Inhalable mixture of polycyclic aromatic hydrocarbons and metals, DNA oxidative stress and nasal ribosomal DNA copy number amplification: Direct and indirect effect analyses among population

The ribosomal DNA (rDNA) plays a crucial role in maintaining genome stability. So far, alterations of rDNA from airborne pollutants exposure remain unclear. Nasal epithelial cells are the earliest respiratory barrier, which has an accessible surrogate for evaluating respiratory impairment. We develo...

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Veröffentlicht in:Journal of hazardous materials 2023-08, Vol.455, p.131538-131538, Article 131538
Hauptverfasser: Wang, Yanhua, Meng, Tao, Zhang, Liya, Lin, Yang, Wu, Nan, Yuan, Huige, He, Zhizhou, Niu, Yong, Dai, Yufei, Zhao, Xing, Duan, Huawei
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container_title Journal of hazardous materials
container_volume 455
creator Wang, Yanhua
Meng, Tao
Zhang, Liya
Lin, Yang
Wu, Nan
Yuan, Huige
He, Zhizhou
Niu, Yong
Dai, Yufei
Zhao, Xing
Duan, Huawei
description The ribosomal DNA (rDNA) plays a crucial role in maintaining genome stability. So far, alterations of rDNA from airborne pollutants exposure remain unclear. Nasal epithelial cells are the earliest respiratory barrier, which has an accessible surrogate for evaluating respiratory impairment. We developed a mixture-centered biomarkers study integrated epidemiological and biological evidence among 768 subjects, a mixture of polycyclic aromatic hydrocarbons (PAHs) and metals. We identified the mixed exposure of PAHs and metals by environmental and biological monitoring, selected urinary 8-hydroxy-2′-deoxyguanosine as DNA oxidative stress marker, and measured their rDNA copy number (rDNA CN) in nasal epithelial cells. We performed linear regression, adaptive elastic net regression, BKMR, and mediation analyses to assess the direct and indirect effects. We found a 10% elevation in urinary 1-hydroxypyrene was correlated with a separate 0.31% and 0.82% amplification of nasal 5S and 45S rDNA CN, respectively (all P 
doi_str_mv 10.1016/j.jhazmat.2023.131538
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So far, alterations of rDNA from airborne pollutants exposure remain unclear. Nasal epithelial cells are the earliest respiratory barrier, which has an accessible surrogate for evaluating respiratory impairment. We developed a mixture-centered biomarkers study integrated epidemiological and biological evidence among 768 subjects, a mixture of polycyclic aromatic hydrocarbons (PAHs) and metals. We identified the mixed exposure of PAHs and metals by environmental and biological monitoring, selected urinary 8-hydroxy-2′-deoxyguanosine as DNA oxidative stress marker, and measured their rDNA copy number (rDNA CN) in nasal epithelial cells. We performed linear regression, adaptive elastic net regression, BKMR, and mediation analyses to assess the direct and indirect effects. We found a 10% elevation in urinary 1-hydroxypyrene was correlated with a separate 0.31% and 0.82% amplification of nasal 5S and 45S rDNA CN, respectively (all P &lt; 0.05). A 10% increment of urine nickel was associated with a separate 0.37% and 1.18% elevation of nasal 5S and 45S rDNA CN, respectively (all P &lt; 0.05). BKMR results also confirmed our findings of PAHs and nickel. Our findings suggested that DNA oxidative stress might trigger rDNA instability induced by inhaled PAHs and metals. [Display omitted] •The nasal rDNA CN amplification presented in PAHs and metals exposed population.•PAHs and Ni in the mixture played a substantial role in expanding nasal rDNA.•DNA oxidative stress might trigger rDNA instability induced by inhaled PAHs and Ni.•Nasal rDNA alteration may serve as the predictive biomarker of respiratory impairment.</description><identifier>ISSN: 0304-3894</identifier><identifier>EISSN: 1873-3336</identifier><identifier>DOI: 10.1016/j.jhazmat.2023.131538</identifier><identifier>PMID: 37156045</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>8-Hydroxy-2'-Deoxyguanosine ; Biomarkers ; DNA Copy Number Variations ; DNA, Ribosomal ; Humans ; Metals ; Metals - toxicity ; Nasal epithelial cell ; Nickel ; Oxidative Stress ; Polycyclic aromatic hydrocarbons ; Polycyclic Aromatic Hydrocarbons - analysis ; Polycyclic Aromatic Hydrocarbons - toxicity ; Ribosomal DNA instability</subject><ispartof>Journal of hazardous materials, 2023-08, Vol.455, p.131538-131538, Article 131538</ispartof><rights>2023</rights><rights>Copyright © 2023. 