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Health Effects (Temperature -- Cardiovascular) -- Summary
Climate alarmists would have people believe that global warming will pose numerous challenges to human health, including premature death due to heat-induced cardiovascular problems. In this Summary we thus present the results of a number of studies conducted over the past decade or so that deal with this important subject.

A good place to begin a review of temperature-related mortality is a cold location like Siberia. Hence, we start with the study of Feigin et al. (2000), who 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 entire world. Analyzing the health records of 2208 patients with a sex and age distribution similar to that of the whole of Russia over the period 1982-93, Feigin et al. found a statistically significant association between stroke occurrence and low ambient temperature. For ischemic stroke (IS), which accounted for 87% of all strokes recorded, they found that the risk of IS occurrence on days with low ambient temperature was 32% higher than it was on days with high ambient temperature. Hence, they suggested the implementation of "preventive measures ... such as avoiding low temperature."

Hong et al. (2003) observed much the same thing 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, further noting that "even a moderate decrease in temperature can increase the risk of ischemic stroke." In addition, they noted that "risk estimates associated with decreased temperature were greater in winter than in the summer," which suggests, in their words, that "low temperatures as well as temperature changes are associated with the onset of ischemic stroke."

Nafstad et al. (2001) studied another cold place: Oslo, Norway. Thanks to Norwegian law, which requires that all deaths 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. Their analysis showed that the average daily number of cardiovascular-related deaths was 15% 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."

To see if relationships between cold temperatures and cardiovascular mortality are preceded by an even more general health-temperature relationship, Hajat and Haines (2002) set out to determine if mere cardiovascular-related doctor visits by the elderly bore a similar relationship to cold temperatures. Based on data obtained between January 1992 and September 1995 for registered patients aged 65 and older from several practices in London, England, they did indeed find that the 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 think that such findings are only to be expected in cold climates. So what about warm climates, where summer maximum temperatures are often extreme, but summer minimum temperatures are typically mild?

In Israel, research conducted by Green et al. (1994) revealed that between 1976 and 1985, mortality from cardiovascular disease was higher by 50% in mid-winter than in mid-summer, both in men and in women, as well as in different age groups, in spite of the fact that summer temperatures in the Negev -- where much of the work was conducted -- often exceeded 30°C, while winter temperatures typically did not drop below 10°C. These findings have also been substantiated by several other Israeli studies, including those that were reviewed by Behar (2000), who wrote 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 additionally been noted in the relatively 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% higher than those observed in the period June through September. Likewise, based on a study of the Hunter region of New South Wales, Australia, which 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% more common in winter and spring than at other times of year," while with respect to 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% more likely to occur than at moderate temperatures."

In a study of both "hot" and "cold" cities in the United States -- where Atlanta, Georgia; Birmingham, Alabama; and Houston, Texas comprised the "hot" group, and where 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 both the acute effects and lagged influence of temperature on cardiovascular-related deaths, finding 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 with 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 Braga et al. observed a deficit of deaths a few days later, which they did not observe for the cold-day effect.

Working in Sao Paulo, Brazil, with data collected over the period 1991-1994, Gouveia et al. (2003) determined that the number of cardiovascular-related deaths in adults (15-64 years of age) increased by 2.6% 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% increase in deaths; but a 1°C cooling below 20°C led to a 6.3% increase in deaths, or more than three times as many cardiovascular-related deaths due to cooling than to warming in the elderly.

For the period 1974-1999, McGregor et al. (2004) obtained data on ischaemic heart disease (IHD) and temperature for five English counties aligned on a north-south transect (Tyne and Wear, West Yorkshire, Greater Manchester, West Midlands, and Hampshire) and analyzed them in such a way as to reveal any relationships that might exist between the two parameters. In doing so, they determined that "the seasonal cycles of temperature and mortality are inversely related," and that "the first harmonic accounts for at least 85% (significant at the 0.01 level) of the variance of temperature and mortality at both the climatological and yearly time scales." They also found that "years with an exaggerated mortality peak are associated with years characterized by strong temperature seasonality," and that "the timing of the annual mortality peak is positively associated with the timing of the lowest temperatures." Why? Because, in the words of McGregor et al., "frequent exposure to cold causes a rise in IHD risk factors (Lloyd, 1991) through increasing blood pressure and viscosity, vasoconstriction, heart rate and angina (Morgan and Moran, 1997)."

