Trends in work-related respiratory diseases attributed to nickel, chromium and cobalt in the UK: descriptive findings from The Health and Occupation Research (THOR) network 1996-2019.

BACKGROUND: Occupational exposure to metals can be associated with respiratory diseases which can adversely affect the individual's health, finances and employment. Despite this, little is known about the incidence of these respiratory conditions over prolonged periods of time. AIMS: This study aimed to investigate the trends in the incidence of work-related respiratory diseases attributed to nickel, chromium and cobalt in the UK. METHODS: Cases of occupational respiratory diseases caused by nickel, chromium or cobalt reported to Surveillance of Work-related and Occupational Respiratory Disease (SWORD), the UK-based surveillance scheme between 1996 and 2019 (inclusive), were extracted and grouped into six 4-year time periods. Cases were characterised by causative metal exposure, occupational and industrial sector. Incidence rates diseases (adjusted for physician participation and response rate) were calculated using ONS employment data. RESULTS: Of cases reported to SWORD during the study period, 1% (173 actual cases) of respiratory problems were attributed to nickel, chromium or cobalt. Diagnoses of asthma compromised the largest proportion of diagnoses (74.4%), followed by lung cancer (8.9%) and pneumoconiosis (6.7%). Cases had a mean age of 47 years (SD 13); 93% were men. The annual incidence fell from 1.6 per million employed in the first 4-year period, to 0.2 in the most recent period. CONCLUSIONS: Over 24 years, a decline in the incidence of metal-related occupational respiratory diseases was observed in the UK. This could be attributed to improvements in working conditions which resulted in reduced metal exposure but could also be due to closure of industries that might have generated case returns.

Pathology and Mineralogy of the Pneumoconioses.

Pneumoconioses represent the spectrum of lung diseases caused by inhalation of respirable particulate matter small enough (typically <5-µm diameter) to reach the terminal airways and alveoli. Pneumoconioses primarily occur in occupational settings where workers perform demanding and skilled manual labor including mining, construction, stone fabrication, farming, plumbing, electronics manufacturing, shipyards, and more. Most pneumoconioses develop after decades of exposure, though shorter latencies can occur from more intense particulate matter exposures. In this review, we summarize the industrial exposures, pathologic findings, and mineralogic features of various well-characterized pneumoconioses including silicosis, silicatosis, mixed-dust pneumoconiosis, coal workers' pneumoconiosis, asbestosis, chronic beryllium disease, aluminosis, hard metal pneumoconiosis, and some less severe pneumoconioses. We also review a general framework for the diagnostic work-up of pneumoconioses for pulmonologists including obtaining a detailed occupational and environmental exposure history. Many pneumoconioses are irreversible and develop due to excessive cumulative respirable dust inhalation. Accurate diagnosis permits interventions to minimize ongoing fibrogenic dust exposure. A consistent occupational exposure history coupled with typical chest imaging findings is usually sufficient to make a clinical diagnosis without the need for tissue sampling. Lung biopsy may be required when exposure history, imaging, and testing are inconsistent, there are unusual or new exposures, or there is a need to obtain tissue for another indication such as suspected malignancy. Close collaboration and information-sharing with the pathologist prior to biopsy is of great importance for diagnosis, as many occupational lung diseases are missed due to insufficient communication. The pathologist has a broad range of analytic techniques including bright-field microscopy, polarized light microscopy, and special histologic stains that may confirm the diagnosis. Advanced techniques for particle characterization such as scanning electron microscopy/energy dispersive spectroscopy may be available in some centers.

The impact of coal mine dust characteristics on pathways to respiratory harm: investigating the pneumoconiotic potency of coals.

