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|Year : 2005 | Volume
| Issue : 28 | Page : 41--50
Confounding or aggravating factors in noise-induced health effects : Air pollutants and other stressors
D Schwela1, S Kephalopoulos1, D Prasher2,
1 Commission of the European Communities, Joint Research Centre, Institute for Health and Consumer Protection, 21020- Ispra(VA), Italy
2 University College London, 330 Gray's Inn Road, London, WC1X 8EE, United Kingdom
Commission of the European Communities, Joint Research Centre, Institute for Health and Consumer Protection, 21020- Ispra(VA)
Different scientific groups have studied and continue to study the health impacts of physical and chemical agents in the environment. In most cases, every study group has considered the health effect as being solely due to the air pollutant(s) under investigation, for example air pollution without due regard for the simultaneous presence of noise pollution whereas both have an impact on the cardiovascular system. Or in the case of noise studies the contribution of solvent, asphyxiant or metal exposures has not been considered, which can have an impact on hearing impairment. One can, therefore, question the stringency of the available evidence of epidemiological studies in both fields to warrant the consideration of air pollutants as confounding or aggravating factors in studies of specific effects due to noise (and vice versa). In this paper we weigh the existing evidence on the association of noise and air pollutant exposure and associated health impacts. In forthcoming publications, the authors will consider the influence of other factors, which can confound noise studies but are currently not included in the analysis.
|How to cite this article:|
Schwela D, Kephalopoulos S, Prasher D. Confounding or aggravating factors in noise-induced health effects : Air pollutants and other stressors.Noise Health 2005;7:41-50
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Schwela D, Kephalopoulos S, Prasher D. Confounding or aggravating factors in noise-induced health effects : Air pollutants and other stressors. Noise Health [serial online] 2005 [cited 2021 Jan 17 ];7:41-50
Available from: https://www.noiseandhealth.org/text.asp?2005/7/28/41/31630
There is a lack of interaction between the scientific community dealing with health impacts due to exposure to noise and that dealing with air pollution. This lack means that the health impact of the combined exposures is usually ignored in epidemiological studies in both fields. Combined exposures occur, for example, when people are exposed to road traffic where noise and air pollution co-exist. In this paper we weigh the existing evidence on the association of noise exposure and air pollution on cardiovascular health.
Health effects of exposure to noise include
hearing impairment,speech interference,sleep disturbance,cardiovascular and other physiological effects,psychological effects including those on performance and memory,effects on residential behaviour, andannoyance.
Health effects from exposure of people to the "classical" air pollutants sulphur dioxide, nitrogen dioxide, ozone, carbon monoxide, and suspended particulate matter include
respiratory and cardiovascular morbidity and mortalitychanges in lung function parametersexacerbation of respiratory and cardiovascular symptoms,effects on development,effects on the central nervous system, andodour annoyance.
With respect to cardiovascular effects, noise and air pollution may affect the same health endpoint. Annoyance may also be an effect, which may be influenced by noise concurrent with annoying odors. Agents that can influence the cardiovascular system besides noise include particulate matter, carbon monoxide and sulphur dioxide.
Particularly in the occupational environment, research on the effects that simultaneous exposure to noise and chemicals might have on the auditory system has increased significantly since the 1980s (Barregard and Axelsson, 1984; Bergstrom and Nystrom, 1986; Johnson et al., 1988; Morata, 1989; Lataye et al., 1997, 2000; Teixeira et al., 2002; Morioka et al., 2000; Sliwinska-Kowalska et al., 2001; Morata, 2002). Ototoxic chemicals, however, do also occur in the indoor environment of people's homes. A range of products including adhesives, biocides, glues, grease and spot removers, insulation, lacquers, liquid correction fluids, paint and paint thinners, resins, room deodorizers, rug cleaners, spray paint, varnishes and wood preservatives release ototoxic chemicals. The intrusion of vehicle emissions from garages and streets with heavy traffic may also contribute ototoxic chemicals. Ototoxic organic solvents include benzene, benzyl alcohol, butyl alcohol, carbon disulphide, carbon tetrachloride, heptane, hexane, styrene, toluene, trichloroethylene and xylenes. Ototoxic heavy metals include arsenic, cobalt, lead, manganese, mercury and organic tin compounds. According to the above studies chemicals that can be considered as ototoxicants were divided into priority lists. The placement of a chemical in the high priority list category took into consideration available evidence of ototoxicity, severity of the problem, accessibility and number of occupationally exposed workers. High priority ototoxics include toluene, xylenes, styrene, n-hexane, mixtures containing the above, trichloroethylene, lead and derivatives, carbon monoxide, cyanide. Additional ototoxics include mercury and derivatives, stoddard solvent, arsenic, carbon disulfide, benzene and manganese. These results were obtained in occupational environments. It is an open question whether other environmental concentrations of these chemicals can also lead to ototoxic health impacts.
