2008 Canlii 18365

WCAT Decision Number: WCAT-2008-00782
2008 CanLII 18365 (BC W.C.A.T.)

WCAT Decision Date: March 11, 2008
Panel: Randy Lane, Vice Chair
_____________________________________________________________________
Introduction
The worker’s widow, Ms. M (not her real initial), has appealed to WCAT from the
October 12, 2006 decision of a review officer with the Review Division of the Workers’
Compensation Board, operating as WorkSafeBC (Board). The review officer confirmed
January 4, 2006, February 8, 2006, and March 2, 2006 Board decisions that the
worker’s lung cancer was not due to the nature of his employment as a groundskeeper.
While the appeal was launched beyond the applicable appeal period, WCAT granted
Ms. M an extension of time in which to appeal. While the worker’s employer was
notified of the appeal, it did not indicate it wished to participate.
Ms. M’s lawyer provided an October 1, 2007 submission which was accompanied by,
among other matters, an undated opinion from Dr. S, a list of references, an October 1,
2007 opinion from Dr. B, and a September 20, 2007 report from Dr. S2. Ms. M’s
lawyer’s October 1, 2007 note was accompanied by additional material which included a
September 29, 2007 submission from Ms. M, a September 27, 2007 letter from the
worker’s mother, an October 1, 2007 letter from Dr. R, September 29 and 30, 2007
letters from Mr. N (not his real initial), copies of June 10, 2005, February 13, 2007 and
July 3, 2007 letters from the Canadian Cancer Society to newspapers and a city council,
an October 8, 2003 newspaper article regarding pesticides, a September 17, 2007
newspaper article regarding a national environmental health strategy, copies of the
worker’s pesticide applicator certificates, a newspaper article about the worker, a copy
of Ms. M’s March 21, 2007 letter to a local newspaper, a November 30, 2006 report
from Mr. L, a November 9, 2006 letter from a representative of the employer,
a November 8, 2006 letter from Mr. G (not his real initial), a March 15, 2007 newspaper
article regarding the use of pesticides, a November 2, 2005 letter from Dr. W (the
worker’s family physician) which had been previously received by the Board, and a copy
of a March 15, 2007 newspaper article regarding pesticides and the worker.
By letter of October 3, 2007 Ms. M’s lawyer provided copies of several articles cited by
Dr. S. By letter of October 5, 2007 submissions were declared complete. By letter of
October 8, 2007 Ms. M’s lawyer provided WCAT with a copy of Dr. S’s invoice. By letter
of October 11, 2007 Ms. M’s lawyer provided WCAT with an October 1, 2007 letter from
Dr. I, as well as, among other documents, an English translation of Dr. I’s January 30,
2006 letter to the Government of Québec, a copy of an April 27, 2004 newspaper article
regarding a national cancer strategy, a copy of an October 21, 2003 newspaper article
regarding the meeting of a federal-provincial-territorial committee
1
Workers’ Compensation Appeal Tribunal 150, 4600 Jacombs Road, Richmond, B.C. V6V 3B1
Telephone: (604) 664-7800; 1-800-663-2782; Fax (604) 664-7898
2008 CanLII 18365 (BC W.C.A.T.)

on pest management and pesticides, a copy of a July 23, 2007 newspaper article
regarding Dr. I, an English translation of a March 4, 1998 newspaper article regarding
Dr. I, and a chart prepared by the United States Navy regarding emergency medical
treatment for acute pesticide poisoning. I have accepted the material submitted to
WCAT after submissions were declared complete.
By letter July 25, 2007 Ms. M was advised that the appeal would proceed by way of
written submissions. That decision does not bind me if I consider an oral hearing is
necessary. I have considered the rule regarding the holding of an oral hearing set out in
item #8.90 of WCAT’s Manual of Rules of Practice and Procedure (MRPP) and the other
criteria set out in that item. WCAT will normally conduct an appeal on a read and
review basis where the issues are largely medical, legal or policy based, and the appeal
does not involve significant issues of credibility. I have reviewed the issues, evidence,
and submissions on the worker’s file and have concluded that this appeal may be
determined without an oral hearing.
Issue(s)
At issue is whether the worker’s lung cancer was due to the nature of his employment.
Jurisdiction
WCAT has exclusive jurisdiction to inquire into, hear and determine all those matters
and questions of fact, law, and discretion arising or required to be determined in an
appeal before it (section 254 of the Workers Compensation Act (Act)). It is not bound
by legal precedent (subsection 250(1) of the Act). WCAT must make its decision on the
merits and justice of the case, but, in so doing, it must apply a policy of the board of
directors of the Board that is applicable in the case.
This is an appeal by way of rehearing, rather than a hearing de novo or an appeal on

the record. WCAT has jurisdiction to consider new evidence, and to substitute its own
decision for the decision under appeal.
Background
The worker was employed as a groundskeeper for a regional district from April 1996
until May 2005. He was responsible for the maintenance of slightly less than 30 acres
of public green space. His position included grounds and park maintenance, equipment
operation, and sundry maintenance. Pursuant to the Pesticide Control Act, the worker
was issued a pesticide applicator certificate in March 1997. He held such a certificate at
the date of his death. The worker was the only district employee who possessed such a
certificate. He sprayed pesticides for eight to 12 days each season. He was also the
first aid attendant and lead hand. He last worked on January 28, 2005.
2
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2008 CanLII 18365 (BC W.C.A.T.)

The worker died on May 16, 2005. The medical certification of death indicated that he
died of a cessation of respiration due to, or as a consequence of, metastatic cancer due
to, or as a consequence of, bronchogenic cancer.
Ms. M contacted the Board in October 2005. She considered that the worker’s cancer
had been caused by his exposure to pesticides. The Board gathered medical records
from a hospital and from Dr. W. In September 1999 the worker had been referred to
a specialist regarding folliculitis of his arms and chest that was worse with heat
and perspiration. In his September 24, 1999 report Dr. H, a dermatologist, noted that
the worker had a problem with recurrent skin eruptions over his shoulders and chest
through the summer months in the previous three to four years. Dr. H considered
the worker had “a true delayed hypersensitivity reaction to a specific wavelength of
ultraviolet light.” 1
In October 2000 the worker was referred to a specialist regarding oral ulcers. In his
October 26, 2000 report Dr. B, an otolaryngologist, confirmed that the worker suffered
recurrent aphthous stomatitis. He noted the worker’s advice that he had experienced
recurrent bouts of ulcers during the previous year.
In his March 14, 2001 report Dr. A, a specialist in internal medicine and respirology,
noted that the worker had been referred to him regarding a ten-year history of chronic
recurrent, almost continuous, canker stores which occurred anywhere in his mouth and
sometimes in the back of his pharynx. He noted that the worker had experienced
eczema as a child and still continued to “have occasional eczematous area.” He noted
that the worker had smoked cigars for ten years but had stopped the previous year. He
confirmed that the worker had local recurrent bucal mucosal ulcers.
Starting in late 2004, the worker developed right-sided headaches. A January 2005
pathology report of skin taken from the worker’s right frontoparietal area revealed
infiltration by a moderately poorly differentiated carcinoma. Diagnostic imaging
performed in 2005 established that the worker had lung cancer which had metastasized
to his brain and his spinal column. In a February 18, 2005 history and consultation
report Dr. R, a radiation oncologist, noted that the worker had not been a heavy smoker
in the past but did have a period during which he smoked cigars.
In mid-December 2005 a case manager requested an opinion from Dr. G, the Board’s
internal medicine consultant and a specialist in internal medicine, as to whether
the worker’s lung cancer could be related to his history of exposure to a number
of pesticides used in the course of his employment. In his December 28, 2005
memorandum Dr. G noted Dr. R’s reference to the worker having smoked cigars. He
could find no other references to the worker’s smoking history.
1
All quotations in this decision are reproduced as written, save for changes noted.
3
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2008 CanLII 18365 (BC W.C.A.T.)

Dr. G commented it was possible to find references in the literature which indicated
that exposure to pesticides/insecticides/herbicides conferred an increased risk of lung
cancer. The odds ratios reported for such exposures were relatively small and certainly
nowhere near the magnitude of the increased risks for lung cancer conferred by
smoking. He commented that, since the worker was reported to have been a smoker,
it was likely the most important carcinogen exposure involved the worker’s smoking
habit rather than his pesticide exposure. Smoking constituted by far the most important
cause of lung cancer, and the dose of smoking-induced carcinogen exposure usually far
outweighed any occupational carcinogen exposures.
By decision of January 4, 2006 the case manager denied Ms. M’s claim for benefits. He
referred to Dr. G’s opinion.
On January 13, 2006 an employee of the British Columbia Cancer Agency (BCCA)
sent the case manager a copy of an article by Alavanja et al. concerning pesticides
and lung cancer.2 On January 17, 2006 the Board received a November 2, 2005 letter
from Dr. W addressed “To Whom it May concern.” While he observed that there were
no known direct links between pesticides/herbicides and oncogenic properties, Dr. W
thought it “worthwhile for the possibility to be considered.” He referred to the article by
Alavanja et al. and commented that the increased number of lung cancers found in
groups using the insecticides chlorpyrifos and diazinon warranted further investigation.
Dr. W’s letter was accompanied by a copy of a February 25, 2004 invoice regarding a
purchase by the worker’s employer of a herbicide called Diphenoprop BK 700 and
a copy of a “chemicalWATCH Factsheet” regarding 2,4-D (2,4-Dichlorophenoxyacetic
acid), a widely used herbicide.
In his January 17, 2006 memorandum, in which he asked Dr. G for a further medical
opinion, the case manager noted that Ms. M advised him that the worker was a
non-smoker:
…She indicates that she had known her husband since he was 15 years of age
and in that time she could only remember him smoking a cigar in recognition of
the birth of their children but that he did not smoke the whole cigar nor did he
really inhale.…
Ms. M indicated that the worker had worked with a number of carcinogenic agents,
including “BK 700” and “244D.” The case manager believed that one of those products
was a herbicide known as metolachlor and the other was an insecticide known as
diazinon. He noted that Ms. M indicated that the BCCA had advised there was a
correlation between the use of pesticides/insecticides and the development of lung
cancer.
2
Alavanja, MC. et al. Pesticides and Lung Cancer Risk in the Agricultural Health Study Cohort. American Journal of
Epidemiology. 2004 Nov 1;160(9):876-85.
4
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2008 CanLII 18365 (BC W.C.A.T.)

