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Noise pollution has grown to be a major public health issue worldwide. We sought to profile serum metabolite expression changes related to occupational noise exposure by untargeted metabolomics, as well as to evaluate the potential roles of serum metabolites in occupational noise-associated arterial stiffness (AS). Our study involved 30 noise-exposed industrial personnel (Lipo group) and 30 noise-free controls (Blank group). The untargeted metabolomic analysis was performed by employing a UPLC-HRMS. The associations of occupational noise and significant differential metabolites (between Blank/Lipo groups) with AS were evaluated using multivariable-adjusted generalized linear models. We performed the least absolute shrinkage and selection operator regression analysis to further screen for AS's risk metabolites. We explored 177 metabolites across 21 categories significantly differentially expressed between Blank/Lipo groups, and these metabolites were enriched in 20 metabolic pathways. Moreover, 15 metabolites in 4 classes (including food, glycerophosphocholine, sphingomyelin [SM] and triacylglycerols [TAG]) were adversely associated with AS (all P < 0.05). Meanwhile, five metabolites (homostachydrine, phosphatidylcholine (PC) (32:1e), PC (38:6p), SM (d41:2) and TAG (45:1) have been proven to be useful predictors of AS prevalence. However, none of these 15 metabolites were found to have a mediating influence on occupational noise-induced AS. Our study reveals specific metabolic changes caused by occupational noise exposure, and several metabolites may have protective effects on AS. However, the roles of serum metabolites in noise-AS association remain to be validated in future studies., 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.)

Objective: Whether coal mine dust exposure increases cardiovascular diseases (CVDs) risk was rarely explored. Our objective was to examine the association between coal mine dust exposure and cardiovascular risk., Methods: We estimated cumulative coal mine dust exposure (CDE) for 1327 coal miners by combining data on workplace dust concentrations and work history. We used brachial-ankle pulse wave velocity (baPWV, a representative indicator of arterial stiffness) and ten-year atherosclerotic cardiovascular disease (ASCVD) risk to assess potential CVD risk, exploring their associations with CDE., Results: Positive dose-response relationships of CDE with baPWV and ten-year ASCVD risk were observed after adjusting for covariates. Specifically, each 1 standard deviation (SD) increase in CDE was related to a 0.27 m/s (95% CI: 0.21, 0.34) increase in baPWV and a 1.29 (95% CI: 1.14, 1.46) elevation in OR (odds ratio) of risk of abnormal baPWV. Moreover, each 1 SD increase in CDE was associated with a 0.74% (95% CI: 0.63%, 0.85%) increase in scores of ten-year ASCVD and a 1.91 (95% CI: 1.62, 2.26) increase in OR of risk of ten-year ASCVD. When compared with groups unexposed to coal mine dust, significant increase in the risk of arterial stiffness and ten-year ASCVD in the highest CDE groups were detected., Conclusion: The study suggested that cumulative exposure to coal mine dust was associated with elevated arterial stiffness and ten-year ASCVD risk in a dose-response manner. These findings contribute valuable insights for cardiovascular risk associated with coal mine dust., (© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Aims: We aimed to evaluate the association of occupational noise with metabolic syndrome (MetS) and its components, and to assess the potential role of miRNAs in occupational noise-associated MetS., Methods: A total of 854 participants were enrolled in our study. Cumulative noise exposure (CNE) was estimated in conjunction with workplace noise test records and research participants' employment histories. Logistic regression models adjusted for potential confounders were used to assess the association of CNE and miRNAs with MetS and its components., Results: We observed linear positive dose-response associations between occupational noise exposure and the prevalence of MetS (OR: 1.031; 95 % CI: 1.008, 1.055). And linear and nonlinear relationship were also found for the association of occupational noise exposure with high blood pressure (OR: 1.024; 95 % CI: 1.007, 1.041) and reduced high-density lipoprotein (OR: 1.051; 95 % CI: 1.031, 1.072), respectively. MiR-200a-3p, miR-92a-3p and miR-21-5p were inversely associated with CNE, or the prevalence of MetS and its components (all P < 0.05). However, we did not find any statistically significant mediation effect of miRNAs in the associations of CNE with MetS. Furthermore, the prevalence of bilateral hearing loss in high-frequency increased (OR: 1.036; 95 % CI: 1.008, 1.067) with CNE level rising, and participants with bilateral hearing loss in high-frequency had a significantly higher risk of MetS (OR: 1.727; 95 % CI: 1.048, 2.819)., Conclusion: Our study suggests that occupational noise exposure is associated with MetS and its components, and the role of miRNAs in noise-induced increasing MetS risk needs to be confirmed in future studies., 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 B.V. All rights reserved.)

Evidence on the association between occupational noise exposure and blood pressure is inconsistent, and the underlying mechanism remains unknown. This study aimed to evaluate the association between occupational noise exposure and blood pressure, and explore the potential role of miRNAs in the association. A total of 894 subjects from two companies in Wuhan, China were included. Occupational noise exposure was assessed using cumulative noise exposure (CNE), and six candidate plasma miRNAs (miR-92a-3p, miR-21-5p, miR-200a-3p, miR-200b-3p, miR-200c-3p, and miR-1-3p) which were not only associated with blood pressure/hypertension but also related to oxidative stress were selected according to previous studies and tested. A linear dose-response relationship was found between occupational noise exposure and blood pressure, including systolic blood pressure (SBP) and diastolic blood pressure (DBP). Each 1-unit increase in CNE levels was significantly associated with a 0.130 (95 % confidence interval [CI] = 0.026, 0.234) unit increase in SBP and a 0.141 (95 % CI = 0.063, 0.219) unit increase in DBP. However, the association between occupational noise and hypertension is not statistically significant (P > 0.05). In the meanwhile, occupational noise exposure was negatively associated with miRNA-92a-3p (β = -0.019, 95 % CI = -0.032, -0.006) and miRNA-21-5p (β = -0.031, 95 % CI = -0.052, -0.010), and miRNA-92a-3p mediated 24.66 % of the association between occupational noise exposure and DBP. In addition, bilateral high-frequency hearing loss was not only positively associated with occupational noise exposure (OR = 1.974, 95 % CI = 1.084, 3.702) but also DBP (β = 2.546, 95 % CI = 0.160, 4.932). Our study suggests that occupational noise exposure is positively associated with SBP and DBP, and miRNA-92a-3p partially mediate the association between occupational noise exposure and DBP., 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 © 2023 Elsevier B.V. All rights reserved.)

