Haloxyfop (aryloxyphenoxypropionates)

Clethodim (cyclohexanediones)

Pinoxaden (phenylpyrazolines)

ACCase inhibitors (A⁽¹⁾)

Alachlor (chloroacetanilides)

Diphenamid (acetamides)

Flufenacet (oxyacetamides)

Fentrazamide (tetrazolinones)

Mitosis inhibitors (K₃⁽¹⁵⁾)

Bensulfuron-methyl (sulfonylureas)

Imazethapyr (imidazolinones)

Cloransulam-methyl (triazolopyrimidines)

ALS inhibitors (B⁽²⁾)

Atrazine (symmetrical triazines)

Photosynthesis II inhibitors (C₁⁽⁵⁾)

Dicamba (benzoic acids)

Synthetic auxins (O⁽⁴⁾)

Glufosinate (organophosphorus)

Glutamine synthetase inhibitor (H⁽¹⁰⁾)

Glyphosate (organophosphorus)

Enolpyruvyl shikimate-3-phosphate (EPSP) synthase inhibitor (G⁽⁹⁾)

Inhibitor of acetyl coenzyme-A carboxylase (ACCase), a pivotal enzyme in plant fatty acid biosynthesis.

Varies based on specific chemical compound; likely to be carcinogenic to humans according to EPA Proposed EPA Weight-of-the-Evidence Categories (US-EPA, 2009a).

Inhibition of cell division (long-chain fatty acid inhibitor).

Slightly toxic; oral RfD* of 1 × 10^–2 mg/kg-day. Critical effects: hemosiderosis, hemolytic anemia (US-EPA, 2009b).

Inhibition of the acetolactate synthase (ALS) enzyme resulting in cessation of the biosynthesis of essential branched chain amino acids (leucine, valine, and isoleucine).

Varied; generally low acute and chronic toxicity to humans and not likely to be carcinogenic.

Inhibit photosynthesis by binding with a specific protein in the photosystem II complex.

Slightly to moderately toxic; oral RfD of 3.5 × 10^–2 mg/kg-day. Critical effects: decreased body weight gain (other effect: cardiac toxicity and moderate-to-severe dilation of the right atrium (EXTOXNET, 2009a; US-EPA, 2009c)).

The specific mode of action is not well defined, however these herbicides mimic the endogenous auxin indoleacetic acid, a plant hormone that stimulates growth and appears to negatively affect cell wall plasticity and nucleic acid metabolism.

Relatively nontoxic. Acute oral LD₅₀† in rats is 1707 mg/kg, dermal LC₅₀^§ in rabbits is >2000 mg/kg. However, eye irritation in rabbit is extreme.

Inhibits the activity of glutamine synthetase, which causes ammonia buildup in the cell. The ammonia destroys cell membranes.

Practically nontoxic by ingestion; some increase in absolute and relative kidney weights in males. No observed carcinogenesis. Oral RfD of 4 × 10^–4 mg/kg-day (NPIC, 2009; US-EPA, 2009d).

Amides, pyridiazinones, pyridines, isoxazoles, pyrazoles, triazoles, triketones, and others

Carotenoid biosynthesis inhibitors

Fluridone (unclassified)

(F₁⁽¹²⁾)

Mesotrione (triketones)

(F₂⁽²⁸⁾)

Amitrole (triazoles)

(F₃⁽¹¹⁾)

Metribuzin (triazinones, asymmetrical triazines)

Photosynthesis II inhibitors (C₁⁽⁵⁾)

Inhibit the catabolic degradation of tyrosine to plastoquinones (important for photosynthesis and carotenoid biosynthesis) and tocopherol (vitamin E, which protects biological membranes against oxidative stress and the photosynthetic apparatus against photo-inactivation).

Varied; developmental toxicity, probable human carcinogen, phytotoxic (US-EPA, 2004, 2006, 2009f, 2009g).

Inhibition of phytoene desaturase, an enzyme essential for carotenoid biosynthesis.

Inhibition of hydroxyphenylpyruvate dioxygenase (HPPD), an enzyme involved in the synthesis of plastoquinone (PQ) and tocopherol (vitamin E).

Target site is generally considered unknown with the exception of amitrole, which inhibits lycopene cyclase and clomazone that is reported to inhibit an early step in the nonmevalonic acid isoprenoid pathway ultimately leading to carotenoid synthesis.

Inhibit photosynthesis by binding with a specific protein in the photosystem II complex.

A slightly toxic compound in EPA toxicity class III. Liver and kidney effects, decreased body weight, mortality; no indications of carcinogenic effects. RfD of 2.5 10–² mg/kg-day (EXTOXNET, 2009b; US-EPA, 2009h).

2,4-D (phenoxyacetic herbicide)

Synthetic auxins (O⁽⁴⁾)