Archive for the ‘Parkinson’s’ Category

h1

Pesticides, Parkinsons, Healthy Homes

April 13, 2011

Dr. Al Sears is a holistic practitioner in the US, who, like a few others, has a national practice, a newsletter and daily e-bulletin, a line of specialized supplements and who also promotes the products of others when he approves of them. His bulletins on the health hazards of many pharmaceuticals, as well as other everyday chemicals, are well-reserached and presented. Here is a piece he sent out April 13, 2011 on pesticides and Parkinson’s disease. If you’re interested in alternatives to pesticides at home, read to the bottom.

PESTICIDES AND PARKINSONS and HOW I KEEP THE CRITTERS OUT

DR. AL SEARS      http://www.alsearsmd.com

When you think “organic,” you probably have a picture in your head of produce – organically grown fruits and vegetables.

But I want you to know about organic pesticides because of the growing evidence that chemical pesticides are linked to Parkinson’s disease.

In a study published by the journal Archives of Neurology, researchers were looking at people’s occupations, and how likely they were to get Parkinson’s disease.
What they found shocked them.

There was almost no increased risk for Parkinson’s regardless of what kind of work people did. But they did find that anyone who used at least one of eight different kinds of pesticides was more than twice as likely to get Parkinson’s.

And if you used the insecticide permethrin, you were three times more likely to develop the disease.1 Permethrin is a common insect killer widely sold for use on clothing. It’s also put in a pharmaceutical cream meant to be rubbed on the skin to kill mites.

Another study by the University of California at Berkeley found that people exposed to maneb, a common pesticide used in gardens, were 75 percent likelier to develop Parkinson’s.2

Then there are the findings of the huge Agricultural Health Study. Have you heard about it? They closely follow about 90,000 licensed pesticide applicators and their spouses, and monitor them for illnesses. Researchers published results showing that people who used commercial herbicides/pesticides like rotenone or paraquat developed Parkinson’s disease 2.5 times more often than non-users.3

These pesticides damage your cells. Rotenone, for example, impairs the ability of your mitochondria to make energy. And paraquat increases oxygen-induced damage to cells.
Some of the cells hardest hit by these pesticides are in an area of the brain that is also damaged by Parkinson’s.

ALTERNATIVES

If you’d like to avoid this kind of damage from pesticides and keep your brain working just as well as it does right now, here’s what I recommend:

•    Stay away from products that claim to be “eco-friendly” or “natural,” when they clearly are not. 

For example, avoid synthetic pyrethroids. They’re similar to pyrethrins, which are natural insect-killing extracts from the flower chrysanthemum. But pyrethroids are created in a lab. Permethrin, which I mentioned earlier, is one of them.

•    Also, stay away from “geraniol.” It’s billed as natural because it’s made from roses, lemons and geraniums, but it’s been banned in Europe because of its toxicity to humans.
Here’s what to use instead:

1.    In my garden, I use neem oil to keep out pests. This extract from the fruit of the neem tree has been used for pest control in parts of Asia and India for over 2,500 years. It’s completely non-toxic. When the Environmental Protection Agency went to test neem for toxicity, it found zero reactions, even at the highest exposure.

In fact, you can use any part of the tree for pest control – the twigs, the leaves or the berries. The tree will grow in Florida. In other places and colder climates, I’ve seen it grown indoors in pots. Even sitting in a pot, it’ll serve to keep the bugs out. You can take a couple leaves and put them in your cabinets to keep cockroaches out. Or you can fray up the ends of the stems (so that the twigs are like brushes) and leave those around to work, too.

2.    I also get rid of the critters that try to crawl into my house with a pesticide that uses diatomaceous earth. It causes the pests to wither up and die.

3.    For a bug spray that’s good for spot use if I do see bugs in the house, I like to use a mint and herbal oil spray. It kills bugs within a few minutes and even smells pleasant, unlike those chemical sprays.

4.    For hard-to-kill bugs, look for pesticides with natural pyrethrins, which are made from chrysanthemums. They act fast, aren’t toxic to pets and degrade within a day.

