Prenatal Pesticide Exposure Research Articles

First trimester pesticide-related exposure behaviors and NNNS scores in infants from the SAWASDEE birth cohort

Background: Prenatal pesticide exposures have been associated with adverse neurodevelopmental outcomes in several studies. A prospective birth cohort, the Study of Asian Women and their Offspring’s Development and Environmental Exposures (SAWASDEE) evaluated the association between self-reported pesticide exposure behaviors during early pregnancy and neurodevelopment in infants. We examined behaviors associated with pesticide exposures in occupational settings to further understand potential sources of prenatal pesticide exposure and the implications for neurobehavioral outcomes in infants. Methods: Pregnant women working in agricultural settings provided information on pesticide-related exposures through detailed questionnaires. We investigated their pesticide-related exposure behaviors during the first trimester and their offspring’s neurobehavioral outcomes measured by the NICU Network Neurobehavioral Scales (NNNS). Results: Among those with first trimester exposure information, 272 women reported working since their last menstrual cycle. 58% of working women handled and applied fertilizers and 38% handled containers of pesticides. Common crop types were fruit (tangerines and/or longan; 44.41%) and rice (23.90%). Participants reported wearing long-sleeved shirts (84.93%), other protective clothing (boots, apron, waterproof pants; 67.28%) and face covers (i.e. scarf/handkerchief; 52.94%) for personal protection against pesticide exposures. For NNNS scale scores ranging from 1 to 9, average summary scores were 5.72±0.81 for attention, 3.69±0.54 for arousal, and 6.02±0.60 for regulation. Handling scores ranged between 0 and 1, and the average was 0.20±0.23. Maternal handling of pesticide containers did not increase infant’s OR of having poorer attention (crude OR: 1.06; 95% CI: 0.41, 2.69) or arousal scores (crude OR: 1.02, 95% CI: 0.49, 2.13). However, working with tangerines during the first trimester increased infant’s OR of having poorer handling scores (crude OR: 3.62; 95% CI: 1.44, 9.11). Conclusions: Prenatal pesticide-related behaviors in agricultural settings can lead to poorer neurobehavioral outcomes in the offspring, as demonstrated with the standardized NNNS summary scores.

Report of prenatal maternal demoralization and material hardship and infant rhinorrhea and watery eyes

BackgroundPreviously, we found that reported infant rhinorrhea and watery eyes without a cold (RWWC) predicted school age exercise-induced wheezing, emergency department visits, and respiratory-related hospitalizations for asthma. These findings appeared independent of infant wheezing and allergy. Overall, we theorize that prenatal material hardship and psychosocial distress can induce infant dysregulation in the autonomic nervous system leading to infant RWWC and school age exercise-induced wheezing. ObjectiveTo test the hypotheses that indicators of prenatal stress and measures of maternal demoralization, which can alter infant autonomic nervous system responses, would predict infant RWWC. MethodsIn a prospective birth cohort of urban children (n = 578), pregnant women were queried in the third trimester about material hardship and maternal demoralization using validated instruments. Child RWWC was queried every 3 months in infancy. ResultsNotably, 44% of the mothers reported not being able to afford at least one of the basic needs of daily living during pregnancy, and children of those mothers were more likely to have infant RWWC (P < .001). The children had an increased risk of RWWC with increasing maternal demoralization during pregnancy (P < .001). In models controlling for sex, race and ethnicity, maternal asthma, maternal allergy, smoker in the home (pre- or postnatal), prenatal pesticide exposure, and older siblings, RWWC was predicted by mother's report of material hardship (relative risk, 1.22; P = .021) and maternal demoralization (relative risk, 1.14; P = .030). ConclusionThese results suggest an association between material hardship and psychological distress during pregnancy and RWWC in infancy, further supporting a link between infant autonomic dysregulation and RWWC.

Prenatal pesticide exposure and childhood leukemia - A California statewide case-control study.

