Abstract

One of the most significant causes of poor water quality is the presence of pathogens. To reduce the cost of human exposure to microbial contamination, monitoring of Fecal Indicator Bacteria (FIB), as a surrogate for the presence of pathogens in natural waters, has become the norm. A total maximum daily load (TMDL) framework is used to establish limits for microbial concentrations in impaired waterbodies. In order to meet microbial loads determined by the TMDLs, reductions in microbial sources varying from 50% to almost complete elimination are required. Such targets are fairly difficult, if not impossible, to achieve. A natural attenuation (NA) framework is proposed that takes into account the connectivity between freshwater streams and their receiving coastal estuaries. The framework accounts for destructive and non-destructive mechanisms and defines three regimes: NA 1 - reaction-dilution mixing at the freshwater-tidal interface, NA 2 - advection-reactions within the tidally influenced coastal stream, and NA 3 - dilution-discharge at the interface with the estuary. The framework was illustrated using the Houston Metropolitan area freshwater streams, their discharge into the Houston Ship Channel (HSC) and into Galveston Bay. FIB concentrations in Galveston Bay were much lower when compared to FIB concentrations in Houston streams. Lower enterococci concentrations in tributary tidal waters were found compared to their counterparts in fresh waters (NA1 regime). Additionally, 70% reduction in FIB loads within the HSC was demonstrated as well as a decreasing trend in enterococci geometric means, from upstream to downstream, on the order of 0.092 day−1 (NA2 regime). Lower enterococci concentrations in Galveston Bay at the confluence with the HSC were also demonstrated (NA3 regime). Statistical testing showed that dilution, tide-associated processes, and salinity are the most important NA mechanisms and indicated the significant effect of ambient temperature and rainfall patterns on FIB concentrations and the NA mechanisms.

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