Telomeres as targets for the toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and polychlorinated biphenyls (PCBs) in rats

VanEtten, Samantha L.; Bonner, Matthew; Ren, Xuefeng; Birnbaum, Linda S.; Kostyniak, Paul J.; Wang, Jie; Olson, James R.

doi:10.1016/j.taap.2020.115264

Cited by 3 publications

(4 citation statements)

References 45 publications

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“…While differences are not explained by behavioral factors, such as diet or smoking 30 , 44 , a growing body of evidence suggests social structural factors like residential 48 , 49 and occupational 52 , 53 segregation are important contributors to racial disparities in exposure to environmental chemicals 78 . Given recent observational and experimental studies linking exposure to POPs with longer LTL 26 , 27 – 33 , 36 , we hypothesized that Black/White differences in LTL are explained by differences in exposure to PCBs, furans, and dioxins. Using various analytic methods, we found support for the hypothesis that exposure to POPs, and PCBs in particular, partially mediates Black/While differences in LTL.…”

Section: Discussionmentioning

confidence: 99%

“…In the only in vivo study to date, researchers found that exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and several PCB congeners, both alone and in combination, resulted in an increased LTL. Specifically, rats exposed to PCBs and TCDD had increased LTL in their liver and lung tissues as well as altered expression of genes related to telomere maintenance in their livers 36 .…”

Section: Introductionmentioning

confidence: 99%

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Persistent organic pollutant exposure contributes to Black/White differences in leukocyte telomere length in the National Health and Nutrition Examination Survey

Roberts

Boss

Mukherjee

et al. 2022

Sci Rep

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Despite racial disparities in diseases of aging and premature mortality, non-Hispanic Black Americans tend to have longer leukocyte telomere length (LTL), a biomarker of cellular aging, than non-Hispanic White Americans. Previous findings suggest that exposure to certain persistent organic pollutants (POPs) is both racially-patterned and associated with longer LTL. We examine whether Black/White differences in LTL are explained by differences in exposure to 15 POPs by estimating the indirect effect (IE) of self-reported race on LTL that is mediated through nine polychlorinated biphenyls (PCBs), three furans, and three dioxins, as well as their mixtures. Our study population includes 1,251 adults from the 1999–2000 and 2001–2002 cycles of the cross-sectional National Health and Nutrition Examination Survey. We characterized single-pollutant mediation effects by constructing survey-weighted linear regression models. We also implemented various approaches to quantify a global mediation effect of all POPs, including unpenalized linear regression, ridge regression, and examination of three summary exposure scores. We found support for the hypothesis that exposure to PCBs partially mediates Black/White differences in LTL. In single-pollutant models, there were significant IEs of race on LTL through six individual PCBs (118, 138, 153, 170, 180, and 187). Ridge regression (0.013, CI 0.001, 0.023; 26.0% mediated) and models examining summative exposure scores with linear combinations derived from principal components analysis (0.019, CI 0.009, 0.029; 34.8% mediated) and Toxic Equivalency Quotient (TEQ) scores (0.016, CI 0.005, 0.026; 28.8% mediated) showed significant IEs when incorporating survey weights. Exposures to individual POPs and their mixtures, which may arise from residential and occupational segregation, may help explain why Black Americans have longer LTL than their White counterparts, providing an environmental explanation for counterintuitive race differences in cellular aging.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Persistent organic pollutant exposure contributes to Black/White differences in leukocyte telomere length in the National Health and Nutrition Examination Survey

Roberts

Boss

Mukherjee

et al. 2022

Sci Rep

View full text Add to dashboard Cite

show abstract

“…of treatment accompanied with AhR activation and induction of ethoxyresorufin O-deethylase (EROD) activity (an early marker of PCBs induced oxidative stress) [67]. Moreover, by using a quantitative polymerase chain reaction (qPCR) to quantify relative telomere length in lung and liver samples collected from rats treated with different PCBs (126, 153 and a mixture of them) showed larger relative telomere length, which is an early indication of euplastic or non-neoplastic pathogenic disease development [68].…”

