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Marinaccio A.,INAIL Italian Workers Compensation Authority Research Area | Scarselli A.,INAIL Italian Workers Compensation Authority Research Area | Merler E.,Padua Local Health Unit | Iavicoli S.,INAIL Italian Workers Compensation Authority Research Area
BMC Public Health | Year: 2012

Background: Malignant mesothelioma is an aggressive and lethal tumour strongly associated with exposure to asbestos (mainly occupational). In Italy a large proportion of workers are protected from occupational diseases by public insurance and an epidemiological surveillance system for incident mesothelioma cases. Methods: We set up an individual linkage between the Italian national mesothelioma register (ReNaM) and the Italian workers compensation authority (INAIL) archives. Logistic regression models were used to identify and test explanatory variables. Results: We extracted 3270 mesothelioma cases with occupational origins from the ReNaM, matching them with 1625 subjects in INAIL (49.7%); 91.2% (1,482) of the claims received compensation. The risk of not seeking compensation is significantly higher for women and the elderly. Claims have increased significantly in recent years and there is a clear geographical gradient (northern and more developed regions having higher claims rates). The highest rates of compensation claims were after work known to involve asbestos. Conclusions: Our data illustrate the importance of documentation and dissemination of all asbestos exposure modalities. Strategies focused on structural and systematic interaction between epidemiological surveillance and insurance systems are needed. © 2012 Marinaccio et al.; licensee BioMed Central Ltd.


Ursini C.L.,INAIL Italian Workers Compensation Authority Research Area | Cavallo D.,INAIL Italian Workers Compensation Authority Research Area | Fresegna A.M.,INAIL Italian Workers Compensation Authority Research Area | Ciervo A.,INAIL Italian Workers Compensation Authority Research Area | And 5 more authors.
BioMed Research International | Year: 2014

Functionalized MWCNTs are used in many commercial and biomedical applications, but their potential health effects are not well defined. We investigated and compared cytotoxic, genotoxic/oxidative, and inflammatory effects of pristine and carboxyl MWCNTs exposing human respiratory (A549 and BEAS-2B) cells to 1-40 g/mL of CNTs for 24 h. Both MWCNTs induced low viability reduction (by WST1 assay) in A549 cells and only MWCNTs-COOH caused high viability reduction in BEAS-2B cells reaching 28.5% viability at 40 g/mL. Both CNTs induced membrane damage (by LDH assay) with higher effects in BEAS-2B cells at the highest concentrations reaching 20% cytotoxicity at 40 g/mL. DNA damage (by Fpg-comet assay) was induced by pristine MWCNTs in A549 cells and by both MWCNTs in BEAS-2B cells reaching for MWCNTs-COOH a tail moment of 22.2 at 40 g/mL versus 10.2 of unexposed cells. Increases of IL-6 and IL-8 release (by ELISA) were detected in A549 cells exposed to MWCNTs-COOH from 10 g/mL while IL-8 increased in BEAS-2B cells exposed to pristine MWCNTs at 20 and 40 g/mL. The results show higher cytogenotoxicity of MWCNTs-COOH in bronchial and of pristine MWCNTs in alveolar cells. Different inflammatory response was also found. The findings suggest the use of in vitro models with different end points and cells to study CNT toxicity. © 2014 Cinzia Lucia Ursini et al.


Ursini C.L.,INAIL Italian Workers Compensation Authority Research Area | Cavallo D.,INAIL Italian Workers Compensation Authority Research Area | Fresegna A.M.,INAIL Italian Workers Compensation Authority Research Area | Ciervo A.,INAIL Italian Workers Compensation Authority Research Area | And 5 more authors.
Journal of Applied Toxicology | Year: 2014

The toxicity of titanium dioxide nanoparticles (TiO2-NPs), used in several applications, seems to be influenced by their specific physicochemical characteristics. Cyto-genotoxic and inflammatory effects induced by a mixture of 79% anatase/21% rutile TiO2-NPs were investigated in human alveolar (A549) and bronchial (BEAS-2B) cells exposed to 1-40μgml-1 30min, 2 and 24h to assess potential pulmonary toxicity. The specific physicochemical properties such as crystallinity, NP size and shape, agglomerate size, surface charge and specific surface area (SSA) were analysed. Cytotoxic effects were studied by evaluating cell viability using the WST1 assay and membrane damage using LDH analysis. Direct/oxidative DNA damage was assessed by the Fpg-comet assay and the inflammatory potential was evaluated as interleukin (IL)-6, IL-8 and tumour necrosis factor (TNF)-α release by enzyme-linked immunosorbant assay (ELISA). In A549 cells no significant viability reduction and moderate membrane damage, only at the highest concentration, were detected, whereas BEAS-2B cells showed a significant viability reduction and early membrane damage starting from 10μgml-1. Direct/oxidative DNA damage at 40μgml-1 and increased IL-6 release at 5μgml-1 were found only in A549 cells after 2h. The secretion of pro-inflammatory cytokine IL-6, involved in the early acute inflammatory response, and oxidative DNA damage indicate the promotion of early and transient oxidative-inflammatory effects of tested TiO2-NPs on human alveolar cells. The findings show a higher susceptibility of normal bronchial cells to cytotoxic effects and higher responsiveness of transformed alveolar cells to genotoxic, oxidative and early inflammatory effects induced by tested TiO2-NPs. This different cell behaviour after TiO2-NPs exposure suggests the use of both cell lines and multiple end-points to elucidate NP toxicity on the respiratory system. © 2014 John Wiley & Sons, Ltd.

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