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Essay on Human Health and Vehicular Pollution
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Essay Contents:
- Essay on the Introduction to Human Health and Vehicular Pollution
- Essay on How are Health Effects Estimated?
- Essay on the Confounding Factors Effecting Human Health
- Essay on Economic Valuation of the Health Benefits of Reduction in Air Pollution
- Essay on the Health Impacts of Particulate Matter
- Essay on the Health Effects of Carbon Monoxide (CO)
- Essay on the Health Effects of Nitrogen Oxides (NOx)
- Essay on the Health Effects of Ozone
- Essay on the Health Effects of Sulphur Dioxide (SO2)
- Essay on the Health Effects of Lead
- Essay on the Pollutants with Potential Carcinogenic Effect from Vehicles
1. Introduction
to Human Health and Vehicular Pollution:
An important reason for controlling air pollutants in the ambient air is the damaging effects they have on human health. These effects include premature death as well as increases in the incidence of chronic heart and lung diseases. There is strong evidence linking urban air pollution to acute and chronic illnesses and premature death, and these adverse health impacts in turn carry high economic costs to the society.
Estimates of the health damages associated with air pollution are important because they can provide both an impetus for environmental controls and a means of evaluating the benefits of specific control policies. The health impacts of air pollution depend on the sensitivity and exposure level of the susceptible population to the pollutants.
The World Health Organisation (WHO) estimates that as many as 1.40 billion urban residents breathe air exceeding the WHO guidelines. The World Health Organisation estimates that every year 800,000 people die prematurely from lung cancer, cardiovascular and respiratory diseases caused by outdoor air pollution. WHO also estimates that about 8 million avoidable deaths will occur world-wide by 2020 due to air pollution. Deaths from air pollution have been ranked as one of top ten causes of disability by the WHO.
Other adverse health effects include increased incidence of chronic bronchitis and acute respiratory illness, exacerbation of asthma and coronary disease, and impairment of lung function. When different health end points of air pollution exposure are brought to one denominator through the valuation exercise, recent World Bank studies in India indicate that premature deaths account for about 40 percent of the health costs and various illnesses provide for the balance 60 percent. Chronic bronchitis and acute respiratory symptoms are the largest contributors to the economic costs associated with morbidity.
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The most significant health effects of air pollution have been associated with particulate matter (PM). Most of the recent studies have examined the health effects based on particle size. The largest health impacts have been associated with particles small enough to penetrate deep into the respiratory tract- respirable suspended particulate matter (PM10), fine particles (PM2.5) and ultra-fine particles (PM0.1). Studies indicate that vehicular pollution is the main source of these small particles.
Recent World Bank studies reported that emissions from motor vehicles are specially hazardous to humans because they include a number of toxic substances and extremely small sized particles. Diesel vehicles and two – stroke engine two and three wheelers are responsible for the elevated fine particulate concentrations and health consequences in Indian cities.
2. How are Health Effects Estimated?
Based on certain assumptions, the quantification of pollutants that are emitted every day can be done for a city or a region. Along with the mass, the level of concentration (micrograms of pollutant per cubic metre of air) as well as the duration of exposure of an individual to a pollutant needs to be known for gauging the health effects of emissions. Thus quantity, concentrations and exposure are crucial components in any exercise that is designed to measure the health effects of air pollution.
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In view of the complications and uncertainties in urban air quality modeling, most assessments of human exposure to date have used measurement techniques and not modeling. The simplest approach is to use data from air quality monitoring stations as a surrogate for the daily level of air pollution to which the population of the city is exposed. To represent the complete city and its population, the number of data points are to be large.
Estimating the health impacts of air pollution can be through extrapolation of studies from other similar cities or through acute exposure studies. First, the demographic groups susceptible to air pollution and associated health outcomes are identified based almost exclusively on epidemiological studies. Those studies determine relationships-referred to as concentration-response (CR) functions between air pollution and health effects in human populations.
Concentration -response function may apply to the whole population or to specific demographic groups only. It is assumed that each unit decrease in the ambient concentration of a pollutant results in a fixed percentage change in the case of deaths or illnesses.
Ideally, cities considering policy changes should conduct an epidemiological study locally. In practice, the complexity’ and costs of undertaking these studies have limited the number of such studies. Instead, cities typically transfer information or extrapolate on health impacts of pollutants on the susceptible demographic groups from existing studies conducted elsewhere.