Background: The World Health Organization (WHO) and the International Labour Organization (ILO) are developing joint estimates of the work-related burden of disease and injury (WHO/ILO Joint Estimates), with contributions from a large number of individual experts. Evidence from human, animal and mechanistic data suggests that occupational exposure to dusts and/or fibres (silica, asbestos and coal dust) causes pneumoconiosis. In this paper, we present a systematic review and meta-analysis of the prevalences and levels of occupational exposure to silica, asbestos and coal dust. These estimates of prevalences and levels will serve as input data for estimating (if feasible) the number of deaths and disability-adjusted life years that are attributable to occupational exposure to silica, asbestos and coal dust, for the development of the WHO/ILO Joint Estimates., Objectives: We aimed to systematically review and meta-analyse estimates of the prevalences and levels of occupational exposure to silica, asbestos and coal dust among working-age (≥ 15 years) workers., Data Sources: We searched electronic academic databases for potentially relevant records from published and unpublished studies, including Ovid Medline, PubMed, EMBASE, and CISDOC. We also searched electronic grey literature databases, Internet search engines and organizational websites; hand-searched reference lists of previous systematic reviews and included study records; and consulted additional experts., Study Eligibility and Criteria: We included working-age (≥ 15 years) workers in the formal and informal economy in any WHO and/or ILO Member State but excluded children (< 15 years) and unpaid domestic workers. We included all study types with objective dust or fibre measurements, published between 1960 and 2018, that directly or indirectly reported an estimate of the prevalence and/or level of occupational exposure to silica, asbestos and/or coal dust., Study Appraisal and Synthesis Methods: At least two review authors independently screened titles and abstracts against the eligibility criteria at a first stage and full texts of potentially eligible records at a second stage, then data were extracted from qualifying studies. We combined prevalence estimates by industrial sector (ISIC-4 2-digit level with additional merging within Mining, Manufacturing and Construction) using random-effects meta-analysis. Two or more review authors assessed the risk of bias and all available authors assessed the quality of evidence, using the ROB-SPEO tool and QoE-SPEO approach developed specifically for the WHO/ILO Joint Estimates., Results: Eighty-eight studies (82 cross-sectional studies and 6 longitudinal studies) met the inclusion criteria, comprising > 2.4 million measurements covering 23 countries from all WHO regions (Africa, Americas, Eastern Mediterranean, South-East Asia, Europe, and Western Pacific). The target population in all 88 included studies was from major ISCO groups 3 (Technicians and Associate Professionals), 6 (Skilled Agricultural, Forestry and Fishery Workers), 7 (Craft and Related Trades Workers), 8 (Plant and Machine Operators and Assemblers), and 9 (Elementary Occupations), hereafter called manual workers. Most studies were performed in Construction, Manufacturing and Mining. For occupational exposure to silica, 65 studies (61 cross-sectional studies and 4 longitudinal studies) were included with > 2.3 million measurements collected in 22 countries in all six WHO regions. For occupational exposure to asbestos, 18 studies (17 cross-sectional studies and 1 longitudinal) were included with > 20,000 measurements collected in eight countries in five WHO regions (no data for Africa). For occupational exposure to coal dust, eight studies (all cross-sectional) were included comprising > 100,000 samples in six countries in five WHO regions (no data for Eastern Mediterranean). Occupational exposure to silica, asbestos and coal dust was assessed with personal or stationary active filter sampling; for silica and asbestos, gravimetric assessment was followed by technical analysis. Risk of bias profiles varied between the bodies of evidence looking at asbestos, silica and coal dust, as well as between industrial sectors. However, risk of bias was generally highest for the domain of selection of participants into the studies. The largest bodies of evidence for silica related to the industrial sectors of Construction (ISIC 41-43), Manufacturing (ISIC 20, 23-25, 27, 31-32) and Mining (ISIC 05, 07, 08). For Construction, the pooled prevalence estimate was 0.89 (95% CI 0.84 to 0.93, 17 studies, I 2 91%, moderate quality of evidence) and the level estimate was rated as of very low quality of evidence. For Manufacturing, the pooled prevalence estimate was 0.85 (95% CI 0.78 to 0.91, 24 studies, I 2 100%, moderate quality of evidence) and the pooled level estimate was rated as of very low quality of evidence. The pooled prevalence estimate for Mining was 0.75 (95% CI 0.68 to 0.82, 20 studies, I 2 100%, moderate quality of evidence) and the pooled level estimate was 0.04 mg/m 3 (95% CI 0.03 to 0.05, 17 studies, I 2 100%, low quality of evidence). Smaller bodies of evidence were identified for Crop and animal production (ISIC 01; very low quality of evidence for both prevalence and level); Professional, scientific and technical activities (ISIC 71, 74; very low quality of evidence for both prevalence and level); and Electricity, gas, steam and air conditioning supply (ISIC 35; very low quality of evidence for both prevalence and level). For asbestos, the pooled prevalence estimate for Construction (ISIC 41, 43, 45,) was 0.77 (95% CI 0.65 to 0.87, six studies, I 2 99%, low quality of evidence) and the level estimate was rated as of very low quality of evidence. For Manufacturing (ISIC 13, 23-24, 29-30), the pooled prevalence and level estimates were rated as being of very low quality of evidence. Smaller bodies of evidence were identified for Other mining and quarrying (ISIC 08; very low quality of evidence for both prevalence and level); Electricity, gas, steam and air conditioning supply (ISIC 35; very low quality of evidence for both prevalence and level); and Water supply, sewerage, waste management and remediation (ISIC 37; very low quality of evidence for levels). For coal dust, the pooled prevalence estimate for Mining of coal and lignite (ISIC 05), was 1.00 (95% CI 1.00 to 1.00, six studies, I 2 16%, moderate quality of evidence) and the pooled level estimate was 0.77 mg/m 3 (95% CI 0.68 to 0.86, three studies, I 2 100%, low quality of evidence). A small body of evidence was identified for Electricity, gas, steam and air conditioning supply (ISIC 35); with very low quality of evidence for prevalence, and the pooled level estimate being 0.60 mg/m 3 (95% CI -6.95 to 8.14, one study, low quality of evidence)., Conclusions: Overall, we judged the bodies of evidence for occupational exposure to silica to vary by industrial sector between very low and moderate quality of evidence for prevalence, and very low and low for level. For occupational exposure to asbestos, the bodies of evidence varied by industrial sector between very low and low quality of evidence for prevalence and were of very low quality of evidence for level. For occupational exposure to coal dust, the bodies of evidence were of very low or moderate quality of evidence for prevalence, and low for level. None of the included studies were population-based studies (i.e., covered the entire workers' population in the industrial sector), which we judged to present serious concern for indirectness, except for occupational exposure to coal dust within the industrial sector of mining of coal and lignite. Selected estimates of the prevalences and levels of occupational exposure to silica by industrial sector are considered suitable as input data for the WHO/ILO Joint Estimates, and selected estimates of the prevalences and levels of occupational exposure to asbestos and coal dust may perhaps also be suitable for estimation purposes. Protocol identifier: https://doi.org/10.1016/j.envint.2018.06.005. PROSPERO registration number: CRD42018084131., Competing Interests: Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Professor Vivi Schlünssen was the Chair of the Danish Quality Committee for Occupational Exposure Limits of the Danish Working Environment Authority from the year 2016, up until 30 June 2022. The other authors declare no conflicts of interest., (Copyright © 2023 World Health Organization, International Labour Organization. Published by Elsevier Ltd.. All rights reserved.)

Carbon disulfide (CS 2 ) exposure has been associated with lung function reduction in occupational population. However, evidence on the general population with relatively low CS 2 exposure is lacking and the mechanism involved remains largely unknown. Urinary CS 2 metabolite (2-mercaptothiazolidine-4-carboxylic acid, TTCA) and lung function were determined in the urban adults from the Wuhan-Zhuhai cohort at baseline in 2011-2012 and were repeated every 3 years. Cross-sectional and longitudinal associations between TTCA and lung function were estimated using linear mixed models. Inflammation and oxidative damage biomarkers in blood/urine were measured to evaluate their potential mediating roles involved. Cross-sectionally, participants in the highest quartile of TTCA level showed a 0.64% reduction in FEV 1 /FVC and a -308.22 mL/s reduction in PEF, compared to those in the lowest quartile. Longitudinally, participants with consistently high TTCA level had annually -90.27 mL/s decline in PEF, compared to those with consistently low TTCA level. Mediation analysis revealed that plasma protein carbonyl mediated 49.89% and 22.10% of TTCA-associated FEV 1 /FVC and PEF reductions, respectively. Conclusively, there was a cross-sectional and longitudinal association between CS 2 exposure and lung function reduction in the general urban adults, and protein carbonylation (oxidative protein damage) partly mediated lung function reduction from CS 2 exposure., 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 © 2023 Elsevier B.V. All rights reserved.)

Silicosis not a disease of the past. It is an irreversible, fibrotic lung disease specifically caused by exposure to respirable crystalline silica (RCS) dust. Over 20,000 incident cases of silicosis were identified in 2017 and millions of workers continue to be exposed to RCS. Identified case numbers are however a substantial underestimation due to deficiencies in reporting systems and occupational respiratory health surveillance programmes in many countries. Insecure workers, immigrants and workers in small businesses are at particular risk of more intense RCS exposure. Much of the focus of research and prevention activities has been on the mining sector. Hazardous RCS exposure however occurs in a wide range of occupational setting which receive less attention, in particular the construction industry. Recent outbreaks of silicosis associated with the fabrication of domestic kitchen benchtops from high-silica content artificial stone have been particularly notable because of the young age of affected workers, short duration of RCS exposure and often rapid disease progression. Developments in nanotechnology and hydraulic fracking provide further examples of how rapid changes in technology and industrial processes require governments to maintain constant vigilance to identify and control potential sources of RCS exposure. Despite countries around the world dealing with similar issues related to RCS exposure, there is an absence of sustained global public health response including lack of consensus of an occupational exposure limit that would provide protection to workers. Although there are complex challenges, global elimination of silicosis must remain the goal., (© 2022 The Authors. Respirology published by John Wiley & Sons Australia, Ltd on behalf of Asian Pacific Society of Respirology.)

Background: The potential role of occupational exposures in the development of nasopharyngeal carcinoma (NPC) remains unclear, particularly in high-incidence areas., Methods: The authors conducted a population-based case-control study, consisting of 2514 incident NPC cases and 2586 randomly selected population controls, in southern China from 2010 to 2014. Occupational history and other covariates were self-reported using a questionnaire. Multivariate logistic regression was used to estimate odds ratios (ORs) with 95% confidence intervals (CIs) for the risk of NPC associated with occupational exposures. Restricted cubic splines were used to evaluate potentially nonlinear duration-response relations., Results: Individuals who had exposure to occupational dusts (OR, 1.45; 95% CI, 1.26-1.68), chemical vapors (OR, 1.37; 95% CI, 1.17-1.61), exhausts/smokes (OR, 1.42; 95% CI, 1.25-1.60), or acids/alkalis (OR, 1.56; 95% CI, 1.30-1.89) in the workplace had an increased NPC risk compared with those who were unexposed. Risk estimates for all 4 categories of occupational exposures appeared to linearly increase with increasing duration. Within these categories, occupational exposure to 14 subtypes of agents conferred significantly higher risks of NPC, with ORs ranging from 1.30 to 2.29, including dust from metals, textiles, cement, or coal; vapor from formaldehyde, organic solvents, or dyes; exhaust or smoke from diesel, firewood, asphalt/tar, vehicles, or welding; and sulfuric acid, hydrochloric acid, nitric acid, and concentrated alkali/ammonia., Conclusions: Occupational exposures to dusts, chemical vapors, exhausts/smokes, or acids/alkalis are associated with an excess risk of NPC. If the current results are causal, then the amelioration of workplace conditions might alleviate the burden of NPC in endemic areas., Lay Summary: The role of occupational exposures in the development of nasopharyngeal carcinoma (NPC) remains unclear, particularly in high-incidence areas. The authors conducted a population-based study with 2514 incident NPC cases and 2586 population controls in southern China and observed that occupational exposures were associated with an increased risk of NPC. Duration-response trends were observed with increasing duration of exposure. These findings provide new evidence supporting an etiologic role of occupational exposures for NPC in a high-incidence region., (© 2021 The Authors. Cancer published by Wiley Periodicals LLC on behalf of American Cancer Society.)

