Traffic related air pollutants: risks to human health - Essay Example

Traffic-Related Air Pollutants: Risks to Human Health Introduction Transport has a major role to play in the lives of most people and also societies, all over the world, including Europe. It increases mobility and influences various aspects of living like interaction between individuals and groups, employment, entertainment, development and basic amenities. Because of these attributes of transport, more and more vehicles have come up in all sectors: transport, road, railways, air and water. However, this has contributed to certain consequences like increased consumption of fuel, noise pollution, road-traffic accidents and injuries, sedentary lifestyle and related health problems, increased emission of air pollutants and increased exposure of people to toxic substances leading to serious health issues (WHO, 2005). Of these, health hazards of toxic air pollutants from traffic are of major concern and they affect population disproportionately, with the elderly people and children being more prone to them. Several public health organizations, including the World Health Organization have become aware of these threats in the wake of rising traffic to accommodate increased mobility and comfort. The organizations have identified health hazards due to traffic related air pollution as a major health challenge which demands emergency understanding and action from various governments, environmental authorities, institutions and organizations (WHO, 2005). According to Kunzli (2002), "the methods to quantify the health impact of air pollution require assumptions and have to deal with inherent uncertainties. Prudent estimates of the impact confirm that even in regions with moderate pollution, compared with “hot spots” like the emerging mega-cities in the Far East, air pollution considerably contributes to morbidity and mortality throughout Europe. Abatement strategies are political in nature, thus, health professionals, such as clinicians, must raise their voices in the political decision process to give strong support for clean air policies, on both a national and an international level." In this research paper, the health hazards of pollutants from traffic will be reviewed through suitable review of literature. Factors that determine emissions As of now, road transport is the main contributor to pollution of air in cities and other places. Catalytic converters which are present in the vehicles are not operational to full force during the the initial distance of travel and when people travel to short distances frequently, more emissions of pollutants happen. Another important factor that determines emission is maintenance of the vehicle. Poorly maintained vehicles lack proper after treatment systems and hence contribute to pollution (WHO, 2005). Several studies over decades have indicated the risks of air pollution on human health, most of it coming from air pollution due to transport. The impact depends on several factors like intensity of emissions from vehicles, type of primary emissions, secondary emissions and patterns of exposure to humans. Pollution contributed by traffic Traffic emits many gaseous pollutants of air and also a wide range of suspended particulate matter of different composition and sizes. Emissions from the tailpipe of the vehicle account for more than 30 percent of fine particulate matter in many urban areas. Particle size less than 2.5µm in diameter are considered to be fine particles. Other sources of particulate matter with reference to traffic include brake linings, wear of tyres and road dust that is resuspended. These emit coarse particulate matter of the range 2.5–10 µm. The main dangerous gaseous emissions include benzene and nitrogen dioxide and these gases are emitted when the manufacture of the vehicle is not in compliance with current European Union (EU) limit values (WHO, 2005). According to Raaschou-Nielsen O et al. (2002), "the average population PM10 exposure to be about 22 micrograms/m3, about one third of which can be attributed to natural (not man-made) PM10." During heavy traffic, street canyons and traffic jams, pollutants are trapped in the air over the region of high traffic and they pollutants are present at much higher levels than other areas. In major urban highways which are prone for heavy traffic, black smoke, nitrogen dioxide and ultrafine particles are present in higher concentrations when compared to other areas. However, other transport related air pollutants remain uniform all over the city. According to WHO (2005), "the concentration in 2010 is expected to be roughly 50% of that in 1995. Also, in 2010, 90% of the urban population in the 15 countries belonging to the EU before 1 May 2004 are expected to live in areas meeting the EU air-quality limit values for nitrogen dioxide (hourly value), carbon monoxide, benzene and lead." Several improvements in technology and implementation of strict standards of emission have infact decreased vehicle related emissions. However, many other factors like increase in vehicles operating diesel, growth of transport, increase in short trips and rampant traffic congestion