Chang et al. (2004) analyzed data from the World Health Organization (WHO) Collaborative Study of Cardiovascular Disease and Steroid Hormone Contraception (WHO, 1995) to determine the effects of monthly mean temperature on rates of hospitalization for arterial stroke and acute myocardial infarction (AMI) among young women aged 15-49 from seventeen different countries in Africa, Asia, Europe, Latin America and the Caribbean. These efforts revealed that "among young women from 17 countries, the rate of hospitalized AMI, and to a lesser extent stroke, was higher with lower mean environmental air temperature." More specifically, they say that "on average, a 5°C reduction in mean air temperature was associated with a 7 and 12% increase in the expected hospitalization rates of stroke and AMI, respectively." They also note that "the findings of an inverse association between mean air temperature and hospitalization rate of AMI in this study are in agreement with several other studies," citing those of Douglas et al. (1990), Douglas et al. (1991), Mackenbach et al. (1992), Douglas et al. (1995), Seto et al. (1998), Danet et al. (1999) and Crawford et al. (2003). Last of all, they note that "lagging the effects of temperature suggested that these effects were relatively acute, within a period of a month."

Contemporaneously, Bartzokas et al. (2004) "examined the relationship between hospital admissions for cardiovascular (cardiac in general including heart attacks) and/or respiratory diseases (asthma etc.) in a major hospital in Athens [Greece] and meteorological parameters for an 8-year period." By these means they discovered that over the whole year, "there was a dependence of admissions on temperature," and that low temperatures were "responsible for a higher number of admissions." Specifically, they say "there was a decrease of cardiovascular or/and respiratory events from low to high values [of temperature], except for the highest temperature class in which a slight increase was recorded."

In Japan, Nakaji et al. (2004) evaluated seasonal trends in deaths due to various diseases, using nationwide vital statistics from 1970 to 1999 and recorded weather data, specifically, mean monthly temperature. According to the nine researchers, Japan has "bitterly cold winters," and their analysis indicated that the numbers of deaths due to infectious and parasitic diseases including tuberculosis, respiratory diseases including pneumonia and influenza, diabetes, digestive diseases and cerebrovascular and heart diseases rise to a maximum during that cold time of year. Of the latter two categories, in fact, they found that peak mortality rates due to heart disease and stroke were 1.5 to 2 times greater in winter (January) than what they were at the time of their yearly minimums (August and September). As a result, they concluded that "to reduce the overall mortality rate and to prolong life expectancy in Japan, measures must be taken to reduce those mortality rates associated with seasonal differences." They also wrote that "it has long been recognized that cold temperature acts as a trigger for coronary events," and that "major infectious diseases are epidemic in winter." Hence, it is clear that to achieve the scientists' stated objectives, it is necessary to bring about a "reduction in exposure to cold environments," as they put it, which is precisely what global warming does, and what it does best when it warms more in winter than in summer, as Nakaji et al. demonstrated to be the case in Japan, where winter warming over the past 30 years was twice as great as what it was during the rest of the year.

Back in Sao Paulo, Brazil, where 12,007 fatal events were observed from 1996 to 1998, Sharovsky et al. (2004) investigated "associations between weather (temperature, humidity and barometric pressure), air pollution (sulfur dioxide, carbon monoxide, and inhalable particulates), and the daily death counts attributed to myocardial infarction." Their efforts revealed "a significant association of daily temperature with deaths due to myocardial infarction (p<0.001), with the lowest mortality being observed at temperatures between 21.6 and 22.6°C." For all practical purposes, however, their data showed little variation in death rates from 18°C to just over 25°C, the latter of which values represents the typical upper limit of observed temperature in Sao Paulo, which is located on the Tropic of Capricorn at an altitude of 800 m. As mean daily temperature dropped below 18°C, however, death rates rose in essentially linear fashion to attain a value at 12°C (the typical lower limit of observed temperature in Sao Paulo) that was more than 35% greater than the minimum baseline value registered between 21.6 and 22.6°C.

