Spanish Influenza in the City of Vancouver, British Columbia, 1918-1919

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Spanish Influenza in the City of Vancouver, British Columbia, 1918-1919

by

Sarah Buchanan

B.Sc., Queen‟s University, 2007

A Thesis Submitted in Partial Fulfillment of the Requirements for the Degree of

MASTER OF SCIENCE

in the Department of Geography

 Sarah Buchanan, 2012 University of Victoria

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Supervisory Committee

Spanish Influenza in the City of Vancouver, British Columbia, 1918-1919

by

Sarah Buchanan

B.Sc., Queen‟s University, 2007

Supervisory Committee

Dr. Aleck Ostry, (Department of Geography, University of Victoria) Supervisor

Dr. Denise Cloutier, (Department of Geography, University of Victoria) Departmental Member

Dr. Mary-Ellen Kelm, (Department of History, Simon Fraser University) Additional Member

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Abstract

Supervisory Committee Supervisor

Dr. Aleck Ostry, Department of Geography, University of Victoria Departmental Member

Dr. Denise Cloutier, Department of Geography, University of Victoria Additional Member

Dr. Mary-Ellen Kelm, Department of History, Simon Fraser University

During the last year of World War I (1918), a second deadly foe was causing

mortality around the world. Spanish Influenza killed an estimated 50-100 million people

worldwide, including 50,000 people in Canada during the 1918-1919 pandemic. This

thesis examines the impact of Spanish Influenza on people living in Vancouver, British

Columbia, Canada between June of 1918 and June of 1919. Statistical analysis with SPSS

was used to determine the association between influenza-caused deaths and

socio-demographic characteristics such as age, gender, immigration status, and employment. In

Vancouver, those who were between the ages of 19 to 39, and those who were employed,

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List of Tables

Table 1. Overview of Canadian provincial and city mortality rates from the literature. ... 15

Table 2. Primary cause of death in 1918-19 and 1921-22. ... 36

Table 3. Secondary cause of death for 1918-19 and 1921-22. ... 37

Table 4. Influenza versus non influenza deaths by time period. ... 38

Table 5. Influenza versus non influenza deaths by residence and time period. ... 38

Table 6. Influenza versus non influenza deaths by gender and time period. ... 39

Table 7. Influenza versus non influenza deaths by age category and time period. ... 40

Table 8. Influenza versus non influenza deaths by place of death and time period... 41

Table 9. Influenza versus non influenza deaths by birthplace and time period. ... 42

Table 10. Influenza versus non influenza deaths by employment status and time period. 42 Table 11. Influenza versus non influenza deaths by employed occupation and time period. ... 43

Table 12. Influenza versus non influenza deaths by marital status and time period... 44

Table 13. Influenza versus non influenza deaths by race and time period. ... 44

Table 14. Influenza versus non influenza deaths by simple immigration status and time period. ... 45

Table 15. Influenza versus non influenza deaths by length of residence in Canada and time period. ... 45

Table 16. Mortality Rates for Gender, Age Group, Immigrants, and the Employed, 1918-1919. ... 50

Table 17. Chi-square test for gender and influenza deaths in 1918-1919. ... 51

Table 18. Chi-square test for gender and influenza deaths in 1921-1922. ... 51

Table 19. Chi-square test for age category and influenza for 1918-19 and 1921-22. ... 52

Table 20. Chi-square test for place of death and influenza in 1918-19 and 1921-22. ... 53

Table 21. Chi-square test for birthplace and influenza in 1918-19 and 1921-22. ... 53

Table 22. Chi-square test for employment status and influenza in 1918-19. ... 54

Table 23. Chi-square test for employment status and influenza 1921-22. ... 54

Table 24. Chi-square test for occupation and influenza in 1918-19 and 1921-22. ... 55

Table 25. Chi-square test for marital status and influenza in 1918-19 and 1921-22. ... 55

Table 26. Chi-square test for immigration status and influenza in 1918-19. ... 56

Table 27. Chi-square test for immigration status and influenza in 1921-22. ... 56

Table 28. Chi-square test for race and influenza in 1918-19. ... 57

Table 29. Chi-square test for race and influenza in 1921-22. ... 57

Table 30. Chi-square test for length of residence in Canada and influenza in 1918-19 and 1921-22. ... 58

Table 31. Correlation between age, gender, birthplace, immigration status, length of residence in Canada, and employment status for Vancouver residents in 1918-19. ... 59

Table 32. Multivariate analysis showing odds ratio‟s for age category, marital status, gender, and employment status in 1918-19. ... 60

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List of Figures

Figure 1. Crowd outside of Hotel Vancouver, November 1918. ... 7

Figure 2. The SEF leaving the Port of Vancouver. ... 14

Figure 3. Vancouver, 1915. ... 22

Figure 4. City of Vancouver boundary in 1915... 35

Figure 5. Influenza versus non influenza deaths by time period.. ... 47 Figure 6. Location of residence for Vancouver residents dying of influenza in 1918-19. 49

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Acknowledgments

First and foremost, I would like to extend my heartfelt thanks to my supervisor Aleck

Ostry for his guidance and encouragement throughout this project. To my committee

members, Denise Cloutier and Mary-Ellen Kelm, thank you for your time, feedback, and

support toward this work; I have truly appreciated your perspectives. Additionally, a big

thank you to Ashley LeBourveau who so carefully transcribed the death certificates from

microfiche into Excel for me. And finally, Patrick Lucey and Cori Barraclough, thank

you for your total support and keen interest in all that I do and for teaching me to see the

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Dedication

I dedicate this thesis to my family for their never-ending love, support, encouragement,

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Chapter 1: Introduction

From the spring of 1918 until the spring of 1919 the world was under siege from a deadly

influenza virus known as Spanish Influenza. As an H1N1 influenza A strain, the virus caused “severe infection in the upper and lower respiratory tract, resulting in fatal respiratory

complications and bacterial pneumonia” (Pica et al., 2010, p. 125). During this period, the

pandemic killed an estimated 50 to 100 million people worldwide (Johnson and Mueller, 2002).

In Canada, approximately 50,000 people died from Spanish Influenza resulting in a mortality

rate of 6.1 per 1,000 people (Fahrni, 2004; Jenkins, 2007; Johnson and Mueller, 2002; Jones,

2005; Pettigrew, 1983; Patterson and Pyle, 1991). The social consequences of the pandemic were

severe and altered the way in which public health was understood.

While there is a plethora of historical research on the Spanish Influenza around the world,

there is little research that takes a geographical and epidemiological approach, especially in Canada. Furthermore, very little research has been conducted on the influenza‟s effect on cities

in British Columbia. This research sought to fill this knowledge gap by taking a medical

geography approach in conjunction with epidemiological methods to characterize the timing,

extent, and socio-demographic determinants of influenza mortality in the City of Vancouver,

British Columbia, Canada.

