Date of this Version
Page et al. appear to have missed our point that the teratogenic effects of oil on fish derive from embryonic exposure to environmentally persistent 3- and 4-ring polycyclic aromatic hydrocarbons (PAHs). They regard our conclusions as incorrect because we failed to demonstrate causality or a clear dose-response relationship. As evidence for lack of causality, they indicate that our data were not replicated. However, our report was a companion paper to a similar one demonstrating PAH-induced teratogenesis in herring embryos, also in the low ppb. Current literature corroborates our data and careful consideration of our conclusion demonstrates that their inclusion of low molecular weight PAHs in their dose-response relationship is counter to their thesis that dose measures should only include toxic compounds.
When we published this work 12 years ago, the concept that PAHs with high octanol-partition coefficient (KOW) were teratogenic at concentrations below their solubility was considered novel. Since then, the sensitivity of developing fish embryos to ppb concentrations of PAHs dissolved in water has been confirmed for fish embryos exposed to oiled sediments, dissolved mixtures of PAHs derived from oiled sediments, and specific high molecular weight PAHs dissolved in water; additional references will be found in the Supplemental Data. More recently, experiments involving specific PAHs with partition-controlled delivery systems also have demonstrated toxic effects at levels below aqueous solubility limits. At least eleven reports replicate our findings in seven different fish species and support our conclusion that accumulation of PAHs by embryos depends on the kinetics of the transfer of PAHs from oil to egg rather than PAH solubility.