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Objectives: The study aimed to estimate the role of liver fibrosis in the association between occupational physical activity (OPA) and blood pressure (BP), which is modified by lifestyle factors., Methods: The questionnaire survey and physical examination were completed among 992 construction workers in Wuhan, China. Associations between OPA or lifestyle factors and liver fibrosis indices and blood pressure were assessed using generalized additive models. The mediation analysis was used to evaluate the role of liver fibrosis in the association between OPA and lifestyle factors and BP., Results: Moderate/high OPA group workers had an increased risk of liver fibrosis [odds ratio (OR) = 1.69, 95% confidence intervals (CI): 1.16-2.47, P < 0.05] compared with low OPA group workers. Smoking or drinking alcohol was related to liver fibrosis (aspartate aminotransferase to platelet ratio index: OR = 2.22, 95% CI: 1.07-4.62 or OR = 2.04, 95% CI: 1.00-4.15; P < 0.05). Compared with non-drinkers, drinkers were related to a 2.35-mmHg increase in systolic blood pressure (95% CI: 0.09-4.61), and a 1.60-mmHg increase in diastolic blood pressure (95% CI: 0.08-3.13; P < 0.05). We found a significant pathway, "OPA → liver fibrosis → blood pressure elevation," and lifestyle factors played a regulatory role in the pathway., Conclusion: OPA or lifestyle factors were associated with liver fibrosis indices or BP in construction workers. Furthermore, the association between OPA and BP may be partially mediated by liver fibrosis; lifestyle factors strengthen the relationship between OPA and BP and the mediation role of liver fibrosis in the relationship., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Zhang, Chen, Jiang, Zhou, Liu, Liu, Dai, Lu, Yi and Yin.)

Fine particulate matter (PM 2.5 ) contributes to the risk of cardiovascular events, partially owing to its deposition in the human respiratory tract. To investigate short-term effects of ambient PM 2.5 exposure on alternation of blood pressure (BP), this study was conducted during the winter-summer period between 2014 and 2015. The study included 106 community residents in Wuhan city, China. We repeatedly monitored the household and outdoor PM 2.5 concentrations as well as individual-level PM 2.5 in each season, and then assessed personal PM 2.5 exposure (including deposited doses of PM 2.5 in the human respiratory tract) by using different methodology (such as using a dosimetry model). All participants took part in the physical examination, including the inflammatory indicators, BP and lung function parameters measurements. Subsequently, we assessed the health damage of exposure to PM 2.5 using generalized additive models. We observed increased BP at 2-day lag for an interquartile range increase in ambient fixed-site, households, individual-level PM 2.5 exposure and the corresponding lung deposited doses of each exposure concentration (p < 0.05), decreased BP at 3-day lag for an interquartile range increase in ambient fixed-site, households PM 2.5 and the corresponding lung deposited doses of each exposure concentration (p < 0.05). The estimated deposited doses of PM 2.5 by the deposition fractions in this study and the referenced deposition fractions by previous reported method were equivalent associated with alternation in BP. In conclusion, lung deposited dose of PM 2.5 as a quantitative indicator may be used to assess adverse cardiovascular effects following the systemic inflammation. However, we require careful assessment of acute adverse cardiovascular effects using ambient fixed-site PM 2.5 after short-term PM 2.5 exposure., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Occupational exposure is a significant source of metal contact; previous studies have been limited regarding the effect of occupational metal exposure on the development of hypertension. This study was conducted to assess the levels of exposure of certain metals (chromium (Cr), iron (Fe), manganese (Mn), and nickel (Ni)) in hypertensive and non-hypertensive workers and to assess the relationship between the risk of hypertension and metal exposure level. Our study included 138 hypertensive patients as case groups and 138 non-hypertensive participants as controls. The exposure risk level was divided according to the limit value after collecting and testing the metal dust in the workshop. Considering the influence of single- and poly-metal, single factor analysis and conditional logistic regression analysis of poly-metal were carried out. The results of the model indicated that the incidence of hypertension increased with an increase in Cr exposure level, and the risk of hypertension was 1.85 times higher in the highest exposure than in the lowest exposure (95% CI: 1.20–2.86, p < 0.05). Mn has the same effect as Cr. There was no significant correlation between Fe or Ni and hypertension. Our findings suggested that Cr and Mn exposure in the work environment might increase the risk of hypertension, while no effect of Fe and Ni on blood pressure was found. Prospective study designs in larger populations are needed to confirm our findings. [ABSTRACT FROM AUTHOR]

Exposure to polycyclic aromatic hydrocarbons (PAHs) could cause high blood pressure (BP) and increased risk for atherosclerotic cardiovascular disease (ASCVD). However, the mechanisms underlying the relationship between them were unclear. We investigated potential mediation effect of obesity on the association of exposure to PAHs with high BP and increased risk for ASCVD. In the repeated measures study, 106 community-dwelling residents in Wuhan, China finished the physical examination in the winter and summer seasons, eight urinary PAHs metabolites were measured. Associations of urinary PAHs with high BP and increased risk for ASCVD were assessed using either linear mixed effect models or generalized estimating equations models. Mediation analysis was performed to evaluate the mediating effect of obesity on the association of urinary PAHs metabolites with high BP or increased risk of ASCVD. We observed the positive association between urinary PAHs metabolites and BP or the odds ratios for high BP (all P < 0.05). Additionally, each one-unit increase in ln-transformed urinary levels of 4-hydroxyphenanthrene or the total of PAH metabolites was associated with a 12.63% or 11.91% increase in the estimated 10-year ASCVD risk (both P < 0.05). The waist-to-height ratio mediated 29.0% of the association of urinary 4-hydroxyphenanthrene with increased risk of ASCVD ( P < 0.05). The findings suggest that PAHs exposure may be associated with elevated BP and an increased risk of ASCVD. Obesity may partially mediate the association between PAHs exposure and higher BP or increased risk of ASCVD. [ABSTRACT FROM AUTHOR]

When evaluating noise-related cardiovascular risk, noise is generally solely assessed as the major stressor. However, cardiovascular effect of other simultaneous exposure events, such as unhealthy lifestyle and genetic variation, is easily neglected. The aim of this study is to estimate the combined effect of noise and lifestyle on blood pressure alteration, particularly under different genetic background. This study included 536 workers from a tobacco factory in Wuhan, China, who were divided into high exposure group and low exposure group according to noise measurement in their working area. All participants took annual physical examination and questionnaire survey to provide information on individual systolic and diastolic blood pressure (SBP and DBP) and lifestyle (smoking, drinking and physical activity). Single nucleotide polymorphism at genes related to stress hormone production were determined. Moderated moderation models were constructed to investigate the interaction effect of noise exposure and lifestyle factors on blood pressure with regard to different genetic background. We identified an expected trend in association between noise exposure and SBP among active smokers (P = 0.086). The moderated moderation analysis showed significant three-way interaction effect (COMT rs4680 × smoking status × noise exposure levels) on SBP or DBP (both P < 0.05). For COMT rs4680 GA+AA genotype carriers, active smoking significantly moderated the association between noise exposure and SBP or DBP (both P < 0.05). The results indicated that for COMT rs4680 A allele carriers, tobacco and noise exposure contribute collectively to blood pressure alteration, supporting that stress hormone production may play a certain role in the smoke-and-noise-induced cardiovascular effect. [ABSTRACT FROM AUTHOR]