Besides total mortality, the cohort studies described above also presented data on mortality from cardiopulmonary diseases. Further, a Swedish case-control study provided results on the relation between long-term PM exposure and fatal (and non-fatal) myocardial infarction. A summary of European studies providing data on mortality from cardiovascular and respiratory diseases is presented in Table .
Analytical studies investigating the relation between long-term PM exposure and cardiovascular and respiratory mortality.
In the Netherlands Cohort Study [6
], most of the excess risk observed in total mortality appeared to be attributable to cardiopulmonary causes of death. The RR of cardiopulmonary mortality for subjects living near a major road was 1.95 (95% CI, 1.09-3.51). Updated analyses [7
] showed RR near to unity for high traffic intensity on the nearest road using the case-cohort approach, and RRs of 1.06 (95% CI, 1.00-1.12) for cardiopulmonary mortality and 1.10 (95% CI, 0.95-1.26) for respiratory mortality in the whole cohort. With reference to BS exposure, the RRs for a 10 μg/m3
increase were 1.04 (95% CI, 0.90-1.20) for cardiopulmonary and 1.16 (95% CI, 0.91-1.48) for respiratory mortality using the case-cohort approach. The corresponding RRs calculated on the whole cohort, adjusted for age, sex, smoking and area-level socio-economic status, were 1.06 (95% CI, 0.98-1.15) and 1.22 (95% CI, 0.99-1.49).
In the PAARC study [8
], causes of death were available until 1998 for 96% of the sample. No association was found between cardiopulmonary mortality (International Classification of Diseases, ICD-9 codes: 401-440 or 460-519) and long-term exposure to BS (RR = 1.00) and TSP (RR = 1.01). When the analysis was restricted to 18 areas, the RRs for all cardiopulmonary causes were 1.06 (95% CI, 1.01-1.12) for a 10 μg/m3
increase in TSP and 1.05 (95% CI, 0.98-1.12) for BS.
Similarly to the findings of the Netherlands Cohort Study, in the German study conducted in North Rhine Westphalia the effects of PM and traffic appeared stronger for - or limited to - cardiopulmonary mortality (ICD-9 codes: 400-440 or 460-519) [9
]. The adjusted RRs for a 7 μg/m3
increase in PM10
in the baseline year was 1.34 (95% CI, 1.06-1.71), while the RR was 1.59 (95% CI, 1.23-2.04) when exposure was measured for five years. Women living near a major road had a 70% (95% CI, 2%-181%) increased risk of dying from cardiopulmonary causes. Mutual adjustment of PM10
level and proximity to major roads did not materially change these estimates. Another analysis was conducted on the same data to investigate the impact of respiratory health on the association between PM10
exposure and cardiovascular mortality [11
]. Findings from that study suggested that impaired respiratory health and long-term exposure to air pollution are independently associated with an increase in cardiovascular mortality.
A population-based case-control study on 1397 cases with first myocardial infarction and 1870 population controls resident in Stockholm county, aged 45-70 years, was conducted between 1992 and 1994 [12
]. Response rates to the mailed questionnaire varied between 70% and 81% depending on sex and case-control status. For each subject, exposure to PM10
was reconstructed from 1960 to a year prior to enrolment (1992-1994), i.e., for over 20 years, using data on traffic around the home address. Only data for long-term exposure to PM10
were used in the analysis, given the high correlation between PM10
(r = 0.998). Logistic regression models adjusted for the matching variables, i.e. age, sex and hospital catchment area, smoking, physical inactivity, diabetes and socio-economic status were used to compute odds ratios (OR). Hypertension, body mass, job strain, diet, passive smoking, alcohol and coffee intake, and occupational exposure to motor exhaust and other combustion products were also evaluated, but did not appear to confound the relation with PM. With reference to fatal cases of myocardial infarction (n = 272), the OR was 1.39 (95% CI, 0.94-2.07) for an increase of 5 μg/m3
exposure. A borderline significant association was found when fatal cases were further restricted to 84 subjects who died out of hospital (OR = 1.84, 95% CI, 1.00-3.40), while the OR was 1.21 (95% CI, 0.75-1.94) for in-hospital deaths. Though this finding can be interpreted as supportive of an association between air pollution exposure and mortality, random variation in small subgroups cannot be excluded.
The Norwegian record-linkage study presented cause- and sex-specific HRs for PM10
]. The crude HRs for cardiovascular mortality (ICD-9 codes: 390-459) for a quartile increase of PM2.5
were 1.11 (95% CI, 1.06-1.16) in 51-70 year old men, 1.06 (95% CI, 1.03-1.09) in 71-90 year old men, 1.16 (95% CI, 1.09-1.24) in 51-70 year old women, and 1.02 (95% CI, 1.00-1.05) in 71-90 year old women. With reference to mortality from chronic obstructive pulmonary disease (COPD, ICD-9 codes: 490-496), the corresponding HRs were 1.32 (95% CI, 1.17-1.49), 1.14 (95% CI, 1.04-1.24), 1.18 (95% CI, 1.03-1.34), and 1.09 (95% CI, 1.00-1.18). Further, the HRs for PM2.5
exposure adjusted for occupation and education (given in Table ) and those for PM10
exposure were almost unchanged. In the same record-linkage investigation, another study considered the socio-economic correlates of PM exposure in subjects aged 50-74 years [13
]. Overall, the risk of death from cardiovascular diseases (RR = 1.11, 95% CI, 1.07-1.15 for a quartile increase) and COPD (RR = 1.17, 95% CI, 1.09-1.25) was associated with PM2.5
exposure. When deprivation indicators were included in the models, however, the RRs became closer to unity. The authors concluded that more deprived neighbourhoods have higher levels of air pollution, and thus deprivation accounts for some of the excess mortality from several diseases, including cardiovascular and respiratory conditions, associated with air pollution in these neighborhoods.