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- Anand, MP, et al.
(author)
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Clinical, Epidemiological and Experimental Approaches to Assess Adverse Health Outcomes of Indoor Biomass Smoke Exposure: Conclusions from An Indo-Swedish Workshop in Mysuru, January 2020
- 2020
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In: Toxics. - : MDPI AG. - 2305-6304. ; 8:3
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Journal article (other academic/artistic)abstract
- This report summarizes the outcome of a workshop held in Mysuru, India in January 2020 addressing the adverse health effects of exposure to biomass smoke (BMS). The aim of the workshop was to identify uncertainties and gaps in knowledge and possible methods to address them in the Mysuru study on Determinants of Health in Rural Adults (MUDHRA) cohort. Specific aims were to discuss the possibility to improve and introduce new screening methods for exposure and effect, logistic limitations and other potential obstacles, and plausible strategies to overcome these in future studies. Field visits were included in the workshop prior to discussing these issues. The workshop concluded that multi-disciplinary approaches to perform: (a) indoor and personalized exposure assessment; (b) clinical and epidemiological field studies among children, adolescents, and adults; (c) controlled exposure experiments using physiologically relevant in vitro and in vivo models to understand molecular patho-mechanisms are warranted to dissect BMS-induced adverse health effects. It was perceived that assessment of dietary exposure (like phytochemical index) may serve as an important indicator for understanding potential protective mechanisms. Well trained field teams and close collaboration with the participating hospital were identified as the key requirements to successfully carry out the study objectives.
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- Ganguly, K, et al.
(author)
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Addressing the challenges of E-cigarette safety profiling by assessment of pulmonary toxicological response in bronchial and alveolar mucosa models
- 2020
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In: Scientific reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 10:1, s. 20460-
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Journal article (peer-reviewed)abstract
- Limited toxicity data on electronic cigarette (ECIG) impede evidence-based policy recommendations. We compared two popular mixed fruit flavored ECIG-liquids with and without nicotine aerosolized at 40 W (E-smoke) with respect to particle number concentrations, chemical composition, and response on physiologically relevant human bronchial and alveolar lung mucosa models cultured at air–liquid interface. E-smoke was characterized by significantly increased particle number concentrations with increased wattage (25, 40, and 55 W) and nicotine presence. The chemical composition of E-smoke differed across the two tested flavors in terms of cytotoxic compounds including p-benzoquinone, nicotyrine, and flavoring agents (for example vanillin, ethyl vanillin). Significant differences in the expression of markers for pro-inflammation, oxidative stress, tissue injury/repair, alarm anti-protease, anti-microbial defense, epithelial barrier function, and epigenetic modification were observed between the flavors, nicotine content, and/ or lung models (bronchial or alveolar). Our findings indicate that ECIG toxicity is influenced by combination of multiple factors including flavor, nicotine content, vaping regime, and the region of respiratory tree (bronchial or alveolar). Toxic chemicals and flavoring agents detected in high concentrations in the E-smoke of each flavor warrant independent evaluation for their specific role in imparting toxicity. Therefore, multi-disciplinary approaches are warranted for comprehensive safety profiling of ECIG.
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- Upadhyay, S, et al.
(author)
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Establishment of Repeated In Vitro Exposure System for Evaluating Pulmonary Toxicity of Representative Criteria Air Pollutants Using Advanced Bronchial Mucosa Models
- 2022
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In: Toxics. - : MDPI AG. - 2305-6304. ; 10:6
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Journal article (peer-reviewed)abstract
- There is mounting evidence that shows the association between chronic exposure to air pollutants (particulate matter and gaseous) and onset of various respiratory impairments. However, the corresponding toxicological mechanisms of mixed exposure are poorly understood. Therefore, in this study, we aimed to establish a repeated exposure setting for evaluating the pulmonary toxicological effects of diesel exhaust particles (DEP), nitrogen dioxide (NO2), and sulfur dioxide (SO2) as representative criterial air pollutants. Single, combined (DEP with NO2 and SO2), and repeated exposures were performed using physiologically relevant human bronchial mucosa models developed at the air–liquid interface (bro-ALI). The bro-ALI models were generated using human primary bronchial epithelial cells (3–4 donors; 2 replicates per donor). The exposure regime included the following: 1. DEP (12.5 µg/cm2; 3 min/day, 3 days); 2. low gaseous (NO2: 0.1 ppm + SO2: 0.2 ppm); (30 min/day, 3 days); 3. high gaseous (NO2: 0.2 ppm + SO2: 0.4 ppm) (30 min/day, 3 days); and 4. single combined (DEP + low gaseous for 1 day). The markers for pro-inflammatory (IL8, IL6, NFKB, TNF), oxidative stress (HMOX1, GSTA1, SOD3,) and tissue injury/repair (MMP9, TIMP1) responses were assessed at transcriptional and/ or secreted protein levels following exposure. The corresponding sham-exposed samples under identical conditions served as the control. A non-parametric statistical analysis was performed and p < 0.05 was considered as significant. Repeated exposure to DEP and single combined (DEP + low gaseous) exposure showed significant alteration in the pro-inflammatory, oxidative stress and tissue injury responses compared to repeated exposures to gaseous air pollutants. The study demonstrates that it is feasible to predict the long-term effects of air pollutants using the above explained exposure system.
