Food chain, plant poisons

Environmental risk assessment examines the potential adverse effects to ecosystems from exposure of the aquatic, terrestrial and air components. Initial assessment normally focuses on the aquatic compartment, including effects on microorganisms in waste water treatment plants. This first tier risk assessment can be extended to cover the sediment part of the aquatic compartment and the soil compartment. At higher tonnage levels, effects relevant to the food chain are evaluated, i.e., secondary poisoning. Diderich in Chapter 8 of (73) discusses the principles of EU environmental risk assessment. 

It turns out that most of these compounds have similar characteristics that contribute to their toxicity to both humans and other species of plants and animals. First, the compounds are environmentally persistent. Many of the early pesticides, and certainly the metals, do not break down in the environment or do so only very slowly. If persistent chemicals are released continually to the environment, the levels tend to rise ever higher. This means they are available to cause harm to other organisms, often not even the target of the pesticide. Second, the early pesticides were broad acting and toxic to many species, not just the target species. These poisons often killed beneficial insects or plants. Third, many of these compounds would bioaccumulate or concentrate in species as they moved up the food chain. The chlorinated pesticides accumulate in the fat of animals. Animals that consumed other animals accumulated more and more of these pesticides. Most species could not metabolize or break down the compounds. Lead accumulates in bone and methyl mercury in muscle. And finally, because of their persistence in the environment and accumulation in various species, the persistent toxicants spread around the world even to places that never used them. Animals at the top of the food chain, such as polar bears and beluga whales, routinely have fat PCB levels greater that 6 ppm. 

Toxic organic chemicals can harm organisms in a variety of ways. Many animals simply become ill after feeding on poisoned plants. Others survive but are then eaten by larger animals that prey on them. The toxins accumulate in predators bodies over time as they consume affected prey animals. Thus, the concentration of a toxic chemical tends to increase as it moves up the food chain in a process known as biomagnification. In one study, for example, the concentration of DDT was found to be 0.25 ppm in the phytoplankton in a body of water, 0.123 ppm in zooplankton, 1.04 ppm in small fish, 4.83 ppm in larger fish, and 124 ppm in birds that fed on the fish. 

How can this scattered taxonomic occurrence of the picrotoxanes be explained Many of the apparent chemical convergences in animal toxins have been explained as toxins received via the food chain e.g. brevetoxin, pederin, saxitoxin, tetrodo-toxin, and the toxins of the arrow-poison frogs). This may explain the occurrence of picrotoxanes in both parasitic animals and plants, but further research will be necessary for a better understanding of this phenomenon. 

Metallic mercury is relatively benign compared to the cilkyl compounds of mercury, which are mainly nervous system poisons. Methylmercury is the most potent of these and also the most prevalent because of its presence in fish. It now is known that microorganisms in the bottom sediment of lakes cind rivers convert inorganic mercury into the more toxic methyl form. Taken up by plants and plankton, it ascends the food chain to humans. Predatory marine fish, such as tuna and swordfish, also contain sub-stantied levels. Although most of our knowledge of human toxicity... 

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