Dioxin

EPA Must Finish the Job of Protecting People from Dioxin

Tuesday, July 13, 2010

Dioxin

EPA Must Finish the Job of Protecting People from Dioxin

After nearly 30 years of delays caused by pressure from chemicals and defense industries, the US Environmental Protection Agency (EPA) is moving forward on setting a safety limit for exposure to dioxin, a ubiquitous, highly toxic and carcinogenic chemical that people of all ages ingest daily with their food – starting at a mother’s breast.

The Environmental Working Group applauds the EPA for taking significant steps to set a long-overdue exposure limit for dioxin, a byproduct of combustion and various industrial processes that is found everywhere in the environment and in people’s bodies. EWG researchers say, however, that the allowable exposure levels may well need to be tightened in the future because of growing evidence that dioxin is even more dangerous than scientists had thought.

Nine animal studies conducted between 1973 and 2008 show that dioxin is harmful at levels even lower than in the human studies on which EPA based its proposal. Those human studies, conducted in 2008, explored the toxic legacy of a 1976 chemical plant explosion in Seveso, Italy, which exposed thousands of people to dioxin in unprecedented intensity and left large quantities of the chemical in the soil.

There is an urgent need for EPA to finalize its assessment and the safety standard that is part of it. EWG research found that the amount of dioxin a nursing infant ingests daily is up to 77 times higher than the level the agency has defined as harmless to the endocrine and immune systems. For cancer risk, the situation is even more dire: the general public is exposed to up to 1,200 times more dioxin than regulatory agencies typically consider safe. Only when EPA finally issues these long-delayed safety standards can public health agencies finish the job of reducing industrial emissions and cleaning up the food supply and the environment in order to protect the health of Americans.

EWG has submitted its analyses and recommendations to EPA’s Science Advisory Board, which scheduled two public meetings in Washington in July and October 2010 to discuss EPA’s long-awaited “Reanalysis of Key Issues Related to Dioxin Toxicity.”

Chlorinated dioxins form as an unintended byproduct of waste incineration and a variety of industrial processes, including smelting, chlorine paper bleaching and pesticide manufacturing. Burning household waste and even forest fires can also produce dioxins. Sometimes described as the most toxic contaminant ever found, dioxin has been linked to multiple outbreaks of disease and cancer triggered by high-level exposures at least as far back as 1949.

More recently, scientists have recognized that continuous, low-dose exposure to dioxin-like compounds, which include the notorious PCB’s, is also a health threat. EPA’s “reanalysis” noted that these low-level exposures are all but unavoidable because dioxins are widespread in the environment, break down very slowly, build up in the food chain and accumulate in the tissues of animals, especially in fat. As a consequence, exposures begin in the womb when dioxins cross the placenta, and newborn infants begin to ingest them from the very first days of life.

The EPA, which began its efforts to set safety limits for dioxin exposure almost 30 years ago, is focusing on a particular form called tetrachlorodibenzo-p-dioxin, or TCDD, the most toxic and best studied of this family of chemicals. EWG’s analysis noted that TCDD “has been associated with a panoply of adverse health effect in people,” including heart disease, diabetes, cancer, endometriosis, early menopause, reduced testosterone and thyroid hormones, immune system disorders and abnormalities of the skin, teeth and nails.

EWG supports EPA’s risk assessment approach to the available science, which was informed by a 2006 evaluation the agency sought from the National Academy of Sciences. However, EWG’s analysis finds that a 130-pound adult who eats a cheeseburger and drinks a glass of milk can consume a third of EPA’s proposed safe daily dose of dioxin and dioxin-like compounds…”

In comments to EPA, EWG writes that the primary source of dioxin contamination in people is food, starting with breast milk and formula for infants and continuing to dioxin exposure from meat, dairy products, fish and shellfish…” Because children consume more food than adults in relation to their body weight, EWG's Dr. Olga Naidenko has found (see EWG analysis):

Infants and children 1-to-10 years of age are the groups with the highest relative dietary exposure.

Breast-fed infants in particular receive a high dose of dioxin during the first months of their life, when breast milk is their only, or primary, food source… developmental and/or early-life dioxin exposure has been linked to neurological alterations, including effects on hearing, psychomotor function, cognition and gender-specific behaviors; effects on the reproductive organs; and hormonal changes.

Despite these concerns, breast milk is still considered by pediatricians to be the best food for infants by far. The presence of dioxin in breast milk (and formula as well) makes it even more important that EPA complete its assessment and begin to take measures to help reduce exposures across the population.

EWG is urging the Science Advisory Board and the EPA to move ahead rapidly “to establish a safety level for dioxin that will truly protect the health of Americans, particularly the youngest and most vulnerable.”

 

Dioxin Timeline

EPA'S Dioxin Assessment: No Safety Standard After Nearly Three Decades of Work

Dioxin and related dioxin-like contaminants form as byproducts of processes that involve chlorine and chlorine-containing substances, including pesticide manufacturing and municipal waste incineration.

Scientists first learned of dioxin's toxicity since the late 19th century, when German chemical industry workers exposed to it developed painful, oozing skin lesions known as chloracne. In the 1980s the U.S. Environmental Protection Agency (EPA) began a protracted process in order to issue a comprehensive human health risk assessment for dioxin. To date this process has included four Science Advisory Board (SAB) reviews (1984, 1988, 1995, and 2001) and a National Academy of Sciences review (2006). Plagued by delays forced by pressure from the chemical and defense industries, EPA has not yet completed that assessment.

EPA first declared 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD, often referred to as dioxin) to be a probable human carcinogen in 1985. In 1997 the International Agency for Research on Cancer classified dioxin as "carcinogenic to humans," and in 2001 the National Toxicology Program, a government research agency that is part of the National Institutes of Health, also classified dioxin as a known human carcinogen. EPA has proposed updating its own classification to deem dioxin a definite "human carcinogen." Both the defense and chemical industries are objecting, continuing a decades-long pattern of trying to slow EPA's review and weaken its findings.

The shackling of EPA's efforts to protect public health from dioxin has a long history.

  • 1949: The first recorded case of human exposure in the United States occurs when an explosion at a Monsanto plant exposes more than 200 workers to dioxin-contaminated herbicides, causing severe skin lesions.

  • 1962-1970: The American military in Vietnam extensively sprays Agent Orange, a potent defoliant and herbicide contaminated with dioxin. Decades later, exposed veterans have an increased risk of developing diabetes and multiple cancers.

  • 1971: The entire town of Times Beach, Missouri, is exposed to dioxin from contaminated waste oils spread on dirt roads to suppress dust. Residents are later evacuated and the location is declared a Superfund site. In the same year, scientists at the National Institute of Environmental Health Sciences determine that fetal exposure to dioxin causes developmental abnormalities in laboratory animals, including cleft palates and kidney malformations.

  • 1976: Dioxin is released in an accident at a pesticide manufacturing plant in Seveso, Italy, contaminating people, air, soil and water. Decades later, scientists find adverse effects on reproductive function, including infertility and low sperm counts; lowered male/female sex ratio in newborns; changes in hormones; diabetes; cardiovascular effects; and elevated incidence of certain cancers (Baccarelli 2008; Eskenazi 2010; Mocarelli 2008; Pesatori 2003; Pesatori 2009)

  • 1978: Scientists at Dow Chemical publish the first study of dioxin carcinogenicity in laboratory animals (Kociba 1978). In the same year, the New York Times publishes a story on the plight of residents near Love Canal, N.Y., where industrial dumping released dozens of toxic substances, many suspected carcinogens. Dioxin and dioxin-like chemicals are among them.

  • 1982: EPA's National Human Monitoring Program begins testing Americans' tissues for the presence of dioxin and dioxin-like chemicals, polychlorinated dibenzo-p-dioxins and dibenzofurans (EPA 1987).

  • 1983: Responding to mounting public concern over dioxin contamination, Congress directs the EPA to launch the National Dioxin Study to determine the extent of pollution nationwide (Barnes 1986). The EPA survey focuses on plants producing herbicides, incinerators and waste dumps.

  • 1985: EPA publishes its "Health Assessment Document for Polychlorinated Dibenzo-p-dioxins," classifying dioxin as a known animal carcinogen and probable human carcinogen (EPA 1985). The EPA's Science Advisory Board reviews EPA's assessment, the first of five reviews of dioxin's toxicity and carcinogenicity that SAB conducts between 1985 and 2010. SAB agrees with the EPA's overall approach but calls the evidence for carcinogenicity of dioxins in humans "uncertain" (SAB 1985).

  • 1986: A joint publication of the EPA and the Midwest Research Institute based on EPA biomonitoring data concludes that dioxin-like pollutants "are prevalent in the general U.S. population" (Stanley 1986).

  • 1986: Research by Greenpeace and other activist groups uncovers collusion between EPA and the paper bleaching industry to keep secret the detection of dioxin in discharges from paper mills and in finished paper products (Van Strum & Merrell 1987; Weisskopf 1987).

  • 1987: Leaked documents from the American Paper Institute reveal industry's strategy to "Get EPA to 'rethink' dioxin risk assessment" so as to avoid liability and "unnecessary changes" in production processes prompted by "unsound scientific data" (Weisskopf 1987).

  • 1988-1989: The Science Advisory Board reviews for the second time EPA's dioxin assessment, presented in two draft documents: “A Cancer Risk-specific Dose Estimate for 2,3,7,8-TCDD” and “Estimating Exposure to 2,3,7,8-TCDD” (SAB 1989).

  • 1990: The Chlorine Institute, an industry trade group, starts a public campaign claiming that dioxin is "much less toxic to humans thasn originally believed," misrepresenting scientific opinion on its dangers (Roberts 1991).

  • 1991: EPA administrator Bill Reilly tells The New York Times: "We are now seeing new information on dioxin that suggests a lower risk assessment for dioxin should be applied" (Schneider 1991). EPA launches its second reassessment of dioxin.

  • 1992: The International Joint Commission (IJC) for the U.S. and Canada issues its Sixth Biennial Report on Great Lakes Water Quality, highlighting evidence that the developing fetus is likely more sensitive to toxic contaminants than adults are (IJC 1992).

  • 1994: EPA releases a draft Health Assessment Document for 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) and Related Compounds. The draft assessment concludes that these chemicals may be harmful at levels similar to those found in the general public, increasing the risk of cancer and causing potential damage to the immune, nervous and reproductive systems (EPA 1994).

  • 1995: EPA's Science Advisory Board completes its third review of EPA's dioxin assessment and agrees with the agency that “the margin of safety (between background exposures and levels of exposure where effects have been observed in test animals) for dioxin-like compounds is smaller than the EPA usually sees for many other compounds” (SAB 1995).

  • 1997: The International Agency for Research on Cancer declares dioxin a known human carcinogen (IARC 1997).

  • 1999: The United Nations Environment Programme warns that dioxin is a concern for all countries and drafts an international treaty that would ban, phase out or limit production of 12 "persistent organic pollutants" (POPs). POPs are chemicals that resist degradation, bioaccumulate through the food web and have a variety of adverse effects on human health and the environment. The United Nations POP list includes, among other substances, dioxin and other polychlorinated dioxins and furans (UNEP 1999).

  • 2000: EPA publishes its Draft Final Report on “Exposure and Human Health Reassessment of 2,3,7,8-Tetrachlorodibenzo-P-Dioxin (TCDD) and Related Compounds.”

