Organophosphate Exposure Research Articles

LC-MS/MS-Profiling of Human Serum Unveils Significant Increase in Neuroinflammation and Carcinogenesis Following Chronic Organophosphate Exposure.

The utilization of organophosphate pesticides (OPs) has escalated in response to the growing global food demand driven by a rapidly increasing population and the environmental disruptions caused by climate change. While acute exposure leads to cholinergic poisoning, chronic OP exposure has been linked to organ dysfunction, inflammation, and carcinogenesis. Serum samples from healthy individuals (n = 11), patients with acute OP exposure (n = 12), and those with chronic OP exposure (n = 31) were analyzed to discern the differentially expressed pathways after acute and chronic OP exposure. Differential expression analysis identified 132 proteins altered in chronic exposure vs control, 86 in acute exposure vs control, and 124 in chronic vs acute exposure. Pathway analysis revealed increased blood coagulation and reduced LXR/RXR activation and DCHR24 signaling in both acute and chronic exposures. Elevated levels of pro-inflammatory proteins, such as S100A8, VWF, and GPIBA, were observed, particularly in chronic exposure, highlighting significant inflammatory effects of OP exposure. These findings provide insights into the pathological mechanisms underlying chronic OP exposure and its contribution to inflammation and long-term health risks.

A review on oxidative stress in organophosphate-induced neurotoxicity.

Acetylcholinesterase inhibition, the principal mechanism of acute organophosphorus compound toxicity, cannot explain neuropsychiatric symptoms occurring after exposure to low organophosphate concentrations causing no cholinergic symptoms. Organophosphate-triggered oxidative stress has increasingly come into focus, occurring when the action of reactive oxygen species, generated from free radicals, is not compensated by antioxidant free radical scavengers. Being nucleophilic, organophosphates can easily accept an electron, thereby generating free radicals. Organophosphates inhibit the antioxidant paraoxonase, and reactive oxygen species are produced during organophosphate metabolism. Organophosphates disrupt the function of mitochondria, the principal source of free radicals. Organophosphates also induce neuroinflammation, which generates reactive oxygen species, and reactive oxygen species in turn stimulate neuroinflammation. Markers of reactive oxygen species are elevated in vitro and in vivo after exposure to organophosphates and in individuals professionally exposed to organophosphates. This most probably contributes to the pathogenesis of the intermediate syndrome and chronic organophosphate-induced neuropsychiatric disorders occurring in patients after organophosphate exposure. Evidence for beneficial effects of antioxidants in organophosphate poisoning is discussed.

Exploring the reproductive exposure risks of phthalates and organophosphates in atmospheric particulate matter based on quantitative structure-activity relationships and network toxicology models.

Minimal study focused on the association between mixed pollutants in atmospheric particulate matter (PM2.5) and their reproductive health risks. Utilizing a novel quantitative structure-activity relationship (QSAR) integrated machine learning algorithms, we evaluated the mixed reproductive health risks associated with phthalates (PAEs) and organophosphates (OPEs) exposure by assessing the affinities of these compounds binding to estrogen receptors (ER) and androgen receptors (AR). The mixed toxicity equivalent factor (TEFmix) and mixed toxicity equivalent quantity (TEQmix) by the QSAR model were all smaller than the sum TEF and TEQ of individual PAEs and OPEs, which may be due to the antagonistic effect of PAEs and OPEs monomers on reproductive toxicity. Based on network toxicology approach, a total of 590 potential targets associated with PAEs and OPEs affecting sex hormones were initially identified, with an additional 50 core targets, including AR and ER. Di-2-ethylhexyl phthalate (DEHP), triphenyl phosphate (TPHP) and mono-(2-ethylhexyl) phthalate (MEHP) were key components to disrupt AR and ER signaling pathway, and was confirmed by molecular docking analysis. In addition to ER and AR, serine/threonine kinase 1 (AKT1) and heat shock protein 90α family A member 1 (HSP90AA1) might be key targets for reproductive toxicity, which have hardly mentioned before. Our study provided precious information on the mixed reproductive exposure risk of PAEs and OPEs in PM2.5, and innovatively explored the potential mechanisms of PAEs and OPEs affecting human reproductive health using network toxicology.

Neurobehavioral Performance in Preschool Children Exposed Postnatally to Organophosphates in Agricultural Regions, Northern Thailand.

