| 1. |
- Ekberg, Olle, et al.
(författare)
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Investigating the presence of mold in wood treated with chlorophenol
- 2020
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Ingår i: 12th Nordic Symposium on Building Physics (NSB 2020). - : EDP Sciences. - 2555-0403. ; 172
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Konferensbidrag (refereegranskat)abstract
- A common moisture-related problem in Sweden and other countries, is mold odor indoors. The general perception is that mold odor indicates hazardous hidden mold. However, some grey literature studies indicate that the source of mold odor might not be substantial amounts of mold, but rather chloroanisoles (CAs) which are biomethylated from chlorophenols (CPs) in moist conditions. Products containing CPs were commonly used world-wide as wood preservatives in the 1960-70s and problems with indoor mold odor have been reported in buildings where such products have been used. In Sweden, one of the main uses of CPs in buildings was in wooden constructions exposed to big moisture loads, such as sill plates and crawl space ceilings. Here we aimed to determine the potential presence and level of mold growth on wood treated with CPs in one school building with reported odor problems built in the stated time period. Odorous wooden samples were taken and analyzed for mold growth. No mold was detected by the naked eye, but some growth was seen using a microscope. We presently investigate more schools and samples, but so far our results question that mold odor depends on substantial amounts of mold.
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| 2. |
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| 3. |
- Guo, Jian Ping, et al.
(författare)
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Profound and paradoxical impact on arthritis and autoimmunity of the rat antigen-presenting lectin-like receptor complex
- 2008
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Ingår i: Arthritis and Rheumatism. - : Wiley. - 0004-3591 .- 1529-0131. ; 58:5, s. 1343-1353
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: The antigen-presenting lectin-like receptor complex (APLEC) was recently identified as a genetic determinant for arthritis susceptibility. We undertook this study to define mechanisms underlying the impact of APLEC on arthritis, to determine whether sex effects occur, and to determine whether APLEC influences different types of arthritis and phenotypes other than susceptibility. METHODS: Arthritis-susceptible DA rats were compared with sex-matched congenic rats in which APLEC alleles were substituted with alleles from arthritis-resistant PVG rats. Six different arthritogenic agents were injected at the base of the tail: Freund's incomplete adjuvant, pristane, squalene, killed mycobacteria, yeast beta-glucan, or rat type II collagen (CII). Arthritis was visually scored, body weight was measured, and anti-CII IgG and cytokine messenger RNA (mRNA) levels were determined by enzyme-linked immunosorbent assay and reverse transcription-polymerase chain reaction, respectively. RESULTS: In 5 models of rheumatoid arthritis (RA), congenic rats deviated profoundly from DA rats by having reduced arthritis susceptibility, delayed onset, decreased severity, and/or reduced body weight loss. Paradoxical opposite genetic effects were noted, including a more severe disease course in congenic males in pristane-induced arthritis and decreased clinical signs in collagen-induced arthritis despite increased autoantibody levels. Interestingly, the anti-CII IgG isotype profile was skewed in congenic rats, and markedly reduced lymph node mRNA levels for interleukin-17 suggested that the cytokine profile of autoreactive T helper cells was also skewed in a less pathogenic direction. CONCLUSION: Rat APLEC regulates autoimmunity and multiple phenotypes in several types of arthritis. However, delineating the genetic impact may require stratification for sex or mode of arthritis induction. This pathogenetic complexity should be considered when evaluating APLEC in inflammatory and autoimmune diseases, including RA.
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| 4. |
- Gustafsson, Åsa, et al.
(författare)
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Genetic variation influences immune responses in sensitive rats following exposure to TiO2 nanoparticles
- 2014
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Ingår i: Toxicology. - : Elsevier. - 0300-483X .- 1879-3185. ; 326, s. 74-85
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- This study examines the immunological responses in rats following inhalation to titanium dioxide nanoparticles (TiO2 NPs), in naïve rats and in rats with induced allergic airway disease. The responses of two different inbred rat strains were compared: the Dark Aguoti (DA), susceptible to chronic inflammatory disorders, and the Brown Norwegian (BN), susceptible to atopic allergic inflammation. Naïve rats were exposed to an aerosol of TiO2 NPs once daily for 10 days. Another subset of rats was sensitized to the allergen ovalbumin (OVA) in order to induce airway inflammation. These sensitized rats were exposed to TiO2 NPs before and during the allergen challenge. Naïve rats exposed to TiO2 NPs developed an increase of neutrophils and lymphocytes in both rat strains. Airway hyperreactivity and production of inflammatory mediators typical of a T helper 1 type immune response were significantly increased, only in DA rats. Sensitization of the rats induced a prominent OVA-specific-IgE and IgG response in the BN rat while DA rats only showed an increased IgG response. Sensitized rats of both strains developed airway eosinophilia following allergen challenge, which declined upon exposure to TiO2 NPs. The level of neutrophils and lymphocytes increased upon exposure to TiO2 NPs in the airways of DA rats but remained unchanged in the airways of BN rats. In conclusion, the responses to TiO2 NPs were strain-dependent, indicating that genetics play a role in both immune and airway reactivity. DA rats were found to be higher responder compared to BN rats, both when it comes to responses in naïve and sensitized rats. The impact of genetically determined factors influencing the inflammatory reactions pinpoints the complexity of assessing health risks associated with nanoparticle exposures.
