> Thinking of poisons in binaries is false - the dose makes the poison. This is true, but by itself this model presents an incomplete picture for assessing the

> Thinking of poisons in binaries is false - the dose makes the poison. This is true, but by itself this model presents an incomplete picture for assessing the risk of PFAS. Two additional models are important: bioaccumulation and half-life. PFAS stick around (pardon the pun) in the environment. They are biomagnified upwards through the food chain. If we are releasing them into the environment at a greater rate than they are degrading, then the biosphere is building up a reservoir of PFAS whose acute effects in humans will lag their release into the environment. Additionally, it is hard to assess the lethal dose of something over a lifespan vs. an acute exposure. This is because slow poisons tend to pick up correlations and interactions with other illnesses as they progress over time (e.g. someone who struggles to get out of bed because of a persistent infection will also get less exercise and sunlight). So the long-term effects of things on the body tend to be less tractable research questions and thus have a negative bias in the scientific literature, which can easily be mistaken for "evidence of absence". This is why the precautionary principle is important for anything that is as pervasive as PFAS.