• Home
• Environmental Health
• Health, Diseases & Disabilities
• Learning and Developmental Disabilities

Learning and Developmental Disabilities Research and Resources

We share here a summary of several common learning and developmental disabilities, focusing on those which are known or suspected to have environmental factors as contributors.

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 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  

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

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

Vulnerable Populations and Timing of Exposures

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 various anatomical systems, including the central nervous system, 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

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

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

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

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

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

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

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

ID causal pathways include these:

• Conditions due to genetic mutations or chromosomal abnormalities, including fragile X syndrome, Rett syndrome and Down syndrome.⁸⁵
• Adverse pregnancy outcomes (such as preterm birth and inter-uterine growth retardation)⁸⁶
• Some other developmental disabilities (such as cerebral palsy, autism spectrum disorders)⁸⁷ and epilepsy.⁸⁸

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

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

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

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. 

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

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.

CHE’s Work on Learning and Developmental Disabilities

Mind, Disrupted: How Toxic Chemicals May Change How We Think and Who We Are, 2010

Scientific Consensus Statement on Environmental Agents Associated with Neurodevelopmental Disorders, 2008

Policy Implications Based on the Scientific Consensus Statement on Environmental Agents Associated with Neurodevelopmental Disorders, 2008

Article in the Journal of Intellectual and Developmental Disability summarizing and updating these two statements: Scientific and policy statements on environmental agents associated with neurodevelopmental disorders, 2010

Resolution of the Learning and Developmental Disabilities Initiative, 2003
explores the emerging science investigating environmental impacts on neurological development and health. We provide this forum for health professionals, scientists, researchers, community groups, government agents, and the health-affected to connect, share and discuss evidence-based research regarding environmental contributors to a wide range of learning and developmental disabilities. In addition to posting influential research articles and other relevant materials, participants will find information about CHE Partnership calls, which feature the latest science on environmental factors that can lead to neurodevelopmental problems.

This page was last revised by practicum student Maggie Lind and Nancy Hepp in September 2016. 

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.

