216 SCHULTZ, DUMONT, AND KYTE 



to the cultures probably represents an interaction of the toxicant and 

 the medium rather than a respiratory effect (see Fig. 2). After the 

 sharp initial decline of oxygen saturation, however, the oxygen 

 consumption rate declined again; this indicated a reduction in 

 respiration of the population. 



Population growth rates and final stationary-phase population 

 densities were sensitive to lower concentrations of product water 

 than were either cytological changes or respiration rates. The 

 exponential growth rates (slopes) for cultures exposed to as little as 

 0.2% toxicant were significantly reduced from those of controls. 

 That this was not observed for cells grown in the presence of 5 to 25 

 mg/liter of pure phenol (Schultz and Dumont, 1977) suggests that 

 some component of the gasifier condensate other than phenol 

 affected the rate of population growth (cell division). On the other 

 hand, the lengthened lag phase and the premature onset of stationary 

 growth at higher concentrations is consistent with data obtained 

 from the growth rates of phenol- treated cells (Schultz and Dumont, 

 1977). Since the cessation of population growth atsuboptimum levels 

 is characteristic of Tetrahymena cultures exposed to a variety of 

 compounds (Blum, Kirshner, and Utley, 1966; Satir, 1967; Meyer 

 et al., 1972; Schultz and Dumont, 1977), it is difficult to determine 

 precise modes of action that bring about this effect. 



Finally, attempts to relate the observed effects of gasifier 

 condensate to one or a group of its specific identified components 

 focus attention immediately on the fact that very high concentra- 

 tions of phenol (2100 mg/hter) and methylated phenols (3120 

 mg/liter) were present in the sample (Ho, Clark, and Guerin, 1976). 

 Although effects were almost certainly elicited by many of the other 

 components present, it is interesting to compare the data presented 

 here with data previously obtained for pure phenol or some methyl 

 phenols. For example, the point at which respiration plateaued in 

 populations exposed to 5% condensate (263 mg/Uter total phenols) 

 was comparable to that in populations exposed to 100 mg/liter 

 phenol (Schultz and Dumont, 1977), 400 mg/liter 3-methyl phenol, 

 300 mg/liter 2,6- and 3,5-dimethyl phenol, and 200 mg/liter 4-ethyl 

 phenol. There is no assurance that phenol per se and/or the other 

 phenolic compounds present were primarily responsible for this 

 effect. Nonetheless, they were the major organic components, and 

 we can be reasonably confident that they had the greatest influence 

 on the parameters measured. Although correlation of toxicity with n 

 and o of selected phenolic compounds has been successful (Kopper- 

 man, Carlson, and Caple, 1974), the compounds that the investi- 

 gators chose for testing had no ortho substitution; the Hammett 



