Chlorpyrifos-induced delayed myelopathy and pure motor neuropathy: a case report.

INTRODUCTION: Organophosphate (OP) poisoning is known to cause delayed neurological manifestations. Chlorpyrifos, an OP, causes a delayed syndrome that is characterized by a motor sensory polyneuropathy. Pure motor neuropathy with intact sensory conduction is rarely documented. Rapidly evolving delayed myelopathy is extremely uncommon. CASE REPORT: A healthy 15-year-old female was admitted to hospital with cholinergic crisis due to ingestion of a large dose of chlorpyrifos (OP). She was treated with atropine and recovered completely without any neurological symptoms or signs. She came to hospital 6 weeks later with upper and lower motor neuron signs involving the lower limbs without sensory loss. By the end of 7 weeks, there was urinary incontinence. At 2-month follow-up, she had progressive spasticity. Electrophysiological studies revealed a pure motor neuropathy. Spine magnetic resonance imaging showed early signs of thoracic cord atrophy. Other causes of myelopathy were excluded. CONCLUSIONS: Chronic neurotoxicity due to OP poisoning is dependent on several factors: chemical composition of the OP, dose systematized, and the administration of anitcholinergics for cholinergic crisis. The pathology of OP-induced delayed neuropathy involves a central-peripheral distal axonopathy. Peripheral distal axonopathy results in a predominantly motor polyneuropathy. Axonopathy of the central nervous system results in myelopathic features that makes for a poorer prognosis.

A simple and sensitive GC/MS method for the determination of atropine during therapy of anticholinesterase poisoning in serum samples.

Atropine is used in the daily clinical practice for the treatment of poisonings caused by anticholinesterase pesticides, due to its sympathomimetic action. The investigation of the cause of the adverse effects that appear during atropine administration showed the necessity for the development and validation of a simple, rapid, sensitive, and specific method for the determination of atropine levels in serum samples. The developed method includes liquid-liquid extraction with ethyl acetate: dichloromethane (3:1, v/v) and derivatization using N,O-bis(trimethylsilyl)-trifluoracetamide (BSTFA) with 1% trimethylchlorsilane (TMCS) in acetonitrile environment. The method was found to be selective, linear, accurate, and precise according to international guidelines. The recovery was higher than 85.9%, the limit of quantification was 2.00 ng/ml, and the calibration curve was linear within the range of 2.00-500 ng/ml (R(2) ≥ 0.992). Accuracy and precision were also calculated and were found to be less than 5.2 and 8.7%, respectively. The developed method was applied in a real case of accidental poisoning with chlorpyrifos in order to determine the atropine serum levels of the patient. The proposed method proved to be useful for the investigation of adverse effects that appear during atropine treatment of patients poisoned by anticholinesterase pesticides and it can also be used for the investigation of poisonings caused after consumption of atropine containing plants.

Severe and prolonged neurologic toxicity following subcutaneous chlorpyrifos self-administration: a case report.

INTRODUCTION: Organophosphate poisoning by oral or inhalation routes is characterized by a typical time-course of clinical features. CASE PRESENTATION: We report a case of subcutaneous chlorpyrifos self-injection leading to a delayed cholinergic phase, prolonged coma, and severe permanent neurologic injury with electrophysiological patterns suggestive of overlapping intermediate syndrome and distal peripheral neuropathy. Time-course and severity of clinical features were not altered by either atropine or pralidoxime administration. Due to prolonged and severe alteration in consciousness, we used brain multimodal nuclear magnetic imaging and auditory cognitive event-related potentials to assess the patient's potential for awakening. Electrophysiological testing used to monitor muscle weakness showed the coexistence of 20 Hz-decremental responses in proximal muscles and severe denervation in distal muscles. Red blood cell acetylcholinesterase activity progressively normalized on day 60, while plasma butyrylcholinesterase activity remained low until day 100. Chlorpyrifos was detectable in serum until day 30 and urine metabolites for up to three months, supporting the hypothesis of a continuous chlorpyrifos release despite repeated surgical debridement. We suggest that adipose and muscle tissues acted as a chlorpyrifos reservoir. At one-year follow-up, the patient exhibited significant neuromuscular sequelae. CONCLUSION: Subcutaneous chlorpyrifos self-injection may result in severe toxicity with prolonged neurologic injury, atypical overlapping electrophysiological patterns, and a poor final outcome.

