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Abstract

  1. Top of page
  2. Abstract
  3. 1 Introduction
  4. 2 Coupled Complex Systems
  5. 3 Climate Change in Relation to Disease
  6. 4 Disease Impacts due to Climate
  7. 5 Conclusions
  8. Short Biography
  9. Acknowledgements
  10. References

What kinds of climate-mediated diseases exist, and how are projected climate changes expected to alter their spread and timing? Disease is produced in a complex way, through coupled interactions between natural and human systems. Climate is a major factor controlling ecosystem variability and therefore the potential for outbreaks of certain diseases. Yet, the concept of vulnerability shows how overall disease risk depends not only on the environmental exposure, but also on the sensitivity and adaptive capacity of the group and place experiencing it. These interactions between environment and society are highlighted through a set of climate-related diseases, ranging from direct to complex relationships, including extreme heat, air pollution, aeroallergens, fungi, water- and food-borne diseases, influenza, rodent-borne diseases, and insect-borne diseases.


1 Introduction

  1. Top of page
  2. Abstract
  3. 1 Introduction
  4. 2 Coupled Complex Systems
  5. 3 Climate Change in Relation to Disease
  6. 4 Disease Impacts due to Climate
  7. 5 Conclusions
  8. Short Biography
  9. Acknowledgements
  10. References

Sensational headlines trumpeted the recent march of West Nile virus across the United States, as well as outbreaks of foot-and-mouth disease in the UK. Such news plays off our well-founded fear of another global disease epidemic, or pandemic. For example, the devastating 1918 influenza pandemic led to 50 million deaths worldwide. The mortality reached 2.5% instead of a typical value less than 0.1%, and the disease struck the 20–40 age group disproportionately (Barry 2004; Earn et al. 2002). Nowadays, we watch the advance of H5N1 avian influenza and worry if it will evolve into a similar nightmare.

Added to these are concerns about global climate change. The World Health Organization (WHO) estimates that 150,000 lives have been lost annually over the last 30 years that are directly attributable to climate change; this number is based on a partial list of outcomes for diseases, flooding, and malnutrition and it represents a conservative estimate (Patz et al. 2005). Many of these deaths are in developing countries within the world's tropical regions. Future impacts of climate change on human health could also be dramatic, especially if some tropical diseases expand into formerly temperate areas. What kind of effects can we expect? Who will be affected and where and when might they be experienced?

2 Coupled Complex Systems

  1. Top of page
  2. Abstract
  3. 1 Introduction
  4. 2 Coupled Complex Systems
  5. 3 Climate Change in Relation to Disease
  6. 4 Disease Impacts due to Climate
  7. 5 Conclusions
  8. Short Biography
  9. Acknowledgements
  10. References

Health is defined as ‘a state of complete physical, mental, and social well-being and not merely the absence of disease or infirmity’ (WHO 2006). Disease pertains more specifically to abnormal physiological function as a result of infection by a pathogen, a genetic problem, or environmental stress. Climate change can modify ecosystems in ways that not only increase physical disease but also create health burdens that affect mental and social well-being via flood and drought impacts on housing, food security, and livelihoods. Recognizing that climate change clearly relates to mental and social health, for the sake of brevity, this article emphasizes the physical dimensions of health and human disease relating to the natural environment and climate.

Nonetheless, understanding the people and places that are influenced by climate-related health impacts requires an appreciation of how disease is produced. It is useful to think of human diseases existing at the intersection of two complex systems of interaction: society and ecology (Figure 1). Disease is one example of many environmental issues that are produced by coupled natural and human systems. Coupling implies feedback between system components. For example, the natural environment in an area might lead to irrigation, which in turn might increase mosquito populations and disease. It typically takes interdisciplinary research from not only geography but also epidemiology, disease ecology, other social sciences, and climatology to solve the complex problems at this interface.

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Figure 1. Disease is complexly determined, because it exists at the intersection of coupled natural and human systems that are themselves complex systems.

