyme inhibitors"[MeSH Terms] OR 

("enzyme"[tw] AND inhibitor*[tw]) OR "enzyme inhibitors"[tw] OR "enzyme inhibitor"[tw] OR 

"herbicides"[Pharmacological Action] OR "herbicides"[MeSH Terms] OR "herbicides"[tw] 

OR "herbicide"[tw] OR "uncoupling agents"[Pharmacological Action] OR "uncoupling 

agents"[MeSH Terms] OR ("uncoupling"[tw] AND agent*[tw]) OR "uncoupling agent"[tw] 

OR "uncoupling agents"[tw] OR "pesticides"[mh] OR pesticide*[tw])) NOT 

(("glyphosate"[nm]) OR (("1071-83-6"[tw] OR "(Carboxymethylamino)methylphosphonic 

acid"[tw] OR "Carboxymethylaminomethanephosphinic acid"[tw] OR "C-K Yuyos FAV"[tw] 

OR "CP 67573"[tw] OR "Folusen"[tw] OR "Forsat"[tw] OR "Glialka"[tw] OR "Glifoglex"[tw] 

OR "Glifosan 747"[tw] OR "gliphosate"[tw] OR "Gliz"[tw] OR "Glyfos"[tw] OR "GlyGran"[tw] 

OR "Glyphodin A"[tw] OR "Glyphomax"[tw] OR "Glyphosate"[tw] OR "Glyphosphate"[tw] 

OR "Ground Bio"[tw] OR "Herbatop"[tw] OR "HM 2028"[tw] OR "Kickdown"[tw] OR "Lancer 

herbicide"[tw] OR "MON 2139"[tw] OR "MON 3539"[tw] OR "MON 6000"[tw] OR "N-

(Phosphonomethyl)glycine"[tw] OR "N-(phosphonomethyl)-Glycine"[tw] OR "NPhosphomethylglycine"[tw] OR "N-Phosphonomethylglycine"[tw] OR "Phorsat"[tw] OR 

"Phosphonomethylglycine"[tw] OR "Phosphonomethyliminoacetic acid"[tw] OR 

"Pondmaster"[tw] OR "Rebel Garden"[tw] OR "Roundup Max"[tw] OR "Safal"[tw] OR 

"Scout herbicide"[tw] OR "Silglif"[tw] OR "yerbimat"[tw]) AND (to[sh] OR po[sh] OR ae[sh] 

OR pk[sh] OR (me[sh] AND ("humans"[mh] OR "animals"[mh])) OR ci[sh] OR bl[sh] OR 

cf[sh] OR ur[sh] OR "environmental exposure"[mh] OR "endocrine system"[mh] OR 

"hormones, hormone substitutes, and hormone antagonists"[mh] OR "endocrine 

disruptors"[mh] OR (("Computational biology"[mh] OR "Medical Informatics"[mh] OR 

Genomics[mh] OR Genome[mh] OR Proteomics[mh] OR Proteome[mh] OR 

Metabolomics[mh] OR Metabolome[mh] OR Genes[mh] OR "Gene expression"[mh] OR 

Phenotype[mh] OR genetics[mh] OR genotype[mh] OR Transcriptome[mh] OR ("Systems 

Biology"[mh] AND ("Environmental Exposure"[mh] OR "Epidemiological Monitoring"[mh] 

OR analysis[sh])) OR "Transcription, Genetic "[mh] OR "Reverse transcription"[mh] OR 

"Transcriptional activation"[mh] OR "Transcription factors"[mh] OR ("biosynthesis"[sh] AND 

(RNA[mh] OR DNA[mh])) OR "RNA, Messenger"[mh] OR "RNA, Transfer"[mh] OR 
GLYPHOSATE B-6

APPENDIX C

Table B-2. Database Query Strings Pre-Public Comment Searches

Database

search date Query string

"peptide biosynthesis"[mh] OR "protein biosynthesis"[mh] OR "Reverse Transcriptase 

Polymerase Chain Reaction"[mh] OR "Base Sequence"[mh] OR "Trans-activators"[mh] OR 

"Gene Expression Profiling"[mh])) OR cancer[sb] OR "pharmacology"[Majr])) OR (("1071-

83-6"[tw] OR "(Carboxymethylamino)methylphosphonic acid"[tw] OR 

"Carboxymethylaminomethanephosphinic acid"[tw] OR "C-K Yuyos FAV"[tw] OR "CP 

67573"[tw] OR "Folusen"[tw] OR "Forsat"[tw] OR "Glialka"[tw] OR "Glifoglex"[tw] OR 

"Glifosan 747"[tw] OR "gliphosate"[tw] OR "Gliz"[tw] OR "Glyfos"[tw] OR "GlyGran"[tw] OR 

"Glyphodin A"[tw] OR "Glyphomax"[tw] OR "Glyphosate"[tw] OR "Glyphosphate"[tw] OR 

"Ground Bio"[tw] OR "Herbatop"[tw] OR "HM 2028"[tw] OR "Kickdown"[tw] OR "Lancer 

herbicide"[tw] OR "MON 2139"[tw] OR "MON 3539"[tw] OR "MON 6000"[tw] OR "N-

(Phosphonomethyl)glycine"[tw] OR "N-(phosphonomethyl)-Glycine"[tw] OR "NPhosphomethylglycine"[tw] OR "N-Phosphonomethylglycine"[tw] OR "Phorsat"[tw] OR 

"Phosphonomethylglycine"[tw] OR "Phosphonomethyliminoacetic acid"[tw] OR 

"Pondmaster"[tw] OR "Rebel Garden"[tw] OR "Roundup Max"[tw] OR "Safal"[tw] OR 

"Scout herbicide"[tw] OR "Silglif"[tw] OR "yerbimat"[tw]) NOT medline[sb]))

("34494-03-6"[tw] OR "MON 0459"[tw] OR "40465-66-5"[tw] OR "MON 14420"[tw] OR 

"MON 8750"[tw] OR "Roundup Hi-Load"[tw] OR "Roundup PRODry"[tw] OR "70393-85-

0"[tw] OR "MON 8000"[tw] OR "Monsanto 8000"[tw] OR "Polado"[tw] OR "Trisodium 

hydrogen bis(N-(phosphonatomethyl)aminoacetate"[tw]) AND (to[sh] OR po[sh] OR ae[sh] 

OR pk[sh] OR (me[sh] AND ("humans"[mh] OR "animals"[mh])) OR ci[sh] OR bl[sh] OR 

cf[sh] OR ur[sh] OR "environmental exposure"[mh] OR "endocrine system"[mh] OR 

"hormones, hormone substitutes, and hormone antagonists"[mh] OR "endocrine 

disruptors"[mh] OR (("Computational biology"[mh] OR "Medical Informatics"[mh] OR 

Genomics[mh] OR Genome[mh] OR Proteomics[mh] OR Proteome[mh] OR 

Metabolomics[mh] OR Metabolome[mh] OR Genes[mh] OR "Gene expression"[mh] OR 

Phenotype[mh] OR genetics[mh] OR genotype[mh] OR Transcriptome[mh] OR ("Systems 

Biology"[mh] AND ("Environmental Exposure"[mh] OR "Epidemiological Monitoring"[mh] 

OR analysis[sh])) OR "Transcription, Genetic "[mh] OR "Reverse transcription"[mh] OR 

"Transcriptional activation"[mh] OR "Transcription factors"[mh] OR ("biosynthesis"[sh] AND 

(RNA[mh] OR DNA[mh])) OR "RNA, Messenger"[mh] OR "RNA, Transfer"[mh] OR 

"peptide biosynthesis"[mh] OR "protein biosynthesis"[mh] OR "Reverse Transcriptase 

Polymerase Chain Reaction"[mh] OR "Base Sequence"[mh] OR "Trans-activators"[mh] OR 

"Gene Expression Profiling"[mh])) OR cancer[sb] OR "pharmacology"[Majr])

("39600-42-5"[tw] OR "Glyphosate potassium"[tw] OR "Glyphosate monopotassium 

salt"[tw] OR "Glyphosate potassium"[tw] OR "Glyphosate-potassium"[tw] OR 

"Monopotassium glyphosate"[tw] OR "Roundup Attack"[tw] OR "Roundup Energy"[tw] OR 

"Roundup Maxload"[tw] OR "Roundup Original Max"[tw] OR "Roundup Power Max"[tw] OR 

"Roundup Ultramax II"[tw] OR "Roundup Weathermax"[tw] OR "Touchdown Forte 

HiTech"[tw] OR "Transorb R"[tw] OR "Weathermax"[tw] OR "Zapp Qi"[tw] OR "70901-12-

1"[tw] OR "Glyphosate-potassium"[tw] OR "Potassium glyphosate"[tw] OR "Potassium N-

(phosphonomethyl)glycine"[tw] OR "Uragan Forte"[tw] OR "VisionMAX"[tw] OR "N-

(phosphonomethyl)glycine potassium salt"[tw] OR "114370-14-8"[tw] OR "Glyphosate 

ammonium"[tw] OR "N-(phosphonomethyl)glycine ammonium salt"[tw] OR "69254-40-

6"[tw] OR "Glyphosate-diammonium"[tw] OR "Diammonium N-

(phosphonomethyl)glycine"[tw] OR "N-(phosphonomethyl)glycine diammonium salt"[tw]) 

NOT (("glyphosate"[nm]) OR (("1071-83-6"[tw] OR 

"(Carboxymethylamino)methylphosphonic acid"[tw] OR 

"Carboxymethylaminomethanephosphinic acid"[tw] OR "C-K Yuyos FAV"[tw] OR "CP 

67573"[tw] OR "Folusen"[tw] OR "Forsat"[tw] OR "Glialka"[tw] OR "Glifoglex"[tw] OR 

"Glifosan 747"[tw] OR "gliphosate"[tw] OR "Gliz"[tw] OR "Glyfos"[tw] OR "GlyGran"[tw] OR 
GLYPHOSATE B-7

APPENDIX C

Table B-2. Database Query Strings Pre-Public Comment Searches

Database

search date Query string

"Glyphodin A"[tw] OR "Glyphomax"[tw] OR "Glyphosate"[tw] OR "Glyphosphate"[tw] OR 

"Ground Bio"[tw] OR "Herbatop"[tw] OR "HM 2028"[tw] OR "Kickdown"[tw] OR "Lancer 

herbicide"[tw] OR "MON 2139"[tw] OR "MON 3539"[tw] OR "MON 6000"[tw] OR "N-

(Phosphonomethyl)glycine"[tw] OR "N-(phosphonomethyl)-Glycine"[tw] OR "NPhosphomethylglycine"[tw] OR "N-Phosphonomethylglycine"[tw] OR "Phorsat"[tw] OR 

"Phosphonomethylglycine"[tw] OR "Phosphonomethyliminoacetic acid"[tw] OR 

"Pondmaster"[tw] OR "Rebel Garden"[tw] OR "Roundup Max"[tw] OR "Safal"[tw] OR 

"Scout herbicide"[tw] OR "Silglif"[tw] OR "yerbimat"[tw]) AND (to[sh] OR po[sh] OR ae[sh] 

OR pk[sh] OR (me[sh] AND ("humans"[mh] OR "animals"[mh])) OR ci[sh] OR bl[sh] OR 

cf[sh] OR ur[sh] OR "environmental exposure"[mh] OR "endocrine system"[mh] OR 

"hormones, hormone substitutes, and hormone antagonists"[mh] OR "endocrine 

disruptors"[mh] OR (("Computational biology"[mh] OR "Medical Informatics"[mh] OR 

Genomics[mh] OR Genome[mh] OR Proteomics[mh] OR Proteome[mh] OR 

Metabolomics[mh] OR Metabolome[mh] OR Genes[mh] OR "Gene expression"[mh] OR 

Phenotype[mh] OR genetics[mh] OR genotype[mh] OR Transcriptome[mh] OR ("Systems 

Biology"[mh] AND ("Environmental Exposure"[mh] OR "Epidemiological Monitoring"[mh] 

OR analysis[sh])) OR "Transcription, Genetic "[mh] OR "Reverse transcription"[mh] OR 

"Transcriptional activation"[mh] OR "Transcription factors"[mh] OR ("biosynthesis"[sh] AND 

(RNA[mh] OR DNA[mh])) OR "RNA, Messenger"[mh] OR "RNA, Transfer"[mh] OR 

"peptide biosynthesis"[mh] OR "protein biosynthesis"[mh] OR "Reverse Transcriptase 

Polymerase Chain Reaction"[mh] OR "Base Sequence"[mh] OR "Trans-activators"[mh] OR 

"Gene Expression Profiling"[mh])) OR cancer[sb] OR "pharmacology"[Majr])) OR (("1071-

83-6"[tw] OR "(Carboxymethylamino)methylphosphonic acid"[tw] OR 

"Carboxymethylaminomethanephosphinic acid"[tw] OR "C-K Yuyos FAV"[tw] OR "CP 

67573"[tw] OR "Folusen"[tw] OR "Forsat"[tw] OR "Glialka"[tw] OR "Glifoglex"[tw] OR 

"Glifosan 747"[tw] OR "gliphosate"[tw] OR "Gliz"[tw] OR "Glyfos"[tw] OR "GlyGran"[tw] OR 

"Glyphodin A"[tw] OR "Glyphomax"[tw] OR "Glyphosate"[tw] OR "Glyphosphate"[tw] OR 

"Ground Bio"[tw] OR "Herbatop"[tw] OR "HM 2028"[tw] OR "Kickdown"[tw] OR "Lancer 

herbicide"[tw] OR "MON 2139"[tw] OR "MON 3539"[tw] OR "MON 6000"[tw] OR "N-

(Phosphonomethyl)glycine"[tw] OR "N-(phosphonomethyl)-Glycine"[tw] OR "NPhosphomethylglycine"[tw] OR "N-Phosphonomethylglycine"[tw] OR "Phorsat"[tw] OR 

"Phosphonomethylglycine"[tw] OR "Phosphonomethyliminoacetic acid"[tw] OR 

"Pondmaster"[tw] OR "Rebel Garden"[tw] OR "Roundup Max"[tw] OR "Safal"[tw] OR 

"Scout herbicide"[tw] OR "Silglif"[tw] OR "yerbimat"[tw]) NOT medline[sb]) OR 

("Roundup"[tw] AND (monsanto[tw] OR "antifungal agents"[Pharmacological Action] OR 

"antifungal agents"[MeSH Terms] OR "antifungal"[tw] OR "anti-fungal"[tw] OR "enzyme 

inhibitors"[Pharmacological Action] OR "enzyme inhibitors"[MeSH Terms] OR 

("enzyme"[tw] AND inhibitor*[tw]) OR "enzyme inhibitors"[tw] OR "enzyme inhibitor"[tw] OR 

"herbicides"[Pharmacological Action] OR "herbicides"[MeSH Terms] OR "herbicides"[tw] 

OR "herbicide"[tw] OR "uncoupling agents"[Pharmacological Action] OR "uncoupling 

agents"[MeSH Terms] OR ("uncoupling"[tw] AND agent*[tw]) OR "uncoupling agent"[tw] 

OR "uncoupling agents"[tw] OR "pesticides"[mh] OR pesticide*[tw])))

((("glyphosate, isopropyl amine salt"[nm]) OR ("N-(phosphonomethyl)glycine 

trimethylsulfonium salt"[nm])) NOT (("glyphosate"[nm]) OR (("1071-83-6"[tw] OR 

"(Carboxymethylamino)methylphosphonic acid"[tw] OR 

"Carboxymethylaminomethanephosphinic acid"[tw] OR "C-K Yuyos FAV"[tw] OR "CP 

67573"[tw] OR "Folusen"[tw] OR "Forsat"[tw] OR "Glialka"[tw] OR "Glifoglex"[tw] OR 

"Glifosan 747"[tw] OR "gliphosate"[tw] OR "Gliz"[tw] OR "Glyfos"[tw] OR "GlyGran"[tw] OR 

"Glyphodin A"[tw] OR "Glyphomax"[tw] OR "Glyphosate"[tw] OR "Glyphosphate"[tw] OR 

"Ground Bio"[tw] OR "Herbatop"[tw] OR "HM 2028"[tw] OR "Kickdown"[tw] OR "Lancer 
GLYPHOSATE B-8

APPENDIX C

Table B-2. Database Query Strings Pre-Public Comment Searches

Database

search date Query string

herbicide"[tw] OR "MON 2139"[tw] OR "MON 3539"[tw] OR "MON 6000"[tw] OR "N-

(Phosphonomethyl)glycine"[tw] OR "N-(phosphonomethyl)-Glycine"[tw] OR "NPhosphomethylglycine"[tw] OR "N-Phosphonomethylglycine"[tw] OR "Phorsat"[tw] OR 

"Phosphonomethylglycine"[tw] OR "Phosphonomethyliminoacetic acid"[tw] OR 

"Pondmaster"[tw] OR "Rebel Garden"[tw] OR "Roundup Max"[tw] OR "Safal"[tw] OR 

"Scout herbicide"[tw] OR "Silglif"[tw] OR "yerbimat"[tw]) AND (to[sh] OR po[sh] OR ae[sh] 

OR pk[sh] OR (me[sh] AND ("humans"[mh] OR "animals"[mh])) OR ci[sh] OR bl[sh] OR 

cf[sh] OR ur[sh] OR "environmental exposure"[mh] OR "endocrine system"[mh] OR 

"hormones, hormone substitutes, and hormone antagonists"[mh] OR "endocrine 

disruptors"[mh] OR (("Computational biology"[mh] OR "Medical Informatics"[mh] OR 

Genomics[mh] OR Genome[mh] OR Proteomics[mh] OR Proteome[mh] OR 

Metabolomics[mh] OR Metabolome[mh] OR Genes[mh] OR "Gene expression"[mh] OR 

Phenotype[mh] OR genetics[mh] OR genotype[mh] OR Transcriptome[mh] OR ("Systems 

Biology"[mh] AND ("Environmental Exposure"[mh] OR "Epidemiological Monitoring"[mh] 

OR analysis[sh])) OR "Transcription, Genetic "[mh] OR "Reverse transcription"[mh] OR 

"Transcriptional activation"[mh] OR "Transcription factors"[mh] OR ("biosynthesis"[sh] AND 

(RNA[mh] OR DNA[mh])) OR "RNA, Messenger"[mh] OR "RNA, Transfer"[mh] OR 

"peptide biosynthesis"[mh] OR "protein biosynthesis"[mh] OR "Reverse Transcriptase 

Polymerase Chain Reaction"[mh] OR "Base Sequence"[mh] OR "Trans-activators"[mh] OR 

"Gene Expression Profiling"[mh])) OR cancer[sb] OR "pharmacology"[Majr])) OR (("1071-

83-6"[tw] OR "(Carboxymethylamino)methylphosphonic acid"[tw] OR

"Carboxymethylaminomethanephosphinic acid"[tw] OR "C-K Yuyos FAV"[tw] OR "CP 

67573"[tw] OR "Folusen"[tw] OR "Forsat"[tw] OR "Glialka"[tw] OR "Glifoglex"[tw] OR 

"Glifosan 747"[tw] OR "gliphosate"[tw] OR "Gliz"[tw] OR "Glyfos"[tw] OR "GlyGran"[tw] OR 

"Glyphodin A"[tw] OR "Glyphomax"[tw] OR "Glyphosate"[tw] OR "Glyphosphate"[tw] OR 

"Ground Bio"[tw] OR "Herbatop"[tw] OR "HM 2028"[tw] OR "Kickdown"[tw] OR "Lancer 

herbicide"[tw] OR "MON 2139"[tw] OR "MON 3539"[tw] OR "MON 6000"[tw] OR "N-

(Phosphonomethyl)glycine"[tw] OR "N-(phosphonomethyl)-Glycine"[tw] OR "NPhosphomethylglycine"[tw] OR "N-Phosphonomethylglycine"[tw] OR "Phorsat"[tw] OR 

"Phosphonomethylglycine"[tw] OR "Phosphonomethyliminoacetic acid"[tw] OR 

"Pondmaster"[tw] OR "Rebel Garden"[tw] OR "Roundup Max"[tw] OR "Safal"[tw] OR 

"Scout herbicide"[tw] OR "Silglif"[tw] OR "yerbimat"[tw]) NOT medline[sb]) OR 

("Roundup"[tw] AND (monsanto[tw] OR "antifungal agents"[Pharmacological Action] OR 

"antifungal agents"[MeSH Terms] OR "antifungal"[tw] OR "anti-fungal"[tw] OR "enzyme 

inhibitors"[Pharmacological Action] OR "enzyme inhibitors"[MeSH Terms] OR 

("enzyme"[tw] AND inhibitor*[tw]) OR "enzyme inhibitors"[tw] OR "enzyme inhibitor"[tw] OR 

"herbicides"[Pharmacological Action] OR "herbicides"[MeSH Terms] OR "herbicides"[tw] 

OR "herbicide"[tw] OR "uncoupling agents"[Pharmacological Action] OR "uncoupling 

agents"[MeSH Terms] OR ("uncoupling"[tw] AND agent*[tw]) OR "uncoupling agent"[tw] 

OR "uncoupling agents"[tw] OR "pesticides"[mh] OR pesticide*[tw])))) OR (("38641-94-

0"[tw] OR "Glyphosate-isopropylammonium"[tw] OR "Glyphosate isopropylamine salt"[tw] 

OR "Azural AT"[tw] OR "CP 70139"[tw] OR "Fosulen"[tw] OR "Glifosato estrella"[tw] OR 

"Glycel"[tw] OR "Glycine, N-(phosphonomethyl)-, cmpd with 2-propanamine (1:1)"[tw] OR 

"Glyfos AU"[tw] OR "Glyfos BIO"[tw] OR "Glyphosate isopropylamine salt"[tw] OR 

"Glyphosate mono(isopropylamine) salt"[tw] OR "Glyphosate-isopropylammonium"[tw] OR 

"Glyphosate-mono(isopropylammonium)"[tw] OR "Landmaster"[tw] OR "MON 139"[tw] OR 

"MON 39"[tw] OR "N-(Phosphonomethyl)glycine isopropylamine salt"[tw] OR "N-

(Phosphonomethyl)glycine isopropylammonium salt"[tw] OR "N-(Phosphonomethyl)glycine 

monoisopropylamine salt"[tw] OR "Nitosorg"[tw] OR "Ron-do"[tw] OR "Utal"[tw] OR "Utal 

(herbicide)"[tw] OR "Vision (herbicide)"[tw] OR "2-Propanamine, compd, with N-
GLYPHOSATE B-9

APPENDIX C

Table B-2. Database Query Strings Pre-Public Comment Searches

Database

search date Query string

(phosphonomethyl)glycine (1:1)"[tw] OR "Glycine, N-(phosphonomethyl)-, compd. with 2-

propanamine (1:1)"[tw] OR "N-(Phosphonomethyl)glycine, compound with 2-propylamine 

(1:1)"[tw] OR "Isopropylamine glyphosate"[tw] OR "81591-81-3"[tw] OR "Glyphosatetrimesium"[tw] OR "Glyphosphate-trimesium"[tw] OR "Avans 330"[tw] OR "Glyphosate 

mono(trimethylsulfonium) salt"[tw] OR "Glyphosate trimethylsulfonium salt"[tw] OR 

"Glyphosate-trimesium"[tw] OR "Medallon"[tw] OR "Ouragan"[tw] OR "R 50224"[tw] OR 

"SC 0224"[tw] OR "Sulfosate"[tw] OR "Sulphosate"[tw] OR "Touchdown herbicide"[tw] OR 

"Trimethylsulfonium carboxymethylamino-methylphosphonate"[tw] OR "Trimethylsulfonium 

glyphosate"[tw] OR "Glycine, N-(phosphonomethyl)-, ion(1-), trimethylsulfonium"[tw] OR 

