Pesticides, toxic effects

For carckiogen pesticides (70,71), animal testkigs are subject to maximum tolerated doses (M I L)). M I D is the maximum amount of a substance that can be administered to an experimental animal without causkig extreme health consequences, such as death, to occur but while continuing to produce some measurable toxic effects. Current regulatory theory holds that carckiogen effects do not have a threshold and caimot be related to reference doses. 

The fungicides are among the chemicals of wide use as plant diseases control agents in intensive agriculture. At the same time these pesticides could have toxic effects, when accumulated in man and animals. Because of general society concern about fungicides use, they should be monitored in waters, soils and crops. 

Hazard identification, step one, means identification of new chemicals or other factors that may cause harmful health effects. Previously, novel hazards were usually observed in case studies or after accidents or other excessive exposures, usually in occupational environments. Today, thorough toxicity studies are required on all pesticides, food additives, and drugs. New chemicals also have to be studied for their potential toxic effects. Thus, earlier hazards were in most cases identified after they had caused harmful effects in humans. Today, most chemical products have been evaluated for their toxicity with experimental animals. Therefore, hazard identification has become a preventive procedure based on safety studies conducted before a chemical compound or product reaches the market, and before individuals are exposed to it. ... 

Ecobichon, D. J. (1996). Toxic effects of pesticides. In Casarett and DouU s Toxicology The Basic Science of Poisons (C. D. Klaassen, Ed.), pp. 643-689. McGraw-Hill, New York. 

Provides access to detailed information on all categories of pesticides including herbicides, fungicides, insecticides, and rodenticides. Included is information on pesticide toxicity, health effects, residual data, efficacy, and other information. NPIC is a cooperative effort of the U.S. EPA and the Oregon State University Department of Agricultural Chemistry. NPIC is staffed from 6 30 a.m to 4 30 p.m. Pacific Standard Time. 

MurphySD. 1986. Toxic effects of pesticides. In Casarett and Doull s toxicology, 3rd ed. 519-581. 

By definition, any pesticide has toxic effects on organisms. Listed pesticides are those that combine high toxicity with resistance to degradation in the environment. Moore and Ramamoorthy109 review the behavior of chlorinated pesticides in natural waters. 

Aniline, which is used not only to synthesise drugs, pesticides and explosives but also as a building block for materials such as polyurethane foams, rubber, azo dyes, photographic chemicals and varnishes, is manufactured at a quantity of approximately three million tons each year [61]. The toxic effects of aniline include increased nitration of proteins in the spleen [62]. 

Although bicyclophosphates do not inhibit acetylcholinesterase, they exhibit a synergistic toxic effect with materials that do. Individuals who have had previous exposure to cholinesterase inhibitors such as nerve agents and commercial organophosphate or carbamate pesticides may be at a greater risk from exposure to bicyclophosphates. 

Murphy, S.D. 1986. Toxic effects of pesticides. Pages 519-581 in C.D. Klaassen, M.O. Amdur, and J. Doull (eds.). Casarett and Doull s Toxicology, Third Edition. Macmillan, New York. 

The Food Quality Protection Act (FQPA) of 1996 mandated that the US EPA carry out risk assessments that consider the cumulative effects of exposure to pesticides having a common mechanism of toxicity, as well as consider exposure to each pesticide by various routes of exposure (e.g., dermal, dietary, inhalation) and sources (e.g., residues in food and water) in an aggregate manner [19]. To accomplish this, there needs to be sufficient evidence supporting a common adverse effect that is associated with a common mechanism of action in specific target tissues. To date, the required criteria necessary to establish a common mechanism of toxicity with a specific toxic effect for the pyrethroids are not available [1,8,98]. 

Thus the total soil pollution was connected with a respiratory system and a digestive tract. Both systems were also sensitive to such urban pollutants as heavy metals and PAH. For radionuclides the correlation with the given nosologies was not revealed. The asthma morbidity was mostly connected with soil pollution rates. This circumstance, apparently, can be related to nonspecific action of pollutants on a human organism, because the etiology of asthma is connected with the human immune defense system and allergy state (Roite, 1991). The last was shown for pesticides (Nikolaev et al., 1988) and heavy metals (Drouet et al., 1990). The sensitized immune system is, apparently, responsible for chronic toxic effects of other pollutants at low doses (Sidorenko et al., 1991 Novak and Magnussen, 1993). 

The toxic effects of pesticides can be diverse and depend on the sensitivity of organisms to these toxicants, and the pesticide concentration or bioavailability. Typically, the short- and long-term effects of pesticides have been evaluated through acute or chronic toxicity bioassays, respectively, using lethality endpoints and sublethal endpoints (e.g., growth and reproduction), particularly these last in chronic bioassays. 

Most commonly, bioassays for the evaluation of the acute toxic effects of pesticides are based on single aquatic species selected to be representative of a range of taxonomic and functional groups, i.e., bacteria, algae, invertebrates or fish [ 53,54]. Generally, toxicity evaluation using a single species is the alternative of choice rather than the use of multiple species, because extrapolation of effects to an ecosystem is more difficult and can often lead to incorrect conclusions. 

Episodic pollution events can adequately be addressed by acute toxicity bioassays, however these are not sufficient to investigate the water quality for delayed toxicity effects of chemicals present. Chronic effects of pesticides can include carcinogenicity, teratogenicity, mutagenicity, neurotoxicity, and reproductive effects (endocrine disruption). 

Table 2 Combined toxicity effects of pesticides evaluated by three toxicity bioassays... 

Historically, organic environmental pollutants were hydrophobic, often persistent, neutral compounds. As a consequence, these substances were readily sorbed by particles and soluble in lipids. In modern times, efforts have been made to make xenobiotics more hydrophilic - often by including ionisable substituents. Presumably, these functional groups would render the compound less bioaccumulative. In particular, many pesticides and pharmaceuticals contain acidic or basic functions. However, studies on the fate and effect of organic environmental pollutants focus mainly on the neutral species [1], In the past, uptake into cells and sorption to biological membranes were often assumed to be only dependent on the neutral species. More recent studies that are reviewed in this chapter show that the ionic organic species play a role both for toxic effects and sorption of compounds to membranes. 

Around 600 substances are covered in this book which includes 70 pesticides. Details covered in the entries includes composition/structure, physical properties, sources, environmentally relevant reactions and pathways, detection and toxic effects, and regulatory limits. Many of the entries also include short case histories. 

---