Executive Summary


In Harm's Way

This report examines the contribution of toxic chemicals to neurodevelop-mental, learning, and behavioral disabilities in children. These disabilities are clearly the result of complex interactions among genetic, environmental and social factors that impact children during vulnerable periods of development. Toxic exposures deserve special scrutiny because they are preventable causes of harm.

  1. An epidemic of developmental, learning, and behavioral disabilities has become evident among children.

These trends may reflect true increases, improved detection, reporting or record keeping, or some combination of these factors. Whether new or newly recognized, these statistics suggest a problem of epidemic proportion.

  1. Animal and human studies demonstrate that a variety of chemicals commonly encountered in industry and the home can contribute to developmental, learning, and behavioral disabilities.

Developmental neurotoxicants are chemicals that are toxic to the developing brain. They include the metals lead, mercury, cadmium, and manganese; nicotine; pesticides such as organophosphates and others that are widely used in homes and schools; dioxin and PCBs that bioaccumu-late in the food chain; and solvents, including ethanol and others used in paints, glues and cleaning solutions. These chemicals may be directly toxic to cells or interfere with hormones (endocrine disruptors), neurotransmitters, or other growth factors. 





Dioxins and PCBs



  1. A deluge of highly technical information has created communication gaps within the field of child development.

    Some pyrethroids cause permanent hyperactivity in animals exposed to small doses on a single critical day of development.

  1. Although genetic factors are important, they should not be viewed in isolation. 

Breast-fed infants are exposed to levels of dioxin that exceed adult exposures by as much as a factor of 50.


Certain genes may be susceptible to or cause individuals to be more susceptible to environmental “triggers.” Particular vulnerability to a chemical exposure may be the result of a single or multiple interacting genes. For example:

  1. Neurotoxicants are not merely a potential threat to children. In some instances, adverse impacts are seen at current exposure levels.

  1. Vast quantities of neurotoxic chemicals are released into the environment each year.  

  1. Environmental releases often lead to human exposures with potential for harm. Dispersion of these chemicals is global.

  1. The historical record clearly reveals that our scientific understanding of the effects of toxic exposures is not sufficiently developed to accurately predict the impact of toxicants, and that our regulatory regime has failed to protect children.

a.     As testing procedures advance, we learn that lower and lower doses are harmful.

The historical record shows that “safe thresholds” for known neurotoxicants have been continuously revised downward as scientific knowledge advances. For example, the initial “safe” blood lead level was set at 60 micrograms/deciliter (ug/dl) in 1960. This was revised down to 10 ug/dl in 1990. Current studies suggest that lead may have no identifiable exposure level that is “safe.” The estimated “toxic threshold” for mercury has also relentlessly fallen, and like lead, any level of exposure may be harmful. Such results raise serious questions about the adequacy of the current regulatory regime, which, by design, permits children to be exposed up to “toxic thresholds” that rapidly become obsolete.

b.     Most chemicals are not tested for their general toxicity in animals or humans, not to mention toxicity to a child’s developing brain specifically.

Nearly 75% of the top high production and volume chemicals have undergone little or no toxicity testing. However, the EPA estimates that up to 28% of all chemicals in the current inventory of about 80,000 have neurotoxic potential. In addition:

c.     Even when regulated, the risks from chemical exposure are estimated for one chemical at a time, while children are exposed to many toxicants in complex mixtures throughout development. Multiple chemical exposures often interact to magnify damaging effects or cause new types of harm. 

With the exception of pesticides used on the food supply, current regimes regulate only one chemical at a time and do not take into account the potential for interactions. Since real world exposures are to multiple chemicals, current regulatory standards, based on single chemical exposures, are inherently incapable of providing adequate margins of safety.

d.     Animal studies generally underestimate human vulnerability to neurotoxicants.

  1. Protecting our children from preventable and potentially harmful exposures requires a precautionary policy that can only occur with basic changes in the regulatory process.


Learning, behavior, and developmental disabilities in children are clearly the result of complex interactions among chemical, genetic and social-environmental factors that influence children during vulnerable periods of development. This report focuses on the role of toxic exposures since they are a preventable cause of harm. The cognitive and behavioral characteristics that result from these interacting influences can be described as traits or abilities, such as attention or memory, which can be measured quantitatively using a variety of neuropsychological tests. Aggregates of these traits are often described using diagnostic labels that identify clinical syndromes, such as attention deficit/hyperactivity disorder, autism or learning disability. Such labels are useful for the purpose of providing clinical interventions. However, traits are generally better suited to research since they can be readily defined, quantitatively measured, and are more amenable to animal models. As a result, a large body of scientific data has begun to describe the effects of chemicals or other influences on neurodevelopment in terms of effects on traits, rather than on clinical syndromes associated with diagnostic labels. In addition, traits provide a common denominator between different fields of research, and allow us to acknowledge influences on the neurocognitive function of “normal” populations, as well as on those with diagnostic labels.

Full Report and Executive Summary are available for pdf download at:  http://www.preventingharm.org/harmswayreadmore.html

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