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Herbicides
Published in Frank A. Barile, Barile’s Clinical Toxicology, 2019
Structurally, the chlorophenoxy herbicides consist of a simple aliphatic carboxylic acid moiety attached to a chlorine- or methyl-substituted aromatic ring through an ether bond. The mechanism of neurotoxicity is not known.
Pesticides and Chronic Diseases
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
Several hundred commercial products contain chlorophenoxy herbicides (Figure 7.58) in various concentrations and combinations. The following are names of widely advertised formulations (in some cases, the same name is used for products with different ingredients; exact composition must, therefore, be determined from product labels): 2,4-D; Agrotec; Amoxone; Aqua-Kleen; BH 2,4-D; Chipco Turf Herbicide “D”; Chloroxone Crop Rider; D50; Dacamine 4D; Ded-Weed; Desoromone; Dinoxol; DMA4, Dormone; Emulsamine BK; Emulsamine E-3; Envert DT or 171; Esteron 99 Concentrate; Esteron 4; Esteron Brush Killer; Estone; Fernoxone; Fernimine; Ferxone; Fernesta; Formula 40; Hedonal; Herbidal; Lawn-Keep; Macondray; Miracle; Netagrone 600; Pennamine D; Planotox; Plantgard; Rhodia; Salvo (a product of identical name marketed by the Crystal Chemical Company contains cacodylic acid as the active ingredient); Spritz-Hormin/2,4-D; Spritz-Hormit/2,4-D; Superoromone Concentre; Super D Weedone; Transamine; U46; Verton 2D; Visko-Rhap; Weed-B-Gon; Weedar; Weed-Rhap, Weed Tox; Weedtrol; De Broussaillant 600; Lithate; Dicotox; Field Clean Weed Killer. 2,4-DB is the butyric acid homolog of 2,4-D. Dichlorprop is the propionic acid homolog. 2,4,5-trichlorophenoxyacetic acid (2,4,5-T) (Brush-Rhap, Dacamine 4T, De Broussaillant Concentre, Ded-Weed Brush Killer, Esteron 245, Fence Rider, Forron, Inverton 245, Line Rider, Spontox, Super D Weedone, Transamine, Trinoxol, Trioxone, U46, Veon 245, Verton 2T, Weedar, Weedone Envert T).4
The Paradox of Herbicide 2,4-D Epidemiology
Published in Rhoda G. M. Wang, James B. Knaak, Howard I. Maibach, Health Risk Assessment, 2017
Gregory G. Bond, Ralph R. Cook
A few investigators have suggested that the chlorophenoxy herbicides may produce a carcinogenic response secondary to a suppression of the immune system mediated by their dioxin contaminants.23 Although TCDD has been shown to cause immunosuppression in some animal studies,24 there is no evidence of it causing similar effects in highly exposed humans.25-26 The dioxin isomers which have been found at low levels in some samples of 2,4-D are orders of magnitude less biologically active and toxic than TCDD.13
The antioxidant study proprieties of Thymus munbyanus aqueous extract and its beneficial effect on 2, 4-Dichlorophenoxyacetic acid -induced hepatic oxidative stress in albino Wistar rats
Published in Toxicology Mechanisms and Methods, 2021
Lazhari Tichati, Fouzia Trea, Kheireddine Ouali
Pesticides include a heterogeneous group of chemicals mainly used in agricultural activities to improve agricultural yields. The high requirements for these chemicals for diet, as well as their non-controlled use in agriculture as a fertilizer, herbicide, and insecticide, causes severe human health problems and diseases, including neurodegeneration and cancers (Singh et al. 2018). These molecules of thousand advertising virtues are currently, pointed at, due to their proven toxicity (Kim et al. 2017). 2,4- dichlorophenoxyacetic acid (2,4-D) is a selective chlorophenoxy herbicide belonging to the synthetic auxins, and used against dicotyledonous weeds which can grow in cereals (e.g., common wheat, durum wheat, rye, barley, oats) and in industrial sites (Busi et al. 2018). Humans and animals are exposed to 2,4-D via consumption of polluted drinking water and foodstuffs, the 2,4- D product handling, and environmental exposure to 2,4- D treated areas (Islam et al. 2018).
2-Methyl-4-chlorophenoxyacetic acid (MCPA) and bromoxynil herbicide ingestion
Published in Clinical Toxicology, 2018
Angela L. Chiew, Colin B. Page, David Clancy, Ahmed Mostafa, Michael S. Roberts, Geoffrey K. Isbister
The clinical course and herbicide concentrations in both cases parallel a previously reported fatal intentional BIN-DIE® ingestion [3]. A 37-year-old male ingested 200 mL of BIN-DIE® and developed severe hyperthermia and hypercapnia approximately 12 h post-ingestion. MCPA and bromoxynil concentrations were 100 µg/ml and 78.8 µg/ml, respectively, just prior to death 19 h post-ingestion. MCPA concentrations in this and our case were low (Figure 2). Severe MCPA toxicity has been reported to be associated with MCPA concentrations greater than 500 µg/ml [2]. However, the relationship between plasma chlorophenoxy herbicide concentrations and toxicity is not clear, with a case series of MCPA ingestions showing poor correlation between admission plasma MCPA concentrations and toxicity [1], with low toxicity at very high presenting MCPA concentrations (>500 µg/ml) and deaths with presenting concentrations much lower than this. The authors hypothesised this may be due to a poor correlation between plasma (measured) and intracellular (mitochondrial) concentrations [1].