have offset the advantages of recent technology and emission norms. Other factors which contribute to increased exposure of humans to air pollution include spread of urban area, increased traffic congestion and increase in commuting time (Health Canada, 2010). Emissions from road transport vehicles can be categorized into four components: 1. Hot emissions 2.Cold start emissions 3. Emissions from fuel evaporation 4. Particulate emissions that arise due to wear and tear and abrasion on road. Exposure of humans to air pollutants Human exposure is dependent on several conditions including spatial and volume distribution of the emitted gases and conditions in which dispersion has occurred. Other factors which influence exposure to pollution are number of people in the region of pollution, duration of stay in that area and their job. People who reside or work near roads that are busy, or those who spend more time in traffic are at increased risk of exposure to pollutants. Infact, travelers in busy areas are often exposed to pollution levels that are atleast 3 times the levels in background. Particulate matter and primary exhaust gases are high in in-vehicle exposure. Other groups of people who are subjected to high levels of exposure include those who live in houses that are ventilated from the road that has heavy traffic, users of road like drivers, pedestrians and commuters and those whose employment demands spending long hours on roads. The development and planning of urban areas also influences exposure to traffic pollutants (WHO, 2005). Health effects of traffic-related pollution The health effects of air pollutants related to traffic has been ascertained based on several toxicological, biological and epidemiological studies on humans and animals. However, epidemiological studies have more value because of their relevance to real life. Studies using cell-culture experiments help in the identification of the hazards with reference to their pathogenesis. The impact of the pollutants will be discussed topic iwse below with relevance to research and studies. The US department of transportation (Claggett, 2009) has identified seven mobile-source air toxics or MSATs, namely, acetaldehyde, acrolein, benzene, 1,3-butadiene, formaldehyde, naphthalene and polycyclic organic matter. Acetaldehyde is basically not the principle exposure source. However, it is a significant component of air pollution. the concentrations of this chemical is lowest out door and highest inside the vehicles. It is also present in many foods. Acetaldehyde is an irritant and a confirmed carcinogen in rodents. There is not much evidence to ascertain the role of this toxic compound in carcinogenecity in humans. There is some evidence about implications for respiratory problems. But they are not very strong. Currently, acetaldehyde is not present in concentrations that affect health. However, increase in the use of ethanol as fuel in future may increase its concentrations (Claggett, 2009). Acrolein may not be present in elevated proportion outside and inside vehicles. It is most likely to be formed from 1,3-butadiene. One of the major indoor sources is tobacco smoke in the environment. The compound is very irritating to the respiratory system. However, there is no evidence to incriminate this substance in the development of cancer. there is insufficient data to assess exposure levels that are ambient for human health. As of now, levels in the atmosphere are much lower than those which cause significant irritation of the respiratory system (Claggett, 2009). Benzene is present in highest concentrations at urban road side and locations of urban in-vehicle. Exposures of this toxic compound have been linked to acute myeloid leukemia. However, reports from various studies are mixed in this regard and as of now, there is uncertainity about hematological effects of this compound (Claggett, 2009). 1,3-Butadiene concentrations are higher indoor than outdoor. It is highly reactive and can produce acetaldehyde, acrolein and formaldehyde. There is clear evidence of carcinogenecity in animals following exposure to this pollutant. In human beings, very few studies have associated this compound with lymphohematopoietic cancers (Claggett, 2009). Formaldehyde occurs in highest concentrations on urban road sides. It has photochemical activity. It is basically a known irritant for eyes, respiratory tract and skin. there is some evidence of association of this compound with nasopharyngeal cancer. There is also limited exposure of asthma occurrence in children. In ambient concentrations however, there are no known health effects (Claggett, 2009). Naphthalene is present in higher concentration indoor than outdoor. Though there is evidence of development of nasal and olfactory tumors in rodents following exposure to this compound, there is no such evidence in human beings. However, some studies have reported effects on blood cells. This compound does not have any health effects when present in ambient concentrations (Claggett, 2009). Polycyclic organic matter or POM are derived mainly from diesel vehicles. Components of this matter are animal carcinogens and suspected human