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Is Dioxin dangerous?

Adverse Health Effects of Dioxin in Humans ( a few examples from around the world )

bullet Figure 5- Breast cancer cases per 100,000 females, and purely spatial clustersClick here to view study which indicates locally high breast cancer cases and elevated dioxin soil levels in Midland and Tittabawassee flood plain may be related
bulletClick here to listen to more from Dr. Linda Birnbaum of the EPA describing dioxin and its effects on humans.
bullet Click here to view the The Long Shadow documentary chronicling the dioxin discovery and the subsequent river residents plight.
bullet It's not just dioxin anymore, click here to see what's the EPA says in the Tittabawassee River besides contaminated fish.

Effects on children
Immune System New
Respiratory System 
Endocrine System  
Reproductive System  
Mechanism of action
Risk Characterization
Body Burdens
Other concerns

American Peoples Dioxin

EPA "Dioxin, are we at risk?"

CHEJ Dioxin Research References
TASC Dioxin Research References
TASC Dioxin and Cancer References

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To counter all the recent misinformation being feed the local community, the following is a summary of dioxins effects on human health as presented on the Coming Clean sites Body Burden Dioxin Case study page.

Exposure to dioxin can lead to a wide array of adverse health effects including cancer, birth defects, diabetes, learning and developmental delays, endometriosis, and immune system abnormalities. 

Dioxin is a known carcinogen. IARC, the International Agency for Research on Cancer, which is part of the World Health Organization, classified it as a known human carcinogen in 1997. In January 2001, the Department of Health and Human Services' National Toxicology Program classified dioxin as a known human carcinogen. The September 2000 draft of the U.S. EPA's Health Assessment document on dioxin also classifies dioxin as a known human carcinogen. In that same report, the U.S. EPA projected an excess cancer risk of one in 100 for the most sensitive people who consume a diet high in animal fats. In other words, the risk of getting cancer from dioxin--over and above the risk of cancer from other sources—is one in 100 for some people. This is a worst-case scenario. It's for the most sensitive people among the five percent of the population who consume the most dioxin. For the average person, EPA estimates a risk level of one in 1,000, which is also a serious risk level. The EPA’s generally "acceptable" risk level is one-in-one-million.

Dioxin also causes a wide range of non-cancer effects including reproductive, developmental, immunological, and endocrine effects in both animals and humans. Animal studies show that dioxin exposure is associated with endometriosis, decreased fertility, inability to carry pregnancies to term, lowered testosterone levels, decreased sperm counts, birth defects, and learning disabilities. In children, dioxin exposure has been associated with IQ deficits, delays in psychomotor and neurodevelopment, and altered behavior including hyperactivity. Studies in workers have found lowered testosterone levels, decreased testes size, and birth defects in offspring of Vietnam veterans exposed to Agent Orange.

Effects on the immune system appear to be among the most sensitive endpoints studied. Animal studies show that dioxin decreased immune response and increased susceptibility to infectious disease. In human studies, dioxin was associated with immune system depression and alterations in immune status leading to increased infections. Dioxin can also disrupt the normal function of hormones—chemical messengers that the body uses for growth and regulation. Dioxin interferes with thyroid levels in infants and adults, alters glucose tolerance, and has been linked to diabetes.

A 2005 study of humans finds epidemiological evidence of an association between increased PCDD/PCDF and PCB body burden and endometriosis.

10/24/09  VA adds three more diseases associated with Agent Orange

New to the list:

bulletB Cell Leukemia's, such as “Hairy Cell Leukemia”
bulletParkinson’s Disease
bulletIschemic Heart Disease: Any condition in which heart muscle is damaged or works inefficiently because of an absence or relative deficiency of its blood supply; most often caused by atherosclerosis, it includes angina pectoris, acute myocardial infarction, chronic ischemic heart disease, and sudden death
Previous list:
bulletAcute and Subacute Transient Peripheral Neuropathy: A nervous system condition that causes numbness, tingling and motor weakness.
bulletAL Amyloidosis: A rare disease caused when an abnormal protein, amyloid, enters tissues or organs.
bulletChloracne: A skin condition that occurs soon after dioxin exposure and looks like common forms of acne seen in teenagers.
bulletChronic Lymphocytic Leukemia: A disease that progresses slowly with increasing production of excessive numbers of white blood cells.
bulletDiabetes Mellitus (Type 2): A disease characterized by high blood sugar levels from the body’s inability to respond properly to the hormone insulin.
bulletHodgkin’s Disease: A malignant lymphoma (cancer) characterized by progressive enlargement of the lymph nodes, liver and spleen, and by progressive anemia.
bulletMultiple Myeloma: A cancer of specific bone marrow cells that is characterized by bone marrow tumors in various bones of the body.
bulletNon-Hodgkin’s Lymphoma: A group of cancers that affect the lymph glands and other lymphatic tissue.
bulletPorphyria Cutanea Tarda: A disorder characterized by liver dysfunction and by thinning and blistering of the skin in sun-exposed areas.
bulletProstate cancer: Cancer of the prostate, one of the most common cancers among men.
bulletRespiratory cancers: Cancers of the lung, larynx, trachea and bronchus.
bulletSoft tissue Sarcoma: A group of different types of cancers in body tissues such as muscle, fat, blood and lymph vessels and connective tissues.

Source: York News Times


Dioxins effects on children

bulletWhy be concerned about dioxin? "For the children"

"Dioxin concerns me, the more I read about it, the more concerned I become.  Why am I here?  I can sum it up in three words - for the children." Dr. Suzanne White, M.D., Medical director for Children's Hospital of Michigan Regional Poison Control Center Detroit, MichiganDr.

Whites comments where made during her presentation at the Freeland High School public meeting hosted by the MDCH August 20, 2003.

Dr. White went on to say:

bulletthat dioxin especially can interfere with childhood development and have lifelong consequences.  There is even a hazard to a child playing the the back yard if the soil has high dioxin content.
bulletisolated studies suggest dioxin can increase a person's chances of getting cancer by 40 to 100 percent.
bulletdata shows a higher than expected incidence of cancer near Midland.
bulletmany studies show a link between the substance and cancer and birth defects in humans as well as a host of other ailments.

Click here for the powerpoint presentation used during the meeting.

Her recommendations to limit exposure: do not eat fish caught in river, washing and peeling produce grown near river, and discouraging children from placing toys or dirty items in their mouths.  For additional precautions recommended by the Michigan Department of Agriculture, click here.

bulletIt should also be noted that the head of the ATSDR, Dr. Henry Falk, M.D.  attended the meeting to make a presentation and to meet with local residents to hear their concerns.  The following day he made a tour to the entire flood plain as well as Dow Chemicals Midland plant.  During his presentation, Dr. Falk said his agency receives 400-500 new cases each year.  He went on to say that he personally could not visit every site and therefore limited visits to those sites with the greatest potential for exposing the public to harm.
bulletState MDEQ warns schools to limit children's exposure to park soils
In a letter dated 12/3/03, the MDEQ notified schools in the area to plan activities so that students are not in direct contact with dioxin laden soils.  The soils of frequently flood parks located in the Tittabawassee River flood plain  have been found by the MDEQ to contain dioxin contamination with levles almost 38 times the states Residential Direct Contact Criteria of 90 ppt. 
bulletClick here for levels discovered in Phase 2 sampling. 
bulletEffects of prenatal exposure (before birth while in mother's womb)
bulletThe health effects most likely to be associated with low level exposures relate to the developing embryo/fetus
bulletDioxin possible cause of Attention Deficit Hyperactivity Disorders (ADD or ADHD)

In the January 1998 issue of the scientific journal Toxicology and Industrial Health, Dr. Peter Hauser and colleagues summarize recent studies that suggest links between perinatal exposure to dioxin-like substances and developmental abnormalities in learning and attention. They propose that the genetic condition known as resistance to thyroid hormone (RTH) may be a useful model for further study of the disruptive effects of dioxin and PCBs on brain development.

Hauser is professor of psychiatry at the UM School of Medicine and chief of psychiatry at the Baltimore Veterans Affairs Medical Center. Co-authors are Drs. J. Michael McMillin and Vinod S. Bhatara of the University of South Dakota School of Medicine.

