Population aging increases the need for knowledge on positive aspects of aging, and contributions of older people to their own wellbeing and that of others. We defined active aging as an individual's striving for elements of wellbeing with activities as per their goals, abilities and opportunities. This study examines associations of health, health behaviors, health literacy and functional abilities, environmental and social support with active aging and wellbeing. We will develop and validate assessment methods for physical activity and physical resilience suitable for research on older people, and examine their associations with active aging and wellbeing. We will examine cohort effects on functional phenotypes underlying active aging and disability.
For this population-based study, we plan to recruit 1000 participants aged 75, 80 or 85 years living in central Finland, by drawing personal details from the population register. Participants are interviewed on active aging, wellbeing, disability, environmental and social support, mobility, health behavior and health literacy. Physical activity and heart rate are monitored for 7 days with wearable sensors. Functional tests include hearing, vision, muscle strength, reaction time, exercise tolerance, mobility, and cognitive performance. Clinical examination by a nurse and physician includes an electrocardiogram, tests of blood pressure, orthostatic regulation, arterial stiffness, and lung function, as well as a review of chronic and acute conditions and prescribed medications. C-reactive protein, small blood count, cholesterol and vitamin D are analyzed from blood samples. Associations of factors potentially underlying active aging and wellbeing will be studied using multivariate methods. Cohort effects will be studied by comparing test results of physical and cognitive functioning with results of a cohort examined in 1989-90.
The current study will renew research on positive gerontology through the novel approach to active aging and by suggesting new biomarkers of resilience and active aging. Therefore, high interdisciplinary impact is expected. This cross-sectional study will not provide knowledge on temporal order of events or causality, but an innovative cross-sectional dataset provides opportunities for emergence of novel creative hypotheses and theories.
Existing studies of the association between air pollution, aeroallergens and emergency department (ED) visits have generally examined the effects of a few pollutants or aeroallergens on individual conditions such as asthma or chronic obstructive pulmonary disease. In this study, we considered a wide variety of respiratory and cardiac conditions and an extensive set of pollutants and aeroallergens, and utilized prospectively collected information on possible effect modifiers which would not normally be available from purely administrative data. The association between air pollution, aeroallergens and cardiorespiratory ED visits (n = 19,821) was examined for the period 1992 to 1996 using generalized additive models. ED visit, air pollution and aeroallergen time series were prefiltered using LOESS smoothers to minimize temporal confounding, and a parsimonious model was constructed to control for confounding by weather and day of week. Multipollutant and multi-aeroallergen models were constructed using stepwise procedures and sensitivity analyses were conducted by season, diagnosis, and selected individual characteristics or effect modifiers. In single-pollutant models, positive effects of all pollutants but NO2 and COH were observed on asthma visits, and positive effects on all respiratory diagnosis groups were observed for O3, SO2, PM10, PM2.5, and SO4(2-). Among cardiac conditions, only dysrhythmia visits were positively associated with all measures of particulate matter. In the final year-round multipollutant models, a 20.9% increase in cardiac ED visits was attributed to the combination of O3 (16.0%, 95% CI 2.8-30.9) and SO2 (4.9%, 95%CI 1.7-8.2) at the mean concentration of each pollutant. In the final multipollutant model for respiratory visits, O3 accounted for 3.9% of visits (95% CI 0.8-7.2), and SO2 for 3.7% (95% CI 1.5-6.0), whereas a weak, negative association was observed with NO2. In multi-aeroallergen models of warm season asthma ED visits, Ascomycetes, Alternaria and small round fungal spores accounted for 4.5% (95% CI 1.8-7.4), 4.7% (95% CI 1.0-8.6) and 3.0% (95% CI 0.8-5.1), respectively, of visits at their mean concentrations, and these effects were not sensitive to adjustment for air pollution effects. In conclusion, we observed a significant influence of the air pollution mix on cardiac and respiratory ED visits. Although in single-pollutant models, positive associations were noted between ED visits and some measures of particulate matter, in multipollutant models, pollutant gases, particularly ozone, exhibited more consistent effects. Aeroallergens were also significantly associated with warm season asthma ED visits.
