CANADA ) Q.B. No.

956 of 2006
PROVINCE OF SASKATCHEWAN )

COURT OF QUEEN’S BENCH FOR SASKATCHEWAN,

JUDICIAL CENTRE OF REGINA

Between:
FRANK BROOKS,
Plaintiff,

HER MAJESTY THE QUEEN, ATTORNEY GENERAL OF

CANADA, GOVERNMENT OF CANADA, and the MINISTER OF NATIONAL
DEFENCE,
Defendants,
- and -

THE DOW CHEMICAL COMPANY and

PHARMACIA CORPORATION,
Third Parties.

Brought under The Class Actions Act.

AFFIDAVIT OF MARGARET E. SEARS, Ph.D

(sworn January_____, 2009)

I, Dr. Margaret E. Sears, of the City of Dunrobin, in the Province of

Ontario, MAKE OATH AND SAY:

1) I have personal knowledge of the matters hereinafter deposed, except where stated to
be based upon information and belief, and where so stated I have stated the grounds
for my belief and do verily believe the same to be true.

2) I received my Ph.D. from McGill University in 1985. I also have a Master of

Engineering degree (Chemical Engineering, 1981; McGill University) and a
 3

Bachelor of Applied Chemistry and Chemical Engineering degree (1979; University

of Toronto). I have attached to this my affidavit as Exhibit 1, my current Curriculum
Vitae.

3) I am a published research scientist, science analyst and medical writer, and an

Adjunct Investigator at the Children’s Hospital of Eastern Ontario Research Institute
in Ottawa. I have knowledge and experience in chemical engineering, applied
chemistry, industrial hygiene, health, and diverse environmental matters. Exhibit 2
to this my Affidavit is a copy of an article from the peer reviewed journal of the
Canadian Paediatric Society, Paediatrics and Child Health, entitled “Pesticide
Assessment: Protecting Public Health on the Home Turf” by myself, Dr. C. Robin
Walker, Dr. Richard H. van der Jagt and Dr. Paul Claman. This article discusses the
health effects and the Canadian federal regulatory assessment of the herbicide
2,4-dichlorophenoxyacetic acid (2,4-D).

4) I have been awarded a grant as a Principal Investigator by the Canadian Institutes of

Health Research (CIHR) to conduct a Scoping Review regarding health and
environmental toxic metals. The CIHR is the Government of Canada's health
research funding agency. It awards grants in funding competitions, based upon peer
review by a committee that reaches consensus. According to the CIHR, only
applications that meet internationally accepted standards of excellence are funded.

5) I am lecturing in the third-year Environment and Health course HSS 3303A at the
University of Ottawa, Winter 2009, on several topics, including epidemiology,
toxicology and chemical assessment.

6) I am assisting Merchant Law Group LLP by providing an environmental medical

perspective regarding the chemicals used at Canadian Forces Gagetown, and the
medical conditions that are the subject of this Class Action.
 4

7) In this Affidavit, some acronyms are used. For convenience, they are defined as
follows:
2,3,7,8-TCDD 2,3,7,8-tetrachlorodibenzo-p-dioxin (the form of dioxin that binds the
AhR most strongly, so is considered the most toxic)
2,4-D 2,4-dichlorophenoxyac-etic acid
2,4,5-T 2,4,5-trichlorophenoxyacetic acid
2,7-DCDD 2,7-dichlorodibenzo-p-dioxin (a principal contaminant of 2,4-D)
AhR Aryl hydrocarbon receptor (a protein in the cytoplasm of cells. When
bound to a chemical such as dioxin, the AhR is transported into the cell
nucleus, where it affects expression of many genes. This affects
development as well as enzymes for metabolism and excretion of toxic
substances.)
ATSDR Agency for Toxic Substances and Disease Registry, within the US
Department of Human and Health Services
CFB Canadian Forces Base
EPA Environmental Protection Agency (in the United States)
IOM Institutes of Medicine (US)
OCDD octochlorodibenzo-p-dioxin (dioxin with chlorine atoms at every
possible location on the molecule)
PCDD/F Polychlorinated dioxins (PCDD) and furans (PCDF)
PMRA Pest Management Regulatory Agency (within Health Canada, the
PMRA is responsible for pesticide assessment and registration for sales
and use in Canada)
ppb parts per billion
ppm parts per million
ppt parts per trillion (may be per total mass of sample, or per lipid content
when reporting lipophylic chemical contamination)
TEF Toxic equivalent factor. This chemical-specific factor is multiplied by
the concentration of the particular AhR binding chemical to estimate the
equipotent quantity of 2,3,7,8-TCDD, called the toxic equivalent (TEQ).
TEQ Toxic equivalent. The AhR-binding toxicity of a mixture of chemicals
is estimated as the sum of the TEQs.
TM17 Total mass of the 17 reportable dioxins and furans that bind with the
AhR
US United States of America
 5

Health Effects

8) The United States Department of Veterans Affairs offers compensation and health
care to veterans for certain diseases that have been determined according to various
independent panels constituted by the American National Academy of Science’s
Institute of Medicine to be associated with exposure to herbicides used in Vietnam.
Exposure is presumed to have occurred with service in Vietnam. The webpage is
reproduced as Exhibit 4. The health effects include:

• acute and subacute peripheral

• porphyria cutanea tarda
neuropathy

• chloracne • prostate cancer

• respiratory cancers (lung, bronchus,

• chronic lymphocytic leukemia
larynx and trachea)

• Hodgkin's disease • soft-tissue sarcoma, acute

• multiple myeloma • Type II diabetes mellitus

• Spina bifida in offspring, and

• non-Hodgkin’s lymphoma additional birth defects in children
of women who served in Vietnam

These same health effects are included in the present Claim.

The conclusions regarding the relationship between these conditions and the
exposure to the chemicals sprayed in Vietnam relied upon thorough review of the
scientific literature and extensive consideration, coordinated by the Institute of
Medicine. A series of books about Veterans and Agent Orange, as well as an Air
Force Health Study may be read online, and are available at:
http://books.nap.edu/openbook.php?record_id=11906&displayrelated=1.
 6

9) This affidavit will not recap all of these findings, but will highlight some key points
and recent updates in the medical literature. I will also discuss the interpretation in
general of scientific studies of complex conditions with long latency periods, such as
cancer.

10) The most well known herbicides sprayed in Vietnam were the “Rainbow
Herbicides,” named for the colours of the stripes on the barrels. They included
Agent Orange (2,4-D and 2,4,5-T), Agent Purple (an earlier mixture of 2,4-D and
2,4,5-T), Agent Pink (2,4,5-T), Agent Green (2,4,5-T), Agent White (2,4-D and
picloram, also known as Tordon 101), and Agent Blue (cacodylic acid). At the time,
these chemicals were also in use domestically. Referring to Exhibit 3,
commonalities of chemicals used in Vietnam and the most-used chemicals at CFB
Gagetown are evident. Other herbicides were also in use, as summarized in Exhibit
3.

Chemicals used at Canadian Forces Base Gagetown

11) The chemicals discussed in this, my Affidavit, are those mentioned in the Statement
of Claim (amended, dated 7th November, 2008).

12) In August 2005 the Department of National Defence, Veterans Affairs Canada,
Health Canada and additional departments and agencies, initiated a fact-finding
mission to gain information on the history of herbicides tested and used at CFB
Gagetown from 1952 to 2004. Extensive documentation of “tasks” – works
commissioned by what I herein call the “Fact Finder project,” are available via an
internet homepage at: http://www.forces.gc.ca/site/Reports/defoliant/index_e.asp.
Upon information and belief, the chemicals listed in the Statement of Claim were
derived from information provided by the Fact Finder project.

13) One of the tasks of the Fact Finder project was to document all of the herbicides
applied at CFB Gagetown, from 1952 to 2004. A collection of toxicological profiles
 7

for the various active ingredients is available on the internet at:

http://www.forces.gc.ca/site/Reports/defoliant/FFReports/task3A1_tier3_final_repor
t.asp.

14) Exhibit 3 to this, my Affidavit, lists the active ingredients of herbicides applied, and
shows their chemical structures. As well, contaminants such as hexachlorobenzene
and chlorinated dibenzo-p-dioxin are included. Information was gathered also from
the Pest Management Regulatory Agency (PMRA), within Health Canada website
(www.pmra-arla.gc.ca), as well as the Toxicological Information Service of the
National Library of Medicine in the United States (www.toxnet.nlm.nih.gov) and a
Compendium of Pesticide Common Names – Herbicides
(www.alanwood.net/pesticides/class_herbicides.html). The quantities and areas
sprayed, and the years of application as reported by the Fact Finder project, are also
presented in Exhibit 3.

15) The active ingredients belong to various groups of pesticides known to have
common mechanisms of action. The 24 pesticide ingredients are listed according to
this established mechanistic grouping, as identified by the PMRA. In Exhibit 3, I
have further grouped the active ingredients according to chemical structure.

16) Some chemicals have been classified by the International Agency for Cancer
Research (IARC) as to the probability that they cause cancer. Classification
information, and the monographs on which the classifications are based, are
available online at: http://monographs.iarc.fr/ENG/Classification/index.php. If
IARC has assessed the carcinogenic potential of a chemical, it is also indicated on
Exhibit 3. Of the chemicals used at Gagetown, the arsenic-containing pesticides and
dioxins in mixtures are known human carcinogens. The phenoxy herbicides,
pentachlorophenol and hexachlorobenzene are possible human carcinogens (Group
2B). Many of the chemicals have not been assessed by the IARC.
 8

17) The years when particular pesticides were used and the total quantities applied, as
provided to the Fact Finder project, are graphed for the chemicals used in greatest
quantities, over multiple years, in a Figure provided at the end of Exhibit 2. Clearly
2,4-D, picloram, dicamba, 2,4,5-T and very recently glyphosate were the mainstays
of the herbicide program. Thus, regardless of exposure at particular occasions to the
other chemicals listed in Exhibit 3, people in and around CFB Gagetown would have
been exposed to 2,4-D, dicamba, dichlorprop, 2,4,5-T, picloram and more recently
glyphosate, as well as the components that accompany them such as contaminants,
adjuvants and breakdown products. These chemicals are the main focus of this
affidavit. Only dichlorprop and glyphosate were not used in Vietnam, meaning that
a vast majority of the herbicide types and quantities sprayed at CFB Gagetown were
also used in Vietnam. Scientific literature regarding dichlorprop and dicamba is
limited compared with 2,4-D, picloram and 2,4,5-T, and some contaminants.