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One useful theoretical framework to aid understanding of these links is the concept of vulnerability, which grew out of work by geographers and others on risk and hazards to society (McCarthy et al. 2001; Turner et al. 2003). Vulnerability (V) can be expressed conceptually as the function

  • V = f(E, S, A)

where E is exposure, S is sensitivity and A is adaptive capacity. Exposure is typically a physical or environmental stimulus (e.g. a heat wave). Sensitivity or the degree of impact related to that stimulus will differ across groups of people because of their social characteristics and environment (e.g. age, socioeconomic status, behavior, land use, and health care). Adaptive capacity or the ability to recover following an event will differ among groups for the same reasons. S and A thus represent social resilience to the environmental stimulus, and vulnerability to risk of a hazard or disease will therefore differ across places and groups depending on the interplay of these three components in space and time.

For example, consider the city of Nogales that straddles the US–Mexico border in the states of Arizona and Sonora. For a heavy rainfall event, exposure to extreme precipitation is the same on both sides of the border; sensitivity to floods and waterborne disease will differ because of drainage infrastructure, land use patterns, and sanitation systems; adaptive capacity will differ because of socioeconomic status and other factors such as access to health care. While socioeconomic status and the associated levels of physical and social infrastructures are often closely (and inversely) aligned with vulnerability, that is not always true. In the case of disease, age and behavior or occupation are frequently major determinants of sensitivity.

It is important to note that disease vulnerability or risk is therefore socially constructed. It is constructed in material sense, via the built environment, land cover/land use, transportation and migration, demographics, social and environmental justice, economic conditions, and public health services. Disease is also constructed in a social theoretic sense (Berger and Luckmann 1966; Giddens 1984; Demeritt 2002), through social institutions and our concepts of what disease represents. The social construction of disease is beyond the scope of this article, but consider your reaction to the term ‘leper’ or society's initial reactions to AIDS and its early victims who were predominantly gay; disease is as much a construction of our minds and of society as it is a brute biological fact. However, because disease is in part determined by complex social systems, this opens up opportunities for us to mitigate it.

Recall that disease is produced through coupled social and natural systems. Ecosystems are a classic example of natural complexity; they comprise vast arrays of organisms and environments that are often interdependent and which interact dynamically. One dimension of these interactions is conceptualized via the notion of a food chain (or food web). For example, certain insects may eat plants or prey on animals, and these insects may in turn be infected by or carry microbes, some of which may be pathogens. The ecological dynamics of a particular pathogen are therefore complexly determined by many environmental factors. Furthermore, because humans are animals and are participants within an ecosystem, our interaction with these pathogens depends in part on systems of biological complexity.

One way to simplify this situation is to examine infectious disease transmission in relation to humans. Diseases among animals are called zoonoses; some zoonoses may also be diseases in humans. Diseases among humans are called anthroponoses. Anthroponoses and zoonoses may be transmitted either directly between host individuals, or indirectly via a vector such as an insect that carries the disease between hosts (National Research Council 2001). We thus obtain four categories: (i) human diseases transmitted directly, like tuberculosis or measles; (ii) human diseases with indirect transmission, such as malaria and dengue transmitted by mosquitoes; (iii) diseases transmitted directly among animal hosts, like rabies, where humans are incidental hosts; and (iv) diseases transmitted indirectly among animals via a vector, such as bubonic plague (fleas) or Lyme disease (ticks), where humans are also incidental hosts.

Disease agents (pathogens), human hosts, and disease vectors are all linked in a multifactorial relationship to environment. Figure 2 illustrates this arrangement, known as the epidemiologic triangle of disease. The behavior of a disease will be determined by its relative location within the triangle, which in turn depends on time and place. Naturally, climate is a major determinant of environmental variability and change, and climate therefore has an important, albeit contingent, role in disease. As a result, changes in the prevalence of disease in particular places or quasi-cyclic patterns of disease over time may be related to climate fluctuations. Direct health impacts of climate, such as heat stroke and hypothermia, can be thought of as interactions along the edge of the triangle without a pathogen or vector. The triangle is also useful for highlighting how different disciplines can contribute to this field. For geography, the human-environment side of the triangle is clearly a place to become engaged, as well as aspects of the biogeography of disease vectors.

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Figure 2. The epidemiologic triangle of disease.

