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Human Health: and Pesticides

This document provides an overview of the potential health effects of two common pesticides, 2,4-D and glyphosate. It discusses risks of both acute and chronic exposure to these pesticides, including increased risks for children, impacts on reproductive health and pregnancy outcomes, neurological effects, and several types of cancer. The document also notes that pesticide exposure can have intergenerational impacts through epigenetic changes and that residential and municipal exposure presents health risks beyond just occupational exposure.

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0% found this document useful (0 votes)
111 views26 pages

Human Health: and Pesticides

This document provides an overview of the potential health effects of two common pesticides, 2,4-D and glyphosate. It discusses risks of both acute and chronic exposure to these pesticides, including increased risks for children, impacts on reproductive health and pregnancy outcomes, neurological effects, and several types of cancer. The document also notes that pesticide exposure can have intergenerational impacts through epigenetic changes and that residential and municipal exposure presents health risks beyond just occupational exposure.

Uploaded by

Laney Sommer
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
You are on page 1/ 26

HUMAN HEALTH

AND PESTICIDES:
GLYPHOSATE AND 2,4-D

Midwest Pesticide Action Center


2015

Contents
Introduction..................................................................................................................2
I.

2,4-Dichlorophenoxyacetic acid (2,4-D)................................................................3


Acute & Chronic Exposure........................................................................................... 3

II. Glyphosate...........................................................................................................3

Acute & Chronic Exposure........................................................................................... 4
III.


Childhood-Specific Risks.......................................................................................4
Childhood-Specific Risks: Neurodevelopmental Impairments..................................... 5
Childhood-Specific Risks: Cancer................................................................................ 6
Childhood-Specific Risks: Asthma................................................................................ 6

IV.









Reproductive Health/Pregnancy...........................................................................7
Reproductive Health: Endocrine Disruption................................................................ 7
Glyphosate and 2,4-D Endocrine Disruption............................................................... 7
Reproductive Health: Importance of Prenatal Development....................................... 8
2,4-D and Prenatal Development................................................................................ 9
Glyphosate and Prenatal Development....................................................................... 9
Reproductive Health: Autism....................................................................................... 10
Reproductive Health: Neurodevelopmental Impairments from Prenatal Exposure..... 10
Glyphosate and Neurodevelopmental Impairments.................................................... 10
Reproductive Health: Male Fertility............................................................................. 11
2,4-D and Male Fertility............................................................................................... 11

V.

Epigenetics: Inheritance of Pesticide Damage.....................................................11

2,4-D and Genetics.............................................................................................................. 12



Glyphosate and Genetics............................................................................................. 12
VI.






Health Effects on the General Population............................................................13


General: Neurological and Parkinsons........................................................................ 13
General: Cancer........................................................................................................... 14
2,4-D and Cancer......................................................................................................... 14
Non-Hodgkin Lymphoma............................................................................................ 15
Prostate Cancer............................................................................................................ 15
Pancreatic Cancer........................................................................................................ 16
Breast Cancer............................................................................................................... 16

VII. Systematic Concerns............................................................................................16


VIII. Moving Forward...................................................................................................18
References....................................................................................................................19

MIDWEST PESTICIDE ACTION CENTER

Introduction
Pesticides are a wide array of chemicals that are used to prevent unwanted pests, including insects,
plants, molds, and animals. The term pesticide is an umbrella term that includes insecticides,
herbicides, fungicides, and rodenticides. Most pesticides contain chemicals that can be harmful
to humans,1 and exposure to these chemicals can cause illnesses (ranging from mild irritation to
severe poisoning, seizures, and death2). Pesticides are a class of biocides, designed to interfere with
the biological processes of living beings. An unintended consequence of their ability to kill pests,
pesticides have been found to injure the human body as well, affecting critical bodily functions
such as the nervous system and hormone regulation.3
This report will provide an overview of the health effects associated with the use of 2,4-D and
glyphosate, two pesticides commonly found in Weed and Feed products. Weed and Feed products
(combination herbicide-fertilizers) merit attention due to the high volume of their use in the U.S.,
Weed and Feed products are commonly used on gardens, lawns, parks, recreational fields, and
playgrounds, and the potential human health risks of exposure. In the most recent year of U.S.
Environmental Protection Agency (EPA) data, approximately 89 million pounds of Weed and
Feed-type products were used in the non-agricultural sector, comprised of the home and garden,
industrial, government, and commercial markets. 4 2,4-D and glyphosate are toxins that have been
linked to a variety of cancers, as well as reproductive, neurological, and respiratory health issues,
and are especially harmful to children.2
Pesticide use and exposure can have serious short and long-term effects on human health, with
increased risks for continued contact. In addition to exposure to Weed and Feed products, humans
face pesticide exposure indoors in homes, schools, places of work, and from agriculture, as well
as from pesticide spray drift, the airborne movement of pesticide applications to contaminate other
areas. Those at the highest risk are workers who are exposed to pesticides on a regular basis, as well
as children, pregnant women, those living in agricultural areas, the elderly, asthmatics, and those
with chronic illnesses.5 Studies have shown, however, that pesticide exposure is a serious health
risk not only for those with daily occupational contact typically farmworkers and professional
landscapers but also for those who encounter pesticides at chronic low levels through residential
or municipal exposure. Associated chronic health risks include cancer, and neurodegenerative,
neurobehavioral, and reproductive effects. A report led by the National Cancer Institute (NCI), a
branch of the National Institutes of Health, states that evidence clearly suggests that at current
exposures pesticides adversely affect human health.6
Much of the research exploring the health effects of pesticides has been conducted in agricultural
regions, due to those regions having both higher rates of pesticide application and more reliable data
measuring pesticide use. These studies are still helpful in understanding the effects of pesticide use
on the general public health. Though applied in a different manner and at different concentrations,
the same active ingredients used in most home and garden pest control products can be found in
large-scale agricultural operations. Furthermore, it is not certain that those living in agricultural
areas face the highest level of ambient pesticide exposure inexpert pesticide users tend to face far

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higher levels of exposure than intended by safety regulations.7 Misuse and overuse of pesticides in
domestic situations is common. A study by the Australian Environment Protection Authority found
private residents applying herbicides at five times the recommended rate.7 This study also found
that homeowners tend to apply pesticides at higher than recommended rates, using more pesticides
per hectare than farmers, likely due to a lack of expertise and training. Pesticides are easily tracked
indoors via adherence to shoes and clothing, which can result in increased and continued exposure
in the home.8 Urban environments also pose unique health hazards, since pesticides take far longer
to biodegrade indoors and exposure is concentrated.9

I.

2,4-Dichlorophenoxyacetic acid (2,4-D)


2,4-D is one of the most commonly used active ingredients in herbicides, and is the most
used active ingredient in the entire U.S. non-agricultural sector; ranking first in the home
and garden market, as well as the industrial, commercial, and government sectors.4 2,4-D
is a synthetic plant hormone which kills plant life by changing the way plant cells grow,
causing the plant cells to divide and grow uncontrollably until tissue damage and plant
death occurs.10 It was first developed by scientists for its potential in chemical warfare,
and was one of the active ingredients in Agent Orange used in the Vietnam War. The EPA
estimates annual domestic usage of 2,4-D is approximately 46 million pounds per year,
used for weed control.11 Annually, 30 million pounds are used in agriculture and 16 million
pounds are used in non-agricultural settings. Approximately 8,740,000 pounds (19% of
total annual 2,4-D use in the U.S.) of 2,4-D are applied by homeowners and landscapers
every year.11

Acute & Chronic Exposure


According to the EPA chemical toxicity report on 2,4-D, acute exposure to high concentrations
of this chemical can cause stupor, coma, coughing, burning sensations in lungs, loss of
muscular coordination, nausea, vomiting, and dizziness.12 Acute exposure to 2,4-D can
result in skin and eye irritation. Fatal outcomes from 2,4-D exposure have resulted from
renal failure, electrolyte imbalance, and multiple organ failures.13 2,4-D is highly toxic and
has been linked to increased incidence of cancer and damage to reproductive systems. The
human health effects of chronic 2,4-D exposure reported for adults include blood, liver,
and kidney toxicity; a reduction in hemoglobin and red blood cell numbers, decreased liver
enzyme activity, and increased kidney weight.12

II.

Glyphosate
Glyphosate is the most used active ingredient in pesticides used within the U.S. agricultural
sector, and has been for the most recent six years of EPA data. Over 180 million pounds
were applied to agricultural lands in the most recent year of recorded data.4 Glyphosate is
the second-most used active ingredient in the U.S. non-agricultural sector 13-15 million
pounds are used annually by the industrial and government sectors, and 5-8 million pounds
are used in the home and garden market alone. Glyphosate is more commonly known by

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its most popular brand name, Roundup, though it is contained in many other products.
Glyphosate is a popular active ingredient in Weed and Feed products, present in over 750
products in the U.S. alone.14 The EPA has stated that, based on its current level of use in
the U.S., both occupational and residential exposure to glyphosate can be expected for the
general population.15
Glyphosate is a broad spectrum herbicide, which kills most types of plants by preventing
plant cells from producing proteins critical for growth and stripping micronutrients
necessary for the plant immune system function.

Acute & Chronic Exposure


Glyphosate has been ranked as a chemical of relatively low toxicity by the EPA since its
primary mechanism of action is upon plant cells; its high toxicity is often due to the inactive
ingredients which accompany it in a product.16 Pesticide products are a combination of an
active ingredient, the primary chemical responsible for killing or repelling pests, and an
undisclosed amount of other inert ingredients. Current regulations require neither the
inert ingredients nor the complete pesticide product to be tested for their effects on human
health. The inert ingredients are not chemically or toxicologically inert; rather, they are
protected as trade secrets, and remain unnamed to the public. In Roundup, one such
accompanying toxin has been identified as the surfactant TN-20, which greatly enhances
the cytotoxic (destructive to cells) effect of glyphosate.17 There is debate over whether
glyphosate itself is acutely toxic to humans; while agricultural companies point to the
EPA finding that glyphosate is low-toxicity, both glyphosate in isolation and Roundup
have been clinically proven to trigger placental and embryonic cell death in humans,18
and have been connected to many other health hazards. According to the EPA, acute
exposure to glyphosate can cause eye irritation, skin irritation, congestion of the lungs,
and increased breathing rate.19 Chronic exposure to glyphosate is known to cause kidney
damage, neurological impairment, and negative reproductive health effects. In the most
recent EPA re-registration of glyphosate, the agency did not include information regarding
acute inhalation toxicity or a study of occupational and residential exposure to glyphosate,
though both are usually required for chemical re-registration.20

III.

