Crystalline Silica Exposure Research Articles

Exposure to Respirable Crystalline Silica in the GB Brick Manufacturing and Stone Working Industries.

The aim of this work was to benchmark respirable crystalline silica (RCS) exposures in brick manufacturing and stone working sectors in Great Britain. This will contribute to a larger programme of work, which will be used to better understand the role of health surveillance in preventing the development of further cases of silicosis and chronic obstructive pulmonary disease. This work was undertaken by means of site visits to measure RCS and respirable dust exposures and assess exposure controls. In addition, historic exposure reports from the sites were collated to allow assessment of exposure trends. The survey, which was conducted in 20 sites (10 from each sector), found that in both sectors over 20% of the measured exposures exceeded the UK RCS 8-hour time-weighted averaged workplace exposure limit (WEL) of 0.1 mg/m3. In the stone sector over 40% of the 8 h time-weighted average RCS exposures were above the RCS WEL compared to 20% in the brick manufacturing sector. In the stone sector, 61% of RCS exposures where water suppression was present exceeded the RCS WEL. This indicates that a variety of exposure controls will be required to control RCS exposures, including respiratory protective equipment (RPE). The use of RPE in situations where RCS exposure exceeded the RCS WEL was more prevalent in stone working than in the brick sector. There were differences associated with RPE and the use of other exposure controls in both sectors. The contextual information in historic consultant's exposure reports was generally limited, with exposure controls either not mentioned or not fully described. This affects the usefulness of exposure monitoring to dutyholders. This work will provide information on exposures allowing construction of lifetime exposure estimates for use in analysis of the health effects data. A second survey to the sites is planned to determine how exposures have altered.

Quantitative Risk Assesment of Crystalline Silica Exposure in Ceramics Industry

Crystalline silica can be found in Ceramics Industry. Ceramics are basically made of clay, feldspar and silica sand. Ceramics manufacturing process starts from the processing of materials, forming, drying, burning and gazing. Crystalline silica consists of three types of quartz, tridymite and cristobalite which are distinguished by their forming temperature. Crystaline silica dust is very dangerous for health workers are exposed continuously it can cause a silicosis. Prevention and control efforts can be done one of them by conducting a risk analysis study on crystalline silica exposure. In this research will be discussed about the analysis of crystalline silica exposure into production workers in the ceramics industry. The purpose of this study was to assess the risk level of crystalline silica due to silicosis. Subjects in this study were 47 production workers with the exposure to crystalline silica between 0,007 � 0,4 mg / m 3 . From the result of risk analysis, it was found that 42,6 of workers had unsafe risk which was confirmed by radiology examination was 6,4 of workers with abnormal condition. Complaints experienced by workers include shortness of breath, cough and phlegm. Long term exposure to 5-20 years to the next tends to increase the risk of the effects caused by exposure to crystalline silica. Based on the results of this study it is recommended that decision makers take action to implement effective risk management strategies to prevent the long-term effects of crystalline silica exposure to the workplace. © 2019, Indian Journal of Public Health Research and Development. All rights reserved.

Respirable Crystalline Silica Exposure among Concrete Finishing Workers at Apartment Complex Construction Sites

ABSTRACT The objective of this study was to evaluate the level of exposure to respirable crystalline silica (RCS) among concrete finishers and to identify the size distribution of particles from concrete finishing work at apartment complex construction sites. Active personal air sampling (n = 129) was conducted at eight sites using filters with aluminum cyclones, and local air sampling for the size distribution of the particles (n = 6) was conducted using a Mylar substrate with cascade impactors. Crystalline silica was analyzed by Fourier-transform infrared spectroscopy (FT-IR). The collected personal samples were sorted by the type of task (concrete chipping, grinding, or plastering) for four kinds of working places (exterior walls, interior walls of apartment units, staircases, and underground parking lots). The geometric mean (GM) of the RCS concentration was highest, although varying according to the type of structure, for concrete grinding (2.06 mg m–3), followed by chipping (0.12 mg m–3) and plastering (0.003 mg m–3). The maximum RCS concentration was measured in the staircases (4.18 mg m–3), followed by the interior walls of apartment units (2.76 mg m–3), underground parking lots (1.30 mg m–3), and exterior walls (0.89 mg m–3). The mass fraction of inhalable, thoracic, and respirable crystalline silica was respectively 73.9%, 40.2%, and 17.9% in chipping and 76.0%, 46.3%, and 19.7% in grinding. Concrete finishing workers at apartment complex construction sites are exposed to unacceptably high concentrations of RCS. To protect workers’ health, dust-minimizing construction methods as well as high-efficiency respirators paired with local exhaust ventilation systems or wet methods must be employed. Further efforts to reduce the total working time and to use full-faced air-purifying respirators are required.

