Relationship between occupational noise exposure and hypertension: Cross-sectional evidence from real-world.

Background: Occupational noise is one of the most common and prevalent occupational hazards worldwide and may induce adverse auditory and/or non-auditory health effects. However, the relationship between occupational noise exposure and hypertension is controversial and has long been debated. Methods: Based on large sample cross-sectional data from all registered occupational health examination units from 2021 to 2022 (N = 101,605), this study aimed to analyze the prevalence of hearing loss and hypertension and to explore the influencing factors of hypertension of workers in Wuhan. Descriptive statistics, univariate analyses and multivariate analyses were used. Forest plot and nomograms were constructed for the visualization of predictive results. The ROC curve, AUC, C-index and calibration curves were used to assess the predictive accuracy and validity. DCA was performed to evaluate the net benefit that workers could receive. Results: Higher rate of high-frequency hearing loss (25.3%), speech frequency hearing loss (8.8%), ECG abnormalities (31.9%) and hypertension (21.0%) were found in workers exposed to occupational noise in Wuhan. Occupational noise exposure (OR = 1.09, 95% CI: 1.01-1.18, p = 0.04), growth of age (OR: 1.07, 95% CI: 1.07-1.07, p < 0.001), overweight (OR: 1.82, 95% CI: 1.73-1.92, p < 0.001), obesity (OR: 3.62, 95% CI: 3.42-3.83, p < 0.001), hyperglycemia (OR: 1.84, 95% CI: 1.73-1.96, p < 0.001), hypercholesterolemia (OR = 1.34; 95% CI 1.22-1.48; p < 0.001), ECG abnormalities (OR = 1.11; 95% CI 1.07-1.15; p < 0.001) and family history of hypertension (OR = 1.69; 95% CI 1.58-1.81; p < 0.001) were risk factors of hypertension for workers. Male workers had a relatively higher hypertension risk than female workers (OR = 1.61; 95% CI 1.54-1.69; p < 0.001). Ear protective measures could not reduce the risk of hypertension in workers. Our nomogram has good predictive accuracy and validity. A dynamic nomogram to predict the workers' risk of hypertension was established publicly available online. Conclusion: Occupational noise exposure may elevate workers' hypertension risk. More effective and relevant prevention measures should be taken. Our nomogram may help identify high-risk workers and facilitate timely interventions.

Stress hormone biosynthesis-based genes and lifestyle moderated the association of noise exposure with blood pressure in a cohort of Chinese tobacco factory workers: A cross-sectional analysis.

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

Effect of thallium exposure and its interaction with smoking on lung function decline: A prospective cohort study.

BACKGROUND: Thallium (Tl) is a cumulative high toxicant in the environment, but few longitudinal studies have investigated the respiratory impairment of Tl exposure. OBJECTIVES: This study aimed to evaluate the effect of Tl and its interaction with smoking on lung function decline, and explore the potential mechanisms. METHODS: The baseline and follow-up lung functions were measured from a prospective cohort study of 1243 workers, who were followed from 2010 to 2014. Their baseline urinary levels of Tl were determined. We also measured the plasma C-reactive protein (CRP) and urinary 8-iso-prostaglandin-F2α (8-iso-PGF2α) in a randomly selected subcohort of 474 subjects. RESULTS: The results showed that a 2-fold increase in urinary Tl was associated with 29.81 mL (95%CI: 3.83-55.80) increased decline in forced expiratory volume in 1 s (FEV1). The effect was more pronounced among heavy-smokers (≥15 pack-years) [ß(95%CI) = 56.42 mL (9.66-103.19)]. In particular, compared to never-smokers with low Tl, heavy-smokers with high Tl had a separate 158.44 mL (95%CI: 54.88-262.00) and 4.58% (95%CI: 1.40-7.76) increased declines in FEV1 and percentage of predicted (ppFEV1), respectively. There was a significant interaction between Tl and smoking intensity on ppFEV1 decline (Pint = 0.034). More importantly, the increasing level of urinary Tl was correlated with elevated CRP and 8-iso-PGF2α. CONCLUSION: Our prospective cohort study identified that exposure to high Tl had a deleterious effect on lung function, and this effect may be enhanced by tobacco smoking. Increased inflammation may partly contribute to the joint effects of Tl and smoking on impaired lung function, but the biological mechanisms need further explorations.

