Abstract  OBJECTIVE: This article reviews panel studies of air pollution on children's respiratory health and proposes future research directions.

METHODS: The PubMed electronic database was used to search published original epidemiological studies in peer-reviewed journals from 2000 to November 2011. Children's age was limited to ≤18 years old. A total of 33 relevant articles were obtained, with 20 articles relating to lung function, 21 articles relating to respiratory symptoms, and 8 articles examining both.

RESULTS: Most studies suggested the adverse effects of air pollution on children's lung function and respiratory symptoms. Particles and NO(2) showed more significant results, whereas effects of SO(2) were not consistent. A few studies indicated that O(3) interacted with temperature and sometimes seemed to be a protective factor for children's respiratory health. Negative associations between air pollutants and pulmonary health were more serious in asthmatic children than in healthy subjects. However, many outcomes depended on the number of lag days. Peak expiratory flow (PEF) was the most usual measurement for children's lung function, followed by forced expiratory volume in 1 second (FEV(1)).

CONCLUSIONS: There are significant adverse effects of air pollution on children's pulmonary health, especially for asthmatics. Future studies need to examine the lag effects of air pollution on children's lung function and respiratory symptoms. Ambient temperature is predicted to change worldwide due to climate change, which will threaten population health. Further research is needed to examine the effects of ambient temperature and the interactive effects between air pollution and ambient temperature on children's lung function and respiratory symptoms.

Abstract  Ozonolysis is a major tropospheric removal mechanism for unsaturated hydrocarbons and proceeds via "Criegee intermediates"--carbonyl oxides--that play a key role in tropospheric oxidation models. However, until recently no gas-phase Criegee intermediate had been observed, and indirect determinations of their reaction kinetics gave derived rate coefficients spanning orders of magnitude. Here, we report direct photoionization mass spectrometric detection of formaldehyde oxide (CH(2)OO) as a product of the reaction of CH(2)I with O(2). This reaction enabled direct laboratory determinations of CH(2)OO kinetics. Upper limits were extracted for reaction rate coefficients with NO and H(2)O. The CH(2)OO reactions with SO(2) and NO(2) proved unexpectedly rapid and imply a substantially greater role of carbonyl oxides in models of tropospheric sulfate and nitrate chemistry than previously assumed.

Abstract  The usage of novel LED-light sources for spectrometric application is shown and described in this paper. The utilization of fiber optical linkage to a simple open path absorption cell and a proper control of the light sources is the key to a robust and high resolved measurement system. A novel optical sensor system based on this approach is realized to measure the concentration of nitrogen dioxide, sulfur dioxide with a resolution below 1 ppm and ozone down to 30 ppb at a 4 cm single reflection cell in a fraction of a second measurement time. In this setup the emitted light from Light Emitting Diodes in the ultraviolet to the visible wavelength range was used. The optoelectronics and the control electronics are separated from the optical sensor head where the pure optical sensor effect takes place. Therefore the sensor can be used in harsh environment for instance in an exhaust tailpipe system or close to discharge plasma in strong electromagnetic fields or at high temperature. Furthermore the sensor design is potentially low cost, quite small, long life and well suited for a large number of applications - from small battery powered hand held devices to industrial process control implementation. An LED-based sensor does not compete to laboratory chemical analytical devices but in many cases it is well suited for high resolved and fast online concentration measurements.

Abstract  Rationale: Cohort evidence linking long-term exposure to outdoor particulate air pollution and mortality has come largely from the United States. There is relatively little evidence from nationally representative cohorts in other countries. Objectives: To investigate the relationship between long-term exposure to a range of pollutants and causes of death in a national English cohort. Methods: A total of 835,607 patients aged 40-89 years registered with 205 general practices were followed from 2003-2007. Annual average concentrations in 2002 for particulate matter with a median aerodynamic diameter less than 10 (PM10) and less than 2.5 μm (PM2.5), nitrogen dioxide (NO2), ozone, and sulfur dioxide (SO2) at 1 km(2) resolution, estimated from emission-based models, were linked to residential postcode. Deaths (n = 83,103) were ascertained from linkage to death certificates, and hazard ratios (HRs) for all- and cause-specific mortality for pollutants were estimated for interquartile pollutant changes from Cox models adjusting for age, sex, smoking, body mass index, and area-level socioeconomic status markers. Measurements and Main Results: Residential concentrations of all pollutants except ozone were positively associated with all-cause mortality (HR, 1.02, 1.03, and 1.04 for PM2.5, NO2, and SO2, respectively). Associations for PM2.5, NO2, and SO2 were larger for respiratory deaths (HR, 1.09 each) and lung cancer (HR, 1.02, 1.06, and 1.05) but nearer unity for cardiovascular deaths (1.00, 1.00, and 1.04). Conclusions: These results strengthen the evidence linking long-term ambient air pollution exposure to increased all-cause mortality. However, the stronger associations with respiratory mortality are not consistent with most US studies in which associations with cardiovascular causes of death tend to predominate.

