Silica Hazards Research Articles

Nearly free silanols drive the interaction of crystalline silica polymorphs with membranes: Implications for mineral toxicity.

Crystalline silica (CS) is a well-known hazardous material that causes severe diseases including silicosis, lung cancer, and autoimmune diseases. However, the hazard associated to crystalline silica is extremely variable and depends on some specific characteristics, including crystal structure and surface chemistry. The crystalline silica polymorphs share the SiO2 stoichiometry and differentiate for crystal structure. The different crystal lattices in turn expose differently ordered hydroxyl groups at the crystal surface, i.e., the silanols. The nearly free silanols (NFS), a specific population of weakly interacting silanols, have been recently advanced as the key surface feature that governs recognition mechanisms between quartz and cell membrane, initiating toxicity. We showed here that the nearly free silanols occur on the other crystalline silica polymorphs and take part in the molecular interactions with biomembranes. A set of crystalline silica polymorphs, including quartz, cristobalite, tridymite, coesite, and stishovite, was physico-chemically characterized and the membranolytic activity was assessed using red blood cells as model membranes. Infrared spectroscopy in highly controlled conditions was used to profile the surface silanol topochemistry and the occurrence of surface nearly free silanols on crystalline silica polymorphs. All crystalline silica polymorphs, but stishovite were membranolytic. Notably, pristine stishovite did not exhibited surface nearly free silanols. The topochemistry of surface silanols was modulated by thermal treatments, and we showed that the occurrence of nearly free silanols paralleled the membranolytic activity for the crystalline silica polymorphs. These results provide a comprehensive understanding of the structure-activity relationship between nearly free silanols and membranolytic activity of crystalline silica polymorphs, offering a possible clue for interpreting the molecular mechanisms associated with silica hazard and bio-minero-chemical interfacial phenomena, including prebiotic chemistry.

Self-reported exposure to hazards and mitigation strategies among oil and gas extraction workers in three U.S. states

Numerous health and safety hazards exist at U.S. onshore oil and gas extraction worksites. Higher fatal injury rates have been reported among drilling and servicing companies, which are more likely to employ workers in construction and extraction occupations, compared to operators that employ more workers in management and office and administrative support roles. However, there is little information describing the extent to which workers encounter these hazards, are provided hazard mitigation strategies by their employers, or use personal protective equipment (PPE). A cross-sectional survey of 472 U.S. oil and gas extraction workers was conducted to identify and characterize factors related to on-the-job fatalities, injuries, and illnesses and determine workers’ health and safety concerns. Workers were employed by servicing companies (271/472, 57.4%), drilling contractors (106/472, 22.5%), and operators (95/472, 20.1%). The likelihood of contact with hazardous substances varied by substance and company type. Drilling and servicing employees had significantly higher odds of self-reported contact with pipe dope (ORdrilling = 10.07, 95% CI: 1.74–63.64; ORservicing = 5.95, 95% CI: 2.18–18.34), diesel exhaust (ORdrilling = 2.28, 95% CI: 1.15–5.05; ORservicing = 4.93, 95% CI: 2.73–10.32), and drilling mud (ORdrilling = 24.36, 95% CI: 4.45–144.69; ORservicing = 3.48, 95% CI: 1.24–12.20), compared to operators. Safety policies, programs, and trainings were commonly reported by workers, although substance-specific training (e.g., respirable crystalline silica hazards) was less common. Differences in self-reported employer PPE requirements and worker use of PPE when needed or required for safety highlight a need for novel strategies to improve the use of PPE. Overall, this study highlights differences in work conditions by company type and uncovers gaps in employer administrative controls and PPE use.

Highly efficient method of utilizing waste silica hazards

Silica gels are the significant commodity solid waste produced by organic laboratories and pharmaceutic industries. Although use of silica gels is continuously growing, the proper methods of re-utilizing silica waste are yet limited. Hence, it demands a non-traditional approach to transform these silica waste into some other useful products apart from using them as a well-known road construction materials. Hereby, we report the fabrication and applications of monolithic polymer-silica composites by ice-templating technique from laboratory waste silica-gels, using green approach. To the best of our knowledge, the fabrication of organic-inorganic hybrid sponges from the particles of hundreds of microns is not reported to date. Scaffolds S60, S120, S180, and S300, were prepared from laboratory discarded silica gels. The morphological, physicochemical, flame-retardant, and liquid absorbent properties of these self-standing scaffolds were analyzed. Results showed that the incorporation of silica particles in the scaffolds turned them into a flame-retardant sponge. These properties make the sponges ideal for making non-flammable cushions, applicable in automobiles, aircrafts, chemical laboratories, hospitals, and other areas of applications. Due to the large porous structures, these scaffolds possess excellent absorption properties and may absorb almost every kind of liquid ranging from oils to acids. Therefore, these scaffolds are also a remarkable absorber for oils and hazardous liquids spillage, such as acids, and can be used as foam for chemical packing applications.