  • 2000: EPA updates its 1994 draft and submits its revised Dioxin Reassessment to the SAB. This is the SAB's fourth review of the dioxin assessment and culminates in publication of an SAB review document in 2001.

  • 2000: The Food Industry Dioxin Working Group, representing beef producers, food processing, farming and retailing, urges the EPA to revise its dioxin assessment to lessen the chance that the assessment will "create a health scare."

  • 2003: The EPA asks the National Academy of Sciences (NAS) to review the agency's draft dioxin reassessment, “Exposure and Human Health Reassessment of 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) and Related Compounds."

  • 2003: The Food Industry Dioxin Working Group again pushes EPA to delay its dioxin assessment, calling for "additional research, data collection and more comprehensive government coordination... before any government action is contemplated."

  • 2005: Japanese scientists publish a study finding that TCDD and related dioxins cross the human placenta and are detectable in cord blood (Suzuki 2005). EWG scientists report finding dioxin-like compounds in cord blood samples from 10 of 10 newborns tested (EWG 2005), further confirming the transfer of a mother's dioxin load to her child in utero.

  • 2006: NAS publishes its report, “Health Risks from Dioxin and Related Compounds: Evaluation of the EPA Reassessment.” NAS issues a press release titled "EPA assessment of dioxin understates uncertainty about health risks and may overstate human cancer risk" (NAS 2006). In its 2010 draft, EPA has carefully considered the NAS recommendations by documenting alternative assessments; evaluating sources of uncertainty; and providing the rationale for its proposed decisions.

  • 2009: EPA releases its Science Plan for Activities Related to Dioxins in the Environment, promising to “accelerate the long-delayed scientific process to complete the assessment of the health risks dioxins pose to the public” and to publish a final report and assessment by the end of 2010 (EPA 2009).

  • 2009: EPA Administrator Lisa Jackson pledges strong federal action to clean up a dioxin-contaminated Dow Chemical site in Michigan and to accelerate the assessment of dioxins’ human health impacts (EPA 2009; EPA 2010; Melzer 2009).

  • May 2010: The agency publishes “EPA’s Reanalysis of Key Issues Related to Dioxin Toxicity and Response to NAS Comments.” The SAB initiates its fifth review of EPA's dioxin assessment.

  • June 2010: The SAB and EPA announce that the SAB review will be extended into Fall 2010.

  • The chemical industry and the Department of Defense submit extensive comments seeking to delay or weaken the proposed EPA standards for dioxin. Some of the submitted comments include:

    • General Electric Company: "In order for this newly-anticipated dioxin risk assessment scheme to quantify the risk of real-world mixtures of dioxins and dioxin-like compounds, the EPA should, at the very least, attempt to reduce some of the inherent uncertainty by dealing with the clear species differences in TEFs [Toxic Equivalency Factor]. Without such adjustments significant misallocation of limited societal resources will occur in order to address unfounded human health concerns regarding, for example, the safety of the US food supply.

    • American Chemistry Council: "EPA's failure to meet its self-imposed deadline for issuing the Draft Report should not circumvent the public's need for an adequate comment period, and the SAB's need for a complete picture of the relevant science before expert deliberations begin... We urge the Chair of the SAB Dioxin Review Panel to reschedule the July face-to-face meeting until at least two weeks after the close of the public comment period."

    • American Chemistry Council: submits extensive comments on "whether or not EPA consistently and appropriately applied a weight of evidence approach to dioxin toxicity and risk."

    • Department of Defense: "We disagree with the characterization for TCDD as “carcinogenic to humans” for all doses; and believe that two classifications should be presented... We suggest that “carcinogenic to humans” be limited to very high exposures and that lower exposures be classified as “likely to be carcinogenic to humans”.

References for the timeline

Baccarelli A, Giacomini SM, Corbetta C, Landi MT, Bonzini M, Consonni D, et al. 2008. Neonatal thyroid function in Seveso 25 years after maternal exposure to dioxin. PLoS Med 5(7): e161.

Barnes D, McBride A, Jaworski N, Harless R, Dupuy A. 1986. A status report on the U.S. national dioxin study. Chemosphere 15(9-12): 1401-04.

EPA. 1985. Health Assessment Document for Polychlorinated Dibenzo-P-Dioxins EPA/600/8-84/014F. Available: http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=38484

EPA. 1987. National Human Adipose Tissue Survey (NHATS). Available: http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=55204

EPA. 1994. Health assessment document for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related compounds EPA/600/BP-92/001c. Available: http://cfpub.epa.gov/ncea/CFM/nceaQFind.cfm?keyword=Dioxin

EPA. 2009. News Releases – Research. EPA Administrator Pledges Strong Federal Cleanup Presence at Dow Dioxin Site in Michigan and Accelerated Assessment of Dioxins’ Human Health Impacts. Available: http://yosemite.epa.gov/opa/admpress.nsf/48f0fa7dd51f9e9885257359003f5342/3ffa6e8e70763f28852575c20064b26b! OpenDocument

EPA. 2010. Seven Priorities for EPA’s Future. Available: http://blog.epa.gov/administrator/2010/01/12/seven-priorities-for-epas-future/

Eskenazi B, Warner M, Marks AR, Samuels S, Needham L, Brambilla P, et al. 2010. Serum dioxin concentrations and time to pregnancy. Epidemiology 21(2): 224-31.

IARC (International Agency for Research on Cancer). 1997. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. Volume 69. Polychlorinated Dibenzo-para-Dioxins and Polychlorinated Dibenzofurans. Available: monographs.iarc.fr/ENG/Monographs/vol69/volume69.pdf

IJC. 1992. International Joint Commission. Sixth Biennial Report Under the Great Lakes Water Quality Agreement of 1978 to the Governments of the United States and Canada and the State and Provincial Governments of the Great Lakes Basin. Available: http://www.ijc.org/php/publications/html/6bre.html

Kociba RJ, Keyes DG, Beyer JE, Carreon RM, Wade CE, Dittenber DA, et al. 1978. Results of a two-year chronic toxicity and oncogenicity study of 2,3,7,8-tetrachlorodibenzo-p-dioxin in rats. Toxicol Appl Pharmacol 46(2): 279-303.

Melzer EJ. 2009. EPA pledges ‘expeditious action’ on Dow dioxin clean-up, but Superfund status not in the works. The Michigan Messenger 5/27/09. Available: http://michiganmessenger.com/19834/epa-pledges-expeditious-action-on-dow-dioxin-clean-up-but-superfund-status-not-in-the-works

Mocarelli P, Gerthoux PM, Patterson DG, Jr., Milani S, Limonta G, Bertona M, et al. 2008. Dioxin exposure, from infancy through puberty, produces endocrine disruption and affects human semen quality. Environ Health Perspect 116(1): 70-7.

NAS. 2006. EPA assessment of dioxin understates uncertainty about health risks and may overstate human cancer risk. Available: http://www8.nationalacademies.org/onpinews/newsitem.aspx?RecordID=11688

NTP. 2005. National Toxicology Program 11th Report on Carcinogens. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD); "Dioxin". Available: http://ntp.niehs.nih.gov/index.cfm?objectid=32BA9724-F1F6-975E-7FCE50709CB4C932

Pesatori AC, Consonni D, Bachetti S, Zocchetti C, Bonzini M, Baccarelli A, et al. 2003. Short- and long-term morbidity and mortality in the population exposed to dioxin after the "Seveso accident". Ind Health 41(3): 127-38.

Pesatori AC, Consonni D, Rubagotti M, Grillo P, Bertazzi PA. 2009. Cancer incidence in the population exposed to dioxin after the "Seveso accident": twenty years of follow-up. Environ Health 8: 39.

Roberts L. 1991. Flap Erupts Over Dioxin Meeting. Science 251(22 February): 866-67.

SAB. 1985. Technical Report of the Environmental Health Committee of EPA's Science Advisory Board Regarding a Draft Health Assessment Document for Polychlorinated Dibenzo-p-dioxins EPA-SAB-EHC-85-009. Available: http://yosemite.epa.gov/sab/sabproduct.nsf/WebBOARD/advisoryreports?OpenDocument

SAB. 1989. Letter from Raymond C. Loehr, Ph.D., Chair, Executive Committee, Science Advisory Board to Mr. William Reilly, Administrator, US Environmental Protection Agency. EPA-SAB-EC-90-003.

SAB. 1995. Letter from Dr. Genevieve Matanoski, Chair, Science Advisory Board, to Honorable Carol M. Browner, Administrator, U.S. Environmental Protection Agency regarding Science Advisory Board's review of the Draft Dioxin Exposure and Health Effects Reassessment Documents, "A Second Look at Dioxin." EPA-SAB-EC-95-021. Available: http://cfpub.epa.gov/ncea/CFM/nceaQFind.cfm?keyword=Dioxin

Schneider K. 1991. U.S. Backing Away from Saying Dioxin is a Deadly Peril. New York Times, August 12 1991.

Stanley JS, Boggess KE, Onstot J, Sack TM, Remmers JC, Breen J, et al. 1986. PCDDs and PCDFs in human adipose tissue from the EPA FY82 NHATS repository. Chemosphere 15(9-12): 1605-12.

Suzuki G, Nakano M, Nakano S. 2005. Distribution of PCDDs/PCDFs and Co-PCBs in human maternal blood, cord blood, placenta, milk, and adipose tissue: dioxins showing high toxic equivalency factor accumulate in the placenta. Biosci Biotechnol Biochem 69(10): 1836-47.

UNEP. 1999. UNEP executive director urges global action on dioxin, and other POPs. New Report Issued on Dioxin, Furan Inventories. Available: http://www.chem.unep.ch/Pops/POPs_Inc/press_releases/pressrel-99/unepnr99-69.htm

Van Strum C, Merrell P. 1987. No Margin of Safety: A Preliminary Report on Dioxin Pollution and the Need for Emergency Action in the Pulp and Paper Industry. Washington, DC: Greenpeace.

Weisskopf M. 1987. Paper Industry Campaign Defused Reaction to Dioxin Contamination. Washington Post October 25, 1987 (Washington, DC).

 

EWG Research on Dioxin

Environmental Working Group research on the ubiquity of dioxin in the human body, and the potential health risks from these exposures that begin in utero, is summarized below.

January 2012 — EWG calls on EPA to Finish Assessment of Dioxin Toxicity

EWG letter to EPA administrator Jackson. Click here to download PDF.

Febuary 2011 — EWG to Dioxin Review Panel

EWG Comments to Dioxin Review Panel

October 2010 — EWG to EPA: Put public health first.

EWG urges EPA’s Science Advisory Board to support the agency’s efforts to finally set a health standard for dioxin, a critical first step to protecting public health from this common food pollutant.

EWG Comments to EPA science board

July 2010 — EWG to EPA: Three decades is long enough.

EWG analysis finds that nursing infants swallow up to 77 times more dioxin than EPA believes is safe; EWG urges EPA to finalize its dioxin assessment begun nearly 30 years ago. Read EWG's analysis, presented to the EPA's Science Advisory Board during its fifth review of EPA's dioxin analysis.

EWG Comments to EPA science board | News release

2003-2009 — Dioxin pollution in people

EWG's body burden studies have found dioxin and other chlorinated dioxins and furans in blood samples from 34 of 34 Americans tested, including cord blood samples collected from 20 newborns at the moment of birth.

