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Environmental Chemicals and Impairment in Children

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Environmental Chemicals and Impairment in Children

Catherine Csaky

The link between environmental toxicants and developmental disabilities in children is discussed.  The effects of environmental agents on the nervous system are described.   Research findings regarding the effect of lead, methylmercury and commercial chemicals on development are also presented.  The relationship between chemical exposure and low-income families is highlighted.  It is concluded that psychologists can play an important role in the assessment and treatment of impairment associated with environmental chemical exposure.

According to the Centers for Disease Control and Prevention (2004), approximately 17% of U.S. children under the age of 18 are affected by one or more developmental disabilities that have an impact on emotional state, cognitive function, learning ability, a variety of behaviors, or physical growth.  Research shows that developmental disabilities frequently occur with anxiety disorders and a variety of psychiatric conditions affecting mood, emotion, and behavior (National Institute of Mental Health, 1999).  Although the etiology of developmental disabilities includes factors such as genetics, nutrition, and social influences, current research indicates a link between environmental toxicants and developmental disabilities (Koger et al., 2005).

Koger et al. (2005) note that the developing nervous system is highly vulnerable to environmental agents.  More specifically, brain development begins early in the fetus, as cell division, migration, differentiation, and synapse formation proceed in sequences with variable timing in different portions of the brain (Koger et al.).  Neural migration and myelination continue through infancy and the second year of life, and overall brain development continues into adolescence (Koger et al.).  The researchers point out that many substances easily penetrate the placenta during prenatal development, and because the fetal blood-brain barrier is not fully formed, toxicants can enter and impact brain development through direct toxicity or through interference with a variety of mechanisms, including the endocrine system (Koger et al.).

Heavy metals, such as mercury, lead, and manganese, commercial chemicals such as some pesticides, and contaminants like dioxins are all of concern because of their direct neurotoxic potential as well as their ability to interfere with biochemical mechanisms (Koger et al.).  Neurotoxicants also target developmental processes, including cell replication, cell differentiation, and neural communication (Koger et al.).  Because normal neurologic development is based on specific sequences of cellular events, such chemical disruption has been related to disabilities, including mental retardation, cerebral palsy, epilepsy, and deficits of learning, memory, and attention, attention-deficit/hyperactivity disorder, and possibly even autism (Koger et al.).

Lead is one of the most frequently studied neurodevelopmental toxicant and regulatory decisions have significantly reduced exposures (Canfield et al., 2003).  The researchers point out that despite legislation, exposures continue.  For example, lead is still used in many industrial, commercial, and military products and applications; deterioration or renovation of homes and complexes constructed prior to 1980 can result in exposure to contaminated paint chips or dust; and lead-tainted soils can persist as long as 2,000 years (Canfield et al.).  Contaminated house dust is a significant source of lead exposure, particularly for children in urban communities (Canfield et al.).

Research shows that there is no “safe” level of lead exposure.  A recent study indicated that concentrations falling below levels of concern set by the Centers for Disease Control and the World Health Organization were found to inversely correlate with intellectual function (Canfield et al.).  In one interesting study, the researchers measured blood lead concentration in 172 children and administered the Stanford-Binet Intelligence Scale at the ages of 3 and 5 years.  The results showed that the blood lead concentration was inversely and significantly associated with IQ.  These findings suggest that more U.S. children may be adversely affected by environmental lead than previously estimated (Canfield et al.).  The researchers assert that lead exposure is associated with a variety of behavioral and cognitive problems in children, including antisocial and delinquent behavior, violence, criminality and unwed pregnancy, and is known to produce deficits in motor coordination, intelligence, language function, learning, memory, attention, and executive function, as well as mental retardation at higher doses (Canfield et al.).

Methylmercury, one of the organic forms of mercury, can also influence both pre-and postnatal brain development depending on the level of exposure (Clarkson et al., 2003).  In the developing brain, methylmercury interferes with cell proliferation and migration.  In severe poisoning cases in children, mental retardation or cerebral palsy may result (Clarkson et al.).  The researchers note that its less obvious effects include disordered cognitive development as reflected by lowered IQ scores, impairments of memory and attention, and coordination deficits (Clarkson et al.).  One recent study assessed the degree of risk to brain development posed by methylmercury exposure in a community that consumed large quantities of seafood.  The researchers investigated the relationship between maternal exposure to methylmercury on the basis of hair or cord blood levels and offspring development.  The results showed subtle adverse effects including performance on the Boston Naming Test (Clarkson et al.).