1. National Institute of Neurological Disorders and Stroke. Learning Disabilities Information Page. September 11, 2015. Viewed July 12, 2016; National Center on Birth Defects and Developmental Disabilities. Specific Conditions | Developmental Disabilities. CDC. Viewed July 12, 2016; National Center on Birth Defects and Developmental Disabilities. Facts | Developmental Disabilities. CDC. September 22, 2015. Viewed July 12, 2016; Institute on Community Integration. About Developmental Disabilities. University of Minnesota. March 30, 2016. Viewed July 12, 2016; Janssen S, Solomon G, Schettler T. Toxicant and Disease Database. Collaborative on Health and the Environment. 2011.
2. AIDD. The Developmental Disabilities Assistance and Bill of Rights Act of 2000 (DD Act). DHHS, ACL. Viewed July 12, 2016; National Center on Birth Defects and Developmental Disabilities. Developmental Disabilities. CDC. Viewed July 11, 2016.
3. AIDD. The Developmental Disabilities Assistance and Bill of Rights Act of 2000 (DD Act). DHHS, ACL. Viewed July 12, 2016.
4. National Institute of Neurological Disorders and Stroke. Learning Disabilities Information Page. September 11, 2015. Viewed July 12, 2016.
5. Health & Consumer Protection Directorate-General. Some elements about the prevalence of Autism Spectrum Disorders (ASD) in the European Union. European Commission. February 2005. Viewed August 30, 2016.
6. World Bank. Disability: Overview. April 4, 2016. Viewed September 13, 2016.
7. World Health Organization. World Report on Disability. 2011. Viewed September 13, 2016.
8. World Health Organization. Autism spectrum disorders. January 2016. Viewed August 31, 2016.
9. Shah PM. Prevention of mental handicaps in children in primary health care. Bulletin of the World Health Organization. 1991;69(6):779-89.
10. World Health Organization. Prevention of blindness and deafness. Viewed August 31, 2016.
11. World Health Organization. Prevention of blindness and deafness. Viewed Augut 31, 2016.
12. National Center on Birth Defects and Developmental Disabilities. Developmental Disabilities Prevalence Trends | Key Findings. CDC. February 12, 2015. Viewed July 12, 2016.
13. Boyle C et al.Trends in the prevalence of developmental disabilities in US children, 1997-2008. Pediatrics. June 2011; 127(6): 1034–1042.
14. Visser S et al.Trends in the parent-report of health care provider-diagnosed and medicated attention-deficit/hyperactivity disorder: United States, 2003–2011. Journal of the American Academy of Child & Adolescent Psychiatry. January 1, 2014; 53(1): 34–46.e2; CDC. Facts about ASDs: Autism and Developmental Disabilities Monitoring (ADDM) Network. Viewed July 12, 2016.
15. McKeown R et al.The impact of case definition on ADHD prevalence estimates in community-based samples of school-aged children. Journal of the American Academy of Child and Adolescent Psychiatry. January 2015; 54(1): 53–61; Hertz-Picciotto I, Delwiche L. The rise in autism and the role of age at diagnosis. Epidemiology. 2009 Jan;20(1):84-90.
16. Boyle C et al.Trends in the prevalence of developmental disabilities in US children, 1997-2008. Pediatrics. June 2011; 127(6): 1034–1042; National Center on Birth Defects and Developmental Disabilities. Research and Tracking | Hearing Loss. CDC. August 13, 2015. Viewed July 13, 2016.
17. Boyle C et al.Trends in the prevalence of developmental disabilities in US children, 1997-2008. Pediatrics. June 2011; 127(6): 1034–1042.
18. Task Force on Major and Chronic Diseases of DG SANCO's Health Information Strand. Major and Chronic Diseases Report 2007. European Commission. 2008. Viewed August 30, 2016.
19. Task Force on Major and Chronic Diseases of DG SANCO's Health Information Strand. Major and Chronic Diseases Report 2007. European Commission. 2008. Viewed August 30, 2016.
20. Public Health Agency of Canada. Report: The State of Public Health in Canada 2009. October 20, 2009. Viewed August 30, 2016.