On January 18, 2006 the Board received some materials entitled “Cancersmart
Pesticides” published by the Labour Environmental Alliance Society3. The materials
noted the dangers associated with various pesticides and the efforts undertaken by
municipalities to adopt by-laws to restrict the use of pesticides.
In his January 30, 2006 memorandum Dr. G commented that, when he originally
evaluated the file, he had performed a literature search regarding the risks associated
with pesticide and herbicide use. A number of studies showed a “slight increased
cancer incidence in exposed workers.” The magnitude of the risk was “quite low” and
nowhere near a relative risk of 2.0, the criterion generally accepted by the Board.
Metolachlor was not listed as a carcinogen by the International Agency for Research on
Cancer (IARC)4, the United States Department of Health and Human Services National
Toxicology Program (NTP)5, materials associated with the California Safe Drinking
Water and Toxic Enforcement Act of 1986 (Proposition 65)6, or the United States
Environmental Protection Agency (EPA) Toxics Release Inventory (TRI) Program7. It
was listed as a “possible” carcinogen by the EPA8. Diazinon was not listed as a
carcinogen by IARC, NTP, Proposition 65 or TRI. It was listed as “not likely” a
carcinogen by the EPA. Dr. G did not think it was reasonably possible to attribute the
worker’s lung cancer to his occupational exposures.
By decision of February 8, 2006 the case manager advised that the January 4, 2006
decision would not be changed.
On February 15, 2006 Ms. M advised the Board that the worker had used “Killex”
products which contained 2,4-D. He also had used “Weed n feed” and diazinon. She
noted that a number of municipalities across the country had passed by-laws restricting
the use of toxic pesticides. She also provided the Board with copies of invoices
associated with purchases of pesticides by the worker’s employer.
In his February 27, 2006 memorandum Dr. G commented that exposure to pesticides
and herbicides had been shown to produce a “slight increased risk for cancer incidents
in exposed workers.” He observed that an odds ratio of 1.3 or 1.4 indicates that,
out of 130 or 140 people with cancer, 30 or 40 of them would have likely developed
cancer as a result of toxic exposure. The other 100 people would likely have
developed cancer from other non-exposure causes. Randomly choosing one individual
out of a total population of 130 or 140 would likely involve the selection of “a
non-exposure malignancy” as there are many more of them present. An odds ratio of
2.0 would mean that, out of 200 people, 100 malignancies were related to exposure
3
See http://www.ecoflair.com/articles/CancerSmartConsumerGuide.pdf for a slightly different version of the
materials.
4
http://www.iarc.fr/
5
http://ntp.niehs.nih.gov/
6
http://www.oehha.org/prop65.html
7
http://www.epa.gov/tri/
8
http://www.epa.gov/
5
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2008 CanLII 18365 (BC W.C.A.T.)

and 100 malignancies were not related to exposure. Randomly choosing one individual
from that population of 200 would involve a 50/50 chance of finding an exposure-related
cancer. An odds ratio of 2.0 with a 50/50 risk is a threshold the Board uses to decide
whether it is likely such an exposure would be significant. He considered the pesticide
exposure as experienced by the worker did not reach that critical threshold; the worker’s
disease was more likely due to non-occupational factors than occupational factors.
Dr. G observed that determining whether any specific chemical has the potential to
cause cancer is not as straightforward as it would seem. Most animal studies are done
with rats whose exposure levels to a substance are hundreds, sometimes thousands, of
times greater than that associated with the usual exposure of humans. He commented
that a number of agencies have been charged with the problem of identifying probable
carcinogens in the environment and identifying substances that should not be used. He
considered that IARC was a well-respected scientific agency that provided the best
information available on potential carcinogens. He noted the other agencies which he
had discussed in his earlier memorandum.
Dr. G commented that, as mentioned in his previous memorandum, metolachlor and

diazinon were not considered to be carcinogens by any of the agencies noted by him.
IARC had given chlorophenoxy herbicides (which includes 2,4-D) a group 2B rating,
indicating that there was limited evidence for carcinogenicity in humans. The EPA
considered that such herbicides were not classifiable as to human carcinogenicity, and
a recent review by the World Health Organization (WHO) concluded 2,4-D was not a
carcinogen.
Dr. G observed that, although the above-noted pesticides may be regulated or, in the
case of diazinon, actually banned, they were banned for reasons other than producing
cancer. Diazinon had been banned because of its acute toxicity, not its ability to induce
cancer. All of the above-noted pesticides have toxic side-effects, some of which are
quite serious, but none of them are considered to be carcinogens.
The case manager’s March 2, 2006 decision referred to Dr. G’s most recent opinion.
Ms. M requested reviews of the January 4, 2006, February 8, 2006, and March 2,
2006 decisions. Her lawyer provided a September 5, 2006 submission which
was accompanied by an “August 31, 2005 report” prepared by Dr. S, who holds an
M. Eng. (Chemical) and a Ph.D. Her curriculum vitae indicated that her then current
employment involved preparing peer-reviewed journal articles for medical researchers
in Ottawa. Dr. S’s report was accompanied by (i) a table which listed the worker’s
medical and work history, (ii) a table which listed pesticides purchased for use by the
worker, (iii) a table which documented medical information relevant to pesticides used
by the worker, (iv) a table which listed some of the organizations calling for municipal
pesticide by-laws, and (v) a list of 45 references. The last document appears to involve
a collection of abstracts of articles published in peer-reviewed journals.
6
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2008 CanLII 18365 (BC W.C.A.T.)

In his October 12, 2006 decision the review officer reviewed the history of the claim and
the submissions. His summary of Dr. S’s report noted the following:
Dr. S’s report is dated August 31, 2006. She states that it is possible
that the worker exhibited signs of pesticide toxicity in the form of chronic
skin rashes and canker sores, both of which he developed subsequent to
his employment with the municipality. If this exposure did cause these
symptoms, he would necessarily have been exposed to very large doses
of these substances. She also suggests a possible link between these
chronic inflammatory conditions and the subsequent development of
cancer. With regard to the specific evidence relating lung cancer risk
to pesticide exposure, she notes two specific pesticides (Diazinon and
Chlorpyrifos) with odds ratios “…close to or greater than two…”
Dr. S’s submission includes a number of charts, the first of which

shows the various pesticides the worker would have been exposed to
during his employment as well as the amounts purchased. She has
estimated the number of grams of these substances the worker would
have used between 1998 and 2004. In a second table, she provides a list
of medical problems associated with each chemical (with bibliographical
references) identified in the first table. Some exposures, such as for
example, the 2,4-D mentioned by the worker’s widow, showed increased
levels for non-Hodgkin’s lymphoma or for cancers with genetic markers.
Other substances were associated with cancers other than lung cancer or,
for example, skin irritations. The two substances associated specifically
with lung cancer are Diazinon (to which she estimates the worker was
exposed to a total of 13 grams) and Chlorpyifos (to which she estimates
the worker was exposed to a total of 5 grams).
The review officer noted subsection 6(3) of the Act and entries in Schedule B of the Act
with respect to carcinoma of the lung and primary cancer of the lung. He also noted
subsection 6(1) of the Act and items #26.22 and #100.50 of the Rehabilitation Services
and Claims Manual, Volume II (RSCM II). He also noted item #B4.5 of the Review
Division’s Practices and Procedures.
The review officer considered that subsection 6(3) of the Act was not applicable to the
claim; there was no radiological or histological evidence that the worker had asbestosis
or had been exposed to asbestos (item #4(a) of Schedule B). Further, there was
no evidence that the worker had been exposed to any of the substances listed in
item #4(e) of Schedule B: aerosols and gases containing arsenic, chromium, nickel or
their compounds; bis (chloromethyl) ether; the dust of uranium, or radon gas and its
decay products; or particulate polycyclic aromatic hydrocarbons.
7
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2008 CanLII 18365 (BC W.C.A.T.)

As part of his consideration of the claim under subsection 6(1) of the Act, the review
officer observed that there was no doubt that cigarette smoking was the primary cause
of lung cancer. (He cited comments found in The Merck Manual of Diagnosis and
Therapy, 17th ed.) He provided the following comments in support of his determination
that the worker’s smoking history was “non-contributory”:
As noted by Dr. G, the information regarding this worker’s smoking history

is scant and I would add, confusing. Two physicians have indicated that
the worker had a limited history of cigar smoking, although one suggests
this totaled 10 years. The worker’s widow, who was acquainted with the
worker from age 15, has stated that he was essentially a non-smoker. I
am unable to explain this discrepancy or to recommend a further
investigation that would likely shed further light on this matter. I do note
that the reference to a 10-year history of cigar smoking is from Dr. A who
also indicated that the worker had a 10-year history of canker sores. This
is contrary to all other information on the file which indicates that the
worker’s complaints in this regard were of much shorter duration. I am
going to assume from this that Dr. A’s information is may be inaccurate
and that the worker’s smoking history is non-contributory.
The review officer considered there was an absence of detail regarding the nature of the
worker’s job or the likely exposures he may have had to herbicides/pesticides. It was
not known how often the worker used pesticides or the manner in which he used them.
He queried whether the worker had used protective equipment, including respiratory
protection. He noted the information that was available:
The available information from the employer indicates that the worker
was a groundskeeper and had a variety of duties beyond the application of
pesticides/herbicides in public parks. Information supplied in the
applicant’s submission lists the chemicals that were purchased during
most of the worker’s employment history. For agents which Dr. S has
specifically related to lung cancer risk, the amounts purchased were
very low (13 grams for Diazinon and 5 grams for Chlorpyifos). Although
as Dr. S has suggested, these records may not be complete, they are
all that are available. There is little in this information that would indicate a
significant exposure to any of these chemicals.
The review officer was not persuaded by Dr. S’s opinion:
I acknowledge that the epidemiological information submitted by Dr. S

does in some cases show a higher incidence of lung cancer among
workers exposed to pesticides. However, the relevance of these studies
8
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2008 CanLII 18365 (BC W.C.A.T.)

is limited on the issue before me. First, four out of nine articles are
based on one 2004 study of agricultural workers in the U.S. and the vast
majority of workers in this study were farmers. I would suspect that their
exposures, both in terms of specific chemicals as well as exposure
amounts, would be significantly different than the worker in the matter
before me. Two other German studies are very old and refer to potential
exposures to asbestos, DDT and arsenic; there is no evidence the worker
on this claim had any such exposure. The one study that did look at
municipal workers dealt with pest control; the exposures were to different
chemicals and, in any event, risk factors for lung cancer were low.
Common to all of these studies suggesting a link between lung cancer and
pesticide exposure are discussions of dose response. In other words,
when a link is established the studies indicate that this occurs in heavily
exposed workers. Several studies referred to exposures of greater than 20
years or of latency periods exceeding 17 years. The worker on this claim
only worked for the accident employer for a total of less than nine years
which would also be the period of time between first exposure and the
diagnosis of lung cancer. Moreover, as previously discussed, there is no
indication that the worker’s exposure to those chemicals specifically linked
to lung cancer would have been substantial.
I find Dr. G’s opinion persuasive largely because of his reference to

various regulatory groups responsible for determining the carcinogenicity
of various substances. These include WHO, the U.S. Environmental
Protection Agency and especially, IARC which is an internationally
recognized organization dedicated solely to this subject. As Dr. G noted,
none of these agencies has recognized any of the substances to which
this worker was likely exposed as carcinogens.
As noted earlier, there is currently no means by which to identify the cause

of cancer in individuals. The best that can be done is to identify trends
based on the results of epidemiological studies. Based on the studies
currently available, I accept that there is possibly a relationship between
pesticide exposure and the development of lung cancer. However, as is
described in policy item #26.22, this evidence is not sufficient to establish
that the worker had an occupational disease due to the nature of his
employment. As a result, I also deny the applicant’s request under section
6(1).
9
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2008 CanLII 18365 (BC W.C.A.T.)