 

EWG Dioxin Analysis

July 12, 2010

Download the PDFDownload the PDF with Full Scientific Analysis and References.

Dr. Timothy Buckley, Chair
Dioxin Review Panel
Science Advisory Board
Environmental Protection Agency (EPA)
Washington, DC

Dear Dr. Buckley,

Twenty-five years after publishing its first assessment of dioxin, a common industrial pollutant and food contaminant, the Environmental Protection Agency (EPA) has yet to establish a safe daily dose for human exposure to this potent chemical.

Dioxin (2,3,7,8-Tetrachlorodibenzo-p-dioxin, also known as 2,3,7,8-TCDD, or TCDD) may well be one of the most-studied of all chemical pollutants. The U.S. National Toxicology Program has listed dioxin as a known human carcinogen since 2001 (NTP 2005), and the U.S. Environmental Protection Agency has proposed to do the same (EPA 2010a). There is a large and persuasive body of research dating from the 1950s showing that dioxin undermines fetal development, damages the reproductive and immune systems and causes severe skin ailments and other disorders.

As U.S. industrial data demonstrate, dioxin is released from municipal waste incinerators; industrial and military hazardous waste treatment facilities; pesticide manufacturing and paper bleaching plants; and a wide range of other industrial processes. In the 1970s, dioxin was identified as a contaminant in Agent Orange, the notorious defoliant deployed by the U.S. during the Vietnam War and blamed for diabetes and other diseases among exposed personnel (Chamie 2008; Cranmer 2000; Gupta 2006).

This widespread, persistent pollutant accumulates in animal and human fat. It contaminates meat, fish, milk, cheese, and human breast milk.

We applaud EPA Administrator Jackson’s commitment to complete the long-awaited dioxin assessment this year (EPA 2009a; EPA 2010b). We urge the Science Advisory Board (SAB) to expedite its review of EPA’s latest dioxin assessment and help the agency meet its goal. This important assessment, once completed, would serve as a cornerstone and working model for the agency’s efforts to protect public health from chemical contaminants.

We recommend that the EPA Science Advisory Board:

  • Urge EPA to finalize its proposed safety standard that would protect Americans from the carcinogenic effects of dioxin. EWG estimates that the general public may be exposed to as much as 1,200 more dioxin contamination in common foods than the amount considered negligible as a cancer risk.

  • Confirm EPA’s decision that the best current human data for determining the safe exposure limit (technically, reference dose, or RfD) for dioxin lies in two key studies, Mocarelli 2008 and Baccarelli 2008, of infants and children in Seveso, Italy, where a 1976 chemical plant explosion exposed thousands of people to dioxin in unprecedented intensity and left large quantities of the chemical in the soil (Cerlesi 1989).

  • Support EPA’s characterization of dioxin as carcinogenic to humans. This definition would be consistent with the National Toxicology Program classification of dioxin as a known human carcinogen in 2001 and the 1997 classification of dioxin as a group 1 carcinogen by the International Agency for Research on Cancer (IARC). The classification is amply supported by the weight of evidence presented by the EPA draft dioxin reanalysis.

  • Advise EPA on how best to strengthen the proposed safe daily dose (RfD) for dioxin over time, to protect children from early life exposures to this contaminant, as data continues to emerge further illuminating the unique sensitivity of the fetus, infant and child to this toxic compound.

Detailed suggestions and technical comments on the EPA draft reassessment are provided in the attached Science Analysis on dioxin’s risks to human health and the need for expedited action. Briefly, EWG’s review of the scientific literature on dioxin has determined that EPA should accelerate its dioxin assessment on these grounds:

  • The U.S. food supply is widely contaminated with dioxins, including beef, pork, chicken, turkey, fish, milk, eggs, butter and other foods Americans eat daily (FDA 2006; Huwe 2009; Schaum 2003).

  • As a result, dioxin is a ubiquitous pollutant in the human body. Authoritative studies by the U.S. Centers for Disease Control and Prevention (CDC) and the EPA’s National Center for Environmental Assessment have determined that at least 13 percent of Americans test positive for dioxin (2,3,7,8-TCDD) (Lorber 2009). Furthermore, CDC has found all Americans tested to be contaminated with dioxin-like compounds, including polychlorinated dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDF) and polychlorinated biphenyls (PCBs), which exhibit toxic properties similar to those of TCDD (Lorber 2009; Patterson 2009). Environmental Working Group's biomonitoring studies have detected TCDD in 11 of 34 Americans tested (EWG 2005). As a category, chlorinated dioxins and furans were found in 34 of 34 Americans tested, including all 20 tested cord blood samples from newborn babies. Clearly, the fetus is exposed to dioxins in utero (EWG 2005).

  • Americans are routinely exposed to dioxins from popular foods at levels close to EPA’s proposed safe daily dose. EWG analysis of data from the peer-reviewed literature finds that a 130-pound adult who eats a cheeseburger and drinks a glass of milk once a day can consume a third of EPA’s proposed safe daily dose of dioxin and dioxin-like compounds, and over time would accumulate an incremental dose of the carcinogens 270 times greater than that which EPA considers acceptable for the general population.

  • Breast-fed infants are among the most endangered Americans of all. Studies detect dioxin and dioxin-like compounds in human breast milk in amounts similar to highly contaminated foods such as beef, cheese and fish (Schecter 2001). Since newborns can consume nothing but breast milk for a number of months, their exposure to dioxins is greater, for their body weight, than that of older children and adults (Charnley 2006). EWG analysis of data from peer-reviewed scientific reports has found that a breast-fed infant three to six months old, with an average weight of 16 pounds, consumes up to 77 times more dioxin and dioxin-like compounds than EPA’s proposed safe daily dose (RfD).

  • Until EPA completes its assessment, other government agencies and environmental cleanup efforts lack guidance to implement remediation measures critical to public health. Finalizing the dioxin assessment is essential for strong, coordinated federal and industry efforts towards cleaning up numerous Superfund sites fouled with dioxin and similar compounds. According to EPA, 123 U.S. bodies of water are so contaminated with dioxins and other bioaccumulative chemical contaminants that the public has been warned to limit or avoid eating certain fish and water-dependent wildlife species caught there (EPA 2009c). Numerous communities across the country are plagued by dioxin pollution from historical industrial and military activities that created and released dioxin-containing hazardous wastes (Casanova 1987; EPA 2009d). Efforts to restore environmental quality at these sites will continue to languish until EPA sets a firm dioxin exposure standard.

Every year, 4 million newborns are exposed to dioxin daily, beginning in utero and continuing throughout life. Ubiquitous dioxin contamination of food has a lifelong impact on Americans' health. Government and industry efforts to reduce dioxin emissions since the 1970s have not been enough: Americans are still routinely overexposed to this uniquely toxic food pollutant. Countless manufacturing and incineration facilities continue to release it into the environment.

With the growing number of studies of dioxin, scientists are finding it to exhibit greater toxicity at progressively smaller doses. Thus, EPA’s present findings on the potency of dioxin to spur cancer and non-cancer health effects may still underestimate the true scope of the problem. The proposed safe daily dose is not the most health-protective and most conservative choice, as demonstrated by EPA’s proposal to establish both the RfD and exposure limits to protect against cancer in the mid-range of values supported by the scientific literature. Also, EPA’s proposed limits may well become obsolete in the future as more scientific evidence adds to our knowledge of the deleterious effects of long-term exposure to dioxin. Such facts support the need for EPA to finish its dioxin assessment and consider plans for strengthening its recommendations as new data emerge.

The societal cost of the dioxin-induced health burden may never be fully understood. But we know this much: it is already too high. It is EPA’s responsibility to address this problem with resolve, making decisions based only on the public good, without regard to pressure from special interests who stand to benefit financially from weak standards and regulations.

After 25 years of study and three previous, in-depth SAB reviews, the EPA has still not completed its dioxin assessment. In this fourth SAB review, we urge you to support the agency by helping it stand by the findings and health standards presented in the current draft. We hope that the Science Advisory Board’s timely, focused review will serve as a closing step in guiding EPA to establish a safety level for dioxin that will truly protect the health of Americans, particularly the youngest and most vulnerable.

Thank you for your attention and for your service on this important panel.

Sincerely,

Jane Houlihan, MSCE
Senior Vice President for Research

Olga V. Naidenko, PhD
Senior Scientist

References:

Casanova JN, Olfenbuttel RF. 1987. Military Sites Contaminated with 2,3,7,8-Tetrachlorodibenzo-pdioxin: Permitting Remedial Action Research. In: Solving Hazardous Waste Problems: Learning from Dioxins (Exner JH, ed): American Chemical Society, 229-43.

Cerlesi S, Di Domenico A, Ratti S. 1989. 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) persistence in the Seveso (Milan, Italy) soil. Ecotoxicol Environ Saf 18(2): 149-64.

Chamie K, DeVere White RW, Lee D, Ok JH, Ellison LM. 2008. Agent Orange exposure, Vietnam War veterans, and the risk of prostate cancer. Cancer 113(9): 2464-70.

Charnley G, Kimbrough RD. 2006. Overview of exposure, toxicity, and risks to children from current levels of 2,3,7,8-tetrachlorodibenzo-p-dioxin and related compounds in the USA. Food Chem Toxicol 44(5): 601-15.

Cranmer M, Louie S, Kennedy RH, Kern PA, Fonseca VA. 2000. Exposure to 2,3,7,8-tetrachlorodibenzop-dioxin (TCDD) is associated with hyperinsulinemia and insulin resistance. Toxicol Sci 56(2): 431-6.

Environmental Working Group (EWG). 2005. Human Toxome Project. 2,3,7,8-TCDD (tetradioxin). Available: https://www.ewg.org/sites/humantoxome/chemicals/chemical.php?chemid=40001

FDA. 2006. PCDD/PCDF Exposure Estimates from TDS Samples Collected in 2001-2004. Available: http://www.fda.gov/Food/FoodSafety/FoodContaminantsAdulteration/ChemicalContaminants/DioxinsPCBs/ ucm077498.htm

Gupta A, Ketchum N, Roehrborn CG, Schecter A, Aragaki CC, Michalek JE. 2006. Serum dioxin, testosterone, and subsequent risk of benign prostatic hyperplasia: a prospective cohort study of Air Force veterans. Environ Health Perspect 114(11): 1649-54.

Huwe J, Pagan-Rodriguez D, Abdelmajid N, Clinch N, Gordon D, Holterman J, et al. 2009. Survey of polychlorinated dibenzo-p-dioxins, polychlorinated dibenzofurans, and non-ortho-polychlorinated biphenyls in U.S. meat and poultry, 2007-2008: effect of new toxic equivalency factors on toxic equivalency levels, patterns, and temporal trends. J Agric Food Chem 57(23): 11194-200.

Lorber M, Patterson D, Huwe J, Kahn H. 2009. Evaluation of background exposures of Americans to dioxin-like compounds in the 1990s and the 2000s. Chemosphere 77(5): 640-51.

NTP. 2005. National Toxicology Program 11th Report on Carcinogens. 2,3,7,8-Tetrachlorodibenzo-pdioxin (TCDD); "Dioxin". Available: http://ntp.niehs.nih.gov/index.cfm?objectid=32BA9724-F1F6-975E-7FCE50709CB4C932

Patterson DG, Jr., Wong LY, Turner WE, Caudill SP, Dipietro ES, McClure PC, et al. 2009. Levels in the U.S. population of those persistent organic pollutants (2003-2004) included in the Stockholm Convention or in other long range transboundary air pollution agreements. Environ Sci Technol 43(4): 1211-8.

