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Sunday, September 2, 2012

Chemicals and Our Health: Learning and Developmental Disabilities

From SaferChemicals.org - Healthy Families

NOTE: This is an excerpt from an impressively well-researched and much more exhaustive paper on the health risks posed to children and adults by low-level toxic chemical exposures. You can download and read the study in its entirety HERE, or read the Executive Summary HERE.

The number of American children with learning and developmental disabilities has been climbing over the past decade, reaching nearly one in six by 2008.[1] The increasing prevalence of autism and attention deficit hyperactivity disorder accounts for most of this change.[2]

The National Academy of Sciences estimates that combinations of environmental factors, including exposure to toxic chemicals, along with genetic susceptibility, cause or contribute to at least 25% of learning and developmental disabilities.

Intellectual disability (formerly referred to as mental retardation) affects 2%, or approximately 1.4 million, children in the United States.[4] As of 2009, 9% of children—roughly 50 million kids—were diagnosed with attention deficit hyperactivity disorder (ADHD).[5][6]According to the U.S. Centers for Disease Control and Prevention (CDC), an estimated 1 in 88 children in the United States have an autism spectrum disorder.[7] Between 1997 and 2008, the prevalence of autism increased nearly 300% nationally.[8]

In a seminal study of California’s dramatic rise in autism rates, researchers found that about 30% of the rise could not be explained by changes in the age of diagnosis or the inclusion of milder cases.[9]

These conditions impose tremendous psychological and economic costs on the affected children, their families, and communities. On average, it costs twice as much to educate a child who has a learning or developmental disability as to educate a child who does not.[10] According to the CDC, individuals with an autism spectrum disorder have average medical expenditures that exceed those without the disorder by $4,110–$6,200 per year.[11] A 2006 study reported that the economic costs associated with autism in the U.S. are approximately $35 billion dollars per year.[12]

The Human Brain: More Susceptible During Development

Much of what we know about chemicals that can cause neurological problems comes from studies of adults—often in the workplace—and from animal studies. For example, lead, mercury, and various organic solvents have been identified in the peer-reviewed, scientific literature as causing neurological effects in adults, mostly through occupational exposures (see Table 2).[13]

Many of these chemicals are in common use and are produced in high volumes,[14] but for many, we have very little knowledge about their neurologic impact in children. A large number of chemicals have never been evaluated for their neurological impacts in children or adults.

"A large number of chemicals have never been evaluated for their neurological impacts in children or adults."

In the last few decades, extensive evidence has accumulated showing that neurotoxic chemicals can have a profound effect on the developing brain at levels that were once thought to be safe, and that may have little or no discernible impacts in adults.[15] Beginning in utero and continuing through adolescence, exposures to certain chemicals during particular time windows of vulnerability can disrupt normal developmental processes with profound and often life-long consequences.[16][17]

Lead, mercury, arsenic, PCBs, certain flame-retardants (PBDEs), and pesticides are among the chemicals for which the special vulnerability of the developing brain has been extensively demonstrated.[18][19]

Our understanding of the developing brain’s unique vulnerability suggests that there may be hundreds or even thousands of additional chemicals that can have an impact. We have no authoritative estimate of the actual number, primarily because relatively few chemicals have been examined for effects in the developing brain of laboratory animals or children.

Ten Chemicals Suspected of Causing Developmental Neurotoxicity

In spring 2012, scientists from the National Institute of Environmental Health Sciences and the Mount Sinai School of Medicine listed “10 chemicals and mixtures widely distributed in the environment that are already suspected of causing developmental neurotoxicity.” These are:

