Amicus Curiae Brief — Monsanto Company, Petitioner v. John L. Durnell

No. 24-1068

In the

Supreme Court of the United States

MONSANTO COMPANY,

Petitioner,

v.

JOHN L. DURNELL,

Respondent.

On Writ of Certiorari to the

Missouri Court of A ppeals, Eastern District

BRIEF OF CHILDREN’S HEALTH DEFENSE AS

AMICUS CURIAE IN SUPPORT OF RESPONDENT

Kim Mack Rosenberg

General Counsel

Risa Evans

Senior Staff Attorney

Eileen Hansen

Legal Fellow

Children’s Health Defense

852 Franklin Avenue,

Suite 511

Franklin Lakes, NJ 07417

Mary S. Holland

Counsel of Record

Chief Executive Officer

Children’s Health Defense

852 Franklin Avenue,

Suite 511

Franklin Lakes, NJ 07417

(202) 417-6971

mary.holland@

childrenshealthdefense.org

Counsel for Amicus Curiae

391818

A

(800) 274-3321 • (800) 359-6859

i

TABLE OF CONTENTS

Page

TABLE OF CONTENTS . . . . . . . . . . . . . . . . . . . . . . . . . . i

TABLE OF CITED AUTHORITIES . . . . . . . . . . . . . . iii

STATEMENT OF INTEREST . . . . . . . . . . . . . . . . . . . . 1

I N T RODUC T ION A N D SU M M A RY OF

ARGUMENT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3

STATEMENT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6

I.

Children Are Uniquely Vulnerable to

Harm from Chemical Exposures, so

Extra Caution is Required in Protecting

Children from the Risks Posed by Pesticides . . . . 6

II. Because of Children’s Vulnerability to

Harm from Chemical Exposures, the

EPA is Required to Use a Presumptive

10X Safety Factor to Protect Children

from the Risks Posed by Pesticides . . . . . . . . . . 17

III. Since 1998, the EPA has Declined to

Use the 10X Safety Factor to Protect

Ch i ld r en f r om H a r m f u l L e vel s of

Glyphosate Exposure Based on a Handful

of Outdated Animal Studies . . . . . . . . . . . . . . . . 18

IV. Studies of the Past 20 Years Strongly

S u g g e s t G l y p h o s a t e H a s Ne u r o development a l a nd O t her Ha r m f u l

Effects on Children . . . . . . . . . . . . . . . . . . . . . . . 25

ii

Table of Contents

Page

ARGUMENT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38

T his Cou r t Should A llow St at es to

P rotect Chi ld ren f rom Exposu re to

Chemicals, Including Glyphosate, Whose

Ha r mf ul Effects on Children the EPA

has Failed to Recognize . . . . . . . . . . . . . . . . . . . . . . . 38

CONCLUSION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 39

iii

TABLE OF CITED AUTHORITIES

Page

CASES:

Bates v. Dow Agrosciences L.L.C.,

544 U.S. 431 (2005) . . . . . . . . . . . . . . . . . . . . . . . . 38, 39

Bruesewitz v. Wyeth LLC,

562 U.S. 223 (2010) . . . . . . . . . . . . . . . . . . . . . . . . . . . 40

Cohen v. Apple Inc.,

46 F.4th 1012 (9th Cir. 2022) . . . . . . . . . . . . . . . . . . . 39

Duke Power Co. v. Carolina Envt’l. Study Group,

438 U.S. 59 (1978) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5

Envtl. Health Trust v. FCC,

9 F.4th 893 (D.C. Cir. 2021) . . . . . . . . . . . . . . . . . . . . 40

NRDC v. United States EPA,

38 F.4th 34 (9th Cir. 2022) . . . . . . . . . . . . . . . . . . . . . 20

Pruneyard Shopping Ctr. v. Robins,

447 U.S. 74 (1980) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5

United Construction Workers v.

Laburnum Construction Corp.,

347 U.S. 656 (1954) . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5

STATUTES AND OTHER AUTHORITIES:

21 U.S.C. § 346a(a) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17

iv

Cited Authorities

Page

21 U.S.C. § 346a(b)(2)(A)(i) . . . . . . . . . . . . . . . . . . . . . . . 17

21 U.S.C. § 346a(b)(2)(A)(ii) . . . . . . . . . . . . . . . . . . . . . . . 17

21 U.S.C. § 346a(b)(2)(C) . . . . . . . . . . . . . . . . . . . . . . . 3, 18

21 U.S.C. § 346a(b)(2)(C)(ii) . . . . . . . . . . . . . . . . . . . . . . . 17

Michael N. Antoniou et al., Teratogenic Effects of

Glyphosate-Based Herbicides: Divergence of

Regulatory Decisions from Scientific Evidence,

4 J. of Envtl. & A nal. Toxicol. 006 (2012) . . . . . . . 37

María-Aránzazu Martínez et al., Neurotransmitter

Changes in Rat Brain Regions Following

Glyphosate Exposure, 161 Envtl. Res. 212 (2018) . . . 34

Yassine Ait Bali et al., Learning and Memory

Impairments Associated to Acetylcholinesterase Inhibition and Oxidative Stress

Following Glyphosate Based-Herbicide

Exposure in Mice, 415 Toxicol. 18 (2019) . . . . . . . . 33

Jacqueline A. Barnett et al., Is the Use of

Glyphosate in Modern Agriculture Resulting

in Increased Neuropsychiatric Conditions

Through Modulation of the Gut-BrainMicrobiome Axis?, 9 Front. Nutr. 827384 (2022) . . . 29

v

Cited Authorities

Page

Samantha K. Bartholomew et al., Glyphosate

Exposure Exacerbates Neuroinflammation

and Alzheimer’s Disease-Like Pathology

Despite a 6-Month Recovery Period in Mice,

21 J. Neuroinflamm. 316 (2024) . . . . . . . . . . . . . . . . 27

Joseph M. Braun, Early-Life Exposure to

Endocrine Disrupting Chemicals and Role

in Childhood Obesity and Neurodevelopment,

13 Nature Rev. Endocrinology 161 (2017) . . . . . . . 10

Bożena Bukowska et al., Glyphosate Disturbs

Various Epigenetic Processes In Vitro and

In Vivo - A Mini Review, 851 S ci . Total

Environ. 158259 (2022) . . . . . . . . . . . . . . . . . . . . . . . 28

Carol J. Burns et al., Pesticide Exposure and

Neurodevelopmental Outcomes: Review of

the Epidemiologic and Animal Studies, 16 J.

Toxicol. & Envtl. Health, Part B 127 (2013) . . 11-12

Mingjun Cao et al., Melatonin Rescues the

Reproductive Toxicity of Low-Dose GlyphosateBased Herbicide Dur ing Mouse Oocyte

Ma tur a ti o n Vi a th e GPER Si g n a lin g

Pathway, 70 J. Pineal Res. e12718 (2021) . . . . . . . . 30

Maria J. Carroquino et al., Environmental

Toxicology: Children at Risk, Envtl. Toxicol. 239

(Edward A. Laws ed., Springer 2013) . . . . . . . . . . . 11

vi

Cited Authorities

Page

Daiane Cattani et al., Developmental Exposure

t o G l y p h o s a t e - B a s e d He r b i c i d e a n d

Depressive-Like Behavior in Adult Offspring:

Implication of Glutamate Excitotoxicity

and Oxidative Stress, 387 Toxicol. 67 (2017) . . . . . 35

Daiane Cattani et al., Long-Ter m Ef fects

of Perinatal Exposure to a GlyphosateBased Herbicide on Melatonin Levels and

Oxidative Brain Damage in Adult Male Rats,

12 A ntioxidants (Basel) 1825 (2023) . . . . . . . . . . . . 28

Daiane Cattani et al., Mechanisms Underlying

the Neurotoxicity Induced by GlyphosateB a s e d He r b i c i d e i n Im m a t u r e R a t

Hippocampus: Involvement of Glutamate

Excitotoxicity, 320 Toxicol. 34 (2014) . . . . . . . . . . . 36

CDC, Managing Chronic Conditions, https://

www.cdc.gov/school-health-conditions/chronicconditions/index.html . . . . . . . . . . . . . . . . . . . . . . . . . . 1

Warren Cornwall, ‘Journal retracts weed killer

study backed by Monsanto, citing ‘serious ethical

concerns,’ Science Advisor, Dec. 5, 2025 . . . . . . . . . 25

Carmen Costas-Ferreira et al., Toxic Effects of

Glyphosate on the Nervous System: A Systematic

Review, 23 Int’l J. Mol. Sci. 4605 (2022) . . . . . . . . 28

vii

Cited Authorities

Page

Eliane Dallegrave et al., The Teratogenic Potential

of the Herbicide Glyphosate–Roundup in

Wistar Rats, 142 Toxicol. Lett. 45 (2003) . . . . . . . . 37

Giada Di Pietro et al., Endocrine Disruptor

Chemicals and Children’s Health, 24 Int’l J.

Molecular Sci. 2671 (2023) . . . . . . . . . . . . . . . . . . . . 10

Débora Dummer Meira et al., Laying the

Groundwork: Exploring Pesticide Exposure

and Genetic Factors in South-Eastern Brazilian

Farmers, 8 Curr. Res. Toxicol. 100215 (2025) . . . . 26

Christopher B. Forrest et al., Trends in US children’s

mortality, chronic conditions, obesity, functional

status, and symptoms, 334 JAMA 6:509 (2025) . . . . 1

FQPA, Pub. L. No. 104-170, 110 Stat. 1489

(Aug. 3, 1996) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3, 17

Cristina Eugenia Gallegos et al., Perinatal

Glyphosate-Based Herbicide Exposure in

Rats Alters Brain Antioxidant Status,

Glutamate and Acetylcholine Metabolism and

Affects Recognition Memory, 34 Neurotox.

