Effects of environmental lead exposure on T-helper cell-specific cytokines in children

Abstract

Lead (Pb) may alter T-lymphocyte reactivity in situ by preferentially enhancing the development of T-helper 2 (TH2)- and inhibiting TH1-lymphocyte development. These effects could result in dysregulation of the presence/availability of TH1- and TH2-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 TH1 and TH2 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 TH1 and TH2 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 TH2 cytokine levels significantly higher and TH1 cytokine levels significantly lower than their healthy counterparts. Oddly, though having elevated Pb levels, healthy refinery students did not display altered TH1 or TH2 cytokine levels relative to control student values. From this, we conclude that substantively increased whole blood Pb levels may promote TH cell dysregulation and alter the availability of key TH1 and TH2 cytokines, effects that could ultimately contribute to development of pulmonary allergic diseases.