Non-dioxin-like Polychlorinated Biphenyls Research Articles

Endometriosis and Organochlorinated Environmental Pollutants: A Case–Control Study on Italian Women of Reproductive Age

BackgroundEndometriosis is a common gynecologic disease characterized by the ectopic growth of endometrial tissue. In industrialized countries, it affects approximately 10% of women of reproductive age. Its etiology is unclear, but a multifactorial origin is considered to be most plausible. Environmental organochlorinated persistent pollutants, in particular dioxins and polychlorinated biphenyls (PCBs), have been hypothesized to play a role in the disease etiopathogenesis. However, results of studies carried out on humans are conflicting.ObjectiveWe evaluated the exposure to organochlorinated persistent pollutants as a risk factor for endometriosis.MethodsWe conducted a case–control study in Rome on 158 women comprising 80 cases and 78 controls. In all women, serum concentrations of selected non-dioxin-like PCBs (NDL-PCBs) and dioxin-like PCBs (DL-PCBs), 1,1-dichloro-2,2,-bis(4-chlorophenyl)-ethene (p,p′-DDE), and hexachlorobenzene (HCB) were determined by ion-trap mass spectrometry. DR-CALUX bioassay was employed to assess the 2,3,7,8-tetrachlorodibenzo-p-dioxin toxicity equivalent (TEQ) concentrations of polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), and DL-PCBs.ResultsWe found an increased risk of endometriosis for DL-PCB-118 [odds ratio (OR) = 3.79; 95% confidence interval (CI), 1.61–8.91], NDL-PCB-138 (OR = 3.78; 95% CI, 1.60–8.94), NDL-PCB-153 (OR = 4.88; 95% CI, 2.01–11.0), NDL-PCB-170 (OR = 3.52; 95% CI, 1.41–8.79), and the sum of DL-PCBs and NDL-PCBs (OR = 5.63; 95% CI, 2.25–14.10). No significant associations were observed with respect to HCB or to the sum of PCDDs, PCDFs, and DL-PCBs given as total TEQs.ConclusionsThe results of this study show that an association exists between increased PCB and p,p′-DDE serum concentrations and the risk of endometriosis.

Accumulation features and temporal trends of PCDDs, PCDFs and PCBs in Baikal seals ( Pusa sibirica)

This study investigated the accumulation features and temporal trends of PCDD/Fs, dioxin-like PCBs (DL-PCBs) and non-dioxin-like PCBs (NDL-PCBs) in the blubber of Baikal seals collected in 1992 and 2005. DL-PCBs (480–3600 ng/g) and NDL-PCBs (980–35,000 ng/g) were dominant contaminants. Concentrations of PCDDs and PCBs in males were significantly higher than in females. In males, age-dependent accumulation was observed for PCDDs, mono- ortho PCBs and NDL-PCBs. PCDFs and non- ortho PCBs showed no such trends, implying that exposure of seals to these contaminants has been decreasing in recent years. No decreasing temporal trend was observed for PCDDs, mono- ortho PCBs and NDL-PCBs, suggesting that Baikal seals are still exposed to PCDDs and PCBs. TEQs of PCDDs and mono- ortho PCBs in seals collected in 2005 accounted for 62–77% of total TEQs. The TEQ levels in 40% of the specimens exceeded the threshold level for immunosuppression observed in harbor seals (209 pg/g).

The 2,2′,4,4′,5,5′-Hexachlorobiphenyl–Enhanced Degradation of Connexin 43 Involves Both Proteasomal and Lysosomal Activities

One of the toxic effects of non-dioxin-like polychlorinated biphenyls (NDL-PCBs) is the acute inhibition of gap junctional intercellular communication (GJIC), an event possibly associated with tumor promotion. The model NDL-PCB-2,2',4,4',5,5'-hexachlorobiphenyl (PCB 153)-induces a sustained GJIC inhibition in rat liver epithelial WB-F344 cells. As this effect might be related to deregulation of connexin 43 (Cx43) synthesis, trafficking, or degradation, we investigated the impact of PCB 153 on these events. Although PCB 153 had no effect on Cx43 mRNA levels, it induced a gradual loss of Cx43 protein and significantly decreased the amount of gap junction plaques in plasma membrane. PCB 153 contributed to extracellular signal-regulated kinases 1 and 2 (ERK1/2)-dependent accumulation of hyperphosphorylated Cx43-P3 form, thus indicating that ERK1/2 activation by PCB 153 might contribute to its effects on Cx43 internalization or degradation. Inhibition of either proteasomes or lysosomes with their specific inhibitors largely restored total Cx43 protein levels, thus suggesting that both proteasomes and lysosomes may participate in the PCB 153-enhanced Cx43 internalization and degradation. However, neither the proteasomal nor the lysosomal inhibitors restored normal GJIC or number/size of gap junction plaques. Finally, PCB 153 also interfered with restoration of gap junction plaques following the inhibition of Cx43 transport to plasma membrane. Taken together, multiple modes of action seem to contribute to downregulation of Cx43 in PCB 153-treated rat liver epithelial cells. The enhanced degradation of Cx43, together with persistent inhibition of GJIC, might contribute to tumor-promoting effects of NDL-PCBs.

