In addition to the breaking of the cells by waves, "K. brevis" cells can die because N-limitation directly affects the growth potential of blooms and the toxicity of "K. brevis" cells that comprise them. When N-limitation is present, intracellular brevetoxin concentrations (fg/μm3) increased up to 2.5-fold in laboratory cultures, implying that during periods of N-limitation of algal growth, there is a higher chance of brevetoxin influx into the marine food web. The toxin content per cell increases when algal growth becomes P-limited. Various field measurements collected in the Gulf of Mexico have shown that the brevetoxin content of "K. brevis" cells is between 1 and 68 pg/cell; however, Hardison et al. discovered that during periods of transient P- and N-limitation, there is a 2- to 5-fold increase in brevetoxins per mole of cell carbon or unit of cell volume. Hardison concluded that this data suggest that the exposure of marine ecosystems to significantly different toxin levels depends on the nutrient status of the "K. brevis" cells. While brevetoxins remain intracellular during early stages of bloom development, the triggering of apoptosis and cell lysis with age release the toxins into the surrounding waters, implying that greater P-limitation that results in more cell death ultimately elevates brevetoxin levels. These high levels may persist in a food chain long after a bloom has subsided due to brevetoxin's high affinity for adsorbing to biological surfaces like sea grass fronds, and thereby accumulating in consuming organisms.