Parathion discussion

Death from a combination of inhalation and dermal exposures has been reported by Fazekas (1971) in four individuals who used methyl parathion (Wofatox) spray in a careless manner. These individuals were part of a larger series of 30 cases (20 men, 10 women) of fatal methyl parathion intoxication reported by Fazekas (1971). Since 26 of these fatalities followed oral exposure, this report is discussed in detail in Sections 3.2.2.1 and 3.2.2.2. 

Cardiovascular Effects. Eesions in the heart and blood vessels have been reported in humans acutely intoxicated with methyl parathion (Wofatox) (Fazekas 1971) and are discussed in Section 3.2.2.2. However, many of these lesions may be secondary to the effects of methyl parathion on the conduction system of the heart, to other components ingested, or to therapeutic regimens that some of these patients received. 

Hepatic Effects. Liver lesions have been reported in humans acutely intoxicated by methyl parathion formulation (Wolfatox) (Fazekas 1971 Fazekas and Rengei 1964). These studies are discussed in detail in Section 3.2.2.1. Liver lesions were hepatocellular swelling, degeneration, and fatty change. 

Neurologic signs did not occur over a 30-day period in male prisoner volunteers in California who ingested daily doses of methyl parathion ranging from 1.0 to 19 mg. There were no uniform changes in plasma or erythrocyte cholinesterase levels at any of these doses (Rider et al. 1969). By increasing concentrations of methyl parathion administered to the same experimental population and using the same protocol, a dose that inhibited cholinesterase values was established. These additional studies were published nearly 20 years ago in abstract form only therefore, they are not discussed in this section. 

Often, absorption occurs by multiple routes in humans. Dean et al. (1984) reported deaths and toxic effects as well as lowered blood cholinesterase levels and excretion of urinary 4-nitrophenol in several children who were exposed by inhalation, oral, and possibly dermal routes after the spraying of methyl parathion in a house. In the same incident (Dean et al. 1984), absorption was indicated in adults who also excreted 4-nitrophenol in the urine, though at lower levels than some of the children, and in the absence of other evidence of methyl parathion exposure. In this study, the potential for age-related differences in absorption rates could not be assessed because exposure levels were not known and the children may have been more highly exposed than the adults. Health effects from multiple routes are discussed in detail in Section 3.2. 

Methyl paraoxon may also be made unavailable by binding to noncritical tissue and plasma constituents (Benke and Murphy 1975), including cholinesterase (Parkinson 1996). In addition, the parent compound is bound to albumin, in serum, as discussed previously in Section 3.4.2.4, but this binding does not appear to limit the availability of methyl parathion to the tissues, indicating that it is reversible. Tissue binding appears to be more important than serum binding (Braeckman et al. 1980, 1983). 

Almost all systemic effects of methyl parathion are related to the action of this compound on the nervous system or are secondary to this primary action. It is therefore necessary to preface a description of the mechanisms of toxicity of methyl parathion with a brief discussion of the nervous system and neuro-humoral transmitters (excerpted from Lefkowitz et al. 1996). 

A susceptible population will exhibit a different or enhanced response to methyl parathion than will most persons exposed to the same level of methyl parathion in the environment. Reasons may include genetic makeup, age, health and nutritional status, and exposure to other toxic substances (e g., cigarette smoke). These parameters result in reduced detoxification or excretion of methyl parathion, or compromised fimction of organs affected by methyl parathion. Populations who are at greater risk due to their imusually high exposure to methyl parathion are discussed in Section 6.7 Populations With Potentially High Exposures. 

This section will describe clinical practice and research concerning methods for reducing toxic effects of exposure to methyl parathion. However, because some of the treatments discussed may be experimental and unproven, this section should not be used as a guide for treatment of exposures to methyl parathion. When specific exposures have occurred, poison control centers and medical toxicologists should be... 

EPA (1988a) has discussed the results of another carcinogenicity bioassay on methyl parathion in rats. Results of this study have not been presented in a peer-reviewed scientific journal and are not available to the public. 

A discussion of the results reported should take into consideration both the pharmacological and toxicological aspects per se, and their interpretation in terms of the health hazards presented by parathion. 