This study was designed to examine differences in the respiratory health status of preadolescent school children, aged 7-11 years, who resided in 10 rural Canadian communities areas of moderate and low exposure to regional sulfate and ozone pollution. Five of the communities were located in central Saskatchewan, a low-exposure region, and five were located in southwestern Ontario, an area with moderately elevated exposures resulting from long-range atmospheric transport of polluted air masses. In this cross-sectional study, the child's respiratory symptoms and illness history were evaluated using a parent-completed questionnaire, administered in September 1985. Respiratory function was assessed once for each child in the schools between October 1985 and March 1986, by the measurement of pulmonary function for forced vital capacity (FVC), forced expiratory volume in 1 sec (FEV1.0), peak expiratory flow rate (PEFR), mean forced expiratory flow rate during the middle half of the FVC curve (FEF25-75), and maximal expiratory flow at 50% of the expired vital capacity (V50max). The 1986 annual mean of the 1-hr daily maxima of ozone was higher in Ontario (46.3 ppb) than in Saskatchewan (34.1 ppb), with 90th percentile concentrations of 80 ppb in Ontario and 47 ppb in Saskatchewan. Summertime 1-hr daily maxima means were 69.0 ppb in Ontario and 36.1 ppb in Saskatchewan. Annual mean and 90th percentile concentrations of inhalable sulfates were three times higher in Ontario than in Saskatchewan; there were no significant differences in levels of inhalable particles (PM10) or particulate nitrates. Levels of sulfur dioxide (SO2) and nitrogen dioxide (NO2) were low in both regions. After controlling for the effects of age, sex, parental smoking, parental education, and gas cooking, no significant regional differences were observed in rates of chronic cough or phlegm, persistent wheeze, current asthma, bronchitis in the past year, or any chest illness that kept the child at home for 3 or more consecutive days during the previous year. Children living in southwestern Ontario had statistically significant (P 0.05).
We examined the role that ambient air pollution plays in exacerbating cardiac disease by relating daily fluctuations in admissions to 134 hospitals for congestive heart failure in the elderly to daily variations in ambient concentrations of carbon monoxide, nitrogen dioxide, sulfur dioxide, ozone, and the coefficient of haze in Canada's 10 largest cities for the 11-year period 1981-1991 inclusive. We adjusted the hospitalization time series for seasonal, subseasonal, and weekly cycles and for hospital usage patterns. The logarithm of the daily high-hour ambient carbon monoxide concentration recorded on the day of admission displayed the strongest and most consistent association with hospitalization rates among the pollutants, after stratifying the time series by month of year and adjusting simultaneously for temperature, dew point, and the other ambient air pollutants. The relative risk for a change from 1 ppm to 3 ppm, the 25th and 75th percentiles of the exposure distribution, was 1.065 (95% confidence interval = 1.028-1.104). The regression coefficients of the other air pollutants were much more sensitive to simultaneous adjustment for either multiple pollutant or weather model specifications.
This study was undertaken to determine whether variations in concentrations of particulates in the ambient air of Montreal, Quebec, during the period 1984 to 1993, were associated with daily variations in cause-specific daily mortality. Fixed-site air pollution monitors in Montreal provided daily mean levels of various measures of particles and gaseous pollutants. Total sulfate was also measured daily (1986-1993) at a monitoring station 150 km southeast of the city (Sutton, Quebec). We used coefficient of haze (COH), extinction coefficient, and sulfate from the Sutton station to predict fine particles and sulfate from fine particles for days that were missing. We estimated associations between cause-specific mortality and PM(2.5), PM(10), predicted fine particles and fine sulfate particles, total suspended particles, coefficient of haze, extinction coefficient, and total sulfate measured at the Sutton station. We selected a set of underlying causes of death, as recorded on the death certificates, as the endpoint and then regressed the logarithm of daily counts of cause-specific mortality on the daily mean levels for the above measures of particulates, after accounting for seasonal and subseasonal fluctuations in the mortality time series, non-Poisson dispersion, weather variables, and gaseous pollutants. We found positive and statistically significant associations between the daily measures of ambient particle mass and sulfate mass and the deaths from respiratory diseases and diabetes. The mean percentage change in daily mortality (MPC), evaluated at the interquartile range for pollutants averaged over the day of death and the preceding 2 days, for deaths from respiratory diseases was MPC(COH)=6.90% (95% CI: 3.69-10.21%), MPC(Predicted PM2.5)= 9.03% (95% CI: 5.83- 12.33%), and MPC(Sutton sulfate)=4.64% (95% CI: 2.46-6.86%). For diabetes, the corresponding estimates were MPC(COH)=7.50% (95% CI: 1.96-13.34%), MPC(Predicted PM2.5)=7.59% (95% CI: 2.36-13.09%), and MPC(Sutton sulfate)=4.48% (95% CI: 1.08-7.99%). Among individuals older than 65 years at time of death, we found consistent associations across our metrics of particles for neoplasms and coronary artery diseases. Associations with sulfate mass were also found among elderly persons who died of cardiovascular diseases and of lung cancer. These associations were consistent with linear relationships. The associations found for respiratory diseases and for cardiovascular diseases, especially in the elderly, are in line with some of the current hypotheses regarding mechanisms by which ambient particles may increase daily mortality. The positive associations found for cancer and for diabetes may be understood through a general hypothesis proposed by Frank and Tankersley, who suggested that persons in failing health may be at higher risk for external insults through the failure of regulating physiological set points. The association with diabetes may be interpreted in light of recent toxicological findings that inhalation of urban particles in animals increases blood pressure and plasmatic levels of endothelins that enhance vasoconstriction and alter electrophysiology. Further research to confirm these findings and to determine whether they are causal is warranted.
