Waste collection is a critical sector, and maintaining a healthy working environment is essential. This study aimed to (i) characterize waste collectors' exposure to bioaerosols, (ii) examine associations between workday exposure to bioaerosols and serum inflammatory markers, and between week-exposure and self-reported symptoms, and (iii) identify hygiene practices, work tasks, and waste types associated with reported symptoms. In a cross-sectional study, exposure was measured among 56 waste collectors using personal air samplers. Blood samples collected at the end of the workday were analyzed for three inflammatory markers. Participants completed a questionnaire on health symptoms, hygiene practices, and work tasks. Individual week-exposure estimates were derived from exposure measurements among 105 collectors, accounting for season, waste type, and work task. Inflammatory markers indicated low-grade systemic inflammation and were positively associated with workday exposure to anaerobic bacteria. Week-exposure to anaerobic bacteria was associated with increased odds of runny nose and sore throat. Eating in the truck cab was associated with eye symptoms and diarrhea. Use of hand sanitizer was associated with lower odds of nasal symptoms and colds. Cleaning of the truck waste compartment was associated with higher exposure and increased odds of eye and airway symptoms. These findings suggest that anaerobic bacterial exposure, work tasks, and hygiene behaviors may contribute to inflammatory responses and symptoms among waste collectors. The results should be interpreted as hypothesis-generating and support the need for confirmatory intervention studies to evaluate causal relationships and preventive measures related to residual and biowaste collection, truck cleaning, and hygiene practices.

AIMS:Early-life environment is crucial for foetal programming and later-life development. Exposure to particulate air pollution during gestation may increase the risk of cardiovascular diseases (CVD) later in life. We investigated the association between exposure to PM2.5 (particulate matter with a diameter of 2.5 μm or less) during gestation and pulse wave velocity (PWV) in children. METHODS AND RESULTS:In the prospective ENVIRONAGE (ENVIRonmental influence ON early AGEing) birth cohort (Belgium), mother-child pairs were recruited at birth, and 244 children between 9 and 11 years were followed up. Arterial stiffness was assessed using carotid-femoral PWV via the Vicorder® (Skidmore Medical, Bristol, UK). A high-resolution spatiotemporal model was used to model daily prenatal and postnatal PM2.5 exposure levels. Associations between prenatal PM2.5 exposures and PWV were tested using linear regression models followed by fitting weekly prenatal exposures to distributed lag non-linear models (DLNM). Among the 244 children [132 girls (54.1%); mean (S) age, 10.2 (0.8) years], a 5 μg/m3 increment in prenatal PM2.5 exposure during trimester two was significantly associated with a 0.09 m/sec higher PWV (95% CI, 0.01 to 0.17; P = 0.03). Accounting for entire childhood PM2.5 exposure, PM2.5 exposure during trimester two remained a predictor of PWV (0.08 m/sec, 95% CI: -0.0006 to 0.16; P = 0.05). CONCLUSION:PWV is an independent predictor of future CVD and all-cause mortality in the general population. Therefore, associations of air pollution exposure during gestation with childhood PWV highlight the potential long-term consequences on the child's cardiovascular system from early life onwards.

