Air Pollutant Effects

Authored by: Edward F. Ferrand

Encyclopedia of Environmental Science and Engineering

Print publication date:  June  2012
Online publication date:  June  2012

Print ISBN: 9781439804421
eBook ISBN: 9780203757659
Adobe ISBN:




Air pollutants may be pervasive throughout areas because they are the products of daily-life activities, or generated by activities whose pollutant by-products tend to be localized in nearby areas by specific processes. They may be caused by point sources, area sources, or mobile sources. The primary standards for cleaner air are intended to protect health, and the secondary standards protect public-welfare interests. The standards often reflect a conservative approach in favor of the protection of health.

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Air Pollutant Effects

Air Pollutants

Air pollutants fall into two main categories: (1) those that are pervasive throughout areas because they are the products of daily‐life activities such as transportation, power generation, space and water heating, and waste incineration, and (2) those generated by activities such as chemical, manufacturing, and agricultural processing whose pollutant by‐products tend to be localized in nearby areas or are spread long distances by tall stacks and prevailing winds.

Air pollutants are also categorized by their emission characteristics: (1) point sources, such as power plants, incinerators, and large processing plants; (2) area sources, such as space and water heating in buildings; and (3) mobile sources, mainly cars and trucks, but also lawn mowers and blowers and airplanes.

The United States has established National Ambient Air Quality Standards (NAAQS) for seven pollutants that are pervasive and are threats to public health and welfare. The Clean Air Act, which initiated this program, was passed in 1963 and was last amended in 1990. The primary standards are intended to protect health, and the secondary standards protect public‐welfare interests such as visibility and danger to animals, crops, and buildings.[ 1 ]

The standards reflect, for the most part but not always, a conservative approach in favor of the protection of health. It is notable that the public, who in the final analysis must pay the cost, appears to be firmly committed to enforcement of the standards without overwhelming concern for costs.

The act requires the states to determine the status of their air quality and to find and introduce the controls that will enable them to meet these standards. Their proposal describing how and when the standards will be met is submitted to the U.S. Environmental Protection Agency (EPA) as an implementation plan for approval. Meeting target dates for air quality standards has been problematic because the complex system that has to be managed includes important socioeconomic and political factors. For example, the close connection between air quality and daily activities such as transportation, waste disposal, and the heating of homes and workplaces requires education of the population to obtain their support for alternative and perhaps costly lifestyle choices in the vehicles they purchase, the packaging of articles they choose, and the type and cost of the fuels they use—choices they may be reluctant to make, even if they will improve the quality of their air environment. Choices benefiting air quality that carry disadvantages for important sectors of the economy are usually skillfully discouraged by some of those sectors.

Control of Criteria Pollutants

Control of the criteria pollutants requires a measurement program to determine the daily and short‐term patterns of the ambient concentrations, identification of the emitting sources, and design and implementation of strategies for their control. A detailed inventory of the sources causing the pollution is prepared. The effectiveness of control technology and potential regulatory strategies is evaluated and their availability is determined with consideration given to the economic and political restraints on their implementation. In other words, the total system to be managed and its interactions have to be detailed and understood in order to evaluate the potential for successful control of the air pollution in an area.

The amount of exposure to the pollutants from independent or grouped sources depends upon the intensity of the activities producing the emissions, the effectiveness of the controls, and the quality of the surveillance instituted to ensure the continued proper use and maintenance of the controls. A factor that can be overwhelming is the pattern of the local meteorology and its effectiveness in dispersing emitted pollutants. The effects of dispersions from one area upon downwind areas should also be considered.

National ambient air quality standards.

Fig. 1   National ambient air quality standards.

Detailed analysis of data accumulated over many years using unchanging analytical methods has shown that very significant changes in an area's air pollution can take place from year to year without significant changes in controls, primarily as the result of changes in the local weather patterns. The combination of 10 years of data at three sampling sites in New York City showed that its sulfur dioxide pollution problems was clearly related to the sulfur content of the fuel that was burned in the city. The data for a 10‐year period were combined on a week‐by‐week basis, with the result that the shape of the 10‐year curve for ambient sulfur dioxide concentrations and the long‐term temperature curve for the city could be superimposed with significant success. Therefore, the sometimes great variations found between years when little change occurred in controls were caused by variations in the local atmosphere, demonstrating that the success or failure of control strategies cannot be evaluated with security over short intervals of time.

The primary standards to protect health and the secondary standards to protect welfare (Fig. 1) have improved with increasing knowledge about the effects of exposures and measurement technology.


Epidemiology is the study of the occurrence and distribution of disease within a population as opposed to its study on an individual basis. An epidemiologist who undertakes to determine the acute and chronic effects caused by exposures of a population to a particular component of local air pollution faces complex problems that can be itemized as follows:

  • In a community study the subjects under scrutiny are subjected to pollutants, known and unknown, other than the ones being investigated.
  • Supporting clinical studies guiding the investigation are seldom based upon human data, but must depend upon studies using surrogate species that were exposed to much higher doses without the contaminants that may contribute to the effects found in the epidemiological study.
  • The true dose is not always the simple product of the measured concentration and the duration of exposure, because of the complexity that can exist between exposure and response—the biologically active dose can be quite different.
  • Individuals whose exposure and symptoms are being correlated very often spend the major part of their time indoors or traveling, where they may be subjected to different pollutants and different concentrations.
  • Different pollutants will disperse and interact differently with the surroundings, introducing a location factor caused by the relationship of exposed individuals to the measurement site—for example, sulfur dioxide concentrations will not vary as much as ozone concentrations, because the higher reactivity of ozone with structural materials and other compounds will affect its concentration at the receptor.

