The refinery of the future.

Fossil fuels-coal, oil and gas-supply most of the world's energy and also form the basis of many products essential for everyday life. Their use is the largest contributor to the carbon dioxide emissions that drive global climate change, prompting joint efforts to find renewable alternatives that might enable a carbon-neutral society by as early as 2050. There are clear paths for renewable electricity to replace fossil-fuel-based energy, but the transport fuels and chemicals produced in oil refineries will still be needed. We can attempt to close the carbon cycle associated with their use by electrifying refinery processes and by changing the raw materials that go into a refinery from fossils fuels to carbon dioxide for making hydrocarbon fuels and to agricultural and municipal waste for making chemicals and polymers. We argue that, with sufficient long-term commitment and support, the science and technology for such a completely fossil-free refinery, delivering the products required after 2050 (less fuels, more chemicals), could be developed. This future refinery will require substantially larger areas and greater mineral resources than is the case at present and critically depends on the capacity to generate large amounts of renewable energy for hydrogen production and carbon dioxide capture.

Radon activity concentration RnCA and workers lung cancer risks in SENA coal mines, Colombia.

The risk of lung cancer or pneumoconiosis mortality, increases with radioactive radon gas exposures. This article report health risk for underground workers exposed to radioactive gas and radon daughters carried by airborne dust at the coal mining in the Central Mountainous Region of Colombia. A set of 33 measurement points located in that mine galleries were selected to monitor radon gas concentration activity, by passive LR-115 detectors, during two months. Resulting values provided radon concentrations, absorbed dose, environmental equivalent dose and the effective dose; miners increased risk of contracting lung cancer is included. It is concluded that the mine ventilation system satisfies the conditions required by the current radiological protection of the miners. Our study point out that Colombia can effectively address the potential risks associated with radon exposure and ensure a safer living environment for its citizens.

A nested case-control study of the effects of dust exposure, smoking on COPD in coal workers.

BACKGROUND: Chronic obstructive pulmonary disease (COPD) represents a prevalent ailment, progressively surging within the ranks of coal mine laborers. The current study endeavors to elucidate the effects of dust exposure and smoking on COPD incidence amongst coal mine workers, while concurrently devising preventive strategies for this affliction. METHOD: A nested case-control study was conducted encompassing 1,416 participants aged ≥ 18 years, spanning the duration from (2017-2018) until 2020. A meticulous matching process yielded a cohort of 708 COPD patients, each paired with a control subject, forming a harmonious 1:1 ratio. Multiple logistic regression analysis was employed to scrutinize the associations between smoking, dust exposure with COPD among coal workers. RESULTS: The COPD prevalence within the cohort of coal workers under investigation amounted to 22.66%, with an accompanying incidence density of 0.09/person-year. Following meticulous adjustment for confounding variables, it was discerned that cumulative dust exposure within the range of 47.19 ~ (OR: 1.90, 95% CI: 1.05, 3.44), 101.27 ~ (OR: 1.99, 95% CI: 1.17, 3.39), as well as smoking indices of 72 ~ (OR: 1.85, 95% CI: 1.19, 2.88), 145 ~ (OR: 1.74, 95% CI: 1.17, 2.61), 310 ~ (OR: 1.85, 95% CI: 1.23, 2.77) engender an escalated vulnerability to COPD among coal workers. Furthermore, interaction analysis discerned an absence of both multiplicative and additive interactions between dust exposure, smoking, and COPD occurrence amidst coal workers. CONCLUSION: Dust exposure and smoking were unequivocally identified as precipitating risk factors for COPD incidence within the population of coal workers, albeit devoid of any discernible interaction between these two causal agents.

Historical shift in pathological type of progressive massive fibrosis among coal miners in the USA.

BACKGROUND: Pneumoconiosis among coal miners in the USA has been resurgent over the past two decades, despite modern dust controls and regulatory standards. Previously published studies have suggested that respirable crystalline silica (RCS) is a contributor to this disease resurgence. However, evidence has been primarily indirect, in the form of radiographic features. METHODS: We obtained lung tissue specimens and data from the National Coal Workers' Autopsy Study. We evaluated specimens for the presence of progressive massive fibrosis (PMF) and used histopathological classifications to type these specimens into coal-type, mixed-type and silica-type PMF. Rates of each were compared by birth cohort. Logistic regression was used to assess demographic and mining characteristics associated with silica-type PMF. RESULTS: Of 322 cases found to have PMF, study pathologists characterised 138 (43%) as coal-type, 129 (40%) as mixed-type and 55 (17%) as silica-type PMF. Among earlier birth cohorts, coal-type and mixed-type PMF were more common than silica-type PMF, but their rates declined in later birth cohorts. In contrast, the rate of silica-type PMF did not decline in cases from more recent birth cohorts. More recent year of birth was significantly associated with silica-type PMF. CONCLUSIONS: Our findings demonstrate a shift in PMF types among US coal miners, from a predominance of coal- and mixed-type PMF to a more commonly encountered silica-type PMF. These results are further evidence of the prominent role of RCS in the pathogenesis of pneumoconiosis among contemporary US coal miners.