Abstract  Oil refineries are one of the proven sources of environmental pollution as they emit more than 100 chemicals into the atmosphere including sulfur dioxide (SO2). The dispersion patterns of SO2 from emissions of Sohar refinery was simulated by employing California Puff (CALPUFF) model integrated with state of the art meteorological Mesoscale Model (MM5). The results of this simulation were used to quantify the ground level concentrations of SO2 in and around the refinery. The evaluation of the CALPUFF and MM5 modeling system was carried out by comparing the estimated results with that of observed data of the same area. The predicted concentrations of SO2 agreed well with the observed data, with minor differences in magnitudes. In addition, the ambient air quality of the area was checked by comparing the model results with the regulatory limits for SO2 set by the Ministry of Environment and Climate Affairs (MECA) in Oman. From the analysis of results, it was found that the concentration of SO2 in the nearby communities of Sohar refinery is well within the regulatory limits specified by MECA. Based on these results, it was concluded that no health risk, due to SO2 emissions, is present in areas adjacent to the refinery.

Abstract  Spatiotemporal models for sulphur dioxide pollution over Europe are considered within an additive model framework. A suitable description of the spatiotemporal correlation structure of the data is constructed and incorporated in the analysis of the additive model, to ensure that standard errors and other forms of analysis reflect the form of variation that is exhibited by the data. To deal with the large sample size, an updating formula based on binning is derived to provide a computationally manageable implementation of the back-fitting algorithm. Interaction terms involving space, time and seasonal effects are also considered. This requires three-dimensional smoothing which is implemented by repeated application of lower dimensional marginal smoothing operations. The properties of this form of smoothing are examined and the estimators are shown to have first-order behaviour, inherited from the marginal operations, which is equivalent to the full multivariate versions. These models and methods are applied to the sulphur dioxide data, allowing detailed and informative descriptions of the spatiotemporal patterns to be created.

Abstract  Ambient air pollution has been associated with increased mortality and morbidity; however, few studies have examined the short-term effect of air pollution specifically on chronic obstructive pulmonary disease (COPD), which is an important cause of mortality and morbidity world wide. In this analysis, we examined the associations between daily air pollution levels [particulate matter less than 10 microns in aerodynamic diameter (PM10), sulfur dioxide (SO2) and nitrogen dioxide (NO2)] and COPD mortality in four Chinese cities. We used Poisson regression models with natural spline smoothing functions to adjust for long-term and seasonal trends of COPD mortality, as well as other time-varying covariates. We did a meta-analysis to obtain the 4-city average estimates. Air pollution (PM10, SO2, and NO2) was found to be associated with increased risk of COPD mortality in these four cities. Using the random-effects model, an increase of 10 mu g m(-3) of 2-day moving average concentrations of PM10, SO2 and NO2 corresponded to a 0.78% (95% CI, 0.13-1.42), 1.30% (95% CI, 0.61-1.99), and 1.78% (95% CI, 1.10-2.46) increase of COPD mortality, respectively. The concentration response curves indicated linear associations without threshold. Only NO2 remained significant in the multi-pollutant models. To our knowledge, this is the first multi-city study in Asian developing region to report the short-term effect of air pollution on COPD mortality. Our results contribute to very limited data on the effects of air pollution on COPD mortality for high exposure settings typical in developing countries. (C) 2013 Elsevier Ltd. All rights reserved.

Abstract  CONTEXT: Investigations of cell/molecular level effects of in vivo exposure of airway mucosa of experimental animals to common irritant gases have demonstrated structural and physiological changes reflective of breaches in epithelial barrier function, presence of inflammatory cell infiltrate and compromised ciliary function. These experimental animal studies provided useful perspectives of plausible, but more subtle pathologic outcomes having relevance to lifestyle exposure to gaseous environmental irritants including tobacco smoke.

