The effect of air pollution on the lung function of adults with asthma remains unclear to date. This study followed 112 patients with asthma at 3-month intervals for 2 years. The pollutant exposure of the participants was estimated using the inverse distance weight method. The participants were divided into three groups according to their lung function level at every visit. A linear mixed-effect model was applied to predict the change in lung function with each unit change in pollution concentration. Exposure to carbon monoxide (CO) and particles less than 2.5 micrometers in diameter (PM_2.5) was negatively associated with large airway function in participants. In the severe group, exposure to chronic sulfur dioxide (SO2) was negatively associated with post-bronchodilator forced expiratory flow at 50%, between 25% and 75% of vital capacity % predicted (change of 95% CI per unit: -0.34 (-0.55, -0.12), -0.24 (-0.44, -0.03), respectively). In the mild group, the effect of SO₂ on the small airways was similar to that in the severe group, and it was negatively associated with large airway function. Exposure to CO and PM_2.5 was negatively associated with the large airway function of adults with asthma. The negative effects of SO₂ were more evident and widely observed in adults with severe and mild asthma than in adults with moderate asthma. Patients with asthma react differently to air pollutants as evidenced by their lung function levels.
Adult ; Air Pollutants/analysis* ; Air Pollution/adverse effects* ; Asthma/epidemiology* ; Beijing/epidemiology* ; Environmental Exposure/adverse effects* ; Humans ; Lung ; Particulate Matter/analysis* ; Sulfur Dioxide/adverse effects*

BackgroundAsthma is a common chronic respiratory disease and is related to air pollution exposure. However, only a few studies have concentrated on the association between air pollution and adult asthma. Moreover, the results of these studies are controversial. Therefore, the present study aimed to analyze the influence of various pollutants on hospitalization due to asthma in adults.

MethodsA total of 1019 unrelated hospitalized adult asthma patients from Northeast China were recruited from 2014 to 2016. Daily average concentrations of air pollutants (particulate matter <2.5 μm [PM], particulate matter <10 μm [PM], sulfur dioxide [SO], nitrogen dioxide [NO], and carbon monoxide [CO]) were obtained from the China National Environmental Monitoring Centre website from 2014 to 2016. Cox logistic regression analysis was used to analyze the relationship between air pollutants and hospital admissions in adult asthma.

ResultsThe maximum odds ratio (OR) value for most air pollutants occurred on lag day 1. Lag day 1 was chosen as the exposure period, and 8 days before onset was chosen as the control period. Three pollutants (PM, CO, and SO) were entered into the regression equation, and the corresponding OR (95% confidence interval) was 0.995 (0.991-0.999), 3.107 (1.607-6.010), and 0.979 (0.968-0.990), respectively.

ConclusionsA positive association between hospital admissions and the daily average concentration of CO was observed. CO is likely to be a risk factor for hospital admissions in adults with asthma.

Air Pollutants ; toxicity ; Air Pollution ; adverse effects ; Asthma ; epidemiology ; Carbon Monoxide ; toxicity ; China ; Environmental Monitoring ; statistics & numerical data ; Female ; Hospitalization ; statistics & numerical data ; Humans ; Male ; Odds Ratio ; Particulate Matter ; toxicity ; Risk Factors ; Sulfur Dioxide ; toxicity

OBJECTIVETo explore acute effects of SO(2) and NO(2) on mortality in the six cities of China.

METHODSSurveillance data on daily air quality, meteorology and the cause of death were collected from January 1, 2007 to December 31, 2009 in Beijing, Tianjin, Xi'an, Shanghai, Guangzhou and Wuhan. Generalized additive model was used to explore the relationship between the daily average concentration of SO(2) and NO(2) and daily mortality, after adjusting the effects of long-term and seasonal trend and weather conditions.

