Short-term effects of air pollutants on outpatient volume of respiratory diseases in Guiyang / 环境与职业医学

Background Affected by concentration, composition, and population tolerance of air pollutants, the relationship between air pollutants and population health has regional differences. There is still a research gap in Guiyang. Objective To explore the short-term effects of air pollutant concentrations in low-pollution areas on the outpatient volume of respiratory diseases. Methods Spearman correlation analysis was used to evaluate the correlation between air pollutants, meteorological factors, and respiratory outpatient volume from January 1, 2013 to December 31, 2020 in Guiyang City. A single pollutant distribution lag nonlinear model and a multi-pollutant interaction model were established based on Poisson distribution. A three-dimensional diagram was drawn to display the relationship between air pollutants and respiratory outpatient volume. Quantitative analysis was conducted on the attribution risk and lag effect of air pollutant concentration on outpatient volume of respiratory diseases in Guiyang City. Results The results of the single pollutant model showed that fine particulate matter (PM2.5), nitrogen dioxide (NO2), carbon monoxide (CO), and sulfur dioxide (SO2) elevated the outpatient volume of respiratory diseases. The maximum relative risk (RR) and 95%CI values of PM2.5, NO2,CO, and SO2 appeared on Day 2, 0, 5, and 6, respectively, which were 1.019 (1.015, 1.023), 1.146 (1.122, 1.171), 1.129 (1.116, 1.143), and 1.046(1.040, 1.052), respectively. For every quartile concentration increment of PM2.5, NO2, CO, or SO2, the outpatient volume of respiratory diseases increased by 0.943% (0.111%, 1.782%), 4.050% (3.573%, 4.529%), 0.595% (0.317%, 0.874%), or 0.667% (0.235%, 1.100%), respectively. The maximum RR (95%CI) of O3 was 1.015 (1.007, 1.023) and appeared on Day 0. The results of multi-pollutant model showed that PM2.5, NO2, CO, SO2, and O3 all elevated the outpatient volume of respiratory diseases. The maximum RR values of PM2.5, NO2, CO, SO2 and O3 appeared on Day 14, 0, 5, 7 and 0, respectively, which were 1.027 (1.021, 1.034), 1.213 (1.179, 1.248), 1.059 (1.043, 1.074), 1.016 (1.005, 1.026), and 1.024 (1.015, 1.033), respectively. Compared with the single pollutant model, the RR values of PM2.5, NO2, and O3 on the outpatient volume of respiratory diseases in the multi-pollutant model showed an upward trend, while the RR values of CO and SO2 in the multi-pollutant model showed a downward trend. Conclusion The impact of low concentrations of PM2.5, NO2, CO, and SO2 on human health cannot be ignored.

Source analysis and health risk assessment of polycyclic aromatic hydrocarbons in atmospheric PM2.5 in a district of Taizhou City from 2019 to 2021 / 环境与职业医学

Background Polycyclic aromatic hydrocarbons (PAHs), one of the main components of fine particulate matter (PM2.5), have a certain impact on ambient air quality, and long-term exposure to PAHs may pose potential health risks to human beings. Objective To identify the distribution characteristics and sources of PAHs in atmospheric PM2.5 in a district of Taizhou City from 2019 to 2021, and to evaluate the health risks of PAHs to the population in the area through the inhalation pathway. Methods From 2019 to 2021, air PM2.5 sampling was carried out at a state-controlled surveillance point in a district of Taizhou City for 7 consecutive days on the 10th-16th of each month, the sampling time was 24 h·d−1, and the sampling flow rate was 100 L·min−1. PM2.5 mass concentration was calculated by gravimetric method. A total of 16 PAHs were determined by ultrasonic extraction-liquid chromatography. Kruskal-Wallis H test was used to compare the distribution charac teristics of PAHs concentrations by years and seasons, characteristic ratio and principal component analysis (PCA) was used to analyze their sources, and a lifetime carcinogenic risk (ILCR) model was used to assess the health risk of PAHs. Results From 2019 to 2021, the annual average concentrations [M (P25, P75)] of ∑PAHs in atmospheric PM2.5 in the selected district of Taizhou City were 6.52 (2.46, 10.59), 8.52 (4.56, 12.29), and 3.72 (1.51, 7.11) ng·m−3, respectively, and the annual benzo[a]pyrene (BaP) excess rates (national limit: 1 ng·m−3) were 27.38% (23/84), 47.62% (40/84), and 19.04% (16/84), respectively, both presenting 2020> 2019 > 2021 (P<0.001, P<0.05). The ∑PAHs concentration distribution showed a seasonal variation, with the highest value in winter and the lowest value in summer (P<0.05). Among the atmospheric PM2.5 samples, the proportion of 5-ring PAHs was the highest, the proportion of 2-3-ring PAHs was the lowest; the proportion of 2-4-ring PAHs showed a yearly upward trend, and the proportion of 5-6-ring PAHs showed yearly downward trend (P<0.05). The characteristic ratio and PCA results suggested that the sources of sampled PAHs were mainly mixed sources such as dust, fossil fuel (natural gas), coal combustion, industrial emissions, and motor vehicle exhaust emissions. The ILCR (RILCR) of PAHs by inhalation for men, women, and children were 1.83×10−6, 2.35×10−6, and 2.04×10−6, respectively, and the annual average RILCR was 2.07×10−6, all greater than 1×10−6. Conclusion For the sampled time period, the main sources of PAHs pollution in atmospheric PM2.5 in the target district of Taizhou City are dust, fossil fuel (natural gas), coal combustion, industrial emissions, motor vehicle emissions, etc., and PAHs may have a potential carcinogenic risk to local residents.

