Source apportionment of polychlorinated biphenyls in the sediment of the Newtown Creek superfund site.

Polychlorinated biphenyls (PCBs) are a primary contaminant of potential concern at the Newtown Creek superfund site. Measurements of PCBs in hundreds of samples of sediment (surface and cores) within Newtown Creek and at nearby reference locations were obtained from the Remedial Investigation (RI) databases. This data set was analyzed using Positive Matrix Factorization (PMF). A weight-of-evidence approach was used to attribute the PMF-generated fingerprints to sources. The PMF analysis generated eight factors (fingerprints or sources) that represent primary sources, such as Aroclors, as well as secondary sources, including the East River and Combined Sewer Outfalls (CSOs). In addition to the high-production volume Aroclors (1016/1242, 1248, 1254, and 1260), some less-widely used Aroclors (1232 and 1268) were found in Newtown Creek sediment. Aroclor 1268 is disproportionately abundant in the deepest sediments, while PCBs likely from CSOs are relatively more abundant in surface sediment.

Dynamic regulation of airway surface liquid pH by TMEM16A and SLC26A4 in cystic fibrosis nasal epithelia with rare mutations.

In cystic fibrosis (CF), defects in the CF transmembrane conductance regulator (CFTR) channel lead to an acidic airway surface liquid (ASL), which compromises innate defence mechanisms, predisposing to pulmonary failure. Restoring ASL pH is a potential therapy for people with CF, particularly for those who cannot benefit from current highly effective modulator therapy. However, we lack a comprehensive understanding of the complex mechanisms underlying ASL pH regulation. The calcium-activated chloride channel, TMEM16A, and the anion exchanger, SLC26A4, have been proposed as targets for restoring ASL pH, but current results are contradictory and often utilise nonphysiological conditions. To provide better evidence for a role of these two proteins in ASL pH homeostasis, we developed an efficient CRISPR-Cas9-based approach to knock-out (KO) relevant transporters in primary airway basal cells lacking CFTR and then measured dynamic changes in ASL pH under thin-film conditions in fully differentiated airway cultures, which better simulate the in vivo situation. Unexpectantly, we found that both proteins regulated steady-state as well as agonist-stimulated ASL pH, but only under inflammatory conditions. Furthermore, we identified two Food and Drug Administration (FDA)-approved drugs which raised ASL pH by activating SLC26A4. While we identified a role for SLC26A4 in fluid absorption, KO had no effect on cyclic adenosine monophosphate (cAMP)-stimulated fluid secretion in airway organoids. Overall, we have identified a role of TMEM16A in ASL pH homeostasis and shown that both TMEM16A and SLC26A4 could be important alternative targets for ASL pH therapy in CF, particularly for those people who do not produce any functional CFTR.

Exploring intrinsic variability between cultured nasal and bronchial epithelia in cystic fibrosis.

The nasal and bronchial epithelium are unified parts of the respiratory tract that are affected in the monogenic disorder cystic fibrosis (CF). Recent studies have uncovered that nasal and bronchial tissues exhibit intrinsic variability, including differences in mucociliary cell composition and expression of unique transcriptional regulatory proteins which relate to germ layer origin. In the present study, we explored whether intrinsic differences between nasal and bronchial epithelial cells persist in cell cultures and affect epithelial cell functioning in CF. Comparison of air-liquid interface (ALI) differentiated epithelial cells from subjects with CF revealed distinct mucociliary differentiation states of nasal and bronchial cultures. Moreover, using RNA sequencing we identified cell type-specific signature transcription factors in differentiated nasal and bronchial epithelial cells, some of which were already poised for expression in basal progenitor cells as evidenced by ATAC sequencing. Analysis of differentiated nasal and bronchial epithelial 3D organoids revealed distinct capacities for fluid secretion, which was linked to differences in ciliated cell differentiation. In conclusion, we show that unique phenotypical and functional features of nasal and bronchial epithelial cells persist in cell culture models, which can be further used to investigate the effects of tissue-specific features on upper and lower respiratory disease development in CF.

