Pralidoxime is the only oxime antidote to organophosphate poisoning stocked in the United Kingdom, produced by rational drug design in the 1950s. Typically, it is used alongside atropine, to reverse the effects of acetylcholinesterase inhibition. However, its efficacy has been questioned by recent meta-analyses of use treating attempted suicides in less economically developed countries, where organophosphate poisoning is more common. This policy analysis assesses the likely efficacy of pralidoxime in the United Kingdom, in scenarios largely different from those evaluated in meta-analyses. In all scenarios, the UK delay in antidote administration poses a major problem, as pralidoxime acts in a time-critical reactivation mechanism before “ageing” of acetylcholinesterase occurs. Additionally, changes in the organophosphates used today versus those pralidoxime was rationally designed to reverse, have reduced efficacy since the 1950s. Finally, the current dosage regimen may be insufficient. Therefore, one must re-evaluate our preparedness and approach to organophosphate poisoning in the United Kingdom.

Field and greenhouse experiments in 1981 and 1982 determined the potential interactions of three preemergence and three postemergence herbicides with four granular insecticides in soybeans [Glycine max (L.) Merr.]. Generally, metribuzin [4-amino-6-tert-butyl-3-(methylthio)-as-triazin-5(4H)-one] increased soybean injury and lowered yields when applied to plots treated with an organophosphate insecticide at planting. Soybean injury from these treatments and from aldicarb [2-methyl-2-(methylthio)-propionaldehyde-o-(methylcarbamoyl)oxime] plus metribuzin applied in the field was greater in 1982 than 1981 due to excessive rainfall immediately after planting. Oryzalin (3,5-dinitro-N4,N4 -dipropylsulfanilamide) plus several of the in-furrow insecticide treatments in the greenhouse increased injury to soybeans. Other than this, the method of insecticide application, banded or in-furrow, had no effect on that caused by each pesticide combination.

Oryzaephilus mercator and O. surinamensis are stored grains and processed food pests, the latter being responsible for major economical losses. Polyacrylamide gel electrophoresis was used to analyse esterase patterns during insect development. Seven esterases, three cholinesterases, two carboxylesterases and two acetylesterases, were identified in O. mercator, one of which was proper to adults. Five esterases, of which four were cholinesterases, occurred in O. surinamensis. Strains of O. mercator and O. surinamensis were also exposed to malathion and chlorpyrifos-methyl. According to the LC50 estimates, OmLC-M and OmLA strains of O. mercator and OsLB strain of O. surinamensis were the most resistant to both insecticides. However, higher sensitivity to malathion and chlorpyrifos-methyl has also been verified in some of its esterases. Cholinesterases OmEST-1 and OsEST-5 seem to be involved in this resistance. These results suggest that organophosphate tolerance may be related to genetic variability in esterase isoenzymes.

The susceptibility of representative pyrethroid (cypermethrin, deltamethrin, lambdacyhalothrin, bifenthrin), organophosphate (chlorpyriphos, triazophos, profenophos) and new chemistry insecticides (spinosad, indoxacarb and emamectin) was investigated for 18 field populations of Plutella xylostella (Linnaeus) from three different zones in Pakistan. The LC50 (mg ml−1; 48 h) values of pyrethroids for various populations ranged from 0.19–1.88 for cypermethrin, 0.31–2.64 for deltamethrin, 0.08–1.16 for lambdacyhalothrin and 0.07–0.88 for bifenthrin. The LC50 (mg ml−1; 48 h) of organophosphates ranged from 0.52–5.67 for chlorpyriphos, 0.37–4.14 for triazophos and 0.03–2.65 for profenophos. The most probable reason for low toxicity of organophosphates and pyrethroids is the evolution of multiple resistance mechanisms; however, further studies are required to establish these mechanisms. When these same products were tested against a susceptible laboratory population (Lab-Pak), the new chemistry compounds were significantly more toxic than pyrethroids and organophosphates. The results are discussed in relation to integrated pest management and insecticide resistance management strategies for P. xylostella.

On 14 July 1991, at 2150 h, a train derailment occurred near the Cantara rail curve about six miles above Dunsmuir in Northern California. The derailment spilled approximately 19,000 gallons of metam-sodium into the Sacramento River. When mixed with loater, metam-sodium degrades to methylisothiocyanate (MITC) and other gases. The contaminated river water passed the town of Dunsmuir and other occupied areas exposing residents to MITC gas.

From 15 July to 20 July (five days), a total of 360 people underwent triage. The majority of patients displayed minor exposure symptoms that did not require hospital care. Mercy Mt. Shasta Hospital, a small rural hospital close to Dunsmuir, received the majority of patients. As of 29 July, 15 days after the incident, Mercy Mt. Shasta Hospital had seen 244 exposed patients in its emergency department, and had admitted five. Three had symptoms that could have been spill-related. Three Regional Poison Control Centers provided medical toxicology advice.

Medical management of the emergency medical services (EMS) response to the event was piecemeal and weak. There did not appear to be a medical operations component at local Emergency Operations Centers (EOC). Most health care personnel interviewed complained about inadequate information about the substance and the situation. Local fire service mutual- aid agreements to obtain additional fire service and ambulance personnel worked well. It is important to emphasize that everyone who believed they had been exposed to the chemical underwent triage and received appropriate acute medical care.