Fecal Sterol Research Articles

Cimetidine, acetaminophen, and 1,7-dimethylxanthine, as indicators of wastewater pollution in marine sediments from Masan Bay, Korea

Concerns have emerged regarding the presence of human-use pharmaceuticals in aquatic environments. We investigated the status of contamination by 29 human-use pharmaceuticals as well as wastewater indicator compounds, fecal sterols and the synthetic endocrine disruptor nonylphenol, in marine sediments from Masan Bay, one of the most contaminated bays in Korea as a result of untreated and/or treated sewage. Among the 29 pharmaceuticals determined, 10 including antacid, analgesic, antibiotic, and antipruritic compounds, and metabolites of caffeine and nicotine were detected in all sediment samples. Cimetidine, acetaminophen, and 1,7-dimethylxanthine were the most frequently detected pharmaceuticals (frequency > 50%), and at high concentrations. The highest concentrations and detection frequencies were at stations located close to wastewater treatment plant (WWTP) outfalls and at the river mouth. The spatial distributions of pharmaceutical were significantly correlated with those of wastewater compounds. These results indicate that occurrence of the pharmaceuticals in marine environments is likely associated with direct sewage inputs, such as WWTP effluents and with other sewage-influenced sources, such as river discharge.

Capsaicinoids but not their analogue capsinoids lower plasma cholesterol and possess beneficial vascular activity.

Capsaicinoids exist in chili peppers, whereas capsinoids are present in some sweet peppers. The present study investigated the effects of capsaicinoids and capsinoids on plasma lipids, relaxation of the aorta, atherosclerotic plaque development, and fecal sterol excretion in hamsters fed a high-cholesterol diet. Five groups of male hamsters were given the control diet or one of the four experimental diets containing 1.3 mmol of capsaicinoids (NL), 2.6 mmol of capsaicinoids (NH), 1.3 mmol of capsinoids (OL), or 2.6 mmol of capsinoids (OH), respectively. Results showed capsaicinoids but not capsinoids could decrease plasma total cholesterol (TC), reduce the formation of atherosclerotic plaque, and relax the aortic artery. This was accompanied by a 28-175% increase in fecal excretion of acidic sterols in hamsters fed the diets containing capsaicinoids. Similarly, capsaicinoids but not capsinoids could decrease the pad weights of epididymal and prerenal adipose tissues. It was concluded that capsaicinoids but not capsinoids could favorably modulate plasma lipids and possess beneficial vascular activity.

Assessment of historical fecal contamination in Curitiba, Brazil, in the last 400 years using fecal sterols

A 400-year sedimentary record of the Barigui River was investigated using fecal biomarkers and nutrient distribution. The temporal variability in cholesterol, cholestanol, coprostanol, epicoprostanol, stigmastanol, stigmasterol, stigmastenol, sitosterol, and campesterol between 1600 and 2011 was assessed. Anthropogenic influences, such as deforestation and fecal contamination from humans and livestock, were observed from 1840. The sterol ratios exhibit evidence of hens, horses, cows, and an unknown herbivore, which may be a capybara (Hydrochoerus hydrochaeris), from 1820 and has been observed more markedly from 1970 onward. Human fecal contamination was detected from 1840 and was observed more markedly from 1930 due to population growth. Thus, the sanitation conditions and demographic growth of Curitiba seemed to be the main factors of human sewage pollution, as the coprostanol concentration over time was strongly correlated with the population growth (r=0.71, p<0.001) although diagenetic processes have also been observed.11Capsule: Record of fecal contamination in the Barigui River over time with an indication of potential sources and the relationship with demographic growth.

Novel use of faecal sterols to assess human faecal contamination in Antarctica: a likelihood assessment matrix for environmental monitoring

AbstractWastewater containing human sewage is often discharged with little or no treatment into the Antarctic marine environment. Faecal sterols (primarily coprostanol) in sediments have been used for assessment of human sewage contamination in this environment, butin situproduction and indigenous faunal inputs can confound such determinations. Using gas chromatography with mass spectral detection profiles of both C27and C29sterols, potential sources of faecal sterols were examined in nearshore marine sediments, encompassing sites proximal and distal to the wastewater outfall at Davis Station. Faeces from indigenous seals and penguins were also examined. Faeces from several indigenous species contained significant quantities of coprostanol but not 24-ethylcoprostanol, which is present in human faeces.In situcoprostanol and 24-ethylcoprostanol production was identified by co-production of their respectiveepi-isomers at sites remote from the wastewater source and in high total organic matter sediments. A C29sterols-based polyphasic likelihood assessment matrix for human sewage contamination is presented, which distinguishes human from local fauna faecal inputs andin situproduction in the Antarctic environment. Sewage contamination was detected up to 1.5 km from Davis Station.

