Salidroside Ameliorates Lung Injury Induced by PM 2.5by Regulating SIRT1-PGC-1α in Mice.

Objective: This study aimed to clarify the intervention effect of salidroside (SAL) on lung injury caused by PM 2.5 in mice and illuminate the function of SIRT1-PGC-1ɑ axis. Methods: Specific pathogen-free (SPF) grade male C57BL/6 mice were randomly assigned to the following groups: control group, SAL group, PM 2.5 group, SAL+PM 2.5 group. On the first day, SAL was given by gavage, and on the second day, PM 2.5 suspension was given by intratracheal instillation. The whole experiment consist of a total of 10 cycles, lasting 20 days. At the end of treatment, blood samples and lung tissues were collected and analyzed. Observation of pathological changes in lung tissue using inverted microscopy and transmission electron microscopy. The expression of inflammatory, antioxidants, apoptosis, and SIRT1-PGC-1ɑ proteins were detected by Western blotting. Results: Exposure to PM 2.5 leads to obvious morphological and pathologica changes in the lung of mice. PM 2.5 caused a decline in levels of antioxidant-related enzymes and protein expressions of HO-1, Nrf2, SOD2, SIRT1 and PGC-1ɑ, and an increase in the protein expressions of IL-6, IL-1ß, Bax, caspase-9 and cleaved caspase-3. However, SAL reversed the aforementioned changes caused by PM 2.5 by activating the SIRT1-PGC-1α pathway. Conclusion: SAL can activate SIRT1-PGC-1ɑ to ameliorate PM 2.5-induced lung injury.

Acute Effects of Individual Exposure to Fine Particulate Matter on Pulmonary Function in Schoolchildren.

OBJECTIVE: This panel study aimed to determine the acute effects of exposure to fine particulate matter (PM 2.5) on schoolchildren's pulmonary function. METHODS: We selected 51 schoolchildren aged 9-12 years attending a full-time boarding school in Beijing, China, measured the indoor and outdoor PM 2.5 concentrations for five consecutive days, calculated the PM 2.5 time-weighted individual exposure levels based on the school micro-environmental concentrations and the time activity pattern recorded by schoolchildren, measured schoolchildren's pulmonary function on the fifth day. The survey was performed three times from December 2018 to April 2019. We used a linear mixed-effects model to evaluate the associations between PM 2.5 and pulmonary function. RESULTS: During the three surveys, the median PM 2.5 time-weighted individual exposure concentrations were 15.30 µg/m 3, 48.92 µg/m 3, and 42.89 µg/m 3, respectively. There was a significant difference between the three surveys in vital capacity (VC), forced vital capacity (FVC), forced expiratory volume in one second (FEV 1) and forced expiratory volume in one second/forced vital capacity (FEV 1/FVC) ( P < 0.05). The relevance analysis found that PM 2.5 had lag effect on schoolchildren's pulmonary function, each 10 µg/m 3increase in PM 2.5could cause largest decreases in FEF 25%-75%, FEV 1/FVC, FEF 75%, and FEV 1 on lag 0-1 d (80.44 mL/s, 35.85%, 78.58 mL/s, and 61.34 mL, respectively), and largest decreases in FEF 25% on lag 1 d (83.68 mL/s), in VC on lag 4 d (32.34 mL), and in FVC on lag 0-4 d (37.76 mL). Gender subgroup analysis revealed that the increase in PM 2.5 caused a decrease in FEV 1/FVC and VC on the day of physical examination only in boys, and on lag days it caused changes in different pulmonary function indicators, both for boys and girls, but most of the pulmonary function indicators decreased more in boys than in girls. CONCLUSION: Our findings show that acute PM 2.5 exposure has significant effects on pulmonary function within 0-4 d, on both small airway indicators and large airway indicators. Boys' pulmonary function is more sensitive to PM 2.5 than girls.

PM2.5 exposure induces vascular dysfunction via NO generated by iNOS in lung of ApoE-/- mouse.

