Pneumoconiosis and advanced occupational lung disease among surface coal miners--16 states, 2010-2011

Coal workers' pneumoconiosis (CWP) is a chronic occupational lung disease caused by long-term inhalation of dust, which triggers inflammation of the alveoli, eventually resulting in irreversible lung damage. CWP ranges in severity from simple to advanced; the most severe form is progressive massive fibrosis (PMF). Advanced CWP is debilitating and often fatal. To prevent CWP, the Coal Mine Health and Safety Act of 1969 established the current federal exposure limit for respirable dust in underground and surface coal mines. The Act also established a surveillance system for assessing prevalence of pneumoconiosis among underground coal miners, but this surveillance does not extend to surface coal miners. With enforcement of the exposure limit, the prevalence of CWP among underground coal miners declined from 11.2% during 1970-1974 to 2.0% during 1995-1999, before increasing unexpectedly in the last decade, particularly in Central Appalachia. Exposure to respirable dust is thought to be less in surface than underground coal miners. Although they comprise 48% of the coal mining workforce, surface coal miners have not been studied since 2002. To assess the prevalence, severity, and geographic distribution of pneumoconiosis among current surface coal miners, CDC obtained chest radiographs of 2,328 miners during 2010-2011 through the Coal Workers' Health Surveillance Program of the National Institute for Occupational Safety and Health (NIOSH). Forty-six (2.0%) of 2,257 miners with >1 year of surface mining experience had CWP, including 37 who had never worked underground. Twelve (0.5%) had PMF, including nine who had never worked underground. A high proportion of the radiographs suggested silicosis, a disease caused by inhalation of crystalline silica. Surface coal mine operators should monitor worker exposures closely to ensure that both respirable dust and silica are below recommended levels to prevent CWP. Clinicians should be aware of the risk for advanced pneumoconiosis among surface coal miners, in addition to underground coal miners, to facilitate prompt disease identification and intervention.     

Airways obstruction, coal mining, and disability.

It has recently been suggested that the inhalation of coal in the absence of complicated coal workers' pneumoconiosis (CWP) or smoking can lead to disabling airways obstruction. The cause of such obstruction has been variously attributed to emphysema or bronchitis. The frequency of significant airways obstruction in a group of United States coal miners seeking compensation for occupationally induced pulmonary impairment was therefore determined. In a sample of 611 "Black Lung" claimants there was only one subject who was a non-smoker and who in the absence of other non-occupationally related diseases,--for example, asthma and bronchiectasis--had sufficient airways obstruction to render it difficult for him to carry out hard labour. An alternative explanation for his reduced ventilatory capacity other than coal dust or smoking may be available. If the inhalation of coal dust in the absence of smoking and complicated CWP ever induces sufficient ventilatory impairment to preclude a miner from working, it is indeed rare.     

An investigation into the relationship between coal workers' pneumoconiosis and dust exposure in U.S. coal miners.

The National Study of Coal Workers' Pneumoconiosis (NSCWP) is a large, continuing epidemiologic study of the respiratory health of U.S. coal miners. By using information from the study, prevalence of coal workers' pneumoconiosis (CWP) was related to indexes of dust exposure obtained from research and compliance sampling data. Clear relationships between prevalences of both simple CWP and progressive massive fibrosis (PMF) and estimated dust exposure were seen. Additional effects independently associated with coal rank (% carbon) and age were also seen. Logistic model fitting indicated that between 2% and 12% of miners exposed to a 2-mg/m3 dust environment in bituminous coal mines would be expected to have Category 2 or greater CWP after a 40-yr working life; PMF would be expected for between 1.3% and 6.7%. The risks for anthracite miners appeared to be greater. There was a suggestion of a background level of abnormality, not associated with dust exposure, but increasing with age. Although there are certain weaknesses in the data used to derive these exposure estimates, the results are in general agreement with, but somewhat greater than, some recent findings for British coal miners.     

Epidemiological evaluation of release of monocyte TNF-alpha as an exposure and effect marker in pneumoconiosis: a five year follow up study of coal workers.