Managing Risks and Exposures to Silica in Training and Assessment Activities in Vocational Education and Training

A number of activities in workplaces, such as such as those including cutting, grinding, sanding, drilling, loading or demolishing products that contain silica, can produce respirable particles of crystalline silica dust that are small enough to inhale. Inhalation of crystalline silica can cause silicosis which is incurable. Work practices are critical to prevent the condition from occurring and safe work practices are as relevant to workplaces as they are to training environments. This study considers methods of risk control and training practices such that silicosis is prevented.Training requirements are profiled in a vocational education and training setting and must include: crystalline silica hazards and health risks, including silicosis; effective use controls; use and maintenance of personal protective equipment, including Respiratory Protective Equipment; safe waste disposal; and, practices for personal decontamination. The training environment must be designed in a manner to allow for engineering controls, such as on-tool water suppression or on-tool dust extraction, to be utilised.

Beyond silicosis, is the world failing on silica hazards?

Collis and Yule 1 stated in 1933, that “silica is such a body poison as is lead, even though it exerts its maleficent influence, especially with regard to tuberculosis, mainly on the respiratory organs, through which it gains access to the body”. This statement invites us to question the editorial 2 entitled “The world is failing on silicosis” in The Lancet Respiratory Medicine. As clinicians, radiologists, toxicologists, and social scientists working on health hazards related to crystalline silica exposure, we delve beyond silicosis, to learn of other dangers associated with silica.

Unveiling the Variability of "Quartz Hazard" in Light of Recent Toxicological Findings.

The variability of quartz hazard stands as one of the most puzzling issues in particle toxicology, notwithstanding the fact that silicosis, the most ancient occupational disease, was the very topic from which the study of the toxicity of particulates developed. Over the years, other adverse effects of silica particles (i.e., lung cancer and autoimmune diseases) were detected and described. However, a few gaps are still present in the physicochemical determinants and cellular pathways involved in the mechanisms of silica pathogenicity. In this perspective, we illustrate how pooling together studies in occupational health and nanotoxicology might fill such gaps, yielding a consistent picture of what imparts toxicity to a given silica source. Recent investigations have shown that crystallinity is not implied in the pathogenic process of silica per se, while patches of disorganized silanols at the surface of both crystalline and amorphous particles can promote membrane damage and inflammation, a process at the origin of silica-related diseases. Introducing these new findings into the accepted multistep model of silica pathogenicity, we obtain a picture of the chemical features of silica governing each cellular step in agreement with the outcomes of major previous studies. We ascribe the origin of the variability of silica hazard mainly to the distribution of various moieties at the particle surface, with silanols playing the major role. Toxicity turns out to be likely predictable by an ad hoc surface characterization. Tailored modifications of the surface can be envisaged to prepare safe materials or blunt toxicity in existing ones.

The in vitro respiratory toxicity of cristobalite-bearing volcanic ash

Ash from dome-forming volcanoes poses a unique hazard to millions of people worldwide due to an abundance of respirable cristobalite, a crystalline silica polymorph. Crystalline silica is an established respiratory hazard in other mixed dusts, but its toxicity strongly depends on sample provenance. Previous studies suggest that cristobalite-bearing volcanic ash is not as bio-reactive as may be expected for a dust containing crystalline silica. We systematically address the hazard posed by volcanic cristobalite by analysing a range of dome-related ash samples, and interpret the crystalline silica hazard according to the mineralogical nature of volcanic cristobalite. Samples are sourced from five well-characterized dome-forming volcanoes that span a range of magmatic compositions, specifically selecting samples rich in cristobalite (up to 16wt%). Isolated respirable fractions are used to investigate the in vitro response of THP-1 macrophages and A549 type II epithelial cells in cytotoxicity, cellular stress, and pro-inflammatory assays associated with crystalline silica toxicity. Dome-related ash is minimally reactive in vitro for a range of source compositions and cristobalite contents. Cristobalite-based toxicity is not evident in the assays employed, supporting the notion that crystalline silica provenance influences reactivity. Macrophages experienced minimal ash-induced cytotoxicity and intracellular reduction of glutathione; however, production of IL-1β, IL-6 and IL-8 were sample-dependent. Lung epithelial cells experienced moderate apoptosis, sample-dependent reduction of glutathione, and minimal cytokine production. We suggest that protracted interaction between particles and epithelial cells may never arise due to effective clearance by macrophages. However, volcanic ash has the propensity to incite a low, but significant, and sample-dependent response; the effect of this response in vivo is unknown and prolonged exposure may yet pose a hazard.

