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Kirsten McSweeny, Atalie Colman, Nick Fancourt, Melinda
Parnell, Sara Stantiall, Geoffrey Rice, Michael Baker, Nick Wilson
With the potential threat of pandemic influenza, there is
growing interest in examining public-health interventions that may temporarily
isolate remote communities and use social distancing as prevention or control
strategies. Historically the evidence that influenza pandemics had a greater
impact in towns and cities compared to rural areas is incomplete.
Some studies of the 1918 pandemic have suggested higher
mortality rates in urban settings—e.g. for
Nigeria1 and South
Africa.2 The picture for the latter is not
entirely clear however, given the potential confounding by high mortality rates
for particular ethnic groups in cities and the association between high
mortality rates and linkages with the railway network. However, higher rural
mortality in the 1918 pandemic has been described for
Iran.3
Extreme remoteness (combined with some control measures)
appears to have protected some populations in towns from infection in 1918 in
Canada,4 the continental United
States,5 and in
Alaska.6 Also some military installations on
islands offshore the United States appear to have escaped this
pandemic,5 as did the remote island of St
Helena in the South Atlantic.7 Remoteness may
also have protected some island groups in the South Pacific—e.g. the Lau
Islands and the Yasawas in Fiji.8 A detailed
study in Yap in the South Pacific also reported that most of the “outer
islands” escaped a 1964 influenza
epidemic.9
To further explore the impact of rurality for the 1918
influenza pandemic, we examined New Zealand data from this period. We
hypothesised that mortality rates (as a proxy for risk of infection) would be
higher in towns and cities than counties.
MethodsData on deaths from pandemic influenza for New Zealand
Europeans were obtained from previously published work by one of the
authors.10 The period covered was 17 October
1918 (date of first epidemic death) to 27 December 1918 (date of the last
epidemic death). These numerator data were collected from the examination of
individual death certificates throughout New Zealand (together with Auckland
data collected by another historian, Linda Bryder). Denominator data for the New
Zealand European population was obtained from the 1916
census.11 To examine the effect of geography on
mortality rates, the country was divided into cities (population >20,000),
large towns (population >2000), small towns (population <2000) and
counties (representing rural areas).
For 11 counties, it was not possible to separate the
data for towns and the surrounding county and so these were excluded from the
analyses. These counties were: Cook County (and Gisborne), Sounds County (and
Picton), Woodville County (and Woodville), Waipukurau County (and Waipukurau),
Eketahuna County (and Eketahuna), Wairoa County (and Wairoa), Rodney County (and
Warkworth), Waipawa County (and Waipawa), Hobson County (and Dargaville),
Waitemata County (and Hellensville) and Whangarei County (and Whangarei).
Statistical analyses were performed using Microsoft Excel and OpenEpi (Emory
University, 2005) software.
Data was available from the 1916
census11 on mean occupants per dwelling for a
total of 81 towns and counties. However, it was considered that this was too
crude a proxy for crowding at the individual household level to make further
analysis worthwhile.
ResultsThe cities and towns had significantly higher influenza
mortality rates than the counties, which represented rural settings (Table 1).
Considering all towns and cities together, the mortality rate ratio (RR) was
2.13 (95% confidence interval (CI) = 2.00–2.27) when compared to counties.
However, larger towns (population >2000 people) had a significantly lower
mortality rate than smaller towns (RR = 0.81, 95% CI = 0.74–0.88).
Similarly, cities had a lower mortality rate than larger towns (RR = 0.89, 95%CI
= 0.83–0.95). Within the cities, the mortality rates were significantly
higher in the two North Island cities than the South Island cities (eg, the RR
for Auckland relative to Dunedin was 1.92 (95% CI = 1.68–2.19).
Within counties there was no statistically significant
association between population size of the county and with the mortality
rate.
Table 1. Influenza mortality rates in cities,
towns and counties for the 1918 pandemic influenza in New Zealand (European
only)
*These are counties exclusive of any towns associated with
them; **For the 3-month period: October to December 1918.
DiscussionMain
findings and interpretation—This analysis identified a
statistically significant protective association for mortality from pandemic
influenza with rural living in a county relative to towns and cities. We are not
aware of these relationships being tested statistically for previous influenza
pandemics.
This pattern is consistent with the limited evidence that
remoteness provided some protection in past influenza pandemics (as detailed in
the introduction). It is biologically plausible that these relationships reflect
a reduced risk of infection among rural dwellers with lower levels of
person-to-person contact or poorer spread of infection from towns into rural
areas (i.e. protection via remoteness). Nevertheless, there is a need for
additional morbidity data on this and other influenza pandemics to clarify these
possible roles further.
