, 2011). Thus, it is not surprising that a monotonic dose response was not found, particularly for endpoints related to the development of the embryos. Carls et al. (1999) stated, but did not demonstrate, that all measured aqueous PAH were freely dissolved and none were associated with oil droplets, which leads to the assumption that all the individual PAH in exposure water were bioconcentrated independent

of each other and other chemicals in the effluent. However, the analytical methods used by Carls et al. (1999) and in related studies, did not distinguish between freely dissolved and particulate oil (see Page et al., 2012). These assumptions are critical to the selection of TPAH as a dose metric and render the findings questionable because the effluents from the different oil-on-gravel loadings Volasertib contained different initial concentrations and compositions of the measured Selleckchem PCI 32765 alkanes and PAH that changed during both of the 16-day experiments. The presence of low solubility alkanes and high molecular weight alkyl PAH in the effluents from the oiled gravel column studies

(EVOSTC, 2009, Brannon et al., 2012 and Page et al., 2012; Supplementary data) is indicative of the presence of a non-dissolved or micro droplet oil phase in the column effluents that probably contained all or most of the higher molecular weight PAH (Faksness et al., 2004 and Redman et al., 2012). Therefore, the uptake and toxicity of PAH in the Carls et al. (1999) study likely cannot be attributed solely to a freely dissolved fraction of the oil PAH, and the likely presence of oil droplets represents an additional confounding factor that would affect the accumulated dose and that was not reported or discussed as part of the toxicology evaluation. Thus, total aqueous PAH, as measured, represented both freely dissolved and unknown amounts of PAH associated with oil droplets. TPAH concentrations in exposure water declined rapidly and PAH composition changed continuously over the course of the 16-day exposures in all doses of LWO and MWO (Carls et al., 1997, Carls et al., 1999 and EVOSTC, 2009; Supplementary data). The rapid decline of TPAH concentration in the LWO and MWO effluents during the 16-day

exposures (Fig. 1) was largely the result of losses medroxyprogesterone of lower molecular weight PAH, particularly naphthalene and alkyl-naphthalenes (Table 1). The relative concentrations of different individual PAH and PAH congener groups, as a percentage of TPAH concentration (%TPAH), changed in all effluent doses during the 16-day exposures, with percent alkyl-naphthalenes declining and percent alkyl-phenanthrenes, alkyl-dibenzothiophenes, and alkyl-chrysenes increasing in the low, mid, and high doses during the first 4 days of exposure (Table 1) and during the remainder of the two 16-day experiments. Thus, PAH exposure concentration declined and relative compositions were different for each dose during the course of the LWO and MWO experiments (EVOSTC, 2009).