Free HealthE Newsletter

Developmental and Neurological Problems

Neurotoxic substances are chemical compounds that, depending on the dose, may have harmful effects on brain function and interfere with the workings of the nervous system. Neurotoxics may affect intelligence, language ability, and attention.^1,2,3,4 They may cause behavioral problems and affect mood and social adjustment. At very high doses, neurotoxics may produce such effects as coma, convulsions, respiratory paralysis, and death.⁵ Lead, mercury, and polychlorinated biphenyls (PCBs) are among the substances suspected of having harmful and possibly permanent neurological effects on children.

Abnormal development is a major concern in children because it may result in birth defects and lasting changes in intelligence, behavior, and reproductive capability. A child's nervous system, reproductive organs, and immune system grow and develop rapidly during the first months and years of life. As organ structures develop, vital connections between cells are established. These delicate developmental processes in children may easily and irreversibly be disrupted by toxic environmental substances, such as lead.⁶

Neurotoxics that may have only a temporary ill effect on an adult brain can cause enduring damage to a child's developing brain.^7,8 The immaturity of children's internal systems especially in the first few months of life, affects their ability to neutralize and rid their bodies of certain toxics. If cells in the developing brain are destroyed by lead, mercury, or other neurotoxic chemicals, or if vital connections between nerve cells fail to form, the damage is likely to be permanent and irreversible. This may mean a loss of intelligence and alteration of normal behavior.^9,10,11,12

Lead is a neurotoxic metal that affects areas of the brain associated with regulating behavior by altering the output of neurotransmitters and disrupting the development of nerve cells. Lead poisoning in children may cause lowered intelligence, reading and learning disabilities, impaired hearing, reduced attention span, hyperactivity, and antisocial behavior. Pregnant women exposed to lead may transfer the metal to a developing fetus resulting in developmental problems. While the fetus is developing, there are critical periods for each organ system, including the nervous system. During these critical periods, the cells of the body are especially sensitive to environmental toxics that may interfere with the normal development of organ structure and function.

A growing body of evidence suggests a number of synthetic and naturally occurring organic chemicals may disrupt the endocrine (hormonal) systems of humans and wildlife. A variety of chemicals cause endocrine disruption in laboratory animals, and some scientists have hypothesized that these effects also may occur in humans. Although further research is needed before such effects can be either demonstrated or ruled out, theoretically children would be at particular risk from very low levels of endocrine disrupting chemicals because of the important role the endocrine system plays in development. Concern exists about the potential for adverse developmental effects because chemicals that block or "mimic" reproductive and thyroid hormones may determine the course of prenatal development.^13,14

Possible Environmental Factors

Lead

Endocrine Disruptors

PCBs and Dioxins

Mercury

Manganese

Lead

Lead is a major environmental health hazard for young children. In 1997, the Centers for Disease Control and Prevention (CDC) reported that between 1991 and 1994, about 900,000 children in the United States under the age of six had elevated blood lead levels.^15,16

Approximately 75 percent of U.S. homes built prior to 1978 contain some lead paint.^17,18,19 Children living in older homes are threatened by chipping or peeling lead paint, and by excessive amounts of lead-contaminated dust resulting from efforts to remove paint during remodeling. Children may be exposed to lead through drinking water that has elevated concentrations from lead plumbing materials and corrosive water. They may breathe air contaminated from nearby smelters, battery plants, and industrial facilities that process lead. Exposure to lead from nearby hazardous waste sites also is a concern.^15,20

Childhood Lead Facts

• 900,000 American children have elevated blood lead levels of concern¹⁵
• Lead paint in older housing is the principal source of lead exposure today ^15,16
• Drinking water can be a significant source of lead exposure in some homes and buildings ^15,20
• In the fetus and young children, elevated lead may damage the brain, resulting in persistent neurological dysfunction¹²

Endocrine Disruptors

Increasing scientific and public attention has been focused on substances that have the potential of disrupting the endocrine systems of wildlife, laboratory animals, and possibly humans.²¹ Disruption of the endocrine system may occur in various ways. Some chemicals may mimic a natural hormone, in effect fooling the body into over-responding to the hormone. Other chemicals may block the effects of a hormone in parts of the body normally sensitive to it. Still others may indirectly stimulate or inhibit the endocrine system, leading to overproduction or underproduction of hormones. Endocrine disruptors may also play a role in reproductive cancers.²²

Scientific questions remain, however, about which chemicals are involved in disruption of the endocrine system and how children may be exposed to those chemicals. It is not yet known whether health effects similar to those observed in laboratory animals are produced in humans, and what methods are best for testing for these effects. EPA is investing significant resources to find answers to these questions.