Household air pollution and epigenetic aging in Xuanwei, China.

BACKGROUND: Household air pollution (HAP) from indoor combustion of solid fuel is a global health burden linked to lung cancer. In Xuanwei, China, lung cancer rate for nonsmoking women is among the highest in the world and largely attributed to high levels of polycyclic aromatic hydrocarbons (PAHs) that are produced from combustion of smoky (bituminous) coal used for cooking and heating. Epigenetic age acceleration (EAA), a DNA methylation-based biomarker of aging, has been shown to be highly correlated with biological processes underlying the susceptibility of age-related diseases. We aim to assess the association between HAP exposure and EAA. METHODS: We analyzed data from 106 never-smoking women from Xuanwei, China. Information on fuel type was collected using a questionnaire, and validated exposure models were used to predict levels of 43 HAP constituents. Exposure clusters were identified using hierarchical clustering. EAA was derived for five epigenetic clocks defined as the residuals resulting from regressing each clock on chronological age. We used generalized estimating equations to test associations between exposure clusters derived from predicted levels of HAP exposure, ambient 5-methylchrysene (5-MC), a PAH previously found to be associated with risk of lung cancer, and EAA, while accounting for repeated-measurements and confounders. RESULTS: We observed an increase in GrimAge EAA for clusters with 31 and 33 PAHs reflecting current (ß = 0.77 y per standard deviation (SD) increase, 95 % CI:0.36,1.19) and childhood (ß = 0.92 y per SD, 95 % CI:0.40,1.45) exposure, respectively. 5-MC (ng/m3-year) was found to be associated with GrimAge EAA for current (ß = 0.15 y, 95 % CI:0.05,0.25) and childhood (ß = 0.30 y, 95 % CI:0.13,0.47) exposure. CONCLUSIONS: Our findings suggest that exposure to PAHs from indoor smoky coal combustion, particularly 5-MC, is associated with GrimAge EAA, a biomarker of mortality.

Association between household fuel combustion and diabetes among middle-aged and older adults in China: A cohort study.

BACKGROUND: Few studies examined the associations of household fuel combustion with incident diabetes. The current study emphasizes the association of domestic fuel combustion with diabetes among middle- and older- Chinese. METHODS: The data was extracted from a national and prospective cohort, the China Health and Retirement Longitudinal Study (CHARLS), which enrolled adults ≥ 45 years. A total of 4610 and 5570 participants were involved in heating and cooking-related analyses. Multivariable logistic models were conducted to assess the association of domestic fuel combustion for heating and cooking with diabetes. Furthermore, we also examined whether it differed from switching fuel types. Subgroup and interaction analyses were performed based on covariates to examine the robustness and find potential effect modifiers. RESULTS: After about 5-year follow-up, 592 and 716 diabetes were diagnosed in heating and cooking-related analyses. Compared to cleaner fuel users, those who used solid fuel for heating [OR (95 % CI):1.32 (1.05-1.66)] maintained higher risks of incident diabetes. In addition, participants who were exposed to solid fuel for both heating and cooking [OR (95 % CI):1.55 (1.17-2.06)] might have further elevated diabetic risk. Those risks are likely to be attenuated if people switched cooking fuel from solid to cleaner [OR (95 % CI): 0.68 (0.53-0.89)]. CONCLUSIONS: Home solid fuel use for heating is associated with an increased risk of incident diabetes. If solid fuel was concurrently used for both cooking and heating, those risks might be further elevated. Interestingly, as compared to solid fuel users, the participants switching cooking fuel types from solid to cleaner presented reduced diabetic risk.

Where there are fumes, there may be lung cancer: a systematic review on the association between exposure to cooking fumes and the risk of lung cancer in never-smokers.

