The association of air pollution and depressed mood in 70,928 individuals from four European cohorts.

BACKGROUND: Exposure to ambient air pollution may be associated with impaired mental health, including depression. However, evidence originates mainly from animal studies and epidemiological studies in specific subgroups. We investigated the association between air pollution and depressed mood in four European general population cohorts. METHODS: Data were obtained from LifeLines (the Netherlands), KORA (Germany), HUNT (Norway), and FINRISK (Finland). Residential exposure to particles (PM2.5, PM2.5absorbance, PM10) and nitrogen dioxide (NO2) was estimated using land use regression (LUR) models developed for the European Study of Cohorts for Air Pollution Effects (ESCAPE) and using European wide LUR models. Depressed mood was assessed with interviews and questionnaires. Logistic regression analyses were used to investigate the cohort specific associations between air pollution and depressed mood. RESULTS: A total of 70,928 participants were included in our analyses. Depressed mood ranged from 1.6% (KORA) to 11.3% (FINRISK). Cohort specific associations of the air pollutants and depressed mood showed heterogeneous results. For example, positive associations were found for NO2 in LifeLines (odds ratio [OR]=1.34; 95% CI: 1.17, 1.53 per 10 µg/m(3) increase in NO2), whereas negative associations were found in HUNT (OR=0.79; 95% CI: 0.66, 0.94 per 10 µg/m(3) increase in NO2). CONCLUSIONS: Our analyses of four European general population cohorts found no consistent evidence for an association between ambient air pollution and depressed mood.

Hourly variation in fine particle exposure is associated with transiently increased risk of ST segment depression.

OBJECTIVES: To evaluate whether hourly changes in fine particle (PM(2.5), diameter<2.5 microm) exposure or outdoor particle concentrations are associated with rapid ischaemic responses. METHODS: 41 non-smoking elderly people with coronary heart disease were followed up with biweekly clinic visits in Helsinki, Finland. The occurrence of ST segment depressions >0.1 mV was recorded during submaximal exercise tests. Hourly variations in personal PM(2.5) exposure and outdoor levels of PM(2.5) and ultrafine particles (<0.1 microm) were recorded for 24 h before a clinic visit. Associations between particulate air pollution and ST segment depressions were evaluated using logistic regression. RESULTS: Both personal and outdoor PM(2.5) concentrations, but not outdoor ultrafine particle counts, were associated with ST segment depressions. The odds ratio (per 10 microg/m(3)) for personal PM(2.5) concentration during the hour preceding a clinic visit was 3.26 (95% CI 1.07 to 9.99) and for 4 h average outdoor PM(2.5) it was 2.47 (95% CI 1.05 to 5.85). CONCLUSIONS: Even very short-term elevations in fine particle exposure might increase the risk of myocardial ischaemia. The precise mechanism is still unknown but could involve changes in autonomic nervous control of the heart.

Urban air pollution, and asthma and COPD hospital emergency room visits.

BACKGROUND: There is little previous information of the effects of size fractioned particulate air pollution and source specific fine particles (PM(2.5); <2.5 microm) on asthma and chronic obstructive pulmonary disease (COPD) among children, adults and the elderly. OBJECTIVES: To determine the effects of daily variation in levels of different particle size fractions and gaseous pollutants on asthma and COPD by age group. METHODS: Levels of particulate air pollution, NO(2) and CO were measured from 1998 to 2004 at central outdoor monitoring sites in Helsinki, Finland. Associations between daily pollution levels and hospital emergency room visits were evaluated for asthma (ICD10: J45+J46) in children <15 years old, and for asthma and COPD (ICD10: J41+J44) in adults (15-64 years) and the elderly (>or=65 years). RESULTS: Three to 5 day lagged increases in asthma visits were found among children in association with nucleation (<0.03 microm), Aitken (0.03-0.1 microm) and accumulation (0.1-0.29 microm) mode particles, gaseous pollutants and traffic related PM(2.5) (7.8% (95% CI 3.5 to 12.3) for 1.1 microg/m(3) increase in traffic related PM(2.5) at lag 4). Pooled asthma-COPD visits among the elderly were associated with lag 0 of PM(2.5), coarse particles, gaseous pollutants and long range transported and traffic related PM(2.5) (3.9% (95% CI 0.28 to 7.7) at lag 0). Only accumulation mode and coarse particles were associated with asthma and COPD among adults. CONCLUSIONS: Among children, traffic related PM(2.5) had delayed effects, whereas among the elderly, several types of particles had effects that were more immediate. These findings suggest that the mechanisms of the respiratory effects of air pollution, and responsible pollutants, differ by age group.

Associations of traffic related air pollutants with hospitalisation for first acute myocardial infarction: the HEAPSS study.