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The appropriateness of transferring these functions depend on whether the confounding factors, base line pollution and base line health for the city are similar to those for the cities included in the transferred epidemiological studies.
Ambient PM concentrations are significantly higher in most of the Indian cities than those found in the cities of U.S and Europe. Similarly the confounding factors, especially smoking and poverty levels are significantly different. Hence extrapolation of results from US and Europe may not be relevant to India.
Human Health Impacts of Acute Exposure to PM Air Pollution:
Epidemiological studies can be grouped according to how exposure is measured – acute exposure studies and chronic exposure studies. Most studies in the scientific literature have examined acute and not chronic health consequences.
Acute exposure studies examine the associations between short- term (daily) variations in PM concentrations and short-term counts of daily total of deaths, cause-specific deaths or specific illnesses in a city, the popularity of these studies stem from their minimal data requirements compared to other study designs. Problems of confounding factors are reduced in these studies because they do not change significantly during the study period in the same city.
Studies carried out by Maureen Cropper and others on behalf of World Bank in Delhi in 1996 are the studies of mortality rates of acute exposure to PM pollution in Delhi area.
3. Confounding Factors
Effecting Human Health:
Association between air pollution and adverse health effects is influenced by several potential and confounding factors such as overcrowding, poverty, malnutrition, tobacco smoking, indoor air pollution, lack of access to health care, etc.
One of the recent studies in Delhi have indicated that the prevalence of chronic obstructive pulmonary disease (COPD) and chronic bronchitis was substantially greater in subjects living in slums and low income areas. With an increase in economic level, the prevalence of respiratory symptoms decreased significantly.
The following confounders are specially important:
1. Differences in life styles that affect exposure to outdoor air pollutants. Population in India spend more time outdoors and are more exposed to air pollutants and are at a greater health risk than those in U.S or U.K. Hence for a given ambient concentration of an air pollutant, population in India are at greater health risk than the population in the United States because they spend more time outdoors.
2. Difference in exposure to pollutants from other sources. For example, exposure to indoor cooking fires in developing countries like India is a major health risk factor especially for women. It affects their lungs and may cause acute respiratory diseases in children. This problem may not be faced by children and women in United States and United Kingdom.
3. Differences in smoking habits. Recent studies found a higher mortality risk from air pollution in smokers than in non- smokers.
4. Differences in geographic and climate conditions – such as altitude, extreme temperature and humidity, -that may exacerbate the adverse health effects of air pollution.
5. Difference in nutritional status and deficiencies in vitamin C and E, which weaken the body’s defenses against air pollutants.
6. Differences in access to medical care that influence the relationship between pollutant levels and hospital admissions or emergency room visits. Lack of appropriate medical facility and treatment can increase the susceptibility of people at risk. (especially elder people with previous respiratory problems).
7. Difference in age distributions. Populations with a higher proportion of very young and old people are more effected by air pollution.
4. Economic Valuation of the Health Benefits of Reduction in Air Pollution
:
Reduction in ambient levels of the common air pollutants (such as particulate matter) have been associated with reduction in premature mortality as well as reductions in chronic bronchitis, asthma attacks and other forms of heart and lung diseases.
To economists, the value of avoiding an illness episode such as an asthma attack, consists of the following four components:
1. The value of the work time lost due to the attack.
2. The medical costs of treating the attack.
3. The amount the patient would pay to avoid the pain and suffering associated with the attack, and
4. The value of the leisure time lost due to the attack.
Medical costs and productivity losses are often estimated by asking about the cost of treatment and the number of days the patient could not perform his duties. Lost work time is then valued at the wage rate and medical costs are imputed based on the full social costs of providing the care, not just the costs to the patient. This is popularly known as cost of illness (COI).
The people are asked what they would pay to avoid the discomfort and inconvenience of illness. This approach is referred to as willingness to pay (WTP) or contingent valuation method (CVM). When estimates of the value of pain and suffering and lost leisure time are unavailable, medical costs and productivity losses are often used to provide a lower bound to the value of avoiding illness (COI) approach to valuing morbidity. In practice, the cost-of- illness (COI) approach is often used to value illness, since empirical estimates of what people are willing to pay to avoid the pain and discomfort tend to be lacking.
