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Pneumoconiosis

Pneumoconiosis is a lung condition caused by the inhalation of dust, characterized by formation of nodular fibrotic changes in lungs. more...

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Medicines

Many substances can cause pneumoconiosis including asbestos, silica, talc and metals.

Depending on the type of dust, variants of the disease are considered. For example there are silicosis, also known as grinders' disease; and pneumosilicosis, which is caused by the inhalation of the dust of stone, sand, or flint containing silica. Because many common minerals contain silica, there are different types of silicosis.

The term Pneumonoultramicroscopicsilicovolcanoconiosis and some variants thereof turned out to be a hoax created as a word puzzle.

Incidents

The Hawk's Nest incident was one of the earliest and most prominent incidents of large-scale silicosis deaths. But while stringent occupational reforms have largely eliminated it in Europe, the US National Institute for Occupational Safety and Health (NIOSH) estimates that a million workers remain at risk to silicosis, 100,000 of whom are at high risk. They estimate 59,000 will develop adverse effects.

But due to pressure from industry groups, its effects are little known and hardly acted upon. A 1992 Houston Chronicle investigation found "silicosis is often misdiagnosed by doctors, disdained by industry officials and unknown to the very workers who stand the greatest chance of getting it. ... Old warnings and medical studies have been ignored, products falsely advertised and government rules flouted--especially with regard to sandblasting, an activity so hazardous that NIOSH recommended its banning in 1974."

Types

  • Bauxite pneumoconiosis
  • Black lung disease

Read more at Wikipedia.org


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Pneumoconiosis and pulmonary function defects in silica-exposed fire brick workers
From Archives of Environmental Health, 5/1/96 by Saou-Hsing Liou

REFRACTORIES, or firebricks, are used widely in the heating processes of many industries (e.g., lining material in the furnace, hearth, or kiln; insulation material of heating containers, such as ladle, retort, tank). Different shapes and sizes of firebricks are designed to fit the workpiece. Raw materials used for the manufacture of fireproof bricks are selected according to characteristics required by various conditions. Raw materials include silica, fire clay, rock high alumina, chrome, magnesite chrome, or zirconium. Silica bricks are very heat resistant at high temperatures and have a low specific gravity; therefore, they are used often in open hearths, glass tanks, and coke oven retorts. During the past 10-20 y, silica bricks were the main type of firebricks used in Taiwan. Workers in the firebrick manufacturing factories were potentially exposed to silica dust. The health hazards of silica dust have been well documented.[1-4] The purpose of the present study was to evaluate the specific health hazards to workers who engaged in the manufacture of firebricks.

Material and Method

Manufacturing processes. In firebrick plants, manufacturing processes include the transport of raw materials, crushing and grinding, screening, mixing, molding, drying, burning, and packing. During the processes of crushing, grinding, screening, and mixing, dusts are usually generated if a dry process is used. Workers engaged in these processes are exposed to high levels of silica dust and are collectively classified as the "crushing group."

Bricks are molded either manually or by machine. Less dust is generated in the molding process than in the crushing process because water or liquid is added to the mixture of raw materials prior to molding. The molding process workers are exposed to much lower levels of silica than are crushing workers. During the process of drying and burning, the bricks are relayed in layers to the carts, which are then transported into a tunnel kiln that is fired with mineral oil. In addition to silica dust, the workers in the burning process may also be exposed to combustion products of mineral oil. The burning process facilitates moderate exposure to silica dust because the heating process may generate more toxic products from silica (i.e., tridymite and cristobalite).