Dichlorvos, chlorpyrifos oxon and Aldicarb adducts of butyrylcholinesterase, detected by mass spectrometry in human plasma following deliberate overdose.

The goal of this study was to develop a method to detect pesticide adducts in tryptic digests of butyrylcholinesterase in human plasma from patients poisoned by pesticides. Adducts to butyrylcholinesterase in human serum may serve as biomarkers of pesticide exposure because organophosphorus and carbamate pesticides make a covalent bond with the active site serine of butyrylcholinesterase. Serum samples from five attempted suicides (with dichlorvos, Aldicarb, Baygon and an unknown pesticide) and from one patient who accidentally inhaled dichlorvos were analyzed. Butyrylcholinesterase was purified from 2 ml serum by ion exchange chromatography at pH 4, followed by procainamide affinity chromatography at pH 7. The purified butyrylcholinesterase was denatured, digested with trypsin and the modified peptide isolated by HPLC. The purified peptide was analyzed by multiple reaction monitoring in a QTRAP 4000 mass spectrometer. This method successfully identified the pesticide-adducted butyrylcholinesterase peptide in four patients whose butyrylcholinesterase was inhibited 60-84%, but not in two patients whose inhibition levels were 8 and 22%. It is expected that low inhibition levels will require analysis of larger serum plasma volumes. In conclusion, a mass spectrometry method for identification of exposure to live toxic pesticides has been developed, based on identification of pesticide adducts on the active site serine of human butyrylcholinesterase.

Non-accidental chlorpyrifos poisoning-an unusual cause of profound unconsciousness.

Chlorpyrifos is an organophosphorus anticholinesterase insecticide, and organophosphate intoxication can induce symptoms such as miosis, urination, diarrhea, diaphoresis, lacrimation, excitation of central nervous system, salivation, and consciousness disturbance (MUDDLES). Although accidental poisoning of children with drugs and chemicals is a common cause for consciousness disturbance in children, the possibility of deliberate poisoning is rarely considered. We report on a healthy 5-year 6-month-old boy with recurrent organophosphate intoxication. Reports of chlorpyrifos intoxication in children are quite rare. This case report demonstrates decision-making process and how to disclose deliberate chlorpyrifos poisoning of the toddler by the stepmother, another example of Munchausen syndrome by proxy.

Combined effects of atrazine and chlorpyrifos on susceptibility of the tiger salamander to Ambystoma tigrinum virus.

Several hypotheses have been examined as potential causes of global amphibian declines, including emerging infectious diseases and environmental contaminants. Although these factors are typically studied separately, animals are generally exposed to both stressors simultaneously. We examined the effects of the herbicide atrazine and the insecticide chlorpyrifos on the susceptibility of tiger salamander larvae, Ambystoma tigrinum, to a viral pathogen, Ambystoma tigrinum virus (ATV). Environmentally relevant concentrations of atrazine (0, 20, 200 microg/L) and chlorpyrifos (0, 2, 20, 200 microg/L) were used along with ATV in a fully factorial experimental design whereby individually housed, 4-week-old larvae were exposed for 2 weeks. Atrazine alone was not lethal to larvae, and chlorpyrifos alone was lethal only at the highest concentration. When combined with ATV, chlorpyrifos increased susceptibility to viral infection and resulted in increased larval mortality. A significant interactive effect between atrazine and ATV was detected. Atrazine treatments slightly decreased survival in virus-exposed treatments, yet slightly increased survival in the virus-free treatments. These findings corroborate earlier research on the impacts of atrazine, in particular, on disease susceptibility, but exhibit greater effects (i.e., reduced survival) when younger larvae were examined. This study is the first of its kind to demonstrate decreases in amphibian survival with the combination of pesticide and a viral disease. Further examination of these multiple stressors can provide key insights into potential significance of environmental cofactors, such as pesticides, in disease dynamics.

Extreme variability in the formation of chlorpyrifos oxon (CPO) in patients poisoned by chlorpyrifos (CPF).