21. National Center on Birth Defects and Developmental Disabilities. Facts | Developmental Disabilities. CDC. September 22, 2015. Viewed July 12, 2016; MedlinePlus. Developmental Disabilities. NIH. Viewed July 11, 2016; Rhine S. Twelve New Genetic Causes of Developmental Disabilities – Sam Rhine Genetics. Viewed July 11, 2016.
22. Lanphear BP. The impact of toxins on the developing brain. Annual Review of Public Health. 2015 Mar 18;36:211-30.
23. Grandjean P, Landrigan PJ. Neurobehavioural effects of developmental toxicity, The Lancet Neurology. March 2014; 13(3): 330–338; Jarjour IT. Neurodevelopmental outcome after extreme prematurity: a review of the literature. Pediatric Neurology. February 2015; 52(2): 143–152; Soleimani F, Zaheri F, Abdi F .Long-term neurodevelopmental outcomes after preterm birth. Iranian Red Crescent Medical Journal. June 2014; 16(6): e17965.
24. Jarjour IT. Neurodevelopmental outcome after extreme prematurity: a review of the literature. Pediatric Neurology. February 2015; 52(2): 143–152; Soleimani F, Zaheri F, Abdi F .Long-term neurodevelopmental outcomes after preterm birth. Iranian Red Crescent Medical Journal. June 2014; 16(6): e17965; United States General Accounting Office. Reproductive and Developmental Toxicants: Regulatory Actions Provide Uncertain Protection. October 1991. Viewed July 11, 2016; National Center on Birth Defects and Developmental Disabilities. Developmental Disabilities. CDC. Viewed July 11, 2016.
25. Janssen S, Solomon G, Schettler T. Toxicant and Disease Database. Collaborative on Health and the Environment. 2011.
26. Janssen S, Solomon G, Schettler T. Toxicant and Disease Database. Collaborative on Health and the Environment. 2011.
27. Janssen S, Solomon G, Schettler T. Toxicant and Disease Database. Collaborative on Health and the Environment. 2011.
28. Bennett D et al. Project TENDR: targeting environmental neuro-developmental risks. The TENDR Consensus Statement. Environmental Health Perspectives. 2016 Jul 1;124(7):A118-22.
29. Minnes S, Lang A, Singer L. Prenatal tobacco, marijuana, stimulant, and opiate exposure: outcomes and practice implications. Addiction Science & Clinical Practice. July 2011; 6(1): 57–70; Goldschmidt L et al. Prenatal marijuana exposure and intelligence test performance at age 6. Journal of the American Academy of Child and Adolescent Psychiatry. March 2008; 47(3): 254–263.
30. Lanphear BP. The impact of toxins on the developing brain. Annual Review of Public Health. 2015 Mar 18;36:211-30.
31. Grandjean P, Landrigan PJ. Developmental neurotoxicity of industrial chemicals. The Lancet. December 22, 2006; 368(9553): 2167–2178.
32. Endocrine Disruption Exchange. Critical windows of development timeline. http://endocrinedisruption.org/prenatal-origins-of-endocrine-disruption/critical-windows-of-development/timeline-test/ Viewed June 16, 2016.
33. Endocrine Disruption Exchange. Home. http://endocrinedisruption.org/.
34. National Center on Birth Defects and Developmental Disabilities. Facts | Developmental Disabilities. CDC. September 22, 2015. Viewed July 12, 2016. Duley L. The global impact of pre-eclampsia and eclampsia. Seminars in Perinatology. 2009 Jun;33(3):130-7.
35. Nebraska Department of Health and Human Services. Nutrition and Lead Poisoning Prevention. June 11, 2013. Viewed September 5, 2016.
36. Council on Environmental Health et al. Iodine deficiency, pollutant chemicals, and the thyroid: new information on an old problem. Pediatrics. 2014 Jun;133(6):1163-6; Vandenberg LN et al. Hormones and endocrine-disrupting chemicals: low-dose effects and nonmonotonic dose responses. Endocrine Reviews. 2012 Jun;33(3):378-455.
37. Bello S et al. Routine vitamin A supplementation for the prevention of blindness due to measles infection in children. Cochrane Database of Systematic Reviews. 2016 Aug 31;8:CD007719.
38. Proceedings of the EPA workshop on interactions between social stress and environmental hazards. Environmental Protection Agency. May 14-15, 2012. Prepared by Industrial Economics, Incorporated.
