交通噪音外文翻譯

1、<p><b>　　附錄</b></p><p><b>　　英文文獻(xiàn)原文</b></p><p>　　Traffic noise causes a lot of concern in the population. It annoys, disturbs sleep andcan cause cardiovascular proble

2、ms in chronically noise-exposed subjects.Approximately 50 million people in the European community are exposed to soundlevels from road traffic at home, that are suspected of increasing the risk ofcardiovascular disorder

3、s. The noise effects hypothesis is based on the general stressmodel. The mechanism includes arousal of the sympathetic and endocrine system.Heart rate, blood press</p><p>　　ischaemic heart disease (IHD) are

4、affected by the noise. In epidemiological studies,subjects who live in noise exposed areas show a higher prevalence of high bloodpressure and IHD (including myocardial infarction). It is estimated thatapproximately 3 per

5、 cent of IHD cases in the general population may be attributed totraffic noise.</p><p>　　1. Introduction</p><p>　　It is common experience that noise is unpleasant and affects the quality of life

6、. Itdisturbs and interferes with activities of the individual including concentration,communication, relaxation and sleep (WHO, 2000a and 2000b; Schwela, 2000).Besides the psychosocial effects of community noise, there i

7、s concern about theimpact of noise on public health, particularly regarding cardiovascular outcomes(Suter, 1992; Passchier-Vermeer and Passchier, 2000; Stansfeld et al., 2000a).Nonauditoryhealth effec</p><p>

8、;　　1.1. Traffic noise level</p><p>　　The A-weighted long-term average sound pressure level is used to describe the noiseexposure at the facades of the people’s homes (LAeq). A distinction is often madebetwee

9、n the exposure during the day (6-22 hr) and the night (22-6 hr). To assess anoverall indicator of the noise exposure, a weighted average was usually calculated(Ldn), giving a 10 dB(A) penalty to the night period. The new

10、 directive of theEuropean Union on the assessment and management of environmental noiseconsiders a weighted lo</p><p>　　65 dB(A) during the day and 55 dB(A) during the night. For such noise levels</p>

11、<p>　　considerable annoyance occurs (WHO European Centre for Environment and</p><p>　　Health, 1995), and the cardiovascular risk tends to increase (Babisch, 2002). Only afew European countries have ass

12、essed the noise exposure completely. In EuropeanUnion countries approximately 13 per cent of the population are exposed to suchlevels at the facades of their houses due to road traffic (EEA, 1999). For the wholeof Europe

13、 the estimate is approximately 20 per cent (Schwela）</p><p>　　1.2. Noise annoyance</p><p>　　Figure 1 shows the relationships between the noise level (outdoors) and thepercentage of ‘highly’ anno

14、yed people due to road, air and rail traffic. The doseresponsecurves are taken from Miedema and Vos (1998). They are derived frommeta-analyses considering a large number of social surveys that were carried out over the r

15、ecent decades in different countries. For the same noise level, aircraft noise is more annoying than road traffic noise and railway noise. However, there are limitations regardin</p><p>　　environmental and c

16、ultural settings (Ouis, 2002; Diaz et al., 2001; Finegold and Finegold, 2003). Therefore it was suggested by a WHO working group on noise and health indicators that countries should assess their individual dose-response

17、curves(WHO, 2003).From the results of nationwide representative surveys carried out regularly in Germany, it is known that road traffic noise is the predominant source of annoyance</p><p>　　for the populatio

18、n. Table 2 gives the results of the year 2000 (Ortscheid and Wende,2002). Eighteen percent of the population are ‘highly’ annoyed by road traffic noise(categories ‘extremely’ and ‘very’ on a five-point scale). Annoyance

19、due to noise from neighbours (6.5 percent) and air traffic (5.7 percent) follow next in the ranking.</p><p>　　2. Noise and stress</p><p>　　The auditory system is continuously analysing acoustic

20、information, which is filtered and interpreted by different cortical and sub-cortical brain structures. The limbic system, including the hippocampus and the amygdala, plays an important role in the emotional processing p