Exposure to dust from the mining environment has historically resulted in epidemic levels of mortality and morbidity from pneumoconiotic diseases such as silicosis, coal workers' pneumoconiosis (CWP), and asbestosis. Studies have shown that CWP remains a critical issue at collieries across the globe, with some countries facing resurgent patterns of the disease and additional pathologies from long-term exposure. Compliance measures to reduce dust exposure rely primarily on the assumption that all "fine" particles are equally toxic irrespective of source or chemical composition. For several ore types, but more specifically coal, such an assumption is not practical due to the complex and highly variable nature of the material. Additionally, several studies have identified possible mechanisms of pathogenesis from the minerals and deleterious metals in coal. The purpose of this review was to provide a reassessment of the perspectives and strategies used to evaluate the pneumoconiotic potency of coal mine dust. Emphasis is on the physicochemical characteristics of coal mine dust such as mineralogy/mineral chemistry, particle shape, size, specific surface area, and free surface area-all of which have been highlighted as contributing factors to the expression of pro-inflammatory responses in the lung. The review also highlights the potential opportunity for more holistic risk characterisation strategies for coal mine dust, which consider the mineralogical and physicochemical aspects of the dust as variables relevant to the current proposed mechanisms for CWP pathogenesis.

A case of welder's lung with end-stage pulmonary fibrosis.

BACKGROUND: Welding, performed regularly by more than a million workers worldwide, is associated with exposures to irritative, fibrogenic and carcinogenic fumes and gases. METHODS AND RESULTS: We present the case of a welder who had worked under extremely poor hygiene conditions for nearly 20 years and had developed end-stage lung fibrosis, finally requiring lung transplantation. Detailed histopathology and scanning electron microscopy/energy dispersive X-ray spectroscopy (SEM/EDS) analyses of his lungs showed advanced interstitial fibrosis and dust deposits in the lungs and in peribronchial lymph nodes containing welding type bodies, Fe, Si (silica), Ti (titanium), SiAl (aluminum silicates), Fe with Cr (Steel), and Zr (Zirkonium). CONCLUSION: In the absence of a systemic disorder and the failure to meet the criteria for diagnosis of idiopathic pulmonary fibrosis (IPF), these findings suggest welder's lung fibrosis as the most likely diagnosis.

A Descriptive Study of a Turkish Pneumoconiosis Case-Series.

BACKGROUND: The study aimed to examine the conditions and factors affecting pneumoconiosis cases to determine the dimensions of the pneumoconiosis problem. METHODS: This retrospective study was conducted in a tertiary research hospital between January 1, 2014, and December 31, 2021. Five hundred ninety-seven patients with pneumo- coniosis were included in the study. RESULTS: Large opacities were detected in 157 cases. When we compared cases with and without Pulmonary Massive Fibrosis (PMF), age and concomitant pulmonary disease were higher in PMF cases, which also showed lower FEV1, FVC, and FEV1/FVC. PMF was more frequent in subjects with long dust exposure duration (more than 20 years) and concomitant pulmonary diseases, particularly tuberculosis. Three occupations, sandblasters, dental technicians, and ceramic workers, showed the earliest onset of pneumoconiosis. CONCLUSIONS: The study presents pneumoconiosis data in a mixed and large population and contributes to the imple- mentation of evidence-based policies and interventions for countries like Turkey striving to cope with the problem of pneumoconiosis.

Effects of chemical composition on the lung cell response to coal particles: Implications for coal workers' pneumoconiosis.

BACKGROUND AND OBJECTIVE: Coal mine dust has a complex and heterogeneous chemical composition. It has been suggested that coal particle chemistry plays a critical role in determining the pathogenesis of coal workers' pneumoconiosis (CWP). In this study, we aimed to establish the association between the detrimental cellular response and the chemical composition of coal particles. METHODS: We sourced 19 real-world coal samples. Samples were crushed prior to use to minimize the impact of particle size on the response and to ensure the particles were respirable. Key chemical components and inorganic compounds were quantified in the coal samples. The cytotoxic, inflammatory and pro-fibrotic responses in epithelial cells, macrophages and fibroblasts were assessed following 24 h of exposure to coal particles. Principal component analysis (PCA) and stepwise regression were used to determine which chemical components of the coal particles were associated with the cell response. RESULTS: The cytotoxic, inflammatory and pro-fibrotic response varied considerably between coal samples. There was a high level of collinearity in the cell responses and between the chemical compounds within the coal samples. PCA identified three factors that explained 75% of the variance in the cell response. Stepwise multiple regression analysis identified K2 O (p <0.001) and Fe2 O3 (p = 0.011) as significant predictors of cytotoxicity and cytokine production, respectively. CONCLUSION: Our data clearly demonstrate that the detrimental cellular effects of exposure to coal mine dusts are highly dependent on particle chemistry. This has implications for understanding the pathogenesis of CWP.