Protocol for generating airway organoids from 2D air liquid interface-differentiated nasal epithelia for use in a functional CFTR assay.

We present a protocol to generate organoids from air-liquid-interface (ALI)-differentiated nasal epithelia. We detail their application as cystic fibrosis (CF) disease model in the cystic fibrosis transmembrane conductance regulator (CFTR)-dependent forskolin-induced swelling (FIS) assay. We describe steps for isolation, expansion and cryostorage of nasal brushing-derived basal progenitor cells, and their differentiation in ALI cultures. Furthermore, we detail the conversion of differentiated epithelial fragments into organoids of healthy controls and CF subjects for validating CFTR function and modulator responses. For complete details on the use and execution of this protocol, please refer to Amatngalim et al.1.

Airway Epithelial Cultures of Children with Esophageal Atresia as a Model to Study Respiratory Tract Disorders.

Esophageal atresia (EA) is a rare birth defect in which respiratory tract disorders are a major cause of morbidity. It remains unclear whether respiratory tract disorders are in part caused by alterations in airway epithelial cell functions such as the activity of motile cilia. This can be studied using airway epithelial cell culture models of patients with EA. Therefore, the aim of this study was to evaluate the feasibility to culture and functionally characterize motile cilia function in the differentiated air-liquid interface cultured airway epithelial cells and 3D organoids derived from nasal brushings and bronchoalveolar lavage (BAL) fluid from children with EA. We demonstrate the feasibility of culturing differentiated airway epithelia and organoids of nasal brushings and BAL fluid of children with EA, which display normal motile cilia function. EA patient-derived airway epithelial cultures can be further used to examine whether alterations in epithelial functions contribute to respiratory disorders in EA.

PFAS in municipal landfill leachate: Occurrence, transformation, and sources.

To understand sources and processes affecting per- and polyfluoroalkyl substances (PFAS), 32 PFAS were measured in landfill leachate from 17 landfills across Washington State in both pre-and post-total oxidizable precursor (TOP) assay samples, using an analytical method that was the precursor to EPA Draft Method 1633. As in other studies, 5:3FTCA was the dominant PFAS in the leachate, suggesting that carpets, textiles, and food packaging were the main sources of PFAS. Total PFAS concentrations (Σ32PFAS) ranged from 61 to 172,976 ng/L and 580-36,122 ng/L in pre-TOP and post-TOP samples, respectively, suggesting that little or no uncharacterized precursors remained in landfill leachate. Furthermore, due to chain-shortening reactions, the TOP assay often resulted in a loss of overall PFAS mass. Positive matrix factorization (PMF) analysis of the combined pre- and post-TOP samples produced five factors that represent sources and processes. Factor 1 consisted primarily of 5:3FTCA (intermediate of 6:2 fluorotelomer degradation and characteristic of landfill leachate), while factor 2 was dominated by PFBS (degradant of C-4 sulfonamide chemistry) and, to a lesser extent, by several PFCAs and 5:3FTCA. Factor 3 consisted primarily of both short-chain PFCAs (end-products of 6:2 fluorotelomer degradation) and PFHxS (derived from C-6 sulfonamide chemistry), while the main component of factor 4 was PFOS (dominant in many environmental media but minor in landfill leachate, perhaps reflecting a production shift from longer to shorter chain PFAS). Factor 5, highly loaded with PFCAs, was dominant in post-TOP samples and therefore represented the oxidation of precursors. Overall, PMF analysis suggests that the TOP assay approximates some redox processes which occur in landfills, including chain-shortening reactions which yield biodegradable products.

Sources of polychlorinated biphenyls to Upper Hudson River fish post-dredging.

