Diseases

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From Climate Change Reconsidered, a work of the Nongovernmental International Panel on Climate Change

Which is more deadly: heat or cold? Rising temperatures or falling temperatures? The IPCC claims warming is the primary danger to be avoided at all costs. Real-world data, however, indicate the opposite.

Systematic research on the relationship between heat and human health dates back to the 1930s (Gover, 1938; Kutschenreuter, 1950; Kutschenreuter, 1960; Oechsli and Buechley, 1970). Early studies by Bull (1973) and Bull and Morton (1975a,b) in England and Wales, for example, demonstrated that normal changes in temperature typically are inversely associated with death rates, especially in older subjects. That is, when temperatures rise, death rates fall; when temperatures fall, death rates rise. Bull and Morton (1978) concluded “there is a close association between temperature and death rates from most diseases at all temperatures,” and it is “very likely that changes in external temperature cause changes in death rates.”

Since this early research was published, a large number of studies have confirmed the original findings. Contrary to the IPCC’s highly selective reading of the literature, the overwhelming majority of researchers in the field have found that warmer weather reduces rather than increases the spread and severity of many diseases and weather-related mortality rates. We review this literature in the following order: cardiovascular diseases, respiratory diseases, malaria, tick-borne diseases, and finally cold- and heat-related mortality from all diseases.

Additional information on this topic, including reviews on the health effects of CO2 not discussed here, can be found at http://www.co2 science.org/ subject/h/subject_h.php under the heading Health Effects.


Contents

Cardiovascular Diseases

A good place to begin a review of temperature-related mortality is a cold location … like Siberia. Feigin et al. (2000) examined the relationship between stroke occurrence and weather parameters in the Russian city of Novosibirsk, which has one of the highest incidence rates of stroke in the world. Analyzing the health records of 2,208 patients with a sex and age distribution similar to that of the whole of Russia over the period 1982-93, they found a statistically significant association between stroke occurrence and low ambient temperature. For ischemic stroke (IS), which accounted for 87 percent of all strokes recorded, they report that the risk of IS occurrence on days with low ambient temperature is 32 percent higher than on days with high ambient temperature. They recommend implementing “preventive measures … such as avoiding low temperature.”

Hong et al. (2003) studied weather-related death rates in Incheon, Korea over the period January 1998 to December 2000, reporting that “decreased ambient temperature was associated with risk of acute ischemic stroke,” with the strongest effect being seen on the day after exposure to cold weather. They found that “even a moderate decrease in temperature can increase the risk of ischemic stroke.” In addition, “risk estimates associated with decreased temperature were greater in winter than in the summer,” suggesting that “low temperatures as well as temperature changes are associated with the onset of ischemic stroke.”

Nafstad et al. (2001) studied weather-related death rates in Oslo, Norway. Thanks to a Norwegian law requiring all deaths to be examined by a physician who diagnoses cause and reports it on the death certificate, they were able to examine the effects of temperature on mortality due to all forms of cardiovascular disease for citizens of the country’s capital over the period 1990 to 1995. They found that the average daily number of cardiovascular-related deaths was 15 percent higher in the winter months (October-March) than in the summer months (April-September), leading them to conclude that “a milder climate would lead to a substantial reduction in average daily number of deaths.”

Hajat and Haines (2002) set out to determine if cardiovascular-related doctor visits by the elderly bore a similar relationship to cold temperatures. Based on data obtained for registered patients aged 65 and older from several London, England practices between January 1992 and September 1995, they found the mean number of general practitioner consultations was higher in the cool-season months (October-March) than in the warm-season months (April-September) for all cardiovascular diseases.

Of course, one might say, such findings are only to be expected in cold climates. What about warm climates, where summer maximum temperatures are often extreme, but summer minimum temperatures are typically mild? Research conducted by Green et al. (1994) in Israel revealed that between 1976 and 1985, mortality from cardiovascular disease was 50 percent higher in mid-winter than in mid-summer, both in men and women and in different age groups, in spite of the fact that summer temperatures in the Negev, where much of the work was conducted, often exceed 30°C, while winter temperatures typically do not drop below 10°C. These findings were substantiated by other Israeli studies reviewed by Behar (2000), who states that “most of the recent papers on this topic have concluded that a peak of sudden cardiac death, acute myocardial infarction and other cardiovascular conditions is usually observed in low temperature weather during winter.”

Evidence of a seasonal variation in cardiac-related mortality has been found in the mild climate of southern California in the United States. In a study of all 222,265 death certificates issued by Los Angeles County for deaths caused by coronary artery disease from 1985 through 1996, Kloner et al. (1999) found that death rates in December and January were 33 percent higher than those observed in the period June through September.

Likewise, based on a study of the Hunter region of New South Wales, Australia that covered the period 1 July 1985 to 30 June 1990, Enquselassie et al. (1993) determined that “fatal coronary events and non-fatal definite myocardial infarction were 20-40 percent more common in winter and spring than at other times of year.” Regarding daily temperature effects, they found that “rate ratios for deaths were significantly higher for low temperatures,” noting that “on cold days coronary deaths were up to 40 percent more likely to occur than at moderate temperatures.”

In a study of “hot” and “cold” cities in the United States—where Atlanta, Georgia; Birmingham, Alabama; and Houston, Texas comprised the “hot” group, and Canton, Ohio; Chicago, Illinois; Colorado Springs, Colorado; Detroit, Michigan; Minneapolis-St. Paul, Minnesota; New Haven, Connecticut; Pittsburgh, Pennsylvania; and Seattle and Spokane, Washington comprised the “cold” group—Braga et al. (2002) determined the acute effects and lagged influence of temperature on cardiovascular-related deaths. They found that in the hot cities, neither hot nor cold temperatures had much impact on mortality related to cardiovascular disease (CVD). In the cold cities, on the other hand, they report that both high and low temperatures were associated with increased CVD deaths, with the effect of cold temperatures persisting for days but the effect of high temperatures restricted to the day of the death or the day before. Of particular interest was the finding that for all CVD deaths the hot-day effect was five times smaller than the cold-day effect. In addition, the hot-day effect included some “harvesting,” where the authors observed a deficit of deaths a few days later, which they did not observe for the cold-day effect.