PM2.5 exposure exacerbates cardiovascular diseases via oxidative stress and inflammation, the detailed mechanism of which is unclear. In this study, the effects of oxidative stress and inflammation, as well as vascular structure and function were studied by multiple PM2.5 exposure model of ApoE-/- mice. The results indicated that NO produced by iNOS not cNOS might play important roles in inducing vascular dysfunction after PM2.5 exposure. The occurrence order and causality among NO, other oxidative stress indicators and inflammation is explored by single PM2.5 exposure. The results showed that NO generated by iNOS occurred earlier than that of other oxidative stress indicators, which was followed by the increased inflammation. Inhibition of NOS could effectively block the raise of NO, oxidative stress and inflammation after PM2.5 exposure. All in all, we firstly confirmed that NO was the initiation factor of PM2.5 exposure-induced oxidative stress, which led to inflammation and the following vascular dysfunction.

PM2.5 aggravates diabetes via the systemically activated IL-6-mediated STAT3/SOCS3 pathway in rats' liver.

PM2.5 exposure aggravates type 2 diabetes, in which inflammatory factors play an important role. In this study, we aimed to explore the mechanisms responsible for aggravating diabetes after PM2.5 exposure, and study the roles of inflammatory factors in insulin-resistant type 2 diabetes. Our study indicated that short-time PM2.5 exposure enhances insulin resistance in type 2 diabetic rats and significantly raises inflammatory factors, including IL-6, TNF-α, and MCP-1, in lungs. However, we found that of these inflammatory factors only IL-6 levels are elevated in blood, liver, adipose tissue, and macrophages, but not in skeletal muscle. IL-6 induced activation of the STAT3/SOCS3 pathway in liver, but not other downstream pathways including STAT1, ERK1/2, and PI3K. Both STAT3 inhibition and IL-6 neutralization effectively alleviated the disorders of glucose metabolism after PM2.5 exposure. Taken together, this suggests that the systemic increase in IL-6 may play an important role in the deterioration of the type 2 diabetes via IL-6/STAT3/SOCS3 pathway in liver after short-time exposure to PM2.5. Besides, we unexpectedly found a stronger resistance to the PM2.5 exposure-induced increase in IL-6 in skeleton muscle than those of many other tissues.

Measurement Uncertainty Assessment for Determination of Allura Red in Puffed Food by HPLC.

This study aimed to assess the measurement uncertainty of a new method for determination of allura redin food by high performance liquid chromatography (HPLC). The uncertainty of mathematical model of allura red is based on Europe for Analytical Chemistry(EURACHEM) guidelines. The sources and components of uncertainty were calculated, including recovery, working solution, sample mass, final volume, response of standard solution, response of sample solution. The expanded uncertainty was 0.0024 (k=2). Uncertainty of working solution was the most significant factor contributing to the total uncertainty, accounting for 86.2%. The uncertainty of volume accounted for the minimum at 0.025%. The developed method is simple and accurate, which can be used for the determination of allura redin puffed samples.

PM2.5 induces autophagy-mediated cell death via NOS2 signaling in human bronchial epithelium cells.

The biggest victim of ambient air pollution is the respiratory system. Mainly because of the harmful components, especially the particulate matters with an aerodynamic diameter of ≤ 2.5µm (PM2.5), can be directly inhaled and deeply penetrate into the lung alveoli, thus causing severe lung dysfunction, including chronic cough, bronchitis and asthma, even lung cancer. Unfortunately, the toxicological mechanisms of PM2.5 associations with these adverse respiratory outcomes have still not been clearly unveiled. Here, we found that PM2.5 rapidly induced inflammatory responses, oxidative injure and cell death in human bronchial epithelium cells through upregulation of IL-6 expression, ROS production and apoptosis. Furthermore, PM2.5 specifically induced nitric oxide synthase 2 (NOS2) expression and NO generation to elevate excessive autophagy. Finally, disruption of NOS2 signaling effectively blocked autophayosome formation and the subsequent cell death. Our novel findings systemically reveled the role of autophagy-mediated cell death in PM2.5-treated human bronchial epithelium cells and provided potential strategy for future clinic intervention.