In discussing their findings, Sharovsky et al. said they "demonstrated a strong association between daily temperature and myocardial infarction in Sao Paulo, Brazil," which suggests that "an acclimatization of the population to the local climate occurs and that myocardial infarction deaths peak in winter not only because of absolute low temperature but possibly secondary to a decrease relative to the average annual temperature," which indeed must be true, for deaths due to heart attacks are consistently greater in winter than in summer, as they wrote, "across many regions of the world (Marshall et al., 1998; Douglas et al., 1991; Seto et al., 1998; Sheth et al., 1999)." Hence, it can be appreciated that the global warming of the past century, which increased minimum temperatures considerably more than maximum temperatures almost everywhere, likely prevented -- or significantly forestalled -- the deaths of many people around the world who otherwise would have succumbed to this deadly scourge of the human race, i.e., (relatively) cold temperature.

In another study conducted in the same year, Kovats et al. (2004) analyzed patterns of temperature-related hospital admissions and deaths in Greater London during the mid-1990s. For the three-year period 1994-1996, cardiovascular-related deaths were approximately 50% greater during the coldest part of the winter than during the peak warmth of summer, while respiratory-related deaths were nearly 150% greater in the depths of winter cold than at the height of summer warmth. Also, with respect to heat waves that climate alarmists typically portray as being ferocious killers, it is revealing to note that the mortality impact of the notable heat wave of 29 July to 3 August 1995 was so tiny that it could not be discerned amongst the random scatter of plots of three-year-average daily deaths from cardiovascular and respiratory problems versus day of year.

With still more information from 2004, Keatinge and Donaldson, in a review article published in the Southern Medical Journal, began the main body of their text with a clear declaration of the relative dangers of heat and cold when it comes to human mortality, writing that "cold-related deaths are far more numerous than heat-related deaths in the United States, Europe, and almost all countries outside the tropics, and almost all of them are due to common illnesses that are increased by cold." So what are the major mechanisms by which cold kills?

Keatinge and Donaldson report that coronary and cerebral thrombosis account for about half of all cold-related deaths, and that respiratory diseases account for approximately half of the rest. With respect to the first of these sets of problems, they say that cold stress causes an increase in arterial thrombosis "because the blood becomes more concentrated, and so more liable to clot during exposure to cold." The sequence of events, as they describe it, is that "the body's first adjustment to cold stress is to shut down blood flow to the skin to conserve body heat," which "produces an excess of blood in central parts of the body," and that to correct for this effect, "salt and water are moved out from the blood into tissue spaces," leaving behind "increased levels of red cells, white cells, platelets and fibrinogen" that lead to increased viscosity of the blood and a greater risk of clotting.

With respect to respiratory-related deaths, the British scientists report that the infections that cause them spread more readily in cold weather as people "crowd together in poorly ventilated spaces when it is cold." In addition, they say that "breathing of cold air stimulates coughing and running of the nose, and this helps to spread respiratory viruses and bacteria." The "train of events leading to respiratory deaths," as they continue, "often starts with a cold or some other minor infection of the upper airways," which "spreads to the bronchi and to the lungs," whereupon "secondary infection often follows and can lead to pneumonia." They also note that cold stress "tends to suppress immune responses to infections," and that respiratory infections typically "increase the plasma level of fibrinogen, and this contributes to the rise in arterial thrombosis in winter."

