Effect of previous-winter mortality on the association between summer temperature and mortality in South Korea.

BACKGROUND: It has recently been postulated that low mortality levels in the previous winter may increase the proportion of vulnerable individuals in the pool of people at risk of heat-related death during the summer months. OBJECTIVES: We explored the sensitivity of heat-related mortality in summer (June-August) to mortality in the previous winter (December-February) in Seoul, Daegu, and Incheon in South Korea, from 1992 through 2007, excluding the summer of 1994. METHODS: Poisson regression models adapted for time-series data were used to estimate associations between a 1 °C increase in average summer temperature (on the same day and the previous day) above thresholds specific for city, age, and cause of death, and daily mortality counts. Effects were estimated separately for summers preceded by winters with low and high mortality, with adjustment for secular trends. RESULTS: Temperatures above city-specific thresholds were associated with increased mortality in all three cities. Associations were stronger in summers preceded by winters with low versus high mortality levels for all nonaccidental deaths and, to a lesser extent, among persons ≥ 65 years of age. Effect modification by previous-winter mortality was not evident when we restricted deaths to cardiovascular disease outcomes in Seoul. CONCLUSIONS: Our results suggest that low winter all-cause mortality leads to higher mortality during the next summer. Evidence of a relation between increased summer heat-related mortality and previous wintertime deaths has the potential to inform public health efforts to mitigate effects of hot weather

Health effects of milder winters: a review of evidence from the United Kingdom.

Cold-related mortality and morbidity remains an important public health problem in the UK and elsewhere. Health burdens have often reported to be higher in the UK compared to other countries with colder climates, however such assessments are usually based on comparison of excess winter mortality indices, which are subject to biases. Daily time-series regression or case-crossover studies provide the best evidence of the acute effects of cold exposure. Such studies report a 6% increase in all-cause deaths in England & Wales for every 1 °C fall in daily mean temperature within the top 5% of the coldest days. In major Scottish cities, a 1 °C reduction in mean temperature below 11 °C was associated with an increase in mortality of 2.9%, 3.4%, 4.8% and 1.7% from all-causes, cardiovascular, respiratory, and non-cardio-respiratory causes respectively. In Northern Ireland, a 1 °C fall during winter months led to increases of 4.5%, 3.9% and 11.2% for all-cause, cardiovascular and respiratory deaths respectively among adults. Raised risks are also observed with morbidity outcomes. Hip fractures among the elderly are only weakly associated with snow and ice conditions in the UK, with the majority of cases occurring indoors. A person's susceptibility to cold weather is affected by both individual- and contextual-level risk factors. Variations in the distributions of health, demographic, socio-economic and built-environment characteristics are likely to explain most differences in cold risk observed between UK regions. Although cold-related health impacts reduced throughout much of the previous century in UK populations, there is little evidence on the contribution that milder winters due to climate change may have made to reductions in more recent decades. Intervention measures designed to minimise cold exposure and reduce fuel poverty will likely play a key role in determining current and future health burdens associated with cold weather

Heat and risk of myocardial infarction: hourly level case-crossover analysis of MINAP database.

OBJECTIVE: To quantify the association between exposure to higher temperatures and the risk of myocardial infarction at an hourly temporal resolution. DESIGN: Case-crossover study. SETTING: England and Wales Myocardial Ischaemia National Audit Project (MINAP) database. PARTICIPANTS: 24,861 hospital admissions for myocardial infarction occurring in 11 conurbations during the warmest months (June to August) of the years 2003-09. MAIN OUTCOME MEASURE: Odds ratio of myocardial infarction for a 1 °C increase in temperature. RESULTS: Strong evidence was found for an effect of heat acting 1-6 hours after exposure to temperatures above an estimated threshold of 20 °C (95% confidence interval 16 °C to 25 °C). For each 1 °C increase in temperature above this threshold, the risk of myocardial infarction increased by 1.9% (0.5% to 3.3%, P=0.009). Later reductions in risk seemed to offset early increases in risk: the cumulative effect of a 1 °C rise in temperature above the threshold was 0.2% (-2.1% to 2.5%) by the end of the third day after exposure. CONCLUSIONS: Higher ambient temperatures above a threshold of 20 °C seem to be associated with a transiently increased risk of myocardial infarction 1-6 hours after exposure. Reductions in risk at longer lags are consistent with heat triggering myocardial infarctions early in highly vulnerable people who would otherwise have had a myocardial infarction some time later ("short term displacement"). Policies aimed at reducing the health effects of hot weather should include consideration of effects operating at sub-daily timescales