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3 Climate Change in Relation to Disease

  1. Top of page
  2. Abstract
  3. 1 Introduction
  4. 2 Coupled Complex Systems
  5. 3 Climate Change in Relation to Disease
  6. 4 Disease Impacts due to Climate
  7. 5 Conclusions
  8. Short Biography
  9. Acknowledgements
  10. References

Climate is continually changing, locally, regionally, and globally in space, as well as from minutes to millennia in time. By extension, there is no such thing as a ‘normal’ climate, a concept that climatologists describe in statistical terms as nonstationarity. This means that although we are accustomed to our climate being a particular way based on recent human experience, the current state of the climate reflects the happenstance of climate system dynamics. Note that climate is not simply average weather, but the long-term integral of the range of weather including extremes. Furthermore, year to year climate variability such as El Niño is superimposed upon longer-term trends. At the local scale, we have done much to modify climate (e.g. see urban heat islands below) and now we also know that we are changing global climate (Intergovernmental Panel on Climate Change (IPCC) 2007). Not only are the current average conditions changing, but the range of extremes is shifting, too. In fact, relatively small shifts in the mean imply relatively large changes in extreme climate conditions. Figure 3 illustrates how such a change in temperature leads both to more hot weather in general and to much more record heat.

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Figure 3. A relatively small increase in mean temperature leads to many more extreme high temperatures. The effect is exacerbated if the variability (spread) about the mean also increases, as in this example.

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A dramatic change in extremes may have unpredictable outcomes for health effects. One characteristic of complex systems is the notion of threshold behavior, that is, amplified responses when a particular set of relationships cross a critical point. The result may include unanticipated outbreaks of disease because a previously unconsidered disease transmission cycle or vector suddenly has an expanded range or season. One example is the recent outbreak of bluetongue disease in northern Europe, a livestock virus originating in Africa (Enserink 2006). More fundamental climate changes and health-related impacts are also underway. Observed climate warming in the latter decades of the 20th century has led to shrinking mountain glaciers in the tropics and mid-latitudes, with warmer conditions and associated ecological habitat migrating upslope along with mosquito-borne disease (Epstein and Mills 2005). Cold extremes are becoming less frequent (IPCC 2007), which will lead presumably to a reduction in related impacts from climate change.

Increased heat and greater variability in temperature and precipitation can generally be expected to lead to more health impacts, especially for heat waves, air quality, and water- and food-borne diseases (Patz et al. 2001). However, because of the greater complexity involved in vector- and rodent-borne diseases, the direction and severity of health impacts for these categories of disease are not as clear (Patz et al. 2001). Furthermore, our ability to make projections of diseases and their impacts under future climate scenarios is very limited at present. We may be able to project changes in, for example, the range of a disease vector, but given the uncertainties of social change it is challenging to calculate future disease impacts beyond simple extrapolation.

4 Disease Impacts due to Climate

  1. Top of page
  2. Abstract
  3. 1 Introduction
  4. 2 Coupled Complex Systems
  5. 3 Climate Change in Relation to Disease
  6. 4 Disease Impacts due to Climate
  7. 5 Conclusions
  8. Short Biography
  9. Acknowledgements
  10. References

This section reviews a set of climate-mediated diseases that represent the range of effects and interactions. Eight categories are used, moving from relatively simple and direct climate–disease relationships such as heat waves through complex ones such as rodent- and insect-borne disease.

4.1 extreme heat and cold

Extreme weather events such as heat waves and cold spells lead to mortality ratios 10% or higher than for average temperatures (Huynen et al. 2001). Typically, weather stress does not kill directly; instead, it is a ‘last straw’ of additional stress for people with other conditions such as heart or lung disease. The elderly and infirm are therefore at greater risk, as are those individuals exposed to thermal stress via their occupation (e.g. outdoor laborers). Presumably, there will be direct temperature change impacts on heatstroke and hypothermia cases, the latter perhaps mitigated by urban heat island effects. The frequency of heavy precipitation events has increased (IPCC 2007), creating the potential for direct health-related impacts from flooding and blizzards. As mentioned above, cold extremes are becoming less frequent, and therefore the focus below is on heat waves.

