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Pesticides have for many decades been used by farmers and other professionals in different activities to achieve various agricultural goals. Pesticides have been responsible for the eradication of many pests, which has in turn had a positive effect on farming practices around the world. For many farmers, pesticides have been a necessity in farming as they have proven to be the most effective way of dealing with pests. Pesticides have mainly been used in agriculture to protect crops against harmful pests. Pesticides have also been greatly used domestically to guard against pests and insects. Pesticides, however, have been known to have a negative effect on human health. In recent years, research has been conducted to investigate the effect of pesticides on human health and the extent to which a link between the two exists. This paper specifically addresses the link between pesticides and the causation of Parkinsonís disease in human beings. The paper explores the various ways and settings in which pesticides are used and the involvement of human beings in that use.

Understanding Pesticides

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Pesticides can generally be viewed as a possible set of interventions whose main goal is to eradicate or, at least, reduce the numbers of pests to manageable levels. Pesticide action is not just limited to insects, but extends to all kind of plant pests, pathogens, and various weed populations. This means that pesticides contain in them insecticides, herbicides, fungicides, and other forms of pest controlling chemicals. Pests around the world account for the destruction of about 40% of the worldís crops (Microsoft Encarta, 2007). This happens both when crops are in the fields and after they are harvested. Various kinds of insects, rodents, birds, and microorganisms are responsible for this damage and are the reason for the necessity of pesticide use. It is therefore easy to understand the popularity of pesticides among farmers. They save farmers millions of dollars in losses resulting from crop destruction by pesticides. Some studies show that for every 1 million invested in pesticides, 4 million is saved in monetary returns (Microsoft Encarta, 2007). These savings in cash should, however, be weighed against the overall cost to human health brought about by the use of pesticides.

Understanding Parkinsonís Disease (PD)

Parkinsonís Disease (PD) is a†nervous system disease or dysfunction. It mainly affects muscular control. The decreased integrity of the muscular system generally results in the involuntary shaking of body appendages, stiffness of muscles, and compromised balance (Rosenbaum, 2006). The disease progresses slowly overtime, getting worse consistently, until it has severely compromised all the main functionalities of a human being. It eventually makes some of the most basic activities impossible, including the ability to think. The disease does not have a cure but may be controlled through a variety of drug therapy and surgical interventions. The drugs are majorly used to control some of the major symptoms of the disease. Although the beginning of the disease as well as its progression are well known, the exact cause of it is still unclear.† †

Statistics estimate that there are around one and a half million people in the U.S.A. who are suffering from Parkinsonís disease. These numbers are courtesy of The†National†Parkinson Foundation. However, sometimes symptoms of the disease may be confused with those experienced during the onset of old age. At other times, the disease may be misdiagnosed and confused with another disease (Rosenbaum, 2006). Parkinsonís disease (PD) usually occurs in older people past the age of sixty. Increase of incidence is directly proportional to increase in age. The term Ďparkinsonismí refers to a group of diseases whose symptoms mainly mimic those of Parkinsonís disease. The link between the development of these diseases and the use of pesticides are also of interest to this paper because of the connection to Parkinsonís diseases. Although Parkinsonism is often misdiagnosed as Parkinsonís disease, it does not fully respond to similar interventions.

Causes of Parkinsonís Disease

Genetic Factors

Parkinsonís could be caused by several different factors. One of the causative factors is a genetic predisposition to the disease inherited from a parent or a close relative. Studies have shown that genetic predisposition may increase a personís chances of developing Parkinsonís disease. 15% of individuals with the disease have a close relative who also has it (Foltynie et al., 2002). Gene coding, which is somewhat similar among family members, may undergo mutation, which may result in the degeneration of the cells and lead to the development of Parkinsonís. Studies conducted with twins reveal that an identical twin is more likely to develop Parkinsonís disease if the other one develops it too. The case is not similar for fraternal twins who unlike identical twins do not have similar genetic makeup (Microsoft Encarta, 2007). According to Foltynie (2002),† in young onset of PD, twin studies† reveal high rates of concordance in monozygotic twins, suggesting that the development of PD in younger peplum may be influenced by genetic factor (Tanner, 2003).