Chlorpyrifos (CPF) is a pesticide that causes tens of thousands of deaths per year worldwide. Chlorpyrifos oxon (CPO) is the active metabolite of CPF that inhibits acetylcholinesterase. However, this presumed metabolite has escaped detection in human samples by conventional methods (HPLC, GC-MS, LC-MS) until now. A recently developed enzyme-based assay allowed the determination of CPO in the nanomolar range and was successfully employed to detect this metabolite. CPO and CPF were analysed in consecutive plasma samples of 74 patients with intentional CPF poisoning. A wide concentration range of CPO and CPF was observed and the ratio of CPO/CPF varied considerably between individuals and over time. The ratio increased during the course of poisoning from a mean of 0.005 in the first few hours after ingestion up to an apparent steady-state mean of 0.03 between 30 and 72h. There was a hundred-fold variation in the ratio between samples and the interquartile range (between individuals) indicated over half the samples had a 5-fold or greater variation from the mean. The ratio was independent of the CPF concentration and the pralidoxime regimen. CPO was present in sufficient quantities to explain any observed acetylcholinesterase inhibitory activity. The effectiveness of pralidoxime in reactivating the inhibited acetylcholinesterase is strongly dependent on the CPO concentration. Differences in clinical outcomes and the response to antidotes in patients with acute poisoning may occur due to inter-individual variability in metabolism.

Guillain-Barre syndrome due to organophosphate compound poison.

Acute manifestations of Organophosphate Compound (OPC) poison are due to effect cholinergic excess. Others are intermediate syndrome [IMS], organophosphate induced delayed neuropathy [OPIND] and chronic organophosphate induced neuropsychiatric disorder [COPIND]. All these manifestation have specific period of occurrence and duration. There are very sparse reports of toxic demylination due to OPC poisoning. We report a case of Guillain-Barre Syndrome (GBS) due to toxic demyelination following OPC poison.

Ethanol poisoning together with organophosphate exposure: a difficult clinical diagnosis because of physician anchoring.

AIMS: Organophosphorus pesticide poisoning occurs frequently in China and can be diagnosed easily based on the history of ingestion and the cholinergic toxic syndrome. Yet, when combined with other toxins, organophosphorus poisoning may appear different. METHODS: Here, we present a case of acute ethanol poisoning together with a dermal organophosphorus exposure. RESULTS: Based on the history and a misinterpretation of the physical examination, the patient was treated as an organophosphorus poisoning. Ultimately, serum analysis helped clarify the diagnosis. CONCLUSIONS: Toxicologist should be aware of the error known as anchoring and take appropriate precautions to limit its occurrence.

Enzyme-based assay for quantification of chlorpyrifos oxon in human plasma.

Chlorpyrifos oxon (CPO) is the active metabolite of the pesticide chlorpyrifos that inhibits cholinesterases at high reaction rates. Chlorpyrifos is of major concern because it causes some ten thousand fatalities each year, mostly due to suicidal attempts. Notwithstanding, toxicokinetic studies on chlorpyrifos in humans are scarce and CPO has not been detected hitherto in human blood. Knowledge of the concentration and the time course of CPO in poisonings would be helpful to better design antidotal strategies, particularly with oximes. Owing to the exceptionally fast covalent binding to butyrylcholinesterase we searched for an enzyme-based assay for CPO determination. We succeeded in a simple procedure where CPO is titrated with purified equine butyrylcholinesterase. The assay requires less than 0.2 mL EDTA plasma and allows the quantification of CPO down to 0.5 nM. CPO is first extracted from plasma with n-pentane, thereby largely excluding the majority of the more hydrophilic pesticide oxons from possible cross-reactions. When chlorpyrifos incorporation is ascertained the assay may be considered largely specific. The new procedure enabled the assessment of the extent of reversible binding of CPO to human albumin, amounting to 85% under physiological conditions. The assay allowed the quantification of CPO in the plasma of a poisoned patient, where the active metabolite was about two orders of magnitude lower than chlorpyrifos. Similar to the parent compound its oxon showed the same tendency to persist for longer periods, thus calling for a change of the usual oxime dosage regimen.

Predicting outcome using butyrylcholinesterase activity in organophosphorus pesticide self-poisoning.