PCBs and Dioxins

PCBs and dioxins produce a number of toxic effects in animals.^23,24 They have been linked to such health concerns as decreased gestational age, lower birth weight, depressed immune responses, impaired mental development, and growth retardation.^24,25,26 Dioxin is considered by EPA to be a known human carcinogen and as such may have adverse effects on children that do not become apparent until many years after exposure occurs.^24,27 However, no direct causal relationship has been established between PCB exposure and human health effects.

EPA banned PCBs over 20 years ago, and the Agency has taken steps to regulate over 95 percent of known sources of dioxin in the United States. Unfortunately, these chemicals are highly persistent in the environment. Because PCBs accumulate in fish and in humans, additional exposures to infants and young children may occur through ingesting contaminated fish and breast milk.²²

Mercury

Mercury is another neurotoxic substance that can produce a wide range of health effects depending on the amount and timing of exposure. Mercury is a liquid at room temperature but vaporizes readily; in vapor form it is readily absorbed through the lungs. Repeated exposures to low levels of mercury vapor over long periods have been associated with tremors, irritability, impulsiveness, drowsiness, impaired memory, and sleep disturbances.²⁸ These effects may occur at lower levels of exposure in children than adults.

When mercury attaches to an organic molecule, it may be absorbed into the body through the digestive tract. Methylmercury, which is produced naturally by certain bacteria, is such a molecule. It can cross the placenta and enter the brain, causing severe brain damage in fetuses. High mercury levels in fish consumed by pregnant women have been linked to severe brain damage and cerebral palsy in newborns.^28,29

Children are exposed to mercury primarily from eating contaminated fish. However, children eating soil contaminated with mercury or accidental exposures to mercury, also have been documented.

Manganese

Airborne manganese particles emitted from industrial and natural sources or from a fuel additive (methylcyclopentadienyl manganese tricarbonyl or MMT) may be neurotoxic. Although MMT was banned by EPA as a gasoline additive in 1994, a recent court ruling allowed the additive to be used while being tested for health effects. Laboratory studies show that manganese disturbs normal functioning of brain cells in rats. Manganese compounds also cross the placenta and may retard growth in fetal rodents. Evidence of developmental effects from chronic inhalation of manganese compounds in humans comes from manganese miners, who have high rates of psychosis and frequently suffer from a condition similar to Parkinson's disease.^30,31

References

1. Bellinger, D., A. Leviton, and C. Waternaux. 1987. Longitudinal Analyses of Prenatal and Postnatal Lead Exposure and Early Cognitive Development. New England Journal of Medicine. Volume 316, Pages 1037-1043.
   
2. Needleman, H.L., A. Schell, and D. Bellinger. 1990. The Long-Term Effects of Exposure to Low Doses of Lead in Childhood: 11-Year Follow-Up Report. New England Journal of Medicine. Volume 322, Pages 83-88.
   
3. McLaughlin, J.F., R.W. Telzrow, and C.M. Scott. 1980. Neonatal Mercury Vapor Exposure in an Infant Incubator. Pediatrics. Volume 66, Number 6, Pages 988-990.
   
4. Maker, E.L., T.J. Smith, and P.L. Landrigan. 1985. The Neurotoxicity of Industrial Solvents: A Review of the Literature. American Journal of Industrial Medicine. Volume 8, Pages 207-217.
   
5. Morgan, D.P. 1989. Recognition and Management of Pesticide Poisonings (4^th Edition). Publication Number EPA 540-9-88-001. U.S. Environmental Protection Agency.
   
6. Schardein, J.L. and K.A. Keller. 1989. Potential Human Developmental Toxicants and the Role of Animal Testing in their Identification and Characterization. CRC Review and Toxicology. Volume 19, Pages 251-339.
   
7. NRC. 1993. Pesticides in the Diets of Infants and Children. National Research Council. Washington, DC: National Academy Press.
   
8. Needleman, H.L. and C.A. Gatsonis. 1990. Low-Level Lead Exposure and the IQ of Children: A Meta-Analysis of Modern Studies. Journal of American Medical Association. Volume 263, Pages 673-678.
   
9. ATSDR. 1993. Toxicological Profile for Arsenic. U.S. Department of Health and Human Services, Public Health Service, Agency for Toxic Substances and Disease Registry.
   
10. ATSDR. 1993. Toxicological Profile for Lead. U.S. Department of Health and Human Services, Public Health Service, Agency for Toxic Substances and Disease Registry.
    