Autophagy Induced FHL2 Upregulation Promotes IL-6 Production by Activating the NF-κB Pathway in Mouse Aortic Endothelial Cells after Exposure to PM2.5.

Epidemiological and clinical studies have increasingly shown that fine particulate matter (PM2.5) is associated with cardiovascular morbidity and mortality, which share the common feature of PM2.5-induced vascular inflammation; however, the underlying mechanisms of how PM2.5 triggers increased inflammatory response in vascular endothelial cells are not well understood. After treating mouse aortic endothelial cells (MAECs) with different concentrations of PM2.5, we assessed interleukin (IL)-6 and four and a half LIM domains 2 (FHL2) expression in cell supernatant by enzyme-linked immunosorbent assay and Western blot, respectively, as well as activation of nuclear factor (NF)-κB and immune-response signaling pathways. Additionally, changes in pathway activation, IL-6 expression, and autophagy were evaluated under PM2.5 exposure, following FHL2 knockdown with small interfering RNA. Our results indicated that PM2.5 exposure induced FHL2 expression and IL-6 secretion, as well as activation of pathways associated with immune response. Additionally, following FHL2 knockdown, the activation of NF-κB-related pathways and IL-6 secretion was inhibited under PM2.5 exposure, although the Akt- and p38-signaling pathways were not affected. Furthermore, PM2.5 exposure induced autophagy, whereas autophagy inhibition eventually inhibited PM2.5-induced FHL2 expression. These findings suggested a novel link between autophagy induced FHL2 upregulation and IL-6 production in MAECs under PM2.5 exposure.

[Application of ICP-MS and ICP-AES for Studying on Source Apportionment of PM2.5 during Haze Weather in Urban Beijing].

To investigate the characteristics of chemical constitute and pollution sources of aerosol fine particulate matter during haze-fog day in Beijing in winter 2013. The samples of PM2.5 were collected in Beijing from January to February, 2013. The technique of ICP-MS and ICP-AES coupled with procedure of bathing-ultrasonic extraction was applied to determine the concentration of 40 elements in the aerosol samples to analyze the characteristics of elements distribution statistically. The absolute principal factor method was used to apportion the pollution sources of PM2.5 during the haze weather in Beijing city in winter 2013. The results showed that during the period of sampling, the volume concentration of Li, Mn, Pb, S etc. obeyed normal distribution approximately, and according to National Ambient Air Quality Standard issued by Ministry of Environmental Protection of the People's Republic of China, the geometric mean concentration of As was twice the annual limit of standard reference, while Pb of some aerosol samples beyond the annual limit of standard reference respectively. The mass fraction of Fe, Zn, Pb, Ti accounted for over 0.1%, while that of Mn, Cu, As, Se etc. 0.01%. These elements were primary inorganic pollutants, and especially the hazards and sources of As and Pb should be concerned. There were 6 main pollution sources were chosen by the factor analysis method, including industrial dust and human beings activities, biomass combustion and building dust, soil and sand dusts, fossil fuel, electronic waste and metal smelting, with the variance contribution rate of 40.3%, 27.0%, 9.1%, 4.9%, 4.8% and 4.6% respectively. ICP-MS and ICP-AES can be applied to analyzing multi-elements in PM2.5 accurately and quickly to facilitate source apportionment, and it indicated that the relevant pollution sources should be considered and the effect of regional transferring of haze pollution sources should be taken into account, and specific measures should be taken for control.

Prevalence and Treatment of Children's Asthma in Rural Areas Compared with Urban Areas in Beijing.