RESULTSIn Beijing, Tianjin, Xi'an, Shanghai, Guangzhou and Wuhan, the daily average concentration of SO(2) and NO(2) were in the range of 39.8-59.5 µg/m(3) and 41.4-60.1 µg/m(3) respectively; the daily mortality for non-accidental were 174.5, 101.4, 27.7, 108.4, 50.6, 17.8, cardiovascular were 86.9, 53.3, 12.8, 34.8, 16.3, 8.1 and respiratory were 18.3, 8.6, 2.6, 18.6, 9.0, 1.8 respectively. The daily average concentration of SO(2) were negatively correlated with daily average temperature in Beijing, Tianjin, Xi'an and Wuhan (the correlation coefficients were -0.66, -0.73, -0.67 and -0.39 respectively, P<0.05). The daily average concentration of SO(2) were negativeiy correlated with relative humidity in Tianjin, Shanghai and Wuhan (the correlation coefficients were -0.26, -0.46 and -0.28 respectively, P<0.05). The daily average concentration of NO(2) were negative correlated with daily average temperature in Beijing, Tianjin, Xi'an and Wuhan (the correlation coefficients were -0.27, -0.49, -0.45 and -0.38 respectively, P<0.05). When the day concentration of SO(2) increased every 10 µg/m(3), the non-accidental mortality in Tianjin and Wuhan raised 0.44%(95%CI: 0.11%-0.78%) and 0.96%(95%CI: 0.22%-1.72%) respectively. When the 1 day-lag concentration of SO(2) increased every 10 µg/m(3), the non-accidental mortality in Shanghai, Guangzhou and Wuhan raised 0.28% (95% CI: 0.02%-0.54% ), 0.41% (95% CI: 0.04%-0.79% ) and 1.14% (95% CI: 0.44%-1.84%) respectively. When the day and 1 day-lag concentration of SO(2) increased every 10 µg/m(3), the non-accidental mortality and the cardiovascular mortality at the six cities scale raised 0.40% (95% CI: 0.13%-0.67%) and 0.48% (95% CI: 0.11%-0.85%) respectively. When the day concentration of NO2 increased every 10 µg/m(3), the non-accidental mortality in Beijing, Tianjin, Shanghai, Guangzhou and Wuhan raised 0.60% (95% CI: 0.26%-0.95%), 0.96% (95% CI: 0.29%-1.64%), 0.43% (95% CI: 0.09%-0.78%), 1.17%(95%CI: 0.69%-1.66%) and 1.23%(95%CI: 0.19%-2.28%) respectively; the cardiovascular mortality in Beijing, Tianjin, Xi'an, Guangzhou and Wuhan raised 0.83% (95% CI: 0.34%-1.32%), 1.09% (95% CI: 0.25%-1.94%), 1.98% (95% CI: 0.00%-4.01%), 1.52% (95% CI: 0.70%-2.36%) and 2.04% (95% CI: 0.54%-3.56%) respectively. When the 1 day-lag concentration of NO(2) increased every 10 µg/m(3), the non-accidental mortality in Guangzhou and Wuhan raised 0.97% (95% CI: 0.49%-1.46%) and 1.67% (95% CI: 0.66%-2.70%)respectively; the cardiovascular mortality in Guangzhou and Wuhan raised 1.06% (95% CI: 0.24%-1.89%)and 2.42% (95% CI: 0.97%-3.89%) respectively. When the day and 1 day-lag concentration of NO(2) increased every 10 µg/m(3), the non-accidental mortality and the cardiovascular mortality at the six cities scale raised 0.81% (95% CI: 0.35%-1.28%), 1.03% (95% CI: 0.40%-1.66%) respectively.

CONCLUSIONExposure to SO(2) and NO(2) was significantly associated with daily non-accidental morality and cardiovascular morality at the multi-city scale in China.

