Analyzed the data: WC YL HW SW TW. Wrote the first draft of the manuscript: WC YL. Contributed to the writing of the manuscript: WC YL EH YS TW.
The authors have declared that no competing interests exist.
A retro-prospective cohort study by Weihong Chen and colleagues provides new estimates for the risk of total and cause-specific mortality due to long-term silica dust exposure among Chinese workers.
Human exposure to silica dust is very common in both working and living environments. However, the potential long-term health effects have not been well established across different exposure situations.
We studied 74,040 workers who worked at 29 metal mines and pottery factories in China for 1 y or more between January 1, 1960, and December 31, 1974, with follow-up until December 31, 2003 (median follow-up of 33 y). We estimated the cumulative silica dust exposure (CDE) for each worker by linking work history to a job–exposure matrix. We calculated standardized mortality ratios for underlying causes of death based on Chinese national mortality rates. Hazard ratios (HRs) for selected causes of death associated with CDE were estimated using the Cox proportional hazards model. The population attributable risks were estimated based on the prevalence of workers with silica dust exposure and HRs. The number of deaths attributable to silica dust exposure among Chinese workers was then calculated using the population attributable risk and the national mortality rate. We observed 19,516 deaths during 2,306,428 person-years of follow-up. Mortality from all causes was higher among workers exposed to silica dust than among non-exposed workers (993 versus 551 per 100,000 person-years). We observed significant positive exposure–response relationships between CDE (measured in milligrams/cubic meter–years, i.e., the sum of silica dust concentrations multiplied by the years of silica exposure) and mortality from all causes (HR 1.026, 95% confidence interval 1.023–1.029), respiratory diseases (1.069, 1.064–1.074), respiratory tuberculosis (1.065, 1.059–1.071), and cardiovascular disease (1.031, 1.025–1.036). Significantly elevated standardized mortality ratios were observed for all causes (1.06, 95% confidence interval 1.01–1.11), ischemic heart disease (1.65, 1.35–1.99), and pneumoconiosis (11.01, 7.67–14.95) among workers exposed to respirable silica concentrations equal to or lower than 0.1 mg/m3. After adjustment for potential confounders, including smoking, silica dust exposure accounted for 15.2% of all deaths in this study. We estimated that 4.2% of deaths (231,104 cases) among Chinese workers were attributable to silica dust exposure. The limitations of this study included a lack of data on dietary patterns and leisure time physical activity, possible underestimation of silica dust exposure for individuals who worked at the mines/factories before 1950, and a small number of deaths (4.3%) where the cause of death was based on oral reports from relatives.
Long-term silica dust exposure was associated with substantially increased mortality among Chinese workers. The increased risk was observed not only for deaths due to respiratory diseases and lung cancer, but also for deaths due to cardiovascular disease.
Walk along most sandy beaches and you will be walking on millions of grains of crystalline silica, one of the commonest minerals on earth and a major ingredient in glass and in ceramic glazes. Silica is also used in the manufacture of building materials, in foundry castings, and for sandblasting, and respirable (breathable) crystalline silica particles are produced during quarrying and mining. Unfortunately, silica dust is not innocuous. Several serious diseases are associated with exposure to this dust, including silicosis (a chronic lung disease characterized by scarring and destruction of lung tissue), lung cancer, and pulmonary tuberculosis (a serious lung infection). Moreover, exposure to silica dust increases the risk of death (mortality). Worryingly, recent reports indicate that in the US and Europe, about 1.7 and 3.0 million people, respectively, are occupationally exposed to silica dust, figures that are dwarfed by the more than 23 million workers who are exposed in China. Occupational silica exposure, therefore, represents an important global public health concern.
Although the lung-related adverse health effects of exposure to silica dust have been extensively studied, silica-related health effects may not be limited to these diseases. For example, could silica dust particles increase the risk of cardiovascular disease (diseases that affect the heart and circulation)? Other environmental particulates, such as the products of internal combustion engines, are associated with an increased risk of cardiovascular disease, but no one knows if the same is true for silica dust particles. Moreover, although it is clear that high levels of exposure to silica dust are dangerous, little is known about the adverse health effects of lower exposure levels. In this cohort study, the researchers examined the effect of long-term exposure to silica dust on the risk of all cause and cause-specific mortality in a large group (cohort) of Chinese workers.
