Derivation of shellfish harvest reopening criteria following the New Carissa oil spill in Coos Bay, Oregon.

Oil spills in Alaska, California, Maine, and other states have raised concerns regarding potential contamination of fish and shellfish, and have led to temporary closures of seafood harvests while health risks are assessed. Lacking standardized protocols, these assessments are generally ad hoc, site-specific efforts, with significant differences in risk evaluation criteria. This article describes the response of a state health agency to shellfish contamination following an oil spill on the Oregon coast, and discusses some of the factors that can complicate the evaluation of potential health risks from consumption of oil-contaminated shellfish. On 4 February 1999, the Japanese-owned cargo ship M/V New Carissa, carrying an estimated 400,000 gallons of light diesel and heavy fuel oil, ran aground 2 miles north of Coos Bay, Oregon. Damage to the ship's hull from the grounding and pounding surf caused the release of an estimated 25,000 to 70,000 gallons of oil. Concern for potential contamination of local recreational shellfish and commercial oyster beds prompted the Oregon Department of Agriculture (ODA) to close shellfish harvesting in Coos and Douglas counties. ODA requested assistance from the Oregon Health Division in the derivation of risk-based criteria for reopening the shellfish harvest. Criteria were developed for the primary contaminants of concern, polycyclic aromatic hydrocarbons (PAHs) expressed as total benzo[a]-pyrene (BaP) equivalents. "Safe" (<10 microg/kg) and "unsafe" (>45 microg/kg) BaP equivalent levels were derived based on upper end (32.5 g/d) and average (7.5 g/d) estimates of shellfish consumption, respectively. Composite samples of oysters, clams, and mussels (15-20 per composite) were collected from target areas and analyzed for PAHs by gas chromatography/mass spectroscopy (GC/MS). Carcinogenic PAHs were converted to total BaP equivalents (wet weight) and compared with criteria. Two oyster samples, collected from a slough off of Coos Bay, contained 33.9 and 34.5 microg/kg BaP equivalents; all other samples had less than 10 microg/kg BaP equivalents. An evaluation of the PAH profiles in the two higher oyster samples indicated a primary source other than the New Carissa oil. Because shellfish sample BaP equivalents attributable to the New Carissa oil spill did not exceed 10 microg/kg, shellfish harvesting was reopened on 4 March 1999. This study revealed some of the inherent difficulties in attempting to quantify health risks from contaminated shellfish following an oil spill and demonstrated the clear need for standardized protocols for responding to such events.

Assessing potential health risks from microcystin toxins in blue-green algae dietary supplements.

The presence of blue-green algae (BGA) toxins in surface waters used for drinking water sources and recreation is receiving increasing attention around the world as a public health concern. However, potential risks from exposure to these toxins in contaminated health food products that contain BGA have been largely ignored. BGA products are commonly consumed in the United States, Canada, and Europe for their putative beneficial effects, including increased energy and elevated mood. Many of these products contain Aphanizomenon flos-aquae, a BGA that is harvested from Upper Klamath Lake (UKL) in southern Oregon, where the growth of a toxic BGA, Microcystis aeruginosa, is a regular occurrence. M. aeruginosa produces compounds called microcystins, which are potent hepatotoxins and probable tumor promoters. Because M. aeruginosa coexists with A. flos-aquae, it can be collected inadvertently during the harvesting process, resulting in microcystin contamination of BGA products. In fall 1996, the Oregon Health Division learned that UKL was experiencing an extensive M. aeruginosa bloom, and an advisory was issued recommending against water contact. The advisory prompted calls from consumers of BGA products, who expressed concern about possible contamination of these products with microcystins. In response, the Oregon Health Division and the Oregon Department of Agriculture established a regulatory limit of 1 microg/g for microcystins in BGA-containing products and tested BGA products for the presence of microcystins. Microcystins were detected in 85 of 87 samples tested, with 63 samples (72%) containing concentrations > 1 microg/g. HPLC and ELISA tentatively identified microcystin-LR, the most toxic microcystin variant, as the predominant congener.

Methylmercury in fish from Owyhee Reservoir in southeast Oregon: scientific uncertainty and fish advisories.

Data collected during 1987-1994 showed elevated levels of mercury (Hg) in fish tissue from the Owyhee Reservoir in southeastern Oregon. Sixty-five percent of the samples analyzed had total Hg levels exceeding the US Environmental Protection Agency's (EPA) health screening value of 0.6 mg/kg. Eighteen out of 89 (20%) fish tissue samples also had total Hg levels greater than the US Food and Drug Administration's (FDA) mercury action level of 1.0 mg/kg. The overall mean Hg content for all fish collected from the reservoir was 0.75 mg/kg wet weight (wet wt.). Fish muscle taken from largemouth bass (Micropterus salmoides), smallmouth bass (Micropterus dolomieu) and channel catfish (Ictalurus punctatus) had the highest mean Hg levels of 0.92, 0.87 and 0.82 mg/kg, respectively. In contrast, rainbow trout (Salmo gairdneri) had the lowest mean Hg content of 0.37 mg/kg. Increases in total Hg concentrations were found to be positively correlated with size for rainbow trout and yellow perch. A weak but significant correlation was also observed between total mercury content and age for smallmouth bass. Based on these data, in 1994 the Oregon Health Division (OHD) issued a fish consumption advisory for the Owyhee Reservoir using a conservative risk-based approach. The process of defining and communicating these consumption limits is the subject of this paper.