Expert opinions submitted by Ms. M
I have read the opinions. The following summaries do not purport to be exhaustive.
Dr. S’s August 31, 2006 opinion (misdated as August 31, 2005)
Dr. S’s assertions stem from general statements regarding carcinogenesis and her
review of articles published in peer-reviewed journals. She stated that chemicals such
as pesticides may play a role in the eventual development of cancer through the
following steps:
- causing genetic damage;

- acting in a manner similar to hormones to stimulate growth that may
in turn lead to additional genetic changes as unstable DNA is quickly
replicated;
- irritating tissue, causing abnormal cell division and/or immune activity;
- suppressing the immune system, that would otherwise eradicate the
abnormal cells; or
- interfering with cell death mechanisms (apoptosis), so that cancer
cells build up.
[footnotes deleted]
Dr. S asserted that experts such as Dr. Alavanja, who in the past had published articles
minimizing the links between pesticides and cancers, are now saying the links
between pesticides and cancer should be dramatically reassessed, taking into account
the multiple steps in the evolution of a clinical case of cancer. She observed that
Dr. Alavanja, the lead author of an article previously submitted to the Board, had
recently published another important discussion of pesticides and cancer9 which
indicated that pesticide carcinogenicity may be underestimated and is, to date, poorly
assessed. She commented that traditional animal toxicology experiments are of limited
relevance to humans, and epidemiology is “diluted” with multiple confounding variables.
Dr. S asserted that pesticide-related ills are often not recognized and are
under-diagnosed. Additionally, pesticide human toxicity data may be skewed by factors
such as the “healthy worker effect”10, poor exposure information, and the fact that
pesticides are now ubiquitous in our environment and food, so an unexposed cohort is
impossible to find.
9
Alavanja, MC et al. Health effects of chronic pesticide exposure: cancer and neurotoxicity. Annual Review of Public
Health. 2004;25:155-97.
10
The “healthy worker effect” is a possible bias which results from the fact that workers at the outset of their careers
are much healthier than the average person in the general population, as that population includes people who are not
able to work owing to illness. A second “healthy worker effect” occurs when workers who become unfit because of
illness or the effect of risk factors that later predispose them to premature mortality are removed from the workplace
or reassigned to other duties and are lost to follow-up or misclassified.
10
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2008 CanLII 18365 (BC W.C.A.T.)

Dr. S asserted that, historically, pesticides had been linked to lung cancer. In support
she cited two articles by Barthel.11 (Those articles from 1976 and 1981 concerned
German agricultural workers who were also exposed to arsenic, asbestos, and DDT.)
At least four pesticides used by the worker have been linked to cancer, including lung
cancer, and those links were becoming steadily stronger in emerging research. 2,4-D
has been linked with non-Hodgkin’s lymphoma. Furthermore, pesticide exposure has
now been linked to cancer with particular genetic damage. There was no genetic
testing of the worker’s tumour, so it was unknown whether his tumour exhibited genetic
changes associated with pesticide exposure.
Dr. S contended that the clinical context further strengthens the hypothesis that the
worker’s pesticide exposure was critical in the development of his cancer. Cancers
commonly evolve from chronic irritation, and it is “obvious” from the persistent canker
sores that the worker’s airway was indeed compromised in this manner. The combined
effects of toxic chemicals are frequently synergistic, rather than additive. The worker
was exposed to herbicides that cause irritation, possibly cancer, and neurological
symptoms. (She cited three articles in support of that last statement. The abstracts of
the articles do not mention lung cancer.)
Dr. S declared that the worker had been exposed to insecticides that affect the nervous
and immune systems and are linked to cancer. (In support she cited four articles,
but only one abstract referred to lung cancer12.) It was impossible to examine in
the laboratory all the combinations of toxic chemicals. However, lawn care chemical
use is associated with increased cancers, to the extent that many organizations are
calling for an end to their use. The worker’s cancer was only diagnosed after it had
metastasized extensively, and it was a very short time afterwards that he passed away
from this aggressive malignancy. She observed there was some evidence that
malignancies arising from pesticide exposure tend to be very aggressive. (In support of
that observation she cited an article dealing with acute myeloid leukemia13 rather than
lung cancer.)
Dr. S contended that the worker was responsible for all pesticide applications,
which meant he carried out all mixing, spreading, spraying, and cleanup operations.
Those activities result in exposure to dust and mists that would penetrate the lungs,
11
Barthel, E. [High incidence of lung cancer in persons with chronic professional exposure to pesticides in
agriculture] E Zeitschrift für Erkrankungen der Atmungsorgane 1976 Sep;146(3):266-74.
Barthel, E. Increased risk of lung cancer in pesticide-exposed male agricultural workers.
Journal of Toxicology and Environmental Health. 1981 Nov-Dec;8(5-6):1027-40.
12
Lee, WJ et al. Cancer incidence among pesticide applicators exposed to chlorpyrifos in the Agricultural Health
Study. Journal of the National Cancer Institute. 2004 Dec 1;96(23):1781-9.
13
Cuneo, A. et al. Morphologic, immunologic and cytogenetic studies in acute myeloid leukemia following
occupational exposure to pesticides and organic solvents. Leukemia Research. 1992 Aug;16(8):789-96.
11
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2008 CanLII 18365 (BC W.C.A.T.)

increasing the likelihood of carcinogenesis in this particular location. The worker
used a small hand-held or backpack sprayer, so that he had to mix pesticides more
frequently. He was closer to the spray than he would have been if he had used a
tank-mounted sprayer that had been towed.
Dr. S noted that it is recommended to wet turf before the application of granular
materials, but this was generally not done, particularly where no irrigation was available:
“…exposure to dusts would have been higher than otherwise.” The worker wore
disposable coveralls when applying pesticides, but these were generally re-used a
few times. (Dr. S did not document the source of her information with respect to
the worker’s work activities.) The re-wearing of work clothes is associated with
higher pesticide exposures; residues from clothing and footwear contaminate indoor
environments, which may lead to considerable ongoing exposure because pesticides do
not break down indoors.
Dr. S summarized her opinion at the conclusion of her initial report. The worker
experienced, and was unsuccessfully treated for, lesions of his skin and respiratory tract
for years before the diagnosis of his lung cancer (irritation may increase the probability
of malignancy developing). He used pesticides that may cause these symptoms, as
well as neurological symptoms that he also exhibited. The worker had worked with, and
presumably inhaled, at least three pesticides that are linked to irritation similar to what
he experienced, as well as to cancers. He used two pesticides that are associated with
odds ratios close to, or greater than, 2.0 for lung cancer (diazinon and chlorpyrifos) and
other pesticides that have been seen to more than double the risk of other
malignancies, alone and in combination. The worker used a large number of pesticides
which have been seen to compound the probability of adverse health effects,
particularly lung cancer.
Dr. S concluded her initial report by stating as follows:
... the evidence very strongly suggests that the pesticides used in the
course of his work were an important contributor to the development of his
cancer and therefore to his death. In my opinion, having reviewed the
medical history, the number and types of pesticides used and the manner
in which they were applied, it is highly likely that pesticide exposures, in
the course of his work, led to [the worker’s] lung cancer.
Table 3 which accompanied Dr. S’s initial report provided information found in the
journal articles as to the effects of exposure to (i) the herbicides 2,4-D, mecoprop, and
glyphosate, and (ii) the insecticides diazinon, dimethoate, and chlorpyrifos. In
particular, she noted that the article by Alavanja et al. previously submitted to the Board
12
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2008 CanLII 18365 (BC W.C.A.T.)

indicated that lung cancer risk was significantly associated with diazinon use. She also
cited an article by Beane Freeman et al.14 which documented increased risks for the
highest tertile of exposure to diazinon and significant tests for trend for lung cancer.15
Also in Table 3 Dr. S documented information found in journal articles as to the effect of
pesticides in combination. She noted Barthel’s 1976 article which documented that the
incidence of lung cancers was 20 times higher in the pesticide-exposed population
compared to an age-matched control population. She noted a study by Pesatori et al.16
which she indicated had documented that lung cancer among pest-control operators
was associated with reported exposure to numerous substances which included
diazinon and DDT. Odds ratios for lung cancer were greater for workers first licensed
before age 40. She noted a report by Ambroise et al.17 which documented that
standardized mortality ratios (SMRs) for all causes of death and for all cancer causes
were significantly greater in municipal pest-control workers. Non-significant18 excesses
were observed for most cancer sites, except for lung cancer which had a low SMR.19
14
Beane Freeman, LE et al. Cancer incidence among male pesticide applicators in the Agricultural Health Study
cohort exposed to diazinon. American Journal of Epidemiology. 2005 Dec 1;162(11):1070-9.
15
In this context, “significant” means that the p value was less than 0.05. A p value is the probability of getting a
value of the test outcome equal to or greater than that observed in the study when in truth there is no association.
(The absence of an association is often called the null hypothesis, that is, the hypothesis that there is no association
between an agent and a disease.) An outcome is statistically significant when the observed p value for the study falls
below the pre-selected significance value. The lower the value the less likely that random error would have produced
the observed relative risk if the true relative risk is 1.0. Statistical significance does not address the magnitude of any
association found in a study but rather assesses the role of random error. A very common significance level is 0.05.
A 0.05 value means that the probability is 5% of observing an association as large as the one found in the study as an
association when in truth there is not one. Thus, if one conducted an examination of a large number of associations
in which the true relative risk equals 1.0, on average 1 in 20 associations found to be statistically significant at a 0.05
level would be spurious.
16
Pesatori, AC. Cohort mortality and nested case-control study of lung cancer among structural pest control workers
in Florida (United States). Cancer Causes Control. 1994 July 5(4):310-318.
17
Ambroise, D. et al. Cancer mortality among municipal pest-control workers. International Archives of Occupational
and Environmental Health. 2005 Jun;78(5):387-93.
18
In this context, “non-significant” referred to a confidence interval which is a range of values calculated from the
results of a study within which the true value is likely to fall. The width of the interval reflects random error. If the
limits of the interval do not include 100 (a relative risk of 1.0), the risk is statistically significant. The larger the sample
size in a study (all other things being equal), the narrower the confidence boundaries will be (indicating greater
statistical stability), thereby reflecting the decreased likelihood that an association found in the study would occur if
the true association is 1.0. Confidence intervals are often noted in connection with relative risks. A 95% confidence
interval means that the range set by the interval will contain the true risk 95% of the time.
19
In cancer mortality studies where cohort mortality is compared to mortality in the general population, SMR refers to
“standardized mortality ratio”. In cancer morbidity studies using the same comparison, SMR refers to “standardized
morbidity ratio”. SMR is defined as a "standardized mortality ratio, equivalent to relative risk (observed cases divided
by expected cases)." An SMR may be expressed in two ways: for example, 150 or 1.5.
Relative risk (RR) is the ratio of the disease incidence or death among people exposed to an agent to the disease
incidence or death among the unexposed. A relative risk of 2.0 is often equated with a 50% likelihood that an
exposed person’s disease was caused by the agent, and a relative risk greater than 2.0 would permit an inference
that an individual’s disease was more likely than not caused by the implicated agent. As noted in "Protocol for the
Assessment of Medical/Scientific Information - Industrial Diseases Standing Committee, Workers’ Compensation
Board of British Columbia" (9 W.C.R. 429, at 445), a relative risk of 1.4 or 1.5 (an SMR of 140 or 150), by itself, is not
very impressive because there are so many confounding variables.
13
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Dr. S’s undated opinion submitted to WCAT
Dr. S reiterated conclusions found in her earlier report. She considered the review
officer had dismissed the possibility of pesticides having caused the worker’s cancer on
the basis that the worker had used only small amounts of diazinon and chlorpyrifos.
She contended that his decision failed to address or take into account the following
points, which I have paraphrased as follows:
• the complete clinical picture (the worker had symptoms consistent with adverse
effects of pesticides indicating that he had biologically significant exposures,
possibly because he was particularly susceptible to their effects, perhaps due to a
genetic predisposition);
• the actual toxicity of chemicals (these insecticides are so toxic they are no longer
permitted on lawns and gardens in Canada, not all pesticides are equally toxic, and
low-dose effects may be very different from high-dose effects); and
• additional information about glyphosate, a substance which causes skin lesions