OBJECTIVES--To determine (a) reproducibility with previous cross sectional findings, and (b) the predictive value of initial release of tumour necrosis factor-alpha (TNF-alpha) towards later progression of coalworkers' pneumoconiosis (CWP). METHODS--Release of monocyte TNF-alpha after in vitro stimulation with coal mine dust, silica, and endotoxin was measured in 104 retired miners and was related to stage of CWP (chest radiograph) and cumulative exposure. A subgroup of 46 miners was screened by high resolution computed tomography (HRCT). Prospective analysis of TNF-alpha (40 out of 104 miners involved in the previous TNF-alpha study) was done by relating initial TNF-alpha to five year progression of CWP measured by comparison of paired chest radiographs. RESULTS--As observed previously, dust stimulated release of TNF-alpha was increased in miners, especially in the early stages of pneumoconiosis. Cumulative exposure was related to pneumoconiotic stage but not to release of TNF-alpha. This excluded TNF-alpha as an exposure marker. Initial concentrations (1987) of TNF-alpha were related to later progression of CWP. Miners who showed abnormally high dust stimulated release of TNF-alpha had an increased risk of progression in CWP (relative risk 8.1). CONCLUSIONS--These results show (a) the significant involvement of TNF-alpha in pneumoconiosis in humans induced by coal dust and (b) that this routine test possibly constitutes a powerful tool to estimate individual prognosis of pneumoconiotic disease, even after the end of occupational exposure.     

Erythrocyte antioxidant enzyme activities in coal miners from three French regions

This study investigated whether differences in the prevalence and severity of coal workers' pneumoconiosis (CWP) between three coal mines could be related to differences in oxidative stress exposure as evaluated in vivo through red-blood-cell antioxidant enzyme activities. Blood samples were obtained from 229 miners selected according to their occupation and their pneumoconiotic status. The following biomarkers were evaluated: erythrocyte catalase, Cu²⁺/Zn²⁺ superoxide dismutase (Cu²⁺/Zn²⁺ SOD), and glutathione peroxidase activities. Antioxidant enzyme activities did not differ significantly between the group of surface workers in Lorraine and the group of underground miners without CWP in Lorraine and in the other coal mines. Erythrocyte Cu²⁺/Zn²⁺ SOD activity was slightly decreased in the group of active underground miners with simple pneumoconiosis as compared with the group of miners without CWP in Nord/Pas-de-Calais. No effect was seen between retired miners at different stages of CWP. Our findings indicate that differences in the prevalence and severity of CWP do not seem to be related to various oxidative activities of coal dust particles, at least as reflected by measurements of antioxidant enzyme activities in circulating erythrocytes in this study. Received: 3 March 1997 / Accepted: 14 October 1997     

Exposure-response analysis of mortality among coal miners in the United States

The quantitative relationship between exposure to respirable coal mine dust and mortality from nonmalignant respiratory diseases was investigated in a study of 8,878 working male coal miners who were medically examined from 1969 to 1971 and followed to 1979. Exposure-related mortality was evaluated using Cox proportional hazards modeling for underlying or contributing causes of death and modified lifetable methods for underlying causes. For pneumoconiosis mortality, the lifetable analyses showed increasing standardized mortality ratios (SMRs) with increasing cumulative exposure category. Significant exposure-response relationships for mortality from pneumoconiosis (P < 0.001) and from chronic bronchitis or emphysema (P < 0.05) were observed in the proportional hazards models after controlling for age and smoking. No exposure-related increases in lung cancer or stomach cancer were observed. Pneumo coniosis mortality was found to vary significantly by the rank of coal dust to which miners were exposed. Miners exposed at or below the current U.S. coal dust standard of 2 mg/m³ over a working lifetime, based on these analyses, have an elevated risk of dying from pneumoconiosis or from chronic bronchitis or emphysema.     

Pneumoconiosis prevalence among working coal miners examined in federal chest radiograph surveillance programs--United States, 1996-2002

Coal workers' pneumoconiosis (CWP) is a chronic lung disease caused by inhalation of coal mine dust. To characterize the prevalence of CWP, the National Institute for Occupational Safety and Health (NIOSH) analyzed recent radiographic information from the U.S. National Coal Workers' X-ray Surveillance Program (CWXSP). Established under the Federal Coal Mine Health and Safety Act of 1969, CWXSP is administered by NIOSH under federal regulations. NIOSH is responsible for approving coal miner examination plans, submitted approximately every 5 years by companies that operate underground coal mines. This report summarizes the results of the analysis, which indicate that the overall prevalence of CWP among participating miners continues to decline; however, new cases are occurring among miners who have worked exclusively under current dust exposure limits. An evaluation of the mining conditions that have resulted in these cases is underway.     

