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Toxicology Reflections

2,4-D: Bad for Me?

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Author –

Used widely for domestic and agricultural purposes, 2,4-dichlorophenoxyacetic acid (2,4-D) has been well known commercial herbicide since the 1940s.  According to Statistics Canada (2006), almost half of Canadian farms reported use of herbicides, including 2,4-D, on over 24 million hectares of land in addition to its domestic use for aesthetic purposes in yards and gardens.  Used to control broadleaf plants, 2,4-D is found commercially in three main forms: alkali salts, amine salts and esters (HC 1993).  As a herbicide, 2,4-D is applied directly for weed control but has the potential to enter the environment through many pathways including accidental spills, excessive application, runoff and aerial drift (HC 1993).

For humans, potential pathways to 2,4-D exposure include: ingestion of residuals on food or in water, direct accidental ingestion, dermal exposure most often through the workplace or application, and inhalation by volatilization (HC 1993EPA 2005).  The US Environmental Protection Agency (2005) identifies sensitive populations including toddlers and pregnant women; however, individuals producing or using the chemical have potential for exposure.  Toxicological research on 2,4-D often focuses on its potential association with cancer; however, in a recent review of the literature, Burns and Swaen (2012) summarized historical research into four additional human health endpoints including reproductive toxicology, genotoxicity, neurotxicity, and general toxicity.

The effects of 2,4-D on human health have been a long standing public controversy, likely partly due to its historical association with the war-time chemical Agent Orange and 2,4,5-trichlorophenoxyacetic acid (2,4,5-T) (ACS 2013), and the lack of evidence linking human health effects when used according to guidelines (Burns and Swaen 2012HC 2008).  As a result, both Health Canada and the US Environmental Protection Agency have conducted re-evaluations of 2,4-D in an effort to determine, using scientifically defensible research, the potential risk posed by 2,4-D and the subsequent regulations or management required to minimize that risk (EPA 2005HC 2008).

Despite the large number of studies looking at the toxicity of 2,4-D, the lack of conclusive evidence that 2,4-D is cancer causing (HC 2008) may be contributing to international, national and public perceptions regarding 2,4-D to differ.  The limited epidemiological evidence on which to base guidelines (WHO 2003) and history of public perceptions of 2,4-D has perhaps led to extreme viewpoints on the use of 2,4-D.  For example, the Sierra Club, an environmental activist organization, is opposed to the use of 2,4-D (2005).  Despite reviews of 2,4-D by Health Canada and other world national health organizations to determine the safety of 2,4-D under proper use conditions, there currently exists uncertainty with regard its potential risk to human health.

The purpose of this article is to further discuss the potential human health risks posed by exposure to 2,4-D, and is 2,4-D really ‘bad’ for humans under normal use conditions.  In addition, discussion will explore how the past research has informed the guidelines and reference values used by relevant health organizations.  Due to the relevance of public perception associated with acceptance of risk (Siegrist and Cvetkovich 2000), the current perspectives on the use of 2,4-D by the public and national/international governments will be discussed.  Lastly, a short summary of current research and comment on future direction of 2,4-D research or use will be provided.

References

American Cancer Society. 2013. Agent Orange and cancer.  Website http://www.cancer.org/cancer/cancercauses/othercarcinogens/intheworkplace/agent-orange-and-cancer

Burns, C.J. and G.M.H. Swaen. 2012. Review of 2,4-dichlorophenozyacetic acid (2,4-D) biomonitoring and epidemiology. Critical Reviews in Toxicology. 42(9):768-786

Health Canada. 1993. Fact sheet on the chemical/physical parameters of 2,4-dichlorophenoxyacetic acid. Health Canada.

Health Canada. 2008. Information note: Health Canada releases final re-evaluation decision on 2,4-D. Health Canada.

Siegrist, M. and Cvetkovich, G. 2000. Perception of Hazards: The Role of Social Trust and Knowledge. Risk Analysis. 20: 713–720.

Sierra Club. 2005. Overview of the toxic effects of 2,4-D. Sierra Club of Canada.

Statistics Canada. 2006. Area of commercial fertilizer, herbicides, insecticides and fungicides applied, in Canada from 1996-2006. Statistics Canada.

United States Environmental Protection Agency. 2005. Reregistration eligibility decision for 2,4-D. Prevention, Pesticides and Toxic Substances. EPA 738-R-05-002.

World Health Organization. 2003. 2,4-D in drinking-water: background document for the development of WHO guidelines for drinking-water quality. World Health Organization.

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20 thoughts on “2,4-D: Bad for Me?

  1. Interesting topic and relevant to us here in Ontario. The province of Ontario has banned the use of pesticides for residential cosmetic use and the controversy around 2,4-D was a one of the pillars of the push to ban. You hit on an important point related to 2,4-D being associated with Agent Orange. I’ve read numerous newspaper articles that mention 2,4-D and immediately associate it with Agent Orange. When most people think about Agent Orange, they think about the possible teratogenic and carcinogen effects that have been observed in Vietnam that could be linked to Agent Orange use during the war (1). Agent Orange was composed of two herbicides, 2,4-D and 2,4,5-T, so in the publics mind, with no help of the media, 2,4-D is associated with carcinogenic effects. However, a number of studies have shown that in the manufacturing process, 2,4,5-T was contaminaed with the dioxin, 2,3,7,8-TCDD, which has been shown to be a potent carcinogen in mammals (2,3). Thus, it comes down to what you mentioned in my thread, what is the actual risk relative to the risk perceived by the public.

    On another note, the province of Ontario commissioned a panel to investigate the link between use of herbicides (2,4-D and 2,4,5-T) by provincial ministries from the 50’s through to the 80’s and illnesses observed in employees (Toronto Star article). I think the panels report further supports that contamination of 2,4,5-T by dioxins is the issue, not 2,4-D (Report on the Independent Fact-Finding Panel on Herbicide 2,4,5-T).

    References

    (1) Ngo, A.D., Taylor, R., Roberts, C.L., Nguyen, T.V. 2006. Association between Agent Orange and birth defects: systematic review and meta-analysis. International Journal of Epidemiology, 35, 1220-1230. http://ije.oxfordjournals.org/content/35/5/1220.short

    (2) Boffetta, P., Mundt, K.A., Adami, H., Cole, P., Mandel, J.S. 2011. TCCD and cancer: a critical review of epidemiological studies. Critical Reviews in Toxicology, 41, 622-636. http://informahealthcare.com/doi/abs/10.3109/10408444.2011.560141

    (3) Kogevinas et al. 1997. Cancer mortality in workers exposed to phenoxy herbicides, chlorophenols, and dioxins an expanded and updated international cohort. American Journal of Epidemiology, 145, 1061-1075. http://aje.oxfordjournals.org/content/145/12/1061.short

  2. Yup, everything you state regarding Agent Orange and contamination with dioxins is right in line with what I have read. You will see it again when I cover public perceptions of 2,4-D!

