Changes in mortalities and hospital admissions associated with holidays and respiratory illness: implications for medical services.

RATIONALE AND OBJECTIVES: To see whether net mortalities increase during and after reductions in medical services, either at average weekends, or at Christmas when pressure from illness is unusually high. METHODS: (1) Paired t-tests to compare mean daily deaths and hospital admissions during and after weekends (Saturday-Tuesday) with means for the week, in south-east England; (2) Linear regressions to see whether trends of daily deaths change when admissions are reduced at Christmas. RESULTS: Neither mean daily all-cause, respiratory or ischaemic heart deaths exceeded weekly averages during weekends, or during Saturday-Monday or Saturday-Tuesday, despite falls in daily elective and daily emergency hospital admissions at weekends that averaged 61-72% and 14-22%, respectively. During 19-24 December, daily deaths were above annual means, respiratory deaths by 49% (29, 1-58), but elective admissions fell and although emergency admissions tended to rise, total admissions rose only for respiratory disease, and only by 33% (376, -47 to 799). On Christmas Day (25 December), even emergency admissions fell sharply below previous trends, respiratory emergency admissions by 18% (P<0.01). Respiratory deaths alone then immediately increased (P<0.01) above trend, by 5.9% (5.8 deaths/day) on 26 December and by 12.9% (12.9) on 27 December. CONCLUSIONS: No adverse effect on mortality was apparent within 2 days from reduction in medical services at weekends. However, respiratory deaths accelerated sharply after reduction in elective and emergency admissions at Christmas, when rates of infection and mortality from respiratory disease were high. Implications for medical services during respiratory epidemics are discussed.

The impact of global warming on health and mortality.

Initial concern about the possible effects of global warming on infections has declined with the realization that the spread of tropical diseases is likely to be limited and controllable. However, the direct effects of heat already cause substantial numbers of deaths among vulnerable people in the summer. Action to prevent these deaths from rising is the most obvious medical challenge presented by a global rise in temperature. Strategies to prevent such deaths are in place to some extent, and they differ between the United States and Europe. Air conditioning has reduced them in the United States, and older technologies such as fans, shade, and buildings designed to keep cool on hot days have generally done so in Europe. Since the energy requirements of air conditioning accelerate global warming, a combination of the older methods, backed up by use of air conditioning when necessary, can provide the ideal solution. Despite the availability of these technologies, occasional record high temperatures still cause sharp rises in heat-related deaths as the climate warms. The most important single piece of advice at the time a heat wave strikes is that people having dangerous heat stress need immediate cooling, eg, by a cool bath. Such action at home can be more effective than transporting the patient to hospital. Meanwhile, it must not be forgotten that cold weather in winter causes-many more deaths than heat in summer, even in most subtropical regions, and measures to control cold-related deaths need to continue.

Cardiovascular responses to heat stress and their adverse consequences in healthy and vulnerable human populations.

This paper reviews the basic thermoregulatory physiology of healthy people in relation to hazards from external heat stress and internal heat loads generated by physical exercise or radiofrequency (RF) radiation. In addition, members of the population are identified who may be particularly vulnerable to the effects of heat stress. These data are examined in relation to current international guidance on occupational and public exposure to RF radiation. When body temperature rises, heat balance of the body is normally restored by increased blood flow to the skin and by sweating. These responses increase the work of the heart and cause loss of salt and water from the body. They impair working efficiency and can overload the heart and cause haemoconcentration, which can lead to coronary and cerebral thrombosis, particularly in elderly people with atheromatous arteries. These adverse effects of thermoregulatory adjustments occur with even mild heat loads and account for the great majority of heat-related illness and death. They are, therefore, particularly relevant to determination of safe population exposures to additional sources of heat stress. It is concluded that exposure to RF levels currently recommended as safe for the general population, equivalent to heat loads of about one tenth basal metabolic rate, could continue to be regarded as trivial in this context, but that prolonged exposures of the general population to RF levels higher than that could not be regarded as safe in all circumstances.

Changes in summer temperature and heat-related mortality since 1971 in North Carolina, South Finland, and Southeast England.

