Lead is a well-known neurotoxin. At extreme levels of exposure, it can kill people. Even at weaker levels, lead exposure is thought to lead to a wide variety of cognitive and psychological problems. Some have suggested that lead’s negative effect on intelligence may play a role in the Black/White IQ gap.
In this article, I’m going to review the evidence linking lead exposure to poor cognitive functioning and then show that the degree of racial differences in lead exposure is not nearly large enough to cause any significant difference in IQ.
The negative effect of lead on cognitive ability has been shown in both monkeys and rats. Bushnell and Browman (1979) fed groups of infant Rhesus monkeys one of three kinds of milk: lead-free milk, milk with low levels of lead, and milk with high levels of lead. Once the monkeys were older children, their blood lead levels (BLLs) were the same. Nonetheless, those who were fed lead as infants scored worse on cognitive tests suggesting that it had done permanent damage to them during development. Levin and Browman (1986) confirmed that this effect lasted into adulthood.
Rice (1985) dosed one group of infant monkeys with lead. Later, when each group’s BLL had fallen to 12 mg/dl or lower, they found that the group exposed to lead in infancy did poorly on cognitive tasks when compared with the control group. Gilbert and Rice (1987) confirmed that this effect lasted into adulthood.
Slechta, Weiss, and Cox (1985) and Brockel and Slechta (1998) found that experimentally exposing rats to lead caused an increase in their impulsivity and a decrease in their performance on cognitive tasks.
Schawrtz (1994) examined 4 cross-sectional and 3 longitudinal studies on the relationship between blood lead levels and IQ in school-age children. Combining data from all seven studies, Schwartz found that an increase in blood lead from 10 ug/dl to 20 ug/dl predicted a decrease in IQ of 2.57 points.
The reported effect sizes did not differ between cross-sectional and longitudinal studies. However, studies with samples from populations with lower overall BLLs produced larger effect sizes suggesting that a given absolute increase in BLL will cause more damage among low BLL individuals than among high BLL individuals. In other words, its damage diminishes as your BLL rises.
Tong et al. (1996) addressed the possibility that low IQ causes lead exposure rather than the other way around. Because they followed the same participants for an extended period of time, Tong et al were able to show not only that BLL was related to low scores on intelligence tests but also that scores on cognitive tests for infants did not predict BLL in 10-13 year olds. This suggests that having a low initial IQ did not cause children to have higher than average BLL.
Weitzman et al. (2004) conducted a review of 23 separate studies and also found a consistent negative relationship between childhood BLL and cognitive ability. Unlike the other reviews we’ve seen here, Weitzman et al. did not find that the effects of BLL on IQ were larger for in samples with lower mean BLL.
This report also reviewed studies showing a negative relationship between BLL and height, female sexual maturation, and head size, which supports the idea that lead disrupts the developmental process.
Lanphear et al. (2005) combined data from 7 longitudinal studies which looked at lead and childhood IQ. These studies controlled for an impressive list of potentially confounding variables including race, sex, birth weight, birth order, maternal education, maternal IQ, maternal age, marital status of parents, prenatal smoking status, prenatal alcohol use, and HOME inventory score which is a measurement of how cognitively stimulating a child’s home environment is.
As can be seen, like Schwartz, Lanphear et al. found that lead’s effect on IQ lessened the more lead a person already had in their blood.
Lanpher et al. also found that current levels of lead predict IQ even after controlling for pre natal levels of IQ. By contrast, pre natal levels of lead does not predict IQ after controlling for current levels of lead. Unlike studies in non-human animals, this suggests that current lead levels damage IQ while lead levels from infancy do not.
Needleman et al. (1990) also looked how chilchood lead exposure related to adult intelligence. In a sample of 160 individuals they found that lead levels at age 11 predicted cognitive ability at age 18.
Similarly, Mazumdar (2011) found that childhood BLL predicted adult IQ scores. This association was reduced to statistical insignificance after controlling for maternal IQ, but this may be due to the fact that their sample only included 43 people.
