Propoxur toxicity

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. 

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. 

Figure 1. Relationship between the mosquito larvicidal toxicity (log LC50) of the thiocarbamate derivatives of carbofuran, propoxur and m-isopropylphenyl methylcarbamate (MIP) and logarithm of the octanol/water partition coefficient (log P).

Arylsulfenylated methylcarbamates also may have other interesting types of selectivity. An example is given in the honey bee and house fly toxicity data in Table II for several derivatives of propoxur (13). Propoxur and most of the derivatives were highly toxic to the honey bee in fact, compounds 10-15 were substantially more toxic to the honey bee than to the house fly (also see Table I). The order of toxicity, however, was reversed with the 4-jt-butylphenyl analog (16) and the 2-methyl-4- t-butylphenyl analog (17) was virtually nontoxic to the honey bee, although it was still effective against the house fly. 

Toxicity of N-AryIsulfenyl Derivatives of Propoxur to the Honey Bee and House Fly... 

Toxicity Propoxur is highly toxic via the oral route. The acute oral LD50 is 50 mg/kg in rats and mice and 40 mg/kg for guinea pigs. Propoxur is only slightly toxic via the dermal route, with acute dermal LD50 of more than 5,000 mg/kg in rats. The acute LC50 for rats (4 hours) is more than 0.5 mg/L. Studies have shown that propoxur does not cause skin or eye irritation in rabbits. 

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... 

The most important inhibitors of CarbEs are organo-phosphorus insecticides (malathion, parathion, para-oxon, methyl parathion, EPN, and others), nerve agents (DFP, soman, sarin, tabun, and VX) and carbamate insecticides (carbofuran, carbaryl, aldicarb, propoxur, oxamyl, methomyl, and others). Organo-phosphorus toxicants inhibit CarbEs irreversibly by phosphorylation and carbamates inhibit CarbEs reversibly by carbamylation similar to the basic mechanism (i.e., acylation of the active site) ... 

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. 

Gupta RC and Kadel WL (1990) Toxic interaction of tet-raisopropylpyrophosphoramide and propoxur Some insights into the mechanisms. Archives of Environmental Contamination and Toxicology 19 917-920. 

Considerable research effort has been paid to the problems of the persistence of chemical means for the plant protection. Many of the studies have been aimed at the persistence of pesticides in the soil. Insecticides based on chlorinated hydrocarbons are particularly persistent, for instance DDT, BHC isomers and so-called polychlorinated cyclodiene compounds, aldrin, dieldrin, andrin, heptachlor. In many countries the use of these pesticides has been either restricted or even prohibited on account of their persistence in the environment. For chemical protection of plants they are gradually being replaced by organophosphate and carbamate substances, which are more toxic, but are less stable in the environment (e.g. parathion, dichlor-vos, carbaryl, propoxur). 

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