Postexposure progression of pneumoconiosis among former Appalachian coal miners.

BACKGROUND: The prevalence of pneumoconiosis among working United States underground coal miners has been increasing for the past two decades, with the highest rates of disease observed among miners in the central Appalachian states of Kentucky, Virginia, and West Virginia. Surveillance for this disease in the United States focuses on working coal miners, who continue to be occupationally exposed to dust. This study examines the radiographic evidence for postexposure progression of pneumoconiosis in a population of former coal miners no longer occupationally exposed to coal mine dust who were seen at a community radiology clinic in eastern Kentucky. METHODS: Data were obtained and analyzed from clinical records of former coal miners who had a clinic encounter during January 1, 2017-August 1, 2019, a recorded final year of employment, and ≥2 postemployment digital chest radiographs. Radiographs were classified according to the International Labour Office guidelines by at least two B Readers. A final summary pneumoconiosis severity score (range, 0-13), accounting for both small and large opacities, was assigned to each chest radiograph. Progression was defined as an increase in severity score between a miner's radiographs over time. RESULTS: Data for 130 former coal miners were analyzed. All miners were male and most (n = 114, 88%) had worked primarily in Kentucky. Information on race/ethnicity was not available. The most common job types were roof bolters (n = 51, 39%) and continuous miner operators (n = 46, 35%). Forty-one (31.5%) miners had evidence of radiographic disease progression after leaving the workforce, with a median of 3.6 years between first and latest postretirement radiograph. A total of 80 (62%) miners had evidence of pneumoconiosis on their latest radiograph, and two-thirds (n = 53) of these were classified as progressive massive fibrosis (PMF), the most severe form of the disease. CONCLUSIONS: Postexposure progression can occur in former coal miners, emphasizing the potential benefits of continued radiographic follow-up postemployment. In addition to participating in disease screening throughout their careers to detect pneumoconiosis early and facilitate intervention, radiographic follow-up of former coal miners can identify new or progressive radiographic findings even after workplace exposure to respirable coal mine dust ends. Identification of progressive pneumoconiosis in former miners has potential implications for clinical management and eligibility for disability compensation.

Trends in pneumoconiosis in Brazil, 1979-2019.

BACKGROUND: Pneumoconiosis is a lung disease related to exposure to dust in the workplace. The disease can induce irreversible damage to health, especially in lung tissue, and can cause progressive and permanent physical disabilities. AIMS: This study evaluated the temporal and spatial distribution of mortality rates (1979-2019) and hospital admissions (1995-2019) for pneumoconiosis in Brazil. METHODS: The outcomes were hospitalization and death due to pneumoconiosis: codes 500-506 according to the ICD-9 and J60-J66 according to the ICD-10. Data from this retrospective ecological study were collected from the Brazilian Ministry of Health database. RESULTS: Hospitalization for pneumoconiosis has decreased in all regions of Brazil. Hospitalizations occurred predominantly in men aged over 40 years. Death rates showed a temporal increase in all regions. Deaths occurred predominantly in men aged over 50 years. The highest hospitalization and death rates were in the states of the Midwest and South Regions. CONCLUSIONS: Pneumoconiosis is a preventable occupational disease, and ongoing occurrences of hospitalizations and deaths highlight the importance of inspecting industries and controlling occupational and environmental exposures.

Demonstrating the protective effect of a 70-year-old occupational exposure limit against pneumoconiosis caused by mica.

