Summerised by Homeopathy with Edel of an Article from Jill Stein, Ted Schettler, David Wallinga and Maria Valenti Year 2000
Child development can be better protected by more precautionary regulation of household and environmental chemicals.Meanwhile, health care providers and parents can play an important role in reducing exposures to a wide variety of known and suspected neurodevelopmental toxicants that are widely present in consumer products, food, the home, and wider community.
Developmental disabilities result from complex interactions of genetic, toxicologic (chemical), and social factors. Among these various causes, toxicologic exposures deserve special scrutiny because they are readily preventable. Lead, mercury, and polychlorinated biphenyls (PCBs) have been extensively studied and found to impair development at levels of exposure currently experienced by significant portions of the general population. High-dose exposures to each of these chemicals cause catastrophic developmental effects.
Brain development begins early in embryonic life and continues well beyond birth into adolescence. During development, brain cells divide, migrate, differentiate, establish synaptic connections, and undergo programmed cell death (apoptosis) in an orchestrated sequence of events controlled by neuro- transmitters and other neurotrophic factors. Interference with any stage of this cascade of events may alter subsequent stages, so that even short-term disruptions may have long- term effects later in life.
Mercury (Hg) is a potent neurodevelopmental toxicant commonly encountered as dietary methylmercury, which adversely affects enzymes, cellular membrane function, and neurotransmitter levels. In a prolonged poisoning episode in Japan and a more acute episode in Iraq, large prenatal methylmercury exposures were associated with psychomotor retardation, seizures, developmental delays, and mental retardation. Much smaller prenatal exposures from maternal consumption of contaminated fish in New Zealand (mean maternal hair level Hg 8.3 ppm) and the Faroe Islands (mean maternal hair level Hg 4.3 ppm) adversely affected IQ, language development, visual–spatial skills, gross motor skills, memory, and attention in offspring.
As with lead, a historical review of our understanding of the neurodevelopmental toxicity of mercury shows that more refined testing has resulted in a steady decline in the exposure level thought to be “safe” and without adverse effects. The U.S. Environmental Protection Agency (U.S. EPA) has recently developed a reference dose for mercury of 0.1 μg Hg/kg/day and estimates that mercury exposures at this level are likely to result in hair mercury levels of about 1.0 ppm. Maternal exposures at or below this level are thought unlikely to increase the risk of harm to the developing fetal brain.
The central nervous toxicity of manganese (Mn) due to occupational exposures is well characterized. Symptoms include gait and movement disorders, and in some cases, inappropriate behavior. More recently, the developmental neurotoxicity of manganese has emerged as a significant public health concern. In several small epidemiologic studies of children, manganese hair levels are associated with ADHD (27–29). Developmental exposure to manganese in laboratory animals is associated with hyperactivity.
At low levels, manganese is an essential dietary trace element necessary for critical enzymatic reactions. The concentration of manganese in human breast milk is about 6 μg Mn/L, whereas infant formula may contain 77–100 μg Mn/L, depending on whether it has been supplemented; soy formula may naturally contain as much as 200–300 μg Mn/L (31,32). In
infants, manganese easily gains access to the developing brain because of an immature blood–brain barrier. These observations raise questions about the wisdom of supplementing infant formula with manganese and the widespread use of infant soy formula containing naturally high concentrations of manganese.
They are also further concerns about the use of gasoline supplemented with an organic manganese compound as an octane enhancer in the United States and Canada. The Ethyl Corporation (Richmond, VA, USA), the U.S.-based manufacturer of the additive, claims there is no evidence to support concerns that manganese in gasoline represents a threat to public health—an argument that is eerily reminiscent of their position on the use of tetraethyl lead many years ago. Present data indicates that the brain is vulnerable to long-lasting effects from developmental exposures to manganese.
The adverse neurodevelopmental impacts of polychlorinated biphenyls (PCBs) have been examined in several large epidemiologic studies. In humans, developmental exposures to PCBs at ambient environmental levels cause hyporeflexia, psychomotor delays, delayed cognitive development, and IQ deficits. Impaired learning, altered behavior, and hyperactivity have been demonstrated in laboratory animals. PCBs also alter thyroid hormone metabolism and may interfere with thyroid hormone-induced gene transcription. In humans, seals, rodents, and birds, PCB exposure causes decreased thyroid hormone levels. Some PCBs also alter neurotrans- mitter levels (47). For example, ortho-PCBs decrease dopamine synthesis, whereas non-ortho-PCBs increase dopamine levels.
Because thyroid hormone is essential for normal brain development, the effects of PCBs and other chemicals that interfere with thyroid hormone homeostasis are of particular concern. Children with learning disabilities are often alienated, isolated, and misunderstood. Some developmental disabilities increase the risk of substance abuse, delinquency, criminal behavior, and suicide.
As the science of neurodevelopment slowly evolves, questions about appropriate preventive actions deserve consideration. The neurodevelopmental effects of relatively few compounds encountered in the ambient environment are well characterized. Yet, even these limited data highlight the profound vulnerability of the developing brain.
Comparisons of animal and human data for lead, mercury, and PCBs show that laboratory animal studies tend to underestimate human neurodevelopmental sensitivity by 2–4 orders of magnitude. In each case, reference or benchmark doses were continuously revised downward as human data were developed because:
1. Neurodevelopmental data are lacking for the large majority of known or suspected neurotoxicants.
2. Regulatory agencies have generally failed to require neurodevelopmental testing of chemicals before they are marketed. 3. None of the voluntary testing programs proposed by the chemical industry in the United States includes neurodevelopmental testing.
In its Sixth Biennial Report on Great Lakes Water Quality, the International Joint Commission (IJC) advocated a weight of evidence approach to the identification of substances that may cause harm. They found it disingenuous that science must prove with 100% certainty that an exposure will result in an adverse health effect before taking precautionary action. They concluded, “. . . the focus must be on preventing the generation of persistent toxic substances in the first place, rather than trying to control their use, release, and disposal after they are produced.” They endorsed the precautionary principle that, with evidence of threats of significant harm, even in the face of scientific uncertainty, precautionary action should be taken to protect public health and the environment. However, Gordon Durnil, former chair of the IJC, described the response strategy of industry lobbyists as the three Ds—deny, divert, delay. Although we can do little about genetic contributions to many of these developmental disorders, we have enormous opportunities to mitigate environmental factors.
Sufficient evidence has been accumulated to permit better understanding of the hazards of exposure to neurotoxic chemicals. Clearly, more comprehensive pre- and postmarket neurodevelopmental testing of chemicals to which humans and wildlife are likely to be exposed is essential. Residual uncertainties, however, cannot be an excuse for avoiding precautionary action when available evidence establishes the plausibility of harm.
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