Estimating pesticide exposure in tidal streams of Leadenwah Creek, South Carolina.

This article estimates the potential exposure of estuarine organisms to two pesticides (azinphosmethyl and fenvalerate) in a tidal stream of Leadenwah Creek near the Edisto River, South Carolina, during four runoff episodes. Exposure is calculated from simulation runs of the one-dimensional transport equation solved by an implicit finite difference method. Calibration was done for each episode by adjusting three conditions (runoff starting time, duration, and flow) and a correction to the dispersion coefficient in order to match the continuously measured salinity transients. First-order rate constants used by the fate component were calculated from half-life values reported in the literature. Baseline scenarios for each episode and each pesticide were derived by using the same conditions obtained in the salinity runs and adjusting the pesticide loading in order to mimic the few data points of measured pesticide concentrations. In all baseline scenarios, pesticide concentration rises following the initial burst of runoff (also noticeable as an abrupt drop in salinity) and then oscillates, forced by the tidal cycle. These oscillations are dominated by transport, while fate imposes a secular decaying trend. Ten additional scenarios for each episode were obtained from the baseline scenario by randomly varying three pesticide load parameters (starting time and duration of runoff, and pesticide discharge) using a Latin hypercubes design. Two exposure metrics were calculated from the simulated and the measured pesticide concentration: maximum and time average, which was obtained by integrating the curve and dividing by the time period. The metrics calculated from the baseline runs are relatively close to the data-derived metrics, because the baseline runs attempted to mimic the data. For each one of the two metrics and all pesticide-episode combinations, several statistics of the set of 11 scenarios were also calculated: minimum and maximum, mid-range, mean, standard deviation, and median. The mean +/- standard deviation interval of the simulation-derived value consistently brackets the data-derived value for the maximum metric, but not for the time-average metric. This may indicate that even if the maximum value is correctly captured in the field sample, the time-average exposure could be in error when calculated directly from the field data due to undersampling of the pesticide time series. The methodology developed here attempts to reconstruct the possible exposure from the sparse sampling of the pesticide concentration during the runoff episodes; only when the number of field samples is high and regularly spaced is it possible to have confidence in the reconstruction of the curve. The shape of the curve cannot be inferred from the field measurements alone; as expected, tidal movement makes the pesticide concentration swing up and down. This result has important implications because the biological community would be subject to repetitive pulses of exposure to the chemicals. The baseline simulations can be used to derive a pulse-exposure metric by calculating the sum of ratios of the time average of the threshold-exceeding concentrations to the time average of the toxic threshold during intervals of above-threshold concentration. This metric is species specific and extrapolates laboratory toxicity data in order to compare pulse exposure to mortality rates measured in the field.

Evidence against transmission of human T-lymphotropic virus/lymphadenopathy-associated virus (HTLV-III/LAV) in families of children with the acquired immunodeficiency syndrome.

Six children with the acquired immunodeficiency syndrome (AIDS) and 12 of their household contacts were investigated serologically for evidence of infection with human T-lymphotropic virus/lymphadenopathy-associated virus (HTLV-III/LAV), the presumed etiologic agent of AIDS. All six children had antibody against HTLV-III/LAV, as measured by enzyme-linked immunosorbent assay, in each specimen tested. Of the two mothers studied both were seropositive; one was diagnosed with and died from AIDS. Four of the remaining 10 household members were seropositive, including three adults in groups at high risk for the development of AIDS and one sibling who was younger than the child with AIDS. Among the seronegative household contacts were four foster mothers or grandmothers of the children with AIDS, three of whom had cared for the children since infancy. Household contact with children with AIDS may include persons in groups at high risk for AIDS who have been infected with HTLV-III/LAV. However, the negative findings in household contacts without risk factors for AIDS suggest that horizontal transmission of the virus within households by means other than sexual contact must be infrequent.