Gene-environment interactions in specific references to PD have not been exhaustively researched and there exists a large possibility that interactions between certain kinds of genetic makeup with environmental influences, such as pesticides, could be responsible for the occurrence of PD (Kelada et al., 2006). Approximately 10 to 30% of PD patients are recorded to have relatives who have suffered from the disease. Although this may occur due to the same exposure, it is widely thought that the genetic factors are at play. Genetic causes account for about 10 to 20% of PD patients (Betarbet, 2000).

Free Radicals

Free radicals, naturally found in the body, may also play a part in the development of the disease. They interfere with normal cell activities in the body, damaging cell organelles, and eventually triggering cell death. This ultimately compromises body organs. Free radicals mainly flourish when inadequate amounts of antioxidants are unavailable in the body.

Environmental factors

Parkinsonís disease is thought to have environmental factors that are the main cause of its development. Industrial and other artificially produced chemicals have been found detrimental and seriously threatening to human health. The numerous environmental pollutants and toxins have led to an increase in the number of PD occurrences. Most of these chemicals come from the substances used in technological and other activities, as well as the by-products of those activities. Various harmful substances that mimic the clinical presentation of PD have in recent years been identified by researchers and physicians; these include certain microorganisms, medicines, and chemicals. MPTP, for instance, is a chemical that is normally created during the production of heroin. The same chemical is found in certain pesticides and exposure to the same is thought to have a connection with the development of PD. Individuals who are exposed to certain pesticides for significant durations of time record more cases of PD, even though a link of direct causation cannot be authoritatively claimed. Other environmental factors, possibly responsible for the development of PD, include a repeated head trauma and the extended use of neuroleptic drugs. Manganese toxicity has also been thought to induce Parkinsonism (Addler, 1999). Inflammation of brain tissue earlier in life is said to result in PD later in life.

It is worth noting that exposure to pesticides does not necessarily have to be through airborne ways, such as breathing it in. It may occur through the interaction with contaminated water, soil, and food. Couteur et al. (2000) have suggested that there is a connection between the development of PD and the drinking of pesticide-contaminated water, as based on the high prevalence of the disease in certain hydrographic regions in Canada, which all seemed to have connections with farming and pesticide use. In one particular case, well water was found to be directly, positively, and independently associated with PD development (Zorzon et al., 2002). Jimenez-Jimenez et al. (1992) note that studies show a positive correlation between the exposure to the pesticide-contaminated well water and the development of PD.

It has also been noted that there are inverse associations of some factors with the occurrence of PD. The sustained use of cigarettes (smoking), as well as the sustained use of caffeine, are inversely proportional to the risk of PD development (Couteur et al., 2012; Powers et al., 2008). However, it is possible that this protection from PD may be a result of the interaction of nicotine and caffeine with certain genetic makeup. The issue, therefore, may need more investigation. Ross and Smith (2007) further assert that gene-environment interaction may influence vulnerability to PD development.

The Link between Parkinsonís and Pesticide Use

A cause-and-effect relationship between environmental neurotoxins and Parkinson's is difficult to prove. This is particularly difficult because it involves the study of different populations, which presents difficulties in methodology of study. Moreover, other factors tend to come into play when studies involve many people and it is difficult to isolate required data that is uninfluenced by these other factors. It is therefore hard to authoritatively state that certain factors are the sole cause of PD. However, epidemiological and etiological research points to strong correlations between exposure to pesticides and the development of PD (Tanner et al., 2003).

Due the increasing incidence of exposure to pesticides with the development of Parkinsonís in individuals who are thus exposed, it is possible to conceive of a connection between the two. Scientists and other professionals have for a long time hypothesized about the existence of a connection between the two. In this regard, many studies have been conducted in a bid to study the disease and its possible causative factors. Other studies have been conducted on the side effects of the use of pesticides on human beings. Others still have tried to connect the two. Research concerning the same is done mainly by testing the effect of suspect chemicals on animals and using the findings to establish the possible effects of the same chemicals on human beings. Other researchers study select populations that are significantly exposed to the suspect chemicals and compare their incidence rates of Parkinsonís to control populations of unexposed individuals. Many researchers over the last few years have established a link between the two. Scientists have isolated 3 main types of chemicals that are suspected to trigger the development of PD. Each of these pesticideís mechanisms of damage to cells are different.