煤矿工人慢性支气管炎的病理分析

目的了解煤矿工人慢性支气管炎的病变特点。方法对１８０例煤矿工人的尸检材料进行病理分析。结果在１８０例煤矿工人中，患慢性支气管炎的１５５例，检出率为８６．１％，与是否患煤工尘肺无关。其好发部位主要在小支气管和细支气管。煤矿工人慢性支气管炎最显著的特点是在各级支气管管壁有粉尘沉积和尘细胞浸润，支气管壁周围可有尘性纤维化，特别是在呼吸性细支气管处尘性病变最重。结论煤矿工人慢性支气管炎主要表现为尘性和尘性与炎性混合性（占８０．０％），单纯的炎性支气管炎数量较少     

Respiratory outcomes among South African coal miners at autopsy

BACKGROUND: Studies of dose-response relationships between respiratory outcomes at autopsy and coal dust exposure are limited. The Pathology Automation System (PATHAUT) database of South African miners, is one of the largest autopsy databases of occupational lung disease. This study described the prevalence of respiratory outcomes among South African coal miners at autopsy, and determined whether dose response relationships existed between emphysema and exposure. METHODS: Autopsies conducted from 1975 to 1997 on coal miners with exclusive coal mining exposure and having exposure duration information (n = 3,167) were analyzed from PATHAUT. Logistic regression was used to determine relationships between exposure and outcomes, controlling for race, smoking and age on a subset for whom smoking history was available (n = 725). RESULTS: The mean duration of exposure was 11.0 years. Most were black miners (75.3%) with significant differences in the mean ages of black and white miners (37.9 and 55.3 years, respectively). Only 22.9% of cases had information on smoking. The prevalence of silicosis, tuberculosis (TB), coal workers' pneumoconiosis (CWP), and moderate and marked emphysema were 10.7%, 5.2%, 7.3%, and 6.4%, respectively. All diseases, except TB, were associated with exposure duration. Black miners had 8.3 and 1.2 fold greater risks for TB and CWP, respectively, than white miners. White miners had an increased risk of 1.4 and 5.4 for silicosis and moderate to marked emphysema, respectively. In models unadjusted for age, and including smoking, moderate to marked emphysema was strongly associated with exposure duration (OR = 3.4; 95% CI = 1.9-5.9 for highest tercile of exposure duration). Exposure-related risk estimates were reduced when age was introduced into the model. However, age and duration of exposure were highly correlated, (r = 0.68) suggesting a dilution of the exposure effect by age. CONCLUSIONS: There were significant dose related associations of disease, including emphysema, with coal dust exposure.     

Mortality of Dutch coal miners in relation to pneumoconiosis, chronic obstructive pulmonary disease, and lung function.

OBJECTIVES: To analyse the mortality patterns of former Dutch coal miners, focusing on coal workers' pneumoconiosis (CWP) and chronic obstructive pulmonary diseases (COPD) in relation to pre-existing impairment of lung function. METHODS: 3790 selected miners, medically examined between 1952 and 1963, were followed up to the end of 1991 with the municipal population registries and the causes of death from the death certificates were ascertained and converted to the codes from the ninth revision of the international classification of diseases (ICD-9). Mortality comparisons were made with the male population in The Netherlands, resulting in standardised mortality ratios (SMRs). 3367 miners had radiological manifestation of CWP at medical examinations. RESULTS: 80% of the miners died during the follow up period. Excess mortalities from CWP (SMR 4523) and COPD (SMR 179) were found. Coal miners without CWP also showed an increased mortality from COPD (SMR 2913). A diminished lung function (forced expiratory volume in one second (FEV1), or FEV1/FVC (forced vital capacity) ratio) at medical examination resulted in a significantly increased SMR for COPD (322 and 212 respectively) whereas normal lung function yielded expected mortalities from COPD. A positive correlation also emerged between diminished lung function and the SMR due to CWP. The body mass index (BMI) at the moment of medical examination was correlated with the risk of dying of COPD and CWP: a decreasing BMI resulting in an increased SMR. CONCLUSIONS: Not only infectious diseases and CWP but also COPD is an important cause of occupational mortality in miners with extensive exposure to coal mine dust. No obvious connection between pre-existing CWP and the COPD mortality exists. Impaired FEV1 and FEV1/FVC ratios are predictors of an increased risk of COPD death. The BMI seems to indicate the severity of the COPD, resulting in premature death.     

