Exposure to bioaerosols in poultry houses at different stages of fattening: use of real-time PCR for airborne bacterial quantification

Previous studies have demonstrated that poultry-house workers are exposed to very high levels of organic dust and consequently have an increased prevalence of adverse respiratory symptoms. However, the influence of the age of broilers, on bioaerosol concentrations has not been investigated. To evaluate the evolution of bioaerosol concentration during the fattening period, bioaerosol parameters (inhalable dust, endotoxin and bacteria) were measured in 12 poultry confinement buildings in Switzerland, at 3 different stages of the birds' growth; Samples of air taken from within the breathing zones of individual poultry-house employees as they caught the chickens ready to be transported for slaughter, were also analysed. Quantitative PCR (Q-PCR) was used to assess the quantity of total airborne bacteria and total airborne Staphylococcus species. Bioaerosol levels increased significantly during the fattening period of the chickens. During the task of catching mature birds, the mean inhalable dust concentration for a worker was 31 ± 4.7 mg/m3, and endotoxin concentration was 11'080 ± 3436 UE/m3 air, more than ten-fold higher than the Swiss occupational recommended value (1000 UE/m3). The mean exposure level of bird catchers to total bacteria and Staphylococcus species measured by Q-PCR is also very high, respectively reaching values of 72 (± 11) x107 cells/m3 air and 70 (± 16) x106/m3 air. It was concluded that in the absence of wearing protective breathing apparatus, chicken catchers in Switzerland risk exposure beyond recommended limits for all measured bioaerosol parameters. Moreover, the use of Q-PCR to estimate total and specific numbers of airborne bacteria is a promising tool for evaluating any modifications intended to improve the safety of current working practices.

Health consultation : Review of on-site air monitoring data during the removal action at Le Mars coal gas site, Le Mars coal gas plant Le Mars, Plymouth County, Iowa EPA facility ID: IA0001032556 (2005)

The Iowa Department of Public Health (IDPH), Hazardous Waste Site Health Assessment Program was asked by the US Environmental Protection Agency (EPA) to review a round of air sampling data. The air data was collected and analyzed during a removal action at the Le Mars Coal Gas Site in Le Mars, Iowa. EPA asked IDPH to determine from the air data if additional monitoring is necessary throughout the removal action to protect nearby residents from exposure.

Secondhand tobacco smoke exposure in open and semi-open settings: a systematic review

Background: Some countries have recently extended smoke-free policies to particular outdoor settings; however, there is controversy regarding whether this is scientifically and ethically justifiable. Objectives: The objective of the present study was to review research on secondhand smoke (SHS) exposure in outdoor settings. Data sources: We conducted different searches in PubMed for the period prior to September 2012. We checked the references of the identified papers, and conducted a similar search in Google Scholar. Study selection: Our search terms included combinations of"secondhand smoke,""environmental tobacco smoke,""passive smoking" OR"tobacco smoke pollution" AND"outdoors" AND"PM" (particulate matter),"PM2.5" (PM with diameter ≤ 2.5 µm),"respirable suspended particles,""particulate matter,""nicotine,""CO" (carbon monoxide),"cotinine,""marker,""biomarker" OR"airborne marker." In total, 18 articles and reports met the inclusion criteria. Results: Almost all studies used PM2.5 concentration as an SHS marker. Mean PM2.5 concentrations reported for outdoor smoking areas when smokers were present ranged from 8.32 to 124 µg/m3 at hospitality venues, and 4.60 to 17.80 µg/m3 at other locations. Mean PM2.5 concentrations in smoke-free indoor settings near outdoor smoking areas ranged from 4 to 120.51 µg/m3. SHS levels increased when smokers were present, and outdoor and indoor SHS levels were related. Most studies reported a positive association between SHS measures and smoker density, enclosure of outdoor locations, wind conditions, and proximity to smokers. Conclusions: The available evidence indicates high SHS levels at some outdoor smoking areas and at adjacent smoke-free indoor areas. Further research and standardization of methodology is needed to determine whether smoke-free legislation should be extended to outdoor settings.

