Environmental exposure to pesticides and the risk of Parkinson's disease in the Netherlands

Brouwer, Maartje; Huss, Anke; Mark, Marianne van der; Nijssen, Peter C.G.; Mulleners, Wim M.; Sas, Antonetta M. G.; Laar, Teus van; Snoo, G.R. de; Kromhout, Hans; Vermeulen, Roel

doi:10.1016/j.envint.2017.07.001

Cited by 136 publications

(55 citation statements)

References 27 publications

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“…Epidemiological studies indicated that some of these factors, including exposure to environmental toxins (e.g. pesticides), could increase the risk of developing PD (Brouwer, Huss, Mark, Nijssen & Mulleners, 2017;Dick et al, 2007). Conversely, other factors, including coffee consumption or physical activity, are associated with a lower risk of developing PD (Bellou et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

Genetically engineered animal models of Parkinson's disease: From worm to rodent

Breger

Fuzzati-Armentero²

2018

Eur J of Neuroscience

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Parkinson's disease (PD) is a progressive neurological disorder characterised by aberrant accumulation of insoluble proteins, including alpha‐synuclein, and a loss of dopaminergic neurons in the substantia nigra. The extended neurodegeneration leads to a drop of striatal dopamine levels responsible for disabling motor and non‐motor impairments. Although the causes of the disease remain unclear, it is well accepted among the scientific community that the disorder may also have a genetic component. For that reason, the number of genetically engineered animal models has greatly increased over the past two decades, ranging from invertebrates to more complex organisms such as mice and rats. This trend is growing as new genetic variants associated with the disease are discovered. The EU Joint Programme – Neurodegenerative Disease Research (JPND) has promoted the creation of an online database aiming at summarising the different features of experimental models of Parkinson's disease. This review discusses available genetic models of PD and the extent to which they adequately mirror the human pathology and reflects on future development and uses of genetically engineered experimental models for the study of PD.

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Section: Discussionmentioning

confidence: 99%

Genetically engineered animal models of Parkinson's disease: From worm to rodent

Breger

Fuzzati-Armentero²

2018

Eur J of Neuroscience

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“…First, we assessed the possible linear association between residential air pollution and PD by using the exposure as a continuous variable. Second, as pesticide exposure has previously been found to be relevant to PD risk, we evaluated the impact of residential exposure to specific pesticides -selected on the basis of prior relevance to PD risk (Benomyl, Lindane, Paraquat, and Maneb) -used on commercial crops within 100 m of a participant's residence on any relationship between air pollution and PD risk (Brouwer et al, 2017). Third, we explored the possible selection bias among the controls and their diseases by excluding each control disease one at a time.…”

Section: Discussionmentioning

confidence: 99%

“…The residential history listed all addresses the participant lived at for at least one year, and the first and last year the participant inhabited each address. The addresses were subsequently geocoded to assess residency-based environmental exposures (Brouwer et al, 2017).…”

Section: Data Collectionmentioning

confidence: 99%

Parkinson'S Disease And Long-Term Exposure To Outdoor Air Pollution: A Matched Case-Control Study In The Netherlands.

Campos¹,

Seelen²,

Hoek³

et al. 2015

ISEE Conference Abstracts

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Background: There is some evidence to suggest an association between ambient air pollution and development of Parkinson's disease (PD). However, the small number of studies published to date has reported inconsistent findings. Objectives: To assess the association between long-term exposure to ambient air pollution constituents and the development of PD. Methods: Air pollution exposures (particulate matter with aerodynamic diameter < 10 μm [PM 10 ], < 2.5 μm [PM 2.5 ], between 2.5 μm and 10 μm [PM coarse ], black carbon, and nitrogen oxides [NO 2 and NO x ]) were predicted based on land-use regression models developed within the "European Study for Air Pollution Effects" (ESCAPE) study, for a Dutch PD case-control study. A total of 1290 subjects (436 cases and 854 controls). were included and 16 years of exposure were estimated (average participant starting age: 53). Exposures were categorized and conditional logistic regression models were applied to evaluate the association between ambient air pollution and PD. Results: Overall, no significant, positive relationship between ambient air pollutants and PD was observed. The odds ratio (OR) for PD associated with an increase from the first quartile of NO 2 (< 22.8 μg/m 3 ) and the fourth (> 30.4 μg/m 3 ) was 0.87 (95% CI: 0.54, 1.41). For PM 2.5 where the contrast in exposure was more limited, the OR associated with an increase from the first quartile PM 2.5 (< 21.2 μg/m3) to the fourth (> 22.3 μg/m3) was 0.50 (95% CI: 0.24, 1.01). In a subset of the population with long-term residential stability (n = 632), an increased risk of PD was observed (e.g. OR for Q4 vs Q1 NO 2 :1.37, 95% CI: 0.71, 2.67). Conclusions:We found no clear association between 16 years of residential exposure to ambient air pollution and the development of PD in The Netherlands.

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“…76 Paraquat, besides being the second most widely used herbicide, 77 also has been associated with an increased risk of Parkinson's disease. 78 Another of the pesticides used by the exposed group is Carbosulfan. This insecticide is a potent genotoxic agent and a potent germ cell mutagen.…”

Section: Cin (%)mentioning

confidence: 99%

“…77 The high frequency of CVs and CAs observed in the exposed group might result from pesticide-induced oxidative stress. Oxidative stress is known to cause DNA damage, which in turn may cause health disorders including Parkinson's disease, 78 endocrine disruption, 80 respiratory and reproductive disorders, 81 Hodgkin's disease, non-Hodgkin lymphoma, 82 leukemia, Burkitt lymphoma, ovarian cancer, neuroblastoma, soft tissue sarcoma, 83 and cancers of the lung, rectum, stomach, bladder, colon and breast. 84,85 Considering that the mutagenic risk of various cigarette components is considered a confounding factor that can influence the frequency of CVs and CAs, we analyze whether smoking and alcohol consumption in both the exposed and unexposed individuals affect the frequency of chromosomal damage.…”

Section: Cin (%)mentioning

confidence: 99%

<p>Chromosomal Instability in Farmers Exposed to Pesticides: High Prevalence of Clonal and Non-Clonal Chromosomal Alterations</p>

Cepeda

Forero-Castro

Cárdenas-Nieto

et al. 2020

RMHP

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Environmental exposure to pesticides and the risk of Parkinson's disease in the Netherlands

Cited by 136 publications

References 27 publications

Genetically engineered animal models of Parkinson's disease: From worm to rodent

Genetically engineered animal models of Parkinson's disease: From worm to rodent

Parkinson'S Disease And Long-Term Exposure To Outdoor Air Pollution: A Matched Case-Control Study In The Netherlands.

<p>Chromosomal Instability in Farmers Exposed to Pesticides: High Prevalence of Clonal and Non-Clonal Chromosomal Alterations</p>

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