METHODS: Freeze-fracture technology was applied to ultrastructural examination of large airway epithelium, with appropriate controls, from guinea pigs exposed to ozone and of nasal mucosa of human subjects exposed to ozone or sulfur dioxide, and nasal mucosa of active smokers.

RESULTS: We documented substantive membrane structural changes to tight junctional complexes and cilia as well as an infiltrate of neutrophils into the surface mucosal layer in exposed animals. These patterns also were evident but not as pervasive among human subjects acutely exposed experimentally to irritant gases and those chronically exposed by their lifestyle to tobacco smoke.

DISCUSSION: Our intent was to characterize respiratory tract mucosal membrane disorganization associated with high level acute irritant exposures in an experimental animal model and to evaluate evidence of similar but perhaps more subtle pathologic change associated with lower level experimental or lifestyle exposures. Our studies demonstrate continuity, albeit subtle, of pathologic change from high dosage experimental animal exposure to low dosage human exposures.

CONCLUSIONS: This study represents the first report of ultrastructural airway epithelial membrane anomalies associated with lifestyle exposure to tobacco smoke irritants.

Abstract  BACKGROUND: Respiratory irritants represent a major cause of occupational obstructive airway diseases. We provide an overview of the evidence related to irritative agents causing occupational asthma or occupational COPD.

METHODS: We searched MEDLINE via PubMed. Reference lists of relevant reviews were also screened. The SIGN grading system was used to rate the quality of each study. The modified RCGP three-star system was used to grade the body of evidence for each irritant agent regarding its causative role in either occupational asthma or occupational COPD.

RESULTS: A total of 474 relevant papers were identified, covering 188 individual agents, professions or work-sites. The focus of most of the studies and the predominant diagnosis was occupational asthma, whereas occupational COPD arose only incidentally.The highest level assigned using the SIGN grading was 2+ (well-conducted systematic review, cohort or case-control study with a low risk of confounding or bias). According to the modified RCGP three-star grading, the strongest evidence of association with an individual agent, profession or work-site ("**") was found for 17 agents or work-sites, including benzene-1,2,4-tricarboxylicacid-1,2-anhydride, chlorine, platinum salt, isocyanates, cement dust, grain dust, animal farming, environmental tobacco smoke, welding fumes or construction work. Phthalic anhydride, glutaraldehyde, sulphur dioxide, cotton dust, cleaning agents, potrooms, farming (various), foundries were found to be moderately associated with occupational asthma or occupational COPD ("*[+]").

CONCLUSION: This study let us assume that irritant-induced occupational asthma and especially occupational COPD are considerably underreported. Defining the evidence of the many additional occupational irritants for causing airway disorders will be the subject of continued studies with implications for diagnostics and preventive measures.

Abstract  Recent studies have shown that the reaction of stabilized Criegee intermediates (CIs, formed from the ozonolysis of alkenes) with SO2 may be an important source sulfuric acid vapor (H2SO4) in alkene-rich regions. We use a global atmospheric chemistry model, GEOS-Chem, with the online aerosol microphysics module, TOMAS, to investigate the impact of CI+SO2 chemistry on cloud condensation nuclei (CCN) concentrations. To get an upper bound for the effect of CI+SO2 chemistry, we use the fastest published rate constants in our simulations. The addition of CI+SO2 chemistry increases H2SO4 globally by 4%, but by over 100% in forested regions, particularly the tropics. However, changes in CCN due to CI+SO2 chemistry were significantly lower, less than 1% globally and no more than 15% in any region. The estimated change in the brightness aerosol indirect effect (AIE) due to the addition of CI+SO2 chemistry was -0.03 W m(-2) globally, which is over an order-of-magnitude smaller than many other model uncertainties such as nucleation mechanisms, primary emissions, SOA and deposition. Thus, we conclude that the details of CI+SO2 chemistry are relatively unimportant in predicting the aerosol indirect effect and have only a minor impact on climate.