and genetic damage and a recently reported link between dicamba and lung
cancer.
Dr. S commented that new information has become available since 2006. As well,
additional information has emerged which clarifies inconsistencies in the worker’s health
history. I have summarized her points in that regard as follows:
• Letters have clarified and confirmed that the worker was a non-smoker and have
addressed the misapprehension that the worker had childhood eczema. This is
important information because the worker’s dermatitis and folliculitis, as well as
canker sores, were temporally linked to pesticide use and were not a recurrence of
a previous condition.
• Dr. S2, a pathologist, has established that the worker had metastatic
adenocarcinoma of pulmonary origin. This had not been previously confirmed.
Additional pathology results pertaining to pesticide exposure may be forwarded
pending further testing. (I note, at this juncture, that submissions have been
declared complete.)
• The supply store from which the worker purchased the Weed 'N Feed mixtures has
clarified the content of the Weed 'N Feed granular product.
• Recent articles include reports of (i) genetic damage related to exposure

to glyphosate (a dose-response20 relationship), (ii) lung cancer related to
20
Higher exposed groups have higher rates of disease.
14
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2008 CanLII 18365 (BC W.C.A.T.)

exposure to dicamba (also dose-dependent), and (iii) an extensive review of
endocrine-disrupting pesticides, including pesticides used by the worker.
Under the heading “Proof”, Dr. S documented her analysis. Since cancer from pesticide
exposure is not explicitly recognized by the Board, it is necessary to piece together a
variety of evidence to establish that, on the balance of probabilities, the worker’s lung
cancer arose as a result of his exposure to the various pesticides. Much of the
information was covered in her first report. She reiterated her comment that the review
officer did not address the fact the worker had other symptoms that could be temporally
related to his pesticide exposure and could be considered to be evidence that he had
physiologically significant exposures. As the worker was a non-smoker, “...we must
look for evidence of other causes of his lung cancer.”
Dr. S contended that the high prevalence of smoking-related lung cancer “swamps” the
statistics within the epidemiological literature; only the largest and strongest studies may
discern other causes. She notes comments by Dr. Guidotti21 that the relative risk of
lung cancer for a non-smoking firefighter would be 3.3 as opposed to the relative risk of
1.5 for firefighters as a whole. She comments that Dr. Guidotti’s observations establish
that difficulties and confounding factors inherent in epidemiological studies cause
measured risks to tend toward unity. She asserts, “... in the case of a non-smoker
positive findings in epidemiological studies should be sufficient.” She observes that
another important point is that measurement of a dose-response indicates a very strong
study.
Dr. S commented that the measured effects of occupational exposures are diluted by
the “healthy worker effect” which could stem from differences in levels of exercise and
lifestyle. Reported odds ratios actually increase as study methods improve. She
contended there must be a very strong effect by pesticides on the occurrence of lung
cancer for a link to emerge as significant, no matter how sophisticated the statistics.
Studies that show a dose-dependent relationship are considered to be very strong
indeed. Studies cited by her had this characteristic. The “healthy worker effect” is real
and important and should be considered when assessing any epidemiological evidence.
Dr. S asserts that Dr. Alavanja recently concluded22 that we must take a multi-pronged
approach to assessment of the relationship between cancers and pesticides and that
links have been underestimated in the past. At least as important as epidemiological
evidence is the vast amount of research describing the effects by which pesticides
contribute to the genesis and promotion of cancers. The pesticides used by the worker
contributed to the development of clinical cancer in many ways. Important mechanisms
are DNA damage, immune system suppression, irritation, hormonal promotion of
growth, and interference with cell death mechanisms. The various chemicals that
the worker used, along with their breakdown products and contaminants, have been
21
http://www.bcpffa.org/docs/BCPFFA%20report%20Dr.%20Guidotti%20-%20final.pdf
22
Alavanja, MC and Bonner MR. Pesticides and human cancers. Cancer Investigations. 2005;23(8):700-11.
15
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2008 CanLII 18365 (BC W.C.A.T.)

identified in the scientific literature as playing all of these contributing roles in the
development of cancer, with the possible exception of cell death mechanisms, a
relatively new area of research. Some individuals’ abilities to metabolize the chemicals
and to repair DNA vary widely, making some people inherently more prone to
developing a clinical malignancy.
With respect to any suggestion that the worker had not worked long enough
with pesticides to have developed a work-related malignancy, she declared, “This is
not necessarily true.” Latency, the time from the exposure to the time of clinical
manifestation of disease, is highly variable. Childhood cancers have a very short
latency, while the conventional understanding is that some adult onset malignancies
occur much longer after exposure to the carcinogenic substances. Dr. Guidotti has
explained that latency has been observed to be shorter for more aggressive tumours.
The worker’s tumour was “undoubtedly aggressive”, with less than four months having
passed between diagnosis and death. Latency may also be shorter if there is “a high
exposure.” The worker’s prolonged record of cankers, rashes, and neurological
difficulties reasonably related to pesticide exposure reasonably indicate that, regardless
of the absolute exposure level, for his particular physiology, he was most probably
exposed to damagingly high levels of pesticides.
Under the heading “In summary”, Dr. S makes a number of observations.

Epidemiological studies involving pesticides used by the worker show positive
associations between lung cancer, with odds ratios greater than 2.0, as well as with
dose-responses. She expands on this point:
These are all the more important since lung cancer is one of the most
difficult conditions to examine using epidemiological methods because
smoking is such a strong confounder. Epidemiological studies showing
any positive result for lung cancer must be accorded great weight when
considering a non-smoker.
Other scientific information is also important with piecing together

the possibility that lung cancer arose from exposure to multiple toxic
chemicals, particularly from inhalation exposures. There is ample
evidence that the pesticides used by [the worker] contribute to the
initiation and promotion of cancer. This greatly strengthens the probability
that [the worker’s] cancers arose from these chemicals.
Dr. S addresses the criteria identified in the Board’s “Protocol for the Assessment
of Medical/Scientific Information - Industrial Diseases Standing Committee, Workers’
Compensation Board of British Columbia”, 9 W.C.R. 429, (Protocol). Regarding the
strength of association, odds ratios of 2.0 or higher have been reported for some
pesticides; “…lower odds ratios for lung cancer in a non-smoker are calculated to be an
appropriate bar.” Confounding by smoking makes consistency a difficult issue and
16
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2008 CanLII 18365 (BC W.C.A.T.)

there are relatively few studies reporting lung cancer specifically, but several are
positive. A dose-response was reported in two studies. Regarding coherence,
pesticides used by the worker are not only epidemiologically linked to lung cancer and
other cancers, they have many effects that would result in the initiation and promotion of
cancers. Regarding a temporal relationship, the worker applied pesticides for nine
seasons before his lung cancer was diagnosed. Although this is a relatively short
latency period, it is not unreasonable given that latency may be inversely related to both
dose and the aggressiveness of the cancer. Regarding specificity, many cancers have
been reported as a consequence of exposure to the pesticides used by the worker, but
with inhalation exposures it is reasonable to expect lung cancers. As for statistical
significance, statistically significant and dose-related links between exposure to the
classes of pesticides and the specific pesticides used by the worker had been
demonstrated in both genetic damage and lung cancer.
Dr. S concludes that the worker’s lung cancer was “... most probably the result of
exposure to the pesticides that he applied during the course of his employment.”
Copies of numerous articles were submitted to WCAT. I have listed them as follows:
Paz-y-Miño et al.23, McKinlay et al.24, Goode et al.25, Sears et al.26, Nielsen et al.27,
Bolognesi28, Holsapple et al.29, Lee et al.30, Beane Freeman et al.31, Chiu et al.32, and
Samanic et al.33
Mr. L’s November 30, 2006 opinion
Mr. L, a mechanical engineer with 50 years of experience in the areas of engineering,

environmental control in the public and private sector, technology evaluation and
transfer, manufacturing, management, and international activities, indicated that he had
read Dr. S’s report. He noted a 2000 re-evaluation of diazinon by Health Canada’s Pest
23
Paz-y-Miño, C et al. Evaluation of DNA damage in an Ecuadorian population exposed to glyphosate. Genetics and
Molecular Biology, 2007;30, 2, 456-460.
24
McKinlay, R et al. Endocrine disrupting pesticides: Implications for risk assessment. Environmental International.
2008 Feb;34(2):168-83.
25
Goode, EL. et al. Polymorphisms in DNA repair genes and associations with cancer risk. Cancer Epidemiology
Biomarkers and Prevention. 2002 Dec;11(12):1513-30. Review. Erratum in: Cancer Epidemiology Biomarkers and
Prevention. 2003 Oct;12(10):1119.
26
Sears, M et al. Pesticide assessment: Protecting public health on the home turf. Paediatric Child Health 2006;
11(4):229-234.
27
Nielsen, SS et al. Risk of Brain Tumors in Children and Susceptibility to Organophosphorus Insecticides: The
Potential Role of Paraoxonase (PON1). Environmental Health Perspectives. 2005;113(7):909-913.
28
Bolognesi, C. Genotoxicity of pesticides: a review of human biomonitoring studies.
Mutation Research. 2003 Jun;543(3):251-72.
29
Holsapple, MP et al. Immunosuppression without liver induction by subchronic exposure to 2,7-dichlorodibenzo-p-
dioxin in adult female B6C3F1 mice. Toxicology and Applied Pharmacology. 1986 May;83(3):445-55.
30
Citation found at footnote #12.
31
Citation found at footnote #14.
32
Chiu, BC et al. Agricultural pesticide use and risk of t(14;18)-defined subtypes of non-Hodgkin lymphoma. Blood.
2006 Aug 15;108(4):1363-9.
33
Samanic, C et al. Cancer incidence among pesticide applicators exposed to dicamba in the Agricultural Health
Study. Environmental Health Perspectives. 2006 Oct;114(10):1521-6.
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2008 CanLII 18365 (BC W.C.A.T.)