Thyroid hormone plays an essential role in prenatal brain growth and development, as well as in normal behavioral and intellectual development. Even moderate impairment of thyroid hormone function has been associated with various problems in behavioral and intellectual development, and certain thyroid diseases such as RTH are associated with attention deficit hyperactivity disorder (ADD or ADHD) and language disorders.   Click here for details.

bulletEffects of prenatal PCB and dioxin background exposure on cognitive and motor abilities in Dutch children at school age.  Click here for copy of article as published in  January 2002 Journal of Pediatrics, Volume 140 number 1

Neurotoxic effects of prenatal PCB and dioxin exposure may persist into school age, resulting in subtle cognitive and motor developmental delays. More optimal intellectual stimulation provided by a more advantageous parental and home environment may counteract these effects of prenatal exposure to PCBs and dioxins on cognitive and motor abilities. (J Pediatr 2002;140:48-56)

bulletPerhaps the most important, and most disturbing, new evidence about dioxin's toxicity is the neurodevelopmental and reproductive effects observed in children.  Read the entire report Dioxin: Children are most vulnerable 
bullet Body Burdens: The pollution in newborns

A benchmark investigation of industrial chemicals, pollutants and pesticides in umbilical cord blood by the Environmental Working Group, July 14, 2005:

bulletA developing child's chemical exposures are greater pound-for-pound than those of adults.
bulletAn immature, porous blood-brain barrier allows greater chemical exposures to the developing brain.
bulletChildren have lower levels of some chemical-binding proteins, allowing more of a chemical to reach "target organs."
bulletA baby's organs and systems are rapidly developing, and thus are often more vulnerable to damage from chemical exposure.
bulletSystems that detoxify and excrete industrial chemicals are not fully developed.
bulletThe longer future life span of a child compared to an adult allows more time for adverse effects to arise.

Breast Milk: "When a woman becomes pregnant, the dioxins in her body can cause irreversible changes in the development of the central nervous system, immune system, reproductive system and endocrine system of the fetus. The dioxins in a woman’s body are also passed to her nursing infant in her milk"    Listen to the EPA's Dr. Linda Birnbaum's comments on this topic, click here

The above are excerpts from Green Peace's report on the global effort to eliminate the sources of dioxin worldwide.  Chapter 8 (page 30) focuses on Dioxin and it's effect on human health.  Read the entire report Dioxin Elimination (pdf)

bulletTooth Development in children.

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In the Jan. 16 1999 Lancet, Alaluusua's team reports that children who had encountered the most dioxin in their mother's milk had the highest rate of these tooth defects. Breast-milk exposure to polychlorinated biphenyls, another group of dioxin-like chemicals, played little if any role.  Article published in Science News Online

bulletIn addition to being carcinogenic, dioxin disrupts the way human hormones and chromosomes work.  Because of its endocrine-disrupting qualities, dioxin also causes a host of other illnesses and problems, including reproductive, neurotoxic, immune system, other hormonal and developmental effects.  Remember that most literature on dioxin's health effect is based on exposure levels of the "General Population" via the food chain.  Would you consider yourself the "General Population" when levels in the vicinity of your back yard have been recorded as the HIGHEST ever found in Michigan & up to 80 times the level for which the MDEQ recommends cleanup?   Many opinions exist on whether the health effects are demonstrated in High or Low levels of exposure or somewhere in-between.  Which ones are correct?  A properly conducted Health Study may provide insight into the answer.  Then again, it may find it's conclusion "Indeterminate".  Until then, follow recommended guidelines to reduce your exposure in the MDCH Dioxin Fact Sheet.pdf, Information about dioxin and the Tittabawassee river flood plain, and MDA Food and gardening dioxin guide  brochures.
bullet"The appropriate way to view dioxin is as a modulator of growth and development. … Dioxin appears to perturb normal homeostasis and hormonal balance leading to alterations in proliferation and differentiation. In the adult, such changes may lead to cancer, immunosuppression, chloracne, and endometriosis." 


bullet08/03/11  New dioxin cancer risk study of women in the Seveso Italy supports report of Breast Cancer increase in Midland and Tittabawassee River area?

 "Dioxin Exposure and Cancer Risk in the Seveso Women’s Health Study", a recent peer reviewed paper published by the National Institute of Public Health, provides an update on it's  study of 800+ women exposed to the highest levels of dioxin in a human population on July 10, 1976, during a chemical plant explosion in Seveso, Italy" 

"Individual serum TCDD is significantly positively related with all cancer incidence in the SWHS cohort, more than 30 years later. This all-female study adds to the epidemiologic evidence that TCDD is a multi-site carcinogen. "

The study seems to reinforce the conclusion of another peer reviewed study published in April 2011 (see TRW Current News 4/2/11) which identified higher breast cancer rates in women living in the city of Midland and in the vicinity of the Tittabawassee River:

"These findings suggest that increased breast cancer incidences are spatially associated with soil dioxin contamination. Aging is a substantial factor in the development of breast cancer. Findings can be used for heightened surveillance and education, as well as formulating new study hypotheses for further research."




Dioxin Exposure and Cancer Risk in the Seveso Women’s Health Study

Background: 2,3,7,8-Tetrachlorodibenzo-para-dioxin (TCDD), a widespread environmental contaminant, disrupts multiple endocrine pathways. The International Agency for Research on Cancer classified TCDD as a known human carcinogen, based upon predominantly male occupational studies of increased mortality from all cancers combined.

Objectives: After a chemical explosion on July 10, 1976, in Seveso, Italy, residents experienced some of the highest levels of TCDD exposure in a human population. In 1996, we initiated the Seveso Women’s Health Study (SWHS), a retrospective cohort study of the reproductive health of the women. We previously reported a significant increased risk for breast cancer and a non-significant increased risk for all cancers combined with individual serum TCDD, but the cohort averaged only 40 years old in 1996. Herein we report results for risk of cancer from a subsequent follow-up of the cohort in 2008.

Methods: In 1996, we enrolled 981 women who were 0 to 40 years in 1976, lived in the most contaminated areas, and had archived sera collected near the explosion. Individual TCDD concentration was measured in archived serum by high-resolution mass spectrometry. A total of 833 women participated in the 2008 follow-up study. We examined the relation of serum TCDD with cancer incidence using Cox proportional hazards models.

Results: In total, 66 (6.7%) women had been diagnosed with cancer. The adjusted hazard ratio (adj-HR) associated with a ten-fold increase in serum TCDD for all cancers combined was significantly increased (adj-HR=1.80 (95% CI 1.29, 2.52)). For breast cancer, the HR was increased, but not significantly ((adj-HR=1.44 (95% CI 0.89, 2.33)).

Conclusions: Individual serum TCDD is significantly positively related with all cancer incidence in the SWHS cohort, more than 30 years later. This all-female study adds to the epidemiologic evidence that TCDD is a multi-site carcinogen.


10/21/08 Local breast cancer rates elevated, study finds statistical relationship to elevated dioxin levels

Spatial variations in the incidence of breast cancer and potential risks associated with soil dioxin contamination in Midland, Saginaw, and Bay Counties, Michigan, USA

Dajun Dai  and Tonny J Oyana

Environmental Health 2008, 7:49doi:10.1186/1476-069X-7-49

Published: 21 October 2008

Abstract (provisional)

Figure 5- Breast cancer cases per 100,000 females, and purely spatial clustersBackground

High levels of dioxins in soil and higher-than-average body burdens of dioxins in local residents have been found in the city of Midland and the Tittabawassee River floodplain in Michigan. The objective of this study is threefold: (1) to evaluate dioxin levels in soils; (2) to evaluate the spatial variations in breast cancer incidence in Midland, Saginaw, and Bay Counties in Michigan; (3) to evaluate whether breast cancer rates are spatially associated with the dioxin contamination areas.


We acquired 532 published soil dioxin data samples collected from 1995 to 2003 and data pertaining to female breast cancer cases (n = 4,604) at ZIP code level in Midland, Saginaw, and Bay Counties for years 1985 through 2002. Descriptive statistics and self-organizing map algorithm were used to evaluate dioxin levels in soils. Geographic information systems techniques, the Kulldorff's spatial and space-time scan statistics, and genetic algorithms were used to explore the variation in the incidence of breast cancer in space and space-time. Odds ratio and their corresponding 95% confidence intervals, with adjustment for age, were used to investigate a spatial association between breast cancer incidence and soil dioxin contamination.


High levels of dioxin in soils were observed in the city of Midland and the Tittabawassee River 100-year floodplain. After adjusting for age, we observed high breast cancer incidence rates and detected the presence of spatial clusters in the city of Midland, the confluence area of the Tittabawassee, and Saginaw Rivers. After accounting for spatiotemporal variations, we observed a spatial cluster of breast cancer incidence in Midland between 1985 and 1993. The odds ratio further suggests a statistically significant (alpha = 0.05) increased breast cancer rate as women get older, and a higher disease burden in Midland and the surrounding areas in close proximity to the dioxin contaminated areas.