"Sulfosate"[tw]) NOT (("glyphosate"[nm]) OR (("1071-83-6"[tw] OR 

"(Carboxymethylamino)methylphosphonic acid"[tw] OR 

"Carboxymethylaminomethanephosphinic acid"[tw] OR "C-K Yuyos FAV"[tw] OR "CP 

67573"[tw] OR "Folusen"[tw] OR "Forsat"[tw] OR "Glialka"[tw] OR "Glifoglex"[tw] OR 

"Glifosan 747"[tw] OR "gliphosate"[tw] OR "Gliz"[tw] OR "Glyfos"[tw] OR "GlyGran"[tw] OR 

"Glyphodin A"[tw] OR "Glyphomax"[tw] OR "Glyphosate"[tw] OR "Glyphosphate"[tw] OR 

"Ground Bio"[tw] OR "Herbatop"[tw] OR "HM 2028"[tw] OR "Kickdown"[tw] OR "Lancer 

herbicide"[tw] OR "MON 2139"[tw] OR "MON 3539"[tw] OR "MON 6000"[tw] OR "N-

(Phosphonomethyl)glycine"[tw] OR "N-(phosphonomethyl)-Glycine"[tw] OR "NPhosphomethylglycine"[tw] OR "N-Phosphonomethylglycine"[tw] OR "Phorsat"[tw] OR 

"Phosphonomethylglycine"[tw] OR "Phosphonomethyliminoacetic acid"[tw] OR 

"Pondmaster"[tw] OR "Rebel Garden"[tw] OR "Roundup Max"[tw] OR "Safal"[tw] OR 

"Scout herbicide"[tw] OR "Silglif"[tw] OR "yerbimat"[tw]) AND (to[sh] OR po[sh] OR ae[sh] 

OR pk[sh] OR (me[sh] AND ("humans"[mh] OR "animals"[mh])) OR ci[sh] OR bl[sh] OR 

cf[sh] OR ur[sh] OR "environmental exposure"[mh] OR "endocrine system"[mh] OR 

"hormones, hormone substitutes, and hormone antagonists"[mh] OR "endocrine 

disruptors"[mh] OR (("Computational biology"[mh] OR "Medical Informatics"[mh] OR 

Genomics[mh] OR Genome[mh] OR Proteomics[mh] OR Proteome[mh] OR 

Metabolomics[mh] OR Metabolome[mh] OR Genes[mh] OR "Gene expression"[mh] OR 

Phenotype[mh] OR genetics[mh] OR genotype[mh] OR Transcriptome[mh] OR ("Systems 

Biology"[mh] AND ("Environmental Exposure"[mh] OR "Epidemiological Monitoring"[mh] 

OR analysis[sh])) OR "Transcription, Genetic "[mh] OR "Reverse transcription"[mh] OR 

"Transcriptional activation"[mh] OR "Transcription factors"[mh] OR ("biosynthesis"[sh] AND 

(RNA[mh] OR DNA[mh])) OR "RNA, Messenger"[mh] OR "RNA, Transfer"[mh] OR 

"peptide biosynthesis"[mh] OR "protein biosynthesis"[mh] OR "Reverse Transcriptase 

Polymerase Chain Reaction"[mh] OR "Base Sequence"[mh] OR "Trans-activators"[mh] OR 

"Gene Expression Profiling"[mh])) OR cancer[sb] OR "pharmacology"[Majr])) OR (("1071-

83-6"[tw] OR "(Carboxymethylamino)methylphosphonic acid"[tw] OR 

"Carboxymethylaminomethanephosphinic acid"[tw] OR "C-K Yuyos FAV"[tw] OR "CP 

67573"[tw] OR "Folusen"[tw] OR "Forsat"[tw] OR "Glialka"[tw] OR "Glifoglex"[tw] OR 

"Glifosan 747"[tw] OR "gliphosate"[tw] OR "Gliz"[tw] OR "Glyfos"[tw] OR "GlyGran"[tw] OR 

"Glyphodin A"[tw] OR "Glyphomax"[tw] OR "Glyphosate"[tw] OR "Glyphosphate"[tw] OR 

"Ground Bio"[tw] OR "Herbatop"[tw] OR "HM 2028"[tw] OR "Kickdown"[tw] OR "Lancer 

herbicide"[tw] OR "MON 2139"[tw] OR "MON 3539"[tw] OR "MON 6000"[tw] OR "N-

(Phosphonomethyl)glycine"[tw] OR "N-(phosphonomethyl)-Glycine"[tw] OR "NPhosphomethylglycine"[tw] OR "N-Phosphonomethylglycine"[tw] OR "Phorsat"[tw] OR 

"Phosphonomethylglycine"[tw] OR "Phosphonomethyliminoacetic acid"[tw] OR 

"Pondmaster"[tw] OR "Rebel Garden"[tw] OR "Roundup Max"[tw] OR "Safal"[tw] OR 

"Scout herbicide"[tw] OR "Silglif"[tw] OR "yerbimat"[tw]) NOT medline[sb]) OR 

("Roundup"[tw] AND (monsanto[tw] OR "antifungal agents"[Pharmacological Action] OR 

"antifungal agents"[MeSH Terms] OR "antifungal"[tw] OR "anti-fungal"[tw] OR "enzyme 
GLYPHOSATE B-10

APPENDIX C

Table B-2. Database Query Strings Pre-Public Comment Searches

Database

search date Query string

inhibitors"[Pharmacological Action] OR "enzyme inhibitors"[MeSH Terms] OR 

("enzyme"[tw] AND inhibitor*[tw]) OR "enzyme inhibitors"[tw] OR "enzyme inhibitor"[tw] OR 

"herbicides"[Pharmacological Action] OR "herbicides"[MeSH Terms] OR "herbicides"[tw] 

OR "herbicide"[tw] OR "uncoupling agents"[Pharmacological Action] OR "uncoupling 

agents"[MeSH Terms] OR ("uncoupling"[tw] AND agent*[tw]) OR "uncoupling agent"[tw] 

OR "uncoupling agents"[tw] OR "pesticides"[mh] OR pesticide*[tw]))))

Toxline

9/2017

( "lancer herbicide" OR "mon 2139" OR "mon 3539" OR "mon 6000" OR "phorsat" OR 

"phosphonomethyliminoacetic acid" OR "rebel garden" OR "roundup max" OR "safal" OR 

"scout herbicide" ) AND 2014:2017 [yr] AND ( ANEUPL [org] OR BIOSIS [org] OR CIS 

[org] OR DART [org] OR EMIC [org] OR EPIDEM [org] OR FEDRIP [org] OR HEEP [org] 

OR HMTC [org] OR IPA [org] OR RISKLINE [org] OR MTGABS [org] OR NIOSH [org] OR 

NTIS [org] OR PESTAB [org] OR PPBIB [org] ) AND NOT PubMed [org] AND NOT pubdart 

[org] 

( " ( carboxymethylamino ) methylphosphonic acid" OR 

"carboxymethylaminomethanephosphinic acid" OR "c k yuyos fav" OR "cp 67573" OR 

"folusen" OR "forsat" OR "glialka" OR "glifosan 747" OR "glygran" OR "glyphodin a" OR 

"glyphomax" OR "ground bio" OR "herbatop" OR "hm 2028" OR "kickdown" ) AND 

2014:2017 [yr] AND ( ANEUPL [org] OR BIOSIS [org] OR CIS [org] OR DART [org] OR 

EMIC [org] OR EPIDEM [org] OR FEDRIP [org] OR HEEP [org] OR HMTC [org] OR IPA 

[org] OR RISKLINE [org] OR MTGABS [org] OR NIOSH [org] OR NTIS [org] OR PESTAB 

[org] OR PPBIB [org] ) AND NOT PubMed [org] AND NOT pubdart [org]

( "glifoglex" OR "gliphosate" OR "gliz" OR "glyfos" OR "glyphosate" OR "glyphosphate" OR 

"n ( phosphonomethyl ) glycine" OR "n ( phosphonomethyl ) glycine" OR "n 

phosphomethylglycine" OR "n phosphonomethylglycine" OR "phosphonomethylglycine" 

OR "pondmaster" OR "silglif" OR "yerbimat" ) AND 2014:2017 [yr] AND ( ANEUPL [org] 

OR BIOSIS [org] OR CIS [org] OR DART [org] OR EMIC [org] OR EPIDEM [org] OR 

FEDRIP [org] OR HEEP [org] OR HMTC [org] OR IPA [org] OR RISKLINE [org] OR 

MTGABS [org] OR NIOSH [org] OR NTIS [org] OR PESTAB [org] OR PPBIB [org] ) AND 

NOT PubMed [org] AND NOT pubdart [org]

1071-83-6 [rn] AND 2014:2017 [yr] AND ( ANEUPL [org] OR BIOSIS [org] OR CIS [org] 

OR DART [org] OR EMIC [org] OR EPIDEM [org] OR FEDRIP [org] OR HEEP [org] OR 

HMTC [org] OR IPA [org] OR RISKLINE [org] OR MTGABS [org] OR NIOSH [org] OR 

NTIS [org] OR PESTAB [org] OR PPBIB [org] ) [not] PubMed [org] [not] pubdart [org] 

( #7 NOT #4 ) AND NOT PubMed [org] AND NOT pubdart [org] 

"roundup" AND 2014:2017 [yr] AND ( ANEUPL [org] OR BIOSIS [org] OR CIS [org] OR 

DART [org] OR EMIC [org] OR EPIDEM [org] OR FEDRIP [org] OR HEEP [org] OR HMTC 

[org] OR IPA [org] OR RISKLINE [org] OR MTGABS [org] OR NIOSH [org] OR NTIS [org] 

OR PESTAB [org] OR PPBIB [org] ) [not] PubMed [org] [not] pubdart [org]

( "mon 0459" OR "40465 66 5" OR "mon 14420" OR "mon 8750" OR "roundup hi load" OR 

"roundup prodry" OR "mon 8000" OR "monsanto 8000" OR "polado" OR "trisodium 

hydrogen bis ( n ( phosphonatomethyl ) aminoacetate ) " ) AND 2014:2017 [yr] AND ( 

ANEUPL [org] OR BIOSIS [org] OR CIS [org] OR DART [org] OR EMIC [org] OR EPIDEM 

[org] OR FEDRIP [org] OR HEEP [org] OR HMTC [org] OR IPA [org] OR RISKLINE [org] 

OR MTGABS [org] OR NIOSH [org] OR NTIS [org] OR PESTAB [org] OR PPBIB [org] ) 

AND NOT PubMed [org] AND NOT pubdart [org] 

( 34494-03-6 [rn] OR 70393-85-0 [rn] ) AND 2014:2017 [yr] AND ( ANEUPL [org] OR 

BIOSIS [org] OR CIS [org] OR DART [org] OR EMIC [org] OR EPIDEM [org] OR FEDRIP 

[org] OR HEEP [org] OR HMTC [org] OR IPA [org] OR RISKLINE [org] OR MTGABS [org] 
GLYPHOSATE B-11

APPENDIX C

Table B-2. Database Query Strings Pre-Public Comment Searches

Database

search date Query string

OR NIOSH [org] OR NTIS [org] OR PESTAB [org] OR PPBIB [org] ) AND NOT PubMed 

[org] AND NOT pubdart [org]

( "glyphosate diammonium" OR "diammonium n ( phosphonomethyl ) glycine" OR "n ( 

phosphonomethyl ) glycine diammonium salt" ) AND 2014:2017 [yr] AND ( ANEUPL [org] 

OR BIOSIS [org] OR CIS [org] OR DART [org] OR EMIC [org] OR EPIDEM [org] OR 

FEDRIP [org] OR HEEP [org] OR HMTC [org] OR IPA [org] OR RISKLINE [org] OR 

MTGABS [org] OR NIOSH [org] OR NTIS [org] OR PESTAB [org] OR PPBIB [org] ) AND 

NOT PubMed [org] AND NOT pubdart [org] 

( "roundup weathermax" OR "touchdown forte hitech" OR "transorb r" OR "weathermax" 

OR "zapp qi" OR "glyphosate potassium" OR "potassium glyphosate" OR "potassium n ( 

phosphonomethyl ) glycine" OR "uragan forte" OR "visionmax" OR "n ( phosphonomethyl ) 

glycine potassium salt" OR "glyphosate ammonium" OR "n ( phosphonomethyl ) glycine 

ammonium salt" ) AND 2014:2017 [yr] AND ( ANEUPL [org] OR BIOSIS [org] OR CIS [org] 

OR DART [org] OR EMIC [org] OR EPIDEM [org] OR FEDRIP [org] OR HEEP [org] OR 

HMTC [org] OR IPA [org] OR RISKLINE [org] OR MTGABS [org] OR NIOSH [org] OR 

NTIS [org] OR PESTAB [org] OR PPBIB [org] ) AND NOT PubMed [org] AND NOT pubdart 

[org] 

( "glyphosate potassium" OR "glyphosate monopotassium salt" OR "glyphosate potassium" 

OR "glyphosate potassium" OR "monopotassium glyphosate" OR "roundup attack" OR 

"roundup energy" OR "roundup maxload" OR "roundup original max" OR "roundup power 

max" OR "roundup ultramax ii" ) AND 2014:2017 [yr] AND ( ANEUPL [org] OR BIOSIS 

[org] OR CIS [org] OR DART [org] OR EMIC [org] OR EPIDEM [org] OR FEDRIP [org] OR 

HEEP [org] OR HMTC [org] OR IPA [org] OR RISKLINE [org] OR MTGABS [org] OR 

NIOSH [org] OR NTIS [org] OR PESTAB [org] OR PPBIB [org] ) AND NOT PubMed [org] 

AND NOT pubdart [org] 

( 39600-42-5 [rn] OR 39600-55-0 [rn] OR 39600-56-1 [rn] OR 39600-58-3 [rn] OR 40465-

59-6 [rn] OR 40465-64-3 [rn] OR 40465-67-6 [rn] OR 40465-70-1 [rn] OR 40465-90-5 [rn] 

OR 40465-91-6 [rn] OR 70901-12-1 [rn] OR 114370-14-8 [rn] OR 69254-40-6 [rn] ) AND 

2014:2017 [yr] AND ( ANEUPL [org] OR BIOSIS [org] OR CIS [org] OR DART [org] OR 

EMIC [org] OR EPIDEM [org] OR FEDRIP [org] OR HEEP [org] OR HMTC [org] OR IPA 

[org] OR RISKLINE [org] OR MTGABS [org] OR NIOSH [org] OR NTIS [org] OR PESTAB 

[org] OR PPBIB [org] ) AND NOT PubMed [org] AND NOT pubdart [org] 

( "sulphosate" OR "touchdown herbicide" OR "trimethylsulfonium carboxymethylamino 

methylphosphonate" OR "trimethylsulfonium glyphosate" OR "glycine n ( phosphonomethyl 

) ion ( 1 ) trimethylsulfonium" ) AND 2014:2017 [yr] AND ( ANEUPL [org] OR BIOSIS [org] 

OR CIS [org] OR DART [org] OR EMIC [org] OR EPIDEM [org] OR FEDRIP [org] OR 

HEEP [org] OR HMTC [org] OR IPA [org] OR RISKLINE [org] OR MTGABS [org] OR 

NIOSH [org] OR NTIS [org] OR PESTAB [org] OR PPBIB [org] ) AND NOT PubMed [org] 

AND NOT pubdart [org] 

( "isopropylamine glyphosate" OR "glyphosate trimesium" OR "glyphosphate trimesium" 

OR "avans 330" OR "glyphosate mono ( trimethylsulfonium ) salt" OR "glyphosate 

trimethylsulfonium salt" OR "glyphosate trimesium" OR "medallon" OR "ouragan" OR "r 

50224" OR "sc 0224" OR "sulfosate" ) AND 2014:2017 [yr] AND ( ANEUPL [org] OR 

BIOSIS [org] OR CIS [org] OR DART [org] OR EMIC [org] OR EPIDEM [org] OR FEDRIP 

[org] OR HEEP [org] OR HMTC [org] OR IPA [org] OR RISKLINE [org] OR MTGABS [org] 

OR NIOSH [org] OR NTIS [org] OR PESTAB [org] OR PPBIB [org] ) AND NOT PubMed 

[org] AND NOT pubdart [org] 
GLYPHOSATE B-12

APPENDIX C

Table B-2. Database Query Strings Pre-Public Comment Searches

Database

search date Query string

( "n ( phosphonomethyl ) glycine monoisopropylamine salt" OR "nitosorg" OR "utal" OR 

"utal ( herbicide ) " OR "vision ( herbicide ) " OR "2 propanamine compd with n ( 

phosphonomethyl ) glycine ( 1 1 ) " OR "glycine n ( phosphonomethyl ) compd with 2 

propanamine ( 1 1 ) " OR "n ( phosphonomethyl ) glycine compound with 2 propylamine ( 1 

1 ) " ) AND 2014:2017 [yr] AND ( ANEUPL [org] OR BIOSIS [org] OR CIS [org] OR DART 

[org] OR EMIC [org] OR EPIDEM [org] OR FEDRIP [org] OR HEEP [org] OR HMTC [org] 

OR IPA [org] OR RISKLINE [org] OR MTGABS [org] OR NIOSH [org] OR NTIS [org] OR 

PESTAB [org] OR PPBIB [org] ) AND NOT PubMed [org] AND NOT pubdart [org] 

( "glyphosate mono ( isopropylamine ) salt" OR "glyphosate isopropylammonium" OR 

"glyphosate mono ( isopropylammonium ) " OR "landmaster" OR "mon 139" OR "mon 39" 

OR "n ( phosphonomethyl ) glycine isopropylamine salt" OR "n ( phosphonomethyl ) 

glycine isopropylammonium salt" ) AND 2014:2017 [yr] AND ( ANEUPL [org] OR BIOSIS 

[org] OR CIS [org] OR DART [org] OR EMIC [org] OR EPIDEM [org] OR FEDRIP [org] OR 

HEEP [org] OR HMTC [org] OR IPA [org] OR RISKLINE [org] OR MTGABS [org] OR 

NIOSH [org] OR NTIS [org] OR PESTAB [org] OR PPBIB [org] ) AND NOT PubMed [org] 

AND NOT pubdart [org] 

( "glyphosate isopropylammonium" OR "glyphosate isopropylamine salt" OR "azural at" OR 

"cp 70139" OR "fosulen" OR "glifosato estrella" OR "glycel" OR "glycine n ( 

phosphonomethyl ) cmpd with 2 propanamine ( 1 1 ) " OR "glyfos au" OR "glyfos bio" OR 

"glyphosate isopropylamine salt" ) AND 2014:2017 [yr] AND ( ANEUPL [org] OR BIOSIS 

[org] OR CIS [org] OR DART [org] OR EMIC [org] OR EPIDEM [org] OR FEDRIP [org] OR 

HEEP [org] OR HMTC [org] OR IPA [org] OR RISKLINE [org] OR MTGABS [org] OR 

NIOSH [org] OR NTIS [org] OR PESTAB [org] OR PPBIB [org] ) AND NOT PubMed [org] 

AND NOT pubdart [org] 

( 38641-94-0 [rn] OR 81591-81-3 [rn] ) AND 2014:2017 [yr] AND ( ANEUPL [org] OR 

BIOSIS [org] OR CIS [org] OR DART [org] OR EMIC [org] OR EPIDEM [org] OR FEDRIP 

[org] OR HEEP [org] OR HMTC [org] OR IPA [org] OR RISKLINE [org] OR MTGABS [org] 

OR NIOSH [org] OR NTIS [org] OR PESTAB [org] OR PPBIB [org] ) AND NOT PubMed 

[org] AND NOT pubdart [org] 

2/2015 "Glifoglex" OR "gliphosate" OR "Gliz" OR "Glyfos" OR "Glyphosate" OR "Glyphosphate" 

OR "N-(Phosphonomethyl)glycine" OR "N-(phosphonomethyl)-Glycine" OR "NPhosphomethylglycine" OR "N-Phosphonomethylglycine" OR "Phosphonomethylglycine" 

OR "Pondmaster" OR "Silglif" OR "yerbimat" 

"(Carboxymethylamino)methylphosphonic acid" OR 

"Carboxymethylaminomethanephosphinic acid" OR "C-K Yuyos FAV" OR "CP 67573" OR 

"Folusen" OR "Forsat" OR "Glialka" OR "Glifosan 747" OR "GlyGran" OR "Glyphodin A" 

OR "Glyphomax" OR "Ground Bio" OR "Herbatop" OR "HM 2028" OR "Kickdown"

"Lancer herbicide" OR "MON 2139" OR "MON 3539" OR "MON 6000" OR "Phorsat" OR 

"Phosphonomethyliminoacetic acid" OR "Rebel Garden" OR "Roundup Max" OR "Safal" 

OR "Scout herbicide"

"roundup"

34494-03-6[rn] OR 70393-85-0[rn]

"MON 0459" OR "40465-66-5" OR "MON 14420" OR "MON 8750" OR "Roundup Hi-Load" 

OR "Roundup PRODry" OR "MON 8000" OR "Monsanto 8000" OR "Polado" OR 

"Trisodium hydrogen bis(N-(phosphonatomethyl)aminoacetate)"
GLYPHOSATE B-13

APPENDIX C

Table B-2. Database Query Strings Pre-Public Comment Searches

Database

search date Query string

39600-42-5[rn] OR 39600-55-0[rn] OR 39600-56-1[rn] OR 39600-58-3[rn] OR 40465-59-

6[rn] OR 40465-64-3[rn] OR 40465-67-6[rn] OR 40465-70-1[rn] OR 40465-90-5[rn] OR 

40465-91-6[rn] OR 70901-12-1[rn] OR 114370-14-8[rn] OR 69254-40-6[rn]

"Glyphosate potassium" OR "Glyphosate monopotassium salt" OR "Glyphosate 

potassium" OR "Glyphosate-potassium" OR "Monopotassium glyphosate" OR "Roundup 

Attack" OR "Roundup Energy" OR "Roundup Maxload" OR "Roundup Original Max" OR 

"Roundup Power Max" OR "Roundup Ultramax II"

"Roundup Weathermax" OR "Touchdown Forte HiTech" OR "Transorb R" OR 

"Weathermax" OR "Zapp Qi" OR "Glyphosate-potassium" OR "Potassium glyphosate" OR 

"Potassium N-(phosphonomethyl)glycine" OR "Uragan Forte" OR "VisionMAX" OR "N-

(phosphonomethyl)glycine potassium salt" OR "Glyphosate ammonium" OR "N-

(phosphonomethyl)glycine ammonium salt"

"Glyphosate-diammonium" OR "Diammonium N-(phosphonomethyl)glycine" OR "N-

(phosphonomethyl)glycine diammonium salt"

38641-94-0[rn] OR 81591-81-3[rn]

"Glyphosate-isopropylammonium" OR "Glyphosate isopropylamine salt" OR "Azural AT" 

OR "CP 70139" OR "Fosulen" OR "Glifosato estrella" OR "Glycel" OR "Glycine, N-

(phosphonomethyl)-, cmpd with 2-propanamine (1:1)" OR "Glyfos AU" OR "Glyfos BIO" 

OR "Glyphosate isopropylamine salt" 

"Glyphosate mono(isopropylamine) salt" OR "Glyphosate-isopropylammonium" OR 

"Glyphosate-mono(isopropylammonium)" OR "Landmaster" OR "MON 139" OR "MON 39" 

OR "N-(Phosphonomethyl)glycine isopropylamine salt" OR "N-(Phosphonomethyl)glycine 

isopropylammonium salt"

"N-(Phosphonomethyl)glycine monoisopropylamine salt" OR "Nitosorg" OR "Utal" OR "Utal 

(herbicide)" OR "Vision (herbicide)" OR "2-Propanamine, compd, with N-

(phosphonomethyl)glycine (1:1)" OR "Glycine, N-(phosphonomethyl)-, compd. with 2-

propanamine (1:1)" OR "N-(Phosphonomethyl)glycine, compound with 2-propylamine 

(1:1)"

"Isopropylamine glyphosate" OR "Glyphosate-trimesium" OR "Glyphosphate-trimesium" 

OR "Avans 330" OR "Glyphosate mono(trimethylsulfonium) salt" OR "Glyphosate 

trimethylsulfonium salt" OR "Glyphosate-trimesium" OR "Medallon" OR "Ouragan" OR "R 

50224" OR "SC 0224" OR "Sulfosate" 

"Sulphosate" OR "Touchdown herbicide" OR "Trimethylsulfonium carboxymethylaminomethylphosphonate” OR “Trimethylsulfonium glyphosate” OR “Glycine, N- Nphosphonemethyl)-, ion(1-), trimethylsulfonium”

Toxcenter

9/2017

L1 9995 SEA 1071-83-6 

L2 92 SEA 34494-03-6 OR 40465-66-5 OR 70393-85-0 

L3 80 SEA 39600-42-5 OR 39600-55-0 OR 39600-56-1 OR 39600-58-3 OR 

 40465-59-6 OR 40465-64-3 OR 40465-67-6 OR 40465-70-1 OR 

 40465-90-5 OR 40465-91-6 

L4 101 SEA 70901-12-1 OR 114370-14-8 OR 69254-40-6 

L5 2022 SEA 38641-94-0 OR 81591-81-3 

L6 10037 SEA L1 OR L2 OR L3 OR L4 

L7 6132 SEA L6 NOT (TSCATS/FS OR PATENT/DT) 

L8 2048 SEA L6 AND (PY>2013 OR ED>=20150201) 

L9 1260 SEA L7 AND (PY>2013 OR ED>=20150201) 

L10 751 SEA L5 NOT L6 
GLYPHOSATE B-14

APPENDIX C

Table B-2. Database Query Strings Pre-Public Comment Searches

Database

search date Query string

L11 530 SEA L10 NOT (TSCATS/FS OR PATENT/DT) 

L12 63 SEA L11 AND (PY>2013 OR ED>=20150201) 

L13 56 SEA L9 AND (CANCER? OR CARCINOG? OR CARCINOM? OR 

COCARCINOG? 