Evidence of the effects of postnatal exposure to organophosphates (OPs) on children's neurodevelopment remains limited but crucial. This cross-sectional study evaluated exposure to OPs and neurobehavioral performance in 172 preschool children. Urinary dialkyl phosphate (DAP) metabolites, biomarkers for exposure to OPs, were measured. The neurobehavioral assessments included motor skills, memory, and cognitive function, measured using the Purdue pegboard test, digit span test, object memory test, and visual-motor integration. Multiple linear regression models were employed to explore the associations between urinary DAP metabolite levels and neurobehavioral performance, adjusting for potential confounders. Findings revealed that children of farming parents had higher urinary levels of dimethylphosphate (DMP) (Beta = 0.730, 95% CI = 0.138, 1.322, p value = 0.016) and diethylphosphate (DEP) (Beta = 0.668, 95% CI = 0.044, 1.291, p value = 0.036). Additionally, high fruit consumption correlated with increased urinary DEP levels (Beta = 0.398, 95% CI = 0.063, 0.733, p value = 0.020). Critically, elevated urinary DEP was associated with poorer fine motor coordination, affecting performance in the Purdue pegboard test for the dominant hand (Beta = -0.428, 95% CI = -0.661, -0.194, p value < 0.001), the preferred hand (Beta = -0.376, 95% CI = -0.603, -0.149, p value = 0.001), and both hands (Beta = -0.524, 95% CI = -0.773, -0.276, p value < 0.001). These findings highlight the role of parental occupation and diet in children's OP exposure and suggest that OP exposure negatively impacts fine motor coordination. Targeted interventions, such as promoting organic diets, enhancing workplace safety, and ongoing biomonitoring, are vital to reduce neurodevelopmental risks for vulnerable populations.

A scoping review to determine if adverse human health effects are associated with use of organophosphates for mosquito control.

Organophosphate insecticides are widely used for adult mosquito control. Although proven effective in reducing mosquito populations and limiting arbovirus transmission, public concern exists regarding potential human health effects associated with organophosphate exposure. The aim of this scoping review was to describe any reported human health conditions associated with organophosphates during their use for adult mosquito control in the United States and Canada. Original peer-reviewed articles published in English language journals from 1 January 2000 to 22 May 2024, were obtained by searching from the databases MEDLINE, EMBASE, Agricultural & Environmental Science Collection, CAB Abstracts, and Scopus. The search identified 6,154 screened articles. Following an independent review, 10 studies were identified that described human health conditions associated with organophosphate exposure during adult mosquito control applications. Of the 10 included studies, only two articles were published within the last 11 years (2013 to 22 May 2024). Three types of study design were represented in the included studies: cohort (n = 5), case study (n = 1), and risk assessment (n = 4). The included studies could not determine causality between exposure to adulticides and development of illness or adverse impacts. Exposure to organophosphates did not contribute to an observed increase in metabolic toxicity, hospitalization rates, or self-reported symptoms and exposure. The available and limited evidence indicates that organophosphates can be used safely to control nuisance mosquitoes or mosquitoes that transmit arboviruses. Continued research regarding the human health effects associated with organophosphate applications for adult mosquito control could help evaluate the basis of the public's concerns and inform public health decision-making.

Isoflurane-lipid emulsion injection as an anticonvulsant and neuroprotectant treatment for nerve agent exposure.

We have shown that briefly inhaled isoflurane rapidly halts convulsions and protects the central nervous system (CNS) from organophosphate-induced neuronal loss when administered at 5% for 5min, even as late as 1h after organophosphate exposure. In the current study we investigated if an injectable form of isoflurane was as effective as inhaled isoflurane. We used a mixture of 10% isoflurane dissolved in an IV-compatible lipid-water emulsion for intravenous administration. Rats with an implanted jugular vein cannula were infused with 1,000μL of the 10% isoflurane-lipid emulsion (ILE) mixture at a rate of 200μL per minute, which achieved full anesthesia lasting approximately 10min. When administered 30min after a highly lethal dose of the organophosphate insecticide paraoxon (POX), the short-duration administration halted convulsions over the course of the study and prevented the great majority of neuronal loss as shown by Fluoro-Jade B staining (FJB). Our results indicate that injectable isoflurane is very effective for treating organophosphate poisoning, negating the need for vaporizer equipment and enabling intravenous therapy.