Analytical challenges in breath analysis and its application to exposure monitoring

There is an increasing interest in the use of breath analysis for monitoring human physiology and exposure to toxic substances or environmental pollutants. This review focuses on the current status of the sampling procedures, collection devices and sample-enrichment methodologies used for exhaled breath-vapor analysis. We discuss the different parameters affecting each of the above steps, taking into account the requirements for breath analysis in exposure assessments and the need to analyze target compounds at sub-ppbv levels. Finally, we summarize the practical applications of exposure analysis in the past two decades

Indoor air quality at a waste incineration plant in Finland

Waste has been incinerated for energy utilization for more than a hundred years, but the harmful emissions emitted from the incineration plants did not begin to cause concern until the 1980s. Many plants were shutdown and the waste incineration plant in Kyläsaari Helsinki was one of them. In later years, new landfill regulations have increased the interest in waste incineration. During the last year, four new plants were taken into operation in Finland, Westenergy in Vaasa among them. The presence of dust has been observed indoors at Westenergy waste incineration plant. Dust is defined as particles with a diameter above 10 μm, while fine particles have a diameter smaller than 2.5 μm, ultrafine under 0.1 μm and nanoparticles under 0.05 μm. In recent years, the focus of particle health research has been changed to investigate smaller particles. Ultrafine particles have been found to be more detrimental to health than larger particles. Limit values regulating the concentrations of ultrafine particles have not been determined yet. The objective of this thesis was to investigate dust and particles present inside the Westenergy waste incineration facility. The task was to investigate the potential pollutant sources and to give recommendations of how to minimize the presence of dust and particles in the power plant. The total particle number concentrations and size distributions where measured at 15 points inside the plant with an Engine Exhaust Particle Sizer (EEPS) Spectrometer. The measured particles were mainly in the ultrafine size range. Dust was only visually investigated, since the main purpose was to follow the dust accumulation. The measurement points inside the incineration plant were chosen according to investigate exposure to visitors and workers. At some points probable leakage of emissions were investigated. The measurements were carried out during approximately one month in March–April 2013. The results of the measurements showed that elevated levels of dust and particles are present in the indoor air at the waste incineration plant. The cleanest air was found in the control room, warehouse and office. The most polluted air was near the sources that were investigated due to possible leakage and in the bottom ash hall. However, the concentrations were near measured background concentrations in European cities and no leakage could be detected. The high concentrations were assumed to be a result of a lot of dust and particles present on surfaces that had not been cleaned in a while. The main source of the dust and particles present inside the waste incineration plant was thought to be particles and dust from the outside air. Other activities in the area around the waste incineration facility are ground work activities, stone crushing and traffic, which probably are sources of particle formation. Filtration of the outside air prior entering the facility would probably save personnel and visitors from nuisance and save in cleaning and maintenance costs.

Effects of formaldehyde on the frog's mucociliary epithelium as a surrogate to evaluate air pollution effects on the respiratory epithelium

The increasing use of alcohol as an alternative fuel to gasoline or diesel can increase emission of formaldehyde, an organic gas that is irritant to the mucous membranes. The respiratory system is the major target of air pollutants and its major defense mechanism depends on the continuous activity of the cilia and the resulting constant transportation of mucous secretion. The present study was designed to evaluate the effects of formaldehyde on the ciliated epithelium through a relative large dose range around the threshold limit value adopted by the Brazilian legislation, namely 1.6 ppm (1.25 to 5 ppm). For this purpose, the isolated frog palate preparation was used as the target of toxic injury. Four groups of frog palates were exposed to diluted Ringer solution (control, N = 8) and formaldehyde diluted in Ringer solution at three different concentrations (1.25, 2.5 and 5.0 ppm, N = 10 for each group). Mucociliary clearance and ciliary beat frequency decreased significantly in contact with formaldehyde at the concentrations of 2.5 and 5.0 ppm after 60 min of exposure (P<0.05). We conclude that relatively low concentrations of formaldehyde, which is even below the Brazilian threshold limit value, are sufficient to cause short-term mucociliary impairment.