These findings suggest that increased breast cancer incidences are spatially associated with soil dioxin contamination. Aging is a substantial factor in the development of breast cancer. Findings can be used for heightened surveillance and education, as well as formulating new study hypotheses for further research.

Click here to view Environmental Health website posting of this study and peer review comments

Click here to view complete study


bullet 4/19/05 EPA finds breast cancer link from dioxin
EPA research on three high-profile pollutants -- dioxin, atrazine and perfluorooctanoic acid (PFOA) -- suggests a link to the trend of early puberty among U.S. girls, and one agency scientist involved in the studies says the findings may also shed light on breast cancer risk factors.

The findings could result in the compounds being given a high priority in the agency’s Endocrine Disruptor Screening Program (EDSP), for which the agency is still developing a research strategy. In the studies, carried out by the Office of Research and Development (ORD), female mice subjected to prenatal exposure to each of the substances demonstrated an effect on mammary gland development, said ORD researcher Suzanne Fenton in a presentation of the findings at the Society of Toxicology’s annual meeting March 7.

Source: Superfund Report via
Date: March 28, 2005
Issue: Vol. 19, No. 7
Inside Washington Publishers

bullet 7/12/04  New evidence supports IARC classification as Class I carcinogen

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. In Press. doi:10.1289/ehp.7219 (available at

In 1997 the International Agency for Research on Cancer (IARC) classified 2,3,7,8-TCDD

(tetrachlorodibenzo-para-dioxin, the most potent dioxin congener, hereafter referred to as simply TCDD) as a Group 1 carcinogen based on limited evidence in humans, sufficient evidence in experimental animals, and extensive mechanistic information indicating that TCDD acts through a mechanism involving the Ah receptor which is present in both humans and animals. The judgment of limited evidence in humans was based primarily on an elevation of all cancers combined in four industrial cohorts. The Class 1 classification has been somewhat controversial, and has been challenged in the literature in recent years. Here we review the epidemiologic and mechanistic evidence which has emerged since 1997. New epidemiologic evidence consists primarily of positive exposure-response analyses is several of the industrial cohorts, as well as evidence of excesses from several specific cancers in the Seveso accident cohort. There are also new data regarding how the Ah receptor functions in mediating the carcinogenic response to TCDD. We conclude that the new evidence generally supports the 1997 IARC classification.

bulletCancer Risk; Re-analysis of data finds no evidence of dioxin cancer threshold

Recently published paper (Oct 2003) found no threshold for dioxin's cancer causing effects, in other words, there is no level below which one can say dioxin is safe.    Click here for details

The researchers concluded: "We have reexamined the threshold analysis and found that the data have been incorrectly weighted by cohort size. In our reanalysis, without the incorrect weighting, the threshold effect disappears."

Environ Health Perspect 2003;111(9):1145-1147)

bulletRisk of soft tissue sarcomas and residence in the neighbourhood of an incinerator of industrial wastes.
bulletAuthors: Comba P ; Ascoli V ; Belli S ; Benedetti M ; Gatti L ; Ricci P ; Tieghi A 
        Affiliation: National Institute of Health (ISS), Viale Regina Elena 299, 00161 Rome, Italy.
bulletSource: Occup Environ Med (Occupational and environmental medicine.) 2003 Sep; 60(9): 680-3
Additional Info: England
bulletStandard No: ISSN: 1351-0711; NLM Unique Journal Identifier: 9422759
bulletAbstract: AIMS: To investigate the association between occurrence of soft tissue sarcomas (STS) in Mantua and residence near an incinerator of industrial wastes. METHODS: Cases were subjects with histologically confirmed primary malignant STS diagnosed 1989-98 in the population resident in Mantua and in the three neighbouring municipalities. Controls were randomly extracted from population registries, matched for age and sex. Residential history was reconstructed for all study subjects since 1960. Main residence was geographically positioned according to GPS standards. RESULTS: The study included 37 STS cases (17 men and 20 women) and 171 controls. The incidence of STS in the area of study was estimated as 8.8 per 100 000 in men and 5.6 per 100 000 in women. The odds ratio associated with residence within 2 km, standardised by age and sex, was 31.4 (95% CI 5.6 to 176.1), based on five exposed cases. At greater distances, risk rapidly decreased, showing a fluctuation around the null value of 1. CONCLUSION: The study shows a significant increase in risk of STS associated with residence within 2 km of an industrial waste incinerator; an aetiological role of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) can be hypothesised.
bulletJune 2003: National Toxicology Program Lists Dioxin As a Known Human Carcinogen

This past January, the National Toxicology Program announced an addendum to
the Ninth Report on Carcinogens adding dioxin to the list of substances it
considers "known to be human carcinogens." The NTP had planned to reclassify
dioxin as a known human carcinogen when the original report was released in
May 2000 but was prevented from doing so by a lawsuit filed by Jim Tozzi,
former OMB staffer and frequent industry consultant. The lawsuit was
dismissed by the U.S. Court of Appeals for the District of Columbia. The NTP
is the second major international scientific body, following the World
Health Organization's International Agency for Research on Cancer (IARC), to
declare that dioxin is a human carcinogen. The U.S. EPA has come to the same
conclusion in its draft reassessment report on dioxin.  Click here for all the details (pdf file)
bulletJune 2003: Cancer Rates in Seveso Are Up

The latest update on the health of residents of Seveso, Italy, who were
exposed to dioxin from an explosion at a pesticide manufacturing plant in
1976, was released in June. The study shows that people who lived in the
areas of highest exposure died more often from cancer than an unexposed
population and that there was an excess of leukemia and Non-Hodgkins
lymphoma. The incidence of diabetes was also higher, as was chronic
circulatory and respiratory disease. These cancer findings further support
the EPA's decision to classify dioxin as a human carcinogen. See Bertazzi,
P.A.,et al., "Health effects of dioxin exposure: A 20-year mortality study,"
American Journal of Epidemiology, 153 (11): 1031-1044, June 1, 2001.

bulletFollow-up study in Seveso indicates breast cancer risks increased significantly.

Warner et al. found that a 10-fold increase in dioxin levels was associated with a 2.1 increase in risk for breast cancer. Despite the small number of cases, the increase was statistically significant.   

Previous work in the aftermath of the 1976 Seveso, Italy, pesticide factory accident failed to establish links between dioxin exposure and breast cancer incidence. This new study of Seveso residents by Warner et al. finds that breast cancer risk increases significantly with higher dioxin exposures. The authors suggest that an earlier study, covering only the first decade after the accident, had not allowed sufficient time to pass since exposure for dioxin's impacts to be manifest.

Click her for all the details

Authors:  Warner, M, B Eskenazi, P Mocarelli, PM Gerthoux, S Samuels and L Needham. 2002. Serum Dioxin Concentrations and Breast Cancer Risk in the Seveso Women’s Health Study. Environmental Health Perspectives 110:625–628.

TRW note:

The EPA estimated body burden for the general population in the  USA ranges from 10 - 40 ppt TEQ.  Research in the   EPA and the CHEJ American Dioxin Report indicates people who live near dioxin release sites, children, nursing infants, and people who eat fish as a main staple of their diet are likely to be exposed to at least 3 - 10 times as much dioxin as the general populaiton.  Simple extrapolation of these numbers indicate serum TCDD levels of some floodplain residents will be in the range of 30-400 ppt TEQ.  While it's true the Seveso event exposed people to very high levels of dioxin, the low end of the studies TCDD serum range suggests breast cancer risks at contamination levels found in the Tittabawasse flood plain and the city of Midland.