Informing the Public

The aerometric networks established by cities and states have been gathering and analyzing data about air pollutants for many years. During these years, attempts were made to inform the public about the quality of its air environment, which can change from day to day and even hour to hour, and about the possible impact that local concentrations are having upon their health. The relationship between raw air pollution data and its health impact significance is complex; therefore, the attempt is made to present the information in a simplified manner that is understandable to the public. Toward this goal, the EPA has developed an Air Quality Index for daily reporting about what has been found in the air together with some indication of its potential effects on health. Important considerations are the variability in the susceptibility of the exposed population, meaning that what may have little or no effect on one group can be a serious concern for others, and that personal patterns of behavior of the exposed can affect the amounts of pollutants that they breathe. Individuals whose lifestyle requires them to move throughout an area (indoors, outdoors, and in vehicles) will receive very different exposures from those who stay at home, depending upon the pervasiveness of the pollutants. In particular, exposures to carbon monoxide will be much greater for those whose daily activities requires them to be in the vicinity of motor vehicles than for those who stay indoors or travel on railroads and subways.

The Air Quality Index designed by EPA reports the daily levels of ozone, particulate matter, carbon monoxide, sulfur dioxide, and nitrogen dioxide on a scale of 0–500. The range corresponds to six different categories of health concern that are also characterized by colors in Table 1.

Table 1   Air quality index definitions.

Air Quality Index

Health Concerns

0–50: Good (green)

Little or no risk

51–100: Moderate (yellow)

Concern for unusually sensitive people

101–150: Unhealthy for sensitive groups (orange)

The general public is unaffected, but people with health problems such as lung and heart disease may be affected

151–200: Unhealthy (red)

Everyone is affected to some degree, especially those in sensitive groups

201–300: Very unhealthy (purple)

A health alert exists; everyone should take precautions, especially those in sensitive groups

301–500: Hazardous (maroon)

Everyone is affected and everyone should take precautions

Risk Reduction

Air pollution affects people primarily through the respiratory system; therefore, the logical way to start minimizing risk is by avoidance of activities that increase one's inhalation of polluted air. When air pollution levels are high, activities that cause increases in breathing rate should be minimized as much as possible, depending upon the importance and necessity of the activity and the seriousness of the pollution episode. As an example, jogging in the vicinity of vehicles where local ventilation is poor, as in the canyon streets of cities, should be avoided because of the high concentrations of carbon monoxide and other pollutants usually found in those areas. This is of special importance to people with asthma or heart diseases such as angina.

Children who spend their time playing outdoors should be restrained from overexerting themselves when ozone levels are high during warm weather episodes, as should individuals with asthma or other respiratory diseases or those who are hypersensitive to ozone.

Effects of Exposure to Criteria Pollutants

Respiratory System Overview

An elementary understanding of studies describing the adverse health effects caused by the inhalation of gaseous or particulate air pollutants requires at least an elementary familiarity with respiratory tract anatomy and dynamics. The respiratory tract can be considered to include three sections:

  • Nasopharynx—nose and mouth down to epiglottis and larynx
  • Tracheobronchial—bronchi down to terminal bronchiole
  • Pulmonary—respiratory bronchiole, alveoli ducts, and alveoli

The trachea divides into left and right bronchi, which divide many times into smaller and smaller tubes down to the respiratory bronchioles. These feed about 65,000 lobules, each containing approximately 5000 thin‐walled air sacs called alveoli. Thus, in an adult there are approximately 300 million alveoli whose thin walls, totaling 70 m2 in area, contain hundreds of miles of tiny capillaries. Oxygen is added to and carbon dioxide is removed from the blood through the walls of these capillaries. The transfer of toxic chemicals into the blood can also take place in the alveoli.

Starting in the nose, where the air is conditioned for proper temperature and humidity, the direction of airflow is changed many times, thereby causing the impaction and deposition of particles on the surfaces of the branching airways. These surfaces contain hairlike ciliary cells whose rapid, wavelike motion, over 15 times per second, carry impacted particles on a mucus layer upward into the trachea for subsequent ingestion.

The velocity of the airflow decreases from about 150 cm/s at the start to almost zero in the alveoli; the smaller the particles, the greater the ease with which they turn corners, thus escaping impaction to penetrate to the alveoli, where they are collected via sedimentation. The larger particles and soluble gases will be trapped in the upper airways, where tissues and their defense mechanisms can be damaged reversibly or irreversibly depending upon the nature, intensity, and duration of the attack.

The amounts of a water‐soluble gas or suspended particles that reach the pulmonary region are strongly dependent upon their inhalation pathway into the body. When inhaled through the nose instead of the mouth, they experience a number of chances of removal by impaction. In the case of sulfur dioxide, this process is greatly enhanced by its very rapid dissolution in the watery fluids on the surface of nasal tissues. The greater tendency for mouth breathing combined with the greater intake of air that accompanies increased exertions contraindicates strenuous activity wherever pollutant levels are high.

Particle removal by deposition along the upper and lower respiratory system is strongly dependent upon particle size.

Particles with an aerodynamic diameter above 10 µm are removed in the convoluted, moist passages of the nose and tracheobronchial region. While almost all those below 2 µm reach the pulmonary region, intermediate sizes tend to distribute themselves along both regions. When the particles are insoluble, they are removed in a few days from the upper respiratory system by mucociliary action; however, those that penetrate down farther can remain for many months or even years. Removal of particles also occurs by phagocytosis through the scavenging action of macrophages.

The size distribution of particles suspended in the atmosphere exhibits a log‐normal behavior. The distribution by mass tends to separate into a fine and a coarse group depending principally upon whether they are formed by condensation of very small precursors, such as those produced in combustion, or are produced from larger particles by mechanical breakdown processes.


