|Minimizing Harm to Human Health Resultant from Persistent Organic Pollutants Contamination of the Environment: Focus on Akwesasne
||Exposure minimization is a key paradigm of public health protection. The Akwesasne
Reserve located along the St. Lawrence River at the mouths of the Grasse, Raquette
and St. Regis rivers is a place of above average exposures to persistent organic
pollutants (POPs). This exposure has resulted from the contamination of the region
with PCBs, which were used and disposed of at the ALCOA West facility, the former
Reynolds Metals facility and the former GM Powertrain facility. The region has received
additional inputs of POPs as a result of being located downstream and downwind from
the Great Lakes Basin.
Considering the excess exposure that has occurred here, POPs exposure minimization
is merited. Two important strategies of exposure minimization are: (1) contaminant
removal and (2) educational outreach on exposure minimization, which involves making
known the existence of the POPs exposure health hazard constituted by contamination
of all animal fats, including both fats present in local wild caught fish and wildlife as well
as fats present in the meats, fish, dairy products and eggs available in the mainstream
Contamination of the Global Environment
During the past 100 years the manufacture and use of certain halogenated
hydrocarbons has gradually led to the contamination of the global environment. These
substances are highly resistant to natural break-down processes. They are also soluble
in fats. Because of these two characteristics, POPs accumulate to the highest levels in
organisms at the top of food chains. Many species of organisms have body burdens of
POPs. Consumption of animal fats is the major exposure route for this group of
All peoples of the Earth bear body burdens of POPs, but those who consume relatively
large quantities of animal fats have the greatest accumulation of POPs in their fat
tissues. First Nations peoples with diets composed largely of fish and wildlife have
received particularly heavy POPs exposures.
POPs are not evenly distributed throughout the world. These substances evaporate at
elevated temperatures and condense out of cold air to redeposit onto the surface of the
planet. The boreal and arctic ecosystems are reservoirs of POPs. The sediments of
the Great Lakes are another vast POPs reservoir. "Across many of the Great Waters
net fluxes of PCB are in the direction of volatilization from surface water to the
surrounding atmosphere. Making these waterbodies sources of PCB to the
atmosphere." This statement is found in the US Environmental Protection Agency
(EPA), December 2007 report, "Survey of New Findings in Scientific Literature Related
to Atmospheric Deposition to the Great Waters: Polychlorinated Biphenyls (PCB)". ( US
EPA, 2007) Thus, the outdoor air of the Great Lakes region contains elevated
concentrations of POPs. Those First Nations peoples living in the Great Lakes region
and downwind from the Great Lakes on the St. Lawrence River receive respiratory
POPs exposures in addition to the POPs exposures resultant from consumption of fish
and wildlife produced in these ecosystems.
Excess Exposures of the People of Akwesasne
The people of Akwesasne, a First Nations reserve located on the St. Lawrence River
East of Massena, New York, have a long history of consuming fish from the St.
Lawrence River. Akwesasne is not only downwind from Great Lakes POPs. It is
downwind also from nearby POPs contaminated waste disposal sites on the ALCOA
West property, the former Reynolds Metals property and the former GM Powertrain site.
All three properties contain areas that were classified as Superfund sites. Major
remedial activities have taken place at these sites, but remediation was conducted
many years after disposal activities contaminated soils and sediments. Large quantities
of PCBs remain on all three sites. All sites were sources of PCB releases to the outdoor
atmosphere leading to respiratory exposures for decades. The people of Akwesasne
have received oral and respiratory exposure to POPs that is considerably in excess of
the average exposure of residents of North America. This fact was confirmed by State
University of New York University at Albany scientists who found PCB levels twice the
national average in the blood of adolescent Mohawk residing on the Akwesasne
Reserve. (Gallo, 2011)
Damages to Human Health
The scientific research literature of POPs exposure impacts on human health is vast
and rapidly growing. Scientific knowledge now supports the conclusion that POPs
exposure at current levels of food supply contamination imposes a significant quantity of
disease risk upon the average consumer of animal based foods. Damages to health
associated with POPs exposure include: cancer, type 2 diabetes, cardiovascular
disease, immune system dysfunction, impairment of sexual function, autoimmune
diseases, impairment of cognitive function and obesity.
Akwesasne residents experience high rates of type 2 diabetes, cardiovascular disease
and cancer. Epidemiological studies have demonstrated a connection between PCB
exposure and elevated incidence of type 2 diabetes and cardiovascular disease at
Akwesasne. Anecdotal evidence supports the conclusion that cancer incidence is far
above average in this place where so much exposure to POPs has occurred for so very
Minimization of Harm to Human Health
A groundbreaking public health policy document titled, “Persistent Organic Pollutants:
Impact on Child Health” was published in 2010 by the World Health Organization
(WHO). This report recommends that health arena leaders take action to minimize the
exposure that children receive to POPs.
POPs exposure minimization can be accomplished via a number of strategies. The
strategies involving action to reduce the presence of POPs in the environment and food
supply include: banning the production and use of POPs such as brominated flame
retardants, clean-up of POPs contaminated sites and establishing a prohibition against
the use of animal fats in the feeding of food animals. POPs exposure minimization can
also be accomplished by implementing strategies that motivate exposure avoidance
behaviors. Principal among these strategies is POPs exposure minimization education.
Such education involves providing the general public with a clearly set forth warning
describing the POPs exposure health hazard and recommending limited animal fat
"Persistent Organic Pollutants: Impact on Child Health", World Health
Restricting consumption of all animal fats is highlighted as a priority strategy for POPs
exposure minimization. Simona Surdu, PhD is the report's major author. David O.
Carpenter, MD, Director of the SUNY Albany Institute for Health and the Environment is
a contributing author. The WHO recently designated the Institute for Health and the
Environment as one of its world-wide centers.
