aerosolizing the subsequent brevetoxins which cause respiratory illnesses in humans. in 2018, mote marine in sarasota, fl updated their frequently asked questions to make it more clear that nutrients (nitrogen is a nutrient found in fertilizer) can grow k. brevis. along the west coast of florida, the early phase of k. brevis blooms are initiated by northerly winds, resulting in upwelling events that cause nutrients to rise towards the surface of the water and transport multiple karenia cell species towards the shore. here they concentrate and either continue to grow or are taken up by onshore winds that spread the cells over beaches and near shore communities. it has been shown that k. brevis blooms are limited by available nitrogen (n) or phosphorus (p), but until recently it was not clear what sources k. brevis was utilizing for these key developmental nutrients. the most likely proposition is some combination of the upwelling of subsurface nutrients, land runoff (agricultural and sugar plantations, cattle ranches, golf courses, theme parks, septic systems, etc.) n2-fixation, drainage from phosphate mines and atmospheric deposition provides the necessary support for the blooms. 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. overall, brevetoxins seem to increase under n- and p-limitation, however, the concentration of brevetoxins per cell under p-limitation has been reported to be roughly twice that under n-limitation. one major concern of this is that management of shellfish bed closures operating under the assumption that brevetoxin concentrations per cell do not vary may compromise public safety if a bloom became nutrient limited.