Abstract  Elevated outdoor ozone levels are associated with adverse health effects. Because people spend the vast majority of their time indoors, reduction in indoor levels of ozone of outdoor origin would lower population exposures and might also lead to a reduction in ozone-associated adverse health effects. In most buildings, indoor ozone levels are diminished with respect to outdoor levels to an extent that depends on surface reactions and on the degree to which ozone penetrates the building envelope. Ozone enters buildings from outdoors together with the airflows that are driven by natural and mechanical means, including deliberate ventilation used to reduce concentrations of indoor-generated pollutants. When assessing the effect of deliberate ventilation on occupant health one should consider not only the positive effects on removing pollutants of indoor origin but also the possibility that enhanced ventilation might increase indoor levels of pollutants originating outdoors. This study considers how changes in residential ventilation that are designed to comply with ASHRAE Standard 62.2 might influence indoor levels of ozone. Simulation results show that the building envelope can contribute significantly to filtration of ozone. Consequently, the use of exhaust ventilation systems is predicted to produce lower indoor ozone concentrations than would occur with balanced ventilation systems operating at the same air-exchange rate. We also investigated a strategy for reducing exposure to ozone that would deliberately reduce ventilation rates during times of high outdoor ozone concentration while still meeting daily average ventilation requirements. Published by Elsevier Ltd.

Abstract  Human exposure and dose models often require a quanti. cation of oxygen consumption for a simulated individual. Oxygen consumption is dependent on the modeled individual's physical activity level as described in an activity diary. Activity level is quantified via standardized values of metabolic equivalents of work (METS) for the activity being performed and converted into activity-specific oxygen consumption estimates. However, oxygen consumption remains elevated after a moderate-or high-intensity activity is completed. This effect, which is termed excess post-exercise oxygen consumption (EPOC), requires upward adjustment of the METS estimates that follow high-energy expenditure events, to model subsequent increased ventilation and intake dose rates. In addition, since an individual's capacity for work decreases during extended activity, methods are also required to adjust downward those METS estimates that exceed physiologically realistic limits over time. A unified method for simultaneously performing these adjustments is developed. The method simulates a cumulative oxygen deficit for each individual and uses it to impose appropriate time-dependent reductions in the METS time series and additions for EPOC. The relationships between the oxygen deficit and METS limits are nonlinear and are derived from published data on work capacity and oxygen consumption. These modi. cations result in improved modeling of ventilation patterns, and should improve intake dose estimates associated with exposure to airborne environmental contaminants.

Abstract  The atmospheric pollutant sulfur dioxide (SO(2)) is endogenously generated from the normal metabolism of sulfur-containing amino acids through the aspartate aminotransferase pathway. SO(2) is produced in cardiovascular tissues, and the aspartate aminotransferase mRNA is localized in endothelia and in vascular smooth muscle cells near the endothelial layer. Recent studies explored the physiological and pathophysiological effects of endogenous SO(2) on the cardiovascular system, and various potential mechanisms were found. These discoveries suggest a novel role of endogenous SO(2) in the modulation of the cardiovascular system and provide a basis for new treatments for cardiovascular diseases.

Abstract  Eruption at Kilauea Volcano, Hawai'i, has continued since 1983, emitting sulfurous air pollution into nearby communities. The purpose of this cohort study was to estimate the relative risk (RR) of acute bronchitis over a period from January 2004 to December 2006 in communities exposed to the volcanic air pollution. A community-based case review was conducted using medical records from clinics and emergency rooms in exposed and unexposed study areas. Initial visits by local residents for diagnosed acute bronchitis were clinically reviewed. The cumulative incidence rate for the 3-yr period was 117.74 per 1000 in unexposed communities and 184.63 per 1000 in exposed communities. RR estimates were standardized for age and gender, revealing an elevated cumulative incidence ratio (CIR) of 1.57 (95% CI = 1.36-1.81) for acute bronchitis in the exposed communities. Highest risk [CIR: 6.56 (95% CI = 3.16-13.6)] was observed in children aged 0-14 yr who resided in the exposed communities. Exposed middle-aged females aged 45-64 yr had double the risk for acute bronchitis than their unexposed counterparts. These findings suggest that communities continuously exposed to sulfurous volcanic air pollution may have a higher risk of acute bronchitis across the life span.