In a recent study, Ising et al. (2003) observed that the pathogenesis of allergies may be stimulated by adjuvant effects - i.e. air pollutants such as particulate matter from diesel exhaust and NO 2 as well as noise - especially during night-time. They investigated the combined effects of chronic exposure to traffic related air pollution and noise, on the risk of skin and respiratory diseases in children. The pediatricians' diagnoses of 400 children together with their parents' answers were analysed with regard to the density of road traffic on their street and several confounding factors. Multiple regression analyses resulted in relative risks of asthma, chronic bronchitis and neuro-dermatitis, which increased significantly with increasing traffic load. A comparison with the literature on such effects caused by air pollution as the only stressor, showed that traffic noise during the night might have an adjuvant effect on the pathogenesis of the mentioned diseases.
In this paper we discuss the evidence of noise air-pollution interaction and corresponding adverse health impacts.
Evidence on air pollution as a risk factor for cardiovascular diseases
Suspended particulate matter, carbon monoxide and sulphur dioxide are important air pollutants with respect to the development or exacerbation of cardiovascular diseases. Studies on short-term exposure to elevated concentrations of fine particulate matter are associated with acute changes in cardio-pulmonary health. Epidemiological studies on mortality rates and life expectancy have shown strong associations to long-term exposure to fine particulate matter and sulphate.
Time-series studies in Athens and two French cities indicate that sulphur dioxide (SO 2 ) exposure has independent acute adverse health effects on mortality for males and females in the age group of 65 years and over (Hatzakis et al., 1986; Deriennic et al., 1989). A study (Kamat and Doshi, 1987) in Mumbai also showed effects of SO 2 on mortality due to cardio-respiratory diseases but the data were insufficient to isolate the separate or combined effects of SO 2 and suspended particulate matter (SPM). In a Chinese study in Beijing, a highly significant association was found between air levels of SO 2 and daily number of deaths due to corpulmonale (Gao, 1993).
Several studies (Touloumi et al., 1994; Xu et al., 1994; Spix and Wichmann, 1996; Sunyer et al., 1996; Zmirou et al., 1996; 1998) have shown a significant increase in cardiovascular mortality with increase in sulphur dioxide. However, multi-pollutant models were not applied in all studies. Other studies, however, could not establish a significant increase in total mortality with increase in SO 2 in the presence of other pollutants, except under special seasonal conditions (Schwartz and Dockery, 1992; Spix et al., 1993; Dab et al., 1996; Anderson et al., 1996). More recently, Mar et al. (2000) evaluated the association between mortality outcome in elderly individuals and particulate matter of varying aerodynamic diameters and gaseous pollutants in Phoenix, Arizona. Cardiovascular mortality was significantly associated with Sulphur dioxide (SO 2) , Nitrogen dioxide (NO 2) , Carbon monoxide (CO), Particulate Matter of varying sizes(PM2.5), (PM10,) (PM10-2.5), and elemental carbon. By factor analysis it was shown that cardiovascular mortality was associated with both combustion related pollution and sulphate.
Cardiovascular responses to exercise under low-level carbon monoxide (CO) exposures of healthy subjects and of patients with ischaemic heart disease have been investigated and reviewed in several studies (Maynard and Waller, 1999; Bascom et al., 1996; Romieu, 1999; WHO, 1999). Post-exposure carbon monoxide haemoglobin (COHb) levels of 2.95.9% have been associated with a significant shortening in the time to onset of angina, with increased electro-cardiographic changes and with impaired left ventricular function during exercise (Bascom et al. 1996). In addition, ventricular arrhythmias may be increased significantly at a mean post-exercise COHb level of 5 percent (Sheps et al. 1990). Epidemiological and clinical data indicate that CO from smoking and environmental or occupational exposures may contribute to cardiovascular mortality and to the early course of myocardial infarction (WHO, 1999).
