4
BEFORE IT STARTS
The Urgency of Banning Specific Pesticides to Lower Our Risk
The farmers spoke of much illness among their families. In the town the doctors had become more and more puzzled by new kinds of sickness appearing among their patients.
—Rachel Carson, Silent Spring, 19621
OVER THE PAST FORTY YEARS, FIVE MEMBERS OF TERRI MCGRATH’S extended family, including her beloved grandfather, developed Parkinson’s disease. In 2005, McGrath, then a forty-nine-year-old special education teacher, noticed that when she walked, her left arm was not swinging and her left foot was dragging. Three years later, she became the sixth member of her family, and the first woman, to receive the same diagnosis.
In the 1920s, McGrath’s grandfather, Alex Adent, and nine of his brothers and sisters emigrated from Lithuania to the United States. Most of the sisters became seamstresses, and most of the brothers, including McGrath’s grandfather, became farmers in southwestern Michigan. Ever since then, McGrath’s family life has centered on a farm in St. Joseph, a small town on the eastern shore of Lake Michigan. Her eighty-six-year-old mother spent her entire life within two miles of that farm.
As a child, McGrath was always playing outside with her grandparents. The family regularly used pesticides on its farm, including DDT, until it was banned in the United States in 1972.2 When the older family members sprayed the chemicals, McGrath stayed inside because her grandmother did not want her to breathe them in. But McGrath would often slip outside soon after, while the pesticides still lingered in the air.3 She, her siblings, and cousins would all pick apples, currants, and grapes that were covered with a white film. Only after her diagnosis did McGrath learn how dangerous some of those pesticides were and how some were linked to Parkinson’s.4
McGrath loved growing up on that farm. Despite her diagnosis, she says that had she known about the harmful effects of pesticides, she is not certain she would have done anything differently. Her children, who now are all “super conscious” of what they eat, are surprised that their mother did not think more about the risk of pesticides.5 McGrath says, “I just didn’t think about [it]. I thought farming was fun.”
McGrath no longer lives on the farm, but her uncle and cousin do. Both are embracing organic farming. McGrath herself remains active. Now retired, she still tutors, is planning a camping trip along the Natchez Trail in the southern United States, and is awaiting the birth of her ninth grandchild. Although she is doing well currently, could she and her family have avoided Parkinson’s disease?
The answer is likely yes. Farmers who are exposed to certain pesticides have a higher risk of developing the disease.6 In one study, the risk of developing the disease for farmers was 170% greater than that for nonfarmers.7 And the longer the farmers worked with the pesticides, the greater their risk.8
Pesticide risks are not limited to farmers. People who simply live in rural areas have high rates of Parkinson’s disease.9 These individuals may be exposed to pesticides in the air that can drift into residential communities.10 In addition, pesticides can contaminate groundwater or well water.11 Private wells are often shallow and may be especially at risk for contamination from nearby pesticides.12 Moreover, in the United States, private well water is not subject to the same regulations as water that comes from public systems.13
Agricultural areas have the highest rates of Parkinson’s. In Nebraska, the rates of the disease are two to four times higher in the state’s rural, agricultural parts than in urban Omaha.14 In Canada, investigators have found an almost perfect correlation between areas with the highest pesticide use and the highest rates of disease.15 In France, rural areas have the highest rates of Parkinson’s, as do the regions with the most vineyards, which often require intense pesticide use.16
And then there is the rest of us. We eat fruits, vegetables, nuts, and grains every day that have been doused in pesticides. What kind of risk are we all exposed to? We do not know. Assessing pesticide exposure from foods and documenting individuals’ dietary habits over a lifetime—given that Parkinson’s takes decades to unfold—are challenging. But this research is needed.
