Congenital anomalies associated with maternal exposure to oxydemeton-methyl

Cholinergic Pesticides

“…Moreover, in animal experiments, AChE activity was shown to be involved in limb bud chondrogenesis (Falugi & Raineri, 1985), and the amount of AChE and ChE present in blood was shown to be depleted for several months in persons exposed to organophosphate pesticides in USA (Romero et al, 1989). In one case, the consequence of the depletion of AChE activity (due to professional OP exposure) in the maternal blood, lasting throughout the pregnancy, caused the birth of a baby with only one eye, brain and heart anomalies, who died after some days (Romero et al, 1989).…”

“…Moreover, in animal experiments, AChE activity was shown to be involved in limb bud chondrogenesis (Falugi & Raineri, 1985), and the amount of AChE and ChE present in blood was shown to be depleted for several months in persons exposed to organophosphate pesticides in USA (Romero et al, 1989). In one case, the consequence of the depletion of AChE activity (due to professional OP exposure) in the maternal blood, lasting throughout the pregnancy, caused the birth of a baby with only one eye, brain and heart anomalies, who died after some days (Romero et al, 1989). During the last decades, neurotransmitter systems (Buznikov, 1990;Buznikov and Shmukler, 1996) and in particular the cholinergic systems (Drews, 1975;Minganti et al, 1981;Fluck et al, 1980 andFalugi, 1993) have been found responsible for cell interactions leading early development.…”

“…The same author reported that OPs are detected in soils years after application, probably due to sorption of the OPs to soil particles, making them unavailable for microbial metabolism (Ragnarsdottir, 2000). As far as living organisms are concerned, the effects of such compounds may last much more, because the AChE of blood may be affected up to several months (see the case report Romero et al 1989). …”

Acute Effects of Organophosphorous Compounds on the Ovine Fetus

“…These include inhibition of protein synthesis in fetal guinea pigs after maternal exposure to parathion (Gupta et al, 1984), presumptive neurotoxicity in human offspring due to exposure of the mother to organophosphorous anticholinesterase insecticides (Romero et al, 1989) and in vitro inhibition of fetal brain acetylcholinesterase by organophosphorous anticholinesterase pesticides (Banerjee et al, 1991). Mehl et al (1994) demonstrated reductions in brain weight of offspring of guinea pigs exposed to trichlorfon or dichlorvos but not to triortho-cresyl phosphate or soman.…”

Acetylcholinesterase plays a non-neuronal, non-esterase role in organogenesis

“…Consistent with this expression, embryo exposure to chemical inhibitors of AChE is associated with structural defects not only in the nervous system, but also in the heart and digestive tract of vertebrates (Pamanji et al, 2015a,b;Snawder and Chambers, 1989;Wyttenbach and Thompson, 1985), including humans (Carmichael et al, 2014;Romero et al, 1989;Sherman, 1995). Although such teratogenicity implicates AChE in non-neuronal organogenesis, genetic evidence is inconclusive.…”