The researchers estimated the cumulative silica dust exposure for 74,040 workers at 29 metal mines and pottery factories from 1960 to 2003 from individual work histories and more than four million measurements of workplace dust concentrations, and collected health and mortality data for all the workers. Death from all causes was higher among workers exposed to silica dust than among non-exposed workers (993 versus 551 deaths per 100,000 person-years), and there was a positive exposure–response relationship between silica dust exposure and death from all causes, respiratory diseases, respiratory tuberculosis, and cardiovascular disease. For example, the hazard ratio for all cause death was 1.026 for every increase in cumulative silica dust exposure of 1 mg/m3-year; a hazard ratio is the incidence of an event in an exposed group divided by its incidence in an unexposed group. Notably, there was significantly increased mortality from all causes, ischemic heart disease, and silicosis among workers exposed to respirable silica concentrations at or below 0.1 mg/m3, the workplace exposure limit for silica dust set by the US Occupational Safety and Health Administration. For example, the standardized mortality ratio (SMR) for silicosis among people exposed to low levels of silica dust was 11.01; an SMR is the ratio of observed deaths in a cohort to expected deaths calculated from recorded deaths in the general population. Finally, the researchers used their data to estimate that, in 2008, 4.2% of deaths among industrial workers in China (231,104 deaths) were attributable to silica dust exposure.
These findings indicate that long-term silica dust exposure is associated with substantially increased mortality among Chinese workers. They confirm that there is an exposure–response relationship between silica dust exposure and a heightened risk of death from respiratory diseases and lung cancer. That is, the risk of death from these diseases increases as exposure to silica dust increases. In addition, they show a significant relationship between silica dust exposure and death from cardiovascular diseases. Importantly, these findings suggest that even levels of silica dust that are considered safe increase the risk of death. The accuracy of these findings may be affected by the accuracy of the silica dust exposure estimates and/or by confounding (other factors shared by the people exposed to silica such as diet may have affected their risk of death). Nevertheless, these findings highlight the need to tighten regulations on workplace dust control in China and elsewhere.
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Crystalline silica is one of the most ubiquitous minerals on earth, with widespread exposure in working and living environments. Multiple serious diseases and increased mortality have been associated with exposure to crystalline silica, making it a high-priority public health concern. Occupational silica exposure and its related health effects rank among the most important public health concerns in developing and developed nations. Recent reports indicate that more than 23 million workers are exposed to crystalline silica in China
Adverse health effects from exposure to silica dust are of increasing public health concern worldwide, and have been studied for many years
Therefore, we present results from a retro-prospective cohort study of 74,040 Chinese workers followed from January 1, 1960, to December 31, 2003. Cumulative silica dust exposure (CDE) was calculated for each worker using a job–exposure matrix (JEM) based on a large number of measurements broken down by job title and collected since 1950. Our objectives were to quantify the health effects of silica exposure on cause-specific mortality and to determine population attributable risks (PARs) of mortality associated with the exposure in Chinese workers.
We identified 74,040 workers from 20 metal mines and nine pottery factories in central and southern China. All individuals were unrelated ethnic Han Chinese. We selected workplaces with systematically collected data on silica dust exposure and workers' health condition. The study included ten tungsten mines in Jiangxi and Hunan provinces, six iron and copper mines in Hubei province, four tin mines in Guangxi province, and nine pottery factories in Jiangxi, Hunan, and Henan provinces (
Trained investigators used a questionnaire to collect data on demographic information, cigarette use, and drinking habits since 1986. In 2004, occupational history and other updates were collected from survivors or those still employed. We defined positive silica dust exposure status as employment in a silica-dust-exposed job for 6 mo or more. Work histories for silica-dust-exposed workers were taken from company occupational records. Data included job titles, work start and end dates, and reasons for leaving (e.g., retirement or workplace change).
All individuals were tracked for their vital status by local hygienists (or occupational health doctors) from January 1, 1960, through December 31, 2003. We classified cause of death evidence by levels of confidence in the data: Level 1—medical record from a hospital or a personal doctor at a local hospital (60.5%); Level 2—cause of death recorded in an employment register, accident record, or death certificate (35.2%); and Level 3—oral reports from relatives (4.3%). Results did not change materially after excluding Level 3 deaths. We used the 10th International Classification of Diseases (ICD-10) to code causes of death.
