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Epidemiological evidence concerning effects of simultaneous exposure to noise and benzene, toluene, ethylbenzene, xylene, and styrene (BTEXS) on renal function remains uncertain. In 2020, a cross-sectional study was conducted among 1160 petrochemical workers in southern China to investigate effects of their co-exposure on estimated glomerular filtration rate (eGFR) and mild renal impairment (MRI). Noise levels were assessed using cumulative noise exposure (CNE). Urinary biomarkers for BTEXS were quantified. We found the majority of workers had exposure levels to noise and BTEXS below China's occupational exposure limits. CNE, trans, trans -muconic acid (tt -MA), and the sum of mandelic acid and phenylglyoxylic acid (PGMA) were linearly associated with decreased eGFR and increased MRI risk. We observed U-shaped associations for both N-acetyl-S-phenyl-L-cysteine (SPMA) and o-methylhippuric acid (2-MHA) with MRI. In further assessing the joint effect of BTEXS (β , −0.164 [95% CI, −0.296 to −0.033]) per quartile increase in all BTEXS metabolites on eGFR using quantile g-computation models, we found SPMA, tt -MA, 2-MHA, and PGMA played pivotal roles. Additionally, the risk of MRI associated with tt -MA was more pronounced in workers with lower CNE levels (P = 0.004). Multiplicative interaction analysis revealed antagonisms of CNE and PGMA on MRI risk (P = 0.034). Thus, our findings reveal negative dose-effect associations between noise and BTEXS mixture exposure and renal function in petrochemical workers. With the exception of toluene, benzene, xylene, ethylbenzene, and styrene are all concerning pollutants for renal dysfunction. Effects of benzene, ethylbenzene, and styrene exposure on renal dysfunction were more pronounced in workers with lower CNE. [Display omitted] • Noise exposure was associated with renal dysfunction in petrochemical workers. • BTEXS metabolites mixture was dose-dependently associated with eGFR decline. • SPMA, tt -MA, 2-MHA, and PGMA were key contributors to joint associations. • SPMA and 2-MHA exhibited nonlinear associations with renal dysfunction. • In workers with lower CNE, tt -MA and PGMA had stronger impacts on renal dysfunction. [ABSTRACT FROM AUTHOR]

Objectives: The objective of our study was to evaluate the association between occupational exposure to trichloroethylene (TCE), a suspected lymphomagen, and serum levels of miRNAs in a cross-sectional molecular epidemiology study of TCE-exposed workers and comparable unexposed controls in China. Methods: Serum levels of 40 miRNAs were compared in 74 workers exposed to TCE (median: 12 ppm) and 90 unexposed control workers. Linear regression models were used to test for differences in serum miRNA levels between exposed and unexposed workers and to evaluate exposure–response relationships across TCE exposure categories using a three-level ordinal variable [i.e., unexposed, < 12 ppm, the median value among workers exposed to TCE) and ≥ 12 ppm)]. Models were adjusted for sex, age, current smoking, current alcohol use, and recent infection. Results: Seven miRNAs showed significant differences between exposed and unexposed workers at FDR (false discovery rate) < 0.20. miR-150-5p and let-7b-5p also showed significant inverse exposure–response associations with TCE exposure (Ptrend= 0.002 and 0.03, respectively). The % differences in serum levels of miR-150-5p relative to unexposed controls were − 13% and − 20% among workers exposed to < 12 ppm and ≥ 12 ppm TCE, respectively. Conclusions: miR-150-5p is involved in B cell receptor pathways and let-7b-5p plays a role in the innate immune response processes that are potentially important in the etiology of non-Hodgkin lymphoma (NHL). Further studies are needed to replicate these findings and to directly test the association between serum levels of these miRNAs and risk of NHL in prospective studies. [ABSTRACT FROM AUTHOR]

[Display omitted] • Atmospheric environmental issues in workplaces should be taken seriously. • Evidence is scarce on the interaction between environmental and occupational factors. • We conducted a cross-sectional study among 363,788 workers in south China in 2020. • PM 2.5 and its components were positively associated with an increased risk of OVD. • Less-dust workers and those exposed to occupational noise and heat were more susceptible. The new round of WHO/ILO Joint Estimates of the Work-related Burden of Disease assessment requires futher research to provide more evidence, especially on the health impact of ambient air pollution around the workplace. However, the evidence linking obstructive ventilatory dysfunction (OVD) to fine particulate matter (PM 2.5) and its chemical components in workers is very limited. Evidence is even more