"Children are more sensitive than adults to almost all dangerous substances, and that
particularly is true for persistent organic pollutants (POPs). Prenatal and early life
exposure to POPs results in reduced cognitive function, suppressed immune system
function and altered development of the reproductive system as well as increased risk
of development of other diseases, such as cancer, later in life."-David O. Carpenter, MD
Multiple exposure to POPs and resultant unquantified total damages to health are
addressed in the 2010 WHO policy document. Use of precaution is advised in the face
of incomplete yet substantial knowledge of serious damages to health resulting from
POPs exposure. Concerns involving gestational, lactational, childhood and adolescent
exposures are raised. This is the first time that a governmental public health entity has
provided leadership on the use of scientific knowledge to minimize the harm that will
result from global POPs contamination. Focus on action to minimize exposure makes
this a highly important public health protection document.
During the course of the past 100 years the global environment has become heavily
polluted with a large number of man-made chemicals, many of which persist in the
environment and accumulate to the highest levels at the top of food chains. POPs are a
major part of global contamination. Human beings are heavily impacted by POPs
exposures: cancers, type 2 diabetes, heart disease, obesity, ADHD, reduced cognitive
function, impaired immune system function and altered reproductive function. The time
is upon us for cooperative efforts by governmental public health entities and nongovernment
environmental health organizations to conduct educational outreach
programs focusing on POPs exposure minimization. Such educational outreach is a
crucial part of the overall effort to minimize the harm that will result from POPs
contamination of our world.
Gallo, M V, Chemosphere. 2011 May; 83(10): 1374-82. Levels of persistent organic
pollutants and their predictors among young adults; http://www.ncbi.nlm.nih.gov/
US Environmental Protection Agency, December 2007. Survey of New Findings in
Scientific Literature Related to Atmospheric Deposition to the Great Waters:
Polychlorinated Biphenyls (PCB); http://www.epa.gov/oaqps001/gr8water/pdfs/
Existing Scientific Knowledge Supports the Conclusion
that Persistent Organic Pollutants (POPs) Exposure Reduction Education Would Empower
Behavior Changes Leading to Reductions in Cancer Incidence-Donald L. Hassig,
February 25, 2011
In the industrialized world, cancer incidence is relatively
high. Cancer is the number one cause of
death worldwide. The American Cancer Society has reported that one in two
men and one in three women will develop cancer during their lifetime. When one observes the relative uniformity of
the existence of high cancer incidence throughout the industrialized world, it
is reasonable to conclude that the major sources of causation are similar for
the global population. Even in a hot spot, the majority of cancers are
very likely to be caused by the same exposures that are causing the majority of
cancers in the rest of the industrialized world. Exposure to persistent
organic (hydrocarbon) pollutants (POPs), which takes place as a result of
consumption of animal fat and exposure to exhaust carcinogens are widespread
and involve a large quantity of pollutant carcinogen intake. It is reasonable to conclude that these two
exposure categories constitute major contributors to cancer causation in the
The excess amount of cancer that exists in a hot spot
can be attributed to unique exposures occurring in the hot spot.
The excess cancer incidence that exists in a particular hot spot is likely to
result from the unique exposures that occur there: living downwind from
large facilities that emit pollutant carcinogens into the atmosphere, living downstream
from large facilities that discharge pollutant carcinogens into surface waters,
living in the vicinity of hazardous waste disposal sites, etc.
To make use of existing scientific knowledge for the purpose of reducing cancer
incidence to a minimum, it is essential that the general public be provided
with the following information: the names of the carcinogenic POPs and
exhaust constituents, the places where these pollutants exist in the
environment, and strategies to avoid exposure to these carcinogens. It is
the responsibility of government public health agencies to provide this
information to the public in an effective and timely manner. Posting
health hazard advisories in the market places, in supermarkets and at gas
stations, would be highly effective in building this cancer prevention public
Chlorinated dioxins, furans and dioxin-like PCBs are the
most studied of POPs. Much of the
scientific research literature describes findings involving these
substances. Polybrominated diphenyl
ethers (PBDEs), other brominated flame retardants, hexachlorobenzene, hexachlorocyclohexane,
Mirex, Toxaphene, chlordane, DDT, and numerous other pesticides are also
POPs. The limited research that exists
for these substances indicates that they are carcinogenic and that they are
endocrine disruptors. Therefore, adverse
effects including cancer are imposed via gestational exposure and lifelong
POPs are contaminants of animal fat due to the lipophilic
character of these substances. According
to the US Environmental Protection Agency's draft dioxin reassessment, over 95
percent of dioxin exposure takes place as a result of animal fat consumption.
A simple public health message is evident in the existing scientific
knowledge. POPs are toxic. POPs exposure causes cancer. Nearly everyone bears a body burden of
POPs. POPs are contaminants of animal
fat. Reducing animal fat consumption
reduces POPs exposure thereby lowering cancer risk.
Scientific Research Findings and Government Reports Supporting the Conclusion
that the Establishment of a Persistent Organic Pollutants (POPs) Exposure
Reduction Education Program Within the Federal and State Government Health
Agencies is of Importance in the Protection of Public Health in the United
States of America Due to the Cancer Preventive Benefit of Such an Educational
Agency for Toxic Substances and Disease Registry Public Health
Statement on Dioxins
The Agency for Toxic Substances and
Disease Registry (ATSDR) publishes a series of Toxicological Profiles. A
Toxicological Profile for dioxins was published in 1998. The ATSDR
website currently makes available a Public Health Statement on Dioxins, which
was created as a central message of the Toxicological Profile. The Public
Health Statement on Dioxins explains how dioxin exposure takes place and sets
forth a science based recommendation for reducing dioxin exposure, that
recommendation being to reduce consumption of animal fat containing
foods. However, this document lacks state of knowledge science on dioxin
exposure cancer risk, much of which has been published since the period covered
in the Profile.
US EPA Dioxin Reassessment
The US EPA Dioxin Reassessment is a
highly detailed compilation of dioxin exposure and adverse health effects science.
Part III of the dioxin reassessment provides a mathematical determination of
dioxin exposure cancer risk. Utilizing the US EPA's cancer risk slope
factor it is possible to calculate approximate population level cancer risk for
dioxin exposure. For the US population of 308 million, dioxin exposure
will cause approximately 308,000 cancer deaths in 70 years. The quantity
of exposure used in the calculation of this quantity of cancer mortality is 1
pg dioxin TEQ/kg bw/day.