 OR LYMPHOMA? OR NEOPLAS? OR ONCOGEN? OR PRECANCER? OR 

TUMOR? 

 OR TUMOUR?) 

L14 6 SEA L12 AND (CANCER? OR CARCINOG? OR CARCINOM? OR 

COCARCINOG? 

 OR LYMPHOMA? OR NEOPLAS? OR ONCOGEN? OR PRECANCER? OR 

TUMOR? 

 OR TUMOUR?) 

L15 16 SEA L13 AND MEDLINE/FS 

L16 40 SEA L13 NOT L15 

L17 44 DUP REM L15 L16 (12 DUPLICATES REMOVED)

 ANSWERS '1-44' FROM FILE TOXCENTER

L*** DEL 16 S L13 AND MEDLINE/FS

L*** DEL 16 S L13 AND MEDLINE/FS

L18 16 SEA L17 

L*** DEL 40 S L13 NOT L15

L*** DEL 40 S L13 NOT L15

L19 28 SEA L17 

L20 28 SEA (L18 OR L19) NOT MEDLINE/FS 

 D SCAN L20

L21 401072 SEA 14 NOT MEDLINE/FS 

L22 6 SEA L14 NOT MEDLINE/FS 

L23 6 DUP REM L22 (0 DUPLICATES REMOVED)

 ANSWERS '1-6' FROM FILE TOXCENTER

 D SCAN L23

 FILE 'MEDLINE' ENTERED AT 19:10:42 ON 14 SEP 2017

CHARGED TO COST=EH011.10.01 

L24 QUE ACROCHORDON OR ACROCHORDONS OR ADENOMATOSIS OR 

ADENOMATOUS 

 OR ADENOSIS OR AMYLOIDOSES OR AMYLOIDOSIS OR ANAPLASIA OR 

 ANGIOENDOTHELIOMATOSIS OR ANGIOMATOSIS OR BUSCHKELOWENSTEIN 

 OR CANCER OR CANCEROUS OR CANCERS OR CARCINOGEN 

L25 QUE CARCINOGENESIS OR CARCINOGENIC OR CARCINOGENICITY OR 

 CARCINOGENS OR CARCINOID OR CARCINOMATOSIS OR CHERUBISM 

OR CIN 

 OR CLL OR COCARCINOGENESIS OR DERMOID OR DYSMYELOPOIESIS 

OR 

 ENCHONDROMATOSIS OR EPIDERMOID OR ERYTHROLEUKAEMIA OR 

ERYTHROLE

 UKAEMIAS 

L26 QUE ERYTHROLEUKEMIA OR ERYTHROLEUKEMIAS OR 

ERYTHROPLAKIA OR 

 ERYTHROPLAKIAS OR ERYTHROPLASIA OR ESSENTIALTHROMBOCYTHEMIA 

 OR EXOSTOSIS OR FIBROADENOSIS OR FIBROID OR FIBROIDS OR 
GLYPHOSATE B-15

APPENDIX C

Table B-2. Database Query Strings Pre-Public Comment Searches

Database

search date Query string

 FIBROMATOSIS OR GLIOMATOSIS OR GLOMANGIOMATOSIS OR 

GRANULOMATOS

 IS 

L27 QUE GYNAECOMASTIA OR GYNECOMASTIA OR HEMANGIOMATOSIS 

OR 

 HODGKIN OR HODGKINS OR LEIOMYOMATOSIS OR LEUKAEMIA OR 

LEUKAEMIA

 S OR LEUKEMIA OR LEUKEMIAS OR LEUKOPLAKIA OR LEUKOPLAKIAS 

OR 

 LEUKOSTASIS OR LIPOBLASTOMATOSIS OR LIPOMATOSIS 

L28 QUE LYMPHANGIOLEIOMYOMATOSIS OR LYMPHANGIOMATOSIS OR 

LYMPHANGIO

 MYOMATOSIS OR LYMPHOPROLIFERATION OR 

LYMPHOPROLIFERATIONS OR 

 LYMPHOPROLIFERATIVE OR LYMPHOSCINTIGRAPHIC OR 

LYMPHOSCINTIGRAPH

 Y OR MACROGLOBULINEMIA OR MACROGLOBULINEMIAS 

L29 QUE MALIGNANCIES OR MALIGNANCY OR MALIGNANT OR 

MASTOCYTOSIS OR 

 MEIGS-SYNDROME OR MELANOMATOSIS OR MENINGIOMATOSIS OR 

METAPLASI

 A OR MICROMETASTASES OR MICROMETASTASIS OR MYCOSISFUNGOIDES 

 OR MYELODYSPLASIA OR MYELODYSPLASIAS 

L30 QUE MYELODYSPLASTIC OR MYELOFIBROSIS OR MYELOMATOSIS OR 

 MYELOPROLIFERATION OR MYELOPROLIFERATIONS OR 

MYELOPROLIFERATIVE

 OR MYELOSUPPRESSION OR MYOFIBROMATOSIS OR NEOPLASIA OR 

 NEOPLASM OR NEOPLASMS OR NEOPLASTIC OR NEURILEMMOMATOSIS 

L31 QUE NEUROFIBROMATOSIS OR NEURONEVUS OR NONHODGKIN OR 

NONHODGKIN

 S OR NONSEMINOMATOUS OR NSCLC OR ONCOGENE-FUSION OR 

OPSOCLONUS-

 MYOCLONUS OR PAPILLOMATA OR PAPILLOMATOSIS OR 

PARANEOPLASTIC 

 OR PEUTZ-JEGHERS OR POLYPOSIS OR PRECANCER 

L32 QUE PRECANCEROUS OR SARCOMATOSIS OR SCHWANNOMATOSIS 

OR 

 SEMINOMATOUS OR SEZARY-SYNDROME OR STRUMA-OVARII OR 

TUMOR OR 

 TUMORGENESIS OR TUMORGENIC OR TUMORIGENESIS OR 

TUMORIGENIC OR 

 TUMOR-MARKER OR TUMOR-MARKERS OR TUMOROGENESIS 

L33 QUE TUMOROGENIC OR TUMORS OR TUMOUR OR TUMOURS OR 

WALDENSTROM 

 OR WALDENSTROMS OR "5Q-SYNDROME" OR "WAGR SYNDROME" OR 

(ASCO 

 NOT FUNGI) OR (SENTINEL-LYMPH-NODE NOT BIOPSY) 

L34 QUE L24 OR L25 OR L26 OR L27 OR L28 OR L29 OR L30 OR L31 OR 

 L32 OR L33 
GLYPHOSATE B-16

APPENDIX C

Table B-2. Database Query Strings Pre-Public Comment Searches

Database

search date Query string

 DIS COST

 FILE 'TOXCENTER' ENTERED AT 19:12:52 ON 14 SEP 2017

CHARGED TO COST=EH011.10.01 

L47 1 SEA L9 AND ?IOMA 

 DIS COST

L48 26 SEA L9 AND (?AOMA OR ?BOMA OR ?COMA OR ?DOMA OR ?EOMA OR 

?FOMA 

 OR ?GOMA OR ?HOMA OR ?IOMA OR ?JOMA OR ?KOMA OR ?LOMA OR 

?MOMA 

 OR ?NOMA OR ?OOMA OR ?POMA OR ?QOMA OR ?ROMA OR ?SOMA OR 

?TOMA 

 OR ?UOMA OR ?VOMA OR ?WOMA) 

L49 0 SEA L9 AND (?XOMA OR ?YOMA OR ?ZOMA OR ?AOMAS OR ?BOMAS 

OR 

 ?COMAS OR ?DOMAS OR ?EOMAS OR ?FOMAS OR ?GOMAS OR ?HOMAS 

OR 

 ?IOMAS OR ?JOMAS OR ?KOMAS OR ?LOMAS OR ?MOMAS OR ?NOMAS 

OR 

 ?OOMAS OR ?POMAS OR ?QOMAS OR ?ROMAS) 

L50 0 SEA L9 AND (?SOMAS OR ?TOMAS OR ?UOMAS OR ?VOMAS OR 

?WOMAS OR 

 ?XOMAS OR ?YOMAS OR ?ZOMAS) 

L51 48 SEA L9 AND L34 

L52 68 SEA L48 OR L49 OR L50 OR L51 

L53 16 SEA L52 NOT L13 

L54 20 SEA L52 AND MEDLINE/FS 

L55 7 SEA L53 AND MEDLINE/FS 

L56 12 DUP REM L53 (4 DUPLICATES REMOVED)

 ANSWERS '1-12' FROM FILE TOXCENTER

 D SCAN L56

L57 6 SEA L12 AND L34 

L58 2 SEA L12 AND (?AOMA OR ?BOMA OR ?COMA OR ?DOMA OR ?EOMA OR 

 ?FOMA OR ?GOMA OR ?HOMA OR ?IOMA OR ?JOMA OR ?KOMA OR 

?LOMA OR 

 ?MOMA OR ?NOMA OR ?OOMA OR ?POMA OR ?QOMA OR ?ROMA OR 

?SOMA OR 

 ?TOMA OR ?UOMA OR ?VOMA OR ?WOMA) 

L59 0 SEA L12 AND (?XOMA OR ?YOMA OR ?ZOMA OR ?AOMAS OR ?BOMAS 

OR 

 ?COMAS OR ?DOMAS OR ?EOMAS OR ?FOMAS OR ?GOMAS OR ?HOMAS 

OR 

 ?IOMAS OR ?JOMAS OR ?KOMAS OR ?LOMAS OR ?MOMAS OR ?NOMAS 

OR 

 ?OOMAS OR ?POMAS OR ?QOMAS OR ?ROMAS) 

L60 0 SEA L12 AND (?SOMAS OR ?TOMAS OR ?UOMAS OR ?VOMAS OR 

?WOMAS OR 

 ?XOMAS OR ?YOMAS OR ?ZOMAS) 

L61 8 SEA L57 OR L58 

L62 8 SEA L61 NOT (L13 OR L52) 

L63 7 DUP REM L62 (1 DUPLICATE REMOVED)
GLYPHOSATE B-17

APPENDIX C

Table B-2. Database Query Strings Pre-Public Comment Searches

Database

search date Query string

 ANSWERS '1-7' FROM FILE TOXCENTER

 D SCAN L63

2/2017 FILE 'TOXCENTER' ENTERED AT 19:21:56 ON 18 FEB 2015

CHARGED TO COST=EH011.05.01.01

L1 8342 SEA 1071-83-6 

L2 63 SEA 34494-03-6 OR 40465-66-5 OR 70393-85-0 

L3 8 SEA L2 NOT L1 

L4 53 SEA 39600-42-5 OR 39600-55-0 OR 39600-56-1 OR 39600-58-3 OR 

 40465-59-6 OR 40465-64-3 OR 40465-67-6 OR 40465-70-1 OR 

 40465-90-5 OR 40465-91-6 

L5 59 SEA 70901-12-1 OR 114370-14-8 OR 69254-40-6 

L6 1828 SEA 38641-94-0 OR 81591-81-3 

L7 8369 SEA L1 OR L2 OR L4 OR L5 

L8 5041 SEA L7 NOT (PATENT/DT OR TSCATS/FS) 

 ACT TOXQUERY/Q

 ---------

L9 QUE (CHRONIC OR IMMUNOTOX? OR NEUROTOX? OR TOXICOKIN? OR 

 BIOMARKER? OR NEUROLOG?) 

L10 QUE (PHARMACOKIN? OR SUBCHRONIC OR PBPK OR 

EPIDEMIOLOGY/ST,CT,

 IT) 

L11 QUE (ACUTE OR SUBACUTE OR LD50# OR LD(W)50 OR LC50# OR 

 LC(W)50) 

L12 QUE (TOXICITY OR ADVERSE OR POISONING)/ST,CT,IT 

L13 QUE (INHAL? OR PULMON? OR NASAL? OR LUNG? OR RESPIR?) 

L14 QUE ((OCCUPATION? OR WORKPLACE? OR WORKER?) AND EXPOS?) 

L15 QUE (ORAL OR ORALLY OR INGEST? OR GAVAGE? OR DIET OR DIETS 

OR 

 DIETARY OR DRINKING(W)WATER?) 

L16 QUE (MAXIMUM AND CONCENTRATION? AND (ALLOWABLE OR 

PERMISSIBLE))

L17 QUE (ABORT? OR ABNORMALIT? OR EMBRYO? OR CLEFT? OR FETUS?) 

L18 QUE (FOETUS? OR FETAL? OR FOETAL? OR FERTIL? OR MALFORM? 

OR 

 OVUM?) 

L19 QUE (OVA OR OVARY OR PLACENTA? OR PREGNAN? OR PRENATAL?) 

L20 QUE (PERINATAL? OR POSTNATAL? OR REPRODUC? OR STERIL? OR 

 TERATOGEN?)

L21 QUE (SPERM OR SPERMAC? OR SPERMAG? OR SPERMATI? OR 

SPERMAS? OR 

 SPERMATOB? OR SPERMATOC? OR SPERMATOG?) 

L22 QUE (SPERMATOI? OR SPERMATOL? OR SPERMATOR? OR 

SPERMATOX? OR 

 SPERMATOZ? OR SPERMATU? OR SPERMI? OR SPERMO?) 

L23 QUE (NEONAT? OR NEWBORN? OR DEVELOPMENT OR 

DEVELOPMENTAL?) 

L24 QUE (ENDOCRIN? AND DISRUPT?) 

L25 QUE (ZYGOTE? OR CHILD OR CHILDREN OR ADOLESCEN? OR 

INFANT?) 

L26 QUE (WEAN? OR OFFSPRING OR AGE(W)FACTOR?) 
GLYPHOSATE B-18

APPENDIX C

Table B-2. Database Query Strings Pre-Public Comment Searches

Database

search date Query string

L27 QUE (DERMAL? OR DERMIS OR SKIN OR EPIDERM? OR CUTANEOUS?) 

L28 QUE (CARCINOG? OR COCARCINOG? OR CANCER? OR PRECANCER? 

OR 

 NEOPLAS?) 

L29 QUE (TUMOR? OR TUMOUR? OR ONCOGEN? OR LYMPHOMA? OR 

CARCINOM?) 

L30 QUE (GENETOX? OR GENOTOX? OR MUTAGEN? OR 

GENETIC(W)TOXIC?) 

L31 QUE (NEPHROTOX? OR HEPATOTOX?) 

L32 QUE (ENDOCRIN? OR ESTROGEN? OR ANDROGEN? OR HORMON?) 

L33 QUE (OCCUPATION? OR WORKER? OR WORKPLACE? OR EPIDEM?) 

L34 QUE L9 OR L10 OR L11 OR L12 OR L13 OR L14 OR L15 OR L16 OR L17 

 OR L18 OR L19 OR L20 OR L21 OR L22 OR L23 OR L24 OR L25 OR L26 

 OR L27 OR L28 OR L29 OR L30 OR L31 OR L32 OR L33 

L35 QUE (RAT OR RATS OR MOUSE OR MICE OR GUINEA(W)PIG? OR 

MURIDAE 

 OR DOG OR DOGS OR RABBIT? OR HAMSTER? OR PIG OR PIGS OR 

SWINE 

 OR PORCINE OR MONKEY? OR MACAQUE?) 

L36 QUE (MARMOSET? OR FERRET? OR GERBIL? OR RODENT? OR 

LAGOMORPHA 

 OR BABOON? OR CANINE OR CAT OR CATS OR FELINE OR MURINE) 

L37 QUE L34 OR L35 OR L36 

L38 QUE (HUMAN OR HUMANS OR HOMINIDAE OR MAMMALS OR MAMMAL? 

OR 

 PRIMATES OR PRIMATE?) 

L39 QUE L37 OR L38 

 ---------

L40 2675 SEA L8 AND L37 

L41 525 SEA L40 AND MEDLINE/FS 

L42 833 SEA L40 AND BIOSIS/FS 

L43 1263 SEA L40 AND CAPLUS/FS 

L44 0 SEA L40 AND IPA/FS 

L45 54 SEA L40 NOT (L41 OR L42 OR L43) 

L46 2064 DUP REM L41 L42 L43 L45 (611 DUPLICATES REMOVED)

 ANSWERS '1-2064' FROM FILE TOXCENTER

L*** DEL 525 S L40 AND MEDLINE/FS

L*** DEL 525 S L40 AND MEDLINE/FS

L47 525 SEA L46 

L*** DEL 833 S L40 AND BIOSIS/FS

L*** DEL 833 S L40 AND BIOSIS/FS

L48 644 SEA L46 

L*** DEL 1263 S L40 AND CAPLUS/FS

L*** DEL 1263 S L40 AND CAPLUS/FS

L49 859 SEA L46 

L*** DEL 54 S L40 NOT (L41 OR L42 OR L43)

L*** DEL 54 S L40 NOT (L41 OR L42 OR L43)

L50 36 SEA L46 

L51 1539 SEA (L47 OR L48 OR L49 OR L50) NOT MEDLINE/FS 

L52 1532 SEA L51 AND L1 
GLYPHOSATE B-19

APPENDIX C

Table B-2. Database Query Strings Pre-Public Comment Searches

Database

search date Query string

L53 7 SEA L51 NOT L52 

 D SCAN L53

L54 688 SEA L6 NOT L7 

L55 485 SEA L54 NOT (PATENT/DT OR TSCATS/FS) 

L56 314 SEA L55 AND L37 

L57 0 SEA L56 AND MEDLINE/FS 

L58 85 SEA L56 AND BIOSIS/FS 

L59 218 SEA L56 AND CAPLUS/FS 

L60 1 SEA L56 AND IPA/FS 

L61 274 DUP REM L56 (40 DUPLICATES REMOVED)

 ANSWERS '1-274' FROM FILE TOXCENTER

 D SCAN L52

Table B-3. Strategies to Augment the Literature Search

Source Query and number screened when available

TSCATSa

9/2017; 2/2015 Compounds searched: 1071-83-6; 34494-03-6; 40465-66-5; 70393-85-0; 38641-94-0; 

81591-81-3

NTP

9/2017 glyphosate AND cancer; Limited to 2010-2017

2/2015 "1071-83-6" OR "Glifoglex" OR "gliphosate" OR "Gliz" OR "Glyfos" OR "Glyphosate" 

OR "Glyphosphate" OR "N-(Phosphonomethyl)glycine" OR "N-(phosphonomethyl)-

Glycine" OR "N-Phosphomethylglycine" OR "N-Phosphonomethylglycine" OR 

"Phosphonomethylglycine" OR "Pondmaster" OR "Silglif" OR "yerbimat"

"34494-03-6" OR "40465-66-5" OR "70393-85-0" OR "MON 0459" OR "MON 14420" 

OR "MON 8750" OR "Roundup Hi-Load" OR "Roundup PRODry" OR "MON 8000" OR 

"Monsanto 8000" OR "Polado" OR "Trisodium hydrogen bis(N-

(phosphonatomethyl)aminoacetate)"

"38641-94-0" OR "Glyphosate-isopropylammonium" OR "Glyphosate isopropylamine 

salt" OR "Azural AT" OR "Buggy" OR "CP 70139" OR "Fosulen" OR "Glifosato estrella" 

OR "Glycel" OR "Glyfos AU" OR "Glyfos BIO" OR "Glyphosate isopropylamine salt" 

OR "Glyphosate mono(isopropylamine) salt" OR "Glyphosate-isopropylammonium" OR 

"Glyphosate-mono(isopropylammonium)" OR "Landmaster" OR "MON 139" OR "MON 

39" OR "N-(Phosphonomethyl)glycine isopropylamine salt" OR "N-

(Phosphonomethyl)glycine isopropylammonium salt" OR "N-(Phosphonomethyl)glycine 

monoisopropylamine salt" OR "Nitosorg" OR "Ron-do" OR "Utal" OR "Vision 

(herbicide)" OR "Roundup" OR "Isopropylamine glyphosate" OR "81591-81-3" OR 

"Glyphosate-trimesium" OR "Glyphosphate-trimesium" OR "Avans 330" OR 

"Glyphosate mono(trimethylsulfonium) salt" OR "Glyphosate trimethylsulfonium salt" 

OR "Glyphosate-trimesium" OR "Medallon" OR "Ouragan" OR "R 50224" OR "SC 

0224" OR "Sulfosate" OR "Sulphosate" OR "Touchdown" OR "Trimethylsulfonium 

carboxymethylamino-methylphosphonate" OR "Trimethylsulfonium glyphosate"

NPIRS

9/2017; 2/2015

PC Codes searched: 417300; 103603; 103613; 103604; 103607; 103601; 128501
GLYPHOSATE B-20

APPENDIX C

Table B-3. Strategies to Augment the Literature Search

Source Query and number screened when available

NIH RePORTER

4/2017 Text Search: "Carboxymethylamino)methylphosphonic acid" OR "2-Propanamine, 

compd, with N-(phosphonomethyl)glycine (1:1)" OR "Avans 330" OR "Azural AT" OR 

"C-K Yuyos FAV" OR "Carboxymethylaminomethanephosphinic acid" OR "CP 67573" 

OR "CP 70139" OR "Diammonium N-(phosphonomethyl)glycine" OR "Folusen" OR 

"Forsat" OR "Fosulen" OR "Glialka" OR "Glifoglex" OR "Glifosan 747" OR "Glifosato 

estrella" OR "gliphosate" OR "Gliz" OR "Glycel" OR "Glycine, N-(phosphonomethyl)-, 

cmpd with 2-propanamine (1:1)" OR "Glycine, N-(phosphonomethyl)-, compd. with 2-

propanamine (1:1)" OR "Glycine, N-(phosphonomethyl)-, ion(1-), trimethylsulfonium" 

OR "Glyfos" OR "Glyfos AU" OR "Glyfos BIO" OR "GlyGran" OR "Glyphodin A" OR 

"Glyphomax" OR "Glyphosate" OR "Glyphosphate" OR "Ground Bio" OR "Herbatop" 

OR "HM 2028" OR "Kickdown" OR "Lancer herbicide" OR "Landmaster" OR 

"Medallon" OR "MON 0459" OR "MON 139" OR "MON 14420" OR "MON 2139" OR 

"MON 3539" OR "MON 39" OR "MON 6000" OR "MON 8000" OR "MON 8750" OR 

"Monsanto 8000" OR "N-(phosphonomethyl)-Glycine" OR "N-

(Phosphonomethyl)glycine" OR "N-(phosphonomethyl)glycine ammonium salt" OR "N-

(phosphonomethyl)glycine diammonium salt" OR "N-(Phosphonomethyl)glycine 

isopropylamine salt" OR "N-(Phosphonomethyl)glycine isopropylammonium salt" OR 

"N-(Phosphonomethyl)glycine monoisopropylamine salt" OR "N-

(phosphonomethyl)glycine potassium salt" OR "N-(Phosphonomethyl)glycine, 

compound with 2-propylamine (1:1)" OR "N-Phosphomethylglycine" OR "NPhosphonomethylglycine" OR "Nitosorg" OR "Ouragan" OR "Phorsat" OR 

"Phosphonomethylglycine" OR "Phosphonomethyliminoacetic acid" OR "Polado" OR 

"Pondmaster" OR "Potassium N-(phosphonomethyl)glycine" OR "R 50224" OR "Rebel 

Garden" OR "Ron-do" OR "Roundup" OR "Safal" OR "SC 0224" OR "Scout herbicide" 

OR "Silglif" OR "Sulfosate" OR "Sulphosate" OR "Touchdown Forte HiTech" OR 

"Touchdown herbicide" OR "Transorb R" OR "Trimethylsulfonium 

carboxymethylamino-methylphosphonate" OR "Trisodium hydrogen bis(N-

(phosphonatomethyl)aminoacetate" OR "Uragan Forte" OR "Utal" OR "Vision 

herbicide" OR "VisionMAX" OR "Weathermax" OR "yerbimat" OR "Zapp Qi" 

(Advanced), Search in: Projects AdminIC: All, Fiscal Year: Active Projects, 

2017, 2016, 2015, 2014, 2013, 2012

Other Identified throughout the assessment process

aSeveral versions of the TSCATS database were searched, as needed, by CASRN including TSCATS1 via Toxline 

(no date limit), TSCATS2 via https://yosemite.epa.gov/oppts/epatscat8.nsf/ReportSearch?OpenForm (date restricted 

by EPA receipt date), and TSCATS via CDAT (date restricted by ‘Mail Received Date Range’), as well as google for 

recent TSCA submissions.

