Crystalline silica is also known as free silica is a very stable compound of silicon and oxygen, where silicon is completely polymerized through silicon-oxygen bonds in three dimensions. Crystalline silica represents a form of silica, which is highly organized, framework pattern. Quartz is the most common crystalline form of silica encountered in nature. It is present in alpha and beta (high temperature) forms. Alpha quartz is commonly found in large quantities in many rocks and soils worldwide. Tridymite and cristobalite are other forms of crystalline silica found in rocks formed at high temperature. Coesite and stishovite are two rare polymorphs formed at high pressures. Microcrystalline varieties of silica also include small grains of this material, possibly combined with amorphous silica. Tripoli, flint, chert, jasper, chalcedony, agate, onyx and silica flour are examples. Silica is typically only one of many constituents of mineral dust and represents a large fraction of the respirable dust present in metalliferous dust, blasting dust, drilling dust, quarry dust and excavation dust.  Most human exposure to crystalline silica occurs in the workplace and regulations exist in form of allowable and acceptable exposure limits which are constantly revised as standards in Australia. As of 2021, with a three-month grace period, employers are now required to provide a low-dose high resolution computed tomography (HRCT) scan, by an appointed medical practitioner, instead of the previously required chest X-ray. This article discusses silica and its problems, evolution of silica exposure standards in Australia, the cost of complacency and best industry practice from GRT.

History of silica exposure and record of cases in an Australian context.

An Australian commission of medical experts published valuable contribution to tuberculous silicosis in 1920. Their findings were based on careful examination of miners employed at the Broken Hill Mines. Inhalation of dust arising from metalliferous mining led to presence of lead, manganese, zinc and silica in the lung tissues of the miners. The Medical Journal of Australia published factors contributing to silicosis in 1933. The publication listed the following:

  • Exposure to silica dust 
  • Length of exposure 
  • The extent of the exposure period plus the latent period and the relation of these to each other 
  • The influence of other dusts on the occurrence and course of silicosis
  • The physique of the worker 

Clinically they identified three stages of silicosis. In the first stage respiratory symptoms may be slight or absent: capacity for work may be slightly impaired. Some departure from normal may be noted in percussion and auscultatory signs, X-ray showing an increased density of linear shadows and the presence of discrete shadows, indicative of nodulation. In the second stage the above physical signs are increased, and the radiographic shadows show an increase in number and size. Working capacity is impaired. In the third stage all the signs and symptoms are more and indications of areas of massive fibrosis are usual. Pulmonary tuberculosis may be present in any of these stages of silicosis.

The injurious dust particles in mine air are so fine as to be invisible to the naked eye. Historically, toxicity of various silica forms has been studied extensively revealing that silica particles pose significant health risks to the human respiratory system causing a variety of debilitating lung diseases such as silicosis.

Are environmental regulations, health and safety concerns or potential profit loss a concern right now?

The cost of complacency – Silicosis in Australia.

At the beginning of 2019, the Australian news network ABC reported the results of an audit of the stonecutting industry in Queensland following the identification of several cases of silicosis in 2018. After the audit, the government agency Workplace Health and Safety Queensland issued 552 compliance notices across 138 stonecutting premises that were found not to be implementing measures to prevent the development of the disease among workers. The Queensland government moved in to put in place a screening program. Of the 799 workers screened, 98 were found to have silicosis. 

What is silicosis? – it is progressive lung damage caused by inhalation of dust containing particles of silica particles. The problem arises from the fact that particles small enough end up in the alveoli, parts of the lungs devoted to gaseous exchange. The areas of so-called lower lung cannot be cleared by coughing and so-called mucus escalator because the ciliated epithelium ends way before the gas exchange begins, and the mucus ends even earlier. The only way to remove contaminants from is by the macrophages, that patrol the lower lung environment and phagocytize the particles. They try to do it with silica, but here a major problem begins. Silica is lethal for macrophages. Macros that consume silica die before they can get to a point where they can move up, passively or actively, so they die in the alveoli. Prior to their death, they secrete compounds that activate other cells, and this initiates inflammation. Lung tissue does not regenerate, the inflammation causes the proliferation of fibrocytes, that lay down fibers, and create scar tissue. The risk of silicosis is present in jobs such as abrasive manufacturing, glass manufacturing, mining, quarrying, road and building construction, sandblasting and stone cutting. 


Types and progression of silicosis.  

Silicosis is the oldest known occupational lung diseases. There are three types of silicosis namely chronic, accelerated, and acute silicosis. Chronic silicosis, results from long term exposure (more than 20 years) to low amounts of silica dust. The silica dust causes swelling in the lungs and chest lymph nodes. This disease may cause people to have trouble breathing. This is the most common form of silicosis. In chronic silicosis, you may only have an abnormal chest X-ray in the beginning and then slowly develop a cough and breathing difficulty. Accelerated silicosis, occurs after exposure to larger amounts of silica over a shorter period (5 to 15 years). Swelling in the lungs and symptoms occur faster than in simple silicosis. Acute silicosis, results from short-term exposure to very large amounts of silica. The term acute means exposure is only limited time, months, weeks or even days, only happen if the amount of silica is so massive. The lungs become very inflamed and can fill with fluid, causing severe shortness of breath and a low blood oxygen level. In acute silicosis, you may experience fever and sharp chest pain along with breathing difficulty. These symptoms can come on suddenly. More than a third of people with silicosis have phlegm production and cough. Chronic bronchitis-like symptoms may occur, and the lungs have additional sounds such as wheezes and crackles. As extensive scarring progresses over time, you may see signs of chronic lung disease such as leg swelling, increased breathing rate, and bluish discolouration of the lips. 

Prevention is better than cure (as there is none)

Silica possesses a wide spectrum in terms of physicochemical size, hydrophobicity, and surface charge properties. Proximity to silica generating activities was once assumed to be mainly affecting mine and quarry workers alone but most recently news of a mother of two that contracted silicosis from a nearby quarry increases the sphere of risk to nearby communities. To take a common mining, quarrying, and civil construction example, drilling and blasting are key to operations and dust generated from them should be eliminated/managed at the source. GRT has recently answered the call for drill and blast dust control through of their new drill and blast control innovatory products GRT: DC Binder for blast pattern dust control and GRT: 12X for drilling dust control. GRT commits to saving lives through their dust control products and now more than ever is the time to harness technological advancement to the benefit of workplace safety and health. 

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Arick et al. 2015. Effects of nanoparticles on the mechanical functioning of the lung. Advances in Colloid and Interface Science. 1-11. 

McMahon, H.E. 1933. Silicosis. Med. Journ. Australia. 15(1), 39-40. 

Perkins et al. 2014. Pathogenesis and Mechanisms of Asbestosis and Silicosis. Pathobiology of Human Disease: A Dynamic Encyclopedia of Disease Mechanisms. 2654-2665.

Southard et al. 2014. Silica, Crystalline. Encyclopedia of Toxicology. 4, 255-259. 

The Lancet. 1922. Tuberculous silicosis in Australia and Elsewhere. 199(5146), 753-

The Lancet. 2019. The world is failing on silicosis. Lancet Respir Med.