1.1 Purpose/Objectives

The purpose of this research was to conduct an in-depth geographical and

epidemiological analysis of Spanish Influenza in Vancouver, British Columbia, during the

pandemic of 1918-1919 and identify its demographic and geographical characteristics. One

investigation of Spanish Influenza in Vancouver, British Columbia, estimated, using newspaper

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than the Canadian average of 6.1 per 1,000 (Andrews, 1977). This same rate is quoted by Kelm (1999) and O‟Keefe and MacDonald (2004). However, in all these publications, it is unclear

whether this is a maximum or an average rate and the methods are not detailed enough to

determine how these rates were calculated. Additionally, there is no indication as to which

populations were most affected or whether socio-economic status or location (separately or

interactively) played a role in either contracting the disease or dying from this virulent strain of

influenza. This research was based on detailed and comprehensive analysis of all Vancouver

deaths from influenza during the epidemic and two years after the epidemic. The study sought to

determine the timing of the epidemic, clearly define mortality rates and demographic/population

risk factors for contracting Spanish Influenza. As well, adoption of a “case” and a “control”

period permitted a comparison of the characteristics of the pandemic influenza with the more

normal influenza season, which occurred in 1921-1922.

Based on the literature, six categories of questions were used to guide the analysis of Spanish

Influenza in Vancouver for 1918-1919. These questions are:

1. Did the first wave of Spanish Influenza in Vancouver occur in the Fall of 1918 and how many waves of the infection occurred?

2. Was the Fall 1918 wave of influenza more deadly than the other waves?

3. Were the effects of influenza consistent across all areas of Vancouver or did some locations experience a more severe mortality rate?

4. Were employed people more likely to die of Spanish Influenza? Were there specific occupations that experienced higher numbers of deaths?

5. Were young adults in Vancouver more likely to die of influenza than other age groups? 6. Did foreign born populations experience higher mortality rates than Canadian born

citizens?

In order to answer these questions, the thesis is organized into five sections. Chapter two, the

literature review, grounds this thesis in medical geography and highlights the story of the

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of influenza in the United States and Canada. Chapter three explains the methods used to answer

the research questions while chapter four reveals the results of the analysis. Finally, chapter five

(Discussion) and chapter six (Conclusions) link the results back to the specific research questions

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Chapter 2: Literature Review

2.1 Understanding Spanish Influenza through the Lens of Medical Geography Medical geography is defined by the Encyclopedia of Geography as the “application of

geographical methods and techniques to the study of health” (Jordan, 2012, p.1). While the term

medical geography suggests a relationship to medicine, Mayer (2010) points out that this may be

a misnomer due to the fact that the research has little to do with diagnoses and treatment but is

more of an examination of the geography of disease and health service delivery with an

epidemiological view point. Medical geography first arose in 1952 with the production of a

report by the Commission on Medical Geography (Ecology) of Health and Disease to the

International Geographic Union (Meade and Earickson, 2000), with a focus on disease ecology,

disease distribution, and health care service delivery and provision. However, as Meade and

Emch (2010) indicate, medical geography goes beyond just the simple presence of disease and

also allows for the inclusion of social, political, and economic factors that influence the

susceptibility of a population to disease and overall population health in general.

One of the key elements of medical geography is its biomedical perspective, a way of

viewing issues of health using biological mechanisms of illness and disease (Moon, 2009). The

idea of a biomedical gaze is attributed to the works of Michael Foucault, a philosopher of history

(or historical philosopher) who has written extensively on theoretical/methodological approaches

related to the medical field (Bishop, 2009). The biomedical gaze involves

examining/understanding a person based on their illness and the way that illness is biologically

manifested within their body (Frank and Jones, 2003; Hick, 1999).

Consequently, the major critique of medical geography is not the research focus itself but

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Elliot, 2009). What is interesting to note is that Meade and Earickson (2000) in the preface to

their medical geography textbook specifically state that medical geography has become “less

concerned with the optimization of health service delivery or a dichotomy between health service

and disease ecology” in favour of becoming more “concerned with health geography as a

behavioral and social construction and disease ecology as an interface between the natural

(physical world) and cultural dimensions of existence” (Meade and Earickson, 2000, p.v). This

advancement in the field of medical geography has allowed, as part of this research, the inclusion

of socio-demographic characteristics that help contextualize the quantitative results.

Furthermore, in their identification of questions of medical geography, Meade and Earickson

(2000) include a question regarding place which is typically associated with health geography as one of that discipline‟s central themes rather than a key element of medical geography. This

suggests that medical geographers are distinctly aware of the prominent critique in their field of

being dehumanizing and reductionist and that this is an evolving methodology moving toward a

more broadly conceptualized health geography.

The framework of medical geography forms the basis of this research because it focuses

on disease and illness (factors of ill-health) rather than health promotion and incorporates the use

of quantitative analysis of disease. Due to the nature of the data being used to undertake this

research, quantitative analysis is necessary as death certificates do not provide the opportunity

for interviews nor qualitative analysis. Consequently, a medical geography approach was taken

as opposed to a health geography approach.

2.2 Spanish Influenza around the World

During the last year of World War One (1918), the world experienced a horrendous death

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referred to as the Spanish Flu. While the Spanish Influenza did not originate in Spain, it is

believed by many authors that neutral Spain was the first to publicize its emergence because of

less wartime censorship (Canadian Medical Association Journal, 1918; Rogers, 1968; Dickin

McGinnis, 1981; Kreiser, 2006).

Between the spring of 1918 and the following spring of 1919, Spanish Influenza spread

around the world killing millions of people. First estimates of the worldwide death toll in the

1920s suggested that 20 million people died (Jordan, 1927). However, this mortality estimate has

increased over time. For example, Patterson and Pyle (1991) estimated 24.7-39.3 million people

died and, more recently, Johnson and Mueller (2002) estimated somewhere from 50 to 100

million may have died in the pandemic. Regardless of which estimate is deemed reliable, as

Tuckel et al. (2006) point out, this worldwide pandemic was unique as it killed millions of

people in a very short time altering the way in which public health was viewed and understood.

For the purposes of this literature review, only material from the United States of

America and Canada were referenced in support of specific research to determine the effect of

Spanish Influenza on people living in Vancouver, British Columbia. The global mortality

highlights the effect Spanish Influenza had during the period between the spring of 1918 and the

spring of 1919. While the focus of this literature review was Canada, and to a lesser extent, the

United States, Spanish Influenza was not unique to North America, nor were mortality rates the

highest in this part of the world (Canada 6.1 per 1,000; USA 6.5 per 1,000; Mexico 20.6 per

1,000) (Johnson and Mueller, 2002). In fact, the most deaths attributed to this disease occurred in

India with a recorded estimate of 18 million deaths (6.1 per 1,000) while the highest morality

rates (between 10.7 and 445 per 1,000) were likely experienced in Africa (Johnson and Mueller,

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2.3 Public Health and the Response to Spanish Influenza

Beyond discussions of mortality rates and death tolls, specific themes relating to this

epidemic appear and reappear throughout the Canadian and US literature, regardless of the

location being examined. These themes include greater emphasis on waging war than on dealing

with the public health problems created by the pandemic; the ineffectiveness of quarantine; a

lack of hospital beds, equipment, and personnel; the use of influenza fears to market so-called

curative or preventative treatments; and, finally, the mobilization of ordinary citizens into

volunteer organizations to take care of the sick.