Three climatically diverse regions were studied to determine the impact of temperature change on heat-related mortality from 1971 to 1997. Median regressions showed that May-August temperatures in North Carolina rose by 1.0 degrees C (95% CL 0.0-2.0 degrees C) from 23.5 degrees C (74.3 degrees F), were unchanged in South Finland at 13.5 degrees C (56.3 degrees F), and rose in Southeast England 2.1 degrees C (0.3-4.0 degrees C) from 14.9 degrees C (58.8 degrees F). After determining for each region the daily temperature (as a 3 degrees C band) at which the mortality was the lowest, annual heat-related mortality was obtained as excess mortality per million at temperatures above this. Annual heat-related mortality per million (among the population at risk, aged 55+) fell in North Carolina by 212 (59-365) from 228 (140-317) to only 16 (not significant, NS); fell in South Finland by 282 (66-500) from 382 (257-507) to 99 (NS); and fell in Southeast England by 2.4 (NS) from 111 (41-180) to 108 (41-176). The falls in North Carolina and South Finland remained significant after allowances were made for changes in age, sex, and baseline mortality. Increased air conditioning probably explains the virtual disappearance of heat-related mortality in the hottest region, North Carolina, despite warmer summers. Other lifestyle changes associated with increasing prosperity probably explain the favorable trends in the cooler regions.

Winter mortality and its causes.

In the 1970s scientific research focussed for the first time on dramatic rises in mortality every winter, and on smaller rises in unusually hot weather. Following the recent decline in influenza epidemics, approximately half of excess winter deaths are due to coronary thrombosis. These peak about two days after the peak of a cold spell. Approximately half the remaining winter deaths are caused by respiratory disease, and these peak about 12 days after peak cold. The rapid coronary deaths are due mainly to haemoconcentration resulting from fluid shifts during cold exposure; some later coronary deaths are secondary to respiratory disease. Heat related deaths often result from haemoconcentration resulting from loss of salt and water in sweat. With the possible exception of some tropical countries, global warming can be expected to reduce cold related deaths more than it increases the rarer heat related deaths, but statistics on populations in different climates suggest that, given time, people will adjust to global warming with little change in either mortality. Some measures may be needed to control insect borne diseases during global warming, but current indications are that cold will remain the main environmental cause of illness and death. Air pollution in cities may also still be causing some deaths, but these are hard to differentiate from the more numerous deaths due to associated cold weather, and clear identification of pollution deaths may need more extensive data than is currently available.

Hypothermia during sports swimming in water below 11 degrees C.

OBJECTIVES: To assess precautions needed to avoid dangerous hypothermia in endurance sports swims in water below 11 degrees C, using rectal temperature, anthropometric measurements, and voluntary swim times during a six day marathon relay swim. METHODS: The time in the water and the decrease in rectal temperature were measured during the longest of three to five relay swims by each of eight experienced swimmers in 9.4-11.0 degrees C water. Height, weight, and four skinfold thicknesses were measured. RESULTS: Swimmers with less subcutaneous fat terminated their swims after significantly less time in the water than those with thicker skinfold thickness, even though their rectal temperatures were not significantly lower. The lowest rectal temperature recorded was 34.3 degrees C. CONCLUSIONS: Subjective sensation in these experienced swimmers gave reliable guidance on safe durations for swims, and all voluntarily left the water with rectal temperatures that present no threat to people able to rewarm in safe surroundings. Endurance swims in highly competitive conditions or water below 9 degrees C may require continuous temperature monitoring for safety.

Mortality related to cold and air pollution in London after allowance for effects of associated weather patterns.

We looked for atypical weather patterns that could confound, and explain large inconsistencies in, conventional estimates of mortality due to SO(2), CO, and smoke. Using Greater London data for 1976-1995 in the linear temperature/mortality range 0-15 degrees C we determined weather patterns associated with pollutants (all deseasonalized) by single regressions of daily temperature, wind, rain, humidity, and sunshine at successive days advance and delay. Polluted days were colder (P<0.01 for SO(2), CO, and smoke) and less windy and rainy than usual, and this cold weather was more prolonged than usual with 50% maximum temperature depression 5.9 days (95% interval 4.0-7.7) before high SO(2), compared to 2.0 (1.6-2.3) days before average cold days. We also used multiple regression of mortality at 50+ years of age on all these weather factors and pollutants at 0-, 1-, 2- to 4-, 5- to 13-, and 14- to 24-day delays to allow for the atypical weather patterns. This showed cold weather associated with 2.77 excess deaths per million during 24 days following a 1 degrees C fall for 1 day, but no net excess deaths with SO(2) (mean 28.0 ppb) or CO (1.26 ppm). It suggested (P>0.05) some increase with smoke, perhaps acting as surrogate for PM(10), for which data were too scanty to analyze.