Institute of Medicine Report,
"Dioxins and Dioxin-Like Compounds in the Food Supply: Strategies to
The Institute of Medicine of the
National Academies published the report titled, "Dioxins and Dioxin-Like
Compounds in the Food Supply: Strategies to Decrease Exposure" in
2003. This report presents several strategies for reducing dioxin
exposure. A key recommendation is that girls and women of child-bearing
age reduce consumption of animal fat containing foods so as to reduce their
dioxin exposure. This group was given particular attention due to the
health damaging effects imposed by gestational exposure.
Toxicological Sciences 67, 63-74 (2002)
Copyright © 2002 by the Society of Toxicology
Persistent Abnormalities in the Rat Mammary
Gland following Gestational and Lactational Exposure to
Suzanne E. Fenton*,1 , Jonathan T.
Hamm,,2 , Linda S.
Geri L. Youngblood*,3
* Division of Reproductive Toxicology and Division
of Experimental Toxicology, Office of Research and Development, National
Health and Environmental Effects Research Laboratory, U.S.
Environmental Protection Agency, Research Triangle Park, North Carolina 27711;
in Toxicology, University of North Carolina, Chapel Hill, North Carolina 27599
Received September 17,
2001; accepted November 14, 2001
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) exposure during gestation has
revealed reproductive anomalies in rat offspring, including inconclusive
reports of stunted mammary development in females (Brown et
al., 1998,Carcinogenesis 19, 1623–1629; Lewis et
al., 2001, Toxicol. Sci. 62, 46–53). The current
studies were designed to examine mammary-gland development in
female offspring exposed in utero and lactationally
to TCDD, and todetermine a critical exposure period and cellular source of these
effects. Long-Evans rats were exposed to 1 µg TCDD/kg body
weight (bw) or vehicle on gestation day (GD) 15. TCDD-exposed females
sacrificed on postnatal days (PND) 4, 25, 33, 37, 45, and 68
weighed significantly less than control litter mates, and
peripubertal animals exhibited delayed vaginal opening andpersistent vaginal
threads, yet did not display altered estrous cyclicity. Mammary
glands taken from TCDD-exposed animals on PND 4 demonstrated
reduced primary branches, decreased epithelial elongation, and
significantly fewer alveolar buds and lateral branches. This
phenomenon persisted through PND 68 when, unlike fully
developed glands of controls, TCDD-exposed rats retained undifferentiated
terminal structures. Glands of offspring exposed to TCDD or oil
on gestation days 15 and 20 or lactation days 1, 3, 5, and 10
were examined on PND 4 or 25 to discern that GD 15 was
a critical period for consistent inhibition of epithelial development.
Experiments using mammary epithelial transplantation between
control and TCDD-exposed females suggested that the stroma
plays a major role in the retarded development of the mammary
gland following TCDD exposure. Our data suggest that exposure
to TCDD prior to migration of the mammary bud into the fat pad
permanently alters mammary epithelial development in female rat
Reprod Toxicol. 2007
Apr-May;23(3):391-6. Epub 2006 Nov 10.
Prenatal TCDD exposure predisposes
for mammary cancer in rats.
Jenkins S, Rowell C, Wang J, Lamartiniere CA.
Department of Pharmacology and
Toxicology, University of Alabama at Birmingham, Birmingham, AL,
Epidemiological data are conflicting
in the link between 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure
and breast cancer causation. We have hypothesized that timing of
exposure to endocrine disruptors, such as TCDD, will alter breast cancer
susceptibility. Using a carcinogen induced rat mammary cancer model, we have
shown that prenatal exposure to TCDD alters mammary gland differentiation and
increases susceptibility for mammary cancer. Investigations into imprinting
via DNA methylation mechanisms showed that there were no changes in
protein expression in DNA methyltransferases, ER-alpha, ER-beta, GST-pi, or
MDGI. Using 2D gels and mass spectrometry, we have found seven proteins to
be differentially regulated, including a decrease in superoxide dismutase 1
(SOD1). Down-regulation of SOD1 could provide an environment ill equipped to
deal with subsequent free radical exposure. We conclude that prenatal TCDD can
predispose for mammary cancer susceptibility in the adult offspring by altering
the mammary proteome.
Volume 73, Issue 6, October
2008, Pages 999-1004
Delayed initiation of
breast development in girls with higher prenatal dioxin exposure; a
longitudinal cohort study
Marike M. Leijsa, b, Janna G. Koppec, Kees Olieb, Wim M.C. van Aalderena, Pim de Voogtb, d, Tom Vulsmaa, Matthijs Westrae and Gavin W. ten Tusscherf, ,
aDepartment of Paediatrics and Neonatology,
Emma Children’s Hospital Academic Medical Centre, Amsterdam, The
bIBED/ESPM, University of Amsterdam, The
cEcobaby Foundation, Loenersloot, The Netherlands
dKIWA Water Research, P.O. Box 1072, 3430 BB
Nieuwegein, The Netherlands
eDepartment of Paediatrics, Zaans Medical
Centre, Zaandam, The Netherlands
fDepartment of Paediatrics and Neonatology, Westfriesgasthuis,
Maelsonstraat 3, 1624 NP Hoorn, The Netherlands
Received 11 February
revised 21 May
accepted 22 May
Available online 15
While many studies have
assessed the health impacts of PCDD/Fs and PCBs on animals and humans,
long-term consequences for especially adolescents, have not (yet) been well
documented. This is certainly also true for the effects of PBDE exposure. As
part of a longitudinal cohort study, now well into its second decade, effects
of perinatal and current PCDD/F exposure, as well as current dl-PCB and PBDE
exposures, on puberty, were assessed.
and current PCDD/F, dl-PCB and PBDE concentrations were determined using GC–MS.
Pubertal development and growth were assessed by means of physical examination
and the Tanner scale. 33 Children (born between 1986 and 1991) consented to the
current follow-up study. Outcomes were evaluated using linear regression or the
non parametric Spearman’s correlation coefficient.