18) Exposure and subsequent internal doses of the population at CFB Gagetown would
have been widespread for many reasons. For instance:
a) Chemicals drift during and following application, in smoke, on dust in the wind,
in sediments that are washed downstream, and as chemicals are volatilized and
redeposited from day to night.
b) Burning would also generalize exposure. Prange examined dioxins in
Queensland in Australia, and stated, “This study demonstrated that although
forest fires influence atmospheric PCDD/F concentrations substantially, forest
fires are not the source of PCDDs in Queensland; rather they are an important
mechanism for the redistribution of PCDDs and may have attributed [sic] to the
widespread PCDD contamination” (Origin of Dioxins in Queensland, Australia.
Investigations into the distribution and sources of polychlorinated dibenzo-p-
dioxins in the Queensland terrestrial environment thesis summary attached as
Exhibit 5). This group has published several studies in this regard.
c) Chemicals on clothing would be brought into common areas. Once indoors, the
chemicals are very persistent. Take-home chemicals would also expose the
spouse and family, as chemicals are shed from footwear and deposited in dust,
 9

where children playing and mouthing fingers and toys would be

disproportionately affected. Laundering clothes distributes chemicals to others’
clothes, particularly if the family’s clothes are laundered together, and results in
exposure of other family members. These issues are discussed in Nishioka MG,
Lewis RG, Brinkman MC, Burkholder HM, Hines CE, Menkedick JR.
Distribution of 2,4-D in air and on surfaces inside residences after lawn
applications: comparing exposure estimates from various media for young
children. Environ Health Perspect. 2001;109:1185-1191, attached as Exhibit 6;
and Gladen BC, Sandler DP, Zahm SH, Kamel F, Rowland AS, Alavanja MC.
Exposure opportunities of families of farmer pesticide applicators. Am J Ind
Med. 1998;34:581-587, attached as Exhibit 7. (Notably, these types of exposures
were not assessed in the Fact Finder Task 3A.)
d) Animals accumulate toxic chemicals and move them about, and chemicals move
up the food chain. Thus, contamination of fauna represents an averaged dose
across the animal’s range, and across its food sources, as discussed by Blanco et
al. (Blanco GA, Cooper EL. Immune systems, geographic information systems
(GIS), environment and health impacts. J Toxicol Environ Health B Crit Rev.
2004;7:465-480, attached as Exhibit 8). No land animals were analysed in the
Fact Finder work.

19) While deforestation was carried out at CFB Gagetown, similar herbicides may have
been used for other applications such as controlling growth along utility corridors or
controlling weeds along roadsides. However, exposure at Gagetown would be
expected to be higher than elsewhere because:
a) A much higher herbicide application rate is necessary to kill brush than to kill
herbaceous weeds. According to the label for a Dow 2,4-D product for forestry,
attached as Exhibit 9, as little as one litre of concentrate per hectare may be used
to control broad-leafed weeds, while up to 24 litres per hectare may be needed to
kill brush up to 2.5 metres tall.
b) As described in the Fact Finder Task 3A reports by Cantox, the sprayed brush
was cleared by hand and burned, rather than left untouched.
 10

c) In the same context, the areas at CFB Gagetown were cleared for use, and the
men were engaged in prolonged exercises around the clock. During training, a
high degree of contact with contaminated soil and water, and probable
contamination of foods under unhygienic conditions, represent greater direct
exposures, compared with exposures of the general population to chemicals
sprayed along uninhabited rights of way.
d) 2,4,5-T is moderately mobile as it can vaporize or dissolve in water, and it has a
half-life in soils of up to 24 weeks according to the Rotterdam Convention
document (attached as Exhibit 10). 2,4,5-T has not been registered for use in
Canada for over 20 years, yet it was found in the soil at CFB Gagetown.
Conservatively, after 30 half-lives, 2,4,5-T would be at levels approximately 1
billionth (thousand millionth) of its original level and thus undetectable. This
means that extraordinarily high levels of 2,4,5-T were present at one time and/or
the half-life model and other mathematical models are of limited reliability. It
must be validated that model results agree with reality.

20) Chemical half life refers to the time for half of the molecules of a chemical to no
longer be the original chemical. The result is that the chemical moves one step along
the breakdown pathway. The new chemical in turn has its own half life. Thus,
degradation of a dioxin would entail half lives for each degradation step – losing
individual chlorine atoms, opening up of rings, and final degradation. Passage of
time does not necessarily mean that chemicals become less toxic. For example,
during its half life, half of the OCDD molecules would lose one chlorine atom and
become a more toxic heptachlorodibenzo-p-dioxin that has its own half life
measured in years. The resulting dioxin binds the AhR more strongly, with a higher
TEF, as summarized by van den Berg et al. (Van den Berg M, Birnbaum LS,
Denison M et al. The 2005 World Health Organization reevaluation of human and
Mammalian toxic equivalency factors for dioxins and dioxin-like compounds.
Toxicol Sci. 2006;93:223-241, attached as Exhibit 11).

21) 2,3,7,8-TCDD has been found to be detectable in the body decades after exposure:
 11

a) Ryan JJ, Schecter A, “Exposure of Russian Phenoxy Herbicide Producers to

Dioxins,” J Occup Environ Med 2000;42:861 870, attached as Exhibit 12; and

b) Kerger BD, Leung HW, Scott P et al., “Age and Concentration Dependent
Elimination Half Life of 2,3,7,8-Tetrachlorodibenzo-p-dioxin in Seveso
children,” Environ Health Perspect 2006;114:1596 1602, attached as Exhibit 13.

Herbicide-related Health Effects

Cancers

22) Cancerous cells have damaged genetic material (DNA). DNA alteration can occur
because cells sometimes make mistakes when replicating, or chemicals may be
“genotoxic” and damage DNA. As cells with altered DNA proliferate, more genetic
damage may accrue. Cancer develops when such a cell successfully, repeatedly
replicates to form a clinically significant malignancy. Chemicals such as pesticides
may play one or more of several different roles in the eventual development of
cancer. The following are provided to introduce an overview or sample of some of
the relevant areas of science:
a) causing genetic damage (Bolognesi C., “Genotoxicity of pesticides, a review of
human biomonitoring studies,” Mutat Res 2003;543:251 272, attached as Exhibit
14);
b) acting in a manner similar to hormones, thereby stimulating growth of normal
and abnormal cells. This may also lead in turn to increased “mistakes” in DNA
replication, and further genetic changes as unstable DNA is quickly replicated.
(Andersen HR, Vinggaard AM, Rasmussen TH, Gjermandsen IM, Bonefeld
Jorgensen EC, “Effects of Currently Used Pesticides in Assays for Estrogenicity,
Androgenicity, and Aromatase Activity in vitro,” Toxicol Appl Pharmacol
2002;179:1 12, attached as Exhibit 15);
c) irritating tissue, causing abnormal cell division and/or immune activity
(Coussens LM, Werb Z., “Inflammation and cancer,” Nature 2002;19
26;420:860 867, attached as Exhibit 16);
 12

d) suppressing the immune system, that would otherwise eradicate abnormal cells
and stop the progression of cancer (Li Q, Kawada T, “The mechanism of
organophosphorus pesticide induced inhibition of cytolytic activity of killer
cell,” Cell Mol Immunol 2006;3:171 178, attached as Exhibit 17); or
e) interfering with cell death mechanisms (apoptosis), so that cancer cells
accumulate (Garry VF, Tarone RE, Long L. Griffith J, Kelly JT, Burroughs B,
“Pesticide appliers with mixed pesticide exposure: G banded analysis and
possible relationship to non Hodgkin's lymphoma,” Cancer Epidemiol
Biomarkers Prev 1996;5:11 16, attached as Exhibit 18).

23) Links between cancers and pesticides have been of great interest to Canadians for
decades. Two very recent reviews highlight relatively consistent effects seen,
particularly for the most common cancers for which linkages are more readily
ascertained. (Bassil KL, Vakil C, Sanborn M, Cole DC, Kaur JS, Kerr KJ. Cancer
health effects of pesticides: systematic review. Can Fam Physician. 2007;53:1704-
1711), attached as Exhibit 19, and (Buka I, Koranteng S, Osornio Vargas AR.
Trends in childhood cancer incidence: review of environmental linkages. Pediatr
Clin North Am. 2007;54:177-203), attached as Exhibit 20.

24) According to the US EPA in 2005, the carcinogenicity of 2,4-D is undetermined (the
Re-Evaluation Decision Fact Sheet is attached as Exhibit 21). The Canadian PMRA
reached similar conclusions in its 2005 document (Pest Management Regulatory
Agency. Re-evaluation of the Lawn and Turf Uses of (2,4-Dichlorophenoxy)acetic
Acid [2,4-D] PACR2005-01, excerpt attached as Exhibit 22). However, unlike the
US EPA, the Canadian PMRA did not re-register diethanolamine (DEA) salts of 2,4-
D, as the DEA posed excessive risks to human health (Pest Management Regulatory
Agency. RVD2008-11 Re-evaluation Decision. (2,4-Dichlorophenoxy) acetic Acid
[2,4-D], excerpts attached as Exhibit 23).

25) 2,4,5-T was added to the Rotterdam Convention for Prior Informed Consent in part
because of concerns regarding carcinogenicity, in recognition that 2,4,5-T will
 13

inevitably be contaminated with the carcinogen 2,3,7,8-TCDD (attached as Exhibit

10).

Haematological cancers (leukemia and lymphoma)

26) Immune system dysfunction, such as auto-immunity and immune suppression, has
been linked to the development of non-Hodgkin lymphoma (nHL). (Grulich AE et
al., “Altered immunity as a risk factor for non-Hodgkin’s lymphoma,” Cancer
Epidemiol Biomarkers Prev 2007;16(3), attached as Exhibit 24). Most importantly,
Grulich et al. postulate that “the potential exists that a highly prevalent, subclinical
form of immune deficiency might be associated with a substantial proportion of
nHL.” As discussed below in this Affidavit, persistent organic pollutants such as
dioxins and hexachlorobenzene contaminating the 2,4-D, 2,4,5-T, and picloram may
be a “missing link” as they disrupt the immune system. This may seem counter-
intuitive, but to explain, one of two phenomena may come into play. Immune
surveillance is important for eradicating early pre-cancerous or cancerous cells, and
cancers are more prevalent in people with suppressed immune systems. On the other
hand, cancers are also more likely to develop when a cell type is over-stimulated to
reproduce, causing increased numbers of transcription errors in DNA replication and
outstripping the effectiveness of immune surveillance. Thus, in individuals with
autoimmune diseases caused by over-activity of the immune system, lymphoma is
also more likely to ensue.

27) In families with a predisposition to developing lymphoma, non-Hodgkin lymphoma

and Hodgkin lymphoma may develop in first degree relatives, with both lymphomas
developing within a particular family, in unpredictable sequences. In an update of a
long study of familial haematological malignancies (Alexandrescu DT, Garino A,
Brown Balem KA, Wiernik PH. “Anticipation in families with Hodgkin's and non
Hodgkin's lymphoma in their pedigree,” Leuk Lymphoma 2006;47:2115 2127),
attached as Exhibit 25, it is stated, “these data suggest that anticipation occurs in
families that exhibit both HL and nHL and that both neoplasms may have a common
 14

genetic basis.” In other words, a single genetic basis is common to sub-types of

lymphomas.

