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Widespread decline and mortality of eastern hemlock, Tsuga canadensis (L.) Carrière, have been caused by hemlock woolly adelgid, Adelges tsugae (Annand) (HWA) (Hemiptera: Adelgidae). The current study is a retrospective analysis conducted in collaboration with Great Smoky Mountains National Park (GRSM) to determine longevity of imidacloprid and its insecticidal metabolites (imidacloprid olefin, 5-hydroxy, and dihydroxy) in GRSM's HWA integrated pest management (IPM) program. Foliage samples were collected from three canopy strata of hemlocks that were given imidacloprid basal drench treatments 4-7 yr prior to sampling. Foliage was analyzed to assess concentrations in parts per billion (ppb) of imidacloprid and its metabolites. Imidacloprid and its olefin metabolite were present in most, 95 and 65%, respectively, branchlets 4-7 yr post-treatment, but the 5-hydroxy and dihydroxy metabolites were present in only 1.3 and 11.7%, respectively, of the branchlets. Imidacloprid and olefin concentrations significantly decreased between 4 and 7 yr post-treatment. Concentrations of both imidacloprid and olefin were below the LC50 for HWA 5-7 yr post-treatment. Knowledge of the longevity of imidacloprid treatments and its metabolite olefin can help maximize the use of imidacloprid in HWA IPM programs.

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Induction of the hepatic detoxification enzyme cytochrome P4501A has been observed in fish exposed to bleached‐kraft mill effluents (BKME). P4501A content was examined in three species of wild fish exposed to BKME in a western Canadian river as part of an extensive program that included chemical monitoring, fish population studies, and other fish biochemical and physiological measurements. The Rocky Mountain whitefish Prosopium williamsoni exhibited marked induction of P4501A compared to reference whitefish, as measured by both catalytic activity and immunoreactive protein content. Similar P4501A induction was observed 4 d after reference fish were treated with 20 mg/kg β‐naphthoflavone. Whitefish P4501A levels have declined from a peak in spring 1991, following mill process modifications and concurrent with reductions in body burdens of hydrophobic compounds. Whitefish collected near the mill, moved upstream of effluent discharges, and held for 8 d showed no significant loss of hepatic P4501A‐related (ethoxyresorufin O‐deethylase, EROD) enzyme activity or P4501A protein levels. For spring 1991, correlations were found between EROD activity and measures of chronic exposure to BKME (e.g., muscle 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin content), but not between EROD and measures of acute exposure (e.g., bile content of resin acids or chlorophenolic metabolites). These and other lines of evidence indicate that the P4501A‐inducing agent(s) at this site may be neither waterborne nor rapidly eliminated. A second species, longnose sucker (Catostomus catostomus), collected near the mill exhibited modest (two‐ to threefold) P4501A induction. For both species, no significant correlations between P4501A induction and trends in other biological responses were found, as described in a companion paper. Burbot (Lota lota) had hepatic EROD activities generally in the range of reference values, despite substantial exposure to mill‐related compounds. In contrast to studies at historically degraded pulp mill sites, P4501A induction is the only major biological response observed to date at this site. As P4501A induction is not related to adverse effects, it could be best classified as an indicator of exposure to BKME.

Hemlock woolly adelgid (Adelges tsugae [Annand]), an invasive insect in the eastern United States, has caused widespread decline of eastern hemlock, Tsuga canadensis (L.) Carriére. Imidacloprid basal drench treatments were assessed 4-7 yr after a single treatment to determine hemlock woolly adelgid population suppression and effects on hemlock canopy health. The effects of sampling site, years post-treatment, and hemlock diameter at breast height (DBH) size classes were evaluated relative to imidacloprid treatment on hemlock woolly adelgid populations and hemlock canopy health characteristics. The influence of hemlock woolly adelgid populations on canopy health characteristics was also assessed. Imidacloprid treatments resulted in low-level hemlock woolly adelgid populations 7 yr post-treatment. Hemlock woolly adelgid was present on more hemlocks 7 yr compared with 4-6 yr post-treatment. Smaller hemlocks, dosed with 0.7 g active ingredient (AI)/2.5 cm DBH, had higher populations of hemlock woolly adelgid than the largest size class, which were treated at twice that dosage. Concentrations of imidacloprid and its olefin metabolite below the LC were sufficient for suppression of hemlock woolly adelgid populations, which suggests an additive effect of imidacloprid and olefin that compounds hemlock woolly adelgid mortality over many generations. Hemlock woolly adelgid populations observed in this study were too low to have an observable effect on hemlock canopy health, indicating that application intervals of up to 7 yr may be adequate to protect hemlocks.