Do you want to wait 30 years to find out if this is true in our area?  There is a viable alternative to Dow's "risk assessment science", it's called the "Precautionary Principle", please read it and then get out there and promote it!.  The precautionary system urges a "better safe than sorry" approach to decisions instead of the risk assessment method of "barging ahead until you can line up the dead bodies".   Polluting Corporations hate the precautionary principle and are spending a lot of time & money to counteract it.   Let's help Dow find the right way to protect the community they contaminated: Dow, clean it up NOW!

bulletShort- and long-term morbidity and mortality in the population exposed to dioxin after the "Seveso accident".
bulletSource: Ind Health (Industrial health.) 2003 Jul; 41(3): 127-38
Additional Info: Japan
bulletStandard No: ISSN: 0019-8366; NLM Unique Journal Identifier: 2985065R
bulletAbstract: The early effects of 2,3,7,8-tetrachlorodibenzo-para-dioxin (TCDD) exposure in the population involved in the Seveso, Italy, incident in 1976, have been examined in numerous studies. Chloracne was the only effect linked with sufficient certainty to dioxin exposure. The possible long-term consequences were investigated with mortality and cancer incidence studies. Mortality and morbidity findings during the 20-year period following the accident showed increased risk from lymphoemopoietic neoplasm, digestive system cancer (rectum in males, and biliary tract among females, in particular) and respiratory system cancer (lung, among males). In the incidence analyses, also thyroid gland and pleura cancer appeared suggestively increased. Soft tissue sarcomas showed an increase in the largest, yet least exposed, exposure sub-cohort. Several hypotheses associating non-cancer effects with dioxin exposure were corroborated by findings in the Seveso population: this was the case with cardiovascular effects (possibly linked to both chemical exposure and stressful disaster experience), endocrine effects (diabetes among females) and reproductive effects: exposure of men to TCDD was linked to a lowered male/female sex ratio in their offspring. The results of many Seveso studies point to possible gender effects, in accordance with animal models. Notwithstanding the acknowledged study limitations (lack of individual exposure markers, short latency, and small population size for certain cancer types), results of previous experimental and epidemiological studies, along with mechanistic knowledge on dioxin toxicity, support the hypotheses that the observed excesses might be associated with dioxin exposure. The mortality and cancer incidence follow-up of the Seveso cohort are continuing
bulletCancer and Developmental Exposure to Endocrine Disruptors

Linda S. Birnbaum1 and Suzanne E. Fenton2

1Experimental Toxicology and 2Reproductive Toxicology Divisions, National Health and Environmental Effects Research Laboratory, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina, USAAbstract
Developing organisms have increased susceptibility to cancer if they are exposed to environmental toxicants during rapid growth and differentiation. Human studies have demonstrated clear increases in cancer after prenatal exposure to ionizing radiation, and there is suggestive evidence that brain tumors and leukemia are associated with parental exposures to chemicals. Animal experiments have demonstrated increased tumor formation induced by prenatal or neonatal exposure to a variety of chemicals, including direct-acting carcinogens and drugs. Recently, natural estrogens have been classified as known human carcinogens. Prenatal exposure to natural and synthetic estrogens is associated with increases in breast and vaginal tumors in humans as well as uterine tumors in animals. Synthetic halogenated chemicals increase liver tumors after early life-stage exposure. Recently, a prototypical endocrine-disrupting compound, 2,3,7,8-tetrachlorodibenzo-p-dioxin, has been shown to be a developmental toxicant of the mammary gland in rodents. Dioxin alters multiple endocrine systems, and its effects on the developing breast involve delayed proliferation and differentiation of the mammary gland, as well as an elongation of the window of sensitivity to potential carcinogens. Implications of these new findings suggest that causes of endocrine-related cancers or susceptibility to cancer may be a result of developmental exposures rather than exposures existing at or near the time of tumor detection. Key words: animal models, atrazine, carcinogenesis, childhood cancers, development, dioxin, endocrine disrupters.

bulletIn February 1997, the International Agency for Cancer Research confirmed 2,3,7,8 TCDD Dioxin as a Class 1 carcinogen.  A 1996 study by the National Research Council estimates dioxin to be 300,000 times more carcinogenic than DDT.   Many cancers are associated with these organochlorines, especially soft tissue and hormone-related cancers.  A 1999 German study concluded that dioxin may be responsible for 12% of all human cancers in industrialized countries.
bullet2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) inhibits growth factor withdrawal-induced apoptosis in the human mammary epithelial cell linDavis JW 2nd, Melendez K, Salas VM, Lauer FT, Burchiel SW. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) inhibits growth factor withdrawal-induced apoptosis in the human mammary epithelial cell line, MCF-10A. Carcinogenesis 2000 May;21(5):881-6 Toxicology Program, The University of New Mexico College of Pharmacy, Albuquerque, NM 87131
bullet10/07/05 Death comes to  Midland?

While corporations crank up the PR and politicians ponder and labor over their next steps, and
we fight our daily environmental battles, we often forget that real people with families and children
are the victims of the chemical trespass we are all forced to live in. My hope is that Dave will continue
to share these stories with all of us. Dave Linhardt is author of

Michelle Hurd Riddick
Lone Tree Council


Dow's mortality studies provide ample evidence that employee death rates from certain cancers are elevated,
some being statistically significant. Due to a lack of data, we do not know if a similar increase in mortality
 has been experienced by persons living in Midland and riverside neighborhoods which have high levels of
dioxin contamination.

Statistics have definite value but they do not provide any information about the persons that died prematurely
or the pain and loss suffered by their family and friends. In fact, "medical privacy" laws prohibit the release of
personal information. Perhaps, if a name and a history was associated with each premature death, the long
 overdue correct action would have been already implemented.

In the spring, I placed an ad in the Midland Daily News requesting contact with anyone that believes his/her
 illness or a death is related to dioxin exposure. The response was far greater than expected.

From time to time, I would like to share what I know about a person whose death may have been related
to dioxin exposure and whose death came too early.

Let me introduce you to "Sarah"

Dave Linhardt

bullet Study finds dioxin increases liver tumors and lung metaplasia

Epidemiological studies indicated that people exposed to dioxins were prone to the development of lung diseases including lung cancer. Animal studies demonstrated that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) increased liver tumors and promoted lung metaplasia in females. ... [more]


bulletDisruption of endocrine function (the bodies chemical messenger system) appears to occur at body levels approximately 100 times lower than those associated with cancer.  International peer-approved research demonstrates that dioxin-like compounds can have transgenerational effects in wildlife and humans.   Included are: reproductive illnesses such as endometriosis, fertility problems and impotence; birth defects; developmental and immune system disorders and more.
bulletClick here to visit an excellent web site devoted to the topic of Hormone Disruption.  Excerpts:
bulletThe development and functioning of the human - and animal - body depends on a complex interaction of chemicals, in which everything must happen at the right time.
bulletThree crucial parts of the human body are the immune system, the hormonal system and the nervous system. It is easy to detect abnormalities in many other parts of the body - if you break your leg, or are bleeding, it is pretty obvious. Detecting changes in these systems is far harder. This is one of the reasons that providing proof of harm to any of these systems is difficult, unless the harm is very substantial - e.g. the damage to the immune system due to HIV. These three systems also affect each other, particularly during the development of the body.
bulletMany of the interactions within and between these systems depend on fairly simple chemicals - all potential targets for imitation by man - made chemicals. The pharmaceutical industry deliberately produces chemicals that affect these systems - the chemical industry does it accidentally - Every chemical is potentially a pharmaceutical.
bulletNew research shows that the environment is more important to health than anyone had imagined. Recent information indicates that toxic effects on health can be inherited by children and grandchildren even when there are no genetic mutations involved.[1] These inherited changes are caused by subtle chemical influences, and this new field of scientific inquiry is called "epigenetics." RACHEL'S ENVIRONMENT & HEALTH NEWS #819, June 9, 2005.
bulletClick here for the Rachel entire article or visit their website
bullet Click here for 9 articles about epigenetics from the Wall Street Journal, New York Times,  New Scientist, Washington State University News Service, Forbes, Times Magazine, and the Seattle Post - Intelligencer.
bulletExcerpt from Skinner Study:
"The transient exposure of a pregnant female at the time of embryonic sex determination to an environmental toxin (endocrine disruptor) can induce an epigenetic transgenerational disease phenotype in all subsequent generations. This has a significant impact on our understanding of factors that influence human disease and the basic concepts of evolutionary biology." Matthew D. Anway, Andrea S. Cupp, Mehmet Uzumcu, and Michael K. Skinner, Science 3 June 2005; 308: 1466-1469 [DOI: 10.1126/science.1108190
bulletClick here for a copy of the studies abstract or visit their website
bullet 32 years later, study finds Serveso babies 6x likely to suffer thyroid malfunction   New!

As the authors conclude, these findings suggest that maternal exposure to dioxins such as TCCD in the environment produces damaging effects on the thyroid function of their babies "far apart in time from the initial exposure."

release date: 28-Jul-2008
Contact: Andrew Hyde
Public Library of Science

Long-lasting effects of the Seveso disaster on thyroid function in babies
Three decades after an accident at a chemical factory in Seveso, Italy in 1976, which resulted in exposure of a residential population to the most dangerous type of dioxin, newborn babies born to mothers living in the contaminated area at the time of the accident are over six times more likely to have altered thyroid function than those born to mothers in a non-contaminated area. The study finding these results is published in the open access journal PLoS Medicine this week by Andrea Baccarelli (of the University of Milan) and colleagues from the United States and Italy.


bulletHigh dioxin levels linked to reduced thyroid hormone FT4 ?

