Aims: To investigate the lagged effects of cold temperature on cardiorespiratory mortality and to determine whether ''wind chill'' is a better predictor of these effects than ''dry bulb'' temperature. Methods: Generalised linear Poisson regression models were used to investigate the relation between mortality and ''dry bulb'' and ''wind chill'' temperatures in the three largest Scottish cities (Glasgow, Edinburgh, and Aberdeen) between January 1981 and December 2001. Effects of temperature on mortality (lags up to one month) were quantified. Analyses were conducted for the whole year and by season (cool and warm seasons). Main results: Temperature was a significant predictor of mortality with the strongest association observed between temperature and respiratory mortality. There was a non-linear association between mortality and temperature. Mortality increased as temperatures fell throughout the range, but the rate of increase was steeper at temperatures below 11˚C. The association between temperature and mortality persisted at lag periods beyond two weeks but the effect size generally decreased with increasing lag. For temperatures below 11˚C, a 1˚C drop in the daytime mean temperature on any one day was associated with an increase in mortality of 2.9% (95% CI 2.5 to 3.4), 3.4% (95% CI 2.6 to 4.1), 4.8% (95% CI 3.5 to 6.2) and 1.7% (95% CI 1.0 to 2.4) over the following month for all cause, cardiovascular, respiratory, and ''other'' cause mortality respectively. The effect of temperature on mortality was not observed to be significantly modified by season. There was little indication that ''wind chill'' temperature was a better predictor of mortality than ''dry bulb'' temperature. Conclusions: Exposure to cold temperature is an important public health problem in Scotland, particularly for those dying from respiratory disease. M ortality rates for cardiovascular and respiratory disease typically exhibit distinct seasonal variation with the highest rates occurring in the winter months.1 For Scotland, the percentage summer to winter difference in weekly all cause mortality rates is estimated to be in the order of 30%.2 The main factor considered to be influencing the observed seasonal pattern is the relation between mortality and temperature. The association between low temperature and increased morbidity and mortality is well recognised.3 4 What is less clear is the exact nature of the relation. Research has shown that the effect of temperature on mortality can exhibit significant variation from region to region. 5 6 For example, some studies have reported a U or V-shaped relation between temperature and mortality with the maximum number of deaths occurring at each end of the temperature scale 7 8 whereas others have reported a more linear or reverse J-shaped relation, with mortality typically increasing as temperature drops.

URL: http://www.clinicaltrials.gov. Unique identifier: NCT00120003.

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Objectives-To examine possible associations between daily concentrations of urban air pollutants and hospital emergency admissions and mortality due to cardiac and pulmonary disease. Methods-A time series study was conducted in the City of Edinburgh, which has a population of about 450 000. Poisson log linear regression models were used to investigate the relation of the daily event rate with daily air pollution concentrations of sulphur dioxide (SO 2 ) and black smoke from 1981 to 1995, and of nitrogen dioxide (NO 2 ), ozone (O 3 ), carbon monoxide (CO), and particulate matter (PM 10 ) from 1992 to 1995. Adjustments were made for seasonal and weekday variation, daily temperature, and wind speed. Results-The most significant findings were positive associations over the period 1981-95 between black smoke as a mean of the previous three days and daily all cause mortality in people aged >65, and respiratory mortality also in this age group (3.9% increase in mortality for a 10 µg/m 3 increment in black smoke). For hospital emergency admissions between 1992 and 1995 the two most significant findings (p<0.05) were for cardiovascular admissions of people aged >65 which showed a positive association with PM 10 as a mean of the 3 previous days, and a negative association with O 3 as a mean of the previous three days. Analyses of outcomes based on linkage with previous cardiorespiratory emergency admissions did not show substantially diVerent results. Conclusion-These data suggest that in the City of Edinburgh, after correction for confounders, there was a small but significant association between concentrations of black smoke and respiratory mortality in the older age group, probably attributable to higher pollution levels in the early part of the study period. There were also generally weak and variable associations between day to day changes in concentrations of urban air pollutants at a single central point and emergency hospital admission rates from cardiac and respiratory disease. (Occup Environ Med 1998;55:697-704)

Objectives: To determine whether the effect of black smoke on cardiorespiratory mortality is modified by cold temperatures. Methods: Poisson regression models were used to investigate the relationship between lagged black smoke concentration and daily mortality, and whether the effect of black smoke on mortality was modified by cold temperature for three Scottish cities from January 1981 to December 2001.Main results: For all-cause respiratory and noncardiorespiratory mortality, there was a significant association between mortality and lagged black smoke concentration. Generally the maximum black smoke effect occurred at lag 0, although these estimates were not statistically significant. A 10 mgm 23 increase in the daily mean black smoke concentration on any given day was associated with a 1.68% (95% CI 0.72 to 2.65) increase in all-cause mortality and a 0.43% (95% CI 20.97 to 1.86), 5.36% (95% CI 2.93 to 7.84) and 2.13% (95% CI 0.82 to 3.47) increase in cardiovascular, respiratory and noncardiorespiratory mortality, respectively, over the ensuing 30-day period. The effect of black smoke on mortality did not vary significantly between seasons (cool and warm periods). For all-cause, cardiovascular and non-cardiorespiratory mortality the inclusion of interaction terms did not improve the models, although for all-cause and noncardiorespiratory mortality there was a suggestion for interaction between temperature and recent black smoke exposure. Conclusions: The results of this study suggested a greater effect of black smoke on mortality at low temperatures. Since extremes of cold and particulate pollution may coexist, for example during temperature inversion, these results may have important public health implications.

