Australia has banned the production of 2,4-D HVE active constituent, also known as agent orange. The latest risk assessment of data from the Department of Sustainability, Environment, Water, Population and Communities (DSEWPAC) determined the risks of the use of 2,4-D HVE products were unacceptable and cannot be mitigated.
The Australian Pesticides and Veterinary Medicines Authority has taken immediate steps to cancel the registration of 11 high volatile ester products (HVE) products and two active constituents.
The decision means the following:
• supply of the cancelled 2,4-D HVE active constituent is to cease immediately (August 21, 2013)
• from August 31, 2013 the supply of product containing 2,4-D HVE manufactured up to August 21, 2013 is to cease
• people can use products they have already bought until August 31, 2014 under the same permit instructions (PER14329) which restricts use to winter only and under strict conditions
• use of these products after August 31, 2014 will be illegal.
Agent Orange is the name given to a potent herbicide and defoliant used by the US military during the Vietnam war from 1961-1971. The product is a 50/50 mixture of 2,4,5,-T and 2,4-D, the main ingredients, manufactured by Monsanto Corporation and Dow Chemical. Agent Orange has been associated with wide range toxic health effects ranging from cancer, leukemia, birth defects and other serious side effects and complications that to this day still plague Vietnam war veterans and the Vietnamese population directly targeted with the herbicide.
Monsanto has recently reached a proposed class action settlement, in February 2012, in the town in which agent orange originated.
The case was filed in 2008 on behalf of people who lived, worked and went to school in the small town of Nitro, West Virginia. For about two decades ending in 1971, Monsanto produced the herbicide 2,4,5-T there, which was used in Agent Orange. The lawsuit claims the company polluted the town with toxic substances, including dioxins, and asks the court to award medical monitoring for residents. The judge presiding over the case has placed a sweeping gag order on the case where details of the case are prohibited from being released. The suit claims poisonous residues from the chemical have polluted the area, putting residents’ health and the environment at serious risk. According to the Republic Broadcasting Network:
“Monsanto is alleged to have burned dioxin waste in open pits, spewing dioxin and its ash into the air and polluting land … The EPA recommended that Monsanto be criminally investigated for fraud in covering-up dioxin contamination in its products, including 2,4,5-T herbicide. Monsanto failed to report contamination, substituted false information to show no contamination or sent in ‘doctored’ samples of their products devoid of dioxin to government regulators.”
Monsanto has tentatively agreed to a $93 million settlement with some of the residents. The settlement would include $21 million for medical testing, $63 million for additional screening, and $9 million for the cleanup of 4,500 homes.
Monsanto and Dow Chemicals have once again revitalized agent orange with the current field trials of GMO crops containing resistance to the main ingredients found in Agent Orange. Dow’s new GM product, dubbed “Enlist,” has been engineered to be resistant to glyphosate, the active ingredient in Monsanto’s popular Roundup herbicide, along with glufosinate and 2,4-D.
What are the toxic effects of 2, 4 -D and the concern of ingesting a GMO product that is resistant to the 2-4-D product? It raises the concern and the possibility that farmers will now begin spraying the herbicide year round to kill weeds also at the same lacing the GMO corn with agent orange. However, the possibility exists of transferring the 2,4-D resistance genes to other plants, nullifying the effect of trying to create a herbicide resistant plant, in particular as the pervasive contamination and spread of GMO products was documented by the Union of concerned scientist.
The Union of concerned scientists was the first organization to evaluate the impact of the transgenic contamination of GMO corn products in its 2005 report quite conclusively demonstrating that they found low levels of transgenically derived sequences in most of the samples of non-engineered corn, canola, and soybean seeds that were tested. Their results suggest that the contamination of traditional varieties of corn, soybeans and canola is pervasive and originates from genetic sequences originating predominantly form genetically modified plants.
What is the impact on the consumer?
Several research studies have documented the toxic effect of 2,4-D as follows:
In mammals, 2,4-D disrupts energy production, depleting the body of its primary energy molecule, ATP (adenosine triphosphate). 2,4-D has been shown to cause cellular mutations which can lead to cancer. This mutagen contains dioxins, a group of chemicals known to be hazardous to human health and to the environment.
