Background: Elevated blood pressure (BP) has been associated with particulate matter (PM) air pollution, but associations with PM chemical constituents are still uncertain. Objectives: We investigated associations of BP with various chemical constituents of fine PM (PM2.5) during 460 repeated visits among a panel of 39 university students. Methods: Resting BP was measured using standardized methods before and after the university students relocated from a suburban campus to an urban campus with different air pollution contents in Beijing, China. Air pollution data were obtained from central monitors close to student residences. We used mixed-effects models to estimate associations of various PM2.5 constituents with systolic BP (SBP), diastolic BP (DBP), and pulse pressure. Results: An interquartile range increase of 51.2 μg/m3 in PM2.5 was associated with a 1.08-mmHg (95% CI: 0.17, 1.99) increase in SBP and a 0.96-mmHg (95% CI: 0.31, 1.61) increase in DBP on the following day. A subset of PM2.5 constituents, including carbonaceous fractions (organic carbon and elemental carbon), ions (chloride and fluoride), and metals/metalloid elements (nickel, zinc, magnesium, lead, and arsenic), were found to have robust positive associations with different BP variables, though robust negative associations of manganese, chromium, and molybdenum with SBP or DBP also were observed. Conclusions: Our results support relationships between specific PM2.5 constituents and BP. These findings have potential implications for the development of pollution abatement strategies that maximize public health benefits.

Background Nitrogen dioxide (NO₂), an oxidant gas that contaminates both outdoor and indoor air, is considered to be a potential risk factor for asthma. We investigated concurrently the effects of outdoor and indoor NO₂ on the prevalence and incidence of respiratory symptoms among children. Methods A cohort study was carried out over 3 years on 842 schoolchildren living in seven different communities in Japan. Indoor NO₂ concentrations over 24 hours were measured in both winter and summer in the homes of the subjects, and a 3-year average of the outdoor NO₂ concentration was determined for each community. Respiratory symptoms were evaluated every year from responses to questionnaires. Results The prevalence of bronchitis, wheeze, and asthma significantly increased with increases of indoor NO₂ concentrations among girls, but not among boys. In neither boys nor girls were there significant differences in the prevalence of respiratory symptoms among urban, suburban, and rural districts. The incidence of asthma increased among children living in areas with high concentrations of outdoor NO₂. Multiple logistic regression analysis showed that a 10 parts per billion (ppb) increase of outdoor NO₂ concentration was associated with an increased incidence of wheeze and asthma (odds ratios [OR] = 1.76, 95% CI : 1.04–3.23 and OR = 2.10, 95% CI : 1.10–4.75, respectively), but that no such associations were found with indoor NO₂ concentration (OR = 0.73, 95% CI : 0.45–1.14 and OR = 0.87, 95% CI : 0.51–1.43, respectively). Conclusions These findings suggest that outdoor NO₂ air pollution may be particularly important for the development of wheeze and asthma among children. Indoor NO₂ concentrations were associated with the prevalence of respiratory symptoms only among girls. Girls may be more susceptible to indoor air pollution than boys.

Background: Ambient air pollution has been associated with activation of systemic inflammation and hypercoagulability and increased plasma homocysteine, but the chemical constituents behind the association are not well understood. We examined the relations of various chemical constituents of fine particles (PM_2.5) and biomarkers of inflammation, coagulation and homocysteine in the context of traffic-related air pollution. Methods: A panel of 40 healthy college students underwent biweekly blood collection for 12 times before and after their relocation from a suburban campus to an urban campus with changing air pollution contents in Beijing. Blood samples were measured for circulatory biomarkers of high-sensitivity C reactive protein (hs-CRP), tumor necrosis factor alpha (TNF-α), fibrinogen, plasminogen activator inhibitor type 1 (PAI-1), tissue-type plasminogen activator (t-PA), von Willebrand factor (vWF), soluble platelet selectin (sP-selectin), and total homocysteine (tHcy). Various air pollutants were measured in a central air-monitoring station in each campus and 32 PM_2.5 chemical constituents were determined in the laboratory. We used three different mixed-effects models (single-constituent model, constituent-PM_2.5 joint model and constituent residual model) controlling for potential confounders to estimate the effects of PM_2.5 chemical constituents on circulatory biomarkers. Results: We found consistent positive associations between the following biomarkers and PM_2.5 chemical constituents across different models: TNF-α with secondary organic carbon, chloride, zinc, molybdenum and stannum; fibrinogen with magnesium, iron, titanium, cobalt and cadmium; PAI-1 with titanium, cobalt and manganese; t-PA with cadmium and selenium; vWF with aluminum. We also found consistent inverse associations of vWF with nitrate, chloride and sodium, and sP-selectin with manganese. Two positive associations of zinc with TNF-α and of cobalt with fibrinogen, and two inverse associations of nitrate with vWF, and of manganese with sP-selectin, were independent of the other constituents in two-constituent models using constituent residual data. We only found weak air pollution effects on hs-CRP and tHcy. Conclusions: Our results provide clues for the potential roles that PM_2.5 chemical constituents may play in the biological mechanisms through which air pollution may influence the cardiovascular system.