21、athways (Spreng, 2000). It has a close connection to the hypothalamus that controls the autonomic nervous system and the hormonal balance of the body. In laboratory studies, changes in blood flow, blood pressure and hear

22、t rat</p><p>　　the catecholamines adrenaline and noradrenaline, and the corticosteroid cortisol (Babisch, 2003; Berglund and Lindvall, 1995; Maschke et al., 2000). Such changes also occur during sleep withou

23、t involvement of cortical structures due to the capacity of the amygdala to learn (plasticity), particularly with respect to adverse sound stimuli (Spreng, 2000 and 2004). Noise is an unspecific stressor that arouses the

24、 autonomous nervous system and the endocrine system. The generalised psycho-physiologica</p><p>　　prepare the organism to cope with a demanding stressor. Any arousal of the sympathetic and endocrine system i

25、s associated with changes in physiological functions and the metabolism of the organism, including blood pressure, cardiac output, blood lipids (cholesterol, triglycerides, free fatty acids, phosphatides) and carbohydrat

26、es (glucose), electrolytes (magnesium, calcium), blood clotting factors</p><p>　　(thrombocyte aggregation, blood viscosity, leukocyte count) and others (Friedman and Rosenman, 1975; Lundberg, 1999; Cohen et

27、al., 1995). In the long term functional changes and dysregulation due to changes of physiological set points may occur, thus increasing the risk of manifest diseases. Since many of the above factors are known to be class

28、ical cardiovascular risk factors, the hypothesis has emerged that chronic noise exposure increases the risk of hypertension, arteriosclerosis and</p><p>　　ischaemic heart disease (Suter, 1992). Figure 2 show

29、s the reaction schema used in epidemiological noise research for hypothesis testing (Babisch, 2002). It simplifies the cause-effect chain i.e.: sound - annoyance (noise) - physiological arousal (stress indicators) - (bio

30、logical) risk</p><p>　　factors - disease - and mortality (the latter is not explicitly considered in the graph). Principally, the effects of environmental noise cannot be extrapolated from results of occupat

31、ional noise studies. The two noise environments cannot be merged into one sound energy-related dose-response model (e. g., a simple 24 hour average noise level measured with a dose-meter). Noise effects do not only depen

32、d on the sound intensity but also on the frequency spectrum, the time pattern of the sound and t</p><p>　　individuals’ activities, which are affected. For example, it may very well be that a truck driver rea

33、cts little to the sound of his engine, but is affected more if disturbed by traffic noise at home or during sleep although the exposure levels are much lower. Therefore, epidemiological studies carried out under real-lif

34、e conditions areneeded to assess the impact of a specific noise source on the health outcomes and provide the basis for a quantitative risk assessment. Other noise sources might a</p><p>　　3. Epidemiological

35、 traffic noise studies</p><p>　　A number of epidemiological studies have been carried out in children and adults regarding changes of mean blood pressure, hypertension and ischaemic heart disease due to long

36、-term exposure to road or aircraft noise. Most of them are cross-sectional. The few observational analytic investigations (case-control and cohort studies) refer to road traffic noise. For reviews see: Babisch (2000); Pa

37、sschier-Vermeer and Passchier (2000); van Kempen et al. (2002). With regard to hypertension, the relative</p><p>　　average sound pressure level in the range of 60-70 dB(A) or more. However, also significantl

38、y negative associations were found. Across all studies no consistent pattern for the relationship between traffic noise level and prevalence of hypertension can be seen. Dose-response relationships, which may support a c

39、ausal interpretation of the findings, were rarely studied. When subjective ratings of noise or disturbances due to traffic noise were considered, the relative risks ranged from</p><p>　　0.8 to 2.3. With rega

40、rd to ischaemic heart disease (IHD), there is not much indication of an increased risk for subjects who live in areas with a daytime average sound pressure level of less than 60 dB(A) across the studies. For higher noise

41、 categories increases in risk were relatively consistently found amongst the studies. However, statistical significance was rarely achieved. Some studies permit reflections on dose-response relationships. These mostly pr