Andrews (1977), Byerly (2005),

and Kreiser (2006) point out that despite

warnings about public gatherings, people

still congregated in city streets to welcome

soldiers home from the war. These authors

claim that these public gatherings resulted

in a spike in influenza cases in the days

following. Furthermore, Kreiser (2006)

calls attention to the fact that the desire to

provide people and supplies to the war

effort precluded precautions, such as

quarantine, from being implemented in the early days of the epidemic. Hence, activities

specifically related to the war effort were not hampered by quarantine protocols leading to the

conclusion that quarantine measures were not implemented effectively. The inability to

effectively implement quarantine measures is also illustrated by the Toronto experience, whereby

Figure 1. Crowd outside of Hotel Vancouver, November 1918. Thomson, Stuart. (Photographer). Armistice Day crowd outside Hotel Vancouver, Georgia Street. [Online image]. Retrieved from City of Vancouver Archives, http://searcharchives.vancouver.ca/armistice-day-crowd-outside-hotel-vancouver-georgia-street;rad.

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the disease spread so quickly to so many people that quarantine and isolation became impractical

almost immediately (MacDougall, 2007).

Additionally, hospitals were badly understaffed during the war and communities had to

compensate by opening other buildings such as schools and hotels to care for the sick (Boucher,

1918; Dickin McGinnis, 1976; Andrews, 1977; Jones, 2005; MacDougall, 2007). As well,

personnel were difficult to find with large numbers of citizens overseas, and provisioning was

more difficult because the military had first access to materials. Finally, many medical

professionals became ill with the flu further straining resources for caring for the sick (Dickin

McGinnis, 1981).

As a result of the widespread concern about contracting Spanish Influenza, many

businesses and other organizations cashed in on the panic to promote and market products as

essential flu prevention and protection techniques (Andrews, 1977; Jenkins, 2007). Pettigrew

(1983) spends a whole chapter describing these different products. Some of the more interesting

remedies included: lard mixed with turpentine, gin pills, goose grease, camphor, sulphur, and oil

of cinnamon (Pettigrew, 1983; Jones, 2007). However, none of these products proved to be

consistently effective remedies.

One of the most impressive feats throughout the epidemic was the mobilization of

volunteers and organizations to care for the sick. The lack of medical personnel resulting from

the war effort was well recognized and entire communities responded to supply the labour and

care necessary to help those who were ill in the community. Dickin McGinnis (1976, p. 7)

undertook a study of Calgary, Alberta, and noted that volunteering to help with influenza was viewed as an opportunity for “women to do their bit for war and for civilization”. These women

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also reflected by Jones‟ work on influenza in Winnipeg (Jones, 2002, 2005, 2006, 2007). For

more information see Jones (2007) who examines in her book the role of women and

volunteering in aiding in the care of those ill with influenza.

So what made Spanish Influenza so deadly and unique? Researchers such as Herring

(1993) and Kelm (1999) hypothesize that part of its virulence was because it was a virgin soil

epidemic so no one had immunity to it. Others postulate that it was not necessarily the flu itself

that was deadly but the secondary pneumonia infection that caused fatality (Canadian Medical

Association Journal, 1918; MacDougall, 2007; Robertson, 1919). Perhaps, as Dickin McGinnis

(1981) suggests, the conditions created by the war, the transportation of large numbers of people

in a short amount of time, and the dismal conditions of the war trenches produced an

environment ripe for the influenza virus to thrive. Additionally, it could have been that the

medical world was not clear on what the cause of influenza was. The Spanish Influenza strain

was not identified until 1933 by British scientists (MacDougall, 2007; Noymer and Garenne,

2000) and is still being analyzed genetically by researchers such as Taubenberger today. The

genetic analysis of the influenza virus gathered from the frozen lung tissue of victims of

influenza indicates that the 1918 virus was an H1N1-subtype influenza A virus (Taubenberger,

2003). Taubenberger (2003 and 2006) further classifies this Spanish Influenza virus as

containing genes from avian-influenza strains and suggests that pigs may have acted as the

intermediary host between birds and humans. Furthermore, the flu is an illness that consistently

infects populations, often with high morbidity but low mortality so it may not have been taken

seriously at the outset; i.e.an attitude of “after all, it‟s only the flu” may have set in (Kreiser,

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2.4 Origins, Timing, and Mortality from the Epidemic

There is much debate within the literature regarding where Spanish Influenza originated.

Some researchers suggest that the flu began in China in February 1918 and was brought to

Western Europe by Chinese labourers before being disseminated by troops fighting throughout

Europe and, from there, back to soldiers‟ countries of origin (Dickin McGinnis, 1981; Pettigrew,

1983). The virus requires an intermediate host, such as pigs, to be transmitted from the avian

population to the human population. The close proximity between the natural influenza reservoir

of birds, the intermediate hosts (pigs), and humans in Asia has resulted in that area being

considered an influenza epicentre (Shortridge and Stuart-Harris, 1982; Webby and Webster,

2001). Consequently, China as the origin makes sense biologically.

Now consider how the virus could have been transmitted from China to the western front.

A recently published book by Guoqi (2011) documents the journey of upwards of 80,000

Chinese labourers across the Pacific Ocean to Vancouver. From Vancouver they boarded onto

railway cars being transported across Canada to the eastern ports for passage to the Western

front. This transportation of Chinese labourers occurred between March 1917 and March of 1918

and was considered to be of utmost secrecy with a complete blackout of the media. At the time, a

$500 head tax was required from any Chinese person entering Canada; however, because these

labourers were enroute to Europe, the Government of Canada waived the tax on the condition the

labourers did not get off the trains (Guoqi, 2011). Not all of the 140,000 – 200,000 Chinese

labourers, sought to address manpower shortages in Western Europe, travelled through Canada

on their way to France. King (1918) indicates that some of them were sent through the

Mediterranean although the majority are said to have passed through Canada and the United

States. Whatever the route, perhaps some of these labourers harboured a precursor to the deadly

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Another hypothesis of the origin of Spanish Influenza comes from Oxford (2001) who

suggests that an acute respiratory infection at Etaples, France, in the winter of 1916 was an

influenza virus of a type similar to the 1918 flu. However, most authors suggest that this strain of

influenza actually originated in the United States in Haskell County and spread to the Camp

Funston army base in north central Kansas where the illness was first reported on March 5, 1918

(Vaughan, 1921; Patterson and Pyle, 1991; Crosby 2003; Barry, 2004). From there it was carried

by troops transported by ships to serve on the European battlefields and then to the rest of the

world. However, Erkoreka (2009, p.192) cautions that it is “problematic to assign such a specific

date to the beginnings of the pandemic, since its origins are likely to be much more complex and varied”. This statement leaves room for continued debate on where the Spanish Influenza strain

first developed.

