BACKGROUND: Although we have gained much information about leadinduced organ damage, the effect of blood lead level on T cell subgroup is yet to be determined.OBJECTIVE: To assess the effect of blood lead level on T cell subgroup of children, and the association of T cell subgroup with threshold limit value of blood lead level.DESIGN: Comparative observation.SETTING: The Institute of Molecular Microorganism, Maternity and Child Care Hospital, Shanxi Provincial Children Hospital.PARTICIPANTS: Sixty children, (32 boys and 28 girls), aged 3-6 years with a mean of (4.5±1.5) years old, were selected from the suburbs of Taiyuan city between May 2003 and October 2003. Informed consents were obtained from all their guardians. The enrolled children according to their blood lead levels were assigned into three groups, 13 in Group Ⅰ with blood lead level ≥ 0.48 μmol/L, 20 in Group 2 with lead level ≥ 0.24 μmol/L but ＜ 0.48 μmoL/L and 27 in Group 3 with lead level ＜ 0.24 μmol/L.METHODS: Blood lead level and expression of T cell subgroup were measured with graphite furnace atomic absorption spectroscopy and immunofluorescence methods respectively. Student t test was used in data analysis, and linear correlation analysis was used to assess the correlation between blood lead level and expression of T cell subgroup.level and expression of T cell subgroup.pression of CD3 and ratio of CD4 to CD8 were lower in Group 1 (lead level ≥0.48 μmol/L) than Group 3 (lead level ＜ 0.24 μmol/L) (t=3.27,blood lead level showed had significant inverse correlation with CD3 expression and the ratio of CD4 to CD8(r=-0.689,-0.674,P ＜ 0.01).CONCLUSION: A blood lead level ≥ 0.48 μmol/L, is shown to significantly decrease the expression of CD3 and ratio of CD4 to CD8 in peripheral blood, which may impair the children's immunological function.

BACKGROUND: Although we have gained much information about leadinduced organ damage, the effect of blood lead level on T cell subgroup is yet to be determined.OBJECTIVE: To assess the effect of blood lead level on T cell subgroup of children, and the association of T cell subgroup with threshold limit value of blood lead level.DESIGN: Comparative observation.SETTING: The Institute of Molecular Microorganism, Maternity and Child Care Hospital, Shanxi Provincial Children Hospital.PARTICIPANTS: Sixty children, (32 boys and 28 girls), aged 3-6 years with a mean of (4.5±1.5) years old, were selected from the suburbs of Taiyuan city between May 2003 and October 2003. Informed consents were obtained from all their guardians. The enrolled children according to their blood lead levels were assigned into three groups, 13 in Group Ⅰ with blood lead level ≥ 0.48 μmol/L, 20 in Group 2 with lead level ≥ 0.24 μmol/L but ＜ 0.48 μmoL/L and 27 in Group 3 with lead level ＜ 0.24 μmol/L.METHODS: Blood lead level and expression of T cell subgroup were measured with graphite furnace atomic absorption spectroscopy and immunofluorescence methods respectively. Student t test was used in data analysis, and linear correlation analysis was used to assess the correlation between blood lead level and expression of T cell subgroup.level and expression of T cell subgroup.pression of CD3 and ratio of CD4 to CD8 were lower in Group 1 (lead level ≥0.48 μmol/L) than Group 3 (lead level ＜ 0.24 μmol/L) (t=3.27,blood lead level showed had significant inverse correlation with CD3 expression and the ratio of CD4 to CD8(r=-0.689,-0.674,P ＜ 0.01).CONCLUSION: A blood lead level ≥ 0.48 μmol/L, is shown to significantly decrease the expression of CD3 and ratio of CD4 to CD8 in peripheral blood, which may impair the children's immunological function.

Human epidemiological and animal studies have demonstrated that excess iron is a risk for cancer. The responsible mechanisms are: 1) increased intracellular iron catalyzes the Fenton reaction to generate hydroxyl radicals, leading to mutagenic oxidative DNA lesions; 2) iron is necessary for cellular proliferation as cofactors of many enzymes. Thus, iron-excess milieu promotes selecting cellular evolution to ferroptosis-resistance, a major basis for carcinogenesis. Ferritin is a 24-subunit nanocage protein required for iron storage under the regulation of the iron-regulatory protein (IRP)/iron-responsive element (IRE) system. Ferritin is a serum marker, representing total body iron storage. However, how ferritin is secreted extracellularly has been unelucidated. We recently discovered that an exosomal marker CD63 is regulated by the IRP/IRE system and that iron-loaded ferritin is secreted as extracellular vesicles under the guidance of nuclear receptor coactivator 4 (NCOA4). On the other hand, we found that macrophages under asbestos-induced ferroptosis emit ferroptosis-dependent extracellular vesicles (FedEVs), which are received by nearby mesothelial cells, resulting in significant mutagenic DNA damage. Therefore, cells, including macrophages, can share excess iron with other cells, via iron-loaded ferritin packaged in extracellular vesicles as safe non-catalytic iron. However, similar process, such as one involving FedEVs, may cause accumulation of excess iron in other specific cells, which may eventually promote carcinogenesis.