Indoor measurements of air pollutants in residential houses in urban and suburban areas: Indoor versus ambient concentrations.

Indoor exposure to air pollutants was assessed through 99 visits to 51 homes located in downtown high-rise buildings and detached houses in suburban and rural areas. The ambient concentrations of ultrafine particles (UFP), black carbon (BC), particulate matter smaller than 2.5 µm in diameter (PM2.5), and trace elements were concurrently measured at a central monitoring site in downtown Toronto. Median hourly indoor concentrations for all measurements were 4700 particles/cm3 for UFP, 270 ng/m3 for BC, and 4 µg/m3 for PM2.5, which were lower than ambient outdoor levels by a factor of 2-3. Much higher variability was observed for indoor UFP and BC across the homes compared to ambient levels, mostly due to the influence of indoor cooking emissions. Traffic emissions appeared to have a strong influence on the indoor background (i.e., outdoor-originated) concentrations of BC, UFP, and some trace elements. Specifically, 85% and 34% of the indoor concentrations of BC and UFP were predominantly from outdoor sources, respectively. Moreover, a positive correlation was observed between indoor concentrations of BC and UFP and total road length within a 300 m buffer zone. There was no significant decrease in indoor air pollution with increasing floor level among high-rise residences. In addition to the influence of outdoor sources on indoor air quality, indoor sources contributed to elevated concentrations of K, Ca, Cr, and Cu. A factor analysis was performed on trace elements, UFP, and BC in homes to further resolve possible sources. Local traffic emissions, soil dust, biomass burning, and regional coal combustion were identified as outdoor-originated sources, while cooking emissions was a dominant indoor source. This study highlights how outdoor sources can contribute to chronic exposure in indoor environments and how indoor activities can be associated with acute exposure to temporally varying indoor-originated air pollutants.

Development of a Novel Simulation Reactor for Chronic Exposure to Atmospheric Particulate Matter.

Epidemiological studies have shown that air pollution is associated with the morbidity and mortality from cardiopulmonary diseases. Currently, limited experimental models are available to evaluate the physiological and cellular pathways activated by chronic multi-pollutant exposures. This manuscript describes an atmospheric simulation reactor (ASR) that was developed to investigate the health effects of air pollutants by permitting controlled chronic in vivo exposure of mice to combined particulate and gaseous pollutants. BALB/c mice were exposed for 1 hr/day for 3 consecutive days to secondary organic aerosol (SOA, a common particulate air pollutant) at 10-150 µg/m3, SOA (30 µg/m3) + ozone (65 ppb) or SOA + ozone (65 ppb) + nitrogen dioxide (NO2; 100 ppb). Daily exposure to SOA alone led to increased airway hyperresponsiveness (AHR) to methacholine with increasing SOA concentrations. Multi-pollutant exposure with ozone and/or NO2 in conjunction with a sub-toxic concentration of SOA resulted in additive effects on AHR to methacholine. Inflammatory cell recruitment to the airways was not observed in any of the exposure conditions. The ASR developed in this study allows us to evaluate the chronic health effects of relevant multi-pollutant exposures at 'real-life' levels under controlled conditions and permits repeated-exposure studies.

Syk Regulates Neutrophilic Airway Hyper-Responsiveness in a Chronic Mouse Model of Allergic Airways Inflammation.

BACKGROUND: Asthma is a chronic inflammatory disease characterized by airways hyper-responsiveness (AHR), reversible airway obstruction, and airway inflammation and remodeling. We previously showed that Syk modulates methacholine-induced airways contractility in naïve mice and in mice with allergic airways inflammation. We hypothesize that Syk plays a role in the pathogenesis of AHR; this was evaluated in a chronic 8-week mouse model of house dust mite (HDM)-induced allergic airways inflammation. METHODS: We used the Sykflox/flox//rosa26CreERT2 conditional Syk knock-out mice to assess the role of Syk prior to HDM exposure, and treated HDM-sensitized mice with the Syk inhibitor, GSK143, to evaluate its role in established allergic airways inflammation. Respiratory mechanics and methacholine (MCh)-responsiveness were assessed using the flexiVent® system. Lungs underwent bronchoalveolar lavage to isolate inflammatory cells or were frozen for determination of gene expression in tissues. RESULTS: MCh-induced AHR was observed following HDM sensitization in the Syk-intact (Sykflox/flox) and vehicle-treated BALB/c mice. MCh responsiveness was reduced to control levels in HDM-sensitized Sykdel/del mice and in BALB/c and Sykflox/flox mice treated with GSK143. Both Sykdel/del and GSK143-treated mice mounted appropriate immune responses to HDM, with HDM-specific IgE levels that were comparable to Sykflox/flox and vehicle-treated BALB/c mice. HDM-induced increases in bronchoalveolar lavage cell counts were attenuated in both Sykdel/del and GSK143-treated mice, due primarily to decreased neutrophil recruitment. Gene expression analysis of lung tissues revealed that HDM-induced expression of IL-17 and CXCL-1 was significantly attenuated in both Sykdel/del and GSK143-treated mice. CONCLUSION: Syk inhibitors may play a role in the management of neutrophilic asthma.

A serological survey of Herpes Simplex Virus type 1 and 2 immunity in pregnant women at labor stage in Tehran, Iran.

This study was carried out to determine the prevalence of neutralizing antibodies to Herpes Simplex Virus type 1 (HSV-I) and type 2 (HSV-2) in pregnant women at labor stage. Blood samples from umbilical cord of four hundred women aging 16 to 40 years at labor stage were collected. After sera separation quantity of anti HSV-1 and HSV-2 antibodies were measured by serum neutralization test. Antibody quantification was assayed by two fold dilution of sera (from 1/2 to 1/256) with 500 Tissue Culture Infective Dose fifty percent (TCID50) of the HSV-1 and HSV-2, separately. Three hundred sixty three (90.75%) of women had neutralizing antibody against HSV-1. Thirty three (8.25%) tested women were seropositive for HSV-2 antibodies. Our results indicate that there is positive correlation between increase of age and seroprevalence of anti-HSV-2 infection in pregnant women. Furthermore, the pattern of HSV-2 infection is similar with other Sexual Transmitted Disease (STD). These results also show that seroprevalence of anti-HSV-1 antibody in our tested population was remarkable. However, the seroprevalence of anti-HSV-1 antibody in different age groups statistically were not significant. These results also showed that most women before fertility age have infections with HSV-1.