Silica Standards: Policy Delays and Future Implications

The Occupational Safety and Health Administration (OSHA) was created in the year 1971 with the passage of the Occupational Safety and Health Act on December 29, 1970. Signed into law by President Nixon, OSHA was created to protect the health and safety of American workers from the hazards of their work environments. A significant workplace health hazard, especially in the construction industry, is crystalline silica, or silica dust. Only recently was an official rule on crystalline silica exposure signed into law. The OSH Act was published in the Federal Register on March 25, 2016, issued on June 23, and effective a year later on June 23, 2017. Previous guidelines and standards on proactive measures to reduce the health effects of silica on workers included federal, state and local programs and initiatives. A systematic review of crystalline silica resources was conducted, including the history of crystalline silica as an occupational health hazard, the history of governmental and non-governmental standards and guidelines on silica, and the anticipated physical adjustments that industries, specific companies, and other entities plan to implement for future compliance with the new standards. The economic consequences of implementing the new practices and permissible exposure limits have yet to be measured, and there were conflicting outlooks between the data published by OSHA and the studies released by groups representing the affected industries. In April 2017, the effective date of the new silica rule was delayed by three months to September 23, 2017.

Characterization of Occupational Exposures to Respirable Silica and Dust in Demolition, Crushing, and Chipping Activities.

Exposures to respirable crystalline silica (RCS) and respirable dust (RD) were investigated during demolition, crushing, and chipping at several Massachusetts construction sites. Personal breathing zone samples (n = 51) were collected on operating engineers working at demolition and crushing sites, laborers performing miscellaneous tasks at demolition sites, crushing machine tenders at crushing sites, and chipping workers at substructure bridge repair sites. Area samples (n = 33) were collected at the perimeter of demolition and crushing sites to assess potential bystanders' exposures. Exposures 'with' and 'without' the use of dust suppression methods were compared when possible. RD samples were analyzed for crystalline silica content with Fourier Transform Infrared Spectrophotometry (FT-IR) according to the National Institute for Occupational Safety and Health (NIOSH) Method 7602. Statistical analyses of the exposure data were performed in SAS version 9.4. Chipping workers had the highest exposure levels [the geometric mean (GM) time-weighted average (TWA) for RCS was 527 µg/m3 and the GM for RD was 4750 µg/m3]. The next highest exposures were among crushing machine tenders (RCS GM of 93.3 µg/m3 and RD GM of 737.6 µg/m3), while laborers and operating engineers had the lowest exposures (RCS GM of 17.0 and 6.2 µg/m3, respectively). Personal 8-h TWA RCS exposures were higher than the new OSHA permissible exposure limit (PEL) of 50 µg/m3 for 80% of samples collected on chipping workers (n = 31) and 50% of samples collected on crushing machine tenders (n = 8). Operating engineers (n = 9) and laborers (n = 3) had RCS exposures lower than OSHA PEL. The highest concentrations measured would have exceeded the PEL within 15 min chipping and within 2 h of crushing with no further exposure. Chipping workers' RCS exposures were higher than OSHA PEL even when they were adjusted to account for the assigned protection factor of the half-face N95 cartridge respirators used during chipping. Exposures of crushing tenders were reduced to levels under the OSHA PEL when a water spraying system in crushing machines was utilized, but not when a water cannon machine was used. Area samples at demolition and crushing sites indicate overall lower exposures than the PEL, however, bystander workers at crushing sites could be exposed to higher levels compared to demolition sites. Real-time dust monitoring during demolition indicate very high short-term peak exposures. Controlling or reducing crystalline silica exposures to levels under the new OSHA PEL of 50 µg/m3 remains challenging for chipping workers and crushing machine tenders. Even with the use of dust suppression controls, respiratory protection may be required for various tasks.