Management Regulatory Agency, but did not indicate that that document linked
exposure to diazinon to lung cancer. He also referred to other materials regarding
pesticides, but did not refer to any material linking pesticides to lung cancer. He
concluded there is sufficient information to prove that there is a health danger from the
use of pesticides for lawn care. He commented that the phasing out of indoor uses and
non-agricultural uses of diazinon certainly raises “health concerns” regarding that
pesticide. He contended that (i) the banning of pesticides for cosmetic lawn care, and
(ii) a Québec study which indicated that children from municipalities that have banned
the use of lawn care herbicides did not have traces of these herbicides in their blood,
provides “... in my opinion, substantial support that the conclusion of the WCB [Workers’
Compensation Board] should be reversed.”
Dr. B’s October 1, 2007 opinion
Dr. B is a medical doctor who has a special interest in environmental influences on

human health. He has taught courses in the subject to family physicians and others.
He is the past founding president of the Canadian Association of Physicians for the
Environment. He indicated that his remarks were directed primarily to addressing the
quality of evidence regarding the risks, or lack thereof, associated with the use of
pesticides, with particular reference to the worker’s situation.
Dr. B observed that, in general terms, the overwhelming majority of cases of lung
cancer are causally associated with personal cigarette smoking, with a significant
minority caused by environmental pollutants, second-hand cigarette smoke, urban air
pollution, and a small group of recognized and specific pulmonary toxins such asbestos.
In the absence of any of those known causative agents, lung cancer is unusual, and its
occurrence merits special consideration as to etiology. Given that the worker was a
non-smoker and a resident of a rural community without significant air pollution
problems, any unusual feature of his lifestyle or personal behaviour deserved to be
considered.
Dr. B stated that synthetic pesticides are designed to be harmful. While that harm
is purported to be primarily limited to “target” species, there is overwhelming evidence
that it is not. Given the worker’s unusually close and prolonged association with
the preparation, and use, of pesticides, “…there is prima facie interest in these agents
as potential causes of his lung cancer.” A significant portion of Dr. B’s opinion involves
his comments regarding the Health Canada’s Pest Management Regulatory Agency.
As I do not consider that such comments are of significant assistance to the resolution
of this appeal, I have not summarized them. I appreciate that Dr. B indicated he was
attempting to “…supply some context and background to the decision-making process
about the quality of evidence relevant to this claim, so that the process may be more
rational and its outcome more accurate.” However, any determinations as to pesticide
safety by the Health Canada’s Pest Management Regulatory Agency were not relied
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2008 CanLII 18365 (BC W.C.A.T.)

upon by the Board in its decision-making. As well, I have not relied on that the agency’s
classifications of any substances to which the worker was exposed.
Dr. B concluded that assumptions about the benign nature of the worker’s exposures to
occupational chemicals have to be considered “suspect.” He considered such
assumptions to be “simply illogical.” He asserted as follows:
A far more logical posture to adopt is that any reasonable evidence,

however modest, that significant adverse effects (including cancer) might
have arisen from [the worker's] exposures, is likely to be accurate.
Dr. I’s October 1, 2007 opinion and accompanying materials
Dr. I, a dermatologist, observed that a 1986 publication of the Government of Québec

listed the possible effects of pesticide exposure on man. Cancer of the lungs was one
of the effects. “The Merck Manual for Physicians” lists non-arsenical pesticides as a
cause of lung cancer. She commented that, until an authority across Canada registers
all lung cancer cases and documents all occupational exposures, it appears evident that
the case of the worker should remain open in the interest of “academic veracity.”
In her January 30, 2006 letter to the Government of Québec, Dr. I asserted that it was
essential that authorities continue measures necessary to provide all citizens with
the right to live in pesticide-free communities. Her letter did not expressly address lung
cancer.
Other materials submitted as part of the review and appeal process
While I have not summarized other pieces of evidence submitted as part of the review
and appeal process, I have reviewed those materials.
Reasons and Decision
Subsection 6(3) and Schedule B of the Act
Ms. M’s lawyer asserts that this claim satisfies the terms of subsection 6(3) of the Act.
The effect of subsection 6(3) of the Act is that if a worker, at or immediately before
the date of the disablement, is employed in a process or industry mentioned in the
second column of Schedule B, and the disease contracted is the disease listed in the
first column of the Schedule set opposite to the description of the process or industry,
the disease is deemed to have been due to the nature of that employment unless the
contrary is proved.
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2008 CanLII 18365 (BC W.C.A.T.)

The worker’s condition could be referred to as carcinoma of the lung or primary cancer
of the lung. Thus, one could say that, subject to further comments below, his condition
satisfied at least two descriptions of disease set out in the first column of Schedule B.
Yet, I find that the evidence does not establish that the claim satisfies the terms
of item #4(a) of Schedule B. The evidence does not support a finding that the worker
suffered from carcinoma of the lung in conjunction with (i) asbestosis or (ii) bilateral
pleural thickening or fibrosis. Thus, the claim does not meet the complete description
of disease set out in item #4(a).
As for item #4(e) of Schedule B, I do not consider that the evidence establishes the
worker had prolonged exposure to aerosols and gases containing arsenic, chromium,
nickel or their compounds; bis (chloromethyl) ether; the dust of uranium, or radon gas
and its decay products; or particulate polycyclic aromatic hydrocarbons. Thus, the
worker’s employment does not meet the description of the process or industry set out in
the second column of Schedule B.
As for item #1(m) of Schedule B, I do not consider that this is a case of poisoning by
“other toxic substances.” The worker was not diagnosed with poisoning; he was
diagnosed with cancer. I consider there is little scope for the review of a claim for
primary cancer of the lung under item #1(m); Schedule B has a specific entry applicable
to primary cancer of the lung. To permit such a review would amount to circumventing
the clear language of items #4(a) and #4(e) and to relieve a claim for benefits of the
need to satisfy the terms of the descriptions of the processes or industries found in the
second column of Schedule B associated with items #4(a) and #4(e).
I find that the terms of Schedule B and subsection 6(3) of the Act have not been
satisfied.
Subsection 6(1) of the Act
As established by the decisions of the case manager and the review officer, that the
claim does not meet the requirements of subsection 6(3) does not end the matter. The
claim must be considered under subsection 6(1), as to whether the worker’s cancer was
due to the nature of his employment.
• Smoking history
I attach some significance to the fact that Dr. A in 2001 and Dr. R in 2005 referred to the
worker’s consumption of cigars. There is little suggestion that Dr. R had access to Dr.
A’s report when she issued her February 18, 2005 report. Had she had access to Dr.
A’s report, one would expect that she would have referred to a ten-year period of
20
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2008 CanLII 18365 (BC W.C.A.T.)

cigar smoking. Her report does not contain that particular detail. Further, the volume of
information in her report suggests that Dr. R conducted a detailed interview of the
worker.
Dr. A’s March 14, 2001 report refers to a ten-year period of cigar smoking which ended
in 2000. I note that in her September 29, 2007 letter Ms. M seeks to explain Dr. A’s
reference to the worker having smoked for ten years: “(there was confusion between
his comment on [the worker’s] canker sore duration, which [the worker] estimated the
time on) to be about 10 years.).” I can appreciate how a physician who had confirmed
the existence of smoking and canker sores might confuse their respective durations.
Yet, it is most unclear to me as to how Dr. A could have been mistaken as to the worker
having smoked cigars.
It would seem quite unlikely that two physicians, who produced reports some four years
apart, would have completely erred with respect to documenting the worker’s
consumption of cigars.
The case manager accepted Ms. M’s declaration that the worker had only smoked a
cigar in recognition of the birth of their children. Of note is the fact that Ms. M later
declared in her September 29, 2007 letter that the information regarding the worker
having smoked a cigar on the occasion of the birth of their children was “wrong.” She
asserted that both children were born prematurely and airlifted to hospital. They did not
celebrate the birth of those children by smoking a cigar. I am struck by the unlikelihood
that the case manager would fabricate a story about the worker having smoked a cigar
in connection with the birth of his children or had so misunderstood Ms. M’s advice to
him that he documented such a story.
Further efforts to persuade decision-makers that the worker did not smoke are found in
a September 27, 2007 letter from the worker’s mother who advised that the worker did
not smoke: “I do not ever remember seeing him with smoking materials in hand.” An
October 1, 2007 letter from Dr. R who treated the worker between February 2005 and
May 2005 asserts that “the medical history did not show that this man was a smoker.”
Dr. R does not identify the nature of the “medical history.” It is not clear whether he
asked the worker at the commencement of treatment in February 2005 if he smoked or
whether he conducted a detailed interview of the worker which canvassed his complete
medical history. In a September 29, 2007 letter Mr. N declared that since the day
the worker started working for the employer he had never seen the worker smoking or
using any tobacco products. I note that no document has been provided from Dr. W
regarding any information he may have had as to the whether the worker was a smoker.
While Ms. M’s lawyer submitted to WCAT that the reports of Drs. R and W supported
the conclusion that the worker was a non-smoker, Dr. W’s November 2, 2005 letter
does not address the issue of smoking.
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2008 CanLII 18365 (BC W.C.A.T.)

The acceptance of this claim does not hinge on whether I find that the worker was a
smoker. I find that it is not necessary that I resolve the issue of whether the worker
smoked. It is not necessary that I point to an alternative cause of the worker’s lung cancer.
I stress that the fact there may be no obvious non-occupational cause of cancer does not
mean there must have been an occupational cause.
The key issue is whether I find that the evidence establishes that the worker’s lung cancer
was due to the nature of his employment.
• Substances to which the worker was exposed
This claim is notable for the fact that the initial January 4, 2006 adjudication was performed
without the Board having confirmed the specific substances to which the worker had been
exposed.
Information was gathered later. The case manager’s January 17, 2006 memorandum
documents Ms. M’s advice that the worker was exposed to “BK 700” and “244D.”
He thought that the products were metolachlor and diazinon. According to a material
safety data sheet (MSDS), Diphenoprop BK 700 does not contain either of those
two substances34. The MSDS for Diphenoprop BK 700 establishes that it contains, among
other substances “low volatile butoxy ethanol esters of 2,4-D.”
I assume that the case manager’s reference to “244D” was actually a reference to
2,4-D (2,4-Dichlorophenoxyacetic acid), a herbicidal member of the phenoxy class of
chemicals. 2,4-D does not contain diazinon or metolachlor.
According to an MSDS, metolachlor is a chlorocetanilide herbicide.35 According to an

MSDS, diazinon (O,O-diethyl-O-(2-isopropyl-6-methyl-4-pyrimidinyl) phosphorothioate)
is an organophosphate insecticide.36
In her note received by the Board on February 15, 2006 Ms. M referred to
(i) Killex products which contain 2,4-D, (ii) “Weed n feed”, and (iii) diazinon. (An MSDS
confirms that Killex contains 2,4-D, mecoprop, and dicamba.37 An MSDS confirms that
Weed 'N Feed contains 2,4-D and mecoprop.38)
A more complete understanding of the nature of the substances to which the worker was
exposed may be gleaned from Table 2 which accompanied Dr. S’s report submitted to the
Review Division. It is asserted that the worker worked with products whose active
ingredients included dimethoate, dichloroprop, glyphosate, 2,4-D, mecoprop, chlorpyrifos
(O,O-diethyl O-(3,5,6-trichloro-2-pyridinyl) phosphorothioate), and diazinon. That table
34
http://terralink-horticulture.com/Attachments/msds/diphenoprop.htm
35
http://www.cdms.net/LDat/mp0G6008.pdf
36
http://www.growercentral.com/UPLOADS/PDFS/diazinon%205g%20msds%20(01-05).pdf
37
http://www.growercentral.com/UPLOADS/PDFS/killex%20msds%20(10-03).pdf
38
http://www.hardwarestore.com/media/msds/186445.pdf
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2008 CanLII 18365 (BC W.C.A.T.)

