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Frontiers in Microbiology 2020Acephate is an organophosphate pesticide that has been widely used to control insect pests in agricultural fields for decades. However, its use has been partially... (Review)
Review
Acephate is an organophosphate pesticide that has been widely used to control insect pests in agricultural fields for decades. However, its use has been partially restricted in many countries due to its toxic intermediate product methamidophos. Long term exposure to acephate and methamidophos in non-target organisms results in severe poisonous effects, which has raised public concern and demand for the removal of these pollutants from the environment. In this paper, the toxicological effects of acephate and/or methamidophos on aquatic and land animals, including humans are reviewed, as these effects promote the necessity of removing acephate from the environment. Physicochemical degradation mechanisms of acephate and/or methamidophos are explored and explained, such as photo-Fenton, ultraviolet/titanium dioxide (UV/TiO) photocatalysis, and ultrasonic ozonation. Compared with physicochemical methods, the microbial degradation of acephate and methamidophos is emerging as an eco-friendly method that can be used for large-scale treatment. In recent years, microorganisms capable of degrading methamidophos or acephate have been isolated, including sp., , , , and Enzymes related to acephate and/or methamidophos biodegradation include phosphotriesterase, paraoxonase 1, and carboxylesterase. Furthermore, several genes encoding organophosphorus degrading enzymes have been identified, such as , , and . However, few reviews have focused on the biochemical pathways and molecular mechanisms of acephate and methamidophos. In this review, the mechanisms and degradation pathways of acephate and methamidophos are summarized in order to provide a new way of thinking for the study of the degradation of acephate and methamidophos.
PubMed: 33013750
DOI: 10.3389/fmicb.2020.02045 -
Chemical Research in Toxicology Sep 2022Exposure to organophosphorus pesticides (OP) can have chronic adverse effects that are independent of inhibition of acetylcholinesterase, the classic target for acute OP...
Exposure to organophosphorus pesticides (OP) can have chronic adverse effects that are independent of inhibition of acetylcholinesterase, the classic target for acute OP toxicity. In pure proteins, the organophosphorus pesticide chlorpyrifos oxon induces a cross-link between lysine and glutamate (or aspartate) with loss of water. Tubulin is particularly sensitive to OP-induced cross-linking. Our goal was to explore OP-induced cross-linking in a complex protein sample, MAP-rich tubulin from and to test 8 OP for their capacity to promote isopeptide cross-linking. We treated 100 μg of MAP-rich tubulin with 100 μM chlorpyrifos, chlorpyrifos oxon, methamidophos, paraoxon, diazinon, diazoxon, monocrotophos, or dichlorvos. Each sample was separated using sodium dodecyl sulfate-polyacrylamide gel electrophoresis and stained with Coomassie blue. Five gel slices (at about 30, 50, 150, and 300 kDa, and the top of the separating gel) were removed from the lanes for each of the eight OP samples and from untreated control lanes. These gel slices were subjected to in-gel trypsin digestion. MSMS fragmentation spectra of the tryptic peptides were examined for isopeptide cross-links. Sixteen spectra yielded convincing evidence for isopeptide cross-linked peptides. Ten were from the chlorpyrifos oxon reaction, 1 from dichlorvos, 1 from paraoxon, 1 from diazinon, and 3 from diazoxon. It was concluded that catalysis of protein cross-linking is a general property of organophosphorus pesticides and pesticide metabolites. Data are available via ProteomeXchange with identifier PXD034529.
Topics: Acetylcholinesterase; Aspartic Acid; Chlorpyrifos; Diazinon; Dichlorvos; Glutamates; Lysine; Monocrotophos; Organophosphorus Compounds; Paraoxon; Peptides; Pesticides; Sodium Dodecyl Sulfate; Trypsin; Tubulin; Water
PubMed: 36048166
DOI: 10.1021/acs.chemrestox.2c00194 -
BMC Public Health Apr 2023Poisoning of children after exposure to pesticides is a major public health concern, particularly in countries with poorer urban populations, such as South Africa. This... (Review)
Review
BACKGROUND
Poisoning of children after exposure to pesticides is a major public health concern, particularly in countries with poorer urban populations, such as South Africa. This may stem from the illegal distribution and domestic use of street pesticides, which are highly hazardous agricultural pesticides. The aim of this study was to profile paediatric deaths due to acute pesticide poisoning in the west-metropole of Cape Town, South Africa; to identify whether the active ingredients were highly hazardous pesticides according to the FAO and WHO; and to inform policy and public health interventions to prevent future exposures and mortality.
METHODS
A retrospective and descriptive analysis of forensic post-mortem records (2010 to 2019) was conducted to identify cases of paediatric deaths (< 18 years old) in the west metropole of Cape Town, involving pesticide poisoning admitted to the Salt River mortuary (one out of 16 mortuaries in the Western Cape province). Demographic, circumstantial, autopsy, and toxicological information was captured. Descriptive statistics, together with chi-square tests, Fisher's probability tests, and Mann-Whitney U tests were used to analyse the data.
