Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by dopaminergic neuron loss in the substantia nigra and the presence of intraneuronal inclusions of α-synuclein (αSyn) aggregates known as Lewy bodies. Epidemiological evidence has linked environmental toxicant exposures to elevated PD risk, but their mechanistic effects on αSyn pathology remain largely unknown. This study examined the influence of industrial solvents trichloroethylene (TCE) and perchloroethylene (PCE), as well as pesticides permethrin, simazine, atrazine, lindane, and trifluralin on αSyn aggregation in vitro and in SK-MEL-28 human melanoma cells. Cytotoxicity was assessed using the MTT assay, which revealed dose-dependent toxicity of all toxicants and identified subtoxic concentrations. The seed amplification assay (SAA) was then used to evaluate direct effects of toxicants on αSyn fibrillization. While TCE, PCE, permethrin, and atrazine did not alter seeding activity, lindane, simazine, and trifluralin were found to inhibit fibril formation at 1 µM. Immunofluorescence was used to analyze toxicant effects on preformed fibril (PFF)-induced inclusion formation in SK-MEL-28 cells. Notably, PCE (1 and 10 µM) and atrazine (0.25 and 1 µM) increased the number of αSyn inclusions per cell and TCE (0.1, 1, and 10 µM) increased average αSyn inclusion size despite having no observable effects in the SAA, suggesting indirect promotion of αSyn pathology via disrupted proteostasis or clearance mechanisms that can be further explored.