Res. 363 (2018) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 34

Carey Gillam, How Monsanto manipulates

journalists and academics, The Guardian,

June 2, 2019 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25

viii

Cited Authorities

Page

Glyphosate Pesticide Tolerances Rule, 65 Fed. Reg.

57957 (Sept. 27, 2000) . . . . . . . . . . . . . . . . . . . . . . 19-20

Glyphosate Pesticide Tolerances Rule, 69 Fed. Reg.

65081 (Nov. 10, 2004) . . . . . . . . . . . . . . . . . . . . . . . . . . 20

Glyphosate Pesticide Tolerances Rule, 71 Fed. Reg.

76180 (Dec. 20, 2006) . . . . . . . . . . . . . . . . . . . . . . . . . 20

Glyphosate Pesticide Tolerances Rule, 73 Fed. Reg.

73586 (Dec. 3, 2008) . . . . . . . . . . . . . . . . . . . . . . . . . . 20

Glyphosate Pesticide Tolerances Rule, 78 Fed. Reg.

25396 (May 1, 2013) . . . . . . . . . . . . . . . . . . . . . . . . . . . 20

Bryan Gonzalez et al., Scoping Review of the

Relationship Between Glyphosate-Based

Herbicide Exposures and Autism Spectrum

Disorder, 204 Food Chem. Toxicol. 115621 (2025) . . . 26

Ph i l l ip e Gra ndjea n & Ph i l ip La nd r ig a n,

Neurobehavioural effects of developmental

toxicity, 13 Lancet 330 (2014) . . . . . . . . . . . . . . . . . . 24

Ha ley M. Jen k i ns et a l., Gest a ti o n a l

Glyphosate Exposure and Early Childhood

Neurodevelopment in a Puerto Rico Birth

Cohort, 246 Envtl. Res. 118114 (2024) . . . . . . . . . . 26

Ersen Karakiliç et al., Endocrine Disruptors and

Children’s Health, 55 Turk. J. Med. Sci. 1671

(2025) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9

ix

Cited Authorities

Page

Ertuğrul Kiykim, Neurodevelopmental Impact

of Pesticides: A Silent Threat, 60 Turk. A rch.

Pediatrics 114 (2025) . . . . . . . . . . . . . . . . . . . . . . . . . . 9

Deepika Kubsad et al., Assessment of Glyphosate

Induced Epigenetic Transgenerational

Inher itance of Pathologies and Sper m

Epimutations: Generational Toxicology,

9 Sci. Rep. 6372 (2019) . . . . . . . . . . . . . . . . . . . . . . . . 31

Ph i l ip J. La nd r ig a n, Env ir o nm e nt a l

Hazards for Children in USA, 11 Int’l J.

Occupational Med. & Envtl. Health 189 (1998) . . . 14

Cor ina Lesseur et al., Mater nal Ur inar y

Levels of Glyphosate During Pregnancy

and Anogenital Distance in Newbor ns

in a US Multicenter Pregnancy Cohort,

280 Envtl. Pollut. 117002 (2021) . . . . . . . . . . . . . . . 30

Jianghong Liu & Er in Schela r, Pesticide

Exposure and Child Neurodevelopment:

Summary and Implications, 60 Workplace

Health & Saf. 235 (2012) . . . . . . . . . . . . . . . . . . . . . . 12

Fabiana Manser visi et al, The Ramazzini

Institute 13-Week Pilot Study GlyphosateBased Herbicides Administered at HumanEquivalent Dose to Sprague Dawley Rats:

Effects on Development and Endocrine

System, 18 Envtl. Health 15 (2019) . . . . . . . . . . . . 33

x

Cited Authorities

Page

Quixing Mao et al., The Ramazzini Institute

13-Week Pilot Study on Glyphosate and

Roundup Administered at Human-Equivalent

Dose to Sprague Dawley Rats: Effects on

the Microbiome, 17 Envtl. Health 50 (2018) . . 33-34

Grant McFa rland et a l., Acute Exposure

an d Chr o ni c Ret enti o n of Aluminum

in Three Vaccine Schedules and Effects

of Genetic and Environmental Variation,

58 J. Trace Elem. Med. Biol. 126444 (2020) . . . . . .10

Katiuska Marins et al., Maternal Exposure

t o Gly ph os a t e In c r e a s e d t h e Ri sk of

Adverse Neurodevelopmental Outcomes in

Rodent Offspring: A Systematic Review,

363 Envtl. Pollution 125086 (2024) . . . . . . . . . . . . 26

Muhammad Irfan Masood et al., Environment

Permissible Concentrations of Glyphosate

in Drinking Water Can Influence the Fate of

Neural Stem Cells from the Subventricular

Zone of the Postnatal Mouse, 270 Env tl .

Pollut. 116179 (2021) . . . . . . . . . . . . . . . . . . . . . . . . . 29

Maria M. Milesi et al., Perinatal Exposure

to a Glyphosate-Based Herbicide Impairs

Fe m a l e R e p r o d u c t iv e O u t c o m e s a n d

Induces Second-Generation Adverse Effects

in Wistar Rats, 92 A rch.Toxicol. 2629 (2018) . . . . 35

xi

Cited Authorities

Page

Monsanto Papers, https://w w w.wisnerbaum.

com /t ox ic -t or t -l aw/monsa nt o -rou ndup lawsuit/monsanto-papers/ . . . . . . . . . . . . . . . . . . . . . 25

Juan P. Munoz et al., Glyphosate and the Key

Characteristics of an Endocrine Disruptor:

A Review, 270 Chemosphere 128619 (2020) . . . . 10, 31

María Teresa Muñoz-Quezada et al., Neurodevelopmental Effects in Children Associated

with Exposure to Organophosphate Pesticides:

A Systematic Review, 39 NeuroToxicology 158

(2013) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12

NAFTA Technical Working Group on Pesticides

Developmental Neurotoxicity Study (DNT)

Guidance Document (Dec. 2016) . . . . . . . . . . . . . . . 24

National Academies of Sciences, Environmental

Neurotoxicology (1992) . . . . . . . . . . . . . . . . . . . . . 9, 24

National Research Council, Pesticides in the Diets of

Infants and Children (1993) . . . . . . 6, 8, 14, 15, 16, 17

Thu Ha Pham et al., Perinatal Exposure to

Gl y p h o s a t e a n d a Gl y p h o s a t e - Ba s e d

Herbicide Affect Spermatogenesis in Mice,

169 Toxicol. Sci. 260 (2019) . . . . . . . . . . . . . . . . . . . . 32

xii

Cited Authorities

Page

Ya oy u P u e t a l . , Ma t e r n a l Gl y p h o s a t e

Exposure Causes Autism-Like Behaviors in

Offspring Through Increased Expression

of Soluble Epoxide Hydrolase, 117 P roc .

Natl. Acad. Sci. U.S.A. 11753 (2020) . . . . . . . . . . . . 29

Xin Ren et al., Effects of Chronic Glyphosate

Exposure to Pregnant Mice on Hepatic

L i p i d Me t a b o l i s m i n O f f s p r i n g,

254 Envtl. Pollut. 112906 (2019) . . . . . . . . . . . . . . . 32

Retraction notice to “Long term toxicity of

a Roundup herbicide and a Rounduptolerant genetically modified maize,” 63 Food

& Chem. Tox. 244 (Jan. 2014) . . . . . . . . . . . . . . . . . . . 35

R e t r a c t i o n Wa t c h , Un e a r t h e d e m a i l s :

Mo n s a n t o c o n n e c t e d t o c a m p ai g n t o

retract GMO paper, https://retractionwatch.

com/2017/08/10/unearthed-docs-monsantoconnected-campaign-retract-gmo-paper/ . . . . . . . . 36

Enrique Rivero, Pediatric chronic disease

has risen nearly 30% in the last 20 years,

UCLA Health (March 10, 2025), https://www.

uclahealth.org/news/release/pediatric-chronicdisease-prevalence-has-risen-nearly-30 . . . . . . . . . . . 1

James R. Roberts & Catherine J. Karr, Pesticide

Exposure in Children, 130 Pediatrics e1765

(2012) (Council on Envtl. Health) (2013) . . . . . . . . . . 12

xiii

Cited Authorities

Page

María Florencia Rossetti et al., Epigenetic Changes

Associated With Exposure to GlyphosateBased Herbicides in Mammals, 12 F ront.

Endocrinol. 671991 (Lausanne) (2021) . . . . . . . . . . 30

Anthony Samsel & Stephanie Seneff, Glyphosate,

Pathways to Modern Diseases II: Celiac

Sprue and Gluten Intolerance, 6 Interdiscip.

