Phthalates, plasticizers that maintain plastic’s durability and flexibility, are chemicals that leach from plastics into the environment. As endocrine disruptors, they can bind to nuclear receptors regulating metabolism and growth. Filter-feeding fin whales (Balaenoptera physalus) consume vast amounts of plastic particles, leading to detectable levels of phthalates and phthalate metabolites in their tissues. This thesis assesses in vitro experimentation on fin whale fibroblast cells as a method of studying the impact that phthalates, phthalate metabolites, and phthalate replacements have on fin whales. Gene expression along nuclear receptor pathways was the chosen endpoint. At tested concentrations, plasticizers/metabolites were not cytotoxic to the fibroblasts, but instead stimulated enzymatic activity. Unexpected results included variation in fibroblast subcultures from the same individual and visible interactions between phthalates and plastic laboratory materials. Overall, gene expression in lipid metabolism (peroxisome proliferator-activated receptors) and thyroid hormone pathways was unresponsive and showed no specific distinction between phthalates and metabolites. However, the glucocorticoid receptor (GR) pathway was affected by DEHP ((bis(2-ethylhexyl) phthalate) downregulating GR expression and DEHA ((bis(2-ethylhexyl) adipate) significantly upregulating it. These findings highlight the need for environmental monitoring of all plasticizer classes. Further research should examine fibroblast-specific pathways, cellular reprogramming, and chemical mixture effects.
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