Another interesting thing about cold-related deaths, as Keatinge and Donaldson describe it, is that "cold spells are closely associated with sharp increases in mortality rates," and that "deaths continue for many days after a cold spell ends." On the other hand, they report that "increased deaths during a few days of hot weather are followed by a lower than normal mortality rate," because "many of those dying in the heat are already seriously ill and even without heat stress would have died within the next 2 or 3 weeks."

So what are the implications of global warming for human mortality? Keatinge and Donaldson state that "since heat-related deaths are generally much fewer than cold-related deaths" -- and, we note, are comprised primarily of deaths that typically would have occurred a few weeks later even in the absence of excess heat -- "the overall effect of global warming on health can be expected to be a beneficial one." As an example, and even including the early heat-harvesting of naturally-expected deaths, they report that "the rise in temperature of 3.6°F expected over the next 50 years would increase heat-related deaths in Britain by about 2,000 but reduce cold-related deaths by about 20,000."

In concluding their treatise, Keatinge and Donaldson state that "even in climates as warm as southern Europe or North Carolina [USA], cold weather causes more deaths than hot weather." They report that "global warming will reduce this at first," but they say "the improvement is not likely to continue without action to promote defenses against cold." For example, they report that "people in regions with mild winters become careless about cold stress, protect themselves less effectively against cold, and generally have more winter deaths than people in colder regions," noting that "climatic warming therefore calls for action to control cold stress as well as heat stress," and stating that if appropriate precautions are taken, "rising temperatures could reduce overall mortality rates." Consequently, as they conclude, "the overall effect of global warming on health can be expected to be a beneficial one."

Moving one year closer to the present, while noting that "anomalous cold stress can increase blood viscosity and blood pressure due to the activation of the sympathetic nervous system which accelerates the heart rate and increases vascular resistance (Collins et al., 1985; Jehn et al., 2002; Healy, 2003; Keatinge et al., 1984; Mercer, 2003; Woodhouse et al., 1993)," and reminding us that "anomalously cold winters may also increase other risk factors for heart disease such as blood clotting or fibrinogen concentration, red blood cell count per volume and plasma cholesterol" -- and in light of the strong causative relationship that exists between cold weather and ischaemic heart disease (IHD) -- McGregor (2005) conducted an analysis to determine if there was any association between the level of IHD mortality in three English counties (Hampshire, West Midlands and West Yorkshire) and the winter-season North Atlantic Oscillation (NAO), which exerts a fundamental control on the nature of winter climate in Western Europe, focusing on the winters of 1974-1975 through 1998-1999. In doing so, he found that "generally below average monthly and all-winter IHD mortality is associated with strong positive values of the monthly or winter climate index which indicates the predominance of anomalously warm moist westerly flows of air over England associated with a positive phase of the NAO," while at the other extreme he found that "winters with elevated mortality levels ... have been shown to be clearly associated with a negative NAO phase and anomalously low temperatures," adding that "the occurrence of influenza ... helps elevate winter mortality above that of summer."

Contemporaneously, Carder et al. (2005) used generalized linear Poisson regression models to investigate the relationship between outside air temperature and deaths due to all non-accident causes in the three largest cities of Scotland (Glasgow, Edinburgh and Aberdeen) that occurred between January 1981 and December 2001. In doing so, they observed "an overall increase in mortality as temperature decreases," which "appears to be steeper at lower temperatures than at warmer temperatures," while they say "there is little evidence of an increase in mortality at the hot end of the temperature range." They also report that "the observed relation between cold temperature and mortality was typically stronger among the elderly," and they state that one of the important findings of their study was that "cold temperature effects on mortality persist with lag periods of beyond two weeks." That is to say, the seven scientists found that for temperatures below 11°C, a 1°C drop in the daytime mean temperature on any one day was associated with an increase in cardiovascular-caused mortality of 3.4% over the following month. Consequently, it can be appreciated that at any season of the year, a decline in air temperature in the major cities of Scotland leads to increases in deaths due to cardiovascular causes, while there is little to no such increase in mortality associated with heat waves.

