The toxicological profile of polychlorinated naphthalenes (PCNs)

Fernandes, Alwyn; Kilanowicz, Anna; Stragierowicz, Joanna; Klimczak, Michał; Falandysz, Jerzy

doi:10.1016/j.scitotenv.2022.155764

Cited by 37 publications

(8 citation statements)

References 134 publications

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“…In previous studies, the overexposure of many physical and chemical pollutants (Fernandes et al, 2022;Gamrad-Streubel et al, 2022;Nie et al, 2022) was reported to be associated with the dysregulations of the immune system. In a recent study, the causal association between diesel exhaust exposure and dysfunction of immune response was confirmed, and the usefulness of metabolomic analysis was shown (Cheng et al, 2022).…”

Section: Discussionmentioning

confidence: 99%

Plasma metabolomics analyses highlight the multifaceted effects of noise exposure and the diagnostic power of dysregulated metabolites for noise-induced hearing loss in steel workers

Zhang

Cui

et al. 2022

Front. Mol. Biosci.

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Noise exposure can lead to various kinds of disorders. Noise-induced hearing loss (NIHL) is one of the leading disorders confusing the noise-exposed workers. It is essential to identify NIHL markers for its early diagnosis and new therapeutic targets for its treatment. In this study, a total of 90 plasma samples from 60 noise-exposed steel factory male workers (the noise group) with (NIHL group, n = 30) and without NIHL (non-NIHL group, n = 30) and 30 male controls without noise exposure (control group) were collected. Untargeted human plasma metabolomic profiles were determined with HPLC-MS/MS. The levels of the metabolites in the samples were normalized to total peak intensity, and the processed data were subjected to multivariate data analysis. The Wilcoxon test and orthogonal partial least square-discriminant analysis (OPLS-DA) were performed. With the threshold of p < 0.05 and the variable importance of projection (VIP) value >1, 469 differential plasma metabolites associated with noise exposure (DMs-NE) were identified, and their associated 58 KEGG pathways were indicated. In total, 33 differential metabolites associated with NIHL (DMs-NIHL) and their associated 12 KEGG pathways were identified. There were six common pathways associated with both noise exposure and NIHL. Through multiple comparisons, seven metabolites were shown to be dysregulated in the NIHL group compared with the other two groups. Through LASSO regression analysis, two risk models were constructed for NIHL status predication which could discriminate NIHL from non-NIHL workers with the area under the curve (AUC) values of 0.840 and 0.872, respectively, indicating their efficiency in NIHL diagnosis. To validate the results of the metabolomics, cochlear gene expression comparisons between susceptible and resistant mice in the GSE8342 dataset from Gene Expression Omnibus (GEO) were performed. The immune response and cell death-related processes were highlighted for their close relations with noise exposure, indicating their critical roles in noise-induced disorders. We concluded that there was a significant difference between the metabolite’s profiles between NIHL cases and non-NIHL individuals. Noise exposure could lead to dysregulations of a variety of biological pathways, especially immune response and cell death-related processes. Our results might provide new clues for noise exposure studies and NIHL diagnosis.

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Section: Discussionmentioning

confidence: 99%

Plasma metabolomics analyses highlight the multifaceted effects of noise exposure and the diagnostic power of dysregulated metabolites for noise-induced hearing loss in steel workers

Zhang

Cui

et al. 2022

Front. Mol. Biosci.

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“…TEFs reevaluated by the WHO in 2005 were used for PCDD/Fs and dl-PCBs. For PCNs, due to the absence of consensus on TEFs, raw data, the relative potencies (REPs) were from the recent review of Fernandes et al, 10 listing REPs for 24 tetra-to octaCNs on the basis of values used in recent works on human exposure, originating from several in vitro studies.…”

Section: Dietary Exposure and Associated Health Riskmentioning

confidence: 99%

“…The predominance of lower chlorinated congeners in products of animal origin reflects recent/chronic exposure since these congeners are metabolized. 10 As mentioned in section 3.4.1, lower chlorinated PCNs are also associated with thermal emissions; 40 to investigate this source, the fractions of some combustion-related PCN congeners ( CR PCNs) to ∑PCNs were calculated and are presented in Table SI13. The ratios of ∑17 CR PCNs/∑70 PCNs described by Lee et al indicate re-emissions of historical Halowax mixtures (ratio <0.11) or combustion-related sources (ratio > 0.5).…”

Section: Linking Compositional Profiles To Emission Sources In Francementioning

confidence: 99%

“…8 PCNs cause multiple toxic responses in organisms, including hepatotoxicity or endocrine disruption, 9 most of them being related to dioxin-like effects mediated through their binding to the aryl hydrocarbon receptor (AhR). 10 This toxic potential is usually evaluated through toxic equivalent (TEQ), a concept in which the dioxin-like effects are recognized as additive. Moreover, it implies considering all the chemicals with the ability to exhort such effects.…”

Section: Introductionmentioning

confidence: 99%

“…6,7 This variety of sources led to the ubiquitous occurrence of PCNs in all the environmental compartments, including food. 8 PCNs cause multiple toxic responses in organisms, including hepatotoxicity or endocrine disruption, 9 most of them being related to dioxin-like effects mediated through their binding to the aryl hydrocarbon receptor (AhR). 10 This toxic potential is usually evaluated through toxic equivalent (TEQ), a concept in which the dioxin-like effects are recognized as additive.…”

Section: Introductionmentioning

confidence: 99%

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Polychlorinated Naphthalenes in Foods from the French Market: Occurrence, Dietary Exposure, and Evaluation of Relative Contributions to Dioxin-like Contaminants

Godéré,

Cariou,

Padioleau

et al. 2024

Environ. Sci. Technol.