Individual and interactive effects of atmospheric PM2.5 and O3 on mortality of circulatory system diseases in Ningxia / 环境与职业医学

Background The impact of atmospheric fine particulate matter (PM2.5) and ozone (O3) on the mortality of circulatory system diseases cannot be ignored. However, whether the interaction between PM2.5 and O3 can affect population health is rarely reported and requires study. Objective To investigate the individual and interactive impacts of atmospheric PM2.5 and O3 on the mortality of circulatory system diseases in the population of Ningxia region. Methods The data of 119647 deaths due to circulatory system diseases, daily average concentrations of atmospheric pollutants, and meteorological data in Ningxia from 2013 to 2020 were retrieved. PM2.5 was divided into low, medium, and high concentrations according to the primary and secondary national limits (35 and 75 μg·m−3) of the Ambient air quality standards. Similarly, O3 was divided into low, medium, and high concentrations according to the national limits (100 and 160 μg·m−3). Using a generalized additive mixed model based on quasi Poisson distribution, the impacts of atmospheric PM2.5 and O3 as well as their interaction on the mortality of circulatory system diseases were analyzed using the population data of Ningxia region. Results During the target period, males and the ≥ 65 year group accounted for larger proportions of deaths due to circulatory system diseases (55.47% and 79.87% respectively). The daily average concentration of PM2.5 (40.25 μg·m−3) exceeded the national primary limit. In the single pollution model, the highest cumulative lag effects for mortality from circulatory system diseases were PM2.5 exposure over previous 1 d (lag01) and O3 exposure for previous 2 d (lag02), and their excess risk (ER) values were 1.03% (95%CI: 0.67%, 1.40%) and 1.02% (95%CI: 0.57%, 1.50%), respectively. The results of concentration stratification analysis showed that the most significant risks of death from circulatory system diseases [ER (95%CI): 1.12% (0.32%, 1.92%) and 0.95% (0.13%, 1.79%) respectively] were found at medium PM2.5 and O3 concentrations. The interaction analysis revealed that under, a synergistic effect on the risk of death from circulatory system diseases was identified (relative excess risk due to interaction=3.08%, attributable proportion of interaction=2.90%, synergy index=1.89) when considering the coexistence of PM2.5 and O3 above the primary limit. As the concentrations of PM2.5 and O3 increased, the synergistic effect increased the risk of death from circulatory system diseases in the general population, men, women, and the ≥ 65 years group. Conclusion Both atmospheric PM2.5 and O3 can increase the risk of death from circulatory system diseases, and the two pollutants have a synergistic effect on the risk of death from circulatory system diseases.

Advances on effects and mechanisms of PM2.5 on occurrence and development of kidney diseases / 环境与职业医学

Air pollution is a serious global public health problem. Air pollutants, especially fine particulate matter (PM2.5), are associated with increased risks of various diseases. In recent years, studies have confirmed that PM2.5 is closely related to chronic kidney disease, secondary kidney disease, and end-stage renal disease. This review summarized the effects of PM2.5 and its components on kidney diseases, and the potential mechanism of kidney injury induced by PM2.5 exposure from the aspects of inflammatory injury and oxidative stress, renal hemodynamic changes, and DNA damage and methylation, aiming to provide an insight for further mechanism research and the prevention and control of air pollution-induced kidney damage.