Air Pollution ; adverse effects ; China ; Cities ; Humans ; Mortality ; Nitric Oxide ; adverse effects ; Particulate Matter ; Sulfur Dioxide ; adverse effects ; Temperature ; Weather

BACKGROUND/AIMS: Although indoor air pollution is a well-known risk factor for tuberculosis (TB), the possible link between outdoor air pollution and TB development has not been examined fully. We assessed the impact of outdoor air pollution on TB development in the Seoul metropolitan area, South Korea. METHODS: The mean concentrations of ambient particulate matter (PM) with an aerodynamic diameter < or = 10 microm (PM10), O3, CO, NO2, and SO2 levels in Seoul, between January 1, 1997 and December 31, 2006, were determined. Furthermore, their association with the risk of developing TB after adjusting for socioeconomic status, between January 1, 2002 and December 31, 2006, was investigated. RESULTS: Between January 1, 2002 and December 31, 2006, a total of 41,185 TB cases were reported in Seoul. Concentrations of PM10, O3, CO, and NO2 were not associated with TB incidence in males or females. However, the interquartile increase in SO2 concentration was associated with a 7% increment in TB incidence (relative risk [RR], 1.07; 95% credible interval [CrI], 1.03 to 1.12) in males but not in females (RR, 1.02; 95% CrI, 0.98 to 1.07). CONCLUSIONS: Long-term exposure to ambient SO2 increased the risk of TB in males.
Adult ; Aged ; Air Pollution, Indoor/*adverse effects ; Female ; Humans ; Incidence ; Inhalation Exposure/adverse effects ; Male ; Middle Aged ; Odds Ratio ; Particle Size ; Particulate Matter/adverse effects ; Republic of Korea/epidemiology ; Retrospective Studies ; Risk Assessment ; Risk Factors ; Sex Factors ; Sulfur Dioxide/*adverse effects ; Time Factors ; Tuberculosis, Pulmonary/diagnosis/*epidemiology/microbiology ; *Urban Health

No abstract available.
Air Pollution, Indoor/*adverse effects ; Female ; Humans ; Male ; Sulfur Dioxide/*adverse effects ; Tuberculosis, Pulmonary/*epidemiology ; *Urban Health

To compare the differences of the active ingredient contents and the sulfur dioxide residue in Astragali Radix before and after sulfur fumigation and provide a basis for establishing an alternative processing method. Astragali Radix, harvested at the same time in Longxi Gansu, were processed with different methods. high performance liquid chromatography (HPLC) was used to determine the contents of the active ingredients in Astragali Radix and the revised method of the pharmacopoeia of China in 2011 was applied to determine the sulfur dioxide residue. The results show that the three-fold sulfur-fumigation group has the highest level of astragaloside IV and the dried sulfur-fumigation group with 10% water has the lowest level; the content of calycosin-7-O-β-D-glucoside is the highest in naturally dried group and the lowest in the group of sulfur fumigating for 3 times; the sulfur dioxide residue of all sulfur-fumigation groups exceeds certain limit significantly and the group of sulfur fumigating for 3 times reaches the highest level.
Astragalus Plant ; chemistry ; Chromatography, High Pressure Liquid ; Drugs, Chinese Herbal ; chemistry ; Fumigation ; adverse effects ; Sulfur Dioxide ; analysis ; Technology, Pharmaceutical ; methods

Air pollution in China comes from multiple sources, including coal consumption, construction and industrial dust, and vehicle exhaust. Coal consumption in particular directly determines the emissions of three major air pollutants: dust, sulfur dioxide (SO(2)), and nitrogen oxide (NOx). The rapidly increasing number of civilian vehicles is expected to bring NOx emission to a very high level. Contrary to expectations, however, existing data show that the concentrations of major pollutants [particulate matter-10 (PM10), SO(2), and nitrogen dioxide (NO(2))] in several large Chinese cities have declined during the past decades, though they still exceed the national standards of ambient air quality. Archived data from China does not fully support that the concentrations of pollutants directly depend on local emissions, but this is likely due to inaccurate measurement of pollutants. Analyses on the cancer registry data show that cancer burden related to air pollution is on the rise in China and will likely increase further, but there is a lack of data to accurately predict the cancer burden. Past experience from other countries has sounded alarm of the link between air pollution and cancer. The quantitative association requires dedicated research as well as establishment of needed monitoring infrastructures and cancer registries. The air pollution-cancer link is a serious public health issue that needs urgent investigation.
Air Pollutants ; toxicity ; Air Pollution ; adverse effects ; Carcinogens, Environmental ; toxicity ; China ; Coal ; Humans ; Neoplasms ; etiology ; Nitrogen Dioxide ; toxicity ; Particulate Matter ; toxicity ; Sulfur Dioxide ; toxicity ; Vehicle Emissions ; toxicity