Ozone is a very reactive chemical that readily attacks other molecules, including those in the tissues of the respiratory system. Exertions that increase the need for oxygen will increase air intake and allow ozone molecules to penetrate and damage the sensitive areas of the lungs. Ozone can aggravate asthma attacks by making individuals more sensitive to allergens that promote the attacks and more susceptible to respiratory infections. Lung tissue can be scarred by continued exposure to ozone over the years. Researchers at Johns Hopkins found that an increase of 10 ppb in weekly ozone levels in cities whose average level was 26 ppb was associated with a 0.52% daily increase in deaths the following week. They calculated that a 10 ppb reduction in daily ozone levels could save nearly 4000 lives throughout the 95 urban communities included in the study. Out of 296 metropolitan areas, 36 have significant upward trends in the criteria pollutants; however, of these, only trends involving ozone had values over the level of air quality standards.

The presence of ozone and other photochemical pollutants depends upon atmospheric conditions, notably temperature, as experience shows that this type of pollution is associated with warm temperatures. The precursors that are affected by elevated temperatures are volatile organic compounds (VOCs) and nitric oxide. Natural sources for these compounds are a less important factor than the emissions produced by human activities, but the long‐range transport of the precursors while atmospheric conditions are converting them to photochemical oxidants means that there is a possibility of picking up precursor material from natural sources en route. Control of this type of air pollutant is focused on controlling emissions of VOCs and nitrogen oxides. It should be noted that ambient concentrations of the criteria pollutant nitrogen dioxide have been found to be generally below the levels considered to be health‐damaging; therefore, efforts to control its presence in the atmosphere are driven by the need to control ozone. The combustion of fuels and other materials provides sufficient energy to cause the nitrogen and oxygen in the air to react to form nitric oxide. The slow air oxidation of nitric oxide to nitrogen dioxide results in a mixture described as nitrogen oxides (NO x ).

The chemical reactions involved in the formation of photochemical oxidants from these precursors are complex. The basic reactions are

N O 2 + h v = N O + O O + O 2 + M = O 3 + M *
where hv represents a photon and M and M* represent material before and after absorbing energy from the ozone formation reaction. In the absence of other molecules capable of reacting with the nitric oxide, the ozone is removed by the rapid reaction
N O + O 3 = N O 2 + O 2

Therefore, concentrations of ozone will remain quite small unless there is a competing reaction for rapid removal of the nitric oxide.

Many organic compounds can play the role of nitric oxide remover in forming photochemical oxidants such as peroxyacetylnitrate (PAN, CH3COO2NO2). VOCs possessing varying reactivities are able to remove nitric oxide and thus make possible the buildup of ozone:

V O C + N O N O 2 + organic nitrates

Although ozone is the major component, peroxynitrates, peracids, hydroperoxides, aldehydes, and a variety of other compounds are found in photochemical smog. Among the major sources releasing reactive organic compounds are automobile engines and tailpipes; gasoline stations; the use of solvents, paints, and lacquers; and a variety of industrial operations. Thus, the control of ozone is complicated by the variety of sources and the distances that can occur between high‐ozone areas and the sources. Suburban and rural areas downwind of urban sources will often have higher ozone levels than source areas because of the transport that occurs while ozone is being formed. Both ozone and PAN cause serious injury to vegetation, but PAN does so at much lower concentrations.

Particulate Matter

“Fine particles” are less than 2.5 mm in size and require electron microscopy for detection; nevertheless, they are much larger than molecules such as ozone and other gaseous pollutants, which are thousands of times smaller and cannot be seen even with electron microscopy. Fine particles are formed by the condensation of molecules into solids or liquid droplets, whereas larger particles are mostly formed by mechanical breakdown of material. “Coarse particles” are between 2.5 and 10 µm in diameter and cannot penetrate as readily as fine particles; nevertheless, they have been found to cause serious deterioration of health. The severity of effects will vary with the chemical nature of the particles; however, since their nature can be so varied and difficult to determine, coarse and fine particles are considered in terms of what epidemiological studies have shown.

The inhalation of particles has been linked with illnesses and deaths from heart and lung disease as a result of both short‐ and long‐term exposures. People with heart disease may experience chest pain, palpitations, shortness of breath, and fatigue when exposed to particulate matter pollutants. Exposures have been linked to cardiac arrhythmias and heart attacks. Inhalation of particulate matter can increase susceptibility to respiratory infections such as asthma and chronic bronchitis. The EPA has found that nearly 100 million people in the United States live in areas that have not met the standard for particulate matter with a diameter less than 2.5 µm. It estimates that compliance by 2010 will prevent 15,000 premature deaths, 75,000 cases of chronic bronchitis, 20,000 cases of acute bronchitis, 10,000 hospital admissions for respiratory and cardiovascular disease, and the loss of 3.1 million days worked.

Emissions from diesel fuel combustion in vehicles and equipment are a special problem, especially for those individuals breathing in close proximity to the exhausts. Cars, trucks, and off‐road engines emit more than half a million tons of diesel particulate matter per year. Emissions of 2.5‐mm particles have decreased in the United States from 2.3 million tons in 1990 to 1.8 million tons in 2003.

Sulfur Dioxide

The combustion of sulfur‐containing fuels is the main source of sulfur dioxide air pollution. The oil and coal burned to heat homes and water and to produce electrical power are the main sources that affect the general population, but individuals who live near metal smelting and other industrial processes can be heavily exposed. Sulfur dioxide exposures are usually accompanied by exposures to particulate matter, which together exacerbate the effects.

Emissions of sulfur compounds from motor vehicles have increased in importance as those from oil and coal burning have been reduced. The diesel fuel used in vehicles can contain up to 500 ppm by weight of sulfur. California, which has the unfortunate combination of high emissions and poor atmospheric ventilation, hopes to reduce the allowable sulfur content of fuels to 15 ppm by 2007. It must be noted that California is the only state that is not preempted by the federal government in controlling pollution, because its efforts anteceded those of the federal government. Emissions of sulfur dioxide in the United States decreased from 31 million tons in 1970 to 16 million tons in 2003.