Acute sterol o-acyltransferase 2 (SOAT2) knockdown rapidly mobilizes hepatic cholesterol for fecal excretion.

The primary risk factor for atherosclerotic cardiovascular disease is LDL cholesterol, which can be reduced by increasing cholesterol excretion from the body. Fecal cholesterol excretion can be driven by a hepatobiliary as well as a non-biliary pathway known as transintestinal cholesterol efflux (TICE). We previously showed that chronic knockdown of the hepatic cholesterol esterifying enzyme sterol O-acyltransferase 2 (SOAT2) increased fecal cholesterol loss via TICE. To elucidate the initial events that stimulate TICE, C57Bl/6 mice were fed a high cholesterol diet to induce hepatic cholesterol accumulation and were then treated for 1 or 2 weeks with an antisense oligonucleotide targeting SOAT2. Within 2 weeks of hepatic SOAT2 knockdown (SOAT2HKD), the concentration of cholesteryl ester in the liver was reduced by 70% without a reciprocal increase in hepatic free cholesterol. The rapid mobilization of hepatic cholesterol stores resulted in a ∼2-fold increase in fecal neutral sterol loss but no change in biliary cholesterol concentration. Acute SOAT2HKD increased plasma cholesterol carried primarily in lipoproteins enriched in apoB and apoE. Collectively, our data suggest that acutely reducing SOAT2 causes hepatic cholesterol to be swiftly mobilized and packaged onto nascent lipoproteins that feed cholesterol into the TICE pathway for fecal excretion.

Differential impact of hepatic deficiency and total body inhibition of MTP on cholesterol metabolism and RCT in mice

Because apoB-containing lipoproteins are pro-atherogenic and their secretion by liver and intestine largely depends on microsomal triglyceride transfer protein (MTP) activity, MTP inhibition strategies are actively pursued. How decreasing the secretion of apoB-containing lipoproteins affects intracellular rerouting of cholesterol is unclear. Therefore, the aim of the present study was to determine the effects of reducing either systemic or liver-specific MTP activity on cholesterol metabolism and reverse cholesterol transport (RCT) using a pharmacological MTP inhibitor or a genetic model, respectively. Plasma total cholesterol and triglyceride levels were decreased in both MTP inhibitor-treated and liver-specific MTP knockout (L-Mttp(-/-)) mice (each P < 0.001). With both inhibition approaches, hepatic cholesterol as well as triglyceride content was consistently increased (each P < 0.001), while biliary cholesterol and bile acid secretion remained unchanged. A small but significant decrease in fecal bile acid excretion was observed in inhibitor-treated mice (P < 0.05), whereas fecal neutral sterol excretion was substantially increased by 75% (P < 0.001), conceivably due to decreased intestinal absorption. In contrast, in L-Mttp(-/-) mice both fecal neutral sterol and bile acid excretion remained unchanged. However, while total RCT increased in inhibitor-treated mice (P < 0.01), it surprisingly decreased in L-Mttp(-/-) mice (P < 0.05). These data demonstrate that: i) pharmacological MTP inhibition increases RCT, an effect that might provide additional clinical benefit of MTP inhibitors; and ii) decreasing hepatic MTP decreases RCT, pointing toward a potential contribution of hepatocyte-derived VLDLs to RCT.