The pest control situation in California and Florida is reviewed, with particular attention to mechanical developments and the introduction of new fungicides and insecticides, such as the insoluble coppers and parathion, and the outstanding unsolved problems such as control for nematodes which will not injure the plant and the need for a systemic material which will control virus diseases. Emphasis is on needed lines of investigation. Pest control problems in Central America, the Caribbean Islands, and South America are discussed, with special reference to lack of suitable equipment and material because of dollar exchange problems. 

Percents volatilized in one day for the various media were calculated using initial pesticide amounts and the overall volatilization rate constants, obtained from the half life for volatilization as output by EXAMS. Mevlnphos results are not included here, for as discussed previously, methods for calculation used in EXAMS are not appropriate for water miscible compounds. The experimental and computer predicted percents volatilized in one day are qualitatively similar (Figure 2). Quantitatively, experimental and predicted percents volatilized agreed within a factor of three for diazlnon, methyl parathion, and malathion, and within a factor of five for parathion. Considering the fact that EXAMS was not intended for use with wet soil systems, these results are encouraging. 

The development of pesticides, for instance, led to the development of genetically engineered organisms and enzymes to handle particularly difficult or uncoimnon organics. Organophosphate pesticides (malathion, diazinon, parathion, etc.) are examples that will be discussed in detail in subsequent chapters. To develop this technology commercially, however, many of the microorganisms must be isolated because they are expensive or are not safe to release to effluent streams. 

Fish have a relatively poor ability for oxidative metabolism compared with the commonly used laboratory animals such as rats and mice. Insects such as flies have microsomal enzymes, and these are involved in the metabolism of the insecticide parathion to the more toxic paraoxon as discussed in the previous chapter (chap. 4, Fig. 25). 

Desulfuration is the term given to removal of sulfur from a molecule. One of the most common desulfuration reactions occurs with sulfur bonded to phosphorus. A common desulfuration reaction is the enzyme-mediated conversion of parathion to paraoxon (see discussion of organophosphate insecticides in Section 18.7) ... 

OPs are chemicals used in agriculture as acaricides, herbicides, and insecticides (Appendix 5-A-l). Because of their toxicity, several of these chemicals are being phased out from use parathion (ethyl) is an example. Many have been now classified by the United States Environmental Protection Agency (USEPA) as a restricted use pesticide (RUP) or a general use pesticide (GUP). Pesticide chemistry has taken a turn for the synthesis, manufacture, and use of still safer compounds. A list of OPs considered for banning has been identified by the USEPA (Table 5-3). The following pages will briefly discuss the uses and toxicity of different OPs. 

Therefore, manufacturing and processing industries are sources of the nitrophenols in soils and may cause groundwater contamination near the disposal sites. As has been discussed in Section 5.2.2, the application of parathion formulations to foliage could be an additional source of 4-nitrophenol in soil. Atmospheric to terrestrial transfer, primarily through rainwater and snow, will be secondary sources of the nitrophenols in water and soil (Luenberger et al. 1988). Deposition of vehicular exhaust on roadways is another source of nitrophenols in soil. No quantitative estimate of the amounts of the two nitrophenols released into soil from the latter three sources is available. 

Space does not permit further discussion of the fate of various organic pesticides in mans environment. Some of the fate reactions involving the older pesticides have been extensively studied, but the picture is far from complete, even for such compounds as DDT and parathion. However, increasingly greater emphasis on more fundamental research is being made, particularly with the recently introduced pesticides, to determine all their possible metabolites under varying environmental conditions. 

There is a vast chemistry of organophosphorus compounds, and even for arsenic, antimony, and bismuth, the literature is voluminous. Consequently only a few topics can be discussed here. It must also be noted that we discuss only the compounds that have P—C bonds. Many compounds sometimes referred to as organophosphorus compounds that are widely used as insecticides, nerve poisons, and so on, as a result of their anticholinesterase activity, do not, in general, contain P—C bonds. They are usually organic esters of phosphates or thiophosphates examples are the well-known malathion and parathion, (EtO)2Pv(S)(0C6H4NO2). Compounds with P—C bonds are almost entirely synthetic, though a few rare examples occur in Nature. 

Chronic toxicity of organophosphates may be discussed under four different areas carcinogenicity, delayed neurotoxicity, experimental myopathy, and, in humans, psychiatric disorders. In 1983, the IARC (International Agency for Research on Cancer) evaluated the carcinogenic potential of, among other pesticides, five organophosphate insecticides/acaricides (malathion, methyl parathion, parathion,... 

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