Progress on toxicity of co-exposure to ambient fine particulate matter and e-cigarettes / 环境与职业医学

Ambient fine particulate matter (PM2.5) is particulate matter with an aerodynamic diameter less than 2.5 μm, and has an extremely wide range of sources. It affects the environmental quality in many cities and regions around the world, and associates with lots of negative effects on public health. E-cigarettes, a group of products that atomize e-liquid by an atomizer and then deliver nicotine and/or other substances to the respiratory system, have been introduced as smoking cessation products or replacement of tobacco cigarettes in recent years. The usage rate of e-cigarettes has grown rapidly all over the world. When these two pollutants coexist in the same atmosphere, they would induce certain adverse health effects not only on the e-cigarette users, but also on the people around them. Besides causing cardiopulmonary toxicity, the co-existing pollutants may associate with higher risks of developmental toxicity and carcinogenicity. In addition, the combined exposure may be related with the occurrence of depression. Therefore, there is an urgent need to conduct studies on the toxic potential of the combined exposure to PM2.5 and e-cigarettes, which is also important for the evaluation and control of the atmospheric compound pollution associated health risk. This paper reviewed the current situation of PM2.5 pollution and e-cigarettes use, introduced the epidemiological studies of PM2.5 and e-cigarette combined exposure, their toxic effects in vivo and in vitro, and possible mechanisms, aiming to provide a reference for subsequent toxicity studies.

Research progress on effects and mechanisms of short-term exposure to ambient fine particulate matter and its components on blood pressure / 环境与职业医学

Elevated blood pressure is one of the major contributors to cardiovascular disease and premature death. The exposure to ambient fine particulate matter (PM2.5) is closely associated with changes in blood pressure, and even short-term exposure to PM2.5 can lead to an increase in blood pressure. PM2.5 is a complex mixture that exerts different toxicities and triggers increased blood pressure through various mechanisms. Therefore, in this article, we provided a comprehensive review of published studies on the effects of short-term exposure to PM2.5 and its components on blood pressure, and elaborated potential mechanisms from four aspects, including oxidative stress and inflammatory response, endothelial dysfunction, autonomic nervous system disorders and hypothalamus-pituitary-adrenal axis activation, and epigenome alteration. Given the limitations of existing research, future prospective studies can be conducted on diverse populations, using more precise exposure measurement methods and multi-omics approaches, to further elucidate the mechanisms underlying the effects of PM2.5 and its various components on blood pressure. The findings would provide a theoretical foundation for effective protection of public health, particularly vulnerable groups.

Ambient Fine Particulate Matter Exposure and Blood Pressure: Evidence from a Large Chinese Multiple Follow-Up Study / 生物医学与环境科学（英文）

OBJECTIVE@#This study aimed to investigate the association of ambient PM2.5 exposure with blood pressure (BP) at the population level in China.@*METHODS@#A total of 14,080 participants who had at least two valid blood pressure records were selected from the China Health and Retirement Longitudinal Survey during 2011-2015. Their long-term PM2.5 exposure was assessed at the geographical level, on the basis of a regular 0.1° × 0.1° grid over China. A mixed-effects regression model was used to assess associations.@*RESULTS@#Each decrease of 10 μg/m3 in the 1 year-mean PM2.5 concentration (FPM1Y) was associated with a decrease of 1.24 [95% confidence interval (CI): 0.84-1.64] mmHg systolic BP (SBP) and 0.50 (95% CI: 0.25-0.75) mmHg diastolic BP (DBP), respectively. A robust association was observed between the long-term decrease in PM2.5 and decreased BP in the middle-aged and older population. Using a generalized additive mixed model, we further found that SBP increased nonlinearly overall with FPM1Y but in an approximately linear range when the FPM1Y concentration was < 70 µg/m3; In contrast, DBP increased approximately linearly without a clear threshold.@*CONCLUSION@#Efficient control of PM2.5 air pollution may promote vascular health in China. Our study provides robust scientific support for making the related air pollution control policies.

Characteristics and Differences of Household Fine Particulate Matter Pollution Caused by Fuel Burning in Urban and Rural Areas in China / 中国医学科学院学报

Objective To explore the overall level,distribution characteristics,and differences in household fine particulate matter (PM2.5) pollution caused by fuel burning in urban and rural areas in China. Methods The relevant articles published from 1991 to 2021 were retrieved and included in this study.The data including the average concentration of household PM2.5 and urban and rural areas were extracted,and the stoves and fuel types were reclassified.The average concentration of PM2.5 in different areas was calculated and analyzed by nonparametric test. Results The average household PM2.5 concentration in China was (178.81±249.91) μg/m3.The mean household PM2.5 concentration was higher in rural areas than in urban areas[(206.08±279.40) μg/m3 vs. (110.63±131.16) μg/m3;Z=-5.45,P<0.001] and higher in northern areas than in southern areas[(224.27±301.66) μg/m3 vs.(130.11±140.61) μg/m3;Z=-2.38,P=0.017].The north-south difference in household PM2.5 concentration was more significant in rural areas than in urban areas[(324.19±367.94) μg/m3 vs.(141.20±151.05) μg/m3,χ2=-5.06,P<0.001].The PM2.5 pollution level showed differences between urban and rural households using different fuel types (χ2=92.85,P<0.001),stove types (χ2=74.42,P<0.001),and whether they were heating (Z=-4.43,P<0.001).Specifically,rural households mainly used solid fuels (manure,charcoal,coal) and traditional or improved stoves,while urban households mainly used clean fuels (gas) and clean stoves.The PM2.5 concentrations in heated households were higher than those in non-heated households in both rural and urban areas (Z=-4.43,P<0.001). Conclusions The household PM2.5 pollution caused by fuel combustion in China remains a high level.The PM2.5 concentration shows a significant difference between urban and rural households,and the PM2.5 pollution is more serious in rural households.The difference in the household PM2.5 concentration between urban and rural areas is more significant in northern China.PM2.5 pollution in the households using solid fuel,traditional stoves,and heating is serious,and thus targeted measures should be taken to control PM2.5 pollution in these households.

