Aldicarb exposure

The Mil by report listed 18 reentry cases from 1949 to 1971 in California citrus (2). Gunther and coworkers cited 47 reentry incidents from 1949 to 1976 in California citrus (3). Peoples et al. reported 38 cases of occupational illness in California Hue to aldicarb exposure from 1974 to 1976 (4). Approximately 14 of these cases were due to exposure to aldicarb residues. 

The acute effects of aldicarb exposure are due to cholinergic overstimulation and may include the SLUDGE syndrome (salivation, lacrimation, urination, diarrhea, gastrointestinal cramping, and emesis), respiratory depression, bronchospasms, increased bronchial secretions, pulmonary edema, blurred vision, miosis, headache, tremors, muscle fasciculations, convulsions, mental confusion, coma, and death due to respiratory failure. Recovery from nonlethal exposures occurs very rapidly, usually within a few hours. 

Researchers have examined the possible effects of aldicarb on the induction of peripheral neuropathies. Currently, insufficient evidence exists to indicate any significant long-term health risk associated with aldicarb exposure. The US Environmental Protection Agency s (EPA) Office of Pesticide Programs has classified aldicarb as group E - evidence of noncarcinogenicity for humans. 

Farmer Farm Family Exposure. Last year, the U. S. Environmental Protection Agency warned women of childbearing age to avoid farm fields recently treated with the herbicide dinoseb because the chemical might cause birth defects. Another study, conducted by a team of medical scientists, found that Kansas farmers exposed to a widely-used corn and wheat herbicide for 20 days or more a year had a sixfold increase in a certain kind of lymph cancers compared to non-farmers. And a third study from Wisconsin noted possible immune-system suppression due to aldicarb exposure. 

Table VI. Suimary of aldicarb exposure assessment PRZM simulations.

Information about exposure to infants, children, and other subgroups is then combined with toxicity information to determine the potential risks posed. If risks are unacceptable, the FDA and EPA will not approve the tolerances. Some of the EPA s recent important regulatory decisions, for example, were based on concerns about childhood or infant exposures, such as the elimination of the use of aldicarb on bananas and EBDCs on a number of fruits and vegetables. 

Edmiston, C.E., Jr., Goheen, M., Malaney, G.W., and Mills, W.E. Evaluation of carbamate toxicity acute toxicity in a culture of Paramecium multlmlcronucleatum upon exposure to aldicarb, carbaryl, and mexacarbate as measured by a Warburg respirometry and acute plate assay. Environ. Res., 36(2) 338-350, 1985. 

The general chemical structure of N-methyl carbamate is shown in Fig. 4.4. Common N-methyl carbamates in use today include aldicarb, carbofuran, methiocarb, oxamyl, and carbaryl. N-methyl carbamates share with organophosphates the capacity to inhibit cholinesterase enzymes and, therefore, share similar symptomology during acute and chronic exposure. 

The UK Pesticide Safety Directorate (PSD) has decided to use the TEF approach for assessment of combined risk from exposure to mixtures of acetyl cholinesterase inhibitors (organophosphate (OP) compounds and carbamates) (PSD 1999). Despite clear differences in the action of carbamates and OP compounds, the index compounds selected for all acetyl cholinesterase inhibitors were either aldicarb (carbamate) or chlorpyrifos (OP). The POD for determining relative potency was predetermined as the dose level that produced 20% inhibition of red blood cell cholinesterase in a 90-day dietary study in rats. 

Carbamates (carbaryl, benomyl, carbofuran, aldicarb, methomyl). Symptoms of exposure were nausea, dizziness, b listers, dermatitis, malaise, sweating, tearing, breathing difficulty, and chest tightness. Usually, incidents have occurred within 1 to 2 days after application except for aldicarb (up to 4 days after application). 

Aldicarb is readily absorbed from all routes of exposure. Oxidation reactions rapidly convert aldicarb to aldicarb sulfoxide, of which a small portion may then be slowly oxidized to aldicarb sulfone. Both the parent compound and its oxidized metabolites can be converted to their respective oximes and nitriles, which may ultimately be converted to aldehydes, acids, and alcohols. Animal studies have indicated aldicarb and its metabolites are distributed to many different tissues but no evidence of accumulation has been found. In the various tissues examined, aldicarb residues were not detected more than 5 days after exposure. The presence of aldicarb in fetal tissue indicates placental transfer in pregnant rats. Various aldicarb metabolites have been found in the milk of cows acutely treated with aldicarb. 