    It is interesting to note that at the provincial and municipal levels of government, decisions to ban chemicals can take place with little to no scientific defense but rather due to the political winds.

    The video you posted was heartbreaking. A video of Noam Chomsky talking about Agent Orange in Vietnam https://www.youtube.com/watch?v=V3qUAHQUQlM has quite a environmentalist spin to it but it is another example of how the human health risks were not clearly understood before it was used on a large scale. I think that despite 2,4-D not being identified as a major carcinogenic contributor to the adverse health effects associated with Agent Orange, some members of the public will still have difficultly accepting it as ‘non-toxic when used appropriately’.

  3. I found it interesting that human health studies where not the most dominant result in search engines when researching 2,4-dichlorophenoxyacetic acid (2,4-D). As a herbicide, the perception of human health effects might not be as apparent due to the targeted use of 2,4,-D on plants and its mode of actions (MoA) which is to alter plant hormones. However, the Insecticide Resistance Action Committee (IRAC) has classified 2,4-D as a group II-B carcinogenic agent (Sandal and Yilmaz, 2011). In humans, the major target organ system if 2,4-D toxicity is the central nervous system and the cardiovascular system (Sandal and Yilmaz, 2011). The uncertainty associated with 2,4-D toxicity in humans lies in the understanding of the MoA causing carcinogenicity, mutagenicity, or genotoxicity. Have you come across any studies that have investigated the MoA of these effects in humans?

    References:

    Sandal, S., & Yilmaz, B. (2011). Genotoxic effects of chlorpyrifos, cypermethrin, endosulfan and 2, 4‐D on human peripheral lymphocytes cultured from smokers and nonsmokers. Environmental toxicology, 26(5), 433-442. http://onlinelibrary.wiley.com.cyber.usask.ca/doi/10.1002/tox.20569/pdf

  4. Thanks for the article. I will look into a few of the other studies mentioned in the paper as well regarding 2,4-D and cell aberrations.

    It is odd that 2,4-D has been licensed since the 1940s and there still isn’t enough conclusive evidence to confidently call it a carcinogen. I think that studies have pointed to MoA in animals that hint at potential MoA in humans but I am not sure that is convincing enough. From my reading, it appears as though studies involving human subjects are usually very small in size thereby limiting the robustness of the results.

    Sandal and Yilmaz (2011) do state that in the past there has been mixed results with respect to 2,4-D and development of tumors which is consistent with other points of view. Furthermore, they point out the lack of literature available for discussion which seems to be a repeating theme.

  5. Interesting topic! In 2012 the US EPA released new data that might be of use for you to address more information about risk related to 2,4-D (EPA 2012). Also this is an interesting paper discussing the 2,4-D exposure and risk assessment for both acute and chronic scenarios (Hays et al. 2012).

    When I first started reading your topic I thought that cancer should be the main focus of 2,4-D studies. However, you addressed that there is a lack of evidence linking the studied compound and cancer in humans. For PAHs, cancer risk is still the main focus of research, however, it has been much discussed that cardiotoxicity resulting from exposure to PAHs might be of greater concern. However, one of the mechanisms responsible for cardiovascular disease is a similar pathway as that of cancer development: mutation. Thus, I wonder if the mechanism of other human health endpoints addressed by you, specifically, genotoxicity, are associated with the cancer pathway (e.g. mutation), or they have independent pathways.

    References
    Hays SM, Aylward LL, Driver J, Ross J, Kirman C (2012) 2,4-D Exposure and risk assessment: Comparison of external dose and biomonitoring based approaches. Regulatory Toxicology and Pharmacology, 64:481-489.
    EPA (US Environmental Protection Agency) (2012) Petitions to Revoke Tolerances; Denials: Natural Resources Defense Council, 2,4-dichlorophenoxyacetic acid (2,4-D).
    See also http://www.epa.gov/oppfead1/cb/csb_page/updates/2012/2-4d-petition.html

  6. Author –
    Yes, I had seen the EPAs denial to the Natural Resources Defense Council’s petition to cancel all product registrations and eliminate tolerances as they relate to food for 2,4-D. I think it was prudent of the USEPA to re-assess the scientific literature; however, I was unable to identify the exact studies that confirmed their previous conclusion that 2,4-D does not cause endocrine disruption, neurotoxic and immunotoxic effects. That being said, I did find an interesting study by Coady et al. (2013) that conducted in vitro analysis on frogs and fish to determine any reproductive or histopathological effects of 2,4-D. Results indicated that there is no specific MoA specific to the endocrine system as a result of 2,4-D exposure, and the decreased fecundity seen at the highest 2,4-D exposure concentrations in the fish assay is likely due to other stressors rather than chemical exposure (Coady et al. 2013). In summary, the USEPA still stand by their initial conclusion that the use of 2,4-D under normal use circumstances and safety guidelines is of little risk to public health under normal use conditions. For your information, I have put in a request to the EPA to provide me with a list of the particular studies that supported their decision. Let’s hope I hear from them before class ends!

    Thank you for the Hays et al. paper. I had read it and will be including some of their conclusions in future posts. Much appreciated.

    Coady, K., T. Marino, J. Thomas, L. Sosinski, B. Neal and L. Hammond. 2013.An evaluation of 2,4-dichlorophenozyacetic acid in the amphibian metamorphosis assay and the fish short-term reproduction assay. Ecotoxicology and Environmental Safety. 90:143-150

  7. Author –
    Wanted to let you know that USEPA got back to me! Here was their response with links to the studies that supported the decision to deny the petition request.

    I received your voice message the other day requesting copies of the studies EPA evaluated in considering the petition from NRDC to revoke the tolerances for 2,4-D. EPA completed a response to that petition in June 2012 and cited a number of studies in our response. The one I believe you may be interested in is the extended one-generation reproduction study. I have provided a link to the reviews of that study below.
    If you need to review the study in the original format, please contact the EPA FOIA office since there are specific procedures that must be followed before the original study can be released.
    If you have any additional questions, please let me know.

