D3.507 - Impact of chemical warfare agents on immune response

Acute inhalation poisoning (AIP) caused by irritant chemical warfare agents, carbon monoxide, and pyrogenic combustion byproducts triggers extensive bronchopulmonary tissue damage and initiates systemic toxic cascades. A critical aspect of such exposure is the induction of allobiosis — a state of altered biological reactivity. This phenomenon potentially modulates the immune profile and exacerbates systemic allergic sensitization, necessitating a deeper investigation into the immunological shifts following toxic inhalation. Aim: To evaluate the influence of acute inhalation exposure to toxic agents on the immune response as a clinical manifestation of allobiotic transformation.

A clinical assessment was conducted on 27 male participants, categorized into two cohorts: Group 1 (G1): 17 patients with confirmed AIP (median age: 43 [41–47] years). Group 2 (G2): 10 healthy individuals (control group; median age: 44 [42–50] years).

Immunological parameters included absolute eosinophil count (E) and serum concentrations of immunoglobulins (IgA, IgM, IgG, IgE). Statistical processing was performed using non-parametric methods, with data expressed as Me (LQ-UQ).

Results: comparative analysis of immunological markers is summarized in the table below.

Analysis revealed a clear upward trend in IgE concentrations and absolute eosinophil counts in Group 1 compared to the control. However, despite these clinical tendencies toward hypersensitization, the differences did not reach statistical significance (p≥0.05).

Acute inhalation poisoning induces a shift in immune reactivity, characterized by a tendency toward elevated serum IgE and eosinophilia. These findings suggest the initiation of an allobiotic response; however, further large-scale studies are required to fully elucidate the mechanisms of long-term immunological dysregulation following toxic exposure.