Morphological changes in Tencel through crosslinking
Abdullah, Department of Polymer Engineering, National Textile
The crosslinking agents which impart crease resistance to
cellulosic fabrics bring morphological changes to fibres. In
this case the fibrillation tendency of tencel fibres is
greatly modified. Fibrillation not only brings undesirable
difficulties during wet processing it also affects the wear
life of tencel fabric. During washing, the fibrillation
process causes greying and creasing of the fabric, resulting
from the joint action of the washing liquor and abrasion
against the walls of rotating washing drum. Therefore,
abrasion is important consideration in wear life of the
tencel fabrics, and thus tencel garment useful life is
affected in two ways.
- It renders the fabric so hairy/fuzzy that it becomes
- It produces a progressive deterioration in strength until
a level is reached at which the fabric is no longer able to
withstand the stress of usage without rupture.
The mode of fracture of tencel fibres in abrasion was
observed using scanning electron microscopy (SEM). The fibres
rupture by multiple splitting revealing the internal fibrillar
structure of tencel fibres as shown in Figure 1. This rupture
resulted from the tensile stress due to frictional forces. The
particular length of fibres that raised the surface of the
fabric after breakage of individual fibres was much more
vulnerable to further attack by repeated abrasion action.
Multiple cracks along raised fibres indicated the repeated
bending and flexing of fibres, shown Figure 1. Further abrasion
results in rounded fibre ends produced from the multiple split
ends and axially split rounded ends.
Figure 1: Dry abrasion morphology of
untreated sample: (a) multiple split fibre end; (b)
transversely and axially fractured; (c) rounded and
axially split ends; (d) propagation of transverse
There is also some evidence of transverse crack linked by
axial split as shown in Figure 1b. There are usually three
possible combinations of transverse and axial crack as shown in
Figure 2. Axial cracks appear first and thus divide the fibre
into two parts, which break independently, giving the form of
break shown in Figure 2a. Transverse cracks form first and then
join with an axial split (Figure 2b), which then breaks
independently giving form shown in Figure 2c. The propagation of
breaks shown in Figure 1e, and continuation of split suggest
that axial split occurs first.
Figure 2. Three possible
combinations of transverse
and axial cracks.
Morphology of fabric at the breakage point is shown in Figure
3. As fibres in the crowns were broken down in succession, this
not only caused reduction in yarn strength, but also the
frictional forces holding the rest of the fibres together were
reduced; the plucking action pulled the more loosely held end of
the fibre from the yarn body and raised it to the surface of the
fabric. This particular raised length of the fibre was no longer
an effective component of the fabric and was, additionally, more
vulnerable to further abrasive attack. Towards the end point,
the whole yarn structure was pulled out (Figure 3a) and fibre
ends at break appeared mangled, twisted and mashed as shown in
Figure 3b and Figure 3c.
Figure 3. Morphology of fabric at
the breakage point: (a) breakage of yarn; (b) detail of
(a) mangled and axially split fibres; (c) detail of (a)
crushed fibres; (d) smeared fibres at the yarn crown.
During laundering i.e. in wet state it was observed that
fibrillation starts from minor cracks (Figure 4a), which with
further abrasion caused the complete disintegration of fibre
structure (Figure 4b). Macro-fibrils were liberated individually
or in groups held in fibre structure by relatively weak hydrogen
bonding and van der Waals forces. Considerable damage to the
fabric also resulted from creasing. Maximum stresses developed
at the outer curvature of the crease, which rubbed against the
fabric and inner surface of washing drum, caused successive
localized fibrillation as shown in Figure 4d. The fibres which
were pulled out due to the abrasive action of washing drum were
massively fibrillated. The fibre ends also appeared stepped
broke and rounded off as shown in Figure 4e and Figure 4f.
Figure 4. Fibrillation observed in
untreated sample: (a) start of the fibrillation after
first wash; (b) extensive fibrillation; (c) inner side of
the crease; (d) outer side of the crease; (e) stepped
(f) rounded fibre end.
Change in morphology through
Two different resin treated fabrics were examined to see the
effect of crosslinking on morphological behaviour of fibres.
Scanning electron microscopic studies on Fabric A; treated with
50g dm-3 Reaktant DH indicated that the mode of fracture was not
distinctly different from untreated fabric as shown in Figure 5.