PURPOSE: Lung cancer in never-smokers (LCINS) is the seventh leading cause of cancer, and exposure to cooking fumes has recently emerged as a potential risk factor. This systematic review is the first to summarize and evaluate the relationship between exposure to cooking fumes and the risk of LCINS. METHODS: This study conducted an online literature search of PubMed, CINAHL, and PsychInfo databases. Inclusion criteria were original research articles published in English, that assessed the relationship between exposure to cooking fumes and the risk of lung cancer between 1 January 2012 and 6 December 2022, and that included never-smokers. RESULTS: Thirteen case-control studies and three prospective cohort studies, focusing mostly on women with LCINS, met the inclusion criteria. Seven case-control studies reported an association between exposure to cooking oil fumes and an increased risk of LCINS. Two case-control studies found that using a fume extractor was associated with a decreased risk of LCINS. In other case-control studies, coal use was linked to an increased risk of LCINS, and participants who did not use a ventilator in their kitchens had a higher risk for LCINS. Poor ventilation [Adjusted Hazard Ratio (AHR) = 1.49; 95% CI: 1.15, 1.95] and poor ventilation in combination with coal use (AHR = 2.03; 95% CI: 1.35, 3.05) were associated with an increased risk for LCINS in one prospective cohort study. CONCLUSION: The evidence reviewed underscores the need to develop culturally-tailored interventions that improve access to affordable and clean fuel through engaging relevant stakeholders.

Exposure to smoky coal combustion emissions and leukocyte Alu retroelement copy number.

Household air pollution (HAP) from indoor combustion of solid fuel is a global health burden that has been linked to multiple diseases including lung cancer. In Xuanwei, China, lung cancer rate for non-smoking women is among the highest in the world and largely attributed to high levels of polycyclic aromatic hydrocarbons (PAHs) that are produced from combustion of smoky (bituminous) coal. Alu retroelements, repetitive mobile DNA sequences that can somatically multiply and promote genomic instability have been associated with risk of lung cancer and diesel engine exhaust exposure. We conducted analyses for 160 non-smoking women in an exposure assessment study in Xuanwei, China with a repeat sample from 49 subjects. Quantitative PCR was used to measure Alu repeat copy number relative to albumin gene copy number (Alu/ALB ratio). Associations between clusters derived from predicted levels of 43 HAP constituents, 5-methylchrysene (5-MC), a PAH previously associated with lung cancer in Xuanwei and was selected a priori for analysis, and Alu repeats were analyzed using generalized estimating equations. A cluster of 31 PAHs reflecting current exposure was associated with increased Alu copy number (ß:0.03 per standard deviation change; 95% confidence interval (CI):0.01,0.04; P-value = 2E-04). One compound within this cluster, 5-MC, was also associated with increased Alu copy number (P-value = 0.02). Our findings suggest that exposure to PAHs due to indoor smoky coal combustion may contribute to genomic instability. Additionally, our study provides further support for 5-MC as a prominent carcinogenic component of smoky coal emissions. Further studies are needed to replicate our findings.

A global review of the state of the evidence of household air pollution's contribution to ambient fine particulate matter and their related health impacts.

Direct exposure to household fine particulate air pollution (HAP) associated with inefficient combustion of fuels (wood, charcoal, coal, crop residues, kerosene, etc.) for cooking, space-heating, and lighting is estimated to result in 2.3 (1.6-3.1) million premature yearly deaths globally. HAP emitted indoors escapes outdoors and is a leading source of outdoor ambient fine particulate air pollution (AAP) in low- and middle-income countries, often being a larger contributor than well-recognized sources including road transport, industry, coal-fired power plants, brick kilns, and construction dust. We review published scientific studies that model the contribution of HAP to AAP at global and major sub-regional scales. We describe strengths and limitations of the current state of knowledge on HAP's contribution to AAP and the related impact on public health and provide recommendations to improve these estimates. We find that HAP is a dominant source of ambient fine particulate matter (PM2.5) globally - regardless of variations in model types, configurations, and emission inventories used - that contributes approximately 20 % of total global PM2.5 exposure. There are large regional variations: in South Asia, HAP contributes âˆ¼ 30 % of ambient PM2.5, while in high-income North America the fraction is âˆ¼ 7 %. The median estimate indicates that the household contribution to ambient air pollution results in a substantial premature mortality burden globally of about 0.77(0.54-1) million excess deaths, in addition to the 2.3 (1.6-3.1) million deaths from direct HAP exposure. Coordinated global action is required to avert this burden.