To clarify the health effects of ozone exposure in young children, the authors studied the association between air pollution and hospital admissions for acute respiratory problems in children less than 2 years of age during the 15-year period from 1980 to 1994 in Toronto, Canada. The daily time series of admissions was adjusted for the influences of day of the week, season, and weather. A 35% (95% confidence interval: 19%, 52%) increase in the daily hospitalization rate for respiratory problems was associated with a 5-day moving average of the daily 1-hour maximum ozone concentration of 45 parts per billion, the May-August average value. The ozone effect persisted after adjustment for other ambient air pollutants or weather variables. Ozone was not associated with hospital admissions during the September-April period. Ambient ozone levels in the summertime should be considered a risk factor for respiratory problems in children less than 2 years of age.
The effects of tropospheric ozone on lung function and respiratory symptoms have been well documented at relatively high concentrations. However, previous investigations have failed to establish a clear association between tropospheric ozone and respiratory diseases severe enough to require hospitalization after controlling for climate, and with gaseous and particulate air pollution at the lower concentrations typically observed in Canada today. To determine if low levels of tropospheric ozone contribute to hospitalization for respiratory disease, air pollution data were compared to hospital admissions for 16 cities across Canada representing 12.6 million people. During the 3927-day period from April 1, 1981, to December 31, 1991, there were 720,519 admissions for which the principle diagnosis was a respiratory disease. After controlling for sulfur dioxide, nitrogen dioxide, carbon monoxide, soiling index, and dew point temperature, the daily high hour concentration of ozone recorded 1 day previous to the date of admission was positively associated with respiratory admissions in the April to December period but not in the winter months. The relative risk for a 30 ppb increase in ozone varied from 1.043 (P
Although some consensus has emerged among the scientific and regulatory communities that the urban ambient atmospheric mix of combustion related pollutants is a determinant of population health, the relative toxicity of the chemical and physical components of this complex mixture remains unclear. Daily mortality rates and concurrent data on size-fractionated particulate mass and gaseous pollutants were obtained in eight of Canada's largest cities from 1986 to 1996 inclusive in order to examine the relative toxicity of the components of the mixture of ambient air pollutants to which Canadians are exposed. Positive and statistically significant associations were observed between daily variations in both gas- and particulate-phase pollution and daily fluctuations in mortality rates. The association between air pollution and mortality could not be explained by temporal variation in either mortality rates or weather factors. Fine particulate mass (less than 2.5 microns in average aerometric diameter) was a stronger predictor of mortality than coarse mass (between 2.5 and 10 microns). Size-fractionated particulate mass explained 28% of the total health effect of the mixture, with the remaining effects accounted for by the gases. Forty-seven elemental concentrations were obtained for the fine and coarse fraction using nondestructive x-ray fluorescence techniques. Sulfate concentrations were obtained by ion chromatography. Sulfate ion, iron, nickel, and zinc from the fine fraction were most strongly associated with mortality. The total effect of these four components was greater than that for fine mass alone, suggesting that the characteristics of the complex chemical mixture in the fine fraction may be a better predictor of mortality than mass alone. However, the variation in the effects of the constituents of the fine fraction between cities was greater than the variation in the mass effect, implying that there are additional toxic components of fine particulate matter not examined in this study whose concentrations and effects vary between locations. One of these components, carbon, represents half the mass of fine particulate matter. We recommend that measurements of elemental and organic carbon be undertaken in Canadian urban environments to examine their potential effects on human health.
