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Sulfonamide PFAS cause developmental abnormalities in mummichogs (Fundulus heteroclitus)
Citation:
Heyder, C., T. Burke, Y. Rericha, A. Champagne, K. Wells, L. Mills, D. Nacci, AND B. Clark. Sulfonamide PFAS cause developmental abnormalities in mummichogs (Fundulus heteroclitus). 30th NACSETAC Annual Meeting, Woods Hole, MA, April 11 - 12, 2024.
Impact/Purpose:
Per- and polyfluoroalkyl substances (PFAS) are long-lasting environmental contaminants with known adverse impacts on fish and other taxa. However, understanding of their impacts on coastal environments, including the effect of chemical structure on toxicity in estuarine and marine organisms is lacking. To examine the effect of structural difference on toxicity during a sensitive life stage, we conducted developmental exposures in an ecologically important estuarine minnow, the mummichog (Fundulus heteroclitus) to perfluorohexanesulfonamide (FHxSA) and perfluorooctanesulfonamide (FOSA). Investigating the mechanistic basis for organismal effects will contribute to goals of connecting modes of action to adverse outcomes, extrapolating across species, and predicting ecological impacts of PFAS contamination
Description:
Per- and polyfluoroalkyl substances (PFAS) are long-lasting environmental contaminants with known adverse impacts on fish and other taxa. However, understanding of their impacts on coastal environments, including the effect of chemical structure on toxicity in estuarine and marine organisms is lacking. To examine the effect of structural difference on toxicity during a sensitive life stage, we conducted developmental exposures in an ecologically important estuarine minnow, the mummichog (Fundulus heteroclitus) to perfluorohexanesulfonamide (FHxSA) and perfluorooctanesulfonamide (FOSA). These compounds both have sulfonamide functional groups but differ in carbon chain length. Embryos were aqueously exposed to FHxSA (0, 1, 10, 30, 60, 100 μM) or FOSA (0, 1, 10, 25, 100 μM) across initial range-finding experiments and subsequent experiments to pinpoint bioactive concentrations. Static exposure occurred from 1-7 days post-fertilization (dpf). A variety of non-destructive endpoints were assessed through 30 dpf, including survival, developmental phenotypic abnormalities, hatching, and growth. Increasing instances of pericardial edema, heart abnormalities, abnormal body head size, and elongated sinus venosus were present in FHxSA exposures as concentration increased, while similar effects were seen in FOSA at lower concentrations. FOSA exposures caused higher instances of both embryonic and larval mortality from 10 - 25 μM. This suggests FOSA may be more acutely toxic when compared to FHxSA at equal nominal concentrations. These results support a role of chain length in developmental toxicity of sulfonamide PFAS in mummichogs, as has been observed elsewhere. Ongoing work investigating the mechanistic basis for organismal effects will contribute to goals of connecting modes of action to adverse outcomes, extrapolating across species, and predicting ecological impacts of PFAS contamination.