The defense mechanisms of the lung are challenged by sulfur dioxide; however, its rapid solution in water irritates tissues but reduces the concentrations that reach the deeper parts of the lung. Inhalation of particulate matter together with sulfur dioxide increases the hazard to the lungs. Asthmatic children and active adults can experience breathing difficulties in high concentrations of sulfur dioxide, and individuals with cardiovascular disease can have their symptoms exacerbated. The conversion in the atmosphere of sulfur dioxide into sulfite and sulfate acidic aerosol particles increases its threat to health.

Sulfur dioxide harms the body's defense system against particulate pollution and the ingress of bacteria into the body through the respiratory system. It also increases the harmful effects of ozone when both these gases are present. Asthmatics, the elderly, and those already suffering from respiratory problems are affected at lower concentrations than the general population. Studies have shown that in the 1950s and 1960s, when ambient concentrations were sometimes higher than 1 ppm and mixed with particulate matter, the occurrence of lasting atmospheric inversions resulted in thousands of excess deaths.

Carbon Monoxide

Carbon monoxide has afflicted the human race since the discovery of fire. Nature contributes very significant quantities, but it does so in such a highly dispersed fashion that human exposures from this source are insignificant. Nature has provided sinks for this insoluble, relatively unreactive gas; otherwise, background concentrations would rise much more rapidly as human contributions added their burden. The oceans, which at one time were believed to be a major sink, are now considered to be a source, because certain marine organisms release enough carbon monoxide to supersaturate the surface layer. The important removal mechanism is believed to be the action of microorganisms that live in soils and plants and the reaction of carbon monoxide with hydroxyl radicals in the atmosphere.

The rapid growth in the use of internal combustion engines has created an outdoor problem as indoor problems were decreased by improvements in space‐heating equipment. The problem is concentrated in urban areas where traffic congestion is combined with canyonlike streets. Emissions of carbon monoxide in the United States decreased from 197 million tons in 1970 to 94 million tons in 2003.

Criteria for a recommended standard occupational exposure to carbon

Fig. 2   Criteria for a recommended standard occupational exposure to carbon monoxide.

Source: Adapted from NIOSH.[ 2 ]

With the exception of exposures resulting from the breakdown or misuse of indoor heating equipment that produces fatalities or serious injuries, carbon monoxide exposures of significance occur in the vicinity of congested traffic. People whose occupation requires them to be near such traffic receive the highest exposures, as do those who jog or bicycle in these areas. Malfunctions in the exhaust system of vehicles also can result in high exposures to their occupants. Exposure to carbon monoxide results in the buildup of carboxyhemoglobin in the blood, which will interfere with the transport of oxygen to cells in the body.

Criteria for recommended standard occupational exposure to carbon

Fig. 3   Criteria for recommended standard occupational exposure to carbon monoxide.

Source: Adapted from NIOSH.[ 2 ]

Carbon monoxide molecules attach themselves to the hemoglobin molecules in the blood with much greater tenacity than do oxygen molecules. The Haldane equation attempts to approximate this competition:

( H b C O ) ( H b O 2 ) = 2 1 0 P C O P O 2

(HbCO) and (HbO2) are the concentrations of carboxyhemoglobin and oxyhemoglobin, and PCO and PO2 are the partial pressures of carbon monoxide and oxygen. Inspiration of air containing high concentrations of carbon monoxide results in its preferential absorption in the blood, thereby interfering with oxygen delivery to the cells in the body. Exposure to carbon monoxide causes a gradual increase in the percentage of carboxyhemoglobin in the blood until an equilibrium value dependent upon the ambient air concentration is reached. The rate of intake is dependent upon the breathing rate; therefore, the more quickly the equilibrium is reached, the greater the exertion. Up to 50 ppm, the equilibrium values of car‐boxyhemoglobin corresponding to different concentrations of inspired carbon monoxide can be estimated from the equation

%HbCO = 0 . 4 + P P M CO 7

The 0.4 constant is in the equation to account for the endogenous carbon monoxide, that is, the carboxyhemoglobin that results from the body's own production of carbon monoxide.

Graphic representations of the conversion of hemoglobin to carboxyhemoglobin in the presence of different concentrations of ambient carbon monoxide and the effect of various levels of activity on the rate of uptake are presented in Figs. 2 and 3.

The level of HbCO in the blood (Table 2) is the important measurement in the evaluation of carbon monoxide pollution. High levels of HbCO are associated with cigarette smokers, firemen, garage workers, foundry workers, and individuals who spend extended periods of time in heavy congested traffic or in vehicles with faulty exhaust systems. Ambient carbon monoxide measurements at a monitoring site can be very misleading as an index of exposure, because study populations are usually mobile and carbon monoxide concentrations can vary significantly, both horizontally and vertically, throughout an urban area.

Exposures to the high concentrations of carbon monoxide sometimes encountered in community atmospheres, even those well above the national standards, are not believed to be sufficient to initiate cardiopulmonary disease; however, individuals whose pulmonary functions are already significantly impaired because of anemia or damage to the heart, vascular system, or lungs can suffer adverse health effects from such exposures.

Table 2   Carboxyhemoglobin levels resulting from steady-state exposure to increasing concentrations of CO in ambient air.