listed the dates of the purchases of particular products, the quantities of the purchases, the
active ingredients, the concentration of the active ingredients, and the quantity of active
ingredients. That list of active ingredients was based on information gathered from
invoices which documented pesticide products purchased for use by the worker.
As evidenced by Attachment 2 which accompanied Dr. S’s report submitted to WCAT,

the initial list in Table 2 was revised to include dicamba. (Dicamba is an acronym
for 3,6-dichloro-2-methoxybenzoic acid). It appears that dicamba may have been
overlooked when the initial list was composed. Dr. S commented that the supplier
“clarified” the content of a Weed 'N Feed granular product. Information on the website
for Scotts Canada confirms that Weed 'N Feed contains dicamba.39 The list of substances
purchased for use by the worker includes Scotts Weed 'N Feed. Two other Weed 'N Feed
purchases were made.
Dr. S did not assert that the literature links exposure to dicamba to lung cancer. She did
note in Attachment 2 that exposure to dicamba is associated with suppression of the
immune system. I consider it likely that she has erred in her comments and that she meant
to point to literature linking dicamba to lung cancer. I say that because, while in
Attachment 2 Dr. S indicated that there is a link between mecoprop and lung cancer, she
cites the study by Samanic et al. which actually deals with dicamba. I note that a search of
the website for PubMed40, using the terms “mecoprop” and “cancer”, reveals very few
articles, let alone any articles which link mecoprop to cancer.
A further revision to the initial list of substances to which the worker was exposed concerns
mecoprop. Table 2 list referred to mecoprop, but it did not identify the concentration of
mecoprop or the quantity of active ingredients. Attachment 2 identified the quantity of
grams of mecoprop associated with the worker’s work activities. Mecoprop is found in
Weed 'N Feed. I accept that an analysis of the product information for Weed 'N Feed
would permit one to determine the concentration of mecoprop in the product and its
quantity.
Dr. S commented in her initial report that it is quite possible that the records are incomplete
with the result that the exposure figures identified by her represent a minimum quantity of
pesticides applied by the worker. In the absence of more than speculation to the contrary, I
have adjudicated this appeal on the basis that the records are complete.
• Extent of exposure
I accept as accurate the contents of the employer’s November 9, 2006 letter which
indicated the worker spent approximately 8 to 12 days per season spraying, as
39
See the following:
http://www.scottscanada.ca/index.cfm/event/ProductGuide.product/documentId/57AD934A0730861278693548576AB
C93
40
A database of the United States National Library of Medicine and the National Institutes of Health that may be
accessed at http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed.
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required. I accept the employer’s evidence that the worker wore protective equipment
involving a suit, gloves, and a mask with a rubber seal. He held a license to spray and
was the only employee to hold such a license during his employment. I further accept
as accurate the contents of Mr. G’s November 8, 2006 letter. Mr. G and his wife lived
near the local cemetery. On numerous occasions Mr. G observed the worker
performing various tasks. One of the tasks involved the application of herbicides and
pesticides. The worker was “always fully protected in wearing his white suit, gloves,
and mask.” Mr. N, who worked with the worker, indicated that anytime he saw
the worker, he always wore protective clothing. The worker “…always followed proper
safety measures.”
In her September 29, 2007 letter Ms. M indicated that the worker “...strictly followed the
safety rules and procedures that were required in obtaining in his Pesticides Applicators
Certificate.” He “...followed the manufacturers’ Labels.” The worker “...wore all the
proper protective clothing while handling and using these pesticides....” Later in that
letter, she declared that the worker “...always wore his proper protective applicators
clothing.”
As noted above, in her initial report Dr. S documented information as to the worker’s
handling and use of pesticides. While I observed above that Dr. S did not document the
source of her information with respect to the worker’s work activities, it appears that she
interviewed Ms. M. I say that, because the March 15, 2007 newspaper article submitted
to WCAT quotes Ms. M to the effect that Dr. S wanted to know every single detail.
That March 15, 2007 article also quotes Ms. M as having advised that there were times
when special gear was not necessary. She indicated that when the worker applied
“weed and feed” at the downtown park he did not don all his gear because it was not
required.
I find that the evidence supports a conclusion that the worker wore protective gear
almost every occasion he applied pesticides.
• Non-carcinogenic effect of exposure
In her initial report Dr. S contended it seems quite likely that, given the timing of the
onset of symptoms for which he sought medical treatment, and the documented links
between medical conditions and pesticides he used, the worker suffered symptoms of
pesticide toxicities other than cancer. With respect, Dr. S is not a physician. I note
that there is no report on file from a physician who has linked the worker’s various
non-cancer symptoms to his occupational exposure.
That the worker’s symptoms such as skin lesions could be associated with exposure to
pesticides does not establish that those symptoms were, indeed, related to pesticide
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exposure. In particular, I query whether such speculation by Dr. S provides a basis
to ignore Dr. H’s September 24, 1999 assessment that the worker’s recurrent skin
eruptions mainly over the shoulders and chest during the summer months involved true
delayed hypersensitivity reaction to a specific wavelength of ultraviolet light.
In considering whether the worker suffered non-cancer reactions to his occupational

exposure, I have taken into account the fact that Dr. A’s March 4, 2001 report noted that
the worker’s canker sores in his mouth and pharynx had been occurring for ten years
prior to March 2001. That would mean that his canker sores commenced around 1991.
That ten-year duration is notable, given that the employment history record completed
by Ms. M at the outset of the claim establishes that the worker did not commence
working for the employer until 1996. He did work as a landscape worker/foreman in a
nursery between 1993 and 1995; however, even that employment post-dates the
commencement of his canker sores. Between 1989 and 1993 the worker was
employed as a trim technician and body shop manager. Neither employment would
have involved exposure to pesticides.
I appreciate that the review officer apparently had some concern as to the accuracy of Dr.
A’s report regarding the duration of the worker’s canker sores. He commented that the
information was contrary to all other information in the file which indicated that the worker’s
complaints were of much shorter duration. I note that Ms. M’s lawyer submitted to WCAT
that the canker sores started in 1999.
I strongly question the extent to which one can reliably infer from the worker’s canker
stores, skin conditions, and possible neurological symptoms that he had significant
exposure to pesticides. However, even if those symptoms were due to pesticide
exposure, such circumstances would not establish that the worker’s lung cancer was
due to his occupational exposure to pesticides.
• Carcinogenic effect of exposure
I do not doubt that the various substances handled by the worker have the capacity to
be harmful. The issue is whether the substances were of causative significance to his
lung cancer.
Ms. M notes Dr. G’s observation that diazinon was not listed as a carcinogen by
a number of recognized agencies. She declares, “This is wrong.” I note that she
does not expressly assert that diazinon was listed by IARC, NTP, TRI or EPA as a
carcinogen. She refers to the Canadian Cancer Society’s statement that scientific
studies have linked pesticide exposure to some lung cancers. It is not clear how such
a statement establishes that Dr. G erred in his evaluation of how diazinon had been
classified by various agencies.
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As noted above, Dr. S linked the active ingredients of mecoprop (likely she meant
dicamba), chlorpyrifos and diazinon to lung cancer. I note that she did not assert that
any of the agencies noted by Dr. G had identified those substances as carcinogenic or
had linked exposure to those substances to the development of lung cancer.
As further noted above, Dr. S links the worker’s lung cancer to his occupational
exposure on the basis of journal articles and other information regarding
carcinogenesis. Of particular interest is the worker’s use of dicamba, chlorpyrifos, and
diazinon. She described other effects associated with other products, but did not expressly
refer to lung cancer.
I have reviewed the materials cited by Dr. S in Table 3 and Attachment 2 in support
of her assertions as to a link between lung cancer and the three listed substances:
dicamba (Samanic et al.), chlorpyrifos (Lee et al. and Alavanja et al.), and diazinon
(Nielsen et al., Beane Freeman et al., and Alavanja et al.).
I have also looked at the article by Ambroise et al.41 cited by Dr. S in Table 3, and I have
looked at the abstract for the article by Pesatori et al. cited by Dr. S in Table 3. I note
that Lee et al. published an article about mortality and chlorpyrifos exposure well before
the conclusion of submissions.
I have considered the notion that the worker’s cancer was not just the product of
exposure to one substance but to a combination of many substances. As well, I have
considered the notion that while there may not be a direct link between exposure to
a particular substance(s) and cancer, exposure to a particular substance(s) initiated,
triggered, or set the stage for the development of the worker’s cancer.
Many of the articles concerning any link between pesticides and cancer stem
from the Agricultural Health Study which involves an assessment of private and
commercial pesticide applicators in Iowa and North Carolina. A search of PubMed
reveals numerous articles which have evaluated the risk of cancer in this cohort. The
private applicators were farmers or nursery workers.
Alavanja et al. noted that epidemiologic data supporting an association for non-arsenical
pesticides and lung cancer risk in humans are mixed. They reviewed the effect of two
herbicides and two insecticides on members of the Agricultural Health Study cohort.
The insecticides were diazinon and chlorpyrifos. Smoking of cigarettes was a strong
risk factor for lung cancer in the cohort. Private applicators experienced a significantly
lower risk of lung cancer compared with the general population, likely due to lower
smoking rates. The two herbicides and two insecticides were associated with a
significant excess lung cancer risk. Three other pesticides, including dicamba, exhibited
an increasing lung cancer risk with increasing lifetime days of use when
41
Ambroise, D et al. Cancer mortality among municipal pest-control workers. International Archives of Occupational
and Environmental Health. 2005 Jun;78(5):387-93.
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2008 CanLII 18365 (BC W.C.A.T.)