The Excess Winter Deaths Measure: Why Its Use Is Misleading for Public Health Understanding of Cold-related Health Impacts.

BACKGROUND: Excess winter deaths, the ratio between average daily deaths in December-March versus other months, is a measure commonly used by public health practitioners and analysts to assess health burdens associated with wintertime weather. We seek to demonstrate that this measure is fundamentally biased and can lead to misleading conclusions about health impacts associated with current and future winter climate. METHODS: Time series regression analysis of 779,372 deaths from natural causes in London over 15 years (1 August 1997-31 July 2012),collapsed by day of death and linked to daily temperature values. The outcome measures were the excess winter deaths index, and daily and annual deaths attributable specifically to cold. RESULTS: Most of the excess winter deaths are driven by cold: The excess winter deaths index decreased from 1.19 to 1.07 after excluding deaths attributable to low temperatures. Over 40% of cold-attributable deaths occurred outside of the December-March period, leading to bias in the excess winter deaths measure. Although there was no relationship between winter severity and annual excess winter deaths, there was a clear correlation with annual cold-attributable deaths. CONCLUSIONS: Excess winter deaths is not an appropriate indicator of cold-related health impacts, and its use should be discontinued. We advocate alternative measures. The findings we present bring into doubt previous claims that cold-related deaths in the UK will not reduce in future as a result of climate change

Comparative assessment of the effects of climate change on heat- and cold-related mortality in the United Kingdom and Australia.

BACKGROUND: High and low ambient temperatures are associated with increased mortality in temperate and subtropical climates. Temperature-related mortality patterns are expected to change throughout this century because of climate change. OBJECTIVES: We compared mortality associated with heat and cold in UK regions and Australian cities for current and projected climates and populations. METHODS: Time-series regression analyses were carried out on daily mortality in relation to ambient temperatures for UK regions and Australian cities to estimate relative risk functions for heat and cold and variations in risk parameters by age. Excess deaths due to heat and cold were estimated for future climates. RESULTS: In UK regions, cold-related mortality currently accounts for more than one order of magnitude more deaths than heat-related mortality (around 61 and 3 deaths per 100,000 population per year, respectively). In Australian cities, approximately 33 and 2 deaths per 100,000 population are associated every year with cold and heat, respectively. Although cold-related mortality is projected to decrease due to climate change to approximately 42 and 19 deaths per 100,000 population per year in UK regions and Australian cities, heat-related mortality is projected to increase to around 9 and 8 deaths per 100,000 population per year, respectively, by the 2080s, assuming no changes in susceptibility and structure of the population. CONCLUSIONS: Projected changes in climate are likely to lead to an increase in heat-related mortality in the United Kingdom and Australia over this century, but also to a decrease in cold-related deaths. Future temperature-related mortality will be amplified by aging populations. Health protection from hot weather will become increasingly necessary in both countries, while protection from cold weather will be still needed

Early-Life Air Pollution Exposure, Neighborhood Poverty, and Childhood Asthma in the United States, 1990⁻2014.