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| 5. |
- Gustafsson, Åsa, 1975-
(författare)
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Nanomaterials : respiratory and immunological effects following inhalation of engineered nanoparticles
- 2014
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Background Nanotechnology is an important and promising field that can lead to improved environment and human health and contribute to a better social and economic development. Materials in nanoscale have unique physiochemical properties which allow for completely new technical applications. Enlarged surface area and properties due to quantum physics are among the properties that distinguish the nanoscale. Nano safety has evolved as a discipline to evaluate the adverse health effects from engineered nanomaterials (ENMs). The prevalence of allergic diseases is increasing in the society. An additional issue is the influence of inherited factors on the health responses to ENMs. The aim of this thesis was to investigate the respiratory, inflammatory, and immunological effects following inhalation of ENMs; both sensitive and genetically susceptible individuals were used. Sensitive individuals refer to individuals with pre-existing respiratory diseases, such as allergic asthma, and genetically susceptible individuals refer to individuals prone to autoimmune and allergic diseases. Methods In vivo models of mice and rats were used. In study I the inflammatory and immune responses following exposure to titanium dioxide nanoparticles (TiO2 NPs) were investigated. The effect of when the TiO2 NP exposure occurs during the development of allergic airway inflammation was investigated in study II, with regards to respiratory, inflammatory, and immune responses. In study III, the influence of the genetics on the respiratory, inflammatory, and immune responses, following TiO2 NP exposure to naïve and sensitive rats was evaluated. In study IV, the inflammatory and immune responses of naïve mice and mice with an allergic airway inflammation were studied in lung fluid and lymph nodes draining the airways following inhalation to hematite NPs (α-Fe2O2).Results Exposure to TiO2 NPs induced a long-lasting lymphocytic response in the airways, indicating a persistent immune stimulation. The dose and timing of TiO2 NP exposure affected the airway response in mice with allergic airway disease. When the mice were exposed to particles and an allergen during the same period, a decline in general health was observed. By comparing different inbred rat strains it was demonstrated that genetically determined factors influence the immune and respiratory responses to TiO2 NP exposure in both naïve and sensitive individuals. Exposure to hematite NPs resulted in different cellular responses: naïve mice had increased numbers of cells while mice with allergic airway inflammation had decreased cell numbers in BALF. Analogous cell responses were also observed in the lung draining lymph nodes.Conclusion Altogether, this thesis emphasises the complexity of assessing health risks associated with nanoparticle exposure and the importance of including sensitive populations when evaluating adverse health effects of ENMs.
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| 6. |
- Gustafsson, Åsa, et al.
(författare)
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Strain differences influence timing and magnitude of both acute and late inflammatory reactions after intratracheal instillation of an alkylating agent in rats
- 2014
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Ingår i: Journal of Applied Toxicology. - : John Wiley & Sons. - 0260-437X .- 1099-1263. ; 34:3, s. 272-280
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Tidskriftsartikel (refereegranskat)abstract
- The acute pulmonary responses after exposure to sulfur and nitrogen mustards are well documented whereas the late pulmonary effects are not. With a novel focus on the immune system this paper investigate whether late phase pulmonary effects developed in rats exposed to the nitrogen mustard melphalan are linked to the acute responses and whether the reactions are genetically regulated. The DA rat strain was used to establish a lung exposure model. Five other inbred rat strains (PVG, PVG.1AV1, LEW, WF and F344) were compared within the model at selected time points. All rat strains displayed a biphasic pattern of leukocyte infiltration in the lungs, dominated by neutrophils 2days after exposure and a second peak dominated by macrophages 29days after exposure. The number of macrophages was higher in the DA rat compared with the other strains. The infiltration of lymphocytes in the lungs varied in both time of appearance and magnitude between strains. The quantity of collagen deposition in the lungs varied between strains at day 90; LEW and WF displayed high collagen content which coincided with an increased level of cytotoxic T cells. LEW further displayed an increased number of T helper cells and natural killer (NK) T cells in the lungs. The results in this study suggest there is a link between the development of lung fibrosis and high cytotoxic cell responses and that there is a genetic influence, as there are variations in acute and late adverse reactions between rat strains in both timing and magnitude.Copyright (c) 2013 John Wiley & Sons, Ltd.
