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Exposure to Home Pesticides Linked to Parkinson Disease

JAMA. 2000;283(23):3055-3056. doi:10.1001/jama.283.23.3055
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People exposed to pesticides in the home or garden may have a significantly higher risk of Parkinson disease, according to a new study presented in San Diego last month at the American Academy of Neurology's annual meeting.

Although other studies have linked occupational exposure to these chemicals as a risk factor for Parkinson disease, the study is the "largest yet of newly diagnosed people with the illness and the first to show a significant association between home pesticide use and the risk of developing Parkinson's disease," said Lorene Nelson, PhD, a neuroepidemiologist at Stanford University School of Medicine, who presented the findings.

The study involved 496 patients diagnosed with Parkinson disease within the Kaiser Permanente Medical Care Program of Northern California during the years 1994-1995, and 541 age- and sex-matched controls from the same population.

HOME PESTICIDE USE
HOME PESTICIDE USE

Using in-person, structured interviews, members of a research team led by Nelson collected information about the patients' lifetime history of exposure to home pesticides (herbicides, insecticides, and fungicides) prior to diagnosis.

HOME PESTICIDE USE

The patients were asked detailed questions about whether they had used or been exposed to insecticides in the house or garden, herbicides in the garden, or fungicides to control mold or mildew in the house or garden. The researchers also inquired about lifestyle factors, including cigarette smoking and alcohol and coffee consumption.

HOME PESTICIDE USE

After controlling for known risk factors, such as family history of the disorder, occupational exposure to pesticides and herbicides, and cigarette smoking, the investigators found that home exposure to insecticides and herbicides was associated with an increased risk of Parkinson's disease, said Nelson. Fungicide exposure was not linked with an increased risk of the disorder.

HOME PESTICIDE USE

Individuals who had high-level herbicide exposure, involving an average of 160 exposure days, had a statistically significant 70% increased risk of the disorder, compared with those who were not so exposed. The group with the lowest level of contact with herbicide, fewer than 30 total days of exposure, had a 40% increased risk compared with nonusers, although the effect was not statistically significant.

HOME PESTICIDE USE

Handling or applying insecticides also was linked with significantly elevated rates of Parkinson disease. Those who used insecticides in the garden showed a 50% increased risk of the disorder compared with those who had never been exposed to home pesticides of any type.

HOME PESTICIDE USE

In-home use of insect-killing chemicals was associated with a 70% increased risk of Parkinson disease, compared with no use of pesticide. This reflects an average level of exposure of 77 days in which the person either actively handled or applied in-home insecticides but does not include subsequent days of exposure to residues after they had been applied.

HOME PESTICIDE USE

Because a previous study had found a substantially increased rate of Parkinson disease among city dwellers who gardened for a hobby, the researchers analyzed the data to see if those whose only significant exposure was using insecticides in their homes had an increased risk.

HOME PESTICIDE USE

"Individuals who were not gardeners had a greater than two-fold increased risk of Parkinson's disease after exposure to in-home insecticides," said Nelson.

BIOLOGICAL PLAUSIBILITY
BIOLOGICAL PLAUSIBILITY

The idea that pesticides might be linked with Parkinson disease is biologically plausible. Many pesticides are neurotoxic and may affect various aspects of central nervous system function, possibly even resulting in cell death.

BIOLOGICAL PLAUSIBILITY

"Some of them are specific for certain neuronal cell populations and can cause specific nerve cell death, at least in [tissue] cultures," said Nelson. "So it's biologically plausible that one or more specific pesticide agents could, for some reason, have an affinity for the substantia nigra and would preferentially affect that region of the brain."

BIOLOGICAL PLAUSIBILITY

The investigators did not collect information on which pesticides were used and therefore cannot implicate any specific chemicals or brands of pesticides.

BIOLOGICAL PLAUSIBILITY

"The whole concept is tantalizing, but there's never been a single agent or even a class of agents that have been identified as a risk factor," said Parkinson disease expert William Koller, MD, PhD, of the University of Miami School of Medicine. In the absence of data implicating any particular product or chemical agent, people should take the usual commonsense precautions that are advised when working with any potential toxin, such as avoiding inhalation of the substance and taking care to prevent skin contact.