Ambient particulate air pollution from vehicles promotes lipid peroxidation and inflammatory responses in rat lung

Oxidative stress plays a major role in the pathogenesis of particle-dependent lung injury. Ambient particle levels from vehicles have not been previously shown to cause oxidative stress to the lungs. The present study was conducted to a) determine whether short-term exposure to ambient levels of particulate air pollution from vehicles elicits inflammatory responses and lipid peroxidation in rat lungs, and b) determine if intermittent short-term exposures (every 4 days) induce some degree of tolerance. Three-month-old male Wistar rats were exposed to ambient particulate matter (PM) from vehicles (N = 30) for 6 or 20 continuous hours, or for intermittent (5 h) periods during 20 h for 4 consecutive days or to filtered air (PM <10 µm; N = 30). Rats continuously breathing polluted air for 20 h (P-20) showed a significant increase in the total number of leukocytes in bronchoalveolar lavage compared to control (C-20: 2.61 x 105 ± 0.51;P-20: 5.01 x 105 ± 0.81; P < 0.05) and in lipid peroxidation ([MDA] nmol/mg protein: C-20: 0.148 ± 0.01; P-20: 0.226 ± 0.02; P < 0.05). Shorter exposure (6 h) and intermittent 5-h exposures over a period of 4 days did not cause significant changes in leukocytes. Lipid damage resulting from 20-h exposure to particulate air pollution did not cause a significant increase in lung water content. These data suggest oxidative stress as one of the mechanisms responsible for the acute adverse respiratory effects of particles, and suggest that short-term inhalation of ambient particulate air pollution from street with high automobile traffic represents a biological hazard.

Indoor NO2 air pollution and lung function of professional cooks

Studies of cooking-generated NO2 effects are rare in occupational epidemiology. In the present study, we evaluated the lung function of professional cooks exposed to NO2 in hospital kitchens. We performed spirometry in 37 cooks working in four hospital kitchens and estimated the predicted FVC, FEV1 and FEF25-75, based on age, sex, race, weight, and height, according to Knudson standards. NO2 measurements were obtained for 4 consecutive days during 4 different periods at 20-day intervals in each kitchen. Measurements were performed inside and outside the kitchens, simultaneously using Palm diffusion tubes. A time/exposure indicator was defined as representative of the cumulative exposure of each cook. No statistically significant effect of NO2 exposure on FVC was found. Each year of work as a cook corresponded to a decrease in predicted FEV1 of 2.5% (P = 0.046) for the group as a whole. When smoking status and asthma were included in the analysis the effect of time/exposure decreased about 10% and lost statistical significance. On predicted FEF25-75, a decrease of 3.5% (P = 0.035) was observed for the same group and the inclusion of controllers for smoking status and asthma did not affect the effects of time/exposure on pulmonary function parameter. After a 10-year period of work as cooks the participants of the study may present decreases in both predicted FEV1 and FEF25-75 that can reach 20 and 30%, respectively. The present study showed small but statistically significant adverse effects of gas stove exposure on the lung function of professional cooks.

Short-term exposure of mice to cigarette smoke and/or residual oil fly ash produces proximal airspace enlargements and airway epithelium remodeling

Chronic obstructive pulmonary disease (COPD) is associated with inflammatory cell reactions, tissue destruction and lung remodeling. Many signaling pathways for these phenomena are still to be identified. We developed a mouse model of COPD to evaluate some pathophysiological mechanisms acting during the initial stage of the disease. Forty-seven 6- to 8-week-old female C57/BL6 mice (approximately 22 g) were exposed for 2 months to cigarette smoke and/or residual oil fly ash (ROFA), a concentrate of air pollution. We measured lung mechanics, airspace enlargement, airway wall thickness, epithelial cell profile, elastic and collagen fiber deposition, and by immunohistochemistry transforming growth factor-β1 (TGF-β1), macrophage elastase (MMP12), neutrophils and macrophages. We observed regional airspace enlargements near terminal bronchioles associated with the exposure to smoke or ROFA. There were also increases in airway resistance and thickening of airway walls in animals exposed to smoke. In the epithelium, we noted a decrease in the ciliated cell area of animals exposed to smoke and an increase in the total cell area associated with exposure to both smoke and ROFA. There was also an increase in the expression of TGF-β1 both in the airways and parenchyma of animals exposed to smoke. However, we could not detect inflammatory cell recruitment, increases in MMP12 or elastic and collagen fiber deposition. After 2 months of exposure to cigarette smoke and/or ROFA, mice developed regional airspace enlargements and airway epithelium remodeling, although no inflammation or increases in fiber deposition were detected. Some of these phenomena may have been mediated by TGF-β1.

