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  • NIH study finds two pesticides associated with Parkinson’s disease (Media release), National Institutes of Health, February 11, 2011.
    • Debunked. In this study of self-reported exposures to 31 pesticides, the researchers have no idea how much of any pesticide (or whatever else) any of the study subjects were exposed to — so they really can't link Parkinson's Disease with anything, let alone paraquat and rotenone. That the researchers collected data on 31 pesticides means that the study is subject to the multiple comparisons problem. The study is also very small — only 72 cases of PD may have been exposed to paraquat; only 51 cases may have been exposed to rotenone. The study is internally inconsistent with respect to the hypothesized modes of the pesticides causing PD (i.e., oxidative stress or mitrochondiral dysfunction). That is, other than paraquat, no other oxidative stressor was associated with PD. Similarly, no mitochondrial inhibitor other than rotenone was associated with PD. Finally, of the nine other published studies, none link paraquat with PD. Rotenone was not linked with PD in the only other published study of a potential association.

Related Topics

Studies and Reports

  • Firestone J et al., Occupational factors and risk of Parkinson's disease: A population-based case-control study, Am J Ind Med. 2010 Mar;53(3):217-23.
    • Conclusion. "These findings do not provide support for the hypothesis that workplace factors affect the risk of PD."
    • Comment. "There was no association with paraquat use.
  • Berry C et al., Paraquat and Parkinson's disease, Cell Death Differ. 2010 Jul;17(7):1115-25. Epub 2010 Jan 22.
    • Abstract. "As evidence emerges that complex gene alterations are involved in the onset of Parkinson's disease (PD), the role of environmental chemicals in the pathogenesis of this disease becomes intensely debated. Although it is undisputed that acute exposure to certain chemicals such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is sufficient to cause human parkinsonism, the evidence that the risk for PD increases because of environmental exposure is generally weaker. Several studies have suggested that pesticide exposure and life in rural areas are significant risks factors for PD. Among other pesticides, paraquat (PQ) has been linked to PD by epidemiological studies and experimental work in rodents, in which it causes lesions in the substantia nigra, pars compacta. However, the evidence that human exposure to the chemical results in an increased risk for PD is rather limited and based on insufficient epidemiological data. This review critically analyses the evidence that implicates PQ in parkinsonism and discusses the limitations of chemical modelling of PD."
  • Tanner C et al., Occupation and risk of parkinsonism: a multicenter case-control study, Arch Neurol. 2009 Sep;66(9):1106-13.
    • Results. The odds ration between occupational exposure and Parkinson's disease was not statistically significant on the confidence interval, OR=2.80 (0.81, 9.72).
  • Kamel F et al., Pesticide exposure and self-reported Parkinson's disease in the agricultural health study, Am J Epidemiol. 2007 Feb 15;165(4):364-74. Epub 2006 Nov 20.
    • Abstract. "Previous studies based on limited exposure assessment have suggested that Parkinson's disease (PD) is associated with pesticide exposure. The authors used data obtained from licensed private pesticide applicators and spouses participating in the Agricultural Health Study to evaluate the relation of self-reported PD to pesticide exposure. Cohort members, who were enrolled in 1993-1997, provided detailed information on lifetime pesticide use. At follow-up in 1999-2003, 68% of the cohort was interviewed. Cases were defined as participants who reported physician-diagnosed PD at enrollment (prevalent cases, n = 83) or follow-up (incident cases, n = 78). Cases were compared with cohort members who did not report PD (n = 79,557 at enrollment and n = 55,931 at follow-up). Incident PD was associated with cumulative days of pesticide use at enrollment (for highest quartile vs. lowest, odds ratio (OR) = 2.3, 95% confidence interval: 1.2, 4.5; p-trend = 0.009), with personally applying pesticides more than half the time (OR = 1.9, 95% confidence interval: 0.7, 4.7), and with some specific pesticides (ORs > or = 1.4). Prevalent PD was not associated with overall pesticide use. This study suggests that exposure to certain pesticides may increase PD risk. Findings for specific chemicals may provide fruitful leads for further investigation."
    • Comment. The associations for paraquat and prevalent and incident cases were statistically insignificant on the confidence intervals.
  • Cooper S et al., A survey of actinic keratoses among paraquat production workers and a nonexposed friend reference group, Am J Ind Med. 1994 Mar;25(3):335-47.