Study population. A total of 852 workers at 34 factories was recruited for this study. Detailed current and past histories of occupations and diseases were collected via questionnaires. The workers who engaged in the manufacturing processes were the "exposed group," whereas office workers and administrative personnel who spent less than one-third of working hours in the manufacturing workplace were the "control group." Application of this criteria resulted initially in 605 (71 %) of the workers being categorized as exposed, and the remaining 247 (29%) comprised the control group. Some of the exposed workers, however, were excluded from the group either because they had been employed in other factories where potential exposure to silica dust may have occurred (e.g., coal mining, foundry, cement or glass production); had potentially been exposed to other toxic gases or fumes in the making of steel or production of asbestos cement; or had a history of chronic obstructive pulmonary disease prior to employment at the firebrick plants. In addition, some of the controls were excluded because they had been employed in the firebrick factories or at other factories in which potential exposure to silica may have occurred, or they reported a history of chronic obstructive pulmonary disease prior to their current employment. Application of the exclusion criteria effected removal of 79 workers from the exposed group and 83 workers from the control group; therefore, there remained 526 and 164 individuals in the exposed and control groups, respectively.

Medical examination. Medical examinations included a respiratory symptom questionnaire, pulmonary function test, and chest x-ray. The respiratory symptom questionnaire was adopted from the questionnaire of the American Thoracic Society.[5] The symptoms identified in this questionnaire included cough, phlegm, wheezing, shortness of breath, and other chest conditions. Pulmonary function was tested by a HI-298 spirometer (Chest, Japan).[6] Each participant was provided with the same instruction prior to completing three acceptable spirograms. The largest value of the sum of forced vital capacity (FVC) and forced expiratory volume in 1 s ([FEV.sub.1.0]) was coded for the test result. A 35- x 35-cm chest film (P-A view) was taken for each participant. The chest films were read by an experienced chest radiologist, who was blind to exposure status, according to the 1980 ILO classification.

Statistical methods. The prevalence of respiratory symptoms and x-ray abnormalities was expressed as a percentage. Pulmonary functions were expressed as a percentage of predicted values (observed/predicted), after adjustment for age, sex, and height.[6] A test for linear trend and Mantel-Haenszel extension chi-square were used to test for a dose-response relationship.

Results

Silica content of raw material. The silica content of the bulk samples of raw material from these 34 factories was analyzed by another investigator, who used the x-ray diffraction method.[7] The silica content of silica sand or quartz was 97%-99%, but content of the clay and rock varied, depending on the source. In general, the silica content of the clay and rock from the Taiwan local area was higher (i.e., between 20% and 50%) than the content found in the imported clay and rock (between 0% and 20%).

Characteristics of the study population. The study population comprised 526 exposed workers and 164 nonexposed control workers. The distribution of personal characteristics among the study population is listed in Table 1. Two-thirds of the study population was male, and the mean age of the exposed workers was 42.7 [+ or -] 10.3 y, which was significantly older than the control group (36.1 [+ or -] 12.4 y). The predominant age range of the exposed workers was 31-50 y, whereas in the control group it was 21-40 y. Duration of employment for exposed workers (8.0 y) was also significantly greater than in the controls (6.6 y). The proportion of smokers in the exposed group (45.6%) was significantly higher than in the control group (34.1%). In addition, workers in the exposed group had smoked for a longer period (mean = 23.3 y), compared with the controls (18.9 y); however, the two groups did not differ with respect to the quantity of cigarettes smoked each day. Given the above-described characteristics, age and smoking status were stratified in the data analysis.

The prevalence of pneumoconiotic abnormalities, stratified by job title, was highest in the crushing group (10.5%), followed by the burning group (5.9%) and molding group (5.2%). The proportion of abnormalities were also correlated with the estimated exposure levels of silica dust, which was considered to be highest in the crushing group, moderate in the burning group, and lowest in the molding group. Two workers who exhibited large opacities in the chest film had been employed in the crushing group; 1 worker had been employed for more than 10 y in crushing, and the other worker had worked for less than 5 y in a small, dusty factory, at which industrial hygiene was insufficient. Engineering controls of dusts were lacking in the semiclosed room, and the worker did not wear protective respiratory apparatus; therefore, the level of dust to which he was exposed was very high.