Chronic exposure to dioxin-like compounds and thyroid function among New York anglers.

Experimental studies suggest that dioxin-like compounds influence thyroid function, although human studies have presented equivocal results. Great Lakes sportfish consumers represent a population with greater potential for exposure to dioxin-like compounds than non-consumers. Thirty-eight licensed anglers participating in a dioxin exposure study, consumers and non-consumers, conducted as part of the New York Angler Cohort Study, donated blood and completed questionnaires regarding demographic, clinical, and sportfish consumption data. ....

The results of this study are preliminary but suggest an inverse association between dioxin-like compounds and fT4.

Source: Bloom, M., Vena, J., Olson, J., Moysich, K., 2006. Chronic exposure to dioxin-like compounds and thyroid function among New York anglers. Environ. Toxicol. Pharmacol. 21: 260-267.

Click here for the entire abstract

bulletLarge Effects from Small Exposures. I. Mechanisms for Endocrine-Disrupting Chemicals
    with Estrogenic Activity.


Information concerning the fundamental mechanisms of action of both natural and environmental hormones, combined with information concerning endogenous hormone concentrations, reveals how endocrine-disrupting chemicals with estrogenic activity (EEDCs) can be active at concentrations far below those currently being tested in toxicological studies. Using only very high doses in toxicological studies of EEDCs thus can dramatically underestimate bioactivity. Specifically: a) The hormonal action mechanisms and the physiology of delivery of EEDCs predict with accuracy the low-dose ranges of biological activity, which have been missed by traditional toxicological testing. b) Toxicology assumes that it is valid to extrapolate linearly from high doses over a very wide dose range to predict responses at doses within the physiological range of receptor occupancy for an EEDC; however, because receptor-mediated responses saturate, this assumption is invalid. c) Furthermore, receptor-mediated responses can first increase and then decrease as dose increases, contradicting the assumption that dose-response relationships are monotonic. d) Exogenous estrogens modulate a system thatis physiologically active and thus is already above threshold, contradicting the traditional toxicological assumption of thresholds for endocrine responses to EEDCs. These four fundamental issues are problematic for risk assessment methods used by regulatory agencies, because they challenge the traditional use of extrapolation from high-dose testing to predict responses at the much lower environmentally relevant doses. These doses are within the range of current exposures to numerous chemicals in wildlife and humans. These problems are exacerbated by the fact that the type of positive and negative controls appropriate to the study of endocrine responses are not part of traditional toxicological testing and are frequently omitted, or when present, have been misinterpreted. Key words: dose response, endocrine disruptors, estrogen action, estrogen receptors, fetal development, inverted U, MCF-7 cells. Environ Health Perspect 111:994-1006 (2003). doi:10.1289/ehp.5494 available via [Online 2 February 2003] . 

Wade V. Welshons,1 Kristina A. Thayer,2 Barbara M. Judy,1 Julia A. Taylor,1 Edward M. Curran,1 and Frederick S. vom Saal2

bulletDioxin body burden significantly affects estrogen metabolism

This is the first report on the association of human body burdens of PCDDs/PCDFs and PCBs with estrogen metabolites. The information presented is crucial to understand their hormonally related health effects in women, such as the risk for breast cancer.

Dioxins (PCDDs), furans (PCDFs), and biphenyls (PCBs) are environmental endocrine disruptors that have half-lives of 7–10 years in the human body and have toxicities that probably include carcinogenesis. ...  In this cohort study of maternal–fetal pairs, we examined the relationship of PCDD/PCDF and PCB exposure to levels of estrogen metabolites in the sera of 50 pregnant women 25–34 years of age from central Taiwan. ... We measured 17 dioxin congeners, 12 dioxin-like PCBs, and 6 indicator PCBs in placenta ... Altered estrogen catabolism might be associated with body burdens of PCDDs/PCDFs. Our study suggests that exposure to PCDDs/PCDFs significantly affects estrogen metabolism. Therefore, PCDD/PCDF exposure must be considered when using the OH-E2 ratio as a breast cancer marker.

Body Burdens of Polychlorinated Dibenzo-p-dioxins, Dibenzofurans, and Biphenyls and Their Relations to Estrogen Metabolism in Pregnant Women




Dioxin Exposure, from Infancy through Puberty, Produces Endocrine Disruption
and Affects Human Semen Quality

This study on men from Seveso published in January 2008 provides evidence
 of a permanent disruptive effect of TCDD on the human male reproductive system,
depending on the age at exposure.

Conclusions: Exposure to TCDD in infancy reduces sperm concentration and motility, and an
opposite effect is seen with exposure during puberty. Exposure in either period leads to
permanent reduction of estradiol and increased FSH. These effects are permanent and
occur at TCDD concentrations < 68 ppt, which is within one order of magnitude of those
in the industrialized world in the 1970s and 1980s and may be responsible at least in part
for the reported decrease in sperm quality, especially in younger men.

Paolo Mocarelli,1,2 Pier Mario Gerthoux,1 Donald G. Patterson Jr.,3 Silvano Milani,4 Giuseppe Limonta,1 Maria Bertona,1 Stefano Signorini,
1 Pierluigi Tramacere,1 Laura Colombo,1 Carla Crespi,1 Paolo Brambilla,1 Cecilia Sarto,1 Vittorio Carreri,5 Eric J. Sampson,3 Wayman E. Turner,3
and Larry L. Needham3
1University Department of Laboratory Medicine, Hospital of Desio, Milano, Italy;
2School of Medicine, University Milano- Bicocca, Milano, Italy; 3National Center for Environmental Health, Centers for Disease Control and
Prevention, Atlanta, Georgia, USA; 4Institute of Medical Statistics and Biometrics, University of Milano, Milano, Italy; 5Department for Preventive
Medicine, Ministry of Health of Regione Lombardia, Milano, Italy

Environmental Health Perspectives Volume 116, Number 1, January 2008

bulletThe mystery of the missing boys ...

It is a question posed by a new 2007 study that has found the proportion of boys born over
the past three decades has unexpectedly dropped in both the United States and Japan. I
n all, more than a quarter of a million boys are missing, compared to what would have been
expected had the sex ratio existing in 1970 remained unchanged.

The study also says the world's most skewed sex ratio is in Canada, in a native community
surrounded by petrochemical plants in Sarnia, Ont., where the number of boys born has
 plunged since the mid-1990s at a rate never seen. ... [more]


bulletRespiratory disease in relation to patient residence near to hazardous waste sites.
Kudyakov, R., Baibergenova, A., Zdeb, M., Carpenter, D., 2004.
Environ. Toxicol. Pharmacol. 18: 249-257

We have examined rates of hospitalization for respiratory diseases in relation to residences in zip codes with hazardous waste sites, as well as socio-economic status. Chronic bronchitis and chronic airway obstruction were elevated in persons who live in zip codes containing persistent organic pollutants (POPs) (PCBs and persistent pesticides) as compared to "clean" zip codes without hazardous waste sites or zip codes with hazardous waste sites containing other kinds of wastes, but the differences could be due to socio-economic status and behavioral risk factors since these are also important risk factors for respiratory diseases. Therefore, we investigated rates of hospitalization for individuals living in zip codes along the Hudson River, because here the average per capita income is higher than in the rest of the state, and there is less smoking, better diet and more exercise. We found a similar elevation of chronic bronchitis and chronic airway obstruction along the Hudson.

These observations are consistent with the possibility that living near a POPs-contaminated site poses a risk of exposure and increased risk of chronic respiratory disease, probably secondary to suppression of the immune system.


bulletToxin exposure may cause rise in asthma 10/10/05


Immune suppression

One of the primary toxic effects of dioxin in laboratory animals is immune suppression, which results in decreased resistance to infectious agents and some cancers. The mechanisms and relationship between altered host resistance and immune dysfunction is complex, poorly defined, but extremely important to understanding health effects. NIEHS researchers are examining the mechanisms of immune suppression. Other studies are examining alterations in immune cell function in several human populations exposed to dioxin at both high levels and at low levels similar to that seen in the general US population.