GENES + TOXINS = DISEASE?
GENES + TOXINS = DISEASE?

Researchers believe that Parkinson disease may be triggered when individuals who have an inherited vulnerability to certain toxins in the environment are exposed to such agents. "But without knowing your genetic predisposition, the only thing you can do is protect yourself against a putative environmental toxin," Koller noted.

GENES + TOXINS = DISEASE?

Nelson and her colleagues plan to reinterview their study subjects to elicit additional details, such as brands and types of pesticides used and whether the patients wore protective clothing. Also in the works are plans to search for genes that confer susceptibility to Parkinson disease and to analyze DNA samples from patients in the study to determine whether there are genetic differences between people with the disorder and controls.

GENES + TOXINS = DISEASE?

If such differences exist, the next step would involve looking for correlations between the study subjects' exposure histories and their genetic makeup to look for significant gene-environment interactions that could increase an individual's risk of developing Parkinson disease.

GENES + TOXINS = DISEASE?

For now, however, the investigators say it is still much too early to say for certain whether in-home use of pesticides represents an important health hazard.

GENES + TOXINS = DISEASE?

"As this was the first study to investigate pesticide exposure in the home or garden, our findings are only suggestive, and no firm conclusions can be drawn until additional studies confirm our results," said Nelson.

Boston—The State Child Health Insurance Program (SCHIP), introduced in 1997, is the largest commitment the US government has made to children's health since it established Medicaid in 1965. Under SCHIP, Congress has authorized $40 billion over 10 years for states to purchase health insurance for low-income uninsured children. While this program promised to provide access to health care for millions of uninsured children, experts point out that the complex issues of poverty can frustrate this laudable goal.

Since SCHIP's inception, about 2 million children have been enrolled in the program, said Richard Bucciarelli, MD, of the University of Florida College of Medicine, at the Pediatric Academic Societies and American Academy of Pediatrics Joint Meeting, held here in May. However, despite this increase in public coverage, the numbers of uninsured children are not declining, said Bucciarelli.

STAGNANT SITUATION
STAGNANT SITUATION

A big part of the problem is the erosion of private sector coverage for low-income families, said Irwin Redlener, MD, of Montefiore Hospital and Medical Center, Bronx, NY, who is president of the Children's Health Fund, a philanthropic initiative dedicated to developing and supporting health programs for medically underserved children. Redlener said recent data from the Center for Studying Health System Change (HSC) illustrate this trend.

STAGNANT SITUATION

According to a study entitled "Recent Trends in Children's Health Insurance Coverage" published in the April 2000 HSC Issue Brief, the percentage of low-income children covered by SCHIP or Medicaid increased from 29% to 33% between 1997 and 1999, while the percentage with private coverage dropped from 47% to 42%. During the same period, the rate of uninsured low-income parents increased from 31% to 35%. So although the SCHIP program has been helpful, said Redlener, "in essence, we have a stagnant situation."

STAGNANT SITUATION

Bucciarelli said many low-income families are losing health insurance not because employers are dropping coverage but because, as premiums increase, employers require workers to pay a larger percentage of the cost to participate in the health care plan. "Where previously the employer covered 60% of the plan, it's now often down in the 30% to 40% range, with the family being responsible for the rest," he said.

STAGNANT SITUATION

Because many of the working poor are not able to pick up an increased share of the premium, families drop their coverage. "And that really is why we're not seeing the number of uninsured children decrease, despite this tremendous input of funds at the federal level," he added.

STAGNANT SITUATION

Another important factor, said Bucciarelli, is documented in a 1998 Institute of Medicine committee report, America's Children: Health Insurance and Access to Care, which stated that after having an insurance card, the most important determinant of whether a child accessed the health care system was whether the family was insured. If a family is not insured, it is likely that the child will not see a physician, even if that child has an insurance card, he said, "because as a family, they're used to not having insurance and not having access."