To investigate the influence of sulfur dioxide (SO₂) on lipopolysaccharide (LPS)-induced acute lung injury (ALI), we examined the influence of exogenous SO₂ on pulmonary tissue inflammatory response. A rat model of ALI induced by intravenous (IV) injection of LPS was developed. Male Sprague-Dawley (SD) rats were divided into four groups randomly: control group, LPS group, LPS plus SO₂ group (IV injection of 0.5 mL Na₂SO₃/NaHSO₃ 10 min before LPS administration) and SO₂ group (only given Na₂SO₃/NaHSO₃). Animals were sacrificed 6 h after agent administration. Lung weight/body weight ratio (LW/BW) was measured and calculated. Morphological changes of lung tissues were observed. The number of polymorphonuclear neutrophil (PMN) in the bronchoalveolar lavage fluid (BALF), intercellular adhesion factor-1 (ICAM-1) expression in the lung tissue and IL-1, IL-6 and IL-10 levels in the serum were tested. The results showed that, compared to control rats, the LPS-treated rats had severe injuries of lung tissues and an increased LW/BW, increased index of quantitative assessment (IQA) score, increased PMN number in the BALF, increased ICAM-1 expression in the lung tissue and increased IL-1, IL-6 and IL-10 levels in the serum 6 h after LPS injection. Administration of the SO₂ donor, Na₂SO/₃NaHSO₃, into LPS-treated rats reduced the LW/BW, PMN number and ICAM-1 expression, and alleviated the degree of ALI (measured by the IQA score). In addition, Na₂SO₃/NaHSO₃ decreased IL-1 and IL-6 levels, but increased IL-10 level in the serum. There were no significant differences in the above indexes between SO₂-treated rats and control rats. These results suggest that exogenous SO₂ could inhibit the pulmonary tissue inflammatory response in rats with LPS-induced ALI.
Acute Lung Injury ; chemically induced ; drug therapy ; Animals ; Bronchoalveolar Lavage Fluid ; cytology ; Inflammation ; drug therapy ; metabolism ; Intercellular Adhesion Molecule-1 ; metabolism ; Interleukin-1 ; blood ; Interleukin-10 ; blood ; Interleukin-6 ; blood ; Lipopolysaccharides ; adverse effects ; Lung ; pathology ; Male ; Neutrophils ; cytology ; Rats ; Rats, Sprague-Dawley ; Sulfur Dioxide ; pharmacology

AIMTo explore the physiopathological mechanisms of airway injury and the effect on the airway responsiveness of rat by inhaled sulfur dioxide(SO2).

METHODSSixteen SD male rats were divided randomly into 2 groups (n = 8): the control group and SO2 group. The control group was exposed o pure air. SO2 group was exposed to SO2 of the content 1.0 mg/(m(3) x h) 6h daily for consecutive 3 d. At 4th day, we determined the airway responsiveness, collected the bronchoalveolar lavage fluid (BALF), plasma and lung tissue. Then we counted the total cellular score in BALF, measured the plasma SP content and made the immunohistochemistry staining on the lung tissue (HE and SP methods).

RESULTSCompared with the control group, the total cellular score in BALF and plasma SP content in SO2 group's increased significantly ( P < 0.01). HE staining showed there were a great deal of inflammatory cells infiltration under the tunica mucosa bronchiorum; and SP immunohistochemistry staining indicated there were significant changes in numbers of SP-IR positive fibers of SO2group.

CONCLUSIONExposure to low concentration of SO2 would injure healthy rat's airway, and induce airway hyperresponsiveness, neurogenic inflammation is one of its critical pathophysiological mechanisms.