Polychlorinated biphenyls (PCBs) are persistent, bioaccumulative, and toxic chemicals that are the dominant contaminant in the Upper Hudson River (UHR) in New York State where two General Electric (GE) plants historically discharged PCBs to the river. Portions of the UHR were dredged from 2009 to 2015 to address PCB contamination. In 2017, the first post-dredging survey of yearling feeder fish and sediment PCB contamination was conducted to establish a baseline for the recovery of the river. Prior analysis of the sediment data from the 2017 survey indicated that ∼2% of the PCBs in the surface sediment were higher in molecular weight than the formulation used by GE and therefore arose from non-GE sources. In this work, the fish PCB data from the 2017 survey were analyzed using Positive Matrix Factorization (PMF). Empirical Bayesian Kriging (EBK) was used to estimate PCB concentrations in the sediment at the locations where fish were collected. The results suggest that PCBs that are the products of microbial dechlorination bioaccumulate in the fish and represent 7% of the PCB mass in the fish data set. Further, the results suggest that about 13% of the PCBs in the fish may have come from non-GE sources. This is higher than the percentage of non-GE PCBs in the sediment, but can be explained by the higher molecular weight of the non-GE mixture which causes it to bioaccumulate more effectively than GE PCBs. Concentrations of the non-GE PCBs averaged about 240 ppb wet weight (whole body) in yearling feeder fish. The remedial goals range from 50 to 400 ppb ww in fillet for fish including piscivorous species that are likely to have higher PCB concentrations than feeder fish.

The SLC26A9 inhibitor S9-A13 provides no evidence for a role of SLC26A9 in airway chloride secretion but suggests a contribution to regulation of ASL pH and gastric proton secretion.

The solute carrier 26 family member A9 (SLC26A9) is an epithelial anion transporter that is assumed to contribute to airway chloride secretion and surface hydration. Whether SLC26A9 or CFTR is responsible for airway Cl- transport under basal conditions is still unclear, due to the lack of a specific inhibitor for SLC26A9. In the present study, we report a novel potent and specific inhibitor for SLC26A9, identified by screening of a drug-like molecule library and subsequent chemical modifications. The most potent compound S9-A13 inhibited SLC26A9 with an IC50 of 90.9 ± 13.4 nM. S9-A13 did not inhibit other members of the SLC26 family and had no effects on Cl- channels such as CFTR, TMEM16A, or VRAC. S9-A13 inhibited SLC26A9 Cl- currents in cells that lack expression of CFTR. It also inhibited proton secretion by HGT-1 human gastric cells. In contrast, S9-A13 had minimal effects on ion transport in human airway epithelia and mouse trachea, despite clear expression of SLC26A9 in the apical membrane of ciliated cells. In both tissues, basal and stimulated Cl- secretion was due to CFTR, while acidification of airway surface liquid by S9-A13 suggests a role of SLC26A9 for airway bicarbonate secretion.

Drug Repurposing for Cystic Fibrosis: Identification of Drugs That Induce CFTR-Independent Fluid Secretion in Nasal Organoids.

Individuals with cystic fibrosis (CF) suffer from severe respiratory disease due to a genetic defect in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, which impairs airway epithelial ion and fluid secretion. New CFTR modulators that restore mutant CFTR function have been recently approved for a large group of people with CF (pwCF), but ~19% of pwCF cannot benefit from CFTR modulators Restoration of epithelial fluid secretion through non-CFTR pathways might be an effective treatment for all pwCF. Here, we developed a medium-throughput 384-well screening assay using nasal CF airway epithelial organoids, with the aim to repurpose FDA-approved drugs as modulators of non-CFTR-dependent epithelial fluid secretion. From a ~1400 FDA-approved drug library, we identified and validated 12 FDA-approved drugs that induced CFTR-independent fluid secretion. Among the hits were several cAMP-mediating drugs, including ß2-adrenergic agonists. The hits displayed no effects on chloride conductance measured in the Ussing chamber, and fluid secretion was not affected by TMEM16A, as demonstrated by knockout (KO) experiments in primary nasal epithelial cells. Altogether, our results demonstrate the use of primary nasal airway cells for medium-scale drug screening, target validation with a highly efficient protocol for generating CRISPR-Cas9 KO cells and identification of compounds which induce fluid secretion in a CFTR- and TMEM16A-indepent manner.

