BOSTON -- Protecting children's developing brains from neurotoxicity should be the No. 1 priority of regulation of chemicals used in industry, researchers here said.
BOSTON, Nov. 9 -- Protecting children's developing brains from neurotoxicity should be the No. 1 priority of regulation of chemicals used in industry, researchers here have urged.
Only a few chemicals have been proven to hinder neurodevelopment, but they represent the "the tip of a very large iceberg" of known neurotoxins and untested chemicals, according to a literature review published online in The Lancet.
"The vulnerability of the human nervous system and its special susceptibility during early development suggest that protection of the developing brain should be a paramount goal of public health protection," wrote Philippe Grandjean, M.D., of Harvard, and Philip J. Landrigan, M.D., of Mount Sinai in New York.
Lower exposures can harm the developing brain because the placenta is not an effective barrier against environmental pollutants and the blood-brain barrier does not finish development until about six months after birth.
"If a developmental process in the brain is halted or inhibited, there is little potential for later repair, and the consequences can therefore be permanent," Drs. Grandjean and Landrigan wrote.
However, they cautioned that causal associations can be difficult to prove and may take decades, especially given the slow pace of current testing.
"As physicians, we should use prudence when counseling our patients, especially pregnant mothers, about avoidance of exposures to chemicals of unknown and untested neurotoxic potential," they wrote.
In their review, the researchers identified 201 known human neurotoxins and more than 1,000 chemicals shown to harm neurodevelopment in laboratory animals but without human data because of lack of testing or reporting.
Because testing substances for their effects on the developing brain has been progressing slowly through the more than 80,000 registered chemicals, new stronger regulatory strategies are needed, they said.
"The two main impediments to prevention of neurodevelopmental deficits of chemical origin are the great gaps in testing chemicals for developmental neurotoxicity and the high level of proof required for regulation," the authors wrote. "New, precautionary approaches that recognize the unique vulnerability of the developing brain are needed for testing and control of chemicals."
They suggested that exposure limits for chemicals should be set at levels that would be safe for pregnant women and young children and aimed at protecting brain development rather than the current strategy of setting exposure limits for the general population. This kind of strategy is called a precautionary approach.
"A precautionary approach, which is now beginning to be used in the [European Union], would mean that early indications of a potential for a serious toxic effect, such as developmental neurotoxicity, should lead to strict regulation, which could be relaxed, should subsequent documentation show less harm than anticipated," they added.
The investigators searched the hazardous substances database of the National Library of Medicine, fact sheets by the Agency for Toxic Substances and Disease Registry, and the integrated risk information system of the Environmental Protection Agency.
They found that the largest groups of neurotoxic compounds were metals, solvents, and pesticides, but those that mainly cause chronic or delayed disease were likely to be underrepresented in the list.
Drs. Grandjean and Landrigan then used the list to search published data for developmental neurotoxicity in humans. The neurodevelopmentally toxic substances were:
•Lead, for which low exposures "seem to cause surprisingly large functional decrements."
•Methylmercury, which has been shown to decrease IQ, memory, attention, language, and visuospatial perception.
•Arsenic, which is present in groundwater and industrial pollution and causes cognitive deficits.
•Polychlorinated biphenyls (PCBs), which were widely used in electrical equipment and are now known to cause IQ as well as subclinical cognitive decrements.
•Solvents, such as ethanol that causes fetal alcohol syndrome and toluene.
•Pesticides, that even at common rural exposures may impair motor speed and latency compared to urban children.
The researchers also reported that emerging data on "three obvious candidate substances deserve particular attention, including two that have not seemed to cause neurotoxicity in adults." These chemicals were:
•Manganese, which has been added to gasoline in Australia and Canada despite several studies in which it was associated with impaired neurobehavioral development,
•Fluoride, which may impair IQ when at high concentrations in drinking water, and
•Perchlorate, which is a widespread groundwater contaminant in the United States and can block maternal iodine uptake and potentially brain development.
In most cases, scientific documentation of developmental neurotoxicity began with recognition of adult neurotoxicity or acute, high-dose poisoning in children, the researchers noted. Accumulation of epidemiologic evidence usually followed to show that lower prenatal exposures are associated with neurobeharioral deficits in children.
Among the 80,000 chemicals registered with the U.S. Environmental Protection Agency for commercial use, most (62,000) were already in use when mandated testing began with the Toxic Substances Control Act in 1977. Fewer than half of the most common chemicals in commercial use have been subjected to even minimal laboratory testing.
The review was supported by the National Institute of Environmental Health Sciences, the. Environmental Protection Agency, and the Danish Medical Research Council.