39. Proceedings of the EPA workshop on interactions between social stress and environmental hazards. Environmental Protection Agency. May 14-15, 2012. Prepared by Industrial Economics, Incorporated.
40. Vishnevetssky J, Tang, D., Chang, H et al. Combined effects of prenatal polycyclic aromatic hydrocarbons and material hardship on child IQ. Neurotoxicology and Teratology. 2015:49;74-80.
41. Lee A. Early influences and childhood development. Does helicobacter play a role? Helicobacter. 2007 Nov;12 Suppl 2:69-74; Black MM, Pérez-Escamilla R, Rao SF. Integrating nutrition and child development interventions: scientific basis, evidence of impact, and implementation considerations. Advances in Nutrition. 2015 Nov;6(6):852-9; Goyal MS et al. Feeding the brain and nurturing the mind: linking nutrition and the gut microbiota to brain development. Proceedings of the National Academy of Sciences USA. 2015 Nov 17; 112(46): 14105–14112.
42. Pavlakis AE et al. Brain imaging and electrophysiology biomarkers: is there a role in poverty and education outcome research? Pediatric Neurology. 2015 Apr;52(4):383-8.
43. Berens AE, Nelson CA. The science of early adversity: is there a role for large institutions in the care of vulnerable children? Lancet. 2015 Jul 25;386(9991):388-98.
44. Brietzke E. Impact of childhood stress on psychopathology. Revista Brasileira de Psiquiatria. 2012 Dec;34(4):480-8.
45. Blair C, Raver CC. Child development in the context of adversity: experiential canalization of brain and behavior. The American Psychologist. 2012 May-Jun;67(4):309-18; Tshala-Katumbay D et al. A global perspective on the influence of environmental exposures on the nervous system. Nature. 2015 Nov 19;527(7578):S187-92.
46. World Bank. Disability: Overview. April 4, 2016. Viewed September 13, 2016.
47. National Ataxia Foundation. Frequently Asked Questions about...Ataxia. June 2016. Viewed September 2, 2016.
48. Centers for Disease Control and Prevention. Facts about Cerebral Palsy. July 13, 2015. Viewed July 12, 2016.
49. Eunice Kennedy Shriver National Institute of Child Health and Human Development, Cerebral Palsy: Overview. NIH. Viewed July 12, 2016.
50. National Institute of Neurological Disorders and Stroke. Cerebral Palsy Information Page. Viewed February 13, 2023.
51. Centers for Disease Control and Prevention. What You Need to Know about Cerebral Palsy. March 3, 2014. Viewed July 12, 2016.
52. Tamburlini G, Ehrenstein O, Bertollini R. Children’s Health and Environment: A Review of Evidence. European Environment Agency and WHO Regional Office for Europe. 2002. Viewed July 7, 2016.
53. Jarjour IT. Neurodevelopmental outcome after extreme prematurity: a review of the literature. Pediatric Neurology. February 2015; Soleimani F, Zaheri F, Abdi F .Long-term neurodevelopmental outcomes after preterm birth. Iranian Red Crescent Medical Journal. June 2014; 16(6): e17965; Sundrum R et al. Cerebral palsy and socioeconomic status: a retrospective cohort study. Archives of Disease in Childhood. 90(1): 15. Viewed July 12, 2016; Spencer NJ, Blackburn CM, Read JM. Disabling chronic conditions in childhood and socioeconomic disadvantage: a systematic review and meta-analyses of observational studies. BMJ Open. 2015 Sep 3;5(9):e007062.
54. National Down Syndrome Society. What Is Down Syndrome? Viewed September 2, 2016.
55. Mayo Clinic. Down Syndrome Causes. Mayo Foundation for Medical Education and Research. Viewed July 12, 2016; Hunter J et al. The association of low socioeconomic status and the risk of having a child with Down syndrome: a report from the National Down Syndrome Project. Genetics in Medicine. September 2013; 15(9): 698–705; March of Dimes. Down Syndrome. Viewed July 12, 2016.
56. Sherman S et al. Risk factors for nondisjunction of trisomy 21. Cytogenetic and Genome Research. 2005; 111(3–4): 273–280.
57. Epilepsy Foundation. What Is Epilepsy? January 2014. Viewed September 3, 2016.
58. Epilepsy Foundation. Who Gets Epilepsy? July 2013. Viewed September 3, 2016.
    
