CUTANEOUS BARRIER FUNCTION AFTER COLD-EXPOSURE IN HAIRLESS MICE - A MODEL TO DEMONSTRATE HOW COLD INTERFERES WITH BARRIER HOMEOSTASIS AMONGWORKERS IN THE FISH-PROCESSING INDUSTRY
L. Halkiersorensen et al., CUTANEOUS BARRIER FUNCTION AFTER COLD-EXPOSURE IN HAIRLESS MICE - A MODEL TO DEMONSTRATE HOW COLD INTERFERES WITH BARRIER HOMEOSTASIS AMONGWORKERS IN THE FISH-PROCESSING INDUSTRY, British journal of dermatology, 132(3), 1995, pp. 391-401
Dry skin and eczema only seldomly occur in workers in the Danish fish-
processing industry (FPI) during work, when their fingers and palms ha
ve a low skin surface temperature, low transepidermal water loss (TEWL
), and a high capacitance. However, shortly after work, when the skin
temperature has become normal, TEWL levels increase to above normal, a
nd capacitance decreases to below normal, followed by the development
of dry skin or chapping, which subsequently revert to normal over a pe
riod of hours. These observations suggest that workers in the FPI may
have a defect in skin barrier function, which is, however, masked by a
low skin temperature, resulting in misleadingly low TEWL levels durin
g work. To test this hypothesis, we disrupted the permeability barrier
in hairless mice with topical acetone, and exposed the treated skin t
o ice for 3 . 5 h. Although TEWL rates immediately after cold exposure
were low, suggesting normal barrier recovery, TEWL increased to level
s slightly above pre-cold exposure levels (i.e. levels just after the
barrier was disrupted with acetone) when the skin temperature reverted
to normal (greater than or equal to 15 min). The changes in TEWL were
paralleled by equivalent changes in percutaneous penetration of the e
lectron-dense tracer lanthanum nitrate. This indicates that cold masks
a defective barrier, and inhibits barrier repair. After a few hours a
t ambient temperatures, normal barrier recovery was observed. Electron
microscopy revealed empty or partially empty lamellar bodies during t
he first 30 min post-cold exposure. After Ih the majority of nascent L
Bs displayed normal morphology. Moreover, histochemical studies showed
a delayed reappearance of stratum corneum intercellular lipids follow
ing cold exposure. These results demonstrate that cold exposure preven
ts barrier recovery after acetone disruption, and provide an explanati
on for the occupatonal dermatosis observed in the fish-processing indu
stry and related occupations.