General Toxic Mechanisms

Many oil components require phase I metabolism (via oxidation) to generate reactive metabolites; for instance, PAHs are metabolized by cytochrome P450 isozymes to form reactive epoxides which target important macromo-lecules such as nucleic acids (i.e., DNA, RNA) and proteins (Figure 3). While phase II conjugative enzymes can further metabolize reactive metabolites to more water-soluble forms that can be excreted, some conjugates can also react with macromolecules and lead to cellular damage. In general, invertebrates lower on the food web (such as mollusks) have lower metabolic activity when compared with vertebrates such as fishes.

P450

Glutathione S-transferase

1,2-Oxide

Covalently bind to macromolecules

1,2-Oxide

1,2-Quinone OH OH

Covalently bind to macromolecules

1,2-Quinone OH OH

1,4-Quinone

Figure 3 Naphthalene metabolism and resultant reactive metabolite generation.

1,4-Quinone

Figure 3 Naphthalene metabolism and resultant reactive metabolite generation.

The most basic form of acute oil toxicity is narcosis (i.e., the general solvent effect). Exposure to a variety of petroleum hydrocarbons, including alkanes, MAHs, and PAHs, can lead to this reversible state of nervous system sedation. Both polar and nonpolar hydrocarbons can lead to narcosis, while polar organics exhibit higher toxicity. In order to predict total oil toxicity via narcosis, some researchers have applied toxic unit models which assume that toxicity is additive (i.e., total oil toxicity can be summed by the toxi-cities of the individual components). Once the sum reaches a threshold concentration which is species specific, mortality occurs. However, the narcosis model likely underestimates chronic oil toxicity, since narcosis is not the primary mode of action. Mortality is the most common way to access the acute impact of an oil spill on a given aquatic population. In laboratory studies, LC50 (the lethal concentration to 50% of a population) is also most commonly used to characterize the acute toxicological impacts on a species.

The long-term genotoxic impacts of oil can be assessed by studying the mortality of embryos from both invertebrates (such as sea urchins and mussels) and vertebrates (such as fish). Embryo mortality is linked to an increase in toxic oil components in a direct dose-dependent manner. In addition, micronucleus frequency, indicators of chromosomal damage, and DNA single-strand breaks are used as biomarkers for assessing genetic impacts. Some studies have reported significant genotoxic damage and impairment of development and/or reproduction in offspring of species living in the originally impacted area years after an oil spill. This demonstrates that residual levels of potentially genotoxic carcinogens from the spill may exist and continue to cause impacts, even though the extent of cytogenetic damage becomes less noticeable as recovery progresses.

Since petroleum and its products are complex mixtures of hydrocarbons, toxicologists have examined model components to try to predict the toxicity of these classes of compounds. Each group, such as the aliphatic hydrocarbons, PAHs, or metals, may potentially cause adverse health effects. Moreover, there are synergistic and antagonistic interactions of the various components. Therefore, it is very difficult to determine the cumulative toxicological effects among variable classes of chemicals. However, PAHs are believed to be the major contributors to oil toxicity.

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