Schaum J, Schuda L, Wu C, Sears R, Ferrario J, Andrews K. 2003. A national survey of persistent, bioaccumulative, and toxic (PBT) pollutants in the United States milk supply. J Expo Anal Environ Epidemiol 13(3): 177-86.

U.S. EPA. 2009a. News Releases – Research. EPA Administrator Pledges Strong Federal Cleanup Presence at Dow Dioxin Site in Michigan and Accelerated Assessment of Dioxins’ Human Health Impacts. Available:http://yosemite.epa.gov/opa/admpress.nsf/48f0fa7dd51f9e9885257359003f5342/3ffa6e8e70763f28852575 c20064b2 6b!OpenDocument

U.S. EPA. 2009b. EPA’s Science Plan for Activities Related to Dioxins in the Environment. Available: http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=209690

U.S. EPA. 2009c. The National Listing of Fish Advisories. Available: http://www.epa.gov/waterscience/fish/advisories/

U.S. EPA. 2009d. Development of Draft Recommended Interim Preliminary Remediation Goals for Dioxin in Soil. Available: http://www.epa.gov/superfund/policy/remedy/sfremedy/remedies/dioxinsoil.html

U.S. EPA. 2010a. EPA’s Reanalysis of Key Issues Related to Dioxin Toxicity and Response to NAS Comments (External Review Draft). Available: http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=222203

U.S. EPA. 2010b. News Release: EPA Releases Draft Dioxin Report for Peer Review and Public Comment. Available: http://yosemite.epa.gov/opa/admpress.nsf/0/6FB73A1C778FE16A8525772A0055AC5A

EWG Science Analysis

Dioxin’s Risks to Human Health and the Need for Expedited Action

by Olga V. Naidenko, PhD, Senior Scientist

Environmental Working Group (EWG) is a non-profit public health and environmental research and advocacy organization based in Washington, DC. We focus much of our research on human and environmental health risks from chemical contamination.

The purpose of this document is to provide estimates of the implications of dioxin exposures for the general population, including breast-fed infants, children, and adults who ingest dioxin in a wide range of dioxin-contaminated foods; and to lay out the many reasons for the Environmental Protection Agency (EPA) to expedite the completion of its dioxin assessment begun 25 years ago and still unfinished.

Dioxin (2,3,7,8-Tetrachlorodibenzo-p-dioxin, also known as 2,3,7,8-TCDD, or TCDD) may well be one of the most-studied chemical pollutants. An unprecedented range and depth of human and animal studies have systematically explored various aspects of dioxin toxicity. Indeed, as more research is done, scientists are finding dioxin to be more, not less, toxic than what was determined by earlier studies.

As the Science Advisory Board (SAB) launches its fourth analysis of EPA’s dioxin assessment in the past quarter century, EWG urges the board to expedite its review process and help EPA finalize this important document that will serve as a cornerstone for the agency’s efforts to protect public health from chemical contaminants.

EWG strongly supports the scientific rationale of the “Draft EPA's Reanalysis of Key Issues Related to Dioxin Toxicity.” We urge the SAB and the members of the Dioxin Review Panel to uphold the EPA’s risk assessment approach and to help speed the agency’s efforts to establish the safety standard for oral exposure to dioxin, as presented in the draft reanalysis.

About dioxin. Chlorinated dioxins are a family of persistent, highly toxic compounds that form as byproducts of waste incineration (Shibamoto 2007) and various industrial processes, such as smelting, chlorine paper bleaching and pesticide manufacturing (Rappe 1990; Weber 2008). The most toxic and most extensively studied member of this family, 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) has been associated with a panoply of adverse health effect in people including cardiovascular disease; diabetes; cancer; endometriosis; early menopause; reduced testosterone and thyroid hormones; altered immune responses; and skin, tooth, and nail abnormalities (Birnbaum 2000; Schecter 2006; White 2009).

Similar harmful effects, though of lesser magnitude, are associated with exposure to related compounds, including various polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs), which generally co-occur with TCDD (Lorber 2009). For these contaminants, the World Health Organization and health agencies in a number of countries apply Toxic Equivalency Factors that represent the relative potency of PCDDs and PCDFs relative to TCDD toxicity (Van den Berg 2006; WHO 2005). These toxicity-weighted concentrations are then summed to give a single, adjusted PCDD/PCDF concentration expressed as a Toxic Equivalent (TEQ) (U.S. EPA 2007).

EWG strongly supports an expedited SAB review of this document so that EPA can meet its goal of finishing the project in 2010. This timely completion is essential because:

  1. Infants and young children receive the highest dose of dioxins from food exposures, relative to their body weight, of any other segment of the population, in significant excess of the EPA’s estimated reference dose (RfD), safe daily dose, of 0.7 picograms per kilogram of body weight per day (pg/kg-day).

  2. At the current contamination levels of dioxins in food, the cancer risk is orders of magnitude above the EPA’s benchmark one-in-one-million risk level that provides a reasonable certainty of no harm. Americans are routinely exposed to dioxins from popular foods at levels close to EPA’s proposed reference dose.

  3. EPA’s proposed standards indicate a need for rapid action towards restricting dioxin exposures.

Details and rationale for our recommendations are listed below.

1. Infants and young children receive the highest dose of dioxins from food exposures, relative to their body weight, of any other segment of the population, in significant excess of the EPA’s estimated reference dose (RfD), safe daily dose, of 0.7 pg/kg-day.

Outside of known dioxin-contaminated industrial and military hazardous waste sites (Casanova 1987; Garabrant 2009) and industrial accidents (Pesatori 2003), the primary source of dioxin contamination in people is from food, starting with breast milk and formula for infants and continuing to dioxin exposure from meat, dairy products, fish and shellfish for children and adults (Schecter 2001; WHO 2010). Infants and children between 1 and 10 years of age have the highest relative dietary exposure, since children consume more food than adults in relation to their body weight (Charnley 2006; Gies 2007).

Breast-fed infants in particular receive a high dose of dioxin during their first months of life, when breast milk is their only, or primary, food source (LaKind 2007). Adverse impacts of dioxins on children’s health are of great concern, because developmental and/or early-life dioxin exposure has been linked to neurological alterations, including effects on hearing, psychomotor function, cognition, and gender- specific behaviors; effects on the reproductive organs; and hormonal changes (Baccarelli 2008; Mocarelli 2008; Wormley 2004).

Two recent, key human studies have clarified and expanded our understanding of the heightened susceptibility of the developing fetus and young children to dioxin:

  • A study of 51 mother-child pairs in Seveso, Italy exposed to TCDD from an industrial explosion. In the study, infants born to mothers in the highly contaminated Seveso region 18 to 29 years after the explosion showed elevated blood levels of thyroid-stimulating hormone (TSH), an indicator of neonatal primary hypothyroidism. Higher maternal serum TCDD concentration correlated with elevated TSH levels in newborns, confirming the specificity of the association (Baccarelli 2008). The thyroid hormone tests were performed 72 hours after birth, indicating that effects observed by the scientists were due to fetal exposure to TCDD that had crossed the placenta.

  • A study of 71 men exposed at a young age to TCDD from the Seveso explosion showed a reduction in various sperm parameters, such as sperm concentration and motility, and changes in the levels of two hormones, estradiol and follicle-stimulating hormones. These reproductive changes were particularly noticeable among a group of men exposed before the age of 10 (mean age of exposure 6.2 years), compared to control groups of men exposed after the age of 10 (mean age at exposure, 13.2 years) and men exposed as adults (mean age at exposure, 21.5 years) (Mocarelli 2008). The authors of the study suggested that TCDD exposure during sensitive developmental windows may “permanently alter the programming of the primordial germ cells” (Mocarelli 2008), with adverse reproductive health consequences for the rest of the person’s life.

EWG scientists carefully reviewed the EPA’s method for estimating a reference dose (RfD) for the oral safety standard, considering both human and animal studies of TCDD toxicity. We support the agency’s methods. We agree with the EPA’s conclusion that the Baccarelli 2008 and Mocarelli 2008 studies have been conducted with the necessary level of scientific rigor to render them adequate and appropriate for the derivation of an RfD protective for non-cancer health effects. Both studies produced a comparable Point of Departure (POD, defined as the Lowest Observed Adverse Effect level (LOAEL) detected in these studies) for oral exposure from contaminated food at 0.02 nanograms of dioxin per kilogram of body weight per day (ng/kg/day). EPA then applied an uncertainty factor of 30-fold, which included a 10-fold factor for lack of a No Observed Adverse Effect Level (NOAEL) and a 3-fold factor for interindividual variability. The resultant RfD, calculated as POD/30, was determined to be 0.7 picograms (pg) per kg/day (pg/kg-day).

EWG notes that this RfD based on human epidemiological studies is, in fact, in the middle of the candidate RfD array derived by EPA from a wide range of animal toxicity studies (Figure 4-4 in the Draft Reanalysis). An argument can be made that, in view of very high toxicity of TCDD, the most conservative and health-protective RfD should be adopted. The RfD recommended by the EPA is based on sound science, is consistent with the full range of available data and would constitute an important step forward for protecting public health and decreasing dioxin exposures from contaminated foods. Of note, our analysis of the amount of TCDD and related compounds (polychlorinated dibenzodioxins (PCDD) and polychlorinated dibenzofurans (PCDF)) that infants and children ingest daily indicates these vulnerable groups of kids would be significantly overexposed for the first several, critical years of their lives (Tables I and II).

Table I. Dioxin contamination in human breast milk – US data a

Reference Dioxin toxic equivalent (TEQ) b levels in breast milk (on a lipid basis) Dioxin TEQ levels (whole- milk basis) and total TEQ exposure from breast milk for 6 months-old infant c Dioxin TEQ dose for 6 month-old breast-fed infant d Infant exposures relative to "safe" daily dose (RfD of 0.7 pg/kg-day e)
(Malisch 2003), cited in (LaKind 2007) 7.18 ppt (pg/g) PCDD+PCDF TEQs (as reported) 0.14-0.35 parts per trillion (ppt) PCDD+PCDF TEQs for 2-5% milk lipid contentf, corresponding to 109-273 pg dioxin TEQ from breast milk/day 15-37 pg/kg- day 21-52 times higher than RfD
(Schecter 2001) not reported 0.35 ppt PCDD+PCDF TEQ (3.7% milk lipid content), corresponding to 273 pg dioxin TEQ from breast milk/day 37 pg/kg-day 52 times higher than RfD
(Charnley 2006) not reported Daily intake of 80-400 ppt PCDD+PCDF TEQs from breast milk/day 11-54 pg/kg- day 15-77 times higher than RfD

Source: EWG analysis of dioxin exposures considering breast milk tests and infant exposure factors from EPA and the peer-reviewed scientific literature.