Methylated polycyclic aromatic hydrocarbons from household coal use across the life course and risk of lung cancer in a large cohort of 42,420 subjects in Xuanwei, China.

BACKGROUND: We previously showed that exposure to 5-methylchrysene (5MC) and other methylated polycyclic aromatic hydrocarbons (PAHs) best explains lung cancer risks in a case-control study among non-smoking women using smoky coal in China. Time-related factors (e.g., age at exposure) and non-linear relations were not explored. OBJECTIVE: We investigated the relation between coal-derived air pollutants and lung cancer mortality using data from a large retrospective cohort. METHODS: Participants were smoky (bituminous) or smokeless (anthracite) coal users from a cohort of 42,420 subjects from four communes in XuanWei. Follow-up was from 1976 to 2011, during which 4,827 deaths from lung-cancer occurred. Exposures were predicted for 43 different pollutants. Exposure clusters were identified using hierarchical clustering. Cox regression was used to estimate exposure-response relations for 5MC, while effect modification by age at exposure was investigated for cluster prototypes. A Bayesian penalized multi-pollutant model was fitted on a nested case-control sample, with more restricted models fitted to investigate non-linear exposure-response relations. RESULTS: We confirmed the strong exposure-response relation for 5MC (Hazard Ratio [95% Confidence Interval] = 2.5 [2.4, 2.6] per standard-deviation (SD)). We identified four pollutant clusters, with all but two PAHs in a single cluster. Exposure to PAHs in the large cluster was associated with a higher lung cancer mortality rate (HR [95%CI] = 2.4 [2.2, 2.6] per SD), while exposure accrued before 18 years of age appeared more important than adulthood exposures. Results from the multi-pollutant model identified anthanthrene (ANT) and benzo(a)chrysene (BaC) as risk factors. 5MC remained strongly associated with lung cancer in models that included ANT and BaC and also benzo(a)pyrene (BaP). CONCLUSION: We confirmed the link between PAH exposures and lung cancer in smoky coal users and found exposures before age 18 to be especially important. We found some evidence for the carcinogen 5MC and non-carcinogens ANT and BaC.

Increased odds of mortality from non-malignant respiratory disease and lung cancer are highest among US coal miners born after 1939.

OBJECTIVES: Coal miners suffer increased mortality from non-malignant respiratory diseases (NMRD), including pneumoconioses and chronic obstructive pulmonary disease, compared with the US population. We characterised mortality trends from NMRD, lung cancer and ischaemic heart disease (IHD) using data from the Federal Black Lung Program, National Coal Workers' Health Surveillance Program and the National Death Index. METHODS: We compared mortality ORs (MORs) for NMRD, lung cancer and IHD in former US coal miners to US white males. MORs were computed for the study period 1979-2017 by birth cohort (<1920, 1920-1929, 1930-1939, ≥1940), with a subanalysis restricted to Central Appalachia. RESULTS: The study population totalled 235 550 deceased miners, aged >45 years. Odds of death from NMRD and lung cancer across all miner birth cohorts averaged twice those of US males. In Central Appalachia, MORs significantly increased across birth cohorts. There was an eightfold increase in odds of death from NMRD among miners born after 1940 (MORBC≥1940 8.25; 95% CI 7.67 to 8.87). Miners with progressive massive fibrosis (PMF) were younger at death than those without PMF (74 vs 78 years; p<0.0001). We observed a pattern of reduced MORs from IHD in coal miners compared with national and regional counterparts. CONCLUSION: US coal miners have excess mortality from NMRD and lung cancer compared with total US and Appalachian populations. Mortality is highest in the most recent birth cohorts, perhaps reflecting increased rates of severe pneumoconiosis.

Indoor air pollution from coal combustion and tobacco smoke during the periconceptional period and risk for neural tube defects in offspring in five rural counties of Shanxi Province, China, 2010-2016.

Indoor air pollution may increase the risk for neural tube defects (NTDs) in Chinese rural populations. However, this association remains a subject of debate. We conducted a population-based case-control study of 222 NTD and 517 control mothers recruited between 2010 and 2016 in five rural areas in northern China. An indoor air pollution exposure evaluation index (IAPEEI) was used to evaluate mothers' exposure to tobacco-sourced and coal-sourced indoor air pollution. Essential characteristics were collected using structured questionnaires within 10 days of delivery. We found that exposure to indoor air pollution (IAPEEI ≥ 1) can lead to 3.41 times the risk of conceiving NTD fetuses compared with the no-exposure group (IAPEEI = 0) (adjusted odds ratio and 95 % confidence interval: 3.41 [2.34-5.02]). The risk increased with increasing IAPEEI score, indicating a clear dose-response trend (P < 0.001). Using a coal stove for heating (especially in the bedroom) and passive smoking are significantly associated with an increased likelihood of NTD occurrence. Exposure to indoor air pollution is a daily reality for rural women in China, and its impact on reproductive health deserves extensive attention.