scarce on the interactive effects between occupational factors and particle exposures. We aimed to fill these gaps based on a large ventilatory function examination of workers in southern China. We conducted a cross-sectional study among 363,788 workers in southern China in 2020. The annual average concentration of PM 2.5 and its components were evaluated around the workplace through validated spatiotemporal models. We used mixed-effect models to evaluate the risk of OVD related to PM 2.5 and its components. Results were further stratified by basic characteristics and occupational factors. Among the 305,022 workers, 119,936 were observed with OVD. We found for each interquartile range (IQR) increase in PM 2.5 concentration, the risk of OVD increased by 27.8 (95 % confidence interval (CI): 26.5–29.2 %). The estimates were 10.9 % (95 % CI : 9.7–12.1 %), 15.8 % (95 % CI : 14.5–17.2 %), 2.6 % (95 % CI : 1.4–3.8 %), 17.1 % (95 % CI : 15.9–18.4 %), and 11 % (95 % CI : 9.9–12.2 %), respectively, for each IQR increment in sulfate, nitrate, ammonium salt, organic matter and black carbon. We observed greater effect estimates among females, younger workers, workers with a length of service of 24–45 months, and professional skill workers. Furthermore, it is particularly noteworthy that the noise-exposed workers, high-temperature-exposed workers, and less-dust-exposed workers were at a 5.7–68.2 % greater risk than others. PM 2.5 and its components were significantly associated with an increased risk of OVD, with stronger links among certain vulnerable subgroups. [ABSTRACT FROM AUTHOR]

• Occupational exposures were associated with DNA methylation aging biomarkers. • Benzene and trichloroethylene exposures increased epigenetic age acceleration. • Epigenetic aging biomarkers capture impacts of environmental chemicals on health. Epigenetic aging biomarkers are associated with increased morbidity and mortality. We evaluated if occupational exposure to three established chemical carcinogens is associated with acceleration of epigenetic aging. We studied workers in China occupationally exposed to benzene, trichloroethylene (TCE) or formaldehyde by measuring personal air exposures prior to blood collection. Unexposed controls matched by age and sex were selected from nearby factories. We measured leukocyte DNA methylation (DNAm) in peripheral white blood cells using the Infinium HumanMethylation450 BeadChip to calculate five epigenetic aging clocks and DNAmTL, a biomarker associated with leukocyte telomere length and cell replication. We tested associations between exposure intensity and epigenetic age acceleration (EAA), defined as the residuals of regressing the DNAm aging biomarker on chronological age, matching factors and potential confounders. Median differences in EAA between exposure groups were tested using a permutation test with exact p -values. Epigenetic clocks were strongly correlated with age (Spearman r > 0.8) in all three occupational studies. There was a positive exposure-response relationship between benzene and the Skin-Blood Clock EAA biomarker: median EAA was −0.91 years in controls (n = 44), 0.78 years in workers exposed to <10 ppm (n = 41; mean benzene = 1.35 ppm; p = 0.034 vs. controls), and 2.10 years in workers exposed to ≥10 ppm (n = 9; mean benzene = 27.3 ppm; p = 0.019 vs. controls; p trend = 0.0021). In the TCE study, control workers had a median Skin-Blood Clock EAA of −0.54 years (n = 71) compared to 1.63 years among workers exposed to <10 ppm of TCE (n = 27; mean TCE = 4.22 ppm; p = 0.035). We observed no evidence of EAA associations with formaldehyde exposure (39 controls, 31 exposed). Occupational benzene and TCE exposure were associated with increased epigenetic age acceleration measured by the Skin-Blood Clock. For TCE, there was some evidence of epigenetic age acceleration for lower exposures compared to controls. Our results suggest that some chemical carcinogens may accelerate epigenetic aging. [ABSTRACT FROM AUTHOR]

It remains unclear how ambient air pollution may affect the prevalence of obstructive ventilatory dysfunction (OVD) among workers. We aim to assess the association of a comprehensive set of ambient air pollutants with OVD prevalence in workers and to explore the potential interactive effects of the occupational factors. This is a population-based cross-sectional study among 305,022 participants from the Guangdong Province, China. Mixed-effects models were used to obtain differences in the OVD risk associated with a 10 μg/m 3 increase in ambient air pollution. We found that for each 10 μg/m 3 increase in PM 2.5 , PM 10 , PM coarse , O 3 , and NO 2 concentrations, the odds ratio (OR) for OVD in workers is 1.324 (95 % confidence interval (CI), 1.282-1.367), 1.292 (95 % CI, 1.268-1.315),1.666 (95 % CI, 1.614-1.719), 1.153 (95 % CI, 1.142-1.165), and 1.023 (95 % CI, 1.012-1.033). We observed that young participants (18-38 years old), women, participants with longer years of service (>48 months), participants working in large enterprises, professional skills workers, and production and manufacturing workers have higher estimated effects. In addition, we also found that workers exposed to high temperatures have higher estimated effects under air pollutants exposure, while workers exposed to noise have higher estimated effects under PM 2.5 , PM 10 , NO 2 , and O 3 exposure. Workers exposed to dust have a lower risk of developing OVD under exposure to ambient air pollutants compared to those not exposed. Our results indicate that ambient air pollution increases the risk of OVD in workers. Moreover, air pollutants exhibit a greater estimated effect among workers exposed to high temperatures or noise. Our research findings highlight the importance of fully considering the impact of ambient air pollution on protecting the respiratory health of workers., Competing Interests: Declaration of competing interest The authors have declared no conflict of interest., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Introduction: An increasing number of original studies suggested that occupational noise exposure might be associated with the risk of hypertension, but the results remain inconsistent and inconclusive. In addition, the attributable fraction (AF) of occupational noise exposure has not been well quantified. We aimed to conduct a large-scale occupational population-based study to comprehensively investigate the relationship between occupational noise exposure and blood pressure and different hypertension subtypes and to estimate the AF for hypertension burden attributable to occupational noise exposure., Methods: A total of 715,135 workers aged 18-60 years were included in this study based on the Key Occupational Diseases Surveillance Project of Guangdong in 2020. Multiple linear regression was performed to explore the relationships of occupational noise exposure status, the combination of occupational noise exposure and binaural high frequency threshold on average (BHFTA) with systolic and diastolic blood pressure (SBP, DBP). Multivariable logistic regression was used to examine the relationshipassociation between occupational noise exposure status, occupational noise exposure combined with BHFTA and hypertension. Furthermore, the attributable risk (AR) was calculated to estimate the hypertension burden attributed to occupational exposure to noise., Results: The prevalence of hypertension among occupational noise-exposed participants was 13·7%. SBP and DBP were both significantly associated with the occupational noise exposure status and classification of occupational noise exposure combined with BHFTA in the crude and adjusted models (all P < 0·0001). Compared with workers without occupational noise exposure, the risk of hypertension was 50% greater among those exposed to occupational noise in the adjusted model (95% CI 1·42-1·58). For participants of occupational noise exposed with BHFTA normal, and occupational noise exposed with BHFTA elevated, the corresponding risks of hypertension were 48% (1·41-1·56) and 56% (1·46-1·63) greater than those of occupational noise non-exposed with BHFTA normal, respectively. A similar association was found in isolated systolic hypertension (ISH) and prehypertension. Subgroup analysis by sex and age showed that the positive associations between occupational noise exposure and hypertension remained statistically significant across all subgroups (all P < 0.001). Significant interactions between occupational noise status, classification of occupational noise exposure combined with BHFTA, and age in relation to hypertension risk were identified (all P for interaction < 0.001). The associations of occupational noise status, classification of occupational noise exposure combined with BHFTA and hypertension were most pronounced in the 18-29 age groups. The AR% of occupational noise exposure for hypertension was 28·05% in the final adjusted model., Conclusions: Occupational noise exposure was positively associated with blood pressure levels and the prevalence of hypertension, ISH, and prehypertension in a large occupational population-based study. A significantly increased risk of hypertension was found even in individuals with normal BHFTA exposed to occupational noise, with a further elevated risk observed in those with elevated BHFTA. Our findings provide epidemiological evidence for key groups associated with occupational noise exposure and hypertension, and more than one-fourth of hypertension cases would have been prevented by avoiding occupational noise exposure., (© 2024. The Author(s).)