Assessment of the dietary exposure to non-dioxin-like PCBs of the Italian general population

The dietary intake of non-dioxin-like polychlorinated biphenyls (NDL-PCBs) has been estimated using the sum of six indicator PCBs (Σ 6(PCBs)) in the Italian general population. Data from a national food consumption survey were combined with the mean concentration values of the individual six indicator PCBs (IUPAC Nos. 28, 52, 101, 138, 153, and 180) in foodstuffs available on the European market. Mean concentrations were estimated from the raw data set provided by the European Commission (DG SANCO). The purpose was to describe the distribution of NDL-PCB dietary intake in the Italian population, and to investigate to what extent the variability in dietary habits may cause higher exposures to the aforesaid contaminants. Results indicated a mean dietary intake of Σ 6(PCBs) corresponding to 24.6, 16.1, and 10.9 ng kg-bw −1 day −1 for toddlers (0.5–6 years old, excluding breastfeeding), children (7–12 year old), and adults (13–94 years old), respectively. Fish and fishery products and milk and dairy products were the major contributors to the total dietary intake. The highest exposures due to variation in dietary habits were in general two–three times higher than the corresponding mean values and they were generally due to a higher fish consumption rate. The NDL-PCB dietary intake decreased with age until about 10–12 years; afterwards it appeared to remain constant. The tolerable daily intake (TDI) has not been established for these contaminants; however, action and maximum allowed levels in feeding stuffs and food recently established by the European Commission for dioxin-like PCBs could also protect consumers from exposure to NDL-PCBs.

Serum levels of PCDDs, PCDFs and PCBs in non-occupationally exposed population groups living near two incineration plants in Tuscany, Italy

A pilot study was carried out in Tuscany, Italy, to provide preliminary information on the concentrations of polychlorinated dibenzodioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), dioxin-like polychlorobiphenyls (DL-PCBs), and selected non-dioxin-like PCBs (NDL-PCBs) in groups of subjects living in the vicinity of two incineration plants. Seventy-four volunteers were enrolled from areas identified as under a potential impact from incinerator emissions and from not exposed areas. No significant differences were observed between subjects living in the two types of areas. Total concentrations of PCDDs, PCDFs, and DL-PCBs resulted to be in the range 23–30 pg WHO–TEQ g −1, lipid base, for subjects in the 27–54 year age groups, while concentrations increased to 40–44 pgTEQ g −1 for the two 55–67 year age groups. The levels of PCDDs and PCDFs were in good agreement with those observed for unexposed population groups in Italy, while the contribution to total TEQ from DL-PCBs was appreciably higher than those currently observed in the general population in Italy and other countries. As to NDL-PCBs, serum levels of the six “indicator” congeners were in the range 240–300 ng g −1, lipid base, for subjects in the 27–54 year age groups. A raise in NDL-PCB body burden (430–470 ng g −1, lipid base) was observed for the two 55+ year age groups, in agreement with the expected age-dependent increase. The findings from this study do not show an incremental exposure to PCDDs and PCDFs in the samples from subjects living around the two incineration plants, whereas PCB congener profiles in all samples suggest a possible impact on the area of interest of industrial activities from near industrial settlements.