On the whole, there is a strong case for the view that childhood lead exposure has a causal impact on childhood IQ. Holding maternal IQ and education constant significantly reduces the probability of genetics confounding these studies. Controlling for HOME inventory scores makes it unlikely that low SES can explain the association between BLL and IQ. Studies done on non-human animals and research showing that infant intelligence does not predict childhood BLL provide good evidence that lead really does cause low IQ rather than the other way around.
The evidence suggesting that childhood lead exposure has an impact on adult IQ is weaker. Some research supports this contention while other research does not. I haven’t been able to find any meta-analysis of these results and some of the research I have reviewed here has not been of particularly high quality. The evidence in this area is not strong enough to justify taking a firm position.
Racial Differences in BLL
In America, African Americans have higher BLLs than do Whites and Hispanics during childhood. White et al. (2015) reviewed 5 national samples taken between 1998 and 2004 and found that African American children had a mean BLL about 1.4 ug/dl higher than non-Hispanic White American children did.
More recent data from the CDC shows that in 1999-2004 Black children had a mean BLL which was 1 ug/dl higher than White children and that this BLL gap shrank to 0.9 ug/dl in samples taken between 2003 and 2006, and to 0.5 ug/dl in samples taken between 2007 and 2010.
Interestingly, both of these studies also looked at White/Hispanic children differences in BLL and both found that there were no consistent differences between these groups.
Black/White differences in BLL during childhood are real, but slight. Their size can be exaggerated by looking at what proportion of each race has a BLL which exceeds some arbitrary threshold. Consider, for instance, this chart from Drum (2016):
That these differences seem larger is not surprising. Small mean differences lead to large differences at the tails of distributions. However, there is no justification for the thresholds used here. In fact, these thresholds are so arbitrary this one chart uses three different standards. This reflects changes in the CDC guidelines about safe levels of lead. For decades, the CDC has been lowering this “safe threshold” as better research has come in with larger samples and more presise measures which has allowed researchers to document the damage that lead does even at very low levels.
Further more, this slight racial gap in blood lead levels diminishes to virtually nothing by adulthood. CDC numbers [taken from Tsoi et al. (2016) and Pricket et al.(1994)] show that BLL levels no longer differ significantly by race among the total population.
Lead and Racial IQ Differences
In the United States, Blacks score about 15 points lower than Whites on IQ tests (Roth et al., 2001). There is debate about the degree to which this gap is due to environmental and genetic factors. Lead is one environmental factor which is sometimes pointed to in order to explain this gap.
Based on the analysis from Lanphear et al., a 7.6 ug/dl difference in BLL (2.4 to 10.0) leads to an IQ difference of 3.9 points. The most recent CDC data available suggests that Black children have a mean BLL about 0.5 ug/dl higher than Whites which is 6.57% as large as a 7.6 ug/dl difference. This, in turn, should have an effect on IQ about 6.57% as large as -3.9 points, which is -0.26 points.
One complication is that the effect of lead on IQ may even be stronger at this very low level of BLL (1.8 vs 1.3) than is indicated by Lanphear’s estimate of the effect within the 2.4-10.0 ug/dl range. However, this effect is almost certainly less than one IQ point.
And this, of course, is in children. Among adults, there is no racial difference in BLL and so it can cause no IQ disparity.The effect of the childhood gap in BLL may persist into adulthood, but, as I reviewed above, research on this is far from conclusive or even consistent. And even if it does, it’s still going to be an effect of less than one point.
On the other hand, there was a small racial gap in adult lead exposure in the 70s and a larger childhood gap. The narrow of racial gaps in lead exposure may have played a role in the Black/White IQ gap slightly shrinking between the 1970s and 1980s.
In conclusion, lead does not play a major role in the B/W IQ gap. It may have played a larger role 40+ years ago, but today it contributes nearly nothing to racial intelligence differences.