5.    There are also bug baits made with boric acid, from the mineral boron. These aren’t toxic to people or pets either, and are great for getting rid of ants.

h1

Are Pesticides Causing Parkinson’s Disease?

February 1, 2011

Are pesticides causing Parkinson’s disease?

30-plus years of research sheds light on a hidden connection…

By Robin Marantz Henig, OnEarth Magazine Posted Jun 22, 2009

Excerpted from the article which appeared in OnEarth Magazine.

Jackie Christensen was 32 when her body began to betray her. She had just returned to work after the birth of her second son and when she tried to type, two fingers on her left hand refused to cooperate. “They wouldn’t go where I would want them to on the keyboard,” says Christensen, who at the time — it was 1997 — was co-director of the food and health program at the Institute for Agriculture and Trade Policy, a Minneapolis think tank. “I also had what they frequently call frozen shoulder, with a very low range of motion in my left arm.”

The first neurologist Christensen went to responded flippantly to her suggestion that she might have multiple sclerosis, which she had self-diagnosed because of her relatively young age and the fact that she was female. “If you want me to write that down, I will,” she remembers him saying, refusing to pursue the matter further. A second neurologist thought it was all in Christensen’s mind and referred her to a psychiatrist. Over the next several months, her symptoms got progressively worse, and she finally consulted neurologist number three. His startling diagnosis: Parkinson’s disease.

“I thought, ‘I can’t have Parkinson’s because I’m not old,’” Christensen recalls. But a trial of the standard treatment, a drug called L-dopa, seemed to work. Based on that clinical observation, the diagnosis was confirmed. This was in 1998, when Christensen was not quite 35, and she has been on L-dopa, with varying degrees of success, ever since.

Why did a disease that usually affects people in their sixties and seventies, and that affects men more often than women, strike this vibrant young mother? Christensen, a lifelong environmental activist, suspected an environmental cause — not only because she was politically inclined to, but because she knew that accumulating scientific information was pointing in that direction. In the past few years, Christensen has been part of a movement exploring a possible connection between exposure to environmental toxins — in particular, the organophosphate pesticides — and Parkinson’s disease, through her work with the Collaborative on Health and the Environment, a national network of advocacy and scientific organizations. She is co-founder of CHE’s working group on Parkinson’s Disease and the Environment.

A cause-and-effect relationship between environmental neurotoxins and Parkinson’s is difficult to prove. As with many other scientific efforts to establish disease causation through population studies, there will probably never be a smoking gun that settles things once and for all. Population studies can detect associations between certain suspected agents and diseases such as cancer, but it’s hard to draw conclusions about what causes a disease from studies that can register only correlations. In the case of Parkinson’s and the environment, however, there has been a steadily mounting consensus about such a connection, and the pace has quickened in the past year or so.

A January 2009 consensus statement from CHE, in collaboration with the Parkinson’s Action Network, a patient advocacy group, found that there was “limited suggestive evidence of an association” between pesticides and Parkinson’s, and between farming or agricultural work and Parkinson’s. This followed by just a few months the publication of Environmental Threats to Healthy Aging, a report co-authored by the Science and Environmental Health Network, a consortium of advocacy groups based in Ames, Iowa; it included a summary of 31 population studies that have looked at the possible connection between pesticide exposure and Parkinson’s. Twenty-four of those studies, according to the report, found a positive association, and in 12 cases the association was statistically significant. In some studies, the group found, there was as much as a sevenfold greater risk of Parkinson’s in people exposed to pesticides. In addition, in April 2009, scientists at the University of California, Los Angeles published a provocative study connecting the disease not only to occupational pesticide exposure but also to living in homes or going to schools that were close to a pesticide-treated field.

Taken together, 30-plus years of research add up to an increasingly persuasive conclusion: exposure to pesticides and other toxins increases the risk of Parkinson’s disease, and we are only now beginning to wrestle with the true scope of the damage.

