Pesticide neurological effects

The answer is D. Organophosphates react with the active site serine residue of hydrolases such as acetylcholinesterase and form a stable phosphoester modification of that serine that inactivates the enzyme toward substrate. Inhibition of acetylcholinesterase causes overstimulation of the end organs regulated by those nerves. The symptoms manifested by this patient reflect such neurologic effects resulting from the inhalation or skin absorption of the pesticide diazinon. 

Generally, it takes some five to seven years to bring a pesticide to market once its pesticidal properties have been verified. Many tests must be conducted to determine such things as the compound s synthesis, its chemical and physical properties, and its efficacy. In addition, in order for registration for use by the US EPA, numerous toxicity tests are undertaken including those for acute toxicity, those for chronic effects such as reproductive anomalies, carcinogenesis, and neurological effects and those for environmental effects. 

The CNS is the target organ disturbed by all organophosphorus pesticides in different formulations used for the control of crop pests or household pests. It has been observed that exposure to organophosphorous pesticides has caused many neurologic effects. Animals exposed to organophosphorous pesticides have... 

Steenland K 1996 Chronic neurological effects of organophosphate pesticides. British Medical Journal 312 1312-1313... 

Neurological effects are not the only ones that result from low level pesticide exposure. Endocrine and immunological effects have also been reported. 

Ruitjen et al. (1994) studied 131 flower-bulb farmers (average age, 43 years) for neurological effects subsequent to 20 years (mean exposure, SD = 7) of exposure to a mixed pesticide including maneb and zineb for an average length of 20 years. The authors observed exposure-related decreases in conduction velocities in motor fibers of the median and peroneal nerves, and in the sensory fibers of the median and sural nerves. 

There are two studies showing neurological effects following occupational exposures to manganese-containing pesticides (Ferraz et al. 1988 Meco et al. 1984). The Ferraz et al. (1988) study is negahvely impacted by the likely exposure of the subjects to a wide variety of peshcides and the lack of a well-matched control group. Addihonal studies in occupationally-exposed persons with restricted exposure to only maneb and mancozeb are needed. 

Stccnland, K. (1996), Chronic neurological effects of organophos-phatc pesticides. Rr. Med J- 312,312-313. 

Neurological Effects. A major incident of occupationally-related illness associated with a pesticide involved Kepone. Kepone is a chlorinated hydrocarbon insecticide used domestically as an ant and roach poison. In 1975, after workers at a plant... 

Of the 16 POPs listed in the 1998 Aarhus Protocol [27], 11 are organochloride pesticides, which have now been banned in several countries. Most concerns regarding these products relate to their toxicity, with health effects to humans ranging from lung damage and neurological problems to death. Many organochloride pesticides are lipophilic, and they accumulate in the adipose tissues. 

Evidence is similar for humans but limited, and includes male sterility, spontaneous abortions in human females, premature human fetuses, severe neurologic and CNS effects, blood dyscrasias, hepatotoxicity, accumulation of organohalogen pesticides in human lipid tissue—and, perhaps even more important, their presence in human breast milk, whence they can continue to exert influences on growth, development and hormonal, CNS and enzyme systems. Aldrin, dieldrin, chlordane, chlordecone (Kepone), heptachlor epoxide, hexachlorobenzene (HCB) and Mirex are all excreted via breast milk in the human female. This is also true for the related PCBs and PBBs that resist biodecomposition and maintain persistent residence in mammalian tissues. For them, excretion via breast milk may constitute the main—if not sole—elimination route. 

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