Abstract  While sulfur dioxide (SO(2)) has been previously known for its toxicological effects, it is now known to be produced endogenously in mammals from sulfur-containing amino acid L-cysteine. L-cysteine is catalyzed by cysteine dioxygenase (CDO) to L-cysteinesulfinate, which converts to β-sulfinylpyruvate through transamination by aspartate aminotransferase (AAT), and finally spontaneously decomposes to pyruvate and SO(2). The present study explored endogenous SO(2) production, and AAT and CDO distribution in different rat tissue. SO(2) content was highest in stomach, followed by tissues in the right ventricle, left ventricle, cerebral gray matter, pancreas, lung, cerebral white matter, renal medulla, spleen, renal cortex and liver. AAT activity and AAT1 mRNA expression were highest in the left ventricle, while AAT1 protein expression was highest in the right ventricle. AAT2 and CDO mRNA expressions were both highest in liver tissue. AAT2 protein expression was highest in the renal medulla, but CDO protein expression was highest in liver tissue. In all tissues, AAT1 and AAT2 were mainly distributed in the cytoplasm rather than the nucleus. These observed differences among tissues endogenously generating SO(2) and associated enzymes are important in implicating the discovery of SO(2) as a novel endogenous signaling molecule.

Abstract  Pulmonary hypertension (PH) is an important pathophysiological process in the development of many diseases. However, the mechanism responsible for the development of PH remains unknown. The objective of the study was to explore the possible impact of sulfur dioxide (SO2) on the endogenous hydrogen sulfide (H2S) pathway in rats with PH induced by high pulmonary blood flow. Compared with sham group, the systolic pulmonary artery pressure (SPAP) in the shunt group was significantly increased, along with the increased percentage of muscularized arteries and partially muscularized arteries of small pulmonary arteries. Compared with the shunt group, SPAP in the shunt+SO2 group was significantly decreased, and the percentage of muscularized pulmonary arteries was also decreased. Additionally, rats that developed PH had significantly lower levels of SO2 concentration, aspartate aminotransferase (AAT) activity, protein and mRNA expressions of AAT2 in pulmonary tissues. Administration of an SO2 donor could alleviate the elevated pulmonary arterial pressure and decrease the muscularization of pulmonary arteries. At the same time, it increased the H2S production, protein expression of cystathionine-γ-lyase (CSE), mRNA expression of CSE, mercaptopyruvate transsulphurase (MPST) and cystathionine-β-synthase (CBS) in the pulmonary tissue of the rats. The results suggested that endogenous SO2/AAT2 pathway and the endogenous H2S production were downregulated in rats with PH induced by high pulmonary blood flow. However, SO2 could reduce pulmonary arterial pressure and improve the pulmonary vascular pathological changes in association with upregulating endogenous H2S pathway.

Abstract  OBJECTIVES: This report presents health statistics from the 2010 National Health Interview Survey (NHIS) for the civilian noninstitutionalized adult population, classified by sex, age, race and Hispanic origin, education, family income, poverty status, health insurance coverage, marital status, and place and region of residence. Estimates are presented for selected chronic conditions and mental health characteristics, functional limitations, health status, health behaviors, health care access and utilization, and human immunodeficiency virus testing. Percentages and percent distributions are presented in both age-adjusted and unadjusted versions.

DATA SOURCE: NHIS is a household, multistage probability sample survey conducted annually by interviewers of the U.S. Census Bureau for the Centers for Disease Control and Prevention's National Center for Health Statistics. In 2010, data were collected on 27,157 adults in the Sample Adult questionnaire. The conditional response rate was 77.3%, and the final response rate was 60.8%. The health information for adults in this report was obtained from one randomly selected adult per family. In very rare instances where the sample adult was not able to respond for himself or herself, a proxy was used.

HIGHLIGHTS: In 2010, 61% of adults aged 18 years and over had excellent or very good health. Twelve percent of adults had been told by a doctor or health professional that they had heart disease, 25% had been told on two or more visits that they had hypertension, 9% had been told they had diabetes, and 22% had been told they had some form of arthritis, rheumatoid arthritis, gout, lupus, or fibromyalgia. Twenty-one percent of adults were current smokers, and 21% were former smokers. Based on estimates of body mass index, 35% of adults were overweight and 27% were obese.