Parkinson’s is the second most common neurodegenerative disease (after Alzheimer’s) in the United States, affecting between 1 million and 1.5 million Americans. The majority of cases occur in people over 65, about 60 percent of them male. It leads to uncontrollable tremors, muscle rigidity, and the inability to direct your arms or legs to move when you want them to. People with Parkinson’s often have a masklike, impassive expression. They may have difficulty speaking clearly and develop a characteristic shuffling gait. Cognitive skills usually are not affected, though some functions like memory and decision-making can be impaired, and, in the face of the gradual and inevitable encroachment of physical limitations, people with Parkinson’s often become depressed.

In part because it can take many forms, Parkinson’s disease is difficult to diagnose. Several movement disorders have been classified in the general category known as Parkinson’s-like syndrome, or parkinsonism. Scientists are divided about whether Parkinson’s disease and parkinsonism are even related in any meaningful way, beyond sharing some symptoms. The two conditions may not even involve the same brain defects. The strict definition of Parkinson’s disease is a loss of cells in the substantia nigra, a small structure in the basal ganglia region of the midbrain (though other brain structures are now thought to be involved as well). The substantia nigra ordinarily secretes the neurotransmitter dopamine, which is involved in many of the brain’s functions, including the control of motor activity.

Often a diagnosis of Parkinson’s disease is made the way it was made for Christensen: by a trial run of L-dopa, which boosts dopamine in the brain. If it works, the problem must be Parkinson’s. It’s a circular kind of logic, but it’s all that most doctors have. There still are no definitive blood tests or brain scans to make the diagnosis.

“Despite remaining uncertainties and data gaps,” wrote the authors of a 2008 report by the Science and Environmental Health Network — Jill Stein, Ted Schettler, Ben Rohrer, and Maria Valenti — “the body of evidence linking pesticide exposure to Parkinson’s disease fulfills generally accepted criteria for establishing causation.” When combined with “extensive laboratory animal data” specifying the underlying biology of this relationship, they wrote, “collectively, this evidence supports the conclusion that pesticide exposures can cause Parkinson’s disease in some people.”

Like most other population studies, this one has no way of proving that, for any one individual, X definitely led to Y — that Jackie Christensen’s early-onset Parkinson’s disease, for instance, was caused by her exposure to pesticides as a teenager. To Christensen, however, the causal connection is clear. Growing up in rural Minnesota, she spent summers working on local farms. In her early teens, this meant engaging in a practice known as “walking beans.” A pickup truck would drop off a bunch of youngsters, including Christensen, at one end of a field, and they would walk the rows of soybeans, weeding as they went. Later, Christensen and her friends rode a “bean buggy,” a rig attached to the front of a tractor from which they would spray the herbicide Roundup, sometimes dyed purple so they could see where it was landing, carefully aiming for the weeds and trying to avoid the beans. Often she was dressed in nothing more than a bathing suit and a baseball cap. “I had a great tan those summers,” she wrote in the introduction to her book, The First Year: Parkinson’s Disease; An Essential Guide for the Newly Diagnosed, “and I had no idea nor gave any thought whatsoever to what I might be exposing myself to, or what the effects might be. After the first day or two of spraying, I could no longer smell the odor of the herbicide. I do remember that when I would come home, my mother would immediately tell me to take a shower because I smelled like chemicals.”

As a young adult, Christensen had a single massive chemical exposure, during a political demonstration that involved wading into the Mississippi River in St. Louis. Wastewater treatment runoff made the water as neon green as Mountain Dew. She says it’s “anybody’s guess” what was in the water, but since many of the industries in St. Louis at the time discharged their wastes into the river, she says the brew probably included organophosphate pesticides, dry cleaning solvents, and other compounds. “After that action, within an hour I had a headache,” she says, “and I was nauseated and felt fatigued and lousy for a week. I know now that those are common symptoms of acute pesticide poisoning. At the time I didn’t think about what was causing it. I was 25 and thought I was bulletproof.”

