Pesticide Exposure - HH-RA.org

Bibliography Tag: pesticide exposure

Payne et al., 2012

Payne, K, Andreotti, G., Bell, E., Blair, A., Coble, J., & Alavanja, M., “Determinants of high pesticide exposure events in the agricultural health cohort study from enrollment (1993-1997) through phase II (1999-2003),” Journal of Agricultural Safety and Health, 2012, 18(3), 167-179.

ABSTRACT:

We conducted an analysis of the determinants of high pesticide exposure events (HPEEs), which are defined as self-reported incidents of high exposure to pesticides, fertilizers, or other chemicals in the Agricultural Health Study, a cohort of private applicators and their spouses residing in North Carolina or Iowa, and commercial applicators residing in Iowa. We examined the risk of HPEEs occurring between enrollment (phase 1: 1993-1997) and follow-up (phase II: 1999-2003) among participants who completed the phase II questionnaire (n=43,149) by calculating hazard rate ratios and 95% confidence intervals using Cox proportional-hazard regression. During the followup period, 1,582 HPEEs were reported (3.8%). HPEE risk was significantly higher among Iowa residents, younger participants, those with a hearing deficit, a risk-taking personality, and an HPEE prior to enrollment. Among private applicators (n=30,102), larger farm size, higher frequency and duration of pesticide use, spraying pesticides with open cab windows, using a tractor cab without a charcoal filter, repairing spray equipment, wearing work clothing more than two days without changing, not removing work boots before entering the home, and storing pesticides in the home were associated with significantly higher HPEE risk. Among commercial applicators (n=2326), higher frequency of pesticide use was associated with a significantly higher HPEE risk. Among spouses (n=10,721), higher frequency of pesticide use, using an application vehicle with a cab, and storing pesticides in the home were associated with a significantly higher HPEE risk. Our findings indicate that HPEEs were associated with several modifiable pesticide handling procedures that can be targeted in safety training and education. FULL TEXT

Klarich Wong et al., 2019

Klarich Wong, Kathryn L., Webb, Danielle T., Nagorzanski, Matthew R., Kolpin, Dana W., Hladik, Michelle L., Cwiertny, David M., & LeFevre, Gregory H., “Chlorinated Byproducts of Neonicotinoids and Their Metabolites: An Unrecognized Human Exposure Potential?,” Environmental Science & Technology Letters, 2019, 6(2), 98-105. DOI:10.1021/acs.estlett.8b00706.

ABSTRACT:

We recently reported the initial discovery of neonicotinoid pesticides in drinking water and their potential for transformation through chlorination and alkaline hydrolysis during water treatment. The objectives of this research were: (1) to determine if neonicotinoid metabolites are relevant to drinking water exposure and (2) to identify the products formed from chlorination of neonicotinoids and their metabolites. Desnitro-imidacloprid and imidacloprid-urea, two known metabolites of imidacloprid, are documented for the first time in drinking water. Desnitro-imidacloprid was present above the lower level of detection (0.03 ng/L) in 67% of samples (six of nine) from drinking water systems but detectable in all samples (up to 0.6 ng/L). Although concentrations of desnitro-imidacloprid were lower than concentrations of the parent neonicotinoids, desnitro-imidacloprid exhibits significantly greater mammalian toxicity than imidacloprid. Using LC-HR-ToF-MS/MS analysis of results from laboratory experiments, we propose structures for novel transformation products resulting from the chlorination of clothianidin, imidacloprid, desnitro-imidacloprid, imidacloprid-urea, and hydrolysis products of thiamethoxam. Formation of chlorinated neonicotinoid byproducts occurs at time scales relevant to water treatment and/or distribution for the imidacloprid metabolites (t1/2 values from 2.4 min to 1.0 h) and thiamethoxam hydrolysis products (4.8 h). Neonicotinoid metabolites in finished drinking water and potential formation of novel disinfection byproducts during treatment and/or distribution are relevant to evaluating the exposure and potential impacts of neonicotinoids on human health.

