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An investigation of cell wall micropore blocking as a possible mechanism for the decay resistance of anhydride modified wood.

Hill, Callum A S; Forster, S C; Farahani, M R M; Hale, M D C; Ormondroyd, G A; Williams, G R

Authors

Callum A S Hill

S C Forster

M R M Farahani

M D C Hale

G A Ormondroyd

G R Williams



Abstract

Corsican pine (Pinus nigra) sapwood was chemically modified with acetic, or hexanoic anhydride to a variety of weight percentage gains. The cell wall microporosity of the wood before and after chemical modification was determined using the technique of solute exclusion. The results showed that the cell wall microporosity decreased as the level of substitution increased, but the cell wall remained accessible at high levels of substitution. Values of the fibre saturation point (FSP) calculated from solute exclusion data ranged from c. 40% (for unmodified wood) to c. 20% at approx. 25% weight percentage gain, but were dependent to some degree upon the calculation method. Evidence is presented suggesting that the reduction in FSP may be attributable to bulking of the cell wall by bonded acyl adduct. It is concluded that the level of hydroxyl substitution in the cell wall is not the primary mechanism for giving decay protection in anhydride-modified wood.

Citation

Hill, C. A. S., Forster, S. C., Farahani, M. R. M., Hale, M. D. C., Ormondroyd, G. A., & Williams, G. R. (2005). An investigation of cell wall micropore blocking as a possible mechanism for the decay resistance of anhydride modified wood. International biodeterioration & biodegradation, 55, 69-76. https://doi.org/10.1016/j.ibiod.2004.07.003

Journal Article Type Article
Publication Date Jan 1, 2005
Deposit Date May 27, 2008
Electronic ISSN 0964-8305
Publisher Elsevier
Peer Reviewed Peer Reviewed
Volume 55
Pages 69-76
DOI https://doi.org/10.1016/j.ibiod.2004.07.003
Keywords Wood; Acetylation; Decay resistance; Solute exclusion; Fibre saturation point;
Public URL http://researchrepository.napier.ac.uk/id/eprint/1907
Publisher URL http://dx.doi.org/10.1016/j.ibiod.2004.07.003