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Inhibition of methanogenesis by C1- and C2-polychlorinated aliphatic hydrocarbons

✍ Scribed by Zhongtang Yu; Geoffrey B. Smith

Publisher
John Wiley and Sons
Year
2000
Tongue
English
Weight
102 KB
Volume
19
Category
Article
ISSN
0730-7268

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✦ Synopsis

Abstract

Inhibition of methanogenesis in ananaerobic wastewater digester sample by four common polychlorinated aliphatic hydrocarbons (dichloromethane, chloroform, trichloroethylene, and perchloroethylene) was investigated. Chloroform was shown to be the most inhibitory, and an aqueous concentration of chloroform as low as 0.09 mg/L completely inhibited methanogenesis. Dichloromethane inhibited methanogenesis at 3.9 mg/L, trichloroethylene at 18 mg/L, but 14.5 mg/L of perchloroethylene did not inhibit methanogenesis. The following order of inhibition was determined (in descending potencies): chloroform ≫ dichloromethane > trichloroethylene > perchloroethylene. The wastewater consortium dechlorinated chloroform, trichloroethylene, and perchloroethylene but not dichloromethane. Our results suggest that inhibition of methanogenesis and dechlorination is determined by both the extent of chlorination and the molecular structure of polychlorinated hydrocarbons. A model is presented, proposing that polychlorinated hydrocarbons inhibit methanogenesis directly and/or indirectly by binding to corrinoid/porphinoid enzymes and free corrinoids/porphinoids in the cell, respectively. Polychlorinated methanes would lead to both direct and indirect inhibition, whereas polychlorinated ethylenes would only inhibit methanogenesis indirectly. The model predicts that direct inhibition of methanogenesis is more potent than indirect inhibition.

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