Gouveia et al. (2003), in a study conducted in Sao Paulo, Brazil using data from 1991-1994, found that the number of cardiovascular-related deaths in adults (15-64 years of age) increased by 2.6 percent for each 1°C decrease in temperature below 20°C, while there was no evidence for any heat-induced deaths due to temperatures rising above 20°C. In the elderly (65 years of age and above), however, a 1°C warming above 20°C led to a 2 percent increase in deaths; but a 1°C cooling below 20°C led to a 6.3 percent increase in deaths, or more than three times as many cardiovascular-related deaths due to cooling than to warming in the elderly.

Wichmann et al. (2011) investigated the association between the daily three-hour maximum apparent temperature (which reflects the physiological experience of combined exposure to humidity and temperature) and deaths due to cardiovascular disease (CVD), cerebrovascular disease (CBD) and respiratory disease (RD) in Copenhagen, Denmark over the period 1999-2006. In conducting their analysis, the researchers found, during the warm half of the year (April-September), an inverse or protective effect with respect to CVD mortality (a 1% decrease in death in response to a 1°C increase in apparent temperature), while they found no association with RD and CBD mortality. During the cold half of the year, all three associations were inverse or protective, which is "consistent with other studies (Eurowinter Group, 1997; Nafstad et al., 2001; Braga et al., 2002; O'Neill et al., 2003; Analitis et al., 2008)." Accordingly, the number of warming-induced deaths avoided in winter significantly overcompensates for the number of deaths caused by an equivalent warming in summer.

Similar results have been found in Australia (Enquselassie et al., 1993), Brazil (Sharovsky et al., 2004), England (McGregor, 2005; Carder et al., 2005; McGregor et al., 2004; and Kovats et al., 2004), Greece (Bartzokas et al., 2004), Japan (Nakaji et al., 2004), the United States (Cagle and Hubbard, 2005), and parts of Africa, Asia, Europe, Latin America and the Caribbean (Chang et al., 2004).

These studies demonstrate that global warming reduces the incidence of cardiovascular disease related to low temperatures and wintry weather by a much greater degree than it increases the incidence associated with high temperatures and summer heat waves.

Additional information on this topic, including reviews of newer publications as they become available, can be found at http://www.co2 science.org/subject/h/healtheffectscardio.php.

Respiratory Diseases

As was true of cardiovascular-related mortality, deaths due to respiratory diseases are more likely to be associated with cold conditions in cold countries. In Oslo, where Nafstad et al. (2001) found winter deaths due to cardiovascular problems to be 15 percent more numerous than similar summer deaths, they also determined that deaths due to respiratory diseases were fully 47 percent more numerous in winter than in summer. Likewise, the London study of Hajat and Haines (2002) revealed that the number of doctor visits by the elderly was higher in cool-season than warm-season months for all respiratory diseases. At mean temperatures below 5°C, in fact, the relationship between respiratory disease consultations and temperature was linear, and stronger at a time lag of six to 15 days, such that a 1°C decrease in mean temperature below 5°C was associated with a 10.5 percent increase in all respiratory disease consultations.

Gouveia et al. (2003) found that death rates in Sao Paulo, Brazil due to a 1°C cooling were twice as great as death rates due to a 1°C warming in adults, and 2.8 times greater in the elderly. Donaldson (2006) studied the effect of annual mean daily air temperature on the length of the yearly respiratory syncytial virus (RSV) season in England and Wales for 1981-2004 and found “emergency department admissions (for 1990-2004) ended 3.1 and 2.5 weeks earlier, respectively, per 1°C increase in annual central England temperature (P = 0.002 and 0.043, respectively).” He concludes that “the RSV season has become shorter” and “these findings imply a health benefit of global warming in England and Wales associated with a reduction in the duration of the RSV season and its consequent impact on the health service.”

The study of hot and cold cities in the United States by Braga et al. (2002) found that increased temperature variability is the most significant aspect of climate change with respect to respiratory-related deaths in the U.S. Why is this finding important? Because Robeson (2002) has clearly demonstrated, from a 50-year study of daily temperatures at more than 1,000 U.S. weather stations, that temperature variability declines with warming, and at a very substantial rate. The reduced temperature variability in a warmer world would lead to reductions in temperature-related deaths at both the high and low ends of the daily temperature spectrum at all times of the year.

These studies show that a warming world would improve people’s health by reducing deaths related to respiratory disease.

Additional information on this topic, including reviews of newer publications as they become available, can be found at http://www.co2 science.org/subject/h/healtheffectsresp.php.


Malaria

Rogers and Randolph (2000) note that “predictions of global climate change have stimulated forecasts that vector-borne diseases will spread into regions that are at present too cool for their persistence.” Such predictions are a standard part of the narrative of those who believe global warming would have catastrophic effects. However, even the IPCC states “there is still much uncertainty about the potential impact of climate change on malaria in local and global scales” and “further research is warranted” (IPCC, 2007-II, p. 404).