RESULTS
In total, 54 paediatric pesticide deaths were identified, including 22 (40.7%) males and 32 (59.3%) females, out of 5,181 paediatric unnatural deaths admitted over the 10-year period. The median age of the decedents was 8.3 years (range: 1 day to 17.9 years), with the majority under five years (42.6%) or between 15 and 18 years old (40.7%). All incidents occurred in peri-urban areas of Cape Town, with most individuals being admitted to hospital (88.9%) for a median survival time of 4.8 h. Toxicological analysis was requested in 50 cases (92.6%) with the organophosphate pesticides terbufos (n = 29), methamidophos (n = 2) and diazinon (n = 2) detected most frequently. Adolescent (15-18 years) suicides (29.6%) and accidental child deaths (< 4 years) (18.5%) were common.
CONCLUSIONS
Terbufos and methamidophos are highly hazardous pesticide (HHP) active ingredients registered in South Africa for agricultural uses, yet commonly sold as street pesticides for domestic use in lower socioeconomic areas. Reducing access and availability of toxic pesticides, especially through the illegal selling of street pesticides, and providing low toxic alternatives to poorer communities, may support mortality reduction initiatives. Mortality and toxicology data provide important, often overlooked, surveillance tools for informing policy and public health interventions to reduce toxic pesticide harm in local communities.
Topics: Adolescent; Child; Female; Humans; Infant, Newborn; Male; Pesticides; Retrospective Studies; South Africa; Suicide
PubMed: 37118778
DOI: 10.1186/s12889-023-15652-5 -
Scientific Reports Jun 2021This study analysed the clinical patterns and outcomes of elderly patients with organophosphate intoxication. A total of 71 elderly patients with organophosphate...
This study analysed the clinical patterns and outcomes of elderly patients with organophosphate intoxication. A total of 71 elderly patients with organophosphate poisoning were seen between 2008 and 2017. Patients were stratified into two subgroups: survivors (n = 57) or nonsurvivors (n = 14). Chlorpyrifos accounted for 33.8% of the cases, followed by methamidophos (12.7%) and mevinphos (11.3%). Mood, adjustment and psychotic disorder were noted in 39.4%, 33.8% and 2.8% of patients, respectively. All patients were treated with atropine and pralidoxime therapies. Acute cholinergic crisis developed in all cases (100.0%). The complications included respiratory failure (52.1%), aspiration pneumonia (50.7%), acute kidney injury (43.7%), severe consciousness disturbance (25.4%), shock (14.1%) and seizures (4.2%). Some patients also developed intermediate syndrome (15.5%) and delayed neuropathy (4.2%). The nonsurvivors suffered higher rates of hypotension (P < 0.001), shock (P < 0.001) and kidney injury (P = 0.001) than survivors did. Kaplan-Meier analysis indicated that patients with shock suffered lower cumulative survival than did patients without shock (log-rank test, P < 0.001). In a multivariate-Cox-regression model, shock was a significant predictor of mortality after intoxication (odds ratio 18.182, 95% confidence interval 2.045-166.667, P = 0.009). The mortality rate was 19.7%. Acute cholinergic crisis, intermediate syndrome, and delayed neuropathy developed in 100.0%, 15.5%, and 4.2% of patients, respectively.
Topics: Acute Kidney Injury; Affect; Aged; Antidotes; Atropine; Chlorpyrifos; Female; Humans; Insecticides; Male; Mevinphos; Middle Aged; Organophosphate Poisoning; Organothiophosphorus Compounds; Pneumonia, Aspiration; Pralidoxime Compounds; Psychotic Disorders; Respiratory Insufficiency; Retrospective Studies; Seizures; Shock; Survival Analysis; Treatment Outcome
PubMed: 34079035
DOI: 10.1038/s41598-021-91230-2 -
Journal of UOEH 2021We gave mice a 540 mg/kg dose of LD50 acephate, followed by an assessment of acephate, methamidophos (MP), and choline esterase (ChE) activity for up to 4 hours (hr) in...
We gave mice a 540 mg/kg dose of LD50 acephate, followed by an assessment of acephate, methamidophos (MP), and choline esterase (ChE) activity for up to 4 hours (hr) in order to investigate the time course of acephate intoxication. At 1 hr, the blood acephate and MP levels were 428 ± 90 µg/ml (mean ± SEM) and 4.2 ± 0.4 µg/ ml, respectively. The liver acephate levels were similar to those in the blood, but the liver MP levels were approximately 3.5 times that of the blood at 1 hr. The brain MP level tended to be higher than the blood MP at 1 hr. These levels decreased gradually over 4 hr, but the brain acephate and MP levels surpassed the blood levels significantly at 4 hr, and after 2 hr, respectively. Serum, liver, cerebrum, cerebellum, and brainstem cholinesterase activity (ChE) were inhibited at 1 hr, and remained inhibited in all but the cerebellum until the end of the experiment. The obtained data were applied to previously reported autopsy cases of acephate intake. Experimental data suggest that brain MP is involved in acute acephate-induced poisoning, even after a reduction in blood acephate. In autopsy cases with suspected acephate poisoning, the MP level in the brain should be considered in addition to the ChE activity to diagnose the cause of death.