Whether Spanish Influenza originated in Kansas or not, the infection‟s presence there

was a factor in the dissemination of the virus and kicked off the first of three influenza waves

beginning in the spring of 1918, the fall of 1918, and the winter of 1918-1919 (Crosby, 2003).

By June of 1919, 675,000 people had perished in the United States as a result of Spanish

Influenza that, according to Kreiser (2006), is more than the total number of American military

deaths incurred during World War One, World War Two, the Korean War, and the Vietnam War

combined.

Part of the reason for this high death toll, and the speed with which the epidemic spread

throughout the United States, is attributed to the efforts of supplying as many soldiers as possible

to the battlefields in Europe, which ruled out a public health approach of complete quarantine.

Crosby (2003, p. 56) indicates that the American armed services (Army and Navy) were affected “earlier and more severely than the civilian population and to a certain extent were the foci from

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which the civilian population received the disease”. Furthermore, Byerly (2005) and Kreiser

(2006) propose that quarantine (the only public health measure that could be used to effectively

combat the epidemic) would have counteracted efforts to rapidly deploy US forces in Europe.

The war was deemed a more important task and troops were dispersed despite illness among the

ranks.

Overall, the US mortality rate directly attributable to Spanish Influenza between 1918

and 1919 is 6.5 deaths per 1,000 people (Johnson and Mueller, 2002). However, as we will see

for Canada, this rate was not consistent across the country. Rogers (1968) identifies mortality

rates for five cities: Philadelphia (158 per 1,000), Baltimore (109 per 1,000), Washington (109

per 1,000), Boston (100 per 1,000), and New York (60 per 1,000). These rates suggest that while

the overall mortality rate for the United States may have been relatively low, certain centers were

more severely impacted. This is also reflected in a study conducted by Noymer and Garenne

(2000) who reveal that in the United States the life expectancy at birth dropped by 11.8 years in

1918 showing the disproportionate impact of the epidemic on young people.

Influenza did not reach Canada until late summer/early fall of 1918; although Dickin

McGinnis suggests it could have arrived earlier in June or July 1918, her hypothesis is refuted by

Humphries (2005). Therefore, it appears that the first wave of the pandemic did not involve

Canada directly. Despite this, the second wave was still destructive to Canadian populations

when it did arrive. The most commonly cited estimate for the Canadian death toll caused by

Spanish Influenza and the pneumonia that accompanied it is 50,000 people out of a total

population of about eight million, a mortality rate of approximately 6.1 deaths per 1,000 people

(Fahrni, 2004; Jenkins, 2007; Johnson and Mueller, 2002; Jones, 2005; Pettigrew, 1983;

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While this mortality rate of 6.1 per 1,000 is consistently documented, it is unclear when

Spanish Influenza first arrived in Canada. This is because of an unresolved debate about how the

epidemic arrived and spread throughout the country. Early researchers such as Dickin McGinnis

(1976, 1981), Pettigrew (1983), and early works of Jones (2002), support the belief that the

epidemic originated with Canadian soldiers returning from Europe on troop ships. The broader

implication of this origin is that American troops infected in the first wave went to Europe where

they infected Canadian troops who then brought the illness to Canada.

However, Humphries (2005) makes a strong case, based on military archives and ship

records, that ships thought to have brought ill soldiers back from Europe were actually sitting

empty in quarantine waiting to be sent to Europe. Thus, these ships could not have brought

Spanish Influenza to Canada. Instead, he presents a new hypothesis that the “physical path taken

by pandemic influenza in Canada was determined by the intensification of the war effort, not by its waning” (Humphries, 2005, p. 241). In short, he theorizes that Spanish Influenza entered

Canada in late August 1918 with newly trained American recruits who were to be sent overseas

via Canada. The “greatest single factor in the diffusion of the disease” according to Humphries

(2005, p.252) was the creation of the Siberian Expedition Force, which was to travel to Russia

from Vancouver and included both American and Canadian troops. This expeditionary force was

recruited during late August and early September of 1918, around the same time that the first

influenza cases appeared in Ontario, Quebec, and Nova Scotia. This force was assembled in

Eastern Canada and transported via rail to Vancouver on October 2, 1918 (Humphries, 2005).

However, according to Humphries (2005), and corroborated by Jones (2007), the train

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drop off military members sick with influenza to the local hospitals. Accordingly, this railway

expeditionary force seeded the epidemic across Western Canada in the early fall of 1918.

The theory of an August 1918 arrival of influenza in Canada is in conflict with research

conducted by Palmer et al. (2007) who show that influenza was present in Newfoundland as

early as May 1918. Thus, it is possible that influenza entered Atlantic and Eastern Canada a few

months prior to August 1918; however, the train

journey of September 1918 was the primary route that

seeded the influenza virus into the west.

As influenza made its way across Canada,

different localities had dissimilar experiences with the

illness. Some areas such as Newfoundland (Palmer et

al., 2007) experienced two long waves of the illness (May – July 1918, September 1918 – June 1919) while

other locations like Winnipeg experienced two shorter

waves (October – December 1918 and February –

April 1919) (Jones, 2005). This discrepancy implies a

geographical determination of the character and timing of the illness as it could have been

shaped by different regional attributes such as the make-up of the social organization in the

cities, towns, and communities‟ Spanish Influenza affected.

Such local or regional heterogeneity appears to also be reflected in mortality rates across

Canada. As shown in Table 1, rates varied from a low of 3.6 per 1,000 (in Ontario) to a high of

780 per 1,000 in one small town in Newfoundland). Why certain regions experienced higher

mortality is unclear as the methods of prevention were similar across Canada with quarantine,

Figure 2. The SEF leaving the Port of

Vancouver. Thomson, Stuart. (Photographer). “Monteagle” leaving Vancouver with Siberian Expeditionary Force. [Online image]. Retrieved from City of Vancouver Archives,

http://searcharchives.vancouver.ca/monteagle- leaving-vancouver-with-siberian-expeditionary-forces;rad.

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reduction of business hours, closure of theatres, picture shows, and schools, sanitation agendas,

and provision of vaccines being the common medical and public health practices (Andrews,

1977; Jenkins, 2007; Jones, 2006; McCullough, 1918; Dickin McGinnis, 1976).

Table 1. Overview of Canadian provincial and city mortality rates from the literature.