Numerous epidemiological studies have linked 2,4-D to non-Hodgkin’s lymphoma (NHL) among farmers. Multi-center studies in Canada and in Sweden of members of the general public found a 30-50% higher odds of 2,4-D exposure among people with NHL.
The teratogenic, neurotoxic, immunosuppressive, cytotoxic and hepatoxic effects of 2,4-D have been well documented and other researchers publishing in the open scientific literature have reported oxidant effects of 2,4- D, indicating the potential for cytotoxicity or genotoxicity. For example, Bukowska (2003) reported that treatment of human erythrocytes in vitro with 2,4-D at 250 and 500 ppm resulted in decreased levels of reduced glutathione, decreased activity of superoxide dismutase, and increased levels of glutathione peroxidase. These significant changes in antioxidant enzyme activities and evidence of oxidative stress indicate that 2,4-D should be taken seriously as a cytotoxic and potentially genotoxic agent.
2,4-D causes significant suppression of thyroid hormone levels in ewes dosed with this chemical (Rawlings et al., 1998). Similar findings have been reported in rodents, with suppression of thyroid hormone levels, increases in thyroid gland weight, and decreases in weight of the ovaries and testes (Charles et al., 1996). The increases in thyroid gland weight are consistent with the suppression of thyroid hormones, since the gland generally hypertrophies in an attempt to compensate for insufficient circulating levels of thyroid hormones. Thyroid hormone is known to play a critical role in the development of the brain. Slight thyroid suppression has been shown to adversely affect neurological development in the fetus, resulting in lasting effects on child learning and behavior (Haddow et al., 1999).
2,4-D causes slight decreases in testosterone release and significant increases in estrogen release from testicular cells (Liu et al., 1996). In rodents, this chemical also increases levels of the hormones progesterone and prolactin, and causes abnormalities in the estrus cycle (Duffard et al., 1995). Male farm sprayers exposed to 2,4-D had lower sperm counts and more spermatic abnormalities compared to men who were not exposed to this chemical (Lerda & Rizzi, 1991). In Minnesota, higher rates of birth defects have been observed in areas of the state with the highest use of 2,4-D and other herbicides of the same class. This increase in birth defects was most pronounced among infants who were conceived in the spring, the time of greatest herbicide use (Garry et al, 1996).
2,4-D also interferes with the neurotransmitters serotonin and dopamine. In young organisms, exposure to 2,4-D results in delays in brain development and abnormal behavior patterns, including apathy, decreased social interactions, repetitive movements, tremor, and immobility (Evangelista de Duffard et al, 1995). Females are more severely affected than males. Rodent studies have revealed a region-specific neurotoxic effect on the basal ganglia of the brain,resulting in an array of effects on critical neurotransmitters and adverse effects on behavior (Bortolozzi et al., 2001).
A peer-reviewed, developmental neurotoxicity study demonstrated severe neurotoxicity in young rats exposed to 2,4-D from postnatal days 12 to 25 at doses of 70 mg/kg/day. These pups showed decreases in GM1 level, diminution in myelin deposition and alterations in all behavioral tests at all doses (Rosso et al, 2000). This herbicide specifically appears to impair normal deposition of myelin in the developing brain (Duffard et al., 1996). The neurotoxic and anti thyroid effects of 2,4-D make it highly likely that fetuses, infants, and children will be more susceptible to long term adverse health effects from exposure to this chemical although they may appear normal at birth.
Young animals can also be exposed to 2,4-D through maternal milk. Recent research has revealed that 2,4-D is excreted in breast milk, thereby resulting in potentially significant exposures to the nursling. The researchers detected 2,4-D residues in stomach content, blood, brain and kidney of 4-day-old neonates fed by 2,4-D exposed mothers (Sturtz et al., 2000). When maternal exposures stopped, the chemical continued to be excreted in maternal milk for a week. Thus, postnatal exposures to this chemical during the critical period for development of the infant brain are of serious scientific concern.
Union of Concerned Scientists, 2005 Seed Report. Gone to Seed, transgenic contaminants in the traditional seed supply.
Barnekow DE, AW Hamburg, V Puvanesarajah, M Guo. Metabolism o 2,4-dicholorophenoxyacetic acid in laying hens and lactating goats. Journal of Agricultural and Food Chemistry. 2000, 49(1):156-163.
