A Biomonitoring Pilot Study in Workers from a Paints Production Plant Exposed to Pigment-Grade Titanium Dioxide (TiO2).

Among particulate matter composing paints, titanium dioxide (TiO2) forms about 20% of the final suspension. Although TiO2 is broadly used in many applications, TiO2 powders represent an established respiratory hazard for workers with long-term exposure. In 35 workers of a paints production plant (15 exposed and 20 not exposed), we assessed pro-inflammatory cytokines (IL-1ß, TNF-α, IL-10, IL-17), surfactant protein D (SP-D) and Krebs von den Lungen-6 glycoprotein (KL-6) in exhaled breath condensate (EBC). In urine samples, we measured 8-isoprostane (Isop) and Malondialdehyde (MDA) as biomarkers of oxidative stress, and Titanium (Ti-U) as a biomarker of exposure. Health status, habits and occupational history were recorded. Airborne respirable dusts and Ti were quantified. Particle number concentration and average diameter (nm) were detected by a NanoTracer™ monitoring device. Ti was measurable in filters collected at the respiratory breathing zone (0.11−0.44 µg/m3 8-h TWA). IL-1ß and IL-10 values were significantly higher in exposed workers, whereas SP-D was significantly lower (p < 0.001). KL-6 was significantly higher in workers than in controls (p < 0.01). MDA levels were significantly increased in exposed workers and were positively correlated with Ti-U. Exposure to TiO2 in paint production is associated with the subtle alterations of lung pathobiology. These findings suggest the need for an integrated approach relying on both personal exposure and biomarker assessment to improve the hazard characterisation in occupational settings.

The formation of SCEs as an effect of occupational exposure to formaldehyde.

Formaldehyde (FA) is a ubiquitous toxic chemical employed worldwide due to its disinfectant and preservative properties. Despite being classified as a human carcinogen, FA is still employed as formalin in pathology wards as standard fixative. We evaluated its relationship with the formation of sister-chromatid exchanges (SCEs) in cultured peripheral blood lymphocytes on 57 pathologists and 48 controls and the risk/protective role played by several genetic polymorphisms. All subjects were assessed for SCEs and genotyped for the most common cancer-associated gene polymorphisms: CYP1A1 exon 7 (A > G), CYP1A1*2A (T > C), CYP2C19*2 (G > A), GSTT1 (presence/absence), GSTM1 (presence/absence), GSTP1 (A > G), XRCC1 (G399A), XRCC1 (C194T), XRCC1 (A280G), XPC exon 15 (A939C), XPC exon 9 (C499T), TNFα - 308 G > A), IL10 - 1082 (G > A), and IL6 - 174 (G > C). Air-FA concentration was assessed through passive personal samplers. Pathologists, exposed to 55.2 µg/m3 of air-FA, showed a significantly higher SCEs frequency than controls, exposed, respectively, to 18.4 µg/m3. Air-FA was directly correlated with SCEs frequency and inversely with the replication index (RI). Regression models showed FA exposure as a significant predictor in developing SCEs, while did not highlight any role of the selected polymorphisms. Our study confirms the role of low air-FA levels as genotoxicity inductor, highlighting the importance to define exposure limits that could be safer for exposed workers.

The role of phase I, phase II, and DNA-repair gene polymorphisms in the damage induced by formaldehyde in pathologists.