Studies of the air pollution effects on premature mortality predict how many fewer people are likely to die if air pollution is reduced. For example studies may indicate that a 10 percent reduction in PM10 in Delhi might result in 1,000 fewer deaths each year. Hence if reducing air pollution in Delhi results in 1000 fewer deaths in a population of 10 million, this is equivalent on an average to reducing risk of deaths annually by 1 in 1000 (0.0001) for each person in the population (calculated from dividing 1,000 deaths by 10 million people or 0.0001).
Since reducing air pollution reduces risk of deaths by a small amount for each person in an exposed population, what economists wish to estimate is what each person in the entire population would pay for this small risk reduction. If this willingness to pay (WTP) were added across all the 10 million residents of Delhi, it would represent the value of saving 1,000 statistical lives.
Dividing the total willingness to pay by the number of statistical lives saved yields the average value of statistical Life (VSL). The goal of calculating VSL is to estimate what people themselves would pay for risk reductions. The VSL is not intended to estimate the intrinsic value of human life. U.S. Environmental Protection Agency studies in 1999 indicate that in U.S, the value of statistical life is approximately U.S $5 million. This is also known as willingness to pay approach.
The human capital approach values loss of lite based on the foregone earnings associated with premature mortality. This is similar to the methodology used in valuing the person killed in a road accident. It is similar to cost – of illness approach used in valuing morbidity. The notion is that people should be willing to pay at least as much as the value of the income they would lose by dying prematurely.
Studies in the United States indicate that the value of statistical life obtained from willingness to pay is about 8 to 23 times larger than foregone earnings. Studies indicate that in the absence of detailed empirical studies in developing countries, it is desirable to provide lower bound limits of the value of health benefits based on the COI approach for morbidity and “human capital approach” for mortality.
5. Health Impacts of Particulate Matter:
Indian cities record some of the highest levels of outdoor particulate matter. Scientific research over the last two decades has demonstrated that particulate matter is the major pollutant of concern from the health perspective. Current research is focusing on questions relating to particulate matter characteristics such as size, number and composition, and the mechanisms by which it causes health impacts.
Available data indicate that the pollutants with the most damaging health impacts are fine particulate matter (causing serious respiratory illness and premature deaths). Studies indicate that in India about 60,000 years are lost annually due to premature death caused by particulate matter.
The particulate matter damage to lung defenses manifests itself in the form of health effects such as respiratory infection (both upper and lower tract infections), chronic obstructive lung diseases (bronchitis), asthma attacks, cardiovascular disease, and lung cancer. The association of particulates and cardio vascular deaths from myocardial infraction and stroke is one of the most puzzling of the adverse effects of particulates.
Classically these are caused by the production of clots in the coronary vessel in the case of myocardial infraction and in the brain in case of stroke. Studies indicate that the inflammation arising in the lungs of the persons inhaling particulates frequently could impact on the coagulation system via the local production of procoagulant factors in the lungs.
A link has been established between respiratory infection or inflammation of lungs and cardiovascular disease owing to a systematic procoagulant effect. Further recent research has increasingly shown that particles can also effect other parts of the body, including the nervous system, by physically moving out of the air ways into blood stream. Thus particle deposition in the air ways can set off a chain of events, potentially affecting parts of the body other than just the respiratory tract.
The main components of urban PM are metals, organic compounds (including HCS and PAHS), and the particle core which is often composed of pure or elemental carbon. Studies indicate lung damages due to metallic PM. Organic compounds especially polycyclic aromatic hydrocarbons (PAHS) are known to lead to mutations and even cause cancer. Sulphate and nitrate ions lead to significant impairment of respiratory tract because of their acidic potential.
Carbonaceous core of the particulate by itself lead to lung irritation and damage and can cause lung cancer. In general, fine and ultra-fine particles from vehicles are composed mainly of particles with a carbon core that contain a variety of metals, organic compounds and sulphates and nitrates. The surface area of the elemental carbon core is considerably increased by its porous nature, greatly enhancing the adsorption probability of these components on air ways and lungs.
A recent study by the U.S. Environmental Protection Agency (EPA) highlighted the likely cancer risk from diesel emissions, declaring it as a potential carcinogen. The diesel particles, many of which are smaller than one micron in diameter, have a carbonaceous core with a large surface area to which various organic compounds including polycyclic hydrocarbons are adsorbed.