42、ospective studies suggest an increase i</p><p>　　risks between 0.8 and 2.7 were found (Babisch, 2000). Figure 3 sums up the results regarding IHD (Babisch, 2000). The entries are estimates of the relative ri

43、sks with 95%-confidence intervals for the comparisons of</p><p>　　extreme groups of noise exposure as given in the publications. The dark-shaded bars in the diagram refer to studies where the noise exposure

44、was determined objectively (sound levels), the light-shaded bars where it was determined subjectively (annoyance). Road traffic and aircraft noise studies are viewed here together. No corresponding results are available

45、for rail traffic studies. (Note: If different subgroups of the population were taken into account (males/females) or different final health</p><p>　　Babisch, 2000; Berglund and Lindvall, 1995; Health Council

46、 of the Netherlands,1994; Health Council of the Netherlands, 1999). Furthermore, an attempt tosummarise the findings using the approach of the meta-analyses was undertakenvan Kempen et al., 2002). The evidence as conclud

47、ed in the literature wascharacterised as follows: biochemical effects: limited evidence, hypertension:limited evidence, ischaemic heart disease: limited/sufficient (Babisch, 2002). Newstudies are on their way, which may

48、im</p><p>　　the evidence for an association tends to increase, since new studies revealedsignificant relative risks in exposed subjects of 1.6 (aircraft noise) and 1.9 (roadtraffic noise) (Rosenlund et al.,

49、2001; Maschke, 2003). With respect to myocardialinfarction a new large case-control study revealed a relative risk of 1.3 in men highlyexposed to traffic noise (average noise level during day > 65 dB(A)), which was<

50、;/p><p>　　significant in the sub-sample of men who had been living for at least 10 years attheir present address (Babisch et al., 2003; Umweltbundesamt, 2004). In future,noise studies should distinguish explici

51、tly between the noise exposureduring theday and during the night because some study results suggest, that nightly noiseexposure plays a fundamentally stronger role in the emergence of health disorders</p><p>

52、;　　than noise during daytime (Maschke, 2003). Three study examples are given below.</p><p>　　3.1. The ‘Caerphilly & Speedwell heart disease studies’</p><p>　　Two cohorts of 2512 (Caerphilly,

53、 South Wales) and 2348 (Speedwell, England)middle-aged men (45 to 59 years) in the United Kingdom were recruited to study the predictive power of already known and of new risk factors for ischaemic heart disease (IHD). T

54、he subjects were followed-up for approx. ten years to collect new</p><p>　　IHD cases during that period (Babisch et al., 1993; Babisch et al., 1998). The subjects were grouped according to 5-dB(A)-categories

55、 of the outdoor A-weighted average sound pressure level, from 6-22 hr (Lday). Due to the high correlationbetween day and night noise levels in the communities (correlation coefficient r =0.94, mean difference 8 dB(A)), t

56、his noise level was used as an indicator for theoverall traffic noise exposure of the streets in the study. All statistical analyses onthe relations</p><p>　　Figure 4 shows the relative prevalence (prevalenc

57、e odds ratio and 95%-confidenceintervals) of high values of biological risk factors (upper quintiles of thedistributions) for the extreme group comparison of road traffic noise exposure (Lday:>65 to 70 dB(A) versus &g

58、t;50 to 55 dB(A)). Bars ‘shifted to the right’ indicate a higherprevalence in the high exposed group of men. Blood clotting factors and blood lipidfactors were more prevalent in the highest exposed group compared with th

59、e lowest.</p><p>　　However, regarding blood pressure, an opposite association was found. All in all, itwas estimated that the risk for subsequent IHD was slightly higher in the exposed group (Babisch et al.,

60、 1993). Although statistically not significant, the ten-year follow-up investigations revealed that the incidence in IHD was higher in subjectsfrom the high noise exposed group (Babisch et al., 1998). The estimate of the

61、 relative risk increased from 1.1 to 1.6 when effect-modifiers of exposure such asroom orien</p><p>　　This is illustrated in Figure 5.</p><p>　　3.2. The ‘Berlin traffic noise studies’</p>

