| Abstract |
The aim of this study was to evaluate fetal exposure to
organophosphate pesticides by measuring their non-specific dialkylphosphate
metabolites (DAPs) in amniotic fluid, and to examine the
potential association between prenatal exposure and fetal growth.
The study was carried out between August 2006 and May 2008.
Amniotic fluid samples were collected from 415 women carrying a
singleton pregnancy during the second trimester of pregnancy via
amniocentesis (for medical indications), to the Fetal-Maternal Unit,
Department of Obstetrics and Gynecology, University Hospital of
Heraklion, Crete, Greece. The samples were analyzed to the laboratory of
Toxicology, Medical School, University of Crete.
The determined organophosphate pesticides metabolites were dimethyl
phosphate (DMP), dimethyl thiophosphate (DMTP), diethyl phosphate
(DEP), diethyl thiophosphate (DETP) and diethyl dithiophosphate
(DEDTP). DAPs were extracted by liquid–liquid extraction and measured
by gas chromatography– mass spectrometry.
Twenty two pregnancies resulted in either fetal demise or termination
of pregnancy due to chromosomal abnormalities or major fetal defects.
Mean maternal age was 32.7 (SD = 5.7). The mean gestational age at
amniocentesis was 18.5 weeks (SD = 2.5).
Exposure to organophosphate pesticides expressed as sums of DMPs,
DEPs, DAPs in amniotic fluid samples ranged from 0.07 to 222.9 ng/ml,
0.19 to 254.3 ng/ml, and 0.05 to 252.6 ng/ml, respectively. DEP was the
metabolite with the higher frequency of detection (90.5%), followed by
DETP (74.0%), DMP (60.0%) and DEDTP (39.5%). Almost all amniotic
fluid samples (97.8%) provided at least one positive metabolite of pesticides (DMP, DEP, DMTP, DETP, DEDTP), which are common
metabolites of about 75% of organophosphate pesticides. DAPs levels did
not differ between urban and rural areas (97.8% in urban areas versus
97.9% in rural areas). This makes difficult to pinpoint if the dominant
source of exposure is the diet and home pesticide use or agriculture.
Maternal age does not affect levels of sumDAPs (p> 0.400).
All measured DAPs in the amniotic fluid seem positively associate
with each other (p <0.002) and this could potentially be attributed to the
simultaneous exposure of the participants to methyl and ethyl
organophosphate pesticides.
There was no statistically significant difference with neonatal gender
and the percentage of the head circumference in the levels of DAPs.
Macrosomic neonates had significantly higher sum levels of DMPs (p=
0.043), which exerted a linear positive association with birth-weight
centile (b= 4.43, p= 0.016).
There is also a seasonal variation in the levels of DAPs which can be
explained by the use of specific organophosphate pesticides in certain
types of cultivations. The sumDMPs showed elevated levels in autumn of
2006 and 2007 and spring 2008. DMPs derived of O,Odimethylsubstituted
organophosphate pesticides such as malathion and dimethoate.
The most probable cause of increased dimethyl phosphate metabolite
levels in the autumns of 2006 and 2007 is the systematic spraying of olive
oil trees for dacus oleae using fenthion and dimethoate during the period
between August and September which was approved by the Ministry of
Rural Development & Food in Greece. The sumDEPs showed elevated
levels in winter 2006–2007 and autumn 2007. DEPs derived from O,Odiethyl-
substituted organophosphate pesticides such as chlorpyrifos and
diazinon and their elevated levels may be due to the widespread use of
diazinon in vineyards and fruit. Conclusively, as DAPs are detectable in amniotic fluid they may be
used as a potential biomarker of fetal exposure to organophosphate
pesticides. Sum levels of DMPs appear to be associated with birth weight
independently of other covariates.
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