Truncating a disease. The reduction of silica hazards to silicosis at the 1930 international labor office conference on silicosis in Johannesburg.

The current nosology and etiology of silicosis were officially adopted by the 1930 International Labor Office (ILO) Conference on silicosis in Johannesburg. Convened by the International Labor Office and by the Transvaal Chamber of Mines, it paved the way to the adoption of a 1934 ILO convention which recognized silicosis as an occupational disease. Even though it constituted a social and sanitary turning point, the Johannesburg conference, strongly influenced by South African physicians working for the gold mining industry, reduced silica hazards to silicosis, an equation which is questioned nowadays. While the definition of silicosis adopted in 1930 was a major step in the recognition of occupational pneumoconioses, it also led to the under-identification of some pathogenic effects of silica. Going back to history opens new avenues for contemporary medical research.

Does the crystal habit modulate the genotoxic potential of silica particles? A cytogenetic evaluation in human and murine cell lines

Crystalline silica inhaled from occupational sources has been classified by IARC as carcinogenic to humans; in contrast, for amorphous silica, epidemiological and experimental evidence remains insufficient. The genotoxicity of crystalline silica is still debated because of the inconsistency of experimental results (“variability of silica hazard”), often related to the features of the particle surfaces. We have assessed the role of crystal habit in the genotoxicity of silica powders. Pure quartz (crystalline) and vitreous silica (amorphous), sharing the same surface features, were used in an in vitro study with human pulmonary epithelial (A549) and murine macrophage (RAW264.7) cell lines, representative of occupational and environmental exposures. Genotoxicity was evaluated by the comet and micronucleus assays, and cytotoxicity by the trypan blue method. Cells were treated with silica powders for 4 and 24h. Quartz but not vitreous silica caused cell death and DNA damage in RAW264.7 cells. A549 cells were relatively resistant to both powders. Our results support the view that crystal habit per se plays a pivotal role in modulating the biological responses to silica particles.

The structure of volcanic cristobalite in relation to its toxicity; relevance for the variable crystalline silica hazard.

BackgroundRespirable crystalline silica (RCS) continues to pose a risk to human health worldwide. Its variable toxicity depends on inherent characteristics and external factors which influence surface chemistry. Significant population exposure to RCS occurs during volcanic eruptions, where ashfall may cover hundreds of square km and exposure may last years. Occupational exposure also occurs through mining of volcanic deposits. The primary source of RCS from volcanoes is through collapse and fragmentation of lava domes within which cristobalite is mass produced. After 30 years of research, it is still not clear if volcanic ash is a chronic respiratory health hazard. Toxicological assays have shown that cristobalite-rich ash is less toxic than expected. We investigate the reasons for this by determining the physicochemical/structural characteristics which may modify the pathogenicity of volcanic RCS. Four theories are considered: 1) the reactivity of particle surfaces is reduced due to co-substitutions of Al and Na for Si in the cristobalite structure; 2) particles consist of aggregates of cristobalite and other phases, restricting the surface area of cristobalite available for reactions in the lung; 3) the cristobalite surface is occluded by an annealed rim; 4) dissolution of other volcanic particles affects the surfaces of RCS in the lung.MethodsThe composition of volcanic cristobalite crystals was quantified by electron microprobe and differences in composition assessed by Welch’s two sample t-test. Sections of dome-rock and ash particles were imaged by scanning and transmission electron microscopy, and elemental compositions of rims determined by energy dispersive X-ray spectroscopy.ResultsVolcanic cristobalite contains up to 4 wt. % combined Al2O3 and Na2O. Most cristobalite-bearing ash particles contain adhered materials such as feldspar and glass. No annealed rims were observed.ConclusionsThe composition of volcanic cristobalite particles gives insight into previously-unconsidered inherent characteristics of silica mineralogy which may affect toxicity. The structural features identified may also influence the hazard of other environmentally and occupationally produced silica dusts. Current exposure regulations do not take into account the characteristics that might render the silica surface less harmful. Further research would facilitate refinement of the existing simple, mass-based silica standard by taking into account composition, allowing higher standards to be set in industries where the silica surface is modified.

