Parkinson's disease in diphenyl-exposed workers—A causal association?

Wastensson, Gunilla; Hagberg, S; Andersson, Eva; Johnels, Bo; Barregård, Lars

doi:10.1016/j.parkreldis.2005.06.010

Cited by 10 publications

(6 citation statements)

References 25 publications

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“…Thirty-one studies fulfilling good scientific standards (Armon class II–III) contributed data to meta-analyses of risk rates for pesticide exposure: five studies on ALS [33,44,45,46,47], four on Alzheimer’s disease [33,48,49,50] and 24 on Parkinson’s disease [23,33,51,52,53,54,55,56,57,58,59,60,61,62,63,64,65,66,67,68,69,70,71,72]. Figure 5 shows an increased overall risk of 50% for contracting these neurodegenerative diseases following exposure to pesticides.…”

Section: Resultsmentioning

confidence: 99%

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Occupational Exposures and Neurodegenerative Diseases—A Systematic Literature Review and Meta-Analyses

Gunnarsson

Bodin

2019

IJERPH

117

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Objectives: To carry out an integrated and stratified meta-analysis on occupational exposure to electromagnetic fields (EMFs), metals and pesticides and its effects on amyotrophic lateral sclerosis (ALS) and Parkinson’s and Alzheimer’s disease, and investigate the possibility of publication bias. Methods: In the current study, we updated our recently published meta-analyses on occupational exposures in relation to ALS, Alzheimer’s and Parkinson’s disease. Based on 66 original publications of good scientific epidemiological standard, according to the Meta-analysis of Observational Studies in Epidemiology (MOOSE) and the Grading of Recommendations, Assessment, Development and Evaluations (GRADE) guidelines, we analysed subgroups by carrying out stratified meta-analyses on publication year, statistical precision of the relative risk (RR) estimates, inspection of the funnel plots and test of bias. Results: Based on 19 studies the weighted RR for occupational exposure to EMFs was 1.26 (95% confidence interval (CI) 1.07–1.50) for ALS, 1.33 (95% CI 1.07–1.64) for Alzheimer’s disease and 1.02 (95% CI 0.83–1.26) for Parkinson’s disease. Thirty-one studies concerned occupational exposure to pesticides and the weighted RR was 1.35 (95% CI 1.02–1.79) for ALS, 1.50 (95% CI 0.98–2.29) for Alzheimer’s disease and 1.66 (95% CI 1.42–1.94) for Parkinson’s disease. Finally, 14 studies concerned occupational exposure to metals and only exposure to lead (five studies) involved an elevated risk for ALS or Parkinson’s disease and the weighted RR was 1.57 (95% CI 1.11–2.20). The weighted RR for all the non-lead exposures was 0.97 (95% CI 0.88–1.06). Conclusions: Exposure to pesticides increased the risk of getting the mentioned neurodegenerative diseases by at least 50%. Exposure to lead was only studied for ALS and Parkinson’s disease and involved 50% increased risk. Occupational exposure to EMFs seemed to involve some 10% increase in risk for ALS and Alzheimer’s disease only.

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Section: Resultsmentioning

confidence: 99%

“…The twelve estimates with the highest precision, in studies [23,33,53,55,57,58,61,62,63,68,71,72], had a weighted RR of 1.39 (95% CI 1.20–1.62). For the low precision estimates, in studies [51,52,54,56,59,60,64,65,66,67,69,70], the corresponding RR was 2.14 (95% CI 1.66–2.74).…”

Section: Resultsmentioning

confidence: 99%

Occupational Exposures and Neurodegenerative Diseases—A Systematic Literature Review and Meta-Analyses

Gunnarsson

Bodin

2019

IJERPH

117

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“…Previously, ten cohort studies – six occupational - examined associations between PD and occupational pesticide exposures or work in occupations involving pesticide exposures,[3, 6, 8, 21-27] and reported relative risk estimates ranging from 0.66 to 5.6. However, since PD is a rare event in all but very large cohorts, these studies relied on as few as 1 and a maximum of 134 exposed incident PD cases.…”

Section: Discussionmentioning

confidence: 99%

“…However, since PD is a rare event in all but very large cohorts, these studies relied on as few as 1 and a maximum of 134 exposed incident PD cases. Exposure assessment in these studies was based on self-report, broad occupational categories listed in national databases, and few used employee records[21, 26] or job-exposure matrices. [3, 6] The Agricultural Health Study[8] and a French (PAQUID) study[3] performed the most detailed exposure assessments, but still only had 68 and 8 exposed PD cases available for analysis, respectively.…”