Blakley PM, JS Kim, GD Firneisz. Effects of preconceptional and gestational exposure to Tordon 202c on fetal growth and development of CD-1 mice. Teratology, 1989, 39:547-553.
Bortolozzi A, AM Evangelista de Duffard, F Dajas, R Duffard, R Silveira. Intracerebral administration of 2,4-diclorophenoxyacetic acid induces behavioral and neurochemical alterations in the rat brain. Neurotoxicology, 2001, 22(2):221-32.
Brand RM, AR Charron, L Dutton, TL Gavlik, et al. Effects of chronic alcohol consumption on dermal penetration of pesticides in rats. J Toxicol Environ Health A, 2004, 67(2):153-61.
Brand RM, Spalding M, Mueller C. Sunscreens can increase dermal penetration of 2,4- dichlorophenoxyacetic acid. J Toxicol Clin Toxicol, 2002, 40(7):827-32.
Bukowska B. Effects of 2,4-D and its metabolite 2,4-dichlorophe nol on antioxidant enzymes and level of glutathione in human erythrocytes. Comp Biochem Physiol C Toxicol Pharmacol, 2003, 135(4):435-41.
Charles JM, TR Hanley Jr., TR Wilson, B van Ravenzwaay, JS Bus. Developmental toxicity studies in rats and rabbits on 2,4-dichlorophenoxyacetic acid and its forms. Toxicological Sciences, 2001, 60(1):121-131.
Charles JM, HC Cunny, RD Wilson, JS Bus. Comparative subchronic studies on 2,4-dichlorophenoxyacetic acid, amine, and ester in rats. Fundamental & Applied Toxicol, 1996, 33:161-165.
Donald DB, J Syrgiannis, F Hunter, G Weiss. Agricultural pesticides threaten the ecological integrity of northern prairie wetlands. Sci Total Environ. 1999, Jul 1;231(2-3):173-81.
Duffard R, G Garcia, S Rosso, A Bortolozzi, M Madariaga, O di Paolo, AM Evangelista de Duffard. Central nervous system myelin deficit in rats exposed to 2,4-dichlorophenoxyacetic acid throughout lactation. Neurotoxicol Teratol, 1996, 18(6):691-696.
Fenske RA. Pesticide exposure assessment of workers and the ir families. Occup Med, 1997, 12:221-37.
de Duffard AME, A Bortolozzi, RO Duffard. Altered behavioral responses in 2,4- dichlorophenoxyacetic acid treated and amphetamine challenged rats. Neurotoxicology, 1995, 16(3):479-488.
Fontana A, Picoco C, Masala G, Prastaro C, Vineis P. Incidence rates of lymphomas and environmental measurements of phenoxy herbicides: ecological analysis and case-control study. Arch Environ Health, 1998, 53:384-7.
Forsyth DJ, PA Martin, GG Shaw. Effects of herbicides on two submersed aquatic macrophytes, Potamogeton pectinatus L. and Myriophyllum siviricum Komarov, in a prairie wetland. Environmental Pollution, 1997, 90:259-268.
Garcia G, P Tagliaferro, A Bortolozzi, MJ Madariaga, A Brusco, AME de Duffard, R Duffard, JP Saavedra. Morphological study of 5-ht neurons and astroglial cells on brain of adult rats perinatal or chronically exposed to 2,4-dichlorophenoxyacetic acid. Neurotoxicology, 2001, 22:733-741.
Garry VF, D Schreinemachers, ME Harkins, et al. Pesticide appliers, bio cides, and birth defects in rural Minnesota. Environ Hlth Perspect, 1996, 104:394-399.
Haddow JE, GE Palomaki, WC Allan, JR Williams, GJ Knight, J Gagnon, CE O’Heir, ML Mitchell, RJ Hermos, SE Waisbren, JD Faix, RZ Klein. Maternal thyroid deficiency during pregnancy and subsequent neuropsychological development of the child. New Eng J Med, 1999, 341(8):549-555.
Hardell L, Eriksson M. A case-control study of non-Hodgkin lymphoma and exposure to pesticides. Cancer, 1999, 85: 1353-60.
