Individual PM2.5 exposure is associated with the impairment of cardiac autonomic modulation in general residents.

Fine particulate matter (PM2.5) is one of the major pollutants in metropolitan areas. The current study was conducted to observe the effects of PM2.5 on cardiac autonomic modulation. The participants included 619 men and women aged from 35-75 in a residential area in Shanghai, China. All the participants were divided into four categories according to the distance between their apartments and major road. In addition, individual PM2.5 was measured using SIDEPAKTM AM510 (TSI, USA) from 8:00 am to 6:00 pm. At the end of the individual PM2.5 measurement, the systolic pressure, diastolic pressure, heart rate (HR), low-frequency (LF), high-frequency (HF), and LF/HF were determined. The association between individual PM2.5 level and the above health effects was analyzed using generalized linear regression. The results showed that the average concentration of individual PM2.5 was 95.5 and 87.0 µg/m(3) for men and women. Residential distance to major road was negatively correlated with the individual PM2.5. The results indicated that per 1.0 µg/m(3) increase of individual PM2.5 was associated with a 2.3 % increase for systolic pressure, 0.3 % increase for diastolic pressure, 0.4 % decrease for LF, and 0.4 % decrease for HF. Nevertheless, there was no statistical association between individual PM2.5 and heart rate and LF/HF in the total model. In addition, the similar results were found in men and women excluding a significant association between PM2.5 and the heart rate in men. The alterations of cardiac autonomic modulation hinted that PM2.5 exposure might be associated with the potential occurrence of cardiovascular disease, such as arrhythmia and ischemic heart diseases.

Preexposure to PM2.5 exacerbates acute viral myocarditis associated with Th17 cell.

BACKGROUND: It is increasingly recognized that exposure to ambient fine particles (PM(2.5)) is a risk factor for the development of cardiovascular events. This study was to explore the link between PM(2.5) exposure and viral myocarditis in the functional mechanism of Th17 cells. METHODS: Male BALB/c mice were administered an intratracheal (i.t.) instillation of 10 mg/kg b.w. PM(2.5) particles. Twenty-four hours later, the mice were injected intraperitoneally (i.p.) with 100 µl of coxsackievirus B3 (CVB3) diluted in Eagle's minimal essential medium (EMEM). Seven days after the treatment, pulmonary and cardiac tissues were examined. RESULTS: The results showed that preexposure to PM(2.5) increased the cardiac and pulmonary injuries and viral replication in the heart of CVB3-infected mice along with an increase in CD4(+) IL-17(+) cells in the spleen and heart. The mRNA expressions of interleukin-17A (IL-17A), perforin, transforming growth factor-ß (TGF-ß) and RORγt were up-regulated in PM(2.5)-pretreated mice than that in the virus-treated mice. Additionally, compared to virus-treated mice, the cardiac protein expressions of IL-17A and matrix metalloproteinases-2 (MMP-2) were increased, but interferon-γ (IFN-γ) and metalloproteinases-1 (TIMP-1) were decreased in PM(2.5)-pretreated mice. Interestingly, PM(2.5) caused IFN-γ decreased, whereas CVB3 caused a dramatic increase in IFN-γ. Subsequently, preexposure to PM(2.5) induced a slight increase of IFN-γ in the sera of CVB3-infected mice. CONCLUSIONS: These results demonstrated that PM(2.5) exposure exacerbated virus-induced myocarditis possibly through the increase in Th17-mediated viral replication, perforin response and imbalance of MMP-2/TIMP-1. These findings provided supportive evidence for the epidemiological research that ambient particles could increase the occurrence and development of cardiovascular diseases.

The biological effects of individual-level PM(2.5) exposure on systemic immunity and inflammatory response in traffic policemen.

BACKGROUND: Ambient fine-particle particulate matter (PM2.5) exposure is associated with the decline in pulmonary function, prevalence of coronary heart disease and incidence of myocardial infarction. The study is to observe the effects of ambient PM2.5 on the cardiovascular system and to explore the potential inflammatory and immune mechanisms. METHODS: The subjects included 110 traffic policemen in Shanghai, China, who were aged 25-55 years. Two-times continuous 24 h individual-level PM2.5 measurements were performed in winter and summer, respectively. The inflammatory marker (high-sensitivity C-reactive protein, hs-CRP), immune parameters (IgA, IgG, IgM and IgE) and lymphocyte profiles (CD4 T cells, CD8 T cells, CD4/CD8 T cells) were measured in blood. The associations between individual-level PM2.5 and inflammatory marker and immune parameters were analysed by multiple linear regression. RESULTS: The average concentration of 24 h personal PM2.5 for participants was 116.98 µg/m(3) and 86.48 µg/m(3) in winter and summer, respectively. In the main analysis, PM2.5 exposure is associated with the increases in hs-CRP of 1.1%, IgG of 6.7%, IgM of 11.2% and IgE of 3.3% in participants, and decreases in IgA of 4.7% and CD8 of 0.7%, whereas we found no statistical association in CD4 T cells and CD4/CD8 T cells. In the adjusted model, the results showed that the increase of PM2.5 was associated with the changes of inflammatory markers and immune markers both in winter and summer. CONCLUSIONS: Traffic policeman have been a high-risk group suffering inflammatory response or immune injury because of the high exposure to PM2.5. These findings provided new insight into the mechanisms linking ambient PM2.5 and inflammatory and immune response.