HYPERSENSITIVITY MARKERS IN CHILDREN UNDER ENVIRONMENTAL ALUMINUM EXPOSURE

Abstract

The studies in the organism adaptation for the conditions of technogenic environmental changes, especially in child population, will allow to design a set of diagnostic markers for assessing the health status and early detection of pathological trends for development of hypersensitivity to environmental substances and improve efficiency of therapeutic and preventive measures. Metals are capable to alter functional activity of immune system by producing both immunostimulating and suppressive effects on immune reactivity, dependent on the properties of the given metal, its environmental concentration, source and duration of exposure. The aim of the present study was to investigate the features of hypersensitivity markers in children under the conditions of external exposure to aluminum. We have conducted a survey of the schoolchildren aged from 7 to 11 y.o. (a mean of 8.82±0.11 years), permanently inhabiting the territory of active industrial exposure associated with environmental contamination with aluminum compounds. The comparison group consisted of children from a “conventionally clean” area, with acceptable parameters of environmental quality. Specific features of sensitization developing to aluminum were evaluated, including both reactive and alternative mediator mechanisms (leukotrienes and prostaglandins), as well as participation of the cytokines in evolving sensitivity to the metal in the ex vivo experiments. We have shown a 1.43-fold increased level of metal in peripheral blood of the observation group, than in comparison group (respectively, observation group, 0.020±0.005 μg/ml; comparison group 0.014±0.003 μg/ml). Enhanced levels of IgE antibodies were found to be 2.13-fold higher compared to the reference values (213.55±88.10 IU/ml against normal rates of < 100.0 IU/ml) accompanied by increased specific IgG antibodies to aluminum (1.55-fold relative to the controls, i.e., 0.157±0.054 cu in observation group versus 0.101±0.041 cu for the comparison group), as well as a 2.09-fold increased spontaneous production of leukotrienes C4/D4/E4 (80.60±19.44 pg/ml for observation group; 38.51±2.40 pg/ml in the comparison group), which was 1.67-fold enhanced by experimental aluminum stimulation. Prostaglandin F2α levels among the children from observation group were increased 1.9-fold (observation group, 892.62±97.20 pg/ml; comparison group, 457.11±132.99 pg/ml, p < 0.05). Under the ex vivo experimental conditions, we observed mostly suppressive effects of aluminum upon the cytokine production. E.g., IL-4 production was inhibited by 2.13-fold, as compared with control values (observation group, 0.64±0.23 pg/ml; comparison group, 1.36±0.09 pg/ml); the suppression for IL-17 was 1.90 times (observation group, 1.08±0.27 pg/ ml; comparison group, 2.05±0.37 pg/ml, p < 0.05). The parameters studied may be used as aluminum hypersensitivity markers and used for monitoring and predictions in public health care.