BARRIERS TO CARE
BARRIERS TO CARE

Such evidence supports the notion that a child's access to health care depends on more than just having health insurance. Access, said Redlener, is the ability to obtain appropriate, affordable, comprehensive health care in a timely fashion on a 24-hour basis, including referrals for special service needs. Many children in this country are medically underserved, he said, because they do not have access to a "medical home" that provides these services in this way.

BARRIERS TO CARE

Redlener said he emphasizes this definition of medically underserved children because he has been struck by how many politicians, elected officials, and policy makers do not understand the situation in this way. Even those who have worked in the area for a long time, he said, seem to think access to health care means having an insurance card or being able to reach an emergency department when that is needed. As an advocate for improving children's health care, he thinks it is crucial that such views be broadened.

BARRIERS TO CARE

Financial barriers to care are not the only barriers, said Redlener. Access to health care can be impeded by a number of other factors, such as lack of available physicians. A large number of people live in health professional–shortage areas (HPSAs), defined as regions in which there is less than one physician for 3500 people. More than 71 million people live in the 2700 federally designated HPSAs in the United States, 70% of which are in rural areas. Children who live in such areas, regardless of insurance status, will have difficulty finding a medical home, said Redlener.

BARRIERS TO CARE

Insufficient transportation is also a barrier to health care, he noted. "There are places in Kentucky, West Virginia, and all over rural America where there's a fantastically well-qualified community health center 4, 6, or 10 miles from where a person lives, but if there's no reliable transportation or no public transportation, it might as well be 150 miles away."

BARRIERS TO CARE

Taking into consideration these barriers and others, Redlener said his group estimates that as many as 21 million children are at serious risk of having no health care or are currently experiencing access problems. Of 74 million children in the country, this represents a substantial percentage of the population that is medically underserved. Redlener stressed that "the approach that only focuses on insurance systems will not help to get to our goal of universal access for kids."

WHAT'S TO BE DONE?
WHAT'S TO BE DONE?

To address these issues, there are a number of efforts that can be made to meet particular needs within communities, said Redlener. For example, one solution to the transportation barrier is a mobile medical unit that brings health care to children, an approach the Children's Health Fund has been studying in rural areas in Mississippi and Arkansas. He added that his group is also planning to go before Congress sometime this year to argue that communities shown to have transportation-based access barriers to care should be entitled to a special fund for building a transportation network.

WHAT'S TO BE DONE?

But while many things can be done by people working locally to address the needs of their communities, Redlener stressed the need for physicians who understand the complex issues of medically underserved children to be involved in making public policy decisions. "We need to emphasize [to the policy makers and legislators] that the needs of underserved children are not all the same, and there's not a homogenous approach to strategies for dealing with their issues."

Boston—A number of toxins, such as lead, polychlorinated biphenyls (PCBs), and organophosphate pesticides are disproportionately concentrated in environments where disadvantaged children live, said Philip Landrigan, MD, chair of the Department of Community and Preventive Medicine at Mount Sinai School of Medicine in New York City, at the joint meeting of the Pediatric Academic Societies and American Academy of Pediatrics. "As it turns out, many of the children who are most heavily exposed in our society to environmental toxins are the same children who are poor, the same children who have either no access or inadequate access to medical care."

The notion that there exist disparities in the level of protection from environmental health hazards among children and adults of different races, ethnicities, and socioeconomic backgrounds is called environmental injustice, said Landrigan.

LEAD STILL A PROBLEM
LEAD STILL A PROBLEM

Lead exposure provides one example of this sort of inequity. A neurotoxin that causes a spectrum of symptoms depending on the blood lead level concentration, lead has been reduced in the environment in the last 25 years in large part because of its removal from gasoline in the 1970s and 1980s. Great declines in blood lead levels in children have been observed, with mean blood lead levels falling from 0.77 µmol/L (16 µg/dL) in 1976 to less than 0.14 µmol/L (3 µg/dL) today. Despite this achievement, there are still areas in the United States where blood lead levels are too high, said Landrigan.