Section: Possible Hepatocarcinogenic Mechanisms Of Pcbsmentioning

confidence: 99%

Impact of PCBs, Furan and Dioxin on Hepatocarcinogenesis

Helal¹,

Ghanem²,

El-Sikaily³

2022

Environmental Sciences

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Stockholm Convention defined polychlorinated biphenyls (PCBs) as a group of persistent organic pollutants (POPs) such as dioxin/furan, dichlorodiphenyltrichloroethane, polychlorinated biphenyls, polychlorinated dibenzo-p-dioxins, aldrin, polychlorinated dibenzofurans and organometallic compounds (such as organotin and organomercury) which share the same characteristics of being persistent, bioaccumulative and toxic and can travel long distance through various media. They have diverse health impacts with different underlined molecular mechanisms. Recently, PCBs were referred as potent carcinogens with persistent existence in the environment. As the liver is the organ of detoxification, it is the major target organ for toxic effects induced by environmental contaminants, including PCBs. PCBs, furan and dioxin exert their hepatocarcinogenic effect through different mechanisms such as induction of oxidative stress, an increase of reactive oxygen species (ROS), mutagenic induction to oncogenes and epigenetic alteration to hepatic cells. In this chapter, we will provide an updated overview about PCBs, furan and dioxins, their impact on liver cancer initiation and progression on various in vivo and in vitro systems and its underlined molecular mechanisms. Also, a special emphasis will be directed to highlight zebrafish as in vivo model system to analyse the hepatocarcinogenic effect of these pollutants.

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“…Despite the large variety of POPs, they all have common properties, such as resistance to decomposition, extreme toxicity even at very low concentrations, abilities to bioaccumulate, transboundary transfer and deposition [VanEtten S.L. et al, 2020;Treger, 2011].…”

Section: Introductionmentioning

confidence: 99%

Estimation of Input of Unintentionally Produced Persistent Organic Pollutants into the Air Basin of the Odessa Industrial-and-Urban Agglomeration

Mykhailenko¹,

Safranov²

2021

J. Ecol. Eng.

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The environmental legislation in Ukraine is changing rapidly. These changes are related to the adaptation of Ukrainian laws to the requirements of the European Union. In this regard, the paper considers the unintentional production of Persistent Organic Pollutants (POPs) in the Odessa Industrial-and-Urban Agglomeration (next -Odessa agglomeration) in the context of new regulatory and legal requirements of Ukraine. In many countries around the world, the issue of pollution of environmental components by POPs has a large focus, because POPs pose a global threat to the environment and human health. The work aims to assess the main sources of unintentional production of POPs in the Odessa agglomeration during one year (2017), taking into account the new territorial features of the Odessa agglomeration. For the first time for Odessa agglomeration, the mass of POPs formed by main sources using the newest European methodological approach was calculated, sources of unintentional production of POPs on volumes of these substances were ranked, and their total mass of generation on the territory of Odessa agglomeration was calculated. The number of POPs molecules equivalent to 2,3,7,8-TСDD, which infiltrate into the air basin of the Odessa agglomeration, hence into the organisms of the agglomeration inhabitants, was calculated. The obtained results were compared with the allowable number per capita of the agglomeration, the relevant conclusions were drawn. Priority sources of unintentional production of POPs were identified, which allows taking appropriate preventive measures to reduce the scale of their generation.

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Telomeres as targets for the toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and polychlorinated biphenyls (PCBs) in rats

Cited by 3 publications

References 45 publications

Persistent organic pollutant exposure contributes to Black/White differences in leukocyte telomere length in the National Health and Nutrition Examination Survey

Persistent organic pollutant exposure contributes to Black/White differences in leukocyte telomere length in the National Health and Nutrition Examination Survey

Impact of PCBs, Furan and Dioxin on Hepatocarcinogenesis

Estimation of Input of Unintentionally Produced Persistent Organic Pollutants into the Air Basin of the Odessa Industrial-and-Urban Agglomeration

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