Another possible factor in contributing to lower rural
mortality rates could have been that there were higher case-fatality rates in
towns and cities relating to poverty (e.g. where these residents faced
additional stress from food shortages after days of illness by breadwinners). We
did not have the data to test this and indeed any such effect may have been
countered by other factors. For example, there is some historical work that
suggests that community support for sick people was organised more quickly in
towns and cities than for rural areas.10
Furthermore, the protective effect of cities versus large
towns, and for large towns over small towns, might possibly have also
represented better community care and medical care available with greater levels
of civic infrastructure and resources.10 For
some small towns there may have been additional factors that compromised the
host resistance of their populations such as work in the mining industry. For
example, the mining towns of Nightcaps (Southland) and Denniston (West Coast)
had extremely high mortality rates of 46.0 and 18.5 per 1000 population
respectively. Public health measures to reduce the spread of influenza may have
helped one town,12 but these measures were
rarely applied.
It is also plausible that some of the differences found in
this analysis may relate to differences in the age-sex structure of the
population groupings involved. Such differences would probably favour lower
mortality rates in the cities given that the European female mortality rate was
lower overall in New Zealand10 and the urban
population had a female bias (i.e. 115 females to 100 males in the 1916 census
in metropolitan areas, versus 99 to 100
nationally11).
Findings from this analysis are also consistent with what we
know about the behaviour of influenza in populations. If the whole population is
susceptible to infection before the epidemic, then the proportion of an
unstructured population infected during the epidemic depends only on the
reproduction number
(R0).13
When R0=2.0, then
about 80% of the population will be infected by the end of the epidemic
(cumulative incidence rate) and the R0
for this 1918 pandemic in one setting in New Zealand was estimated to be in the
1.3 to 3.1 range.14 If, as seems likely, a
large majority of people in towns and cities in New Zealand became infected,
then mortality rate differences would be dependent on factors that influenced
survivability, such as access to nursing care. Protection from actual infection
probably only became evident from the remoteness and higher levels of social
distance experienced in rural areas.
Limitations—As detailed above, there
are limitations of using crude mortality and denominator data that were not
adjusted by age or sex. Furthermore, there was no adjustment for socioeconomic
position which was found to be important in a Norwegian study of this
pandemic15 and an Australian
study.16 Another limitation was that we did not
consider data for the Māori population, given concerns around the
under-reporting of Māori deaths and of under-recording in the 1916 census
(partly as a protest against officialdom associated with wartime
conscription).10
Indeed, Māori had particularly high mortality rates in
this epidemic,10,17 even though they were a
predominantly rurally-based population at this time. Nevertheless, many
Māori settlements would probably have equated more to small towns as
opposed to rurally isolated families on farms.
Even for the European population, the denominator data from
the 1916 census may not have been fully accurate due to both population growth
over the subsequent 2-year period and the population movements associated with
World War I (i.e. troops and healthcare workers overseas or in military training
camps).
Implications for further research and
policy—Detailed statistical examination of the 1918 pandemic can
potentially provide insights into the potential behaviour of a future influenza
pandemic. It is likely that the severity of the 1918 pandemic was at least
partly a function of the low population immunity to this new strain of virus.
This situation contrasts with seasonal influenza which infects a population with
relatively high levels of full and partial immunity. Consequently, seasonal
influenza may provide a less valid model for the behaviour of future pandemics
than can be obtained from analysis of past pandemics.
We are planning future work with individual-level data to
clarify some of the limitations with this ecological-level analysis. This work
may also include an attempt to analysis Māori data in those areas where
there is greater confidence around the quality of numerator and denominator
data. Others may also want to consider applying modern epidemiological methods
to existing mortality datasets from 1918 in other countries to further explore
any impacts of rurality and social distancing.
In the meantime, however, this work offers some limited
evidence that rurality might have provided some protection from this influenza
pandemic. This may support public health efforts in a future pandemic for remote
rural populations to consider isolating themselves for a few weeks if they deem
the costs of socioeconomic disruption are worth the benefits of either delaying
or preventing the arrival of pandemic influenza in their communities.
Preparations such as improved Internet access for rural
areas may facilitate home-schooling and working from home during such a period.
Nevertheless, all communities of whatever size probably need to be involved in
strengthening planning and civic infrastructure given the risk that a future
pandemic may not be adequately stopped at borders (even of island nations) or
contained within just parts of a country.
Competing interests: None.
Author information: Kirsten McSweeny,
Atalie Colman, Nick Fancourt, Melinda Parnell, Sara Stantiall, Medical
Students, University of Otago, Wellington; Michael Baker and Nick Wilson, Senior
Lecturers, University of Otago, Wellington; Geoffrey Rice, Associate Professor
and Head of Department, Department of History, Canterbury University,
Christchurch
Acknowledgements:
This study had organisational support and some minor financial support
from the Department of Public Health, University of Otago, Wellington (as part
of medical student training in public health). Some of the ongoing work on this
article by two of the authors (NW & MB) was also part of background work for
a Centers for Disease Control and Prevention (USA) grant (1 U01 CI000445-01). We
also thank Linda Bryder for her past work in collecting mortality data for
Auckland and the two anonymous reviewers for their helpful comments.
Correspondence: Dr Nick Wilson, Department
of Public Health, University of Otago, Wellington, PO Box 7343, Wellington;
Email: nick.wilson@otago.ac.nz
References:
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