What dioxin does to our immune system.  The immune system is a complex set of specialized cells and organs that defends the body against attack. When it functions properly, the immune system fights off diseases caused by bacteria, viruses, fungi, parasites and cancer cells. "When it malfunctions, however, it can unleash a torrent of diseases, from allergy to arthritis to cancer to AIDS", according to the US National Institutes of Health (NIH).


Links to Autoimmune Disease– Diabetes, Lupus, Multiple Sclerosis and Arthritis
        NATIONAL INSTITUTES OF HEALTH Reports from Special Environmental Health Issue

A study by scientists at Johns Hopkins University concludes that at least ten million Americans are affected by one of 80 known autoimmune diseases – conditions such as type 1 (insulin-dependent) diabetes, lupus, multiple sclerosis and even Takayasu's arteritis, which attacks the aorta and its branches. These conditions result when a person's immune system mounts an attack against one's own tissues.

Immunotoxic effects that result from prenatal exposure to environmental chemicals may be more dramatic or persistent than those from exposure during adult life. For example, prenatal exposure to the insecticide chlordane, or the aromatic hydrocarbon benzopyrene, produces what appears to be lifelong immunosuppression in mice. Furthermore, when mice genetically predisposed to develop autoimmune disease were treated with the environmental contaminant tetrachlorodibenzo-p-dioxin (TCDD) before birth, their postnatal autoimmunity was increased.

Dioxin affects ability to fight Flu infections
Hogaboam, J, A Moore and BP Lawrence. 2008. The aryl hydrocarbon receptor affects distinct tissue 
compartments during ontogeny of the immune system. Toxicological Sciences 102(1):160-170.

Researchers find for the first time that mice exposed to the contaminant dioxin during development or while nursing have a diminished capacity to fight a flu infection later in life. Mouse pups born to pregnant mice that were exposed to a small amount of the ubiquitous and persistent pollutants had fewer white blood cells that normally kill the flu virus and more of a different kind that increases lung inflammation. The increased inflammation can make the disease more severe and recovery more difficult. ...

This study looked at the long term immune effects of dioxin when exposure occurs during development. The authors tried to identify the critical windows of exposure where fetuses are most sensitive to dioxin's harmful effects. ...

The number of specialized white blood cells -- referred to as CD8+ T-cells specifically recognize and kill the flu virus, were significantly reduced in the pups but not their moms, who had been exposed to dioxin. ...

Dioxin exposure in the womb, and/or during nursing, impacts the development of the immune system in mouse pups. Ultimately, the immune system of the pups is permanently changed such that their response to an infection later in life is seriously impaired. These results demonstrate the importance of the critical windows of exposure for dioxin induced immune suppression: there are periods in life where individuals are especially sensitive to exposure to harmful chemicals potentially resulting in long-term. ...

Immune system toxins

In 1987, about 45% of Americans were living with one or more
chronic conditions (a term that includes chronic diseases and
impairments).  In 1935, the proportion was 22%, so chronic
conditions have approximately doubled during the last 60 years.
The majority of people with chronic conditions are not disabled,
nor are they elderly.  In fact, one out of every four children in
the U.S. (25%) now lives with a chronic condition.[1]

Dioxins and PCBs are carcinogenic and powerfully immunotoxic in many animals, including humans.                                          


bulletDioxin: Potent immune system poison (pdf file):  
U.S. Environmental Protection Agency's (EPA's) 1994 draft
reassessment of dioxin emphasized that dioxin damages the
immune system directly and indirectly. From studies of rats, mice,
guinea pigs, rabbits, cattle, marmosets, monkeys, and humans, EPA
concludes that even low doses of dioxin attack the immune system.
Dioxin directly reduces the number of B cells (immune cells that
develop in the bone marrow, then circulate throughout the blood
and lymph, fighting off invaders). And it reduces the number of T
cells (immune cells that develop in the thymus, then circulate
throughout the body, attacking invaders), but dioxin's attack on T
cells seems to be indirect. EPA says, "One potentially important
indirect mechanism is via effects on the endocrine system. Several
endocrine hormones have been shown to regulate immune
responses, including glucocorticoids, sex steroids, thyroxine,
growth hormone, and prolactin. Importantly, TCDD [dioxin] and
other related compounds have been shown to alter the activity of
these hormones."[2,pg.9-49]


bulletMichigans Midland County incidence of diabetes is higher than Michigan and National averages

mchd_diabetes.jpg (42941 bytes)

Click graph for larger view, use Back button to return to this page

bulletThe Midland County Health Director, Mike Krecek, stated in the Cities May 26th Midland meeting [more]
bulletMidland county residents have a higher incidence of Diabetes than State and National averages
bulletIronically, he also stated that the citizens of Midland County overall health is better than most.
bulletExtensive research exists which documents the link between diabetes and dioxin. 
bulletSummary of 66 studies linking PCB's and Dioxins to diabetes (about half are specific to dioxin)
bulletAbstracts of studies 1-33
bulletAbstracts of studies 34-66
bulletNAS Institute of Medicine 2000: Veterans & Agent Orange Dioxin exposure and type 2 diabetes

Strength of Evidence in Epidemiologic Studies Based on material presented in the papers and reports reviewed here, as well as the cumulative findings of research reviewed in Veterans and Agent Orange (1994), Veterans and Agent Orange: Update 1996, and Veterans and Agent Orange:Update 1998, the committee finds that there is limited/suggestive evidence of an association between exposure to the herbicides used in Vietnam or the contaminant dioxinand Type 2 diabetes. No one paper or study was determinative in reaching this decision. Instead, the committee found that the information accumulated over years of research now meets the definition established for limited/suggestive evidence—that is, evidence is suggestive of an association between herbicides and the outcome, but limited because chance, bias, and confounding could not be ruled out with confidence.


Federal Register: 2001 VA 38 CFR part 3: Disease associated with exposure to certain herbicide agents: Type 2 diabetes

bulletDioxin in the City of Midland soils and the flood plain downstream are higher than any other city in the State of Michigan.
bulletSo, if a County of people with excellent health habits have the highest rate if diabetes in the nation, what could be the cause?
bulletCommon sense indicates a possibility dioxin is causing the diabetes and the National Academy of Sciences agrees.
bulletMr. Krecek noted the elevated levels of diabetes back in 2002 when he 1st was hired.  To date, if a study is in progress, it's behind closed doors.
bulletJuly 2005: Department of Defense links Adult onset diabetes to agent orange
bulletJune 2003: Dioxin Linked To Diabetes
The Department of Veterans Affairs (VA) has proposed adding type 2 diabetes
to the list of diseases positively associated with exposure to Agent Orange
and other herbicides used in Vietnam during the war. Dioxin is found in
Agent Orange and other similar herbicides. If approved by the VA, veterans
who served in Vietnam who develop adult-onset diabetes will be able to file
claims for compensation without having to prove that their diabetes was
specifically caused by exposure to herbicides sprayed in Vietnam. The
proposal follows a review by the Institute of Medicine of the National
Academy of Sciences that evaluated mounting evidence supporting the
possibility of a link between Agent Orange/dioxin and type 2 diabetes. The
review found new "limited or suggestive" evidence of an association, though
this evidence was not conclusive. For more information see Veterans and
Agent Orange: Herbicide/Dioxin Exposure and Diabetes, available from the
National Academy Press, Washington, DC for $18. Call 202-334- 3313 or
bulletDiabetes is increasing The finding that an endocrine-disrupting chemical like dioxin may be able to promote diabetes opens up new avenues for thought about this rapidly-increasing disease. Perhaps it isn't fat itself that causes diabetes --perhaps it is the toxic chemicals stored in our fat that cause disease. It has been known for a long time that human fat accumulates toxic chemicals. For example, the U.S. Public Health Service has been collecting samples of fat from humans for 20 years and analyzing them for halogenated hydrocarbons, including dioxin, beta-hexachlorocyclohexane, heptachlor, DDT, DDD, DDE, PCBs, trichloroethylene, perchloroethylene, 2,4-D, methyl chloride, vinyl chloride, polyvinyl chloride (PVC), and chloroform, among others. We each carry literally hundreds of exotic toxic chemicals in our body fat. For any particular chemical, our fat often has a concentration 100 times as high as the concentration in our blood serum. It is also known that chemicals can be released from fat to re-circulate in the blood stream during times of pregnancy, stress, illness or fasting. Many fat-stored organohalogens are known to interfere with our endocrine systems by mimicking or blocking natural hormones.
bulletCalvert GM, Sweeney MH, Deddens J, Wall DK. Evaluation of diabetes mellitus, serum glucose, and thyroid function among United States workers exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin. Occup Environ Med 1999 Apr;56(4):270-6. Division of Surveillance, Hazard Evaluations and Field Studies, Centers for Disease Control and Prevention, Cincinnati, Ohio 45226, USA. JAC6@CDC.GOV
bulletCranmer M, Louie S, Kennedy RH, Kern PA, Fonseca VA. Exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is associated with hyperinsulinemia and insulin resistance. Toxicol Sci 2000 Aug;56(2):431-6. The Department of Pharmacology and Toxicology, the University of Arkansas for Medical Sciences, Little Rock, USA.


