Single-cell transcriptomics reveals the pulmonary inflammation induced by inhalation of subway fine particles.

People generally take the subway and inevitably inhale the fine particles (PM2.5) on subway platforms. This study revealed whether and how subway PM2.5 causes lung inflammation. Herein, the pulmonary inflammatory response to subway PM2.5 was observed in mice, manifesting as the inflammatory cells infiltration and collagen deposition in tissue, inflammatory cytokine enhancement in bronchoalveolar lavage fluid and Toll-like receptors signal pathway activation in the lungs. Furthermore, single-cell RNA sequencing unearthed subway PM2.5-induced cell-specific responses in the lungs. Twenty immune subsets were identified by the molecular and functional properties. Specific cell populations of CD4+ T and γδ T cells were regarded as the predominant sources of pneumonitis induced by subway PM2.5. Moreover, we demonstrated that the lung inflammatory injury was significantly more attenuated in Rag1-/- mice lacking functional T cells and B cells than that in wild type mice. We proved the slight inflammation of lung tissue in Rag1-/- mice may be dependent on monocytes and neutrophils by activation of the intracellular molecular network. This is the first experimental study on subway PM2.5 causing pulmonary inflammatory damage. It will set an alarm for people who usually travel by subway and efficient measures to reduce PM2.5 should be developed in subway stations.

Inhalation of subway fine particles induces murine extrapulmonary organs damage.

Because of its speed and convenience, the subway has become the first choice for travel by many residents. However, the concentration of fine particles (PM2.5) in the air of a subway platform is higher than that of the ground level or carriage. Moreover, the composition and source of subway PM2.5 differ from those of atmospheric PM2.5. Currently, there is insufficient research on the impact of subway PM2.5 on health. In this study, intratracheally subway PM2.5-inoculated wild type (WT) and Rag1-/- mice, lacking functional T cells and B cells, were used to investigate the potential of subway PM2.5 exposure to cause extrapulmonary organ injuries. Subway PM2.5 increased inflammatory cells infiltration, tumor necrosis factor (TNF)-α, interleukin (IL)-6, as well as monocyte chemotactic protein (MCP)-1 gene and protein expression, cyclooxygenase-2 (COX-2) induction, and Toll-like receptor (TLR)-2, TLR4, myeloid differentiation factor 88 (MyD88), and nuclear factor (NF)-κB levels in liver, kidney, spleen, and thymus in a dose-dependent fashion in WT mice. Subway PM2.5 exposure resulted in slight macrophage (F4/80+) and neutrophil (Ly6G+) infiltration and caused no increase in the protein levels of TNF-α, IL-6, MCP-1, or COX-2 in the liver, kidneys, spleen, and thymus of Rag1-/- mice. These results demonstrate a dose-response manner between subway PM2.5 exposure and inflammatory injuries of extrapulmonary organs, which could be related to the TLR/MyD88/NF-κB signaling pathway. Subway PM2.5-induced extrapulmonary organ damage was dependent on T cells and B cells; this finding may provide insight for research on the mechanisms responsible for the health hazards posed by air pollution.

Impact of ambient fine particulate matter on emergency department admissions for circulatory system disease in a city in Northeast China.

The cardiovascular impact of fine particles has caused great concern worldwide. However, evidences on the impact of fine particulate matter (PM2.5) on emergency department (ED) admissions for circulatory system disease in Northeast China is limited. We assessed the acute, lag, cumulative, and harvesting effects of PM2.5 on ED admissions for circulatory system diseases and their exposure-response relationship. A total of 26,168 ED admissions, including those for hypertension, ischemic heart disease (IHD), arrhythmia, heart failure (HF), and cerebrovascular events (CVE), were collected from the Shenyang Emergency Center from 1 January 2017 to 31 December 2018. The relationship between PM2.5 and ED admissions for circulatory system disease was estimated using a distributed lag non-linear model and a generalized additive quasi-Poisson model. We stratified the analyses by temperature. Air pollution was positively correlated with daily ED admissions for circulatory system disease or other cause-specific diseases under different lag structures. For every 10-µg/m3 increase in the PM2.5 concentration, the relative risk of daily ED admissions for circulatory system disease was 1.007 [95% confidence interval (CI), 1.001-1.013] in lag0, 1.007 (95%CI, 1.000-1.013) in lag1, and 1.011 (95%CI, 1.002-1.021) in lag03. A lag effect was found in IHD, a cumulative effect was found in CVE, and both lag and cumulative effects were found in hypertension and arrhythmia. A harvesting effect was observed in daily ED admissions for circulatory system disease and HF. We found no interaction between pollutants and temperature. We observed a monotonic and almost linear exposure-response relationship between PM2.5 and circulatory system disease with no threshold effect.PM2.5 contributes to obvious acute, lag, cumulative, and harvesting effects on circulatory system disease. PM2.5 was associated with the risk of daily ED admissions for circulatory system disease, hypertension, IHD, arrhythmia, HF, and CVE. Therefore, air quality management must be strengthened.