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- Ernstgard, L, et al.
(author)
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Acute effects of exposure to vapours of dioxane in humans
- 2006
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In: Human & experimental toxicology. - : SAGE Publications. - 0960-3271 .- 1477-0903. ; 25:12, s. 723-729
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Journal article (peer-reviewed)abstract
- Information on the acute effects associated with the handling of 1,4-dioxane is sparse. Our aim was to evaluate the acute effects of 1,4-dioxane vapours. In a screening study, six healthy volunteers rated symptoms on a visual analogue scale (VAS), while exposed to stepwise increasing levels of 1,4-dioxane, from 1 to 20 ppm. The initial study indicated no increased ratings at any of the exposure levels; we decided to use 20 ppm (72 mg/m3) as a tentative no observed adverse effect level (NOAEL). In the main study, six female and six male healthy volunteers were exposed to 0 (control exposure) and 20 ppm 1,4-dioxane vapour, for 2 hours at rest. The volunteers rated 10 symptoms on VAS before, during, and after the exposure. Blink frequency was monitored during exposure. Pulmonary function, and nasal swelling, was measured before, and at 0 and 3 hours after exposure. Inflammatory markers in plasma (C-reactive protein, and interleukin-6) were measured before and at 3 hours after exposure. In conclusion, exposure to 20 ppm 1,4-dioxane for 2 hours did not significantly affect symptom ratings, blink frequency, pulmonary function, nasal swelling, or inflammatory markers in the plasma of the 12 volunteers in our study.
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| 19. |
- Ernstgard, L, et al.
(author)
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Down-regulation of the inflammatory response after short-term exposure to low levels of chemical vapours
- 2019
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In: Occupational and environmental medicine. - : BMJ. - 1470-7926 .- 1351-0711. ; 76:7, s. 482-487
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Journal article (peer-reviewed)abstract
- To investigate the relation between signs and symptoms of irritation and biomarkers of inflammatory markers in blood in healthy volunteers exposed to different chemical vapours for 2 or 4 hours in an exposure chamber.MethodsThe investigated chemicals were: acetic acid (5 and 10 ppm), acrolein (0.05 and 0.1 ppm), 1,4-dioxane (20 ppm), n-hexanal (2 and 10 ppm), hydrogen peroxide (0.5 and 2.2 ppm), 2-propanol (150 ppm), m-xylene (50 ppm), standard and dearomatised white spirit (100 and 300 mg/m3). C reactive protein (CRP), serum amyloid A protein and interleukin 6 were measured in plasma immediately before and 2 or 4 hours after the exposures. Symptoms were rated from 0 to 100 mm in Visual Analogue Scales and covered 10 questions whereof four related to irritation: discomfort in the eyes, nose and throat and dyspnoea. The effect measurements included blink frequency by electromyography, nasal swelling by acoustic rhinometry and lung function by spirometry.ResultsLogistic quantile regression analyses revealed no significant associations except a negative relation between ratings of irritation and CRP.ConclusionThe results suggest a down-regulation of CRP after short-term exposure to low levels of vapours of irritating chemicals. This response might be mediated by the cholinergic anti-inflammatory pathway and further studies are recommended in order to refute or confirm this hypothesis.
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| 22. |
- Ernstgard, L, et al.
(author)
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Liquid-air partition coefficients of 1,1-difluoroethane (HFC152a), 1,1,1-trifluoroethane (HFC143a), 1,1,1,2-tetrafluoroethane (HFC134a), 1,1,1,2,2-pentafluoroethane (HFC125) and 1,1,1,3,3-pentafluoropropane (HFC245fa)
- 2010
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In: Journal of applied toxicology : JAT. - : Wiley. - 1099-1263 .- 0260-437X. ; 30:1, s. 59-62
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Journal article (peer-reviewed)
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| 40. |
- Lorentzen, JC, et al.
(author)
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Chloroanisoles and Chlorophenols Explain Mold Odor but Their Impact on the Swedish Population Is Attributed to Dampness and Mold
- 2020
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In: International journal of environmental research and public health. - : MDPI AG. - 1660-4601. ; 17:3
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Journal article (peer-reviewed)abstract
- We recently reported that mold odor may be explained by chloroanisoles (CAs) formed by microbial biotransformation of chlorophenols (CPs) in legacy wood preservatives. Here we examine psychophysical aspects of CAs and trace their historic origins in buildings. Our exposure of healthy volunteers shows that 2,4,6-triCA is often perceived as unpleasant, characterized as musty or moldy and is detected at 13 ng/m3 or lower. Similar concentrations are reported in buildings with odor complaints. Scrutiny of written records reveal that new building construction methods were introduced in the 1950s, namely crawlspaces and concrete slabs on the ground. These constructions were prone to dampness and attack from wood decay fungi, prompting chemical companies and authorities to advocate preservatives against rot. Simultaneously, CPs became household chemicals used for example in indoor paints. When large-scale odor problems evolved, the authorities that once approved the preservatives attributed the odor to hidden mold, with no evidence that substantial microbial biomass was necessary for odor formation. Thereby the public remained unaware of problematic exposure to CPs and CAs. We conclude that the introduction of inappropriate designs of house foundations and CP-based preservatives once ignited and still provide impetus for indoor air research on “dampness and mold”.
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