The association of silica dust exposure with mortality among never smokers has not been well established. We aimed to evaluate the association of silica dust exposure with mortality among never smokers. We studied 17,130 workers employed for at least 1 year between January 1, 1960 and December 31, 1974, with follow-up until the end of 2013. Cumulative respirable silica dust exposure (CDE) was estimated by linking a job-exposure matrix to personal work history. We observed 3937 deaths during 589,357.26 person-years of follow-up. Significant positive exposure-response relationships were found between CDE and mortality from all cause (HR = 1.01, 95%CI = 1.01-1.02), respiratory tuberculosis (HR = 1.04, 95%CI = 1.02-1.06), CVDs (HR = 1.03, 95%CI = 1.02-1.04), and diseases of the respiratory system (HR = 1.06, 95%CI = 1.04-1.07). We found higher standardized mortality ratios for respiratory tuberculosis (2.62, 2.32-2.95), CVDs (1.43, 1.32-1.54), and pneumoconiosis (77.75, 68.21-88.25) among silica dust exposed workers. In addition, we estimated that 4.19%, 20.69%, 7.48% and 34.06% of deaths for all cause, respiratory tuberculosis, CVDs, and diseases of the respiratory system among Chinese workers were attributed to silica, after adjusting for other covariates. With regard to lung cancer, compared with unexposed group, the HRs and 95% CI were 0.94 (0.52-1.71), 1.86 (1.15-3.00), 1.65 (0.95-2.86) for low, medium, and high exposed workers, respectively. Long-term silica dust exposure is associated with increased mortality in the absence of cigarette smoking., (Copyright © 2021 Elsevier GmbH. All rights reserved.)

We aimed to explore the association of occupational noise exposure with atherosclerotic cardiovascular disease (ASCVD) risk in Chinese adults. We included 21,412 participants from the Dongfeng-tongji Cohort Study, occupational noise exposure was evaluated through workplace noise level and/or the job titles, hearing loss was defined as a pure-tone mean of 25 dB or higher at 0.5, 1, 2, and 4 kHz in any ear. Compared with participants without occupational noise exposure, the 10-year ASCVD risk was significantly higher for noise exposure duration ≥20 years (OR = 1.20, 95%CI = 1.05-1.32) after adjusting for potential confounders. In the subgroup analysis, the association was only statistically significant in males (OR = 1.86, 95%CI = 1.12-3.14) and participants aged equal to or over 60 years old (OR = 1.20, 95%CI = 1.05-1.33), but not in females (OR = 1.15, 95%CI = 0.71-1.92) and aged below 60 (OR = 1.51, 95%CI = 0.75-2.85). In the subsample analyses (N = 10,165), bilateral hearing loss was associated with a higher risk of 10-year ASCVD (OR = 1.72, 95%CI = 1.30-2.30), especially for participants who were males (OR = 2.40, 95%CI = 1.61-3.42) and aged equal to or over 60 (OR = 1.85, 95%CI = 1.40-2.44). The present study suggests that occupational noise exposure may be a potential risk factor for ASCVD, especially for males and older participants., (Copyright © 2021 Elsevier GmbH. All rights reserved.)

Objectives: To investigate the effect of sex on the risk of silicosis and to explore any interaction between cigarette smoking and sex in the development of silicosis., Methods: The cohort was selected from eight Chinese pottery factories. Diagnoses of silicosis were based on 1986 Chinese pneumoconiosis Roentgen diagnostic criteria. Data on cigarette smoking were collected by face-to-face interviews in 1989 and 2003., Results: Eight thousand eight hundred and eighty seven dust-exposed workers were included. Men had a 77% higher incidence of silicosis than women. At lower pack-years of smoking, men were 72% more at risk than women. The latency period was found to be longest in female never-smokers and shortest in female ever-smokers., Conclusions: Men had a higher risk of developing silicosis than women. Cigarette smoking increased the risk in both sexes, more so in women., Competing Interests: Conflicts of Interest: None declared., (Copyright © 2020 American College of Occupational and Environmental Medicine.)

Background: Little is known about the different risk of silicosis in metal mines and pottery factories. We aimed to compare the silicosis risks among silica-exposed workers in different industrial circumstances., Research Question: Are the silicosis risks among silica-exposed workers in industrial circumstances different?, Study Design and Methods: We studied 39,808 workers followed up from January 1, 1960 to December 31, 2003 in China. Cumulative respirable silica dust exposure (CDE) was estimated by linking a job-exposure matrix to personal work history. Silicosis of stage I or higher was diagnosed by Chinese pneumoconiosis Roentgen diagnostic criteria., Results: A total of 9,377 silicosis patients were diagnosed during 1,153,580.9 person-years' follow-up in the cohort. Hazard ratios of silicosis for each 1 mg/m 3 -year increase in CDE were 1.08 (1.07-1.08) for tungsten mines, 1.41 (1.33-1.48) for iron and copper mines, 1.14 (1.11-1.17) for tin mines, and 1.03 (1.02-1.04) for pottery factories, respectively. When exposed to 0.05 mg/m 3 of respirable silica dust for 45 years, the cumulative risks in metal mines (2.3%, 9.9%, 1.5% for tungsten mines, iron and copper mines, and tin mines, respectively) were still higher than those in pottery factories (0.6%). The joint effect of silica and smoking on silicosis was more than multiplicative., Interpretation: The risk of silicosis in metal miners is higher than that in pottery workers when exposed to the same level of silica dust. The silica dust exposed years should be under 10 years for metal miners and 40 years for pottery workers at 0.05 mg/m 3 to keep lifetime risk within 0.1%. Current exposure limits should take into account differences in various industrial circumstances. Smoking cessation could help reduce silicosis risk for silica-exposed workers., (Copyright © 2020 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.)

Dimethylformamide (DMF) is a volatile organic compound listed as one of the four toxicants with the highest priority for human field study. However, the effect of DMF exposure on lung function and the underlying mechanisms remain unknown. We aimed to investigate the exposure-response relationship and possible mechanism between internal DMF exposure and lung function alteration. We studied 3701 Chinese adults from the Wuhan-Zhuhai cohort with a 3-year follow-up. The cross-sectional relationship between urinary biomarker of DMF exposure (N-Acetyl-S-(N-methylcarbamoyl)-L-cysteine, AMCC) and lung function, and the mediating role of plasma C-reactive protein (CRP) were assessed. We also convened a sub-cohort (N = 138) to assess the stability of AMCC in repeated urine samples collected for continuous 3 days and intervals of 1, 2 and 3 years. The longitudinal association between AMCC and lung function change in 3 years was further assessed. We found a dose-response relationship between AMCC and lung function reduction. Each 2-fold increase in AMCC was cross-sectionally associated with a 23.12-mL (95% CI: -36.68, -9.55) decrease in FVC and a 19.01-mL (95% CI: -31.08, -6.93) decrease in FEV 1 . Increased CRP significantly mediated 5.39% and 5.87% of the AMCC-associated FVC and FEV 1 reductions, respectively. With 3-year follow-up, AMCC showed a fair to excellent stability (intra-class correlation coefficients were 0.88, 0.55, 0.60 and 0.50 for continuous 3 days, intervals of 1, 2 and 3 years, respectively) and was dose-dependently associated with longitudinal lung function decline. Compared with those with persistent low AMCC levels, participants with persistent high AMCC levels had a 101.09-mL/year (95% CI: -167.40, -34.77) decline in FVC and a 66.27-mL/year (95% CI: -114.14, -18.41) decline in FEV 1 in the sub-cohort. Similar results were found in the full-cohort. Our findings suggest that exposure of general population to environmental DMF may impair lung function, and systematic inflammation may be an underlying mechanism., 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 © 2020 Elsevier B.V. All rights reserved.)

Objectives Shift work is associated with metabolic disorders as it disturbs circadian rhythms. However, the potential association of shift work with knee osteoarthritis (KOA), a metabolic-related disease, has not been confirmed. The objective of this study was to quantify the association of shift work with the risk of KOA. Methods This retrospective cohort study comprising 13 741 retired workers from the Dongfeng Motor Corporation. KOA was defined by knee pain and clinical X-ray radiographs. Occupational history, including job description and shift work, was collected from face-to-face interviews using questionnaires. Cox proportional hazards regression models were used to estimate exposure-response relationships. Results During the 590 085 person-years of follow-up, a total of 847 cases of KOA (incidence of KOA was 143.5 per 100 000 person-years) were identified. After adjusting for potential confounders, shift work was independently associated with an elevated risk of KOA [hazard ratio (HR) 1.19, 95% confidence interval 1.03-1.36]. Compared with daytime workers, the risk of KOA increased with prolonged periods of shift work; the HR of KOA for participants with 1-9 years, 10-19 years, and ≥20 years shift work were 1.03 (95% CI 0.84-1.26), 1.19 (95% CI 0.98-1.46), and 1.42 (95% CI 1.15-1.76), respectively. The HR for KOA associated with shift work gradually decreased as the period after finishing shift work increased. Conclusion Our results indicated that shift work could be an independent risk factor for KOA.