Background: Air pollution–mortality risk estimates are generally larger at longer-term, compared with short-term, exposure time scales.Objective: We compared associations between short-term exposure to black smoke (BS) and mortality with long-term exposure–mortality associations in cohort participants and with short-term exposure–mortality associations in the general population from which the cohorts were selected.Methods: We assessed short-to-medium–term exposure–mortality associations in the Renfrew–Paisley and Collaborative cohorts (using nested case–control data sets), and compared them with long-term exposure–mortality associations (using a multilevel spatiotemporal exposure model and survival analyses) and short-to-medium–term exposure–mortality associations in the general population (using time-series analyses).Results: For the Renfrew–Paisley cohort (15,331 participants), BS exposure–mortality associations were observed in nested case–control analyses that accounted for spatial variations in pollution exposure and individual-level risk factors. These cohort-based associations were consistently greater than associations estimated in time-series analyses using a single monitoring site to represent general population exposure {e.g., 1.8% [95% confidence interval (CI): 0.1, 3.4%] vs. 0.2% (95% CI: 0.0, 0.4%) increases in mortality associated with 10-μg/m3 increases in 3-day lag BS, respectively}. Exposure–mortality associations were of larger magnitude for longer exposure periods [e.g., 3.4% (95% CI: –0.7, 7.7%) and 0.9% (95% CI: 0.3, 1.5%) increases in all-cause mortality associated with 10-μg/m3 increases in 31-day BS in case–control and time-series analyses, respectively; and 10% (95% CI: 4, 17%) increase in all-cause mortality associated with a 10-μg/m3 increase in geometic mean BS for 1970–1979, in survival analysis].Conclusions: After adjusting for individual-level exposure and potential confounders, short-term exposure–mortality associations in cohort participants were of greater magnitude than in comparable general population time-series study analyses. However, short-term exposure–mortality associations were substantially lower than equivalent long-term associations, which is consistent with the possibility of larger, more persistent cumulative effects from long-term exposures.

In patients complying with treatment as per protocol, CR oxycodone⁄CR naloxone was effective for the management of chronic low back pain of moderate or severe intensity.

Background: The recommended maximum age and time window for intravenous alteplase treatment of acute ischemic stroke differs between the Europe Union and United States. Aims:We compared the effects of alteplase in cohorts defined by the current Europe Union or United States marketing approval labels, and by hypothetical revisions of the labels that would remove the Europe Union upper age limit or extend the United States treatment time window to 4.5 h. Methods: We assessed outcomes in an individual-patient-data meta-analysis of eight randomized trials of intravenous alteplase (0.9 mg/kg) versus control for acute ischemic stroke. Outcomes included: excellent outcome (modified Rankin score 0-1) at 3-6 months, the distribution of modified Rankin score, symptomatic intracerebral hemorrhage, and 90-day mortality.Results: Alteplase increased the odds of modified Rankin score 0-1 among 2449/6136 (40%) patients who met the current European Union label and 3491 (57%) patients who met the age-revised label (odds ratio 1.42, 95% CI 1.21À1.68 and 1.43, 1.23À1.65, respectively), but not in those outside the age-revised label (1.06, 0.90À1.26). By 90 days, there was no increased mortality in the current and age-revised cohorts (hazard ratios 0.98, 95% CI 0.76À1.25 and 1.01, 0.86-1.19, respectively) but mortality remained higher outside the age-revised label (1.19, 0.99-1.42). Similarly, alteplase increased the odds of modified Rankin score 0-1 among 1174/6136 (19%) patients who met the current US approval and 3326 (54%) who met a 4.5-h revised approval (odds ratio 1.55, 1.19À2.01 and 1.37, 1.17À1.59, respectively), but not for those outside the 4.5-h revised approval (1.14, 0.97À1.34). By 90 days, no increased mortality remained for the current and 4.5-h revised label cohorts (hazard ratios 0.99, 0.77À1.26 and 1.02, 0.87-1.20, respectively) but mortality remained higher outside the 4.5-h revised approval (1.17, 0.98-1.41).Conclusions: An age-revised European Union label or 4.5-h-revised United States label would each increase the number of patients deriving net benefit from alteplase by 90 days after acute ischemic stroke, without excess mortality.