59. Epilepsy Foundation. Who Gets Epilepsy? July 2013. Viewed September 3, 2016.
60. Epilepsy Foundation. Who Gets Epilepsy? July 2013. Viewed September 3, 2016.
61. Epilepsy Foundation. Who Gets Epilepsy? July 2013. Viewed September 3, 2016.
62. Epilepsy Foundation. Is Epilepsy Inherited? July 2013. Viewed September 3, 2016.
63. CDC. Facts about FASDs. April 16, 2015. Viewed August 31, 2016.
64. CDC. Facts about FASDs. April 16, 2015. Viewed August 31, 2016.
65. Substance Abuse and Mental Health Services Administration. Preventing FASD: Healthy Women, Healthy Babies. US Department of Health and Human Services. 2007. Viewed August 31, 2016.
66. CDC. Vital Signs: Alcohol and Pregnancy. February 2, 2016. Viewed July 12, 2016.
67. CDC. State-Specific Alcohol Consumption Rates for 2013. September 24, 2015. Viewed August 31, 2016.
68. CDC.
    Fetal Alcohol Spectrum Disorders (FASDs): Facts about FASDs. April 16, 2015. Viewed September 1, 2016.
69. Tan CH et al. Alcohol use and binge drinking among women of childbearing age — United States, 2011–2013. Morbidity and Mortality Weekly Report. September 25, 2015; 64(37);1042-1046.
70. CDC. Fetal Alcohol Spectrum Disorders (FASDs): Data & Statistics. November 17, 2015. Viewed September 1, 2016.
71. O'Neil E. Developmental timeline of alcohol-induced birth defects. The Embryo Project at Arizona State University. April 24, 2011. Viewed September 1, 2016.
72. Tyler C et al. Environmental health and developmental disabilities: a life span approach. Family & Community Health. December 2008; 31(4): 287–304; National Institute on Alcohol Abuse and Alcoholism. Fetal Alcohol Exposure. CDC. Viewed July 15, 2016.
73. Fragile X Association of Southern California. What is Fragile X? Viewed September 4, 2016.
74. CDC. Facts about Fragile X Syndrome. April 15, 2015. Viewed September 4, 2016.
75. World Health Organization. Genes and human disease. Viewed August 31, 2016.
76. World Health Organization. Deafness and hearing loss. March 2015. Viewed September 1, 2016.
77. World Health Organization. Deafness and hearing loss. March 2015. Viewed September 1, 2016.
78. Cohen BE, Durstenfeld A, Roehm PC. Viral causes of hearing loss: a review for hearing health professionals. Trends in Hearing. 2014 Jul 29;18; Scasso CA, Bruschini L, Berrettini S, Bruschini P. [Progressive sensorineural hearing loss from infectious agents]. Acta Otorhinolaryngologica Italica. 1998 Aug;18(4 Suppl 59):51-4.
79. WebMD. Medicines That Cause Hearing Loss. Viewed September 1, 2016.
80. Ryan AF et al. Temporary and permanent noise-induced threshold shifts: a review of basic and clinical observations. Otology and Neurotology. 2016 Sep;37(8):e271-5.
81. ICD9DATA.com. 2012 ICD-9-CM Diagnosis Code 318.0 : Moderate Intellectual Disabilities. Viewed July 12, 2016.
82. National Center on Birth Defects and Developmental Disabilities. Case Definitions | Developmental Disabilities. CDC. Viewed July 12, 2016.
83. National Center on Birth Defects and Developmental Disabilities. Case Definitions | Developmental Disabilities. CDC. Viewed July 12, 2016; Arizona Department of Education. Rosa’s Law: Intellectual Disability Terminology Changes. May 29, 2013. Viewed July 12, 2016.
84. MedlinePlus. Intellectual Disability. NIH. Viewed July 12, 2016.
85. MedlinePlus. Intellectual Disability. NIH. Viewed July 12, 2016; Eunice Kennedy Shriver National Institute of Child Health and Human Development. What Causes IDDs? NIH. Viewed July 12, 2016; Sherman S et al. Risk factors for nondisjunction of trisomy 21. Cytogenetic and Genome Research. 2005; 111(3–4): 273–280; Vinceti M et al. Does maternal exposure to benzene and PM10 during pregnancy increase the risk of congenital anomalies? A population-based case-control study. Science of the Total Environment. 2016 Jan 15;541:444-50.
86. Jarjour IT. Neurodevelopmental outcome after extreme prematurity: a review of the literature. Pediatric Neurology. February 2015; Soleimani F, Zaheri F, Abdi F. Long-term neurodevelopmental outcomes after preterm birth. Iranian Red Crescent Medical Journal. June 2014; 16(6): e17965; Gouin K, Murphy K, Shah PS. Effects of cocaine use during pregnancy on low birthweight and preterm birth: systematic review and metaanalyses. American Journal of Obstetrics and Gynecology. 2011 Apr;204(4):340.e1-12; National Center on Birth Defects and Developmental Disabilities. Facts | Developmental Disabilities. CDC. September 22, 2015. Viewed July 12, 2016.
87. Tamburlini G, Ehrenstein O, Bertollini R.  Children’s Health and Environment: A Review of Evidence. European Environment Agency and WHO Regional Office for Europe. 2002. Viewed July 7, 2016; National Institute of Neurological Disorders and Stroke. Cerebral Palsy Information Page. Viewed July 12, 2016; MedlinePlus. Intellectual Disability. NIH. Viewed July 12, 2016; Suades-González E et al. Air pollution and neuropsychological development: a review of the latest evidence. Endocrinology. October 2015; 156(10): 3473–3482.
88. Nickels KC et al. Cognitive and neurodevelopmental comorbidities in paediatric epilepsy. Nature Reviews. Neurology. 2016 Aug;12(8):465-76.
89. Miller MD, Crofton KM, Rice DC, Zoeller RT. 2009. Thyroid-disrupting chemicals: interpreting upstream biomarkers of adverse outcomes. Environmental Health Perspectives. 117:1033–1041.