Objective:The mucosal origin hypothesis in rheumatoid arthritis (RA) posits that inhalant exposures, such as cigarette smoke and crystalline silica (c-silica), trigger immune responses contributing to disease onset. Despite the established risk posed by these exposures, the mechanistic link between inhalants, lung inflammation, and inflammatory arthritis remains poorly understood, partly from the lack of a suitable experimental model. As c-silica accelerates autoimmune phenotypes in lupus models and is a recognized risk factor for several autoimmune diseases, we investigated whether c-silica exposure could induce RA-like inflammatory arthritis in mice. Methods:Two arthritis-prone mouse strains, BXD2/TyJ and HLA-DR4 transgenic (DR4-Tg), were exposed to c-silica or PBS via oropharyngeal instillation. Arthritis was evaluated by clinical signs and histopathology. Autoimmunity was further evaluated by serological analysis, including autoantibodies and cytokines and chemokines. Lung pathology was evaluated by histopathology and immunofluorescent staining for lymphocyte and macrophages. Results:C-silica exposure induced chronic pulmonary silicosis in all mice. In BXD2 mice, this was associated with rapid arthritis development, marked by synovitis, bone erosion, and elevated serum autoantibody levels targeting various antigens, including snRNP and citrullinated protein. Additionally, BXD2 mice exhibited inducible bronchus-associated lymphoid tissue (iBALT) formation and elevated autoantibodies in bronchoalveolar lavage fluid (BALF). Conversely, DR4-Tg mice had no significant arthritis, negligible autoantibody responses, and milder lung inflammation lacking iBALT. Conclusion:We introduce a novel model of c-silica-mediated inflammatory arthritis, creating a novel platform to unravel the molecular and cellular underpinnings of RA and advance understanding of the mucosal origin hypothesis.

Occupational exposure to respirable crystalline silica (RCS) is a significant health concern associated with pulmonary and systemic diseases, mediated in part through lung macrophage toxicity. In this study, we employed an ex vivo indirect exposure model, to explore potential links between silica-induced macrophage toxicity and changes in innate and adaptive immune cell phenotypes, that may contribute to systemic effects of RCS. THP-1 derived macrophages served as a macrophage model and were exposed to crystalline silica particles. Whole blood was subsequently exposed ex vivo to conditioned medium (CM) from these particle-exposed cells. We then characterized immune cell responses via soluble cytokine analysis and single cell profiling by mass cytometry. Two crystalline silica types were compared, Min-U-Sil 5 quartz (Minusil) and synthetic quartz (gQ), that differ in "nearly free silanols" (NFS)-functional groups linked to RCS pathogenicity. In one set of experiments, an immune stimulation cocktail was added during the last 4 h of exposure to observe potential Minusil-induced changes in cellular immune responses. The findings demonstrated that exposing whole blood to Minusil CM significantly elevated soluble pro-inflammatory cytokines levels. At the single cell level, Minusil CM exposure altered monocyte and dendritic cell subpopulation frequencies and increased frequencies of several lymphocyte populations with high expression of the early activation marker CD38. Following immune stimulation, two cytotoxic effector memory T cell subpopulations showed increased frequencies: one polyfunctional and one characterised by a high expression of CD161. This study provides novel data on immune cell profiles associated with ex vivo exposure to RCS.

Systemic sclerosis (SSc) is an autoimmune chronic connective tissue disorder with a complex pathogenesis and a strong gene-environment interaction. Despite the low prevalence of SSc, with around 100-250 cases per million, the morbidity and mortality are high and disproportionately affecting women. In this context, we review the influence of the external and internal exposome on the "immunome" in SSc. While several studies have addressed aspects of exposure-induced autoimmunity in general, very few have focused on SSc-specific phenotypes. In epidemiological studies, targeted characterization of the external exposome component in relation to SSc has often been limited to a single exposure. Despite the selective characterization of exposure, such studies play an important role in providing evidence that can be used towards reduction of exposure of modifiable factors, and can lead to proper management and prevention of SSc. Additionally, there is an effort towards integration of external exposome data with health data (health records, medical imaging, diagnostic results, etc.), to significantly improve our understanding of the environmental and occupational causes of SSc. A limited number of studies have identified biological processes related to the vascular homeostasis, fibrotic processes and the immune system. The key findings of the current review show advances in our understanding of the SSc disease phenotype and associated biomarkers in relation to specific pathophysiological features, however most often such studies are not supplemented with external exposome data.