LEAD STILL A PROBLEM

"Lead is a problem that has been ghettoized," he said. Deteriorating housing units in which lead paint still remains are the culprits, and these environments disproportionately affect African American children in the inner city. He pointed out that in 1991, 35% of African American children in New York's inner city areas had elevated blood lead levels, compared with 4% to 5% of white children in the suburbs. While numbers have dropped in the intervening years—to about 27% for inner city children and 2% for suburban children—"this is a 10-fold discrepancy, which is an enormous difference," he said.

LOWER LEVELS AT FAULT
LOWER LEVELS AT FAULT

Recent research shows that cognitive defects can be caused by blood lead levels lower than the currently acceptable level of 10 µg/dL. Using data from the National Health and Nutrition Examination Survey (NHANES) III collected from 1988 to 1994, Bruce Lanphear, MD, MPH, of the Children's Hospital Medical Center at the University of Cincinnati, and others assessed the relationship between lead exposure and cognitive defects in math, reading, short-term memory, and visual construction skills in 4853 children between 6 and 16 years of age.

LOWER LEVELS AT FAULT

The researchers found an inverse relation between blood lead concentration and all cognitive function scores, a result that was seen in math and reading scores for concentrations as low as 2.5 µg/dL. They concluded that many more children than have previously been thought have been adversely affected by lead exposure. Lanphear said these results argue for cutting the acceptable blood lead level in half, if not more.

TOXIC TABLE FOOD
TOXIC TABLE FOOD

Another type of toxic substance disproportionally concentrated in the environments where poor minority inner city children live are PCBs, said Landrigan. Cities such as New York, Cleveland, Detroit, Buffalo, and Chicago have been heavily polluted by PCBs, which were prinicipally used as liquid insulation in electrical transformers, generators, and capacitors. These heavy, oily compounds were made in vast quantities in this country from the mid 1940s until 1976, when their manufacture was banned.

TOXIC TABLE FOOD

PCBs may no longer be in use, but they still wreak their effects on biological organisms, said Landrigan. These compounds persist for years without breaking down, and therefore are still as toxic today as they were when they first entered the environment. Because of their indestructability, PCBs bioaccumulate in the food chain.

TOXIC TABLE FOOD

This phenomenon means that when the toxins wash into river or lake beds, they are taken up by plankton whole and not broken down. Then the plankton are eaten by fish, and those fish in turn are eaten by larger fish, with PCB concentrations increasing through each level of this aquatic food chain. The result is that top predator species such as striped bass, blue fish, and lobsters have very high concentrations of these intact toxins.

TOXIC TABLE FOOD

How does this relate to environmental justice? Landrigan explained that it is predominantly people who are poor or who do not work who find that a good source of cheap food can be supplied by fishing. But if the fish they bring home are contaminated by PCBs, the lipophilic chemicals pass up the food chain into humans to bioaccumulate in the adipose tissue. If a woman who has eaten fish contaminated with PCBs becomes pregnant, these accumulated PCBs can cross the placenta into the fetus. Studies have shown, said Landrigan, that infants exposed in utero to PCBs have dose-related deficits in IQ and alterations in behavior similar to those produced by lead. The mechanism is almost certainly different, but the end product is the same, he added.

TOXIC TABLE FOOD

Landrigan said his group has done surveys in New York City and found that the people who are most likely to eat East River fish are not fishermen from Connecticut, who come down to fish the river because the fish are biting. "They throw what they catch back," he said, "but poor people take them home, serve them to their families, and share them with their neighbors. We're just now organizing an epidemiological study to look at the long-term consequences of that."

TOXIC CLASSROOMS
TOXIC CLASSROOMS

A third neurotoxin that is disproportionately concentrated in inner cities are organophosphate pesticides. Landrigan said survey data from all of New York state looking at pesticide use county by county showed that the two counties with the highest use are Manhattan and Brooklyn.

TOXIC CLASSROOMS

"It turns out pesticides are being heavily applied in daycare centers, apartments, and schools, and they're being most heavily applied in poor neighborhoods because their principal target is cockroaches."