  • Lead: a heavy metal banned from gasoline in the 1970s, found in old paint, lead pipes and sinkers, toys, jewelry, and other items made of vinyl plastic. 
  • Methylmercury: released into the air from coal-burning power plants; also found in some medical equipment, switches, personal care products, and fluorescent bulbs. 
  • Polychlorinated biphenyls (PCBs): used in electrical transformers; banned in the late 1970s but still widely found in lakes, rivers, soil, fish, and people. 
  • Organophosphate pesticides: pesticides containing phosphorous that work by disrupting the nervous system; used to kill insects on crops and lawns, and in buildings. 
  • Organochlorine pesticides: pesticides containing chlorine that work by disrupting the nervous system; used to kill insects on crops and lawns, and in buildings; many but not all have been banned in the United States. 
  • Endocrine disruptors: chemicals that disrupt the hormone system, including phthalates and Bisphenol-A (both widely used in plastics), PCBs, brominated flame retardants, perfluorinated compounds, dioxins, organochlorine pesticides, among others. 
  • Automotive exhaust. 
  • Polycyclic aromatic hydrocarbons: air pollutants from fuel combustion in vehicles, coal-fired power plants, heating, and cooking; also found in tobacco smoke. 
  • Brominated flame retardants: flame retardant chemicals added to furniture, electronics, building materials, bedding, and a wide range of other products. 
  • Perfluorinated compounds: used in stain-resistant and nonstick products. 
Lead, methylmercury, PCBs, some endocrine disruptors, brominated flame retardants, and perfluorinated compounds are among chemicals subject to regulation by the Toxic Substances Control Act.[39]

Toxic Flame Retardants Example

Scientists continue to identify chemicals with enough evidence to raise serious concern over their effects on brain development. A category of flame-retardant chemicals called polybrominated diphenyl ethers (PBDEs) provides a clear illustration of how current chemical laws fail to protect public health.

PBDEs are used in many products, including upholstery, electronics, carpet, building materials, bedding, and mattresses.[20][21] Despite some regulatory restrictions on PBDEs, these chemicals remain a serious problem because they break down into more toxic forms and are used in many recycled products like carpet padding. In addition, they persist in the environment for a long time, build up in people’s bodies and in breast milk, and are often found at higher levels in children than adults.[22][23]

An extensive body of scientific literature documents the neurodevelopmental impacts of PBDEs in laboratory animals. In laboratory studies, low doses of some PBDEs cause deficits in learning, memory and hearing, changes in behavior, and delays in sensory-motor development in mice and rats.[24][25][26][27][28][29][30]

A landmark study published in 2010 provided the first evidence of the adverse effects of these chemicals on human brain development. The study tracked 329 women who gave birth in lower Manhattan hospitals following the terrorist attacks of September 11, 2001. The researchers found an association between levels of PBDE flame retardants in the babies’ cord blood and delays in mental and physical development measured at 1, 2, 3, 4, and 6 years of age.[31]

In 2004 and 2009, the U.S. government reached a voluntary agreement with chemical manufacturers to begin phasing out three commercial mixtures of PBDEs.[32][33] Since 2002, at least twelve states have banned one or more of these flame retardants due to the mounting evidence of harm to human health.[34]

Some manufacturers have responded by replacing the three PBDE mixtures with different chemicals that they claimed were safer, with no publicly available information to support their claims.

These replacement flame retardants are now showing up in the environment, in the atmosphere, sediments and seagull eggs around the Great Lakes, raising concerns that we have simply moved from one dangerous set of chemicals to another, without adequate safety testing.[35][36]

And, to the extent that these new chemicals are also persistent and bioaccumulative, we will be living with their toxic consequences for years to come.

How Chemical Policy Reform Can Help

There is solid and mounting scientific evidence on a limited number of chemicals, including those described above, to show that they are harmful to brain development. Where the weight of the evidence warrants concern, TSCA reform should include swift action to replace known toxic chemicals with safer alternatives.

However, for most of the thousands of chemicals on the market, we have virtually no information about their effects on the developing nervous system. Of the 3,000 chemicals produced in highest volume (over one million pounds per year), few have been adequately tested for toxicity to the developing brain.[37]

To ensure healthy brain development for future generations, TSCA must be updated to require that all existing and new chemicals are evaluated for their safety for pregnant women, children, workers, and other vulnerable populations.