BACKGROUND: The prevalence of childhood asthma has been increasing in China. This study aimed to compare the prevalence, diagnosis, and treatment of asthmatic children from urban and rural areas in Beijing, China. METHODS: Schools, communities, and kindergartens were randomly selected by cluster random sampling from urban and rural areas in Beijing. Parents were surveyed by the same screening questionnaires. On-the-spot inquiries, physical examinations, medical records, and previous test results were used to diagnose asthmatic children. Information on previous diagnoses, treatments, and control of symptoms was obtained. RESULTS: From 7209 children in rural areas and 13,513 children in urban areas who completed screening questionnaires, 587 children were diagnosed as asthma. The prevalence of asthma in rural areas was lower than in urban areas (1.25% vs. 3.68%, χ2 = 100.80, P < 0.001). The diagnosis of asthma in rural areas was lower than in urban areas (48.9% vs. 73.9%, χ2 = 34.6, P < 0.001). Compared with urban asthmatic children (56.5%), only 35.6% of rural asthmatic children received inhaled corticosteroids (P < 0.05). The use of bronchodilators was also lower in rural areas than in urban areas (56.5% vs. 66.4%, χ2 = 14.2, P < 0.01). CONCLUSION: The prevalence of asthma in children was lower in rural areas compared with children in the urban area of Beijing. A considerable number of children were not diagnosed and inadequately treated in rural areas.

[Assessment of haze-related human health risks for four Chinese cities during extreme haze in January 2013].

OBJECTIVE: To evaluate the human health risks (premature death risk as an indicator) in Beijing, Shanghai, Guangzhou and Xi'an during extreme haze in January 2013. METHODS: The daily average particulate matter ≤ 2.5 µm in aerodynamic diameter (PM2.5) concentrations of Beijing, Shanghai, Guangzhou and Xi'an in January 2013 were collected and their characteristics explored. The populations and mortality rate of four cities in 2010 were collected from the statistical yearbook, the exposure-response relationships selected from the reference and then the premature death calculated according to the proportion risk model of Poisson regression. RESULTS: In January 2013, the 24 h mean concentrations of PM2.5 in Beijing, Shanghai, Guangzhou and Xi'an were (240 ± 165) , (83 ± 27), (94 ± 49) and (210 ± 98) µg/m(3) respectively and they were all above the secondary level of Ambient Air Quality Standards (GB 3095-2012). The 24 h mean concentrations of PM2.5 in Beijing and Xi'an were much higher than those in Shanghai and Guangzhou. Approximately 86.4% (19/22) , 58.1% (18/31), 54.8% (17/31) and 93.5% (29/31) of 24 h mean PM2.5 concentrations in Beijing, Shanghai, Guangzhou and Xi'an respectively exceeded the secondary level of Ambient Air Quality Standards (GB 3095-2012). The number of premature death due to the exposure to haze were 725 (95%CI: 457-977) for Beijing, 296 (95%CI: 96-502) for Shanghai, 310 (95%CI: 189-434) for Guangzhou and 85 (95%CI: 21-141) for Xi'an respectively in January 2013. CONCLUSION: The PM2.5 pollutions of four cities in January 2013 were serious enough to pose elevated risks of human health.

[Epidemiological survey of children asthma prevalence in Beijing urban area].

OBJECTIVE: To explore the prevalence, diagnosis and management of childhood asthma in Beijing urban area. METHODS: Multi-stage, stratified and random cluster sampling was used to recruit children born during November 1, 1995 to October 31, 2010 from Beijing or other provinces but residing in Beijing for over half a year. The same screening questionnaires for the third national epidemiological survey of children's asthma were distributed to parents of children at schools, kindergartens and communities during October 2010 to March 2011. Asthmatic children were picked among the screening-positive children based on on-the-spot inquiries, physical examinations, medical records and supporting test results. Further survey of asthmatics was carried out to investigate the diagnosis and treatment status of childhood asthma and other associated allergic diseases. All data required double entry by Epi-Info 3.5.3 software and were processed by SPSS 19.0. RESULTS: Among a total of 14 085 questionnaires, 13 513 were completed with a response rate of 95.94%. And 497 (3.68%) children were diagnosed with typical (n = 451, 3.34%) and cough variant (n = 46, 0.34%) asthma. Among them, 40.64% (202/497) were newly diagnosed and 59.36% (295/497) had been previously diagnosed with asthma. The prevalence of asthma was higher in boys than in girls (4.80% (345/1790) vs 2.40% (152/6323), χ(2) = 54.446, P < 0.01). The asthma prevalence of preschoolers (3 - < 7 years old) was the highest (5.05% (180/3563)). In the past two years, the symptoms of 69.42% (345/497) children persisted and the current two-year prevalence of asthma was 2.55% (345/13513). Among the 295 children with previous asthma, only 46.44% (137/295) received inhaled corticosteroids according to the Global Initiative for Asthma (GINA) and 82.37% (243/295) of them used antibiotics. CONCLUSIONS: The prevalence of asthma is 3.68% in children under 14 years old in Beijing urban area and it varies in children with different genders and ages. A considerable number of children are not diagnosed or treated properly. And the management of asthma requires further improvement.