A number of epidemiologic studies with a variety of exposure assessment approaches have implicated pesticides as risk factors for childhood cancers. Here we explore the association of pesticide exposure in pregnancy and early childhood with childhood acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML) utilizing land use and pesticide use data in a sophisticated GIS tool. We identified cancer cases less than 6 years of age from the California Cancer Registry and cancer-free controls from birth certificates. Analyses were restricted to those living in rural areas and born 1998-2011, resulting in 162 cases of childhood leukemia and 9,805 controls. Possible carcinogens were selected from the Environmental Protection Agency's classifications and pesticide use was collected from the California Department of Pesticide Regulation's (CDPR) Pesticide Use Reporting (PUR) system and linked to land-use surveys. Exposures for subjects were assessed using a 4000m buffer around the geocoded residential addresses at birth. Unconditional logistic and hierarchical regression models were used to assess individual pesticide and pesticide class associations. We observed elevated risks for ALL with exposure to any carcinogenic pesticide (adjusted Odds Ratio (aOR): 2.83, 95% CI: 1.67-4.82), diuron (Single-pesticide model, adjusted (OR): 2.38, 95% CI: 1.57-3.60), phosmet (OR: 2.10, 95% CI: 1.46-3.02), kresoxim-methyl (OR: 1.77, 95% CI: 1.14-2.75), and propanil (OR: 2.58, 95% CI: 1.44-4.63). Analyses based on chemical classes showed elevated risks for the group of 2,6-dinitroanilines (OR: 2.50, 95% CI: 1.56-3.99), anilides (OR: 2.16, 95% CI: 1.38-3.36), and ureas (OR: 2.18, 95% CI: 1.42-3.34). Our findings suggest that in rural areas of California exposure to certain pesticides or pesticide classes during pregnancy due to residential proximity to agricultural applications may increase the risk of childhood ALL and AML. Future studies into the mechanisms of carcinogenicity of these pesticides may be beneficial.

Prenatal pesticide exposure and respiratory health outcomes in the first year of life: Results from the infants' Environmental Health (ISA) study.

Growing evidence suggests that pesticide exposure may influence respiratory health, but data in young children are very limited. We examined the association of prenatal pesticide exposure with lower respiratory tract infections (LRTIs) and wheeze at one year of age in children from the Infants' Environmental Health (ISA) study in Costa Rica. We measured seven pesticide metabolites, including ethylenethiourea (ETU, metabolite of mancozeb), in maternal urine samples collected repeatedly during pregnancy. For each woman, we averaged pesticide concentrations during each half of pregnancy (≤20 and>20 weeks of gestation) and across repeated samples collected over the course of pregnancy. We collected information about LRTIs (n=355) and wheezing (n=272) during the first year of life from mothers when their children were 11-19 months old. We fit multivariable logistic regression models using high (quartile 4) vs. low (quartiles 1-3) urinary pesticide concentrations as exposures and adjusted models for maternal age, education, parity, gestational age at birth, and child sex. Ten percent of the children had at least one LRTI and 39% had at least one episode of wheezing during their first year of life. Median (25-75th percentile) specific gravity-corrected urinary ETU concentrations during the first half, second half, and over the course of pregnancy were 3.4 (2.1-5.0), 3.3 (2.2-4.7), and 3.4 (2.4-5.0) ng/mL, respectively. We observed that high urinary ETU concentrations during the first half of pregnancy were associated with increased odds of LRTI (OR=2.45; 95% CI: 0.96, 6.26), whereas high urinary ETU concentrations during the second half of pregnancy were associated with decreased odds of wheezing (OR=0.50; 95% CI: 0.26, 0.96). We found that the association between high urinary ETU concentrations during the first half of pregnancy and LRTIs persisted among mother-child pairs with either high or low ETU concentrations during the second half. In contrast, the association of high urinary ETU concentrations during the second half of pregnancy with wheezing was attenuated when we simultaneously adjusted for urinary ETU concentrations during the first half. We observed null associations between other pesticide metabolites measured during pregnancy and respiratory outcomes. Our data indicate that exposure to mancozeb/ETU during the first half of pregnancy may be associated with respiratory outcomes in the first year of life.