The 2015 and 2017 results were: 

• Number of records identified from PubMed, TOXLINE, and TOXCENTER (after duplicate 

removal): 5,592

• Number of records identified from other strategies: 211

• Total number of records to undergo literature screening: 5,803

Following the publication of the draft profile and receipt of public comments, ATSDR conducted an 

updated literature review to capture any references published after the conclusion of the original literature 

review. The updated literature review searches occurred in September and October 2019 using the 

following sources:
GLYPHOSATE B-21

APPENDIX C

• Toxline

• IPA

• Science Direct

• PubMed

• BIOSIS

• MEDLINE

• SciFinder

In each database, searches were limited to references published from 2017 (i.e., the year the literature 

searches for glyphosate were last conducted) to the present date. Table B-4 includes the search strings 

used in each of these searches. 

Table B-4. Database Query Strings Post-Public Comment Searches

Database 

search date Query String

Toxline 

9/2019

( "lancer herbicide" OR "mon 2139" OR "mon 3539" OR "mon 6000" OR "phorsat" OR 

"phosphonomethyliminoacetic acid" OR "rebel garden" OR "roundup max" OR "safal" OR 

"scout herbicide" )

( " ( carboxymethylamino ) methylphosphonic acid" OR 

"carboxymethylaminomethanephosphinic acid" OR "c k yuyos fav" OR "cp 67573" OR 

"folusen" OR "forsat" OR "glialka" OR "glifosan 747" OR "glygran" OR "glyphodin a" OR 

"glyphomax" OR "ground bio" OR "herbatop" OR "hm 2028" OR "kickdown" )

( "glifoglex" OR "gliphosate" OR "gliz" OR "glyfos" OR "glyphosate" OR "glyphosphate" OR "n 

( phosphonomethyl ) glycine" OR "n ( phosphonomethyl ) glycine" OR "n 

phosphomethylglycine" OR "n phosphonomethylglycine" OR "phosphonomethylglycine" OR 

"pondmaster" OR "silglif" OR "yerbimat" )

1071-83-6 [rn]

"roundup"

( "mon 0459" OR "40465 66 5" OR "mon 14420" OR "mon 8750" OR "roundup hi load" OR 

"roundup prodry" OR "mon 8000" OR "monsanto 8000" OR "polado" OR "trisodium hydrogen 

bis ( n ( phosphonatomethyl ) aminoacetate ) " )

( 34494-03-6 [rn] OR 70393-85-0 [rn] )

( "glyphosate diammonium" OR "diammonium n ( phosphonomethyl ) glycine" OR "n ( 

phosphonomethyl ) glycine diammonium salt" )

(roundup weathermax OR touchdown forte hitech OR transorb r OR weathermax OR zapp qi 

OR glyphosate potassium OR potassium glyphosate OR potassium n ( phosphonomethyl ) 

glycine OR uragan forte OR visionmax OR n ( phosphonomethyl ) glycine potassium salt OR 

glyphosate ammonium OR n ( phosphonomethyl ) glycine ammonium salt)

( "glyphosate potassium" OR "glyphosate monopotassium salt" OR "glyphosate potassium" 

OR "glyphosate potassium" OR "monopotassium glyphosate" OR "roundup attack" OR 

"roundup energy" OR "roundup maxload" OR "roundup original max" OR "roundup power 

max" OR "roundup ultramax ii" )

(39600-42-5 [rn] OR 39600-55-0 [rn] OR 39600-56-1 [rn] OR 39600-58-3 [rn] OR 40465-59-6 

[rn] OR 40465-64-3 [rn] OR 40465-67-6 [rn] OR 40465-70-1 [rn] OR 40465-90-5 [rn] OR 

40465-91-6 [rn] OR 70901-12-1 [rn] OR 114370-14-8 [rn] OR 69254-40-6 [rn])

IPA

9/2019

("1071-83-6" or "38641-94-0").rn. and ("Glyphosate" or "glyphosate isopropylamine" or 

"Glyphosphate" or "N-(phosphonomethyl)glycine " or "glycine, N-(phosphonomethyl)-, 

compound with 2-propanamine (1:1)" or "phosphonomethyliminoacetic acid" or "glyphosate 

acid" or "glyphosate-isopropylammonium" or "glyphosate mono(isopropylamine) salt" or 

"glyphosate-mono(isopropylammonium)" or "N-(phosphonomethyl)glycine, isopropylamine 

salt" or "Pondmaster" or "Roundup Max" or "Glifoglex" or "Glycel" or "Rondo" or "Spasor" or 

"Tumbleweed" or "MON-0573" or "CP 67573" or "Roundup" or "Glifonox" or "MON-0139" or 

"CP 70139").rw. and ("Glyphosate" or "glyphosate isopropylamine").sh.
GLYPHOSATE B-22

APPENDIX C

Table B-4. Database Query Strings Post-Public Comment Searches

Database 

search date Query String

Science 

Direct

9/2019

Glyphosate OR Glyphosphate OR "N phosphonomethyl glycine" OR 

"phosphonomethyliminoacetic acid" OR "glyphosate acid"

"Glyphosate isopropylamine" OR "Glycine, N-phosphonomethyl-, compound with 2-

propanamine 1:1" OR "glyphosate-isopropylammonium" OR "glyphosate monoisopropylamine 

salt" OR "glyphosate-monoisopropylammonium" OR "N phosphonomethyl)glycine, 

isopropylamine salt"

"Pondmaster" OR "Roundup Max" OR Glifoglex OR Glycel OR Rondo OR Spasor OR 

Tumbleweed OR "MON-0573" OR "CP 67573"

Roundup OR Rondo OR Glifonox OR Glycel OR "MON-0139" OR "CP 70139"

(Sonic AND Herbicide NOT Ultrasonic) OR (Rodeo and Herbicide)

PubMed

9/2019

("glyphosate"[nm] OR "1071-83-6"[tw] OR "(Carboxymethylamino)methylphosphonic acid"[tw] 

OR "Carboxymethylaminomethanephosphinic acid"[tw] OR "C-K Yuyos FAV"[tw] OR "CP 

67573"[tw] OR "Folusen"[tw] OR "Forsat"[tw] OR "Glialka"[tw] OR "Glifoglex"[tw] OR "Glifosan 

747"[tw] OR "gliphosate"[tw] OR "Gliz"[tw] OR "Glyfos"[tw] OR "GlyGran"[tw] OR "Glyphodin 

A"[tw] OR "Glyphomax"[tw] OR "Glyphosate"[tw] OR "Glyphosphate"[tw] OR "Ground Bio"[tw] 

OR "Herbatop"[tw] OR "HM 2028"[tw] OR "Kickdown"[tw] OR "Lancer herbicide"[tw] OR "MON 

2139"[tw] OR "MON 3539"[tw] OR "MON 6000"[tw] OR "N-(Phosphonomethyl)glycine"[tw] OR 

"N-(phosphonomethyl)-Glycine"[tw] OR "N-Phosphomethylglycine"[tw] OR "NPhosphonomethylglycine"[tw] OR "Phorsat"[tw] OR "Phosphonomethylglycine"[tw] OR 

"Phosphonomethyliminoacetic acid"[tw] OR "Pondmaster"[tw] OR "Rebel Garden"[tw] OR 

"Roundup Max"[tw] OR "Safal"[tw] OR "Scout herbicide"[tw] OR "Silglif"[tw] OR "yerbimat"[tw] 

OR "Roundup"[tw] OR "34494-03-6"[tw] OR "MON 0459"[tw] OR "40465-66-5"[tw] OR "MON 

14420"[tw] OR "MON 8750"[tw] OR "Roundup Hi-Load"[tw] OR "Roundup PRODry"[tw] OR 

"70393-85-0"[tw] OR "MON 8000"[tw] OR "Monsanto 8000"[tw] OR "Polado"[tw] OR 

"Trisodium hydrogen bis(N-(phosphonatomethyl)aminoacetate"[tw] OR "39600-42-5"[tw] OR 

"Glyphosate potassium"[tw] OR "Glyphosate monopotassium salt"[tw] OR "Glyphosate 

potassium"[tw] OR "Glyphosate-potassium"[tw] OR "Monopotassium glyphosate"[tw] OR 

"Roundup Attack"[tw] OR "Roundup Energy"[tw] OR "Roundup Maxload"[tw] OR "Roundup 

Original Max"[tw] OR "Roundup Power Max"[tw] OR "Roundup Ultramax II"[tw] OR "Roundup 

Weathermax"[tw] OR "Touchdown Forte HiTech"[tw] OR "Transorb R"[tw] OR 

"Weathermax"[tw] OR "Zapp Qi"[tw] OR "70901-12-1"[tw] OR "Glyphosate-potassium"[tw] OR 

"Potassium glyphosate"[tw] OR "Potassium N-(phosphonomethyl)glycine"[tw] OR "Uragan 

Forte"[tw] OR "VisionMAX"[tw] OR "N-(phosphonomethyl)glycine potassium salt"[tw] OR 

"114370-14-8"[tw] OR "Glyphosate ammonium"[tw] OR "N-(phosphonomethyl)glycine 

ammonium salt"[tw] OR "69254-40-6"[tw] OR "Glyphosate-diammonium"[tw] OR 

"Diammonium N-(phosphonomethyl)glycine"[tw] OR "N-(phosphonomethyl)glycine 

diammonium salt"[tw]) AND (cancer[sb] OR "neoplasms"[mh] OR "carcinogenicity tests"[mh] 

OR "carcinogens"[mh] OR "cell division/drug effects"[mh] OR "cell cycle/drug effects"[mh] OR 

"cell line, tumor/drug effects"[mh] OR "gene expression regulation, neoplastic"[mh] OR 

"neoplasm proteins/drug effects"[mh] OR "angiogenesis inducing agents"[mh] OR 

"myelodysplastic-myeloproliferative diseases"[mh] OR cancer*[tw] OR carcinog*[tw] OR 

carcinom*[tw] OR cocarcinog*[tw] OR lymphoma*[tw] OR neoplas*[tw] OR oncogen*[tw] OR 

precancer*[tw] OR tumor*[tw] OR tumour*[tw]) AND (2017/01/01 : 3000[dp])

("glyphosate, isopropyl amine salt"[nm] OR "N-(phosphonomethyl)glycine trimethylsulfonium 

salt"[nm] OR "38641-94-0"[tw] OR "Glyphosate-isopropylammonium"[tw] OR "Glyphosate 

isopropylamine salt"[tw] OR "Azural AT"[tw] OR "CP 70139"[tw] OR "Fosulen"[tw] OR 

"Glifosato estrella"[tw] OR "Glycel"[tw] OR "Glycine, N-(phosphonomethyl)-, cmpd with 2-

propanamine (1:1)"[tw] OR "Glyfos AU"[tw] OR "Glyfos BIO"[tw] OR "Glyphosate 

isopropylamine salt"[tw] OR "Glyphosate mono(isopropylamine) salt"[tw] OR "Glyphosateisopropylammonium"[tw] OR "Glyphosate-mono(isopropylammonium)"[tw] OR 

"Landmaster"[tw] OR "MON 139"[tw] OR "MON 39"[tw] OR "N-(Phosphonomethyl)glycine 
GLYPHOSATE B-23

APPENDIX C

Table B-4. Database Query Strings Post-Public Comment Searches

Database 

search date Query String

isopropylamine salt"[tw] OR "N-(Phosphonomethyl)glycine isopropylammonium salt"[tw] OR 

"N-(Phosphonomethyl)glycine monoisopropylamine salt"[tw] OR "Nitosorg"[tw] OR "Rondo"[tw] OR "Utal"[tw] OR "Utal (herbicide)"[tw] OR "Vision (herbicide)"[tw] OR "2-

Propanamine, compd, with N-(phosphonomethyl)glycine (1:1)"[tw] OR "Glycine, N-

(phosphonomethyl)-, compd. with 2-propanamine (1:1)"[tw] OR "N-(Phosphonomethyl)glycine, 

compound with 2-propylamine (1:1)"[tw] OR "Isopropylamine glyphosate"[tw] OR "81591-81-

3"[tw] OR "Glyphosate-trimesium"[tw] OR "Glyphosphate-trimesium"[tw] OR "Avans 330"[tw] 

OR "Glyphosate mono(trimethylsulfonium) salt"[tw] OR "Glyphosate trimethylsulfonium 

salt"[tw] OR "Glyphosate-trimesium"[tw] OR "Medallon"[tw] OR "Ouragan"[tw] OR "R 

50224"[tw] OR "SC 0224"[tw] OR "Sulfosate"[tw] OR "Sulphosate"[tw] OR "Touchdown 

herbicide"[tw] OR "Trimethylsulfonium carboxymethylamino-methylphosphonate"[tw] OR 

"Trimethylsulfonium glyphosate"[tw] OR "Glycine, N-(phosphonomethyl)-, ion(1-), 

trimethylsulfonium"[tw] OR "Sulfosate"[tw]) AND (cancer[sb] OR "neoplasms"[mh] OR 

"carcinogenicity tests"[mh] OR "carcinogens"[mh] OR "cell division/drug effects"[mh] OR "cell 

cycle/drug effects"[mh] OR "cell line, tumor/drug effects"[mh] OR "gene expression regulation, 

neoplastic"[mh] OR "neoplasm proteins/drug effects"[mh] OR "angiogenesis inducing 

agents"[mh] OR "myelodysplastic-myeloproliferative diseases"[mh] OR cancer*[tw] OR 

carcinog*[tw] OR carcinom*[tw] OR cocarcinog*[tw] OR lymphoma*[tw] OR neoplas*[tw] OR 

oncogen*[tw] OR precancer*[tw] OR tumor*[tw] OR tumour*[tw]) AND (2017/01/01 : 3000[dp])

("glyphosate"[nm]) OR (("1071-83-6"[tw] OR "(Carboxymethylamino)methylphosphonic 

acid"[tw] OR "Carboxymethylaminomethanephosphinic acid"[tw] OR "C-K Yuyos FAV"[tw] OR 

"CP 67573"[tw] OR "Folusen"[tw] OR "Forsat"[tw] OR "Glialka"[tw] OR "Glifoglex"[tw] OR 

"Glifosan 747"[tw] OR "gliphosate"[tw] OR "Gliz"[tw] OR "Glyfos"[tw] OR "GlyGran"[tw] OR 

"Glyphodin A"[tw] OR "Glyphomax"[tw] OR "Glyphosate"[tw] OR "Glyphosphate"[tw] OR 

"Ground Bio"[tw] OR "Herbatop"[tw] OR "HM 2028"[tw] OR "Kickdown"[tw] OR "Lancer 

herbicide"[tw] OR "MON 2139"[tw] OR "MON 3539"[tw] OR "MON 6000"[tw] OR "N-

(Phosphonomethyl)glycine"[tw] OR "N-(phosphonomethyl)-Glycine"[tw] OR "NPhosphomethylglycine"[tw] OR "N-Phosphonomethylglycine"[tw] OR "Phorsat"[tw] OR 

"Phosphonomethylglycine"[tw] OR "Phosphonomethyliminoacetic acid"[tw] OR 

"Pondmaster"[tw] OR "Rebel Garden"[tw] OR "Roundup Max"[tw] OR "Safal"[tw] OR "Scout 

herbicide"[tw] OR "Silglif"[tw] OR "yerbimat"[tw]) AND (to[sh] OR po[sh] OR ae[sh] OR pk[sh] 

OR (me[sh] AND ("humans"[mh] OR "animals"[mh])) OR ci[sh] OR bl[sh] OR cf[sh] OR ur[sh] 

OR "environmental exposure"[mh] OR "endocrine system"[mh] OR "hormones, hormone 

substitutes, and hormone antagonists"[mh] OR "endocrine disruptors"[mh] OR 

(("Computational biology"[mh] OR "Medical Informatics"[mh] OR Genomics[mh] OR 

Genome[mh] OR Proteomics[mh] OR Proteome[mh] OR Metabolomics[mh] OR 

Metabolome[mh] OR Genes[mh] OR "Gene expression"[mh] OR Phenotype[mh] OR 

genetics[mh] OR genotype[mh] OR Transcriptome[mh] OR ("Systems Biology"[mh] AND 

("Environmental Exposure"[mh] OR "Epidemiological Monitoring"[mh] OR analysis[sh])) OR 

"Transcription, Genetic "[mh] OR "Reverse transcription"[mh] OR "Transcriptional 

activation"[mh] OR "Transcription factors"[mh] OR ("biosynthesis"[sh] AND (RNA[mh] OR 

DNA[mh])) OR "RNA, Messenger"[mh] OR "RNA, Transfer"[mh] OR "peptide 

biosynthesis"[mh] OR "protein biosynthesis"[mh] OR "Reverse Transcriptase Polymerase 

Chain Reaction"[mh] OR "Base Sequence"[mh] OR "Trans-activators"[mh] OR "Gene 

Expression Profiling"[mh])) OR cancer[sb] OR "pharmacology"[Majr])) OR (("1071-83-6"[tw] 

OR "(Carboxymethylamino)methylphosphonic acid"[tw] OR 

"Carboxymethylaminomethanephosphinic acid"[tw] OR "C-K Yuyos FAV"[tw] OR "CP 

67573"[tw] OR "Folusen"[tw] OR "Forsat"[tw] OR "Glialka"[tw] OR "Glifoglex"[tw] OR "Glifosan 

747"[tw] OR "gliphosate"[tw] OR "Gliz"[tw] OR "Glyfos"[tw] OR "GlyGran"[tw] OR "Glyphodin 

A"[tw] OR "Glyphomax"[tw] OR "Glyphosate"[tw] OR "Glyphosphate"[tw] OR "Ground Bio"[tw] 

OR "Herbatop"[tw] OR "HM 2028"[tw] OR "Kickdown"[tw] OR "Lancer herbicide"[tw] OR "MON 

2139"[tw] OR "MON 3539"[tw] OR "MON 6000"[tw] OR "N-(Phosphonomethyl)glycine"[tw] OR 
GLYPHOSATE B-24

APPENDIX C

Table B-4. Database Query Strings Post-Public Comment Searches

Database 

search date Query String

"N-(phosphonomethyl)-Glycine"[tw] OR "N-Phosphomethylglycine"[tw] OR "NPhosphonomethylglycine"[tw] OR "Phorsat"[tw] OR "Phosphonomethylglycine"[tw] OR 

"Phosphonomethyliminoacetic acid"[tw] OR "Pondmaster"[tw] OR "Rebel Garden"[tw] OR 

"Roundup Max"[tw] OR "Safal"[tw] OR "Scout herbicide"[tw] OR "Silglif"[tw] OR "yerbimat"[tw]) 

NOT medline[sb]) AND (2017/01/01 : 3000[dp])

("Roundup"[tw] AND (monsanto[tw] OR "antifungal agents"[Pharmacological Action] OR 

"antifungal agents"[MeSH Terms] OR "antifungal"[tw] OR "anti-fungal"[tw] OR "enzyme 

inhibitors"[Pharmacological Action] OR "enzyme inhibitors"[MeSH Terms] OR ("enzyme"[tw] 

AND inhibitor*[tw]) OR "enzyme inhibitors"[tw] OR "enzyme inhibitor"[tw] OR 

"herbicides"[Pharmacological Action] OR "herbicides"[MeSH Terms] OR "herbicides"[tw] OR 

"herbicide"[tw] OR "uncoupling agents"[Pharmacological Action] OR "uncoupling 

agents"[MeSH Terms] OR ("uncoupling"[tw] AND agent*[tw]) OR "uncoupling agent"[tw] OR 

"uncoupling agents"[tw] OR "pesticides"[mh] OR pesticide*[tw])) NOT (("glyphosate"[nm]) OR 

(("1071-83-6"[tw] OR "(Carboxymethylamino)methylphosphonic acid"[tw] OR 

"Carboxymethylaminomethanephosphinic acid"[tw] OR "C-K Yuyos FAV"[tw] OR "CP 

67573"[tw] OR "Folusen"[tw] OR "Forsat"[tw] OR "Glialka"[tw] OR "Glifoglex"[tw] OR "Glifosan 

747"[tw] OR "gliphosate"[tw] OR "Gliz"[tw] OR "Glyfos"[tw] OR "GlyGran"[tw] OR "Glyphodin 

A"[tw] OR "Glyphomax"[tw] OR "Glyphosate"[tw] OR "Glyphosphate"[tw] OR "Ground Bio"[tw] 

OR "Herbatop"[tw] OR "HM 2028"[tw] OR "Kickdown"[tw] OR "Lancer herbicide"[tw] OR "MON 

2139"[tw] OR "MON 3539"[tw] OR "MON 6000"[tw] OR "N-(Phosphonomethyl)glycine"[tw] OR 

"N-(phosphonomethyl)-Glycine"[tw] OR "N-Phosphomethylglycine"[tw] OR "NPhosphonomethylglycine"[tw] OR "Phorsat"[tw] OR "Phosphonomethylglycine"[tw] OR 