Air pollution and cardiovascular hospital admissions in a medium-sized city in São Paulo State, Brazil

The objective of the present study was to estimate the contribution of environmental pollutants to hospital admissions for cardiovascular disease. A time series ecological study was conducted on subjects aged over 60 years and living in São José dos Campos, Brazil, with a population near 700,000 inhabitants. Hospital admission data of public health patients (SUS) were obtained from DATASUS for the period between January 1, 2004 and December 31, 2006, according to the ICD-10 diagnoses I20 to I22 and I24. Particulate matter with less than 10 µm in aerodynamic diameter, sulfur dioxide and ozone were the pollutants examined, and the control variables were mean temperature and relative humidity. Data on pollutants were obtained from the São Paulo State Sanitary Agency. The generalized linear model Poisson regression with lags of up to 5 days was used. There were 1303 hospital admissions during the period. Exposure to particulate matter was significantly associated with hospitalization for cardiovascular disease 3 days after exposure (RR = 1.006; 95%CI = 1.000 to 1.010) and an increase of 16 µg/m³ was associated with a 10% increase in risk of hospitalization; other pollutants were not associated with hospitalization. Thus, it was possible to identify the role of exposure to particulate matter as an environmental pollutant in hospitalization for cardiovascular disease in a medium-sized city inSoutheastern Brazil.

Association of sulfur dioxide exposure with circulatory system deaths in a medium-sized city in Brazil

There is a demonstrable association between exposure to air pollutants and deaths due to cardiovascular diseases. The objective of this study was to estimate the effects of exposure to sulfur dioxide on mortality due to circulatory diseases in individuals 50 years of age or older residing in São José dos Campos, SP. This was a time-series ecological study for the years 2003 to 2007 using information on deaths due to circulatory disease obtained from Datasus reports. Data on daily levels of pollutants, particulate matter, sulfur dioxide (SO2), ozone, temperature, and humidity were obtained from the São Paulo State Environmental Agency. Moving average models for 2 to 7 days were calculated by Poisson regression using the R software. Exposure to SO2 was analyzed using a unipollutant, bipollutant or multipollutant model adjusted for mean temperature and humidity. The relative risks with 95%CI were obtained and the percent decrease in risk was calculated. There were 1928 deaths with a daily mean (± SD) of 1.05 ± 1.03 (range: 0-6). Exposure to SO2 was significantly associated with mortality due to circulatory disease: RR = 1.04 (95%CI = 1.01 to 1.06) in the 7-day moving average, after adjusting for ozone. There was an 8.5% decrease in risk in the multipollutant model, proportional to a decrease of SO2 concentrations. The results of this study suggest that residents of medium-sized Brazilian cities with characteristics similar to those of São José dos Campos probably have health problems due to exposure to air pollutants.

Relationship between pulmonary function and indoor air pollution from coal combustion among adult residents in an inner-city area of southwest China