carcinogens. there is some evidence of lung cancer in those exposed to occupational injury. But in ambient concentrations, no such association is noted (Claggett, 2009). Mortality Several epidemiological studies use mortality as an indicator of adverse effects of traffic related air pollution. Several studies in the Europe, United States and other parts of the world have associated mortality with air pollution risk. The pollutants incriminated in this effect are ozone and fine particulate matter and the main cause of mortality being cardiopulmonary cause. In a study by Katsouyanni et al (2001) which was a huge project involving 29 European cities, it was found that an increase in daily black smoke by 10-µg/m3, simultaneously increased the number of deaths everyday by 0.6 percent. The study stressed on the fact that more often than not, black sooth polluted air in combination with nitrogen dioxide and the effect of black sooth was much lower than that of nitrogen dioxide. In cities with higher concentrations of the gas, the combined effect was higher. The study inferred that nitrogen dioxide could be used as an indicator of presence of traffic-derived toxic particles in air. In yet another similar study by Samet et al (2000), the popular National Morbidity, Mortality, and Air Pollution Study conducted in the US, no evidence was found to ascertain the role of nitrogen dioxide in modifying the association between particulate matter and daily mortality. Some studies like Le Terte et al (2002), found a strong association between black sooth and mortality. The cause of mortality was attributed to development of cardiovascular and respiratory complications. According to the Netherlands Cohort Study (NLCS) by Brunekreef et al (2009), "estimated overall exposure concentrations of black smoke, NO2, NO, and PM2.5 were associated with mortality. For a 10-microg/m3 increase in the black smoke concentration, the relative risk (RR) (95% confidence interval [CI]) was 1.05 (1.00-1.11) for natural-cause (nonaccidental) mortality, 1.04 (0.95-1.13) for cardiovascular mortality, 1.22 (0.99-1.50) for respiratory mortality, 1.03 (0.88-1.20) for lung cancer mortality, and 1.04 (0.97-1.12) for noncardiopulmonary, non-lung cancer mortality. Results were similar for NO2, NO, and PM2.5. For a 10-microg/m3 increase in PM2.5 concentration, the RR for natural-cause mortality was 1.06 (95% CI, 0.97-1.16)." These reports, according to the authors are similar to those reported by the American Cancer Society. In a study by Sunyer et al (2000), the researchers found a strong association between air levels of black smoke and mortality. Mortality in this study was related to all causes. In another study on the impact of particulate matter on motality of human beings, Scwartz et al (2002) opined that particulate matter of 2.5micrometers had linear association with mortality of people exposed to it. For every 10-µg/m3 increase in this size particulate matter, mortality increased by 3.4 percent. The authors compared the effects of 2.5 particulate matter with those derived from non-combustion and opined that non-combustion particles were associated with lesser mortality and health problems. Some studies have shown the association between distance from road to residence and risk of mortality Hoek et al (2002) conducted a cohort study and opined that residing near major roads increases the risk of death. According to the study, for every 10-µg/m3 increase in black smoke, the risk of death due to cardiopulmonary problem increased by 1.34. There has been immense research indicating the association between occupational exposure of traffic toxic substances and mortality. Stern et al (1988) conducted a retrospective study in which he ascertained the risk of death due to heart disease in tunnel workers exposed to carbon monoxide through occupation. The study revealed that this population had increased risk of atherosclerosis which contributed to their mortality. Kunzli et al (2000), reported that "air pollution caused 6% of total mortality or more than 40,000 attributable cases per year. About half of all mortality caused by air pollution was attributed to motorised traffic, accounting also for: more than 25,000 new cases of chronic bronchitis (adults); more than 290,000 episodes of bronchitis (children); more than 0.5 million asthma attacks; and more than 16 million person-days of restricted activities." Respiratory health effects Traffic pollutants can cause both allergic and non-allergic respiratory problems. In a study by Steerenberg et al. (2001), the researchers conducted a study to ascertain the implications of exposure to black smoke in causing nonallergic respiratory problems. The main outcome measures in this study were markers for inflammation in the nose: interleukins-8, urea, uric acid, nitric oxide metabolites and albumin. The study compared these outcomes in children living in schools located in areas of background black smoke of 53 µg/m3 as against those going to school in low black smoke level regions: less than 18 µg/m3. This study revealed that those exposed to high levels of smoke are at risk of developing non-allergic respiratory problems. Kunzli