  1. For comparison, similar range of PCDD/PCDF concentrations in breast milk was reported by several other studies conducted in North America (all numbers are on the lipid basis): 2.6 pg/g (ppt) for a selected group of 8 PCDD/F TEQs (did not include TCDD) (LaKind 2009); 12 ng/kg (ppt) PCDD/F and PCBs TEQs (Wang 2003), cited in (Charnley 2006); and 15 ppt (ng/kg) PCDD/PCDF TEQs, based on Canadian data for 1986-87 (Ryan 1993).
  2. Overall toxic equivalency (TEQ) for body burden of TCDD and related compounds, PCDDs and PCDFs as reported in the individual studies. For a PCDD/PCDF mixture, total TEQ is the sum of the product of the concentration of an individual dioxin- like compound and the corresponding TCDD TEF for that compound. TCDD commonly comprises ~10% of total dioxin TEQs in different matrices such as food, body burden, etc. (Lorber 2009; Van den Berg 1998).
  3. According to EPA's Exposure Factors Handbook (U.S. EPA 2009), mean breast milk intake for infants 1-6 months of age is in the range of 673-896 ml/day. For this analysis, we used the volume of 780 ml/day located in the middle of the range and typical for 3-6 months-old infants, as identified in other studies (LaKind 2000; Neville 1988). Human breast milk density is 1.03 g/ml (LaKind 2000).
  4. For infants from 3 to less than 6 months of age, EPA recommends assuming a mean body weight of 7.4 kg (U.S. EPA 2009).
  5. Proposed in the EPA's 2010 Draft Reanalysis (U.S. EPA 2010).
  6. The total fat content of 24-hour human breast milk sample is typically in the range of 20-50 g/L. National Academy of Sciences (NAS). 1991. Nutrition during lactation. http://www.iom.edu/Reports/1991/Nutrition-During-Lactation.aspx

Table II. Estimates of dietary exposure to PCDD/F TEQs for U.S. children up to 10 years of age a

Age Average intake, pg/kg-day Children's average exposures relative to "safe" daily dose (RfD of 0.7 pg/kg-day) High intake (95%), pg/kg-day b Children's high exposures relative to "safe" daily dose (RfD of 0.7 pg/kg- day)
2 years (Charnley 2006) 0.7-1.2 c 1-1.7 times higher than RfD 1.5-2.2 2.1-3.1 times higher than RfD
2 years (FDA 2006) 0.78 1.1 times higher than RfD not reported  
6 years (Charnley 2006) 0.6-0.9 0.9-1.3 times higher than RfD 1.3-1.8 1.8-2.5 times higher than RfD
6 years (FDA 2006) 0.62 0.9 of the RfD not reported  
10 years (FDA 2006) 0.44 0.6 of the RfD not reported  
General US population (Charnley 2006) 0.2-0.4 0.3-0.6 of the RfD 0.8-1.2 1.1-1.7 times higher than RfD

Source: EWG compilation of dioxin exposure estimates for the U.S. population from the FDA data and the peer-reviewed scientific literature.

  1. FDA Total Diet Study (TDS) did not include breast milk. Thus we could not estimate exposures for infants 6-11 months of age, a group that ingests breast milk in addition to other foods.
  2. As reported by Charnley 2006 study.
  3. Charnley 2006 reported two estimates for each category of PCDD/F exposure, one estimate assuming that non-detect samples included the tested compound at 1⁄2 of the limit of detection, corresponding to the higher estimate listed; and a second estimate assuming that non-detect samples did not contain the analyte in question (assigned zero value), corresponding to the lower estimate listed.

As demonstrated by the data in Table I, all breast-fed infants and children up to 2 years of age are currently ingesting amounts of PCDD/F TEQs significantly greater than the proposed RfD (U.S. EPA 2010). Higher dietary intakes persist for children 2-10 years of age and, in the highest exposure group (95% or top 5% of exposure), remain above RfD, as shown in Table II. These elevated exposures for children compared to adults are of serious concern, since younger humans or laboratory animals appear to be more sensitive to dioxin’s effects on hormones (Mocarelli 2008; Su 2010). The full range of health effects that would be triggered by the early, high-dose exposure to dioxin in infants is still incompletely understood. However, as new research on dioxin toxicity in humans is conducted, scientists are finding evidence of adverse changes at progressively lower doses of dioxin, as evidenced by the long-term follow up studies from the Seveso cohort (Alaluusua 2004; Baccarelli 2008; Mocarelli 2008).

Children eliminate TCDD from their bodies faster than adults and have a shorter TCDD half-life, possibly due to differences in the relative contribution of toxicant clearance pathways (Kerger 2006). However, the rate of dioxin clearance from the body is inversely related to the proportion of adipose tissue in the body, the Body-Mass Index (BMI). In people of all ages, greater BMI is associated with longer residence times of TCDD and related compounds in the body (Collins 2007; Kerger 2006; Landi 1998). For example, the half-life of TCDD is longer in females compared to males, due to higher BMI (Landi 1998). Due to the rising numbers of overweight and obese American children and adolescents (Balistreri 2010), children’s cumulative exposure to TCDD and related contaminants would also increase, with negative effects on their reproductive and hormonal systems and general metabolism.

Appropriate, balanced nutrition is important for human health from the moment of birth. Numerous studies have found that, despite the presence of industrial chemical contaminants in breast milk, breast- feeding remains an essential foundation for growth; resistance to infections; neurological development; and many other parameters of wellbeing (Massart 2008; Mead 2008). While scientific evidence indicates that the advantages of breast-feeding generally outweigh the health risks from contaminants, it is essential to work towards decreasing life-time exposures to these pollutants and thereby lessen infant ingestion of pollutants from breast milk (Gies 2007; WHO 2009).

2. At the current contamination levels of dioxins in food, the cancer risk is orders of magnitude above the EPA’s benchmark one-in-one-million risk level that provides a reasonable certainty of no harm. Americans are routinely exposed to dioxins from popular foods at levels close to EPA’s proposed reference dose.

Dioxin carcinogenicity to humans has been demonstrated by several large-scale occupational studies (Becher 1998; Cheng 2006; Ott 1996; Steenland 2001); cancer findings in the Seveso cohort (Pesatori 2009) and supporting animal data (La Merrill 2010; McGregor 1998; Steenland 2004). EWG agrees with EPA’s scientific rationale for characterizing TCDD as “carcinogenic to humans.” We find this description to be well supported by the multiple lines of evidence outlined in the EPA draft. The definition “carcinogenic to humans” would apply equally to intense exposures for people contaminated in workplace settings or industrial explosions, as well as for lower exposures from contaminated food typical for general population, as determined by the U.S. National Toxicology Program and the International Agency for Research on Cancer (IARC 1997; NTP 2005).

In the draft reanalysis, EPA determined an oral cancer slope factor of 1 x 106 per (mg/kg-day). After reviewing the EPA’s cancer risk assessment method, EWG agrees with the appropriateness of this slope factor and finds it consistent with carcinogenicity data from both human and animal studies.

In its earlier assessment, EPA estimated that dioxin exposures for the general population would be above the risk level that assures a reasonable certainty of no harm (one-in-a-million risk level) (U.S. EPA 1994). Same findings have been made by government agencies in other countries (Gies 2007). As reported by a study published in 1990s, based on the cancer slope factors from EPA’s 1994 assessment, 7,800-78,000 excess cancers over a lifetime could be attributed to dioxin exposure from food (Schecter 1997).

Studies of dioxin carcinogenicity published over the past decade only deepen concerns about dioxin’s toxicity and carcinogenicity. The table below presents some estimates for the excess number of cancer cases that would arise from the levels of dioxin exposure found in the general population.

Table III. Excess cancer risk associated with ingestion of dioxins (PCDD/F) from food for the U.S. population.

Exposed group Daily ingestion dose for PCDD/F TEQ, pg/kg bw-day Excess cancer risk, method 1 a Number of cancer cases per million b Excess cancer risk, method 2 c Number of Americans developing cancer from dioxin exposure, per million people b
General population (FDA 2006) 0.32 2.1x10-4 210 3.2x10-4 320
General population, 95% exposure (Charnley 2006) 0.8-1.2 d 4.1x10-4 to 5.5x10-4 410-550 8x10-4 to 12x10-4 800-1200
At the draft RfD (EPA 2010) 0.7 3.7x10-4 370 7x10-4 700

Source: EWG analysis of cancer risk considering typical daily dioxin intakes and exposure factors from EPA, FDA and the peer-reviewed scientific literature.

  1. Excess cancer risk (ER) calculated according to the formula ER = [exp(AUC*6.04E-6)*0.112-0.112]/0.888, as described in the EPA Draft Reanalysis Table 5-3.
  2. This number of excess cancer cases corresponds to lifetime (70 years) exposure to dioxins.
  3. Excess cancer risk (ER) according to the formula that utilizes Oral Slope Factor (OSF) of 1 x 106 per (mg/kg-day). OSF = 1E6*ER/daily ingestion dose (D), as described in the EPA Draft Reanalysis Table 5-3. Based on this formula, we calculated ER=OSF*D/1E6
  4. Range of values for the PCDD/F TEQ ingestion described in footnote 2 in Table II above.

The excess cancer risk due to dioxin exposure represents a significant public health concern. As demonstrated by the data in Table III, excess lifetime cancer risk ranges from 320 to 1,200 per million people exposed. People within the highest 5% of dietary exposure to dioxin would face 2-4 fold greater cancer risk compared to the general population with average exposures. Across the population, the estimated cancer risk is 2 to 3 orders of magnitude above one-in-a-million cancer risk that regulatory agencies associate with a virtually safe dose for carcinogens in food (Edler 2005; Gaylor 1997; Wardlaw 1985). These findings clearly point to the urgent need for restricting dioxin exposures and decreasing the human health burden from dioxin contamination in food (WHO 2010).

EWG analysis of data from the peer-reviewed literature finds that a 130-pound adult eating a single hamburger or drinking two glasses of milk per day can be exposed to dioxin and dioxin-like compounds (PCDDs and PCDFs, excluding PCBs) at levels very close to EPA’s proposed reference dose. For example:

  • One quarter-pound hamburger (90% lean ground beef) = 15% of the RfD for dioxin
  • Two 8-ounce glasses of whole milk = 17% of the RfD
  • One 4-ounce block of cheese = 39% of the RfD
  • One cheeseburger (1 ounce of cheese) and an 8-ounce glass of whole milk = 33% of the RfD

For this analysis, typical amounts of fat in the representative foods were identified from USDA and EPA reports as well as published literature (U.S. EPA 2003; USDA 2010a, b). Mean concentration of PCDD/PCDF TEQs in beef at 0.55 pg/gram lipid was reported in the 2007-2008 USDA survey of dioxins and furans in U.S. meat and poultry (Huwe 2009). Mean concentration of dioxins and furans in milk at 14.3 pg PCDD/F TEQs per liter was reported in the EPA’s national survey of persistent, bioaccumulative, and toxic (PBT) pollutants in the United States milk supply (Schaum 2003).

According to EPA’s estimates of TCDD carcinogenicity, these routine, daily exposures correspond to a cancer risk between 0.5x10-4 and 2.7x10-4, up to 270 times greater than the one-in-a-million cancer risk considered acceptable for the general population. Thus, these common foods that contain PCDD/F at levels close to, but below, the RfD would be associated with an incremental cancer risk well above the levels expected to provide a reasonable certainty of no harm. 3. EPA’s proposed standards indicate a need for rapid action towards restricting dioxin exposures.