Association of prenatal pesticide exposures with adverse pregnancy outcomes and stunting in rural Bangladesh

BackgroundPesticide exposure during pregnancy is thought to adversely affect fetal growth, which in turn may impact child growth, but results have been inconsistent across studies and few have explored these effects in developing countries. ObjectivesTo quantify urinary concentrations of pesticide biomarkers in early pregnancy (<16 weeks’ gestation), and to estimate the association of these concentrations with preterm birth, low birth weight, small for gestational age, and stunting at ~1 and 2 years of age. MethodsEight pesticide biomarkers were quantified in urine collected from 289 pregnant women (aged 18–40 years) participating in a birth cohort study in Bangladesh. Anthropometry measurements were conducted on the index child at birth and approximately 1 and 2 years of age. A directed acyclic graph was used to identify minimal sufficient adjustment sets. Log-binomial regression was used to estimate the relative risk (RR) with 95% confidence intervals (CI). Results3,5,6-trichloro-2-pyridinol (TCPY), a metabolite of chlorpyrifos and chlorpyrifos methyl, and 4-nitrophenol, a metabolite of parathion and methyl parathion, were detected in nearly all women with geometric mean (95% CI) values of 3.17 (2.82–3.56) and 18.66 (17.03–20.46) µg/g creatinine, respectively. 3-phenoxybenzoic acid (3-PBA), a non-specific metabolite of several pyrethroids, and 2-isopropyl-4-methyl-6-hydroxypyrimidine (IMPY), a diazinon metabolite, were detected in 19.8% and 16.1% of women, respectively. The remaining four pesticide biomarkers were detected in <10% of women. Women in the highest quartile of 4-nitrophenol were more than 3 times more likely to deliver preterm than women in the lowest quartile: unadjusted RR (95% CI), 3.57 (1.65, 7.73). Women in the highest quartile of 4-nitrophenol were also at increased risk of having a child born small for gestational age: RR (95% CI) adjusted for household income, maternal education, and maternal total energy and meat intake, 3.81 (1.10, 13.21). Women with detectable concentrations of IMPY were at increased risk of having a child born with low birth weight compared to women with non-detectable concentrations: adjusted RR (95% CI), 2.13 (1.12, 4.08). We observed no association between any of the pesticide biomarkers and stunting at 1 or 2 years of age. DiscussionExposure to the insecticides parathion and diazinon during early pregnancy may increase the risk of adverse birth outcomes.

Organophosphate Exposures, Financial Hardship and Child Neurodevelopmental Outcomes in the CHARGE study

OPS 55: Pesticides and neurological outcomes, Room 412, Floor 4, August 26, 2019, 1:30 PM - 3:00 PM In-utero exposure to organophosphate pesticides has been associated with neurodevelopmental delay. This study examined whether maternal report of inability to pay for basic needs (food, housing, medical care and heating) modified the relationship between prenatal pesticide exposure and autism spectrum disorder (ASD). Methods: We studied 488 children with ASD and 329 typically-developing controls aged 2-5 years enrolled between 2003 and 2008 in the CHARGE (Childhood Autism Risks from Genetics and the Environment) study, a population-based, case-control investigation. Diagnoses were confirmed by standardized assessments and information regarding maternal factors was determined from a structured interview with the mother. Residential proximity to agricultural application of organophosphate pesticides, based on California Department of Pesticide Regulation data, was determined by spatial analysis of maternal residence before and during pregnancy. Multiple logistic regression was used to examine the association between exposure during several time points during the pregnancy, and effect modification by the experience of financial hardship. Results: 213 (26%) CHARGE study mothers lived within 1.5 km of agricultural application of organophosphate compounds during their pregnancies. ASD odds were elevated in those exposed to pesticides between the 3 months prior to conception up through delivery (adjusted odds ratio (aOR) 2.44; 95% CI [1.05, 5.63]). Odds for mothers with 2nd trimester organophosphate exposure was higher for women with financial hardship compared to those without, 3.01; 95% CI [1.34, 6.75] vs 1.92; 95% CI [1.35, 2.76], respectively. This disparity was particularly pronounced for chlorpyrifos exposure, where those with financial hardship exhibited odds ratios ranging from 5 to 15 at all pregnancy timepoints. Conclusions: This study identified financial hardship as an amplifier of the association between organophosphate pesticide exposures during pregnancy and offspring ASD. It adds to the existing evidence highlighting the importance of studying the co-exposure of social and environmental factors affecting children at early developmental stages.