Workers involved in crushing, milling, screening, and bagging of mica scrap are at increased risk to develop pneumoconiosis, a progressive material overloading of the lung that can lead to fibrosis and, in the later stages, to dyspnea. Pneumoconiosis is only seen after 10-20 years of respiratory mica exposure, and it can have a latency period of up to 40 years-today's cases date back to exposures during the second half of the 20th century. An occupational lifetime exposure level of 3 mg/m3 respirable mica dust has been considered to present no risk of pneumoconiosis since 1951 when the American Conference of Governmental Industrial Hygienists (ACGIH) established a 20 million particles per cubic foot (mppcf) (3.5 mg/m3 respirable particles) exposure limit. As a result, numbers of unspecified and other pneumoconioses in the United States have steadily declined since the early 1970s. Data from the National Institute for Occupational Safety and Health documents a 91% decrease between 1972 and 2014 (i.e., the peak of documented cases and the latest reported data) for combined cases of aluminosis, berylliosis, stannosis, siderosis, and fibrosis from production and use of bauxite, graphite fibers, wollastonite, cadmium, Portland cement, emery, kaolin, antimony, and mica. Ample evidence indicates that the 70-year-old occupational lifetime exposure level of 3 mg/m3 respirable mica dust is protective of workers' health.

[Occupational health risk assessment of pneumoconiosis caused by dust exposure at 18 quarries in a given area of Hubei Province].

OBJECTIVE: To explore the occupational health risk level of pneumoconiosis caused by dust exposure in a given area of Hubei province. METHODS: From April 2021 to October 2021, 18 quarries were randomly selected in the areas where quarries were concentrated in Hubei Province to conduct on-site hygiene investigation and detection. A total of 384 workers were employed in the above quarries, and 293 workers were exposed to dust. The International Mining and Metals Commission's risk rating table method and occupational hazard risk index method were used to analyze the occupational health risk level from total and respirable dust views, respectively. Meanwhile, the square weighted Kappa test was performed to analyze the consistency between two risk assessment method. RESULTS: The median dust exposure rate of workers in the above18 enterprises was 73.22%, small, underground mining, and barite quarries had relatively higher dust exposure rates(all median were 100.00%). The medians of daily dust exposure time, personal protective equipment wearing rate, free silica content of dust, 8-hour time weighted average exposure concentration of total dust and respirable dust in each assessment indicator were 6-8 hours, 0%-24.00%, 1.69%-35.30%, 0.56-3.70 mg/m~3, and 0.33-1.20 mg/m~3, respectively. Occupational health risk assessment result showed the overall occupational health risk levels of quarries, as well as different production scales and mining method, were all low. Among different positions, wind driller and tunneling worker had high and medium occupational health risk, respectively, and the rest of the positions had low or very low risk. International Council on Mining and Mentals(ICMM) risk rating table method and the INDEX method consistency analyses showed that these two risk assessment method had strong consistency in terms of total dust(Kappa value was 0.65(95%CI 0.57-0.73)), and general consistency in term of respirable dust(Kappa value was 0.51(95%CI 0.39-0.62)). CONCLUSION: The overall occupational health risk level of pneumoconiosis caused by dust exposure in quarries was low, but risk levels were higher for wind driller and tunneling worker.

Early signs of pneumoconiosis in a dental technician in Italy: a case report.

BACKGROUND: Dental technicians are at high risk of pneumoconiosis, usually driven by inhalation of mixed dusts, including metals. An etiological diagnosis is not easy to be performed, particularly in advanced stages. CASE PRESENTATION: We describe the case of an early pneumoconiosis occurring in a 47-year-old dental technician who developed respiratory symptoms shortly after beginning work. She described the work environment as dusty and lacking relevant primary prevention tools. A chest CT showed multiple peripheral pseudonodular lesions in both lower lobes; bronchoalveolar lavage and bronchial aspirate evidenced numerous macrophages with reflective metal bodies included into the cytoplasm, that at scanning electron microscopy coupled to Energy Dispersive X-Ray Analysis resulted Zirconium and Aluminum, whereas Tungsten (W) was localized outside cells. End of shift urinary concentrations of W were substantially raised as compared to pre-shift (1.1 vs. 0.2 µg/L). CONCLUSIONS: We concluded for diagnosis of early work-related pneumoconiosis due to abnormal occupational exposure to metals. The case demonstrates the need also for dental professionals to comply with industrial hygiene standards and to be monitored by occupational health physicians.

Trends in global, regional and national incidence of pneumoconiosis caused by different aetiologies: an analysis from the Global Burden of Disease Study 2017.