EWG commends EPA for preparing a thorough, rigorous, and scientifically justified risk assessment for TCDD and for developing an RfD and cancer slope factor based on the key studies published over the past five years. We also note that this year’s external peer review of EPA’s Draft Reanalysis is the fourth time that the Science Advisory Board has reviewed EPA’s dioxin assessment, with the first one in 1988, followed by reviews in 1995, 2001, and the current, 2010 review.

Dioxins and related synthetic chemical pollutants accumulate in the bodies of people from daily ingestion of dioxin-contaminated fatty foods, such as beef, pork, poultry and other meats; milk and dairy products; fish; and eggs (FDA 2006; Lorber 2009; Schecter 2001; USDA 2009). Based on the National Health and Nutrition Examination Survey (NHANES) 2001-2002 data, EPA and USDA researchers determined that the blood levels of PCDD/F in the general population are in the range of 12.9-17.5 pg/g (on a lipid basis) and the background intake is ~ 0.5 pg TEQ/kg-day at the 50th percentile (Lorber 2009). Several research groups have reported that background human exposures from dioxins and other chemical pollutants in food have declined in the U.S. population over the past two decades (LaKind 2009; Patterson 2008). These findings are encouraging; yet, dioxins remain as persistent, highly toxic pollutants that threaten the health of all Americans and especially the health of infants and children.

TCDD may well be one of the most-studied chemical pollutants with an unprecedented range and depth of human and animal studies that have systematically explored various aspects of dioxin toxicity. As more research is done, scientists are finding dioxin to be more, not less toxic than what was determined by earlier studies. Thus, EWG urges the SAB to expedite its review process and help EPA finalize this important document that will serve as a cornerstone for the Agency’s efforts to protect public health from chemical contaminants.

References for the attachment

Alaluusua S, Calderara P, Gerthoux PM, Lukinmaa PL, Kovero O, Needham L, et al. 2004. Developmental dental aberrations after the dioxin accident in Seveso. Environ Health Perspect 112(13): 1313-8.

Baccarelli A, Giacomini SM, Corbetta C, Landi MT, Bonzini M, Consonni D, et al. 2008. Neonatal thyroid function in Seveso 25 years after maternal exposure to dioxin. PLoS Med 5(7): e161.

Balistreri KS, Van Hook J. 2010. Trajectories of Overweight Among US School Children: A Focus on Social and Economic Characteristics. Matern Child Health J: in press.

Becher H, Steindorf K, Flesch-Janys D. 1998. Quantitative cancer risk assessment for dioxins using an occupational cohort. Environ Health Perspect 106 Suppl 2: 663-70.

Birnbaum LS, Tuomisto J. 2000. Non-carcinogenic effects of TCDD in animals. Food Addit Contam 17(4): 275-88. Casanova JN, Olfenbuttel RF. 1987. Military Sites Contaminated with 2,3,7,8-Tetrachlorodibenzo-p-dioxin: Permitting Remedial Action Research. In: Solving Hazardous Waste Problems: Learning from Dioxins (Exner JH, ed): American Chemical Society, 229-43.

Charnley G, Kimbrough RD. 2006. Overview of exposure, toxicity, and risks to children from current levels of 2,3,7,8-tetrachlorodibenzo-p-dioxin and related compounds in the USA. Food Chem Toxicol 44(5): 601-15. Cheng H, Aylward L, Beall C, Starr TB, Brunet RC, Carrier G, et al. 2006. TCDD exposure-response analysis and risk assessment. Risk Anal 26(4): 1059-71.

Collins JJ, Bodner K, Burns CJ, Budinsky RA, Lamparski LL, Wilken M, et al. 2007. Body mass index and serum chlorinated dibenzo-p-dioxin and dibenzofuran levels. Chemosphere 66(6): 1079-85.

Edler L, Kitsos CP, eds. 2005. Recent Advances in Quantitative Methods in Cancer and Human Health Risk Assessment: John Wiley & Sons.

FDA. 2006. PCDD/PCDF Exposure Estimates from TDS Samples Collected in 2001-2004. Available: http://www.fda.gov/Food/FoodSafety/FoodContaminantsAdulteration/ChemicalContaminants/DioxinsPCBs/ ucm077498.htm [accessed June 23, 2010].

Garabrant DH, Franzblau A, Lepkowski J, Gillespie BW, Adriaens P, Demond A, et al. 2009. The University of Michigan Dioxin Exposure Study: predictors of human serum dioxin concentrations in Midland and Saginaw, Michigan. Environ Health Perspect 117(5): 818-24.

Gaylor DW, Axelrad JA, Brown RP, Cavagnaro JA, Cyr WH, Hulebak KL, et al. 1997. Health risk assessment practices in the U.S. Food and Drug Administration. Regul Toxicol Pharmacol 26(3): 307-21.

Gies A, Neumeier G, Rappolder M, Konietzka R. 2007. Risk assessment of dioxins and dioxin-like PCBs in food-- comments by the German Federal Environmental Agency. Chemosphere 67(9): S344-9.

Huwe J, Pagan-Rodriguez D, Abdelmajid N, Clinch N, Gordon D, Holterman J, et al. 2009. Survey of polychlorinated dibenzo-p-dioxins, polychlorinated dibenzofurans, and non-ortho-polychlorinated biphenyls in U.S. meat and poultry, 2007-2008: effect of new toxic equivalency factors on toxic equivalency levels, patterns, and temporal trends. J Agric Food Chem 57(23): 11194-200.

IARC. 1997. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. Volume 69. Polychlorinated Dibenzo-para-Dioxins and Polychlorinated Dibenzofurans. Available: http://monographs.iarc.fr/ENG/Monographs/vol69/volume69.pdf [accessed July 6, 2010].

Kerger BD, Leung HW, Scott P, Paustenbach DJ, Needham LL, Patterson DG, Jr., et al. 2006. Age- and concentration-dependent elimination half-life of 2,3,7,8-tetrachlorodibenzo-p-dioxin in Seveso children. Environ Health Perspect 114(10): 1596-602.

La Merrill M, Harper R, Birnbaum LS, Cardiff RD, Threadgill DW. 2010. Maternal dioxin exposure combined with a diet high in fat increases mammary cancer incidence in mice. Environ Health Perspect 118(5): 596-601.

LaKind JS. 2007. Recent global trends and physiologic origins of dioxins and furans in human milk. J Expo Sci Environ Epidemiol 17(6): 510-24.

LaKind JS, Berlin C, Sjodin A, Turner WE, Wang RY, Needham L, et al. 2009. Do Human Milk Concentrations of Persistent Organic Chemicals Really Decline During Lactation? Chemical Concentrations During Lactation and Milk/Serum Partitioning Environ Health Perspec 117(10): 1625-31.

LaKind JS, Berlin CM, Park CN, Naiman DQ, Gudka NJ. 2000. Methodology for characterizing distributions of incremental body burdens of 2,3,7,8-TCDD and DDE from breast milk in North American nursing infants. J Toxicol Environ Health A 59(8): 605-39.

LaKind JS, Hays SM, Aylward LL, Naiman DQ. 2009. Perspective on serum dioxin levels in the United States: an evaluation of the NHANES data. J Expo Sci Environ Epidemiol 19(4): 435-41.

Landi MT, Consonni D, Patterson DG, Jr., Needham LL, Lucier G, Brambilla P, et al. 1998. 2,3,7,8- Tetrachlorodibenzo-p-dioxin plasma levels in Seveso 20 years after the accident. Environ Health Perspect 106(5): 273-7.

Lorber M, Patterson D, Huwe J, Kahn H. 2009. Evaluation of background exposures of Americans to dioxin-like compounds in the 1990s and the 2000s. Chemosphere 77(5): 640-51.

Malisch R, van Leeuwen FXR. 2003. Results of the WHO-coordinated exposure study on the levels of PCBs, PCDDs and PCDFs in human milk. Organohalogen Compd 64: 136-40.

Massart F, Gherarducci G, Marchi B, Saggese G. 2008. Chemical Biomarkers of Human Breast Milk Pollution. Biomark Insights 3: 159-69.

McGregor DB, Partensky C, Wilbourn J, Rice JM. 1998. An IARC evaluation of polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans as risk factors in human carcinogenesis. Environ Health Perspect 106 Suppl 2: 755-60.

Mead MN. 2008. Contaminants in Human Milk: Weighing the Risks against the Benefits of Breastfeeding. Environ Health Perspec 116(10): A427-A34.

Mocarelli P, Gerthoux PM, Patterson DG, Jr., Milani S, Limonta G, Bertona M, et al. 2008. Dioxin exposure, from infancy through puberty, produces endocrine disruption and affects human semen quality. Environ Health Perspect 116(1): 70-7.

Neville MC, Keller R, Seacat J, Lutes V, Neifert M, Casey C, et al. 1988. Studies in human lactation: milk volumes in lactating women during the onset of lactation and full lactation. Am J Clin Nutr 48(6): 1375-86.

NTP. 2005. National Toxicology Program 11th Report on Carcinogens. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD); "Dioxin". Available: http://ntp.niehs.nih.gov/index.cfm?objectid=32BA9724-F1F6-975E-7FCE50709CB4C932 [accessed July 7 2010].

Ott MG, Zober A. 1996. Cause specific mortality and cancer incidence among employees exposed to 2,3,7,8-TCDD after a 1953 reactor accident. Occup Environ Med 53(9): 606-12.

Patterson DG, Jr., Turner WE, Caudill SP, Needham LL. 2008. Total TEQ reference range (PCDDs, PCDFs, cPCBs, mono-PCBs) for the US population 2001-2002. Chemosphere 73(1 Suppl): S261-77.

Pesatori AC, Consonni D, Bachetti S, Zocchetti C, Bonzini M, Baccarelli A, et al. 2003. Short- and long-term morbidity and mortality in the population exposed to dioxin after the "Seveso accident". Ind Health 41(3): 127-38.

Pesatori AC, Consonni D, Rubagotti M, Grillo P, Bertazzi PA. 2009. Cancer incidence in the population exposed to dioxin after the "Seveso accident": twenty years of follow-up. Environ Health 8: 39.

Rappe C. 1990. Environmentally stable chlorinated contaminants from the pulp and paper industry. IARC Sci Publ(104): 341-53.

Ryan JJ, Lizotte R, Panopio LG, Shewchuk C, Lewis DA, Sun WF. 1993. Polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) in human milk samples collected across Canada in 1986-87. Food Addit Contam 10(4): 419-28.

Schaum J, Schuda L, Wu C, Sears R, Ferrario J, Andrews K. 2003. A national survey of persistent, bioaccumulative, and toxic (PBT) pollutants in the United States milk supply. J Expo Anal Environ Epidemiol 13(3): 177-86.

Schecter A, Birnbaum L, Ryan JJ, Constable JD. 2006. Dioxins: an overview. Environ Res 101(3): 419-28.

Schecter A, Cramer P, Boggess K, Stanley J, Papke O, Olson J, et al. 2001. Intake of dioxins and related compounds from food in the U.S. population. J Toxicol Environ Health A 63(1): 1-18.

Schecter A, Olson JR. 1997. Cancer risk assessment using blood dioxin levels and daily dietary TEQ intake in general populations of industrial and non-industrial countries. Chemosphere 34(5-7): 1569-77.

Shibamoto T, Yasuhara A, Katami T. 2007. Dioxin formation from waste incineration. Rev Environ Contam Toxicol 190: 1-41.

