AIR POLLUTION – MONITORING MODELLING AND HEALTH

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340 Air Pollution – Monitoring, Modelling and Health PM 2.5 (Loomis 2000). While investigation of the health effects of particulate matter should continue, it would be unwise to focus too narrowly to the exclusion of other components of air pollution. The preoccupation with the smallest particles may be due in part to the tendency to look where the light is: although most researchers live in North America and western Europe and most previous studies on the health effects of air pollution have been conducted in those areas, many of the world’s largest cities and much of the population currently exposed to high levels of air pollution are located in developing countries. For public health purposes, it is clearly important to examine the health effects of air pollution in these areas. Research in these settings may also yield far-reaching scientific benefits by allowing the effects of air pollution to be understood in a context more representative of the world’s climate and health. 2.2 Sulfur dioxide (SO 2 ) Sulfur dioxide (SO 2 ), which is commonly from combustion of fuel containing sulfur-mostly coal and oil, metal selting, and other industrial process, is a highly water soluble irritant gas and is rapidly taken up in the nasal passages during normal, quiet breathing. Studies in human volunteers found that, after inhalation at rest of an average of 16 ppm SO 2 , less than 1% of the gas could be detected at the oropharynx (Speizer and Frank 1966). Penetration to the lungs is greater during mouth breathing than nose breathing, and also is greater with increased ventilation such as during exercise (Costa and Amdur 1996). Since individuals with allergic rhinitis and asthma often experience nasal congestion, mouth breathing is practiced at a greater frequency in these individuals perhaps making them more vulnerable to the effects of water soluble gasses such as SO 2 (Ung et al. 1990). Despite the potential for high-level SO 2 exposures to cause adverse health effects is well recognized, epidemiologic studies of children have not demonstrated convincing evidence that ambient SO 2 exposure at typical current levels are associated with asthma outcomes, even the results from the same nationality’s children were also inconsistent. Four Chinese Cities study performed in 1997 did not present any associations between outdoor SO 2 exposure and asthma or asthma related symptoms (Zhang et al. 2002); also, Zhao et al. authors reported that indoor SO 2 , but not outdoor SO 2 , was a risk factor for wheeze, daytime breathlessness in Chinese children (Zhao et al. 2008). However, the results from the Northeast Chinese Children Health study present some evidence that ambient levels of SO 2 were positively associated with children’s asthma outcomes (Dong et al. 2011). Multi-pollutant regression analyses indicated that SO 2 risk estimates for asthma outcomes were not sensitive to the inclusion of co-pollutants, including PM, NO 2 , O 3 and CO, and concluded that the observed health associations for SO 2 might be attributed partly to co-pollutants, with a focus on PM and NO 2 as these pollutants tend to be moderately to highly correlated with SO 2 and have known respiratory health effects (U.S. EPA 2008). Although the studies show that co-pollutant adjustment had varying degrees of influence on the SO 2 effect estimates, among the studies with tighter confidence intervals (an indicator of study power), the effect of SO 2 on respiratory health outcomes appears to be generally robust and independent of the effects of ambient particles or other gaseous co-pollutants. In spite of all the research investigating the relationship between SO 2 exposure and responses in individuals with asthma, the mechanism of the SO 2 response is still not very clear. SO 2 may act as an aspecific bronchoconstrictor agent, similar to inhaled histamine or methacholine: the rapid onset of bronchoconstriction after exposure suggests a neural
Air Pollution and Health Effects in Children 341 mechanism of action for SO 2 in asthma, but airway inflammation may result from shortterm SO 2 exposure (U.S. 1998). Results from the animal studies indicated that SO 2 -induced bronchoconstriction was mediated by the activation of a muscarinic (cholinergic) reflex via the vagus nerves (part of the parasympathelic branch of the autonomic nervous system (Nadel et al. 1965); However, there is some evidence from studies of human asthmatics for the existence of both muscarinic and nonmuscarinic components (Sheppard 1988), with the nonmuscarinic component possibly involving an effect of sulfur dioxide on airway mast cells. Also, injection of atropine, which counteracts the effects of the parasympathetic nervous system, prevented the increase in airway resistance and increased airway conductance in healthy subjects exposed to SO 2 but had no effect on asthmatics (Nadel et al. 1965; Snashall and Baldwin 1982). In conclusion, sulfur dioxide-induced bronchoconstriction and respiratory inhibition appear to be mediated through vagal reflexes by both cholinergic and non-cholinergic mechanisms. Non-cholinergic components include but are not limited to tachykinins, leukotrienes, and prostaglandins. The extent to which cholinergic or noncholinergic mechanisms contribute to sulfur dioxide-induced effects is not known and may vary between asthmatic and healthy individuals and between animal species (U.S. 1998). So, the mechanism of why SO 2 elicits such a dramatic effect on the bronchial airways of subjects with asthma is still needed further study. 2.3 Nitrogen oxides (NOx) Nitrogen oxides (NOx), a mixture of nitric oxide (NO) and nitrogen dioxide (NO 2 ), are produced from natural sources, motor vehicles and other fuel combustion processes. NO is colourless and odourless and is oxidised in the atmosphere to form NO 2 which is an odourous, brown, acidic, highly-corrosive gas. NO 2 are critical components of photochemical smog and produces the yellowish-brown colour of the smog. In urban areas, most of NO 2 in the ambient air arises from oxidization of emitted NOx from combustion mainly from motor engines, and it is considered to be a good marker of traffic-related air pollution. Many epidemiological studies have reported associations between NOx, NO, NO 2 and asthma outcomes. Nordling et al. (2008) prospectively followed children in Stockholm, Sweden, from birth until 4 years of age and found that exposure to traffic-related air pollution during the first year of life was associated with an excess risk of persistent wheezing of 1.60 (95% confidence interval, 1.09–2.36) for a 44-µg/m3 increase in traffic NOx. Brauer et al. used LUR models to estimate the effect of traffic-derived pollutants on asthma incidence among 4-year-old children in the Netherlands and found odds ratios (ORs) of 1.20 per 10-µg/m 3 increase in NO 2 (Brauer et al. 2007). Also, a population-based nested case– control study in southwestern British Columbia indicated, comparing with the industrialrelated pollutants (PM 10 , SO 2 , black carbon), traffic-related pollutants were associated with the highest risks for asthma diagnosis: adjusted OR=1.08 (95%CI, 1.04-1.12) for a 10-µg/m3 increase of NO, and 1.12 (95%CI, 1.07-1.17) for a 10-µg/m 3 increase in NO 2 (Clark et al. 2010). However, epidemiological evidence about these associations is still inconsistent. Four Chinese Cities study did not find any associations between NOx and asthma outcomes (Zhang et al. 2002); No statistically significant NO 2 effect on asthma exacerbation was provided in the study from Greece (Samoli et al. 2011). This inconsistence may be partly due to methodological problems, confounding or effect modification by other pollutants, and a lack of prospective data. To some extent, this inconsistency in epidemiological studies also relates to the differences between the groups of people who have been studied. Despite
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AIR POLLUTION - MONITORING, MODELLI
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Contents Preface IX Chapter 1 Urban
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Preface This book provides a compre
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AIR POLLUTION – MONITORING MODELLING AND HEALTH

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