Until then, we are left with educated guesses. We do know that organic foods have much lower levels of pesticide residues than conventional choices.17
DDT ON THE FARM
The insecticide DDT was once considered a miracle. In the 1930s, the Swiss chemist Dr. Paul Hermann Müller was looking for a chemical that could kill insects that were destroying crops and spreading disease—without harming the plants. Müller, a nature lover, tested hundreds of chemicals before coating the inside of a glass box with DDT, a colorless, tasteless, and almost odorless nerve toxin.18 He placed houseflies into the container, and they bit the dust. Müller had found his answer.19
During World War II, DDT, which kills a wide range of insects, slowed the spread of malaria and other diseases among Allied forces in Europe and in the South Pacific. Winston Churchill said in 1944, “The excellent DDT powder which had been fully experimented with and found to yield astonishing results will henceforth be used on a great scale by the British forces in Burma and by the American and Australian forces in the Pacific and India.”20 According to the historian Dr. James Whorton, “When the war ended, DDT was given a hero’s welcome, hailed throughout the land as ‘Killer of Killers’ and ‘the atomic bomb of the insect world.’”21
In 1948, Müller received the Nobel Prize for Medicine. The Nobel Committee said, “Without any doubt, the material [DDT] has already preserved the life and health of hundreds of thousands.” Today, DDT is still used to help control the spread of malaria in parts of Africa.22
During the war, DDT was also used at home. Dr. Guy Wilcox’s father supplied food for soldiers from his family’s farm in the small hamlet of Sauquoit in upstate New York. Wilcox’s father raised dairy cows and grew grain. To protect the oats and barley, they used pesticides, including DDT. The chemical was stored in an old barn where Wilcox spent many hours as a boy. The can of DDT was often covered in cobwebs that kept away flies but not his young hands. Wilcox would pry open the can, play with the powder, and often make a mess in the barn.
DDT was easy to use and inexpensive. Wilcox helped his dad mix it with fertilizer for the crops. They would then spread the mixture over the fields while undoubtedly breathing it in.
In 2008, Wilcox began dragging his right foot. He developed a tremor in his right hand and was diagnosed with Parkinson’s. A decade later, the progression of his disease forced him to stop practicing medicine.
DDT was not the miracle chemical that Müller had envisioned. Beginning as early as the 1940s, its harmful effects on the health of wildlife, humans, and the environment were identified and detailed, including in Rachel Carson’s 1962 book Silent Spring.23 Even though it was banned half a century ago, DDT persists in the environment—and in our food supply. It becomes more concentrated as it makes its way up the chain to human consumption. The pesticide is then stored in our fatty tissues, as is the case with other animals.24
Because of the widespread use of DDT and related chemicals, some are detectable in nearly everyone.25 In 2003 and 2004, more than thirty years after the insecticide was banned, the US Centers for Disease Control tested the blood of about 2,000 people ages twelve and older. The researchers were looking for DDT and its metabolite, or breakdown product, DDE. The body converts chemicals in food and medications to often simpler molecules that are sometimes referred to as “metabolites.” They found that “a small proportion of the population had measurable DDT [and] most of the [US] population had detectable DDE” in their blood.26 For Parkinson’s, what matters more are the concentrations of chemicals in the brain. Because DDT dissolves in fat, “levels of DDT or metabolites may occur in fatty tissues [such as the brain] at levels up to several hundred times that seen in the blood.”27
AGENT ORANGE IN VIETNAM
Vietnam veterans and up to 4 million Vietnamese came into contact with Agent Orange during the war. Named for the color of the 208-liter barrels in which it was stored, Agent Orange was an herbicide mixture designed to kill vegetation and crops in the tropical forests so that aircraft fighters could spot the enemy below.
From 1965 to 1970, an estimated 45 million liters of Agent Orange were sprayed in Vietnam (Figure 1).28 There has been no large-scale study of the effect of this exposure on the health of the Vietnamese or war veterans.29 Smaller studies, however, have linked Agent Orange to many problems in these populations, including birth defects, cancer, and Parkinson’s.30 People who were exposed to Agent Orange during the war have been found to have a higher risk of developing the disease.31 Studies looking at Korean veterans who were in Vietnam also show an association between Agent Orange exposure and subsequent development of Parkinson’s. The evidence is sufficient that veterans who were exposed to Agent Orange and now have Parkinson’s are eligible for disability compensation and health care from the US Department of Veterans Affairs.32
Richard Stewart, the son of a World War II veteran, is a seventy-one-year-old former Green Beret who has Parkinson’s disease. At the time of the Vietnam War draft, Stewart was working for Eastman Kodak developing reconnaissance tools, so he was eligible for occupational deferment. But he chose to enlist and deployed to Vietnam in 1970. He later became a platoon leader in the US Army’s famous 101st Airborne Division. He remembers being in and out of areas treated with Agent Orange. “Pretty nasty stuff,” Stewart recalls.
Four decades later, he noticed that he was beginning to lose his sense of smell, and later he developed a tremor in his left hand. He was diagnosed with Parkinson’s. Stewart had become a mathematics educator at age fifty-one, but he was forced to retire early due to progression of the disease.
