Where there’s poverty, you’ll often find lead poisoning.
Decades before the Flint water crisis, pediatrician Herb Needleman knew the relationship between poverty and lead poisoning all too well. When he began practicing medicine in the 1950s, lead was everywhere—in pipes, paint, gasoline, and countless other consumer products. It affected children from every social stratum, but poor children were hit the hardest. “He would have been disheartened to hear of the Flint crisis,” says his son Joshua, “but probably not surprised.”
Throughout the 1960s, ’70s, and ’80s, Needleman crusaded for more stringent lead safety standards after his groundbreaking research showed that chronic, low-level lead poisoning could cause devastating neurological impairments in children. Before the publication of his work, researchers believed that lead poisoning was a short-term problem that could easily be treated. Yet his work showed that the effects could be lingering and devastating—even if a child didn’t show overt signs of lead poisoning.
Lead poisoning continues to disproportionately affect impoverished, minority communities.
Now 90, Needleman has advanced Alzheimer’s disease and couldn’t be interviewed for this piece. But public health experts like Philip Landrigan credit Needleman’s work with lowering average blood lead levels in American children by 78% between 1976 and 1991.
“We used to think that lead poisoning was like the flu—either you had it or you didn’t,” Landrigan says. Thanks to Needleman, we know that lead poisoning can be a serious problem even at very low levels of exposure.
The lead crisis in Flint serves as a reminder that Herb Needleman’s work isn’t finished. There, lead poisoning travels on old pipes. As a result of an April 2014 switch to the corrosive Flint River as the source of the city’s drinking water, the protective crust that coated the inside of the pipes dissolved, and lead worked its way into homes throughout the area. Just over a year after the switch, pediatrician Mona Hanna-Attisha reported an epidemic of lead poisoning in the city’s children, with 3% of local kids showing blood lead levels higher than the Centers for Disease Control and Prevention’s recommended cutoff of 5 µg/dL.
Today, just as it was in Needleman’s day, lead poisoning continues to disproportionately affect impoverished, minority communities. What we lack, Landrigan says, is not an understanding of the dangers of lead but rather the political will to fix the problem.
A Long History
For nearly 10,000 years, humans have turned to lead for medicines and cosmetics, used it to line aqueducts, shaped it for cooking and eating utensils, and even added it as a sweetener. Since the time of the ancient Greeks, physicians have recognized the tell-tale signs of acute lead poisoning in children and adults: vomiting, confusion, seizures, fever, rash, fatigue, and changes in behavior.
The Industrial Revolution, however, turned lead poisoning into an epidemic. Paint manufacturers, taking a cue from artists, who had used white leaded pigments for centuries, began using lead in mass produced home paints in the late 19th century. Even baby cribs were coated with white lead paint, its slightly sweet taste tantalizingly tasty to infants and children. Children unknowingly ingested or inhaled tiny pieces of paint that flaked off their cribs or the windows, doors, and walls of their homes. By 1904, early reports linked cases of childhood lead poisoning to these household leaded paints.
Twenty years later, a new, more pervasive source of lead pollution appeared. Gasoline manufacturers had turned to lead to solve the problem of engine knock, the premature detonation of gasoline inside a cylinder that was slowly destroying the millions of new cars taking to the roads. Adding a chemical called tetraethyl lead eliminated the problem, but it also spewed tons upon tons of lead directly into the atmosphere. Industry claimed the gasoline additive was safe, but cases of severe, acute lead poisoning in workers who produced the stuff immediately challenged that notion. Concerns about chronic, low-level exposure to lead in the atmosphere also arose. Less than a year after tetraethyl lead hit the market, biochemist William Mansfield Clark noted that leaded gasoline could cause widespread air pollution, creating “a menace to public health.” But most attention remained focused on preventing overt cases of acute lead poisoning.
The first challenge to the belief that only severe, acute lead poisoning could cause harm came when pediatric neurologist Randall Byers noticed that several of the children he saw with cognitive and behavioral issues shared one thing in common: previous lead poisoning. Throughout the 1930s, Boston psychologist Elizabeth Lord kept immaculate records of children admitted to the pediatric ward for acute lead poisoning. Many children were hospitalized with symptoms of anemia, loss of appetite, itchy palms and feet, stomach pains, brain swelling, and paralysis. X-rays revealed bones stippled with bright white blotches of lead.