A comparison of respirable crystalline silica concentration measurements using a direct-on-filter Fourier transform infrared (FT-IR) transmission method vs. a traditional laboratory X-ray diffraction method

Evaluation and control of respirable crystalline silica (RCS) exposures are critical components of an effective mine industrial hygiene program. To provide more timely exposure data in the field, an end-of-shift Fourier transform infrared (FT-IR) spectrometry method has been developed for evaluation of direct-on-filter RCS. The present study aimed to apply this FT-IR method using field samples collected in three Northwestern U.S. metal/nonmetal mines and compare the results to traditional laboratory X-ray diffraction analysis (XRD). Seventy-five dust samples were analyzed using both methods. Samples for each mine were split in half by random assignment, with half used to create a calibration factor for the FT-IR analysis and half used to apply the calibration. Nonparametric correlational and two-sample comparative tests were used to assess the strength of association and the level of agreement between the two methods. Strong, positive correlations were observed between FT-IR and XRD RCS concentrations, with Spearman rank correlation coefficients ranging between 0.84 and 0.97. The mean RCS concentrations determined through FT-IR analysis were lower than through XRD analysis, with mean differences ranging from −4 to −133 ug/m3 and mean percent errors ranging from 12% to 28%. There was a statistically significant improvement in the level of agreement between log FT-IR and log XRD RCS concentrations following calibration at two of the three mines, with mean differences of −0.03 (p = 0.002) and −0.02 (p = 0.044) in the log scale. The reduction in mean difference following calibration at the other mine was not statistically significant (mean log scale difference = −0.05, p = 0.215), but the differences between FT-IR and XRD were not significantly different without calibration (mean log scale difference = −0.07, p = 0.534). The results indicate that mine-specific calibration factors can improve the level of agreement between RCS concentrations determined via a field-based, end-of-shift FT-IR method in metal/non-metal mines as compared to traditional XRD analysis.

4-1BB Signaling Promotes Alveolar Macrophages-Mediated Pro-Fibrotic Responses and Crystalline Silica-Induced Pulmonary Fibrosis in Mice.

Silicosis is caused by exposure to crystalline silica (CS). We have previously shown that blocking 4-1BB signaling attenuated CS-induced inflammation and pulmonary fibrosis. However, the cells that express 4-1BB, which plays a vital role in promoting fibrosis, are still unknown. In this study, we demonstrated that the expression of 4-1BB is elevated in alveolar macrophages (AMs) in the lungs of CS-injured mice. CS exposure also markedly enhanced the expression of 4-1BB in macrophage-like, MH-S cells. In these cells, activation of the 4-1BB signaling with an agonist antibody led to upregulated secretion of pro-fibrotic mediators. Consistently, blocking 4-1BB downstream signaling or genetic deletion of 4-1BB alleviated pro-fibrotic responses in vitro, while treatment with a 4-1BB fusion protein promoted pro-fibrotic responses. In vivo experiments showed that blocking 4-1BB signaling decreased the expressions of pro-fibrotic mediators and fibrosis. These data suggest that 4-1BB signaling plays an important role in promoting AMs-mediated pro-fibrotic responses and pulmonary fibrosis. Our findings may provide a potential molecular target to reduce CS-induced fibrotic responses in occupational lung disease.

