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Query: UMLS:C0032273 (pneumoconiosis)
 1,578 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Asthma is receiving increased attention as a cause of occupational disability, both by virtue of occupational causation and by interactions between work and pre-existing asthma. Reasons for the failure of pneumoconiosis-related disability evaluation systems to be applicable to asthma are discussed, including the inherent variability of asthma, its responsiveness to treatment, and its variable time course with respect to occupational exacerbation. A distinction is made between the trait of airway hyperresponsiveness and the disease of asthma. A scheme for organizing reports about asthma-related disability clearly specifies the questions that need to be addressed.
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PMID:Assessing occupational disability from asthma. 159 66

A random sample of 342 workers engaged in chipping and grinding of agate stones were surveyed in a cross-sectional study to assess the prevalence of respiratory morbidity in the agate industry. The findings were compared with those obtained in controls. The study showed a significantly higher prevalence of lung diseases among agate workers than among controls (63.4% vs 35.5%, P less than 0.001). The respiratory morbidity in agate workers and controls was maximal in the group aged 31+ years (83.3% and 42.2%, respectively). The prevalence of pneumoconiosis in agate workers (18.4%) was highly significant as compared with controls, in whom not a single case was found (P less than 0.001). However, there was no significant difference between the prevalence of pneumoconiosis in men and women of the exposed group (17.9% vs 19.6%). Among the cases of pulmonary diseases in agate workers, pneumoconiosis formed the largest group (18.4%), whereas among controls it was tuberculosis (12.1%). The prevalence of pulmonary tuberculosis was very high in both agate workers and controls (15.5% and 12.1%, respectively), probably because of poor socio-economic and unhygienic living conditions. The prevalence of chronic bronchitis was found to be higher among the control population as compared with the exposed group (6.7% vs 2.6%). It therefore appeared that agate dust had no role in precipitating chronic bronchitis. However, bronchial asthma appeared to have been aggravated due to agate dust, as the risk among agate workers was 7-fold that found among the controls. The prevalence of pneumoconiosis showed a dose-response relationship in both male and female agate workers.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A study of the prevalence of respiratory morbidity among agate workers. 164

The harmful effect of cement dust upon living organisms consists in irritating, sensitizing and pneumoconiotic properties of its components. In animal studies it has been observed that cement dust induces atrophic and hypertrophic changes in nasal and pharyngeal mucosa and chronic exfoliative bronchitis. In the lungs of experimental animals slight tissue fibrosis and some emphysema foci were found. The examination of workers exposed to cement dust has shown that disorders of the upper respiratory airways they suffer from include most often chronic rhinitis, laryngitis and pharynx catarrh. Also, it has been noticed that chronic bronchitis in the exposed workers was 1.7 times more frequent compared to those non-exposed, and that asthma was diagnosed in some of the exposed workers. Chronic bronchitis was usually characterized by the symptoms of impaired, obstructive lung ventilation. Defects in lung ventilation were strictly related to the duration of mild cases of cement pneumoconiosis diagnosed in a small percentage of workers who were exposed for at least 10 years to high dust concentrations. Long-term contact of skin with cement results in inflammatory changes or, in some cases, in chemical burns. Etiological factors of inflammatory skin changes are allergenic elements (Cr, Nr, Co) and irritating agents found in cement.
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PMID:[Biological effect of cement dust]. 181 89

This study examines the early efforts of the United Mine Workers of America to illuminate the problem of occupational respiratory diseases in the coal fields. The union used the hearings of the US Anthracite Coal Strike Commission of 1902-3 to draw public attention to "miners' asthma." In 1915, it began to agitate for the provision of workers' compensation benefits for victims of this disorder. Throughout the 1950s and 1960s, the union's Welfare and Retirement Fund disseminated information on advances in understanding chronic pulmonary diseases of mining. In particular, the miners' fund promoted the British conceptualization of a distinctive coal workers' pneumoconiosis. At the same time, the staff of the union health plan pressed the US Public Health Service and the Pennsylvania Department of Health to investigate the prevalence of occupational respiratory diseases among bituminous miners. Taken together, these endeavors contributed significantly to growing recognition of the severity and extent of this important public health problem and thus helped lay the foundation for the Federal Coal Mine Health and Safety Act of 1969.
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PMID:The United Mine Workers of American and the recognition of occupational respiratory diseases, 1902-1968. 182 71

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.
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PMID:Silicosis and lung cancer in North Carolina dusty trades workers. 186 18

Alveolar macrophages (AM) represent a lung border system bringing about the protection of the organ from the environmental hazards, regulating cell and humoral response in the lungs, and eliminating endogenous toxic substances. However, in some situations AM are involved in the pathologic processes and even may serve as an initiating factor in the development of lung pathology. They realize their pathogenic effect in the bronchial asthma, acute respiratory distress-syndrome, pneumoconiosis releasing various biologically active compounds which take part in the formation of bronchial hyperreactivity, chemotaxis disturbances, haemostasis pathology. Particularly interesting is the possibility of lung tissue damage by AM when they interact with endotoxin-positive granulocytes.
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PMID:[Alveolar macrophages in lung physiology and pathology]. 187 89