    Copy of full petition response:
    http://www.regulations.gov/#!documentDetail;D=EPA-HQ-OPP-2008-0877-0446
    Excerpt from the petition response above:

    “….As to endocrine effects, the extended one-generation reproduction study examined: Potential effects on parental male and female reproductive function, offspring survival and growth including endocrine and systemic toxicity parameters such as estrous cyclicity (female adult rats and offspring); sperm parameters; anogenital distance; nipple retention; puberty onset (vaginal opening and balano-preputial separation); adrenal weight, thyroid/parathyroid gland weight, pituitary gland weight, testes and ovarian weight, thyroid hormone effects; and histopathology of a wide range of tissues including the thyroid, adrenal, pituitary, testes, and ovary. (Refs. 31 and 32). The endpoints examined in the extended one-generation reproduction study meet or exceed the specifications in the latest guideline (1998) for the two-generation reproduction study. (Ref. 33). Specifically, this extended one-generation study included evaluation of sperm parameters and thyroid assays across various age groups, which are not part of the two-generation study. The main design difference between an extended one-generation study and a two-generation study is that the latter study is run for a full two generations no matter what results are seen in the first generation. On the other hand, an extended one-generation study is not continued into the second generation if triggers on the key endpoints do not indicate there is a potential concern. This design eliminates the needless destruction of animals, but does not reduce the scientific value of the data…..”

    Links to the reviews of the extended one-generation reproduction study:
    31. Risk Assessment Branch VII, Health Effects Division (7509P), EPA, 2,4-D: Review of Extended 1-Generation Reproduction Study and Dose-Range-Finding and Pharmacokinetic Titration Studies. D376556. MRID 47972101, 47417901, 47417902. (November 30, 2010). http://www.regulations.gov/#!documentDetail;D=EPA-HQ-OPP-2008-0877-0463
    32. Office of Chemical Safety and Pollution Prevention, EPA, Memorandum from Linda Taylor to Katie Weyrauch, “2,4-D: Revised Executive Summary of the Data Evaluation record of the Extended 1-Generation Reproduction Study” (June 1, 2011).
    http://www.regulations.gov/#!documentDetail;D=EPA-HQ-OPP-2008-0877-0464

  8. Author –
    Hazard Assessment
    According to Health Canada (1993) 2,4-D is classified as a threshold substance; however, despite the conclusion that it is non-genotoxic, it remains categorized in Group III due to the possibility that it is carcinogenic to humans. Organizations such as the USEPA and the WHO have also concluded that there is a lack of carcinogenic effects resulting from exposure to 2,4-D (FAO/WHO 1997 cited in WHO 2003). Health Canada (2010) considers an oral Acceptable Daily Intake (ADI) of 0.1 mg/kg-bw/day based on a NOAEL of 100mg//kg-bw/day (Kobayashi et al. 1972 cited in HC 2010). Health Canada indicates that uncertainty factors are applied for interspecies and intraspecies variation; however, an uncertainty factor related to incomplete information or lack of information was not found but is assumed.
    The US EPA summarizes that 2,4-D has a low acute toxicity through oral, dermal or inhalation pathways of exposure; however, when doses are chronically delivered above renal clearance capacity there have been health effects have been seen in animals ( 2005). Timchalk (2004) suggests that evidence of health effects in animals does not provide a reliable indication of human health endpoints. The persistence of 2,4-D is limited both in the environment and human body (WHO 1989, Sandmann et al. 1988, Ou 1984 cited in HC 1993; Sauerhoff et al. 1977). Therefore, chronic exposure is only likely when repeatedly exposed. For example, seasonally during chemical application on farms or daily exposure through occupations involving products containing 2,4-D.
    There are a plethora of studies attempting to link 2,4-D exposure to many human health endpoints in various categories including: cancer, reproductive toxicity, genotoxicity, neurotoxicity, and general toxicity (i.e. respiratory and heart disease). These studies are well summarized in Burns and Swaen (2012) but were largely found to be statistically insignificant or insufficient. Interestingly, organizations such as Health Canada (2010) and the US EPA (2005) have also reviewed the literature and find minimal health affects likely to be experienced by humans. For example, Health Canada (2010) identifies only hepatic cellular hyperplasia as a critical health effect associated with oral exposure to 2,4-D. In summary, historical epidemiological studies have been insufficient to support the proposed health effects of exposure to 2,4-D; however, health agencies worldwide continue to periodically re-consider the current research should it better inform toxicological reference values and protect human health.

    Burns, C.J. and G.M.H. Swaen. 2012. Review of 2,4-dichlorophenozyacetic acid (2,4-D) biomonitoring and epidemiology. Critical Reviews in Toxicology. 42(9):768-786
    Health Canada. 2010. Federal Contaminated Site Risk Assessment in Canada, Part II: Health Canada Toxicological Reference Values (TRVs) and Chemical-Specific Factors. Version 2.0. Health Canada. Ottawa, Ontario.
    Kobayashi, S., S. Toida, H. Kawamura, H.S. Chang, T. Fukuda and K. Kawaguchi. 1972. Chronic toxicity of 2,4-dichlorophenol in mice: a simple design for the toxicity of residual metabolites of pesticides. J. Med. Soc. 19(3-4):356
    Sauerhoff, M.W., W.H.Braun, G.E. Blau and P.J. Gehring. 1977. The fate of 2,4-dichlorophenoxyacedtic acid following oral administration to man. Toxicology. 8:3
    Timchalk, C. 2004. Comparative inter-species pharmacokinetics of phenoxyacetic acid herbicides and related organic acids: evidence that the dog is not a relevant species for evaluation of human health risk. Toxicology. 200:1-19
    US Environmental Protection Agency. 2005. 2,4-D RED Facts. Website: http://www.epa.gov/oppsrrd1/REDs/factsheets/24d_fs.htm (updated on May 09/2012)
    World Health Organization. 2003. 2,4-D in drinking-water: background document for development of WHO Guidelines for Drinking-water Quality. World Health Organization. Geneva, Switzerland.