Three ways have been suggested as to how pesticides may play a role in the development of Parkinsonís disease. The first is that pesticides are directly neurotoxic, which cells cannot handle. MPTP is the prototype Parkinsonís disease neurotoxin (Couteur et al., 1999). This toxicity interferes with the functioning of cell organelles, notably the mitochondria. They also inhibit dopamine transmission between brain cells and this largely impairs cell functions. Secondly, pesticides may cause PD through the induction or inhibition of certain important xenobiotic metabolizing enzymes. This then impairs metabolic activities, which ultimately leads to cell death. Lastly, it is thought that pesticides could be a conduit through which other naturally occurring neurotoxins are able to enter the body and cause PD. In this theory, pesticides themselves do not result in PD development but rather act as a host for PDĖcausing neurotoxins. These neurotoxins may be naturally occurring in farms or certain water sources (Couteur et al., 1999).


These are generally chemicals designed to eradicate weeds and other unwanted plants, mainly herbs, so as to ensure that they do not compete with the farmerís crop for essential nutrients. Herbicides stop the weedsí growth and kill them. Paraquat is one such chemical, whose main action is the destruction of broad leaf weeds. This chemical is thought to interfere with brain proteins and destroy brain cells, ultimately resulting in Parkinsonism (Tanner, 2003). Trifluralin is also a herbicide known to have similar effects. Organochloride- and organophosphate-containing pesticides are especially suspected for the causation of PD.


As their name suggests, insecticides are designed to kill insects by the direct damage of their brain cells. Rotenone, which belongs to this class, is particularly destructive to cell mitochondria and has been known to induce oxidative stress to the brain. It may also increase the production of certain brain chemicals, which lead to the ultimate destruction of brain cells.


These are chemicals that act against fungal organisms that pose a threat to crops and lead to plant diseases. Maneb and Benomyl are the examples of fungicides that are thought to have a negative effect on the brain cellís mitochondrial functions. They also impair the ability of brain cells to repair themselves, thus accelerating cell death.

Because of their different mechanisms of action, exposure to multiple types of pesticides poses an increased risk of PD development as compared to the exposure to only one type. Research suggests evidence that there is indeed a link between the two. Rotenone and Paraquat are some of the major pesticides thought to play a part in the causation of Parkinsonís disease development.

Animal Test Evidence

The effect of pesticides on animal cells and structures has been known to trigger neurodegenerative processes in targeted pests. Research by scientists at the University of California Los Angeles revealed that the same effect that certain pesticides have on insects, rodent sand certain microorganisms also occur in human beings (Tanner, 2003). Certain chemicals work synergistically from neurotoxic agents, although each of the chemicals used separately is relatively safe. Researchers at the University of Pennsylvania exposed a rat to rotenone, a common pesticide for a period of time. The rat gradually began to display symptoms of Parkinsonís disease. The mitochondrial inhibiting action of the chemical severely compromised the animalís neurological functions and led to its Parkinsonism. Betarbet et al. (2000) similarly assert that chronic administration of rotenone induces major symptoms of Parkinsonís disease in rats. Tests revealed that the exposure led to the degeneration of animal brain tissue. This has led to the hypothesis that this particular chemical, which is very widely used, could actually be exposing its users to the risk of Parkinsonís disease development. The researchers, however, observed a difference in the level of vulnerability to rotenone among different populations, suggesting that there might also be other factors at play, along with exposure to the pesticide, such as genetic makeup. Pesticidal activity has been observed to induce cell death in animals by initiating pathological processes which result in irreparable damage. The effects of this pesticide on animal brain cells can be used to suggest a link between the presence of certain pesticides and the occurrence of Parkinsonís, especially where the incidence of the disease is high in regions where the chemical is present. The study can also be used to make inquiry into a possibly similar effect of other pesticides on human beings.

Mechanistic Evidence

Another way to draw evidence that there exists a link between pesticides and the development of Parkinsonís disease is in the cell functions. Individuals experiencing the disease are known to have certain symptoms in their cells. The cell mitochondrion, which converts cell nutrients into energy, is usually fairly destroyed. In other cells, oxidative stress, which often causes cell self-destruction, occurs. By investigating the prior presence of chemicals (pesticides) known to have this effect on animal cells, researchers are able to conclude that a connection exists. Control populations of individuals from the same region are also considered. Using statistical methods, researchers are able to draw meaningful conclusions. Such a study was conducted and revealed that the incidence of Parkinsonís disease was 2.5 times more likely in individuals who had been exposed to toxic pesticides than those who had not.