Measuring cystic fibrosis drug responses in organoids derived from 2D differentiated nasal epithelia.

Cystic fibrosis is caused by genetic defects that impair the CFTR channel in airway epithelial cells. These defects may be overcome by specific CFTR modulating drugs, for which the efficacy can be predicted in a personalized manner using 3D nasal-brushing-derived airway organoids in a forskolin-induced swelling assay. Despite of this, previously described CFTR function assays in 3D airway organoids were not fully optimal, because of inefficient organoid differentiation and limited scalability. In this report, we therefore describe an alternative method of culturing nasal-brushing-derived airway organoids, which are created from an equally differentiated airway epithelial monolayer of a 2D air-liquid interface culture. In addition, we have defined organoid culture conditions, with the growth factor/cytokine combination neuregulin-1<i>ß</i> and interleukin-1<i>ß</i>, which enabled consistent detection of CFTR modulator responses in nasal-airway organoid cultures from subjects with cystic fibrosis.

Recurrent Respiratory Syncytial Virus Infection in a CD14-Deficient Patient.

BACKGROUND: Recurrent respiratory syncytial virus (RSV) infection requiring hospitalization is rare and the underlying mechanism is unknown. We aimed to determine the role of CD14-mediated immunity in the pathogenesis of recurrent RSV infection. METHODS: We performed genotyping and longitudinal immunophenotyping of the first patient with a genetic CD14 deficiency who developed recurrent RSV infection. We analyzed gene expression profiles and interleukin (IL)-6 production by patient peripheral blood mononuclear cells in response to RSV pre- and post-fusion (F) protein. We generated CD14-deficient human nasal epithelial cells cultured at air-liquid interface (HNEC-ALI) of patient-derived cells and after CRISPR-based gene editing of control cells. We analyzed viral replication upon RSV infection. RESULTS: Sanger sequencing revealed a homozygous single-nucleotide deletion in CD14, resulting in absence of the CD14 protein in the index patient. In vitro, viral replication was similar in wild-type and CD14-/- HNEC-ALI. Loss of immune cell CD14 led to impaired cytokine and chemokine responses to RSV pre- and post-F protein, characterized by absence of IL-6 production. CONCLUSIONS: We report an association of recurrent RSV bronchiolitis with a loss of CD14 function in immune cells. Lack of CD14 function led to defective immune responses to RSV pre- and post-F protein without a change in viral replication.

Effect of membrane filtration on the fate of polychlorinated biphenyls in wastewater treatment.

The Spokane River is impacted by levels of polychlorinated biphenyls (PCBs) that have triggered fish consumption advisories and exceed water quality standards. Select wastewater treatment plants (WWTPs) on the river have been upgraded from secondary (biological) treatment to tertiary treatment in the form of membrane filtration to address phosphorus contamination. Because membrane filtration is effective at removing particles, it is likely to reduce PCB concentrations in the effluent as well. In this work, PCBs measured in the influents and effluent of several WWTPs discharging to the river were examined. Implementation of membrane filtration reduced PCB concentrations in the effluent (and therefore PCB loads to the river) by 33% at a facility that produces recycled and virgin paper and by ∼55% at municipal WWTPs, compared to secondary (activated sludge) treatment. Largest reductions in concentrations in effluent and loads were achieved for higher molecular weight (MW) PCB congeners (i.e. those with six or more chlorines), homologs, and formulations. The more modest reductions in effluent concentrations achieved at the paper WWTP may be due to the mix of PCBs in the wastewater there: it contained primarily the low MW Aroclor 1242 (presumably from carbonless copy paper) and PCB 11 (3,3'-dichlorobiphenyl) possibly from pigments. PCBs that appear to be associated with silicone products such as caulk, tubing, and o-rings are relatively more abundant in the effluent of some plants compared to the influent, suggesting that these congeners arise from contamination during sampling or from within the plant itself. At some WWTPs, this contamination accounts for nearly a third of PCBs measured in the effluent.