Few studies evaluate the amount of particulate matter less than 2.5 mm in diameter (PM2.5) in relation to a change in lung function among adults in a population. The aim of this study was to assess the association of coal as a domestic energy source to pulmonary function in an adult population in inner-city areas of Zunyi city in China where coal use is common. In a cross-sectional study of 104 households, pulmonary function measurements were assessed and compared in 110 coal users and 121 non-coal users (≥18 years old) who were all nonsmokers. Several sociodemographic factors were assessed by questionnaire, and ventilatory function measurements including forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), the FEV1/FVC ratio, and peak expiratory flow rate (PEFR) were compared between the 2 groups. The amount of PM2.5 was also measured in all residences. There was a significant increase in the relative concentration of PM2.5 in the indoor kitchens and living rooms of the coal-exposed group compared to the non-coal-exposed group. In multivariate analysis, current exposure to coal smoke was associated with a 31.7% decrease in FVC, a 42.0% decrease in FEV1, a 7.46% decrease in the FEV1/FVC ratio, and a 23.1% decrease in PEFR in adult residents. The slope of lung function decrease for Chinese adults is approximately a 2-L decrease in FVC, a 3-L decrease in FEV1, and an 8 L/s decrease in PEFR per count per minute of PM2.5 exposure. These results demonstrate the harmful effects of indoor air pollution from coal smoke on the lung function of adult residents and emphasize the need for public health efforts to decrease exposure to coal smoke.

Association between NOx exposure and deaths caused by respiratory diseases in a medium-sized Brazilian city

Exposure to nitrogen oxides (NOx) emitted by burning fossil fuels has been associated with respiratory diseases. We aimed to estimate the effects of NOx exposure on mortality owing to respiratory diseases in residents of Taubaté, São Paulo, Brazil, of all ages and both sexes. This time-series ecological study from August 1, 2011 to July 31, 2012 used information on deaths caused by respiratory diseases obtained from the Health Department of Taubaté. Estimated daily levels of pollutants (NOx, particulate matter, ozone, carbon monoxide) were obtained from the Centro de Previsão de Tempo e Estudos Climáticos Coupled Aerosol and Tracer Transport model to the Brazilian developments on the Regional Atmospheric Modeling System. These environmental variables were used to adjust the multipollutant model for apparent temperature. To estimate association between hospitalizations owing to asthma and air pollutants, generalized additive Poisson regression models were developed, with lags as much as 5 days. There were 385 deaths with a daily mean (±SD) of 1.05±1.03 (range: 0-5). Exposure to NOx was significantly associated with mortality owing to respiratory diseases: relative risk (RR)=1.035 (95% confidence interval [CI]: 1.008-1.063) for lag 2, RR=1.064 (95%CI: 1.017-1.112) lag 3, RR=1.055 (95%CI: 1.025-1.085) lag 4, and RR=1.042 (95%CI: 1.010-1.076) lag 5. A 3 µg/m3 reduction in NOx concentration resulted in a decrease of 10-18 percentage points in risk of death caused by respiratory diseases. Even at NOx concentrations below the acceptable standard, there is association with deaths caused by respiratory diseases.

Ag dopedWO(3)-based powder sensor for the detection of NO gas in air

WO3-based materials as sensors for the monitor of environmental gases such as NO2 (NO + NO2) have been rapidly developed for various potential applications (stationary and mobile uses). It has been reported that these materials are highly sensitive to NOx with the sensitivity further enhanced by adding precious group metals (PGM such as Pt, Pd, Au, etc.). However, there has been limited work in revealing the sensing mechanism for these gases over the WO3-based sensors. In particular, the role of promoter is not yet clear though speculations on their catalytic, electronic and structural effects have been made in the past. In parallel to these PGM promoters here we report,for the first time, that Ag promotion can also enhance WO3 sensitivity significantly. In addition, this promotion decreases the optimum sensor temperature of 300 degreesC for Most WO3-based sensors, to below 200 degreesC. Characterizations (XRD, TEM, and impedance measurement) reveal that there is no significant bulk structure change nor particle size alteration in the WO3 phases during the NO exposure. However, it is found that the Ag doping creates a high concentration of oxygen vacancies in form of coordinated crystallographic shear (CS) planes onto the underneath WO3. It is thus proposed that the Ag particle facilitates the oxidative conversion of NO to NO2 followed by a subsequent NO2 adsorption on the defective WO, sites created at the Ag-WO3 interface; hence, accounting for the high molecular sensitivity. (C) 2002 Elsevier Science B.V. All rights reserved.