Do targeted bans of insecticides to prevent deaths from self-poisoning result in reduced agricultural output?

BACKGROUND: The pesticides monocrotophos, methamidophos, and endosulfan were a very common cause of severe poisoning in Sri Lanka during the 1980s and early 1990s, before they were banned in 1995 and 1998. Now, the most commonly used insecticides are the less toxic World Health Organization Class II organophosphorus pesticides and carbamates. These bans were followed by a large reduction in both fatal poisonings and suicide in Sri Lanka. OBJECTIVE: We aimed to see if these bans adversely affected agricultural production or costs. METHODS: We used data from the World Resources Institute to compare the yields of the main crop groups in Sri Lanka with those from surrounding South Asian countries for 1980-2005. We also examined data from the Sri Lankan Department of Census and Statistics to examine the yields of 13 specific vegetable crops and rice for 1990-2003, along with the costs of rice production. RESULTS: We found no drop in productivity in the years after the main bans were instituted (1995, 1998). We observed substantial annual fluctuation in estimated yields in all data sources, but these did not coincide with the bans and were no larger than the fluctuations in other countries. Also, there was no sudden change in costs of rice production coinciding with bans. CONCLUSIONS: Countries aiming to apply restrictions to reduce deaths from pesticide poisoning should evaluate agricultural needs and develop a plan that encourages substitution of less toxic pesticides. If farmers have an affordable alternative for pest control for each crop, there is no obvious adverse effect on agricultural output.

Pesticide poisoning in south India: opportunities for prevention and improved medical management.

OBJECTIVE: Warangal district in Andhra Pradesh, southern India, records >1000 pesticide poisoning cases each year and hundreds of deaths. We aimed to describe their frequency and distribution, and to assess quality of management and subsequent outcomes from pesticide poisoning in one large hospital in the district. METHODS: We reviewed data on all patients admitted with pesticide poisoning to a district government hospital for the years 1997 to 2002. For 2002, details of the particular pesticide ingested and management were abstracted from the medical files. FINDINGS: During these 6 years, 8040 patients were admitted to the hospital with pesticide poisoning. The overall case fatality ratio was 22.6%. More detailed data from 2002 revealed that two-thirds of the patients were <30 years old, 57% were male and 96% had intentionally poisoned themselves. Two compounds, monocrotophos and endosulfan, accounted for the majority of deaths with known pesticides in 2002. Low fixed-dose regimens were used in the majority of cases for the most commonly used antidotes (atropine and pralidoxime). Inappropriate antidotes were also used in some patients. CONCLUSIONS: It is likely that these findings reflect the situation in many rural hospitals of the Asia Pacific region. Even without an increase in resources, there appear to be significant opportunities for reducing mortality by better medical management and further restrictions on the most toxic pesticides.

Efficacy of trimedoxime in mice poisoned with dichlorvos, heptenophos or monocrotophos.

The aim of the study was to examine antidotal potency of trimedoxime in mice poisoned with three direct dimethoxy-substituted organophosphorus inhibitors. In order to assess the protective efficacy of trimedoxime against dichlorvos, heptenophos or monocrotophos, median effective doses and efficacy half-times were calculated. Trimedoxime (24 mg/kg intravenously) was injected 5 min. before 1.3 LD50 intravenously of poisons. Activities of brain, diaphragmal and erythrocyte acetylcholinesterase, as well as of plasma carboxylesterases were determined at different time intervals (10, 40 and 60 min.) after administration of the antidotes. Protective effect of trimedoxime decreased according to the following order: monocrotophos > heptenophos > dichlorvos. Administration of the oxime produced a significant reactivation of central and peripheral acetylcholinesterase inhibited with dichlorvos and heptenophos, with the exception of erythrocyte acetylcholinesterase inhibited by heptenophos. Surprisingly, trimedoxime did not induce reactivation of monocrotophos-inhibited acetylcholinesterase in any of the tissues tested. These organophosphorus compounds produced a significant inhibition of plasma carboxylesterase activity, while administration of trimedoxime led to regeneration of the enzyme activity. The same dose of trimedoxime assured survival of experimental animals poisoned by all three organophosphorus compounds, although the biochemical findings were quite different.

Mortality of globally threatened Sarus cranes Grus antigon from monocrotophos poisoning in India.

Globally threatened Sarus cranes Grus antigon are resident at Keoladeo National Park World Heritage site and the surrounding area near Bharatpur, Western Rajasthan, India. In winter, they are joined by c. 200 wintering common cranes Grus grus. On 23 November 2000, 15 Sarus cranes and three common cranes were found dead in a field adjacent to the park, where wheat seed had been sown the previous day. Chemical analyses of seed samples from the field and the cranes' alimentary tract contents identified residues of the organophosphate insecticide monocrotophos. Monocrotophos concentrations of 0.8 and 1.8 ppm were found in wheat samples, and 0.2-0.74 ppm (x=0.33) in the alimentary tract contents of five of the seven cranes examined. No other organophosphate or organochlorine pesticides were detected. We conclude that the cranes died from monocrotophos poisoning after eating treated seed. We discuss similar incidents of avian mortality, and recommend that measures be taken to reduce these.

The importance of electrodiagnostic studies in acute organophosphate poisoning.