A delay in initiation of
breast development was found in girls (n = 18) with higher prenatal (p = 0.023)
and lactational PCDD/F exposure (p = 0.048).
The males revealed a
negative trend with age at first ejaculation. For other endpoints on puberty
and growth (pubic hair, axillary hair, genital stage, length, BMI, testicular
volume, menarche) no significant relation was found with any of the measured
Discussion and conclusion
A relation between prenatal PCDD/F exposure and
later initiation of breast development was seen. A Belgian study found a delay
in breast development with higher current serum concentrations of dioxin-like
compounds. The initiation of puberty is a complex process and it is yet not
clear how dioxin-like compounds precisely affect this process prenatally.
Further follow-up into adulthood is warranted, in order to detect the
possibility of developing malignancies and fertility problems.
Perspect. 2002 July; 110(7): 625–628.
concentrations and breast cancer risk in the Seveso Women's Health Study.
Brenda Eskenazi, Paolo Mocarelli, Pier Mario Gerthoux, Steven Samuels, Larry
Needham, Donald Patterson, and Paolo Brambilla
School of Public
Health, University of California at Berkeley, Berkeley, California 94720, USA. email@example.com
This article has been cited by
other articles in PMC.
(TCDD or dioxin), a widespread environmental contaminant, has been shown to
disrupt multiple endocrine pathways. The International Agency for Research on
Cancer classified TCDD as a known human carcinogen, primarily based on
occupational studies of increased mortality from all cancers combined. Using
data from the Seveso Women's Health Study (SWHS), we examined the association
between individual serum TCDD levels and breast cancer risk in women residing
around Seveso, Italy, in 1976, at the time of an industrial explosion that
resulted in the highest known population exposure to TCDD. The SWHS cohort
comprises 981 women who were infants to 40 years old in 1976, resided in the
most contaminated areas at the time of the explosion, and had archived sera
that was collected soon after the explosion. For each woman, serum TCDD
exposure was measured by high-resolution mass spectrometry. Cancer cases were
identified during interview and confirmed by medical record. At interview, 15
women (1.5%) had been diagnosed with breast cancer and serum TCDD levels for
cases ranged from 13 to 1,960 ppt. Cox proportional hazards modeling showed
that the hazard ratio for breast cancer associated with a 10-fold increase in
serum TCDD levels (log(subscript)10(/subscript) TCDD) was significantly
increased to 2.1 (95% confidence interval, 1.0-4.6). Covariate-adjusted results
were not different. Individual serum TCDD is significantly related with breast
cancer incidence among women in the SWHS cohort. Continued follow-up of the
cohort will help shed light on the possible role of TCDD in the pathogenesis of
Perspect. 1998 April; 106(Suppl 2): 663–670.
risk assessment for dioxins using an occupational cohort.
H Becher, K Steindorf,
and D Flesch-Janys
German Cancer Research
Center, Division of Epidemiology, Heidelberg, Germany. firstname.lastname@example.org
This article has been cited by
other articles in PMC.
We consider a cohort
of 1189 male German factory workers (production period 1952-1984) who produced
phenoxy herbicides and were exposed to dioxins. Follow-up until the end of 1992
yielded a significantly increased standardized mortality ratio (SMR) for total
cancer (SMR 141; 95% confidence interval 117-168).
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) concentrations up to 2252 ng/kg body
fat were measured in 275 cohort members. Other higher chlorinated dioxins and
furans also occurred in high concentrations. For quantitative analysis, the integrated
TCDD concentration over time was used as an exposure variable, which was
calculated using results from half-life estimation for TCDD and workplace
history data. The other congeners were expressed as toxic equivalency (TEQ) and
compared to TCDD using international toxic equivalency factors. Poisson and Cox
regressions were used to investigate dose-response relationships. Various
covariables (e.g., exposure to beta-hexachlorocyclohexane, employment
characteristics) were considered. In all analyses, TCDD and TEQ exposures were
related to total cancer mortality. The power model yielded a relative risk (RR)
function RR(x) = (1 + 0.17x)0.326 for TCDD (in microgram/kilogram blood fat x
years)--only a slightly better fit than a linear RR function--and RR(x) = (1 +
0.023x)0.795 for TEQ. Investigations on latency did not show strong effects.
Different methods were applied to investigate the robustness of the results and
yielded almost identical results. The results were used for unit risk
estimation. Taking into account different sources of variation, an interval of
10(-3) to 10(-2) for the additional lifetime cancer risk under a daily intake
of 1 pg TCDD/kg body weight/day was estimated from the dose-response models
considered. Uncertainties regarding the dose-response function remain. These
data did not indicate the existence of a threshold value; however, such a value
cannot be excluded with any certainty.
J Occup Environ Med. 2004 Feb;46(2):123-36.
Cancer in US Air Force veterans of the Vietnam War.
Akhtar FZ, Garabrant DH, Ketchum NS, Michalek JE.
Spec-Pro, Inc, San Antonio, TX, USA.
J Urol. 2005 Jan;173(1):87.
Cancer incidence and mortality were summarized in Air Force
veterans of the Vietnam War. The index subjects were Operation Ranch Hand
veterans who sprayed 2,3,7,8 tetrachlorodibenzo-p-dioxin (dioxin)-contaminated
herbicides in Vietnam. Comparisons served in Southeast Asia during the same
period but did not spray herbicides. We assessed cancer incidence and mortality
using national rates and contrasted cancer risk in each of three Ranch Hand
dioxin exposure categories relative to comparisons. The incidence of melanoma
and prostate cancer was increased among white Ranch Hand veterans relative to
national rates. Among veterans who spent at most 2 years in Southeast Asia, the
risk of cancer at any site, of prostate cancer and of melanoma was increased in
the highest dioxin exposure category. These results appear consistent with an
association between cancer and dioxin exposure.
