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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 7:00 AM EST

This story originally appeared on the OnEarth website.

Carlos Jusino grew up a typical kid in Harlem, rollerblading near the Hudson River, eating at the McDonald's on 145th Street and Broadway, hanging out with friends in his building. Also typical was the fact that many of Jusino's neighbors and family members, including his mother, had asthma. "When I was growing up, she went to the hospital about once a month for asthma," he says. Although he didn't know it at the time, more than 30 percent of the kids in Harlem have asthma, one of the highest rates in the country.

Jusino's family was worried about the air quality around Harlem, but most of its attention was directed to a sewage treatment facility built in 1985 along the West Side Highway next to the Hudson, where a foul-smelling settling tank lay exposed. The plant galvanized the community, including a group of environmental justice activists known as the Sewage Seven. They sued the city and won a settlement in 1994 that helped establish air-monitoring stations around the plant.

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Harlem is plagued by health conditions not uncommon among the urban poor. In addition to suffering from asthma, children here have high rates of obesity and, perhaps most alarming, significant learning disabilities. Increasingly, medical researchers are discovering that all of these syndromes are linked at least in part to environmental factors, from nutrition to tobacco smoke to industrial chemicals. Jusino, like many, was stunned to learn that pollution's biggest target may be not our lungs but our brains.

Researchers are finding the Harlem population to be a valuable source of data, and what they're learning is both illuminating and worrisome. And if you think poor air quality is limited to disadvantaged urban neighborhoods, think again. Harlem's problems are shared by the rest of the country. If clues can be found here, the lessons can apply elsewhere.

If you think poor air quality is limited to disadvantaged urban neighborhoods, think again.

As many as one in six children nationwide has a neurodevelopmental disability, including autism, speech and language delays, and attention deficit hyperactivity disorder. The Centers for Disease Control and Prevention estimates that ADHD alone affects 14 percent of children, although experts debate whether it may be overdiagnosed. In any case, the number of children needing special education services has increased 200 percent in the past 25 years. In a 2000 report, the National Research Council of the National Academy of Sciences estimated that 3 percent of brain disorders are caused outright by environmental toxicity and an additional 25 percent by environmental exposures interacting with genetic susceptibilities.

Every day, America's pregnant women and young children are exposed to a trifecta of suspected neurotoxicants in the form of pesticides (mostly via food and water but also home, lawn, and farm applications), polycyclic aromatic hydrocarbons, or PAH (mostly via exposure to vehicle exhaust), and polybrominated diphenyl ethers, or PBDEs (flame retardants, mostly in upholstered furniture and electronics). The CDC routinely samples Americans for these and other industrial by-products in our bodies, so we know their reach is pervasive. But we are not all equally exposed, and some of us appear to be more vulnerable to them for reasons that may include genetic susceptibility, poor nutrition, stress, and age.

Andrei Zveaghintev/Shutterstock

Jusino joined a youth group through his high school in Washington Heights in 1994 and started mapping, block by block, local sources of pollution, including dry cleaners and diesel-spewing bus depots. In 1997 he joined the staff of West Harlem Environmental Action (We Act), a group co-founded by Peggy Shepard, one of the Sewage Seven. Today, as a GIS mapping specialist and technician, he is the proud chief caretaker of Aethan, a retro-looking black box that records real-time black carbon pollution. The size of a microwave oven, the Aethalometer (from the Greek word meaning "blacken with soot") sends out several feet of PVC pipe through a window overlooking the corner of 152nd Street and Amsterdam Avenue, where the We Act offices occupy a light-filled, redbrick former police precinct house.

Aethan looks retro, but he has a Twitter account, where he says things like "Holy pollution, Batman! Look, the WE ACT Aethalometer reading is at 2,780 nanograms per cubic meter." (For perspective, during low-traffic weekends, the readings hover around 1,200.)

"The readings get really high around 3:00 p.m.," said Jusino, who, at age 35, sports silver-rimmed glasses and a trim goatee. Outside, it was early evening, and the machine was reading in the mid-700s. I couldn't help imagining dark whorls of goblin-faced spirits wafting up to choke us at the windows. It's a misconception, though, that the worst air pollution is visible. We tend to equate it with smog. Smog exists, of course, but it was largely knocked back under the air-quality controls of the 1970s. Over its 40-year life, the Clean Air Act has radically cut many ingredients of smog: carbon monoxide emissions are down 82 percent, sulfur dioxide 76 percent, and ozone concentrations 28 percent.

The monitor's pollution readings "get really high around 3:00 p.m."