Endocrine disruption (reproductive harms and diabetes)

28) When chemicals affect fundamental biological functions they may precipitate
diverse consequences. Binding of the aryl hydrocarbon receptor (AhR), the common
feature of “dioxin-like” toxicities, results in several effects on the endocrine,
immune and neurological systems, that lead to health effects including cancers.
Apart from overt toxic effects, some other health effects reported include diabetes
and endometriosis (which is linked to adverse reproductive outcomes):
a) Remillard RB, Bunce NJ, “Linking Dioxins to Diabetes: Epidemiology and
Biologic Plausibility,” Environ Health Perspect 2002;110:853 858, attached as
Exhibit 26;
b) Fierens S, Mairesse H, Heilier F et al., “Dioxin/polychlorinated biphenyl body
burden, diabetes and endometriosis: findings in a population-based study in
Belgium,” Biomarkers, 2003;8:529 534, attached as Exhibit 27; and
c) Rier S, Foster WG “Environmental dioxins and endometriosis,” Toxicol Sci
2002;70:161 170, attached as Exhibit 28.

29) Remillard et al. also question the “long-standing dogma that all the toxic effects of
[dioxin-like compounds] are mediated by the Ah receptor.” Most epidemiological
studies only measured 2,3,7,8-TCDD. I fully expect that dioxins and related
compounds exert other toxic effects in living organisms. In particular, this was
confirmed in studies of the immunotoxic effects of the non-AhR binding dioxin 2,7-
DCDD as well as 2,3,7,8-TCDD, discussed in paragraph 72.

30) A recent study of Vietnam Veterans was published following all Institutes of
Medicine reports in this regard, by Michalek et al. (Michalek JE, Pavuk M.
Diabetes and cancer in veterans of operation ranch hand after adjustment for
calendar period, days of spraying, and time spent in southeast Asia. J Occup
Environ Med. 2008;50:330-340), attached as Exhibit 29) Diabetes and cancer
 15

among Vietnam veterans were more strongly linked to herbicide exposures by

factoring in the time of year (herbicide spraying was seasonal) for better exposure
ascertainment. This not only adds weight to scientific “evidence” regarding these
health outcomes, it illustrates the previous of Remillard et al. that relative risks are
underestimated in epidemiological studies.

31) Lee et al. addressed cause versus effect of persistent organic pollutants in obesity,
metabolic syndrome and type 2 diabetes mellitus (Lee DH, Lee IK, Song K et al. A
strong dose-response relation between serum concentrations of persistent organic
pollutants and diabetes: results from the National Health and Examination Survey
1999-2002. Diabetes Care. 2006;29:1638-1644, attached as Exhibit 30; and Lee DH,
Lee IK, Porta M, Steffes M, Jacobs DR, Jr. Relationship between serum
concentrations of persistent organic pollutants and the prevalence of metabolic
syndrome among non-diabetic adults: results from the National Health and Nutrition
Examination Survey 1999-2002. Diabetologia. 2007;50:1841-1851, attached as
Exhibit 31). They found that these conditions were correlated with blood levels of
persistent organic pollutants, including dioxin-like chemicals. Most importantly,
directly addressing a common belief that lifestyle and diet, rather than toxic
chemicals, are the most important determinants of development of metabolic
syndrome or type 2 diabetes mellitus, Lee et al. found that obesity was correlated
with diabetes and metabolic syndrome only in the relative absence of pollutants.
There was no correlation between obesity and metabolic abnormalities when higher
levels of pollutants were detectable in the blood. This raises the possibility that
obesity may result from the body diluting lipophylic toxic chemicals that are
resistant to metabolism and excretion. Thus, dioxins may have a more important
role in metabolic syndrome and diabetes than previously thought, with obesity
playing a secondary role, protecting the body by sequestering toxins.

32) Lee et al.’s findings were largely replicated in two 2008 reports by Uemura et al. In
a large, population-based Japanese study, dioxin-like chemicals in the blood were
 16

highly significantly correlated with metabolic syndrome and diabetes, and most
strongly associated with high blood pressure, elevated triglycerides and glucose
intolerance (Uemura H, Arisawa K, Hiyoshi M et al. Prevalence of Metabolic
Syndrome Associates with Body Burden Levels of Dioxin and Related Compounds
among General Inhabitants in Japan. Environ Health Perspect. 2008, attached as
Exhibit 32; and Uemura H, Arisawa K, Hiyoshi M et al. Associations of
environmental exposure to dioxins with prevalent diabetes among general
inhabitants in Japan. Environ Res. 2008;108:63-68, attached as Exhibit 33).

33) In 2008, Smink et al. reported that children who were exposed to higher levels of
hexachlorobenzene while in utero were three times as likely to be obese at 6.5 years
of age, compared with children with low exposures (Smink A, Ribas-Fito N, Garcia
R et al. Exposure to hexachlorobenzene during pregnancy increases the risk of
overweight in children aged 6 years. Acta Paediatr. 2008;97:1465-1469, attached as
Exhibit 34). Obesity is a symptom of metabolic syndrome, a prelude to diabetes
mellitus. This prospective study design is considered to be a higher grade of medical
information.

34) Frazier recently published a review of reproductive disorders associated with

pesticide exposure, finding that, “Every class of pesticides has at least one agent
capable of affecting a reproductive or developmental endpoint in laboratory animals
or people.” (Frazier LM. Reproductive disorders associated with pesticide exposure.
J Agromedicine. 2007;12:27-37), attached as Exhibit 35.

35) Agent Orange, containing 2,4-D, 2,4,5-T and various dioxins including 2,3,7,8-
tetrachlorodibenzo-para-dioxin (TCDD), has long been associated with birth defects.
This was association was strengthened in a systematic review of this subject. (Ngo
AD, Taylor R, Roberts CL, Nguyen TV. Association between Agent Orange and
birth defects: systematic review and meta-analysis. Int J Epidemiol. 2006;35:1220-
1230), attached as Exhibit 36.
 17

36) Persistent organic pollutants also affect reproduction, with the end result that more
females are born than males. Skewing of the sex ratio of offspring in Italy as a result
of phenoxy herbicide/dioxin contamination is discussed in Mocarelli P, Gerthoux
PM, Ferrari E et al., “Paternal concentrations of dioxin and sex ratio of offspring,”
Lancet 2000;355:1858-1863, attached as Exhibit 37. The percentage of male
offspring was reduced from the national average of 51% to less than 40%.

Phenoxy herbicides – 2,4-D and 2,4,5-T

37) In this section I will discuss links between phenoxy herbicides and cancers, as well
as developmental/reproductive effects.

38) Genetic changes in lymphocytes precede development of lymphoma, and this has
been seen in association with exposure to 2,4-D. Chromosomal and nuclear
abnormalities, as well as hormonal abnormalities, have been seen in vitro and in
vivo, and in foresters in British Columbia using 2,4-D. (Holland NT, Duramad P,
Rothman N et al., “Micronucleus frequency and proliferation in human lymphocytes
after exposure to herbicide 2,4-dichlorophenoxyacetic acid in vitro and in vivo,”
Mutat Res 2002;521:165 178., attached as Exhibit 38; and Garry VF, Tarone RE,
Kirsch IR et al., “Biomarker Correlations of Urinary 2,4-D Levels in Foresters:
Genomic Instability and Endocrine Disruption,” Environ Health Perspect
2001;109:495 500, attached as Exhibit 39.)

39) Bharadwaj et al. examined effects of low concentrations of 2,4-D on expression of

genes in human hepatoma cells. In their study, 87 genes showed significant changes
(two-fold threshold); some were upregulated and some were downregulated.
Changes started to appear at 1.0 nM 2,4-D concentration. Bharadwaj concluded that
2,4-D is associated with altered expression of many genes, such as those involved in
cell-cycle control, stress response, DNA repair and immune function (Bharadwaj L,
Dhami K, Schneberger D, Stevens M, Renaud C, Ali A. Altered gene expression in
 18

human hepatoma HepG2 cells exposed to low-level 2,4-dichlorophenoxyacetic acid

and potassium nitrate. Toxicol In Vitro. 2005;19:603-619, attached as Exhibit 40)

40) Research by Chiu et al. in 2004 strongly links non-Hodgkin lymphoma to herbicide
use on farms. The statistically significant increased risk associated with herbicide
exposure was not modified by family history, and was consistent across types of
non-Hodgkin lymphoma. (Chiu BC, Weisenburger DD, Zahm SH et al.,
“Agricultural pesticide use, familial cancer, and risk of non-Hodgkin lymphoma,”
Cancer Epidemiol Biomarkers Prev 2004;13:525 531, attached as Exhibit 41)

41) Increased mortality from cancer has been linked to chlorophenoxy herbicides, such
as 2,4-D. (Schreinemachers DM, “Cancer Mortality in Four Northern Wheat
Producing States,” Environ Health Perspect 2000;108:873-881, attached as Exhibit
42.)

42) Studies of workers may be biased due to the “healthy worker” effect (those who are
less robust find other employment). Nevertheless, workers exposed to phenoxy
herbicides, chlorophenols and contaminants were more likely to die of cancer than
their less exposed co-workers. (Kogevinas M, Becher H, Benn T et al., “Cancer
Mortality in Workers Exposed to Phenoxy Herbicides, Chlorophenols, and Dioxins.
An Expanded and Updated International Cohort Study,” Am J Epidemiol
1997;145:1061 1075, attached as Exhibit 43; and Kogevinas M., “Human health
effects of dioxins: cancer, reproductive and endocrine system effects,” Hum Reprod
Update 2001;7:331 339, attached as Exhibit 44.) Workers also exhibited other
effects, with endocrine effects possibly being the most sensitive. Endocrine effects
lead to conditions such as Type II Diabetes Mellitus.