The main mode of fracture is multiple splitting of fibres due to
tensile fatigue. However, the surface damage was less pronounced
as the surface resin protected the fibre surface from abrasive
action. Step breakage was also observed as shown in Figure 5b.
According to two possible mechanisms of stepped break, it is not
clear whether two breaks formed and then joined up by an axial
split, or whether the fibre was already split axially into two
parts, which then broke. Further abrasion rounded off the fibre
ends and caused axial splitting as shown in Figure 5c.
Figure 5. Dry abrasion morphology of
Reaktant DH treated sample (a) surface damage and multiply
splitted fibre ends, (b) stepped break, (c) rounded off
and axially splitted fibre ends, (d) detail of fibres at
the breaking point of yarn; mashed, mangled and twisted.
It appears that the main mechanism of failure in Fabric B;
treated with 50g dm-3 Reaktant FC was not rubbing off of the
fibre surface or multiple splitting of fibres, but it was abrupt
rupture of fibres under stress as shown in Figure 6a & 6b.
Figure 6. Fibre fracture observed in Reaktant FC treated
samples: (a) brittle fractures at the crown;
(b) brittle fracture through bending.
Transverse fractures appeared to be brittle fractures; it was
very difficult to draw any conclusion from the side view of
broken fibre ends, but this may be granular fracture. Figure 7
shows an idealized view of granular fracture. When tension
reaches a certain level, elements will begin to break (Figure
7b), but the discontinuity prevents the occurrence of a large
enough stress concentration to cause the crack to continue
propagating across the fibre. However, there is some cohesion
between elements, and excess stress is transferred to
neighbouring elements that are thus more likely to break at a
nearby position. Eventually the failure becomes cumulative over
a cross-section (Figure 7c), and the granular breaks results
Figure 7. (a) Structure of separate
elements, (b) Under tension, elements start to break. (c)
Stress transfer causes cumulative break over a
cross-section. (d) Granular break.
Figure 8 shows the wet mode of fibre fracture in Reaktant DH
and Reaktant FC treated fabrics. Broken ends developed where
fibres were pulled apart leaving frayed fibril bundles as shown
in Figure 8a and Figure 8e. Such damage is typical of wet
abrasion in tencel. Reaktant DH treated fabric showed some
evidence of fibrillation presumably the cumulative swelling and
tearing forces were great enough to tear fibrils and bonded
sheets from the fibres, as shown in Figure 8b. However, the
fibrillation is not strictly fibrillation as observed in
untreated fabric. It seems like peeling away of thick slabs and
ribbons of fibrils from the body of the fibre. Small wedges or
notches at the surface of the fibres (marked by an arrow in
Figure 8c and Figure 8f) indicated the cutting action by the
drum liner. These are potentially the weak regions through which
fibre fracture propagates. In Reaktant FC treated fabric, the
cutting action was progressive and caused removal of fragments
from the surface of the fibres as shown in Figure 8d. The
propagation of fibre rupture by cutting action was also evident
in Figure 10f. In some instances, large segments were peeled
from the fibres revealing the inner fibril structure (Figure
8h), and also skin layer was flaked off showing the resin layer
underneath (Figure 8g). There was no evidence of fibre
fibrillation as observed in the fabric.
Figure 8. Fracture morphology of
Reaktant DH treated fabric: (a) frayed fibril end; (b)
Fibrillation; (c) surface damage through cutting action.
Fracture morphology of Reaktant FC treated fabric: (d)
gradual peeling of thick slab; (e) Frayed fibril end; (f)
propagation of fracture through cutting action; (g) flaked
off fibres; (h) Inner fibril structure of fibre.
The molecular structures introduced into the fibres affect
the fibrillation tendency and mode of fracture of tencel fabric;
however, it is greatly related to the molecular length and
extensibility of the crosslinkages formed in the fibre. The mode
of fracture of Reaktant DH treated fibres was similar to
untreated Tencel fibres because either its monomers were not
able to penetrate far into the fibre interior due to
longer-chain molecule or it formed long-chain crosslinks which
imparted less stiffness to the Tencel fibres compare to
shorter-chain lengths of Reaktant FC crosslinks. When dry
abraded, Reaktant DH treated fibres were multiply splitted,
while Reaktant FC treated fibres were abruptly ruptured. When
wet abraded, in both fabrics fibre ends were pulled apart
leaving frayed fibril ends. However, cutting abrasion action was
more progressive in Reaktant FC treated fabric.