Since the British physician James Parkinson first described the “shaking palsy” in 1817, Parkinson’s disease has been linked to a variety of possible environmental causes, both natural and artificial. It has been linked, too, to genetic factors, dating back to the beginning of the twentieth century, when early-onset Parkinson’s was first found to run in a few scattered, unlucky families. Those who study the connection between Parkinson’s and the environment suggest that it’s probably the combined result of having a genetic predisposition to the disease and a dangerous exposure to some sort of neurotoxin. A favorite expression of people in this field is that “genetics loads the gun and environment pulls the trigger.”

To read entire article in On Earth magazine, click here.

Robin Marantz Henig is a contributing writer to the New York Times Magazine. She is the recipient of a 2009 Guggenheim Foundation fellowship, and is the author of eight books on science, including The Monk in the Garden (Houghton Mifflin), a finalist for the National Book Critics Circle Award.

h1

“Toxins, Brain Chemistry, and Behavior”

February 9, 2009

Toxins, Brain Chemistry, and Behavior
http://www.dartmouth.edu/~rmasters/tbcba.htm

ROGER D. MASTERS
Research Professor
Dartmouth College
Hanover, New Hampshire 03755

I. The Problem

During the last two decades, evidence has accumulated that the interaction of environmental pollution, poor diet, and lifestyle contributes to the exceptionally high rates of violent crime in many American cities. Lead intoxication, even at low levels, correlates with aggressive behavior as well as learning disabilities. Manganese, a toxin that at high levels of exposure contributes to Parkinsonism, has also been linked to violent behavior. Effects of lead and manganese interact, moreover, so that individuals exposed to both show stronger effects than those exposed to either one alone. Alcohol and drug use, often associated with violent crime, increase the deleterious effects of toxic metals through complex biochemical interactions at the cellular level. These chemicals compromise the serotonin, dopamine, and other neurotransmitter systems that are integral to self-control due to their effects in lowering thresholds for violent behavior.

Environmental pollution does not impact everyone equally. Brain cells absorb toxic metals when diets are low in calcium, iron, zinc, Vitamin D, and other essential nutrients. Prenatal exposure to lead and alcohol can result in premature or low weight births, small head circumferences and learning or behavioral deficits. Bottle-feeding with commercial formulas exposes infants to four or five times as much manganese uptake as breast milk, a finding that suggests why studies show breast fed infants have IQ scores 2 to 8 points higher than comparable babies fed infant formula. In addition to direct effects of poor diet on children’s behavior, nutritional deficits thus probably combine with exposure to toxic metals to increase the likelihood of attention deficit disorder (ADD), hyperactivity, and other learning deficits. In addition, because the problems of poverty and broken families often co-vary with inadequate diet, housing with lead paint, and aging water systems, as well as inadequate prenatal health care, high rates of bottle feeding, and exposure to industrial pollution, poor urban populations are at risk for neurotoxicity in multiple ways.

The neurotoxicity hypothesis is strongly grounded in findings from a number of laboratory studies and observations of human behavior. In seven different groups of prison inmates, violent criminals had substantially higher levels of lead or manganese in their hair than nonviolent criminals or law-abiding controls. Otherwise puzzling geographical differences in rates of violent crime in the U.S. are highly correlated with environmental pollution and death rates from alcoholism. Counties in which the EPA did not report industrial releases of either lead or manganese, and where alcoholism was lower than average, had a rate of 228 violent crimes per 100,000 people (well under the national average). In contrast, counties with industrial releases of lead and manganese and higher than average alcoholism had rates of violent crime of 969 per 100,000 (three times above the national average). (The statistics linking differences in the rate of violent crime to lead, to manganese, and to alcoholism would each occur by chance less than once per 10,000 times.) Controlling for 17 other factors, including population density, poverty, and ethnic composition, the three sources of neurotoxicity are significantly associated with violent crime.