Toxicol. 159 (2013) . . . . . . . . . . . . . . . . . . . . . . . . . . . 11

Anthony Samsel & Stephanie Seneff, Glyphosate’s

Suppression of Cytochrome P450 Enzymes

and Amino Acid Biosynthesis by the Gut

Microbiome: Pathways to Modern Diseases

15 Entropy 1416 (2013) . . . . . . . . . . . . . . . . . . . . . . . . 36

Norman R. Saunders et al., Barrier Mechanisms in

the Developing Brain, 3 Front. Pharmacol. 46

(2012) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13

R o b e r t S c h e u p l e i n e t a l . , D i f fe r e n t i a l

Sensitiv ity of Chil dren an d Adults to

Chemical Toxicity: I. Biological Basis,

35 Regul. Toxicol. Pharmacol. 429 (2002) . . . . . . . 13

Stephanie Seneff et al., Is Autism a PIN1 Deficiency

Syndrome? A Proposed Etiological Role

for Glyphosate, 168 J. Neurochem. 2124 (2024) . . . 27

xiv

Cited Authorities

Page

Stephanie Seneff, PhD, Toxic Legacy: How the

Weedkiller Glyphosate is Destroying our

Health and the Environment - One Scientist’s

Deter mined Quest to Reveal the Tr uth

(Chelsea Green Publishing 2021) . . . . . . . . . . . . . 4, 24

Gilles-Eric Séralini et al., Republished study:

Long-term Toxicity of a Roundup Herbicide

and a Roundup-tolerant Genetically Modified

Maize, 26 Envtl. Sci. Eur. 14 (2014) . . . . . . . . . 35-36

Peter D. Sly & Felicity Flack, Susceptibility

of Children to Environmental Pollutants,

1140 A nn. N.Y. Acad. Sci. 163 (2008) . . . . . . . . . . . . 13

Jakeline Liara Teleken et al., Glyphosate-Based

Herbicide Exposure dur ing Pregnancy

and La ctation Malp rograms the Male

Reproductive Morphfunction in F1 Offspring,

16 J. of Dev. Orig. Health & Dis. 1 (2019) . . . . . . . . 32

U. S . G . S . Pe s t i c i d e Na t i o n a l S y n t h e s i s

P roject , https: // wat er.usg s.gov/nawqa /

p n s p / u s a g e / m a p s /s ho w_ m a p . p hp? ye a r

=1992&map=GLYPHOSATE&hilo=L . . . . . . . . . . . 4

U.S. Environmental Protection Agency Policy on

Children’s Health (March 2026) . . . . . . . . . . . . . . . . . 6

U.S. Envtl. Prot. Agency, Children Are at

Greater Risks from Pesticide Exposure, https://

archive.epa.gov/pesticides/regulating/laws/

fqpa/web/html/kidpesticide.html . . . . . . . . . . . . . . . 18

xv

Cited Authorities

Page

U.S. Envtl. Prot. Agency, Glyphosate Human

Health Risk Assessment for Proposed Use on

Indian Mulberry and Amended Use on Pea, Dry,

Decision No. 360557 (2006) . . . . . . . . . . . . . . . . . 18, 19

U.S. Envtl. Prot. Agency, Glyphosate Interim

Registration Review Registration Decision

(2020) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20

U.S. Envtl. Prot. Agency, Glyphosate: Draft

human health risk assessment in support

of registration review, Decision No. 487242

(2017) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20, 21, 22

U.S. Envtl. Prot. Agency, Glyphosate: Response

to Comments on the Human Health Draft

Risk Assessment, Decision No. 5 4 2736

(Apr. 23, 2018) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9-10

U.S. Envtl. Prot. Agency, Office of Chemical Safety

and Pollution Prevention, EDSP Weight

of Evidence Conclusions on the Tier 1

Screening Assays for the List 1 Chemicals

(June 29, 2015) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22

U.S. EPA Memorandum, Withdrawal of the

Glyphosate Interim Registration Review

Decision, Sept. 21, 2022 . . . . . . . . . . . . . . . . . . . . . . . 20

U.S. Patent No. 316032, awarded Dec. 8, 1964 . . . . . . . . 4

xvi

Cited Authorities

Page

Ondine S. von Ehrenstein et al., Prenatal and Infant

Exposure to Ambient Pesticides and Autism

Spectrum Disorder in Children: Population

Based Case-Control Study, 364 BMJ 1962 (2019) . . 31

World Health Organization, Principles for

Evaluating Health Risks in Children Associated

with Exposure to Chemicals (2006) . . . 6, 8, 14, 15, 16

1

STATEMENT OF INTEREST1

Over the last thirty years, chronic illness among

children has reached epidemic proportions. 2 Children’s

Health Defense (“CHD”) is a nonprofit organization whose

mission is to end the childhood chronic disease epidemic by

reducing the toxic environmental exposures that underlie

it, especially where those exposures are involuntary.

CHD seeks to hold responsible parties accountable and to

establish safeguards to prevent future harm to children’s

health.

CHD is interested in the outcome of this case for two

primary reasons. First, glyphosate is the most widely

used biocide on the planet and infants and young children

are the sub-populations most exposed to glyphosate and

particularly vulnerable to its harms. Second, children’s

health is undermined when federal preemption works in

tandem with regulatory failure to protect children from

toxic agents, as is threatened in this case.

1. Under Supreme Court Rule 37.6, CHD states that no counsel

for any party authored this brief in whole or in part and no entity

or person, aside from CHD, its members, and counsel, made any

monetary contribution toward the preparation or submission of

this brief.

2. See Christopher B. Forrest et al., Trends in US children’s

mortality, chronic conditions, obesity, functional status, and

symptoms, 334 JAMA 6:509–516 (2025); Enrique Rivero, Pediatric

chronic disease has risen nearly 30% in the last 20 years, UCLA

Health (March 10, 2025), https://www.uclahealth.org/news/release/

pediatric-chronic-disease-prevalence-has-risen-nearly-30; CDC,

Managing Chronic Conditions, https://www.cdc.gov/school-healthconditions/chronic-conditions/index.html.

2

Since the 1990s, use of glyphosate-based pesticides

has skyrocketed. Indeed, it is now so widespread that

glyphosate residue is regularly ingested by children

through food and drink, as well through play on treated

parks and lawns, in swimming pools and ponds where

runoff may occur, and through oral contact with unwashed

hands and toys and other objects that are contaminated

with residue.

Mounting scientific evidence suggests that such

exposure harms children. Yet since 1998, based on a

handful of short-term, industry-funded, unpublished

animal studies conducted mostly before the turn of the

century, the EPA has concluded that glyphosate poses

no more risk to infants and children than to adults, and

refuses to provide children with the default-level of extra

protection required under federal law.

Policymakers must use extra caution when evaluating

the impact of environmental exposures on children

because children are not merely little adults; rather, their

biology leaves them more susceptible to health effects from

chemical exposures, and those effects may be lifelong. The

EPA’s outdated science notwithstanding, the States must

be able to use the tort system to protect their youngest

and most vulnerable citizens from known pesticide risks

by requiring warning labels that acknowledge the full

extent of those risks.

3

INTRODUCTION AND SUMMARY

OF ARGUMENT

The EPA has failed to protect children from risks

associated with glyphosate, a now-ubiquitous pesticide

chemical that presents special and increasingly evident

dangers to children. A question presented by this case

is, should the federal government preclude states from

requiring pesticide manufacturers to warn of those risks?

Biology and other factors render children more

susceptible than adults to injuries from toxins, and

experts recognize that extra caution must be used

when managing children’s exposure to potential toxins.

The Food Quality Protection Act (“FQPA”) writes this

recognition into federal law, requiring EPA to apply an

additional tenfold (10X) safety factor to protect infants

and children when it conducts the risk assessments that

underlie pesticide residue tolerance limits on agricultural

commodities, unless reliable data justify a different factor.

See 21 U.S.C. § 346a(b)(2)(C).

The EPA has ignored both the needs of children and

federal law when it comes to glyphosate. When assessing

the risks of glyphosate to children and setting residue

tolerance limits for glyphosate, the EPA has opted not to

study developmental neurotoxicity and other potentially

serious effects of glyphosate on children. Instead, relying

on a handful of unpublished, industry-funded, decades-old

animal studies with endpoints limited to a small set of

immediately observable, physical effects such as skeletal

malformation, the Agency has determined that glyphosate

exposure poses no more risks to children than to adults.

Thus, since 1998, the Agency has assessed glyphosate

4

risk and set tolerance limits without using the 10X FQPA

safety factor that would provide crucial added protection

for children.

The use of glyphosate has increased dramatically over

the years, 3 and infants and children under five are the

populations most highly exposed. Despite the EPA turning

a blind eye to glyphosate’s effects on children, a growing

body of evidence suggests that glyphosate poses a greater

risk to children than to adults, including negative effects

that can be both profound and permanent. The EPA has

failed to identify these effects for the simple reason that

it has refused to look for them.

Where the EPA has failed to adequately account

for the effects of glyphosate on children, and in the face

of children’s increasing and long-term exposure to this

chemical and mounting evidence of harm, states must

3. The U.S.G.S. Pesticide National Synthesis Project

provides pesticide use maps graphically depicting the increased

use of glyphosate. See https://water.usgs.gov/nawqa/pnsp/usage/

maps/show_map.php?year=1992&map=GLYPHOSATE&hilo=L.

Glyphosate was originally patented in 1964 as a chelating agent,

and used to strip mineral deposits in commercial hot-water systems.

Toxic Legacy: How the Weedkiller Glyphosate is Destroying our

Health and the Environment - One Scientist’s Determined Quest

to Reveal the Truth, by Stephanie Seneff, PhD (Chelsea Green

Publishing 2021) (“Toxic Legacy”), 9; see also U.S. Patent No.

316032, awarded Dec. 8, 1964. Use as an herbicide began in the early

1970s, and in the mid 1990s, with the advent of “Roundup Ready”

crops genetically-engineered to resist glyphosate, glyphosate’s

use began to increase dramatically. In more recent years, use has

expanded from weedkilling to harvest-aid, and it is now sprayed as

a desiccant on many types of crops immediately before harvest. See

Toxic Legacy, 9-11.

5

retain their power to require that pesticide warning labels

are adequate to protect children’s health. There are sound

legal arguments as to why the failure-to-warn claim in

this case is not preempted;4 in addition, this Court should

uphold the lower court’s decision to ensure that states

retain the ability to protect their most vulnerable citizens.