Genetic polymorphisms of MnSOD, GSTM1, GSTT1, and OGG1 in coal workers' pneumoconiosis

Little is known about the genetic susceptibility to coal workers' pneumoconiosis (CWP). We investigated the association between genetic polymorphisms of MnSOD, GSTM1, GSTT1, or OGG1 and susceptibility to CWP. The study population was composed of 259 Chinese retired coal miners who had similar dust exposure histories. Of these, there were 99 cases with International Labor Organization chest radiologic criteria for CWP and 160 controls (with no radiologic criteria for CWP). Individual dust exposure variables were estimated from work histories, and smoking information was obtained from interviews. Polymerase chain reaction-based techniques evaluated the genotypes of all study subjects. There were no differences in genotype frequency of MnSOD, GSTM1, GSTT1, and OGG1 between miners with CWP and miners without CWP, by logistic regression analysis. Cumulative dust exposures, but not genetic polymorphisms, were associated significantly with the presence of CWP. This study illustrates the complexity of factors that may contribute to the development of CWP.     

Respiratory impairments due to dust exposure: A comparative study among workers exposed to silica,asbestos, and coalmine dust

We conducted a comparative study of pulmonary dysfunction among workers who were exposed to silica, asbestos, or coalmine dust. The results showed that all three groups of dust-exposed workers, even those without radiographic signs of pneumoconiosis, had decreased spirometric parameters and diffusing capacity (DLco) in both nonsmokers and smokers. Pulmonary function was further decreased when pneumoconioses were present in the three groups. In accord with increasing radiographic categories, pulmonary function in the workers' pneumoconiosis (CWP), it changed relatively little. Workers with mild to moderate (radiographic category I–II) silicosis or asbestosis showed similarly decreased DLco, but those with silicosis showed lower FEV₁/FVC than those with asbestosis. The workers with CWP also showed a lower FEV₁/FVC than those with asbestosis. The major impairment patterns for silica workers, asbestos workers, and coal miners were mixed, restrictive and mixed, and obstructive, respectively. Smoking obviously increased the prevalence of obstruction for all the groups. We conclude from the present study that all the three dusts cause functional abnormalities that precede radiographic changes of pneumoconiosis. We should pay more attention to respiratory impairment in the initial stage of silicosis and CWP. Am. J. Ind. Med. 31:495–502, 1997. © 1997 Wiley-Liss, Inc.     

煤尘职业接触者和早期煤工尘肺BAL液中表面活性物质研究

目的 探讨煤尘职业接触者和早期煤工尘肺患者BAL液中表面活性物质含量改变特点及其意义。方法 采煤工人23人,按X线诊断煤工尘肺期别分为0期（煤尘接触者）组7人、0^ 组8人和I期组8人,并取健康农民7人为对照组。经纤维支气管肺泡灌洗（BAL）收集BAL液,测定表面活性蛋白A(SP－A）和磷脂（PL）及其组分含量。结果 0期组BAL液中SP－A含量、SP－A／PL和PG／PI明显高于对照组（P＜0．01）,且随煤工尘肺期别增加而有降低趋势。结论 BAL液中SP－A含量、SP－A／PL和PG／PI升高可能是煤尘接触的早期效应指标。     

Evaluation of serum type III procollagen peptide as an exposure marker in retired coal workers

Serum type III procollagen peptide (PIIIP), a degradation product of the type III collagen precursor, has been put forward as an exposure marker for mineral dust. We evaluated PIIIP levels as a marker of exposure to and effects of coal dust in retired coal miners (n = 104). To this end: (a) the individual cumulative dust exposure was calculated from job-exposure matrices, and (b) in addition to routine chest radiography (CR) of all miners according to the criteria of the International Labour Organisation (ILO), a subgroup (n = 46) was screened by high-resolution computed tomography (HRCT). Profusion score (CR and HRCT) tended to increase with cumulative dust exposure, even in the absence of CR evidence for pneumoconiosis (i.e. CR , 0/1, n = 35). In contrast to our previous findings in active miners, PIIIP levels were not increased in miners as compared with non-dust-exposed controls (n = 29), and no differences were observed between miners without (ILO = 0/0) and miners with coal workers' pneumoconiosis (CWP; ILO 0/1). No trend in PIIIP versus pneumoconiosis stage was present, either by CR or by the more sensitive HRCT score. PIIIP was also unrelated to any lung function parameter (FEV₁, FVC, impedance, diffusion capacity). Age, medication, medical history and smoking habits had no significant effect on PIIIP levels. In the miners with CWP (i.e. ILO > 0/0, n = 28) a significant negative correlation was present between PIIIP values and (log) cumulative dust exposure. This decrease in serum PIIIP levels with increasing cumulative exposure may be due to chronic adaptive changes in type III collagen deposition and/or breakdown. Other relations between exposure and PIIIP were not observed. In conclusion, the present findings do not support the use of serum type III procollagen peptide as a marker of exposure to and (early) interstitial or respiratory effects of coal dust.     

