Effects Of PM2 Research Articles

Smaller particular matter, larger risk of female lung cancer incidence? Evidence from 436 Chinese counties

BackgroundMany studies have reported the effects of PM2.5 and PM10 on human health, however, it remains unclear whether particular matter with finer particle size has a greater effect.ObjectivesThis work aims to examine the varying associations of the incidence rate of female lung cancer with PM1, PM2.5 and PM10 in 436 Chinese cancer registries between 2014 and 2016.MethodsThe effects of PM1, PM2.5 and PM10 were estimated through three regression models, respectively. Mode l only included particular matter, while Model 2 and Model 3 further controlled for time and location factors, and socioeconomic covariates, respectively. Moreover, two sensitivity analyses were performed to investigate the robustness of three particular matte effects. Then, we examined the modifying role of urban-rural division on the effects of PM1, PM2.5 and PM10, respectively.ResultsThe change in the incidence rate of female lung cancer relative to its mean was 5.98% (95% CI: 3.40, 8.56%) for PM1, which was larger than the values of PM2.5 and PM10 at 3.75% (95% CI: 2.33, 5.17%) and 1.57% (95% CI: 0.73, 2.41%), respectively. The effects of three particular matters were not sensitive in the two sensitivity analyses. Moreover, urban-rural division positively modified the associations of the incidence rate of female lung cancer with PM1, PM2.5 and PM10.ConclusionsThe effect on the incidence rate of female lung cancer was greater for PM1, followed by PM2.5 and PM10. There were positive modifying roles of urban-rural division on the effects of three particular matters. The finding supports the argument that finer particular matters are more harmful to human health, and also highlights the great significance to develop guidelines for PM1 control and prevention in Chinese setting.

Nucleotide Excision Repair Pathway Activity Is Inhibited by Airborne Particulate Matter (PM10) through XPA Deregulation in Lung Epithelial Cells.

Airborne particulate matter with a diameter size of ≤10 µm (PM10) is a carcinogen that contains polycyclic aromatic hydrocarbons (PAH), which form PAH–DNA adducts. However, the way in which these adducts are managed by DNA repair pathways in cells exposed to PM10 has been partially described. We evaluated the effect of PM10 on nucleotide excision repair (NER) activity and on the levels of different proteins of this pathway that eliminate bulky DNA adducts. Our results showed that human lung epithelial cells (A549) exposed to 10 µg/cm2 of PM10 exhibited PAH–DNA adducts as well as an increase in RAD23 and XPD protein levels (first responders in NER). In addition, PM10 increased the levels of H4K20me2, a recruitment signal for XPA. However, we observed a decrease in total and phosphorylated XPA (Ser196) and an increase in phosphatase WIP1, aside from the absence of XPA–RPA complex, which participates in DNA-damage removal. Additionally, an NER activity assay demonstrated inhibition of the NER functionality in cells exposed to PM10, indicating that XPA alterations led to deficiencies in DNA repair. These results demonstrate that PM10 exposure induces an accumulation of DNA damage that is associated with NER inhibition, highlighting the role of PM10 as an important contributor to lung cancer.

Effect of PM2.5 exposure on gestational hypertension, fetal size in preeclampsia-like rats.

Studies have shown intriguing associations between gestational PM2.5 exposure and preeclampsia (PE), as well as fetal growth restriction (FGR). This study investigated the impact of PM2.5 exposure on gestational hypertension and fetal outcome in a preeclampsia-like rat model. Pregnant Sprague Dawley rats were exposed to either filtered (FA) or PM2.5-contaminated air during the whole pregnancy period. A PE-like rat model was established by intraperitoneal injection of L-NAME (300mg/kg) from gestational day (GD) 12 to until GD20. Systolic blood pressure (SBP), weight gain, pup weight and placental weight were measured. The percentages of rat Treg/Th17 cells and Th17-related cytokines were examined by flow cytometry. Gene expression profiles were analyzed by microarray, and the expression of differentially expressed genes was validated by qRT-PCR. The results showed that maternal PM2.5 exposure had no effect on SBP but was associated with low birth weight (LBW) and a higher labyrinth/basal zone ratio. The percentages of splenic Th17 cells from the PM2.5 group of PE-like rats were higher than those from the FA or PM2.5 groups of healthy controls. A significantly decreased Treg/Th17 cell ratio was found in the PM2.5 group of PE-like rats. The mRNA expression of Foxp3 was downregulated, while the mRNA expression of RORα and RORγτ was upregulated after PM2.5 exposure. Furthermore, we observed that both the mRNA and protein levels of TNF-a, CCL2, CCL3 and CCR1 increased in the PM2.5 groups. Our study suggested that systemic inflammation may contribute to the development of FGR associated with PM2.5 exposure throughout pregnancy.