The potential impact of PM2.5 on the covid-19 crisis in the Brazilian Amazon region

ABSTRACT OBJECTIVE This study aims to assess covid-19 morbidity, mortality, and severity from 2020 to 2021 in five Brazilian Amazon states with the highest records of wildfires. METHODS A distributed lag non-linear model was applied to estimate the potential exposure risk association with particulate matter smaller than 2.5-µm in diameter (PM2.5). Daily mean temperature, relative humidity, percentual of community mobility, number of hospital beds, days of the week, and holidays were considered in the final models for controlling the confounding factors. RESULTS The states of Para, Mato Grosso, and Amazonas have reported the highest values of overall cases, deaths, and severe cases of covid-19. The worrying growth in the percentual rates in 2020/2021 for the incidence, severity, and mortality were highlighted in Rondônia and Mato Grosso. The growth in 2020/2021 in the estimations of PM2.5 concentrations was higher in Mato Grosso, with an increase of 24.4%, followed by Rondônia (14.9%). CONCLUSION This study establishes an association between wildfire-generated PM2.5 and increasing covid-19 incidence, mortality, and severity within the studied area. The findings showed that the risk of covid-19 morbidity and mortality is nearly two times higher among individuals exposed to high concentrations of PM2.5. The attributable fraction to PM2.5 in the studied area represents an important role in the risk associated with covid-19 in the Brazilian Amazon region.

Association between exposure to air pollutants and hospitalization for SARS-Cov-2: an ecological time-series study

ABSTRACT BACKGROUND: Exposure to air pollutants and illness by severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2) infection can cause serious pulmonary impairment. OBJECTIVE: To identify a possible association between exposure to air pollutants and hospitalizations due to SARS-Cov-2. DESIGN AND SETTING: Ecological time-series study carried out in Taubaté, Tremembé, and Pindamonhangaba in 2020 and 2021. METHODS: Study with Sars-Cov-2 hospitalizations with information on hospitalization date, sex and age of the subjects, duration of hospitalization, type of discharge, and costs of these hospitalizations. Statistical analysis was performed through a negative binomial regression, with data on pollutant concentrations, temperature, air relative humidity, and hospitalization date. Coefficients obtained by the analysis were transformed into relative risk for hospitalization, which estimated hospitalizations excess according to an increase in pollutant concentrations. RESULTS: There were 1,300 hospitalizations and 368 deaths, with a predominance of men (61.7%). These data represent an incidence rate of 250.4 per 100,000 inhabitants and 28.4% hospital lethality. Significant exposure (P value < 0.05) occurred seven days before hospital admission (lag 7) for nitrogen dioxide (NO2) (relative risk, RR = 1.0124) and two days before hospital admission for PM2.5 (RR = 1.0216). A 10 μg/m3 in NO2 concentration would decrease by 320 hospitalizations and ¼ US $ 240,000 in costs; a 5 μg/m3 in PM2.5 concentration would decrease by 278 hospitalizations and ¼ US $ 190,000 in costs. CONCLUSION: An association between exposure to air pollutants and hospital admission due to Sars-Cov-2 was observed with excess hospitalization and costs for the Brazilian public health system.

Recognition models of cigarette smoking behavior by real-time indoor PM2.5 concentrations in public places / 环境与职业医学

