5 resultados para Ventilated patients

em eResearch Archive - Queensland Department of Agriculture


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In Australia, factors such as local planning processes, urban encroachment into rural areas and intensification of the poultry industry have increased the potential for odour and dust nuisance. At present, accurate estimates of odour emissions from mechanically ventilated poultry housing systems do not exist for Australian conditions. This has made the poultry industry vulnerable to unsubstantiated criticism. Recently, the Australian poultry industry have made a significant investment in research to obtain accurate estimates of odour, dust and volatile chemical emission rates from typical poultry housing systems. This paper describes the measurement of odour emissions from tunnel ventilated poultry housing systems in different climatic zones in Queensland and Victoria, Australia (humid sub-tropical and Mediterranean respectively) during two seasons (summer and winter). Samples were collected at defined intervals over typical batch production cycles to define the odour emission profiles. These samples were analysed using dynamic olfactometry according to the Australian Standard 4323.3 to derive the odour concentration values. Ventilation rates were measured concurrently, allowing the calculation of odour emission rates. Odour concentration and emission rates were assessed in terms of ventilation rate, ambient and shed air temperature and relative humidity and litter moisture status. Odour emission rates varied with bird age. Seasonal differences in odour emission rate were also observed.

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This study assessed the levels of two key pathogens, Salmonella and Campylobacter, along with the indicator organism Escherichia coli in aerosols within and outside poultry sheds. The study ranged over a 3-year period on four poultry farms and consisted of six trials across the boiler production cycle of around 55 days. Weekly testing of litter and aerosols was carried out through the cycle. A key point that emerged is that the levels of airborne bacteria are linked to the levels of these bacteria in litter. This hypothesis was demonstrated by E. coli. The typical levels of E. coli in litter were similar to 10(8) CFU g(-1) and, as a consequence, were in the range of 10(2) to 10(4) CFU m(-3) in aerosols, both inside and outside the shed. The external levels were always lower than the internal levels. Salmonella was only present intermittently in litter and at lower levels (10(3) to 10(5) most probable number [MPN] g(-1)) and consequently present only intermittently and at low levels in air inside (range of 0.65 to 4.4 MPN m(-3)) and once outside (2.3 MPN m(-3)). The Salmonella serovars isolated in litter were generally also isolated from aerosols and dust, with the Salmonella serovars Chester and Sofia being the dominant serovars across these interfaces. Campylobacter was detected late in the production cycle, in litter at levels of around 107 MPN g(-1). Campylobacter was detected only once inside the shed and then at low levels of 2.2 MPN m(-3). Thus, the public health risk from these organisms in poultry environments via the aerosol pathway is minimal.

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Odour emission rates were measured from nine tunnel-ventilated broiler farms in south-eastern Queensland, Australia. At one farm, odour emission rates were measured over two sequential batches approximately weekly, while at the remaining farms, odour emission rates were measured just before the first pickup (around Day 35 of the batch) when bird liveweight was greatest and peak odour emission rates were expected. Odour samples were analysed using dynamic olfactometry (to AS/NZS 4323.3:2001), and an artificial olfaction system was used to continuously monitor odour emission rates at one farm. Odour emission rates ranged from 330 to 2960 ou/s per 1000 birds and from 0.19 to 2.12 ou/s.kg, with a significant amount of variability observed throughout the batch and throughout each sampling day. While the wide range in odour emission rates was primarily due to changes in bird liveweight and ventilation requirements, other factors were also involved. The artificial olfaction system proved useful for quantifying the range and variability of odour emission rates, especially when olfactometry analysis was impractical.

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An observational study was undertaken to measure odour and dust (PM10 and PM2.5) emission rates and identify non-methane volatile organic compounds (NMVOCs) and odorants in the exhaust air from two tunnel-ventilated layer-chicken sheds that were configured with multi-tiered cages and manure belts. The study sites were located in south-eastern Queensland and the West Gippsland region of Victoria, Australia. Samples were collected in summer and winter on sequential days across the manure-belt cleaning cycle. Odour emissions ranged from 58 to 512 ou/s per 1000 birds (0.03-0.27 ou/s.kg) and dust emission rates ranged 0.014-0.184 mg/s per 1000 birds for PM10 and 0.001-0.190 mg/s per 1000 birds for PM2.5. Twenty NMVOCs were identified, including three that were also identified as odorants using thermal desorption-gas chromatography-mass spectrometry/olfactometry analysis. Odour emission rates were observed to vary with the amount of manure accumulation on the manure belts, being lowest 2-4 days after removing manure. Odour emission rates were also observed to vary with diurnal and seasonal changes in ventilation rate. Dust emissions were observed to increase with ventilation rate but not with manure accumulation. Some NMVOCs were identified at both farms and in different seasons whereas others were observed only at one farm or in one season, indicating that odorant composition was influenced by farm-specific practices and season.

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Background and Aim The etiology of Crohn's disease (CD) implicates both genetic and environmental factors. Smoking behavior is one environmental risk factor to play a role in the development of CD. The study aimed to assess the contribution of the interleukin 23 receptor (IL23R) in determining disease susceptibility in two independent cohorts of CD, and to investigate the interactions between IL23R variants, smoking behavior, and CD-associated genes, NOD2 and ATG16L1. Methods Ten IL23R single-nucleotide polymorphisms (SNPs) were genotyped in 675 CD cases, and 1255 controls from Brisbane, Australia (dataset 1). Six of these SNPs were genotyped in 318 CD cases and 533 controls from Canterbury, New Zealand (dataset 2). Case–control analysis of genotype and allele frequencies, and haplotype analysis for all SNPs was conducted. Results We demonstrate a strong increased CD risk for smokers in both datasets (odds ratio 3.77, 95% confidence interval 2.88–4.94), and an additive interaction between IL23R SNPs and cigarette smoking. Ileal involvement was a consistent marker of strong SNP–CD association (P ≤ 0.001), while the lowest minor allele frequencies for location were found in those with colonic CD (L2). Three haplotype blocks were identified across the 10 IL23R SNPs conferring different risk of CD. Haplotypes conferred no further risk of CD when compared with single SNP analyses. Conclusion IL23R gene variants determine CD susceptibility in the Australian and New Zealand population, particularly ileal CD. A strong additive interaction exists between IL23R SNPs and smoking behavior resulting in a dramatic increase in disease risk depending upon specific genetic background.