The effects of air pollution on the lung cancer mortality in rural areas of eastern China: a multi-region study.

Recently, the burden of lung cancer (LC) has attracted global attention. Meanwhile, LC has become the leading cause of death in China. Many studies found a strong link between air pollutants and the risk of LC mortality in some large cities, but the results have been inconsistent, and most studies have only focused on the daily effects of six pollutants in large cities, ignoring their potential cumulative effects. This study was to investigate the weekly effects of six air pollutants (CO, NO2, O3, PM2.5, PM10, and SO2) on LC mortality in rural areas of eastern China and to further clarify which population groups were susceptible to air pollution and seasonal trends. First, a generalized additive model was combined with a distributed lag nonlinear model to evaluate the individual impact of air pollution on LC deaths in each area. The random-effect model was then used to pool the associations between air pollutants and LC mortality risk in ten counties or districts. The results showed that six air pollutants had a statistically significant effect on the risk of LC mortality at different lag weeks. The effects of NO2, PM10, and CO on weekly LC mortality were strongest at a cumulative lag of 1, 0, and 1 week, respectively, the maximum cumulative risk ratio (RR) of 1.37 (95%CI: 1.23 to 1.52), 1.30 (95%CI: 1.15 to 1.46), and 1.30 (95%CI: 1.17 to 1.43), with interquartile concentrations increasing. In summary, air pollution was an important factor in LC mortality, and the effect was stronger on males, the elderly, and during cold season. It was suggested that relevant departments should formulate air pollution management measures for the elderly, males, and in different seasons in rural areas and reduce the burden of lung cancer caused by air pollution.

Particulate matter (PM10) destabilizes mitotic spindle through downregulation of SETD2 in A549 lung cancer cells

Air pollution represents an environmental problem, impacting negatively in human health. Particulate matter of 10 μm or less in diameter (PM10) is related to pulmonary diseases, including lung cancer. Mitotic spindle is made up by chromosome-microtubule (MT) interactions, where SETD2 plays an important role in MT stability. SETD2 binds and activates α-TUBULIN sub-unit and promotes MT polymerization. Alongside this mechanism, the spindle assembly checkpoint (SAC) senses the adequate mitotic progression through proteins such as BUBR1, AURORA B and SURVIVIN. Alterations in MT dynamics as well as in SAC cause aneuploidy and chromosomal instability, a common phenotype in cancer cells. In this study, we evaluated the effect of PM10 in the expression and protein levels of SETD2, as well as the effect in the expression and protein levels of SAC and mitotic components involved in chromosomal segregation/mitosis, using the A549 lung cancer cell line. A549 cell cultures were exposed to PM10 (10 μg/cm2) for 24 h to evaluate the expression and protein levels of SETD2 (SETD2), TUBA1A (α-TUBULIN), CCNB1 (CYCLIN B1), BUB1B (BUBR1), AURKB (AURORA B) and BIRC5 (SURVIVIN). We observed that PM10 decreases the expression and protein levels of SETD2, α-TUBULIN and BUBR1 and increases the levels of AURORA B and SURVIVIN in A549 cells, compared with non-treated cells. PM10 also caused a decrease in mitotic index and in the percentage of cells in G2/M when compared with control group. Co-localization of SETD2/α -TUB was lower in PM10-treated cells in comparison with non-treated cells. Finally, micronuclei (MN) frequency was higher in PM10-treated cells in contrast with non-treated cells, being whole chromosomes more common in PM10-treated MN than in non-treated MN. Our results suggest that PM10 causes missegregation and aneuploidy through downregulation of SETD2 and SAC components, inducing aneuploidy and predisposing to the generation of chromosomal instability in transformed cells.