Background Inhalation of airborne particulate matter, such as silica and diesel exhaust particles, poses serious long-term respiratory and systemic health risks. Silica exposure can lead to silicosis and systemic autoimmune diseases, while DEP exposure is linked to asthma and cancer. Combined exposure to silica and DEP, common in mining, may have more severe effects. This study investigates the separate and combined effects of occupational-level silica and ambient-level DEP on lung injury, inflammation, and autoantibody formation in two genetically distinct mouse strains, thereby aiming at understanding the interplay between genetic susceptibility, particulate exposure, and disease outcomes. Silica and diesel exhaust particles were administered to mice via oropharyngeal aspiration. Assessments of lung injury and host response included in vivo lung micro-computed tomography, lung function tests, bronchoalveolar lavage fluid analysis including inflammatory cytokines and antinuclear antibodies, and histopathology with particle colocalization. Results The findings highlight the distinct effects of silica and diesel exhaust particles (DEP) on lung injury, inflammation, and autoantibody formation in C57BL/6J and NOD/ShiLtJ mice. Silica exposure elicited a well-established inflammatory response marked by inflammatory infiltrates, release of cytokines, and chemokines, alongside mild fibrosis, indicated by collagen deposition in the lungs of both C57BL/6J and NOD/ShilLtJ mice. Notably, these strains exhibited divergent responses in terms of respiratory function and lung volumes, as assessed through micro-computed tomography. Additionally, silica exposure induced airway hyperreactivity and elevated antinuclear antibody levels in bronchoalveolar lavage fluid, particularly prominent in NOD/ShiLtJ mice. Moreover, antinuclear antibodies correlated with extent of lung inflammation in NOD/ShiLTJ mice. Lung tissue analysis revealed DEP loaded macrophages and co-localization of silica and DEP particles. However, aside from contributing to airway hyperreactivity specifically in NOD/ShiLtJ mice, the ambient-level DEP did not significantly amplify the effects induced by silica. There was no evidence of synergistic or additive interaction between these specific doses of silica and DEP in inducing lung damage or inflammation in either of the mouse strains. Conclusion Mouse strain variations exerted a substantial influence on the development of silica induced lung alterations. Furthermore, the additional impact of ambient-level DEP on these silica-induced effects was minimal.

Rising plastic consumption leads to widespread microplastic (MP) contamination. Raman spectroscopy is widely used for MP identification due to its ability to analyse particles as small as 1 μm. However, it faces challenges such as interference from pigments and additives. In this study, we aim to assess the accuracy of Raman micro-spectroscopy in identifying coloured plastic samples by applying various oxidative treatments to eliminate the possible interference effect caused by colourants associated with the sample. Standard and coloured microplastics were analysed using a Raman imaging microscope. Coloured plastics were treated with H2O2 30%, Sodium hypochlorite 5%, and Fenton reagent (H2O2 30% and Ferrous sulphate 0.2 M) for 24, 48, and 72 h. The Raman spectra were acquired after treatment to assess the impact of the treatment procedure on the polymer identification. Our results revealed that colourants significantly impact Raman spectra by peak broadening and/or fluorescence effects, which reduces identification accuracy and match scores Red pigments particularly obscure polymer identification. Treatments like oxidation and Fenton's reagent showed limited effectiveness. Additives in plastic samples can affect the accuracy of polymer identification by the Raman spectroscopy technique. Common treatment procedures do not improve the accuracy of identification. In order to improve the reliability of Raman analysis, essential factors such as utilizing multiple excitation lasers and appropriate CCD detectors, establishing a comprehensive reference library of colourants and additives, and employing advanced techniques like time-gated Raman spectroscopy or Surface-Enhanced Raman Spectroscopy (SERS) should be considered.

The adverse outcome pathway (AOP) framework plays a crucial role in the paradigm shift of toxicity testing towards the development and use of new approach methodologies. AOPs developed for chemicals are in theory applicable to nanomaterials (NMs). However, only initial efforts have been made to integrate information on NM-induced toxicity into existing AOPs. In a previous study, we identified AOPs in the AOP-Wiki associated with the molecular initiating events (MIEs) and key events (KEs) reported for NMs in scientific literature. In a next step, we analyzed these AOPs and found that mitochondrial toxicity plays a significant role in several of them at the molecular and cellular levels. In this study, we aimed to generate hypothesis-based AOPs related to NM-induced mitochondrial toxicity. This was achieved by integrating knowledge on NM-induced mitochondrial toxicity into all existing AOPs in the AOP-Wiki, which already includes mitochondrial toxicity as a MIE/KE. Several AOPs in the AOP-Wiki related to the lung, liver, cardiovascular and nervous system, with extensively defined KEs and key event relationships (KERs), could be utilized to develop AOPs that are relevant for NMs. However, the majority of the studies included in our literature review were of poor quality, particularly in reporting NM physicochemical characteristics, and NM-relevant mitochondrial MIEs were rarely reported. This study highlights the potential role of NM-induced mitochondrial toxicity in human-relevant adverse outcomes and identifies useful AOPs in the AOP-Wiki for the development of AOPs for NMs.