a low-exposure group was used as a reference group, but not when a non-exposed
group was used as a reference group. The two herbicides and two insecticides had a
significant exposure-response relation with lung cancer, but did not have as strong an
exposure response when intensity-weighted exposure days were used as an exposure
metric. They observed that the results suggest that a substantial portion of farmers and
commercial pesticide applicators may be at an enhanced risk of lung cancer from
working with pesticides currently registered for use in the United States and other
countries.
Alavanja et al. observed that almost all of lung cancer cases that occurred in the
cohort were observed in current or former smokers. It was not possible to rule out
residual confounding from cigarette smoking. It was also not yet possible to assess
effect-modification between pesticide exposure and cigarette smoking.
In Table 4 of their article, Alavanja et al. documented the odds ratios associated
with use of various pesticides as categorized by lifetime exposure days. Using
the non-exposed group as a reference group, the odds ratios for dicamba were
below 1.1 for three categories of lifetime exposure days, including the category of
106.6 to 224.7 days. Only the category of greater than 224.7 lifetime exposure days
was moderately elevated. However, the associated figure of 1.6 was not statistically
significant. When the low-exposure group of less than 24.5 days was used as a
reference group, the odds ratios increased to 1.3 for the category of 24.5 to 108.5 days,
1.7 for 106.6 to 224.7 days, and 3.1 for greater than 224.7 days. Only the final figure
was statistically significant.
Using the non-exposed group as a reference group, the odds ratios for chlorpyrifos
were 1.0 or less for the categories of (i) fewer than 24.5 lifetime exposure days and
(ii) between 24.5 and 103.0 lifetime exposure days. The odds ratios for the categories
of 103.1 to 116.0 days and greater than 116.0 days were both 1.7. Neither figure was
statistically significant. When a low-exposure group of fewer than 24.5 days was used
as a reference group, the odds ratios increased slightly. The only notable increase was
an increase to 1.9 for the category of greater than 116.0 days. That figure was not
statistically significant.
Using a non-exposed group as a reference group, the odds ratios for diazinon were less
than 1.4 for the exposure categories of fewer than 20.0 days and 20.0 to 108.5 days.
The odds ratio for the category of greater than 108.5 days was 2.7. That last figure was
statistically significant. Using the low-exposure category of less than 20.0 days as a
reference group, the odds ratios for the categories of 20.0 to 108.5 days and greater
than 108.5 days were 1.6 and 3.2 respectively. Only the latter figure was statistically
significant.
I pause, at this juncture, to note that the worker’s career with the employer would
have involved between 72 and 108 lifetime exposure days to all pesticides (8 to 12 days
27
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2008 CanLII 18365 (BC W.C.A.T.)

a season x 9 seasons). Even if he had been exposed to diazinon, dicamba, and
chlorpyrifos on every possible day out of a maximum 108 days, his exposure would not
have put him in an exposure category for any one of those substances associated with
a statistically significant relative risk of 2.0 or greater.
Shortly after the publication of the article by Alavanja et al., Lee et al.
published their article regarding cancer incidence and exposure to chlorpyrifos in the
Agricultural Health Study cohort. They observed that there was little epidemiologic
evidence of an association between chlorpyrifos exposure and human cancer. Some
experimental studies had detected chlorpyrifos-induced mutagenicity. Chlorpyrifos
exposure was associated with increased risks of several cancers, including cancers
of the lung, although not one of the increases was statistically significant. The
relative risk for lung cancer of 1.36 for all enrolled applicators increased slightly to 1.49
associated with applicators who completed a take-home questionnaire which gathered
further information about exposures. Statistically significant trends in increasing lung
cancer incidence were seen with both lifetime exposure days and intensity-weighted
exposure days, with the rate in the highest exposure categories (equal to or greater
than 56.1 lifetime exposure days and equal to or greater than 417.7 intensity-weighted
exposure days) being approximately twice that of the rate in the non-exposed category.
The relative risk figures were 2.18 and 1.80 respectively; both figures were statistically
significant.
Lee et al. observed that the trend did not change when information as to total years
of pesticide application was added to the multivariable analysis as a surrogate measure
of other potential farming exposures or when the figures were adjusted for smoking
history using number of packs smoked per year or years smoked as separate variables.
The chlorpyrifos-lung cancer association was further investigated by calculating
odds ratios for lung cancer according to lifetime exposure-days stratified by state of
residence, histologic type, and smoking history. There was a statistically significant
exposure-response trend among current smokers. The authors were unable to
investigate risk trends among non-smokers because of the small number of cases.
Another evaluation which examined lung cancer risks associated with the combined
effect of chlorpyrifos and other agents revealed that the interaction rate ratio for lung
cancer with chlorpyrifos and smoking was limited to a comparison of current smokers
versus non-smokers. The latter category was composed of never and former smokers
combined because of the small number of never-smoking patients with lung cancer in
the cohort.
In the discussion section of their article Lee et al. observed that individuals in the
highest quartile of chlorpyrifos use (that is, with more than 56 lifetime exposure-days)
had twice the risk of lung cancer of applicators who never used chlorpyrifos,
although that elevation in risk “... may be restricted to current smokers.” The authors
noted that most previous studies had shown lower lung cancer rates for farmers than for
the general population, probably due to a lower prevalence of smoking among
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2008 CanLII 18365 (BC W.C.A.T.)

farmers. The cohort had a lower risk of lung cancer than the populations of Iowa and
North Carolina, but the authors did detect an exposure-response pattern between
chlorpyrifos exposure and lung cancer risk after controlling for other known cancer risk
factors.
Lee et al. noted that a limitation of the analysis as it related to lung cancer was the
possible confounding effect of smoking. Because of the small number of lung cancer
patients who had been exposed to chlorpyrifos, they could not analyze data separately
for women or non-smokers. Only four non-smokers had developed lung cancer. They
declared that the lung cancer findings were unlikely to be due to smoking because other
smoking-related cancers showed no exposure-response relationship with chlorpyrifos
use after accounting for cigarette smoking, whether adjusted by pack-years, number of
packs smoked per day, or years smoked. They declared that confounding by smoking
was not likely to be an important issue in their study.
Lee et al. concluded their article by observing that the findings “...suggest an
association between chlorpyrifos use and incidence of lung cancer among applicators
in the Agricultural Health Study.” They observed that lung cancer was not an a priori
hypothesized site linked to chlorpyrifos exposure, and thus the “…results must be
interpreted cautiously, pending confirmatory studies in the Agricultural Health Study and
elsewhere.”
Beane Freeman et al. studied cancer incidence among male pesticide applicators in
the Agricultural Health Study cohort exposed to diazinon. They observed that standard
assays of mutagenicity and cytotoxicity for diazinon have generally been negative. In
1997 the EPA classified diazinon as not likely a human carcinogen. Some laboratory
and epidemiologic data suggest potential carcinogenicity. They noted that Alavanja et
al. and Pesatori et al. had reported an association between diazinon use and lung
cancer. IARC had not reviewed the carcinogenicity of diazinon in particular; however, it
had stated that spraying and application of non-arsenical insecticides falls in the
category of “probably carcinogenic to humans,” indicating that further investigation was
warranted.
Beane Freeman et al. noted that there were increased risks for the highest exposure
category of greater than 38.8 exposure days compared with a non-exposed category
regarding the incidence of lung cancer. The relative risk was 2.41; it was statistically
significant. There was a significant increasing linear trend for the incidence of lung
cancers. When the low-exposed tertile of fewer than 20 days of exposure was used as
the reference group, association with lung cancer remained significant. The relative risk
was 3.19.
Beane Freeman et al. explored associations that might exist at higher levels of exposure
by splitting the highest tertile of exposure at the median of that tertile. They split the
category of greater than 38.8 days into categories of 38.9 to 108.8 days and
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2008 CanLII 18365 (BC W.C.A.T.)

greater than 108.8 days of lifetime and intensity-weighted exposure days. Using
the non-exposed category as a reference group, the figures were 1.82 and 3.46. The
latter figure was statistically significant. Using the low-exposed category of fewer than
20 days as a reference group, the relative risk figures were 2.53 and 4.16 respectively.
The latter figure was statistically significant.
Beane Freeman et al. observed that, since lung cancer was highly associated
with tobacco use, it was possible that the association observed in the study was due
to uncontrolled confounding by smoking. They observed that they modelled the risk
estimates by using a variety of smoking metrics and the results were unchanged,
suggesting that confounding due to smoking probably did not explain the elevated risks
of lung cancer. They observed that the point estimates for diazinon reported in their
analysis did not change when other pesticides were included in the model, suggesting
that their results were not due to residual confounding by those other pesticides.
Beane Freeman et al. noted that their study was only one of a few to examine
the effects of diazinon exposure and the risk of cancer. They noted that they found
evidence of an association of lung cancer risk with increasing lifetime exposure to
diazinon. While approaching statistical significance, the observed associations were not
significantly elevated when an intensity-weighted exposure algorithm was used. They
observed that, as more cases of cancer accrued in the cohort among those exposed to
diazinon, analyses that further explore and refine potential associations will be
performed.
Samanic et al. studied cancer incidence among pesticide applicators exposed to

dicamba in the Agricultural Health Study. They observed that the EPA regarded
dicamba as not classifiable as to human carcinogenicity. There was no experimental
evidence that dicamba was mutagenic or carcinogenic. They observed that existing
evaluations of dicamba-related health effects were inadequate.
Samanic et al. observed that they found no strong associations between any cancer site
and dicamba exposure for either lifetime exposure days or intensity-weighted exposure
days. They observed a trend of increasing lung cancer risk with increasing lifetime
exposure days when the reference group was low-exposed participants (1.0 to fewer
than 20.0 days of lifetime exposure), with a relative risk 2.16 for the upper half of the
highest tertile (greater than 116 days). The number of non-smoking dicamba-exposed
lung cancer cases (five) was too small to assess risk among non-smokers. In an
analysis based on intensity-weighted exposure days, those with exposure in the top two
tertiles of (i) between 86.6 and less than 344.25 days and (ii) greater than 344.25 days
had nearly twice the risk as those with low exposure, but no dose-response was
evident. There was no evidence of increased lung cancer risk with either lifetime
exposure days or intensity-weighted lifetime days when applicators unexposed to
dicamba served as the reference. Samanic et al. noted the figures
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2008 CanLII 18365 (BC W.C.A.T.)

obtained by Alavanja et al. and noted the similarity of their figures based on calculations
with reference to the low-exposed group as a reference group. When a non-exposed
group was used, the relative risks for all exposure tertiles were less than 1.5.
Samanic et al. noted that there were limitations to their study. They observed that the
patterns of association observed for lung cancer warranted further attention.
I question whether the worker would have had 108 days of lifetime exposure to
dicamba. However, even that number of days of exposure would not put the worker in
the upper half of the highest tertile (greater than 116 days) used by Samanic et al.
I have read the other articles submitted by Ms. M. I understand how some may be
relevant, but I consider that the above articles are the most relevant to the issue
before me. As an example, the article by Paz-y-Miño et al. concerns DNA damage
in an Ecuadorian population exposed to glyphosate. That there may have been
such damage does not mean that that population experienced, or will experience,
an increased incidence of cancer. The article by McKinlay et al. concerned a risk
assessment of endocrine-disrupting pesticides, but it did not draw a persuasive link
between pesticides to which the worker was exposed and lung cancer. The article
by Goode et al. concerned polymorphism in DNA repair genes and associations with
cancer risk. The article by Sears et al. examined the assessment of 2,4-D by Health
Canada’s Pest Management Regulatory Agency. The authors noted that while the
medical literature did not uniformly indicate that harms arise from phenoxy herbicide
exposure, given the strengths and limitations of epidemiological, toxicological, and
ecological research, it appears that cancer, neurological impairment, and reproductive
problems are persuasively linked to phenoxy herbicide exposure. Nielsen et al.
examined the risk of brain tumours in children exposed to organophosphorus
insecticides. Bolognesi reviewed human biomonitoring studies and the genotoxicity
of pesticides. Holsapple et al. studied mice exposed to a low-molecular-weight
halogenated aromatic hydrocarbons. Chiu et al. examined whether the association
between pesticides and non-Hodgkin’s lymphoma differed for molecular subtypes of
non-Hodgkin’s lymphoma.
In reviewing the appeal, I observe that the persuasiveness of Dr. S’s opinions linking the
worker’s lung cancer to his occupational exposure is limited by the fact that she is not a
medical doctor. In referring to Dr. S’s reports, Ms. M’s lawyer uses such terms as
“medical report” and “expert medical evidence.” Yet, Dr. S is not a medical doctor. Her
opinions are not medical reports or medical evidence. Dr. G is a medical doctor, as is
Dr. B. Yet, Dr. B’s opinion is not especially persuasive as it does not include a
considered opinion regarding causation. Mr. L is not a medical doctor and his opinion
adds little to the adjudication of this appeal.
This is not to say that only the opinions of physicians are relevant to the adjudication
of appeals involving cancer. I appreciate that opinions of non-physicians may be
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2008 CanLII 18365 (BC W.C.A.T.)