Pulmonary function. There was no difference in the observed/predicted ratio of forced vital capacity (FVC), adjusted for height, age, and sex, between the exposed and control groups (Table 3). In the exposed group, however, forced expiratory volume in 1 s (FEV.sub.1.0)/FVC (%) was significantly lower than in the control group. In addition, the mean maximal expiratory flow (MMEF), forced expiratory flow at 50% vital capacity (FEF.sub.50%), and forced expiratory flow at 75% vital capacity (FEF.sub.75%) were lower in the exposed group, compared with controls. The pulmonary function parameters (i.e., FEV.sub.1.0/FVC, MMEF, FEF.sub.50%, and FEF.sub.75%) in both smoking and nonsmoking exposed workers stratified by smoking status, were significantly lower than in the comparable controls. These results suggested that pulmonary function defects in the firebrick workers were obstructive.

[TABULAR DATA 3 OMITTED]

A dose-response relationship, stratified by duration of employment, was found between defects in pulmonary function and duration of employment (Table 4). We adjusted for smoking, and FEV.sub.1.0/FVC, MMEF, FEF.sub.50%, and FEF.sub.75% were most compromised in workers who had been employed for more than 10 y, followed by those employed for 5-10 y, and, finally, those employed for less than 5 y. The pulmonary functions were the least compromised in the controls. These results indicated that pulmonary function decreased as duration of exposure increased. This finding provided further evidence of health hazards in the firebrick industries.

[TABULAR DATA 4 OMITTED]

Pulmonary function, stratified by job titles, was the most decreased in the crushing group, followed by the burning group, molding group, and control group (Table 5 [adjusted for smoking!). Therefore, as levels of silica dust increased, pulmonary function decreased. These findings accorded with pneumoconiotic abnormalities evident in the chest x-rays.

[TABULAR DATA 5 OMITTED]

Prevalence of respiratory symptoms. There were no differences between the exposed and control groups with respect to cough, phlegm, and shortness of breath (Table 6). The prevalence of wheezing in the exposed group, however, was significantly higher than in controls. Symptoms of cough and phlegm in the smokers and ex-smokers, stratified by smoking status, were significantly higher in the exposed-group nonsmokers; this effect of smoking status, however, was not found in the control group. Prevalence of respiratory symptoms in the exposed group, stratified by smoking status, was not significantly higher than in the controls, except for wheezing, which occurred significantly more in the exposed workers who were nonsmokers, compared with nonsmoking control-group members.

[TABULAR DATA 6 OMITTED]

There was no difference in the prevalence of respiratory symptoms among the control, molding, burning, and crushing groups. Wheezing occurred most frequently among the burning workers, but this finding was not significant statistically when comparisons were made with the other groups. Perhaps the frequency of wheezing among burning workers resulted from inhalation of the irritant gases created during the combustion process.

Discussion

Development of silicosis in firebrick workers was reported in Missouri.[8] An association between silica exposure in firebrick or refractory brick workers and cancer risk has been noted in studies from Russia and Italy.[9-11] In our study, silica sand and silica-containing clay or rock were used to manufacture silica firebricks. Silica sand or quartz is 97%-99% silica, and clay or rock contains 0%-50% silica.[7] During the crushing and grinding operations, silica dust was generated in the workplace, especially when a dry process was used. Employees in such a work environment have an increased risk of silicosis. In our study, 6.9% of the firebrick workers had pneumoconiosis.

