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How We're Destroying Our Kids' Brains

As many as one in six children has a neurodevelopmental disability, and scientists are finding links to pollution.

| Sat Dec. 7, 2013 6:00 AM EST

The environmental trail of brain damage extends far back in history. Accounts of lead toxicity date to the Greek physician Nicander of Colophon in 200 B.C. In more recent times, a French physician in 1848 described ill-tempered infants who'd been sucking on lead soldiers. More examples of damaged childhoods came to light after twentieth-century commercial and industrial exposures. A cheap, arsenic-laced stabilizer was added to powdered milk in Japan during the spring of 1955, causing sickness, epilepsy, or lowered IQ in more than 12,000 victims, most of them infants. (Studies of nerve cells in a Petri dish suggest that arsenic inhibits cell growth and, in the developing brain, reduces the branching of dendrites—the structures of neurons that send and receive signals.) Also in the 1950s, a factory in Minamata, Japan, began releasing mercury into the local bay, ultimately causing severe physical and cognitive problems in children whose mothers ate contaminated fish while pregnant.

By the mid-1970s researchers around the world had documented cases of lowered IQ in children exposed to lead from air pollution, mercury-based preservatives in grain, and polychlorinated biphenyls (PCBs) in fish, as well as in those exposed to alcohol in utero. The effects were much greater in children than in exposed adults. These were, as the neurotoxicologist Pam Lein of the University of California, Davis, puts it, "the blunt ones"—exposures whose effects became apparent after some concerted research. But no one really understood how the toxins worked, and they didn't know if other, more subtle, discoveries awaited.

In 1972, a Danish medical student named Philippe Grandjean saw a young woman on television who was suffering from so-called Minamata disease. Exposed to mercury in the womb, she could hardly talk and was afflicted by a severe spastic limb condition. Grandjean wondered why he wasn't being taught about environmental exposures if they could cause so much damage. He decided to spend his life researching neurotoxicants, which he terms "brain drainers." Since then he has written more than 100 papers on mercury, taught a couple of generations of scientists, and as both a physician and a researcher has an understanding of the micro and macro scope of the problem. What he told me wasn't comforting.

"Because the human brain is so complex, it's incredibly vulnerable."

"Because the human brain is so complex, it's incredibly vulnerable," says Grandjean, now an adjunct professor at the Harvard School of Public Health and the author of the 2013 book Only One Chance: How Environmental Pollution Impairs Brain Development and How to Protect the Brains of the Next Generation. "Even if something goes a little bit wrong, you don't get a second chance," he says. "You're stuck with it, and even small deficiencies can be quite significant."

As Grandjean explains it, shortly after conception, the brain begins to form from a tiny strip of cells. At its fetal growth peak, 12,000 cells are generated every minute, or 200 per second. These cells start sending and receiving messages and migrating to specific locations. By the time the brain is fully baked, it has close to 100 billion nerve cells and roughly as many caretaking glia cells, which provide nutrients, sweep out dead cells, and insulate nerve fibers. "If cells are in the wrong place or they don't form the right connections," Grandjean says, "that's what you've got for your whole life."

In a groundbreaking review published in the Lancet in 2006, Grandjean and his co-author, Philip Landrigan, of Mount Sinai Hospital in New York City, identified 201 heavy metals, solvents, pesticides, and endocrine disruptors known to have toxic effects in the human brain (at least 1,000 other substances are neurotoxic in animals but haven't been tested in humans). Of those 201, about half are "high production volume" chemicals, made in or imported to the United States in excess of one million pounds per year. At the time, the authors could point to only half a dozen as showing evidence of developmental toxicity in the fetal brain, but the count is now up to 10 and growing. All of these neurotoxicants are relatively common, routinely found in the blood of pregnant women. They include the usual suspects—lead, methylmercury, and PCBs—but also organochlorine pesticides like DDT (which was banned in the 1970s but still persists in soil and water), organophosphate chemicals like the roach-killer chlorpyrifos, PAH, PBDEs (this pervasive class of flame retardants is now being phased out), arsenic, ethanol, and the solvent toluene.

We are beginning to learn more about how these substances may alter brain development. Their strategies are complex and varied. Under the influence of methylmercury, for example, the brain's nerve cells "are lying helter-skelter, not in their usual logical locations," says Grandjean. Pesticides are designed to be neurotoxicants—that's the whole point—and some, like chlorpyrifos, work by inhibiting cholinesterase, an enzyme critical to brain-cell communication. Different neurotoxicants affect children differently. At high levels, methylmercury appears to cause memory deficits, while lead primarily decreases attention span and pesticides tend to impair spatial perception. Black carbon apparently affects attention and processing speed.