Table 2: Some Chemicals Known to be Neurotoxic to Humans[38]*
Metals and inorganic compounds
Organic solvents
Other organic substances
Aluminum compounds
Arsenic and arsenic compounds
Azide compounds
Barium compounds
Bismuth compounds
Carbon monoxide
Cyanide compounds
Fluoride compounds
Hydrogen sulphide
Lead and lead compounds
Lithium compounds
Manganese and manganese compounds
Mercury and mercuric compounds
Nickel carbonyl
Selenium compounds
Tellurium compounds
Thallium compounds
Tin compounds
Benzyl alcohol
Carbon disulphide
Dichloroacetic acid
Diethylene glycol
2-Ethoxyethyl acetate
Ethyl acetate
Ethylene dibromide
Ethylene glycol
Isopropyl alcohol
Isopropyl acetone
Methyl butyl ketone
Methyl cellosolve
Methyl ethyl ketone
Methylene chloride
Propyl bromide
Vinyl chloride
Acetone cyanohydrin
Allyl chloride
Butylatedtriphenyl phosphate
Dibutyl phthalate
Diethylene glycol diacrylate
Dimethyl sulphate
Ethylene oxide
Fluoroacetic acid
Methyl chloride
Methyl formate
Methyl iodide
Methyl methacrylate
Polybrominated biphenyls
Polybrominated diphenyl ethers
Polychlorinated biphenyls
Propylene oxide
Tributyl phosphate
Trimethyl phosphate
Tri-o-tolyl phosphate
Triphenyl phosphate
*It is important to note that the listed chemicals are industrial chemicals. Table 2 does not include neurotoxic pesticides, which are regulated under a different federal statue.


Boyle C, et al. Trends in the prevalence of developmental disabilities in U.S. children, 1997–2008. Pediatrics 2011;127(6):1034-1042.

Boyle C, et al. Trends in the prevalence of developmental disabilities in U.S. children, 1997–2008. Pediatrics 2011;127(6):1034-1042.

Scientific Frontiers in Developmental Toxicology and Risk Assessment [Internet]. Washington, DC: National Academy of Sciences Committee on Developmental Toxicology; [cited 2000] Available from: http://www.nap.edu/openbook.php?record_id=9871&page=R1.

Gilbert S, et al. The scientific consensus statement on environmental agents affiliated with neurodevelopmental disorders. Neurotoxicology and Teratology 2009;31(4)241-242.

Akinbami LJ, et al. Attention deficit hyperactivity disorder among children aged 5–17 years in the United States, 1998–2009. NCHS data brief, no 70. Hyattsville, MD: National Center for Health Statistics 2011.

POP 1 Child population: Number of children (in millions) ages 0–17 in the United States by age, 1950–2010 and projected 2030–2050 [Internet]. Washington, DC: U.S. Census Bureau, U.S. Department of Commerce; [accessed May 31, 2012]. Available from: http://www.childstats.gov/americaschildren/tables/pop1.asp.

Prevalence of Autism Spectrum Disorders — Autism and developmental disabilities monitoring network [Internet]. Atlanta: U.S. Centers for Disease Control and Prevention; [updated 2012 March 30]. Available from: http://www.cdc.gov/mmwr/preview/mmwrhtml/ss6103a1.htm?s_cid=ss6103a1_w.
Boyle C, et al. Trends in the prevalence of developmental disabilities in U.S. children, 1997-2008. Pediatrics 2011;127(6):1034-1042.

Hertz-Picciotto I, et al. The rise in autism and the role of age in diagnosis. Epidemiology 2009;20(1):84-90.
Individuals with Disabilities Education Act: Funding Distribution [Internet]. Federal Education Budget Project, New America Foundation; [2012 January 10] Available from: http://febp.newamerica.net/background-analysis/individuals-disabilities-education-act-funding-distribution.

Shimabukuro T, et al. Medical expenditures for children with an autism spectrum disorder in a privately insured population. Journal of Autism and Developmental Disorders 2008;38(3):546-552.

Ganz M. Understanding Autism: From basic neuroscience to treatment, First Edition. Boca Raton, Florida: CRC Press; 2006:475-502.

Grandjean P, et al. Developmental neurotoxicity of industrial chemicals. Lancet 2006; 368(9553):2167-2178.

High Production Volume Information System [Internet]. Washington, D.C: U.S. Environmental Protection Agency; [updated 2012 March 22]. Available from: http://www.epa.gov/hpv/hpvis/index.html.
Grandjean P, et al. Developmental neurotoxicity of industrial chemicals. Lancet 2006; 368(9553):2167-2178.

Grandjean P, et al. Developmental neurotoxicity of industrial chemicals. Lancet 2006; 368(9553):2167-2178.
Adams J, et al. Workshop to identify critical windows of exposure for children’s health: Neurobehavioral work group summary. Environmental Health Perspectives 2000;108(3):535-544.

Grandjean P, et al. Developmental neurotoxicity of industrial chemicals. Lancet 2006; 368(9553):2167-2178.
Herbstman JB, et al. Prenatal exposure to PBDEs and neurodevelopment. Environmental Health Perspectives 2010;118(5):712-719.