All workers exposed to silica dust received chest radiographs every 2 to 4 y, even after cessation of dust exposure. National diagnostic criteria for pneumoconiosis were standardized as stage I, II, or III. These categories have been previously described
We conducted a detailed quantitative occupational exposure evaluation using data from historical industrial health records. Industrial health record-keeping for occupational hazards in each mine or factory started in the early 1950s, when the Chinese government enforced systematic dust sampling regulations that required monthly measurement of dust concentrations in workplaces. The dust monitoring scheme involved measuring total airborne dust concentration by a gravimetric method for each dust-exposed job title, and using a microscopic sizing method to determine particle size distribution and crystalline silica content (quartz by X-ray diffraction method) in bulk samples of settled dust
For the purpose of this study, more than 4,200,000 environmental measurements of total dust concentrations from 29 mines and factories from 1950 to 2003 were used to create a JEM. In this matrix, the total dust concentrations associated with each job title were averaged by year, then listed, along with specific facility and job titles, for each calendar year
We used the JEM of total dust concentrations to estimate silica dust exposure for each worker. In this matrix, total silica dust concentrations were listed along with specific facility and job titles for each calendar year. We used all available total dust concentrations for each job to create this JEM. The results indicated good agreement for measured total dust concentrations (
Complete work histories for each study individual were taken from personal employment records in mine/factory files. Work histories include job titles and calendar years for each worker's full duration of employment. They were used with the JEM to estimate CDE for individual workers as follows:
We used data from a standardized monitoring program in all industrial facilities to track potential environmental hazards, including radon, polycyclic aromatic hydrocarbons, asbestos, talc, and metal elements. Findings indicated very low exposure to asbestos, nickel, talc, and cadmium in the studied workplaces.
We used Cox proportional hazards regressions to estimate the hazard ratios (HRs) and 95% confidence intervals (CIs) for selected causes of death by different levels of CDE compared with no exposure. CDE was categorized into low, medium, and high levels based on equally spaced percentiles from the exposure distribution in the entire cohort. Further, tests of linear trend were conducted by including the median value for each level of CDE as a continuous variable in the models. We also estimated the HRs associated with a 1 mg/m3-y increase in CDE by entering CDE into the models as a continuous variable. In addition, nonlinear association was assessed by adding a quadratic term (CDE and square of CDE, continuous) to the model. Other covariates included in the model were gender, year of hire (five categories, 1955 or earlier, 1956–1960, 1961–1965, 1966–1970, and 1970 or later), age at hire (continuous), and type of mine/factory (four categories, tungsten, iron/copper, tin, and pottery) as potential confounders. For mortality with possible nonlinear associations, we further examined the detailed exposure–response relationship of mortality risk across the range of CDEs using a penalized spline regression model