Prenatal organophosphorus pesticide exposure and childhood adiposity in the Mount Sinai Children’s Environmental Health Study

Prenatal organophosphorus pesticide exposure and childhood adiposity in the Mount Sinai Children’s Environmental Health Study

Residential sources of pesticide exposure during pregnancy and the risks of hypospadias and cryptorchidism: the French ELFE birth cohort

ObjectivesPrenatal occupational exposure to pesticides has been associated with male reproductive tract abnormalities. Little is known about the possible impact of non-occupational pesticide exposure on fetal and child development in...

Prenatal pesticide exposure associated with glycated haemoglobin and markers of metabolic dysfunction in adolescents

BackgroundPesticide exposure has been associated with increased risk of diabetes mellitus in adults, but potential effects of prenatal exposure on glucose regulation have not been investigated.The aim of this study was to investigate if maternal occupational pesticide exposure in pregnancy was associated with glycated haemoglobin A1c (HbA1c) in adolescents and whether an association was modified by sex and paraoxonase-1 (PON1) Q192R polymorphism. MethodsA prospective cohort study of children whose mothers were either occupationally exposed or unexposed to pesticides in early pregnancy. At age 10-to-16 years, the children (n = 168) underwent clinical examinations including pubertal stage assessment (accepted by 141 children) and blood sampling. PON1 Q192R genotype was available for 139 children and 103 mothers.The main outcome measure was HbA1c but other relevant biomarkers were also included. ResultsPrenatal pesticide exposure was associated with a 5.0% (95% confidence interval: 1.8; 8.2) higher HbA1c compared to unexposed children after adjustment for confounders. After stratification, the association remained significant for girls (6.2% (1.6; 11.1)) and if the child or the mother had the PON1 192R-allele (6.1% (1.6; 10.8) and 7.1% (2.0; 12.6), respectively). Besides, an exposure-related increase was seen for the leptin-to-adiponectin ratio, for plasminogen activator inhibitor type-1 in girls, and for interleukin-6 in children whose mothers had the R-allele. ConclusionPrenatal pesticide exposure was associated with higher HbA1c and changes in related biomarkers in adolescents. Our results suggest an adverse effect on glucose homeostasis and support previous findings from this cohort of an exposure-associated metabolic risk profile with higher susceptibility related to female sex and the PON1 192R-allele.

Combined Prenatal Pesticide Exposure and Folic Acid Intake in Relation to Autism Spectrum Disorder.

Background:Maternal folic acid (FA) protects against developmental toxicity from certain environmental chemicals.Objective:We examined combined exposures to maternal FA and pesticides in relation to autism spectrum disorder (ASD).Methods:Participants were California children born from 2000–2007 who were enrolled in the Childhood Autism Risks from Genetics and the Environment (CHARGE) case–control study at age 2–5 y, were clinically confirmed to have ASD () or typical development (), and had information on maternal supplemental FA and pesticide exposures. Maternal supplemental FA and household pesticide product use were retrospectively collected in telephone interviews from 2003–2011. High vs. low daily FA intake was dichotomized at (median). Mothers’ addresses were linked to a statewide database of commercial applications to estimate agricultural pesticide exposure.Results:High FA intake () during the first pregnancy month and no known pesticide exposure was the reference group for all analyses. Compared with this group, ASD was increased in association with and any indoor pesticide exposure {adjusted odds ratio [95% confidence interval (CI): 1.3, 4.7]} compared with low FA [ (95% CI: 0.7, 2.2)] or indoor pesticides [ (95% CI: 1.1, 2.8)] alone. ORs for the combination of low FA and regular pregnancy exposure () to pet pesticides or to outdoor sprays and foggers were 3.9 (95% CI: 1.4, 11.5) and 4.1 (95% CI: 1.7, 10.1), respectively. ORs for low maternal FA and agricultural pesticide exposure 3 mo before or after conception were 2.2 (95% CI: 0.7, 6.5) for chlorpyrifos, 2.3 (95% CI: 0.98, 5.3) for organophosphates, 2.1 (95% CI: 0.9, 4.8) for pyrethroids, and 1.5 (95% CI: 0.5, 4.8) for carbamates. Except for carbamates, these ORs were approximately two times greater than those for either exposure alone or for the expected ORs for combined exposures under multiplicative or additive models.Conclusions:In this study population, associations between pesticide exposures and ASD were attenuated among those with high versus low FA intake during the first month of pregnancy. Confirmatory and mechanistic studies are needed. https://doi.org/10.1289/EHP604