Abstract  This study aimed to investigate the effect of alpha-lipoic acid (LA) administration on sulfite-induced alterations in visual evoked potentials (VEPs). Fifty two male albino Wistar rats were randomized into four experimental groups as follows; control (C), LA treated (L), sodium metabisulfite (Na(2)S(2)O(5)) treated (S), Na(2)S(2)O(5)+LA treated (SL). Na(2)S(2)O(5) (260 mg/kg/day) and LA (100 mg/kg/day) were given by intragastric intubation for 5 weeks. The latencies of VEP components were significantly prolonged in the S group and returned to control levels following LA administration. Thiobarbituric acid reactive substances (TBARS) levels in the S group were significantly higher than those detected in controls. LA significantly decreased brain and retina TBARS levels in the SL group compared with the S group. Sulfite caused a significant decrease in retina and brain glutathione peroxidase (GPx) activities which was restored to control levels via LA administration. Brain glutathione (GSH):glutathione disulfide (GSSG) ratio was significantly increased in rats jointly treated with sulfite and LA compared to rats treated with sulfite alone. Though not significant, a similar increase in GSH:GSSG ratio was also observed in the retina of SL group. This study showed that LA is protective against sulfite-induced VEP alterations and oxidative stress in the brain and retina. (C) 2008 Elsevier Inc. All rights reserved.

Abstract  Sulfur dioxide (SO2) is a ubiquitous air pollutant which causes kinds of damage to human and other organisms. However, the effects and mechanisms on the plasma membrane when cells and tissues were exposed to SO2 were still unknown. The results herein showed a gradual reduction in body weight and dry lung weight for rats exposed to SO2. The wet lung weights were increased. The changes indicated SO2 inhalation caused pulmonary tissue permeability edema. The pulmonary permeability was increased by the determination of protein contents in BALs and pulmonary permeability index (PPI). The intracellular proteins were penetrated into extracellular matrix. The total leukocytes in BALs of rats in each group exposed to SO2 were significantly increased, and the granulocytes were also increased significantly. However, the lymphocytes in BALs of rats exposed SO2 were to some extent different to the control groups. The activities of acid phosphatase (ACP), alkaline phosphatase (AKP) and lactic dehydrogenase (LDH) in BALs were increased to some extent. The results showed that the functions of plasma membrane were damaged with the damage of membrane structure, parts of the membrane bound enzymes and intracellular enzymes were released into BALs. The membrane fluidity in AM cells were significantly decreased by the determination of steady-state fluorescent polarization degree (P) and fluorescence microviscosity (eta) of the AM.

Abstract  Sodium metabisulfite (Na(2)S(2)O(5)) is used as an antioxidant and antimicrobial agent in a variety of drugs and functions as a preservative in many food preparations. This study was performed to elucidate the dose-dependent effects of sodium metabisulfite ingestion on rat gastric tissue apoptotic changes and lipid peroxidation. Forty male wistar rats, aged 3 months were used. They were randomly divided into four groups: control (C), the group treated with Na(2)S(2)O(5) (10 mg/kg; S1), the group treated with Na(2)S(2)O(5) (100 mg/kg; S2), the group treated with Na(2)S(2)O(5) (260 mg/kg; S3). Na(2)S(2)O(5) was given by intragastric intubation for 35 days. In the S2 and S3 groups, malondialdehyde (MDA) levels increased markedly when compared with the control group. High doses of sulfite administration elevated number of apoptotic cells both in mucosa and submucosa layers of stomach in parallel with increased MDA levels. These results suggest that sodium metabisulfite increased lipid peroxidation and thus number of apoptotic cells on gastric tissue in dose-dependent manner.

Abstract  Sulfites are compounds commonly used as preservatives in foods, beverages and pharmaceuticals. Sulfite is also endogenously generated during the metabolism of sulfur-containing amino acids and drugs. It has been shown that sulfite is a highly toxic molecule. Many studies have examined the effects of sulfite toxicity, but the effect of ingested sulfite on the number of neurons in the hippocampus has not yet been reported. The present study was undertaken to investigate the effect of ingested sulfite on pyramidal neurons by counting cells in CA1 and CA3-2 subdivisions of the rat hippocampus. For this purpose, rats were assigned to one of four groups (6 rats per group): control (C), sulfite (S), deficient (D) and deficient+sulfite (DS). Sulfite oxidase deficiency was established by feeding rats a low molybdenum diet and adding 200ppm tungsten (W) to their drinking water. Sulfite (70mg/kg) was also administered to the animals via their drinking water. At the end of the experimental period, the rats were sacrificed by exsanguination under anesthesia, and their brains and livers quickly removed. The livers were used for a SOX activity assay, and the brains were used for neuronal counts in a known fraction of the CA1 and CA3-2 subdivisions of the left hippocampus using the optical fractionator method, which is a stereological method. The results showed that sulfite treatment caused a significant decrease in the total number of pyramidal neurons in three subdivisions of the hippocampus (CA1 and CA3-2) in the S, D and DS groups compared with the control group. It is concluded that exogenous administration of sulfite causes loss of pyramidal neurons in CA1 and CA3-2 subdivisions in both normal and SOX deficient rat hippocampus. This finding provides supporting evidence that sulfite is a neurotoxic molecule.