Indices of atmospheric particulate matter (PM) have been reported to be associated with daily mortality and morbidity in a large number of recent time-series studies. However, the question remains as to which components of PM are responsible for the reported associations. Multiple PM components rarely are measured simultaneously. To investigate PM effects on mortality and morbidity, we used the multiple PM components measured in Windsor, Ontario, at a site only a few miles from downtown Detroit, Michigan. This study focused primarily on two study periods in which multiple PM components were measured in Windsor: 1985 to 1990, when levels of total suspended particles (TSP), sulfate from TSP (TSP-SO4(2-)), PM less than 10 microns in diameter (PM10), and nonthoracic TSP (TSP-PM10) were measured throughout the year; and 1992 to 1994, when data on PM10, PM2.5 (PM less than 2.5 microns in diameter), PM10-2.5 (PM10 minus PM2.5), particle acidity (H+), and artifact-free sulfates (SO4(2-)) were available for mostly summer months. Mortality data were analyzed for the 1985 to 1990 study period, and data on both mortality and hospital admissions of elderly patients were analyzed for the 1992 through 1994 period. Poisson regressions were used to estimate the effects of these PM components and gaseous criteria pollutants on mortality (nonaccidental, circulatory, respiratory, and nonaccidental without circulatory and respiratory) and on hospital admissions of elderly patients (for pneumonia, chronic obstructive pulmonary disease [COPD], ischemic heart disease, dysrhythmias, heart failure, and stroke), adjusting for temperature and humidity, trends and seasonal cycles, and day of the week. Both PM10 and TSP were associated significantly with respiratory mortality for the 1985 to 1990 period, with similar relative risk (RR) estimates for PM10 (RR = 1.123; 95% confidence interval [CI] 1.0361-1.218) and TSP (RR = 1.109; 95% CI 1.028-1.197), per 5th to 95th percentile increment. The effect-size estimates for TSP-SO4(2-) and TSP-PM10 were smaller and less significant. In two-pollutant models, simultaneous inclusion of gaseous pollutants with PM10 or TSP reduced PM coefficients by 0 to 34%. The effect-size estimates for total mortality, circulatory mortality, and total minus circulatory and respiratory mortality were less than those for respiratory mortality. Ozone (O3) and nitrogen dioxide (NO2) also were associated significantly with total and circulatory mortality, but a simultaneous consideration of these pollutants with PM10 reduced PM10 coefficients only slightly, or even increased them. In these results, pollution coefficients often were positive at multiple lag days (0-day through 3-day lags were examined), but for PM indices, 1-day lag coefficients were most significant. However, when all combinations of multiple-day average exposures were examined, for cases in which multiple lag days were positive, the choice of single-day or multiple-day average exposure did not appreciably change the estimated effect sizes. An examination of temporal correlation showed that the order of spatial uniformity as expressed by the median site-to-site correlation was O3 (0.83), PM10 (0.78), TSP (0.71), NO2 (0.70), carbon monoxide (CO) (0.50), and sulfur dioxide (SO2) (0.49), which suggests less exposure error for O3 and PM10 than for the other measured pollutants. Thus, these results suggest that spatially homogeneous pollution indices show higher associations with measured health outcomes.
The association of daily cardiac and respiratory admissions to 168 acute care hospitals in Ontario, Canada, with daily levels of particulate sulfates was examined over the 6-year period 1983-1988. Sulfate levels were recorded at nine monitoring stations in regions of southern and central Ontario spanned by three monitoring networks. A 13-micrograms/m3 increase in sulfates recorded on the day prior to admission (the 95th percentile) was associated with a 3.7% (p
To profile participants based on reported outdoor physical activity barriers using a data-driven approach, describe the profiles and study their association with unmet physical activity need.
Cross-sectional analyses of 848 community-dwelling men and women aged 75-90 living in Central Finland in 2012. Barriers to outdoor physical activity and unmet physical activity need were enquired with a questionnaire. The latent profiles were identified by profiling participants into latent groups using a mixture modeling technique on the multivariate set of indicators of outdoor physical activity barriers. A path model was used to study the associations of the profiles with unmet physical activity need.