"Phosphonomethyliminoacetic acid"[tw] OR "Pondmaster"[tw] OR "Rebel Garden"[tw] OR 

"Roundup Max"[tw] OR "Safal"[tw] OR "Scout herbicide"[tw] OR "Silglif"[tw] OR "yerbimat"[tw]) 

AND (to[sh] OR po[sh] OR ae[sh] OR pk[sh] OR (me[sh] AND ("humans"[mh] OR 

"animals"[mh])) OR ci[sh] OR bl[sh] OR cf[sh] OR ur[sh] OR "environmental exposure"[mh] 

OR "endocrine system"[mh] OR "hormones, hormone substitutes, and hormone 

antagonists"[mh] OR "endocrine disruptors"[mh] OR (("Computational biology"[mh] OR 

"Medical Informatics"[mh] OR Genomics[mh] OR Genome[mh] OR Proteomics[mh] OR 

Proteome[mh] OR Metabolomics[mh] OR Metabolome[mh] OR Genes[mh] OR "Gene 

expression"[mh] OR Phenotype[mh] OR genetics[mh] OR genotype[mh] OR 

Transcriptome[mh] OR ("Systems Biology"[mh] AND ("Environmental Exposure"[mh] OR 

"Epidemiological Monitoring"[mh] OR analysis[sh])) OR "Transcription, Genetic "[mh] OR 

"Reverse transcription"[mh] OR "Transcriptional activation"[mh] OR "Transcription factors"[mh] 

OR ("biosynthesis"[sh] AND (RNA[mh] OR DNA[mh])) OR "RNA, Messenger"[mh] OR "RNA, 

Transfer"[mh] OR "peptide biosynthesis"[mh] OR "protein biosynthesis"[mh] OR "Reverse 

Transcriptase Polymerase Chain Reaction"[mh] OR "Base Sequence"[mh] OR "Transactivators"[mh] OR "Gene Expression Profiling"[mh])) OR cancer[sb] OR 

"pharmacology"[Majr])) OR (("1071-83-6"[tw] OR "(Carboxymethylamino)methylphosphonic 

acid"[tw] OR "Carboxymethylaminomethanephosphinic acid"[tw] OR "C-K Yuyos FAV"[tw] OR 

"CP 67573"[tw] OR "Folusen"[tw] OR "Forsat"[tw] OR "Glialka"[tw] OR "Glifoglex"[tw] OR 

"Glifosan 747"[tw] OR "gliphosate"[tw] OR "Gliz"[tw] OR "Glyfos"[tw] OR "GlyGran"[tw] OR 

"Glyphodin A"[tw] OR "Glyphomax"[tw] OR "Glyphosate"[tw] OR "Glyphosphate"[tw] OR 

"Ground Bio"[tw] OR "Herbatop"[tw] OR "HM 2028"[tw] OR "Kickdown"[tw] OR "Lancer 

herbicide"[tw] OR "MON 2139"[tw] OR "MON 3539"[tw] OR "MON 6000"[tw] OR "N-

(Phosphonomethyl)glycine"[tw] OR "N-(phosphonomethyl)-Glycine"[tw] OR "NPhosphomethylglycine"[tw] OR "N-Phosphonomethylglycine"[tw] OR "Phorsat"[tw] OR 

"Phosphonomethylglycine"[tw] OR "Phosphonomethyliminoacetic acid"[tw] OR 

"Pondmaster"[tw] OR "Rebel Garden"[tw] OR "Roundup Max"[tw] OR "Safal"[tw] OR "Scout 

herbicide"[tw] OR "Silglif"[tw] OR "yerbimat"[tw]) NOT medline[sb])) AND (2017/01/01 : 

3000[dp])
GLYPHOSATE B-25

APPENDIX C

Table B-4. Database Query Strings Post-Public Comment Searches

Database 

search date Query String

("34494-03-6"[tw] OR "MON 0459"[tw] OR "40465-66-5"[tw] OR "MON 14420"[tw] OR "MON 

8750"[tw] OR "Roundup Hi-Load"[tw] OR "Roundup PRODry"[tw] OR "70393-85-0"[tw] OR 

"MON 8000"[tw] OR "Monsanto 8000"[tw] OR "Polado"[tw] OR "Trisodium hydrogen bis(N-

(phosphonatomethyl)aminoacetate"[tw]) AND (to[sh] OR po[sh] OR ae[sh] OR pk[sh] OR 

(me[sh] AND ("humans"[mh] OR "animals"[mh])) OR ci[sh] OR bl[sh] OR cf[sh] OR ur[sh] OR 

"environmental exposure"[mh] OR "endocrine system"[mh] OR "hormones, hormone 

substitutes, and hormone antagonists"[mh] OR "endocrine disruptors"[mh] OR 

(("Computational biology"[mh] OR "Medical Informatics"[mh] OR Genomics[mh] OR 

Genome[mh] OR Proteomics[mh] OR Proteome[mh] OR Metabolomics[mh] OR 

Metabolome[mh] OR Genes[mh] OR "Gene expression"[mh] OR Phenotype[mh] OR 

genetics[mh] OR genotype[mh] OR Transcriptome[mh] OR ("Systems Biology"[mh] AND 

("Environmental Exposure"[mh] OR "Epidemiological Monitoring"[mh] OR analysis[sh])) OR 

"Transcription, Genetic "[mh] OR "Reverse transcription"[mh] OR "Transcriptional 

activation"[mh] OR "Transcription factors"[mh] OR ("biosynthesis"[sh] AND (RNA[mh] OR 

DNA[mh])) OR "RNA, Messenger"[mh] OR "RNA, Transfer"[mh] OR "peptide 

biosynthesis"[mh] OR "protein biosynthesis"[mh] OR "Reverse Transcriptase Polymerase 

Chain Reaction"[mh] OR "Base Sequence"[mh] OR "Trans-activators"[mh] OR "Gene 

Expression Profiling"[mh])) OR cancer[sb] OR "pharmacology"[Majr]) AND (2017/01/01 : 

3000[dp])

("39600-42-5"[tw] OR "Glyphosate potassium"[tw] OR "Glyphosate monopotassium salt"[tw] 

OR "Glyphosate potassium"[tw] OR "Glyphosate-potassium"[tw] OR "Monopotassium 

glyphosate"[tw] OR "Roundup Attack"[tw] OR "Roundup Energy"[tw] OR "Roundup 

Maxload"[tw] OR "Roundup Original Max"[tw] OR "Roundup Power Max"[tw] OR "Roundup 

Ultramax II"[tw] OR "Roundup Weathermax"[tw] OR "Touchdown Forte HiTech"[tw] OR 

"Transorb R"[tw] OR "Weathermax"[tw] OR "Zapp Qi"[tw] OR "70901-12-1"[tw] OR 

"Glyphosate-potassium"[tw] OR "Potassium glyphosate"[tw] OR "Potassium N-

(phosphonomethyl)glycine"[tw] OR "Uragan Forte"[tw] OR "VisionMAX"[tw] OR "N-

(phosphonomethyl)glycine potassium salt"[tw] OR "114370-14-8"[tw] OR "Glyphosate 

ammonium"[tw] OR "N-(phosphonomethyl)glycine ammonium salt"[tw] OR "69254-40-6"[tw] 

OR "Glyphosate-diammonium"[tw] OR "Diammonium N-(phosphonomethyl)glycine"[tw] OR 

"N-(phosphonomethyl)glycine diammonium salt"[tw]) NOT (("glyphosate"[nm]) OR (("1071-83-

6"[tw] OR "(Carboxymethylamino)methylphosphonic acid"[tw] OR 

"Carboxymethylaminomethanephosphinic acid"[tw] OR "C-K Yuyos FAV"[tw] OR "CP 

67573"[tw] OR "Folusen"[tw] OR "Forsat"[tw] OR "Glialka"[tw] OR "Glifoglex"[tw] OR "Glifosan 

747"[tw] OR "gliphosate"[tw] OR "Gliz"[tw] OR "Glyfos"[tw] OR "GlyGran"[tw] OR "Glyphodin 

A"[tw] OR "Glyphomax"[tw] OR "Glyphosate"[tw] OR "Glyphosphate"[tw] OR "Ground Bio"[tw] 

OR "Herbatop"[tw] OR "HM 2028"[tw] OR "Kickdown"[tw] OR "Lancer herbicide"[tw] OR "MON 

2139"[tw] OR "MON 3539"[tw] OR "MON 6000"[tw] OR "N-(Phosphonomethyl)glycine"[tw] OR 

"N-(phosphonomethyl)-Glycine"[tw] OR "N-Phosphomethylglycine"[tw] OR "NPhosphonomethylglycine"[tw] OR "Phorsat"[tw] OR "Phosphonomethylglycine"[tw] OR 

"Phosphonomethyliminoacetic acid"[tw] OR "Pondmaster"[tw] OR "Rebel Garden"[tw] OR 

"Roundup Max"[tw] OR "Safal"[tw] OR "Scout herbicide"[tw] OR "Silglif"[tw] OR "yerbimat"[tw]) 

AND (to[sh] OR po[sh] OR ae[sh] OR pk[sh] OR (me[sh] AND ("humans"[mh] OR 

"animals"[mh])) OR ci[sh] OR bl[sh] OR cf[sh] OR ur[sh] OR "environmental exposure"[mh] 

OR "endocrine system"[mh] OR "hormones, hormone substitutes, and hormone 

antagonists"[mh] OR "endocrine disruptors"[mh] OR (("Computational biology"[mh] OR 

"Medical Informatics"[mh] OR Genomics[mh] OR Genome[mh] OR Proteomics[mh] OR 

Proteome[mh] OR Metabolomics[mh] OR Metabolome[mh] OR Genes[mh] OR "Gene 

expression"[mh] OR Phenotype[mh] OR genetics[mh] OR genotype[mh] OR 

Transcriptome[mh] OR ("Systems Biology"[mh] AND ("Environmental Exposure"[mh] OR 

"Epidemiological Monitoring"[mh] OR analysis[sh])) OR "Transcription, Genetic "[mh] OR 

"Reverse transcription"[mh] OR "Transcriptional activation"[mh] OR "Transcription factors"[mh] 
GLYPHOSATE B-26

APPENDIX C

Table B-4. Database Query Strings Post-Public Comment Searches

Database 

search date Query String

OR ("biosynthesis"[sh] AND (RNA[mh] OR DNA[mh])) OR "RNA, Messenger"[mh] OR "RNA, 

Transfer"[mh] OR "peptide biosynthesis"[mh] OR "protein biosynthesis"[mh] OR "Reverse 

Transcriptase Polymerase Chain Reaction"[mh] OR "Base Sequence"[mh] OR "Transactivators"[mh] OR "Gene Expression Profiling"[mh])) OR cancer[sb] OR 

"pharmacology"[Majr])) OR (("1071-83-6"[tw] OR "(Carboxymethylamino)methylphosphonic 

acid"[tw] OR "Carboxymethylaminomethanephosphinic acid"[tw] OR "C-K Yuyos FAV"[tw] OR 

"CP 67573"[tw] OR "Folusen"[tw] OR "Forsat"[tw] OR "Glialka"[tw] OR "Glifoglex"[tw] OR 

"Glifosan 747"[tw] OR "gliphosate"[tw] OR "Gliz"[tw] OR "Glyfos"[tw] OR "GlyGran"[tw] OR 

"Glyphodin A"[tw] OR "Glyphomax"[tw] OR "Glyphosate"[tw] OR "Glyphosphate"[tw] OR 

"Ground Bio"[tw] OR "Herbatop"[tw] OR "HM 2028"[tw] OR "Kickdown"[tw] OR "Lancer 

herbicide"[tw] OR "MON 2139"[tw] OR "MON 3539"[tw] OR "MON 6000"[tw] OR "N-

(Phosphonomethyl)glycine"[tw] OR "N-(phosphonomethyl)-Glycine"[tw] OR "NPhosphomethylglycine"[tw] OR "N-Phosphonomethylglycine"[tw] OR "Phorsat"[tw] OR 

"Phosphonomethylglycine"[tw] OR "Phosphonomethyliminoacetic acid"[tw] OR 

"Pondmaster"[tw] OR "Rebel Garden"[tw] OR "Roundup Max"[tw] OR "Safal"[tw] OR "Scout 

herbicide"[tw] OR "Silglif"[tw] OR "yerbimat"[tw]) NOT medline[sb]) OR ("Roundup"[tw] AND 

(monsanto[tw] OR "antifungal agents"[Pharmacological Action] OR "antifungal agents"[MeSH 

Terms] OR "antifungal"[tw] OR "anti-fungal"[tw] OR "enzyme inhibitors"[Pharmacological 

Action] OR "enzyme inhibitors"[MeSH Terms] OR ("enzyme"[tw] AND inhibitor*[tw]) OR 

"enzyme inhibitors"[tw] OR "enzyme inhibitor"[tw] OR "herbicides"[Pharmacological Action] 

OR "herbicides"[MeSH Terms] OR "herbicides"[tw] OR "herbicide"[tw] OR "uncoupling 

agents"[Pharmacological Action] OR "uncoupling agents"[MeSH Terms] OR ("uncoupling"[tw] 

AND agent*[tw]) OR "uncoupling agent"[tw] OR "uncoupling agents"[tw] OR "pesticides"[mh] 

OR pesticide*[tw]))) AND (2017/01/01 : 3000[dp])

((("glyphosate, isopropyl amine salt"[nm]) OR ("N-(phosphonomethyl)glycine 

trimethylsulfonium salt"[nm])) NOT (("glyphosate"[nm]) OR (("1071-83-6"[tw] OR 

"(Carboxymethylamino)methylphosphonic acid"[tw] OR 

"Carboxymethylaminomethanephosphinic acid"[tw] OR "C-K Yuyos FAV"[tw] OR "CP 

67573"[tw] OR "Folusen"[tw] OR "Forsat"[tw] OR "Glialka"[tw] OR "Glifoglex"[tw] OR "Glifosan 

747"[tw] OR "gliphosate"[tw] OR "Gliz"[tw] OR "Glyfos"[tw] OR "GlyGran"[tw] OR "Glyphodin 

A"[tw] OR "Glyphomax"[tw] OR "Glyphosate"[tw] OR "Glyphosphate"[tw] OR "Ground Bio"[tw] 

OR "Herbatop"[tw] OR "HM 2028"[tw] OR "Kickdown"[tw] OR "Lancer herbicide"[tw] OR "MON 

2139"[tw] OR "MON 3539"[tw] OR "MON 6000"[tw] OR "N-(Phosphonomethyl)glycine"[tw] OR 

"N-(phosphonomethyl)-Glycine"[tw] OR "N-Phosphomethylglycine"[tw] OR "NPhosphonomethylglycine"[tw] OR "Phorsat"[tw] OR "Phosphonomethylglycine"[tw] OR 

"Phosphonomethyliminoacetic acid"[tw] OR "Pondmaster"[tw] OR "Rebel Garden"[tw] OR 

"Roundup Max"[tw] OR "Safal"[tw] OR "Scout herbicide"[tw] OR "Silglif"[tw] OR "yerbimat"[tw]) 

AND (to[sh] OR po[sh] OR ae[sh] OR pk[sh] OR (me[sh] AND ("humans"[mh] OR 

"animals"[mh])) OR ci[sh] OR bl[sh] OR cf[sh] OR ur[sh] OR "environmental exposure"[mh] 

OR "endocrine system"[mh] OR "hormones, hormone substitutes, and hormone 

antagonists"[mh] OR "endocrine disruptors"[mh] OR (("Computational biology"[mh] OR 

"Medical Informatics"[mh] OR Genomics[mh] OR Genome[mh] OR Proteomics[mh] OR 

Proteome[mh] OR Metabolomics[mh] OR Metabolome[mh] OR Genes[mh] OR "Gene 

expression"[mh] OR Phenotype[mh] OR genetics[mh] OR genotype[mh] OR 

Transcriptome[mh] OR ("Systems Biology"[mh] AND ("Environmental Exposure"[mh] OR 

"Epidemiological Monitoring"[mh] OR analysis[sh])) OR "Transcription, Genetic "[mh] OR 

"Reverse transcription"[mh] OR "Transcriptional activation"[mh] OR "Transcription factors"[mh] 

OR ("biosynthesis"[sh] AND (RNA[mh] OR DNA[mh])) OR "RNA, Messenger"[mh] OR "RNA, 

Transfer"[mh] OR "peptide biosynthesis"[mh] OR "protein biosynthesis"[mh] OR "Reverse 

Transcriptase Polymerase Chain Reaction"[mh] OR "Base Sequence"[mh] OR "Transactivators"[mh] OR "Gene Expression Profiling"[mh])) OR cancer[sb] OR 

"pharmacology"[Majr])) OR (("1071-83-6"[tw] OR "(Carboxymethylamino)methylphosphonic 
GLYPHOSATE B-27

APPENDIX C

Table B-4. Database Query Strings Post-Public Comment Searches

Database 

search date Query String

acid"[tw] OR "Carboxymethylaminomethanephosphinic acid"[tw] OR "C-K Yuyos FAV"[tw] OR 

"CP 67573"[tw] OR "Folusen"[tw] OR "Forsat"[tw] OR "Glialka"[tw] OR "Glifoglex"[tw] OR 

"Glifosan 747"[tw] OR "gliphosate"[tw] OR "Gliz"[tw] OR "Glyfos"[tw] OR "GlyGran"[tw] OR 

"Glyphodin A"[tw] OR "Glyphomax"[tw] OR "Glyphosate"[tw] OR "Glyphosphate"[tw] OR 

"Ground Bio"[tw] OR "Herbatop"[tw] OR "HM 2028"[tw] OR "Kickdown"[tw] OR "Lancer 

herbicide"[tw] OR "MON 2139"[tw] OR "MON 3539"[tw] OR "MON 6000"[tw] OR "N-

(Phosphonomethyl)glycine"[tw] OR "N-(phosphonomethyl)-Glycine"[tw] OR "NPhosphomethylglycine"[tw] OR "N-Phosphonomethylglycine"[tw] OR "Phorsat"[tw] OR 

"Phosphonomethylglycine"[tw] OR "Phosphonomethyliminoacetic acid"[tw] OR 

"Pondmaster"[tw] OR "Rebel Garden"[tw] OR "Roundup Max"[tw] OR "Safal"[tw] OR "Scout 

herbicide"[tw] OR "Silglif"[tw] OR "yerbimat"[tw]) NOT medline[sb]) OR ("Roundup"[tw] AND 

(monsanto[tw] OR "antifungal agents"[Pharmacological Action] OR "antifungal agents"[MeSH 

Terms] OR "antifungal"[tw] OR "anti-fungal"[tw] OR "enzyme inhibitors"[Pharmacological 

Action] OR "enzyme inhibitors"[MeSH Terms] OR ("enzyme"[tw] AND inhibitor*[tw]) OR 

"enzyme inhibitors"[tw] OR "enzyme inhibitor"[tw] OR "herbicides"[Pharmacological Action] 

OR "herbicides"[MeSH Terms] OR "herbicides"[tw] OR "herbicide"[tw] OR "uncoupling 

agents"[Pharmacological Action] OR "uncoupling agents"[MeSH Terms] OR ("uncoupling"[tw] 

AND agent*[tw]) OR "uncoupling agent"[tw] OR "uncoupling agents"[tw] OR "pesticides"[mh] 

OR pesticide*[tw])))) OR (("38641-94-0"[tw] OR "Glyphosate-isopropylammonium"[tw] OR 

"Glyphosate isopropylamine salt"[tw] OR "Azural AT"[tw] OR "CP 70139"[tw] OR "Fosulen"[tw] 

OR "Glifosato estrella"[tw] OR "Glycel"[tw] OR "Glycine, N-(phosphonomethyl)-, cmpd with 2-

propanamine (1:1)"[tw] OR "Glyfos AU"[tw] OR "Glyfos BIO"[tw] OR "Glyphosate 

isopropylamine salt"[tw] OR "Glyphosate mono(isopropylamine) salt"[tw] OR "Glyphosateisopropylammonium"[tw] OR "Glyphosate-mono(isopropylammonium)"[tw] OR 

"Landmaster"[tw] OR "MON 139"[tw] OR "MON 39"[tw] OR "N-(Phosphonomethyl)glycine 

isopropylamine salt"[tw] OR "N-(Phosphonomethyl)glycine isopropylammonium salt"[tw] OR 

"N-(Phosphonomethyl)glycine monoisopropylamine salt"[tw] OR "Nitosorg"[tw] OR "Rondo"[tw] OR "Utal"[tw] OR "Utal (herbicide)"[tw] OR "Vision (herbicide)"[tw] OR "2-

Propanamine, compd, with N-(phosphonomethyl)glycine (1:1)"[tw] OR "Glycine, N-

(phosphonomethyl)-, compd. with 2-propanamine (1:1)"[tw] OR "N-(Phosphonomethyl)glycine, 

compound with 2-propylamine (1:1)"[tw] OR "Isopropylamine glyphosate"[tw] OR "81591-81-

3"[tw] OR "Glyphosate-trimesium"[tw] OR "Glyphosphate-trimesium"[tw] OR "Avans 330"[tw] 

OR "Glyphosate mono(trimethylsulfonium) salt"[tw] OR "Glyphosate trimethylsulfonium 

salt"[tw] OR "Glyphosate-trimesium"[tw] OR "Medallon"[tw] OR "Ouragan"[tw] OR "R 

50224"[tw] OR "SC 0224"[tw] OR "Sulfosate"[tw] OR "Sulphosate"[tw] OR "Touchdown 

herbicide"[tw] OR "Trimethylsulfonium carboxymethylamino-methylphosphonate"[tw] OR 

"Trimethylsulfonium glyphosate"[tw] OR "Glycine, N-(phosphonomethyl)-, ion(1-), 

trimethylsulfonium"[tw] OR "Sulfosate"[tw]) NOT (("glyphosate"[nm]) OR (("1071-83-6"[tw] OR 

"(Carboxymethylamino)methylphosphonic acid"[tw] OR 

"Carboxymethylaminomethanephosphinic acid"[tw] OR "C-K Yuyos FAV"[tw] OR "CP 

67573"[tw] OR "Folusen"[tw] OR "Forsat"[tw] OR "Glialka"[tw] OR "Glifoglex"[tw] OR "Glifosan 

747"[tw] OR "gliphosate"[tw] OR "Gliz"[tw] OR "Glyfos"[tw] OR "GlyGran"[tw] OR "Glyphodin 

A"[tw] OR "Glyphomax"[tw] OR "Glyphosate"[tw] OR "Glyphosphate"[tw] OR "Ground Bio"[tw] 

OR "Herbatop"[tw] OR "HM 2028"[tw] OR "Kickdown"[tw] OR "Lancer herbicide"[tw] OR "MON 

2139"[tw] OR "MON 3539"[tw] OR "MON 6000"[tw] OR "N-(Phosphonomethyl)glycine"[tw] OR 

"N-(phosphonomethyl)-Glycine"[tw] OR "N-Phosphomethylglycine"[tw] OR "NPhosphonomethylglycine"[tw] OR "Phorsat"[tw] OR "Phosphonomethylglycine"[tw] OR 

"Phosphonomethyliminoacetic acid"[tw] OR "Pondmaster"[tw] OR "Rebel Garden"[tw] OR 

"Roundup Max"[tw] OR "Safal"[tw] OR "Scout herbicide"[tw] OR "Silglif"[tw] OR "yerbimat"[tw]) 

AND (to[sh] OR po[sh] OR ae[sh] OR pk[sh] OR (me[sh] AND ("humans"[mh] OR 

"animals"[mh])) OR ci[sh] OR bl[sh] OR cf[sh] OR ur[sh] OR "environmental exposure"[mh] 