According to Reiter (2000), claims that malaria resurgence is the product of CO2-induced global warming ignore the disease’s history and an extensive literature showing factors other than climate are known to play more important roles in the disease’s spread. For example, historical analysis reveals that malaria was an important cause of illness and death in England during the Little Ice Age. Its transmission began to decline only in the nineteenth century, during a warming phase when, according to Reiter, “temperatures were already much higher than in the Little Ice Age.”

Why was malaria prevalent in Europe during some of the coldest centuries of the past millennium? And why have we only recently witnessed malaria’s widespread decline at a time when temperatures are warming? Other factors are at work, such as the quality of public health services, irrigation and agricultural activities, land use practices, civil strife, natural disasters, ecological change, population change, use of insecticides, and the movement of people (Reiter, 2000; Reiter, 2001; Hay et al., 2002). Models employed by the IPCC predict widespread future increases in malaria because nearly all of the analyses they cite used only one, or at most two, climate variables to make predictions of the future distribution of the disease over the earth, and they generally do not include any non-climatic factors.

In one modeling study that used more than just one or two variables, Rogers and Randolph (2000) employed five climate variables and obtained very different results. Briefly, they used the present-day distribution of malaria to determine the specific climatic constraints that best define that distribution, after which the multivariate relationship they derived from this exercise was applied to future climate scenarios derived from state-of-the-art climate models, in order to map potential future geographical distributions of the disease. They found only a 0.84 percent increase in potential malaria exposure under the “medium-high” scenario of global warming and a 0.92 percent decrease under the “high” scenario. They state that their quantitative model “contradicts prevailing forecasts of global malaria expansion” and “highlights the use [we would say superiority] of multivariate rather than univariate constraints in such applications.” This study undercuts the claim that any future warming of the globe will allow malaria to spread into currently malaria-free regions.

Hay et al. (2002) investigated long-term trends in meteorological data at four East African highland sites that experienced significant increases in malaria cases over the past couple decades, reporting that “temperature, rainfall, vapour pressure and the number of months suitable for P. falciparum transmission have not changed significantly during the past century or during the period of reported malaria resurgence.” Therefore, these factors could not be responsible for the observed increases in malaria cases. Likewise, Shanks et al. (2000) examined trends in temperature, precipitation, and malaria rates in western Kenya over the period 1965-1997, finding no linkages among the variables.

Also working in Africa, Small et al. (2003) examined trends in a climate-driven model of malaria transmission between 1911 and 1995, using a spatially and temporally extensive gridded climate data set to identify locations where the malaria transmission climate suitability index had changed significantly over this time interval. Then, after determining areas of change, they more closely examined the underlying climate forcing of malaria transmission suitability for those localities. This protocol revealed that malaria transmission suitability did increase because of climate change in specific locations of limited extent, but in Southern Mozambique, which was the only region for which climatic suitability consistently increased, the cause of the increase was increased precipitation, not temperature.

In fact, Small et al. say that “climate warming, expressed as a systematic temperature increase over the 85-year period, does not appear to be responsible for an increase in malaria suitability over any region in Africa.” They concluded that “research on the links between climate change and the recent resurgence of malaria across Africa would be best served through refinements in maps and models of precipitation patterns and through closer examination of the role of nonclimatic influences.” The great significance of this has recently been demonstrated by Reiter et al. (2003) for dengue fever, another important mosquito-borne disease.

Examining the reemergence of malaria in the East African highlands, Zhou et al. (2004) conducted a nonlinear mixed-regression model study that focused on the numbers of monthly malaria outpatients of the past 10-20 years in seven East African highland sites and their relationships to the numbers of malaria outpatients during the previous time period, seasonality and climate variability. They say that “for all seven study sites, we found highly significant nonlinear, synergistic effects of the interaction between rainfall and temperature on malaria incidence, indicating that the use of either temperature or rainfall alone is not sensitive enough for the detection of anomalies that are associated with malaria epidemics.” This has also been found by Githeko and Ndegwa (2001), Shanks et al. (2002) and Hay et al. (2002). Climate variability—not just temperature or warming—contributed less than 20 percent of the temporal variance in the number of malaria outpatients, and at only two of the seven sites studied.

In light of their findings, Zhou et al. concluded that “malaria dynamics are largely driven by autoregression and/or seasonality in these sites” and that “the observed large among-site variation in the sensitivity to climate fluctuations may be governed by complex interactions between climate and biological and social factors.” This includes “land use, topography, P. falciparum genotypes, malaria vector species composition, availability of vector control and healthcare programs, drug resistance, and other socioeconomic factors.” Among these are “failure to seek treatment or delayed treatment of malaria patients, and HIV infections in the human population,” which they say have “become increasingly prevalent.”

Kuhn et al. (2003) say “there has been much recent speculation that global warming may allow the reestablishment of malaria transmission in previously endemic areas such as Europe and the United States.” To investigate the robustness of this hypothesis, they analyzed the determinants of temporal trends in malaria deaths within England and Wales from 1840-1910. Their analysis found that “a 1°C increase or decrease was responsible for an increase in malaria deaths of 8.3 percent or a decrease of 6.5 percent, respectively,” which explains “the malaria epidemics in the ‘unusually hot summers’ of 1848 and 1859.” Nevertheless, the long-term near-linear temporal decline in malaria deaths over the period of study, in the words of the researchers, “was probably driven by nonclimatic factors.” Among these they list increasing livestock populations (which tend to divert mosquito biting from humans), decreasing acreages of marsh wetlands (where mosquitoes breed), as well as “improved housing, better access to health care and medication, and improved nutrition, sanitation, and hygiene.” They additionally note that the number of secondary cases arising from each primary imported case “is currently minuscule,” as demonstrated by the absence of any secondary malaria cases in the UK since 1953.