Childhood-Specific Risks
Pesticides are often used in school and childcare facilities, as well as on parks and playing
fields, though they pose a heightened health risk to children. Because they eat and drink
more than adults in proportion to their body weight, children receive higher doses of toxic
chemicals when exposed to pesticides in their surrounding environment, or through food
and water. As another result of their body size, children are closer to the floor and ground,
and this lower breathing zone increases their exposure if pesticides are present. Children
have a more rapid respiratory rate, taking in a greater volume of air per body weight
compared to adults, leaving them more vulnerable to the respiratory illnesses associated
with pesticide exposure.21 Prenatal and early childhood exposure is especially hazardous,

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as internal organs are still developing, are less able to detoxify chemicals, and are therefore
more vulnerable toxic exposures.22 Childhood activity patterns, including a high level of
hand-to-mouth activity, likely contribute to an increased oral ingestion of the pesticides in
their environment.23
Children exposed to pesticides indoors face heightened health risks. According to the U.S.
Centers for Disease Control and Prevention (CDC), humans spend approximately 90% of
their time indoors, and the air indoors can often be more polluted than outdoor air, even
in industrial city centers. The CDC asserts that for many people, especially children, risks
to health from indoor air pollution are greater than from outdoor air pollution.24 Children
exposed to pesticides indoors suffer from higher concentrations of the toxins to which
they are especially sensitive. Pesticide application is unlikely to remain isolated to the
area to which it is applied in a two-year long study conducted on Midwestern homes,
levels of 2,4-D inside the home were found to be ten times higher after an application
of 2,4-D to the lawn.25 The lack of exposure to external elements like sunlight, which
promote chemical degradation, leads to pesticides persisting longer indoors. As a result,
indoor exposure for young children in the home by non-dietary means of ingestion from
contact with floors, table tops, and contaminated dust in the air was ten times higher after
a lawn application. Children whose parents used garden insecticides were found to have
significantly higher levels of pesticide metabolites in their urine, for months after the last
application.26 Researchers concluded that garden pesticides and pesticide ingestion via diet
were the sources of elevated pesticide levels in children, and recommended that pesticide
use be avoided in areas where children play.
In a 2012 report, the American Academy of Pediatrics (AAP) recognized that the association
between pesticide exposure and childhood cancer, abnormal neurodevelopment,
asthma, perturbation of gestational growth, and endocrine-mimicking effects is greatly
concerning.27 Pesticides that affect the endocrine system like glyphosate are particularly
dangerous for children, as they disrupt the glands and hormones that facilitate regular
growth and development.28 The AAP noted specifically that the most comprehensive
reviews of the existing literature implicate an association of pesticides with leukemia and
brain tumors. The AAP as a whole, comprised of 60,000 primary care pediatricians and
pediatric specialists, issued a recommendation in 2012 that a serious effort be made to
reduce childhood contact with pesticide.29 As it stands, almost all children have contact
with pesticides in a study of pre-school aged children in Seattle, pesticide metabolites
(detectible pesticide residues found in urine samples) were found in 99% of children tested,
with at least two different pesticides present in approximately 75% of children tested.26

Childhood-Specific Risks: Neurodevelopmental Impairments


The brain and nervous system of a fetus, infant, or child, are particularly susceptible to
the effects of neurotoxic substances during vulnerable periods of development. During
the period of neurological development in utero through adolescent years exposure
to neurotoxins can result in developmental neurotoxicity. This can manifest as changes in

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functionality of the nervous system, including changes in cognition and behavior.30 Many
pesticides are neurotoxins the entire class of organophosphate pesticides, which includes
most insecticides, is neurotoxic. Even a very low level of exposure to neurotoxic pesticides,
during critical periods of fetal development, has been shown to fundamentally alter brain
architecture.31 Children with little or no pesticide exposure have a lower probability of
neurologic health risks.32
A 2010 study by the AAP found that children exposed to organophosphate pesticides are
more likely to meet the diagnostic criteria for ADHD.33 American Academy of Pediatrics
researchers examined over 1,100 children aged 8 to 15 as a representative sample of children
across the U.S., and found that children with higher than median levels of pesticide in their
urine were twice as likely to have ADHD. This study concluded that pesticide exposure, at
levels common among U.S. schoolchildren, may contribute to the prevalence of ADHD.
In 2008 the International Journal of Occupational Medicine and Environmental Health
published a study which found an association between childhood pesticide exposure and
neurodevelopmental and behavioral impairments.34 This study found that children exposed
to organophosphate pesticides, both prenatally and during childhood, may have difficulties
performing tasks that involve short-term memory, and may show increased reaction time,
impaired mental development or pervasive developmental problems. In newborns, the
effects of pesticide exposure were found to manifest as an increased number of abnormal
reflexes and increased reaction time; in adolescents, as mental and emotional problems.

Childhood-Specific Risks: Cancer


Childhood cancer risk is significantly increased by pesticide exposure at home and at
school facilities. A 2005 publication from the CDC National Institute for Occupational
Safety and Health found that pesticide exposure at schools produces acute illnesses among
students, and recommended that schools reduce child pesticide exposure and pesticiderelated illnesses by creating pesticide spray buffer zones around schools.35 A 2009 study
led by Georgetown University researchers found exposure to household pesticides to be
associated with a two-fold increase in risk for acute lymphoblastic leukemia (ALL), the most
common childhood cancer. Parents of children with ALL were twice as likely to be using
pesticides in the home.36 Children newly diagnosed with ALL were found to have elevated
levels of pesticide toxins in their urine. In a systematic review of all studies concerning
residential pesticide exposure and childhood leukemia from 1950-2009, prenatal and
childhood exposures to residential pesticides, insecticides, and herbicides were positively
associated with childhood leukemia.37 For children under ten, garden pesticide use has
been associated with an almost seven-fold increase in risk of leukemia.38

Childhood-Specific Risks: Asthma


Asthma is the most common chronic disease for children, whose lungs and airways are
still developing and are thus more vulnerable to respiratory illnesses.39 From 1980 to 1996,
childhood asthma prevalence in the U.S. doubled, and rates continue to rise.40 As of 2005,
nine percent of U.S. children have asthma. Many studies correlate pesticide exposure with

MIDWEST PESTICIDE ACTION CENTER

the development of childhood asthma, and may prove insightful in understanding why
asthma has become so widespread. Typically, the earlier in life that pesticide exposure
occurs, the more likely a child is of becoming asthmatic. In 2004, researchers from the
University of Southern Californias Keck School of Medicine found that children exposed
to herbicides in their first year of life were four and a half times more likely to be diagnosed
with asthma by the age of five.41 Children exposed to any pesticides in the first year of life
were approximately two and a half times more likely to be diagnosed with asthma by the
age of five. Researchers emphasized that infancy and early childhood is time when children
are most vulnerable to developing asthma.

IV.

Reproductive Health/Pregnancy
Reproductive health encompasses the diseases and disorders that affect the reproductive
system during all stages of life. Such disorders include reduced fertility, birth defects,
developmental disorders, preterm birth, and impotence. Pesticide exposure has been linked
to damage to reproductive health and the endocrine system. The herbicide atrazine, for
example, has been linked to abnormal sperm, menstrual disorders, and low birth weight.42
According to the National Institutes of Health, exposure to environmental pollutants and
endocrine disruptors may pose the greatest threat to reproductive health.43 The weight of
scientific evidence shows pesticide-related damage to human reproductive health, with
particularly high risks for pregnant women and fetuses.

Reproductive Health: Endocrine Disruption


The endocrine system is the collection of glands in the human body responsible for
regulating hormone levels. Many pesticides are endocrine disruptors, affecting critical
processes of hormone production that the body needs in order to maintain homeostasis,
the state of stable internal bodily functions.44 The EPA has found that disruption of the
endocrine system can result in reproductive disorders, birth defects, immune suppression,
and other harmful effects.45

Glyphosate and 2,4-D Endocrine Disruption


Both 2,4-D and glyphosate have been linked to disruption of the endocrine system. The
EPA has stated that based on current data regarding effects to the thyroid and gonads, there
is concern regarding the potential of 2,4-D to disrupt the human endocrine system.46 In
2009, the glyphosate herbicide Roundup was confirmed as both genotoxic (damaging to
cellular DNA) and an endocrine disruptor.47 At doses lower than what is commonly applied
in agriculture, Roundup caused endocrine disruption and cell death in human liver cells,
within 24 hours of introduction. Scientists observed endocrine system disruption which
had the potential to alter metabolism, development, and reproduction, as well as cause
hormone-dependent diseases like prostate and breast cancer. An additional university study
found Roundup disruptive to steroidogenesis (the production of steroids) in testicular cells
which produce testosterone, which plays a crucial role in male reproductive function.48
Exposure to Roundup disrupted StAR protein expression and reduced sex hormone

MIDWEST PESTICIDE ACTION CENTER

production in human testicular cells by 94 percent. The StAR protein, susceptible to


environmental pollutants, is responsible for the process by which all steroid hormones are
synthesized.
A 2005 study observed Roundups endocrine disrupting and toxic effects in the disruption
of human estrogen synthesis and messenger DNA.49 Exposure to Roundup, at subagricultural doses, was found toxic to human placental cells within 18 hours of exposure.
This study is an excellent example of the role inert ingredients play in pesticide toxicity, as
the commercial product Roundup (which is a combination of glyphosate and unspecified
inert ingredients) was found to be more toxic to placental cells than glyphosate alone. In
a follow-up study conducted in 2007, it was determined that although Roundup is more
toxic to embryonic and placental cells than glyphosate alone, glyphosate does act directly
as a partial inactivator of aromatase, the estrogen-producing enzyme. It was concluded
that Roundup exposure may affect human reproduction and fetal development, and that
chemical mixtures in formulations appear to be underestimated regarding their toxic or
hormonal impact.50