OBJECTIVES: Pneumoconiosis remains a major global occupational health hazard and illness. Accurate data on the incidence of pneumoconiosis are critical for health resource planning and development of health policy. METHODS: We collected data for the period between 1990 and 2017 on the annual incident cases and the age-standardised incidence rates (ASIR) of pneumoconiosis aetiology from the Global Burden of Disease Study 2017. We calculated the average annual percentage changes of ASIR by sex, region and aetiology in order to determine the trends of pneumoconiosis. RESULTS: Globally, the number of pneumoconiosis cases increased by a measure of 66.0%, from 36 186 in 1990 to 60 055 in 2017. The overall ASIR decreased by an average of 0.6% per year in the same period. The number of pneumoconiosis cases increased across the five sociodemographic index regions, and there was a decrease in the ASIR from 1990 to 2017. The ASIR of silicosis, coal workers' pneumoconiosis and other pneumoconiosis decreased. In contrast, measures of the ASIR of asbestosis displayed an increasing trend. Patterns of the incidence of pneumoconiosis caused by different aetiologies were found to have been heterogeneous for analyses across regions and among countries. CONCLUSION: Incidence patterns of pneumoconiosis which were caused by different aetiologies varied considerably across regions and countries of the world. The patterns of incidence and temporal trends should facilitate the establishment of more effective and increasingly targeted methods for prevention of pneumoconiosis and reduce associated disease burden.

Unusual pneumoconiosis in two patients with heavy print toner, and paper dust exposure.

Workers in a print shop are exposed to photocopier toner dust and paper dust over a prolonged period of time. However, there are only rare case reports of toner and paper dust induced lung damage in humans. We reviewed our consultation files for a period of 30 years from 1987 to 2018 to look for cases with a diagnosis of giant cell interstitial pneumonia (GIP), printer toner exposure and paper dust exposure resulting in lung disease. There were two cases which met our inclusion criteria. Slides, clinical histories and imaging were reviewed. Both the patients had worked in print shops, and had no history of exposure to hard metals. Patient 1 presented with shortness of breath and cough over several months, while patient 2 was asymptomatic at presentation. Both the patients underwent surgical lung biopsies. Histopathologic examination from both the cases showed a spectrum of pathology, including features of GIP, desquamative interstitial pneumonia, chronic bronchiolitis with lymphoid hyperplasia, and particulate matter consistent with toner. Energy dispersive spectroscopy was performed on one case, and it revealed no cobalt or tungsten particles. The unusual combination of findings is very suggestive that toner particles with or without paper dust exposure were responsible for the pathologic changes in the lungs of these patients. This possibility should be explored further with additional patients who work in print shops where they are exposed to paper dust and paper toner and have signs or symptoms of diffuse lung disease.

Pneumoconiosis with a Sarcoid-Like Reaction Other than Beryllium Exposure: A Case Report and Literature Review.

Background: Chronic beryllium disease (CBD) is a granulomatous disease that resembles sarcoidosis but is caused by beryllium. Clinical manifestations similar to those observed in CBD have occasionally been reported in exposure to dusts of other metals. However, reports describing the clinical, radiographic, and pathological findings in conditions other than beryllium-induced granulomatous lung diseases, and detailed information on mineralogical analyses of metal dusts, are limited. Case presentation: A 51-year-old Japanese man with rapidly progressing nodular shadows on chest radiography, and a 10-year occupation history of underground construction without beryllium exposure, was referred to our hospital. High-resolution computed tomography showed well-defined multiple centrilobular and perilobular nodules, and thickening of the intralobular septa in the middle and lower zones of both lungs. No extrathoracic manifestations were observed. Pathologically, the lung specimens showed 5-12 mm nodules with dust deposition and several non-necrotizing granulomas along the lymphatic routes. X-ray analytical electron microscopy of the same specimens revealed aluminum, iron, titanium, and silica deposition in the lung tissues. The patient stopped smoking and changed his occupation to avoid further dust exposure; the chest radiography shadows decreased 5 years later. Conclusion: The radiological appearances of CBD and sarcoidosis are similar, although mediastinal or hilar lymphadenopathy is less common in CBD and is usually seen in the presence of parenchymal opacities. Extrathoracic manifestations are also rare. Despite limited evidence, these findings are similar to those observed in pneumoconiosis with a sarcoid-like reaction due to exposure to dust other than of beryllium. Aluminum is frequently detected in patients with pneumoconiosis with a sarcoid-like reaction and is listed as an inorganic agent in the etiology of sarcoidosis. It was also detected in our patient and may have contributed to the etiology. Additionally, our case suggests that cessation of dust exposure may contribute to improvement under the aforementioned conditions.