Heat waves are relative to typical temperatures for a location, as is their impact. Thus, record heat in one city may be normal for another at lower latitude. Heat stress occurs because residents are not acclimatized or adapted to the unusual conditions, due to a lack of cooling, unfavorable building design and physical tolerance. Chicago experienced a major heat wave in July 1995, resulting in over 400 excess deaths. As is typical of such events, a lag of 2–3 days between the very high temperatures and the resulting peak in deaths was seen (Patz et al. 2001). A similar pattern was noted in the record heat wave that struck Europe in the summer of 2003. Temperatures ran as high as 10 °C above average for about 10 days, especially in France where there were approximately 15,000 excess deaths nationally and about 1000 in Paris alone (Kalkstein et al. 2007). An analogous heat wave projected onto New York City would lead to almost 3000 excess deaths (Epstein and Mills 2005). By comparison, annual tornado deaths in the United States are less than 100, with the largest single annual total just over 500 (National Oceanographic and Atmospheric Administration 2007).

Extreme heating, and therefore its negative effects, are exacerbated by the urban heat island. This term describes the well-known climatic effects of urbanization that lead to cities being warmer than the surrounding areas, especially overnight (Comrie 2000). Daily minimum temperatures can be 5 °C or more warmer, meaning fewer winter frosts, an earlier thermal springtime, and of course higher overnight minimum temperatures in summer. Depending on the city and humidity levels, the latter can reduce the relief from daytime high temperatures and increase weather stress. Climate model projections of overnight lows for the next century show the warmest night of the year increasing by 10 °C (Christidis et al. 2005), before accounting for the additional urban heat island effect in cities. While local conditions may modulate these projections higher or lower, the overall potential for increases in heat deaths is high.

4.2 air pollution

Connections between air quality and health have been known for a long time, although the precise effects of specific pollutants are still actively researched (Pope et al. 2002). Health effects were self-evident from the thousands of deaths in the infamous London smogs of the 1950s (about 4000 were estimated for the December 1952 smog), when smoke concentrations were tens and even hundreds of times higher than today (Harrison 2006), turning buildings black. The word ‘smog’ is a contraction of ‘smoke’ and ‘fog’ although we use it more broadly to include ground-level ozone pollution (photochemical smog) today. These events led to the mid-1950s Clean Air Acts in the UK and similar developments in the United States, and constituted some of the earlier manifestations of the modern environmental movement. These laws and their descendants, such as the landmark 1970 Clean Air Act in the United States, led to dramatic air quality improvements in subsequent decades (Bureau of Transportation Statistics 1999), a testament to the effectiveness of environmental regulation.

But, will climate change undo the progress? Higher temperatures increase ground-level ozone pollution (Patz et al. 2001), because the chemical reactions that produce ozone from its precursor pollutants proceed faster under warmer conditions. If cloud-free conditions increase, then more available solar radiation will further increase ozone levels. Ozone health effects include breathing problems, airway inflammation, and reduced resistance to infections. Climate change projections indicate the likelihood for a longer, more severe, and more widespread high-ozone season each year (Fiore et al. 2002; Hogrefe et al. 2004). A relatively unexplored climate change impact may involve dust pollution from particulate matter. Warming will, in areas without a matching increase in moisture, lead to dryer conditions and increased chances for higher dust concentrations, and possibly even long-range dust transport, due to desiccation of the soil. Particulate pollution is linked to premature death, respiratory illness, aggravated asthma, chronic bronchitis, and decreased lung function (American Lung Association 2001).

4.3 aeroallergens

The direct fertilization effects of increased carbon dioxide on plants are well known to increase biomass, but this effect also leads to greatly increased pollen production. Ragweed is a common aeroallergen; when it is grown under doubled carbon dioxide plant height increases by 9% but 61% more pollen is produced (Wayne et al. 2002). Not only does the amount of pollen increase, but warmer springs have already lengthened the growing season for many allergen-producing plants. For example, Sambucus (Elder) first pollen dates in Europe remained consistent in mid-June from 1900 through the 1970s. Since then, these dates have shifted over 3 weeks earlier into mid-late May (Van Vliet et al. 2002).

