Effect of Pt nanoparticle size on resistance to chloride-induced inhibition for hydrodechlorination of trichloroethylene in water


KARAHAN S., ÇELİK G.

Journal of Environmental Chemical Engineering, cilt.12, sa.2, 2024 (SCI-Expanded) identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 12 Sayı: 2
  • Basım Tarihi: 2024
  • Doi Numarası: 10.1016/j.jece.2024.112467
  • Dergi Adı: Journal of Environmental Chemical Engineering
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, CAB Abstracts, Chemical Abstracts Core, Compendex, INSPEC, Veterinary Science Database
  • Anahtar Kelimeler: Deactivation, Hydrodechlorination, Inhibition, Structure sensitivity, Trichloroethylene
  • Orta Doğu Teknik Üniversitesi Adresli: Evet

Özet

Catalysts used for hydrodechlorination (HDC) of trichloroethylene (TCE) undergo partial or complete loss of catalytic activity due to inhibition by inevitable reaction product HCl. Changing the size of Pt NPs could be used as a strategy to prevent inhibition of HDC catalysts if the structure sensitivity of the reaction was known. This study aims to obtain structure-sensitivity of aqueous-phase HDC of TCE and investigate the effect of Pt NPs’ size on resistance to chloride inhibition. The research encompassed the synthesis of Pt NPs, characterization studies, and catalytic activity measurements at 30 °C & 1 atm H2 in batch or discontinuous pulse mode. Characterization results showed that targeted Pt NPs were successfully synthesized with average particle sizes of 3.0 nm, 5.8 nm, 8.9 nm, and 60.9 nm. Catalytic activity experiments revealed that initial turnover frequency values exhibited a decrease with increasing particle size of Pt NPs, indicating that aqueous-phase HDC of TCE is a structure sensitive reaction. The fastest kinetics and the highest resistance to HCl inhibition were observed over the smallest Pt NPs employed in this study. This information can serve as a rational synthesis parameter for designing catalysts that could mitigate chloride inhibition caused by the reaction product HCl.