Relationship between organophosphate and pyrethroid pesticides and metabolic syndrome in Korean farmers.

The global use of pesticides steadily increased until the early 2010s. Pesticides play a significant role in agriculture in Korea. Metabolic syndrome is more prevalent in rural areas than in urban areas. This study explored the potential association between organophosphate and pyrethroid pesticide exposure and metabolic syndrome. This study enrolled 1,317 individuals who participated in the Pesticide Exposure and Intoxication Study conducted by the Dankook University Hospital Center for Farmers' Safety and Health from 2014 to 2019. Urinary levels of dimethylphosphate, dimethylthiophosphat, diethylphosphate, and diethylthiophosphate were measured to assess organophosphate pesticide exposure and urinary levels cis-3-(2,2-dichlorovinyl)-2,2-dimethylcyclopropane carboxylic acid, trans-3-(2,2-dichlorovinyl)-2,2-dimethylcyclopropane carboxylic acid, cis-3-(2,2-dibromovinyl)-2,2-dimethylcyclopropane carboxylic acid, and 3-phenoxybenzoic acid were measured to assess pyrethroid pesticide exposure. The odds ratio for the 4th quartile group of organophosphate metabolites concentration was 1.48 (95% confidence interval: 1.06-2.09) compared to the 1st quartile group after adjustment for general factors. In addition, a positive trend was observed across the quartile groups of organophosphate metabolites concentration. A positive trend was noted across the quartile groups of organophosphate metabolites in males, while no significant association was observed in females. Furthermore, no significant associations were observed between metabolic syndrome and pyrethroid metabolites concentration. A positive correlation was observed between the prevalence of metabolic syndrome and the concentrations of urinary organophosphate metabolites, consistent with previous research finding. This association may be attributed to the action of organophosphates as acetylcholinesterase inhibitors, stimulating beta cells in the islets of Langerhans. This can lead to alterations in lipid metabolism and insulin resistance, ultimately leading to metabolic syndrome development. Metabolic syndrome is a major contributor to cardiovascular disease; therefore, it is necessary to identify the risk factors unique to rural areas, such as pesticide exposure.

Organophosphate insecticide exposure and respiratory symptoms among school children in Northern Thailand: Interaction by biomass burning, dampness and season

The aim was to study associations between dialkylphosphates (DAPs), organophosphate (OP) metabolites in urine, biomarkers of OP insecticide exposure, and respiratory symptoms among children in upper northern Thailand. We recruited junior high school children in randomly selected schools in four cities (N = 337), with repeated data collection in wet and dry seasons. Urine was collected and analyzed for six OP metabolites, with creatinine adjustment. Total DAP was expressed as sum of DAPs. Data on respiratory symptoms was collected by a standardized questionnaire. Associations were analyzed by multiple logistic regression. Totally 11.3 % lived in farm families. Total DAPs concentration was higher in dry season (p = 0.002) but did not differ between farm and non-farm children. Total DAPs in wet season was associated with current wheeze (p = 0.019), current asthma attacks (p = 0.012) and attacks of breathlessness in last 12 months (p = 0.021). Total DAPs in dry season was associated with current wheeze (p = 0.042), and associations between DAPs and respiratory symptoms were stronger for dimethylphosphate metabolites (DMPs) than for diethylphosphate metabolites (DEPs). DMPs are produced by certain OP pesticides. Biomass burning inside or outside the home, and dampness or mold at home, enhanced the association between total DAPs and attacks of breathlessness.In conclusion, OP pesticide exposure, measured as urinary DAPs, was higher in dry season and similar in farm and non-farm children. OPs exposure, especially to DMP related pesticides, can increase asthmatic symptoms, especially in wet season. Combined exposure to OP and smoke from biomass burning, or dampness and mold, can further increase the prevalence of attacks of breathlessness. There is a need to reduce OP insecticide and biomass smoke exposure among Thai children. Since different pesticides can be used in different seasons, studies on respiratory health effects of OPs pesticide exposure should be done in different seasons.

Multiomics Screening Identified CpG Sites and Genes That Mediate the Impact of Exposure to Environmental Chemicals on Cardiometabolic Traits.

