Ceramics manufacturing contributes to ambient silica air pollution and burden of lung disease

Abstract

Inhalation of silica (SiO2) in occupational exposures can cause pulmonary fibrosis (silicosis), lung function deficits, pulmonary inflammation, and lung cancer. Current risk assessment models, however, cannot fully explain the magnitude of silica-induced pulmonary disease risk. The purpose of this study was to assess human health risk exposed to airborne silica dust in Taiwan ceramics manufacturing. We conducted measurements to characterize workplace-specific airborne silica dust in tile and commodity ceramic factories and used physiologically based alveolar exposure model to estimate exposure dose. We constructed dose-response models for describing relationships between exposure dose and inflammatory responses, by which health risks among workers can be assessed. We found that silica contents were 0.22-33.04 % with mean concentration ranges of 0.11-5.48 and 0.46-1763.30 μg m(-3), respectively, in commodity and tile ceramic factories. We showed that granulation workers in tile ceramic factory had the highest total SiO2 lung burden (∼1000 mg) with cumulative SiO2 lung burden of ∼4 × 10(4) mg-year. The threshold estimates with an effect on human lung inflammation and fibrosis are 407.31 ± 277.10 (mean ± sd) and 505.91 ± 231.69 mg, respectively. For granulation workers, long-term exposure to airborne silica dust for 30-45 years was likely to pose severe adverse health risks of inflammation and fibrosis. We provide integrated assessment algorithms required to implement the analyses and maintain resulting concentration of silica dust at safety threshold level in the hope that they will stimulate further analyses and interpretation. We suggest that decision-makers take action to implement platforms for effective risk management to prevent the related long-term occupational disease in ceramics manufacturing.

ROS-Dependent Activation of EGFR/Akt/p38 MAPK and JNK1/2/FoxO1 and AP-1 Pathways in Human Pulmonary Alveolar Epithelial Cells Leads to Up-Regulation of COX-2/PGE2 Induced by Silica Nanoparticles

“…It has been verified that prolonged inhalation of crystalline silica may cause lung inflammation and lead to multiple diseases, such as chronic bronchitis, lung fibrosis, and silicosis [38,39]. The expression of COX-2 and PGs has been observed to be significantly induced in inflammatory pulmonary diseases such as COPD, acute lung injury, and asthma [11,12].…”

Reactive Oxygen Species-Dependent Activation of EGFR/Akt/p38 Mitogen-Activated Protein Kinase and JNK1/2/FoxO1 and AP-1 Pathways in Human Pulmonary Alveolar Epithelial Cells Leads to Up-Regulation of COX-2/PGE2 Induced by Silica Nanoparticles

“…It has been established that prolonged inhalation of crystalline silica can lead to lung inflammation and the development of various diseases, including chronic bronchitis, lung fibrosis, and silicosis [38,39]. Moreover, the expression of COX-2 and PGs has been observed to be significantly induced in inflammatory pulmonary diseases such as COPD, acute lung injury, and asthma [11,12].…”

Predictive risk factors for development of silicosis in Turkish ceramic workers

“…The variances of occupational health and safety practices between developed and developing countries should be concerned. The risk of inflammation is higher in workers those exposed to more silica due to longer duration of work and as the exposure lasts pulmonary diseases such as pneumoconiosis and fibrosis might occur (7,14).…”

“…As the employment in coal mining industry has declined recently, cases of silicosis began to be reported from sectors such as sandblasting, stone breaking, construction, mining, cement and glass production. The ceramics industry is also one of the sectors where silicosis cases commonly reported (7). It has been shown that exposure levels for crystalline silica have exceeded and were associated with high exposure levels almost in all ceramic process steps such as raw material preparation, mixing, molding, casting and retouching (8).…”