USGS1975
Summary: Pollutants tend to simplify plant and animal communities by causing a progressive loss of species. At the extreme, this leads to erosion and loss of soil fertility. Weedy, broadly adapted species increase. Among animals, carnivorous species and groups are often the first to suffer. This is partly because of their exposure at the top of the food chain, and partly, it appears, because of physiological differences. Species differences in susceptibility are abundant and are often critical. One result is that when one pest is controlled another is likely to flare up. Resistance appears commonly in insects and is known in other fast-breeding forms, including fishes, frogs, and rodents. Resistant individuals can carry toxicant loads that make them dangerous food for other animals. Some groups, including mollusks and annelids, are naturally resistant to many organohalogens and tend to accumulate them. Animals such as birds may carry lipophilic pollutants in large amounts with apparent safety until forced to draw upon their fat. They may then suffer delayed mortality, and no doubt suffer reproductive or behavioral effects at sublethal levels. Lipophilic pollutants in the brain rise when body lipids decrease and fall when body lipids increase. Mutagenesis can be caused by some common pollutants and the mutagenic properties of most chemicals are far too little known. Fortunately, common pesticides are not likely to be strong mutagens. Mutagenicity may be affecting certain long-lived and slow-breeding species in the wild, but most species have enough population turnover to swamp an occasional mutagenic event. Behavioral changes can be caused by relatively low levels of contaminants, but it is often hard to demonstrate them without using high dosages. Reproduction may or may not be affected adversely by low exposures. At certain exposures that are below the toxic levels of a chemical, a biostimulatory effect is to be expected. Food chain accumulations definitely do occur when persistent chemicals enter organisms that eliminate them poorly. However, loss of chemicals in the food chain must be more common than accumulation. The great concentration from water to aquatic organism is chiefly a physical phenomenon, not a food chain effect, but it affords high starting levels for these chains. Terrestrial food chains often start at a high level with heavily contaminated, struggling prey. Litter feeders are another important base. Vegetation may be contaminated enough to be dangerous to animals that eat it. Dermal and respiratory routes of intoxication occur in the wild, but the oral route is far more important at most times and places. The organisms that govern soil fertility and texture are affected more by cultivation than by pesticides. Above ground, growing knowledge of resistance, species differences, and biological controls is leading to integrated control, in which use of chemicals is limited and specific. We do not know what is happening to most nontarget invertebrates. Amphibians and reptiles may be killed by applications of insecticides, but are not highly sensitive and can carry large residues. Effects of these residues on reproduction are little known. Heavy kills of birds by pesticides still occur in the field. Fish-eating and bird-eating birds also undergo shell thinning and related reproductive troubles in many areas, sometimes to the point of population decline and local or regional extermination. DDE most often correlates with shell thinning in the wild and in experiments. No other known chemical approaches DDE in causing severe and lasting shell thinning. Herbivorous birds seem to be largely immune to this effect. It is uncertain how much dieldrin and PCBs contribute to embryotoxicity in carnivorous birds. Mammals may be killed by the more toxic pesticides, but some of the commonest small rodents are so resistant, and lose their residues so rapidly, that they are of little