II. Current Research

With the support of a grant from the Environmental Protection Agency, current work is exploring a number of ways that toxic pollution affects the public. Data from a number of surveys of children’s blood lead are being combined with socio-economic and demographic data from the U.S. Census Bureau, health data from the Center of Disease Control, pollution data from the EPA, and crime data from the FBI. Our research will focus on the extent to which lead is being absorbed by humans due to: a) water treatment procedures; b) industrial releases of lead and other toxins; c) plumbing systems, leaded paint, and other sources of lead associated with old housing; d) other sources, such as lead residues in soil, that are particularly common in the center of some American cities; and e) dietary habits (such as shortages of calcium and iron) and demographic factors (such as poverty, stress, and minority ethnicity) which are known to be associated with increased risk of lead uptake. The resulting geographical variations in lead levels in children’s blood will also be studied as a factor that might explain rates of crime, educational failure and disease that are unusually high.

We are also studying “risk co-factors” that make lead and other toxic metals in the environment more dangerous to local residents. Here our emphasis will be on the use of silicofluorides as agents in water treatment. There are two reasons for this focus. First, both fluosilicic acid and sodium silicofluoride are toxins — and both leave potentially toxic residues if they do not dissociate completely. In studying the correlations between the use of these chemicals and crime, disease, and behavioral dysfunction, we seek to establish clearly whether or not these compounds are poisoning the public. Second, the silicofluorides apparently function to increase the cellular uptake of lead and other toxic metals, such as manganese; confirming correlations between silicofluorides and lead uptake should thus clarify the extent to which these compounds are risk co-factors for toxicity and other hazardous effects.

III. Results to date.

Our analysis of data from Massachusetts has revealed several important findings which are confirmed, where evidence is available, by preliminary analyses of the 129 cities covered in the September 1992 EPA News Release and of county data in West Virginia.

1. Communities with a higher percentage of children having blood lead over 10 mg/dL are significantly more likely to have higher rates of violent crime and higher rates of educational failure.

2. Communities using either fluosilicic acid (H2SiF6) or sodium silicofluoride (NaSiF6) have significantly higher rates of crime than those using sodium fluoride or delivering unfluoridated water (with the exception of towns with naturally fluoridated water).

3. The use of fluosilicic acid (H2SiF6) to fluoridate public water supplies significantly increases the amounts of lead in the water (whereas the use of sodium silicofluoride (NaSiF6) or sodium fluoride (NaF) does not.

4. There is no linear relationship between the amount of lead in a community’s public water supply (as measured by current methods of determining “90th percentile first draw water lead”) and the rates of violent or property crime.

IV. Implications

If these research hypotheses are confirmed, it should be possible to target both criminal and civil environmental enforcement strategies in a way that produces major public health benefits by reducing exposure and absorption of lead pollution and thereby reducing violent crime, learning disorders. and such diseases as hypertension. In the past, questions have been raised about the need to regulate industrial releases of lead and some have doubted that chronic exposure to low levels of lead pollution actually harm humans. Other efforts, such as the removal of leaded paint from old houses, have also been subjected to criticism on the grounds that they actually release more lead into the environment. If the hypotheses tested in this study are confirmed, efforts to remove lead from the environment will be validated and their effectiveness improved. In addition, this study may also suggest some relatively inexpensive non-enforcement interventions, such as ending or modifying water fluoridation procedures using silicofluorides. For all these reasons, environmental protection will be greatly enhanced by the acquisition of more comprehensive evidence of how environmental sources of lead and the risk co-factors for lead uptake are correlated with disease, crime, and behavioral dysfunction. The neurotoxicity hypothesis implies the benefits of a biomedical and dietary approach to educational failure, crime, and social deviance. Studies show IQ increases of as much as 15 points among children with poor diets who are given vitamin supplements. Removal of lead (“chelation”) and other methods of biochemical normalization have also been found to improve behavior and learning. Other studies indicate that the successes of Head Start are due in good part to its nutritional component. Because many children do not continue to benefit from balanced diets after Head Start, poor nutrition may explain the frequently observed declines in educational performance after these programs have been completed. Interventions such as good neonatal care, breast-feeding, vitamin supplements, and school lunches might therefore improve educational performance, as well as reduce violence and social disintegration.