4.4 fungi and molds

Changing temperature and moisture patterns can be expected to change the spatial distribution and timing of fungi and molds. For example, in the arid and semi-arid regions of North and South America the pathogenic soil fungi Coccidioides spp. cause a disease called valley fever (coccidioidomycosis). Occupations such as archeology or building construction involve soil disturbance, and can thus lead to increased exposure to fungal spores (Kolivras and Comrie 2004). Climate is linked to coccidioidomycosis presumably by changes in soil moisture and subsequent dispersion of spores. A sequence of wetting and drying of the soil in key seasons leads to fungal growth followed by desiccation and spore formation; spore dispersion can then occur during subsequent dusty conditions (Comrie 2005).

4.5 water- and food-borne diseases

Precipitation and temperature fluctuations can directly impact pathogens and diseases in water and food. Two examples from New Zealand illustrate these links. Natural flood events cause increases in fecal bacteria (Escherichia coli) as water levels rise and debris is washed into the stream. Bacteria counts spike in the first few hours of an event as the initial water rise and washout takes place (Davies-Colley et al. 2004). Higher mean temperatures lead to more monthly Salmonella cases (WHO 2003), most likely resulting from improper refrigeration and exacerbation of food contamination.

Water-borne pathogens are numerous and widespread; some examples include giardia, cholera, cryptosporidium, rotaviruses, enteroviruses, Coxsackie viruses, cyclospora, and hepatitis A and E viruses. Health risks range from wound infections to diarrhea to organ failure (Rose et al. 2001). The more complex effects of climate are illustrated via shellfish poisoning (Vibrio vulnificus in oysters) in Florida. A clear summer peak in infections and deaths is seen over multiple years, where the pathogen is controlled in part by the seasonal temperature and salinity of estuaries (Rose et al. 2001). With projected greater climate variability in rainfall and runoff, there will likely be an increased risk of contamination events as salinity and temperature patterns change.

Cholera is a major water-borne disease. It is caused by the bacterium Vibrio cholerae that attaches to marine and estuarine copepods (zooplankton). Fresh water is affected via fecal contamination from prior infection. A landmark early geographic and epidemiological study was made by John Snow, who mapped cholera cases in London during the 1854 epidemic in which over 10,000 deaths occurred. He detected a concentration of cases around a specific public water pump on Broad Street, and deduced that the water from that pump was contaminated. Cholera–climate links occur via zooplankton blooms resulting from changes in ocean temperatures, pH and salinity (Colwell 1996). For example, cholera prevalence in Bangladesh has been linked to fluctuations in nearby sea surface temperatures (Colwell 1996), which are in turn linked to climate which further affects pH and salinity via rainfall and runoff.

4.6 influenza

Influenza is a highly seasonal disease, but it comes as a surprise to many that the root cause of influenza seasonality is unknown. Outbreaks and virulence of influenza from year to year are undoubtedly closely linked to the circulating viral subtype. The timing of the winter outbreak each year is remarkably synchronized across individual countries and even hemispheres, within days in many instances (Viboud et al. 2004a), due in part to rapid transmission via air travel. The Southern Hemisphere peak is 6 months out of phase with the Northern Hemisphere, and it does not consistently lead or lag (Viboud et al. 2004a), while the tropics have a mixed pattern. Clearly, some kind of seasonal control must be at work, but none of the simpler hypotheses (such as indoor crowding in winter or return of children to school) have stood up to analysis. There is limited evidence that colder winters show increased morbidity and mortality, at least in France (Viboud et al. 2004b).

There are numerous hypotheses on the role of climate in influenza seasonality, many of which are hard to examine given current health data. One possibility is ecological seasonality, because the native hosts of the virus are wild water fowl such as duck, but other birds and animals carry the virus, including domesticated species such as pigs, cows, cats, and chickens (White 2006). Seasonality might be introduced via increased human–animal contact in source regions for new viral subtypes, annual feeding or reproductive cycles, or migration. Alternatively, our susceptibility to the virus may be seasonal (Dowell 2001).