TOXIC CLASSROOMS

Landrigan pointed out that if something is not done to address the disproportionate concentration of such toxins in the environment, "we're going to perpetuate a population of poor minority kids whose intellects are eroded by toxins like lead, and who will continue for generations to come to be environmentally, medically, and economically disadvantaged in relation to majority kids."

Philip Elton Gunby, who died on May 21, 2000, just 9 days short of his 68th birthday, played a major role in American Medical Association (AMA) publications for nearly 33 years. He retired in May 1997 as director of the Division of Medical News and Humanities, Journal of the American Medical Association (JAMA), but continued to write a quarterly column and occasional other articles for the Medical News & Perspectives (MN&P) section until this month.

Grahic Jump LocationImage not available.

Philip Elton Gunby (1932-2000) on assignment in Bosnia-Herzegovina in February 1997.

After graduating from Michigan State University in East Lansing and starting his journalism career as a reporter with the Associated Press in Columbus, Ohio, for 8 years, Phil and his wife, Mary Ellen, moved in late 1964 to Evanston, Ill, from which he would spend the next third of a century commuting to AMA headquarters in Chicago. His first position at the Association was with AMA News, but he is perhaps best remembered for his work as a reporter and then as editor for 13 years of MN&P.

In the course of his career, Phil won awards for medical writing from many organizations, such as the American Medical Writers Association, American Heart Association, Radiological Society of North America, and numerous others. He was a member of the Sigma Delta Chi professional journalism society and taught medical journalism at Northwestern University's Medill School of Journalism and other local institutions.

A quintessential "people person," Phil made and kept hundreds of friends during every stage of his life. He was the one who organized reunions of his Lockport (NY) Senior High School graduating class and the relative who tracked down far-flung members of the Gunby clan in Canada, England, Norway, and elsewhere in the world. M. Therese Southgate, MD, who was deputy editor of JAMA during much of his tenure, recalls that in an era rampant with competition and ambition, "Phil was the glue that held people together."

And he kept abreast of everything at all newsworthy. "Phil Gunby was the eyes and ears of the world to me. If anything happened in the world and I didn't hear from Phil, I knew it was not important," George Lundberg, MD, former editor of JAMA, said recently, adding, "I put him in charge of the whole front part of THE JOURNAL."

Phil's devotion to and interest in international medical matters did not end at the office door. Throughout the years, he and his wife opened their hearts and their home to several physicians from abroad who spent time working at JAMA. In addition, his work allowed him to nurture a love of travel—combined with an alliance with the military—that began when the US Air Force sent him to France for a time in the 1960s. He rose to the rank of brigadier general in the Illinois Air National Guard, from which he retired in 1985. On JAMA assignments overseas, he cultivated relationships with members of the international medical community that continually proved helpful to THE JOURNAL.

Friendships he developed with the surgeons general of the Army, Navy, and Air Force (including current AMA head E. Ratcliffe Anderson, MD, a former Air Force surgeon general) enabled Phil to be JAMA's front-line reporter on the medical aspects of the conflicts in the Persian Gulf and the former Yugoslavia. Closer to home, he initiated and for a decade arranged an annual JAMA dinner for these military medical chiefs in conjunction with the AMA annual meeting.

A dedicated family man as well as an intrepid newshound, Phil cherished the time he spent in such pursuits as riding a tandem bicycle with his wife (affectionately known as Wig from the days when she was tennis champion Mary Ellen Wigman) or decorating an Easter egg tree at their Evanston home with his three children, Cathy Gunby Vaughn, RN, Mark Gunby, MD, and Craig Gunby, their spouses, and six grandchildren. The Gunbys retired to Oklahoma in 1997, where Mary Ellen Gunby resides at 5801 S Atlanta Ave, Tulsa, OK 74105-7544.

Susan Crawford contributed to this article.

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Philip Elton Gunby (1932-2000) on assignment in Bosnia-Herzegovina in February 1997.

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