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NEWS & INFORMATION
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Source To Surgery - January 1996, Vol. 4 Issue I
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Contact Dermatitis Due to Chemical Hypersensitivity
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Kevin J. Kelly, MD., Associate Professor of Pediatrics & Medicine
Medical College of Wisconsin and Children's Hospital of Wisconsin, Milwaukee, USA
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Previous articles have concentrated on the emergence, prevalence and understanding of
latex protein allergy. However, contact dermatitis from chemicals in natural rubber
latex products remains an even more important cause of disability and loss of work. Type IV
cell-mediated delayed hypersensitivity is a common adverse reaction to natural rubber
latex (NRL) products manifested as contact dermatitis of the skin. This problem is more
common than IgE antibody-mediated Type I immediate hypersensitivity to N~L although it
may precede this problem in up to 40% of individuals with latex protein allergy. Acute
contact dermatitis is due to an immunological reaction to a residual chemical leached from the
finished latex products. The chemical involved penetrates the skin, and is
ingested and processed by dermal macrophage (Langerhans Cells). These
cells migrate to regional lymph nodes where T-cells are sensitized and
migrate back to the dermis. Upon second exposure to the chemical, T-
lymphocyte cells and mast cells are activated resulting in vesiculation,
erythema, swelling, cracking and itching of the skin at the site of contact.
This dermatitis frequently extends beyond this area of contact (e.g., the
forearm in a patient wearing a NRL glove). Continued exposure may lead
to chronic dermatitis manifested as dry, irritated, cracked, pruritic skin
with erythema.
Chemical residuals in gloves manufactured from NRL are frequently
responsible for the development of contact dermatitis. These chemicals
used in the manufacture of gloves fall into broad classifications of
accelerators, accelerator activators, stabilizers, antidegradants, retarders,
fillers and extenders. It is the accelerator group chemicals (especially
thiurams and carbamates) that induce the majority of the skin
dermatitis reactions.
A diagnosis is made by a medical history, physical exam, and patch
testing with the offending rubber chemicals. In the past, the FDA has
allowed specific gloves, low in chemical additives, and which passed a
modified Draize test to be labeled as "hypoallergenic." The emergence of
latex protein allergy has rendered this simple labeling process obsolete
and misleading. In addition, the modified Draize test does not always
identify gloves with low levels of chemicals that may induce continued
dermatitis. Specific measurement of extractable residual chemicals is
more desirable since threshold concentrations for developing dermatitis
could be established. However, a physiologic extraction method that
mimics the clinical setting as well as a technique for analytical
measurement of the residual chemical is difficult due to changes in the
configuration of chemicals during manufacture. At the present time,
volatile chemical extractions can be used but use of artificial sweat is
likely to be more desirable.
An understanding of the relationship of chemicals from NRL products to
the development of IgE-mediated protein allergy is incomplete. Whether
chemical sensitivity induces IgE mediated allergy, merely breaking down
the skin allowing proteins access to the immune system, or whether
haptenation or adjuvant activity occurs to increase immediate
hypersensitivity is unknown. Further research will be necessary to clarify
answers to multiple questions surrounding the role of chemical additives
in finished rubber products as producing human disease.
Individuals experiencing recurrent or persistent dermatitis should consult
with their doctor in order to establish a specific diagnosis.
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