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Learning and Developmental Disabilities Research and Resources

Image from US Pacific Fleet at Creative Commons: Engineman 1st Class Floyd Johnson draws a picture with a child during a Community Service (COMSERV) event at the Bukit Harapan Children's Home, a nonprofit organization that houses mentally and physically disabled children who have been orphaned, abandoned due to their disabilities, or come from unstable family backgrounds.

Common developmental disorders and disabilities, with some conditions and classifications overlapping:1

*These conditions are described in more detail on other pages on this site and have only limited discussion here.

Environmental exposures are not necessarily linked to all the disabilities included here. On this page we focus on the connections between environmental exposures and disabilities.

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Developmental disabilities (DD) are broadly defined as severe, chronic conditions due to mental and/or physical impairments that develop by the age of 22.2 According to The Developmental Disability Assistance and Bill of Rights Act of 2000, the term developmental disabilities applies only to conditions with functional limitations in at least three of the following areas: self-care, receptive and expressive language, learning, mobility, self-direction, independent living or economic self-sufficiency.3

Learning disabilities are conditions which impact an individual's ability to use written or spoken language, perform mathematical calculations, coordinate movements or direct attention. Under the legal definition of the Developmental Disability Assistance and Bill of Rights Act of 2000, learning disabilities are a subset of developmental disabilities. Other specific conditions, such as intellectual disabilities, attention deficit hyperactivity disorder (ADHD) Down syndrome and blindness, are also subsets of developmental disabilities.4

Prevalence

Comparisons across countries or across time can be extremely difficult, in part because different definitions or diagnostic criteria are used among entities.5 Tracking and recording of data are also quite variable across entities and time.

On this page we provide some general statistics about developmental disabilities globally and in the US, Europe and Canada.

Global Prevalence

Disability prevalence is higher for developing countries, although specific data are difficult to secure. One-fifth of the estimated global total population, or between 110 million and 190 million people, experience significant disabilities.6 Disability is also higher among women than men, and children from poorer households in many countries and those in ethnic minority groups are at significantly higher risk of disability than other children.7

  • Globally, one in 160 children has an autism spectrum disorder (ASD).8
  • 1991 prevalence estimates for children seven to ten years old are that two in 1000 children are identified with cerebral palsy, four in 1000 with moderate to profound intellectual disability (IQ<50) and five in 1000 with epilepsy.9
  • 2012 estimates are that 5.3 percent of the world's population have a disabling hearing loss; nine percent of these are children.10
  • Visual impairment is a major global health issue: estimates are that 285 million people of all ages are visually impaired (in 2010), of whom 39 million are blind.11

United States

According to the CDC, approximately one in every six 3- to 17-year-old children within the US has one or more developmental disabilities.12 Developmental disabilities do not affect all children equally, disproportionately more common among males versus females, non-Hispanics versus Hispanics, and low-income children versus middle- and high-income children.

prevalence of DDs in the USA

Prevalence of developmental disabilities in children has been increasing. From 1997 to 2008 prevalence increased an estimated 17 percent across all developmental disabilities within the United States despite a decrease in the prevalence of moderate to profound hearing loss.13 The increase is largely driven by the increase in ADHD and autism prevalence over the past twenty to thirty years.14 However, there is scientific debate about how much of the increase is due to changes in diagnostic definitions versus actual increases in the number of affected children.15 For more information on autism and ADHD please refer to CHE’s Autism and Mental Health pages.

prevalence of DDs over time

According to the CDC, blindness affects an estimated 0.13 percent of American children, while moderate to profound hearing loss affects between 0.1 and 0.5 percent.16 A 2011 study found that the prevalence of hearing loss decreased by 30.9 percent and the prevalence of blindness increased by 18.1 percent from 1997 to 2008.17

European Union

Prevalence rates have been estimated in different European countries but due to the
different methodologies and definitions used, comparisons are not possible. A study
published in 2004 looked at the surveys carried out worldwide and suggests that the rise in incidence of autism should be a matter of urgent public concern. A 2005 epidemiological survey mentions epilepsy as the most frequent comorbid conditions to autism spectrum disorder, followed by hearing or visual impairments, cerebral palsy, Down syndrome, tuberous sclerosis and fragile X syndrome, among others.18