BACKGROUND: The usefulness of a low butyrylcholinesterase (BuChE) activity on admission for predicting severity in acute organophosphorus (OP) insecticide poisoning has long been debated. Previous studies have been confounded by the inclusion of multiple insecticides with differing inhibitory kinetics. AIM: We aimed to assess the usefulness of admission BuChE activity, together with plasma OP concentration, for predicting death with two specific organophosphorus insecticides. DESIGN: A prospective cohort of self-poisoned patients. METHODS: We prospectively studied 91 and 208 patients with proven dimethoate or chlorpyrifos self-poisoning treated using a standard protocol. Plasma butyrylcholinesterase activity and OP concentration were measured on admission and clinical outcomes recorded. RESULTS: The usefulness of a plasma BuChE activity <600 mU/ml on admission varied markedly--while highly sensitive in chlorpyrifos poisoning (sensitivity 11/11 deaths; 100%, 95% CI 71.5-100), its specificity was only 17.7% (12.6-23.7). In contrast, while poorly sensitive for deaths in dimethoate poisoning [12/25 patients; 48%, (27.9-68.7)] it was reasonably specific [86.4% (75.7-93.6)]. A high OP concentration on admission was associated with worse outcome; however, a clear threshold concentration was only present for dimethoate poisoning. CONCLUSION: Plasma BuChE activity on admission can provide useful information; however, it must be interpreted carefully. It can only be used to predict death when the insecticide ingested is known and its sensitivity and specificity for that insecticide has been studied. Plasma concentration of some OP insecticides predicts outcome. The development of rapid bedside tests for OP detection may aid early assessment of severity.

Evaluation of subchronic chlorpyrifos poisoning on hematological and serum biochemical changes in mice and protective effect of vitamin C.

Chlorpyrifos (CPF) is one of the most widely used organophosphorous insecticides in agriculture with its attendant adverse health outcomes. This study aimed at evaluating the effect of subchronic oral CPF administration on hematological and serum biochemical indices, and the possible ameliorating effect of vitamin C on the indices in mice. Thirty mice divided into 3 groups of 10 mice each were used for this study. Mice in group I (control) were dosed with vegetable oil, while those in group II were given CPF (21.3 mg/kg~ 1/5(th) LD(50)) only. Mice in group III were pretreated with vitamin C (100 mg/kg) prior to dosing with CPF 30 min later (Vitamin C + CPF-treated group). This regime was given to each group of mice three times a week for a period of ten weeks. During the study period, mice were examined for signs of toxicity, and weight of each mouse was measured every week. At the end of the study period, blood samples were collected from the mice and analyzed for packed cell volume (PCV), total red blood cell (RBC), white blood cell (WBC) and total protein (TP). Serum obtained from the blood was analyzed for Na( +, K+ and Cl-), urea, creatinine, alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP). The results showed that mice in the vitamin C + CPF-treated group exhibited milder signs of toxicity and significant increase in weight gain (p<0.01) compared to the CPF-treated group. No significant increase in weight in the CPF-treated group was observed compared to the control. There was a significant increase in PCV, RBC, Hb, TP and creatinine, but a significant decrease was obtained in WBC, ALT and AST in the CPF-treated group compared to the control. All the parameters with the exception of WBC, ALT and AST (which increased significantly), were significantly decreased in the vitamin C + CPF-treated group compared to CPF-treated group. ALP was significantly elevated in the CPF-treated group compared to both the control and vitamin C + CPF-treated group. No significant changes in urea and the measured electrolytes in all three groups, except a significant decrease in the concentration of Na(+) was observed in the CPF-treated group compared to the control. The study demonstrated that pretreatment of CPF-administered mice with vitamin C significantly altered some important hematological and serum biochemical parameters, revealing the protective action of the vitamin against some organ damage induced by CPF.

Acute chlorpyrifos poisoning in pregnancy: a case report.

BACKGROUND: Pesticide exposures and poisoning are common and generally under-reported in poorly resourced countries where women are mainly involved in agricultural work. Cases of organophosphate poisoning in pregnancy are unusual. CASE REPORT: A 22-year-old woman in her 29th week of pregnancy presented to King Edward VIII Hospital, Durban, South Africa having had multiple generalized tonic-clonic seizures at home. An initial presumptive diagnosis of eclampsia was made and treatment using intravenous MgSO(4) was initiated. Signs of OP toxicity included a garlic odor; vomiting, diarrhea, fecal incontinence; hypersecretions with airway compromise, diffuse rhonchi; pinpoint pupils; and muscle weakness and fasciculations. The patient responded to intravenous doses of atropine; oximes were not available. Although the mother survived, the infant was born prematurely and died two days after birth without showing any OP signs. CONCLUSIONS: Organophosphate poisoning may mimic acute complications in pregnancy, such as eclampsia and seizures. Immediate management includes general supportive measures and use of specific pharmacological agents such as atropine and oximes. Poisoning during pregnancy may result in serious adverse effects for both mother and the fetus or neonate. Prompt diagnosis and treatment are necessary to avoid adverse outcomes.