Bradman et al., 2003

Bradman A, Barr DB, Claus Henn BG, Drumheller T, Curry C, Eskenazi B, “Measurement of pesticides and other toxicants in amniotic fluid as a potential biomarker of prenatal exposure: a validation study,” Environmental Health Perspectives, 2003, 111:1779-1782. DOI:10.1289/ehp.6259.

ABSTRACT:

Prenatal pesticide exposures may adversely affect children’s health. However, exposure and health research is hampered by the lack of reliable fetal exposure data. No studies have been published that report measurements of commonly used nonpersistent pesticides in human amniotic fluid, although recent studies of pesticides in urine from pregnant women and in meconium indicate that fetuses are exposed to these chemicals. Amniotic fluid collected during amniocentesis is the only medium available to characterize direct fetal exposures early in pregnancy (approximately 18 weeks of gestation). As a first step in validating this exposure biomarker, we collected 100 amniotic fluid samples slated for disposal and evaluated analytical methods to measure organophosphate and carbamate pesticides and metabolites, synthetic pyrethroid metabolites, herbicides, and chlorinated phenolic compounds. The following six phenols were detected (detection frequency): 1- and 2-naphthol (70%), 2,5-dichlorophenol (55%), carbofuranphenol (5%), ortho-phenylphenol (30%), and pentachlorophenol (15%), with geometric mean concentrations of 0.72, 0.39, 0.12, 0.13, and 0.23 microg/L, respectively, for positive values. The organophosphate metabolites diethylphosphate and dimethylphosphate were detected in two (10%) samples, and dimethylthiophosphate was detected in one (5%) sample, with geometric mean concentrations of 0.31, 0.32, and 0.43 microg/L, respectively, for positive values. These levels are low compared with levels reported in urine, blood, and meconium in other studies, but indicate direct exposures to the young fetus, possibly during critical periods of development. Results of this pilot study suggest that amniotic fluid offers a unique opportunity to investigate fetal exposures and health risks. FULL TEXT

Mao et al., 2018

Mao, Q., Manservisi, F., Panzacchi, S., Mandrioli, D., Menghetti, I., Vornoli, A., Bua, L., Falcioni, L., Lesseur, C., Chen, J., Belpoggi, F., & Hu, J., “The Ramazzini Institute 13-week pilot study on glyphosate and Roundup administered at human-equivalent dose to Sprague Dawley rats: effects on the microbiome,” Environmental Health, 17(1), 50, 2018. doi:10.1186/s12940-018-0394-x.

ABSTRACT:

BACKGROUND: Glyphosate-based herbicides (GBHs) are broad-spectrum herbicides that act on the shikimate pathway in bacteria, fungi, and plants. The possible effects of GBHs on human health are the subject of an intense public debate for both its potential carcinogenic and non-carcinogenic effects, including its effects on microbiome. The present pilot study examines whether exposure to GBHs at doses of glyphosate considered to be “safe” (the US Acceptable Daily Intake – ADI – of 1.75 mg/kg bw/day), starting from in utero, may modify the composition of gut microbiome in Sprague Dawley (SD) rats.

METHODS: Glyphosate alone and Roundup, a commercial brand of GBHs, were administered in drinking water at doses comparable to the US glyphosate ADI (1.75 mg/kg bw/day) to F0 dams starting from the gestational day (GD) 6 up to postnatal day (PND) 125. Animal feces were collected at multiple time points from both F0 dams and F1 pups. The gut microbiota of 433 fecal samples were profiled at V3-V4 region of 16S ribosomal RNA gene and further taxonomically assigned and assessed for diversity analysis. We tested the effect of exposure on overall microbiome diversity using PERMANOVA and on individual taxa by LEfSe analysis.