BACKGROUND: Acute myocardial infarction (AMI) is the leading cause of death attributed to cardiovascular diseases. An association between traffic related air pollution and AMI has been suggested, but the evidence is still limited. OBJECTIVES: To evaluate in a multicentre study association between hospitalisation for first AMI and daily levels of traffic related air pollution. METHODS: The authors collected data on first AMI hospitalisations in five European cities. AMI registers were available in Augsburg and Barcelona; hospital discharge registers (HDRs) were used in Helsinki, Rome and Stockholm. NO2, CO, PM10 (particles <10 microm), and O3 were measured at central monitoring sites. Particle number concentration (PNC), a proxy for ultrafine particles (<0.1 microm), was measured for a year in each centre, and then modelled retrospectively for the whole study period. Generalised additive models were used for statistical analyses. Age and 28 day fatality and season were considered as potential effect modifiers in the three HDR centres. RESULTS: Nearly 27,000 cases of first AMI were recorded. There was a suggestion of an association of the same day CO and PNC levels with AMI: RR = 1.005 (95% CI 1.000 to 1.010) per 0.2 mg/m3 and RR = 1.005 (95% CI 0.996 to 1.015) per 10000 particles/cm3, respectively. However, associations were only observed in the three cities with HDR, where power for city-specific analyses was higher. The authors observed in these cities the most consistent associations among fatal cases aged <75 years: RR at 1 day lag for CO = 1.021 (95% CI 1.000 to 1.048) per 0.2 mg/m3, for PNC = 1.058 (95% CI 1.012 to 1.107) per 10000 particles/cm3, and for NO2 = 1.032 (95% CI 0.998 to 1.066) per 8 microg/m3. Effects of air pollution were more pronounced during the warm than the cold season. CONCLUSIONS: The authors found support for the hypothesis that exposure to traffic related air pollution increases the risk of AMI. Most consistent associations were observed among fatal cases aged <75 years and in the warm season.

Associations between ambient, personal, and indoor exposure to fine particulate matter constituents in Dutch and Finnish panels of cardiovascular patients.

AIMS: To assess the relation between ambient, indoor, and personal levels of PM2.5 and its elemental composition for elderly subjects with cardiovascular disease. METHODS: In the framework of a European Union funded study, panel studies were conducted in Amsterdam, the Netherlands and Helsinki, Finland. Outdoor PM2.5 concentrations were measured at a fixed site. Each subject's indoor and personal PM2.5 exposure was measured biweekly for six months, during the 24 hour period preceding intensive health measurements. The absorbance of PM2.5 filters was measured as a marker for diesel exhaust. The elemental content of more than 50% of the personal and indoor samples and all corresponding outdoor samples was measured using energy dispersive x ray fluorescence. RESULTS: For Amsterdam and Helsinki respectively, a total of 225 and 238 personal, and 220 and 233 indoor measurements, were analysed from 36 and 46 subjects. For most elements, personal and indoor concentrations were lower than and highly correlated with outdoor concentrations. The highest correlations (median r>0.9) were found for sulfur and particle absorbance, which both represent fine mode particles from outdoor origin. Low correlations were observed for elements that represent the coarser part of the PM2.5 particles (Ca, Cu, Si, Cl). CONCLUSIONS: The findings of this study provide support for using fixed site measurements as a measure of exposure to particulate matter in time series studies linking the day to day variation in particulate matter to the day to day variation in health endpoints, especially for components of particulate matter that are generally associated with fine particles and have few indoor sources. The high correlation for absorbance of PM2.5 documents that this applies to particulate matter from combustion sources, such as diesel vehicles, as well.

Personal exposure to fine particulate matter in elderly subjects: relation between personal, indoor, and outdoor concentrations.

The time-series correlation between ambient levels, indoor levels, and personal exposure to PM2.5 was assessed in panels of elderly subjects with cardiovascular disease in Amsterdam, the Netherlands, and Helsinki, Finland. Subjects were followed for 6 months with biweekly clinical visits. Each subject's indoor and personal exposure to PM2.5 was measured biweekly, during the 24-hr period preceding the clinical visits. Outdoor PM2.5 concentrations were measured at fixed sites. The absorption coefficients of all PM2.5 filters were measured as a marker for elemental carbon (EC). Regression analyses were conducted for each subject separately, and the distribution of the individual regression and correlation coefficients was investigated. Personal, indoor, and ambient concentrations were highly correlated within subjects over time. Median Pearson's R between personal and outdoor PM2.5 was 0.79 in Amsterdam and 0.76 in Helsinki. For absorption, these values were 0.93 and 0.81 for Amsterdam and Helsinki, respectively. The findings of this study provide further support for using fixed-site measurements as a measure of exposure to PM2.5 in epidemiological time-series studies.