BODIPY-derived ratiometric fluorescent sensors: pH-regulated aggregation-induced emission and imaging application in cellular acidification triggered by crystalline silica exposure

Modification of classic fluorophore to possess the emission transitions between aggregation-induced emission (AIE) and intrinsic emission offers reliable approach to the design of ratiometric fluorescent sensors. In this study, a proton acceptor benzimidazole was integrated with BODIPY to form three compounds, BBI-1/2/3, which demonstrated the AIE (~595 nm, Iagg) in neutral aqueous medium and intrinsic BODIPY emission (~510 nm, Iint) in acidic medium. All the three showed the ratiometric pH sensing behavior in a dual excitation/dual emission mode, yet BBI-3 displayed still the dual emission ratiometric pH sensing ability. The pH-dependent emission ratio Iint/Iagg of the three were fully reversible, and no interference was observed from normal abundant chemical species in live cells. Their different pKa (BBI-1, pKa 4.4; BBI-2, pKa 2.7; BBI-3, pKa 3.6) suggested that the substituents on benzimidazole moiety were essential to govern their functioning pH range. The ratiometric imaging of BBI-1 in A549 cells provided an effective intracellular pH (pHi) calibration formula corresponding to emission ratio of Iint/Iagg. Ratiometric pHi imaging in A549 cells upon small particle exposure confirmed the particle-induced cellular acidification with this formula. Both particle size and the chemical nature of the particle contribute to the observed acidification effect. The synchronization of lysosome disruption to cellular acidification in A549 cells upon crystalline silica exposure was directly observed for the first time with BBI-1, showing the potential application of BBI-1 in the study of silicosis and other related diseases. This study demonstrated that endowing fluorophore with AIE/intrinsic emission transition could be a promising strategy for ratiometric sensor design.

Silicosis and Silica-Induced Autoimmunity in the Diversity Outbred Mouse.

Epidemiological studies have confidently linked occupational crystalline silica exposure to autoimmunity, but pathogenic mechanisms and role of genetic predisposition remain poorly defined. Although studies of single inbred strains have yielded insights, understanding the relationships between lung pathology, silica-induced autoimmunity, and genetic predisposition will require examination of a broad spectrum of responses and susceptibilities. We defined the characteristics of silicosis and autoimmunity and their relationships using the genetically heterogeneous diversity outbred (DO) mouse population and determined the suitability of this model for investigating silica-induced autoimmunity. Clinically relevant lung and autoimmune phenotypes were assessed 12 weeks after a transoral dose of 0, 5, or 10 mg crystalline silica in large cohorts of DO mice. Data were further analyzed for correlations, hierarchical clustering, and sex effects. DO mice exhibited a wide range of responses to silica, including mild to severe silicosis and importantly silica-induced systemic autoimmunity. Strikingly, about half of PBS controls were anti-nuclear antibodies (ANA) positive, however, few had disease-associated specificities, whereas most ANAs in silica-exposed mice showed anti-ENA5 reactivity. Correlation and hierarchical clustering showed close association of silicosis, lung biomarkers, and anti-ENA5, while other autoimmune characteristics, such as ANA and glomerulonephritis, clustered separately. Silica-exposed males had more lung inflammation, bronchoalveolar lavage fluid cells, IL-6, and autoantibodies. DO mice are susceptible to both silicosis and silica-induced autoimmunity and show substantial individual variations reflecting their genetic diverseness and the importance of predisposition particularly for autoimmunity. This model provides a new tool for deciphering the relationship between silica exposure, genes, and disease.

Crystalline silica alters Sulfatase-1 expression in rat lungs which influences hyper-proliferative and fibrogenic effects in human lung epithelial cells

Lung epithelial cells are the first cell-type to come in contact with hazardous dust materials. Upon deposition, they invoke complex reactions in attempt to eradicate particles from the airways, and repair damage. The cell surface is composed of a heterogeneous network of matrix proteins and proteoglycans, which act as scaffold and control cell-signaling networks. These functions are controlled, in part, by the sulfation patterns of heparin-sulfate proteoglycans (HSPGs), which are enzymatically regulated. Although there is evidence of altered HSPG-sulfation in idiopathic pulmonary fibrosis (IPF), this is not investigated in silicosis.Our previous studies revealed down-regulation of Sulfatase-1 (SULF1) in human bronchial epithelial cells (BECs) by crystalline silica (CS). In this study, CS-induced down-regulation of SULF1, and increases in Sulfated-HSPGs, were determined in human BECs, and in rat lungs. By siRNA and plasmid transfection techniques the effects of SULF1 expression on silica-induced fibrogenic and proliferative gene expression were determined.These studies confirmed down-regulation of SULF1 and subsequent increases in sulfated-HSPGs in vitro. Moreover, short-term exposure of rats to CS resulted in similar changes in vivo. Conversely, effects were reversed after long term CS exposure of rats. SULF1 knockdown, and overexpression alleviated and exacerbated silica-induced decrease in cell viability, respectively. Furthermore, overexpression of SULF1 promoted silica-induced proliferative and fibrogenic gene expression, and collagen production.These findings demonstrate that the HSPG modification enzyme SULF1 and HSPG sulfation are altered by CS in vitro and in vivo. Furthermore, these changes may contribute to CS-induced lung pathogenicity by affecting injury tolerance, hyperproliferation, and fibrotic effects.

