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

To analyze the prevalence characteristics and influence factors of pneumoconiosis of workers exposed to dusts in an iron mine, to provide the base of preventive measures for pneumoconiosis of iron mine.The subjects of cohort study were all workers exposed to dusts for at least one year registered in an iron mine during 1960 to 1974, and followed-up to the end in 2003. The cases with pneumoconiosis were diagnosed by the local diagnosis group of pneumoconiosis, according to the national diagnostic criteria of pneumoconiosis. The risk factors were analyzed with Cox risk model.A total of 3647 miners were included in the cohort study and were followed up by 132 574.4 person years. There were 316 cases with pneumoconiosis, and the incidence of pneumoconiosis for a year was 0.24 per thousand. There were 274 cases (86.7%) with pneumoconiosis in workers exposed to dusts before 1960, the incidence of pneumoconiosis for a year was 0.40 per thousand, which was significantly higher than that (0.07 per thousand) of workers exposed to dusts after 1960. The average latency of pneumoconiosis was 26.0 +/- 7.3 years. The average durations of upgrade from stage 0(+) to I , I to II and II to III were 5.3 +/- 3.2, 6.6 +/- 5.2 and 11.3 +/- 5.0 years, respectively. However, 164 cases with pneumoconiosis were diagnosed after ceasing exposure to dusts for mean 8.3 years. The risk of pneumoconiosis in iron miners increased with exposure doses, and there was an obvious dose-effect relationship. The average cumulative exposure dose of cases with pneumoconiosis was 173.7 +/- 91.6 mg/m3 x y, which was significantly higher than that (112.1 +/- 64.8 mg/m3 x y) of workers without pneumoconiosis. Also the tuberculosis (HR = 5.9, P0.001) and smoking (HR = 1.7, P0.01) were the main risk factors.There was an obvious dose-effect relationship between the cumulative exposure dose and pneumoconiosis incidence. Tuberculosis and smoking were the main risk factors influencing the pneumoconiosis incidence.

To assess biological response and health adverse effects of industrial dusts from pottery factories and tungsten mines on alveolar macrophages (AM) in vitro.AM acquired from bronchoalveolar lavage of guinea pigs were used as the target cells. AM were then co-cultured with respirable dust particles (15, 30, 60 and 120 μg/10⁶) from pottery factories and tungsten mines. LDH activity, cell viability, the release of ROS and TNF-α were determined to assess the biological responses of the dusts. China Standard Quartz was used as control.Dose- response relationships between the dust concentrations and the enhancement of LDH activity, the release of ROS and TNF-α were found in both dusts from pottery factories and tungsten mines. The cell viability decreased when the dusts' concentrations increased. Differences of biological response were observed in the dust particles from different mines or factories. Compared with the pottery dusts, higher LDH activity and the release of TNF-α induced by tungsten dust were observed. In the 120 μg/10⁶ group, the TNF-α induced by tungsten dust, pottery dusts and China Standard Quartz was (5.2 +/- 2.0) ng/ml, (3.3 +/- 1.6) ng/ml and (2.8 +/- 0.5) ng/ml respectively. However, the impact on the cell viability induced by pottery dust was higher than that by tungsten mine.Industrial dusts from various sources could induce different biological effects. The results of the biological effects of dusts in laboratory tests may be of potential use to provide base data for their adverse effects evaluation.