Differential expression profile of microRNAs in the lung tissues of coal workers with pneumoconiosis and patients with silicosis.

The purpose of this study was to characterize the microRNA (miRNA) profile of the lung tissues from coal workers' pneumoconiosis (CWP) and silicosis and to analyze the changes in downstream genes, biological processes, and signaling pathways based on the differently expressed miRNAs. Lung tissues from three CWP patients, eight silicosis patients, and four healthy controls were collected and analyzed for their miRNA profiles using Affymetrix® GeneChip® miRNA Arrays. Differentially expressed miRNAs (DEMs) were identified between the different groups. The miRanda and TargetScan databases were used to predict the putative target genes, and volcano and heat maps were drawn. Gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) pathway enrichment analyses were then performed to screen the DEMs-associated biological process and signaling pathways, respectively. Further identification with a comprehensive literature research involving particle exposure, fibrosis, inflammation and lung cancer were used to further screen DEMs of CWP and silicosis. Microarray data showed that 375 and 88 miRNAs were differentially expressed in CWP and silicosis lung tissues compared with healthy lung tissues, while 34 miRNAs were differentially expressed in CWP compared with silicosis lung tissues. The GO and KEGG pathway analyses showed that, the target genes were mainly enriched in the TGF-ß, MAPK, p53 and other signal pathways. These results provided insight into the miRNA-related underlying mechanisms of CWP and silicosis, and they provided new clues for miRNAs as biomarkers for the diagnosis and differential diagnosis of these two diseases.

Association of Exposure to Ambient Fine Particulate Matter Constituents With Semen Quality Among Men Attending a Fertility Center in China.

Ambient fine particulate matter (PM2.5) exposure has been linked to decreased semen quality, but the associations between PM2.5 constituent exposures and semen quality remain unknown. We enrolled 1081 men whose partners underwent assisted reproductive technology procedures in Wuhan, China in 2014-2015, and examined their semen quality. Daily average concentrations of PM2.5 constituents including 10 metals/metalloid elements and 4 water-soluble ions were continuously determined for 1 week per month at 2 fixed monitoring stations. Linear mixed models were used to examine the associations of exposures to PM2.5 and its constituents with semen quality. Each interquartile range (36.5 µg/m3) increase in PM2.5 exposure was significantly associated with 8.5% (95% CI: 2.3%, 14.4%) and 8.1% (95% CI: 0.7%, 15.0%) decrease in sperm concentration and total sperm number, respectively. Antimony, cadmium, lead, manganese, and nickel exposures were significantly associated with decreased sperm concentration, whereas manganese exposure was also significantly associated with decreased total motility. Nonsmokers were more susceptible to PM2.5 constituent exposures, especially for antimony and cadmium (all P for effect modification <0.05). These findings suggest that PM2.5 and certain constituents may adversely affect semen quality, especially sperm concentration, and provide new evidence to formulate pollution abatement strategies for male reproductive health.

Inverse Association between Ambient Sulfur Dioxide Exposure and Semen Quality in Wuhan, China.

Evidence concerning the association between ambient gaseous air pollutant exposures and semen quality is sparse, and findings in previous studies remain largely inconsistent. We enrolled 1759 men and performed 2184 semen examinations at a large reproductive medical center in Wuhan, China, between 2013 and 2015. Inverse distance weighting interpolation was performed to estimate individual exposures to SO2, NO2, CO, and O3 during the entire period (lag 0-90 days) and key periods (lag 0-9, 10-14, 70-90 days) of sperm development. Linear mixed models were used to analyze exposure-response relationships. SO2 exposure with 0-90 days lag was significantly associated with monotonically decreased sperm concentration (ß for each interquartile range increase of exposure: -0.14; 95% CI: -0.23, -0.05), sperm count (-0.21; -0.30, -0.12) and total motile sperm count (-0.16; -0.25, -0.08). Significant associations were observed for total and progressive motility only when SO2 exposure was at the highest quintile (all Ptrend < 0.05). Similar trends were observed for SO2 exposure with 70-90 days lag. NO2, CO, or O3 exposure was not significantly associated with semen quality. Our results suggest that ambient SO2 exposure adversely affects semen quality and highlight the potential to improve semen quality by reducing ambient SO2 exposure during early stages of sperm development.