Also reporting in 2005, Cagle and Hubbard described what they learned in examining the relationship between temperature and cardiac-related deaths in King County, Washington (USA) over the period 1980-2000 using Poisson regression analysis, based on information provided by the Washington State Department of Health on out-of-hospital deaths of all adults over the age of 54, plus historical meteorological data obtained from the National Climate Data Center for the Seattle-Tacoma International Airport. Based on this work they determined there was an average of 2.86 cardiac-related deaths per day for all days when the maximum temperature fell within the broad range of 5-30°C. For days with maximum temperatures less than 5°C, however, the death rate rose by 15% to a mean value of 3.30, while for days with maximum temperatures greater than 30°C death rates rose not at all, actually dropping by 3% to a mean value of 2.78. In addition, they found that "the observed association between temperature and death rate is not due to confounding by other meteorological variables," and they learned that "temperature continues to be statistically significantly associated with death rate even at a 5-day time lag."

So why is cold so effective in killing people? Cagle and Hubbard mention a number of human haematological changes that occur upon exposure to cold, including a decrease in blood plasma volume (Bass and Henschel, 1956; Chen and Chien, 1977; Fregley, 1982; Collins et al., 1985) that is accompanied by "a sympathetic nervous system reflex response to cold-induced stress (LeBlanc et al., 1978; Collins et al., 1985; LeBlanc, 1992)," as well as "an increase in packed cell volume due to increased numbers of red cells per unit volume (Keatinge et al., 1984), increased platelet counts and platelet volume (Finkel and Cumming, 1965; Keatinge et al., 1984), increased whole blood viscosity (Keatinge et al., 1984), increased serum lipid levels (Keatinge et al., 1984; Woodhouse et al., 1993; Neild et al., 1994), and increased plasma fibrinogen and factor VII clotting activity values (Keatinge et al., 1984; Woodhouse et al., 1994)." These various haemodynamic and vasoconstrictive factors combine, in their words, "to produce what Muller et al. (1994) refer to as 'acute risk factors' that may trigger a cardiac event." Vasoconstriction and concomitant increases in central blood volume and systolic blood pressure, for example, "put additional workload on the heart which may lead to increased arrhythmias (Amsterdam et al., 1987), decreased thresholds for angina and abnormal myocardial contractions (De Lorenzo et al., 1999), as well as increasing the risk of dislodging a vulnerable plaque which could lead to thrombosis (Muller et al., 1994)," which "may occur through increased cardiac filling pressure and stroke volume which in turn increases cardiac oxygen requirements while lessening cardiac access to oxygen (Muza et al., 1988; De Lorenzo et al., 1999)." In addition, the Washington researchers report that "greater blood viscosity also works to increase the load on the heart through greater resistance to flow (Frisancho, 1993) and increasing blood pressure (Keatinge et al., 1984)."

Jumping all the way to 2009, Tam et al. employed daily mortality data for the period 1997 to 2002, which they obtained from the Hong Kong Census and Statistics Department, to examine the association between diurnal temperature range (DTR = daily maximum temperature minus daily minimum temperature), focusing on cardiovascular disease among the elderly (people aged 65 and older). This work revealed "a 1.7% increase in mortality for an increase of 1°C in DTR at lag days 0-3," which results they describe as being "similar to those reported in Shanghai." And in discussing their findings, the four researchers state that "a large fluctuation in the daily temperature -- even in a tropical city like Hong Kong -- has a significant impact on cardiovascular mortality among the elderly population." In addition, we note that it has long been known that the DTR has declined significantly over many parts of the world as mean global temperature has risen over the past several decades (Easterling et al., 1997), which is perhaps another reason why colder temperatures are a much greater risk to human life than are warmer temperatures.

In distilling the results of these several studies into a single take-home message, it is clear that they demonstrate that global warming is actually beneficial to humanity, in that it reduces the incidence of cardiovascular diseases related to low temperatures and wintry weather by a much greater degree than it increases the incidence of cardiovascular diseases associated with high temperatures and summer heat waves.

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Last updated 21 April 2010