ENVIRONMENTAL FACTORS AFFECTING THE PERSISTENCE OF WASTE-WATER INDICATOR COMPOUNDS IN STREAMS

Suitable tracers for the biological and chemical components of waste water effluent are needed to identify the sources and track the fates of waste water compounds in surface water. Effective surrogate compounds reflect the source and magnitude of contamination and are readily detectable under surface water conditions. Caffeine and cotinine are two of the most commonly proposed indicators of human-derived waste in surface- and ground-water systems. Caffeine is arguably the most widely consumed non-prescription, human drug in the world. Cotinine is a by-product of nicotine metabolism in humans and, consequently, detection of cotinine in surface water environments is a common indicator of human waste impacts. Caffeine and cotinine are ubiquitous in WWTP effluent in the United States and are detectable in surface waters at ng/L concentrations using existing analytical methods.

The utilization of caffeine and cotinine as indicators of human waste impacts in surface water systems, however, requires a fundamental understanding of their fates in this environment. Little is known about the potential for biotransformation of caffeine and cotinine in waste-water-impacted streams, but the fact that both chemicals derive from natural flora suggests a potential for biotransformation in the environment. This study assessed the potential impact of in situ biotransformation on the proposed use of caffeine and cotinine as indicators of human waste impacts in streams. A series of microcosm studies were conducted with ¹⁴C-substrates and sediment/water samples from three, effluent-impacted streams in order to assess: 1) the relative efficiency of caffeine biotransformation in sediments under oxic and anoxic conditions, 2) the potential for significant biotransformation of caffeine in the water-column, 3) the impact of sediment location (relative to WWTP outfall) on the efficiency of caffeine biotransformation, and 4) the potential for biotransformation of cotinine and its metabolic precursor, nicotine, in sediment.