Effects of silica exposure on the cardiac and renal inflammatory and fibrotic response and the antagonistic role of interleukin-1 beta in C57BL/6 mice.

Current epidemiological studies suggest that crystalline silica exposure is associated with an increased risk of cardiovascular and renal disease; however, the potential pathological damage of the heart and kidney and its underlying mechanisms have not been completely elucidated. This study tried to investigate the silica-induced inflammatory and fibrotic changes in the heart and kidney and evaluate the role of interleukin (IL)-1 beta (ß) in silica-induced cardiac and renal damage. In this study, a silica-exposed model was generated by intratracheally instilling silica dust in mice. The anti-IL-1ß monoclonal antibody (mAb) was used to neutralise IL-1ß in the pulmonary alveolus and serum. The real-time PCR studies showed that (1) inhalational silica induced inflammatory responses in the heart and kidney by elevated mRNA levels of TNF-α, IL-6 and MCP-1; (2) early fibrotic responses in the heart were observed as elevated mRNA levels of collagen I and fibronectin. What is more, fibrosis of the kidney was demonstrated by pathological results and significantly increased mRNA levels of TGF-ß, collagen I, collagen III and fibronectin. Further studies showed that usage of anti-IL-1ß mAb decreased the inflammatory response of the heart and kidney induced by inhalational silica and also attenuated fibrosis in the mouse kidney. In conclusion, this study found that inhaled silica induced inflammatory and early fibrotic responses in the mouse heart and inflammatory response and fibrosis in the mouse kidney. Neutralisation of IL-1ß attenuated the silica-induced inflammatory response of the heart and kidney and decreased fibrosis in the mouse kidney.

Plasma LncRNA-ATB, a Potential Biomarker for Diagnosis of Patients with Coal Workers' Pneumoconiosis: A Case-Control Study.

LncRNA-ATB (lncRNA was activated by transforming growth factor-ß) has been reported to be involved in specific physiological and pathological processes in human diseases, and could serve as biomarkers for cancers. However, the role of lncRNA-ATB in coal workers' pneumoconiosis (CWP) is still unknown. This study aimed to investigate the association between lncRNA-ATB and CWP. Quantitative real-time polymerase chain reaction was performed to detect plasma lncRNA-ATB expression in 137 CWP patients, 72 healthy coal miners and 168 healthy controls. LncRNA-ATB was significantly upregulated in CWP (p < 0.05). Compared with the healthy controls and healthy coal miners, the odds ratios (ORs) (95% confidence interval (CI)) for CWP were 2.57 (1.52-4.33) and 2.17 (1.04-4.53), respectively. LncRNA-ATB was positively associated with transforming growth factor-ß1 (TGF-ß1) (r = 0.30, p = 0.003) and negative correlated with vital capacity (VC) (r = -0.18, p = 0.033) and forced vital capacity (FVC) (r = -0.18, p = 0.046) in CWP patients. Compared with healthy controls, the area under the curve (AUC) was 0.84, resulting in a 71.17% sensitivity and 88.14% specificity. When compared with healthy coal miners, the AUC was 0.83, the sensitivity and specificity were 70.07% and 86.36%, respectively. LncRNA-ATB expression is commonly increased in CWP and significantly correlates with the TGF-ß1 in CWP patients. Furthermore, elevated lncRNA-ATB was associated with CWP risk and may serve as a potential biomarker for CWP.

[Oxidative stress and mitochondrion-related cell apoptosis in human bronchial epithelial 16HBE cells induced by silica dust].

