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Crab zoeae ( Rhithropanopeus harrisii ) were exposed to water-soluble fractions of jet fuel (JP5) for the first 5 days or for the duration of zoeal development (11 to 14 days). Short-term exposure or continuous exposure to low concentrations of petroleum hydrocarbons caused no increase in mortality or changes in development rate, and increased megalopal weight was characteristic of such groups. This phenomenon, termed "hormesis," is probably a generalized aspect of environmental stress etiology but has seldom been reported as such.

Both biologically active and autoclaved sediments convert trimethyltin hydroxide to the volatile tetramethyltin. Larger amounts of tetramethyltin were formed in the bioactive sediments than in the sterile sediments. No volatile tin compounds were detected in the absence of trimethyltin hydroxide or from trimethyltin hydroxide in seawater or in seawater containing bentonite. The formation of tetramethyltin is slow, taking over 80 days at 16 degrees C to reach a maximum. The extent of conversion, although significant, is not extensive. The formation of tetramethyltin occurs in estuarine sediments by both abiotic and biologically enhanced pathways. A redistribution mechanism accounts for at least the abiotic pathway and possibly both formation pathways.

The LC50 concentrations of a series of 15 structurally distinct diorganotins (R2SnX2) and triorganotins (R3SnX) were determined for zoeae of the mud crab Rhithropanopeus harrisii. Zoeae were exposed from hatching until metamorphosis, at ˜14 d. The LC50 values varied by almost 4 orders of magnitude, from the least toxic aquated species, dimethyltin (LC50 = 92,276 nM) to the most toxic, tricyclohexyltin (LC50 = 19.8 nM). Within a homologous series, the diorganotin was less toxic than the corresponding triorganotin, but the toxicity of the two classes overlapped, e.g., dicyclohexyltin was more toxic than trimethyltin and about as toxic as triethyltin. Correlations between the Hansch π parameter and the LC50, and between total surface area and the LC50, suggest that aqueous thermodynamic activity (hydrophobicity), a function of the organic ligand attached to tin, controls bioconcentration and thus the lethal dose. This conclusion is substantiated by the observation of a single linear relationship between a sum of Hansch fragment constants and the LC50 values for both the di‐ and triorganotins. The difference in toxicity between di‐ and trialkyltins results from a decrease in hydrophobic character when a hydroxyl group is substituted for an organic ligand in the former. Any electronic effect of the organic ligand is overwhelmed by the factors that control hydrophobic behavior, as evidenced by the observed poor correlations with χ.