One investigation found that the age standardized incidence ratios of autism and other pervasive developmental disorders (PDD) in the United Kingdom increased from 35 in 1991 to 365 in 2001, more than a ten-fold increase in 10 years. The increase for PDD was around ten-fold; but the increase in autism was also striking. The authors conclude that better ascertainment of diagnosis is likely to have contributed to this increase but that a real increase cannot be ruled out.19

Canada

The prevalence of pervasive developmental disorders, including autism, Rett syndrome and Asperger syndrome, is estimated to be between 27.5 and 70 per 10,000 children aged one to 14 years. The estimated prevalence of ADHD in 2001 was 4.8 in children aged four to 17 years.20

Causes and Contributors

Common causes of developmental disabilities include genetic or chromosomal abnormalities, substance exposure, preterm birth, low birth weight and specific infectious diseases.21 Environmental toxicants have the ability to play a role in each of these causal mechanisms.

Environmental Exposures and Developmental Disability

Mechanisms of Toxicants

The impacts of toxicants on the developing brain are through various mechanisms. Mercury causes cell death and alters cell migration and proliferation. Lead disrupts neurotransmission, synaptogenesis and synaptic trimming. DDT, PCBs, polybrominated diphenyl ethers (PBDEs), phthalates and bisphenol A appear to act—at least in part—by disrupting estrogenic or thyroid hormones.22

Research has found associations between environmental toxicants and developmental disabilities through both direct and indirect pathways,23 with the indirect associations through  genetic mutation, preterm birth and intrauterine retardation.24

Prenatal and childhood exposures that are associated with developmental disabilities are summarized here. This list of environmental toxicants is not exhaustive and does not include other exposures, such as electromagnetic radiation, linked to neurodevelopmental problems.

A “strong” association indicates a known causal link between the exposure and a condition while a “good” association indicates a well-documented association without a well-documented human causal link. Unless noted otherwise, information is from CHE's Toxicant and Disease Database.25

Chemical Toxicants Associated with Development Disabilities
Disease/Disorder Strong Evidence26 Good Evidence27

Altered neurodevelopment with changes in behavior

  Bisphenol A (BPA)

Cerebral palsy

Mercury  
Cognitive impairment (including learning impairments, intellectual disability and developmental delay)

Carbon disulfide

Cocaine

Ethyl alcohol

Lead

Mercury

Nicotine

PCBs (polychlorinated biphenyls)

Tobacco smoke

1,1-Dichloroethane

Air pollution, including PAHs, nitrogen dioxide and particulate matter28

Carbon monoxide

Marijuana29

Nitrates/nitrites

PBDEs30

Pentachlorophenol (PCP)

Pesticides, including carbamates, DDT/DDE, methyl bromide,

organochlorine pesticides, organophosphate pesticides

Solvents, including styrene,

tetrachloroethylene (PCE) and

xylene

Decreased coordination / dysequilibrium (ataxia)

Acrylamide

Carbon disulfide

Lead

Mercury

Aluminum
Manganese

Pesticides, including chlordecone,

methyl bromide, organochlorine pesticides and organophosphate pesticides

Solvents, including tetrachloroethylene (PCE)

Delayed growth

Ethyl alcohol

Lead

Mercury

PCBs

Toluene

Fetal alcohol syndrome/fetal solvent syndrome

Ethyl alcohol

Toluene

Solvents

Hearing loss (not limited to developmental loss)

Carbon disulfide

Cobalt

Ethyl alcohol

Lithium

Metals, including arsenic, lead, mercury and thorium

Noise (loud sounds)

 

Anilines

Carbon monoxide

Carbon tetrachloride

Cyanide

DDT/DDE

Dimethyl sulfoxide

Dinitrophenols

Iodine

Jet fuel, including JP-4

Organotins

Propylene glycol

Solvents, including

benzene, styrene, toluene, trichloroethylene (TCE) and xylene

Minamata disease Mercury  
Seizures/epilepsy

Carbon monoxide
Cyanide
Lead
Mercury

Aluminum
Halogenated hydrocarbons
Pesticides, including methyl bromide, organochlorine pesticides and organophosphates
Phosphine