Although simplistic model simulations may suggest that the increase in temperature predicted for Britain by 2050 is likely to cause an 8-14 percent increase in the potential for malaria transmission, Kuhn et al. say “the projected increase in proportional risk is clearly insufficient to lead to the reestablishment of endemicity.” Expanding on this statement, they note that “the national health system ensures that imported malaria infections are detected and effectively treated and that gametocytes are cleared from the blood in less than a week.” For Britain, they conclude that “a 15 percent rise in risk might have been important in the 19th century, but such a rise is now highly unlikely to lead to the reestablishment of indigenous malaria,” since “socioeconomic and agricultural changes” have greatly altered the cause-and-effect relationships of the past.

Zell (2004) states that many people “assume a correlation between increasing disease incidence and global warming.” However, “the factors responsible for the emergence/reemergence of vector-borne diseases are complex and mutually influence each other.” He cites as an example the fact that “the incidence and spread of parasites and arboviruses are affected by insecticide and drug resistance, deforestation, irrigation systems and dams, changes in public health policy (decreased resources of surveillance, prevention, and vector control), demographic changes (population growth, migration, urbanization), and societal changes (inadequate housing conditions, water deterioration, sewage, waste management).” Therefore, as he continues, “it may be over-simplistic to attribute emergent/re-emergent diseases to climate change and sketch the menace of devastating epidemics in a warmer world.” Indeed, Zell states that “variations in public health practices and lifestyle can easily outweigh changes in disease biology,” especially those that might be caused by global warming.

Rogers and Randolph (2006) ask if climate change could be responsible for recent upsurges of malaria in Africa. They demonstrate that “evidence for increasing malaria in many parts of Africa is overwhelming, but the more likely causes for most of these changes to date include land-cover and land-use changes and, most importantly, drug resistance rather than any effect of climate,” noting that “the recrudescence of malaria in the tea estates near Kericho, Kenya, in East Africa, where temperature has not changed significantly, shows all the signs of a disease that has escaped drug control following the evolution of chloroquine resistance by the malarial parasite.” They then go on to explain that “malaria waxes and wanes to the beat of two rhythms: an annual one dominated by local, seasonal weather conditions and a ca. 3-yearly one dominated by herd immunity,” noting that “effective drugs suppress both cycles before they can be expressed,” but that “this produces a population which is mainly or entirely dependent on drug effectiveness, and which suffers the consequence of eventual drug failure, during which the rhythms reestablish themselves, as they appear to have done in Kericho.”

Childs et al. (2006) present a detailed analysis of malaria incidence in northern Thailand from January 1977 through January 2002 in the country’s 13 northern provinces. Over this time period, when the IPCC claims the world warmed at a rate and to a level that were unprecedented over the prior two millennia, Childs et al. report a decline in total malaria incidence (from a mean monthly incidence of 41.5 to 6.72 cases per hundred thousand people. Noting “there has been a steady reduction through time of total malaria incidence in northern Thailand, with an average decline of 6.45 percent per year,” they say this result “reflects changing agronomic practices and patterns of immigration, as well as the success of interventions such as vector control programs, improved availability of treatment and changing drug policies.”

Finally, some researchers have studied the effect of rising CO2 concentrations on the mosquitos that transmit malaria. Tuchman et al. (2003) took leaf litter from Populus tremuloides (Michaux) trees that had been grown out-of-doors in open-bottom root boxes located within open-top above-ground chambers maintained at atmospheric CO2 concentrations of either 360 or 720 ppm for an entire growing season, incubated the leaf litter for 14 days in a nearby stream, and fed the incubated litter to four species of detritivorous mosquito larvae to assess its effect on their development rates and survivorship. This work revealed that larval mortality was 2.2 times higher for Aedes albopictus (Skuse) mosquitos that were fed leaf litter that had been produced in the high-CO2 chambers than it was for those fed litter that had been produced in the ambient-air chambers.

In addition, Tuchman et al. found that larval development rates of Aedes triseriatus (Say), Aedes aegypti (L.), and Armigeres subalbatus (Coquillett) were slowed by 78 percent, 25 percent, and 27 percent, respectively, when fed litter produced in the high-CO2 as opposed to the ambient-CO2 chambers, so that mosquitoes of these species spent 20, 11, and nine days longer in their respective larval stages when feeding on litter produced in the CO2-enriched as compared to the ambient-CO2 chambers. As for the reason behind these observations, the researchers suggest that “increases in lignin coupled with decreases in leaf nitrogen induced by elevated CO2 and subsequent lower bacterial productivity [on the leaf litter in the water] were probably responsible for [the] decreases in survivorship and/or development rate of the four species of mosquitoes.”

What is the significance of these findings? In the words of Tuchman et al., “the indirect impacts of an elevated CO2 atmosphere on mosquito larval survivorship and development time could potentially be great,” because longer larval development times could result in fewer cohorts of mosquitoes surviving to adulthood; and with fewer mosquitoes around, there should be lower levels of mosquito-borne diseases.

A 2011 study in Biology Letters finds that warmer temperatures seem to slow transmission of malaria-causing parasites, by reducing their infectiousness. Paaijmans et al. incubated mosquitoes infected with Plasmodium yoelii, which causes rodent malaria, at 20, 22, 24 and 26 degrees Celsius for 5–14 days. The researchers then examined the salivary glands of the mosquitoes — where the parasite travels when it is mature — and found that the parasite developed more quickly in warmer temperatures. But they also found fewer sporozoites — the infectious form of the parasite — indicating that the mosquitoes were less infectious at higher temperatures. Although parasite development peaked at 26 ºC, malaria risk was higher at 24 ºC, because parasite survival rates peaked at a lower temperature of 22 ºC.

