Propoxur exposure

Currently, insufficient evidence exists to indicate any significant long-term health risk associated with propoxur exposure. 

The internal dose of propoxur was measured by assessing the total amount of 2-isopropoxyphenol (IPP) excreted in the urine, collected over a period of 24 hr from the start of exposure, and described in detail in previous studies (Brouwer et al., 1993 Meuling et al., 1991). Volunteer kinetics studies revealed a one-to-one relationship of absorbed propoxur and excreted IPP on a mole basis. Based on the results by Machemer et al. (1982), a pulmonary retention of 40% was used to calculate the relative contribution of the respiratory exposure to the internal exposure. To estimate the contribution of the dermal exposure, the calculated respiratory portion was subtracted from the total amount of IPP excreted in urine. 

Figure 1 Distribution of the potential dermal exposure of applicators (N = 3, n = 9) to propoxur and of harvesters (N = 6, n = 18).

Table 2 Ranges (and Medians) of Actual Exposure of the Hands (in pg Propoxur)...

Concentrations of propoxur in the breathing zone ranged from 0.6 to 25 (median, 0.7) pg/m3, and from 0.4 to 29.4 (median, 1.2) pg/m3 for applicators in exposure scenarios without and with protective clothing, respectively. For... 

Table 4 Internal Exposure (Dose) of Propoxur Expressed as Excreted Amount of 2-Isopropoxyphenol (nmol IPP)...

In 1985, Berteau and Mengle (1985) of the California Department of Health Services and Maddy of the Department of Food and Agriculture conducted a preliminary review of pesticides used indoors. They noted several cases (six) from the Pesticide Illness Surveillance system in which illness was reported after structural pest control. Hypothetical exposure estimates for infants, children, and adults following label use for propoxur, DDVP, and chlorpyrifos were sometimes greater than toxic levels. In 1987, Berteau et al. (1989) reiterated the concern about the potential magnitude of indoor exposures, particularly for children. 

Most insecticides, especially the organophosphate group, cause neurotoxicity as their major mode of action. Assessment of the neurotoxicity includes neurochemical endpoints such as cholinesterase (including acetylcholinesterase, which is the major neurotransmitter in vertebrates such as fish, and other enzymes such as butyrylcholinesterase) inhibition and behavioral endpoints such as swimming speed [79]. Studies done in rats show the neurotoxic action of insecticides such as dimethoate, methyl parathion, dichlorvos, ethyl parathion or propoxur after a prolonged exposure [80,81]. 

Turfgrass chemicals are by no means the only toxic hazard faced by average people, nor indeed the most unjust or egregiously unfair one, of course. Consider, for example, the disproportionately high exposure of inner city residents to propoxur, chlorpyrifos, diazinon, and permethrin used to treat the insects and pests that are an everyday part of life in poorly maintained structures, rented by absent and indifferent landlords. The use of such chemicals in lawn management is far less directly utilitarian than in inner city homes, however such urban residents face a health hazard where lawn managers face a mere nuisance, if that. 

When propoxur in ethanol was irradiated by UV light, only one unidentified cholinesterase inhibitor formed. Exposure to sunlight for 3 h yielded no photodecomposition products (Crosby et ah, 1965). 

Like other carbamates, propoxur can inhibit the action of cholinesterase and disrupt nervous system function. Depending on the severity of exposure, this effect may be short-term and reversible. 

Human adults have ingested single doses of 50 mg of propoxur without apparent symptoms. Prolonged or repeated exposure to propoxur may cause symptoms similar to acute effects. Propoxur is very efficiently detoxified (transformed into less toxic or practically nontoxic forms), making it possible for rats to tolerate long periods of daily doses approximately equal to the LD50 of the insecticide, provided that the dose is spread out over the entire day, rather than ingested all... 

Cross-resistance refers to a situation in which a strain that becomes resistant to one insecticide automatically develops resistance to other insecticides to which it has not been exposed. For example, selection of a strain of Spodoptera littoralis with fenvalerate resulted in a 33-fold increase in tolerance to fenvalerate. The resistant strain also showed resistance to other pyrethroids (11- to 36-fold) and DDT (lower than for the pyrethroids). Exposure of Cidex qninquefasciatus to fenitrothion resulted in the development of resistance to the carbamate insecticide propoxur. Similarly, selection of a housefly strain with permethrin resulted in a 600-fold increase in resistance to permethrin. The resistant strain also showed resistance to methomyl, DDT, dichlorvos, and naled (Hassall, 1990). 

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. 

Dermal absorption of propoxur in humans has been estimated to be 16% estimated absorption from the gastrointestinal tract in experimental studies with humans has been complicated due to propoxur-induced emesis. A biological half-life of 3.1 h has been determined and 2-isopropoxyphenol is the major metabolite. The majority of the dose undergoes urinary excretion within 48 h of exposure. In rats, both the parent compound and 2-isopropoxyphenol appear to be eliminated primarily in the urine as sulfate conjugates. 

Institoris L, Siroko O, Undeger U, et al. Detection of the effects of repeated dose combined propoxur and heavy metal exposure by measurement of certain toxicological, haematological and immune function parameters in rats. Toxicology2001 163(2 3) 185 93. 

Institoris, L Papp, A Siroki, O., and Banerjee, B, D, (2004), Comparative inve,stigation of behavioral, neurotoxicological, and immunotoxicological Indices in detection of subacute combined exposure with methyl parathion and propoxur in rats. Ecotoxicol Environ. Safety 57,270-277. 

Photolytic. Though no products were identified, the half-life in UV irradiated water (X >290 nm) was 87.9 hours (Jensen-Korte et al, 1987). When propoxur in ethanol was irradiated by UV light, only one unidentified cholinesterase inhibitor formed. Exposure to sunlight for 3 hours yielded no photodecomposition products (Crosby et al., 1965). 

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