Estimating Counterfactual Risk Under Hypothetical Interventions in the Presence of Competing Events: Crystalline Silica Exposure and Mortality From 2 Causes of Death.

Exposure to silica has been linked to excess risk of lung cancer and nonmalignant respiratory disease mortality. In this study we estimated risk for both these outcomes in relation to occupational silica exposure as well as the reduction in risk that would result from hypothetical interventions on exposure in a cohort of exposed workers. Analyses were carried out using data from an all-male study population consisting of 2,342 California diatomaceous earth workers regularly exposed to crystalline silica and followed between 1942 and 2011. We estimated subdistribution risk for each event under the natural course and interventions of interest using the parametric g-formula to adjust for healthy-worker survivor bias. The risk ratio for lung cancer mortality, comparing an intervention in which a theoretical maximum exposure limit was set at 0.05 mg/m3 (the current US regulatory limit) with the observed exposure concentrations, was 0.86 (95% confidence interval: 0.63, 1.22). The corresponding risk ratio for nonmalignant respiratory disease mortality was 0.69 (95% confidence interval: 0.52, 0.93). Our findings suggest that risks from both outcomes would have been considerably lower if historical silica exposures in this cohort had not exceeded current regulatory limits.

Determinants of Respirable Crystalline Silica Exposure among Sand-stone Workers

Objective: Our aim was to determine the occupational exposure level for respirable crystalline silica (RCS) and respirable dust (RD) among sandstone workers. Materials and methods: This study was a descriptive analysis of the occupational exposure to respirable crystalline silica (RCS) and respirable dust (RD), utilizing personal air sampling from the breathing zone. The samples were collected throughout the 8-h working day: 88 samples were collected from workers performing stone cutting in mines and at home (wetting system), as well as stone chiseling and stone carving (22 samples each). Twenty-two samples were collected of the RD using the Gravimetric method (NIOSH 600), while for occupational exposure, the level of RCS was measured using a NIOSH7601 spectrophotometer. Results: Sand-stone workers had a geometric mean occupational exposure to RD of GM 1.84 mg/m3. The highest respiratory dust (RD) concentration (2.83 mg/m3) was found among the stone carvers. Those cutting stone at the mines had the next highest GM (2.65 mg/m3), while the lowest occupational exposure was seen among those chiseling stone(GM 0.9 mg/m3). The occupational exposure to RCS had a geometric mean of 0.10 mg/m3. The highest exposure group was for those cutting stone in the mines (GM = 0.14 mg/m3) followed by those carving stone (GM = 0.10 mg/m3). The moderate exposure group was for those chiseling stone (GM 0.05 mg/m3 ) followed by those cutting stone at home (GM = 0.03 mg/m3). The low exposure group had a GM of 0.03 mg/m3 for RCS. We found the quartz silica concentrations of the sandstone used in this area high (≤90%) as was the percentage of quartz silica in the airborne particulates for stone carving (≤71.4% by volume). Conclusion: The stone cutting in mines group and the stone carving group reached occupational exposure limits to RCS which exceeded the 0.05 mg/m3 OSHA PEL. It is essential to prevent such high exposure through engineering controls, by adapting tools and implementing medical surveillance. All groups had a RCS occupational exposure which would warrant medical surveillance as each group exceeded the OSHA action level of 0.0025 mg/m3.