GLIS3 mediated by the Rap1/PI3K/AKT signal pathway facilitates real-ambient PM2.5 exposure disturbed thyroid hormone homeostasis regulation

Exposure to fine particulate matter (PM2.5) could damage multiple organs and systems. Recent epidemiological studies have shown that PM2.5 can disrupt dynamic balance of thyroid hormone (TH). However, the underlying mechanism by which PM2.5 interferes with TH remains unclear. This study evaluated the role of Gli-similar3 (GLIS3) in the effect of PM2.5 on TH synthesis in mice using a real-ambient exposure system, in Shijiazhuang City, Hebei Province. The PM2.5exposure group (PM) and filtered air group (FA) were placed in the exposure device for four and eight weeks. The results showed that the PM2.5 exposure altered the structure of the thyroid gland. Moreover, after PM2.5 exposure for eight weeks, the exposure level of free thyroxine (FT4) increased and the expression level of thyroid stimulating hormone (TSH) decreased in serum of mice. In addition, PM2.5 exposure significantly increased the expression of proteins related to thyroid hormone synthesis, such as sodium iodide transporter (NIS), thyroid peroxidase (TPO) and thyroglobulin (TG). Next, we found that GLIS3 and thyroid transcription factor Paired box 8 (PAX8) also increased after PM2.5 exposure. In order to further explore the potential molecular mechanism, we carried out transcriptome sequencing. KEGG analysis of the top 10 pathways revealed that the Ras-associated protein 1 (Rap1) signaling pathway could activate transcription factors and is related to thyroid cell survival. Additionally, PM2.5 exposure significantly increased the protein levels of Rap1 and its active form (Rap1 +GTP). We speculate that the active state of Rap1 is believed to be involved in activating the expression of transcription factor GLIS3. In conclusion, PM2.5 exposure induces histological changes in the thyroid gland and thyroid dysfunction in mice. The exposure activates GLIS3 through the Rap1/PI3K/AKT pathway to promote the expression of proteins related to thyroid hormone synthesis, leading to increased dysregulating TH homeostasis.

Association between traffic-related air pollution and anxiety hospitalizations in a coastal Chinese city: are there potentially susceptible groups?

Motor vehicle exhaust emissions have become the main source of urban air pollution in China, but few studies have explored the association of short-term exposure to traffic-related air pollutants (TRAPs) with anxiety disorders. Thus, we used an overdispersed, generalized additive model (GAM) to investigate the association between TRAPs and hospital admissions (HAs) for anxiety in Qingdao, a coastal Chinese city with high vehicle ownership. In addition, stratified analyses were performed by gender, age, season and hospitalization frequency (first admission and readmission). A positive association between TRAPs and HAs for anxiety was observed. Both inhalable particulate matter (PM10) and nitrogen dioxide (NO2) showed significant effects at lag 3 in the single-day lag structure, and each 10 μg/m3 increase in the concentrations was significantly associated with increases of 0.88% [95% confidence interval (CI): 0.04%, 1.72%] for PM10 and 2.74% (0.45%, 5.08%) for NO2 on anxiety hospitalizations. For fine particulate matter (PM2.5) and carbon monoxide (CO), the strongest effects were found at lag05 and lag04 [2.67% (0.77%, 4.62%) and 0.19% (0.04%, 0.34%), respectively] in the multiday lag structure. The estimates of PM2.5 were relatively robust after adjusting for other pollutants in the two-pollutant model. Stratified analyses indicated that the associations were stronger in females and younger individuals (<45 in age) than in males and elderly individuals (≥45 in age). Furthermore, the effects of PM2.5 and CO were most obvious during the cold season. Regarding hospitalization frequency, only PM2.5 was found to have a significant effect in the first-admission group. The results showed that short-term exposure to TRAPs, especially to PM2.5, was significantly associated with the increased risk of daily HAs for anxiety, which can help clinicians and policymakers better understand the effects of TRAPs to implement targeted interventions.

Rural-urban differences in associations between air pollution and cardiovascular hospital admissions in Guangxi, southwest China.