No Evidence of Dioxin Cancer Threshold
David Mackie,1 Junfeng
Liu,1 Yeong-Shang Loh,2 and Valerie Thomas3
1Woodrow Wilson School of Public and International Affairs, 2Department
of Physics, and 3Princeton Environmental Institute, Princeton
University, Princeton, New Jersey, USA
The U.S. Environmental Protection Agency (EPA) has developed an estimate of the
human cancer risk from dioxin, using the standard low-dose linear extrapolation
approach. This estimate has been controversial because of concern that it may
overestimate the cancer risk. An alternative approach has been published and
was presented to the U.S. EPA Science Advisory Board's Dioxin Review Panel in
November 2000. That approach suggests that dioxin is a threshold carcinogen and
that the threshold is an order of magnitude above the exposure levels of the
general population. 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. Key words:
cancer, dioxin, TCDD, threshold. Environ Health Perspect 111:1145-1147
Utilization of Quantitative Cancer Risk Assessment to Assist Decision
Making on Public Health and POPs Exposure-Donald L. Hassig, April 2,
Beginning in the early 1900s, the entire biosphere has
gradually become contaminated with persistent organic pollutants (POPs).
POPs are persistent, man made, toxic substances. Many of the POPs are
classified as know to cause cancer in humans or reasonably anticipated
to cause cancer in humans.
POPs are contaminants of all animal
fat. Exposure takes place largely through consumption of animal fat.
All humans bear a body burden of POPs. This has been the case for
several generations. Gestational exposure has taken place repeatedly,
creating a current generation that has been shaped to a considerable
extent by whatever genetic and morphological changes are imposed by
gestational POPs exposure. In animal studies gestational POPs exposure
predisposes offspring to increased cancer susceptibility. It is
reasonable to suspect that gestational POPs exposure contributes to the
breast cancer cases that are now being diagnosed in girls throughout the
United States. Breast cancer in the 14 to 19 year old age group is a
new phenomenon. Consecutive generations of gestational POPs exposure is
also a new phenomenon.
Governments around the world have failed
to warn their citizens of the POPs contamination problem. This has
happened because of the tremendous amount of influence that corporations
exert over government. The corporate polluters will not allow
government public health agencies to inform the public about POPs
contamination of the food supply and the damages to heath that are
associated with POPs exposure.
Government environmental health
agencies have produced quantitative cancer risk assessments for a few of
the POPs. A quantitative cancer risk assessment is a document that
describes the use of epidemiological research findings to develop
estimates of how much cancer is caused by exposure to various quantities
of a carcinogen. Cancer incidence in low, medium and high exposure
groups is plotted against the quantities of exposure. The slope of the
line that best approximates this data is called the cancer slope factor.
The cancer slope factor is a number that describes the amount of
cancer caused by a unitary quantity of exposure to the carcinogen.
Multiplying the quantity of exposure by the cancer slope factor yields
an estimate of the amount of cancer risk imposed by that particular
quantity of exposure.
The US EPA has developed a process for
making available to the public the limited risk information. EPA's
Integrated Risk Information System (IRIS) is accessible on the agency's
Very little scientific knowledge exists upon which to
base quantitative cancer risk assessments for the vast majority of
POPs. It is not possible at the current state of scientific knowledge
to produce quantitative cancer risk assessments for all of the POPs
that one is exposed to as a result of animal fat consumption. Thus, POPs
exposure imposes an unknown quantity of cancer risk. However, by
simply taking into account the quantity of cancer risk that is imposed
by exposure to those POPs for which quantitative risk assessments exist
it is clear that more than an acceptable amount of cancer risk is
imposed by total POPs exposure.
Dioxin exposure cancer risk has
been quantified by US EPA in Part III of the Agency's 2003 draft dioxin
reassessment. This risk is greater than 1 in 1000 for current
background levels of exposure. However, due to the EPA's failure to
finalize the draft dioxin reassessment, no quantitative cancer risk
assessment information for dioxin is available through the IRIS program.
Greater than 1 in 1000 is an unacceptable quantity of cancer risk.
Quantitative cancer risk assessments have been produced by IRIS for
several of the POPs, including: Chlordane, DDE, DDT, Dieldrin,
Hexachlorobenzene, alpha-Hexachlorocyclohexane and Toxaphene. The oral
exposure cancer slope factors for these substances are provided below.
Multiplying the quantity of exposure by the cancer slope factor
produces an estimate of cancer risk.
Chlordane 3.5 x10-1 per mg/kg-day
DDE 3.4 x10-1 per mg/kg-day
DDT 3.4 x10-1 per mg/kg-day
Dieldrin 1.6 x10-1 per mg/kg-day
Hexachlorobenzene 1.6 per mg/kg-day
alpha-Hexachlorocyclohexane 6.3 per mg/kg-day
Toxaphene 1.1 per mg/kg-day
order to calculate the cancer risk imposed by exposure to each of the
substances listed above it is necessary to determine how much exposure
is taking place on a daily basis. Analysis of animal fat foods for POPs
contaminants is the process that generates the basic exposure data
needed. However, such testing is not being conducted to the extent that
reliable data is available.
No scientific knowledge exists on
the subject of synergies that cause multiple POPs exposure to impose
more than an additive quantity of cancer risk. Simply adding the cancer
risk for those POPs that have been assessed is likely to produce an
underestimate of actual cancer risk.
The only reasonable course
of action open to public health departments is warning the public of the
significant and unquantified cancer risk imposed by the POPs exposure
resultant from animal fat consumption. The United Nations' Safe Planet
Campaign has begun to educate citizens of the world on the subject of
POPs body burden. Hopefully, Safe Planet will soon begin to set before
the public the facts of POPs in the food supply and the unacceptable
quantity of cancer risk that this contamination imposes.
Partial List of the Persistent Organic Pollutants (POPs) Named on the US Environmental Protection Agency's Integrated Risk Information System (IRIS) Website
Click on A to Z List of IRIS Substances
Quantitative Estimate of Carcinogenic Risk from Oral Exposure
- Not Assessed under the IRIS Program.
*TCDD is not named on the IRIS website.