Background Public places are frequently polluted by cigarette smoking, and there is a lack of accurate, real-time, and intelligent monitoring technology to identify smoking behavior. It is necessary to develop a tool to identify cigarette smoking behavior in public places for more efficient control of cigarette smoking and better indoor air quality. Objective To construct a model for recognizing cigarette smoking behavior based on real-time indoor concentrations of PM2.5 in public places. Methods Real-time indoor PM2.5 concentrations were measured for at least 7 continuous days in 10 arbitrarily selected places (6 public service providers and and 4 office or other places) from Oct. to Nov. 2022 in Pudong New Area, Shanghai. Indoor nicotine concentrations were monitored with passive samplers simultaneously. Outdoor PM2.5 concentration data were obtained from three municipal environmental monitoring stations which were nearest to each monitoring point during the same period. Mann-Whitney U test was used to compare indoor and outdoor means of PM2.5 concentrations, and Spearman rank correlation was used to analyze indoor PM2.5 and nicotine concentrations. An interactive plot and a random forest model was applied to examine the association between video observation validated indoor smoking behavior and real-time indoor PM2.5 concentrations in an Internet cafe. Results The average indoor PM2.5 concentration in the places providing public services [(97.5±149.3) µg·m−3] was significantly higher than that in office and other places [(19.8±12.2) µg·m−3] (P=0.011). The indoor/outdoor ratio (I/O ratio) of PM2.5 concentration in the public service providers ranged from 1.1 to 19.0. Furthermore, the indoor PM2.5 concentrations in the 10 public places were significantly correlated with the nicotine concentrations (rs=0.969, P<0.001). Among them, the top 3 highly polluted places were Internet cafes, chess and card rooms, and KTV. The results of random forest modeling showed that, for synchronous real-time PM2.5 concentration, the area under the curve (AUC) was 0.66, while for PM2.5 concentration at a lag of 4 min after the incidence of smoking behavior, the AUC increased to 0.72. Conclusion The indoor PM2.5 concentrations in public places are highly correlated with smoking behavior. Based on real-time indoor PM2.5 monitoring, a preliminary recognition model for smoking behavior is constructed with acceptable accuracy, indicating its potential values applied in smoking control and management in public places.

Correlation between dietary approaches to stop hypertension pattern and central obesity affected by PM2.5 exposure / 环境与职业医学

Background There is a lack of evidence on whether exposure to PM2.5 and its constituents would affect the relationship between the dietary approaches to stop hypertension (DASH) and central obesity. Objective To investigate the effect of exposure to PM2.5 and its constituents on the correlation between the DASH dietary pattern and the prevalence of central obesity. Methods The data were obtained from the baseline survey of the "Xinjiang Multi-Ethnic Natural Population Cohort Construction and Health Follow-Up Study" in Urumqi. A DASH score was calculated according to intake frequency of 8 food groups, and summed from intake frequency of recommended food groups scored from 1 to 5 from low to high, and intake frequency of restricted food groups scored from 1 to 5 from high to low. A higher DASH score indicates better compliance with the DASH dietary pattern. We estimated exposure using satellite-derived PM2.5 and a chemical transport model (GEOS-Chem) for its constituents, including organic carbon (OC), black carbon (BC), sulfate (SO42−), nitrate (NO3−), ammonium (NH4+), and soil dust. Central obesity was defined by waist circumference: ≥90 cm for men or ≥85 cm for women according to Criteria of weight for adults (WS/T 428—2013). A logistic regression model was used to analyze the effects of the DASH dietary pattern as well as PM2.5 and its constituents on central obesity, and a stratified analysis was used to explore the effects of PM2.5 and its constituents on the association between the DASH dietary pattern and central obesity. Results The study included 9 565 urban residents, aged (62.30±9.42) years, with a central obesity prevalence rate of 60.75%. After adjusting for selected confounders, the DASH score Q5 group had a 17.5% lower risk of central obesity than the Q1 group (OR=0.825, 95%CI: 0.720-0.947). PM2.5 and its constituents OC, BC, SO42−, NH4+, and soil dust were positively associated with the prevalence of central obesity, but no association was observed between constituent NO3− exposure and central obesity. The stratified analysis revealed that the prevalence of central obesity was reduced in the DASH score Q5 group in participants exposed to low concentrations of PM2.5 and its constituents NO3−, NH4+, and soil dust, while the protective effect of the DASH pattern on central obesity disappeared in subjects exposed to high concentrations of PM2.5 and its constituents NO3−, NH4+, and soil dust. Conclusion Exposure to PM2.5 and its constituents NO3−, NH4+, and soil dust could attenuate the protective effect of the DASH pattern on central obesity.

Research progress on adverse health effects of fine particulate matter constituents in China / 环境与职业医学

Air pollution has always been an important factor threatening population health, and with the acceleration of urbanization in China, the adverse health effects associated with air pollution is becoming more and more serious. Numerous scientific studies have shown that chemical components of fine particulate matter are closely related to human health damage. This paper elaborated reported human health outcomes of PM2.5 chemical components, including fatality, morbidity, reproduction & development, and physiological indexes or biomarkers, reviewed the research progress of PM2.5 chemical constituents on human health in China, and summarized the deficiencies of current research, aiming to provide useful clues for future relevant studies.