From a chemical standpoint, lead and calcium are similar. Both atoms occupy the same column of the periodic table, calcium near the top and lead closer to the bottom. If lead gets in the body, it can disrupt a multitude of cellular processes that rely on calcium. Neurons use calcium to send messages, which is one of the reasons the nervous system receives the brunt of lead’s toxic effects. The presence of lead hijacks the brain’s calcium pathways, causing decreased signals from some neurons, while increasing signals in others. In children, this can alter brain development, leading to the behavioral and neurological issues that Lord and Needleman saw. Treatment, such as it was, consisted of removing the source of lead from the child and administering a high calcium diet along with liberal doses of cod liver oil. If they recovered from the initial bout of brain swelling, Lord and other physicians initially assumed the children would be fine.
There’s no such thing as a short-term exposure to lead.
When Lord began to pore over her records, however, that’s not what she found. With Byers, Lord found that hopes for a full recovery after acute lead poisoning were misplaced. The children’s marked improvements while hospitalized masked ongoing neuropsychological problems. Many children developed behavioral problems like aggression and angry outbursts. Others had difficulty in school, or with sensory and motor skills. Lord and Byers’s data on nearly 100 lead poisoning cases in Boston children, published in 1943, provided the first hints that exposure could have long-lasting effects.
There’s no such thing as a short-term exposure to lead, says Nick Newman, a pediatrician at Cincinnati Children’s Hospital and director of their lead clinic. “Lead is the archetypal poison. It stays in the body for years, and even a small amount can become significant over a long time,” he says.
Building His Case
As a newly minted pediatrician at the Children’s Hospital of Philadelphia, Herb Needleman treated an endless parade of lead poisoned children. It all seemed like just part of the job until he told a mother whose infant daughter lay comatose in the ICU that her child’s health depended on her finding a new place to live. The mother replied, “Where else am I going to go?”
That moment reverberated throughout Needleman’s life. “I suddenly realized that the issue was not just making diagnoses and treating them. The issue was in the life story of people,” he said in an interview 50 years later.
As Needleman bounced from position to position early in his career, he found he couldn’t escape the long reach of lead poisoning. Patient interactions like this, combined with the Lord and Byers’s study, suggested to Needleman that the effects of lead poisoning may linger far beyond a child’s hospital stay. A short stint as an adult psychiatrist only reinforced this belief: The problems affecting many of his adult patients mimicked those he saw in young, lead poisoned children.
What set Needleman apart from other physicians of the time, his son says, was his natural curiosity and deep-seated sense of justice. “He just wouldn’t let any kind of injustice stand. That’s how he was,” Joshua says.
Most of his colleagues ridiculed the idea that the slow buildup of lead in the body could create chronic health problems even in the absence of overt symptoms. They could buy the idea that acute lead poisoning might have long-term effects, but Needleman’s idea of low-level chronic poisoning seemed a reach.
Before Needleman could test his hypothesis that longstanding lead exposure decreased IQ and increased behavioral problems, he needed a way to measure long-term lead levels in the body. Blood lead levels only told him current lead exposure, and Needleman needed a measurement that would capture this over a much longer period. Bone biopsies would give him the information that he needed, but they were too invasive and expensive. Finally, as he transitioned away from treating patients directly to researching lead poisoning as a young professor at the University of Pittsburgh, Needleman hit on an accessible and cheap stand-in for bone: baby teeth.
Calcium deposits in teeth just like it does in bone. Because lead mimics calcium, and teeth and bone are similar, Needleman realized that baby teeth could provide the same information about long-term lead exposure as bone biopsies. Needleman collaborated with several Philadelphia dental clinics, including one in the suburbs and two in the inner city. The researchers found that the poor, mostly African-American kids from the inner city had lead levels five times higher than their wealthier suburban counterparts. The resulting 1972 Nature paper revealed that baby teeth could readily identify long-term lead burden.