The European Food Safety Authority (EFSA) has a goal to efficiently conduct aggregate exposure assessments (AEAs) for chemicals using both exposure models and human biomonitoring (HBM) data by 2030. To achieve EFSA's vision, a roadmap for action for advancing aggregate exposure (AE) in the EU was developed. This roadmap was created by performing a series of engagement and data collection activities to map the currently available methods, data, and tools for assessing AE of chemicals, against the needs and priorities of EFSA. This allowed for the creation of a AEA framework, identification of data and knowledge gaps in our current capabilities, and identification of the challenges and blockers that would hinder efforts to fill the gaps. The roadmap identifies interdependent working areas (WAs) where additional research and development are required to achieve EFSA's goal. It also proposes future collaboration opportunities and recommends several project proposals to meet EFSA's goals. Eight proposal projects supported by SWOT analysis are presented for EFSA's consideration. The project proposals inform high-level recommendations for multi-annual and multi-partner projects. Recommendations to improve stakeholder engagement and communication of EFSA's work on AEA were gathered by surveying stakeholders on specific actions to improve EFSA's communication on AE, including webinars, virtual training, social media channels, and newsletters.

Assessing dermal exposure to volatile organic compounds (VOCs) is becoming increasingly important in industrial settings. This study evaluated the applicability of a novel custom-made activated charcoal cloth (ACC) patch in various workplaces. Forty-nine workers carrying out different tasks were included in this assessment: desk working (“no VOC exposure”), sandblasting (“no VOC exposure”), cherry-picker driving (“dermal vapour exposure”), repairing (“low liquid exposure), degreasing (“medium liquid exposure”), spray painting (“high liquid exposure”), and immersing (“immersion exposure”). Each participant wore three ACC patches (thumb, index finger and neck). Additionally, two glove types were tested during the immersion task: all-round nitrile gloves and highly chemical-resistant gloves. One extra patch was placed on the outside of the glove to assess the ingress of VOCs. In general, the ACC patches captured various levels of VOCs ranging from levels below LOQ (“no VOC exposure”) to 0.4 mg/cm^2 (“dermal vapour exposure”) and 6.5 mg/cm^2 (“immersion exposure”). Furthermore, the ACC patches allowed us to differentiate the level of direct hand contact by comparing the amount of VOCs found on the fingers versus the neck. Workers carrying out direct liquid handling tasks, such as spray painting, showed over 75% hand versus neck exposure than workers only exposed via vapour (1-30%). Finally, the percentage of ingress could be calculated during the immersion task by comparing the outer patch with the inner patches. When wearing nitrile gloves, 5% of ingress was observed versus nearly 0% when wearing chemical-resistant gloves. These findings demonstrate the applicability of the custom-made ACC patches to measure dermal VOC exposure in different work conditions.