However, there are virtually no regulations governing the black carbon component of fine particulate matter smaller than 2.5 microns, known as PM 2.5. Black carbon is responsible for two million premature deaths globally each year. It also contributes substantially to climate change. A recent study by a team of 31 geophysicists found that black carbon is "the second most important human emission in terms of its climate forcing in the present-day atmosphere."

Black carbon is a component of particulate matter left over from the incomplete combustion of fuels in vehicle engines, apartment-building boilers, cooking stoves, and other sources. Aethan's 3:00 p.m. peak is the product of diesel-powered vehicles, including school buses. Harlem has one of the highest levels of black carbon in New York. In part, this is because of the high density of older buildings, which tend to have older, less efficient, and poorly maintained heating systems. But diesel fuel is also a major source of black carbon, and Harlem is home to six of Manhattan's seven transit bus depots as well as commercial trucking routes. By 2006, after a big public campaign spearheaded by the Natural Resources Defense Council (NRDC), city transit buses that had previously used dirty diesel switched to a combination of filters and cleaner fuel. But plenty of other fleet vehicles, older school buses, and ships passing close by still burn the bad stuff.

A host of ills has been attributed to fine particulate pollution, including heart and lung disease, sometimes causing premature death. Black carbon is considered a reliable co-conspirator of PAH, a class of compounds that are also by-products of combustion. (Black carbon is easier to measure than PAH and, depending on location and source, tends to be highly correlated with them.) When inhaled, fine particulates go deep into the lungs, but they also travel to the brain, where they can alter DNA expression, cause inflammation, and possibly gum up neuronal circuitry. Jusino and others wondered: Could these and other common contaminants be contributing to the high incidence of neurodevelopmental delays in the children of Harlem?

* * *

Northern Manhattan is home to not only some of the best music, soul food, and dance troupes in the city but also one of its most venerated medical research institutions, Columbia University Medical Center. Frederica Perera was a young cancer researcher there in the 1980s when she decided to collect tissue samples from human placentas, expecting that they would be "pristine," or untouched by environmental exposures. "But we found there were fingerprints on these samples of DNA damaged by pollution, even in women who weren't smokers," she recalled from her office at the Columbia Center for Children's Environmental Health on West 168th Street. "It made me concerned about fetal exposures. I really wanted to look more closely at this window." Although she started out looking for cancer markers, she was soon curious about other pressing health conditions in the Harlem community.

Alexander Mak/Shutterstock

That Perera was even looking at environmental causes of illness was both unusual and unfashionable. For the past two decades, cancer researchers and other molecular biologists have spent much of their time riveted by the genome, believing it would unlock the secrets of disease. But cellular life isn't determined simply by the blueprints of DNA. It's now understood that cells are designed to interact nimbly with the outside world and that genes get turned on or off—and are sometimes mutated altogether—by environmental exposures from diet, inhalation, even transmission through the skin. To truly understand human health and disease, scientists need to look at both the genome and—to use a term coined in 2005 by Christopher Wild, a cancer epidemiologist—the "exposome."

Perera decided to do just that.

Today, as director of the Columbia center, she oversees what has become one of the most respected epidemiological data troves in the country. (She is also a trustee of NRDC.) Starting in late 1998, Perera and her colleagues recruited more than 700 pregnant women from hospitals in Harlem, Washington Heights, and the South Bronx for what's known as the Mothers and Children Study. Now, 15 years later, the team has retained three-quarters of its original participants, and the first babies are entering their teenage years. Such "prospective" studies, which follow a group over time and measure their health outcomes, are considered the gold standard in scientific research because they don't rely on retrospective memory or old, imperfect medical records. Blood and urine samples have been banked since the mothers' pregnancies and deliveries, as have samples from the children, and researchers can go back to these as they ponder new questions.

It's now known that many chemicals can cross the placenta, once believed to be a sacrosanct barrier.

It's now known that many chemicals can cross the placenta, once believed to be a sacrosanct barrier. This is disquieting, because the vast majority of these chemicals have never been tested for human health effects. Furthermore, the medical community agrees that many diseases and conditions, including obesity, cancer, and autism, are modulated by both genes and fetal exposures. In September, the American College of Obstetricians and Gynecologists and the American Society for Reproductive Medicine issued a joint statement saying, "The scientific evidence over the last 15 years shows that exposure to toxic environmental agents before conception and during pregnancy can have significant and long-lasting effects on reproductive health." (The chemical industry, however, is seeding doubt. The American Chemistry Council's chief medical officer responded that ACOG's evidence was based on "a limited number of flawed studies.") It makes sense to developmental biologists that fetal exposures matter; this is when the cells in the body and brain are on the biggest adventure of their lives, differentiating and replicating like a one-way train. Once it's left the station, it doesn't go back.