Heat related mortality in warm and cold regions of Europe: observational study.

OBJECTIVES: To assess heat related mortalities in relation to climate within Europe. DESIGN: Observational population study. SETTING: North Finland, south Finland, Baden-Württemberg, Netherlands, London, north Italy, and Athens. SUBJECTS: People aged 65-74. MAIN OUTCOME MEASURES: Mortalities at temperatures above, below, and within each region's temperature band of minimum mortality. RESULTS: Mortality was lowest at 14.3-17.3 degrees C in north Finland but at 22.7-25.7 degrees C in Athens. Overall the 3 degrees C minimum mortality temperature bands were significantly higher in regions with higher than lower mean summer temperatures (P=0.027). This was not due to regional differences in wind speeds, humidity, or rain. As a result, regions with hot summers did not have significantly higher annual heat related mortality per million population than cold regions at temperatures above these bands. Mean annual heat related mortalities were 304 (95% confidence interval 126 to 482) in North Finland, 445 (59 to 831) in Athens, and 40 (13 to 68) in London. Cold related mortalities were 2457 (1130 to 3786), 2533 (965 to 4101), and 3129 (2319 to 3939) respectively. CONCLUSIONS: Populations in Europe have adjusted successfully to mean summer temperatures ranging from 13.5 degrees C to 24.1 degrees C, and can be expected to adjust to global warming predicted for the next half century with little sustained increase in heat related mortality. Active measures to accelerate adjustment to hot weather could minimise temporary rises in heat related mortality, and measures to maintain protection against cold in winter could permit substantial reductions in overall mortality as temperatures rise.

Winter mortality in relation to climate.

We report further details of the Eurowinter survey of cold related mortalities and protective measures against cold in seven regions of Europe, and review these with other evidence on the relationship of winter mortality to climate. Data for the oldest subject group studied, aged 65-74, showed that in this vulnerable group, high levels of protection against indoor and outdoor cold at given outdoor temperatures were found mainly in countries with cold winters, and were associated with low levels of excess mortality at a given level of outdoor cold. Regions such as London that had poor protection against cold and/or high baseline mortalities had higher levels of winter excess mortality than expected for the coldness of their winters.

Cold related mortalities and protection against cold in Yakutsk, eastern Siberia: observation and interview study.

OBJECTIVE: To assess how effectively measures adopted in extreme cold in Yakutsk control winter mortality. DESIGN: Interviews to assess outdoor clothing and measure indoor temperatures; regressions of these and of delayed cause-specific mortalities on temperature. Setting Yakutsk, east Siberia, Russia. SUBJECTS: All people aged 50-59 and 65-74 years living within 400 km of Yakutsk during 1989-95 and sample of 1002 men and women who agreed to be interviewed. MAIN OUTCOME MEASURES: Daily mortality from all causes and from ischaemic heart, cerebrovascular, and respiratory disease. RESULTS: Mean temperature for October-March 1989-95 was -26.6 degreesC. At 10.2 degrees C people wore 3.30 (95% confidence interval 3.08 to 3.53) layers of clothing outdoors, increasing to 4.39 (4.13 to 4.66; P<0. 0001) layers at -20 degrees C. Thick coats, often of fur, replaced anoraks as temperature fell to -48.2 degrees C. 82% of people went out each day when temperatures were 10.2 degrees C to -20 degrees C, but below -20 degrees C the proportion fell steadily to 44% (35% to 53%) at -48.2 degrees C (P<0.001), and overall shivering outdoors did not increase. Living room temperature was 17.9 (17.2 to 18.5) degrees C at 10.2 degrees C outdoors, 19.6 (18.8 to 20.4) degrees C at -20 degrees C, and 19.1 (18.6 to 19.6) degrees C at -48.2 degrees C. Mortality from all causes and from ischaemic heart and respiratory disease was unaffected by the fall in temperature. Mortality from respiratory disease (daily deaths per million) rose from 4.7 (4.3 to 5.1) to 5.1 (4.4 to 5.7) (P=0.03), but this was offset by a fall in deaths from injury. CONCLUSIONS: People in Yakutsk wore very warm clothing, and in extremely cold weather stayed indoors in warm housing, preventing the increases in mortality seen in winter in milder regions of the world. Only respiratory mortality rose, perhaps because of breathing cold air.