very useful. Many epidemiologists are not physicians, and yet their opinions may be
highly relevant. As an example, epidemiologists may be in a much better position
than physicians to conduct an analysis of available literature concerning whether a link
generally exists between an exposure and a disease. Dr. S is not an epidemiologist.
Her gathering of information in the literature relevant to the effects of pesticides is, of
course, relevant to the issue before me. Her opinion as to whether the worker’s cancer
is due to the nature of his employment is less relevant. The persuasiveness of opinions
of non-physicians is limited when non-physicians seek to provide opinions on causative
significance.
Ms. M advised in her September 29, 2007 submission that the BCCA and the Canadian
Cancer Society were “…offering to do a complete documentary of [the worker],
pertaining to his work with Pesticides and his Cancer. Within the documentary it will be
presented and identified that [the worker’s] untimely death was a result of exposure to
Pesticides, and that we have to start keeping records of such diseases to prevent it from
happening to others.” She also advises that “…a major media is interested in my
research and [the worker’s] story.” Such a documentary may indeed be undertaken, yet
as of the adjudication of this appeal, no medical opinion has been submitted from a
physician from either of the societies mentioned by Ms. M.
After having reviewed the matter, I find that the evidence is insufficient to find that the
worker’s lung cancer was due to the nature of his employment. I accept that the worker
may have sprayed pesticides for nine seasons at 8 to 12 days per season. The
spraying, and any associated mixing, would have exposed him to such substances as
dicamba, chlorpyrifos, and diazinon. There is some indication in recent articles that
there is an increased risk of lung cancer associated with exposure to such substances.
Yet, I question whether the worker in the case before me would have had the
same form of exposure to pesticides as the members of the Agricultural Health Study
cohort. He was not a farmer, a nursery worker or a commercial pesticide applicator. I
appreciate that a review of the various articles establishes that the authors sought to
measure the number of days members of the cohort used particular pesticides. Thus,
one could seek to compare the relative risk of members of the cohort associated with a
certain number of days of exposure to a particular pesticide to the number of days the
worker used pesticides in the course of his employment.
In addition to my comments noted above regarding the significance of the most

relevant studies cited by Dr. S, I observe that the data gathered by Alavanja et al.
does not support a finding that the worker’s lung cancer is due to his pesticide
exposure. The worker did not have sufficient lifetime days of exposure to produce a
doubling of his lung cancer risk. In turn, the results of the study by Alavanja et al.
raise questions about the persuasiveness of the study by Lee et al. which found a
doubling of risk associated with more than 56.1 exposure days when compared to a
non-exposed group. In contrast, Alavanja et al. documented a relative risk of 1.0 for
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2008 CanLII 18365 (BC W.C.A.T.)

those members of the cohort with 24.5 to 103.0 lifetime days of exposure to chlorpyrifos
when compared to a non-exposed group. The figures calculated by Alavanja et al.
also contrast with the calculations of Beane Freeman et al. While Alavanja et al.
documented odds ratios of 1.4 or less for the exposure categories of fewer than 20 days
and between 20.0 and 108.5 days when compared to a non-exposed group, Beane
Freeman et al. calculated a relative risk of 2.41 for the highest exposure category of
greater than 38.8 days when compared to a non-exposed group.
Also of interest, in a consideration of the persuasiveness of the studies that have

emerged from the Agricultural Health Study cohort, is the fact that a comparison
between the highest exposed groups to the non-exposed groups yields lower figures
than comparisons between the highest exposed groups and the lowest exposed groups.
Intuitively, one would consider that a comparison between non-exposed groups and
highest exposed groups would result in a greater odds ratio or relative risk. I note that
Alavanja et al. observed that, in other contexts, authors had ascribed the phenomenon
to hormesis, that is, the protective effect resulting from exposure to a subtoxic
concentration of a chemical. They considered that the phenomenon was due to
unidentified factors present in the non-exposed group, but not in the exposed group,
which might elevate risk among the non-exposed. They observed that additional
epidemiologic and mechanistic data would be necessary before the question could be
rigorously addressed.
The authors of the studies of the Agricultural Health Study cohort addressed the
question of whether the results were due to confounding by cigarette smoking. Notably,
very few members of the cohort who developed lung cancer were non-smokers.
Further study is needed. It should be kept in mind that the authors noted an
association. That term is not the same as causation. The authors did not declare a
causal link between the substances they examined and lung cancer.
The substances to which the worker was exposed apparently have not been classified
as human carcinogens by various agencies. This is not to say that a substance can
only be found to be a carcinogen if the agencies noted by Dr. G determine that a
particular substance is a carcinogen. However, I attach some significance to the fact
that Dr. G observed that the agencies charged with assessing carcinogenicity have not
determined that the substances to which the worker was exposed are, in fact,
carcinogenic.
I have considered the criteria set out in the Board’s Protocol. I do not consider that the
evidence is sufficiently robust to find that there is a causal link between the substances
to which the worker was exposed, either singly or in combination, and his lung cancer.
It may be that articles and assessments produced in ensuing years will provide support
for finding that the substances to which the worker was exposed are indeed
33
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2008 CanLII 18365 (BC W.C.A.T.)

carcinogenic. However, at this point, I am not satisfied that the evidence supports a
conclusion that the worker’s lung cancer was due to the nature of his employment.
I have kept in mind section 250 of the Act which provides at subsection (2) that
WCAT must make its decision on the merits and justice of the case, and provides
at subsection (4) that where evidence supporting different findings is evenly weighted
WCAT must resolve the issue in a manner that favours the worker.
Subsection 250(4) refers to a “worker”, but not to a “dependant”. On its face,

that subsection does not apply to the claims of dependants, unless one wanted
to contend that the word “worker” must be taken to include a worker’s dependant(s).
Yet, the statute contains many instances where the word “worker” cannot be taken
to include a dependant. A clear example of that is subsection 6(10) which clearly
indicates that the claims of workers and dependants are subject to the restriction
found in subsection 6(8). If the claims of workers were considered to include those of
dependants, there would be no need to refer to both workers and their dependants. It is
not necessary for me to resolve whether subsection 250(4) applies to the claims of
dependants, as I find that the evidence in this case is not evenly weighted such that the
issue should be resolved in Ms. M’s favour.
Conclusion
Ms. M’s appeal is denied. I confirm the review officer’s October 12, 2006 decision. I find
that the worker’s lung cancer was not due to the nature of his employment.
Reimbursement has been requested in connection with expenses of $300.00 and

$1,361.00 incurred for the reports of Drs. B and S, respectively. I consider
that reimbursement of those expenses associated with the reports would be
appropriate. Item #13.23 of WCAT’s MRPP provides that WCAT will generally order
reimbursement of expenses for attendance of witnesses or obtaining written evidence,
regardless of the results in the appeal, where (1) the evidence was useful or helpful to the
consideration of the appeal or (2) it was reasonable for the party to have sought such
evidence in connection with the appeal.
Randy Lane
Vice Chair
RL/jy
34
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2008 Canlii 18365

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WCAT Decision Number: WCAT-2008-00782

2008 CanLII 18365 (BC W.C.A.T.)

2008 CanLII 18365 (BC W.C.A.T.)

This is an appeal by way of rehearing, rather than a hearing de novo or an appeal on

2008 CanLII 18365 (BC W.C.A.T.)

2008 CanLII 18365 (BC W.C.A.T.)

2008 CanLII 18365 (BC W.C.A.T.)

2008 CanLII 18365 (BC W.C.A.T.)

Dr. G commented that, as mentioned in his previous memorandum, metolachlor and

2008 CanLII 18365 (BC W.C.A.T.)

Dr. S’s submission includes a number of charts, the first of which

2008 CanLII 18365 (BC W.C.A.T.)

As noted by Dr. G, the information regarding this worker’s smoking history

The review officer was not persuaded by Dr. S’s opinion:

I acknowledge that the epidemiological information submitted by Dr. S

2008 CanLII 18365 (BC W.C.A.T.)

I find Dr. G’s opinion persuasive largely because of his reference to

As noted earlier, there is currently no means by which to identify the cause

2008 CanLII 18365 (BC W.C.A.T.)

- causing genetic damage;

2008 CanLII 18365 (BC W.C.A.T.)

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Dr. S concluded her initial report by stating as follows:

2008 CanLII 18365 (BC W.C.A.T.)

2008 CanLII 18365 (BC W.C.A.T.)

• additional information about glyphosate, a substance which causes skin lesions

• Recent articles include reports of (i) genetic damage related to exposure

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Under the heading “In summary”, Dr. S makes a number of observations.

Other scientific information is also important with piecing together

2008 CanLII 18365 (BC W.C.A.T.)

Mr. L’s November 30, 2006 opinion

Mr. L, a mechanical engineer with 50 years of experience in the areas of engineering,

2008 CanLII 18365 (BC W.C.A.T.)

Dr. B’s October 1, 2007 opinion

Dr. B is a medical doctor who has a special interest in environmental influences on

2008 CanLII 18365 (BC W.C.A.T.)

A far more logical posture to adopt is that any reasonable evidence,

Dr. I’s October 1, 2007 opinion and accompanying materials

Dr. I, a dermatologist, observed that a 1986 publication of the Government of Québec

Other materials submitted as part of the review and appeal process

Reasons and Decision

Subsection 6(3) and Schedule B of the Act

2008 CanLII 18365 (BC W.C.A.T.)

Subsection 6(1) of the Act

2008 CanLII 18365 (BC W.C.A.T.)

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• Substances to which the worker was exposed

According to an MSDS, metolachlor is a chlorocetanilide herbicide.35 According to an

2008 CanLII 18365 (BC W.C.A.T.)

As evidenced by Attachment 2 which accompanied Dr. S’s report submitted to WCAT,

2008 CanLII 18365 (BC W.C.A.T.)

• Non-carcinogenic effect of exposure

2008 CanLII 18365 (BC W.C.A.T.)

In considering whether the worker suffered non-cancer reactions to his occupational

• Carcinogenic effect of exposure

2008 CanLII 18365 (BC W.C.A.T.)

2008 CanLII 18365 (BC W.C.A.T.)

2008 CanLII 18365 (BC W.C.A.T.)

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2008 CanLII 18365 (BC W.C.A.T.)