Effects of pre-pregnancy PM2.5 exposure on vascular remodeling in mother-fetal interface of mice via HIF-1α/VEGF axis / 环境与职业医学

Background Atmospheric fine particulate matter (PM2.5) can induce abnormal early embryo development, resulting in adverse pregnancy outcomes such as embryo damage and spontaneous abortion. The vascular remodeling of maternal-fetal interface regulated by hypoxia inducible factor-1α (HIF-1α)/vascular endothelial growth factor (VEGF) axis is a key link in early embryo development. Objective To investigate the effects of pre-pregnancy PM2.5 exposure on the uterine state of mice before conception and the vascular remodeling of maternal-fetal interface after conception, and to further explore the regulatory role of the HIF-1α/VEGF axis. Methods Forty eight-week-old C57BL/6J sexually mature female mice and several males (for mating, without any treatment) were adaptive fed for 1 week. The female mice were divided into a PM2.5 exposure group and a control group, 20 mice per group. The PM2.5 exposure group was given 3 mg·kg−1 PM2.5 suspension by nasal instillation, once every other day for four weeks; the control group were treated with the same dose of blank sampling membrane suspension. Body weight of the mice was recorded every week during the experimental period. At the end of the exposure, six mice from each group were sacrificed. Then the uterus was weighted and its organ coefficients were calculated, a histopathological morphology evaluation was conducted by HE staining, and the mRNA expressions of HIF-1α, VEGF and its receptors Flt-1 and Flk-1 in the uterus samples were further examined. The remaining 14 female mice in each group were caged with male mice overnight with a sex ratio of 2:1, then we calculated the pregnancy rate. On gestation day 10 (GD10), the female mice were decapitated and the uterus was dissected, the histopathological morphology of embryo and placenta were observed by HE staining, and the mRNA expressions of HIF-1α, VEGF and its receptors Flt-1 and Flk-1 were detected as well in the uterus samples. Results Compared with the control group, the pre-pregnancy PM2.5 exposure had no significant effect on body weight gain of the female mice, but decreased uterine organ coefficient, accompanied by pathological damage such as endometrium thinning as well as decreased mRNA expressions of HIF-1α, VEGF and its receptors Flt-1 and Flk-1 (all Ps<0.05). After mating, the pre-pregnancy PM2.5 exposure induced a decrease of the pregnancy rate (control group: 9/14; exposure group: 5/14) and abnormal embryo arrangement, small placenta, narrowing of spiral arteries (control group: 1.00±0.06; exposure group: 0.86±0.08; P=0.01), as well as significant decreases in HIF-1α, VEGF and its receptor Flk-1 mRNA expressions. (all Ps <0.05). Conclusion Pre-pregnancy PM2.5 exposure has adverse effects on the pathological structure and angiogenesis in female mice uterus, leading to abnormal vascular network remodeling at the mother-fetal interface after conception, and the HIF-1α/VEGF axis may play a regulatory role.

Exosomes from PM 2.5-treated Human Bronchial Epithelial Cells Increase Lung Cancer Metastatic Potential / 生物医学与环境科学（英文）

Objective@#Fine particulate matter (PM 2.5) is an air pollutant that has become of great concern in recent years. Numerous studies have found that PM 2.5 may contribute to lung cancer, but the pathogenesis has not yet been fully elucidated. In this study, we explored the roles of exosomes from bronchial epithelial cells in PM 2.5-promoted lung cancer metastasis.@*Methods@#Exosomes were isolated from cell supernatants. An animal model of lung metastasis (established by tail vein injection of A549-luc) and in vitro studies with lung cancer cell lines were used to investigate the effects of exosomes derived from PM 2.5-treated human bronchial epithelial cells (PHBE-exo).@*Results@#The animal experiments revealed that PHBE-exo-treated mice showed stronger luciferase activity and a larger relative metastatic region in the lungs, thus indicating that PHBE-exo promoted the metastatic potential of lung cancer. Additionally, PHBE-exo promoted the migration, invasion and epithelial-to-mesenchymal transition of lung cancer cells, in a manner mediated by activation of c-Jun N-terminal kinase.@*Conclusion@#These results implied that PM 2.5 may promote the development of lung cancer through exosomes derived from bronchial epithelial cells, thus providing a potential interventional target for lung cancer. These findings broadened our understanding of cancer-promoting mechanisms of environmental pollutants.