RESULTS: Microbiome profiling revealed that low-dose exposure to Roundup and glyphosate resulted in significant and distinctive changes in overall bacterial composition in F1 pups only. Specifically, at PND31, corresponding to pre-pubertal age in humans, relative abundance for Bacteriodetes (Prevotella) was increased while the Firmicutes (Lactobacillus) was reduced in both Roundup and glyphosate exposed F1 pups compared to controls.

CONCLUSIONS: This study provides initial evidence that exposures to commonly used GBHs, at doses considered safe, are capable of modifying the gut microbiota in early development, particularly before the onset of puberty. These findings warrant future studies on potential health effects of GBHs in early development such as childhood. FULL TEXT

Harari et al., 2010

Harari, Raul, Julvez, Jordi, Murata, Katsuyuki, Barr, Dana, Bellinger, David C., Debes, Frodi, & Grandjean, Philippe, “Neurobehavioral deficits and increased blood pressure in school-age children prenatally exposed to pesticides,” Environmental Health Perspectives, 118, 890-896, 2010, doi:10.1289/ehp.0901582.

ABSTRACT:

BACKGROUND: The long-term neurotoxicity risks caused by prenatal exposures to pesticides are unclear, but a previous pilot study of Ecuadorian school children suggested that blood pressure and visuospatial processing may be vulnerable.

OBJECTIVES: In northern Ecuador, where floriculture is intensive and relies on female employment, we carried out an intensive cross-sectional study to assess children’s neurobehavioral functions at 6-8 years of age.

METHODS: We examined all 87 children attending two grades in the local public school with an expanded battery of neurobehavioral tests. Information on pesticide exposure during the index pregnancy was obtained from maternal interview. The children’s current pesticide exposure was assessed from the urinary excretion of organophosphate metabolites and erythrocyte acetylcholine esterase activity.

RESULTS: Of 84 eligible participants, 35 were exposed to pesticides during pregnancy via maternal occupational exposure, and 23 had indirect exposure from paternal work. Twenty-two children had detectable current exposure irrespective of their prenatal exposure status. Only children with pre-natal exposure from maternal greenhouse work showed consistent deficits after covariate adjustment, which included stunting and socioeconomic variables. Exposure-related deficits were the strongest for motor speed (Finger Tapping Task), motor coordination (Santa Ana Form Board), visuospatial performance (Stanford-Binet Copying Test), and visual memory (Stanford-Binet Copying Recall Test). These associations corresponded to a developmental delay of 1.5-2 years. Prenatal pesticide exposure was also significantly associated with an average increase of 3.6 mmHg in systolic blood pressure and a slight decrease in body mass index of 1.1 kg/m2. Inclusion of the pilot data strengthened these results.

CONCLUSIONS: These findings support the notion that prenatal exposure to pesticides-at levels not producing adverse health outcomes in the mother-can cause lasting adverse effects on brain development in children. Pesticide exposure therefore may contribute to a “silent pandemic” of developmental neurotoxicity. FULL TEXT

Mattix et al., 2007

Mattix KD, Winchester PD, Scherer LR, “Incidence of abdominal wall defects is related to surface water atrazine and nitrate levels,” Journal of Pediatric Surgery, 2007, 42:6, DOI: 10.1016/j.jpedsurg.2007.01.027

ABSTRACT:

BACKGROUND: Gastroschisis and omphalocele are congenital abdominal wall defects (AWD). Atrazine and nitrates are common agricultural fertilizers.

METHODS: The Centers for Disease Control and Prevention natality data set was used to collect data for patients with AWD born between January 1990 and December 2002. Similar data were obtained from the Indiana State Department of Health. An estimated date of conception was calculated by birth date and gestational age. Surface water nitrate and atrazine levels for Indiana were collected from US Geological Survey data. Midwest was defined as Indiana, Illinois, Iowa, Ohio, and Nebraska. Statistical analysis was performed by chi2 test and Pearson correlation for P < or = .05.

