Browsing by Author "Pacheco, Solange"
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- Disclosing effects of tobacco smoke on occupationally exposed workers at Lisbon restaurantsPublication . Pacheco, Solange; Simoes, Tania; Torres, Vukosawa; Lopes, Carlos; Almeida, Bugalho; Penque, DeborahThis study represents a global assessment of IAQ in Lisbon smoking entertainment places and health effects on exposed workers. Most importantly, it may contribute to the better understanding of pathogenesis mechanisms due to SHS exposure. In addition it may lead to the discovery of specific biomarkers for occupational SHS-exposure that might precede respiratory diseases on their employees and promote more effective therapies.
- Exposição ocupacional ao fumo de tabaco ambiental: um estudo em restaurantes na cidade de LisboaPublication . Pacheco, Solange; Aguiar, Fátima; Proença, Carmo; Penque, Deborah; Simões, Tânia
- Exposição ocupacional ao fumo de tabaco: alterações subclínicas em proteínas de inflamação agudaPublication . Pacheco, Solange; Simões, Tânia; Penque, Deborah
- Occupational exposure to environmental tobacco smoke in hospitality venues: are genetic- or proteomics-based biomarkers predictive of respiratory diseases?Publication . Silva, M.J.; Vital, Nádia; Pacheco, Solange; Antunes, Susana; Neves, Sofia; Louro, Henriqueta; Torre, Vukosava M.; Vaz, Fátima; James, Peter; Lopes, Carlos; Marçal, Nelson; Bugalho de Almeida, António; Simões, Tânia; Penque, DeborahEnvironmental tobacco smoke (ETS) is recognized as an occupational hazard in the hospitality industry. Although Portuguese legislation banned smoking in most indoor public spaces, it is still allowed in some restaurants/bars, representing a potential risk to the workers’ health, particularly for chronic respiratory diseases. The aims of this work were to characterize biomarkers of early genetic effects and to disclose proteomic signatures associated to occupational exposure to ETS and with potential to predict respiratory diseases development. A detailed lifestyle survey and clinical evaluation (including spirometry) were performed in 81 workers from Lisbon restaurants. ETS exposure was assessed through the level of PM 2.5 in indoor air and the urinary level of cotinine. The plasma samples were immunodepleted and analysed by 2D-SDSPAGE followed by in-gel digestion and LC-MS/MS. DNA lesions and chromosome damage were analysed innlymphocytes and in exfoliated buccal cells from 19 cigarette smokers, 29 involuntary smokers, and 33 non-smokers not exposed to tobacco smoke. Also, the DNA repair capacity was evaluated using an ex vivo challenge comet assay with an alkylating agent (EMS). All workers were considered healthy and recorded normal lung function. Interestingly, following 2D-DIGE-MS (MALDI-TOF/TOF), 61 plasma proteins were found differentially expressed in ETS-exposed subjects, including 38 involved in metabolism, acute-phase respiratory inflammation, and immune or vascular functions. On the other hand, the involuntary smokers showed neither an increased level of DNA/chromosome damage on lymphocytes nor an increased number of micronuclei in buccal cells, when compared to non-exposed non-smokers. Noteworthy, lymphocytes challenge with EMS resulted in a significantly lower level of DNA breaks in ETS-exposed as compared to non-exposed workers (P<0.0001) suggestive of an adaptive response elicited by the previous exposure to low levels of ETS. Overall, changes in proteome may be promising early biomarkers of exposure to ETS. Likewise, alterations of the DNA repair competence observed upon ETS exposure deserves to be further understood. Work supported by Fundação Calouste Gulbenkian, ACSS and FCT/Polyannual Funding Program.