A number of studies have investigated the association between CO exposure and daily mortality and hospital admissions due to cardiovascular diseases. An early study (Hexter and Goldsmith, 1971) found a positive significant association between CO and mortality in Los Angeles. More recent studies in this city established an association between daily mortality and CO, total hydrocarbons, and particulate matter (Shumway et al., 1988) and CO, NO 2 , and particulate matter (Kinney and Ozkaynak, 1991). These studies, however, noted the strong correlation between the three respective pollutants and could not separate their individual influence. No relationship was found between CO and daily mortality due to cardiovascular diseases in Los Angeles, or Chicago, after adjustment for PM 10 in later studies (Ito et al., 1995; Kinney et al. 1995; Ito and Thurston, 1996). No relationship between CO and daily mortality, with or without adjustment for other pollutants, was found in other cities (Saldiva et al., 1994; 1995; Verhoeff et al., 1996; Kelsall et al., 1997). Other studies established a small association between CO exposure and daily mortality for all causes (Touloumi et al., 1994; 1996; Salinas and Vegas, 1995; Wietlisbach et al., 1996; Burnett et al., 1998a;b). Other pollutants and environmental variables, however, were also significant. Schwartz (1996) raised the question of whether the demonstrated association was causal and asked whether CO might be acting as a proxy for particulate matter.
Studies in the USA (Morris et al., 1995; Schwartz, 1995; Morris and Naumova, 1998), Canada (Burnett et al., 1997) and Greece (Pantazopoulou et al., 1995) show an association between ambient CO and mortality and hospital admissions due to cardiovascular diseases. This association persists even at very low CO levels indicating no threshold for the onset of these effects. A strong association between cardiovascular mortality and CO was also found by Mar et al. (2000).
More recently Tarkiainen et al. (2003) investigated the association between acute CO exposure and cardiac autonomic function as measured by heart rate variability in subjects with stable coronary artery disease. Acute CO exposure which most likely represented exposure derived from traffic seemed to modify cardiac autonomic control in patients with stable coronary artery disease.
Suspended particulate matter
An extensive body of experimental and epidemiological literature demonstrates significant associations between concentration of suspended particulate matter (SPM) and the rates of mortality and morbidity in the human population (Bascom et al., 1996; Wilson and Spengler 1996; WHO 1996; Romieu, 1999; Ghio and Samet, 1999; Cohen and Nikula, 1999; Schwela, 2000; Pope and Dockery, 1999; Pope 2000a;b). Current time-series epidemiological studies do not indicate a threshold below which no effects occur. Recent daily time-series mortality studies have observed associations between changes in daily death counts and fluctuations in suspended particulate matter (Pope, 2000a;b). Increased mortality occurred concurrently or within a time lag of 1-5 days after increase of suspended particulate matter concentrations. Studies that provided a breakdown of mortality by respiratory, cardiovascular and other diseases observed a high percentage of excess death attributable to exposure to particulate matter. Studies in the 1990s suggest that even at low levels of SPM (less than 100 µg/m 3 ), short-term exposure is associated with daily mortality and daily hospital admissions related to cardiovascular diseases (Burnett et al., 1995; 1999; Poloniecki et al. 1997; Schwartz, 1997; 1999; Schwartz and Morris, 1995). This is also supported by the findings of Mar et al. (2000).
Goldberg et al. (2001) undertook a study to determine whether variations in concentrations of particulates in the ambient air of Montreal, Quebec, during the period 1984 to 1993, were associated with daily variations in cause-specific daily mortality. They estimated associations between cause-specific mortality and fine particulate matter (PM2.5, PM 10) , predicted fine particles and fine sulphate particles, total suspended particles and total sulphate. Associations with sulphate mass were found among elderly persons who died of cardiovascular diseases. They stated that the associations found for cardiovascular diseases, especially in the elderly, are in line with some of the current hypotheses regarding mechanisms by which ambient particles may increase daily mortality.