Reproductive Health: Importance of Prenatal Development


A mothers environmental and dietary pesticide exposures may translate directly to increased
toxic exposure for her fetus or newborn, in a process known as placental transfer. Certain
pesticide metabolites easily cross the placenta to reach the fetus. In 2011, researchers
found that when pregnant women consumed potatoes, corn, and soybeans that had been
genetically modified to be pesticide-tolerant, metabolites of one of the herbicides showed
up in the cord blood of 100 percent of their babies.51 Pregnant women exposed to pesticides
have been linked to a variety of adverse birth outcomes, including miscarriage, fetal death,
birth malformations, lowered birth weight, and embryonic cell death.
While the long-term health consequences of maternal pesticide exposure during pregnancy
are not fully known, research suggests that prenatal (in utero) and neonatal (in infancy)
exposure can manifest itself in a myriad of grave health consequences. Low-dose exposure
to neurotoxic pesticides in infancy may create modified responses to environmental
contaminants as adults. When exposed to toxic substances later in life, it can result in
hastened age-related degenerative changes, accelerating dysfunctional processes such as
impairment of learning and memory.52
In 2012, a group of childrens health experts published a study that measured the effects
of exposure to pesticides at low levels typical of ingestion through food or residential
exposure on pregnant women. The study found that the amount of pesticide exposure of
a pregnant woman was inversely proportional to length of gestational period and her babys
birth weight. The pregnant women with the highest exposure to pesticides delivered their
babies on average half a week earlier, with a starting birth weight on average one third of
a pound lighter.53 A team of scientists from Columbia Universitys School of Public Health
have also found that mother-newborn pairs with higher levels of insecticide detected in
their umbilical cord plasma at delivery had a birth weight on average 0.4 pounds lighter.54

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These researchers found that the level of pesticide in umbilical cord plasma was inversely
associated with birth length, with birth length decreasing by 0.24 cm for additional every
log unit of insecticide present in the plasma. This study concluded that insecticide exposure
impaired fetal growth, and emphasized the importance of phasing out residential use of
insecticide. Lowered birth weights are known to be associated with increased rates of
heart disease, stroke, hypertension, and diabetes.55 Scientists believe these negative health
associations are the result of fetal programming, whereby deficiency or damage at critical
stages of development has permanent effects on the bodys physiology and metabolism.
Exposure to toxins such as pesticides may be one type of damage that produces fetal
programming.

2,4-D and Prenatal Development


In 2005, Californias Office of Environmental Health Hazard Assessment formally
identified 2,4-D and its associated compounds to be reproductive toxicants, and lists 2,4D as a substance known to the State to cause reproductive toxicity.56 Maternal exposure
to 2,4-D has been linked to birth malformations in a major EPA study. In an examination
of the wheat-producing regions of the Midwest, this study found that infants conceived
from April to June the time of peak herbicide application had an increased chance
of circulatory and respiratory malformations.57 In regions with higher rates of herbicide
application, infant musculoskeletal anomalies increased, and male infant death resulting
from birth defects significantly increased. 2,4-D, at both agricultural and residential levels
of exposure, has been shown to produce developmental injury to embryos, by increasing
the incidence of embryonic cell death and reducing early gestation cell development in the
period corresponding to the first five to seven days of conception.58 Even at concentrations
assumed to be without adverse health consequences by regulatory agencies, reflecting
typical human exposure in the Midwest, exposure was damaging to reproduction and early
fetal development.

Glyphosate and Prenatal Development


Studies point to the hazard glyphosate poses to pregnant women and their fetal development.
A 2001 study by the Canadian Public Health department examined the effect of increased
pesticide exposure on embryonic and fetal death by tracking miscarriage in women who
reside on farms where pesticides are used. The study found that pre-conception maternal
exposure to glyphosate, along with other pesticides, increased risk of miscarriage.59 The
same study found an elevated risk of early-stage miscarriage (less than 12 weeks after
conception) associated with exposure to a family of herbicides that include 2,4-D. An
elevated risk of late-stage miscarriage (12-19 weeks after conception), or fetal death, was
associated with preconception exposure to glyphosate. The science suggests that exposure
to multiple pesticides leads to heightened risk, as the combination of certain chemicals may
be far more toxic than either in isolation. The human body now encounters this exposure
even before birth a 2005 study found an average of 200 industrial chemicals and pollutants
in the umbilical cord blood of newborns in the U.S, including waste products, flame
retardants, and pesticides.60 The general population faces exposure to pesticides and other

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toxins from both indoor and outdoor environments throughout a lifetime, many of which
bio-accumulate in the body long after exposure.61 Regarding miscarriage, exposure to more
than one type of pesticide among women over 35 led to a drastically increased risk. These
varied toxic inputs are health hazards, as many chemicals have the potential to amplify the
negative health effects of other chemicals. Specifically, those exposed to carbaryl and 2,4D together had 27 times the risk of miscarriage compared to similar women exposed only
to carbaryl.62

Reproductive Health: Autism


Autism, which the CDC reveals has increased 289.5% between 1997 and 2008,63 has been
extensively linked to both prenatal and neonatal pesticide exposure. A team of public
health experts recently identified a list of ten contaminants most likely to be linked to
the development of autism organophosphate pesticides, organochlorine pesticides, and
endocrine disruptors were all included on the list.64 Maternal residence during pregnancy
near pesticide applications has been linked to the development of autism spectrum disorders
in children. Mothers whose proximity to agricultural areas exposed them to pesticide drift
during early gestation (the first one to eight weeks of pregnancy) were found to be six
times more likely to have children with Autism Spectrum Disorders.65 Risk for autism
spectrum disorders in children increased with the number of pounds of pesticide applied,
and decreased with maternal distance from crop sites.

Reproductive Health:
Neurodevelopmental Impairments from Prenatal Exposure
Scientific studies suggest a troubling connection between prenatal pesticide exposure and
neurodevelopmental damage. In a 2006 study published by the AAP, children exposed
prenatally to higher levels of an insecticide were found to be significantly more likely
to experience delays in psychomotor (wherein children learn the relationship between
cognitive function and physical movement) and mental development, attention problems,
attention deficit/hyperactivity disorders, and pervasive developmental disorders by the age
of three.66 Children exposed to higher levels of the insecticide studied were five times more
likely to experience delays on the Psychomotor Development Index. This study focused on
children living in inner-city areas, where insecticides are more common than herbicides,
and is a helpful illustration of the fact that although the population faces different types of
pesticide exposure across the U.S., the human health impact is similarly destructive.

Glyphosate and Neurodevelopmental Impairments


Glyphosate and Roundup have been linked to negative neurodevelopmental health effects,
particularly for prenatal exposure. In a detailed examination of the effects of pesticide
exposure on reproductive outcomes in an agricultural region of Minnesota, scientists found
that conceptions in spring, at the height of pesticide application, resulted in significantly
more children with birth defects than found in any other season (7.6% vs. 3.7%). Fortytwo percent of children from families with recurrent birth defects were conceived in
spring, a significantly higher rate than that for any other season.67 Specifically, adverse

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10

neurobehavioral developmental effects were almost four times as likely for children with
parental glyphosate exposure. Roundup was found to be uniquely associated with specific
adverse birth or developmental outcomes 43% of children with ADD/ADHD had parents
who reported using Roundup.

Reproductive Health: Male Fertility


Male fertility has consistently been shown to suffer when confronted with pesticide
exposure. A 2013 systematic review of 17 studies on the effect of pesticides on sperm
found that there are significant associations between exposure to pesticide and semen
quality indicators.68 The most common finding, among all pesticide classes investigated,
was a decrease in sperm concentration. Decreased sperm motility and an overall decrease
in sperm health was also associated with exposure to all pesticides investigated.

2,4-D and Male Fertility


The EPA has listed a variety of negative effects that 2,4-D has on male sex organs, including
atrophy of the testes, degeneration of sperm-producing tissues, and decreased number of
sperm in the testes.69 Though it is well known that exposure to pesticides at occupational
levels can adversely affect semen quality, chronic low-level environmental exposure
to 2,4-D has also been linked decreased male fertility.70 Men from agrarian areas in the
U.S., merely by living in regions with higher ambient levels of pesticides, were found
to have higher levels of 2,4-D present in their body than men from urban centers, which
corresponded with poor semen quality and lower sperm concentration.

V.

Epigenetics: Inheritance of Pesticide Damage


The scientific study of the effects of pesticides on epigenetics is an important emerging
field that helps us understand the long-term, multi-generational consequences of pesticide
exposure. Epigenetics is the process of changing gene expression, while maintaining the
same DNA sequence, which occurs throughout everyones lifetime. This separate cellular
process regulates if and when certain genes are expressed, and is driven by the interaction
between genes and the environment. Epigenetic changes can include inactivation of
normally active genes, or the expression of genes that are typically silent such changes
in gene behavior can be responsible for the development of a wide variety of health issues,
from fetal growth restriction to diabetes and cancer. Persistent Organic Pollutants, or
POPs, are long-lasting chemicals like DDT that persist for decades in the environment.71
For their longevity, POPs are considered a potential source of environmental modification
of epigenetic responses in humans.
It is theorized that pesticide exposure is one environmental influence that can influence
transgenerational epigenetics when environmental cues result in heritable alterations to
genetic expression. In 2012, biologists researching inheritance of epigenetic responses
found that pesticide exposure in mice altered the way certain genes were activated, and that
change was passed down along generations, resulting in mental disorders and obesity.72

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Exposure to a pesticide as far as three generations back caused adverse health effects.
Studies demonstrate the same effect on human health. Parental exposure to pesticide
has already been linked to childhood cancer risk. Being the child of a licensed pesticide
applicator has been shown to increase risk of all childhood cancers. The risk of all
lymphomas increased two-fold and the risk of Hodgkins lymphoma specifically increased
as well for children of pesticide applicators.73 Parental failure to use chemically resistant
gloves in the course of pesticide application was associated with a further increased risk of
childhood cancer. Understanding epigenetics is especially important when considering the
effects of pesticides on reproductive health, as the most vital time for genetic development
is in the womb.