43) 2,4-D, other phenoxy herbicides and their associated dioxins have also been linked
to increased incidence of non-Hodgkin lymphoma in humans, in numerous studies.
As studies are improved to include larger numbers of people and to better ascertain
exposures, relationships become clearer. Some of these studies are:
 19

(1) Hardell L, Eriksson M, Lenner P, Lundgren E, “Malignant lymphoma and

exposure to chemicals, especially organic solvents, chlorophenols and phenoxy
acids: a case control study,” Br J Cancer (1981);43:169 176, attached as Exhibit
45;
(2) Ibrahim MA, Bond GG, Burke TA et al., “Weight of the evidence on the
human carcinogenicity of 2,4-D,” Environ Health Perspect 1991;96:213 22.:213
222, attached as Exhibit 46;
(3) Becher H, Flesch Janys D, Kauppinen T et al., “Cancer mortality in
German male workers exposed to phenoxy herbicides and dioxins,” Cancer
Causes Control 1996;7:312 321, attached as Exhibit 47;
(4) Hooiveld M, Heederik DJ, Kogevinas M et al., “Second Follow up of a
Dutch Cohort Occupationally Exposed to Phenoxy Herbicides, Chlorophenols,
and Contaminants,” Am J Epidemiol 1998;147:891 901, attached as Exhibit 48;
(5) Bertazzi PA, Zocchetti C, Pesatori AC, Guercilena S, Sanarico M, Radice
L, “Ten year mortality study of the population involved in the Seveso incident in
1976,” Am J Epidemiol 1989;129:1187 1200, attached as Exhibit 49;
(6) Hardell L, Eriksson M, “Is the decline of the increasing incidence of non
Hodgkin lymphoma in Sweden and other countries a result of cancer preventive
measures?” Environ Health Perspect, 2003;111:1704 1706, attached as Exhibit
50;
(7) McDuffie HH, Pahwa P, McLaughlin JR et al., “Non Hodgkin's
Lymphoma and Specific Pesticide Exposures in Men: Cross Canada Study of
Pesticides and Health,” Cancer Epidemiol Biomarkers Prev 2001;10:1155 1163,
attached as Exhibit 51; and
(8) Mills PK, Yang R, Riordan D, “Lymphohematopoietic cancers in the
United Farm Workers of America (UFW), 1988-2001,” Cancer Causes Control,
2005;16:823 830, attached as Exhibit 52. This recent work is particularly
important because a dose-response effect was seen, with higher incidence at
higher exposures. Observation of a dose-response increases the certainty
regarding causality, as does repeated findings.
 20

44) In 2006, Chiu identified genetic translocations in non-Hodgkin lymphoma that were
much more prevalent in patients who had been exposed to 2,4-D. This follicular
lymphoma is the type that is most difficult to treat in advanced stages. (Chiu BC,
Dave BJ, Blair A, Gapstur SM, Zahm SH, Weisenburger DD, “Agricultural pesticide
use and risk of t(14;18)-defined subtypes of non-Hodgkin lymphoma,” Blood
2006;108:1363-1369, attached as Exhibit 53)

45) Dicamba is a phenoxy herbicide that would also be contaminated with dioxins.
There is comparatively very little research into this chemical specifically, although it
is very commonly used in combination with other phenoxy herbicides such as 2,4-D.
Nevertheless, it was recently linked to lung and colon cancers in a study of 41,969
applicators. (Samanic C, Rusiecki J, Dosemeci M et al. Cancer incidence among
pesticide applicators exposed to dicamba in the agricultural health study. Environ
Health Perspect. 2006;114:1521-1526), attached as Exhibit 54.

46) As reviewed by the US Institute of Medicine, there is substantial research

demonstrating significant correlations between cancers and exposure to Rainbow
herbicides; the ingredients and contaminants. The active ingredients of Agents
Orange, Purple, Pink and Green are the phenoxy herbicides 2,4,5-
trichlorophenoxyacetic acid (2,4,5 T) and 2,4-dichlorophenoxyacetic acid (2,4-D).
2,4-D was also in Agent White.

Dioxin Contamination of Phenoxy herbicides

47) During the manufacture of these two phenoxy herbicides, 2,4-D and 2,4,5-T,
chlorinated dibenzo-p-dioxins are formed. At higher reactor temperatures during
synthesis of phenoxy herbicides, both the speed and efficiency of the reaction, and
the degree of dioxin contamination in the final product increase. Dow Chemical
manufactured Agent Orange as well as the phenoxy herbicides used in registered
pesticide products.

48) Dibenzo-para-dioxins ("dioxins") are toxic chemicals that are very persistent in the
environment. There are 75 different dioxins, distinguished by the number and
 21

arrangement of chlorine atoms around dioxin's three ring structure. They are among
the most toxic compounds made by man, and some are targeted for elimination
under the Canadian Environmental Protection Act. In 1990, Environment Canada
and Health Canada reported, for the Government of Canada, that phenoxy herbicides
were the largest source of dioxins in the environment. Dioxins containing more than
one chlorine atom are almost exclusively man-made. Excerpts from this report,
prepared under the Canadian Environmental Assessment Act, are attached as Exhibit
55.

49) The World Health Organization INCHEM Environmental Health Criteria 88 on

Polychlorinated dibenzo-para-dioxins and dibenzofurans, lists chemicals with these
contaminants in Table 12, which is reproduced as Exhibit 56. Specifically, 2,4-
dichlorophenoxyacetic acid, 2,4-dichlorophenoxybutyric acid, 3,6-dichloro-2-
methoxybenzoic acid, 2,4-Dichlorophenoxy propionic acid, Hexachlorobenzene,
Nitrofen, Pentachlorophenol and other chlorinated phenols, all of which were used
at CFB Gagetown to a greater or lesser degree, may be contaminated with 2,3,7,8-
TCDD. Additionally, it is noted that contaminants of chlorinated phenols and
products in which they were used (e.g. polychlorinated phenoxy herbicides) were
estimated to be the major source of higher chlorinated dioxins in the Canadian
environment. 2,3,7,8-tetrachlorodibenzo-para-dioxin (2,3,7,8-TCDD), with four
symmetrically placed chlorine atoms, is the predominant dioxin formed as a by-
product of 2,4,5-T manufacture, and 2,3,7,8-TCDD was historically also a
significant contaminant of 2,4-D.

50) The World Health Organization and the International Agency for Research on
Cancer evaluated carcinogenicity of chlorinated dibenzo-para-dioxins. They
concluded that 2,3,7,8-TCDD has been demonstrated to be carcinogenic at multiple
sites in experimental animals, with tumour promotion following binding to the Ah
receptor. The Ah receptor functions the same way in humans as in experimental
animals; and tissue concentrations in heavily exposed human populations in which
an increased overall cancer risk was observed are similar to those in rats exposed to
 22

carcinogenic dosage regimens in bioassays. Studies of 2,3,7,8-TCDD, as well as

phenoxy herbicides are discussed. 2,3,7,8-TCDD was given the most severe
designation, a “known human carcinogen.” 2,7-DCDD was not evaluable at the
time, due to a paucity of data. (IARC Monographs on the Evaluation of
Carcinogenic Risks to Humans. Volume 69. Polychlorinated Dibenzo-para-Dioxins
and Polychlorinated Dibenzofurans. Summary of Data Reported and Evaluation. 8-
12-1997.), attached as Exhibit 57.

51) 2,7-diclorodibenzo-p-dioxin (2,7-DCDD) is a dioxin that is formed during

manufacture of 2,4-D. Excerpts describing the dioxin contaminants of 2,4-D and
other phenoxy herbicides including 2,4,5-T, from the World Health Organization
International Programme on Chemical Safety, “Environmental Health Criteria 29,
2,4-dichlorophenoxyacetic acid (2,4-D) are attached as Exhibit 58, and excerpts
from Environmental Health Criteria 84 are attached as Exhibit 59. 2,7-DCDD is not
subject to regulation or monitoring by Canada’s agencies. To my knowledge,
manufacturers’ analyses of this contaminant are not public.

52) At a meeting on August 11, 2006 in Ottawa, I asked the executive director (Dr.
Karen Dodds) of Canada’s Pest Management Regulatory Agency (PMRA), and staff
representing laboratory services, health evaluation, re-evaluation and other divisions,
about levels of 2,7-DCDD in today’s 2,4-D. Neither Dr. Dodds nor her staff had any
recent information that they could offer regarding recent concentrations of
2,7-DCDD in herbicides. They informed me, and I do verily believe to be true, that
the levels of 2,7-DCDD are orders of magnitude higher than the levels of TCDD.
The PMRA carries out 2,3,7,8-TCDD analyses, and I asked them to analyze the
2,7-DCDD at the same time. Staff told me that they cannot do this because if they
attempted to measure the 2,7-DCDD in the same analytical run as the TCDD it
would swamp their detectors. The PMRA is not required to monitor 2,7-DCDD, and
does not measure it because this would require separate, expensive repeat dioxin
analyses. This substantiates what I understand and know about the manufacturing
processes, that to this day 2,4-D is highly contaminated with 2,7-DCDD. Other
 23

phenoxy herbicides are manufactured using chemically similar feedstocks and have
the same issues regarding manufacturing, so I expect that the same would be true for
them.

53) The chemical manufacturing background of the 2,4-D contamination with 2,4,7,8-
TCDD is that the 2,4-dichlorophenol feedstock was contaminated with the chemical
used to make 2,4,5-T (i.e. 2,4,5-trichlorophenol). Currently, purer feedstock means
that less 2,3,7,8-TCDD is formed. Changes in manufacturing to reduce 2,3,7,8-
TCDD and dioxins in general are noted in the PMRA assessment of 2,4-D
(PACR2005-01), in footnote 5, on page 11 (attached as Exhibit 22).

54) The historical contamination of 2,4-D samples with 2,3,7,8-TCDD and the ongoing
contamination with other dioxins, particularly 2,7-DCDD, have been confirmed to
me not only by PMRA staff, but also by the late Mr. Don Page, past head of the
Industry Task Force II for 2,4-D Research.

55) In 1986, Hagenmaier measured 6.8 ppb of 2,3,7,8-TCDD as a contaminant in 2,4-D

(Hagenmaier H. Determination of 2,3,7,8-tetrachlorodibenzo-p-dioxin in commercial
chlorophenols and related products. Fresenius Z Anal Chem. 1986;325:603-606,
attached as Exhibit 60).

56) Tetrachlorodibenzo-p-dioxins as well as dioxins with 2 and 3 chlorine atoms were

measured in 2,4-D at Agriculture Canada in Ottawa, during development of the
standard measurement technique (gas chromatography - mass spectrophotometry) by
Cochrane et al. in 1981 (Cochrane WP, Singh J, Miles W, Wakeford B.
Determination of chlorinated dibenzo-p-dioxin contaminants in 2,4-D products by
gas chromatography-mass spectrometric techniques. J Chromatography.
1981;217:289-299, attached as Exhibit 61). Unlike previous work referenced in this
paper, the 2,3,7,8-TCDD congener was not found in this work, although high levels
 24

of 2,7-DCDD were. Very high levels of total dioxins were measured, up to 23.8
ppm in ester products.

57) In the Task 3 Fact Finder report (Task 2, Appendix A), Cantox assumed a non-zero
value for 2,3,7,8-TCDD contamination of 2,4-D based upon information provided by
Health Canada.

Picloram
58) Picloram is highly carcinogenic in rats and mice, yielding neoplasms in all sites.
(Reuber MD, “Carcinogenicity of picloram,” J Toxicol Environ Health 1981;7:207
222, abstract attached as Exhibit 62.)

59) Tordon in its various forms, is a mixture of 2,4-D and picloram. Picloram was
historically contaminated with high levels of hexachlorobenzene (HCB).

60) HCB may be contaminated with highly chlorinated forms of dioxin, that have been
detected at high levels at CFB Gagetown. These dioxins with seven or eight
chlorine atoms are also more persistent in the environment.

Adjuvants
61) The herbicide that is sprayed is generally a mixture of one or more pesticides, plus
other ingredients called “adjuvants.” Adjuvant ingredients are used to improve the
performance of the pesticide, as described by Green, in “Adjuvant Outlook for
Pesticides” by DuPont Crop Protection, Newark, Delaware USA, attached as Exhibit
63. The use of additional tank-mix adjuvants is described, including for products
that already include surfactant ingredients.

