The zebrafish chorion is a tough acellular envelope perforated by funnel-shaped pore canals roughly 0.5–0.7 µm across. Below hatching, this is the only route a foreign particle has into the embryo: anything that cannot fit through a pore is physically excluded, regardless of its chemistry. This is the size-exclusion mechanism reported for engineered nanoparticles crossing the chorion (e.g. Lee et al. 2007, silver nanoparticle imaging in early zebrafish development).
Because the pore population itself varies in size, whether a given particle gets through is modeled as a probability rather than a hard cutoff — a logistic function of how its effective diameter compares to the chorion's mean pore diameter:
d_eff = d_primary × agglomeration factor
P(pass) = 1 / (1 + exp((d_eff − d_pore) / w))
w = 60 nm (pore-to-pore biological spread)
- Primary particle diameter — the size of one dispersed nanoparticle as manufactured.
- Medium ionic strength — higher salt concentration screens surface charge and drives colloidal agglomeration, multiplying the effective diameter that actually reaches the chorion by up to 20×. This is the same aggregation mechanism raised for nanomaterial risk assessment: dispersion state, not just primary size, decides fate.
- Chorion pore diameter — moves the mean of the biological pore-size distribution across its documented 0.5–0.7 µm range.
- Particles that pass accumulate in the perivitelline space and can go on to contact the embryo proper (internal dose); particles that fail stay bound to the outer chorion surface and never reach the embryo — a purely physical gate that happens before any cellular toxicity (oxidative stress, membrane damage) has a chance to occur.
Real-world relevance: the OECD fish embryo acute toxicity test (FET) and countless nanosafety screens rely on this chorion barrier — a nanomaterial's agglomeration state in the exposure medium can be the single biggest lever on whether it is developmentally toxic at all.