While a statistical association has been found between adverse health effects and PM10, some of the recent studies using PM2.5 data have shown an even stronger association between health outcomes and particles in this size range. Evidence that smaller particles are more harmful is supported by medical and toxicological research, which is increasingly focused on understanding the role of particle size (in the fine and ultra-fine range) and composition in PM toxicity.
Studies indicate that ultra-fine particles tend to behave more like gases and hence travel to the lower region of the lungs as compared to larger particles which tend to get deposited in the upper or middle region of the respiratory tract. Particles larger than about 10 microns in diameter are deposited almost exclusively in the nose and throat.
The human nostrils filter out more than 99 percent of the inhaled large and medium sized particulates. Smaller particles enter the wind pipe and lungs, when some of them cling to the protective mucous and are removed. Fine particles less than one micron are able to reach the lower regions of the lungs and are likely to react with lungs. The fine and ultra-fine particulates may trend to be deposited in the alveoli (tiny air sacs in the lungs) and are of serious health concern.
Recent studies by World health organization across a wide array of cities, including those in developing countries indicate that the health gains indeed result from PM pollution reductions.
These studies indicate that every 10 g/m3 increase in the daily average concentrations of PM10 increase:
1. Non – trauma deaths by 0.8 percent.
2. Hospital admissions for respiratory and cardiovascular diseases by 1.4 and 0.6 percent respectively.
3. Emergency room visits by 3.1 percent
4. Restricted activity days by 7.7 percent and
5. Cough in children with phlegm by 3.3 to 4.5 percent.
6. Health Effects of Carbon Monoxide (CO)
:
Of all the air pollutants, the toxicology of carbon monoxide is perhaps the best understood. Inhaled carbon monoxide has no direct toxic effects on lungs, but rather appears to exert its effects by interfering with oxygen transport system in the body. It is generally accepted that carbon monoxide exerts its effects by binding to haemoglobin and reducing the capacity of the blood to transport and release the oxygen at the tissues.
Carbon monoxide that enters the blood stream combines with haemoglobin in the blood forming carboxy haemoglobin, which reduces the capacity of blood to carry oxygen. Carbon monoxide has 245 times more affinity than oxygen to haemoglobin, and hence if haemoglobin is exposed to CO, it takes up the CO in precisely the same way as it would take up oxygen. The carboxy hemoglobin level in the blood is normally 1.2 to 1.5 per cent. At about 5 per cent level, the carboxy haemoglobin begins to induce adverse health effects.
Excess CO uptake impairs perception and thinking, slows reflexes, and may cause drowsiness, angina, unconsciousness, or death. An exposure to concentrations of 45 g/m3 of CO for more than two hours adversely effects a person’s ability to make judgments. Convulsions may occur when carboxy haemoglobin saturations exceed 60% and may even cause death. Rapid recovery is possible when exposed to oxygen or fresh air but results in nausea, vomiting, head ache and extreme “depression”.
Severe poisoning by carbon monoxide often results in lasting damage to the central nervous system. A wide range of neurological effects may develop following CO poisoning. They may range from loss of concentration, dullness or depression to a parkinsonian syndrome. Exposure of pregnant women to excessive CO has been linked to low birth weights, increased premature birth and retarded development after birth.
Recent studies have found positive correlation between CO concentrations and hospital admissions for heart failure. This is due to the fact that more blood is needed to supply the same amount of oxygen and the heart must work harder.
Studies involving people with deficient blood supply to the heart, (Ischemic heart disease) who were engaged in exercise during exposure to CO have shown that carboxy haemoglobin (COHb) levels as low as 2.2 percent can lead to earlier on set of Electro Cardiogram (ECG) changes, indicative of increased deficiency of oxygen supply to the heart and earlier on set of chest pain, etc. Hence exposure to higher levels CO may precipitate death due to myocardial infraction and heart failure.
7. Health Effects of Nitrogen Oxides (NOx)
:
Nitrogen oxide (NO2) is the key component among oxides of nitrogen in the ambient air. NO2 is a gaseous pollutant and its effects on health include damage to the cells lining the lung, also contributing to greater difficulty in removing bacteria and other agents, thus increasing susceptibility to respiratory infections.