62) Surfactants and other ingredients are added to pesticide formulations to improve
spreading over and penetration of foliage. Effects of adjuvants may be diverse and
species-specific, as described by Lui et al. (Liu Z. Effects of surfactants on foliar
uptake of herbicides - a complex scenario. Colloids Surf B Biointerfaces.
 25

2004;35:149-153), attached as Exhibit 64. Similarly, pesticide penetration of skin is

enhanced by surfactants, lotions and even insect repellents, as described by Pont et
al. (Pont AR, Charron AR, Brand RM. Active ingredients in sunscreens act as
topical penetration enhancers for the herbicide 2,4-dichlorophenoxyacetic acid.
Toxicol Appl Pharmacol. 2004;195:348-354.), attached as Exhibit 65.

63) When spraying from an aircraft, droplet size is difficult to control. Smaller droplets
fall more slowly and drift further, as described in the textbook Environmental
Chemistry, an excerpt attached as Exhibit 66. Importantly from the point of view of
pulmonary disease and cancer, smaller particles (droplets, or dried residues)
penetrate more deeply into lungs, as described by Foos et al. (Foos B, Marty M,
Schwartz J et al. Focusing on children's inhalation dosimetry and health effects for
risk assessment: an introduction. J Toxicol Environ Health A. 2008;71:149-165),
reproduced in part (pages 149, 152-154) as Exhibit 67.

Contaminants and breakdown products

64) The pesticide ingredients of concern are known to have been contaminated to a
greater or lesser extent, at various times, depending at least in part upon the
particular conditions of manufacturing. Contamination may arise in a variety of
ways. The feedstocks of herbicide manufacture could have been contaminated, the
conditions of herbicide manufacturing may have caused formation of high levels of
contaminants (particularly when the temperature is higher than ideal) or the two
factors could have worked together to cause formation of toxic contaminants. As
well, when herbicides break down the resulting chemicals may be toxic.

65) Chlorinated phenols are used in the manufacture of phenoxy herbicides, and when
the herbicides break down they reverts to these chemicals. Chlorinated phenols are
possible human carcinogens. As described in references below, they may also
dimerize (two molecules may join together) in the environment to form dioxins.
 26

Dioxins
66) Dioxins bioaccumulate - they collect in fatty tissue and the liver, and become
concentrated in animals higher up the food chain. According to the US Centres for
Disease Control, dioxins are in people's bodies, as measured in the blood (excerpts
attached as Exhibit 68). Indeed, according to the Environmental Working Group,
dioxins enter the womb, and are in mothers' milk, as shown in excerpts of “Across
Generations. Industrial chemicals in mothers and daughters: The pollution we share
and inherit,” excerpts attached as Exhibit 69.

67) 2,3,7,8-TCDD binds with a protein in cells in the body, at a site called the aryl
hydrocarbon receptor (AhR). As discussed above, when this happens, it sets in
motion cellular machinery that affects many body systems and organs. These are
sometimes referred to as “dioxin-like” toxicities, since other chemicals with a similar
arrangement of chlorine atoms, including some furans and polychlorinated
biphenyls, also bind with the AhR and elicit similar toxic effects. Some long-term
effects of this AhR binding is described by Landi et al. in “TCDD-mediated
alterations in the AhR-dependent pathway in Seveso, Italy, 20 years after the
accident,” attached as Exhibit 70.

68) 2,3,7,8-TCDD binds the AhR most strongly, and is considered the most toxic dioxin.
The other 16 AhR-binding dioxins, and other dioxin-like chemicals, are pro-rated
using “toxic equivalent factors” (TEF) according to how strongly they bind the AhR.
Using this method, toxicity of various chemicals or mixtures may be reported as
“toxic equivalents” (TEQ) – the mass of 2,3,7,8-TCDD that would bind the AhR in
an equivalent manner. AhR binding “accounting” of toxicities is a convenient
regulatory tool, allowing regulation of a large number of toxic chemicals according
to in vitro tests. The TEQ/TEF method is described in Van den BM, Birnbaum LS,
Denison M et al., “The 2005 World Health Organization re-evaluation of human and
mammalian toxic equivalency factors for dioxins and dioxin-like compounds,”
Toxicol Sci 2006;93:223-241, attached as Exhibit 11. As acknowledged, this scheme
is based upon the assumption that all of these molecules act through the AhR, and
 27

not via other mechanisms that may not be common to the entire group of chemicals.
As useful as this approach is from a regulatory point of view, it is naïve and
simplistic to believe that chemicals such as dioxins would bind with only one site
(the AhR) in a body. The articles discussing dioxin toxicities all mention that
dioxins could potentially also bind to other sites and that toxic effects that would
ensue are not accounted for in the TEQ system.

69) Population-wide effects of 2,3,7,8-TCDD exposure are diverse, and some depend
upon the timing of the exposure. A recent study by Mocarelli of citizens in Seveso,
Italy where a 1976 accident released large quantities of 2,3,7,8-TCDD highlights
some of this complexity. Exposure during infancy eventually resulted in reduced
sperm concentration and motility, while exposure during puberty resulted in the
opposite. However, exposure in either infancy or puberty consistently resulted in
reduced estradiol and increased follicle-stimulating hormone (Mocarelli P, Gerthoux
PM, Patterson DG, Jr. et al. Dioxin exposure, from infancy through puberty,
produces endocrine disruption and affects human semen quality. Environ Health
Perspect. 2008;116:70-77, attached as Exhibit 71).

70) A recent update of the Seveso cohort confirmed excess mortality from lymphatic and
hematopoietic tissue neoplasms (lymphoma and leukemia), as well as increased
mortality from circulatory diseases in the first years after the accident, from chronic
obstructive pulmonary disease, and from diabetes mellitus. (Consonni D, Pesatori
AC, Zocchetti C et al. Mortality in a population exposed to dioxin after the Seveso,
Italy, accident in 1976: 25 years of follow-up. Am J Epidemiol. 2008;167:847-858.),
attached as Exhibit 72.

71) A frequently observed effect of 2,3,7,8-TCDD is chloracne, as discussed in the

following citations:
a) Baccarelli A, Pesatori AC, Consonni D et al., “Health status and plasma dioxin
levels in chloracne cases 20 years after the Seveso, Italy accident,” Br J
Dermatol 2005;152:459 465, attached as Exhibit 73; and
 28

b) Panteleyev AA, Bickers DR, “Dioxin induced chloracne reconstructing the

cellular and molecular mechanisms of a classic environmental disease,” Exp
Dermatol 2006;15:705 730, attached as Exhibit 74.

72) Hexachlorobenzene may also be contaminated with dioxins, to the extent that
chloracne has occurred in workers. (Coenraads PJ, Olie K, Tang NJ. Blood lipid
concentrations of dioxins and dibenzofurans causing chloracne. Br J Dermatol.
1999;141:694-697), attached as Exhibit 75.

73) Exhibit 76 contains excerpts from the Toxicological Profile for Chlorinated
Dibenzo-p-dioxins from the Agency for Toxic Substances and Disease Registry of
the United States Department of Health and Human Services. It summarizes animal
studies, including some on 2,7-dichlorodibenzo-p-dioxin (2,7-DCDD). In many
tests 2,7-DCDD was found to be less toxic than 2,3,7,8-TCDD, but it was reported to
have developmental effects similar to 2,3,7,8-TCDD, with considerable variation
amongst species and strains. 2,7-DCDD affected the heart, liver and antibody
response. Cancers, including leukemias, lymphomas, hemangiosarcomas and
hemangiomas, as well as dose-related increased incidences of hepatocellular
adenomas and carcinomas were also observed. Most significantly, 2,7-DCDD was
noted to be “equipotent” to TCDD in suppressing response of neutrophils (a kind of
white blood cell) to antibodies in mice and in vitro. This type of phenomenon is
implicated in development of lymphoma and leukemia. These studies are attached as
Exhibits 77 and 78 (Holsapple MP, Dooley RK, McNerney PJ, McCay JA. Direct
suppression of antibody responses by chlorinated dibenzodioxins in cultured spleen
cells from (C57BL/6 x C3H)F1 and DBA/2 mice. Immunopharmacology.
1986;12:175-186 and Holsapple MP, McCay JA, Barnes DW. Immunosuppression
without liver induction by subchronic exposure to 2,7-dichlorodibenzo-p-dioxin in
adult female B6C3F1 mice. Toxicol Appl Pharmacol. 1986;83:445-455). This type
of effect would feed directly into development of cancers, as discussed above.
 29

Hexachlorobenzene (HCB)
74) Hexachlorobenzene (HCB) has been used as a pesticide, and is a contaminant and
by-product of the manufacture of other pesticides such as picloram. HCB is
extremely persistent in the environment, and bioaccumulates in adipose tissue and
the liver. As depicted in Exhibit 3, the World Health Organization accorded HCB its
highest rating, 1A Extremely Hazardous, in its Recommended Classification of
Pesticides (2004).

75) The international trade of HCB is regulated by the Rotterdam convention on Prior
Informed Consent (see http://www.pic.int/), which entered into force on 24 February
2004.

76) HCB has caused a serious outbreak of porphyria in humans. The use and production
of hexachlorobenzene is severely restricted by the Stockholm convention on
persistent organic pollutants, which entered into force on May 17, 2004. This is
described at the international website: http://www.pops.int.

77) According to the World Health Organization International Agency for Research on
Cancer, there is sufficient evidence that HCB causes cancer in animals, and
information that suggests carcinogenicity in humans, so it is classified as a possible
human carcinogen, 2B. The HCB section is appended as Exhibit 79.

78) High levels of exposure to hexachlorobenzene in a community has been associated

with high prevalence of soft tissue sarcoma and thyroid cancer. (Grimalt JO, Sunyer
J, Moreno V et al., “Risk excess of soft tissue sarcoma and thyroid cancer in a
community exposed to airborne organochlorinated compound mixtures with a high
hexachlorobenzene content,” Int J Cancer 1994;56:200 203, attached as Exhibit 80.)

79) Hexachlorobenzene has been found to be immunotoxic, affecting immunoglobulins,

neutrophils and T-cells in a variety of locations including the skin, liver and lung.
Observations in animals and humans were reviewed by Michielsen et al. in “The role
 30

of the immune system in hexachlorobenzene induced toxicity,” Environ Health

Perspect 1999;107 Suppl 5:783 92, attached as Exhibit 81.

80) Picloram was contaminated with HCB, although manufacturing changes were made
to reduce this contamination. (United Nations Environment Programme,
International Labour Organisation, World Health Organization. International
Programme on Chemical Safety, “Environmental Health Criteria 195
Hexachlorobenzene,” (1997), available at:
http://www.inchem.org/documents/ehc/ehc/ehc195.htm, attached as Exhibit 82).

81) The Institute of Medicine examined health effects of the three herbicide ingredients
2,4-D, 2,4,5-T, and picloram (in combination), concluding that they are associated
with an increase in lymphomas (also in combination) as seen in their publication
“Veterans and Agent Orange. Update 2000” available at
http://www.iom.edu/Object.File/Master/4/122/AOrange20004pager.pdf. This
grouping of all lymphomas and an underlying immune dysfunction etiology is
pervasive in the scientific literature. These themes are well represented in a recent
article (Fisher SG, Fisher RI. The emerging concept of antigen-driven lymphomas:
epidemiology and treatment implications. Curr Opin Oncol. 2006;18:417-424),
attached as Exhibit 83. Discerning fundamental differences or commonalities in
aetiology is different from classifying lymphomas according to clinical distinctions
once they have developed. Clinical differences that arise during the progression of
lymphoma are important to choose a course of treatment, but should not be equated
with fundamental differences in aetiology.