Five barrier profiles were identified. Profile A was characterized with minor barriers, profile B with weather barriers, profile C with health and weather barriers, profile D with barriers concerning insecurity, health and weather; and profile E with mobility and health barriers. The participants in the profiles differed in the proportion of individual and environmental barriers. The risk for unmet physical activity need was highest among people whose severe mobility difficulties restricted their outdoor physical activity.
Outdoor physical activity barriers reflect the imbalance in person-environment fit among older people, manifested as unmet physical activity need.
In older adults, mobility limitations often coexist with overweight or obesity, suggesting that similar factors may underlie both traits. This study examined the extent to which genetic and environmental influences explain the association between adiposity and mobility in older women. Body fat percentage (bioimpedance test), walking speed over 10 m, and distance walked in a 6-min test were evaluated in 92 monozygotic (MZ) and 104 dizygotic (DZ) pairs of twin sisters reared together, aged 63-76 years. Genetic and environmental influences on each trait were estimated using age-adjusted multivariate genetic modeling. The analyses showed that the means (and s.d.) for body fat percentage, walking speed, and walking endurance were 33.2+/-7.3%, 1.7+/-0.3 m/s and 529.7+/-75.4 m, respectively. The phenotypic correlation between adiposity and walking speed was -0.32 and between adiposity and endurance it was -0.33. Genetic influences explained 80% of the association between adiposity and speed, and 65% of adiposity and walking endurance. Cross-trait genetic influences accounted for 12% of the variability in adiposity, 56% in walking speed, and 34% in endurance. Trait-specific genetic influences were also detected for adiposity (54%) and walking endurance (13%), but not speed. In conclusion, among community-living older women, an inverse association was found between adiposity and mobility that was mostly due to the effect of shared genes. This result suggests that the identification of genetic variants for body fat metabolism may also provide understanding of the development of mobility limitations in older women.
The aim of this study was to analyze whether the associations between perceived environmental and individual characteristics and perceived walking limitations in older people differ between those with intact and those with poorer lower extremity performance.
Persons aged 75 to 90 ( N = 834) participated in interviews and performance tests in their homes. Standard questionnaires were used to obtain walking difficulties; environmental barriers to and, facilitators of, mobility; and perceived individual hindrances to outdoor mobility. Lower extremity performance was tested using Short Physical Performance Battery (SPPB).
Among those with poorer lower extremity performance, the likelihood for advanced walking limitations was, in particular, related to perceived poor safety in the environment, and among those with intact performance to perceived social issues, such as lack of company, as well as to long distances.
The environmental correlates of walking limitations seem to depend on the level of lower extremity performance.
Assess associations between short-term exposure to gaseous pollutants and asthma hospitalisation among boys and girls 6 to12 years of age.
A bi-directional case-crossover analysis was used. Conditional logistic regression models were fitted to the data for boys and girls separately. Exposures averaged over periods ranging from one to seven days were used to assess the effects of gaseous pollutants on asthma hospitalisation. Estimated relative risks for asthma hospitalisation were calculated for an incremental exposure corresponding to the interquartile range in pollutant levels, adjusted for daily weather conditions and concomitant exposure to particulate matter.
Toronto, Ontario, Canada.
A total of 7319 asthma hospitalisations for children 6 to 12 years of age (4629 for boys and 2690 for girls) in Toronto between 1981 and 1993.
A significant acute effect of carbon monoxide on asthma hospitalisation was found in boys, and sulphur dioxide showed significant effects of prolonged exposure in girls. Nitrogen dioxide was positively associated with asthma admissions in both sexes. The lag time for certain gaseous pollutant effects seemed to be shorter in boys (around two to three days for carbon monoxide and nitrogen dioxide), as compared with girls (about six to seven days for sulphur dioxide and nitrogen dioxide). The effects of gaseous pollutants on asthma hospitalisation remained after adjustment of particulate matter. The data showed no association between ozone and asthma hospitalisation in children.
The study showed positive relations between gaseous pollutants (carbon monoxide, sulphur dioxide, and nitrogen dioxide) at comparatively low levels and asthma hospitalisation in children, using bi-directional case-crossover analyses. Though, the effects of certain specific gaseous pollutants were found to vary in boys and girls.