OBJECTIVE: To investigate oxidative stress and mitochondria-related cell apoptosis induced by silica dust in human normal bronchial epithelial 16HBE cells. METHODS: Cell viability, lactate dehydrogenase (LDH), superoxide dismutase (SOD), cell apoptotic rate, the expression level of Bax and Bcl-2 mRNA were measured after 16HBE cells were exposed to 37.5, 75, 150, 300 µg/mL respirable silica dust (diameter<2 µm, d50=1 µm)for 24 h in vitro. Reactive oxygen species (ROS)were tested after 16HBE cells were exposed to silica dust at above concentrations for 1.5, 3, 6, 12 h, respectively. RESULTS: Dose-dependent decreases of cell viability and the activity of SOD were observed when silica concentrations increased. The activity of LDH increased when silica concentrations elevated. Compared with the control group, cell viability significantly reduced in 75, 150, 300 µg/mL silica-treated groups (P<0.05). The activity of LDH significantly increased in 150, 300 µg/mL silica-treated groups when compared with the control group (P<0.05). The activity of SOD in all silica-treated groups were significantly lower in comparison with controls (P<0.05). Intracellular ROS levels reached peak values at 1.5 h of silica exposure and gradually dropped to the base level at 12 h. The relationship between ROS levels and silica exposure were dose-response at 1.5 h, 3 h and 6 h of exposure (P<0.05). Similar dose-dependent increase were observed for apoptotic rate and silica exposure (P<0.05). The expression levels of Bcl-2 mRNA decreased, and the expression levels of Bax mRNA increased when silica concentrations increased. The results showed that significantly positive correlations between ROS level and apoptotic rate (r=0.892,P<0.05)or the expression level of Bax mRNA (r=0.850,P<0.05). There was a negative correlation between ROS level and the expression level of Bcl-2 mRNA (r=-0.703,P<0.05). CONCLUSION: Silica dust could induce cytotoxicity, oxidative stress and mitochondria-related cell apoptosis in 16HBE cells. Oxidative stress may play role in the processes of mitochondria-related apoptosis.

The Wuhan-Zhuhai (WHZH) cohort study of environmental air particulate matter and the pathogenesis of cardiopulmonary diseases: study design, methods and baseline characteristics of the cohort.

BACKGROUND: Particulate air pollution has been recognized to be associated with a wide range of adverse health effects, including increased mortality, morbidity, exacerbation of respiratory conditions. However, earlier physiological or pathological changes or long-term bodies' reaction to air pollutants have not been studied in depth in China. The Wuhan-Zhuhai (WHZH) cohort study is designed to investigate the association between air pollutants exposure and physiological or pathological reactions on respiratory and cardiovascular system. METHODS/DESIGN: The cohort is a community-based prospective study that includes 4812 individuals aged 18-80 years. The collections of data were conducted from April to May 2011 in Wuhan city and in May 2012 in Zhuhai city. At baseline, data on demographic and socioeconomic information, occupational history, family disease history, lifestyle, cooking mode, daily travel mode, physical activity and living condition have been collected by questionnaires. Participants underwent an extensive physical examination, including anthropometry, spirometry, electrocardiography, and measurements of blood pressure, heart rate, exhaled nitric oxide and carbon monoxide. Potential conditions in the lung, heart, liver, spleen, and skin were synchronously performed. In addition, samples of morning urine, fasting blood serum and plasma were collected during physical health examination. DNA were extracted and were stored at -80°C. Environment concentrations of particulate matter and chemicals were determined for 15 days in each of four seasons. Participants are followed for physiological or pathological changes or incidence of cardiopulmonary diseases every 3 years. DISCUSSION: The results obtained in WHZH cohort study may increase a better understanding of the relationship between particulate air pollution and its components and possible health damages. And the potential mechanisms underlying the development of cardiopulmonary diseases has implications for the development of prevention and treatment strategies.

Respiratory Toxicology of Graphene-Based Nanomaterials: A Review.

Graphene-based nanomaterials (GBNs) consist of a single or few layers of graphene sheets or modified graphene including pristine graphene, graphene nanosheets (GNS), graphene oxide (GO), reduced graphene oxide (rGO), as well as graphene modified with various functional groups or chemicals (e.g., hydroxyl, carboxyl, and polyethylene glycol), which are frequently used in industrial and biomedical applications owing to their exceptional physicochemical properties. Given the widespread production and extensive application of GBNs, they can be disseminated in a wide range of environmental mediums, such as air, water, food, and soil. GBNs can enter the human body through various routes such as inhalation, ingestion, dermal penetration, injection, and implantation in biomedical applications, and the majority of GBNs tend to accumulate in the respiratory system. GBNs inhaled and substantially deposited in the human respiratory tract may impair lung defenses and clearance, resulting in the formation of granulomas and pulmonary fibrosis. However, the specific toxicity of the respiratory system caused by different GBNs, their influencing factors, and the underlying mechanisms remain relatively scarce. This review summarizes recent advances in the exposure, metabolism, toxicity and potential mechanisms, current limitations, and future perspectives of various GBNs in the respiratory system.