The association between shift work and hearing loss is unclear. We aimed to evaluate this association in a Chinese population independently and in combination with occupational noise. A total of 11,196 participants of the Dongfeng-Tongji cohort study were included. Shift work was self-reported and hearing loss was defined as a pure-tone mean of 25 dB or higher at 0.5, 1, 2, and 4 kHz in any ear. The Robust Poisson method were used to assess the relationship between shift work and hearing loss, and the prevalence ratios (PRs) were calculated. Compared to individuals who reported no shift work, the PRs of bilateral hearing loss were significantly higher for a shift work duration of fewer than 10 years in women, (PR = 1.024, 95% confidence interval [CI] = 1.002-1.053), but not in men (PR = 1.016, 95% confidence interval [CI] = 0.998-1.035). The association between short duration of shift work and bilateral hearing loss was just statistically significant in women when those with occupational noise exposure were excluded (PR = 1.067, 95%CI = 1.015-1.122). When shift work and occupational noise exposure were combined, the PRs for hearing loss were highest among individuals with the longest shift work (≥10 years) and longest noise exposure (≥20 years) durations, whether for bilateral (PR = 1.114, 95%CI = 1.068-1.162) or any ear (PR = 1.065, 95%CI = 1.034-1.096). A short duration of shift work may be a risk factor for hearing loss in women and could increase the prevalence of hearing loss when combined with occupational noise., (Copyright © 2019 Elsevier B.V. All rights reserved.)

Polychlorinated dibenzo-dioxins and polychlorinated dibenzo-furans (PCDD/Fs) have been reported to induce reactive oxygen species and oxidative stress, but the dose-response relationships have not been explored in molecular epidemiological studies. In this study, a total of 602 participants were recruited, comprising of 215 foundry workers, 171 incineration workers and 216 residents living more than 5 km away from the plants as the reference group. Individual PCDD/Fs exposures were estimated according to PCDD/Fs levels of working and living ambient air and daily foods. Urinary 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) and 8-iso-prostaglandin-F2α (8-isoPGF2α) were determined to reflect oxidatively generated damage to DNA and lipid. Generalized linear models were used to access the associations between PCDD/Fs exposure and oxidative stress biomarkers. We found that PCDD/Fs exposure and urinary oxidative stress biomarkers of workers were all higher than those of the reference group. Significantly positive exposure-response relationships between individual PCDD/Fs exposures and urinary 8-oxodG and 8-iso-PGF2α were found. Each 1-unit increase in ln-transformed levels of PCDD/Fs exposure generated a 0.78 nmol/mmol creatinine increase in ln-transformed 8-oxodG and a 0.50 ng/mmol creatinine increase in ln-transformed 8-isoPGF2α in foundry workers, a 0.49 nmol/mmol creatinine increase in ln-transformed 8-oxodG and a 0.26 ng/mmol creatinine increase in ln-transformed 8-isoPGF2α in incineration workers, compared with the reference group. And such associations were not modified by tobacco use. Our findings could help to understand the dose-response relationships between PCDD/Fs and oxidatively generated damage to DNA and lipid, and provide an epidemiologic basis for conducting research on the carcinogenesis and other toxicity mechanisms of PCDD/Fs., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Background: The World Health Organization (WHO) and the International Labour Organization (ILO) are developing a joint methodology for estimating the national and global work-related burden of disease and injury (WHO/ILO joint methodology), with contributions from a large network of experts. In this paper, we present the protocol for two systematic reviews of parameters for estimating the number of deaths and disability-adjusted life years attributable to pneumoconiosis from occupational exposure to dusts and/or fibres, to inform the development of the WHO/ILO joint methodology., Objectives: We aim to systematically review studies on occupational exposure to dusts and/or fibres (Systematic Review 1) and systematically review and meta-analyse estimates of the effect of occupational exposure to dusts and/or fibres on pneumoconiosis (Systematic Review 2), applying the Navigation Guide systematic review methodology as an organizing framework., Data Sources: Separately for Systematic Reviews 1 and 2, we will search electronic academic databases for potentially relevant records from published and unpublished studies, including Medline, EMBASE, Web of Science and CISDOC. We will also search electronic grey literature databases, Internet search engines and organizational websites; hand-search reference list of previous systematic reviews and included study records; and consult additional experts., Study Eligibility and Criteria: We will include working-age (≥15 years) study participants in the formal and informal economy in any WHO and/or ILO Member State but exclude children (<15 years) and unpaid domestic workers. Eligible risk factors will be dusts and/or fibres from: (i) asbestos; (ii) silica; and/or (iii) coal (defined as pure coal dust and/or dust from coal mining). Included outcomes will be (i) asbestosis; (ii) silicosis; (iii) coal worker pneumoconiosis; and (iv) unspecified pneumoconiosis. For Systematic Review 1, we will include quantitative prevalence studies of occupational exposure to dusts and/or fibres (i.e. no versus any exposure) stratified by country, sex, age and industrial sector or occupation. For Systematic Review 2, we will include randomized controlled trials, cohort studies, case-control studies and other non-randomized intervention studies with an estimate of any occupational exposure to dusts and/or fibres on the prevalence of, incidence of or mortality due to pneumoconiosis, compared with the theoretical minimum risk exposure level of no exposure., Study Appraisal and Synthesis Methods: At least two review authors will independently screen titles and abstracts against the eligibility criteria at a first stage and full texts of potentially eligible records at a second stage, followed by extraction of data from qualifying studies. At least two review authors will assess risk of bias and the quality of evidence, using the most suited tools currently available. For Systematic Review 2, if feasible, we will combine relative risks using meta-analysis. We will report results using the guidelines for accurate and transparent health estimates reporting (GATHER) for Systematic Review 1 and the preferred reporting items for systematic reviews and meta-analyses guidelines (PRISMA) for Systematic Review 2., Prospero Registration Number: CRD42018084131., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

Background: Both cigarette smoking and long-term exposure to crystalline silica dust were reported to be associated with increased mortality. However, the combined effect of both factors has not been well evaluated., Methods: We investigated a retro-prospective cohort of 7,665 workers from one Chinese iron mine with a median follow-up of 42.8 years. Cumulative silica exposure was estimated for each worker by linking work histories with a job-exposure matrix. Cigarette smoking information was collected through face-to-face questionnaires. Hazard ratios (HRs) for total and cause-specific mortality due to silica exposure and smoking were estimated using Cox proportional hazards models., Results: A total of 2,814 deaths occurred during 315,772.9 person-years of follow-up. Significantly elevated mortality from all causes, cardiovascular disease, non-malignant respiratory disease and lung cancer was observed among silica-exposed workers, while elevated mortality from non-malignant respiratory disease and lung cancer was observed among smokers. Combined exposure to silica dust and cigarette smoking elevated the proportion of mortality and accounted for 21.2, 76.0, 35.7 and 81.4% of all causes, non-malignant respiratory disease, cardiovascular disease, and lung cancer, respectively. Significant additive joint effects of silica exposure and cigarette smoking on mortality from lung cancer (HR 1.893, 95% CI 0.628 to 3.441) and pneumoconiosis (6.457, 0.725 to 39.114), together with a significant multiplicative joint effect from all causes (1.002, 1.000 to 1.004) were observed., Conclusions: The present findings indicated that silica exposure in combination with cigarette smoking accounted for a fraction of extra deaths in our cohort. Our research showed the urgent need for smoking cessation and silica control among iron miners.

Objective: The aim of this study was to explore the potential role of extracellular matrix (ECM) regulated by miRNAs in lung function decline., Methods: We convened 270 silica dust exposed subjects and divided them into three groups according to lung function data. MiRNAs were measured by real-time quantitative polymerase chain reaction detecting system and ECM-related proteins were detected by enzyme linked immunosorbent assay. Data were analyzed by t test, Chi-squared tests, nonparametric Mann-Whitney U test, and Spearman rank correlation coefficient., Results: Lower miR-200c and miR-29c were observed in subjects with severe lung function decline and higher ECM proteins were observed in subjects with mild or severe lung function decline. MiRNA and ECM were significantly correlated with FVC%, FEV1%, MMF%, and PEF% (r: 0.204 to 0.458, P < 0.01) and that miRNA were significantly correlated with ECM (r: 0.309 to 0.687, P < 0.01)., Conclusion: The abnormal ECM regulated by miRNAs may play an important role in lung function decline associated with silica dust exposure.

The association between occupational noise exposure and hypertension is unclear. We aimed to explore the association in a Chinese population and to summarize our findings with previous published articles. The cross-sectional study included 22,450 participants from Dongfeng-Tongji Cohort Study. In a subsample of 10,636 subjects, we assessed the association between hearing loss and hypertension. For the meta-analysis, we searched PubMed and EMBASE until April 2017, and the pooled odds ratio (OR) was combined using a random effect model. Compared with participants without occupational noise exposure, the risk of hypertension was significantly higher for noise exposure duration ≥20 (OR = 1.09, 95% confidence interval [CI] = 1.00-1.18). In the sex-specific analysis, the association was only significantly pronounced in males (OR = 1.16, 95% CI = 1.03-1.31), but not in females (OR = 1.01, 95% CI = 0.88-1.14). In the subsample analyses, hearing loss, which was an indicator for exposure to loud noise, was associated with a higher risk of hypertension, especially for participants who were bilateral hearing loss (OR = 1.39, 95% CI = 1.24-1.54). In the meta-analysis, the pooled OR for the association between occupational noise exposure and hypertension was 1.25 (95% CI = 1.10-1.42). On the basis of an indicator for exposure to occupational noise, the cross-sectional study and meta-analysis identified occupational noise exposure as a potential risk factor for increased hypertension risk., (Copyright © 2017 American Society of Hypertension. Published by Elsevier Inc. All rights reserved.)