Transient receptor potential vanilloid 2 (TRPV2), a potential novel biomarker in childhood asthma.

BACKGROUND: The presence of transient receptor potential vanilloid 2 (TRPV2) in human peripheral blood cells may suggest a role under pathological conditions. The aim of this study was to explore the relationship between the expression profile of TRPV2 gene and childhood asthma in the north of China. The effects of allergens exposure on the expression of TRPV2 gene were also investigated. METHODS: Sixty asthmatics children confirmed by physician diagnosis and 60 healthy children as a control group were recruited. Serum total IgE and specific IgE were measured. Using quantitative Reverse Transcription Polymerase Chain Reaction (qRT-PCR), TRPV2 was detected in total RNA extracted from peripheral blood lymphocytes. Student's t-test and chi-square test were used to analyze the relationship between TRPV2 transcript and different parameter variables on susceptibility of childhood asthma. Multiple logistic regression was used to analyze the associations between TRPV2 gene and allergens. RESULTS: The expression level of TRPV2 gene was increased 2.6 times in asthmatic children compared with controls (p < .01). The up-regulation of TRPV2 gene and sensitization to one of three the allergens-spring pollen, dust mite, and dog and cat hair-were correlated with childhood asthma. In addition, the hypersensitivity to spring pollen, cockroach, and dust mite and up-regulation of TRPV2 gene expression may be the risk factors for the childhood asthma in Beijing. CONCLUSIONS: The increased expression of TRPV2 gene in peripheral lymphocytes is closely correlated with childhood asthma in the north of China. This study provides a potential new biomarker of childhood asthma and lays the basis for further clarification of the pathogenesis underlying asthma.

[Determination of trace elements Be, Cd, as and Pb in air of residential areas by inductively coupled plasma-mass spectrometry coupled with ultrasonic leaching].

In the present paper, the method for determining the trace elements Be, Cd, As and Pb in air of residential areas by inductively coupled plasma-mass spectrometry was established. Ultrasonic leaching procedures were applied to extract the trace elements from the filter membrane of the atmospheric particulates. The operating condition of the instrument was optimized. 72Ge, 115s In and 204Tl were chosen as the internal elements and the effect of matrix, interface and fluctuation of instrument was overcome effectively. Satisfactory linearity of working curves of four elements was obtained, giving all the correlation coefficients over 0.9995, and the detection limit of the method was between 0.006 and 0.045 ng x m(-3). The mean values of National Standard Reference Material GBW(E)080212 were in agreement with the certified values. The sampling filters membranes, divided into four equal parts and with added standard solution with different concentions were analyzed, and the recovery rate of samples were in the range of 91.6%-109.7% with the related standard deviation between 0.7% and 4.8%. The obtained results showed that the method of determining the trace elements Be, Cd, As and Pb in air of residential areas by inductively coupled plasma-mass spectrometry proved to be simple, accurate, sophisticated and stable.

Association of polymorphisms of STAT6 and SO(2) with Chinese childhood asthma: a case-control study.