62、<p>　　In the Berlin case-control studies, interviews were conducted with 645 male patientswith acute myocardial infarction (MI) collected from 17 clinics and 3390 controlstaken from the population registers (Babisc

63、h et al., 1994). The men were aged 41-70years. The traffic noise exposure outdoors at the facades of the homeswas takenfrom noise maps of the city authorities. In the subgroup of men who lived in their</p><p&g

64、t;　　homes for at least fifteen years, the odds ratio (95%-confidence interval) of IHDincidence was 1.3 when the two highest categories of the noise level during the daywere taken together (>70 to 80 dB(A)) as compared

65、 to the lowest noise category(≤60 dB(A)), after adjustment for potentially confounding factors. This is illustrated in Figure 6.</p><p>　　Figure 6. Relative risk of the incidence of ischaemic heart disease i

66、n middle aged mencompared with the road traffic outdoor noise level [‘Berlin Traffic Noise Studies’] (Babisch et al., 1994).</p><p>　　3.3. The ‘Spandau health survey’</p><p>　　In the Spandau hea

67、lth survey, the road traffic noise exposure at the homes of 1718 subjects who took part in a follow-up investigation on the development of clinical health endpoints, was assessed using official noise maps of the area (Ma

68、schke et al., 2003; Maschke 2003). The subjects, males and females, were aged 18 to 90 years. After adjustment for potentially confounding factors, cross-sectional analyses revealed a significantly higher prevalence of h

69、igh blood pressure (hypertension)</p><p>　　with increasing noise level outside the bedroom. This is shown in Figure 7. A significant increase in the risk was noted for the prevalence, if the equivalent conti

70、nuous sound pressure level of the nocturnal street traffic noise exceeded 55 dB(A). The relative risk was 1.9 in comparison with locations where the equivalent continuous sound pressure level was below 50 dB(A). With reg

71、ard to the</p><p>　　4. Risk evaluation process</p><p>　　A conceptual framework for the regulation of environmental hazards was given by the US National Research Council (National Research Counci

72、l, 1983; Neus and Boikat, 2000; Patton, 1993). The process of risk assessment (risk evaluation) comprises hazard identification (‘Which health outcome is relevant?’), exposure assessment (‘How many are affected’) and dos

73、e-response assessment (‘Threshold of effect?’) (Babisch, 2002). This information is summarised in, and is called, ‘risk characterisation’ or ‘</p><p>　　other scientific disciplines, and is subject to the dis

74、cussion of uncertainties including chance, bias and validity of studies as well as transparency, replicability and comprehensiveness of reviews. As a result of the risk evaluation process, a quantitative estimate about t

75、he likelihood that the hazard will affect exposed people will be derived. Usually attributable risk percentages will be calculated (Walter, 1998). This will serve as key information for any kind of risk management includ

76、ing r</p><p>　　5. Conclusion</p><p>　　Nowadays the noise and cardiovascular risk hypothesis is well established. The biological plausibility is based on clinical and experimental research and ha

77、s been established for a long time on the basis of laboratory and animal experiments. For reviews see for example: Borg (1981); Kjellberg (1990); Berglund and Lindvall (1995); Babisch (2003). However, a quantitative risk

78、 assessment requires epidemiological research in this field. Only some studies of the relationship between</p><p>　　road traffic noise and cardiovascular endpoints permit reflections on dose-response relatio

79、nships. The mostly prospective studies regarding ischaemic heart diseases (IHD) suggest an increase in risk for outdoor noise levels above 65-70 dB(A) during the daytime (Lday), the relative risks (RR) ranging from 1.1 t

80、o 1.5. Approximately 13-20 per cent of the European population and 16 per cent of the German population are exposed (Pe) to such road traffic noise levels during the day at the facades of</p><p>　　their home

81、s. Assuming a 20 per cent increase in the IHD risk in these subjects (relative risk of 1.2), 17 per cent of the IHD cases would be attributable to the noise. With regard to the entire population (using the German figure

