02 · Impacts
From plankton to people.
PFAS do not partition into fat the way classical persistent organics do. Instead they bind to serum proteins and fatty-acid binding proteins in liver — concentrating in the same tissues we use to regulate metabolism and immunity. Three case studies illustrate the climb up the food web.
Rainbow trout (Oncorhynchus mykiss)
Laboratory studies (Martin et al., 2003) show PFOS bioconcentration factors of 1 100 L/kg whole body and over 4 000 L/kg in liver — orders of magnitude greater than in muscle, because of strong binding to liver fatty-acid binding protein (L-FABP). The consequence is a fish that cannot clear what it absorbs: PFOS half-life in trout plasma exceeds 20 days, and dietary exposure of just 500 ng/g feed is enough to disrupt the hypothalamic–pituitary–thyroid axis within weeks (Benskin et al., 2009; Wang et al., 2011).
- 96 h LC50 (juvenile, PFOS): ≈ 7.8 mg/L — acute mortality at spill concentrations
- Hepatomegaly & steatosis: livers swell 30–60 % and accumulate lipid droplets, mimicking non-alcoholic fatty liver disease (Martin et al., 2003)
- Endocrine disruption: plasma T4 drops > 50 %, slowing growth and smoltification
- Feminisation: vitellogenin induced in male trout — a biomarker of estrogenic injury
- Immune suppression: reduced lymphocyte counts and impaired response to Aeromonas challenge
- Reproductive failure: ≥ 1 µg/L chronic exposure cuts egg viability and produces larval skeletal deformities
Trophic transfer of PFOS from contaminated trout
A single contaminated trout is not the end-point. PFOS persists through digestion and partitions into the liver and serum of every predator that eats one — concentrating with each step up the food web. This is observed as bioaccumulation.
Bottlenose dolphin (Tursiops truncatus)
Dolphins integrate decades of PFAS exposure through their fish-rich diet. Plasma ΣPFAS exceeds 1 000 ng/mL in many populations — among the highest concentrations measured in any wild mammal. In Charleston (SC) and the Indian River Lagoon (FL), mean plasma PFOS reaches 1 360 ng/mL, roughly 100× the level shown to suppress immune function in laboratory mammals (Houde et al., 2006; Fair et al., 2013).
- Trophic magnification factor (PFOS): ~ 5.9 per level — concentrations roughly sextuple each step up the food web
- Immune collapse: T- and B-lymphocyte proliferation reduced > 40 %, with elevated rates of Lobomycosis, morbillivirus, and bacterial pneumonia (Fair et al., 2013)
- Endocrine disruption: suppressed thyroid hormones and altered cortisol, linked to poor body condition and stranding
- Liver pathology: stranded dolphins from PFAS hot-spots show hepatocellular hypertrophy, necrosis, and biliary hyperplasia (Schwacke et al., 2012)
- Reproductive harm: PFOS crosses the placenta and is excreted in milk — calf survival in contaminated estuaries falls below 75 % in the first year
- Population decline: NOAA designated Charleston bottlenose dolphins a “depleted stock” partly due to contaminant-linked mortality
The C8 community — Parkersburg, West Virginia
From the 1950s to 2002 the DuPont Washington Works plant released PFOA (“C8”) into the Ohio River and groundwater. Approximately 69 000 residents drank contaminated water for years. The court-ordered C8 Science Panel (2005–2013) sampled blood from 69 030 people and concluded a “probable link” between PFOA exposure and six conditions:
- Kidney cancer
- Testicular cancer
- Thyroid disease
- Ulcerative colitis
- Pregnancy-induced hypertension
- Hypercholesterolaemia
In 2023 the IARC reclassified PFOA as Group 1 (carcinogenic to humans) and PFOS as Group 2B.