Visual impairment

Carbon monoxide

Methanol

Carbon disulfide

Copper

Fungicides
Mercury

Methyl bromide

n-Hexane

Organotins

Paucity of Research

Research on developmental neurotoxicity is limited due to an absence of systematic testing. Although more than 200 industrial chemicals have been found to be neurotoxicants in adults, and 1,000 chemicals have been reported as neurotoxicants in laboratory animal studies, only a fraction of those are recognized to cause neurodevelopmental disorders.31

Disabilities and disorders with no known strong or good environmental contributors are not listed here. In addition to the associations above, the following toxicants are associated with unspecified neurodevelopmental effects:

Some associations with limited or conflicting evidence are listed in CHE's Toxicant and Disease Database.

Vulnerable Populations and Timing of Exposures

Brain Development: An Analogy

Imagine that the development of the human brain is a journey on a convoluted and branching path, such as a complex hiking trail.

brain development map

image from Nathalie Babineau-Griffiths at Creative Commons, modified

There are many turns and decision points along the way. A change of direction closer to the beginning of the journey is more likely to take you to a place far away from your intended destination than a change toward the end of the journey.

An environmental factor that alters brain development—whether a chemical or radiation exposure, lack of adequate nutrition, an injury, inadequate nurturing or stimulation, a hormone imbalance or something else—will generally have a greater effect earlier in brain development than later on.

This analogy does not imply that the ultimate "destination" of brain development after exposure or injury is less valuable than the typical or intended destination. However, it generally is different.

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The developmental stage of an individual at the time of an exposure can make a huge difference in the outcome. An exposure that could cause severe malformations for a fetus could be harmless to an individual later in life. In general, exposures early in life (embryo, fetus, infant and child) are more likely to cause harm to the developing and maturing brain and nervous system than exposures later in life.

Critical windows. According to the World Health Organization, a critical window of susceptibility is a "sensitive time interval during development when environmental exposures can interfere with physiology of cell, tissue, or organ." These windows include periods in which cells are growing rapidly, tissues are forming, and the young body is still without most protective capabilities, such as an immune system, blood brain barrier, or DNA repair system.

The Critical Windows of Development32 timeline from the Endocrine Disruption Exchange33 shows how exposures to certain chemicals can affect different anatomical systems, including the central nervous systems, at different stages of prenatal development.

Preterm Birth and Impaired Fetal Growth

Several adverse pregnancy events and birth outcomes are associated with an increased risk of many developmental disabilities.34 Of these, both preterm birth and impaired fetal growth (low birth weight and intrauterine growth retardation) can be caused by prenatal chemical exposure. For more information regarding the toxicant causes of preterm birth and impaired fetal growth please refer to the Reproductive Health Research and Resources webpage.

Other Contributors

Interacting Factors

These nutritional, disease, infection, stress and other factors can interact with chemical exposures and with each other. For example, children who are deficient in the nutrients calcium and iron absorb more lead when exposed to this powerful neurotoxicant.35

Iodine deficiency can interfere with normal brain development in fetuses, but women who are deficient in iodine are also more vulnerable to the effects of perchlorate. Exposure to perchlorate contributes to thyroid hormone deficiency, which limited evidence suggests in a pregnant woman can lead to intellectual disability in her child.36

A deficiency of vitamin A increases the risk of blindness in children infected with the measles virus.37

Animal models indicate that exposure to air pollution and stress in utero can harm cognitive abilities later in life more than either pollution or stress alone.38

Rodent models demonstrate that lead exposure before birth might affect the stress response system in a way that harms the body and may lead to greater impulsivity.39

In a study of children from birth to age seven, children who experienced high levels of air pollution in utero had lower IQ scores than those not exposed, but  only when their mothers experienced material hardship.40

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Brain development is greatly influenced by a child's or mother's nutrition,41  experience with injury, infectious disease and/or infection. Poverty,42 institutional environments43 stress44 and other adverse environments45 contribute to cognitive impairment.

