Disulfoton detection limit

The primary method for the disposal of liquid pesticide wastes in California in the past has involved soil evaporation pits, ditches, and ponds (Winterlin et al. 1989). A core soil sample taken from one such pit in northern California contained 44 mg/kg disulfoton at a depth of 90 cm (Winterlin et al. 1989). Disulfoton was detected in six of seven bottom soil samples from tail water pits used to collect irrigation runoff in Haskell County, Kansas, in 1974. The maximum and mean concentrations of disulfoton in these samples were 32.7 and 13.42 pg/kg respectively (Kadoum and Mock 1978). At a detection limit of 0.01 mg/kg, disulfoton was not detected in sediment samples collected from Lakes Superior and Huron, including Georgian Bay, in 1974 (Glooschenko et al. 1976). 

The purpose of this chapter is to describe the analytical methods that are available for detecting, and/or measuring, and/or monitoring disulfoton, its metabolites, and other biomarkers of exposure and effect to disulfoton. The intent is not to provide an exhaustive list of analytical methods. Rather, the intention is to identify well-established methods that are used as the standard methods of analysis. Many of the analytical methods used for environmental samples are the methods approved by federal agencies and organizations such as EPA and the National Institute for Occupational Safety and Health (NIOSH). Other methods presented in this chapter are those that are approved by groups such as the Association of Official Analytical Chemists (AOAC) and the American Public Health Association (APHA). Additionally, analytical methods are included that modify previously used methods to obtain lower detection limits, and/or to improve accuracy and precision. 

The presence of disulfoton and/or its metabolites in the liver appears to be a sensitive indicator of disulfoton exposure, despite the limited data. Supporting evidence from animal studies indicates that disulfoton exposure will result in detectable levels in the liver (Bull 1965 Puhl and Fredrickson 1975). However, monitoring of liver levels would require biopsy, which is not practical. 

Urine catecholamines may also serve as biomarkers of disulfoton exposure. No human data are available to support this, but limited animal data provide some evidence of this. Disulfoton exposure caused a 173% and 313% increase in urinary noradrenaline and adrenaline levels in female rats, respectively, within 72 hours of exposure (Brzezinski 1969). The major metabolite of catecholamine metabolism, HMMA, was also detected in the urine from rats given acute doses of disulfoton (Wysocka-Paruszewska 1971). Because organophosphates other than disulfoton can cause an accumulation of acetylcholine at nerve synapses, these chemical compounds may also cause a release of catecholamines from the adrenals and the nervous system. In addition, increased blood and urine catecholamines can be associated with overstimulation of the adrenal medulla and/or the sympathetic neurons by excitement/stress or sympathomimetic drugs, and other chemical compounds such as reserpine, carbon tetrachloride, carbon disulfide, DDT, and monoamine oxidase inhibitors (MAO) inhibitors (Brzezinski 1969). For these reasons, a change in catecholamine levels is not a specific indicator of disulfoton exposure. 

Increased levels of urinary catecholamines may also be associated with accumulation of acetylcholine that resulted from acetylcholinesterase inhibition by disulfoton. No human data were located to support this, but limited animal data provide some evidence. Disulfoton exposure caused a 173% and 313% increase in urinary noradrenaline and adrenaline levels in rats, respectively, within 72 hours (Brzezinski 1969). The major metabolite of catecholamine metabolism, HMMA, was also detected in the urine from rats given acute doses of disulfoton (Wysocka-Paruszewska 1971). 

---