bulletNew 2005 study: 1st epidemiological evidence of dioxin body burden & endometriosis in humans
bulletThe results provide the first epidemiological evidence of an association between increased PCDD/PCDF and PCB body burden and endometriosis.
bulletFertil Steril. 2005 Aug;84(2):305-12.
Heilier JF, Nackers F, Verougstraete V, Tonglet R, Lison D, Donnez J.
Industrial Toxicology and Occupational Medicine Unit, Universite Catholique de Louvain, Brussels, Belgium.
bulletOBJECTIVE: To investigate the possible association between the body burden of dioxin-like compounds and endometriotic disease.
bulletDESIGN: Case-control study.
bulletSETTING: Gynecology ward in a university hospital.
bulletPATIENT(S): Seventy-one women with peritoneal endometriosis (n = 25) or deep endometriotic (adenomyotic) nodules (n = 25) and controls (n = 21).
bulletINTERVENTION(S): Collection of 200 mL of blood (fasted) and face-to-face interview.
bulletMAIN OUTCOME MEASURE(S): Assessment of dioxin (PCDD), furan (PCDF), and dioxin-like PCB serum concentrations (picograms toxic equivalent [TEQ]/g lipids).
bulletRESULT(S): Age and body mass index were traced by linear multiple regression as determinants of total TEQ levels. After standardization for these variables (30 years and 22.5 kg/m2), the mean TEQ levels were 24.21 (controls), 30.62 (peritoneal endometriosis), and 37.60 (deep endometriotic [adenomyotic] nodules) pg TEQ/g lipids. Logistic regressionanalysis indicated a significantly increased risk of deep endometriotic (adenomyotic) nodules (odds ratio [OR], 3.3; 95% confidence interval [CI], 1.4-7.6) for an increment of 10 pg in total TEQ levels/g lipids. An increased risk was also found for peritoneal endometriosis (OR, 1.9; 95% CI, 0.9-3.8) for total TEQ levels and for dioxins alone (OR, 3.2; 95% CI, 1.0-9.9).
bulletCONCLUSION(S): The results provide the first epidemiological evidence of an association between increased PCDD/PCDF and PCB body burden and endometriosis.
bulletEndometriosis is a disease in which tissue similar to the lining of the uterus, the endometrium, implants and grows outside of the uterus, often in the abdominal cavity, frequently causing pain, infertility, pain with sex, and bowel or bladder problems. Endometriosis requires involvement of hormones and immune system malfunction in order to develop, and is associated with increased risk of other immune system disorders and certain cancers. Although genetic factors may contribute to the risk of endometriosis in some women, human and animal studies indicate a potentially important role for environmental factors as well, including exposure to dioxins, furans, PCBs, chemicals that mimic estrogen, and radiation. It is important to consider that combinations of chemical and radiation exposures may add up to increase the risk more than would be expected from any one alone.
Ted Schettler, MD, Science Director and Chair, Science Work Group, CHE
Science and Environmental Health Network
bullet Click here to review entire report
bullet Click here to review references cited in report
bullet New! Increased levels of polychlorobiphenyls in Italian women with endometriosis.
bulletThe results obtained clearly show an increase of PCB congeners most abundant in human tissues in women with endometriosis.

Porpora, M., Igelido, A., de Dominico, A., Ferro, A., Crobu, M., Pallante, D., Cardelli, M., Cosmi, E., De Felip, E., 2006.  Chemosphere. In Press.

Abstract Endometriosis has been hypothesised to be linked to persistent and toxic organochlorinated chemicals. Dioxins and dioxin-like compounds have in particular been associated with the disease, mainly on the basis of experimental studies. Data in women are conflicting. A case-control study on 80 Italian nulliparous women of reproductive age was carried out to assess whether there is a correlation between the presence of endometriosis and blood levels of polychlorobiphenyls (PCBs), a family of ubiquitary environmental pollutants which comprises congeners with dioxin-like activity. Higher levels of PCBs were found in women with endometriosis. A mean cumulative value of 410 ng g -1, lipid base, was found in cases versus the value of 250 ng g- 1 observed in the control group (odds ratio for upper tertile 4.0, CI 95% 1.3-13; p = 0.0003). PCB increase involved both dioxin-like (PCBs 105, 118, 156, and 167) and non-dioxin-like congeners (PCBs 101, 138, 153, 170, 180). Š The results obtained clearly show an increase of PCB congeners most abundant in human tissues in women with endometriosis. The interpretation of these results is made particularly difficult by the fact that the observed increase involves congeners of both dioxin-like and non-dioxin-like type, this making necessary to considerate the broad range of different and not fully elucidated mechanisms of action pertinent to both groups of congeners. Further studies are ongoing aimed to understand the complex network of factors and the mechanisms that may be thought to be responsible of the association we observed, with a particular attention to polymorphism in genes encoding enzymes involved in PCB detoxification

DIOXIN and Neurological function

bulletEffect of dioxins on regulation of tyrosine hydroxylase gene expression by aryl hydrocarbon receptor: a neurotoxicology study

Dioxins and related compounds are suspected of causing neurological disruption. Epidemiological studies indicated that exposure to these compounds caused neurodevelopmental disturbances such as learning disability and attention deficit hyperactivity disorder, which are thought to be closely related to dopaminergic dysfunction.

Although the molecular mechanism of their actions has not been fully investigated, a major participant in the process is aryl hydrocarbon receptor (AhR). This study focused on the effect of 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD) exposure on the regulation of TH, a rate-limiting enzyme of dopamine synthesis, gene expression by AhR.

Methods: N2a-R beta cells were established by transfecting murine neuroblastoma Neuro2a with the rat AhR cDNA.

TH expression induced by TCDD was assessed by RT-PCR and Western blotting. Participation of AhR in TCDD-induced TH gene expression was confirmed by suppressing AhR expression using the siRNA method.

Catecholamines including dopamine were measured by high-performance liquid chromatography. A reporter gene assay was used to identify regulatory motifs in the promoter region of TH gene.

Binding of AhR with the regulatory motif was confirmed by an electrophoretic mobility shift assay (EMSA).

Results: Induction of TH by TCDD through AhR activation was detected at mRNA and protein levels. Induced TH protein was functional and its expression increased dopamine synthesis.

The reporter gene assay and EMSA indicated that AhR directly regulated TH gene expression. Regulatory sequence called aryl hydrocarbon receptor responsive element (AHRE-) was identified upstream of the TH gene from 285 bp to 167 bp.

Under TCDD exposure, an AhR complex was bound to AHRE-as well as the xenobiotic response element (XRE), though AHRE-was not identical to XRE, the conventional AhR-binding motif.

Conclusions: Our results suggest TCDD directly regulate the dopamine system by TH gene transactivation via an AhR- AHRE--mediated pathway. The AhR- mediated pathway could have a particular AhR-mediated genomic control pathway transmitting the effects of TCDD action to target cells in the development of dopaminergic disabilities.