82) Recent research on roles of aromatic hydrocarbon solvents (phenols are of this class)
suggests an immunological mechanism could be involved in development of
lymphoma from exposure to solvents such as benzene. (Vineis P, Miligi L,
Constantini AS, “Exposure to Solvents and Risk of Non-Hodgkin Lymphoma: Clues
on Putative Mechanisms,” Cancer Epidemiol Biomarkers Prev 2007;16:381 384,
attached as Exhibit 84.)
 31

Hormone-linked cancers (prostate)

83) Dioxins and the pesticides of interest in this Class Action have been linked to
cancers in multiple sites. It is interesting that pesticides may act similarly to
hormones, which can promote the growth of cancers. These hormonal or “endocrine
disrupting” effects may also cause reproductive, developmental, and neurological
problems. Hormonal effects are described in:
a) Xie L, Thrippleton K, Irwin MA et al., “Evaluation of Estrogenic Activities of
Aquatic Herbicides and Surfactants Using an Rainbow Trout Vitellogenin
Assay,” Toxicol Sci 2005;87:391 398, attached as Exhibit 85; and
b) Kim HJ, Park YI, Dong MS, “Effects of 2,4-D and DCP on the DHT Induced
Androgenic Action in Human Prostate Cancer Cells,” Toxicol Sci 2005;88:52 59,
attached as Exhibit 86.

84) Prostate cancer can be promoted by chemicals that act in a manner similar to
hormones (hormone mimics), that disrupt the endocrine system (endocrine
disruptors). As described in this Affidavit, dioxins and hexachlorobenzene are
known endocrine disruptors.

Cancers linked to herbicides

85) The attention of the medical and scientific community was drawn to the adverse
health effects associated with 2,4-D and 2,4,5-T in the 1970s. In September 1973,
an entire issue of Environmental Health Perspectives was devoted to health effects of
dioxins, with papers authored by Dow Chemical employees. One example (Schwetz
BA, Norris JM, Sparschu GL et al., “Toxicology of chlorinated dibenzo-p-dioxins,”
Environ Health Perspect 1973;5:87-99:87-99) is attached as Exhibit 87.

86) By the 1970's, toxicology studies, even among chemical company funded
researchers, indicated that dioxin was a potent carcinogen. (Kociba, R.J. et al.,
“Results of a Two-Year Chronic Toxicity and Oncogenicity Study of
2,3,7,8-tetrachlorofibenzen-p-Dioxin in Rats,” Toxicol. Applied Phamacol
 32

1978;469:179-303, attached as Exhibit 88.) The lead author and other authors of the
articles attached as Exhibits 87 and 88 were Dow Chemical employees and the work
was funded by Dow Chemical.

87) Hardell has researched extensively the etiology of non Hodgkin’s lymphoma (nHL),
and has discussed how this cancer of lymphocytes has at its root disruption of the
immune system. (Hardell L, Lindstrom G, Van BB, Fredrikson M, Liljegren G,
“Some Aspects of the Etiology of Non-Hodgkin's Lymphoma,” Environ Health
Perspect 1998;106 Suppl 2:679 81, attached as Exhibit 89.) A role of persistent toxic
chemicals in the etiology of non-Hodgkin’s lymphoma is discussed in Hardell L,
Lindstrom G, Van BB et al, “Adipose Tissue Concentrations of Dioxins and
Dibenzofurans, Titers of Antibodies to Epstein Barr Virus Early Antigen and the
Risk for Non Hodgkin Lymphoma,” Environ Res 2001;87:99 107, attached as
Exhibit 90. Studies of the relationship between Epstein Barr virus and dioxin-like
chemicals (that bind the AhR) in development of non-Hodgkin lymphoma revealed
that virus-linked cancer progressed when there were also significant levels of
persistent organic pollutants such as dioxins in the body. Thus, toxic chemicals and
the immune suppression they cause may underlie apparently distinct causes of
non-Hodgkin lymphoma.

88) Dioxins along with herbicide exposure have been correlated with increased risk for
“all cause” cancer (cancers in any site), as described in:
a) Becher H et al., “Cancer mortality in German male workers exposed to phenoxy
herbicides and dioxins, Cancer Causes Control 1996;7:312 321, attached as
Exhibit 47;
b) Steenland K, Bertazzi P, Baccarelli A, Kogevinas M, “Dioxin Revisited:
Developments Since the 1997 IARC Classification of Dioxin as a Human
Carcinogen,” Environ Health Perspect, 2004;112:1265 1268, attached as Exhibit
91;
 33

c) Kogevinas M, “Human health effects of dioxins: cancer, reproductive and

endocrine system effects,” Hum Reprod Update 2001;7:331 339, attached as
Exhibit 44; and
d) Bertazzi PA, Consonni D, Bachetti S et al., “Health Effects of Dioxin Exposure:
A 20 Year Mortality Study,” Am J Epidemiol 2001;153:1031 1044, attached as
Exhibit 92.

89) There has been much research and debate about health effects of exposure to
herbicides in Vietnam. According to Frumkin H, “Agent Orange and Cancer: an
Overview for Clinicians,” CA Cancer J Clin. 2003;53:245-255, attached as Exhibit
93, “There is sufficient evidence for an association between Agent Orange exposure
and the malignancies: soft tissue sarcoma; non Hodgkin lymphoma; Hodgkin
disease; and chronic lymphocytic leukemia (CLL). Evidence is limited or suggestive
that there are links with respiratory cancers (lung, trachea/bronchus, larynx), prostate
cancer and multiple myeloma.”

90) Arsenic, including the form cacodylic acid that was applied at Gagetown, has long
been a known human carcinogen, according to the International Agency for
Research on Cancer (IARC) (Arsenic and Arsenic Compounds (Group 1) -
Summaries & Evaluations, attached as Exhibit 94).

Epidemiology and Interpretation of Studies

91) Scientific uncertainty in epidemiology translates into lower estimation of risks, as

the estimate is obscured by confounding or unrecognized factors. This arises in part
due to the limitations of our understanding of the roots of cancers. On a general
level, cancer ultimately amounts to the uncontrolled proliferation of genetically
abnormal cells. Multiple steps are involved in producing the genetic
abnormality(ies), and to prod the initial abnormal cells both to reproduce and not to
die. (Luch A, “Nature and Nurture Lessons from Chemical Carcinogenesis,” Nat Rev
Cancer 2005;5:113 125, attached as Exhibit 95.)
 34

92) In analyses of epidemiological studies, there are two possible types of erroneous
conclusions that scientists might draw. A harmful effect might be reported when it
in fact only occurred by chance (false positive), or a true effect might be missed
(false negative). Mathematically, there is an unavoidable trade-off between these
two types of error. If you want to be extremely certain that you do not conclude that
a pesticide causes harm when it really does not, you increase the possibility that real
harm will be deemed insignificant during the statistical analyses. The probability of
“missing” a real effect due to the mathematical “noise” also increases as the
frequency of the event decreases (e.g. for cancers, which are relatively rare events).
Most importantly, the standards for error testing for these statistical tests are entirely
subjective.

93) A standard assumption in toxicological research has been that “the dose makes the
poison.” This simplistic (albeit convenient) truism is now known to be inaccurate.
Chronic low doses may have adverse biological effects in addition to those
associated with acute high doses, which is why regulatory bodies doing chemical
assessment (e.g. Canada’s Pest Management Regulatory Agency) require not only
acute and chronic of testing in animals, but also multi-generational testing.
Unfortunately, regulatory testing does not explore the entire dose-response curve.
One reason that low-dose effects occur is that at high doses, protective mechanisms
are triggered in the body to rid it of the chemical, while at low doses the chemical is
"below the radar" and these metabolic and excretion mechanisms may not be
triggered. Some chemicals that bind with receptor sites (e.g. endocrine disrupting,
hormone mimicking chemicals) may cause different effects depending upon degree
of saturation. Tiny doses during gestation may have life-time consequences.
Endocrine (hormonal) effects and suppression of the immune system may arise at
very low chronic levels, but not be detected with higher acute exposures. Of course,
this immune suppression is what may be the link to lymphomas. In a very readable
summary, Myers compiled many examples of low-dose effects as reported in high
quality, peer-reviewed publications (Meyers P and Hessler W. Does 'the dose make
 35

the poison?' Extensive results challenge a core assumption in toxicology.

Environmental Health News, 30-4-2007), attached as Exhibit 96.

94) Thus, soldiers who were exposed to areas that had been defoliated on a repeated
basis during the years between when those chemicals were directly applied to a
specific area, could reasonably be equally at risk of developing a lymphoma as an
individual who had direct contact with the specific chemicals at the time they were
applied.

95) Dr. Warren Porter has studied pesticides and low dose exposures. One example of
the unexpected results of low doses of commercially available herbicide containing
2,4-D is in an article he co-authored (Cavieres MF et al., “Developmental Toxicity
of a Commercial Herbicide Mixture in Mice: I. Effects on Embryo Implantation and
Litter Size,” Env Health Persp 2002;110(11):1081-1085, attached as Exhibit 97.)
Rather than seeing a steadily more severe effect with increasing exposure, a
U-shaped dose-response curve was found for reproductive toxicity of a mixture of
herbicides.

96) In summary, results reported in the peer-reviewed literature attached to this Affidavit
are more likely to be understating than overstating connections between chemicals
and health outcomes. As well, high-exposure studies showing mixed results cannot
automatically disprove studies where significant effects were seen, at lower
exposures.

97) Scientific thought is evolving in the subject of cancer epidemiology as it is

recognized that, even in the seemingly straightforward cases where treatment of a
virus or bacterium may result in a cure, cancers are not generally caused by a simple
mechanism or a single biological agent. As well, cancers evolve in individuals
during the course of the disease, such that a malignancy that initially responds to
therapy may eventually develop resistance, with fatal consequences. Established
epidemiologists have published a discussion of cancer and neurological harms from
 36

chronic exposure to pesticides, including phenoxy herbicides, explaining how and

why epidemiological links may be under estimated. (Alavanja MC, Hoppin JA,
Kamel F., “Health effects of chronic pesticide exposure: cancer and neurotoxicity,”
Annu Rev Public Health, 2004;25:155 97), attached as Exhibit 98.

Incrementally increased risk

98) Some argue that it is both necessary and impossible to assess numerous chemicals,
environmental concentrations, routes of exposure, internal doses and diseases to
establish that particular chemical(s) caused health condition(s) for individuals. In
this Affidavit I explain why I believe that the crucial point is that the toxic chemical
exposures in and around CFB Gagetown were above the norm of the day, such that
they specifically would contribute significantly to ill health among members of the
proposed class.