Six patients with acute organophosphate pesticide poisoning in whom electrodiagnostic studies influenced or supported specific decisions in management are described. One patient was admitted to hospital with a diagnosis of acute alcoholic intoxication. Electrodiagnostic studies revealed single stimulus induced repetitive responses and decrement-increment responses at 30 and 50 Hz repetitive nerve stimulation, findings that are indicative of a depolarization block due to inactivation of acetylcholinesterase at the motor end-plate. The patient was subsequently treated as a case of acute organophosphate poisoning. The administration of edrophonium (0.1 mg) to another patient with normal neuromuscular transmission studies unmasked the latent electrophysiological abnormalities. Three instances are described in which electrodiagnostic studies were useful in predicting whether pralidoxime administration was likely to be useful and for how long was pralidoxime therapy to be continued. Phrenic nerve conduction study in one patient with impending respiratory failure revealed an unstimulable phrenic nerve. The potential role of phrenic nerve conduction studies and neuromuscular transmission studies in influencing decisions like intubation and mechanical ventilation is discussed.

Monocrotophos--worker safety.

Monitoring data on field-worker exposure studies show that prolonged or continued use of monocrotophos in plant protection may lead to significant dermal exposure with an impact on cholinesterase activity. Although oral uptake (suicide) is more hazardous than dermal exposure (spray work), both exposure routes may be potentially fatal. On the other hand, prompt therapy is successful even after a heavy oral dose. The epidemiological review did not reveal a prominent risk scenario. Justification of monocrotophos use depends on agricultural need and appropriate safety measures. Eighteen cases of monocrotophos poisoning have been identified in the literature and from the manufacturer's case file. Seven cases were occupational, and nine resulted from suicide attempts. One case was a nonprofessional accident, and one was recorded without details. Further monocrotophos poisoning cases may be concealed in the unspecified data on poisoning among tropical farming communities. However, the fact remains, that only a small number of reliably reported poisoning cases are attributable to monocrotophos products, and the reports confirm the efficacy of basic medical attention to poisoning. This is in contrast to the high hazard classification and to the high perceived hazard of the products in question. Safetywise, monocrotophos appears to be better than its reputation. A level of safety precautions normally recommended for pesticide work is sufficient, even under large-scale professional use conditions, to utilize monocrotophos safely.

Type II paralysis or intermediate syndrome following organophosphorous poisoning.

Three cases of type II paralysis or intermediate syndrome following organophosphorous poisoning are reported. Two patients had an initial improvement followed by development of paralysis of neck flexors, cranial nerves, proximal muscles of the limbs and respiratory muscles, which occurred 48 to 96 hours after the poisoning. All the patients recovered completely.

Respiratory failure from severe organophosphate toxicity due to absorption through the skin.

Organophosphates are the most common group of chemicals involved in poisoning in Sri Lanka. Usually, poisoning is by ingestion for suicidal purposes, although accidental poisoning is not uncommon. Poisoning due to absorption through intact or damaged skin is rare. A 32-year-old man was admitted to a peripheral hospital following assault with a 100-ml bottle of insecticide called Monocrotophos, an organophosphate. He had a 2-in. long laceration just above his left eyebrow and there was spilling of the liquid contained in the bottle over his head and face. The liquid was wiped off but the head or face was not washed. After about 3 h the patient developed symptoms and signs of early organophosphate poisoning which were treated with atropine and pralidoxime. On the 3rd day, while on therapy, the patient developed severe weakness of limbs and respiratory distress needing intubation and assisted ventilation. The patient was transferred to the neurology intensive care unit of the General Hospital, Colombo, on the eighth day. His serum potassium levels were low and an ECG showed prominent U waves in all leads. The plasma cholinesterase levels were within 37.5-50% of normal even on the 20th day indicating severe exposure.

Neurotoxic effects of organophosphorus insecticides. An intermediate syndrome.

Acute neurotoxic effects during the cholinergic phase of organophosphorus insecticide poisoning and delayed neurotoxic effects appearing two to three weeks later are well recognized. We observed 10 patients who had paralysis of proximal limb muscles, neck flexors, motor cranial nerves, and respiratory muscles 24 to 96 hours after poisoning, after a well-defined cholinergic phase. The compounds involved were fenthion, monocrotophos, dimethoate, and methamidophos. Four patients urgently required ventilatory support. The paralytic symptoms lasted up to 18 days. A delayed polyneuropathy later developed in one patient. Three patients died. Electromyographic studies showed fade on tetanic stimulation, absence of fade on low-frequency stimulation, and absence of post-tetanic facilitation, suggestive of a postsynaptic defect. This neuromuscular junctional defect may have been the predominant cause of the paralytic symptoms, with neural and central components contributing to various degrees. Our patients appeared to have a distinct clinical entity (a so-called intermediate syndrome) that developed after the acute cholinergic crisis and before the expected onset of the delayed neuropathy.

Fatal poisoning with a plant protective containing monocrotophos, dodine and dinocap.

The toxicological findings after fatal poisoning with a plant protective containing monocrotophos, dodine and dinocap are described and discussed. While monocrotophos could be measured in all tissues and in blood 12 microgram/g, lung 13 microgram/g, brain 13 microgram/g, kidney 11 microgram/g, liver 1.8 microgram/g), measurable amounts of dodine (detection limit approx. 3 microgram/g) and dinocap (detection limit approx. 4 microgram/g) were not detected in these materials. The gastric contents contained 52 mg of monocrotophos, 7.5 mg of dodine and 20 mg of dinocap.

Treatment of monocrotophos-poisoned birds of prey with pralidoxime iodide.

Monocrotophos, and organophosphorus insecticide, was sprayed by farmers to control a plague of levant voles in alfalfa fields. Large numbers of birds of prey attracted by the dying and dead voles developed secondary poisoning after eating the voles. Paralysis of skeletal muscles was the principal clinical finding in these birds. Many of the birds died but some were treated with pralidoxime iodide, 100 mg/kg of body weight, given by intramuscular injection. All treated birds recovered, some in a very short time.