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Despite the growing interest in PCNs and the dioxin-like toxicity exhibited by a number of congeners, a comprehensive assessment of their contribution to the cocktail of dioxin-like contaminants is still lacking. To address such a shortcoming, this study investigated the PCN contamination in foodstuffs recently acquired in France, together with that of the regulatory polychlorinated dibenzodioxins/furans (PCDD/Fs) and polychlorinated biphenyls (PCBs). PCNs were ubiquitous at levels (∑70 PCNs = 2.5−150 pg g −1 wet weight) similar to those reported in other countries, with maximum concentrations observed in fish and fishery products from the North-East Atlantic Ocean. Their congener patterns further suggested unintentional releases of PCNs, while those of the other foodstuffs were correlated to the historical PCN profiles. Low risk from dietary exposure was estimated (∑70 PCNs-EDIs of 60−360 pg kg −1 bw d −1 , ∑24 PCNs-TEQ-EDIs of 8 × 10 −3 −2.2 × 10 −2 pg TEQ kg −1 bw d −1 ), with milk and dairy products being the highest contributors, followed by meat and meat products. Finally, the rather high contributions of PCNs to the total PCNs+PCDD/Fs +PCBs concentrations (0.9−50%, average of 9%) and the toxic equivalents (0.2−24%, average of 5%) show that these substances are not minor components of the PCNs+PCDD/Fs+PCBs cocktail.

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WHO- and UNEP-Coordinated Exposure Studies 2000–2019: Findings of Polychlorinated Naphthalenes

Tschiggfrei,

Schächtele,

Fernandes

et al. 2023

Persistent Organic Pollutants in Human Milk

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The concentrations of polychlorinated naphthalenes (PCN) were determined in 40 pooled human milk samples from 39 countries covering all five of the United Nations regional groups. The samples were collected in the 2016–2019 exposure studies on persistent organic pollutants coordinated by the United Nations Environment Programme (UNEP).The median concentration of the sum of 26 PCN was 55 pg/g lipid (range 27 pg/g to 170 pg/g). Human milk from European countries showed considerably higher levels than those found in milk from countries in the African, Asia-Pacific, and Latin America/Caribbean regions. The most abundant congeners were the congener pairs PCN 52/60 and PCN 66/67 (inseparable by conventional chromatography) and to a lesser extent PCN 28/36, PCN 42, PCN 46, PCN 48, PCN 59, and PCN 69.Among other adverse biological effects, a critical response of many PCN congeners is dioxin-like toxicity. So, in addition to reporting concentrations of individual congeners, the toxic equivalents (TEQ) were also calculated in these samples, using two sets of relative effect potency (REP) values: a set that has been used in a number of human exposure studies and another set reported by Falandysz et al. (J Environ Sci Health, Part C: Environ Carcinogenesis Ecotoxicol Rev 32(3):239–272, 2014). The median PCN-TEQ concentration in human milk was 0.07 pg PCN-TEQ/g lipid (range 0.03 pg/g to 0.23 pg/g), when calculated using the human biomonitoring study REPs, and 0.03 pg PCN-TEQ/g lipid (range 0.01 pg/g to 0.10 pg/g), when calculated with other suggested REPs. The vast majority, about 90%, of this TEQ can be attributed to the PCN 66/67 congener pair. Individual REPs for PCN 66 and 67 from in vivo studies are quite different, but a chromatographic separation of these two congeners is not possible under routine GC conditions. Different approaches to estimate the uncertainties showed that the value of the REPs used is more important than the analytical problem to separate PCN 66 and PCN 67. PCN-TEQ based on the two sets of REPs differ approximately by a factor of 2.2, whereas the congener-specific determination was estimated to result in approximately 30% lower concentrations in comparison with the standard method.The assessment of PCN 66 and PCN 67 in order to obtain confirmed TEF would be most important for calculations of the dioxin-like toxicity of PCN, followed by PCN 69. Minor contributions to PCN-TEQ concentrations in human milk come from PCN 52/60, PCN 64/68, PCN 70, and PCN 73.On average, the contribution of PCN-TEQ to the cumulative TEQ (including the overall sum of toxic equivalents of PCDD, PCDF, and dioxin-like PCB [WHO2005-TEQ]) is between 1% and 2%, with a wider range of up to 5% for the 39 countries of this study. This is about an order of magnitude lower than the contribution of dioxin-like PCB to the cumulative TEQ (median 26%). In line with the observed higher total PCN concentrations, European countries also showed considerably higher levels of PCN-TEQ than found in the other regions. PCN-TEQ calculated with REPs used in human biomonitoring studies add on average about 2% to the cumulative TEQ of dioxin-like contaminants in Africa, the Asia-Pacific region, and Latin American and Caribbean countries and about 4% in European countries. The corresponding contribution of PCN-TEQ calculated using the other set would be 1% in non-European countries and 2% in European countries.

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The toxicological profile of polychlorinated naphthalenes (PCNs)

Cited by 37 publications

References 134 publications

Plasma metabolomics analyses highlight the multifaceted effects of noise exposure and the diagnostic power of dysregulated metabolites for noise-induced hearing loss in steel workers

Plasma metabolomics analyses highlight the multifaceted effects of noise exposure and the diagnostic power of dysregulated metabolites for noise-induced hearing loss in steel workers

Polychlorinated Naphthalenes in Foods from the French Market: Occurrence, Dietary Exposure, and Evaluation of Relative Contributions to Dioxin-like Contaminants

WHO- and UNEP-Coordinated Exposure Studies 2000–2019: Findings of Polychlorinated Naphthalenes

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