Because poverty increases the risk of inadequate access to education and health care, unsafe working conditions, polluted environments, and lack of access to safe water and sanitation, its contribution to disability is considerable.46

A brief summary of what we know of these contributors, plus any genetic contributions, is included in the discussion of each disorder and condition below.

Specific Disorders and Conditions

Focusing on conditions and disorders with known connections to environmental exposures, in alphabetical order.

Ataxia (Decreased Coordination)

Ataxia refers to clumsiness or a loss of balance and coordination that is not due to muscle weakness. This loss of coordination may be caused by a number of different medical or neurological conditions:

  • Injury (head trauma, brain hemorrhage)
  • Neurologic conditions
  • Certain viral infections
  • Exposure to toxicants (listed in the table above)
  • Diet (deficiencies of certain vitamins, especially Vitamin E or Vitamin B12, or sensitivity to gluten
  • Other medical conditions affecting the nervous system (stroke, brain tumor and other cancers, diabetes, multiple sclerosis, neurosyphilis (Tabes dorsalis), immune system problems)
  • Genetic disorders47

Cerebral Palsy

Types of Cerebral Palsy

Symptoms define the type of CP:48

  • Spastic (stiff muscles), the most prevalent form, comprising 77 percent of all CP cases
  • Dyskinetic (uncontrollable movements)
  • Ataxic (poor balance and coordination)
  • Mixed

Cerebral palsy (CP) is a neurological disorder that primarily affects mobility but in severe cases can cause intellectual disabilities.49 Other common symptoms include seizures, hearing loss, impaired vision, and impaired bladder and bowel control.50

CP is the most common motor disability in children, with about one in 323 children US children diagnosed.51 The onset of CP symptoms occurs from infancy to early childhood.

Causes and Risk Factors

CP is caused by malformation of the brain or brain injury.52 Other than exposure to mercury as listed in the table above, environmental risk factors include preterm birth and lower maternal socioeconomic status.53

Down Syndrome

Down syndrome occurs when an individual has a full or partial extra copy of chromosome 21. Common physical traits of Down syndrome are low muscle tone, small stature, an upward slant to the eyes and a single deep crease across the center of the palm. Individuals with Down syndrome possess varying degrees of cognitive delays, from very mild to severe.54

Causes and Risk Factors

Strong associations have been found between maternal socioeconomic status, maternal age and chromosome 21-nondisjunction, the cause of 95 percent of Down syndrome cases.55 Results regarding smoking, alcohol, maternal irradiation, fertility drugs, oral contraceptives and spermicides remain inconsistent.56

Epilepsy

Epilepsy is a chronic disorder marked by recurrent, unprovoked seizures. Many people with epilepsy have more than one type of seizure and may have other neurological symptoms.57 Epilepsy is the fourth most common neurological condition, and epilepsy affects more than 65 million people worldwide. New cases of epilepsy are most common among children, especially during the first year of life, and then also increase after age 55.58

Causes and Risk Factors

A traumatic injury to the brain can lead to either short-term temporary seizures shortly after the initial trauma or longer-term post-traumatic epilepsy that is caused by scarring. Military combat-associated brain injuries increase the risk of post-traumatic epilepsy.59 Toxicant exposures connected with seizures are listed in the table above.

Hispanic individuals are at greater risk of epilepsy than non-Hispanics, and Blacks have higher lifetime prevalence than Whites. However, active epilepsy—in which seizures are not completely controlled—is more common in Whites than in Blacks. People with lower socioeconomic status have a higher rate of developing seizures and epilepsy.60

Strokes, brain tumors and Alzheimer's disease can all cause epilepsy.61 Genetic predisposition also seems to be a factor.62

Signs and symptoms of FASD63

  • Abnormal facial features, such as a smooth ridge between the nose and upper lip
  • Small head size
  • Shorter-than-average height
  • Low body weight
  • Poor coordination
  • Hyperactive behavior
  • Difficulty with attention
  • Poor memory
  • Difficulty in school, especially with math
  • Learning disabilities
  • Speech and language delays
  • Intellectual disability or low IQ
  • Poor reasoning and judgment skills
  • Sleep and sucking problems as a baby
  • Vision or hearing problems
  • Problems with the heart, kidneys, or bones
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Fetal Alcohol Spectrum Disorders

Defined by the CDC as conditions which occur in individuals whose mothers drank alcohol during pregnancy, fetal alcohol spectrum disorders are marked by physical, behavioral and learning problems. These intellectual and behavioral problems often cause lifelong issues, including problems with mental health, substance use, getting and keeping a job, and the law.64

Cause and Risk Factors

The only cause of FASD is prenatal alcohol exposure. Alcohol consumed at any stage of pregnancy—including before a woman knows she's pregnant—can cause FASD.65 Thus there is no pregnancy period in which it is safe to drink alcohol.