Selection of non-dioxin-like PCBs for in vitro testing on the basis of environmental abundance and molecular structure

The non-dioxin-like polychlorinated biphenyls (NDL-PCBs) constitute the major proportion of PCBs found in food and human tissues. It is important to improve our understanding of the toxicity, environmental and human risks associated with the NDL-PCBs, since their toxicology is incompletely characterized and a human health risk assessment is required. This paper discusses the selection of a training set of 20 tri- to hepta-chlorinated biphenyls, PCBs 19,28,47,51,52,53,74,95,100,101,104,118,122,128,136,138,153,170,180, and 190. Suggested for comprehensive screening using in vitro assays to identify critical mechanisms of toxicological action. The selected PCBs form a balanced basis for developing of quantitative structure-activity relationship (QSAR) models for prediction of physicochemical and toxicological properties of non-tested PCB congeners. Chemical and physical properties, environmental abundance and toxicological activities of the congeners were considered during the selection process. A complementary set of PCBs, a reference set, was selected using D-optimal onion design including PCBs 18,20,28,30,37,40,50,54,60,77,82,99,122,132,153,161,170,188,192, and 193. Congeners of this set are well suited for validation of QSAR models developed using the training set. For visualization of the chemical diversity of environmentally abundant PCBs and congeners of the training and reference sets, principal component analysis (PCA) was used. Statistical molecular design was used to verify the structural representation. As a reference structure for dioxin-like PCBs, PCB 126 was added in the training set. The selected set of NDL-PCBs is proposed for use in toxicological testing programs to provide rational basis for risk assessment of the NDL-PCBs.

Non-dioxin-like polychlorinated biphenyls induce a release of arachidonic acid in liver epithelial cells: A partial role of cytosolic phospholipase A 2 and extracellular signal-regulated kinases 1/2 signalling

Non-dioxin-like polychlorinated biphenyls (NDL-PCBs) have been shown to act as tumor promoters in liver; however, the exact mechanisms of their action are still only partially understood. One of the interesting effects of NDL-PCBs is the acute inhibition of gap junctional intercellular communication (GJIC), an effect, which has been often found to be associated with tumor promotion. As previous studies have suggested that NDL-PCB-induced disruption of lipid signalling pathways might correspond with GJIC inhibition, we investigated effects of PCBs on the release of arachidonic acid (AA) in the rat liver epithelial WB-F344 cell line, a well-established model of liver progenitor cells. We found that both 2,2′,4,4′-tetrachlorobiphenyl (PCB 47) and 2,2′,4,4′,5,5′-hexachlorobiphenyl (PCB 153), but not the dioxin-like, non- ortho-substituted, 3,3′,4,4′,5-pentachlorobiphenyl (PCB 126), induce a massive release of AA. The AA release, induced by PCB 153, was partially inhibited by extracellular signal-regulated kinases 1/2 (ERK1/2) signalling inhibitor, U0126, and by cytosolic phospholipase A 2 (cPLA 2) inhibitor, AACOCF 3. Although PCB 153 induced both ERK1/2 and p38 activation, the specific p38 kinase inhibitor, SB203580, had no effect on AA release. Inhibitors of other phospholipases, including phosphatidylcholine-specific phospholipase C or phosphatidylinositol-specific phospholipase C, were also without effect. Taken together, our findings suggest that the AA release, induced by non-dioxin-like PCBs in liver progenitor cell line, is partially mediated by cytosolic PLA 2 and regulated by ERK1/2 kinases. Our results suggest that more attention should be paid to cell signalling pathways regulated by AA or eicosanoids after PCB exposure, which might be involved in their toxic effects.

Pesticide and non-dioxin-like polychlorinated biphenyls (NDL-PCBs) residues in foodstuffs from Ismailia city, Egypt

Samples of vegetables and cereals from Egypt were screened for 113 pesticides, of which 68 were quantified, using gas chromatography-mass spectrometry (GC/MS) with limits of detection (LODs) ranging from 0.02 to 1.9 µg kg−1. In addition, the residues of 17 non-dioxin-like polychlorinated biphenyls (NDL-PCBs) were measured in samples of animal origin (meat, dairy products and seafood) using high-resolution gas chromatography (HRGC)/high-resolution mass spectroscopy (HRMS). None of the cereal samples and 72.7% of the vegetables contained any detectable levels of the pesticides. Detectable residues, not exceeding the current European Union maximum residue limits (MRLs) were found in 27.3% of vegetables. The estimated daily intake for detected pesticides was well below their corresponding acceptable daily intake (ADI), with exposure ranges between 0.002% of the ADI for profenofos and 0.2% of the ADI for lambda-cyhalothrin. The sum concentration of 17 PCBs congeners varied between 2.5 and 322 ng g−1 fat, corresponding to 1.7-216 ng g−1 fat for the seven indicator PCBs. The highest values were measured in seafood, the lowest in dairy products. Hexa-CB 153, 138 and hepta-CB180 were the congeners with the highest contribution. PCBs congener profiles found in most of the samples were consistent with the expected profile for Aroclor 1260 and 1262. PCBs’ contamination levels reported in this paper were many times lower than in developed countries, except for chicken samples. Also, the dietary intake of seven indicator PCBs due to the consumption of food of animal origin (4.84 ng kg−1 body weight day−1) from Ismailia city, Egypt, is several times lower than the intake in European Union countries.

