Explore chapters and articles related to this topic
Biomarkers in Occupational Neurotoxicology
Published in Lucio G. Costa, Luigi Manzo, Occupatinal Neurotoxicology, 2020
Organophosphorus compounds are among the most widely used insecticides; their mechanism of action involves inhibition of acetylcholinesterase (AChE), which leads to accumulation of acetylcholine at cholinergic synapses with an ensuing cholinergic crisis.104 AChE is widely distributed throughout the body and is also present in blood cells, such as erythrocytes and lymphocytes, though its physiological role in these cells, which are devoid of synaptic contacts, has not been elucidated. Inhibition of AChE, as well as of pseudocholinesterase in plasma, has been extensively used as a biomarker of exposure to, and effect of, organophosphates.105,106 When used as a marker of exposure in populations studies, one should consider the issue of interpersonal variability in the activity of these enzymes. In the best circumstances, baseline values should be obtained for each individual, and variations below these activity levels, rather than absolute levels, should be utilized to assess exposure. In the absence of pre-exposure measurements, repeated post-exposure measurements at different intervals should be obtained, rather than comparison with population ranges. If acute exposure to an organophosphate has occurred, AChE activity would increase over time to reach a level considered normal for that individual.107
Organophosphorous Compounds
Published in Fina P. Kaloyanova, Mostafa A. El Batawi, Human Toxicology of Pesticides, 2019
Fina P. Kaloyanova, Mostafa A. El Batawi
Diagnosis of the intoxication can be difficult in mild cases, when only myosis, nausea, vomiting, weakness, headache, and giddiness are observed. In such cases a good anamnesis and ChEA determination will help very much. Unusual toxicological features in poisoning by fat-soluble OPs are reported by Davies et al.4 In 5 suicidal patients who used dichlorfenthion, the initial symptoms were mild, and cholinergic crisis appeared at 40 to 48 h after ingestion. Two patients died and in the other three ChE inhibition persisted for 48 d. In one patient almost total inhibition of both plasma and erythrocyte ChE was noted for 66 d. This corresponded to pesticide presence in fat tissue at the 54th d and in blood at the 75th d. The levels of dichlorfenthion in adipose tissues in this case were, respectively, 65, 58, and 0.63 ppm on d 4, 7, and 54 after poisoning. Leptophos is more fat soluble and produces a more protracted clinical picture.
Toxicology
Published in Martin B., S.Z., of Industrial Hygiene, 2018
The organophosphates are one of the few classes of neurotoxins in which the target enzymes are known. These compounds inhibit both acetylcholinesterase, which explains the central nervous system and neuromuscular toxicity, and neuropathy target esterase, an enzyme that is inhibited in neuropathy. Acute poisoning by inhalation, ingestion, or skin absorption produces a cholinergic crisis characterized by encephalopathy in which convulsions, muscle twitching, weakness, lacrimation, and involuntary defecation and urination are common. In milder cases, there is nausea, vomiting, and diarrhea lasting from a few hours to days. The severity of these cholinergic features depends on the severity of exposure and the particular organophosphate. With some organophosphates, if the acute episode is survived, a delayed neuropathy develops. There is little relationship between the severity of the acute effects and subsequent development of neuropathy, which in fact may develop in the absence of obvious acute effects.