et al (1997) reported that traffic related air polution increased the risk of bronchitis in children and chronic bronchitis in adults. In another study on school children by Janssen et al (2003), the researchers found that 2.5 particulate matter, nitrogen dioxide and soot were associated with development of non-allergic respiratory symptoms like bronchitis and phlegm. Children whose schools were located near roads where high counts of lorries traveled demonstrated more symptoms as against those who were lcoated away from the roads. This study however did not demonstrate changes in lung function and bronchial hyper-reactivity. According to Forsberg et al (1997), exposure of human beings to sulphur dioxide levels above 1.7µg/m3 leads to respiratory symptoms like phlegm, cough and upper respiratory symptoms. The study reported that exposure to nitrogen dioxide contributed to nose irritation, throat irritation and cough and these symptoms are not caused by black smoke. Some studies have reported bronchitis and morning cough subsequent to exposure to pollutants like carbon monoxide, benzene and nitrogen dioxide (WHO, 2005). Nitrogen dioxide has been strongly linked to cough, but not to bronchitis. A couple of Norwegian studies have reported an association between higher levels of benzene and increased chances of hospital admissions. benzene has also been linked to impaired lung function. There are also some reports of development of bronchial hyperreactivity in children exposed to high levels of carbon monoxide and nitrogen dioxide (WHO, 2005). Some studies have demonstrated epidemiological evidence of respiratory illness like increased bronchitis prevalence in children, increased cough and increased wheeze in children in those exposed to traffic pollution. Even this fact has been disputed by several other studies like Lercher et al (1995). Whatever may be the association, manifestations related to traffic pollution exposure is more predominant in children than in adults. According to Zhou et al (2001), those employed in transport like conductors, bus drivers and taxi drivers were at increased risk of development of acute respiratory symptoms and chronic respiratory health problems. As far as occupational exposure is concerned, studies have shown that street cleaners have increased prevalence of asthma and chronic bronchitis unlike cemetery workers who are not much exposed to pollution. In a study by Yang et al (2002), workers employed in toll booths of highways developed increased symptoms like dry throat, irritation of the eyes, head ache and nasal congestion. There is some evidence that customs officers, who are exposed to high levels of diesel-engine emissions have changes in mucus membranes like dysplastic epithelia, goblet cell hyperplasia and metaplastic epithelia (WHO, 2005). Controlled studies with reference to allergic respiratory manifestation of exposure to traffic pollution indicate that exposure to motor vehicle exhaust even for 2 hours increased neutrophil count and inflammatory mediators like interleukins, fibronectin, prostaglandin and antitrypsin in broncho-alveolar lavage, suggestive of mild airway inflammatory. Lung function tests however, remained normal. According to WHO (2005), "rather substantial evidence points to transport-related air pollution’s increasing the risk of non-allergic respiratory symptoms and suggests that inflammatory processes are related to exposure to such pollution." Allergic respiratory illness There is mounting evidence to ascertain the role of air pollution in the development of asthma. Several epidemiological and experimental studies on animals have supported an intimate relationship between traffic related pollution and IgEmediated sensitization (Koren, 1995). Many studies have demonstrated the association between exposure to traffic pollutants and other allergic respiratory problems too. There is some evidence that exposure to these air pollutants during the first two years of life increases the chances of development of asthma. However, studies like those by Gehring et al (2002) failed to demonstrate any association between air pollution and asthma. The inconsistency in the results is mainly due to lack of definite diagnostic criteria for asthma in children. While most studies have employed wheezing as a sign of astham, wheezing can be just due to reactice airways and not really due to asthma. Some studies have tried to find an association between another allergic problem, Hay fever and traffic pollutants. However, no consistent results were available that could link the two. According to WHO (2005), "with the review restricted to studies that used measured or modelled exposure to indicators of transport-related air pollution and allergic sensitization assessed by antibody measurements or skin-prick testing, the overall results remain inconsistent." Some controlled studies on human beings and experimental studies on mice have provided substantial evidence about the risk of exacerbation of allergy and development of allergy subsequent to exposure to air pollutants related to transport. However, there is not much evidence with regard to study on population and