Source apportionment of perfluoroalkyl substances in Great Lakes fish.

Due to the complex sources and fate of perfluoroalkyl substance (PFAS), their source apportionment in the environment remains a challenge. A data set of 11 straight-chain PFAS in 139 samples of fish in the Great Lakes was analyzed using positive matrix factorization (PMF) to investigate their primary sources, whose spatial variations were examined against the surrounding environmental factors. PMF analysis produced five fingerprints. Factor 1 (72% of Σ11PFAS, dominated by PFOS) probably represented emissions from primary sources (such as consumer products) and secondary sources (precursors), and increased in average abundance from west to east across the Great Lakes. Factor 2 (13% of Σ11PFAS) and factor 3 (7% of Σ11PFAS), highly loaded with long-chain PFAS and PFNA, respectively, were thought to represent PVDF manufacture or processing in metal plating. They showed higher contributions in sparsely populated Lakes Superior and Huron. Factor 4 (5% of Σ11PFAS, highly loaded with PFOS and PFHxS) presented hot spots near current and former air force bases, suggesting it was related to aqueous film-forming foams (AFFFs). Factor 5 (4% of Σ11PFAS) contained primarily PFOS and PFOSA, which may imply metabolism of precursors (PFOSA) to PFOS in vivo. Unexpectedly, the spatial trends of the five sources all showed abnormally low values near the more urbanized Chicago and Milwaukee in Lake Michigan, which may be due to their unique wastewater and stormwater infrastructure or may arise from atmospheric transport of precursors. Our study indicated that PMF was an effective tool to identify sources of PFAS in fish despite absorption, distribution, metabolism, and excretion (ADME) processes which might alter fingerprints in fish relative to their surrounding environment.

Concentration of polychlorinated biphenyls in serum from New Jersey biomonitoring study: 2016-2018.

The first statewide New Jersey Biomonitoring (NJBM) of serum polychlorinated biphenyls (PCBs) was conducted from 2016 to 2018. Forty ortho-substituted PCBs were measured in serum samples collected from 920 NJ residents in compliance with the CDC method. The lipid adjusted geometric mean (GM) of ∑40PCB concentration for all the 920 measured subjects was 65.5 ng/g lipid (95% CIs: 56.9-75.4 ng/g lipid). Age stratified serum concentration showed that the lowest GM (33.3 ng/g lipid) was observed in the 20-39 years age group (n = 282), followed by a concentration of 76.05 ng/g lipid (n = 382) in the 40-59 years age group, and the highest GM (168.4 ng/g lipid) was found in the 60-74 years age group (n = 256). A survey regression model revealed that ∑40PCBs was significantly associated with age, moderately associated with geographic region, and not significantly associated with sex. The comparison of serum PCB levels in NJBM with the sequential National Health and Nutrition Examination Survey (NHANES) data suggested that the serum PCBs in NJ adults declined 52-59% at all age groups over the last decade. Positive Matrix Factorization (PMF) suggests that ongoing and recent exposure to lower molecular weight PCBs contributes about 15% to total serum PCB levels and more in younger subjects, while higher molecular weight PCBs contribute 52% of the total serum PCB levels and more in older subjects.

Isolating different natural and anthropogenic PAHs in the sediments from the northern Bering-Chukchi margin: Implications for transport processes in a warming Arctic.