OBJECTIVE: To investigate the association of polymorphisms of STAT6 gene and air pollutants of PM(10), NO(2), and SO(2), with asthma in Chinese children. METHODS: 418 subjects aged 14 years and under were recruited in a case-control study. The association between STAT6 polymorphisms and childhood asthma were tested by allele frequency, genotype analysis, and MDR analysis. Exposure to outdoor air pollutants was estimated by a 5-day moving average level. Statistical analyses were performed with SAS 9.1 software. RESULTS: Only 3 alleles of GT repeats at exon 1 of STAT6 were found in Chinese children. C258T and T710C were 2 new SNPs of STAT6 at 3'-UTR. Children who carried T allele of C258T were more common in asthma children than in control subjects (P<0.05). The MDR analysis showed that GT repeats, C258T and T710C of STAT6 polymorphisms interacted together in leading to susceptibility to childhood asthma among Chinese people. After confounding factors were controlled, such as SNP C258T, family history of asthma, frequency of influenza within a year, the 5-day average of SO(2) was tested to be a key risk factor of asthma in Chinese children (P<0.05). CONCLUSION: Chinese children differed in polymorphisms of STAT6 and in its relation with childhood asthma.

Immunological effect of PM2.5 on cytokine production in female Wistar rats.

OBJECTIVE: To investigate the immunological effect of PM2.5 on cytokine production in female Wistar rats. METHODS: Female Wistar rats were given 0.3 mg, 0.75 mg, 2 mg, 5 mg of PM2.5 per 0.5 mL saline, respectively. Saline was used as the negative control. TNF-alpha and IL-6 levels in the branchoalveolar lavage were measured by ELISA, and mRNA expression levels in lung tissue were detected by RT-PCR. Alveolar macrophages were collected for testing phogacytic function. RESULTS: Exposure to PM2.5 stimulated TNF-alpha production in a dose-dependent manner (P < 0.05), However, no statistically significant difference was found. No time-dependent change in TNF-a and IL-6 production was found. TNF-alpha and IL-6 mRNA expressions were induced by PM2.5-exposure. The phagocytic rate (PR) was significantly decreased by PM2.5 treatment. CONCLUSION: PM2.5 exposure increases inflammation response of the lung in a dose-dependent manner. Moreover, tissue injury induced by PM2.5 may be related to altered production of cytokines. PMz2.5 may impair the phagocytic activity of alveolar macrophages.

[Histopathology of lung of rats exposed to suspension of PM(2.5) with silver staining].

OBJECTIVE: To observe the histopathological changes of the lung of rats which exposed to the suspension of PM(2.5) and detect the effect of silver staining showing dust particles deposited in the lungs. METHODS: The dissociative PM(2.5) of Beijing city was collected to make suspension. The rats were divided into different groups and exposed to different dosage of PM(2.5) (0.3 mg/0.2 ml per rat, 0.75 mg/0.2 ml per rat, 2 mg/0.2 ml per rat) by intratracheal instillation every week. These rats were sacrificed at 4, 12 weeks and 24 weeks (total dosage: 7.2 mg per rat, 18 mg per rat, 48 mg per rat) after the treatment, and their lungs were sampled. The pathological varieties and the situation of these rats' lungs were observed macroscopically and using hematoxylin and eosin (HE) staining, Warthin-Starry (WS) silver stain, as well as the transmission electron microscope (TEM). The dust particles in these rats' lungs were observed by x-ray spectrum chemical element analysis (X-RSA). The granulomatous lesion in the lungs of the rats was counted, and the deposition degree, integrated optical density (IOD) value and integrated area density (IAD) value of the dust particles deposited in the lungs were measured. The variance, least significance difference, and the unitary linear related and regression were analyzed. RESULTS: The number of the granulomatous lesion in the lungs of the rats became more and more with time. In WS staining the dust particles were dark brown and became clearer. The IOD and IAD value of these dust particles were much higher in WS staining than that in HE staining (P < 0.05). The IOD value of the dust particles was positively correlated with the number of the granulomatous lesion (R = 0.639, P < 0.01). The ultrastructure of the dust particles in the rats' lungs and the dissociative PM(2.5) was basically same in TEM. Their main compositions were similar, by X-RSA, and both of them were silicon. CONCLUSION: The suspension of PM(2.5) could result in the granulomatous lesion in the lung of rats. WS silver staining is a good method to show PM(2.5) phagocytized by macrophage, and is better than HE staining.

