The differences in Enterococcus species composition across shore are consistent with the results of the hindcast model ( Rippy et al., in press, their Fig. 3), which identified two sources of Enterococcus (a northern onshore source and a southern offshore source) at Huntington Beach. These results also lend credence to the source-specific mortality formulations in the ADS and ADSI models, which parameterize the mortality of onshore and offshore FIB differently based on the

assumption that FIB from different sources can have different exposure histories or species compositions, and thus different mortality rates ( Sinton et al., 2002). October 16th, 2006, was partially cloudy with JQ1 maximum solar insolation levels of 445 J m−2 s−1 measured at 13:00. No significant relationship was detected between solar insolation dose (J m−2, integrated over the 20 min sampling interval) and E. coli decay rate at any station over the study period. Measured Enterococcus decay rates, however, increased significantly with solar insolation dose, but only at offshore

stations (50–150 m offshore) ( Fig. 2). The general lack of correlation ALK inhibitor between solar insolation dose and FIB decay (especially for E. coli) was unexpected, as prior research has indicated a clear relationship between sunlight and FIB mortality in seawater ( Boehm et al., 2005, Sinton et al., 2002 and Troussellier et al., 1998). It is possible, however, that solar insolation

did contribute to FIB decay at Huntington Beach, and that detection of this effect was obscured by the contribution of physical dilution (via advection and diffusion) to decay ( Rippy et al., in press). The significant correlation found between solar insolation dose and FIB decay for offshore Enterococcus ( Fig. 2) supports the role of solar insolation in regulating Enterococcus mortality seaward of the surfzone. This finding motivates testing insolation-dependent mortality models for this FIB group, particularly those that allow the relationship between solar insolation dose and FIB decay to vary across shore (ADSI and ADGI models). All mortality models were sensitive to the selection of mortality parameters: m for the one-parameter models (ADC and ADI) and m0 and m1 (surfzone and offshore mortality) for the two-parameter models (ADS, ADSI, ADG and ADGI) ( SI Figs. 3–6). For all two-parameter Forskolin mouse mortality models, skill was more sensitive to changes in the offshore mortality parameter than the surfzone mortality parameter ( SI Figs. 5 and 6). This indicates that mortality may be a dominant processes contributing to FIB decay offshore, where the influences of advection and diffusion are weaker ( Rippy et al., in press). Mortality parameters for Enterococcus were larger overall than those for E. coli for every model ( Table 1). This is consistent with the slower overall decay observed for E. coli during the HB06 study ( Rippy et al., in press).