Pesticide exposure Fatalities

Pharmacologically, carbofuran inhibits cholinesterase, resulting in stimulation of the central, parasympathetic, and somatic motor systems. Sensitive biochemical tests have been developed to measure cholinesterase inhibition in avian and mammalian brain and plasma samples and are useful in the forensic assessment of carbamate exposure in human and wildlife pesticide incidents (Bal-lantyne and Marrs Hunt and Hooper 1993). Acute toxic clinical effects resulting from carbofuran exposure in animals and humans appear to be completely reversible and have been successfully treated with atropine sulfate. However, treatment should occur as soon as possible after exposure because acute carbofuran toxicosis can be fatal younger age groups of various species are more susceptible than adults (Finlayson et al. 1979). Carbofuran labels indicate that application is forbidden to streams, lakes, or ponds. In addition, manufacturers have stated that carbofuran is poisonous if swallowed, inhaled, or absorbed through the skin. Users are cautioned not to breathe carbofuran dust, fumes, or spray mist and treated areas should be avoided for at least 2 days (Anonymous 1971). Three points are emphasized at this juncture. First, some carbofuran degradation... 

Two fatal cases of occupational exposure to 1,2-dibromoethane were reported by Letz et al. (1984). A worker collapsed shortly after entering a pesticide storage tank containing residues of 1,2-dibromoethane he remained in the tank for 45 minutes. A supervisor attempting to rescue the worker also collapsed and was exposed for 20-30 minutes prior to rescue. Both men died 12 and 64 hours after collapse, respectively. The primary route of exposure was postulated to be dermal, with inhalation also playing a potentially important role. Neither worker had been wearing protective clothing or respirators. 

Figure 2-4 graphically depicts the information that currently exists on the health effects of 1,2-dibromoethane in humans and animals by various routes of exposure. The vast majority of literature reviewed concerning the health effects of 1,2-dibromoethane in humans described case reports and longer-term studies of pesticide workers and case reports of accidental or intentional ingestion of 1,2-dibromoethane. The predominant route of exposure in the occupational studies is belived to be inhalation, with dermal exposure also implied. In a case report of fatalities, dermal exposure was considered the primary route (Letz et al. 1984). The information on human exposure is limited in that the possibility of concurrent exposure to other pesticides or other toxic substances cannot be excluded, and the duration and level of exposure to 1,2-dibromoethane generally cannot be quantified from the information presented in these reports. 

In order to reach a conclusion when and how and, and to some extent, how much of a particular insecticide was administered, the form and quantity in which the insecticide exists in different tissues and in blood and urine may give valuable clues. Indeed, an intelligent deduction is also based on the knowledge of metabolic pathways and formation of other derivatives. Thus, as parathion is excreted in the urine ultimately as p-nitro-phenol, urinary p-nitrophenol levels may indicate the extent of exposure to parathion ). In cases of mild and moderate exposure, the excreted p-nitrophenol in urine was found to be of the order of 0.057 to 0.322 mg. percent. In severe and fatal cases of poisoning by parathion, the level of p-nitrophenol in urine was from 0.16 to 1.16 mg. percent. para-Nitrophenol thus is rapidly excreted in urine and no longer detected 48 hours after the exposure to the pesticide. 

Carbamates and OPs are chemicals that are often used as fungicides, insecticides, or pesticides and possess actions similar to nerve agents. These compounds are considered weapons of opportunity since their primary use is not by conventional militaries. In the USA, toxicity from these compounds is fairly rare. In 2006, there were approximately 1,200 cases of carbamate exposures and 1,500 organophosphate exposures documented for children 19 years old and younger (Bronstein et al, 2007). Although there were a few fatalities reported in 2006 from these substances, these fatalities occurred only in older individuals. 

It is estimated that there are 3.8 million cases of occupational diseases due to exposure to chemicals in the world each year. Of these, acute pesticide poisoning accounts for about 3 million cases. About 220,ci00 of these are fatal. Over 90 % of exposure incidents and about 99% of deaths take place in the third world countries [13]. German Development expert reports on the careless use of pesticides, in Sri Lanka — there they spread DDT with bare hands, people are powdered white , On the Antilles island of Trinidad a total... 

The transfer of pesticides to beverage containers also appears amongst cases of accidental poisoning, and may have particularly disastrous sequelae, especially in the case of paraquat. Decanting paraquat into soft drink or beer bottles has featured in New Zealand paraquat fatalities. The addition of both a stenching agent and an emetic in paraquat formulations was introduced to minimize unintentional exposures of this nature. 

National Poi.son Center in Taiwan indicate that the fatality rate is much higher in Taiwan than in most Western countries, with 5.65% of all poisoning exposure.s resulting in death. There were 6872 cases of pesticide intoxication among 223,436 total cases of various intoxications from 1985 to 1993 (Tabic 6>, and these accounted for approximately 22-30% of the total incidences, from 1991 to 1996. The incidence of pesticide poisoning gradually declined during this time. 

Suicide (7511 patients, 66.7%) was the most common intent of exposure. The oral route (8930 patients, 79.2%) was the most common route of exposure. Table 8 shows increased age. suicide attempt, oral exposure, and concurrent exposure with a higher risk of fatality. In terms of age differences, people 19-39 years old comprised the largest number of injured patients. Acute pesticide poisoning mainly involved adults, and the mean age of patients was 43,3 18.9 years. Acute pesticide poisoning was associated with a very high case fatality rate (14.5%), and there was a wide range of differences in clinical severity among various pesticides. 

A highly toxic substance by ingestion, and possibly by most other routes of exposure moderately toxic by inhalation and skin contact cholinesterase inhibitor toxic effects are similar to those of other carbamate pesticides and include excessive salivation, lacrimation, slow heart rate, blurred vision, twitching of muscle and lack of coordination, nausea, weakness, diarrhea and abdominal pain oral intake of probably 1.5-3 g could be fatal to adult humans a teratogenic substance, producing adverse reproductive effects in experimental animals. 

Althongh strnctural feature in the molecule varies from most other organophosphorus pesticides, the toxic actions are similar to parathion and other phosphate esters. Extremely toxic by all routes of exposure cholinesterase inhibitor can present a serious inhalation hazard, if spilled, due to relatively high vapor pressure exhibits acute, delayed, and chronic effects symptoms of cholinergic effects similar to those of other organophosphates death can result from respiratory arrest ingestion of 0.3-2 g could be fatal to adult human. 

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