4. In addition to respondent’s arguments as to why the

failure-to-warn claim is not preempted, federal preemption of

any state remedy for damages from nonconsensual exposure

without inclusion of an adequate federal remedy for those

harms would present significant substantive and procedural

due process problems. See Pruneyard Shopping Ctr. v. Robins,

447 U.S. 74, 93-94 (1980) (Marshall, concurring) (“Quite

serious constitutional questions might be raised if a legislature

attempted to abolish certain categories of common-law rights

in some general way. Indeed, our cases demonstrate that there

are limits on governmental authority to abolish ‘core’ commonlaw rights, including rights against trespass, at least without a

compelling showing of necessity or a provision for a reasonable

alternative remedy.”); United Construction Workers v. Laburnum

Construction Corp., 347 U.S. 656, 663-64 (1954) (“Here Congress

has neither provided nor suggested any substitute for the

traditional state court procedure for collecting damages for

injuries caused by tortious conduct. For us to cut off the injured

respondent from this right of recovery will deprive it of its property

without recourse or compensation.”); Duke Power Co. v. Carolina

Envt’l. Study Group, 438 U.S. 59, 87-92 (1978) (sustaining federal

statute preempting state law remedies and providing alternative

federal remedy with reasonable liability caps).

6

STATEMENT

I.

Children Are Uniquely Vulnerable to Harm from

Chemical Exposures, so Extra Caution is Required

in Protecting Children from the Risks Posed by

Pesticides.

No one would dispute that extra caution is required

in protecting children from the harmful effects of

chemical exposures, because children are not simply

little adults; rather, profound biological differences exist

between children and adults that leave children even

more vulnerable than adults to injuries from chemical

exposures. Even the EPA acknowledges “the scientific

understanding that children may be at greater risk to

environmental pollutants than adults due to differences

in behavior and biology, and that the effects of early

life exposures may also arise in adulthood or in later

generations.” U.S. Environmental Protection Agency

Policy on Children’s Health, (March 2026).

In its 1993 publication Pesticides in the Diets of

Infants and Children (“NRC Pesticides”), the National

Research Council (“NRC”) thoroughly explored special

characteristics of children that render them uniquely

vulnerable to injuries from toxic exposures, and the

corresponding need for extra caution in assessing and

managing the risks created by such exposures. More

recently, in its 2006 Principles for Evaluating Health

Risks in Children Associated with Exposure to Chemicals

(“WHO Principles”), the World Health Organization

(“ WHO”) discussed both the basis for children’s

vulnerability and recommendations for assessing and

managing risks created by chemical exposures.

7

As explained by the WHO:

Children have different susceptibilities during

different life stages owing to their dynamic

growth and developmental processes as well

as physiological, metabolic, and behavioural

d i f fer ence s . F rom concept ion t h r ough

adolescence, rapid growth and developmental

processes occur that can be disrupted by

exposures to environmental chemicals. These

include anatomical, physiological, metabolic,

functional, toxicokinetic, and toxicodynamic

processes. Exposure pathways and exposure

patterns may also be different in different

stages of childhood. Exposure can occur in

utero through transplacental transfer of

environmental agents from mother to fetus or

in nursing infants via breast milk. Children

consume more food and beverages per kilogram

of body weight than do adults, and their dietary

patterns are different and often less variable

during different developmental stages. They

have a higher inhalation rate and a higher body

surface area to body weight ratio, which may

lead to increased exposures. Children’s normal

behaviours, such as crawling on the ground and

putting their hands in their mouths, can result

in exposures not faced by adults. Children’s

metabolic pathways may differ from those of

adults. Children have more years of future life

and thus more time to develop chronic diseases

that take decades to appear and that may be

triggered by early environmental exposures.

8

They are often unaware of environmental risks

and generally have no voice in decision-making.

WHO Principles, 2.

Along with more current studies, WHO Principles

and NRC Pesticides confirm that infants and children are

uniquely susceptible to harm from toxic chemical exposures

in at least four ways. First, unlike adults, they may be

exposed to toxins during critical windows of development

during which development of organs and systems may be

disrupted, leading to a cascade of harms. See, e.g., NRC

Pesticides, 3, 24 (“toxicity to a functional system . . . prior to

its full development may permanently affect that system,

resulting in altered function . . . in the mature animal”);

WHO Principles, 39-128 (discussing “Developmental

State-Specific Susceptibilities and Outcomes”). Second,

infants and young children have immature defense

systems, rendering them less able to eliminate some

toxins and metabolites that can affect development of

important systems. See, e.g., WHO Principles, 26, 33;

NRC Pesticides, 78, 87, 90, 95-96. Third, children may

receive higher relative doses of toxins per exposure than

adults due to lesser body weight, greater relative surface

area, and other factors. See, e.g., NRC Pesticides, 4;

WHO Principles, 31-33 and 36-38. Finally, the ill-effects

of toxic exposures on children may unfold over time and

be difficult to ascertain through short-term observation

or testing. See, e.g., WHO Principles, 78 (discussing

evidence that “neurotoxic insults during development

that result in no observable phenotype at birth or during

childhood could manifest later in life as earlier onset of

neurodegenerative diseases, such as Parkinson disease”);

NRC Pesticides, 7 (noting possibility of chronic effects

9

that are expressed only after long latency periods, such

as cancer, neurodevelopmental impairment, and immune

dysfunction); National Academies of Sciences (“NAS”),

Environmental Neurotoxicology 4 (1992) (observing

that neurotoxic effects of environmental exposures are

difficult to ascertain because “[t]he changes are often

subtle and subclinical, and months or years can elapse

between exposure to a neurotoxicant and the appearance

of dysfunction or disease”).

The following more recent studies address children’s

unique vulnerability to toxic insult and differences between

children and adults that may explain this vulnerability:

• Ertuğrul Kıykım, Neurodevelopmental

Impact of Pesticides: A Silent Threat, 60

Turk. A rch. Pediatrics 114 (2025) (discussing

evidence that chronic low dose exposure to

organophosphate pesticides interferes with

various biochemical pathways, causing

impaired neurodevelopment and cognitive

deficits);

• Ersen Karakiliç et al., Endocrine Disruptors

and Children’s Health, 55 T urk. J. Med.

Sci. 1671 (2025) (reviewing risks posed by

endocrine disruptors and factors making

early-life exposures more harmful to

children, including immature blood–brain

barrier and detoxification enzymes, higher

intake of air, food, and water per kg, thinner

skin, and higher surface-to-volume ratio);5

5. Although EPA holds that glyphosate is not an endocrine

disruptor (see EPA, Glyphosate: Response to Comments on the

Human Health Draft Risk Assessment, Decision No. 542736 (Apr.

10

• Giada Di Pietro et al., Endocrine Disruptor

Chemicals and Children’s Health, 24 Int ’l

J. Molecular Sci. 2671 (2023) (discussing

differences between adults and children

that potentially render health effects from

early-life exposure to endocrine-disrupting

chemicals more severe and long-lasting than

exposure in adulthood);

• Grant McFarland et al., Acute Exposure and

Chronic Retention of Aluminum in Three

Vaccine Schedules and Effects of Genetic

and Environmental Variation, 58 J. Trace

Elem. Med. Biol. 126444 (2020) (analyzing

expected acute exposures and longer-term

whole-body accumulation/clearance across

three vaccination schedules, indicating,

inter alia, that children experience greater

health risks than adults due to immature

detoxification, renal, gut, and neurological

systems);

• Joseph M. Braun, Early-Life Exposure

to Endocr ine Disr upting Chemicals

and Role in Childhood Obesity and

Neurod evel op m ent, 13 N a t u r e R e v.

E n docrinolo g y 161 (2017) (review ing

epidemiolog ical studies of endocr ine

disrupting chemicals, indicating fetuses

and children may have greater vulnerability

23, 2018), 5-6), some evidence suggests otherwise. See Juan P. Munoz

et al., Glyphosate and the Key Characteristics of an Endocrine

Disruptor: A Review, 270 Chemosphere 128619 (2020) (review of

research indicating glyphosate exhibits 8 of 10 key characteristics

of an endocrine disruptor).

11

due to hormone-dependent developmental

processes occurring only in early life, lower

levels of detoxification enzymes, and higher

intake of food and water per kilogram,

increasing r isk of obesity, metabolic

d i sor der s , a nd neu r o development a l

conditions);

• A nthony Samsel & Stephanie Seneff,

Glyphosate, Pathways to Modern Diseases

II: Celiac Sprue and Gluten Intolerance, 6

Interdiscip. Toxicol. 159 (2013) (indicating

glyphosate exposure poses greater health

risk to children than adults in part due to

immature detoxification, renal, gut, and

neurological systems, resulting in various

biochemical disruptions most consequential

during fetal/early childhood development

when these systems are forming);

• Maria J. Carroquino et al., Environmental

Toxicology: Children at Risk, in Envtl.

Toxicol. 239 (Edward A. Laws ed., Springer

2013) (orig. pub. online 2012) (discussing

findings from several major scientific

reports that risks to children differ from

adults, due to developmental timing of organ

formation, underdeveloped metabolism and

excretion capabilities, and higher exposure

per body weight);

• Carol J. Burns et al., Pesticide Exposure

and Neurodevelopmental Outcomes:

Review of the Epidemiologic and Animal

Studies, 16 J. Toxicol. & Envtl. Health,

12

Part B 127 (2013) (synthesizing human and

animal studies on pesticide exposure during

development; finding developing animals

and children can be more sensitive to

pesticide neurotoxicity than adults, causing

permanent neurological changes);

• Jianghong Liu & Erin Schelar, Pesticide

Exposure and Child Neurodevelopment:

Summary and Implications, 60 Workplace

Health & Saf. 235 (2012) (review indicating

even low levels of pesticide exposure in

pre-natal and early childhood is linked

to cognitive deficits, behavioral problems

and developmental delays, due in part to

vulnerable windows of development and

higher exposure relative to body weight);

• James R. Roberts & Catherine J. Karr,

Pesticide Exposure in Children, 130

Pediatrics e1765 (2012) (Council on Envtl.