2,4-D and Genetics


2,4-D exposure has been associated with genetic damage. In 2004, medical researchers
discovered that a 2,4-D herbicide had genotoxic (damaging to cellular DNA) effects,
causing chromosome breakage in human blood cells.74In 2005, researchers found that
human exposure to 2,4-D, at environmentally realistic levels, can elicit gene expression
changes in genes that affect stress response, cell cycle control, immunology and DNA
repair.75 University of Minnesota researchers studying U.S. pesticide applicators found that
the men with the highest level of 2,4-D metabolites in their urine had elevated hormone
levels and altered genomic stability. Frequency of chromosome aberrations correlated
to the volume of pesticide to which they were exposed.76 A study produced by Egyptian
geneticists found that 2,4-D caused chromosome breakage in bone marrow cells of mice.77
Though is not known how damaging the cumulative effect of such genetic alterations may
be, genetic damage has the potential to cause irreversible adverse effects, which is why
many health experts advise that all efforts be made to limit pesticide exposure.

Glyphosate and Genetics


Recent science has associated glyphosate, isolated from any accompanying inert
ingredients, with dangerous consequences for human genetics. A 2013 study found
that ingesting glyphosate residues through diet is biologically disruptive, damaging gut
bacteria necessary for detoxification, and inducing disease.78 Researchers at MIT found
that glyphosates damage to the immune system and the gastrointestinal tract facilitates the
development of most diseases associated with the Western diet, including obesity, diabetes,
heart disease, depression, autism, infertility, cancer and Alzheimers disease. Researchers
characterized glyphosates negative impact as insidious, causing slow and steady damage
to cellular systems by blocking enzymes the body relies on for detoxification. The study
concluded that glyphosate is the textbook example of a disruption of homeostasis by an
environmental toxin.

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VI.

Health Effects on the General Population


Studies have shown that the negative health effects of pesticide exposure reach not only
higher-risk groups such as children and pregnant women, but the general population as
well, particularly in the form of cancers and neurological effects. Significantly, many
studies have founds links to these serious diseases in otherwise healthy groups of people
who face elevated pesticide exposure by means of occupational contact, and even those
who encounter only ambient (non-occupational) levels of pesticide.

General: Neurological and Parkinsons


There is extensive scientific literature showing strong associations between pesticide
exposure and serious neurological damage, particularly Parkinsons disease. Individuals
exposed to pesticides have been found to be 70% more likely to contract Parkinsons
than those not exposed.79 According to an NCI review of scientific literature concerning
the health effects of chronic pesticide exposure, there is very strong support for the link
between pesticide exposure and Parkinsons disease. 80
Parkinsons disease is a degenerative central nervous system disorder, which progresses
from motor function decline to cognitive decline and dementia, with a high associated
mortality risk. In a 2013 meta-analysis of over 100 studies, researchers found that exposure
to pesticides and solvents is associated with an elevated risk of Parkinsons disease.81 Rural
living in general, for its increased environmental exposure to pesticides, also increases risk
of Parkinsons. In another meta-analysis, public health experts concluded that in a majority
of peer-reviewed studies, environmental factors such as rural living and farming elevate
risk of Parkinsons. Pesticide exposure elevated risk an average of two-fold across all
studies examined.82 Still another meta-analysis found that 17 out of 19 studies examined,
exposure to pesticide was linked to an increased risk of Parkinsons, with risk increasing
with increased duration of exposure.83
A 2011 study led by researchers at the University of California Los Angeless School of
Public Health found that ambient residential (home or garden) and workplace pesticide
exposure can greatly increase risk of Parkinsons.84 In this study, those with ambient
workplace exposure to certain pesticides had a three-times higher risk of Parkinsons.
Younger onset Parkinsons was associated with those who faced both ambient workplace
exposure and ambient residential exposure. Those exposed to certain combinations of
pesticides experienced the greatest increase in Parkinsons risk, which led the authors
of this study to suggest that pesticides affecting different mechanisms that contribute to
neuron death may act together to increase the risk of Parkinsons disease considerably.
With regards to neurobehavioral performance and neurological disease, NCI researchers
found that studies indicate chronic pesticide exposure is associated with deficits in cognitive
function and psychomotor function, as well as Alzheimers disease and dementia.85
In another study, chronic exposure to pesticides has been associated with impaired
performance on neuropsychological tests; scores for memory, attention, verbal fluency and

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abstract thinking were all lowered with increased pesticide exposure. Low performance
on neuropsychological tests was found to be more than twice as likely for those who had
chronic pesticide exposure. Information selection and information processing were the
most affected.86 The authors concluded that these results may be indicative of long-term
progressive neurological degenerative changes brought on by pesticide exposure.

General: Cancer
The weight of scientific evidence suggests that occupational exposure to pesticides is
carcinogenic. A carcinogen is a substance or exposure capable of causing cancer in living
tissue.87 The World Health Organizations International Agency for Research on Cancer,
responsible for the most widely used carcinogenic classification system, has been one of
many expert agencies to have cautioned about the carcinogenic effects of pesticide. The
IARC has designated the spraying and application of insecticides a probable human
carcinogen, its second-highest classification cancer-causing potential.88 Using its own
evaluator model, the EPA has found dozens of pesticides likely to be carcinogenic
to humans.89 2,4-D still has not yet undergone a complete evaluation by the EPA for its
carcinogenic potential,90 though the EPA acknowledges that 2,4-D has demonstrated
neurotoxic and developmentally toxic effects.91 The EPA has set a deadline of 2015 to
review the available science on glyphosate and determine whether use of the chemical
should be controlled or restricted.92
According to a review by the NCI, existing scientific literature supports an association
between pesticides and the following types of cancer: non-Hodgkin lymphoma, leukemia
(particularly childhood leukemia), multiple myeloma (a malignancy of the plasma cells),
soft-tissue sarcoma, prostate cancer, pancreatic cancer, lung cancer, and ovarian cancer.93 In
a 2007 review of 10 years of studies on the relationship between pesticides and various types
of cancer, researchers found that pesticide exposure was positively associated with nonHodgkin lymphoma and leukemia in most studies.94 The most consistent associations for
pesticide exposure were brain and prostate cancer, and many studies also showed positive
associations between exposure and the development of solid tumors. Though most cancer
studies have been conducted on rural populations, pesticide use in other environments
carries the same risk. In a sixty year-long study of the mortality of pesticide applicators in
urban Rome, university researchers found a significantly increased risk for cancer of the
liver, gallbladder, and nervous system.95

2,4-D and Cancer


Other health effects of 2,4-D are more universally understood, such as the link to increased
cancer risk. In 2007, scientists studying the Cancer Registry of Central California found
that working in fields treated with 2,4-D is associated with increased rates of gastric
cancer.96 Agricultural workers who were routinely exposed to 2,4-D were found to be
almost twice as likely to develop gastric cancer. A study conducted by the EPAs National
Health and Environmental Effects Research Laboratory found increased cancer mortality
in the Midwest wheat-growing region, where chlorophenoxy herbicides, of which 2,4-D is

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the most prominent, usage is high.97 2,4-D is heavily used in wheat production, and high
wheat acreage regions are associated with statistically significantly higher rates of cancer
and cancer deaths. EPA scientists, assuming widespread ambient exposure of 2,4-D, have
indicted an association between 2,4-D exposure and general cancer mortality.

Non-Hodgkin Lymphoma
Exposure to herbicides generally leads to a significantly increased risk of non-Hodgkin
lymphoma.98 Two Swedish case-control studies showed an increased risk of non-Hodgkin
lymphoma from exposure to a wide range of pesticides. Herbicides, insecticides, and
fungicides were all found to be risk factors for lymphoma.99 Glyphosate exposure in
particular had a strong association, carrying a three-times higher risk for non-Hodgkin
lymphoma. The highest incidence of non-Hodgkin lymphoma occurred within 10 years of
exposure to the toxins. Like the U.S., Canada has seen a decades-long rise in non-Hodgkin
lymphoma. The Canadian Cancer Registries Epidemiology Research Group investigated
this matter in 2000, and found an increased risk of non-Hodgkin lymphoma for men exposed
to pesticides, with increased risk corresponding with increased duration of exposure to
herbicides. Excess risk of non-Hodgkin lymphoma among females was associated with
exposure to pesticides.100 Men and women who were exposed to herbicides for 15 years
or longer were 50 percent more likely to develop non-Hodgkin lymphoma. The authors
concluded that exposure to pesticides and other toxins plays an important role in the rise
of non-Hodgkin lymphoma, and that residential pesticide and herbicide use is of concern.

