PESTICIDE REPORT BY MERIEL WATTS

Reprinted from Soil & Health 2001, Vol 60 No.1, p.16-18.

PARKINSON'S DISEASE, PESTICIDES AND DERRIS DUST

In September last year we reported on the medical finding of Parkinson's disease as a result of exposure to 2,4-D in Northland. In November, the mainstream media published the results of a laboratory study linking the disease to rotenone, more commonly known as Derris Dust. There is a gathering body of evidence and worldwide concern that exposure to pesticides might be an important triggering factor in the development of this devastating and irreversible condition of the nervous system. We take a closer look at the problem.

For much of the last 20 years, concerns about pesticides have been focussed on cancer, the "dread disease". However, attention has recently begun to switch to the complicated effects of pesticides on the nervous system, in particular the chronic neurological problems, of which Parkinson's disease is just one. It has been projected that neurodegenerative diseases will overtake cancer as the second most common cause of death among the elderly by the year 2040 (Lang & Lozano 1998).

What is Parkinson's disease? Parkinson's disease is the most common degenerative disease of the nervous system, currently affecting about one per cent of the population. It is usually a late onset disease characterised by progressive and irreversible symptoms of muscular rigidity, shaking hands, facial tics, and tremors. Muhammad Ali, Michael J Fox, and athlete John Walker exhibit these characteristic symptoms. As the disease progresses, speaking becomes difficult, a shuffling gait develops, and there may be symptoms of senility and severe depression: the suffering can go on for many years. It also shortens life span. The symptoms result from the death of neurons in the brain, particularly dopaminergic neurons - that part of the brain involved in producing dopamine, a chemical messenger that helps control muscle activity.

The cause of this death of neurons is still largely unknown, even though the disease was first described in 1817 by James Parkinson. Early studies concentrated on finding a possible genetic link to the disease, but a massive study of nearly 20,000 identical twins has virtually ruled out the genetic causation theory, with fewer than 10 per cent of cases thought to have a genetic component (Tanner et al. 1999).

Environmental causes have long been suspected and attention has increasingly turned towards pesticides (Giasson & Lee 2000). In fact, one of James Parkinson's original patients was a gardener thought to have been exposed to arsenic and nicotine pesticides (Le Couteur et al. 1999). One of the classic symptoms of Parkinson's, the muscle tremor, is also a classic symptom of exposure to organophosphate insecticides. The current hypothesis, backed by strong evidence from scientific studies, is that damage to mitochondria is the cause of Parkinson's disease. Mitochondria are tiny organelles that exist in all cells and are involved in metabolism and the provision of energy for cells to carry out their functions. There is substantial evidence that a number of plant extracts, drugs, pesticides and other chemicals damage mitochondria, and in particularly interfere with its enzyme complex, known as "complex I", and hence can cause Parkinson's disease (Schapira 1998; Le Couteur et al. 1999; Betarbet et al. 2000). Suspect pesticides "A steady stream of studies from around the world have shown again and again that a common thread among victims of Parkinson's is a history of exposure to insecticides and herbicides" (Montague 1999). Fungicides do not appear to be quite so heavily implicated, although there is some evidence of the involvement of dithiocarbamate fungicides like maneb (Ritz & Yu 2000). Industrial solvents are also implicated, and many pesticide formulations contain solvents. Studies on the link between Parkinson's and pesticides began in the early 1980s when it was discovered that users of an opiate drug (MPTP), chemically similar to the herbicide paraquat, developed Parkinson's Disease (Pfohman 1992). Most of the evidence linking Parkinson's to pesticides comes from retrospective studies of populations with elevated levels of the disease. Because of the immense difficulties involved in establishing cause and effect, these studies have been able to establish links only to general classes of pesticides rather than to specific chemicals. The first reported association of this kind was in 1978 and involved a crop duster routinely exposed to organophosphate insecticides. Other studies have linked Parkinson's to carbamate insecticides, carbon disulphide-based fumigants, organochlorine insecticides, household fumigation, chlorphenoxy herbicides, or herbicides generally (Semchuk et al. 1993; Le Couteur et al. 1999; Ritz & Yu 2000).