Today, Stewart lives in upstate New York with his wife, a self-described “flower child who peacefully protested the war,” who was ready to demonstrate again after her husband’s diagnosis. Stewart remains physically active, walking 2.5 miles and doing two hundred push-ups a day. He is also an enthusiastic member of veterans’ groups and says, “I only have Parkinson’s disease. A lot of people are a lot worse off.”
CONTAMINATED MILK
On March 20, 1982, a New York Times headline read, “Hawaii Recalls Pesticide-Laced Milk from Stores and Schools.”33 Farmers in Oahu had fed dairy cattle the tops of pineapple plants known as “green chop.” The problem was that the leaves had been sprayed with heptachlor, a pesticide that had been banned by the Environmental Protection Agency (EPA). Heptachlor was considered a potential carcinogen, or cancer-causing chemical, and it persists in the environment.34 In the 1960s, the Food and Drug Administration had set a zero tolerance level for heptachlor in foods.
In 1978, the Pineapple Growers Association of Hawaii and the state of Hawaii argued that heptachlor was needed to protect pineapples, the state’s largest source of agricultural revenue, from ants. At the time heptachlor could be found in the fat cells of virtually every American.35 The attorney representing the state of Hawaii and the pineapple growers said that his clients “do not concur or accept… that heptachlor use to control ants on pineapple poses a significant risk of exposure to man or the environment.”36 They were granted an exemption and started using the pesticide.
The exemption allowed heptachlor to be sprayed on pineapples but prohibited the use of green chop as feed within one year of spraying it with the chemical. Then, in 1982, it was discovered that some of the contaminated tops apparently had slipped into the feed before the year was up and the heptachlor had broken down at least partially.37 Testing found that seven of the nineteen dairies on Oahu had heptachlor levels in their milk that were three to six times the acceptable state level. Two months after the contamination was detected, Hawaii’s state health director ordered all fresh milk removed from stores and schools.38
During those two months, Hawaiians were exposed to high levels of the pesticide. Leland Parks, a scientist at the Pacific Biomedical Research Center in Honolulu, tested samples of breast milk from nursing mothers and found that the average level of heptachlor contamination had increased fourfold.39 He said, “It appears that there is a relationship between exposure to the contaminated store-bought milk and the increase in human breast milk.… There is enough information to make me and many others uncomfortable.”40
Another scientist suggested that the infants exposed to milk with high levels of heptachlor be followed to assess the long-term health risks of the exposure. According to the scientist, “A natural experiment has been foisted on the people of Hawaii.”41
In 2016, a research team in Japan was ready to evaluate the results of this “natural experiment” to see whether there was a connection between heptachlor exposure and Parkinson’s disease.42 By coincidence, Japanese researchers had launched a Honolulu Heart Program in the 1960s to follow more than 8,000 men of Japanese ancestry living on Oahu for the development of heart disease. As part of that study, individuals completed diet surveys including questions on milk consumption. A subset had agreed to have autopsies performed at the time of their death. The research team examined the brains of 449 of them.
The investigators’ findings were remarkable. They found that the density of nerve cells in the substantia nigra, the area of the brain affected by Parkinson’s, was lowest in those who consumed the most milk.43 Researchers also found a potential clue. The brains of those with Parkinson’s were more likely to have the remains of heptachlor.44
The study had limitations. One was that the researchers did not have samples of milk that the participants may have drunk during the heptachlor contamination.45 But its findings were supported by other studies. Some have found that levels of a related pesticide called dieldrin—which was widely sprayed on corn and cotton in the United States until 1970 (all uses were banned in 1987)—are also more likely to be found in the brains of people with Parkinson’s.46 The blood levels of these pesticides that dissolve in fat, such as DDT, heptachlor, and dieldrin, are also higher in individuals with Parkinson’s.47 Finally, in animal experiments, dieldrin kills dopamine-producing nerve cells.48
These pesticides have saturated the globe. While DDT, heptachlor, and dieldrin were banned from use on crops in the United States and other industrialized countries in the late twentieth century, use of the pesticides shifted to less industrialized nations, including India and China.49 Even though China, for example, has now banned these pesticides, it used to be a major producer and consumer of them. As a result, the Chinese have high concentrations of the residues in milk from nursing mothers and increasing rates of Parkinson’s.50
The effects may be felt for years to come, especially in middle- and low-income nations. Remnants of the chemicals are still found in the milk supply of many countries, including Brazil, China, Ethiopia, and Uganda.51
The accumulation of these pesticides in the body is not limited to adults who were exposed. They can be passed on to subsequent generations. As the Hawaii case showed, nursing women who ingest these chemicals from dairy or meat products can deliver them to their babies through their breast milk (Figure 2). DDT and similar pesticides were found in the breast milk of women living in Spain, Nicaragua, Taiwan, and the Spanish Canary Islands as recently as 2014.52
This class of pesticides may also cross the placenta into the developing fetus. Dieldrin then accumulates in body fats and is detectable in the brains of fetuses.53 Twenty years ago, a report said that this “could pose a risk to the developing brain.”55 Such exposure may impair “motor and cognitive development in newborns and infants.”56 The long-term effects of DDT, heptachlor, and dieldrin on fetuses and breastfed children—and whether they can increase risk of developing Parkinson’s—are unknown but concerning.