90. Centers for Disease Control and Prevention. Facts about Jaundice and Kernicterus. February 23, 2015. Viewed September 3, 2016.
91. Centers for Disease Control and Prevention. Facts about Jaundice and Kernicterus. February 23, 2015. Viewed September 3, 2016; Mayo Clinic Staff. Infant jaundice. Mayo Clinic. Viewed September 3, 2016.
92. Centers for Disease Control and Prevention. Facts about Jaundice and Kernicterus. February 23, 2015. Viewed September 3, 2016; Mayo Clinic Staff. Infant jaundice. Mayo Clinic. Viewed September 3, 2016.
93. Healthy Children. Types of Learning Problems. American Academy of Pediatrics. November 21, 2016. Viewed August 29, 2016; National Institute of Neurological Disorders and Stroke. Learning Disabilities Information Page. September 11, 2015. Viewed July 12, 2016.
94. National Institute of Neurological Disorders and Stroke. Learning Disabilities Information Page. September 11, 2015. Viewed July 12, 2016.
95. National Institute of Mental Health. Attention Deficit Hyperactivity Disorder. NIH. March 2016. Viewed July 12, 2016.
96. Schettler T. Learning Disabilities, Behavioral/Emotional Disorders, and Other Brain Disorders: What We Know. The Collaborative on Health and the Environment. Viewed July 11, 2016.
97. National Center on Birth Defects and Developmental Disabilities. Developmental Disabilities Prevalence Trends | Key Findings. CDC. February 12, 2015. Viewed July 12, 2016.
98. Eunice Kennedy Shriver National Institute of Child Health and Human Development. What Causes Learning Disabilities? NIH. Viewed July 12, 2016.
99. Tyler C et al. Environmental health and developmental disabilities: a life span approach. Family & Community Health. December 2008; 31(4): 287–304.
100. World Health Organization. Microcephaly. March 2, 2016. Viewed August 31, 2016.
101. Sustainability@BU. Minamata Disease. Boston University. Viewed September 4, 2016; World Health Organization. Mercury and health. January 2016. Viewed September 4, 2016
102. Mayo Clinic Staff. Muscular dystrophy. Mayo Clinic. November 27, 2014. Viewed September 5, 2016.
103. Kobayakawa M. [Social cognitive impairment in myotonic dystrophy type 1]. Brain and Nerve. 2016 Feb;68(2):137-44.
104. Ishigaki K. [Central nervous involvement in patients with Fukuyama congenital muscular dystrophy].Brain and Nerve. 2016 Feb;68(2):119-27; Matsumura T. [Clinical importance of central nervous system dysfunction in myopathy]. Brain and Nerve. 2016 Feb;68(2):109-18.
105. Mayo Clinic Staff. Muscular dystrophy. Mayo Clinic. November 27, 2014. Viewed September 5, 2016.
106. Woods R et al. Long-lived epigenetic interactions between perinatal PBDE exposure and Mecp2308 mutation. Human Molecular Genetics. 2012 Jun 1;21(11):2399-411.
107. Lesiak A et al. The environmental neurotoxicant PCB 95 promotes synaptogenesis via ryanodine receptor-dependent miR132 upregulation. The Journal of  Neuroscience. 2014 Jan 15;34(3):717-25.
108. Tourette Association of America. About Tourette: What Is Tourette? Viewed September 5, 2016.
109. Gunduz A, Okun MS. A review and update on Tourette syndrome: where is the field headed? Current Neurology and Neuroscience Reports. 2016 Apr;16(4):37.
110. World Health Organization. Visual impairment and blindness. August 2014. Viewed September 1, 2016.
111. World Health Organization. Visual impairment and blindness. August 2014. Viewed September 1, 2016.
112. Congdon NG, Friedman DS, Lietman T. Important causes of visual impairment in the world today. JAMA. 2003;290(15):2057-2060; Bailey G. Cataracts. AllAboutVision.com. July 20, 2016. Viewed September 5, 2016.
113. Tamburlini G, Ehrenstein O, Bertollini R.  Children’s Health and Environment: A Review of Evidence. European Environment Agency and WHO Regional Office for Europe. 2002. Viewed July 7, 2016; Jarjour IT. Neurodevelopmental outcome after extreme prematurity: a review of the literature. Pediatric Neurology. February 2015; 52(2): 143–152; Soleimani F, Zaheri F, Abdi F .Long-term neurodevelopmental outcomes after preterm birth. Iranian Red Crescent Medical Journal. June 2014; 16(6): e17965.
114. Congdon NG, Friedman DS, Lietman T. Important causes of visual impairment in the world today. JAMA. 2003;290(15):2057-2060; Whitcher JP, Srinivasan M, Upadhyay MP. Corneal blindness: a global perspective. Bulletin of the World Health Organization. 2001;79(3):214-21.
115. White NH. Long-term outcomes in youths with diabetes mellitus. Pediatric Clinics of North America. 2015 Aug;62(4):889-909.
116. Bello S et al. Routine vitamin A supplementation for the prevention of blindness due to measles infection in children. Cochrane Database of Systematic Reviews. 2016 Aug 31;8:CD007719; Wright CB, Redmond TM, Nickerson JM. A history of the classical visual cycle. Progress in Molecular Biology and Translational Science. 2015;134:433-48; Mayo-Wilson E et al. Vitamin A supplements for preventing mortality, illness, and blindness in children aged under 5: systematic review and meta-analysis. BMJ. 2011 Aug 25;343:d5094.
117. Administration on Intellectual and Developmental Disabilities (AIDD). History of the DD Act. Administration for Community Living. September 19, 2013. Viewed July 15, 2016. 
     