It is thus well established that exposure to air pollution, especially fine particulate matter and carbon monoxide is a risk factor for cardiovascular morbidity and mortality (Pope 2000a;b; Maynard and Waller 1999; WHO, 1999; 2000b; Maynard, 2004).
Noise as a risk factor for cardiovascular diseases
In 1980, WHO noted that vasoconstriction and significantly increased levels of blood pressure or vasodilatation of blood vessels have been reported in persons exposed acutely to high levels of noise (WHO 1980). However, the associations were weak and their medical significance unclear. More recently, expert groups in WHO's normative work on guidelines for environmental noise reviewed the overall evidence for associations between noise exposure and cardiovascular morbidity (WHO, 2000a; Berglund and Lindvall, 1995). According to these publications noise may have a large temporary and permanent impact on physiological functions in man and may act as an environmental stressor.
Epidemiological studies involve general populations (including children) living in noisy areas around airports, industries and on noisy streets. Such studies more often also investigate the exposure of workers to higher levels of noise in the occupational environment. Short-term exposures to high noise levels activate the autonomic and hormonal systems leading to temporary changes such as increases in blood pressure and heart rate and vasoconstriction. After prolonged exposure, susceptible individuals in the general population may develop permanent effects, such as hypertension and ischemic heart disease associated with exposures to high sound pressure levels (WHO, 2000a; Berglund and Lindvall, 1995). Individual characteristics, lifestyle behaviour and environmental conditions determine in part also the magnitude and duration of effects. Other authors also noted that besides annoyance, sleep disturbance and decreased school performance, evidence exists that living in noisy areas may present a risk for the onset of cardiovascular diseases, predominantly arterial hypertension and ischemic heart disease (e.g., Stansfeld, 2000]).
Laboratory experiments and field quasi experiments show that if noise exposure is temporary, the physiological system usually returns, after the exposure terminates, to a normal or pre-exposure state within a time in the range of the exposure duration. If the exposure is sufficiently intense and unpredictable, cardiovascular and hormonal responses may appear, including increases in heart rate and peripheral vascular resistance, changes in blood pressure, blood viscosity, blood lipids, and shifts in electrolytes (Mg/Ca) and hormonal levels (epinephrine, norepinephrine, cortisol). The great interest in the first four outcomes comes from an interest in noise-related coronary heart disease (Ising and Giinter, 1997).
A number of occupational and community noise studies have considered noise as a risk factor for cardiovascular disease. Many of the studies in occupational settings have indicated that workers exposed to high levels of industrial noise during 5 to 30 years have increased blood pressure and statistically significant increase in risk for hypertension compared to workers in control areas (Passchier-Vermeer, 1993). Only a few studies on environmental noise have shown increased risk for hypertension in populations living in noisy areas around airports and on noisy streets. The overall evidence suggests a weak association between long-term environmental noise exposure and hypertension (Berglund and Lindvall, 1995; HCN, 1994; IEH, 1997). Although a weak association was found, no dose-response relationships could be established.
For ischemic heart disease, Babisch (1998a;b) has presented an updated summary of available studies. The studies reviewed include case control and cross-sectional designs as well as three longitudinal studies. It was not yet possible to conduct the most advanced quantitative integrated analysis of the available studies. The calculated relative risks and accompanying confidence intervals presented relate to classes of high noise levels (mostly >65 dBA during daytime) versus low levels (mostly <55 dBA during daytime) rather than a range of exposure levels. Due to methodological factors identified in the meta-analysis, a cautious interpretation of the results is warranted (Lercher et al., 1998). Prospective studies that controlled for confounding factors suggest an increase in ischemic heart disease at noise levels of LAeq(612h) above 65-70 dB when orientation of the bedroom, window opening habits and years of exposure are taken into account, the risk of heart disease is slightly higher (Babisch et al., 1998a). Moderation and mediation through disposition and behavioural or environmental factors have not been sufficiently accounted for in the analyses carried out to date. On average in epidemiological studies, the lowest level at which an effect from exposure to traffic noise on ischemic heart disease has been observed is 70 dB LAeq,24h (HCN, 1994 ).