82、of 16 per cent exposed), the population attributable risk percentage (PAR%) would be approximately 3, meaning that 3 per cent of all IHD cases would be attributable to the traffic noise (PAR% = [Pe * (RR-1)] / [Pe * (RR-

83、1) + 1] * 100) (Hennekens and Buring, 1987). These</p><p><b>　　英文文獻(xiàn)譯文</b></p><p>　　交通噪音造成的人口關(guān)注。它苦惱，擾亂睡眠，可引起慢性噪聲心血管問題。大約有50萬歐洲市民有機(jī)會(huì)接觸社會(huì)的聲音，那增加心血管疾病風(fēng)險(xiǎn)。隔音效果的假設(shè)是基于一般應(yīng)力模型。該機(jī)制包括使交感神經(jīng)和內(nèi)分泌系統(tǒng)

84、興奮。心率，血壓，應(yīng)激激素和古典生物風(fēng)險(xiǎn)因素缺血性心臟?。↖HD）受噪音影響。在流行病學(xué)研究中，在噪聲暴露區(qū)現(xiàn)場表演的人有高發(fā)病率如血壓力和缺血性心臟?。òㄐ募」Ｋ溃?。據(jù)估計(jì)，大約3分之一案例（占總?cè)丝诘陌俜种┛赡苁怯捎诮煌ㄔ胍魧?dǎo)致的。</p><p><b>　　簡介</b></p><p>　　這是共同的經(jīng)驗(yàn)不是愉快的噪音，它影響生活質(zhì)量、擾亂個(gè)人、包括集中

85、活動(dòng)的溝通、放松和睡眠（世界衛(wèi)生組織，2000年和2000年b; Schwela，2000）。除了社區(qū)噪聲的心理影響，有關(guān)注影響公眾健康的噪音，特別是關(guān)于心血管事件（蘇特，1992年; Passchier- Vermeer和Passchier，2000; Stansfeld等人，2000年。）Nonauditory對噪音健康的影響的研究，是用人類如需使用實(shí)驗(yàn)室和幾十年的經(jīng)驗(yàn)方法來進(jìn)行研究的。生物反應(yīng)模型已經(jīng)推導(dǎo)出以總務(wù)應(yīng)力概念為基礎(chǔ)的噪

86、聲的假設(shè)，大型的流行病學(xué)已經(jīng)研究了很久（Babisch，2000）。</p><p>　　1.1。交通噪音水平 加權(quán)長期平均聲壓水平是用來描述噪音暴露在人民的面面。往往都是有區(qū)別的接觸（6-22小時(shí)）和夜間（22-6小時(shí)）。為了評估噪聲暴露的綜合指標(biāo)，通常以加權(quán)平均來計(jì)算，以10分貝（A）為夜間罰款時(shí)期。歐洲聯(lián)盟關(guān)于評估環(huán)境噪音管理的新的指令是考慮加權(quán)長期平均聲壓級（如19-23小時(shí)，罰款5分貝（A））和

87、非加權(quán)夜間噪聲指標(biāo)指令。</p><p>　　在表1住宅噪聲的分布中，由于德國的公路和鐵路交通是給定的（Umweltbundesamt，2001）。根據(jù)模型計(jì)算，約占德國人口的百分之十六的人口是生活在“噪音區(qū)”的（世衛(wèi)組織歐洲區(qū)域辦事處，2000年），道路交通噪音水平在戶外超過65分貝（A）在白天和夜間超過55分貝（甲）。對于這樣的噪音水平相當(dāng)大的地區(qū)（世衛(wèi)組織歐洲中心及環(huán)境生，1995年）和心血管風(fēng)險(xiǎn)水平呈上升

88、趨勢的地區(qū)（Babisch，2002）。在歐洲歐盟國家約百分之十三的人口有機(jī)會(huì)接觸這些地區(qū)。對于整個(gè)歐洲的估計(jì)大約是百分之二十（Schwela，2000）。</p><p>　　1.2。噪音滋擾 表1顯示了室外的噪音水平和百分比的關(guān)系。該曲線取自Miedema和沃斯（1998）的研究。他們分析考慮了大量的社會(huì)調(diào)查，在不同國家進(jìn)行了近十年的研究。對于同樣的噪聲水平，飛機(jī)噪音比道路交通噪聲和鐵路噪聲更煩人。但