OR "endocrine system"[mh] OR "hormones, hormone substitutes, and hormone 
GLYPHOSATE B-28

APPENDIX C

Table B-4. Database Query Strings Post-Public Comment Searches

Database 

search date Query String

antagonists"[mh] OR "endocrine disruptors"[mh] OR (("Computational biology"[mh] OR 

"Medical Informatics"[mh] OR Genomics[mh] OR Genome[mh] OR Proteomics[mh] OR 

Proteome[mh] OR Metabolomics[mh] OR Metabolome[mh] OR Genes[mh] OR "Gene 

expression"[mh] OR Phenotype[mh] OR genetics[mh] OR genotype[mh] OR 

Transcriptome[mh] OR ("Systems Biology"[mh] AND ("Environmental Exposure"[mh] OR 

"Epidemiological Monitoring"[mh] OR analysis[sh])) OR "Transcription, Genetic "[mh] OR 

"Reverse transcription"[mh] OR "Transcriptional activation"[mh] OR "Transcription factors"[mh] 

OR ("biosynthesis"[sh] AND (RNA[mh] OR DNA[mh])) OR "RNA, Messenger"[mh] OR "RNA, 

Transfer"[mh] OR "peptide biosynthesis"[mh] OR "protein biosynthesis"[mh] OR "Reverse 

Transcriptase Polymerase Chain Reaction"[mh] OR "Base Sequence"[mh] OR "Transactivators"[mh] OR "Gene Expression Profiling"[mh])) OR cancer[sb] OR 

"pharmacology"[Majr])) OR (("1071-83-6"[tw] OR "(Carboxymethylamino)methylphosphonic 

acid"[tw] OR "Carboxymethylaminomethanephosphinic acid"[tw] OR "C-K Yuyos FAV"[tw] OR 

"CP 67573"[tw] OR "Folusen"[tw] OR "Forsat"[tw] OR "Glialka"[tw] OR "Glifoglex"[tw] OR 

"Glifosan 747"[tw] OR "gliphosate"[tw] OR "Gliz"[tw] OR "Glyfos"[tw] OR "GlyGran"[tw] OR 

"Glyphodin A"[tw] OR "Glyphomax"[tw] OR "Glyphosate"[tw] OR "Glyphosphate"[tw] OR 

"Ground Bio"[tw] OR "Herbatop"[tw] OR "HM 2028"[tw] OR "Kickdown"[tw] OR "Lancer 

herbicide"[tw] OR "MON 2139"[tw] OR "MON 3539"[tw] OR "MON 6000"[tw] OR "N-

(Phosphonomethyl)glycine"[tw] OR "N-(phosphonomethyl)-Glycine"[tw] OR "NPhosphomethylglycine"[tw] OR "N-Phosphonomethylglycine"[tw] OR "Phorsat"[tw] OR 

"Phosphonomethylglycine"[tw] OR "Phosphonomethyliminoacetic acid"[tw] OR 

"Pondmaster"[tw] OR "Rebel Garden"[tw] OR "Roundup Max"[tw] OR "Safal"[tw] OR "Scout 

herbicide"[tw] OR "Silglif"[tw] OR "yerbimat"[tw]) NOT medline[sb]) OR ("Roundup"[tw] AND 

(monsanto[tw] OR "antifungal agents"[Pharmacological Action] OR "antifungal agents"[MeSH 

Terms] OR "antifungal"[tw] OR "anti-fungal"[tw] OR "enzyme inhibitors"[Pharmacological 

Action] OR "enzyme inhibitors"[MeSH Terms] OR ("enzyme"[tw] AND inhibitor*[tw]) OR 

"enzyme inhibitors"[tw] OR "enzyme inhibitor"[tw] OR "herbicides"[Pharmacological Action] 

OR "herbicides"[MeSH Terms] OR "herbicides"[tw] OR "herbicide"[tw] OR "uncoupling 

agents"[Pharmacological Action] OR "uncoupling agents"[MeSH Terms] OR ("uncoupling"[tw] 

AND agent*[tw]) OR "uncoupling agent"[tw] OR "uncoupling agents"[tw] OR "pesticides"[mh] 

OR pesticide*[tw])))) AND (2017/01/01 : 3000[dp])

BIOSIS

9/2019

CH=(Glyphosate OR "glyphosate isopropylamine" OR Glyphosphate OR "N-

(phosphonomethyl)glycine " OR "glycine, N-(phosphonomethyl)-, compound with 2-

propanamine (1:1)" OR "phosphonomethyliminoacetic acid" OR "glyphosate acid" OR 

"glyphosate-isopropylammonium" OR "glyphosate mono(isopropylamine) salt" OR 

"glyphosate-mono(isopropylammonium)" OR "N-(phosphonomethyl)glycine, isopropylamine 

salt" OR Pondmaster OR "Roundup Max" OR Glifoglex OR Glycel OR ((Muster) AND 

(pesticide OR herbicide)) OR Rondo OR ((Sonic) AND (pesticide OR herbicide)) OR Spasor 

OR ((Sting) AND (pesticide OR herbicide)) OR Tumbleweed OR "MON-0573" OR "CP 67573" 

OR Roundup OR ((Rodeo) AND (pesticide OR herbicide)) OR Glifonox OR "MON-0139" OR 

"CP 70139" OR ((Shackle) AND (pesticide OR herbicide)) OR "1071-83-6" OR "38641-94-0")

Indexes=BCI Timespan=2017-2019

MEDLINE

9/2019

("glyphosate" OR "1071-83-6" OR "(Carboxymethylamino)methylphosphonic acid" OR 

"Carboxymethylaminomethanephosphinic acid" OR "C-K Yuyos FAV" OR "CP 67573" OR 

"Folusen" OR "Forsat" OR "Glialka" OR "Glifoglex" OR "Glifosan 747" OR "gliphosate" OR 

"Gliz" OR "Glyfos" OR "GlyGran" OR "Glyphodin A" OR "Glyphomax" OR "Glyphosate" OR 

"Glyphosphate" OR "Ground Bio" OR "Herbatop" OR "HM 2028" OR "Kickdown" OR "Lancer 

herbicide" OR "MON 2139" OR "MON 3539" OR "MON 6000" OR "N-

(Phosphonomethyl)glycine" OR "N-(phosphonomethyl)-Glycine" OR "NPhosphomethylglycine" OR "N-Phosphonomethylglycine" OR "Phorsat" OR 

"Phosphonomethylglycine" OR "Phosphonomethyliminoacetic acid" OR "Pondmaster" OR 

"Rebel Garden" OR "Roundup Max" OR "Safal" OR "Scout herbicide" OR "Silglif" OR 
GLYPHOSATE B-29

APPENDIX C

Table B-4. Database Query Strings Post-Public Comment Searches

Database 

search date Query String

"yerbimat" OR "Roundup" OR "34494-03-6" OR "MON 0459" OR "40465-66-5" OR "MON 

14420" OR "MON 8750" OR "Roundup Hi-Load" OR "Roundup PRODry" OR "70393-85-0" 

OR "MON 8000" OR "Monsanto 8000" OR "Polado" OR "Trisodium hydrogen bis(N-

(phosphonatomethyl)aminoacetate" OR "39600-42-5" OR "Glyphosate potassium" OR 

"Glyphosate monopotassium salt" OR "Glyphosate potassium" OR "Glyphosate-potassium" 

OR "Monopotassium glyphosate" OR "Roundup Attack" OR "Roundup Energy" OR "Roundup 

Maxload" OR "Roundup Original Max" OR "Roundup Power Max" OR "Roundup Ultramax II" 

OR "Roundup Weathermax" OR "Touchdown Forte HiTech" OR "Transorb R" OR 

"Weathermax" OR "Zapp Qi" OR "70901-12-1" OR "Glyphosate-potassium" OR "Potassium 

glyphosate" OR "Potassium N-(phosphonomethyl)glycine" OR "Uragan Forte" OR 

"VisionMAX" OR "N-(phosphonomethyl)glycine potassium salt" OR "114370-14-8" OR 

"Glyphosate ammonium" OR "N-(phosphonomethyl)glycine ammonium salt" OR "69254-40-6" 

OR "Glyphosate-diammonium" OR "Diammonium N-(phosphonomethyl)glycine" OR "N-

(phosphonomethyl)glycine diammonium salt" ) AND MH (("neoplasms" OR "carcinogenicity 

tests" OR "carcinogens" OR "cell division/drug effects" OR "cell cycle/drug effects" OR "cell 

line, tumor/drug effects" OR "gene expression regulation, neoplastic" OR "neoplasm 

proteins/drug effects" OR "angiogenesis inducing agents" OR "myelodysplasticmyeloproliferative diseases") OR AB (cancer* OR carcinog* OR carcinom* OR cocarcinog* 

OR lymphoma* OR neoplas* OR oncogen* OR precancer* OR tumor* OR tumour*))

("glyphosate, isopropyl amine salt" OR "N-(phosphonomethyl)glycine trimethylsulfonium salt" 

OR "38641-94-0" OR "Glyphosate-isopropylammonium" OR "Glyphosate isopropylamine salt" 

OR "Azural AT" OR "CP 70139" OR "Fosulen" OR "Glifosato estrella" OR "Glycel" OR 

"Glycine, N-(phosphonomethyl)-, cmpd with 2-propanamine (1:1)" OR "Glyfos AU" OR "Glyfos 

BIO" OR "Glyphosate isopropylamine salt" OR "Glyphosate mono(isopropylamine) salt" OR 

"Glyphosate-isopropylammonium" OR "Glyphosate-mono(isopropylammonium)" OR 

"Landmaster" OR "MON 139" OR "MON 39" OR "N-(Phosphonomethyl)glycine 

isopropylamine salt" OR "N-(Phosphonomethyl)glycine isopropylammonium salt" OR "N-

(Phosphonomethyl)glycine monoisopropylamine salt" OR "Nitosorg" OR "Ron-do" OR "Utal" 

OR "Utal (herbicide)" OR "Vision (herbicide)" OR "2-Propanamine, compd, with N-

(phosphonomethyl)glycine (1:1)" OR "Glycine, N-(phosphonomethyl)-, compd. with 2-

propanamine (1:1)" OR "N-(Phosphonomethyl)glycine, compound with 2-propylamine (1:1)" 

OR "Isopropylamine glyphosate" OR "81591-81-3" OR "Glyphosate-trimesium" OR 

"Glyphosphate-trimesium" OR "Avans 330" OR "Glyphosate mono(trimethylsulfonium) salt" 

OR "Glyphosate trimethylsulfonium salt" OR "Glyphosate-trimesium" OR "Medallon" OR 

"Ouragan" OR "R 50224" OR "SC 0224" OR "Sulfosate" OR "Sulphosate" OR "Touchdown 

herbicide" OR "Trimethylsulfonium carboxymethylamino-methylphosphonate" OR 

"Trimethylsulfonium glyphosate" OR "Glycine, N-(phosphonomethyl)-, ion(1-), 

trimethylsulfonium" OR "Sulfosate" ) AND (MH ("neoplasms" OR "carcinogenicity tests" OR 

"carcinogens" OR "cell division/drug effects" OR "cell cycle/drug effects" OR "cell line, 

tumor/drug effects" OR "gene expression regulation, neoplastic" OR "neoplasm proteins/drug 

effects" OR "angiogenesis inducing agents" OR "myelodysplastic-myeloproliferative 

diseases") OR AB(cancer* OR carcinog* OR carcinom* OR cocarcinog* OR lymphoma* OR 

neoplas* OR oncogen* OR precancer* OR tumor* OR tumour* ) )

AB ("glyphosate" OR "1071-83-6" OR "(Carboxymethylamino)methylphosphonic acid" OR 

"Carboxymethylaminomethanephosphinic acid" OR "C-K Yuyos FAV" OR "CP 67573" OR 

"Folusen" OR "Forsat" OR "Glialka" OR "Glifoglex" OR "Glifosan 747" OR "gliphosate" OR 

"Gliz" OR "Glyfos" OR "GlyGran" OR "Glyphodin A" OR "Glyphomax" OR "Glyphosate" OR 

"Glyphosphate" OR "Ground Bio" OR "Herbatop" OR "HM 2028" OR "Kickdown" OR 

"Lancer herbicide" OR "MON 2139" OR "MON 3539" OR "MON 6000" OR "N-

(Phosphonomethyl)glycine" OR "N-(phosphonomethyl)-Glycine" OR "NPhosphomethylglycine" OR "N-Phosphonomethylglycine" OR "Phorsat" OR 

"Phosphonomethylglycine" OR "Phosphonomethyliminoacetic acid" OR "Pondmaster" OR 
GLYPHOSATE B-30

APPENDIX C

Table B-4. Database Query Strings Post-Public Comment Searches

Database 

search date Query String

"Rebel Garden" OR "Roundup Max" OR "Safal" OR "Scout herbicide" OR "Silglif" OR 

"yerbimat") AND (MH ("humans" OR "animals" OR "environmental exposure" OR 

"endocrine system" OR "hormones, hormone substitutes, and hormone antagonists" OR 

"endocrine disruptors" OR "Computational biology" OR "Medical Informatics" OR Genomics 

OR Genome OR Proteomics OR Proteome OR Metabolomics OR Metabolome OR Genes 

OR "Gene expression" OR Phenotype OR genetics OR genotype OR Transcriptome OR 

"Systems Biology") OR AB ("toxicity" OR "poisoning" OR "adverse effects" OR 

"pharmacokinetics" OR "metabolism" OR "chemically induced" OR "blood" OR 

"cerebrospinal fluid" OR "urine")) AND MH (("Environmental Exposure" OR "Epidemiological 

Monitoring" OR "Transcription, Genetic " OR "Reverse transcription" OR "Transcriptional 

activation" OR "Transcription factors") OR AB (Analysis OR Biosynthesis)) AND MH ((RNA 

OR DNA OR "RNA, Messenger" OR "RNA, Transfer" OR "peptide biosynthesis" OR 

"protein biosynthesis" OR "Reverse Transcriptase Polymerase Chain Reaction" OR "Base 

Sequence" OR "Trans-activators" OR "Gene Expression Profiling" OR "pharmacology") OR 

AB (cancer OR "1071-83-6" OR "Carboxymethylamino)methylphosphonic acid" OR 

"Carboxymethylaminomethanephosphinic acid" OR "C-K Yuyos FAV" OR "CP 67573" OR 

"Folusen" OR "Forsat" OR "Glialka" OR "Glifoglex" OR "Glifosan 747" OR "gliphosate" OR 

"Gliz" OR "Glyfos" OR "GlyGran" OR "Glyphodin A" OR "Glyphomax" OR "Glyphosate" 

OR "Glyphosphate" OR "Ground Bio" OR "Herbatop" OR "HM 2028" OR "Kickdown" OR 

"Lancer herbicide" OR "MON 2139" OR "MON 3539" OR "MON 6000" OR "N-

(Phosphonomethyl)glycine" OR "N-(phosphonomethyl)-Glycine" OR "NPhosphomethylglycine" OR "N-Phosphonomethylglycine" OR "Phorsat" OR 

"Phosphonomethylglycine" OR "Phosphonomethyliminoacetic acid" OR "Pondmaster" OR 

"Rebel Garden" OR "Roundup Max" OR "Safal" OR "Scout herbicide" OR "Silglif" OR 

"yerbimat"))

AB ("Roundup" ) AND (AB ((monsanto OR "antifungal agents" OR "antifungal" OR "antifungal" OR ("enzyme" AND inhibitor* ) OR "enzyme inhibitors" OR "enzyme inhibitor" OR 

"herbicides" OR "herbicide" OR ("uncoupling" AND agent* ) OR "uncoupling agent" OR 

"uncoupling agents" OR pesticide*) OR MH ("antifungal agents" OR "enzyme inhibitors" OR 

herbicides OR "uncoupling agents" OR pesticides)) (NOT (("glyphosate" OR "1071-83-6" OR 

"(Carboxymethylamino)methylphosphonic acid" OR 

"Carboxymethylaminomethanephosphinic acid" OR "C-K Yuyos FAV" OR "CP 67573" OR 

"Folusen" OR "Forsat" OR "Glialka" OR "Glifoglex" OR "Glifosan 747" OR "gliphosate" OR 

"Gliz" OR "Glyfos" OR "GlyGran" OR "Glyphodin A" OR "Glyphomax" OR "Glyphosate" 

OR "Glyphosphate" OR "Ground Bio" OR "Herbatop" OR "HM 2028" OR "Kickdown" OR 

"Lancer herbicide" OR "MON 2139" OR "MON 3539" OR "MON 6000" OR "N-

(Phosphonomethyl)glycine" OR "N-(phosphonomethyl)-Glycine" OR "NPhosphomethylglycine" OR "N-Phosphonomethylglycine" OR "Phorsat" OR 

"Phosphonomethylglycine" OR "Phosphonomethyliminoacetic acid" OR "Pondmaster" OR 

"Rebel Garden" OR "Roundup Max" OR "Safal" OR "Scout herbicide" OR "Silglif" OR 

"yerbimat" )) AND AB ("toxicity" OR "poisoning" OR "adverse effects" OR "pharmacokinetics" 

OR "metabolism") AND (MH ("humans" OR "animals" OR "environmental exposure" OR 

"endocrine system" OR "hormones, hormone substitutes, and hormone antagonists" OR 

"endocrine disruptors" OR (("Computational biology" OR "Medical Informatics" OR 

Genomics OR Genome OR Proteomics OR Proteome OR Metabolomics OR Metabolome 

OR Genes OR "Gene expression" OR Phenotype OR genetics OR genotype OR 

Transcriptome OR "Transcription, Genetic " OR "Reverse transcription" OR "Transcriptional 

activation" OR "Transcription factors" OR "RNA, Messenger" OR "RNA, Transfer" OR 

"protein biosynthesis" OR "Reverse Transcriptase Polymerase Chain Reaction" OR "Base 

Sequence" OR "Trans-activators" OR "Gene Expression Profiling" OR "pharmacology") OR 

AB ("chemically induced" OR "blood" OR "cerebrospinal fluid" OR "urine" OR cancer OR 

"1071-83-6" OR "(Carboxymethylamino)methylphosphonic acid" OR 
GLYPHOSATE B-31

APPENDIX C

Table B-4. Database Query Strings Post-Public Comment Searches

Database 

search date Query String

"Carboxymethylaminomethanephosphinic acid" OR "C-K Yuyos FAV" OR "CP 67573" OR 

"Folusen" OR "Forsat" OR "Glialka" OR "Glifoglex" OR "Glifosan 747" OR "gliphosate" OR 

"Gliz" OR "Glyfos" OR "GlyGran" OR "Glyphodin A" OR "Glyphomax" OR "Glyphosate" 

OR "Glyphosphate" OR "Ground Bio" OR "Herbatop" OR "HM 2028" OR "Kickdown" OR 

"Lancer herbicide" OR "MON 2139" OR "MON 3539" OR "MON 6000" OR "N-

(Phosphonomethyl)glycine" OR "N-(phosphonomethyl)-Glycine" OR "NPhosphomethylglycine" OR "N-Phosphonomethylglycine" OR "Phorsat" OR 

"Phosphonomethylglycine" OR "Phosphonomethyliminoacetic acid" OR "Pondmaster" OR 

"Rebel Garden" OR "Roundup Max" OR "Safal" OR "Scout herbicide" OR "Silglif" OR 

"yerbimat" OR "peptide biosynthesis") OR (AB("biosynthesis") AND MH(RNA OR DNA )) 

OR MH ("Systems Biology" AND ("Environmental Exposure" OR "Epidemiological 

Monitoring"))

AB ("34494-03-6" OR "MON 0459" OR "40465-66-5" OR "MON 14420" OR "MON 8750" 

OR "Roundup Hi-Load" OR "Roundup PRODry" OR "70393-85-0" OR "MON 8000" OR 

"Monsanto 8000" OR "Polado" OR "Trisodium hydrogen bis(N-

(phosphonatomethyl)aminoacetate") AND AB ("toxicity" OR "poisoning" OR "adverse effects" 

OR "pharmacokinetics" OR "metabolism") AND (AB ("chemically induced" OR "blood" OR 

"cerebrospinal fluid" OR "urine") OR MH ("humans" OR "animals" OR "environmental 

exposure" OR "endocrine system" OR "hormones, hormone substitutes, and hormone 

antagonists" OR "endocrine disruptors" OR "Computational biology" OR "Medical 

Informatics" OR Genomics OR Genome OR Proteomics OR Proteome OR Metabolomics 

OR Metabolome OR Genes OR "Gene expression" OR Phenotype OR genetics OR 

genotype OR Transcriptome OR "Systems Biology")) AND MH (("Environmental Exposure" 

OR "Epidemiological Monitoring" OR analysis )) OR "Transcription, Genetic " OR "Reverse 

transcription" OR "Transcriptional activation" OR "Transcription factors" OR ("biosynthesis" 

AND (RNA OR DNA )) OR "RNA, Messenger" OR "RNA, Transfer" OR "peptide 

biosynthesis" OR "protein biosynthesis" OR "Reverse Transcriptase Polymerase Chain 

Reaction" OR "Base Sequence" OR "Trans-activators" OR "Gene Expression Profiling" OR 

"pharmacology") OR AB (cancer))

("39600-42-5" OR "Glyphosate potassium" OR "Glyphosate monopotassium salt" OR 

"Glyphosate potassium" OR "Glyphosate-potassium" OR "Monopotassium glyphosate" OR 

"Roundup Attack" OR "Roundup Energy" OR "Roundup Maxload" OR "Roundup Original 

Max" OR "Roundup Power Max" OR "Roundup Ultramax II" OR "Roundup Weathermax" 

OR "Touchdown Forte HiTech" OR "Transorb R" OR "Weathermax" OR "Zapp Qi" OR 

"70901-12-1" OR "Glyphosate-potassium" OR "Potassium glyphosate" OR "Potassium N-

(phosphonomethyl)glycine" OR "Uragan Forte" OR "VisionMAX" OR "N-

(phosphonomethyl)glycine potassium salt" OR "114370-14-8" OR "Glyphosate ammonium" 

OR "N-(phosphonomethyl)glycine ammonium salt" OR "69254-40-6" OR "Glyphosatediammonium" OR "Diammonium N-(phosphonomethyl)glycine" OR "N-

(phosphonomethyl)glycine diammonium salt" ) NOT (("glyphosate" ) OR (("1071-83-6" OR 

"(Carboxymethylamino)methylphosphonic acid" OR 

"Carboxymethylaminomethanephosphinic acid" OR "C-K Yuyos FAV" OR "CP 67573" OR 

"Folusen" OR "Forsat" OR "Glialka" OR "Glifoglex" OR "Glifosan 747" OR "gliphosate" OR 

"Gliz" OR "Glyfos" OR "GlyGran" OR "Glyphodin A" OR "Glyphomax" OR "Glyphosate" 

OR "Glyphosphate" OR "Ground Bio" OR "Herbatop" OR "HM 2028" OR "Kickdown" OR 

"Lancer herbicide" OR "MON 2139" OR "MON 3539" OR "MON 6000" OR "N-

(Phosphonomethyl)glycine" OR "N-(phosphonomethyl)-Glycine" OR "NPhosphomethylglycine" OR "N-Phosphonomethylglycine" OR "Phorsat" OR 

"Phosphonomethylglycine" OR "Phosphonomethyliminoacetic acid" OR "Pondmaster" OR 

"Rebel Garden" OR "Roundup Max" OR "Safal" OR "Scout herbicide" OR "Silglif" OR 

"yerbimat") AND AB ("toxicity" OR "poisoning" OR "adverse effects" OR "pharmacokinetics" 

OR "metabolism") AND MH (("humans" OR "animals" OR "environmental exposure" OR 
GLYPHOSATE B-32

