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The Selection and Use of Gloves against Pesticides
Published in Robert N. Phalen, Howard I. Maibach, Protective Gloves for Occupational Use, 2023
The chemical form of the pesticide appears to be of some importance. For example, 4-chloro-2-methylphenoxyacetic acid (MCPA) had no appreciable permeation through gloves of natural rubber, Neoprene, nitrile, or Viton coated Neoprene when used in a salt formulation, whereas MCPA permeated through the same four glove materials with reduced lag-times when applied in an ester form.20
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
2,4,5-TP (Silvex) is the propionic acid homolog of 2,4,5-T. Kuron is a low-volatility ester of 2,4,5-TP. 2,4,5-TB is the butyric acid homolog of 2,4,5-T. Fenac or clorfenac is 2,3,6-trichlorophenylacetic acid. Dicamba (Banvel) is dichloroanisic acid. MCPA, MCPB, MCPB-ethyl, MCPCA, and MCPP (Mecoprop) are 2-methyl,4-chlorophenoxy aliphatic acids and esters.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
These same authors linked records of more than 20,000 licensed pesticide applicators in Sweden to the central cancer registry.67–68 An estimated 72% of the applicators had exposure to phenoxy herbicides, mainly MCPA, MCPP, and 2,4-DP but also 2,4-D and 2,4,5-T. No excess incidence of STS, NHL, or HD was observed in the total group of applicators nor in subsets defined by latency or year of licensing.
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
2-Methyl-4-chlorophenoxyacetic acid (MCPA) is a chlorophenoxy herbicide. In a case series of 181 self-poisonings most patients developed only mild toxicity and deaths were rare [1]. Bromoxynil, a nitrile herbicide is available in many countries worldwide, including many countries in Europe. Its use is restricted in the United States, but is readily available in Australia. We found no reports of bromoxynil monointoxication, but from limited data available it appears ingestion of the combination of MCPA and bromoxynil may be associated with a higher mortality [2,3]. The combination appears to result in severe toxicity characterized by tachycardia, tachypnoea, rising CO2, metabolic acidosis, hyperthermia and cardiac arrest [2,3]. Dialysis has been proposed as a treatment, but there is no evidence to support whether it increases elimination. We present two cases of MCPA/bromoxynil ingestion whose management included continuous venovenous haemodiafiltration (CVVHDF) and present clearances of both herbicides.
Microbiota-derived butyrate is an endogenous HIF prolyl hydroxylase inhibitor
Published in Gut Microbes, 2021
Ruth X. Wang, Morkos A. Henen, J. Scott Lee, Beat Vögeli, Sean P. Colgan
To more fully understand the relationship between butyrate and HIF, we examined whether butyrate influences PHD activity by monitoring 2-OG levels. Olenchock et al.17 established that PHD2 inhibition directly leads to 2-OG accumulation, as PHD2 decarboxylates 2-OG at a high rate of ~200 pmol/min/g of tissue, with 1 mole of PHD2 estimated to decarboxylate 45 moles of 2-OG in 1 min. In this, we considered such 2-OG accumulation as a metabolic biomarker of PHD inhibition (Figure 3a). Butyrate significantly increased 2-OG levels in T84 IECs compared to control after 3 h, as did the PHD inhibitor IOX2, albeit to lesser extent than butyrate at this time point (Figure 3b). In the presence of MCPA and butyrate, which eliminated the β-oxidation of butyrate, 2-OG levels were also significantly increased, expectedly to a significantly lesser level compared to butyrate alone (Figure 3b). MCPA, through eliminating β-oxidation of butyrate, not only stops the increase in oxygen consumption, but also prevents the increased TCA cycle production of metabolites such as 2-OG (figure 1f). Because 2-OG is also a TCA cycle metabolite, the additional increase in 2-OG with butyrate compared to IOX2 and butyrate with MCPA represents the 2-OG produced from the TCA cycle because of butyrate β-oxidation. Butyrate treatment over 4 days has been shown to significantly increase acetyl-CoA and 2-OG levels in other model IECs.18 Our findings here suggest that while butyrate metabolism contributes to increased 2-OG, butyrate additionally increases 2-OG levels in a manner independent of β-oxidation that is possible through direct PHD inhibition.
Bromoxynil and 2-methyl-4-chlorophenoxyacetic acid (MCPA) poisoning could be a bad combination
Published in Clinical Toxicology, 2018
Betty S. H. Chan, Angela L. Chiew, Sarah Grainger, Colin B. Page, Alan Gault, Ahmed Mostafa, Michael S. Roberts, Nicholas A. Buckley, Geoffrey K. Isbister
We would like to provide further research findings following the case reports on “2-methyl-4-chlorophenoxyacetic acid (MCPA) and bromoxynil herbicide ingestion” by Chiew et al. [1]. This reported a characteristic toxicity profile of hyperthermia, hypercapnia and metabolic acidosis in two patients that responded to aggressive active cooling and supportive treatment.