Not all kids are equally vulnerable. Other factors matter, like genes, psychosocial stress, and, interestingly, gender. Boys tend to be more vulnerable than girls to the deficits associated with PAH. Studies of prenatal exposures to phthalates and bisphenyl-A (BPA), both endocrine disruptors, also show gender differences. Phthalates are considered anti-androgens, while BPA acts like an estrogen, and the developing brain takes important cues from both hormones. With chlorpyrifos exposure, for example, boys have greater difficulty than girls with working memory.

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Many of these substances disproportionately affect the poor, but not all. Poor kids are exposed to more lead and first- and secondhand tobacco smoke. More affluent populations accumulate more mercury from their diet. Urban kids may be exposed to more PAH and black carbon, farm kids to more pesticides and arsenic from well water.

Of all the suspects, brominated flame retardants may be the most democratic. Although levels of PBDEs are now dropping in pregnant women, Americans still have the highest levels tested anywhere in the world. Flammability standards enacted in California in the 1970s resulted in the addition of PBDEs to everything from electronics to home furnishings nationwide. Unfortunately, the molecules easily migrate, accumulating in blood and breast milk and persisting for years. Structurally similar to PCBs in some cases, they appear to interfere with thyroid hormone signaling, either by directly altering the amounts of hormone or by blocking the hormone transporters. As researchers learned from studying cretinism, thyroid hormones are critical to brain development, among other functions.

A University of California, Berkeley, study of children in the state's Salinas Valley reported that those born to mothers with the highest levels of PBDEs during pregnancy averaged six points lower in verbal IQ and had lower scores for fine motor skills and a higher risk of hyperactivity. And PBDEs probably don't act in isolation. Per Eriksson, a Swedish toxicologist, has found that when lab animals are exposed to both PBDEs and mercury, the neurological effects are significantly stronger than those of mercury alone.

Philip Landrigan directs the children's environmental Health Center at Mount Sinai Hospital. Like Grandjean, he is a pillar in the field; in the 1970s, he linked childhood IQ deficits to low levels of lead. More recently he's been integral to health studies of rescue workers who were exposed to toxic particles during 9/11. Caps from the New York City police and fire departments and the US Navy decorate his office on East 102nd Street.

But do a few IQ points matter? Should society care if a boy behaves a few shades more or less aggressively?

What worries Landrigan is how easily many neurological effects can fly under the radar. These are not the kinds of acute poisonings that land kids in emergency rooms. Most doctors are not trained to look for prenatal or childhood environmental exposures. If parents ask them about it, he says, "they tend to offer bland reassurance." But for the individuals and families involved, learning, psychological, and behavioral impairments can have dramatic, lifelong impacts on meaningful measures from happiness to income.

But do a few IQ points matter? Should society care if a boy behaves a few shades more or less aggressively? These are questions that currently interest epidemiologists more than family physicians. One of Landrigan's associates at Mount Sinai, research scientist Megan Horton, who worked previously with Perera, told me that an average drop of five IQ points in the United States translates into 2.4 million gifted kids instead of 6 million, and 9.4 million mentally retarded children instead of 6 million, or a 57 percent increase. Leonardo Trasande, a pediatrician formerly at Mount Sinai and now at the New York University School of Medicine, has estimated that mercury exposures alone have led to losses of 0.59 to 3.2 IQ points in several hundred thousand children born every year in the United States, resulting in decreased lifetime economic productivity valued at $8.7 billion annually. Thanks in large part to the laws spurred by Landrigan's epidemiological sleuthing, airborne lead pollution has declined 90 percent since 1980. With the decline has come a concomitant improvement in IQ scores and an intriguing drop in youth aggression and urban crime.

Landrigan argues that the field of environmental health must become a centerpiece of public health. Mount Sinai has one of just 11 children's environmental health centers nationwide. He's disappointed that Congress last year pulled substantial funding from the once-promising National Children's Study, which aimed to follow the exposures and health of thousands of children. At the same time, federal legislation that would strengthen the way chemicals are tested and regulated gets repeatedly stalled.

"Clearly there's a need for a new regulatory apparatus for testing chemicals, and the backlog is huge," says Miriam Rotkin-Ellman, a senior scientist specializing in public health at NRDC. "There are also a lot of gaps in the science, both in terms of characterizing the health end points, such as autism, and in terms of understanding the mechanisms by which chemicals can interact with neurodevelopment. What's the timing and what are the pathways of exposure?"

Recognizing the need for more data, Landrigan's program is about to launch its own $20 million prospective study following children from the womb through childhood. It will complement the work being done at Columbia and also at the University of Utah. "We will in some instances combine and pool our data in order to increase our ability to discover links between environmental exposures and disease," says Landrigan.