The PAR was calculated with the following equation:
Standardized mortality ratios (SMRs) were defined as the ratio of observed to expected deaths
The cohort included 74,040 individuals (63,529 males, 85.8%). The average age was 27.2 y for individuals entering into the cohort. And 16.2% were still working at the end of follow-up (
Type of Mine/Factory | End of Follow-Up | Number of Mines/Factories | Median Period of Follow-Up (Years) | Number of Workers | Number of Workers Exposed to Silica Dust | Number of Pneumoconiosis Cases | Number of Deaths |
Tungsten mines | December 31, 1994 | 4 | 29.9 | 13,857 | 10,787 | 3,650 | 3,678 |
Tungsten mines | December 31, 2003 | 6 | 34.7 | 19,061 | 15,170 | 4,238 | 7,138 |
Iron and copper mines | December 31, 1989 | 4 | 20.2 | 7,368 | 4,355 | 356 | 438 |
Iron and copper mines | December 31, 2003 | 2 | 35.5 | 11,214 | 4,666 | 406 | 2,293 |
Tin mines | December 31, 1994 | 1 | 28.9 | 2,717 | 1,838 | 621 | 548 |
Tin mines | December 31, 2003 | 3 | 35.5 | 5,526 | 3,109 | 466 | 1,391 |
Pottery factories | December 31, 1989 | 1 | 30.0 | 826 | 496 | 39 | 178 |
Pottery factories | December 31, 1994 | 4 | 31.7 | 6,098 | 4,050 | 477 | 1,404 |
Pottery factories | December 31, 2003 | 4 | 38.0 | 7,373 | 4,838 | 742 | 2,448 |
Entire cohort | 29 | 33.1 | 74,040 | 49,309 | 10,995 | 19,516 |
Respirable silica dust levels in the four types of mines/factories from 1960 to the end of 2003 are shown in
Characteristic | Entire Cohort ( |
Levels of CDE |
|||
Unexposed ( |
Low ( |
Medium ( |
High ( |
||
|
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Tungsten mines | 32,918 (44.5) | 6,961 (28.1) | 7,255 (47.0) | 9,626 (57.0) | 9,076 (53.4) |
Iron and copper mines | 18,582 (25.1) | 9,561 (38.7) | 5,272 (34.1) | 2,041 (12.1) | 1,708 (10.1) |
Tin mines | 8,243 (11.1) | 3,296 (13.3) | 2,082 (13.5) | 2,478 (14.7) | 387 (2.3) |
Pottery factories | 14,297 (19.3) | 4,913 (19.9) | 829 (5.4) | 2,733 (16.2) | 5,822 (34.3) |
|
63,529 (85.8) | 17,879 (72.3) | 14,432 (93.5) | 15,659 (92.8) | 15,559 (91.6) |
|
1937.1±11.1 | 1939.4±10.9 | 1941.6±9.6 | 1935.7±10.2 | 1930.9±10.5 |
|
|||||
1900–1919 | 5,719 (7.7) | 1,470 (5.9) | 453 (2.9) | 1,175 (7.0) | 2,621 (15.4) |
1920–1929 | 12,389 (16.7) | 2,849 (11.5) | 1,459 (9.5) | 3,216 (19.1) | 4,865 (28.6) |
1930–1939 | 25,441 (34.4) | 7,758 (31.4) | 4,019 (26.0) | 7,108 (42.1) | 6,556 (38.6) |
1940–1949 | 20,627 (27.9) | 8,064 (32.6) | 6,413 (41.5) | 3,832 (22.7) | 2,318 (13.6) |
1950–1963 | 9,864 (13.3) | 4,590 (18.6) | 3,094 (20.0) | 1,547 (9.2) | 633 (3.7) |
|
1961.8±7.4 | 1963.1±7.2 | 1965.3±6.6 | 1960.5±6.9 | 1958.0±6.9 |
|
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1915–1954 | 16,181 (21.9) | 3,884 (15.7) | 969 (6.3) | 4,406 (26.1) | 6,922 (40.7) |
1955–1959 | 21,383 (28.9) | 6,702 (27.1) | 3,852 (25.0) | 5,683 (33.7) | 5,146 (30.3) |