Health) (2013) (comprehensive American

Association of Pediatrics technical report

reviewing scientific evidence on pesticide

exposure in children, finding children

are uniquely vulnerable to uptake and

adverse effects of pesticides because of

developmental, dietary, and physiologic

factors);

• Mar ía Teresa Muñoz- Quezada et al.,

Ne u r o d e v e l o p m e n t a l E f f e c t s i n

Children Associated with Exposure to

Organophosphate Pesticides: A Systematic

Review, 39 NeuroToxicology 158 (2013)

13

(sy nthesis of repor ted ev idence over

previous decade on neurodevelopmental

effects of organophosphate pesticide

exposure in children, indicating critical

developmental windows make children more

susceptible than adults to neurotoxic effects

of pesticides);

• Nor man R . Saunders et al., Bar r ier

Mechanisms in the Developing Brain, 3

F ront. Pharmacol . 46 (2012) (scientific

analysis and review of literature suggesting

developing brains may be more vulnerable

to drugs, toxins, and pathological conditions,

contributing to cerebral damage and later

neurological disorders);

• Peter D. Sly & Felicity Flack, Susceptibility

of Children to Environmental Pollutants,

1140 A n n . N.Y. A ca d . S ci . 163 (2008)

(concluding children more likely to suffer

adverse hea lth outcomes f rom same

exposure level, due to exposures during

critical developmental windows where

toxins can cause permanent structural or

functional damage; discussing immature

metabolic and detoxification pathways;

and higher internal doses for the same

environmental concentration);

• Robert Scheuplein et al., Differential

Sensitivity of Children and Adults to

Chemical Toxicity: I. Biological Basis,

3 5 R e gu l . T ox ic ol . P h a r m ac ol . 4 2 9

(2002) (recognizing dietary exposure is

14

compounded by children’s immature livers

and excretory systems, which may be unable

to effectively remove pesticide metabolites);

• Philip J. Landr igan, Environmental

Hazards for Children in USA, 11 Int’l J.

Occupational Med. & Envtl. Health 189

(1998) (analysis of biological sensitivities

indicating children are generally more

susceptible to environmental toxicants than

adults, due in part to rapid organ growth

and development).

As the WHO notes, due to the potential for dramatically

different effects of chemical exposures on children, “the

full spectrum of effects from childhood exposures cannot

be predicted from adult data,” and adult-based safety data

relating to such exposures often cannot be readily applied

to the pediatric population. WHO Principles, 2. Thus,

risk assessment paradigms must “evaluate exposures

relevant to children from preconception to adolescence,

taking into account the specific susceptibilities at each

developmental stage” and “[r]isk assessment approaches

for exposures in children must be linked to life stages.”

Id. Along similar lines, the NRC notes it is important

to “enhance understanding of developmental toxicity,

especially in humans, during critical periods of postnatal

development, including infancy and puberty.” NRC

Pesticides, 9.

The NRC adds “[o]f particular importance are tests

for neurotoxicity and toxicity to the developing immune

and reproductive systems. Extrapolation of toxicity data

from adult and adolescent laboratory animals to young

humans may be inaccurate.” Id. The NRC also cautions

15

that because of differences in maturation rates across

species, “cross-species comparisons of potential toxicity

for pesticides in the very young animal, although helpful,

cannot be used in the same manner that cross-species

comparisons are used with adult animals because of

differences in developmental patterns.” Id., 25.

The WHO Principles recommend various childprotective risk-assessment approaches, including the

following:

• Conduct prospective cohort studies of

pregnant women, infants, and children with

longitudinal capture of exposures at critical

windows and sensitive health end-points

along the continuum of human development.

• Continue to develop and enhance populationbased surveillance systems for real-time

capture of sentinel health end-points.

• Strengthen exposure monitoring efforts

in children during different developmental

stages, including assessment of aggregate

and cumulative exposures.

• Develop validated, sensitive, and coste f fe c t i ve b i o m a rk e r s o f e x p o s u r e ,

susceptibility, and effects, particularly

during early developmental stages.

• Improve characterization of differences in

toxicokinetic and toxicodynamic properties

of xenobiotics at different developmental

stages. Develop databases of stage -

16

specific physiological and pharmacokinetic

parameters in both human and animal

studies.

• Study mechanisms of action during different

developmental stages by which exposures

may cause adverse outcomes.

• Develop endpoints that can be used to assess

organ system functions in both humans and

animal species and to identify analogous

periods of development across species.

• Improve characterization of windows of

susceptibility of different organ systems in

relation to structural and functional endpoints.

• Develop and validate biological models and

animal testing guidelines that can address

health outcomes at different developmental

stages.

WHO Principles, 4-6.

The NRC offers this precautionary principle as an

overall guide: “In the absence of data to the contrary,

there should be a presumption of greater toxicity to

infants and children.” NRC Pesticides, 9 (emphasis

added).

17

II. Because of Children’s Vulnerability to Harm from

Chemical Exposures, the EPA is Required to Use a

Presumptive 10X Safety Factor to Protect Children

from the Risks Posed by Pesticides.

The EPA is required to set tolerance limits for

pesticide chemical residue on food, including raw

agricultural commodities and processed foods. See 21

U.S.C. § 346a(a). Residue tolerance limits are “the single

most important tool by which the U.S. Government

regulates pesticide residues in food.” NRC Pesticides, 18

(emphasis in original).

The EPA is required to set tolerance limits such

that “there is a reasonable certainty that no harm will

result from aggregate exposure to the pesticide chemical

residue, including all anticipated dietary exposures and all

other exposures for which there is reliable information.”

21 U.S.C. § 346a(b)(2)(A)(i) and (ii). Additionally, the limits

must ensure “a reasonable certainty that no harm will

result to infants and children from aggregate exposure

to the pesticide chemical residue.” See 21 U.S.C. § 346a(b)

(2)(C)(ii).

In 1996, through the Food Quality Protection Act,

Congress wrote into federal law the recognition of

children’s unique vulnerabilities and the need to specially

protect them from harmful pesticide exposures. See

FQPA, Pub. L. No. 104-170, 110 Stat. 1489 (Aug. 3, 1996).

The FQPA directs the EPA to use “an additional tenfold

margin of safety for the pesticide chemical residue and

other sources of exposure . . . to take into account potential

18

pre- and post-natal toxicity and completeness of the data

with respect to exposure and toxicity to infants and

children.” 21 U.S.C. § 346a(b)(2)(C).

In other words, the EPA is required to assume that

the risk to children from the use of a particular pesticide

is ten times greater than for adults when assessing risks

and setting residue tolerance limits for pesticide chemicals

like glyphosate. The EPA may “use a different margin of

safety for the pesticide chemical residue only if, on the

basis of reliable data, such margin will be safe for infants

and children.” Id. (emphasis added).

III. Since 1998, the EPA has Declined to Use the 10X

Safety Factor to Protect Children from Harmful

Levels of Glyphosate Exposure Based on a Handful

of Outdated Animal Studies.

The EPA has long recognized that infants and children

under five years old are the population most highly exposed

to glyphosate, through multiple routes of exposure.6 See

U.S. Envtl. Prot. Agency, Glyphosate Human Health Risk

Assessment for Proposed Use on Indian Mulberry and

Amended Use on Pea, Dry, Decision No. 360557 (2006)

(“2006 Risk Assessment”), 3, 21. However, according to

EPA documents, in 1998, the EPA concluded that infants

6. They are exposed not only through what they eat and drink,

but also through outdoor play in treated areas and where runoff may

accumulate, such as lawns, turf, playgrounds, and pools, and through

incidental exposures, including hand-to-mouth and object-to-mouth

exposures. See EPA, Children Are at Greater Risks from Pesticide

Exposure, https://archive.epa.gov/pesticides/regulating/laws/fqpa/

web/html/kidpesticide.html.

19

and children are no more vulnerable to glyphosate than

adults, and should be afforded no extra protection. Based

on this conclusion, the EPA reduced the FQPA children’s

safety factor for glyphosate from the presumptive 10X to

1X, thereby eliminating the statute’s additional tenfold

child-protective safety margin. See id., 17-18.

The 1998 decision to eliminate the children’s safety

factor was based primarily on a handful of rat and rabbit

studies where pregnant animals were exposed to varied

levels of glyphosate, and the lowest observed adverse

events levels (“LOAEL”) for fetuses and offspring

were compared with the LOAELs for the mothers.

From these studies, the Agency concluded, “There is

no evidence of quantitative or qualitative increased

susceptibility of the young demonstrated in the prenatal

developmental studies in rats and rabbits and pre/post

natal reproduction study in rats.” Id. (emphasis added).

According to the EPA, the additional bases for eliminating

the safety factor were: “2. The toxicology database is

complete; 3. A developmental neurotoxicity study is not

required; and 4. The dietary (food and drinking water)

exposure assessments will not underestimate the potential

exposures for infants and children.” Id., 17-18, 11-13,

16 (discussing developmental and reproductive toxicity

studies available in the toxicity database).

Since 1998, as use of glyphosate has increased,

the EPA has maintained its decision to eliminate the

10X FQPA safety factor each time it has added residue

tolerance limits for new types of foods and agricultural

commodities or increased existing limits, apparently

based on the same set of rat and rabbit studies. See,

e.g., Glyphosate Pesticide Tolerances Rule, 65 Fed. Reg.