- Occupational Exposure to Environmental Tobacco Smoke: A Study in Lisbon RestaurantsPublication . Pacheco, Solange; Aguiar, Fátima; Proença, Maria do Carmo; Penque, Deborah; Ruivo, Patricia; Simoes, TaniaEnvironmental tobacco smoke (ETS), also referred to as secondhand smoke (SHS), is a major threat to public health and is increasingly recognized as an occupational hazard to workers in the hospitality industry. Therefore, several countries have implemented smoke-free regulations at hospitality industry sites. In Portugal, since 2008, legislation partially banned smoking in restaurants and bars but until now no data have been made available on levels of indoor ETS pollution/exposure at these locations. The aim of this study was to examine the occupational exposure to ETS/SHS in several restaurants in Lisbon, measured by indoor fine particles (PM2.5) and urinary cotinine concentration in workers, after the partial smoking ban in Portugal. Results showed that the PM2.5 median level in smoking designated areas was 253 μg/m3, eightfold higher than levels recorded in canteens or outdoor. The nonsmoking rooms of mixed restaurants exhibited PM2.5 median level of 88 μg/m3, which is higher than all smoke-free locations studied, approximately threefold greater than those found in canteens. Importantly, urinary cotinine concentrations were significantly higher in nonsmoker employees working in those smoking designated areas, confirming exposure to ETS. The proportion of smokers in those rooms was found to be significantly positively correlated with nonsmoker urinary cotinine and indoor PM2.5 levels, establishing that both markers were occupational-ETS derived. The use of reinforced ventilation systems seemed not to be sufficient to decrease the observed ETS pollution/exposure in those smoking locations. Taken together, these findings demonstrate that the partial restrictions on smoking in Portuguese venues failed to provide adequate protection to their employees, irrespective of protective measures used. Therefore, a smoke-free legislation protecting individuals from exposure to ETS/SHS in all public places and workplaces is urgently needed in Portugal.
- Occupational second-hand smoke exposure: A comparative shotgun proteomics study on nasal epithelia from healthy restaurant workersPublication . Neves, Sofia; Pacheco, Solange; Vaz, Fátima; James, Peter; Simões, Tânia; Penque, Deborah; NevesNon-smokers exposed to second-hand smoke (SHS) present risk of developing tobacco smoke-associated pathologies. To investigate the airway molecular response to SHS exposure that could be used in health risk assessment, comparative shotgun proteomics was performed on nasal epithelium from a group of healthy restaurant workers, non-smokers (never and former) exposed and not exposed to SHS in the workplace. HIF1α-glycolytic targets (GAPDH, TPI) and proteins related to xenobiotic metabolism, cell proliferation and differentiation leading to cancer (ADH1C, TUBB4B, EEF2) showed significant modulation in non-smokers exposed. In never smokers exposed, enrichment of glutathione metabolism pathway and EEF2-regulating protein synthesis in genotoxic response were increased, while in former smokers exposed, proteins (LYZ, ATP1A1, SERPINB3) associated with tissue damage/regeneration, apoptosis inhibition and inflammation that may lead to asthma, COPD or cancer, were upregulated. The identified proteins are potential response and susceptibility/risk biomarkers for SHS exposure.
- Occupational secondhand smoke effect on nasal epithelial proteomaPublication . Pacheco, Solange; Vaz, Fatima; Torres, Vukosava; Penque, Deborah; Simões, Tania; James, PeterThe tobacco is one of the biggest public health threats, smoking kills more than 7 million people/year worldwide and more than 890,000 are deaths resulting from exposure to Secondhand Smoke (SHS). In adults, SHS is associated to cardiovascular and respiratory diseases, including coronary heart disease and lung cancer, through pathological and molecular mechanisms not yet understood. In this study, we aimed to investigate the SHS effects on nasal epithelial proteome in exposed workers.
- Occupational secondhand smoke exposure - A proteomic analysisPublication . Neves, Sofia; Pacheco, Solange; Vaz, Fátima; Simões, Tania; James, Peter; Simões, Tânia; Penque, DeborahBackground: WHO have stated that near 900 000 deaths per year result from exposure to Second- Hand Smoke (SHS). SHS exposure has been linked to cancer, respiratory and cardiovascular diseases and diabetes. However, the associated underlying molecular mechanisms remain to be elucidated. The objective of this proteomics study is to uncover putative key molecules involved in these mechanisms that can be used to predict and monitor diseases risks associated with occupational SHS exposure. Methods: In total, 25 Lisbon restaurants agreed to participate. Nasal epithelium and urine samples were collected from their employees (n=52) for proteomics analysis and cotinine evaluation of SHS exposure, respectively. The subjects were classified as never smoker (N), former smoker (F) and smoker (S); exposed (NE=11; FE=10; SE=4) or non-exposed (N=11; F=8; S=8) to SHS. All subjects were healthy and showed no significant differences in parameters like age, time in the workplace, tobacco smoking habits and spirometry evaluation of pulmonary function. Urine cotinine levels showed significantly elevated in the exposed subjects compared to non-exposed, confirming SHS exposure. Nasal epithelium samples were analyzed by shotgun proteomics using an ESI-LTQOrbitrap mass spectrometer. The “MS raw data” was submitted to “PatternLab for Proteomics” software, with “Comet” search machine algorithm, from where the identified proteins were submitted to a “ClueGO” functional annotation & enrichment analyses in “Cytoscape” software, with the propose to shed some light about the molecular biology involved in the cellular response to the SHS exposition. Results: In NE subjects the SHS is associated with the biologic terms of “Lactate dehydrogenase complex” and “Pentose-Phosphatase Shunt”, also with “Glutathione peroxidase activity” and “Tcell apoptotic process”. At the other end the FE individuals present a specific proteome enriched in biologic information with terms as the “L-Lactate dehydrogenase complex” and the “Peroxisome” as was expected by the results above for the NE cohort; but there were also other different terms as: “Peripheral T cell lymphoma”, “Central carbon metabolism in cancer”, “Myelodysplastic syndrome”, “Monocyte & Granulocyte & Macrophage & Leukocyte Chemotaxis”, Nucleossome, variant H3.1-H2A2-H2B.1&Others” and finally “DNA replication-dependent chromatin assembly”. Conclusions: Proteome of nasal epithelium seems to be modulated by SHS exposure and this is a different and perhaps cumulative process between NE and FE individuals.