The Impact of Prenatal Organophosphate Pesticide Exposures on Thai Infant Neurodevelopment.

A birth cohort was begun to investigate the levels and sources of pesticide exposure in pregnant women living in Thailand, and to examine the effects of pesticide exposure on infant neurodevelopment at five months of age. Subjects were interviewed using questionnaires regarding their demographic characteristics, educational background, and work and home activities related to pesticide exposures. Spot urine samples were collected at 28 weeks gestation and analyzed by gas chromatography-mass spectrometry to determine maternal metabolite levels of organophosphate pesticides including dimethyl phosphate (DMP); total DEP (diethyl phosphate (DEP), diethyl thiophosphate (DETP), and diethyl dithiophosphate (DEDTP), and total DAP (the sum of all metabolite levels). At five months of age, infant development was evaluated using the Bayley Scales of Infant and Toddler Development-III (Bayley-III). Higher total DEP and total DAP metabolite levels from the mother at 28 weeks’ gestation were significantly associated with reduced motor composite scores on the Bayley-III at five months of age. The total DEP levels were also significantly associated with reduced cognitive composite scores. Prenatal concentrations of maternal urinary metabolites were associated with infant cognitive and motor development. The results of several studies now suggest the need for public health intervention to reduce prenatal pesticide exposures from both agricultural and domestic use.

Interaction between prenatal pesticide exposure and a common polymorphism in the PON1 gene on DNA methylation in genes associated with cardio-metabolic disease risk\u2014an exploratory\xa0study

BackgroundPrenatal environmental conditions may influence disease risk in later life. We previously found a gene-environment interaction between the paraoxonase 1 (PON1) Q192R genotype and prenatal pesticide exposure leading to an adverse cardio-metabolic risk profile at school age. However, the molecular mechanisms involved have not yet been resolved. It was hypothesized that epigenetics might be involved. The aim of the present study was therefore to investigate whether DNA methylation patterns in blood cells were related to prenatal pesticide exposure level, PON1 Q192R genotype, and associated metabolic effects observed in the children.MethodsWhole blood DNA methylation patterns in 48 children (6–11 years of age), whose mothers were occupationally unexposed or exposed to pesticides early in pregnancy, were determined by Illumina 450 K methylation arrays.ResultsA specific methylation profile was observed in prenatally pesticide exposed children carrying the PON1 192R-allele. Differentially methylated genes were enriched in several neuroendocrine signaling pathways including dopamine-DARPP32 feedback (appetite, reward pathways), corticotrophin releasing hormone signaling, nNOS, neuregulin signaling, mTOR signaling, and type II diabetes mellitus signaling. Furthermore, we were able to identify possible candidate genes which mediated the associations between pesticide exposure and increased leptin level, body fat percentage, and difference in BMI Z score between birth and school age.ConclusionsDNA methylation may be an underlying mechanism explaining an adverse cardio-metabolic health profile in children carrying the PON1 192R-allele and prenatally exposed to pesticides.