11. Gilbert, S.G. and K.S. Grant-Webster. 1995. Neurobehavioral Effects of Developmental Methylmercury Exposure. Environmental Health Perspectives. Volume 103 (Suppl. 6), Pages 135-142.
    
12. ATSDR. 1993. Case Studies in Environmental Medicine: Lead Toxicity. U.S. Department of Health and Human Services, Public Health Service, Agency for Toxic Substances and Disease Registry.
    
13. ATSDR. 1989. Toxicological Profile for PCBs. U.S. Department of Health and Human Services, Public Health Service, Agency for Toxic Substances and Disease Registry.
    
14. ATSDR. 1994. Toxicological Profile for 4,4'-DDT, 4,4'-DDE, 4,4'-DDD (Update). U.S. Department of Health and Human Services, Public Health Service, Agency for Toxic Substances and Disease Registry.
    
15. ATSDR. 1997. Healthy Children­Toxic Environments. Report of the Child Health Workgroup. U.S. Department of Health and Human Services, Public Health Service, Agency for Toxic Substances and Disease Registry.
    
16. CDC. 1997. Update: Blood Lead Levels­United States, 1991-1994. Morbidity and Mortality Weekly Report. Volume 46, Number 7, Pages 141-145.
    
17. Sargent, J.D., M.J. Brown, J.L. Freeman, A. Bailey, et al. 1995. Childhood Lead Poisoning in Massachusetts Communities: Its Association with Sociodemographic and Housing Characteristics. American Journal of Public Health. Volume 85, Pages 528-534.
    
18. Gemmel, D. 1994. Association of Housing Age and Condition with Blood Lead Levels. In: Proceedings of the 25^th Public Health Conference on Record and Statistics.
    
19. USEPA. 1996. Lead Hazard Prevention in Homes: Fact Sheet. Publication Number EPA 747-F-96-003. U.S. Environmental Protection Agency, Office of Prevention, Pesticides, and Toxic Substances.
    
20. ATSDR. 1995. A Case-Control Study to Determine Risk Factors for Elevated Blood Levels in Children. U.S. Department of Health and Human Services, Public Health Service, Agency for Toxic Substances and Disease Registry.
    
21. Kavlock, R.J. and G.T. Ankley. 1996. A Perspective on the Risk Assessment Process for Endocrine-Disruptive Effects on Wildlife and Human Health. Risk Analysis. Volume 16, Pages 731-739.
    
22. USEPA. 1997. Special Report on Endocrine Disruption: An Effects Assessment and Analysis. Publication Number EPA 630-R-96-012. U.S. Environmental Protection Agency, Office of Research and Development.
    
23. Kimbrough, R.D. 1995. Polychlorinated biphenyls (PCBs) and Human Health: An Update. Critical Reviews of Toxicology. Volume 25, Pages 133-163.
    
24. ATSDR. 1992. Congressional Testimony: Public Health Implications of Dioxins. Department of Health and Human Services, Public Health Service, Agency for Toxic Substances and Disease Registry.
    
25. Schantz, S.L. 1996. Developmental Neurotoxicity of PCBs in Humans: What Do We Know and Where Do We Go From Here? Neurotoxicology and Teratology. Volume 18, Pags 217-227.
    
26. Silbergeld, E.K. 1993. Evaluating the Success of Environmental Health Programs in Protecting the Public's Health. In: Hazardous Waste Conference 1993. Agency for Toxic Substances and Disease Registry.
    
27. ATSDR. 1989. Public Health Statement: PCBs. U.S. Department of Health and Human Services, Public Health Service, Agency for Toxic Substances and Disease Registry.
    
28. Amler, R.W., D.A. Rice, and B.L. Johnson. 1996. Assessment of Mercury Neurotoxicity Through Psychometric and Neurobehavioral Testing. Neurotoxicology. Volume 17, Pages 237-240.
    
29. Koos, B.J. and L.D. Longo. 1976. Mercury Toxicity in Pregnant Women, Fetuses, and Newborn Infants. Obstetrics and Gynecology. Volume 126, Pages 390-409.
    
30. Mena, L., O. Meurin, S. Feunzobda, and G.C. Cotzias. 1969. Chronic Manganese Poisoning­Clinical Picture and Manganese Turnover. Neurology. Volume 17, Pages 128-136.
    
31. Mena, L., H. Kazuko, K. Burke, and G.C. Cotzias. 1969. Chronic Manganese Poisoning­Individual Susceptibility and Absorption of Iron. Neurology. Volume 19, Pages 1000-1006.

Information provided by the US Environmental Protection Agency

Path: Home>Education>Health Information>Developmental and Neurological Problems