Neutralization of interleukin-1 beta attenuates silica-induced lung inflammation and fibrosis in C57BL/6 mice.

The inflammation and fibrosis induced by silica dust are considered to be substantial responses in silicosis progression. Interleukin-1 beta (IL-1ß) plays an important role in silica-induced lung inflammation, but the mechanisms that underlie the influence of IL-1ß on the progression of silicosis remain unclear. In this study, the role of IL-1ß in silica-induced inflammation and fibrosis was evaluated by administering a suspension of 2.5-mg silica dust, either with or without 40 µg anti-mouse IL-1ß monoclonal antibody (mAb), to the lungs of male C57BL/6 mice. Silica + anti-IL-1ß mAb-treated mice showed the depletion of IL-1ß as well as the attenuation of inflammation, as evaluated in the bronchoalveolar lavage fluid (BALF) and histological sections from 1 to 84 days after silica exposure. Further study of the BALF indicated that inhibition of IL-1ß could reduce the contents of tumor necrosis factor-alpha and monocyte chemoattractant protein-1. The real-time PCR and pathology results showed that the neutralization of IL-1ß attenuated silica-induced fibrosis by inhibiting the gene expression of transforming growth factor-beta 1, collagen I and fibronectin. The examination of Th1-cytokine and Th2-cytokine suggested that depletion of IL-1ß decelerated the Th1/Th2 balance toward a Th2-dominant response. In conclusion, the present study suggests that the neutralization of IL-1ß attenuates silica-induced inflammation and fibrosis by inhibiting other inflammatory and fibrogenic mediators and modulating the Th1/Th2 balance.

[The role of interleukin-1ß on the pulmonary fibrosis in mice exposed to crystalline silica].

OBJECTIVE: This study was designed to evaluate the role of interleukin (IL)-1ß in the development of fibrosis in mice exposed to silica. METHODS: The total of 96 Male C57BL/6 mice were divided into four groups. (1) blank control group, (2) PBS group in which mice were instilled with PBS only, (3) silica + IL-1ß mAb group in which mice were instilled with 2.5 mg silica dust and 40 µg anti-IL-1ß mAb, (4) silica group in which mice were instilled with 2.5 mg silica dust and 40 µg IgG. The final volume of suspension or PBS instilled into the mouse was 50 µl. At 7, 28 and 84 days after treatment, 8 mice were sacrificed in each group. Then BALF was collected for the count of inflammatory cells and cytokines determination. The lung tissues were collected for the detecting of mRNA levels of fibrogenic molecules. RESULTS: The collagen deposition induced by silica in the lung tissues was partly inhibited by anti-IL-1ß. A intensely pulmonary cytokines such as IL-1ß, TNF-α, MCP-1 were induced by crystalline silica exposure, and partly inhibited by anti-IL-1ß. The levels of TGF-ß and fibronectin in silica exposed mice were significantly elevated than those in control mice at days 28 and 84 after treatment (P < 0.01). And the mRNA levels of TGF-ß, collagen I and fibronectin were significantly decreased in silica+IL-1ß mAb group when compared with those in silica group at days 7, 28 and 84 (P < 0.01). There was a significant decrease of the ratios of IFN-γ/IL-4 in both silica+anti-IL-1ß mAb and silica groups when compared with those in control mice at the above three time points (P < 0.01). However, the IFN-γ/IL-4 ratios in silica+anti-IL-1ß group were significantly higher than those in silica group at 7, 28 and 84 days (P < 0.05 or P < 0.01). CONCLUSION: IL-1ß may promote the pulmonary fibrosis in mice exposed to silica.

[Protective performance and subjective evaluation of N95 filtering-facepiece respirators].