Study on DNA methylation in HEB cells exposed to PM(2.5) by application of methylation chip technology / 中华劳动卫生职业病杂志

Objective: To screen the differential methylation sites, genes and pathways of air pollution fine particles (PM(2.5)) on human bronchial epithelial (HBE) cells by methylation chip and bioinformation technology, so as to provide scientific basis for further study of the toxicological mechanism of PM(2.5) on HBE cells. Methods: In August 2020, HBE cells were infected with 10 μg/ml and 50 μg/ml PM(2.5) aqueous solution for 24 h, namely PM(2.5) 10 μg/ml exposure group (low dose group) and PM(2.5) 50 μg/ml exposure group (high dose group) ; uninfected HBE cells were used as control group. The DNA fragments were hybridized with the chip, the chip scanned and read the data, analyzed the data, screened the differential methylation sites, carried out GO analysis and KEGG analysis of the differential methylation sites, and analyzed the interaction relationship of the overall differential methylation sites by functional epigenetic modules (FEMs). Results: Compared with the control group, 127 differential methylation sites were screened in the low-dose group, including 89 genes, including 55 sites with increased methylation level and 72 sites with decreased methylation level. The differential methylation sites were mainly concentrated in the Body region and UTR region. Compared with the control group, 238 differential methylation sites were screened in the high-dose group, including 168 genes, of which 127 sites had increased methylation level and 111 sites had decreased methylation level. The differential heterotopic sites were mainly concentrated in the Body region and UTR region. Through FEMs analysis, 8 genes with the most interaction were screened, of which 6 genes had significant changes in methylation level. MALT1 gene related to apoptosis was found in the heterotopic site of methylation difference in low-dose group; PIK3CA and ARID1A genes related to carcinogenesis were found in the heterotopic sites of methylation difference in high-dose group; TNF genes related to tumor inhibition were found in the results of FEMs analysis. Conclusion: After PM(2.5) exposure to HBE cells, the DNA methylation level is significantly changed, and genes related to apoptosis and carcinogenesis are screened out, suggesting that the carcinogenic mutagenic effect of PM(2.5) may be related to DNA methylation.

Research progress on effects of PM2.5 exposure during pregnancy on maternal and infant thyroid function / 环境与职业医学

Ambient air pollution has become a widespread global public health problem. As one of the main components of ambient air pollution, fine particulate matter (PM2.5), with its small diameter and large surface area, can carry a variety of toxic substances and enter the blood circulation directly through the blood-air barrier, damaging various tissues and organs of human body. Studies have shown that PM2.5 exposure during pregnancy can disrupt the mother's and child's thyroid function. Since the fetal thyroid gland does not begin to develop until around the sixth week of pregnancy, the fetal thyroid hormone is almost entirely dependent on the mother during early stages of pregnancy, and maternal thyroid hormone level play a crucial role in the growth and development of fetus. When a mother is exposed to PM2.5 during pregnancy, placenta, the "bridge" between mother and fetus, is also affected to some extent, including changes in placental iodine uptake and oxidative stress, inflammation, and DNA methylation in placental tissue. Exposure to PM2.5 during pregnancy also alters maternal thyroid hormone level and normal placental function, which can have a detrimental effect on pregnancy outcomes, such as preterm birth, low birth weight, and neurological abnormalities. This paper reviewed the effects of PM2.5 exposure during different trimesters on maternal and infant thyroid function, placental function, and pregnancy outcomes, aiming to provide more accurate protection of maternal and fetal health.

Meta-analysis of effects of long-term exposure to PM2.5 on C-reactive protein levels / 环境与职业医学

Background Fine particulate matter (PM2.5) is a serious air pollutant associated with elevated levels of C-reactive protein (CRP), an inflammatory indicator. Objective To assess the potential impacts of long-term exposure to PM2.5 on CRP levels based on previous epidemiological studies. Methods PubMed, Embase, Web of Science, CNKI, and Wanfang databases were searched to screen the cohort studies published from January 1, 2000 to January 1, 2022 on the effects of long-term exposure to PM2.5 on CRP levels. "Fine Particulate Matter", "PM2.5", "Particulate Air Pollutants", "Ambient Particulate Matter", "CRP", "C-reactive Protein", and "High Sensitivity C-reactive Protein" in English or Chinese were the key words used in the search. The percentage change in CRP level per 10 μg·m−3 increase in PM2.5 concentration in each study was extracted, followed by meta-analysis, subgroup analysis, and sensitivity analysis. Results A total of 1241 articles were retrieved, and 7 articles were included. Random-effects models were used to merge the included data, and it was found that the percentage of CRP level increased by 10.41% (95%CI: 2.24%-18.57%, P<0.05), when PM2.5 concentration increased by 10 μg·m−3, І2=84.2%. The subgroup analysis conducted with grouping based on the annual mean concentration of PM2.5 long-term exposure showed that the intra-group heterogeneity was significantly reduced in the <15 μg·m−3 and the 15- μg·m−3 groups, and the subgroup forest analysis showed differences between the two groups. The results of sensitivity analysis showed that there was a high degree of heterogeneity among the 7 studies, and the 2 papers with the highest annual average PM2.5 concentration were the sources of heterogeneity. The Egger test and the funnel plot indicated that no obvious publication bias was found. Conclusion Long-term exposure to PM2.5 can raise levels of CRP in human body.