Now, Needleman needed detailed cognitive and behavioral testing to link lead to neuropsychological issues. He gathered more data in Boston, this time collecting more than 3,000 teeth from 2,500 kids. With colleagues from the Boston Children’s Hospital, they administered half-day psychometric tests to kids with the highest and lowest lead levels. They also surveyed teachers, asking about the kids’ ability to follow directions and manage their emotions. On every level, the data were clear: the greater a child’s exposure to lead, the greater their neurological damage.
“Needlman showed through innovative research that neurological damage could occur at much lower levels of lead than anyone thought,” says Gerald Markowitz, a public health historian at the City University of New York.
By the time Needleman published these results in the New England Journal of Medicine in 1979, other scientists had been working on the issue of chronic lead exposure in children, including Philip Landrigan. As a young officer with the Epidemic Intelligence Service in 1971, Landrigan traveled to El Paso, Texas, after public officials discovered that a local lead smelter had released 1,116 tons of lead, 560 tons of zinc, 12 tons of cadmium, and 1.2 tons of arsenic into the soil and air. Atmospheric tests revealed airborne lead levels almost 50 times the EPA’s limit at the time. Landrigan was placed in charge of testing blood lead levels in the local populace, and he found that two-thirds of kids under the age of 10 who lived within a mile of the smelter had evidence of lead poisoning.
“Every kid we tested who lived on the west side of the city had lead poisoning,” Landrigan says.
Results in hand, both Landrigan and Needleman began pushing for stronger rules around acceptable blood lead levels and for eliminating lead from gasoline and paint, which continued to be the largest contributors to lead poisoning in children. As the momentum behind their work began to build, industry struck back.
By the 1970s, the U.S. produced more than 250,000 metric tons of tetraethyl lead, which was mixed with 90% of all gasoline sold in the country. Industry assembled an array of experts to prove to the government and the public alike that their gasoline was safe. Industry scientists tried to sow doubt about the potential for negative health effects from tetraethyl lead or gasoline fumes. Experts described workers who became sick after working with the additive as “careless” for not following instructions. As the years passed, industry efforts grew more savvy, involving clever marketing campaigns and relying on an army of public relations firms and industry consultants that actively lobbied Congress and the Environmental Protection Agency. The producers of leaded gasoline also produced the science on its safety, and leaded gasoline got a clean bill of health through the 1960s.
Needleman and Landrigan’s studies appeared just as the burgeoning environmental movement began pushing to remove lead from pesticides, paint, gasoline, and other consumer products. Eventually, lead paint was banned by the EPA in 1978. Gasoline refiners, determined not to see their industry follow suit, struck back, aiming their blows at Needleman and Landrigan.
“Industry didn’t see the public health crisis, just a public relations one. They were determined to kill the messenger as well as the message,” Markowitz says.
Industry marshaled an army of paid experts to pick apart Needleman’s work. Throughout the 1980s, they criticized his data collection and analysis. They also tried to counter his findings by publishing studies of their own.
“These battles can get very messy. When the economic issues are very strong, industry doesn’t listen to science,” says Virginia Rauh, an environmental health scientist at Columbia University.
Things hit a fever pitch in 1991, when, spurred by PR firms and industrial consultants, the University of Pittsburgh, with the National Institutes of Health, who had funded much of Needleman’s research, opened a formal investigation of scientific misconduct. During the multi-year investigation, Needleman couldn’t access any of the decades of data on childhood lead poisoning, which ground his research—and sense of purpose—to a complete halt.
Needleman’s work was influential, forming a foundation on which other scientists could do their research. “In 1990, there were now 30 papers from around the world all saying the same thing…The [lead industry] couldn’t contest that, so what were they going to do? If they could discredit my work, the whole thing would collapse or be fundamentally revised,” Needleman said in a 2003 interview.
Needleman tried to shield his young family from the venom directed towards him, but the stress nevertheless leaked out. He had no problem with questions about the science itself, but the attacks became personal. To Needleman, the university investigation was the lowest blow because it signaled that his employers didn’t stand by his decades of service.
“Had he not been so willing to defend himself, his work would have quickly been discredited,” Joshua says.