Intermediate syndrome after organophosphate intoxication in patient with end-stage renal disease.

A 42-year-old woman with a 24-year history of systemic lupus erythematous and lupus nephritis for 8 years who had been receiving regular hemodialysis for 4 years for nonoligoric end-stage renal disease (ESRD) ingested about 100 mL of 40.8% chlorpyrifos in a suicide attempt. On admission to our emergency department, she was drowsy. Gastric lavage, activated charcoal, pralidoxime (PAM), and atropine were administered 4 h later. Her consciousness level improved gradually with treatment, which included hemodialysis. However, on the second hospital day, intermittent fever to 38.4 degrees C, sore throat, and trismus were noted. About 45 h after chlorpyrifos ingestion, the patient developed profound motor paralysis followed by respiratory arrest, consistent with the diagnosis of intermediate syndrome (IMS), even with adequate atropine and PAM. Chorealike involuntary movements of her upper limbs were noticed on the fifth day. Intermittent tonic-clonic seizures, each attack lasting for 3 to 5 min, appeared on the 13th day, which responded well to intravenous diazepam and phenytoin. She was discharged on the 18th day. This case suggests that patients with ESRD suffering chlorpyrifos intoxication are at risk of IMS. Prompt endotracheal intubation, intensive care, and hemodialysis are necessary for life support.

Differences between organophosphorus insecticides in human self-poisoning: a prospective cohort study.

BACKGROUND: Although more than 100 organophosphorus insecticides exist, organophosphorus poisoning is usually regarded as a single entity, distinguished only by the compound's lethal dose in animals. We aimed to determine whether the three most common organophosphorus insecticides used for self-poisoning in Sri Lanka differ in the clinical features and severity of poisoning they cause. METHODS: We prospectively studied 802 patients with chlorpyrifos, dimethoate, or fenthion self-poisoning admitted to three hospitals. Blood cholinesterase activity and insecticide concentration were measured to determine the compound and the patients' response to insecticide and therapy. We recorded clinical outcomes for each patient. FINDINGS: Compared with chlorpyrifos (35 of 439, 8.0%), the proportion dying was significantly higher with dimethoate (61 of 264, 23.1%, odds ratio [OR] 3.5, 95% CI 2.2-5.4) or fenthion (16 of 99, 16.2%, OR 2.2, 1.2-4.2), as was the proportion requiring endotracheal intubation (66 of 439 for chlorpyrifos, 15.0%; 93 of 264 for dimethoate, 35.2%, OR 3.1, 2.1-4.4; 31 of 99 for fenthion, 31.3%, 2.6, 1.6-4.2). Dimethoate-poisoned patients died sooner than those ingesting other pesticides and often from hypotensive shock. Fenthion poisoning initially caused few symptoms but many patients subsequently required intubation. Acetylcholinesterase inhibited by fenthion or dimethoate responded poorly to pralidoxime treatment compared with chlorpyrifos-inhibited acetylcholinesterase. INTERPRETATION: Organophosphorus insecticide poisoning is not a single entity, with substantial variability in clinical course, response to oximes, and outcome. Animal toxicity does not predict human toxicity since, although chlorpyrifos is generally the most toxic in rats, it is least toxic in people. Each organophosphorus insecticide should be considered as an individual poison and, consequently, patients might benefit from management protocols developed for particular organophosphorus insecticides.

A case study of acute human chlorpyrifos poisoning: novel aspects on metabolism and toxicokinetics derived from liquid chromatography-tandem mass spectrometry analysis of urine samples.