Children, of course, are harder to study than lab animals, because they are exposed to so many different conditions that can confound the results. That's why large, prospective epidemiological studies are so critical. Perera knows both what's in these babies' bloodstreams and what happens to them as they age. The larger the study, the stronger the statistical power. Even so, epidemiological findings are necessarily couched in terms of "associations" rather than causal links. So epidemiologists often look to better-controlled animal studies as a guide, as well as to molecular lab investigations of human blood and tissue samples.

With enough replication and diverse strategies, a picture begins to emerge. The center's early studies found significant associations between pollutants measured in the mothers and difficult birth outcomes, including low birth weight and small head circumference. The main culprits were PAH and chlorpyrifos, a then-common organophosphate pesticide used indoors to kill roaches and bedbugs. (Later the team would look at flame retardants.) Perera also documented that these chemicals damaged cellular DNA. Chlorpyrifos was found in the umbilical cords of virtually every mother in the early samples. Since 2001 it has been phased out of residential use, but exterminators are still caught using it. It also remains a common agricultural pesticide and so ends up as a residue in food. Perera and her colleagues knew that reduced head circumference had been linked to lower IQ scores, and animal experiments had shown that chlorpyrifos killed developing brain cells and induced behavioral changes in rats. In some well-known experiments, for example, rats given low doses of the pesticide while in the womb or shortly after birth later had trouble learning their way around a maze.

Although Perera and her team didn't know how these chemicals might be changing the brain, they were determined to find out all they could about the children's growth and development. The children (now teenagers), who are mostly Dominican and African American, would be regularly tested on everything from reading ability and motor skills to psychological yardsticks like aggression, risk-taking, and depression.

By the time they were 3 years old, the children with the highest exposures to the pesticide tested as much as six points lower on motor skills and three points lower on mental development and were significantly more likely than those with lower exposures to suffer from attention and hyperactivity problems. These findings were published in 2006 in Pediatrics. Other studies showed that children most exposed to PAH were nearly three times as likely to show cognitive developmental delays. By the time they were 7, the children most exposed to chlorpyrifos were showing deficits in working memory, a key component of IQ. Their working memory declined by 2.8 percent and their full-scale IQ by 1.4 percent, after adjusting for variables like tobacco smoke and maternal intelligence.

The center's findings on the cognitive impacts of PAH and pesticides bolster what other researchers have found in Boston, Cincinnati, and California. Perera led a similar cohort study with researchers in Poland and found that higher prenatal exposure corresponded to an average 3.8-point drop in IQ in 5-year-olds. This drop is comparable to the effects of lead, the discovery of which, in the 1970s, eventually triggered a massive public health response in the form of laws removing lead from automobile gasoline, restricting it in household paint, and, to this day, requiring lead tests in children in many parts of the country.

Now that the Harlem children are older, the team is examining whether the ill effects of fetal and cumulative exposures play out in other ways—poor academic performance, impaired social skills, anxiety and depression, and self-destructive behavior.

Now that the Harlem children are older, the team is examining whether the ill effects of fetal and cumulative exposures play out in other ways—poor academic performance, impaired social skills, anxiety and depression, and self-destructive behavior.

On the day I visited the center this fall, a mom—let's call her Michelle—and her 14-year-old son came in for a couple of hours of assessments. They were both greeted by a tremendous hug from Diurka Maria Diaz, a researcher and counselor who has followed the families from the beginning. "You're taller than I am now!" she teased the boy. Hefty, dressed in black pants and a black sweatshirt, he towered over his toddler sister. She is also in the study, which continues to recruit new participants who likely have different exposomes. While Michelle's placenta absorbed chlorpyrifos during her son's gestation, it probably absorbed replacement pesticides during her daughter's. The replacements come from a class of chemicals known as pyrethroids, whose neurodevelopmental effects remain largely unstudied.

Diaz, who is known to the families as Didi, exudes warmth and charisma as well as concern for the challenges faced by kids in the study. "It's hard to be a 14-year-old," she says. "Many of these kids are overweight, many are depressed. We've referred about 40 percent for counseling." Furthermore, a remarkable 24 percent of the cohort children at age 2 had a potentially diagnosable developmental delay. About 70 percent of these children qualified for New York City’s early intervention services.

Such delays are typically attributed to growing up in impoverished environments with relatively low parental involvement, low mental stimulation, and pervasive psychological stress. Perera's team, though, is convinced that fetal environmental exposures play a role and that their effects may be aggravated when combined with maternal stress, as well as when combined with one another.

"In the past, we took a reductionist approach," Perera says, "a single exposure, a single effect. But now we think that pollution interacts with nutritional and social susceptibility factors. We're making heroic attempts to measure these. We're building the exposome."

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