1960–1964 | 8,611 (11.6) | 2,933 (11.9) | 1,917 (12.4) | 2,010 (11.9) | 1,751 (10.3) |
1965–1969 | 11,219 (15.2) | 4,228 (17.1) | 3,197 (20.7) | 1,975 (11.7) | 1,819 (10.7) |
1970–1974 | 16,646 (22.5) | 6,984 (28.2) | 5,503 (35.6) | 2,804 (16.6) | 1,355 (8.0) |
|
24.8±7.6 | 23.9±7.4 | 23.8±6.2 | 24.9±7.3 | 27.2±8.7 |
|
|||||
Current smokers—number (percent) | 21,438 (48.0) | 5,878 (37.9) | 5,998 (54.7) | 5,397 (57.2) | 4,165 (47.5) |
Current smokers—pack-years | 33.9±17.1 | 33.1±17.6 | 33.3±16.7 | 35.9±17.5 | 33.2±16.0 |
Former smokers—number (percent) | 6,141 (13.7) | 1,458 (9.4) | 1,387 (12.6) | 1,278 (13.5) | 2,018 (23.0) |
Former smokers—pack-years | 28.5±14.0 | 30.9±15.6 | 26.8±13.7 | 28.5±13.2 | 27.9±13.3 |
Never smokers—number (percent) | 17,130 (38.3) | 8,188 (52.7) | 3,587 (32.7) | 2,764 (29.3) | 2,591 (29.5) |
|
18.7±10.4 | 0.0±0.0 | 14.6±9.6 | 18.1±9.4 | 23.4±10.3 |
|
3.9±4.2 | 0.0±0.0 | 0.6±0.3 | 2.5±0.9 | 8.5±4.1 |
|
0.2±0.2 | 0.0±0.0 | 0.1±0.1 | 0.2±0.2 | 0.4±0.2 |
|
10,995 (22.3) | 0 (0.0) | 678 (4.4) | 3,550 (21.0) | 6,767 (39.8) |
|
|||||
1955–1959 | 1,210 (11.0) | NA | 19 (2.8) | 331 (9.3) | 860 (12.7) |
1960–1969 | 4,344 (39.5) | NA | 90 (13.3) | 1,317 (37.1) | 2,937 (43.4) |
1970–1979 | 2,663 (24.2) | NA | 198 (29.2) | 873 (24.6) | 1,592 (23.5) |
1980–2003 | 2,778 (25.3) | NA | 371 (54.7) | 1,029 (29.0) | 1,378 (20.4) |
|
44.2±10.4 | NA | 47.8±9.8 | 43.6±10.9 | 44.3±10.1 |
|
21.3±10.2 | NA | 21.1±8.7 | 18.6±9.7 | 22.7±10.3 |
Values expressed as mean ± standard deviation, unless otherwise indicated. Percentages may not total 100 due to rounding.
Levels are tertiles of CDE of all the workers with exposure to silica dust: low, 0.01–1.23 mg/m3-y; medium, 1.24–4.46 mg/m3-y; and high, >4.46 mg/m3-y.
Data were available for the sub-cohorts that had been followed through the end of 2003. Smokers were defined as those who had smoked regularly for over 1 y. Smokers who stopped smoking within 1 y before the end of follow-up were defined as current smokers.
These characteristics were calculated among workers exposed to silica dust. Mean silica dust concentration was calculated as CDE divided by duration of silica dust exposure.
These characteristics were calculated among workers diagnosed with pneumoconiosis. Latency of pneumoconiosis was defined as the period between the year of first exposure to dust and the year of first diagnosis of pneumoconiosis.
NA, not applicable.
The numbers of deaths and the HRs for the main mortality causes are shown in
HRs and 95% CIs were derived from penalized spline regression models to examine the nonlinear relation of CDE to mortality. The vertical solid line in each panel represents the 95th percentile of CDE. Dashed lines represent the point estimate of the HR adjusted for duration of follow-up (time-dependent, continuous) and calendar time (time-dependent, continuous); solid lines represent HR further adjusted for smoking (never smoked/ever smoked), with dotted lines indicating the 95% CI; the rug plots along the horizontal axes give the distribution of CDE values. For simplicity of presentation, the reference value of CDE was set to 0 mg/m3-y (0.01 mg/m3-y for pneumoconiosis).