  9. Author –
    Exposure Assessment: Routes, Pathways and Concentrations

    As mentioned previously, 2,4-D is commonly used for the elimination of broad-leaved weeds in agricultural, industrial (e.g. forestry) and domestic settings (HC 1993; WHO 2003). 2,4-D is also used for elimination of aquatic weeds and is applied in and around water sources (WHO 2003). Despite this widespread use throughout the environment, the persistence of 2,4-D results in minimal environmental concentrations with exception of direct consumption, chronic/acute workplace exposure, or chemical spills. For example, the concentrations of 2,4-D in the air, water, soil and food are summarized below in Table 1 (not exhaustive but represents those studies from North America that are identified and used by HC and the WHO):

    In 2003, the WHO stated that there was insufficient data available to determine if the greatest exposure to humans was due to food or water consumption. At that time, they suggested a lower ADI than Health Canada of 0.01 mg/kg-bw/day which translates to a drinking water guideline of 30 µg/L (2003). If you compare the drinking water guideline to the table above, even the highest concentration in water does not exceed the guideline according to the WHO.

    In 2005, the US EPA determined that acute exposure to 2,4-D through diet, residential use, and swimming posed little to no risk to human health. In addition, the US EPA suggests that acute concentrations of 432 µg/L or greater for the most sensitive population (females 13-49 years old) is much higher than maximum concentration produced by modeling estimates (2005). Furthermore, individuals working with and manufacturing 2,4-D can reduce their risk to acceptable levels simply by using the chemical according to safety standards and ensuring the use of protective equipment (2005). Overall, environmental and occupational exposure is generally extremely low when 2,4-D is applied correctly and personal protective equipment is used and current exposures are below current guidelines (Aylward et al. 2009).

    Despite government reassurance that exposure risks are minimal, there remains uncertainty regarding exposure to 2,4-D. Since the WHO, US EPA and HC determined that 2,4-D poses a minimal risk to human health, researchers continue to explore ways to accurately determine exposure concentrations to 2,4-D (Hays et al. 2012). While some governments, such as the Australian Pesticides and Veterinary Medicines Authority, continue to review the human health and toxicological implications of the widespread use of 2,4-D (APVMA 2013). Next week’s post will be a continuation of exposure assessment including information regarding the fate of 2,4-D in the human body and methods used to establish or estimate 2,4-D exposure concentrations in humans using biomonitoring.

    References

    Australian Pesticides and Veterinary Medicines Authority. 2013. 2,4-D Review. Website: http://www.apvma.gov.au/products/review/current/2_4_d.php (accessed September 23, 2013)
    Aylward, L.L., M.K. Morgan, T.E. Arbuckle, D.B. Barr, C.J. Burns, B.H. Alexander and S.M. Hays. 2009. Biomonitoring data for 2,4-dichlorophenoxyacetic acid in the United States and Canada: interpretation in a public health risk assessment context using biomonitoring equivalents. Environmental Health Perspectives. 118:177-181
    Grover, R., Kerr, L.A., Wallace, K., Yoshida, K. and Maybank, J. Residues of 2,4-D in air samples from Saskatchewan: 1966-1975. J. Environ. Sci. Health, B11(4): 331 (1976).
    Hays, S.M., L.L. Aylward, J. Driver, J. Ross and C. Kirman. 2012. 2,4-D exposure and risk assessment: comparison of external dose and biomonitoring based approaches. Regulatory Toxicology and Pharmacology. 64:481-489
    Health Canada. 1993. Fact sheet on the chemical/physical parameters of 2,4-dichlorophenoxyacetic acid. http://www.hc-sc.gc.ca/ewh-semt/pubs/water-eau/index-eng.php#tech_doc
    Hiebsch, S.C. The occurrence of thirty-five pesticides in Canadian drinking water and surface water. Unpublished report prepared for the Environmental Health Directorate, Department of National Health and Welfare (1988).
    McLeod, H.A., Smith, D.C. and Bluman, N. Pesticide residues in the total diet in Canada, V: 1976 to 1978. J. Food Saf., 2: 141 (1980).
    US Environmental Protection Agency. 2005. 2,4-D RED Facts. Website: http://www.epa.gov/oppsrrd1/REDs/factsheets/24d_fs.htm (updated on May 09/2012)
    Waite, D.T., A.J. Cessna, R. Grover, L.A. Kerr and A.D. Snihura. 2002. Environmental concentrations of agricultural herbicides: 2,4-D and triallate. J. Environ. Qual. 31:129-144
    World Health Organization. 2003. 2,4-D in drinking-water: background document for development of WHO Guidelines for Drinking-water Quality. World Health Organization. Geneva, Switzerland.

  10. Great start to your exposure assessment! I have a question regarding the sensitive population you mentioned in your reflection above. I am wondering what characteristics of females between the age of 13-49 make them the most sensitive population for exposure to 2,4-D. Does it have to do with the mode of action of 2,4-D on some specific physiological pathway only present in females? I am guessing that it may be related to estrous cycling as that age group seems to be when puberty starts to when menopause begins. The link you provided states that they are the most sensitive but does not say why1. Maybe you could address this in the second half of your exposure assessment?

    US Environmental Protection Agency. 2005. 2,4-D RED Facts. Website: http://www.epa.gov/oppsrrd1/REDs/factsheets/24d_fs.htm (updated on May 09/2012)

  11. From the table in your post, it looks like water is a potentially important source for 2,4-D given its relatively long half life in this medium. You may be planning on covering this along the way, but do you have a sense of how important this might be in agricultural areas where there might be run off into water supplies? I noticed it is one of the pesticides for which Saskatchewan specified a drinking water standard.

  12. You are right, i did also noticed 2,4-D on the list while i was looking for the values for Fluoride. I gotta say i was a bit curious when i saw it, i wonder if any specific past cases prompted the incorporation of the compound on the list or if it is one of those case where you have to include highly produced/used compounds. In my personal experience, i have been collaborating with my former group from back home on a series of studies evaluating pharmaceutical compounds in river and drinking water, and we did detect a number of compounds. Usually they showed up in low concentrations, but the presence in treated drinking water did tell us something about the effectiveness of these facilities. I join last comment on our curiosity about 2,4-D in drinking water.

  13. Author –

    I am also mostly interested in 2,4-D in drinking water. I will review the information specific to that topic and consider a post dedicated to it.

    I do think that seasonally one can see spikes in herbicides, especially in rivers that flow through areas of intense agriculture. I’ll see what I can find in the literature to back that up.

    I did read that charcoal filters are sufficient to remove 2,4-D but have my doubts that charcoal filtration is used in most municipal treatment plants. I recently took a tour of the Saskatoon treatment plant and don’t recall charcoal filtration. I’ll check into it.