Unlike the other disabilities discussed on this page, FASDs are completely preventable. Despite this, three out of four women who want to get pregnant as soon as possible report drinking. This puts more than 3 million women in the US at risk of exposing their developing babies to alcohol.66

LDDmap

Weighted data from the CDC from the Behavioral Risk Factor Surveillance System (BRFSS);67 click to zoom

Types of FASDs68

  • Fetal Alcohol Syndrome (FAS), the most involved end of the FASD spectrum, is characterized by abnormal facial features, growth problems and central nervous system problems. People with FAS can have problems with learning, memory, attention span, communication, vision, or hearing, or a mix of these problems.
  • Alcohol-Related Neurodevelopmental Disorder (ARND) is marked by intellectual disabilities and problems with behavior and learning.
  • Alcohol-Related Birth Defects (ARBD), associated with hearing loss or with problems with the heart, kidneys, or bones, or with a mix of these.

Within the 2011-2013 pregnant population in the US, the Behavioral Risk Factor Surveillance System (BRFSS) estimates that one in 10 women consumed alcohol, and as many as two percent to five percent of first-grade students in the United States might have an FASD.69

The lifetime cost for one individual with FAS in 2002 was estimated at $2 million. People with severe problems, such as profound intellectual disability, have much higher costs. The estimated cost to the United States for FAS alone exceeds $4 billion annually.70

While alcohol is the only causal factor of FASDs, not all alcohol consumption is the same. The quantity, frequency and timing of consumption all impact the effect of alcohol on a developing baby.71 The impact  of prenatal alcohol exposure can also be altered by nutrition, parity (number of pregnancies of at least 24 weeks), smoking, genetics, maternal stress and age.72

Fragile X Syndrome

Fragile X syndrome (FXS) is the most common single-gene cause of intellectual disability and can also cause behavioral challenges and assorted physical characteristics:

  • Intellectual disabilities, including learning disabilities
  • Behavior challenges, including ADD or ADHD, autism and autistic-like behaviors, anxiety, hand-biting/flapping, aggression, poor eye contact, and sensory issues
  • Challenges with speech and language
  • Physical abnormalities

According to the Fragile X Association of Southern California, FXS is the leading known cause of autism. Other associated conditions are fragile X-associated tremor/ataxia syndrome (FXTAS) and fragile X-associated premature ovarian insufficiency (FXPOI).73

Cause and Risk Factors

FXS is caused by a mutation in the FMR1 gene, which makes a protein the body requires for brain development.74 Because boys have only one X chromosome, FXS is more common in boys than in girls. According to the Fragile X Association of Southern California, fragile X syndrome is found in one in 2000-3600 males and one in 4000 to 6000 females with full mutation worldwide.75 See the website of the Fragile X Association of Southern California for more details.

Hearing Impairment or Loss

hearing impaired child

 

image from PAD Pittsburgh Association of the Deaf at Creative Commons

The World Health Organization defines hearing loss as the inability to hear as well as someone with normal hearing—hearing thresholds of 25 dB or better in both ears. Hearing loss may be mild, moderate, severe or profound. It can affect one ear or both ears and leads to difficulty in hearing conversational speech or loud sounds. Half of all cases of hearing loss are avoidable through primary prevention.76

Causes and Risk Factors

Hearing loss may result from genetic causes, complications at birth and aging.77 Infectious disease, including rubella, cytomegalovirus, herpes, syphilis and Zika, as well as chronic ear infections, can contribute to hearing impairments.78 Some medications can cause hearing loss,79 and intense sounds can also cause both temporary and permanent hearing impairment.80 Toxicant exposures contributing to hearing impairment are listed in the table above.