[Effects of formaldehyde on the activity of superoxide dismutases and glutathione peroxidase and the concentration of malondialdehyde].

This review focus on the effects of formaldehyde on the activity of superoxide dismutases (SOD), glutathione peroxidase (GSH-Px) and the concentration of malondialdehyde (MDA) in recent years. It is showed formaldehyde having effect on lipid peroxidation by many studies of animal experiment and occupational group, it can decrease the activity of SOD and GSH-Px, increase the concentration of MDA, there are dose-response relationship between those lipid peroxidation index and the concentration of formaldehyde too. In future study, the animal experiment and the people's late effect of low dose formaldehyde exposure should be pay more attention.

Characteristics and seasonal variations of PM2.5, PM10, and TSP aerosol in Beijing.

OBJECTIVE: To investigate the seasonal characteristics and the sources of elements and ions with different sizes in the aerosols in Beijing. METHODS: Samples of particulate matters (PM2.5), PM10, and total suspended particle (TSP) aerosols were collected simultaneously in Beijing from July 2001 to April 2003. The aerosol was chemically characterized by measuring 23 elements and 18 water-soluble ions by inductively coupled plasma-atomic emission spectroscopy (ICP-AES) and ion chromatography (IC), respectively. RESULTS: The samples were divided into four categories: spring non-dust, spring dust, summer dust, and winter dust. TSP, PM10, and PM2.5 were most abundant in the spring dust, and the least in summer dust. The average mass ratios of PM > 10, PM2.5-10, and PM2.5 to TSP confirmed that in the spring dust both the large coarse (PM > 10) and fine particles (PM2.5) contributed significantly in summer PM2.5, PM2.5-10, and PM > 10 contributed similar fractions to TSP, and in winter much PM2.5. The seasonal variation characteristics of the elements and ions were used to divide them into four groups: crustal, pollutant, mixed, and secondary. The highest levels of crustal elements, such as Al, Fe, and Ca, were found in the dust season, the highest levels of pollutant elements and ions, such as As, F-, and Cl-, were observed in winter, and the highest levels of secondary ions (SO4(2-), NO3-, and NH4+) were seen both in summer and in winter. The mixed group (Eu, Ni, and Cu) showed the characteristics of both crustal and pollutant elements. The mineral aerosol from outside Beijing contributed more than that from the local part in all the reasons but summer, estimated using a newly developed element tracer technique.

[Preliminary study on the relationship between chronic sinusitis histomorphology and aerosol].

OBJECTIVE: To observe the relationship between histomorphological changes in mucosa of chronic sinusitis (CS) and aerosol particles. METHODS: The ethmoidal sinus mucus specimens of 60 patients with CS type I, II and III, and 16 cases of normal controls were collected. Meanwhile the pulmonary specimens in autopsy of 5 adult and 5 fetus cases were also collected. The specimens were stained by HE staining and Warthin-Starry (W-S) special aerosol particles staining method respectively, the ethmoidal sinus mucosa basement membrane were displayed by Van Gieson's (VG) special staining method, and its thickness was measured. RESULTS: By the W-S staining, some black aerosol particles were found depositing on the epithelial cells layer of damaged mucosa and in the plasm of the epithelial cells. The degree of deposition was gradually increased in type I, II and III of CS. The number of cases of slight, medium and heavy depositing in type I were 11/20, 7/20, 2/20, in type II 5/20, 9/20, 6/20, and in type III 3/20, 6/20, 11/20 respectively; the more particles deposited, the more thickening the basement membrane. The thickness of the basement membrane in type I, II and III of CS were (12.15 +/- 4.73), (16.67 +/- 2.22), (23.75 +/- 3.48) microm respectively. There were significant differences among type I, II and III (P < 0.01). The black particles in the mucosa epithelium tissues of normal control group and non-damaged mucosa epithelium and desquamation area were seldom seen. On the other hand, the aerosol particles were not seen in the pulmonary specimens of the fetal autopsy. CONCLUSION: In damaged mucosa epithelial cells of the CS, there are aerosol particles existing which may relate with the morphological changes of CS.