Author: Eiichi AkahoshiSeiko YoshimuraSaeko UrunoMitsuko Ishihara-Sugano Credits/Source: Environmental Health 2009, 8:24


bulletOne explanation:

The way in which dioxin affects cells is similar in some way to the way in which hormones such as estrogen work. Dioxin enters a cell and binds to a protein present in cells known as the Ah receptor. The receptor when bound to dioxin can then bind to DNA and alter the expression of some genes. This can lead to alterations in the level of specific proteins and enzymes in the cell. While it is not known exactly how changes in the levels of these different proteins cause the toxicity of dioxin, it is believed by most scientists that the initial binding of dioxin the Ah receptor is the first step. Another explaination:

The highly toxic group of dioxins and dioxin-like chemicals (also called ligands) enter the cell and bind to a protein in the cytoplasm called Ah receptor (AhR). This ligand-AhR complex, after further exchange of some smaller proteins (e.g., AhR translocator, ARNT) to become 'transformed', enters the nucleus to bind to a specific 'dioxin receptor element' (or enhancer) (DRE) of DNA. This DNA interaction occurs 'upstream' of genes which then are activated to produce certain enzymes, some of which are highly correlated with the subsequent toxicity events.

bullet wpe5.jpg (30886 bytes)


bulletScientists are most concerned about exposures to fetuses, nursing infants and children, due to the delicate balance in the developing body.  Children in the U.S. are believed to receive up to 12% of their lifetime exposure to dioxin in their first year of life.  People of color suffer disproportionate exposure to these chemicals, as do others who live or work near incinerators, paper mills, chemical plants and toxic dumps.
bulletDioxin Levels In Food Are NOT Going Down

A newly published report shows that the amount of dioxin in food has
remained at the same dangerous level it was more than a decade ago. This
finding directly contradicts the assurances of the U.S. EPA that dioxin
levels in food are not a public health concern because dioxin levels in food
are down from what they were a few years ago. The EPA's strategy of not
having to reduce levels in meat and dairy, the primary sources of dioxin in
food, now needs to be re-evaluated. See "Schecter, A., et al., "Intake of
dioxins and related compounds from food in the U.S. population," Journal of
Toxicology and Environmental Health, Part A, 63: 101-118, 2001.
bulletRisk Characterization of Dioxin     Dr. Linda Birnbaum of the EPA slide show on
latest research into Dioxin and it's effects on human health.
bullet..for any particular community, understanding the potential health threats that could result from toxic releases is a nearly impossible task. Public health officials often lack sufficient understanding of how citizens have been exposed to toxic substances, how those substances work within the body, and how many people have contracted chronic disease within a community to render conclusive judgments as to whether particular toxic exposures have led—or can lead—to increases in disease"  The above is an excerpt of a report mentioned in a 1/22/02  USPIRG Press Release.  The report (a very large PDF file), is titled "Toxic Releases and Health: A Review of Pollution Data and Current Knowledge on the Health Effects of Toxic Chemicals". A section specific to dioxin starts on page 25.
bulletThe EPA and WHO (World Health Organization) have been investigating Dioxin for years.   The EPA's DRAFT Reassessment of Dioxin April 2002  (pdf).  Interesting comparisons between EPA and WHO findings can be found starting on page 43.  The EPA's final report is due out late 2002 or early 2003.  Note that most of document focuses on exposures to the "general population" via the food chain.  Citizens living in highly contaminated Tittabawassee flood plain probably have a much higher exposure.   The point is, we are expected to sit in the middle of the most dioxin contaminated land found in Michigan until they figure it out.

Body Burden

bulletBody Burden studies indicate dioxin/furan pollution maybe present in almost EVERYONE.  Low dose exposure produces health problems.  See Body Burden: The Pollution in People (very large pdf file)
bulletEPA research: Body burdens associated with effects
bullet Body Burdens: The pollution in newborns

A benchmark investigation of industrial chemicals, pollutants and pesticides in umbilical cord blood by the Environmental Working Group, July 14, 2005:

bulletA developing child's chemical exposures are greater pound-for-pound than those of adults.
bulletAn immature, porous blood-brain barrier allows greater chemical exposures to the developing brain.
bulletChildren have lower levels of some chemical-binding proteins, allowing more of a chemical to reach "target organs."
bulletA baby's organs and systems are rapidly developing, and thus are often more vulnerable to damage from chemical exposure.
bulletSystems that detoxify and excrete industrial chemicals are not fully developed.
bulletThe longer future life span of a child compared to an adult allows more time for adverse effects to arise.
bullet New! Body burden of dioxins and dioxin-like polychlorinated biphenyls in pregnant women residing in a contaminated area
bullet doi:10.1016/j.chemosphere.2006.02.020

Jein-Wen Chena, Shu-Li Wanga, b, Hui-Yen Yua, Po-Chi Liaoc and Ching-Chang Leec, ,

Division of Environmental Health and Occupational Medicine, National Health Research Institute, 35 Keyan Road, Zhunan Town, Miaoli County 350, Taiwan Institute of Occupational Safety and Health, Kaohsiung Medical University, Kaohsiung, Taiwan Department of Environmental and Occupational Health, College of Medicine, National Cheng Kung University, 138 Sheng-Li Road, Tainai 704, Taiwan

Received 24 September 2005; revised 11 February 2006; accepted 13 February 2006. Available online 4 April 2006.


A large pentachlorophenol (PCP)-manufacturing plant located in southwestern Taiwan operated between 1965 and 1982. The present study was conducted to ascertain whether an increased body burden of dioxins existed in pregnant women living in an area of Tainan city contaminated by chemicals from this plant. Twenty-eight pregnant subjects, 2139 years of age and residing in the study area between March and December of 2004 with a mean dwelling time of 6.07 6.11 years, were recruited. Concentrations of polychlorinated dibenzo-p-dioxins, dibenzofurans (PCDD/Fs), and dioxin-like polychlorinated biphenyls (PCBs) in serum of recruited residents were determined. Pregnant women residing in the study area >3 years had significantly higher PCDD (7.48 versus 5.13 pg-toxic equivalents [TEQ]/g-lipid) and dioxin-like PCB (6.70 versus 3.74 pg-TEQ/g-lipid) values as compared to those residing 3 years. Furthermore, dioxin concentrations increased with increasing dwelling time. Statistical analyses performed according to demographic characteristics and socioeconomic and dietary habits revealed that total TEQ values were significantly associated with fish consumption and smoking status. Dioxin congeners with greater degrees of chlorine substitution (e.g., HpCDD/F and OCDD/F) partitioned to greater degrees in the subjects of this study as compared to subjects in the general Taiwanese population. The findings of this study strongly implicate the activity of the PCP manufacturing plant in the observed increase in dioxin body burden. Investigation of the health consequences of this increased body burden is recommended.

Keywords: Serum; Exposure; Polychlorinated dibenzo-p-dioxins; Polychlorinated dibenzofurans; Pentachlorophenol production; Pregnancy

Abbreviations: PCBs, Polychlorinated biphenyls; PCDDs, Polychlorinated dibenzo-p-dioxins; PCDFs, Polychlorinated dibenzofuran; PCP, Pentachlorophenol production; TEQ, Toxic equivalence; TEF, Toxic equivalent factor



bulletThe most clearly established health effect of dioxin in humans is a skin eruption called Chloracne. The Seveso incident in 1976 contaminated the vicinity with dioxin and caused many cases of chloracne.

Image copied without permission from

                                             Viktor Yushchenko (Before and After dioxin poisoning )

Other Research into Health Effects of Dioxin


bulletIn 1996 the Environmental Protection Agency (EPA) relocated some members of the Pensacola community in Florida whose dioxin soil levels reached or exceeded 200 ppt TEQ. 
bulletIn the spring of 2002, the MDEQ took 36 samples from downriver areas lying within the Tittabawassee River floodplain. The sampling in Phase 1 found dioxin levels ranging from 35 ppt to 7,261 ppt TEQ, with an average level of 998 pptThat summer, Phase 2, with over 150 samplesaveraged 799 ppt with a max of 3,400 ppt in soils downstream of Dow and actually in the floodplain.  A floodplain residents yard averaged 529 ppt with a high of 1,400 ppt.  Eggs from freerange chickens on this residents property had dioxin levels of 16 - 48 ppt in each egg! According to the Michigan Department of Community Health, the EPA draft dioxin reassessment report will require MDEQ to revise its residential direct contact criteria for dioxin downward, not upward, from 90 ppt to somewhere between 12 and 53 ppt.
bulletThe now defunct Dow sponsored Corrective Action Consent Order would have raised the human contact level from 90 ppt to 831 pptDoes this sound dangerous to you? Can we trust Dow to act in our best interests in the future?

In addition:

bullet"At higher risk of exposure to dioxin are children, nursing infants, some workers and farmers, people who eat fish as a main staple of their diet such as some indigenous peoples and fishermen, and people who live near dioxin release sites. These groups of people are likely exposed to at least 10 times as much dioxin as the general population. "

The statement was made in the American Peoples Dioxin Report published by the  Center for Health, Environment, and Justice, a group which evolved out of the Love Canal incident.  The section of the report titled "Science" has an excellent description of dioxin and and how it is measured (TEQ's).  A supporting document Technical Support Document provides the scientific basis and support for the conclusions and recommendations made in the report.

Dow's message to the public is simple: dioxin poses no threat to humans in the flood plain.  Research from non-Dow scientists from around the world disagree.  Click here


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