Abstract 32: Liver-Specific Transgenic Expression of Cholesteryl Ester Hydrolase Reduces Atherosclerosis in LDLR-/- Mice

Liver plays a central role in the final elimination of cholesterol from the body either as bile acids or as free cholesterol (FC) and lipoprotein cholesterol is the major source of total biliary cholesterol. HDL is the major lipoprotein responsible for removal and transport of cholesterol mainly as cholesteryl esters (CE) from the peripheral tissues to the liver. While HDL-FC is rapidly secreted into bile, the fate of HDL-CE remains unclear. We have earlier demonstrated the role of human cholesteryl ester hydrolase (CEH, CES1) in hepatic hydrolysis of HDL-CE and increasing bile acid synthesis, a process dependent on SR-BI expression. In the present study, we examined the hypothesis that by enhancing the elimination of HDL-CE into bile/feces liver-specific transgenic expression of CEH will be anti-atherogenic. Increased CEH expression in the liver led to significant increase in flux of HDL-CE to bile acids. In LDLR-/- background, this enhanced elimination of cholesterol led to attenuation of diet-induced atherosclerosis in LDLR-/-LCEH2 mice (Figure) with a consistent increase in fecal sterol secretion primarily as bile acids. Taken together with the observed reduction in atherosclerosis by increasing macrophage CEH-mediated cholesterol efflux, these studies establish CEH as an important regulator in enhancing cholesterol elimination and also as an anti-atherogenic target.

Liver-specific transgenic expression of cholesteryl ester hydrolase reduces atherosclerosis in Ldlr−/− mice

The liver plays a central role in the final elimination of cholesterol from the body either as bile acids or as free cholesterol (FC), and lipoprotein-derived cholesterol is the major source of total biliary cholesterol. HDL is the major lipoprotein responsible for removal and transport of cholesterol, mainly as cholesteryl esters (CEs), from the peripheral tissues to the liver. While HDL-FC is rapidly secreted into bile, the fate of HDL-CE remains unclear. We have earlier demonstrated the role of human CE hydrolase (CEH, CES1) in hepatic hydrolysis of HDL-CE and increasing bile acid synthesis, a process dependent on scavenger receptor BI expression. In the present study, we examined the hypothesis that by enhancing the elimination of HDL-CE into bile/feces, liver-specific transgenic expression of CEH will be anti-atherogenic. Increased CEH expression in the liver significantly increased the flux of HDL-CE to bile acids. In the LDLR(-/-) background, this enhanced elimination of cholesterol led to attenuation of diet-induced atherosclerosis with a consistent increase in fecal sterol secretion primarily as bile acids. Taken together with the observed reduction in atherosclerosis by increasing macrophage CEH-mediated cholesterol efflux, these studies establish CEH as an important regulator in enhancing cholesterol elimination and also as an anti-atherogenic target.

Intestinal Cgi-58 Deficiency Reduces Postprandial Lipid Absorption

Comparative Gene Identification-58 (CGI-58), a lipid droplet (LD)-associated protein, promotes intracellular triglyceride (TG) hydrolysis in vitro. Mutations in human CGI-58 cause TG accumulation in numerous tissues including intestine. Enterocytes are thought not to store TG-rich LDs, but a fatty meal does induce temporary cytosolic accumulation of LDs. Accumulated LDs are eventually cleared out, implying existence of TG hydrolytic machinery in enterocytes. However, identities of proteins responsible for LD-TG hydrolysis remain unknown. Here we report that intestine-specific inactivation of CGI-58 in mice significantly reduces postprandial plasma TG concentrations and intestinal TG hydrolase activity, which is associated with a 4-fold increase in intestinal TG content and large cytosolic LD accumulation in absorptive enterocytes during the fasting state. Intestine-specific CGI-58 knockout mice also display mild yet significant decreases in intestinal fatty acid absorption and oxidation. Surprisingly, inactivation of CGI-58 in intestine significantly raises plasma and intestinal cholesterol, and reduces hepatic cholesterol, without altering intestinal cholesterol absorption and fecal neutral sterol excretion. In conclusion, intestinal CGI-58 is required for efficient postprandial lipoprotein-TG secretion and for maintaining hepatic and plasma lipid homeostasis. Our animal model will serve as a valuable tool to further define how intestinal fat metabolism influences the pathogenesis of metabolic disorders, such as obesity and type 2 diabetes.

An integrated evaluation of molecular marker indices and linear alkylbenzenes (LABs) to measure sewage input in a subtropical estuary (Babitonga Bay, Brazil)

Babitonga Bay is a South Atlantic estuary with significant ecological function; it is part of the last remaining areas of mangrove communities in the Southern Hemisphere. The aim of this study was to determine the spatial distribution of the faecal sterols and linear alkylbenzenes (LABs) in surface sediments and to perform an integrated evaluation of several molecular marker indices to assess the sewage contamination status in the study area. The highest observed concentrations of faecal sterols (coprostanol + epicoprostanol) and LABs were 6.65 μg g−1 and 413.3 ng g−1, respectively. Several faecal sterol indices were calculated and correlated with coprostanol levels; these analyses showed that the index limits presented in the current literature could underestimate the sewage contamination in this study area. For the overall estuarine system, a low sewage impact may be assumed based on the low total mass inventories calculated for coprostanol (between 1.4% and 4.8%).