City Mortality Rate (per 1,000) Source

Newfoundland (Nfld) 5.0 Palmer et al., 2007

New Brunswick 4.0 Jenkins, 2007

Ontario (ON) 3.6 Jenkins, 2007

Quebec 7.0 Jenkins, 2007

Winnipeg, Manitoba 6.0 to 6.5 Jones, 2006

South Winnipeg 4.0 Jones, 2005

North Winnipeg 6.7 Jones, 2005

Saskatchewan cities 6.0 Lux, 1997

Rural Saskatchewan > 10 Lux, 1997

Alberta 11.5 Jenkins, 2007

British Columbia: non-native population

6.2 Kelm, 1999

Vancouver, British Columbia 23.3 Andrews, 1977

Aboriginal Communities

Hebron, Nfld 680 Palmer et al., 2007

Okak, Nfld 780 Palmer et al., 2007

Norway House, Manitoba 183 Herring and Sattenspiel, 2003

British Columbia: native population

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One of the difficulties in understanding these marked differences in rates is that the

methods used to obtain them are not clearly stated. Most of these rates appear to have been

derived from the media (especially newspapers). It is therefore impossible to determine their and

to assess the suitability of the methods used to obtain them.

For example, Jenkins (2007), while providing mortality rates for New Brunswick,

Ontario, Quebec, Saskatchewan and Alberta, is unclear which populations were used as the

denominator in the rate calculation. Jenkins extracts the total number of deaths from influenza

from various other authors, and then (it appears) calculates rates using the quoted numbers as

numerators. For example, the total number of influenza deaths for Quebec was extracted from

Patterson and Pyle (1991). Jenkins then calculated a rate but does not say which denominator

was utilized; therefore, this calculation cannot be repeated and its accuracy is unknown.

Lux (1997) provides an overview of the impact of Spanish Influenza on Saskatchewan

cities and rural regions. Influenza rates were lower in urban than in rural Saskatchewan,

however, as with many of these historical accounts of influenza, the methods used to calculate

rates are not explicit. The only clue provided by Lux is that the mortality data were based on

information from the Saskatchewan Board of Public Health.

A similar conundrum is presented with the work of Jones (2005 and 2006). Rates for

Winnipeg are extracted from City Health Department records. While these may be good

secondary sources, it is not indicated whether the mortality data obtained was raw, with rates

calculated by Jones, or whether the rates were obtained directly from the City Hall records.

Either way, it is unclear how the rates were determined.

While methods were not explicit for Jones and Lux, they were based on “official” health

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than 10 in rural Saskatchewan. These studies have the advantage of being based on official data

rather, than in some of the other studies quoted in Table 1, on media reports and appear to put a

range on rates in the prairies in 1918-19 of 4 to 10 deaths per 1,000 population, much lower than

the extremely high rates of 780 per 1,000 observed in one Newfoundland study.

There are very few studies that undertake an examination of the impact of Spanish

Influenza in British Columbia. Two commonly cited papers discussing the influenza epidemic in

British Columbia were written by Andrews (1977) and Kelm (1999). Andrews (1977),

specifically examines influenza in the City of Vancouver. While she specifically acknowledges “precise morbidity and mortality figures are not available for Vancouver for the six-month

epidemic period” she does provide a mortality rate of 23.3 per 1,000 (Andrews, 1977, p. 27).

This rate is based upon information provided by the Vancouver Daily Province newspaper and

the 1918 annual report for the City of Vancouver. The period of the epidemic this rate represents

is from the beginning of the epidemic to the end of January 1919. Unfortunately, it is not clear

when the beginning of the epidemic is, as numerous cities are included within the same

timeframe but not all cities were infected at the same time. Nor is it clear whether Andrews

herself calculated the rate or if it was provided by the newspaper or annual report. While the

mortality rate of 23.3 per 1,000 has been quoted in other historical discussions of Spanish

Influenza, its accuracy is unclear. My research will, by using death certificates and clear

denominators, be able to calculate the mortality rate associated with Spanish Influenza for the

City of Vancouver with greater accuracy.

Kelm (1999) quotes an overall B.C. mortality rate of 6.21 per 1,000 (based on Vital

Statistics Sessional papers for May of 1919) and the same Vancouver mortality rate of 23.3 per

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population was 46 per 1,000 implying that Aboriginals suffered much more severely than the

non-Aboriginal population. The Aboriginal mortality rate is based on Department of Indian

Affairs and Vital Statistics population information at the band level and mortality from

flu-related illness (Kelm, (1999); Kelm, 2011, pers. comm.). It is not clear from Kelm‟s article what

year the population totals represent or what mortality figures were used (Vital Statistics versus

Department of Indian Affairs) as part of the rate calculation.

One of Kelm‟s key findings is that, among Aboriginals in BC, young children and older

adults were most affected whereas mortality from Spanish flu appears to have been greater

among young adults in the non-Aboriginal populations. One reason for these differences may be that at this time “one-third of the total population of British Columbia‟s First Nations were under

the age of fifteen” (Kelm, 1999, p. 30). However, that does not explain the greater impact among

older Aboriginal adults versus older non-Aboriginal adults she observed.

The studies that do clearly identify how the rates were calculated are Palmer et al. (2007)

and Herring and Sattenspiel (2003). Palmer et al. (2007) used 1911 census population data to

calculate death rates per 10,000 for districts across Newfoundland by wave of influenza

infection. Sources of information to determine mortality rates included death records, interviews

with island residents, census data, vital statistics, records of international shipping, newspapers,

local museums, and government correspondence about the influenza epidemic. Accordingly, the

overall mortality rate for Newfoundland came from a fairly rigorous methodological

investigation. However, the rates provided for Hebron and Okak (small towns in Newfoundland)

were not calculations conducted by the authors but sourced elsewhere. Consequently, the

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Herring and Sattenspiel (2003) undertook a slightly different approach to determining

mortality rates for the isolated, primarily Aboriginal community of Norway House in Manitoba.

The authors used parish records to estimate the mortality rate of Norway House (183 per 1,000)

and performed a more detailed analysis using Treaty Annuity Pay Lists for population estimates

to examine family distributions of mortality. The analysis of family distribution reveals that

while there is a high community mortality rate, the impact of influenza was concentrated within seven nuclear families (25% of the deaths) and within “families related through the male line”

(56% of the deaths) (Herring and Sattenspiel, 2003, p. 169). Therefore, the high mortality rate is

more of a result of the impact on these particular families than on the impact of influenza on the

community as a whole.