Epidemiological studies found that exposure to air pollution increases cardiovascular hospitalizations. However, studies on rural-urban differences in associations between hospitalizations for cardiovascular diseases and air pollution are limited. The generalized linear model (GLM) was applied to investigate the associations between cardiovascular hospitalizations and air pollution (SO2, NO2, PM2.5, PM10, CO, and O3) in Guangxi, southwest China, in 2015 (January 1-December 31). The relative risk of pollutants (SO2, NO2) on cardiovascular hospital admissions was significantly different between urban and rural areas. The effect of SO2 on cardiovascular hospitalizations was higher in urban areas than in rural areas at lag0 to lag3 and cumulative lag01 to lag03. In urban areas, there were positive associations between NO2 and cardiovascular hospitalizations at lag0, lag1 and cumulative lag01, lag02. In contrast, the effect of NO2 on cardiovascular hospitalizations was not significant in rural areas. Urban residents were more sensitive than rural residents to SO2 and NO2. Subgroup analyses showed statistically significant differences between rural and urban areas in the association between SO2 and NO2 and cardiovascular hospitalizations for males. For age groups, people aged ≥ 65 years appeared to be more vulnerable to SO2 and NO2 in urban areas. The effects of PM2.5 PM10, CO, and O3 on cardiovascular hospitalizations were consistently negative for all groups. Our findings indicated that there were rural-urban differences in associations between cardiovascular hospitalizations and air pollutants. In rural areas, the risk of cardiovascular hospitalizations was mainly influenced by SO2. Therefore, we expect to pay attention to protecting people from air pollution, particularly for those aged ≥ 65 years in urban areas.

Nonlinear effect of air pollution on adult pneumonia hospital visits in the coastal city of Qingdao, China: A time-series analysis

Many studies have illustrated adverse effects of short-term exposure to air pollution on human health, which usually assumes a linear exposure-response (E-R) function in the delineation of health effects due to air pollution. However, nonlinearity may exist in the association between air pollutant concentrations and health outcomes such as adult pneumonia hospital visits, and there is a research gap in understanding the nonlinearity. Here, we utilized both the distributed lag model (DLM) and nonlinear model (DLNM) to compare the linear and nonlinear impacts of air pollution on adult pneumonia hospital visits in the coastal city of Qingdao, China. While both models show adverse effects of air pollutants on adult pneumonia hospital visits, the DLNM shows an attenuation of E-R curves at high concentrations. Moreover, the DLNM may reveal delayed health effects that may be missed in the DLM, e.g., ozone exposure and pneumonia hospital visits. With the stratified analysis of air pollutants on adult pneumonia hospital visits, both models consistently reveal that the influence of air pollutants is higher during the cold season than during the warm season. Nevertheless, they may behave differently in terms of other subgroups, such as age, gender and visit types. For instance, while no significant impact due to PM2.5 in any of the subgroups abovementioned emerges based on DLM, the results from DLNM indicate statistically significant impacts for the subgroups of elderly, female and emergency department (ED) visits. With respect to adjustment by two-pollutants, PM10 effect estimates for pneumonia hospital visits were the most robust in both DLM and DLNM, followed by NO2 and SO2 based on the DLNM. Considering the estimated health effects of air pollution relying on the assumed E-R functions, our results demonstrate that the traditional linear association assumptions may overlook some potential health risks.

Effect of Airborne Particulate Matter on the Immunologic Characteristics of Chronic Rhinosinusitis with Nasal Polyps.

The inflammatory mechanisms of environmental pollutants in chronic rhinosinusitis (CRS) have recently been proposed. However, the mechanisms underlying the inflammatory effects of particulate matter (PM) on nasal polyp (NP) tissues remain unknown. Here we investigated the mechanism underlying the inflammatory effects of PM10 on human nasal polyp-derived fibroblasts (NPDFs). We isolated NPDFs from human NP tissues obtained from patients with CRS with NPs (CRSwNP). The NPDFs were exposed to PM10 in vitro. Immunologic characteristics were assessed using real-time polymerase chain reaction, enzyme-linked immunosorbent assay, Western blot, and flow cytometry. Additionally, we investigated the effect of NPDF-conditioned media (CM) on the expression of CD4+ T cell inflammatory mediators. PM10-treated NPDFs significantly upregulated interleukin (IL)-6, IL-4, and IL-33 expression and CXCL1 protein levels than PM10-treated normal tissues. MAP kinase, AP-1, and NF-kB were the primary cell signaling proteins. Immune cells in NPDF-CM had elevated IL-13, IL-17A, and IL-10 expression, but no significant difference in IFN-γ, TNF-α, and IL-4 expression. Moreover, under a Th2 inducing condition, NPDF-CM-treated CD4+ T cells had increased expression of IL-13, IL-10, and IL-17, which was reversed on ST2 inhibitor addition. Our study suggests that PM10 exposure could significantly increase the Th2 inflammatory pathway in NP tissues, specifically the IL-33/ST2 pathway-mediated immune response.

Association between atmospheric particulate matter and emergency room visits for cerebrovascular disease in Beijing, China.

