Pesticides human fatalities

The effects of pollution can be direct, such as toxic emissions providing a fatal dose of toxicant to fish, animal life, and even human beings. The effects also can be indirect. Toxic materials which are nonbiodegradable, such as waste from the manufacture of insecticides and pesticides, if released to the environment, are absorbed by bacteria and enter the food chain. These compounds can remain in the environment for long periods of time, slowly being concentrated at each stage in the food chain until ultimately they prove fatal, generally to predators at the top of the food chain such as fish or birds. 

Available records Indicate that worldwide each year, there are about 1,000,000 accidental human poisonings and about 20,000 human deaths (50). In the U.S. there are 20,000 reported human pesticide poisonings and about 35 reported fatalities each year (Blondell,... 

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... 

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. 

A cellular toxicant like arsenic. Fatal human dose is about 500 mg of thallium. Intake of thallium causes depilation. Many reported fatalities. An experimental teratogen. When heated to decomposition it emits very toxic fumes of SOx and Tl. Pesticide for control of rats, moles, and house mice. See also THALLIUM COMPOUNDS and SULFATES. 

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. 

Many of these are phosphate or thiophosphate esters. Some organophosphorus insecticides and other pesticide products are almost immediately toxic to humans, while others appear to be nontoxic, at least in the short and medium term. Specialised references need to be consulted. Best known of the extremely toxic varieties are Parathion and tetraethylpyrophosphate (TEPP), both of which can be rapidly fatal by inhalation, ingestion or skin absorption. Potential long-term hazards from residual traces of relatively non-toxic pesticides (or their breakdown products) are currently the subject of much investigation and concern. 

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