Section: Discussionmentioning

confidence: 99%

Occupational pesticide use and Parkinson's disease in the Parkinson Environment Gene (PEG) study

Narayan

Liew

Bronstein³

et al. 2017

Environment International

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Objective To study the influence of occupational pesticide use on Parkinson's disease (PD) in a population with information on various occupational, residential, and household sources of pesticide exposure. Methods In a population-based case control study in Central California, we used structured interviews to collect occupational history details including pesticide use in jobs, duration of use, product names, and personal protective equipment use from 360 PD cases and 827 controls. We linked reported products to California's pesticide product label database and identified pesticide active ingredients and occupational use by chemical class including fungicides, insecticides, and herbicides. Employing unconditional logistic regression, we estimated odds ratios and 95% confidence intervals for PD and occupational pesticide use. Results Ever occupational use of carbamates increased risk of PD by 455%, while organophosphorus (OP) and organochlorine (OC) pesticide use doubled risk. PD risk increased 110-211% with ever occupational use of fungicides, herbicides, and insecticides. Using any pesticide occupationally for >10 years doubled the risk of PD compared with no occupational pesticide use. Surprisingly, we estimated higher risks among those reporting use of personal protective equipment (PPE). Conclusions Our findings not only provide additional evidence that occupational pesticide exposures increase PD risk, but do so even after controlling for other sources of pesticide exposure; specifically, occupational use of carbamates, OPs, and OCs, as well as of fungicides, herbicides, or insecticides as a group increased risk. Interestingly, PPE use, particularly use of gloves, did not provide protection in this population.

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“…Epidemiological investigations of possible associations between exposure to biphenyl and health outcomes in humans are limited to two studies of workers exposed to biphenyl during production of biphenyl-impregnated fruit wrapping paper at mills in Finland and Sweden at concentrations above the occupational threshold limit value (1.3 mg/m 3 ; ACGIH 2001 ) ( Seppäläinen and Häkkinen 1975 ; Wastensson et al 2006 ). These studies provide limited evidence of nervous system effects (i.e., abnormal electroencephalography and electroneuromyography; increased prevalence of Parkinson’s disease) associated with occupational biphenyl exposure.…”

Section: Effects Other Than Cancermentioning

confidence: 99%

Human Health Effects of Biphenyl: Key Findings and Scientific Issues

Hogan

Cai

et al. 2016

Environ Health Perspect

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Background:In support of the Integrated Risk Information System (IRIS), the U.S. Environmental Protection Agency (EPA) has evaluated the human health hazards of biphenyl exposure.Objectives:We review key findings and scientific issues regarding expected human health effects of biphenyl.Methods:Scientific literature from 1926 through September 2012 was critically evaluated to identify potential human health hazards associated with biphenyl exposure. Key issues related to the carcinogenicity and noncancer health hazards of biphenyl were examined based on evidence from experimental animal bioassays and mechanistic studies.Discussion:Systematic consideration of experimental animal studies of oral biphenyl exposure took into account the variety of study designs (e.g., study sizes, exposure levels, and exposure durations) to reconcile differing reported results. The available mechanistic and toxicokinetic evidence supports the hypothesis that male rat urinary bladder tumors arise through urinary bladder calculi formation but is insufficient to hypothesize a mode of action for liver tumors in female mice. Biphenyl and its metabolites may induce genetic damage, but a role for genotoxicity in biphenyl-induced carcinogenicity has not been established.Conclusions:The available health effects data for biphenyl provides suggestive evidence for carcinogenicity in humans, based on increased incidences of male rat urinary bladder tumors at high exposure levels and on female mouse liver tumors. Kidney toxicity is also a potential human health hazard of biphenyl exposure.Citation:Li Z, Hogan KA, Cai C, Rieth S. 2016. Human health effects of biphenyl: key findings and scientific issues. Environ Health Perspect 124:703–712; http://dx.doi.org/10.1289/ehp.1509730

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Parkinson's disease in diphenyl-exposed workers—A causal association?

Cited by 10 publications

References 25 publications

Occupational Exposures and Neurodegenerative Diseases—A Systematic Literature Review and Meta-Analyses

Occupational Exposures and Neurodegenerative Diseases—A Systematic Literature Review and Meta-Analyses

Occupational pesticide use and Parkinson's disease in the Parkinson Environment Gene (PEG) study

Human Health Effects of Biphenyl: Key Findings and Scientific Issues

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