The interaction effects of polycyclic aromatic hydrocarbons exposure and TERT- CLPTM1L variants on longitudinal telomere length shortening: A prospective cohort study.

Telomere length (TL) is an index of cellular aging and can predict the incidences of many age-related diseases. Change of TL might be affected by environmental pollution and individual's genetic background. In this cohort study, we aimed to evaluate the associations between polycyclic aromatic hydrocarbons (PAHs) exposure and longitudinal TL shortening, and investigate whether genetic variations in TERT-CLPTM1L can modify these associations. We measured the baseline concentrations of twelve urinary PAH metabolites and genotyped six variants at TERT-CLPTM1L among 1243 coke-oven workers. The relative leukocyte TL was detected in both baseline and follow-up (4 years later) visits. The TL shortening were estimated by TL decline and TL ratio. We found that the urinary level of 1-hydroxypyrene (1-OHP) had significant dose-response relationships with increased TL decline [ß(95%CI) = 0.078(0.023, 0.133), P = 0.005] and TL ratio [ß(95%CI) = 0.096(0.037, 0.155), P = 0.002]. Besides, urinary 1-hydroxynaphthalene (1-OHNa) was marginally dose-related with elevated TL decline [ß(95%CI) = 0.053(-0.001, 0.107), P = 0.055] and TL ratio [ß(95%CI) = 0.057(-0.002, 0.116), P = 0.058]. Analyses of TERT-CLPTM1L variants showed that the rs401681 and rs465498 could modify the effect of 1-OHP on increasing TL decline (Pinteraction = 0.012 and 0.035, respectively) and TL ratio (Pinteraction = 0.014 and 0.067, respectively), which were pronounced among rs401681TT and rs465498CC carriers, but not seen among rs401681TC + CC and rs465498CT + TT carriers. In conclusion, elevated exposure to PAHs can accelerate the TL shortening and this effect can be modified by TERT-CLPTM1L variants. These results may add potential evidence for gene-environment interactions on dynamic changes of telomere length. Further studies are warranted to validate these findings and uncover the underlying mechanisms.

A genetic variant in long non-coding RNA MALAT1 associated with survival outcome among patients with advanced lung adenocarcinoma: a survival cohort analysis.

BACKGROUND: Recently studies have demonstrated that the long non-coding RNA (lncRNA) metastasis associated lung adenocarcinoma transcript 1 (MALAT1) may participate in the development and progression of lung cancer. In this study, we hypothesized that genetic variant of this lncRNA may affect the prognosis of lung cancer patients. METHODS: We conducted a follow-up study for 538 patients with non-small cell lung carcinoma (NSCLC), including 140 early-staged (stage I and II) and 398 advanced staged (stage III and IV) patients. The genetic variant rs3200401 in MALAT1 was then genotyped among this population by using TaqMan assay. The association of this variant with overall survival of these patients was further analyzed. RESULTS: It was shown that among the advanced lung adenoma patients, subjects carrying rs3200401 CT and CT + TT genotypes had significantly longer median survival time (MST = 29.9, 28.9 vs. 19.3 month, Long-rank P = 0.019 and 0.024, respectively) and decreased death risks [crude HR (95% CI) = 0.65 (0.43-0.98) and 0.64 (0.44-0.95), P = 0.040 and 0.025, respectively], when compared to subjects wtih the MALAT1 rs3200401 CC genotype. However, the beneficial effect of rs3200401 was not seen among early NSCLC and advanced lung squamous cell carcinoma patients. We further tested the TCGA data, and found that a higher expression of MALAT1 was associated with metastatic of advanced lung adenocarcinoma but not with lung squamous cell carcinoma. CONCLUSIONS: The rs3200401 T allele located on the lncRNA MALAT1 was associated with a better survival for advanced lung adenocarcinoma patients, which may offer a novel prognostic biomarker for this patient subgroup. However, these results need to be validated in larger populations of lung cancer and the biological function of this variant still warrants further investigation.