infact, the results are inconsistent. As of now, it has not been possible to identify the main component of traffic related pollution that has the possibility of triggering allergic problems. While some experts attribute to whatever minimal allergic problems present to nitrogen dioxide, some others attribute it to ozone. Impact on lung function There are very few studies which have evaluated the impact of traffic pollution on lung function. According to a review conducted by WHO (2005), there is evidence to prove that increased density of lorry traffic causes decrease in lung function. Such an association was noted even with black smoke. Cardiovascular morbidity Many time-series studies have evaluated and ascertained the impact of chronic exposure to air pollution with regard to cardiovascular related hospital admissions. The studies have demonstrated the association between black smoke and development of cardiovascular problems in elderly patients, especially in hotter semesters. The cardiovascular problems which have been studied in this regard are angina, myocardial infarction and circulatory diseases. In an interesting study by Poloniecki et al (1997), the researchers found a strong association between myocardial infarction and presence of high levels of black smoke in air. They however, could not find any evidence to incriminate traffic pollution in the development of circulatory diseases and angina. In yet another study by Le Tertre et al (2002), an increase in atmospheric black smoke by 10-µg/m3 increases the risk of cardiac admissions by 1.1 percent for all age groups and by 1.3 percent in the elderly population. The main pollutant that has been incriminated in the development of cadiovascular disease is black smoke. However, it is yet unclear whether carbon monoxide and nitrogen dioxide also can contribute to cardiovascular morbidity. Some studies have demonstrated an association between increase in ultra fine and fine particulate matter concentrations and risk of cardiac ischemia, a couple of days after exposure, as indicated by depression in the ST segment on ECG. Riedecker et al (2004) conducted a study to evaluate the physiological changes in state troopers who were healthy. They conducted several blood tests before, during and after a patrol shift. Data from the study showed that in-vehicle exposure to particulate matter 2.5 decreased lymphocyte count, increased red blood cell indices, increased neutrophils and increased C-reactive protein and von Willebrand factor. As far as the function of the heart was concerned exposure to in-vehicle particulate matter caused ectopic beats, increased the variability of the heart and increased the length of the cycle of heart beat. Some longitudinal studies have indicated an association between time spent in traffic and risk of myocardial infarction. Even in professional drivers, there is an increased risk of myocardial infarction and causes underlying this risk are not fully understood. Some attribute psychological demands of the profession and various individual risk factors to the increased risk of myocardial infarction. Most experts agree on the fact that traffic related air pollution causes cardiovascular problems due to inflammatory mediators that originate in the respiratory system. These particles can also have implications in the nervous system. Cancer Another important health hazard related to traffic air pollution is cancer. Of the several types of cancer that have been studied in relation to traffic pollution, lung cancer is the most studied and prevalent one. Studies on cancer mainly use benzene or nitrogen dioxide as indicators of traffic related air pollution. In a study by Nyberg et al (2000), the researchers conducted a retrospective assessment of long term exposure to nitrogen dioxide released into air from traffic. The RR for development of lung cancer following exposure to traffic pollution for 30 years was 1.2, after adjusting for other confounding factors. In yet another study by Nafstad et al (2003), the researchers found that for every 10-µg/m3 rise in nitrogen dioxide in atmosphere, the risk of development of lung cancer increased by 1.08 and with similar rise of sulphur dioxide, the risk increased by 1.01. While these studies have been conducted on adults, there are not many studies which have studied the association between traffic pollution and risk of cancer in children, or rather the evidence has been inconsistent. Other cancers which have been found to be associated with traffic pollution are leukemias, all types of cancer and central nervous system tumors. There are conflicting opinions about the risk of cancers in children following exposure to traffic pollution. While researchers like Feychting et al. (1998) reported a rise in the risk of all types of cancers subsequent to exposure to traffic related air pollution, others like Raaschou-Nielsen et al. (2001) have refuted such reports. The latter study however found an association between exposure to nitrogen dioxide and benzene and lymphomas. There is some evidence to ascertain the increased risk of development of leukemia in children living close to sources of air pollution. But