- Occupational secondhand smoke exposure may modify the proteoma expression of human nasal epitheliumPublication . Neves, Sofia; Pacheco, Solange; Vaz, Fátima; Martins, Inês; James, Peter; Simões, Tânia; Penque, DeborahThe tobacco is one of the biggest public health threats, smoking kills more than 7 million people/year worldwide and more than 890,000 are deaths resulting from exposure to Second Hand Smoke (SHS). In adults, SHS is associated to cardiovascular and respiratory diseases, including coronary heart disease and lung cancer, through pathological and molecular mechanisms not yet understood. In this study, we aimed to investigate the SHS effects on airway proteome in exposed workers. Nasal epithelium was collected from hospitality workers (non-smokers=40; smokers=12) long-term exposed and non-exposed to SHS at the workplace. Samples were analyzed by shotgun proteomics using an ESI-LQT Orbitrap XL mass spectrometer. The generated MS raw data was submitted to ‘PatternLab for Proteomics 4.0’ for peptide identification and relative quantification by label-free - extracted ion chromatograms (XIC). Golden rules were applied to obtain reliable data such as the inferred proteins must have at least one unique peptide identified to be considered and be detected in at least 80% of the cohort. Two proteins were found to be differentially expressed in the no-smokers exposed to SHS compared with the control: BPI fold-containing family A member 1 (BPIFA1) and Heat shock Protein Beta-1 (HSPB1). The first protein plays a role in the airway inflammatory response after exposure to irritants substances and the second is associated as a regulator of actin filament dynamics. Our findings support the indication that in non-smokers the prolonged exposure to SHS can lead to airway proteome modulation. When validated, the uncovered proteins can be promising candidates to “susceptibility/risk” and/or “response” biomarkers for SHS exposure.
- Occupational secondhand smoke exposure may modify the proteoma expression of human nasal epitheliumPublication . Neves, Sofia; Pacheco, Solange; Vaz, Fátima; Torres, Vukosava Milic; James, Peter; Simões, Tânia; Penque, DeborahThe tobacco is one of the biggest public health threats, smoking kills more than 7 million people/year worldwide and more than 890,000 are deaths resulting from exposure to Second Hand Smoke (SHS). In adults, SHS is associated to cardiovascular and respiratory diseases, including coronary heart disease and lung cancer, through pathological and molecular mechanisms not yet understood. We aimed to investigate the SHS effects on airway proteome in exposed workers. Nasal epithelium was collected from hospitality workers (non-smokers=40; smokers=12), long-term exposed and non-exposed to SHS at the workplace. Samples were analyzed by shotgun proteomics using an ESI-LQT Orbitrap XL mass spectrometer. The generated MS raw data was submitted to ‘PatternLab for Proteomics’ for peptide identification and relative quantification by label-free - extracted ion chromatograms (XIC). Golden rules were applied to obtain reliable data: in the identification of a protein at least one unique peptide must had to be present in more than 80% of the individuals, and consequently each inferred protein had to be detected in 80% to 100% of the cohort. Two proteins were found to be differentially expressed in the no-smokers exposed to SHS compared with the control: BPI fold-containing family A member 1 (BPIFA1) and Heat shock Protein Beta-1 (HSPB1). The first protein plays a role in the airway inflammatory response after exposure to irritants substances and the second is associated as a regulator of actin filament dynamics. Our findings support the indication that in non-smokers the prolonged exposure to SHS can lead to airway proteome modulation. When validated, the uncovered proteins can be promising candidates to “susceptibility/risk” and/or “predictive” biomarkers for SHS exposure.