Toxins and the Brain
April 4, 2012
This essay is in response to the question: How does the environment influence brain development? What are the exposures of greatest concern? What is the latest science and how can we translate that science into protective public health policy?
In 1979 Needleman and colleagues reported that children with elevated concentrations of lead in their baby teeth had reduced IQ relative to less exposed children. The relationship between tooth lead and IQ could only be clearly seen in population studies. Not every child exposed to lead was severely impaired, and in fact some children with high lead also had relatively high IQ. But when plotting the data for the full population, it became apparent that in lead-exposed children the IQ distribution curve was shifted downward by about 5-7 IQ points. Thus, irregardless of other factors relating to intelligence, a child exposed to lead had lower cognitive function than he or she would have had otherwise. Later evidence has indicated that these reductions in cognitive function are permanent, and last for life.
The same study reported a variety of other effects of lead exposure. Exposed children were more distractable, less persistent, more dependent, hyperactive, frustrated, and had a lower overall functioning. These behavioral differences raise an important question still unanswered more than 30 years later. Is the reduction in IQ in lead-exposed children a consequence of their inability to pay attention, or does lead impact directly the different areas of the brain involved in cognitive function, attention, and multiple behaviors?
Later very similar effects on cognitive function were seen in children born to mothers who had eaten polychlorinated biphenyl (PCB)-contaminated cooking oil. The exposed children had a similar reduction in cognitive function, with the IQ curve shifted downward by about 5-7 IQ points. There was no recovery with time, indicating a permanent decrement in cognitive function. Subsequent studies showed that children exposed to PCBs before birth exhibited reduced attention span and elevated rates of anti-social and disruptive behavior. It is really surprising that two chemicals as dissimilar as lead and PCBs do exactly the same thing to both cognition and behavior.
And it doesn’t stop there. Children exposed to methylmercury as a consequence of prenatal exposure from maternal consumption of contaminated seafood showed both reduced IQ and shortened attention. Cognitive deficits have been reported for several metals, including arsenic and manganese, as well as fluoride. In addition to PCBs, cognitive deficits have been reported for dioxins, chlorinated pesticides like DDT, organophosphate pesticides, polybrominated diphenyl ethers (PBDEs), and polyaromatic hydrocarbons. Pre- and early post-natal exposure to environmental tobacco smoke results in reduced IQ. The behavioral effects of all of these contaminants have not been as thoroughly studied as is the case for lead and PCBs, but many of these chemicals have been reported to be elevated in children with attention deficit hyperactivity disorder (ADHD). There are publications that implicate exposure to lead, PCBs, methyl mercury, other persistent organic pollutants like dioxins and chlorinated pesticides, organophosphate pesticides, PBDEs, perfluorinated chemicals, chlorophenols, phthalates, organic solvents, and environmental tobacco smoke and risk of ADHD.
These observations raise some very important questions. Do all chemicals that cause a reduction in IQ also shorten attention span and increase hyperactivity and frustration? Do they all act by a common mechanism? What happens if a child is exposed to more than one of these chemicals? Are the effects additive or even synergistic? Is the decrement in function greater with prenatal exposure, or are there also decrements from exposures any time in life? We need much more study on these issues. The present evidence suggests that prenatal exposure is most damaging, but that even adults will suffer some decrements of memory function if exposed to many of these chemicals. But no one has systematically investigated the effects of multiple exposures.
There is increasing evidence, again strongest for lead, that early life exposure to contaminants that alter ability to deal with frustration increase the risk of anti-social and criminal behavior later in life. We tend to think that criminals are a product of poverty, poor education and poor family support. These are certainly documented risk factors. However these are also documented risk factors for greater than average exposure to a variety of environmental chemicals associated with reduced IQ and increased anti-social and disruptive behavior. Perhaps we need to begin to consider at least some criminal behavior as an environmentally-induced disease! Crime rates have fallen rather dramatically in recent years, and police and politicians are quick to take credit for that. However at least a part of the real reason may be that the progress we have made in reducing exposure to lead, PCBs and some other contaminants in children born today has resulted in a generation more able to deal with frustration later in life.
In spite of progress, levels of exposure to environmental contaminants are still too high and still are altering brain function. Again the best case in point is that of lead. It was major progress when in 1991 CDC set as a national goal to reduce the blood lead concentration of children to 10 µg/dl or less, implying that this was the boundary between safe and unsafe. But we now know that there is no concentration of lead that does not cause harm to nervous system function. We still have 10% of pregnant women in the US with levels of methyl mercury in their body that pose harm to their unborn child. While levels of PCBs and organochlorine pesticides have declined in the average person, we all still have measurable concentration distributed in our body fat. But recent studies show that even at current low concentrations of serum PCBs, the higher the concentration the poorer children do on cognitive function tests. Furthermore the knowledge of how dangerous these chemical are in increasing risk of many different diseases, not just to the brain, grows more rapidly than the concentrations in the average person declines.
These facts only make it ever more important that we find ways of reducing human exposure to neurotoxic chemicals, find cost-effective and efficient methods to remove them from the environment, and develop requirements for adequate testing of new chemicals for adverse effects on nervous system function before they come onto the market. Many of the chemicals listed above, like PCBs and chlorinated pesticides, have not been manufactured for many years, yet they are present in our bodies and still causing harm. The old adage that an ounce of prevention is worth a pound of cure is particularly relevant here. We must not manufacture, use, and distribute chemicals that will adversely affect the cognitive function and behavior of future generations.
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