Winter mortality and cold stress in Yekaterinburg, Russia: interview survey.

OBJECTIVES: To evaluate how mortality and protective measures against exposure to cold change as temperatures fall between October and March in a region of Russia with a mean winter temperature below -6 degrees C. DESIGN: Interview to assess factors associated with cold stress both indoors and outdoors, to measure temperatures in living room, and to survey unheated rooms. SETTING: Sverdlovsk Oblast (district), Yekaterinburg, Russia. SUBJECTS: Residents aged 50-59 and 65-74 living within approximately 140 km of Yekaterinburg in Sverdlovsk Oblast. Survey of sample of 1000 residents equally distributed by sex and age groups. MAIN OUTCOME MEASURES: Regression analysis was used to relate data on indoor heating and temperatures, the amount of clothing worn, the amount of physical activity, and shivering while outside, to outdoor temperature; results were compared with mortality patterns for ischaemic heart disease, cerebrovascular disease, respiratory disease, and mortality from all causes. RESULTS: As mean daily temperatures fell to 0 degree C the amount of clothing worn outdoors increased, physical activity while outdoors became more continuous, and only 11 (6.6%) of the 167 people surveyed who went outdoors at temperatures above 0 degree C reported shivering. The mean temperature in living rooms in the evening remained above 21.9 degrees C. Mortality from ischaemic heart disease, cerebrovascular disease, respiratory disease, and all causes did not change. As the temperature fell below 0 degree C the number of items of clothing worn plateaued at 16.0 and the number of layers at 3.7. With regression analysis, shivering outdoors was found to increase progressively to 34.6% (P < 0.001) of excursions at -25 degrees C, and mortality (after declining slightly) rose progressively (all cause mortality rose by 1.15% for each 1 degree C drop in temperature from 0 degree C to -29.6 degrees C, 95% confidence interval 0.97% to 1.32%). 94.2% of bedrooms were directly heated, and evening temperatures in the living room averaged 19.8 degrees C even when outside temperatures reached -25 degrees C. CONCLUSIONS: Outdoor cold stress and mortality in Yekaterinburg increased only when the mean daily temperature dropped below 0 degree C. At temperatures down to 0 degree C cold stress and excess mortality were prevented by increasing the number of items of clothing worn and the amount of physical activity outdoors in combination with maintaining warmth in houses.

Early increases in ischaemic heart disease mortality dissociated from and later changes associated with respiratory mortality after cold weather in south east England.

STUDY OBJECTIVE: To identify the time courses and magnitude of ischaemic heart (IHD), respiratory (RES), and all cause mortality associated with common 20-30 day patterns of cold weather in order to assess links between cold exposure and mortality. DESIGN: Daily temperatures and daily mortality on successive days before and after a reference day were regressed on the temperature of the reference day using high pass filtered data in which changes with a cycle length < 80 days were unaffected (< 2%), but slower cyclical changes and trends were partly or completely suppressed. This provided the short term patterns of both temperature and mortality associated with a one day displacement of temperature. The results were compared with simple regressions of unfiltered mortality on temperature at successive delays. STUDY POPULATION AND SETTING: Population of south east England, including London, over 50 years of age from 1976-92. MAIN RESULTS: Colder than average days in the linear range 15 to 0 degrees C were associated with a "run up" of cold weather for 10-15 days beforehand and a "run down" for 10-15 days afterwards. The increases in deaths were maximal at 3 days after the peak in cold for IHD, at 12 days for RES, and at 3 days for all cause mortality. The increase lasted approximately 40 days after the peak in cold. RES deaths were significantly delayed compared with IHD deaths. Excess deaths per million associated with these short term temperature displacements were 7.3 for IHD, 5.8 for RES, and 24.7 for all cause, per one day fall of 1 degree C. These were greater by 52% for IHD, 17% for RES, and 37% for all cause mortality than the overall increases in daily mortality per degree C fall, at optimal delays, indicated by regressions using unfiltered data. Similar analyses of data at 0 to -6.7 degrees C showed an immediate rise in IHD mortality after cold, followed by a fall in both IHD and RES mortality rates which peaked 17 and 20 days respectively after a peak in cold. CONCLUSION: Twenty to 30 day patterns of cold weather below 15 degrees C were followed:(1) rapidly by IHD deaths, consistent with known thrombogenic and reflex consequences of personal cold exposure; and (2) by delayed increases in RES and associated IHD deaths in the range 0 to 15 degrees C, which were reversed for a few degrees below 0 degree C, and were probably multifactorial in cause. These patterns provide evidence that personal exposure to cold has a large role in the excess mortality of winter.