An understanding of the molecular mechanism whereby an environmental chemical causes a disease is important for the purposes of future applications. In this study, a multiomics workflow was designed to combine several publicly available datasets in order to identify CpG sites and genes that mediate the impact of exposure to environmental chemicals on cardiometabolic traits. Organophosphate and prenatal lead exposure were previously reported to change methylation level at the cg23627948 site. The outcome of the analyses conducted in this study revealed that, as the cg23627948 site becomes methylated, the expression of the GNA12 gene decreases, which leads to a higher body fat percentage. Prenatal perfluorooctane sulfonate exposure was reported to increase the methylation level at the cg21153102 site. Findings of this study revealed that higher methylation at this site contributes to higher diastolic blood pressure by changing the expression of CHP1 and GCHFR genes. Moreover, HKR1 mediates the impact of B12 supplementation → cg05280698 hypermethylation on higher kidney function, while CTDNEP1 mediates the impact of air pollution → cg03186999 hypomethylation on higher systolic blood pressure. This study investigates CpG sites and genes that mediate the impact of environmental chemicals on cardiometabolic traits. Furthermore, the multiomics approach described in this study provides a convenient workflow with which to investigate the impact of an environmental factor on the body's biomarkers, and, consequently, on health conditions, using publicly available data.

ScL-2PAM: A Novel Countermeasure That Ameliorates Neuroinflammation and Neuronal Losses in Mice Exposed to an Anticholinesterase Organophosphate.

Due to their inhibition of acetylcholinesterase, organophosphates are among the most toxic of chemicals. Pralidoxime (a.k.a 2-PAM) is the only acetylcholinesterase reactivator approved in the U.S., but 2-PAM only poorly traverses the blood-brain barrier. Previously, we have demonstrated that scL-2PAM, a nanoformulation designed to enter the brain via receptor-mediated transcytosis, is superior to unencapsulated 2-PAM for reactivating brain acetylcholinesterase, ameliorating cholinergic crisis, and improving survival rates for paraoxon-exposed mice. Here, we employ histology and transcriptome analyses to assess the ability of scL-2PAM to prevent neurological sequelae including microglial activation, expression of inflammatory cytokines, and ultimately loss of neurons in mice surviving paraoxon exposures. Levels of the mRNA encoding chemokine ligand 2 (CCL2) were significantly upregulated after paraoxon exposures, with CCL2 mRNA levels in the brain correlating well with the intensity and duration of cholinergic symptoms. Our nanoformulation of 2-PAM was found to be superior to unencapsulated 2-PAM in reducing the levels of the CCL2 transcript. Moreover, brain histology revealed that scL-2PAM was more effective than unencapsulated 2-PAM in preventing microglial activation and the subsequent loss of neurons. Thus, scL-2PAM appears to be a new and improved countermeasure for reducing neuroinflammation and mitigating brain damage in survivors of organophosphate exposures.

Quantification of 11 metabolites in rat urine after exposure to organophosphates

BackgroundThe aim of the study was to develop a technique for quantitative determination of rat urine metabolites by HPLC–MS/MS, which can be used to search for biomarkers of acute intoxication with organophosphates (OPs).ResultsThe content of metabolites in the urine of rats exposed to a single dose of paraoxon (POX1x); interval, twice daily administration of paraoxon (POX2x); exposure to 2-(o-cresyl)-4H-1, 3, 2-benzodioxaphosphorin-2-oxide and paraoxon (CBPOX) was investigated. New data were obtained on the content in the urine of intact rats as well as rats in 3 models of OP poisoning: 3-methylhistidine, threonine, creatine, creatinine, lactic acid, acetylcarnitine, inosine, hypoxanthine, adenine, 3-hydroxymethyl-butyrate and 2-hydroxymethyl-butyrate.ConclusionsThe proposed assay procedure is a simple and reliable tool for urine metabolomic studies. Within 1–3 days after OP exposure in all three models of acute intoxication, the concentration of metabolites in rat urine, with the exception of adenine, changes similarly and symmetrically, regardless of the method of poisoning modeling, in all three models of acute intoxication. Further studies are needed to determine the specificity and reliability of using urinary metabolite concentration changes as potential biomarkers of acute organophosphate intoxication.Graphical

