• Cristian Cobilinschi 1Carol Davila University of Medicine and Pharmacy, Bucharest, Romania 2 Bucharest Clinical Emergency Hospital, Intensive Care Unit, Romania
  • Andrei Cosmin Andrei 2 Bucharest Clinical Emergency Hospital, Intensive Care Unit, Romania
  • Radu Tincu 1Carol Davila University of Medicine and Pharmacy, Bucharest, Romania 2 Bucharest Clinical Emergency Hospital, Intensive Care Unit, Romania
Keywords: herbicides, 2,4-dichlorphenoxyacetic acid, acute poisoning, urine alkalinization, critical care


Herbicides are widely used to control the growth of broadleaf plants and among these 2,4-dichlorphenoxyacetic acid (2,4-D) has become dominant in both agriculture and households. However, despite being rare, acute intoxication with 2,4-D has lethal potential if early diagnosis and management are misguided. 2,4-D poisoning can mimic OP intoxication, so neuromuscular toxicity and coma can orient towards a correct symptom identification. We report the case of a 46-year-old male patient brought into the emergency department after voluntary herbicide ingestion that family confirmed as 2,4-D. Initial assessment revealed an agitated, confused, drowsy patient with a CGS of 9. Laboratory tests revealed mild metabolic acidosis and rhabdomyolysis. Patient management included early sodium bicarbonate administration, low dose mannitol, injectable furosemide and supplemental potassium to induce urine alkalinization. He was discharged five days later in good clinical condition. Acute 2,4-D intoxication has an increased risk of mortality, especially since no antidote is available. Diagnosis should be made promptly and urine alkalinization to accelerate poison clearance is the mainstay treatment.


[1] S. M. Bradberry, B. E. Watt, A. T. Proudfoot, and J. A. Vale, “Mechanisms of toxicity, clinical features, and management of acute chlorophenoxy herbicide poisoning: A review,” J. Toxicol. - Clin. Toxicol., vol. 38, no. 2, pp. 111–122, 2000.
[2] “2,4-dichlorophenoxyacetic acid (2,4-D) in drinking water: Guideline technical document for public consultation -” .
[3] T. N. C. Weed Control Methods Handbook, “2,4-D.”
[4] B. Bukowska, “Effects of 2,4-D and its metabolite 2,4-dichlorophenol on antioxidant enzymes and level of glutathione in human erythrocytes,” Comp. Biochem. Physiol. - C Toxicol. Pharmacol., vol. 135, no. 4, pp. 435–441, 2003.
[5] A. Adeyinka and L. Pierre, Organophosphates. StatPearls Publishing, 2018.
[6] G. Serrano et al., “Degradation and mechanism of 2,4-dichlorophenoxyacetic acid (2,4-D) by thermally activated persulfate oxidation.”
[7] D. B. Barr and B. Buckley, “In Vivo Biomarkers and Biomonitoring in Reproductive and Developmental Toxicity,” Reprod. Dev. Toxicol., pp. 253–265, 2011.
[8] M. O. Oghabian Z, Ghanbarzadeh N, Sharifi MD, “Treatment of 2, 4-Dichlorophenoxyacetic Acid (2, 4-D) Poisoning; a Case Study,” Int. J. Med. Toxicol. Forensic Med., vol. 4, no. 300190, pp. 104–107, 2014.
[9] S. Hiran and S. Kumar, “30 2, 4-D Dichlorophenoxyacetic Acid Poisoning.”
[10] A. Bhalla, V. Suri, N. Sharma, S. Mahi, and S. Singh, “2,4-D (ethyl ester) poisoning: Experience at a tertiary care centre in Northern India,” Emerg. Med. J., vol. 25, no. 1, pp. 30–32, 2008.
[11] L. Prescott, J. Park, and I. Darrien, “Treatment of severe 2,4‐D and mecoprop intoxication with alkaline diuresis.,” Br. J. Clin. Pharmacol., vol. 7, no. 1, pp. 111–116, 1979.
[12] D. Roberts and N. Buckley, “Urinary alkalinisation for acute chlorophenoxy herbicide poisoning,” Cochrane Database Syst. Rev., 2005.
[13] M. E. Peterson, Toxicologic Decontamination. 2012.