Characterization of sources and temporal variation in the organic matter input indicated by n-alkanols and sterols in sediment cores from Admiralty Bay, King George Island, Antarctica

The Antarctic continent is one of the most protected areas on the planet, but is dynamically responding to environmental change on a global scale. Change in the air temperature may affect the organic matter production in the area. Biomarkers such as sterols, n-alkanols and phytol in three sediment cores from Admiralty Bay, Antarctica, were determined to identify the type of organic matter, variation in input and possible relationship with general temperature changes over the past decades. The concentrations ranged from 0.91 to 13.99 μg g−1 (dry weight) of total sterols, 0.20–2.14 μg g−1 of total n-alkanols and 0.13–2.38 μg g−1 of phytol. Cholest-5-en-3β-ol was the most abundant sterol. The fecal sterols, 5β-cholestan-3β-ol and 5β-cholestan-3α-ol, occurred at low concentration (<0.01–0.15 μg g−1), below the baseline values for this region. The lower carbon chain n-alkanols were more abundant, which suggested that algae, bacteria and zooplankton were the primary sources of the sedimentary organic matter. Phytol exhibited little variation across all of the cores, which appears to be the result of degradation. Variation in the concentration of compounds in one core was compared with the variation in mean air temperature (MAT) over time; this preliminary association showed a tendency toward increased concentration during the period in which the MAT was more elevated.

Algal Sterols are as Effective as β-Sitosterol in Reducing Plasma Cholesterol Concentration

The present study examined the cholesterol-lowering activity of sterol extract (SE) derived from alga Schizochytrium sp. and its interaction with gene expression of transporters, receptors, and enzymes involved in cholesterol absorption and metabolism. GC-MS analyses found that SE was a mixture of various sterols including lathosterol, ergosterol, stigmasterol, 24-ethylcholesta-5,7,22-trienol, stigmasta-7,24(24(1))-dien-3β-ol, and cholesterol. Results showed that SE at doses of 0.06 and 0.30 g/kg diet were able to decrease plasma cholesterol concentration by 19.5 and 34%, respectively, compared with the control, in hamsters maintained on a 0.1% high-cholesterol diet. SE at a dose of 0.30 g/kg diet was as effective as β-sitosterol in reducing plasma total cholesterol (TC). SE-induced reduction in plasma TC was accompanied by down-regulation of intestinal acyl-CoA:cholesterol acyltransferase 2 (ACAT2) and hepatic 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase and up-regulation of hepatic low-density lipoprotein (LDL) receptor. Addition of SE to the diet increased the excretion of total fecal sterols. It was concluded that SE possessed the same cholesterol-lowering activity as β-sitosterol and the underlying mechanisms were mediated by increasing sterol excretion and decreasing cholesterol absorption and synthesis.

Reconstructing long-term trends in municipal sewage discharge into a small lake in northern Manitoba, Canada

Ross Lake lies within the City of Flin Flon (Manitoba, Canada), a mining community originally formed by the Hudson Bay Mining and Smelting Company (now Hudbay Minerals Inc.) in 1927. At the time of this investigation, a continuous effluent stream from Hudbay Minerals (approximately 80years) and a discontinuous and unknown amount of raw and minimally treated municipal sewage (>20years, likely ending in 1951) was discharged into the north basin of the lake. Maximum concentrations of fecal sterols, such as coprostanol and terrestrial phytosterols, such as: β-sitosterol, campesterol, stigmastanol were measured in vertical sections of sediment cores, collected from Ross Lake, in the 15–16-cm section, which likely corresponds to the 1930s. Concentrations of coprostanol increased from <1μgg−1 in older sediments, to 252.3μgg−1 organic carbon at the peak. Observed changes in concentrations of sterols, in combination with radiometric dating and changes to sediment physicochemical characteristics, support the conclusion that sediments of a depth of less than 17.5-cm depth were deposited during the post-industrial era from approximately 1930 onwards. Ratios of coprostanol to cholesterol >1, peaking at 3.6 are consistent with anecdotal information that municipal sewage was discharged into Ross Lake during the early years of urbanization, prior to changes in treatment of sewage and discharge practices that began in 1951. Finally, historical concentrations of terrestrial phytosterols followed trends similar to those of coprostanol and cholesterol and may possibly be the result of an increase in the flux of terrestrial organic matter into Ross Lake as the result of regional deforestation due to logging and fire.