Prenatal Pesticide Exposure and Autism in Children – a California Statewide Population Based Study

Prenatal Pesticide Exposure and Autism in Children – a California Statewide Population Based Study

Pesticides, Neurodevelopmental Disagreement, and Bradford Hill’s Guidelines

ABSTRACTNeurodevelopmental disorders such as autism affect one-eighth of all U.S. newborns. Yet scientists, accessing the same data and using Bradford-Hill guidelines, draw different conclusions about the causes of these disorders. They disagree about the pesticide-harm hypothesis, that typical United States prenatal pesticide exposure can cause neurodevelopmental damage. This article aims to discover whether apparent scientific disagreement about this hypothesis might be partly attributable to questionable interpretations of the Bradford-Hill causal guidelines. Key scientists, who claim to employ Bradford-Hill causal guidelines, yet fail to accept the pesticide-harm hypothesis, fall into errors of trimming the guidelines, requiring statistically-significant data, and ignoring semi-experimental evidence. However, the main scientists who accept the hypothesis appear to commit none of these errors. Although settling disagreement over the pesticide-harm hypothesis requires extensive analysis, this article suggests that at least some conflicts may arise because of questionable interpretations of the guidelines.

Prenatal pesticide exposure and PON1 genotype associated with adolescent body fat distribution evaluated by dual X-ray absorptiometry (DXA).

Many modern pesticides have endocrine disrupting abilities and early-life exposure may affect growth and disease risk later in life. Previously, we reported associations between prenatal pesticide exposure and higher childhood body fat content measured by anthropometry. The associations were affected by child PON1 Q192R genotype. We aimed to study whether prenatal pesticide exposure was still associated with body fat content and distribution in the children at puberty and the potential impact of both maternal and child PON1 Q192R genotype. In this prospective cohort study of 247 children born by occupationally exposed or unexposed women (greenhouse workers and controls) two follow-up examinations (age 10-15 and 11-16years) including simple anthropometry, skinfold measurements, pubertal staging and blood sampling were performed. Total and regional fat% was determined by dual X-ray absorptiometry (DXA) at age 10-15. Prenatal pesticide exposure was associated with increased total, android, and gynoid fat percentage (DXA) at age 10-15years after adjustment for sex, socioeconomic status, and puberty (all β=0.5 standard deviation score (SDS) p<0.05). Stratified by sex, the associations were significant in girls (total fat: β=0.7 SDS, android-gynoid ratio: β=0.1, both p<0.05), but not in boys. Carrying the R-allele (child or mother, separately, or both) augmented the differences between exposed and unexposed children (total fat: β=1.0 SDS, β=0.8 SDS, p<0.05, respectively, and β=1.2 SDS, p<0.01). No exposure-related differences were found if either the child or mother had the QQ wild-type. At age 11-16, exposed children tended to have a higher total fat% estimated by skinfolds than unexposed children (p=0.06). No significant associations between prenatal exposure and body mass index or waist circumference were found. Prenatal pesticide exposure was associated with higher adolescent body fat content, including android fat deposition, independent of puberty. Girls appeared more susceptible than boys. Furthermore, the association depended on maternal and child PON1 Q192R genotype.

Prenatal exposure to multiple pesticides is associated with auditory brainstem response at 9 months in a cohort study of Chinese infants

BackgroundPesticides are associated with poorer neurodevelopmental outcomes, but little is known about the effects on sensory functioning. MethodsAuditory brainstem response (ABR) and pesticide data were available for 27 healthy, full-term 9-month-old infants participating in a larger study of early iron deficiency and neurodevelopment. Cord blood was analyzed by gas chromatography–mass spectrometry for levels of 20 common pesticides. The ABR forward-masking condition consisted of a click stimulus (masker) delivered via ear canal transducers followed by an identical stimulus delayed by 8, 16, or 64 milliseconds (ms). ABR peak latencies were evaluated as a function of masker-stimulus time interval. Shorter wave latencies reflect faster neural conduction, more mature auditory pathways, and greater degree of myelination. Linear regression models were used to evaluate associations between total number of pesticides detected and ABR outcomes. We considered an additive or synergistic effect of poor iron status by stratifying our analysis by newborn ferritin (based on median split). ResultsInfants in the sample were highly exposed to pesticides; a mean of 4.1 pesticides were detected (range 0–9). ABR Wave V latency and central conduction time (CCT) were associated with the number of pesticides detected in cord blood for the 64ms and non-masker conditions. A similar pattern seen for CCT from the 8ms and 16ms conditions, although statistical significance was not reached. Increased pesticide exposure was associated with longer latency. The relation between number of pesticides detected in cord blood and CCT depended on the infant's cord blood ferritin level. Specifically, the relation was present in the lower cord blood ferritin group but not the higher cord blood ferritin group. ConclusionsABR processing was slower in infants with greater prenatal pesticide exposure, indicating impaired neuromaturation. Infants with lower cord blood ferritin appeared to be more sensitive to the effects of prenatal pesticide exposure on ABR latency delay, suggesting an additive or multiplicative effect.