Effect of posture on body temperature of young men in cold air.

We studied eight young adult men to see whether a supine posture caused a fall in body core temperature in the cold, as it does in thermoneutral conditions. In air at 31 degrees C (thermoneutral), a supine posture for 3 h reduced mean aural, gastric, oesophageal and rectal temperatures by 0.2-0.4 degree C, compared to upright and increased femoral artery blood flow from 278 (SEM 42)ml.min-1 whilst upright to 437 (SEM 42) ml.min-1 whilst supine. In cold air (8 degrees C) the supine posture failed to reduce these temperatures [corrected] significantly, or to increase femoral blood flow: it reduced heart rate, and increased arterial systolic and pulse pressures adjusted to carotid sinus level, less than in thermoneutral conditions. However, the behaviour of core temperature at the four sites was significantly nonuniform between the two postures in the cold, mainly because the supine posture tended to reduce rectal temperature. It may have done so by reducing heat production in the muscles of the pelvis, since it reduced overall metabolic rate from 105 (SEM 8) to 87 (SEM 4) W.m-2 in the cold. In other respects the results indicated that posture ceased to have an important effect on body core temperatures during cold stress.

Cardiovascular mortality in winter.

Ischaemic heart disease is the biggest single cause of excess mortality in winter, accounting for approximately half of all the excess deaths. Most of these deaths take place hours or a day or two after exposure to cold suggesting that some result from thrombosis starting during or shortly after cold exposure, although some can result from immediate reflex effects of cold, and some can occur in association with respiratory deaths which are delayed many days after cold weather. Changes in blood composition observed in the cold that may explain the rapid thrombotic deaths include increased red cell count, plasma cholesterol, and plasma fibrinogen, which are all thrombogenic. The protective protein C does not increase significantly. British data suggests that cold housing particularly affects respiratory mortality in winter, and outdoor cold exposures mortality from arterial thrombosis. A Europe-wide survey is now being run as part of the EC- funded project "Eurowinter" to assess such factors.

Cold-induced increases in erythrocyte count, plasma cholesterol and plasma fibrinogen of elderly people without a comparable rise in protein C or factor X.

1. Six elderly (66-71 years) and six young (20-23 years) subjects (half of each group women) were cooled for 2 h in moving air at 18 degrees C to investigate possible causes of increased mortality from arterial thrombosis among elderly people in cold weather. Compared with thermoneutral control experiments, skin temperature (trunk) fell from 35.5 to 29.5 degrees C, with little change in core temperature. 2. Erythrocyte count rose in the cold from 4.29 to 4.69 x 10(12)/l, without a change in mean corpuscular volume, indicating a 14% or 438 ml decline in plasma volume; increased excretion of water, Na+ and K+ accounted for loss of only 179 ml of extracellular water. 3. Plasma cholesterol and fibrinogen concentrations rose in the elderly subjects from 4.90 mmol/l and 2.97 g/l (control) to 5.45 mmol/l and 3.39 g/l in the cold, and in the young subjects from 3.33 mmol/l and 1.84 g/l (control) to 3.77 mmol/l and 2.07 g/l in the cold. Increases were significant for the elderly subjects, the young subjects and the group as a whole, except for cholesterol in the young subjects, and all were close to those expected from the fall in plasma volume. 4. Plasma levels of Protein C and factor X did not increase significantly in the cold in the elderly subjects, young subjects, or the group as a whole. 5. The results suggest that loss of plasma fluid in the cold concentrates major risk factors for arterial thrombosis, while small molecules, including protective Protein C, redistribute to interstitial fluid.