Quantitative Estimate of Carcinogenic Risk from Oral Exposure
- Assessed Under the IRIS Program
Cancer Slope Factors
Chlordane 3.5 x10-1 per mg/kg bw-day
DDE 3.4 x10-1 per mg/kg bw-day
DDT 3.4 x10-1 per mg/kg bw-day
Dieldrin 1.6 x10-1 per mg/kg bw-day
Hexachlorobenzene 1.6 per mg/kg bw-day
alpha-Hexachlorocyclohexane 6.3 per mg/kg bw-day
Toxaphene 1.1 per mg/kg bw-day
Cancer Action News Network
Donald L. Hassig, Producer
Loving the Earth Environmental Revolution
Quantitative Cancer Risk Assessment Science is
Insufficient to Produce an Estimate of Cancer Risk for Total POPs
Exposure Imposed by Consumption of Animal Fat
The unedited interview is available here.
Dr. Vincent Cogliano is the scientist responsible for
running US EPA's Integrated Risk Information System (IRIS). Dr.
Cogliano describes the current state of
scientific knowledge on the subject of quantitative cancer risk
persistent organic pollutants (POPs). Few quantitative cancer risk
have been produced for POPs. It is not possible to produce a
quantitative cancer risk assessment for total POPs exposure imposed by
consumption of animal fat.
The only reasonable action government public health agencies have open
to them is educating the general public about POPs exposure cancer risk
and exposure reduction strategies. This action has not been taken
despite the fact that the federal government has been aware of POPs
contamination of the food supply since the 1970s. The US government has
allowed corporations to dictate silence on the subject of POPs exposure
cancer risk. The government health entities must throw off all
corporate control and begin immediately to educate the general public on
the subject of POPs exposure avoidance via restricting consumption of
|An Interview with Arnold J. Schecter, MD, U Texas at Dallas, School of Public Health, Reduce Cancer Risk Via Restricting Consumption of Animal Fat: POPs Exposure Reduction Education for the General Public
Dr. Schecter is a member of the faculty of
the University of Texas at Dallas School of Public Health. Dr.
Schecter states that sufficient scientific knowledge exists upon which
to base a public health educational outreach setting before the
general public strategies for POPS exposure reduction.
The simple message of that educational outreach is this. POPs are
toxic, man made chemicals. All people have body burdens of POPs.
POPs are contaminants of all animal fat. Consuming less animal fat
reduces POPs exposure. POPs exposure reduction decreases the
individual's risk of developing cancer, cardiovascular disease and
type II diabetes. POPs exposure reduction among members of a
population will lead to decreases in the incidence of cancer,
cardiovascular disease and type II diabetes in that population.
Dr. Schecter's interview strongly supports government action to
establish and conduct public health educational outreach on POPs
February 24, 2011 Interview with Arnold J. Schecter, MD, U Texas at
Dallas, School of Public Health
Donald L. Hassig (DH): Good evening, Dr. Schecter.
Arnold Schecter, MD (AS): Good evening.
DH: Dr. Schecter is a scientist who has devoted his career, decades,
to studying the levels of POPs, persistent organic pollutants,
chemicals like dioxins, PCBs, brominated flame retardants. He has
dedicated much of his life to studying the levels of these chemicals
in the US food supply. Tell us about some of your more recent
research Dr. Schecter.
AS: What we have been looking at recently is levels of certain man
made chemicals that are toxic and in some cases persistent in humans
and in food. For example, in the past we have looked at dioxins and
PCBs in this country in Vietnam veterans and everyone in the US we
have loooked at and others have looked at where dioxins seeem to be
contaminating all of us as do PCBs. These are described by many as
persistent organic pollutants or POPs because they are persistent in
the environment or people. They are toxic. They bioaccumulate. They
cause a number of health problems. Lately, we have been interested in
what are now known as emerging POPs and chemicals that are similar to
the emerging POPs. We started looking not too long ago at a certain
type of flame retardant, PBDE, polybrominated diphenyl ether. We
looked first in nursing mothers' breast milk, because of reports from
Sweden that the levels of these were going up. At the same time,
dioxin levels and PCB levels were decreasing in the people they
studied. We did a study here in Texas. We found that every nursing
mother had milk that was contaminated with PBDE type flame retardants.
By comparing it with other countries we found that the levels were
higher than had been measured in any other country. We had three
findings. PBDEs are in nursing mothers' breast milk. The levels are
the highest in the world. We found no one who did not have this
contamination. We realized that this meant that babies before birth
were being contaminated as some moved through the placenta. We
realized that if an infant was getting all of his or her food by
nursing that child was going to be getting a dose of PBDEs and flame
retardants are not what babies need in their bodies. We later looked
at PBDEs in food and found that some foods particularly with animal
fats, whether they were animals or fish or dairy products were
contaminated with PBDEs. These are fat soluble chemicals. When we
looked at fish with higher fat levels like salmon or sardines we found
higher levels of PBDEs.
We also were interested in looking at another popular brominated flame
retardant. In America we use more PBDEs than in most other countries.
Another brominated flame retardant, which is believed to be toxic,
hexabromocyclododecane, was found at the same levels in nursing
mothers' breast milk in the US as in Europe. The levels are lower
than PBDEs in the US but we did find them in the milk of every woman
that we looked at. We then looked at hexabromocyclododecane in food
purchased from American supermarkets. We found that a number of
foods were contaminated with hexabromocyclododecane.
We also were interested in perfluorinated chemicals. We looked in
foods. These are chemicals found in Teflon and ScotchGuard that
resist stains or resist water. We found that a number of foods had
some of these perfluorinated chemicals.
We looked at dust vacuumed from floors in the US and Germany. We
found that PBDEs were at fairly high levels in dust and also that they
were much higher in the US than in Germany in a small study that we
DH: How do the PBDEs get from where they are put when used in
manufacturing? How do they get out of the material good into the
dust and get into the food?
AS: Yes, a very key question, of course. What is believed now is
that PBDEs, which are found in electronics and also in mattresses,
sofas, chairs, break off from what they are put in so that if your
were to lie down on your mattress tonight if PBDEs were used to
prevent fire, then as you lie down on the mattress this may release
dust containing PBDEs. Food also somehow gets contaminated. I do not
know what the route is for getting into the food.