Polycyclic aromatic hydrocarbons (PAHs) have become the dominating burden in the Arctic ecosystems, but their transport pathways and relative importance of different sources in the Arctic remained unclear, and this would be further complicated by climate change. Here we interpreted 27 PAHs in 34 surface sediments from the northern Bering-Chukchi margin. We integrated source apportionment methods (including diagnostic ratios, principal component analysis, hierarchical analysis, and positive matrix factorization (PMF) model) together with geochemistry parameters, which reveal a gradually clear picture of the spatial patterns of different sources. The total PAH concentrations (50.4 to 896.0 ng/g dw) exhibited a "hilly" shape with the increase of latitude, showing the highest level of PAHs in the northeast Chukchi Sea. The total BaP toxic equivalent quotient (TEQ) for carcinogenic compounds was from 1.06 to 33.3 ng TEQ/g. Most PAHs showed positive correlations with silt content, total organic carbon, stable carbon isotopes and black carbon (p < 0.01 or 0.05). Generally, source apportionment methods revealed an increasing petrogenic source of PAHs with latitudes. The PMF model further differentiated two petrogenic (36.7%), two pyrogenic (softwood and fossil fuel combustion, 35.5%) and one in-situ biogenic source (Perylene, 27.8%). An extremely high petrogenic signal was captured in the Canada Basin margin, possibly originating from the Mackenzie River via ice drifting with Beaufort Gyre, while another petrogenic source may come from coal deposit erosion by deglaciation. Softwood combustion (characterized by Retene) exhibited exclusively higher contribution in the northeast Chukchi Sea and might result from the increasing wildfire in Alaska due to climate change, whereas fossil fuel combustion exhibited similar contributions across different latitudes. Our results revealed natural PAHs as important "inside sources" in the Arctic, which are highly sensitive to global warming and deserves more attention.

Sources of polychlorinated biphenyls to Upper Hudson River sediment post-dredging.

The Upper Hudson River (UHR) has been contaminated with polychlorinated biphenyls (PCBs) since the 1940s due to the manufacture of capacitors at two plants near Hudson Falls and Fort Edward, NY by General Electric (GE). Dredging of portions of the UHR was conducted from 2009 to 2015 as a partial remedy for this contamination. In 2017, the New York State Department of Environmental Conservation undertook a comprehensive post-dredging survey of sediment contamination in the UHR. Thousands of samples were collected, and 130 of these were analyzed for PCBs using EPA method 1668A. This data set was analyzed using Positive Matrix Factorization. Six factors were observed. One factor resembled the dominant Aroclors used by GE with little alteration. Three factors represented different pathways and/or extents of microbial dechlorination. One factor resembled a mixture of microbial dechlorination products and a higher molecular weight Aroclor used by GE. The congener patterns of the dechlorination factors suggest that removal of chlorines at the ortho position does occur in the UHR sediment, in agreement with several laboratory studies showing that such ortho dechlorination is possible. This ortho dechlorination could theoretically lead to complete dechlorination of PCBs to biphenyl in UHR sediment. Only one factor was not attributable to GE. It represents inputs of PCBs from tributaries and urban areas and explains 1.7% of the PCB mass in the sediments. The small contribution from the non-GE PCB source suggests that recontamination of the sediment after dredging was minor.

Perfluoroalkyl substances in sediments from the Bering Sea to the western Arctic: Source and pathway analysis.

