Humans are constantly exposed to low concentrations of inorganic mercury and even some organic forms present in the atmosphere, however, the majority of mercury that remains in the human body is in the form of methylmercury, coming from ingestion [4].
From the MeHg journey we learned that its concentration grows the higher in the food web we go (a.k.a. biomagnification and bioaccumulation). Higher animals consume the polluted preys and accumulate that mercury in their tissues; humans are just the last step in this process. EPA (and like the world) warns about consuming fish and shellfish with methylmercury in their tissues, given that a high concentration of Hg in the human body leads to mercury poisoning (e.g., Minamata disease).
Yes, they have - but that's only one piece of the puzzle.
MeHg concentrations in fish consumed by humans have increased over time due to ongoing changes in aquatic ecosystems, namely overfishing and increases in seawater temperature [6]. These connections are less straightforward as saying that more Hg in the environment equals more MeHg exposure, but analyses of food webs relationships and the overall availability of food for fish in higher trophic levels help explaining why MeHg human exposure has not really eased.
Overfishing of some species (eg. herring) leaves higher trophic levels without much options for prey, hence, they end up focusing on some species which may result in worsening bioaccumulation.
Prey niches are highly dependent on water temperature; predators feed on other species that might also be very specialized to some physicochemical conditions. Thus, changing temperature changes availability of prey.
Now, these food web modifications are not easy to predict as the opposite effect can also be found as lower MeHg bioaccumulation can also result from changes in prey availability... the key point here is that even though reducing Hg emissions is a great starting point, prevention of human exposure to methylmercury won't be solved by just one strategy.