Organophosphate pesticide exposure and risk of SARS-CoV-2 infection

Several studies have reported immune modulation by organophosphate (OP) pesticides, but the relationship between OP exposure and SARS-CoV-2 infection is yet to be studied. We used two different measures of OP pesticide exposure (urinary biomarkers (N = 154) and residential proximity to OP applications (N = 292)) to examine the association of early-childhood and lifetime exposure to OPs and risk of infection of SARS-CoV-2 using antibody data. Our study population consisted of young adults (ages 18–21 years) from the Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS) Study, a longitudinal cohort of families from a California agricultural region. Urinary biomarkers reflected exposure from in utero to age 5 years. Residential proximity reflected exposures between in utero and age 16 years. SARS-CoV-2 antibodies in blood samples collected between June 2022 and January 2023 were detected via two enzyme linked immunosorbent assays, each designed to bind to different SARS-CoV-2 antigens. We performed logistic regression for each measure of pesticide exposure, adjusting for covariates from demographic data and self-reported questionnaire data. We found increased odds of SARS-CoV-2 infection among participants with higher urinary biomarkers of OPs in utero (OR = 1.94, 95% CI: 0.71, 5,58) and from age 0–5 (OR = 1.90, 95% CI: 0.54, 6.95).

Sex and adrenal hormones in association with insecticide biomarkers among adolescents living in ecuadorian agricultural communities

BackgroundOrganophosphate, pyrethroid, and neonicotinoid insecticides have resulted in adrenal and gonadal hormone disruption in animal and in vitro studies; limited epidemiologic evidence exists in humans. We assessed relationships of urinary insecticide metabolite concentrations with adrenal and gonadal hormones in adolescents living in Ecuadorean agricultural communities. MethodsIn 2016, we examined 522 Ecuadorian adolescents (11-17y, 50.7% female, 22% Indigenous; ESPINA study). We measured urinary insecticide metabolites, blood acetylcholinesterase activity (AChE), and salivary testosterone, dehydroepiandrosterone (DHEA), 17β-estradiol, and cortisol. We used general linear models to assess linear (β = % hormone difference per 50% increase of metabolite concentration) and curvilinear relationships (β2 = hormone difference per unit increase in squared ln-metabolite) between ln-metabolite or AChE and ln-hormone concentrations, stratified by sex, adjusting for anthropometric, demographic, and awakening response variables. Bayesian Kernel Machine Regression was used to assess non-linear associations and interactions. ResultsThe organophosphate metabolite malathion dicarboxylic acid (MDA) had positive associations with testosterone (βboys = 5.88% [1.21%, 10.78%], βgirls = 4.10% [-0.02%, 8.39%]), and cortisol (βboys = 6.06 [-0.23%, 12.75%]. Para-nitrophenol (organophosphate) had negatively-trending curvilinear associations, with testosterone (β2boys = −0.17 (−0.33, −0.003), p = 0.04) and DHEA (β2boys = −0.49 (−0.80, −0.19), p = 0.001) in boys. The neonicotinoid summary score (βboys = 5.60% [0.14%, 11.36%]) and the neonicotinoid acetamiprid-N-desmethyl (βboys = 3.90% [1.28%, 6.58%]) were positively associated with 17β-estradiol, measured in boys only. No associations between the pyrethroid 3-phenoxybenzoic acid and hormones were observed. In girls, bivariate response associations identified interactions of MDA, Para-nitrophenol, and 3,5,6-trichloro-2-pyridinol (organophosphates) with testosterone and DHEA concentrations. In boys, we observed an interaction of MDA and Para-nitrophenol with DHEA. No associations were identified for AChE. ConclusionsWe observed evidence of endocrine disruption for specific organophosphate and neonicotinoid metabolite exposures in adolescents. Urinary organophosphate metabolites were associated with testosterone and DHEA concentrations, with stronger associations in boys than girls. Urinary neonicotinoids were positively associated with 17β-estradiol. Longitudinal repeat-measures analyses would be beneficial for causal inference.

Model acetylcholinesterase-Fc fusion glycoprotein biotechnology system for the manufacture of an organophosphorus toxicant bioscavenging countermeasure.

Organophosphate (OP) toxicants remain an active threat to public health and to warfighters in the military. Current countermeasures require near immediate administration following OP exposure and are reported to have controversial efficacies. Acetylcholinesterase (AChE) fused to the human immunoglobulin 1 (IgG1) Fc domain (AChE-Fc) is a potential bioscavenger for OP toxicants, but a reproducible AChE-Fc biomanufacturing strategy remains elusive. This report is the first to establish a comprehensive laboratory-scale bioprocessing strategy that can reproducibly produce AChE-Fc and AChE(W86A)-Fc which is a mutated AChE protein with reduced enzymatic activity. Characterization studies revealed that AChE-Fc and AChE(W86A)-Fc are N-glycosylated dimeric fusion glycoproteins but only AChE-Fc had the capability to bind to paraoxon (a model OP). This AChE-Fc fusion glycoprotein bioprocessing strategy can be leveraged during industrial biomanufacturing development, while the research-grade AChE-Fc proteins can be used to determine the potential clinical relevance of the countermeasure against OP toxicants.