Glyphosate and Non-Hodgkin Lymphoma


Glyphosate has been extensively linked to non-Hodgkins lymphoma. A 2008 study
published in the International Journal of Cancer found that in a broad population sample
of males and females aged 18 to 74, those who had been exposed to glyphosate over the
course of their lifetime were over twice as likely to have non-Hodgkins lymphoma.101
Glyphosate was found specifically to be associated with a more than two-fold increase
in risk of in T-cell lymphomas, and an over three-fold increase in risk of lymphocytic
lymphoma. The risk of non-Hodgkins lymphoma for men exposed to glyphosate for just
two or more days per year was twice as high as the risk for men who were unexposed
or exposed for less than two days per year.102 Still another study labeled glyphosate as
potentially carcinogenic and found the chemical to be significantly associated with an
increased risk of non-Hodgkins lymphoma.103

Prostate Cancer
Researchers have concluded that certain pesticides have strong associations with prostate
carcinogenesis.104 In 2003, a major study led by an NCI researcher examined the relationship
between 45 common pesticides and incidence of prostate cancer, studying over 55,000
male pesticide applicators in the U.S. with no prior history of prostate cancer. 105 Compared
to prostate cancer rates of the general population, the men who regularly handled pesticides
were at a significantly increased risk of developing prostate cancer. Another study found
that Californian farm workers, who face higher environmental levels of pesticide exposure

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despite not being directly involved in pesticide application, have been found to experience
an elevated risk of prostate cancer.106 In 2011 the Keck School of Medicine at the University
of Southern California, using a population-based cancer registry, found evidence of an
association between ambient pesticide exposures in and around homes in agricultural areas
and prostate cancer. Environmental exposure to certain pesticide compounds was found to
have a role in prostate carcinogenesis.107

Pancreatic Cancer
Occupations with high level pesticide exposure have been associated with an increased
risk of pancreatic cancer. In a study of occupational hazards in Spain, of all occupations
studied, pesticide exposure was one of only a few occupational hazards to be associated
with a three-fold increase in risk of pancreatic cancer.108 Most individuals with highest
risk of pancreatic cancer were farmers, workers employed in agricultural industries, or
landscapers. Authors concluded that pesticide exposure leads to an increased risk of
pancreatic cancer. National Cancer Institute researchers confirmed this finding, in a study
that demonstrated occupational exposure to fungicides and herbicides led to excess risks
for pancreatic cancer. Authors concluded that increased amounts of pesticide exposure were
associated with a significantly increased risk of pancreatic cancer, and that the evidence
supports a finding of pesticides playing a role in human pancreatic carcinogenesis.109

Breast Cancer
Studies examining women in living in U.S. agricultural areas have shown an increased risk
of breast cancer. A 2004 study by NIH researchers found an elevated risk of breast cancer
for women who lived closest to sites of pesticide application.110A case-control study in
North Carolina found that women who reported being present in the fields during or shortly
after a pesticide application had elevated risk of breast cancer.111 Analyzing three years of
reported data on breast cancer rates, the authors concluded that women with higher pesticide
exposure may be more likely to develop breast cancer. Using acres of crops planted as a
proxy measure for level of pesticide exposure, one study found evidence for an association
between pesticide exposure and risk of breast cancer mortality.112

VII. Systematic Concerns


Overall, pesticide use in the U.S. has increased by about 7% since 1996, a change which
equates to the additional use of millions of pounds of pesticides per year.113 The U.S.
Geological Survey has found that in the U.S., over 90% of streams and over 50% of all
groundwater, both sources of drinking water, in both urban and agricultural areas contain
pesticides.114 Herbicide-resistant crop technology has led to a 527 million pound increase
in herbicide use in the U.S. between 1996 and 2011. This increased volume of pesticide
application is driven in particular by the spread of glyphosate-resistant weeds, as well as
genetically modified crops intended to withstand glyphosate treatment. The pervasiveness
of pesticides means that, increasingly, even those who choose not to use pesticides in
their homes will face ambient exposure. In the American Association of Pesticide Control

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Officials three most recent years of reported data (2002-2004) from the Pesticide Drift
Enforcement Survey given to state pesticide regulatory agencies, 2,4-D and glyphosate
were the two active ingredients most commonly involved in state-confirmed occurrences
of pesticide drift.115 Additionally, the total number of reports of pesticide drift received by
state pesticide regulatory agencies rose every year.
The EPA is the agency that assesses pesticides and other toxic chemicals for whether their
active ingredients pose unreasonable risks to humans. The EPA then sets limits on how
an approved pesticide may be used, including who may use it, how frequently it may
be used, where it may be used, and what protective clothing must be worn when in use.
Pesticides are considered for both their short term (acute) and long term (chronic) health
consequences. To learn what chemicals are at work in any given pesticide product, one
can look to the active ingredients and their concentrations as listed on the product label.
The same active ingredient can be found in hundreds of differently named products, while
products of similar names or brands can have entirely different active ingredients.
Pesticides are also labeled by the EPA as belonging to one of four Toxicity Categories which
are based on immediate risks brought on by exposure.116 Acute exposure to pesticides of
Toxicity Categories I and II is known to be fatal in high doses. Packaging for pesticides
in order of the three most severe Toxicity Categories are required to bear the signal words
danger-poison, warning, or, caution. Immediate health effects of pesticides can
range from mild, like slight skin irritation, to extremely serious, like irreversible damage
to ocular and skin tissue. While much is known by the medical community regarding
immediate treatment of acute exposure, understanding the long-term health effects and
carcinogenity of repetitive low-level exposure to pesticides remains a matter of grave
concern for scientists and regulators.
The pesticide toxicity ranking system currently in use in the U.S. is likely not sensitive
enough to the human health effects shown to be brought on by even low-dose exposure.
Chemical regulations are based on the assumption that higher doses are always more
dangerous, as such, any level of exposure below the safe dosage is assumed to be
without health risks. Yet a 2012 study found that endocrine-disrupting chemicals, including
pesticides, function in such a way that moderate doses are the least damaging, while very
low and very high doses are most dangerous to the human body.117 This means that the
chronic low-level exposure to pesticide which most Americans face may not be safe at
all, and that there may be no such thing as a safe dosage of endocrine-disrupting chemicals.
Scientists have suggested that another inadequate aspect of the EPAs model of premarket
toxicologic testing is its reliance on relatively short-term administration of a single active
ingredient to inbred strains of animals. This, scientists argue, does not reflect the reality of
human exposure to pesticides, which is far more likely to be a complex mix of compounds
over a lifetime, and may lead to products that negatively affect human health gaining
regulatory approval.118 It is impossible to fully see the human health impact of pesticide
exposure when utilizing an incomplete strategy, testing each chemicals effects in isolation.

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Though this report was limited to the effects of pesticides on human health, it is important
to note that pesticides have long-lasting damaging effects on the natural environment, by
contaminating ground water, lakes, and rivers, and disturbing the ecosystem by killing nontarget species.

VIII. Moving Forward


The scientifically demonstrated health effects of pesticide exposure call for a reduction in
use of these toxic chemicals. The precautionary principle is a scientific principle which states
that in situations where substances have a serious risk of harm but there exists scientific
uncertainty regarding the degree of risk, the danger should be assumed, and preventative
measures should be taken to protect the public health.119 The American Academy of
Pediatrics, American Public Health Association, World Health Organization, and California
EPA all advise limiting toxic chemical exposure under the precautionary principle.120121122
The European Union has codified the precautionary principle as law, specifically applied
to preventing pesticide exposure.123 The Los Angeles Unified School District, the second
largest school district in the U.S., has adopted the precautionary principle as a long-term
objective to reduce risk to students and employees as well as Integrated Pest Management
(IPM) as a pest control strategy.124 Integrated Pest Management is a strategy for pest control
which avoids the need for using chemical products by correcting the underlying sources of
pest problems, and can be applied to both indoor and outdoor environments. By adopting
the preventative mentality of the precautionary principle and IPM, the grave health risks of
pesticide exposure can be mitigated.

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References
1 What is a Pesticide? U.S. Environmental Protection Agency. May 2012. http://www.epa.gov/kidshometour/pest.htm
2 James R. Roberts, M.D., M.P.H; J. Routt Reigart, M.D. Recognition and Management of Pesticide Poisonings: 6th Edition.
U.S. Environmental Protection Agency. 2013.
http://www2.epa.gov/sites/production/files/documents/rmpp_6thed_final_lowresopt.pdf
3 James R. Roberts, M.D., M.P.H; J. Routt Reigart, M.D. Chronic Effects, Recognition and Management of Pesticide
Poisonings: 6th Edition. U.S. Environmental Protection Agency. 2013.
http://www2.epa.gov/sites/production/files/documents/rmpp_6thed_ch21_chroniceffects.pdf
4 A Grube, D Donaldson, T Kiely, L Wu. Pesticides Industry Sales and Usage: 2006 and 2007 Market Estimates. U.S.
Environmental Protection Agency. February 2011.
http://www.epa.gov/opp00001/pestsales/07pestsales/market_estimates2007.pdf
5 What are the Potential Health Effects of Pesticides? Recognizing and Reporting Pesticide Problems. California Department
of Pesticide Regulation. http://www.cdpr.ca.gov/docs/dept/comguide/effects_excerpt.pdf
6 M Alavanja, J Hoppin, F Kamel. Health Effects of Chronic Pesticide Exposure: Cancer and Neurotoxicity. Annual Review of
Public Health 2004; 25: 15597. DOI: 10.1146/annurev.publhealth.25.101802.123020
7 EPA Guidelines for Responsible Pesticide Use. Environment Protection Authority. December 2005.
http://www.epa.sa.gov.au/xstd_files/Water/Guideline/guide_pesticides.pdf
8 Marcia G. Nishioka, Robert G. Lewis, Marielle C. Brinkman, Hazel M. Burkholder, Charles E. Hines, John R. Menkedick.
Distribution of 2,4-D in Air and on Surfaces inside Residences after Lawn Applications: Comparing Exposure Estimates from
Various Media for Young Children. Environmental Health Perspectives 2001; 109: 11851191.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1240481/pdf/ehp0109-001185.pdf
9 P Landrigan et al. Pesticides in Inner-City Children: Exposures, Risk, and Prevention. Environmental Health Perspectives
1999; 107(3): 431-437. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1566233/pdf/envhper00520-0047.pdf
10 Re-registration Eligibility Decision for 2,4-D. U.S. Environmental Protection Agency. June 2005.
http://www.epa.gov/oppsrrd1/REDs/24d_red.pdf
11 2,4-D RED Facts. U.S. Environmental Protection Agency. June 2005.
http://www.epa.gov/oppsrrd1/REDs/factsheets/24d_fs.htm
12 2,4-Dichlorophenoxyacetic Acid (2,4-D) Chemical Summary. U.S. Environmental Protection Agency. March 2007.
http://www.epa.gov/teach/chem_summ/24D_summary.pdf
13 James R. Roberts, M.D., M.P.H; J. Routt Reigart, M.D. Chlorophenoxy Herbicides, Recognition and Management of
Pesticide Poisonings: 6th Edition. U.S. Environmental Protection Agency. 2013.
http://www2.epa.gov/sites/production/files/documents/rmpp_6thed_ch10_chlorophenoxys.pdf
14 Glyphosate. National Pesticide Information Center. Oregon State University and U.S. Environmental Protection Agency,
September 2010. http://npic.orst.edu/factsheets/glyphogen.pdf
15 R.E.D. Facts: Glyphosate. U.S. Environmental Protection Agency. September 1993.
http://www.epa.gov/oppsrrd1/REDs/factsheets/0178fact.pdf
16 James R. Roberts, Catherine J. Karr, and Council on Environmental Health. Technical Report: Pesticide Exposure in
Children. American Academy of Pediatrics. Pediatrics 2012; 130(6): e1765-e1788.
17 Glyphosates Suppression of Cytochrome P450 Enzymes and Amino Acid Biosynthesis by the Gut Microbiome: Pathways to
Modern Diseases, Entropy, 2013; 15(4): 1416-1463. http://www.mdpi.com/1099-4300/15/4/1416
18 Benachour N, Seralini GE. Glyphosate formulations induce apoptosis and necrosis in human umbilical, embryonic, and
placental cells. Chemical Research in Toxicology 2009; 22(1): 97-105. http://www.ncbi.nlm.nih.gov/pubmed/19105591

