Lead (Pb) may alter T-lymphocyte reactivity in situ by preferentially enhancing the development of T-helper 2 (T(H)2)- and inhibiting T(H)1-lymphocyte development. These effects could result in dysregulation of the presence/availability of T(H)1- and T(H)2-associated cytokines. The aim of this study was two-fold, that is, to assess whole blood Pb levels in schoolchildren from Taiwanese communities that varied in degree of potential for Pb exposure and then ascertain if there were relationships between Pb exposure and changes in levels of key T(H)1 and T(H)2 cytokines. Grades 5 and 6 students were selected from four different community schools, i.e., one from: urban area with new homes; urban area with old homes; rural site with old homes; and area located near an oil refinery. Students at each site were further divided into healthy and respiratory allergy subgroups. Blood was collected and whole blood Pb levels and serum interferon (IFN)-γ, interleukin (IL)-12, -4, and -5 levels were determined. The results indicate no differences in whole blood Pb levels (<4 µg/dl) among students from urban and rural sites; these values were similar in the healthy and allergic subjects. Serum T(H)1 and T(H)2 cytokine levels also did not differ among/within the groups. In contrast, refinery children had significantly increased Pb levels (5.2-8.8 µg/dl) relative to any of the other sets' levels. Of these, children with allergies had serum T(H)2 cytokine levels significantly higher and T(H)1 cytokine levels significantly lower than their healthy counterparts. Oddly, though having elevated Pb levels, healthy refinery students did not display altered T(H)1 or T(H)2 cytokine levels relative to control student values. From this, we conclude that substantively increased whole blood Pb levels may promote T(H) cell dysregulation and alter the availability of key T(H)1 and T(H)2 cytokines, effects that could ultimately contribute to development of pulmonary allergic diseases.