    Yes, 2,4-D has a Canadian Drinking Water Quality Guideline of 0.1 mg/L due to the use of the pesticide on agricultural land in Canada. The Federal-Provincial-Territorial Committee on Drinking Water (which has representatives from each province and territory) have determined that guideline. In a future post, I can look into how that decision was made but for now what I can tell you is that the use of 2,4-D across the prairies means that on a provincial level, most governments are likely to include 2,4-D in their guidelines. Basically, most provinces/territories adopt the Federal guidelines unless they have some reason to change them due to the nature of the water quality in their province (e.g. pH objective in SK for drinking water is more alkaline than the federal aesthetic objective because our water quality is influenced by our geology).

    Thanks for posting!

  14. During the classes we have seen that the risk of exposure can be categorized by age group. I am very interested on this right now, since recently a paper gained my attention. Reviewing the PAH dietary exposure in different age groups, authors found that adult males had highest estimated dietary intake of total PAHs (Falco et al. 2003).
    It was also described that for some other chemicals, infants and children may be highly exposed due to their mouth behavior. I wonder if you read any paper that describes any difference in risk of exposure due to age group.

    Falco et al. Polycyclic Aromatic Hydrocarbons in Foods: Human Exposure through the Diet in Catalonia, Spain. Journal of Food Protection, Vol. 66, No. 12, 2003, Pages 2325–2331

  15. Author –

    Exposure Assessment: Fate of 2,4-D in the Human Body

    Having discussed the concentrations of 2,4-D in the environment and the routes and pathways by which 2,4-D can enter the human body, it is pertinent to follow up with the fate of 2,4-D within the human body and how it is measured. Therefore, this week’s topic will be the Fate of 2,4-D in the Human Body, followed by Measuring Human Exposure to 2,4-D next week.

    As mentioned in previous posts, quantifying human exposure using environmental concentrations of 2,4-D introduces uncertainty because of its lack of persistence in the environment. Furthermore, it is a challenge to determine the exposure from all routes and pathways given how different environmental characteristics can change the persistence of 2,4-D in the environment. However, once 2,4-D has entered the body through oral, dermal or inhalation pathways, its fate appears to be reliably the same within the human body. The following discussion will explore the fate of 2,4-D within the human body; however, animals studies will be frequently referenced because of their availability and quality relative to human studies.

    In oral exposure studies on animals, 2,4-D is readily absorbed and distributed throughout the body in mice, rats and goats (WHO2003, Khanna and Fang 1966, Pelletier et al. 1988 cited in HC 1993, Sauerhoff et al. 1977). The WHO (2003) summarizes a few studies that suggest up to 86-94% is absorbed within the gastrointestinal tract of rats. In addition to the high percentage and rate of 2,4-D absorption into the body of rats, it has not been found to bioaccumulate in the body and is rapidly cleared through excreta (WHO 2003). Similar to studies on animals, 2,4-D is absorbed and excreted quickly by the human body with approximately 75-82% of the dose excreted within 96 hours, followed by the rest in conjugate form (Kohli et al. 1974, Sauerhoff et al. 1977). Kohli et al. (1974) conclude that like rats, accumulation of 2,4-D in the human body is ‘unlikely’. Munro et al. (1992) later confirmed that 2,4-D may be found throughout the human body but it does not appear to accumulate in any tissue.

    Munro et al. 1992 suggest that dermal exposure is most likely to result from using products containing 2,4-D as opposed to oral exposure. Unlike oral exposure, dermal absorption in humans is slow and variable depending on the point of contact and whether protective clothing is worn (Frank et al.1985, Moody et al. 1990, Moody et al. 1992). Frank et al.1985 summarizes several studies that confirm that inhalation of 2,4-D is excreted from the human body unchanged and at the same rate of dermal absorption and excretion.

    While in the body, animal studies indicate that 2,4-D does not break down into metabolites, and as discussed above, up to 94% of it is passes through the urine within the first 48 hours (Khanna and Fang 1966). In a review of the literature conducted by Garabant and Philbert in 2002, they conclude that 2,4-D was not found to have reactive intermediate metabolic products within the various species exposed (including humans). That said, at extremely high lethal doses Bradberry et al. 2000 explore mechanisms of toxicity for the family of chlorophenoxy herbicides which may not specifically be relevant to 2,4-D. The approach of looking at the toxicity of a group of chemicals is something that will be discussed in a future post.

    At different doses, the extent to which 2,4-D is found through the body does change. For instance, 2,4-D can be found in the kidneys, liver, blood and lungs of animals exposed to low doses of 2,4-D; however, at higher doses it can also be detected in the brain (Khanna and Fang 1966). This movement of 2,4-D through the body at different dosages appears to also apply to humans (NRCC 1978 cited in HC 1993). At sub-chronic exposures in animals, 2,4-D can also be found in the eye, thyroid, adrenal glands and reproductive organs (EPA 2005). In rats, doses above 50 mg/kg bw/day represent clearance saturation of the kidneys which results in movement of 2,4-D to more places in the body before it can be removed (Khanna and Fang 1966). That said, it does not bioaccumulate in humans and is eventually excreted through the urine as described above (Munro et al. 1992).

    In summary, 2,4-D enters the body through oral, dermal or inhalation pathways depending on environmental circumstances. Once in the body, the dose determines the extent to which it is found throughout the tissues while the rate of excretion is limited by the capacity of the kidneys. 2,4-D does not appear to breakdown into metabolites within human or animals and therefore, almost all of it eventually leaves the body through urination. Next week’s discussion will explore how 2,4-D exposure is measure and quantified.

    Bradberry, S.M., B.E. Watt, A.T. Proudfoot and J.A. Vale. 2000. Mechanisms of toxicity, clinical features, and management of acute chlorophenoxy herbicide poisoning: a review. Clinical Toxicology. 38(2):111-122

    Frank, R., R.A. Campbell and G.J. Sirons. 1985. Forestry workers involved in aerial application of 2,4-dichlorophenoxyacetic acid: exposure and urinary excretion. Arch. Environ. Contam. Toxicol. 14:427

    Garabant, D.H. and M.A. Philbert. 2002. Review of 2,4-dichlorophenoxyacetic acid epidemiology and toxicology. Crit. Rev. Toxicol. 32(4):233-257

    Health Canada. 1993. Fact sheet on the chemical/physical parameters of 2,4-dichlorophenoxyacetic acid. Health Canada.