Combined effect of cigarette smoking and occupational noise exposure on hearing loss has rarely been evaluated among Chinese population, especially among females. This cross-sectional study was conducted in 11196 participants of Dongfeng-Tongji cohort study. Smoking status was self-reported through questionnaire and occupational noise exposure was evaluated through workplace noise level and/or the job titles. Hearing loss was defined as a pure-tone mean of 25 dB or higher at 0.5, 1, 2, and 4 kHz in both ears. Compared with participants without occupational noise exposure, the risk of hearing loss was significantly higher for noise exposure duration ≥20 (OR = 1.45, 95%CI = 1.28-1.65). The association was particularly evident among individuals who were males (OR = 1.74, 95%CI = 1.45-2.08) and aged ≥ 70 (OR = 1.74, 95%CI = 1.30-2.33). Similarly, the risks increased with the increasing of pack-years in males and all age groups except for those aged <60. As to the combined effect, the hearing loss risk was highest for noise exposure duration ≥20 and pack-years ≥25 (OR = 2.41, 95%CI = 1.78-3.28), especially among males (OR = 2.42, 95%CI = 1.74-3.37) and those aged ≥70 (OR = 2.76, 95%CI = 1.36-5.60). Smoking may be an independent risk factor for hearing loss. And it may synergistically affect hearing when combined with occupational noise exposure, especially among males and older participants.

The association between low-level crystalline silica (silica) exposure and mortality risk is not well understood. We investigated a cohort of 44,807 Chinese workers who had worked in metal mines or pottery factories for at least 1 year from January 1, 1960, to December 31, 1974, and were followed through 2003. Low-level silica exposure was defined as having a lifetime highest annual mean silica exposure at or under a permissible exposure limit (PEL). We considered 3 widely used PELs, including 0.05 mg/m3, 0.10 mg/m3, and 0.35 mg/m3. Cumulative silica exposure was estimated by linking a job exposure matrix with each participant's work history. For the 0.10-mg/m3 exposure level, Cox proportional hazards models showed significantly increased risk of mortality from all diseases (for each 1-ln mg/m3-years increase in logged cumulative silica exposure, hazard ratio (HR) = 1.05, 95% confidence interval (CI): 1.03, 1.07), malignant neoplasms (HR = 1.06, 95% CI: 1.03, 1.09), lung cancer (HR = 1.08, 95% CI: 1.02, 1.14), ischemic heart disease (HR = 1.09, 95% CI: 1.02, 1.16), pulmonary heart disease (HR = 1.08, 95% CI: 1.00, 1.16), and respiratory disease (HR = 1.20, 95% CI: 1.14, 1.26). The 0.05-mg/m3 and 0.35-mg/m3 exposure levels yielded similar associations. Long-term exposure to low levels (PELs ≤0.05 mg/m3, ≤0.10 mg/m3, or ≤0.35 mg/m3) of silica is associated with increased total and certain cause-specific mortality risk. Control of ambient silica levels and use of personal protective equipment should be emphasized in practice., (© The Author(s) 2017. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Background: Crystalline silica is considered as one of the most common and serious occupational hazards to workers' health. Although its association with lung cancer has been studied for many decades, the conclusion remains somewhat controversial. Our objectives are to review and summarize the epidemiological evidence on the relationship between occupational silica exposure and risk of lung cancer and to provide an update on this major occupational health concern., Methods: Eligible studies up to 29 April 2016 were identified. Pooled effect estimates were calculated according to the reported outcome and the study design. Cohort, case control and proportional mortality studies were examined separately. Studies reporting results according to silicotic status were grouped together and analyzed. Due to the significant amount of heterogeneity expected, random effects models were implemented. Subgroup and meta-regression analyses (both univariate and multivariate) were performed in an attempt to explain heterogeneity. Studies which had adequate exposure characterization were selected to find out whether there was an exposure-response relationship between silica and lung cancer., Results: The risk of lung cancer was found to be elevated in both silicotics and non-silicotics. The pooled standardized mortality ratio (SMR) was 2.32 with a 95 % confidence interval (95 % CI) of 1.91-2.81 and 1.78 (95 % CI 1.07-2.96) respectively. The pooled standardized incidence ratio (SIR) was 2.49 (95 % CI 1.87-3.33) and 1.18 (95 % CI 0.86-1.62) respectively. Subgroup analysis showed that workers in the mining industry had the highest risk of lung cancer with a pooled SMR of 1.48 (95 % CI 1.18-1.86) and the weakest association was seen in potteries with a pooled SMR of 1.14 (95 % CI 1.05-1.23). A positive exposure-response relation was found between cumulative silica exposure and risk of lung cancer., Conclusion: The results of our meta-analysis supported the carcinogenic role of silica on the lungs, which was more pronounced at higher levels of exposure, in the presence of silicosis and in the mining industry. Further research is needed to evaluate whether non-silicotics are truly at risk, whether a predisposing factor would explain this potential risk, and to determine the mechanism of carcinogenicity of silica in humans.

Objectives: To evaluate the effects of the interactions between polymorphisms in Nalp3, caspase-1, and interleukin(IL)-1β genes and occupational dust exposure on the risk of silicosis., Methods: We conducted a population-based case-control study in a large iron mine in China. Between January 2006 and December 2009, we identified 179 patients with silicosis to evaluate as cases and 201 individuals without silicosis to evaluate as controls. We estimated cumulative dust exposure (CDE) for all subjects and we genotyped polymorphisms in Nalp3, caspase-1, and IL-1β genes. We estimated odds ratios(ORs), 95% confidence intervals(95%CIs), and p-values using logistic regression models adjusted for selected confounders., Results: After adjusting for age, smoking status, and CDE, subjects with the CT genotype of Ex4-849C>T in Nalp3 and the GA genotype of Ex2+37G>A in caspase-1 had increased risks of silicosis (adjusted ORs[95%CIs] = 2.40 [1.12-5.12] and 3.62 [1.63-8.02], respectively). Among subjects younger than 70 years old, those with the CC genotype of IVS8-7652A>C in Nalp3 had a lower risk of silicosis than those with other genotypes (adjusted OR[95%CI] = 0.24[0.06-0.88]). Among subjects aged 70 years and older, those with the CT genotype of Ex4-849C>T in Nalp3 and those with the GA genotype of Ex2+37G>A in caspase-1 had a higher risk of silicosis than those with other genotypes (adjusted ORs [95%CI] = 2.52[1.04-6.12] and 5.19[1.88-14.35], respectively). Among subjects with CDE greater than 120 mg/m3×year and among smokers, those with the GA genotype of Ex2+37G>A in caspase-1 had a higher risk of silicosis than those with other genotypes (adjusted ORs[95%CIs] = 26.37[3.35-207.39] and 3.47[1.40-8.64], respectively)., Conclusions: Genetic polymorphisms in Nalp3 and caspase-1 may be associated with individual susceptibility to silicosis, especially when the polymorphisms interact with age, CDE, or smoking status.

This study aims to develop a prognostic risk prediction model for the development of silicosis among workers exposed to silica dust in China. The prediction model was performed by using retrospective cohort of 3,492 workers exposed to silica in an iron ore, with 33 years of follow-up. We developed a risk score system using a linear combination of the predictors weighted by the LASSO penalized Cox regression coefficients. The model's predictive accuracy was evaluated using time-dependent ROC curves. Six predictors were selected into the final prediction model (age at entry of the cohort, mean concentration of respirable silica, net years of dust exposure, smoking, illiteracy, and no. of jobs). We classified workers into three risk groups according to the quartile (Q1, Q3) of risk score; 203 (23.28%) incident silicosis cases were derived from the high risk group (risk score ≥ 5.91), whilst only 4 (0.46%) cases were from the low risk group (risk score < 3.97). The score system was regarded as accurate given the range of AUCs (83-96%). This study developed a unique score system with a good internal validity, which provides scientific guidance to the clinicians to identify high-risk workers, thus has important cost efficient implications.

