The effects and potential mechanisms of essential metals on the associations of polycyclic aromatic hydrocarbons with blood cell-based inflammation markers

Polycyclic aromatic hydrocarbons (PAHs) are well-acknowledged pro-inflammatory chemicals, but their associations with blood cell-based inflammatory biomarkers need further investigation. Moreover, the effects and mechanisms of essential metals on PAH-related inflammation remain poorly understood. To...

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Veröffentlicht in:Environmental pollution (1987) 2024-05, Vol.349, p.123856-123856, Article 123856
Hauptverfasser: Liao, Xiaojing, Wu, Haimei, Liu, Kang, Bai, Yansen, Wu, Degang, Guo, Chaofan, Liu, Xin, Zhang, Zhaorui, Huang, Yongshun, Zhao, Na, Xiao, Yongmei, Deng, Qifei
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container_title Environmental pollution (1987)
container_volume 349
creator Liao, Xiaojing
Wu, Haimei
Liu, Kang
Bai, Yansen
Wu, Degang
Guo, Chaofan
Liu, Xin
Zhang, Zhaorui
Huang, Yongshun
Zhao, Na
Xiao, Yongmei
Deng, Qifei
description Polycyclic aromatic hydrocarbons (PAHs) are well-acknowledged pro-inflammatory chemicals, but their associations with blood cell-based inflammatory biomarkers need further investigation. Moreover, the effects and mechanisms of essential metals on PAH-related inflammation remain poorly understood. To elucidate the associations of PAHs on inflammatory biomarkers, as well as the effects and mechanisms of essential metals on these associations. A cross-sectional study was conducted on 1388 coke oven workers. We analyzed the modification effects of key essential metal(s) on PAHs-inflammatory biomarkers associations. To explore the possible mechanisms from an inflammation perspective, we performed a bioinformatic analysis on the genes of PAHs and essential metals obtained from the Comparative Toxicogenomics Database (CTD) and performed a mediation analysis. We observed associations of PAHs and essential metals with lymphocyte-to-monocyte ratio (LMR) (P 
doi_str_mv 10.1016/j.envpol.2024.123856
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Moreover, the effects and mechanisms of essential metals on PAH-related inflammation remain poorly understood. To elucidate the associations of PAHs on inflammatory biomarkers, as well as the effects and mechanisms of essential metals on these associations. A cross-sectional study was conducted on 1388 coke oven workers. We analyzed the modification effects of key essential metal(s) on PAHs-inflammatory biomarkers associations. To explore the possible mechanisms from an inflammation perspective, we performed a bioinformatic analysis on the genes of PAHs and essential metals obtained from the Comparative Toxicogenomics Database (CTD) and performed a mediation analysis. We observed associations of PAHs and essential metals with lymphocyte-to-monocyte ratio (LMR) (P &lt; 0.05). PAH mixtures were inversely associated with LMR (βQGC-index = −0.18, P &lt; 0.001), with 1-hydroxypyrene (1-OH-Pyr) being the most prominent contributor (weight = 63.37%), whereas a positive association between essential metal mixtures and LMR was observed (βQGC-index = 0.14, P &lt; 0.001), with tin being the most significant contributor (weight = 51.61%). An inverse association of 1-OH-Pyr with LMR was weakened by increased tin exposure (P &lt; 0.05). The CTD database showed that PAHs and tin compounds co-regulated 22 inflammation-associated genes, but they regulated most genes in opposite directions. Further identified the involvement of oxidative stress and mediation analysis showed that the mediation effect of 8-hydroxydeoxyguanosine (8-OHdG) on 1-OH-Pyr-LMR association presented heterogeneity between low and high tin tertile groups (I2 = 37.84%). 1-OH-Pyr and tin were significantly associated with LMR. Modification effects indicated that the inverse association of 1-OH-Pyr with LMR was mitigated with an increase in tin. The mediation effect of 8-OHdG on the inverse association of 1-OH-Pyr with LMR may be partially dependent on tin. [Display omitted] •PAH mixtures were related to decreased LMR, with pyrene contributing the most.•Essential metals had joint effects on elevated LMR, with tin being predominant.•Tin had a modifying effect on pyrene-LMR association.•Pyrene and tin regulated inflammation-related common genes in opposite directions.•8-OHdG mediated pyrene-LMR association and partially dependent on the dose of tin.</description><identifier>ISSN: 0269-7491</identifier><identifier>EISSN: 1873-6424</identifier><identifier>DOI: 10.1016/j.envpol.2024.123856</identifier><identifier>PMID: 38556152</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Essential metals ; Inflammation ; Modification effect ; Polycyclic aromatic hydrocarbons ; Regulatory network</subject><ispartof>Environmental pollution (1987), 2024-05, Vol.349, p.123856-123856, Article 123856</ispartof><rights>2024 Elsevier Ltd</rights><rights>Copyright © 2024 Elsevier Ltd. 