The neurotoxicity hypothesis provides a new and potentially crucial dimension to accepted theories of crime. Factors like poverty, population density, social disintegration, race, easy access to guns, and violence on TV are obviously important contributors to violence, yet they do not effect everyone the same way. Studies of the behavioral impact of heavy metals can increase our knowledge of why these factors influence some individuals more than others. Crime prevention, better systems for screening prison inmates for potential violence, and cost-effective parole or probation options are all attractive. At the same time, the implications of the neurotoxicity hypothesis for our social, education, and legal systems are enormous. This approach does not excuse crime on the grounds of biochemistry. If poor diet and alcoholism contribute to learning disabilities and crime, this information ought to have the same status as knowing that drinking and driving do not mix. Given advances in neuroscience, dare we ignore the behavioral effects of neurotoxicity when this knowledge promises more effective crime prevention — and perhaps also more effective rehabilitation — than current methods?

h1

Exposures – and justice (or the lack thereof)

February 7, 2009

[Quotes:
"there is a huge gap between what researchers are discovering about environmental contaminants and what they can prove about their impact on disease. The gap has ensured that only a tiny fraction of worker's compensation payments are received by those who were exposed to harmful substances at work. "
"E. Donald Elliott, a Yale Law School professor specializing in these cases, said that simply being exposed to a risk in the workplace "should in itself be a compensable injury. From a policy standpoint, does it make sense for the entire burden of uncertainty or unknown science to fall on the injured parties rather than falling on the business or industry involved?" "]

NY Times, January 25, 2009

Exposed to Solvent, Worker Faces Hurdles

By FELICITY BARRINGER

BEREA, Ky. — When the University of Kentucky published new research in 2008 suggesting that exposure to a common industrial solvent might increase the risk for Parkinson’s disease, the moment was a source of satisfaction to Ed Abney, a 53-year-old former tool-and-die worker.

Mr. Abney, now sidelined by Parkinson’s, had spent more than two decades up to his elbows in a drum of the solvent, trichloroethylene, while he cleaned metal piping at a now-shuttered Dresser Industries plant here.

The university study had focused on him and his factory co-workers who worked near the same 55-gallon drum of the vaguely sweet-smelling chemical. It found that 27 workers had either the anxiety, tremors, rigidity or other symptoms associated with Parkinson’s, or had motor skills that were significantly impaired, compared with a healthy peer group. The study, Mr. Abney thought, was the scientific evidence he needed to claim worker’s compensation benefits.

He was wrong. The medical researchers would not sign the form attesting that Mr. Abney’s disease was linked to his work.

Individuals like Mr. Abney are caught between the conflicting imperatives of science and law — and there is a huge gap between what researchers are discovering about environmental contaminants and what they can prove about their impact on disease. The gap has ensured that only a tiny fraction of worker’s compensation payments are received by those who were exposed to harmful substances at work.

“It’s awfully difficult for any doctor or researcher to say to an individual: ‘You have this disease because you were exposed at this time,’ ” said J. Paul Leigh, a professor of public health sciences at the University of California, Davis.

How many people are caught in the same bind as Mr. Abney, “nobody really knows,” said Rafael Metzger, a California lawyer who specializes in cases involving diseases contracted in the workplace.

“Most workers who have an occupational disease don’t think they have an occupational disease,” Mr. Metzger said, adding that “the few who might think it are mostly not successful” in getting compensation “because there isn’t a robust body of literature to support the claim.”

Mr. Abney’s wife, Anita Susan Abney, is frustrated by the high standard of proof required. “If you’re saying in your study, ‘Yes, the dots have been connected,’ you should be able to say it in a court of law,” Ms. Abney said. “You should be able to say it at all levels.” She added, “I don’t blame it on the doctors, but on the strictness of the research.”

Trichloroethylene was nearly ubiquitous in American industry in the latter part of the 20th century. Production grew from to 321 million pounds in 1991 from 260,000 pounds in 1981, according to the Environmental Protection Agency.

The National Toxicology Program has declared that the solvent, also known as TCE, can “reasonably be anticipated” to be a carcinogen. It is a contaminant in drinking water in some areas of the country and is found in more than half the 1,430 priority Superfund sites listed by the E.P.A.