Intellectual Disabilities

Categories

Intellectual Disabilities are categorized by severity:81

  • Mild: IQ 50-70
  • Moderate: IQ 35-49
  • Severe: IQ 20-34
  • Profound: IQ less than 20

Intellectual disabilities (IDs) are any conditions marked by an intelligence quotient (IQ) of 70 or less.82 Up until 2010 and the passage of  Rosa’s Law (Intellectual Disability Terminology Changes), ID was termed mental retardation.83 Between one and three percent of American children have an ID.84

Causes and Risk Factors

Little Things Matter: The Impact of Toxins on the Developing Brain, from the Canadian Environmental Health Atlas

ID causal pathways include these:

In addition to directly impacting brain development, environmental toxicants (listed in the table above) can play a role in these causal pathways.

Low levels of thyroid hormones in a pregnant woman can lead to adverse neuropsychological development, including intellectual disability, in her child.89

Kernicterus

In some babies, the liver is not sufficiently developed to efficiently get rid of excess bilirubin, a yellow-colored pigment of red blood cells. When bilirubin builds up in a baby's blood, the skin and whites of the eyes might look yellow and is called jaundice. Kernicterus is a type of brain damage that can result from high levels of bilirubin in a baby’s blood. It can cause athetoid cerebral palsy and hearing loss, as well as problems with vision and teeth and sometimes intellectual disabilities.90

Causes and Risk Factors

About 60 percent of all babies have jaundice. When severe jaundice goes untreated, kernicterus can result.91  

Babies at higher risk of jaundice and kernicterus include preterm births, babies with dark skin color (because jaundice may not be as noticeable) and those of East Asian or Mediterranean descent. Also, babies who suffer significant bruising during birth, whose blood type does not match their mothers', and who are breastfed are at higher risk. Genetic predisposition also plays a role.92

Common Learning Disabilities93

Learning Disabilities

Learning disability (LD) is a broad term applied to individuals with disorders that impact their ability to utilize language, perform calculations, coordinate movements, or direct attention.94

Although attention deficit/hyperactivity disorder (ADHD) is a developmental disability that can impact an individual’s ability to learn, it is not classified as a learning disability.95 Impairments in one's ability to learn due to intellectual disabilities, vision or hearing loss, or emotional disturbances are also not considered learning disabilities.96

The National Center on Birth Defects and Developmental Disabilities (NCBDDD) estimates that  one in 13 American has a learning disability.97

Causes and Risk Factors

According to the Eunice Kennedy Shriver National Institute of Child Health and Human Development,  current causal hypotheses include genetic, toxicant exposure (as described in the table above) and nonchemical environmental factors such as malnutrition and poor prenatal health care.98

cover of A Story of Health

Amelia's story within A Story of Health highlights how environment is connected to learning disabilities; click to open the PDF.

Other nontoxicant environmental exposures associated with learning and intellectual disabilities include infectious disease (such as HiB, Haemophilus influenzae type B) and trauma.99 Microcephaly (a smaller than normal head, usually a sign of diminished brain growth), can also lead to learning and developmental disabilities.100 Microcephaly has been of growing concern because of its causal connection to the Zika virus and its spread via mosquitoes but also through direct transmission between humans.

Minamata Disease

Minimata disease case

Akio Mizoguchi celebrates victory in having his mother's case of Minamata disease officially recognized in 2013. Cases are still being diagnosed decades after the mercury discharge stopped. Image from Timothy Takemoto at Creative Commons.

Minamata disease is a neurological syndrome whose symptoms include ataxia, numbness in the hands and feet, general muscle weakness, narrowing of the field of vision and damage to hearing and speech. Severe cases involve brain damage, paralysis, incoherent speech and delirium. In extreme cases, insanity, paralysis, coma and death follow within weeks of the onset of symptoms. A congenital form of the disease can also affect fetuses.101 Minamata disease is named for Minamata, Japan, where the Chisso Co. Ltd. discharged waste liquid with high concentrations of methylmercury into Minamata Bay starting in 1932 and lasting until at least 1968.