Exposure-Lag-Response in Longitudinal Studies: Application of Distributed-Lag Nonlinear Models in an Occupational Cohort.

Prolonged exposures can have complex relationships with health outcomes, as timing, duration, and intensity of exposure are all potentially relevant. Summary measures such as cumulative exposure or average intensity of exposure may not fully capture these relationships. We applied penalized and unpenalized distributed-lag nonlinear models (DLNMs) with flexible exposure-response and lag-response functions in order to examine the association between crystalline silica exposure and mortality from lung cancer and nonmalignant respiratory disease in a cohort study of 2,342 California diatomaceous earth workers followed during 1942–2011. We also assessed associations using simple measures of cumulative exposure assuming linear exposure-response and constant lag-response. Measures of association from DLNMs were generally higher than those from simpler models. Rate ratios from penalized DLNMs corresponding to average daily exposures of 0.4 mg/m3 during lag years 31–50 prior to the age of observed cases were 1.47 (95% confidence interval (CI): 0.92, 2.35) for lung cancer mortality and 1.80 (95% CI: 1.14, 2.85) for nonmalignant respiratory disease mortality. Rate ratios from the simpler models for the same exposure scenario were 1.15 (95% CI: 0.89, 1.48) and 1.23 (95% CI: 1.03, 1.46), respectively. Longitudinal cohort studies of prolonged exposures and chronic health outcomes should explore methods allowing for flexibility and nonlinearities in the exposure-lag-response.

Exceedance of environmental exposure limits to crystalline silica in communities surrounding gold mine tailings storage facilities in South Africa

BackgroundUnlike occupational silica exposures, the association between non-occupational silica exposures and adverse health effects is not well researched, despite its occurrence in communities close to dust-generating sources such as tailings storage facilities (TSFs). Recent studies have shown that communities surrounding TSFs in South Africa often complain about the onset of dust-related health effects. Even though international interim non-occupational crystalline silica limits have been established, South Africa is yet to enforce its own limits for residential areas close to TSF sites. ObjectiveThe objective of the study was to assess the need to enforce non-occupational crystalline silica limits for South Africa. MethodsThe methods involved (1) Quantifying the silica polymorph content in bulk dust collected from TSFs in South Africa; (2) Assessing the possibility of the dust to reach surrounding communities through ambient and personal filter sampling and; (3) Conducting risk characterisation for both cancer and non-cancer endpoints. ResultsAll bulk dust samples consisted mostly of crystalline silica (73.14–87.09%). Large percentages of nanoparticles were identified in all bulk samples (66.8–70.7%) indicating the possibility of the dust to lodge deep within the lungs. The crystalline silica levels obtained from ambient PM10 sampling and personal PM4 sampling all exceeded the international crystalline silica interim limits and reached maximum levels of 90 and 50.9μg·m−3, respectively. For three TSFs, sampling sites close to the TSFs showed higher PM4 silica levels compared to sites further from TSFs. Risk characterisation revealed the possibility of cancer and non-cancer health effects when chronically exposed to silica levels recorded during the study. ConclusionThe results indicate unacceptable crystalline silica exposures in surrounding communities and the need for enforcement of an ambient silica limit for South Africa.

The effect of aluminium and sodium impurities on the in vitro toxicity and pro-inflammatory potential of cristobalite