Abstract  A noticeable effect of sulfite treatment was observed on the plasma ceruloplasmin ferroxidase activity of rats with normal sulfite oxidase activity when compared to normal controls. The plasma levels of selenium, iron, and zinc were unaffected by sulfite in normal and sulfite oxidase (SOX)-deficient rats. While plasma level of Mn was decreasing, plasma Cu level increased in SOX-deficient rats. Treating SOX-deficient groups with sulfite did not alter plasma level of Mn but made plasma level of Cu back to its normal level. This is the first evidence that Cu and Mn status were affected in experimental sulfite oxidase deficiency induced by low molybdenum diet with tungsten addition deserving further research to determine the underlying mechanisms of these observations in experimental sulfite oxidase deficiency.

Abstract  In this work we used daily outpatient data from the Landseed Hospital in a heavily industrial area in northern Taiwan to study the associations between daily outpatient visits and air pollution in the context of a heavily polluted atmospheric environment in Chung-Li area during the period 2007-2011. We test the normality of each data set, control for the confounding factors, and calculate correlation coefficient between the outpatient visits and air pollution and meteorology, and use multiple linear regression analysis to seek significance of these associations. Our results show that temperature and relative humidity tend to be negatively associated with respiratory diseases. NO and NO2 are two main air pollutants that are positively associated with respiratory diseases, followed by PM10, PM2.5, O-3, CO, and SO2. Young outpatients (age 0-15 years) are most sensitive to changing air pollution and meteorology factors, followed by the eldest (age >= 66 years) and age 16-65 years of outpatients. Outpatients for COPD diseases are most sensitive to air pollution and meteorology factors, followed by allergic rhinitis, asthma, and pneumonia diseases. In the context of sex difference to air pollution and meteorological factors, male outpatients are more sensitive than female outpatients in the 16-65 age groups, while female outpatients are more sensitive than male outpatients in the young 0-15 age groups and in the eldest age groups. In total, female outpatients are more sensitive to air pollution and meteorological factors than male outpatients.

Abstract  BACKGROUND: Mt. Oyama in Miyakejima Island erupted in June, 2000. All Miyake villagers were forced to evacuate from the island in September, 2000, due to continuous eruptions and emissions of unsafe amounts of volcanic gas, mainly SO2. From February, 2005, Miyake villagers returned to the island despite volcanic gas still being emitted.

OBJECTIVES: This study examines the 2-yr changes in Miyake residents' respiratory systems from autumn 2004 to November 2006.

METHODS: The study population was 823 Miyake adult residents who participated in the health check-up in 2006. Respiratory effects were evaluated by a questionnaire for respiratory symptoms and spirometry. SO2 has been continuously monitored at 7 sampling points of the inhabited area. The mean SO2 concentration from February 2005 to November 2006 was 0.031 ppm. The area was categorized into 4 areas by SO2 concentration, namely, areas L, H-1, H-2 and H-3, where average SO2 concentrations were 0.019, 0.026, 0.032, and 0.045 ppm, respectively.

RESULTS: The study subjects showed no deterioration in lung function. Prevalence of cough and phlegm among all participants were significantly higher in 2006 than in 2004, and age-, sex- and smoking-adjusted odds ratios of cough and phlegm were 1.75 (95%CI 1.33-2.30) and 1.44 (1.12-1.87). Prevalence of chronic bronchitis-like symptoms among normosusceptive subjects in 2006 was 4.1% which was significantly higher than that of 2.1% in 2004 (p=0.035). Compared to area L, the frequencies of phlegm and irritation of the nose were significantly increased in areas H-2 and H-3.

CONCLUSION: SO2 exposure-related respiratory symptoms were observed in adult Miyakejima residents after returning to the island.