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So far, alterations of rDNA from airborne pollutants exposure remain unclear. Nasal epithelial cells are the earliest respiratory barrier, which has an accessible surrogate for evaluating respiratory impairment. We developed a mixture-centered biomarkers study integrated epidemiological and biological evidence among 768 subjects, a mixture of polycyclic aromatic hydrocarbons (PAHs) and metals. We identified the mixed exposure of PAHs and metals by environmental and biological monitoring, selected urinary 8-hydroxy-2′-deoxyguanosine as DNA oxidative stress marker, and measured their rDNA copy number (rDNA CN) in nasal epithelial cells. We performed linear regression, adaptive elastic net regression, BKMR, and mediation analyses to assess the direct and indirect effects. We found a 10% elevation in urinary 1-hydroxypyrene was correlated with a separate 0.31% and 0.82% amplification of nasal 5S and 45S rDNA CN, respectively (all P &lt; 0.05). A 10% increment of urine nickel was associated with a separate 0.37% and 1.18% elevation of nasal 5S and 45S rDNA CN, respectively (all P &lt; 0.05). BKMR results also confirmed our findings of PAHs and nickel. Our findings suggested that DNA oxidative stress might trigger rDNA instability induced by inhaled PAHs and metals. [Display omitted] •The nasal rDNA CN amplification presented in PAHs and metals exposed population.•PAHs and Ni in the mixture played a substantial role in expanding nasal rDNA.•DNA oxidative stress might trigger rDNA instability induced by inhaled PAHs and Ni.•Nasal rDNA alteration may serve as the predictive biomarker of respiratory impairment.</description><subject>8-Hydroxy-2'-Deoxyguanosine</subject><subject>Biomarkers</subject><subject>DNA Copy Number Variations</subject><subject>DNA, Ribosomal</subject><subject>Humans</subject><subject>Metals</subject><subject>Metals - toxicity</subject><subject>Nasal epithelial cell</subject><subject>Nickel</subject><subject>Oxidative Stress</subject><subject>Polycyclic aromatic hydrocarbons</subject><subject>Polycyclic Aromatic Hydrocarbons - analysis</subject><subject>Polycyclic Aromatic Hydrocarbons - toxicity</subject><subject>Ribosomal DNA instability</subject><issn>0304-3894</issn><issn>1873-3336</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc9u1DAQxi0EokvhEUA-ciCLvY7zhwuqWmgrVXCBszWxJ6xXjh3spGp4OJ4Nd7Nw5WR79PvmG89HyGvOtpzx6v1he9jDrwGm7Y7txJYLLkXzhGx4U4tCCFE9JRsmWFmIpi3PyIuUDowxXsvyOTkTNZcVK-WG_L71e3DQOaSDfZjmiDT0dAxu0Yt2VlOIIZvky34xMWiIXfCJgjd0wAlcekevvlzQ8GBNpu6RpiliWgEPCRyNtgsp93BHUIdxoX4eOowUhtHZ3uosDP4DvbIR9XRUWm_WB_b9WgO3JMxth-B_5PHG2R1VL8mzPg-Br07nOfn--dO3y5vi7uv17eXFXaFFJadCYCUb07bSdK2oyxpqCQ1IMJ3WRlR9U7bMVKzJxRa1YRVmGrDvWL2rOWfinLxd-44x_JwxTWqwSaNz4DHMSe0anjda1YJnVK6ojiGliL0aox0gLooz9RidOqhTdOoxOrVGl3VvThZzN6D5p_qbVQY-rgDmj95bjCppi17juitlgv2PxR89z7IS</recordid><startdate>20230805</startdate><enddate>20230805</enddate><creator>Wang, Yanhua</creator><creator>Meng, Tao</creator><creator>Zhang, Liya</creator><creator>Lin, Yang</creator><creator>Wu, Nan</creator><creator>Yuan, Huige</creator><creator>He, Zhizhou</creator><creator>Niu, Yong</creator><creator>Dai, Yufei</creator><creator>Zhao, Xing</creator><creator>Duan, Huawei</creator><general>Elsevier B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-2717-7936</orcidid><orcidid>https://orcid.org/0009-0008-9527-2936</orcidid></search><sort><creationdate>20230805</creationdate><title>Inhalable mixture of polycyclic aromatic hydrocarbons and metals, DNA oxidative stress and nasal ribosomal DNA copy number amplification: Direct and indirect effect analyses among population</title><author>Wang, Yanhua ; Meng, Tao ; Zhang, Liya ; Lin, Yang ; Wu, Nan ; Yuan, Huige ; He, Zhizhou ; Niu, Yong ; Dai, Yufei ; Zhao, Xing ; Duan, Huawei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c365t-3e658d995db93747a75a8a5adbccd36f8490d608a8a9ecd06e8d9aefb07271103</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>8-Hydroxy-2'-Deoxyguanosine</topic><topic>Biomarkers</topic><topic>DNA Copy Number