Pesticides and Skin Diseases in Man - Pesticides: Evaluation of Environmental Pollution - page 532

16.5.4 Allergic Contact Dermatitis
When analyzing the data on contact allergy (CA) and allergic contact dermatitis (ACD)
to pesticides, one must not forget the difference between these two terms, which are
too frequently mixed up—contact allergy (synonym: contact hypersensitivity) and allergic
contact dermatitis (synonym: allergic contact eczema). CA is the body's readiness to
develop an inflammatory reaction against specific haptens (low-molecular-weight chemicals).
This state of hypersensitivity is acquired during previous skin exposures to the hapten.
The presence of altered immune reactivity does not necessarily imply the existence of any
disease. A group of people with CA will never develop clinical symptoms. Among those
symptomatic, a vast majority will indeed develop the inflammatory skin disease—ACD;
however, some sensitized people may also develop allergic contact stomatitis, conjuncti-
vitis, urticaria, asthma, allergic rhinitis, or systemic reactions (Spiewak 2008). Typically,
numerous exposures are necessary to induce hypersensitivity to haptens (Vandenberg
and Epstein 1963). The duration of this induction phase depends on the individual
predisposition of the exposed person and the sensitizing potency of the hapten (Schlede
et al. 2003; Basketter et al. 2006). Some pesticides are potent sensitizers; parathion was
even utilized as a model hapten in animal studies (Lisi et al. 1987). Strong-to-extreme
sensitizing potency in animal models was also reported for maneb, mancozeb, zineb,
and benomyl (Matsushita et al. 1976, 1977). This property is reflected in the reports
on “epidemics” of ACD among farmers caused by nematin (Helmdach and Schlenzka
1984), 2,4-dichloro-6-(o-chloroanilino)-s-triazine anilazine (Schuman and Dobson 1985),
and propargite (Saunders et al. 1987). In Japan, out of 815 pesticide-related diseases and
poisonings registered from 1968 to 1970, ACD was diagnosed in 34% (Matsushita et al.
1980). Among all the occupational dermatoses compensated by the Polish Farmers' Social
Insurance Fund, 18% were caused by pesticides (Spiewak 2003). In a study of Taiwanese
fruit farmers spraying pesticides on a regular basis, contact hypersensitivity to pesticides
was found in 40% and clinical symptoms of contact dermatitis was found in 30% (Guo et al.
1996). An anecdotal yet striking report suggests that susceptibility to pesticide sensitiza-
tion might be race-dependent: in a Californian flower plantation, all seven coworkers of
Japanese ancestry developed ACD to benomyl, while all ten Mexican coworkers remained
unaffected. Moreover, one Japanese volunteer in the control group developed positive
reaction to benomyl, while two Caucasians remained negative (Savitt 1972).
The above observations indicate that CA and ACD to pesticides are a relevant problem.
However, prophylactic screening and further diagnosis of pesticide-related contact derma-
titis is complicated by the dynamic changes in pesticide use in agriculture, industry, and
households. New pesticides are continuously allowed while old ones are being withdrawn
from the market. However, even if a pesticide is no longer on the market, sensitization
of humans may persist for years and decades, eventually to reappear as cross-reactivity
with a new pesticide structurally related to the primary sensitizer (Matsushita et al. 1976;
Matsushita and Aoyama 1981; Peluso et al. 1991; Koch 1996). Numerous products of daily
use (rubber, medications, housekeeping products) contain pesticides or chemically related
substances that may provoke relapses of the disease. Allergizing properties may be due to
pesticides themselves or due to additives such as emulgators or preservatives. Skin reac-
tions may be provoked by degradation products of the active substances or additives, as
in the case of workers sorting potatoes previously treated with metham sodium (sodium
N-methyl dithiocarbamate), which underwent hydrolytic decomposition to form sensitiz-
ing methyl isothiocyanate (Schubert et al. 1993). The diagnosis should be based on clini-
cal symptoms, history of exposure, and positive patch test reaction with the substance in