[14] T. Keller, G. Skopp, M. Wu, and R. Aderjan, “Fatal overdose of 2,4-dichlorophenoxyacetic acid (2,4-D),” Forensic Sci. Int., vol. 65, no. 1, pp. 13–18, 1994.
[15] P. G. Jorens, L. Heytens, R. J. De Paep, L. Bossaert, M. I. Selala, and P. J. C. Schepens, “A 2,4-dichlorophenoxyacetic acid induced fatality,” Eur. J. Emerg. Med., vol. 2, no. 1, pp. 52–55, 1995.
[16] R. Kamanyire and L. Karalliedde, “Organophosphate toxicity and occupational exposure,” Occup. Med. (Chic. Ill)., vol. 54, no. 2, pp. 69–75, 2004.
[17] A. J. Bednarska, M. Choczyński, R. Laskowski, and M. Walczak, “Combined effects of chlorpyriphos, copper and temperature on acetylcholinesterase activity and toxicokinetics of the chemicals in the earthworm Eisenia fetida,” Environ. Pollut., vol. 220, pp. 567–576, 2017.
[18] C. Cobilinschi et al., “Histopathological features of low-dose organophosphate exposure,” Rom. J. Morphol. Embryol., vol. 61, no. 2, 2020.
[19] C. Cobilinschi, R. Tincu, A. Totan, Z. Ghiorghiu, P. Neagu, and R. Macovei, “Thyroid dysfunction caused by organophosphate,” Toxicol. Lett., no. S169, p. 473, 2017.
[20] E. C. Aromataris, D. S. J. Astill, G. Y. Rychkov, S. H. Bryant, A. H. Bretag, and M. L. Roberts, “Modulation of the gating of ClC-1 by S-(-) 2-(4-chlorophenoxy)propionic acid,” Br. J. Pharmacol., vol. 126, no. 6, pp. 1375–1382, 1999.
[21] V. R. Beasley, E. K. Arnold, R. A. Lovell, and A. J. Parker, “2,4-D toxicosis I: A pilot study of 2,4-dichlorophenoxyacetic acid- and dicamba-induced myotonia in experimental dogs,” Vet. Hum. Toxicol., vol. 33, no. 5, pp. 435–440, 1991.
[22] R. D.M. et al., “Intentional self-poisoning with the chlorophenoxy herbicide 4-chloro-2-methylphenoxyacetic acid (MCPA),” Ann. Emerg. Med., vol. 46, no. 3, pp. 275–284, 2005.
[23] J. R. Reigart and J. R. Roberts, “Recognition and Management of Pesticide Poisonings,” in United States Environmental Protection Agency, vol. 46, no. 18, Washington:, 1999, pp. 156–169.
[24] Z. Durakovic, A. Durakovic, S. Durakovic, and D. Ivanovic, “Poisoning with 2,4-dichlorophenoxyacetic acid treated by hemodialysis,” Arch. Toxicol., vol. 66, no. 7, pp. 518–521, 1992.
[25] M. Moshiri, S. R. Mousavi, and L. Etemad, “Management of 2, 4- Dichlorophenoxyacetic Acid Intoxication by Hemodialysis: A Case Report,” Iran. J. Toxicol., vol. 10, no. 1, pp. 53–55, 2016.
[26] S. Hellman, “Stopping metastases at their source,” N Engl J Med., vol. 337, pp. 996–997, 1997.
[27] M. W. Sauerhoff, W. H. Braun, G. E. Blau, and P. J. Gehring, “The fate of 2,4-dichlorophenoxyacetic acid (2,4-D) following oral administration to man,” Toxicology, vol. 8, no. 1, pp. 3–11, 1977.
[28] J. D. Kohli, R. N. Khanna, B. N. Gupta, M. M. Dhar, J. S. Tandon, and K. P. Sircar, “Absorption and excretion of 2,4-dichlorophenoxyacetic acid in man,” Xenobiotica, vol. 4, no. 2, pp. 97–100, 1974.
[29] I. C. Munroe et al., “A comprehensive, integrated review and evaluation of the scientific evidence relating to the safety of the herbicide 2,4-D,” J. Am. Coll. Toxicol., vol. 11, no. 5, 1992.