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      Risk Assessment of Exposure to Silica Dust in Building Demolition Sites

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          Abstract

          Background

          Building demolition can lead to emission of dust into the environment. Exposure to silica dust may be considered as an important hazard in these sites. The objectives of this research were to determine the amount of workers' exposure to crystalline silica dust and assess the relative risk of silicosis and the excess lifetime risk of mortality from lung cancer in demolition workers.

          Methods

          Four sites in the Tehran megacity region were selected. Silica dust was collected using the National Institute for Occupational Safety and Health method 7601 and determined spectrophotometrically. The Mannetje et al and Rice et al models were chosen to examine the rate of silicosis-related mortality and the excess lifetime risk of mortality from lung cancer, respectively.

          Results

          The amount of demolition workers' exposure was in the range of 0.085–0.185 mg/m 3. The range of relative risk of silicosis related mortality was increased from 1 in the workers with the lowest exposure level to 22.64/1,000 in the employees with high exposure level. The range of the excess lifetime risk of mortality from lung cancer was in the range of 32–60/1,000 exposed workers.

          Conclusion

          Geometric and arithmetic mean of exposure was higher than threshold limit value for silica dust in all demolition sites. The risk of silicosis mortality for many demolition workers was higher than 1/1,000 (unacceptable level of risk). Estimating the lifetime lung cancer mortality showed a higher risk of mortality from lung cancer in building demolition workers.

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          Most cited references29

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          Application of toxicological risk assessment principles to the chemical constituents of cigarette smoke.

          To provide a hazard prioritisation for reported chemical constituents of cigarette smoke using toxicological risk assessment principles and assumptions. The purpose is to inform prevention efforts using harm reduction. International Agency for Research on Cancer Monographs; California and US Environmental Protection Agency cancer potency factors (CPFs) and reference exposure levels; scientific journals and government reports from the USA, Canada, and New Zealand. This was an inclusive review of studies reporting yields of cigarette smoke constituents using standard ISO methods. Where possible, the midpoint of reported ranges of yields was used. Data on 158 compounds in cigarette smoke were found. Of these, 45 were known or suspected human carcinogens. Cancer potency factors were available for 40 of these compounds and reference exposure levels (RELs) for non-cancer effects were found for 17. A cancer risk index (CRI) was calculated by multiplying yield levels with CPFs. A non-cancer risk index (NCRI) was calculated by dividing yield levels with RELs. Gas phase constituents dominate both CRI and NCRI for cigarette smoke. The contribution of 1,3-butadiene (BDE) to CRI was more than twice that of the next highest contributing carcinogen (acrylonitrile) using potencies from the State of California EPA. Using those potencies from the USEPA, BDE ranked third behind arsenic and acetaldehyde. A comparison of CRI estimates with estimates of smoking related cancer deaths in the USA showed that the CRI underestimates the observed cancer rates by about fivefold using ISO yields in the exposure estimate. The application of toxicological risk assessment methods to cigarette smoke provides a plausible and objective framework for the prioritisation of carcinogens and other toxicant hazards in cigarette smoke. However, this framework does not enable the prediction of actual cancer risk for a number of reasons that are discussed. Further, the lack of toxicology data on cardiovascular end points for specific chemicals makes the use of this framework less useful for cardiovascular toxicity. The bases for these priorities need to be constantly re-evaluated as new toxicology information emerges.
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            Chronic obstructive pulmonary disease due to occupational exposure to silica dust: a review of epidemiological and pathological evidence.

            Occupational exposure is an important risk factor for chronic obstructive pulmonary disease (COPD), and silica dust is one of the most important occupational respiratory toxins. Epidemiological and pathological studies suggest that silica dust exposure can lead to COPD, even in the absence of radiological signs of silicosis, and that the association between cumulative silica dust exposure and airflow obstruction is independent of silicosis. Recent clinicopathological and experimental studies have contributed further towards explaining the potential mechanism through which silica can cause pathological changes that may lead to the development of COPD. In this paper we review the epidemiological and pathological evidence relevant to the development of COPD in silica dust exposed workers within the context of recent findings. The evidence surveyed suggests that chronic levels of silica dust that do not cause disabling silicosis may cause the development of chronic bronchitis, emphysema, and/or small airways disease that can lead to airflow obstruction, even in the absence of radiological silicosis.
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              Silica induces NLRP3 inflammasome activation in human lung epithelial cells

              Background In myeloid cells the inflammasome plays a crucial role in innate immune defenses against pathogen- and danger-associated patterns such as crystalline silica. Respirable mineral particles impinge upon the lung epithelium causing irreversible damage, sustained inflammation and silicosis. In this study we investigated lung epithelial cells as a target for silica-induced inflammasome activation. Methods A human bronchial epithelial cell line (BEAS-2B) and primary normal human bronchial epithelial cells (NHBE) were exposed to toxic but nonlethal doses of crystalline silica over time to perform functional characterization of NLRP3, caspase-1, IL-1β, bFGF and HMGB1. Quantitative RT-PCR, caspase-1 enzyme activity assay, Western blot techniques, cytokine-specific ELISA and fibroblast (MRC-5 cells) proliferation assays were performed. Results We were able to show transcriptional and translational upregulation of the components of the NLRP3 intracellular platform, as well as activation of caspase-1. NLRP3 activation led to maturation of pro-IL-1β to secreted IL-1β, and a significant increase in the unconventional release of the alarmins bFGF and HMGB1. Moreover, release of bFGF and HMGB1 was shown to be dependent on particle uptake. Small interfering RNA experiments using siNLRP3 revealed the pivotal role of the inflammasome in diminished release of pro-inflammatory cytokines, danger molecules and growth factors, and fibroblast proliferation. Conclusion Our novel data indicate the presence and functional activation of the NLRP3 inflammasome by crystalline silica in human lung epithelial cells, which prolongs an inflammatory signal and affects fibroblast proliferation, mediating a cadre of lung diseases.
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                Author and article information

                Contributors
                Journal
                Saf Health Work
                Saf Health Work
                Safety and Health at Work
                Occupational Safety and Health Research Institute
                2093-7911
                2093-7997
                02 January 2016
                September 2016
                02 January 2016
                : 7
                : 3
                : 251-255
                Affiliations
                [1 ]Department of Occupational Health Engineering, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
                [2 ]Department of Occupational Health Engineering, School of Public Health, Shahid Beheshti University of Medical Sciences, Tehran, Iran
                [3 ]Department of Epidemiology and Biostatistics, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
                Author notes
                []Corresponding author. Department of Occupational Health Engineering, School of Public Health, Tehran University of Medical Sciences, Poorsina Street, Tehran, Iran. omidileila@ 123456yahoo.com omidil@ 123456razi.tums.ac.ir
                Article
                S2093-7911(15)00118-3
                10.1016/j.shaw.2015.12.006
                5011095
                27630796
                d737bfde-525e-4601-9d08-0ce415697637
                Copyright © 2016, Occupational Safety and Health Research Institute. Published by Elsevier.

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 9 February 2015
                : 3 December 2015
                : 17 December 2015
                Categories
                Original Article

                Occupational & Environmental medicine
                dust,lung cancer,occupational exposure,silica,silicosis
                Occupational & Environmental medicine
                dust, lung cancer, occupational exposure, silica, silicosis

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