OBJECTIVE: To evaluate the protective performance of N95 filtering-facepiece respirators (FFRs) used widely in China and to investigate participants' subjective evaluation about them. METHODS: Four models (A1, A2, B1, B2) of N95 FFRs from two manufactures were chosen to measure the filter penetration and inhalation resistance. Inward leakage was measured by Condensation Nuclei Counting method (CNC) in 50 participants selected using the Chinese respirator fit test panel. Each participant was asked subjective feelings after wearing a respirator by questionnaire survey. RESULTS: The filter penetration and inhalation resistance of four FFRs complied with national standard (GB 2626-2006). The geometric mean fit factors (GMFFs) for four models were 20.9, 14.6, 74.0, 49.1 and there passing rates were 4%, 4%, 42%, 10%. All of four models had bad seal performance, especially the passing rate of A1 and A2 were lower than 10%. The self-feelings about the resistance for FFRs had no significant difference (P > 0.05). The results indicated that B (B1 and B2) has a better fit than A (A1 and A2) according to participants' subject evaluation (P < 0.05). The folding style respirator (B2) was significant more comfortable than the cup style respirator (B1). The subjective feeling of respirators leakage by participant was poor consistent with objective inward leakage test. The kappa index was 0.067 (95%CI: -0.029∼0.163, P = 0.18) and the consistent rate was 50%. CONCLUSION: The poor seal performance was the biggest problem of N95 FFRs in Chinese market. Respirators should be resigned or improved rely on Chinese facial features. Dust workers should choice a fit respirator according to the result of objective leakage test rather than subjective feeling of leakage.

Blood volatile organic aromatic compounds concentrations across adulthood in relation to total and cause specific mortality: A prospective cohort study.

OBJECTIVE: We aimed to evaluate the relationship between blood volatile organic aromatic compounds (VOACs) across adulthood and mortality. METHODS: A total of 16,968 participants from the National health and Nutrition Examination Surveys (NHANES 1988-1994 and 1999-2014) were included in the present study. Cox proportional hazards models were used to explore the associations between VOACs and total or cause-specific mortality. RESULTS: A total of 1,282 deaths occurred among 16,968 participants with a median follow-up of 8.06 years. We observed significant positive dose-response relationship between VOACs including benzene, ethylbenzene, o-xylene, m-/p-xylene and BEX (the sum of benzene, ethylbenzene, m-/p-and o-xylene concentrations) and total mortality, the multiple adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) were 1.24 (1.13, 1.36), 1.15 (1.04, 1.27), 1.10 (1.00, 1.23), 1.09 (1.01, 1.19) and 1.21 (1.08, 1.35), respectively. In addition, all VOACs significantly elevated risk of the mortality from cancer, and benzene was associated with risk of the mortality from heart disease and the HRs and 95% CIs was 1.39 (1.09-1.77). For non-smokers, benzene, ethylbenzene and BEX were associated with elevated risk of total mortality and the mortality from cancer, and benzene was associated with risk of the mortality from heart disease. CONCLUSIONS: Blood VOACs are associated with increased risks of total and specific-cause mortality, which are also observed among non-smokers.

Short-Term Effects of Low-Level Ambient Air NO2 on the Risk of Incident Stroke in Enshi City, China.

Previous studies found that exposure to ambient nitrogen dioxide (NO2) was associated with an increased risk of incident stroke, but few studies have been conducted for relatively low NO2 pollution areas. In this study, the short-term effects of NO2 on the risk of incident stroke in a relatively low-pollution area, Enshi city of Hubei Province, China, were investigated through time-series analysis. Daily air-pollution data, meteorological data, and stroke incidence data of residents in Enshi city from 1 January 2015 to 31 December 2018 were collected. A time-series analysis using a generalised additive model (GAM) based on Poisson distribution was applied to explore the short-term effects of low-level NO2 exposure on the risk of incident stroke and stroke subtypes, as well as possible age, sex, and seasonal differences behind the effects. In the GAM model, potential confounding factors, such as public holidays, day of the week, long-term trends, and meteorological factors (temperature and relative humidity), were controlled. A total of 9122 stroke incident cases were included during the study period. We found that NO2 had statistically significant effects on the incidence of stroke and ischemic stroke, estimated by excess risk (ER) of 0.37% (95% CI: 0.04-0.70%) and 0.58% (95% CI: 0.18-0.98%), respectively. For the cumulative lag effects, the NO2 still had a statistically significant effect on incident ischemic stroke, estimated by ER of 0.61% (95% CI: 0.01-1.21%). The two-pollutant model showed that the effects of NO2 on incident total stroke were still statistically significant after adjusting for other air pollutants (PM2.5, PM10, SO2, CO, and O3). In addition, the effects of NO2 exposure on incident stroke were statistically significant in elderly (ER = 0.75%; 95% CI: 0.11-1.40%), males (ER = 0.47%; 95% CI: 0.05-0.89%) and cold season (ER = 0.83%; 95% CI: 0.15-1.51%) subgroups. Our study showed that, as commonly observed in high-pollution areas, short-term exposure to low-level NO2 was associated with an increased risk of incident stroke, including ischemic stroke. Males and elderly people were more vulnerable to the effects of NO2, and the adverse effects might be promoted in the cold season.