DH: I have been familiar with this to the extent that I understand
how dioxins get into the animal food supply. It is my understanding
that minute particulates settle upon the vegetation or the aqueous.
In the terrestrial, when these particles settle upon vegetation cattle
consume the forage that has minute particles that contain dioxins
which then accumulate in their bodies. I wondered about the PBDEs.
Is it possible that the PBDEs would be minute particles in the outdoor
atmosphere and that they would come down like that?
AS: Well, the PBDEs are not chemically bound to the products that
they are in. They are added so that they can break off. The plastic
could break off with the PBDEs. It is not as well worked out right
now how PBDEs are migrating through the environment, food and us as
what we seem to know about dioxins.
DH: What is known about the health impacts? With babies that are
during gestation being exposed to PBDEs and then after gestation they
begin their own individual life and they are nursing the mother
getting more PBDEs. Then they are in the house crawling around on
the floor in the dust with the PBDEs. What is know about the health
impacts of these exposures?
AS: This is a relatively new field where investigations have been
done on laboratory animals like rats and mice and now more recently on
people, human epidemiology studies. It is interesting that PBDEs seem
similar in some of the health outcomes to PCBs. For example, it is
believed that both can cause cancer, both PCBs and PBDEs. It is
believed that both can have effects on the nervous system such as
lowering IQ if the baby has been exposed or the child has been
exposed, or emotional changes in children. Endocrine disruption,
changes in the levels of hormones. Problems with reproduction or
development such as less fetuses carried to normal delivery;
spontaneous abortions can happen. As best we know now, these POPs,
the PBDEs seem somewhat similar to PCBs. The literature now is coming
out with new papers very frequently on various POPs or chemicals that
are sort of like POPs but are not POPs. For example, bisphenol-A,
which is not persistent, but because we get an intake into our body
every day it's something like POPs, we've got it in us and we are
getting it in us. So BPA which is not persistent is sometimes called
a POPs-like chemical.
DH: I see. Because it is continuously present in our body. It
doesn't persist, but by being constantly exposed it is continuously
present in our body.
DH: We have talked about the presence of these chemicals, where they
are at and that they end up being part of the human body and that
there is some scientific knowledge about the diseases that can be
associated with these exposures. Is there sufficient scientific
knowledge and this would be your expert opinion? Is there sufficient
scientific knowledge on the subject of POPs exposure and disease
outcome to create, to produce public health statements on these
AS: There are POPs networks that have been producing public health
statements warning about health hazards. There is an international
POPs network and the Stockholm Convention meets periodically. (The
Stockholm Convention) targeted first what they call the "Dirty Dozen"
and has been adding to it. For example PBDEs went on the list
relatively recently. I think both persistent organic pollutants and
endocrine disruptors, some of which are the same chemicals have been
described by many people and many organizations as being a public
DH: What is the public health message that exists in the scientific
literature from your viewpoint?
AS: Ok. I will give you my personal opinion as someone who works in
the field. Different scientists will not alway agree on how toxic
something is or almost anything else in science there are areas of
disagreement. My own personal feeling is that these are man made
chemicals and they are toxic and bioaccumulate so they present a
hazard. If at all possible, we should be using non-hazardous
chemicals or phasing out those we know to be hazardous and trying to
replace them, if we need to replace them with less hazardous
chemicals. It may be that we could use other materials in our
mattresses to make them soft and flame resistant where you don't need
to add man made chemicals.
DH: This is kind of a regulatory matter, where we're deciding what
chemicals to use. What about the public health matter, this matter of
what do you tell the people? What would you tell the public about
AS: I think I would find myself in the group of scientists who feel
that if you have something that is toxic and persistent and man made
that you don't necessarily have to use that we should do whatever we
can do to decrease the amount in the environment and in people, but
also be thoughtful about what we replace the dangerous chemicals with.
We don't want to replace one dangerous chemical with another. We
want to make sure that before a new chemical is introduced that it has
been thoroughly tested for safety.
DH: Considering the fact that numerous POPs are contaminants of
animal fat, what is the public health message on POPs that exists in
AS: Well I think that raises a very interesting point. What you just
mentioned is that some of the POPs are fat soluble and they are found
in animal fats. In public health and medicine for quite some time now
there has been a general consensus among most that the less animal
fats the better for a person's health, whether we are talking about
colon cancer, heart attacks, or heart disease, or strokes. Now we can
add one more reason to eat less animal fat and perhaps more vegetables
and fruits and that is to decrease the intake of toxic POPs,
persistent organic pollutants or other toxic chemicals.
DH: What would the likely outcome be of reducing your exposure to
these chemicals? Isn't it the point of this being addressed by public
health that having less of these chemicals in your body, less body
burden of POPs would reduce disease risk for some of these chronic
AS: The way I see it as a public health physician who does research
and practice in the field, in my opinion, what is happening when we
reduce toxic chemicals whether it is lead in gasoline or cigarette
smoke or dioxin, or mercury at high levels or lead at certain levels,
is that we will be reducing in the population disease. It does not
mean that every person who ingests a certain number of molecules of a
toxic chemical is going to get sick. It does mean that in the general
population of the six billion people on the Earth or 360 million
living in America, whatever the figure is these days, there should be
less disease and better health.
DH: I am very hopeful that your research and the research of others
will lead to wide spread public knowledge of these matters. We do
this work. Our organization makes it our practice to conduct
information tables at colleges and in high schools and educate policy
makers. We have been educating town board members all around St.
Lawrence County where our group is located, where we started up. We
are finding that there is an interest. People want to reduce the
incidence of these diseases, particularly cancer. We go to a town
board and talk to them about POPs and the cancer risk that is
associated with exposure to chemicals like dioxins and PCBs. We have
been hesitant to say very much about the cancer risk associated with
the PBDEs, just because as you say its a newer field of research and
there is not as much known about cancer outcome. I don't think there
is any epidemiology on cancer outcome with PBDE exposure. There is so
much epidemiology on cancer outcome with dioxin exposure and a little
less with PCB exposure.