Cites: Environ Res. 1994 Oct;67(1):1-197925191
Cites: Environ Res. 1994 Apr;65(1):56-688162885
Cites: N Engl J Med. 1995 Jan 19;332(3):133-87800004
Cites: Environ Health Perspect. 1995 Mar;103 Suppl 2:97-1027614954
Cites: Epidemiology. 1995 Sep;6(5):476-848562622
Cites: Thorax. 1995 Oct;50(10):1051-67491552
Cites: Thorax. 1995 Sep;50(9):948-548539674
Cites: Thorax. 1995 Nov;50(11):1188-938553276
Cites: Thorax. 1996 Jan;51 Suppl 1:S3-68658385
Cites: Thorax. 1996 Jan;51(1):13-228658362
Cites: J Epidemiol Community Health. 1996 Apr;50 Suppl 1:S3-118758217
Cites: J Epidemiol Community Health. 1996 Apr;50 Suppl 1:s22-98758220
Cites: J Epidemiol Community Health. 1996 Apr;50 Suppl 1:s42-68758223
Cites: J Epidemiol Community Health. 1996 Apr;50 Suppl 1:s63-708758227
Cites: J Epidemiol Community Health. 1996 Apr;50 Suppl 1:s71-58758228
Cites: Environ Health Perspect. 1996 Dec;104(12):1354-609118879
Cites: Environ Health Perspect. 1997 Feb;105(2):216-229105797
Cites: Epidemiology. 1997 Mar;8(2):162-79229208
Cites: Thorax. 1997 Sep;52(9):760-59371204
Cites: J Expo Anal Environ Epidemiol. 1998 Apr-Jun;8(2):129-449577746
Cites: Biometrics. 1998 Jun;54(2):596-6059629646
Cites: J Air Waste Manag Assoc. 1998 Aug;48(8):689-7009739623
Cites: Am J Public Health. 1998 Dec;88(12):1761-69842371
Cites: Epidemiology. 1999 Jan;10(1):23-309888276
Cites: Health Rep. 1998 Winter;10(3):9-21 (ENG); 9-22 (FRE)9926344
Cites: Arch Environ Health. 1999 Mar-Apr;54(2):130-910094292
Cites: Environ Health Perspect. 1999 Jun;107(6):489-9310339450
Cites: Environ Health Perspect. 1999 Jun;107 Suppl 3:421-910423388
Cites: Environ Health Perspect. 1999 Aug;107(8):629-3110417359
Cites: Environ Health Perspect. 1999 Aug;107(8):633-610417360
Determine the risk of premature mortality due to the urban ambient air pollution mix in Canada.
The number of daily deaths for non-accidental causes were obtained in 11 cities from 1980 to 1991 and linked to concentrations of ambient gaseous air pollutants using relative risk regression models for longitudinal count data.
Nitrogen dioxide had the largest effect on mortality with a 4.1% increased risk (p
Comment In: Can J Public Health. 1998 Jul-Aug;89(4):228, 238, 240 passim9735513
To investigate the acute respiratory health effects of ambient air pollution, the number of emergency of urgent daily respiratory admissions to 168 acute care hospitals in Ontario were related to estimates of exposure to ozone and sulfates in the vicinity of each hospital. Ozone levels were obtained from 22 monitoring stations maintained by the Ontario Ministry of the Environment for the period January 1, 1983 to December 31, 1988. Daily levels of sulfates were recorded at nine monitoring stations representing three different networks operated by the Ontario Ministry of the Environment and Environment Canada. Positive and statistically significant associations were found between hospital admissions and both ozone and sulfates recorded on the day of admission and up to 3 days prior to the date of admission. Five percent of daily respiratory admissions in the months of May to August were associated with ozone, with sulfates accounting for an additional 1% of these admissions. Ozone was a stronger predictor of admissions than sulfates. Positive and statistically significant (P
We obtained data on daily numbers of admissions to hospital in Toronto, Canada, from 1980 to 1994 for respiratory, cardiac, cerebral vascular, and peripheral vascular diseases. We then linked the data to daily measures of particulate mass less than 10 microns in aerodynamic diameter (PM10), particulate mass less than 2.5 microns in aerodynamic diameter (PM2.5), and particulate mass between 2.5 and 10 microns in aerodynamic diameter (PM10-2.5), ozone, carbon monoxide, nitrogen dioxide, and sulfur dioxide. Air pollution was only associated weakly with hospitalization for cerebral vascular and peripheral vascular diseases. We controlled for temporal trends and climatic factors, and we found that increases of 10 microg/m3 in PM10, PM2.5, and PM10-2.5 were associated with 1.9%, 3.3%, and 2.9% respective increase in respiratory and cardiac hospital admissions. We further controlled for gaseous pollutants, and the percentages were reduced to 0.50%, 0.75%, and 0.77%, respectively. Of the 7.72 excess daily hospital admissions in Toronto attributable to the atmospheric pollution mix, 11.8% resulted from PM2.5, 8.2% to PM10-2.5, 17% to carbon monoxide, 40.4% to nitrogen dioxide, 2.8% to sulfur dioxide, and 19.8% to ozone.
