The Impact of Pesticides - Academy Publish

The acute dermal toxicity of carbamates is generally low to moderate; an exceptionis aldicarb, which is highly toxic. Data are available for only a limited number ofsubstances (IPCS, 1986).Short- and long-term toxicity studies have been carried out. Some carbamates arevery toxic and others are less toxic in long-term studies. For many years, long-termtoxicity data on carbamates have been evaluated by the FAO/WHO Joint Meetingon Pesticide Residues (JMPR), and a number of ADI (the estimate of the amount ofa substance in food, mg/kg body weight/day, that can be ingested daily over alifetime without appreciable health risk to the consumer (WHO 1997)) forcarbamates have been established (IPCS, 1986).Among other pesticides, carbamates have been included in the list of knownendocrine disruptor compounds (Schulte-Oehlmann et al., 2011). In this welldesignedreview authors provide a databanks of a wide range of pesticides withpotentially endocrine-disrupting properties, discussion on some key questionsregarding the multiplicity of variables involved.The onset of clinical effects subsequent to carbamate exposure depends on the dose,route of exposure, type of carbamate involved, use of protective gear, and thepremorbid state of the victim (Rosman et al., 2009). Ingestion or inhalation ofcarbamates results in a more rapid onset of clinical effects as compared with dermalexposure. Acute carbamate poisoning episodes were recently described amongpesticide sprayers due to inadequate personal protection (Jensen et al., 2010). Thereis an increase of pesticide exposure and poisoning in children around the world withconsequent morbidity and mortality (El-Naggar 2009; Balme et al., 2010; Jayashreeet al., 2011) Clinical manifestations for carbamates (excluding herbicides) resultfrom accumulation of ACh in the synapses and overstimulation of muscarinic andnicotinic receptors throughout target organs. The main clinical manifestations of thecarbamate intoxication are muscarinic signs (miosis, salivation, sweating,lacrimation, rhinorrhea, abdominal cramping, vomiting, diarrhea, urinaryincontinence, bronchospasm, dyspnea, hypoxemia, bradycardia, bronchialsecretions, pulmonary edema and respiratory failure), nicotinic signs (less frequent;muscular twitching, fasciculations, muscle weakens including the respiratorymuscles, paralysis, tachycardia, hypertension) and central nervous system signs(rare) (Rosman et al., 2009). The large demand for educational materials thatsummarize the acute toxicity of pesticides is illustrated by the publication of fiveeditions of the Environmental Protection Agency’s Recognition and Management ofPesticide Poisonings (US EPA, 1999; Frazier, 2007).The medical management of carbamate poisoning consists of supportive measuresand specific antidotal treatment, that is, the anticholinergic compound atropine(Rosman et al., 2009). Recovery without medical treatment of cases of accidentaloverexposure with various carbamate pesticides spontaneously occurred, generally,within 4 h of exposure that caused symptoms of headache, dizziness, weakness,excessive salivation, nausea, or vomiting. For accidental or intentional poisoningthat produced symptoms such as visual disturbances, profuse sweating, abdominalpain, incoordination, fasciculations, breathing difficulties, or changes in pulse rate,treatment with atropine combined with general supportive treatment, such asartificial respiration and administration of fluids, has resulted in recovery ofAcademyPublish.org - The Impact of Pesticides23