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Moreover, the effects and mechanisms of essential metals on PAH-related inflammation remain poorly understood. To elucidate the associations of PAHs on inflammatory biomarkers, as well as the effects and mechanisms of essential metals on these associations. A cross-sectional study was conducted on 1388 coke oven workers. We analyzed the modification effects of key essential metal(s) on PAHs-inflammatory biomarkers associations. To explore the possible mechanisms from an inflammation perspective, we performed a bioinformatic analysis on the genes of PAHs and essential metals obtained from the Comparative Toxicogenomics Database (CTD) and performed a mediation analysis. We observed associations of PAHs and essential metals with lymphocyte-to-monocyte ratio (LMR) (P &lt; 0.05). PAH mixtures were inversely associated with LMR (βQGC-index = −0.18, P &lt; 0.001), with 1-hydroxypyrene (1-OH-Pyr) being the most prominent contributor (weight = 63.37%), whereas a positive association between essential metal mixtures and LMR was observed (βQGC-index = 0.14, P &lt; 0.001), with tin being the most significant contributor (weight = 51.61%). An inverse association of 1-OH-Pyr with LMR was weakened by increased tin exposure (P &lt; 0.05). The CTD database showed that PAHs and tin compounds co-regulated 22 inflammation-associated genes, but they regulated most genes in opposite directions. Further identified the involvement of oxidative stress and mediation analysis showed that the mediation effect of 8-hydroxydeoxyguanosine (8-OHdG) on 1-OH-Pyr-LMR association presented heterogeneity between low and high tin tertile groups (I2 = 37.84%). 1-OH-Pyr and tin were significantly associated with LMR. Modification effects indicated that the inverse association of 1-OH-Pyr with LMR was mitigated with an increase in tin. The mediation effect of 8-OHdG on the inverse association of 1-OH-Pyr with LMR may be partially dependent on tin. 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Moreover, the effects and mechanisms of essential metals on PAH-related inflammation remain poorly understood. To elucidate the associations of PAHs on inflammatory biomarkers, as well as the effects and mechanisms of essential metals on these associations. A cross-sectional study was conducted on 1388 coke oven workers. We analyzed the modification effects of key essential metal(s) on PAHs-inflammatory biomarkers associations. To explore the possible mechanisms from an inflammation perspective, we performed a bioinformatic analysis on the genes of PAHs and essential metals obtained from the Comparative Toxicogenomics Database (CTD) and performed a mediation analysis. We observed associations of PAHs and essential metals with lymphocyte-to-monocyte ratio (LMR) (P &lt; 0.05). PAH mixtures were inversely associated with LMR (βQGC-index = −0.18, P &lt; 0.001), with 1-hydroxypyrene (1-OH-Pyr) being the most prominent contributor (weight = 63.37%), whereas a positive association between essential metal mixtures and LMR was observed (βQGC-index = 0.14, P &lt; 0.001), with tin being the most significant contributor (weight = 51.61%). An inverse association of 1-OH-Pyr with LMR was weakened by increased tin exposure (P &lt; 0.05). The CTD database showed that PAHs and tin compounds co-regulated 22 inflammation-associated genes, but they regulated most genes in opposite directions. Further identified the involvement of oxidative stress and mediation analysis showed that the mediation effect of 8-hydroxydeoxyguanosine (8-OHdG) on 1-OH-Pyr-LMR association presented heterogeneity between low and high tin tertile groups (I2 = 37.84%). 1-OH-Pyr and tin were significantly associated with LMR. Modification effects indicated that the inverse association of 1-OH-Pyr with LMR was mitigated with an increase in tin. The mediation effect of 8-OHdG on the inverse association of 1-OH-Pyr with LMR may be partially dependent on tin. [Display omitted] •PAH mixtures were related to decreased LMR, with pyrene contributing the most.•Essential metals had joint effects on elevated LMR, with tin being predominant.•Tin had a modifying effect on pyrene-LMR association.•Pyrene and tin regulated inflammation-related common genes in opposite directions.•8-OHdG mediated pyrene-LMR association and partially dependent on the dose of tin.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>38556152</pmid><doi>10.1016/j.envpol.2024.123856</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0002-2326-0468</orcidid></addata></record>
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source Elsevier ScienceDirect Journals
subjects Essential metals
Inflammation
Modification effect
Polycyclic aromatic hydrocarbons
Regulatory network
title The effects and potential mechanisms of essential metals on the associations of polycyclic aromatic hydrocarbons with blood cell-based inflammation markers
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