APPENDIX C

Table B-4. Database Query Strings Post-Public Comment Searches

Database 

search date Query String

"endocrine system" OR "hormones, hormone substitutes, and hormone antagonists" OR 

"endocrine disruptors" OR (("Computational biology" OR "Medical Informatics" OR 

Genomics OR Genome OR Proteomics OR Proteome OR Metabolomics OR Metabolome 

OR Genes OR "Gene expression" OR Phenotype OR genetics OR genotype OR 

Transcriptome OR ("Systems Biology" OR (AB ("chemically induced" OR "blood" OR 

"cerebrospinal fluid" OR "urine")) AND MH("Environmental Exposure" OR "Epidemiological 

Monitoring" OR analysis )) OR "Transcription, Genetic " OR "Reverse transcription" OR 

"Transcriptional activation" OR "Transcription factors") OR AB ("biosynthesis")) AND (RNA 

OR DNA OR "RNA, Messenger" OR "RNA, Transfer" OR "peptide biosynthesis" OR "protein 

biosynthesis" OR "Reverse Transcriptase Polymerase Chain Reaction" OR "Base 

Sequence" OR "Trans-activators" OR "Gene Expression Profiling" OR "pharmacology" OR 

"antifungal agents"[Pharmacological Action] OR "antifungal agents"[ Terms] OR "antifungal" 

OR "anti-fungal" OR "enzyme inhibitors" OR AB (cancer OR "1071-83-6" OR 

"(Carboxymethylamino)methylphosphonic acid" OR 

"Carboxymethylaminomethanephosphinic acid" OR "C-K Yuyos FAV" OR "CP 67573" OR 

"Folusen" OR "Forsat" OR "Glialka" OR "Glifoglex" OR "Glifosan 747" OR "gliphosate" OR 

"Gliz" OR "Glyfos" OR "GlyGran" OR "Glyphodin A" OR "Glyphomax" OR "Glyphosate" 

OR "Glyphosphate" OR "Ground Bio" OR "Herbatop" OR "HM 2028" OR "Kickdown" OR 

"Lancer herbicide" OR "MON 2139" OR "MON 3539" OR "MON 6000" OR "N-

(Phosphonomethyl)glycine" OR "N-(phosphonomethyl)-Glycine" OR "NPhosphomethylglycine" OR "N-Phosphonomethylglycine" OR "Phorsat" OR 

"Phosphonomethylglycine" OR "Phosphonomethyliminoacetic acid" OR "Pondmaster" OR 

"Rebel Garden" OR "Roundup Max" OR "Safal" OR "Scout herbicide" OR "Silglif" OR 

"yerbimat" OR "Roundup") AND AB (monsanto OR "enzyme") AND AB ((inhibitor* OR 

"enzyme inhibitors" OR "enzyme inhibitor" OR "herbicides" OR "herbicide" OR "uncoupling 

agents" OR "uncoupling") OR MH (herbicides OR "uncoupling agents")) AND AB (agent* OR 

"uncoupling agent" OR "uncoupling agents" OR Pesticide*) OR MH (Pesticides)

(TX ("glyphosate, isopropyl amine salt" OR "N-(phosphonomethyl)glycine trimethylsulfonium 

salt”) ) NOT TX ("glyphosate") OR ( TX ("1071-83-6"OR 

"(Carboxymethylamino)methylphosphonic acid" OR "Carboxymethylaminomethanephosphinic 

acid”OR "C-K Yuyos FAV" OR "CP 67573” OR "Folusen" OR "Forsat" OR "Glialka" OR 

"Glifoglex" OR "Glifosan 747" OR "gliphosate" OR "Gliz" OR "Glyfos" OR "GlyGran" OR 

"Glyphodin A" OR "Glyphomax" OR "Glyphosate" OR "Glyphosphate" OR "Ground Bio" OR 

"Herbatop" OR "HM 2028" OR "Kickdown" OR "Lancer herbicide" OR "MON 2139" “MON 

3539" OR "MON 6000" OR "N-(Phosphonomethyl)glycine" OR "N-(phosphonomethyl)-

Glycine" OR "N-Phosphomethylglycine" OR "N-Phosphonomethylglycine” OR "Phorsat" OR 

"Phosphonomethylglycine" OR "Phosphonomethyliminoacetic acid" OR "Pondmaster" OR 

"Rebel Garden"OR "Roundup Max" OR "Safal" OR "Scout herbicide" OR "Silglif" OR 

"yerbimat") ) AND ( MH ("humans" OR "animals") OR MH ("environmental exposure" OR 

"endocrine system" OR "hormones, hormone substitutes, and hormone antagonists" OR 

"endocrine disruptors") OR MH ("Computational biology" OR "Medical Informatics" OR 

Genomics OR Genome OR Proteomics OR Proteome OR Metabolomics OR Metabolome OR 

Genes OR "Gene expression" OR Phenotype OR genetics OR genotype OR Transcriptome 

OR "Transcription, Genetic " OR "Reverse transcription" OR "Transcriptional activation" OR 

"Transcription factors" OR "RNA, Messenger" OR "RNA, Transfer" OR "peptide biosynthesis" 

OR "protein biosynthesis" OR "Reverse Transcriptase Polymerase Chain Reaction" OR "Base 

Sequence" OR "Trans-activators" OR "Gene Expression Profiling") OR MH ("Systems 

Biology") ) AND ( MH ("Environmental Exposure" OR "Epidemiological Monitoring") OR MW 

(analysis) OR MW ("biosynthesis") ) AND ( MH (RNA OR DNA) OR AB (cancer) OR MM 

("pharmacology") ) AND ( MH ("humans" OR "animals") OR MH ("environmental exposure" 

OR "endocrine system" OR "hormones, hormone substitutes, and hormone antagonists" OR 

"endocrine disruptors" OR (("Computational biology" OR "Medical Informatics" OR Genomics 
GLYPHOSATE B-33

APPENDIX C

Table B-4. Database Query Strings Post-Public Comment Searches

Database 

search date Query String

OR Genome OR Proteomics OR Proteome OR Metabolomics OR Metabolome OR Genes OR 

"Gene expression" OR Phenotype OR genetics OR genotype OR Transcriptome OR 

("Systems Biology" AND ("Environmental Exposure" OR "Epidemiological Monitoring") OR 

MW (analysis) OR MH ("Transcription, Genetic" OR "Reverse transcription" OR 

"Transcriptional activation" OR "Transcription factors") OR MW ("biosynthesis") ) AND ( MH 

((RNA OR DNA) OR "RNA, Messenger" OR "RNA, Transfer" OR "peptide biosynthesis" OR 

"protein biosynthesis" OR "Reverse Transcriptase Polymerase Chain Reaction" OR "Base 

Sequence" OR "Trans-activators" OR "Gene Expression Profiling") OR AB (cancer) OR MM 

("pharmacology") OR TX (("1071-83-6" OR "(Carboxymethylamino)methylphosphonic acid" 

OR "Carboxymethylaminomethanephosphinic acid" OR "C-K Yuyos FAV" OR "CP 67573" OR 

"Folusen" OR "Forsat" OR "Glialka" OR "Glifoglex" OR "Glifosan 747" OR "gliphosate" OR

"Gliz" OR "Glyfos" OR "GlyGran" OR "Glyphodin A" OR "Glyphomax" OR "Glyphosate" OR 

"Glyphosphate" OR "Ground Bio" OR "Herbatop" OR "HM 2028" OR "Kickdown" OR "Lancer 

herbicide" OR "MON 2139" OR "MON 3539" OR "MON 6000" OR "N-

(Phosphonomethyl)glycine" OR "N-(phosphonomethyl)-Glycine" OR "NPhosphomethylglycine" OR "N-Phosphonomethylglycine" OR "Phorsat" OR 

"Phosphonomethylglycine" OR "Phosphonomethyliminoacetic acid" OR "Pondmaster" OR 

"Rebel Garden" OR "Roundup Max" OR "Safal" OR "Scout herbicide" OR "Silglif" OR 

"yerbimat") OR TX ("Roundup" AND (Monsanto)) OR MH ("antifungal agents")OR TX 

("antifungal" OR "anti-fungal") OR MH ("enzyme inhibitors") OR TX ("enzyme" AND inhibitor*) 

OR TX ("enzyme inhibitors" OR "enzyme inhibitor")OR MH ("herbicides") OR TX ("herbicides" 

OR "herbicide") OR MH ("uncoupling agents”) OR TX ("uncoupling" AND agent*) OR TX 

("uncoupling agent" OR "uncoupling agents") OR MH ("pesticides" OR pesticide*) )

SciFinder

9/2019

Substance Identifier "1071-83-6; 38641-94-0; Glyphos...">substances (27)>get references 

(19597)>refine "2017-2019" (2591)>refine "Clinical Trial Dissertation Jo..." (1111)>remove 

198 references (913)

The results of the 2019 updated literature review were: 

• Number of records identified (after duplicate removal): 2,636

• Number of records identified from government websites: 0

• Total number of records to undergo literature screening: 2,636

B.1.2 Literature Screening 

A two-step process was used to screen the literature search to identify relevant studies on glyphosate: 

• Title and abstract screen

• Full text screen

Title and Abstract Screen. Within the reference library, titles and abstracts were screened manually for 

relevance. Studies that were considered relevant (see Table B-1 for inclusion criteria) were moved to the 

second step of the literature screening process. Studies were excluded when the title and/or abstract 

clearly indicated that the study was not relevant to the toxicological profile. 

2015/2017 literature review:

• Number of titles and abstracts screened: 5,803

• Number of studies considered relevant and moved to the next step: 628
GLYPHOSATE B-34

APPENDIX C

2019 literature review

• Number of titles and abstracts screened: 2,636

• Number of studies considered relevant and moved to the next step: 135

Full Text Screen. The second step in the literature screening process was a full text review of individual 

studies considered relevant in the title and abstract screen step. Each study was reviewed to determine 

whether it was relevant for inclusion in the toxicological profile. 

2015/2017 literature review: 

• Number of studies undergoing full text review: 628

• Total number of studies cited in the profile: 329

2019 literature review:

• Number of studies undergoing full text review: 135

• Total number of studies cited in the profile: 60

A summary of the results of the literature search and screening is presented in Figure B- and Figure B-2.. 
GLYPHOSATE B-35

APPENDIX C

Figure B-1. February 2015 and September 2017 Literature Search Results and 

Screen for Glyphosate
GLYPHOSATE B-36

APPENDIX C

Figure B-2. September 2019 Supplemental Literature Search Results and Screen 

for Glyphosate

Number of records identified via database searches

(see Table B-4)

MEDLINE IPA PubMed Science Direct SciFinder TOXLINE BIOSIS 

 20 6 889 205 913 6 1,204 

n=2,636 (after duplicates removed) Literature Search Title/Abstract Screen Full-Text Screen

Number of Records Screened: 2,636

Number of Articles Screened: 135

Number of Records Excluded as Not Relevant: 3,342

Number of Studies for Qualitative Review: 89

Number of articles excluded for Criteria: 46
GLYPHOSATE C-1

APPENDIX C. USER'S GUIDE

Chapter 1. Relevance to Public Health

This chapter provides an overview of U.S. exposures, a summary of health effects based on evaluations of 

existing toxicologic, epidemiologic, and toxicokinetic information, and an overview of the minimal risk 

levels. This is designed to present interpretive, weight-of-evidence discussions for human health 

endpoints by addressing the following questions:

1. What effects are known to occur in humans?

2. What effects observed in animals are likely to be of concern to humans?

3. What exposure conditions are likely to be of concern to humans, especially around hazardous 

waste sites?

Minimal Risk Levels (MRLs)

Where sufficient toxicologic information is available, ATSDR derives MRLs for inhalation and oral 

routes of entry at each duration of exposure (acute, intermediate, and chronic). These MRLs are not 

meant to support regulatory action, but to acquaint health professionals with exposure levels at which 

adverse health effects are not expected to occur in humans.

MRLs should help physicians and public health officials determine the safety of a community living near 

a hazardous substance emission, given the concentration of a contaminant in air or the estimated daily 

dose in water. MRLs are based largely on toxicological studies in animals and on reports of human 

occupational exposure.

MRL users should be familiar with the toxicologic information on which the number is based. 

Section 1.2, Summary of Health Effects, contains basic information known about the substance. Other 

sections, such as Section 3.2 Children and Other Populations that are Unusually Susceptible and 

Section 3.4 Interactions with Other Substances, provide important supplemental information.

MRL users should also understand the MRL derivation methodology. MRLs are derived using a 

modified version of the risk assessment methodology that the Environmental Protection Agency (EPA) 

provides (Barnes and Dourson 1988) to determine reference doses (RfDs) for lifetime exposure. 

To derive an MRL, ATSDR generally selects the most sensitive endpoint which, in its best judgement, 

represents the most sensitive human health effect for a given exposure route and duration. ATSDR 

cannot make this judgement or derive an MRL unless information (quantitative or qualitative) is available 

for all potential systemic, neurological, and developmental effects. If this information and reliable 

quantitative data on the chosen endpoint are available, ATSDR derives an MRL using the most sensitive 

species (when information from multiple species is available) with the highest no-observed-adverse-effect 

level (NOAEL) that does not exceed any adverse effect levels. When a NOAEL is not available, a 

lowest-observed-adverse-effect level (LOAEL) can be used to derive an MRL, and an uncertainty factor 

of 10 must be employed. Additional uncertainty factors of 10 must be used both for human variability to 

protect sensitive subpopulations (people who are most susceptible to the health effects caused by the 

substance) and for interspecies variability (extrapolation from animals to humans). In deriving an MRL, 
GLYPHOSATE B-2

APPENDIX C

these individual uncertainty factors are multiplied together. The product is then divided into the 

inhalation concentration or oral dosage selected from the study. Uncertainty factors used in developing a 

substance-specific MRL are provided in the footnotes of the levels of significant exposure (LSE) tables 

that are provided in Chapter 2. Detailed discussions of the MRLs are presented in Appendix A.

Chapter 2. Health Effects

Tables and Figures for Levels of Significant Exposure (LSE)

Tables and figures are used to summarize health effects and illustrate graphically levels of exposure 

associated with those effects. These levels cover health effects observed at increasing dose 

concentrations and durations, differences in response by species and MRLs to humans for noncancer 

endpoints. The LSE tables and figures can be used for a quick review of the health effects and to locate 

data for a specific exposure scenario. The LSE tables and figures should always be used in conjunction 

with the text. All entries in these tables and figures represent studies that provide reliable, quantitative 

estimates of NOAELs, LOAELs, or Cancer Effect Levels (CELs).

The legends presented below demonstrate the application of these tables and figures. Representative 

examples of LSE tables and figures follow. The numbers in the left column of the legends correspond to 

the numbers in the example table and figure.

TABLE LEGEND

See Sample LSE Table (page C-5)

(1) Route of exposure. One of the first considerations when reviewing the toxicity of a substance 

using these tables and figures should be the relevant and appropriate route of exposure. 

Typically, when sufficient data exist, three LSE tables and two LSE figures are presented in the 

document. The three LSE tables present data on the three principal routes of exposure 

(i.e., inhalation, oral, and dermal). LSE figures are limited to the inhalation and oral routes. Not 

all substances will have data on each route of exposure and will not, therefore, have all five of the 

tables and figures. Profiles with more than one chemical may have more LSE tables and figures.

(2) Exposure period. Three exposure periods—acute (<15 days), intermediate (15–364 days), and 

chronic (≥365 days)—are presented within each relevant route of exposure. In this example, two 

oral studies of chronic-duration exposure are reported. For quick reference to health effects

occurring from a known length of exposure, locate the applicable exposure period within the LSE 

table and figure.

(3) Figure key. Each key number in the LSE table links study information to one or more data points 

using the same key number in the corresponding LSE figure. In this example, the study 

represented by key number 51 identified NOAELs and less serious LOAELs (also see the three 

"51R" data points in sample LSE Figure 2-X).

(4) Species (strain) No./group. The test species (and strain), whether animal or human, are identified 

in this column. The column also contains information on the number of subjects and sex per 

group. Chapter 1, Relevance to Public Health, covers the relevance of animal data to human 

toxicity and Section 3.1, Toxicokinetics, contains any available information on comparative 

toxicokinetics. Although NOAELs and LOAELs are species specific, the levels are extrapolated 

to equivalent human doses to derive an MRL.
GLYPHOSATE B-3

APPENDIX C

(5) Exposure parameters/doses. The duration of the study and exposure regimens are provided in 

these columns. This permits comparison of NOAELs and LOAELs from different studies. In 

this case (key number 51), rats were orally exposed to “Chemical X” via feed for 2 years. For a 

more complete review of the dosing regimen, refer to the appropriate sections of the text or the 

original reference paper (i.e., Aida et al. 1992).

(6) Parameters monitored. This column lists the parameters used to assess health effects. Parameters 

monitored could include serum (blood) chemistry (BC), behavioral (BH), biochemical changes 

(BI), body weight (BW), clinical signs (CS), developmental toxicity (DX), enzyme activity (EA), 

food intake (FI), fetal toxicity (FX), gross necropsy (GN), hematology (HE), histopathology 

(HP), lethality (LE), maternal toxicity (MX), organ function (OF), ophthalmology (OP), organ 

weight (OW), teratogenicity (TG), urinalysis (UR), and water intake (WI).

(7) Endpoint. This column lists the endpoint examined. The major categories of health endpoints 

included in LSE tables and figures are death, body weight, respiratory, cardiovascular, 

gastrointestinal, hematological, musculoskeletal, hepatic, renal, dermal, ocular, endocrine, 

immunological, neurological, reproductive, developmental, other noncancer, and cancer. "Other 

noncancer" refers to any effect (e.g., alterations in blood glucose levels) not covered in these 

systems. In the example of key number 51, three endpoints (body weight, hematological, and 

hepatic) were investigated.

(8) NOAEL. A NOAEL is the highest exposure level at which no adverse effects were seen in the 

organ system studied. The body weight effect reported in key number 51 is a NOAEL at 

25.5 mg/kg/day. NOAELs are not reported for cancer and death; with the exception of these two 

endpoints, this field is left blank if no NOAEL was identified in the study.

(9) LOAEL. A LOAEL is the lowest dose used in the study that caused an adverse health effect. 

LOAELs have been classified into "Less Serious" and "Serious" effects. These distinctions help 

readers identify the levels of exposure at which adverse health effects first appear and the 

gradation of effects with increasing dose. A brief description of the specific endpoint used to 

quantify the adverse effect accompanies the LOAEL. Key number 51 reports a less serious 

LOAEL of 6.1 mg/kg/day for the hepatic system, which was used to derive a chronic exposure, 

oral MRL of 0.008 mg/kg/day (see footnote "c"). MRLs are not derived from serious LOAELs. 

A cancer effect level (CEL) is the lowest exposure level associated with the onset of 

carcinogenesis in experimental or epidemiologic studies. CELs are always considered serious

effects. The LSE tables and figures do not contain NOAELs for cancer, but the text may report 

doses not causing measurable cancer increases. If no LOAEL/CEL values were identified in the 

study, this field is left blank.

(10) Reference. The complete reference citation is provided in Chapter 8 of the profile.

(11) Footnotes. Explanations of abbreviations or reference notes for data in the LSE tables are found 

in the footnotes. For example, footnote "c" indicates that the LOAEL of 6.1 mg/kg/day in key

number 51 was used to derive an oral MRL of 0.008 mg/kg/day.
GLYPHOSATE B-4

APPENDIX C

FIGURE LEGEND

See Sample LSE Figure (page C-6)

LSE figures graphically illustrate the data presented in the corresponding LSE tables. Figures help the 

reader quickly compare health effects according to exposure concentrations for particular exposure 

periods.

(13) Exposure period. The same exposure periods appear as in the LSE table. In this example, health 

effects observed within the chronic exposure period are illustrated.

(14) Endpoint. These are the categories of health effects for which reliable quantitative data exist. 

The same health effect endpoints appear in the LSE table.

(15) Levels of exposure. Concentrations or doses for each health effect in the LSE tables are 

graphically displayed in the LSE figures. Exposure concentration or dose is measured on the log 

scale "y" axis. Inhalation exposure is reported in mg/m3 or ppm and oral exposure is reported in 

mg/kg/day.

(16) LOAEL. In this example, the half-shaded circle that is designated 51R identifies a LOAEL 

critical endpoint in the rat upon which a chronic oral exposure MRL is based. The key number 

51 corresponds to the entry in the LSE table. The dashed descending arrow indicates the 

extrapolation from the exposure level of 6.1 mg/kg/day (see entry 51 in the sample LSE table) to 

the MRL of 0.008 mg/kg/day (see footnote "c" in the sample LSE table).

(17) CEL. Key number 59R is one of studies for which CELs were derived. The diamond symbol 

refers to a CEL for the test species (rat). The number 59 corresponds to the entry in the LSE 

table.

(18) Key to LSE figure. The key provides the abbreviations and symbols used in the figure.
GLYPHOSATE

C-5

APPENDIX C
GLYPHOSATE

C-6

APPENDIX C
GLYPHOSATE D-1

APPENDIX D. QUICK REFERENCE FOR HEALTH CARE PROVIDERS 

Toxicological Profiles are a unique compilation of toxicological information on a given hazardous 

substance. Each profile reflects a comprehensive and extensive evaluation, summary, and interpretation 

of available toxicologic and epidemiologic information on a substance. Health care providers treating 

patients potentially exposed to hazardous substances may find the following information helpful for fast 

answers to often-asked questions.

Primary Chapters/Sections of Interest

Chapter 1: Relevance to Public Health: The Relevance to Public Health Section provides an overview 

of exposure and health effects and evaluates, interprets, and assesses the significance of toxicity 

data to human health. A table listing minimal risk levels (MRLs) is also included in this chapter.

Chapter 2: Health Effects: Specific health effects identified in both human and animal studies are 

reported by type of health effect (e.g., death, hepatic, renal, immune, reproductive), route of 

exposure (e.g., inhalation, oral, dermal), and length of exposure (e.g., acute, intermediate, and 

chronic). 

NOTE: Not all health effects reported in this section are necessarily observed in the clinical 

setting. 

Pediatrics: 

Section 3.2 Children and Other Populations that are Unusually Susceptible

Section 3.3 Biomarkers of Exposure and Effect

ATSDR Information Center 

Phone: 1-800-CDC-INFO (800-232-4636) or 1-888-232-6348 (TTY) 

Internet: http://www.atsdr.cdc.gov

The following additional materials are available online:

Case Studies in Environmental Medicine are self-instructional publications designed to increase primary 

health care providers’ knowledge of a hazardous substance in the environment and to aid in the 

evaluation of potentially exposed patients (see https://www.atsdr.cdc.gov/csem/csem.html). 

Managing Hazardous Materials Incidents is a three-volume set of recommendations for on-scene 

(prehospital) and hospital medical management of patients exposed during a hazardous materials 

incident (see https://www.atsdr.cdc.gov/MHMI/index.asp). Volumes I and II are planning guides 

to assist first responders and hospital emergency department personnel in planning for incidents 

that involve hazardous materials. Volume III—Medical Management Guidelines for Acute 

Chemical Exposures—is a guide for health care professionals treating patients exposed to 

hazardous materials.

Fact Sheets (ToxFAQsTM) provide answers to frequently asked questions about toxic substances (see 

https://www.atsdr.cdc.gov/toxfaqs/Index.asp).
GLYPHOSATE D-2

APPENDIX D

Other Agencies and Organizations

The National Center for Environmental Health (NCEH) focuses on preventing or controlling disease, 

injury, and disability related to the interactions between people and their environment outside the 

workplace. Contact: NCEH, Mailstop F-29, 4770 Buford Highway, NE, Atlanta, GA 

30341-3724 • Phone: 770-488-7000 • FAX: 770-488-7015 • Web Page: 

https://www.cdc.gov/nceh/.