First Case Report Of Anca-Associated Vasculitis And Anthracosis Coexistence.

Anthracosis is a type of mild pneumoconiosis secondary to harmless carbon dust deposits. Although anthracosis was previously associated with inhaled coal particles, such as coal workers' pneumoconiosis, this hypothesis was later abandoned; pathology has been associated with inhaled dust particles. Our paper is the first case report of ANCA-associated vasculitis and anthracosis coexistence. In addition, it aims to highlight that histopathologically proven anthracotic granulomatous nodules can show high FDG uptake in PET/CT contrary to expectation. We present a case of a 73-year-old male with p-ANCA-associated vasculitis and anthracotic lung nodules accompanied by radiological and clinical findings. The patient got diagnosis with p-ANCA-associated vasculitis with serological and rheumatological tests. Atypically, the clinical findings of the patient were weak (No dyspnoea, cough or additional pulmonary complaints). Nodules were present on X-ray graphics and nodules' contours were irregular on CT. On PET/CT, SUV values of the nodules were high [12 kBq/mL]. Histopathological specimens showed multiple lung granulomas including anthracosis particles. Until performing the biopsy, we could not exclude the possibility of malignancy. Conclusion: When lung involvement of vasculitis is superimposed by anthracosis, it can create granulomas with high SUV values. The relationship between anthracosis and parenchymal lung diseases is a current topic and many recently published papers are present on this subject. To the best of our knowledge, our paper is the first paper showing the relationship between parenchymal involvement of vasculitis and anthracosis in the literature. Environmental pollution and dust particles are the known reasons for anthracosis particles in the nodules. It is open to future research on whether air pollution triggers new atypical cases or not.

Overall and cause-specific mortality rates among men and women with high exposure to indoor air pollution from the use of smoky and smokeless coal: a cohort study in Xuanwei, China.

OBJECTIVES: Never-smoking women in Xuanwei (XW), China, have some of the highest lung cancer rates in the country. This has been attributed to the combustion of smoky coal used for indoor cooking and heating. The aim of this study was to evaluate the spectrum of cause-specific mortality in this unique population, including among those who use smokeless coal, considered 'cleaner' coal in XW, as this has not been well-characterised. DESIGN: Cohort study. SETTING: XW, a rural region of China where residents routinely burn coal for indoor cooking and heating. PARTICIPANTS: Age-adjusted, cause-specific mortality rates between 1976 and 2011 were calculated and compared among lifetime smoky and smokeless coal users in a cohort of 42 420 men and women from XW. Mortality rates for XW women were compared with those for a cohort of predominately never-smoking women in Shanghai. RESULTS: Mortality in smoky coal users was driven by cancer (41%), with lung cancer accounting for 88% of cancer deaths. In contrast, cardiovascular disease (CVD) accounted for 32% of deaths among smokeless coal users, with 7% of deaths from cancer. Total cancer mortality was four times higher among smoky coal users relative to smokeless coal users, particularly for lung cancer (standardised rate ratio (SRR)=17.6). Smokeless coal users had higher mortality rates of CVD (SRR=2.9) and pneumonia (SRR=2.5) compared with smoky coal users. These patterns were similar in men and women, even though XW women rarely smoked cigarettes. Women in XW, regardless of coal type used, had over a threefold higher rate of overall mortality, and most cause-specific outcomes were elevated compared with women in Shanghai. CONCLUSIONS: Cause-specific mortality burden differs in XW based on the lifetime use of different coal types. These observations provide evidence that eliminating all coal use for indoor cooking and heating is an important next step in improving public health particularly in developing countries.

The recognition of lung disease in coal workers: The role of Gough-Wentworth whole lung sections.