Functional variant of the carboxypeptidase M (CPM) gene may affect silica-related pneumoconiosis susceptibility by its expression: a multistage case-control study.

OBJECTIVES: In a genome-wide association study, we discovered chromosome 12q15 (defined as rs73329476) as a silica-related pneumoconiosis susceptibility region. However, the causal variants in this region have not yet been reported. METHODS: We systematically screened eight potentially functional single-neucleotide polymorphism (SNPs) in the genes near rs73329476 (carboxypeptidase M (CPM) and cleavage and polyadenylation specific factor 6 (CPSF6)) in a case-control study including 177 cases with silicosis and 204 healthy controls, matched to cases with years of silica dust exposure. We evaluated the associations between these eight SNPs and the development of silicosis. Luciferase reporter gene assays were performed to test the effects of selected SNP on the activity of CPM in the promoter. In addition, a two-stage case-control study was performed to investigate the expression differences of the two genes in peripheral blood leucocytes from a total of 64 cases with silicosis and 64 healthy controls with similar years of silica dust exposure as the cases. RESULTS: We found a strong association between the mutant rs12812500 G allele and the susceptibility of silicosis (OR=1.45, 95% CI 1.03 to 2.04, p=0.034), while luciferase reporter gene assays indicated that the mutant G allele of rs12812500 is strongly associated with increased luciferase levels compared with the wild-type C allele (p<0.01). Moreover, the mRNA (peripheral blood leucocytes) expression of the CPM gene was significantly higher in subjects with silicosis compared with healthy controls. CONCLUSIONS: The rs12812500 variant of the CPM gene may increase silicosis susceptibility by affecting the expression of CPM, which may contribute to silicosis susceptibility with biological plausibility.

Respirable coal mine dust in underground mines, United States, 1982-2017.

BACKGROUND: This study summarized the mass concentration and quartz mass percent of respirable coal mine dust samples (annually, by district, and by occupation) from underground coal mines during 1982-2017. METHODS: Respirable dust and quartz data collected and analyzed by Mine Safety and Health Administration (MSHA) were summarized by year, coal mining occupation, and geographical area. The older (before August 2016) 2.0 mg/m 3 respirable dust MSHA permissible exposure limit (PEL) was used across all years for comparative purposes. For respirable dust and quartz, geometric mean and percent of samples exceeding the respirable dust PEL (2.0 mg/m 3 or a reduced standard for samples with >5% quartz content) were calculated. For quartz samples, the average percent quartz content was also calculated. RESULTS: The overall geometric mean concentration for 681 497 respirable dust samples was 0.55 mg/m 3 and 5.5% of the samples exceeded the 2.0 mg/m 3 PEL. The overall respirable quartz geometric mean concentration for 210 944 samples was 0.038 mg/m 3 and 18.7% of these samples exceeded the applicable standard. There was a decline over time in the percent of respirable dust samples exceeding 2.0 mg/m 3 . The respirable dust geometric mean concentration was lower in central Appalachia compared to the rest of the United States. However, the respirable quartz geometric mean concentration and the mean percent quartz content were higher in central Appalachia. CONCLUSION: This study summarizes respirable dust and quartz concentrations from coal mine inspector samples and may provide an insight into differences in the prevalence of pneumoconiosis by region and occupation.

Pneumoconiosises: modern view.

The article is devoted to the actual problem - dust diseases of the lungs. The peculiarities of occurrence and course of pulmonary lesions that have a significant place in the overall structure of occupational morbidity are considered. Modern approaches to treatment, diagnostics and prevention issues in pneumoconiosis are discussed.

[Research of epigenetic modifications in pathogenesis of pneumoconiosis].