They also conducted a travel-based analysis using Hudson‟s Bay Company journals to

establish the travel patterns between Norway House and other trading posts where influenza was

contracted. These journals indicate that travel occurred more frequently during the warmer

months when waterways were open, to accommodate travel by water, while in winter months

travel was less frequent, and took longer, which delayed the dissemination of influenza into the

community. However, after running computer simulations on the movement of influenza

between communities, in the vicinity of Norway House, the author‟s note that while travel (i.e.

rate of travel and patterns of travel) influenced the timing of influenza infection it did not affect

the number of cases experienced by the community. The study did not provide seasonal mortality

rates so there is no discussion on how mortality rates were influenced by travel patterns.

My research follows a similar method, in determining mortality rates, to that of Palmer et

al. (2007) by also utilizing census populations, census information, and death records. Death certificates were used as the primary source of information to identify the number of deaths

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caused by Spanish Influenza in Vancouver. The key difference is that this study will utilize the

census population from 1921, rather than from 1911, as it is closer in time to the period of the

epidemic (1918-1919) so the population numbers should be more reflective of 1918 – 1919 than

the 1911 census numbers.

2.5 Groups Most Vulnerable to the Epidemic

Perhaps the most commonly cited unique feature of this strain of influenza is that it

resulted in high mortality rates among young adults. Noymer and Garenne (2000) and Palmer et

al. (2007) discuss the W-shaped age-specific mortality curve where high mortality rates are experienced in the youngest and oldest populations, as well as a peak between the ages of 15 to

45. Additionally, virtually all authors cited in this literature review indicate at some point within

their research that young adults were most affected. The use of the term „young adult‟ in these

studies is not consistent. For example, Jones (2006) identifies that 60% of all deaths in the city of

Winnipeg occurred in people between the ages of 20 to 39. On the other hand, Humphries (2005)

suggests that the majority of deaths in Canada were healthy males and females between the ages

of 15 and 35. Tuckel et al. (2006) in their analysis of Hartford, Connecticut indicate that there

was a higher mortality rate among males and for young adults between the ages of 25 to 35

years.

In addition to the age-specific population effects, there is some discussion within the

literature that socio-economic status may have played a role. This suggestion is primarily based

on observed differences in mortality rates between immigrant populations and non-immigrant

populations in American cities. The most detailed examination of this population difference is

conducted by Tuckel et al. (2006) in their study of Hartford, Connecticut. They demonstrated

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nativity and higher among those with Canadian, Russian, Austrian, and Polish maternal nativity.

Those people with Italian maternal nativity experienced the highest mortality rates in Hartford.

Tuckel et al. (2006) concluded that a higher proportion of immigrants, renters, and the less

educated tended to have higher mortality rates in Hartford. Accordingly, this suggests that

socio-economic status may indeed have been a risk factor for death caused by influenza in 1918-19

with those of a lower socio-economic status more at risk. Moreover, a similar immigrant effect is

proposed by Jones (2002, 2005, 2006, and 2007) in her analysis of Winnipeg, where the

mortality rate for northern Winnipeg, with a population primarily composed of immigrants and

the poor, was higher than southern Winnipeg where the wealthier, Canadian-born citizens lived

(see Table 1). However, it is important to keep in mind that the way that Jones calculated the

mortality rates is unclear so the accuracy of these rates is undeterminable.

2.6 Spanish Influenza in British Columbia and Vancouver

Very little can be found in the literature specifically related to British Columbia; the most

widely quoted papers are written by Andrews (1977) and Kelm (1999) and a book written by O‟Keefe and MacDonald (2004). Andrews (1977), and O‟Keefe and MacDonald (2004),

concentrate on the City of Vancouver, while Kelm (1999) conducts her analysis on the First

Nations populations of British Columbia.

Andrews (1977) investigated the influenza epidemic in the city of Vancouver using

newspaper articles published in 1918 and 1919 as her primary references. From these, she quotes

the mortality rate as 23.3 per 1,000 (a total of 795 deaths) and suggests miners and pregnant

women suffered the highest mortality rates. The same mortality rate is also referenced in

O‟Keefe and MacDonald (2004) but does not explain where this figure originated. Additionally,

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America but, as suggested by Keiser (2006, p.

130) in her review of this book, these rates “beg analysis”.

O‟Keefe and MacDonald (2004) in their

book exploring the actions of Vancouver‟s

medical health officer, Dr. Underhill, reveal that

his assessments of mortality rates show that the

white population of Vancouver was most

affected in contrast to other ethnicities such as

the Chinese, Japanese, and Hindu populations. If this is correct, then Vancouver‟s ethnic

mortalities are in opposition to other locations in Canada, and also the United States, where

studies indicate that the highest mortality rates occurred among immigrant populations (Tuckel et

al., 2006; Jones, 2002, 2005, 2006, and 2007). However, O‟Keefe and MacDonald were not clear whether the white population was composed of Canadians only or if it also includes white

immigrants. Consequently, analysis of race (based on immigration status and Caucasian versus

non-Caucasian) in order to clarify this point will be part of the forthcoming research.

Furthermore, Andrews indicates that there were three waves of Spanish Influenza in

Vancouver, the first in October of 1918, the second in January of 1919, and the third in March of

1919. This observation is consistent with Humphries‟ hypothesis of spread of influenza from the

American military to a location in Eastern Canada and subsequent early fall spread, via train,

across to Vancouver (Humphries, 2005). However, without clear methods and a more precise

investigation of mortality in Vancouver this cannot be ascertained with any reliability.

Figure 3. Vancouver, 1915. Calder, Walter H. (Photographer). View of north west area of downtown Vancouver, showing parts of Stanley Park, Burrard Inlet, and the North Shore. [Online image]. Retrieved from City of Vancouver Archives,

http://searcharchives.vancouver.ca/view-of- north-west-area-of-downtown-vancouver- showing-parts-of-stanley-park-burrard-inlet-and-north-shore;rad.

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Kelm (1999), in her examination of the 1918-1919 influenza epidemic in the Aboriginal

populations of British Columbia, highlights the varied mortality rates stated for these populations

depending on who is doing the reporting; for example, the Department of Indian Affairs (600

deaths) versus the Vital Statistics Branch (700 deaths) versus agent reports (over 1,000 deaths),

and suggests that under reporting is likely. Additionally, Kelm indicates that First Nations

populations experienced higher relative mortality rates (46 per 1,000) as compared to non-Native

populations (6.21 per 1,000). However, it is not clear on the exact method with which these rates

were calculated other than that native mortality rate is based on Department of Indian Affairs and

Vital Statistics population information at the band level and mortality information from

flu-related illness (Kelm, (1999); Kelm, 2011, pers. comm.).

Similar to the rest of the literature, transportation routes such as railways and shipping

lines are highlighted as key influenza dissemination vectors in British Columbia with Kelm

(1999) also citing the closure of canneries and the exodus of ill workers back to the reserves as

an example.

