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Público·95 miembros

Air Pollution By Mn Rao Pdf

Comprehensive book presenting the fundamentals of air pollution. The coverage includes the important principles and practices of pollution sampling, analysis and control. The types, sources and effects of air pollution on human health animals, plants and materials are also dealt with in great detail. Also discussed is the part played by meteorological factors in dispersion of atmospheric effluents. Miscellaneous topics like acid rain, greenhouse effect, indoor air pollution and occupational diseases, such as silicosis and asbestosis, have also been covered.An attempt has been made to make the book Indian-oriented. Included are the Pollution Control Acts of India, air pollution problems in Indian cities, Indian Standards pertaining to air quality, and specific case studies of effects of air pollution in India such as the effect of the Taj Mahal.

air pollution by mn rao pdf

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The quality of ambient air is a noticeable demonstration because the ambient air plays a cardinal preface on the human activities and most of environmental processes. The monitoring of the quality of air is an important part of the pollution control because the ambient air was confirmed as an affected branch on the earth from both anthropogenic activities and natural phenomena. In the existing investigation, there were expected to test the selected important air quality parameters of the ambient air at around the Peradeniya region in Sri Lanka which is known as relatively populous region with the traffic. The ambient air samples were collected through a glass fiber filter paper which was attached to the high volume air sampler and both PM10 concentration and concentration total suspended particles (TSP) of the ambient air were determined using weight differences of air collection bottle and filter paper. Beside of that the lead (Pb) concentrations and NOX concentrations of the ambient air were investigated using hot acid extraction method while having the contribution of atomic absorption spectrometer (AAS) and of absorbing method in to a liquid with the aid of UV- visible spectrometer. As the results, there were obtained 0.0141 ppm of PM10 concentration, 0.0214 ppm of total suspended particles (TSP) concentration, 0.151 μg/m3 of NOX concentration and 0.015μg Pb/ m3 of lead (Pb) concentration of the ambient air at around the Peradeniya region at that moment. When comparing of those results with the air quality standards and norms, it was identified the non hazardous atmosphere at the selected region at that occasion.

Prenatal exposure to PM2.5 impacts lung development and respiratory health in a variety of ways that may persist throughout childhood [5]. Developmental PM2.5 exposure can lead to disturbed alveolarization, impaired lung function, and pulmonary immune differentiation, which may influence acute and chronic health outcomes. In a meta-analysis of multiple European birth cohorts, MacIntyre et al. [19] concluded there was consistent evidence for an association between air pollution and pneumonia in early childhood. The link between prenatal PM2.5 exposure and the development of asthma has also become increasingly recognized as epidemiologic studies have reported positive associations [6, 20]. Hehua et al. [6] reviewed 18 studies and found that children prenatally exposed to multiple air pollutants had increased risk of wheeze and asthma during childhood. However, only a weak association was identified in the five existing studies that evaluated prenatal PM2.5 exposure. These findings highlight a research gap and the need for future studies to examine PM2.5 exposure and contribution to asthma etiology, as well as mechanistic studies to tease apart the complex gene-environment interactions involved in asthma development.

Based on the numerous epidemiological studies summarized above, it is clear that prenatal exposure to fine PM is associated with numerous adverse effects in children, including acute birth outcomes and chronic respiratory effects, with a growing body of literature indicating cognitive and metabolic dysfunction. Although not currently regulated through air quality standards, ultrafine particles (UFPs, PM0.1) are postulated to exert enhanced toxicities due to their larger surface area/mass ratio, enhanced oxidative capacity and ability to translocate into systemic circulation [46]. In general, there is a lack of human evidence on the specific effects from prenatal exposure to UFPs, in part due to the lack of monitoring and models to estimate UFP exposure [47]. In the first large-scale epidemiologic study, Lavigne et al. [48] demonstrated in addition to PM2.5 and nitrate exposure, prenatal UFP exposure was independently associated with childhood asthma incidence. Wright et al. [49] also observed prenatal UFP exposure was associated with asthma development in children in the Northeastern USA, independent of NO2 and temperature. These emerging findings emphasize the need to fill the current gap in the literature interrogating the relationship between prenatal UFP exposure and adverse health outcomes in offspring, particularly immune, neurological, and cardiometabolic endpoints. Further data will help verify the independent risk of UFP exposure on developmental endpoints, as well as inform the effects from multi-pollutant models. In the scarcity of human evidence, a variety of recent studies in animal models have investigated the specific effects of UFP exposure. Described in more detail in the next section, phenotypic and mechanistic data gleaned from animal models help support improved knowledge and encourage further regulation of air pollution exposure during this critical window of development.