20

57957, 57961-63 (Sept. 27, 2000) (maintaining FQPA factor

at 1X while expanding and restructuring tolerances);

Glyphosate Pesticide Tolerances Rule, 69 Fed. Reg. 65081,

65085 (Nov. 10, 2004) (maintaining FQPA factor at 1X

while setting new and increased tolerances); Glyphosate

Pesticide Tolerances Rule, 71 Fed. Reg. 76180, 76183 (Dec.

20, 2006) (maintaining FQPA factor at 1X while setting

new tolerances); Glyphosate Pesticide Tolerances Rule,

73 Fed. Reg. 73586, 73591 (Dec. 3, 2008) (maintaining

FQPA factor at 1X while setting new and increased

tolerances); Glyphosate Pesticide Tolerances Rule, 78

Fed. Reg. 25396, 25398 (May 1, 2013) (maintaining FQPA

factor at 1X while setting new and increased tolerances).

In its 2017 draft glyphosate risk assessment, EPA

reiterated the conclusion that “there is no evidence of

quantitative or qualitative fetal susceptibility in rats or

rabbits following in utero exposure in the developmental

studies” and maintained its elimination of the FQPA

safety factor.7 U.S. Envtl. Prot. Agency, Glyphosate:

Draft human health risk assessment in support of

registration review, Decision No. 487242, (2017) (“2017

Risk Assessment”), 4.

7. The EPA discussed risk in its Glyphosate Inter im

Registration Review Registration Decision of 2020, but in 2022, the

human health portion of the Decision was vacated because the Agency

did not adequately consider whether glyphosate causes cancer. See

NRDC v. United States EPA, 38 F.4th 34 (9th Cir. 2022). The Agency

subsequently withdrew the 2020 Decision, leaving the 2017 Draft

Risk Assessment as the most current non-withrawn glyphosate

risk assessment. See U.S. EPA Memorandum, Withdrawal of the

Glyphosate Interim Registration Review Decision, Sept. 21, 2022.

21

The Agency’s 2017 conclusion relied on “two prenatal developmental toxicity studies in rats and rabbits

and three reproductive toxicity studies (two studies

performed for two generations, 1 study performed for

three generations),” which the Agency characterized,

collectively, as “Evidence of Sensitivity/Susceptibility in

the Developing or Young Animal.” 2017 Risk Assessment,

12-14.

Four of the studies underlying the 2017 conclusion are

the same ones the Agency has relied on since eliminating

the 10X safety factor in 1998, and of those, three predate

the EPA’s 1983 adoption of Good Laboratory Practice

standards (“GLP”). The most recent study is dated 2007.

All of the studies were industry-funded.

As shown in Table 1, the studies underlying the 2017

conclusions regarding glyphosate effects on infants and

children considered only immediate, physically observable

adverse effects on offspring of maternal exposure to

glyphosate.

22

Table 1: Studies Referenced in EPA’s 2017 Draft

Risk Assessment as Evidence that Developing and

Young Children are No More Sensitive/Susceptible to

Glyphosate’s Adverse Effects than Adults Are8

Study Date

Sponsor

EPA MRID

#

1980 (preGLP)

Monsanto

#46362

Study Type

Study Endpoints:

Offspring Effects

Considered at LOAEL

Rat:

Developmental

Toxicity

Fetuses examined

after gestational day

20 for visceral softtissue and skeletal

alterations

1980 (preRabbit:

Fetuses examined

GLP)

Developmental

after gestational day

Monsanto # Toxicity

28 for visceral and

46363

skeletal malformations

1982 (preRat:

Offspring examined

GLP)

Three Generation for sex distribution,

Monsanto

Reproduction

body weights, survival,

#105995

and gross postmortem

findings.

8. See 2017 Risk Assessment, 30-31; see also U.S. Envtl. Prot.

Agency, Office of Chemical Safety and Pollution Prevention, EDSP

Weight of Evidence Conclusions on the Tier 1 Screening Assays for

the List 1 Chemicals (June 29, 2015), 27-29; 47-48; 50-52.

23

1990

Monsanto

#41621501

Rat:

Two Generation

Reproduction

2007

Safepharm

Labs, Ltd.

#48865101

Rat:

Two Generation

Reproduction

Offspring examined

for mortality, clinical

signs (e.g., soft stool),

body and organ weight,

food-consumption;

reproduction-fertility

indices (pre-coital

interval, gestation

length, litter size,

dead pups/litter, pup

survival), and selected

tissues.

Offspring organs

weighed and tissues

examined for gross and

microscopic pathology;

also considered

mortality, clinical

signs, body weight,

food consumption,

reproduction-fertility

indices, developmental

landmarks and

reflexes, ano-genital

distance.

There are many sound bases for critiquing the Agency’s

decision to eliminate the FQPA safety factor and the

animal studies that underlie it.9 Here, suffice it to say that

9. Indeed, there are many sound bases for challenging the

Agency’s conclusions about glyphosate safety for human beings

and other life forms. For comprehensive discussion of the human

and environmental impacts of glyphosate and the ways glyphosate

24

crucial studies are missing from the EPA’s risk assessment

for children.

To begin, absent are studies of developmental

neurotoxicity, which would assess cognitive, behavioral,

and neurobiological effects over time, for different

exposure windows. See generally, NAS, Environmental

Neurotoxicology, 18, 54 (1992) (“a chemical cannot be

regarded as free of neurotoxicity merely because data on

its toxicity are lacking”‘ and “[t]o maximize detection of

toxicity, some toxicity studies encompassing the full life

span of experimental animals should be encouraged”).

These studies are important; as the EPA recognizes,

“The developing nervous system is especially vulnerable

to certain chemicals, and exposures may result in altered

neural development with consequences that may be quite

unlike the chemical’s effects in an adult nervous system.”

See NAFTA Technical Working Group on Pesticides

Developmental Neurotoxicity Study (DNT) Guidance

Document, 1 (Dec. 2016); see also Phillipe Grandjean

& Philip Landrigan, Neurobehavioural effects of

developmental toxicity, 13 Lancet 330, 334 (2014) (brain

damage caused by developmental neurotoxicity is “too

often untreatable and frequently permanent”).

Also absent are studies of endpoints where children

may have unique vulnerabilities, including oxidative stress

and other biochemical effects; endocrine, immune system,

fails to meet FIFRA’s safety standard, see Petition to cancel all

registrations of glyphosate herbicide, filed with the EPA on Dec.

13, 2023 by six farmworker, environmental, and agriculture public

interest organizations. For another comprehensive discussion

of glyphosate’s harmful effects on all life forms and proposed

biochemical mechanisms of harm, see Toxic Legacy, supra, n. 3.

25

and microbiome-mediated effects; and adult-onset disease

following early-life exposure. Also missing: studies of the

long-term or cumulative effects of glyphosate on infants

and children and of real-world exposures to glyphosate

formulations that include surfactants and adjuvants.

IV. Studies of the Past 20 Years Strongly Suggest

Glyphosate Has Neurodevelopmental and Other

Harmful Effects on Children.

The EPA’s failure to meaningfully study the effects

of glyphosate on the health of infants and children hardly

means that health effects do not occur.10 Indeed, over the

last two decades, a growing body of literature points to

myriad ill effects of glyphosate on infants and children,

from both prenatal and post-natal exposure. The EPA has

not acknowledged these effects for the simple reason that

it has refused even to consider them. Relevant literature

includes the following:

10. The EPA’s dereliction of duty has resulted in an

underestimate of the risks posed by glyphosate. However,

Monsanto plays a role here too by its “deceptive efforts to defend

the safety of its top-selling Roundup herbicide.” See Carey Gillam,

How Monsanto manipulates journalists and academics, The

Guardian, June 2, 2019; see also Warren Cornwall, ‘Journal

retracts weed killer study backed by Monsanto, citing ‘serious

ethical concerns,’ Science Advisor, Dec. 5, 2025; Monsanto

Papers, https://www.wisnerbaum.com/toxic-tort-law/monsantoroundup-lawsuit/monsanto-papers/ (internal documents obtained

in discovery “reveal a systematic, decades-long campaign” by

Monsanto to “manipulate scientific research, corrupt regulatory

processes, and deceive the public about the safety of its flagship

herbicide, Roundup”). Monsanto’s malfeasance is beyond the scope

of this brief, but should not be ignored.

26

• Bryan Gonzalez et al., Scoping Review

of the Relationship Between GlyphosateBased Herbicide Exposures and Autism

Spectr um Disorder, 204 Fo od C h em .

Toxicol . 115621 (2025) (scientific review

demonstrates strong relationship between

deleterious effects of exposure to glyphosate

herbicides and autism spectrum disorder

in children, particularly during critical

neurodevelopmental windows);

• Débora Dummer Meira et al. , Laying

the Groundwork: Exploring Pesticide

Exposure and Genetic Factors in SouthEastern Brazilian Farmers, 8 Curr. Res.