This case-control study aimed to investigate whether the levels of Hsp70 (HSPA1A) and Hsp27 (HSPB1) in plasma and lymphocytes were associated with the risk of chronic obstructive pulmonary disease (COPD) among coal workers. A total of 76 COPD cases and 48 age-matched healthy controls from a group of coal workers were included. The case group consisted of 35 COPD patients whose condition was complicated with coal workers' pneumoconiosis (CWP) and 41 COPD patients without CWP. Heat shock proteins (Hsps) in plasma and lymphocytes were detected by ELISA and flow cytometry, respectively. Multiple logistic regression models were applied to estimate the association between Hsp levels and COPD risk. Our results showed that plasma Hsp70 and lymphocyte Hsp27 levels were significantly higher and plasma Hsp27 levels were significantly lower in COPD cases than in controls (p < 0.01). No significant differences in lymphocyte Hsp70 levels were found between COPD cases and the matched subjects. Higher plasma Hsp70 levels (odds ratio (OR) = 13.8, 95 % confidence interval (CI) = 5.7-33.5) and lower plasma Hsp27 levels (OR = 4.6, 95 % CI = 2.0-10.5) were significantly associated with an increased risk of COPD after adjusting for confounders. Higher lymphocyte Hsp27 levels were only associated with an increased risk of COPD with CWP (OR = 6.6, 95 % CI = 2.0-22.1) but not with an increased risk of COPD without CWP (OR = 3.0, 95 % CI = 0.9-8.9). Additionally, there were strong joint effects of different Hsps on COPD risk. These results showed that higher levels of plasma Hsp70 and lower levels of plasma Hsp27 might be associated with an increased risk of COPD among coal workers. They may have the potential to serve as monitoring markers for COPD in coal workers.

Pneumoconiosis is the most serious occupational disease in China and its leading cause is occupational silica exposure. Pneumoconiosis takes several years to develop depending on the exposure level of silica. However, individual variation in the susceptibility to pneumoconiosis has been observed among the subjects with similar exposure. We conducted a genome-wide screening with 710,999 single nucleotide polymorphisms (SNPs) in a cohort of 400 coal workers (202 cases and 198 exposed controls) for pneumoconiosis susceptible loci. Seven promising variants were evaluated in an independent cohort of 568 coal workers (323 cases and 245 exposed controls), followed by a second replication on 463 iron ore workers (167 cases and 296 exposed controls). By pooling all of the genome-wide association studies and replication stages together, we found a genome-wide significant (P < 5.0 × 10(-8)) association for rs73329476 (P = 1.74 × 10(-8), OR = 2.17, 95% CI = 1.66-2.85) and two additional replicated associations for rs4320486 (P < 0.05) and rs117626015 (P < 0.05) with combined P-values of 4.29 × 10(-6) and 5.05 × 10(-6), respectively. In addition, the risk allele T of rs73329476 was significantly associated with lower mRNA expression levels of carboxypeptidase M (CPM) in total cellular RNA from whole blood of 156 healthy individuals (P = 0.0252). The identified pneumoconiosis susceptibility loci may provide new insights into the pathogenesis of pneumoconiosis, and may also have some clinical utility for risk prediction for pneumoconiosis and high-risk population screening for workers with occupational silica exposure., (© The Author 2014. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)

Background: The association between crystalline silica exposure and risk of heart disease mortality remains less clear., Methods: We investigated a cohort of 42,572 Chinese workers who were potentially exposed to crystalline silica and followed from 1960 to 2003. Cumulative silica exposure was estimated by linking a job-exposure matrix to each person's work history. Low-level silica exposure was defined as never having held a job with an exposure higher than 0.1 mg/m. We estimated hazard ratios (HRs) in exposure-response analyses using Cox proportional hazards model., Results: We identified 2846 deaths from heart disease during an average of 35 years follow-up. Positive exposure-response trends were observed for cumulative silica exposure associated with mortality from total heart disease (HRs for increasing quartiles of cumulative silica exposure compared with the unexposed group = 0.89, 1.09, 1.32, 2.10; P for linear trend < 0.001) and pulmonary heart disease (0.92, 1.39, 2.47, 5.46; P for linear trend < 0.001). These positive trends remained among workers with both high- and low-level silica exposure. There was also a positive trend for ischemic heart disease among workers with low-level exposure, with quartile HRs of 1.04, 1.13, 1.52, and 1.60 (P for linear trend < 0.001)., Conclusion: Low-level crystalline silica exposure was associated with increased mortality from heart disease, including pulmonary heart disease and ischemic heart disease, whereas high-level exposure mainly increased mortality from pulmonary heart disease. Current permissible exposure limits for crystalline silica in many countries may be insufficient to protect people from deaths due to heart disease.

Objective: Workplace aerosol sampling is challenged by its influencing factors and methodological limitations. Some factors, including blank setting, electrostatic effect, sample mass gain, and limit of detection (LOD), were studied to characterize them further and thereby to improve the sampling method., Methods: Through a field sampling in two shipyards and by an analysis of a large amount of dust data from different industries, the influencing factors were comparatively studied with emphasis on their effect on the final result., Results: After calibration with field blanks, the concentrations of most sample types in the shipyards decreased significantly, varying by as much as -24.3% of the final measurements. After laboratory blank calibration, dust concentrations increased or decreased without a definite change trend. With a variation of -1.8%, only the measurements of Chinese "total dust" sampled with polypropylene filters were significantly influenced by the electrostatic effect. The LOD coincidence rate was only 17.3% for American respirable dust in different industries and 12.2% for respirable particles collected by normal flow rate samplers (FSP2) in the shipyards. The latter increased to 73.9% when high flow samplers (FSP10) were used., Conclusions: It was suggested that field blank calibration was the predominant influencing factor in comparison with electrostatic effect and laboratory blank adjustment. The LOD coincidence rate was too low for reliable sampling, and this might be improved by use of high flow samplers.

Crystalline silica has been classified as a human carcinogen by the International Agency for Research on Cancer (Lyon, France); however, few previous studies have provided quantitative data on silica exposure, silicosis, and/or smoking. We investigated a cohort in China (in 1960-2003) of 34,018 workers without exposure to carcinogenic confounders. Cumulative silica exposure was estimated by linking a job-exposure matrix to work history. Cox proportional hazards model was used to conduct exposure-response analysis and risk assessment. During a mean 34.5-year follow-up, 546 lung cancer deaths were identified. Categorical analyses by quartiles of cumulative silica exposure (using a 25-year lag) yielded hazard ratios of 1.26, 1.54, 1.68, and 1.70, respectively, compared with the unexposed group. Monotonic exposure-response trends were observed among nonsilicotics (P for trend < 0.001). Analyses using splines showed similar trends. The joint effect of silica and smoking was more than additive and close to multiplicative. For workers exposed from ages 20 to 65 years at 0.1 mg/m(3) of silica exposure, the estimated excess lifetime risk (through age 75 years) was 0.51%. These findings confirm silica as a human carcinogen and suggest that current exposure limits in many countries might be insufficient to protect workers from lung cancer. They also indicate that smoking cessation could help reduce lung cancer risk for silica-exposed individuals.

BACKGROUND.: The detailed lung radiographic response to silica exposure has not been described. In estimating the exposure-response relationship in silicosis with statistical models, the absence of baseline (unattributable) risk can disable relative-rate estimation or produce widely varying estimates. This obstructs identification of optimum exposure metrics and invalidates comparisons and meta-analyses, which assume a common background rate. METHODS.: A cohort of 3,000 Chinese tin miners with more than 1,000 cases of silicosis was analyzed for the period 1961-1994. Regular surveillance documented three stages of silicosis. To examine the exposure-response relationship, the intercept in relative-rate models was fixed to correspond to 1% of the observed silicosis rate. Exposure metrics for contributions in different time-windows were simultaneously evaluated, as were burden and cumulative burden metrics. RESULTS.: Silica exposures that most contributed to silicosis onset occurred in the period 5-10 years prior (excess annual rate per 10 mg-year/m(3) , ER = 0.158, 95% CI = 0.125-0.192, or 16% per year). During 10-20 year prior, the excess rate contribution was much smaller (ER = 0.048, 95% CI = 0.037-0.060) but larger again during 20-30 year prior to onset (ER = 0.112, 95% CI = 0.098-0.126). For advanced silicosis, all time periods contributed about equally to the rate of onset. CONCLUSIONS.: Reliable estimates of parameters were observed, demonstrating exposure contributions over time. Burden metrics with different half-lives suggested some reversibility for silicosis onset with a half-life of 20 years. Advanced silicosis was best predicted with a cumulative burden metric which was consistent with prior observations that previously deposited silica continues to cause pulmonary damage., (Copyright © 2012 Wiley Periodicals, Inc.)

Polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) have been reported as possible carcinogenic hazards to humans. However, epidemiological studies on their carcinogenic roles are limited. The current study was designed to determine the concentrations and characteristics of PCDD/Fs and evaluate their association with cancer mortality in exposed workers in one automobile foundry factory. PCDD/F levels in factory and surrounding environment were analyzed through air and settling dust sampling. The cancer mortalities among workers in this foundry factory were calculated using data from a cohort study. The results showed that the PCDD/F concentrations of air in workplace ranged 0.36-2.25 pg World Health Organization-Toxic Equivalent (WHO-TEQ) Nm(-3) (average 1.01 pg WHO-TEQ Nm(-3)), which were 1.16-7.26 times higher than those outside the factory. The PCDD/F concentrations of settling dust in the workplace ranged 3.34-18.64 pg WHO-TEQ g(-1) (average 8.25 pg WHO-TEQ g(-1)), which were lower than those just outside the factory (average 16.13 pg WHO-TEQ g(-1)). Furthermore, a cohort study of workers in this factory with average follow-up of 24.52 years showed that cancer was the leading cause of death, with significant elevated mortality (standardized mortality ratio (SMR)=1.70, 95% confidence interval (CI): 1.35-2.13) among workers, when compared with Chinese national mortality. The cancer mortality among front-line workers was increased significantly (adjusted relative risk (RR)=1.73, 95% CI: 1.14-2.60), particularly among melting and casting workers, when compared with that among assistant workers. Our results indicated that there was a dose-response relationship between PCDD/F exposure and cancer mortality among foundry workers., (Copyright © 2012 Elsevier B.V. All rights reserved.)