The effect is complex: as temperature rises, parasites do develop faster, but fewer of them become infectious. Paaijmans et al. say that there are several possible explanations for why parasite survival falls as temperature increases: the parasite may not be able to cope with the higher temperatures, or mosquito immune systems may work better at warmer temperatures. The researchers plan to repeat the experiments with human malaria. But it should also be replicated outside of the lab with wild mosquitoes. “The [reduced transmission] effects might be even stronger if mosquitoes in the wild are in poorer condition than in the lab.” It is also possible that the results will apply to other mosquito-borne diseases such as dengue fever and West Nile virus.


In conclusion, research that takes into account more than one or two variables typically shows little or no relationship between the incidence of malaria and temperature. Many factors are more important than temperature, and those that are subject to human control are being used to steadily reduce the incidence of deaths from this disease. In the words of Dye and Reiter (2000), “given adequate funding, technology, and, above all, commitment, the campaign to ‘Roll Back Malaria,’ spearheaded by the World Health Organization, will have halved deaths related to [malaria] by 2010” – independent of whatever tack earth’s climate might take in the interim.

Current research that supports this conclusion was quantied by Béguin et al. (2011). In this study, the researchers showed that GDP per capita has a much stronger effect on malaria transmission than climate change. Specifically, they estimated populations at risk of malaria based on climatic variables, population growth and GDP per capita. GDP is an approximation for per capita income for 1990, 2010 and 2050, based on a sensitivity analyses for the following three scenarios: (1) a worst-case scenario, in which income declines to 50% of its 2010 values by 2050, (2) a growth reduction scenario, in which income declines by 25% in 2030 and 50% in 2050, relative to the A1B scenario, and (3) a scenario in which income stays constant at 2010 values. Their results show that populations at risk will continue to decrease from now until 2030 and 2050 if GDP increases, regardless of the impact of climate change (from 3.52 billion people in 2030 to 1.74 billion people in 2050 with no climate change or from 3.58 billion people in 2030 to 1.95 billion people in 2050 with climate change). Despite making a gratuitous claim that the results are "dependent on optimistic, and potentially unsustainable, economic growth,” it is still more important to pursue economic development rather than to pursue reductions in climate change.

Additional information on this topic, including reviews of newer publications as they become available, can be found at at http://www.co2 science.org/subject/m/malaria.php

Tick-Borne Diseases

The IPCC claims that one of the likely consequences of the increase in temperature would be expanded geographic ranges of tick-borne diseases, although once again this prediction is highly qualified. “Climate change alone is unlikely to explain recent increases in the incidences of tick-borne disease in Europe or North America,” the IPCC admits, and “other explanations cannot be ruled out” (IPCC 2007-II, p. 403).

Randolph and Rogers (2000) reported that tick-borne encephalitis (TBE) “is the most significant vector-borne disease in Europe and Eurasia,” having “a case morbidity rate of 10-30 percent and a case mortality rate of typically 1-2 percent but as high as 24 percent in the Far East.” The disease is caused by a flavivirus (TBEV), which is maintained in natural rodent-tick cycles; humans may be infected with it if bitten by an infected tick or by drinking untreated milk from infected sheep or goats.

Early writings on the relationship of TBE to global warming predicted it would expand its range and become more of a threat to humans in a warmer world. However, Randolph and Rogers indicate that “like many vector-borne pathogen cycles that depend on the interaction of so many biotic agents with each other and with their abiotic environment, enzootic cycles of TBEV have an inherent fragility,” so that “their continuing survival or expansion cannot be predicted from simple univariate correlations.” The two researchers decided to explore the subject in greater detail than had ever been done before.

Confining their analysis to Europe, Randolph and Rogers first correlated the present-day distribution of TBEV to the present-day distributions of five climatic variables: monthly mean, maximum, and minimum temperatures, rainfall and saturation vapor pressure, “to provide a multivariate description of present-day areas of disease risk.” Then, they applied this understanding to outputs of a general circulation model of the atmosphere that predicted how these five climatic variables may change in the future. The results of these operations indicated that the distribution of TBEV might expand both north and west of Stockholm, Sweden in a warming world. For most other parts of Europe, however, the two researchers say “fears for increased extent of risk from TBEV caused by global climate change appear to be unfounded.” They found that “the precise conditions required for enzootic cycles of TBEV are predicted to be disrupted” in response to global warming, and that the new climatic state “appears to be lethal for TBEV.” This finding, in their words, “gives the lie to the common perception that a warmer world will necessarily be a world under greater threat from vector-borne diseases.” In the case of TBEV, in fact, they report that the predicted change “appears to be to our advantage.”

Similarly, Estrada-Peña (2003) evaluated the effects of various abiotic factors on the habitat suitability of four tick species that are major vectors of livestock pathogens in South Africa. This work revealed “year-to-year variations in the forecasted habitat suitability over the period 1983-2000 show a clear decrease in habitat availability, which is attributed primarily to increasing temperature in the region over this period.” In addition, when climate variables were projected to the year 2015, Estrada-Peña found that “the simulations show a trend toward the destruction of the habitats of the four tick species.” This is the opposite of what is predicted by those who warn of catastrophic consequences from global warming.

Zell (2004) determined that “the factors responsible for the emergence/reemergence of vector-borne diseases are complex and mutually influence each other,” citing as an example that “the incidence and spread of parasites and arboviruses are affected by insecticide and drug resistance, deforestation, irrigation systems and dams, changes in public health policy (decreased resources of surveillance, prevention, and vector control), demographic changes (population growth, migration, urbanization), and societal changes (inadequate housing conditions, water deterioration, sewage, waste management).”