    • Abstract. "Follow-up on two reports of an excess of keratoses among paraquat production workers was conducted to evaluate the contribution of occupational exposures to the prevalence of keratoses among workers in a paraquat production plant in Texas. A cross-sectional study design was used to compare the prevalence of keratoses among current workers to an age, race, and sex frequency-matched group of their friends who had never worked at the plant. The analysis is based on 112 workers and 232 friends. Exposure, outcome, and covariables used in the analyses were obtained from an interview questionnaire, dermatology exam, and company records. Overall, the prevalence proportion of the presence of any actinic keratoses among workers and friends was similar (0.30 and 0.28, respectively). Among high cumulative exposed workers, the prevalence of any actinic keratoses was 0.40 compared to 0.20 among low-exposed workers and 0.28 among friends. These results were further explored using a multiple logistic regression approach to adjust for known risk and possibly confounding variables. Statistically significant high risks of actinic keratoses were demonstrated for freckling before age 16 years, older age, suntanning behaviors, occupational exposure to polycyclic aromatic hydrocarbons (PAH), and Fitzpatrick skin type. There was no significant contribution of overall exposure status (worker vs. friend). Similar to the crude analysis, the odds of actinic keratoses of high-exposed workers compared to friends was 1.9 (confidence interval [CI] = 0.9-4.2) whereas the comparable odds ratio for low-exposed workers vs. friends was 0.6 (CI = 0.2-1.7). These data do not demonstrate an excess of actinic keratoses overall nor any consistent increase in the odds of keratoses with an increase in plant exposure level."
  • Firestone J et al., Pesticides and risk of Parkinson disease: a population-based case-control study, Arch Neurol. 2005 Jan;62(1):91-5.
    • Conclusion. "... the lack of significant associations, absence of associations with home-based exposures, and weak associations with rural exposures suggest that pesticides did not play a substantial etiologic role in this population."
  • Hertzman C et al., A case-control study of Parkinson's disease in a horticultural region of British Columbia, Mov Disord. 1994 Jan;9(1):69-75.
    • Abstract. "We compared personal histories of 127 cases and 245 controls to identify possible environmental risk factors for idiopathic parkinsonism (IP). Of our controls, 121 had cardiac disease (CD) and 124 were randomly selected from electoral lists (voters). Using logistic regression and adjusting for sex and age, we ran separate analyses: IP versus CD and IP versus voters. A full occupational history was collected, as was known contact with all pesticides associated with the tree fruit sector of the agricultural industry. We found a significant association between IP and having had an occupation in which exposure through handling or directly contacting pesticides was probable, but no specific chemicals were associated with IP. We conclude that although occupations involving the use of agricultural chemicals may predispose to the development of IP, it seems likely that the pathogenesis is multifactorial rather than related to a specific agent."
    • Comment. No association between exposure to paraquat and Parkinson's disease was found.
  • Hertzman C et al., Parkinson's disease: a case-control study of occupational and environmental risk factors, Am J Ind Med. 1990;17(3):349-55.
    • Abstract. "We compared personal histories of 57 cases and 122 age-matched controls to identify possible environmental determinants of Parkinson's disease (PD). Odds ratios (OR) adjusted for sex, age, and smoking were computed using stepwise logistic regression. We found a statistically significant increased risk for working in orchards (OR = 3.69, p = 0.012, 95% CI = 1.34, 10.27) and a marginally significant increased risk associated with working in planer mills (OR = 4.11, p = 0.065, 95% CI = 0.91, 18.50). A Fisher's exact test of the association between PD development and (1) paraquat contact, and (2) postural tremor gave statistically significant probability estimates of 0.01 and 0.03, respectively. The relative risk of PD decreased with smoking, an inverse relationship supported by many studies."
    • Comment. The planer mill worker odds ratio is not statistically significant on the confidence interval. On the orchard worker odds ratio, the confidence interval or margin of error is more than twice as large as the reported effect. These are essentially non-results.
  • Rajout A et al., Geography, drinking water chemistry, pesticides and herbicides and the etiology of Parkinson's disease, Can J Neurol Sci. 1987 Aug;14(3 Suppl):414-8.
    • Abstract. "In 1984 we made the first observation of a correlation between early age exposure to rural environment (and drinking well water) and development of idiopathic Parkinson's disease (IPD). These findings were subsequently confirmed elsewhere (Barbeau, 1985;25 Tanner, 1985). Analysis of all early age onset IPD (EPD) cases born and raised in Saskatchewan revealed that 20 of 22 had exclusively rural exposure during the first 15 years of life. This distribution was significantly different from the general population (p = 0.0141). Further study of the EPD group included sampling and metal analysis of childhood sources of drinking water in 18 cases and 36 age and sex-matched controls. Water collected from the two groups was analyzed for 23 metals (including 7 elements implicated in the etiology of IPD). There was no difference in the metal composition of the water between the two groups. Finally, a review of herbicide and pesticide use in Saskatchewan agriculture was undertaken to determine if there was an increased incidence of EPD following utilization of any particular chemical. No increase was found in the incidence of EPD with the introduction of any pesticide or herbicide, including Paraquat, for agricultural use. We conclude that there is a strong correlation between early age rural environmental exposure and development of IPD. We believe well water is a likely vehicle for the causal agent, but neither water metal concentration nor any of the herbicides and pesticides used in Saskatchewan agriculture are related to the cause."

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