Characteristics of Diagnosed and Death Cases of Pneumoconiosis in Hubei Province, China, 1949-2019.

OBJECTIVE: This study aims to summarize the characteristics of diagnosed pneumoconiosis and pneumoconiosis death in the Hubei Province of China, between the years 1949 and 2019, and provide clues for the scientific prevention of pneumoconiosis. METHODS: We recruited 23,069 pneumoconiosis cases in Hubei Province, China, from 1949 to 2019. Basic information and occupational surveillance information were obtained from the Hubei Occupational Diseases and Health Risk Factors Information Surveillance System. RESULTS: The annually diagnosed pneumoconiosis cases showed an overall increasing trend from 1949 to 2019 in Hubei Province. The major types of pneumoconiosis were coal workers' pneumoconiosis (CWP, 49.91%) and silicosis (43.39%). Pneumoconiosis cases were mainly engaged in mining (75.32%) and manufacturing (12.72%), and were distributed in Huangshi (35.48%), Yichang (16.16%), and Jingzhou (7.97%). CWP (47.50%) and silicosis (44.65%) accounted for most of the deaths. CONCLUSIONS: The number of pneumoconiosis cases and deaths in Hubei increased in the period of 1949 to 2019. Silicosis and CWP contributed to the predominant types of pneumoconiosis. Prevention and control measures should continue to be taken to reduce the morbidity and mortality of pneumoconiosis.

Association of body mass index with serum anti-Müllerian hormone and inhibin B levels among 8323 women attending a reproductive medical center: a cross-sectional study.

PURPOSE: To assess the association of body mass index (BMI) with serum anti-Müllerian hormone (AMH) and inhibin B (InB) levels among women attending a reproductive medical center. METHODS: We conducted a cross-sectional study of 8323 women (96.4% were Han race) without polycystic ovary syndrome (PCOS) from the reproductive medical center of Tongji Hospital in Wuhan, China for assisted reproductive technology treatment between January 2016 and May 2018. For each participant, BMI and levels of serum AMH and InB were measured at entry by trained clinical technicians. Multivariate linear regression models were used to quantitatively estimate the associations of continuous and categorical BMI with serum AMH and InB levels. RESULTS: Each 1 kg/m2 increase in BMI was significantly associated with a 1.02% (95% CI: 0.40, 1.65%) and 3.59% (3.11, 4.06%) reduction in AMH and InB levels, respectively. No departure from linearity was observed for either AMH or InB (both P for nonlinear trend >0.05). Overweight and obesity were significantly associated with a 6.01% (0.70, 11.04%) and 18.64% (2.29, 32.26%) reduction in AMH level, and were significantly associated with a 18.80% (15.23, 22.23%) and a 35.44% (25.47, 44.08%) reduction in InB level, respectively. In addition, the association between BMI and AMH level was significantly stronger among women ≥32 years. CONCLUSIONS: BMI was linearly and inversely associated with AMH and InB levels among women without PCOS. Both overweight and obesity were significantly associated with lower AMH and InB levels.

Association between short-term exposure to ambient air pollution and dementia mortality in Chinese adults.

