Epidemiological studies have demonstrated an association between use o
f carbamate insecticides, including carbaryl, and increased incidence
of allergic asthma in farmers. In this study the effect of oral carbar
yl exposure on the development of allergic responses to house dust mit
e (HDM) was examined in female Brown Norway rats. Rats were gavaged fo
r 2 weeks with 0, 2, 10, or 50 mg/kg/day of carbaryl. They were sensit
ized with a subcutaneous injection of HDM in aluminum hydroxide adjuva
nt 3 days after the beginning of carbaryl exposure and challenged with
antigen via the trachea 1 day after the final carbaryl ingestion. Two
days after challenge, antigen-specific cell proliferation in pulmonar
y lymph nodes was significantly higher in the 50 mg/kg group than in c
ontrols, while antigen-specific splenocyte proliferation was decreased
in groups dosed with 2, 10, and 50 mg/kg carbaryl. Total protein and
lymphocyte number in bronchoalveolar lavage (BAL) fluid were also incr
eased in the 50 mg/kg group. By 7 days after challenge, immune-mediate
d pulmonary inflammation (eosinophils), antigen-specific immunoglobuli
n (Ig)E level in serum, and antigen-specific IgE and IgA levels in BAL
fluid were significantly elevated in the 50 mg/kg group. No apparent
change was observed for lactate dehydrogenase and eosinophil peroxidas
e in BAL fluid, while the number of BAL macrophages were decreased in
groups dosed with 10 and 50 mg/kg carbaryl. The results suggest that c
arbaryl may cause systemic immune suppression, while enhancing pulmona
ry allergic responses to house dust mite antigen, (C) 1998 Society of
Toxicology.