The association between atmospheric particulate matter and emergency room visits for cerebrovascular disease were evaluated in Beijing. A generalized additive model was used to evaluate the associations between particulate matter and cerebrovascular disease, based on the daily data of meteorological elements, PM concentrations, and emergency room (ER) visits for cerebrovascular disease in Beijing from 2009 to 2012. Long-term trends and the effects of holidays, the day of the week, and confounding factors were controlled to determine the lag effect at 0-6days. Single- and double-pollutant models were employed for different age and sex groups. The effect of PM2.5 concentration on the number of daily ER visits for cerebrovascular disease was much stronger than that of PM10 concentration. PM2.5 and PM10 had maximum RR values of 1.096 and 1.054 at lag 6 for patients aged 61-75years. For each inter-quartile range (IQR) increase in PM10 concentration, the maximum RR values for the total, males, females, aged 15-60years, aged 61-75years, and aged > 75years were 1.024, 1.044, 1.043, 1.038, 1.054, and 1.032, respectively. For each IQR increase in PM2.5 concentration, the maximum RR values for the total, males, females, aged 15-60years, aged 61-75years, and aged > 75years were 1.038, 1.064, 1.076, 1.054, 1.096, and 1.049, respectively. The RR values of the double-pollutant models were lower than those of the single-pollutant models. This study showed that the effects of PM pollution on cerebrovascular disease were different among different gender and age groups, and aged 61-75years were mostly sensitive to particulate matters. The effects of PM2.5 on cerebrovascular disease were stronger than those of PM10. Our results can provide scientific evidence for the local government to take effective measures to improve air quality and the health of residents. The online version contains supplementary material available at 10.1007/s40201-021-00776-w.

Long-Term Exposure to Ambient PM2.5, Sunlight, and Obesity: A Nationwide Study in China.

BackgroundAccumulated researches revealed that both fine particulate matter (PM2.5) and sunlight exposure may be a risk factor for obesity, while researches regarding the potential effect modification by sunlight exposure on the relationship between PM2.5 and obesity are limited. We aim to investigate whether the effect of PM2.5 on obesity is affected by sunlight exposure among the general population in China.MethodsA sample of 47,204 adults in China was included. Obesity and abdominal obesity were assessed based on body mass index, waist circumference and waist-to-hip ratio, respectively. The five-year exposure to PM2.5 and sunlight were accessed using the multi-source satellite products and a geochemical transport model. The relationship between PM2.5, sunshine duration, and the obesity or abdominal obesity risk was evaluated using the general additive model.ResultsThe proportion of obesity and abdominal obesity was 12.6% and 26.8%, respectively. Levels of long-term PM2.5 ranged from 13.2 to 72.1 μg/m3 with the mean of 46.6 μg/m3. Each 10 μg/m3 rise in PM2.5 was related to a higher obesity risk [OR 1.12 (95% CI 1.09-1.14)] and abdominal obesity [OR 1.10 (95% CI 1.07-1.13)]. The association between PM2.5 and obesity varied according to sunshine duration, with the highest ORs of 1.56 (95% CI 1.28-1.91) for obesity and 1.66 (95% CI 1.34-2.07) for abdominal obesity in the bottom quartile of sunlight exposure (3.21-5.34 hours/day).ConclusionLong-term PM2.5 effect on obesity risk among the general Chinese population are influenced by sunlight exposure. More attention might be paid to reduce the adverse impacts of exposure to air pollution under short sunshine duration conditions.

Exposure to environmentally relevant concentrations of ambient fine particulate matter (PM2.5) depletes the ovarian follicle reserve and causes sex-dependent cardiovascular changes in apolipoprotein E null mice

