More than half of the US population has clinically troubling blood lead levels that lower IQ scores

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In 1923, lead was first added to gasoline to help keep car engines healthy. However, automotive health came at the great expense of our own well-being.

A new study calculates that exposure to car exhaust from leaded gas during childhood stole a collective 824 million IQ points from more than 170 million Americans alive today, about half the population of the United States.

The findings, from Aaron Reuben, a Ph.D. candidate in clinical psychology at Duke University, and colleagues at Florida State University, suggest that Americans born before 1996 may now be at greater risk for lead-related health problems, such as faster aging of the brain. Leaded gas for cars was banned in the U.S. in 1996, but the researchers say that anyone born before the end of that era, and especially those at the peak of its use in the 1960s and 1970s, had concerningly high lead exposures as children.

The team’s paper appeared the week of March 7 in the journal Proceedings of the National Academy of Sciences.

Lead is neurotoxic and can erode brain cells after it enters the body. As such, there is no safe level of exposure at any point in life, health experts say. Young children are especially vulnerable to lead’s ability to impair brain development and lower cognitive ability. Unfortunately, no matter what age, our brains are ill-equipped for keeping it at bay.

“Lead is able to reach the bloodstream once it’s inhaled as dust, or ingested, or consumed in water,” Reuben said. “In the bloodstream, it’s able to pass into the brain through the blood-brain barrier, which is quite good at keeping a lot of toxicants and pathogens out of the brain, but not all of them.”

One major way lead used to invade bloodstreams was through automotive exhaust.

To answer the complex question of how leaded gas use for more than 70 years may have left a permanent mark on human health, Reuben and his co-authors Michael McFarland and Mathew Hauer, both professors of sociology at Florida State University, opted for a fairly simple strategy.

Using publicly available data on U.S. childhood blood-lead levels, leaded-gas use, and population statistics, they determined the likely lifelong burden of lead exposure carried by every American alive in 2015. From this data, they estimated lead’s assault on our intelligence by calculating IQ points lost from leaded gas exposure as a proxy for its harmful impact on public health.

The researchers were stunned by the results.

“I frankly was shocked,” McFarland said. “And when I look at the numbers, I’m still shocked even though I’m prepared for it.”

As of 2015, more than 170 million Americans (more than half of the U.S. population) had clinically concerning levels of lead in their blood when they were children, likely resulting in lower IQs and putting them at higher risk for other long-term health impairments, such as reduced brain size, greater likelihood of mental illness, and increased cardiovascular disease in adulthood.

Leaded gasoline consumption rose rapidly in the early 1960s and peaked in the 1970s. As a result, Reuben and his colleagues found that essentially everyone born during those two decades are all but guaranteed to have been exposed to pernicious levels of lead from car exhaust.

Even more startling was lead’s toll on intelligence: childhood lead exposure may have blunted America’s cumulative IQ score by an estimated 824 million points—nearly three points per person on average. The researchers calculated that at its worst, people born in the mid-to-late 1960s may have lost up to six IQ points, and children registering the highest levels of lead in their blood, eight times the current minimum level to initiate clinical concern, fared even worse, potentially losing more than seven IQ points on average.

Dropping a few IQ points may seem negligible, but the authors note that these changes are dramatic enough to potentially shift people with below-average cognitive ability (IQ score less than 85) to being classified as having an intellectual disability (IQ score below 70).

Moving forward, McFarland is analyzing the racial disparities of childhood lead exposure, hoping to highlight the health inequities suffered by Black children, who were exposed more often to lead and in greater quantities than white children.

Reuben’s next step will be to examine the long-term consequences of past lead exposure on brain health in old age, based on previous findings that adults with high childhood lead exposure may experience accelerated brain aging.

“Millions of us are walking around with a history of lead exposure,” Reuben said. “It’s not like you got into a car accident and had a rotator cuff tear that heals and then you’re fine. It appears to be an insult carried in the body in different ways that we’re still trying to understand but that can have implications for life.”


Higher neighborhood-level risks of childhood lead exposure were associated with smaller mid-anterior, central, and mid-posterior corpus callosal volumes (i.e., the genu, truncus/body, and anterior splenium, respectively); to a lesser extent, lead-exposure risk was associated with smaller posterior corpus callosal volumes (i.e., posterior splenium) [56,58,59]. These associations were absent for ADI, but present for housing age.

Thus, the lead-risk associations were likely attributable to factors associated with elevated lead-exposure risk (e.g., residual lead paint in older homes) [1,27]. Because ABCD enrolled 9- to 10-year-old participants at baseline, we cannot know whether these associations existed prior to baseline (i.e., pre- vs. postnatal insults) or disentangle them from other unmeasured confounding factors. However, the relationships between lead risk and callosal volume in mid-anterior to posterior, but not anterior, callosal regions are consistent with research showing earlier development of anterior than posterior corpus callosum, with the latter continuing to grow through adolescence (i.e., anterior-to-posterior maturation) [60–63].

While we recently reported the strongest inverse associations between lead-exposure risk and cortical structure in children of low-income families [28], the nonspecific inverse associations in callosal structure observed here suggest differential socioeconomic and environmental modulation of cortical and subcortical developmental trajectories, which is consistent with known spatially and temporally variable structural brain maturation [30,64].