    Khanna, S. and S.C. Fang. 1966. Metabolism of C-14 labeled 2,4-dichlorophenoxyacetic acid in rats. J. Agric. Food Chem. 14:500-503

    Kohli, J.D., R.N. Khanna, B.N. Gupta, M.M. MDhar, J.S. Tandon and K.P. Sircar. 1974. Absorption and excretion of 2,4-dichlorophenoxyacetic acid in man. Xenobiotica. 4(2):97-100

    Moody, R.P., C.A. Franklin, L. Ritter, and H.I. Maibach. 1990. Dermal absorption of the phenoxy herbicides 2,4-D, 2,4-D amine,2,4-D isooctyl, and 2,4,5-T in rabbits, rats, rhesus monkeys, and humans: a cross-species comparison. J. Toxicol. Enviorn. Health. 29:237

    Moody, R.P., R.C. Wester, J.L. Melendres and H.I. Maibach. 1992. Dermal absorption of the phenoxy herbicide 2,4-D dimethylamine in humans: effect of DEET and anatomic site. J. Toxicol. Environ. Health. 36:241

    Munro, I.C., G.L. Carlo, J.C. Orr, K.G. Sund, R.M. Wilson, E. Kennepohl, B.S. Lynch, M. Jablinske and N.L. Lee. 1992. A comprehensive, integrated review and evaluation of the scientific evidence relating to the safety of the herbicide 2,4-D. J. Am. Coll. Toxicol. 11(5):559-664

    National Research Council of Canada. 1978. Phenoxy herbicides – their effects on environmental quality, with accompanying scientific criteria for 2,3,8-tetrachlorodibenxo-p-dioxin(TCDD). Associate Committee on Scientific Criteria for Environmental Quality, Ottawa.

    Pelletier, O., L. Ritter, J. Caron and D. Somers. 1988. Pharmacokinetics of 2,4-dichlorophenoxyacetic acid dimethylamine salt in rats: dermal versus oral exposure. Agro(Am. Chem. Soc.) 79

    Sauerhoff, M.W., W.H. Braun, G.E. Blau and P.J. Ghering. 1977. The fate of 2,4-dichlorophenoxyacetic acid following oral administration to man. Toxicology. 8:3

    US Environmental Protection Agency. 2005. 2,4-D RED Facts. Website: http://www.epa.gov/oppsrrd1/REDs/factsheets/24d_fs.htm (updated on May 09/2012)

    World Health Organization. 2003. 2,4-D in drinking-water: background document for development of WHO Guidelines for Drinking-water Quality. World Health Organization. Geneva, Switzerland

  16. The knowledge of 2,4-D fate in the body would certainly be useful in assessing the risk of exposure to humans. With most of the compound excreted through the urine, is there much of a concern for absorption or are there any known sites of toxicant absorption in the human body? In class we discussed the uses of incorporating an adsorption factor in our estimates of daily exposure and I wonder if this would or has been applied to 2,4-D exposure.

    Based on what you have mentioned with excretion above as well as the elimination rates noted in case studies (Kohli et al., 1974; Sauerhoff et al., 1977) where individual males volunteered to ingest oral doses of 2,4-D (recognizing variability in different exposure routes), I am wondering what cause for concern there is for human exposure? Do these small and quick adsorption events, followed by excretion, lead to long-term chronic effects that result in potential carcinogenic endpoints? Sorry if I am jumping the gun, I realize effects will likely come after your discussion on exposure. This is just an interesting topic having mostly thought of 2,4-D as a plant targeting contaminant used in an agricultural setting. I am interested to see how different (daily) exposures will affect the variety and extent of endpoints mentioned above and methods of measuring human exposure.

    Kohli, J. D., Khanna, R. N., Gupta, B. N., Dhar, M. M., Tandon, J. S., & Sircar, K. P. (1974). Absorption and excretion of 2, 4-dichlorophenoxyacetic acid in man. Xenobiotica, 4(2), 97-100. http://informahealthcare.com.cyber.usask.ca/doi/abs/10.3109/00498257409049349

    Sauerhoff, M. W., Braun, W. H., Blau, G. E., & Gehring, P. J. (1977). The fate of 2, 4-dichlorophenoxyacetic acid (2, 4-D) following oral administration to man. Toxicology, 8(1), 3-11. http://www.sciencedirect.com.cyber.usask.ca/science/article/pii/0300483X7790018X

  17. Author –
    Exposure Assessment: Measuring Human Exposure to 2,4-D

    As determined in Week #4, in humans, a large proportion of 2,4-D is excreted in urine regardless of the route and pathway into the body (Frank et al.1985, Kohli et al. 1974, Munro et al. 1992, Sauerhoff et al. 1977). The ubiquitous nature of low concentrations of 2,4-D in the environment make it difficult to accurately calculate exposure, thereby introducing uncertainty. Using a biomarker such as urine to measure the cumulative exposure of humans to 2,4-D would seem to be an ideal approach that provides a proxy for the total concentration of 2,4-D to which someone was exposured. The purpose of this post is to discuss the use of biomonitoring to measure the cumulative exposure of 2,4-D in humans.

    The US EPA (2005) describes aggregate risk as the “combined risk from dietary exposure (food and drinking water pathways), as well as exposure from non-occupational sources (e.g. residential uses)”. Therefore, in order to accurately determine the aggregate risk you need to consider the total exposure to 2,4-D which can be accomplished by examining the sum of the background concentrations as suggested by Sexton et al. (2004). As described by Hays et al. (2012), integrated exposure ‘from all routes and pathways’ can accomplish this by using biomonitoring. Furthermore, concentrations of 2,4-D determined through biomonitoring can be found to correspond to the external exposure concentrations (Hays and Aylward 2009).

    In the case of 2,4-D, the use of urine as a biomarker provides total the exposure dose while reducing the uncertainty associated with estimated exposure and absorption in traditional external exposure calculations (Sexton et al. 2004). Sexton et al. (2004) provides a graphic showing the components of a traditional exposure assessment which depicts the many components required to accurately determine exposure (Figure 1). Each of these components have the potential to add to the uncertainty depending on the error associated with the measurements and assumptions made.

    Figure 1. Multiple variables contributing to the overall exposure as depicted in Sexton et al. (2004).

    Although the relationship between external exposure concentrations of 2,4-D and urine concentration is non-linear (Munro et al. 1992), the use of biomonitoring methods has proven to be a valuable way to determine exposure to 2,4-D in humans (Hays et al. 2012). In fact, Hays et al. (2012) summarize that traditional estimates of exposure overestimate the risk by 4 to 40 times that determined by biomonitoring methods of exposure assessment. Hays et al. (2012) further conclude that the determination of overall low aggregate risk exposure to humans, based on traditional exposure assessments, is providing a very conservative estimation of the human health risk associated with 2,4-D when compared to the risk from a biomonitoring approach.