Variations</topic><topic>DNA, Ribosomal</topic><topic>Humans</topic><topic>Metals</topic><topic>Metals - toxicity</topic><topic>Nasal epithelial cell</topic><topic>Nickel</topic><topic>Oxidative Stress</topic><topic>Polycyclic aromatic hydrocarbons</topic><topic>Polycyclic Aromatic Hydrocarbons - analysis</topic><topic>Polycyclic Aromatic Hydrocarbons - toxicity</topic><topic>Ribosomal DNA instability</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Yanhua</creatorcontrib><creatorcontrib>Meng, Tao</creatorcontrib><creatorcontrib>Zhang, Liya</creatorcontrib><creatorcontrib>Lin, Yang</creatorcontrib><creatorcontrib>Wu, Nan</creatorcontrib><creatorcontrib>Yuan, Huige</creatorcontrib><creatorcontrib>He, Zhizhou</creatorcontrib><creatorcontrib>Niu, Yong</creatorcontrib><creatorcontrib>Dai, Yufei</creatorcontrib><creatorcontrib>Zhao, Xing</creatorcontrib><creatorcontrib>Duan, Huawei</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of hazardous materials</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Yanhua</au><au>Meng, Tao</au><au>Zhang, Liya</au><au>Lin, Yang</au><au>Wu, Nan</au><au>Yuan, Huige</au><au>He, Zhizhou</au><au>Niu, Yong</au><au>Dai, Yufei</au><au>Zhao, Xing</au><au>Duan, Huawei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhalable mixture of polycyclic aromatic hydrocarbons and metals, DNA oxidative stress and nasal ribosomal DNA copy number amplification: Direct and indirect effect analyses among population</atitle><jtitle>Journal of hazardous materials</jtitle><addtitle>J Hazard Mater</addtitle><date>2023-08-05</date><risdate>2023</risdate><volume>455</volume><spage>131538</spage><epage>131538</epage><pages>131538-131538</pages><artnum>131538</artnum><issn>0304-3894</issn><eissn>1873-3336</eissn><abstract>The ribosomal DNA (rDNA) plays a crucial role in maintaining genome stability. So far, alterations of rDNA from airborne pollutants exposure remain unclear. Nasal epithelial cells are the earliest respiratory barrier, which has an accessible surrogate for evaluating respiratory impairment. We developed a mixture-centered biomarkers study integrated epidemiological and biological evidence among 768 subjects, a mixture of polycyclic aromatic hydrocarbons (PAHs) and metals. We identified the mixed exposure of PAHs and metals by environmental and biological monitoring, selected urinary 8-hydroxy-2′-deoxyguanosine as DNA oxidative stress marker, and measured their rDNA copy number (rDNA CN) in nasal epithelial cells. We performed linear regression, adaptive elastic net regression, BKMR, and mediation analyses to assess the direct and indirect effects. We found a 10% elevation in urinary 1-hydroxypyrene was correlated with a separate 0.31% and 0.82% amplification of nasal 5S and 45S rDNA CN, respectively (all P &lt; 0.05). A 10% increment of urine nickel was associated with a separate 0.37% and 1.18% elevation of nasal 5S and 45S rDNA CN, respectively (all P &lt; 0.05). BKMR results also confirmed our findings of PAHs and nickel. Our findings suggested that DNA oxidative stress might trigger rDNA instability induced by inhaled PAHs and metals. [Display omitted] •The nasal rDNA CN amplification presented in PAHs and metals exposed population.•PAHs and Ni in the mixture played a substantial role in expanding nasal rDNA.•DNA oxidative stress might trigger rDNA instability induced by inhaled PAHs and Ni.•Nasal rDNA alteration may serve as the predictive biomarker of respiratory impairment.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>37156045</pmid><doi>10.1016/j.jhazmat.2023.131538</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0002-2717-7936</orcidid><orcidid>https://orcid.org/0009-0008-9527-2936</orcidid></addata></record>
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subjects 8-Hydroxy-2'-Deoxyguanosine
Biomarkers
DNA Copy Number Variations
DNA, Ribosomal
Humans
Metals
Metals - toxicity
Nasal epithelial cell
Nickel
Oxidative Stress
Polycyclic aromatic hydrocarbons
Polycyclic Aromatic Hydrocarbons - analysis
Polycyclic Aromatic Hydrocarbons - toxicity
Ribosomal DNA instability
title Inhalable mixture of polycyclic aromatic hydrocarbons and metals, DNA oxidative stress and nasal ribosomal DNA copy number amplification: Direct and indirect effect analyses among population
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