The National Institute for Occupational Safety and Health (NIOSH) conducts research on occupational 

diseases and injuries, responds to requests for assistance by investigating problems of health and 

safety in the workplace, recommends standards to the Occupational Safety and Health 

Administration (OSHA) and the Mine Safety and Health Administration (MSHA), and trains 

professionals in occupational safety and health. Contact: NIOSH, 395 E Street, S.W., Suite 9200, 

Patriots Plaza Building, Washington, DC 20201 • Phone: 202-245-0625 or 1-800-CDC-INFO 

(800-232-4636) • Web Page: https://www.cdc.gov/niosh/.

The National Institute of Environmental Health Sciences (NIEHS) is the principal federal agency for 

biomedical research on the effects of chemical, physical, and biologic environmental agents on 

human health and well-being. Contact: NIEHS, PO Box 12233, 104 T.W. Alexander Drive, 

Research Triangle Park, NC 27709 • Phone: 919-541-3212 • Web Page: 

https://www.niehs.nih.gov/.

Clinical Resources (Publicly Available Information)

The Association of Occupational and Environmental Clinics (AOEC) has developed a network of clinics 

in the United States to provide expertise in occupational and environmental issues. Contact: 

AOEC, 1010 Vermont Avenue, NW, #513, Washington, DC 20005 • Phone: 202-347-4976 

• FAX: 202-347-4950 • e-mail: AOEC@AOEC.ORG • Web Page: http://www.aoec.org/.

The American College of Occupational and Environmental Medicine (ACOEM) is an association of 

physicians and other health care providers specializing in the field of occupational and 

environmental medicine. Contact: ACOEM, 25 Northwest Point Boulevard, Suite 700, Elk 

Grove Village, IL 60007-1030 • Phone: 847-818-1800 • FAX: 847-818-9266 • Web Page: 

http://www.acoem.org/.

The American College of Medical Toxicology (ACMT) is a nonprofit association of physicians with 

recognized expertise in medical toxicology. Contact: ACMT, 10645 North Tatum Boulevard, 

Suite 200-111, Phoenix AZ 85028 • Phone: 844-226-8333 • FAX: 844-226-8333 • Web Page: 

http://www.acmt.net.

The Pediatric Environmental Health Specialty Units (PEHSUs) is an interconnected system of specialists 

who respond to questions from public health professionals, clinicians, policy makers, and the 

public about the impact of environmental factors on the health of children and reproductive-aged 

adults. Contact information for regional centers can be found at http://pehsu.net/findhelp.html.

The American Association of Poison Control Centers (AAPCC) provide support on the prevention and 

treatment of poison exposures. Contact: AAPCC, 515 King Street, Suite 510, Alexandria VA 

22314 • Phone: 701-894-1858 • Poison Help Line: 1-800-222-1222 • Web Page: 

http://www.aapcc.org/.
GLYPHOSATE E-1

APPENDIX E. GLOSSARY

Absorption—The process by which a substance crosses biological membranes and enters systemic 

circulation. Absorption can also refer to the taking up of liquids by solids, or of gases by solids or liquids.

Acute Exposure—Exposure to a chemical for a duration of ≤14 days, as specified in the Toxicological 

Profiles.

Adsorption—The adhesion in an extremely thin layer of molecules (as of gases, solutes, or liquids) to the 

surfaces of solid bodies or liquids with which they are in contact.

Adsorption Coefficient (Koc)—The ratio of the amount of a chemical adsorbed per unit weight of 

organic carbon in the soil or sediment to the concentration of the chemical in solution at equilibrium.

Adsorption Ratio (Kd)—The amount of a chemical adsorbed by sediment or soil (i.e., the solid phase) 

divided by the amount of chemical in the solution phase, which is in equilibrium with the solid phase, at a 

fixed solid/solution ratio. It is generally expressed in micrograms of chemical sorbed per gram of soil or 

sediment.

Benchmark Dose (BMD) or Benchmark Concentration (BMC)—is the dose/concentration 

corresponding to a specific response level estimate using a statistical dose-response model applied to 

either experimental toxicology or epidemiology data. For example, a BMD10 would be the dose 

corresponding to a 10% benchmark response (BMR). The BMD is determined by modeling the doseresponse curve in the region of the dose-response relationship where biologically observable data are 

feasible. The BMDL or BMCL is the 95% lower confidence limit on the BMD or BMC. 

Bioconcentration Factor (BCF)—The quotient of the concentration of a chemical in aquatic organisms 

at a specific time or during a discrete time period of exposure divided by the concentration in the 

surrounding water at the same time or during the same period.

Biomarkers—Indicators signaling events in biologic systems or samples, typically classified as markers 

of exposure, effect, and susceptibility.

Cancer Effect Level (CEL)—The lowest dose of a chemical in a study, or group of studies, that 

produces significant increases in the incidence of cancer (or tumors) between the exposed population and 

its appropriate control.

Carcinogen—A chemical capable of inducing cancer.

Case-Control Study—A type of epidemiological study that examines the relationship between a 

particular outcome (disease or condition) and a variety of potential causative agents (such as toxic 

chemicals). In a case-control study, a group of people with a specified and well-defined outcome is 

identified and compared to a similar group of people without the outcome.

Case Report—A report that describes a single individual with a particular disease or exposure. These 

reports may suggest some potential topics for scientific research, but are not actual research studies.
GLYPHOSATE E-2

APPENDIX E

Case Series—Reports that describe the experience of a small number of individuals with the same 

disease or exposure. These reports may suggest potential topics for scientific research, but are not actual 

research studies.

Ceiling Value—A concentration that must not be exceeded. 

Chronic Exposure—Exposure to a chemical for ≥365 days, as specified in the Toxicological Profiles.

Clastogen—A substance that causes breaks in chromosomes resulting in addition, deletion, or 

rearrangement of parts of the chromosome.

Cohort Study—A type of epidemiological study of a specific group or groups of people who have had a 

common insult (e.g., exposure to an agent suspected of causing disease or a common disease) and are 

followed forward from exposure to outcome, and who are disease-free at start of follow-up. Often, at 

least one exposed group is compared to one unexposed group, while in other cohorts, exposure is a 

continuous variable and analyses are directed towards analyzing an exposure-response coefficient.

Cross-sectional Study—A type of epidemiological study of a group or groups of people that examines 

the relationship between exposure and outcome to a chemical or to chemicals at a specific point in time.

Data Needs—Substance-specific informational needs that, if met, would reduce the uncertainties of 

human health risk assessment.

Developmental Toxicity—The occurrence of adverse effects on the developing organism that may result 

from exposure to a chemical prior to conception (either parent), during prenatal development, or 

postnatally to the time of sexual maturation. Adverse developmental effects may be detected at any point 

in the life span of the organism.

Dose-Response Relationship—The quantitative relationship between the amount of exposure to a 

toxicant and the incidence of the response or amount of the response.

Embryotoxicity and Fetotoxicity—Any toxic effect on the conceptus as a result of prenatal exposure to 

a chemical; the distinguishing feature between the two terms is the stage of development during which the 

effect occurs. Effects include malformations and variations, altered growth, and in utero death.

Epidemiology—The investigation of factors that determine the frequency and distribution of disease or 

other health-related conditions within a defined human population during a specified period. 

Excretion—The process by which metabolic waste products are removed from the body. 

Genotoxicity—A specific adverse effect on the genome of living cells that, upon the duplication of 

affected cells, can be expressed as a mutagenic, clastogenic, or carcinogenic event because of specific 

alteration of the molecular structure of the genome.

Half-life—A measure of rate for the time required to eliminate one-half of a quantity of a chemical from 

the body or environmental media.

Health Advisory—An estimate of acceptable drinking water levels for a chemical substance derived by 

EPA and based on health effects information. A health advisory is not a legally enforceable federal 

standard, but serves as technical guidance to assist federal, state, and local officials.
GLYPHOSATE E-3

APPENDIX E

Immediately Dangerous to Life or Health (IDLH)—A condition that poses a threat of life or health, or 

conditions that pose an immediate threat of severe exposure to contaminants that are likely to have 

adverse cumulative or delayed effects on health.

Immunotoxicity—Adverse effect on the functioning of the immune system that may result from 

exposure to chemical substances. 

Incidence—The ratio of new cases of individuals in a population who develop a specified condition to 

the total number of individuals in that population who could have developed that condition in a specified 

time period. 

Intermediate Exposure—Exposure to a chemical for a duration of 15–364 days, as specified in the 

Toxicological Profiles.

In Vitro—Isolated from the living organism and artificially maintained, as in a test tube.

In Vivo—Occurring within the living organism.

Lethal Concentration(LO) (LCLO)—The lowest concentration of a chemical in air that has been reported 

to have caused death in humans or animals.

Lethal Concentration(50) (LC50)—A calculated concentration of a chemical in air to which exposure for 

a specific length of time is expected to cause death in 50% of a defined experimental animal population.

Lethal Dose(LO) (LDLo)—The lowest dose of a chemical introduced by a route other than inhalation that 

has been reported to have caused death in humans or animals.

Lethal Dose(50) (LD50)—The dose of a chemical that has been calculated to cause death in 50% of a 

defined experimental animal population.

Lethal Time(50) (LT50)—A calculated period of time within which a specific concentration of a chemical 

is expected to cause death in 50% of a defined experimental animal population.

Lowest-Observed-Adverse-Effect Level (LOAEL)—The lowest exposure level of chemical in a study, 

or group of studies, that produces statistically or biologically significant increases in frequency or severity 

of adverse effects between the exposed population and its appropriate control.

Lymphoreticular Effects—Represent morphological effects involving lymphatic tissues such as the 

lymph nodes, spleen, and thymus.

Malformations—Permanent structural changes that may adversely affect survival, development, or 

function.

Metabolism—Process in which chemical substances are biotransformed in the body that could result in 

less toxic and/or readily excreted compounds or produce a biologically active intermediate.

Minimal Risk Level (MRL)—An estimate of daily human exposure to a hazardous substance that is 

likely to be without an appreciable risk of adverse noncancer health effects over a specified route and 

duration of exposure.
GLYPHOSATE E-4

APPENDIX E

Modifying Factor (MF)—A value (greater than zero) that is applied to the derivation of a Minimal Risk 

Level (MRL) to reflect additional concerns about the database that are not covered by the uncertainty 

factors. The default value for a MF is 1.

Morbidity—The state of being diseased; the morbidity rate is the incidence or prevalence of a disease in 

a specific population.

Mortality—Death; the mortality rate is a measure of the number of deaths in a population during a 

specified interval of time.

Mutagen—A substance that causes mutations, which are changes in the DNA sequence of a cell’s DNA. 

Mutations can lead to birth defects, miscarriages, or cancer.

Necropsy—The gross examination of the organs and tissues of a dead body to determine the cause of 

death or pathological conditions.

Neurotoxicity—The occurrence of adverse effects on the nervous system following exposure to a 

hazardous substance.

No-Observed-Adverse-Effect Level (NOAEL)—The dose of a chemical at which there were no 

statistically or biologically significant increases in frequency or severity of adverse effects seen between 

the exposed population and its appropriate control. Although effects may be produced at this dose, they 

are not considered to be adverse.

Octanol-Water Partition Coefficient (Kow)—The equilibrium ratio of the concentrations of a chemical 

in n-octanol and water, in dilute solution.

Odds Ratio (OR)—A means of measuring the association between an exposure (such as toxic substances 

and a disease or condition) that represents the best estimate of relative risk (risk as a ratio of the incidence 

among subjects exposed to a particular risk factor divided by the incidence among subjects who were not 

exposed to the risk factor). An odds ratio that is greater than 1 is considered to indicate greater risk of 

disease in the exposed group compared to the unexposed group.

Permissible Exposure Limit (PEL)—An Occupational Safety and Health Administration (OSHA) 

regulatory limit on the amount or concentration of a substance not to be exceeded in workplace air 

averaged over any 8-hour work shift of a 40-hour workweek.

Pesticide—General classification of chemicals specifically developed and produced for use in the control 

of agricultural and public health pests (insects or other organisms harmful to cultivated plants or animals).

Pharmacokinetics—The dynamic behavior of a material in the body, used to predict the fate 

(disposition) of an exogenous substance in an organism. Utilizing computational techniques, it provides 

the means of studying the absorption, distribution, metabolism, and excretion of chemicals by the body.

Pharmacokinetic Model—A set of equations that can be used to describe the time course of a parent 

chemical or metabolite in an animal system. There are two types of pharmacokinetic models: data-based 

and physiologically-based. A data-based model divides the animal system into a series of compartments, 

which, in general, do not represent real, identifiable anatomic regions of the body, whereas the 

physiologically-based model compartments represent real anatomic regions of the body.
GLYPHOSATE E-5

APPENDIX E

Physiologically Based Pharmacodynamic (PBPD) Model—A type of physiologically based doseresponse model that quantitatively describes the relationship between target tissue dose and toxic 

endpoints. These models advance the importance of physiologically based models in that they clearly 

describe the biological effect (response) produced by the system following exposure to an exogenous 

substance. 

Physiologically Based Pharmacokinetic (PBPK) Model—A type of physiologically based doseresponse model that is comprised of a series of compartments representing organs or tissue groups with 

realistic weights and blood flows. These models require a variety of physiological information, including 

tissue volumes, blood flow rates to tissues, cardiac output, alveolar ventilation rates, and possibly 

membrane permeabilities. The models also utilize biochemical information, such as blood:air partition 

coefficients, and metabolic parameters. PBPK models are also called biologically based tissue dosimetry 

models.

Prevalence—The number of cases of a disease or condition in a population at one point in time. 

Prospective Study—A type of cohort study in which a group is followed over time and the pertinent 

observations are made on events occurring after the start of the study. 

Recommended Exposure Limit (REL)—A National Institute for Occupational Safety and Health 

(NIOSH) time-weighted average (TWA) concentration for up to a 10-hour workday during a 40-hour 

workweek.

Reference Concentration (RfC)—An estimate (with uncertainty spanning perhaps an order of 

magnitude) of a continuous inhalation exposure to the human population (including sensitive subgroups) 

that is likely to be without an appreciable risk of deleterious noncancer health effects during a lifetime. 

The inhalation RfC is expressed in units of mg/m3 or ppm.

Reference Dose (RfD)—An estimate (with uncertainty spanning perhaps an order of magnitude) of the 

daily oral exposure of the human population to a potential hazard that is likely to be without risk of 

deleterious noncancer health effects during a lifetime. The oral RfD is expressed in units of mg/kg/day. 

Reportable Quantity (RQ)—The quantity of a hazardous substance that is considered reportable under 

the Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA). RQs are 

(1) ≥1 pound or (2) for selected substances, an amount established by regulation either under CERCLA or 

under Section 311 of the Clean Water Act. Quantities are measured over a 24-hour period.

Reproductive Toxicity—The occurrence of adverse effects on the reproductive system that may result 

from exposure to a hazardous substance. The toxicity may be directed to the reproductive organs and/or 

the related endocrine system. The manifestation of such toxicity may be noted as alterations in sexual 

behavior, fertility, pregnancy outcomes, or modifications in other functions that are dependent on the 

integrity of this system.

Retrospective Study—A type of cohort study based on a group of persons known to have been exposed 

at some time in the past. Data are collected from routinely recorded events, up to the time the study is 

undertaken. Retrospective studies are limited to causal factors that can be ascertained from existing 

records and/or examining survivors of the cohort.

Risk—The possibility or chance that some adverse effect will result from a given exposure to a hazardous 

substance.
GLYPHOSATE E-6

APPENDIX E

Risk Factor—An aspect of personal behavior or lifestyle, an environmental exposure, existing health 

condition, or an inborn or inherited characteristic that is associated with an increased occurrence of 

disease or other health-related event or condition.

Risk Ratio/Relative Risk—The ratio of the risk among persons with specific risk factors compared to the 

risk among persons without risk factors. A risk ratio that is greater than 1 indicates greater risk of disease 

in the exposed group compared to the unexposed group.

Short-Term Exposure Limit (STEL)—A STEL is a 15-minute TWA exposure that should not be 

exceeded at any time during a workday. 

Standardized Mortality Ratio (SMR)—A ratio of the observed number of deaths and the expected 

number of deaths in a specific standard population.

Target Organ Toxicity—This term covers a broad range of adverse effects on target organs or 

physiological systems (e.g., renal, cardiovascular) extending from those arising through a single limited 

exposure to those assumed over a lifetime of exposure to a chemical.

Teratogen—A chemical that causes structural defects that affect the development of an organism.

Threshold Limit Value (TLV)—An American Conference of Governmental Industrial Hygienists 

(ACGIH) concentration of a substance to which it is believed that nearly all workers may be repeatedly 

exposed, day after day, for a working lifetime without adverse effect. The TLV may be expressed as a 

Time-Weighted Average (TLV-TWA), as a Short-Term Exposure Limit (TLV-STEL), or as a ceiling 

limit (TLV-C).

Time-Weighted Average (TWA)—An average exposure within a given time period. 

Toxicokinetic—The absorption, distribution, metabolism, and elimination of toxic compounds in the 

living organism.

Toxics Release Inventory (TRI)—The TRI is an EPA program that tracks toxic chemical releases and 

pollution prevention activities reported by industrial and federal facilities. 

Uncertainty Factor (UF)—A factor used in operationally deriving the Minimal Risk Level (MRL), 

Reference Dose (RfD), or Reference Concentration (RfC) from experimental data. UFs are intended to 

account for (1) the variation in sensitivity among the members of the human population, (2) the 

uncertainty in extrapolating animal data to the case of human, (3) the uncertainty in extrapolating from 

data obtained in a study that is of less than lifetime exposure, and (4) the uncertainty in using lowestobserved-adverse-effect level (LOAEL) data rather than no-observed-adverse-effect level (NOAEL) data. 

A default for each individual UF is 10; if complete certainty in data exists, a value of 1 can be used; 

however, a reduced UF of 3 may be used on a case-by-case basis (3 being the approximate logarithmic 

average of 10 and 1).

Xenobiotic—Any substance that is foreign to the biological system.
GLYPHOSATE F-2

APPENDIX F

APPENDIX F. ACRONYMS, ABBREVIATIONS, AND SYMBOLS

AAPCC American Association of Poison Control Centers

ACGIH American Conference of Governmental Industrial Hygienists

ACOEM American College of Occupational and Environmental Medicine

ACMT American College of Medical Toxicology

ADI acceptable daily intake

ADME absorption, distribution, metabolism, and excretion

AEGL Acute Exposure Guideline Level

AIC Akaike’s information criterion 

AIHA American Industrial Hygiene Association 

ALT alanine aminotransferase

AOEC Association of Occupational and Environmental Clinics

AP alkaline phosphatase

AST aspartate aminotransferase

atm atmosphere

ATSDR Agency for Toxic Substances and Disease Registry

AWQC Ambient Water Quality Criteria

BCF bioconcentration factor

BMD/C benchmark dose or benchmark concentration

BMDX dose that produces a X% change in response rate of an adverse effect

BMDLX 95% lower confidence limit on the BMDX

BMDS Benchmark Dose Software 

BMR benchmark response

BUN blood urea nitrogen 

C centigrade

CAA Clean Air Act

CAS Chemical Abstract Services

CDC Centers for Disease Control and Prevention

CEL cancer effect level

CERCLA Comprehensive Environmental Response, Compensation, and Liability Act

CFR Code of Federal Regulations

Ci curie

CI confidence interval

cm centimeter

CPSC Consumer Products Safety Commission

CWA Clean Water Act

DHHS Department of Health and Human Services

DNA deoxyribonucleic acid

DOD Department of Defense

DOE Department of Energy

DWEL drinking water exposure level

EAFUS Everything Added to Food in the United States

ECG/EKG electrocardiogram

EEG electroencephalogram

EPA Environmental Protection Agency

ERPG emergency response planning guidelines 

F Fahrenheit

F1 first-filial generation

FDA Food and Drug Administration
GLYPHOSATE F-3

APPENDIX F

FIFRA Federal Insecticide, Fungicide, and Rodenticide Act

FR Federal Register

FSH follicle stimulating hormone

g gram

GC gas chromatography

gd gestational day

GGT γ-glutamyl transferase 

GRAS generally recognized as safe

HEC human equivalent concentration 

HED human equivalent dose 

HHS Department of Health and Human Services 

HPLC high-performance liquid chromatography

HSDB Hazardous Substance Data Bank 

IARC International Agency for Research on Cancer

IDLH immediately dangerous to life and health

IRIS Integrated Risk Information System 

Kd adsorption ratio

kg kilogram

kkg kilokilogram; 1 kilokilogram is equivalent to 1,000 kilograms and 1 metric ton

Koc organic carbon partition coefficient

Kow octanol-water partition coefficient

L liter

LC liquid chromatography

LC50 lethal concentration, 50% kill

LCLo lethal concentration, low

LD50 lethal dose, 50% kill

LDLo lethal dose, low

LDH lactic dehydrogenase

LH luteinizing hormone

LOAEL lowest-observed-adverse-effect level

LSE Level of Significant Exposure

LT50 lethal time, 50% kill

m meter

mCi millicurie

MCL maximum contaminant level

MCLG maximum contaminant level goal

MF modifying factor

mg milligram

mL milliliter

mm millimeter

mmHg millimeters of mercury

mmol millimole

MRL Minimal Risk Level

MS mass spectrometry

MSHA Mine Safety and Health Administration

Mt metric ton

NAAQS National Ambient Air Quality Standard

NAS National Academy of Science

NCEH National Center for Environmental Health

ND not detected

ng nanogram
GLYPHOSATE F-4

APPENDIX F

NHANES National Health and Nutrition Examination Survey

NIEHS National Institute of Environmental Health Sciences

NIOSH National Institute for Occupational Safety and Health

NLM National Library of Medicine

nm nanometer

nmol nanomole

NOAEL no-observed-adverse-effect level

NPL National Priorities List

NR not reported

NRC National Research Council

NS not specified

NTP National Toxicology Program

OR odds ratio

OSHA Occupational Safety and Health Administration

PAC Protective Action Criteria

PAH polycyclic aromatic hydrocarbon

PBPD physiologically based pharmacodynamic 

PBPK physiologically based pharmacokinetic 

PEL permissible exposure limit

PEL-C permissible exposure limit-ceiling value

pg picogram

PEHSU Pediatric Environmental Health Specialty Unit

PND postnatal day

POD point of departure

ppb parts per billion

ppbv parts per billion by volume

ppm parts per million

ppt parts per trillion

REL recommended exposure level/limit

REL-C recommended exposure level-ceiling value

RfC reference concentration

RfD reference dose

RNA ribonucleic acid

SARA Superfund Amendments and Reauthorization Act

SCE sister chromatid exchange

SD standard deviation

SE standard error

SGOT serum glutamic oxaloacetic transaminase (same as aspartate aminotransferase or AST)

SGPT serum glutamic pyruvic transaminase (same as alanine aminotransferase or ALT)

SIC standard industrial classification

SMR standardized mortality ratio

sRBC sheep red blood cell

STEL short term exposure limit

TLV threshold limit value

TLV-C threshold limit value-ceiling value

TRI Toxics Release Inventory

TSCA Toxic Substances Control Act

TWA time-weighted average

UF uncertainty factor

U.S. United States

USDA United States Department of Agriculture
GLYPHOSATE

F-5

APPENDIX F

USGS United States Geological Survey

USNRC U.S. Nuclear Regulatory Commission

VOC volatile organic compound

WBC white blood cell

WHO World Health Organization > greater than ≥ greater than or equal to = equal to < less than ≤ less than or equal to % percent α alpha β beta γ gamma δ delta

μm micrometer

μg microgram q1*

cancer slope factor

– negative + positive

(+) weakly positive result (–) weakly negative result