    In summary, the use of biomonitoring methods to determine cumulative exposure to 2,4-D is more accurate for the overall determination of risk to human health. Using urine as a biomarker, we can measure the concentration of 2,4-D from all exposure pathways and routes while eliminating much of the uncertainty associated with attempting to determine environmental concentrations, duration of exposure, and absorption into the human body. Lastly, research by Hays et al. (2012) confirms that the use of traditional exposure assessment methods provide a very conservative estimation of overall risk as confirmed by risk assessments based on biomonitoring.

    The second post this week will summarize the uncertainty associated with the use of 2,4-D as it relates to human health and provide a conclusion as to the overall risk posed by 2,4-D in society.

    Frank, R., R.A. Campbell and G.J. Sirons. 1985. Forestry workers involved in aerial application of 2,4-dichlorophenoxyacetic acid: exposure and urinary excretion. Arch. Environ. Contam. Toxicol. 14:427

    Hays, S.M. and L.L. Aylward. 2009. Using biomonitoring equivalents to interpret human biomonitoring data in a public health risk context. J. Appl.Toxicol. 29(4):275-288

    Hays, S.M., L.L. Aylward, J. Driver, J. Ross and C. Kirman. 2012. 2,4-D exposure and risk assessment: comparison of external dose and biomonitoring based approaches. Regulatory Toxicology and Pharmacology. 64:481-489

    Kohli, J.D., R.N. Khanna, B.N. Gupta, M.M. MDhar, J.S. Tandon and K.P. Sircar. 1974. Absorption and excretion of 2,4-dichlorophenoxyacetic acid in man. Xenobiotica. 4(2):97-100

    Munro, I.C., G.L. Carlo, J.C. Orr, K.G. Sund, R.M. Wilson, E. Kennepohl, B.S. Lynch, M. Jablinske and N.L. Lee. 1992. A comprehensive, integrated review and evaluation of the scientific evidence relating to the safety of the herbicide 2,4-D. J. Am. Coll. Toxicol. 11(5):559-664

    Sauerhoff, M.W., W.H. Braun, G.E. Blau and P.J. Ghering. 1977. The fate of 2,4-dichlorophenoxyacetic acid following oral administration to man. Toxicology. 8:3

    Sexton, K., L.L. Needham and J.L. Pirkle. 2004. Human biomonitoring of environmental chemicals. Am.Sci.92:38-45

    US Environmental Protection Agency. 2005. 2,4-D RED Facts. Website: http://www.epa.gov/oppsrrd1/REDs/factsheets/24d_fs.htm (updated on May 09/2012)

  18. Author –

    Summary of Uncertainty and Conclusion of Risk

    The domestic and agricultural use of 2,4-D throughout North America since the 1940s has resulted in the widespread exposure of humans to this well-known commercial herbicide. As discussed previously, 2,4-D is a herbicide that eliminates broadleaf plants from our agricultural fields, recreational areas, and water ways. Given its wide-spread use there is much uncertainty associated with 2,4-D because of its potential to effect human health; however, conclusive evidence has yet to be determined. As a result, governments and the public want to determine the human health risks associated with direct exposure during application and accidental exposure, or indirect exposure through air, water and food over both short and long term exposure.

    The purpose of this post is to summarize the uncertainty, acknowledge current risk management, and conclude the overall risk associated with the use of 2,4-D. Please note that public perception is included in uncertainty despite the lack of extensive previous discussion because but remains an important aspect of uncertainty in my opinion.

    Hazard Uncertainty

    Although individual studies may suggest associations between 2,4-D exposure and human health end points, large reviews of the literature by government and researchers have determined that the evidence is insufficient to draw conclusions (Burns and Swaen 2012, HC 2008). However, to account for the unknown, and intra and inter-species variations, governments include uncertainty factors in their determination of Acceptable Daily Intake (ADI) to be conservative and provide a large margin of safety for the public. Furthermore, the classification of 2,4-D by government agencies reflects the uncertainty around its toxicity to humans. For example, Health Canada categorized 2,4-D as possibly carcinogenic to humans because of the lack of conclusive epidemiological evidence.

    Exposure Uncertainty

    The wide-spread use of 2,4-D throughout the environment makes it difficult to attain empirical measurements on the concentrations found throughout the air, water and food. Once 2,4-D is released into the environment its persistence changes based on several environmental factors which makes it difficult to determine the exact concentration humans are exposed to over time based on the concentration released. Furthermore, the uncertainty is increased as we attempt to estimate the proportion of 2,4-D that is absorbed into the human body.

    Research indicates that 2,4-D enters the human body through an inhalation, dermal or ingestion pathway and is then readily absorbed (WHO2003, Khanna and Fang 1966, Pelletier et al. 1988 cited in HC 1993, Sauerhoff et al. 1977). In addition, several studies show that 2,4-D does not bioaccumulate and almost completely leaves the human body within 96 hours limited only by kidney clearance capacity (Kohli et al. 1974, Sauerhoff et al. 1977, Khanna and Fang 1966). That said, the uncertainty around the specific toxicological effects of 2,4-D on the human body (given that most studies are on animals) causes some to question whether it is toxic to humans at low concentratons on chronic or sub chronic exposure levels. To address the uncertainty associated with external exposure assessment there is a movement towards using biomonitoring for a more integrated approach (Sexton et al. 2004, Hays and Aylward 2009, Hays et al. 2012).

    Public Perceptions and Uncertainty

    Lack of conclusive evidence that 2,4-D is not carcinogenic and its past association with chemicals such as Agent Orange are likely influencing public perceptions and increasing the perceived uncertainty around the use of 2,4-D (ACS 2013). As a result, researchers continue to study the potential effects of 2,4-D on human health, and governments continue to review 2,4-D as new research develops. In this case, as with many chemicals, the uncertainty is leading to the collection of more information and continued critical review of the research. However, a proportion of the public and special interest groups remain cautious with regard to the use of 2,4-D and actively push for the elimination or restriction of its use (Sierra Club 2005, Globe and Mail 2012). As a form of risk management, some government agencies taken measures to protect the public by banning certain forms of 2,4-D and restricting the use of 2,4-D under certain conditions (APVMA 2013, HC 2008, EPA 2005).