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| 7. |
- Holmdahl, Rikard, et al.
(författare)
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Arthritis induced in rats with non-immunogenic adjuvants as models for rheumatoid arthritis
- 2001
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Ingår i: Immunological Reviews. - : Wiley. - 1600-065X .- 0105-2896. ; 184
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Forskningsöversikt (refereegranskat)abstract
- Rat models are useful for studies of the pathogenesis of rheumatoid arthritis (RA) since rats are extraordinarily sensitive to induction of arthritis with adjuvants. Injection of not only the classical complete Freund's adjuvant but also mineral oil without mycobacteria and pure adjuvants such as pristane and squalene, induce severe arthritis in many rat strains. Models like pristane-induced arthritis in rats are optimal models for RA since they fulfill the RA criteria including a chronic relapsing disease course. Arthritogenic adjuvants like pristane, avridine, squalene and mineral oil are not immunogenic since they do not contain major histocompatibility complex (MHC) binding peptides. Nevertheless, the diseases are MHC-associated and dependent on the activation of alphabetaTCR (T-cell receptor)-expressing T cells. However, it has not been possible to link the immune response to joint antigens or other endogenous components although immunization with various cartilage proteins induce arthritis but with different pathogeneses. To unravel the mechanisms behind adjuvant-induced arthritis, a disease-oriented genetic approach is optimal. Several loci that control onset of arthritis, severity and chronicity of the disease have been identified in genetic crosses and most of these have been confirmed in congenic strains. In addition, many of these loci are found in other autoimmune models in the rat as well as associated with arthritis in mice and humans.
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| 8. |
- Juran, Stephanie A, et al.
(författare)
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Odor thresholds for 2,4,6 -trichloroanisole reviewed in the context of indoor air quality
- 2015
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Ingår i: Proceedings - Healthy Buildings 2015 America: Innovation in a Time of Energy Uncertainty and Climate Adaptation, HB 2015. - : International Society of Indoor Air Quality and Climate. - 9781510821286 ; , s. 415-418
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Konferensbidrag (refereegranskat)abstract
- Chloroanisoles have received minimal attention in research on indoor air quality (IAQ) although they can affect comfort and maybe also health when levels are sufficiently high to evoke malodor. Here, we review the literature for odor thresholds (OT) for 2,4,6-trichloroanisole to estimate at which concentrations air is perceived as malodorous, and discuss the caveats in measuring and comparing OTs. In general, reported OTs for 2,4,6-trichloroanisole are extremely low but still in the range measured in indoor air of problem buildings, as we reported recently (Lorentzen et. al., 2015). However, OTs vary considerably due to methodological constraints such as different methods of stimulus presentation. Only one study (not published in a peer reviewed journal) reports OTs in air, and the data suggest that 2,4,6-trichloroanisole can be among the most potent microbial odors. Additional studies are therefore warranted. It will also be important in future studies to investigate the perceived odor quality of CAs in the context of IAQ problems with dampness and mold.
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| 9. |
- Larsson, E, et al.
(författare)
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Corticosteroid treatment of experimental arthritis retards cartilage destruction as determined by histology and serum COMP
- 2004
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Ingår i: Rheumatology. - : Oxford University Press (OUP). - 1462-0332 .- 1460-2172 .- 1462-0324. ; 43:4, s. 428-434
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Tidskriftsartikel (refereegranskat)abstract
- Objective. To examine if changes in serum cartilage oligomeric matrix protein (COMP) correlate with the development of cartilage damage, as measured by histological grading, in corticosteroid-treated animals with collagen-induced arthritis (CIA). Methods. DA rats with established CIA were treated with corticosteroids (betamethasone, 0.1 mg/kg body weight) or placebo (saline) intraperitoneally once daily after reaching an arthritis score exceeding 1. The treatment continued throughout the study. Arthritis progression was monitored by clinical scoring of paws, serial measurements of serum COMP and fibrinogen, and histological grading of paws. Results. Corticosteroid treatment reduced clinical signs of arthritis compared with placebo (arthritis score reduced, P < 0.01 at day 25). Corticosteroid treatment also reduced fibrinogen levels compared with placebo (P < 0.01). The morphological changes in the joint were less severe in the corticosteroid-treated animals (median cartilage score 4 in the placebo group, 0 in the corticosteroid-treated group; P < 0.01). The levels of COMP remained unchanged during treatment in the corticosteroid-treated arthritic animals, whereas an increase in levels of COMP was observed in rats treated with placebo (P < 0.01). There was a correlation between serum COMP and the extent of cartilage destruction at day 25 after immunization (r=0.77, P < 0.001). Conclusions. Corticosteroids given therapeutically to arthritic rats diminish joint destruction histologically, and stable serum COMP levels reflect this effect.
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