Occupational silica exposure can cause silicosis and is associated with systemic autoimmune diseases such as rheumatoid arthritis (RA). The connection between silicosis and systemic effects remains unclear, but a role for ectopic lymphoid structures in the lung is hypothesized as an early event in the initiation of autoimmunity leading to systemic disease including arthritis. The objective was to investigate the relationship between pulmonary silica exposure, silicosis and the development of systemic autoimmunity in an established model of silica-mediated arthritis in the BXD2/TyJ mouse, with a focus on local autoimmunity development in lung and draining lymph node. Male and female mice were transorally exposed to 5 mg of silica or PBS and examined 1, 2 or 6 weeks later. BAL fluid and serum was collected for autoantibody assessment. Tracheobronchial lymph node (TBLN) and lungs were collected for histology and immunofluorescent staining for B (B220+), helper T cells (CD4+), and non-alveolar macrophages (Iba1+). Silica-exposed mice demonstrate silicosis with marked alveolitis, present at 1 week post-exposure (PE), while peribronchial and perivascular infiltrates are observed starting 6 weeks PE. TBLN enlargement occurs by 2 weeks PE. Autoantibodies were found in BALF before serum. T, B and macrophage-containing accumulations are present in the lung 2 weeks PE, intensifying by 6 weeks PE. Clusters of CD4+ T cells and Iba1+ cells appear to precede involvement of B cells. Preliminary findings of lymphoid accumulations and local autoantibody formation in the lung suggests this mouse model provides a platform to study the role of silica-induced pulmonary inflammation in the initiation of systemic autoimmunity including arthritis.

In low-income countries, a widespread but poorly studied type of cottage industry consists of melting scrap metal for making cookware. We assessed the exposure to lead (Pb) among artisanal workers, and their families, involved in manufacturing cookware from scrap metal. In a cross-sectional survey, we compared artisanal cookware manufacturing foundries with carpentry workshops (negative controls) and car battery repair workshops (positive controls), all located in residential areas, in Lubumbashi (DR Congo). We collected surface dust in the workspaces, and blood and urine samples among workers, as well as residents living in the cookware workshops. Trace elements were quantified in the samples by Inductively Coupled Plasma Mass Spectrometry (ICP-MS). In surface dust, median Pb concentrations were higher in cookware foundries (347 mg/kg) than in carpentries (234 mg/kg) but lower than in battery repair workshops (22,000 mg/kg). In workers making the cookware (n = 24), geometric mean (GM) Pb blood cencentration was 118 μg/L [interquartile range (IQR) 78.4-204], i.e. nearly twice as high as among carpenters [60.2 μg/L (44.4-84.7), n = 33], and half the concentration of battery repair workers [255 μg/L (197-362), n = 23]. Resident children from the cookware foundries, had higher urinary Pb [6.2 μg/g creatinine (2.3-19.3), n = 6] than adults [2.3 (2.2-2.5), n = 3]. Our investigation confirms the high Pb hazard linked to car battery repair and reveals a high exposure to Pb among artisanal cookware manufacturers and their families, especially children, in residential areas of a city in a low-income country.

Abstract Introduction Evaluation of dermal and respiratory exposure to volatile organic compounds in occupational settings is becoming increasingly important. Methods This study assessed the dermal exposure contribution (versus inhalation exposure) to the overall exposure of seven workers employed in a spray paint company. Stoffenmanager®V8 was used to model inhalation exposure, followed by air measurements with active charcoal tubes and dermal exposure assessment using three custom-made activated charcoal cloth patches (neck, thumb and index finger) of xylene and ethylbenzene. Internal exposure was assessed by pre- and post-shift urine samples of mandalic acid (ethylbenzene), phenyl glyoxylic acid (ethylbenzene), and methyl hippuric acid (xylene). We divided the workers into painters (n=3) and drivers (n=4). Results The predicted concentrations from stoffenmanager®V8 were lower than the measured values of the painters, namely, estimated=18.4 mg/m3 versus measured=36.2±23.3 mg/m3 (ethylbenzene) and estimated=34.6 mg/m3 versus measured=161.5±102.14 mg/m3 (xylene). Subsequently, the inhalation samples were evaluated for compliance with the Belgian TLV using expostats, showing well-controlled air exposure for all scenarios except the painter’s xylene exposure, where two measurements (220 mg/m3) were almost the TLV (222 mg/m3). Dermal measurements indicated that painters experienced dermal liquid exposure (hands) ranging from 30 to 42 times higher and 2.5 times higher vapour exposure (neck) than drivers. However, no significant differences were found in the urinary post samples of both groups, 177.10±89.0 mg/g creatinine versus 51.2±32.7 mg/g creatinine (ethylbenzene) and 35.7±15.5 mg/g creatinine versus 16.9±4.0 mg/g creatinine (xylene). Discussion and conclusion drivers who did not have liquid dermal contact can still have overall exposure comparable to the painters.

