Introduction:
Scientific knowledge has accumulated during the course of the past
several decades so as to provide a basis for concluding that exposure
to persistent organic (hydrocarbon) pollutants (POPs) is a major
contributor to cancer causation. Now is the time for making use of
this knowledge by way of public educational outreach on POPs exposure
reduction.
Materials and Methods:
The work of creating this paper was conducted via reading and
understanding scientific research articles and government
publications. The availability of these documents on the internet has
greatly facilitated this work.
Results and Discussion:
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 POPs, which
takes place as a result of consumption of animal fat is widespread and
involves a relatively large quantity of pollutant carcinogen intake.
It is reasonable to conclude that POPs exposure is a major contributor
to cancer causation in the industrialized world.
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.
POPs are contaminants of all animal fat due to the lipophilic
character of these substances. 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.
Adverse health effects including cancer are imposed via gestational
exposure and the exposures that take place during the lifetime of the
independent organism.
Several epidemiological studies have been conducted for populations
with excess dioxin exposure. The 1976 chemical production facility
explosion that occurred in Seveso, Italy released a large quantity of
dioxins, resulting in widespread exposure of the regional population.
Occupational exposures have taken place among workers engaged in the
production of phenoxy acid herbicides, particularly in the case of
manufacture of 2,4,5-T. Additionally, United States military forces
received excess exposure resultant from the aerial spraying of
defoliants containing dioxin contaminants during the Vietnam War.
In the 2002 paper titled, “Serum Dioxin Concentrations and Breast
Cancer Risk in the Seveso Women’s Health Study”, researchers Marcella
Warner et al reported a statistically significant positive association
between serum dioxin levels and breast cancer risk.1 The group of
women with highest blood serum dioxin concentrations exhibited a
higher rate of breast cancer incidence than groups with lower serum
dioxin levels.
Several cohorts of factory workers employed in the manufacture of the
penoxy acid herbicide, 2,4,5-T, have been assessed for dioxin exposure
cancer outcome. Becher, et al published the paper, “Quantitative
Cancer Risk Assessment for Dioxins Using an Occupational Cohort” in
1998.2 The authors reported a statistically significant link between
dioxin exposure and cancer mortality. Mathematical modeling of the
data led this team to conclude that dioxin exposure cancer risk was of
a magnitude existing in the range 1 x 10 E-3 to 1 x 10 E-2 for
exposure in the amount of 1 pg TCDD/kg body weight/day. Other
research groups have investigated cancer mortality among herbicide
production and application workers. The results of these studies
serve to create consensus on the connection between dioxin exposure
and elevated cancer risk.
Operation Ranch Hand was the code name for US military activities
involving aerial spraying of defoliants during the Vietnam conflict.
Agent Orange, a defoliant containing relatively high concentrations of
dioxins, was utilized extensively. In 2004, Akhtar et al published
the study titled, “Cancer in US Air Force Veterans of the Vietnam
War”.3 Increased incidence of melanoma and prostate cancer were
positively associated with dioxin exposure.
Animal studies have demonstrated that a relation exists between
gestational dioxin exposure and increased breast cancer susceptibility
in female offspring.4,5 A study published in 2008 reported delayed
initiation of breast development in girls with higher prenatal dioxin
exposure.6 These research results provide a plausible explanation of
the breast cancer cases, which have been diagnosed among American
girls as young as ten years of age during the 2000s.
Certain reports produced by United States federal government agencies
contain scientific information supporting the conclusion that POPs
exposure is a major contributor to cancer causation. However, no US
government report provides a comprehensive analysis of the cancer risk
imposed by the POPs exposure resultant from consumption of animal fats
contaminated at current background levels.
The Agency for Toxic Substances and Disease Registry (ATSDR) published
a Toxicological Profile for Dioxins in 1998.7 At the same time, ATSDR
also published a companion document, titled “Public Health Statement
on Dioxins”. These documents recommend reduced animal fat consumption
due to the existence of scientific knowledge describing associations
between dioxin exposure and increased cancer risk.
The United States Environmental Protection Agency (EPA) has been
endeavoring to produce a reassessment of dioxins since April 1991.
The most recent draft of the reassessment, titled, “Exposure and Human
Health Reassessment for 2,3,7,8-Tetrachlorodibenzo-p-dioxin and
Related Compounds” is dated 2003.8 The EPA draft dioxin reassessment
is a highly detailed compilation of dioxin exposure and adverse health
effects science. According to the EPA, over 95 percent of dioxin
exposure takes place as a result of animal fat consumption.
Part III of the dioxin reassessment provides a mathematical
determination of dioxin exposure cancer risk. EPA’s choice of a
linear model for dioxin exposure cancer risk is supported by research
findings reported in 2003 by Mackie, et al.9 The Mackie study found
no evidence of a threshold for dioxin exposure cancer risk. Utilizing
the US EPA’s cancer 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.
The Institute of Medicine (IoM) of the National Academies published
the report titled, “Dioxins and Dioxin-Like Compounds in the Food
Supply: Strategies to Decrease Exposure” in 2003.10 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. The IoM
report did not address dioxin exposure cancer outcome. Its
recommendations were based upon findings of other diseases endpoints.
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 knowledge.
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.
Acknowledgements:
Cancer Action NY is a grassroots environmental protection/cancer risk
reduction organization. I serve as director of this small group of
dedicated individuals because I believe in doing this work. I am able
to do this work because of the frugality and generosity of my father,
William John Hassig, DVM.
References:
1. Warner M, et al. Serum dioxin concentrations and breast cancer risk in
the Seveso Women’s Health Study. Environmental Health Perspectives.
(2002) July; 110(7): 625–628.
2. Becher H, et al. Quantitative cancer risk assessment for dioxins using
an occupational cohort. Environmental Health Perspectives. (1998)
April; 106(Suppl 2): 663–670.
3. Akhtar FZ, et al. Cancer in US Air Force veterans of the Vietnam War.
Journal of Occupational Environmental Medicine. 2004 Feb;46(2):123-36.
4. Fenton SE, et al. Persistent Abnormalities in the Rat Mammary Gland
following Gestational and Lactational Exposure to
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD). Toxicological Sciences 67,
63-74 (2002)
5. Jenkins S, et al. Prenatal TCDD exposure predisposes for mammary
cancer in rats. Reproductive Toxicology. (2007) Apr-May;23(3):391-6
6. Leijsa MM, et al. Delayed initiation of breast development in girls
with higher prenatal dioxin exposure; a longitudinal cohort study.
Chemosphere Volume 73, Issue 6, October (2008), Pages 999-1004
7. The Agency for Toxic Substances and Disease Registry. (1998)
Toxicological Profile for Dioxins. www.atsdr.gov
8. U S Environmental Protection Agency. (2003 Draft) “Exposure and Human
Health Reassessment for 2,3,7,8-Tetrachlorodibenzo-p-Dioxin and
Related Compounds”. www.epa.gov
9. Mackie D, et al. No Evidence of Dioxin Cancer Threshold. (2003)
Environmental Health Perspectives 111:1145-114
10. The Institute of Medicine of the National Academies of Sciences.
“Dioxins and Dioxin-Like Compounds in the Food Supply: Strategies to
Decrease Exposure”. (2003). www.nas.edu
Prevent Cancer Now 
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