CO in Atmosphere (ppm)

COHb in blood (%)

Signs and Symptoms






No appreciable effect, except shortness of breath on vigorous exertion; possible tightness across the forehead; dilation of cutaneous blood vessels



Shortness of breath on moderate exertion; occasional headache with throbbing in temples



Headache; irritable; easily fatigued; judgment disturbed; possible dizziness; dimness of vision



Headache; confusion; collapse; fainting on exertion



Unconsciousness; intermittent convulsion; respiratory failure; death if exposure is long continued



Rapidly fatal

Source: Adapted from Ellenhorn's Medical Toxicology 2nd Ed., Baltimore, MD: Lippincott Williams & Wilkins.[ 3 ]

In order to maintain normal function, the tissues of the body must receive oxygen at a rate that depends upon their nature and functions. Those with a high rate of oxygen demand are more susceptible to the oxygen‐depriving action of carbon monoxide. For example, studies of the brain and liver show a decrease in oxygen pressure at those sites even at levels as low as 2% carboxyhemoglobin. Cardiopulmonary system abnormalities, such as shunts that have developed that allow venous blood to mix directly with arterial blood, cause the individuals affected to be explicitly sensitive to carbon monoxide. Angina pectoris patients who experienced exposures that raised their carboxyhemoglobin level to 2.5%—that is, approximately to the level produced by an 8‐hour exposure at the concentration set as the air quality standard—suffered the onset of chest pain from exercise significantly sooner than did other angina patients not similarly exposed. The reduction in risk of heart attack that is observed soon after the cessation of the cigarette smoking habit indicates that carbon monoxide may be an important factor in precipitating heart attacks. The inhalation of carbon monoxide during pregnancy is a special concern because a higher concentration of carboxyhemoglobin is generated in the fetus than in the mother, and the elimination of carbon monoxide after exposure is slower in the fetus. The effects of combining exposure to carbon monoxide with sudden significant changes in altitude or the intake of drugs or alcohol upon the performance of body functions should be considered and avoided.

Nitrogen Oxides

“Nitrogen oxides” (NO x ) refers to the mixtures of nitric oxide and nitrogen dioxide that are formed when combustion causes the nitrogen and oxygen in the atmosphere to combine to form nitric oxide, some of which then oxidizes further to nitrogen dioxide; combustion gases contain about 5–10% nitrogen dioxide mixed with nitric oxide. The mechanism for the process is believed to be

O 2 = 2 O N 2 + O = N O + N N + O 2 = N O + O N + O H = N O + H

The overall reaction for the formation of nitrogen dioxide is

2 N O + O 2 = 2 N O 2

Nitric oxide is oxidized rapidly by ozone; therefore, ozone levels tend to be lower in the vicinity of nitric oxide sources, such as the tailpipes of vehicles.

Nitrogen dioxide, the most toxic of the nitrogen oxides, causes damage to lung tissues at concentrations higher than usually found in ambient atmospheres. Exposures above the national standard of 0.053 ppm are rare; therefore, with the exception of activities in the vicinity of industrial sources, nitrogen oxides have not been found to be a cause for community concern. An important consideration in the case of significant exposures is the delay that can occur between exposure and sensations of distress, which may delay prompt treatment. An important effect is the increased susceptibility to pathogens that may result from the destruction of macrophages and general injury to the lung's defense mechanisms.


The major source of lead in the air environment has been motor vehicles; therefore, levels have decreased dramatically as regulations have mandated the elimination of lead from gasoline because of its health effects and its detrimental action on the catalytic converters in vehicles. Metal processing, such as in lead smelters, is currently responsible for most of the lead in the air, but waste incinerators and lead acid battery manufacturing also contribute.

The chief cause of concern about lead is its effect on children. Lead damages the brain, particularly the cerebellum, and the kidneys, liver, and other organs, and can lead to osteoporosis and reproductive disorders. Its effect upon fetuses and young children produces learning disabilities and lowers IQ. Lead exposures result in high blood pressure and can lead to anemia.

The exposure of children occurs not only through the air but also through accidental or intentional eating of paint chips and contaminated food or water.

Toxic Air Pollutants

The Clean Air Act of 1977 required that emission standards be imposed upon air pollutants considered hazardous because they have been found to increase illness or mortality. The complexities encountered in attempts to control pollutants by declaring them to be criteria pollutants and setting air quality standards resulted in the choice of emission controls instead of air quality standards for toxic materials. The EPA has listed 188 pollutants whose emissions must be reduced. Examples are benzene (gasoline), perchlorethylene (used in dry cleaning), and methylene chloride (a solvent and paint stripper), as well as toluene, dioxin, asbestos, cadmium, mercury, and chromium.

The effects of significant exposures to toxic pollutants may be cancer, neurological effects, damage to the immune system, and reproductive effects. The risk of cancer associated with exposure to toxic pollutants in the air for a population is calculated on the basis of two factors. One describes the potency of the air contaminant, the other the magnitude and duration of the exposure, which is commonly assumed to be a lifetime of 70 years. The potency of a hazardous material can be expressed as a unit risk value. The unit risk value for an air pollutant is the increased lifetime cancer risk occurring in a population in which all individuals are exposed continuously from birth (70 years). The following discussion is based on a relatively simple version of risk assessment compared to the more sophisticated methods that are now in use.

The unit risk values are used to compare the potency of carcinogens with each other and to make crude estimates of the risk to populations whose exposures are known or assumed. The unit risk values are calculated so as to represent plausible upper bounds that are unlikely to be higher but could be appreciably lower. The units of unit risk values are (µ/m3)−1. The product of the unit risk value and the ambient concentration is the individual risk, and the product with the population exposed is the aggregate risk. Division of the individual or aggregate risk by 70 results in the corresponding annual risks. The maximum average concentration of the hazardous material in the ambient atmosphere is used in order to be conservative. Thus, if a maximum value of cadmium in the atmosphere in the vicinity of a copper smelter is 0.3 µg/m3, and the unit risk value of cadmium is 2.3 × 10−3(µg/m3)−1, then the probability of cancer (i.e., the maximum individual risk from the inhalation of cadmium) is

2 . 3 × 1 0 - 3 × 0 . 3 = 0 . 6 9 × 1 0 - 3
and the aggregate risk is
1 0 0 0 / 7 0 = 1 4 . 3

Risk assessment has become not only increasingly important but also more complex as the basis for the management of exposures. The EPA issues guidelines for assessing the risks of carcinogens, mutagens, developmental toxicants, and chemical mixtures together with guidelines for estimating exposures. The integrated risk information system (IRIS) is an electronic database maintained by EPA that contains information on the human health effects that can result from exposure to hazardous pollutants. The EPA provides telephone, fax, and e‐mail contacts for obtaining information about hazardous pollutants.