Cause

Minamata disease, sometimes referred to as Chisso-Minamata disease, is caused by severe mercury poisoning. For more information about mercury's effects and the history of this disease, see the Mercury webpage.

Muscular Dystrophy

Muscular dystrophy (MS) is a group of diseases that cause progressive weakness and loss of muscle mass. Symptoms of the most common variety of MS begin in childhood, primarily in boys. Other types don't surface until adulthood.102 Some types of MS affect the brain in addition to muscles and may cause social cognitive impairment,103 intellectual disability and seizures.104

Causes and Risk Factors

MS is caused by genetic mutations that interfere with the production of proteins needed to form healthy muscle. Young boys are at higher risk than girls of the most common form of MS.105

Rett Syndrome

Rett syndrome affects girls almost exclusively and is characterized by normal early growth and development followed by a slowing of development, loss of purposeful use of the hands, distinctive hand movements, slowed brain and head growth, problems with walking, seizures, and intellectual disability. Apraxia—the inability to perform motor functions—is perhaps the most severely disabling feature of Rett syndrome, interfering with every body movement, including eye gaze and speech. Rett syndrome is estimated to affect one in every 10,000 to 15,000 live female births and in all racial and ethnic groups worldwide.

Causes and Risk Factors

Nearly all cases of Rett syndrome are caused by a mutation in the methyl CpG binding protein 2 (MECP2) gene. Scientists have identified mutations in the CDKL5 and FOXG1 genes in individuals who have atypical or congenital Rett syndrome, but the mechanisms are still unknown. Although Rett syndrome is a genetic disorder, fewer than one percent of recorded cases are inherited or passed from one generation to the next. Most cases are spontaneous, with the mutation occurring randomly.

There is some animal evidence that exposures to  toxicants, including a flame retardant (BDE-47)106 and PCBs (PCB 95)107 may influence gene expression, especially regarding learning and memory impairment, in affected individuals.

Tic Disorders

Tics are involuntary, repetitive movements and vocalizations and are the defining feature of a group of childhood-onset, neurodevelopmental conditions known collectively as tic disorders. Tourette syndrome (TS) is one type of tic disorder; the others are chronic tic disorder (motor or vocal type), and provisional tic disorder. These are distinguished by the types of tics present (motor, vocal/phonic, or both) and by the duration of the tics. Current estimates are that one out of every 160 children (0.6 percent) between the ages of five and 17 in the United States has TS.108

Causes and Risk Factors

TS is considered a hereditary disorder, likely modified by environmental factors, but specific genes or environmental influences have not been identified.109

Visual Impairment

Braille reading

image from Exchanges Photo at Creative Commons

The International Classification of Diseases -10 (Update and Revision 2006) lists four levels of visual function:

  1. Normal vision
  2. Moderate visual impairment
  3. Severe visual impairment
  4. Blindness

Moderate and severe visual impairment are grouped under the term "low vision", which taken together with blindness represents all visual impairment. 80 percent of all visual impairment can be prevented or cured.110

Causes and Risk Factors

Globally the major causes of visual impairment:

  • Uncorrected refractive errors (myopia, hyperopia or astigmatism), 43 percent
  • Glaucoma, two percent.111
  • Unoperated cataract, 33 percent. Cigarette smoking, UV-B light, high alcohol consumption and some medications, such as steroids, are associated with cataract, the leading cause of blindness worldwide (although usually associated with aging rather than child development).112

Preterm birth has been linked with visual impairment within children,113 as have both infectious disease, such as measles,114 and diabetes.115 Vitamin A deficiency is a leading cause of blindness in children worldwide.116 Toxicant exposures contributing to visual impairment are listed in the table above. 

Legal History: United States

The mental retardation laws of the 1960s supplied the groundwork for the developmental disability laws we see today. The original laws, the Maternal and Child Health and Mental Retardation Planning Amendments and the Mental Retardation Facilities and Community Mental Health Centers Construction Act of 1963, applied only to individuals with mental retardation. It wasn’t until 2010, however, that Congress passed "Rosa's Law", a federal law that removed the term "mental retardation" in federal education and health and labor statutes, replacing it with "intellectual disability". 