Toxicity of organophosphates can be potentiated 15-20-fold in rats and mice by pretreatment with a metabolite of tri-O-cresylphosphate, CBDP (2-0-cresyl)-4H-l,3,2-benzodioxa-phosphorin-2-oxide), which is an irreversible inhibitor of CarbEs. In similar studies, tetraisopropylpyrophosphoramide (iso-OMPA), or mipafox, an organophosphate-irreversible inhibitor of CarbEs, potentiates three-to fivefold the toxicity of several OPs (soman, DFP, and methylparathion) and carbamates (carbofuran, aldicarb, propoxur, and carbaryl). Inhibition of CarbEs by CBDP, iso-OMPA, or mipafox pretreatment, particularly in plasma, liver, heart, brain, and skeletal muscles, is a major contributory factor in the potentiation of toxicity of organophosphates and carbamates. Thus, the toxicity of any drug, pesticide, or other type of agent that is normally detoxified by CarbEs, could be potentiated by pre-exposure to an organophosphorus or other carboxylesterase inhibitor. 

The introduction in the early 1970 s of the soil-incorporated, water-soluble systemic insecticide/nematicide aldicarb was regarded as a major advance in the technology of pest control. It eliminated the once prevalent hazard of inadvertent exposure of applicators or inhabitants of nearby dwellings, wildlife, and useful insects to toxic chemicals during spraying or aerial application of pesticides. 

As stated earlier, the means by which to test a model are dependent on the biases of the model tester and the purposes of his exercise. The purpose of the calibration in this study is to set up the exposure assessment simulations, which will determine the potential for aldicarb to contaminate the ground water in the scenarios modeled. As will be seen shortly, this potential is represented by model results at a point deep in the unsaturated zone. As such, it becomes Imperative to accurately portray aldicarb fate in the unsaturated zone. Since these field studies showed that high concentrations of aldicarb were maintained near the soil surface, parameters were adjusted to portray that behavior. If anything, this exercise has uncovered a discrepancy between model theory and reality, and a future direction in PRZM development and/or field testing might be to test the theories proposed. Nonetheless, the calibration in this study is valid since the purpose is to duplicate reality, given the limitations of the model. 

The calculated criterion assumes that 100% of exposure to aldicarb is from drinking water, with an average consumption of 2 1/day. 

It. should also be noted that some studies have shown improvements in learning associated with exposure to cholinesterase inhibitors. These effects in rats were either transient during exposure or observed at low doses or after recovery the compounds studied include parathion (water maze Evens et al., 1998), chlorfenvinpho.s (active avoidance Socko et al., 1999), and aldicarb (passive avoidance and water maze Palumbo et al., 2001). These observations probably reflect the memory-enhancing properties of low levels of cholinergic stimulation, the basis for the therapeutic use of some cholinesterase inhibitors in the treatment of Alzheimer s dementia. 

Chronic exposure to aldicarb-contaminated groundwater and human imtnune function. Fnvimn. Res. 41, 633-645. 

Hajoui. 0 Flipo, D Mantiour, S., Fournier, M., and Krzystyniak, K. (1992). Immunotoxicity of. subchionic versus chronic exposure to aldicarb in mice. /nr. 7. Immunopharmacol. 14,1203-11. 

Enzyme-immnnoassay for Aldicarb , in Biological Monitoring of Pesticide Exposure, Measurement, Estimation and Risk Reduction, eds. R.G.M. Wang, C.A. Franklin, R.C. Honeycut, J.C. Reinhert, ACS Symposium Series... 

C. Many of these agents can be absorbed by inhalation and ingestion and through the skin (with the exception of aldicarb, most carbamates are poorly absorbed across the skin compared with organophosphates). Highly lipophilic organophosphates (eg, disulfoton, fenthion, and others) are stored in fat tissue, which may lead to persistent toxicity lasting several days after exposure. 

---