We go to town boards. They have been quick, in wanting to reduce
cancer burden in their jurisdictions, they have been quick to show
their support by passing resolutions and speaking with people at other
levels of government. They show their support for public education on
reducing exposure to POPs by way of limiting animal fat intake. They
want the federal government, the state government and the county
governments to provide this kind of education to the general public.
We tell them that the environmental groups can not get this job done.
We need to have good partners with government to educate the public
about the existence of POPs in the food supply.
It is so good you have this great science that you produce and the
other scientists have been producing. Let's just step back from this
a bit. Tell about the book that you wrote so long ago and tell us
when it was first published and how many editions it has gone through.
This book is titled, "Dioxins and Health". I remember checking that
out of the library quite a long time ago so I know there is quite a
bit of history here.
AS: What is your question?
DH: Tell us about what motivated you to write "Dioxins and Health",
when you first published this book. Tell us about that book. I see
that as the Bible of POPs. It was the starting point. It was a very
important document in the world scientific community, human beings,
dealing with the presence of these persistent organic pollutants in
the environment, in our bodies, in food. Tell us about your work that
went into publishing "Dioxins and Health".
AS: The history of that, and we are working on the third edition now,
was that I went to a number of meetings both of citizens' groups and
scientists and I noticed a great interest in the chemicals, the
dioxins, PCBs, similar chemicals. I noticed a couple of things. One
was even the best scientists did not understand the science that
scientists in different fields were generating. Chemists did not
understand epidemiologist. Physicians spoke to other physicians, not
chemists, not toxicologists who studied animals. I thought it would
be useful to try to edit. I didn't write the book, I edited it to
have a book that spoke to different people and scientists to people
who are not scientists and vice versa. That was the origin.
DH: Great idea. Certainly wonderful that you conceived of that and
set about doing it. When was the first edition published?
AS: I don't remember. The second edition was published in 2003. We
are working on the third edition right now.
DH: When do you think it will become available?
AS: I hope it will be out before this year is over. If not this year.
DH: I certainly would like to know when it comes out.
AS: We're trying.
DH: What changes have you seen? What is the difference between
edition three and edition one or edition two? What is the trend?
What has taken place in the existing scientific knowledge with regards
to dioxins and dioxin-like compounds, including some of the PCBs?
AS: I think, well, I know we have more science on the dioxins and
PCBs. I think what needs to be added in addition is the emerging
persistent organic pollutants such as we have been talking about or
compounds related to them.
DH: So, in the third edition you are going to address PBDEs and the
other brominated flame retardants?
DH: It has been great talking to you. I always enjoy these
interviews with you. There is one thing more that comes to my mind,
if you have time to discuss this. You had looked at the levels of
POPs, specifically, dioxins in the bodies of vegans and compared this
to the levels of these chemicals in the bodies of those who consume.
I am sure that you know and that most of the people in the audience
know. Just for the completeness of this. The term vegan refers to
the fact that people do not consume any animal products. So you
looked at the levels of dioxins and possibly some other POPs in the
bodies of people who do not consume animal products and then you
compare that to the body burdens of these chemicals in people who do
consume animal products. What did you find?
AS: What we found in two small studies, one with dioxins in vegans,
or people who have not eaten any meat or fish or dairy products for a
long time, or eggs, and then with PBDEs, was that the levels were
lower in vegans than in the US general population. In the more recent
study with PBDEs, what we found was that the longer the time since
eating meat or, animal fat, lets put it that way, the lower the
DH: That's certainly interesting. It proves out this matter of if
you recommend that people reduce their intake of animal fat that the
hope is that it would cause these levels to be lower. Then you see
this actually existing in the case of the vegans who have not been
consuming animal fat and they have these lower levels. They certainly
are an example of how one might go about minimizing their body burden
of chemicals like dioxins and PCBs and the brominated flame
I think I have covered everything that I wanted to talk to you about.
I look forward to these interviews with you so much because I know you
are this great source of scientific knowledge on this subject area.
What do you intend? You told me that you were working on a research
proposal earlier today. What are your intentions for future research
in this area, Dr. Schecter?
AS: I would like to continue learning what levels of toxic chemicals
are in people and in food. How does it get into us? And then, what
is the health consequence of these chemicals?
I'm about talked out. My voice is about gone.
DH: Thank you so much, Dr. Schecter. You are a great man. I am so
glad that you are a former New Yorker. We'll always be able to say
that even though it's sunnier in Texas, this is where Arnold Schecter
started his dioxins and his PCBs and his PBDEs research. We are
very proud of that.
AS: Thank you for your kindness and thank you for your probing,
interesting and insightful questions.
DH: Thanks for all the research you are doing. The research is the
very heart of the activism and the public health. It all comes down
to what do we know. What do the scientists know about these chemicals
and about the health of the human beings and the animals? Thanks a
AS: Thank you for your interest.
DH: Have a wonderful evening.
AS: Thanks, same to you.
Cancer Action NY's Cancer Action Network
Donald L. Hassig, Producer
Loving the Earth Pollution Free Revolution
Dr. Arnold J. Schecter on Science Supporting the
Conclusion that POPs Exposure Causes Cancer
This interview is available at the URL found below.http://www.radio4all.net/index.php/program/49736
Arnold J. Schecter, MD is an internationally recognized
expert in the subject area of persistent organic pollutants (POPs) exposure and disease
outcome. He is a public health scientist employed as a member of the faculty of the University of Texas at Dallas School of Public Health. He shares recent research
findings describing the contamination of US mothers' breast milk with
PBDEs, brominated flame retardants, which are believed to impose cancer
risk in ways similar to other endocrine disrupting chemicals.
Dr. Schecter states that sufficient scientific knowledge exists upon
which to base public health educational outreach on POPs exposure
The simple public health message that Dr. Schecter sees in the
scientific literature is this. POPs are toxic, man made chemicals. POPs exposure leads to accumulation of increasing body burden. Many POPs are
carcinogens. POPs contaminate animal fat and therefore, restricting
intake of animal fat will reduce POPs exposure. Reducing POPs exposure
will reduce cancer risk and thus reduce cancer incidence population