    Risk Management

    Not covered in the previous posts, I think a few comments on risk management provide a necessary compliment to the identification of uncertainty above. Risk management of 2,4-D are the activities or actions that take place to minimize or eliminate the potential human health risks associated with its use. Therefore, throughout the reading, I have identified several risk management strategies (in bold and italics) that are intended to reduce the risk.

    In an effort to decrease exposure to certain forms of 2,4-D and/or acute concentrations of the chemical, governments including Health Canada and Australia provide guidelines for pesticide use and/or restrict its use under certain conditions (HC 2008, APVMA 2013). Health authorities continue to review the scientific literature and provide the public with educational materials that to inform them of the potential health risks associated with 2,4-D (WHO2003, APVMA 2013, EPA 2005, HC 1993). Ongoing research continues to support decision making by providing governments with updated information on 2,4-D and its potential human health risks. For example, recent studies suggest that 2,4-D may have immunologic effects in humans (Pahwa et al. 2012), and that it should be studied in combination with other pesticides to more accurately reflect typical human exposure to pesticides (Kachuri et al. 2013). Lastly, efforts to improve risk communication as it relates to the use and potential human health risks associated with 2,4-D are likely ongoing to keep the public informed and safe.

    Risk

    Aside from acute exposures (i.e. workplace accidents and accidental poisonings), the concentrations of 2,4-D in the environment typically do not exceed Acceptable Daily Intake concentrations set by health agencies. Both government agencies and scientific reviews of the literature have confirmed that the risk associated with the use of 2,4-D under normal circumstances in minimal to nil (EPA 2005, HC 2010). Therefore, until research can provide more conclusive evidence that 2,4-D is associated with human health endpoints over short and long term exposure, it is likely that risk management strategies rather than a ban on 2,4-D will ensue. At the more local level of provincial and municipal governments, special interest groups and communities can respond to the uncertainty associated with 2,4-D by banning its use to eliminate risk. Overall, I would conclude that the human health risks associated with background and normal use of 2,4-D is negligible but that 2,4-D requires regular review and re-evaluation, effective risk communication strategies, and the presence of risk management strategies to ensure human health is protected.

    References

    American Cancer Society. 2013. Agent Orange and cancer. Website http://www.cancer.org/cancer/cancercauses/othercarcinogens/intheworkplace/agent-orange-and-cancer

    Australian Pesticides and Veterinary Medicines Authority. 2013. 2,4-D Review. Website: http://www.apvma.gov.au/products/review/current/2_4_d.php (accessed September 23, 2013)

    Burns, C.J. and G.M.H. Swaen. 2012. Review of 2,4-dichlorophenozyacetic acid (2,4-D) biomonitoring and epidemiology. Critical Reviews in Toxicology. 42(9):768-786

    Globe and Mail. 2012. Controversial pesticide 2,4-D deemed not ‘dangerous’, but still banned in Quebec. Written by Barrie McKenna http://www.theglobeandmail.com/news/national/controversial-pesticide-24-d-deemed-not-dangerous-but-still-banned-in-quebec/article581095/ (accessed October 8, 2013)

    Hays, S.M. and L.L. Aylward. 2009. Using biomonitoring equivalents to interpret human biomonitoring data in a public health risk context. J. Appl.Toxicol. 29(4):275-288

    Hays, S.M., L.L. Aylward, J. Driver, J. Ross and C. Kirman. 2012. 2,4-D exposure and risk assessment: comparison of external dose and biomonitoring based approaches. Regulatory Toxicology and Pharmacology. 64:481-489

    Health Canada. 1993. Fact sheet on the chemical/physical parameters of 2,4-dichlorophenoxyacetic acid. Health Canada.

    Health Canada. 2008. Information note: Health Canada releases final re-evaluation decision on 2,4-D. Health Canada.

    Health Canada. 2010. Federal Contaminated Site Risk Assessment in Canada, Part II: Health Canada Toxicological Reference Values (TRVs) and Chemical-Specific Factors. Version 2.0. Health Canada. Ottawa, Ontario.

    Kachuri, L., P.A. Demers, A. Blair, J.J. Spinelli, M. Pahwa, J.R. McLaughlin, P. Pahwa, J.A. Dosman and S.A. Harris. 2013. Multiple pesticide exposures and the risk of multiple myeloma in Canadian men. International Journal of Cancer. 133(8):1846-1958

    Khanna, S. and S.C. Fang. 1966. Metabolism of C-14 labeled 2,4-dichlorophenoxyacetic acid in rats. J. Agric. Food Chem. 14:500-503

    Kohli, J.D., R.N. Khanna, B.N. Gupta, M.M. MDhar, J.S. Tandon and K.P. Sircar. 1974. Absorption and excretion of 2,4-dichlorophenoxyacetic acid in man. Xenobiotica. 4(2):97-100

    Pahwa, M., S. A. Harris, K. Hohenadel, J.R. McLaughlin, J.J. Spinelli, P. Pahwa, J.A. Dosman and A. Blair. 2012. Pesticide use, immunologic conditions, and risk of non-Hodgkin lymphoma in Canadian men in six provinces. International Journal of Cancer. 131(11):2650-2659

    Sauerhoff, M.W., W.H. Braun, G.E. Blau and P.J. Ghering. 1977. The fate of 2,4-dichlorophenoxyacetic acid following oral administration to man. Toxicology. 8:3

    Sexton, K., L.L. Needham and J.L. Pirkle. 2004. Human biomonitoring of environmental chemicals. Am.Sci.92:38-45

    Sierra Club. 2005. Overview of the toxic effects of 2,4-D. Sierra Club of Canada

    United States Environmental Protection Agency. 2005. Reregistration eligibility decision for 2,4-D. Prevention, Pesticides and Toxic Substances. EPA 738-R-05-002.

    World Health Organization. 2003. 2,4-D in drinking-water: background document for development of WHO Guidelines for Drinking-water Quality. World Health Organization. Geneva, Switzerland.

  19. I enjoyed your thread and your conclusions were interesting, especially in the context of the Ontario ban on 2,4-D and other compounds for residential use. This is not an issue in Ontario any longer but I often wonder about effects of exposure to a variety of different pesticides and the possibility of cumulative effects? Individually, the chemicals do not pose a risk but could they pose a risk in combination? This is one area of toxicology and risk assessment for that matter is underdeveloped. We are not exposed to one chemical at a time but a variety of chemicals, not only pesticides.

  20. Author –

    Yup, you are correct. People are starting to wonder if they should be addressed in combination with other chemicals. The study I mentioned in my last post by Kachuri et al. 2013 is suggesting exactly that!

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