99) In awarding assistance to veterans following exposures to herbicides, the Canadian

and US governments have already clearly recognized that among the many
determinants of health (e.g. genetics, epigenetics, nutrition, lifestyle, infections and
toxic exposures), the toxic chemical exposures, and ensuing doses, are a significant
contributor to ill health of those exposed to these chemicals, including at CFB
Gagetown, far beyond the norm of the day.

100) While lifestyle and genetics are determinants of health, environmental contaminants
are extremely important as well (“Genuis SJ. Medical practice and community health
care in the 21st century: a time of change”, Public Health, 2008;122:671-680,
attached as Exhibit 99). Toxic chemical exposures at earlier ages are additionally
important, as development may be affected and the stage is set for health throughout
life. A few examples of a large body of research include immune suppression in
young children who had been exposed to higher levels of dioxins as infants
compared with lower-exposed infants, decreased sperm quality and altered hormone
levels later in life following childhood exposure to dioxins, and altered breast
 37

development (attached as Exhibit 100, Weisglas-Kuperus N, Patandin S, Berbers GA

et al. “Immunologic effects of background exposure to polychlorinated biphenyls
and dioxins in Dutch preschool children”, Environ Health Perspect, 2000;108:1203-
1207; Exhibit 101, Mocarelli P, Gerthoux PM, Patterson DG, Jr. et al., “Dioxin
exposure, from infancy through puberty, produces endocrine disruption and affects
human semen quality”, Environ Health Perspect, 2008;116:70-77; and Exhibit 102,
Fenton SE, “Endocrine-disrupting compounds and mammary gland development:
early exposure and later life consequences”, Endocrinology, 2006;147:S18-S24).
These effects may cause increased incidence and severity of infections, cancers,
reproductive difficulties and limited ability to breastfeed.

101) In addressing environmental determinants of health, comprehensive examinations,

laboratory testing for pollutants and ensuing biochemical abnormalities, and
treatments aimed at reducing underlying toxic chemicals and their effects
(discussed in Exhibit 99, Genuis SJ, “Medical practice and community health care
in the 21st century: a time of change”, Public Health; 2008;122:671-680) may not
be covered by all provincial health care plans.

102) As discussed in Exhibit 99 (Genuis SJ, “Medical practice and community health
care in the 21st century: a time of change”, Public Health; 2008;122:671-680),
labels for diseases reflect symptoms rather than underlying biology. In this
perspective, the medical conditions that are connected with exposures to a
common group of chemicals constitute a class.

103) Weighing scientific information to determine certainty of causality was most

famously addressed by Austin Bradford Hill (e.g. exposure preceded disease;
association is strong with a dose-response, effect has been replicated, etc.).
However, in studying health effects of chemicals in the environment a broad range
of evidence must be considered, from biochemical investigations to animal
 38

research and epidemiological studies, in order to piece together the scientific

picture. Such complex considerations do not readily fit within the Hill Criteria;
nor did Hill propose application of his ideas with great rigidity. As discussed by
Thygesen et al., “The Hill Criteria may therefore to some seem useful and sound
because they in many conditions do hold, while others may find them useless and
misleading, because under other conditions they do not hold” (attached as Exhibit
103, Thygesen LC, Andersen GS, Andersen H, “A philosophical analysis of the
Hill criteria”, J Epidemiol Community Health, 2005;59:512-516). More tersely,
Höfler argues, “the heuristic value of Hill’s consideration converges to zero as the
complexity of a causal system and the uncertainty about the true causal system
increase”(attached as Exhibit 104, Hofler M, “The Bradford Hill considerations on
causality: a counterfactual perspective”, Emerg Themes Epidemiol, 2005;2:11.:11).
The inapplicability and impracticality of a strict Hill Criteria approach led the US
Institutes of Medicine to adopt alternative assignments for strength of association
between the herbicides used in Vietnam and health conditions.

Fact Finder Reports

104) The Fact Finder Task 3B epidemiological study was conducted by Dr. Guernsey.
The author herself depicted it as a preliminary study with substantial limitations.
High quality epidemiological studies are difficult, time-consuming and expensive.
Perhaps in large part due to limited resources and time pressures, this study was
designed in a way that was predestined not to find any significant results. It should
be given no weight, for the following reasons.

a) Exposure was presumed, based upon place of residence at time of diagnosis.

There was no ascertainment of exposures or doses, and no follow-up of
personnel who had actually been at CFB Gagetown. Despite long latency
periods for development of illnesses such as cancers, it was not ascertained
whether people had been residents for sufficient time for a health condition to
be attributable to environmental exposures in the area. If people from the
Gagetown area tended to move elsewhere in the province, for example to St.
 39

John or the coast, they would be counted in the “unexposed” group after they
got sick. If they moved out of province, they would have been lost from the
study.

b) As described in her study, the group presumed to have been exposed was
expanded from that proposed by Dr. Guernsey. An Advisory Committee
including non-scientists expanded the group presumed to have been exposed
to 20% of the population of the province, including all of Fredericton. This
unusual method of research design meant that any effect that might have been
seen with a more tightly constrained or rigorously determined “exposed”
group was diluted to insignificance.

c) The standard method of risk calculation in such epidemiological research is to

compare the incidence of the health outcome in the “exposed” group to the
incidence in the “unexposed” group. Calculations in this study used
provincial statistics as the comparator, which meant that the “exposed” group
was counted in both groups. This diminished the calculated relative risk.

d) To illustrate the effects of these irregularities in experimental design and data

manipulation, I calculated that if the true effect of being in the presumed-
exposed 20% of the provincial population was to increase the probability of
illness by 100%, the method of calculation would indicate an increase of only
70%. Furthermore, if only half of the presumed-exposed group actually had
been exposed, the experimental design would mask an actual 200% increase
in risk.

105) Environmental sampling in the Fact Finder Task 2 was carried out by Jacques
Whitford Ltd. When drafted, the Task 2 work was an exploratory investigation,
preliminary to more extensive testing. In particular, sampling of biota was
recommended to investigate contaminants within the ecosystem. Species at risk
were also discussed within the planning report. The Task 2 field program was a
scaled-down version of the initial proposal.
 40

106) The Task 2 “presence/absence” field program did not include samples that would
be most likely to establish the presence of chemicals of concern. Water and soils
with little organic matter generally contain low levels of dioxins, which bind to
organic compounds. Persistent organic pollutants are concentrated in fatty
materials, and are biomagnified up food chains, so sampling of animals is
preferred in order to demonstrate the presence or absence of persistent,
bioaccumulative chemicals.

107) Vegetation is often less contaminated than the soil. In the Fact Finder report,
samples were recorded as “green plant material,” “woody stems” and “roots,” with
no identification of species. There was no mention that members of the
Curcurbitaceae (melon/squash/gourd) family tend to accumulate persistent organic
pollutants such as dioxins to a greater degree than other plants. Pumpkins and
related plants have been demonstrated to remediate soils at the Sydney Tar ponds
by sequestering persistent organic pollutants such as dioxins (personal
communication from Terry McIntyre, Environment Canada, Science and
Technology Integration Division). It is thought that an exudate from the roots
mobilizes persistent organic pollutants for uptake by zucchini and pumpkin (field
study attached as Exhibit 105, White JC, “Plant-facilitated mobilization and
translocation of weathered 2,2-bis(p-chlorophenyl)-1,1-dichloroethylene (p,p'-
DDE) from an agricultural soil”, Environ Toxicol Chem, 2001;20:2047-2052).
Wild cucumber (Echinocystis lobata) is a member of the Curcurbitaceae family,
and is a native plant that is well established in New Brunswick, according to
“Vascular Plants of New Brunswick” by Richard Fournier at the University of
Moncton (excerpt attached as Exhibit 106, Fournier R, “Plantes Vasculaires du
Nouveau – Brunswick Dicotylédones, Vascular Plants of New Brunswick,
Magnoliopsida (Dicotyledons)”, University of Moncton, 2006; available at
http://www.cuslm.ca/foresterie/plantenb/dicots.pdf). This may well have been a
missed opportunity to identify possible areas of concern by identifying and
 41

sampling plants that would take up dioxins more efficiently. Instead, the
contractor collected and analyzed miscellaneous, unidentified plants.

108) The Fact Finder Task 3 mathematical modelling by Cantox involved comparing a
calculated human dose based upon mathematical models and soil and water
pollutant data, with a supposed “safe” dose. There are many reasons this is a very
uncertain exercise, not least among them that no “safe” dose has been accepted for
TEQs, as well as the difficulty of calculating a past human dose.

109) In any mathematical modelling such as the Fact Finder risk assessment, it is
important that the methods be validated using data, so that the exercise is
demonstrated to have predictive value. There was no validation of mathematical
modelling predictions such as internal doses. This could have been done by
applying models to wildlife and comparing the results with measurements of
dioxins in animals.

110) The Fact Finder Task 3B study would have benefited from meaningful data on
contamination of foods upon which to base the deliberations and models.
Subsequent analyses (Task 4) of aquatic life did show elevated contamination
when calculated using the standard method, on a lipid-normalized basis, but this
data was not available at the time of the Fact Finder risk assessment.

111) Some routes of exposure were not assessed due to lack of data and models. They
include smoke inhalation during burning of brush, and take-home chemicals.

112) In the Fact Finder’s Task 2B report, it was recommended that ecological sampling,
including soil invertebrates and mammals, be carried out, as stated in the report
summary attached as Exhibit 107 (Jacques Whitford Ltd and National Defence and
 42

the Canadian Forces, “Report Summary Task 2B: Environmental Site Assessment
of CFB Gagetown, NB”, National Defence, 2007). Task 4 at CFB Gagetown
involved collection and analysis of fish and molluscs for dioxins. Only the muscle
of the fish was analysed. The pollutants of interest would have collected in the
fatty layer under the skin, and in organs such as the liver. Nevertheless, the data
can be used to calculate the concentration of dioxin in the fat (lipid). I carried out
these calculations, which are presented along with the summary report in Exhibit
108 (G.A Packman & Associates, Environmental Consultants, “Task 4: Fish and
Freshwater Mussel Sampling Summary”, National Defence and the Canadian
Forces, 2008). Lipid-normalized data indicated that Swan Lake Creek was
consistently much more highly contaminated than Brisley Stream or the Nerepis
River. Lipid-normalized dioxin concentrations are a standard presentation for this
type of data.

113) From my review of the Fact Finder reports, a common theme is that research
design, sampling, study execution, calculations and reporting did not maximize the
probability of finding chemicals or discerning significant risks. Rather, the
potential significance of research was minimized, and significant findings were
even obscured in the final report.