Alternatively, other groups have applied DEPs in prenatal exposure models via intranasal application [83, 84], oropharyngeal administration [85], and intratracheal instillation [86, 87]. Outcomes from instillation and inhalation exposures can result in differing pathological consequences [88]; however, in the case of in utero exposures, translocation of the particles into systemic circulation may be of greater consequence to fetal development. Investigators have taken care to apply relevant exposure concentrations using these techniques. For instance, Chen et al. [87] applied 20 μg of a DEP suspension, representing an average daily dose of 8.6 μg/mouse, approximately equating to an inhalational exposure level of 160 μg/m3 PM2.5. Instillation has also been used in general for PM2.5 [89, 90] and PM0.1 [91, 92] dosing using particles collected in urban environments. Oral gavage [93] and intraperitoneal (i.p.) injection of particles [94] are much less commonly used; however, authors cite technical advantages in comparison to intratracheal instillation. While systemic administration of particles does not represent a physiology route of exposure [95], translocation into systemic and placenta circulation may serve as a proxy to investigate fetal/offspring effects. Last, traffic-related air pollution has been extensively studied in animal models via direct exposure to freshly generated diesel exhaust (DE) [96]. Here, rodents are exposed to both particulate and gaseous components. In several prenatal mouse exposure models, DE concentrations have ranged from 90 to 300 μg/m3 PM2.5 [97,98,99,100]. Overall, the many inhalation toxicology methods for generating controlled PM exposures has spurred substantial research in rodent models demonstrating effects on offspring respiratory, immune, neurological, and cardiometabolic development (described in detail in this section). These findings bolster the results gleaned from human epidemiological studies and provide a deeper understanding of the underlying biological mechanisms.

In a rabbit model of diesel exhaust exposure, filtered to generate ultrafine PM (69 nm diameter particles), Valentino et al. [135] observed transplacental transfer of particles using transmission electron microscopy (TEM) analysis. Nanoparticles were visualized in maternal blood spaces of exposed placentae, in trophoblastic cells, and within fetal vessels. Investigators also demonstrated disruption of placental function in exposed animals, which was largely due to reduced placental vascularization. Veras et al. [136] also reported functional morphologic changes in placentae, primarily on the maternal side, from mice exposed to ambient levels of air pollution in São Paulo. Exposure during gestation resulted in smaller fetal weights, reduced volumes, calibers, and surface areas of maternal blood spaces, and greater fetal capillary surfaces and diffusive conductance, which authors discussed as a fetoplacental adaption to maintain and expand oxygen and nutrient delivery. In another mouse model, Paul et al. [106] confirmed decreased placental efficiency with the presence of metallic nanoparticles in the placenta. This correlated with impaired lung development in offspring that persisted into adulthood.

Fine PM exposure induces maternal systemic and placental oxidative stress and inflammation, as evidenced in exposed human populations and in experimental models. Nagiah et al. [154] observed pregnant women living in highly industrialized areas of south Durban, South Africa, had increased markers reflective of oxidative stress in circulating lymphocytes as compared to women living in a less industrialized area in the north with lower pollutant levels. Levels of malondialdehyde (MDA), superoxide dismutase (SOD2), and uncoupling protein 2 (UCP2) mRNA were elevated, whereas Nrf2 and GSH expression was decreased in the higher exposure group. Similarly, Ambroz et al. [155] compared urine and blood markers reflecting oxidative DNA damage and lipid peroxidation in mothers and infants living in the Czech Republic in areas with relatively poor to good air quality. Investigators measured 8-oxo-7,8-dihydro-2-deoxyguanosine (8-oxodG), a common product of DNA oxidation, and 15-F2t-isoprostane (15-F2t-IsoP), an oxidized product of arachidonic acid. Isoprostanes, including 15-F2t-IsoP, as well as 8-iso-prostaglandin F2α (8-iso-PGF2α), are routinely employed as markers of oxidative stress. In newborns from the Czech Republic, PM2.5 concentrations significantly predicted 8-oxodG excretion, and PM2.5 and benzo[a]pyrene concentrations significantly predicted 15-F2t-IsoP levels. In mothers, PM2.5 concentrations were a significant predictor of 8-oxodG levels. Using a metabolomics approach, Yan et al. [132] observed maternal oxidative stress and inflammation-related pathways, including linoleate, leukotriene, and prostaglandin, were altered in response to traffic-related air pollution exposure.

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