Topics: Animals; Brain; Cholinesterase Inhibitors; Insecticides; Mice; Organothiophosphorus Compounds; Phosphoramides
PubMed: 34092764
DOI: 10.7888/juoeh.43.197 -
Toxicology Reports Jun 2024Methamidophos is a highly hazardous organophosphate and is known to cause an acute cholinergic toxidrome. Methamidophos use is not allowed in South Africa and therefore...
Methamidophos is a highly hazardous organophosphate and is known to cause an acute cholinergic toxidrome. Methamidophos use is not allowed in South Africa and therefore local data pertaining to methamidophos poisoning is very limited, with no paediatric clinical cases described. Methamidophos is an active metabolite of acephate, a commonly used organophosphate, registered for agricultural use in South Africa. We present a paediatric case of methamidophos poisoning with prolonged clinical effects. The patient experienced a prolonged cholinergic toxidrome lasting 10 days, with a period of near-full recovery during this time. We discuss the biological plausibility of the detected methamidophos being a byproduct of acephate. In addition, we highlight the importance of closer monitoring of patients with organophosphate poisoning in areas where acephate is commonly used.
PubMed: 38173652
DOI: 10.1016/j.toxrep.2023.12.001 -
Integrated Environmental Assessment and... Sep 2022Intact soil food webs are pivotal to maintaining essential soil functions, such as carbon recycling, sequestering, and biomass production. Although the functional role...
Intact soil food webs are pivotal to maintaining essential soil functions, such as carbon recycling, sequestering, and biomass production. Although the functional role of micro- (e.g., bacteria and fungi) and macrofauna (e.g., earthworms) is comparatively well established, the importance of the mesofauna community (e.g., abundance and diversity of Acari and Collembola) in maintaining soil functionality is less clear. We investigated this question in a six-month field experiment in arable soil by actively manipulating mesofauna abundance and biodiversity through the application of two legacy insecticides (lindane and methamidophos) at sufficiently high doses to reduce mesofauna abundance (well above previously registered application rates; 2.5 and 7.5 kg a.s./ha for lindane, and 0.6 and 3 kg a.s./ha for methamidophos) and measure the impact on organic matter degradation. Our results demonstrate that both insecticides had reduced Collembola and Acari abundances by up to 80% over the study's six-month duration. In addition, we observed less pronounced and more complex changes in mesofauna biodiversity over time. These included insecticide-dependent temporal fluctuations (both reduction and increase) for different estimates (indices) of local (alpha)-diversity over time and no lasting impact for most estimates after six months. Even at these exceptionally high field rates, Collembola and Acari diversity was observed to generally recover by six months. In contrast, considering organic matter breakdown, we found no evidence of a treatment-related effect. These results suggest that organic matter breakdown in arable soils is likely driven by other trophic levels (e.g., microorganisms or earthworms) with only a limited influence of the mesofauna community. We discuss these findings with regard to their implications for our current understanding of soil food web function and future European soil risk assessments. Integr Environ Assess Manag 2022;18:1423-1433. © 2021 The Authors. Integrated Environmental Assessment and Management published by Wiley Periodicals LLC on behalf of Society of Environmental Toxicology & Chemistry (SETAC).
Topics: Animals; Arthropods; Biodiversity; Food Chain; Hexachlorocyclohexane; Insecticides; Oligochaeta; Soil
PubMed: 34878731
DOI: 10.1002/ieam.4563 -
International Journal of Environmental... Dec 2016Methamidophos is a representative organophosphate insecticide. The knowledge of its developmental neurotoxicity is limited, especially for zebrafish in the early stages...
Methamidophos is a representative organophosphate insecticide. The knowledge of its developmental neurotoxicity is limited, especially for zebrafish in the early stages of their life. Four hour post-fertilization (hpf) zebrafish embryos were exposed to several environmentally relevant concentrations of methamidophos (0, 25, and 500 μg/L) for up to 72 hpf. Locomotor behavior was then studied in the zebrafish larvae at this timepoint. Acridine orange (AO) staining was carried out in the zebrafish larvae, and the mRNA levels of genes associated with neural development ( and ) were analyzed by reverse transcription-polymerase chain reaction (RT-PCR). The number of escape responders for mechanical stimulation was significantly decreased in exposed groups. AO staining showed noticeable signs of apoptosis mainly in the brain. In addition, the mRNA levels of and were both significantly down-regulated in exposed groups. Our study provides the first evidence that methamidophos exposure can cause developmental neurotoxicity in the early stages of zebrafish life, which may be caused by the effect of methamidophos on neurodevelopmental genes and the activation of cell apoptosis in the brain.
