Bioaccumulation and Metabolic Effects of the Endocrine Disruptor Methoprene in the Lobster, Homarus americanus

Methoprene is a pesticide that acts as a juvenile hormone agonist.Although developed initially against insects, it has since beenshown to have toxic effects on larval and adult crustaceans.Methoprene was one of several pesticides applied to the WesternLong Island Sound (WLIS) watershed area during the summer of1999; the other pesticides were malathion, resmethrin, and sumethrin.These pesticides were applied as part of a county-by-countyeffort to control the mosquito vector of West Nile Virus. Subsequently,the seasonal lobster catches from the WLIS have decreased dramatically.The lethality of the pesticides to lobsters had been unknown.We studied the effects of methoprene while other investigatorsstudied effects of the other pesticides. We questioned whethermethoprene, through its effects on larvae, adults or both, couldhave contributed to this decline. We found that low levels ofmethoprene had adverse effects on lobster larvae. It was toxicto stage II larvae at 1 ppb. Stage IV larvae were more resistant,but did exhibit significant increases in molt frequency beginningat exposures of 5 ppb. Juvenile lobsters exhibited variationsin tissue susceptibility to methoprene: hepatopancreas appearedto be the most vulnerable, reflected by environmental concentrationsof methoprene inhibiting almost all protein synthesis in thisorgan. Our results indicated that methoprene concentrates in the hepatopancreas,nervous tissue and epidermal cells of the adult lobster. Methoprenealtered the synthesis and incorporation of chitoproteins (cuticleproteins) into adult postmolt lobster explant shells. SDS PAGEanalyses of adult post–molt shell extracts revealed changesin the synthesis of chitoproteins in the methoprene-treatedspecimens, suggesting that methoprene affects the normal pathwayof lobster cuticle synthesis and the quality of the post-moltshell. Although it is likely that a combination of factors ledto the reduced lobster population in WLIS, methoprene may havecontributed both by direct toxic effects and by disrupting homeostaticevents under endocrine control.