BackgroundExposure to crystalline silica (SiO2), in the form of quartz, tridymite or cristobalite, can cause respiratory diseases, such as silicosis. However, the observed toxicity and pathogenicity of crystalline silica is highly variable. This has been attributed to a number of inherent and external factors, including the presence of impurities. In cristobalite-rich dusts, substitutions of aluminium (Al) for silicon (Si) in the cristobalite structure, and impurities occluding the silica surface, have been hypothesised to decrease its toxicity. This hypothesis is tested here through the characterisation and in vitro toxicological study of synthesised cristobalite with incremental amounts of Al and sodium (Na) dopants. MethodsSamples of synthetic cristobalite with incremental amounts of Al and Na impurities, and tridymite, were produced through heating of a silica sol-gel. Samples were characterised for mineralogy, cristobalite purity and abundance, particle size, surface area and surface charge. In vitro assays assessed the ability of the samples to induce cytotoxicity and TNF-α production in J774 macrophages, and haemolysis of red blood cells. ResultsAl-only doped or Al+Na co-doped cristobalite contained between 1 and 4 oxide wt% Al and Na within its structure. Co-doped samples also contained Al- and Na-rich phases, such as albite. Doping reduced cytotoxicity to J774 macrophages and haemolytic capacity compared to non-doped samples. Al-only doping was more effective at decreasing cristobalite reactivity than Al+Na co-doping. The reduction in the reactivity of cristobalite is attributed to both structural impurities and a lower abundance of crystalline silica in doped samples. Neither non-doped nor doped crystalline silica induced production of the pro-inflammatory cytokine TNF-α in J774 macrophages. ConclusionsImpurities can reduce the toxic potential of cristobalite and may help explain the low reactivity of some cristobalite-rich dusts. Whilst further work is required to determine if these effects translate to altered pathogenesis, the results have potential implications for the regulation of crystalline silica exposures.

Total and Cause-Specific Mortality Risk Associated With Low-Level Exposure to Crystalline Silica: A 44-Year Cohort Study From China.

The association between low-level crystalline silica (silica) exposure and mortality risk is not well understood. We investigated a cohort of 44,807 Chinese workers who had worked in metal mines or pottery factories for at least 1 year from January 1, 1960, to December 31, 1974, and were followed through 2003. Low-level silica exposure was defined as having a lifetime highest annual mean silica exposure at or under a permissible exposure limit (PEL). We considered 3 widely used PELs, including 0.05 mg/m3, 0.10 mg/m3, and 0.35mg/m3. Cumulative silica exposure was estimated by linking a job exposure matrix with each participant's work history. For the 0.10-mg/m3 exposure level, Cox proportional hazards models showed significantly increased risk of mortality from all diseases (for each 1-ln mg/m3-years increase in logged cumulative silica exposure, hazard ratio(HR) =1.05, 95% confidence interval (CI): 1.03, 1.07), malignant neoplasms (HR = 1.06, 95% CI: 1.03, 1.09), lung cancer (HR = 1.08, 95% CI: 1.02, 1.14), ischemic heart disease (HR = 1.09, 95% CI: 1.02, 1.16), pulmonary heart disease (HR = 1.08, 95% CI: 1.00, 1.16), and respiratory disease (HR = 1.20, 95% CI: 1.14, 1.26). The 0.05-mg/m3 and 0.35-mg/m3 exposure levels yielded similar associations. Long-term exposure to low levels (PELs ≤0.05 mg/m3, ≤0.10 mg/m3, or ≤0.35mg/m3) of silica is associated with increased total and certain cause-specific mortality risk. Control of ambient silica levels and use of personal protective equipment should be emphasized in practice.

Systemic sclerosis due to crystalline silica exposure among jewelry workers in Korea: two case reports

BackgroundOccupational exposure to crystalline silica is a potential risk factor for various systemic autoimmune diseases including systemic sclerosis. The etiology of systemic sclerosis is not conclusively known, but there are epidemiological studies that show the relationship between exposure to crystalline silica and risk of systemic sclerosis. Here we report, for the first time, two cases of crystalline silica-related systemic sclerosis in patients who worked in crystal processing in the jewelry-manufacturing field.Case presentationCase 1 is a 57-year-old man who had worked mainly in crystal processing for multiple jewelry-processing companies for 17 years, since the age of 15 years. He contracted tuberculosis at the age of 25 years and showed Raynaud’s phenomenon of both the hands and feet at age 32 years. Digital cyanosis and sclerosis developed at approximately age 41 years. The patient was diagnosed with systemic sclerosis at age 48 years.Case 2 is a 52-year-old man who worked in crystal processing for various jewelry-processing companies for 7 years, since the age of 23 years. He first showed signs of cyanosis in the third and fourth digits of both hands at age 32 years, was diagnosed with Raynaud’s syndrome at age 37 years, and was diagnosed with systemic sclerosis at age 38 years.Crystal processing is a detailed process that involves slabbing and trimming the selected amethyst and quartz crystals, which requires close proximity of the worker’s face with the target area. In the 1980s and 1990s, the working hours were 12 h per day, and the working environment involved 15 workers crowded into a small, 70-m2 space with poor ventilation.ConclusionTwo workers who processed crystals with a maximum crystalline silica content of 56.66% developed systemic sclerosis. Considering the epidemiological and experimental evidence, exposure to crystalline silica dust was an important risk factor for systemic sclerosis. An active intervention is necessary to reduce exposure in similar exposure groups in the field of jewelry processing.