Exposures at Canadian Forces Base Gagetown

114) To recap and bring together points discussed above, 17 dioxins with chlorine
atoms in the 2,3,7 and 8 positions on the dioxin structure are subject to regulation
in Canada, and were measured at CFB Gagetown. Other chemicals that cause
"dioxin-like" health effects include hexachlorobenzene, and some furans and
polychlorinated biphenyls (PCBs), and some of which were also measured during
the Fact Finder’s project. Most importantly, many other pollutants, including 2,7-
DCDD, were not measured at all. As described above, according to staff at the
PMRA to this day 2,4-D contains 2,7-DCDD at levels that are orders of magnitude
 43

higher than 2,3,7,8-TCDD. As well, more 2,4-D has been applied, and 2,4-D was
applied more recently than 2,4,5-T (see Exhibit 3). In the very limited research on
this chemical, it was found that 2,7-DCDD disrupts the immune system in a
manner consistent with mechanisms known to instigate haematological
malignancies. Thus, unmeasured dioxins that disrupt the immune system,
including 2,7-DCDD, could be playing a part in the ill health experienced by some
veterans and citizens.

115) It may seem difficult to assess long past exposure of people to bioaccumulative
toxins contaminating herbicides, but biomonitoring (measuring the levels of
pollutants in blood or tissue of people) has an important role to play. There is
extensive literature on this topic. One example is Kerger BD, Leung HW, Scott
PK, Paustenbach DJ, “Refinements on the age-dependent half-life model for
estimating child body burdens of polychlorodibenzodioxins and dibenzofurans,”
Chemosphere. 2007;67:S272-S278, attached as Exhibit 109 (Kerger BD, Leung
HW, Scott PK, Paustenbach DJ, “Refinements on the age-dependent half-life
model for estimating child body burdens of polychlorodibenzodioxins and
dibenzofurans”, Chemosphere, 2007; 67:S272-S278). There are numerous articles
in this issue of Chemosphere, reporting body burdens of dioxins in various
populations.

116) Measurements of these persistent, lipophylic (fat-loving) chemicals may be

misleadingly low if the individual has taken extra steps to eliminate these toxins
from the body. Fortunately, health can be largely restored for many people with
serious medical conditions caused by body burdens of toxic chemicals. (Cecchini
MA, Root DE, Rachunow JR, Gleb PM, “Managing Chronic Illness in Patients.
Health Status of Rescue Workers Improved by Sauna Detoxification,” Townsend
Letter The Examiner of Alternative Medicine, 2006), attached as Exhibit 110. To
my knowledge, levels of dioxins and other contaminants such as
 44

hexachlorobenzene have yet to be systematically measured in the blood or tissues

of veterans or citizens claiming to be harmed by herbicides at CFB Gagetown.

117) At CFB Gagetown, measurements of dioxins and HCB were carried out in soil,
sediment, water and vegetative samples. Some soil samples were excessively
contaminated. However, it is expected that water and vegetation would now not be
overly elevated. The organic contaminants are not very water soluble, and do not
translocate from the roots to leaves. Sampling of vegetation is a standard
measurement to monitor ongoing emissions, for instance from an incinerator or
industrial operation but dioxin levels in leaves fall off much more quickly than
levels in the soil (Domingo JL, Schuhmacher M, Llobet JM, Muller L, Rivera J.
PCDD/F concentrations in soil and vegetation in the vicinity of a municipal waste
incinerator after a pronounced decrease in the emissions of PCDD/Fs from the
facility. Chemosphere. 2001;43:217-226), attached as Exhibit 111 (Domingo JL,
Schuhmacher M, Llobet JM, Muller L, Rivera J, “PCDD/F concentrations in soil
and vegetation in the vicinity of a municipal waste incinerator after a pronounced
decrease in the emissions of PCDD/Fs from the facility”, Chemosphere,
2001;43:217-226).

118) When assessing the environment for toxic materials that bioaccumulate such as
dioxins or hexachlorobenzene, the most efficient and effective way to detect their
presence is to test animals for them. Fish, earthworms, mammals, birds and small
biota in streams accumulate persistent pollutants such as dioxins or
hexachlorobenzene, and embody a sort of average of the contamination over their
range (e.g. earthworms and small aquatic biota do not travel great distances, fish
may remain in a watershed, and birds and foxes range over larger areas).
Potentially contaminated areas may be mapped based upon a variety of measures
of toxins. (Blanco GA, Cooper EL, “Immune systems, geographic information
systems (GIS), environment and health impacts,” J Toxicol Environ Health B Crit
Rev 2004;7:465 480), attached as Exhibit 8.
 45

Commonalities
Chemical exposures

119) Exhibit 3 (Structures, Classification and Toxicities of Herbicides and Related

Chemicals Used at Canadian Forces Gagetown) includes the chemical structures of
the herbicides. Among the highest-volume and longest term herbicides, there is a
commonality of at least one ring structure. Not only do they look similar on paper,
these “aromatic” rings with chlorine atoms attached all have toxicities associated
with them. The members of the proposed Class would have been exposed to a
chemical mixture, but the principle ingredients were similar, with similarities
amongst the chemical structures and the toxicities of the chief contaminants
(phenoxy herbicides and picloram, and their contaminants and breakdown
products).

120) Predominant toxicity may arise from the persistent pollutants – dioxins and
hexachlorobenzene. Their persistence would confer a common type of exposure
over time. These have been researched as a group, and exhibit some common
toxicities. Each substance may be identified and measured in the blood and
adipose tissue many years after exposure. As mentioned, sauna and other
supportive therapies may reduce this body burden.

121) A common thread throughout much of the timeframe is the 2,4-D, that
accompanied both 2,4,5-T and picloram in various herbicide mixtures.
Accompanying 2,4-D is the contaminant 2,7-DCDD.

Health Conditions

122) The Institute of Medicine in the US has already identified the class of health
conditions, in relation to exposure to principally the same chemicals as are the
 46

subject of this present matter. This was further acknowledged by Veterans Affairs
Canada and confirmed in the Fact Finder literature review by Dr. Guernsey.

123) In the scientific literature, health effects of phenoxy herbicides and of dioxins are
necessarily examined in combination. Similarly, toxicities of picloram and its
contaminant hexachlorobenzene are examined in combination. Furthermore,
toxicities of dioxins and hexachlorobenzene are studied in combination because
hexachlorobenzene is a “dioxin-like” chemical.

124) There are many commonalities amongst the origins of the health conditions.
Without recapping all of the above, for example, immune and/or endocrine
disruption may contribute to both the development of cancer, and to diabetes
mellitus. Hormone-mimicking chemicals may promote cancer, or cause
reproductive problems and birth defects.

125) Exposures and ensuing doses of toxic chemicals sustained on and around CFB
Gagetown were significantly greater than the norm of the day.

126) Within the limitations of the Fact Finders data, there are strong indications of past
and continuing significant contamination of CFB Gagetown.

127) The Fact Finder risk assessment and epidemiological study were highly flawed and
do not allay scientific concerns regarding substantial risk to public health.

128) In conclusion, I believe that there are sufficient commonalities amongst the toxic
chemicals that were used, the exposures of individuals in and around CFB
Gagetown, and the root mechanisms of the health conditions included in the Class.
 47

129) I make this Affidavit in support of the Plaintiff’s Motion for Certification of the
present proposed class action.

SWORN BEFORE ME at the )

__________ of _____________, in the )
Province of Ontario this ________ day of )
January, A.D. 2009 ) __________________________
) Margaret E. Sears, PhD.
______________________________ )
A Notary Public in and for the Province of )
Saskatchewan. )

This Affidavit was delivered by:

MERCHANT LAW GROUP LLP

2401 Saskatchewan Drive, #100
Regina, Saskatchewan
S4P-4H8

Lawyer in Charge of File:

E.F. Anthony Merchant, Q.C.

(306) 359-7777
(306) 522-3299
 48

List of Exhibits

(1) Curriculum Vitae of Margaret. E. Sears

(2) Sears M, Walker CR, van der Jagt RHC, Claman P. Pesticide Assessment:
Protecting Public Health on the Home Turf. Paediatr Child Health.
2006;11:229-234.
(3) Structures, Classification and Toxicities of Herbicides and Related Chemicals
Used at Canadian Forces Gagetown.
(4) United States Department of Veterans Affairs. Agent Orange - Herbicide
Exposure Vietnam Veterans Benefit From Agent Orange Rules. United
States Department of Veterans Affairs . 24-4-2007. available from
http://www.vba.va.gov/bln/21/benefits/herbicide/aono1.htm

(5) Prange JA. Origin of Dioxins in Queensland, Australia. Investigations into the
distribution and sources of polychlorinated dibenzo-p-dioxins in the
Queensland terrestrial environment [ 2003.

(6) Nishioka MG, Lewis RG, Brinkman MC, Burkholder HM, Hines CE,
Menkedick JR. Distribution of 2,4-D in air and on surfaces inside residences
after lawn applications: comparing exposure estimates from various media for
young children. Environ Health Perspect. 2001;109:1185-1191.

(7) Gladen BC, Sandler DP, Zahm SH, Kamel F, Rowland AS, Alavanja MC.
Exposure opportunities of families of farmer pesticide applicators. Am J Ind
Med. 1998;34:581-587.

(8) Blanco GA, Cooper EL. Immune systems, geographic information systems
(GIS), environment and health impacts. J Toxicol Environ Health B Crit Rev.
2004;7:465-480.

(9) Pest Management Regulatory Agency. Dow AgroSciences Esteron* 600

Forestry Herbicide. Pest Management Regulatory Agency, Health Canada . 9-
11-2007. http://pr-rp.pmra-arla.gc.ca/PR_SOL/pr_web.ve1?p_ukid=1186

(10) Joint FAO/UNEP Programme for the operation of prior informed consent. 2,4,5-
T and its salts and esters. Rotterdam Convention - Operation of the Prior
Informed Consent Procedure for Banned or Severely Restricted Chemicals.
Decision Guidance Document. Rotterdam Convention . 1996.

(11) Van den Berg M, Birnbaum LS, Denison M et al. The 2005 World Health
Organization reevaluation of human and Mammalian toxic equivalency factors
for dioxins and dioxin-like compounds. Toxicol Sci. 2006;93:223-241.
 49

(12) Ryan JJ, Schecter A. Exposure of Russian phenoxy herbicide producers to

dioxins. J Occup Environ Med. 2000;42:861-870.

(13) Kerger BD, Leung HW, Scott P et al. Age- and concentration-dependent
elimination half-life of 2,3,7,8-tetrachlorodibenzo-p-dioxin in Seveso children.
Environ Health Perspect. 2006;114:1596-1602.

(14) Bolognesi C. Genotoxicity of pesticides: a review of human biomonitoring

studies. Mutat Res. 2003;543:251-272.

(15) Andersen HR, Vinggaard AM, Rasmussen TH, Gjermandsen IM, Bonefeld-
Jorgensen EC. Effects of currently used pesticides in assays for estrogenicity,
androgenicity, and aromatase activity in vitro. Toxicol Appl Pharmacol.
2002;179:1-12.

(16) Coussens LM, Werb Z. Inflammation and cancer. Nature. 2002;19-26;420:860-

867.

(17) Li Q, Kawada T. The mechanism of organophosphorus pesticide-induced

inhibition of cytolytic activity of killer cells. Cell Mol Immunol. 2006;3:171-
178.

(18) Garry VF, Tarone RE, Long L, Griffith J, Kelly JT, Burroughs B. Pesticide
appliers with mixed pesticide exposure: G-banded analysis and possible
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