In light of these many complicating factors, Zell says “it may be over-simplistic to attribute emergent/re-emergent diseases to climate change and sketch the menace of devastating epidemics in a warmer world.” Indeed, he concludes that “variations in public health practices and lifestyle can easily outweigh changes in disease biology,” especially those that might be caused by global warming.


Heat-related Mortality

Keatinge and Donaldson (2001) analyzed the effects of temperature, wind, rain, humidity, and sunshine during high pollution days in the greater London area over the period 1976-1995 to determine what weather and/or pollution factors have the biggest influence on human mortality. Their most prominent finding was that simple plots of mortality rate versus daily air temperature revealed a linear increase in deaths as temperatures fell from 15°C to near 0°C. Mortality rates at temperatures above 15°C were, in the words of the researchers, “grossly alinear,” showing no trend. Days with high pollutant concentrations were colder than average, but a multiple regression analysis revealed that no pollutant was associated with a significant increase in mortality among people over 50 years of age. Indeed, only low temperatures were shown to have a significant effect on both immediate (one day after the temperature perturbation) and long-term (up to 24 days after the temperature perturbation) mortality rates.

Keatinge et al. (2000) examined heat- and cold-related mortality in north Finland, south Finland, southwest Germany, the Netherlands, Greater London, north Italy, and Athens, Greece in people aged 65-74. For each of these regions, they determined the 3°C temperature interval of lowest mortality and then evaluated mortality deviations from that base level as temperatures rose and fell by 0.1°C increments. The result, according to the researchers, was that “all regions showed more annual cold related mortality than heat related mortality.” Over the seven regions studied, annual cold-related deaths were nearly 10 times greater than annual-heat related deaths. The scientists also note that the very successful adjustment of the different populations they studied to widely different summer temperatures “gives grounds for confidence that they would adjust successfully, with little increase in heat related mortality, to the global warming of around 2°C predicted to occur in the next half century.” Indeed, they say their data suggest “any increases in mortality due to increased temperatures would be outweighed by much larger short term declines in cold related mortalities.” For the population of Europe, therefore, an increase in temperature would appear to be a climate change for the better.

Gouveia et al. (2003) conducted a similar study in Sao Paulo, Brazil, where they tabulated the numbers of daily deaths from all causes (excepting violent deaths and deaths of infants up to one month of age), which they obtained from the city’s mortality information system for the period 1991-1994. They then analyzed these data for children (less than 15 years of age), adults (ages 15-64), and the elderly (age 65 and above) with respect to the impacts of warming and cooling. For each 1°C increase above the minimum-death temperature of 20°C for a given and prior day’s mean temperature, there was a 2.6 percent increase in deaths from all causes in children, a 1.5 percent increase in deaths from all causes in adults, and a 2.5 percent increase in deaths from all causes in the elderly. For each 1°C decrease below the 20°C minimum-death temperature, however, the cold effect was greater, with increases in deaths from all causes in children, adults, and the elderly registering 4.0 percent, 2.6 percent, and 5.5 percent, respectively. These cooling-induced death rates are 54 percent, 73 percent, and 120 percent greater than those attributable to warming.

Kan et al. (2003), in a study conducted in Shanghai, China from June 1, 2000 to December 31, 2001, found a V-like relationship between total mortality and temperature that had a minimum mortality risk at 26.7°C. Above this temperature, they note that “total mortality increased by 0.73 percent for each degree Celsius increase; while for temperatures below the optimum value, total mortality decreased by 1.21 percent for each degree Celsius increase.” The net effect of a warming of the climate of Shanghai, therefore, would likely be reduced mortality on the order of 0.5 percent per degree Celsius increase in temperature, or perhaps even more, in light of the fact that the warming of the past few decades has been primarily due to increases in daily minimum temperatures.

Goklany and Straja (2000) studied deaths in the United States due to all causes over the period 1979-97. They found deaths due to extreme cold exceeded those due to extreme heat by 80 percent to 125 percent. No trends were found due to either extreme heat or cold in the entire population or, remarkably, in the older, more susceptible, age groups, i.e., those aged 65 and over, 75 and over, and 85 and over. Goklany and Straja say the absence of any trend “suggests that adaptation and technological change may be just as important determinants of such trends as more obvious meteorological and demographic factors.”

Davis et al. (2003) examined daily mortality rates for 28 major U.S. cities over 29 years between 1964 and 1998. In order to control for changes in the age structure of each city’s population that might bias temporal comparisons, they standardized each day’s mortality count relative to a hypothetical standard city with a population of one million people, with the demographics of that city based on the age distribution of the entire U.S. population in the year 2000. They found “heat-related mortality rates declined significantly over time in 19 of the 28 cities. For the 28-city average, there were 41.0+/- 4.8 (mean +/- SE) excess heat-related deaths per year (per standard million) in the 1960s and 1970s, 17.3 +/- 2.7 in the 1980s, and 10.5 +/- 2.0 in the 1990s.” This 74 percent drop in heat-related deaths occurred despite an average increase in temperature of 1.0°C during the same period. They interpret this to mean that “the U.S. populace has become systematically less affected by hot and humid weather conditions,” and they say this “calls into question the utility of efforts linking climate change forecasts to future mortality responses in the United States,” something the IPCC explicitly does. The four scientists conclude that “there is no simple association between increased heat wave duration or intensity and higher mortality rates in the United States.”

Donaldson et al. (2003) determined the mean daily May-August 3°C temperature bands in which deaths of people aged 55 and above were at a minimum for three areas of the world—North Carolina, USA; South Finland; and Southeast England. They then compared heat- and cold-related deaths that occurred at temperatures above and below this optimum temperature interval for each region, after which they determined how heat-related deaths in the three areas changed between 1971 and 1997 in response to: (1) the 1.0°C temperature rise that was experienced in North Carolina over this period (from an initial temperature of 23.5°C), (2) the 2.1°C temperature rise experienced in Southeast England (from an initial temperature of 14.9°C), and (3) the unchanging 13.5°C temperature of South Finland.