Hardell L, Eriksson M. Is the decline of the increasing incidence of non-hodgkins lymphoma in Sweden and other countries a result of cancer preventive measures? Environ Health Perspect, 2003, 111(14):1704-6.
Hayes HM, RE Tarone and KP Cantor. On the Association between Canine Malignant Lymphoma and Opportunity for Exposure to 2,4-Dichlorophenoxyacetic Acid. Environmental Research, 1995, 70(2):119-125.
Hayes HM, RE Tarone, KP Cantor, CR Jessen, DM McCurrnin, and RC Richardson. Case control study of canine malignant lymphoma: Positive association with dog owner’s use of 2,4- dichlorophenoxyacetic acid herbicide. J. Natl. Cancer. Inst. 1991, 83:1226-1231.
Kogevinas, M. Soft Tissue Sarcoma and non-Hodgkins Lymphoma in Workers exposed to phenoxy-herbicides, chlorophenols, and dioxins – 2 nested case studies. Epidemiology, 1995, 6(4):396-402.
Lerda D, R Rizzi. Study of reproductive function in persons occupationally exposed to 2,4-D. Mutation Research, 1991, 262:47-50.
Littorin, M “Dioxins in Blood from Swedish Phenoxy Herbicide Workers.” In Lancet Vol.344 (8922), August 27, 1994, pp.611-612.
Liu RC, C Hahn, ME Hurtt. The direct effect of hepatic peroxisome proliferators on rat leydig cell function in vitro. Fundamental & Applied Toxicol, 1996, 30:102-108.
Duffard R, Bortolozzi A, Ferri A, Garcia G, Evangelista de Duffard AM. Developmental neurotoxicity of the herbicide 2,4-dichlorophenoxyacetic acid. Neurotoxicology, 1995, 16(4):764.
Lu C, RA Fenske, NJ Simcox, D Kalman. Pesticide exposure of children in an agricultural community: evidence of household proximity to farmland and take home exposure pathways. Environ Res, 2000, 84:290-302.
Madrigal-Bujaidar E, Hernandez-Ceruelos A, Chamorro G. Induction of sister chromatid exchanges by 2,4-dichlorophenoxyacetic acid in somatic and germ cells of mice exposed in vivo. Food Chem Toxicol, 2001, 39(9): 941-6.
McDuffie HH, Pahwa P, McLaughlin JR, et al. Non-Hodgkin’s lymphoma and specific pesticide exposures in men: cross-Canada study of pesticides and health. Cancer Epidemiol Biomarkers Prev., 2001, 10(11): 1155-63.
Miligi L, Adele Seniori Costantini, Vanessa Bolejack, Angela Veraldi, Alessandra Benvenuti, Oriana Nanni, Valerio Ramazzotti, Rosario Tumino, Emanuele Stagnaro, Stefania Rodella, Arabella Fontana, Carla Vindigni, Paolo Vineis. Non-Hodgkin’s lymphoma, leukemia, and exposures in agriculture: Results from the Italian multicenter case-control study. Am J Ind Med. 2003 44(6):627-636.
Moody RP, RC Wester, JL Melendres, HI Maibach. Dermal absorption of the phenoxy herbicide 2,4-D dimethylamine in humans: effect of DEET and anatomic site. J Toxicol Environ Health, 1992, 36(3):241-50.
Morrison HI, Wilkins K, Semenciw R, Mao Y, Wigle D. Herbicides and cancer. J Natl Cancer Inst, 1992, 84:1866-74.
Morrison, H. et al. Farming and Prostate Cancer Mortality. American Journal of Epidemiology, 1993, 137(30):270-280.
National Research Council of Canada. Associate committee on Scientific Criteria for Environmental Quality; Subcommittee on Pesticides and Industrial Organic Chemicals. “2,4-D Some Current Issues” NRCC No. 20647, 1983, Pp. 29-55.
Nishioka MG, Burkholder HM, Brinkman MC, Gordon SM. Measuring lawn transport of lawnapplied herbicide acids from turf to home: Correlation of dislodgeable 2,4-D turf residues with carpet dust and carpet surface residues. Environmental Science and Technology, 1996, 30: 3313- 3320.