FIGURE 2. How pesticides can be passed from cow feed to babies.54
The United States banned DDT, Agent Orange, and heptachlor in the 1970s and 1980s. However, the United States has not banned all pesticides linked to Parkinson’s. The one with perhaps the strongest link to the disease is still in widespread use: paraquat.57
THE DANGEROUS PESTICIDE COATING OUR CROPS TODAY
Paraquat has been used as a pesticide since the 1950s and is marketed as an alternative to the world’s most popular weed killer, glyphosate, more commonly known as Roundup.58 Paraquat takes care of weeds that not even Roundup can kill.59 Today, it is used on farm fields across the United States (Figure 3), and its use continues to rise.60 According to the US Geological Survey, its primary uses are for corn, soybeans, wheat, cotton, and grapes.61
Paraquat may be an excellent weed killer, but its effectiveness comes at an enormous price. A 2009 study found that exposure to paraquat and another pesticide called maneb within five hundred meters of one’s home increased the risk of Parkinson’s disease by a whopping 75%.64 Two years later, another study found that people who used paraquat—most notably farmers—were 2.5 times more likely to have Parkinson’s than those who did not.65 A scientist at the National Institutes of Health who has investigated paraquat said that the data were “about as persuasive as these things can get.”66
In the laboratory, paraquat reproduces the features of Parkinson’s disease.67 In 1999, scientists at the University of Rochester gave paraquat to mice, and their activity decreased. Paraquat also killed dopamine-producing nerve cells in the rodents’ substantia nigras, the same area of the brain affected by Parkinson’s in humans. The greater the amount of paraquat administered, the greater the number of nerve cells lost. The effects mirrored those observed when the researchers gave MPTP, the toxin first linked to Parkinson’s a decade earlier. The researchers concluded that the widely used herbicide causes destruction of dopamine-producing nerve cells in the substantia nigra and a syndrome similar to that caused by MPTP.68
Even beyond Parkinson’s, paraquat has substantial safety concerns. A 2011 report called it “the most highly acutely toxic herbicide to be marketed over the last 60 years.”69 If it touches your eyes, it can damage the cornea and lead to blindness.70 If you breathe it in, it can cause internal bleeding.71 If you swallow a teaspoonful, it is fatal. In fact, paraquat is so toxic and so readily available that it is commonly used to commit suicide in many parts of the world.72
Because of its link to Parkinson’s and its role in the deaths of thousands worldwide, thirty-two countries, including China, have banned its use (Table 1).73 However, while Britain prohibits the use of paraquat, a company there continues to export it to the rest of the world.74 The company indicates that the evidence of whether paraquat increases the risk of Parkinson’s is “fragmentary and insufficient.”75 Colombia, Ecuador, Guatemala, India, Indonesia, Japan, Mexico, Panama, Singapore, South Africa, Taiwan, and the United States are all customers.77
TABLE 1. List of when select countries banned paraquat76
Advocacy groups within and outside the Parkinson’s community have sought to ban paraquat in the United States.78 On July 24, 2017, the Unified Parkinson’s Advocacy Council, which includes the American Parkinson Disease Association, the Davis Phinney Foundation, The Michael J. Fox Foundation, and the Parkinson’s Foundation, wrote to the EPA, “We write to express our concern with paraquat dichloride, which is shown to increase the risk of Parkinson’s disease. We ask the Environmental Protection Agency to deny reregistration of this herbicide based on strong evidence of paraquat’s harm to human health.”79
For pesticides to be sold or distributed in the United States, they have to be registered with the EPA. According to the agency’s own rules, registration is contingent on “scientific studies showing that they can be used without posing unreasonable risks to people or the environment.”80
The EPA itself acknowledges the “high toxicity of paraquat.”82 Its own website reads, “Paraquat Dichloride: One Sip Can Kill” (Figure 4).83 It includes “true stories” involving deaths from accidental ingestion of the chemical, including that of an eight-year-old boy who in 2008 drank paraquat that had been put in a Dr. Pepper bottle that he found in the garage. The child died in the hospital sixteen days later.84
The EPA reviews the safety standards of all herbicides like paraquat every fifteen years. In 2017, the EPA opened paraquat for reconsideration, and it has until October 2022 to make a decision on its future.85 In 2019, in the absence of action by the EPA, The Michael J. Fox Foundation submitted a petition with over 100,000 signatures to the EPA urging it to ban paraquat.86
Meanwhile, paraquat use in the United States has doubled over the last decade (Figure 5).87 It is now, according the EPA, “one of the most widely used herbicides registered in the United States.”88 In 2016, more than 12 million pounds of it were sprayed in the United States.
