Limnol. Oceanogr., 44(3, part 2), 1999, 878–888

The influence of a commercial humic acid (Aldrich; AHA) on the development of anthracene photoinduced toxicity to the duckweed Lemna gibba was examined using both roomand low-temperature (778K) chlorophyll fluorescence assays. Plants were exposed to 2 mg liter21 anthracene both with and without 6.2 mg liter21 of AHA and grown under either visible light or simulated solar radiation that mimics the natural abundance of UV radiation. Exposure periods ranged from 1 to 48 h to examine temporal changes in chlorophyll degradation and chlorophyll a fluorescence induction in response to these light and HA treatments. The onset of anthracene photoinduced toxicity followed a definite sequence; chlorophyll a fluorescence induction parameters (Fv/Fm, and t1⁄2) responded earliest to anthracene exposure, with observable chlorophyll degradation requiring up to 24 to 48 h. Of these, t1⁄2 was the most sensitive, with significant inhibition apparent within 1 h of exposure. Throughout the entire 48-h exposure, 6.2 mg liter21 AHA ameliorated the photoinduced toxicity of anthracene, in terms of both chlorophyll degradation and Fv/ Fm inhibition. In contrast, AHA delayed the complete inhibition of t1⁄2 by only 1 to 24 h rather than permanently protecting the plants from anthracene damage to PS2. This suggests that AHA may slow, but not prevent, the entrance of either intact anthracene or its photooxidized byproducts under these exposure conditions. Predicting the negative impacts of anthropogenic contaminants is often complicated by various chemical and ecological factors that can modify the fate and effects of xenobiotics. For example, the toxicity of both inorganic and organic contaminants to freshwater organisms often is ameliorated in the presence of either natural or commercial forms of dissolved organic carbon (DOC) (Day 1991; Goodrich et al. 1991; Oikari et al. 1992; Steinberg et al. 1992; Hodge et al. 1993; Williamson et al. 1999). The mechanism likely involves chemical partitioning of the contaminant to DOC which diminishes its bioavailability and, hence, biological efficacy (Jaffé 1991; Knulst 1992; Lores et al. 1993; Kukkonen and Pellinen 1994; Kopinke et al. 1995). Polycyclic aromatic hydrocarbons (PAHs), for example, bind to natural forms of DOC (Johnsen and Gribbestad 1991; Schlautman and Morgan 1993; Kopinke et al. 1995), hence diminishing the toxicity and(or) bioavailability of the unmodified parent compounds (Landrum et al. 1985; Kukkonen and Oikari 1991; Kukkonen and Pellinen 1994). Further complicating this scenario, natural levels of ultraviolet radiation (UVR) in sunlight enhance the toxicity of PAHs to aquatic animals (Bowling et al. 1983; Oris and Giesy 1985; Holst and Giesy 1989; Monson et al. 1995) and plants (Greenberg et al. 1993; Huang et al. 1993; Gala and Giesy 1994; Gensemer et al. 1996). However, little work specifically has addressed the extent to which DOC controls PAH bioavailability or toxicity in the presence of natural 1 Corresponding author and current address: ENSR Consulting, 4303 W. LaPorte Ave., Fort Collins, Colorado 80521.