Workers employed in mining, milling, ore-processing, tunneling, quarrying, and other industries in which minerals, clays, or rocks are used, are at risk for exposure to silica dust. Occupations associated with an increased risk of silicosis include sandblaster, miner or tunneler, miller, pottery worker, glassmaker, foundry worker, quarry worker, and abrasives worker.[1-4] Pneumoconiosis has also been identified in other occupations that involve exposure to silica dust.[12-19] At a ceramic plate plant in Poland, 13% of the workers had pneumoconiosis;[14] 3.1% (11/358) of the employees at a South African pottery factory also had pneumoconiosis.[13] Simple pneumoconiosis was found in 13.3% of the workers in a Dutch fine-ceramic plant.[18] Sporadic cases of silicosis were also reported among workers potentially exposed to silica in other raw materials (e.g., slateworkers,[12] gemstone workers,[15] confectionery workers,[16] pottery workers,[17] silica flour and industrial sand workers[19]). The prevalence of pneumoconiosis in the respective industries is determined by the content of silica in raw materials and the types of processing used. Other industries in Taiwan that involved potential exposure to silica dust were compared, and the prevalence of pneumoconiosis in the firebrick workers was higher than in other production workers (i.e., stone production workers, 1.0%; clay, 1.0%; glass, 0.6%; steel, 0.7%; metal, 2.7%, machine, 1.8%, and cement, 4.7%).[20]

A dose-response relationship was shown between prevalence of pneumoconiosis in firebrick workers and estimated levels of exposure, even though no environmental monitoring data were available. Prevalence was highest among workers in the dusty crushing operation, followed by burning and molding operations. A dose-response relationship was also found between duration of employment and prevalence of pneumoconiosis: 14.4% in workers employed 10+ y, 5.1% in workers employed 5-10 y, and 2.0% in workers employed less than 5 y. These results suggested that the risk of developing pneumoconiosis increased with cumulative exposure levels, which were defined either by job title or by duration of employment.

A significant degree of obstructive airway disease (i.e., decreased FEV.sub.1.0/FVC) was found among firebrick workers in our study, compared with controls. Among smokers and nonsmokers, we also noted decreases in MMEF, FEF.sub.50%, and FEF.sub.75% in firebrick workers, compared with controls. These findings suggest the existence of large and small-airway obstruction defects among firebrick workers. Loss of lung function associated with exposure to silica dust has been shown in previous studies.[21-23] Small-airway obstruction has also been found in silica-exposed workers.[24] In their cross-sectional study, Chia et al.[24] also found a dose-response relationship between reduction in pulmonary function and duration of employment or exposure level estimated by job title. These studies also revealed that exposure to silica led to pulmonary function damage, and that the damage was associated with cumulative exposure levels.

The high prevalence of cough, phlegm, and bronchitis in the firebrick workers was associated with smoking. Respiratory symptoms were significantly more numerous in smokers, compared with nonsmokers; however, respiratory symptoms were not associated with exposure. The prevalence of respiratory symptoms in firebrick workers who smoked was not significantly higher than in the controls, with the exception of wheezing, which was not associated with either the estimated level of exposure or duration of employment. Wheezing occurred most frequently among the burning workers. In addition to silica dusts, the burning workers were also exposed to combustion products (e.g., sulfide dioxide, nitrogen oxide).

A weakness of this study was the lack of exposure data to quantify individual risk. From time to time, variations of exposure existed because the factories produced a diversity of products and because production schedules were irregular. Exposure levels were estimated by job titles, and dose-response relationships were shown. This classification was consistent with concentrations of respirable dust and percentages of crystalline silica in the work areas measured in a prior study by Puntoni et al.[10] Our study provided evidence that exposure to silica dust among firebrick workers can lead to pneumoconiosis and pulmonary function damage. Proper respiratory protection should be mandatory. Substitution of the alumina or zirconium bricks for silica firebricks and the installation of ventilation systems--especially in the dusty crushing, grinding, and mixing operations--are recommended.

References

[1.] Ziskind M, Jones RN, Weil H. Silicosis: state of the art. Am Rev Respir Dis 1976; 113:643-65.

[2.] Corn JK. Historical aspects of industrial hygiene-silicosis. Am Ind Hyg Assoc J 1980; 41:125-32.

[3.] Balaan MR, Weber SL, Banks DE. Clinical aspects of coal workers' pneumoconiosis and silicosis. Occup Med (State of the Art Reviews) 1993; 8:19-34. [4.] Parkes WR. Occupational lung disorders. 3rd ed. London, UK: Butterworth-Heinemann Ltd, 1994.