4.7 rodent-borne disease

The infamous Black Death of the 14th century in Europe was an epidemic of bubonic plague. Plague is caused by a bacterium (Yersinia pestis) that is carried by fleas on rodents; social conditions led to strong overlaps between rat habitat and humans in the 14th century. Today, plague is still endemic in humans and animals in many countries around the world, albeit at much lower prevalence, including the United States and parts of Africa, South America, and Asia (Centers for Disease Control and Prevention (CDC) 2006a). Climate affects plague through rodent ecology. For example, in Central Asia (Kazakhstan) warmer springs and wetter summers lead to population increases in gerbils, and therefore fleas, with a 1 °C temperature increase leading to a 50% increase in Y. pestis prevalence (Stenseth et al. 2006).

Hantavirus is carried in rodent feces, and it causes hantavirus pulmonary syndrome in humans. In the United States, there are almost 500 cases annually occurring across much of the country, but with a focus in the Four Corners states of the Southwest (CDC 2006b). In this area of high climate variability, wet winters typically lead to abundant vegetation and rodent food supplies the following spring. Rodent populations increase, the number of infected rodents grows, and therefore so does human contact with rodent feces and urine in and around homes. This sequence was first noted following the El Niño-related wet winter of 1992–1993 in the region, which was followed by a major hantavirus pulmonary syndrome outbreak in summer 1993 (Engelthaler et al. 1999).

4.8 insect vectors of disease

Lyme disease is named for the city of Lyme, Connecticut, where it was first noted. It is caused by the bacterium Borrelia burgdorferi that is carried by the deer tick, Ixodes scapularis, which is found on deer and mice. As deer and mouse habitat and populations have increased with forest edge expansion in the eastern United States, so has the exposure of people to being bitten by the deer tick. Lyme disease is prevalent across many of the eastern and southern states, but climate change projections suggest that the range of suitable habitat will expand to include the Midwestern states and southeastern Canada in coming decades as milder winters move northward (Brownstein et al. 2005).

Malaria is caused by protozoan parasites Plasmodium spp. that are carried by female Anopheles mosquitoes transmitting the disease between human hosts. Malaria has an enormous disease burden around the world, especially in developing countries, with an estimated ~300 million clinical cases, and 1–3 million deaths (including many children) every year worldwide (CDC 2006c). Climate affects malaria via the mosquito lifecycle: precipitation variability and humidity control the amount of standing water for breeding, while higher temperatures lead to increased biting rates as well as a more rapid larval development and possible increases in species range (Epstein and Mills 2005). For example, a major rainfall event in Maputo, Mozambique, in early 2000 led to a malaria outbreak 3–8 weeks later (Epstein and Mills 2005). Climate change projections of areas suitable for malaria transmission show marginal expansion beyond current endemic areas in the tropics, to include parts of the United States gulf coast, Mexico, southeast Brazil, Namibia, as well as Turkey, Central Asia, and southern China; some areas become unsuitable such as parts of India, Somalia, northeast Australia, southwest Brazil, and the central valley of California (Rogers and Randolph 2000). Although these regions are relatively small compared to core endemic regions, the very large disease burden in the population means that the number of new cases is still likely to be large.

Dengue fever is also transmitted via a mosquito, in this case principally Aedes spp., between human and primate hosts. There are four viral strains, and infection with more than one strain can lead to a more severe disease known as dengue hemorrhagic fever (DHF). An estimated 100 million cases per year of dengue occur worldwide, with 250,000 cases per year of DHF; incidence of DHF has increased several fold in recent decades (CDC 2006d). Climate change projections of dengue risk show increases globally, extending from core endemic areas in the tropics into the subtropics (Hales et al. 2002).

Beyond the examples here, there are many other climate-related vector-borne diseases, including schistosomiasis (bilharzia) via flatworms, encephalitis via insects infected with protozoan parasites, West Nile virus via birds and mosquitoes, tularemia via bacteria in insects and spiders, yellow fever virus via mosquitoes, and many more. Each of these diseases presents opportunities for complex interactions between society, the specific disease ecology, and climate.