After a two-tiered investigation by the university and the NIH, Needleman was ultimately exonerated. The small irregularities flagged by the gasoline industry as fraudulent were either honest errors that resulted from the management of large datasets in a pre-computer age or alterations in study design that Needleman had disclosed in the original paper.
By that point, sales of leaded gasoline were in a tailspin and had been for more than a decade. The passage of the Clean Air Act in 1970 gave the Environmental Protection Agency the authority to regulate lead levels in gasoline. In 1974, the EPA required unleaded gasoline in cars with catalytic converters, which emissions standards all but required the following year. More stringent refinery regulations also required that gasoline companies decrease the amount of lead in their automobile fuel beginning in 1979. By the early 1980s, the use of leaded gasoline dropped by more than 80% in the U.S. And in 1996, the EPA outright banned the sale of leaded gasoline in cars. The precipitous drop in sales of leaded gasoline perfectly matched the decline in average blood lead levels in children.
“Levels we thought were safe and innocuous just a few decades ago are now considered harmful,” says Bruce Lanphear, an environmental health scientist at Simon Fraser University in Canada. “Science advances one funeral at a time,”
As blood lead levels continued to decline, scientists determined that no safe level of lead exposure existed. Even small exposures could harm the body.
“In those early studies, we had few children with very low blood lead levels. Almost no preschoolers had blood lead levels below 10 µg/dL,” says David Bellinger, an environmental health scientist at the Harvard School of Public Health who did his training with Needleman. Low levels in the early 1980s are now more than twice as high as the CDC’s current recommendations.
Beginning in the mid-1980s, not long after Needleman’s studies first appeared, Rauh, the Columbia environmental health scientist, and other researchers began to piece together why symptoms of chronic lead exposure didn’t necessarily appear until years later. As children mature, Rauh says, they have to tap into an ever-expanding set of skills that increase in complexity. The neurological effects of lead poisoning become apparent only when children need to tap into more fine-tuned skills. Epidemiological studies revealed that African-American children had a slightly different way of metabolizing lead that made them more prone to lead poisoning. They absorbed calcium 50% more efficiently, and since lead is closely related to calcium, this meant they also absorbed more lead.
Needleman’s pioneering work has also enabled scientists like Quan Lu, an environmental geneticist at the Harvard School of Public Health, to tease apart why lead is so toxic to the developing brain. Lu exposed neural stem cells to levels of lead twice as high as the recommended CDC threshold (although still not enough to cause acute toxicity), and then measured how lead changed which genes were active. The deep sequencing identified 19 changes, 16 of which were involved in the oxidative stress response, a type of chemical stress that can damage key ingredients in just about any cell, including proteins, lipids, and DNA. Insights like these would likely go undiscovered without Needleman’s foundational research.
Although the Flint water crisis appears to be the poster child for modern-day lead poisoning, Lanphear points out that there are hundreds more communities in the United States that are similarly at risk.
“Flint is in the middle of the pack” when it comes to severity, he says. Nonetheless it serves as a classic example of how lead poisoning occurs alongside poverty, and how government and industry often try to cover up the problem. The issue has also served as a reminder that the country has billions of dollars of remediation ahead to truly win the fight against lead.
To Markowitz, spending valuable and increasingly limited research dollars on understanding why lead is poisonous and how it impacts the body is a complete waste of money.
“Lead poisoning is totally preventable. We can take it out of the environment and just stop using it. There are 500,000 kids with elevated blood lead levels—it doesn’t need to be that way. These kids are victims of a society willing to let its least powerful members suffer the effects of lead,” Markowitz says.
Needleman has become a hero to public and environmental health scientists. His work in developing a way to measure for chronic lead exposure and for standing up to an industry determined to bring him to his knees has saved thousands of lives and improved the health of countless others.
“We still have a long way to go to eliminate the threat, but we wouldn’t have made it this far without Needleman,” Bellinger says.
[Carrie Arnold is a freelance science writer and contributing editor for NOVA Next. She has written for Scientific American, Discover, New Scientist, Science News, among others. She can be reached via Twitter.]