Environmental barriers are associated with disability-related outcomes in older people but little is known of the effect of environmental barriers on mortality. The aim of this study was to examine whether objectively measured barriers in the outdoor, entrance and indoor environments are associated with mortality among community-dwelling 80- to 89-year-old single-living people.
This longitudinal study is based on a sample of 397 people who were single-living in ordinary housing in Sweden. Participants were interviewed during 2002-2003, and 393 were followed up for mortality until May 15, 2012.Environmental barriers and functional limitations were assessed with the Housing Enabler instrument, which is intended for objective assessments of Person-Environment (P-E) fit problems in housing and the immediate outdoor environment. Mortality data were gathered from the public national register. Cox regression models were used for the analyses.
A total of 264 (67%) participants died during follow-up. Functional limitations increased mortality risk. Among the specific environmental barriers that generate the most P-E fit problems, lack of handrails in stairs at entrances was associated with the highest mortality risk (adjusted RR 1.55, 95% CI 1.14-2.10), whereas the total number of environmental barriers at entrances and outdoors was not associated with mortality. A higher number of environmental barriers indoors showed a slight protective effect against mortality even after adjustment for functional limitations (RR 0.98, 95% CI 0.96-1.00).
Specific environmental problems may increase mortality risk among very-old single-living people. However, the association may be confounded by individuals' health status which is difficult to fully control for. Further studies are called for.
To study which individual characteristics and environmental factors correlate with fear of moving outdoors and whether fear of moving outdoors predicts development of mobility limitation.
Observational prospective cohort study and cross-sectional analyses.
Community and research center.
Seven hundred twenty-seven community-living people aged 75 to 81 were interviewed at baseline, of whom 314 took part in a 3.5-year follow-up.
Fear of moving outdoors and its potential individual and environmental correlates were assessed at baseline. Perceived difficulties in walking 0.5 km and 2 km were assessed twice a year over a 3.5-year period.
At baseline, 65% of the women and 29% of the men reported fear of moving outdoors. Poor socioeconomic status; musculoskeletal diseases; slow walking speed; and the presence of poor street conditions, hills in the nearby environment, and noisy traffic correlated with fear of moving outdoors. At the first 6-month follow-up, participants with fear of moving outdoors had more than four times the adjusted risk (odds ratio (OR)=4.6, 95% confidence interval (CI)=1.92-11.00) of developing difficulties in walking 0.5 km and a three times greater adjusted risk (OR=3.10, 95% CI=1.49-6.46) for developing difficulty in walking 2 km compared with those without fear. The difference in the prevalence of walking difficulties remained statistically significant over the 3.5-year follow-up (P=.02 and P=.009, respectively).
Fear of moving outdoors is common in older adults and increases the risk of developing self-reported difficulties in walking 0.5 km and 2 km. Knowledge about individual and environmental factors underlying fear of moving outdoors and finding ways to alleviate fear of moving outdoors are important for community planning and prevention of disability.
The aim of the present study was to examine the contribution of genetic and environmental factors to depressive symptoms among older women. The participants were 102 monozygotic and 115 dizygotic female twin pairs aged 64 to 76 years. Depressive symptoms were assessed by the Center for the Epidemiologic Studies Depression Scale. The contribution of genetic and environmental effects was estimated for the constructed depressiveness factor and for the subscales which were depressed mood, psychomotor retardation, lack of wellbeing and interpersonal difficulties. Of the variance in depressiveness, shared environmental influences accounted for 39% and nonshared environmental influences 61%. For the subscales, 24% to 62% of the variance was explained by individual, and 13% to 23% by shared, environmental factors. Lack of wellbeing had its own moderate additive genetic effect explaining 30% of the variance. This study showed that in older women predominantly environmental factors underlay individual differences in depressiveness; however, the factors varied to some extent between dimensions measured by the subscales.