BackgroundFine particulate matter (PM2.5) exposure accelerates atherosclerosis and contains known ovotoxic chemicals. However, effects of exposure to PM2.5 on the finite ovarian follicle pool have hardly been investigated, nor have interactions between ovarian and cardiovascular effects. We hypothesized that subchronic inhalation exposure to human-relevant concentrations of PM2.5 results in destruction of ovarian follicles via apoptosis induction, as well as accelerated recruitment of primordial follicles into the growing pool. Further, we hypothesized that destruction of ovarian follicles enhances the adverse cardiovascular effects of PM2.5 in females.ResultsHyperlipidemic apolipoprotein E (Apoe) null ovary-intact or ovariectomized female mice and testis-intact male mice were exposed to concentrated ambient PM2.5 or filtered air for 12 weeks, 5 days/week for 4 h/day using a versatile aerosol concentration enrichment system. Primordial, primary, and secondary ovarian follicle numbers were decreased by 45%, 40%, and 17%, respectively, in PM2.5-exposed ovary-intact mice compared to controls (P < 0.05). The percentage of primary follicles with granulosa cells positive for the mitosis marker Ki67 was increased in the ovaries from PM2.5-exposed females versus controls (P < 0.05), consistent with increased recruitment of primordial follicles into the growing pool. Exposure to PM2.5 increased the percentages of primary and secondary follicles with DNA damage, assessed by γH2AX immunostaining (P < 0.05). Exposure to PM2.5 increased the percentages of apoptotic antral follicles, determined by TUNEL and activated caspase 3 immunostaining (P < 0.05). Removal of the ovaries and PM2.5-exposure exacerbated the atherosclerotic effects of hyperlipidemia in females (P < 0.05). While there were statistically significant changes in blood pressure and heart rate variability in PM2.5-compared to Air-exposed gonad-intact males and females and ovariectomized females, the changes were not consistent between exposure years and assessment methods.ConclusionsThese results demonstrate that subchronic PM2.5 exposure depletes the ovarian reserve by increasing recruitment of primordial follicles into the growing pool and increasing apoptosis of growing follicles. Further, PM2.5 exposure and removal of the ovaries each increase atherosclerosis progression in Apoe-/- females. Premature loss of ovarian function is associated with increased risk of osteoporosis, cardiovascular disease and Alzheimer’s disease in women. Our results thus support possible links between PM2.5 exposure and other adverse health outcomes in women.

A city-level analysis of PM2.5 pollution, climate and COVID-19 early spread in Spain.

PurpuseThe COVID-19 outbreak has escalated into the worse pandemic of the present century. The fast spread of the new SARS-CoV-2 coronavirus has caused devastating health and economic crises all over the world, with Spain being one of the worst affected countries in terms of confirmed COVID-19 cases and deaths per inhabitant. In this situation, the Spanish Government declared the lockdown of the country.MethodsThe variations of air pollution in terms of fine particulate matter (PM2.5) levels in seven representative cities of Spain are analyzed here considering the effect of meteorology during the national lockdown. The possible associations of PM2.5 pollution and climate with COVID-19 accumulated cases were also analyzed.ResultsWhile the epidemic curve was flattened, the results of the analysis show that the 4-week Spanish lockdown significantly reduced the PM2.5 levels in only one city despite the drastically reduced human activity. Furthermore, no associations between either PM2.5 exposure or environmental conditions and COVID-19 transmission were found during the early spread of the pandemic.ConclusionsA longer period applying human activity restrictions is necessary in order to achieve significant reductions of PM2.5 levels in all the analyzed cities. No effect of PM2.5 pollution or weather on COVID-19 incidence was found for these pollutant levels and period of time.Graphical abstract Supplementary InformationThe online version contains supplementary material available at 10.1007/s40201-022-00786-2.

Short-Term Joint Effects of PM10, NO2 and SO2 on Cardio-Respiratory Disease Hospital Admissions in Cape Town, South Africa.

Background/Aim: In sub-Sahara Africa, few studies have investigated the short-term association between hospital admissions and ambient air pollution. Therefore, this study explored the association between multiple air pollutants and hospital admissions in Cape Town, South Africa. Methods: Generalized additive quasi-Poisson models were used within a distributed lag linear modelling framework to estimate the cumulative effects of PM10, NO2, and SO2 up to a lag of 21 days. We further conducted multi-pollutant models and stratified our analysis by age group, sex, and season. Results: The overall relative risk (95% confidence interval (CI)) for PM10, NO2, and SO2 at lag 0–1 for hospital admissions due to respiratory disease (RD) were 1.9% (0.5–3.2%), 2.3% (0.6–4%), and 1.1% (−0.2–2.4%), respectively. For cardiovascular disease (CVD), these values were 2.1% (0.6–3.5%), 1% (−0.8–2.8%), and −0.3% (−1.6–1.1%), respectively, per inter-quartile range increase of 12 µg/m3 for PM10, 7.3 µg/m3 for NO2, and 3.6 µg/m3 for SO2. The overall cumulative risks for RD per IQR increase in PM10 and NO2 for children were 2% (0.2–3.9%) and 3.1% (0.7–5.6%), respectively. Conclusion: We found robust associations of daily respiratory disease hospital admissions with daily PM10 and NO2 concentrations. Associations were strongest among children and warm season for RD.