BACKGROUND: Short-term exposure to ambient air pollution has been linked to an increased risk of mortality from a variety of causes, but its effects on mortality from dementia remain largely unknown. OBJECTIVES: To investigate the association between short-term exposure to ambient air pollution and dementia mortality, and quantitatively assess the excess mortality. METHODS: In this time-stratified case-crossover study, 47,108 dementia deaths were identified in Jiangsu province, China during 2015-2019. Exposure to particulate matter with an aerodynamic diameter ≤ 2.5 µm (PM2.5), PM10, sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO), and ozone (O3) was assessed by extracting daily concentrations from a validated grid dataset based on each subject's residential address. Conditional logistic regression models were applied for exposure-response analyses. RESULTS: There were 47,108 case days and 159,852 control days during the study period. Each 10 µg/m3 increase of lag 04-day exposure to PM2.5, PM10, and NO2 was significantly associated with a 1.43 % (95 % CI: 0.77, 2.09 %), 1.06 % (0.59, 1.54 %), and 2.80 % (1.51, 4.10 %) increase in odds of dementia mortality, corresponding to an excess mortality of 4.87 %, 5.50 %, and 6.43 %, respectively. We estimated that reducing ambient air pollutant exposures to the WHO air quality guidelines would avoid up to 4.17 % of the dementia deaths, while the ambient air quality standards in China would only help avoid up to 0.39 %. CONCLUSIONS: This study provides consistent evidence that short-term exposure to PM2.5, PM10, and NO2 is associated with increased odds of dementia mortality, which can be translated to a considerable excess mortality. Our findings highlight a potential approach to prevent deaths from dementia by reducing individual exposures to ambient air pollution, especially in areas with high levels of ambient air pollution.

The clinical study of CBCT imaging technology in the restoration of upper anterior teeth of the elderly.

OBJECTIVE: To evaluate and analyze the clinical effect of CBCT imaging technology on the restoration of upper anterior teeth of the elderly. METHODS: 36 elderly patients with upper anterior teeth loss in our hospital from January 2018 to January 2020 were selected for implant restoration. Patients were equally randomized into a curved tomographic restoration group (TR group) and a CBCT restoration group (CR group). Patients in the two groups underwent traditional implant restoration. Then we compared and analyzed the implant migration, the adjustment time of first wearing, and the success rate of axial gingival recession and restoration satisfaction of patients in the two groups. RESULTS: The neck offset and the root offset of the implants in the CR group was (0.77±0.15) mm and (0.83±0.17) mm, respectively, which were significantly lower than (1.25±0.27) mm and (1.73±0.29) mm in the TR group (t=6.593, t=11.359, all P<0.01). The initial wearing adjustment time of patients in the CR group [(8.73±1.94) min] was significantly less than (18.79±4.85) min in the TR group (t=8.171, P<0.01); the CR group had a significantly higher success rate of axial gingival recession as compared to the CR group (94.44% vs 61.11%, χ2=6.0857, P<0.05); The restoration satisfaction rate of patients in the CR group was 100%, which was significantly higher than 77.78% of the TR group (χ2=8.7429, P<0.05). CONCLUSION: The CBCT imaging technology has a significant clinical effect on the restoration of the upper anterior teeth of the elderly, which effectively reduces the deviation of implant placement, shorten the adjustment time of their initial wearing, and greatly improves the success rate of axial gingival recession, effectively guarantees the long-term stability and aesthetics of dental implant restoration, and significantly enhances the satisfaction of patients.

Sources of 24-h personal exposure to PM2.5-bound metals: results from a panel study in Wuhan, China.

Atmospheric PM2.5-bound metals have been widely addressed, but research on the exposure levels and sources of personal PM2.5-bound metals among urban community residents is limited. The aim of this study is to explore the exposure levels and sources of 24-h personal PM2.5-bound metals among community inhabitants in Wuhan, China. We conducted a penal study of 216 observations with measurements of 16 metals bounded to 24-h personal PM2.5 samples in April-May, 2014, 2017. Analyses of covariance were used to compare PM2.5-bound metal levels across different living habits and ambient conditions. Principal component analysis (PCA) with varimax rotation was performed to explore PM2.5-bound metal sources. Personal PM2.5-bound aluminum (Al) (113.41 ng/m3) showed the highest geometric mean (GM) concentration, followed by lead (Pb) (90.89 ng/m3), zinc (Zn) (67.71 ng/m3), and iron (Fe) (51.85 ng/m3). The elevated levels of PM2.5-bound Al, vanadium (V), manganese (Mn), arsenic (As), rubidium (Rb), cadmium (Cd), and thallium (Tl) were found in participants with cigarette smoke exposure, compared with those without. The concentrations of Rb and strontium (Sr) were positively associated with the time spent outdoors. The increased concentration of nickel (Ni) was found in individuals who spent > 30 min/day in traffic. The elevated levels of V, Mn, and cobalt (Co) were associated with a short distance from dwellings to the main road. The results of PCA showed that PM2.5-bound metals might come from five sources: As, selenium (Se), Rb, Cd, Tl, and Pb from cigarette smoke exposure; Al, V, Mn, Fe, and Sr from crustal dust; copper (Cu) and antimony (Sb) from industrial activities; Ni and Co from traffic emission; and Zn from coal combustion. The concentrations of PM2.5-bound metals in this study were at moderate levels. Cigarette smoke exposure, industrial activities, traffic emission, and coal combustion might be major anthropogenic sources of personal PM2.5-bound metal exposures in Wuhan, China.