Silicosis and lung cancer in North Carolina dusty trades workers

Since 1940, 760 cases of silicosis have been diagnosed as part of the State of North Carolina's (NC) pneumoconiosis surveillance program for dusty trades workers. Vital status was ascertained through 1983 for 714 cases that had been diagnosed since 1940 and death certificates were obtained for 546 of the 550 deceased. Mortality from tuberculosis, cancer of the intestine and lung, pneumonia, bronchitis, emphysema, asthma, pneumoconiosis, and kidney disease was significantly increased in whites. Mortality from tuberculosis, ischemic heart disease, and pneumoconiosis was significantly increased in non-whites. The standardized mortality ratio (95% CI) for lung cancer based on U.S. rates was 2.6 (1.8-3.6) in whites, 2.3 (1.5-3.4) in those who had no exposure to other known occupational carcinogens, and 2.4 (1.5-3.6) in those who had no other exposure and who had been diagnosed for silicosis while employed in the NC dusty trades. Age-adjusted lung cancer rates in silicotics who had no exposure to other known occupational carcinogens were 1.5 (.8-2.9) times higher than that in a referent group of coal miners with coalworkers' pneumoconiosis (CWP) and 2.4 (1.5-3.9) times higher than that in a referent group of non-silicotic metal miners. Age- and smoking-adjusted rates in silicotics were 3.9 (2.4-6.4) times higher than that in metal miners. This analysis effectively controls for confounding by age, cigarette smoking, and exposure to other known occupational carcinogens, and it is unlikely that other correlates of silica exposure could explain the excess lung cancer mortality in the silicotics.     

Prevalence of pneumoconiosis and its relationship to dust exposure in a cohort of U.S. Bituminous coal miners and ex-miners

Information on radiographic evidence of coal workers' pneumoconiosis (CWP) is presented for a group of 3,194 underground bituminous coal miners and ex-miners examined between 1985 and 1988. Prevalence of CWP was related to estimated cumulative dust exposure, age, and rank of coal. On the basis of these data, miners of medium to low rank coal, who work for 40 years at the current federal dust limit of 2 mg/m³, are predicted to have a 1.4% risk of having progressive massive fibrosis on retirement. Higher prevalences are predicted for less severe categories of CWP. Miners in high rank coal areas appear to be at greater risk than those mining medium and low rank coals. Ex-miners who said that they left mining for health-related reasons had higher levels of abnormality compared to current miners.     

A cross sectional study of the independent effect of occupation on lung function in British coal miners.

BACKGROUND: Chronic bronchitis and emphysema are now recognised complications of occupational exposure to coal dust, and since 1992 compensation has been available for miners with impaired lung function provided that they also have x ray film evidence of pneumoconiosis. However, many miners with heavy exposure to coal dust and impairment of lung function therefore do not qualify for compensation because they do not have simple pneumoconiosis. In the present study attempts were made to determine whether coal mining is an independent risk factor for impairment of lung function in a group of Nottinghamshire miners with no evidence of simple pneumoconiosis, by comparing these men with a group of local controls who were not occupationally exposed. METHOD: Forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) were obtained on 1286 miners with no evidence of pneumoconiosis on x ray film. Lung function data were also obtained from a random sample of 567 men aged between 40 and 70 living in a district of Nottingham and who had never worked in the mining industry or in any other dusty occupation. Multiple linear regression in SPSS was used to estimate the mean independent effect of mining on FEV1 and FVC after adjustment for age, height, and smoking, in all miners and controls, and in a subgroup of men of 45 and under. In men of 45 and under, the independent effects of mining and smoking on the probability of a deficit of one litre or more from modelled predicted FEV1 values were computed with logistic regression in EGRET. RESULTS: There was a significant mean effect of mining on FEV1 after adjustment for age, height, and smoking of -155 ml (95% confidence interval (95% CI) -74 to -236 ml, P < 0.001), but the size of effect was inversely related to age such that in men of 45 and under the estimated mean effect of mining was -251 ml (95% CI -140 to -361 ml, P < 0.001). In this subgroup of younger men, 4.7% of miners and 0.7% of controls had a deficit of one litre or more from predicted FEV1 values, and in logistic regression, there was a marginally significant independent effect of both smoking (P = 0.05) and mining (P = 0.07) for a deficit of this magnitude. CONCLUSIONS: Occupational exposure to coal dust is associated with a small mean deficit in lung function even in the absence of simple pneumoconiosis, and independently from the effects of smoking. The requirement that miners should have evidence of pneumoconiosis to qualify for compensation for impaired lung function is therefore unjustified.     