Silicosis is a fibrotic lung disease caused by inhalation of free crystalline silicon dioxide or silica. Occupational exposure to respirable crystalline silica dust particles occurs in many industries. Phagocytosis of crystalline silica in the lung causes lysosomal damage, activating the NALP3 inflammasome and triggering the inflammatory cascade with subsequent fibrosis. Impairment of lung function increases with disease progression, even after the patient is no longer exposed. Diagnosis of silicosis needs carefully documented records of occupational exposure and radiological features, with exclusion of other competing diagnoses. Mycobacterial diseases, airway obstruction, and lung cancer are associated with silica dust exposure. As yet, no curative treatment exists, but comprehensive management strategies help to improve quality of life and slow deterioration. Further efforts are needed for recognition and control of silica hazards, especially in developing countries., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

In China, dust samplers were originally designed to collect 'total dust' for a short term during production, which is different from the widely adopted sampling strategy for dust. With the aim to provide the conversion factor from Chinese total dust to US and German respirable dust and to look at the influences on conversion factors from environment, production, and instruments, a comparative field study on the dust concentration measurements by different sampling methods was carried out in the same Chinese industries as in the 1989-1990 study and in some other factories. A supplemental experiment was also conducted in a wind tunnel. Dust concentration was measured with a parallel sampling strategy by using the following samplers: 10-mm nylon cyclone for US respirable dust (AR), FSP-Berufsgenossenschaftliches Institut für Arbeitssicherheit (BIA) cyclone for German respirable dust (GR), and samplers for Chinese total dust (CT). Totally, 1434 samples were collected (269 AR, 198 GR, and 967 CT), from which 429 matched sample pairs (249 pairs of AR/CT, 180 GR/CT) were available to calculate conversion ratios. Industry- and job-based conversion factors are presented in this study. The conversion factor of AR/CT was 0.38 for tungsten mines, 0.19 for copper/iron mines, 0.65 for tin mines, and 0.20 for pottery industry, while the factor of GR/CT was 0.69 for tungsten, 0.37 for copper/iron, and 0.52 for pottery. In the job category, AR/CT factors varied from 0.16 to 0.96 and GR/CT from 0.12 to 0.72. For the industries studied in 1988-1989, the AR/CT and GR/CT factors were 0.29 and 0.45, respectively. Both factors were definitely influenced by production, CT dust concentration, sample gain, and variation of dust concentration. Moreover, the respirable dust concentration by FSP-BIA was significantly higher than that by 10-mm cyclones, 63.27-73.10% more as showed also by the wind tunnel experiment. Meanwhile, the GR/CT ratio was significantly larger than the AR/CT in every industry or job with only few exceptions. The GR/CT estimates should be considered as independent ones. Following these results, there is a need to use 'ideal samplers' (consistent with the internationally accepted respirable fraction) in practice and to assess the existent samplers in order to homogenize the exposure data situation.

Background: Human exposure to silica dust is very common in both working and living environments. However, the potential long-term health effects have not been well established across different exposure situations., Methods and Findings: We studied 74,040 workers who worked at 29 metal mines and pottery factories in China for 1 y or more between January 1, 1960, and December 31, 1974, with follow-up until December 31, 2003 (median follow-up of 33 y). We estimated the cumulative silica dust exposure (CDE) for each worker by linking work history to a job-exposure matrix. We calculated standardized mortality ratios for underlying causes of death based on Chinese national mortality rates. Hazard ratios (HRs) for selected causes of death associated with CDE were estimated using the Cox proportional hazards model. The population attributable risks were estimated based on the prevalence of workers with silica dust exposure and HRs. The number of deaths attributable to silica dust exposure among Chinese workers was then calculated using the population attributable risk and the national mortality rate. We observed 19,516 deaths during 2,306,428 person-years of follow-up. Mortality from all causes was higher among workers exposed to silica dust than among non-exposed workers (993 versus 551 per 100,000 person-years). We observed significant positive exposure-response relationships between CDE (measured in milligrams/cubic meter-years, i.e., the sum of silica dust concentrations multiplied by the years of silica exposure) and mortality from all causes (HR 1.026, 95% confidence interval 1.023-1.029), respiratory diseases (1.069, 1.064-1.074), respiratory tuberculosis (1.065, 1.059-1.071), and cardiovascular disease (1.031, 1.025-1.036). Significantly elevated standardized mortality ratios were observed for all causes (1.06, 95% confidence interval 1.01-1.11), ischemic heart disease (1.65, 1.35-1.99), and pneumoconiosis (11.01, 7.67-14.95) among workers exposed to respirable silica concentrations equal to or lower than 0.1 mg/m(3). After adjustment for potential confounders, including smoking, silica dust exposure accounted for 15.2% of all deaths in this study. We estimated that 4.2% of deaths (231,104 cases) among Chinese workers were attributable to silica dust exposure. The limitations of this study included a lack of data on dietary patterns and leisure time physical activity, possible underestimation of silica dust exposure for individuals who worked at the mines/factories before 1950, and a small number of deaths (4.3%) where the cause of death was based on oral reports from relatives., Conclusions: Long-term silica dust exposure was associated with substantially increased mortality among Chinese workers. The increased risk was observed not only for deaths due to respiratory diseases and lung cancer, but also for deaths due to cardiovascular disease. Please see later in the article for the Editors' Summary.

An analysis was conducted on a cohort of Chinese pottery workers to estimate the exposure-response relationship between respirable crystalline silica dust exposure and the incidence of radiographically diagnosed silicosis, and to estimate the long-term risk of developing silicosis until the age of 65. The cohort comprised 3,250 employees with a median follow-up duration of around 37 years. Incident cases of silicosis were identified via silicosis registries (Chinese X-ray stage I, similar to International Labor Organisation classification scheme profusion category 1/1). Individual exposure to respirable crystalline silica dust was estimated based on over 100,000 historical dust measurements. The association between dust exposure, incidence and long-time risk of silicosis was quantified by Poisson regression analysis adjusted for age and smoking. The risk of silicosis depended not only on the cumulative respirable crystalline silica dust exposures, but also on the time-dependent respirable crystalline silica dust exposure pattern (long-term average concentration, highest annual concentration ever experienced and time since first exposure). A long-term "excess" risk of silicosis of approximately 1.5/1,000 was estimated among workers with all annual respirable crystalline silica dust concentration estimates less than 0.1 mg/m(3), using the German measurement strategy. This study indicates the importance of proper consideration of exposure information in risk quantification in epidemiological studies.

Background: Hsp70, an early-response protein induced when organisms are confronted with simple or complicated environmental stresses, can act as either a cellular protector or a danger signal., Objectives: The goal of this study was to evaluate levels of lymphocyte and/or plasma Hsp70 as biomarkers for assessing exposure response to complex coke oven emissions (COEs)., Methods: We recruited 101 coke oven workers and determined levels of polycyclic aromatic hydrocarbon (PAH) exposure, urinary 1-hydroxypyrene (1-OHP), genotoxic damage by comet assay and micronuclei test, and other markers of damage, including plasma malondialdehyde (MDA) and lactate dehydrogenase (LDH). These were compared to levels of lymphocyte (intra-cellular) and plasma (extracellular) Hsp70 using Western blots and enzyme-linked immunosorbent assays (ELISA), respectively., Results: We observed a COEs-related dose-dependent increase in levels of DNA damage, micronuclei rate, MDA concentration, and LDH activity. Lymphocyte Hsp70 levels increased in the intermediate-exposure group (1.39 +/- 0.88) but decreased in the high-exposure group (1.10 +/- 0.55), compared with the low-exposure group. In contrast, plasma Hsp70 levels progressively increased as the dose of exposure increased. Negative correlations were seen between lymphocyte Hsp70 levels and olive tail moment and LDH activity in the intermediate- and high-exposure groups. However, we observed positive correlations between plasma Hsp70 levels and LDH activity in the low and intermediate groups., Conclusions: In workers exposed to COEs, high lymphocyte Hsp70 levels may provide protection and high plasma Hsp70 levels may serve as a danger marker. Larger validation studies are needed to establish the utility of Hsp70 as a response marker.

Objective: The role of silica in the causation of lung cancer is an ongoing debate. In order to explore whether observed association between silica exposure and lung cancer is confounded by exposure to other occupational carcinogens, we updated a previously nested case-control study among a cohort of male workers in 29 Chinese mines and factories on the basis of an extended follow-up., Methods: Five hundred and eleven lung cancer cases and 1,879 matched controls were selected. Exposure to respirable silica as well as relevant occupational confounders were quantitatively assessed based on historical industrial hygiene data. The relationship between exposure to silica and lung cancer was analyzed by conditional logistic regression analysis adjusted for exposure to arsenic, polycyclic aromatic hydrocarbons (PAHs), radon, and smoking., Results: In a crude analysis adjusted for smoking only, a significant trend of increasing risk of lung cancer with exposure to silica was found for tin, iron/copper miners, and pottery workers. But after adjustment for relevant occupational confounders, no relationship between silica and lung cancer can be observed. Instead, there is a significant association between lung cancer mortality and cumulative exposure to inorganic arsenic (OR = 1.86, 95% CI: 1.14, 3.04 for each mg/m(3)-year increase) and carcinogenic PAHs (OR = 1.35, 95% CI: 1.08, 1.69 for each 100 microg/m(3)-year increase)., Conclusion: This analysis does not provide any evidence to show that exposure to silica causes lung cancer in the absence of confounding factors.