Although perfluoroalkyl substances (PFASs) are ubiquitous in the Arctic, their dominant pathways to the Arctic remain unclear. Most modeling studies support major oceanic transport for PFASs in the Arctic seawater, but this conclusion contradicts the rapid response of PFASs to global emissions in some biota species. Sediments, which act as important PFAS sinks for seawater and potential PFAS source to the benthic food web, are important for interpreting the fate of PFASs in the Arctic. Here we investigate the occurrence of 9 PFASs in one core (1945-2014) and 29 surface sediments from the Bering Sea to the western Arctic. Total PFAS concentrations (0.06-1.73 ng/g dw) in surface sediments were dominated by perfluorooctane sulfonate (PFOS), perfluorononanoic acid (PFNA) and perfluorobutyl sulfonate (PFBS), with higher levels in the Bering Sea slope and the northeast Chukchi Sea. Historical trends in PFASs varied among individuals, with PFOS declining in the early 2000s while PFNA showing an increasing up-core trend. Analysis of positive matrix factorization model identified that the major PFAS sources in the sediment core were dominated by the atmospheric oxidation of consumer use of PFOS precursor-based products (45.0%), while the oceanic transport of fluoropolymer manufacture of polyvinylidene fluoride (mainly PFNA) exhibited an increasing trend over time, becoming dominant in surface sediments (42.8%). Besides, local input of possible aqueous fire-fighting foams (mainly PFOS and PFBS) also acted as an important source currently (30.1%) and historically (34.9%). Our study revealed that the pathways of PFASs in Arctic sediments varied greatly for individuals and the conclusion of PFOS originating from mainly atmospheric oxidation was different from seawater modeling results. This, together with the high possibility of sediments as direct source to Arctic food web (supported by similar PFAS compositions and temporal variations), help provide additional evidence regarding PFAS pathways to the Arctic.

Source Apportionment of Polychlorinated Biphenyls in Atmospheric Deposition in the Seattle, WA, USA Area Measured with Method 1668.

Atmospheric deposition can be an important pathway for the delivery of toxic polychlorinated biphenyls (PCBs) to ecosystems, especially in remote areas. Determining the sources of atmospheric PCBs can be difficult, because PCBs may travel long distances to reach the monitoring location, allowing for a variety of weathering processes that may alter PCB fingerprints. Previous efforts to determine the sources of atmospheric PCBs have been hampered by the electron capture detection methods used to measure PCBs. In this work, EPA method 1668, which is capable of measuring all 209 congeners, was used to measure PCBs in bulk atmospheric deposition at seven locations in the Green-Duwamish River watershed in and near Seattle, WA. Analysis of this data set via Positive Matrix Factorization allowed the identification of six factors that represent PCB sources. Four factors, representing approximately 88% of all PCB mass, are strikingly similar to unweathered Aroclors, suggesting minimal weathering during transport and/or local PCB sources at some sites. A fifth factor contained virtually all of the PCB 11 mass and represents PCBs from pigments. It explained approximately 39% of the Toxic Equivalency Quotient in the atmospheric deposition samples. The remaining factor contained non-Aroclor PCBs and may be related to silicone.

Alterations in fingerprints of polychlorinated biphenyls in benthic biota at the Portland Harbor Superfund Site (Oregon, USA) suggest metabolism.

In order to understand the sources and fate of polychlorinated biphenyls (PCBs) in several species of benthic biota, including clams (Corbicula fluminea), oligochaetes (Lumbriculus variegatus), and mussels (Margaritifera falcata and Anodonta nuttalliana) at the Portland Harbor Superfund Site (PHSS), their congener fingerprints were examined. First, diagnostic ratios of congeners known to be metabolizable vs. recalcitrant in the cytochrome P450 (CYP) pathway were significantly lower in biota than in its co-located sediment, indicating metabolism may have occurred. Next, the congener patterns were analyzed using Positive Matrix Factorization (PMF). The dominant fingerprint (by mass) in benthic biota is related to Aroclor 1260 but displays differences in the fingerprint that are consistent with weathering via absorption, distribution, metabolism, and excretion (ADME). This fingerprint is similar to one isolated from PCBs in fish from Washington State, indicative of common metabolic pathways and consistent with CYP metabolism. When metabolism is taken into account, the spatial distribution of the PMF-isolated PCB fingerprints in biota matches well with those from co-located sediment samples, suggesting that the same mix of sources at one location partitions into biota and sediment. In accordance to their higher hydrophobicity, higher molecular weight (MW) PCB formulations were proportionately more abundant in biota than in sediment, although low MW PCBs (e.g., PCBs 4 and 11) do bioaccumulate in benthic organisms and should not be ignored in risk assessment efforts. Finally, fingerprinting suggests potential reasons why lab-based and field-based biota-sediment accumulation factors (BSAFs) differ substantially for bivalves.