Research indicates that commercial chemicals such as pesticides and plastics, and contaminants like dioxins alter hormone or neurotransmitter function and may interfere with sexual differentiation of the brain, as well as affect cognitive abilities such as memory (Koger et al., 2005).  Pesticides are toxic by design and many insecticides act as direct neurotoxicants, as they are designed to disable the nervous system of insects through mechanisms directly relevant to human physiology.  Many insecticides function by affecting the metabolism of neurotransmitters, or by interfering with endocrine function (U.S. Congress, Office of Technology Assessment, 1990).  Research shows learning and behavioral changes in rodents exposed to organophosphate pesticides (Koger et al.).  The authors note that because of the parallels in brain development between rodents at postnatal Day 10 and humans during the last trimester of pregnancy, there is the potential for similar effects in the offspring of women exposed during pregnancy (Koger et al.).  While little research has assessed the developmental neurotoxicity of pesticides in humans, findings suggest impairments in memory, social interaction, creativity, and motor skills in a population of Mexican children exposed to pesticides relative to a comparable group who lived in an untreated area (Koger et al.).

Both endogenous and exogenous factors and their interactions regulate human child development (Walkowiak et al., 2001).  Among the exogenous factors affecting early neurobehavioral child development is the exposure to chemicals in utero or during the early stages of brain development (Walkowiak et al.).  As previously discussed, some environmental chemicals such as lead or organic mercury, have received attention in the literature, including the polychlorinated biphenyls (PCBs).  PCBs are persistent environmental contaminants consisting of up to 209 individual congeners.  PCB and their metabolites cross the placenta, exposing the vulnerable fetus to PCBs circulating in maternal blood.  After birth the infant is additionally exposed to relatively high PCB concentrations in human milk.  Among a wide range of biological effects, developmental neurotoxicity seems to be a prominent feature of these chemical mixtures (Walkowiak et al.).

In another interesting study, the researchers investigated whether environmental levels of exposure to PCBs adversely affect mental and motor development in early childhood, and if a favorable home environment can counteract this effect.  The results showed negative associations between milk PCB and mental/motor development at all ages, becoming significant from 30 months onwards.  Over 30 months, for a PCB increase from 5th percentile to 95th percentile, there was a decrease in the Bayley Scales of Infant Development mental scores, and a decrease in the Bayley Scales of Infant Development motor scores.  In addition, home environment had a positive effect from 30 months onwards (Walkowiak et al.).  The researchers conclude that prenatal PCB exposure at current European background levels inhibits, and a favorable home environment supports, mental and motor development until 42 months of age (Walkowiak et al.).

Environmental toxicant and chemical exposure has been strongly tied to income in the United States (Evans, 2004).  Research shows that low-income families live closer to toxic waste dumps, and their children carry a heavier body burden of toxins (Evans, 2004).  Research also shows that the prevalence of unsafe lead levels in American children was four times higher in low-income families than in high-income families (Evans, 2004).  Furthermore, studies indicate that low-income homes have higher levels of nitrogen dioxide, carbon monoxide, and radon and allergen exposures associated with asthma (Evans, 2004).  The author contends that exposure to toxins such as lead and pesticides, along with residence in areas with poorer air and water quality, causes physical health problems and cognitive deficits in children (Evans, 2004).  More specifically, residential crowding and noise are associated with socioemotional distress and elevated psychophysiological stress among children; high noise levels interfere with reading acquisition; substandard housing quality causes respiratory morbidity; and low-quality school facilities are associated with poor learning outcomes (Evans, 2004).  It is apparent that low-income children may face physical environmental risks with known adverse developmental outcomes (Evans, 2004).

There are numerous opportunities for psychological interventions in this critical area.  Oskamp (2000) notes that the role of psychology in addressing disability and rehabilitation issues needs to include the role of psychologists in the analysis of environmental toxicants and their effects on children’s development.  Koger et al. (2005) also point out that many areas of psychology are impacted in some way b y the relationship between toxicants and child development or could contribute to diminishing the problem.  For example, neuropsychologists can develop measures of the deficits associated with chemical exposures, and health, biological, clinical, and social psychologists can help examine the stress response associated with living in polluted environments and inform strategies to more effectively cope with such challenges (Koger et al.).

McKenzie-Mohr (2000) has developed a framework called community-based social marketing (CBSM), which uses principles of social psychology to promote community-based efforts toward sustainable practices.  CBSM projects that have been implemented include efforts to reduce pollution and hazardous waste and to protect watersheds (McKenzie-Mohr, 2000).  In sum, the evidence clearly shows a link between environmental chemicals and developmental disabilities, and psychologists can certainly play an important role in the assessment and treatment of impaired behavioral and cognitive function associated with environmental chemical exposure.

References

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National Institute of Mental Health. (1999). Learning disabilities. Retrieved February 26,  2006, from www.nih.gov.

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