MIDWEST PESTICIDE ACTION CENTER

19

19 Technical Factsheet on: Glyphosate. U.S. Environmental Protection Agency.


http://www.epa.gov/safewater/pdfs/factsheets/soc/tech/glyphosa.pdf
20 R.E.D. Facts: Glyphosate. U.S. Environmental Protection Agency. September 1993.
http://www.epa.gov/oppsrrd1/REDs/factsheets/0178fact.pdf
21 G Solomon. Pesticides and Human Health: A Resource for Healthcare Professionals. Physicians for Social Responsibility.
http://www.psr-la.org/files/pesticides_and_human_health.pdf
22 Pesticides and Food: Why Children May be Especially Sensitive to Pesticides. U.S. Environmental Protection Agency.
2012. http://www.epa.gov/pesticides/food/pest.htm
23 James R. Roberts, Catherine J. Karr, and Council on Environmental Health. Technical Report: Pesticide Exposure in
Children. American Academy of Pediatrics. Pediatrics 2012; 130(6): e1765-e1788.
24 Chapter 5: Indoor Air Pollutants and Toxic Materials. Healthy Housing Reference Manual. U.S. Centers for Disease Control
and Prevention. 2009. http://www.cdc.gov/nceh/publications/books/housing/cha05.htm
25 Marcia G. Nishioka, Robert G. Lewis, Marielle C. Brinkman, Hazel M. Burkholder, Charles E. Hines, John R. Menkedick.
Distribution of 2,4-D in Air and on Surfaces inside Residences after Lawn Applications: Comparing Exposure Estimates from
Various Media for Young Children. Environmental Health Perspectives 2001; 109: 11851191.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1240481/pdf/ehp0109-001185.pdf
26 Lu C, Knutson DE, Fisker-Andersen J, Fenske RA. Biological Monitoring Survey of Organophosphorus Pesticide Exposure
Among Pre-School Children in the Seattle Metropolitan Area. Environmental Health Perspectives 2001; 109(3):299-303.
http://www.ncbi.nlm.nih.gov/pubmed/11333193
27 J Roberts, C J. Karr, Council on Environmental Health. Technical Report: Pesticide Exposure in Children. American
Academy of Pediatrics. Pediatrics 2012; 130(6): e1765-e1788.
28 http://www.epa.gov/pesticides/factsheets/kidpesticide.htm
29 AAP Makes Recommendations to Reduce Childrens Exposure to Pesticides. American Academy of Pediatrics. 11/26/12.
http://www.aap.org/en-us/about-the-aap/aap-press-room/Pages/AAP-Makes-Recommendations-to-Reduce-ChildrensExposure-to-Pesticides.aspx
30 D Rice, S Barone Jr. Critical Periods of Vulnerability for the Developing Nervous System: Evidence from Humans and
Animal Models. Environmental Health Perspectives 2000;108(3): 511-533.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1637807/pdf/envhper00312-0143.pdf
31 S G Selevan, CA Kimmel, P Mendola. Identifying critical windows of exposure for childrens health. Environmental Health
Perspectives 2000; 108(3): 451-455.http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1637810/
32 C Lu et al. Organic Diets Significantly Lower Childrens Dietary Exposure to Organophosphorus Pesticides. Environmental
Health Perspectives. 2006; 114(2): 260-263. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1367841/
33 Maryse F. Bouchard, David C. Bellinger, Robert O. Wright, Marc G. Weisskopf. Attention-Deficit/Hyperactivity Disorder and
Urinary Metabolites of Organophosphate Pesticides. Pediatrics 2010. DOI: 10.1542/peds.2009-3058
34 Hankei W, Jurewiczi J. Prenatal and Childhood Exposure to Pesticides and Neurobehavioral Development: Review of
Epidemiological Studies. International Journal of Occupational Medicine and Environmental Health 2008; 21(2):121-132.
DOI: 10.2478/v10001-008-0014-z
35 Alarcon WA,Calvert GM,Blondell JM,Mehler LN,Sievert J,Propeck M,Tibbetts DS,Becker A,Lackovic M,Soileau
SB,Das R,Beckman J,Male DP,Thomsen CL,Stanbury M. Acute illnesses associated with pesticide exposure at schools.
JAMA 2005; 294(4):455-65. http://www.ncbi.nlm.nih.gov/pubmed/16046652
36 O Soldin, H Nsouly-Maktabi, J M Genkinger, C A Loffredo, J A Ortega-Garcia, D Colantino, D B Barr, N L Luban, A T
Shad, D Nelson. Pediatric Acute Lymphoblastic Leukemia and Exposure to Pesticides. Therapeutic Drug Monitoring 2009;
31(4): 495-501. DOI: 10.1097/FTD.0b013e3181aae982

MIDWEST PESTICIDE ACTION CENTER

20

37 M Turner,D Wigle,D Krewski. Residential Pesticides and Childhood Leukemia: A Systematic Review and Meta-Analysis.
Environmental Health Perspectives 2010;118(1): 3341. DOI: 10.1289/ehp.0900966
38 Lowengart RA,Peters JM,Cicioni C,Buckley J,Bernstein L,Preston-Martin S,Rappaport E. Childhood Leukemia and
Parents Occupational and Home Exposures. Journal of the National Cancer Institute 1987; 79(1): 39-46.
http://www.ncbi.nlm.nih.gov/pubmed/3474448
39 Asthma. Media Center, Fact Sheet 307. May 2011, World Health Organization.
http://www.who.int/mediacentre/factsheets/fs307/en/
40 The State of Childhood Asthma, United States, 19802005. Advance Data from Vital and Health Statistics: Number 281. U.S.
Centers for Disease Control and Prevention. December 2006. http://www.cdc.gov/nchs/data/ad/ad381.pdf
41 Muhammad Salam,Yu-Fen Li,Bryan Langholz,Frank Gilliland, Childrens Health Study. Early-life environmental risk
factors for asthma: findings from the Childrens Health Study. Environmental Health Perspectives 2004;112(6): 760765.
DOI: 10.1289/ehp.6662
42 Atrazine. Toxicant and Disease Database. The Collaborative on Health and the Environment.
http://www.healthandenvironment.org/tddb/contam/2452
43 Reproductive Health. National Institute of Environmental Health Sciences. National Institutes of Health.
http://www.niehs.nih.gov/health/topics/conditions/repro-health/index.cfm
44 W Mnif, A Hadj Hassine,A Bouaziz,A Bartegi, O Thomas,B Roig. Effect of Endocrine Disruptor Pesticides: A Review.
International Journal of Environmental Research and Public Health 2011; 8(6): 22652303. DOI:10.3390/ijerph8062265
45 Children Are at Greater Risks from Pesticide Exposure. Health and Safety Fact Sheets. U.S. Environmental Protection
Agency. January 2002. http://www.epa.gov/pesticides/factsheets/kidpesticide.htm
46 Re-registration Eligibility Decision for 2,4-D. U.S. Environmental Protection Agency. June 2005.
http://www.epa.gov/oppsrrd1/REDs/24d_red.pdf
47 Gasnier C,Dumont C,Benachour N,Clair E,Chagnon MC,Sralini GE. Glyphosate-based herbicides are toxic and
endocrine disruptors in human cell lines. Toxicology 2009; 262(3): 184-191. DOI: 10.1016/j.tox.2009.06.006.
48 L. Walsh, C McCormick, C Martin, D Stocco. Roundup Inhibits Steroidogenesis by Disrupting Steroidogenic Acute
Regulatory (StAR) Protein Expression. Environmental Health Perspectives 2000; 108: 769-776.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1638308/pdf/envhper00309-0125.pdf
49 S Richard,S Moslemi,H Sipahutar,N Benachour, GE Seralini. Differential Effects of Glyphosate and Roundup on Human
Placental Cells and Aromatase. Environmental Health Perspectives 2005; 113(6): 716-720. DOI:10.1289/ehp.7728
50 Benachour N,Sipahutar H,Moslemi S,Gasnier C,Travert C,Sralini GE. Time- and dose-dependent effects of roundup on
human embryonic and placental cells. Archives of Environmental Contamination and Toxicology 2007; 53(1): 126-133.
http://www.ncbi.nlm.nih.gov/pubmed/17486286
51 Aris A,Leblanc S. Maternal and fetal exposure to pesticides associated to genetically modified foods in Eastern Townships of
Quebec, Canada. Reproductive Toxicology 2011; 31(4): 528-33. DOI: 10.1016/j.reprotox.2011.02.004
52 Eriksson P,Talts U. Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings.
Neurotoxicology 2000; 21(1-2): 37-47. http://www.ncbi.nlm.nih.gov/pubmed/10794383
53 S Rauch, J Braun, D Barr, A Calafat, J Khoury, M. A Montesano, K Yolton, B Lanphear. Associations of Prenatal Exposure
to Organophosphate Pesticide Metabolites with Gestational Age and Birth Weight. Environmental Health Perspectives 2012;
120:1055-1060. DOI: http://dx.doi.org/10.1289/ehp.1104615
54 R Whyatt, V Rauh, D Barr, D Camann, H Andrews, R Garnkel, L Hoepner, D Diaz, J Dietrich, A Reyes, D Tang, P Kinney,
F Perera. Prenatal Insecticide Exposures and Birth Weight and Length Among an Urban Minority Cohort. Environmental
Health Perspectives 2004; 112: 1125-1132. DOI:10.1289/ehp.6641

