A kinetic model for surfactant inhibition of pentachlorophenol biodegradation.

A kinetic model is used to describe the effect of the nonionic surfactant Tergitol NP-10 (TNP10) on pentachlorophenol (PCP) biodegradation by Sphingomonas chlorophenolica sp. strain RA2. Different initial biomass to initial substrate ratios ranging from 13 to 418 were tested with 23 TNP10 concentrations ranging from 0 to 1500 mg/L. Tests were also conducted at 10 degrees C and 20 degrees C. No PCP biodegradation inhibition was observed at concentrations below the critical micelle concentration (CMC) of 50 mg/L. TNP10 concentrations above 100 to 200 mg/L were increasingly inhibitory to PCP biodegradation rates. This inhibition was best described by the Monod kinetic equation wherein the effect of TNP10 inhibition is reflected in the half-saturation constant (Ks). The value of the Ks increased from between 1.5 and 13.5 mg/L with no surfactant present to 44 to 131 mg/L at 1000 mg/L TNP10. Using a standard competitive inhibition approach, the inhibition constant for TNP10 was approximately 100 mg/L at both 10 degrees C and 20 degrees C.

Nonionic surfactant effects on pentachlorophenol biodegradation.

Several potential mechanisms of surfactant-induced inhibition of pentachlorophenol (PCP) biodegradation were tested using a pure bacterial culture of Sphingomonas chlorophenolicum sp. Strain RA2. PCP degradation, glucose degradation, and oxygen uptake during endogenous conditions and during glucose degradation were measured for batch systems in the presence of the nonionic surfactant Tergitol NP-10 (TNP10). TNP10 did not exert toxicity on RA2 as measured by dissolved oxygen uptake rates under endogenous conditions and glucose biodegradation rates. TNPIO reduced the substrate inhibition effect of PCP at high PCP concentrations, resulting in faster PCP degradation rates at higher concentrations of TNP10. Calculations of a micelle partition coefficient (Kmic) show that PCP degradation rates in the presence of surfactant can be explained by accounting for the amount of PCP available to the cell in the aqueous solution. A model is discussed based on these results where PCP is sequestered into micelles at high TNP10 concentrations to become less available to the bacterial cell and resulting in observed inhibition. Under substrate toxicity conditions, the same mechanism serves to increase the rate of PCP biodegradation by reducing aqueous PCP concentrations to less toxic levels.