The term “dioxin” refers to a group of compounds that cause similar adverse health effects. They belong to three classes of chemicals: chlorinated dibenzo‐p‐dioxins (CDDs), chlorinated dibenzofurans (CDFs), and polychlorinated biphenyls (PCBs). Studies to date indicate that the compound 2,3,7,8‐tetrachlo‐rodibenzo‐p‐dioxin (TCDD) is the more toxic substance. CDDs and CDFs are not created on purpose but result as byproducts of certain activities; PCBs were produced for use in transformers and other purposes, but their use has now been prohibited. Combustion of certain materials, chlorine bleaching of pulp and paper, and certain chemical manufacturing processes all may create small amounts of dioxins.

Dioxins are characterized as likely human carcinogens, with the compound TCDD considered a human carcinogen on the basis of available human and animal data. The cancer risk to the population from exposures to dioxins is estimated to be 1 in 1000, with the likelihood that the risk may be much lower. Adverse health effects have been associated with personnel exposed to Agent Orange in Vietnam because of its dioxin content. Based upon available data, there is no clear indication that the general population is suffering health diseases from exposure to dioxins.

Indoor Air

Indoor air quality became important to those responsible for protection against adverse health effects caused by the inhalation of pollutants when it was realized that most individuals spend 90% of their time indoors and that indoor air quality is deteriorated by a large variety of sources. Four organizations—the American Lung Association, EPA, Consumer Product Safety Commission, and American Medical Association—prepared a document titled Indoor Air Pollution in 1989 that presents a summary of information for health professionals about the causes and effects of indoor air pollution. Fig. 4, taken from this document, provides an overview of the effects of air pollutants and their causes.

From a practical standpoint, the most important factor in the control of indoor air pollution is the quality of the ventilation of occupied space. The reduction of energy costs by cutting down on forced ventilation can lead to “sick building syndrome,” the term applied to outbreaks of complaints as a result of poorly ventilated indoor spaces. The National Institute for Occupational Safety and Health has investigated many cases of indoor air quality health hazards and has published guidelines for such investigations.

In certain cases, air quality standards are met outdoors but not indoors. For example, an investigator who measured indoor versus outdoor levels of suspended particulate matter found that he spent 84% of his time indoors, and that 82.3% of his exposure was attributable to indoor air. The average indoor levels of nitrogen dioxide of 95 homes in rural Wisconsin was higher than the outdoor level, sometimes exceeding the ambient air quality standard.

Secondhand Smoke

The mixture of combustion products from the burning end of tobacco products and the smoke exhaled by smokers is referred to as “environmental tobacco smoke” or “secondhand smoke.” It contains more than 4000 chemicals, more than 50 of which are cancer‐causing agents. It is associated with an increase in lung cancer and coronary heart disease and is particularly dangerous to the not yet fully developed lungs of young children, increasing their risk for sudden infant death syndrome, asthma, bronchitis, and pneumonia. An estimated 3000 lung cancer deaths and 35,000 coronary heart disease deaths occur annually among adult nonsmokers in the United States as a result of exposure to secondhand smoke. In children it is estimated that 8000–26,000 new asthma cases and 15,000–300,000 new cases of bronchitis and pneumonia for those less than 18 months are result from inhaling secondhand smoke.

Indoor Radon Levels

Next to cigarette smoking, the inhalation of radon gas and the products of its radioactive disintegration are considered the most significant cause of lung cancer. The EPA has estimated that 20,000 of the lung cancer deaths expected annually can be ascribed to radon, and the surgeon general has attributed 85% of lung cancer deaths to smoking.[ 4 ]

Radon‐222, an odorless, colorless radioactive gas, is one of the products in the chain of decay of elements starting with uranium‐238 in the soil, which after radon goes on to produce polonium isotopes 218 and 214. Their alpha particle emissions dissipate their energy while destroying lung tissue, which leads to lung cancer. The radioactivity attributable to radon in the air is measured in picocuries per liter, which correspond to two atoms decaying per liter per minute. The concentration of the decay products is measured in “working level units,” where 1 working level unit of decay products is released from approximately 200 pCi/L of radon.

The only certain method of determining the presence of radon is by testing, which should be performed whenever a dwelling is brought or sold. The EPA has prepared the “Home Buyer's and Seller's Guide to Radon,” which provides information about what can be done to protect against this problem.

Biological Contaminants

The New York Academy of Medicine issued a resolution in 1983[ 6 ] expressing its concern about the damage to health caused by the inhalation of biologic agents that points out that “by far the most important substances in indoor air that affect human health are infectious agents, primarily viruses and bacteria in the form of aerosols or as part of droplets or particles. These cause more than 60,000 deaths and 250 million disabling illnesses in the United States each year.” In addition to viruses and bacteria, the indoor air can be contaminated with pollens, fungal sores, algae, amoebas, actinomycetales, arthropod fragments, and droppings and dander from humans and animals. The airborne transfer of disease can involve pathogenic, toxicogenic, or allergenic agents via short‐range direct person‐to‐person transfer or long‐range dispersion throughout rooms sharing a common ventilation system. An important preventive strategy is to isolate other rooms from contamination by the air from rooms containing sources of microbial pollution.