MIDWEST PESTICIDE ACTION CENTER

21

55 Godfrey KM,Barker DJ. Fetal Programming and Adult Health. Public Health Nutrition 2001; 4(2B): 611-24.
http://www.ncbi.nlm.nih.gov/pubmed/11683554
56 Chemicals Meeting the Criteria for Listing Via The Authoritative Bodies Mechanism: (2,4-Dichlorophenoxy) Acetic Acid
(2,4-D), 2,4-D N-Butyl Ester, 2,4-D Isopropyl Ester, 2,4-D Isooctyl Ester, 2,4-D Propylene Glycol Butyl Ether Ester (2,4-D
PGBE), 2,4-D Butoxyethanol Ester and 2,4-D Dimethylamine Salt. Office of Environmental Health Hazard Assessment,
Reproductive and Cancer Hazard Assessment Branch. California Environmental Protection Agency November 2005.
http://oehha.ca.gov/prop65/CRNR_notices/admin_listing/intent_to_list/pdf_zip/24DNOILjust.pdf
57 D Schreinemachers. Birth Malformations and Other Adverse Perinatal Outcomes in Four U.S. Wheat-Producing States.
Environmental Health Perspectives 2003;111(9): 12591264. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1241584/
58 A Greenlee, T Ellis, R Berg. Low-Dose Agrochemicals and Lawn-Care Pesticides Induce Developmental Toxicity in Murine
Pre-implantation Embryos. Environmental Health Perspectives 2004; 112: 703709. DOI:10.1289/ehp.6774 a
59 T Arbuckle, Z Lin, L Mery. An Exploratory Analysis of the Effect of Pesticide Exposure on the Risk of Spontaneous Abortion
in an Ontario Farm Population. Environmental Health Perspectives 2001; 109: 851857.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1240415/pdf/ehp0109-000851.pdf
60 Environmental Working Group. A Benchmark Investigation of Industrial Chemicals, Pollutants and Pesticides in Umbilical
Cord Blood. 2005. http://www.ewg.org/research/body-burden-pollution-newborns
61 Fourth National Report on Human Exposure to Environmental Chemicals. U.S. Centers for Disease Control and Prevention.
2013. http://www.cdc.gov/exposurereport/pdf/FourthReport_UpdatedTables_Mar2013.pdf
62 T Arbuckle, Z Lin, L Mery. An Exploratory Analysis of the Effect of Pesticide Exposure on the Risk of Spontaneous Abortion
in an Ontario Farm Population. Environmental Health Perspectives 2001; 109: 851857
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1240415/pdf/ehp0109-000851.pdf
63 Developmental Disabilities Increasing in the U.S. CDC Features. June 2011. U.S. Centers for Disease Control and
Prevention. http://www.cdc.gov/features/dsdev_disabilities/index.html
64 P Landrigan,L Lambertini,L Birnbaum. A Research Strategy to Discover the Environmental Causes of Autism and
Neurodevelopmental Disabilities. Environmental Health Perspectives 2012; 120(7): a258-a260. DOI:10.1289/ehp.1104285
65 E Roberts, P English, J Grether, G Windham, L Somberg, C Wolff. Maternal Residence Near Agricultural Pesticide
Applications and Autism Spectrum Disorders among Children in the California Central Valley. Environmental Health
Perspectives 2007; 115: 1482-1489.
66 L Hoepner, D Barr, R Whitehead, D Tang and R Whyatt, V Rauh, R Garfinkel, F Perera, H Andrews. Impact of Prenatal
Chlorpyrifos Exposure on Neurodevelopment in the First Three Years of Life Among Inner-City Children. Pediatrics 2006;
118: e1845. DOI: 10.1289/ehp.10168
67 V Garry,M Harkins,L Erickson,L Long-Simpson,S Holland, B Burroughs. Birth Defects, Season of Conception, and sex of
children born to pesticide applicators living in the Red River Valley of Minnesota, USA. Environmental Health Perspectives
2002; 110(3): 441-449. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1241196
68 Martenies SE,Perry MJ. Environmental and occupational pesticide exposure and human sperm parameters: A systematic
review. Toxicology 2013; 307: 66-73. DOI: 10.1016/j.tox.2013.02.005
69 C Cox. Herbicide Factsheet: 2,4-D. Journal of Pesticide Reform 2006; 25(4).
http://www.pesticide.org/get-the-facts/pesticide-factsheets/factsheets/24d-factsheet
70 S Swan, R Kruse, F Liu, D Barr, E Drobnis, J Redmon, C Wang, C Brazil, J Overstreet, Study for Future Families Research
Group. Semen Quality in Relation to Biomarkers of Pesticide Exposure. Environmental Health Perspectives 2003; 111: 14781484. DOI:10.1289/ehp.6417
71 Fourth National Report on Human Exposure to Environmental Chemicals. U.S. Centers for Disease Control and Prevention.
2009. http://www.cdc.gov/exposurereport/pdf/FourthReport.pdf

MIDWEST PESTICIDE ACTION CENTER

22

72 D Crews, R Gillette, S Scarpino, M Manikkam, M Savenkova, M Skinner. Epigenetic Transgenerational Inheritance


of Altered Stress Responses. Proceedings of the National Academy of Sciences of the United States. DOI: 10.1073/
pnas.1118514109
73 K Flower, J Hoppin, C Lynch, A Blair, C Knott, D Shore, D Sandler. Cancer Risk and Parental Pesticide Application in
Children of Agricultural Health Study Participants. Environmental Health Perspectives 2004; 112: 631-635. DOI: 10.1289/
ehp.6586
74 Zeljezic D,Garaj-Vrhovac V. Chromosomal aberrations, micronuclei and nuclear buds induced in human lymphocytes
by 2,4-dichlorophenoxyacetic acid pesticide formulation. Toxicology 2004: 200(1):39-47. http://www.ncbi.nlm.nih.gov/
pubmed/15158562
75 Bharadwaj L,Dhami K,Schneberger D,Stevens M,Renaud C,Ali A. Altered gene expression in human hepatoma HepG2
cells exposed to low-level 2,4-dichlorophenoxyacetic acid and potassium nitrate. Toxicology in Vitro 2005; 19(5): 603-619.
http://www.ncbi.nlm.nih.gov/pubmed/15878651
76 V Garry, R Tarone, I Kirsch, J Abdallah, D Lombardi, L Long, B Burroughs, D Barr, J Kesner. Biomarker Correlations of
Urinary 2,4-D Levels in Foresters: Genomic Instability and Endocrine Disruption. Environmental Health Perspectives 2001;
109: 495-500. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1240309/pdf/ehp0109-000495.pdf
77 Zeljezic D,Garaj-Vrhovac V. Chromosomal aberrations, micronuclei and nuclear buds induced in human lymphocytes by
2,4-dichlorophenoxyacetic acid pesticide formulation. Toxicology 2004l; 15: 200(1): 39-47.
http://www.ncbi.nlm.nih.gov/pubmed/15158562
78 A Samsel,S Seneff. Glyphosates Suppression of Cytochrome P450 Enzymes and Amino Acid Biosynthesis by the Gut
Microbiome: Pathways to Modern Diseases. Entropy 2013; 15(4): 1416-1463. DOI: 10.3390/e15041416
79 Ascherio, et al. Pesticide Exposure and Risk for Parkinsons Disease. Annals of Neurology 2006; 60(2): 197-203.
DOI:10.1002/ana.20904
80 M Alavanja, J Hoppin, F Kamel. Health Effects of Chronic Pesticide Exposure: Cancer and Neurotoxicity. Annual Review of
Public Health 2004; 25: 15597. DOI: 10.1146/annurev.publhealth.25.101802.123020
81 G Pezzoli, E Cereda. Exposure to Pesticides or Solvents and Risk of Parkinsons Disease. Neurology 2013; 80(22): 20352041. DOI:10.1212/WNL.0b013e318294b3c8
82 Priyadarshi A,Khuder SA,Schaub EA,Priyadarshi SS. Environmental Risk Factors and Parkinsons Disease: A Metaanalysis.
Environmental Research 2001; 86(2): 122-127. http://www.ncbi.nlm.nih.gov/pubmed/11437458
83 Priyadarshi A,Khuder SA,Schaub EA,Shrivastava S. A Meta-Analysis of Parkinsons Disease and Exposure to Pesticides.
Neurotoxicology2000; 21(4): 435-40. http://www.ncbi.nlm.nih.gov/pubmed/11022853
84 A Wang,S Costello,M Cockburn,X Zhang,J Bronstein, B Ritz. Parkinsons Disease Risk from Ambient Exposure to
Pesticides. European Journal of Epidemiology 2011; 26(7): 547-555. DOI:10.1007/s10654-011-9574-5
85 M Alavanja, J Hoppin, F Kamel. Health Effects of Chronic Pesticide Exposure: Cancer and Neurotoxicity. Annual Review of
Public Health 2004; 25: 15597. DOI: 10.1146/annurev.publhealth.25.101802.123020
86 I Baldi,L Filleul,B Mohammed-Brahim,C Fabrigoule,J F Dartigues,S Schwall,J P Drevet,R Salamon, andP Brochard.
Neuropsychologic effects of long-term exposure to pesticides: results from the French Phytoner study. Environmental Health
Perspectives 2001; 109(8): 839-844. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1240413/
87 Known and Probable Human Carcinogens. American Cancer Society. June 2011. http://www.cancer.org/cancer/
cancercauses/othercarcinogens/generalinformationaboutcarcinogens/known-and-probable-human-carcinogens
88 Occupational Exposures in Insecticide Application, and Some Pesticides. IARC Monographs on the Evaluation of
Carcinogenic Risks to Humans, Volume 53. International Agency for Research on Cancer, World Health Organization.
http://monographs.iarc.fr/ENG/Monographs/vol53/volume53.pdf