Where Did That Pollution Come From? A Review of Chemical and Microbial Markers of Organic Pollution

This review presents the current range of analytical markers which can be used to identify the sources of organic matter in environmental waters. Both chemical and microbial markers are presented. Applications which have been developed include identification of pollution input from human domestic sources, agriculture, landfills, and urban runoff. DNA and RNA characteristic of individual animal species, fecal sterols and bile acids, artificial sweeteners, commercial chemicals, and isotope ratios of carbon and hydrogen have been found useful as pollution markers. The review is intended to both introduce the reader to this vital area of research, and to present an overview which can be useful to practitioners in the field.

The analysis of faecal sterols in sediment samples by HPLC-UV using ultrasound-assisted treatment

A method was developed for the analysis of faecal sterols in sediment samples by ultrasound-assisted extraction and quantification by HPLC with a UV detector.

Sedimentary biomarkers along a contamination gradient in a human-impacted sub-estuary in Southern Brazil: A multi-parameter approach based on spatial and seasonal variability

The composition and seasonal variations of sedimentary organic matter were investigated along the Cotinga sub-estuary, located in Paranaguá Bay, a large South American estuary where urban activities and the primary Brazilian grain shipping port are sources of pollution. Steroids and hydrocarbons were analyzed in surface sediments collected during the austral winter (2008) and summer (2009) in three distinct sectors, along this sub-estuary in a presumed gradient of fecal contamination. Concentrations ranged from 0.28 to 7.33μgg−1 (in dry sample weight thereafter), <DL (below detection limit) to 57.2ngg−1 and <DL to 1.69μgg−1 for aliphatic hydrocarbons (ΣAHs), polycyclic aromatic hydrocarbons (ΣPAHs) and coprostanol, respectively. Petrogenic inputs may be considered as source of AHs due to the presence of unresolved complex mixture in the majority of sites; however the levels observed do not indicate oil contamination. The highest ΣPAHs concentrations were found during the summer in the middle sector of the sub-estuary but were below the threshold effect levels (TEL), suggesting the absence of contamination by PAHs. Selected PAH isomer ratios indicated pyrolytic sources, whereas fecal sterols indicated decreasing sewage contamination from sub-estuary to the open ocean. The absence of correlation between organic markers and grain-size parameters suggested no preferential deposition sites of organic matter in the study area. The Principal Components Analysis suggested spatial variation in the distribution of sterols and AHs; however, temporal variations were only evident in the distribution of PAHs.

Baseline concentrations of faecal sterols and assessment of sewage input into different inlets of Admiralty Bay, King George Island, Antarctica

The Antarctic region is one of the best preserved environments in the world. However, human activities such as the input of sewage result in the alteration of this pristine site. We report baseline values of faecal sterols in Admiralty Bay, Antarctica. Four sediment cores were collected during the 2006/2007 austral summer at the Ezcurra (THP and BAR), Mackelar (REF) and Martel (BTP) inlets. Concentrations of faecal sterols (coprostanol+epicoprostanol) were <0.16μgg−1, suggesting no sewage contamination and probable “biogenic” contributions for these compounds. Baseline values, calculated using the mean concentration of faecal sterols in core layers for THP, BAR, REF and BTP, were 0.04±0.02, 0.03±0.01, 0.07±0.01 and 0.04±0.02μgg−1, respectively. These results established as natural contributions of faecal sterols, suggesting that these markers can be useful indicators of human-derived faecal input and contributing to monitoring programs to prevent anthropogenic impacts.