Secondary sources of biological contamination can be established indoors by viable organisms that find friendly environments and sources of nourishment in soils, plants, and stagnant water. Pathogens, toxins, and allergens can be brought indoors through air intakes and shoes, clothing, or tools. The human body—mainly from the nose and mouth but also from other parts of the body—is a primary source of biological air contaminants and of nourishment for the growth of microorganisms. For example, it has been reported that the body sheds skin scales at a rate, dependent upon activity level, which averages 7 million scales per minute with an average of four bacteria per scale. Dust mites, derma‐tophagoides, feed on these scales and in turn produce fecal pellets in the respirable size range that can strongly affect sensitive individuals.

Diagnostic quick reference.

Fig. 4   Diagnostic quick reference.

Source: Adapted from American Lung Association, EPA, Consumer Product Safety Commission, and American Medical Association, Indoor Air Pollution.[ 5 ]

Almost all surfaces containing organic material such as cloth fabrics, paper, wood, leather, adhesive ceiling tiles, paint, soaps, and greases under proper conditions can sustain the growth of fungi, bacteria, acarids, and other microbes. Locations indoors where water can stagnate or cause continuous dampness of surfaces—for example, chilled water air‐conditioning systems, refrigerator drip pans, bathrooms, flooded basements, hot tubs, and saunas—are possible sources of biological pollutants.

Aerosol formation originating from water reservoirs is an important mechanism for airborne transmission of disease. The “jet‐drop” phenomenon that occurs in washbasins, bathtubs, toilet bowls, and urinals can generate aerosolized microorganisms, as can the high‐speed water‐cooled drills used by dentists. Humidifiers that generate steam by other than thermal means can be dangerous sources of microorganisms that have grown inside the reservoirs; therefore, they should be sterilized before use and will always form droplets containing the minerals in the water being used. Filters in ventilating systems, if not properly cleaned and maintained, can also become significant sources of infectious diseases.

Some organisms are not able to survive for long periods outside a host and thus require rapid person‐to‐person transfer to cause serious problems, but others can remain viable for long periods and thus carry the diseases that are recognized as transmittable through air. The following are some of the major diseases that are classified as human airborne infections:



Rheumatic fever

Meningococcus meningitis

Scarlet fever

German measles




Chicken pox

Whooping cough

Hemolytic streptococci


Pneumococcus pneumonia

Systemic mycosis

Mycoplasma pneumonia



Common cold

Certain lesser‐known diseases have been brought into focus by investigators of illnesses attributed to indoor air pollution. Some of these have been associated with contaminated water reservoirs in humidifiers, chilled‐water air‐conditioning systems, and other adjuncts to indoor ventilation and climatization.

The most notable infection is Legionnaires' disease, which has caused a number of epidemics, including the one at the Legionnaires Convention in Philadelphia in 1977, which resulted in 182 cases, 25 of which were fatal. The infection is caused by a not‐uncommon soil bacterium, Legionella pneumophila, which survives very well in water and can thus contaminate cooling towers, air conditioners, and other potential sources of aerosols. Drinking water in a hospital has also been implicated in the transmission of this infection. Since its discovery, studies have claimed that 10–15% of pneumonia cases in hospitals are attributable to legionella. A milder, self‐limiting disease with flulike symptoms called Pontiac fever is also attributed to legionella.

Tuberculosis is caused by a virulent microorganism, Mycobacterium tuberculosis, which can survive for long periods in encapsulated form and has been shown to be readily transmitted through ventilation systems. The gradual disappearance of this disease has been reversed in areas where acquired immunodeficiency syndrome (AIDS) is prevalent; therefore, its importance as a public health problem is increasing.

Hypersensitivity pneumonitis and humidifier fever also are associated with aerosols from contaminated water. The former, which is the more serious, is an interstitial lung disease that in its acute form causes fever, chills, cough, and dyspnea 4–6 h after exposure. The more commonly blamed agents are the thermoactinomycetes or the thermophylic micropolyspora. Humidifier fever is self‐limited, with symptoms resembling the flu.

Fungal Diseases

Fungi can cause disease and can also generate highly potent toxins. Treating the diseases is a special problem because available drugs are few in number because of the difficulty of finding ones that will preferentially attack fungal cells in the presence of mammalian cells.

Histoplasma capsulatum and other molds and yeast organisms such as blastomyces, cryptococcus, and coccidioides are pathogenic to humans. The latter is responsible for valley fever, which is causing concern in hot, dry areas such as the Southwest, where it thrives. Cryptococcus, often found in soil contaminated by pigeon droppings, is a killer of AIDS patients, attacking the central nervous system and causing meningitis. Aspergillus fumigatus is a common fungus that invades the lung. When the spores are stirred up and inhaled they can grow fungus balls in the lung. One condition is called “farmer's lung,” but in hospitals where transplant or AIDS patients have suppressed immune systems, the fungus can produce severe infections that must be treated rapidly. Detection of the fungus is difficult because instead of using the bloodstream it attacks by traveling from tissue to tissue. Aspergillus flavus produces aflatoxin, one of the most potent carcinogens known.

As in the case of tuberculosis, immunocompromised individuals are readily susceptible to the acquisition of disease via inhalation. Nosocomial aspergillosis from sources such as contaminated air conditioners should be a special concern in hospitals.[ 7 ]


“Asbestos” is the generic term for silicate materials that occur in fibrous form. A fibrous form that is classified as a serpentine is called “chrysotile” and is the type of asbestos most common in the United States. The length and flexibility of its fibers allow it to be spun and woven. Other types of asbestos are amphiboles that include amosite, crocidolite, tremolite, anthophyllite, and actinide. Their fibers do not lend themselves to weaving, but in general they have higher heat resistance than chrysotile. Asbestos is used in many products, but most of it is used in construction—in floor tiles, cements, roofing felts, and shingles—and was used in very large quantities to protect steel structures from weakening during fires.

Measurements made of asbestos concentrations in the ambient air of New York City led to its banning in 1971 in sprayed material, a ban rapidly adopted nationally and worldwide. Nevertheless, many tons of asbestos will have to be handled with great care when the many buildings that used it to protect their steel structure from fire are finally demolished.

