Methodological Approaches to a Biological Model for Validating Health Damage Criteria Following Wildfire Smoke Exposure

Introduction. Prolonged exposure to smoke from wildland fires causes various health impairments, primarily affecting the respiratory, cardiovascular, and nervous systems. To substantiate safe exposure levels to landscape fire smoke, a biological model closely mimicking natural conditions has been developed.

Materials and Methods. Experiments were conducted on adult Wistar rats. Mean CO concentrations ranged from 20 to 30 mg/m³, and PM2.5 concentrations from 0.37 to 0.93 mg/m³. The total duration of biomass smoke exposure in the experiment was 1, 4, 8, 20 (4 h/day, 5 days), and 80 (4 h/day, 5 days/week, 4 weeks) hours. The cumulative exposure loads for CO and PM2.5 were calculated. Behaviour was assessed using the open‑field test; EEG recordings, histological analysis of the cerebral cortex and testes, and DNA fragmentation and DNA methylation levels in testicular and blood cells were evaluated. First‑generation offspring were examined immediately after birth and at maturity.

Results. A biphasic relationship was observed: lower exposure levels were associated with activation of CNS parameters, whereas further increases in duration or intensity led to significant inhibition of these parameters. Regarding the reproductive system, an adverse response in the form of impaired postnatal development of offspring, in the absence of a pronounced gonadotoxic effect in the parental generation, was detected at cumulative exposure loads ranging from 0.22 to 4 mg. Prolonged exposure to wildland fire smoke for one month was accompanied by marked impairment of spermatogenic function in the testes and increased neonatal mortality in offspring.

Conclusion. Safe smoke exposure levels (based on PM2.5 and CO indicators) were established with regard to the functional state of the central nervous and reproductive systems, genotoxicity parameters, DNA methylation, and offspring health.