The influence of PM2.5 exposure on kidney diseases.

The harm of air pollution to public health has become a research hotspot, especially atmospheric fine-particulate matter (PM2.5). In recent years, epidemiological investigations have confirmed that PM2.5 is closely related to chronic kidney disease and membranous nephropathy Basic research has demonstrated that PM2.5 has an impact on the normal function of the kidneys through accumulation in the kidney, endothelial dysfunction, abnormal renin-angiotensin system, and immune complex deposition. Moreover, the mechanism of PM2.5 damage to the kidney involves inflammation, oxidative stress, apoptosis, DNA damage, and autophagy. In this review, we summarized the latest developments in the effects of PM2.5 on kidney disease in human and animal studies, so as to provide new ideas for the prevention and treatment of kidney disease.

Effects of PM2.5 concentration on mortality in China:A study based on city-level panel data

Effects of PM2.5 concentration on mortality in China:A study based on city-level panel data

Effects of Dust Event Days on Influenza: Evidence from Arid Environments in Lanzhou

Airborne aerosol is believed to be an important pathway for infectious disease transmissions like COVID-19 and influenza. However, the effects of dust event days on influenza have been rarely explored, particularly in arid environments. This study explores the effects of ambient particulate matter (PM) and dust events on laboratory-confirmed influenza in a semi-arid city. A descriptive analysis of daily laboratory-confirmed influenza (influenza) cases, PM (PM10 and PM2.5), meteorological parameters, and dust events were conducted from 2014 to 2019 in Lanzhou, China. The case-crossover design combined with conditional Poisson regression models was used to estimate the lagging effects of PM and dust events on influenza. In addition, a hierarchical model was used to quantitatively evaluate the interactive effect of PM with ambient temperature and absolute humidity on influenza. We found that PM and dust events had a significant effect on influenza. The effects of PM10 and PM2.5 on influenza became stronger as the cumulative lag days increased. The greatest estimated relative risks (RRs) were 1.018 (1.011,1.024) and 1.06 1(1.034,1.087), respectively. Compared with the non-dust days, the effects of dust events with duration ≥ 1 day and with duration ≥ 2 days on influenza were the strongest at lag0 day, with the estimated RRs of 1.245 (95% CI: 1.061-1.463) and 1.483 (95% CI: 1.232-1.784), respectively. Subgroup analysis showed that pre-school children and school-aged children were more sensitive to PM and dust events exposure. Besides, we also found that low humidity and temperature had an interaction with PM to aggravate the risk of influenza. In summary, ambient PM and dust events exposure may increase the risk of influenza, and the risk of influenza increases with the dust events duration. Therefore, more efforts from the government as well as individuals should be strengthened to reduce the effect of PM on influenza, particularly in cold and dry weather.

PM2.5 induces the distant metastasis of lung adenocarcinoma via promoting the stem cell properties of cancer cells

Lung cancer is the most common cancer in China and second worldwide, of which the incidence of lung adenocarcinoma is rising. As an independent factor, air pollution has drawn the attention of the public. An increasing body of studies has focused on the effect of PM2.5 on lung adenocarcinoma; however, the mechanism remains unclear. We collected the PM2.5 in two megacities, Beijing (BPM) and Shijiazhuang (SPM), located in the capital of China, and compared the different components and sources of PM2.5 in the two cities. Vehicle emissions are the primary sources of BPM, whereas SPM is industrial emissions. We found that chronic exposure to PM2.5 promotes the tumorigenesis and metastasis of lung adenocarcinoma in patient-derived xenograft (PDX) models, as well as the migration and invasion of lung adenocarcinoma cell lines. SPM has more severe effects in vivo and in vitro. The underlying mechanisms are related to the stem cell properties of cancer cells, the epithelial-mesenchymal transition (EMT) process, and the corresponding miRNAs. It is hopeful to provide a theoretical basis for improving air pollution in China, especially in the capital area, and is of the significance of long-term survival of lung cancer patients.

Association of long-term exposure to PM2.5 with hypertension prevalence and blood pressure in China: a cross-sectional study

ObjectiveEvidence of the effects of long-term fine particulate matter (PM2.5) exposure on hypertension and blood pressure is limited for populations exposed to high levels of PM2.5. We aim to assess...