Association of shift-work, daytime napping, and nighttime sleep with cancer incidence and cancer-caused mortality in Dongfeng-tongji cohort study.

BACKGROUND: Few studies investigated the combined effects of night-shift work, daytime napping, and nighttime sleep on cancer incidence and mortality. METHODS: A total of 25,377 participants were included in this study. Information on sleep habits, cancer incidences, and mortalities were collected. Cox proportional hazards models were used to calculate the adjusted hazard ratios and 95% confidence intervals (HRs, 95%CIs). RESULTS: Male subjects experienced ≥20 years of night-shift work, or without daytime napping had an increased risk of cancer, when compared with males who did not have night-shift work or napped for 1-30 min [HR (95%CI) = 1.27 (1.01-1.59) and 2.03 (1.01-4.13), respectively]. Nighttime sleep for ≥10 h was associated with a separate 40% and 59% increased risk of cancer [HR (95%CI) = 1.40 (1.04-1.88)] and cancer-caused mortality [HR (95%CI) = 1.59 (1.01-2.49)] than sleep for 7-8 h/night. Combined effects of three sleep habits were further identified. Male participants with at least two above risk sleep habits had a 43% increased risk of cancer [HR (95%CI) = 1.43 (1.07-2.01)] and a 2.07-fold increased cancer-caused mortality [HR (95%CI) = 2.07 (1.25-3.29)] than those who did not have any above risk sleep habits. However, no significant associations were observed among women. CONCLUSIONS: Long night-shift work history, without daytime napping, and long nighttime sleep duration were independently and jointly associated with higher cancer incidence among males. KEY MESSAGES Night-shift work of ≥20 years, without napping, and nighttime sleep of ≥10 h were associated with increased cancer incidence. Nighttime sleep ≥10 h was associated with a 2.07-fold increased cancer-caused mortality among males. Combined effects of night-shift work ≥20 years, without napping, and nighttime sleep ≥10 h on increasing cancer incidence were existed among males.

Polycyclic aromatic hydrocarbons exposure and lung function decline among coke-oven workers: A four-year follow-up study.

OBJECTIVES: This study aimed to investigate quantitative relationships of urinary PAH metabolites with lung function declines among coke-oven workers. METHODS: We performed a prospective investigation involving 1243 workers with follow-up periods from 2010 to 2014. Their lung function measurements, including forced vital capacity (FVC), forced expiratory volume in one second (FEV1), the percentage of predicted FVC (FVC%) and FEV1 (FEV1%), FEV1/FVC ratio, and forced expiratory flow between 25% and 75% of vital capacity (FEF25-75), were detected in both baseline (2010) and follow-up study (2014). We also detected the urinary concentrations of 12 PAH metabolites in the baseline study. The relationships between the baseline urinary PAH metabolites and 4-year lung function declines were analyzed by multivariate linear regressions, with adjustment for potential confounders. RESULTS: We found that the baseline concentrations of urinary 1-hydroxynaphthalene (1-OHNa), 2-OHNa, 2-hydroxyfluorene (2-OHFlu), 9-OHFlu, 1-hydroxyphenanthrene (1-OHPh), 2-OHPh, and ΣOH-PAHs were significantly associated with accelerated decline in FEV1/FVC [all ß>0 and false discovery rate (FDR) P<0.05]. Additionally, the baseline levels of urinary 1-OHNa, 1-OHPh, 2-OHPh, 9-OHPh, 1-hydroxypyrene (1-OHP), and ΣOH-PAHs were associated with significantly deeper decline in FEF25-75 (all ß>0 and FDR P<0.10). When using backward selection to adjustment for 10 urinary PAH metabolites, the most significant determiner for FEV1/FVC decline was 1-OHNa among nonsmokers and 9-OHFlu among smokers, and the significant determiner for FEF25-75 decline was 9-OHPh among nonsmokers and 1-OHP among smokers. CONCLUSIONS: This longitudinal study revealed that higher baseline exposure levels of PAHs could lead to greater decline in lung function over a 4-year follow-up.