Waste crankcase oil (WCO) is a major source of oil pollution in both the aquatic and terrestrial environment and has been implicated in the poisoning of mammals and fish. It is also mutagenic. Since birds' eggs are highly sensitive to external microliter applications of environmentally polluting oils, we examined the developmental effects of external applications of WCO on eggs of the mallard duck (Anas platyrhynchos) and the bobwhite quail (Colinus virginianus). At 48 hr of development, mallard eggs were exposed externally to 2, 5, or 15 :l of WCO or 15 :l of clean crankcase oil (CCO) while bobwhite eggs received proportional doses of 0.5, 1, or 3 :l of WCO and 3 :l of CCO in a similar manner. WCO was highly embryotoxic to both species compared to CCO and resulted in dose-dependent mortality, reduced growth, and abnormal survivors. Application of 15 :l WCO resulted in 84% mortality in mallards and 3 :l WCO resulted in 88% mortality in bobwhites. Abnormal survivors included embryos with subcutaneous edema, incomplete ossification, and eye and brain defects. Red blood cell *-aminolevulinic acid dehydratase (ALAD) activity, liver ALAD activity, and hemoglobin concentration were significantly lower after treatment with WCO in embryos and hatchlings of both species. Plasma uric acid, plasma alanine aminotransferase (ALT), and plasma aspartate aminotransferese (AST) were significantly elevated in WCO-treated mallards after hatching. Biochemical effects, growth retardation, and mortality at proportionally lower dose levels were more pronounced in mallards than in bobwhites. Chemical analysis of the WCO and CCO revealed a considerably higher content of aromatic hydrocarbons in WCO than in CCO. Lead levels were highly elevated in WCO (4600 ppm) compared to CCO (2 ppm).
