Immune and genetic status in children residing in conditions of airogenic exposure to nickel

Introduction. It is quite relevant to assess effects produced on children by chemical factors (exemplified by nickel) associated with specific point single nucleotide replacements in detoxification genes.

Materials and Methods. Children in the observation group (n=44) are exposed to airborne nickel amounting to 1.28 average annual MPC; children in the reference group (n=45) live in a “relatively clean” area (lower than 0.1 average daily MPC). The study relied on using mass spectrometry, enzyme-linked immune assay, allergosorbent assay, flow cytometry, and real-time PCR.

Results. Inhalation exposure to nickel (up to 1.28 average daily MPC) at a dose of 0.00207 mg/kg per day resulted in a 1.73-fold increase in blood contamination in children in the observation group compared to the reference group. In the observation group, a statistically significant (p<0.05) increase in the number of CD4⁺CD25⁺CD127^–-regulatory cells (by 1.5 times), cortisol concentration (by 1.7 times), the level of specific IgE antibodies to nickel (1.3 times) and an increase in the number of CD4⁺ lymphocytes (by 10%) were found relative to the values obtained in the reference group; polymorphism of genes controlling detoxification and apoptosis processes was identified – CYP1A1, GSTP1, TP53 and CPOX (RR=1.39–1.96) (RR=1.96, 95% CI: 1.79–2.12; RR=1.61, 95% CI: 1.31–1.97; RR=1.39, 95% CI: 1.05–2.02 and RR=1.76, 95% CI: 1.53–2.01, respectively). Based on the results of modeling using the “exposure marker – effect marker” system, there was established a relationship reflecting the hyperproduction of nickel-specific IgE, total IgE, and cortisol when nickel was present in blood (RR = 2.42, 95% CI: 1.37–4.27; RR = 2.39, 95% CI: 1.54–3.79; RR = 4.60, 95% CI: 1.05–20.11, respectively).

Limitations. The study limitations include a limited sample size in the examined children groups and sex-related imbalances; this requires additional research to verify the findings.

Conclusion. Therefore, children exposed to airborne nickel (1.28 average daily MPC) and with polymorphism of candidate apoptosis and detoxification genes (CYP1A1, GSTP1, TP53, CPOX) face a risk (RR=1.39–1.96) of excessive nickel bioexposure (2.6 times higher). This affects on immune regulation (suppressive and helper activity of cell clusters, nickel hypersensitivity – IgE), and adaptation (hypercortisolemia). So, we can recommend verified indicators as markers of effect and sensitivity for preventing allergic diseases in children living in environments destabilized by pollutants (using nickel compounds as an example).

Compliance with ethical standards. The study protocol was approved by the Local Ethics Committee of the Federal Scientific Center for Medical and Preventive Health Risk Management Technologies, meeting report No. 7 dated December 19, 2022. All participants and their legal representatives gave informed voluntary written consent to participate in the study.

Contribution:
Dianova D.G. – concept and design of the study, writing text;
Dolgikh O.V. – concept of the study, data analysis and interpretation, editing;
Kazakova O.A., Shirinkina A.S. – data collection and processing, and creating tables.
All authors are responsible for the integrity of all parts of the manuscript and approval of the manuscript final version.

Conflict of interest. The authors declare no conflict of interest.

Funding. The study had no sponsorship.

Received: September 24, 2025 / Accepted: December 2, 2025 / Published: January 15, 2026

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