Topics: Animals; Apoptosis; Embryo, Nonmammalian; Gene Expression Regulation, Developmental; Insecticides; Larva; Neurotoxicity Syndromes; Organophosphorus Compounds; Organothiophosphorus Compounds; RNA, Messenger; Zebrafish
PubMed: 28036051
DOI: 10.3390/ijerph14010023 -
The Science of the Total Environment Mar 2023Pesticide exposure has consistently been associated with Parkinson's disease (PD) onset. Yet, fewer epidemiologic studies have examined whether pesticides influence PD...
BACKGROUND
Pesticide exposure has consistently been associated with Parkinson's disease (PD) onset. Yet, fewer epidemiologic studies have examined whether pesticides influence PD motor and non-motor symptom progression.
OBJECTIVES
Using a geographic information system tool that integrates agricultural pesticide use reports and land use records to derive ambient exposures at residences and workplaces, we assessed associations between specific pesticides previously related to PD onset with PD symptom progression in two PD patient cohorts living in agricultural regions of California.
METHODS
We calculated the pounds of pesticide applied agriculturally near each participant's residential or occupational addresses from 1974 to the year of PD diagnosis, using a geographic information system tool that links the California Pesticide Use Reports database to land use data. We examined 53 pesticides selected a priori as they have previously been associated with PD onset. We longitudinally followed two PD patient cohorts (PEG1 N = 242, PEG2 N = 259) for an average of 5.0 years (SD ± 3.5) and 2.7 years (SD ± 1.6) respectively and assessed PD symptoms using the movement disorder specialist-administered Unified Parkinson's disease Rating Scale part III (UPDRS), Mini-Mental State Examination (MMSE), and Geriatric Depression Scale (GDS). Weighted time-to-event regression models were implemented to estimate effects.
RESULTS
Ten agricultural pesticides, including copper sulfate (pentahydrate), 2-methyl-4-chlorophenoxyacetic acid (MCPA) dimethylamine salt, tribufos, sodium cacodylate, methamidophos, ethephon, propargite, bromoxynil octanoate, monosodium methanearsonate (MSMA), and dicamba, were associated with faster symptom progression. Among these pesticides, residential or workplace proximity to higher amounts of copper sulfate (pentahydrate) and MCPA (dimethylamine salt) was associated with all three progression endpoints (copper sulfate: HRs = 1.22-1.36, 95 % CIs = 1.03-1.73; MCPA: HRs = 1.27-1.35, 95 % CIs = 1.02-1.70).
CONCLUSIONS
Our findings suggest that pesticide exposure may not only be relevant for PD onset but also PD progression phenotypes. We have implicated ten specific pesticide active ingredients in faster PD motor and non-motor decline.
Topics: Humans; Parkinson Disease; Pesticides; Copper Sulfate; 2-Methyl-4-chlorophenoxyacetic Acid; Workplace; California
PubMed: 36526213
DOI: 10.1016/j.scitotenv.2022.160851 -
Industrial Health Feb 2020This study explored the potential association between chronic exposure to pesticide mixtures including paraquat and respiratory outcomes among Colombian farmers....
This study explored the potential association between chronic exposure to pesticide mixtures including paraquat and respiratory outcomes among Colombian farmers. Sociodemographic and occupational data, respiratory symptoms and spirometric data were collected. Paraquat in spot urine samples were quantified with solid-phase extraction high-performance liquid chromatography. Multiple Poisson regressions with robust variance were used to determine factors associated with respiratory outcomes. Profiles of pesticide mixtures used were identified among 217 farmworkers, but profenofos and methamidophos-based mixtures were more frequent. Chronic paraquat exposure was slightly associated with self-reported asthma (PR: 1.06; 95% CI 1.00 to 1.13). Different pesticide mixtures were associated with flu, thoracic pain, allergic rhinitis, and obstructive pattern in spirometry. Although acute exposure to paraquat is low among Colombian farmers participating in the study, associations between respiratory outcomes and chronic pesticide mixtures exposure including profenofos, methamidophos or glyphosate require further specific studies.
Topics: Adolescent; Adult; Aged; Chest Pain; Colombia; Farmers; Female; Humans; Male; Middle Aged; Occupational Exposure; Organothiophosphates; Organothiophosphorus Compounds; Paraquat; Pesticides; Respiratory Tract Diseases; Rhinitis, Allergic; Spirometry
PubMed: 30996154
DOI: 10.2486/indhealth.2018-0111