[5.] Ferris BG. Epidemiology standardization project. Am Rev Respir Dis 1978, 118:1-53. [6.] Dompeling E, van Schayck CP, Folgering H, et al. Accuracy, precision and linearity of the portable flow-volume meter Microspiro HI-298. Europ Respir J 1991; 4:812-15. [7.] Wang SM. The analysis of silica content in the raw material of firebrick manufacturing factories. Taipei, Taiwan: Council of Labor Affairs, 1989. [8.] Lesser M, Zia M, Kilburn KH. Silicosis in kaolin workers and firebrick makers. S Med J 1978; 71:1242 46.

[9.] Katsnelson BA, Mokronosova KA. Non-fibrous mineral dusts and malignant tumors: an epidemiological study of mortality. J Occup Med 1979; 21:15-20.

[10.] Puntoni R, Goldsmith DF, Valerio F, et al. A cohort study of workers employed in a refractory brick plant. Tumori 1988; 74:27-33.

[11.] Merlo F, Costantini M, Reggiardo G, et al. Lung cancer risk among refractory brick workers exposed to crystalline silica: a retrospective cohort study. Epidemiology 1991; 2:299-305.

[12.] Craighead JE, Emerson RJ, Stanley DE. Slateworker's pneumoconiosis. Human Pathol 1992; 23:1098-1105.

[13.] Rees D, Steinberg M, Becker PJ, et al. Dust exposure and pneumoconiosis in a South African pottery. 2. Pneumoconiosis and factors influencing reading of radiological opacities. Br J Ind Med 1992, 49:465-71.

[14.] Gielec L, Izycki J, Wozniak H. Evaluation of long-term occupational exposure to dust and its effect on health during production of ceramic tiles. Medycyna Pracy 1992; 43:25-33.

[15.] White NW, Chetty R, Bateman ED. Silicosis among gemstone workers in South Africa: tiger's-eye pneumoconiosis. Am J Ind Med 1991; 19:205-13.

[16.] Canessa PA, Torraca A, Lavecchia MA, et al. Pneumoconiosis (silicosis) in the confectionery industry. Sarcoidosis 1990; 7:75-77.

[17.] Anonymous. Silicosis among pottery workers-New Jersey. Morbid Mortal Weekly Rep 1992; 41 :405-06.

[18.] Meijers JM, Swaen GM, van Vliet K, et al. Epidemiologic studies of inorganic dust-related lung diseases in the Netherlands. Exper Lung Res 1990; 16:15-23.

[19.] Johnson WM, Busnardo MS. Silicosis following employment in the manufacturing of silica flour and industrial sand. J Occup Med 1993; 35:716 19.

[20.] Liou SH. Occupational disease profile in Taiwan, Republic of China. Ind Health 1994; 32:107-18.

[21.] Prowse K, Allen MB, Bradbury SR Respiratory symptoms and pulmonary impairment in male and female subjects with pottery workers' silicosis. Ann Occup Hyg 1989, 3:375 85.

[22.] Jones RN, Weil H, Ziskind M. Pulmonary function in sandblasters' silicosis. Bull Physiopathol Respir 1975; 11 :589-95.

[23.] Hnizdo E. Loss of lung function associated with exposure to silica dust and with smoking and its relation to disability and mortality in South African gold miners. Br J Ind Med 1992; 49:47279.

[24.] Chia KS, Ng TP, Jeyaratnam J. Small airways function of silica-exposed workers. Am J Ind Med 1992; 22:155-62.

This study was supported by a grant from Taiwan Provincial Health Department, Taichung, Taiwan, Republic of China.

Submitted for publication April 4, 1995; revised; accepted for publication August 23, 1995.

Requests for reprints should be sent to Dr. Saou-Hsing Liou, P.O. Box 90048-509, Taipei, Taiwan, 10107, Republic of China.

COPYRIGHT 1996 Heldref Publications
COPYRIGHT 2004 Gale Group

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