Cause of Death (ICD-10 Codes) | Number of Events | HR Increase per 1 mg/m3-y Increase in CDE | HRs for Levels of CDE versus Unexposed |
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Low | Medium | High | ||||
|
3,621 | 0.982 (0.972–0.991) | 1.20 (1.09–1.32) | 1.13 (1.03–1.24) | 0.97 (0.88–1.07) | 0.06 |
Malignant neoplasm of nasopharynx (C11) | 176 | 0.942 (0.895–0.991) | 0.96 (0.63–1.48) | 0.83 (0.55–1.24) | 0.58 (0.36–0.93) | 0.02 |
Malignant neoplasm of liver and intrahepatic bile ducts (C22) | 1,001 | 0.972 (0.953–0.991) | 1.15 (0.96–1.37) | 1.02 (0.86–1.22) | 0.87 (0.72–1.06) | 0.05 |
Lung cancer (C33–C34) | 949 | 1.005 (0.987–1.023) | 1.45 (1.19–1.75) | 1.53 (1.27–1.84) | 1.46 (1.19–1.78) | 0.01 |
|
3,401 | 1.062 (1.055–1.068) | 1.31 (1.09–1.56) | 2.70 (2.36–3.08) | 3.83 (3.38–4.35) | <0.001 |
|
3,100 | 1.065 (1.059–1.071) | 1.30 (1.06–1.60) | 3.14 (2.71–3.64) | 4.53 (3.94–5.20) | <0.001 |
|
4,425 | 1.031 (1.025–1.036) | 1.08 (0.96–1.21) | 1.42 (1.29–1.57) | 1.86 (1.71–2.03) | <0.001 |
Pulmonary heart diseases (I26–I27) | 2,729 | 1.050 (1.044–1.056) | 1.08 (0.88–1.33) | 2.32 (2.01–2.67) | 3.44 (3.01–3.92) | <0.001 |
Hypertensive heart disease (I11) | 391 | 0.977 (0.955–0.999) | 0.87 (0.62–1.24) | 0.83 (0.63–1.11) | 0.86 (0.66–1.12) | 0.44 |
Ischemic heart disease (I20–I25) | 624 | 0.971 (0.950–0.994) | 1.25 (0.99–1.56) | 1.03 (0.82–1.29) | 0.80 (0.63–1.02) | 0.01 |
Chronic rheumatic heart disease (I05–I09) | 123 | 0.979 (0.934–1.026) | 1.29 (0.74–2.25) | 1.16 (0.70–1.92) | 0.94 (0.56–1.58) | 0.54 |
|
2,662 | 0.997 (0.988–1.006) | 1.01 (0.89–1.13) | 0.89 (0.79–0.99) | 0.90 (0.81–1.00) | 0.05 |
|
4,309 | 1.069 (1.064–1.074) | 1.89 (1.60–2.24) | 4.28 (3.74–4.91) | 6.68 (5.85–7.61) | <0.001 |
Pneumoconiosis (J60–J65)d | 2,857 | 1.060 (1.053–1.067) | 1.0 (referent) | 4.36 (3.49–5.44) | 7.75 (6.21–9.67) | <0.001 |
|
879 | 0.991 (0.973–1.008) | 1.15 (0.94–1.41) | 0.88 (0.73–1.08) | 0.94 (0.78–1.15) | 0.36 |
|
1,180 | 0.983 (0.964–1.002) | 1.47 (1.25–1.72) | 1.17 (0.98–1.39) | 1.06 (0.88–1.27) | 0.34 |
|
19,516 | 1.026 (1.023–1.029) | 1.17 (1.12–1.23) | 1.30 (1.25–1.36) | 1.58 (1.51–1.64) | <0.001 |
All Cox proportional hazards models included age as the time variable. Categorical analyses were based on levels of CDE, including unexposed, low, medium, and high; the unexposed level was used as the reference category (low level for pneumoconiosis). In all models, the HRs associated with CDE were adjusted for gender, year of hire (five categories: 1955 or earlier, 1956–1960, 1961–1965, 1966–1970, and 1970 or later), age at hire (continuous), and type of mine/factory (four categories: tungsten, iron/copper, tin, and pottery).
Levels were tertiles of CDE of all the workers with exposure to silica dust: low, 0.01–1.23 mg/m3-y; medium, 1.24–4.46 mg/m3-y; and high, >4.46 mg/m3-y.
Assessed by including the median values of exposure within each category as a continuous variable in the model, including the reference category.
For a subset of workers with exposures under the respirable silica concentration limit of 0.1 mg/m3 during their lifetime work histories (mean and median CDE were 0.64 and 0.56 mg/m3-y, respectively), each 0.1 mg/m3-y increase in CDE was associated with a 2.1% (95% CI 1.4%–2.7%), 7.2% (5.2%–9.4%), and 2.4% (0.7%–4.1%) increase in the mortality risk for all diseases, respiratory diseases, and CVDs, respectively. After adjusting for gender, year of hire, age at hire, type of mine/factory, and smoking, the respective mortality risk were 0.8% (0.1%–1.5%), 6.3% (4.1%–8.6%), and 2.2% (0.4%–4.1%) for all diseases, respiratory diseases, and CVDs, respectively; for CVDs, the mortality risk of pulmonary heart disease and ischemic heart disease increased by 6.0% (2.8%-9.3%) and 4.2% (1.4%-7.2%), respectively.