89、是，也有關(guān)于限制在不同的曲線普遍適用性環(huán)境和文化環(huán)境。因此有人建議由一位工作組的噪音及衛(wèi)生指標(biāo)，各國應(yīng)評估其個(gè)人劑量反應(yīng)曲線（世界衛(wèi)生組織，2003年）。</p><p>　　從全國代表性的調(diào)查結(jié)果進(jìn)行定期德國，據(jù)了解，道路交通噪音的主要來源的煩惱的人口。表2給出了2000年（Ortscheid與文德的結(jié)果，2002年）。百分之十八的人口是'高'惱火道路交通噪音（類別'非常'和&#

90、39;非常'以5分制）。由于噪音滋擾鄰居（6.5百分比）和空中交通（百分之五點(diǎn)七）按照未來的排名。</p><p>　　2。噪聲和壓力 聽覺系統(tǒng)的不斷聲信息分析，這是不同的過濾和皮層和分皮層的大腦結(jié)構(gòu)解釋。該邊緣系統(tǒng)，包括海馬，杏仁核，在情感（紫莖澤蘭，2000年）處理途徑起著重要的作用。它有一個(gè)緊密連接下丘腦是控制自主神經(jīng)系統(tǒng)和內(nèi)分泌平衡身體。在實(shí)驗(yàn)室研究中，血流量，血壓的變化，心率發(fā)現(xiàn)了壓力荷

91、爾蒙的釋放，同時(shí)增加包括腎上腺素和去甲腎上腺素的兒茶酚胺，皮質(zhì)醇和皮質(zhì)類固醇（Babisch，2003;貝里隆德和Lindvall，1995年;。上的Maschke等，2000）。這種變化也可能發(fā)生在睡眠期間沒有皮質(zhì)結(jié)構(gòu)，參與因杏仁核的學(xué)習(xí)能力（可塑性），特別是關(guān)于不良（紫莖澤蘭，2000年和2004年）的聲音刺激。</p><p>　　噪聲是一種非特異性應(yīng)激能引起自主神經(jīng)系統(tǒng)和內(nèi)分泌系統(tǒng)。廣義的心理和生理概念給

92、予亨利和Stephens可直接應(yīng)用于噪聲引起的應(yīng)激反應(yīng)（亨利和斯蒂芬斯，1977）。應(yīng)力作為該機(jī)制是由基因決定的。這可能是修改經(jīng)驗(yàn)和環(huán)境因素。其生物學(xué)功能是準(zhǔn)備機(jī)體應(yīng)付苛刻的壓力。任何覺醒交感神經(jīng)和內(nèi)分泌系統(tǒng)是與生理變化功能和機(jī)體代謝，包括血壓，心臟輸出，血脂（膽固醇，甘油三酯，游離脂肪酸，磷脂）和碳水化合物（葡萄糖），電解質(zhì)（鎂，鈣），血液凝血因子（血小板聚集，血液粘度，白細(xì)胞計(jì)數(shù)）和其他（弗里德曼和羅森曼，1975;隆貝格，199

93、9;科恩等人。，1995）。從長遠(yuǎn)來看功能失調(diào)的變化，由于生理變化可能設(shè)置點(diǎn)發(fā)生，從而增加了明顯的疾病的風(fēng)險(xiǎn)。由于上述許多因素是已知的心血管風(fēng)險(xiǎn)因素，假設(shè)已經(jīng)出現(xiàn)，長期暴露噪音增加了高血壓，動(dòng)脈硬化的風(fēng)險(xiǎn)，缺血性心臟?。ㄌK特，1992）。</p><p>　　圖2顯示了反應(yīng)，在流行病學(xué)研究中使用的模式噪聲假設(shè)檢驗(yàn)（Babisch，2002）。它簡化了因果鏈，即：聲音-煩惱（噪音） -生理覺醒（壓力指標(biāo)）- （生