Pesticide and non-dioxin-like polychlorinated biphenyls (NDL-PCBs) residues in foodstuffs from Ismailia city, Egypt

Pesticide and non-dioxin-like polychlorinated biphenyls (NDL-PCBs) residues in foodstuffs from Ismailia city, Egypt

Association between Serum Concentrations of Persistent Organic Pollutants and Self-Reported Cardiovascular Disease Prevalence: Results from the National Health and Nutrition Examination Survey, 1999–2002

BackgroundThere is now increasing evidence that exposure to persistent organic pollutants (POPs) can contribute to the development of inflammatory diseases such as atherosclerosis.ObjectiveThe objective of this study was to examine associations of serum concentrations of POPs with self-reported history of cardiovascular disease (CVD).DesignCross-sectional associations of serum POPs concentrations with the prevalence of self-reported CVD were investigated in 889 adults ≥ 40 years of age in the National Health and Nutrition Examination Survey, 1999–2002. We selected 21 POPs [3 polychlorinated dibenzo-p-dioxins (PCDDs), 3 polychlorinated dibenzofurans (PCDFs), 5 dioxin-like polychlorinated biphenyls (PCBs), 6 nondioxin-like PCBs, and 4 organochlorine (OC) pesticides] because they were detectable in ≥ 60% of participants.ResultsDioxin-like PCBs, nondioxin-like PCBs, and OC pesticides were positively associated with the prevalence of CVD only among females. Compared with those in the lowest quartile of serum concentration, the odds ratios for CVD across increasing quartiles were 0.9, 2.0, and 5.0 for dioxin-like PCBs (p for trend < 0.01), 1.2, 1.2, and 3.8 for nondioxin-like PCBs (p for trend < 0.01), and 1.9, 1.7, and 4.0 for OC pesticides (p for trend = 0.03). PCDDs showed positive trends with the prevalence of CVD in both males and females; adjusted odds ratios were 1.4, 1.7, and 1.9 (p for trend = 0.07, males and females combined).ConclusionsOur findings need to be carefully interpreted because of the cross-sectional design and use of self-reported CVD. Prospective studies are needed to clarify these associations.

Extended Analyses of the Association Between Serum Concentrations of Persistent Organic Pollutants and Diabetes

We recently reported on serum concentrations of six persistent organic pollutants (POPs) and prevalence of diabetes in a random U.S. sample (1). Most previous epidemiological studies were restricted from studying several POPs given cost and serum amounts needed. Focus on selected POPs may be appropriate in occupational or accidental high exposure, but, in the general population with only background POP exposure, there is a need to study the concentrations of many interrelated POPs. Our initial approach to risk characterization was to calculate a summary to accumulate risk of exposure across six POPs (1). Even though the summary of six POPs was strongly associated with diabetes, individual POPs had substantial differences in strength of association (1). Thus, it is also of interest to estimate risk within subclasses of POPs that have similar physical and chemical properties. All POPs measured in the National Health and Nutrition Examination Survey (NHANES) can be divided into five subclasses: polychlorinated dibenzo- p -dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), dioxin-like polychlorinated biphenyls (PCBs), nondioxin-like PCBs, and organochlorine (OC) pesticides. Such specificity about diabetogenicity of POP subclasses would be especially important from the viewpoints of both toxicology and regulation. Therefore, in this article we report on the diabetes associations of 19 POPs within five POP subclasses, each detected among at least 60% of study subjects, i.e., in a manner …

Association Between Serum Concentrations of Persistent Organic Pollutants and Insulin Resistance Among Nondiabetic Adults

