Chemically or physically modified wood materials have enhanced resistance to wood decay fungi. In contrast to treatments with traditional wood preservatives, where the resistance is caused mainly by the toxicity of the chemicals added, little is known about the mode of action of nontoxic wood modification methods. This study reviews established theories related to resistance in acetylated, furfurylated, dimethylol dihydroxyethyleneurea-treated, and thermally modified wood. The main conclusion is that only one theory provides a consistent explanation for the initial inhibition of brown rot degradation in modified wood, that is, moisture exclusion via the reduction of cell wall voids. Other proposed mechanisms, such as enzyme nonrecognition, micropore blocking, and reducing the number of free hydroxyl groups, may reduce the degradation rate when cell wall water uptake is no longer impeded.

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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.

Chemical modification of wood increases decay resistance but the exact mechanisms remain poorly understood. Recently, Ringman and coauthors examined established theories addressing why modified wood has increased decay resistance and concluded that the most probable cause of inhibition and/or delay of initiation of brown-rot decay is lowering the equilibrium moisture content. In another recent study, Jakes and coauthors examined moisture-induced wood damage mechanisms, including decay and fastener corrosion, and observed that these mechanisms require chemical transport through wood cell walls. They proposed that chemical transport within wood cell walls is controlled by a moisture-induced glass transition in interconnected networks of hemicelluloses and amorphous cellulose. This paper shows how these models jointly suggest mechanisms by which wood modifications can inhibit brown-rot. Alternative mechanisms are also discussed. These models can be used to understand and further improve the performance of wood modification systems.

Abstract: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 (W Ac ) 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: W Ac 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.

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Environmental concern regarding the use of toxic preservatives such as chromated copper arsenate (CCA) has been put forward. In the European Union, United States, and Japan, CCA has been phased out for residential and water-contact applications. Ecotoxicological studies of wood treated with conventional preservatives were carried out in the late 1990s, and it was concluded that the main impact is to water and aquatic organisms. Today, alternatives to conventional preservation methods, marketed as "environmentally friendly" or "nontoxic," are emerging. Examples of such alternatives are modified wood, e.g., thermally modified, furfurylated, and acetylated wood. To date, not enough hazard characterization has been performed. In the present study, the Microtox assay with the marine bacterium Vibrio fischeri and the Daphtox procedure with the crustacean Daphnia magna were used as screening methods in an effect assessment. Both organisms were exposed to water leachates from furfurylated wood using two different leaching procedures. The results indicate that Microtox is more sensitive to the toxic components from furfurylated wood than Daphtox. Furthermore, the toxicity of treated Pinus radiata was higher than that of treated Pinus sylvestris. The toxicity did not diminish over the test period, as is the case for preservative-treated wood. The present study found that treatment conditions can influence the toxicity considerably, so toxicity studies should be included in the development of new treatment process. The present study also shows that using an intermediate vacuum-drying step, leading to a more efficient curing/polymerization, results in slightly less hydrophobic oligomers in the product, such that the leachates become less toxic to bacteria.

The furfurylation process is an extensively investigated wood modification process. Furfuryl alcohol molecules penetrate into the wood cell wall and polymerize in situ. This results in a permanent swelling of the wood cell walls. It is unclear whether or not chemical bonds exist between the furfuryl alcohol polymer and the wood. In the present study, five different wood species were used, both hardwoods and softwoods. They were treated with three different furfurylation procedures and leached according to three different leaching methods. The present study shows that, in general, the leachates from furfurylated wood have low toxicity. It also shows that the choice of leaching method is decisive for the outcome of the toxicity results. Earlier studies have shown that leachates from wood treated with furfuryl alcohol prepolymers have higher toxicity to Vibrio fischeri than leachates from wood treated with furfuryl alcohol monomers. This is probably attributable to differences in leaching of chemical compounds. The present study shows that this difference in the toxicity most likely cannot be attributed to maleic acid, furan, furfural, furfuryl alcohol, or 2-furoic acid. However, the difference might be caused by the two substances 5-hydroxymethylfurfural and 2,5-furandimethanol. The present study found no difference in the amount of leached furfuryl alcohol between leachates from furfurylated softwood and furfurylated hardwood species. Earlier studies have indicated differences in grafting of furfuryl alcohol to lignin. However, nothing was found in the present study that could support this. The leachates of furfurylated wood still need to be