RESULTS: The Centers for Disease Control and Prevention identified 9871 children with AWD in 1990 and in 1995-2001 of 35,876,519 live births (rate 2.75/10(5)). In Indiana, 358 children from 1990-2001 had AWD of 1,013,286 live births (rate 3.53/10(5)). The AWD rate in Indiana was significantly higher than the national rate in 1996 (P = .0377), 1998 (P = .0005), and 2001 (P = .0365) and significantly higher than the Midwest rate in 1998 (P = .0104). Monthly comparison demonstrated a positive correlation of AWD rate and mean atrazine levels (P = .0125).

CONCLUSION: Indiana has significantly higher rates of AWD compared with national rates. Increased atrazine levels correlate with increased incidence of AWD.

Winston et al., 2016

Jennifer J. Winston, Michael Emch, Robert E. Meyer, Peter Langlois, Peter Weyer, Bridget Mosley, Andrew F. Olshan, Lawrence E. Band, Thomas J. Luben and the National Birth Defects Prevention Study, “Hypospadias and maternal exposure to atrazine via drinking water in the National Birth Defects Prevention study,” Environmental Health, 15:76, DOI: 10.1186/s12940-016-0161-9

ABSTRACT:

BACKGROUND: Hypospadias is a relatively common birth defect affecting the male urinary tract. It has been suggested that exposure to endocrine disrupting chemicals might increase the risk of hypospadias by interrupting normal urethral development.

METHODS: Using data from the National Birth Defects Prevention Study, a population-based case-control study, we considered the role of maternal exposure to atrazine, a widely used herbicide and potential endocrine disruptor, via drinking water in the etiology of 2nd and 3rd degree hypospadias. We used data on 343 hypospadias cases and 1,422 male controls in North Carolina, Arkansas, Iowa, and Texas from 1998–2005. Using catchment level stream and groundwater contaminant models from the US Geological Survey, we estimated atrazine concentrations in public water supplies and in private wells. We assigned case and control mothers to public water supplies based on geocoded maternal address during the critical window of exposure for hypospadias (i.e., gestational weeks 6–16). Using maternal questionnaire data about water consumption and drinking water, we estimated a surrogate for total maternal consumption of atrazine via drinking water. We then included additional maternal covariates, including age, race/ethnicity, parity, and plurality, in logistic regression analyses to consider an association between atrazine and hypospadias.

RESULTS: When controlling for maternal characteristics, any association between hypospadias and daily maternal atrazine exposure during the critical window of genitourinary development was found to be weak or null (odds ratio for atrazine in drinking water = 1. 00, 95 % CI = 0.97 to 1.03 per 0.04 μg/day increase; odds ratio for maternal consumption = 1.02, 95 % CI = 0.99 to 1.05; per 0.05 μg/day increase).

CONCLUSIONS: While the association that we observed was weak, our results suggest that additional research into a possible association between atrazine and hypospadias occurrence, using a more sensitive exposure metric, would be useful. FULL TEXT

Lebov et al., 2016

Jill F. Lebov, MSPH, PhD, Lawrence S. Engel, PhD, David Richardson, PhD, Susan L. Hogan, PhD, Jane A. Hoppin, ScD, and Dale P. Sandler, PhD, “Pesticide use and risk of end-stage renal disease among licensed pesticide applicators in the Agricultural Health Study,” Occupational and Environmental Medicine, 2016, 7, DOI: 10.1136/oemed-2014-102615

ABSTRACT:

OBJECTIVES: Experimental studies suggest a relationship between pesticide exposure and renal impairment, but epidemiological evidence is limited. We evaluated the association between exposure to 41 specific pesticides and end-stage renal disease (ESRD) incidence in the Agricultural Health Study (AHS), a prospective cohort study of licensed pesticide applicators in Iowa and North Carolina.