Methylmercury (MeHg) is a toxicant that mainly originates from in situ microbial methylation of inorganic mercury (Hg) in the environment and poses a severe health risk to the public. However, the characteristics of the Hg-methylating microbial community and its relationship with MeHg production in various environments remain to be understood. In the present study, Hg-methylating microbial communities and genes (hgcAB cluster) in the sediments of the Pearl River (PR), Pearl River Estuary (PRE) and South China Sea (SCS) were investigated at a large spatial scale using high-throughput sequencing-based approaches. The results showed that sulfur-reducing bacteria (SRB) and iron-reducing bacteria (IRB) were consistently the dominant microbial strains responsible for the methylation of inorganic Hg in all three regions investigated. The abundance and diversity of Hg-methylating communities and genes were both found to be higher in the PR sediments compared to that in the PRE and SCS sediments, and in good agreement with the spatial distribution of MeHg. Furthermore, a significant correlation was observed between the MeHg concentration and the abundance of both hgcA and hgcB genes in the sediments of the PR, PRE and SCS regions. Overall, the present study suggested that there was the presence of a close link between MeHg and Hg-methylating communities or genes in the ambient aquatic environment, which could be used to reflect the potential of in situ MeHg production., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Objectives: The occupational exposure limit for trichloroethylene (TCE) in different countries varies from 1 to 100 ppm as an 8-hour time-weighted average (TWA). Many countries currently use 10 ppm as the regulatory standard for occupational exposures, but the biological effects in humans at this level of exposure remain unclear. The objective of our study was to evaluate alterations in immune and renal biomarkers among workers occupationally exposed to low levels of TCE below current regulatory standards., Methods: We conducted a cross-sectional molecular epidemiology study of 80 healthy workers exposed to a wide range of TCE (ie, 0.4-229 ppm) and 96 comparable unexposed controls in China, and previously reported that TCE exposure was associated with multiple candidate biological markers related to immune function and kidney toxicity. Here, we conducted further analyses of all of the 31 biomarkers that we have measured to determine the magnitude and statistical significance of changes in the subgroup of workers (n=35) exposed to <10 ppm TCE compared with controls., Results: Six immune biomarkers (ie, CD4+ effector memory T cells, sCD27, sCD30, interleukin-10, IgG and IgM) were significantly decreased (% difference ranged from -16.0% to -72.1%) and one kidney toxicity marker (kidney injury molecule-1, KIM-1) was significantly increased (% difference: +52.5%) among workers exposed to <10 ppm compared with the control group. These associations remained noteworthy after taking into account multiple comparisons using the false discovery rate (ie, <0.20)., Conclusion: Our results suggest that occupational exposure to TCE below 10 ppm as an 8-hour TWA may alter levels of key markers of immune function and kidney toxicity., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2019. No commercial re-use. See rights and permissions. Published by BMJ.)