Steenland K, Bertazzi P, Baccarelli A, Kogevinas M. 2004. Dioxin revisited: developments since the 1997 IARC classification of dioxin as a human carcinogen. Environ Health Perspect 112(13): 1265-8.

Steenland K, Deddens J, Piacitelli L. 2001. Risk assessment for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) based on an epidemiologic study. Am J Epidemiol 154(5): 451-8.

Su PH, Chen JY, Chen JW, Wang SL. 2010. Growth and thyroid function in children with in utero exposure to dioxin: a 5-year follow-up study. Pediatr Res 67(2): 205-10.

U.S. EPA. 1994. Health assessment document for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related compounds EPA/600/BP-92/001c. Available: http://cfpub.epa.gov/ncea/CFM/nceaQFind.cfm?keyword=Dioxin [accessed June 24, 2010].

U.S. EPA. 2003. Continuing Survey of Food Intakes by Individuals (CSFII) Analysis of Food Intake Distributrions EPA/600/R-03/029. Available: http://oaspub.epa.gov/eims/eimscomm.getfile?p_download_id=132295 [accessed July 2, 2010].

U.S. EPA. 2007. TRI Dioxin and Dioxin-like Compounds Toxic Equivalency (TEQ) Information Rule. Available: http://www.epa.gov/tri/lawsandregs/teq/teqprule.html [accessed July 7 2010].

U.S. EPA. 2009. Exposure Factors Handbook: 2009 Update EPA/600/R-09/052a. Available: http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=209866 [accessed June 23, 2010].

U.S. EPA. 2010. EPA’s Reanalysis of Key Issues Related to Dioxin Toxicity and Response to NAS Comments (External Review Draft). Available: http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=222203 [accessed July 7, 2010].

USDA. 2009. Dioxins and Dioxin-Like Compounds In the U.S. Domestic Meat and Poultry Supply. Available: http://www.fsis.usda.gov/factsheets/Dioxin_Resources/index.asp [accessed July 1, 2010].

USDA. 2010a. Ground Beef Calculator - User selects fat/lean percentage. Available: http://www.nal.usda.gov/fnic/foodcomp/cgi-bin/measure.pl?MSRE_NO=23999 [accessed July 6 2010].

USDA. 2010b. USDA National Nutrient Database for Standard Reference. Available: http://www.nal.usda.gov/fnic/foodcomp/search/ [accessed July 2 2010].

Van den Berg M, Birnbaum L, Bosveld AT, Brunstrom B, Cook P, Feeley M, et al. 1998. Toxic equivalency factors (TEFs) for PCBs, PCDDs, PCDFs for humans and wildlife. Environ Health Perspect 106(12): 775-92.

Van den Berg M, Birnbaum LS, Denison M, De Vito M, Farland W, Feeley M, et al. 2006. The 2005 World Health Organization reevaluation of human and Mammalian toxic equivalency factors for dioxins and dioxin-like compounds. Toxicol Sci 93(2): 223-41.

Wang RY, Needham LL. 2003. Levels of polychlorinated dibenzo- p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs) and polychlorinated biphenyls (PCBs) in human milk at two US locations [Abstract]. Journal of Toxicology—Clinical Toxicology 41(730).

Wardlaw GM. 1985. Assessing the cancer risk from foods. J Am Diet Assoc 85(9): 1122-7.

Weber R, Gaus C, Tysklind M, Johnston P, Forter M, Hollert H, et al. 2008. Dioxin- and POP-contaminated sites-- contemporary and future relevance and challenges: overview on background, aims and scope of the series. Environ Sci Pollut Res Int 15(5): 363-93.

White SS, Birnbaum LS. 2009. An overview of the effects of dioxins and dioxin-like compounds on vertebrates, as documented in human and ecological epidemiology. J Environ Sci Health C Environ Carcinog Ecotoxicol Rev 27(4): 197-211.

WHO. 2005. Project for the re-evaluation of human and mammalian toxic equivalency factors (TEFs) of dioxins and dioxin-like compounds. Available: http://www.who.int/ipcs/assessment/tef_update/en/ [accessed July 1 2010].

WHO. 2009. Biomonitoring of Human Milk for Persistent Organic Pollutants (POPs). Available: http://www.who.int/foodsafety/chem/pops/en/index.html [accessed July 1, 2010].

WHO. 2010. Dioxins and their effects on human health. Available: http://www.who.int/mediacentre/factsheets/fs225/en/ [accessed June 18 2010].

Wormley DD, Ramesh A, Hood DB. 2004. Environmental contaminant-mixture effects on CNS development, plasticity, and behavior. Toxicol Appl Pharmacol 197(1): 49-65.

 

Dioxin Timeline

EPA'S Dioxin Assessment: No Safety Standard After Nearly Three Decades of Work

Dioxin and related dioxin-like contaminants form as byproducts of processes that involve chlorine and chlorine-containing substances, including pesticide manufacturing and municipal waste incineration.

Scientists first learned of dioxin's toxicity since the late 19th century, when German chemical industry workers exposed to it developed painful, oozing skin lesions known as chloracne. In the 1980s the U.S. Environmental Protection Agency (EPA) began a protracted process in order to issue a comprehensive human health risk assessment for dioxin. To date this process has included four Science Advisory Board (SAB) reviews (1984, 1988, 1995, and 2001) and a National Academy of Sciences review (2006). Plagued by delays forced by pressure from the chemical and defense industries, EPA has not yet completed that assessment.

EPA first declared 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD, often referred to as dioxin) to be a probable human carcinogen in 1985. In 1997 the International Agency for Research on Cancer classified dioxin as "carcinogenic to humans," and in 2001 the National Toxicology Program, a government research agency that is part of the National Institutes of Health, also classified dioxin as a known human carcinogen. EPA has proposed updating its own classification to deem dioxin a definite "human carcinogen." Both the defense and chemical industries are objecting, continuing a decades-long pattern of trying to slow EPA's review and weaken its findings.

The shackling of EPA's efforts to protect public health from dioxin has a long history.

  • 1949: The first recorded case of human exposure in the United States occurs when an explosion at a Monsanto plant exposes more than 200 workers to dioxin-contaminated herbicides, causing severe skin lesions.

  • 1962-1970: The American military in Vietnam extensively sprays Agent Orange, a potent defoliant and herbicide contaminated with dioxin. Decades later, exposed veterans have an increased risk of developing diabetes and multiple cancers.

  • 1971: The entire town of Times Beach, Missouri, is exposed to dioxin from contaminated waste oils spread on dirt roads to suppress dust. Residents are later evacuated and the location is declared a Superfund site. In the same year, scientists at the National Institute of Environmental Health Sciences determine that fetal exposure to dioxin causes developmental abnormalities in laboratory animals, including cleft palates and kidney malformations.

  • 1976: Dioxin is released in an accident at a pesticide manufacturing plant in Seveso, Italy, contaminating people, air, soil and water. Decades later, scientists find adverse effects on reproductive function, including infertility and low sperm counts; lowered male/female sex ratio in newborns; changes in hormones; diabetes; cardiovascular effects; and elevated incidence of certain cancers (Baccarelli 2008; Eskenazi 2010; Mocarelli 2008; Pesatori 2003; Pesatori 2009)

  • 1978: Scientists at Dow Chemical publish the first study of dioxin carcinogenicity in laboratory animals (Kociba 1978). In the same year, the New York Times publishes a story on the plight of residents near Love Canal, N.Y., where industrial dumping released dozens of toxic substances, many suspected carcinogens. Dioxin and dioxin-like chemicals are among them.

  • 1982: EPA's National Human Monitoring Program begins testing Americans' tissues for the presence of dioxin and dioxin-like chemicals, polychlorinated dibenzo-p-dioxins and dibenzofurans (EPA 1987).

  • 1983: Responding to mounting public concern over dioxin contamination, Congress directs the EPA to launch the National Dioxin Study to determine the extent of pollution nationwide (Barnes 1986). The EPA survey focuses on plants producing herbicides, incinerators and waste dumps.

  • 1985: EPA publishes its "Health Assessment Document for Polychlorinated Dibenzo-p-dioxins," classifying dioxin as a known animal carcinogen and probable human carcinogen (EPA 1985). The EPA's Science Advisory Board reviews EPA's assessment, the first of five reviews of dioxin's toxicity and carcinogenicity that SAB conducts between 1985 and 2010. SAB agrees with the EPA's overall approach but calls the evidence for carcinogenicity of dioxins in humans "uncertain" (SAB 1985).

  • 1986: A joint publication of the EPA and the Midwest Research Institute based on EPA biomonitoring data concludes that dioxin-like pollutants "are prevalent in the general U.S. population" (Stanley 1986).

  • 1986: Research by Greenpeace and other activist groups uncovers collusion between EPA and the paper bleaching industry to keep secret the detection of dioxin in discharges from paper mills and in finished paper products (Van Strum & Merrell 1987; Weisskopf 1987).

  • 1987: Leaked documents from the American Paper Institute reveal industry's strategy to "Get EPA to 'rethink' dioxin risk assessment" so as to avoid liability and "unnecessary changes" in production processes prompted by "unsound scientific data" (Weisskopf 1987).

  • 1988-1989: The Science Advisory Board reviews for the second time EPA's dioxin assessment, presented in two draft documents: “A Cancer Risk-specific Dose Estimate for 2,3,7,8-TCDD” and “Estimating Exposure to 2,3,7,8-TCDD” (SAB 1989).

  • 1990: The Chlorine Institute, an industry trade group, starts a public campaign claiming that dioxin is "much less toxic to humans thasn originally believed," misrepresenting scientific opinion on its dangers (Roberts 1991).

  • 1991: EPA administrator Bill Reilly tells The New York Times: "We are now seeing new information on dioxin that suggests a lower risk assessment for dioxin should be applied" (Schneider 1991). EPA launches its second reassessment of dioxin.

  • 1992: The International Joint Commission (IJC) for the U.S. and Canada issues its Sixth Biennial Report on Great Lakes Water Quality, highlighting evidence that the developing fetus is likely more sensitive to toxic contaminants than adults are (IJC 1992).

  • 1994: EPA releases a draft Health Assessment Document for 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) and Related Compounds. The draft assessment concludes that these chemicals may be harmful at levels similar to those found in the general public, increasing the risk of cancer and causing potential damage to the immune, nervous and reproductive systems (EPA 1994).

  • 1995: EPA's Science Advisory Board completes its third review of EPA's dioxin assessment and agrees with the agency that “the margin of safety (between background exposures and levels of exposure where effects have been observed in test animals) for dioxin-like compounds is smaller than the EPA usually sees for many other compounds” (SAB 1995).

  • 1997: The International Agency for Research on Cancer declares dioxin a known human carcinogen (IARC 1997).

  • 1999: The United Nations Environment Programme warns that dioxin is a concern for all countries and drafts an international treaty that would ban, phase out or limit production of 12 "persistent organic pollutants" (POPs). POPs are chemicals that resist degradation, bioaccumulate through the food web and have a variety of adverse effects on human health and the environment. The United Nations POP list includes, among other substances, dioxin and other polychlorinated dioxins and furans (UNEP 1999).

  • 2000: EPA publishes its Draft Final Report on “Exposure and Human Health Reassessment of 2,3,7,8-Tetrachlorodibenzo-P-Dioxin (TCDD) and Related Compounds.”