Acceleration of Biliary Cholesterol Secretion Restores Glycemic Control and Alleviates Hypertriglyceridemia in Obese db / db Mice

Recent studies support a role for cholesterol in the development of obesity and nonalcoholic fatty liver disease. Mice lacking the ABCG5 ABCG8 (G5G8) sterol transporter have reduced biliary cholesterol secretion and are more susceptible to steatosis, hepatic insulin resistance, and loss of glycemic control when challenged with a high-fat diet. We hypothesized that accelerating G5G8-mediated biliary cholesterol secretion would correct these phenotypes in obese mice. Obese (db/db) male and their lean littermates were administered a cocktail of control adenovirus or adenoviral vectors encoding ABCG5 and ABCG8 (AdG5G8). Three days after viral administration, measures of lipid and glucose homeostasis were determined, and tissues were collected for biochemical analyses. AdG5G8 increased biliary cholesterol and fecal sterol elimination. Fasting glucose and triglycerides declined, and glucose tolerance improved in obese mice expressing G5G8 compared with mice receiving control adenovirus. These changes were associated with a reduction in phosphorylated eukaryotic initiation factor 2α and c-Jun N-terminal kinase in liver, suggesting alleviation of endoplasmic reticulum stress. Phosphorylated insulin receptor and protein kinase B were increased, indicating restored hepatic insulin signaling. However, there was no reduction in hepatic triglycerides after the 3-day treatment period. Accelerating biliary cholesterol secretion restores glycemic control and reduces plasma triglycerides in obese db/db mice.

LXR Driven Induction of HDL‐Cholesterol is Independent of Intestinal Cholesterol Absorption and ABCA1 Protein Expression

We investigated whether: (1) liver X receptor (LXR)-driven induction of high-density lipoprotein cholesterol (HDL-C) and other LXR-mediated effects on cholesterol metabolism depend on intestinal cholesterol absorption; and (2) combined treatment with the LXR agonist GW3965 and the cholesterol absorption inhibitor ezetimibe results in synergistic effects on cholesterol metabolism that could be beneficial for treatment of atherosclerosis. Mice were fed 0.2% cholesterol and treated with GW3965+ezetimibe, GW3965 or ezetimibe. GW3965+ezetimibe treatment elevated serum HDL-C and Apolipoprotein (Apo) AI, effectively reduced the intestinal cholesterol absorption and increased the excretion of faecal neutral sterols. No changes in intestinal ATP-binding cassette (ABC) A1 or ABCG5 protein expression were observed, despite increased mRNA expression, while hepatic ABCA1 was slightly reduced. The combined treatment caused a pronounced down-regulation of intestinal Niemann-Pick C1-like 1 (NPC1L1) and reduced hepatic and intestinal cholesterol levels. GW3965 did not affect the intestinal cholesterol absorption, but increased serum HDL-C and ApoAI levels. GW3965 also increased Apoa1 mRNA levels in primary mouse hepatocytes and HEPA1-6 cells. Ezetimibe reduced the intestinal cholesterol absorption, ABCA1 and ABCG5, but did not affect the serum HDL-C or ApoAI levels. Thus, the LXR-driven induction of HDL-C and ApoAI was independent of the intestinal cholesterol absorption and increased expression of intestinal or hepatic ABCA1 was not required. Inhibited influx of cholesterol via NPC1L1 and/or low levels of intracellular cholesterol prevented post-transcriptional expression of intestinal ABCA1 and ABCG5, despite increased mRNA levels. Combined LXR activation and blocked intestinal cholesterol absorption induced effective faecal elimination of cholesterol.

분변계 스테롤을 이용한 남해안 패류양식어장(여자만과 강진만)의 퇴적물내 분변오염도 평가

Eight fecal sterols were analyzed in surface sediments collected from shellfish farming areas in Yeoja Bay and Gangjin Bay, Korea, to evaluate sewage-derived fecal pollution. The concentrations of coprostanol, a good marker of sewage-derived organic contamination, in sediments were in the range of 10-530 ng/g-dry in Yeoja Bay, and 10-190 ng/g-dry in Gangjin Bay. Coprostanol levels were markedly higher in the inner bay than in the outer bay. These levels were lower than those reported in urbanized bays in Korea, however, they were comparable to levels in other shellfish farming areas including Gamak Bay. A multivariate analysis of the ratios of other sterols suggested that the sterols originated from sewage and plankton/benthos. Sewage was the dominant source at stations located close to the river mouth and wastewater treatment plant (WWTP) outfalls, and plankton/benthos was the primary source in the outer bay. These results suggest that management of point sources, e.g., WWTP as well as non-point sources, e.g., riverine inputs is important for improving the water quality in Yeoja Bay and Gangjin Bay.