2.7 Summary

In conclusion, the Spanish Influenza pandemic of 1918-1919 circumnavigated the globe

in a very short time frame and killed millions of people worldwide. The Spanish flu targeted

young adult populations, a fact uncommon to the more typical influenza virus strains, and

highlighted the importance of transportation routes as dissemination corridors. What remains

fascinating about this pandemic is the speed at which infectious disease can circle the globe,

which is potentially much greater today with the speed and accessibility of world travel. By

understanding the elements of historical epidemics and identifying susceptible populations,

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As expressed previously, there is still little known about how Spanish Influenza affected

the population of British Columbia and, according to Kelm (pers. comm., 2011), there is

uncertainty about how socio-economic factors may have played a role in the experience of the

disease during and after the epidemic. The purpose of this research was, therefore, to re-examine

Vancouver death certificates from 1918 and 1919 as a case study and determine what

populations in Vancouver were affected the most and whether or not this can be tied to

socio-economic differences at that time.

There are major limitations in the literature on Spanish Influenza. The biggest limitation

is the difficulty in determining the exact number of deaths because of incomplete reporting,

misdiagnosis, and the potential for confusing diagnoses between this particular influenza strain

and pneumonia (Johnson and Mueller, 2001; Palmer et al., 2007; Patterson and Pyle, 1991).

Specifically, when official records indicate the cause of death as pneumonia during 1918-1919 it

is difficult to know whether the individual had Spanish Influenza and then contracted pneumonia

or whether they only had pneumonia. Overall, these limitations culminate in a commonly

suggested underestimate in both the number of cases and number of deaths from Spanish

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Chapter 3: Methods

With the limitation of misdiagnosis in mind, the following methods, grounded in medical

geography, were employed to create as accurate a representation as possible of the impact of

Spanish Influenza in Vancouver.

3.1 Data Collection and Determining Population Size

Death certificates from the City of Vancouver in 1918-1919 and 1921-1922 were

collected from the British Columbia Vital Statistics Agency. The hard copies of these records

were obtained from the microfiche vaults at Simon Fraser University library and the information

on them transcribed to create the excel database used for analysis. Transcription of the records

was conducted by Ashlee LeBourveau at Simon Fraser University. The transcription was verified

by reviewing a random sampling of the original death certificates and comparing it to the created

database. The information provided by these death certificates included some or all of the

following: name of deceased, registered number of the certificate, date of birth of deceased, date

of death, place of death, how long deceased was at place of death, former or usual residence,

cause of death, duration of cause of death, secondary cause of death, duration of secondary cause

of death, sex, age, occupation, parent occupation, race, marital status, birthplace, length of residence in Canada, father, father‟s birthplace, mother, mother‟s birthplace, informant‟s name,

and informant‟s address. In short, the data used for this thesis were Vancouver mortality data for

the period of June 1918 to June 1919 and June 1921 to June 1922.

Mortality rates were calculated for influenza deaths for both of these time periods in

order to determine if Spanish Influenza had a larger affect during the 1918-1919 flu season. The

total population size used for the calculations was based on Government of Canada 1921 census

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completed in 1921. However, the population size for 1918-1919 is also based upon the 1921

population size. Considering population size can change substantially over a short timeframe, it

was necessary to examine what was happening in Vancouver in terms of demographics between

1918-1919 and 1921-1922. As an example Macdonald (1992) states that between the census years of 1911 and 1921, Vancouver‟s population increased by a third to 163,000 people.

One way to do this was to see how fast the city grew or shrank and whether migration

patterns changed over this time period. According to Macdonald (1992), Vancouver experienced

a large population drop between 1910 and 1920 especially around the years of 1913 and 1914 as

a result of the depression and the beginning of World War I when military personnel went

overseas. However, Barman (1986, p. 98) states that by World War I the “socio-demographic

framework of Vancouver was in place and the growth was moderated”. During the 1920s growth

in Vancouver occurred again and between the 1921 and 1931 censuses the population grew from

175,000 to 246,000 (Macdonald, 1992). Because 1921-1922 is still the early part of the 1920s

decade in which the major growth began, the 1921 census should still be a good estimate in

terms of population for 1918-1919. Military personnel would have begun returning home during

this period as well increasing population levels to better match those assessed in 1921. During

this same period, populations in Point Grey and South Vancouver more than doubled to 13,000

and 32,000 respectively (Macdonald, 1992) which becomes important when determining the

boundary of analysis. Or in other words, how should Vancouver be physically defined for the

purposes of this study?

3.2 Boundary of Analysis

Identifying the boundary of Vancouver to use for the analysis of Spanish Influenza

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the City of Vancouver prior to the amalgamation of Point Grey and South Vancouver in 1929

could be used. This boundary, as represented by historical maps in Hayes (2005), would include

Alma Street to the west, Boundary Street to the east, 16th Avenue to the south, and Burrard Inlet

to the north. In this case, only death certificates with place of residence within this geographical

area would be included for analysis. The second option would be to include both South

Vancouver and Point Grey along with the City of Vancouver, which represents the boundary of

present day Vancouver.

Due to the fact that death certificates were only collected for people who died in

Vancouver and excluded certificates that stated death occurred in Point Grey or South

Vancouver, the boundary of analysis is the City of Vancouver proper, prior to amalgamation (i.e.

option one).

3.3 Calculating Mortality Rates

Mortality rates have been selected as a method of analysis as they provide an “index of

the severity of the disease from both clinical and public health standpoints” (Gordis, 2009, p.

67). This provides an indication of how negatively the population of the City of Vancouver was

affected by Spanish Influenza. Three sets of mortality rates, most conservative, moderately

conservative, and least conservative were used to analyze the affect of Spanish Influenza in

Vancouver, British Columbia. All mortality calculations followed the basic epidemiological

calculation of number of resident deaths from Spanish Influenza divided by number of residents

in the population multiplied by 1,000 as shown in Equation 1 (Gordis, 2009). The denominator

used for this calculation will be 117, 217, the population of the City of Vancouver (excluding

South Vancouver and Point Grey) according to the 1921 Canadian census (Government of

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Equation 1. Mortality Rate Formula

The most conservative mortality rate was calculated using only those records that indicated

influenza as the primary cause of death. The moderately conservative mortality rate used only

those records with influenza listed as either the primary cause of death or secondary cause of

death. Finally, the least conservative mortality rate included records having influenza as the

primary or secondary cause of death as well as all pneumonia deaths. Pneumonia deaths were

included in this mortality rate to acknowledge the close association between pneumonia and

Spanish Influenza.

3.4 Managing the Association between Pneumonia and Influenza

In order to manage the close association with Spanish Influenza and pneumonia, the

initial analysis was conducted with the two causes of death categories reviewed separately. By

treating influenza and pneumonia separately and using the 1921-1922 data set as a comparison

any discrepancy in pneumonia deaths can be observed. If pneumonia deaths for 1918-1919 far

exceed the deaths for 1921-1922, it is likely that Spanish Influenza played a role in this

difference. As this was observed, cases having the primary or secondary cause of death as

influenza or primary cause of death as pneumonia are included in the analysis. The

amalgamation of pneumonia and influenza deaths follows methods used by Tuckel et al. (2006)

and Palmer et al. (2007).