Nishioka, M.G. et al. Distribution of 2,4-dichlorophenoxy acetic acid in floor dust throughout homes following homeowner and commercial lawn applications: Quantitative effects of children, pets and shoes. Environ. Sci. Technol., 1999, 33:1359-1365.
Osaki K, JF Mahler, JK Hasemann, CR Moomaw, ML Nicolette, A Nyska. Unique renal tubule changes induced in rats and mice by the peroxisome proliferators 2,4-dicholorophenoxyacetic acid (2,4-D) and WY-1643. Toxicologic Pathology, 2001, 29(4):440-450.
Palmeira, C.M, A.J Moreno and V.M.C. Madeira. Interactions of herbicides 2,4-D and dinoseb with liver mitochondrial bioenergetics. Toxicol. Appl. Pharmacol., 1994, 127:50-57.
Pont AR, Anna R. Charron and Rhonda M. Brand. Active ingredients in sunscreens act as topical penetration enhancers for the herbicide 2,4-dichlorophenoxyacetic acid. Toxicology and Applied Pharmacology, 2004, 195(3):348-354.
Rawlings NC, SJ Cook, D Waldbillig. Effects of the pesticides carbofuran, chlorpyrifos, dimethoate, lindane, triallate, trifluralin, 2,4-D, and pentachlorophenol on the metabolic endocrine and reproductive endocrine system in ewes. J Toxicol Environ Hlth, 1998, 54:21-36.
Riviere JE, Baynes RE, Brooks JD, Yeatts JL, Monteiro-Riviere NA. Percutaneous absorption of topical N,N-diethyl-m-toluamide (DEET): effects of exposure variables and coadministered toxicants. J Toxicol Environ Health A, 2003, 66(2):133-51.
Roberts BL, HW Dorough. Relative toxicity of chemicals to the earthworm. Environ Toxic Chem, 1984, 3:67-78.
Rosso SB, AO Caceres, AM de Duffard, RO de Duffard, S Quiroga. 2,4-dichlorophenoxyacetic acid disrupts the cytoskeleton and disorganizes the Golgi apparatus of cultured neurons. Toxicological Sciences, 2000, 56(1):133-140.
Rosso SB, GB Garcia, MJ Madariaga, AM Evangelista de Duffard, RO Duffard. 2,4- Dichlorophenoxyacetic acid in developing rats alters behaviour, myelination and regions brain gangliosides pattern. Neurotoxicology, 2000, 21(1-2):155-63.
Sterlineg TD, AV Arundel. Health effects of phenoxy herbicides – A review. Scand J Work Environ Health, 1986, 12:161-173.
Sturtz N, AM Evangelista de Duffard, R Duffard. Detection of 2,4-dichlorophenoxyacetic acid (2,4-D) residues in neonates breast-fed by 2,4-D exposed dams. Neurotoxicology, 2000, 21(1- 2):147-54.
Sulik M, W Kisilewski, B Szyaka, A Kemona, M Sulkowska, M Baltziak. Morphological change in mitochondria and lysosome of hepatocytes in acute intoxication with 2,4-
dichlorophenoxyacetic acid (2,4-D). Materia Medica Polona, 1998, 30(1-2):16-19.
Tuschl H, C Schwab. Cytotoxic effects of the herbicide 2,4-dichlorophenoxyacetic acid in HepG2 cells. Food Chem Toxicol, 2003, 41:385-393.
Venkov P, M Topashka-Ancheva, M Georgieva, V Alexieva, E Karanov. Genotoxic effect of substituted phenoxyacetic acids. Arch Toxicol, 2000, 74:560-6.
Zahm SH, Blair A. Pesticides and non-Hodgkin’s lymphoma. Cancer Res, 1992, 52: 5485s-5488s.
Zeljezic D, V Garaj-Vrhovac. Chromosomal aberrations, micronuclei and nuclear buds induced in human lymphocytes by 2,4-dichlorophenoxyacetic acid pesticide formulation. Toxicology, 2004, 200:39-47.
Zychlinkski, L. and S. Zolnierowicz. Comparison of uncoupling activities of chlorophenoxy herbicides in rat liver mitochondria. Toxicol. Lett., 1990, 52:25-34.