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Background: Previous studies have shown that inflammatory and antioxidant dietary patterns can modify the risk of COPD, yet few studies have examined the association of these diets with its early signs (PRISm), and the potential role of metabolic disorders remains to be elucidated., Methods: Data from 9529 individuals who participated in the 2007-2012 National Health and Nutrition Examination Survey (NHANES) were analyzed. The Dietary Inflammation Index (DII) and the Dietary Antioxidant Composite Index (CDAI) were assessed using 24-h dietary recall, multiple metabolic indicators were calculated according to biochemical markers, and lung function parameters defined PRISm cases. Individual and joint effects of DII and CDAI were evaluated by generalized linear models and binary logistic regression models, and mediation effects of metabolic indicators were further explored by causal mediation analysis., Results: Increased DII was associated with decreased lung function (FEV1: β = -18.82, FVC: β = -29.2; OR = 1.04) and increased metabolic indicators (β = 0.316, 0.036, 0.916, 0.033, and 0.145 on MAP, UA, TC, TyG, and MS, respectively). Contrary to this, CDAI were positively and negatively associated with lung function (FEV1: β = 3.42; FVC: β = 4.91; PRISm: OR = 0.99) and metabolic indicators (β < 0), respectively. Joint effects of DII and CDAI indicated the minimal hazard effects of DII on TyG (β = -0.11), FEV1 (β = 72.62), FVC (β = 122.27), and PRISm (OR = 0.79) in subjects with high CDAI when compared with those with low CDAI (low DII + high CDAI vs. high DII + low CDAI). Furthermore, TyG mediated 13.74 %, 8.29 %, and 21.70 % of DII- and 37.30 %, 20.90 %, and 12.32 % of CDAI-FEV1, -FVC, and -PRISm associations, respectively., Conclusions: These findings indicated that CDAI can attenuate the adverse effects of DII on metabolic disorders and lung function decline, which provides new insight for diet modification in preventing early lung dysfunction., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.)

Background: 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., Objects: To elucidate the associations of PAHs on inflammatory biomarkers, as well as the effects and mechanisms of essential metals on these associations., Methods: 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., Results: We observed associations of PAHs and essential metals with lymphocyte-to-monocyte ratio (LMR) (P < 0.05). PAH mixtures were inversely associated with LMR (β QGC-index  = -0.18, P < 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 (β QGC-index  = 0.14, P < 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 < 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 (I 2  = 37.84%)., Conclusion: 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., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Systemic immune-inflammation index (SII) emerged as a biomarker of chronic inflammation and an independent prognostic factor for many cancers. We aimed to investigate the associations of SII level with total and cause-specific mortality risks in the general populations, and the potential modification effects of lifestyle-related factors on the above associations. In this study, we included 30,521 subjects from the Dongfeng-Tongji (DFTJ) cohort and 25,761 subjects from the National Health and Nutrition Examination Survey (NHANES) 1999-2014. Cox proportional hazards regression models were used to estimate the associations of SII with mortality from all-cause, cardiovascular diseases (CVD), cancer and other causes. In the DFTJ cohort, compared to subjects in the low SII subgroup, those within the middle and high SII subgroups had increased risks of total mortality [hazard ratio, HR (95% confidence interval, CI) = 1.12 (1.03-1.22) and 1.26 (1.16-1.36), respectively) and CVD mortality [HR (95%CI) = 1.36 (1.19-1.55) and 1.50 (1.32-1.71), respectively]; those within the high SII subgroup had a higher risk of other causes mortality [HR (95%CI) = 1.28 (1.09-1.49)]. In the NHANES 1999-2014, subjects in the high SII subgroup had higher risks of total, CVD, cancer and other causes mortality [HR (95%CI) = 1.38 (1.27-1.49), 1.33 (1.11-1.59), 1.22 (1.04-1.45) and 1.47 (1.32-1.63), respectively]. For subjects with a high level of SII, physical activity could attenuate a separate 30% and 32% risk of total and CVD mortality in the DFTJ cohort, and a separate 41% and 59% risk of total and CVD mortality in the NHANES 1999-2014. Our study suggested high SII level may increase total and CVD mortality in the general populations and physical activity exerted a beneficial effect on the above associations.