The metabolic fate of the organophosphorothioate-type insecticide chlorpyrifos (CP) in an acutely intoxicated 59 years old female was investigated by liquid chromatography-electrospray ionisation-tandem mass spectrometry (LC-ESI-MS/MS) analysis of urine samples. Fifteen metabolites of CP and its bioactivated intermediate chlorpyrifos-oxon (CPO), respectively, of which only three have been described in man so far, were identified on the basis of characteristic MS/MS transitions, precursor/product ion and/or neutral loss scans, chlorine isotopomer patterns, and partly by synthesis of reference compounds and subsequent structure confirmation. Three distinct biotransformation routes of CP are proposed: (1) cleavage reactions at the aromatic phosphoester bond, (2) cleavage reactions at the alkyl phosphoester bonds, and (3) glutathione (GSH) dependent nucleophilic substitution of the 6-chlorine at the aromatic moiety. Route (2) has not been reported in humans before and (3) is a hitherto completely unknown scheme of CP metabolism. Urinary markers of the latter were chiefly cysteine S-conjugates of mono-dechlorinated CP, CPO, mono-O-deethyl CP, and mono-O-deethyl CPO as well as the 6-mercapturic acid conjugate of 3,5-dichloro-2-pyridinol. The presence of 3,5-dichloro-6-methylthio-2-pyridinol as well as its O-glucuronide suggests further a cysteine S-conjugate beta-lyase mediated degradation. In addition to the qualitative LC-MS/MS screening the renal elimination profiles of the primary products of scheme (1), i.e. diethyl thiophosphate (DETP), diethyl phosphate (DEP), and 3,5,6-trichloro-2-pyridinol (TCP), were monitored over 14 days (n=21). A biphasic first-order excretion mechanism with half-lives of 21.5h (initial fast excretion phase) and 119.5h (terminal phase) for the sum of free DETP and DEP was found. TCP was hardly eliminated in its free form (O-glucuronide identified as phase II conjugate) and half-lives calculated for the total amount of TCP (acidic hydrolysis of urine samples) were 40.8 and 150.7h. The present study gives a more detailed view on the biotransformation of CP and together with the obtained kinetic data adds novel aspects to the limited knowledge of human metabolism of this xenobiotic, in particular at high dosage.

Determination of chlorpyrifos metabolites in human urine by reversed-phase/weak anion exchange liquid chromatography-electrospray ionisation-tandem mass spectrometry.

A liquid chromatography-electrospray ionisation-tandem mass spectrometry (LC-ESI-MS/MS) method for the quantification of major chlorpyrifos (CP) metabolites, i.e. diethyl thiophosphate (DETP), diethyl phosphate (DEP), and 3,5,6-trichloro-2-pyridinol (TCP), in human urine was developed. Simultaneous separation of the parent compound and its primary biotransformation products was achieved within 20 min in gradient elution mode employing a mixed-mode reversed-phase/weak anion exchange (RP/WAX) separation principle. The analytical method was developed for a toxicokinetic study of an acute poisoning incidence with a CP containing pesticide formulation. An initial mass spectrometric screening performed with unprocessed urine samples revealed that CP is not excreted unchanged by the kidney. Hence, the quantitative assay was validated for DETP (quantifier transition: m/z 169-->95, qualifier transition: m/z 169-->141), DEP (m/z 153-->79, 153-->125), and TCP (m/z 196-->35, 198-->35) taking dibutyl phosphate (DBP) (m/z 209-->79, 209-->153) as internal standard. Clean-up of urine samples prior to LC-ESI-MS/MS analysis was carried out by a liquid-liquid extraction step with a mixture of ethylacetate and acetonitrile (70:30; v/v). Linearity was observed between 0.25 and 75 mgL(-1), and the signal-to-noise ratio at 0.25 mgL(-1) was better than six for the individual analytes. Recoveries, precision, and accuracies were all adequate across the validated range of 1-75 mgL(-1) for the present toxicological case study.

Effects of herbicide and insecticide interaction on soil entomofauna under maize crop.

The aim of this study was to evaluate the impact of the herbicide mixture nicosulfuron + atrazine, with or without the insecticide chlorpyrifos, onto soil entomofauna under maize crop. The treatments, applied 25 days after maize emergence, were represented by a weeded control without insecticide and herbicide, a weeded control with chlorpyrifos, and mixtures of nicosulfuron + atrazine, with or without chlorpyrifos. Arthropods populations, on the soil surface, as well as inside the soil under maize, were principally represented by mites (Arachnida: Acari), decomposer collembolans (Hexapoda:Parainsecta:Collembola) and predator ants (Hymenoptera:Formicidae). The nicosulfuron + atrazine mixture with chlorpyrifos and the isolated chlorpyrifos reduced the population dynamics of all insect groups on the soil surface compared to the weeded control. In the soil, mite and ant populations were reduced after application of the herbicide mixture with chlorpyrifos and of the isolated chlorpyrifos.