From the identification of a specific lung disease caused by coal dust exposure in miners in 1831 until the demonstration of the association of that exposure to risk of emphysema in 1984, there was continuous argument about the harmfulness of coal dust. Ill health in miners was attributed variously to tuberculosis, quartz exposure or cigarette smoking. An acceptance that coal dust was harmful only started with investigative radiology and pathology in the 1920s, and physiology in the 1950s. Most of the early investigations were in South Wales, the centre of the most important coal field in Great Britain. Among the investigators was Professor Jethro Gough who, with his technician James Wentworth, introduced a technique for making thick sections of whole, inflated lungs on paper backing. Here, we describe this method and its central role in understanding the relationships between coal dust exposure, pneumoconiosis, emphysema and lung dysfunction in miners.

Coal Miners and Lung Cancer: Can Mortality Studies Offer a Perspective on Rat Inhalation Studies of Poorly Soluble Low Toxicity Particles?

Inhalation studies involving laboratory rats exposed to poorly soluble particles (PSLTs), such as carbon black and titanium dioxide, among others, have led to the development of lung cancer in conditions characterized as lung overload. Lung overload has been described as a physiological state in which pulmonary clearance is impaired, particles are not effectively removed from the lungs and chronic inflammation develops, ultimately leading to tumor growth. Since lung tumors have not occurred under similar states of lung overload in other laboratory animal species, such as mice, hamsters and guinea pigs, the relevance of the rat as a model for human risk assessment has presented regulatory challenges. It has been suggested that coal workers' pneumoconiosis may reflect a human example of apparent "lung overload" of poorly soluble particles. In turn, studies of risk of lung cancer in coal miners may offer a valuable perspective for understanding the significance of rat inhalation studies of PSLTs on humans. This report addresses whether coal can be considered a PSLT based on its composition in contrast to carbon black and titanium dioxide. We also review cohort mortality studies and case-control studies of coal workers. We conclude that coal differs substantially from carbon black and titanium dioxide in its structure and composition. Carbon black, a manufactured product, is virtually pure carbon (upwards of 98%); TiO2 is also a manufactured product. Coal contains carcinogens such as crystalline silica, beryllium, cadmium and iron, among others; in addition, coal mining activities tend to occur in the presence of operating machinery in which diesel exhaust particles, a Type I Human carcinogen, may be present in the occupational environment. As a result of its composition and the environment in which coal mining occurs, it is scientifically inappropriate to consider coal a PSLT. Despite coal not being similar to carbon black or TiO2, through the use of a weight of evidence approach-considered the preferred method when evaluating disparate studies to assess risk- studies of coal-mine workers do not indicate a consistent increase in lung cancer risk. Slight elevations in SMR cannot lead to a reliable conclusion about an increased risk due to limitations in exposure assessment and control of inherent biases in case-control studies, most notably confounding and recall bias. In conclusion, the weight of the scientific literature suggests that coal mine dust is not a PSLT, and it does not increase lung cancer risk.

Glycogen metabolism reprogramming promotes inflammation in coal dust-exposed lung.

Long-term coal dust exposure triggers complex inflammatory processes in the coal workers' pneumoconiosis (CWP) lungs. The progress of the inflammation is reported to be affected by disordered cell metabolism. However, the changes in the metabolic reprogramming associated with the pulmonary inflammation induced by the coal dust particles are unknown. Herein, we show that coal dust exposure causes glycogen accumulation and the reprogramming of glucose metabolism in the CWP lung. The glycogen accumulation caused by coal dust is mainly due to macrophages, which reprogram glycogen metabolism and trigger an inflammatory response. In addition, 2-deoxy-D-glucose (2-DG) reduced glycogen content in macrophages, which was accompanied by mitigated inflammation and restrained NF-κB activation. Accordingly, we have pinpointed a novel and crucial metabolic pathway that is an essential regulator of the inflammatory phenotype of coal dust-exposed macrophages. These results shed light on new ways to regulate CWP inflammation.

[Progress in the epidemiological studies on coal mine dust exposure with workers' health damage].

Coal is one of the major fuels, which brings huge energy and economic benefits to global industry and daily life. large amounts of coal dust produced in the process of coal mining and transportation, which seriously threatens the health of related workers. Productive coal dust exposure not only directly leads to respiratory diseases, but also may cause health damage to various systems throughout the body. Numerous studies have shown that coal dust exposure is closely associated with decreased lung function, coal worker's pneumoconiosis, chronic obstructive pulmonary disease, lung cancer, and cardiovascular diseases, and the severity of diseases is affected by coal rank, coal dust concentration, cumulative dust exposure, coal dust composition, and individual lifestyle, etc. The article comprehensively summarized the progress of the epidemiological studies on the health hazards of coal miners from coal dust exposure, in order to provide clues for further researches on health damage and protect the health of the occupational population.