After adjustment for potential confounders including smoking, we estimated the PAR for silica dust exposure. Silica exposure accounted for 15.2% of mortality from all deaths, 63.9% of mortality from respiratory diseases, and 21.0% of mortality from CVDs among the silica-exposed workers. According to an annual health statistical report in China, the prevalence of silica-dust-exposed workers was 16.3% among Chinese industrial workers in 2008
Cause of Death (ICD-10 Codes) | SMR (95% CI) | |||
1970 to 1974 | 1970 to 1984 | 1970 to 1994 | 1970 to 2003 | |
|
0.69 (0.58–0.82) | 0.79 (0.73–0.85) | 0.85 (0.81–0.89) | 0.82 (0.79–0.85) |
Malignant neoplasm of nasopharynx (C11) | 2.57 (1.47–3.98) | 2.10 (1.57–2.71) | 1.80 (1.45–2.19) | 1.76 (1.45–2.10) |
Malignant neoplasm of liver and intrahepatic bile ducts (C22) | 1.06 (0.77–1.38) | 1.12 (0.98–1.27) | 1.21 (1.11–1.32) | 1.16 (1.08–1.25) |
Lung cancer (C33–C34) | 1.22 (0.74–1.81) | 1.00 (0.83–1.17) | 0.96 (0.87–1.05) | 0.90 (0.84–0.97) |
|
10.40 (9.46–11.38) | 7.87 (7.44–8.31) | 6.96 (6.66–7.27) | 6.83 (6.55–7.11) |
|
4.06 (3.69–4.46) | 3.53 (3.33–3.74) | 4.47 (4.27–4.68) | 4.88 (4.67–5.09) |
|
2.25 (2.02–2.49) | 1.87 (1.76–1.97) | 1.95 (1.87–2.03) | 1.91 (1.85–1.98) |
Pulmonary heart diseases (I26–I27) | 3.49 (3.12–3.88) | 2.79 (2.62–2.97) | 3.77 (3.60–3.95) | 4.03 (3.87–4.20) |
Hypertensive heart disease (I11) | 0.34 (0.11–0.70) | 0.86 (0.63–1.12) | 1.70 (1.44–1.98) | 2.45 (2.17–2.75) |
Ischemic heart diseases (I20–I25) | 0.52 (0.19–1.01) | 0.83 (0.64–1.04) | 0.83 (0.72–0.95) | 1.04 (0.94–1.14) |
Chronic rheumatic heart diseases (I05–I09) | 0.29 (0.13–0.52) | 0.32 (0.22–0.46) | 0.53 (0.41–0.66) | 0.56 (0.45–0.69) |
|
6.52 (5.94–7.12) | 3.71 (3.52–3.92) | 2.61 (2.51–2.72) | 2.32 (2.24–2.40) |
Pneumoconiosis (J60–J65) | 180.20 (163.32–197.90) | 117.11 (110.12–124.31) | 97.44 (92.89–102.11) | 88.13 (84.38–91.97) |
|
0.33 (0.23–0.44) | 0.55 (0.48–0.63) | 0.75 (0.68–0.82) | 0.86 (0.80–0.93) |
|
0.95 (0.79–1.14) | 1.11 (1.00–1.22) | 1.07 (0.99–1.16) | 1.00 (0.93–1.08) |
|
1.32 (1.25–1.39) | 1.20 (1.17–1.23) | 1.23 (1.21–1.26) | 1.21 (1.19–1.23) |
SMRs were estimated based on Chinese national mortality rates (not available before 1970).
The SMR from all causes was 0.83 (95% CI 0.80–0.85) among non-dust-exposed workers. In this group, we observed elevated SMRs for nasopharynx cancer (SMR 1.91, 95% CI 1.41–2.48), liver cancer (1.17, 1.04–1.31), hypertensive heart disease (2.24, 1.84–2.68), pulmonary heart disease (1.17, 1.04–1.32), and infectious diseases (1.98, 1.76–2.22), including respiratory tuberculosis (1.24, 1.08–1.41).
Our findings provide strong evidence that long-term silica dust exposure is associated with substantially increased mortality among Chinese workers. We not only confirmed significant relationships between increased silica dust exposure and heightened risk of death from respiratory diseases and lung cancer, but also found a significant exposure–response relationship between silica dust exposure and mortality from CVD, even at lower exposure levels.
