Current day concentrations of ambient air pollution have been associated with a range of adverse health effects, particularly mortality and morbidity due to cardiovascular and respiratory diseases. In this review, we summarize the evidence from epidemiological studies on long-term exposure to fine and coarse particles, nitrogen dioxide (NO2) and elemental carbon on mortality from all-causes, cardiovascular disease and respiratory disease. We also summarize the findings on potentially susceptible subgroups across studies. We identified studies through a search in the databases Medline and Scopus and previous reviews until January 2013 and performed a meta-analysis if more than five studies were available for the same exposure metric.There is a significant number of new studies on long-term air pollution exposure, covering a wider geographic area, including Asia. These recent studies support associations found in previous cohort studies on PM2.5. The pooled effect estimate expressed as excess risk per 10 μg/m3 increase in PM2.5 exposure was 6% (95% CI 4, 8%) for all-cause and 11% (95% CI 5, 16%) for cardiovascular mortality. Long-term exposure to PM2.5 was more associated with mortality from cardiovascular disease (particularly ischemic heart disease) than from non-malignant respiratory diseases (pooled estimate 3% (95% CI −6, 13%)). Significant heterogeneity in PM2.5 effect estimates was found across studies, likely related to differences in particle composition, infiltration of particles indoors, population characteristics and methodological differences in exposure assessment and confounder control. All-cause mortality was significantly associated with elemental carbon (pooled estimate per 1 μg/m3 6% (95% CI 5, 7%)) and NO2 (pooled estimate per 10 μg/m3 5% (95% CI 3, 8%)), both markers of combustion sources. There was little evidence for an association between long term coarse particulate matter exposure and mortality, possibly due to the small number of studies and limitations in exposure assessment. Across studies, there was little evidence for a stronger association among women compared to men. In subjects with lower education and obese subjects a larger effect estimate for mortality related to fine PM was found, though the evidence for differences related to education has been weakened in more recent studies.

Exposure to traffic-related air pollution is associated with risk of cardiovascular disease and mortality. We examined whether exposure to diesel exhaust increased blood pressure in human subjects. We analyzed data from 45 nonsmoking subjects, age 18–49 in double-blinded, crossover exposure studies, randomized to order. Each subject was exposed to diesel exhaust, maintained at 200 μg/m3 of fine particulate matter, and filtered air for 120 minutes on days separated by at least two weeks. We measured blood pressure pre-exposure, at 30-minute intervals during exposure, and 3, 5, 7 and 24 hours from exposure initiation, and analyzed changes from pre-exposure values. Compared with filtered air, systolic blood pressure increased at all points measured during and after diesel exhaust exposure; the mean effect peaked between 30 and 60 minutes after exposure initiation (3.8 mmHg [95% CI: −0.4, 8.0] and 5.1 mmHg [95% CI: 0.7, 9.5] respectively). Sex and metabolic syndrome did not modify this effect. Combining readings between 30 and 90 minutes, diesel exhaust exposure resulted in a 4.4 mmHg increase in systolic blood pressure, adjusted for participant characteristics and exposure perception (95% CI: 1.1, 7.7, p=0.0009). There was no significant effect on heart rate or diastolic pressure. Diesel exhaust inhalation was associated with a rapid, measurable increase in systolic, but not diastolic, blood pressure in young nonsmokers, independent of perception of exposure. This controlled trial in humans confirms findings from observational studies. The effect may be important on a population basis given the worldwide prevalence of exposure to traffic-related air pollution.

BackgroundExposure to traffic-related air pollution (TRAP) is considered a trigger for acute cardiovascular events. Diesel Exhaust (DE) is a major contributor to TRAP in the world. We evaluated the effect of DE inhalation on circulating blood cell populations, hematological indices, and systemic inflammatory cytokines in humans using a specialized facility.MethodsIn a randomized double-blind crossover study balanced to order, 17 metabolic syndrome (MetS) and 15 healthy subjects inhaled filtered air (FA) or DE exposure in two-hour sessions on different days with a minimum 2-week washout period. We collected blood pre-exposure, 7, and 22 hours after exposure initiation and measured the complete blood count and differential. We performed multiplex cytokine assay to measure the changes in the systemic inflammatory cytokines, and endothelial adhesion molecules (n=15). A paired analysis compared the effect of DE and FA exposures for the change from pre-exposure to the subsequent time points.ResultsA significant increase in the hematocrit was noted 7 hrs after DE [1.4% (95% CI: 0.9 to 1.9%)] compared to FA exposure [0.5% (95% CI: -0.09 to 1.0%); p=0.008. The hemoglobin levels increased non-significantly at 7 hrs post DE [0.3 gm/dL (95% CI: 0.2 to 0.5 gm/dL)] versus FA exposure [0.2 gm/dL (95% CI: 0 to 0.3 gm/dL)]; p=0.06. Furthermore, the platelet count increased 22 hrs after DE exposure in healthy, but not in MetS subjects [DE: 16.6 (95% CI: 10.2 to 23) thousand platelets/mL versus [FA: 3.4 (95% CI: -9.5 to 16.3) thousand platelets/mL)]; p=0.04. No DE effect was observed for WBC, neutrophils, lymphocytes or erythrocytes. Using the multiplex assay, small borderline significant increases in matrix metalloproteinase-9, interleukins (IL)-1beta, 6 and 10 occurred 7 hrs post exposure initiation, whereas E-selectin, intercellular adhesion molecule-1, and vascular cell adhesion molecule -1, and myeloperoxidase 22 hrs post exposure.ConclusionsOur results suggest that short-term DE exposure results in hemoconcentration and thrombocytosis, which are important determinants of acute cardiovascular events. Multiplex assay showed a non-significant increase in IL-1β and IL-6 immediately post exposure followed by myeloperoxidase and endothelial activation molecules. Further specific assays in a larger population will improve our understanding of the systemic inflammatory mechanisms following acute exposure to TRAP.Clinical trials registration numberStudy was conducted between 2004 to 2006, prior to expectation for registration.