Sintered permanent magnets are made from the powdered metals of cobalt, nickel, aluminium, and various rare earths. During production, exposure to respirable crystalline silica and asbestos may also occur. Reported here is a cross sectional study of 310 current and 52 retired hourly employees who worked 10 or more years making sintered magnets. Each participant had a chest radiograph, spirometry, and completed a respiratory questionnaire. Illness logs were also reviewed to calculate the incidence of recorded respiratory disorders. The prevalences of abnormalities in pulmonary function and respiratory symptoms were not higher than found in an external referent population. Although the prevalence of diffuse parenchymal opacities consistent with pneumoconiosis (four workers) was similar to the referent population, one worker had radiographic findings consistent with silicosis and two workers had profusion scores of 1/2 or above, not seen in the referent group. The incidence of reported respiratory conditions in the log, including asthma, was 10 times that of other manufacturers in the same industrial classification category. Excessive exposures to cobalt, nickel, and respirable silica were shown by environmental measurements.
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PMID:Characterisation of respiratory health and exposures at a sintered permanent magnet manufacturer. 191 3

A voluntary scheme for the surveillance of work related and occupational respiratory disease (SWORD) was established in January 1989 with help from the British Thoracic Society and the Society of Occupational Medicine and support from the Health and Safety Executive. Three hundred and fifty four chest physicians representing 90% of the chest clinics in the United Kingdom and 361 occupational physicians submit reports regularly of newly diagnosed cases of work related respiratory illness with information on age, sex, residence, occupation, and suspected causal agent. In 1989 2101 cases were notified, of which frequent diagnoses were asthma (26%), mesothelioma (16%), pneumoconiosis (15%), benign pleural disease (11%), and allergic alveolitis (6%). Incidence rates calculated against denominators from the Labour Force Survey showed very large differences between occupational groups, especially for asthma and asbestos related diseases. Substantial regional variation in the incidence of asthma was not explained by the geographical distribution of high risk industries and was probably due to differing levels of ascertainment. The results imply that the true frequency of acute occupational respiratory disease in the United Kingdom may have been three times greater than that reported.
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PMID:Occupational respiratory disease in the United Kingdom 1989: a report to the British Thoracic Society and the Society of Occupational Medicine by the SWORD project group. 203 41

The authors have carried out a statistical analysis of cases of occupational asthma and other occupational lung diseases submitted to the Ministry of Labour in Quebec between 1986 and 1988. The total number of claims was 913, 993, and 866 respectively for the 3 years of which 61% to 71% were accepted. 41% to 55% were new assessments. Of 228 new claims accepted in 1988, 81 (36%) were for occupational asthma. This number surpassed the number of claims accepted for traditional pneumoconiosis (asbestos = 30, and silicose = 36). Isocyanates were the principle cause of occupational asthma (23% of cases were recognised in 1988) followed by flour, red and white cedar, snow crab process workers, and various pharmaceutical products and grains. In comparison with statistics in 1977, one noticed there was a large reversal of the frequency of certain occupational lung diseases that are recognised, because at that time asbestosis and silicosis were the principle causes of claims put forward and accepted. The authors discuss the statistical bias of occupational lung disease obtained by medico-legal agencies. Although occupational asthma has not been the object of the systematic screening program in the work place and although there is a tendency for workers to avoid or abandon their occupation more often than in the traditional pneumoconioses current protection is sufficient in Quebec to motivate individuals who are possibly suffering from occupational asthma to put in a claim for compensation.
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PMID:[Medico-legal statistics on occupational asthmna in Quebec between 1986 and 1988]. 214 54

The type of lung disease caused by metal compounds depends on the nature of the offending agent, its physicochemical form, the dose, exposure conditions and host factors. The fumes or gaseous forms of several metals, e.g. cadmium (Cd), manganese (Mn), mercury (Hg), nickel carbonyl (Nl(CO)4, zinc chloride (ZnCl2), vanadium pentoxide (V2O5), may lead to acute chemical pneumonitis and pulmonary oedema or to acute tracheobronchitis. Metal fume fever, which may follow the inhalation of metal fumes e.g. zinc (Zn), copper (Cu) and many others, is a poorly understood influenza-like reaction, accompanied by an acute self-limiting neutrophil alveolitis. Chronic obstructive lung disease may result from occupational exposure to mineral dusts, including probably some metallic dusts, or from jobs involving the working of metal compounds, such as welding. Exposure to cadmium may lead to emphysema. Bronchial asthma may be caused by complex platinum salts, nickel, chromium or cobalt, presumably on the basis of allergic sensitization. The cause of asthma in aluminium workers is unknown. It is remarkable that asthma induced by nickel (Ni) or chromium (Cr) is apparently infrequent, considering their potency and frequent involvement as dermal sensitizers. Metallic dusts deposited in the lung may give rise to pulmonary fibrosis and functional impairment, depending on the fibrogenic potential of the agent and on poorly understood host factors. Inhalation of iron compounds causes siderosis, a pneumoconiosis with little or no fibrosis. Hard metal lung disease is a fibrosis characterized by desquamative and giant cell interstitial pneumonitis and is probably caused by cobalt, since a similar disease has been observed in workers exposed to cobalt in the absence of tungsten carbide. Chronic beryllium disease is a fibrosis with sarcoid-like epitheloid granulomas and is presumably due to a cell-mediated immune response to beryllium. Such a mechanism may be responsible for the pulmonary fibrosis occasionally found in subjects exposed to other metals e.g. aluminium (Al), titanium (Ti), rare earths. The proportion of lung cancer attributable to occupation is around 15%, with exposure to metals being frequently incriminated. Underground mining of e.g. uranium or iron is associated with a high incidence of lung cancer, as a result of exposure to radon. At least some forms of arsenic, chromium and nickel are well established lung carcinogens in humans. There is also evidence for increased lung cancer mortality in cadmium workers and in iron or steel workers.
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PMID:Metal toxicity and the respiratory tract. 217 66


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