These findings have important public health implications. Silica dust exposure is very common and is associated with increased morbidity and mortality from pneumoconiosis. Our study showed that the cumulative incidence of pneumoconiosis was 20.3% and the death rate from this disease in those with the disease was very high (61.7%). A report from the Chinese Ministry of Health indicated that the death rate from all reported pneumoconiosis was 23.1% between 1949 and 2008
Dust exposure has been linked to risk of death in previous environmental and occupational health studies. The World Health Organization has estimated that 1.4% of all deaths result from exposure to various dust particles
Our data suggest that silica dust substantially raises the risk of death from respiratory diseases as well as CVDs. Traditionally, non-malignant respiratory diseases were thought to be the main causes of death among dust-exposed workers
Several prior reports on the relationship between ambient particulate matter and cardiovascular mortality have focused on combustion-sourced particulate matter in cities
In addition, we found elevated mortality from all causes, pneumoconiosis, infectious diseases, malignant neoplasms including nasopharynx cancer and liver cancer, and CVDs including ischemic heart disease and hypertensive heart disease among individuals who worked in an environment with respirable silica dust concentrations equal to or lower than 0.1 mg/m3. The 0.1-mg/m3 level is the exposure limit for respirable silica in the workplace specified by the US Occupational Safety and Health Administration. In China, the limit for respirable silica (0.07–0.35 mg/m3, depending on the percentage of silica dust) is similar to the US standard. However, even keeping silica exposure lower than 0.1 mg/m3 may not fully protect workers.
The association of silica dust exposure and lung cancer risk has been controversial for decades. In the present study, silica dust exposure was associated with lung cancer; risk ratios based on exposure levels ranged from 1.45 to 1.53. The penalized spline curve suggested a positive exposure–response association between silica exposure and lung cancer risk, although the HR decreased at higher levels of CDE. Possible explanations for the decrease in lung cancer risk at higher CDE include (1) a depletion of the number of susceptible workers in the cohort at high exposure levels and (2) bias introduced by the healthy worker survivor effect. This phenomenon was also observed in studies of other occupational populations
The strengths of this study include a large sample size, a long duration of follow-up, and a low rate of loss to follow-up (4.6%). We collected detailed information on silica dust exposure and cause-specific mortality; the diversity of mine types provided a wide range of exposures.
There were several limitations to this study. First, we did not collect data on dietary patterns and leisure time physical activity, and, therefore, we were unable to evaluate the confounding influence of these factors, especially on CVDs. However, diet and physical activity patterns were likely to be relatively homogenous in this cohort. Second, long-term exposure to silica dust was estimated carefully, but measurement errors were inevitable. Silica dust concentrations before 1950 were estimated using the concentrations in 1950, which may have led to underestimation of exposure for those who worked before 1950 (6,164 workers). Third, although the majority of deaths were ascertained by reviewing medical or accident records or death certificates, 4.3% of deaths were reported orally by relatives, yielding cause of death data that might not be reliable. However, results did not change after excluding these deaths. Finally, silica dust levels vary across different industries and companies, and thus the use of HRs estimated from this cohort may lead to inaccurate estimation of the PAR due to silica dust exposure for the entire population of Chinese industrial workers.
In summary, in this large cohort study, we found a significant exposure–response relationship between silica dust exposure and mortality from all causes, pneumoconiosis, and respiratory disease. Importantly, we also demonstrated a significant exposure–response relationship between silica dust exposure and CVDs. Findings from this study have important public health implications for improving occupational safety among those exposed to silica dust in China and around the world.
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We are indebted to Dr. Frank B. Hu at the Harvard School of Public Health and Dr. Qingyi Wei at the University of Texas MD Anderson Cancer Center for providing valuable comments. We thank the study participants and field workers at the local study sites for their help. This article is dedicated to the memory of our friend Dr. William Wallace, who provided great support during our data collection and died unexpectedly in July 2008.
cumulative silica dust exposure
confidence interval
cardiovascular disease
hazard ratio
10th International Classification of Diseases
job–exposure matrix
population attributable risk
standardized mortality ratio