Removal and prediction of chemicals in anaerobic–anoxic–aerobic wastewater treatment system: Case study on organophosphates

Distribution and removal of chemicals in wastewater treatment plants (WWTPs) have mainly relied on mathematical models. Existing exposure assessment models such as SimpleTreat, STPWIN are based on conventional activated sludge processes. There is an urgent need to develop an A2/O-based WWTPs exposure assessment model. Organophosphates (OPEs) have different physical and chemical properties and potential environmental risks. The fate and biodegradation kinetics of three types of OPEs, including alkyl OPEs, chlorinated OPEs and triphenyl ester OPEs, were studied in a laboratory-scale anaerobic/anoxic/aerobic (A2/O) sewage treatment system and batch reactors. The three types of OPEs had different anaerobic, anoxic, and aerobic removal characteristics. A compensation mechanism was found between anaerobic and anoxic/aerobic removal. When the hydraulic retention time decreased from 82 to 20.5 h, the removal efficiencies in the anaerobic unit decreased, while those in the anoxic unit increased; as a result, the total removal efficiencies remained high (>80 %) for all OPEs except triphenyl phosphate (65.5%–75.1 %). The concept of effective sludge concentration (MLSSeff) was proposed to illustrate the compensation mechanism and calibrate the second-order kinetic equation for predicting pollutant removal in the A2/O system: MLSSeff = ken × MLSS, where ken is a constant related to the influent total organic carbon content (TOC). The influent TOC contents of the anoxic and aerobic units affected the value of MLSSeff and OPEs removal. The results are of great significance for assessing OPEs exposure and predicting exposure to emerging micropollutants in sewage treatment systems.

Development of Nontargeted Workflow of Occupational Exposure by Infrared Ion Spectroscopy and Silicone Wristbands' Passive Sampling.

A new approach using orthogonal analytical techniques is developed for chemical identification. High resolution mass spectrometry and infrared ion spectroscopy are applied through a 5-level confidence paradigm to demonstrate the effectiveness of nontargeted workflow for the identification of hazardous organophosphates. Triphenyl phosphate is used as a surrogate organophosphate for occupational exposure, and silicone wristbands are used to represent personal samplers. Spectral data of a target compound is combined with spectral data of the sodium adduct and quantum chemical calculations to achieve a confirmed identification. Here, we demonstrate a nontargeted workflow that identifies organophosphate exposure and provides a mechanism for selecting validated methods for quantitative analyses.

Role of PON1 L55M Gene Polymorphism in Parkinson's Disease among North Indian Population.

The role of various genetic markers including alpha synuclein, Parkin, etc., is known in the pathogenesis of Parkinson's disease (PD). Novel genetic markers including paraoxonase 1 (PON1) have also been linked to PD pathogenesis in recent studies. The PON1 L55M allele carriers may have defective clearance of environmental toxins and may result in increased susceptibility to PD. Hence, we studied the role of PON1 L55M polymorphism in PD among a North Indian population. Seventy-four PD patients and 74 age- and sex-matched controls were recruited in this hospital-based case-control study. Baseline characteristics were recorded using structured questionnaire. DNA was extracted from 3-4 ml of venous blood, followed by PCR and restriction digestion. PON1 L55M genotypes were visualized as bands: LL (177 bp), LM (177, 140 bp) and MM (140,44 bp) on 3% agarose gel. Mann-Whitney U test and Chi-squared test were used for comparing two groups of skewed and categorical variables, respectively. Measures of strength of association were calculated by binary regression analysis. P value < 0.05 was considered as significant. Parkinson's disease patients had significantly higher exposure to pesticides (12.2%; P (organophosphate exposure) < 0.001) and well water drinking (28.4%; P = 0.006) compared to controls. Frequency distribution of LL, LM, MM genotypes was 67.5% (50/74), 28.4% (21/74), and 4.1% (3/74), respectively, for cases and 72.6% (54/74), 26% (19/74) and 1.4% (1/74), respectively, for controls. PON1 L55M genotype distribution between Parkinson's disease cases and controls was not significant (P = 0.53). PON1 L55M polymorphism was not associated with PD after adjusting for confounders by binary regression analysis. There was no significant association between PON1 L55M polymorphism and PD. Larger population-based studies would be required from India before drawing any definite conclusions.