Short-Term Exposure to Ambient Air Pollution and Mortality From Myocardial Infarction.

BACKGROUND: Short-term exposure to ambient air pollution has been linked to occurrence of myocardial infarction (MI); however, only a limited number of studies investigated its association with death from MI, and the results remain inconsistent. OBJECTIVES: This study sought to investigate the association of short-term exposure to air pollution across a wide range of concentrations with MI mortality. METHODS: A time-stratified case-crossover study was conducted to investigate 151,608 MI death cases in Hubei province (China) from 2013 to 2018. Based on each case's home address, exposure to particulate matter with an aerodynamic diameter ≤2.5 µm (PM2.5), particulate matter with an aerodynamic diameter ≤10 µm (PM10), sulfur dioxide, nitrogen dioxide (NO2), carbon monoxide, and ozone on each of the case and control days was assessed as the inverse distance-weighted average concentration at neighboring air quality monitoring stations. Conditional logistic regression models were implemented to quantify exposure-response associations. RESULTS: Exposure to PM2.5, PM10, and NO2 (mean exposure on the same day of death and 1 day prior) was significantly associated with increased odds of MI mortality. The odds associated with PM2.5 and PM10 exposures increased steeply before a breakpoint (PM2.5, 33.3 µg/m3; PM10, 57.3 µg/m3) and flattened out at higher exposure levels, while the association for NO2 exposure was almost linear. Each 10-µg/m3 increase in exposure to PM2.5 (<33.3 µg/m3), PM10 (<57.3 µg/m3), and NO2 was significantly associated with a 4.14% (95% confidence interval [CI]: 1.25% to 7.12%), 2.67% (95% CI: 0.80% to 4.57%), and 1.46% (95% CI: 0.76% to 2.17%) increase in odds of MI mortality, respectively. The association between NO2 exposure and MI mortality was significantly stronger in older adults. CONCLUSIONS: Short-term exposure to PM2.5, PM10, and NO2 was associated with increased risk of MI mortality.

Exogenous Clara cell protein 16 attenuates silica particles-induced inflammation in THP-1 macrophages by down-regulating NF-κB and caspase-1 activation.

Inhalation of silica particles leads to pulmonary inflammatory responses. Clara cell protein 16 (CC16) has been reported to played a protective role in inflammatory lung diseases. However, its role on silica particles-induced inflammation has not been fully clarified. In this study, THP-1 macrophages were exposed to 75 µg/cm2 silica particles with or without 2 µg/mL exogenous CC16 (recombinant CC16, rCC16) for 24 hr. The production of inflammatory cytokines, including interleukin (IL)-1ß, tumor necrosis factor (TNF)-α and IL-6, in the cell supernatants of different groups was detected through ELISA kits and real-time RT-PCR, respectively. The nuclear translocation of nuclear factor (NF)-κB, protein levels of pro-IL-1ß, the nucleotide-binding domain-like receptor protein 3 (NLRP3) and caspase-1 were evaluated via immunofluorescence or western blot. Results showed that, at 75 µg/cm2 silica particle concentration, the treatment of rCC16 significantly decreased IL-1ß, TNF-α and IL-6 protein release and mRNA levels in THP-1 macrophages. Compared to those only exposed to silica particles, THP-1 macrophages exposed to both silica particles and rCC16 showed significantly lower nuclear levels and higher cytosol levels of NF-κB p65, as well as lower co-localization coefficients through immunofluorescence. Additionally, the administration of rCC16 significantly attenuated the increase of pro-IL-1ß, NLRP3 and caspase-1 levels induced by silica particle exposure. Our results suggested that exogenous CC16 could inhibit silica particles-induced inflammation in THP-1 macrophages, mainly through suppressing NF-κB pathway and caspase-1 activation.