Toxicol. 100215 (2025) (finding link between

glyphosate use by agricultural workers

in Brazil and high blood pressure, heart

disease, miscarriages, and ADHD);

• Haley M. Jenkins et al., Gestational

Glyphosate Exposure and Early Childhood

Neurodevelopment in a Puerto Rico Birth

Cohort, 246 Envtl. Res. 118114 (2024) (cohort

study measuring glyphosate exposure

during pregnancy finds association between

prenatal exposure and developmental delays

in early childhood);

• Katiuska Marins et al., Maternal Exposure

to Glyphosate Increased the Risk of

Adverse Neurodevelopmental Outcomes

in Rodent Offspring: A Systematic Review,

363 E n v t l . P ollu t ion 125086 (2024)

27

(comprehensive examination of behavioral,

biochemical, morphological, and genetic

a lt erations resulting f rom per inata l

glyphosate exposure, finding exposure

during development can cause oxidative

stress, neuroinflammation, mitochondrial

dysfunction, and behavioral changes,

increasing susceptibility to neurological

disorders later in life);

• Samantha K. Bartholomew et al., Glyphosate

Exposure Exacerbates Neuroinflammation

and Alzheimer’s Disease-Like Pathology

Despite a 6-Month Recovery Period in Mice,

21 J. Neuroinflamm. 316 (2024) (finding

that despite an extended recovery period,

glyphosate exposure elicits long-lasting

pathological consequences; mice dosed with

glyphosate for 14 days showed glyphosate

and major metabolite in brain tissue even

after six months, w ith corresponding

increases in pro-inflammatory factor that

is elevated in neurodegenerative disorders

such as Alzheimer’s);

• Stephanie Seneff et al., Is Autism a

PIN1 Deficiency Syndrome? A Proposed

Etiological Role for Glyphosate, 168

J. Neu rochem . 2124 (2024) (early-life

glyphosate exposure produces permanent

prog ra m m i ng ef fect s not seen w it h

equivalent adult exposure: prenatal /

perinatal exposure reduces melatonin

in rat pups, disrupts PIN1 signaling,

28

impairs autophagy, produces autism-like

morphological features and behaviors;

causes glutamate neuroexcitotoxicity, and

oxidative stress);

• Daiane Cattani et al., Long-Term Effects

of Perinatal Exposure to a GlyphosateBased Herbicide on Melatonin Levels and

Oxidative Brain Damage in Adult Male

Rats, 12 A ntioxidants (Basel) 1825 (2023)

(pregnant rats exposed to glyphosate, where

offspring showed reduction in melatonin,

increased oxidative stress and cellular brain

damage markers associated with increased

risk of neurodegenerative disorders);

• Carmen Costas-Ferreira et al., Toxic Effects

of Glyphosate on the Nervous System:

A Systematic Review, 23 I nt ’l J. Mol .

S ci. 4605 (2022) (analyzing mechanisms

of gly phosat e neu rot ox icity, f i nd i ng

glyphosate may influence neurotransmitter

signaling, oxidative stress pathways,

neuroinflammatory processes);

• Bożena Bukowska et al., Glyphosate

Disturbs Various Epigenetic Processes In

Vitro and In Vivo - A Mini Review, 851

Sci. Total Environ. 158259 (2022) (finding

epigenetic changes caused by glyphosate can

persist over time, be passed on to offspring

in the next generation, and even in third

generation can result in some disorders such

as prostate disease or obesity);

29

• Jacqueline A. Barnett et al., Is the Use

of Glyphosate in Modern Agriculture

Resulting in Increased Neuropsychiatric

Conditions Through Modulation of the

Gut-Brain-Microbiome Axis?, 9 F ront.

Nutr. 827384 (2022) (perspective review

finding glyphosate-resistant microbes

in the g ut have potential to increase

production of pro-inflammatory cytokines

and reactive oxygen species, and can affect

immune and neurodevelopment across

generations through maternal transfer of

gut microbiome);

• Mu ha m mad Ir fa n Masood et a l.,

Environment Permissible Concentrations

of Glyphosate in Drinking Water Can

Influence the Fate of Neural Stem Cells from

the Subventricular Zone of the Postnatal

Mouse, 270 Envtl. Pollut. 116179 (2021)

(in vitro study discussing glyphosate’s

mechanisms of neurotoxicity, suggesting

glyphosate interferes with maturation of

new neurons in the brain);

• Yaoyu Pu et al., Maternal Glyphosate

Exposure Causes Autism-Like Behaviors

in Offspring Through Increased Expression

of Soluble Epoxide Hydrolase, 117 P roc.

Natl. Acad. Sci. U.S.A. 11753 (2020) (mouse

study in which glyphosate administered in

maternal drinking water during pre- and

post-natal period associated with autismlike behavioral abnormalities in juvenile

30

offspring and other biological changes

including disruption of gut microbiome);

• Mingjun Cao et al., Melatonin Rescues

the Reproductive Toxicity of Low-Dose

Glyphosate-Based Herbicide Dur ing

Mouse Oocyte Maturation Via the GPER

Signaling Pathway, 70 J. P ineal R es .

e12718 (2021) (study regarding toxic effects

of low-dose glyphosate-based herbicide

exposure on mature mouse oocytes during

meiotic maturation revealed that low-dose

glyphosate has adverse effect on oocyte

maturation and early embryo cleavage,

highlighting protective role of melatonin);

• María Florencia Rossetti et al., Epigenetic

Changes Associated With Exposure to

Glyphosate-Based Herbicides in Mammals,

12 Front. Endocrinol. (Lausanne) 671991

(2021) (scientific review summarizing

epigenetic changes produced by glyphosate

and like chemicals, finds such changes could

be heritable leading to disease long after the

exposure has ended);

• Corina Lesseur et al., Maternal Urinary

Levels of Glyphosate During Pregnancy

and Anogenital Distance in Newborns

in a US Multicenter Pregnancy Cohort,

280 Envtl. Pollut. 117002 (2021) (finding

statistically significant correlation between

levels of glyphosate in urine of mothers

during late pregnancy and anogenital

31

distance in female offspring; long anogenital

distance associated with a greatly increased

risk to polycystic ovary syndrome, the most

common cause of female infertility);

• Juan P. Munoz et al., Glyphosate and the Key

Characteristics of an Endocrine Disruptor:

A Review, 270 Chemosphere 128619 (2020)

(scientific review indicating glyphosate

exhibits 8 of 10 key characteristics of an

endocrine disruptor, including disruption

of thyroid hormone regulation, suppression

of testosterone synthesis, inhibition of

developmental enzyme for converting

testosterone to estrogen, and enhanced

estrogenic signaling in breast cancer cells);

• Ondine S. von Ehrenstein et al., Prenatal

and Infant Exposure to Ambient Pesticides

and Autism Spectrum Disorder in Children:

Population Based Case-Control Study, 364

BMJ 1962 (2019) (finding women living

within 1.2 miles of pesticide spray areas 30

percent more likely to have children with

severe autism, with highest odds ratio for

children exposed to glyphosate in first year

of life);

• Deepi k a Kubsa d et a l., Assessm ent

of Gl y p h o s a t e In d u c e d Ep i g e n e ti c

T r a n s g e n e r a t i o n a l In h e r i t a n c e of

Pathologies and Sperm Epimutations:

Generational Toxicology, 9 Sci. Rep. 6372

(2019) (study exposing pregnant rats to low

32

doses of glyphosate between eighth and

fourteenth days of gestation, finds dramatic

increase in in several health problems, most

linked to reproduction, in second and third

generation);

• Jakeline Liara Teleken et al., GlyphosateBa s e d He r b i c i d e Ex p os u r e d u r in g

Pregnancy and Lactation Malprograms

the Male Reproductive Morphfunction in

F1 Offspring, 16 J. of Dev. Orig. Health &

Dis. 1 (2019) (male offspring of mice exposed

to glyphosate during gestation and lactation

suffered serious health effects, including

delayed testicular descent, reduced sperm

counts, structural alterations within testes);

• Xin Ren et al., Effects of Chronic Glyphosate

Exposure to Pregnant Mice on Hepatic

Lipid Metabolism in Offspring, 254 Envtl.

Pollut. 112906 (2019) (offspring of pregnant

mice exposed to glyphosate showed fatty

liver and perturbations of various blood

parameters related to fats, cholesterol and

standard liver enzymes, demonstrating that

chronic prenatal exposure to glyphosate

can result in lipid metabolism disruption in

offspring);

• Thu Ha Pham et al., Perinatal Exposure

to Glyphosate and a Glyphosate-Based

Herbicide Affect Sper matogenesis in

Mice, 169 Toxicol. S ci. 260 (2019) (male

rats exposed to glyphosate products in

33

utero had low testosterone, deformed

testes, decreased sperm count, and fertility

problems);

• Fabiana Manservisi et al, The Ramazzini

Institute 13-Week Pilot Study GlyphosateBased Herbicides Administered at HumanEquivalent Dose to Sprague Dawley Rats:

Effects on Development and Endocrine

System, 18 E n v t l . H e a lt h 15 (2019)

(offspring of pregnant rat dams exposed

to glyphosate-based herbicides throughout

gestation and weaning, at doses considered

safe for humans, induced endocrine effects

and altered reproductive developmental

parameters, including androgen-like effects

and increased testosterone in females);

• Yassine Ait Bali et al., Learning and

Memor y Impair ments Associated to

Acetylcholinesterase Inhibition and

Oxidative Stress Following Glyphosate

Ba sed-Herbicid e Exposure in Mice,

415 T ox ic ol . 18 (2 019) (mouse study

finding subchronic and chronic exposure

to glyphosate-based herbicides led to

numerous cognitive abnormalities and

various potentially explanatory biochemical

changes);

• Quixing Mao et al., The Ramazzini Institute

13-Week Pilot Study on Glyphosate and

Ro un dup Admini st ered at Hum anEquivalent Dose to Sprague Dawley Rats:

34

Effects on the Microbiome, 17 E n v tl .

