The Impact of Global Warming on Health and Mortality

W. R. Keatinge, MA, MB, BCHIR, PHD, FRCP; G. C. Donaldson, BA, PHD

Disclosures

South Med J. 2004;97(11) 

In This Article

Causes of Cold-Related and Heat-Related Deaths

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. Coronary and cerebral thrombosis account for about half of the cold-related deaths and respiratory disease for about half the rest.[6] Cold stress causes the increase in arterial thrombosis because the blood becomes more concentrated, and so more liable to clot, during exposure to cold. The sequence of events is that the body's first adjustment to cold stress is to shut down blood flow to the skin, to conserve body heat.[7,8,9] The shift of blood from the skin produces an excess of blood in central parts of the body. To correct that, salt and water are moved out from the blood into tissue spaces and are eventually excreted. This leaves behind increased levels of red cells, white cells, platelets, and fibrinogen, and causes increased viscosity of the blood (Fig. 1). All of these changes promote clotting.

Temperatures and erythrocyte counts of elderly and young adult volunteers exposed to mild surface cooling. Triangles, exposure to turbulent air at 64.4°F, lightly clothed. Circles, control; fully clothed in still air at 71.6°F throughout. Values are mean ± SEM (n = 6); *P < 0.05, **P = < 0.01, ***P < 0.001 compared with control (paired t test), for 0, 2, and 24 hours only. Reproduced, with permission, from Neild PJ, Syndercombe-Court D, Keatinge WR, et al. Clin Sci 1994;86:43-48. The Biochemical Society and the Medical Research Society.

The anticoagulant protein C, which normally hinders intravascular clotting, might be expected to increase in line with the increase in concentration of the thrombogenic elements of blood during exposure to cold. If it did, it would counter the effects of those elements, at least in part. However, it has a small enough molecule to allow it to diffuse through the walls of blood vessels. As a result, it redistributes from the blood into the tissue spaces of the body, and its plasma concentration hardly changes during general hemoconcentration in the cold.

Since cold exposure causes this increase in concentration of thrombogenic factors in the blood of both young and elderly people, it might be expected that it would increase mortality rates in both age groups. In practice, the increase in mortality rate is virtually confined to the elderly. Part of the explanation for this is that baseline fibrinogen levels are much higher in the elderly, so that even in the cold, fibrinogen levels in young adults do not reach the baseline level of the elderly (Fig. 2). A more important reason is that young people are protected from intra-arterial thrombosis by the fact that their arteries have a healthy endothelial lining. The inner surfaces of arteries of elderly people are commonly affected by atheroma and so are much more prone to thrombose.

Effect of cold exposure on plasma fibrinogen and cholesterol concentrations. Triangles, exposure to turbulent air at 64.4°F, lightly clothed. Circles, control; fully clothed in still air at 71.6°F throughout. Values are mean ± SEM (n = 6); *P < 0.05, **P = < 0.01, ***P < 0.001 compared with control (paired t test), for 0, 2 and 24 hours only. Reproduced, with permission, from Neild PJ, Syndercombe-Court D, Keatinge WR, et al. Clin Sci 1994;86:43-48. The Biochemical Society and the Medical Research Society.

The increase in respiratory infections and respiratory deaths in winter is due partly to respiratory infections spreading more readily in cold weather. People crowd together in poorly ventilated spaces when it is cold. Apart from that, breathing of cold air stimulates coughing and running of the nose, and this helps to spread respiratory viruses and bacteria. Cold stress also tends to suppress immune responses to infections. Respiratory infections also increase the plasma level of fibrinogen, and this contributes to the rise in arterial thrombosis in winter.[10]

The train of events leading to respiratory deaths in winter often starts with a cold or some other minor infection of the upper airways. This spreads to the bronchi and to the lungs. Secondary infection often follows and can lead to pneumonia. Anything that ameliorates a cold will therefore reduce more serious respiratory infections. The simplest treatment for a cold is the old remedy of inhaling steam for 30 minutes or so. This not only reduces the symptoms of a cold at once, but moderates the entire subsequent course of the illness.[11,12] The reasons for this are not fully known, but one is that a rise in temperature to around 113°F causes heat shock damage to the rhinoviruses that cause many colds.[13]

Epidemics of influenza used to kill hundreds of thousands of people every 2 or 3 years, often through secondary bacterial pneumonia. Since the 1970s, these epidemics have been much less common and less severe worldwide. The decline mostly occurred before the start of immunization against influenza.[14,15] The reasons for it are not fully known, but an important factor appears to be reduced opportunities for exchanges of genetic material between human, avian, and porcine strains of influenza virus. In the past, particularly in times of war and civil disturbance, there was frequent contact of people with ducks, chickens, and pigs in living spaces. Settled times allow better hygiene, which allows less contact between the different viruses. A potential new risk has appeared with the mass rearing of chickens, which allows epidemics of avian influenza to infect huge flocks of birds. Spread to human beings of these viruses and of the frequently lethal SARS virus has so far been limited by mass slaughter of infected birds. However, there is a risk that one of the new strains of influenza will develop, through contact with human influenza virus, the capacity for rapid transmission from person to person. If this happened, it could trigger a human epidemic on the scale of the influenza pandemic of 1918.

Surprisingly, few of the excess deaths in winter are due to the body simply cooling until vital organs such as the heart and brain cease to function. When hypothermia does occur it is usually a consequence of other illness and it is not a common cause of death in North America[16,17] and is a rare one in Britain.[18,19]

In the past, deficiency of vitamin C in the winter diet may have contributed to winter mortality rates, but winter death is now due to the effects of cold on people. Vitamin C does have a protective action against arterial thrombosis, but fruits and vegetables are now freely available even in winter. Statistical analysis shows that the winter mortality rate is closely associated with cold weather. Time series analysis on deseasonalized data, using multiple single regressions,[6] shows that cold spells are closely associated with sharp increases in mortality rates. The deaths continue for many days after a cold spell ends and account for all of the excess mortality rate in winter.

Heat-related death, like cold-related death, is often due to thermal stress exacerbating conditions that commonly cause deaths among elderly people. This is particularly true of temperate regions with moderate summer temperatures. However, in regions where people are exposed to air close to or above body temperature for long periods, a substantial amount of the heat-related deaths are due to simple hyperthermia, overheating of the body until the body proteins are denatured.[20] A wide range of psychoactive drugs, particularly those with anticholinergic or narcotic actions, increase the risk of this by impairing sweating and other responses to heat. Psychiatric patients are accordingly particularly vulnerable to heat stress.

In regions with cool summers, such as Britain, almost all heat-related deaths are due to other factors. Unlike cold-related deaths, infections play little part in these, but as with cold-related deaths, coronary and cerebral thromboses account for many heat-related deaths. These thromboses again result from hemoconcentration, which in this case has a simple cause, loss of salt and water in sweat.[21] Other heat-related deaths result from a range of other factors that are not well understood but which probably include strain on failing hearts unable to provide the additional blood flow to the skin needed to increase loss of heat from the body. One mitigating factor in relation to heat-related death in relatively cool countries such as Britain is that increased deaths during a few days of hot weather are followed by a lower than normal mortality rate. The likely reason is that 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.

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