Utskrift
Utendørs trekonstruksjoner må beskyttes mot vær og vind. Hovedutfordringen er at de fleste norske treslag er svært lite motstandsdyktige mot nedbrytning. Det finnes i hovedsak fem prinsipper for trebeskyttelse: utnyttelse av trevirkets naturlige holdbarhet, konstruktiv trebeskyttelse, bruk av impregnerte trematerialer, bruk av modifiserte trematerialer og overflatebehandling.
Lone Ross
Avdelingsleder/forskningssjef
-
Divisjon for skog og utmark
(+47) 911 97 268 lone.ross@nibio.no Kontorsted: Ås - Bygg H8
Utendørs testing av tre i Norge er tidkrevende på grunn av klimaet. NIBIO har mange utendørs feltforsøk, som bidrar til økt kunnskap om holdbarhet til tre, og feltene evalueres 1-2 ganger pr år. Felttestene gir resultater som er grunnlaget for holdbarhetsklassifisering av norske treslag benyttet i applikasjoner slik som ytterkledning, terrassedekker og i jordkontakt. Testing viser så langt at den naturlige holdbarheten er lav for eksempelvis lønn, lind, osp, bjørk, or, rogn og selje. Den arten som har vist størst motstand mot råte i felttestene er einer.
I laboratoriene ved NIBIO utføres det en rekke standardiserte og modifiserte tester med hensyn til holdbarhet av tre. Laboratorietesting går raskere enn felttesting, men kan aldri erstatte en reell brukssituasjon. Imidlertid er testing i laboratoriet et viktig supplement som kan gi raske og gode svar på detaljerte problemstillinger. Impregneringsmidler forbedrer den naturlige holdbarheten til tre ved å hindre at treet angripes av sopp og insekter, og dermed får trevirket lengre levetid. De ulike impregneringsmidlene påvirker selve produktegenskapene til treproduktene.
Acetylated wood is a durable and dimensionally stable product with many potential applications in exterior timber structures. Research has shown that acetylated wood can be effectively bonded by various adhesive types. However, one of the most commonly used adhesives for timber constructions, melamine urea formaldehyde (MUF), shows poor performance in combination with acetylated wood in delamination tests based on cyclic wetting and drying. The hydrophobic acetylated wood surface leads to reduced adhesion due to poorer adhesive wetting and fewer chemical bonds between the resin and the wood polymers. The use of a resorcinol-formaldehyde (RF)-based primer on the acetylated wood surface prior to the application of MUF leads to positive gluing results with both acetylated radiata pine and beech, providing significantly improved resistance to delamination. Radial penetration of the primer and MUF in acetylated wood shows higher penetration compared with untreated wood. In addition, a phenol resorcinol-formaldehyde adhesive system showed high resistance against delamination and can be used for gluing of acetylated wood.
The effect of wood modification on wood-water interactions in modified wood is poorly understood, even though water is a critical factor in fungal wood degradation. A previous review suggested that decay resistance in modified wood is caused by a reduced wood moisture content (MC) that inhibits the diffusion of oxidative fungal metabolites. It has been reported that a MC below 23%–25% will protect wood from decay, which correlates with the weight percent gain (WPG) level seen to inhibit decay in modified wood for several different kinds of wood modifications. In this review, the focus is on the role of water in brown rot decay of chemically and thermally modified wood. The study synthesizes recent advances in the inhibition of decay and the effects of wood modification on the MC and moisture relationships in modified wood. We discuss three potential mechanisms for diffusion inhibition in modified wood: (i) nanopore blocking; (ii) capillary condensation in nanopores; and (iii) plasticization of hemicelluloses. The nanopore blocking theory works well with cell wall bulking and crosslinking modifications, but it seems less applicable to thermal modification, which may increase nanoporosity. Preventing the formation of capillary water in nanopores also explains cell wall bulking modification well. However, the possibility of increased nanoporosity in thermally modified wood and increased wood-water surface tension for 1.3-dimethylol-4.5-dihydroxyethyleneurea (DMDHEU) modification complicate the interpretation of this theory for these modifications. Inhibition of hemicellulose plasticization fits well with diffusion prevention in acetylated, DMDHEU and thermally modified wood, but plasticity in furfurylated wood may be increased. We also point out that the different mechanisms are not mutually exclusive, and it may be the case that they all play some role to varying degrees for each modification. Furthermore, we highlight recent work which shows that brown rot fungi will eventually degrade modified wood materials, even at high treatment levels. The herein reviewed literature suggests that the modification itself may initially be degraded, followed by an increase in wood cell wall MC to a level where chemical transport is possible.
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One way to protect timber in service against basidiomycete deterioration is by means of acetylation via reaction with acetic anhydride. The reason why acetylated wood (WAc) is resistant against decay fungi is still not exactly understood. The aim of this study was to contribute to this field of science, and Postia placenta colonisation after 4, 12, 20, 28 and 36 weeks was observed at Three acetylation levels of Pinus spp. sapwood. Mass loss (ML) and wood moisture content (MC) data reflected the acetylation levels. The initial equilibrium MC (EMC) proved to be a good indicator of subsequent ML. Genomic DNA quantification showed P. placenta colonisation in all samples, also in samples where no ML were detectable. The number of expressed gene transcripts was limited, but the findings supported the results of previous studies: WAc seems to have some resistance against oxidative mechanisms, which are part of the metabolism of P. placenta. This leads to a delay in decay initiation, a delay in Expression of genes involved in enzymatic depolymerisation, and a slower decay rate. The magnitudes of these effects are presented for each acetylation level. The data also imply that there is no absolute decay threshold at high acetylation levels, but instead a significant delay of decay initiation and a slower decay rate.