Effects of short-term sub-lethal diazinon® exposure on behavioural patterns and respiratory function in Clarias batrachus: inferences for adaptive capacity in the wild
Published in Chemistry and Ecology, 2022
Shubhajit Saha, Azubuike V. Chukwuka, Dip Mukherjee, Kishore Dhara, Aina O. Adeogun, Nimai Chandra Saha
Behavioural toxicity: The results on the behavioural responses of C. batrachus in the present work may serve as an indicator of the reflection of the toxicity of diazinon in fish. Behavioural distress such as – Loss of balance, erratic swimming and mucous secretion was not observed in the control group. No fish displayed abnormal behaviour in the control group. The excessive mucous secretion on the body surface of fish can be attributed to responses to physical irritation of skin contact with the toxicant. It could also reflect the onset of cholinergic crisis. The activation of muscarinic cholinergic receptors on smooth muscle and gland cells, which results in bronchoconstriction and mucus secretion are typical of cholinergic toxicity [54]. Observations of stress-like erratic fin motion, breathing difficulty, suffocation, hyperactivity, and adherence to the surface particularly at the greater concentrations (22, 24 and 26 mg/L) during 72 and 96 h, are features attributable to progressive neurotoxicity. While such features have been reported in other fish species under similar toxicant exposures [46,55,56], altered fish behavioural patterns including hyperactivity, erratic swimming and seizure in treated fish are traceable to the neurotoxicity of diazinon, via the acetylcholinesterase inhibition pathway [57]. While behavioural changes are valuable sentinels of early toxicity, with integral pointers to underlying neurotoxicity [58], disrupted AChE activity at sublethal concentrations has been implicated [59,60]. In fish, OP compounds have also shown ability to modify complex and ecologically relevant behaviours, such as swimming performance, dark/light preference (scoto-taxis), thigmotaxis (i.e. tendency for animals to stay nearer to the walls of the environment relative to the centre), shoal cohesion, predator avoidance, feeding behaviour and, consequently, growth [61,62]. As such, behavioural changes are valuable sentinels of early toxicity, with integral pointers to underlying neurotoxicity [58].
Pesticide-induced changes in cholinesterase activity and chronic kidney disease of unknown etiology among farmers in Nakhon Ratchasima, Thailand
Published in Human and Ecological Risk Assessment: An International Journal, 2021
Ekarat Sombatsawat, Dana Boyd Barr, Parinya Panuwet, Mark Gregory Robson, Wattasit Siriwong
The findings of this study revealed that the prevalence of pesticide poisoning among farmers in Nakhon Ratchasima province, Thailand was fairly high, with the abnormal erythrocyte AChE and BuChE levels of 55.17% and 46.55%, respectively. Our findings are similar to those of previous research (Nganchamung et al. 2017). The CKDu prevalence in the study location was 24.14%, which was much higher than that reported in the Thai Screening and Early Evaluation of Kidney Disease (SEEK) study, which found a figure of 17.5% (Ingsathit et al. 2010). Several other studies conducted in Egypt (Kamell and El-Minshawy 2010), El Salvador (Peraza et al. 2012), India (Rajapurkar et al. 2012), Central America (Almaguer et al. 2014), and Sri Lanka (Kulathunga et al. 2019) have reported the emergence of CKDu in agricultural workers. In terms of CKDu etiology, recent research has identified pesticide exposure as a risk factor for kidney dysfunction among farm workers (Chandrajith et al. 2011; Singh et al. 2013; Ganguli 2016). Many farmers in developing countries are exposed to OP and carbamate pesticides due to lack of awareness about appropriate pesticide handling behavior. Previous reports provided strong evidence that an acute cholinergic crisis can be developed due to pesticide exposure within a few minutes to hours after exposure (Lameire et al. 2013; Kashani et al. 2017). In the present study, only erythrocyte AChE was significantly associated with the eGFR, which served as a biomarker of kidney function in the participants (p-value = 0.04). Our findings are similar to those reported previously (Singh et al. 2011; Lebov et al. 2016). Also in a previous study, ever use of OP and carbamate pesticides by agricultural workers was associated with a reduced eGFR (García-Trabanino et al. 2015). As proposed before, pesticide exposure affected the neurotransmitter acetylcholine, which significantly altered renal function as a result of alterations in neural, humoral, and metabolic activity (Wedin 1992). A study by Mendley et al. (2019), which based on renal biopsies obtained from agricultural workers, demonstrated a link between a history of exposure to pesticides and herbicides, and potential renal tubular toxicity.