We reported strong relations between serum concentrations of persistent organic pollutants (POPs), especially organochlorine (OC) pesticides or nondioxin-like polychlorinated biphenyls (PCBs), and prevalence of diabetes in a U.S population with background exposure to POPs. Here, we investigated POPs and insulin resistance, a frequent pathogenic precursor of type 2 diabetes. Serum POPs and homeostasis model assessment of insulin resistance (HOMA-IR) were investigated cross-sectionally in 749 nondiabetic participants aged > or = 20 years. Nineteen POPs in five subclasses were selected, detectable in > or = 60% of participants. Among subclasses, OC pesticides were most strongly associated with HOMA-IR. Adjusted geometric means of HOMA were 3.27, 3.36, 3.48, and 3.85 (P for trend <0.01) across quartiles of OC pesticides. The relationship strengthened with increasing HOMA-IR percentile: adjusted odds ratios comparing the highest versus lowest POPs quartile were 1.8 for being > or = 50th percentile of HOMA-IR, 4.4 for being > or = 75th percentile, and 7.5 for being > or = 90th percentile. Associations with elevated HOMA-IR appeared to be specific to oxychlordane and trans-nonachlor but also were found for two nondioxin-like PCBs. No HOMA-IR associations were seen in the other three POP subclasses. The association between OC pesticides and HOMA-IR tended to strengthen as waist circumference increased, with no apparent association in the lowest quartile of OC pesticide concentrations. These findings, coupled with those concerning diabetes prevalence, suggest that OC pesticides and nondioxin-like PCBs may be associated with type 2 diabetes risk by increasing insulin resistance, and POPs may interact with obesity to increase the risk of type 2 diabetes.

Non-Coplanar PCB-Mediated Modulation of Human Leukocyte Phagocytosis: A New Mechanism for Immunotoxicity

Organochlorine (OC) contaminants, notably polychlorinated biphenyls (PCBs) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), are ubiquitous in all ecosystems and found in the tissues of humans and wildlife. Although the immunotoxicity of coplanar, dioxinlike PCBs is well documented, the adverse effects exerted by non-coplanar, non-dioxinlike PCBs have received little attention. Direct causal relationship between PCB and dioxin exposure and the observed detrimental effects on the immune system has yet to be fully established in humans. The immunomodulatory potential of toxic coplanar PCB 169 and TCDD and abundant non-coplanar PCBs 138, 153, and 180 on human leukocyte phagocytosis, an important innate immune function that initiates the clearance of pathogens, was tested upon in vitro exposure. Mixture and concentration-response experiments demonstrated a suppression of phagocytosis by non-coplanar PCBs suggesting a previously unrecognized aryl hydrocarbon receptor (AhR)-independent pathway. Regression analysis revealed that reduction of phagocytosis was mostly explained by the non-coplanar congeners. The effects on phagocytosis could not be accurately predicted by either the currently used toxic equivalence (TEQ) approach or the mouse model, thus undermining the use of the traditional models in the risk assessment for OC mixtures containing non-coplanar congeners. Our results are cause for concern as they suggest an AhR-independent pathway through which non-coplanar PCBs modulate phagocytosis, the immune system's first line of defense, possibly increasing the risk to developing infectious disease.

Consumption advisories for salmon based on risk of cancer and noncancer health effects

The levels of dioxins/furans, polychlorinated biphenyls (PCBs), and chlorinated pesticides were determined in farmed salmon for eight regions in Europe, North America, and South America, in salmon fillets purchased in 16 cities in Europe and North America, and in five species of wild Pacific salmon. Upon application of US Environmental Protection Agency (USEPA) methods for developing fish consumption advisories for cancer from mixtures of all of these substance for which USEPA has reported a cancer slope factor, the most stringent recommendation, for farmed salmon from northern Europe, was for consumption of at most one meal every 5 months in order to not exceed an elevated risk of cancer of more than 1 in 100,000. Farmed salmon from North and South America triggered advisories of between 0.4 and one meal per month. Retail market samples, in general, reflected levels found in regionally farmed fish, although much of the US salmon comes from Chile, which had somewhat lower contaminant levels than the North American farmed samples. Upon consideration of all of these organochlorine compounds as a mixture, even wild Pacific salmon triggered advisories of between one and less than five meals per month. The advisories are driven by the nondioxin-like PCBs and pesticides and not by dioxins/furans and coplanar PCBs. For noncancer effects for contaminants where USEPA has provided a reference dose only endrin and PCBs triggered any significant advisory. For both of these in the worst case, farmed salmon from northern Europe, the advice was not more than three meals per month.