This study aimed to evaluate possible cytotoxic effects of thermoplastic materials commonly used for occlusal splints and orthodontic appliances. Seven thermoplastics were included: three variants of the Essix sheets (C+, Plus, and Tray Rite; Dentsply Sirona), three thermoplastics (Bleach Heavy, Splint, and X-Heavy; Cavex Holland) and Invisalign (Align Technology). Cylindrical specimens (n = 24; 10 mm diameter) were incubated in cell culture medium for 24 h and 14 days. After incubation, the medium was collected, serially diluted, and dosed to primary human gingival fibroblasts in triplicate. Medium processed like the samples was used as negative control. Cell viability was evaluated by XTT and LDH assay to assess metabolic activity and membrane integrity, respectively. Next, cell cycle was assessed with flow cytometry after exposing HGFs to undiluted extracts. The 24-hour and 14-day extracts did not evoke cytotoxicity after 24-hour incubation. No significant differences in cell viability (one-way ANOVA, p > 0.05 ) in the XTT and LDH assays or in cell cycle distribution between the different materials (two-way ANOVA, p > 0.05 ). The thermoplastics tested in the study showed no evident in-vitro cytotoxic effects. Further investigation should focus on determining which compounds are released from thermoplastic materials and assessing potential toxicity related to exposure to these compounds. Our study adds to the growing body of evidence on the biocompatibility of dental thermoplastics. This can aid clinical decision-making, as thermoplastics are expected to be safe to use in terms of cytotoxicity.

Making something FAIR is hard, particularly when you do more than making something findable. We've seen before that making something usefully findable requires deep indexing, and already that continues to be difficult, because we are not seeing it enough. So, when I thought convert a paper led by Hoet's lab in Leuven into machine-actionable RDF to make it FAIR, I gravely underestimated the amount of work.

Abstract Introduction Occupational exposure to crystalline silica is associated with an elevated risk of autoimmune diseases in susceptible individuals, yet underlying mechanisms, likely influenced by gene-environment interactions, remain unclear. We aimed to investigate the immunotoxicological effects of exposure to crystalline silica considering the effect of genetic background in C57BL/6J and NOD/ShiLtJ mice. Methods C57BL/6J and NOD/ShiLtJ mice were oropharyngeally exposed to 4mg quartz (median size about 2 µm) with animal ethics committee approval of KU Leuven (P111/2021). Ten weeks post-exposure, bronchoalveolar lavage fluid (BALF), lungs and serum were collected to evaluate inflammatory cell count, lung histology, lung fibrosis and antinuclear antibody (ANA) presence. Results Silica exposed mice developed a local inflammatory response characterized by inflammatory infiltrates, recruitment of macrophages/neutrophils and mild lung fibrosis, which was more pronounced in the NOD/ShiLtJ mice. In BALF, the silica-exposed NOD/ShiLtJ mice showed significantly high ANA scores with about 40% of mice reaching a score of 3-4, while silica-exposed C57BL/6J mice had lower scores, only reaching up to 2. Silica-exposed NOD/ShiLtJ mice also developed systemic ANAs present in serum, with scores reaching up to 4, whereas silica-exposed C57BL/6J mice only reached scores up to 2-3. Discussion The autoimmune-prone background of NOD/ShiLtJ mice characterized by an H2(g7) MHC haplotype and genetic variants impacting tolerance and T cell functioning seems to render them more susceptible to an inflammatory phenotype facilitating the development of autoantibodies. Conclusion The autoimmune-prone genetic background of the NOD/ShiLtJ mice appears to be a critical factor contributing to their susceptibility to develop silica-induced features of autoimmune disease.