even that is a much debated topic and recent reports have shown no cancer risks on such exposures (Reynolds et al., 2004). According to Duarte-Davidson et al (2001), "overall the evidence from human studies suggests that any risk of leukaemia at concentrations of exposure in the general population of 3.7-42 microg/m(3)-that is at concentrations three orders of magnitude less than the occupational lowest observed effect level-is likely to be exceedingly small and probably not detectable with current methods. This is also likely to be true for infants and children who may be exposed continuously to concentrations of 3.4-5.7 microg/m(3)." In those with occupation exposure to air pollution like drivers increased risk of bladder cancer was noted, especially in lorry drivers. the bladder cancer etiology was attributed to motor exhaust. Some researchers have proved an association between lung cancer and driver occupation. With regard to lung cancer, taxi drivers were the most susceptible population followed by lorry drivers. Similar risk was seen even in road construction workers and railroad workers. Other cancers associated with occupational exposure to traffic pollution include non-Hodgkins lymphoma, kidney and bladder cancers, endocrine glands cancer, male breast cancr and colon carcinoma. Carcinogenic properties of traffic pollution have best been demonstrated in mice. With this regard, inflammatory cell-derived oxidants have been the main etiological factors in the development of cancer. Thus, several studies have indicated the risk of development of various types of cancer following exposure to traffic air pollution either due to resident status or due to employment. Most experts agree that oxidative stress and subsequent DNA damage are the pathological mechanisms of induction of cancer due to these toxic substances in air released in traffic. Effects on fetus Like any other any toxic substances, traffic pollutants have negative outcomes on fetus because of the pattern of exposure and also because of physiologic immaturity. The organ systems of the fetus are in a developing stage with rapid turnover of cells, thus making them more prone to toxic effects of the pollutants. Many researchers have observed a positive association between increased exposure to air pollutants and post natal neonatal mortality. There have been reports about increased risk of low birth weight and premature birth in those exposed to carbon monoxide in the first trimester of pregnancy. Similar reports were found even for sulphur dioxide, particulate matter and nitrogen dioxide. In experimental studies on mice, it was found that exposure to diesel exhaust smoke led to abnormal deliveries of pregnant mice and defects in the development of thymus, testes and ovaries of the fetuses. It was also found that the testesterone and progesterone levels were higher in the maternal mice following exposure to pollutants (WHO, 2005). According to Cetta and Sala (2010), air pollutants can cause perinatal damage to the fetus and lead to fetal malformations, birth defects and developmental anomalies in newborns. Impact on fertility While there are no reports about association between exposure to traffic pollution and female infertility, there is substantial evidence to ascertain the role of these pollutants in causing male infertility. Research has shown that exposure to these toxic substances through occupation causes decrease in the sperm count and decrease in serum levels of various hormones like follicle stimulating hormone, testosterone, and leuteinizing hormones. Also, the motility of the sperms, forward progression of the sperms, sperm kinetics and functional tests also get affected. Of the various pollutants, lead and nitrogen dioxide seem to affect the semen quality (WHO, 2005). Conclusion From the scientific evidence that is available, traffic related air pollution has several negative health putcomes on children, adults, elderly, pregnant women and fetus. The evidence is supported by epidemiological evidence and experimental studies. In many time-series studies the mortality and morbidity was strongly associated with black smoke. Black smoke is a diesel exhaust. other than black smoke, carbon monoxide, nitrogen dioxide, sulphur dioxide and differnt types of particulate matter have been incriminated in various health hazards in human beings. The exhaust from vehicles often comes out as a mixture of these pollutants and even now, it has not been clearly possible the ascertain the composition of the mixture and which componenet in the mixture actually has health implications. However, from whatever information we have, trffic related air pollutants increase mortality and morbidity. the morbidity is associated with several systems including the respiratory system, cardiovascular system, hematopoietic system, genital organs and fetus. While the most studied health effects of traffic pollution are asthma and lung cancer, some amount of substantial evidence is present regarding the ill effects on other systems. References Cetta, F., and Sala, M. (2010). Traffic-Related Air Pollution and Childhood Asthma. 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