Ambient air pollution is a well-known risk factor of various asthma-related outcomes, however, past research has often focused on acute exacerbations rather than asthma development. This study draws on a population-based, multigenerational panel dataset from the United States to assess the association of childhood asthma risk with census block-level, annual-average air pollution exposure measured during the prenatal and early postnatal periods, as well as effect modification by neighborhood poverty. Findings suggest that early-life exposures to nitrogen dioxide (NO₂), a marker of traffic-related pollution, and fine particulate matter (PM2.5), a mixture of industrial and other pollutants, are positively associated with subsequent childhood asthma diagnosis (OR = 1.25, 95% CI = 1.10⁻1.41 and OR = 1.25, 95% CI = 1.06⁻1.46, respectively, per interquartile range (IQR) increase in each pollutant (NO₂ IQR = 8.51 ppb and PM2.5 IQR = 4.43 µ/m³)). These effects are modified by early-life neighborhood poverty exposure, with no or weaker effects in moderate- and low- (versus high-) poverty areas. This work underscores the importance of a holistic, developmental approach to elucidating the interplay of social and environmental contexts that may create conditions for racial-ethnic and socioeconomic disparities in childhood asthma risk

The Effects of Temperature on Accident and Emergency Department Attendances in London: A Time-Series Regression Analysis.

The epidemiological research relating mortality and hospital admissions to ambient temperature is well established. However, less is known about the effect temperature has on Accident and Emergency (A&E) department attendances. Time-series regression analyses were conducted to investigate the effect of temperature for a range of cause- and age-specific attendances in Greater London (LD) between 2007 to 2012. A seasonally adjusted Poisson regression model was used to estimate the percent change in daily attendances per 1 °C increase in temperature. The risk of overall attendance increased by 1.0% (95% CI 0.8, 1.4) for all ages and 1.4% (1.2, 1.5) among 0- to 15-year-olds. A smaller but significant increase in risk was found for cardiac, respiratory, cerebrovascular and psychiatric presentations. Importantly, for fracture-related attendances, the risk rose by 1.1% (0.7, 1.5) per 1 °C increase in temperature above the identified temperature threshold of 16 °C, with the highest increase of 2.1% (1.5, 3.0) seen among 0- to 15-year-olds. There is a positive association between increasing temperatures and A&E department attendance, with the risk appearing highest in children and the most deprived areas. A&E departments are vulnerable to increased demand during hot weather and therefore need to be adequately prepared to address associated health risks posed by climate change

The effects of hourly differences in air pollution on the risk of myocardial infarction: case crossover analysis of the MINAP database.

OBJECTIVES: To investigate associations between air pollution levels and myocardial infarction (MI) on short timescales, with data at an hourly temporal resolution. DESIGN: Time stratified case crossover study linking clinical data from the Myocardial Ischaemia National Audit Project (MINAP) with PM(10), ozone, CO, NO(2), and SO(2) data from the UK National Air Quality Archive. Pollution effects were investigated with delays (lags) of 1-6, 7-12, 13-18, 19-24, and 25-72 hours in both single and multi-pollutant models, adjusted for ambient temperature, relative humidity, circulating levels of influenza and respiratory syncytial virus, day of week, holidays, and residual seasonality within calendar month strata. SETTING: Population based study in 15 conurbations in England and Wales. SUBJECTS: 79,288 diagnoses of myocardial infarction recorded over the period 2003-6. MAIN OUTCOME MEASURES: Excess risk of myocardial infarction per 10 µg/m(3) increase in pollutant level. RESULTS: In single pollutant models, PM(10) and NO(2) levels were associated with a very short term increase in risk of myocardial infarction 1-6 hours later (excess risks 1.2% (95% confidence interval 0.3 to 2.1) and 1.1% (0.3 to 1.8) respectively per 10 μg/m(3) increase); the effects persisted in multi-pollutant models, though with only weak evidence of an independent PM(10) effect (P = 0.05). The immediate risk increases were followed by reductions in risk at longer lags: we found no evidence of any net excess risk associated with the five pollutants studied over a 72 hour period after exposure. CONCLUSIONS: Higher levels of PM(10) and NO(2), which are typically markers of traffic related pollution, seem to be associated with transiently increased risk of myocardial infarction 1-6 hours after exposure, but later reductions in risk suggest that air pollution may be associated with bringing events forward in time ("short-term displacement") rather than increasing overall risk. The well established effect of air pollution on cardiorespiratory mortality may not be mediated through increasing the acute risk of myocardial infarction, but through another mechanism