Role of intestinal flora and 5-HT in depression- and anxiety-like behaviors in mice exposed to PM2.5 / 环境与职业医学

Background Some studies have shown that PM2.5 exposure is closely related to central nervous system diseases that lead to cognitive dysfunction and change the composition of intestinal flora. However, there are few studies on the role of intestinal flora in PM2.5-induced depression- and anxiety-like behaviors in mice. Objective To observe the effects of PM2.5 exposure on depression- and anxiety-like behaviors and the composition of intestinal flora in mice, and to explore the role of intestinal flora in regulating 5-hydroxytryptamine (5-HT) in depression- and anxiety-like behaviors in mice exposed to PM2.5. Methods Eight-week-old male SPF C57BL/6J mice were randomly divided into control group (NS group), probiotic group (LGG group), PM2.5 group (PM group), and combined exposure group (PML group), 6 mice in each group. Mice in the PM group and the PML group were exposed to PM2.5 in a dynamic exposure cabinet for 6 h per day, 6 d a week for 7 consecutive weeks, and the PM2.5 concentrations were approximately 8 times higher than the outdoor concentration. The LGG group and the PML group were orally administered with Lactobacillus rhamnosus while the NS group and the PM group were orally administered with the same amount of saline. Elevated plus maze test and open field test were used to detect depression and anxiety in mice. Fecal samples of mice were collected to evaluate intestinal flora abundance, diversity, and structure between groups using high-throughput sequencing of 16S rRNA. ELISA was employed to detect the levels of 5-HT in serum and hippocampus. Spearman correlation was used to analyze the correlations of differential intestinal flora with 5-HT level in hippocampus and depression- and anxiety-like behavior indicators in mice. Results The percentage of open-arm entry [M(P25, P75)] in the PM group was 0.0% (0.0%, 33.3%), lower than those in the NS group [47.7% (25.0%, 50.8%) ] and the PML group [46.9% (40.0%, 50.0%)], and the differences were statistically significant (P<0.05). The total travelled distance and the time spent in central area (\begin{document}$\bar x \pm s $\end{document}) in the PM group were (2.01±0.90) m and (10.31±1.99) s respectively, shorter than those of the NS group [(3.80±0.89) m, (14.47±3.07) s], the total travelled distance in the PML group [(2.73±1.12) m] was shorter than those of the NS group and the LGG group [(4.21±1.08) m], and the differences were statistically significant (P<0.05). Compared to the NS group, the Simpson index of the PM group significantly increased (P<0.05). Compared to the LGG group, the Simpson index of the PML group significantly decreased (P<0.05). The results of Beta diversity analysis showed that there were differences in the composition of intestinal flora among the four groups of mice. Compared with the NS group and the LGG group, the abundances of Erysipelotrichaceae and Dubosiella in the PM group and the PML group increased, while the abundances of Prevotellaceae_UCG-001 decreased, and the differences were statistically significant (P<0.05). In hippocampus, the level of 5-HT in the PM group [(135.02±10.31) μg·g−1] was lower than those in the NS group [(178.77±43.15) μg·g−1] and the LGG group [(224.85±22.98) μg·g−1], and the level of 5-HT in the PML group [(161.27±15.81) μg·g−1] was lower than that in the LGG group (P<0.05). 5-HT level in hippocampus was significantly positively correlated with the relative abundance of Prevotellaceae_UCG-001 (r=0.6090, P=0.012). The percentage of open-arm entry was significantly negatively correlated with the relative abundance of Dubosiella (r=−0.4630, P=0.023). Conclusion Atmospheric PM2.5 exposure may cause depression- and anxiety-like behaviors in mice. The observed behavior dysfunction may be associated with the changes in diversity and relative abundance of intestinal flora as well as the decrease of 5-HT level. Such depression- and anxiety-like behaviors are alleviated after adding probiotics.

Research progress on adverse effects of fine particulate matter constituent exposure on ischemic heart disease / 公共卫生与预防医学

Ambient fine particulate matter (PM2.5) is a mixture consisting of a wide range of chemical constituents including carbonaceous aerosols, water soluble ions and inorganic elements, and has become the major air pollutant in most cities in China. Evidence suggests that exposure to ambient PM2.5 induces damage on the cardiovascular system and can increase risk of the development and mortality of ischemic heart diseases (IHD). However, the effects of exposure to specific PM2.5 constituents on IHD remain unclear, and its underlying mechanisms are yet to be investigated. Here we reviewed studies investigating the association of short- and long-term exposure to specific PM2.5 constituents with IHD, which may provide useful clues for future relevant studies.