Role of sodium silicate in induction of scleroderma-related autoantibodies in brown Norway rats through oral and subcutaneous administration

Silica hazard is a growing occupational problem and has been reported to be associated with scleroderma via case reports and occupational studies. The aim of this study is to demonstrate whether oral or subcutaneous silicate exposure can induce an autoimmunity and scleroderma susceptibility in immunosensitive rats. Sodium silicate in a dose of 3mg in 0.2ml NS was administered through oral and subcutaneous routes to 20 brown Norway rats. Autoantibodies including ANA, anti-RNP, anti-SCL70 and anti-centromere were measured and compared with pre- and post-challenge serum samples. Serum ANA and anti-RNP were high in significant number of rats (P<0.05) of only the subcutaneous silicate group. There is an increase in the number of positive readings of autoantibodies at 14th week in comparison with the number of positive readings of autoantibodies at 7th week but P values were not significant. It may be concluded that silicate might induce autoimmunity and scleroderma and it seems to be that the longer the duration of exposure the greater the risk. This is probably the first experimental animal study demonstrating the induction of scleroderma-related autoantibodies after challenge with silicate.

Symposium on Jewellery Manufacturing Technology, Santa Fe, USA

Symposium on Jewellery Manufacturing Technology, Santa Fe, USA

Silica hazard of caisson construction in Hong Kong.

Caisson construction work in Hong Kong generates considerable silica dust from granite rock. A survey of 18 sites was aimed at assessing the hazard of silica dust and determining the prevalence of silicosis among caisson workers. Data from 87 air samples confirmed high silica exposure in general with a severe exposure hazard for underground workers drilling rocks under conditions of little or no wet suppression. Of 118 workers radiologically examined, 12 cases of silicosis (including 6 cases of silico-tuberculosis) were found in underground workers (giving an overall prevalence of 16 per cent in this group), and only in those with 10 to 20 years of work experience. The occurrence of tuberculosis in another 6 underground and 2 surface workers appeared to be higher than expected. The findings confirmed a serious occupational health hazard and the need for preventive action.

Some problems in roentgen diagnosis of silicosis.

The roentgenologic aspects of silicosis are well known to many physicians interested in occupational diseases of the chest. The criteria for the roentgen diagnosis of silicosis have been described and effectively correlated with experimental and pathological observations. In spite of all the information available to those who are called upon to give opinions on workers in a silica hazard, oftentimes it is impossible to render a correct interpretation and on other occasions the wrong diagnosis is made. My personal experience with some of these difficulties has prompted the selection of three totally different observations or groups for consideration. ANALYSIS OF OBSERVATIONS It is generally conceded that the roentgen examination, properly done, is the most precise method available for demonstrating visible shadows of pathological changes produced by silicosis. In this country the diagnosis of silicosis is not made, as a rule, in the absence of positive roentgen evidence of the condition.

Anthraco-Silicosis

The term “anthraco-silicosis” is a descriptive title for the form of pneumoconiosis commonly called “miner's asthma.” It is a chronic disease due to breathing air containing dust generated in the various processes involved in the mining and preparation of anthracite coal. It is characterized anatomically by generalized fibrotic changes throughout both lungs with the presence of excessive amounts of carbonaceous and siliceous material, usually by compensating emphysema, and often by cardiac changes in the later stages of the disease. The purpose of this paper is to present a review of some observations made in coal miners with anthraco-silicosis in the anthracite coal fields over a period of twenty-seven years. We will not go into detail as to pathogenesis, as this is discussed elsewhere in this symposium. The presence of the silica particles in a certain concentration, their size, and the changes that ensue in the lungs after they are deposited there are well known to most of you. We have had an opportunity to observe this disease in coal miners during many years. When we were in general practice, most of our male patients were coal miners, and in the years devoted to roentgenology we have personally studied approximately a thousand cases a year for twenty-five years. About fifteen years ago, in association with the late Dr. Byron H. Jackson, we studied one thousand cases from the standpoint of the age and build of the worker, the working conditions, years of exposure, and race. We found no resistance to the disease on the part of any particular race. It was our experience that when a man was exposed to a silica hazard, it took from five to seven years before there were any distinctive changes in the lungs that could be noted on the roentgenogram. This, of course, was in the average case. It is universally conceded that the only way that the diagnosis can be made in the living is by roentgen examination. We believe, however, that a diagnosis of first-stage anthraco-silicosis cannot be made with any degree of assurance on the roentgenogram alone. The history must be obtained. This is not true concerning the second and third stages of the disease. Their roentgenographic appearances are characteristic and the diagnosis can be made with less consideration of the history. During the past several years, we have been associated, in a minor way, with Dr. Lewis Gregory Cole in the study of silicosis. Preliminary reports have already been made and we are anxious to know his final conclusions. One of the most brilliant contributions to American radiology, on the subject of silicosis, was made by the Chairman of this Symposium, Dr. Eugene P. Pendergrass, and his illustrious chief and predecessor, the late Dr. Henry K. Pancoast. No study of this subject can be complete without a review of their work. One of the first papers on this subject in America was contributed by Childs, in 1917, to Lanza's “Miners' Consumption.”