Previous research on lead’s impact on corpus callosal structure has been inconsistent. Stewart and colleagues [19] reported inverse correlations between bone-lead levels and posterior corpus callosal volume in occupationally exposed lead workers. Brubaker et al. [21] reported increased white matter integrity in the callosal genu, body, and splenium in adults exposed to lead during childhood, but Hsieh et al. [65] found nonsignificant differences in corpus callosal white-matter integrity in lead-exposed workers. Lasky et al. [66] reported no significant differences in callosal volume in lead-exposed (pre- or postnatal) versus non-lead-exposed rhesus monkeys, while Rai et al. [67] suggested that exposure to metal mixtures (arsenic, cadmium, and lead) in developing rats may thin the corpus callosum. There are no endogenous lead-exposure data yet in ABCD, but our study suggests that lead-exposure risk and its related environmental factors may be associated with corpus callosal morphology.

Exposures to other neurotoxicants are similarly associated with callosal morphology [68–72]. Prenatal alcohol exposure was most consistently associated with smaller areas of more posterior callosal regions in 8- to 22-year-olds [68,69], and prenatal particulate matter air pollution exposure, especially during the 3rd trimester, was most strongly associated with smaller volumes of the callosal body in 8- to 12-year-olds (mid-anterior + central + mid-posterior) [70].

Posterior corpus callosal size was 3.1% (7.9%) smaller in 12- to 18-year-old males (females) prenatally exposed to cigarette smoking [71], and splenial (posterior corpus callosal) size in 4.5-year-olds was 1.4% smaller given high versus low levels of prenatal polychlorinated-biphenyl exposure [72]. Here, we found a 5.2% mean decrease in mid-posterior, central, and mid-anterior corpus callosal volume in individuals living in census tracts with the highest versus lowest lead-risk score.

Lead’s well-established effects on cognition and potential associations with corpus callosal structure are complemented by relationships between corpus callosal structure, cognition, and intelligence [73]. In our sample, anterior callosal regions were weakly associated with cognitive function whereas posterior regions were more strongly associated with cognitive performance.

The association between mid-posterior callosal structure and processing speed (i.e., the Pattern Comparison Processing Speed Test) corroborates research on callosal volume and processing speed in occupationally lead-exposed and non-exposed adult men [18]. Our reported associations between mid-posterior callosal volume and performances on the Picture Vocabulary Test and the Oral Reading Recognition Test are also consistent with research suggesting that posterior callosal regions are critical for interhemispheric transfer between temporal-parietal-occipital cortical regions involved in language processing [74–77].

The lead-risk metric was primarily a function of the estimated neighborhood-level prevalence of lead-based paint given the age of houses in that neighborhood [25,26]. Even though lead-based house paint and leaded gasoline (for on-road vehicles) were banned in the US in 1978 [78] and 1996 [79], children remain at risk for ingesting lead via (1) drinking water provided through lead service lines (i.e., lead-containing plumbing) [80], (2) lead-contaminated dust and soil given the prior use of lead-based paint in older buildings [27], and (3) lead-contaminated topsoil from past leaded-gasoline vehicle emissions [81].

Indeed, while average blood lead levels have substantially declined over the past several decades, a 2021 study estimated that nearly 400,000 1-to-11-year-olds in 2011–2016 had blood-lead levels exceeding the CDC’s reference level of 5 μg/dL [82]. Here, about one in five houses in our participants’ neighborhoods were estimated to contain lead-based paint hazards, which is consistent with national surveys showing that 25% of United States housing stock contains one or more lead hazards [27].

Of 14 risk factors known to impair neurodevelopment (e.g., medical conditions, low SES), lead exposure was reported as 2nd only to preterm birth in its impact on total reduction in IQ [83]. Lead-associated decrements in IQ have been suggested to contribute to annual costs of approximately $977 billion in low- and middle-income countries [17], many of which do not have regulations as to limits of the concentration of lead in paint [84]. Accordingly, reducing risks of lead exposure (and addressing related environmental factors) will have economic and health benefits that facilitate prosperity in the United States and worldwide.

Lead risk and housing age were distinctly associated with callosal morphology. In contrast, ADI, a metric of neighborhood socioeconomic disadvantage [40,41], was inversely associated with subcortical gray-matter, cerebellar cortical, accumbens area, and amygdalar volumes, but not callosal morphology. Despite research on the effects of neighborhood SES on child development (e.g. ADI) [85] and family-specific SES measures on children’s brain structure [86–88], less is known about how neighborhood-level metrics of disadvantage influence neurocognitive development [87,89].

Our results are consistent with previous reports showing (1) smaller cortical and subcortical volumes in 8- to 21-year-olds living in low-SES neighborhoods [90] and (2) greater age-related increases in right amygdalar volume in adolescents living in more disadvantaged neighborhoods (potentially due to the groups’ lower baseline amygdalar volumes) [91]. Given associations between amygdalar volume and depressive symptoms [92], it will be critical to evaluate longitudinal trajectories of mental health and brain development in ABCD and whether neighborhood characteristics increase risk or promote resilience to developmental insults such as lead neurotoxicity.

reference link :https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC8516269/


More information: Half of US population exposed to adverse lead levels in early childhood, Proceedings of the National Academy of Sciences (2022). DOI: 10.1073/pnas.2118631119.

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