The　emerging　toxicant　N-(1,3-dimethylbutyl)-N＇-phenyl-p-phenylenediamine　quinone　(6PPD-Q)　is　of　wide　concern　due　to　its　ubiquitous　occurrence　and　high　toxicity.　Despite　regular　human　exposure,　limited　evidence　exists　about　its　presence　in　the　body　and　potential　health　risks.　Herein,　we　analyzed　cerebrospinal　fluid　(CSF)　samples　from　Parkinson＇s　disease　(PD)　patients　and　controls.　The　CSF　levels　of　6PPD-Q　were　twice　as　high　in　PD　patients　compared　to　controls.　Immunostaining　assays　performed　with　primary　dopaminergic　neurons　confirm　that　6PPD-Q　at　environmentally　relevant　concentrations　can　exacerbate　the　formation　of　Lewy　neurites　induced　by　alpha-synuclein　preformed　fibrils　(alpha-syn　PFF).　Assessment　of　cellular　respiration　reveals　a　considerable　decrease　in　neuronal　spare　respiratory　and　ATP-linked　respiration,　potentially　due　to　changes　in　mitochondrial　membrane　potential.　Moreover,　6PPD-Q-induced　mitochondrial　impairment　correlates　with　an　upsurge　in　mitochondrial　reactive　oxygen　species　(mROS),　and　Mito-TEMPO-driven　scavenging　of　mROS　can　lessen　the　amount　of　pathologic　phospho-serine　129　alpha-synuclein.　Untargeted　metabolomics　provides　supporting　evidence　for　the　connection　between　6PPD-Q　exposure　and　changes　in　neuronal　metabolite　profiles.　In-depth　targeted　metabolomics　further　unveils　an　overall　reduction　in　glycolysis　metabolite　pool　and　fluctuations　in　the　quantity　of　TCA　cycle　intermediates.　Given　its　potentially　harmful　attributes,　the　presence　of　6PPD-Q　in　human　brain　could　potentially　be　a　risk　factor　for　PD.