Air Pollutants ; adverse effects ; Animals ; Asthma ; chemically induced ; Bronchi ; drug effects ; innervation ; physiopathology ; Bronchial Hyperreactivity ; chemically induced ; physiopathology ; Bronchitis ; chemically induced ; Bronchoalveolar Lavage Fluid ; cytology ; Male ; Nerve Fibers ; drug effects ; physiology ; Neurogenic Inflammation ; chemically induced ; physiopathology ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Substance P ; blood ; Sulfur Dioxide ; adverse effects

OBJECTIVEHypoxic pulmonary hypertension is an important pathophysiologic process of various cardiovascular diseases. Sulfur dioxide (SO2) was considered as a kind of toxic gas previously, but recent studies suggested that SO2 could act as a key bioactive molecule in the pathogenesis of cardiovascular diseases. Therefore, this study was designed to examine the effect of sulfur dioxide on pulmonary vascular structure of hypoxic pulmonary hypertensive rats treated with SO2 donor substances.

METHODSThe rats were randomly divided into 3 groups: control group(n = 8), hypoxic group(n = 8) and hypoxic + SO2 group (n = 10, treated with SO2 donor Na2SO3/NaHSO3). The rats of hypoxic group and hypoxic + SO2 group were under a hypoxic condition for 21 days, while the rats of control group were exposed to room air. The mean pulmonary artery pressure was tested by means of right cardiac catheterization and the content of SO2 in plasma was investigated by high performance liquid chromatography (HPLC). The change in relative medial thickness (RMT) of pulmonary arteries was examined under optical microscope. The ultra-structural changes were observed under a transmission electron microscope. The data were analyzed through one-way analysis of variance (ANOVA) by SPSS 13.0 software.

RESULTSCompared with control group [(2.25 +/- 0.50) kPa], the mean pulmonary artery pressure of hypoxic group [(5.12 +/- 0.51) kPa] raised significantly (t = 5.091, P < 0.01) and RMT of hypoxic group (9.66 +/- 1.27) compared with control group (6.83 +/- 1.57) significantly raised (t = 3.392, P < 0.01). Ultrastructural observation showed the proliferation and degeneration of endothelial cells in small pulmonary arteries in rats with pulmonary hypertension. The internal elastic lamina was irregular. The proliferation of medial smooth muscle cells of arteries was shown at the level of respiratory bronchioles. The collagens also increased. Meanwhile, compared with control group [(33.36 +/- 5.62) micromol/L], the content of SO2 in plasma of hypoxic group [(27.01 +/- 4.17) micromol/L] declined (t = 2.067, P < 0.05). Whereas compared with that of hypoxic group [(5.12 +/- 0.51) kPa], the mean pulmonary artery pressure of hypoxic + SO2 group [(3.94 +/- 0.33) kPa] declined (t = 2.712, P < 0.01) and RMT of hypoxic + SO2 group (6.97 +/- 1.83) decreased compared with hypoxic group (9.66 +/- 1.27) (t = 3.009, P < 0.01). Compared with those of hypoxic group, the pulmonary artery ultrastructural changes in hypoxic group ameliorated obviously after using exogenous sulfur dioxide donor. The endothelial cells became flat and the smooth muscle cells of arteries slightly enlarged and arranged regularly. At the same time, compared with hypoxic group [(27.01 +/- 4.17) micromol/L], the content of SO2 in plasma of hypoxic + SO2 group [(29.89 +/- 4.52) micromol/L] raised (t = 1.263, P > 0.05).

CONCLUSIONSulfur dioxide plays an important role in the regulation of small pulmonary artery structural changes in hypoxic pulmonary hypertensive rats. The hypoxic pulmonary hypertensive damages can be ameliorated significantly after using exogenous SO2 donor.

Animals ; Hypertension, Pulmonary ; blood ; pathology ; physiopathology ; Hypoxia ; blood ; pathology ; physiopathology ; Male ; Pulmonary Artery ; drug effects ; pathology ; Rats ; Rats, Wistar ; Sulfur Dioxide ; adverse effects ; blood