METHODS: Via linkage to the United States Renal Data System, we identified 320 ESRD cases diagnosed between enrollment (1993-1997) and December 2011 among 55,580 male licensed pesticide applicators. Participants provided pesticide use information via self-administered questionnaires. Lifetime pesticide use was defined as the product of duration and frequency of use and then modified by an intensity factor to account for differences in pesticide application practices. Cox proportional hazards models, adjusted for age and state, were used to estimate associations between ESRD and: 1) ordinal categories of intensity-weighted lifetime use of 41 pesticides, 2) poisoning and high-level pesticide exposures, and 3) pesticide exposure resulting in a medical visit or hospitalization.

RESULTS: Positive exposure-response trends were observed for the herbicides alachlor, atrazine, metolachlor, paraquat, and pendimethalin, and the insecticide chlordane. More than one medical visit due to pesticide use (HR = 2.13; 95% CI: 1.17, 3.89) and hospitalization due to pesticide use (HR = 3.05; 95% CI: 1.67, 5.58) were significantly associated with ESRD.

CONCLUSIONS: Our findings support an association between ESRD and chronic exposure to specific pesticides and suggest pesticide exposures resulting in medical visits may increase the risk of ESRD. FULL TEXT

Paz-y-Miño et al., 2007

César Paz-y-Miño, María Eugenia Sánchez, Melissa Arévalo, María José Muñoz, Tania Witte, Gabriela Oleas De-la-Carrera, Paola E. LeoneI, “Evaluation of DNA damage in an Ecuadorian population exposed to glyphosate,” Genetics and Molecular Biology, 2007, 30:2, DOI: 10.1590/S1415-47572007000300026

ABSTRACT:

We analyzed the consequences of aerial spraying with glyphosate added to a surfactant solution in the northern part of Ecuador. A total of 24 exposed and 21 unexposed control individuals were investigated using the comet assay. The results showed a higher degree of DNA damage in the exposed group (comet length = 35.5 µm) compared to the control group (comet length = 25.94 µm). These results suggest that in the formulation used during aerial spraying glyphosate had a genotoxic effect on the exposed individuals. FULL TEXT

Settimi et al., 2008

Laura Settimi PhD Angela Spinelli MSc Laura Lauria MSc Giuseppe Miceli MD Nicoletta Pupp MD Giuliano Angotzi MD Aldo Fedi MD Serena Donati MD Lucia Miligi DSc John Osborn PhD Irene Figà‐Talamanca PhD, “Spontaneous abortion and maternal work in greenhouses,” American Journal of Industrial Medicine, 2008, 51:4, DOI: 10.1002/ajim.20556

ABSTRACT:

BACKGROUND: A positive association between maternal occupational exposure to pesticide and spontaneous abortion has been reported in some studies. Work in greenhouses may imply exposure of pregnant women to pesticides continuously and at elevated level.

METHODS: A total of 717 women working in greenhouses provided information on 973 pregnancies, including 110 spontaneous abortions. These pregnancies were classified as exposed or not exposed according to maternal occupation, re‐entry activities and application of pesticides in greenhouses during at least 1 month in the first trimester of pregnancy. The ORs for spontaneous abortion were estimated through a generalised estimate equations model for all orders of pregnancy together, and through a logistic regression model limited to first pregnancies.

RESULTS: Increased risks of spontaneous abortion were found for maternal re‐entry activities within 24 hr after pesticides were applied (all orders of pregnancy: OR 3.2, 95% CI 1.3–7.7; first pregnancies: OR 3.8, 95% CI 1.0–13.9) and for those who applied pesticides (all orders of pregnancy: OR 2.6, 95% CI 1.0–6.6; first pregnancies: OR 3.7, 95% CI 0.7–20,6)

CONCLUSIONS: The observed results support the hypothesis of an association between maternal work in greenhouses and spontaneous abortion. The main limitations of the study are lack of information on the specific chemicals used and the small number of pregnancies heavily exposed to pesticides.

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