2,4-D

CAS RN:94-75-7

Health Effects

0.2.1 SUMMARY OF EXPOSURE
  • 0.2.1.1 ACUTE EXPOSURE
    • A) USES: Chlorophenoxy compounds are mixed into commercial fertilizers to restrict the growth of broadleaf weeds. Several hundred commercial products contain chlorophenoxy compounds in various forms, concentrations, and combinations. Agent Orange was a mixture of chlorophenoxy compounds. Other chlorophenoxy compounds include MCPA (methylchlorophenoxy acetic acid) and MCPP (Mecoprop, 4-Chloro-2-methylphenoxypropionic acid).
    • B) TOXICOLOGY: In animals, chlorophenoxy compounds have been shown to demyelinate peripheral nerves, depress ribonuclease synthesis, uncouple oxidative phosphorylation, and increase hepatic peroxisomes. They are also moderately irritating to skin and mucous membranes.
    • C) EPIDEMIOLOGY: Thousands of exposures to chlorophenoxy compounds are reported to poison centers every year. The majority of cases have no or only minor effects, but major effects and even death does occur after exposures, usually with deliberate, large ingestions.
    • D) WITH POISONING/EXPOSURE
      • 1) MILD TO MODERATE TOXICITY: Inadvertent/exploratory ingestions by children generally only cause mild irritation of the exposed tissue (eg, gastrointestinal mucosa, skin, eyes, respiratory tract).
      • 2) SEVERE TOXICITY: Large, deliberate ingestions can cause mucosal ulceration, miosis, coma, fever, hypotension, emesis, tachycardia, bradycardia, ECG abnormalities, muscle rigidity, rhabdomyolysis, renal failure, acute lung injury, and respiratory failure. Deaths have occurred secondary to cardiopulmonary arrest, but are rare. After ingestion, fever of sudden but delayed onset may occur. Electrolyte abnormalities, such as hypocalcemia, hyperkalemia, and hypophosphatemia, can develop. Thrombocytopenia and leukopenia have been reported. Hyperglycemia has also been reported in cases of acute 2,4-D poisoning. Direct dermal contact may cause skin irritation. Some chlorophenoxy compounds are also moderately irritating to eyes and respiratory and gastrointestinal linings.
      • 3) CHRONIC EXPOSURE: Local depigmentation has resulted from protracted dermal contact. Albuminuria and porphyria may occur. Chlordioxin may produce chloracne with heavy exposures.
0.2.3 VITAL SIGNS
  • 0.2.3.1 ACUTE EXPOSURE
    • A) WITH POISONING/EXPOSURE
      • 1) Fever of sudden but delayed onset may occur following ingestion.
0.2.20 REPRODUCTIVE HAZARDS
  • A) 2,4-D and 2,4,5-T have caused adverse reproductive effects in experimental animals. Allegations of human birth defects due to these compounds have not been confirmed.
0.2.21 CARCINOGENICITY
  • 0.2.21.1 IARC CATEGORY
    • A) IARC Carcinogenicity Ratings for CAS94-75-7 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
      • 1) Not Listed
    • B) IARC Carcinogenicity Ratings for CAS93-76-5 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
      • 1) Not Listed
    • C) IARC Carcinogenicity Ratings for CAS94-74-6 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
      • 1) Not Listed
    • D) IARC Carcinogenicity Ratings for CAS93-65-2 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
      • 1) Not Listed
  • 0.2.21.2 HUMAN OVERVIEW
    • A) Human studies show conflicting results. Some studies have suggested a relationship between chlorophenoxy herbicides and both soft tissue sarcoma and non-Hodgkin's lymphoma, while others have not. There is limited evidence of an association with prostate carcinoma.
  • 0.2.21.3 ANIMAL OVERVIEW
    • A) Animal studies are limited, but have generally been negative.
0.2.22 GENOTOXICITY
  • A) The chlorophenoxy herbicides have produced mixed negative and positive responses in various genotoxicity test systems. A recent review found no evidence of genotoxic or mutagenic potential in vitro and in vivo for 2,4-D.
  • B) One study was conducted to determine whether or not New Zealand Vietnam War veterans showed evidence of genetic disturbances arising as a consequence of their now confirmed exposure to chlorophenoxy herbicides. During 1965 to 1971, more than 76 million liters of phenoxylic herbicides were sprayed over parts of Southern Vietnam and Laos. A sample group of 24 New Zealand Vietnam War veterans and 23 control volunteers were compared using a sister chromatid exchange (SCE) analysis. The results showed a significant difference between the mean of the experimental group and the mean of the control group (11.05 vs 8.18; p<0.001). The experimental group also had an extremely elevated proportion of cells with high SCE frequencies (HFCs) above the 95th percentile compared to the controls (11% and 0.07%, respectively) (Rowland et al, 2007).
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