MIDWEST PESTICIDE ACTION CENTER

23

89 Chemicals Evaluated for Carcinogenic Potential. U.S. Environmental Pesticide Agency, Office of Pesticide Programs.
November 2012. http://npic.orst.edu/chemicals_evaluated.pdf
90 2,4-Dichlorophenoxyacetic acid (2,4-D) (CASRN 94-75-7). Integrated Risk Information System. U.S. Environmental
Protection Agency. 1987. http://www.epa.gov/iris/subst/0150.htm
91 2,4-D RED Facts. Pesticides: Reregistration. U.S. Environmental Protection Agency. June 2005.
http://www.epa.gov/oppsrrd1/REDs/factsheets/24d_fs.htm
92 Glyphosate Final Work Plan Registration Review Case No. 0178. U.S. Environmental Protection Agency. December 2009.
http://www.epa.gov/oppsrrd1/registration_review/glyphosate/
93 M Alavanja, J Hoppin, F Kamel. Health Effects of Chronic Pesticide Exposure: Cancer and Neurotoxicity. Annual Review of
Public Health 2004; 25: 15597. DOI: 10.1146/annurev.publhealth.25.101802.123020
94 K.L. Bassil, C. Vakil, M. Sanborn, D.C. Cole, J.S. Kaur, K.J. Kerr. Cancer Health Effects of Pesticides. Canadian Family
Physician 2007; 53(10): 17041711. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2231435/
95 Giordano F,DellOrco V,Giannandrea F,Lauria L,Valente P,Fig-Talamanca I. Mortality in a cohort of pesticide applicators
in an urban setting: sixty years of follow-up. International Journal of Immunopathology and Pharmacology 2006; 19(4):6165. http://www.ncbi.nlm.nih.gov/pubmed/17291409
96 Mills PK, Yang RC. Agricultural Exposures and Gastric Cancer Risk in Hispanic Farm Workers in California. Environmental
Research 2007; 104(2): 282-289. http://www.ncbi.nlm.nih.gov/pubmed/17196584
97 D M Schreinemachers. Cancer mortality in four northern wheat-producing states. Environmental Health Perspectives 2000;
108: 873881. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2556929/
98 M Eriksson, L Hardell, M Carlberg, M Akerman. Pesticide exposure as risk factor for non-Hodgkin lymphoma including
histopathological subgroup analysis. International Journal of Cancer 2008; 123(7): 1657-1663. DOI:10.1002/ijc.23589
99 Hardell L, Eriksson M, Nordstrom M. Exposure to pesticides as risk factor for non-Hodgkins lymphoma and hairy cell
leukemia: pooled analysis of two Swedish case-control studies. Leukemia and Lymphoma 2002; 43(5): 1043-1049.
http://www.ncbi.nlm.nih.gov/pubmed/12148884
100 Mao Y,Hu J,Ugnat AM,White K, Canadian Cancer Registries Epidemiology Research Group. Non-Hodgkins lymphoma
and occupational exposure to chemicals in Canada. Annals of Oncology 2000; 11(1): 69-73.

http://www.ncbi.nlm.nih.gov/pubmed/10707783
101 Mikael Eriksson, Lennart Hardell, Michael Carlberg, Mans Akerman. Pesticide Exposure as Risk Factor for Non-Hodgkin
Lymphoma including Histopathological Subgroup Analysis. International Journal of Cancer 2008; 123(7): 16571663
DOI:10.1002/ijc.23589
102 McDuffie H, Pahwa P, McLaughlin J, Spinelli J, Fincham S, Dosman J, Robson D, Skinnider L, Choi N. Non-Hodgkins
Lymphoma and Specific Pesticide Exposures in Men. Cancer Epidemiology, Biomarkers & Prevention 2001;10(11):115563. http://cebp.aacrjournals.org/content/10/11/1155.long
103 A J De Roos, S H Zahm, K P Cantor, D D Weisenburger, F F Holmes, L F Burmeister, A Blair. Integrative assessment of
multiple pesticides as risk factors for non-Hodgkins lymphoma among men. Occupational and Environmental Medicine
2003; 60(11). DOI: 10.1136/oem.60.9.e11
104 Mills PK, Yang R. Prostate Cancer Risk in California Farm Workers. Occupational and Environmental Medicine 2003;
45(3): 249-258. http://www.ncbi.nlm.nih.gov/pubmed/12661182
105

Use of Agricultural Pesticides and Prostate Cancer Risk in the Agricultural Health Study Cohort. American Journal of
Epidemiology. http://aje.oxfordjournals.org/content/157/9/800.full

MIDWEST PESTICIDE ACTION CENTER

24

106 Prostate Cancer Risk in California Farm Workers. Journal of Occupational Environmental Medicine. 2003.

http://www.ncbi.nlm.nih.gov/pubmed/12661182
107 Cockburn M,Mills P,Zhang X,Zadnick J,Goldberg D,Ritz B. Prostate cancer and ambient pesticide exposure in
agriculturally intensive areas in California. American Journal of Epidemiology 2011;173(11):1280-8. DOI: 10.1093/aje/
kwr003
108

J Alguacil, et al. Risk of Pancreatic Cancer and Occupational Exposures in Spain. The Annals of Occupational Hygiene
2000; 44(5): 391-403. http://annhyg.oxfordjournals.org/content/44/5/391.full.pdf

109 Ji BT,Silverman DT,Stewart PA,Blair A,Swanson GM,Baris D,Greenberg RS,Hayes RB,Brown LM,Lillemoe
KD,Schoenberg JB,Pottern LM,Schwartz AG,Hoover RN. Occupational Exposure to Pesticides and Pancreatic Cancer.
American Journal of Industrial Medicine 2001; 39(1): 92-99. http://www.ncbi.nlm.nih.gov/pubmed/11148019
110 E Lawrence et al. Pesticide Use and Breast Cancer Risk among Farmers Wives in the Agricultural Health Study. American
Journal of Epidemiology 2005; 161(2): 121-135. DOI: 10.1093/aje/kwi022
111 Duell EJ,Millikan RC,Savitz DA,Newman B,Smith JC,Schell MJ,Sandler DP. A Population-Based Case-Control Study
of Farming and Breast Cancer in North Carolina. Epidemiology 2000; 11(5): 523-531.

http://www.ncbi.nlm.nih.gov/pubmed/10955404
112 Abdalla MH,Gutierrez-Mohamed ML,Farah IO. Association of pesticide exposure and risk of breast cancer mortality in
Mississippi. Biomedical Sciences Instrumentation 2003; 39: 397-401. http://www.ncbi.nlm.nih.gov/pubmed/12724926
113 Benbrook, Charles. Impacts of genetically engineered crops on pesticide use in the U.S. -- the first sixteen years.
Environmental Sciences Europe2012,24:24.DOI:10.1186/2190-4715-24-24
114 Pesticides in the Nations Streams and Ground Water, 19922001A Summary. Fact Sheet 2006-3028. U.S. Geological
Survey. March 2006. http://pubs.usgs.gov/fs/2006/3028/
115 2005 AAPCO Pesticide Drift Enforcement Survey. American Association of Pesticide Control Officials. 2005.

http://aapco.org/documents/surveys/DriftEnforce05Rpt.html
116 Chapter 7: Precautionary Statements. Label Review Manual. U.S. Environmental Protection Agency. July 2012.

http://www.epa.gov/oppfead1/labeling/lrm/chap-07.pdf
117

L Vandenberg, T Colborn, T Hayes, J Heindel, D Jacobs Jr., D Lee, T Shioda, A Soto, F Saal, W Welshons, R Zoeller,
J Myers. Hormones and Endocrine-Disrupting Chemicals: Low-Dose Effects and Nonmonotonic Dose Responses.
Endocrine Reviews2012; 33(3):378-455. DOI:10.1210/er.2011-1050

118 M Alavanja, J Hoppin, F Kamel. Health Effects of Chronic Pesticide Exposure: Cancer and Neurotoxicity. Annual Review
of Public Health 2004; 25: 15597. DOI: 10.1146/annurev.publhealth.25.101802.123020
119 Grandjean P. Implications of the Precautionary Principle for Primary Prevention and Research. Annual Review of Public
Health 2004; 25: 199-223. http://www.ncbi.nlm.nih.gov/pubmed/15015918
120 The Precautionary Principle and Chemical Exposure Standards for the Workplace. Policy Statement Database. American
Public Health Association. January 1996. http://www.apha.org/advocacy/policy/policysearch/default.htm?id=124
121 October 2004 Environmental Justice Action Plan. California Environmental Protection Agency. October 2004.

http://www.calepa.ca.gov/envJustice/ActionPlan/Documents/October2004/ActionPlan.pdf
122 World Health Organization. The Precautionary Principle: Protecting Public Health, the Environment and the Future of Our
Children. International Journal of Epidemiology 2003; 32: 489-92.

http://www.euro.who.int/__data/assets/pdf_file/0003/91173/E83079.pdf
123 The Precautionary Principle. Summaries of EU Legislation. European Union. December 2011.

http://europa.eu/legislation_summaries/consumers/consumer_safety/l32042_en.htm
124 Los Angeles Unified School District Integrated Pest Management Policy. Los Angeles Unified School District. 2002.

http://www.laschools.org/employee/mo/ipm/docs/ipmpolicyretype.pdf

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