Based on risk estimates for noise-induced myocardial infarction, Neus and Boikat (2000) note that the magnitude of lifetime risk for this health endpoint amounts to between 2000 and 7000 in 100000 persons for equivalent daytime noise levels above 65 dBA and 75 dBA, respectively. These risks are considerably higher than most cancer risks related to air pollutants and almost of the magnitude of the cancer risk of benzo[a]pyrene (about 9000 in 100000) (WHO, 2000b).
In another study (Belojevic et al, 2002) investigated the prevalence of arterial hypertension and myocardial infarction with regard to subjective ratings of traffic noise exposure to ascertain whether there were gender differences in this relationship. This cross sectional interview study showed that highly noise-disturbed adult male residents in a city in Yugoslavia were under increased risk of arterial hypertension and myocardial infarction, compared to subjects slightly annoyed, or not annoyed by noise. Among female residents this relation was not statistically significant.
A recent meta-analysis (Babisch, 2000) revealed that with the exception of a few studies, the results of the environmental noise studies are not statistically significant. One reason for this is a lack of statistical power, but also misclassification of individual exposure may play a role, diluting the true effect if any. The magnitude of the estimates of effect tends to be small, which make the results susceptible to unknown and residual confounding. The available literature provides no epidemiological evidence of a relationship between noise exposure and mean blood pressure in adults. However, noise-related higher blood pressure values have repeatedly been observed in children. As far as hypertension is concerned as the adverse health impact, there is little epidemiological evidence for an association between increased risk and high traffic noise levels. For ischemic heart disease there is some epidemiological evidence of an increased risk in subjects who live in noisy areas with outdoor noise levels higher than 65-70 dBA.
More recently, van Kempen et al. (2002) conducted a meta-analysis of 43 epidemiological studies published between 1970 and 1990 that investigated the relation between noise exposure (both occupational and community) and blood pressure and/or ischemic heart disease. Although it was concluded that noise exposure can contribute to the prevalence of cardiovascular disease, the evidence for a relationship between noise exposure and ischaemic heart disease was found to be still inconclusive because of the limitations in exposure characterization adjustment for important confounders, and bias in the publication of positive findings.
The overall conclusion is that cardiovascular effects have been associated with long term exposure (air and road traffic) to LAeq,24h values in the range of 65 to 70 dB or more. The associations are weak; the effect is somewhat stronger for ischaemic heart disease than for hypertension. Potentially, such small risks are important because a large number of persons are currently exposed to these noise levels or likely to be exposed in the future.
Air pollution as a confounding variable in noise studies
For noise, in epidemiological studies weak associations have been observed between cardiovascular effects and long-term exposure to noise (aircraft and road traffic) with LAeq,24h values of 65-70 dB. The association is somewhat stronger for ischaemic heart disease than for hypertension. Such small risks are important, however, because a large number of persons are currently exposed to these noise levels, or are likely to be exposed in the future. Noise levels are permanently increasing in urban areas with the increase in road traffic and aircraft traffic. Most noise studies did not consider the concomitant effect of air pollution on the cardiovascular system.
Exposure to suspended particulate matter, carbon monoxide, and sulphur dioxide can affect cardiovascular morbidity and mortality. These results have been shown, in some instances, to persist in multi-pollutant models. Epidemiological and clinical data indicate that carbon monoxide from smoking and environmental or occupational exposures may contribute to cardiovascular disease and mortality and to the early course of myocardial infarction. No specific consideration has been given in these studies to the simultaneous presence of noise and air pollution. Future studies clearly need to consider not only the impact of specific pollutants but also consider the combined effects of noise and air pollution, which in the case of road traffic, necessarily occur simultaneously. Noise epidemiological studies need to consider other pollutants as confounding if not aggravating factors.
While it is not known with certainty that noise increases cardiovascular morbidity, the increasing levels of noise may finally lead to such health impacts. In contrast, air pollution of certain compounds is well established to influence cardiovascular diseases. As both air pollution and noise exposure occur in urban areas, investigations on impacts of noise on cardiovascular health should consider air pollution exposure as a potential confounding variable. This is particularly important since associations between noise and cardiovascular diseases are weak while associations between air pollutants and cardiovascular morbidity and mortality are much better established.
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