Navigating the Neurological Abyss: A Comprehensive Review of Organophosphate Poisoning Complications.

Organophosphate poisoning is a significant global health concern with implications for both occupational and environmental settings. This comprehensive review thoroughly explores the biochemical basis, clinical presentation, diagnostic methods, treatment strategies, and long-term effects of organophosphate exposure. The acute phase is characterized by cholinergic crisis, respiratory distress, and neurological manifestations, while delayed complications include the intermediate syndrome and organophosphate-induced delayed neuropathy. Diagnostic approaches involve clinical evaluation, cholinesterase-level assessments, and imaging studies. Treatment strategies encompass decontamination, antidotes such as atropine and pralidoxime, and supportive care. Long-term effects may include cognitive and neurological sequelae, necessitating rehabilitation approaches such as physical and occupational therapy. Prevention strategies include stringent occupational safety guidelines, sustainable agricultural practices, and public awareness initiatives. The implications for clinical practice underscore the importance of a multidisciplinary approach. At the same time, the call to action emphasizes the need for collaborative efforts in prevention and awareness to mitigate the impact of organophosphate poisoning on public health and the environment.

Child exposure to organophosphate and pyrethroid insecticides measured in urine, wristbands, and household dust and its implications for child health in South Africa: A panel study.

Children in agricultural areas are exposed to organophosphate (OP) and pyrethroid (PYR) insecticides. This explorative study investigated child exposure to OPs and PYRs, comparing temporal and spatial exposure variability within and among urine, wristbands, and dust samples. During spraying season 2018, 38 South African children in two agricultural areas (Grabouw/Hex River Valley) and settings (farm/village) participated in a seven-day study. Child urine and household dust samples were collected on days 1 and 7. Children and their guardians were wearing silicone wristbands for seven days. Intraclass correlation coefficients (ICCs) evaluated temporal agreements between repeated urine and dust samples, Spearman rank correlations (Rs) evaluated the correlations among matrices, and linear mixed-effect models investigated spatial exposure predictors. A risk assessment was performed using reverse dosimetry. Eighteen OPs/PYRs were targeted in urine, wristbands, and dust. Levels of chlorpyrifos in dust (ICC = 0.92) and diethylphosphate biomarker in urine (ICC = 0.42) showed strong and moderate temporal agreement between day 1 and day 7, respectively. Weak agreements were observed for all others. There was mostly a weak correlation among the three matrices (Rs = -0.12 to 0.35), except for chlorpyrifos in dust and its biomarker 3,5,6-trichloro-2-pyridinol in urine (Rs = 0.44). No differences in exposure levels between living locations were observed. However, 21% of the urine biomarker levels exceeded the health-risk threshold for OP exposure. Observed high short-term variability in exposure levels during spraying season highlights the need for repeated sampling. The weak correlation between the exposure matrices points to different environmental and behavioral exposure pathways. Exceeding risk thresholds for OP should be further investigated.

Associations between pesticide exposure with biomarkers of stroke risk factors in farmers.

The extensive use of pesticides may cause acute and chronic intoxication. Therefore, this study aimed to reveal the associations between pesticide exposure and serum markers for stroke risk factors in farmers. A cross-sectional study was conducted with farmers, who used chemical pesticides in Seloprojo Village, Ngablak District, Magelang Regency, Central Java Province, Indonesia. A questionnaire containing demographics, pesticide use, and aspects related to work was employed. Measurements of serum cholesterol, uric acid, glucose, cholinesterase, and fibrinogen levels were also conducted. Of the 106 subjects, 31 (29.2%) used organophosphates as chemical pesticides. There was a significant difference between organophosphate and nonorganophosphate groups in plasma fibrinogen levels. The organophosphate group had higher levels of fibrinogen (292.29 ± 67.56 mg/dL) than the non-organophosphate group (255.24 ± 38.90 mg/dL). Of the studied risk factors for stroke, there is a significant association between organophosphate exposure and increased plasma fibrinogen levels.