Short term exposure to NO2 has been associated with a wide range of lower respiratory illnesses in children (cough, running nose, sore throat, etc.), as well as increased sensitivity to urban dust and pollen. Exposure to NO2 is linked with increased air way resistance in asthmatics and decreased pulmonary function. Long term exposure to concentrated NO2 emissions can result in lung cancer.
Recent studies indicate that exposure to a daily mean NO2 concentration of 244 g/m3 was associated with sore throats among adults. The health consequences of NO2 exposure ranges from cough to bronchitis, broncho pneumonia and acute pulmonary edema.
Nitrogen oxide exposure basically increases the susceptibility to viral infections especially in children. It is a respiratory irritant which can reduce lung functions. Asthmatics and children are particularly sensitive to NO2 emissions. Annoyance, cough, throat and nose irritation is generally associated with NO2 exposure.
8. Health Effects of Ozone
:
Ozone is responsible for photochemical smog and has been associated with transient effects on human respiratory system. Of the documented health effects, the most significant is decreased pulmonary function in individuals taking light to heavy exercise. Ozone can cause severe damage to lung tissues and impair defenses against bacteria and viruses.
Short-term adverse health effects have been observed from hourly exposures to ozone concentrations as low as 200 g/m3. These effects include eye, nose and throat irritation, coughing, throat dryness, thoracic pain, increased mucous production, chest tightness, fatigue and nausea.
A study on the long-term health effects of ozone exposure in southern California found that it may reduce pulmonary function. The synergistic effects of ozone and other pollutants (particulates and nitrogen dioxide), and absence of a threshold value for ozone have also been reported.
In 1994 Ostro estimated that for a 1 g/m3 increase in the annual average of 1- hour daily maximum ozone exposure resulted in about 28 to 97 respiratory symptom days (chest discomfort, coughing, wheezing, sore throats cold, flu, etc.) per person per year, 23 to 30 eye irritations per adult per year, and 39 to 190 asthma attacks per asthmatic person per year.
9. Health Effects of Sulphur Dioxide (SO2)
:
Sulphur dioxide is an irritating gas and is associated with reduced lung function and increased risk of mortality and morbidity. Adverse health effects of SO2 include coughing, phlegm, chest discomfort, and bronchitis. Prolonged exposure may result in reduced lung function and increased risk of mortality. Children are more susceptible to SO2 exposure than adults. Studies suggest that asthmatics are more sensitive to SO2, responding with broncho – constriction at much lower exposure levels than normal individuals.
Sulphur dioxide exacerbates the effects of PM, and vice – versa. Correlations between exposure to SO2 and mortality have been established in different parts of the world. The world Health Organisation (WHO) has determined in 1987 that the effects of 24 hour human exposure to SO2 include mortality at ambient concentrations above 250 g/m3. Regular exposure to SO2 causes increased respiratory symptoms or illness at ambient concentrations above 100 g/m3. In recent studies, however, the adverse effects of SO2 have been observed even at lower concentrations.
A statistically significant correlation between ambient SO2 concentrations and acute health effects (coughing) was demonstrated for children. In a study in Los Angeles USA, a significant association was observed between SO2 concentrations and chest discomfort.
Studies by Ostro indicate that 10 g/m3 drop in ambient SO2 concentrations would result in a drop of 15 to 87 deaths per one million population. The same study estimates that a 10 g/m3 change in ambient concentrations of SO2 would cause 10 to 26 cough incidents among one lakh children and 5 to 15 chest discomfort incidents among 100 adults.
10. Health Effects of
Lead:
In cities where leaded gasoline is still used, air borne lead poses a serious threat to human health. Most of the lead in ambient air is in the form of fine particles with an aerodynamic diameter of less than 10 micron (PM10). Motor vehicles are the major source of lead in ambient air in many countries which are using leaded gasoline. Though many countries including India have phased out lead, more than 100 countries (including Bangladesh) still use leaded gasoline.
Lead absorbed in the human body is distributed among bones, teeth, blood and soft tissues. Most of it is concentrated in bones (about 70 per cent for children and 95 per cent for adults). Lead absorption increases in diets with low levels of calcium, vitamin D, iron and zinc.