Formaldehyde (FA) is a human carcinogen used as formalin in hospital laboratories. We evaluated its association with human chromosomal aberrations (CAs) and the risk/protective role played by several genetic polymorphisms in this relationship, on a cohort of 57 exposed pathologists vs 48 controls. All subjects were assessed for CAs on peripheral blood lymphocytes and genotyped for the most common cancer-associated gene polymorphisms which could be related with the genotoxic outcome: CYP1A1 exon 7 (A>G), CYP1A1*2A (T>C), CYP2C19*2 (G>A), GSTT1 (Positive/Null), GSTM1 (Positive/null), GSTP1 (A>G), XRCC1 (G399A), XRCC1 (C194T), XRCC1 (A280G), XPD (A751C), XPC exon 15 (A939C), XPC exon 9 (C499T), TNFα - 308 (G>A), IL10 - 1082 (G>A), IL10 - 819 (C>T) and IL6 - 174 (G>C). Air-FA concentration was assessed through personal samplers. The comparison between pathologists and controls showed a significantly higher CAs frequency in pathologists. Significant positive correlations were found between CAs frequency and air-FA concentration while significant associations were found between variation in CAs frequency and the mutated allele for CYP1A1 exon 7 (A>G), CYP2C19*2 (G>A), GSTT1-positive, GSTM1-positive and XRCC1 (G399A). Our study confirms the role of FA as genotoxicity inductor, even in workers chronically exposed to low air-FA levels and reveals the role played by some genetic polymorphisms in this association, highlighting the importance of individual susceptibility biomarkers assessment in occupational health studies.

Occupational Exposure to Carbon Nanotubes and Carbon Nanofibres: More Than a Cobweb.

Carbon nanotubes (CNTs) and carbon nanofibers (CNFs) are erroneously considered as singular material entities. Instead, they should be regarded as a heterogeneous class of materials bearing different properties eliciting particular biological outcomes both in vitro and in vivo. Given the pace at which the industrial production of CNTs/CNFs is increasing, it is becoming of utmost importance to acquire comprehensive knowledge regarding their biological activity and their hazardous effects in humans. Animal studies carried out by inhalation showed that some CNTs/CNFs species can cause deleterious effects such as inflammation and lung tissue remodeling. Their physico-chemical properties, biological behavior and biopersistence make them similar to asbestos fibers. Human studies suggest some mild effects in workers handling CNTs/CNFs. However, owing to their cross-sectional design, researchers have been as yet unable to firmly demonstrate a causal relationship between such an exposure and the observed effects. Estimation of acceptable exposure levels should warrant a proper risk management. The aim of this review is to challenge the conception of CNTs/CNFs as a single, unified material entity and prompt the establishment of standardized hazard and exposure assessment methodologies able to properly feed risk assessment and management frameworks.

Oxidative stress induction in woodworkers occupationally exposed to wood dust and formaldehyde.

BACKGROUND: Many workers are exposed to wood dust (WD) and formaldehyde (FA), whose carcinogenic activity is supposed to be oxidative stress-mediated. This study aims to assess to what extent the occupational exposure to WD and FA, albeit within regulatory limits, could result in OS induction in a woodworkers' population. METHODS: The sample population consisted of 127 woodworkers from 4 factories and 111 unexposed controls. Individual exposure was assessed by personal air-samplers. Each participant enrolled in the study filled out a questionnaire and provided a urinary sample to quantify OS biomarkers, namely 15-F2t-IsoProstane (15-F2t-IsoP) and 7,8-dihydro-8-oxo-2'-deoxyguanosine (8-oxo-dGuo). The main confounding factor for OS, i.e. tobacco smoking exposure, was assessed by measuring cotinine in urine samples. RESULTS: Woodworkers were exposed to significantly higher amounts of WD and FA as compared to controls (p < 0.001). Among OS biomarkers, 15-F2t-IsoP showed statistically significant higher values in woodworkers compared to controls (p = 0.004). A significant, positive correlation was observed between 15-F2t-IsoP and 8-oxo-dGuo (p = 0.005), cotinine (p = 0.05), FA (p < 0.001) and WD (p = 0.01); 8-oxo-dGuo was significantly correlated with cotinine (p = 0.001) and WD (p = 0.004). In addition, WD and FA were significantly correlated each other (p < 0.001). CONCLUSIONS: The study confirms that WD and FA may induce OS in woodworkers, and highlights that even the compliance with occupational exposure limits can result in measurable biological outcomes.