Pneumoconiosis is the most common and severe occupational disease, has become a major public health problem in the world. Its causes are well known, but the pathogenesis of it is not completely clear and effective therapies are not currently available. Epigenetic modifications have been considered an initial event in the development of pneumoconiosis. Epigenetic regulatory mechanisms in pneumoconiosis include DNA methylation, non-coding RNA (ncRNA) , and histone modification. In recent years, many researchers have studied the effect of dust-induced pulmonary fibrosis-related gene expression at the epigenetic level on macrophage activation, lung fibroblast proliferation, activation, transdifferentiation, and epithelial or endothelial-mesenchymal transition (EMT/EndMT) to further elucidate the pathogenesis of pneumoconiosis. In this review, we discusses the epigenetic modifications in pneumoconiosis, with an aim to provide new insights into the early diagnosis, condition assessment and targeted therapy of this occupational disease.

Artificial stone-associated silicosis: a rapidly emerging occupational lung disease.

INTRODUCTION: Artificial stone is an increasingly popular material used to fabricate kitchen and bathroom benchtops. Cutting and grinding artificial stone is associated with generation of very high levels of respirable crystalline silica, and the frequency of cases of severe silicosis associated with this exposure is rapidly increasing. AIM: To report the characteristics of a clinical series of Australian workers with artificial stone-associated silicosis. METHODS: Respiratory physicians voluntarily reported cases of artificial stone-associated silicosis identified in their clinical practices. Physicians provided information including occupational histories, respiratory function tests, chest radiology and histopathology reports, when available. RESULTS: Seven male patients were identified with a median age of 44 years (range 26-61). All were employed in small kitchen and bathroom benchtop fabrication businesses with an average of eight employees (range 2-20). All workplaces primarily used artificial stone, and dust control measures were poor. All patients were involved in dry cutting artificial stone. The median duration of exposure prior to symptoms was 7 years (range 4-10). Six patients demonstrated radiological features of progressive massive fibrosis. These individuals followed up over a median follow-up period of 16 months (IQR 21 months) demonstrated rapid decline in prebronchodilator forced expiratory volume in 1 s of 386 mL/year (SD 204 mL) and forced vital capacity of 448 mL/year (SD 312 mL). CONCLUSIONS: This series of silicosis in Australian workers further demonstrates the risk-associated high-silica content artificial stone. Effective dust control and health surveillance measures need to be stringently implemented and enforced in this industry.

Occupational emphysema in South African miners at autopsy; 1975-2014.

PURPOSE: To determine the associations between exposure duration, measured by employment tenure, and emphysema presence and severity in black and white South African miners at autopsy. METHODS: We examined the association between mining tenure and emphysema presence or severity using the Pathology Automation (PATHAUT) database, 1975-2014. We used logistic regression models adjusted for age, tuberculosis, HIV status, and year of death. The effect of smoking on the presence and severity of emphysema was assessed in a sub-analysis of white miners. RESULTS: Mining tenure was significantly associated with increased odds of emphysema presence in black and white miners. For every 10-year increase in tenure, black miners had a 17% increase in odds of emphysema [ORblack = 1.17 (95% CI 1.12, 1.22)] and white miners had a 7% increase in odds of the disease [ORwhite = 1.07 (95% CI 1.04, 1.10)]. Tenure was significantly associated with emphysema severity among black miners [ORseverity = 1.16 (95% CI 1.06, 1.28)]. In a subset of white miners with smoking status, we found that for every 10 years of tenure, there is a significant increase in odds of emphysema presence and severity [ORpresence = 1.14 (95% CI 1.09, 1.19); ORseverity = 1.06 (95% CI 1.00, 1.10)] after adjusting for smoking. CONCLUSIONS: We observed a significant relationship between mining tenure and emphysema severity among South African miners in PATHAUT between 1975 and 2014. This relationship was evident in multi-variable analyses adjusted for smoking among white miners. Hazards from long term exposure to inhaled mineral dust leading to lung damage (silicosis, fibrosis, COPD) is evident and warrants further improvement of working conditions and prevention measures in South African mines especially for black workers. Further research is needed to determine if there is an effect of TB and HIV co-infection on the development of emphysema.