https://doi.org/10.1016/j.aquatox.2026.108050
Highlights:
- Chronic exposure to sodium fluoride (NaF) significantly increases viral susceptibility in rainbow trout, nearly doubling mortality rates at higher concentrations.
- NaF exposure induces both temporary thyroid hormone imbalance and long-term structural damage to the thyroid gland, suggesting persistent physiological vulnerability.
Abstract
- NaF disrupts immune function by reducing circulating immune cells, altering leucocyte profiles, and amplifying inflammatory responses.
Endocrine disruptors (EDs) are widely distributed in terrestrial and aquatic ecosystemsand are increasingly recognized for their potential impacts on organism health. Exposure to EDs is known to affect endocrine systems, such as the thyroid hormone system (THS), but can also manipulate the immune system (IS) of organisms.
This study aimed to investigate the potential impact of the ED sodium fluoride (NaF) on the THS and pathogen resistance in rainbow trout exposed for seven months to 1.5 or 5 mg/L of fluoride (F-). Viral resistance was assessed by subjecting the fish to an infectious challenge with the infectious hematopoietic necrosis virus (IHNV). Mortality was monitored daily for six weeks following infection.
Exposure to sodium fluoride (NaF), particularly at 5 mg F-/L, significantly increased the susceptibility of juvenile fish to viral infections, nearly doubling cumulative mortality rates. While early viral replication was not affected, NaF caused lasting changes to cellular immunity, including a reduction in circulating immune cells, disrupted leucocyte profiles and an intensified inflammatory response. The link to thyroid disruption could be drawn by showing that NaF induced temporary disruption of thyroid function (T3 and T4 concentrations) during infection and caused persistent structural changes in the thyroid gland, indicating a lasting physiological vulnerability even after hormonal levels appeared to recover.