Many of these studies involved occupational exposure. However, in May 2000, neuroepidemiologist Dr Lorene Nelson presented to the American Academy of Neurology's annual meeting in San Diego the results of a study on the association between Parkinson's Disease and home use of pesticides. The study confirmed the occupational exposure findings, indicating that home users are just as susceptible to harm from pesticides as are farmers. The worse problem came with use of household insecticides, with a 70 per cent increase in risk of the disease, but exposure to garden insecticides and herbicides also significantly increased the risk. As mentioned already, the vast majority of studies have been able to link Parkinson's only to broad classes of pesticides. However, investigations of some individual Parkinson's cases have shown links to specific pesticides. These include paraquat, maneb, diquat and dieldrin (Le Couteur et al. 1999) - not forgetting the New Zealand case linking Parkinson's to 2,4-D reported in Soil & Health last year (Watts 1999). Other pesticides have been linked with acute but reversible parkinsonism (parkinsonism is a disorder with symptoms like Parkinson's disease, but which may be reversible). These include the organophosphates malathion, dimethoate and chlorpyrifos, and the carbamate propoxur (Bhatt et al. 1999).

One interesting case of reversible parkinsonism supports the study by Nelson on household insecticide use. It involved a 64-year-old woman who used an aerosol organophosphate insecticide twice daily in her kitchen and bedroom over a period of ten years. She developed progressive symptoms of parkinsonism, but recovered after a period in hospital. On returning home she became ill again. The pattern recurred every time she went home. She eventually moved to a new home, then after two years without symptoms she wore clothing that had been stored in her previous home. She again developed parkinsonism, which subsided when she removed the clothing. Her sister and daughter who came to care for her were also affected, but her husband, son, daughter-in-law and grandchildren were unaffected (Bhatt et al. 1999). This episode supports the notion that there may be familial susceptibility to Parkinson's disease as a result of genetic variation in the enzymes involved in detoxifying pesticides (Le Couteur et al. 1999). It also provides a sharp warning for those people who think flysprays are harmless. There is also laboratory evidence that a number of pesticides are toxic to mitochondria or interfere with their function, and are thereby potentially able to cause Parkinson's disease. These include chlordane, cyanide, cyhalothrin, 2,4-D, DDT, dieldrin, dinoseb, endosulfan, ethaphos, glyphosate, heptachlor, paraquat, permethrin, rotenone and 1080 (Le Couteur et al. 1999).

The new generation insecticides are worse. New generation insecticides may be even more of a problem. Since scientists came to the conclusion that it is the target site insensitivity of the old style broad spectrum insecticides that was causing insect resistance, they have sought to develop insecticides that are much more specific in their biochemical activity. And one of the specific sites they have found to be effective in killing insects is that of the complex I enzyme system in mitochondria - the very one that appears to underlie Parkinson's disease (LŸmmen 1998). Such new generation insecticides include fenpyroximate, tebufenpyrad, fenzaquin, pyrimidifen, and pyridaben - all used for mite control and in some cases for other insects (LŸmmen 1998; Espositi 1998). Of these, only fenpyroximate and tebufenpyrad are currently registered in New Zealand. Do not expect that the new registration system soon to start up under ERMA will detect these problems: knowledge of the effects of pesticides on the complex I enzyme system of mitochondria is not required for registration of pesticides.

Derris Dust and Parkinson's

Despite the fact that there is so much evidence linking Parkinson's disease to a number of synthetic chemical pesticides, the subject only hit the news when a recent study linked Parkinson's to a pesticide that is permitted under organics standards: rotenone, more commonly known as Derris Dust, and used principally by home gardeners.