Effects of Occupational Silica Exposure on OXIDATIVE Stress and Immune System Parameters in Ceramic Workers in TURKEY

ABSTRACTSilica is the second most common element after oxygen, and therefore, exposures to crystalline silica dust occur in a large variety of occupations such as metal foundries, constructions, and ceramic, quarry, and pottery industries. Since crystalline silica exposure has been linked with silicosis, lung cancer, and other pulmonary diseases, adverse effect attributed to this element has be a cause for concern worldwide. Silica dust exposure in workers is still considered to be important health problem especially in developing countries. The aim of the study was to investigate the effects of occupational silica exposure on oxidative stress parameters including the activities of superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), glutathione peroxidase (GPx), and levels of total glutathione (GSH) and thiobarbituric acid reactive substance (TBARS) as well as immune system parameters such as interleukin (IL)-1α, IL-1β, IL-2, IL-4, IL-6, and IL-10 and tumor necrosis factor (TNF)-α in Turkish ceramic workers. In this study, nearly 50% of Turkish ceramic workers were diagnosed with silicosis. Eighty-four percent of these silicotic workers were found to present with profusion category 1 silicosis, whereas controls (n = 81) all displayed normal chest radiographs. Data demonstrated a significant decrease in levels of GSH and activities of CAT, SOD, and GPx, but a significant increase in MDA levels and activity of GR in all workers. Further, workers possessed significantly higher levels of IL-1α, IL-1β, IL-2, IL-4, IL-6, IL-10, and TNF-α. These observations suggest that ceramic workers may have impaired antioxidant/oxidant status and activated immune system indicative of inflammatory responses.

Inflammasome Independent Leukotriene B4 Production Drives Crystalline Silica Induced Sterile Inflammation in Lungs

Abstract Occupational exposure to Crystalline Silica (CS) is a major public health concern with millions of workers continuously exposed to CS. Deposition of fine silica particles in the lungs can lead to severe lung inflammation and cancer. Lipid chemokine Leukotriene B4 (LTB4) and IL-1b that mediate leukocyte recruitment to the site of injury, are the key mediators of CS-induced sterile inflammation. Our previous studies have shown that CS exposure increases lung tumor burden in K-rasLA1 mice and that is abrogated in the LTB4 receptor, BLT1 deficient mice. Here, we show that phagocytosis of CS sequentially activates a series of pathways leading to LTB4, IL-1b and CXC chemokine production. CS uptake induces rapid formation of lipid bodies termed “lipidosome” independent of inflammasome activation. Studies with inhibitors suggested that CS-induced lipidosome formation and LTB4 production is linked to the phagocytosis pathway, an observation confirmed by confocal microscopy. We further demonstrated the SiRNA knockdown of cPla2, JNK or Rab40c prevents the formation of lipidosome and production of LTB4. Lastly, we demonstrate using an air pouch model in mice that JNK inhibitor, BI-78D3 is effective in reducing CS induced sterile-inflammation in-vivo. In summary, our studies highlight a novel inflammasome independent and JNK activation dependent lipidosome pathway leading to the production LTB4 as a major regulator of CS-induced sterile inflammation.

Estimating the burden of occupational cancer: assessing bias and uncertainty

Background and objectivesWe aimed to estimate credibility intervals for the British occupational cancer burden to account for bias uncertainty, using a method adapted from Greenland’s Monte Carlo sensitivity analysis.MethodsThe attributable...