When considering dust, three dust fractions are of main concern: the inhalable, thoracic and respirable dust fractions. However, for crystalline silica, the respirable dust fraction is the most important due to its potential health effects in humans.
It is also important to note that national occupational exposure limit values for crystalline silica apply to the respirable dust fraction. This dust fraction corresponds to the proportion of an airborne contaminant, which penetrates to the pulmonary alveolar (gas exchange) region of the lungs. This fraction normally represents 10 to 20% of the inhalable dust fraction, but the proportion can vary considerably.
The following diagram explains the difference between the various dust fractions:
Source: Dichotomous model of aerosol fractionation according to Görner P. and Fabriès J.F.
This illustration identifies the different sections of the lung. The larynx (mentioned in the diagram above) lies between the pharynx (upper part of the airway) and the trachea (windpipe). The pulmonary alveolar region is made up of approximately 300 million alveoli, or air sacs.
The European Standards Organisation (CEN) and the International Standards Organisation (ISO) have agreed standardised conventions for the health-related sampling of dusts or aerosols in workplaces (EN 481, ISO 7708).
These conventions represent target specifications for instruments used to assess the possible health effects due to inhalation of aerosols.
The following figure illustrates the sampling conventions:
The inhalable, thoracic and respirable conventions as percentages of total airborne particles, from EN 481.
The graph shows the probability that a particle of a specific aerodynamic diameter will penetrate the different parts of the human respiratory system.
For example, following the respirable convention, there is a 50% chance (or a probability of 0.5) that a particle of aerodynamic diameter 4 µm will penetrate the pulmonary alveolar region of the lung. Similarly, there is a 30% chance (probability of 0.3) that a particle of aerodynamic diameter 5 µm will penetrate this region of the lung.
|AERODYNAMIC DIAMETER μm||INHALABLE CONVENTION %||THORACIC CONVENTION %||RESPIRABLE CONVENTION %|
Source: EN 481. Numerical values of the conventions, as percentages of total airborne particles
People at work are rarely exposed to pure crystalline silica. The dust they breathe in at the workplace is usually composed of a mixture of crystalline silica and other materials.
The response of an individual is likely to depend on:
Whatever the circumstances, to limit the health effects related to exposure to respirable crystalline silica dust, exposure levels need to be controlled and reduced.
Silicosis is a commonly known health hazard and one of the world’s oldest known occupational diseases (e.g. NIOSH 2002, OSHA 2013, ANSES 2019). Silicosis is historically associated with the inhalation of crystalline silica-containing dust and the causal relationship between silicosis and crystalline silica exposure is well-established (Morfeld 2013). A threshold value for the respirable quartz dust concentration and silicosis incidence (1/1, ILO 1980/2000) is estimated through a statistical model in the German porcelain worker cohort (Morfeld 2013). Silicosis is one of the most common types of pneumoconiosis. It is a nodular progressive fibrosis caused by the deposition in the lungs of fine respirable particles of crystalline silica. The resulting scarring of the innermost parts of the lungs can lead to breathing difficulties and, in some cases, death. Larger (non-respirable) particles are more likely to settle in the main (upper) airways of the respiratory system and may be cleared by mucus and/or ciliary action.
Common silicosis is generally caused by prolonged chronic inhalation of respirable crystalline silica dust generated by a work process. Silicosis can vary greatly in its severity, from “simple silicosis” to “progressive massive fibrosis”. Generally, three types of silicosis are described in literature (EUR 14768; INRS 1997):
Generally, three types of silicosis are described in literature (EUR 14768; INRS 1997):
Future cases of silicosis can be reduced by implementing appropriate measures to reduce exposure to silica-containing dusts. Such measures include improved work practices, engineering controls, respiratory protective equipment and training programmes.
According to a number of epidemiological studies among occupationally exposed populations, under some circumstances there is a relation between lung cancer and exposure to respirable crystalline silica dust.
In 1997, a working group of the International Agency for Research on Cancer (IARC) concluded on the basis of literature review that inhaled respirable crystalline silica from occupational sources is carcinogenic to humans (IARC, 1997).
In making this evaluation, the IARC working group noted also that carcinogenicity was not detected in all industrial circumstances studied and may be dependent on inherent characteristics of the crystalline silica or on external factors affecting its biological activity.
In 2011, IARC updated its Monographs and confirmed that crystalline silica dust, in the form of quartz or cristobalite, is carcinogenic for human (group 1) and that the variable hazard of different types of silica related to its surface properties (IARC, 2011).
According to the French Agency for Sanitary Safety, no other cancer than lung cancer association with exposure to respirable crystalline silica has been proven (ANSES 2019).
A recommendation (SUM DOC 94 final) from the EU Scientific Committee for Occupational Exposure Limits (SCOEL) was adopted in June 2003. The main conclusions were as follows:
The different modes of action of RCS-induced genotoxicity have been evaluated in a series of toxicological studies since 2011. According to an updated review of respirable crystalline silica genotoxicity, the role of inflammation driven by quartz surface after inhalation is confirmed and findings support a practical threshold (secondary effect) (Borm et al 2019).
The role of freshly fractured crystalline silica particles has been outlined in new studies and acknowledged in regulatory evaluations (Turci et al 2016; ANSES 2019). How the chemical features and configuration of the silica surface can trigger variable toxic responses remains to be explained. Promising interdisciplinary research is ongoing to elucidate the puzzling mechanisms of crystalline silica pathogenicity and possibly mitigate or reduce its surface reactivity (Pavan et al 2019).
In scientific literature, papers are published about the possible association between silica exposure and autoimmune disorders (e.g. scleroderma, lupus and rheumatoid arthritis). In its 2019 opinion, the ANSES confirms that while such an association may be observed in some studies for systemic scleroderma, systemic lupus and rheumatoid arthritis, one cannot establish a direct (causal) correlation or dose-response relation between exposure to crystalline silica and auto-immune disease occurrence.
As far as other pathologies are concerned, such as renal and cardio-vascular pathologies, one cannot conclude on a role for crystalline silica particles in the occurrence of these diseases (ANSES 2019).