Few field studies have been reported aimed at evaluating the effects on wild fish populations, but relevant data have been produced in laboratory studies dealing with effects at population level. In particular, PCDD, PCDF, and dioxin-like PCB congeners produce adverse effects that only occur days, weeks, or even months after exposure. Most meaningful comparisons can be made when toxic responses are based on the body burden ofTCDD, and/or the other relevant PCDD and PCDF congeners, and when the fish are observed for many weeks or months after exposure. Fish are more sensitive to TCDD toxicity during very early development. For example, rainbow trout swim-up fry are approximately 10 times more sensitive to the lethal potency of TCDD than juvenile rainbow trout, but rainbow trout are even more sensitive when exposed as newly fertilized eggs, at levels ofsome hundred picograms ofTCDD per gram of body weight, 20 times more sensitive than juveniles. Among the laboratory-tested species, the most sensitive, and most sensitive developmental stage to TCDD-induced lethality, are lake trout (Salvelinus namaycush) during an early development stage, such as newly fertilized eggs. A body burden of 0.04 ngg~ of fresh tissue showed a significant increase of sac fry mortality, with estimated TCDD lethal concentrations ranging from 50 to 60ngg_1 of eggs. Other effects potentially influencing the organism's energy requirements have been detected in fish, and include a decrease in feed consumption following exposure of juvenile fish to TCDD. Decreased feed consumption subsequently results in decreased body weight gain (wasting syndrome), which has been observed in yellow perch (Perca fluviatilis), rainbow trout (Oncorhynchus mykiss), and bluegill
(Lepomis macrochirus), but the importance of these effects in the field still remains to be explained.
The ability oforganisms to develop resistance to toxic chemicals has been recognized for decades, but the studies focused essentially on nonvertebrate groups. Among the few studies on the vertebrate group, researchers focused in particular on fish, and the chemicals most studied are PCDDs, PCDFs, and PCBs. This process, known as 'molecular drive', refers to the development of acquired resistance in geographically isolated wildlife populations, showing how pressure from environmental chemicals may permanently alter gene expression. Some indigenous nonmigratory fish populations from North America and Europe, exposed for generations, have shown resistance which is manifested by reduced mortality, reduced developmental abnormalities, and/or altered expression of toxicant-metabolizing enzymes. Resistance to chemicals like PCBs and TCDD most likely involves metabolic pathways shift, including altered sensitivity of target sites and/or balance of activation/detoxification pathways. The resistance developed may cause severe future environmental problems by reducing population fitness. A reduction of the reproductive output, a compromised immune function, and/or decreased growth rates have been documented. The low genetic heterogeneity found in resistant populations with a reduced fitness may generate resistant organisms very vulnerable to additional stress.
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