There was no question in Mr. Abney’s mind what he was working with.

“It was a good cleaner,” he said in an interview, his cane at his side. His wife recalled, “When he came home at night, he would say, ‘The smell is killing me.’ ”

Mrs. Abney sat next to her husband, with the fat files she has accumulated documenting aspects of his case — communications with doctors and with lawyers (all of whom left after the doctors refused to sign the forms).

Some of the paperwork documents the progression of Mr. Abney’s ailment: the day in 1996 when “on my left hand, a finger was twitching” or the day he could not enunciate the lesson to the Sunday school class he was teaching; and then, the day neither his hands nor his voice would perform his morning devotional rituals.

For five years, he received a series of diagnoses, including Lou Gehrig’s disease, amyotrophic lateral sclerosis, or A.L.S. Doctors at the Mayo Clinic in Jacksonville, Fla., correctly diagnosed his condition in 2001.

He left work and now receives federal disability payments of $1,200 a month. He was referred to Drs. Don M. Gash and John T. Slevin and joined a group of Parkinson’s patients involved in the testing of an experimental drug.

Mr. Abney mentioned that some of his co-workers also had neurological problems. Researchers mailed a questionnaire to 134 former Dresser workers; 65 responded.

Three, including Mr. Abney, had full-fledged Parkinson’s. The researchers found that of 27 others, 14 reported they had symptoms of the kind associated with the disease, and 13 others had significant slowing of motor responses or other symptoms of Parkinson’s.

A parallel study showed that feeding the solvent to rats resulted in injured neurons in the same area of the brain whose degeneration causes Parkinson’s in humans.

The conclusion, published in the Annals of Neurology in February 2008: “These results demonstrate a strong potential link between chronic TCE exposure and Parkinsonism.” But when it came to the specifics of Mr. Abney’s case, Dr. Gash said in an interview, “He started working at Dresser over 25 years ago, maybe 28 years ago. Trying to reconstruct what was going on then is just impossible.”

He added, “Certainly, we focused on one aspect of the toxins he was exposed to, but he was exposed to other toxins,” including agricultural pesticides or fumigants used to kill vermin at the plant.

“Was it the trichloroethylene?” Dr. Gash asked. “It could have been. But it could have been other things, too,” including a genetic predisposition to the disease.

Implicating TCE requires ruling out other potential causes, he said — something that could take years.

Which leaves few options for compensation. Dwight Lovan, Kentucky’s commissioner of worker’s compensation, said, “We are dependent on the scientific and medical communities for the element of causality.”

In other circumstances, proof of causality has been eased or waived. For instance, the Veterans Affairs Department in 2001 added Lou Gehrig’s disease to the list of service-related disabilities for Persian Gulf war veterans; in September 2008 it agreed to consider any service member who served for at least 90 days eligible for disability benefits if they later contracted A.L.S.

A crucial element of this decision, according to a veterans affairs official, was that the agency made no link between the onset of A.L.S. and a service member’s experience — whether exposure to the anthrax vaccine or the fires Saddam Hussein set in the oil wells under his control.

Kentucky officials do not have that option. In the workplace, as John Burton, an emeritus professor at the School of Management and Labor Relations at Rutgers University, said, “You still have the underlying requirement to establish that the workplace was the cause.” Because the burden of proof is so high and the relative benefits are so low, lawyers have little financial incentive to take on a case like Mr. Abney’s.

And scientists like Dr. Gash have little enthusiasm for working with lawyers.

E. Donald Elliott, a Yale Law School professor specializing in these cases, said that simply being exposed to a risk in the workplace “should in itself be a compensable injury.”

“You don’t have to prove you got the Parkinson’s because of the exposure,” Professor Elliott said. “From a policy standpoint, does it make sense for the entire burden of uncertainty or unknown science to fall on the injured parties rather than falling on the business or industry involved?”

For Mr. Abney and his wife, the disappointment still rankles. “You read this study and you hear about it and it builds you up,” he said. “And then you get let down. You get to where you just don’t care.”

Follow

Get every new post delivered to your Inbox.