Quantitation of polychlorinated biphenyls in fish for human cancer risk assessment: A comparative case study

A range of analytical options is available for the quantification of environmental polychlorinated biphenyls (PCBs). The PCBs can be quantified as Aroclor mixtures, as individual PCB congeners, or as PCB homologues. The methodological choice is driven by many considerations, including cost, but it is important to note that the risk assessment methods recommended by the U.S. Environmental Protection Agency (U.S. EPA) have specific and varying requirements for these analytical endpoints. The toxic equivalency approach is recommended for settings where the original Aroclor mixtures have been heavily degraded or weathered. Because this method only addresses the dioxin-like fraction of the PCB mass, the remaining PCB congeners need to be quantified and assessed separately, in a manner that is consistent with current U.S. EPA guidance. In this present analysis, we examined various methods for estimating a total nondioxin-like PCB mass in fish tissue samples from a New Jersey waterway using congener and homologue data: The National Oceanic and Atmospheric Administration estimate of the PCB total based on 18 congeners sigma dioxin-like congeners, an estimate of the PCB total from 38 analyzed congeners--sigma dioxin-like congeners, and the total of nine homologue groups--sigma dioxin-like congeners. These three approaches yielded similar estimates of the total nondioxin-like PCBs for a variety of fish species, whereas the totals quantified as Aroclor 1248, 1254, or 1260 were typically more than fivefold lower. Based on these results, the selection of the PCB analytical endpoints obtained from field investigations of fish and shellfish should be guided by the appropriate risk assessment methodology and by the analytical limitations.

Inhibition of ethoxyresorufin-O-deethylase (EROD) activity in mixtures of 2,3,7,8-tetrachlorodibenzo-p-dioxin and polychlorinated biphenyls

Induction of ethoxyresorufin-O-deethylase (EROD) activity and porphyrin accumulation shows different structure-activity relationships for different polychlorinated biphenyls (PCBs) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Interactions between the two responses can strongly influence the induction and activity of EROD. The results support the conclusion that there are nonadditive interactions between nondioxin-like PCBs and dioxin-like compounds. The interaction between EROD activity and the porphyrin biosynthesis makes the prerequisite of additivity in the toxic equivalency factor concept for environmental mixtures highly spurious. Inhibition of EROD activity caused by non-dioxin like compounds could have a significant impact on the value of EROD activity as a biomarker in the present methods of risk assessment for these compounds.

Immunopotentiation reverses the embryotoxic effect of serum from females with pregnancy loss

The 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) toxic equivalent quantity (TCDD-TEQ) approach was used successfully to predict lethal embryotoxicity in salmonids, but its applicability to sublethal effects of mixtures of organohalogenated compounds in other fish species is poorly known. The sublethal toxicity of two dioxin-like compounds (DLCs), 3,3′,4,4′-tetrachlorobiphenyl (PCB77) and 2,3,4,7,8-pentachlorodibenzofuran (2,3,4,7,8-PnCDF), two non-dioxin-like (NDL) polychlorinated biphenyls (PCBs), 2,2′,5,5′-tetrachlorobiphenyl (PCB52) and 2,3,3′,4′,6-pentachlorobiphenyl (PCB110), and of Aroclor 1254, a complex commercial mixture of PCBs, was assessed in Fundulus heteroclitus embryos exposed by intravitelline injection. At 16 days post-fertilization, the two DLCs and Aroclor 1254 altered prey capture ability in addition to inducing classical aryl hydrocarbon receptor-mediated responses: ethoxyresorufin-O-deethylase (EROD) induction, craniofacial deformities and reduction in body length. None of these responses was induced by the two NDL PCBs, at doses up to 5400 ng g−1 wet weight. Dose–response curves for prey capture ability for the 2 DLCs tested were not parallel to that of TCDD, violating a fundamental assumption for relative potency (ReP) estimation. Dose–response curves for EROD induction were parallel for 2,3,4,7,8-PnCDF and TCDD, but the ReP of 2,3,4,7,8-PnCDF for F. heteroclitus was 5-fold higher than the World Health Organization (WHO) fish toxic equivalent factor (TEF) based on embryolethality in salmonids. The chemically derived TCDD-TEQs of Aroclor 1254, calculated using 3,3′,4,4′,5-pentachlorobiphenyl (PCB126) concentrations and it ReP for F. heteroclitus, overestimated its potency to induce EROD activity possibly due to antagonistic interactions among PCBs. This study highlights the limitations of using TEFs based on salmonid toxicity data alone for risk assessment to other fish species. There is a need to assess the variability of RePs of DLCs in different species for a variety of endpoints and to better understand interactions between DLCs and other toxic chemicals.