A study by Selikoff et al. of mortality among 17,800 asbestos workers from 1967 to 1976 found 675 excess deaths from cancer out of a total of 995. The ratio of observed to expected deaths in such a population was 3.11 for all cancers, 4.60 for lung cancers, and >1 for several other types of cancer. They found 175 deaths from mesothelioma, a cancer rarely found in the general population, and 168 from asbestosis, a form of pneumoconiosis characterized by fibrosis of the lung that often continues after exposure ceases.

Cigarette smoking was found to have a strong multiplicative effect when combined with exposure to asbestos. Based upon a mortality rate of 1 for a nonsmoking, nonexposed comparison group, the mortality ratio for nonsmoking asbestos workers, nonexposed cigarette smokers, and workers exposed to asbestos who also smoked were 5, 11, and 53.

The methods of asbestos analysis differed in that occupational exposures were originally measured by counting the number of fibers longer than 5 µm in a given volume of air using optical microscopy. In the ambient air, the submicroscopic fibers, called “fibrils,” which are the ones that can penetrate deeply into the respiratory system, had to be measured; therefore, the Environmental Science Laboratory, led by Irving Selikoff, at Mount Sinai School of Medicine developed an electron microscopy method that measured the mass of fibrils per cubic meter of air.

Percentage of plant species visibly injured as a function of peak 1 h
                           and 3 h SO

Fig. 5   Percentage of plant species visibly injured as a function of peak 1 h and 3 h SO2 concentrations.

Source: Adapted from Air Quality Criteria for Particulate Matter and Sulfur Oxide, 1981..[ 8 , 9 ]

Asbestos air concentrations are now reported in terms of nanograms per cubic meter—asbestos background concentrations are usually in the range of 0–10 ng/m3.

Table 3   Relative sensitivity of plants to SO2.





Sweet potatoes











Red clover












Sweet pea

Sweet William





Bachelor button







Trembling aspen



Jack pine

Red pine


White pine

Austrian pine


White birch





Large‐toothed aspen

Douglas fir


Ponderosa pine

      Garden Plants












Swiss chard







Cultivated mustard





Asbestos in schools has been a major concern because of the prevalence of its use and the nature of the population involved. A study of chrysotile asbestos in schools known to contain damaged asbestos insulation measured 9–1950 ng/m3. Measurements in schools selected at random found a mean of 179 ng/m3, compared to average outdoor concentrations of 6. The excess risk of death from lung cancer caused by asbestos exposure is proportional to the intensity of the exposure and its duration. One estimate of the cancer incidence rate from asbestos reported by the EPA was that continuous exposure to 0.01 fibrils per mL (about 300 ng/m3) will cause 28 mesotheliomas per million females and 19 per million males, and 5 excess lung cancers per million females and 17 per million males.

Plant Effects

The effects upon the plant surfaces of the contact of vegetation by suspended particulate matter via dry or wet deposition are not well documented. Direct entry of sulfur dioxide gas molecules through the plant stomata, on the other hand, produces effects that are better understood and appear to depend, to a great extent, upon the rate of conversion to sulfate, a natural plant nutrient. As might be expected, the response of a plant to a particular exposure incident is dependent upon the concentration and duration of exposure and, because of the opening and closing patterns of stomata, also on the time in its daily cycle that exposures occur. Data on the injury threshold of 31 species of forest and agricultural plants were plotted to show their relative sensitivity to sulfur dioxide (Fig. 5). The relative sensitivity of specific plants to SO2 is indicated in Table 3.



Carbon Monoxide, 1984—Addendum to the 1979 Air Quality Criteria Document for Carbon Monoxide—Revised Evaluation of Health Effects Associated with Carbon Monoxide Exposure. EPA‐600/8‐83‐033F.
A Guide to Indoor Air Quality 1995, EPA‐402‐K‐93‐007.
Health effects of acid precipitation. Report of NIEHS Conference in Environmental Health Perspectives. 1984.
Lead, 1986—Air Quality Criteria Document for Lead II EPA‐600/8‐83/028bF.
National Air Toxics Information Clearinghouse, Lung cancer risk from passive smoking. Environ. Int., 1985, 11, 3–22.
National Research Council Carbon Monoxide, 1977; Ozone, 1977; Lead, 1972; Nitrogen Oxides, 1977; Polycyclic Organic Matter, 1972, National Academy Press: Washington, DC.
Nitrogen Oxides, 1982—Air Quality Criteria Document for Oxides of Nitrogen. EPA‐600/8‐82.
Repace, J.L. Indoor air pollution. Environment International. 1982, 8, 21–36.
Samet, J.M.; Marbury, M.C.; Spegler, J.D. Health effects and sources of indoor air pollution. Am. Rev. Respir. Dis. 1988, 137 Part I, 1486–1508, Part II, 221–242.
Second Addendum, 1986—Assessment of Newly Available Health Information. 1986, EPA‐600/8‐86/02 OF.
Selikoff Asbestos Lung Disease—A Primer for Patients, Physicians and Lawyers.
Spengler, J.; Hallowell, C.; Moschandreas, D.; Fanger, O. Indoor air pollution. Environ. Int. 1982, 8, 1–534.
Stewart, R.D.; Peterson, J.E.; Baretta, E.D. Experimental human exposure to carbon monoxide. Arch. Environ. Health 1970, 21, 154–164.
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Task Group on Lung Dynamics, Deposition and Retention Models for Internal Pasimetry of the Human Respiratory Tract. Health Physics 1966, 12, 173–207.
USEPA Airborne Asbestos Health Assessment Update. 1985, USEPA‐600/8‐84‐003F.
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Waldbott, G.L. Health Effects on Environmental Pollutants, C.V. Mosby Co.: St. Louis, 1973.
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