Immunosuppressive environmental chemicals may increase the potency of
allergens and thereby play a role in the development of allergic diseases. This study's primary objective was to examine the mechanisms behind the relationship between allergic diseases and the immunosuppression induced by some environmental chemicals. We focused on the modulation of allergic potential in vitro and in mice by the organophosphorus
pesticide O,O-diethyl-O-4-nitrophenyl-thiophosphate (
parathion) and the organochlorine
pesticide 1,1,1-trichloro-2,2-bis(4-methoxy-phenyl)ethane (
methoxychlor), with respect to the T(H)1-type
allergen 2,4-dinitrochlorobenzene (
DNCB) and the T(H)2-type
allergen trimellitic anhydride (TMA). Mice (4-week-old) were orally administered
parathion or
methoxychlor. Four weeks after the final dosing, the mice were sensitized to
DNCB or TMA, and T-lymphocyte proliferation measured in their (using a local lymph node assay [LLNA]). In addition, we analyzed T-lymphocytes via
surface antigen expression and local
cytokine production in auricular lymph nodes
after treatment with 0.1%
DNCB or 0.3% TMA. The estimated concentration of
DNCB and TMA to yield a stimulation index (SI) of cell proliferation of three decreased markedly in
parathion- and
methoxychlor-pre-treated mice.
Pesticide pre-treatment induced marked increases in the number of helper and cytotoxic T-cells, levels of T(H)1 and T(H)2
cytokines, and gene expression in lymph node cells. According to our results, T(H)1- and T(H)2-type
allergies are aggravated by prior exposure to immunosuppressive environmental chemicals.