  • 2000: EPA updates its 1994 draft and submits its revised Dioxin Reassessment to the SAB. This is the SAB's fourth review of the dioxin assessment and culminates in publication of an SAB review document in 2001.

  • 2000: The Food Industry Dioxin Working Group, representing beef producers, food processing, farming and retailing, urges the EPA to revise its dioxin assessment to lessen the chance that the assessment will "create a health scare."

  • 2003: The EPA asks the National Academy of Sciences (NAS) to review the agency's draft dioxin reassessment, “Exposure and Human Health Reassessment of 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) and Related Compounds."

  • 2003: The Food Industry Dioxin Working Group again pushes EPA to delay its dioxin assessment, calling for "additional research, data collection and more comprehensive government coordination... before any government action is contemplated."

  • 2005: Japanese scientists publish a study finding that TCDD and related dioxins cross the human placenta and are detectable in cord blood (Suzuki 2005). EWG scientists report finding dioxin-like compounds in cord blood samples from 10 of 10 newborns tested (EWG 2005), further confirming the transfer of a mother's dioxin load to her child in utero.

  • 2006: NAS publishes its report, “Health Risks from Dioxin and Related Compounds: Evaluation of the EPA Reassessment.” NAS issues a press release titled "EPA assessment of dioxin understates uncertainty about health risks and may overstate human cancer risk" (NAS 2006). In its 2010 draft, EPA has carefully considered the NAS recommendations by documenting alternative assessments; evaluating sources of uncertainty; and providing the rationale for its proposed decisions.

  • 2009: EPA releases its Science Plan for Activities Related to Dioxins in the Environment, promising to “accelerate the long-delayed scientific process to complete the assessment of the health risks dioxins pose to the public” and to publish a final report and assessment by the end of 2010 (EPA 2009).

  • 2009: EPA Administrator Lisa Jackson pledges strong federal action to clean up a dioxin-contaminated Dow Chemical site in Michigan and to accelerate the assessment of dioxins’ human health impacts (EPA 2009; EPA 2010; Melzer 2009).

  • May 2010: The agency publishes “EPA’s Reanalysis of Key Issues Related to Dioxin Toxicity and Response to NAS Comments.” The SAB initiates its fifth review of EPA's dioxin assessment.

  • June 2010: The SAB and EPA announce that the SAB review will be extended into Fall 2010.

  • The chemical industry and the Department of Defense submit extensive comments seeking to delay or weaken the proposed EPA standards for dioxin. Some of the submitted comments include:

    • General Electric Company: "In order for this newly-anticipated dioxin risk assessment scheme to quantify the risk of real-world mixtures of dioxins and dioxin-like compounds, the EPA should, at the very least, attempt to reduce some of the inherent uncertainty by dealing with the clear species differences in TEFs [Toxic Equivalency Factor]. Without such adjustments significant misallocation of limited societal resources will occur in order to address unfounded human health concerns regarding, for example, the safety of the US food supply.

    • American Chemistry Council: "EPA's failure to meet its self-imposed deadline for issuing the Draft Report should not circumvent the public's need for an adequate comment period, and the SAB's need for a complete picture of the relevant science before expert deliberations begin... We urge the Chair of the SAB Dioxin Review Panel to reschedule the July face-to-face meeting until at least two weeks after the close of the public comment period."

    • American Chemistry Council: submits extensive comments on "whether or not EPA consistently and appropriately applied a weight of evidence approach to dioxin toxicity and risk."

    • Department of Defense: "We disagree with the characterization for TCDD as “carcinogenic to humans” for all doses; and believe that two classifications should be presented... We suggest that “carcinogenic to humans” be limited to very high exposures and that lower exposures be classified as “likely to be carcinogenic to humans”.

References for the timeline

Baccarelli A, Giacomini SM, Corbetta C, Landi MT, Bonzini M, Consonni D, et al. 2008. Neonatal thyroid function in Seveso 25 years after maternal exposure to dioxin. PLoS Med 5(7): e161.

Barnes D, McBride A, Jaworski N, Harless R, Dupuy A. 1986. A status report on the U.S. national dioxin study. Chemosphere 15(9-12): 1401-04.

EPA. 1985. Health Assessment Document for Polychlorinated Dibenzo-P-Dioxins EPA/600/8-84/014F. Available: http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=38484

EPA. 1987. National Human Adipose Tissue Survey (NHATS). Available: http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=55204

EPA. 1994. Health assessment document for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related compounds EPA/600/BP-92/001c. Available: http://cfpub.epa.gov/ncea/CFM/nceaQFind.cfm?keyword=Dioxin

EPA. 2009. News Releases – Research. EPA Administrator Pledges Strong Federal Cleanup Presence at Dow Dioxin Site in Michigan and Accelerated Assessment of Dioxins’ Human Health Impacts. Available: http://yosemite.epa.gov/opa/admpress.nsf/48f0fa7dd51f9e9885257359003f5342/3ffa6e8e70763f28852575c20064b26b! OpenDocument

EPA. 2010. Seven Priorities for EPA’s Future. Available: http://blog.epa.gov/administrator/2010/01/12/seven-priorities-for-epas-future/

Eskenazi B, Warner M, Marks AR, Samuels S, Needham L, Brambilla P, et al. 2010. Serum dioxin concentrations and time to pregnancy. Epidemiology 21(2): 224-31.

IARC (International Agency for Research on Cancer). 1997. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. Volume 69. Polychlorinated Dibenzo-para-Dioxins and Polychlorinated Dibenzofurans. Available: monographs.iarc.fr/ENG/Monographs/vol69/volume69.pdf

IJC. 1992. International Joint Commission. Sixth Biennial Report Under the Great Lakes Water Quality Agreement of 1978 to the Governments of the United States and Canada and the State and Provincial Governments of the Great Lakes Basin. Available: http://www.ijc.org/php/publications/html/6bre.html

Kociba RJ, Keyes DG, Beyer JE, Carreon RM, Wade CE, Dittenber DA, et al. 1978. Results of a two-year chronic toxicity and oncogenicity study of 2,3,7,8-tetrachlorodibenzo-p-dioxin in rats. Toxicol Appl Pharmacol 46(2): 279-303.

Melzer EJ. 2009. EPA pledges ‘expeditious action’ on Dow dioxin clean-up, but Superfund status not in the works. The Michigan Messenger 5/27/09. Available: http://michiganmessenger.com/19834/epa-pledges-expeditious-action-on-dow-dioxin-clean-up-but-superfund-status-not-in-the-works

Mocarelli P, Gerthoux PM, Patterson DG, Jr., Milani S, Limonta G, Bertona M, et al. 2008. Dioxin exposure, from infancy through puberty, produces endocrine disruption and affects human semen quality. Environ Health Perspect 116(1): 70-7.

NAS. 2006. EPA assessment of dioxin understates uncertainty about health risks and may overstate human cancer risk. Available: http://www8.nationalacademies.org/onpinews/newsitem.aspx?RecordID=11688

NTP. 2005. National Toxicology Program 11th Report on Carcinogens. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD); "Dioxin". Available: http://ntp.niehs.nih.gov/index.cfm?objectid=32BA9724-F1F6-975E-7FCE50709CB4C932

Pesatori AC, Consonni D, Bachetti S, Zocchetti C, Bonzini M, Baccarelli A, et al. 2003. Short- and long-term morbidity and mortality in the population exposed to dioxin after the "Seveso accident". Ind Health 41(3): 127-38.

Pesatori AC, Consonni D, Rubagotti M, Grillo P, Bertazzi PA. 2009. Cancer incidence in the population exposed to dioxin after the "Seveso accident": twenty years of follow-up. Environ Health 8: 39.

Roberts L. 1991. Flap Erupts Over Dioxin Meeting. Science 251(22 February): 866-67.

SAB. 1985. Technical Report of the Environmental Health Committee of EPA's Science Advisory Board Regarding a Draft Health Assessment Document for Polychlorinated Dibenzo-p-dioxins EPA-SAB-EHC-85-009. Available: http://yosemite.epa.gov/sab/sabproduct.nsf/WebBOARD/advisoryreports?OpenDocument

SAB. 1989. Letter from Raymond C. Loehr, Ph.D., Chair, Executive Committee, Science Advisory Board to Mr. William Reilly, Administrator, US Environmental Protection Agency. EPA-SAB-EC-90-003.

SAB. 1995. Letter from Dr. Genevieve Matanoski, Chair, Science Advisory Board, to Honorable Carol M. Browner, Administrator, U.S. Environmental Protection Agency regarding Science Advisory Board's review of the Draft Dioxin Exposure and Health Effects Reassessment Documents, "A Second Look at Dioxin." EPA-SAB-EC-95-021. Available: http://cfpub.epa.gov/ncea/CFM/nceaQFind.cfm?keyword=Dioxin

Schneider K. 1991. U.S. Backing Away from Saying Dioxin is a Deadly Peril. New York Times, August 12 1991.

Stanley JS, Boggess KE, Onstot J, Sack TM, Remmers JC, Breen J, et al. 1986. PCDDs and PCDFs in human adipose tissue from the EPA FY82 NHATS repository. Chemosphere 15(9-12): 1605-12.

Suzuki G, Nakano M, Nakano S. 2005. Distribution of PCDDs/PCDFs and Co-PCBs in human maternal blood, cord blood, placenta, milk, and adipose tissue: dioxins showing high toxic equivalency factor accumulate in the placenta. Biosci Biotechnol Biochem 69(10): 1836-47.

UNEP. 1999. UNEP executive director urges global action on dioxin, and other POPs. New Report Issued on Dioxin, Furan Inventories. Available: http://www.chem.unep.ch/Pops/POPs_Inc/press_releases/pressrel-99/unepnr99-69.htm

Van Strum C, Merrell P. 1987. No Margin of Safety: A Preliminary Report on Dioxin Pollution and the Need for Emergency Action in the Pulp and Paper Industry. Washington, DC: Greenpeace.

Weisskopf M. 1987. Paper Industry Campaign Defused Reaction to Dioxin Contamination. Washington Post October 25, 1987 (Washington, DC).

 

EWG Research on Dioxin

Environmental Working Group research on the ubiquity of dioxin in the human body, and the potential health risks from these exposures that begin in utero, is summarized below.

January 2012 — EWG calls on EPA to Finish Assessment of Dioxin Toxicity

EWG letter to EPA administrator Jackson. Click here to download PDF.

Febuary 2011 — EWG to Dioxin Review Panel

EWG Comments to Dioxin Review Panel

October 2010 — EWG to EPA: Put public health first.

EWG urges EPA’s Science Advisory Board to support the agency’s efforts to finally set a health standard for dioxin, a critical first step to protecting public health from this common food pollutant.

EWG Comments to EPA science board

July 2010 — EWG to EPA: Three decades is long enough.

EWG analysis finds that nursing infants swallow up to 77 times more dioxin than EPA believes is safe; EWG urges EPA to finalize its dioxin assessment begun nearly 30 years ago. Read EWG's analysis, presented to the EPA's Science Advisory Board during its fifth review of EPA's dioxin analysis.

EWG Comments to EPA science board | News release

2003-2009 — Dioxin pollution in people

EWG's body burden studies have found dioxin and other chlorinated dioxins and furans in blood samples from 34 of 34 Americans tested, including cord blood samples collected from 20 newborns at the moment of birth.