There is a significant association of the use of certain groups of pesticides, which contain substances that disrupt mitochondrial activities or cause oxidative stress, with the occurrence of Parkinsonís. Research by the National Institute of Health indicates that individuals who are exposed to either Rotenone or Paraquat over significant periods of time usually have a two and a half more chance of developing Parkinsonís than those who have not, all other factors being constant (Tanner et al., 2011). In a joint study by the National Institute of Environmental Health Sciences (NIEHS) and the Parkinson's Institute and Clinical Center in California, 110 people with PD, along with 358 control individuals were studied to determine the influence of pesticides on PD development. This was part of a larger study where 90,000 farmers and their spouses were interviewed to assess the life-long effects of pesticide use on them. Findings revealed increased incidences and severity of PD among individuals more often exposed to pesticides both infrequency and in small quantities. Control populations revealed fewer incidences of PD (Tanner et al., 2011).

Proximity Evidence

There is a correlation between the occurrence of PD in individuals and their proximity to areas where pesticides are available or in use. As early as in the 1970s, epidemiologists noticed an increased incidence of PD development in the individuals who had grown up in rural areas, where they were more likely to be exposed to farm pesticides. This was even truer for the individuals who had grown up on farms. The role of pesticides in the possible cause of PD was suggested. Further research has been conducted in recent years, where individuals living or working in areas where they are likely to be exposed to pesticides over a long duration of time are examined for PD, as compared to those who are not. Research has revealed that such individuals report two and a half times more cases of PD as compared to the control populations (Tanner et al., 2011). Some studies have geographically linked pesticide usage to the occurrence of PD (Couteur et al., 1999). Many studies have revealed a positive correlation between the duration of exposure to harmful pesticides and the development of PD. The same studies have also suggested a similar correlation with the increased quantities of exposure. The likelihood of PD development is thought to increase if the exposure to harmful pesticides occurred in an individualís youth and teenage years other than later in life (Nelson, 2000). The fact that farming, rural living, and consumption of well water have been found to be closely linked with many PD patients suggests that pesticides are a causative factor of PD (Brown et al., 2006). Other studies show that continued contact with certain domestic pesticides can also expose individuals to the same fate, as those exposed to industrial herbicides and farm pesticides. In 2009, UCLA published a report linking Parkinsonís to the exposure to both farm and domestic pesticides.†

Drug Use Evidence

There are some substances that have been known to induce Parkinsonís-like symptoms. Such substances have been used in research to establish whether a link between Parkinsonís and PD exists. The chemicals in the substances are compared to the chemicals found in pesticides in order to gauge whether the same substances could be responsible for Parkinsonís.

Certain types of drugs have been known to induce Parkinson-like tremors. Heroin, for instance, has a chemical in it that causes individuals to tremble involuntarily. This makes heroin addicts of particular interest to scientific studies. Investigations into whether similar chemicals found in heroin are found in some pesticides have been done with positive results in some pesticides. Methamphetamines have been known to also induce temporary Parkinsonism in some of its users (Betarbet, 2000). The toxicant 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), usually found in certain quantities in some drug substances taken by human beings, has been known to induce Parkinsonism in its patients, causing symptoms that pathologically and biochemically resemble those in a Parkinsonís patient. This has been true for some drug addicts, however and not for all of them. Pesticides which bear a similar structural or molecular makeup as that in MPTP are therefore thought to be risk factors for PD development. These include pesticides like Rotenone and Paraquat (Goldman & Tanner, 1998). Parkinsonism that results directly from the intentional or accidental ingestion of MPTP is clinically undistinguishable from Parkinsonís disease. The similar structure link exists between Paraquat, a common herbicide, and the chemicals found in MPTP, which both induce Parkinsonism.


Although there are numerous gaps in research about the connection between PD and pesticide use mainly due to methodological inadequacies, it is possible with the amount of data already gathered to suggest that there is indeed a strong link between the two. Epidemiological and etiological studies have revealed that there is an undeniable correlation between the two that appears consistent. This is especially true for long-time exposures. Toxicological studies have revealed that Paraquat and Rotenone in particular exert neurotoxic actions on brain cells, which is thought to cause cell death and result in PD development. Future research on gene-environment interaction and its effect on PD suspect ability, as well as the effect of multiple exposures to pesticides and their consequences, may yield a better understanding of the phenomenon. At present, the amount of research done and the findings therefore are sufficient enough to warrant the conclusion of an association between exposure to pesticides and PD. However, evidence is not sufficient enough to establish a direct causal relationship between the two.

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