Meanwhile, Perera's group has embarked on the next frontier in environmental health: brain imaging. Now that Columbia has data on exposures and cognitive problems, it makes sense to look at the brain structures themselves. Have the chemicals altered the brain in physically obvious ways?

In a nutshell, "yes," says Virginia Rauh, a perinatal epidemiologist at Columbia. Brain images of 5- to 11-year-olds with the highest exposures to chlorpyrifos show subtle deformations in parts of the brain associated with receptive language and social cognition and a thinning of areas of the parietal and frontal cortices, which are involved in executive functions like attention and problem solving.

Using brain imaging to complement large-scale epidemiology is brand new. It's also very expensive, and the technology is still being validated. Although Rauh admits that her team is "far from being able to say these changes are linked to impairment," it's time to focus on that question. "Public health has not really looked at the brain, other than with metals like lead and mercury," she says. "Our challenge is to link particular deficits we're seeing to meaningful impairment so that we can intervene and prevent them."

I took the train back home to Washington, DC, passing through the northeast corridor's confused, tight mix of commercial promise and marginalized decay. Over it all hung the molecular by-products of progress. To get a sense of just how far black carbon reaches into my own family's life, I decided to take a cue from Jusino and his pet Aethan and order up my own air-monitoring companion for a few days. I called Steven Chillrud, co-director of the Exposure Assessment Facility Core at Columbia's Lamont-Doherty Earth Observatory. An environmental geochemist, he tries to figure out how much black carbon people are exposed to by strapping carbon-measuring machines to buildings and sometimes car commuters, pedestrians, and bicyclists. He FedExed me a loaner micro-Aeth patched into a twill vest. I decided to call it Aethchyluth, honoring the urban Greek tragedian with a lisp. Aside from a few lumps, the device was fairly unobtrusive. No one seemed to notice the small sensor stretching upward toward my chin like a playful pet monkey. I wore it for most of three days while walking and driving around Washington in my daily routine.

"Schools and day-cares are typically built on the cheapest land, often next to highways."

After I shipped Aethchyluth back, Chillrud sent me the data graph, which looks like an EKG reading, drawn in thin blue spikes. Then we matched the graph to the record from a GPS app, which had tracked my travels. High spikes occurred on I-495, the Capital Beltway, which wasn't a surprise. Although I avoid it like the plague at peak rush hour, I'd driven it a couple of times at off-hours to visit relatives in southern Maryland. Even in my car with the windows rolled up, my levels hovered around the 6,000 nanograms per cubic meter mark, or more than twice the average reading Jusino was getting on his Harlem corner on a typical weekday.

I pitied the people who drive this twice a day in slow-moving traffic, but they don't get the most sympathy from Chillrud. "Schools and day-cares are typically built on the cheapest land, often next to highways," he says. "That's where developing lungs are, and susceptible kids."

But as my readings made clear, schoolchildren don't need a major freeway to breathe in black carbon and PAH. Aethchyluth got readings equal to the beltway in the parking lots at my kids' schools. That's because idling cars and school buses sit there just as kids are leaving. I was reminded of what a neuroscientist who studies brain inflammation told me: "I hold my breath when I'm behind a diesel bus."

Nineteen percent of Americans live near high-volume roads, and most areas don't monitor the air. So just how bad were my readings? We don't really know, says Chillrud, because the EPA hasn't issued guidelines for black carbon pollution the way it has for other pollutants. Black carbon is complicated because it's a proxy for many pollutants, he explains, and there are no consistent ways to measure it. In the meantime, city and federal officials recommend we reduce it through the use of cleaner fuels, newer engines, and, in New York City's case, mandated higher-quality fuel oil. "It will gradually get better," he says. "But there's still a lot to do."

When I was in Harlem, Frederica Perera had laid out a busy future of continued studies of childhood exposures to everything from PAH to phthalates to BPA to the newer pyrethroid pesticides. Her windows looked out over the Hudson River, a reminder of our collective interdependence on the air and water that both nourish us and transport pollution into our cells. The river glinted as it flowed out to sea. Once ragingly filthy, it is now cleaner than it has been in two generations.

Policy changes work, and some of those changes are quickly mirrored in our bodies. After the residential phaseout of chlorpyrifos, levels in pregnant women fell significantly. A small study published in September in the journal Environmental Science and Technology found that levels of some brominated flame retardants in pregnant Californians were 65 percent lower than in a similar group tested three years earlier (a phaseout began in 2004). By 2006, after converting to cleaner fuel and using filters, New York City's transit buses reduced their emissions of particulate matter by 97 percent.

"If the science is utilized well, policy makers can act. That's why it is enormously helpful," said Perera. "The good news is that by nature these exposures are preventable." She stood up to go to a meeting, passing framed photos of four of her grandchildren. On her way out she sent a warm greeting to Michelle. More families would be arriving soon.

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