ABSTRACT
OBJECTIVE: To determine prolonged effects of organophosphorus (OP) insecticide poisoning on cognitive event-related potentials (ERPs). METHODS: ERPs of a group of 32 patients recovered from cholinergic phase of OP insecticide poisoning were compared with those of two matched control groups: 32 healthy volunteers and nine patients hospitalised with paracetamol overdose. A follow-up assessment was done in 21 patients (66% of the initial sample) 6 months after OP intoxication and the findings were compared with their initial ERP data. RESULTS: Patients showed highly significant prolongation of P300 latency, compared to healthy controls (p=0.003) and the controls with paracetamol overdose (p=0.016). Follow-up ERP findings of the patients revealed that this impairment remained unchanged even 6 months after OP poisoning (p=0.790). There was no significant difference in N100, P200 and N200 latencies or P300 amplitude either among the groups or between the two assessments of the patients with OP poisoning. CONCLUSIONS: Our results suggest that acute OP poisoning causes a delay in cognitive processes involved in stimulus classification, lasting at least for 6 months. SIGNIFICANCE: These findings highlight the possibility of development of long-lasting cognitive deficits following OP insecticide poisoning, and warrant longer-term prospective studies to determine whether this impairment is permanent.
Subject(s)
Cognition Disorders/physiopathology , Evoked Potentials, Auditory/physiology , Organophosphate Poisoning , Poisoning/etiology , Poisoning/physiopathology , Adolescent , Adult , Case-Control Studies , Cognition Disorders/chemically induced , Electroencephalography , Female , Humans , Longitudinal Studies , Male , Neuropsychological Tests , Reaction Time/drug effects , Reaction Time/physiology , Retrospective StudiesABSTRACT
OBJECTIVE: To determine the effect of organophosphate (OP) insecticide poisoning on cognitive processing time of visual stimuli. METHODS: We compared 33 patients who recovered from the cholinergic phase (on average, 15 days after poisoning) with an age- and sex-matched control group. The tests used were simple visual reaction time (SVRT), recognition visual reaction time (RVRT), visual evoked potentials (VEP), and motor evoked potentials (MEP). The term cognitive processing time (CPT) was used to denote the time taken from the initial cortical perception of a stimulus to initiation of the descending motor impulse. CPT of each type of visual reaction was calculated by subtracting the sum of the visual impulse duration and the motor impulse duration from reaction time (CPT = reaction time-[P100 latency + total motor conduction time]). RESULTS: Both the SVRT and RVRT were significantly prolonged in patients. There was no significant difference in P100 latency or total motor conduction time (TMCT) between patients and the controls. However, CPT of simple visual reactions (CPT(SVR)) and the CPT of recognition visual reactions (CPT(RVR)) were significantly prolonged in patients. CONCLUSIONS: Acute organophosphate poisoning may slow higher-order cognitive processing involved in visual stimulus detection and visual stimulus discrimination, even after clinical recovery from the cholinergic phase.
Subject(s)
Cognition Disorders/chemically induced , Insecticides/poisoning , Organophosphate Poisoning , Perceptual Disorders/chemically induced , Acetylcholine/metabolism , Adult , Brain/drug effects , Brain/metabolism , Brain/physiopathology , Cognition Disorders/physiopathology , Cognition Disorders/psychology , Electroencephalography/drug effects , Evoked Potentials, Motor/drug effects , Evoked Potentials, Motor/physiology , Evoked Potentials, Visual/drug effects , Evoked Potentials, Visual/physiology , Female , Humans , Male , Neuropsychological Tests , Perceptual Disorders/physiopathology , Perceptual Disorders/psychology , Reaction Time/drug effects , Reaction Time/physiology , Synaptic Transmission/drug effects , Synaptic Transmission/physiology , Visual Perception/drug effects , Visual Perception/physiologyABSTRACT
Accumulation of sulfur-containing compounds and their bacterial mediated reductions have led to the emission of pungent odors from stagnant water bodies. This study is focused on the contribution of inorganic sulfur compounds in the emission of hydrogen sulfide. The measured dissolved oxygen levels have demonstrated good negative correlations with the dissolved sulfide levels implying the oxygen deficiency is the key for the reduction of sulfate ion and sulfite ion to sulfide ion. Particularly, the dissolved molar fractions of sulfide from the total dissolved sulfur compounds (sulfates, sulfites and sulfides) have a very good correlation with the dissolved oxygen for the stagnant water bodies except the artificially aerated prawn farms. For the stagnant water bodies with significant correlations, linear regressions are reported for them to be utilized in estimating one component of the regression from the measurement of the other. The measured data were further utilized to estimate the levels of hydrogen sulfide gas. The pH of the water bodies has confined much of the dissolved sulfides in the form of bisulfide ion and they can be easily escaped to the atmosphere upon acidification due to industrial discharges and/or acidic precipitations. The estimated levels of hydrogen sulfide just above the water surface were plotted for the most polluted stagnant water body in Sri Lanka for the pH range of 5-10 and temperature range of 25-35 degrees C.