In 1970, the term "developmental disability" was introduced, and neurological conditions, such as cerebral palsy and epilepsy, were included under the protections upheld by these laws. Intellectual disabilities, as well as learning disabilities and ADHD, are now defined as separate subsets under developmental disabilities. 

Over the decades, amendments and new regulations have expanded the legal definition of developmental disabilities with the current definition defined by the Developmental Disabilities Assistance and Bill of Rights Act of 2000. The goal of these laws is to ensure that individuals with developmental disabilities have access to the resources needed to “promote self-determination, independence, productivity, and integration and inclusion in all facets of community life…"117

Additional protection for individuals with disabilities is found under the Americans with Disabilities Act of 1990. This act prohibits the discrimination on the basis of disability applicable to employment, state and local government, public accommodations, commercial facilities, transportation, and telecommunications. While specific impairments are not identified within the ADA, the laws extend to individuals with physical and mental impairments that impacts one or more major life activities.118

Educational services for individuals with developmental disabilities are regulated by the Individuals with Disabilities Education Act (IDEA). First signed in 1975, IDEA ensures that children with disabilities are provided with the “least restrictive environment appropriate to their individual needs.”119  The act distinguished the types of government and public agency intervention into two parts, Parts B and C. IDEA’s Part B applies to school-age children (three to 21 years old) and outlines Individualized Educational Programs (IEPs). Regulating the services available to infants and toddlers, IDEA’s Part C describes early intervention service requirements.120  More than 6.5 million children are eligible for services under IDEA nationwide. For more information regarding IDEA please refer to Disability.gov’s Individuals with Disabilities Education Act (IDEA).121

Ethical, Historical and Social Issues

Prejudice against people with disabilities has long been an issue. Persons with disabilities, considered as a group, are more likely to experience adverse socioeconomic outcomes than persons without disabilities, including less education, worse health outcomes, lower employment and higher rates of poverty.122 Thus adverse environments are both a cause and a consequence of some disabilities.

Along these lines, it wasn't until 2010 that the term "mental retardation," long considered a derogatory designation, was legally changed on the federal level to "intellectual disabilities." (see section on Legal Issues above). But even the term "disabilities" has been controversial because to some it implies that people with certain conditions are "lesser" than those who have what society has deemed as "normal" abilities. In response, "differently abled" was first proposed (in the 1980s) as an alternative to disabled, handicapped, etc. on the grounds that it gave a more positive message and so avoided discrimination towards people with disabilities.

Some have even proposed entirely different terms to promote an even more positive or "neutral" approach. A prime example is "neurodiversity", a term coined by Judy Singer in 1988. It refers to “the diversity of human brains and minds – the infinite variation in neurocognitive functioning with our species.”123  However, the term wasn’t popularized until Harvey Blume’s 1998 article in The Atlantic. In the article Blume states “Neurodiversity may be every bit as crucial for the human race as biodiversity is for life in general. Who can say what form of wiring will prove best at any given moment? Cybernetics and computer culture, for example, may favor a somewhat autistic cast of mind.”124

From the concept of neurodiversity has emerged the neurodiversity paradigm. The fundamental principles of this paradigm are these:

  1. Neurodiversity is naturally occurring and valuable form of human diversity
  2. There is no “right” or “normal” type of brain in the same way that there is no one “right” or “normal” sex or race
  3. The social dynamics around neurodiversity mirror those around other forms of human diversity.125  

This is the philosophy behind the neurodiversity movement.

Along with the Autism Rights Movement (ARM), the neurodiversity movement strives to be inclusive of all neurominorities. There is quite a bit of overlap between these movements as well as ongoing debate about how to best forward these ideas. Those spearheading these efforts see these movements as part of a broader push for human rights. 126  

See more about environmental contributors to developmental disabilities in the list of CHE publications and Dig Deeper resources in the right sidebar.


This page was last revised by practicum student Maggie Lind and Nancy Hepp in September 2016. Read more about Maggie's practicum, including her review summary.

CHE invites our partners to submit corrections and clarifications to this page. Please include links to research to support your submissions through the comment form on our Contact page.

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