Distribution and Predictors of Pesticides in the Umbilical Cord Blood of Chinese Newborns.

Rates of pesticide use in Chinese agriculture are five times greater than the global average, leading to high exposure via the diet. Many are neurotoxic, making prenatal pesticide exposure a concern. Previous studies of prenatal exposure in China focused almost entirely on organochlorines. Here the study goals were to characterize the exposure of Chinese newborns to all classes of pesticides and identify predictors of those exposures. Eighty-four pesticides and 12 metabolites were measured in the umbilical cord plasma of 336 infants. Composite variables were created for totals detected overall and by class. Individual pesticides were analyzed as dichotomous or continuous, based on detection rates. Relationships between demographic characteristics and pesticides were evaluated using generalized linear regression. Seventy-five pesticides were detected. The mean number of detects per sample was 15.3. Increased pesticide detects were found in the cord blood of infants born in the summer (β = 2.2, p = 0.01), particularly in July (β = 4.0, p = 0.03). Similar trends were observed for individual insecticide classes. Thus, a summer birth was the strongest predictor of pesticide evidence in cord blood. Associations were more striking for overall pesticide exposure than for individual pesticides, highlighting the importance of considering exposure to mixtures of pesticides, rather than individual agents or classes.

Prenatal pesticide exposure and otitis media during early childhood in the PELAGIE mother–child cohort

ObjectiveContemporary pesticides, such as triazines or organophosphates, possess immunotoxic properties. We aimed to determine whether prenatal environmental exposure to these current-use pesticides was associated with otitis media (OM) during the...

Characterization of Pesticide Exposure in a Sample of Pregnant Women in Ecuador.

Few studies have detailed the prenatal pesticide exposure levels of women employed in or residing near large-scale agricultural industries. This study reports pesticide metabolite levels during and shortly after pregnancy in a pilot study of workers in Ecuador. Urine samples were collected for 16 rose workers and 10 nonagricultural workers enrolled into the study in early pregnancy. We measured six nonspecific organophosphatedialkylphosphate (DAP) pesticide metabolites, two alkylenebis-dithiocarbamate pesticide metabolites [ethylene thiourea (ETU) and propylene thiourea (PTU)], 3,5,6-trichloro-2-pyridinol (TCPy), malathion dicarboxylic acid, and two pyrethroid metabolites (2,2-dimethylcyclo propanecarboxylic acid and 3-phenooxybenzoic acid). We collected 141 urine samples (mean: 5.4 per woman). We observed high detection frequencies for five DAP metabolites and ETU, PTU, and TCPy. We report elevated levels of ETU in the entire sample (median 4.24ng/mL, IQR 2.23, 7.18), suggesting other possible non-occupational pathways of exposure. We found no statistical differences in pesticide levels by current employment status, although the highest pesticide levels were among rose workers. We observed within-woman correlation in TCPy and PTU levels, but not in ETU or DAP levels. The present study is the first to characterize prenatal pesticide exposure levels among working women in Ecuador. Limitations include a small sample size and use of a convenience sample. Strengths include a longitudinal design and multiple urine samples per woman. Results provide an initial characterization of prenatal pesticide exposure levels and how these levels vary over pregnancy in a community impacted by agricultural industry and will inform further studies in the region.

Prenatal Pesticide Exposure and Neurodevelopmental Disorders

Prenatal Pesticide Exposure and Neurodevelopmental Disorders