First, it was determined that the 3°C temperature band at which mortality was at its local minimum was lowest for the coolest region (South Finland), highest for the warmest region (North Carolina), and intermediate for the region of intermediate temperature (Southeast England). This suggests these three populations were somewhat acclimated to their respective thermal regimes. Second, in each region, cold-related mortality (expressed as excess mortality at temperatures below the region’s optimum 3°C temperature band) was greater than heat-related mortality (expressed as excess mortality at temperatures above the region’s optimum 3°C temperature band).

Third, the researchers found that in the coldest of the three regions (South Finland, where there was no change in temperature over the study period), heat-related deaths per million inhabitants in the 55-and-above age group declined from 382 to 99. In somewhat warmer Southeast England, where it warmed by 2.1°C over the study period, heat-related deaths declined but much less, from 111 to 108. In the warmest of the three regions (North Carolina, USA, where mean daily May-August temperature rose by 1.0°C over the study period), heat-related deaths fell most dramatically, from 228 to a mere 16 per million.

From these observations we learn that most people can adapt to both warmer and cooler climates and that cooling tends to produce many more deaths than warming, irrespective of the initial temperature regime. As for the reason behind the third observation—the dramatic decline in heat-related deaths in response to warming in the hottest region of the study (North Carolina)—Donaldson et al. attribute it to the increase in the availability of air conditioning in the South Atlantic region of the United States, where they note that the percentage of households with some form of air conditioning rose from 57 percent in 1978 to 72 percent in 1997. With respect to the declining heat-related deaths in the other two areas, they say “the explanation is likely to lie in the fact that both regions shared with North Carolina an increase in prosperity, which could be expected to increase opportunities for avoiding heat stress.”

Huynen et al. (2001) analyzed mortality rates in the entire population of Holland. For the 19-year period from January 1979 through December 1997, the group of five scientists compared the numbers of deaths in people of all ages that occurred during well-defined heat waves and cold spells. They found a total excess mortality of 39.8 deaths per day during heat waves and 46.6 deaths per day during cold spells. These numbers indicate that a typical cold-spell day kills at a rate that is 17 percent greater than a typical heat-wave day in the Netherlands.

The researchers note that the heat waves they studied ranged from 6 to 13 days in length, while the cold spells lasted 9 to 17 days, making the average cold spell approximately 37 percent longer than the average heat wave. Adjusting for this duration differential makes the number of deaths per cold spell in the Netherlands fully 60 percent greater than the number of deaths per heat wave. What is more, excess mortality continued during the whole month after the cold spells, leading to even more deaths, while there appeared to be mortality deficits in the month following heat waves, suggesting, in the words of the authors, “that some of the heat-induced increase in mortality can be attributed to those whose health was already compromised” or “who would have died in the short term anyway.” This same conclusion has been reached in a number of other studies (Kunst et al., 1993; Alberdi et al., 1998; Eng and Mercer, 1998; Rooney et al., 1998). It is highly likely, therefore, that the 60 percent greater death toll we have calculated for cold spells in the Netherlands as compared to heat waves is an underestimate of the true differential killing power of these two extreme weather phenomena.

The Dutch could well ask themselves, therefore, “Will global climate change reduce climate-related mortalities in the Netherlands?” … which is exactly what the senior and second authors of the Huynen et al. paper did in a letter to the editor of Epidemiology (Martens and Huynen, 2001). Based on the predictions of nine different GCMs for an atmospheric CO2 concentration of 550 ppm in the year 2050—which implied a 50 percent increase in Dutch heat waves and a 67 percent drop in Dutch cold spells—they calculated a total mortality decrease for Holland of approximately 1,100 people per year at that point in time.

Data from Germany tell much the same story. Laschewski and Jendritzky (2002) analyzed daily mortality rates of the population of Baden-Wurttemberg, Germany (10.5 million inhabitants) over the 30-year period 1958-1997 to determine the sensitivity of the people living in this moderate climatic zone of southwest Germany to long- and short-term episodes of heat and cold. They found the mortality data “show a marked seasonal pattern with a minimum in summer and a maximum in winter” and “cold spells lead to excess mortality to a relatively small degree, which lasts for weeks,” and that “the mortality increase during heat waves is more pronounced, but is followed by lower than average values in subsequent weeks.” The authors’ data demonstrate that the mean duration of above-normal mortality for the 51 heat episodes that occurred from 1968 to 1997 was 10 days, with a mean increase in mortality of 3.9 percent, after which there was a mean decrease in mortality of 2.3 percent for 19 days. Hence, the net effect of the heat waves was a calculated overall decrease in mortality of 0.2 percent over the full 29-day period.

We end with the work of Thomas Gale Moore, an economist at Stanford University USA. In his first publication reviewed here (Moore, 1998), Moore reported the results of two regression analyses he conducted to estimate the effect on the U.S. death rate of a 4.5°F increase in average termperature, the IPCC’s “best estimate” at the time (1992) of likely warming over the course of the next century. For the first analysis, Moore “regressed various measures of warmth on deaths in Washington, DC, from January 1987 through December 1989,” a period of 36 months, and then extrapolated the results for the entire country. He used Washington, DC because temperatures are recorded for major urban areas, not states, while monthly data on deaths is available from the National Center for Health Statistics only for states, but the center treats the nation’s capital as a state. This analysis found a 4.5°F rise “would cut deaths for the country as a whole by about 37,000 annually.”