Appropriate equipment can minimize the harmful health effects of pesticides on humans. For example, protective gloves can reduce the risk of the disease among farmers who are exposed to some (including paraquat), but not all, pesticides.90 This kind of equipment and additional protective measures, such as boots, disposable coveralls, and goggles, could decrease the risk of developing Parkinson’s disease in the United States and globally.
FIGURE 5. Estimated use of paraquat in the United States in millions of pounds, 1992–2016.89
CASE FOR CAUSATION
In 1964, a decade after demonstrating that smoking causes lung cancer, Sir Austin Bradford Hill gave a lecture titled “The Environment and Disease: Association or Causation.”91 In it, the world’s leading medical statistician outlined the criteria that an observed association—those who are exposed to pesticides, for example, have a higher rate of disease than the general population—would have to meet to demonstrate causation.92
Generally, an association—people exposed to certain chemicals have higher rates of Parkinson’s, for example—does not prove that one causes the other. This was the tobacco industry’s argument: that just because smokers had higher rates of lung cancer was not proof that smoking was the cause.93 Hill’s achievement was to show that population studies could prove that one led to the other. The link between the two had to be strong, it had to be supported by other scientific evidence, and it had to meet other criteria.
Chemical companies have pushed back against the science. Following the tobacco industry playbook, according to a 2018 investigation by the New York Times, they have lobbied the EPA not to ban certain pesticides by undermining population studies that show the link to various neurological problems, including Parkinson’s.94 Pesticides and other environmental factors tick most, if not all, of Hill’s criteria. The evidence includes numerous studies demonstrating a strong link between certain pesticides and Parkinson’s, high rates of the disease among those with the greatest exposure (e.g., farmers), and animal studies that replicate the features of the disease in exposed mice.95 Based on his criteria, we can conclude that certain pesticides are not merely associated with Parkinson’s. They likely cause it.
Not surprisingly, this conclusion is not shared by those who sell pesticides. A 2016 review funded by a chemical company that makes pesticides reached a different conclusion with regard to satisfaction of these criteria and the link to causation.96 That review concluded, “There may be risk factors associated with rural living, farming, pesticide use or well-water consumption that are causally related to [Parkinson’s disease], but the studies to date have not identified such factors.”97
The solution to helping end Parkinson’s disease is not to expose more people to chemicals that are linked to the disease and produce the features of Parkinson’s in the lab. The solution is to stop using such chemicals. Other countries with lower incomes and less strict environmental policies have banned paraquat. The United States should do the same.
ECHOES OF SILENT SPRING
Rachel Carson launched the modern environmental movement in the 1960s with the publication of Silent Spring.98 In the book, she described the impact of the indiscriminate use of pesticides. She wrote,
It is ironic to think that man might determine his own future by something so seemingly trivial as the choice of an insect spray.
All this has been risked—for what? Future historians may well be amazed by our distorted sense of proportion. How could intelligent beings seek to control a few unwanted species by a method that contaminated the entire environment and brought the threat of disease and death even to their own kind? Yet this is precisely what we have done.99
Carson went on, “The public must decide whether it wishes to continue on the present road, and it can do so only when in full possession of the facts.”100 Sixty years ago, facts were in short supply, and many consequences were unknown.
Now we know. We recognize the benefits of pesticides in agriculture, but we also know that certain kinds of these chemicals are linked to Parkinson’s, not to mention autism, lung disease, and various cancers.101
When there are other, less toxic options, we have no excuse for using chemicals that make us sick. We can no longer claim ignorance. If we continue to allow the use of these pesticides, we are choosing to permit the spread of Parkinson’s through the farms we tend, the air we breathe, and the water we drink.102