Rotenone is extracted from plants belonging to the legume family, mostly plants of the Derris and Lonchocarpus genera which come from Southeast Asia, Central and South America. Rotenone is found in at least 68 species of legume (Morris & Powell 2000). Apparently it has been known in scientific circles since 1961 that rotenone inhibits the complex I enzyme system of mitochondria (Esposti 1997), and since 1997 that it may be implicated in Parkinson's disease (Morris & Powell 2000). The latest study found that chronic intravenous exposure to rotenone induced the progressive degeneration of the dopaminergic neurons in the brains of rats, and the reduced movement, unsteady movement, hunched posture, rigidity and shaking paws characteristic of Parkinson's (Betardet et al. 2000).

NOTE: Do not take the list of pesticides provided here as any sort of definitive statement on those which cause Parkinson's disease. It is important to remember that there is an immense lack of scientific knowledge about the effects of pesticides on the nervous system and on the enyzme systems involved in metabolism, and that the work on linking specific pesticides to Parkinson's disease is in its infancy. Studies linking Parkinson's to pesticides have implicated most categories of insecticides and herbicides: organochlorines, organophosphates, carbamates, fumigants, synthetic pyrethroids, the new generation miticides, phenoxy herbicides, paraquat, glyphosate, and even natural plant extracts. Those who slavishly adhere to scientific proof before they stop using pesticides will argue there is no definitive proof. Those who do not want to run the risk of developing Parkinson's might take a different view.

What to do instead of using Derris Dust as Derris Dust is a naturally occurring compound? It has long been allowed in organic growing systems. Under the current BIO-GRO standards, Derris Dust is a restricted material, meaning that it may be used "only in accordance with the principles specified in these Standards", with a reduction each year in the dependence on it, and only until more acceptable materials are available. It is also permitted under Demeter and Agriqual/Certenz standards. Its main use is in home gardening, particularly for controlling the caterpillar of white cabbage butterfly. In commercial horticulture it has largely been replaced by Bt preparations. Bt is the short name for Bacillus thuringiensis, the preparation that was used to eradicate the white-spotted tussock moth in Auckland several years ago. Soil & Health will be requesting that BIO-GRO, Demeter and Agriqual/ Certenz no longer allow Derris Dust in certified organic systems. We will report progress on this front as it occurs.

The finding of such drastic health problems from exposure to an age old organic preparation should act as a wake-up call to organic growers. It is a reminder that many natural plant products can be toxic when they are extracted and concentrated. It is a reminder that the philosophy of organic growing is not that of replacing synthetic chemicals with natural chemicals. Rather it is to strive for balance in an agri-ecosystem, or home garden, in which the grower works with nature as much as possible rather than trying to control it. Pesticide preparations, even those of natural occurring substances, should be the last port of call not the first remedy. They may control the pest at that moment in time, but they do not encourage a balanced system that looks after itself. Derris Dust also kills valuable biological control insects like ladybirds. This is counterproductive. In our city garden, we have fed the birds to encourage their presence for many years. We have no problem with white cabbage butterfly, or any other insect pests. After dining on the birdseed and left over bread crusts, the birds make a bee-line to the garden and clean up any insects they can find. Mind you they are also partial to lettuce and silver beet - these we net. If your bird populations are not sufficient for natural control, try squashing the caterpillars with your fingers. It may be messy, but it is preferable to Parkinson's disease. Or use Bt.

Finally, a little bit of good news for the coffee-drinkers out there: research indicates that coffee-drinkers are less likely to develop Parkinson's disease (Ross et al. 2000). It appears to be a direct effect of caffeine intake! On the other hand, high intake of total fats, saturated fats and cholesterol seems to increase the risk of Parkinson's (Johnson et al. 1999).

SUSPECT PESTICIDES Evidence of involvement in Parkinson's disease 2,4-D dieldrin diquat maneb paraquat rotenone

EVIDENCE OF INVOLVEMENT IN PARKINSONISM chlorpyrifos dimethoate malathion propoxur

EVIDENCE OF EFFECTS ON MITOCHONDRIAL

ENZYME SYSTEM chlordane cyanide cyhalothrin 2,4-D DDT dieldrin dinoseb endosulfan ethaphos glyphosate heltachlor paraquat permethrin rotenone 1080