5 Conclusions

  1. Top of page
  2. Abstract
  3. 1 Introduction
  4. 2 Coupled Complex Systems
  5. 3 Climate Change in Relation to Disease
  6. 4 Disease Impacts due to Climate
  7. 5 Conclusions
  8. Short Biography
  9. Acknowledgements
  10. References

Overall, warmer and more extreme climate shifts will lead to direct disease impacts as well as less-direct impacts that are exacerbated or mediated by social and ecological factors. Furthermore, complex system interactions raise the possibility of ‘threshold behavior’ and unexpected events in disease outbreaks. In general, the more complex the multiple factors controlling the disease are, the more uncertain the projected outcome. As socioeconomic conditions change, relationships to disease can also shift with time. Added to this are uncertainties in future climate projections that make climate change-related health projections a challenging task.

The spread and outbreak of disease under climate change are favored by projections of more heat waves and urban warming, with longer and more severe ozone seasons. We expect to see increased pollen allergen production with an earlier start to the season, as well as changes in fungus and mold growth due to swings in precipitation and temperature extremes. The expected changes in climate extremes are likely to exacerbate current relationships that lead to a greater risk of water-borne pathogens via flooding and higher water temperatures. Although influenza is a highly seasonal disease, we currently have a very poor understanding of climate links to the seasonality of influenza. There is evidence to suggest that higher rainfall variability may amplify or alter the temporal patterns of rodent-borne diseases. Finally, although marginal shifts in mosquito vector ranges are projected, they are in areas of the world where the potential disease burden on the population will be high.

It is insightful to note that the relationships between disease and climate are complex, because disease occurs at the intersection of natural and human systems. Disease is one way in which the dynamics of these complex systems are coupled together. Thus, disease should not be viewed as simply produced by nature, with a one-way impact on society; rather, many aspects of disease are socially constructed, both materially through human practice such as modification of our environment, and institutionally through the ways in which we construct the idea of disease. Because disease has both natural and social components, this creates differential vulnerabilities across groups in different places and times. Therein lays some real hope to reduce the impacts of disease, because it is possible to change how we do things as a society to mitigate disease impacts by changing our sensitivity and even our adaptive capacity. This is also an opportunity for geographers to use their expertise in the relationships between society and nature to improve our understanding of environmentally mediated disease.

Short Biography

  1. Top of page
  2. Abstract
  3. 1 Introduction
  4. 2 Coupled Complex Systems
  5. 3 Climate Change in Relation to Disease
  6. 4 Disease Impacts due to Climate
  7. 5 Conclusions
  8. Short Biography
  9. Acknowledgements
  10. References

Andrew Comrie is Professor of Geography and Regional Development, and Professor of Atmospheric Sciences, University of Arizona, Tucson, AZ, USA. He is also Dean of the Graduate College and Associate Vice President for Research at the University of Arizona. His research interests span the interactions of climate, environment, and society, and include subjects such as climate variability, air quality, climate mapping, wildfire, and disease. He has published on these and related topics in the Annals of the Association of American Geographers, Professional Geographer, Bulletin of the American Meteorological Society, Journal of Climate, and Atmospheric Environment. He serves on the editorial boards of Annals of the Association of American Geographers and Atmospheric Environment, and he is the Americas Editor for International Journal of Climatology. He currently continues to do research on climate and health, especially valley fever and mosquito-borne diseases. He holds undergraduate and master's degrees from the University of Cape Town, and a PhD from Pennsylvania State University.

Acknowledgements

  1. Top of page
  2. Abstract
  3. 1 Introduction
  4. 2 Coupled Complex Systems
  5. 3 Climate Change in Relation to Disease
  6. 4 Disease Impacts due to Climate
  7. 5 Conclusions
  8. Short Biography
  9. Acknowledgements
  10. References

This work was originally prepared as part of a global climate change public lecture series, hosted by the College of Science at the University of Arizona. I am grateful to colleagues associated with that series for their valuable comments on early versions of the material.

Note
  • *

    Correspondence address: Andrew Comrie, Department of Geography and Regional Development, University of Arizona, 409 Harvill Building, Tucson, AZ 85721, USA. E-mail: comrie@arizona.edu.

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  1. Top of page
  2. Abstract
  3. 1 Introduction
  4. 2 Coupled Complex Systems
  5. 3 Climate Change in Relation to Disease
  6. 4 Disease Impacts due to Climate
  7. 5 Conclusions
  8. Short Biography
  9. Acknowledgements
  10. References
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