Accumulating evidence has shown that both DNA damage caused by the metabolites of polycyclic aromatic hydrocarbons (PAH) and genetic polymorphisms in PAH-metabolic genes contribute to individual susceptibility to PAH-induced carcinogenesis. However, the functional relevance of genetic polymorphisms in PAH-metabolic genes in exposed individuals is still unclear. In this study of 240 coke-oven workers (the exposed group) and 123 non-coke-oven workers (the control group), we genotyped for polymorphisms in the AhR, CYP1A1, GSTM1, and GSTT1 genes by PCR methods, and determined the levels of DNA damage in peripheral blood lymphocytes using the alkaline comet assay. We found that the ln-transformed Olive tail moment (Olive TM) values in the exposed group were significantly higher than those in the control group (P < 0.001). Furthermore, in the exposed group, the Olive TM values in subjects with the AhR Lys(554) variant genotype were higher than those with the AhR Arg(554)/Arg(554) genotype (P = 0.021). Similarly, the Olive TM values in the non-coke-oven workers with the CYP1A1 MspI CC + CT genotype were lower than the values of those with the CYP1A1 MspI TT genotype (P = 0.005). However, these differences were not evident for GSTM1 and GSTT1. These results suggested that the polymorphism of AhR might modulate the effects of PAHs in the exposed group; however, the underlying molecular mechanisms by which this polymorphism may have affected the levels of PAH-induced DNA damage warrant further investigation.

Background: Mineral dusts that contain crystalline silica have been associated directly or indirectly with the development of pneumoconiosis or silicosis, non-malignant respiratory diseases, lung cancer, and other diseases. The health impacts on workers with silica mixed dust exposure in tin mines and dose-response relationships between cumulative dust exposure and the mortality from lung cancer are investigated., Methods: A cohort of 7,837 workers registered in the employment records in 4 Chinese tin mines between 1972 and 1974 was identified for this study and the mortality follow-up was traced through 1994. Of the cohort, the cause of death was ascertained for 1,061 (97%) of the 1,094 deceased workers. Standardized mortality ratios (SMRs) were calculated for all workers, non-exposed workers, and dust-exposed workers with different exposure levels, silicotics, and non-silicotics based on Chinese national rates., Results: The mortality from all causes in four tin mines was nearly the same as the national mortality. Malignant neoplasm, cerebrovascular disease, and cardiovascular disease accounted for 68.6% of all deaths. Mortality excess from lung cancer, liver cancer, all malignant diseases, and non-malignant respiratory diseases was observed among dust-exposed workers; a 50-fold excess of pneumoconiosis was observed. There was an upward trend for SMRs of lung cancer was noted from no exposure to low, medium, and high exposure levels (SMRs=1.29, 2.65, 2.66, 3.33). The shape of the exposure-response curve for risk of lung cancer at high exposure levels was inconsistent in these four mines., Conclusions: The findings indicated a positive dose-response relation between exposure to cumulative dust and the mortality of lung cancer. High arsenic content in dust particles, together with crystalline silica, may play an important role in causing increased mortality from lung cancer., (Copyright (c) 2005 Wiley-Liss, Inc.)

Epidemiological research has demonstrated the relationship between exposure to quartz dust and an elevated risk of pneumoconiosis and possible elevated risk of cancer. The current study was designed to evaluate the biological responses of workplace particles containing crystalline silica using an in vitro cell test. Respirable particle samples were sampled from four tin mines, where the standardized mortality ratio (SMR) for pneumoconiosis was 51.6 and SMR for lung cancer was 2.2 in dust-exposed miners. Alveolar macrophages (AM) are considered as the target cells for primary dust effects. The samples were then measured at 15, 30, 60 and 120 microg particle per 10(6) AM for cytoxicity with the release of glucuronidase, lactate dehydrogenase, for reactive oxygen damage with H(2)O(2) release, and for ability to induce fibrosis using the secretion of tumor necrosis factor-alpha (TNF-alpha). Pure quartz (DQ12) and corundum were used as controls. The results showed the samples from tin mines caused a higher cytoxicity when compared to corundum, yet lower when compared to quartz. However, reactive oxygen species release (148-177 nmol/3 x 10(5) AM in high concentration of 120 microg/10(6) AM) induced by the samples were significantly higher than that induced by quartz (57 nmol/3 x 10(5) AM) and corundum (62 nmol/3 x 10(5) AM). Furthermore, particle samples induced higher TNF-alpha secretion than corundum, the samples from Limu tin mine induced much higher TNF-alpha levels than that induced by DQ12 quartz. The results from the in vitro tests help elucidate the degree of hazard of dust particles in tin mines. The in vitro reaction patterns of AM also constitute a powerful tool to monitor biological and pathogenic responses of humans following dust particle exposure.

We aimed to explore the association between occupational noise exposure duration and heart rate variability (HRV) and the underlying mechanism. A total of 449 subjects in a manufacturing company in Wuhan, China were included in our study and six candidate miRNAs (miR-200a-3p, miR-200b-3p, miR-200c-3p, miR-1-3p, miR-92a-3p and miR-21–5p) were tested among 200 individuals. Information combining the work histories and the occupational noise monitoring records were used to calculate the exposure of occupational noise, HRV indices were measured by using 3-channel digital Holter monitors, including the standard deviation of all normal R-R intervals (SDNN), the root mean of the square of successive differences between adjacent normal NN intervals (r-MSSD), SDNN index, low-frequency power (LF), high-frequency power (HF) and TP (total power). We found a significant linear negative dose-response relationship between occupational noise exposure duration and HRV indices (P for overall <0.05, P for nonlinear >0.05), including SDNN, r-MSSD, SDNN index, LF and HF. In the continuous models, the β (95% CIs) for each 1-year occupational noise exposure were −0.002 (−0.004, −0.001) for SDNN, −0.002 (−0.004, −0.001) for r-MSSD, −0.002 (−0.004, −0.001) for SDNN index, and −0.006 (−0.012, −0.001) for HF. Meanwhile, we also found that occupational noise exposure duration was significantly associated with lower expression of five miRNAs, when adjusting for other covariates. The β (95% CIs) were −0.039 (−0.067, −0.011) for miRNA-200c-3p, −0.053 (−0.083, −0.022) for miRNA-200a-3p, −0.044 (−0.070, −0.019) for miRNA-200b-3p, −0.032 (−0.048, −0.017) for miRNA-92a-3p, and −0.063 (−0.089, −0.038) for miRNA-21–5p in the continuous models. In addition, we found a positive association between miRNA-1-3p and LF (β = 0.039, 95% CI = 0.002, 0.080). Our study suggests that occupational noise exposure duration is associated with cardiac autonomic dysfunction, and the role of miRNAs in noise induced HRV reduction needs to be confirmed in future studies. [Display omitted] • Occupational noise exposure duration is associated with reduced SDNN, SDNN index, and HF. • Occupational noise exposure duration is associated with lower miR-200c-3p, miR-200a-3p, miR-200b-3p, miR-92a-3p, and miR-21–5p. • The role of miRNAs in noise induced HRV reduction needs to be confirmed. [ABSTRACT FROM AUTHOR]

Long-term noise exposure is reported to damage cardiovascular system, but the relationship between occupational noise exposure and arterial stiffness (AS) and the underlying mechanism is still unclear. We aimed to investigate the association of occupational noise exposure with arterial stiffness (AS), and further explore the mediation roles of microRNAs (miRNAs). A total of 838 workers were recruited from two companies in Wuhan, Hubei, China. Cumulative occupational noise exposure (CNE) was assessed through noise level of job title and work years in occupational noise. The AS for the participants were evaluated using brachial-ankle pulse wave velocity (baPWV) measured by an oscillometric device. Each 1-unit increase in CNE levels was significantly associated with a 0.002 (95% confidence interval (CI) = 0.001–0.003) unit increase in ln-transformed values of baPWV. In the sex-specific analysis, the association was significant in males (β = 0.002, 95%CI = 0.001–0.003). Meanwhile, the risk of bilateral hearing loss at high frequency was significantly higher in the high-exposed group than non-exposed group (OR = 1.895, 95%CI = 1.024–3.508), and participants with bilateral hearing loss at high frequency had a significantly higher level of ln-transformed baPWV (β = 0.032, 95%CI = 0.003–0.061). Occupational noise exposure and AS were both negatively associated with plasma miR-92a-3p and miR-21–5p, and the two miRNAs mediated 15.0% and 16.8% of the association of occupational noise with AS (P < 0.05). Our findings suggest that occupational noise exposure is positively associated with AS, and plasma miR-92a-3p and miR-21–5p may partly mediate such association. [Display omitted] • Occupational noise exposure is positively associated with arterial stiffness. • Bilateral high frequency hearing loss is positively associated with arterial stiffness. • Plasma miR-92a-3p and miR-21–5p mediated the association between occupational noise and arterial stiffness. [ABSTRACT FROM AUTHOR]