Toxicological Profile for Polybrominated Biphenyls and Polybrominated Diphenyl Ethers (PBBs and PBDEs) [Internet]. Atlanta: Agency for Toxic Substances and Disease Registry, U.S. Department of Health and Human Services; [2004 September] Available from: http://www.atsdr.cdc.gov/ToxProfiles/tp68.pdf.

Polybrominated Diphenyl Ethers: Recommendations to reduce exposure in California [Internet]. Sacramento: California Environmental Protection Agency; [2006 February]. Available from: http://oehha.ca.gov/pdf/PBDEWrkgrpRptFeb06.pdf.

Polybrominated diphenylethers (PBDEs) [Internet]. Washington DC: U.S. Environmental Protection Agency; [2010 January 26] Available from: http://www.epa.gov/oppt/pbde/.

Fire Retardants in Toddlers and Their Mothers [Internet] Washington DC: Environmental Working Group; [2008 September]. Available from: http://www.ewg.org/reports/pbdesintoddlers.

Viberg H, et al. Exposure to polybrominated diphenyl ethers 203 and 206 during the neonatal brain growth spurt affects proteins important for normal neurodevelopment in mice. Toxicology Science 2009;109:306-311.

Johansson N, et al. Neonatal exposure to deca-brominated diphenyl ether (PBDE 209) causes dose- response changes in spontaneous behavior and cholinergic susceptibility in adult mice. Neurotoxicology 2008;29(6):911-919.

Costa L, et al. Developmental neurotoxicity of poly- brominated diphenyl ether (PBDE) flame retardants. Neurotoxicology 2007;28(6):1047-1067.

Rice D, et al. Developmental delays and locomotor activity in the C57BL6/J mouse following neonatal exposure to the fully brominated PBDE, deca- bromodiphenyl ether. Neurotoxicology Teratology 2007;29(4):511-20.

Eriksson P, et al. Brominated flame retardants: A novel class of developmental neurotoxicants in our environment? Environmental Health Perspectives 2001;109(9):903-908.

Kuriyama S, et al. Developmental exposure to low-dose PBDE-99: Effects on male fertility and neurobehavior in rat offspring. Environmental Health Perspectives 2005;13(2):149-154.

Viberg H, et al. Neonatal exposure to poly- brominated diphenyl ether (PBDE 153) disrupts spontaneous behaviour, impairs learning and memory, and decreases hippocampal cholinergic receptors in adult mice. Toxicology and Applied Pharmacology 2003;192(2):95-106.

Herbstman JB, et al. Prenatal exposure to PBDEs and neurodevelopment. Environmental Health Perspectives 2010;118(5):712-719.

Polybrominated Diphenylethers (PBDEs) Significant New Use Rule (SNUR) Questions and Answers [Internet]. Washington DC: U.S. Environmental Protection Agency; [updated 2007 August 8] Available from: http://www.epa.gov/oppt/pbde/pubs/qanda.htm.

DecaBDE Phase-out Initiative [Internet] Washington, DC: U.S. Environmental Protection Agency; [updated 2010 April 28] Available from: http://www.epa.gov/oppt/existingchemicals/pubs/actionplans/deccadbe.html.

Healthy States: Protecting families from toxic chemicals while Congress lags behind [Internet] Washington, DC: Safer Chemicals, Health Families and Safer States; [2010 November 17]. Available from: http://www.saferstates.com/attachments/HealthyStates.pdf.

Da Chen R, et al. Novel methoxylated polybrominated diphenoxybenzene congeners and possible sources in herring hull eggs from the laurentian Great Lakes of North America. Environmental Science & Technology 2011;45(22):9523–9530.

Salamova A, et al. Discontinued and alternative brominated flame retardants in the atmosphere and precipitation from the Great Lakes basin. Environmental Science and Technology 2011;15;45(20):8698-8706.

Grandjean P, et al. Developmental neurotoxicity of industrial chemicals. Lancet 2006; 368(9553):2167-2178.

Landrigan P, et al. A research strategy to discover the environmental causes of autism and neurodevelopmental disabilities. Environmental Health Perspectives [Internet]. 2012 [cited 2012 April 25];120:a258-a260. Available from: http://dx.doi.org/10.1289/ehp.1104285.

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