Dieldrin pretreatment alters [14C]dieldrin and [3H]7,12-dimethylbenz[a]anthracene uptake in rainbow trout liver slices.

We previously demonstrated that pretreatment of rainbow trout with the organochlorine insecticide dieldrin altered in vivo disposition of a subsequent [14C]dieldrin dose. This was not explained by changes in total lipid content or the activity of common xenobiotic metabolizing enzymes. We hypothesized that dieldrin induced hepatic proteins responsible for organochlorine (OC) sequestration, transport, or excretion and that these changes reflected an adaptive response of trout to OC exposure. Here, uptake of 1.18 microM [14C]-dieldrin by precision cut liver slices was increased by dieldrin pretreatment of rainbow trout. Uptake of 0.118 and 1.18 microM [3H]-7,12-dimethylbenz[a]anthracene (DMBA) and efflux of 0.118 microM [3H]DMBA were significantly increased in slices from dieldrin-pretreated trout. Liver slice uptake of 10 but not 1.18 microM [3H]-estradiol and [3H]cholic acid was significantly increased by dieldrin pretreatment. There were no such significant differences for [3H]cholesterol, [3H]cholesterol-oleate, or [3H]oleic acid uptake. Dieldrin pretreatment did not alter hepatic microsomal metabolism of [3H]DMBA or [14C]benzo[a]pyrene or content of six cytochrome P450 isozymes, as quantitated by Western Blot analysis. These results provide further evidence that altered disposition of [14C]dieldrin and [3H]DMBA in dieldrin-pretreated trout was not explained by microsomal enzyme induction but reflected altered processes integral to hepatocellular transmembrane kinetics. These changes may have important implications for OC bioaccumulation by rainbow trout and demonstrate an interaction between dieldrin and DMBA in the absence of cytochrome P450 system induction.

Chlordecone pretreatment alters [14C]chlordecone and [14C]cholesterol transport kinetics in the perfused rat liver.

Previous work demonstrated that pretreatment of mice with low doses of the organochlorine insecticide chlordecone (CD) altered the tissue disposition of a subsequent [14C]CD or [14C]cholesterol challenge dose. The profile of these changes was consistent with the induction of a protein integral to hepatic CD/cholesterol turnover. The present study was undertaken to confirm similar in vivo effects in the rat and to analyze potential CD-induced changes in hepatic transport kinetics in the perfused rat liver. For in vivo experiments, male, Sprague-Dawley rats were treated with CD (5, 15, or 40 mg/kg) and challenged 3 or 7 days later with a 5 mg/kg [14C]CD tracer dose. Rats challenged 3 days after treatment and evaluated 16 hr later showed a dose-dependent decrease in hepatic [14C]CD relative to controls. This decrease could not be attributed to alterations in liver mass or total liver lipid. For kinetics studies, rats received 15 mg/kg CD and livers were perfused 3 days later. Following a brief (5-7 min) single-pass perfusion, the perfusate was replaced with recirculating buffer containing albumin-bound [3H]oleic acid or high-density lipoprotein-bound [14C]CD or [14C]cholesterol. Livers from pretreated animals had significantly decreased rates of [14C]CD and [14C]cholesterol uptake. Efflux of [14C]CD and biliary excretion of [14C]cholesterol were increased. No changes were observed in uptake or biliary excretion of [3H]oleic acid. SDS-PAGE of hepatic cytosol revealed an enhanced band intensity corresponding to a M(r) of 25,600 in livers from pretreated rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Chronic dieldrin exposure increases hepatic disposition and biliary excretion of [14C]dieldrin in rainbow trout.

Previous work demonstrated that exposure of laboratory animals including fish to certain organochlorine (OC) insecticides altered the tissue distribution of a subsequent tracer dose of the same [14C]OC. In the present study, 10- to 20-g rainbow trout were exposed to 15 ppm dieldrin in the diet. Fish were subsequently challenged at 2-week intervals with an intraperitoneal injection of 0.1 mg/kg [14C]dieldrin and viscera (liver, bile, mesenteric fat, kidney, and intestine) analyzed for radioactivity, 24 hr later. After 10 and 12 weeks of dieldrin pretreatment, [14C]dieldrin was significantly elevated relative to controls in liver (200%), bile (500%), and fat (500 and 1200% for 10 and 12 weeks, respectively) of pretreated fish. Other tissues were unchanged. Chloroform/methanol extractions revealed a time-dependent increase in label disposition to carcass lipid in controls but not in pretreated fish. Altered disposition could not be explained by changes in total body lipid or induction of total cytochrome P-450 or ethoxyresorufin-O-deethylase, pentoxyresorufin-O-deethylase, glutathione S-transferase, or UDP glucuronosyltransferase activities. In vivo assessment of [14C]dieldrin metabolism revealed no increase in hepatic and only a slight (22%) increase in biliary polar:nonpolar concentration ratio after 9 weeks 20 ppm dieldrin pretreatment. Results suggest that constitutive changes in liver integral to dieldrin sequestration, transport, or excretion may be an adaptive response of trout to chronic OC exposure.