94、物）的風(fēng)險(xiǎn)因素 -疾病 -和死亡率（后者是在圖中沒有明確審議）。</p><p>　　該機(jī)制的運(yùn)作'直接'通過突觸和神經(jīng)的相互作用'間接地通過情感和聲音的認(rèn)知觀感。這應(yīng)該指出的是，'直接'通路有關(guān)即使在低噪音等級特別是在睡眠中，當(dāng)機(jī)體在其最低點(diǎn)是覺醒。我們的目標(biāo)噪聲暴露（音量）和主觀噪聲暴露（煩惱）可作為獨(dú)立變量，在暴露的統(tǒng)計(jì)分析噪聲和健康之間關(guān)系的端點(diǎn)。</p>

95、;<p>　　主要是，對環(huán)境噪聲的影響不能被推斷出來的結(jié)果職業(yè)噪音的研究。噪聲環(huán)境中的兩個(gè)無法合并成一個(gè)健全能源相關(guān)的劑量反應(yīng)模型（例如，一個(gè)簡單的平均噪音二十四小時(shí)量度與劑量米）。隔音效果不僅取決于聲音強(qiáng)度還取決于頻譜，聲音的時(shí)間模式和個(gè)人的活動(dòng)，這些活動(dòng)都受到影響。例如，它很可能是一卡車司機(jī)的反應(yīng)不大，他的引擎聲，但影響更多，如果不安受交通噪音在家里或在睡眠雖然暴露水平遠(yuǎn)遠(yuǎn)低。</p><p>

96、　　3。流行病學(xué)研究的交通噪音 流行病學(xué)研究已經(jīng)開展了兒童和成人平均血壓，高血壓，缺血性心臟疾病方面的變化由于長期暴露在公路或飛機(jī)的噪音。他們大多是橫截面。為數(shù)不多的觀測（病例對照研究和隊(duì)列研究）分析調(diào)查指道路交通噪音。有關(guān)評論見：Babisch（2000）; Passchier- Vermeer和Passchier（2000）;車肯朋等人（2002年）。</p><p>　　對于高血壓，風(fēng)險(xiǎn)相對發(fā)現(xiàn)在四

97、個(gè)顯著的正研究中，介于1.5和3.3科目誰住在同一個(gè)地區(qū)的白天平均在60-70分貝（A）以上范圍內(nèi)的聲壓級。不過，也顯著的負(fù)關(guān)聯(lián)被發(fā)現(xiàn)。在所有的研究并沒有一致的模式之間的交通噪音水平和患病率的關(guān)系高血壓可以看到。劑量反應(yīng)關(guān)系，這可能支持的因果調(diào)查結(jié)果的解釋，很少研究。當(dāng)噪聲的主觀評價(jià)或因交通噪音干擾進(jìn)行了審議，風(fēng)險(xiǎn)相對介于0.8到2.3。</p><p>　　關(guān)于缺血性心臟病（IHD），沒有太多的跡象風(fēng)險(xiǎn)增加科

98、目誰一起生活的地區(qū)白天平均聲壓水平小于60分貝之間的研究（一）。對于更高的噪音類別增加在風(fēng)險(xiǎn)相對一致的研究發(fā)現(xiàn)之一。然而，統(tǒng)計(jì)意義很少實(shí)現(xiàn)。一些研究允許的劑量反應(yīng)的思考關(guān)系。前瞻性研究表明，這些大多是在風(fēng)險(xiǎn)增加以上65-70分貝（A）室外噪音水平在白天，風(fēng)險(xiǎn)相對從1.1至1.5。噪聲影響較大的因素時(shí)，中介度日如年住宅，開放空間定位和窗口中考慮了習(xí)慣分析。關(guān)于干擾和煩惱的主觀反應(yīng)，相對0.8和2.7之間的風(fēng)險(xiǎn)被發(fā)現(xiàn)（Babisch，200