For his second analysis, Moore regressed the death rates in 89 large U.S. counties with various weather variables, including actual average temperatures in 1979, highest summer temperature, lowest winter temperature, number of heating degree days, and number of cooling degree days, and several other variables known to affect death rates (percent of the population over age 65, percent black, percent with 16 years or more of schooling, median household income, per-capita income, air pollution, and health care inputs such as number of hospital beds and physicians per 100,000 population.) He found “the coefficient for average temperature implies that if the United States were enjoying temperatures 4.5 degrees warmer than today, mortality would be 41,000 less. This savings in lives is quite close to the number estimated based on the Washington, DC data, for the period 1987 through 1989.” Moore notes that “a warmer climate would reduce mortality by about the magnitude of highway deaths.”

Two years later, in a report published by the Hoover Institution, Moore estimated the number of deaths that would be caused by the costs associated with reducing U.S. greenhouse gas emissions (Moore, 2000). “Economists studying the relationship of income and earnings to mortality have found that the loss of $5 million to $10 million in the U.S. GDP [gross domestic product] leads to one extra death,” Moore writes. Since the Energy Information Administration (EIA) estimated that meeting the Kyoto Protocol’s goal of reducing greenhouse gas emissions to 7 percent below 1990 levels by 2010-2012 would cost $338 billion annually (without emissions trading), “the EIA estimates imply that somewhere between 33,800 and 67,000 more Americans will die annually between 2008 and 2012.”

These studies of the effects of temperature on human mortality show that cooling, not warming, kills the largest number of people each year. The number of lives saved by warmer weather, if the IPCC’s forecasts of future warming are correct (and we doubt that they are), would far exceed the number of lives lost. The margin in the United States is enormous, with the number of prevented deaths exceeding the number of deaths that occur on the nation’s highways each year. Conversely, attempting to stop global warming by reducing emissions would cost lives—between 33,800 and 67,000 a year in the U.S. alone, according to Moore (2000). These staggering numbers leave little doubt that global warming does not pose a threat to human health.

Terrestrial Animals

Another animal-related concern with respect to global warming is that rising temperatures will increase the prevalence of parasitic and vector-borne diseases, resulting in increasing mortality rates. To date, very little research has been published on this concern. Here, however, we cite two papers that have provided some understanding of the subject.

Writing in Trends in Parasitology, Morgan and Wall (2009) state “global climate change predictions suggest that far-ranging effects might occur in population dynamics and distributions of livestock parasites, provoking fears of widespread increases in disease incidence and production loss.” However, they indicate, “just as development rates of many parasites of veterinary importance increase with temperature, so [too] do their mortality rates [increase].” They further note “temperature will also affect mortality indirectly through the action of predators, parasitoids, pathogens and competitors, whose development and abundance are also potentially temperature sensitive,” so that, in the end, “the net effect of climate change could be complex and far from easily predicted.”

In perusing the subject in greater detail, as they elucidate some of the many complexities involved, the two U.K. researchers indicate “several biological mechanisms (including increased parasite mortality and more rapid acquisition of immunity), in tandem with changes in husbandry practices (including reproduction, housing, nutrition, breed selection, grazing patterns and other management interventions), might act to mitigate increased parasite development rates, preventing dramatic rises in overall levels of diseases.” However, because “optimum mitigation strategies will be highly system specific and depend on detailed understanding of interactions between climate, parasite abundance, host availability and the cues for and economics of farmer intervention,” as they characterize the situation, they conclude “there is a need for research that considers likely effects of climate change and mitigation strategies in terms of the whole host-parasite system, including anthropogenic responses, and not just in terms of parasite population dynamics.” It likely will be some time before the temperature-related parasitic disease relationship for animals is resolved.

Turning to a well-known vector-borne disease, Conte et al. (2009) note “the midge Culicoides imicola is the principal vector of bluetongue virus (BTV) that causes an infectious disease of domestic and wild ruminants,” and “over the last ten years, BTV has invaded Mediterranean countries and much of Northern Europe,” inducing several scientists and others to contend the BTV vector had expanded its range northward “because of rising temperatures,” as suggested by the work of Mellor (2004), Purse et al. (2005), and Mellor et al. (2008). However, a careful examination of Culicoides population data in Italy prior to 2000 was made by Goffredo et al. (2003). They determined “trapping conditions of previous collections would have had very little chance of catching C. imicola,” or detecting its presence, suggesting there was insufficient evidence to make the case for a warming-induced northward expansion of the BTV vector, because it may already have been present there but undetected.

In response to even earlier fears of a potential BTV invasion, a national surveillance program for C. imicola had been established in Italy in the year 2000, where 70,000 light-trap collections were made at about 3,800 different sites. Using the first year of data obtained from this program, Conte et al. defined the spatial distributions of three different C. imicola infection zones: zone I (endemicity), zone II (transition), and zone III (absence). Then, using data from 2002–2007, they quantified how C. imicola populations evolved through time in these three zones, working under the logical assumption that “a species that is undergoing geographical range expansion should have a population that remains stable over time in zone I and increases in zones II and III.”

The three researchers state their results indicated “no detectable range expansion of C. imicola population in Italy over the past six years.” In fact, they report “a weak, but significant reduction was observed in the transition zone.” Conte et al. therefore conclude their data “support the hypothesis that the spread of BTV in Italy is not because of the geographical expansion of its main vector, but due to a modification of the interaction between the virus, the vector and the environment, as may also have been the case in northern Europe.” As for the future, they write, their results indicate “precautions should be taken when inferring range progression for species requiring highly targeted forms of sampling and for which a constant probability of detection over time should be established.” This demonstrates once again that it is easy to blame global warming for the poleward expansion of a vector-spread disease, but it is quite another thing to prove the case.


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