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Attention Deficit Hyperactivity Disorder - could it be related to subtle lead intoxication and maternal smoking About 1.5 million children, ages 4 to 15 years, suffer from Attention Deficit Hyperactivity Disorder (ADHD). The cause is generally not known. Exposure to tobacco smoke while in the uterus has been implicated in several studies. A report in the journal Environmental Health Perspectives in the Fall of 2006 investigated prenatal and postnatal exposure to tobacco smoke and blood lead levels in 4,704 children, ages 4 to 15 years, who participated in a national survey. A single question was asked about whether the mother smoked during her pregnancy though there was no information about exactly how much she smoked. Another question asked about the mother’s or the father’s smoking after the child was born. Lead exposure was determined by performing blood lead levels. A total of 135 children had evidence of ADHD as determined by parent reporting and use of prescribed stimulant drugs. The main findings were a more than fourfold increased risk of ADHD among females and a twofold increased risk among males exposed to a smoking mother during her pregnancy. Although lead levels were well within the normal limit (less than 10 micrograms per 100 milliliters of blood), those in the highest fifth of values (over 2 micrograms, but, for the most part, under 5 micrograms) had a fourfold increased risk of ADHD. There was no increased risk of ADHD associated with exposure to parental tobacco smoke after the child was born. The authors suggest that about one-third of ADHD can be attributed to either in utero tobacco smoke or low level lead exposure. Commentary: This is an interesting study that will require confirmation. The lack of information on how heavily the mother smoked or whether she smoked throughout the pregnancy is unfortunate. Nevertheless, there are several other studies supporting the findings here about in utero tobacco smoke exposure. The blood lead levels were determined at an age when levels have usually fallen markedly from their peak at ages 1 to 3 years. That means we have no idea what those peak levels were and that detracts from the findings. In subsequent studies, it will be important to determine blood levels serially at ages 1 to 3 years, and then determine if the height of those levels is related to the frequency of occurrence of ADHD. Still, this study does give support to the advise to women to not smoke at all during pregnancy and it emphasizes the dangers of low level lead poisoning to the brain. Amazingly, the blood level of lead considered dangerous a few decades ago was 40 micrograms per 100 milliliters of blood. As more evidence accumulated, the level defining toxicity was reduced to 30, then 20, and finally to the current level of 10 micrograms. But, the Cincinnati group involved in the present article has presented impressive evidence that the 10 microgram level is too high and that levels in the range of 2 to 3 micrograms can damage the brain. At present, average lead levels at ages 1 to 3 years are in the 2 microgram range, far lower than in the past as a result of reducing environmental lead exposure (in houses and gasoline). Because the lead levels related to ADHD in this study were above 2 micrograms at ages 4 to 15 years, the assumption is that the levels were substantially higher at ages 1 to 3 years, well above the national average and well above the 2 to 3 microgram levels that appear in some children to be associated with subtle deficits in thinking, attention, academic achievement, and IQ. In other words, it may take higher levels (though still within “normal” limits) to produce ADHD than it takes to cause subtle changes in thinking and brain function. This study, as well as others, does give strong support to continuing efforts to further reduce environmental lead exposure in early childhood from paint in old houses, lead-containing toys, etc.
Braun, J., et al. Exposure to environmental toxicants and Attention Deficit Hyperactivity Disorder in US children. Environmental Health Perspectives. doi:10.1289/ehp.9478 available via http://dx.doi.org/ [Online 19 September 2006] |
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