Adverse effects of lead exposure have been observed in small children, women of reproductive age and male adults. New borne and young children are most vulnerable. Exposure to levels of lead commonly encountered in urban environment constitute a significant hazard for children, especially those less than 6 years old.
Children with high levels of lead accumulated in their baby teeth experience lower intelligent quotients (IQS), short-term memory loss, reading and spelling under achievements, impairment of visual motor function, poor perception integration, disruptive class room behaviour, and impaired reaction time.
Recent studies of children hospitalised in Dhaka, Bangladesh showed blood lead levels ranging between 93 and 200 g/dl, which are 4 to 8 times greater than WHO guidelines. Hence the effect of lead is significant in countries like Bangladesh which have not banned leaded gasoline.
Adult women of reproductive age are also a high risk group because lead levels of pregnant women are closely correlated with those of newborns. Higher levels of lead exposure are associated with impaired renal function, anaemia, loss of central nervous system function and at higher concentrations, coma and death. However such higher concentrations are not possible due to vehicular pollution, but are usually associated with acute exposure to poorly controlled work places.
Among adults, lead levels in blood are linked to an increase of high blood pressure. No threshold level for adverse health effects of lead has been identified. People who are exposed to lead on the job, such as traffic police inhaling air borne lead particles, suffer adverse health effects in places using leaded gasoline.
Based on research studies, Ostro established relationships between lead levels in air and effects on human health. Ostro estimated that a 1 g/m3 increase in ambient lead levels would cause a 0.975 IQ point decrement per child, twenty to sixty five premature deaths and eighteen to fifty non-fatal heart attacks among a lakh of males, and forty five to ninety eight hypertension cases among 1000 males.
11. Pollutants with Potential Carcinogenic Effect from Vehicles
:
The WHO lists PAHS, benzene, 1-3 butadiene, aldehydes and diesel exhaust as carcinogens and provides guidelines for their ambient concentrations.
1. Polycyclic Aromatic Hydrocarbons (PAHS):
PAHS are primarily vehicle related and are produced by both gasoline and diesel vehicles. Diesel vehicles produce higher quantities of PAHS than gasoline vehicles. Diesel particulates consists of carbonaceous core and PAHS are adsorbed on the carbon core.
PAHS absorbed in the lungs and intestines and metabolised in the human body are mutagenic and carcinogenic. Epidemiological studies have identified 50 per cent greater risk of bladder cancer among truck drivers and delivery men exposed to diesel engine exhaust. It is estimated that 9 out of 100,000 people exposed to 1 g/m3 of benzo pyrene, a PAH, over life time, would develop cancer. There is no known threshold level for carcinogenic effects of benzopyrene.
Evaporative and exhaust emissions from gasoline fueled vehicles are the largest known sources of benzene in the ambient air. Benzene has toxic and carcinogenic effects. Exposure to benzene can cause eye irritation and visual blurring. It can cause nausea, vomiting and diarrhea. Continued exposure to low and mild levels may result in impaired gait, nervous irritability and breathlessness. High levels of exposure to benzene can damage the respiratory tract, lung tissue, bone marrow and can cause death.
The carcinogenic effects of benzene include leukemia. The most consistent evidence for causal relationship in humans has been found between benzene exposure and myloid leukemia. Benzene has been classified as group 1 (definite carcinogen) by the International Agency for cancer Research and their studies indicate lung cancer and leukemia from benzene. There is no safe level for air borne benzene.
Vehicle pollution is the major source of 1, 3-butadiene in the ambient air. Exposure to higher levels of 1, 3-butadiene causes irritation of the eyes, nose and throat and affects central nervous system. At ambient levels of exposure, the major concern is the risk of cancer.
Long term inhalation studies in rats and mice have shown that 1, 3-butadiene causes cancer in a variety of organs. International Cancer Research Association has classified 1, 3-butadiene as “probably carcinogenic to humans”.
Aldehydes are absorbed in the respiratory and gastrointestinal tracts and metabolized. Adverse health effects of formaldehyde include eye and nose irritation, irritation of mucous membranes, alteration in respiration, coughing, nausea and shortness of breath. Exposure to formaldehyde is associated with risk of cancer.
Aldehydes are formed mostly during idling of diesel engines. Hence small children waiting for long hours at bus stops and traffic police personnel at traffic signals are exposed more to the risk of aldehydes and consequently to their carcinogenic effect.