Contrasting geographical distribution of mortality from pneumoconiosis and chronic bronchitis and emphysema in British coal miners.

To explore whether the characteristics of coal mine dust that predispose to chronic airways obstruction are the same as those associated with pneumoconiosis, mortality from the two disease was compared in coal miners in 22 counties of England and Wales during 1979-80 and 1982-90. The proportional mortality ratios (PMRs) for coal workers' pneumoconiosis varied from 135 (95% confidence interval (95% CI) 16-488) in Leicestershire to 3825 (95% CI 1538-7881) in South Glamorgan. The PMRs for chronic bronchitis and emphysema were consistently higher than those in other occupations, but showed much less geographical variation and did not correlate geographically with those for pneumoconiosis. These findings indicate that the pathogenetic mechanisms by which coal mine dust causes chronic bronchitis and emphysema depend on different features of the dust from those producing pneumoconiosis. Also, they suggest that current social security regulations in Britain, which require evidence of pneumoconiosis as a condition of compensation for chronic bronchitis and emphysema in coal miners, may discriminate unfairly against claimants from some regions.     

Identification and classification of high risk groups for Coal Workers' Pneumoconiosis using an artificial neural network based on occupational histories: a retrospective cohort study

Background  

Coal workers' pneumoconiosis (CWP) is a preventable, but not fully curable occupational lung disease. More and more coal miners are likely to be at risk of developing CWP owing to an increase in coal production and utilization, especially in developing countries. Coal miners with different occupational categories and durations of dust exposure may be at different levels of risk for CWP. It is necessary to identify and classify different levels of risk for CWP in coal miners with different work histories. In this way, we can recommend different intervals for medical examinations according to different levels of risk for CWP. Our findings may provide a basis for further emending the measures of CWP prevention and control.     

煤工尘肺患者血清中基质金属蛋白酶-9及其抑制因子水平的变化

目的 探讨煤工尘肺患者血清中基质金属蛋白酶(MMP-9)及基质金属蛋白酶抑制剂(TIMP-9)水平的变化及意义.方法 采用双抗体夹心ELISA法检测188例煤工尘肺(煤肺组53例,煤矽肺组67例,矽肺组68例)、57例0期(0~+期组)、64例接尘对照组和50例健康对照组血清中MMP-9及TIMP-9含量;分析血清中MMP-9和TIMP-9水平在各煤工尘肺组及各对照组间的变化,以及二者的相关性;并根据煤工尘肺期别、是否有并发症以及接尘年限等因素进行分析.结果 煤肺组血清中MMP-9水平为17.16 ng/ml、煤矽肺组为15.14ng/ml,矽肺组为17.50 ng/ml,与健康对照组比较,差异均有统计学意义(P<0.05)与接尘对照组、0~+组比较,均呈降低趋势,其中矽肺组及煤矽肺组差异有统计学意义(P<0.05).3组煤工尘肺患者血清中MMP-9水平比较,差异无统计学意义(P>0.05);煤肺组、煤矽肺组和矽肺组血清中TIMP-9水平分别为(330.00±108.42),(312.044±120.09),(366.81±135.50)ng/ml,均低于健康对照组,其中矽肺组和煤肺组血清中TIMP-9水平较接尘对照组、1~+组明显增高,差异有统计学意义(P<0.05),3组煤工尘肺组间比较,矽肺组血清中TIMP-9水平较煤矽肺组升高,差异有统计学意义(P<0.05).3组煤工尘肺患者血清中MMP-9和TIMP-9水平按不同的疾病分期、是否有并发症以及接尘年限进行分析,差异均无统计学意义(P>0.05);矽肺组血清中TIMP-9水平与年龄呈正相关(r=0.249,P<0.05),血清中MMP-9和TIMP-9水平在接尘对照组中呈正相关(r=0.294,P<0.05),其他组中未发现相关性.结论 血清中MMP-9与TIMP-9水平变化与粉尘对机体的损害程度有关,MMP-9与TIMP-9共同参与了煤工尘肺的病理生理过程;动态观察0~+期及健康煤矿工人血清中MMP-9和TIMP-9水平,可为煤工尘肺的预防及早期诊断提供参考.