118. United States Department of Justice. 2010 ADA Regulations. Viewed July 15, 2016.
119. Civil Rights Division. A Guide to Disability Rights Laws Civil Rights Division. Department of Justice. Viewed July 15, 2016.
120. Disability.gov. Individuals with Disabilities Education Act (IDEA). Viewed July 15, 2016; Civil Rights Division. A Guide to Disability Rights Laws Civil Rights Division. Department of Justice. Viewed November 7, 2017.
121. Disability.gov. Individuals with Disabilities Education Act (IDEA). Viewed November 7, 2017.
122. World Bank. Disability: Overview. April 4, 2016. Viewed September 13, 2016.
123. Walker N. Neurodiversity: Some Basic Terms & Definitions. Neurocosmopolitanism. September 27, 2014. Viewed July 15, 2016.
124. Muzikar D. Neurodiversity: A Person, a Perspective, a Movement? The Art of Autism. August 23, 2015. Viewed July 15, 2016.
125. Walker N. Neurodiversity: Some Basic Terms & Definitions. Neurocosmopolitanism. September 27, 2014. Viewed July 15, 2016.
126. Walker N. Neurodiversity: Some Basic Terms & Definitions. Neurocosmopolitanism. September 27, 2014. Viewed July 15, 2016.

View All Footnotes

Blog Posts

CHE Publications

Including those created jointly with other organizations

Dig Deeper