Health 50 (2018) (finding exposure to

glyphosate-based herbicides in utero and for

six days after birth at doses considered safe

for humans significantly altered diversity of

gut microbiota in rat pups, while mothers

were unaffected; describing possibility

of significant downstream health effects

related to microbiome disruption);

• Ma r ía-A ránza zu Ma r tínez et a l.,

Neurotransmitter Changes in Rat Brain

Regions Following Glyphosate Exposure,

161 Envtl . Res . 212 (2018) (finding oral

glyphosate exposure in rats significantly

altered central nervous system (CNS)

monoaminergic neurotransmitters in a brain

regional- and dose-related manner, which

could potentially affect mood, memory, and

motor control);

• Cristina Eugenia Gallegos et al., Perinatal

Glyphosate-Based Herbicide Exposure in

Rats Alters Brain Antioxidant Status,

Glutamate and Acetylcholine Metabolism

and Affects Recognition Memory, 34

Neurotox . R es . 363 (2018) (concluding

exposure to glyphosate-based herbicide

during early stages of rat development

affects brain oxidative stress markers

and activ ity of en z y mes i nvolved i n

biochemical systems, which contribute to

neurotransmission disruption, and cognitive

deficits in offspring);

35

• Maria M. Milesi et al., Perinatal Exposure

to a Glyphosate-Based Herbicide Impairs

Female Reproductive Outcomes and

Induces Second- Generation Adverse

Effects in Wistar Rats, 92 A rch.Toxicol.

2629 (2018) (concluding perinatal exposure

to low doses of glyphosate-based herbicide

in food impaired female reproductive

performance and induced fetal growth

retardation and structural congenital

anomalies in offspring);

• Daiane Cattani, et al., Developmental

Exposure to Glyphosate-Based Herbicide

and Depressive-Like Behavior in Adult

Offspr ing: Implication of Glutamate

Excitotoxicity and Oxidative Stress, 387

Toxicol. 67 (2017) (investigation regarding

effects of subchronic exposure to GBH

on some neurochemical and behavioral

parameters in immature and adult rat

offspring exposed to glyphosate in utero

and through drinking water, finds various

biochemical disruptions and depressive

behaviors);

• Gilles-Eric Séralini et al., Republished11

study: Long-term Toxicity of a Roundup

11

11. The study was retracted after its original publication in

a different journal in 2012. See Retraction notice to “Long term

toxicity of a Roundup herbicide and a Roundup-tolerant genetically

modified maize,” 63 Food & Chem. Tox. 244 (Jan. 2014). Emails later

revealed that prior to the retraction, Monsanto “engaged with a

network of scientists and other commentators to spread the message

36

Herbi c i d e an d a Ro un dup -t ol er ant

Genetically Modified Maize, 26 Envtl .

Sci. Eur. 14 (2014) (First full-lifespan (2

year) rat study finding long-term exposure

to glyphosate-tolerant GM maize and lowdose Roundup in drinking water associated

w ith increased cancer risk, liver and

kidney toxicity, and endocrine/metabolic

disturbances);

• Da i a ne Cat t a n i et a l., Mech ani s m s

Underlying the Neurotoxicity Induced by

Glyphosate-Based Herbicide in Immature

Ra t Hip p o c a mp u s: Inv olv e m e n t of

Glutamate Excitotoxicity, 320 Toxicol. 34

(2014) (investigating whether Roundup leads

to neurotoxicity in hippocampus of immature

rats following acute and chronic (pregnancy

and lactation) exposure, finding Roundup

might lead to excessive extracellular

glutamate levels and consequently to

glutamate excitotoxicity and oxidative

stress in rat hippocampus);

• A nthony Samsel & Stephanie Seneff,

Glyphosate’s Suppression of Cytochrome

P450 Enzymes and Amino Acid Biosynthesis

by the Gut Microbiome: Pathways to

Modern Diseases 15 Entropy 1416 (2013)

that the Seralini paper was bad science and should be retracted.”

Retraction Watch, Unear thed emails: Monsanto connected

to campaign to retract GMO paper, https://retractionwatch.

com/2017/08/10/unearthed-docs-monsanto-connected-campaignretract-gmo-paper/.

37

(linking glyphosate to gut dysbiosis and a

cascade of diseases through disruption of

critical enzyme, which manifests over time

as inflammation, damaging cellular systems

throughout body);

• Michael N. Antoniou et al., Teratogenic

Effects of Glyphosate-Based Herbicides:

Divergence of Regulatory Decisions from

Scientific Evidence, 4 J. of Envtl. & A nal.

Toxicol. 006 (2012) (synthesizing evidence

from existing studies showing glyphosatebased herbicides can interfere with crucial

developmental pathways, causing birth

defects; arguing that European regulatory

agencies favor non-publ ic, industr ysponsored data over independent evidence

that shows developmental toxicity);

• Eliane Dallegrave et al., The Teratogenic

Potential of the Herbicide Glyphosate–

Roundup in Wistar Rats, 142 Toxicol .

Lett. 45 (2003) (pups exposed to varying

doses of glyphosate in utero from days 6-15

of gestation showed congenital deformities

at a rate inversely proportional to dosing

level; nearly all pups had retarded skeletal

development and edema related to organ

failure).

If these studies suggest anything with respect to the

EPA’s glyphosate decisions, it is that the EPA is failing

children, and should have increased the 10X safety factor,

rather than eliminating it.

38

ARGUMENT

This Court Should Allow States to Protect Children

from Exposure to Chemicals, Including Glyphosate,

Whose Harmful Effects on Children the EPA has

Failed to Recognize.

In Bates v. Dow Agrosciences L.L.C., this Court

recognized “the importance of providing an incentive to

manufacturers to use the utmost care in the business of

distributing inherently dangerous items.” 544 U.S. 431,

449-50 (2005). Moreover, the Court noted that in the

context of FIFRA, “tort suits can serve as a catalyst” for

ensuring and improving product safety:

By encouraging plaintiffs to bring suit for

injuries not previously recognized as traceable

to pesticides such as [the pesticide there at

issue], a state tort action of the kind under

review may aid in the exposure of new dangers

associated with pesticides. Successful actions

of this sort may lead manufacturers to petition

EPA to allow more detailed labelling of their

products; alternatively, EPA itself may decide

that revised labels are required in light of

the new information that has been brought

to its attention through common law suits. In

addition, the specter of damage actions may

provide manufacturers with added dynamic

incentives to continue to keep abreast of all

possible injuries stemming from use of their

product so as to forestall such actions through

product improvement.

39

Id. at 431 (brackets in Court’s opinion; internal quotation

marks and citation omitted).

The need for safety incentives is nowhere greater than

in the realm of child welfare, and the rationale from Bates

v. Dow Agrosciences is fully applicable here. Especially

because new information about the ill effects of glyphosate

on children continues to emerge on a regular basis, statelaw failure-to-warn actions are essential catalysts for

safety. States must be allowed to protect children from the

risks of glyphosate by requiring warnings fully disclosing

those risks.

CONCLUSION

Over the last thirty years, two trends in the federal

government have worked synergistically to undermine

protection of children’s health: (1) federal preemption of

state laws that would otherwise incentivize safety and

protect children against potentially harmful products to

which they are routinely exposed (often without informed

consent); and (2) federal regulators’ failure to ensure that

these products are safe for children, a failure due in part to

the regulators’ use of outdated studies that fail to account

for children’s unique vulnerability or their current level

of real-world exposure.

For example, the Telecommunications Act of 1996 is

understood to bar states from regulating in connection

with health effects of radiofrequency (RF) radiation as

long as wireless facilities and devices comply with the

Federal Communications Commission’s RF radiation

emission limits. See, e.g., Cohen v. Apple Inc., 46 F.4th

1012, 1016 (9th Cir. 2022). In 1996, the FCC adopted RF

40

exposure guidelines that were not designed to protect

against what are now well-recognized non-thermal health

effects of RF radiation. Since 1996, the deployment of

wireless facilities and technology and the population’s

exposure to RF radiation have skyrocketed, and in 2021,

the U.S. Court of Appeals for the District of Columbia

ordered the FCC to explain why it ignored compelling

evidence of biological harms from exposure to RF

radiation when it declined an opportunity to update the

1996 guidelines–in particular, with respect to children.

See Envtl. Health Trust v. FCC, 9 F. 4th 893 (D.C. Cir.

2021).12 But despite children’s ever-increasing exposure to

RF radiation and mounting evidence of harm, the FCC has

continued to leave the guidelines in place. Thus, federal

preemption coupled with regulatory failure leaves children

vulnerable to harms from mounting real-world exposure

to wireless radiation.

Vaccines present a structurally similar problem. The

1986 National Childhood Vaccine Injury Act preempts

state laws that would otherwise allow lawsuits on behalf

of children injured by routine childhood vaccines, and

provides essentially blanket liability protection to vaccine

manufacturers and those who administer the vaccines.

This scheme leaves a regulatory vacuum: vaccine

manufacturers have little incentive to monitor and improve

the safety of their products. See Bruesewitz v. Wyeth

LLC, 562 U.S. 223, 250 (2010) (Sotomayor, J., dissenting).

Since 1986, the number of vaccines recommended and

mandated for routine childhood use has skyrocketed.

However, the federal agencies charged with ensuring

vaccine safety have failed to study (among other things)

12. CHD was one of several petitioners in EHT v. FCC.

41

the full safety profiles of individual vaccines, exposure

to multiple vaccines at once, and cumulative exposure to

vaccines over time. Thus, just as with wireless radiation,

federal preemption coupled with regulatory failure leaves

children vulnerable to harms from mounting real-world

exposure to vaccines.

While a similar situation is threatened in the

context of pesticides, this case presents an opportunity

to interrupt these troubling trends.For the sound legal

reasons articulated in the Respondent’s brief, along with

the policy considerations articulated here, this Court

should uphold the decision below.

Respectfully submitted,

Kim Mack Rosenberg

General Counsel

Risa Evans

Senior Staff Attorney

Eileen Hansen

Legal Fellow

Children’s Health Defense

852 Franklin Avenue,

Suite 511

Franklin Lakes, NJ 07417

Mary S. Holland

Counsel of Record

Chief Executive Officer

Children’s Health Defense

852 Franklin Avenue,

Suite 511

Franklin Lakes, NJ 07417

(202) 417-6971

mary.holland@

childrenshealthdefense.org

Counsel for Amicus Curiae