3.5 Analysis using the Statistics Package for Social Sciences (SPSS)

Prior to conducting the analysis, the data from the death certificates were coded to collect

similar variables into larger categories (Appendix 1). Cross-tabulations, univariate and

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version 20. Once coded, cross-tabulations were run for each year to assess the number and

percent of people in each category versus influenza or non-influenza deaths for the whole data

set. Variables with high proportions of influenza deaths are carried over into univariate analysis

focusing only on residents of Vancouver. Univariate statistical analysis uses chi-square tests to

determine if there is any association between influenza deaths and the following

social/geographical characteristics: gender, age, place of death, birthplace, employment status,

type of employed occupation, marital status, race, simple immigration status, and length of

residence in Canada. The Fisher‟s Exact test for statistical significance was used for two-by-two

cross-tabulations and the Pearson Chi-square test for significance was used for cross-tabulations

larger than two-by-two (Field, 2009). Chi-squares were selected as they test whether there is an

association between two categorical variables, the type of variables present in this study. While

one limitation to chi-square tests is that the “sampling distribution of the test statistic has an

approximate chi-square distribution” because there was a large sample size and the expected

frequencies for the analysis run here were above five in each cell, this limitation was overcome

(Field, 2009, p. 690).

Prior to running the multivariate model, a correlation test using the Cramer‟s V statistic

determined whether any of the variables are correlated to each other or acting as confounders

(Field, 2009). Based on the output of the correlation matrix along with the information provided

by the univariate analysis, age, gender, marital status, immigrant status, birthplace, length of

residence in Canada, and employment status were entered into the multivariate model.

The multivariate analysis used logistic regression to determine if the significant

relationships between influenza and the socio-demographic characteristics presented in the

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for age, gender, and marital status were forced into the multivariate model followed by the

introduction of immigrant status, birthplace, and length of residence in a forward stepwise

fashion. This means that:

“[T]he current model is compared to the model when that predictor is removed. If the removal of that predictor makes a significant difference to how well the model fits the observed data, then the computer retains that predictor (because the model is better if the predictor is included). If, however, the removal of the predictor makes little difference to the model then the computer rejects the predictor.” (Field, 2009, p.272)

The SPSS model rejected all three of these variables indicating that neither immigrant status,

length of residence or birthplace could be considered to influence death by influenza when age,

gender, and marital status are controlled.

Employment status was then added to the model, again using the forward stepwise

method, to determine if employment impacted influenza deaths when controlling for age, gender,

and marital status. This variable was retained in the model implying that employment could be

considered to influence death by influenza when age, gender, and marital status are controlled.

3.6 Visual Representation

Finally, maps of Spanish Influenza were created for the City of Vancouver using ArcGIS

9.3. As detailed neighbourhood classification cannot be undertaken, maps pinpointed locations of

residence rather than providing amalgamated mortality rates for communities. An Address

Locator created in ArcGIS used present day street configuration information from the open

source database at the City of Vancouver. The addresses for only the residents of the City of

Vancouver in 1918-1919 were uploaded into the GIS program and the address locator geocoded

them to the current street configuration. Any addresses that showed up outside of the boundaries

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showing the density of deaths in the City of Vancouver during 1918-1919. The mapping was

used as a visual aid due to the limited ability to match the historical addresses to present day

configuration with a high percentage of accuracy.

3.7 Limitations

While death certificates, census data, and mortality rates provide useful information

regarding the affect of Spanish Influenza in Vancouver, it is important to recognize and

acknowledge the limitations of using these sources and methods.

The death certificates collected for the analysis are from 1918-1922 and are hand-written.

While they represent a good primary source of data, in some cases the information provided was

illegible or did not have all sections completed resulting in missing information. If the missing

information excluded important elements such as age or location of death, or the cause of death

was illegible then this record was removed from the analysis when those variables were used.

The higher the number of records that are removed from analysis the less accurately the results

will represent what actually occurred during the 1918-1919 Spanish Influenza epidemic in

Vancouver. For this reason, missing information could be a severe limitation to this study.

Additionally, all death certificates that were from Vancouver were selected; however, it is not

clear what area this actually constitutes, i.e. does it include Point Grey and South Vancouver? As

such, residence information provided by the death certificate was relied upon for the majority of

the study but this information was not consistently recorded. The address locator was also

intended to reduce error in terms of the boundary of analysis. Lastly, at that time, death

certificates were generally not recorded for the Aboriginal population meaning that there is no

analysis of this population component included in this study (Belshaw, 2009). To conclude, the

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factors therefore restricting the understanding of these elements to indirect measures such as

occupation.

The census provides population data for amalgamated areas, for example, British

Columbia, and Vancouver but does not provide information on smaller neighbourhood areas

within Vancouver such as Shaughnessy, Kitsilano, or other smaller neighbourhood units.

Because the census data is limited in what it can provide on the small scale, a neighbourhood

analysis is impossible to undertake. Neighbourhood analysis would have been useful in teasing

out underlying socio-economic risk factors such as poor versus wealthy as some neighbourhoods

are known for the financial attributes of their residents.

Other limitations to the census data, as pointed out by the census itself include error

sources such as the uncertainty of exact age, intentional misstatements, missing information

(missing data/lost data/no response), or collection of information via third parties (i.e. not the

individual themselves) (Census, 1921). Furthermore, within the census itself there is little, to no,

analytical or interpretive discussion of what the data provided represents or what the margin of

error may be. Lastly, the census did not occur during the period of 1918-1919 so analysis for

both sets of death certificate data is conducted using population sizes from 1921. However,

census data are useful as they follow a consistent method of data collection.

As mentioned previously, mortality rates are a good indication of the severity of a disease

in a population; however, these rates do not give any indication of how many people were

affected by the disease, as they only consider those who have died as a result of the disease.

Cases of influenza cannot be analyzed using this method and, as such, the total impact of Spanish

Influenza cannot be fully understood. Furthermore, death certificates do not include any

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out the ability to examine more social impacts or responses to the epidemic. Finally, mortality

rates are restricted by a reliance on population data. As this is a historical analysis, specific

elements such as a neighbourhood analysis had to be left out due to the lack of appropriate

available population information.

Mapping the residence locations also proved to be a challenge and the resulting map does

not capture all the deaths as not all the addresses could be matched to present day street

configurations in Vancouver.

Lastly, the choice to solely use the quantitative data provided by the death certificates and

census population information limited my ability to utilize all the facets of a medical geography

approach which also supports understanding the spatial distributions and patterns of movement

of people within the city, to and from the city, and other more social facets of life in Vancouver

Spanish Influenza in the City of Vancouver, British Columbia, 1918-1919